Professional Documents
Culture Documents
Paedriatics - OK....................................................................................................................................... 7
Immunisation .................................................................................................................................... 26
Orthopedics ...................................................................................................................................... 33
Developmental problems.................................................................................................................. 37
Intoxications ..................................................................................................................................... 43
Antibiotics......................................................................................................................................... 55
Anticoagulants .................................................................................................................................. 72
Pharmacology ................................................................................................................................... 83
Obstetrics - OK ...................................................................................................................................... 87
Amenorrhoea.................................................................................................................................. 168
TB ................................................................................................................................................ 299
PE ................................................................................................................................................ 415
MI ................................................................................................................................................ 428
ECG.............................................................................................................................................. 435
HT................................................................................................................................................ 449
DM .............................................................................................................................................. 489
Paedriatics - OK
- by age
o neonate < 1 mth
o infant 1 mth – 1 yr
o toddler 1-3 yrs
o child
o puberty
boys 12 – 16/18
girls 10 – 15/17
- neonatal conjunctivitis
o immediately after birth, purulent, sticky
o marked conj. oedema = gonococcal
o if at 2nd – 3rd week = chlamydia
- umbillical granuloma – red fleshy tissue at the base of umbilicus + discharge
o topical silver nitrate (caustic pen) – for 5 days
o if yellowish discharge - U/S and surgery (urachus fistula)
- umbilical discharge
o types
mucous
pus
urine
before delivery – communication = urachus; if it remains after delivery =
patent urachus
- Dx
creatining and urea levels from discharge -> confirm it’s
a urinary discharge
U/S – rule out patent urachus
- Mx – refer for surgical correction
faeces
black
o Dx diff
CA
fistula
urachal cyst
umbilical calculus
o Mx
clean debris
apply dressing (wound)
swab for culture and sensitivity
A/B
- night terrors and sleep walking have many features in common – murtagh 789
o sleep walking – child not awake
sit up in bed, walk around, do not acknowledge the parents even though the
eyes might be open
lasts 10-30 min
1-8 yrs
cannot remember the episode next morning
usually within2 hrs after falling asleep
harmless, benign
inherited – family Hx
2% of children
usually grow out of it by 12 yrs
Sx
educate parents, protect the child (unaware)
wake up the child 15 mins before the usualy time of the attacks for a
few days
do not try to calm the child during the attack -> it will aggravate the
situation
no indic. for sleeping pills
o night terror
sharp screams, violent thrashing movts., sweating, tachycardia
Night terror (sleep terror) Sleep walking Nightmare
2-4 yrs 6-9 yrs 3-6 yrs
First 1/3 of the sleep First 1/3 of the sleep Last 1/3 of the sleep
(within 2 hrs of falling
asleep)
Non-REM stage Non-REM stage REM stage
Unarousable Unarousable Easily aroused
Will NOT remember the Will NOT remember the Will remember the dream
dream dream
- breath holding spells
o usually when trying to get something from their parents (getting his own way): they cry
vigorously -> hold their breath -> turn pale -> then blue -> sometimes (rarely)
unconscious, fits or seizures
o 6mths – 6 yrs; MC 2-3 yrs
o can last 10-60 sec -> then they will breathe again
o Rx
reassurance
educate the parents – not harmful, will go away, don’t panic, take any action
during the spell (just ignore the baby – be firm!)
- hypospadiasis = urethral opening on the ventral aspect of the penis
o you cannot do circumcision – they might use that skin later for repair
o look for assoc. abnormalities:
if no urinary stream – refer immediately
if urinary stream present – reassess by 6 mths + surgery by 12 mths
- aspirin in children (otherwise, always Paracetamol)
o Kawasaki
o Rheumatic fever
o Juvenile rheumatic arthritis
- tests for baby at birth: hypothyr., cystic fibrosis, fenylketonuria, homocysteinuria
- septicemia - child unable to feed, sleepy most of the time, high fever 40 degrees, chest
retraction, tracheal tug, incr. resp.
- platelets < 40,000 = risk of intracranial bleeding for infant
- sudden infant death syndrome
o unknown cause
o potential causes/risk factors:
smoking of the parents (passive smoking)
parental narcotic/cocaine abuse
prone position during sleep
artificial feeding
hyperthermia
extreme prematurity
URTI
- cow’s milk lacks
o iron
o vit. C
Respiratory problems
- stridor:
o Croup (acute laryngotracheobronchitis).
o Epiglotitis.
o Inhaled foreign body.
o Laryngomalacia.
- foreign body
o in the oesophagus
wait max. 6 hr – beyond that -> risk of perforation (especially with lithium
batteries)
could be passed in stool in 3 days
Dx – x-ray
Rx – oesophagoscopy to remove the object
o in the resp. tract
always suspect when symptoms on only 1 side
1-3 years of age.
Sx
Coughing or choking episodes while eating solid foods or sucking small
object.
Persistent coughing and wheezing.
Inspiratory stridor.
Sudden onset of first wheezing with no history of allergy.
All symptoms may disappear if the object passes into the lower airways.
- Later, wheeze, infection or obstructive emphysema supervene
causing localized rhonchi, crepitations and breathlessness.
decr. or absent breath sound over whole or part of a lung
Dx
inspir. and expir. chest x-ray
- Organic foreign bodies such as peanuts will not show,
compensatory hyperinflation, collapse and consolidation will
gradually appear.
Rx
examine the nose, etc. under GA
Complete airway obstruction: Hold head down, deliver 5 blows to the
back and five chest thrusts. Attempt removal of the object or proceed
cricothyroid puncture.
- epiglotitis vs. croup vs. bronchiolitis – Jay, Alena – p. 47
o Epiglottitis
Sore thumb / fingerprint sign on lateral neck x-ray film
Treatment:
Oxygen by mask
May intubate or ventilate
Cricothyrotomy or tracheostomy
Antibiotics:
- ceftriaxone
o Croup
Steeple sign on anterior neck x-ray film
most ominous sign of deterioration = retraction of intercostal spaces and
suprasternal fossi
Treatment:
Nebulised adrenaline
Corticosteroid oral/IM/IV
May do intubation
Croup Epiglottitis Bronchiolitis
(Laryngotracheobronchitis)
Cause Viral – Parainfluenza virus (+ Bacterial – Haemophilus RSV
adenov., influenza) influenzae type B
Age 6 mths – (3-)6 years, 6 mths – 6 yrs 2 weeks - 9 mths, < 1 yr
sometimes older (2-7 years - alena)
may also occur in adults
Onset Slow (usually 2 days) – Rapid (hours) Slow (usually 2 days) –
prodrome of URTI prodrome of URTI
Fever Low grade High (> 40) yes
Dysphagia None Severe None
Drooling None Present None
Stridor Harsh inspiratory stridor Soft expiratory stridor
Cough Barking, brassy, spontaneous Absent Yes
Digestive problems
- baby vomits after the first and each feeding
o tracheoesof. fistula - becomes cyanotic
o esophageal atresia – does NOT become cyanotic
o Dx
chest x-ray
- Tracheoesophageal fistulae (TEF)
o 1 in 3,000 births
o Associated with polyhydramnios (16%), cardiac abnormalities, vestibular abnormalities,
imperforate anus, and genital-urinary abnormalities
o Various types:
Distal TEF with upper oesophageal atresia (85%)
Blind upper & lower oesophageal pouches without a connection to the trachea
(8%)
True H-type fistula (4%)
Proximal oesophagus empties to the trachea (1%)
o Dx
Passage of a nasogastric tube that meets an obstruction 9-13cm from the
nares suggests the diagnosis
Chest radiograph with the catheter in place demonstrates the position of the
pouch as well as air in the stomach and intestine
o A standard barium swallow is not recommended because of the possibility of spillage
into the pulmonary tree
- if baby vomits, check K:
o low – pyloric stenosis
o high
congenital adrenal hyperplasia
baby vomits, decr. Na, K incr., CL 80 ?
salt losing congenit. syndrome?
- vomiting in children
o by color
green / bile stained
1 - Duodenal atresia – newborn
- assoc. with Down syndrome
Small bowel obstruction
volvulus – vomiting and abd. distension
- bilious / green vomiting
- several small, seedy, yellowish stools (from the intestine distal
from the volvulus)
- olive shaped mass palpable in epigastrum
- non-projectile bile-stained vomiting
Sepsis.
Infection: UTI, Otitis media.
milk stained (non-bile stained), coffee ground
1 - Pyloric Stenosis
GORD
Infection: UTI, Otitis Media.
o types
1. 1st day baby vomiting bilious content + baby did not pass meconium
duodenal or jejunal atresia
- x-ray: double-bubble sign
small bowel obstruction or malrotation
Hirschprung dis.
imperforated anus
meconium plug
meconium ileus
cystic fibrosis
2. 2-3 weeks with projectile vomiting immediate after the meal
baby lethargic, hungry, dehydrated, visible peristaltic movement
crossing from left to right during feeding, changes with posture and
respiration
usually with olive shaped mass or no mass on exam.
= pyloric stenosis
- complic: metabolic alcalosis: Na decr, K decr, Cl decr, HCO3 incr
Vomiting: Loss of water and HCl.
Resulting condition: Hypovolaemia with hypokalemic
hypochloremic metabolic alkalosis
Na <130 (135-145)
HCO3- >32 (22-28)
pH >7.45
Cl- <100
K normal or low (3.5-5.5)
- 2-6 weeks of age
- risk factors:
male
first born baby
Caucasian
fam. Hx
- baby appears hungry, failure to thrive
- Gastric peristalsis clearly visible in abdominal wall
- vomiting not-bile stained, coffee grounds aspect
- Pyloric tumour
- Dx
1 test – feeding test
Feel tumour (wave left -> right abdomen or
immediately after vomiting)
nd
2 and best test – U/S, as good as surgical exploration
barium meal is not preferred -> risk of aspiration
- Rx
IV fluid replacement: 0.45% (1/2 normal saline) with
5% dextrose (DA).
Potassium: Once the baby is passing urine
20mmol/l KCL if mild
30mmol/l KCL if moderate or severe.
Surgery: Refer to paediatric surgeon for Ramstedt
pylorotomy.
3. morning efortless vomiting + headache
causes:
- posterior fossa tumor
medulloblastoma
5-7 yrs
most frequent tumor in childhood
round cerebellar tumor (from vermix) – midline
Sx
o ataxia, poor balance (frequent falls),
dysmetria, etc.
o Traid Murtagh: dizziness + morning
headache + vomiting
o raised intracranial pressure (ICP):
nausea, vomiting, headache, change in
the behaviour or mental status of the
child
o signs (Awad):
1 - disturbed level of
consciousness
2 - ipsilateral pupillary dil.
3 - papilloedema
most reliable sign of ICP = level
of consciousness
late signs: bradycardia, HT,
papiloedema
Rx: … + hyperventil. (decr. CO2
=> decr. blood sent to the
brain)
- infratentorial tumor
Sx
- headache, vomiting, strabismus, meningismus, blurring of
vision, hydro or macrocephaly, dizziness
4. projectile vomiting + headache + rash (with photo)
meningococcemia (meningitis)
- Kernig, Brudzinski signs poz.
- Rx
next step = A/B = benzyl penicillin
even better or if allergic = i.v. ceftriaxone
5. vomiting after each feeding but child is thriving and happy = GORD
Irritability and crying: sole manifestation.
Vomitus: Just ingested milk.
- Vomitus may be projectile BUT NOT persistent.
- The Majority of babies continue to thrive and gain weight.
- can be:
mild – no complications
severe - w/ complications
Peptic oesophagitis.
Barrett’s oesophagus
Peptic strictures.
adenocarcinoma of oesophagus
Failure to thrive: uncommon.
Pulmonary complications: Persistent cough,
wheeze that may result from aspiration
(aspiration pneumonia)
- Mx
Healthy infant whose main symptoms are vomiting and
regurgitation (mild form):
Reassurance.
upright position after feeding + get rid of air +
decrease spacing between meals, small
frequent meals + gaviscam (milk thickener) +
antacid can be added + sleep with head of bed
elevated
If symptoms persist - severe, w/ complications
Barium oesophagogram: To exclude
anatomical abnormality such as stricture,
gastric outlet obstruction and malrotation.
if Acid-reflux-related symptoms suggestive of
oesophagitis:
o Endoscopy and biopsies (most
appropriate)
if atypical sympt:
Aspiration needs to be considered.
Barium oesophagogram.
CXR
Ambulatory 24-hour pH monitoring: May detect
the presence of GORD but does not prove the
association
- Rx
Medications:
Mylanta – stomach protector
H2 receptor antagonists. – not popular in Aus.,
cause sedation
Proton pump inhibitors.
Surgery: Complications or medical treatment failed.
6. vomiting and diarrhoea and fever
gastroenteritis
- cause
rotavirus
Rotavirus: 40-50%, Winter.
Adenovirus: 7-17%
Bacterial: 5-10%: Salmonella, Campylobacter jejuni,
Yersinia enterocolitica and E. Coli.
salmonella enteritis
o go back to school / work after 3
succesive negative weekly stool
analysis
o MC form = enteric fever
o usual source = meat, poultry
o salmonella choleraesus – causes
gastroenteritis
o ampicilin is used to terminate the
carrier state
o blood cultures are usually not positve in
Salmonella gastroenteritis
o Rx – A/B
- risk – dehydration
Sx - oral rehydration or iv rehydration (if child cannot
drink)
8. child vomiting + bringing the leg to his abdomen (drawing the leg up), looks
pale. The pain is episodic.
on exam. – sausage shape mass
later sign – PR - red currant jelly
= intussuception
Mx
- Dx and Rx = air enema -> repeat -> surgery
9. vomiting + fever + urgency of urination = UTI
10. projectile vomiting + lower abd. pain
incarcarcerated hernia
torsion of testis
- steatorhea
o causes
coeliac dis.
cystiac fibrosis
giardiasis
malabs.
pancr. enzymes problems
o Dx
small bowel biopsy
- failure to thrive
o definition
< 3rd percentile or
drop > 2 percentils
o causes
organic
coeliac dis.
cystic fibrosis
non-organic – more frequent!
psychosocial: negligence, child abuse, etc.
- chronic diarrhoea in kids – diff. Dx
o cystic fibrosis
AR (1 gene involved = carrier, 2 genes involved = disease)
12 common mutations
MC = delta F508 on CFTR gene, on chromosome 7
defect in an ion channel prot. – affects the normal transp. of Cl => decr. Na and
water transfer => incr. viscosity in secretion (lung, pancreas, gut)
Sx
triad: FTT + chronic cough + loose bowel actions
GI and resp sympt
- GI
meconium ileus
then bulky, steatoreic stools
rectal prolapse
- resp
URTIs, cough
recurrent pneumonias
bronchiectasis
sinusitis, polyps
clubbing of fingers
- infertility in males
Dx
on 1st/2nd day – newborn screening -> looking for 1. immunoreactive
trypsin (IRT) – if > 99 percentile = positive => send for 2. DNA analysis:
check to see if 1 or 2 allels are affected ->
if both = disease => refer to cystic fibrosis clinic
if only 1 = carrier -> 3. sweat chloride test: 75 g sweat (>60 mEq/L =
positive) => refer to cystic fibrosis clinic
- 40-60 – suggestive of healthy carrier
Rx
drainage of airway secretions
hypertonic saline solution by nebuliser
A/B for inf.
oral pancr. enzymes
lung and liver transplant
survival in developed countries = 31 yrs (in poor countries – 10 yrs)
o coeliac disease
triad: fatigue + wt. loss + diarrhoea
loose stools
wt. loss
fatigue, due to iron/folate deficiency (due to malabs.) anemia
- microcytic – iron deficiency
- normocytic
- macrocytic – folate deficiency
Irish nurse
Sx
usually start after gastroenteritis – acid, watery diarrhoea, smells like
vinegar
cough
buttock wasting
bulky stool
failure to thrive
Dx
I test - fecal fat estimation (steathorea)
- incr. faecal fat
- fat crystals in stool
IgA
- antigliadin AB – screening only
- antiendomysial – 90% sens./specif. (Maria)
- antitransglutaminase – 90% sens./specif. (Maria)
II test - small bowel biopsy
Cx
increased risk of proximal jejunal lymphoma
Rx
remove gluten from diet
o toddler’s diarrhoea – Hx of loose stools containing undigested food (peas and other
vegetables)
otherwise the child is healthy and gaining weight
resolves spontaneously
- abd pain in children
o 3 mths – 1 year (< 2 yrs)
INTUSSUSCEPTION = Distal ileum telescopes into a distal bowel loop.
usually in the ileocolic region
also at other ages
causes
- metastatic deposit – MC from melanoma
- enlarged Payer patches – in children
- Crohn
- Meckel diverticulum
- lymphoma of the small bowel
- benign sumbucous fibrolipoma
- internal hernia
Sx
- Intestinal obstruction
- Sudden screaming intermittent attacks of pain with vomiting,
drawing the legs up
- sausage mass in the RIF
- Child looks pale, lethargic, anxious and unwell.
- Bleeding (red currant jelly stool): Late sign.
Associations:
- Recent viral gastroenteritis (adenovirus).
- Infantile Spasm.
- H-S Purpura (Arthralgia, skin rash, nephritis).
Dx:
- Plain X-ray: Normal or bowel obstruction. = I step
- Ultrasound.
- gas or barium enema – best - Hydrostatic reduction under
USG.
Rx
- gas or barium enema
if it fails, repeat
risk of recurrence
monitor for 24 hrs in the hospital
- Surgery: If enema failed, peritonitis or septicaemia
o usually over 5 yrs
Appendicitis
Any age, rare under 5 years.
Sx
- Anorexia, vomiting.
- Localized abdominal pain: Epigastrium, periumbilical region, RIF.
- Tenderness and guarding in RIF.
- palpation of the left side of the abd. caused pain in the right
side of the abd.
- Typical march of symptoms (J.B Murphy):
Prodromal mild bowel upset.
Development of abdominal pain, which progressively
worsens.
Anorexia, nausea, vomiting.
Moderate fever.
Signs of focal peritonitis over the inflamed appendix.
Rectal examination – not done in children!
Dx
- Physical examination: Abdominal auscultation, palpation,
percussion.
- first test: FBC and Urinalysis: Leukocytosis, rule out UTI.
- Pregnancy test: Female adolescents
if female patient – next test: USG: Female adolescents
(doubt and no peritonitis).
- CT:
Neurologically impaired
Immunologically suppressed, or
obese (doubt and no peritonitis).
- lactose intolerance –murtagh 477
o normal histology of intest. mucosa
o incr. in Asians
o normal galactose absorbtion
o doesn’t cause steatorhea
o types:
1. genetic – enzyme defficiency / absence
Sx
- often asympt. or
- 30 min.-2 hrs after milk consumption
colicky abd. pain
bloating
diarrhoea
Dx
- hydrogen test (breath test) – if lactose not broken in small
intestine, it will be broken down by bact. in the large intest.,
which also produce gas
- overload test (blood glucose test)
give lactose (50g) then check glucose levels
normal – glucose incr. > 1 mmol/L
sick – glucose the same or incr. < 1 mmol/L
- check reducing substances in stool – Clinitest tablets
2. in children, after acute gastroenteritis
watery, frothy, smell like vinegar stools (acidic) => can cause
excoriations of the buttocks
but happy baby, thriving
vomiting subsides but the diarrhoea continues
Dx
- detection of reducing substances in stool (stool acidity test)
Rx
- continue breastfeeding
- if bottle feed – switch to lactose-free formula for 1 month
(vilous glands will recover)
- galactosemia
o AR
o glycogen storage disease
o cannot metabolize galactose
o Sx
jaundice weeks 2-6, family Hx of jaundice, family Hx of cataract
toxic levels of galactose in the blood, resulting in
hepatomegaly, jaundice, cirrhosis
renal failure
cataracts
brain damage
ovarian failure.
lethragy, vomiting, diarrhoea
failure to thrive
o Dx
during newborn screening – blood (from the heel of the infant) or urine test
Beutler fluorescent spot test
reducing substances (galactose) in the urine
o Rx
eliminate lactose and galactose from the diet
- encopresis
o 4-5 yrs, previously toilet trained
o previously had constipation and anal fissure, so he avoids going to the toilet (e.g. at
school) due to fear => fecal impaction and soiling of the underwear
o Rx
day 1 – enema to empty the bowel
day 2 – laxatives p.r.
day 3 – oral laxatives
then go back to toilet training – tell parents to put child to toilet after bkfast,
before going to school
address constipation: more fiber, more fluids
- necrotising enterocolitis
o in premature newborns
o caused by ischemia of the bowel + inf. (Pseudomonas aeruginosa)
o risk factors
septicemia
low apgar scores
respiratory distress
o Dx
x-ray
pneumatosis intestinalis – air cysts in the intest. wall
finding of air in the portal vein = severe illness
o Rx
supportive
if perforation - remove necrotic intestine
- young child 6 weeks – no stool up to 7 days - still OK
- Hirschprung disease = aganglionosis = congenital megacolon
o narrowed aganglionic portion + proximal distension
o suspect if there is just a delay in passing of meconium
o males
o constipation + distension
o Dx
PR
x-ray, barium enema (distended enema)
full thickness biopsy
o Rx
rezection of the affected portion of colon
preliminary colostomy
Immunisation
- immunisation schedule – additional notes from Neha + Murtagh – p. 79
o premature baby < 32 wks – additional HBV vaccine at 1 yrs
o > 6 mths – can give influenza vaccine
free for:
> 65 age
indigenous population > 50 yrs (+ free pneumococcal vaccine)
indigenous population 15-49 yrs who have a high risk of complic. and
death
o pneumococcal vaccine - indigenous population at 2, 4, 6 mths, 18-24 mths
in chronic heart failure, chronic renal failure, postsplenectomy
not in chronic HT
o post-splenectomy
H. influenza B – Hib – once (if not immunized)
pneumococcal vacc. 2-3 weeks pre-op., repeat after 5 yrs
meningococcal vacc. – every 5 yrs.
e.g.
after 2 yrs, URTI – A/B
Cx
short term:
- incr. platelets
long term
- severe inf.
pneumonia – Rx: amoxycilin
o HepA – indigenous population
1 dose – 12-24 mths
2 dose – 18-24 mths (6 mths later)
- CI for vaccination
o absolute CI for vaccination
encephalopathy after DTP
anaphylaxis after vaccine
o relative CI for vaccination
fever > 38.5 -> defer
- CI of all vaccines
o > 38.5
o anaphylaxis
o live (attenuated) vaccines – not in immunosupressed patients
- CI vaccines – Neha (notes)
o anaphylaxis
o encephalopathy within 7 days of immunization
o live vaccines CI in immunsupressed
C.I. for MMR, varicella, oral polio – if pacient is immunosupressed (e.g. ALL) or
on high C/S or on chemotherapy
after systemic C/S Rx, delay the live vaccines for at least 3 mths
polio vaccine
- live
- inactivated
o in children doing chemotherapy – booster doses 6 mths after Rx
o +/- for all vaccines – fever > 38.5: wait for fever to go down?
Cardiac problems
- cyanosis
o central
heart
lung
o peripheral
- heart malformations
o The major presenting features are:
Murmur
Signs of CHF
Central cyanosis
-
o cyanotic - shunt right -> left
TGA Hypoplastic left TOF
heart syndrome
(HLHS)
Description Aorta and Severe cardiac failure VSD
pulmonary arteries - survival depends on Pulmonary stenosis
arise from the patency of PDA Right ventricle
incorrect ventricles hypertrophy
Overriding of aorta
Cianosis In the first day of 4th – 5th day (after > 3 mths, more
detected birth the PDA closes obvious when crying
down) or on exertion
Cyanotic spells (tet
spells)
Murmur No murmur? No murmur (the only Systolic murmor
one!) (pulmonary stenosis)
Dx U/S U/S X-ray cardiac contour
‘boot-shaped’
U/S
Rx Surgery Prostaglandin to
keep DA open
o acyanotic – shunt left -> right
ASD VSD PDA (can become
cyanotic)
Description 5-7% Most common (25%) Prematurity
not associated with - 2 types:
pulmonary 1. membranous
hypertension 2. muscular
- types: 50% close
1. Septum secundum spontaneously
2. Septum primum (muscular)
Usually asympt. - Small: incidental
Resp. distress with finding
normal SaO2 - Medium:
breathlessness,
failure to thrive,
recurrent chest inf.
MC common cause of
central cyanosis?
Murmur 2nd intercostal space Lower left sternum Continous,
(upper left sternal edge -> machinery
edge) -> loud holoystolic / murmur
mild ejection pansystolic murmur
/systolic murmur can have thrill +3
(incr. blood flow
through the
pulmonary valve)
The aortic and
pulmonary
components of the
second heart sound
are widely separated
(wide fixed splitting).
Dx U/S U/S U/S
Natural history Septum primum - Depends on size:
Assoc with Down Small, moderate –
syndrome closes
No need of Large – might not
prophylaxis for O. close
secundum, but Can have a tinge of
needed for O. cyanosis if with
primum heart failure.
Rx Surgery – never Surgery Indomethacin – to
closes on its own close PDA
Surgery
o q
VSD – SaO2
AD 60%
VD 80% incr.
AS 95%
VS 95%
ASD
AD 75% incr.
VD 75% incr.
AS 95%
VS 95%
hyperoxia test – adm 100% O2 to the baby 10 min
resp. cause – SaO2 will improve
cyanotic heart disease – SaO2 will NOT improve
SaO2 – determined with
blood gas
pulse oximetry
- types of murmur
o Innocent murmur
mid-systolic, no diastolic comp.
musical high-pitched
at the base of the heart
not radiating
changes with posture and respiration
no assoc. thrill
o organic murmur
diastolic
loud
palpable thrill
radiating to axila or neck
with assoc. sympt.
- mitral stenosis – purple book p. 171, Q37
o aboriginals
o diastolic murmur at apex
doesn’t radiate (the only one)
o tappering apex beat
o S1 increased loud and usually palpable sound 1
o loud P2
o opening snap after S2 = mitral valve stenosis
o AF
- mitral regurgitation
o systolic murmur radiates to the axila
- aortic stenosis
o loss of consciousness (syncope) + angina + dyspnoea on exertion
o fatigue
o systolic ejection murmur
systolic murmur = aortic stenosis (MC than mitral regurgitation)
radiates up, in the throat
no radiation & exacerbation with Valsalva manouver = HOCM
o apical impulse is lateral to the mid clavicular line
o aortic stenosis vs. complete heart block
similar, but hBP in aortic stenosis vs. HBP in complete heart block
- aortic regurgitation
o diastolic murmur that radiates down or down and to the left
- (pan) holosystolic murmurs
o VSD
o tricuspid regurgitation
o mitral regurgitation
Urinary problems
- enuresis
o child with:
nocturnal enuresis: night wetting > 5 (6) yrs (by age 5 the child should be dry by
night) or
diurnal enuresis: daytime wetting > 4rs
o types
primary
sec.
psychological factors (transitory)
asympt. urinary inf.
o risk factors
family Hx > 50%
o Dx
urinary exam – inf.?
o Rx
reassurance
step-wise Mx:
1. alarm (conditioning apparatus) in the diaper – bell when the baby
wets the diaper: wakes him up, child feels guity, goes to the bathroom
- 3 mths
- 3 mths break
- 3 mths
- 3 mths break
- most effective in children > 8 yrs old
2. desmopressin acetate (DDAVP) intranasal spray – similar to ADH
3. DDAVP + alarm
4. planned waking
5. TCAs? – purple book
never punish the child!
praise the child when he doesn’t wet the bed
- VUR
o 80% are females
o types
1. congenital abnormality in UV junction
2. boys – post. urethral valves
neuropathic bladder – spinal anomaly – 25%
urinary tract anomaly
o grade 1 – 5
1 proximal ureter distended
2 whole ureter distended
3 ureter and calices distended
4 significant distension of ureter
5 even larger distension and tortuosity of the ureter
o Cx
renal scarring
HT
o Dx
1: urine culture
2: U/S
3. MCUG (micturating cystourethrogram)
o Mx
daily prophylaxis with A/B, daily single dose, 1/3 of required dose
trimethoprim
nitrofurantoin
Orthopedics
- urgent referal conditions in orthopedics:
o Perthes
o slipped capital femoral epiphysis
o DDH
o tumor
- hip pain in kids
Transient Perthes SCFE Osgood- Septic
synovitis (flattening of Schalchter arthritis /
femoral head) osteomyelitis
4-8 yrs, 4-8 yrs, male 10-15 yrs, 10-15 yrs, Any age
female male male
Recent viral Restricted Obese child Tibial - Local point
inf. in Hx movement: Prepuberty tuberosity tenderness –
Self limiting Abduction Restricted pain osteomylitis
Restricted and internal movement: Self limiting - Refuses to
movement: rotation internal walk, doesn’t
Abduction rotation let you touch
and internal his leg –
rotation septic
arthritis
Fever, etc.
Dx Dx – Xray: Dx-xray Dx-x ray Dx – x-ray
x-ray – increased Osteomyelitis:
normal joint space + Early normal
U/S femoral head Late:
too lateral haziness, loss
of density,
subperiostal
elevation,
sequestrium
Mx Urgent Urgent Rx: limit Mx – 1. joint
referral referral: risk activity aspir. (open
(provide of avascular lavage) + rule
crutches): if necrosis of out gout
not Rx can the femoral
lead to head
osteoarthritis
o developmental dysplasia of the hip (DDH) – 0-4 yrs
women: men 6:1
asym. 40%, bilat 1/3
tight adductors & short leg, delay in walking, limping
risk factors:
breech presentation with extended legs
oligohydramnios
congenit. anomalies
1st born female child
Dx:
2 mths – Ortolani, Barlow
- ortolani test (abduction + anterior pressure => reduce the
luxation)
- barlow manouver (the reverse => cause the luxation)
U/S under 3-6 mths
x-ray – helpful after 3 mths
screening
DO!!
- before discharge
- at 6 wks
Mx
ref to specialist
0-6 mths pelvic harness = abduction splint
3-16 mths – reduction & cast (pelvic spica)
> 18 mths - open reduction & possible osteothomy
follow up:
acetabular dysplasia (underdev. roof of hip) -> premature
osteoarthrits
x-ray for teenager
o irritable hip = transient synovitis - Alena
acutely painful hip in kids
MC cause of limp in pre-school age
3-8 yrs
Hx of recent viral URTI (1-2 wks ago)
able to walk, but with pain (refuses to walk)
otherwise afebrile and well
Dx of exclusion after ruling out the other conditions
common
synovial inflamation
self-limiting
sudden onset of limb pain and limp
moderate decr. in range of hip movt. especially internal rotation
if severe limitation of hip movt. – consider septic arthritis
Dx
FBE normal
x-ray normal
orthopedic surgeon can suggest U/S if liquid present
Mx
settles within 7 days
no complic.
follow up in 4-6 mths to rule out Perthes disease
o Perthes dis.
avasc. necrosis of capital femural epiphysis
2-12 yrs (4-8 majority)
20% bilat.
pain + limp + restricted hip movt.
o slipped capital femoral epiphysis – 10-15 yrs
wt. > 90% percentile
pain in knee and hip
hip is externally rotated and shorted
cannot do: internal rotation + abduction
o juvenile arthritis
very rare in the hip
o septic arthrits – any age + fever
consider in any sudden onset of monoarthritis
in doubt, treat as sepsis
cause – MC staf.
Sx
swollen, red, tender joint
all movements are painful (child doesn’t move the leg at all)
Dx
joint aspiration
- will show neutrofils and bacteria
if treated with C/S, bacteria might not be seen
(masking)
Rx
1. arthroscopy and lavage -> blood culture
2. A/B – staf. MC cause
- Flucloxacilin
- in hospital – Ceftriaxone – 3rd gen (covers gram -)
o Osteochondritis of tibial tubercle = Osgood-Schlatter osteochondritis, traction
apophysitis of tibial tubercle
10-14 yrs
common in sports with running, kicking, jumping + after injury / fall
Sx
localized pain in the region of tibial tubercle during and after the
activity
lump, localized swelling, tenderness at the tibial tubercle
pain is present if any attempts to flex or straighten knee against
resistence
Dx
x-ray -> widening of apophysis, fragmentation of bone
Mx
abstain from active sports
acute attack – ice packs, simple analgezics
self limiting, takes 1 yr to resolve
cvadriceps stretching exercises
- growing pains – murtagh 878
o 3-7 yrs
o wake up due to pain in knee, shin, calf
o may recur during the night
o attack lasts 20-30 mins
o fam Hx
o benign – no abnormalities are found
o Rx
reassurance
analgezics, heat packs
- juvenile chronic arthritis = juvenile RA = juvenile arthritis = Still’s disease
o unknown etiol
o < 16 yrs
o types
pauciarticular <= 4 joints, M.C. - large joints: knee, wrist, ankle
assoc with uveitis or sacroileitis
polyarticular > 4 joints
large and small joints
RF can be positive, rheumatoid nodules are often present
cervical spine is involved
with systemic onset (with vasculitis) – with spiking fever, Salmon-pink rash on
trunks and extremities, arthritis, myalgia, hepatosplenomegaly,
lymhpadenopathy, pleuritis, pericarditis
o Dx:
ESR incr., FBE (microcytic anemia, lymphopenia, platelet decr.)
pauciartic – ANA +
U/S – pericarditis?
o Dx diff – rule out septic arthritis -> perform arthrocentesis
o Rx
physiotherapy, occupational therapy
NSAIDs
IV Igs in systemic type with vasculitis
C/S
methotrexate
joint replacement
synovectomy may be required
- osteomyelitis
o causes
haematogenous
MC – staph. aureus – 90%
o Sx
fever
point tenderness over the bone
pain in the joint = septic arthritis
pain in the bone, outside the joint = osteomyelitis
o Rx - flucloxacilin
Developmental problems
Puberty
girls at age 10, boys at age 12.
Girls usually complete puberty by ages 15–17, while boys usually complete puberty by ages 17 or 18
sequence in girls:
first telarche (enlargement of the breast buds)
then growth spurt
then axillary and pubic hair develops
then menarche occurs (2 years after start of puberty)
sequence in boys:
scrotal and testicular growth
pubic hair (after 6 months)
penile enlargement (within 12-18 months)
axillary hair (after 2 years)
deepening of the voice
- dev
o female
I – telarche – 2 yrs till menarche
II – adrenarche - androgen hormons -> axillary and pubic hair, body odor
III – menarche – influenced by her mother’s menarche
IV – pubarche – pubic hair
o male
I – testis
- Simple Tanner scale – printout from Neha
o boys
scrotal & testis growth -> 6 mths -> pubic hair -> 12-18 mths -> penile
enlargement -> Axillary hair (whole process 2 years)
o girls
1st = enlargement of breast buds (9 yrs old) -> growth spurt -> axillary & pubic
hair -> menarche (whole process = 2 yrs)
o average time for puberty = 3 yrs
o based on secondary sexual characters
male
size of testis
pubic and axillary hair
female
breast and nipple dev.
pubic and axillary hair
o stages:
1 – preadolescent, no sec. sexual chars.
2 – 9-11
3 – 11-13
4 – 13-15
5 – 15+
- causes of delayed puberty:
o types
hypogonadotropic hypogonadism
decr. FSH, decr. LH => decr. estr.
pituitary problem
hypergonadotropic hypogonadism
incr. FSH, incr. LH, decr. estr.
o Dx
FSH, LH
- normal percentile: 3 – 97% for height and weight
- speech problems
o delay
causes
mental retardation – MC
deafness
cerebral palsy
infantile autism
social deprivation
o stammering
male 3:1
genetic factors
recover spontaneously before age 16
o elective mutism – occurs only in certain situations
- developmental problems in kids
o precocious puberty – early sexual characters in girls < 8 yrs, boys < 9.5 yrs
o premature telarche – isolated breast dev. in girls < 2 yrs
due to hormonal stimulation from estrogen
sometimes with discharge from nipples
o pubertal gynecomastia – 40-50% boys, transient
st
- 1 year of life wt. calculation
o ¾ kg monthly first 4 mths = ¾ x 4 = 3 kg
o ½ kg monthly next 4 mths = ½ x 4 = 2 kg
o ¼ kg monthly next 4 mths = ¼ x 4 = 1 kg
o total at 1 yr: 6 kg + wt. at birth
- obese children are taller than same age children
o MC assoc. of childhood obesity in Aus. = above average height
- gynecomastia
o causes
physiol.
first 3 weeks – incr. estr. from the mother
puberty – up to 50% of adolescent boys
- hormonal imbalance: estr. / testosterone ratio incr.
elderly
- > 50 yrs – due to decr. test.
drugs = discome
digoxin
isoniazide
spironolactone, steroids
cimetidine
omeprazole
metyhldopa, marijuana
estrogen
+ calcium antagonists, amiodarone, TCAs
NOT: furosemide, labetalol
hypogonadal states:
Klinefelter’s syndrome
sec. testic. failure (torsion, orchitis, orchidectomy, traumatic atrophy)
liver failure
testic. feminisation sydrome
estr.-secreting tumors
adrenal CA
Leydig cell tumor
o Dx
1 - testosterone
2 – estr.
o Rx
< 18 yrs – reassurance
if persists > 18 yrs - find cause: Klinefelter, testic. atrophy, etc.
- developmental delay
o ask if the child lost some skills recently (even more alarming for neurol. involvement)
o after vaccination – very rare, anecdotal
unusual irritability and prolonged crying, due to low grade fever – after DPT
- Growth charts – see p. 210 in my notes
o http://www.cdc.gov/growthcharts/clinical_charts.htm
o http://www.cdc.gov/nccdphp/dnpa/growthcharts/guide.htm interpretation
o this is a wide variation of a normal growth
o 3% of normal children will be above 97th percentile or below 3rd percentile
even below 3rd and above 97th percentile there are normal kids
the range between the 3rd and 97th percentile (-2 SD to +2 SD) includes 94% of
normal children
the other 6% are below 3rd or above 97th percentile
o short stature
1. familial (genetic) short stature
bone age BA = CA chronological age
grow on 3rd percentile or below but the rate of growth is parallel to 3 rd
growth velocity = N
puberty is at the appropriate time
2. constitutional delay
boys
often family Hx of parent being short as a child with delayed puberty
and eventually he caught up
“late bloomers”
BA < CA
puberty is delayed
- e.g. in the recalls
short, with CA = 13, but stature of 9 yrs
good prognosis? if BA = 9 = constitutional delay
3. hypopituitism
usually manifests after 2 yrs
look for relative obesity w/o any other explanation
4. chronic illness or malnutrition
coeliac, cystic fibrosis, etc.
5. iatrogenic
e.g. C/S
- fusion of epyphisis
6. chromosomal abnormality
MC – Turner syndr.
- girl – short stature
- 45X0
o Alena
most kids 25-75 percentile
<10 = concern
> 95 = gigantic
important is the trend from birth
if always high or low percentile = normal!
drop in wt. > 2% at a certain moment, in a short period of time = FTT
- short stature
o genetic
o intraut. causes
o intralabor causes
o postpartum causes
extensive resuscitation
growth hormone retardation
post delivery hypoglycemia
hypothyr.
cystic fibrosis
coeliac dis.
fenylketonuria
o later
child abuse, nutritional defficiences
chronic renal failure
Turner syndr. – female
o MC = constitutional delay
o combinations:
bone age = chronological age => subnormal adult height
cause
- genetic short stature
- low birth wt.
bone age < chronological age + appropriate to the height age => normal adult
height
cause = familial maturation delay
e.g. jul 2009 – q11
bone age below height age => severe growth retardation
cause = endocrine – hypothyr., growth hormone defficiency
o Dx
FBE – anemia, chronic inflam. (ESR, CRP)
thyroid fc.
growth hormone level
blood sugar level
kariotyping – Turner
x-ray of the left wrist -> bone age
if it’s younger than the age of the child => room for it to grow
Milestones - TO DO!
- asked so far – Murtagh 866
o social smile: 2 mths (0-7 wks)
o roll over from back to front position: 4 mths?
o roll over from back to front position: 5 mths
both asked – 4-5 mths
o sits with support: 6 m
o sits alone: 8 m
o standing with support: 5-10 m (10 m)
o walk with support: 7 ½ - 12 ½ (12 m)
o walk without support: 11 ½ - 15 m (15 m)
o walks up steps w/o help: 2 yrs (14-22 m)
climbs stairs with alternate foot: 30 m?
o hops on one foot: 3-5 yrs
o rides a tricycle: 21 m – 3 yrs
o reach for an object: 3 – 5 ½ m
o pass object from hand to hand: 4 ½ - 7 ½ m
o pincer grip: 9 – 15 m
o wave his hand / wave goodbye around: 12 m ??
o drinks from a cup: 10-17 m (1 ½ yr)
o play peakaboo: 10 m
o draw a triangle / square: 4 yrs
o draw a 3 part man: 3-5 yrs
o build a tower of 4 blocks: 15 -26 mths
o build a tower of 8 blocks: 40 mths ??
o says mum, dad w/o meaning: 6-10 mths
o says mum, dad w/ meaning: 9-15 mths
speaks 4 words including mama and dada: 9 – 15 m (15 m)?
o says 3 words other than mum and dad: 1.5 yrs (12-20 mths)
o 3 words sentence: 3 yrs
o give first and last name: 2-4 yrs (4 ys)
o name colors: 3 – 5 yrs (5 yrs)
o teeth - 6-12 mths?
Antibiotics
- A/B used in various conditions:
o scabies
permethrin cream 5% or
benzyl benzoate 25% emulsion
o toxoplasmosis
pyrimethamine + sulfadiazine + folate (to counteract their antifolate activity)
o cellulitis:
strepto. and staf
severe: flucloxacillin IV
less severe: flucloxacillin p.o.
in DM
penicillin + metronidazole + gentamicin (empirical) (Alena)
o mastitis – flucloxacilin (or for candida – fluconazole or nystatin)
o orbital cellulitis – fluclox. + ceftriaxone
o conjunctivitis - cloramphenicol eye drops
gonococcal (hyperacute onset)
IV cephalosporins or penicillin
topical sulfacetamide
Chlamydia
neonates – erythromycin
children > 6 kg: azithromycin
o UTI
Rx - TG (Alena)
1 – trimethoprim – not in pregnancy
2 – amoxyclav. – in pregnancy
3 – cephalosp. - cefalexin
4 – nitrofurantoin – not in pregnancy?
in pregnancy - amoxyclav or cefalexin
o prostatitis: amoxycillin + gentamicin
o epididymo-orchitis
STI (gonococc + chlamydia): cephtriaxone + doxycycline
Instrumentation (E. coli): amoxyclav or trimethoprim
o bacterial vaginosis
1 - metronidazole 400 mg p.o. 12 hourly for 7 days
2 - clindamycin 20% p.o. or vaginal cream – in:
resistant inf.
pregnancy
in pregnancy
1. clindamycin 300 mg orally 12 hourly for 7 days
metronidazole 400 mg p.o. 12 hourly for 7 days
- not very safe – categ B2
o Trichomonas
metronidazole p.o.
pregnancy – clotrimazole vaginal tablets
o candidiasis
topical clotrimazole(miconazole, etc.) – first line, 1-7 days
vaginal tablet + cream
recurrent
nystatin cream + pessaries
recalcitrant, not pregnant
fluconazole or itraconazole p.o.
in pregnancy – clotrimazole pessaries! (local, not systemic)
in Candidata glabrata - boric acid (not in pregnancy)
o Chlamydia
1. azythromycin (preferred) or doxycycline
2. erythromycin – in pregnancy
o trachoma
non-pregnant woman, child – azythromycin
pregnant woman, child < 6 kg – erythromycin or roxythromycin
o Gonorrhoea
if penicillin-resistant gonococci (PPNG)
ceftriaxone + azithromycin or doxycycline
if PPNG prevalence is low
amoxycillin + probenecid + azythromycin (if Chlamydia hasn’t been
ruled out)
in pregnancy
erythromycin or roxythromycin
o syphilis
procaine benzylpenicillin or benzathine penicillin
if sensitive to penicillin
- doxycycline
o STD prophilaxis after unprotected sex
penicillin (gonococal) or azithromycin or doxycycline (chlamydia)–
prophilactically
o PID
mild to moderate / outpatient: Azithromycin 1g orally + ceftriaxone 250 mg IM +
doxycycline 100 mg b.d. orally + metronidazole 400 mg b.d. For 14 days.
severe / hospital: cefotaxime (or ceftriaxone) + doxycycline + metronidazole
in pregnancy: cefotaxime (or ceftriaxone) + roxithromycin + metronidazole
o post-partum endometritis or pyrexia (fever, tender uterus, foul smelling lochia):
ampicilin (or amoxycylin) + metronidazol + gentamycin
o otitis media
first line = amoxycillin
still not resolving after 48 hrs
2. cefaclor or
amoxycillin + clavulanic acid – if resistence is suspected
o bronchitis – amoxycillin or doxycycline
o pneumonia
staph. - flucloxacilin
lower lobe consolid – strept. pn.
Rx – penicillin or amoxyclav
atypical pneumonia
- Azithromycin – the best
covers Mycoplasma, Legionella, Chlamydia
- Erithromycin, roxithromycin
don’t cover Legionella
- doxycycline, tetracycline
pneumocystic - cotrimoxazol
Klebsiella - cefuroxime
o lung abscess
clindamycin + cephalosp. (ceftriaxone)
cephalosp. + flucloxacillin
o tonsilitis – penicilin
o rheumatic fever – penicilin
o scarlet fever – penicillin
o impetigo - topical antiseptic – bactroban (Mupirocin)
if extensive, systemic A/B
flucloxacilin
cephalexin
o meningitis - Ceftriaxone (III generation) + benzylpenicillin
Ceftriaxone (III generation) 2 g IV
plus benzylpenicillin 2.4 g IV (ampicillin for Listeria) in immune-
compromised or Listeria
if penicillin/cephalosporin hypersensitivity:
vancomycin + ciprofloxacin
prophylaxis in contacts: ciprofloxacin or rifampicin
o typhoid fever – ciprofloxacin
o other diarrhoeas – see Diarrhoea chap.
o whooping cough – clarythromycin / erythromycin
o epiglotitis – Cephalosp. III gen: Ceftriaxone, cefotaxime
o inf. endocarditis - start ASAP empiric Rx with benzyl penicillin + flucloxacilin +
gentamycin i.v.
o osteomyelitis – (staph.) flucloxacilin
o septic arthritis (staph.) - Flucloxacilin
in hospital – Ceftriaxone – 3rd gen (covers gram -)
o cholecystitis - gentamicin, ampicillin.
o cholangitis: ceftriaxone, penicillin, aminoglycosides
o peptic ulcer
1st line: PPI + clarythromycin + amoxycilin
2nd line: PPI + metronidazole + amoxycilin
3rd line or if sensitive to penicilin: PPI + clarythromycin + metronidazole
o peritonitis (after viscus rupture): Give gentamicin 5 mg/kg IV, ampicillin 1 g IV and
metronidazole 500 mg IV
o TB
active TB
4 drugs (rifampicin, isoniazid, pyrazinamide, ethambutol) for 2 mths
then 2 drugs (rifampicin and isoniazid) for 4 mths
- total 6 mths
latent TB (Mantoux positive, no sympt., no x-ray)
when active TB is excluded: isoniazid mono-therapy for 6-9 mths
pregnant
isoniazid, rifampicin, ethambutol – 9 mths treatments
isoniazid resistant TB
streptomycin or amikacin instead of isoniazide
- A/B:
o gram pos – penicilin, if allergic erythromycin; cefalosp. I; ampicilin
o gram neg – gentamicin (nefro, neuro, ototox.); cefalosp. II, III (the higher the generation,
the more gram neg. coverage)
o chlamydia, mycoplasma – tetracyclin, doxycicline
o staf – amoxicilin (if resistant staf.) + clav., flucloxacilin, dicloxacilin (penicilins)
o trimetoprim, cefalexin (gen III) – UTI
- cross sensitivity 4-6 % between peniciln and cephalosporin
- no topical A/B in Aus.
o exception – ocular inf. (cloramphenicol)
- A/B
o classif.
bactericidal
- beta lactams
penicilins
cephalosporins
- aminoglicozides
bacteriostatic
macrolides
tetracyclines
o I. beta lactams – interfere with the synthesis of the bacterial wall
1. penicilins
types:
- narrow spectrum (have “penicilin” in the name)
benzyl penicilin
procain penicilin
benzathine penicilin
phenoximethyl penicilin - oral
- broad spectrum – modified in order to have a broad spectrum
ampicilin
amoxycilin
- antistaph. – resistant to beta lactamase
methiciline
cloxaciline
flucloxaciline
SE: cholestatic jaundice
dicloxaciline – preferred over flucloxaciline, but not
very stable
- antipseudomonal
piperacilin
ticarcilin
resistance to penicilin – mechanisms:
- production of beta lactamase enzymes (destroys the beta
lactam ring of a beta lactams)
use of beta lactamase inhibitors: clavulanic acid
(amoxicilin + clavulanic acid = amoxiclav), sulbactam,
tazobactam
- reduction in cell wall permeability
e.g. the gram negative bact.
- occurrence of modified penicilin binding sites
MRSA – methicillin resistant staph. aureus
-> use vancomycin
2. cephalosporin
first gen.
- active on gram + and modest on gram –
- e.g.
cefalexin - oral
cefazolin - iv
second gen.
- strongest on gram + and moderate on gram –
- cefaclor, cefuroxim
third gen.
- strongest on gram – and less than second gen. on gram +
- ex. cefotaxime, cephtriaxone
fourth gen.
- strong on gram -, moderate on gram +, also cover other bact.
- ex. cefclidine, cefepime
3. imipenam – very broad spectrum (gram +, gram -, aerob/anaerob,
pseudomonas, most enterobact. etc. – almost all bact.)
4. meropenam – also very broad spectrum
o II. aminoglicozides
gentamycin, streptomycin, amikacin, kanamycin, neomycin
spectrum: good for gram -, also on gram +
SE
ototoxic - vit. E should be added to prevent the ototoxicity of
gentamycin
nephrotoxic – monitor renal fc.
prefered dosage: once daily
o III. macrolides
erithromycin, claritromycin, azithromycin
spectrum
more on gram +, less on gram –
active on mycoplasma, chlamydia, bordetella
azithromycin – very active on legionella
o IV. tetracyclins
tetracyclin, doxycyclin
spectrum:
gram +, gram -, chlamydia, mycoplasma
A/B of choice for atypical bact.: mycoplasma, chlamydia, malaria
prophylaxis, plague, brucellosis, cholera, Lyme dis. + in mixed inf.
o V. glycopeptides:
vancomycin
to treat multiresistant staph.
- pseudomembranous cholitis (no.2 choice; no. 1 choice =
metronidazol)
o VI. metronidazol
drug of choice for pseudomembranous cholitis
o VII. nitrofurantion
UTI
o VIII. A/B affecting the tropoisomerase 2 enzyme
ciprofloxacin, norfloxacin
SE:
CI in children < 14 yrs: risk of joint difformity (not in growing years)
ciprofloxacin + theophylin interaction => theophylin toxicity
o IX. anti-TB – all are hepatotoxic
first line:
rifampicine
- SE: red urine
isoniaside
- SE: hepatotoxicity
etambutol
- SE: optic neuritis
pyrazinamide
- SE: peripheral neuropathy. (add vit. B12 to prevent it)
- not in pregnancy
second line
streptomycin
ciprofloxacin
Ventricular arrhythmias
fast- Quinidine (Na+) channel block prevention of paroxysmal recurrent
Ia channel Procainamide (intermediate atrial fibrillation (triggered by vagal
blockers Disopyramide association/dissociation) overactivity), *procainamide in
Wolff-Parkinson-White syndrome
In Wolff-Parkinson-White
Amiodarone
syndrome
Sotalol K+ channel blocker
(sotalol:) ventricular tachycardias
III Ibutilide
and atrial fibrillation
Dofetilide Sotalol is also a beta (Ibutilide:) atrial flutter and atrial
E-4031 blocker[6] fibrillation
Anticoagulants
- heparin
o types
unfractioned
LMW (fractioned)
o adm. IV or SC
o monitored by APTT
o inactivates thrombin
o Cx
heparin induced thrombocytopenia (HIT)
Petechiae of the skin, bleeding, haematuria
thrombosis – most characteristic
usually when using unfractioned heparin, rarely with fractioned heparin
decr. platelets, but thrombotic disorder
4-15 days after adm. of heparin -> Sx of thrombosis
Rx
- withdrawal of heparin
- antidote: protamine sulphate
- replacement with warfarin
- warfarin
o antivit. K, depresses fact. II (prothrombin), VII, IX, X
o effect starts after 2-3 days
o full effect after 5-7 days
o antidote:
fresh frozen plasma
vit. K
prothrombin complex concentrate
o monitored with INR (normal INR = 0.8-1.1)
target INR:
2-3 for most indications
2.5-3.5 for mechanical prostetic heart valve
INR measured
before starting –> baseline (modified in certain dis., e.g. liver dis.)
3rd day -> effect started
6-7th day -> max. effect
daily for 1 week – adjust the dose
weekly for next 4 weeks
then monthly
o indic:
prosthetic cardiac valve
DVT, PE
AF selected cases
post-coronary bypass surgery
postop. in lower limb surgery
thrombosis in antiphospholipid antibody syndrome
o CI
active bleeding
intracranial bleeding
uncontrolled HT
impaired liver function
pregnancy
o Cx
skin necrosis
purple toes syndrome
Rx – stop warfarin
o intox.
INR 3-5
lower the dose or omit the next dose of warfarin
resume therapy at a lower dose when INR is in therap. range
INR 5-9:
cease warfarin
give vit. K
measure INR after 24 hrs
INR > 9
low risk of bleeding
- cease warfarin
- give vit. K
- measure INR in 6-12 hrs
high risk of bleeding
- cease warfarin
- give FFP
- give vit K
- measure INR in 6-12 hrs
if bleeding, no matter what the INR is - FFP
o pre-op:
elective surgery
stop it 1 week before surgery + start heparin (LMW heparin)
stop heparin 12-24 hrs before surgery
after surgery, start heparin and warfarin
stop heparin when desired INR has been achieved
emmergency surgery
give FFP + prothrombine concentrate + vit. K
o admin. for
3 months if cause of DVT is known
6 months if cause of DVT is unknown
- anti-platelets
o aspirin
thromboxane A2 inhibitor
100 mg tabl. – 1x / day
o Clopidogrel
ADP inhibitor
75 mg
o dipiridamole
phosphodiesterase inh.
indic. – prostetic valves in young patient
also a vasodilator. (with more SE)
o GP IIb/IIIa glicoproteins
Eptifibatide, Alciximal
for interventional cardiology
antiemetic, nausea:
a. side effect of morphine – haloperidol, prochlorperazine (Stemetil)
b. poor gastric emptying – metclopramide, cisapride, domperidone
c. cytotoxic chomotherapy or radiotherapy – ondansetron (Zofran) =
serotonin receptor antagonist
antivertigo – betahistine - dilate the blood vessels within the middle ear which
can relieve pressure from excess fluid and act on the smooth muscle. In
Meniere’s syndrome.
antipsychotics:
- tranquilizing psychiatric medication primarily used to manage psychosis
(including delusions or hallucinations, as well as disordered thought),
particularly in schizophrenia and bipolar disorder.
- All antipsychotic drugs tend to block D2 receptors in the dopamine pathways
of the brain. This means that dopamine released in these pathways has less
effect. Excess release of dopamine in the mesolimbic pathway has been
linked to psychotic experiences. It is the blockade of dopamine receptors in
this pathway that is thought to control psychotic experiences.
- first generation (typical) antipsychotics – 1950 - the first typical
antipsychotics to enter clinical use were the phenothiazine (chlorpromazine)
o Butyrophenones
Haloperidol (Haldol, Serenace)
Droperidol (Droleptan)
o Phenothiazines
Chlorpromazine (Thorazine, Largactil)
Fluphenazine (Prolixin) - Available in decanoate (long-acting)
form
Perphenazine (Trilafon)
Prochlorperazine (Compazine)
Thioridazine (Mellaril, Melleril)
Trifluoperazine (Stelazine)
Mesoridazine
Periciazine
Promazine
Triflupromazine (Vesprin)
Levomepromazine (Nozinan)
Promethazine (Phenergan)
Pimozide (Orap)
o Thioxanthenes
Chlorprothixene (Cloxan, Taractan, Truxal)
Clopenthixol (Sordinol)
Flupenthixol (Depixol, Fluanxol)
Thiothixene (Navane)
Zuclopenthixol (Cisordinol, Clopixol, Acuphase)
- second generation (atypical) antipsychotics - less likely for causing
extrapyramidal motor control disabilities in patients, which include unsteady
Parkinson's disease-type movements, body rigidity and involuntary tremors.
These abnormal body movements can become permanent even after
medication is stopped. During the course of treatment atypical antipsychotics
are associated with the following benefits; higher rate of responders,
efficiency in patients with refractory disease, lower risk of suicides, better
functional capacity and an improved quality of life
o Clozapine (Clozaril) - Requires weekly to biweekly complete blood
count due to risk of agranulocytosis. – new gold standard in
schizophrenia
o Olanzapine (Zyprexa) - Used to treat psychotic disorders including
schizophrenia, acute manic episodes, and maintenance of bipolar
disorder. Dosing 2.5 to 20 mg per day.
o Risperidone (Risperdal) - Dosing 0.25 to 6 mg per day and is titrated
upward; divided dosing is recommended until initial titration is
completed, at which time the drug can be administered once daily.
Used off-label to treat Tourette syndrome and anxiety disorder.
o Quetiapine (Seroquel) - Used primarily to treat bipolar disorder and
schizophrenia, and "off-label" to treat chronic insomnia and restless
legs syndrome; it is a powerful sedative. Dosing starts at 25 mg and
continues up to 800 mg maximum per day, depending on the severity
of the symptom(s) being treated.
o Ziprasidone (Geodon) - Approved in 2006[citation needed] to treat
bipolar disorder. Dosing 20 mg twice daily initially up to 80 mg twice
daily. Side-effects include a prolonged QT interval in the heart, which
can be dangerous for patients with heart disease or those taking other
drugs that prolong the QT interval.
o Amisulpride (Solian) - Selective dopamine antagonist. Higher doses
(greater than 400 mg) act upon post-synaptic dopamine receptors
resulting in a reduction in the positive symptoms of schizophrenia, such
as psychosis. Lower doses, however, act upon dopamine
autoreceptors, resulting in increased dopamine transmission, improving
the negative symptoms of schizophrenia. Lower doses of amisulpride
have also been shown to have antidepressant and anxiolytic effects in
non-schizophrenic patients, leading to its use in dysthymia and social
phobias. Amisulpride has not been approved for use by the Food and
Drug Administration in the United States.
o Asenapine (Saphris) is a 5-HT2A- and D2-receptor antagonist under
development for the treatment of schizophrenia and acute mania
associated with bipolar disorder.
o Paliperidone (Invega) - Derivative of risperidone that was approved in
2006.
o Iloperidone (Fanapt) - Approved by the FDA on May 6, 2009.
o Zotepine (Nipolept, Losizopilon, Lodopin, Setous)- An atypical
antipsychotic indicated for acute and chronic schizophrenia. It was
approved in Japan circa 1982 and Germany in 1990, respectively.
o Sertindole (Serdolect, and Serlect in Mexico). Sertindole was
developed by the Danish pharmaceutical company H. Lundbeck. Like
the other atypical antipsychotics, it is believed to have antagonist
activity at dopamine and serotonin receptors in the brain.
antidepressants:
- selective serotonin reuptake inhibitors (SSRIs) - current standard of drug
treatment
o A possible cause of depression is an inadequate amount of serotonin,
a chemical used in the brain to transmit signals between neurons.
SSRIs are said to work by preventing the reuptake of serotonin (also
known as 5-hydroxytryptamine, or 5-HT) by the presynaptic neuron,
thus maintaining higher levels of 5-HT in the synapse.
o This class of drugs includes:
Citalopram (Celexa, Cipramil)
Escitalopram (Lexapro, Cipralex, Seroplex, Lexamil)
Fluoxetine (Prozac, Sarafem, Symbyax)
Fluvoxamine (Luvox)
Paroxetine (Paxil, Aropax)
Sertraline (Zoloft)
o These antidepressants typically have fewer adverse effects than the
tricyclics or the MAOIs, although such effects as drowsiness, dry
mouth, nervousness, anxiety, insomnia, decreased appetite, long-term
weight gain and decreased ability to function sexually may occur. Some
side effects may decrease as a person adjusts to the drug, but other
side effects may be persistent. Though safer than first generation
antidepressants, SSRIs may not work on as many patients as previous
classes of antidepressants, suggesting the role of norepinephrine in
depression is still important.
- serotonin-norepinephrine reuptake inhibitors (SNRIs)
o newer form of antidepressant that work on both norepinephrine and 5-
HT. They typically have similar side effects to the SSRIs, though there
may be a withdrawal syndrome on discontinuation that may necessitate
dosage tapering.
o These include:
Desvenlafaxine (Pristiq)
Duloxetine (Cymbalta)
Milnacipram (Ixel)
Venlafaxine (Effexor)
- tricyclic antidepressants (TCAs)
o the oldest class of antidepressant drugs. Tricyclics block the reuptake
of certain neurotransmitters such as norepinephrine (noradrenaline)
and serotonin. They are used less commonly now due to the
development of more selective and safer drugs. Side effects include
increased heart rate, drowsiness, dry mouth, constipation, urinary
retention, blurred vision, dizziness, confusion, and sexual dysfunction.
However, tricyclic antidepressants are still used because of their
effectiveness, especially in severe cases of major depression.
o These include:
Tertiary amine tricyclic antidepressants:
Amitriptyline (Elavil, Endep) – also used in
neuropathies, e.g. in diabetes, shingles, ankylosis
spondilytis, etc.) for pain relief
Clomipramine (Anafranil)
Doxepin (Adapin, Sinequan)
Imipramine (Tofranil)
Trimipramine (Surmontil)
Secondary amine tricyclic antidepressants
Desipramine (Norpramin)
Nortriptyline (Pamelor, Aventyl, Noritren)
Protriptyline (Vivactil)
- tetracyclic antidepressants (TeCAs)
o named after their chemical structure which contains four rings of atoms
and are closely related to the tricyclic antidepressants (TCAs) which
contain three rings of atoms.
o Pharmaceutical Drugs
Amoxapine (Asendin)
Maprotiline (Deprilept, Ludiomil, Psymion)
Mazindol (Mazanor, Sanorex)
Mianserin (Bolvidon, Norval, Tolvon)
Mirtazapine (Remeron, Avanza, Zispin)
Setiptiline (Tecipul)
- monoamine oxidase inhibitors (MAOIs)
o may be used if other antidepressant medications are ineffective. MAOIs
work by blocking the enzyme monoamine oxidase which breaks down
the neurotransmitters dopamine, serotonin, and norepinephrine
(noradrenaline).
o Because there are potentially fatal interactions between this class
of medication and certain foods (particularly those containing
tyramine), as well as certain drugs, classic MAOIs are rarely
prescribed anymore. However, this does not apply to Emsam, the
transdermal patch form of selegiline, which due to its bypassing of the
stomach has a lesser propensity to induce such events.
o MAOIs can be as effective as tricyclic antidepressants, although they
are generally used less frequently due to the fact that they have a
higher incidence of dangerous side effects and interactions. A new
generation of MAOIs has been introduced; moclobemide (Manerix),
known as a reversible inhibitor of monoamine oxidase A (RIMA), acts in
a more short-lived and selective manner and does not require a special
diet.
o The MAOI group of medicines include:
Isocarboxazid (Marplan)
Moclobemide (Aurorix, Manerix)
Phenelzine (Nardil)
Selegiline (Eldepryl, Emsam)
Tranylcypromine (Parnate)
- Noradrenergic and specific serotonergic antidepressants (NaSSAs)
o newer class of antidepressants which purportedly work to increase
norepinephrine (noradrenaline) and serotonin neurotransmission by
blocking presynaptic alpha-2 adrenergic receptors while at the same
time blocking certain serotonin receptors.
o Examples include:
Mianserin (Tolvon)
Mirtazapine (Remeron, Avanza, Zispin)
- Norepinephrine (noradrenaline) reuptake inhibitors (NRIs)
o act via norepinephrine (also known as noradrenaline). NRIs are thought
to have a positive effect on the concentration and motivation in
particular.
o These include:
Atomoxetine (Strattera)
Mazindol (Mazanor, Sanorex)
Reboxetine (Edronax)
Viloxazine (Vivalan)
- Norepinephrine-dopamine reuptake inhibitors (NDRIs)
o inhibit the neuronal reuptake of dopamine and norepinephrine
(noradrenaline).
o These include:
Bupropion (Wellbutrin, Zyban)
- Selective serotonin reuptake enhancers (SSREs)
o Tianeptine (Stablon, Coaxil, Tatinol)
- Norepinephrine-dopamine disinhibitors (NDDIs)
o act by antagonizing the serotonin 5-HT2C receptor which normally acts
to inhibit norepinephrine and dopamine release, thereby promoting
outflow of these neurotransmitters.
o Examples:
Agomelatine (Valdoxan, Melitor, Thymanax)
Lithium:
- mood stabilizing drug, primarily in the treatment of bipolar disorder, where
they have a role in the treatment of depression and particularly of mania, both
acutely and in the long term. As a mood stabilizer, lithium is probably
more effective in preventing mania than depression, and may reduce the
risk of suicide in certain bipolar patients.In depression alone (unipolar
disorder) lithium can be used to augment other antidepressants. Lithium
carbonate (Li2CO3), sold under several trade names, is the most commonly
prescribed, while the citrate salt lithium citrate (Li3C6H5O7), the sulfate salt
lithium sulfate (Li2SO4), lithium aspartate and the orotate salt lithium orotate
are alternatives.
- Upon ingestion, lithium becomes widely distributed in the central nervous
system and interacts with a number of neurotransmitters and receptors,
decreasing norepinephrine release and increasing serotonin synthesis.
antiepileptics:
- carbamazepine (+ trigeminal neuralgia)
- valproate
- ethosuximide
- gabapentin (+ diabetic neuropathy, post-herpetic neuralgia)
anticoagulants:
- warfarin = antivit. K (coumadins)
o oral
o in patients with atrial fibrillation, if > 65 and with no other
contraindications
o full effect reached after 5-7 days
o maintain an INR = 2-3
o antidotes:
vit. K – the effect is not immediate
fresh frozen plasma – brings all the required coagulation factors,
the effect is immediate
- heparin
o long term treatment: start with heparin (sc or iv), until oral warfarin
starts to take effect (5-7 days)
o can be:
unfractioned – short half-life => adm. frequently or as an infusion
low-mollecular-weight (LMW) – daily usage
enoxaparin
dalteparin
o antidote: protamine sulphate - reverses the anticoagulant effects of
heparin by binding to it.
antiplatelet drugs:
- aspirin
o it has half the effectiveness of warfarin in preventing strokes!!!
- dypiridamole
- ticlopidine, clopidogrel
thrombolytics:
- These drugs are most effective if administered immediately after it has been
determined they are clinically appropriate. The advantage of administration is
highest within the first sixty minutes, but may extend up to six hours after the
start of symptoms.
- examples:
o tissue plasminogen activator - t-PA - alteplase (Activase)
o reteplase (Retavase)
o tenecteplase (TNKase)
o anistreplase (Eminase)
o streptokinase (Kabikinase, Streptase)
o urokinase (Abbokinase)
- Side-effects:
o Hemorrhagic stroke is a rare but serious complication of thrombolytic
therapy.
o If a patient has had thrombolysis before, an allergy against the
thrombolytic drug may have developed (especially after
streptokinase).
antispasmodic – hyoscine
Obstetrics - OK
Pregnancy parameters
- implantation:
o 5 days for fertilized egg
o 10 days from ovulation
- don’t monitor baby up to 24 weeks
o until then – only monitor mother
- term baby > 37 weeks
- caracteristic of pregnancy
o immunol. suppresion
o leucocytosis
- gestational age - most appropriate examination:
o U/S in first trimester, 8th - 9th week, before 18 wks (not reliable after 18th week)
the earlier the more accurate
measures the crown-rump legnth (CRL)
o if no U/S, then pelvic / bi-manual examination in first trimester
measures the uterine size
- engagement of the fetal head
o 36-40 wks – in primigravida
o during labor – in multigravida
- FHS
o heard with Doppler amplif. at 9-12 weeks
o heard with the stethoscope at 20 weeks
- fetal movts. felt by
o 18 wks – multigravida
o 20 wks – primigravida
- caracteristic for pregnancy
o LH very elevated – because beta sub-unites of LH and HCG are almost identical, so the
HCG is measured in the LH assays
> 200 mIU/mL -> indicative of pregnancy
- Gravida indicates the total number of times a woman has been pregnant, regardless of whether
these pregnancies were carried to term. A current pregnancy, if any, is included in this count.
- Para indicates the number of viable (>20 wks) births. Pregnancies consisting of multiples, such as
twins or triplets, count as ONE birth for the purpose of this notation.
- Abortus is the number of pregnancies that were lost for any reason, including induced abortions
or miscarriages. The abortus term is sometimes dropped when no pregnancies have been lost.
pregnancy stuff:
duration: 37-42 weeks (40 weeks since last normal menstrual period, LNMP - or 38 weeks from
conception)
prenatal care:
monthly visits during the first two trimesters (from week 1–28)
biweekly from 28 to week 36 of pregnancy
weekly after week 36 (delivery at week 38–40)
total: 14 (can be reduced to 7-10)
suplimentation:
folate 0.5 mg last 3 months before the pregnancy and first 3 months of the pregnancy
iron – in vegans / vegetarians
calcium and vit. D (10 micrograms/day) – maybe
vit. A excess is harmful to the baby!
screening:
- chorionic villus sampling: 9-11 weeks, results in 48 hrs
- amniocentesis: 15 weeks, results in 3 weeks
- ultrasound
- immunisations:
- influenza
- antityphoid or cholera – if travelling abroad
- polio – is not vaccinated yet
symphisis – fundal height: approx. match height in cm = no. of weeks (e.g. at 20 weeks – 20 cm)
evolution:
by 10 weeks (70 days) the placental development is complete
uterus becomes palpable from 12-13 weeks
fetal movements felt after 18 weeks
morphology ultrasound scan at 18-20 weeks
uterine fundus reaches the umbilicus – 20 weeks
Infections in pregnancy
- pregnancy doesn’t lower the woman’s resistance to inf.?
o exception: poliomyelitis
- baby – immunocompetent at 14 wks, but the efficacy is low till the second ½ of the pregn.
- Mx
o offer mother termination of pregnancy if active infection with:
erythema infectiosum
rubella
- types
o a. bacterial
1. GBStrepto
(15) 18-27% of mothers are carriers
during labor > 50% of babies born through an infected vagina are
colonized
- 1% of them will develop early onset GBS neonatal sepsis ->
difficult to treat, with high neonatal death
25-30% of premature babies
2-8% of term babies
15-40% neurol. sequelae in survivors
risk incr. in
- PROM – mother can develop chorioamniotitis
- vaginal delivery – especially in premature babies
Mx – 2 approaches:
- 1. test for it at 36 weeks
swab low vagina + rectum
- 2. treat if positive risk factors
premature labor < 37 weeks
when anticipated ROM > 18 hrs before delivery
intrapartum fever > 38o
previous early onset GBS dis.
GBS bacteriuria during pregnancy
Rx.
- for mother
come to hospital if early labor
benzyl penicillin every 6 hrs during labor or after ROM
- crosses the placenta and goes to the baby
if allergic to penicillin: clindamycin or
erythromycin
- for baby
optional if baby is normal
mandatory if baby is infected or in prolonged PROM
2. gonorrhoea
can cause:
- septic abortion
- chorioamnionitis during pregnancy
- neonatal blindness from conjunctivitis. Neonates coming
through the birth canal are given erythromycin ointment in
eyes to prevent blindness from infection. The underlying
gonorrhea should be treated; if this is done then usually a good
prognosis will follow.
investigate whether mother is infected – culture on Thayer-Martin
medium
treatment:
- erythromycin or roxythromycin
- (this is for non-pregnant woman - currently: doxycycline +
metronidazole – but N. gonorrhoeae increasingly resitent to
tetracyclines, so replace with:
probenecid (increases the acid uric in urine + increases
the serum concentration of antibiotics by inhibiting
their renal excretion) + ceftriaxone + doxycycline
clindamycin
gentamicin
azithromycin)
3. syphilis
extremely rare now
able to penetrate the placenta after the 15th week => congenital
syphilis in 20-50%, perinatal death in 20-30%
can cause early and late congenital syphilis: stillborns, prematurity,
Hutchinson's triad (deafness, Hutchinson's teeth (centrally notched,
widely-spaced peg-shaped upper central incisors), and interstitial
keratitis (IK), an inflammation of the cornea which can lead to corneal
scarring and potentially blindness), mulberry molars (sixth year molars
with multiple poorly developed cusps), frontal bossing, poorly
developed maxillae, enlarged liver and spleen, etc.
screening at first antenatal test + repeated at 30 wks
- VDRL
- rapid plasma reagin (RPR) test
confirmed with more specific tests:
TP haemagglutination test (TPHA)
fluorescent treponamal AB test (FTA-ABS)
TP immobilisation test (TPI)
Rx
- procaine benzylpenicillin or benzathine penicillin
- (in non-pregnant: if sensitive to penicillin
doxycycline)
- in case mother was infected and not fully treated -> baby also
treated with procaine benzylpenicillin for 10 days
since baby’s sympt. are non-specific + serology is
inacurate
o b. viral – smaller than bact. => higher chance of passing through the placenta
most of them infect the baby only if very severe inf. in the mother
exceptions:
- rubella
- CMV
- herpes
1. rubella
very rare now, due to the immunization program
- 85% had the inf. and 90% of them are immune
if active inf. in first 14 wks => fetus will almost certainly be inf. (90%),
with 40% of them being damaged by the virus (5% risk in last trim.)
causes congenital rubella syndrome:
- prematurity
- "blueberry muffin" rash
- cataract, blindness
- deafness
- heart malform. - PDA
- IUGR
- thrombocytopenic purpura, hepatosplenomegaly
- vasculitis, renal artery stenosis
prevention
- immunize all women between 11-13 yrs
- screening
when she wants to get pregnant
if not immune – get the vaccine + don’t get
pregnant in the next 3 mths
at first pregnancy test – if vaccinated now, extremely
small risk of inf.
Mx in case of inf. (rubeliform rash – 50% of rashes are not due to
rubella) or contact with infected person
- pregnancy test neg.
IgM neg., IgG neg. -> immunize + don’t get pregnant in
next 3 mths.
IgM pos., IgG neg. -> supportive Rx + don’t get
pregnant till sympt. disappear and IgG becomes pos.
IgM neg., IgG pos. = immune, safe to get pregnant
- pregnancy test pos.
IgM neg., IgG neg. -> do not immunize + avoid contact
with inf. person + repeat test in 3 weeks
if IgM become pos. -> discuss therapeutic
abortion if first trim.
amniocentesis can be used to confirm the inf.
of the baby
IgM pos., IgG neg. -> discuss therapeutic abortion if
first trim.
IgM neg., IgG pos. = immune, continue pregnancy
2. CMV
MC non-bacterial pregnancy inf. in Aus.
CMV is the most common cause of congenital infection in humans and
intrauterine primary infections are second only to Down's syndrome
as a known cause of mental retardation
1% of women may become inf. during pregnancy
- most of them asympt.
- Cx
incr. perinatal mortality
3-7% with congenital abnormalities
hearing loss, visual impairment, or diminished
mental and motor capabilities
no screening since there is no vaccine available
3. genital herpes
primary inf. is usually asympt.
transm.
- during pregnancy – rare: 1:11.000
- during labor (+ GBS)
40-50% if active primary inf.
5% if active recurrent inf.
Dx – endocervical swabs every 2 wks from wk 34 – can be abandoned
(not a good predictor)
Mx
- if no current active inf. (primary or recurrent lesions have
healed) => vaginal delivery
- if active herpetic lesions during ROM or labor => C-section
- aciclovir prophylactic from week 38?
- + Rx the baby with aciclovir if
clinically ill
positive cultures
Cx - severe neonatal inf.
- 30% risk of neonatal death
- in 40% of survivors - neurol. damage
4. chickenpox (varicella)
80% of women are immune
causes the: malformations, microcephaly, optic atrophy, psychomotor
retardation, etc.
primary inf. during pregnancy
- in first trim. => 0.4% of babies are inf.
- in second trim. => 2% of babies are inf.
congenital varicela syndrome
limb hypoplasia
microcephaly
optic atrophy
cortical atrophy
cataracts
psychomotor retardation
convulsions
IUGR
disem. inf. in baby – if inf. is 7 days before or
after the delivery
Dx
- IgM neg., IgG neg., but sympt. -> give to the mother VZV Ig
12.5 U/kg i.m. within 4 days of exposure + if severe inf.
Aciclovir
- IgM pos., IgG neg. -> give to the mother VZV Ig 12.5 U/kg i.m.
withing 4 days of exposure + if severe inf. Aciclovir
- IgM neg., IgG pos. = Shingles – Rx mother with Aciclovir
- + infected infant
VZV Ig. + Aciclovir
5. HIV
30% chance to pass the inf. to the baby
inf. has no adverse reaction on the pregnancy and viceversa
Mx
- with Rx of the mother => risk drops to 2%
retroviral drugs antenatally and intrapartum
C-section delivery – reduces risk by 50%
vaginal delivery – if viral load < 1000 copies/ml
bottle feeding
coexisting STIs, chorioamniotitis or ROM for > 4 hrs =>
4x risk of transm.
avoid invasive manouvers: CVS, amniocentesis,
cephalic version, etc.
after delivery – baby is washed and given azathioprine
for 6 weeks
Dx
- screening – ELISA:
positive - repeat in 12 weeks
unprotected intercourse + negative – repeat in 12
weeks
- confirmation – Western blot (ELISA can be positive in EBV inf.)
6. hepatitis B
predom. in migrant mothers
transm. to the baby probably during birth (only 1-5% during pregnancy)
incr. risk if both HbS Ag and HbC Ag are pos. in mother’s blood
Rx
- babies are given
hep. B Ig (only if mom is infected) +
(otherwise only) hep. B vaccine at birth + vaccine at 2
mths and 6 mths
dose: 0.5 ml in the anterolat. thigh
o adult: 1 ml, in the deltoid (Engerix B)
- w/o Rx – high risk of liver CA when the babies become adults
7. hepatitis C
prevalence = 1.3%
risk of vertical transm. = 3-7%
- if assoc. with HIV + high viral load => 25%
Rx
- no methods to avoid transm.
avoid fetal scalp blood sampling and fetal scalp
electrode application
- Rx in mother (ribavirin + interferone) is teratogenic
- if HCV RNA is pos. in the baby after 12-18 mths -> refer baby
for Rx
8. parvovirus B19 - erithema infectiosum / slap cheeck disease/arthritis
pregnant lady exposed to this => Hydrops (erithroblastosus) faetalis –
fever, cardiac failure -> discuss termination
if inf. in 2nd trim – U/S of the baby
Dx – check AB
o c. other
toxoplasmosis
rare – 0.2-1%
- highest risk in first trim.
90% asympt.
Cx – in 25% of fetuses
- most asympt. – with delayed sequelae, e.g. dev. delays
- small baby (IUGR)
- eyes and CNS may be severely damaged
- miscarriage
one of the TORCH infections that lead to congenital abnormalities.
These are:
- TOxoplasmosis
- Rubella
- Cytomegalovirus.
- Herpes simplex
screening
- antenatal + retest in each trim.
Px
- avoid touching cat faeces
- when handling raw meat
avoid touching her eyes or mouth
wash her hands
- only eat well-cooked meat
- wash fruits and vegetables thoroughly before eating them
- wear gloves when gardening
Rx
- pyrimethamine + sulfadiazine + folate (to counteract the their
antifolate activity)
o d. UTI
incr. due to urinary stasis
asympt. bacteriuria in pregnant women
6% of women (pregnant or not)
- 30% of them will develop symptomatic UTI = pyelonephritis
screening in early pregnancy
- MSU -> culture
85% - E. coli
Rx for 7 days with amoxiclav or cefalexin
- repeat culture after 7 days
if not cured, continue A/B
pylonephritis
usually after 20 wks
Sx
- mild
tiredness, incr. urinary frequency, dysuria
- more severe
chills and rigors, fever
pain over one/both renal areas
dehydration
nausea
Dx
- MSU -> culture
Cx
- in baby
low birthweight
- in mother
premature labor
PROM
postpartum endometritis
perinatal death
Rx
- correct dehydration
- AB - amoxiclav or cefalexin
repeat culture every 2 wks
o e. vaginitis
Conditions in pregnancy
- I. Early pregnancy
o a. Bleeding
1. ectopic pregnancy
MC location = ampula
RISK FACTORS:
- Previous ectopic pregnancy.
- Pelvic inflammatory disease.
- Previous tubal surgery or scarring
- IVF treatment.
- Intrauterine contraceptive device (IUCD).
- 50% with no predisposing risk factors.
o Sx
- triad: amenorrhoea + lower abd. pain + abnormal vaginal
bleeding
- the mass usually cannot be palpated
- if ruptured: rebound tenderness and a small amount of
guarding
o Dx
U/S
empty uterus (absent gestational sac)
tubal mass, tubal ring
fluid in the pouch of Douglass
o Mx
beta HCG
if < 1500 UI, repeat after 48 hrs
if > 1500 UI, transvaginal U/S
o if gestational sac in uterus = abortion
o otherwise = ectopic pregnancy
Rx
methotrexate
indic.
- beta HCG < 3500 U/L
- dead fetus: transvaginal U/S – no fetal heart
beats
- tubal mass < 3.5 cm
- tube must be intact
- stable pac.
normal LFT
normal U & E
normal FBC
- patient must use contraception (OCP) and not
get pregnant for at least 3 mths
- if methotrexate is CI –> laparoscopic surgery (salpingectomy or
salpingostomy)
o Cx
rupture
MC location of the rupture = isthmus of fallopian tubes
CLINICAL HISTORY:
- 5th – 9th weeks of pregnancy.
- History of breast tenderness, nausea, or recent
unprotected intercourse.
- Predominant feature: Lower abdominal pain
(90%).
- Vaginal bleeding (mild), collapse.
- Tenderness and guarding to one side.
- Discomfort and swelling in that lateral fornix
on vaginal examination.
- Smaller uterus than expected for
amenorrhoea.
- shock: hT, tachycardia
DIAGNOSIS:
- First step: Pregnancy test:
Urinary dipstick in emergency
department and
beta-HCG in blood.
- Next: Transvaginal Ultrasound:
Empty uterus, a tubal ring, adnexal
mass and fluid in the pouch of Douglas.
MANAGEMENT:
- Haemodynamically unstable:
High-flow oxygen.
IV resuscitation.
Urgent referral to the gynaecological
team.
- Haemodynamically stable:
Admission.
Give all rhesus-negative mothers anti-
D immunoglobulin.
Refer for laparoscopy.
2. GESTATIONAL TROPHOBLASTIC DISEASE / NEOPLASIA
o a. benign hydatiform mole (mollar pregnancy)
Most patients (80-90%) follow a benign course with their
disease remitting spontaneously.
Incidence: 1 every 1500-2000 pregnancies.
Higher incidence in women in Asia (Taiwan): 1 every 125-200
pregnancies.
Younger than 20 years, older than 40 years.
Sx
Irregular or heavy vaginal bleeding during first or
second trimester.
Usually painless.
The patient may expel molar ‘vesicles’ from vagina –
clots that look like grapes.
Uterus large to date
Excessive nausea, hyperemesis gravidarum (due to
incr. beta HCG from large placenta).
- also present in multiple pregnancies
Dx
Absence of fetal heart sounds.
Ultrasound: ‘snowstorm’ pattern is diagnostic.
β-hCG titres can be high for early pregnancy.
TREATMENT:
Evac. under GA
Manual evacuation.
dilat. and evac.
D&C
followed by U/S + prophylactic inj. of methotrexate
FOLLOW –UP: Weekly serum (or urine) β-hCG.
They should decline to undetectable levels
within 12-16 weeks after evacuation.
if not back to normal -> oncology assessment
for possible metastases
o MC location = lung
o brain
o bones
no pregnancy for 1 yr (use OCP)
o b. Invasive mole (chorioadenoma destruens).
o c. Choriocarcinoma.
3. spontaneous miscarriage
o intrauterine death – MC cause = unknown
o Expulsion of the products of conception before 24th week of pregnancy.
o Occurs in 10-20% of all early pregnancies.
o Most common in first trimester.
o miscarriage
I trim – chromosomal (MC - 60%, mostly trisomies) and fetal
abnormalities
MC > 35 yrs
II trim
genetic dis.
inf.
uterine malform.
cervical incompetence
20% of women with recurrent misscariage
after 12 weeks have this (usually at 16 wks)
gradual dilatation of internal cervical os ->
pressure of the intrauterine pressure will break
the amniotic bag at the cervical os point
Sx
o recurrent miscarriage: painless leaking
of amniotic fluid (PROM)
o painless cervical dilatation + incr.
cervical mucous discharge
o miscarriage after painless labor
o contr. – only rarely
o usually no or small bleeding – diff.
from other type of miscarriages
Dx
o U/S or vaginal exam. – before
Rx - cervical cerclage – sutures like a ring on
outside of the cervix, at the internal os level
o at 12-14 wks (before they usually
miscarriage)
o not after ROM
o results
10% will still abort
10% will deliver prematurely
80% normal delivery
o sutures removed 7 days before delivery
or when she presents with labor or
ROM
o STAGES of abortion:
Threatened Inevitable (Dx. Incomplete Complete Missed
after clinical (Dx. after U/S) (silent)
exam)
POC Present, alive + Present, alive Some parts are No Present but
Uterine size still present dead
compatible inside the
with the uterus
duration of
pregnancy
Cervix Closed Open >= 0.5 Open Closed Closed
cm
Fetal heart Good Good No No No
sounds
Will Normal Incomplete or Complete a. Abortion
continue pregnancy in complete a.
with 90-95% cases
Rx Observation, - Minimal - Minimal U/S – confirm - expectant
bed rest bleeding: wait bleeding: wait that uterus is Mx if
& watch & watch empty hemodynamic
- Heavy - Heavy stable, no
bleeding: D&C bleeding: D&C signs of inf.,
patient
agrees to wait
+ lives close
to the
hospital
- otherwise ->
D&C
1. Threatened miscarriage.
Most common up to 14 weeks of gestation.
Chance of successful outcome of pregnancy in
threatened abortion: 90-95%, provided ultrasound
examination is normal.
Mild cramps and transient vaginal bleeding.
Uterine size compatible with the duration of
pregnancy.
External cervical os is closed on speculum
examination.
2. Inevitable miscarriage.
Cannot be arrested.
Bleeding is heavier, abdominal cramps more persistent
(typical here).
External cervical os is open (0.5 cm or more).
POC may be found in the vagina or protruding from the
cervical canal.
3. Incomplete miscarriage.
Parts of the fetus of placental material are retained in
the uterus.
The bleeding remains heavy.
The cramps persist even following the passage of clots
and POC.
4. Complete miscarriage.
All the fetal and placental material has been expelled
from the uterus.
Bleeding and cramps stop.
Signs of pregnancy disappear.
Cervical os is closed.
5. Silent or missed micarriage.
All the POC are retained.
Cramps and bleeding are replaced by an asymptomatic
brownish vaginal discharge.
USG fails to detect fetal heart motion.
o Dx
First: Pregnancy test.
If β-hCG is positive, check β-hCG level to assess
usefulness of ultrasound of USG.
- Β-hCG greater than 1000 U/L: USG.
To confirm the gestation.
To check the sac size.
Liquor volume.
Presence or absence of fetal heart
activity.
o MANAGEMENT:
Stable or Unstable?
IV resuscitation.
Transfusion if needed.
Refer to Gynaecological team for surgical or non-surgical
management.
Give rhesus-negative mothers anti-D immunoglobulin.
4. septic abortion
Result of criminal abortion.
Pelvic infection with salpingitis, peritonitis, pelvic and pulmonary
thrombophlebitis.
Can lead to septicaemia, DIC, shock and death.
CLINICAL FEATURES:
- Fever > 37.8
- Abdominal pain
- Foul-smelling vaginal discharge and bleeding.
MANAGEMENT:
- First step: Swabs for microscopic assessment and culture.
- Immediate antibiotic therapy: Gentamicin 5mg/kg IV, ampicillin
2g IV and metronidazole 500 mg IV.
- Refer for curettage or emergency hysterectomy.
- II. late pregnancy
o a. bleeding = ANTEPARTUM HAEMORRHAGE = Vaginal bleeding after 24 weeks of
gestation
1. Placenta praevia
The placenta is implanted, either partially or wholly, in the lower uterine
segment and lies below the fetal presenting part.
-
incidence – 1%
MC obstetric cause of coagulopathy
classif.
- total, complete, central – completely covers the cervical os
- partial
- marginal – edge min. 2 cm away from cervical os
RISK FACTORS:
- Three times as common in multiparous women as in
primiparae.
- Caesarean section.
- Submucous fibroids.
- History of placenta praevia.
- Advanced maternal age
Sx
- PAINLESS vaginal bleeding.
may be precip. by
trauma
coitus
pelvic / vaginal exam
can stop, then resume
- Uterine Hypotonia: Uterus is not tender.
- Fetal head is still mobile above the pelvic brim
- Blood loss is MATERNAL.
- Bleeding in second half of pregnancy is placenta praevia until
proven otherwise.
DIAGNOSIS:
- First: Fetal heart sounds.
- Ultrasound: Dx is confirmed only after 30 weeks of pregnancy
(at 32-34 weeks).
wait till then since usually the lower part of the
placenta atrophies and the upper part hypertrofies =>
placenta migrates up in 80-90% of cases
- NEVER perform a vaginal or speculum examination, as this
may precipitate torrential vaginal haemorrhage!!!
MANAGEMENT:
- First step: Admission
resuscitate mother
give anti-D if mother is Rh neg.
confirm Dx by U/S
aim: prevent prematurity – prolong the pregnancy
wait for fetal lung maturity: confirmed with
amniocentesis – L/S ratio (lecithin-
sphingomyelin ratio)
o >2 lungs are probably mature
o < 1.5 risk of hyaline membr. dis.
- Minor: Continue pregnancy until term.
vaginal delivery can be attempted
if abnormal bleeding starts, change to C-
section
- Major: Caesarean section at 37-38 weeks
before term / labor starts
earlier if severe bleeding.
Cx
- Sheehan’s syndr.
- acute tubular necrosis
- no engagement of the fetal head – blocked by the placenta
praevia
oblique or transversal presentation
2. placental abruption
Premature separation of a normally situated placenta.
incidence – 1%
Risk factors:
- Maternal hypertension, Pre-eclampsia.
- cigarette smoking, cocaine abuse
- History of placental abruption.
- Trauma, MVA
- Multiple pregnancy, polyhydramnios
CLINICAL FEATURES:
- Abdominal pain with or without vaginal bleeding.
usually external bleeding
sometimes concealed placental abruption - internal
bleeding => retroplacental hematoma => increased
fundal height
Dx diff. with
o red degen. of fibroid
o complic. of an ovarian cyst (torsion,
rupture)
shock out of proportion with the vaginal bleeding
- Hard/tense and tender uterus
Dx. diff with polyhydramnios
- Maternal and fetal blood loss.
Fetal distress.
Shock.
DIAGNOSIS:
- Clinical: painful vaginal bleeding + normal implantation
- USG: It is not an accurate tool.
MANAGEMENT:
- Mild: <500 ml.
Mother and fetus are well.
Patient may go home if the bleeding ceases or
induction of labour if pregnancy has advanced to 37
weeks.
- Moderate: 500-1000 ml.
Signs of shock, fetus is hypoxic.
Rapid blood transfusion, possible caesarean.
- Severe: 1500 ml.
Treatment of shock (as pre-eclampsia is associated, BP
may be in the normal range).
most coaglopathies occur here
The fetus is almost always dead: Amniotomy
(spontaneous labour).
If still alive: Urgent delivery.
COMPLICATIONS:
- Maternal:
DIC – release of tissue thromboplastin from ruptured
plac.
hypovolaemic shock.
acute renal failure - ATN
post-partum haemorrhage
- Fetal: IUGR, pre-term delivery, anaemia.
3. vasa previa
rare
when fetal blood vesels traverse the placental membranes => rupture
of fetal blood vessels during the rupture of membranes
risk factors
- multiparity
- placental accesory lobes
Sx
- triad: rupture of membranes + painless vaginal bleeding + fetal
tachycardia, then bradycardia (due to exsanguination)
- loss of fetal blood
- bleeding usually doesn’t stop
- the fetus usually dies
Dx
- clinical
- Apt test – distinguish between fetal blood and maternal blood
Mx
- emmergency C-section, otherwise the fetus will die
4. placenta accreta
rare: 1:500 - 1:2500
- incidence is incr. due to incr. incidence of C-sections
- risk proportionately increased after multiple C-sections
risk factors
- previous C-section + anterior low lying placenta
when placenta implants over a previous C-section scar -> the
trophoblast penetrates through the scarred decidua and myometrium,
becoming morbidly adherent
Sx
- vaginal bleeding + frequently DIC
Mx – caesaren hysterectomy to preserve the mother’s life
5. rupture of the uterus
RESULT OF:
- Obstructed labour – during the uterine contractions
- Trauma.
- Dehiscence of a caesarean scar.
- Inappropriate use of oxytocics.
Sx
- Vaginal bleeding.
- Abdominal pain which becomes constant.
- Shock in some cases.
- Some can be asymptomatic.
TREATMENT:
- Hysterectomy.
- In few cases the uterine tear can be sutured.
6. polyp
Sx
- bleeding can occur after coitus
- more limited bleeding
best way to monitor adequacy of blood volume replacement = urine output
since the body can compensate through vasoconstr. for a while (pulse,
BP normal), but the urinary output will be decr. in hypovolemia
o b. HT in pregnancy – classif:
1. chronic HT
essential HT – prior to conception or in the first ½ of the pregnancy,
w/o an underlying cause
sec. HT – caused by renal, renovasc. or endocrine disorders or aortic
coarctation
2. gestational HT
arises after 20 wks
w/o any features of pre-eclampsia
resolves within 3 mths after delivery
good prognosis
Rx
- monitoring to exclude the dev. of pre-eclampsia
- if BP>140:90, give antihypertensive drugs
maintain BP at 110-140/80-90
3. pre-eclampsia
after 20 wks
multisystem dis.
- HT – usually the first sympt., followed by proteinuria
resolves within 3 months of delivery
RISK FACTORS:
- MC in Primigravida.
1/3 of them will recur
- in multigravida, if
maternal dis.: Family history of hypertension/pre-
eclampsia., DM, chronic renal dis., SLE
placental problems: hydatiform mole, placental
abruption
fetal problems: Multiple pregnancy, Hydrops fetalis.
SEVERE P. = BP > 160/110 mmHg plus proteinuria.
Imminent eclampsia – severe p. +
- Severe headache.
- Blurring of vision.
- Epigastric pain.
- Hyperreflexia.
- Oliguria.
Dx
- Hypertension that arises after 20 weeks of gestation
Hypertension: > 140/90 mmHg or
Rise in blood pressure of more than 25 mmHg systolic
or 15 mm Hg diastolic
- plus one of the following:
Proteinuria: > 300mg/24 hrs or urine protein/creatinine
ratio > 30 mg/mmol
renal insufficiency
serum creatinine > 0.09 mmol/L or
oliguria
liver dis.
raised AST/ALT and/or
severe epigastric/RUQ pain
neurol. problems
convulsions (eclampsia)
hyperreflexia with clonus
severe headaches with hyperreflexia
persistent visual disturbances (scotomata)
haematol. problems
thrombocytopenia
haemolysis
DIC
fetal growth restriction
COMPLICATIONS:
- Mother
HELLP syndrome = severe form of pre-eclampsia
triad:
o Hemolytic anemia
o Elevated Liver enzyme
o Low Platelets.
Rx – deliver the baby
DIC
Oliguria, ARF
Eclampsia (tonico-clonic seizures and coma).
- Baby
Intrauterine death.
IUGR
Premature delivery.
MANAGEMENT:
- Admission: BP > 150/100 (twice), maternal symptoms,
compromised fetal well being.
- Treat HT:
moderate – p.o.
Methyldopa 250 mg two-three times daily.
Labetalol or atenolol
Nifedipine
Severe – i.v
Hydralazine 5 mg IV bolus every 20 min
- < 32 weeks: try to continue pregnancy until 35 weeks
steroids for pulmonary maturity
daily fetal movement count (kick chart)
3 CTGs / week
Doppler umbilical blood flow
platelet count – to detect HELLP syndrome
if platelets > 100.000 – keep monitoring
if platelets < 100.000
o give C/S – 2 doses, 24 hrs apart -> to
prevent hyaline membrane dis.
o correct the thrombocytopenia, then
o induction
- 32-35 weeks: Same management, but if delivery is indicated,
can do C-section or induction of labor
- > 35 wks
pregnancy should be terminated rapidly with induction
of labor or C-section, depending on the cervix and feto-
maternal situation
- eclampsia
delivery
prevent convulsions with MgSO4
can be used first 48-72 hrs after delivery
Initial dose of 4g IV over 5-10 min then infusion
1g/h for at least 24 hours.
if woman has eclampsia, hyperreflexia,
headache or fits
monitor tendon reflexes, resp. rate (>16/min)
and urine output (>25 ml/h)
SE
o diminished or abolished reflexes (knee
jerk = patellar reflex) – first sign
o decr. resp. rate -> resp. paralysis
o decreased urinary output
Rx
o stop MgSO4
o give antidote - Calcium Gluconate.
if convulsions occur, treat with Diazepam 0.1-0.2
mg/kg IV or phenytoin
4. pre-eclampsia superimposed on chronic HT
after 20 wks
systemic features of pre-eclampsia develop on top of an existing chronic
HT
o c. PROM
in most cases (80-90%) the baby is born within 7 days
for best prognosis of the baby, most imp. is the admin. of C/S
Mx
lithmus paper test (nitrizine test) – is there amniotic fluid in the
discharge?
monitor for signs of chorioamniotitis
- cause: anaerobes, GSE
- Sx
fever
tachycardia
abd. pain, tenderness
offensive vaginal discharge
- Dx
FBE: incr. WBC, CRP – every 2-3 days
- Rx
A/B
expedite the delivery
sterile speculum exam. – under strict sterile conditions
NO PV!! – risk of inf.
U/S – amount of amniotic fluid around the baby (oligohydramnios?)
Doppler for umbilical blood flow: is the baby receiving enough blood?
CTG – every 2-3 days
high and low vaginal swab, rectal swab
- then erythromycin – 250 mg every 5 hrs
usually ceased if swabs come back negative
fetal fibronectin – labor?
Valsalva manouver -> examine the pouring of the amniotic fluid in the
fornixes
2 C/S inj. 24 hrs apart (for 48 hrs)
check indic. and CR for tocolitic
- if contr. have started before the C/S therapy is concluded
-> admin. Ca channel blocker (nifedipine) or
Salbutamol
- otherwise rarely used, since the contr. might signify subclinical
uterine inf. -> in this case delivery should be expedited
transport ASAP to tertiary hospital
if OK and no immediate labor, send home
- monitor fever
- no sexual intercourse
- no strenuous exercise
- urgent readmission in the hospital if
fever
vaginal discharge
decr. fetal movt.
> 35 wks
- if cervix is favorable -> induction with oxytocin (Syntocinon)
- if cervix is unfavorable -> delay induction by 48-72 hrs, to give
time to the cervix to ripen (=> induction will be easier)
26-35 wks = PPROM (preterm premature ROM)
- try to delay the delivery but incr. risk of inf.
- immunisation
o severity of blood group sensitisation can be assessed by:
1. maternal serum anti-D titres
not very accurate
useful
- if very low or very high
- in the first pregnancy
2. previous obstetric performance – gets worse with succeeding pregnancies
3. liquor bilirubin levels at 26-34 wks
second best after 4.
4. measurement of fetal haemoglobin sampled from the fetus at 20-36 wks
in order that
- fetal blood transfusion cand be given if Hb is low
- fetal blood group to be determined
- direct Coombs test to be performed
detects RBC AB on the RBCs (direct) or in the serum
(indirect) by using rabbit anti-serum against RBC
the best
5. U/S – looking for ascites and/or hydrops (late signs)
o any jaundice in first 24 hrs is pathol. – ABO, Rh
o Rh incompatibility is the most common and severe cause of HDN. This incompatibility
may occur when an Rh-negative mother and an Rh-positive father have an Rh-positive
baby. Cells from the baby can cross the placenta and enter the mother's bloodstream,
causing the mother to make anti-D antibodies. Unlike ABO antibodies, the structure of
anti-D antibodies makes it likely that they will cross the placenta and enter the baby's
bloodstream. There, they can destroy the baby's red blood cells, causing a severe or
fatal anemia.
o ABO incompat.
when mother is group O and baby is group A or B
more frequent but milder jaundice in the first day
rarely with severe hemolytic anemia in baby
Dx
Coombs test
Rx – to prevent kernicterus
phototherapy
o Rh incompat.
due to the D antigen
present on the erythrocytes of Rh-pos. fetuses as early as 7 weeks => mothers
become immunised if they receive a feto-maternal transfusion as early as 7
weeks (e.g. termination of pregnancy as early as 7 weeks, fetomaternal
transfusion during the pregnancy)
Sx
hemolytic anemia
jaundice in the first 24 hrs
hepatosplenomegaly
heart failure
Cx
MC cause of hydrops faetalis
stillbirth
screening of mothers
at first presentation
at 28 wks
at 34-36 wks
Dx
Coombs test
- direct – from baby
used to detect these anti-RBC antibodies or
complement proteins that are bound to the surface of
red blood cells
- indirect – from mother
detects antibodies against RBCs that are present
unbound in the patient's serum
Kleihauer test - blood test used to measure the amount of fetal
hemoglobin transferred from a fetus to a mother's bloodstream
- performed on Rhesus-negative mothers to determine the
required dose of Rho(D) immune globulin (RhIg) to destroy the
fetal RBCs and thus inhibit formation of Rh antibodies in the
mother and prevent Rh disease in future Rh-positive children.
indic. for anti-D:
all Rh-neg. unsensitised women who have an abortion
- -> inj. 250 IU within 72 hrs of abortion
all Rh-neg. unsensitised women who require/have:
- CVS, amniocentesis
- ectopic pregn.
- threatened abortion
- antepartum haemor.
- abd. trauma
- need an external cephalic version
- -> inj. 250 IU before 20 wks or 625 IU after 20 wks
all Rh-neg. unsensitised women whose pregnancy has progressed to 28
wks or 34 wks
- -> 625 IU prophylactically
all Rh-neg. unsensitised women who gave birth to an Rh-pos. baby
- -> 625 IU within 72 hrs if Coombs test is neg.
- perform Kleihauer test on mother’s blod
if 80 => > 5 ml of fetal blood was transfused to the
mother -> inj. an additional 625 IU
if second pregn. in Rh-neg mother with Rh-pos. baby -> perform amniocentesis
if bilirubin is present -> intrauterine blood exchange
Rx – to prevent kernicterus
before birth
- intrauterine blood transfusion
- early induction of labor – after fetal lungs are mature
- plasma exchange in mother – to reduce the level of ABs by
75%
after birth
- phototherapy
- blood transfusion
- exchange transfusion
- jaundice in pregnancy
o viral hepatitis – 40%
hepatitis A – MC hepatits during pregnancy
similar course as in non-pregnant women
worse prognosis if chronic hepatitis is present
incr. risk of premature labor
o severe pre-eclampsia, eclampsia and hyperemesis gravidorum – can cause hepatic
damage with jaundice
o III trim
1. MC cause - acute fatty liver of pregnancy
rare
high mortality – 50%
causes
- disordered metabolism of fatty acids by mitochondria in the
mother, caused by deficiency in the LCHAD (long-chain 3-
hydroxyacyl-coenzyme A dehydrogenase) enzyme
- admin. of hepatotoxic agents in debilitated mother
week 35-36
Sx
- nausea, anorexia, vomiting
- jaundice
- fever
Cx
- renal failure
- fulminant hepatitis with hepatic encephalopathy
- pancreatitis
- DIC
Dx
- liver and renal failure (urea and uric acid incr.)
- AST and ALT incr. (but not as high as in viral hepatitis: 200 not
400)
- bilirubin incr.
- ALP usually normal
- liver biopsy – confirms the Dx
Rx
- urgent admission to ICU
- urgent termination of pregnancy (life-saving for mother and
baby)
- prevent / treat DIC
- may require liver transplant
2. intrahepatic cholestasis of pregnancy (hepatosis)
MC in third trimester, but can start anytime
- usually in the second ½ of the pregnancy
due to estr. sensitivity
Cx
- fetal distress
- fetal death
- preterm delivery
- meconium ingestion
- meconium aspiration syndrome
Sx
- intense itching, usually without a rash
Generally, the itching is localized to the abdomen, legs,
palms, and soles, but can be generalized.
Itching that increases in the evening
Itching that does not respond favorably to anti-
histamines or other anti-itch remedies
- Often, elevated LFT results as well as serum bile acid counts
- Less common:
Darker urine
Lighter stools
Increased clotting time (due to possibly associated
vitamin K deficiency)
Fatigue
Increased nausea
Decrease in appetite
Jaundice - only occurs in relatively small subset of
cases
Upper right quadrant pain
Dx
- ALP incr.
- AST/ALT and bilirubin only mildly incr.
if bilirubin highly incr. = MC in viral hepatitis
Rx
- monitor fetus – deliver if in distress
prognosis
- usually clears up rapidly after delivery
- often recurs in future pregnancies or if using OCP (which are
CI)
- DM
o 1. existing (pre-gestational) DM
effects on fetus
large for date (macrosomia)
incr. fetal abnormalities
- neural tube defects
- cardiac – VSD, ASD, TGA
- kidney
- small left colon
hypoxia
intrauterine death
miscarriage
malpresentation
IUGR
preterm delivery
postnatal
- early hypoglyc. – jitters, tremors
should be checked @ 4 hrs after delivery or after
second feeding, whatever comes first
- ARDS
- jaundice
effects on mother – incr. risk of:
pre-eclampsia
DKA
polyhydramnios
intercurrent inf.
first trim. miscarriage
obstructed labor (incr. shoulder dystocia)
placental abruption
C-section
aim for diabetic control:
4-7 mmol/L
HbA1c < 7%
type II - stop oral hypoglicaemic pills during pregnancy and breastfeeding -> use
insulin instead
type I – insulin reqs. will incr. (especially in the last trim.), but will go back to
normal after delivery
o 2. gestational DM
screening test is glucose challenge test (non-fasting) at 26-28 wks (not OGTT)
N=8
> 8 is abnormal -> then do OGTT (fasting)
- also do OGTT if high risk:
previous Hx of gestational DM
DM
family Hx of DM or gestational DM
Hx of macrosomia
PCOS
glycosuria
common in pregnancy – 25-50%
only 2-3% of them have DM
if present on 2 occasions, should do OGTT
Rx – like in pre-gestational DM
follow up with OGTT at 6 weeks and then every 5 yrs
likely to recur in subsequent pregnancies
30% of developing DM later in life
- vomiting
o causes
normal pregnancy
multiple pregnancy
hydatiform mole
UTI
intest. obstr.
o Dx
U&E and creatinine – to assess the dehydration
U/S – multiple pregnancy? hydatiform mole?
urine culture – UTI?
single erect abd. X-ray – intest. obstr.?
- acute pancreatitis in pregn. is assoc. with:
o cholelitiasis – MC
o alcohol intake
o cocaine use
o hyperparathyroidism
o abd. trauma
- pain in lumber area while walking, 3rd trimester - refer to physiotherapy
- fetal movts. felt by
o 18 wks – multigravida
o 20 wks - primigravida
- can’t feel fetal movement
o I step – intermittent auscultation
don’t hear anything - >II step = U/S
hear something that worries you (bradycardia, etc.) -> II step = CTG
CTG normal
- Mx
< 32 wks – U/S
> 32 wks – repeat CTG
o (another approach) if normal auscultation (hypoxia)
CTG
if ok, discharge + do kick chart (normal: 10 movements / day)
if abnormal auscultation
CTG + U/S
- multiple pregnancies
o assoc. with
incr. perinatal morbidity and mortality (5-10x)
incr. post-partum haemor. (uterine atony)
incr. IUGR of one or both twins
incr. umbilical cord prolapse (especially for twin 2)
o not assoc. with feto-maternal haemorrhage
- oligohydramnios
o Mx
U/S
RFT
regular CTG
lupus AB
- polyhydramnios
o risks
PROM
preterm labor
cord prolapse
APH
malpresentation
- pubic symphysis diasthasis (pelvic osteoartropathy)
o separation of pubic bones (due to relax. of ligaments during pregnancy)
o II-III trim or early postparthum
o Sx
pubic pain aggravated by walking / moving
pubic joint is very tender
o Dx
confirmed by U/S
post-partum – x-ray
o Rx
bed rest on firm mattress
- abdomen big for date (fundus > age)
o wrong date
o polyhydramnios
fetal malformations
multiple pregnancy (twins)
DM
infection: CMV, toxoplasmosis
chorioangioma of placenta
o DM – macrosomia
o fibroids
o twins
o Rh incompat. – MC cause of hydrops faetalis
o ABO incompat.
- abdomen small for date (fundus < age)
o wrong date
o small baby – in fetal malform.
o oligohydramnios – in fetal malform.
o IUGR
- CTG
o usually performed after 26 weeks (before, not very accurate)
o not usually done
not superior to intermittent auscultation
has not decr. the incidence of cerebral palsy or other neonatal dev. anomalies
rarely a predictor of previous fetal oxigenation – unless profoundly abnormal
poor predictor of current fetal oxigenation - unless profoundly abnormal
o indic
high risk pregnancy: HT mom, DM, etc.
overdue pregnancy > 40 wks (2 times / week)
if on oxytocin
if color of water is brown or green
if bad baby heart beats
o SE
increases the risk of obstetric intervention (instrumental delivery, C-section)
o 2 lines:
above - baby’s heart
below - uterus contractions
o we check fetal heart rate, fetal movements and uterine contr. to identify the presence
of fetal hypoxia
1. baseline FHR = mean level of FHR when this is stable (excluding accelerations
and decelerations)
normal: 110-160 (150?)
<110 bradycardia
- incr. vagal heart tone
- fetal heart block
- cord compression
- fetal hypoxia
>150 tachyc.
- fetal inf.
- fetal hypoxia
- maternal fever
> 200 – fetal arrhythmia
2. baseline variability – minor fluctuations of baseline
normal: 5-25 (10-15?)
reduced or incr. = fetal dystress
lost:
- pre-term fetus who is sleeping
- drug effect – diazepam, morphine
incr.
- maternal fever, drugs, hypoxia
3. accelerations
transient incr. in FHR > 15 bpm lasting at least 15 sec
simultaneous with the uterine contr.
usually present (normal) – at least 2
- if absent, baby might be sleeping
wake up baby, then repeat CTG
4. decelerations
transient decr. in FHR lasting at least 15 sec
a. early – start before the uterus contr., coinciding with uterine contr.
- normal, due to incr. vagal tone in response to uterine contr.
(HEAD compression)
c. variable
- sign of UMBILICAL CORD compression
Rx – change position of the mother
- if severe = severe fetal compromise
b. late (PLACENTA)
- sign of fetal hypoxia (utero-placental insufficiency) -> rule out
placental abruption!
Rx - C-section
- if persistent = severe fetal compromise
o types of results
normal antenatal CTG
baseline FHR = 110-160
variability of FHR – 5-25
decelarations are absent or early
accelerations 2 within 15 mins
- normally present
- if absent, baby might be sleeping
wake up baby, then repeat CTG
stress CTG (in labor)
normal
- baseline FHR 110-160
- variability 5-25
- decel. absent or early
- (accelerations are not considered during labor – their
significance is unknown)
non-reassuring pattern – one of the following features is present:
- baseline FHR 100-109 (slight bradycardia) or 161-170 (slight
tachycardia)
- variability is reduced to 3-5
- variable decelerations
- Mx
non-reassuring pattern in I stage of labor
reposition the woman (left, right position)
give O2 via face mask
if she was on oxytocin, slow it or stop it
-> then check CTG again
o if it didn’t improve -> perform fetal
scalp blood sampling (with
amniotomy)
if ph<7.2 -> C-section
abnormal CTG – 2 of the features in the non-reassuring type are present
or
- baseline FHR< 100 or >170
- variability is absent (<3) = monotonous trace
- late decelerations (especially prolonged > 3 min)
=> immediate delivery
vaginal – if cervix is fully dilated
C-section – if cervix is not fully dilated
most ominous – indicating severe fetal compromise
- 1. persistent late decelerations - worst
- 2. severe variable decelerations
- appendicitis in pregnancy
o Dx
difficult, due to:
the displacement of the appendix by the enlarged uterus – higher the
later the condition occurs during pregnancy
tenderness more difficult to localize, since appendix is behind the large
uterus
confusion with other dis.
- UTI
- hyperemesis gravidarum
- right ovarian cyst complic.
- red degen. of fibroid
- small concealed placental abruption
o Rx – appendicectomy
- DVT in pregnancy
o anticoag. throughout pregnancy
use heparin instead of warfarin
heparin = large molecule => cannot cross the placenta (no anticoag.
effect on the baby)
reversal of its anticoag. effect can be achieved faster than for warfarin
warfarin
SE
- cannot be used in the first trim. (teratogenic)
could be used during weeks 13-36, but its effect is
slower to reverse
- incr. miscarriage risk
- incr. stillbirth
- incr. neurol. problems in the baby
- crosses the placenta and has anticoag. effect on the baby as
well -> incr. haemor. in mother and baby
o 6 weeks post-partum heparin
- impaction of a retroverted uterus (e.g. 16 wks - MCQ)
o Sx
lower abd. pain, urinary ret.
- thrombocytopenia
o causes
incidental thrombocytopenia of pregnancy– MC
not significant unless < 50x109/L
pre-eclampsia – when severe = HELLP syndr.
immune thrombocytopenia
SLE
- maternal mortality
o 1:10.000 in Aus.
o causes
primary pulmonary HT – 50% die during pregnancy or puerperium
severe pre-eclampsia and eclampsia
PE
postpartum haemorrhage
5. amniotic fluid embolism
anesthetic accidents
- IUGR
o part least affected is the brain
o can be
asymmetric
MC
due to placental dysfc.
biparietal head diameter (BPD) is the last one to be affected
symmetric
more rare
causes
- intraut. inf.
- other intraut. abnormalities
biparietal head diameter (BPD) is reduced along with the other
dimensions
- premature delivery
o causes
incr. uterine size
macrosomia
polyhydramnios
multiple pregnancy
shortened cervix < 1.5 cm
open cervix, especially if:
the internal os is open
bacterial vaginosis is present
Hx of premature delivery
o Dx
fetal fibronectin test on cervical secretions is positive, even if the cervix is
closed – most conclusive!
Postpartum pathology
- postpartum haemorrhage
o causes:
1. MC cause = uterine atony
causes:
- previous atony
- big uterus / baby: polyhydramnios, macrosomia, twins, big
fibroids
- after prolonged / obstructed labor
- old age mother
- halothen anesthesia
- oxytocin can cause it
Sx
- massive bleeding
Rx.
- for atony
oxytocin IV
massage the uterus
if failed -> (step ladder approach)
ergometrine
bilat uterus compress. for 3 min
PGs
uterine artery ligation
hysterectomy
- for the bleeding
IV fluids + O2, pulse/BP monitoring every 15 min
urinary catheter – monitor urine output
2. retained placenta – baby was born normal + bleeding
second MC cause of bleeding
Rx – step-ladder approach
- oxytocin drips
- curretage under GA
- uterine artery ligation
- hysterectomy
3. laceration – same as above + placenta delivered normal + BP 80/60
in precipitated (fast) labor (e.g. 4 hrs), elderly grand-multigravida
contracted uterus
4. DIC, cogulopathy
contracted uterus in 3 and 4 (excludes 1 and 2)
5. uterine inversion
due to overtraction on the cord or Dubin expression of the placenta
w/o waiting for firm uterine contr.
placental delivery then vaginal bleeding + profound shock, out of
proportion with the bleeding (due to autonomic stimution caused by
drawing the ovaries and their nerve supply)
pain is not very severe (more shock)
can lead to death through shock + haemorrhage
Rx
- immediate replacement of the uterus
manual
if uterus is firmly contracted – use hydrostatic method
- if unsuccessful - surgery
6. uterine rupture
Hx of C-section + prolonged labor + late second stage: suddenly
bleeding (no delivery of baby)
- the bleeding might not be important (concealed bleeding)
- shock out of proportion with the bleeding (like in inversion)
can also occur after a normal stage 3 (abnormal stage 3 – pulling on
the cord -> inversion)
MC in grand multipara, when delivering a large baby
7. amniotic fluid embolism
very very rare
amniotic fluid, fetal cells, hair, or other debris enters the mother's blood
stream via the placental bed of the uterus and triggers an allergic
reaction. This reaction then results in cardiorespiratory (heart and lung)
collapse and coagulopathy.
On the list of causes of maternal mortality, it is fifth
Sx
- massive bleeding
- convulsions, coma, death
o Dx
evaluation of blood loss with
observation of clotting and estimation of blood clotting time by the
bedside -> giving the most info in the shortest time
- does not clot or clotting time > 8 min – pathol.
FBE – Hb: useful only when low
coag. profile (platelets, fibrinogen, APTT, prothrombin time – PT) –
takes 30-60 min to assess
D-dimers or fibrin degradation product (FDP)
- puerperium – up to 6 weeks after delivery
o vascular and lymphatic engorgement of the breasts
o colostrum secretion: 2-3 days -> then milk secretion
o transient leucocytosis
o lochia - post-partum vaginal discharge, containing blood, mucus, and placental tissue.
Lochia discharge typically continues for 4 to 6 weeks after childbirth
It progresses through three stages:
Lochia rubra (or cruenta) is the first discharge, red in color because of
the large amount of blood it contains.
- It typically lasts no longer than 3 to 5 days after birth.
Lochia serosa is the term for lochia which has thinned and turned
brownish or pink in color. It contains serous exudate, erythrocytes,
leukocytes, and cervical mucus.
- This stage continues until around the tenth day after delivery.
Lochia alba (or purulenta) is the name for lochia once it has turned
whitish or yellowish-white. It contains fewer red blood cells and is
mainly made up of leukocytes, epithelial cells, cholesterol, fat, and
mucus.
- It typically lasts from the second week through the third to
sixth week after delivery.
- puerperal fever / sepsis
o > 38 degrees
o > 24 hrs
o from end of day 1 – end of day 10
o causes
3 Bs
birth canal – endometritis
- post-partum endometritis or pyrexia (fever, tender uterus,
foul smelling lochia):
ampicilin (or amoxycylin) and metronidazol
if not improving, add gentamycin
breast - mastits
bladder – UTI
+ DVT
MC
UTI – E.coli
breast inf – staph. aureus
wound inf. – if C-section
less common
genital – endometritis – strepto.
DVT?
o Dx
U/S: bulky uterus
inspection of lower tract for infected tears or lacerations
MSU for microscopy, culture, sensitivity
vaginal swab
signs of mastitis
o Rx
1 - init. empirical: penicilin + metronidazole + gentamycin
after result, adjust for sensitivity
- after birth - http://en.wikipedia.org/wiki/Fetal_circulation
o umbilical vein closes and becomes ligamentum teres
o closure of the ductus venosus
o lateral umbilical artery becomes lateral umbilical ligament
o ductus arteriosus is closing due to increased local PG
o increased venous return from the lungs causes pressure to increase in the left atrium,
which closes the foramen ovale flap valve
o opening up of the lungs cases a massively increased pulmonary artery blood flow
Congenital anomalies
o eyes far from each other (wide palpebral fissure + wide philtrum + wide face): Down,
chromosomal anomaly
o eyes close to each other (short/narrow palpebral fissure + short/narrow philtrum +
narrow face / microcephaly): alcoholism
- Down syndrome
o types
95% - trisomy 21, due to failure of disjunction (separation) during meiosis
5 % - can be:
translocation involving chromosome 21
- often inherited, risk of recurrence = 10%
mosaicism
o risk factors
increased maternal age
o incidence
20 yrs – 1:2000
30 yrs – 1:700
35 yrs – 1:400
37 yrs - 1:250
40 yrs – 1:100
43 – 1:50
we say increased risk if > 1:300
risk of recurrence = 1%
o Sx
varying degrees of intellectual impairment and dev. delay
premature ageing and Alzheimer-like changes in the brain develop in mid life
(4th - 5th decades)
head
moon-shaped face, with small mouth and teeth
transverse furrowed tongue, high arched palate
sloping / oblique palpebral fissures and epicanthic folds
flattened occiput and face
short squat nose
sparse, coarse hair
hands
short and broad, with hyperextensible fingers
abnornalities of the thumb and little finger
single transverse palmar crease
hypotonia, hyperreflexia
gentle and good natured temperament, lively and affectionate, cheerful and
sociable, with affinity for music, dance, rhythm
associated dis.
very frequent: atlanto-axial subluxation -> sports are CI
- Dx – cervical spine x-ray
congenital heart malformation (septal defects)
duodenal atresia
o screening
first trimester – combined test – triple test:
1. 11-12 wks - U/S – nuchal translucency (if thick > 2 mm: Down; not
compulsory: normally just at 18 wks, at 13 wks woman would have to
pay for it)
10-12 wks – blood tests:
- 2. Beta HCG incr.
- 3. plasma protein decr. – PAPPA (pregnancy associated plasma
protein …)
second trimester
15-18 wks – triple or quadriple test
- 1. beta HCG incr.
- 2. alfa fetoprot. decr.
- 3. unconj. estriol decr.
- 4. inhibin A incr. - optionally
high risk mother: old mother, previous Down, etc. -> invasive methods
amniocentesis – 15-18 wks
- most accurate
- abortion rate: 1 in 200
chorionic villus sampling – 9-11 wks
- less accurate
- abortion rate: 1 in 100
- neural tube defects: AMC clinical assessment p. 105-106
o types:
spina bifida
Dx - U/S can be seen at 16-18 wks
incr. alfa-fetoprot. in mother at 12-15 weeks (screening only – not
diagnostic)
- amniocentesis - incr. alfa fetoprot.
anencephaly
happening during 5-8 wks
Dx - U/S can be seen at 11-12 wks
women are offered the option to
- terminate
- continue the pregnancy
MC Cx = polyhydramnios
o incidence = 1:1000
o recurrence if not taking folate = 2-5%
screening in subsequent pregnancies: alfa fetoprot. in maternal serum at 16
wks
o prevention
folic acid - up to 12 wks
0.5 mg / day
5 mg / day – if:
- previous neural tube defect
- on antiepileptic drugs
- DM?
vit. B (B6, B12)
vit. D
- cleft palate, cleft lip
o MC cranio-facial malform.
o causes
benzodiazepine
antiepileptics - carbamazepine
amphetamines
Rubella
genetic factors
Kalman syndr.
smoking
alcohol
- alcohol abuse
o from 80 g alcohol / day => fetal alcoholic syndrome
microcephaly
mental retardation
poor muscle tone
short palpebral fissure
long and smooth filtrum
underweight till puberty
short stature
septal defect
facial hypoplasia
joint deformities
low IQ
attention deficit
forebrain malform.
- cocaine abuse
o IUGR
o placenta abruption
o premature labor
o still birth
o intraventr. haemor.
o developmental delay
o stillbirth
o teratogenic effect not proven
- fetal malformations can be assoc. with umbilical cord vessel anomalies
o N – 2 arteries, 1 vein (3 vessels)
o MC anomaly assoc. with fetal malformation = only 2 vessels in the cord
1 artery + 1 vein – the baby can survive
otherwise – stillbirth in the first trim.
Antenatal care
o first antenatal checkup
confirm pregnancy
FBE
blood group, RH, Coombs test
blood sugar level
random
fasting
MSU, urine analysis, electrolytes
LFT
inf.
rubella
hep. B
HIV
syphillis - VDRL
CMV
- consider varicella, hep. C
o Hb electroforesis – thalassemia
o for gestational DM
screening test is glucose challenge test (non-fasting) at 26-28 wks (not OGTT)
N=8
> 8 is abnormal -> then do OGTT (fasting)
- also do OGTT if high risk: previous Hx of gestational DM, DM,
family Hx of DM or gestational DM, Hx of macrosomia, PCOS,
glycosuria
insulin requirements
incr. in last trimester
decr. just after the delivery
foetal hypoglycemia
should be checked @ 4 hrs after delivery or after second feeding,
whatever comes first
o international travel
after 28 wks – better to avoid
after 36 wks – prohibited
o pregnancy + cardiac dis.
never give ergometrine
don’t put in lithotomy position
watch for fluid balance
o VSD in pregnancy
if only VSD – can go for vaginal delivery
if VSD + transverse lie – C-section
o >= 42 wks (41 wks + 6 days) = postdated pregnancy
induction and C/S then
U/S – check amniotic fluid index – N > 5
CTG – if CTG abnormal, do pH test (foetal scalp)
meconium stained indicated foetal distress
we have to do CTG before Dx of foetal distress
pH < 7.2 = foetal hypoxia
- have to check cord prolapse too
o after ROM – check for cord prolapse
o C/S in
breech pres.
foetal distress
labor progress is low
Labor
contractions:
before 30 weeks: small localized contractions every 1 min + higher amplitude contraction every 30-30
min
after 30 weeks: more intense (Braxton Hicks contractions)
after 36 weeks: increasing progressively until labour starts
labour starts: 1 contraction every 10 min, lasts 20 sec
late labour: 2-4 contractions every 10 min (1 every 2-4 min), last 40-90 sec
contractions still occur for 48 hrs after delivery, with decreased frequency
cervix dilatation:
anytime after 34 weeks, but usually later (especially in primigravidae)
dilatation of min. 1 cm/h during labor
onset of labour: dilatation of cervix more than 2 cm + painful contractions at least every 10 min and with
increasing frequency
stage I – till complete cervical dilatation (10 cm); only passive uterine contractions
- has a:
o passive phase
o active phase – from cervix dilated 3-4 cm to fully dilated; cervix dilates faster,
contractions become more painful
stage II – till birth: passive uterine contractions + active abdominal contractions
- if it lasts more than 2 hrs -> vacuum extraction or forceps
stage III: placenta expulsion: 15-30 min after the birth of the baby
wait 2-3 min after birth before clamping the umbilical cord
- labor
o epidural – up to 7 cm dilatation
o monitoring of fetal well being
uncomplicated labor – intermittent auscultation (stethoscope with Doppler)
complication - CTG
o There are 3 signs of the onset of labor:
A bloody show
passage of a small amount of blood or blood-tinged mucus through the
vagina near the end of pregnancy
It can occur just before labor or in early labor as the cervix changes
shape, freeing mucus and blood that occupied the cervical glands or
cervical os
Rupture of membranes (waters breaking)
Onset of contractions
st
o 1 stage
starts when
cervix is at least 2 cm dilated
contr. become painful and regular, at progressively shorter intervals
(3-5 min), and lasting > 1 min
duration
average 8.25 hrs in nulliparae, 5.5 hrs in multipare
phases
a. latent: onset -> 4 cm dilat.
b. active: 4 cm -> 10 cm dilat.
- 1 cm / hr dilatation
pulse, temp., BP every 2 hrs
monitor contr.
monitor FHR every 15 min
PV exam every 4 hrs
if ROM – check for cord prolapse
every woman should receive Syntometrine (ergometrine + oxytocin), to
promote contr.
minimize bleeding (16 x less)
nd
o 2 stage – begins when the cervix is fully dilated
duration
< 45 min – multiparous (average 15 min)
< 2 hrs – nulliparous (average 1 hr)
> 2 hrs – can be:
- 1. obstructed labor - very low chance the woman will deliver
naturally
if on epidural (no urge to push) we can wait up to 3 hrs
causes:
pelvic swellings: ovarian tumors, fibroids,
ectopic pelvic kidney, very distended urinary
bladder
o (not cystocel or rectocel – are soft, can
easily be pushed out of the way)
cephalopelvic disproportion
large baby: DM, hydrops, etc.
postterm pregnancy
MCQ: MC finding = 4 cm of head is palpable in the
abd., although the bony head is at the ischial spines on
pelvic assessment
Rx
if good contr. -> assisted delivery
o forceps
more traumatic for mother
incr. in vaginal tears
incr. need for episiotomy
not for the baby
o vacuum extraction
more traumatic for the baby
The baby may be left with a
temporary lump on its head,
known as a chignon.
A possible cephalohematoma
formation, or subgaleal
hemorrhage
if not effective contr. -> give oxytocin drips
o if effective contr. -> assisted delivery
o if still not effective -> C-section
if cephalopelvic disproportion: C-section
e.g. shoulder dystocia
after the delivery of the head, the anterior
shoulder of the infant cannot pass below the
pubic symphysis, or requires significant
manipulation to pass below the pubic
symphysis. It is diagnosed when the shoulders
fail to deliver shortly after the fetal head.
In shoulder dystocia, it is the chin that presses
against the walls of the perineum.
causes
o with a large baby (DM) - MC
o postterm pregnancy – MC
o mid-forceps delivery
Rx – various manouvers – MC – McRobert’s
manouver
Cx
o Shoulder dystocia is an obstetrical
emergency, and fetal demise can occur
if the infant is not delivered, due to
compression of the umbilical cord
within the birth canal
o The major concern of shoulder
dystocia is damage to the upper
brachial plexus nerves.
Klumpke paralysis - form of
paralysis involving the muscles
of the forearm and hand,
resulting from a lower brachial
plexus injury in which C8-T1
nerves are injured - affects,
principally, the intrinsic
muscles of the hand and the
flexors of the wrist and fingers
+/- dilators of the iris and
elevators of the eyelid (both of
which may be seen in the case
of associated Horner's
Syndrome). The classic
presentation of Klumpke's
palsy is the “claw hand” where
the forearm is supinated and
the wrist and fingers are
hyperextended. If Horner
syndrome is present, there is
miosis (constriction of the
pupils) in the affected eye
Erb's Palsy - paralysis of the
arm caused by injury to the
upper group of the arm's main
nerves, specifically the upper
trunk C5-C6 is severed - loss of
sensation in the arm and
paralysis and atrophy of the
deltoid, biceps, and brachialis
muscles. The position of the
limb, under such conditions, is
characteristic: the arm hangs
by the side and is rotated
medially; the forearm is
extended and pronated. The
arm cannot be raised from the
side; all power of flexion of the
elbow is lost, as is also
supination of the forearm. The
resulting biceps damage is the
main cause of this classic
physical position commonly
called "waiter's tip." Risk
factors – breach presentation,
shoulder dystocia
- 2. inefficient or incoordinate labor
Feature on PV exam. Obstructed labor Inefficient or incoordinate
labor
Moulding of fetal head ++ Usually none
Caput formation on the fetal ++ +/-
head
Cervical oedema Anterior lip oedema Usually none
Fetal tachycardia ++ and progressive +
Station of fetal head – relation Just at or above the ischial Can be above or below the
of the lowest part to the spines ischial spines
ischial spines
Amount of head palpable > 2 finger breadths Usually < 1 finger breadth
above the pelvic brim when (most important feature)
the lower point of the head is
at the ischial spines
monitor FHR every 5 min
if FHR falls < 100 + for > 2 min => PV (cord prolapse?)
monitor contr. – normal: 60-90 sec every 2-4 min
if not good, give oxytocin
rd
o 3 stage
duration
15 min in both nulliparae and multiparae (90%)
if still not delivered after 15 min
- encourage contr. by rubbing the uterine fundus
- no effect => manual removal
MC SE = uterine inversion
o total duration of labor:
9.5 hrs in nulliparae
6 hrs in multiparae
o cardinal movements of labor:
engagement
descent
flexion
these first three occur simultaneously
internal rotation
extension
external rotation
expulsion
o sign of progress of labor
incr. strength, duration and frequence of the uterine contr.
descent of fetal head into the pelvis
rotation of the fetal head (occipito-transverse to occipito-anterior) on abd.
palpation
best sign of progress – progressive increase in cervical dilatation
with effacement (shortening) of the cervix
rotation of the fetal head (occipito-transverse to occipito-anterior) on pelvic
exam.
descent of head within and through the pelvis
above the spines -> spines level -> below spines -> coccyx -> vulva
- induction of labor
o indic.
prolonged pregnancy > 42 weeks
hypertensive disorders in pregnancy
pregn. induced HT
pre-eclampsia
eclampsia
PROM
intrauterine foetal death
IUGR
antepartum haemor.
isoimunisation
ABO
Rh
o CI
absolute
cephalopelvic disproportion
placenta praevia
vasa praevia
foetal distress
previous classical C-section (not low segmental)
invasive cervical CA
cord presentation
some abnormal presentations
- breech pres.
complete – ok (bent knee)
frank – ok (knee extended)
incomplete – NOT OK (with feet down)
o when to start: when cervix is ready / favorable -> assesed with Bishop score
1. cervix dilatation
2. cervix length
3. cervix consistency
4. cervix position
5. head station (in raport to ischial spines)
0 1 2 3
Dilatation (cm) <1 2 3 >4
Length (cm) >4 3 2 <1
Consistency Firm Mild Soft
Position Post. Ant. Central
Head station -3 -2 -1 >0
score 0-4 – cervix not ready for induction (very high risk to fail induction)
score at least 5 to start induction (with amniotomy)
o procedure:
start with intravaginal prostaglandin gel
PG E2 – dynoprostone – for alive baby
PG F2 alpha – dynoprost
- indic.
dead foetus
missed abortion
termination of pregnancy
evac. of hydatidiform mole
wait until cervix will be ready (if no foetal distress), with Bishop score >=5
then, do amniotomy
SE
- cord prolapse
- inf.
after amniotomy, deliver within 5-8 hrs
after amniotomy, use oxytocin infusion (drips) to promote contr.
then proceed with normal delivery
- malpresentations
o breech presentation
15% at 30 weeks, but only 3% at birth
incr. risk for the fetus
- due to
intracranial haemor.
asphyxia
fractues of humerus, femur or clavicle
- preterm and lart postterm babies – mortality 12%
- term babies – mortality 1%
types
- with extended legs (frank) – 65-70%
- with flexed legs (complete)
- footling (incomplete) – one foot comes first (rare)
Rx
if still breech pres. at 37 wks, attempt cephalic version - easier if the baby has
flexed legs
ext. cephalic version @ 36 wks or end of 37 week + tocolytic
CI
cephalopelvic disproportion
placenta praevia
multiple pregnancies
antepartum bleeding
Hx of uterine scar, HT, bad obstetric Hx
PE
Hx if unstable lie
small for date baby
absolute indic.
shoulder presentation
face presentation
risk of cord prolapse: first do PV to exclude cord prolapse
- Rx
if the cord is still puslating, push the presenting part
and the cord as far in as possible
place mother in knee – chest position
urgent delivery
C-section – preferred
vaginal delivery with forceps or vacuum
extraction, avoiding cord pressure
- C-section – preferred, with decr. perinatal mortality (from 1.15% to 0.6%)
- normal delivery can also be used
baby with normal size
complete breech or extended legs
eyebrow presentation
head flexed
CPD excluded
labor onset spontaneously
e.g. if unexpected breech presentation with full cervical dilatation
with insufic. time to organize a C-section
o transverse or oblique presentation
may convert to a longitudinal one later on
Dx – 1st - U/S to rule out placenta previa (this is what might be causing the baby
to have this presentation, prevents him from having a cephalic presentation)
Mx
- at 36 weeks – cephalic version
- > 36 weeks: wait for normal labor
if beyond 37 wks (term) best Mx is C-Section
- malpositions
o types
occipito-posterior – MC
11 cm (vs. 9.5 for normal position)
assoc. with poor quality uterine contr.
- if this is excluded – cephalopelvic. disproportion
incoordinate uterine action almost always occurs => incr. fetal distress
- CTG is recommended for monitoring
- even more common when oxytocin and epidural were used
in this case CTG is mandatory
slow labor
- Rx
labor can be stimulated with
amniotomy
oxytocin
epidural is often necessary
C-section may be necessary in case of obstructed labor
or fetal distress
occipito-transverse
(occipito-ant. = N)
face
brow
o Rx
if no other problems – vaginal delivery in most of them (especially in occipito-
post. and occipito-transverse)
exception: face – vaginal delivery may be impossible => C-section
C-section – in prolonged labor with maternal exhaustion, obstructed labor, CPD,
fetal distress, selected primigravida
- anesthesia
o epidural
the anaesthetist conducting an epidural places the catheter in the mid-lumbar,
or lower back region of the spine.
In adults, the spinal cord terminates around the level of the disc between L1 and
L2 (in neonates it extends to L3 but can reach as low as L4), below which lies a
bundle of nerves known as the cauda equina ("horse's tail"). Hence, lumbar
epidurals carry a very low risk of injuring the spinal cord.
A common solution for epidural infusion in childbirth or for post-operative
analgesia is 0.2% ropivacaine or 0.125% bupivacaine, with 2 µg/mL of fentanyl
added. This solution is infused at a rate between 4 and 14 mL/hour, following a
loading dose to initiate the nerve block.
CI (purple book)
previous surgery to the vertebrae in the area
skin infection near the point of intended insertion
significant maternal haemorrhage (it may make the extent of
haemorrhage more difficult to assess)
Bleeding disorder (coagulopathy) or anticoagulant medication (e.g.
warfarin) - risk of spinal cord-compressing hematoma
- e.g. thrombocytopenia < 40.000/mm3
cardiac condition (e.g. primary pulmonary HT) where the heart cannot
cope with the vasodil. caused by the epidural
severe fetal distress – better to give GA and expedite the delivery
SE
slows down the labor significantly
bloody tap
Neurological injury lasting less than 1 year (rare, about 1 in 6,700)
Epidural abscess formation (very rare, about 1 in 145,000).
Epidural haematoma formation (very rare, about 1 in 168,000).
Neurological injury lasting longer than 1 year (extremely rare, about 1 in
240,000).
Paraplegia (1 in 250,000).
Arachnoiditis (extremely rare, fewer than 1000 cases in the past 50
years)
Death (extremely rare, less than 1 in 100,000).
o pudendal anasthetic block
produced by blocking the pudendal nerves (which arise from S2,3,4) near the
ischial spine of the pelvis
a local anesthetic such, as lidocaine or chloroprocaine (Lidocaine is usually
preferred for a pudendal block because it has a longer duration than
chloroprocaine which usually lasts less than one hour), is injected into the
pudendal canal where the pudendal nerve is located.
This allows quick pain relief to the perineum, vulva, and vagina. A pudendal
block is usually given in the second stage of labor just before delivery of the
baby. It relieves pain around the vagina and rectum as the baby comes down
the birth canal. It is also helpful just before an episiotomy.
- oxytocin
o SE
MC: uterine hypertonus and tetany => fetal distress
water intox.
uterine rupture – in multiparous
rare
hT
o CI – if cervix is closed
- Apgar score
o at 1 and 5 min
0 1 2
Appearance / color Absolutely blue Centrally pink, Pink
peripherally blue
Pulse / heart rate Absent < 100 > 100
Grimace / response to No response Some facial Cries
stimulation (place grimace
suction catheter in the
nose of the child)
Activity / muscle tone Limb, floppy, flacid, Some flexion Good active
hypotonic movement
Respiration effort Absent Gasping, irregular, Normal good
slow crying
good > 7
How ready is this child =
heart rate
resp. effort
irritability
tone
colour
low score at 1 and 5 min => the child needs resuscitation
causes
significant hypoxia
perinatal asphyxia
etc.
Apgar score
Gynecology - OK
Breast pathology
- mastalgia
o 30-50 yrs (MC 35-45 yrs)
o causes
MC cause – cyclical mastalgia
pregnancy
caffeine
breast CA
< 10%
e.g. mastitis carcinomatosa – red and hot breast, during lactation
fibroadenoma
mastitis
drugs
OCP
HRT – diffuse bilat. pain
- Rx – estr. dose should be reduced
theophylline
o types
diffuse, bilat. and cyclical = cyclical mastalgia
30-50 (35) yrs
hormonal basis
causes
- MC = benign mammary dysplasia (fibroadenosis, chronic
mastitis, cystic hyperplasia, fibrocystic breast dis.)
30-50 yrs
Dx
mammogram – if diffuse lumpiness > 40 yrs
o shows calcifications
U/S
biopsy
Mx
large cysts - aspiration
Sx
- pain in the breasts (mid-cycle till the end of the period) and
feeling of lumpy breasts
pain extend down the inner aspect of the upper arm
- possible - straw-like or green grey discharge from the nipple
- breasts diffusely nodular or lumpy
Rx – Murtagh 969
- mild
reassurance
rule out the fear of CA in the patient
analgezic (paracetamol)
lifestyle advice
low fat, eliminate caffeine
wear good quality, comfortable bra
lose wt.
- moderate
mefenamic acid (NSAID - inh. of PG synthesis)
add vit B1, Vit B6
(primrose oil – contains an essential fatty acid - Awad)
- no response
danazol (progestogen = modified testosterone – inhibits
the ovarian synthesis of estr.)
norethisterone – progestogen
diffuse, bilat. non-cyclical mastalgia
poorly understood
causes (maybe)
- duct ectasis
- periductal mastitis
Rx
- much more difficult to treat
- exclude caffeine, wt. loss
- vit B1, Vit B6
- norethisterone – progestogen
unilat. difuse non-cyclical
mastitis – cellulits of the interlobular connective tissue
- in lactating women with
cracked nipple
poor milk drainage
- causes
bact
MC cause – staph. aureus coagulase-positive
o Rx
flucloxacilin
erythromycin
E. coli
candida – after A/B
severe breast pain (hot knife, hot shooting
pains)
- Sx
a sore lump at first
then red tender area
fever
- Cx – breast abscess
if persisting > 48 hrs + area of tense induration
develops
Rx
surgical drainage (under GA) or aspiration with
a large bore needle (under LA)
A/B
- Rx
breastfeeding should continue (milk production not
affected)
empty the breast well
flucloxacilin
or cephalexin
for candida – fluconazole
or nystatin
localised
costochondritis (Tietze’s syndrome)
- constochondral junction becomes strained in persistent cough
- palpable swelling about 4 cm from sternal edge (enlargement
of the costochondral cartilage)
- initiated or aggravated by deep breathing and coughing
- self-limiting – may take a few mths
- Rx – infiltration with local anesthetic and C/S
o Dx
mammography > 40 yrs
U/S – for localised pain
not useful in postmenopausal breast – fatty and looks like CA
excision biopsy – in lumps
- nipple discharge: breast CA can produce any tipe of discharge!
o bloody discharge
one breast – benign
both breasts – probably malignant
intraductal papiloma
intraductal carcinoma
mamary dysplasia
o green-grey
mamary duct ectasia (green toothpaste)
mamary dysplasia
o yellow
mamary dysplasia
intraduct. carcinoma (clear, serous)
breast abscess (pus)
o milky white
lactation cyst
lactation
hyperprolactinemia
drug induced e.g. chlorpromazine
o straw like color
fibroadenosis
- cracked nipples
o cause
wrong breastfeeding
aggressive suckling by the baby
o Mx
teach appropriate breastfeeding technique
continue breastfeeding
even in mastitis and with breast abscess, from both breasts
CI – HIV
- breast lumps
o mamary dysplasia – 32%
o fibroadenoma – 23%
15-35 yrs
types:
juvenile – soft, rapidly-growing tumor
adult
Rx
firm, smooth and mobile (“the breast mouse”)
Dx
U/S
FNAC
o carcinoma – 22%
o cysts – 10%
40-50 yrs
assoc. with mammary dysplasia
regress after menopause
Dx
for breast cyst – 1st test is always U/S!
mammography
FNAC
MCQ: 45 yrs, painful solid lump in the breast – breast cyst (tense)
rapid growth – pain
o breast abscess - 2%
o mammary duct ectasia
looks like CA
a whole breast quadrant is indurated and tender
toothpaste-like nipple discharge
Rx – widespread linear and globular calcif.
Dx/Rx - surgery
o duct papilloma
not premalignant
bloody discharge
Rx – excision of duct and affected breast segment
o lactation cyst (galactocele)
Rx - aspiration
o Paget’s syndrome of the nipple
o fat necrosis
after large bruise or trauma (e.g. protracted breastfeeding)
with skin and nipple retraction
looks like CA
it usually disappears
Dx – excision biopsy
- breast CA
o MC CA in women
o lifetime risk: 1 in 11 women in Aus.
1 in 11 women will develop CA by age 75 – max around 60 yrs
o 1 in 25 women die of breast CA
o incidence rises with age and incr. in higher socioeconomic class
o types
MC - non-invasive: intraductal CA
invasive
invasive duct carcinomas – 90%
lobular carcinoma
etc.
o risk factors
sex -100 x more common in women
Caucasian race
low in Asian countries
age:
> 40 yrs (uncommon under 30 yrs)
- mean age of Dx = 60 yrs
greatest risk – positive familial Hx
first degree relatives (mother, sister, daughter) with breast CA,
especially < 50 yrs: highest risk (risk incr. 3x)
strong predisposition from mutations in the genes BRCA1 and BRCA2
personal Hx
Hx of breast CA
- including carcinoma of the other breast
Hx of benign proliferative dis. or lumps - especially mammary displasia
(with cellular atypia)
hormonal facts:
early menarche
late menopause (>53)
nulliparous at 40 yrs – one of the most offending risk factors
- having the first child over 30 yrs
no breastfeeding
HRT > 5 yrs
obesity after menopause
alcohol
ionising radiation
o not risk factors:
OCP
smoking
sedentarism
o screening
monthly self-examination
false positive rate is high < 40 yrs
recommended > 35 yrs
mammography
at least every 2 yrs for all women 50-70 yrs
+ 40-49 yrs – on demand
specificity = 90%
in high risk genetic inheritance pattern: Murtagh 982
monthly self-examination
> 40 yrs - at least annual GP exam.
mammography every 2 yrs > 50 yrs
aspiration of cysts
mammography, U/S and FNAC to Dx any localised mass
U/S for young dense breasts
o Sx
lump: painless, hard, irregular, attached or fixed to underlying tissues or sking
(dimpling)
< 10% with pain
nipple changes: retracted (not inverted), distortion, discharge (blood stained)
skin: dimpling, peau d’orange
Paget’s syndrome of the breast – Dx diff. with eczema
Paget’s syndrome Eczema
Unilat. Bilat.
Older patients Reproductive years / lactation
Possible nipple discharge No discharge
Not pruritic Pruritic
No pustules Pustules
Deformity of the nipple Normal nipple
Possible palpable lump No lump
spread:
local
- skin
- muscles
regional
- I - axillary lymph nodes
- internal mammary
- supraclav. nodes (right side)
(left – gastric; small percentage of gastric – to right as
well)
distal
- 1 - other breast
- 2 - bones
- brain
- liver
- lung – cannonball metastases (many round m.)
o Dx
tripple test
clinical exam.
imaging: mammography +/- U/S
FNAC +/- core biopsy
approach:
< 35 yrs – bilateral U/S
- U/S
in dense breasts (< 35 yrs) especially with cysts
for Dx diff between solid lump and cyst
palpable masses at the periphery of breasts (not
screened with mammography)
> 35 yrs - bilateral mammography + U/S
- mammography
established benefit over 50 yrs!
possible benefit in the 40s
pattern: irregular infiltrating mass with focal spotty
microcalcif.
if
- cystic -> aspirate
- solid -> fine needle biopsy -> only cytology (cannot Dx CA) –
surgeon does this
for
cyst aspiration
solid lumps
90-95% accuracy – better than mammography
indic. for biopsy or excision of lump:
cyst fluid is bloodstained
the lump doesn’t dissapear completely with
aspiration
the swelling recurs within 1 mth
- unsure/suspicion of CA: core biopsy -> histology (can Dx CA) –
radiologist does this under U/S guidance
FNAC cannot distinguish between in situ and invasive!
core biopsy can do that
tumor markers
estr. receptors – in 2/3 of breast CA
- good prognostic factor
progesterone receptors
o Staging
Manchester
I - confined to the breast
II - confined to breast + palpable mobile axillary lymph nodes
III - skin changes (fixation, cutaneous ulcers, peau d’orange) + fixed
axillary nodes, supraclav. nodal involv.
IV - distant metast.
o Rx
workflow (dr. Gaya)
a. for younger women - wide local excision (quadrantectomy), with a 1
cm margin
- “sentinel node” procedure to detect if the first node draining
from the breast (santinel node) is involved
single most powerful predictor of subsequent
metastases and death = lymph node involvment
radioisothopic dye injected at nuclear medicine the day
before the surgery + the day of the surgery we inject
some blue dye close to the nipple:
we remove the santinel node during surgery,
send it to pathology, check it
o if not affected, we don’t remove the
lymph nodes
o if affected, we remove all the nodes
(axillary disection)
if more nodes are involved, we
do chemotherapy
- plus radiotherapy – otherwise 40% chance of recurrence
indic.
tumor > 5 cm
axillary node involvement > 3 nodes
positive of close tumor margins
b. for an older woman or a large tumor - modified radical mastectomy
(compared to the regular radical mastectomy we don’t remove the
pectoralis major muscle) + axillary lymphadenectomy
- no radiotherapy required
if post-menopausal woman with invaded nodes, we do antiestrogen
therapy (tamoxifen)
- will be effective especially if estrogen-receptive, but we will
administer it anyway
advanced stage
- radiotherapy and chemotherapy
pregnancy: terminate pregnancy + radiotherapy and
chemotherapy
breast reconstruction
- rectus abd. or latissimus dorsi flap
- immediate reconstruction
breast surgeon + cosmetic surgeon (8 hr surgery)
- later reconstruction
step 1 - breast surgeon puts in a tissue expander, to
expand the skin
step 2 – cosmetic surgeon – completes the surgery later
in time
for nipple – skin from labia majora
microcalcif. in the breast (lots of small dots) – might be DCIS = ductal
carcinoma in situ
- breast screening – looking for microcalcif.
microcalcif. are irregular (“crushed rock”) or punctuate
- stereotactic biopsy – trydimensional biopsy, with 2 probes to
locate small CAs (core biopsy)
- hook-wire pre-op localization done by the radiologist
area removed -> the radiologyst will do a mammogram
on the tissue to make sure all the microcalcif. were
removed
no chemotherapy, no radiotherapy is required
cancer comes back in the same location
- chest wall radiotherapy + tamoxifen (if menopausal)
types of Rx (Maria)
surgery:
- breast conserving
- modified radical mastectomy – indic.:
> 5 cm
multifocal CA
peau d’orange of the overlying skin is wide (extends
into another quadrant)
previous radiation
patient’s wish
adjuvant
- radiation: after surgery (always), axillary nodes (>3)
- chemotherapy: pre-menopausal
- hormonal Rx: post-menopausal (tamoxifen)
- + aromatase inhibitors: anastrozole, etc.
- + monoclonal AB: trastuzumab (Herceptin)
- + progesterones: medroxyprogesterone acetate
o poor prognostic factors:
tumors > 2 cm
tumors 1-2 cm + estr./progest. receptor negative or high histological grade
lymph node involvement
- suppresion of lactation – if woman doesn’t want to breastfeed or wants to stop breastfeeding
o 1. tight fitting bra +/- fluid restriction
o 2. ice application to relieve pain + simple analgezics
with 1-2 lactation usually subsides in a few days
o 3. bromocriptine
reserved for severe engorgement + if 1+2 failed
risk of severe HT, seizures and strokes in post-partum women
- galactorrhoea
o in multigravid woman, with normal prolactin levels
is common
Rx
reassurance
bromocriptine – if very profuse and troublesome
Amenorrhoea
- primary amenorrhoea
o types
sexually infantile
short stature
- Turner syndr. – 45X0
gonadal disfyc. - infertility
web neck (cystic hygroma)
wide carrying angle
low ear insertion and low hairline
vision and hearing problems
lymphedema
coarctation of aorta, bicuspid aortic valve
horseshoe kidney
- hypothyr.
normal stature
- Kalman syndr. – hypotalamo-hypogonadism
deficit of GnRH => lack of FSH and LH
anosmia, hyposmia
optic problems: color blindness or optic atrophy
cleft palate
- true gonadal agenesis
masculinized
congenital adrenal hyperplasia
- 95% due to 21-hydroxylase defic. - AR
normal male genitalia , ambiguous female genitalia /
enlarged clitoris
baby vomits, decr. Na, K incr. – salt-wasting
- (rare – in 17 hydroxylase deficiency – AR
ambiguous male genitalia, normal female genitalia)
true hermaphrodism
- XX/XY mosaique
androgen-secreting ovarian tumor
normally feminised
Mullerian agenesia
- absent uterus
- vaginal agenesis
- tranverse vaginal septum
- imperforate hymen
cyclical recurrent lower abd. pain
suprapubic mass
may have urinary ret.
androgen insensitivity syndrome
o Dx
1. check breast dev.
2. then U/S -> check for normal uterus
PCOS
PCOS POF Ovarian resistant Menopause
syndr.
FSH Incr. Very incr. Incr. Incr.
LH Very incr. Very incr. Incr.
(LH:FSH =
2:1/3:1)
Estr. N Decr. Incr. Decr.
Testosterone Incr.
(free, DHEA)
U/S > 10 cysts <10 cysts 3-4 cysts
o Sx
irreg. cycles, oligo- or amenorrhoea, infertility
obesity
hirsutism, acne
+/- DM
o MC cause of anovulatory infertility
o causes
insulin resistance
incr. androgens
o risk of endometrial CA (unopposed estrogen)
o Dx.
incr. LH (LH>FSH, LH:FSH = 2:1/3:1) – normally FSH>LH
estr. N
incr. androstendione
+/- insulin incr., blood sugar level incr.
sex hormone binding globulin decr.
transvaginal U/S
if thickness > 5 mm
- hysteroscopy + biopsy
if thickness < 5 mm – CA very unlikely
Rotterdam Dx criteria – at least 2 of the following:
1. oligo- or amenorrhoea
2. signs of hyperandrogenism:
- clinical: acne, hirsutism, deepening of the voice, clitoromegaly
- lab.: incr. testosteron, incr. DHEA
3. U/S >= 10 (12) cysts in any of the ovaries or both (at the periphery)
o Rx
lifestyle modif.
metformin – best Rx
OCP
decr. cyst formation
decr. acne
decr. testost.
for hirsutism
wax
laser
wants to get pregnant: metformin and clomiphene have equal efficacy, but:
BMI incr.> 25 – give metformin
BMI normal – clomiphene
blue book p. 527 says:
- 1. metformin and
- 2. clomiphene, but both are equally effective
- 3. laparoscopic ovarian drilling, IVF, gonadotrophin therapy –
when 1. and 2. have failed
PCOS with normal prolactin:
Rx – clomiphene citrate
- SERM
- stimulates the pituitary gland to produce more FSH and LH =>
ovulation and superovulation
- effects
excessive estr.
fluid retention, breast enlargement
hot flushes (vasomotor sympt.)
o cold and warm feeling on the face,
neck and upper thorax
dev. of more than 1 follicle and release of
more than 1 ovum => multiple pregnancy (5-
10% risk)
inadequate ovulation (corpus luteum dysfc.)
enlarged ovaries with multiple cysts, pain and
incr. risk of torsion
ovarian hyperstim. syndr. – enlarged ovaries,
ascites, hypovolemia, haemo-concentration
NO incr. in birth defects
POF
o causes
autoimmune?
ran out of ovums?
o types
< 12 mths of amenorrhoea
POF
resistant ovarian failure (if no POF option)
> 12 mths of amenorrhoea
premature menopause
o Dx diff
pituitary tumors
prolactinoma – MC
- incr. prolactin
gonadotrophin-producing tumors – extremely rare
craniopharyngioma - brain tumor derived from pituitary gland embryonic
tissue
with deposit of Ca on X-ray
low FSH and LH
double floor of the sella turcica – can be an anatomical variant (if prolactin is
normal)
o Sx
hot flashes, dry vagina, mood swings (like in menopause)
o Rx
HRT
fertility – ovum donor
Bleeding
- menorrhagia
o causes
general
thyroid dis.
liver dis.
renal dis.
coag. / platelet dis.
local
fibroids – with regular periods
- enlarged uterus
adenomyosis – with regular periods
- enlarged uterus
endometrial polyps – with regular periods
endometrial CA – MC postmenopausal
PID
physiological - DUB
- ovulatory
- anovulatory cycles
MCQ: MC cause of menorrhagia + irregular cycles
suddenly occuring in a 45 yrs old woman, previously
OK (disorder of ovulation)
iatrogenic
hormonal – HRT
non-hormonal – IUD
anticoag.
- uterine fibroids
o encapsulated uterine smooth muscle fiber tumors (leiomyoma – pl. is leiomyomata)
o types
intramural - MC
submucosal (in the muscle beneath the endometrium) – MC to cause
menorrahgia
subserosal (underneath the peritoneal surface of the uterus)
intrauterine – pedunculated, causes continuous bleeding
o estr. dep, decrease by menopause
o in fertile women, especially in obese women
o Sx
totally asympt or
menorrhagia
dysmenorrhea, pelvic discomfort (if big)
dysuria, constipation, back pain
if pedunculated – torsion
infertility
calcification
in pregnancy
red degeneration of fibroid
- sometimes, mostly in second trimester of pregnancy
- low grade fever, severe abd. pain, local tenderness, guarding
- but no shock (no blood loss)
- Dx diff. with
torsion of ovarian cyst
placental abruption
effects of pregnancy on the fibroid:
- incr. in size
- softens
effects of fibroid on baby:
- incr. risk of miscarriage
- premature labor
- malposition
- post-partum hemorrhage – lack of contr.
- may prevent vaginal labor (if big and located at inferior uterine
pole)
o Dx
U/S
in case of bleeding, the first step = uterine curettage (Dx and Rx)!
o Rx
in pregnancy
myomectomy – not recommended in pregnancy or during C-section; do
nothing
red degeneration in pregnancy – just analgesics
not pregnant
< 14 wks in size (measured like a baby) + no sympt.
- leave it and observe
> 14 wks or infertile woman, young, wants babies
- Rx: blood transfusion (if needed), then myomectomy
admin. GNRH (for max 6 mths) before surgery, to
decrease size
old lady, doesn’t want babies, severe signs & sympt.
- Rx: hysterectomy
- DUB
o 10-20% women at some stage
o types
ovulatory – 35-45 yrs
anovulatory – 12-16 and 45-55 yrs
o Sx
menstruation > 8 days
heavy bleeding > 4 days
frequent bleeding – periods occur more often than every 21 days
o Dx of exclusion
FBE, coag. profile, FSH, LH, etc.
D & C, hysteroscopy, biopsy
-> if all normal = DUB
o Mx – step-ladder approach:
conservative / medical
1. mefenamic acid (PG inh.) - NSAID
- or naproxen, ibuprofen, indomethacin
- can reduce the bleeding considerably in up to 50% of pacients
(blue book p. 533)
2. tranexamic acid (antifibrinolytic agent)
3. COC
- provided it’s not CI (e.g. in HT)
4. GnRH agonist – induce a medical menopause
- SE – significant menopausal sympt. (when admin. before
menopause)
- e.g.
nasal spray - Synarel
monthly implant – Zoladex
5. oral progest.
- e.g.
norethisterone
blue book p. 532: recommended in a 45 yrs
woman with DUB, HT and regular cycles
(ovulating)
medroxy progesterone acetate (MPA)?
6. Depo-provera
7. Implanon
8. Mirena IUD
- blue book p. 532: recommended in a 45 yrs woman with DUB,
HT and regular cycles (ovulating)
9. danazol
- virilization SE on long term Rx
10. D & C
surgery: for women who have finished their family + DUB Dx is established
11. if fibroid – myomectomy
12. uterine artery embolization
13. uterine a. ligation
14. uterine ablation
- methods
laser
diathermic
- difficult to perform and with poor long-term cure rate if the
uterus is significantly enlarged (blue book)
15. hysterectomy – most invasive but also most effective
- especially if severe bleeding and severe anemia
- postmenopausal bleeding
o causes
in the first 2-3 yrs after LMP – MC = episode of ovarian folicular activity
+ decr. of hot flushes, incr. vaginal lubrication, incr. breast and abd.
size
> 3 yrs after menopause:
1. MC – vaginal atrophy
2. cervical or endometrial polyps
3. endometrial or cervical CA – 10% together – we shouldn’t miss
cystic endometrial hyperplasia – in obese women
ectropion – MC in postcoitus bleeding
o Dx
first step: transvaginal U/S
endometrial thickness < 5 mm -> OK
endometrial thickness > 5 mm -> suspect of CA
- -> do hysteroscopy – most appropriate
- causes of post-coital bleeding
o ectropion - MC cause in young women
the central columnnar epithelium protrudes out through the external os of the
cervix
due to excess estrogen, in
young women ovulating
pregnant women
OCP
CIN is often located inside it
Sx
mucous discharge (not purulent) which can be abundent
lesion that looks like an erosion – used to be called cervical erosion
- red ring around the cervical os
can cause bleeding, e.g. post-coital
Rx
if asympt. - reassurance
if troublesome - cautery
- healing in 4 weeks
o CA – always to rule out in the elderly
o chlamydial cervicitis
o cervical polyp
o trauma
Dysmenorrhoea
o types
primary
common
often commencing 2 yrs after menarche, when ovulatory cycles begin
- not present during the anovulatory cycles
less common after pregnancy or cervical dilatation
Sx
- pain starts before the period and continues 1-2 days into the
period
Rx – success in 95%
- anti-prostglandins, inh. of prostaglandin synthetase
NSAIDs
- OCPs
MCQ: young virgin with severe dysmenorrhea - OCP
placebo is also effective in 20-50%
sec.
Sx
- pain persists through the menses
causes
- submucous fibroids
- endometriosis and adenomyosis
- PID
Rx – treat the primary dis.
Vaginal discharge and infections & STI
- vaginal pH - N = 4-4.7 (acidic)
- Dx
o pH
o smears -> before initiating the Rx
amine or whiff test – add a drop of KOH to vaginal secr. -> for bacterial
vaginosis
wet film
o culture
o STI workup
first-pass urine and ThinPrep samples -> for Chlamydia and gonorrhoea PCR
swabs from cervix for Chlamydia and gonorrhoea: cervix then endocervix
viral culture (herpes simplex)
GBS – swabs from endocervix, urethra, rectum
Pap smear
- causes
Color Consistency Odor pH Wet film Assoc.
sympt.
Physiological Milky- No No (no
discharge white or itchiness)
clear
mucoid
Atrophic Yellowish Non- tenderness,
vaginitis offensive dyspareunia,
post-coital
bleeding
Candida White Thick (cream No 4 Lactobacili, no Itch,
cheese) polymorphs, soreness,
+ spores, redness
hyphae
Trichomonas Yellow- Bubbly, Malodorous, 5- Numerous Soreness,
green profuse fishy 6 polymorphs, itch
(mucopurulent) Trichomonads
(with flagella
and moving)
Bacterial Grey Watery, Malodorous, 5- Numerous Irritation
vaginosis profuse, bubbly fishy 6 polymorphs, (sometimes)
clue cells
o 1. physiological discharge
o 2. atrophic vaginitis – after menopause
vaginal dryness, reduced elasticity and turgor of the vulvar skin
loss of vaginal acidity -> more prone to inf.
yellowish non-offensive discharge
tenderness, dyspareunia
post-coital bleeding
Rx
vaginal estrogen replacement
oral HRT
o 3. bacterial vaginosis – 40-50%
not transmitted sexually
caused by a mixed flora:
Gardnerella vaginalis
Mobiluncus species
Mycoplasma hominis
Sx
fishy, fowly discharge
no pain, no itch
Dx
clue cells – aggregates of squamous vaginal epithelial cells with bact.
attached to them (cytoplasm appears granular and the borders are
obscured)
Rx
1 - metronidazole 400 mg p.o. 12 hourly for 7 days
2 - clindamycin 20% p.o. or vaginal cream – in:
- resistant inf.
- pregnancy
in pregnancy
- 1. clindamycin 300 mg orally 12 hourly for 7 days
- metronidazole 400 mg p.o. 12 hourly for 7 days
not very safe – categ B2
do not need to trace and treat the partners
o 4. Trichomonas – 10-20%
flagellated protozoan
transmitted through sexual intercourse
Sx
soreness, itch
yellow-green profuse thin discharge, with small bubbles in 20-30%
diffuse erythema of cervix and vagina
punctate appearance on cervix – charact.
Dx – culture
Rx
metronidazole p.o.
pregnancy – clotrimazole vaginal tablets
trace and treat the partner!
o 5. candidiasis – 20-30%
Sx
thrush, white discharge (curdy, cheesy, yoghurt), itchy
risk factors
- endogenous
DM
pregnancy
debilitating dis. – immunocompromised, AIDS
- exogenous
A/B
OCP, HRT, IUD
long term use of corticosteroids and other
immunosupressants
carbohydrate-rich diet
orogenital / anogenital intercourse
tight-fitting jeans, nylon underwear, humidity / wet
bathing suit
Dx
high vaginal swab
culture
Rx
topical clotrimazole(miconazole, etc.) – first line, 1-7 days
- vaginal tablet + cream
recurrent
- nystatin cream + pessaries
recalcitrant, not pregnant
- fluconazole or itraconazole p.o.
in pregnancy – clotrimazole pessaries! (local, not systemic)
in Candidata glabrata - boric acid (not in pregnancy)
- resistent to imidazoles
other advice
- good hygiene, no creams, warm water and vinegar, avoid sex
(painful)
- dryness
- no need to trace and treat partners
- change from OCPs to condoms
o 6. GBS
in pregnant woman, during labor - benzylpenicillin
non-pregnant woman – amoxycillin if significant pyogenic inf.
o 7. retained vaginal tampon
extremely offensive vaginal discharge
o 8. tampon toxic shock syndrome
due to exotoxin produced by staph. aureus
- STI
o vaginitis
bacterial vaginosis
candida
Trichomonas v.
o uretritis
Sx
asympt. or
dysuria, penile discharge (clear, white, yellow) – men
dysuria, vaginal discharge
Cx
epididymo-orchitis, prostatithis, urethral stricture in men
PID, infertility in women (MC in NSU)
causes:
Chlamydia
gonorrhoea
non-specific urethritis (NSU)
- C. trachomatis
- Ureaplasma
- Mycoplasma hominis
Chlamydia
most frequent STD in Australia (3x more frequent than gonorrhoea)
- always the first tested for
incubation 1-2 weeks (5 days – 12 weeks)
Sx
- usually asympt. (until severe urethritis or salpingitis occurs) or
- milky-white or clear discharge
Cx
- common cause of infertility due to tubal obstruction
Dx.
- first pass urine (first 10 ml after not urinating for 4 hrs) -> PCR
(95% specificity)
- wire swab (2-3 cm into the urethra + endocervical canal in
women)
PCR and LCR (ligase chain reaction) – in men
Rx.
- 1. azythromycine (preferred) or doxycycline
- 2. erythromycin – in pregnancy
- trace and treat (the same way) all partners (even if asympt.)
no sexual intercourse until healing
Screening for higher risk
- all sexually active females < 25 yrs
- all sexually active tenagers, especially females, Aboriginals and
Torres Islands Islanders
- unsafe sex (no condom)
anal sex
6-12 mths post-inf.
Gonorrhoea
incubation 2-3 days (up to 3 weeks)
Sx – 2-7 days after vaginal/anal/oral sex
- creamy-pus like discharge
- oropharynx – dysphagia, sore throat
- anus – mucopurulent anal discharge, anal discomfort
Dx
- first pass urine -> PCR
less reliable than an endocervical specimen
- urethral standard swab (into the urinary meatus)
- + throat swab
- + rectal swab – gay people
Rx
- if penicillin-resistant gonococci (PPNG)
ceftriaxone + azithromycin or doxycycline
- if PPNG prevalence is low
amoxycillin + probenecid + azithromycin (if Chlamydia
hasn’t been ruled out)
- in pregnancy
erythromycin or roxythromycin
- if it doesn’t respond to Rx – probably suprainf. with Chlamydia
- trace and treat partners
o cervicitis
mucopurulent c. often a foreruner of PID
agents:
C. trachomatis
gonococcus
Rx – as for urethritis
ciprofloxacin + doxycicline
o PID
Includes Endometritis, salpingitis, tubo-ovarian abscess, pelvic peritonitis.
Recurrent infections: Risk of infertility and ectopic pregnancy.
Causes: not always an STI
Sexually transmitted:
- Chlamydia
- Gonococcus
Following instrumentation of the cervix, or recent insertion of an
IUCD.
- Mycoplasma
- vaginal pathogens
- E. coli - sometimes
following a suction curettage for unwanted pregnancy, especially if
having multiple sexual partners
- Chlamydia (15%) + vaginal pathogens
CLINICAL FEATURES:
acute
- for Dx:
must be – all these 3:
moderate to severe bilateral lower abdominal
pain (+/- rebound)
On vaginal examination adnexal tenderness
and
cervical motion tenderness.
one of the following must be present
Fever >= 38
o if fever is present = systemic inf. = PID,
rather then just a local inf. (vaginitis,
etc.)
WBC >= 10.500/mm2
purulent fluid obtained via culdocentesis
inflam. mass present at bimanual pelvic exam.
or U/S
ESR >= 15 mm/h or CRP > 1 mg/dL
evidence for the presence of Chlamydia or
gonococcus in the endocervix
> 5 WBC per oil immersion field on Gram stain
of endocervical discharge
- other sympt.
malaise, dyspareunia, menstrual irregularities and
vaginal discharge, dysuria or frequent urination
chronic PID
- Sx – ache in the lower back, mild lower abd. pain
DIAGNOSIS:
Send endocervical swab for gonococcal and chlamydial culture.
FBE and blood culture.
Pregnancy test.
Cx
infertility
MANAGEMENT:
Remove IUD or retained products of contraception if present.
Admit:
- Systemically unwell.
- Pregnant.
- Intolerant to oral medication.
- Tubo-ovarian abscess.
Antibiotic therapy:
- mild to moderate / outpatient: Azithromycin 1g orally +
ceftriaxone 250 mg IM + doxycycline 100 mg b.d. orally +
metronidazole 400 mg b.d. For 14 days.
- severe / hospital: cefotaxime (or ceftriaxone) + doxycycline +
metronidazole
- in pregnancy: cefotaxime (or ceftriaxone) + roxithromycin +
metronidazole
Follow-up.
Partner needs to be tested and treated.
o ulcers
genital herpes
syphillis
o lumps
warts
o itch
scabies
pubic lice
o extragenital STI
-
o Puberty to menopause: Peak 25-35 years.
o MC in nulliparous women and resolves with pregnancy.
o CLINICAL FEATURES:
most patients are asympt.!!
Dx made when a laparoscopy is done to investigate the infertility
pain
Secondary dysmenorrhoea.
- painful period
- pain usually starts before the period and continues through
the period, then decr.
Acute pain with rupture of endometrioma.
Dyspareunia.
Non-specific pelvic pain or discomfort, low back pain
pain at urination and/or defecation
abnormal bleeding
Menorrhagia.
Premenstrual spotting.
irregular spotting
Infertility.
diarrhoea / constipation, bloating
(almost) never undergoes malignant change
o DIAGNOSIS:
rule out other pathology
PV
size of uterus
Douglass – mass present, lumps that are painful
adnexial masses
retroverted uterus
cervical excitation (motion tenderness)
first exam. – U/S
rule out: ovarian cysts, fibroids, etc.
gold std. of Dx: direct visual inspection at laparoscopy or laparotomy.
o Rx
Analgesics.
MEDICAL:
1. COC: once daily for 6 months
2. Progestogens.
3. GnRH analogues.
4. Danazol (treatment of choice).
SURGICAL:
indic
- if the medical Rx fails
- causing infertility
- if significant impact on patient’s life
Laser or microsurgery
- removal of the tissue
- endometrial ablation or electrodiathermy excision
- hysterectomy
- Adenomyosis
o invasion of the myometrum by the basal endometrium of the uterine cav., with ectopic
glandular tissue (adenomyotic glands) found in the muscle
o 35-50 yrs
o not MC in nulliparous (diff. from endometriosis)
o Sx
dysmenorrhoea
menorrhagia
dyspareunia
slightly enlarged and tender uterus
o Dx
D&C not helpful
core biopsy of the myometrum
removed uterine specimen (after hysterectomy)
o Rx
if severe sympt. -> hysterectomy (adenomyotic glands repond poorly to
hormonal suppression)
Endometrial CA
o risk factors
anovulatory cycles
old age
obesity
nulliparity
late menopause
DM
PCOS
NOT - smoking
o Dx
U/S
if thickness > 5 mm
- hysteroscopy + biopsy
if thickness < 5 mm – CA very unlikely
Cervical CA
o risk factors
all women who were sexually active
higher risk
early age of first intercourse
multiple partners or partner who had multiple partners
smoking
OCP
radiotherapy
diethylstilbestrol (DES)
HPV – especially with high risk strains (16, 18)
- 4 of 5 women get HPV after they start sexual life, most clear the
infection in 1-2 years
- condoms give limited protection from transmitting the disease
o prevention
vaccine = Gardasil – for types 6, 11, 16, 18
6, 11 – anogenital warts
16, 18 - cervical cancer
also prevents some vulval and vaginal cancers
admin. 0, 1-2 mths, 4-6 mths IM
girls – any age (9-26 yrs)
- in school free, then they have to buy it
boys – 9-15 yrs, safe but not proven to be effective
useful until 26 yrs
not in pregnant women
- always do a pregn. test first
S.E. - slight fever, allergy
useful in existing warts
after admin., continue with PAP smears as usually
o screening
PAP smears (cellular level) – every 2 yrs
if (LSIL CIN I) -> repeate PAP in 12 mths
- -> if normal -> repeat in 12 mths
-> if normal > normal screening every 2 yrs
- if LSIL CIN I-> colposcopy + biopsy (tisular level – how deep and
extensive is the lesion)
-> if LSIL -> ablation
crio
laser
sugical
if HSIL (CIN II or CIN III) -> colposcopy + biopsy
- if HSIL -> ablation
crio
laser
sugical
- if invasive -> cone biopsy
SE
bleeding
cervix incompetence
cervix stenosis
premature labor in the future
PROM
in pregnancy – cone biopsy is CI
< 20 wks – termination of pregnancy + Rx the
CA
> 20 wks – discuss with mother:
o terminate pregnancy
o continue, but risk of advanced CA
best to wait till 36 wks, then C-
Section (vaginal delivery is CI)
o stages
I – limited to cervix
II
Iia – upper 2/3 of vagina
IIb – upper 2/3 of vagina + parameters
III – lower vagina
IV
IVa - bladder and rectum
IVb – distant metastases
o Rx
I – cervical conization
II – radiation + chemotherapy
III, IV – radiation + chemotherapy
o
vaginal hernia, which occurs when your small intestine (small bowel) descends
into the lower pelvic cavity and pushes at the top part of your vagina, creating a
bulge.
Enteroceles most commonly occur in women who have had surgery to remove
the uterus (hysterectomy
Rx – surgery
- Rectocele
o
If the muscles behind the vagina are damaged, the rectum will begin pressing
into the vagina. This is called a rectocele.
The most common symptoms of rectocele are:
a bulge in your vagina
constipation and difficulty completing bowel movements
a feeling of rectal pressure
painful sexual intercourse
o Cystocele
If the muscles in front of the vagina are weakened, the bladder will begin to
bulge into the vagina. This is called a cystocele.
The most common symptoms of cystocele are:
difficulty emptying your bladder
leaking of urine, especially when you cough, sneeze or laugh
pain during sexual intercourse
o Urethrocele – urethra bulges into the vagina
Infertility
- male infertility (Murtagh 1108-1110):
o causes
I. decr. sperm prodution
congenital cryptorchidism
- varicocele – does not affect risk (Murtagh)!
inf.: mumps
antispermogenic agents: chemotherapy, iradiations, drug, heat
II. hypothalamic-pituitary dis.
III. disorders or coitus:
ED
retrograde ejaculation
- in DM
- after prostate surgery
psychosexual ejaculation failure
IV. idiopathic
o Dx
normal sperm analysis
volume > 2 ml
sperm concentration
- > 20 million/mL
< 20 mil. = oligospermia -> IVF
< 5 mil. = severe oligospermia -> ICSI
morphology (shape)
- > 20% normal
motility – the most important (> concentration)
- > 40% motility after 4 h
- >25-30 % moving very fast
velocity > 30 microns/s
antibodies against sperm
- < 50 % in cervical mucous
normal hypotal. fc.
GNRH
hormal pituitary fc.
FSH, LH
testosterone
o Rx
inj. with FSH – if sperm analysis isn’t very bad (can improve it)
regular IVF - if sperm analysis isn’t very bad
if very bad – 2% / cycle treated success rate
IVF with ICSI – if very bad
20% per cycle treated success rate
o MCQ
no fructose = no sperm coming from the testicles
0-3 ml – coming from the prostate
- female infertility
o Dx
ovulating?
patency of tubes?
cervical factor?
post-coital test – 2 hrs after check:
- spermatozoids
- cervix – mucus consistency
- IVF
o indic.
males
oligospermia
presence of sperm AB
females
endometriosis
damaged or absent fallopian tubes
unexplained infertility
- ICSI (intracytoplasmic sperm injection)
o indic.
severe oligospermia or azoospermia
failure of IVF
- fertility treatment – Monash IVF
o infertility rate – 15%
o cause of infertility
1/3 woman
1/3 man
1/3 man and woman
o SafetyNet – out of 7500 you get 5000 back
o in vivo
ovulation induction – clomiphene
intrauterine insemination – 2000 AUD
10% success rate
risk of multiple pregnancies
o in vitro
IVF – try this first
no good sperm
donor program
- donor types
known
unknown =altruistic – when child becomes 18 has the
right to find out who his biological mother / father is
- for
sperm
ovum
put sperm and ovum together for (short insem. protocol) 2 or 16 hrs
(long)
Intra Cytoplasmic Sperm Injection – if IVF failed or when we need to do testic.
aspiration, go for this one
low sperm count
inject sperm
o overall success rate in 90% in 3 attempts
Medicine
Orthopedics - OK
General stuff
- most common causes of post-traumatic arterial thrombosis
o 1. fracture of femur
o knee dislocation
o hip fracture
- MC cause of artery anjury – posterior knee dislocation (popliteal a.)
- nerves that regenerate most after traumatic laceration:
o digital n.
o sural n.
- after visit to chiropractor = dissection of vertebral artery: neck pain, facial hemisensory loss,
ataxia
- compartment syndrome – haematoma within a fascia, compressing on close structues (nerves,
arteries, etc.)
o Sx – e.g. leg swollen, post. tibial pulse not felt, pain on moving toes
o Rx - fasciotomy
- MVA
o thoracolumbar pain – transport in supine position on a flat surface
o with blood in urethra -> retrograde urethrogram
o main cause of death after MVA - disruption of great vessels, hypoperfusion and shock
- compound / open fracture – first step = debridement
- internal organ rupture in trauma
o MC source of air under diaphragm = ruptured intestine
o blow in the abdomen – least often organ to rupture = stomach
o MC organ injured in abd. trauma – spleen 45%
2 – liver: 40%
- splenic rupture
o Mx
stable pac.
U/S and CT scan
isolated splenic rapture
conservative Rx
- if it fails -> splenectomy
hT -> splenectomy
other organs are affected -> splenectomy
- greenstick fracture
o Hx of trauma
o usually occur most often during infancy and childhood when one's bones are soft
o Because a child's bones are much more pliable than adult bone, an incomplete, or
'greenstick,' fracture may occur. A "greenstick fracture" means that one side of the
fracture has broken and one side is bent; therefore it is classified as an incomplete
break.
o The name for a greenstick fracture comes from the analogy of breaking a young, fresh
tree branch. The broken branch snaps on one side (the outer side of the bend), while
the inner side is bent, and still in continuity.
o Most often the greenstick fracture must be bent back into the proper position (called a
"reduction") and then casted for about six weeks. Greenstick fractures can take a long
time to heal because they tend to occur in the middle, slower growing parts of bone.
- stress fractures
o normal bone, but repeated stresses/injury on it
diff. from
pathol. fractures
acute traumatic fractures
o athletes, soldiers
o locations
MC – neck and shaft of second metatharsal bone
spinal vertebra in cricket
neck of first rib in COPD (coughing)
neck of fibula and upper end of tibia in runners
perpendicular fracture starts from the cortical in -> advances till it
becomes transversal
Rx – rest!
o Sx – pain worse on weight bearing, point tenderness
o Dx
1. x-ray – usually normal
2. nuclear bone scan – increased uptake at the point of fracture
o Mx
rest
healing takes 6-8 wks
walking boots
- insufficiency fractures
o anorexia
o women from the Middle East all covered (insuf. vit. D)
- flail chest
o 3 or more ribs broken
o Sx
paradoxical resp. -> gas exchanage impaired -> resp. distress
o Rx
immediate intub. and positive pressure ventilation, even if assoc.
pneumothorax (risk of aggravating)
Dislocation / fracture Main problem or MC injured structure
Shoulder disloc. (ant. disloc. 95%) Axillary n. injury
Fracture of shaft of humerus Radial n. palsy
Fracture of surgical neck of humerus Non-union
True pseudo-arthrosis
Supracondylar fracture Impingement of brachial artery
Dislocated elbow Injury of median and ulnar nerve
Fracture of head of radius Elbow stiffness
post-traumatic osteoarthritis
Colles fracture Rupture extensor policis longus tendon
Stiffness of the wrist and fingers
Regional pain syndrome
Scaphoid fracture Avasc. necrosis of proximal fragment
Subcapital fracture of femur Avascular necrosis of femoral head
Hip dislocation (post. MC) Usually no injuries
Femoral n. and vasc. injury
Injury of the knee Popliteal artery injury
Ankle fracture Mortis view – to see if stable or unstable:
If gap between tibia and fibula is uneven =
unstable => Rx - refer
-
External Auditive Conduct laceration with bony debris in the canal
Haemotympanum
CSF otorrhea or rhinorrhea
o Tests
Tuning fork tests
CT scan
Special tests: audiometry, facial nerve testing (nerve excitability test,
electroneuronography)
- Temporal Bone / Basal Skull Fractures
o
o Longitudinal Fractures
70-90% of temporal bone fractures
Extending to EAC, ME, ET, & foramen lacerum
Presentation: bleeding from EAC, CHL, CSF otorrhea, facial paralysis
o Transverse Fractures
20-30% of temporal bone fractures, usually more severe occipital bone injury
Presentation: hemotympanum, CSF rhinorrhea, SNHL, facial paralysis in 50% of
cases
o Treatment
Stabilize for other neurologic & life-threatening injuries
Observation
Antibiotic coverage
Surgery for persistent TM perforation – paper patch myringoplasty or standard
tympanoplasty
CHL – hemotympanum resolves in 3-4 weeks with no sequelae
Facial paralysis – facial nerve decompression & exploration
CSF leak – head elevation, stool softeners, acetazolamide (to decrease CSF
production), placement of a lumbar drain, repair of CSF leak
fracture of the base of skull – CSF leak
- don’t touch the nose (use orogastral tube)
- AB prophylaxis to prevent meningitis
- Orbital floor (blow-out) fractures
o Fracture of the orbital wall caused by blunt, non-penetrating force
o Direct blunt trauma to the globe causes increased intraorbital pressure, causing the thin
bones of the orbit to “blow out”
o Inferior orbital wall is most commonly involved
o Ocular globe is protected by the orbital fat
o Forced duction testing is done to evaluate possible muscle entrapment
o Inferior oblique muscle is tested, other muscles tested if necessary
o Plain films (tear drop sign on Water’s view)
o
o CT scan
o Indications for surgical repair of orbital floor blow-out fractures
Rapid onset of intraorbital bleeding & decreased visual acuity
Entrapment (diplopia)
Enophthalmos of involvement of 1/3 to ½ of the orbital floor
o infraorbital nerve loss in fractured floor of orbit -> diplopia with restricted upward
gaze
- zygomatic fracture
o enophtalmos
Arm
- lateral epicondilitys = tennis elbow = source of extensors tendons (M 683)
o pain on pressing on the lateral epicondyl
o pronated forearm + extended elbow + extend wrist -> pain
o resisting extension of wrist -> pain
o Rx
dumbell exercise with palm facing down
RICE (rest, ice, compression, elevation)
C/S local inj. (1-2)
- medial epicondilitys = golf elbow = source of flexor tendons
o pain on pressing on the medial epicondyl
o resisting flexion of wrist -> pain
o Rx
dumbell exercise with palm facing up
RICE (rest, ice, compression, elevation)
C/S local inj. (1-2)
- DeQuervain tenosynovitis = washerwoman’s sprain– M 689
o tenosynovitis of the first dorsal extensor compartment tendons:
ext. policis brevis
abductor policis longus
o 40-50 yrs
o Sx
tenderness in the thumb, extended along the radial side of the thumb down to
the radial side of the forearm
pain on pinching or writing
triad: tenderness to palpation of proximal radial styloid process + firm tender
localized swelling over the radial styloid + positive Finklestein’s sign
(pathognomonic)
o Dx
Finklestein test = hand with thumb between the other 4 fingers, move hand
medial <-> lateral => causes pain
o Rx
rest in splint that involves the thumb
NSAIDs are CI!
local inj. of C/S under U/S guidance
last resort: surgical release of the tendons
- Dupuytren contracture (palmar aponeuritis)
o risk factors
smoking
alcoholism
heavy manual labor
trauma
DM
phenytoin
o fibroting thickening of palmar fascia with skin puckering & tethering
o ring and little finger diformity (but any finger can be affected)
MCP and PIP are affected, DIP is spared
o often bilat. and symmetrical
o similar
Peyronies dis. = fibrotic dis. of the penis (discomfort and difformity on erection)
plantar fasciitis = subcut. nodule on the feet = rare
o causes
genetic – AD
alcoholism
antiepileptics
o Rx
fasciectomy surgery – remove affected fascia
tendency to recurrence
- carpal tunnel syndrome
o pins and needles, then pain in the median n. teritory (fingers 1-3.5)
awakening from their sleep due to this - pathognomonic
MCQ: man walks up during the night due to painful wrist
o Rx
rest
splinting
C/S infiltration
surgery
- injuries to the wrist and hand
o Colles’ fracture
Fracture of the distal radius usually within 2.5 cm of the wrist.
Most common of the wrist fractures.
Elderly women with osteoporosis.
Fall on the outstretched hand.
Dorsal angulation and dorsal displacement of the distal radial fragment, or
radial displacement.
CLINICAL FEATURES:
Swelling, ecchymosis, tenderness.
‘dinner fork’ deformity.
ASSESS neurovascular status: Acute carpal tunnel syndrome.
common assoc.
- ulna
- scaphoid
- radial or ulnary styloid fracture
X-ray: distal fragment is:
Dorsally displaced with dorsal comminution.
Dorsally tilted fragment with apex or fracture volar.
Supinated.
Radially deviated.
Shortened.
Cx
1. Stiffness of wrist and fingers.
- + Most frequent LATE complication of a Colles facture in an
elderly woman
2. osterarthritic changes
3. malunion
4. non-union – Rx: internal fixation
5. delayed union
MANAGEMENT:
Colles’ backslab: Permit full elbow flexion, thumb movements, extends
from below the elbow to the metacarpal heads (thumb not included)
- include thumb if associated scaphoid fracture
types
- Undisplaced or minimally displaced (stable):
Colles’ backslab.
No manipulation (reduction).
7-10 days.
- Displaced, angulated fractures with radial deviation:
Reduction (Bier’s block = regional nerve block for all the
wrist and hand fractures, using a blood pressure cough
on the arm + injection with anestetic in the hand).
Circumferential plaster cast for 6-8 weeks.
hand fully pronated
full ulnar deviation
with the wrist slightly flexed.
Check within 24 hours: Discoloration, Swelling,
neurovascular status.
too tight plaster
o I – discoloration
o II – tingling and numbness, point
tenderness
Rx – cut the plaster open
Physiotherapy.
o Smith’s fracture
Distal radial fracture.
Volar displacement.
Fall on to the dorsum of the hand, a hyperflexion or a hypersupination injury.
Usually unstable.
Localized swelling.
‘garden spade’ deformity.
The patient is unable to extend the wrist.
Pain on supination and pronation.
Assess for damage to the median nerve.
MANAGEMENT:
Reduction (Bier’s block).
Place a long-arm plaster.
Elbow in 90° flexion, forearm in full supination and the wrist
dorsiflexed.
Extend plaster above the elbow.
o Barton’s fracture-dislocation
Intra-articular fracture of the distal radius with associated subluxation of the
carpus.
It moves in a volar or dorsal direction.
MANAGEMENT:
Refer immediately to the Orthopaedic team as this injury is unstable
and open reduction with internal fixation is required.
o Scaphoid fracture
Most commonly fractured carpal bone.
Fall on to the outstretched hand.
Blood supply is from distal to proximal poles of scaphoid: Risk of avascular
necrosis of the proximal half of the bone..
CLINICAL FEATURES:
Pain on dorsiflexion or ulnar deviation.
Pain and weakness of pinch grip.
Pain and tenderness in palpation of the anatomical snuff box or along
the thumb metacarpal.
DIAGNOSIS:
I - X-RAY: AP/lateral/scaphoid views required.
- X-ray alone may not reveal scaphoid fracture.
Bone scan.
II and best - CT scan.
-
MANAGEMENT:
Normal X-ray: Removable splint 7-10 days, follow up.
if
- Confirmed fracture without displacement or angulation: plaster
from the mid-shaft of the forearm to the metacarpal heads,
and around the base of the thumb to below the
interphalangeal joint.
The wrist should be (like holding an apple – Awad):
Fully pronated.
Radially deviated.
Partially dorsiflexed.
Thumb held in mid-abduction.
- displacement > 2 mm and / or angulation – open reduction
and fixation
COMPLICATIONS:
Non union.
Avascular necrosis of the proximal half of the bone.
- circ. (like for the femur head)
central to periph. – usually closes
periph. to center – from the capsule (the main one)
Osteoarthritis.
o MALLET FINGER:
Injury of the extensor digitorum tendon at the DIP joint.
It results from hyperflexion of the extensor digitorum tendon.
Sx
Full passive, but incomplete active, extension at the distal
interphalangeal joint.
TREATMENT:
Mallet splint for 6-8 weeks.
Elevate hand.
Analgesics.
- Injuries to the elbow
o Pulled elbow - subluxation of radial head
Children 2-6 years.
Axial traction applied to an extended arm.
The radial head is subluxed out of the annular ligament.
CLINICAL FEATURES:
Anxious child.
Local pain.
Loss of use of the arm, particularly supination.
Elbow semi-flexed and pronated on examination.
There is no neurovascular compromise.
Motor activity is normal.
X-RAY:
Only to exclude a fracture if extensive swelling.
Reduction is not successful after two or three attempts.
MANAGEMENT:
Reduction
- Apply pressure to the region of the radial head with one hand.
- Apply axial compression at the wrist.
- Supinate the forearm.
- Gently flex the elbow with the other hand.
supination + force flexion of the elbow while holding
the thumb over radial head, to feel it move into
position, in the anular ligament-> moves into position
No immobilization is required.
- injuries to the shoulder and upper arm
o acromioclavicular dislocation
Fall on to the apex of the shoulder with the arm held in adduction.
types
Subluxation: Causes local tenderness to palpation with minimal
deformity.
Full dislocation: Prominent outer end of the clavicle (step difformity).
CLINICAL FEATURES:
Local tenderness and swelling.
Palpable step between distal clavicle and acromion.
Pain with adduction.
Assess the clavicle and scapula for associated fractures.
DIAGNOSIS:
X-ray: Apparent on stress view. Patient holding a weight in each hand,
compare the shoulders.
TREATMENT:
Minor: Ice, oral analgesics sling immobilization, daily range of motion
exercises.
Complete: Same initial treatment, refer to Orthopaedic team for
possible operative intervention.
o glenohumeral join dislocation
ANTERIOR DISLOCATION - MC
Caused by forced abduction and external rotation of the shoulder.
Young adults from sports, traffic crashes or elderly from a fall.
It tends to become recurrent.
CLINICAL FEATURES:
- ‘Squared off’ shoulder: arm held in slight abduction and
external rotation.
- Loss of deltoid contour.
- Humeral head can be palpated anteriorly.
- Loss of internal rotation.
- Patient cannot rise the arm above the head. (but can move his
head to that position)
most specific – cannot scratch between his scapulas
with his hand
- All shoulder movements are painful.
ASSOCIATED WITH (These result in recurrent dislocations.)
- Hill-Sachs lesion: Flattening or a wedge-shaped defect in the
posterolateral humeral head.
- Bankart lesion – after the first dislocation: Avulsion of capsule
when shoulder dislocates. Occurs in 85% of all anterior
shoulder dislocations.
COMPLICATIONS:
- Look for complications before any attempt of manipulation.
- Axillary nerve damage:
Check sensation over lateral deltoid (police patch)
check motor function with isometric contractions of
deltoid muscle. – Murtagh 1394
- Posterior cord of the brachial plexus.
- Axillary artery damage.
- Fracture of the upper humerus.
DIAGNOSIS:
- X-ray: Always to rule out associated humeral head fracture.
Mercedes Benz sign on lateral oblique view – normal
humeral head displaced ant or post
ant dislocation – humeral head under the
coracoid process of the scapula
post dislocation – humeral head over the
coracoid process of the scapula
- Humeral head is displaced medially and anteriorly with loss of
contact with the glenoid fossa.
TREATMENT:
- Pain relief: Morphine 2.5-5 mg IV.
- Conscious sedation with fentanyl (analgezic) and midazolam
(sedative, muscle relaxant)
or fentanyl and propofol (used currently)
- Perform the reduction:
Kocher’s manoeuvre.
Hippocratic method.
Jay: straight arm, pull forward (in axul bratului) +
upward (flexion) + abduction + supination
- Sling.
- Test again for neurovascular damage.
- X-ray to confirm the reduction.
o fractures of the upper humerus
location:
Greater tuberosity.
Lesser tuberosity.
Surgical neck of humerus.
Supracondylar
Usually in elderly patients.
CLINICAL FEATURES:
Localized pain.
Loss of movements.
Swelling and tenderness.
COMPLICATIONS:
Dislocation of the humeral head.
Complete distraction of the humeral head from the shaft.
Axillary nerve damage causing anaesthesia over lateral deltoid, and loss
of deltoid movement.
Axillary (circumflex) vessel damage.
in supracondylar fracture (just above the epicondyles)
- Sx – huge hematoma
- Cx = brachial artery injury => Volkman contracture
permanent flexion contracture of the hand at the
wrist, resulting in a claw-like deformity of the hand
and fingers. It is more common in children. Passive
extension of fingers is restricted and painful. On
examination the fingers are white or blue and cold and
the Radial pulse is absent.
It is caused by obstruction on the brachial artery near
the elbow
results from acute ischaemia/necrosis of the
muscle fibres of the flexor group of muscles of
the forearm, specially flexor digitorum
profundus and flexor pollicis longus which
become fibrotic and short
causes:
Any fracture in elbow region or upper arm may
lead to Volkmann's ischemic contracture but
commonly caused due to supracondylar
fracture of the humerus.
improper use of a tourniquet
improper use of a plaster cast – too tight
compartment syndrome.
Rx
surgery to fix the damaged tissues
cut open the tight plasters + fasciotomy
MANAGEMENT:
1. check pulse
2. closed reduction of fracture
3. check pulse again
4. put into backslab half-cast at 100 degrees
Immediately refer (high risk of neural / vasculary injury):
- Gross angulation or total distraction of the humeral head.
- Fractures associated with a dislocation: High incidence of
neurovascular injury.
- Associated neurovascular damage.
in elderly with fractures of head of humerus
- usually w/o dislocation => rest arm in sling + shoulder movt. as
early as possible
Pain relief.
Velpeau sling for one week.
Elderly: Social services.
- Torn shoulder rotator cuff mechanism: As an acute injury results in inability to abduct the arm
more than 40° in the presence of an actively contracting deltoid muscle.
o no deformity on the shoulder
Leg
- dislocation of the hip
o Occurs in violent trauma such as:
Traffic crash.
knee strikes dashboard w/ thigh abducted
Blow from the back while in squatting position
Fall from height.
Direct fall on to the hip.
o location
The most common direction to dislocate is posteriorly (85%).
The posterior capsular ligaments are less strong than the anterior ones.
Central and anterior dislocation are rare.
o CLINICAL FEATURES:
The hip is held slightly flexed.
Adducted.
Internally rotated.
externally rotated – for anterior dislocation (rotation is more specific
in determining whether ant. or post. dislocation)
o DIAGNOSIS:
X-ray the pelvis, hip and the shaft of the femur in all cases.
o COMPLICATIONS:
Avascular necrosis of the head of femur: Increases dramatically after 6 hours of
hip dislocated.
Assess L5 and S1 of the ankle and sensation over the medial side of the ankle
(L5) and lateral border of the foot (S1).
Sciatic nerve neurapraxia: 15%
o MANAGEMENT:
Pain relief: Morphine 2.5-5mg and antiemetic.
Refer for immediate reduction under general anaesthesia.
Check associated knee lessions.
- femur fractures
o fractures of the neck of femur
types
subcapital
- internal fixation
- hemiarthroplasty – preferred, especially in the elderly
transcervical (e.g. stress fracture in young person) – dynamic hip screw
(internal fixation)
- high
- med
- low
intertrochenteric – arthroplasty? (Murtagh – pin and plate)
subtrochenteric – arthroplasty?
femoral shaft – intramedullary nail
supracondylar – internal fixation
condyle
- undisplaced – plaster or internal fixation
- displaced – internal fixation
Rx
displaced fracture - best – arthroplasty
- total – better, more expensive, more disclocations
preferred
- hemiarthroplasty
if surgery is CI, intramedullary nailing (if no osteoporosis) – dynamic hip
screw
if displaced – multiple screw fixation
Cx
non-union – most important to discuss
- => best Rx is not internal fixation but hemiarthroplasty
avascular necrosis of the head of femur
- circ.
central to periph. – usually closes
periph. to center – from the capsule (the main one)
- more often if subcapital
- knee exam. (hinge joint, flex-ext)
o effusion
check for skin dimplings lateral from the patella and above it – if they
disappeared = effusion
patellar tap test
patellar bulge test
o medial collat. lig, lateral collat. lig
genu valgum (knocked legs)
stress test
- >10 degrees pathol.
children
- do nothing till 8 yrs
- refer if inter medial malleloar space > 8 cm
genu varum (bowed legs)
where is my horse?
stress test
children
- up to 3 yrs normal
- Mx
reassurance
3 yrs – observe
refer if intercondylar dist. > 6 cm
genu recurvatum
o cruciate ligament
ant (ACL) – more commonly than post.
soccer player accident – MC = injury to anterior cruciate ligament
knee giving way
tests
- ant drawer test – with knee at 90 degrees (> 10 degree pathol.)
- Lachmann’s test – with knee at 15-20 degrees (> 5 mm patol.)
- pivot shift test
post (PCL)
tests
- post drawer test
- post. sac test?
o meniscus – in twisting movts.
medial
more frequent (75%) than lateral
most common knee injury
Sx
- giving away sensation
- locking of joint – MC cause of locking
knee locking in flexion
lateral
tests
Apley grind/distraction test
McMurray test
- knee pain – frequent in hip problems, with the knee joint being normal
- fractures of the patella
o Usually by direct trauma:
Traffic crash.
Fall.
Indirect force from violent quadriceps contraction.
o CLINICAL FEATURES:
Acute knee pain.
Swelling and bruising.
Loss of function, especially inability to extend the knee.
o DIAGNOSIS:
1st: X-ray of both knees.
Confusion may arise from congenital bipartite or tripartite patella but
this are BILATERAL.
Consider CT scan when a suspected fracture is not seen on X-ray.
o MANAGEMENT:
Refer immediately: Distracted or comminuted fractures.
Stable: Aspiration of haemarthrosis.
Place the leg in a padded plaster cylinder from the thigh to the ankle.
Refer to fracture clinic.
- flat feet (pes plano valgus)
o painless, asympt.
o refer if painful, stiff
o majority: physiological
o by 6th birthday: 80% resolve
Bone pathology
- osteosarcoma
o primary – in adolescents: knee (in the metaphysis)
o sec. – metastases
o Sx
pain + swelling
stress fractures
o Dx
x-ray typical:
sunburst appearance
Codman’s triangle – due to periostal elevation
+ new bone formation
o Sx
surgery
chemotherapy
- Paget’s dis. of the bone
o normal bone replaced by new soft bone:
osteoclastic activity, then osteoblastic activity
o 10% at 90 yrs
o Sx
male 2:1
95% asympt.
Dx. during x-ray or incr. ALP level
bone pain, joint pain and stiffness, waddling gait,
MC bones affected: pelvis, femur, skull
his hat doesn’t fit him anymore!
deafness
hyperdynamic circ. -> heart failure
o Dx
marked incr. of ALP (asympt. incr. of ALP)
normal Ca and phosphate
x-ray – dense, expanded bone (bigger, thicker bone)
x-ray features
- larger bone / bony extension
- thickened cortex
- coarse / thicker trabeculation
metastases of the prostate CA, transitional cell CA of the bladder =
osteosclerotic -> have to be excluded (do PSA)
o Cx
fractures
cardiac failure – the bones become arterio-venous shunts, bypassing the
capillaries (more input blood coming back to the heart => higher output
cardiac failure)
osteogenic sarcoma – rarely
deafness
diformities
o Rx
1. bisphosphonates
SE – oesophagitis (don’t go to sleep right after taking it)
Neurology - OK
Nerve roles
- Cranial nerves
o Only the first and the second pair emerge from the cerebrum; the
remaining 10 pairs emerge from the brainstem.
-
Sensory,
Name Motor Origin Nuclei Function
or Both
PARALYSIS: eye is
displaced downwards and
outwardly (“down-and-out”)
PARALYSIS: vertical
diplopia on looking
downward (stays behind)
V Trigeminal nerve Both Pons Principal sensory Receives sensation from the
Sensory trigeminal face and innervates the
and nucleus, Spinal muscles of mastication;
Motor trigeminal Located in superior orbital
nucleus, fissure (ophthalmic nerve -
Mesencephalic V1), foramen rotundum
trigeminal (maxillary nerve - V2), and
nucleus, foramen ovale (mandibular
Trigeminal motor nerve - V3)
nucleus
Supplies branchiomotor
innervation to most laryngeal
and all pharyngeal muscles
(except the stylopharyngeus,
which is innervated by the
glossopharyngeal); provides
parasympathetic fibers to
Nucleus nearly all thoracic and
Both
ambiguus, Dorsal abdominal viscera down to the
Sensory Posterolateral
X Vagus nerve motor vagal splenic flexure; and receives
and sulcus of Medulla
nucleus, Solitary the special sense of taste from
Motor
nucleus the epiglottis. A major
function: controls muscles for
voice and resonance and the
soft palate. Symptoms of
damage: dysphagia
(swallowing problems),
velopharyngeal insufficiency.
Located in jugular foramen
Controls sternocleidomastoid
Accessory nerve and trapezius muscles,
(or cranial Nucleus overlaps with functions of the
Mainly Cranial and
XI accessory nerve or ambiguus, Spinal vagus. Examples of symptoms
Motor Spinal Roots
spinal accessory accessory nucleus of damage: inability to shrug,
nerve) weak head movement;
Located in jugular foramen
o
o Klumpke paralysis - form of paralysis involving the muscles of the forearm and hand,
resulting from a lower brachial plexus injury in which C8-T1 nerves are injured -
affects, principally, the intrinsic muscles of the hand and the flexors of the wrist and
fingers".+/- dilators of the iris and elevators of the eyelid (both of which may be seen
in the case of associated Horner's Syndrome). The classic presentation of Klumpke's
palsy is the “claw hand” where the forearm is supinated and the wrist and fingers are
hyperextended. If Horner syndrome is present, there is miosis (constriction of the
pupils) in the affected eye (complete claw)
o
o syringomyelia
- leg – Murtagh 714, blue book 190-191
o sciatic nerve, coming from the sacral (or lumbosacral) plexus – branches above the
popliteal fossa into:
PED: P=Common Peroneal nerve (at the front of the leg) damaged =>
E=Eversion, D=Dorsiflexion
L5-S1
complic. of lithotomy position -> compression of common peroneal
nerve
branches:
- deep peroneal nerve – dorsiflexors: tibialis ant., extensor
hallucis longus, extensor digito longus, fibularis brevis
- superf. peroneal nerve – eversion muscles: fibularis longus,
fibularis brevis
- L4-L5-S1-S2
Muscles supplied by P:
- Extensor hallucis longus
- Extensor digitorum longus
- Tibialis anterior
- Peroneus brevis
- Short head of biceps femoris
TIP: T=Tibial nerve (at the back of the leg) damaged => I=Inversion, P=Plantar
flexion
L4-L5
SEDIP => sciatic nerve damaged (peroneal nerve and tibial nerve are branches
of sciatic)
Power loss Reflex Sensory loss
C5 Abduction of arm Biceps
C6 Elbow flexion, extension Biceps
of wrist
C7 Elbow extension Triceps
C8 Hand grip
T1 Finger spread (abduction /
adduction of fingers)
L3 Extension of knee Knee jerk Anterior aspect of
thigh
L4 Inversion of foot Knee jerk Medial aspect of the
ankle
L5 Dorsiflexion of great toe - Dorsum of foot
S1 Plantar flexion and Ankle Lateral aspect of the
eversion Plantar ankle
- Nerve roots asked in MCQ – Oxford p. 457
o biceps jerk: C5-C6
o triceps jerk: C7
o hip flexion L1-L2
o knee extension L2-L3
o knee jerk: L3-L4
o ankle jerk: S1
o dorsiflexion: L4 (DIEP – going down)
o inversion: L4
o eversion: L5-S1
o plantar flexion: S1-S2
- foot drop – L5 (common peroneal n.)
- bladder – low sacral nerves
- cvadriceps – L2-L4
- L5 and S1 radiculopathies are MC
- L4
o dorsiflexion (extension)
o inversion
o knee jerk
o skin on medial of the leg below the knee
- L5 (Hx of back pain, sciatica) and common peroneal n. (Hx of knee injury, iatrogenic
compression of the n.)
o dorsiflexion, including dorsiflexion of the great toe
foot drop
o inversion
o eversion
o no reflex
o skin on lateral of the leg below the knee
- S1
o plantar flexion
o eversion
o ankle jerk
o plantar jerk
- sciatic n.
o plantar flexion
o dorsiflexion
foot drop
o widespread sensory loss on the leg
- nerves affected by prolonged stretching / compression during surgery
o common peroneal n. – lithotomy position
o ulnar n. – at the elbow (with abducted and supinated arm)
o radial n. – in the spiral groove
upper limb: Biceps reflex C5/C6 · Brachioradialis reflex C6 · Extensor digitorum reflex
Tendon reflexes C6/C7 · Triceps reflex C7/C8
lower limb: Patellar reflex L2-L4 · Ankle jerk reflex S1/S2 · Plantar reflex L5-S2
- corneal reflex
o V – afferent
o VII – efferent
- gag reflex
o glossopharingeal IX - aferent –
o vagus X – eferent
- oculocephalic reflex (doll’s reflex) – brainstem integrity
Tremor
o types
resting – Parkinson
action or postural
essential tremor
- AD in 50% of cases
- can be present in Parkinson
- Sx
triad: tremor with little disability + normal gait + family
Hx
tremor
begins with slight tremor in one of the hands ->
spreads to the other over time
may involve head (titubation), chin and tongue
interferes with writing, handling of cups, etc.
tremor most marked when arms held out =
postural tremor
exacerbated by anxiety
relieved by alcohol
- Dx diff from Parkinson
faster tremor (8-13 Hz, vs. 4-6 in Parkinson)
normal gait (vs. loss of arm swing and shortened step
in Parkinson)
- Rx
reassurance
drugs
1 – propranolol
benzos – in stress
alcohol – 1 std. drink
anxiety/emotional
hyperthyroidism
alcohol
drugs / drug withdrawal (heroine, cocaine, alcohol)
intention tremor – exacerbated by action and increases as the target is
approached
in cerebellar lesions
flapping tremor (asterixis)
COPD with CO2 narcosis (incr. CO2, decr. O2)
hepatic encephalopathy, Wilson’s disease
uraemia
- Parkinson’s dis.
o MC and disabling chronic neurol. disorder
o male = female
o degeneration of dopaminergic neurons in the substantia nigra => decr. of dopamine in
the basal ganglia -> causes movts. to become smaller and slower
o parkinsonism can be drug induced: phenothiazines (chlorpromazine), butyrophenones
(haloperidol, droperidol), reserpine
CI in Parkinson
o Sx
slow and insidious onset, around 58-62 yrs
only 50% have rest tremor at onset
first signs = loss of dexterity in rapid alternating movts. + absence of
arm swing
triad: rest tremor + rigidity + bradykinesia (poverty of movt.)
tiredness, lethargy, restlessness
tremor
hemi-parkinsonism – at start
4-6 Hz
pill-rolling – severe cases
cogwheel ridigity
slow and shuffling gait with flexed trunk and short steps
no arm swing
bradykinesia
slowness to start the movts.
micrographia
decr. blinking
slow monotonous speech
progressive forward flexion of the trunk
poor balance – suspect Parkinson in a fractured hip
constipation (common)
congnitive impairment – due to:
progressive Parkinson-associated dementia in 30-40% usually after 10
yrs
Alzheimer
medication
normal reflexes
o Dx
clinical!
Dx. diff.
parkinsonsism – doesn’t respond to levodopa
Lewy bodies in the neurones – pathognomonic
o Rx
1. drugs:
types:
- dopaminergic
levodopa – best drug, baseline and gold standard of Rx
initiate Rx ASAP
start low: 100 mg/day
incr. if needed: max. tolerated dose = 450-600
mg/day
+ carbidopa or benserazide – with the onset of
disability (motor disturbances)
improves rigidity, dyskinesia, gait disorder, but not the
tremor
- dopamine agonists
bromocriptine
SE - severe psychiatric disturbances ->not in
elderly with confusion or dementia
pergolide – assoc. in Rx for the levodopa “on-off”
phenomenon
SE - severe psychiatric disturbances ->not in
the elderly with confusion or dementia
cabergoline
- anticholinergic – for tremor (in young people)
benztropine
benzhexol
- COMT inhibitors
entacapone – levodopa potentiation
- others
amantadine
selegiline
approach:
- mild (minimal disability)
levodopa + carbidopa or
selegiline (can be use as first line monotherapy)
amantadine
- moderate (independent but disabled)
levodopa
+ dopamin agonist: pergolide or bromocriptine or
cabergoline
- severe (disabled, dependent on others)
levodopa + pergolide or cabergoline
+ entacapone
long term problems – after 3-5 yrs of Rx with levodopa
- dyskinesia: choreiform, involuntary flickering movt. of the
mouth (lips, tongue), face, eyelids, cheeks, limbs, trunk – 80-
100% of patients
Rx: decr. levodopa and carbidopa + add pergolide or
cabergoline
- end of dose failure (effect lasts for only 2-3 hrs)
Rx:
add entacapone
dosages closer together
- “on-off” phenomenon (sudden inability to move – recovery in
30-90 min)
Rx:
apomorphine (+ domperidone to prevent
vomiting) for off phase
add pergolide
- early morning dystonia (clawing of toes)
Rx – slow release levodopa
- nocturnal akinesia
Rx – slow release levodopa
- sundown effect: patients often go psychotic as the sun goes
down
2. surgery:
alleviates only the tremor and rigidity
does not prevent the progression to bradykinesia, dysarthria and
dementia
types:
- pallidotomy
- stereotactic thalamotomy
indic:
- tremor or rigidity not responding to drugs
- for younger patients with unilat. tremor
Seizures
-
types:
partial (non-convulsive, no loss of consciousness)
- simple
e.g. Jacksonian march: starts from a part of the body
and moves to other area of the body
- complex
with impaired (cloudy, but not lost) consciousness
e.g. temporal lobe epilepsy – with olfactory
hallucinations
generalized (convulsive, with loss of consciousness)
- grand-mal (tonic – clonic)
Sx
usually last 1-2 min
loss of consciousness
tonico-clonic contractions
tongue-biting
incontinence
post-ictal confusion
Dx diff with functional or pseudo-seizures = means of
coping with stress (exams, etc.)
atypical: no loss of consciousness, no tongue-
biting, no incontinence, etc.
nocturnal epilepsy – involuntary vocalisation followed
by grand-mal
blood on the pillow and enuresis noticed in the
morning
- petit-mal = absence
absence seizures: observe child during running and
swimming – might have a seizure and die!
can have a motor component
- myoclonic seizures –> sodium valproate
- febrile seizures
with surprised or scared look (not a blank look), lip-smacking, mouth movement
= temporal lobe epilepsy
valproate:
SE
- liver toxic (LFT done every 2 mths for 6 mths)
- very teratogenic
o EEG features
Absence seizures Infantile spasm
Syncope
o Transient loss of consciousness.
Associated with blurred vision, dizziness, sweating and loss of postural tone,
followed by spontaneous full recovery.
o It is due to reduced cerebral perfusion
o Causes vary from benign to imminently life threatening.
Dx diff.
vaso-vagal: with prodrome – vomiting
- syncope after going to the bathroom or post-op (pain), change
of position
posture change, by standing
pro-drome before the syncope
warning feeling (dizziness), nausea, hot or skin
sensation, blurred vision
sliding to the ground, rapid return to consciousness
Sx
palor, sweating
hBP, bradycardia
trigger factors: emotional upset, pain
hBP Bradycardia Vaso-vagal attack
hBP Tachycardia Shock
If decr. central venous
pressure = hypovolemia,
septic shock
If incr. central venous pressure
and JVP = cardiogenic shock
HBP Bradycardia (but > 50) Incr. intracranian pressure
(ICP)
HBP Bradycardia (but < 50) Complete heart block
cardiac - sudden onset, short duration
- Arrhythmia, either tachycardia or a bradycardia.
complete heart block
pulse 25-50
large volume pulse
increased JVP, cannon wave (large wave
produced by atrial contraction)
systolic murmur
- Myocardial infarction.
- Stenotic valve lesion (aortic stenosis).
aortic stenosis = dyspnea + chest pain + syncope + syst.
murmur
slow rising pulse
non-dysplaced apex beat
aortic thrill
ejection systolic murmur radiated to the
carotids, better heard at upper left sternal age
and aortic area
brain hypoperfusion in presence of fixed decr.
cardiac output => syncope
- Hypertrophic cardiomyopathy.
- Drug toxicity or side effect.
vascular
Carotid sinus hypersensitivity: Hypersensitive baroreceptors cause
excessive reflex bradycardia +/- vasodilatation on minimal stimulation
(Head turning or shaving).
Pulmonary embolism.
Haemorrhage or fluid loss:
- Haematemesis and melaena.
- Concealed haemorrhage (such as an abdominal aortic aneurysm
of ectopic pregnancy).
- Vomiting and diarrhoea with dehydration.
Neurological:
- Subarachnoid haemorrhage.
- Vertebrobasilar insufficiency. – in posterior circular problems
(vertebrobasilar), less from anterior (cerebral) circ.
Postural (orthostatic) hypotension:
- Diabetes, hypoadrenalism (Addison’s).
- Parkinson’s disease and autonomic failure.
- Drugs: antihypertensives, diuretics, nitrates.
- Cough, micturition or defecation syncope.
- Hypoglycaemia (relative).
o DIAGNOSIS:
Priority: Blood glucose test strip and ECG.
Send blood for FBC, U&Es, cardiac biomarkers, pregnancy test, CXR and CT scan.
o TREATMENT:
Underlying condition.
TIA
o cerebral circ. Oxford 452
o origin
80% carotid origin
20% vertebrobasilar
o Episodes of sudden transient focal neurological deficit lasting for less than 24 hours
(usually less than 10 min).
o 12% of patients have a stroke by 1 month (often within 1-7 days).
o types
anterior
usually carotid artery or middle cerebral artery
posterior
vertebral, PICA, basilar
o CAUSES:
Embolic:
Cardiac: Post MI, AF, mitral stenosis, valve prostheses.
Extracranial vessels: Carotid stenosis, narrowed vertebral artery.
Reduced cerebral perfusion:
Hypotension: Hypovolaemia, drugs or cardiac arrhythmia.
Hypertension: Hypertensive encephalopathy.
Hypercoagulable states: Protein C, S or antithrombin III deficiency.
Vasculitis: TA, SLE, PAN.
Lack of nutrients:
Anaemia.
Hypoglycaemia.
o CLINICAL FEATURES:
anterior - Carotid artery dysfunction – unilat. sympt.
Hemiparesis.
Hemianaesthesia.
Homonymous hemianopia.
Dysphasia.
Dysarthria.
Amaurosis fugax (Transitory monocular blindness).
posterior - Vertebrobasilar territory dysfunction:
Bilateral limb paresis.
Crossed sensory symptoms.
Diplopia.
bilat. blurry vision
Bilat. cortical blindness.
homonymous hemianopia?
Nystagmus.
Ataxia.
Vertigo.
cranial nerve paralysis (e.g. IX, X, etc.)
memory loss
PICA – lateral medullary syndrome, due to injury to the lateral part of
the medulla oblongata
- vertigo
- nystagmus
- ataxia
- Horner
- dissociated sensory loss (affecting face and limbs – MCQ: blue
book p. 401)
ipsilat. sensory fibres in the post. columns (for touch,
vibration, posture – they only cross at the pons level ->
from there up all the fibres from the other side are
together)) + contralat. ant. and lateral column
spinothalamic fibres (pain + temperature – they cross
at the spinal cord level)
(corticospinal tract – motor
o 80% of the fibres cross at the medulla
oblongata level)
o DIAGNOSIS:
Glucose test strip.
FBC, ESR, coagulation profile, blood sugar, LFT, electrolytes and lipid profile.
ECG and CXR.
URGENT CT BRAIN SCAN to differentiate
haemorrhage from
infarction and to look for structural non-vascular lesion.
CT aspect:
- infarction – black
- haemorrhage – white
- calcif. – very white
Duplex carotid ultrasound for a suspected carotid territory ischaemic event as
soon as possible.
o Mx
ADMISSION if:
ECG is abnormal.
TIAs are recurring over a period of hours or progress in severity and
intensity.
Significant systemic disorder suspected.
Diastolic BP over 110 mmHg.
Low-dose aspirin 300 mg immediately (all TIAs are ischemic, so we can give
them aspirin).
Then 75-150 mg once daily if complete recovery has occurred.
or Warfarin
indications: Cardiac emboli (AF).
if still having TIAs with aspirin or warfarin, add clopidogrel
Refer to Medical or Neurology outpatients within 7 days.
Patients can present with the consequences of their TIAs (head injury, Colles’
fracture). Do not fail to investigate the true precipitating event (the TIA).
Carotid endarterectomy: If > 70% stenosis.
Stroke
o Due to a vascular disturbance producing a focal neurological deficit over 24 hours.
o location
right handed => dominant hemishpere is left
can’t speak = left parietal lobe affected
o Causes:
Cerebral ischaemia: 80%.
Cerebral thrombosis from atherosclerosis, hypertension or rarely
arteritis.
Cerebral embolism from AF, post MI mitral stenosis, atheromatous
plaques in neck vessels.
Hypotension causing cerebral hypoperfusion.
Cerebral haemorrhage: 20%
Intracerebral haemorrhage associated with hypertension or rarely
intracranial tumour and bleeding disorders including anticoagulation.
Subarachnoid haemorrhage from ruptured berry aneurysm or arteriovenous
malformation.
o RISK FACTORS:
I – Hypertension – 4-6 x incr.
II - Hyperlipidaemia.
Smoking.
DM.
Heart disease (valvular, ischaemic, AF).
Past TIA/stroke.
Peripheral vascular disease.
o DIAGNOSIS:
Presentation may give a clue to aetiology.
Cerebral thrombosis: often preceded by a TIA and the neurological
deficit usually progresses gradually (headache and loss of consciousness
are uncommon).
Cerebral embolism: sudden, complete neurological deficit.
Intracerebral haemorrhage: Sudden onset of headache (suggests
haemorrhage), vomiting, stupor, coma with rapidly progressive
neurological deficit.
Subarachnoid haemorrhage: sudden ‘worst headache ever’ associated
with meningism, confusion and lethargy.
lacunar infarct
- 25% of all ischemic strokes
- caused by occlusion of a single deep penetrating artery that
arises directly from the constituents of the Circle of Willis,
cerebellar arteries, and basilar artery. The corresponding lesions
occur in the deep nuclei of the brain (37% putamen, 14%
thalamus, and 10% caudate) as well as the pons (16%) or the
posterior limb of the internal capsule (10%)
- types (Awad) – 5 syndromes:
1. contralat. pure motor (hemiparesis) –MC - 33-50%
2. contralat. pure sensory
3. sensory-motor
4. ataxic contralat. hemiparesis – second MC
5. clumsy hands + disarthria
- Sx (Maria)
isolated hemipareses.
isolated unilat. sensory deficit
isolated unilat ataxia
isolated unilat. dystonia
isolated unilat. parkinsonism
isolated dysarthria
dysarthria + hemiparesis partic. of face, tongue and
hand
- capsular warning syndrome:
TIA that usually precedes the pure motor type of
lacunar infarction in HT + DM
FBC, ESR, coagulation profile, ELFTs and blood sugar.
ECG and CXR.
1. Urgent CT head scan: This may initially be normal with a cerebral infarct.
o Mx
MANAGEMENT:
If glucose is low give 50% dextrose 50 mL IV.
If the patient is unconscious secure airway, consider endotracheal
intubation if respiratory depression.
Oxygen: aim for oxygen saturation above 94%.
Avoid to treat acutely (first 24-48 hrs) raised blood pressure unless
aortic dissection or hypertensive encephalopathy.
- lower it gradually – risk of cerebral hypoperfusion
cautious use of oral drugs for BP > 220/110
preferably: ACE inh.
- blood pressure is often elevated because of the stroke (90% of
pacients with stroke)
Refer to Stroke unit. – reduces mortality by 20%
2. Antiplatelet agents: Once haemorrhagic stroke is excluded (with CT
scan) give aspirin 300 mg. – if alergic, Clopidogrel
or 2. warfarin, if:
- > 60 yrs
- risk factors
DM, AF
- vertebrobasilar stroke (not carotid)
- recurrent TIA or stroke and patient already on aspirin
Thrombolysis: Onset of symptoms < 4.5 hours, no contraindications.
Alteplase 0.9mg/kg over 1 hour.
- rarely used
- can convert an ischemic stroke into a haemorrhagic stroke
Brain haemorrhage
- EPIDURAL/EXTRADURAL HAEMATOMA:
o sudden
o in MVA
o Neurosurgical emergency if mass effect.
o Arterial bleeding (middle meningeal artery) between skull and dura matter.
o ‘Lucid interval’ of consciousness before CNS deterioration.
o Imaging: lens shaped (biconvex) collection of blood, crosses the mid-line.
o Rx
surgery – burr hole
-
- SUBDURAL HAEMATOMA:
o Neurosurgical emergency if mass effect.
o Most common (20-40%) venous bleeding, slow deterioration.
o in elderly people
o Between dura matter and arachnoid membrane.
o Imaging: Sickle shaped collection of blood. It will NOT cross the mid-line
-
- SAH
o massive pain (worse pain ever)
o Diffuse layering of blood below arachnoid membrane.
o Does not cause mass effect, predisposes to vasospasm.
o PICA aneurysms: Intraventricular haemorrhage.
o
o Causes
Head injury.
Ruptured aneurysm.
in polycystic kidney dis. - AD
Hypertension.
Coarctation of the aorta.
Arteriovenous malformation.
Coagulopathy or vasculitis.
o Sx
Sudden, severe ‘worst headache ever’.
Lethargy, nausea, vomiting, meningism.
A IIIrd nerve oculomotor palsy suggests bleeding from posterior communicating
artery aneurysm.
o DIAGNOSIS:
Arrange a CT head scan urgently to confirm the diagnosis (99% caught - Amit)
Lumbar puncture (1%): If CT scan is negative or unavailable (xantochromia =
blood in CSF)
o MANAGEMENT:
Oxygen
prevent the main Cx = vasospasm
nimodipine (if blood pressure is stable) – to prevent vasospasm with
subsequent ischemic stroke!!
3 H therapy:
- control HT
- hypervolemia – overload the patient
- hemodilution – thin the blood
Refer to neurosurgical unit.
Lorazepam 0.07mg/kg, diazepam 0.2mg/kg or midazolam 0.1mg/kg for seizures
or severe agitation.
Paracetamol 500 mg and codeine phosphate 8 mg two tablets orally.
Meningitis
o CAUSES:
Meningococcus.
Streptococcus pneumoniae.
Listeria monocytogenes (infants under 3 months, adults over 55 years,
immunosuppression).
Viruses.
Cryptococcus neoformans.
TB.
o CLINICAL FEATURES:
Prodromal malaise.
Generalized headache.
Fever, vomiting.
TRIAD: fever + vomiting + headache
Altered mental status with irritability and drowsiness.
Confusion, coma.
Pyrexia.
Photophobia.
Neck stiffness.
Localized cranial nerve palsies or seizures may occur.
Signs of meningeal irritation – neck stiffness (also in SAH).
o Always consider meningitis in:
The confused elderly.
Sick neonate.
Generalized convulsive status epilepticus.
Coma of unknown cause.
o Meningococeal septicemia
early signs
Muscle pain: Legs.
Abnormal skin colour: Pallor or mottling.
Cold hands and feet.
Rigors, vomiting, headache.
late signs
Petechial rash (non-blanching).
Impaired consciousness.
Meningism.
o DIAGNOSIS:
Blood cultures.
CT scan: If focal neurological signs, especially if signs of incr. ICP
LP: If there are no focal neurological signs and no ICP!!! (CI if ICP is suspected)
– to confirm diagn.
CSF findings (table – Jay’s notes)
- bacterial meningitis: WBC - neutrophils incr. (85%), protein incr.
(1 – normal 0.15-0.4), glucose decr.
- viral – lymphocytes incr., normal glucose
- TB – lymphocytes incr., glucose decr.
- GBS - prot. incr., cells normal (WBC are not incr. – 90%,
mononuclear cells incr. – 10%)
o Rx
Oxygen and fluids.
Ceftriaxone (III generation) 2 g IV
+/- benzylpenicillin 2.4 g IV (ampicillin for Listeria) in immune-
compromised or Listeria
if penicillin/cephalosporin hypersensitivity:
vancomycin + ciprofloxaxin
AS SOON AS THE DIAGNOSIS IS SUSPECTED!
+ prophylaxis in contacts: ciprofloxacin or rifampicin
Dexamethasone 10 mg IV if bacterial meningitis is strongly suspected
(decreases the cerebral oedema)!
Headaches / migraine
- Headache – see printout from Jay
o Consider the serious or life-threatening diagnoses first:
Meningitis.
Subarachnoid haemorrhage.
Space-occupying lesion.
Temporal arteritis.
Acute narrow-angle glaucoma.
Hypertensive encephalopathy.
o The majority however will be:
Migraine.
Tension or muscle contraction headache.
Cluster headache.
Post-traumatic headache.
Disease in other cranial structures.
- migraine
o with family Hx!!
o 5-10% of children
o a. Common – without aura
Hx of at least 5 attakcs
lasts 4-72 hrs if untreated
relieved by sleep
Dx
Have at least 2 of the following headache characteristics
- unilat. usually
- pulsating or throbbing
- moderate to severe
- aggravated by movement
- blurred vision in both eyes
have at least 1 of these assoc. symptoms:
- nausea and/or vomiting
- photophobia
- phonophobia
o b. Classic – with aura
less common
similar to common migraine plus a history of at least 2 attacks that:
have a typical aura: reversible visual, sensory or speech symptoms, but
not motor
visual: uni or bilat flashing lights, zigzag lines (teichopsia), central
scotoma
symptoms develop over 5 minutes but less than 60 mins.
headache precedes, accompanies or follows the aura within 60 mins, although
up to 40% can have aura with no headache
less typical aura – very rare
hemiplegia – from which patient recovers completely
ophtalmoplegia
basilar: ataxia, vertigo, tinnitus, nystagus, diplopia, confusion
o Mx
darkened room
oxigen by facemask
oral analgesic: aspirin, ibuprofen, paracetamol and codeine
antiemetic: metoclopramide 10-20 ml IV
if NSAIDs didn’t resolve the headache:
triptan - sumatriptan 6 mg sc
- CI
known coronary artery disease, previous AMI
children – only:
paracetamol
NSAIDs
avoid precip factors:
fatigue, alcohol, caffeine, hunger, chocolate
- tension headache
o women
o assoc. with stress but without prodrome
o pain comes gradually
o never lasts > 1 day
o bilat., dull and band-like
o mild to moderate
o pain in the morning, gets worse during the day
o mild nausea associated, vomiting is rare
o headaches often become chronic
o Mx
paracetamol + codeine
reassurance
- cluster headache
o rare
o men
o provoked by alcohol
o 2-3 hrs after falling asleep
o attacks are shorter in duration: 15 min – 3 hrs
o headache is centred around the orbit, the pain recurring in separate bouts
o NO VOMITING!
o assoc. with unilat rhinorrhoea, lacrimation, conjunctival congestion
o Mx
acute
O2 100% (lower conc. are ineffective) – up to 15 min.
- if no improv., after 15 min. stop O2 (can be toxic)
Sumatriptan 6mg SC
dihydroergotamine 1 mg IM
lignocaine
bridging Rx
often needed while preventive Rx is commenced
C/S have been used to produce rapid suppresion of attacks (within 24-
48 hrs)
- prednisolone oral 50 mg daily for 7-10 days, then taper over 3
weeks
may recur when steroids are tapered so preventive drug must be
initiated in parallel
preventive Rx
Verapamil 160 mg orally daily or
methylsergide 1 mg orally daily or
lithium 250 mg orally twice
Raised ICP
o signs of raised ICP
deteriorating / LOC
deteriorating resp. pattern
HT with bradycardia
progressive headache, worse when waking up in the morning
ataxia
vomiting
lateralizing signs (cranial n. paralysis) – tentorial herniation
3rd n. palsy
- superior eyelid drop = ptosis
- dilated pupils = midriasis
- diplopia - eye looking “down and out”
4 n. palsy
th
Brain tumors
o children
predom. in the post. fossa
midline cerebellar mass = medulloblastoma
MC malignant brain tumour
children
obstructs CSF blood flow => headache
infratentorial
o neurofibromas
supratentorial
neurofibromatosis type I
o meningioma – very slow (slowest)
usually benign
seizures for 3 years, then suddenly worsening (hemiparesis, etc.)
more common
supratentorial
o glioblastoma multiforme – much faster
seizures + hemiparesis at the same time
MC malignant and most aggressive tumor
adults
o astrocytoma - less aggressive
o oligodendroglioma
o ependymoma
Dermatology - OK
- dermatology
o description
general outlook of patient
location and pattern of lesions
morphology of lesions
well defined / poorly defined
mono/poly morphous
red/ salmon pink/ etc.
scaly (epidermal lesion)
ABCDE
- asymmetry
- border
- color
- dimension
- extraordinary (different), evolving
o skin layers
epidermus
dermus
basement membrane
fat
- Wood’s lamp
o UV in dark room
o color
green or bright yellow – tinea capitis (50% of cases)
coral pink – erythrasma
pink gold – pityriasis versicolor (hypopigm.)
yellowish green – pseudomonas species
Strepto pathology
- tonsilitis
o causes
viral - MC
redness with pain
bacterial
15 – 30%: Group A streptococcal (GAS) pharyngitis.
- Bacterial causes for sore throat other than GAS are rare.
e.g. EBV
Sx
- exudate
- high fever
- painful lymphadenepathy
o Cx
scarlet fever
rheumatic fever
retropharingeal abscess
GN
o Rx
< 4 yrs – probably viral – no A/B
> 4 yrs :
if EBV – no A/B
if GAS
- if GAS:
penicillin
if allergic, erithromycin
- scarlet fever (scarlatina)
o children, aboriginals (strepto. inf. in general)
o GAStrepto. pyogenes which produces erythrogenic toxin (exotoxin)
o Sx
prodromal sympt.: fever, sore throat, malaise, then
rash appears on the 2nd day, sand-paper like under touch, blanches on
pressure, spares face and palms and soles
is worse in the skin folds. These Pastia lines (where the rash runs
together in the armpits and groin) appear and can persist after the rash
is gone.
circumoral pallor
strawberry tongue
recovers in 5 days – fine desquam. on recovery
o Dx
PR interval can be prolonged -> may be evolving towards rheumatic fever
o Cx
rheumatic fever
GN
erythema nodosum
o Rx
Phenoxymethylpenicillin 250-500 mg orally q.d.s. for 10 days
- rheumatic fever
o after a streptococcus group A (S. pyogenes) inf.: tonsilitis, scarlet fever
o indigenous population
o Sx
acute onset with fever, joint pains, malaise
flitting arthralgia mainly in leg (knees, ankles) and arms (elbows, wrists)
one joint settles as the other one gets affected
o Dx
2 or more major Jones criteria
1 major + 2 or more minor Jones criteria
major criteria:
polyarthritis
carditis
- MC affected = mitral valve
- can lead to congestive heart failure
Sydenham’s chorea
subcut. nodules
erythema marginatum
minor criteria
arthralgia
ECG – prolonged PR interval
previous RF or rheumatic heart dis.
fever >= 38 degrees
raised ESR > 30 mm/hr or CRP > 30 mg/L
+ raised ASO titre, incr. DNAse B titre, positive throat swab for strepto,
Hx of scarlet fever
o Rx – penicillin
benzathin penicillin IM or phenoxymethylpenicillin p.o.
- impetigo (school sores)
o types
vesico-pustular, with honey-colored crusts
staph. aureus, stepto. pyogenes
bullous impetigo
< 2 yrs
staph. aureus
with blisters
ecthyma – more serious form, penetrating deeper, in the dermis
scars after the ulcers heal
o Rx
topical antiseptic – bactroban (Mupirocin)
if extensive, systemic A/B
flucloxacilin
cephalexin
Atopic dermatitis
Hair disorders
- tinea capitis
o dermatophyte inf.
o children only
o from cats and dogs
o scaly, patchy alopecia
o breaking of hair shafts in one location, scaly
with small broken off hair shafts (not clear)
o Rx
griseofulvin – for up to 6 wks oral, 10 mg/kg/day, max 250 mg
(not amphothericin – only in hospitals – nephrotoxic)
skin - terbinafin cream or imidazol cream
scalp – oral terbinafin (less SE, more effective) or oral griseofulvin
- alopecia
o causes
SLE, autoimmune thyroiditis
nutritional
fungal inf.
…
o types
areata – one or more discrete circular areas of hair loss
can occur anywhere on the body (not just on the head)
triad: patch of complete hair loss + clean scalp + exclamation-mark
hairs
totalis – involves the whole scalp
universalis – involves the eyebrows and eyelids as well
o 20% have familial Hx
o triggers
severe febrile illness
severe emotional stress
o Dx
FBE – Hb, thyroid, iron, zinc
biopsy of the scalp
exam. the hair under microscope
exclamation mark sign
pull hair sign
examine nail – psoriasis
where else in the body is hair loss: eyebrow, chest, etc.
o Rx
aim: regrowth of hair + pyschological support
initial – potent topical C/S betamethasone 0.5% – 1 – 2 times / day
small lesion – intralesional C/S
triamcinolone acetonide
oral C/S if topic failed
topical dithranol
topical minoxidil
adjuvant
topical immunotherapy
UV radiation (PUVA)
drugs – each used for 3-6 mths before switching to another one
o prognostic
33% chance of complete regrowth within 6 mths
50% chance of complete regrowth within 1 yr
80% chance of the cured people will relapse
- 4 conditions that can be confused with alopecia:
o Tinea capitis
is scaly! (not clean skin as in alopecia)
o Trichotillomania
they don’t have clear patches of hair loss, but patches with short / long hair
Hx of stressor (in the family)
o Lichen planus – causes permanent scarring of the scalp
o Discoid cutaneous lupus – causes permanent scarring of the scalp
- any hairy lesion on the skin = benign until proven otherwise
Nail problems
- Ingrowing toe nail /onychocryptosis:
o Very common condition esp in adolescent boys.
o May follow injury or deformity of nail bed.
o Typically located along the lateral edges of great toe nail and represents an imbalance
between the soft tissue of nail fold and the growing nail edge.
o It is exacerbated faulty nail trimming , constricting shoes , poor hygiene.
o Prevention
Instruct on correct foot and nail care.
Foot hygiene.
Correct trimming of toe nails-esp leaving the corners project beyond the skin.
Daily stretch the toe nails with the pads of the thumb.
o Treatment- Elliptical excision of the skin.
Electrocautery of the wedge of tissue.
Phenolisation method.(deep cleaning with the cotton stick soaked in phenol
deep into the nail bed)
- paronychia
o infection where the nail and skin meet at the side or the base of a finger or toenail
o can be assoc. with DM
o can be:
acute
MC staph. aureus
Rx
o elevation of nail fold or puncture of the fold
o removal of nail
o if recurrent – wedge resection of the region, removing the edge
of the nail and the corresponding germianl nail bed
chronic
secondary inf. with Candida
- onychomycosis
o Rx – terbinafine – for 3 mths
- nail problems
o nail clubbing (convex)
pulm. causes: lung CA, chronic lung supuration (empyema, abscess),
bronchiectasis, cystic fibrosis, TB, fibrosing alveolitis
GIT causes: IBS (Crohn, ulcerative cholitis), liver cirrhosis, GIT lymphoma,
malabs. (coeliac dis.)
CV causes: congenital cyanotic heart dis., endocarditis, atrial myxoma,
aneurysms, infected grafts
o koilonychia (flat or concave)– in iron-deficiency anemia
o onycholysis (lifting of the nail plate)
psoriasis
trauma
fungal
o pitting of the nail
psoriasis
o nail apparatus melanoma
2-3% of melanomas
longitudinal pigmented streak in the nail
pigmentation of the proximal nail fold
late Dx
poor prognosis
Skin ulcers
- skin ulcer – Murtagh 1195
o venous ulcerations (gravitational, stasis, varicose ulcers) - MC
location
lower 1/3 of the leg, above medial or lateral malleolei (gaiter area)
more on the medial side of the leg
Hx of trauma, venous insufic. or DVT
always sec. to deep venous thromboflebitis
the assoc. chronic venous HT causes trophic changes:
- hyperpigm.
- fibrotic thickening
- induration
- eczema
- and finally ulcers
ulcers usually shallow, but can reach to periosteum
sometimes you can find the granulation floor
it is slow healing
not tender, but can be painful
pain is relieved by raising the leg
Sx
wet
blue skin
warm leg
varicosities, varicose dermatitis
oedema
ragged edge
often superficial
dermatitis
hyperpigm.
“atropie blanche”
ABI > 0.9 (normal)
o arterial
distal
below the ankles:
- tips of the toes
- point of the heel
- pressure points
heels
head of first metatarsal
malleoli
punched out
often deep
painful
dry
skin atrophy around
no oedema
minimal granulation tissue
cold leg
loss of hair
ABI < 0.5-0.8
Hx of arterial dis., smoking, DM
o Rx
we need the patient’s compliance
promote the clean granulation tissue
appropriate cleansing and dressing
avoid antiseptics
avoid soaps
just wash with NS
use intrasite gel and benzoyl peroxide
occlusive bandages with zinc oxide
in inf. or cellulitis - A/B
compression banding is the mainstay of the Rx
from the base of the toe (toe not included) to just below the knee
depending on the ABI
- ABI < 0.8 – caution
mild compression for 0.6-0.8
bed rest, elevation above the heart level
RICE:
rest
ice
compression
elevation
encourage early mobilization and good nutrition
if oedema elevate the leg + diuretics
ulcers will not heal in oedema
treat varicose veins
unna`s boots - compression stocking + unna`s paste = 15% zinc oxide
o + metabolic
DM – neuropathic = trophic ulcer
These are due to diabetic neuropathy causing loss of sensation which
follows an injury of which patient is unaware.
Deep punched out lesions over pressure points.
Common site – ball of the foot under 1st metatarsal head. Sometimes
heel may also be affected.
These ulcers may extend to the bones and into joints.
They are prone to secondary infections.
Treatment
- Based on controlling the diabetics.
- Clearing infection with appropriate antibiotics.
(iv flucloxacillin+ iv gentamycin +iv metranidazole)
- sensory loss: gloves and stockings
- Dx to confirm cause – arterial Doppler
o + pyoderma gangrenosum
in IBS, rheumatoid arthritis, multiple myeloma, etc.
deep ulcers, usually on the legs
oral C/S as Rx of choice in pyoderma gangrenosum (skin manif. in ulcerative
cholitis)
o inf. – smelly discharge
bact. gram +, -, anaerobs (deeper)
syphillis
deep, chronic
atypical mycobact.
deep fungi
Infectious diseases - OK
TB
- TB
o triad: malaise + cough + wt. loss +/- erythema nodosum
o exposure can give
primary TB
Sx – cough, hemoptysis, sweating , fever, malaise, anorexia
- Murtagh – in most cases asympt.
x-ray: infiltrates in the middle and lower lobes + hilar lymphnodes
(unilat.)
latent TB - MC
Mantoux test – positive
no clinical features
usually no X-ray changes
10% (if weak immune system) will progress (progressive primary TB)
to reactivation =>
active secondary TB, within first 2 yrs of exposure
clinical
- constit. – fatigue, night sweats, wt. loss
- site dependent sympt.
pulmonary TB – MC
Sx
o chronic productive cough
o +/- hemoptisis
x-ray
o infiltration and cavitations in upper
lobes (apical area)
o hilar lymphadenopathy
o pleural effusion
o past. inf. - apical calcif. and scarring –
can still have surviving bact.
miliary TB
x-ray: multiple small bilat. seed-like lesions
extrapulm TB
pericarditis, peritonitis, meningitis,
osteomielitis, epididimitis or tubal TB
o MCQ: constrictive pericarditis with
previous TB exposure (ventr. failure,
oedema, JVP extremely high, abd.
distension)
x-ray - infiltr. in apical lobes +
pleural effusion
o Dx
Mantoux test:
delayed hypersensitivity test
- evaluated after 72 hrs
< 5 mm = negative
- do vaccination!
5-10 mm = past vaccination
> 10 mm = positive
- evidence of inf.
active
inactive – latent TB
chest x-ray
if productive cough
sputum – acid-fast bacili
- stain – Ziehl Nielson
- culture
TB specific – interferon gama release assay
bronchoscopy and biopsy can be considered
pleural effusion – with monocytes
o Mx
only by specialist! (not by GP)
notifiable dis. -> Dept. of Human Services
contact tracing by Dept. of Human Services
bacterial confirmation and drug susceptibility testing first – only then will be
Rx
no isolation!
o Rx
active TB
4 drugs (rifampicin, isoniazid, pyrazinamide, ethambutol) for 2 mths
then 2 drugs (rifampicin and isoniazid) for 4 mths
- total 6 mths
latent TB (Mantoux positive, no sympt., no x-ray)
when active TB is excluded: isoniazid mono-therapy for 6-9 mths
treat only specific groups:
- recent TB converters (Mantoux test neg., recently – within last
2 yrs - became pos.)
- children, adolescents
- close contact with patient smear-TB positive
- patient with HIV, DM uncontrolled, CRF, C liver F
- overseas trained people (immigrants)
pregnant
start Rx ASAP
- pyrazinamide not recommended
- isoniazid, rifampicin, ethambutol – 9 mths treatments
don’t cross placenta
no teratogenic effect
minimal conc. in milk – breast feeding is NOT CI
isoniazid resistant TB
streptomycin or amikacin instead of isoniazide
Food poisoning
- diarrhoea – Murtagh 470, Oxford 390
o staf. aureus - 1-6 hrs
o vibrio cholerae – 2 hrs – 5 days
Rx – doxycycline
in pregnant women: amoxycillin
o Clostridium perfringens – 8-24 hrs
o Clostridium botulinum – 12-36 hrs
honey, canned food
botulusm – descending paralysis
o Salmonella – 12-48 hrs
can return to work after 3 consecutive weekly negative stool cultures
usually no A/B if not inflammatory (no blood, no fever) – just observe, give fluids
if severe: ciprofloxacin
o E. coli – 12-72 hrs
Rx – in moderate / severe cases: norfloxacin, ciprofloxacin
o Shigella – 2-3 days
bacillar dysentery: blood in stool, fever
Rx – moderate to severe: cotrimoxazole., norfloxacin
o campylobacter – 2-5 days
Rx – if prolonged: norfloxacin
o Giardia lamblia – 1-4 weeks
MC non-viral gastroenteritis
profuse watery diarrhoea, with undig. food
no mucous, no blood, no fever
steatorrhoea, malabs. syndrome
abd. distension, cramps
wt. loss, FTT
after camping
Dx – stool microscopy
Rx – tinidazole, metronidazole
o Entamoeba hystolitica – 1-4 weeks
amoebiasis
dysentery (blood, mucous in stool)
Rx - metronidazole
o Clostridium difficile – 1-7 days
pseudomembranous colitis
after antibiotics (clindamycin, cephalosporins, penicillin based AB, like
amoxycilin
bloody diarrhoea, GI perforation, toxic megacolon
Rx:
o stop A/B
o metronidazole
o vancomycin
o rotavirus – 1-7 days
Traveller’s disease
- traveller’s diarrhoea
o 1. E. coli – 12-72 hrs
o 2. campylobacter – 2-5 days
o 3. yersinia & pseudomonas aer.
o Giardia – 1-4 weeks
- travaller’s dis. (Alena)
o travelling to an area with sleeping sickness – Rx – give him vaccine
o after travel
sympt. within 2 wks in most dis.
sympt. > 2 wks -> only HIV
o if GIT sympt.
Dx
1 - stool microscopy
2 - stool culture
o traveller’s diarrhoea
acute (not persistent)
E. coli - MC
6-12 hrs after food intake
lasts for 2-3 days
watery stool +/- vomiting
Mx
- rehydration in mild cases
- A/B only in moderate and severe cases
norfloxacin, ciprofloxacin, azythromycin
persistent diarrhoea
giardiasis
- no mucous and blood
- Mx - metronidazol
amoebiasis
- mucus and blood
- Mx - metronidazol
typhoid fever
Salmonella typhi
incub 3-21 days
spread: faecal –oral
Sx
- triad: stepladder fever (gradually increases over 4 days) + abd.
pain + bradycardia
- insidious onset, headache, dry cough, fever, abd. pain, pea-soup
diarrhoea or constipation
- high fever with relative bradycardia (usually fever causes
tahic.)
- abd. pain, splenomegaly
- rose spots on the trunk (40%) – late sympt.
- CNS signs: confusion, lethargy, coma, meningism = toxic state
- Dx
blood culture - first 10 days
serology
later – urine / stool
- Cx
GIT bleeding
GIT perforation
- Rx
ciprofloxacin
if fever, rigors – MC = malaria
malaria = returned traveller (most of them within 2 months of return) +
fever
- return from Vietnam
- Sx
triad: fever + chills + headache
abrupt onset with high fever, chills, rigors, sweating,
headache, abd. pain
atypical presentation: diarrhoea, abd. pain, cough,
vomiting, jaundice
arrhythmia
huge hepatomegaly, splenomegaly
- Dx
thick and thin films (from blood)
FBE: monocytosis + thrombocytopenia
cerebral malaria: periventricular changes on CT scan
- Rx
admit
supportive
antimalarial drugs
P. vivax, P. ovale, P. malariae – chloroquine +
primaquine
in chloroquine-resistant malaria -> artimisinin,
artemether, mefloquine
o artimisinin also for pregnancy, kids
uncomplicated P. falciparum - quinine +
doxycycline or merflquine
complicated P. falciparum (severe) – quinine IV
- prophylaxis (murtagh 116)
avoid mosquito bites:
keep away from rural areas after dusk
sleep in rooms with mosquito nets
use insect repellent
wear long sleeves and trousers
avoid using perfumes – attract mosquitos
take antimalarial medicines regularly
non-pregnant woman
o chloroquine sensitive area ->
chloroquine
o chloroquine resistant area ->
mefloquine or doxycycline or proguanil
o multidrug resistant area (Thailand,
Cambodia, Myanmar) -> doxycycline
+/- chloroquine
pregnant woman
o preferable and approved in I trim. of
pregn. = chloroquine and proguanil
o mefloquine can be given in II and III
trim.
o other traveller’s dis. w/o diarrhoea
hepatitis A, E
Dengue fever – M 123, 260
triad: fever + severe aching (muscle ache / body ache / pain on
movement of eyes) + rash
endemic in Queensland
flavi virus, part of arbovirus
mosquito transmission
transm. - female Aedes mosquito
children get least severe illness
pain
- starts with pain behind the eye
- severe backache
caract. maculopapular rash – starts from limb - > trunk
fever, malaise, nausea
Dx
- IgM serology
- leucopenia with thrombocytopenia
Rx – symptomatic
convalescence – severe fatigue and depression (suicidal risk)
no vaccination
Ross River fever
from Queensland with fever = Ross River fever
mosquito borne
Ross River virus = alpha virus
fever + polyarthralgia + rash + from Queensland
Yellow fever (bradycardia like in typhoid + jaundice like in malaria)
triad: fever + bradycardia + jaundice
Africa, South America
West Nile River encephalitis
transm. by mosquitos – mosquito nets, repellants
viral disease
more common in US
o immunisations
compulsory
yellow fever
menigococcus
voluntary
hep. A, B, E
typhoid
cholera
japanese B encephalitis
- triad: febrile illness + vomiting + stupor
rabies
typhus
plague
- zoonoses
o Brucellosis (undulant fever, Malta fever)
from cattle
triad: malaise + headache + undullant fever
Cx – chronic fatigue syndrome
o Q fever – Coxiella Burnetti
in cattle (and sheep) farmers and handlers
abattoir workers
triad: fever + headache + prostration
sudden onset with fever, rigors, myalgia
pneumonia, hepatitis, endocarditis – sometimes
Rx – doxycycline
vaccine
o leptospirosis:
in abatoir workers, veterinarians, sewage workers, farmers
Sx
triad: abrupt fever + headache + conjunctivitis
undulant fever?
abrupt headache
severe myalgia
jaundice
petechial rash on the skin
liver and spleen enlarged
- HIV
o chronic diarrhoea, axilar and inguinal lymphadenopathy, failure to thrive
- diarrhoea
o hyponatremic – can cause seizures but less often
o hypernatremic – with less dehydration, but more often seizures
- trachoma
o MC inf. cause of blindness in aboriginals
o direct transm.
o Chlamydia trachomatis
o 5 stages: FISTO
1. folicles > 5
2. inflam.
3. scarring
4. trichiasis (inversion or eversion of the eyelashes)
5. opacity of cornea
o Mx: SAFE
surgery
A/B
non-pregnant woman, child – azythromycin
pregnant woman, child < 6 kg – erythromycin or roxythromycin
facial cleanliness
environmental upgrade: sanitation, hygiene
Hematology - OK
Leukemias
- multiple myeloma (MM)
o multiple myeloma - cancer of plasma cells, a type of white blood cell normally
responsible for the production of antibodies
o elderly – 60 yrs
o Sx
triad: weakness + back pain + wt. loss
CRAB: calcium incr., renal failure, anemia, bone lesions
osteoporosis, back pain (> 80%), bone pain and tenderness
incr. pathol. bone fractures
weakness, tiredness
recurrent inf.
CRF
hyperviscos. syndrome – clots in the brain, dementia, etc.
o Dx
normocytic anemia
next examination: protein electrophoresis in serum and urine -> increased
level of abnormal globulins
serum – M (monoclonal protein) spike in the IgG zone
urine - Bence-Jones protein (composed of free light chains)
ALP is normal, unless fractures present
very high ESR
incr. Ca, normal phosphate
best examination: bone marrow aspiration to confirm Dx: increased plasma
cells, replacing the bone marrow
x-ray: “punched out osteoclastic lesions on the skull”
o Rx
chemotherapy
medial survival = 3 yrs
- leukemias
ALL AML CLL CML
2-10 yrs + 55-60 yrs 65 yrs (older) 40-60 yrs (younger)
second peak at 40 yrs MC type of leukemia
Triad: malaise + pallor Triad: malaise + pallor Triad: fatigue + wt. Triad: fatigue +night
+ bone pain + oral problems loss + sweats + abd.
Lymphadenopathy, Gum hypertrophy, lymphadenopathy fullness
hepato-splenomegaly gingivial bleeding Enlarged rubbery (splenomegaly)
Testic. and CNS involv. CNS involv. at lymphnodes (only in Massive
Pancytopenia with presentation is rare the lymphoid line CA, splenomegaly (due
circulatory blast cells Pancytopenia with not in the myloid line to bleeding
Pallor of normocytic circulatory blast cells CA) in neck, axilla, disorders)
anemia Pallor of normocytic groin Gout features
Susceptibility to inf. anemia Hepatosplenomegaly (purine distruction)
Bruising, petechiae Susceptibility to inf. (50%) Priapism
due to decr. platelets Bruising, petechiae Mild anemia Blast crisis =final
MCQ: ALL post due to decr. platelets stage -> behaves
chemotherapy –> fever like an acute
and pancytopenia –> leukemia, with rapid
admit patient progression and
short survival
Blasts (lymphoblasts) Blasts (myeloblasts) Lymphocytosis > Philadelphia
Positive for TDT AUER rods 15x109 / L mature chromosome t(9:22)
Positive for (BCR/ABL fusion
myeloperoxidase and gene)
Sudan dye WBC very incr. >
100x109 / L
Left shift (immature)
Chemotherapy Chemotherapy Chemotherapy – Chemotherapy -
(vincristine, aspargine, Complic. of chlorambucil Imatinib
daunorubicin) chemotherapy: Radiotherapy – to Stem cell transplant
If CNS involv. –> 1. inf. de-bulk the swollen
intrethecal 2. tumor lysis lymph nodes
methotrexate syndrome (increase Splenectomy
Treat aggressively any serum urea level,
inf. (IV A/B) acute renal failure)
Relapses – bone Relapses – bone
marrow / stem cell marrow / stem cell
transplant transplant
- Hodgkin vs. non-Hodgkin
Hodgkin Non-Hodgkin
Reed-Sternberg cells (50% infected with EBV) No R-S cells
2 peaks: young adults (15-35), elderly (>55)
Rubbery painless lymphnodes (cervical 60- More than 1 region of lymphnodes involved (2-
70%, axillary, inguinal, paraaortic, 3) + extranodal tissues involved:
mediastinal) -> may later become matted Waldeyer’s ring – peritonsilitis
(aglutinate to form a mass) Burkitt’s lymphoma – characteristic jaw
Triad: malaise + drenching night sweats + lymphadenopathy (assoc. with EBV or HIV)
pruritus Skin tumor – cutaneous T cell lymphoma =
Cyclical fever Sezary syndr.
Pain in the enlarged lymphnodes after Hepatosplenomegaly
drinking alcohol
Splenomegaly (considered a lymphnode)
Hepatomegaly
Scenarios:
1. One tonsil enlarged, no fever, no pain
2. tonsil enlarged
- young, non-smoker = lymphoma
- 1 tonsil enlarged, smoker, ulcer on tonsil =
SCC
Dx Dx
1st step: FNAC - cytology 1st step: FNAC - cytology
2nd and the best: lymphnode excisional biopsy 2nd and the best: lymphnode excisional biopsy
- hystology - hystology
Blood: hypochromic anemia, incr. WBC, Blood: pancytopenia
platelets N or decr.
Rx – chemotherapy+/- radiotherapy Rx – chemotherapy+/- radiotherapy
Prognosis: More aggressive than H., poorer progn.
1. lymphocytes predom. – best prognosis
2. nodular sclerosis
3. mixed cellularity
4. lymphocyte depletion
- stem cell
o lymphoid stem cell
lymphoid blast
lymphocyte
o myeloid stem cell
myeloid blast
RBC
WBC
platelets
- types of leukemia:
o acute leukemia – problem at the blast level
o chronic leukemia – problem at the mature cells level
Coagulation problems
INR, PT (extrinsic APTT (intrinsic Platelets Bleeding time
pathway) and common
pathways)
DIC Incr. Incr. Decr. Incr.
Heparin Incr. Incr. N N
Warfarin, vit. K Incr. Incr. N N
deficiency
Hemophillia A N Incr. N N
Von Willebrand N Incr. N Incr.
Thrombocytopenia N N Decr. Incr.
HSP (vasculitis) N N N N
- DIC
o Sx
bleeding from the venopuncture sides, hematuria, incr. bruising
o Dx
decr. platelets
decr. fibrinogen
incr. D-dimer = incr. fibrin degradation products
+ schizocytes = fragmented RBCs
o Rx
fresh frozen plasma
iv heparin – to stop the clotting in the peripheral vessels
- bleeding problems
o Haemophilia – X-linked recessive (only in boys)
A
= fact. VIII deficiency
more common
Sx
- triad: spontaneous hemarthrosis + muscle bleeds + delayed
bleeding
- spontaneous hemarthrosis, MC in knees, ankles and elbows =
pathognomonic
- many are seropos. for HIV, HBV, HCV – transmission through
factor VIII
low platelet count – suspicion of HIV-assoc. ITP
Rx
- avoid aspirin
- cryoprecipitate
- fact. VIII concentrates
B (Christmas dis.)
= fact. IX (Christmas factor) deficiency
less common
Rx
- recombinant fact. IX concentrates
o von Willebrand disease
deficiency of von Willebrand factor =>affects
transport of fact. VIII
platelet adhesion to each other
platelet adhesion to the blood vessel wall
MCQ: in girls, but actually equal in both genders
AD
MC bleeding disorder (1%)
mild, with excellent prognosis
bleeding tendency aggravated by aspirin
Sx
triad: incr. bleeding 1. incision, 2. dental, 3. mucosal
man
- epistaxis
- hemarthrosis (rare)
female
- long and intense first period (menarche) = menorrhagia
- epistaxis
- hemarthrosis (rare)
Dx
prolonged bleeding time
prolonged APTT
Rx
avoid aspirin!
before dental or surgical procedures + to stop existing bleeding use:
- desmopressin acetate (DDAVP – promotes the release of von
Willebrand factor from the blood vessel walls)
- fact. VIII concentrate
- tranexamic acid - antifibrinolytic
- cryoprecipitate (contains, among other factors, fact. VIII and
von Willebrand)
o Petechiae/purpura/ecchymoses:
Vascular
HSP
- non-thrombocytopenic purpura
severe inf. – severe angiitis, usually followed by DIC
- meningococcaemia
- other septicemias
simple purpura (easy bruising syndrome)
- in young women
bruising with minor trauma + heavy periods
Platelet disorders - platelets < 50 x 109/L
Immune thrombocytopenic purpura (ITP) = isolated thrombocytopenia
- Short history of symptoms
- types:
acute thrombocytopenia of childhood
child well otherwise
viral inf. in recent Hx or drugs
cross-reacting AB against platelets
Dx
o BMA: megakariocytes incr.
(compensatory)
Rx of bleeding
o IgG
o C/S
prognosis
o 90% self-limiting in 6 mths
o 10% pass into chronic ITP
chronic ITP
autoimmune disorder
adult women
Rx
o prednisolone
o azothioprine, methotrexate
o splenectomy – in some patients (but
risk of subsequent severe inf., e.g. with
strepto. pn.)
avoided in children
- Sx
triad: bruising + oral bleeding + epistaxis
no splenomegaly (rare)
- Dx
exclude ALL/AML
FBE:
platelets significantly decr.
all else normal
thrombotic thrombocytopenic purpura (TTP)
- assoc. with haemolytic uraemic syndrome (HUS)
after E. coli or Shigella inf. (camping)
hemolysis (low Hb), kidney involv. (high urea, high
creat.), unconj. bilirubin incr., palor, hematuria,
hemoglobinuria, incr. in uric acid
- Sx
HUS
haemol. anemia
ARF
fever (non-inf.)
fluctuating CNS signs
thrombocytopenia
- Rx
plasma exchange
FFP
platelets
SLE – autoimmune purpura, with splenomegaly
portal hypertension – hypersplenism / splenomegaly => decr. platelets
o splenectomy
indic.
chronic ITP
heredit. spherocytosis
hypersplenism
trauma
lymphoma
who will benefit more from splenectomy: chronic ITP
risks
short term
- thrombocytosis
- risk of thrombembolism
long term
- severe inf. with strepto. pn. in the first 2 yrs
Rx – start A/B ASAP: penicillin, amoxycillin
prophylaxis
pneumococcal vacc. 2-3 weeks pre-op. + repeat every 5 yrs
meningococcal vacc. – every 5 yrs.
H. influenza B – Hib – once (if not immunized)
MCQ: after 2 yrs, URTI –> Rx - A/B
o bleeding
from everywhere – DIC
hemarthrosis – haemophilia
petechial rash, bruising – ITP
o epistaxis
causes
HT - MC
local
- cocaine abuse
- chronic rhinitis, chronic sinusitis
- ulcers in nasal cav.
- perforation of nasal septum
- nasal polyps
bleeding disorders: von Willebrand dis., etc.
- thrombophilia – Murtagh 1367
o primary tendency to coagulopathy
o types
inherited
fact. V Leiden gene mutation
prot. C deffic.
prot. S deffic.
prothrombin gene mutation
antithrombin deffic.
acquired
anti-phospholip. AB
lupus anticoagulant
incr. homocystein
o thrombophylia screening – all the factors above:
fact. V Leiden
prot. C
prot. S
prothrombin
antithrombin
antiphosphopholipid AB
lupus anticoag.
homocystein
+ anthrombin C AB?
+ antiocardiolipin AB?
o indic. for investig.
recurrent thrombosis
venous thromboembolism < 40 yrs
arterial thrombosis < 30
skin necrosis on warfarin
recurrent fetal loss
familial thromboembolism
o MCQ:
daugther asking for OCP, mother had DVT
woman with DVT wants to get pregnant
-> do thrombophilia screen
Anemia
- iron studies – Murtagh table p. 146
o 1. serum iron
o 2. transferrin (the major protein carrying the iron in blood)
transferrin conc. = TIBC (total iron-binding capacity)
level rises when iron reserves become depleted
low iron + incr. TIBC = iron deficiency
o 3. tranferrin saturation
= serum iron / TIBC
very incr. in haemochromatosis
o 4. serum ferritin
reflects the iron stores in the body
decr. values even before the serum iron gets decr.
Serum Fe TIBC % Transferrin Ferritin
saturation
Iron deficiency Decr. N or incr. Decr. Very decr.
Anemia of chronic Decr. N or decr. Decr. N or incr.
dis.
Thalassaemia, N or incr. N N or incr. Incr.
Sideroblastic
anemia
Haemochromatosis Incr. Decr. Very incr. Very incr.
- anemia – Murtagh 212
Iron defic. B12 defic. Folate defic. Chronic dis. Haemol.
(B12 decr.) (folate
decr.)
MCV <80 > 98 > 98 N or <80 N
Iron Decr. N or decr. Incr.
TIBC Incr. Decr. Decr.
Transferrin Decr. Decr. Incr.
saturation
Ferritin Decr. (most Incr. Incr.
characteristic)
Other Incr.
findings urobilinogen,
incr.
reticulocytes,
incr. iron
absorbtion,
decr. RBC
survival
- anemia:
o Sx
triad: fatigue + palpitations + exertional dyspnoea
headache, faintness/dizziness
angina on effort
o types:
Microcytic anemia - MCV < 80
- Iron deficiency anemia
causes
chronic blood losses: menorrhagia, GIT bleeding,
malignancy (occult blood losses – colon CA)
incr. demands: prematurity, multiple pregnancies,
adolescence, pregnancy
o iron stores
term baby – 6-8 mths
premature baby – 6 weeks
malabs.: coeliac, postgastrectomy
inadequate intake: drinking a lot of cow’s milk
high risk
children:
o prevention< 6 months, premature and
low wt.
o 1. toddlers 6-36 mths with a diet high
in cow’s milk and low in iron: highest
risk
o exclusively breastfed > 6 mths
o delayed introduction of solids
o lack of vit. C
2. adolescents
adults
o 3. women of child-bearing age
prevention
avoid cow’s milk in the first 12 mths
avoid excessive cow’s milk in the first 24 mths
introduce iron-containing solids early, at 4-5
mths
Rx
correct the cause
iron-rich foods
iron supplements
o types:
oral – 6 months (to replenish
stores)
parenteral (SE – allergic reaction)
o anemia responds in 2 weeks and is
corrected after 2 months
- Hemoglobinopathy
alpha-, and beta-thalassemia
incr. prevalence
o alpha - Asia
o beta - Mediterranean basin, Middle east,
north and central India and South East Asia
(China)
AR
alpha – deletion of 1-4 genes for the 2 alfa globin
chians
o 4 genes – major alpha thalassemia (no
alpha chains; hydrops fetalis)
o 3 genes – haemoglobin H dis. (mild to
moderate anemia; HbH on electroforesis)
o 1-2 genes – symptomless carrier
beta – 2 genes
o minor / heterozygous / trait – 1 gene is
mutated
usually asympt.
o major / homozygous – 2 genes are mutated
very severe haemolytic anemia
triad: pallor + jaundice +
hepatosplenomegaly
neonatal jaundice
Dx
HbA2 (no alpha chains) incr. (> N =2%)
o > 3.5 = trait
Hb F (fetal)
blood film:
o microcytic anemia
o target cells
o nucleated red cells
o reticulocytosis
o basophilic stippling - erythrocytes
display small dots at the periphery.
These dots represent accumulations of
rRNA and are always pathological
Rx (in major)
o transfusions
o desferrioxamine (iron chelation agent)
o folic acid
o splenectomy
HbE syndrome
South-East Asia (like thalassemia)
HbC syndrome
and various other unstable hemoglobin diseases
- Sideroblastic anemia
abnormal production of ringed sideroblasts, caused either
genetically or indirectly as part of myelodysplastic
syndrome, which can evolve into hematological
malignancies (especially acute myelogenous leukemia).
The body has iron available but cannot incorporate it into
hemoglobin. Failure to completely form heme molecules,
whose biosynthesis takes place partly in the mitochondrion.
This leads to deposits of iron in the mitochondria that form
a ring around the nucleus of the developing red blood cell.
types:
Hereditary sideroblastic anemia
Acquired sideroblastic anemia, including lead
toxicity
Reversible sideroblastic anemia
- Anemia of chronic disease (sometimes – but more commonly
presenting as normocytic anemia)
Macrocytic anemia – MCV > 98
with megaloblastic changes:
- deficiency of vitamin B12
body stores: 3-5 mg
causes:
vegans / vegetarians > 3 yrs
Macrocytic anemia can also be caused by
removal of the functional portion of the
stomach, such as during gastric bypass surgery,
leading to reduced vitamin B12/folate
absorption. Therefore one must always be
aware of anemia following this procedure.
Pernicious anemia is caused by a lack of
intrinsic factor. Intrinsic factor is required to
absorb vitamin B12 from food. A lack of intrinsic
factor may arise from:
o an autoimmune condition targeting the
parietal cells (atrophic gastritis) that
produce intrinsic factor or
o against intrinsic factor itself (AB
antiintrinsic and AB antiparietal).
These lead to poor absorption of
vitamin B12.
o Dx - hypersegmented polymorphs?
terminal ileum pathology (where B12 is
absorbed): Crohn, ileitis, tapeworm
blind intest. loop syndrome
H. pylori inf.
H2 receptor blockers, PPI
other drugs: OCP, metformin
chronic alcoholism
HIV
incr. demands
Sx
anemia
neurol. problems
o subacute combined degen. of the
spinal cord
o polyneuritis
o atrophic glossitis
Dx
Schilling test
Rx
vit. B12 IM
- deficiency of folic acid (or both).
not stored in the body
daily requirements: 5-10 micrograms/day
does not produce neurological symptoms, while B12
deficiency does.
causes:
decr. intake: old age, poverty, malnutrition,
alcoholism
malabs.
drugs: phenytoin
incr. demands in pregnancy – pernicious
anemia of pregnancy
o MC cause of anemia in pregnancy
Rx
folate p.o.
- drugs:
cytotoxic: Methotrexate, zidovudine, azathioprin, 5-
fluorouracil
anticonvulsants: phenytoin, phenobarbitone
A/B: co-trimoxazole, pyrimethamine
without megaloblastic changes:
- Alcoholism commonly causes a macrocytosis, although not
specifically anemia.
first indication of alcohol abuse
- Other types of Liver Disease can also cause macrocytosis.
- Myelodysplastic disorders (sideroblastic anemia)
Cx
inf.
haemorrhage
leukaemia (CML)
- Hypothyr. (usually normocytic)
Normocytic anemia - the overall hemoglobin levels are always decreased, but
the red blood cell size (Mean corpuscular volume) remains normal.
Acute blood loss
- causes
haematemesis
melena
- Dx – reticulocytes incr.
Hemolytic anemia
- Dx
incr. unconj. bilirubin
reticulocytosis (polychromasia)
decr. haptoglobin
protein that in humans is encoded by the HP
gene
In blood plasma, haptoglobin binds free
hemoglobin (Hb) released from erythrocytes
with high affinity and thereby inhibits its
oxidative activity. The haptoglobin-hemoglobin
complex will then be removed by the
reticuloendothelial system (mostly the spleen).
In clinical settings, the haptoglobulin assay is
used to screen for and monitor intravascular
hemolytic anemia.
o In intravascular hemolysis free
hemoglobin will be released into
circulation and hence haptoglobin will
bind the Hb. This causes a decline in Hp
levels.
o Conversely, in extravascular hemolysis
the reticuloendothelial system,
especially splenic monocytes,
phagocytose the erythrocytes and
hemoglobin is not released into
circulation and hence haptoglobin
levels are normal.
- types
congenital:
hereditary spherocytosis
o spherocytes -> get stuck in the spleen ->
splenomegaly
o Dx
clinical
incr. MCHC (mean corpuscular
hemoglobin concentration)
osmotic fragility test
o Rx
phototherapy or exchange
transfusion – if kernicterus is
present
folic acid to prevent
megaloblastic crisis
splenectomy
hereditary eliptocytosis
(thalassemia)
sickle cell anemia
defic. of G6PD
o X linked recessive – in boys only
o African (Sudanese), Mediteranean,
Asian
o causes episodic anemia due to decr.
capac. of the RBC to deal with
oxidative stress; precip. by
inf.
antioxidant drugs:
sulphonamides, antimalarial,
nitrofurantoin, vit. C and K,
traditional medicine, high dose
aspirin, naphtalene
broad beans (favism)
o neonatal jaundice
o Dx
Beutler fluorescent spot test
Heinz bodies (bill cell) -
inclusions within red blood
cells composed of denatured
hemoglobin
sometimes with spherocytes
o no Rx
defic. of pyruvate kinase
acquired
ABO/Rh immunis.
drug toxicity
o A/B: antimalarials, sulphametoxazole
o antiinflam.
o penicillin, methyldopa
inf.
o Mycoplasma
o malaria
DIC
autoAB
o cause
idiopathic - 50%
non-Hodgkin lymphomas
SLE
o action
cold agglutinin dis. - IgM
act at body temp. – Ig G -
autoimmune hemol. anemia
o Dx – direct Coombs test pos.
Anemia of chronic disease and malignancy
- enough iron, but intercellular iron transport within the
marrow is suppressed in inflam. => erythropoiesis is
suppressed
- MCQ: boy who looks pale and has chronic diarrhoea
chronic kidney disease – defic. of erythropoietin
- Rx – adm. of erythropoietin
endocrine disorders: hypothyroidism (can be macrocytic as well)
- with bradycardia, fatigue, constipation, lymphocytosis
bone marrow replacement
- metast.
- myelofibrosis
- ALL, AML, CML, CLL, lymphoma
- aplastic anemia
o destruction of hematopoesis
o pancytopenia + hypocellularity in the bone marrow
o types
congenit – Fanconi
acquired
idiopathic – MC
immune
post-viral inf.
- parvovirus B19
- HBV
- Epstein-Barr
- HIV
o Sx
no splenomegaly
no hepatomegaly
no lymphadenopathy
o Rx
supportive
RBCs, platelets transfusion
A/B
immunosuppresion – if immune cause
bone marrow transplant
Digestive system - OK
Pre-hepatic Post-hepatic
Function test Hepatic Jaundice
Jaundice Jaundice
Normal /
Total bilirubin Increased
Increased
Normal
Alanine transferase and
Increased
Aspartate transferase levels
- jaundice
o = bilirubin > 17 micromol/L
o clinical jaundice > 50 micromol/L
- hyperbilirubinemia
o unconjugated
haemolytic jaundice – starts after 4-6 mths
spherocytosis
G6PD deficit
drugs – methyldopa
sickle cell anemia
- sickle cell crisis
sickle cells get plucked inside the capillaries and cause
infarcts
precip. by
inf.
cold weather
hypoxia
dehydr.
acidosis
surgery
types:
vaso-occlusive
splenic sequestration
o => infarction
o severe pain in the LUQ
o Rx
O2 + hydration
aplastic
haemolytic
Cx
unequal digits (infarction in the bones)
Dx
Hb electrophoresis (HbS)
Howell-Jolly bodies = basophilic nuclear
remnants (clusters of DNA) in circulating
erythrocytes
o post-splenectomy
o sickle cell – causes autosplenectomy
o coeliac dis. – splenic atrophy
o spleen radiation therapy - Hodgkin
o + myelodysplasia
o + megaloblastic anemia, B12 defic.
o + severe hemolytic anemia
Rx
pneumococcal vaccine
oral penicillin till 5 yrs
+/- splenectomy
ineffective erythropoiesis - megaloblastic anaemia
polycytemia vera
incr. RBC
incr. viscosity
gross retardation at delivery
MC = Gilbert’s syndr.
AD
3-5%
defic. of glucuronyl transferase => incr. unconj. bilirubin
all other fc. test are normal
jaundice when
- under stress
- fasting
- sick (cold)
- etc.
Dx
- fasting bilirubin
- bilirubin after nicotinic acid
- liver biopsy - normal
no Rx required
drugs:
A/B
- flucloxacillin
- amoxyclav
- erythromycin
- rifampicine
radiographic agent
Crigler Najjar syndrome
very rare
types
- I
AR
UDP-G absent
unconj. bilir. > 340 micromol/L -> kernicterus, unless
treated
Rx
fenobarbital doesn’t help
phototherapy, exchange transfusion, etc.
- II
AR
UDP-G decr.
unconj. bilir. < 340 micromol/L
Rx
fenobarbital helps
hypothyr.
Rx - thyroxine
ABO/Rh hemolysis
breast milk jaundice
physiological
o conjugated
familial disorders
Rotor syndr.
- AR
- rare
- non-itching jaundice
- liver cells are not pigmented
- no Rx is required
Dubin Johnson syndr.
- AR
- defect in the ability of hepatocytes to secrete conjugated
bilirubin into the bile
- liver is pigmented in black
- no Rx is required
hepatitis
both direct and indirect bilir. incr.
FTT, dark urine, pale stools
drug induced
chlorpromazine
OCP
primary biliary sclerosis
biliary atresia
after first week
stools are white
AST/ALT incr.
chronic cholestatic jaundice
neonatal sepsis
galactosemia
postop. jaundice
intraduct problems
gall stones
biliary strictures
infection
malignancy – cholangiocarcinoma
extraduct problems
pancreatic CA
pancreatitis
- Jaundice
o in newborn:
kernicterus if bilirubin > 340 micromol / L
Rx
> 285 micromol/L -> phototherapy
> 360 micromol/L -> consider exchange transfusion
types
first 24 hrs – pathol.
- ABO – MC
Mother is group 0, child is A or B
direct Coombs test pos.
w/ spherocytes
Dx diff: day 1 – incr. unconj. bilirubin + incr.
spherocytes + family Hx of spherocytosis =
spherocytosis
Rx
phototherapy immediately
- Rh – more severe
direct Coombs test pos.
w/o spherocytes
> 24 hrs
- physiological jaundice – MC cause of jaundice in newborn (50%
of term babies and 80% of prematures develop jaundice in the
first week of life)
due to immature liver enzymes
start at 2-3 days, max by day 3-5, finishes in 1-2 weeks
(less than 2 weeks)
not very severe
Rx - phototherapy
- breast milk jaundice
starts on day 4-7, lasts up to 6 weeks
hormones secreted through milk are inhibiting UDP-G
child normal, feeding normal
liver enz. normal
Dx – by suspending breastfeeding for 24-48 hrs =>
serum bilirubine falls = breast milk jaundice
Mx – continue breastfeeding
- hypothyr.
- neonatal sepsis
lethargic baby + jaundice + hepatosplenomegaly at the
end of the first week
Dx
both direct and indirect bilirubin are incr.
Mx
I step: blood culture
A/B
- conjug. bilirubin
neonatal hepatitis
biliary atresia
galactosemia
check bilirubin
in day 1 jaundice (ABO)
in jaundice that persists > 14 days
- biliary problems
o first test - U/S: look for 3 things
dilatation of CBD – most important thing to look for
stones
gall bladder – cholecystits?
AST/ALT ALP (obstr. + bone GGT (alcohol +
dis.) drugs + obstr.)
Cholecystitis: N N N
+ fever, Murphy’s
positive, U/S thick
gall bladder wall
Cholelithiasis N N N
+ RUQ pain, nausea,
vomiting, no fever
Murphy’s negative,
U/S gall bladder
stones
Hepatitis very incr. Incr. Incr.
Cholangitis N or incr. Very incr. Very incr.
(Rx – ERCP)
o congenital hepatic fibrosis – less likely with jaundice
Biliary atresia (progressive sclerosing Neonatal hepatitis:
cholangitis) - Infective (TORCH)
- Idiopathic
- Metabolic (AR)– galactosemia, Wilson,
alpha 1 antitripsine
Assoc. with other anomalies Depends on conc.
No family Hx Family Hx
Term babies Pre-term
Persistent acholic / pale stools Normal color stools
U/S gall bladder not visible Gall bladder visible
- biliary problems
o female + pain in RUQ radiating towards the back after eating fatty foods + U/S with
stones= cholelitiasis with biliary colic
o same + fever = cholecystitis
o jaundice + stones in CBD + pain = choledocolitiasis
pale stools, dark urine
Dx
1 – U/S
ERCP
MRCP – the best
o acute cholangitis = (obstructive) jaundice + fever, chills, rigor + abd pain
Charcot triad:
fever, chills
jaundice
severe pain
Dx
1 – U/S
ERCP
MRCP – the best, less invasive
Rx
IV fluids
A/B: ceftriaxone, penicillin, aminoglycosides
ERCP surgery – gold standard
- biliary litiasis
o Sx
Biliary pain:
Severe, constant pain that can last for hours.
History of episodes of similar pain.
Epigastric
- referred to the scapula
If cholecystitis develops, the pain typically shifts to the right upper
quadrant and becomes more severe. + tenderness, guarding (Murphy’s
sign)
The patient may be jaundiced if the common bile duct is obstructed.
Look for right upper quadrant tenderness.
o DIAGNOSIS:
FBC.
U&E.
LFTs.
Lipase/amylase.
Request an upper abdominal ultrasound.
if equivocal / technically inadequate (obese woman) => HIDA (Tc-IDA)
scan of the gall blader (contrast injected in blood -> liver -> secreted in
the bile)
dilatation of CBD
best seen with:
- I – MRCP
- II – ERCP
o MANAGEMENT:
PAIN relief: Morphine 0.1 mg/kg IV with metoclopramide 10 mg IV.
Advise patients to eat a diet low in saturated fat.
Refer the patient to Surgical outpatients for follow-up.
o Cx
1. cholecystitis = MC
2. choledocolitiasis and jaundice
3. pancreatitis
4. ileus
- acute cholecystitis
o Acute, CONSTANT right upper quadrant pain.
Referred to the scapula.
o Associated with fever, anorexia, nausea and vomiting.
no jaundice
o SIGNS: Localized tenderness with involuntary guarding and rebound tenderness.
Murphy’s sign
o DIAGNOSIS AND MANAGEMENT:
FBC, U&E, blood sugar, LFTs, lipase/amylase and blood culture.
incr. CRP, ESR
USG: thickened wall.
Give gentamicin, ampicillin.
Refer to Surgical team for bed rest, analgesia, antibiotics and cholecystectomy.
surgery not when acute cholecystits or cholangitis, but after treating
the inf.
Liver pathology
- types of hepatitis – table Murtagh p. 625
- liver enzimes, ALP, etc. in various hepatic dis. – table Murtagh p. 622
- hepatitis B – printout with the table
HbsAg Anti HBs HbeAg Anti Hbe AntiHBc HBV ALT, AST
DNA
Acute HBV + - + - IgM + Highly
Highly incr.
infective
Chronic HBV + - + - IgG + Highly
highly incr.
infective
Chronic HBV + - - + IgG Incr.
low infective
Recovery + IgG
Immunization +
o serology guidelines
HbsAg = persistent inf.
anti-HBs = past inf. and immunity
HbeAg, HBV DNA = highly infectious (circulating virus)
anti-Hbe = low titre of HBV (low infectivity)
anti-HBc IgM = recent inf.
anti-HBc IgG = past inf.
o HBc antigen is only found in the liver (biopsy), not in the blood
o transmission
blood
sex
also at risk – sexually active homosexual male
saliva
vertical - perinatal transmission – Asia (Chinese South Asia)
lowest risk = scientist in a pathol lab
o Rx
alpha interferon
Lamivudine
liver transplant – recurrence of HBV
o Cx
chronic hepatitis 5-10%
cirrhosis - 15-40%
- 6-15% in 5 yrs -> CA - risk factor for hepatocellular CA (90-100x
or 223x incr. risk)
- 20-23% in 5 yrs -> liver failure
Rx – liver transplant
o prophylaxis
normal human immunglobulin – in people who sustained a needlestick injury
with blood products from a confirmed HBV donor
vaccine
can be admin. to chronic carriers without harm
types
- recombinant
- plasma-derived
- hepatitis C
o most common type of infective hepatitis in Aus.
o in
IV drug users and tatooing - most frequent
post-transfusion
haemophilia
hemodialisys
sex and vertical - uncommon
o Cx
60-80% chronic hepatitis = MC cause of chronic hepatitis
cirrhosis 10-25% in 20-30 yrs
- CA
- liver failure
o RX
ribavirin
alpha interferon
- hepatitis A
o mild, but can cause fulminant hepatitis as well
o excretion of the virus in the feces diminishes at the onset of the clinical dis.
o Sx
jaundice – more common in childrent than in adults
o Px
gamma-globulin – within 2 wks of exposure decr. the attack rate
vaccine
- chronic liver dis.
o Sx
ascites
central abd. resonance and dullness around it and on the flanks
min. 250 ml in order to be detected clinically
Rx
- bed rest
- < 1.5 L of fluids / day
measure body wt. daily
- spironolactone 100 mg (up to 400 mg) / day
add furosemide if response is inadequate
- paracentesis + albumin infusion
bilat. parotid gland enlargement
pigmentation of the skin
telangiectasis
palmar erythema
easy bruising
spider naevi
muscle wasting
testic. atrophy
gynecomastia
asterixis (hepatic flap)
lymphadenopathy
NO peripheral neuropathy
o Dx
smooth muscle autoantibodies
o poor prognosis factors – Child-Pugh classif. of severity
1. encephalopathy resistant to Rx
2. ascitis resitant to Rx
3. incr. bilirubin
4. low serum albumin
5. incr. INR
o Cx
portal HT
portal pressure gradient (the difference in pressure between the portal
vein and the hepatic veins) of 5 mm Hg or greater
types
- prehepatic
portal vein thrombosis
congenital atresia
- intrahepatic.
congenit. fibrosis
primary biliary stenosis -> primary biliary cirrhosis
haemochromatosis
other infiltrates:
sarcoidosis
Wilson’s dis.
chronic viral inf. – HBV, HCV, HDV
alcohol
- posthepatic
Budd-Chiari = hepatic veins thrombosis (or
thromboflebitis)
can be sec. to polycythemia vera
Cx – cirrhosis, ascitis
inf. vena cava thrombosis
constrictive pericarditis
Sx
- Ascites (free fluid in the peritoneal cavity)
- Hepatic encephalopathy
- Increased risk of spontaneous bacterial peritonitis
- Increased risk of hepatorenal syndrome
- Splenomegaly (enlargement of the spleen) with consequent
sequestration therein of red blood cells, white blood cells, and
platelets, together leading to mild pancytopenia
- Portacaval anastomoses (esophageal varices, gastric varices,
anorectal varices [not to be confused as haemorrhoids], caput
medusae – radiate centrifugally from the umbilicus), with
esophageal varices and gastric varices posing an ongoing risk of
life-threatening hemorrhage, with haematemesis or melaena
Rx
- prophylaxis of varices
endoscopic banding
portosystemic shunt – TIPS (transjugular intrahepatic
portosystemic shunt)
but increased risk of hepatic encephalopathy,
and it does not improve the mortality rate
- Management of ascites
This should be gradual to avoid sudden changes in
systemic volume status which can precipitate hepatic
encephalopathy, renal failure and death. The
management includes salt restriction, diuretics
(spironolactone), paracentensis, TIPS and
peritoneovenous shunt.
- Control of hepatic encephalopathy
This includes reduction of dietary protein, followed by
lactulose and use of oral antibiotics.
- Non-alcoholic fatty liver disease (NAFLD)
o is one cause of fatty liver changes, when fat is deposited (steatosis) in the liver when
this is not due to excessive alcohol use.
o It is related to insulin resistance and the metabolic syndrome, and may respond to
treatments originally developed for other insulin-resistant states (e.g. diabetes mellitus
type 2), such as weight loss, metformin and thiazolidinediones.
o Non-alcoholic steatohepatitis (NASH) is the most extreme form of NAFLD, which is
regarded as a major cause of cirrhosis of the liver of unknown cause.
- liver CA
o massive enlargement
in metastases – not enlarged
o Dx
tumoral markers
alphafeto protein (AFP)
Pancreatic pathology
- acute pancreatitis
o past Hx of gall stones, alcoholism
o previous attacks
o risk factors: GET SMASHED
Gall stones
Ethanol
Trauma
Steroids
Mumps
Autoimmune
Scorpione, snake bites
Hypercalcemia, hyperlipidemia, hypertriglyceridemia, hypothermia
ERCP, emboli
Drugs (azathioprine), duodenal ulcers
o Sx
first simpt = severe and constant pain in epigastrium region, radiating to the
back
pain may be partly relieved by sitting up and leaning forwards.
nausea and vomiting
fever, tachicardia, pale, sweating, anxious (shock)
reduced or absent bowel sounds, abd. distension
Cullen sign – periombilical echimosis (discoloration)
Bluish discoloration in the loins (Grey Turner’s sign): Uncommon and develops
after several days.
o Dx
I - FBE
amylase – early, at least 3x > normal level
- inacurate in people with hyperlipidaemia!
serum lipase – most reliable
if jaundice, high bilirubine, severe pancreatitis, suspicion of stone
II = ERCP – Dx and Rx
MRCP – more acurate, non invasive
if no jaundice, mild pancreatitis
II = abd CT - best
- if stone => do III. ERCP
U/S to identify gall stones
Xray
exclude intraperit. gas as a result of visceral perforation
- usually normal or showing ileus
exclude lower lobar pneumonia
LFT
CRP incr., leucocytosis
glucose incr., Ca decr.
o Rx
admission
hydration:
needle-by-mouth (nothing by mouth) = iv fluids
analgezics – morphine
antiemetics – metoclopramide, prochlorperazine
calcium gluconate (if Ca decr.) – slow IV
o mortality > 20%
o Complic
early
shock
acute renal failure
severe dehydration => renal failure (hypovolemia)
DIC
sepsis
hypocalcaemia, hyperglycemia
resp. problems
- atelectasis
- pneumonia
- pleural effusion
late
pseudocyst
- no epitelial lining: wall = fibroid or granulation tissue
- complic. of acute or chronic pancreatitis
- doesn’t move with resp. (retroperit.)
- size
< 6 cm – small, usually asympt., usually will resolve on
its own
> 6 cm – large, symptomatic, can cause gastric outlet
obstr. or compression of bile ducts
palpable, painful
Mx – if stomach obstr. or bile ducts drainage,
even if < 6 weeks, do drainage into stomach,
duodenum or jejunum
o laparoscopic or laparotomy (depending
on size and surgeon)
- age of cyst
< 6 wks – fragile wall (only granulation tissue), can
break
Mx – wait, will probably disappear on its own
> 6 wks – mature, with fibroid capsule, stronger,
resistant wall
Mx – no matter the size, do drainage
- Dx
best investig: CT scan
abscess
pressure on surrounding organs (if inflamed)
hemorrh.
rupture
portal vein thrombosis
- chronic pancreatitis
o MC assoc. with alcoholism
o Sx
pain
o Dx
amylase is N or slightly incr.
some have calcif.
o if associated DM -> Rx with low doses of insulin
- dilatation of gall ducts
o Dx
first – U/S
ERCP - best
MRCP – even better – if available
- pancreatic CA
o head of pancreas
men
Sx
triad: anorexia + wt. loss + jaundice +/- epigastric pain
distended gall bladder, which moves with respiration
jaundice, pale stools, dark urine
wt. loss
Dx
U/S: distended intrahep. and extrahep. bile ducts
- pancr. duct might be dilated as well
urine: conj. bilirubin, no urobilinogen
blood: AST/ALT moderately elevated, incr. total and conj. bilirubin, incr.
ALP
Abdominal pain
o pancreatitis – Hx or alcoholism or biliary stones
fever + epigastric pain + radiating to the back
no abd. signs except for
Cullen sign
Gray Turner sign
o hemorroids – small amounts of painless rectal bleeding
o anal fissure – small amounts of painFULL rectal bleeding
o rectal CA – tenesmus + rectal bleeding + alternate bowel habits + wt. loss
o pregnant woman with lower abd pain
I trim – ectopic
II trim – ovarian torsion / twisted ovarian cyst
III trim – red degen. or fibroid
o a few weeks Hx of postprandial pain = mesenteric ischemia
Acute mesenteric ischemia Chronic mesenteric ischemia
Hx of aterosclerosis / AF (irregular pulse) / After eating -> abd. pain
digoxin
Acute abd. pain + tenderness + no bowel
sounds
Blood stained stool
o acute abd. pain + tenderness + irregular pulse+ no bowel sounds = acute mesenteric
ischemia = mesenteric infarction (Afshan)
CAUSES:
Mesenteric arterial embolism (often associated with AF).
Mesenteric arterial thrombosis.
Decreased mesenteric blood flow (hypotension).
Mesenteric venous thrombosis.
CLINICAL FEATURES:
Middle-aged or ELDERLY patient.
History of vascular disease elsewhere.
Sudden onset of severe diffuse abdominal pain.
The severity of the pain far exceeds the associated physical signs.
Associated with vomiting and bloody diarrhoea.
Abdominal examination: Distension, generalized tenderness, absent
bowel sounds.
diffuse tenderness and rebound tenderness (diffuse peritonitis)
maybe - a few weeks Hx of postprandial pain = mesenteric ischemia
Rectal examination: Fresh rectal blood.
MCQ: Rx of digoxin (and thiazide) + acute abd. pain + tenderness +
irregular pulse = hypokalemia (with bowel sounds present; no bowel
sounds + PR – dark, blood stained material = acute mesenteric
ischemia)
Dx
Angiography to confirm diagnosis
metabolic acidosis
MANAGEMENT:
IV infusion of normal saline.
Refer to the Surgical team.
Poor prognosis.
o rectus sheath haematoma – common in pregnancy + pain after bouts of cough
rupture of abdominal rectus sheath
elderly
Hx of
- coughing due to URTI, TB, bronchitis, asthma
- anticoag therapy
- trauma
- labor
- vigurous and coordinated rectus muscle contr. due to Valsalva
manouvers, coughing, sneezing, straining from constipation,
intercourse
Sx - severe, sudden, acute abd. pain, guarding and abd.rigidity (due to
bleeding inside the peritoneal cavity)
can cause intest. obstruction
periomb. echimosis = Cullen sign (same as in acute pancreatitis)
Dx
- CT
- U/S in pregnant lady
Mx
- surgery
Dysphagia and oesophageal pathology
o oesophageal rupture (Boerhaave syndrome)
sudden chest pain after prolonged vomiting in alcoholics
forceful vomiting against a closed epiglottis (trying to withold
vomiting)
shock, hT
pleural collection: breath sounds absent on a hemithorax
+ subcut. emphysema, mediastinal gas
Dx
CT
then endoscopy – not prior, since it might cause an incomplete tear to
become complete
- Dysphagia
o oesophagitis
causes
Candida (monilial oesoph.)
reflux
- Rx
PPI – the best
H2- receptor blocker
prokinetic
antacid
lifestyle measures
o myasthenia gravis
o Plummer-Vinson syndrome = syderopenic dysphagia
dysphagia (oesophageal webs) + iron-deficiency anemia + glossitis
risk factor for oesophageal SCC CA
o Parkinson
o peptic stricture
lower 1/3 of oesoph.
Cx of reflux oesophagitis
rare today with the current treatments
Dx
barium swallow
endoscopy
Rx
dilate stricture
treat reflux
o globus hystericus = lump in the throat
psychological disorder
o pharyngeal pouch (Zenker’s diverticulum)
post. pharyngeal diverticulum, pushing in the oesophagus
elderly
Sx
dysphagia, food regurgitation, gurgling in the neck
coughing immediately after eating (food regurgitated in the airways)
halitosis
no pain
o oesophageal diverticulum
usually sec. to an underlying motility problems -> sympt. due to the primary
problem
hiatal hernia
o achalasia
incr. lower oesophageal sphincter tone + failure of muscle relaxation
women, 30-40 yrs
Sx
dysphagia for liquids and solids (organic causes usually have dysphagia
only for solids!)
- if severe: has more difficulty swallowing liquids than solids
- usually not progressive!
wt. loss
regurgitation
- at night
- when lying down
chest pain, hiccups, aspir. pneumonia
Dx
1. plain x-rain
- air-fluid level
- absence of gastric air bubble
2. barium swallow
- distended oesoph. - S-shaped + narrowing of the dye in barium
swallow = “rat-tail” (not charact.) + fluid level
3. manometry - high tension at lower end of esophagus
4. endoscopy – exclude CA
Cx
stricture
oesophageal CA
Rx
botox inj. – short term relief
drugs
- nitrates
- Ca channel blockers
pneumatic dilatation – may recur
laparoscopic cardiomyotomy (Heller’s myotomy) – the best
o oesophageal CA
Barrett oesophagus = premalignant lesion for adenocarcinoma of oesoph.
=metaplasia with columnar-lined epithelium in the lower 1/3 of the
oesophagus + ulcer inside + stricture (blue book mcq 3.106)
due to prelonged reflux
types
SCC
adenocarcinoma
Sx
triad: fatigue + dysphagia + wt. loss
severe dysphagia at beginning of meal+ painful swallowing + severe
wt. loss
- gradual dysphagia, for solids, then for fluids
dysphagia + hoarseness of voice = oesoph. CA
Dx
barium swallow – apple core
endoscopy: narrowing of the oesophagus + ulcer
- + biopsy
if initially negative (especially with premalignant lesion),
repeat
Intestinal pathology
- apendicitis
o CLINICAL FEATURES:
Anorexia, nausea, vomiting, diarrhoea or constipation.
Low-grade pyrexia.
Localized abdominal pain: Epigatrium, periumbilical region, RIF.
Tenderness and guarding in RIF.
Rectal examination: To help diagnose a retrocaecal of pelvic appendix.
o Typical march of symptoms (J.B Murphy):
Prodromal mild bowel upset.
Development of abdominal pain, which progressively worsens.
Anorexia (key word), nausea, vomiting.
Moderate fever.
Signs of focal peritonitis over the inflamed appendix.
o DIAGNOSIS:
Physical examination: Abdominal auscultation, palpation, percussion.
FBC and Urinalysis: Leukocytosis, rule out UTI.
Pregnancy test: Female adolescents.
USG: Female (doubt and no peritonitis).
CT: For doubtful cases only.
o MANAGEMENT:
Normal saline infusion.
Give gentamicin 5 mg/kg IV, ampicillin 1 g IV and metronidazole 500 mg IV if
rupture is suspected with peritonitis.
Refer to the Surgical team.
- Meckel’s diverticulum
o most frequent malformation of the gastrointestinal tract
o rule of 2s
2% population
2 inches in length
2% are symptomatic
usually discovered during abd. surgery for a different problem
2 feet from ileo-caecal valve (distal ileum)
age group – 2 yrs
male:female = 2:1
2 types of ectopic tissue:
gastric
pancreatic
o Sx
painless rectal bleeding (not mixed with faeces)
acute / chronic bleeding
umbilicus fistula
o Dx – Tc99m pertechnetate scan, laparotomy
o Cx
intest. obstr.
o Rx – surgical resection
- diverticular disorder
o 90% in descending colon
o due to lack of fibres
o over 40 yrs
o 1/3 people > 60 yrs
o Sx
usually asympt. = diverticulosis
sometimes - irregular bowel habits, constipation
diverticulits – sympt. (< 10% of people with diverticulosis)
This follows inflammation of one or more colonic diverticulae.
It causes LOWER abdominal pain radiating to the left iliac fossa,
tenderness in LIF
can occur anywhere (e.g. small bowel)
Bloody diarrhoea.
Sometimes with sudden PROFUSE rectal bleeding (without faeces).
Sx
- triad: acute pain + left-sided iradiation + fever
- Low-grade fever.
- Abdominal tenderness in LIF
- pain increased with walking and change of position
- Guarding on the LIF with palpable mass.
Complications:
- Perforation.
- Paracolic abscess
- Severe bleeding (elderly).
- Fistula formation (colovesical fistula + vagina, small bowel)
- Bowel obstruction.
DIAGNOSIS
- Request and erect CXR if perforation is suspected.
- U/S, CT scan – detect fistula or perforation
- Sigmoidscopy
Rx
- Commence an IV infusion to treat dehydration or shock.
- Analgesia.
- Antibiotic therapy: Gentamicin, ampicillin and metronidazole.
- Refer to the surgical team.
- profuse rectal bleeding
o divertic. dis.
o angiodysplasia
o ulcerated CA
o IBD
o ischemic colitis
Site Colon only (begins in rectum, continuesAll GIT, mouth to anus (terminal ileus),
proximally) repeated perianal lesions (abscesses,
fistulas), mouth ulcers – caused from
granulomas (granulomas in Crohn - non-
caseating - and TB - caseating)
½ ileocolic, ¼ - 1/3 small bowel only, ¼-
1/3 colon only
Rectal No rectal involvment, no mass Lump in right iliac fossa + rectal
changes (e.g. fistula)
Systemic Wt. loss, fever, lethargy are UNCOMMON Wt. loss, fever, lethargy, etc.
Sx
Lesions The whole colon mucosa but superficial Skip lesion but affecting the whole
width of the intest. wall
Fine granular mucosa
FBE ESR Incr.
Dx Extensive mucosal ulceration may leave x-ray: Free air associated with
normal mucosal islands (pseudo-polyps) perforation may be seen.
visible on plain film. Stenotic regions are best visualized
with barium follow-through studies or
Dilation of the transverse colon greater
on colonoscopy.
than 6 cm indicates the presence of toxic Sigmoidscopy: cobblestone appearance
megacolon. (patchy mucosal edema)
Sigmoidoscopy: granular red proctitis, Colonoscopy – Dx diff. with UC
with contact bleeding
Intestinal obstruction
- intest. obstruction
o triads
with (and without?) Hx of surgery – adhesions
absolute constipation + without bowel sounds = obstruction
elder came with PAIN + constipation + abd. distension + bowel sounds present
= pseudoobstruction
absolute constipation + with no Hx of bowel sounds absent (bowel sounds
present) +/- no X ray given = MC cause is fecal impaction
MC cause of diarrhoea in a bed-ridden patient = faecal impaction
debut:
small bowel obstr. – pain
large bowel obstr. – constipation, abd. distention
if X-ray:
sigmoid volvulus
multiple gas shadows/ haustration
- with Hx of surgery = adhesions
- without Hx of surgery = indirect inguinal hernia
o MC cause in Aus.
small bowel
adhesions (if Hx of surgery)
obstructed groin hernia
gallstone ileus – with Hx of cholelitiasis + colecystoduodenal fistula
- with free air in the biliary tree on x-ray
large bowel
CA
volvulus
- MC in
neonates (in intest. malrotations)
young paralyzed people, bed-ridden
bed-ridden elderly people, chronic constipation ->
stretching -> twisting
- Dx
x-ray: inverted U, pointing up and right (distended
sigmoid loop)
- Rx
endoscopic – passing the tube beyond the kink
Faecal impaction
- Dx
x-ray: ground glass appearance (colon stuffed with
solid faces)
- Rx
enemas
manual disimpaction
Diverticulitis.
Intussusception.
Mesenteric Infarction.
Crohn’s disease.
o Sx
Colicky pain.
becomes continuous pain in case of strangulation
Periumbilical pain: suggests small bowel origin.
Large bowel obstruction can cause pain anywhere in the abdomen.
Strong association with vomiting, constipation and abdominal distention.
Visible peristalsis may be seen.
Tinkling bowel sounds.
Signs of dehydration.
The pain becomes more continuous and generalized if strangulation occurs (MC
with femoral hernia).
Always examine the hernial orifices and perform a rectal examination.
o
o DIAGNOSIS:
Send blood for FBC.
Urea and electrolytes.
Lipase.
Amylase.
Blood sugar levels.
Request erect and supine abdominal X-rays and look for the following features:
- SMALL BOWEL OBSTRUCTION - LARGE BOWEL OBSTRUCTION
o MANAGEMENT:
Commence an infusion of normal saline to correct dehydration from vomiting
and fluid loss into the bowel.
1. NS before surgery
2. Hartmann before surgery
Pass a nasogastric tube.
Analgesia.
Small and large bowel obstr in elderly - gastrografin enema to Dx. diff.
mecanical obstr. (surgery) vs. pseudobstr.
Refer the patient to the Surgical team.
- intestinal pseudo-obstruction
o Chronic impairment of GI motility.
colon: colonic ileus, Ogilvie syndrome
small intestine
o Patients affected: mainly elderly and taking tricyclics antidepressants (anticholinergics).
o types
primary
sec.
scleroderma (esophageal motility is also impaired)
myxedema
amyloidosis
muscular dystrophy
multiple sclerosis
hypokalemia
chronic renal failure
diabetes mellitus
drugs (anticholinergics – in Parkinson, HT medication, opiates)
after pelvic surgery
severe system illness
o Although may involve any part of the GI tract, typically presents with colonic distention.
o Dx
X-ray: Gas in the bowel all the way to the rectum, maximal in the caecum
(classical obstruction - no air into the rectum).
o Treatment:
repeat rectal exam. or sigmoidoscopy to attempt deflation
then prokinetics
then colonoscopic decompression
- perforation of a viscus
o May occur anywhere in the gastrointestinal tract.
o Common sites are:
1. Peptic ulcer: risk factors.
2. The appendix.
3. Colonic diverticulum.
o Can occur de novo.
o CLINICAL FEATURES:
Severe abdominal pain.
Signs of generalized peritonitis with board-like rigidity.
Shock soon supervenes.
o DIAGNOSIS AND MANAGEMENT:
FBC, U&E, blood sugar and lipase/amylase.
Request an erect CXR:
Look for gas under the diaphragm.
Seen in over 70% of cases.
o Rx
IV normal saline.
Analgesia with morphine 2.5-5 mg.
Pass a nasogastric tube.
Commence broad-spectrum antibiotics such as gentamicin 5 mg/kg once daily,
ampicillin 1 g IV q.d.s. and metronidazole 500 mg IV t.d.s.
Refer the patient immediately to the surgical team.
Colon CA
- colon CA – Murtagh 440
o men > 50 yrs (90% of all cases)
o mortality rate 60%
o incidence
women 1:25 = 0.04
man 1:20 = 0.05
first degree relative - 1:8 = 0.12
o usually arises from an existent adenoma
o 2/3 in descending colon and rectum
o risk factors
family Hx
ulcerative colitis
colonic adenomata
decr. dietary fibre
familial
familial adenomatous polyposis (FAP) – 100% by 50 yrs
- risk factor for colon CA, duodenal and small bowel CA
- assoc. with retinal pigmentation
- + Gardner’s syndrome = most severe form of FAP
multiple (countless) polyps in the colon (predispose to
colon CA) + tum. outside the colon (osteoma of the
skull, thyroid CA, desmoid tumors of the abd. wall,
epidermoid cyst, sebacous cyst, fibroma)
hereditary non-polyposis colorectal CA (HNPCC)
other precancerous lesions
villous adenoma
o Sx:
Right colon Anemia
Dyspepsia
Mass
Left colon Altered bowel movt., Partial obstr.
Pain
Sigmoid Altered bowel movt., Complete obstr.
Rectal bleeding
Rectal Rectal bleeding
Tenesmus
Mass
triad Murtagh: rectal bleeding + mucous discharge + change in bowel habits
MCQ: stool mixed with blood and mucus in elderly person – MC is colon CA
o screening - new mcq book – p. 101 + Murtagh p. 77 + Alena’s printout
colon CA screening – blue book – p.101-102 - > 50 yrs
a. asymptomatic with no risk factors
a. FOB every 1-2 yrs > 50 yrs
b. slightly increased risk (first or second degree relative with colon cancer
after 55 years)
a. FOB annualy > 50 yrs or 10 yrs earlier than the family’s earliest
affected relative
b. sigmoidoscopy every 5 years
c. moderately increased risk (1 first degree relative with cancer before 55
years or 2 first- or second degree relatives with colon cancer at any age)
a. colonoscopy every 5 years
b. FBO annualy in the intervening years
d. high risk
a. 2 or more first or second degree relatives with colon CA < 50 yrs or
3 or more first or second degree relatives with colon CA at at any
age
a. colonoscopy every 2 yrs from 25-30 yrs
b. familial adenomatous polyposis (FAP)
a. annual sigmoidoscopy – from the age of 10
b. then every 3 years - from the age of 35
c. hereditary nonpolyposis colorectal cancer (HNPCC)
- colonoscopy every 1-2 yrs after age of 25
o Dx
colonoscopy – the best
abd. CT scan – might miss some small tumors
not U/S
o Duke’s classif.
Stage Extension 5 yr survival
A Mucosa and submucosa 90%
B Muscularis or serosa 75-85%
C Regional lymph nodes 30-40%
D Distant metastases <5%
Duke A – 75% detected with FOB
o Rx
Duke A, B – surgery
pancolectomy
paucy surgery
C,D – surgery + radiation
- Peutz-Jehgers – AD = hereditary intestinal polyposis syndr.
o dev. of benign hamartomatous polyps in the GIT -> strong tendency to dev. CA in
multiple sites (breast, liver, pancreas, etc.), while the polyps don’t have malignant
tendency
o lowest malignant potential (2%) for colon CA
may undergo malignant transf. into adenocarcinoma
o hyperpigmented (black) macules on the lips and oral mucosa
- tumors in the small bowel – predom. benign
o types
adenocarcinoma
100 x incr. risk in Crohn in the affected portion (distal ileum)
lymphomas
terminal ileum
proximal jejunum – assoc. with coeliac dis.
carcinoids
familial adenomatous polyposis
incr. risk of duodenal and small bowel carcinoma
Peutz-Jehgers – hamartomas, may undergo malignant transf. into
adenocarcinoma
- adenoma with incr. malignant potential (benign tum. of colon)
o villous
o > 2 cm
o multiple
o with dysplasia
- benign villous adenoma
o Sx - clear discharge
o Cx - causing marked electrolyte imbalance = depletion syndrome - prerenal azotemia,
hyponatremia, hypokalemia
Anal pathology
- anal anatomy:
o lower ½ of the anal canal – sensitive, painful
o upper ½ of the anal canal – where the hemorrhoids start from
separated by the dentate line
- anal fissure
o mid-posterior position (6 o’clock)
o MC cause of painful rectal bleeding = anal fissure
o Rx
analgezic creams
local nitroglicerine ointment
SE
- postural hTN
- headaches
surgery – in recurrent fissure or with fibrosis/stenosis
Lord’s procedure – 8 finger dilatation of the anus – breaks down all the scar and
inflam. tissue is broken down -> fissure heals
- perianal abscess and fistula
o blocked anal gland => abscess => fistula – pussy discharge, pain, tenderness
Rx
abscess
- cruciate incision +/- A/B
fistula
- excise the fistulous tract
Cx – fecal incontinence
- perianal hematoma – lower ½ of the anal canal
o rupture of an external haemorrhoidal vein from horseriding, constipation, homosexuals
o Rx
1 day – aspirate with wide gauge needle
1-5 day – incision under local anesthesia (clot already formed),
> 5 days – leave alone except if fever (infected) or severe pain
- hemorrhoids
o 20-50 yrs
o causes:
MC – chronic constipation, lack of dietary fibre
portal hypertension
o Sx
bleeding with blue red blood (venous blood), prolapse, mucous discharge,
itching, incomplete bowel evac.
venous varices starting above the dentate line
degrees
I – above the dentate line
- only bleeding + itching, mucous leak
II – prolapse below the dentate line – will reduce on its own
- bleeding
III – prolapse, needs manual reduction
- bleeding
IV – complicated, cannot be reduced + thrombosis + lots of pain
- strangulated – pain –> refer immediately -> hemoroidectomy
o Mx – Murtagh 361
I degree
high fiber diet, prevent constipation, laxatives
II-IV? or if profuse bleeding or thrombosed or IV (paul)
injecting of sclerosing solution -> clotting of the hemorroids -> drop off
- now not so favored
I. MC (no general anesthesia required) - rubber band ligation – they clot
and drop off
II. cryotherapy
III. best – hemoroidectomy – if severe, recurrent, strangulated
- post-op hot sitz baths – relaxes the spasm of the sphincter
- analgezic - pethidine
don’t give morphine – causes smooth muscle spasm
- pilonidal synus
o abscess midline, in the natal cleft
o more frequent in Greeks (hairy backs)
o due to hair strand which goes out then goes back in the skin
o in drivers in the army (non-padded car seats)
o Rx
acute – incision & drainage (incision and leave open, not incision and stitch)
Karydakis – big incision
chronic - excise the abscess
flatten out the natal cleft
Constipation
- chronic constipation in elderly
o Mx
1st line - Ispagula husk (bulking agent)
2nd line - lactulose syrup
3rd line – glycerine suppository
peristaltic stimulants
docusate (Coloxyl) with senna
bisacodyl (Durolax)
Movicol
Shaw’s cocktail for severe cases
bulkforming agents
Male pathology
- ED – Murtagh 1120
o causes
psychosocial – young
elderly
DM
hyperlip.
- premature ejaculation
o persistent or recurrent ejaculation before, on or shortly after penetration
time from penetration to ejaculation < 2 min
o MC male sexual dysfc.
o MC cause = performance anxiety
o can be
primary – since beginning of sexual life
sec. – developed later
o Rx
short term
topical anesthetics
- lignocaine 2.5% + prilocaine 2.5% cream to glans penis ½ hr
before intercourse
long term
SSRI (fluoxetine, sertraline, paroxetine) + clomipramine => relieve
anxiety
- 3-5 hrs before intercourse
squeeze technique no longer advised
- balanitis
o inflam. of glans penis + foreskin
o MC – candida
o children – wet nappies
o adults – immunocompromised people, DM
o Sx
saline bath
topical C/S
topical nystatin
topical myconazol
- balanitis xerotic obliterans
o thickening of the foreskin + skin pallor
o Sx
topical C/S
circumcision
- prostate CA
o 80% at 80 yrs
o risk factors
1. age > 75 yrs
2. relative Dx with prostate CA < 60 yrs – most important!
family Hx is responsible for 5-10% of cases
o MC CA in men
o structure
central?
transitional -> BPH
periph. -> CA
periphe ral -> doesn’t usually give urinary sympt. (like the BPH or
prostatitis - central)
o metastases
lymphatic -> pelvic nodes (not groin)
blood
osteosclerotic metastases in the bones: pelvis, spine
CA that doesn’t metastasize to the brain = prostate CA
o Sx
obstruction
acute retention
back pain
hematuria, uremia – 5%
o Dx
screening – controversial
PR
- signs of CA:
hard lump
asymmetry
induration
loss of median sulcus
PSA
- > 10 ng/mL suggestive of prostate CA
> 20 – most probably advanced CA, with metastases
> 30 – most probably distant metastases
- 4-10 prostatitis, benign hypertrophy
- normal < 4
serum acid phosphatase – PSA is preferred
biopsy
transurethral
transrectal
- => Gleason score – 2 specimens, score of 1-5 -> combined score
= 2-10
2-4 indolent
5-7 intermediate
8-10 aggressive
- Gleason grade: 1-5
- e.g. 5% undiff. cells – do nothing; decision is made on clinical
basis + Gleason score
o Rx
do nothing – in the elderly > 70 yrs (monitor, “watchful waiting”)
organ-confined dis. (early)
radical prostatectomy (good cure rate)
- indic. < 70 yrs, PSA < 20
- Cx
urinary incontinence – 10%
ED – 70%
locally advanced dis. (organ involved + capsule invasion or seminal vesicles) OR
old debilitated patient
2 mths of androgen deprivation to suppress the gland, then
external beam radiotherapy
- Cx
ED – after 2 yrs
radiation proctitis – faecal urgency, diarrhoea
metastatic disease
androgen deprivation Rx (paleative) – 95% from testicle, 5% from
adrenal glands
- bilat. orchidectomy – gold standard
if spinal cord compression – orchidectomy -> androgen
deprivation -> metastases stop growing
- antiadrogenic tablets
cyproterone acetate
flutamide
- exogenous estr.
stilboestrol
SE – cardiovasc. morbidity
- LHRH and LHRH analogues (goserelin) SC – most commonly
used now due to decr. complic.
- hormonal
ketoconazole -> “medical” orchidectomy and
adrenalectomy
glucocorticoid
- Benign prostate hypertrophy
o Sx
acute on chronic urine retention
bladder outlet obstruction:
triad: poor urine flow + straining to void + frequency
voiding flow rate < 10-15 mL/sec
o Cx
retention
UTI
calculus formation
uraemia
o Rx
acute retention
1. urethral catheter
2. suprapubic drainage if 1 fails
drugs
alpha-adrenergic blocking drugs (inh. the contr. of the muscle in the
bladder neck and urethra)
- phenoxybenzamine
- prazosin
- terazosin
5-alpha-reductase inhibitors (reduce prostatic volume)
- finasteride
surgery
indic.
- renal failure
- upper tract dil.
- retention
- bladder stones
methods:
- TURP
Cx
retrograde ejaculation - MC
ED – 5%
- laser ablation
- transurethral incision of the prostate (TUIP) – for small glands
- open prostatectomy – less used these days (<1%)
- prostatitis
o Sx:
triad: dysuria + fever + perineal pain
PR: very tender prostate, swollen, firm
o Rx:
amoxycillin + gentamicin
Electrolyte disturbances
- electrolyte disorders
o K
Normal: 3.5-5 mmol/l
usually intracellular
hyperkalemia
Most common electrolyte disorder associated with cardiac arrest.
CAUSES:
- Increased potassium intake: banana, low fat milk, beans, sweat
potato.
- Increased production – when cellular membranes are
ruptured!
e.g. rhabdomyolisis, burns, ischaemia, haemolysis.
- Decreased renal excretion: Acute and chronic renal failure,
Addison’s disease, hypoaldosteronism, drugs (K⁺ sparing
diuretics – spironolactone, amiloride; ACE inhibitors and AIIRA,
NSAIDs).
- Transcellular compartmental shift: acidosis, hyperglycaemia,
low insulin, digoxin poisoning, beta blockers
drugs:
digoxin
indomethacin
iv benzyl penicillin (contains K)!
Sx
- Weakness, ascending paralysis, loss of deep tendon reflexes
and respiratory failure
types:
- MILD: 5-6 mmol/L
- MODERATE: 6-7 mmol/L
- SEVERE: more than 7 mmol/L - ECG changes:
(5.5-6.5mmol/L) Tall, peaked T waves.
(6.5-7.5 mmol/l) Prolonged PR interval with flattened P
waves.
ST segment depression.
(7-8 mml/L) - QRS widening, absent P waves and
sinusoidal wave pattern.
VT, VF, PEA and (>8 mmol/L) asystole
- MANAGEMENT:
SEVERE:
Immediate cardioprotection: 10% calcium
gluconate.
Other therapies to shift potassium into the cells,
and eliminate potassium from the body.
MODERATE:
Shift potassium intracellularly with 10%
dextrose 500 mL IV (or glucose) with 25 units
of soluble insulin over 20 minutes.
8.4% sodium bicarbonate 20 ml IV over 5
minutes.
Salbutamol 5-10 mg nebulized.
+ cation exchanging enema while waiting for
dialysis
MILD:
Remove potassium from the body with:
o Furosemide 40-80 mg IV
o Potassium-exchange resin orally or
enema.
hypokalemia
Associated with an increased incidence of cardiac arrhythmias
especially if pre-existing heart disease.
CAUSES:
- Inadequate intake of potassium, e.g. alcoholism, starvation.
- Abnormal gastrointestinal losses: Vomiting, diarrhoea, laxative
abuse.
- Abnormal renal losses: Cushing syndrome, ectopic ACTH
production, hyperaldosteronism, diuretics and steroids.
- Compartmental shift: Metabolic alkalosis, insulin.
types
- normal - Potassium levels less than 3.5 mmol/L
- SEVERE: Serum potassium less than 2.5 mmol/L.
CLINICAL FEATURES:
- muscle weakness, fatigue, leg cramps and constipation.
- Polydipsia, polyuria, rhabdomyolisis, ascending paralysis and
respiratory failure
MCQ: Rx of digoxin (and thiazide) + acute abd. pain + tenderness +
irregular pulse = hypokalemia (with bowel sounds present: no bowel
sounds = acute mesenteric ischemia)
ECG changes:
- broad and flat P
- mild – T waves merging with the the U-waves
- Flat or inverted T waves, prominent U waves.
- QT prolongation
- Prolonged PR interval.
- Ventricular arrhythmias, including Torsades de Pointes
(polymorphic VT) -> VF -> death
MANAGEMENT:
- Immediate replacement: Serum potassium below 3.0 mmol/L
or potassium 3.0-3.5 mmol/L in patients with CHF, MI.
- Give potassium 10-20 mmol/h, DO NOT exceed 40 mmol/h.
- Change to oral supplements when potassium is above 3.5
mmol/L.
- Amit:
> 2.5 or asympt.
give oral K
< 2.5 or sympt.
give iv K
o Na+
Normal: 130-145 mmol/l
usually extracellular
hypernatraemia
Serum sodium level more than 145mmol/L.
CAUSES:
- Decreased fluid intake with normal fluid loss: Inability to
communicate water needs (CVA, infants, intubated patients).
- Hypotonic fluid loss with water loss in excess: Excessive
sweating, dermal burns, gastrointestinal loss, renal loss
(diabetes insipidus).
- Increased salt load: Hyperaldosteronism, ingestion of salt
tablets, administration of hypertonic saline.
CLINICAL FEATURES: neurological
- Increased thirst, weakness, lethargy, irritability.
- Altered mental status, ataxia, tremor and focal neurological
signs.
- Seizures and coma.
MANAGEMENT:
- High-flow oxygen.
- Fluid replacement
- Hypovolaemic patients: IV normal saline without causing too
rapid reduction in the serum sodium.
- Aim to reduce the sodium by 0.5-1.0 mmol/h.
hyponatraemia
Serum sodium level less than 130 mmol/L.
Clinical Features: The more rapid the fall the greater the symptoms:
- >125 mmol/L: usually asymptomatic.
- 115-125 mmol/L: lethargy, weakness, ataxia and vomiting.
- <115 mmol/L: confusion, headache, convulsions and coma.
- PSEUDOHYPONATRAEMIA - Associated with hyperglycaemia, hyperlipidaemia,
(hyper-osmolar hyperproteinaemia, azotaemia.
hyponatraemia)
MANAGEMENT:
- Treat underlying medical condition.
- Aim to increase serum sodium gradually by 0.5 mmol/L per
hour to a maximum rate of 12 mmol/L per 24 hours.
- Neurological symptoms (brain oedema): 3% hypertonic saline,
20% hypertonic saline.
- if significant hyponatraemia: fluid restriction – 1.5 l (same as in
CHF)
- osmolality (blood, urine) = 2Na +glucose + urea
o serum normal value: 275-300
o urine normal value: 500-800
o SIADH (incr. ADH) and diabetes insipidus (low ADH)
opposite effects, affect water only (not electrolyte)
hyponatraemia
SIADH – common post-op.
self-limited
Rx – vasopressin (naso-spray)?
Serum Na Serum Urine Na Urine
osmolality osmolality
- Zinc deficiency
o after prolonged IV fluid admin.
o Zn = component of coenzymes involved in wound healing
o Sx
exanthematous dermatitis
- Copper defic.
o anaemia, neutropenia
o bone demin.
- Cobalt defic.
o vit. B12 defic.
- Magnesium defic.
o vit. K-defic. syndrome
o => bleeding tendency
ABG
- ABG – Oxford 684
o pH = 7.35-7.45
o paCO2 = 35-45 mmHg
o HCO3 = 22-26 (24-28) mmol/L (~25)
o anion gap: (Na+K) – (CL- + HCO3-)
normal: 8-16 (7-14, 10-12)
Na+ normal: 130-145 mmol/L
K+ normal: 3.5-5 mmol/L
Cl- normal: 95-107 mmol/L
HCO3- : 22-26 (24-28) mmol/L (~25)
pH CO2 (acidic) HCO3- (alkaline) Conditions
Resp. acidosis Decr. Incr. Incr. (chronic - to Hypoventil., muscle
(retention) compensate) or N relaxants, myasthenia
(acute) gravis, CNS causes (head
injury), lungs disease
(asthma, COPD - MC)
Resp. Incr. Decr. Decr. (chronic - to Hyperventil. (CO2 washout),
alkalosis compensate) or N aspirin intox.
(acute)
Metab. Decr. Decr. (chronic Decr. a. with increased anion gap
acidosis - to (incr. acids):
compensate) - lactic acid: shock, inf.,
or N (acute) lactic acidosis – tissue
ischemia
- urate: chronic renal failure
- ketone: DM, alcohol
- drugs: salicylates,
biguanides, ethylene glycol,
methanol
- These values vary with the age and height of the person; the values that follow are for a 70 kg
(154 lb), average-sized adult male [2]:
Physiologic = 155 The anatomic dead space plus the alveolar dead
dead volume ml space.
- The tidal volume, vital capacity, inspiratory capacity and expiratory reserve volume can be
measured directly with a spirometer. Determination of the residual volume can be done by
radiographic planemetry, body plethysmography, closed circuit dilution and nitrogen washout.
- These are the basic elements of a ventilatory pulmonary function test. The results (in particular
FEV1/FVC and FRC) can be used to distinguish between restrictive and obstructive pulmonary
diseases:
volumes are essentially often low (Asthma can reduce the ratio
obstructive
asthma or COPD normal but flow rates are to 0.6, Emphysema can reduce the
diseases
impeded ratio to 0.7 - 0.4)
- lung abscess
o MC - staph.
o Sx
sputum with foul odour
pleuritic chest pain
tachyc., tachypneic
bronchial breath
crepitations
fever > 38.5
o Dx
x-ray: shadow of small cavity with fluid level
best investig: CT chest
bronchoscopy
o Rx
O2, strong analgezic
postural drainage, tapping
IV A/B:
clindamycin (active on anaerobs; SE – pseudomembranous colitis) +
cephalosp. (ceftriaxone)
cephalosp. + flucloxacillin
- bronchitis
o acute - sore throat, runny nose, persistent cough especially at night and in the
morning, small amount of yellow sputum
Rx
amoxycillin
doxycycline
o chronic - persistent cough especially at night and in the morning, large amount of
yellow sputum
o Dx
x-ray
- sputum types – Murtagh p. 446
- fibrosis alveolytis – all pulmonary parameters decreased
- idiopathic pulmonary fibrosis
o Hx of shortness of breath and cough
o clubbing with coarse crackles in both lung bases
- sleep apnoea
o types
obstructive:
decr. airway size
- obesity
- tonsillar hypertrophy
- macroglossia
upper airway muscle hypotonia
- alcohol
nasal obstr.
central
neurol. (sleep center affected)
o Dx
sleep study (somnography)
bad when interferring with the REM sleep
o Mx – stepladder
1. lifestyle
wt. loss
2. drugs
stop sedatives
use nasal decongestives
3. C-PAP mask
4. surgery
5. mandibular implants (splint)
6. amytriptilline
- chest findings – Murtagh 529
Dx Trachea Chest wall Percussion Breath Vocal Abnormal
movt. sounds fremitus sounds
(incr. in
consolid.
and
fibrosis)
N Middle Equal Resonant Vesicular N None
expansion
Lung fibrosis Middle Decr. bilat. Resonant Vesicular Incr. Fine
(generalised) crackles
Pneumonia / Middle Decr. Dull Bronchial Incr. Fine late
CA unilat. inspiratory
consolidation crackles
(CA: no fever
and no
crackles)
Lung collapseTowards Decr. Dull Absent or Absent None
the unilat. decr. or decr.
collapse
Pleural Towards Decr. Stony dull Absent or Absent None
effusion the unilat. decr. or decr.
opposite
side
Pneumothorax Towards Decr. Hyperresonant Absent or Absent None
the unilat. decr. or decr.
opposite
side
Emphysema Middle Decr. bilat. Resonant to Vesicular Decr. +/-
hyperresonant crackles
and
wheezing
from
chronic
bronchitis
Asthma Middle Decr. bilat. Resonant Vesicular N or Expiratory
with decr. wheezes
prolonged
expiration
Pneumonia
o types
round lesions with fluid level + pleural effusion + flu-like sympt and dry cough =
staph.
Rx - flucloxacilin
MC = lower lobe consolid – strept. pn.
Rx - amoxyclav
atypical pneumonia
paucity of chest signs (fever, headache, cough, white sputum) +
significant X-ray signs (patchy bilat. infilt.)
causes:
- MC = Mycoplasma
- Legionella, Chlamydia
Rx - erythromycin, doxyciclin, azythromycin (the best)
Rx
- Azithromycin – the best
covers Mycoplasma, Legionella, Chlamydia
- Erithromycin, roxithromycin
don’t cover Legionella
SE – GIT sympt.
- doxycycline, tetracycline
Streptococcal Staph. Mycoplasma Pneumocystic
Popul. / age All, indigenous All Teens, young Immunsuppressed
adults people
Sx Fever, rigor, Fever, rigor, Flu-like sympt., Dry cough,
cough, purulent cough, purulent followed by dry dyspnea, fever,
sputum, pleuritic sputum, cough look toxic/sick
pain pleuritic pain with few other
signs
x-ray Lobar Bilat. cavities Patchy bilat. Can be normal,
consolidation infiltrations even though they
look so sick
Cx MC – empyema MC – abscess Least likely to give
you abscess
Rx Penicillin Flucloxacilin Erythromycin Cotrimoxazol
Klebsiella
newborn, elderly, DM, alcoholics
cavitating pneumonia in the upper lobe (diff. from staph.)
Rx - cefuroxime
Asthma
- asthma
o causes / triggers
inf.
allergies
cigarette smoke
sudden change in weather or temp.
drugs that can exacerbate asthma:
beta blockers
aspirin
NSAIDs
foods causing asthma:
sulfites and metabisulfites preservatives
MSG
sea food
nuts – peanuts
stress
exercise in a cold atmosphere
o Sx
triad: dyspnoea, wheeze and cough.
o lab:
FEV1/FVC (FEV1%) – most accurate test (Forced expiratory volume at 1 second /
Forced vital capacity)
normal 75–80%.
<75% = obstruction
PEFR - maximal flow (or speed) achieved during the maximally forced expiration
initiated at full inspiration, measured in liters per minute. It is measured with a
peak flow meter or mini peak flow meter.
in children over 6 years and adults
compared to graphs of predicted normal values based on a person's sex,
age and height
o types of attack
mild
moderate
severe – dangerous signs:
SaO2 < 90%
- SaO2<92% - give O2
PEF < 100 L/min
FEV1/FVC < 40%
RR > 50 in children or > 25 adults
HR > 120
using access. resp. muscles = chest retractions = intercostal recession
of the muscles
sternal notch
nasal flaring
too breathless to talk or feed
exhaustion, sleep deprivation, drowsiness, confusion
silent chest.
cyanosis
o drugs:
Bronchodilators
beta-2 receptor agonists:
- Short acting beta2-adrenoceptor agonists (SABA) - effect starts
after 1-2 min, max. at 10-20 min.
salbutamol (albuterol USAN)
terbutaline
- Long acting beta2-adrenoceptor agonists (LABA)
salmeterol
eformoterol
- adrenaline – sc, im or iv
Anticholinergic medications:
- ipratropium bromide
Methylxantines – limited use due to side effects and limited efficacy
- theophylline - oral
- aminophylline – injection
anti-IgE agents
- Omalizumab
- Mauzumab
Antiinflammatory - Long term control
Glucocorticoids are the most effective treatment available for long term
control.
- inhaled
beclomethasone
budesonide
ciclesonide (single daily dose)
fluticasone
- oral – for exacerbations
prednisolone
Mast cell stabilizers – inhaled; adverse effects are uncommon!
- sodium cromglycate
- nedocromil sodium
Leukotriene antagonist – chewable tablets
- montelukast
- zafirlukast
o routes of delivery
<3 yrs - metered dose inhalation (MDI) + small volume spacer + face mask
3-5 yrs - MDI + small volume spacer
5-8 yrs – MDI + large volume spacer
> 8 yrs – MDI
o Sx - patterns in children – Murtagh 1280
mild - infrequent, episodic type
not severe
attacks > 6-8 wks apart
Mx
- short acting beta agonists (SABA): Salbutamol, Terbutaline –
when required
moderate - frequent episodic
attacks < 6 wks apart (4-6 weeks)
attacks more severe
Mx:
- SABA during attack
- Montelukast or cromolyn or
- inhaled C/S = ICS
beclometasone
fluticasone
ciclesonide
budesonide
severe - persistent asthma
attacks on most of the days
nocturnal attack > 1/week
multiple ED admissions
Mx:
- SABA in attack
- ICS
- consider LABA (salmeterol, eformoterol)
- if needed:
theophylline
ipratropium bromide
oral prednisolone
status asthmaticus
Rx
- O2
- hydration
- salbutamol
- C/S oral or IV
Mx of attack
monitoring of attack:
- FEV1/FVC
- PEFR
hydration!
O2
- when do you intubate:
after the other Rx have failed
blood gases are affected
inhaled Salbutamol + oral C/S
- wait 20 min and assess
if second attack or sympt. persist -> repeat inhaled
Salbutamol
if third attack or sympt. persist -> repeat
inhaled Salbutamol
o if sympt. persist other drugs:
theophylline
ipratropium bromide
oral prednisolone
IV C/S
moderate / severe asthma attack in children
- a. salbutamol puffs with spacer + prednisone
1 puff / 4 breaths
how many puffs
6 puffs < 6 yrs
o + 2 puffs ipratropium if severe attack
12 puffs > 6 yrs
o + 4 puffs ipratropium if severe attack
then
20 min later – repeat
20 min later – salbutamol (repeat)
o if still not better -> ICU
- or continuous nebulised salbutamol via mask
Salbutamol with nebulizer + O2 (nebulizer better than
spacer)
Salbutamol 2.5 mg < 6 yrs
Salbutamol 5 mg > 6 yrs
- b. O2 through nebuliser
- c. IV infusion of salbutamol + hydrocortison
- d. adrenaline IM
criteria for sending the child home
- off salbutamol > 4 hrs
- off the O2 for > 24 hrs
- eating / drinking normally
- no sign or resp. distress
exercise-induced asthma:
1-2 puffs of Salbutamol before exercise (last for 1-2 hrs)
antihistam. – not in children, except in severe asthma
poor outcome if Hx of severe attacks requiring intubation
COPD
- COPD
o Dx
FEV1/FEV
<70% after bronchodilator
< 80% predicted
o Rx
stop smoking
drugs
SABA
LABA
ipratroprium bromide
C/S - COPD – only 10% respond to steroids
- inhal.
- p.o.
A/B – in inf.
beta blockers in assoc. CV problems
- decr. the need of home O2
- decr. the exacerbations
steroids and salmeterol (LABA) improve the quality of life
O2
if SaO2 < 92%
correct O2 admin in COPD:
- low flow 2-3 L
- prolonged > 15 hrs / day
- low percent 30-40%
CO2 narcosis
- if Rx with too much O2 => CO2 retention => resp. depression
-> anxiety
->progress to confusion: flapping tremors (asterixis)
O2 – best factor for incr. long term prognosis
o sign of poorest prognosis in bronchospasm = high PaCO2
o MCQ: emphysema, V1-4 ST segm depression, normal axis, right bundle block:
RVHypertrophy with right bundle block
o MCQ: COPD with incr. JVP, oedema, decr. O2, incr. CO2, why advise for a home O2
therapy system? because hypoxia is the cause of his heart failure
PE
- acute pulmonary oedema (APO)
o cause: MI, etc.
o Sx – dyspnea, etc.
o Rx
O2
CPAP, PEEP
nitrates (GTN)
morphine
diuretics
- PE – my p.41
o predispoz. factors (same as for DVT):
contraception – OCP
obesity
surgery or immobilisation
thrombophilia
trauma
varicose veins
malignancy
pregnancy
prev. episode of DVT or PE
fam. Hx in first degree relative
o Sx
Small PE: Sudden dyspnoea, pleuritic pain and pleural rub, and possibly
haemoptysis, with few physical signs.
Major PE: Dyspnoea, chest pain and light-headedness or collapse/syncope,
followed by recovery.
Look for cyanosis, tachycardia, hypotension, raised JVP and loud delayed
pulmonary second sound (due to pulmonary HT)
o Dx
FIRST: X-ray: Mainly to exclude pneumonia, pneumothorax.
SECOND and Best: CT Pulmonary angiogram (CTPA).
THIRD - if CTPA unavailable or CI (e.g. renal failure – no contrast): Ventilation-
Perfusion isotope lung scan (V/Q scan).
V/Q ration (ventilation / perfusion)- isotope scanning with Technetium
Tc-99m
Result Interpretation Significance
Excludes pulmonary
Normal No perfusion deficit
thromboembolism
Low probability Perfusion deficit with matched ventilation deficit Non diagnostic
ventilation/perfusion ratio (or V/Q ratio) is a measurement used to assess the efficiency and adequacy
of the matching of two variables:
"V" - ventilation - the air which reaches the lungs
"Q" - perfusion - the blood which reaches the lungs
- A lower V/Q ratio (with respect to the expected value for a particular lung area in a defined
position) impairs pulmonary gas exchange and is a cause of low arterial partial pressure of
oxygen (paO2). Excretion of carbon dioxide is also impaired but a rise in arterial partial pressure
of carbon dioxide (paCO2) is very uncommon because this leads to respiratory stimulation and
the resultant increase in alveolar ventilation returns paCO2 to within the normal range. These
abnormal phenomena are usually seen in chronic bronchitis, asthma and acute pulmonary
oedema.
- A high V/Q ratio increases paO2 and decreases paCO2. This finding is typically associated with
pulmonary embolism (where blood circulation is impaired by an embolus), but can also be
observed in COPD as a maladaptive ventilatory overwork of the undamaged lung parenchyma.
Pleural pathology
- pleural effusion
o Sx
dullness on percution
o Dx
pleural fluid contains
mononuclear cells predom. = TB
transudate vs. exudate
- criteria for exudate:
The ratio of pleural fluid protein to serum protein is
greater than 0.5
The ratio of pleural fluid LDH and serum LDH is greater
than 0.6
Pleural fluid LDH is greater than 0.6 or 2/3 times the
normal upper limit for serum.
Lung CA
- lung CA
o second MC CA in Aus., after non-melanoma skin CA
o most lethal CA in Aus.
o prognosis at 5 yrs – 12-14%
o risk factors
smoking
silicosis, working in a mine
asbestos
o rship with smoking:
smoker
squamous
small cell
non-smoker
adenocarcinoma – MC in non-smokers
o Sx
triad: malaise + wt. loss + cough
hemoptisis
superior vena cava compression syndrome
jugular veins proeminent, subcut veins on upper chest dil.
paraneoplastic phenomena
squamous cell carcinoma
- hypercalcaemia – production of parathyroid hormone-related
peptide (PTHrP)
Sx - fatigue, constipation, polyuria, confusion, coma
small cell carcinoma
- SIADH – hyponatraemia with normal volemia
- ectopic ACTH secr. – Cushing syndrome
Pancoast tumor/syndrome
Horner syndrome +
compression on T1
- all small muscles of the hand, including thenar and hypothenar
eminences
- difficulty of precision grip and opposition of thumb to fingers,
weakness spreading an bringing together the fingers
- in time – claw hand
o types
small cell (SCLC) - 15-20%
Rx
- chemotherapy
- radiotherapy - palliative
non-small cell (NSCLC)
squamous – 20-30%
adenocarcinoma – 20-30%
large cell carcinoma – 20-30%
Rx
- surgery
- chemotherapy
- radiotherapy - palliative
o Dx
sometimes incidental finding at chest x-ray
bronchoscopy and biopsy (if close to a bronchia)
- mesothelioma
o risk factors
asbestosis (boiler worker, electricity-generating plants)
smoking
o Sx
cough
pleuritic pain
massive recurrent hemorrhagic pleural effusion
pleural plaques
o Dx
percutaneous biopsy
o Rx
surgery
chemotherapy
radiotherapy
o prognosis – very poor
- asbestosis
o after a lag of 10-20 yrs or more from the exposure
o fibrosis / scarring of the lungs
o assoc.
mesothelioma
TB more assoc. with silicosis (not asbestosis)
Cardiac pathology - OK
- infective endocarditis
o causes
MC – strepto. viridans > 50% (after dental work)
in IV drug users – MC candida and staph. aureus
MC affected valve = tricuspid (blood goes to right side of the heart
first)
staph. aureus (50% of acute forms)
Coxiella burnetti – Q fever
o predisposing factors
valvular dis.
cardiac defects
prosthetic valves
IV drug use
after
dental work (dental extraction, etc.)
instrumentation (urethral dilatation, etc.)
minor or major surgical procedures (tonsillectomy, abortion)
central venous catheters
o mortality 6-30%
o 15% previously Dx with heart dis.
o Sx
may be with no murmur
triad: fever of unknown origin + cardiac murmur + embolism
presentations
acute endocarditis
subacute endocarditis
prosthetic endocarditis
o Mx
take blood cultures, then
start ASAP empiric Rx with:
benzyl penicillin + flucloxacilin + gentamicin i.v.
- HOCM
o fam. Hx of father who died early – usually AD
o Sx
exertional syncope
collapse during physical effort (plays football) due to arrythmia
ejection systolic murmur (same as aortic stenosis)
no radiation & exacerbation with Valsalva manouver = HOCM
o Dx
1 – echocardiography – every 5 yrs
left ventricular hypertrophy
subaortic septal hypertrophy -> pushes the valve -> similar to aortic
stenosis
o Rx
NO digoxin (can decr. the ejection fraction)
- jugular venous pressure (JVP) – internal jugular vein
o raised if >4 cm
o components:
a wave – atrial systole
c wave – closure of tricuspid valve (not normally visible)
x descent – ventricular systole
v wave – atrial filling agains a closed tricuspid valve
y descent – opening of the tricuspide valve
o pathology:
raised JVP with normal waveform: right heart failure, fluid overload
raised JVP with absent pulsation: Superior Vena Cava obstruction
large a wave – pulmonary hypertension, pulmonary stenosis
cannon a wave – right atrium contracts against a closed tricuspid valve -
complete heart block
absent a wave – atrial fibrillation
larve v wave – tricuspid regurgitation
high plateau of JVP with deep x and y descents – constrictive pericarditis
absent JVP – reduced circulatory volume
o positive abdominojugular reflux sign – rise in JVP presistent after 15-60 sec of abdominal
compression = right ventricular failure
- cardiac tamponade
o Sx
Beck triad
hT
muffled heart sounds
increased JVP, distended neck veins
pulsus paradoxus: exaggeration of normal phyisiological resp. variation in BP
(> 10 mm Hg in inspir.)
o Dx
x-ray
loss of aortic knuckle
widened mediastinum
o Mx - pericardiocentesis
- pericarditis
o types
acute
chronic – with hepatosplenomegaly and jaundice, incr. JVP, ascitis, oedema
o Sx
pain improved when leaning forward
cardiac tamponade signs (see above)
o ECG
ST elevation and PR depression (pathognomonic - Jay) in almost all leads
(except for aVR and V1)!!
Heart failure
o types
left
tachypnoea, pleural effusion, crepitations/bilat. basal crackles, gallop
rhythm (3rd heart sound)
right
incr. JVP, peripheral / ankle oedema, hepatomegaly, ascites
cor-pulmonale
- right heart failure
- secondary chronic pulmonar HT
- Rx
O2 – 3yr survival improved by 50%
systolic
LV ejection fraction < 40
diastolic
impairment of LV filling
o Rx – Murtagh 1335
lifestyle
salt restriction <2 g / day
water restriction < 1.5 L / day
drugs
1. ACE inh (or AIIRA – losartan and other sartans, if cough is a
problem)
- correct neuroendocrine problemes
- decr. the cardiac load
- decr. risk of death
2. add diuretic – if congestion
- furosemide
- hydrochlorothiazide
3. + selective beta blocker
- prolong survival!
- bisoprolol, carvedilol, metoprolol
4. + digoxin
- if indicated
e.g. AF
- CI in bradycardia
5. + spironolactone
- careful when combining with ACE inh. (risk of hyperkalemia)
6. + consider vasodil.
7. + consider transplant
o highest risk for non-cardiac operation: heart failure (>Hx of of DVT or MI)
o 50% will die in 5 yrs
Cardiac arrhythmias
- arrhythmias
o causes:
I - Medications: Side effect.
II - Exclude myocardial ischaemia from ACS as a priority.
III - Electrolyte disturbances: Hyperkalaemia.
Hypoxia
Hypovolaemia.
Thyroid disease.
Septicaemia.
o types:
bradycardia < 60
can be:
- SINUS
Rx
Bolus of atropine 0.5-0.6 mg IV.
o Repeat the atropine if it persists (up to
3 mg IV).
if patient conscious: Consider the insertion of a
temporary transvenous pacemaker (second or
complete heart block)
- JUNCTIONAL
- AV BLOCK = Prolongation of PR interval to > 200 ms
First degree: Benign
PR>0.2 s (5 small boxes)
Rx
o none, unless sympt.
Second degree:
types:
o Mobitz I or Wenckebach – progressive
prolongation of PR interval, then a
drop of a QRS complex (Wenkeback
phenomena)
AV node is blocked
Rx - none
o Mobitz II
intermittently nonconducted P
waves not preceded by PR
prolongation and not followed
by PR shortening
PR is constant (not
progressively prolonged) but
1:1, 1:2, 1:3, … for every 1-3 P
waves, a QRS is dropped
Rx – Pacemaker, especially
after myocardial infarction
Third (complete) – no relationship between P waves
and QRS complexes
HR: 25-50
Large volume pulse
Increased JVP (CANNON WAVE)
Systolic murmur
Rx
o temporary pacemaker, then arrange
for
o permanent pacemaker
o First check drugs, if no response give
treatment
o atropine?
-
- atrioventricular blocks
o grade I – PR extended > 0.20 sec - digitalis
o grade II – PR extended and certain SA impulses are missed (do not make it to the
ventricles)
Mobitz type I (Wenkebach) – digitalis
Mobits type II – usually not from digitalis
o grade III – complete AV block, ventricles contracting at lower rate than the atria
- atrioventricular dissociation
o ventricles contracting at a higher rate than the atria (unlike the AV block grade III)
tachycardia
Broad-complex:
- VT, VF, SVT with block.
VT
broad QRS
> 300 / min, regular
Rx
o pulseless VT or unconscious, unstable:
Give a synchronized DC shock 120-150 J
and repeat up to three times.
o with pulse, conscious, stable:
Amiodarone 300 mg IV over 20-60 min
followed by an infusion of amiodarone
900 mg over 24 hours.
VF
no QRS complex
Rx
o cardioversion
adrenalin
CPR
o drugs: amiodarone, lidocaine
- WPW:
Short PR interval on ECG.
Delta wave.
wide QRS
Rx
radiofrequency ablation of accessory pathway.
stable - IV procainamide (class Ia)
unstable – DC cardioversion
CI
Avoid adenosine, verapamil, digoxin and
diltiazem as they block the AV node and may
worsen a pre-excited AF leading to VT.
Narrow-complex tachycardia: SVT
- sinus rhythm, narrow QRS complexes, 150-200 / min
- if unstable: Synchronized DC cardioversion 70-120 J.
- if stable:
1. Vagal stimulus such as:
carotid sinus massage: Young, stable, with no
carotid bruit, no history of TIA or CVA.
Valsalva manouver
2.a.Adenosine: 6 mg rapidly over 2-5 seconds IV
followed by 12 mg IV after 1-2 min, then further 12 mg
once more if still no response.
SE – cardiac arrest
2.b. Alternatively verapamil 2.5-5 mg as a bolus.
in pregnant woman: iv beta blockers (verapamil
is teratogenic)
Irregular narrow-complex tachycardia: AF
- Prevalence: 0.1% less than 55 years, 10% above the age of 80.
- risk factors
HT – 20% of cases of AF
- More prevalent in men.
- HR = 350-550 / min
- irregularly irregular rhythm + absent P waves
- Common underlying causes: Ischaemic heart disease,
thyrotoxicosis and hypertension (rheumatic fever in
developing countries).
- Risk of stroke: 2.5-3 below the age of 65, over 10 in older
population.
- High risk of femoral artery embolism.
- Rx
Alena
acute onset (<48 hrs), young age (<65 yrs), no
structural damage (no MI), stable -> rhythm
control: amiodarone + heparin
o but first U/S to exclude thrombus in the
heart
o rate control – digoxin (Murtagh) or
beta blocker (Oxford)
unstable – cardioversion
elderly patient, with risk factors, previous MI,
etc.
o rate control: digoxin, beta blocker
o anticoag.
(Maria) Unstable: Synchronized DC cardioversion 120-
150 J.
Stable: more or less than 48 hours?
Acute - less than 48 hours: Rate control, rhythm
control, anticoagulation.
o I - Rate control (Maria?):
1. digoxin – don’t give for low
BP (< 90/60) – Murtagh 779
2. verapamil, diltiazem
3. Beta-blocker – metoprolol,
atenolol
o (Maria) II - Rhythm control (Amit = I =>
rate will be controlled as well):
Murtagh: if symptomatic +
recent onset (< 6 mths)!!
electrical cardioversion – if
unstable
chemical – if stable: Flecainide
(class Ic), Amiodarone (class
IIa), Sotalol (risk of acute heart
failure).
o Anticoagulation - heparin, then
> 60 yrs, with risk factors –
warfarin (Jay)
< 60 yrs, w/o risk factors –
aspirin
2. More than 48 hours
o main goal: rate control
beta blocker
digoxin - AF and signs of
cardiac failure.
o Anticoagulation: Enoxaparin 1 mg/kg or
UF heparin 5000 IV as a bolus followed
by an infusion.
o failure to revert chemically => DC shock
first do transoesoph. U/S
- paroxysmal AF
spontaneously ends in less than 7 days (usually in 24
hrs)
after heavy alcohol, drugs
Rx
if not rapid – don’t need to revert
if rapid - convert
- persistent AF – fails to revert within 7 days
usually converts with DC cardioversion
- permanent AF – elderly, cannot be reverted (permanent
damage in the conduction system in the heart)
just rate control
anticoag.
AV node ablation + permanent permanent pacemaker
AV with rapid ventr. response over a long
period of time -> LV dysfc.
Atrial Flutter:
- Usually asymptomatic.
- Common complication of hypertension and hypertensive heart
disease.
- Regular (or irregular) rhythm.
- flutter waves (saw-tooth)
- Rate 300
- Ventric. rate = 125-175 (150)
- with variable blocks -> is irregular
Dx diff with AF
if no P waves = AF
if P waves = atrial flutter
- Rx
similar with AF (Murtagh)
permanent – radiofrequency ablation
medical – amiodarone, sotalol
o Bundle branch blocks
LBBB (William)
wide QRS > 0.12
broad monomorphic R waves in I and V6
broad monomorphic S waves in V1
Rx
- newly diagnosed LBBB -> MI? -> thrombolise
RBBB (Marrow)
wide QRS
MI
- coronary ischemic syndr.
o stable angina
o acute coronary syndrome (ACS)
STEMI
NSTEACS
NSTEMI
unstable angina
-
- AMI
o STEMI
if coronary block is not relieved, MI will progress over next 6-12 hrs (4 hrs =
window period)
main goal of Rx is reperfusion
causes of new systolic murmur post MI
V septal rupture
papillary muscle rupture
papillary muscle dysfc. in ant. MI
func. mitral regurgitation sec. to LV dil.
pericardial friction rub, limited to systole
Dx
First step in management: ECG within 10 minutes of patient arrival.
- ECG: ST elevation in two or more contiguous leads:
Inferior MI: II, III, aVF
Anterior MI
anteroseptal – V1-V3
anterolateral – V3-V4
Lateral: I, aVL, V5-V6
Posterior: Mirror-image ST depression V1-V4
Repeat ECG after 5-10 min if non-dx ECG.
- repeat ECG every 2-3 hours
Send blood for laboratories: Cardiac biomarkers.
- second step = Troponin I or T
normal < 0.02
rise after 4-6 hours after symptom onset.
Repeat in 6-8 hours if normal.
Indicate myonecrosis.
Remains elevated for 5-14 days (not useful for re-
infarction).
More sensitive for myocard than CK-MB.
can also be elevated in CRF – due to renal destruction
Dx diff with CRF:
o do also CK – not elevated in CRF
o if troponin is gradually increasing – MI
constantly increased = CRF
- + CK-MB, CK.
If troponin is unavailable.
rise after 4 hrs
not specific for myocard
CK-MB is more specific than total CK.
Returns to normal within 72 hours.
May be used to confirm re-infarction.
complic.
LVF: pulm. congestion
- Rx: diuretics
- O2
- morphine
- digoxin is CI – incr. the force of contr. -> risk of rupture
cardiogenic shock – 90% mortality
- Rx – dopamine, dobutamine
aseptic pericarditis (Dressler syndrome)
- Rx
NSAIDS, paracetamol, aspirin
C/S
Mx
I. MONA
- Morphine 2.5 mg IV with antiemetic. – up to 4 times every 10
min. (total 10 mg)
- Oxygen high dose: 40-60%
- GTN 150-300 µg sublingually.
- Aspirin 150-300 mg unless contraindicated.
II. Reperfusion therapy:
- PCI if this is available within 90 minutes of patient arrival. (in
tertiary hospitals) and within 12 hrs of onset of sympt.
angiography/angioplasty (stents)
protocol:
within 60 min of arrival if patient presents
within 1 hr. of sympt.
within 90 min of arrival if patient presents
within 1-3 hrs. of sympt.
within 90-120 min of arrival if patient presents
within 3-12 hrs. of sympt.
o otherwise - thrombolysis
- Thrombolysis: within 12 hours of onset of symptoms
(preferrably within 6 hrs and within 30 minutes of patient
arrival) with rt-PA
pain disappears + ST elevation disappears = MI was
resolved
types:
streptokinase
o 1.5 UI iv infusion over 30-60 min
o under strict control of the BP
if systolic < 70 => stop infusion
Tenecteplase.
Reteplase
Alteplase.
o 15 mg iv bolus, followed by infusion of
50 mg over 30 min, then 35 mg over
next 60 min
SE
severe hT
bleeding
allergic reaction – with streptokinase
o if allergic reaction, don’t use it for at
least 1 yr
reperfusion arrhythmias
o thrombolysis done under strict ECG
control
o as bad as VF
o in the necrotic zone there are all sort
of toxic substances: reperfusion causes
them to mobilize => they iritate the
myocardium => arrhythmias
CI
absolute
o Intracerebral or subarachnoid
haemorrhage
o Intracranial neoplasm ever.
o Stroke in previous 6 months.
o Active GI bleeding in last month.
o Major surgery or trauma in previous 3
weeks.
o Known bleeding diathesis.
o CRP > 10
o Aortic dissection.
first rule out aortic disection
before giving thrombolysis ->
can kill a patient with aortic
dissection
relative
o Oral anticoagulant therapy.
o Pregnancy within 1 week post-partum.
o Central line.
o Refractory hypertension.
o Infective endocarditis.
o Severe hepatic or renal disease.
indic.
ST elevation > 1 mm in limb leads
ST elevation > 2 mm in chest leads
new LBBB
post MI – ST depression in V2-V3 -> ask for V7-
V9
after 12 hrs, thrombolysis is still considered if:
persist. pain
preservation of R waves in infarct-related ECG
leads (not replaced by pathol. Q wave)
major complic. – cardiogenic shock
- antiplatelets
aspirin 300 mg
clopidogrel 300 mg
- heparin.
III. after reperfusion
- antiplatelet agents
- cardioselective beta blockers – increase the survival (MCQ)
Atenolol
Metoprolol
- ACE inh. – within 24-48 hrs after MI
- statin therapy – regardless of the cholesterol level
- + warfarin
drugs that decreased the mortality in MI
1. beta blockers
2. ACE inh. (if no renal failure)
3. aspirin
4. statins
- Neha:
o cardiac chest pain
MONA -> hospital: ECG, Trop
No pain Hx of pain at rest or
repetitive pain or
prolonged pain
No ECG changes or Low risk Intermed. risk
enzyme changes
ECG
- ECG
o normal impulse conduction
sinoatrial node (right atrium) – 60-100 beats/min
AV junction – delay, so A can contract before V (including the atrial kick at the
end of the A contr.)
AV node – 40-60 pacemaker
bundle of His
bundle branches (left and right)
Purkinje fibers
ventricular cells – 20-45 beats / min
o small square=0.04, large square=0.2 sec
o ECG interpretation: RRAHIM
Rate
Rhythm
Axis
Hypertrophy
Interval
MI and miscellaneous
o 1. calculate rate:
vertical bar every 15 large squares
I. count 30 large squares (6 sec) – count the no. of R waves in those squares,
multiply by 10 -> in regular and irregular rhythms
II. look for R wave falling on a line, then see where the next R wave falls – in
regular rhythms only
300 - next line in large square (300:1)
150 – next line … (300:2)
100 (300:3)
75 (300:4)
60 (300:5)
50 (300:6)
…
III. 300 / no. of large squares between 2 QRS complexes – in regular rhythms
o 2. determine rhythm (RR intervals are regular?):
Regular
regularly irregular
irregularly irregular – AF
o 3. assess P waves – do they exist? are they followed by QRS? are they all the same in
size and shape?
MAT = multifocal atrial tachcardia >= 3 P waves, each different, in the same
ECG
o 4. determine PR interval – beginning of P to beginning of R
o 5. determine QRS duration
o 6. QT interval – beginning of Q to end of T (T=terminal)
o Components
P waves = atrial depolarization (contraction) - best appreciated in lead II
Present
absent - AF
relationship to QRS complexes (no rship. = AV block)
PR interval: 0.12-0.2 (3-5 boxes)
QRS complexes = ventricular depolarization = 0.04-0.12 (1-3 boxes)
narrow (supraventric)
widened (>0.12 s) (ventric.)
ST segment
T waves = ventricular repolarization
Elevated
depressed
inverted (ischemia).
U wave = after repolarization
o leads
I, II, III – limb leads
aVR (right arm), aVL (left arm), aVF (feet) = augmented limb leads
V1-V6 = chest leads (V1 = right -> V6 = left)
V1-V2 = medial
V2-V3 = septum
V4-V6 = lateral
rhythm strip = longer strip of II
-
o problems
sinus bradycardia
sinus tachycardia
1 extra atrial focus firing = normal sinus rhythm with PAC – premature atrial
contr.
1 extra ventricular focus = PVC
wide and bizarre QRS (slower conduction of the impulse from the
ectopic foci)
can be
- uniform
bigeminism (normal QRS, weird QRS – repeated)
trigeminism
couplet: normal PVC PVC – repeat
triplet: normal PVC PVC PVC - repeat
- polymorfic
multiple extra atrial foci firing = AF
1. absent Ps
2. irregularly irregular rhythm
3. narrow (normal) QRS
multiple extra foci in V = VF
1. absent Ps
2. irregularly irregular rhythm
3. wide QRS
looping (re-entrant) circuit in A = atrial flutter
picket fence, saw-tooth
regular
flutter P waves
type
- with regular AV block - every 2nd, 3rd or 4th is transmitted to the
V generating a QRS (1:1, 1:2, 1:3)
- with variable AV block
looping circuit in AV = paroxysmal SVT = PSVT– with sudden start, captured on
ECG, triggered by a PAC (which can be seen); comes and goes - can only be
captured with Holter; no P waves
SVT – has P waves
looping circuit in V = VT
regular
- monomophic
- polymorphic
block impulses coming from SA node = AV junctional blocks
1st degree – prolonged PR
2nd degree
- type I Mobitz = Wenkebach phenomena
PR gets longer and longer, until a QRS complex is
dropped
regularly irregular
- type II Mobitz
not all the P waves are transmitted to QRS
tough to be differentiated from 3rd degree
3rd degree
- A contracts at 60-100
- V contracts at 20-45
MI
STEMI:
- ST elev. > 1mm in limb leads (farther from the heart) and
>2mm in chest leads (closer to the heart) in 2 or more
CONTIGUOUS leads or
- or LBBB!
location
- lateral - I, aVL, V5-V6
- inf – II, III, aVF
- ant – V1-V4
septal – V2-V3
or combinations
antlat.
antinf.
nitrates are CI due to hT
- posterior
ST depression in ant. leads (V1-V4) (reciprocal change)
tall R waves in V1-V2 (right side leads)
normally - R wave progression: small in V1 –
gets taller – tallest in V5
+ ST elevation in V7-V9 = post leads (on the back)
- right side MI: V1 + inf. leads (II, III,aVF)
Cx – severe hT!
reciprocal changes
- inf. MI -> reciprocal in lat. leads
- post. MI -> reciprocal in ant. leads
types of MI
- STEMI = Q wave MI = transmural MI (SQT)
stages:
ischemia: ST depression, peaked T waves, then
T-wave inversion
infarction – ST elevation
ongoing infarction – Q waves and T-wave
inversion
fibrosis – persistent Q waves but normal ST
segm. and T waves
- NSTEMI = non-Q wave MI = subendocardial MI
stages:
ischemia: ST depression, T-wave inversion
infarction – ST depression, T-wave inversion
fibrosis –ST returns to baseline, T wave
inversion persists
Q waves in I, II, III = infarct
Q waves
- pathol. if > 1 mm
- can be normal in V1 and aVR
- appear in hrs – days later
ventricular hypertrophy
RVHypertrophy: tall R in V1-V2 taller than 7 mm
LVH: even taller R in V5-V6 + deep S wave in V1-V2 >= 35 mm
- tallest R + deepest S >=35 mm
atrial hypertrophy – P waves
P > 2 ½ small squares in height = RAH (P pulmonale)
P > 2 ½ small squares in length = LAH (P mitrale)
- simple – in II
- notched P (camel hump, biphid) in V1
- biphasic (+ and -) in V1
ST depression in:
post. MI (+ tall R waves)
normal angina (troponins normal)
NSTEMI (troponins incr.)
bundle branch block -> slow conduction through collaterals -> wide QRS
any onset of new bundle branch block = new MI
William Marrow:
- WiLLiaM (W pattern in V1 and or M pattern in V6) = LBBB
M pattern in V5/V6
- MaRRoW = RBBB – sign of RVHypertrophy =
(M) RSR’ in V1/V2
- W = QRS
- M = RSR’
axis deviation -> R wave predom + or – in I and II
I II
Normal + +
In LVH
RAD = Romance (R in V1 - +
and V2 are going towards
each other = kissing)
In RVH
Indeterminate (superior or - -
extreme RAD)
intervals
PR
- incr. in AV block 1st degree and 2nd degree, type I
- decr. in
WPW
high catecholamines (fast rhythm)
QRS
- incr.
bundle branch block
incomplete bundle branch block 0.10-0.12
PVC
ventricular rhythm
QT - QT length is influenced by the heart rate
- adjust:
corrected QT: QTc = QT/square root(RR) – Bazzet’s
formula
prolonged > 0.44
QT>1/2 RR = prolonged
- prolonged QT = risk of Torsades de Pointes (polymorphic VT) ->
VF -> death
causes:
hypokalemia
TCAs
haloperidol, droperidol
WPW syndrome
- mnemonic = wPWS
PR is short
Wide QRS
Slurring (Delta wave)
shortcut with faster conduction ->delta aspect
of first branch of R
PE – S1Q3T3
- I – deep S
- III – deep Q and T wave inversion (positive)
hyperkalemia
- life-threatening
- ECG changes corelate with levels
taller and taller T waves – difficult to sit on
may mimic and ST elevation, but J junction is on
the isoelectric line
P flattens, then disappears
Vascular pathology - OK
- surgery indic.
o carotid occlusion
> 70% carotid occlusion
60-70% - grey area
surgery in DM, elderly, hyperlip., recurrent TIP
<60%
Rx – aspirin low dose
o >50% coronary artery occlusion
- angiodysplasia
o AV malformation in the intestine
o > 55 yrs
o in the caceum + right colon
o Sx
multiple episodes of profuse rectal bleeding
assoc. with CREST syndr.
o Rx
surgical resection
Arterial pathology
- vasculary problems / surgery
o arterial
risk factors
smoking
DM
HT
hypercholest.
family Hx
AF
acute - sudden onset = “cold white leg” – very painful
causes:
- thrombosis
- embolism
- traumatic contusion
MC site – common femoral artery
Sx
- pain, pallor, perishing cold, paralysis, paresthesia,
pulselessness (6Ps)
- most ominous signs – M 716
1. paralysis or paresis (weakness)
2. muscle compartment pain or tenderness
Mx
- reversible if Rx within 4 hrs
iv heparin 5000 U immediately
emmergency embolectomy or stenting
thrombolysis with streptokinase or urokinase
then lifetime anticoag. with warfarin!
- after 6 hrs cannot be reversed -> amputation
chronic
prevention
- stop smoking, wt. loss
types:
- intermittent claudication
pain or tightness in muscles during daytime, with
exercise
o agravating factors: walking, exercise
o relived by rest
sites
o superficial femoral - MC
pain in tighs and calfs after
200-500 m
o profunda femoris – pain after 100 m
o multiple segment involvment – pain
after 40-50 m
o external or common iliacc artery - pain
in buttocks and thighs
o aortic bifurcation = Leriche syndr. –
with ED + bilat. ischemic buttock
claudication
Dx
FBE
first test = ABI
o normal: > 0.9-1.1
> 0.9 venous ulcer
o intermit. claudic. 0.5-0.7
o rest pain: 0.3-0.5
o calcif. >1.1
second test – color Doppler
gold standard = angiography
o reserved for proposed intervention
Mx
control DM and HT
decr. wt.
stop smoking
keep legs warm and dry
proper care of the foot
aspirin
if ABI < 0.3 -> refer for urgent surgery
o endarterectomy or bypass grafting
- rest pain – constant severe burning pain in the forefoot at rest
during night time
pain in the forefoot, toes, heels
relieving factor: hanging the foot out of the bed
emmergency condition => refer to surgeon
immediately
indic. for vascular surgeon – Murtagh 719
o unstable claudic. of recent onset,
deteriorating
o severe claudic. – unable to maintain a
normal life
o rest pain
o tissue loss – ulcers, heel’s cracks, dry
gangrenous patches, inf.
Venous pathology
- varicose veins
o predispoz. factors
family Hx.
female
pregnancy
multiparity
previous DVT
extrinsic venous compression – intraabd. tumors, etc.
occupation – dentist, etc.
diet – low in fibre
o Rx
high-fibre diet
supportive stockings or tights
surgery
sclerotherapy
- for small, isolated veins
surgical ligation and stripping
- DVT
o risk factors
family Hx
Hx of previous thrombembolism
thrombophilia
drugs: OCP, HRT, tamoxifen
> 40 yrs
varicose veins
significant illness: heart failure, CA
malignancy (in idiopathic DVT)
recent surgery
major / orthopedic surgery
immobility
long flights
pregnancy / puerperium
obesity
dehydration
o recurrent DVT – pancr. CA
o unilat. sudden onset of DVT – ovarian CA
o Sx
“hot blue leg” = acute venous obstruction
painful, tender
oedema
o Dx
gold standard = Doppler U/S
contrast venography – if U/S doubtful
D-dimer – to exclude DVT when doubtful (if negative)
don’t do Hoffman sign (plantar dorsiflexion causes pain) since it might
mobilise the thrombus
o Cx
PE
20%
- of these 30% will be fatal
varicose veins => venous ulcer
o Rx
heparin, then
warfarin
3-6 mths
we need to treat at least for 3 mths (with warfarin)
do not give aspirin
mobilisation
compression stockings
- thromboflebitis
o red cord-like vein, tender on palpation
o usually in superficial varicose veins
o migratory superficial thromboflebitis = pancreatic CA
o Rx
early mobilisation
bed rest
compression with uniform pressure over the vein
prevent propagation of the thrombus
limb elevation
NSAIDs
Aortic pathology
- coarctation of the aorta
o narrowing distal of ductus arteriosus and subclavian artery
o male 2:1
o Sx
asympt. always
headache, epistaxis, claudication, cold legs
BP difference between upper and lower limbs
weak delayed pulse in legs
mid to late systolic murmur over aortic area
infraclavicular murmur
o Rx
surgical resection of the narrowed portion – if HT
angioplasty
- widened mediastinum + systolic murmur – can be:
o aortic aneurysm
leaking aneurysm
Sx
- severe abd. pain
- moderate abd. rigidity
- shock
- if leaked posteriorily -> pain irradiates to the back and down
into the genitalia
- intense lower back pain
ruptured aneurysm
Sx
- lower abd. pain, generalised
o aortic dissection – with shock, chest pain, etc.
- aortic abdominal aneurysm
o risk factors
Marfan syndr.
o Sx
pulsating palpable mass in the abd
abd pain, back pain
o Cx
ruptured
Sudden abdominal pain.
Radiating to the back or groin.
Syncope, collapse or unexplained shock.
Feel for a tender mass with expansible pulsation on examination.
Classic triad:
- Abdominal or back pain
- shock
- pulsatile or tender abdominal mass in men over 45 years.
Dx
- Perform a rapid bedside ultrasound to confirm the presence of
abdominal aneurysm.
- X-ray – midline opacity with calcified border
Dx diff. with chronic pancreatitis – calcifications like a
chain (2 parallel lines)
- CT scan.
Rx
- High-flow oxygen by face mask.
- Slow IV infusion: avoid giving massive fluid replacement, as
this leads to coagulopathy, hypothermia, increases the
bleeding.
- Refer urgently to the vascular surgical team.
o Rx
< 5 cm – observating, elective surgery
> 5 cm – urgent surgery
no matter what size + symptoms = urgent surgery
method: stenting
- aortic dissection
o PREDISPOSED BY:
Hypertension.
pre-existing aortic aneurysm
Marfan syndrome.
inflam. vasculitides (temporal arteritis, syphilitic aortitis, Takayasu arteritis)
Bicuspid aortic valve.
Coarctation
Iatrogenic trauma.
o Sx
Abrupt onset with sudden pain.
Sharp or tearing pain, irradiating to the back
Retrosternal, interscapular or lower in the back, migratory, severe, resistant to
opiates.
Unequal radial artery pulses +/- decr. or absent pulses at the femoral arteries
Difference of blood pressure in the arms.
Diastolic murmur if Aortic regurgitation occurred.
o Dx
1. investig. of choice = contrast CT
2. if renal fc. is abnormal -> transoesophageal U/S
x-ray – wide mediastinum
o Rx
morphine
beta blocker – relax the muscle in the aorta, decr. the extension of disection
or Ca channel blockers – if beta blockers are CI
+ sodium nitroprusside – vasodil.
surgery – stent graft
o COMPLICATIONS:
Myocardial Infarction. – disection before origin of coronary arteries; the
dissection will cause the MI
(inferior) MI with wide mediastinum
- Dx: transoesophageal U/S
if aortic dissection, don’t give thrombolysis (can kill the
person with aortic dissection) and don’t give aspirin
(gets worse with aspirin)!!!
Aortic incompetence (regurgitation) – diastolic murmur
Cardiac tamponade.
Pleural effusion.
Intestinal ischaemia.
Oliguria and haematuria.
- steal syndromes
o from the other good leg
o subclavian steal syndrome
retrograde (reversed) flow of blood in the vertebral artery or the internal
thoracic artery, due to a proximal stenosis (narrowing) and/or occlusion of the
subclavian artery. The arm may be supplied by blood flowing in a retrograde
direction down the vertebral artery at the expense of the vertebrobasilar
circulation.
HT
- blood pressure regulation
o autonomous nervous system - baroreceptors are located in the left and right carotid
sinuses and in the aortic arch + under stress, etc
sympathetic system - raises BP
vasoconstriction
increases the force the heart's contractions
increases the speed of the heart's contractions
parasympathetic system – lowers BP (opposite effect to the sympathetic
system)
o renin-angiotensin(-aldosterone) system
angiotensinogen – under the action of renin (kidney) ->
Angiontensin I – under the action of ACE (angiotensin-converting
enzyme, on the surface of pulmonary and renal endothelium) ->
- Angiotensin II ->
Angiotensin III ->
Angiotensin IV
renin: secreted by the kidney from specialized cells called granular cells of the
juxtaglomerular apparatus in response to:
A decrease in arterial blood pressure (that could be related to a
decrease in blood volume) as detected by baroreceptors (pressure
sensitive cells). This is the most causal link between blood pressure and
renin secretion (the other two methods operate via longer pathways).
A decrease in sodium chloride levels in the ultra-filtrate of the nephron.
This flow is measured by the macula densa of the juxtaglomerular
apparatus.
Sympathetic nervous system activity, that also controls blood pressure,
acting through the beta1 adrenergic receptors.
angiotensin II
potent vasoconstrictor of arterioles.
constricts glomerular arterioles, having a greater effect on efferent
arterioles than afferent. The glomerular filtration rate (GFR) is thus
maintained, and blood filtration can continue despite lowered overall
kidney blood flow.
increased Na and Cl reabsorption and K elimination, increased water
reabsorbtion (directly and by increasing the aldosterone)
causes the release of aldosterone
causes the release of ADH
stimulates the sympathetic system
o aldosterone – mineralocorticoid hormone, released from the adrenal cortex in response
to high serum angiotensin II, high ACTH or high serum potassium levels -> increases BP
actions:
increases water reabsorption
increases Na and Cl reabsorption
increases K elimination
increases Ca elimination
modified:
increased in hyperaldosteronism
- Sx
weakness (hypokalemia)
polyuria, polydypsia
HT
- primary (hyporeninemic) hyperaldosteronism
causes:
bilateral adrenal hyperplasia (90%)
adrenal adenoma – Conn’s syndrome
adrenal carcinoma
diagnostic:
low renin: If there is a primary
hyperaldosteronism the decreased renin (and
subsequent decreased angiotensin II) will not
lead to a decrease in aldosterone levels (a very
helpful clinical tool in diagnosis of primary
hyperaldosteronism)
o Usually, renin levels are suppressed,
leading to a very low renin-aldosterone
ratio (<0.0005)
hypertension
hypokalemia (normal Na and Cl)
Rx
spironolactone
rezection of the adrenal adenoma
ACE inh. do not help (aldosterone works
outside the renin-angiotensinogen system)
- secondary (hyperreninemic) hyperaldosteronism
causes
a juxtaglomerular cell tumor (renin producing
tumor) leads to increased aldosterone, as the
body's aldosterone production is normally
regulated by renin levels.
renal artery stenosis in which the reduced
blood supply across the juxtaglomerular
apparatus stimulates the production of renin
diagnostic
high renin
hypertension
hypokalemia (normal Na and Cl)
decreased in Addison’s disease
antagonists:
spironolactone,eplerenone – competitive antagosits for aldosterone’s
receptors
o ADH (vasopressin) – synthesized by the pituitary gland
increases water reabsortion (main effect)
ADH secretion is increased when the body osmolality increases (more
concentrated blood; ADH reabsorbs more water, to dilute the blood) =>
more concentrated urine
ADH defficienty leads to hypernatremia (more water than Na is lost)
increases reabsorption of urea
increases Na and Cl reabsorption
increases peripheral vascular resistance and thus increases arterial blood
pressure
- high blood pressure
o measurement
sphygmomanometer – use 3 sizes:
types
o adult
o child
o large adult (obese)
rules:
o cuff’s
width
at least 40% of the arm circumference
(Murtagh)
cover 2/3 of the arm (not more) – AMC
o children - cuff width should cover 75%
of the arm (Murtagh)
cuffs that are too wide underestimate the BP,
cuffs that are too narrow overestimate it
(AMC)
length
at least double the arm circumference
(Murtagh)
bladder length should not completely encircle the limb
(but only 80%) - AMC
bladder width is half the length of the bladder -
AMC
o types of drugs used
1. diuretics
thiazides
o actions:
increase the Na and Cl elimination (inhibiting
reabsorption of sodium (Na+) and chloride (Cl-) ions
from the distal convoluted tubules in the kidneys by
blocking the thiazide-sensitive Na+-Cl- symporter)
increase the K elimination
increase the serum uric acid
o side effects
hypokalemia, hyponatraemia, loss of Mg
hyperuricemia
hyperglycaemia
dyslipidaemia (increase cholesterol and triglycerides)
impotence
o contraindications
type 2 diabetes
hyperuricaemia
kidney failure
dyslipidaemia
pregnancy
o indications
heart failure
older patients
o examples:
hydrochlorothiazide
chlortalidone (thiazide-like)
indapamide (thiazide-like)
loop diuretics
o action: act on the Na+-K+-2Cl- symporter (cotransporter) in the
thick ascending limb of the loop of Henle to inhibit sodium and
chloride reabsorption
o side effects:
loss of K, Na, Ca, Mg
o examples:
furosemide - Lasix
edema from heart failure, hepatic cirrhosis,
renal failure
hypertension – less potent than thiazides
Bumetanide
Ethacrynic acid
Torsemide
potassium-sparing diuretics
o aldosterone antagonists
spironolactone
o Epithelial sodium channel blockers
amiloride
triamterene
2. beta-blockers
types of beta receptors
o β1-Adrenergic receptors are located mainly in the heart and in
the kidneys
o β2-Adrenergic receptors are located mainly in the lungs,
gastrointestinal tract, liver, uterus, vascular smooth muscle, and
skeletal muscle
o β3-receptors are located in fat cells
actions
o reduction in cardiac output (due to negative chronotropic and
inotropic effects)
o reduction in renin release from the kidneys
o central nervous system effect to reduce sympathetic activity
(for those ß-blockers that do cross the blood-brain barrier, e.g.
Propranolol)
indications:
o hypertension - young patient, anxious patient
o angina, heart attack
o cardiac arrhythmia
side effects
o fatigue, insomnia
o bronchospasm!
o dyslipidaemia
o impotence
o stopping them can precipitate angina at rest!
o not to be used with verapamil / diltiazem (bradycardia)
contraindications
o asthma, COPD
o heart failure
o bradycardia, heart block
o dyslipidaemia
o DM
o periph. vasc. dis.
examples:
o non-selective
propranolol
o selective for β1-Adrenergic receptors
metoprolol
atenolol
pindolol
3. calcium-channel blockers
actions
o negative inotropic and chronotropic effects
o vasodilation
o relaxation of smooth muscle in the bronchi
indications:
o hypertension
o angina, heart attack
o asthma
o cardiac arrhythmia
o peripheral vascular disease
side effects
o congestive cardiac failure (with beta-blockers and digoxin –
verapamil, diltiazem)
o heart blocks
contraindications
o heart failure
o flushing
o constipation (verapamil)
examples:
o dihydropyridine
nifedipine
amlodipine
felodipine
o Phenylalkylamine
verapamil
o Benzothiazepine
diltiazem
4. ACE inhibitors & AIIRA (Angiotensin II receptor antagonist, more selective
than ACE inhibitors, do not produce cough)
actions
o vasodilation
o reduces aldosterone (diuresis)
indications:
o hypertension
o heart failure
o peripheral vascular disease
o diabetes
o cardioprotective after a heart attack
side effects
o cough
o disturbance in taste (dysgeusia)
o rash
o hyperkalemia
o first dose hypotension
o angioedema
contraindications
o bilateral kidney artery stenosis, precaution in chronic kidney
disease
o pregnancy
o hyperkalemia, avoid potassium sparing diuretics
o hypersensitivity to ACE inhibitors
examples:
o ACE inhibitors
captopril
enalapril
lisinopril
o AIIRA
irbesartan
losartan
5. central-acting agents
actions
o a2 adrenergic agonists - stimulate a2 receptors in the brain,
which decreases cardiac output and peripheral vascular
resistance, lowering blood pressure
indications:
o hypertension – in asthma, pregnancy
side effects
o sedation
o dry mouth
o constipation
o impotence
contraindications
o liver disease (methyldopa)
o precaution in depression
examples:
o clonidine
o methyldopa
6. alpha-blockers
actions
o selective for the alpha-1 receptors on vascular smooth muscle.
These receptors are responsible for the vasoconstrictive action
of norepinephrine, which would normally raise blood pressure.
By blocking these receptors, prazosin reduces blood pressure.
indications:
o hypertension – in patients who cannot take diuretics or beta-
blockers (diabetes, asthma, dyslipidaemia), peripheral vascular
disease, heart failure, prostatism (LUTS – lower urinary tract
symptoms)
side effects
o first dose syncope
o orthostatic hypotension
o sedation, weakness
contraindications
o heart failure, orthostatic hypertension
o precaution in elderly patients
examples:
o prazosin
o terazosin
7. alpha- and beta-blockers
labetalol
8. vascular smooth muscle relaxants (other than calcium-channel blockers)
indications:
o refractory hypertensive states
o hypertensive emergencies
examples
- hydralazine
- minoxidil
- diazoxide
- sodium nitroprusside
- HT – Murtagh 1296
o types
essential – 90-95%
sec
kidney dis. – 3-4%
- GN
- reflux nephropathy
- kidney a. stenosis
- DM
endocrine
- primary hyperaldosteronism (Conn’s syndrome)
- Cushing
- phaechromocytoma
- OCP
coarctation of the aorta
drugs
pregnancy
immune disorders
- e.g. polyarteritis nodosa
o approach in Rx
1. lifestyle
SNAP
- smoking
- nutrition
- alcohol
- physical exercise
wt. loss
decr. salt
decr. stress
2. drugs
if lifestyle fails, treat if:
- systolic 140-180
- diastolic 90-110
targets
- < 140-90
>= 65 yrs
w/o
DM
kidney dis.
proteinuria
- < 130/85
< 65 yrs
DM
kidney impairment
proteinuria 0.25-1 g / 24 hrs
- <125/75
proteinuria > 1 g / 24 hrs
strategy
- start with 1 drug
- not responding to Rx
increase the antiHT drug to highest acceptable dose
substitute with another drug from a compatible class
add another drug from another class
- starting strategies – Murtagh 1307 + 1313
thiazide
diuretic +
beta blocker
ACE inh.
DM, dyslipidaemia
ACE inhibitors / AIIRA
calcium channel blockers
o verapamil, diltiazem
o nifedipine, felodipine
coronary heart dis.
beta blockers
nifedipine, felodipine
congestive heart failure
diuretic
ACE inh. / AIIRA
- Cx in HT
o HT retinopathy – stages:
I – silver lining (silver wiring)
II – artery & venous nipping (crossing over)
III
flame-shaped haemorrhages
soft exudate (cotton wool)
IV - papilloedema
o HYPERTENSIVE ENCEPHALOPATHY
Acute and malignant hypertensive crisis.
Severe hypertension (diastolic over 140 mmHg).
very high BP (systolic > 200)
Severe headache, confusion, vomiting and blurred vision.
Focal neurological signs, seizures and coma may develop later.
Fundoscopy: retinal haemorrhages, exudates and papilloedema. (grade IV
changes)
DIAGNOSIS:
ECG and CXR.
Examine an MSU for proteinuria and send it for microscopy to look for
evidence of renal disease, with casts or abnormal urinary red blood
cells (greater than 70% dysmorphic).
MANAGEMENT:
Aim for oxygen of 94%.
Aim to initially reduce main arterial pressure gradually by 25% or aim
for a diastolic BP of 100-110 within the first 24 hours.
Use oral treatment with labetalol 100 mg, atenolol 100 mg or long
acting nifedipine 20-30 mg.
Dyslipidaemia
- hyperlipidaemia
o risk factors for
coronary artery dis.
incr. LDL and decr. HDL
LDLC/HDL > 4
pancreatitis
TG > 10 mmol/L
o goal:
cholest. < 4 mmol/L
LDL < 2.5 mmol/L
< 2.0 in high risk patients
HDL > 1 mmol/L
TG < 1.5 mmol/L
o indic. to initiate the drug therapy: 1317 murtagh
1. existing heart disease + cholest. > 4
2. if one or more of these risk factors + cholest. > 6.5 or cholest. > 5.5 and HDL
<1
DM
familial hypercholesterolemia
family Hx of coronary heart disease: first degree relative < 60 yrs
HT
periph. vasc. disease
3. HDL < 1 + cholest. > 6.5
4. males 35-75 yrs and postmenopausal women < 75 if cholest. > 7.5 or TG > 4
5. anyone if cholest. > 9 or TG > 8
- dyslipidaemia drugs
o first line
1. HMG-CoA reductase inhibitors (statins) - decreased cholesterol synthesis +
increased synthesis of LDL receptors, resulting in an increased clearance of low-
density lipoprotein (LDL) from the bloodstream
atorvastatin, fluvastatin, simvastatin
- also combinations with ezetimibe
SE
- GIT side-effects
- myalgia, myositis
- liver dysfc. – uncommon
monitor
- LFT
- CK
2. Ezetimibe – lowers cholesterol absorbtion in the intestine
if statin-intolerant
3. ezetimibe + statin
4. bile acid sequestrants (resins) - they bind bile acids and sequester them from
enterohepatic circulation. Since bile acid sequesterants are large polymeric
structures, they are not well-absorbed from the gut into the bloodstream. Thus,
bile acid sequestrants, along with any bile acids bound to the drug, are excreted
via the feces
cholestyramine, colestipol
SE
- constipation
- offensive wind
5. fibrates: decrease TG production in the liver + increase HDL (less LDL
reduction effect)
gemfibrozil, fenofibrate
SE
- risk of myopathy
- gallstones
- in combination with the statins can cause rhabdomyolysis
only used if the other drugs are not tolerated
o second line
nicotinic acid (niacin, vit. B3) – lowers cholesterol, increases HDL, lowers TG
probucol – lowers cholesterol absorption
estr. – in postmenopausal women
n-3 fatty acids in fish – lowers TG and cholesterol (VLDL)
o usage:
elevated LDL:
statin + ezetimibe
statin + resin
elevated TG:
fibrates
or nicotinic acid, n-3 fatty acids
+ decr. alcohol
mixed (CT and TG elevated):
if TG < 4 – statin
if TG > 4 – fibrate
- familial hypercholesterolemia - xanthoma on the Achilles
- familial combined hyperlidpidaemia – xantelasma
Rheumatology - OK
- arthritis disorders:
o simple analgezics – aspirin, paracetamol
o NSAID, cyclo-oxygenase-2 (COX-2) specific inhibitors
o disease-modifying agents
rheumatoid arthritis
sulphasalazine
hydroxychloroquine
gold
D-penicillamine
methotrexate
cyclosporin
cyclophosphamide
azathioprine
leflunomide
biological DMARDS
fish oil – omega 3
systemic lupus erythematosus
hydroxychloroquine
azathioprine
spondilarthropaties
sulphasalazine
methotrexate
osterarthritis
glucosamine
chondroitin
o disease-suppresant agents
corticosteroids
o intra-articular injections
corticosteroids
hylan (hyaluronic acid)
o surgery
synovectomy
joint replacement
arthrodesis
- gout
o men
o symptoms:
arthritis
monoarthritis 90%
- metatarsal-phalangeal 75%
- other toes
- ankles
- knees
tophi – in ears, elboyw, big toes, fingers, Achilles tendon
renal calculi
high fever, fatigue
o risk factors:
alcohol
diuretic (thiazides)
beta blockers (?)
niacin, aspirin, ciclosporin
fructose sweetened drinks
meat, seafood (purine-rich)
o precipitate an acute attack of gout in a susceptible indiv.
alcohol
surgery
starvation
drugs
thiazides
frusemide
probenecid
aspirin
sulphinylpyrazone
o Dx
monosodium urate crystals in the synovial fluid or in the tophus with strong
negative birefringence in polarized light microscopy
hyperuricemia – 70%
X-ray – punched out erosions at joints margins
o Rx of attacks
1. indomethacin (or other NSAIDs) 50 mg until sympt. abate (3-5 days), then
taper to 25 mg until cessation of the attack
2. colchicine
SE – diarrhoea
3. C/S intraartic.
ACTH in difficult cases
o Px of attacks
allopurinol
indic.
- frequent acute attacks
- tophi or chronic gouty arthritis
- kidney stones or uric acid nephropathy
- hyperuricaemia
probenecid – a bit less effective than allopurinol
- pseudogout (condrocalcinosis)
o in elderly, on top of osteoarthritis
o Sx
knee
wrist
o Dx
calcium pyrophosphate crystals -> polarized light microscopy of sinovial fluid
shows weakly positively birefringent crystals
x-ray: calcif. of the articular cartilage
o Rx – reverse compared to gout
1 - C/S intraartic.
2 - colchicine
3 – indomethacin
paracetamol
- lordosis
o I test – CT scan
o most appropriate – densitometry
o MRI – best
Autoimmune diseases
- antibodies: Murtagh 284
o RF – RA, Sjogren
o anti-CCP - RA
o ANA – SLE, scleroderma, autoimmune hepatitis
o antidsDNA (double stranded) -> SLE (more specific than ANA)
o antiphospholipids - SLE
o AB to extractable nuclear antigen
Anti Ro (SSA) – Sjogren, SLE
anti La (SSB) – Sjogren, SLE
AntiSm – SLE
Anti Jo-1, Anti MI-2 – polymyositis, dermatomyositis
anti-Scl70 (anti-topoisomerase I) – scleroderma (diffuse)
o anticentromere AB – limited system sclerodema - CREST
o AMA (anti-mitochondrial AB) – primary biliary cirrhosis, autoimmune hepatitis
o anti gastric parietal cell antibodies – pernicious anemia, atrophic gastritis
o anti intrinsic fact. AB: pernicious anemia
o coeliac dis.
antigliadin AB
antitransglutaminase AB
antiendomysial AB
o anti-thyroid microsomal AB - Hashimoto
o ANCA – antineutrophil cytoplasmic AB
c-ANCA – Wegener granulomatosis
p-ANCA – microscopic polyangitis, Churg-Strauss syndr., Goodpasture?
o anti-GBM – Goodpasture
o anti acetycholine receptors AB – myastenia gravis
o anti smooth-muscle – chronic active hepatitis
- Reiter vs. Behcet
Reiter (reactive arthritis) Behcet
Gender Men 10:1 Men 2:1
HLA HLA B27 HLA B51
Triad Triad: non-specific urethritis + vasculitis
conjunctivitis (+/- iritis) +
arthritis
(similar, but w/o ocular and
mucocutanous lesions =
reactive arthrits)
Ulcers Painless ulcers recurrent, painful mouth,
scrotal, labial ulcers
Vision problems Conjunctivitis Uveitis, retinitis (severe pain
in the eye, decr. eye vision)
Long term ocular disability Rare Inevitable – prompt referral
required!
Arthritis – long term Frequent – 50% Rare (knees)
involvement Spondylitis, sacroiliitis
common + knees, ankle, toes
poliarthritis
Cause After an acute inf. with Genetic, race
specific venereal or Multiorgan dis. (vasculitis)
dysenteric organisms:
SARA (Shigella), CARA
(Chlamydia)
Rx NSAIDs C/S, immunosupressants
- uveitis – always part of connective tissue / autoimmune dis. (not inf. dis.)
o causes
Behcet’s dis.
Reiter’s syndrome
ankylosing spond.
IBS
psoriasis
SLE
(sarcoidosis, juvenile RA)
o Rx – treat underlying condition
- connective tissue disorders
o WHEN TO SUSPECT?
Middle aged person.
Female: More common.
Multisystemic involvement.
Skin lesions + arthritis + other features
- SLE
o Most common connective tissue disorder.
o first investig. is always ANA
o Inflammation in several organ systems and production of autoantibodies that
participate in immunologically-mediated tissue injury.
o Incidence F:M = 10:1
o Age of onset: 15-40 years old.
o CLINICAL FEATURES:
Arthritis: Peripheral polyarthritis with symmetric involvement of small and large
joints WITHOUT joint erosion.
Skin lesions: Malar rash, discoid rash, rash on the hands, photosensitivity.
autoimmune thrombocytopenic rash with splenomegaly and
menorrhagia
Other features: Oral/Nasal ulcers (painless), serositis (pleurisy, pericarditis,
peritonitis), renal, haematological and neurological involvement.
alopecia
o DIAGNOSIS:
ANA Test: highly sensitive 98%. – first test
Anti-dsDNA Ab and anti-Sm Ab : highly specific 90%. – most specific
ENA antibodies.
Rheumatoid factor: Positive in 50%.
ESR/CRP: Elevated in proportion to disease activity.
we need at least 4 of these 11 criteria:
1. malar rash
2. discoid rash
3. photosensitivity
4. arthritis
- polyarthritis always – 2 or more joints
- symmetrical, non-erosive
5. serositis: pleuritis, pericarditis
6. nephritis
- MC cause of dis. and death in SLE!
- small proteinuria > 0.5 g/day
- 3+ casts
7. hematol. – anemia, neutropenia
8. neurol. – intractable headache, seizures, psychosis
9. oral ulcers – do not heal
10. immunol. – antidsDNA, anti-Sm, anti-Ro, antiphospholip., anti-
histone (drug induced: hydralazine, procainamide, propylthiouracil,
lithium, chlorpromazine)
11. ANA
o MANAGEMENT:
MILD: NSAIDs for treatment of arthralgia.
MODERATE: Low dose of antimalarials (hydroxychloroquine) specially with
dermatological lesions and constitutional symptoms.
SEVERE: Steroids (oral, topical), Immunosuppressant (azathioprine,
methotrexate) drugs.
UV sunscreen
- Scleroderma
o Progressive systemic sclerosis.
o Generalized disorder characterized by fibrosis and degenerative changes in blood
vessels, visceral organs and skin.
o F:M = 3-4:1.
o Incidence peaks in fifth and sixth decade.
o No inflammation.
o CLINICAL FEATURES:
I. Localized.
Skin: Bilateral symmetrical swelling of fingers leading to skin
tightening.
Raynaud’s phenomenon (90%): Blanching and/or cyanosis of digits
followed by erythema, tingling and pain following cold exposure or
emotional stress.
- typical in scleroderma
II. Generalised (limited or diffuse)
limited cutaneous systemic sclerosis - involves areas distal to the elbow
and knee but may involve the face and neck
- CREST
calcinosis of subcutaneous tissue in the hands
Raynaud syndr.
present in:
o SLE
o RA
o dermatomyositis
o systemic sclerosis
o worker with vibrating tools
o hematol.
thrombocypenia?
polycytemia
cold aglutinin dis.
o drugs - beta blockers
o hypothyroidism
not present in ankylosing spondylitis
esophageal reflux
sclerodactyly
telangiectasia
diffuse cutaneous systemic sclerosis - skin thickening on the trunk and
proximal aspects of the extremities in addition to involvement of the
face and distal aspects of the extremities
skin: hypo- or hyperpigmentation
GI (90%): Decreased motility with secondary dysphagia, GORD, diarrhoea,
constipation.
Joints: Polyarthralgias
Kidneys (10-15%): Hypertension, oliguria.
Lung: Interstitial fibrosis.
Heart: Ventricular dysfunction.
o DIAGNOSIS:
anticentromere AB – limited system sclerodema - CREST
anti-Scl70 (anti-topoisomerase I) – scleroderma (diffuse)
ANA antibodies
Skin biopsy.
- Vasculitis
o Inflammation and necrosis of blood vessels resulting in ischaemia and infarction.
o Any organ system can be involved.
o Keys to diagnosis: Clinical suspicion, laboratories are not specific, biopsy will confirm.
Small vessel Medium-sized vessel Large vessel
Wegener’s vasculitis.
CD8 cell mediated muscle necrosis. B cell and CD4 immune-complex mediated
perifasicular vasculitis.
F>M
F > M.
o CLINICAL FEATURES:
Progressive symmetrical proximal muscle weakness: Shoulder and hip.
The hip extensors are often severely affected, leading to particular
difficulty in ascending stairs and rising from a seated position.
The weakness is generally progressive, accompanied by lymphocytic
inflammation (mainly cytotoxic T lymphocytes).
Atrophy of muscles.
muscle pain (50%)
dermatomyositis
Dermatological involvement:
- Gottron’s papules (70%) - erithematous, scaly eruptions over
the knuckles of interphalangeal and metacarpophalangeal
joints + elbows
- heliotrope rash with oedema
- shawl sign - diffuse, flat, erythematous lesion over the back
and shoulders or in a "V" over the posterior neck and back or
neck and upper chest, worsens with UV light
Cardiac, GI, pulmonary involvement.
o DIAGNOSIS:
1 - Increased muscle enzyme levels: CK, LDH, ALT, AST.
EMG.
Anti Jo-1, Anti MI-2 AB
best - Muscle biopsy.
o TREATMENT:
Physical therapy.
Assessment of organ involvement.
High dose of corticoids.
Immunosuppressive agents.
Intravenous immunoglobulin.
Malignancy surveillance (Ovarian, stomach, prostate, BCC, SCC incr.).
- Sjogren’s syndr.
o Chronic inflammatory disorder.
o CD4/CD8 cell mediated infiltration and destruction of salivary and lacrimal glands.
o Patient’s with Sjogren’s syndrome are at higher risk of non-Hodgkin’s lymphoma.
o MC assoc. with RA
o CLINICAL FEATURES:
Dry mouth: Difficulty swallowing food without drinking, caries, erythema of
oral mucosa.
bilat. swelling of the salivary glands (parotids, submand.)
Ocular: Burning, dry, painful eye relieved by tears, foreign body sensation,
blepharitis.
o DIAGNOSIS:
Autoantibodies: Anti-Ro, Anti-La, RF
Salivary flow measurements.
Salivary gland biopsy.
Schirmer test – shows decr. lacrimal production
o TREATMENT:
Good dental hygiene.
Artificial tears.
Hydroxychloroquine, corticosteroids, immunosuppressant agents for severe
systemic involvement.
- rheumatoid arthritis
o affects multiple joints, most commonly small joints of the hands, feet and cervical
spine, symmetrically, but larger joints like the shoulder and knee can also be involved.
o AB attack the synovium – init. joint space is wider, then becomes narrow (not use it as
an x-ray criterion)
then attack the bone (osteopenia, erosion)
o attack the synovium everywhere => symmetrical
o Sx
Synovitis can lead to tethering of tissue with loss of movement and erosion of
the joint surface causing deformity and loss of function
morning stiffness
afects the tendons and ligaments => ulnar deviation of the hands (subluxation
of joints)
Rx – fixation with metal rod in straight position (arthrodesis)
rheumatoid nodules – often subcutaneous, usually found over bony
prominences / pressure points, such as the olecranon, the calcaneal
tuberosity, the metacarpophalangeal joint, or other areas that sustain
repeated mechanical stress.
Nodules are associated with a positive RF (rheumatoid factor) titer and
severe erosive arthritis
fatigue, malaise
carpal tunnel syndrome
o lab:
rheumatoid factor – if negative, seronegative arthritis – 15% of patients
anti-citrullinated protein antibodies (ACPAs). Like RF, these tests are positive in
only a proportion (67%) of all RA cases, but are rarely positive if RA is not
present, giving it a specificity of around 95%
anti-CCP AB (cyclic citrullinated peptide) test and the Anti-MCV assay
(antibodies against mutated citrullinated Vimentin)
RF and anti-CCP present = worse prognosis
ESR and C-reactive protein are elevated
o diagnostic - The American College of Rheumatology has defined (1987) the following
criteria for the classification of rheumatoid arthritis - at least four criteria have to be met
for classification as RA
Morning stiffness of >1 hour most mornings for at least 6 weeks.
Arthritis and soft-tissue swelling of >3 of 14 joints/joint groups, present for at
least 6 weeks
Arthritis of hand joints, present for at least 6 weeks
Symmetric arthritis, present for at least 6 weeks
Subcutaneous nodules in specific places
Rheumatoid factor at a level above the 95th percentile
Radiological changes suggestive of joint erosion
o Murtagh 355 – Dx diff of various arthritis types
o Rx
Splintage
Exercise
Bed rest
drugs
aspirin, paracetamol, fish oils
C/S
methotraxate
+ sulfasalazine
+ hydrochloroquine
Rheumatoid arthritis Osteoarthritis Gout
Primary joints MCP, PIP, wrist First MCP of the
Symmetrical thumb,DIP
cervical and lumbar
spine, hips and knees
Heberden’s nodes, on Absent Frequently present
the DIP joint
(osteophytes)
+ Bouchard’s nodes
(on PIP joint) much
less common
Joints Soft, warm, tender Hard and bony
Stiffness Worse after resting If present, worse after
(morning) effort (may be
described as evening
stiffness)
RF Positive Negative
anti-CCP AB Positive Negative
ESP and CRP incr. Normal
X-ray 1. Erosion of joint 1. Loss of joint space 1. asymmetrical
margins 2. Periartic. bone 2. punched out
2. Osteopenia sclerosis (dense bone, erosions
3. symmetrical white)
+ Cysts 3. Marginal osteophytes
+ Joint distruction + Cysts
+ Subluxation
- osteoarthritis
o wear and tear of the carthilage (with poor blood supply) -> repair (even poorer in
elderly)
body can’t give more carthilage, so it tries to compensate by producing more
bone
o earliest fc. lost in hip OA – internal rotation
o Rx
NSAIDs, aspirin
COX-2 inh.
C/S intraartic.
glucosamine
- juvenile chronic arthritis = juvenile RA = juvenile arthritis = Still’s disease
o unknown etiol
o < 16 yrs
dis. frequently persists in adults
o types
pauciarticular <= 4 joints, M.C. - large joints: knee, wrist, ankle
assoc with uveitis or sacroileitis
polyarticular > 4 joints
large and small joints
RF can be positive, rheumatoid nodules are often present
cervical spine is involved
with systemic onset (with vasculitis) – with spiking fever, Salmon-pink rash on
trunks and extremities, arthritis, myalgia, hepatosplenomegaly,
lymhpadenopathy, pleuritis, pericarditis
o Dx:
ESR incr., FBE (microcytic anemia, lymphopenia, platelet decr.)
pauciartic – ANA +
U/S – pericarditis?
o Dx diff – rule out septic arthritis -> perform arthrocentesis
o Rx
physiotherapy, occupational therapy
NSAIDs
IV Igs in systemic type with vasculitis
C/S
methotrexate
joint replacement
synovectomy may be required
- rheumatic fever – see above
- ankylosing spondylitis
o yound men
o sacroiliac joints and spine – pain and stiffness
o also hips, shoulders, knees, ankles
o morning stiffness
o iridocyclitis
o Rx
exercise
NSAIDs
- psoriatic arthritis:
o fingers and toes - DIP involvement
o sacroilitis – like in akylosing spondylosis
o RF neg.
- Goodpasture’s syndrome
o hemoptysis + hematuria
o sore throat, cough, runny nose
o anti-glomerular basement membrane AB
o Dx
anti-glomerular basement membrane (anti-GBM) from lungs and kidneys
p-ANCA?
o Rx
C/S
immunosupressants
- Wegener granulomatosis
o triads:
physiopatol.: URT granuloma + fleeting pulmonary shadows (nodules) + GN
sympt.: malaise + URTs (rhinits, sinusitis), LRTs (wheeze, cough)
o 40-50 yrs
o Sx
LRT + URT sympt.
polyarthritis
eye involv. – orbital mass
oral ulcers
GN 75%
o Dx
chest x-ray: multiple nodes and cavitations
c-ANCA (antineutrophil cytoplasm AB)
Dx confirmed by open lung biopsy
o Rx
cyclophosphamide
fatal w/o Rx!
- Takayasu’s arteritis
o young Japanese females
o pulseless disease
o large vessel vasculitis
affects the arch of aorta and other major arteries
o Sx
absence of peripheral pulse
HT
o Dx
ESR, CRP
angiography of the aorta
o Rx – C/S
Myopathies
- proximal muscle weakness, cannot climb stair, cannot comb the hair, no neurol. problems =
myopathy
- polymyositis/dermatomyositis – see above
- Duchenne’s muscular dystrophy – X linked recessive
o 2-5 yrs
o boys
o progressive scheletal muscle degeneration, cardiac muscle involvment
o dystrophin = muscle protein that is missing => muscle fibre fragility, breakdown and
necrosis
o Sx
proximal muscle weakness by age 3
hypertrophy of calf muscles
wasting of thigh muscles
cardiomyopathy
cannot walk upstairs (14-22 months should be able to do that)!
o Dx
1 - CK incr. 50-100 times
2 - muscle biopsy – best for diagn.
EMG
o prognosis
wheelchair by 10-12 yrs
die by age 20
o complic
scoliosis, flexion contractures, incr. risk of fractures
o Rx
supportive
oral prednisolone – slows the progress of the disease
- post-viral myositis
o Rx – analgezia
paracetamol
ibuprofen
- inclusion body myositis – predominantly distal muscle weakness
- myositis = SE of statins
o statins + fibrates = bad combination -> risk of myopathy (simvastatin myopathy)
o even worse with erythromycin – liver enzyme inhibitor
o causes rhabdomyolisis
o check serum CK and urine myoglobin
- rhabdomyolisis
o Sx
muscle pain, swelling, red-brown urine
o causes
burns
trauma
o Dx
CK
urine
blood
myoglobin
o Rx – supportive
- myoglobinuria/hemoglobinuria (not hematuria) – no RBCs on microscopy
Endocrinology - OK
- insulinoma
o incr. insulin, proinsulin and C-peptide levels
o hypoglycemia improved by eating
o U/S – pancr. tumor
- paraneoplastic syndromes
o in Cas of the lung, liver, stomach
o Sx
hypercalcemia
hypokalemia
hypoglycemia
etc.
o e.g.
squamous cell carcinoma
hypercalcaemia – production of parathyroid hormone-related peptide
(PTHrP)
- Sx - fatigue, constipation, polyuria, confusion, coma
small cell carcinoma
SIADH – hyponatraemia with normal volemia
ectopic ACTH secr. – Cushing syndrome
o Dx diff. with carcinoid syndr. –> here Sx appear long before the local growth and metast.
carcinoid syndrome
sympt sec to carcinoid tum. (which can occur anywhere in the GIT +
lung)
- MC in appendix, ileum, rectum, caecum, lungs
due to incr. production of serotonin metabolyte: 5-HIAA
flushing of the skin, wheezing, bronhoconstr., diarrhoea, abd. pain, hT,
right side of heart affected (tricuspid valve dis. syndrome - prolif. of
myocytes on the valve)
Dx
- urine 5HIAA
- chromograffin test
Rx
- octretide
- tumor resection
bouts of flushed face
- w/ diarrhoea – carcinoid syndr. – Dx. 5-HIAA
- w/o diarrhoea – phaeocromocytoma
- acromegaly
o Sx
triad: nasal problems + fitting problems (rings, shoes, etc.) + incr. sweating
excessive growth of hands, tissues (nose, lips, face), feet, jaw and tongue
weakness, sweating, headaches
amenorrhoea, loss of libido
sleep apnoea
glycosuria
o Dx
measurement of growth hormone levels after glucose challenge test (OGTT)
hyperglycemia inhibits the release of growth hormone in normal
people
insuline-like growth factor 1 (IGF-1) – key test
Hyperprolactinemia
o causes
physiol. –pregnancy, breast-feeding, intercourse, sleeping, stress
tumors
prolactin-producing tumor in anterior pituitary gland = prolactinoma
- very high levels of prolactin (especially in macroadenomas)
pituitary adenoma - tum. that compress the stock of the pituitary gland
(which releases dopamin which inhibits the release of hormons from the
anterior pituitary - FSH, LH, ACTH, prolactin - or posterior - vassopresin,
oxytocin)
hypothyroidism, PCOS, POF – through negative feedback, stimulate the pituitary
gland
sarcoidosis
renal failure
cirrhosis
silicosis
breast trauma
breast herpes zoster
drugs
drugs that inhibit the dopamine
- typical antipsychotics (haloperidol) and some atypical
antipsychotics (risperidone, amisulpride)
fluoxetine (SSRI)
metoclopramide
ranitidine
estrogen (HRT) – MC cause
methyldopa
Ca channel blockers
estrogen
- (drugs causing gynecomastia:
- digoxin
- isoniazide
- spironolactone, steroids
- cimetidine
- omeprazole
- metyhldopa, marijuana
- estrogen
- + calcium antagonists, amiodarone, TCAs
- NOT: furosemide, labetalol)
purple book – causes in women:
defic. in the release of dopamine (70%)
pituitary or suprapituitary tumor (25%)
primary hypothyroidism (1%)
other causes (4%)
o Sx
women
galactorhea – if very high levels of prolactine: in pituitary tumors
oligo – amenorhoea
infertility
decreased libido
men
decreased libido
ED
gynecomastia – rare (but not galactorrhoea)
osteopenia
headache
bitemp. hemianopia
o Dx
prolactin – after fasting
check cause: MRI, CT scan – pituitary tumor
microadenoma < 1 cm
- MRI every year – check growth
macroadenoma
- MRI every 6 mths
- test visual field
o Rx
if primary – dopamin agonists (inhibit release of prolactin from the pituitary)
bromocriptine
- stop if woman gets pregnant
cabergoline – better but more expensive
for oligo – amenorhoea -> OCP
drug induced – stop drug
pituitary tumor -> dopamin agonists:
shrink the tumor
stop galactorhoea
Thyroid pathology
- Murtagh – p. 221 – table for Sx
Hypothyr. Hyperthyr.
Risk factors Autoimmune dis. (Hashimoto) Graves’
Down’s Excessive thyroxine
Turner’s Hot nodules
Rx with radioiodine, Amiodarone – less frequently
amiodarone, lithium Inf. (De Quervain’s subacute
Thyroid surgery thyroiditis)
Postpartum (Sheehan’s
syndr.)
Sx general Tiredness, lethargy, cold Anxiety, agitation,
intol. restlessness
Psychiatric Depression, psychosis Psychosis
Musculoskeletal Weakness, decr. reflexes, Weakness, incr. reflexes,
myalgias, carpal tunnel syndr. clonus, proximal myopathy,
fine tremor
Skin Dry, cold, coarse Warm sking, moist or sweaty
Myxoedema (non-gravity
dep.)
Thin hair, brittle
Face puffy Exophtalmos, lid lag
Cardiovasc. Bradycardia, AMI, Tachycardia, heart failure, AF,
cardiomyopathy, HT (systolic)
cardiomegaly
Endocrine Goitre, infertility, Goitre, gynecomastia
galactorrhoea
O&G Menorrhagia, oligo- or Oligo- or amenorrhoea
amenorrhoea
Neurol Ataxia Tremor
Other Decr. libido, constipation, wt. Wt. loss, fever (thyroid storm)
gain, anemia
TSH T4 T3 Rx
Primary hypothyr. Incr. Decr. Decr. Thyroxine:
- non-vasc. patient: start with 50
micrograms/day
- vasc. patient, > 65: do ECG (address
any vasc. problems first), then start
25 micrograms/day (thyroxine can
cause an Acute Coronary Syndr.)
Test TSH, T4 every 4-6 weeks until
you reach the desired level: if needed
increase in increments of 25
micrograms
Then 1-2 times after 6 mths
Then yearly
In pregnancy: check at least every
trimester
Sec. hypothyr. N or decr. Decr. N or decr.
(hypotalamus
cause)
Hyperthyr. Decr. Incr. Incr. 1. Beta blockers (for tachycardia and
palpit.)
2. first try Propylthiouracyl (PTU) or
Carbimazole (in pregnancy)
3. Radio iodine (before surgery)
4. surgery
5. in subacute thyroiditis:
symptomatic
Sick euthyroid N or a bit N or a N or a bit Only symptomatic (self-limited)
(post-op. – decr. bit decr.
response to stress: decr.
cortisol incr. =>
TSH, T3, T4
hormones just a bit
decr. but with
sympt.
- thyroid problems
o Sx
dysphagia
painful in inflamation – Hashimoto
complete – anaplastic carcinoma
stridor – requires urgent surgery
o Dx
blood hormons: T1, T3, TSH, calcitonin, Ca
U/S
FNAC
thyroiditis?
nodules
thyroid scintigraphy - scan
diffusely increased activ.
- Graves dis.
diffusely decreased activ.
- subacute thyroiditis
- silent thyroiditis
- post-partum thyroiditis
diffusely heterogenous activity
- toxic multinodular goitre
focally increased activity
- hyperfc. adenoma
o thyroglossal cyst
o thyroid cyst
Dx – U/S
o nodules
single – benign
multinodular goitre – benign
less likely to be malignant than a single nodule
a multinodular goiter is with hyperthyr.?
Toxic nodule
Dx
- localized increased uptake of radioiodine
Cold nodule
Dx
- localized decreased uptake of radioiodine
- CA?
o thyrotoxicosis
types
primary = Graves disease
- autoimmune
- Sx
diffuse goitre
exophtalmia, lid lag
- Dx
difuse increased uptake of radioiodine
secondary
- hot nodule
- De Quervain’s subacute thyroiditis
post. inf. – viral, URTI
initially hyperthyr., then hypothyr.!
Sx
fever
enlarged painful thyroid
tender lump or swollen goitre
Dx
difuse decreased / absent uptake of
radioiodine
incr. T3 and T4, decr. TSH
no AB
o Dx diff from Graves
Rx
propranolol
paracetamol
self-resolving
-
Sx
triad: anxiety + wt. loss + weakness
amenorrhoea (everything else incr.)
Rx
antithyroid drugs (thyrostatics) - inhibit the production of thyroid
hormones: carbimazole, methimazole, propylthiouracil
beta-blockers: propranolol, metroprolol
radioactive iodine therapy (with iodine-131)
surgery
o thyroid crisis (thyroid storm)
acute hyperthyr. Sx precip. by surgery or inf. in undiagnosed patient
Rx
emmergency admission!
antithyroid drugs
C/S
anti-heart failure and antiarrhythmia drugs
o hyperthyr. in pregnancy
dangerous for the baby
premature delivery
IU growth restriction
fetal death
malformations
Rx
medical
- propilthyouracil
passes less to the baby
risk of hypothyr in mother
check level of T4 in the mother regularly
- carbimazole – if propilthyouracil doesn’t work
long acting thyroid stimulator -> protector? detect
status of baby
if not working -> surgery
radioactive Rx is prohibited!
o hypothyr.
Sx
triad: tiredness + husky voice + cold intol.
menorrahagia (everything else decr.)
Rx
thyroxin – monitor TSH levels:
- check every month, till stable
check every 2-3 months, till stable
check every 2-3 yrs
o Hashimoto’s thyroiditis
autoimmune
initially thyrotoxicosis, then mixedema
MC cause of bilat. non-thyrotoxic goitre in Aus.
Dx
anti-thyroid microsomal AB
aspiration cytology
o non-toxic goitre
puberty – temporary
pregnancy – temporary
menopause
low iodine in water/diet – in Tasmania
o hypothyr in pregnancy
Sx
increased miscarriage
still birth
premature birth
Rx
thyroxine
if woman already with hypothyr, increase dose by 25 micrograms
during pregnancy
- return to normal dose after delivery
o thyroid CA
types
papillary – MC (75-85%)
- excellent prognosis
folicullar – 10-20%
- excellent prognosis
medullary – 5-8%
- part of MEN-2 syndrome (multiple endocryne neoplasia)
- poor prognosis
anaplastic < 5%
- can cause complete dysphagia
- poor prognosis - not responsive to Rx
+ lymphomas, SCC
Sx
painless nodule
hoarseness of voice = spread to soft tissues in the neck, affecting the
recurrent laryngeal nerve = inoperable tumor
Dx
scan - cold nodule
FNAC – investig. of choice
Rx
very high cure rate with Rx!
thyroid ablation
- thyroidectomy
- I 131 ablation
followed by thyroxine replacement Rx for the rest of his life
- causes of unilat. exophtlamia
o Graves dis. - MC
o contralat. Horner?
o cavernous sinus pathology
o intraorbital pathology
- stridor post-thyroidectomy (due to haematoma) -> open wound / all (superficial / deep)
sutures in ward
Hyperparathyroidism
Ca PO4 ALP PTH
Multiple myeloma Incr. Incr. or N N N
Paget’s dis. N N Very very incr. N
Primary Incr. Decr. Slightly incr. or N Very very incr.
hyperparathyr.
Osteoporosis N N N N
Osteomalacia Decr. Decr. N N
(decr. bone
density)
Malignancy Incr. Incr. Incr. N
CRF Decr. Incr. Incr. or N N
o types
primary
PTH increased
Ca incr.
due to a parathyroid adenoma
secondary
PTH increased, Ca can be normal or low
o MC cause of isolated (asympt.) incr. of Ca
o Sx
moans – muscle aching
abd. groans – abd. pain, gastroesof. reflux, constipation
stones - kidney
bones – pain, back pain
psychic overtones - fatigue, depression
o Dx
PTH very incr.
DM
- Murtagh – 194 – Dx + 1320 Rx + Jay’s notes
- Sx
o polyuria + polydipsia + wt. loss
o lethargy
o neuropathy
diabetic foot ulcer is the MC cause of prolonged hospital stay in DM
if DM is properly controlled, amputation can be reduced by 50%
if untreated, 1/3 of DM patients will have amputation due to DM neuropathy
with the presence of normal pedal pulse, the dev. of foot ulcer is unlikely
types:
MCQ: burning pains in the feet, pins and needles in the fingers and
toes, weakness and unsteadiness of the legs, distal wasting and
weakness in all limbs, glove and stocking sensory loss of all modalities,
areflexia
1. sensory polyneuropathy – bilat. perifpheral symmetrical (glove &
stocking distribution) with numbness, tingling, pain often worse at
night
- Rx
paracetamol / aspirin
gabapentin
TCA
2. moneneuritis - cranial nerve neuropathy
- III, IV
- difficult to Rx – C/S
3. amiotrophy – asymetrical motor neuropathy
- a. painful wasting of quadriceps (lumbosacral radiculopathy)
Dx – EMG
- b. focal neuritis – pain & tingling of ant surface of thighs
Rx - Immunglobulins
4. autonomic neuropathy
- heart – orthostatic hypotension, tahicardia
- GIT – gastroparesis (bloating, early satiety)
usually slower GIT movement => bacterial overwgrowth
=> diarrhoea
- urine retention
- ED
Rx
amytriptilline
o HbA1C < 7% normal
control in the last 3 months
o childhood DM
polyuria, polydypsia, wt. loss (despite polyphagia)
Rx
- insulin: 2 divided doses
- 0.5 unit/kg/day - honeymoon period (first 2 weeks after Dx)
- 1 unit/kg/day – older child
- 1.5 unit/kg/day adolescent
2/3 in the morning + 1/3 in the evening
2/3 long / intermed. + 1/3 short acting
Dx – blood sugar
o Rx
types of drugs
o insulin
o oral hypoglycaemic agents
insulin secretagogues
sulfonylureas: glipizide, gliclazide, glibenclamide,
tolbutamide, chlorpropamide
(me)glitinides: repaglinide
insulin sensitisers
biguanides: metformin
glitazones: pioglitazone, rosiglitazone
alpha-glucosidase inhibitors - slow the digestion of starch in the
small intestine, so that glucose from the starch of a meal enters
the bloodstream more slowly, and can be matched more
effectively by an impaired insulin response or sensitivity
acarbose
peptide analogs
incretin mimetics
o GLP analogs: exenatide
DPP-4 inhibitors
o vildagliptin
amylin analogs
approach
type II
- start with lifestyle changes – 2-3 month trial
- if not controlled, then start Metformin – incr. dose to max.
- then add Gliclaside – incr. dose
- then add Acarbose – incr. dose
- then insulin
type I
- insulin
ultra-short: Lispro
short acting: neutral
intermediate acting: Isophane, Protophane
- Cx
o 1. hypoglycemia
glucose < 3 mmol/L
Sx - sweating, anxiety, hunger, palpitations, confusion, drowsiness, seizures,
coma
types
mild-moderate = conscious patient
- oral food containing glucose (20-25 g glucose)
severe = unconscious or delirious
- 20-30 ml of 50% glucose / dextrose IV (hospital) in the cubital
fossa (not in the hand – high glucose concentration could cause
thrombosis of small veins) or
1 ml glucagon IM (at home, in ambulances)
- in kids – 10% glucose (50% could cause complic.?)
- neonatal hypoglycemia
5ml/kg 10% dextrose IV over 5 min
then 100 ml/kg/day IV infusion
- at home – apply instaglucose – rub gel on the gums
o 2. DKA (diabetic ketoacidosis)
hyperglycemia + dehydration + ketonuria
ketonuria = production of ketone bodies is a normal response to a shortage of
glucose, meant to provide an alternate source of fuel from fatty acids.
causes
- in DM – especially type 1
- in significant dehydration and electrolyte loss (e.g. massive
vomiting)
- in starvation
MCQ: K+ shifts to extracel space => K+ in blood is incr., but total body K+ (intra
+ extracel) is low (due to renal loss)
child is very dehydrated (main problem), confused in the morning, with urine
ketones
Rx
10 U insulin IM
DKA 48hrs
+ 2. Maintenance:
85ml/kg (or
Next 10 kg – 50ml/kg
+ 3. Losses:
If hypokalemia:
40 mmol/L < 30 kg
60 mmol/L > 60 kg
o 3. hyperosmolar hyperglycemia
marked hyperglycemia + dehydration + high plasma osmolarity, but w/o
ketonuria
in type 2 DM
Rx
fluids
insulin
o 4. lactic acidosis
metabolic acidosis with large anion gap
DM type 2 Rx with metformin, especially if RF is present
Rx
removal of cause
fluids
alkalinisation with IV sodium bicarbonate
Oral pathology - OK
- submand. vs. parotid gland pathology
o angle of jaw
visible = submand. lesion
Dx
- 1st - bimanual palpation
- most appropriate - intraoral x-ray
- best test = CT
- orthopantogram – panoramic x-ray of all the teeth
can miss small stones
not clearly visible = parotid
Dx – 1st and best = U/S
- parotid and prostate – U/S
no FNAC for scrotum and parotid
o submand. swelling and ear pain
examine what? tongue CA (with retroauric. lymphnodes?)
o pathol.
parotid
tumors
- parotid pleomorphic adenoma – benign
most popular (benign) tumor of the parotids
admixture of polygonal epithelial and spindle-
shaped myoepithelial elements
displaces the ear lobe
does not cause facial nerve palsy
- adenolymphoma (Warthin tum., adenolymphoma,
monomorphic adenoma) – benign tumour of the salivary glands
(e.g. parotids)
second most common benign parotid tumor
- CA
salivary glands (parotid) cancers
mucoepidermoid carcinoma – most popular
Adenoid cystic cancer – second most popular
facial nerve palsy + palpable lymph nodes + later on
pain + lump of parotid
Dx – initial test = U/S
Cx - invasion of the facial nerve -> facial palsy
stones
- painful swelling precipitated by anticipation of food (before
meals)
swelling appears before eating and goes away a few
hours after eating = stone
submand.
tumors
- more commonly CA than parotid tumors
- lower and more anterior than parotid tumors
- do not displace the ear lobe
TRIANGLE TRIANGLE
- Cystic hygroma
- Bronchial sinuses
and cysts
o locations
ant neck triangle
branchial cleft cyst – MC in the ant triangle
- Most common cystic lesion of the anterior triangle of the neck
in children
- Unilocular, cystic mass displacing the submandibular gland
anteriorly and the sternocleidomastoid muscle posteriorly
- Dx diff with submand. gland lesion
when palpating the cyst it will not produce any saliva /
puss /etc in the mouth
closer to the SCM (following its line) than the mandible
(lower)
- Rx
removal of the cyst
carotid body tumor
carotid aneurysm
lateral thyroid tumor (metastases)
post neck triangle
developmental remnants
- cystic hygroma
-
can be huge
soft, transilluminated
May be macrocystic or microcystic
MRI is the gold standard for radiologic evaluation
- bronchial sinuses and cysts
Pancoast tumor (from lung apex)
cervical rib
midline
thyroid nodule
thyroglossal duct cyst
- Midline lesion anywhere from foramen caecum and the thyroid
gland
- May contain ectopic thyroid tissue
- May contain all of the functioning thyroid
- Ultrasound, thyroid scans
- moves with protrusion of the tongue + moves with swallowing
- Rx
Surgical excision - Sistrunk procedure
o
dermoid cyst – beneath the chin
midline cervical lymph node swelling
anywhere / widespread
sebaceous cyst
lipoma
submand.
salivary gland tumor
cervical actynomycosis
sternocleidomastoid tumor
ENT - OK
- uvula is shy (away from the lesion) and the tongue is bold (towards the lesion)
Laryngeal pathology
- laryngitis
o acute
hoarseness
loss of voice
o chronic
due to
smoking
- active
- passive (in barmaids, etc.)
voice abuse
- laryngeal CA
o Hx of chronic laryngitis and smoking
o might be preceeded by leukoplakia
o hoarseness of the voice + lump (cervical lymph node) + sore throat + cough + stridor +
earache
o Rx
radiotherapy, laser therapy
laryngectomy
- laryngomalacia
o MC cause of stridor in infants
Usually presents as inspiratory stridor within the first 6 months of life
o 90% of patients will have spontaneous resolution of symptoms usually by 12 months
of age (18 months – 2 years)
10% require surgery
o Main congenital abnormality of the larynx.
o Immature aryepiglottic folds and glottis.
o Increased tendency of larynx to collapse in inspiration.
o Sx
Stridor is intermittent and variable in intensity
Symptoms are worse during sleep and positional variations occur (worse when
supine, improved when patient is prone)
o Diagnosis
Confirmed upon flexible laryngoscopy with findings of supraglottic tissue into
the laryngeal inlet during inspiration
the tongue and epiglotis falls back causing stridor
Laryngotracheobronchoscopy to rule out any synchronous airway pathology
Polysomnography to detect episodes of hypoxia or hypercapnia
o Management
Most do not require intervention due to a high rate of spontaneous
improvement
10-20% of synchronous airway lesions (patients with more severe symptoms
should undergo direct laryngoscopy & bronchoscopy to assess the entire
tracheobronchial tree)
Gastro-oesophageal reflux can exacerbate laryngomalacia & should be treated
medically
Surgical intervention is indicated for approx. 10% of patients – indications are
severe stridor, apnea, failure to thrive, pulmonary hypertension, and cor
pulmonale
Ear and hearing problems
- screening for hearing loss
o 8-9 mths
o school entry
- Audiologic Testing
o 0-3 months
ABR
Auditory Steady State Response (ASSR)
o 2-12 months
BOA (behavioural observation audiometry)
o 7-30 months
VRA (visual reinforcement audiometry)
o 24 months – 6 years
Play audiometry
o 6 years +
Modified play audiometry
o 8 years +
Standard adult audiometry
- hearing tests
AC < BC =
In conductive hearing loss, bone conduction is better than air negative
Rinne
In sensorineural hearing loss, bone conduction and air conduction are both AC > BC =
equally depreciated, maintaining the relative difference of bone and air positive
conductions Rinne
- Hearing Loss
o degrees
normal: 0-20 dB (20 = soft speaking voice)
mild: loss of 20-40 dB (40 = normal speaking voice)
moderate: 40-70 (70 = shout)
severe: 70-90 dB
profound: > 90 dB
o MC causes
impacted cerumen (wax)
serious otitis media
otitis externa
children – congenital deafness
elderly - presbyacusis
o Types
Conductive Hearing Loss
Conductive hearing loss can be acquired or congenital and is caused by
blockage or damage in the outer and/or middle ear
A conductive hearing loss leads to a loss of loudness and can often be
helped by medical or surgical treatment.
Causes:
- blockages of the ear canal by impacted wax or foreign objects
- Otitis externa
- Middle ear infection (glue ear)
- perforated eardrum (due to infection or trauma)
- otosclerosis
- partial or complete closure of the ear canal.
Sensorineural Hearing Loss
Sensorineural hearing loss can be acquired or congenital and is caused
by damage to, or malfunction of, the cochlea (sensory part) or the
hearing nerve (neural part).
Sensorineural hearing loss leads to a loss of loudness as well as a lack
of clarity. The quantity and the quality of sound are affected and
sometimes may limit the benefit of a hearing aid.
Causes:
- the ageing process – presbyacusis
bilat. high frequency (s, f, th) hearing loss
- excessive noise exposure
- diseases such as meningitis and Meniere's disease
- viruses, such as mumps and measles
- Ototoxic drugs
- head injuries
Mixed Hearing Loss
Mixed hearing loss results when there is a problem in both the
conductive pathway (in the outer or middle ear) and in the nerve
pathway (the inner ear)
An example of a mixed hearing loss is a conductive loss due to a middle-
ear infection combined with a sensorineural loss due to damage
associated with ageing.
o Rx
hearing aid – in conductive hearing loss
cochlear implant - effective if implated early
children > 2 yrs
adults
- otosclerosis
o Disease of the bone surrounding the inner ear and is the most common cause of
conductive hearing loss in the adult with a normal tympanic membrane
o The normal middle ear bone is replaced by vascular, spongy bone that becomes sclerotic
o Progressive disease
o Develops in the 20s and 30s
o Family history (autosomal dominant)
o Unilateral or bilateral
o Female preponderance
o Stapes footplate is affected
o May progress rapidly during pregnancy
o Treatment
Referral to an ENT consultant
Stapedectomy (approximately 90% effective)
Hearing aid fitting (less effective alternative)
while waiting for surgery
- loudness recruitement
- hearing loss causes
o sensorineural – damage to cochlea
presbyacusis
noise exposure
when exposed to noise > 8 hrs / day for 10 yrs
meningitis
Meniere
viruses – mumps, measles
ototoxic drugs
o conductive – blockage in outer or middle
wax
otitis ext.
middle ear inf.
chronic - cholesteatoma
perforated eardrum (inf., trauma)
otosclerosis
- tinnitus
o assoc. sympt. in deafness
o types
non-pulsatile, constant – the cause is in the ear
pulsatile
o Rx
treat cause
betahistine
clonazepam
carbamazepine
acute tinnitus – lignocaine i.v.
- normal otoscopy:
-
- acute otitis media
o
o 2/3 of children have at least one episode by age of 3, 90% by school entry.
o 2 cardinal features
inflam.
effusion
o Clinical Features:
Earache, pulling of the ear, reduced hearing, irritability, anorexia, lethargy
fever, vomiting – bacterial -> A/B
o EXAMINATION:
Usual middle ear landmarks are not well seen.
The TM is dull and opaque, with lost light reflex, and may be bulging, yellow-
grey colour.
fluid level might be seen
On pneumatic otoscopy TM mobility is reduced.
May have associated signs of URTI.
o CAUSES:
Streptococcus pneumonie 35-40%
H. Influenzae 25-30%
Viral: 25%
Moraxella catarrhalis 15-20%
least common – staph.
Do not accept otitis media as the sole diagnosis in a sick febrile young child
without elimination of a more serious cause
meningitis – frequently assoc. with otitis media
o Rx
try to avoid using A/B
never use A/B in children, except for this!
> 1 yr old, mildly unwell, immuncompetent
just observation for 12-24 h, analgezia, no A/B
if symptoms not resolving or severely ill (vomiting, fever)
- first line = amoxycillin
- still not resolving after 48 hrs
2. cefaclor or
amoxycillin + clavulanic acid – if resistence is
suspected
< 1 yr, moderate/severe, immuncompromised
- amoxycillin
- still not resolving after 48 hrs
amoxycillin + clavulanic acid
o complic
Effusion – 70%
Perforation of the TM results in purulent otorrhoea, and usually relief of pain.
Febrile convulsions are commonly related to AOM < 1yr
Repeated suppurative inf. can cause hearing loss
Mastoiditis
swelling, tenderness behind the ear
deterioration
Mx – referral!
serous otitis media (glue ear – the middle ear fluid has become thick and glue-
like) = incomplete resolution of acute otitis media
hearing loss, loss of drum mobility
rarely
suppurative labyrinthitis or intracranial infection (meningitis – child
unwell, extradural or subdural abscess, brain abscess): uncommon.
Facial nerve palsy, lateral sinus thrombosis, and benign intracranial
hypertension.
o aboriginals – frequently chronic otitis media – don’t use A/B
- chronic otitis media
o infected otorrhea through a tympanic membrane perforation or tympanostomy tube
o pain in chronic otitis media – relieved after spontaneous rupture of the tympanic
membrane
o cause
pseudomonas
staph. aureus
proteus
o Treatment:
Antipseudomonal penicillin or cephalosporins (children)
Ear drops & quinolones (adults)
o Safe vs. unsafe perforation
Safe Perforation
Dizziness
o can be with
central cause – brain, cerebellum
acoustic neuroma
MS
head injury
vertebrobasilary insuf.
peripheral cause – inner ear
Meniere
BPPB
vestibular neuritis / labyrhinthitis
o causes:
COMMON
Benign Paroxysmal Positional Vertigo
Vestibular neuritis/labyrinthitis (unilateral peripheral vestibulopathy)
Meniere’s syndrome
Vestibular migraine
Psychogenic
Idiopathic
LESS COMMON
Acoustic neuroma
Vertebro-basilar transient ischaemic attack/stroke
Multiple sclerosis
Posterior fossa tumours
Arnold-Chiari malformations
Autoimmune inner ear disease
Perilymph fistula/semicircular canal dehiscence
Invasive middle/inner ear disease (e.g. otomastoiditis, tumours,
cholesteatoma)
Bilateral peripheral vestibulopathy (if asymmetric)
o Diagnostic Triads (J.Murtagh)
only vertigo caused by movement = BPPV
Acute vertigo + nausea + vomiting = vestibular neuronitis
(acute vertigo + nausea + vomiting) + hearing loss +/- tinnitus = acute
labyrinthitis (similar sympt. to Meniere)
Vertigo + vomiting + tinnitus + hearing loss = Meniere’s syndrome
(unilateral) tinnitus + hearing loss + unsteady gait = acoustic neuroma
- duration of common causes of vertigo
Seconds Benign positional vertigo
Minutes Vertibrobasillar insuf., migraine
Hours Meniere’s disease
Days Vestibular neuritis, labyrinthine infarcts
o 4 common causes
1. Benign paroxysmal positional vertigo (BPPV)
Most common cause of vertigo seen by otolaryngologists (20-40% of
patients with peripheral vestibular disease)
Affects all ages
Approximately 50% of people over the age of 70 have experienced at
least one episode
Symptoms & signs are brought about by changes in head position, 5-
10 sec later, lasts 10-60 sec
May be associated with closed head injury, infections, surgery and
prolonged bed rest
Pathophysiology:
- Otoconia become dislodged and pass through the
endolymphatic space of the vestibule into one of the
semicircular canals
Pathognomonic sign:
- nystagmus toward the affected ear on doing a Dix-Hallpike
test
Treatment:
- Epley repositioning maneuver
- Brandt-Darrof exercises
-
2. vestibular neuronitis – M 508
20-40 yrs
only vestibular portion of nerve VIII is affected
- if both vestibular and auditive portions (hearing loss) are
affected = labyrinthitis
Second most common disorder affecting the labyrinth
Viral etiology with consequent inflammation of the vestibular nerve
Signs/symptoms:
- previously absolutely healthy, sudden onset of severe rotatory
vertigo + nausea and vomiting
vertigo relieved by lying down
- Spontaneous nystagmus and diminished VOR
- Usually subsides over a course of several days or weeks
Differential diagnoses: cerebellar hemorrhage and infarction
Treatment:
- bed rest – mild case
- more severe - vestibular sedatives and anti-emetics in the first
24-72 hours
Dimenhydrinate - Dramamine
Prochloperazine – Stemetil i.m.
Diazepam
- severe
+ short course of C/S
- Vestibular adaptation exercises/rehabilitation in the recovery
phase
3. Meniere’s disease
Meniere’s syndrome is an inner ear disorder marked by spontaneous
attacks of vertigo, fluctuating SNHL, aural fullness and tinnitus
When the syndrome is idiopathic and not attributable to other causes
(i.e. syphilis) it is referred to as Meniere’s disease
Pathophysiology: endolymphatic hydrops
Duration of vertigo during attacks may last from 20-30 minutes up to a
few hours
It is commonest in the 30-50 age group
Characterised by paroxysmal attacks of:
- Vertigo
- Tinnitus
- Nausea and vomiting
- Sweating and pallor
- Deafness (progressive) – sensorineural
- + nystagmus during the attack
Treatment:
- Vestibular sedative, antiemetic for acute episodes
Prochloperazine
urea crystals in orange juice
Diazepam
Betahistine
- Low salt diet +/- diuretic for maintenance treatment
- Meniett device
- Intra-tympanic gentamicin or surgery for refractive cases
4. acoustic neuroma = Vestibular schwannoma
tumor of Schwann cells on 8th cranial n.
slow growing –> brain has time to adjust => less vertigo
78% of all cerebellopontine angle tumors
0.8% to 2.7% of population: 0.7 to 1 per 100,000
Pathology: vestibular division of cranial nerve VIII; Schwann cells
Type 2 Neurofibromatosis
- Bilateral tumors
- Chromosome 22 abnormality
- AD
Symptoms:
- Unilateral progressive SNHL 85%
- Sudden hearing loss 15%
- Tinnitus 56%
- Vertigo 19%
- Midface hypesthesia, cranial nerve V
- absence of the corneal reflex
- Facial paresis
- Diplopia, dysphagia, hoarseness, aspiration, cerebellar ataxia
- if hydrocephalus: headache and vomitting
Treatment:
- Observation
50-55% show little or no growth in 1-3 years
less than 0.2mm per year
Repeat MRI to monitor growth
- Surgical resection
Translabyrinthine, middle fossa, or suboccipital
retrosigmoid approaches
Stereotactic radiosurgery (gamma knife)
- nystagmus
o physiol. = part of the vestibulo-oculo reflex (VOR)
tested with the caloric reflex test
with warm water: eyes will turn towards the contralat. ear +
horizontal nystagmus towards the ipsilateral ear
with cold water – opposite effect
o pathol.
caused by lesions of
inner ear
VIII nerve
brainstem
cerebellum
cortex
Ophtalmology - OK
-
o normal left eye fundus
- Dx
o vision
6/4
6/5
6/6
6/60
…
count fingers at 6 m
count fingers at 1 m
see fingers?
perception of light
o optic disc - nasal
clear contour
o retinal vessels
narrower arteries
wider veins
o macula – temporal
no blood vessels in the middle
darker in color
- cranial nerves for eye muscles
o III
MR
SR
IR
IO
levator palpebral sup.
palsy:
ptosis + fixed pupil dil. + down & out eye
- DM or any ischemic problem – pupil normal (peripheral fibres
will still get supplied, here are the ones for the pupil)
causes
- DM or other ischemic problems
- cavernous sinus lesions
- sup. orbital fissure
o IV
SO
palsy: diplopia on downward (vertical) and lateral gaze
o VI
L.R
palsy: divergent squint on lateral gaze
- diplopia
o monocular – persists after occluding 1 eye
causes: in the same eye!
early cataract
dislocated lens
severe astygmatism
psychogenic / functional
Rx – not urgent
o binocular – (doesn’t persist when ocluding 1 eye)
REFER URGENTLY!!
causes: in the higher nerve centres
ocular nerve palsy – III, IV, VI
- CVA or TIA
- tumor
- aneurysm
- DM
- arthritis
- head injury
- migraine (ophtalmic) - transient
blow out fractures
concussion
MS – recurrent diplopia
myastenia gravis
hyperthyr.
- blocked naso-lacrymal duct
o repeated inf.
o usually self-corrected between 6-12 mths
o Rx
repeated bathing with normal saline
massage over the lacrymal sac
local A/B for inf.
refer – probing of the lacrymal sac, if
severe blockage or
if not self-corrected by 12 mths
o Cx
dacryocystitis – inf. of the lacrymal sac sec. to the obstruction
Rx
systemic A/B – flucloxacillin
drainage
- orbital vs. periorbital cellulitis
Orbital – big emmergency! Perorbital – also urgent
Unilat. swollen red eyelids
Post-septal Pre-septal
Pain on eye movement No pain
Restriction of eye movement No restriction of eye movement
Proptosis No proptosis
Loss of vision No loss of vision
Causes: Cause:
- sinusitis – MC - after an abrasion
- infection of nearby structures
- trauma
- previous surgery.
> 2yrs
Cx: blindness – may develop in hours
Dx - scan of head: possibility of abscess
within the brain (from the ethmoidal sinus) ->
needs to be drained, otherwise the child will
never recover
- refer to ophtalmologist (tertiary hospital) IV cefotaxime until afebrile, then
- IV antibiotics: IV cefotaxime + amoxyclav for 7-10 days
di(flu)cloxacilin until afebrile, then
amoxyclav for 10 days
- surgical decompression of the affected eye
- red eye – Murtagh 554 + Alena’s notes:
Pain Photophobia Vision Pupil Discharge
Conjunctivitis No No N N Yes
- acute conjunctivitis
o lasting < 3 weeks
o causes
infectious - usually bilat., with discharge and a gritty or sandy sensation
bact
- purulent discharge, with sticking together of the eyelashes in
the morning
- hyperemia of the conj.
- causes
str. pn.
str. pyogenes
haem. infl.
staph. aureus
pseudomonas
Rx – genta, tobramycin
gonococcal (hyperacute onset)
very rare and dangerous – immediate referral
o can give severe corneal inf. with
perforation
septicaemia
neonatal conj. (+ chlamydia)
Rx
o IV cephalosporins or penicillin
o topical sulfacetamide
Chlamydia
brick red follicular conj. with stringy mucus
discharge
types
o neonatal
o young patient with venereal inf.
o isolated Aboriginal people with
trachoma
MC cause of blindness in the
world
recurrent and untreated => lid
scarring and inturned lashes
(endtropion) with corneal
ulceration and visual loss
Dx
o swabs for culture and PCR
Rx
o local sulfacetamide eye drops
o systemic
neonates – erythromycin
children > 6 kg: azithromycin
- Dx
clinical
swab
- Rx
severe cases - cloramphenicol eye drops
milder cases
saline irrigation
antiseptic – propamidine isethionate
viral
- MC assoc. with an URTI
- highly contagious –> good hygiene
- Hx of infected contacts
- resolves in 3 weeks
- caused by adenovirus
- Cx – sec. bact. inf.
- preauric. lymphnode
- Rx
symptomatic
C/S are CI
non-infectious
from welding (actinic)
alergic
types
- assoc. with hay fever
Rx
topical antihistam.
topical sodium cromoglycate
topical C/S
- contact hypersensitivity
assoc. with topical ophtalmic drugs (A/B) contact lens
sol., cosmetics, etc.
Rx
remove cause
naphazoline
topical C/S
- episcleritis
o no discharge
o no watering
o N vision
o self-limiting
o Rx
topicl and oral C/S
- scleritis – assoc. with autoimmune dis.
o painful loss of vision
o urgent referral
- uveitis
o acute
anterior uveitis = iritis and iridocyclitis
Sx
- photophobia
- iris is sticky and sticks to the lens => adhesion => constricted /
irregular pupils
- blurred vision, floaters in the field of vision
causes
- 80% isolated
- 20% Reiter, ankylosing sponditlytis, Crohn, IBS, psoriasis
(seronegative arthropaties), SLE – HLA B27
Rx
- referral
- pupil dil. with atropine
- topical C/S
- systemic C/S
frequently recurrs after Rx
post. uveitis = choroiditis
o chronic
Sx
pupil is bound to the lens by synechiae and distorted
Cx – loss of vision due to:
glaucoma
cataract
- refractive errors
o presbyopia
> 45 yrs
o myopia
image formed IN FRONT of the retina (long eye or steep cornea)
Rx – concave lenses
Cx in high myopia
retinal detach.
macular degen.
glaucoma
o hypermetropia
image formed BEHIND the retina (long eye or steep cornea)
Rx – convex lenses
Cx – closed angle glaucoma
o astigmatism
causes – conical corean (keratoconus – e.g. Down)
o pinhole test – 1 mm hole
corrects any refractive error
if not => not just a refraction error!
- acute visual loss
o flashers and floaters
causes
constant – less of a concern
- age
- myopia
- eye surgery
fresh onset = concern
- retinal detachment
o retinal detachment
types
posterior vitrous degen. and detachment – in everybody
- sudden onset of floaters
- flashing lights = traction on the retina
- Rx – urgent referral
some people – pathol. detachment
- causes
trauma
high myopia (thin retina)
previous surgery (e.g. cataract)
DM retinopathy
- Sx
no pain
more dangerous if affecting macula
sudden onset of: (the 4 Fs)
flashes
floaters (spots, dots, cobwebs)
field loss
fall in visual acuity
o partial
o total – if macula detached
then suddenly irevers. blindness
“a curtain came down over the eye”
if revers. = carotid stenosis and embolism
- Dx
opthtalmoscopy: detached retinal fold as a large grey
shadow in the vitreous cav.
- Mx
transport to the hospital ASAP!
can’t transport by air
tilt head back and cover eye
keep pressure on the detached retina
o upper curtain (MC) – lower
detachment – keep head up
o bottom curtain – upper detachment –
lie down
specialist Rx
surgery – sealing of retinal tears
o macular degen. (see below)
o amaurosis fugax
unilat. transient loss of vision due to transient occlusion of the retinal a.
causes
emboli from
- carotid stenosis - MC
- carotid aneurysm
- heart
- temporal arteritis
risk of stroke after an episode of amaurosis fugax = 2% / year
o central retinal artery occlusion (CRAO)
elderly people – smokers, etc.
obstruction by emboli, thrombi, AS
Hx of TIAs or amaurosis fugax
exclude temporal arteritis
Sx
acute painless loss of vision (usually profound), with sudden onset
- “curtain descending over one eye”
- irrevers.
waxy, swollen, pale retina, thin arteries
chilly red spot in the macula – init. still vascularization, but then same
color as the rest of the retina
Rx
lower intraocular pressure (glaucoma medication)
inhale CO2 (paper bag)
poor prognostic, unless treated within 30 min.
o central retinal vein occlusion (CRVO)
in HT, dyslipidamia, DM, anaemia, glaucoma
Sx
similar to CRAO, but milder vision loss
can be sudden but usually more gradual loss of central vision
Dx
hemorrhage in all the 4 quarters, including borders of optical disc
“tomato ketchup and cheese” or “stormy sunset” appearance
Rx
find and treat cause
poor prognostic
better if the initial presentation was better
CRAO CRVO
Unilateral Unilateral
Often hypertensive
Mx: Mx:
Exclude GCA & TIA Elective referral to ophthalmologist within 1
Refer ophthalmologist wk
Ocular massage Screened for HTN, DM, Hypercholesterolemia
Acetazolamide oral – reduce IOP
o ischemic optic neuropathy – irevers.
temporal artheritis
sudden and often bilat. occlusion of the short ciliary aa. supplying the
optic nerve
Sx
- revers. vision of loss, then can lead to irevers.
- sudden loss of central vision
unilat., can rapidly become bilat.
- assoc. temporal headache, temporal aa. tender, thickened and
nonpulsatile
Dx
- ESR (> 40), CRP (sometimes ESR can be normal, then we do CRP)
- FBE (Hb – anemia; gives you higher ESR)
- temporal a. biopsy – confirm Dx
Rx – predisolone for 18-24 mths
- iv if patient has transitory loss of vision
- after 10 days of Rx – changes biopsy result (modif. have
disappeared)
o optic (retrobulbar) neuritis
inflam. of the optic nerve
causes
MS
neurosyphilis
toxins
woman, 20-40 yrs
Sx
retrooc. discomfort with eye movt.
central field loss (central scotoma)
- or peripheral circumferential blindness
Dx
optic disk swollen, then atrophic, then disc pallor
Rx
IV C/S
most patients recover spontaneously, but are left with diminished
acuity
o migraine
zigzag lines and lights
multicolored flashing lights
unilat. or bilat. field deficit
self-resolution within a few hrs
o hysteria
bilat. loss of vision, with tunnel vision
o vitreous haemorrhage
assoc. with
trauma
DM retinopathy
tumor
retinal detach.
Sx
sudden onset of floaters
loss of vision
Dx
clots of blood that move with the vitreous (black swirling cloud)
Mx
urgent referral – exclude retinal detach.
may resolve spontaneously
surgical vitrectomy for persistent haemorr.
o closed angle glaucoma (see below)
- chronic loss of vision
o in children = amblyopia = decr. in the visual acuity due to abnormal visual experience in
early childhood
strabismus
cataracts
refractive errors
retinoblastoma
o Glaucoma
Dx for incr. intraoc. pressure
cup:disc
- N <= 30%
- if > 30% = raised intraocular pressure
tonometry
- normal 10-22 mm Hg
incr. – can go up to 55-60
closed angle glaucoma
acute -> acute loss of vision
- ciliary flush (hyperemia)
- Common in middle aged or elderly hypermetropes.
- Associated with a narrowed anterior chamber.
- Obstruction to the outflow of aqueous humour.
- Precipitated by pupillary dilation – in the evening
- Sx – similar with migraine without aura, but with visual Sx –
diagn diff.!
Severe throbbing pain.
Headache.
Nausea and vomiting.
Weakness.
Visual changes:
Vision is reduced with HALOES around lights.
The cornea is HAZY.
Fixed and DILATED oval pupil.
corneal or scleral injection
On gentle palpation the eye feels hard.
- MANAGEMENT:
Ocular emergency.
Urgent referral to the Ophthalmology team.
1. Commence miotic drops (pilocarpine every 5
minutes for up to 1 hour).
2. Acetazolamide 500 mg slowly IV then 250 mg orally
t.d.s. – diuretic
3. periferal iridotomy – perforation in the iris to
evacuate the liquid
Antiemetic such as metoclopramide 10 mg IV and
analgesia such as morphine 2.5 mg.
chronic
primary open angle glaucoma = “glaucoma”
MC cause of irrevers. blindness in middle age
risk factors:
- age (after 40 yrs – check for glaucoma, especially with fam. Hx)
- fam. Hx
- high myopia
- DM
- HT
screening
- > 40 yrs – every 2-5 yrs
- if family Hx – start from 30 yrs, every 2 yrs
Sx
- progressive restriction of visual field (tunnel vision)
also in
retinitis pigmentosa
hysteria
central vision is N
Rx – for life!
- drugs
beta blockers: timolol, betaxolol
acetazolamide (diuretic)
pilocarpine - parasympathomimetic alkaloid
latanoprost - PG analogue
dipivefrine – prodrug of epinephrine, converted to
epinephrine in the eye
- surgery or laser therapy – if drugs failed
o cataract
cause
age – everybody > 80 yrs have opacities
DM
trauma
C/S
UV light
uveitis
Sx
blurring of vision in bright light
Dx
diminished red reflex
change in the appearance of the lens
Rx
lens extraction + intraoc. lens implant
- CI:
intraoc. inflam.
severe DM retinopathy
Px – UV sunglasses
Cx
hypopyon (puss in ant. chamber of the eye)
-
- causes
in case of endophtalmitis after
penetrating injuries
surgery
cataract
- urgent referral!
- Rx
avoid movt.
avoid smoking / alcohol
don’t give heparin
bed rest 5 days
sedative
check daily
if floaters / flashes -> emmergency!
bleeding 2nd, 3rd, 4th day?
o retinitis pigmentosa
displacement of the melanin-containing cells from the pigment epithelium into
the more superficial parts of the retina
Sx
night blindness in childhood
tunnel vision
blind by adolescence / middle age
Dx
patches of dark pigment especially at the periphery
o macular degeneration
causes / risk factors
age related
high myopia
types
acute – exudative
chronic – pigmentary (slow onset)
drusen (neovasc. membranes which develop under the retina of the macular
area and leek fluid or bleed ) + visual loss
Sx
central visual loss
- acute – sudden fading of central vision
- eventually central vision is completely lost
distorted images = macular degen.!
- lines of the words bend / seem wavy while reading
Dx
screening: using a grid pattern (Amsler chart)
- shows distorted lines
- cannot see the central dot
-
ophtalmoscopy – white exudates, haemorrhage in the retina
fluorescein angiography
can be
wet – acute?
- hemorrh., fluid leaks in macula
- Rx
laser photocoagulation
inj. inside the eye – vascular growth factor inhibitor =
new Rx
stabiliz.
1/3 improve
dry – chronic?
- “worn-out jumper”
- Rx
nutritional supplements
antiox. – vit. A, C, E + Zn
- corneal disorders
o keratoconjunctivitis sicca - “dry eyes”
causes
ageing, menopause
systemic dis.
- RA
- SLE
- Sjogren
drugs
- beta blockers
Rx
artificial tears – hypromellose, polyvinyl alcohol
o keratitis
causes
UV light (“arc eye”)
herpes simplex
herpes zoster ophtalmicus
superficial punctate keratitis
- in various conditions:
e.g. UV light exposure = flash burns
microbiol keratitis
- risk factors
contact lenses – MC with pseudomonas
corneal trauma or surgery
post-herpetic corneal lesion
etc.
Cx
perforation and blindness
Rx
urgent referral!
topical A/B – ciprofloxacin oint.
o abrasion / ulceration
causes
trauma
contact lenses
fingernails
UV burns
dendritic ulcer
- primary herpes simplex I inf.
can also cause follicular conjunctivitis
- Dx
stain with fluorescein
- Rx
aciclovir
atropine – prevent reflex spasm of the pupil
Dx
slit lamp and fluorescein staining
Rx
chloramphenicol oint.
eye pad
- pterygium
o
o fleshy overgrowh of the conjunctiva onto the nasal side of the cornea
o in dry, dusty, windy areas
o Rx
surgical excision
- pinguecula
-
o yellowish elevated nodular growth of the cornea
o Rx
surgery – if uncomfortable
- corneal ulcer with hypopyon - emmergency
o rheumatoid arthritis
o contact lenses abuse
- blepharitis
o inflam. of the lid margins
o freq. assoc. with seborrhoeic and atopic dermatitis, and rosacea
o types
seborrhoeic
staph.
assoc. with rosacea
o Rx
eyelid hygiene – mainstay of Rx
topical C/S
topical A/B
tetracycline
chloramphenicol
- stye (hordeolum ext.) – inflam. external glands
o
o acute abscess of eye lash folicle
o staf. aureus
o red tender swelling of lid margin, usually on medial side
o Rx
hot compress
lash epilation
chloramfenicol oint.
- chalazion (internal hordeolum, meibomian cyst)
o
o granuloma of the Meibomian gland
o inflamed tender irritant lump in the eyelid
o chronic – chalazion
o Rx
hot compress
chloramphenicol oint.
if large and uncomfortable -> surgery – incision and curretage under LA
- herpes zoster ophtalmicus (shingles)
o ophtalmic distribution of the V nerve (trigeminal)
o respects the midline!
o ocular problems: conjunctivitis, uveitis, keratitis, glaucoma
o Rx
topical aciclovir
systemic aciclovir – oral, IV
- penetrating eye injury
o not a lot of pain
o do not give pain killers – morphine, etc. – can cause vomiting, making things worse
small dose + antiemetic (metoclopramide)
o no local anestetic eye drops – can be retinotoxic
o don’t put bandage (pressure), just a shield or cone
o urgent referral!
if delay – give systemic A/B
- ectropion – rolling outward of the eye lid
o cause
age – involution
facial nerve palsy
o Rx – lubricant Rx
- entropion – rolled inward
o iritation of the cornea
o Rx – attach eyelid to the cheek
- lid tumor
o BCC 90 %, SCC 9 %, other 1%
o with loss of eye lashes (madarosis) – serious!
- subluxated lens
o
o Marfan syndrome
o trauma
- MRI – don’t do if metalic foreign body in the eye (magnetic)
- burn
o acid – injury just on the spot
o alkaline – injury keeps evolving
wash with excess water for 30 min
- leukoria
-
- retinoblastoma!
- retinopathy
o typical
cotton wool (intra-retinal infarcts) - DM
flame shaped haemor., AV nicking - HT
o DM
non-prolipherative
Related to ischaemia of blood vessels and include:
- Haemorrhages: Dot and blot.
- Microaneurysms.
- Exudates: Soft and hard.
- hemor., hard exudates (lipids – yellow, clear margins), around
the macula
- cotton wool spots – ischemia of the nerve fiber layers, indistinct
margins
venous beeding – severe
prolipherative
Proliferative: Changes in blood vessels in response to ischaemia to the
retina.
- New vessel formation.
- Vitreal haemorrhage.
- Retinal detachment.
can leak, rupture with hemor in the vitreous, healing with fibrosis,
retractional retinal detachment
- Rx - panretinal argon laser photocoagulation
o HT
Emmergency medicine - OK
- emmergency situations >- rapid primary survey = assess ABCD (disability) E (exposure)
o 1. Airway
secure the airway
consider cervical spine injury (in trauma) – neck collar
airway management
- identify the cause of airway obstruction
- assessment of airway
look for clinical signs of hypoxia
cyanosis, agitation, confusion
look for signs of obstruction
1. stridor
o laryngeal
upper
inspiratory
o tracheal
lower airway
expiratory
2. hoarseness of voice - laryngeal
3. aphonia – cannot speak at all (suffocating)
o most dangerous – may lead to impending
circulatory collapse
breathing patterns
tachypnea, bradypnea, use of accessory muscles
- establishment of the airway
basic Mx
caution with cervical spine injury
anatomical positioning of the patient
sucction of the mouth content, etc.
use of nasopharingeal or oropharingeal tubes
laryngeal mask
transtracheal jet ventilation – crycothyrotomy
definitive Mx
endotracheal intubation
o indic.
unable to protect the airway (risk of
aspiration) – unconscious patient
unadequate spontaneous resp.
SaO2 < 90% with 100% O2 admin.
GCS <= 8
o oro- or nasotracheal
o preferred = rapid sequence intubation (RSI)
in surgery we give 4 drugs: anesthetic,
muscle relaxant of choice (=succinyl
choline=suxamethonium), narcotic
analgesic, benzodiazepine (midazolam)
but here we only give 2: succinyl choline +
midazolam
first preoxigenation 100% O2 with mask
for 3 min (-> then intubate)
w/o doing bimanual valve ventilation (BVM)
– don’t push air in the stomach -> to
prevent aspiration
w/ cricoid pressure = Sellick manouver
o best method to confirm successful intubation:
ventilation (can also be confirmed with
auscultation and chest x-ray) and oxigenation: end
tidal CO2 (ET-CO2) – checks both ventilation and
oxigenation
ET tube size:
in children: uncuffed ET tubes used (cuffed ET
tubes can damage the trachea)
endotracheal tubes
length: age/2 + 12 cm
width
o >1 yr: age/4 + 4mm
o < 1 yr:
< 1kg: 2.5 mm
1-2 kg: 3 mm
2-3 kg: 3-3.5 mm
> 3 kg: 3.5 mm
1 month-1 year: 4 mm
O2 delivery systems
o nasal prongs (canula) – recommended today
flow rate: up to 3 L
max. received 40 % O2 (in emmergency we
always give 100% O2; in other situations –
with smaller conc.)
o simple face mask – used to be the preferred one
flow rate: 10-12 L
max. 60 % O2
o face mask with O2 reservoir
flow: 15 L
max. 90% O2
o ET tube
flow: 15-20 L
100% O2
o 2. breathing
look, feel, listen
pulsoximetry
ABG
o 3. circulation - BP
adm. fluids
cardiopulm. resuscitation
basic life support (BSL)
- DRABC
danger
response
A
B
C
CPR
o how:
30 compress. : 2 breaths
chest depression: 4-5 cm
rate of compressions: 100 /
min
o must important sign of successful
resuscitation: pupillary light reflex OK
o how long to continue CPR: as long as
you can, till the specialized team has
arrived (usually max. 45-50 min)
o if cardioversion is not available, IV
adrenalin should be given every 3 min
Disability
neurological signs
defibrillation
o use it right away if available
o for a witnessed cardiac arrest, using a
manual defibrillator:
give 3 consecutive shocks in
first defibrillation attempt
further shocks –> single shocks
o first shock: 200 J biphasic (before 360 J
monophasic – no longer used)
o continue CPR for 2 min
o second shock: 200 J biphasic -> max. 3
shocks
o shockable rhythms:
pulseless (unstable) VT
VF
o non-shockable rhythms:
asystole
pulseless electrical activity
(PEA)
advanced life support (specialized team has arrived)
- continue CPR
- in shockable rhythms - defibrillate again
- non-shockable rhythms – drugs only
- drugs
adrenalin 1 mg iv or intracardiac repeat every 3 min
during defibrillation
atropine 1-3 mg
in asystole or severe bradycardia
amiodarone – 300 mg bolus
in VT of VF
Mg – muscle relaxation, etc.
in any critical patient
bicarbonate – controversial
1 mmol/kg
- think of and address the reversible causes of cardiac arrest: 4Hs,
4Ts
hypoxemia
hypovolemia
hypo/hyperthermia
hypo/hyperkalemia
tamponade
tension pneumothorax
toxins
thrombosis (pulm., coronary)
- cardiac arrest
o basic life support -> ECG, monitor BP ->
VF
-> defibrilation -> adrenaline 1:10,000 10 ml iv -> defibrilation
- + consider lignocaine
asystole
adrenaline dilute 1 mg 1:10,000 give 10 ml iv from it -> continue CPR,
consider more adrenaline every 10 min -> atropine 1.2 mg i.v.
electromechanical dissociation
causes:
- 4 Ts
cardiac tamponade
PE/thrombembolism
tension pneumothorax
toxic / drug abuse
- 4 Hs
hypoxia
hypovolumia
hypothermia
hypoglycemia
hypokalemia + other electrolyte imbalance
after ruling these out -> treat as asystole
VT
pacient stable – amiodarone, lignocaine
pacient not stable – treat as VF
bradycardia – atropine 0.5 mg i.v.
consider external pacemaker
- CPR
o external cardiac massage – best indication that the massage is effective: size and
reaction of pupils
o most important factor that will result in a successful resuscitation = early
cardioversion
- anesthesics
o ketamine
one of the few analgezics which doesn’t cause hT
incr. everything: BP, ICP, bronhodil.
very good analgezic effect
dissociative anesthtic
SE – unpleasant hallucinations (in high dose), nausea, vomiting
indic.
for small pediatric procedures
anesthetic of choice in patients with low BP
in asthma
CI – head trauma (incr. ICP)
o tiopenthal sodium
decr. BP, decr. ICP
cerebroprotective effect (decr. the O2 consumption of the brain)
indic.
neurosurgery
SE
resp. depression, hT
endogenous histamine release -> careful in asthma
o propofol – very popular and efficient
stable anesthesia
no hallucination
SE – resp. depression, hT
can be contam. very easy (made with eggs) -> careful with antiseptic
procedures
- muscle relaxants
o depolarizing
succinyl choline – MC used in emmergency
cholinergic drug
short acting (3-5 min)
SE
- incr. ICP
CI – head injury
- hyperkalemia
CI in burn injury, crash injury
- bradycardia (Rx – atropin)
- malignant hyperthermia – very rare
non-dose dependant
very high mortality
o non-polarizing
types
intermed.
long acting
curaniums
pancuronium, etc.
- anaphylaxis
o causes:
MC of food alergy:
1. peanuts
2. seafood
in health professionals – latex
o Rx
ABC
seize the suspected allergic trigger
O2 - 6-8 L
adrenalin i.m. or i.v. (not s.c. for anaphylaxis – too slow) + on the endotracheal
tube
ampules contain 1 mg adrenalin (1000 micrograms)
- 1:1,000 conc. = 1 mg adrenalin in 1 ml sol. (1 to 1)
- 1:10,000 = 1 mg in 10 ml (10 times diluted)
admin.
- adults
0.5 mg i.m. 1:1000 (0.5 ml)
0.5 mg i.v. 1:10,000 (5 ml)
- children under 15 kg
10 micrograms / kg
i.m. 1:1000
i.v. 1:10,000
- laryngeal oedema
5 mg (5 ml) 1:1000 throught the endotracheal tube
- repeat after 3-5 min – 1-2 times
if persistent, do adrenalin infusion: 0.25 micrograms /
kg / min
+ antihistamins
+ hydrocortisone
if nothing else worked, especially in kids with asthma taking beta 2 agonists (can
develop adrenaline resistance): glucagon 2 mg i.v. + noradrenaline infusion
o indic for intub. post-severe alergic reaction
wheezing or persistent cough
loss of consciousness or collapse
difficult or noisy breathing
swelling of tongue
swelling or tightness in throat
difficulty in talking or hoarseness of voice
- bee sting:
o local
prometazine (antihistam.) oral
hydrocortisone cream – local
o general sympt. (facial oedema, swollen tongue)
IM adrenaline (vasoconstr. -> reduce oedema)
o if anaphylactic shock – venom immunetherapy
- snake bite – M 1345
o tiger snake – MC
o Sx
nausea and vomiting – reliable sympt.
abd. pain, excessive perspiration, severe headache
blurred vision
difficulty speaking or swallowing
coagulation defect (e.g. haematuria)
tender lymphadenopathy
o Cx
greatests danger: resp. obstruction and failure
neurol. – ptosis
hematol. (anticoag.) – affects clotting
+don’t rely on abd. sympt.!
+ cardiol.
+ nephrol.
o Mx
first aid: firm bandage, starting from distal to proximal + splint the 2 limbs
together
if on buttocks – no bandage, but do not move
not tight, no turniquet, no ice
make window in the bandage to do the swab (don’t displace the
bandage)
no sympt. – no treat.
observe patient for 12 hrs, then release
no helicopter
if sympt. – antivenom + antihistam. + C/S (to avoid serum sickness – if it
happens, use adrenaline)
venom detection kit: take swab (if scratchmarks) or use fresh urine,
and detect the type of snake
- monovalent antivenom preferred (e.g. specific for tiger snake)
over polyvalent (since it can cause anaphylaxia)
- if we cannot detect the type of snake -> polyvalent
- dilute antivenom 1: 10 in NS, prolonged 30 min. infusion
- air transportation
o CI in:
snake bite
retinal detach.
- spider bite
o only one spider is life-threatening – Sydney funnel-web spider (Murtagh 1346)
Sx
muscle fasculation, salivation and lacrimation, piloerection, dyspnoea,
neurol. sympt.
Mx – like for snake bites
resuscitation
specific antivenom
o red-back spider and black widow spider can also cause envenomation
rarely fatal, more serious in the young, frail, elderly
Mx
antihistamine
antivenom i.m.
o the rest – life support
Mx
apply ice pack
do not bandage
CA metastases - OK
- Murtagh p. 242-243
- 1. lymphonodes
o supraclav. nodes
right – 1. breast (women), lung (men)
also lung (Pancoast tumor)
left – gastric (small percentage of gastric – to right as well) – Troisier’s sign
also lung (Pancoast tumor)
o
- by location / destination
o metastases in the brain (same as lungs)
breast
lung
colon
lymphoma
kidney
melanoma
prostate
o metastases in the lungs (same as brain)
1. breast – MC - Murtagh
2. lung
3. colon
4. (MC at MCQ course) kidney – cannonball
5. testis
melanoma
+ thyroid - cannonball
o bone metastases – all are osteolytics, except for prostate CA (osteosclerotic)
from
breast – MC (Murtagh)
prostate CA (+ transitional cell CA of the bladder) = osteosclerotic ->
have to be excluded (do PSA)
lung
Hodgkin’s
(MC at the MCQ course) kidney CA – rarefying bone lesions
Dx - bone scan – with Technetium 99
Rx
1 - paracetamol
2 – NSAIDs + codeine
3 –morphine +/- paracetamol/NSAIDS
(Paget’s dis. of the bone
x-ray features
larger bone / bony extension
thickened cortex
coarse / thicker trabeculation)
o metastasize to the liver:
1. colon
2. pancr
3. liver
4. stomach
5. breast
6. lung
7. melanoma
least likely to metastasize to liver: kidney
o CA metastases in the ovaries (blue book p. 531) – only 5% of the CA in the ovaries
in Aus. MC from colon CA
in underdev. countries – MC from breast CA
in Japan (with a very high incidence of stomac CA) – MC from stomac CA
(Krukenberg tumor in both ovaries)
- by origin
o kidney CA
liver
lungs
brain
bones
o thyr. CA, what makes it inoperable
x-ray - cannon balls metastases in the lung
hoarseness of voice – maybe?
o breast CA
1 – the other breast
2 – bones
lung
liver
o stomach CA
liver
ovary (Krukenberg)
o multiple melanoma
lungs
liver
brain
small bowel
o testicular CA
lungs
liver
o prostate CA
bones: pelvis, spine
brain
- malignant ascitis
o source
ovary - MC
uterus
colorectal
stomach
liver
o can be assoc. with:
nodules on PR
hepatic bruit
supraclav. lymphnodes
absent ankle oedema
Genetic diseases - OK
- inheritance patterns – Murtagh 167
o autosomal dominant AD – anatomy / morphol. defects = 50% of the offspring (male or
female) inherit the dis.
familial adenomatous polyposis
Huntington’s disease
Von Willebrand
neurofibromatosis
Marfan’s syndrome
triad: tall stature + dislocated lens and myopia + aortic root dilatation
tall and thin
long fingers
mitral valve prolapse
Gilbert’s disease
tuberous sclerosis
hereditary spherocytosis
achondroplasia
Noonan’s syndrome
acute intermittent porphyria
o autosomal recessive – enzymes = 1:2:1 inheritance if both mother and father are
carrying the dis.
cystic fybrosis
beta thalassemia
hemochromatosis
Wilson’s disease
Phenylketonuria
if untreated causes intellectual disability, seizures
neonatal screening: Guthrie test
galactosemia
sickle cell anemia
alpha-1 antitrypsin deficiency
o X-linked recessive = 50% males affected, 50% female carriers; 25% affected, 25%
carriers (if just the mother is carrying the gene)
hemophilia A
G6PD deficiency
Duchenne muscular dystrophy
o X-linked dominant
vit. D resistant rickets
o Y-linked
hairy pinna
- fragile X syndrome
o triad: facies (long narrow face, low large ears) + large testes + low IQ
o MC inherited cause of intelectual disability
- 47xxy = Klinefelter syndr.
o tall stature, long limbs
o mild delay in motor and language dev.
o small testes (< 2 cm), infertile, gynecomastia
Pain - OK
- chronic pain management
o pharm.
step-wise approach:
1. Panadol on when required basis
2. Panadol on a regular basis – 4 x 1 g / day
NSAIDs? – depending on the condition
3. Opioids on a self-management approach – PO or self-injected
adjuvant therapy: TCA - Amitryptiline
o non-pharm. Rx
e.g. swimming is good in ankilosing spondylitis
- analgesics
o simple analgezics (actually NSAIDs too):
paracetamol
effects:
- moderate analgezic (same as aspirin)
- moderate antipyretic
- minimal anti-inflammatory
excellent safety: doesn’t affect the stomach (in ulcer) +
doesn’t affect the platelet function -> first line analgezic in
mild to moderate pain
dosage: 1 g 4 hourly (max. 4 g / day)
aspirin
short half-life
effects:
- moderate analgezic
- moderate antipyretic
- anti-inflammatory
side effects:
- affects the stomach (ulcers, stomach bleeding)
- has an antiplatelet effect (by inhibiting the
production of thromboxane, which under normal
circumstances binds platelet molecules together)
dosage:
- 600 mg 4 hourly (max. 4 g / day)
o NSAIDs – it takes 10 days for them to achieve maximal effectiveness
(recommend intermitent 14 day courses). Most NSAIDs act as
nonselective inhibitors of the enzyme cyclooxygenase (COX), inhibiting
both the cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2)
isoenzymes. COX catalyzes the formation of prostaglandins and
thromboxane from arachidonic acid. Prostaglandins act as messenger
molecules in the process of inflammation.
types by chemical structure
Propionic acid derivatives
- Ibuprofen – short half-life
- Naproxen
long half-life – in bony metastases in cancer
- Fenoprofen
- Ketoprofen
- Flurbiprofen
- Oxaprozin
Acetic acid derivatives
- Indomethacin – short half-life
- Sulindac
long half-life – in bony metastases in cancer
- Etodolac
- Diclofenac – short half-life
Enolic acid (Oxicam) derivatives
- Piroxicam - non-selective cox inhibitor - analgesic
antipyretic
long half-life – in bony metastases in cancer
- Meloxicam - preferential inhibitor of COX-2 over
COX-1
- Tenoxicam
long half-life – in bony metastases in cancer
- Droxicam
- Lornoxicam
- Isoxicam
Fenamic acid derivatives
- Mefenamic acid
- Meclofenamic acid
- Flufenamic acid
- Tolfenamic acid
Selective COX-2 inhibitors = coxibs – don’t have the
gastrointestinal side effects of the COX-1 inhibitors,
but they can cause cardiovascular problems (high
blood pressure, thrombosis – fatal myocardial
infarction and stroke, kidney problems)
- Celecoxib (FDA alert)
- Rofecoxib (Vioxx - withdrawn from market)
- Valdecoxib (withdrawn from market)
- Parecoxib (FDA withdrawn)
postoperative pain – IV, IM
- Lumiracoxib (TGA cancelled registration)
- Etoricoxib (FDA withdrawn)
Phenylbutazone
types by mechanism
non-selective inhibitors of COX-1 and COX-2, mainly in
CNS – paracetamol
non-selective inhibitors of COX-1 and COX-2, in CNS and
periphery – aspirin, other NSAIDs
Selective COX-2 inhibitors (see above)
Preferential inhibitors of COX-2 over COX-1 – meloxicam
prevent side-effects:
combine NSAID (e.g. diclofenac) with misoprostol
(synthetic prostaglandine E1 (PGE1) analogue)
to be avoided in significant renal failure or congestive
cardiac failure
o opiods – reserved for severe pain
types
popular weaker opioids
- codeine – strength simililar to aspirine (stronger
when combined with paracetamol)
- oxycodone
synthetic
very effective orally and rectally
in moderate pain (between NSAIDs and
strong opioids)
- dextropropoxyphene – controversial
popular strong opioids
- morphine
most effective in cancer pain
dosage:
orally: 10 mg 4 x / day
IM or SC: 7.5-15 mg
IV: bolus, slow or infusion
- pethidine – synthetic
risk of accumulation of its toxic metabolite
(norpethidine), causing myoclonic and
general seizures
not very used these days
- methadone – oral
in chronic pain – now replaced by long-acting
morphine
used in opiod dependency
other opioids
- fentanyl – synthetic opioid
administration:
IV
SC, IM
transdermal
epidural
efficacy similar to morphine but with fewer
side effects (10 mg morphine SC = 150
micrograms fentanyl SC)
- hydromorphone – 5 - 7 times more potent than
morphine
high risk of dependence
- tramadol – atypical, with opiod and non-opiod
features
more and more popular
analgesia without sedation or
respiratory depression
low abuse / dependence
- buprenorphine
limited use, in opioid dependence
-pentazocine – not recommended
-diamorphine = heroin
side effects:
nausea, vomiting
constipation
respiratory depression
dysphoria
tolerance / physical dependence / psychological
dependence
o combined analgesics: paracetamol / aspirine + opioid (codeine)
not recommended – rather prescribed separately
o methoxyflurane – inhalatory – in emergencies, roadside accidents
(ambulance)
o in neropathic pain:
tricyclic antidepressant (TCA) – amitryptilin – first choice in
diabetic neuropathy
antiepileptics:
carbamazepine - trigeminal neuralgia
gabapentin – newer - diabetic neuropathy (second choice
after TCAs), post-herpetic neuralgia)
o by age:
children
paracetamol
aspirine – should not be used < 18 years – risk of
Reye’s syndrome (fatty liver, encephalopathy)
opioids
- oral
- parenteral
bolus – IM, IV, SC
continuous infusion – IV, SC
elderly – more sensitive, lower doses
- psychogenic pain
o periomb.
o during the day
o not referred
o exclude from Hx: constipation, UTI, dairy product allergy
o Hx – emotional changes in the family
o Rx
enough dietary fibre and fluids, to have normal transit
family meeting to support the child (do not punish the child)
Radiology - OK
- xray
o abd
erect
supine
chest – pneumonia in lower lung lobes, can cause abd. pain
bowel obstruction
location
- small bowel – center
- large bowel – periphery
folds
- small – continuous from side to side
- large – can’t see the whole fold
size
- small – 3 cm
- large – 6 cm
caecum – 9 cm
sigmoid volvulus
inverted U, pointing up and right (distended sigmoid loop)
- bed-ridden elderly people, chronic constipation -> stretching ->
twisting
- young paralyzed people, bed-ridden
caecum volvulus – small bowel obstruction
emphysematous cholecystitis – air in the wall of the gall bladder
gas in the liver
biliary tracts
portal vein
hydatic cyst – multilocular, with multiple daugther cysts inside the big cyst
cyst vs. abscess – abscess might have air inside
U/S cannot see through air – e.g. retrocaecal apendix
o fractures
cortical disruption
Colles - post. dislocation of the distal fragm. compared to the proximal
fragment
fracture through lucency = pathol. fracture (malignancy)
- CT scan brain
o bleeding
intraaxial bleeding – inside the brain
extraaxial bleeding – outside the brain
SAH
- cause
aneurysm
AV malformation
surgery – immediate effect
radiotherapy - after 12 mths they scar; during
these 12 mths they can still bleed
- Dx
CT scan
75% show up on the CT scan
25% - small amount of bleeding not seen on CT
scan
o do a lumbar puncture
to locate the aneurysm or AV malformation
contrast angiogram
U/S through fontanele – till 12 (max. 18) mths
CT angiogram
MRI angiogram
subdural
- elderly
- multiple minor trauma
- Sx – confused
- venous
- sickle-shape (crescent)
- with dark areas inside (chronic, acute –heamor. – on chronic)
- can cause midline shift (if large)
extradural
- young
- major trauma
- Sx – headache
- arterial (middle meningeal)
- biconvex
- can cause midline shift (if large)
scalp haematoma
- Rx – with no loss of consciousness -> observe them for a few
hrs., then discharge them
blood = white
would be at the botton of the pic / bottom of the ventricles as the
patient is in supine position (heavier than CSF)
o stroke
cause
emboli
- if multiple vessels obstructed, MC with emboli (2 emboli
coming from a proximal source)
e.g.
elderly – AF
o Dx U/S – clot in a heart chamber
young
o HOCM
o mitral valve dis.
o DVT + patent foramen ovale -> could
cause an emboli to the brain
thrombus
types
ischemic
- loss of grey (cortex, on the outside) - white matter
differentiation + swelling of the brain
aa.
anterior cerebral a.
middle cerebral a. – from carotid a.
posterior cerebral a. – from vertebral a.
haemor.
o tumors
intraaxial – completely surrounded by brain on 3 axial images (in all the
planes)
MRI better – volume / 3D image
extraaxial – meningioma usually
o calcif.
coroid plexes
produce CSF
can calcify (the 2 lower branches of the ventricle H)
pinal gland – on the mid-line (shifted to one side = sign of midline shift = incr.
ICP)
o older patient – larger ventricles, deeper gyri due to CNS atropy due to old age
- brain MRI
o 1. you can see the skin / scalp - is white
skin cannot be seen on CT (white bone, then brain)
o 2. bone is black
o 3. brain
o method - 2 basic sequences:
T1 – anathomy – CSF is black
the only one that can be done with contrast: contrast will be white on
black background (CSF)
T2 – for pathology (for extra fluid in the brain)
CSF + any fluid is white – high signal
o Dx for MS – white spots = demyelination plaques around the ventricles
Other stuff - OK
- treatment options
o conservative - symptomatic
o medical
o surgical
o others
- planes
o median (midsaggital) plane – divides left/right
o transversal plane - horizontal
o coronal (frontal) plane – divides ventral (ant.) / dorsal (post.)
o
- postural hT = drop of > 10 mm Hg when standing
- intest. absorbtion
o terminal ileum
bile salts
vit. B12
o proximal jejunum
iron
folic acid
vit. C
Ca
etc.
- oedema
o pitting – pressing with the finger leaves an indentation that persists for some time after
the release of the pressure
cardiac
hepatic
renal
varicose veins / thromboflebitis / DVT
o non-pitting oedema
lymphoedema
lymphatic obstruction – do abdmino-pelvic CT to look for tumors
check for DVT - Doppler U/S??
myxedema
- hereditary angioedema – bouts of abd. pain and facial oedema
o Dx – C1 esterase inhibitor
- autonomic nervous system
o sympathetic
originate from the thoracolumbar region of the spinal cord (levels T1 - L2,
specifically) - "thoracolumbar outflow"
o parasympathetic
arise from the central nervous system with the:
III, VII, IX and X tenth cranial nerves
S2, S3, and S4 spinal nerves
"craniosacral outflow"
- central nervous system membranes and spaces
o epidural (or peridural) space – just in the spine
o dura mater
o subdural space – virtual, becomes real in cases of haemorrage (subdural hematoma)
o arachnoid
o subarachnoid space – contains the cerebrospinal fluid
hemorrhage from aneurysms
o pia mater
- Types of tissues
o epithelium is classified as a primary body tissue - cells which line the cavities and
surfaces of structures throughout the body. It is also the type of tissue of which many
glands are formed. Epithelium lines both the outside (skin) and the inside cavities and
lumen of bodies.
o connective tissue
o muscle tissue
o nervous tissue.
- marital disruption – single most powerful sociodemographic predictor of stress-related dis.
- greatest predictor of cardiovasc. dis. and DM = low educational level
- prevention
o primary – prevent the disease from occurring
o secondary – stop or delay the progression of dis.
screening and early detection of dis.
o tertiary – minimise disability in case of irreversible damage from the dis.
rehabilitation
- organ transplant
o storage times
24 hrs – kidney, pancreas, liver
12-24 hrs – lung
max. 6 hrs – heart
o Cx
malignancies
40% will develop a CA within 10 yrs
- universal
o donor - 0 Rh-neg
o recipient – AB Rh-neg.
- sexual abuse
o risk factor for:
mood disorders (depression)
anxiety disorders
eating disorders
substance abuse
- MC causes of death in Aus.
o 1 – circulatory disease: cardiovasc. disease
o 2 – CA
o 3 – accidents, poisoning, violence
o 4 – resp. dis.
o 5 - suicide
- MC causes of suddent death in Aus.
o 1 – MI
o 2 – accidents
o 3 – CVA
o 4 – PE
o 5 – suicide
- Leading causes of death in Australia
Smooth muscle. In
blood vessels the
principal effect is
vasoconstriction.
Blood vessels with
α1 receptors are
present in the skin
and the Gq: (Alpha blockers)
α1: phospholipase noradrenaline phenoxybenzamine
noradrenaline≥ gastrointestinal
ADRA1A, C (PLC) phenylephrine phentolamine
adrenaline >> system, and during
ADRA1B, the fight-or-flight activated, IP3 methoxamine prazosin
isoprenaline
ADRA1D response and calcium Cirazoline tamsulosin
vasoconstriction up terazosin
results in the
decreased blood
flow to these organs.
This accounts for an
individual's skin
appearing pale when
frightened. In the GI
tract, the effect is
relaxation.
Lung, smooth
(Short/long)
muscle, cerebellum,
salbutamol
skeletal muscle. In
(albuterol in
lung, agonists cause
USA)
bronchiole dilation.
Gs: adenylate bitolterol (Beta blockers)
isoprenaline > Agonists can be
β2: cyclase mesylate butoxamine
adrenaline > useful in treating
ADRB2 activated, formoterol propranolol
noradrenaline asthma. In smooth
cAMP up isoproterenol ritodrine
muscle, relaxes
levalbuterol
walls. Relaxes
metaproterenol
uterine muscle and
salmeterol
promotes release of
terbutaline
insulin.
Psychiatry - OK
Main pathology
Defense mechanisms
- types: http://en.wikipedia.org/wiki/Defence_mechanism
o I. pathol.
2. denial = avoid to become aware of some painful aspect of reality, you’re not
ready to accept it
e.g. patient doesn’t accept that he has cancer (“no, you are lying”)
Rx – don’t confront him, just give him time to accept it (unless he’s
dealing with a life-threatening situation)
3. splitting = external objects are divided into “all good” or “all bad”
e.g. patient doesn’t talk to any nurse because doctors are better than
nurses; morning stuff is better than evening stuff
mainly in borderline personalities
o II. immature – MC in adolescents, often also in adults
1. projection = attributing your own vicious thoughts or feelings onto someone
else
e.g. husband is cheating on wife -> tells her “I think you are cheating on
me”
5. somatisation = phsychic derivatives are converted into bodily symptoms
e.g. you think of an exam, and you develop symptoms (e.g. diarrhoea)
o III. neurotic – in adults
6. displacement = an emotion or drive is shifted to another that resembles the
original in some aspect
e.g. stressed from work/boss, get home, take it on your
partner/family/pet
7. intellectualization = excessive use of intelectual processes to avoid affective
expression (mood), but emotions are missing in the talks / arguments
e.g. pacient finds out he has cancer, he researches it, he talks about it
like in a speech, with no emotion
8. rationalization = rational explanations are used to justify unacceptable
attitudes or behaviour (blame game)
e.g. blaming something else for your mistakes
9. isolation = separation of an idea from the emotional effect that
accompanies it
e.g. when seeing the body of her dead son, the mother is very cold and
detached
11. repression
10 suppresion -> after a while you actually forget you ever had a dog
12. reaction formation = unacceptable impulse is transformed its opposite
e.g. we are afraid of an exam, but when asked we tend to say “I’m fine”
15. regression = you don’t behave according to your age (but like a younger
person)
MC in males
e.g. after his parents’ divorce, a 7 yrs old boy starts to wet his bed
again
o IV. normal, healthy, mature
14. sublimation = impulse gratification has been achieved but the aim or object
has been changed from unacceptable to acceptable
the most mature one
e.g. you like pornography, but you achieve satisfaction by focusing on
something else (e.g. you become part of the censorship board – you
watch it, but in an acceptable way)
10. suppresion = conscious forgetting
the only conscious defense mec.
e.g. lost a beloved dog, denies he ever had one (to avoid suffering)
13. humour = something is wrong with you and you are making fun of yourself
before anybody else has the chance to do it
16. introjection (Samir) = identifying with some idea or object so deeply that it
becomes a part of that person
17. identification (Samir) = unconscious modeling of one's self upon another
person's character and behavior
o + 4. blocking (Shipra) = temporary block in thinking (in stressful situation)
e.g. at exam, you know the answer but it just doesn’t come to our mind
Rx – relax, it will pass
o + transference (Samir)
pacients becomes emotionally involved /has negative feelings for her
psychiatrist, based on the patient’s childhood rships (with parents, teachers,
siblings) – transferring to the psychiatrist the feelings originally developed in
her childhood
can be
- positive (with positive feelings)
- negative (with negative feelings)
countertransference – the other way around
therapist develops pos. or neg. feelings because a particular patient
reminded them consciously or unconsciously of another patient or close
person
Personality disorders
o they were like this from the beginning, but can change / control it if they want
o = maladaptive behav.
o men: MC - antisocial
o women: MC – borderline
o key Sx
interpersonal rships are affected
failure to achieve goals at work
chronic unhappiness
o these are not diseases:
they are functioning
no trigger point / beginning for it
no psychotic sympt. (delusions, ellusions, hallucinations, etc.)
o types:
cluster A – isolated, detached, aloof + OK with that (but the surroundings are
not OK)
1. paranoid = suspicious, everybody around is plotting against them
- but not a delusion – accept explanations for their wrong ideas
2. schizoid = loner (happy to be alone), doesn’t talk to you
3. schizotypal = bizarre
- magical thinking
e.g. plants talk to him
- superstitious
- on the verge of getting psychotic
they might get psychotic for a short time under stress
cluster B
4. borderline = “unstable mood + impulsive”
- chronic feeling of emptiness, unhappiness -> suicidal gestures
love to give themselves physical pain to overcome
emotional pain (cut their wrists, etc.)
- sexual promiscuity
- use drugs all the time
- under stress can have psychotic or depression episodes – short
lived
- Dx – must have 5 out of :
frantic effort to avoid real or imagined abandonment
(not including suicide)
a pattern of unstable interpersonal rships
recurrent suicidal behav.
impulsivity in at least 2 areas (promiscuous sex, eating
disorder, binge eating, substance abuse)
identity disturbance
affective disturbance – very fast and strong emotional
responses
chronic feeling of emptiness, worthlessness
inappropriate anger
transient, stress related paranoid ideation, delusions or
dissociation sympt.
5. antisocial – they love to break the law + have no conscience, no
remorse for what they are doing (or they even enjoy it)
- genetic comp. (father -> son)
6. histrionic = “look at me” (center of attention), Paris Hilton
- uses seduction to attract attention
- in celebrities
- sexually frigid
7. narcissisitic – “I am the best”
- don’t take criticism
cluster C
8. anxious avoidant – “loner” but not happy about it (diff. from
schizoid)
- because they are scared of criticism / rejection or getting
embarrased (forced to be alone but don’t wanna be alone)
- obsessed to do everything right
- prone to depression
9. dependent – cannot take decisions, want somebody else to decide
for them
- won’t leave their partner even if abused
- very prone to depression
10. obsessive (ankastic?) – “perfectionist”
- likes order, likes things in a certain way
- very thrifty
- not prone to OCD, but prone to depression
+ passive-aggressive personality? (purple book) – negativistic attitudes and
passive resistance to demands for adequate performance at work or in
othersocial contexts, always complaining about these demands
Types of disorders
o I. anxiety disorder
components
psychological comp. – always worried, hypervigilance, restlessness,
difficulty concentrating, sleep disturbance
physiological comp. – hyperactivity: tahic., hands shaking, dry mouth,
tension headache, constip. or diarhhoea, etc. (adrenal release –
syndrome)
types:
1. panic disorder = unexpected and recurrent panic attacks + avoidance
behaviour (avoiding what could trigger the panic attack)
- MC people coming to the ED
- panicogens: lactate, CO2, caffeine
- young women (mid twenties)
- reach peak within ½ min
- +/- agoraphobia = afraid of public spaces (scared of having
panic attacks in public)
- they fear they will lose their mind / go crazy
- ABG: pH incr., PaCO2 decr., SaO2 normal
- Sx
panic attacks:
Lasts minutes to hours: 20 minutes.
Self-limited.
Occurs in patients with or without chronic
anxiety.
Spontaneous. – no significant trigger
Age of presentation: Mid twenties.
Variety of somatic symptoms (not faked).
o Sympathetic discharge: Release of
noradrenaline with produces
cardiovascular and other autonomic
symptoms.
o Palpitations, chest pain and tightness,
sweating, dizziness, trembling,
chocking, abdominal pain.
o Disorganization, Confusion, Dread,
Terror.
o Hyperventilation: Exhaling carbon
dioxide, lowering pH which affects
neuromuscular transmission (chest
tightness).
DIFFERENTIAL DIAGNOSIS:
o Panic attack secondary to a medical
condition.
o Panic attack secondary to medications.
o Caffeine intox. – no chest tightness
o Other anxiety disorders: Panic attack
are unexpected. The fear is of having an
attack, not of a specific situation.
TREATMENT:
o Antidepressants.
o Cognitive behavioural therapy.
o Benzodiazepines may be needed on a
short-term basis to provide more
immediate relief.
long term – between attacks
1. breathe in paper bags or relaxation
techniques
2. SSRIs
3. TCAs
2. phobic disorder
- irrational fear focused on certain things (not generalized like in
the generalized anxiety) disorder
- with insight – the person recognizes that the fear is irrational
and out of proportion with the real danger
- resistance is usually minimal and unsuccessful
- types:
agora phobia – fear of the marketplace/public
places/busses/confined places, far from home, you
cannot run away from there
untreated may culminate in a panic attack
social phobia – talking / eating / socializing with people;
ok 1 on 1, but not with a larger group of people
may be a predisposing factor for alcoholism
(alcohol is anxiolytic)
specific phobias
fear of spiders, snakes, illness, contamination,
etc.
- Rx
1. CBT:
systematic desensitization
assertive thinking
2. SSRI
in social phobia (stage fear):
beta blockers (control the physiological comp.)
3. OCD
- recurrent and obtrusive and false thoughts, with insight, they
know it’s wrong but can’t help it + action required to calm the
thoughts
- Rx
1. CBT
exposure and response prevention therapy
2. SSRI
4. post-traumatic stress disorder (PTSD)
- something major happened that threated his existance or
affected his integrity (impressed him very much)
+ reexperiencing – horrific intrusive image in his life,
occuring unexpectedly (not a halucination) + avoidance
of the places related to that event
flash-backs – during the day
nighmares – during the night
- hypervigilance – always on edge
- types:
acute < 1 mth
chronic > 1 mth
- 3 clusters of sympt.:
1. intrusive phenomenon: recollections, nightmares,
flashbacks
2. hyperarousal phenom. = exagerated startle response
(e.g. when you call their name a little loudly)
3. avoidance or reminders and emotional numbning
(they avoid the topic)
- Rx
1. CBT
crisis intervention therapy - goal: bring the
patient back to pre-crisis status
2. group therapy
3. SSRI
for nightmares: zopiclone, zolpidem (non-benzos
anxiolytics)
5. generalized anxiety disorder – anxious about everything
- mild, > 6 mths
- caract. = anticipatory feelings, especially in the morning (things
will go wrong today) + physical sympt.
- difficulty falling asleep (thinking about what happened during
the day) and then walking up during the night
- women
- Rx
1. CBT
2. SSRI
6. adjustment (reactive) disorder
- something changed in your life and you can’t adjust to it + get
anxious about it
Rx
all antidepressents: SSRI, SNRI, TCA
benzodiapines – with a clear time limit (otherwise – addicted)
CBT
- relaxtion + gradual exposure to the trigger
o II. Somatoform disorder
physical sympt. with no medic al explanation
transform psychological emotions to physical problems, without being
able to connect the 2
types:
1. somatisation disorder – classical form - never seen
- young women (starts < 30 yrs)
- 8 or more complaints:
4 of pain
2 GI
1 neurol.
1 sexual
- + atypical forms – with less complaints
- Rx
CBT
keep rescheduling their appts., don’t confront
2. conversion disorder
- women
- MC on the left side of the body
- may precede the dev. of somatisation disorder
- stressors cause neurol. sympt.
e.g. see something bad => they go blind; they are upset
and want to shout out their anger, but they respect
their father, so they lose their voice
- with “Labelle indifference” – their medical/neurol. problem
doesn’t bother them (because it helps them deal with their
problem)
- Rx
CBT – comforting
- better prognosis
no premorbid personality
no secondary gain
identifiable precipitating factor
blindness, paralysis, speech difficulty (aphonia)
young age
abrupt onset
3. hypochondriasis
- convinced they have 1 disease + tell you the diagnostic, despite
examinations and investigations denying his diagnostic
- Rx
psychotherapy
keep rescheduling their appts., don’t confront
4. body dysmorphic disorder
- one part of their body is not correct / sick
- MCQ: keeps looking in the mirror, changing clothes
- diff. from body image disturbance = eating disturbance (the
whole body is not correct)
5. psychological pain – persistent pain even though the etiology doesn’t
match
- e.g. torn ligament – Rx – should go away – but they still have
pain (they have no motivation to get well – others, well
motivate, like sportsmen, get well in 1 week)
Rx
drugs + psychotherapy
- conversion – good prognosis
- the others – bad prognosis
o III. Factitious disorder (Munchausen disease)
they simulate sympt. in order to get admitted in the hospital
variant: Munchausen by proxy - they simulate sympt. in a relative (their kids)
order to get admitted in the hospital
diff. from malingering = they simulate sympt. in order to achieve obvious gain
or to avoid punishment or responsability
o IV. impulse control disorders – cannot control their impulses + are anxious about it (they
have to do it)
1. intermittent explosive disorder
out of proportion uncontrolled reaction of anger / violence at small
triggers
followed by remorse
cannot control their anger
2. cleptomania
cannot control their impulse to steal objects they do not require ->
relived after they do it
¼ of the bulimics are also cleptomaniacs
Rx
- CBT: systematic desensitization
3. pyromania
love to put things on fire + get sexual gratification from doing it
usually low IQ
4. trichotillomania
pull their hair out when stressed
life change (parents separated, new father, etc.)
some also eat their hair => bezoars of hair causing intest. obstr.
with unequal areas of balding
Dx diff – KOH preparation to exclude a fungal inf.
o V. adjustment disorder
temporary disorder of varying severity, occurring as an acute reaction to
overwhelming stress, at any age, who have no underlying mental disorder
= inability or maladaptive reaction to an identifiable stressful life event like:
divorce, family crisis, failing exams, etc.
Sx must occur within 3 mths of the event and shouldn’t persist longer than 6
mths
females
genetic comp.
Sx = variety of disturbances at home or work, like: rage, shame, guilt, anxiety,
depression
o VI. delusionals disorder
just delusions – non-bizarre, initially seem reasonable, but upon investig. no
foundation is found for them
no insight
personality doesn’t desintegrate, well inserted in society
types
paranoid disorder (MC)
- subtype – pathological jealousy
- can occur as a psychological reaction to deafness
tinnitus may produce or aggravate auditory
hallucinations
erotomanic – they believe a celebrity is in love with them
can be dangerous – if their delusion refers to another person
e.g. pathological jealousy, Othello`s syndrome, attracted to a celebrity
could kill the person they fantasize about
Rx very difficult, don’t usually respond to antypsychotics
early detection is very important
o VII. eating disorders – feeling fat, overvalued idea of body image – even tough they are
skin on bone
anorexia nervosa – feeling fat
90% women
11-21 yrs -MC
Sx
- stop eating
subtype / some patients – binge eating (like in bulimia)
- heavy exercise – this keeps them healthy for a long time!
- amenorrhea (more often then in bullimia)
- purging: laxatives, vomiting
- motivation:
tired of family control, broke up with her boyfriend
(who were telling her to eat more)
don’t like food
- lanugo hair – due to emaciation
- hT, hypothermia, bradycardia
- parotid gland hypertrophy
- dental enamel erosion of the post. surface of the teeth
- lost shivering response to cold
- loss of breast dev.
associated psychopathology:
- depression
suicidal ideation
- anxiety sympt. focused on eating
- social withdrawal
- obsessional behav. concerning food, diet, wt. and exercise
- perfectionistic and preoccupied with external appearance
Cx
- liver, thyroid fc. abnormalities
- normocytic anemia, iron defficiency
BMI < 17.5 (or body wt. with 15% less than expected for the person’s
height, sex and age)
DSM criteria
- 1. failure maintain 85% of wt. according to age / height/
physical activity
- 2. intense fear of putting on wt.
- 3. body image disturbance = unrealistic self-evaluation (they are
really thin but believe they are overweight
- 4. amenorrhoea
risk of hypokalemia
bulimia :
binge eating, then induce vomiting
motivation:
- love food but feel bad because of their weight (they used to be
fat at one point in the past)
BMI - normal
Sx
- anemia
- teeth decay
- parotid enlargement
- teeth marks on dorsum of hand, calloused knuckles on the
back of the 2nd and 3rd fingers
- dental decay
- irregular cycles, oligo - rarely amenorrhoea
DSM criteria
- I. recurrent episodes of binge eating, consuming abnormal
amounts of food compared to normal persons + lack of control
during the binge
- II. recurrent inapropriate compensatory behav. to prevent wt.
gain
self induced vomiting, laxatives, fasting, excessive
exercise
- III. self-eval. is influenced by their body size and shape
- IV. disturbance doesn’t occur only during an episode of anorexia
nervosa (one of the 2 types of anorexia is the bulimic type)
complic
- lose HCl – electrolytes imbalances
- oesoph. lacerations
Investig (for both)
electrolytes – decr. K+
excessive laxatives cause metabolic acidosis
Rx
electrolyte correction – give K, Ca, Mg, vit. D
parenteral nutrition
family support
refer to eating disorder clinic: CBT
drugs:
- SSRI
- never prescribe TCAs!!! (they can decr. K)
Cx
can be life-threatening: they take lots of multivit. which can cause
hypophosphatemia!
o VIII. brief psychotic disorder
1-30 days
a stressor is always present
o IX. schizophreniform disorder
sympt. 1-6 mths
> 6 mths = schizophrenia
1-30 days = brief psychotic disorder
much better prognosis than schizophrenia
o X. schizoaffective disorder
psychotic (predom). + mania or depression
diff. from psychogenic depression = depression (predom.) with psychotic
elements
Rx – ECT
Rx
antypsychotics first, then treat depression
o XI. cyclothimic disorder = minor form of bipolar going on for > 2 yrs
o XII. dysthimic disorder = minor form of depression going on for > 2 yrs
no suicidal ideation
Schizophrenia
o very complicated, difficult to diagnose, takes a long time (4-5 long sessions)
o point prevalence = 1%
o good prognosis in schizofrenia
late age of onset
female
shizoid – poor prognosis
extroverted personality – better
abrupt onset = good
insidious = bad
positive without negative sympt. = good
good response to Rx early on = good
o MC causes of death:
I – cardiovasc. disease
II – suicide – 10%
o genetic fact.
o male
o late teen, early 20s
later in women (estr. protection)
o young people – drop in grades at school
o the more you delay the Rx, the poorer the prognosis
o they can leave a normal life with Rx!
not bad news these days anymore!
o tend to drift down the social scale due to their disease
o stigma for life – don’t diagnose: refer to specialist
o Dx – sympt. > 6 mths
o Sx
positive
lack of insight – MC sympt. in acute schizophrenia (97%)
delusions
- paranoid
- grandiose
- passivity phenomena – thought insertion / extraction /
broadcasting
thought insertion – believe someout outside is inserting
ideas in their heads
thought extraction – believe someout outside is
extracting ideas from their heads
thought broadcasting – his thoughts are not private but
shared with everyone (people are reading their minds)
- idea of reference – believe that irrelevant unrelated things in
the world are referring to them directly or indirectly
TV, radio is telling you to do something
they are special and the radio / TV / newspapers are
talking about them + they are followe around
hallucinations
- auditory – characteristic types:
1. audible thoughts (hearing his thoughts spoken out)
2. hearing voices - hear 2 people talking about the
patient or quarelling
3. voices commenting the patient’s actions
+ hearing commands – in depression as well
(illusions are not characteristic in s.)
disorganized speech
- “word salad” = incoherent sequence of words
- derailment – they keep changing the subject
- “loose association” – with some connection between the ideas
(diff. from “flight of ideas” with no connection between ideas –
in mania)
formal thought disorder – disturbance in the way
thoughts are linked together
types:
o flight of ideas – in mania
o perseveration – persistent repetition of
the same responses to a series of
different Qs – in dementia
o loose association – in schizophrenia
difficult communication: as though a “pane of glass” is between the
doctor and the patient
disorganized behaviour
psychomotor disturbance
- agitation
- retardation – catatonic
saccidic eye movement – when asked to follow an object with their
eyes, they do it in steps
negative sympt.
lack of motivation
blunted affect
poverty of thoughts
concrete interpretation of proverbs
social withdrawal
o types:
paranoid
disorganized – bizarre
catatonic
psychomotor disturbance (agitation or retardation)
catalepsy - keep their body in weird positions for a long time, e.g. with
the head above the pillow
- diff. from cataplexy – sudden loss of muscle tone + temporary
episodes of paralysis
part of the narcolepsy syndrome
o Rx
typical (conventional) antypsychotics – not used very much; very few used these
days (5-6 out of 25-30) due to SE
work primarily on dopamine (dopaminergic)
- dopamine hypothesis in schizophrenia: positive features in s.
are due to overactivity of dopaminergic pathways
e.g.
- haloperidol – tablet, inj long or short acting
- droperidol – p.o. only
- chlorpromazine
- trifluperazine
- flupenentixole – inj long acting
- zuclupentixol – inj long acting
SE
- extrapyramidal
1. acute dystonia – within hrs to days of Rx
in 20% of young males taking potent
antypsychotics
severe sustained painful agonizing spastic
contr. of axial muscles: around the eyes
(oculogyric crisis – eyes rolled up and open –
“the look-ups”), tongue (protrudes to 1 side),
spasm of the masticatory muscles (trismus),
neck (torticolis), dysarthria, dysphonia,
dysphagia
MC after haloperidol and fluphenazine +
chlorpromazine
cased by effect on the nigrostriatal tract
(dopamine decr. => incr. acetylcholine)
prophylaxis + Rx – inj. of anticholinergic:
benzatropine (cogentin) 2 mg IM or IV bolus –
quick response to it (5 min)
o if no response, repeat in 30 min
o then continued for a week or longer
2. parkinsonism – rigidity and tremor
within 1-4 weeks
parkinsonism – extrapir. – Murtagh 296
o rest tremor
o cogwheel ridigity
o bradikinezia
o shuffling gait
Rx – inj. of anticholinergic: atropine or
benzatropine
3. akathisia – restlessness (extra energy in my legs),
generalized restlessness, always moving (confused
with anxiety)
also caused by antiemetics and SSRI
Rx
o beta blockers
o benzodiazepines
o + lower the dose
o + indic. to change the drug!
4. tardive diskinezia - choreoatethetosis = involuntary
movements: grimaces, protruding the mouth, lip
smacking, winking, etc. + stiffness
after 3-6 mths or yrs of using them
irevers.
involuntary movements disappear when
sleeping
lots of dopamine supression => supersensitive
dopamine
3:1 = female:male, in the 40s-50s
no Rx
o even if stopping Rx
o change to another antipsychotic
(atypical)
o indic. for Clozapine
o tetrabenazine – cau cause Parkinson
- photosensitivity – discol. of exposed skin
- retinal deposits
- jaundice
- leucopenia
- ECG changes
- neuroleptic malignant syndrome – acute medical condition:
degen. of the muscle (CK very much incr.), fever, rigor,
shivering, disturbed consciousness, seizure and death
atypical
work on dopamine and serotonin (serotonergic)
e.g.
- clozapine – 1976
can cause death due to agranulocytosis
Sx – inf. (URTI)
Dx - FBE
reintroduced in 1992 US / 1994 Aus.
Aus. very good system - patient / doctor / pathology /
lab – all registered
blood test for WCC every week for 16 wks, then every 4
wks
drugs dispensed based on the blood results
only used as the third option (1 and 2 failed or bad SE)
very potent, very strong SE (“very dirty”)
blocks every receptor in the brain (shuts it
down)
- olanzapine
SE - wt. gain
not dose related
we won’t change the dose (as GP we cannot
change the dose – the psychiatrist only can
decide this)
Rx
o lifestyle modif. advice
- quetiapine
- risperidone – causes hyperprolactinemia
- amisulpride – causes hyperprolactinemia
replace with quetiapine or olanzapine
- aripiprazol
- ziprazadone
- sertindol – just listed
similar SE – but much less often
- extrapir.
- bone marrow problems
- liver problem
- MC = metabolic syndr. – incr. wt., hyperlip., hyperglyc. –
especially olanzapine
- sedation
- cardiac SE – prolonged QT interval – ziprazadone
- antipsychotic medication
o effects:
block dopamine receptors => dopamine goes down =>prolactin increases =
hypreprolactinemia = gynecomastia, galactorrhea, amenorrhea
block the muscarinic cholinergic receptors (M blockers) => anticholinergic
effects: dry mouth, constipation, urinary ret., confusion
avoided in elderly
block histamine => sedation, wt. gain
block the alpha adrenergic receptors => hypotension
o act on 3 tracts in the brain:
1. tuberoinfundibular tract -> decr. dopamin -> incr. prolactin
2. nigrostriatal tract
important in Parkinson: dopamine goes down, acethycholine goes up
cause extrapiramidal effects
3. meso-limbic tract -> clozapine works only here => no endocr. effects (1), no
extrapyr. effects (3)
but not a first line drug (but as the 3rd line of attack, after 2 drug failure),
due to the life-threatening risk of agranulocytosis
- I choice in psychosis = risperidone
- II – e.g. olanzapine
- III – clozapine = indic. no. 1
also indicated in tardive dyskinezia = indic no. 2
SE:
hypersalivation, drooling of saliva
wt. gain
diabetogenic
leucopenia or agranulocytosis – 3% (0.6% -
purple book) of patients
o 85% in the first 9 months
o FBC once a week
o Check FBC for neutropenia in any
patient presenting with fever, sore
throat or other infection.
CI
myeloprolif. disorders
severe CNS depression
previous Hx of leucopenia or agranulocytosis
o types:
typical = pure D2-antagonists
butyrophenones
- haloperidol – the only one available IV
e.g. ED – pacient with agitation
1 – lorazepam (other benzodiapines)
2 – haloperidol – available IV
- droperidol – p.o. only
phenotiazine
- chlorpromazine
atypical
D2-5HT2 (serotonin)
- risperidone
D2-D4-5HT2
- clozapine
- olanzapine – drug of choice in newly Dx schizophrenia
- quetiapine
o SE
risperidone - hyperprolactinemia
risperidone – postural hT
olanzapine, clozapine, quetiapine
dramatic wt. gain, abnormal lipid profile, abnormal glucose tolerance
and DM type 2
- must be monitored for these
- Rx
lifestyle changes
prophylactic metformin
- indic. to change the antypsychotic – if HbA1C is elevated
quetiapine – used if insomnia is a major problem in psychoses
causes sedation but also wt. gain
exprapir. – see above
- neuroleptic malignant syndrome
o uncommon but most dangerous
o due to low dopamine caused by the dopamine receptor blockage
o caused by:
antypsychotics: haloperidol, trifluoperazine
Rx with dopaminergic drugs in Parkinson, stopped abruptly
o Sx
gradual onset with:
1st - muscle rigidity, then
fever
vitals (BP) unstable
encephalopathy, delirium - then
coma
o life-threatening situation, mortality = 50%
o especially with antidopaminergic antypsychotics – haloperidol: patient with fever and
rigidity -> send to ICU
Dx: order CK - incr. (thousands)
Rx:
immediately stop the medication
resp. and circ. support
Dantrolene (muscle relaxant)
Bromocriptine (dopamine agonist)
- first psychotic episode
o ASSESSMENT: make sure there is no organic cause
A thorough psychiatric history.
Mental status examination.
Physical examination, with particular attention to neurological assessment.
It is critical to assess the patient's risk of self-harm or danger to others.
Rule out drug-induced or drug-withdrawal states.
o Rx
Clinical practice is generally to start treatment in first episode psychosis with an
oral form of a second-generation antipsychotic.
Amisulpride.
Aripiprazole.
Olanzapine.
Quetiapine.
Risperidone.
Parenteral treatment:
Should be avoided if at all possible in the acute care of patients with
schizophrenia.
If necessary:
- Olanzapine.
- Haloperidol.
Once a patient has responded to a drug it is usually possible to use once-daily
dosing.
It is essential to monitor closely for adverse effects of antipsychotic drugs.
Mood disorders
o +/- psychotic symp. = reality check problems
delusions of sin, etc.
o with risk of self harm, suicide
we need to do a risk assessment!
o a rship breakup would cause depression, not a psychosis
o classification
Major mood disorders.
Major depressive disorder.
Bipolar disorder.
Other specific mood disorders.
Dysthymic disorder: Depression alone – no other sympt.
Cyclothymic disorder: depressive and hypomanic disorders
(consistently over the past two years).
Mood disorder due to a general medical condition.
Adjustment disorder with depressed mood.
o major depression (hypomania) = pseudodementia
mental symptoms (memory loss, etc.) + mood instability, but normal MMSE =>
pseudodementia (depression)
min. 2 weeks
as a mood = very common, not necessarily pathol.
Lifetime prevalence: 13-20%.
can be present in other diseases
strokes – especially in the left anterior hemisphere
aphasia – types:
- Broca aphasia in the ant. speech area (middle and inf. frontal
gyri) – MC in middle cerebral a. infarcts
with dysarthria, other motor defficits
many of them are depressed or agitated
- Wernicke aphasia in the post. speech area (sup. temporal gyrus
and post. temporo-parietal areas)
rambling, incomprehensible speech, full of neologisms
with euphoria or paranoid combativeness
Parkinson’s dis. – in 40% of cases
Alzheimer – in 25-33% of cases
Mood disorders are familial but the exact mode of transmission is not
understood.
May begin at any age with an average age at onset in the mid-teens to late 20s.
good prognosis in bipolar depression
female
late onset
not extroverted
acute onset
not biological (bad appetite, bad sleep, etc.)
not melancholic (anhedonia)
not psychotic
good response to treatment
Sx
1. depressed mood most of the day
2. anhedonia – lack of pleasure for activities that were pleasureable
before
3. significant wt. gain or wt. loss
4. incr. or decr. appetite
5. insomnia or hypersomnia
- sleep problems
wakes up early in the morning (middle insomnia) and
cannot fall back asleep = depression
cannot go to sleep, keeps thinking about what
happened during the day (initial insomnia) = OCD
- typical D. – 3,4,5 all decr.
- atypical D. – 3,4,5 all incr.
6. feelings of guilt and worthlessness
7. suicidal ideation
children, teens
- tearful child, poor performance at school = depression
- irritability (rather than depressed mood)
- insomnia
- lack of concentration
- psychomotor agitation
Dx - disease:
Cardinal feature is depressed mood that predominates for at least 2
WEEKS and causes significant impairment in the individual’s areas of
functioning.
+ Must also exhibit at least 4 of the following:
- Anhedonia.
- Change in appetite.
- Change in sleep.
- Change in body activity.
- Loss of energy.
- Feelings of worthlessness and excessive or inappropriate guilt.
- Decreased concentration.
- Suicidal ideation.
total: 5 sympt. out of 9 (not just 1 = feeling depressed)
exclude dis. causing D.
- hypothyr.
- thiamine defficiency (Wernicke – Korsakoff)
DIFFERENTIAL DIAGNOSIS:
Medical conditions: They present to the GP often with a somatic
complaint ‘I can’t sleep’ or ‘I have no energy’.
Bipolar disorder.
Schizoaffective disorder.
Grief reaction
- normal
stage 1 – few hrs – few days
denial generally
disbelief and emotional numbness
stage 2 – few weeks – 6 mths
sadness, restlessness, poor sleep, guilt or
blame, anxiety, somatic sympt., auditory and
visual hallucinations
stage 3 – from 6 mths
all sympt. resolved
only memory of good time left
- abnormal
stage 2 > 6 mths
stage 3 with anniversary reactions
- anniversary grief reaction vs. hypochondriasis
hypochondriasis = multiple admissions, multiple
doctors, all negative
anniversary reaction, it only started on the anniversary
Grief (bereavment) Depression
Right after delivery -> goes Starts a few (2-3)weeks post- Starts a few (2-3) weeks post-
away in max. 1 week (3-5 partum, during the partum, during the
days) puerperium (until week 6) – puerperium (until week 6) –
when the high level of when the high level of
hormones during pregnancy hormones during pregnancy
have fallen abruptly have fallen abruptly
Due to hormonal changes Mother doesn’t want the Mother has psychotic sympt.:
baby to be sad / unhappy like believes or hears voices
Mother a bit sad, depressed her – she thinks life is not telling her that the baby is
worth living evil (the devil) and she must
kill him. They may also harm
themselves.
Baby is at risk!
(purple book)
- 1 in 500 births
- MC in primiparous women, Hx of major psychiatric illness or
family Hx of major psychiatric history
- clinical pictures: organic, affective (MC – predom. with manic
disorders) and schizophrenic
- abrupt onset with insomnia, followed by confusion,
fluctuating agitation and labile mood.
Recurrence in future pregnancies – as high as 20%
Also risk of relapse of mood disorder independent of future
pregnancies.
Rx – just family support Rx: Rx:
- antidpressants in milder - antipsychotics
forms - if not responding early ->
- ECT in severe depression ECT
type - psychogenic depression = depression (predom.) with psychotic elements
Rx – ECT
Rx
antidepressants
- 1. TCA – not used so much anymore
e.g.
amitriptyline
nortriptyline
imipramine
clomipramine
dophiepin
clomipramin
SE – not used anymore due to their SE (risk of overdose
– patients might use them to comit suicide)
anticholinergic SE: dry mouth, constipation,
flatulatence, urinar ret.
tachycardia, HT then postural hTN, blurred
vison, wt. gain
hypokalemia, prolongation of QT interval,
arrhythmias
- 2. SSRI
e.g.
Fluoxetine
o first indic. in adolescents with major
depression
monitor for suicidal ideation,
violence
paroxetine
Citalopram
Scitalopram
Fluvoxamine
- 3. SNRI (serotonin-norepinephrine reuptake inhibitor)
e.g.
venlafaxine
duloxetine
mirtazapine – not commonly used (Samir
Ibrahim = part of a SSRI subgroup - serotonin
agonists)
o heavy sedation, crazy stimulation of
appetite, wt. gain
o takes effect very fast compared with
the other drugs
Venlavaxan
Desvenlavaxan
SE for SSRI and SNRI
headache, nausea (serotonin surge)
drowsiness, sedation, lack of sleep
impotence (10-35%) – become depressed over
this
SNRI – more cholinergic side effects
- 4. MAOI – not used today
SE - food with thyramine (cheese reaction) – surge in
catecolamines – HT emmergency -> crisis (can cause
death)
pacients had to avoid 50% of the the food items
subtype: RIMA (reversable inhibitor of MAO)
just 1 drug – moclobemide
weak antidepressant, but used when SSRIs
cause ED
SE – same as SSRI
o but no ED!!
- 5. lithium – mood stabilizer
SE
fybrosis of the thyroid -> hypothyroidism
(check every 3 mths)
renal failure (check every 3 mths)
- 6. dopaminergic
wilberton (Zyben) – used only for cessation of smoking
very expensive
not used in Aus. for depression
- if stopping antidepressive medication, do it gradually over 2
weeks
ECT
- consent from the patient is required
- done under GA + muscle relaxants (succinyl choline)
usually with the electrods on the right lobes
- 2-3 times / week for a few months
- indic.
primary indic. = major depression, in these types:
(Murtagh 189)
melancholic depression unresponsive to
antidepressants
psychotic depression
substantial suicide risk
depression or severe psychomotor agitation
causing life-threatening refusals (refusing to
eat)
ineffective antidepressant medication
+ (purple book) post-partum depression, when
the mother should return quickly to the care of
her baby
recent onset (not chronic) of schizophrenia
catatonic stupor and lethal catatonia
mania and especially lithium-resistant manic episodes
- SE
muscle aches from relaxant
headaches and transient confusion
short-term amnesia – for the period of time when
doing the ECT
loss of memory – forget some of the good things in their
lives
- drug interaction
e.g.
benzos should be tapered and seized – they
raise the seizure threshold and may impair the
efficacity of ECT
o if sedation is required before ECT
(cannot go to sleep), use zopiclone,
zolpidem (non-benzos anxiolytics)
taper and discontinue all the antidepressants
before ECT
lithium doesn’t affect the efficacity but causes
severe post-ictal confusion
all drugs are resumed after ECT
+ counseling
- supportive counselling
- CBT
change
thinking – change negative into positive
thinking
o identify the negative thoughts - written
at the top of the page
o discuss the evidence for that thought
o try to reverse that thought
behaviour – moreimportant for OCD, anxiety,
phobia, etc.
- psychoanalytic
o mania
min. of 4 days
More often requires involuntary admission (at least overnight) – brought by
their relatives
Sx
Pathological elevation of mood combined with:
- Overactivity.
- Irrationality.
- Poor judgement.
- Lack of insight.
Severe disruption of relationships, employment or finances.
everything incr.
ONSET:
- Acute or insidious.
- Can arise spontaneously or follow:
Depressive illness.
Severe stress.
Surgery.
Infection.
Childbirth.
Precipitants:
- Antidepressant medication.
- ECT.
- Steroids.
- Amphetamines.
- Lithium withdrawal.
Primary features
- Overcheerfulness - high mood = euphoria
- Overtalkativeness – but there is logic in what they say
Pressured speech – not smooth
- Overactivity.
too many activities
less need to sleep – doesn’t need to sleep, has too
many things to do (not insomnia = wants to go to sleep
but can’t)
Other features
- Irritability.
- Flight of ideas.
- Distractibility.
- Grandiosity.
- Delusions (mood-congruent) – but not bizarre like in
schizophrenia
- Hallucinations.
- Impaired judgement - e.g. buys 5 cars, goes bankrupt
- Gambling.
DIFFERENTIAL DIAGNOSIS:
Schizophrenia: Can present with disorganised behaviour, violent
excitement, delusions, incomprehensible speech.
- The content of delusions (bizarre rather than mood-
congruent), will help to distinguish this from mania.
Rx
Best managed in hospital to avoid self-harm and to the others.
with mood stabilizers
- 1. Benzodiazepines: First and oral if possible.
- 2. antypsychotics
Haloperidol
atypical
- 3. lithium - mainly for prophylaxis
- 4. anticonvulsants/antiepileptics
all of them
SE
liver
bone marrow
skin rash (Steven – Johnson)
ECT: Severe cases.
no psychotherapy – they are too agitated
o bipolar
very strong genetics and linkage with substance abuse
mania + depression
- antidepressant medication:
o indic.
for mood disorders: depression
adjustment disorders
anxiety disorders
eating disorders
impulse control disorders
chronic pain (amytriptilline – increases the endogenous opioids)
o take 2-6 weeks to kick in
used for min. 4-6 weeks (unless SE) before changing it, increasing the dose
if they still didn’t work after 6 weeks of usage, change the drug
o categ.
1. TCA
work on
- norepinephrine, serotonin, dopamine receptors (block their
reuptake) -> they increase in the brain
- alpha receptors
- muscarinic rec.
- histamine
e.g.
- Imipramine – panic disorders
- Clomipramine – OCD, premature ejaculation
- Amitryptiline – chronic pain
2. MAOI – MAO breaks down norepinephrine, serotonin, dopamine; MAOI
causes incr. in norepinephrine, serotonin, dopamine
e.g. Tranycypromine
cannot have cheese, red wine, chocolate, sausages – contain tyramine
=> HT crisis: headaches, nose bleeds, palpitations
3. SSRI – only work on serotonin (hence the name SSRI)
1,2,3 have the same efficiency, but SSRI preferred due to less SE
- Fluoxetine (Prozac)
- paroxetine (Aropax)
- sertraline (Zoloft)
- citalopram
- escitalopram
4. newer antidepressants
Trazadone - used if insomnia is a major problem
Buproprion - least sexual dysfc.
- also used in quiting smoking
acts on dopamine, which is responsible for causing
craving
o general SE
sedation (antihistaminic effect) – less with SSRIs
hT – more with TCAs
anticholinergic – more with TCAs
cardiac problems – only with TCAs (prolongation of QT interval -> risk for
torsade de pointes)
decr. the seizure threshold -> should be stopped before ECT
depending on the washout period: 2-3 days in SSRI, 2-3 weeks TCA
if anxious, non-benzodiazepine anxiolitic = zolpidem (because BD also
decr. the seizure threshold)
sexual dysfc. (ED, ejaculatory dysfc.) – more with SSRIs, less with escitalopram
nausea, vomiting, abd. bloating – SSRIs (especially sertraline)
o TCA intox
SE
anticholinergic
cardiotoxic: cardiac arrythmias, prolong. of QT interval
overdose:
observation and supportive measures
activated charcoal
convulsions –> diazepam
cardiotoxic effect -> IV sodium bicarbonate
- if no improvement of the arrythmia, use lidocaine
- serotonin syndrome – emmergency condition caused by excessive serotonin in CNS when
combining antidepressants (SSRI, TCA, MAOI)
o Sx
rapid onset with:
fever
agitation
incr. reflexes
tremor
tachycardia, HT
dilated pupils
then confusion, coma
o Dx - clinically
o most dangerous combinations:
I. SSRI (sertraline, fluoxetine, paroxetine) + MAOI (phenelzine, moclobemide)
II. SSRI + TCA (amitriptyline, imipramine, clomipramine)
III. SSRI + opiates
IV. SSRI + anticonvulsants
also SSRI + OTC drugs (e.g. NSAIDs)
o Rx
don’t stop the SSRI, but the other drug
stabilize pacient -> urgent referal to ICU
serotonin antagonist:
methylsergide
cyproheptadine
o changing drugs
antipsychotics (taper gradually drug one, while gradually increasing drug two,
no break)
antidepressants (stop first one abruptly – or even better taper, allow for break
and washout time, then start the second one)
-
- washout periods
From To Washout period
Short acting SSRI Short acting SSRI Nil
Fluoxetine Short acting SSRI 1 week
TCA 2 weeks
MAOI 5 weeks
TCAs Short acting SSRI 2-4 days
Fluoxetine 2-4 days
MAOIs 1 week
MAOIs Anything 2 weeks
- switch antidepressant (Amit):
o SSRI to MAOI
wait 4-5 weeks
o MAO-I to SSRI
wait 2-3 weeks
- suicide and self-harm
o self harm
80% using drugs
5% using self-cutting
MC – wrists
o suicide
seasons
MC in spring
2 – summer
3 – fall
4 – winter
weekdays
men – Mon
women - Fri
- mood stabilizers = antiepileptics
o used in:
bipolar – in mania
seizures
impluse control disorder
violence
o types:
1. lithium – drug of choice
discovered in 1949 in Melbourne – John Caid (Nobel prize – 1962)
neither habit forming, nor addictive
indic.
- bipolar
Rx of choice in acute mania
prophylaxis of bipolar disorder (depression and mania)
less effective in patients with rapid cycling
mood disorders (women)
if discontinued, patients responding to it in the
past might not respond anymore
in treatment refractory depression: lithium + TCAs
in aggressiveness associated with developmental
disability (mental handicap)
- schizoaffective disorder
- adjustment disorder
admin.
- 750-1000 mg p.o. in 2-3 divided doses
incr. by max. 250-500 mg/day
- plasma level
normal at start 0.8-1.4 mmol/L
chronic users 0.6-0.8 mmol/L
samir ibrahim: very narrow therapeutic range – keep
the blood level at 0.6-1 (<0.6 not effective, 1.2 toxic, 1.6
fatal)
- monitor every 1-3 mths!
CI - in kidney disease
SE
- nausea, vomiting, diarrhoea
- erythroderma
- metalic taste
- headache
- wt. gain
- acne
- afects the cardiac conduction
- hypothyroidism (used in hyperthyr.)
- kidney failure
test thyroid and kidney evey 2-3 months!
- leucocytosis
- polyuria/polydypsia – nephrogenic diabetes insipidus
- teratogenic (especially in the first trimester) – Ebstein’s
anomaly in babies
toxicity
- sympt. – indic. to decr. the dose
fine tremor
apathy, lethargy, slurred speach
muscle weakness
ataxia, anorexia, nausea
muscle fasciculations
choreoatetosis, convulsions, coma, death
- for patient - important not to get:
dehydrated
hyponatraemic
-> both incr. lithium toxicity (by increasing the
renal reabsorbtion)
- Rx
stop drug
dialysis
indic.
o convulsions, coma
o lithium > 4 mmol/L
o in renal failure
2. valproic acid (sodium valproate)
indic.:
- kidney disease (where we cannot give Li)
- pregnancy as mood stabilizer!
SE
- sedation
- cognitive impairment
- GI distrub.
- hepatotoxic
- teratogenic -> causes spina bifida
3. carbamazepine
indic. in pregnancy as antiepileptic!
SE
- hepatotoxic
- rashes
- agranulocytosis
- teratogenic
- Benzodiazepins
o enhance the effect of the neurotransmitter gamma-aminobutyric acid (GABA - the chief
inhibitory neurotransmitter in the mammalian central nervous system), which results in:
sedative
hypnotic (sleep-inducing)
anxiolytic (anti-anxiety)
anticonvulsant
muscle relaxant
amnesic action.
o These properties make benzodiazepines useful in treating:
anxiety, agitation
insomnia
seizures
muscle spasms
alcohol withdrawal
premedication for medical or dental procedures
o not metab. in the liver -> safe to use in liver dis.
e.g. lorazepam, temazepam, oxazepam
o types
short acting (1/2 life = 1-12 hrs)– alprazolam, midazolam,
intermediate acting (1/2 life = 12-40 hrs) – clonazepam, lorazepam
short and intermed. – Rx for insomnia, seizures
long acting (1/2 life = 40-250 hrs) – diazepam (NOT i.m.)
Rx. for anxiety
o SE
resp. depression, paradoxical disinhibition, chronic dependence on oral benzos
o antidote = flumazenil
DEMENTIA
Behavioral emmergencies
o Situations where patients show behaviour that potentially places themselves or other
people at risk of physical harm.
o Requires immediate intervention.
o The criteria for defining behavioural emergencies are vague.
o WORKING DEFINITION:
Refusal to cooperate.
Intense staring.
Motor restlessness.
Purposeless movements.
Affective lability.
Loud speech.
Irritability.
Intimidating behaviour.
Aggression to property.
Signs of imminent intentional or unintentional self-harm.
Demeaning or hostile verbal behaviour.
o DIAGNOSIS: May be unknown or provisional:
1. Medical disorders: Usually associated with delirium.
2. Substance intoxication or withdrawal with or without delirium.
3. Psychiatric disorders – after ruling out 1 and 2:
Schizophrenia.
Mania.
Psychotic depression.
Personality disorder.
Post-traumatic stress disorder.
o LEGAL AND PROFESIONAL OBLIGATIONS:
Treatment without consent is conducted under the relevant mental health act.
Those treating an acutely disturbed person in such an emergency will need to be
aware of the provisions of relevant legislation and be satisfied that the person
meets criteria for involuntary treatment.
When the situation is too dangerous for medical personnel to intervene (when
weapons are involved or there is a high likelihood of extreme violence)
emergency personnel such as security staff or police will be required to disarm
and restrain the patient.
o Rx
INITIAL STEPS IN MANAGEMENT:
In approaching the patient, care should be taken to ensure the safety of
yourself, of other patients and staff, and of the patient.
Measures that can reduce the risk of harm include:
- Room with two exits.
- Furniture that cannot be thrown.
- Adequate backup from staff.
- Alarm.
-Placing yourself at a safe distance between the patient and an
exit.
PHARMACOLOGICAL TREATMENT:
acutely disturbed patient = Murtagh 488
- 1. diazepam p.o.
- 2. midazolam i.m.
- 3. diazepam i.v. (never i.m.)
- 4. haloperidol i.m. (or droperidol i.m. – blue book: no longer
available)
In acute medical settings the usual problem is violence in the context of
acute delirium, often secondary to substance intoxication or
withdrawal. The immediate objective is to achieve SEDATION (put to
sleep).
- IV route is preferred for achieving acute sedation because it
allows titration of the dose and provide a more immediate
effect of the drug.
IV medication:
first choice - Diazepam: 2.5-5 mg increments
repeated every 3-5 minutes.
second choice - Droperidol: 5-10 mg IV. (less SE
than haloperidol)? – blue book says it’s no
longer available parenterally
- If patient cannot be physically restrained IM route is
appropriate (higher incidence of over and undersedation).
IM medication:
Midazolam 10-15 mg.
Droperidol 5 mg. - blue book: no longer
available
In contrast, behavioural emergencies in acute psychiatric settings vary
widely in their nature and severity, and encompass a broad spectrum of
psychiatric diagnoses, typically psychotic illnesses. In these settings the
immediate objective is to achieve TRANQUILLISATION (do not put to
sleep).
- The oral route is preferred for medication as it encourages
engagement between patient and staff, allows the patient to
feel more in control, aids future medication adherence and
reduces the risk of adverse effects.
- If not possible IM or IV medication
- drugs:
Benzodiazepines are generally the drugs of first choice
in tranquillisation, as they have fewer adverse effects
than antipsychotic drugs.
diazepam p.o.
Antipsychotics if:
Patient already taking antipsychotics.
Adequate tranquillisation is not achievable
with a benzodiazepine alone.
- Delirium
o confusion + hypo or hyperactive behavior
o Usually affects elderly people admitted to hospital.
o 10% to 15% are delirious on arrival.
o 5% to 40% will develop delirium while inpatients.
o Patients with dementia are at particular risk.
o Children and the seriously ill are also more likely to develop delirium.
o Impaired cognitive function (especially in orientation and memory) and reduced ability
to focus, sustain or shift attention.
o Psychomotor changes:
Agitation or withdrawal.
Drowsiness.
Illusions, hallucinations, delusions.
o Symptoms develop over hours to days.
o CAUSES:
Infection: especially systemic, but also pulmonary, urinary, or ear infections.
Toxicity due to drugs: especially anticholinergic drugs or narcotic analgesics.
Withdrawal from sedative drugs or alcohol: This should be suspected when
tremors, sweating and visual hallucinations are present
o DIFFERENTIAL DIAGNOSIS:
Mania.
Schizophrenia.
Dementia: especially dementia with Lewy-bodies.
o PREVENTION is the most important
Adequate hydration and nutrition.
Adequate pain relief.
Promotion of sleep.
Correction of visual and hearing impairments.
Avoidance of restraints.
Provision of lighting appropriate to the time of day.
Close involvement of family members.
o MANAGEMENT:
Identification.
Treatment of its underlying cause.
The delirious patient must be nursed in a setting where they can be observed at
all times, because behaviour may be unpredictable.
UTI (most common cause of confusion in elderly)
FBE – U & E, blood sugar
x-ray
o Rx
Frequently no medication will be needed.
If delusions or hallucinations are causing distress, or if behavioural disturbance
threatens the patient's treatment or care, or is causing significant threat to
others, then use Haloperidol 1-5 mg orally.
If oral administration is impossible: Haloperidol 2.5-5 mg IM.
If significant extrapyramidal adverse effects:
- Benztropine 1 to 2 mg orally.
- Benzhexol 2 mg orally.
- Avoid chlorpromazine.
Child psychiatry
- ADHD
o boys 6:1
o 5 % of school age children
o in 60% no complete recovery
o cannot be Dx < 4 yrs
o Age: 7 yrs, going to school
o Dx. of exclusion
o Dx diff. with autism
o family Hx
o very common
o Sx
very easily distracted – can only focus for 1 min to the TV
usually only picked up in school (not noticed by parents)
attention + behavior: attention deffict +
with hyperkinesis ADHD
- non-goal directed behav. (he doesn’t want to achieve
something specific)
- can’t help it
without hyperkinesis ADD
impulsiveness and hyperactivity
inattention
hyperactivity, impulsiveness
o Dx
first exclude other causes
always need to check eyes, hearing, lead level first
exclude outside causes for the child’s behavior: e.g. if his parents
divorced, etc. – talk to both parents
psychometric assessment – exclude intellectual impairment and
learning disorders
2 situations – home and school
obtain behavioral rating scales from both
sympt. present for at least 6 mths, causing significant functional impairement
o Dx diff. with conduct disorder – were antisocial during childood
angry child
abused by parents – friends
is goal directed + full of anger
o Mx
refer to child phychiatryst
confirm if from family / home or school
exclude social causes, social disruption
speech therapist
involve teacher
audiometry
drugs:
dexamphetamine
methylphenidaze (ritalin)
Autism ADHD
36 mths 7 yrs
No family Hx. Family Hx – boy inherited from the
father
Criteria: 2 situations – home and school
autistic spectrum 3 specific issues: Impulsiveness + overactivity + loss of
1. verbal problems concentration
2. non-verbal communication and
social interaction (hugging, etc.)
3. fixation / specific focus on
something (e.g. he likes dinosaurs)
and doesn’t like when his life is
changing
- Asperger – only 2 and 3
Any sex Boys
Rx - Refer to child psychiatrist Ask for school report
Dexamphetamine –> decr. the
hyperactivity
o autism
autistic spectrum disorder – many subtypes
e.g. Asperger syndrome – very mild form of autism
- many will have an almost normal life
- sedentary, isolated life
- avoid eye contact
- normal speech
- some are very good in mathematics
- communication through language is preserved
Autism Asperger
Boys 4:1 Boys 8:1
Onset < 3 yrs (30 mths), after a period of
normal dev.
Low IQ Normal or high IQ
No social interaction Can speak, likes friends
Lack joint attention: Fascination with things
No eye contact No eye contact
No pointing
Lack of pretend play (feeding doll)
Lack of social interest
Lack of social play
Lack of communication (verbal, non-verbal)
Lack of peer-rship
Lack of spontaneous seeking
Stereotype repetitive behav.
Don’t like any disruption from normal routine Rigid to routine
Assoc. with: tuberous sclerosis, epilepsy,
rubella, Tourette syndr.
No Rx Rx: behav. therapy, individual assessment,
Need regular check-ups (don’t complain even speech therapists
when sick, in pain)
used to be called childhood schizophrenia
25% develop epilepsy during adolescence
can be sec. to rubella, phenylketonuria, tuberous sclerosis, neurolipoidoses
main problem: no communication, no normal rship with the ones around + like
to be on their own
no eye contact, no seeking behav. (looking for a hug), no playing with
other children
doesn’t want to be kissed, embraced
play with toys in an unusual ways
odd in many ways
onset
early – 6 mths
- doesn’t start the language
late
- started talking, then loses the talk
Doesn’t enjoy peekaboo
stereotypical movts. – rocking, spinning, etc.
restricted repetitive interest:
have fixations for certain things - likes dinosaurs and Bob the builder
doesn’t like changes to his routine – throws tantrums and explosive
outbursts if change is attempted
Other conditions
- CBT
opackage of treatments, useful in many/most psychiatric disorders
oindic.
chronic pain – due to the associated anxiety, depression and avoidance behav.
phobias
depression
eating disorders
etc.
- depersonalization
o Sx
the patient feels unreal, detached from his own experience and unable to feel
emotion
time distortion
changes in body image
out of body experience (autoscopy)
reality testing is intact (knows the border between inner experience and the
outer world)
often + derealisation = the external world is strange and unreal
o occurs in:
healthy people – when tired or sleep-deprived (lasting only a few min.)
anxiety disorders
panic disorder
post-traumatic stress disorder (PTSD)
agoraphobia
schizophrenia
depression
acute intox. or withdrawal from alcohol, hallucinogens, etc.
ecstatic and trance practices – e.g. religioius
epilepsy – especially temporal epilepsy
- seasonal affective disorder
o young women
o in areas with decr. sunlight
o mediated by melatonin
o onset and remission of major depressive episodes at certain time durin the year
MC onset in winter, recovery in spring
o Sx
irritability, hypersomnia, hyperphagia with carbohydrate craving, wt. gain,
energy loss
- Capgras syndrome – person believes that a relative or close friend has been replaced by a
double or impostor pretending to be that person
o in schizophrenia, etc.
- Fregoli syndrome – person misidentifies or recognizes familiar people in other people
(strangers)
o in schizophrenia
- De Clerambault syndrome (erotomania)
o women
o they believe an important or famous person is in love with them and comunicaticates
their love in obscure, indirect ways
o in schizophrenia
- querulant paranoia – person keeps having litigations with the civil authorities, then also with the
lawyers and judges involved in the earlier trials (suspects conspiration)
- migrant psychosis – in people who have just immigrated in a another country
- Irritable bowel syndrome (IBS)
o very frequent in Aus.
o women
o triggered by a gastroenteritis or a major stress
o at least 2 of the following:
abd. pain relieved by defecation
onset of abd. pain is assoc. with change in bowel frequency (diarrhoea or
constip.)
onset of abd. pain is assoc. with change in consistency of stools (loose , watery,
pellet)
o MCQ: pain in the left iliac fossa
o urgency, straining, tenesmus, bloating, passage of mucus
o almost always assoc. with depression or anxiety
o Rx
dietary modif. – identify the specific food that triggers IBS in them and remove it
from the diet
CBT
SSRI
fluoxetine (blue book)
mebeverine – controls the spastic peristalsys e.g. in diarrhoea before
an exam (serotonin receptor antagonist)
- limbic encephalitis
o autoimmune dis. – AB to nerve cell antigens
a large proportion are paraneoplastic (small cell lung CA, non-Hodgkin
lymphoma, etc.)
o Sx
recent onsef of irritability, angry outbursts, anxiety sympt. or depression
which precede the memory problems and confusional episodes
memory disturbance
short term memory only is affected
long term / autobiografic memory is preserved
episodic confusion
hallucinations
paranoid ideation
insomnia
psychomotor seizures
history: recent onset of irritability, anger outbursts, anxiety or depression ->
then memory and confusional problems
o Rx
C/S
plasma exchange
immunomodulation
cyclophosphamide
- hypnagogic hallucinations – vivid dreamlike hallucinations occuring at the onset of sleep
- REM sleep disorder – acting out (yelling, punching, etc.) of dreams that are vivid and intense
Ekbom syndrome
o types
1 - they believe they have an insect on their body
2 - restless legs syndrome
middle-aged, elderly
up to 10% of population
familial Hx – AD with variable penetrance
precip. factors
- anemia
- hypothyroidism
- renal failure
- DM
Sx
- irresistible urge to move the legs, “tingling, burning and
crawling” of the skin, from thighs to the feet
- occurs when sitting down or lying in bed
- worse during the evening and at night
- relieved by walking
- typically patient complaints of limb discomfort at rest and then
urge to move the affected part
Rx
- mild
lifestyle changes – good sleep hygiene (bed just for
sleeping: no reading, TV, etc.)
levodopa
benserazide
dopamine agonists – amantadine, selegilin
- illusion - there is something there, but incorrectly interpreted
o diff. from hallucination (there’s nothing there)
- types of thoughts
o overvalued idea – quantitatively different from reality
in anorexia nervosa, morbid jealousy, hypochondriasis, querulous paranoia,
body image disturbance
o delusion – qualitatively different from reality
o phobia – with excessive arousal or anxiety in presence of the trigger, with minimal
resistance to it
o obsession – recognized by the patient as senseless and irrational and is resisted by him
rumination – more complex obsessional thoughts, which are repetitive,
intrusive, unwanted and upsetting
- reassurance should only be offerred when the patient’s concerns have been fully understood
and investigated
- vaginismus
o spasm of the perineal musculature of the lower 1/3 of the vagina
o young women, of high socioeconomic standard
o can be caused by:
a sexual trauma (rape, childhood sexual abuse) or very strict upbringing (sex =
sin)
scarring following episiotomy
o can be assoc. with a phobic anxiety of anticipating vaginal intercourse, e.g. in the
presence of an inexperienced partner
- Diogenes – people who like to collect garbage
- Charles Bonnet - visual hallucinations due to organic reasons
o if organic reason is resolved, the hallucinations will go away
- Cotard syndrome – they believe they have lost body parts, blood, their soul
- folie-a-deux
o rare
o one psychotic sympt. is transm. from one person to another (sympt. manifest only when
they are together)
- amygdala – in the temporal lobe, regulates affects
o regulates limbic system
- corpus calossum – responsible for sexual dimorphysm
- cingulate gyrus – part of limbic system, involved in emotion formation, processing, learning and
memory
- transient global amnesia < 8 hrs
o loss of both recent and biographical memory
o in vertebro-basilar insufficiency
- which psychiatric dis. is increasing in incidence = dementia (incr. ageing population)
- Paraphilias
o unusual sexual preferences, “perverts”
o types:
1. exhibitionism – recurrent urge to expose oneself to strangers
2. fetishism – use / collection of non-living objects (e.g. bras, etc.) usually assoc.
with the human body
3. pedophilia – recurrent urge or arousal towards pre-pubescents
4. frotteurism - recurrent urge or arousal involving touching or rubbing against a
non-consenting partner
5. voyeurism (peeping tom) - recurrent urge or arousal involving the act of
observing an unsuspecting person who is engaging in sexual activity
6. masochism - recurrent urge or arousal involving the act of humiliationg (the
love to receive pain)
7. sadism - recurrent urge or arousal involving the act of giving pain
8. transvestic fetishism - recurrent urge or arousal involving cross dressing (but
don’t feel they belong to the opposite sex)
- gender identity disorders – persistent discomfort and sense of inappropriateness regarding their
assigned sex
o + preoccupied with wearing opposite gender’s clothes
o feel trapped in their body – they feel they are girls in boys’ body or vice versa (born
with the wrong body)
+ experience anxiety, depression and suicidal thoughts because of this =
gender dysphoria
o from birth
o will have preferences for friends of the opposite sex
o request surgery to change their sex
o adopt the opposite gender’s behavior
Ethics - OK
- mental health act (1986) + mental health regulations (2008)
o only for mentally ill persons
o consent is not required – treatment will be involuntary
o criteria for involuntary treatment
a. person appears to be mentally ill
b. person’s mental illness requires immediate treatment
c. treatment is necessary for safety or protection of member of the public
d. person has refused or is unable to consent to treatment
e. person can’t receive treatment in less restrictive manner
o involuntary treatment order (ITO)
involuntary vs. voluntary patient
- sexual rships between doctors and patients
o are usually initiated by the doctors
- rape
o presents right after rape – call police
o presents a while after rape – call child protection agency
- domestic violence
o step 1 – take photos
o step 2 – refer to safe shelter
- patient refuses to pay for the consultation
o select “free of charge” or
o send the bill to her home
- parents can give consent until 18
o as long as it’s in the best interest in the child
- consent in minors
o legal age of consent in Aus. = 18 yrs
legal age for sex, including abortion and ocp – 16 yrs (south aus. and tasmania
– 17)
> 16 yrs – OK to prescribe OCPs or perform abortion at her request /
with only her consent
14-16 Gillick test (or the stem will tell me that she lives alone, she is
mature, etc.) – asses whether:
- mature minor – treat as a 16 yrs old
lives independently of her parents + is mature and
understands the potential risks and complications of
the required medical procedure
e.g. pregnant girl, 14 yrs, asking for abortion – blue
book 573
if she is mature (Gillick test)
and if it was by consent
o OK
even if > 2 yrs between her and
her boyfriend
even though it’s illegal, she is
under 16 yrs
- immature minor – treat as a kid and request her parents’
consent
< 14 yrs - request her parents’ consent
- mom wants her mentally retarded girl to have an hysterectomy
o we cannot do that (we refuse) – the girl is entitled to have her uterus (human rights)
o mom can make a request to the child health court (?)
she will probably be refused
- mentally retarded girl - contraception
o under institutional care – OCP
o alone – contact guardianship court
- consent form checked by
o HMO
o nurse
o anesthetist
o surgeon – he is the only one legally responsible
- adopted children have the right to be informed they were adopted
o but this remains the decision of their parents at least until the child is 18 yrs old
- consent in incompetent patients (e.g. elderly demented people)
o 1. advance directive from the patient
The first source of guidance for doctors on the treatment to be offered to an
incompetent patient is the patient’s own advance directive given BEFORE he or
she became incompetent.
This may state whether the patient wishes to have particular treatment or to
refuse it
o 2. Surrogate decision maker appointed by the patient (Health attorney, medical agent
or enduring guardian).
If a patient is incompetent and has not previously consented to treatment or
refuse it, a person appointed in advance by the patient may have authority to
decide on the patient’s behalf.
Most Australian jurisdictions now have legislation enabling patients who are
over the age of 18, while competent, to appoint someone else to make
medical decisions for them if they later become incompetent
o 3. Guardian appointed by a board, tribunal or court.
If a patient is not competent (and, in jurisdictions that have legislation allowing
people to make advance directive or to appoint their own substitute decision
maker, has not done so), it may be necessary for a substitute decision maker to
be appointed by a guardianship body.
A guardianship body will not intervene by appointing a guardian unless that is
NECESSARY.
IF THE PERSON’S RELATIVES ARE CARING FOR THE PERSON
SATISFACTORILY, IT IS GENERALLY CONSIDERED THAT THERE IS NO
NEED FOR A GUARDIAN.
If, however, there is a dispute between family members about the
person’s care, a formally appointed guardian may be needed to make or
review decision about the person.
o 4. The bottom line: Relatives and carers.
If there is no person who has been formally appointed as a surrogate decision
maker, either by the patient or by a guardianship body, a relative or carer may
be able to consent.
This Acts set out a hierarchy of people to decide the ‘person responsible’
including relatives and carers, for consenting to treatment (different
depending on state).
e.g. Victoria:
1. A person appointed by the patient under the Medical
Treatment Act.
2. A person appointed by the Victorian Civil and Administrative
Tribunal to male decisions in relation to the proposed
treatment.
3. A person appointed under a guardianship order with power to
make such decisions.
4. An enduring guardian appointed by the patient while
competent.
5. A person appointed by the patient with power to make such
decisions.
6. The patient’s spouse of domestic partner.
7. The patient’s primary carer.
8. The patient’s nearest relative.
Statistics - OK
- prevalence = total no. of old and new cases
o point prevalence = measure of the proportion of population having the condition at a
particular time
o period prevalence = measure of the proportion of population having the condition over
a period of time
- incidence = no. of new cases
Prevalence Incidence
New vaccine introduced Decr. Decr.
Disease that kills patients Decr. Constant
Drug that cures a dis. Decr. Constant
Drug that doesn’t cure the dis. Incr. Constant
but extends life
- sensitivity and specificity
Dis. present Dis. absent
Test pos. A = true pos. B = false pos.
Test neg. C = false neg. D = true neg.
o sensitivity – ability to detect the true positives
sensitivity = A / (A + C) (true pos. / total pos.)
not related to prevalence
o specificity – ability to detect the true negatives
specificity = D / (B + D) (true net. / total neg.)
not related to prevalence
o positive predictive value – proportion of true positives identified in a defined population
positive predictive value = A / (A + B) (true pos. / total population)
PPV = (no. true positives)/(no. of true positives + no. of false positives) =
(sensitivity x prevalence)/(sensitivity x prevalence) + (1 – specificity) x (1 –
prevalence)
computation of sensitivity, specificity and prevalence
tests lose PPV when the prevalence is low
o negative predictive value – proportion of true negatives identified in a defined
population
negative predictive value = D / (C + D) (true neg. / total population)
computation of sensitivity, specificity and prevalence
- std. dev.
o mean BP + 2 std. dev. = systolic
o mean BP – 2 std. dev. = diastolic
- types of studies:
o case report – least in evidence
o case-control studies
type of retrospective, epidemiological, clinical study design. In a case-control
study, people with a disease (often, a specific diagnosis, perhaps lung cancer)
are matched with people who do not have the disease (the 'controls'). Further
data is then collected on those individuals and the groups are compared to find
out if other characteristics (perhaps a history of smoking) are also different
between the two groups.
non-randomised
retrospective
provide circumstantial evidence
o cross-sectional studies
type of one-dimensional data set. Cross-sectional data refers to data collected
by observing many subjects (such as individuals, firms or countries/regions) at
the same point of time, or without regard to differences in time. Analysis of
cross-sectional data usually consists of comparing the differences among the
subjects.
For example, we want to measure current obesity levels in a population. We
could draw a sample of 1,000 people randomly from that population (also
known as a cross section of that population), measure their weight and height,
and calculate what percentage of that sample is categorized as obese. For
example, 30% of our sample were categorized as obese. This cross-sectional
sample provides us with a snapshot of that population, at that one point in
time. Note that we do not know based on one cross-sectional sample if
obesity is increasing or decreasing; we can only describe the current
proportion.
Cross-sectional data differs from time series data also known as longitudinal
data, which follows one subject's changes over the course of time.
o longitudinal case series – can be:
cohort studies
form of longitudinal study (a type of observational study) used in
medicine, econometrics, actuarial science and ecology. It is an analysis
of risk factors and follows a group of people who do not have the
disease, and uses correlations to determine the absolute risk of subject
contraction. It is one type of clinical study design and should be
compared with a cross-sectional study.
A cohort is a group of people who share a common characteristic or
experience within a defined period (e.g., are born, are exposed to a
drug or a vaccine, etc.). Thus a group of people who were born on a day
or in a particular period, say 1948, form a birth cohort. The comparison
group may be the general population from which the cohort is drawn,
or it may be another cohort of persons thought to have had little or no
exposure to the substance under investigation, but otherwise similar.
Alternatively, subgroups within the cohort may be compared with each
other.
In medicine, a cohort study is often undertaken to obtain evidence to
try to refute the existence of a suspected association between cause
and effect; failure to refute a hypothesis strengthens confidence in it.
Crucially, the cohort is identified before the appearance of the disease
under investigation. The study groups follow a group of people who do
not have the disease for a period of time and see who develops the
disease (new incidence).
panel study - sample a cross-section, and survey it at (usually regular) intervals.
o randomised controlled trial
some authors distinguish between:
"RCTs" which compare treatment groups with control groups not
receiving treatment (as in a placebo-controlled study), and
"randomized trials" which can compare multiple treatment groups with
each other
- all studies have to be approved by the Human Research Ethics Committee
Normal values
Australia: (Murtagh – p. 148)
adult male:
17-50 years 1-10 mm/h
> 50 years 2-15 mm/h
adult woman:
17-50 years 3-12 mm/h
> 50 years 5-20 mm/h
> 100 mg/L 80% sensitivity and 88% specificity for bacterial infection
10-40 mg/L 69& sensitivity and 54% specificity for viral infection
renal fc.
creatinine: 0.04 – 0.1 mmol/L
urea: 3-8 mmol/L
eGFR > 60 ml/min/1.72 m2
normal urinary output = Normal 1 ml / kg / hr
haematology
red cells 4.5-6 x 1012/L male, 4-5.5 female
reticulocytes 0.5 – 2 % (1%)
leucocytes 4.5-11 x 109 / L
platelets 150-400 x 109 / L
neutrophils 2-7.5 x 109 / L
eosinophils 0.2-0.4 x 109 / L (<0.44)
lymphocytes 1-4 x 109 / L (<4.5)
monocytes 0.2-0.8 x 109 / L (<0.8)
basophils ?
coagulation
bleeding time 2-8.5 min
fibriongen
prothrombin time – (12-15) seconds
prothorombin international normalized ratio (INR) 1-1.2
- The prothrombin time is the time it takes plasma to clot after addition of tissue factor
(obtained from animals). This measures the quality of the extrinsic pathway (as well as the
common pathway) of coagulation.
- The speed of the extrinsic pathway is greatly affected by levels of factor VII in the body.
Factor VII has a short half-life and its synthesis requires vitamin K.
- The prothrombin time can be prolonged as a result of deficiencies in vitamin K, which can be
caused by warfarin, malabsorption, or lack of intestinal colonization by bacteria (such as in
newborns). In addition, poor factor VII synthesis (due to liver disease) or increased
consumption (in disseminated intravascular coagulation) may prolong the PT.
- A high INR level such as INR=5 indicates that there is a high chance of bleeding, whereas if
the INR=0.5 then there is a high chance of having a clot. Normal range for a healthy person
is 0.9–1.3, and for people on warfarin therapy, 2.0–3.0, although the target INR may be
higher in particular situations, such as for those with a mechanical heart valve, or bridging
warfarin with a low-molecular weight heparin (such as enoxaparin) perioperatively.
Serum electrolytes
Na+ normal: 130-145 mmol/L
K+ normal: 3.5-5 mmol/L
Cl- normal: 95-107 mmol/L
HCO3- : 22-26 (24-28) mmol/L (~25)
anion gap: (Na+) – (CL- + HCO3-) normal: 8-16
pH = 7.35-7.45
paCO2 = 35-45 mmHg
PaO2 = (75) 85-100 (105) mmHg
can be > 100 since this is partial pressure
SaO2 = 98%
lipids
plasma cholesterol: < 5.5 mmol/L (recommended < 4)
triglycerides: <2 mmol/L (< 1.5)
HDL cholesterol > 1mmol/L (> 1)
LDL cholesterol <3.5 mmol/L (< 2.5)
BMI
mass (kg) / height(m)2
N 20-25
young women N 19-24
25-30 overweight
30-39 obese
> 40 morbidly obese
mean BMI in Aus. = 25
glucose
fasting (after 12 hrs of fasting) 3.5-6 mmol/L (>7 diabetes)
random (no fast, at least 2 hours after a meal) 3.5-9 mmol/L (>11.1 diabetes)
oral glucose tolerance test (OGTT) – after a 12 hrs fast; measures glucose at 0 hrs (before glucose
administration) and at 2 hrs after glucose administration (75 g)
glycosylated haemoglobin 4-6% of total haemoblogin (> 7 diabetes)
Contents
Pediatrics - OK .............................................................................................................................................. 6
Digestive problems....................................................................................................................... 12
Immunisation ............................................................................................................................... 23
Orthopedics ................................................................................................................................. 29
Intoxications ................................................................................................................................ 38
Antibiotics ................................................................................................................................... 48
Anticoagulants ............................................................................................................................. 64
Pharmacology .............................................................................................................................. 72
Obstetrics - OK ............................................................................................................................................ 76
Pregnancy parameters.................................................................................................................. 76
Bleeding..................................................................................................................................... 149
Infertility.................................................................................................................................... 170
TB ...................................................................................................................................................... 256
PE ...................................................................................................................................................... 353
MI ...................................................................................................................................................... 364
DM..................................................................................................................................................... 416
Pediatrics - OK
- By age
o Neonate < 1 mth
o Infant 1 mth – 1 yr
o Toddler 1-3 yrs
o Child
o Puberty
Boys 12 – 16/18
Girls 10 – 15/17
- Neonatal Conjunctivitis:
oImmediately after birth, purulent, sticky
oMarked conjunctival edema = Gonococcal
oIf at 2nd to 3rd wk = Chlamydia
- Umbillical granuloma – Red fleshy tissue at base of umbilicus + discharge
o Topical Silver Nitrate (Caustic pen) ------ for 5 days (MCQ)
o If yellowish (urine) discharge - USG and Surgery (Urachus fistula)
- Umbilical discharge
o types
Mucous
7
Pus
Urine
before delivery – communication = Urachus; if it remains after delivery =
patent urachus
- Dx
Creatinine and urea levels from discharge -> confirm it’s
a urinary discharge
USG – to rule out patent urachus
- Mx – Refer for surgical correction
Feces
Black----Meconium?
o Dx diff
CA
Fistula
Urachal cyst
Umbilical calculus
o Mx
Clean debris
Apply dressing (wound)
Swab for culture and sensitivity
A/B
- Night terrors and sleep walking have many features in common – Murtagh 789
o Sleep walking: – child not awake
sits up in bed, walks around, don’t acknowledge parents even though eyes
might be open
lasts 10-30 min
1-8 yrs, (child is neurologically & developmentally normal)
Can’t remember episode next morning
usually within 2 hrs after falling asleep
harmless, benign
inherited – family Hx
2% of children
usually grow out of it by 12 yrs
Rx
Reassure and educate parents, protect the child (unaware), self limiting
wake up the child 15 mins before the usual time of attacks for a few dys
don’t try to calm the child during attack--> it will aggravate the situation
no indication for sleeping pills, anti-epileptics or sleep EEG.
no relation with TV viewing or day’s activity
o Night terror:
Sharp screams, violent thrashing movements, sweating, tachycardia
3N for night terror and sleep walking. No N for nightmate
Night (sleep) terror Sleep walking Nightmare
2-4 yrs 6-9 yrs 3-6 yrs
First 1/3 of sleep (within 2 hrs of First 1/3 of sleep Last 1/3 of sleep
falling asleep)
Non-REM stage Non-REM stage REM stage
8
Rx:
O2 by mask
May intubate or ventilate
Cricothyrotomy or tracheostomy
Antibiotics:
- Ceftriaxone
o Croup: (acute laryngo-tracheo-bronchitis)
Steeple sign on anterior neck X Ray film
10
Most ominous sign of deterioration = Retraction of intercostal spaces and
suprasternal fossi and use of accessory muscles. Rx:
Nebulized Adrenaline
Corticosteroid Oral/ IM/ IV
May do intubation
Croup Epiglottitis Bronchiolitis
(Laryngotracheobronchitis)
Cause Viral – Parainfluenza virus (+ Bacterial – H. influenzae type B RCV
adenov., influenza)
Age 6 mths – (3-) 6 years, 6 mths – 6 yrs 2 wks - 9 mths, < 1 yr
sometimes older may also occur in adults
Onset Slow (usually 2 days) – Rapid (hrs) Slow (usually 2 days) –
prodrome of URTI prodrome of URTI
Fever Low grade High (> 40) yes
Dysphagia None Severe None
Drooling None Present None
Stridor Harsh inspiratory stridor Soft expiratory stridor
Cough Barking, brassy, spontaneous Absent Yes
Voice Hoarse Soft, clear to muffled
Wheeze Bilat. Inspiratpry crackles and
or expiratory wheeze
Posture Recumbent/ lying back Sitting forward, quietly & still,
while his eyes follow you
around the room (limited head
movt. to protect obstructive
airway), sits with neck
hyperextended and chin
protruding (“sniffing dog”
position) & lean forward in a
“tripod” position to maximize
air entry
Toxemia Mild Severe
Other Indication of emergency Cherry-Red epiglottis Resp. distress (tachypnea,
intervention: Child is restless It’s a true emergency and can intercostal recession, nasal
& irritable lead to life-threatening airway flaring) widespread fine
obstruction so time should not inspir. crackles (not in
be wasted on ordering an X Ray asthma) hyperinflated chest –
11
o 3 causes:
Infantile respiratory distress Transient tachypnoea of Meconium aspiration
syndrome (Hyaline membrane newborn (Wet lungs – can’t syndrome (with meconium
disease) eliminate/squeeze fluids from all over his body)
lungs because delivered by C/S)
Premature, usually < 30 wks wt Term baby, C section Post term baby (Jay – in
<2.5kg (can be in term babies too) prolonged labor)
Not improving with O2 < 30% O2 (< 40% other sources) Sympt. from birth
Longer course, worst prognosis Quick recovery within 72 hrs Usually they improve
X-Ray – ground-glass haze, Coarse streaking/ fluid in lung Hyperinflation, bilateral
fine granularity with hypoareated fissures consolidation because of
lung fields, slightly elevated both inspiration of meconium
hemidiaphragms
Rx:
- Betametasone to mothers up to
34 wks (↑secr. of surfactant)
- Surfactant (Survanta) on ETT for
baby
Digestive problems
- Baby vomits after first and each feeding
o Tracheoesophageal fistula - becomes cyanotic
o Esophageal atresia – does NOT become cyanotic
o Dx
chest X Ray
- Tracheoesophageal fistulae (TEF):
o 1 in 3,000 births
o Associated with polyhydramnios (16%), cardiac abnormalities, vestibular abnormalities,
imperforate anus, and genital-urinary abnormalities
o Various types:
Distal TEF with upper esophageal atresia (85%)
Blind upper & lower oesophageal pouches without a connection to the trachea
(9%)
True H-type fistula (6%)
Proximal esophagus empties to trachea (1%)
o Dx
Passage of a NG tube that meets obstruction 9-13 cm from nares suggests
diagnosis
Chest X Ray with catheter in place demonstrates position of pouch as well as
air in stomach and intestine.
o A standard Ba swallow is not recommended because of possibility of spillage into
pulmonary tree.
- If baby vomits, check serum K:
o Low K – Pyloric Stenosis
o High K
Congenital adrenal hyperplasia (salt losing) presents soon after birth
Baby vomits, marked decr. Na and Cl, K incr.
Salt losing congenital syndrome?
13
- Vomiting in children
o By color
Green (bile stained):
1- Duodenal atresia – newborn
- assoc. with Down syndrome
Small bowel obstruction
Volvulus – Vomiting and abdominal distension
- Bilious/ green vomiting
- Several small, seedy and yellowish stools (from intestine distal
to point of volvulus)
- Olive shaped mass palpable in epigastrum
- Non-projectile bile-stained vomiting
Sepsis
Infection: UTI, Otitis media
Milk stained (Non-bilious), Coffee ground
1 - Pyloric Stenosis ----- Projectile
GERD
Infection: UTI, Otitis media
o types
1. 1st day baby vomiting bilious content + baby did not pass meconium
duodenal or jejunal atresia
- X Ray: Double-bubble sign
small bowel obstruction or malrotation
Hirschprung dis.
imperforated anus
meconium plug & ileus
cystic fibrosis
2. 2-3 wks with projectile vomiting immediately after meal
14
Dx
On 1st/2nd day – Newborn screening --> looking for
1. Immunoreactive Trypsin (IRT ) – if > 99 percentile = positive => send
for 2. DNA analysis: Check to see if 1 or 2 allels are affected -->
If both + = Diseased => refer to Cystic Fibrosis Clinic
If only 1 + = Carrier--> 3. Sweat Cl- Test: 75 g Sweat (> 60 mEq/L =
positive) => Refer to Cystic Fibrosis Clinic.
- 40-60 – Suggestive of healthy carrier
Rx
Drainage of airway secretions
Hypertonic saline solution by nebulizer
A/B for infection
Oral pancreatic enzymes
Lung and liver transplant
Survival in developed countries = 31 yrs (in poor countries – 10 yrs)
o Celiac disease: (Fe deficiency is MC than other metabolits)
triad: fatigue + wt. loss + diarrhoea +hyperactive bowel sounds
loose stools
wt. loss (failure to thrive)
fatigue, due to iron/ folate deficiency (due to malabs.) anemia
- Microcytic – iron deficiency
- Normocytic
- Macrocytic – folate deficiency
- ↑INR due to Vit K malabsorption
- Osteoprosis due to Vit D and calcium malabsorption
Irish nurse
Sx
usually start after gastroenteritis – acid, watery diarrhoea, smells like
vinegar
cough
buttock wasting
bulky stool
failure to thrive
Dx
I test - fecal fat estimation (Steathorea)
- ↑fecal fat
- fat crystals in stool
IgA
- Anti-gliadin AB – Screening only
- Anti-endomysial – 90% sens./specif. (Maria)
- Anti-transglutaminase – 90% sens./specif. (Maria)
II test - Small bowel biopsy (best)
Cx
Increased risk of proximal jejunal lymphoma
Rx
Remove gluten from diet
19
o Toddler’s diarrhea: Hx of loose stools containing undigested food (peas & other
vegetables)
otherwise child is healthy and gaining weight
resolves spontaneously
- Abdominal pain in children
o 3 mths – 1 year (< 2 yrs)
INTUSSUSCEPTION = Distal ileum telescopes into a distal bowel loop.
usually in the ileocolic region
also at other ages
causes
- Metastatic deposit – MC from melanoma
- Enlarged Pyer’s patches – in children
- Crohn’s
- Meckel’s diverticulum
- lymphoma of small bowel
- benign sumbucous fibrolipoma
- Internal hernia
Sx
- Intestinal obstruction
- Sudden screaming intermittent attacks of pain with vomiting,
drawing legs up
- Sausage mass in the RIF
- Child looks pale, lethargic, anxious and unwell.
- Bleeding (Red Currant Jelly Stool): Late sign.
Associations:
- Recent viral gastroenteritis (Adenovirus)
- Infantile Spasm.
- H-S Purpura (Arthralgia, skin rash, nephritis)
Dx:
- Plain X Ray: Normal or bowel obstruction = I step
- Ultrasound: Target sign
- Barium Enema: Claw sign
- Air or Barium enema – best - Hydrostatic reduction under USG
Rx
- Air or Barium enema
if it fails, repeat for at least 3 times
risk of recurrence
monitor for 24 hrs in the hospital
- Surgery: If enema failed, peritonitis or septicaemia
o Usually over 5 yrs
Appendicitis
Any age, rare under 5 years.
Sx
- Anorexia, vomiting.
- Localized abdominal pain: Epigastrium, periumbilical region, RIF.
- Tenderness and guarding in RIF
20
o Rx
Day 1 – enema to empty bowel
Day 2 – laxatives PR
Day 3 – oral laxatives
then go back to toilet – put child to toilet after breakfast, before going to school
address constipation: more fiber, more fluids
- Necrotising enterocolitis:--- in premature newborns
o caused by ischemia of the bowel + inf. (Pseudomonas aeruginosa)
o Risk factors
Septicemia
Low apgar scores
Respiratory distress
o Dx
X Ray
Pneumatosis intestinalis – air cysts in the intestinal wall
finding of air in the portal vein = severe illness
o Rx
Supportive
if perforation - remove necrotic intestine
- young child 6 wks – no stool up to 7 days - still OK
- Hirschprung disease = Aganglionosis = congenital megacolon
o Narrowed aganglionic portion + proximal distension
o There is just a delay in passing of meconium (usually on 4 th day) and bilious vomiting on
7th day.
o MC in male
o Constipation + distension
o Dx
PR
X ray, Barium enema (distended enema)
full thickness biopsy
o Rx
Resection of affected portion of colon
Preliminary colostomy
Immunisation
- Immunisation schedule – additional notes from Neha + Murtagh – p. 79
o Premature baby < 32 wks – additional HBV vaccine at 1 yr
o > 6 mths – can give Influenza vaccine
free for:
> 65 age
indigenous population > 50 yrs (+ free pneumococcal vaccine)
indigenous population 15-49 yrs who have a high risk of complication
and death.
o Pneumococcal vaccine - Indigenous population at 2, 4, 6 mths, 18-24 mths
in chronic heart failure, chronic renal failure, postsplenectomy
not in chronic HT
o Post-splenectomy
H. influenza B – Hib once (if not immunized)
24
-
o Cyanotic (Blue babies) - Shunt Right --> Left 5Ts (TOF, TGA, Tricuspid Atresia, Tingle
Ventricle, Truncus areteriosus)
TGA Hypoplastic left heart TOF
DiGeorge syndrome syndrome (HLHS) MC cyanotic heart disease of
(CATCH 22) childhood (DiGeorge
syndrome) presents e nail
clubbing
26
Sequence in girls:
first telarche (enlargement of breast buds)
then growth spurt
then axillary and pubic hair develops
then menarche occurs (2 years after start of puberty)
Sequence in boys:
Scrotal and testicular growth
Pubic hair (after 6 months)
Penile enlargement (within 12-18 months)
axillary hair (after 2 years)
deepening of voice
Tanner stages
Boys Girls
Prepubescent Basal Growth, No penile/ testicular Basal growth, breast buds
Stage 1 enlargement, No pubic hair
Stage 2 Testicular/ scrotal enlargement (9- Growth spurt (8-13 yrs
11 yrs)
Stage 3 Growth spurt/ Pubic hair Axillary and pubic hair
Stage 4 Penile enlargement,axillary hair Coarse pubic hair and menarche
Stage 5 Deepening of voice and facial hair Adult pubic hair distribution
- Development
o Female
I – Telarche 2 yrs till menarche
II – Adrenarche androgen hormones --> axillary & pubic hair, body odor
III – Menarche influenced by her mother’s menarche
IV – Pubarche pubic hair
o Male
I – Testis
- Simple Tanner scale – printout from Neha
o Boys
Scrotal & testis growth --> 6 mths --> pubic hair --> 12-18 mths --> penile
enlargement --> Axillary hair (whole process 2 yrs)
o Girls
1st = enlargement of breast buds (9 yrs old) -> growth spurt -> axillary & pubic
hair --> menarche (whole process = 2 yrs)
o Average time for puberty = 3 yrs
o Based on secondary sexual characters
Male
34
size of testis
pubic and axillary hair
Female
breast and nipple dev.
pubic and axillary hair
o Stages:
1– Preadolescent, no sec. sexual chars.
2– 9 - 11
3– 11-13
4– 13-15
5– 15+
- Causes of delayed puberty:
o types
Hypogonadotropic hypogonadism
↓FSH ↓ LH ↓ estrogen
Pituitary problem
Hypergonadotropic hypogonadism
↑FSH ↑LH ↓ estrogen
o Dx
FSH LH
- Normal percentile: 3 – 97% for height & weight
- Speech problems
o Delay
Causes
Mental retardation – MC
Deafness
Cerebral palsy
Infantile autism
Social deprivation
o Stammering
Male 3:1
Genetic factors
Recover spontaneously before age 16
o Elective mutism – occurs only in certain situations
- Developmental problems in kids
o Precocious puberty – early secondary sexual characters in girls < 8 yrs, boys < 9.5 yrs
Investigation of preco. Puberty:
1. FSH, LH and Estradiol (usually raised in precocious puberty)
2. Bone age X Ray (Left wrist and elbow)
3. MRI brain (to exclude pituitary tumor) if FSH and LH are ↑
o Premature telarche – isolated breast dev. in girls < 2 yrs
due to hormonal stimulation from estrogen
sometimes with discharge from nipples
o Pubertal gynecomastia – 40-50% boys, transient
- 1st yr of life weight calculation
o ¾ kg monthly first 4 mths = ¾ x 4 = 3 kg
o ½ kg monthly next 4 mths = ½ x 4 = 2 kg
35
Even below 3rd & above 97th percentile there are normal kids.
o Short Stature:
1. Familial (Genetic) short stature
Bone age BA = CA Chronological age
Grow on 3rd percentile or below but the rate of growth is parallel to 3 rd
Growth velocity = Normal
Puberty is at appropriate time
2. Constitutional delay (delayed puberty) MC
Boys
Growth velocity is slower bw 6m and 3yrs
often family Hx of parent being short as a child with delayed puberty
and eventually he caught up ----- “Late bloomers”
BA < CA
Puberty is delayed
1st bone age then (testosterone & plasma gonadotrophin levels MCQ)
- e.g. in the recalls
Short with CA = 15 but stature of 12 yrs
good prognosis? if BA = 9 = constitutional delay
3. Hypopituitrism
Usually manifests after 2 yrs
look for relative obesity w/o any other explanation
4. Chronic illness or malnutrition
Celiac, Cystic fibrosis, etc.
5. Iatrogenic
e.g. C/S
- fusion of epiphysis
6. Chromosomal abnormality
MC – Turner Syndrome
- Girl – Short stature -- 45XO
7. Skeletal Dysplasia—Short limbs
o Alena
most kids 25-75 percentile
<10 = Concern
> 95 = Gigantic
important is trend from birth
if always high or low percentile = normal!
drop in wt. > 2% at a certain moment, in a short period of time = FTT
- Short stature
o Genetic
o Intrauterine causes
o Intralabor causes
o Postpartum causes
extensive resuscitation
Growth hormone retardation
Post delivery hypoglycemia
Hypothyroidism
37
Cystic Fibrosis
Celiac disease
Phenylketonuria
o later
child abuse, nutritional defficiences
CRF
Turner syndrome – female (45XO)
o MC = Constitutional delay
o Combinations:
Bone age = Chronological age => Subnormal adult height
cause
- Genetic short stature
- low birth weight
Bone age < Chronological age + appropriate to height age => Normal adult
height
Cause = familial maturation delay
e.g. jul 2009 – q11
Bone age below height age => severe growth retardation (only height is short,
GH is diagnostic)
cause = endocrine – hypothyr., growth hormone defficiency
o Dx
FBE – anemia, chronic inflammation (ESR, CRP)
Thyroid function
Growth Hormone level
Blood sugar Level
Karyotyping – Turner
X Ray of left wrist -> bone age
if it’s younger than age of child => room for it to grow
Milestones - TO DO!(MCQ 2145 P 94)
- Asked so far – Murtagh 866
o Social Smile: 2 mths (0-7 wks)
o Roll over from back to front position (prone to supine): 4 months?
o Roll over from front to back position: 5 mths
Both asked – 4-5 mths
o sits with support: 6m
o sits alone: 8m
o standing with support: 5-10 m (10 m)
o walks with support: 7 ½ - 12 ½ (12 m)
o walks without support: 11 ½ - 15 m (15 m)
o walks up steps w/o help: 2 yrs (14-22 m)
Climbs stairs with alternate foot: 30 m
o hops on one foot: 3-5 yrs
o rides a tricycle: 21m – 3 yrs
o reach for an object: 3 – 5½m
o pass object from hand to hand: 4½-7½m
o pincer grip: 9 –15 m
o wave his hand/ wave goodbye around: 12 m ??
38
Admit
o 1 Standard drink = 10g
250 ml glass of Beer 4.8%
100 ml glass of Wine 13.5%
30 ml glass of Spirit 40%
http://www.health.gov.au/internet/alcohol/publishing.nsf/Content/standard
o High risk/ harmful drinking
> 6 standard drinks for men
> 4 standard drinks for women
o Alcohol limit for driving in Australia: < 0.05 g/ 100ml (2.5 g alcohol/ 5L blood volume)
for a 70 kg man, this means not to drink more than:
2 std drinks in 1h
3 std drinks in 2h
4 std drinks in 3h (1 std drink eliminated in 1 h)
o Lethal dose: 0.45-0.5 g/100 ml (%)
o Intoxication
Potentially fatal
BAC is around 0.45% to 0.5%
Use a breath analyzer to estimate BAC & observe pt, until BAC falls below 0.2%.
BAC normally declines at a rate of 0.015% to 0.02%/ hr, although rate of decline
may be ↑in heavy drinkers.
Sx
hearing voices (like in Schizophrenia)
TREATMENT:
Supportive and symptomatic
Careful monitoring of:
- BAC
- Level of consciousness
- Responsiveness
- O2 saturation
o Alcohol withdrawal:
Characterised by:
Anxiety
Tremor
Sweating
Nausea & vomiting
Agitation
Headache and perceptual disturbances
Seizures: Uncommon
Alcoholic hallucinosis
- rare complication of alcohol withdrawal in alcoholics. This
develops about 12 to 24 hrs after drinking stops and involves
auditory hallucinations (accusatory or threatening voices).
these begin with simple sounds (whispering, muted
laughter, clink of glasses, simple words)
43
TREATMENT:
- Hospitalization
- Correct dehydration and infection if any
- Benzodiazepine loading dose technique.
Diazepam 10 to 20 mg orally, 2 hrly until symptoms
subside.
- Thiamine 100 mg IM as a single dose, followed by 300 mg orally,
daily in 3 divided doses.
- Haloperidol 1.5 to 10 mg orally If psychotic features (e.g.
hallucinations and delusions). Add haloperidol– only if
benzodiazepines didn’t work.
- Wernicke’s Encephalopathy:
o in alcoholics due to thiamine defficiency
o Sx – CONA
Confusion
Opthtalmoplegia
Nystagmus
Ataxia
Nystagmus & Ataxia (DD)
- with alcohol – Wernicke’s encephalopathy
- cerebellar stroke
no tongue fasciculations
Korsakoff amnestic confabulatory syndrome
Anterograde amnesia
Retrograde amnesia
Confabulation – to make up missing details from affected memory
meager content in conversation
lack of insight
apathy
o Rx
Thiamin IV or IM
followed by glucose/ dextrose
if we administer glucose first, before thiamin, it might cause
dehydrogenation of piruvate, which will consume thiamin
- Drug intox.
o CNS depressors, stupor, coma
miosis, bradycardia, hT
Drugs:
OPIODS:
- 1. Morphine
SE
Miosis (pin-point pupils)
drowsiness & respiratory depression – most
dangerous
o in high single dose adm.
o usually in terminal patients
45
- Effects in prenancy
IUGR
placental abruption
premature labor
intraventricular hemorrhage
developmental delay
stillbirth
teratogenic effect not proven
- Post-withdrawal – can cause depression
- RX Cold blanket and cool normal saline MCQ party intoxication
Amphetamine
- Sx
rush with grandiosity, feelings of well-being and
overconfidence, heightened sense of sexual feeling
can aggravate or produce a paranoid schizophreniform
psychosis - “stimulant psychosis” (by increasing
dopamine in the synaptic clefts of brain)
paranoia and persecutory delusions
ideas of reference
auditory and visual hallucinations
persecutory auditory hallucinations
visual illusions and hallucinations
tactile hallucinations of bugs or vermin crawling under
the skin (formication) – can lead to scratching
anxiety, hostility, aggressiveness
- Rx
admission
cessation of amphetamines
antipsychotics – haloperidol, phenothiazines
- In pregnancy
amphetamines - MC associated with congenital
anomalies and
cleft palate
HT and pre-eclampsia
IUGR
preterm labor
- withdrawal – with depression and high suicidal risk
- Ecstasy – type of amphetamine
euphoria, anxiety, agitation
dehydration
sec. hyponatremia due to excessive water
consumption
muscle jerks
Marijuana (Cannabis)
- only drug that has its own receptor
- potentiates the effect of sleeping pills – risk of overdose
- mix of stimulant/ depressant / hallucinogen effects
47
Pneumocystic - Cotrimoxazol
Klebsiella - Cefuroxime
o Lung abscess
Cephalosporin (Ceftriaxone) + Clindamycin
Cephalosporin + Flucloxacillin
o Tonsilitis – Penicilin
o Rheumatic fever Penicilin
o Scarlet fever Penicillin
o Impetigo Topical antiseptic – Bactroban (Mupirocin)
if extensive, systemic A/B
Flucloxacilin
Cephalexin
o Meningitis - Ceftriaxone (3rd gen) + Benzylpenicillin
Ceftriaxone 2 g IV
+ Benzylpenicillin 2.4 g IV (ampicillin for Listeria) in immune-
compromised or Listeria
if Penicillin/Cephalosporin hypersensitivity:
Vancomycin + Ciprofloxacin
prophylaxis in contacts: Ciprofloxacin or Rifampicin
o Typhoid fever – Ciprofloxacin
o other diarrhoeas – see Diarrhoea chap.
o Whooping Cough – Clarithromycin/ Erythromycin
o Epiglotitis – Cephalosporin (3rd gen): Ceftriaxone, Cefotaxime
o Infective endocarditis - start ASAP empiric Rx with Benzyl Penicillin + Flucloxacilin +
Gentamycin IV
o Osteomyelitis – (staph.) Flucloxacilin
o Septic arthritis (staph.) Flucloxacilin
in hospital – Ceftriaxone – 3rd gen (covers gram -ve)
o Cholecystitis - Gentamicin, Ampicillin.
o Cholangitis: Ceftriaxone, Penicillin, Aminoglycosides
o Peptic ulcer
1st line: PPI + Clarythromycin + Amoxycilin
2nd line: PPI + Metronidazole + Amoxycilin
3rd line if sensitive to Penicilin: PPI + Clarythromycin + Metronidazole
o Peritonitis (after viscus rupture): Gentamicin 5 mg/kg IV + Ampicillin 1 g IV +
Metronidazole 500 mg IV
o TB
Active TB
4 drugs (rifampicin, isoniazid, pyrazinamide, ethambutol) for 2 mths
then 2 drugs (rifampicin and isoniazid) for 4 mths
- total 6 mths
Latent TB (Mantoux positive, no symptoms, no X Ray findings)
when active TB is excluded: Isoniazid mono-therapy for 6-9 mths
Pregnant
Isoniazid, Rifampicin, Ethambutol – 9 mths treatments
Isoniazid resistant TB
52
e.g.
- Penicilin
- Cephalosporin (cross-reaction with penicilin)
- Sulphur drugs
- IV contrast mediums (CT, etc.)
type II – Cytotoxic
sub-types
- hemol. anemia – sulphonamides (sulfur drugs), peniciline – rare,
quinidine (anti-arrhythmic), methyldopa
- Agranulocytosis – clozapine, carbimazole, ACE inh.
- Thrombocytopenia – heparin (HIT), quinidine
type III – Immune-complex mediated
e.g.
- penicilin
- sulphur drugs
- thiazides
type IV – T-cell mediated
e.g.
- penicilin
- cephalosporin
- local anesthetics
- phenitoin
- Drugs to be avoided in pregnancy – Murtagh 1063
o A/B
Tetracyclines (e.g. doxycycline) – incorporated into fetal bones and teeth
Aminoglycosides
Trimethoprim
o Anti-HTN
ACE inhibitors
Diuretics – as in pre-eclampsia and pregnancy induced HT the intravasc. volume
is already low.
Beta blockers – have potential problems
(best evaluated to use in pregnancy = Methyldopa)
Verapamil
o C/S systemic
o Anticonvulsants
Phenytoin – hydantoin syndrome (facial, nail and other abnormalities)
o Estrogen
Diethystilbestrol
causes reproductive tract abnormalities in both genders
↑risk of clear cell carcinoma of vagina in female children
↑ abortion rate
o Danazol – Androgenisation: Clitoral hypertrophy & labial fusion in female fetuses
- Drugs to be used in Breastfeeding
o Antiphyschotic
Olanzapine
Risperidone
56
No typical antipsychotics
Clozapine – as much as possible avoid but can be given
o Antidepressants
SSRI except fluoxetine
prefer short acting SSRIs (Paroxetine, Sertraline)
o Bipolar drugs
Na valpropate---- Drug of choice
Lithium – CI (blue book), but Shipra said: as much as possible avoid, but can be
given (check level in the infant as well)
o Benzodiazepines
short acting cause sedation and poor sucking in baby
long acting, like diazepam, cause floppy infant syndrome
o Opioids – safe
- Danazol
o Androgenic SE, especially in long term Rx
Weight gain
Fluid retention
Voice change
in pregnancy: androgenisation: clitoral hypertrophy & labial fusion in female
fetuses
- Inotrop drugs
o Positive inotrops
Ca
Ca sensitizer – levosimendan (in CHF)
Cardiac glycosides – Digoxin
Catcholamines – adrenaline, noradrenaline, dopamine, dobutamine
PG
Phosphodiesterase inh. – theophylline
o Negative inotrops
Beta blockers
Ca channel blockers – only diltiazem, verapamil
amlodpidine (long acting metabolite of nifedipine) – replacing nifedipine
decr. the afterload resitance (vasodil.)
SE:
- edema – nifedipine
- reactive tachycardia
- Chronotrop. neg. Drugs (decreasing HR)
o digoxin
o verapamil, diltiazem
o adenosine
o beta blockers
- Antiarrhythmic Drugs - http://en.wikipedia.org/wiki/Antiarrhythmic_agent
Known [5]
Class Examples Mechanism Clinical uses
as
57
Ventricular arrhythmias
fast- Quinidine +
(Na ) channel block prevention of paroxysmal recurrent
channel Procainamide (intermediate atrial fibrillation (triggered by vagal
Ia
blockers Disopyramide association/dissociation) overactivity), *procainamide in
Wolff-Parkinson-White syndrome
verapamil intox.
AV block I-III
LBBB, RBBB
- Beta Blockers
o Types
Non-selective: Propranolol (acts on both heart and lung)
Selective: Metoprolol, Atenolol, Sotalol (acts only on heart)
o Indications
HTN
heart failure – decr. Mortality (cardioselective only)
after MI – decr. mortality
rate control
rhythm control – sotalol
o CI
Pregnancy
heart block
Prinzmetal angina (due to coronary spasm)
asthma, COPD (propranolol – neselective)
DM
peripheral vascular disease
o SE
bronchospasm – non-selective
hyperkalemia
hyponatraemia
↑risk of DM
- ACE inhibitors
o Indications
HTN
Heart failure – ↓mortality
MI – ↓ mortality
especially with:
- renal condition
- HTA
- DM
Renal condition (renoprotectors)
DM nephropathy in beginning stage (microalbuminuria)
Progressive renal failure
o SE
Dry cough
Angioedema (C1 estrase)
Agranulocytosis (cytotoxic)
Hyperkalemia
Acute renal failure – in (unilateral or bilateral) renal artery stenosis
Orthostatic hypotension
o CI
Pregnancy
59
Renal failure (in advanced stages when creatinine > 3.5 & worsening with their
use)
Renal artery stenosis
Diastolic heart failure (hypertrophic heart) – M 1337
hypertrophic cardiomyopathy
aortic stenosis
HT
Rx
- Beta blocker
- Calcium antagonists
- Spironolactone (causes hyperkalemia)
o indic.:
Diuretic
Heart failure
HTN
Antiandrogen (Aldosterone antagonist) causes gaynocomastia
- Thiazides
o SE
hypokalemia
hyperuricaemia
impaired glucose tolerance –↑risk of DM (like the Beta Blockers)
hypercholestrolemia
o indic.
diuretic
HTN
heart failure
protect from oxalate stones (renal stones)
- Nitrates
o Types
o Short acting
GTN – spray, patch
duration of action – 30 min
Long acting
isosorbid mononitrate
isosorbid dinitrate
o SE
Postural hypotension and Headaches – bc of vasodilation
reflex tachycardia (prevent with β blockers)
- Hyperkalemia
o causes
Drugs
K⁺ sparing diuretics (spironolactone & amiloride)
ACE inhibitors & AIIRA
Digoxin
Beta Blockers
NSAIDs: Indomethacin, etc.
IV Benzyl Penicillin (contains K)!
60
- tachycardia
various arrythmias
- shortened QRS complex, atrial or ventricular extrasystoles,
paroxysmal atrial tachycardia with AV block, heart block
- PR interval prolongation
- Pulses bigeminy, V. tach. or fibrillation
nodal bradycardia, bradyarrythmia
ST depression with T negative wave (“sagging” )
hypokalemia – small T wave, proeminent U wave
- hyperkalemia – tall tented T wave, widened QRS complex, absent
P waves
hypocalcemia: long QT, small T wave
- hypercalcemia: short QT
ventricular ectopics
never prolonged QTc (corrected QT -> predispose to torsade de pointes)
Rx
Stop digoxin
Check K+
Treat arrythmias
Consider giving digibind IV – AB to digoxin
- NSAIDs:
o not in renal failure/ insufficiency
↓ GFR
↑ proximal tubular reabsorption
can ↓ Lithium clearance -> Lithium toxicity (MCQ)
- Oral antidiabetics
o Glibenclamide
SE
hypoglycemia
cholestatic jaundice
o Metformin
GI upset
diarrhoea, ↑flatulence
no hypoglycemia
- Amphotericin B IV
o only in potentially lethal fungal infection, as a last resort
o SE
Phlebitis at the site of infusion
anemia
hypokalemia
renal problems (irreversible)
renal failure
renal tubular necrosis
- Azathioprine
o hepatotoxic
o acute pancreatitis
62
- Phenytoin
SE
o P 450 inducer
o Gum hypertrophy
o Teratogenic --hydantoin syndrome (facial, nail and other abnormalities)
o Osteomalacia & osteopenia (not osteoporosis)
o interferes with folate metabolism – Megaloblastic anemia
o neuropathies (vertigo, headache and nystagmus)
o Yellow-brown pigmentation of skin
o hirsutism
o lymphadenopathy
o risk of cardiac arrythmias when injected rapidly
- Valproate
o Hepatotoxic (monitored in plasma)
o Teratogenic
- Benzodiazepines
o SE
drowsiness, dizziness
upset stomach
blurred vision
dreaming
depression
- Amitryptilline (TCA)
o SE
ED
↑ QT interval
- Erythromycin:
o Abdominal Pain
o Anorexia
o Loose bowel motions
- CorticoSteroids
o SE – Oxford 371
Short term
mood changes: euphoria, depressive
mild hypokalemia
mild hyperglycemia – counter-insulin effect
Long term (Cushing – like syndrome)
insomnia, increased appetite
fluid retention – mineralocorticoid effect
HTN
adrenal suppression
avascular necrosis of the bone
myopathy
cataract
gynecomastia?
osteoporosis
growth suppression
63
pancreatitis
oesophageal and peptic ulceration
infections – ↑frequency and severity
candidiasis
chickenpox
- Teratogenic drugs
o class
A – safe
B – not fully studied, Metronidazole
C
Lithium – defintely teratogenic in the 1 st trimester and should always
be suspended, preferrably before an intended pregnancy!
Methadone
- should be taken during the 1st trimester
- discontinue gradually in the 2nd trimester
- taken again during breastfeeding to prevent or minimise
withdrawal or abstinence in the neonate
Phenytoin and all entiepileptics
Warfarin
ACE inh.
Danazol (androgenisation) Clitoral hypertrophy & labial fusion
Retinoids
A/B:
- tetracyclines (growth retardation, etc.)
- metronidazole (its now proven to be safe)
- chloramphenicol
- aminoglycozides
- Drugs causing pulmonary infiltration
o Amiodarone -> fibrosis, alveolitis
other SE:
hypothyroidism (inf. the conversion of T4 -> T3)
photosensitivity
skin pigmentation
peripheral neuropathy
ARDS
o Bleomycin
o Busulphan
o Gold compounds (rheumatoid arthritis)
o Nitrofurantoin
o Methotrexate
o Methylsergide
- Nephrotoxic drugs
o A/B
Aminoglycosides: gentamycin, etc.
Cephalosporins – some
worst combinations causing ARF (acute tubular necrosis):
- Gentamycin + Cefazolin (1st gen)
64
- Toxoplasmosis
o Pyrimethamine + Sulfadiazine (+ folic acid, to counteract their antifolate activity)
- Clostridium difficile
o 1. Metronidazole
o 2. Vancomycin– if 1 fails
o Antiemetic, nausea:
a. side effect of morphine – haloperidol, prochlorperazine (Stemetil)
b. poor gastric emptying – metclopramide, cisapride, domperidone
c. cytotoxic chomotherapy or radiotherapy – ondansetron (Zofran) = serotonin receptor
antagonist
Antivertigo – Betahistine - dilate blood vessels within middle ear which can relieve pressure from
excess fluid and act on smooth muscle. In Meniere’s syndrome.
Antipsychotics:
- Tranquilizing psychiatric medication primarily used to manage psychosis (including delusions or
hallucinations, as well as disordered thought) particularly in schizophrenia and Bipolar Disorder.
- All antipsychotic drugs tend to block D2 receptors in dopamine pathways of brain. This means
that dopamine released in these pathways has less effect. Excess release of dopamine in
mesolimbic pathway has been linked to psychotic experiences. It is blockade of dopamine
receptors in this pathway that is thought to control psychotic experiences.
- 1st generation (Typical) antipsychotics – 1950 - the first typical antipsychotics to enter clinical
use were the Phenothiazine (Chlorpromazine)
o Butyrophenones
Haloperidol (Haldol, Serenace)
Droperidol (Droleptan)
o Phenothiazines
Chlorpromazine (Thorazine, Largactil)
Fluphenazine (Prolixin) - Available in decanoate (long-acting) form
Perphenazine (Trilafon)
Prochlorperazine (Compazine)
Thioridazine (Mellaril, Melleril)
Trifluoperazine (Stelazine)
Mesoridazine
Periciazine
Promazine
Triflupromazine (Vesprin)
Levomepromazine (Nozinan)
Promethazine (Phenergan)
Pimozide (Orap)
o Thioxanthenes
Chlorprothixene (Cloxan, Taractan, Truxal)
Clopenthixol (Sordinol)
Flupenthixol (Depixol, Fluanxol)
Thiothixene (Navane)
Zuclopenthixol (Cisordinol, Clopixol, Acuphase)
68
o Examples:
Agomelatine (Valdoxan, Melitor, Thymanax)
Lithium:
- A mood stabilizing drug, primarily in treatment of Bipolar Disorder, where it has a role in
treatment of depression and particularly mania, both acutely and in the long term. As a mood
stabilizer, it is probably more effective in preventing mania than depression and may ↓ risk of
suicide in certain bipolar patients. In depression alone (unipolar disorder) Lithium can be used to
augment other antidepressants. Lithium carbonate (Li2CO3), sold under several trade names is
MC prescribed while the citrate salt lithium citrate (Li3C6H5O7) the sulfate salt lithium sulfate
(Li2SO4), lithium aspartate and the orotate salt lithium orotate are alternatives.
- Upon ingestion, it becomes widely distributed in CNS and interacts with a number of
neurotransmitters and receptors, ↓ norepinephrine release and increasing serotonin synthesis.
Parkinson: Levo-dopa (precursor of cathecolamines: dopamine, epinephrine, norepinephrine),
Quetiapine (at night, = antipsychotic,= Seroquel, also used in Schizophrenia, Bipolar syndrome, restless
legs syndrome and chronic insomnia )
Antiepileptics:
- Carbamazepine (+ also used in Trigeminal neuralgia)
- Valproate
- Ethosuximide
- Gabapentin (+ diabetic neuropathy, post-herpetic neuralgia)
- Aspirin
o it has half the effectiveness of warfarin in preventing strokes!!!
- Dypiridamole
- Ticlopidine, Clopidogrel
Thrombolytics:
- These drugs are most effective if administered immediately. The advantage of administration is
highest within first 60 minutes, but may extend up to 6 hrs after start of symptoms.
- examples:
o tissue plasminogen activator - t-PA - alteplase (Activase)
o reteplase (Retavase)
o tenecteplase (TNKase)
o anistreplase (Eminase)
o Streptokinase (Kabikinase, Streptase)
o urokinase (Abbokinase)
- Side-effects:
o Hemorrhagic stroke is a rare but serious complication of thrombolytic therapy.
o If a patient has had thrombolysis before, an allergy against the thrombolytic drug may
have developed (especially after streptokinase).
Antispasmodic – hyoscine
diarrhoea
dermatitis
dementia
- Regular monitoring of plasma level of drugs – for:
o Lithium
o Digitalis
o Theophylline
Therapeutic value Toxic value
Digitalis 0.5-1.5 2
Lithium 0.6-1.2 2
Theophylline 10-12 20
o Clozapine
monitor FBE (neutropenia) and glucose tolerance (DM)
o nortryptiline
o (Amit) +
Aminoglycosides: gentamicin
Antiepileptics: phenytoin, valproate, carbamazepine
antiarrhythmics
antidepressants
- Drug interactions
o Erythromycin and Theophylline
o ACE inhibitors and Diuretics
o Amiodarone and Beta Blockers
o NOT - Digoxin and Warfarin
- Drug administration changes in pre-op for elective surgery
o Oral hypoglycemic
No change for minor procedure
Switch over to insulin at least 48 hrs before surgery
o OCP
Combined OCPs: Stop pill 4 weeks before surgery (risk of DVT due to ↑
estrogen in OCP)
Mini-pill: can be continued
o Oral anticoagulants
Warfarin
Elective surgery
- Stop it 1 week before surgery + start heparin (LMW heparin)
- Stop heparin 12-24 hrs before surgery
- After surgery, start heparin and warfarin
- Stop heparin when desired INR has been achieved
Emmergency surgery
- Give FFP + prothrombine concentrate + Vit. K
o Aspirin, Clopidogrel - Stop 1 week before surgery
o Antianginal, Anti-HT – continued
o Antidepresants
MAOI – Stop 3 weeks before surgery
Lithium – Stop 48-72 hrs before surgery
o C/S
76
if taken for > 1 week in last year (external C/S have suppressed the endogenous
production of C/S): give hydrocortison supplement before or during surgery to
keep up with the stress of the surgery
- Drugs that can be delivered by endotracheal tube
o O2
o Naloxone
o Lignocaine
o Atropine
o Adrenaline
o Asthma
Beta 2 agonists: Salbutamol (Ventoline)
Cholinergic blockers: Iprotropium bromide (Atrovent)
- Statin (HMG-CoA inh.)
o SE
Hepatotoxic
Myositis
Statins + fibrates = bad combination -> risk of myopathy (simvastatin
myopathy)
- even worse with erythromycin – liver enzyme inhibitor
- causes rhabdomyolysis:
check serum CK and urine myoglobin
hemoglobinuria (not hematuria) – no RBCs on
microscopy
o CI in pregnancy
o Dx
LFT, CK – follow up for 6 mths
- Follow up LFT test
o Anti-TB drugs
o Anti-epileptics
o Li
o Statins
Obstetrics - OK
Pregnancy parameters
- Implantation:
o 5 days for fertilized egg
o 10 days from ovulation
- Don’t monitor baby up to 24 weeks
o until then – only monitor mother
- Term baby > 37 weeks
- Characteristic of pregnancy
o immunological suppresion
o leucocytosis
- Gestational age - most appropriate examination:
o U/S in first trimester, 8th to 9th week, before 18 wks (not reliable after 18th week)
the earlier the more accurate
measures the crown-rump legnth (CRL)
o if no U/S then pelvic/ bi-manual examination in first trimester
77
Gravida/ para/ abortus (GPA) or sometimes just gravida/ para (GP), is a shorthand notation for a
woman's obstetric history.
- Gravida indicates the total number of times a woman has been pregnant, regardless of whether
these pregnancies were carried to term. A current pregnancy, if any, is included in this count.
- Para indicates the number of viable (>20 wks) births. Pregnancies consisting of multiples, such as
twins or triplets, count as ONE birth for the purpose of this notation.
- Abortus is the number of pregnancies that were lost for any reason, including induced abortions
or miscarriages. The abortus term is sometimes dropped when no pregnancies have been lost.
Pregnancy stuff:
duration: 37-42 wks (40 weeks since last normal menstrual period, LNMP or 38 wks from conception)
Prenatal care:
monthly visits during the first two trimesters (from week 1–28)
biweekly from 28 to week 36 of pregnancy
weekly after week 36 (delivery at week 38–40)
total: 14 (can be reduced to 7-10)
Supplimentation:
Folate 0.5 mg last 3 months and first 3 months of the pregnancy
Iron – in vegans/ vegetarians
Calcium and vit. D (10 µgrams/ day) – maybe
Vit. A excess is harmful to the baby!
Screening:
- Chorionic villus sampling: 9-11 weeks, result in 48 hrs
- Amniocentesis: 15 weeks, result in 3 weeks
- Ultrasound
- Immunisations:
78
- Influenza
- Typhoid or cholera – if travelling abroad
- Polio – if not vaccinated yet
Symphisis – Fundal height: approx. match height in cm = No. of weeks (e.g. at 20 weeks – 20 cm)
Evolution:
by 10 weeks (70 days) the placental development is complete
uterus becomes palpable from 12-13 weeks
fetal movements felt after 18 weeks
morphology ultrasound scan at 18-20 weeks
uterine fundus reaches the umbilicus – 20 weeks
Infections in pregnancy
- Pregnancy doesn’t lower the woman’s resistance to inf.?
o exception: poliomyelitis
- baby – immunocompetent at 14 wks, but the efficacy is low till the second ½ of the pregn.
- Mx
o offer mother termination of pregnancy if active infection with:
Erythema infectiosum (Slppped cheek, 5th disease)
Rubella
- Types
o a. Bacterial
1. Group B Streptococcus:
(15) 18-27% of mothers are carriers
during labour > 50% of babies born through an infected vagina are
colonized
- 1% of them will develop early onset GBS neonatal sepsis ->
difficult to treat with high neonatal death
25-30% of premature babies
2-8% of term babies
15-40% neurological sequelae in survivors
risk incr. in
- PROM – mother can develop chorioamniotitis
- Vaginal delivery – especially in premature babies
Mx – 2 approaches:
- 1. test for it at 36 weeks
Swab low vagina + rectum
- 2. treat if positive risk factors
premature labor < 37 weeks
when anticipated ROM > 18 hrs before delivery
intrapartum fever > 38o C
previous early onset GBS dis.
GBS bacteriuria during pregnancy
Rx.
- for mother
come to hospital if early labor
79
Rx
- Procaine benzylpenicillin or benzathine penicillin
- Non-pregnant: if sensitive to penicillin
Doxycycline
- in case mother was infected and not fully treated -> baby also
treated with procaine benzylpenicillin for 10 days
since baby’s sympt. are non-specific + serology is
inacurate
o b. Viral – smaller than bact. => higher chance of passing through the placenta
most of them infect baby only if very severe infection in mother
exceptions:
- Rubella
- CMV
- Herpes
1. Rubella (German Measles)
very rare now, due to the immunization program
- 85% had the inf. and 90% of them are immune
if active inf. in first 14 wks => fetus will almost certainly be inf. (90%),
with 40% of them being damaged by virus (5% risk in last trim.)
causes “Congenital Rubella Syndrome”:
- Prematurity
- "blueberry muffin" rash
- Cataract, blindness
- Deafness
- Heart malformation - PDA
- IUGR
- Thrombocytopenic purpura, hepatosplenomegaly
- Vasculitis, renal artery stenosis
Prevention
- Immunize all women between 11-13 yrs
- Screening
when she wants to get pregnant
if not immune – get vaccine and don’t get
pregnant in next 3 months
at first pregnancy test – if vaccinated, extremely small
risk of infection
Mx in case of inf. (rubelliform rash – 50% of rashes are not due to
rubella) or contact with infected person
- Pregnancy test neg.
IgM neg., IgG neg. -> immunize and don’t get pregnant
in next 3 mths
IgM pos., IgG neg. -> supportive Rx + don’t get
pregnant till sympt. disappear and IgG becomes pos.
IgM neg., IgG pos. = immune, safe to get pregnant
- Pregnancy test pos.
IgM neg., IgG neg. -> do not immunize + avoid contact
with inf. person + repeat test in 3 weeks
81
D&C
followed by U/S + prophylactic inj. of methotrexate
FOLLOW –UP: Wkly serum or urine β-hCG.
They should fall to undetectable levels within
12-16 wks after evacuation
if not back to normal -> oncology assessment
for possible metastases
o MC location = lung
o brain
o bones
Precaution: no pregnancy for 1 yr (use OCP)
o b. Invasive mole (chorioadenoma destruens).
o c. Choriocarcinoma.
3. Spontaneous miscarriage
o Intrauterine death – MC cause = Unknown
o Expulsion of products of conception before 24th wks of pregnancy
o Occurs in 10-20% of all early pregnancies
o MC in 1st trimester
o Miscarriage
1st trimester – Chromosomal (MC - 60%, mostly trisomies) and
fetal abnormalities
MC > 35 yrs
nd
2 trimester
genetic disease
infection
uterine malformation
Fetal fibronectin test: if + even when cervix is still
closed risk of premature delivery is markedly ↑.
cervical incompetence
20% of women with recurrent misscariage
after 12 wks have this (usually at 16 wks)
gradual dilatation of internal cervical OS ->
intrauterine pressure will break amniotic bag at
cervical OS.
Sx
o Recurrent miscarriage: painless leaking
of amniotic fluid (PROM)
o painless cervical dilatation + ↑ cervical
mucous discharge
o miscarriage after painless labour
o contractions – only rarely
o usually no or small bleeding – differ
from other type of miscarriages
Dx
o U/S or vaginal examination – before
Rx - Cervical Cerclage – sutures like a ring on
outside of cervix at internal OS
88
Can’t be arrested/stopped
Bleeding is heavier, abdominal cramps more persistent
(typical here)
External OS is open (5 mm ≥).
POC may be found in vagina or protruding from cervical
canal.
3. Incomplete miscarriage.
Parts of fetus/placental material retained in uterus
The bleeding remains heavy.
Cramps persist even following passage of clots and
POC
4. Complete miscarriage.
All fetal and placental material has been expelled from
uterus
Bleeding and cramps stop.
Signs of pregnancy disappear.
Cervical OS is closed.
5. Silent or missed micarriage.
All the POC are retained
Cramps and bleeding are replaced by an asymptomatic
brownish vaginal discharge
USG fails to detect fetal heart motion.
o Dx
First: Pregnancy test.
If β-hCG is positive, check β-hCG level to assess
usefulness of ultrasound of USG.
- Β-hCG greater than 1000 U/L: USG.
To confirm the gestation.
To check the sac size.
Liquor volume.
Presence or absence of fetal heart
activity
o MANAGEMENT:
Stable or Unstable?
IV resuscitation
Transfusion if needed
Refer to Gynaecological team for surgical or non-surgical
management
Give Rh negative mothers anti-D immunoglobulin
4. Septic abortion
Result of criminal abortion.
Pelvic infection with salpingitis, peritonitis, pelvic and pulmonary
thrombophlebitis.
Can lead to septicaemia, DIC, shock and death.
CLINICAL FEATURES:
- Fever > 37.8
90
- Abdominal pain
- Foul-smelling vaginal discharge and bleeding.
MANAGEMENT:
- First step: Swabs for microscopic assessment and culture.
- Immediate antibiotic therapy: Gentamicin 5mg/kg IV, ampicillin
2g IV and metronidazole 500 mg IV
- Refer for curettage or emergency hysterectomy
- II. Late pregnancy
o a. Bleeding = ANTEPARTUM HEMORRHAGE = Vaginal bleeding after 24 wks of gestation
1. Placenta praevia
The placenta is implanted, either partially or wholly, in the lower uterine
segment and lies below the fetal presenting part.
incidence – 1%
MC obstetric cause of coagulopathy
classif.
- total, complete, central – completely covers the cervical os
- partial
- marginal – edge min. 2 cm away from cervical os
-
RISK FACTORS:
- Three times as common in multiparous women as in primiparae.
- Cesarian section.
- Submucous fibroids.
- History of placenta praevia.
- Advanced maternal age
Sx
- PAINLESS vaginal bleeding
may be precipitated by
trauma
coitus
pelvic/ vaginal exam
can stop then resume
- Uterine Hypotonia: Uterus is non tender
- Fetal head is still mobile above the pelvic brim
- Blood loss is MATERNAL.
- Bleeding in 2nd half of pregnancy is placenta praevia until proven
otherwise.
DIAGNOSIS:
- First: Fetal heart sounds
- Ultrasound: Dx is confirmed only after 30 weeks of pregnancy (at
32-34 weeks)
91
Dx
- clinical
- Apt test – distinguish between fetal blood and maternal blood
Mx
- emmergency C-section, otherwise fetus will die
4. Placenta Accreta
rare: 1:500 - 1:2500
- incidence is ↑due to↑incidence of C-sections
- risk proportionately increases after multiple C-sections
risk factors
- previous C-section + anterior low lying placenta
when placenta implants over a previous C-section scar -> trophoblast
penetrates through scarred decidua and myometrium becoming
morbidly adherent.
Sx
- Excessive vaginal bleeding leading to frequent DIC
Mx – Cesaren hysterectomy to preserve mother’s life
5. Rupture of uterus
RESULT OF:
- Obstructed labour – during uterine contractions
- Trauma
- Dehiscence of a cesarean scar
- Inappropriate use of oxytocins
Sx
- Vaginal bleeding
- Abdominal pain which becomes constant
- Shock in some cases
- Some can be asymptomatic
TREATMENT:
- Hysterectomy
- In few cases uterine tear can be sutured
6. Polyp
Sx
- Bleeding can occur after coitus
- More limited bleeding
best way to monitor adequacy of blood volume replacement = urine output
since body can compensate through vasoconstriction for a while (Pulse,
BP normal) but urinary output will be ↓ in hypovolemia.
o b. HTN in pregnancy – Classification:
1. Chronic HT
Essential HT – prior to conception or in 1st ½ of the pregnancy, without
an underlying cause
Secondary HT – caused by renal, renovasc. or endocrine disorders or
aortic coarctation
2. Gestational HT
arises after 20 wks
without any features of pre-eclampsia
94
Thrombocytopenia
hemolysis
DIC
fetal growth restriction
COMPLICATIONS:
- Mother
HELLP syndrome = severe form of pre-eclampsia
triad:
o Hemolytic anemia
o Elevated Liver enzyme
o Low Platelets
Rx – deliver the baby
DIC
Oliguria, ARF
Eclampsia (tonico-clonic seizures and coma)
- Baby
Intrauterine death.
IUGR
Premature delivery.
MANAGEMENT:
- Admission: BP > 150/100 (twice), maternal symptoms,
compromised fetal well being.
- Treat HTN:
moderate – Oral
Methyldopa 250 mg two-three times daily.
Labetalol or atenolol
Nifedipine
Severe – IV
Hydralazine 5 mg IV bolus every 20 min
- < 32 wks: try to continue pregnancy until 35 wks
steroids for pulmonary maturity
daily fetal movement count (kick count chart)
3 CTGs/ week
Doppler umbilical blood flow
Platelet count – to detect HELLP syndrome
if platelets > 100.000 – keep monitoring
if platelets < 100.000
o Give C/S – 2 doses, 24 hrs apart -> to
prevent hyaline membrane disease
o Correct thrombocytopenia, then
o induction
- 32-35 wks: Same management, but if delivery is indicated, can
do C-section or induction of labor
- > 35 wks
pregnancy should be terminated rapidly with induction
of labor or C-section, depending on cervix and feto-
maternal situation.
96
- Eclampsia
delivery
prevent convulsions with MgSO4
can be used in first 48-72 hrs after delivery
Initial dose of 4g IV over 5-10 min then infusion
1g/ h for at least 24 hrs.
if woman has eclampsia, hyperreflexia, fits or
headache
monitor tendon reflexes, resp. rate (>16/min)
and urine output (>25 ml/h)
SE/toxicity
o diminished or abolished reflexes (knee
jerk = patellar reflex) – first sign
o decr. resp. rate -> resp. paralysis
o decreased urinary output
Rx
o stop MgSO4
o give antidote – Cal. Gluconate
if convulsions occur, treat with Diazepam 0.1-0.2
mg/kg IV or Phenytoin
4. Pre-eclampsia superimposed on chronic HT
after 20 wks
systemic features of pre-eclampsia develop on top of existing chronic HT
o c. PROM
in most cases (80-90%) the baby is born within 7 days
for best prognosis of baby, most important is administartion of C/S
Mx
lithmus paper test (Nitrizine test) – is there amniotic fluid in discharge?
monitor for signs of Chorioamniotitis
- cause: anaerobes, GSE
- Sx
fever
tachycardia
abd. pain, tenderness
offensive vaginal discharge
- Dx
FBE: incr. WBC, CRP – every 2-3 days
- Rx
A/B
expedite the delivery
Sterile speculum exam. – under strict sterile conditions
NO PV!! – risk of inf.
U/S – amount of amniotic fluid around the baby (oligohydramnios?)
Doppler for umbilical blood flow: is the baby receiving enough blood?
CTG – every 2-3 days
WBC and C reactive protein every 2-3 days.
high and low vaginal swab, rectal swab
97
Week 35-36
Sx
- nausea, anorexia, vomiting
- jaundice and fever
Cx
- renal failure
- fulminant hepatitis with hepatic encephalopathy
- pancreatitis
- DIC
Dx
- liver and renal failure (urea and uric acid ↑)
- AST and ALT ↑(but not as high as in viral hepatitis: 200 not 400)
- Bilirubin ↑
- ALP usually normal
- liver biopsy – confirms Dx
Rx
- urgent admission to ICU
- urgent termination of pregnancy (life-saving for mother and
baby)
- prevent/ treat DIC
- may require liver transplant
2. Intrahepatic cholestasis of pregnancy (hepatosis)
MC in 3rd trimester, but can start anytime
- usually in second ½ of pregnancy
due to estrogen sensitivity
Cx
- fetal distress
- fetal death
- preterm delivery
- meconium ingestion
- meconium aspiration syndrome
Sx
- intense itching, usually without a rash
Generally, itching is localized to abdomen, legs, palms,
and soles, but can be generalized.
Itching that increases in evening
Itching that doesn’t respond favorably to anti-
histamines or other remedies
- Often, elevated LFTs and serum bile acid counts
- Less common:
Darker urine
Lighter stools
↑ clotting time (due to associated vitamin K deficiency)
Fatigue
Increased nausea
Decrease in appetite
Jaundice - only in relatively small subset of cases
101
o 2. Gestational DM
screening test is glucose challenge test (non-fasting) at 26-28 wks (not OGTT)
N = 8 mmol/l
> 8 abnormal -> then do OGTT (fasting)
Criteria for diagnosis of gestational DM: Fasting > 5.5mmol/l and >
8mmol/l 2hrs after 75gms oral glucose.
- also do OGTT if high risk:
previous Hx of gestational DM
DM
family Hx of DM or gestational DM
Hx of macrosomia
PCOS
glycosuria
common in pregnancy – 25-50%
only 2-3% of them have DM
if present on 2 occasions, should do OGTT
Rx – like in pre-gestational DM
follow up with OGTT at 6 weeks and then every 5 yrs
likely to recur in subsequent pregnancies
30% developing DM later in life
- Vomiting
o causes
normal pregnancy
multiple pregnancy
hydatiform mole
UTI
intestinal obstruction
o Dx
U&E and creatinine – to assess the dehydration
U/S – multiple pregnancy? hydatiform mole?
urine culture – UTI?
single erect abd. X-ray – intest. obstr.?
- Acute pancreatitis in pregn. is assoc. with:
o cholelithiasis – MC
o alcohol intake
o cocaine use
o hyperparathyroidism
o abdominal trauma
- pain in lumber area while walking, 3rd trimester - refer to physiotherapy
- fetal movements felt by
o 18 wks –multigravida
o 20 wks - primigravida
- can’t feel fetal movement
o 1st step – intermittent auscultation
don’t hear anything -> 2nd step = U/S
hear something that worries you (bradycardia, etc.) -> II step = CTG
CTG normal
103
- Mx
< 32 wks – U/S
> 32 wks – repeat CTG
o (another approach) if normal auscultation (hypoxia)
CTG
if ok discharge + do kick count chart (normal: 10 movements/day)
if abnormal auscultation
CTG + U/S
- Multiple pregnancies
o assoc. with
↑perinatal morbidity and mortality (5-10x)
↑post-partum hemorrhage (uterine atony)
↑IUGR of one or both twins
↑umbilical cord prolapse (esp. for 2nd twin)
o not associated with feto-maternal hemorrhage
- Oligohydroamnios
o Mx
U/S
RFT
regular CTG
lupus AB
- Polyhydroamnios
o risks
PROM
preterm labor
cord prolapse
APH
malpresentation
- Pubic symphysis diastasis (pelvic osteoarthropathy)
o separation of pubic bones (due to relaxation of ligaments during pregnancy)
o II-III trim or early postparthum
o Sx
pubic pain aggravated by walking/ moving
pubic joint is very tender
o Dx
confirmed by U/S
post-partum – X Ray
o Rx
bed rest on firm mattress
- Abdomen big for date (fundus > age)
o wrong date
o polyhydramnios
fetal malformations
multiple pregnancy (twins)
DM
infection: CMV, toxoplasmosis
chorioangioma of placenta
104
o DM – macrosomia
o fibroids
o twins
o Rh incompat. – MC cause of hydrops fetalis
o ABO incompatibility
- Abdomen small for date (fundus < age)
o Wrong date
o Small baby – in fetal malformation
o Oligohydramnios– in fetal malformation
o IUGR
- CTG:
o usually performed after 26 weeks (before not very accurate)
o not usually done
not superior to intermittent auscultation
has not ↓ incidence of cerebral palsy or other neonatal developm. anomalies
rarely a predictor of previous fetal oxygenation – unless profoundly abnormal
poor predictor of current fetal oxygenation - unless profoundly abnormal
o Indications
high risk pregnancy: HT and DM mom, etc.
overdue pregnancy > 40 wks (2 times/ week)
on Oxytocin
color of water is brown or green
bad baby heart beats
o Side Effects
↑ risk of obstetric intervention (instrumental delivery or C-section)
o 2 lines:
above - baby’s heart
below - uterus contractions
o we check fetal heart rate, fetal movements and uterine contractions to identify the
presence of fetal hypoxia
1. Baseline FHR = mean level of FHR when this is stable (excluding accelerations
and decelerations)
Normal: 110-160 (150?)
< 110 Bradycardia
- ↑ vagal heart tone
- fetal heart block
- cord compression
- fetal hypoxia
>150 Tachycardia
- fetal inf.
- fetal hypoxia
- maternal fever
> 200 – fetal arrhythmia
2. Baseline variability – minor fluctuations of baseline
normal: 5-15 (10-15?)
reduced or incr = fetal distress
lost:
105
- Mx
non-reassuring pattern in I stage of labor
reposition woman (left, right position)
give O2 via face mask
if she was on oxytocin, slow it or stop it
-> then check CTG again
o if it didn’t improve -> perform fetal
scalp blood sampling (with
amniotomy)
if Ph <7.2 -> C-section
Abnormal CTG – 2 of the following features in the non-reassuring type
are present or
- baseline FHR < 100 or > 170
- variability is absent (<3) = monotonous trace
- late decelerations (especially prolonged > 3 min)
=> immediate delivery
vaginal – if cervix is fully dilated
C-section – if cervix is not fully dilated
Most ominous – indicating severe fetal compromise
- 1. persistent late decelerations - worst
- 2. severe variable decelerations
- Appendicitis in pregnancy:
o Dx
difficult, due to:
the displacement of appendix by enlarged uterus – higher the later the
condition occurs during pregnancy
tenderness more difficult to localize, since appendix is behind large
uterus
confusion with other diseases
- UTI
- hyperemesis gravidarum
- right ovarian cyst complication
- red degeneration of fibroid
- small concealed placental abruption
o Rx – Appendicectomy
- DVT in pregnancy
o Anticoagulant throughout pregnancy
use Heparin instead of Warfarin (therapeupric doses for 3 months then prophylactic
doses for remainder of pregnancy until 6 wks postpartum)
Heparin = Large molecule size => can’t cross placenta (no anticoagulant
effect on baby). Therapeutic dose = 2 times prophylactic dose.
reversal of anticoagulant effects can be achieved faster than warfarin
Warfarin
SE
- Can’t be used in 1st trimester (Teratogenic)
can be given during 13-36 wks but its effect is slower
to reverse
107
- miscarriage risk
- stillbirth
- neurological problems in baby
- crosses placenta and has anticoagulant effects on baby as well ->
hemorrhg. in mother and baby
o 6 wks post-partum heparin
- Impaction of a retroverted uterus (e.g. 16 wks - MCQ)
o Sx
lower abd. pain, urinary retention
- Thrombocytopenia
o causes
incidental thrombocytopenia of pregnancy– MC
not significant unless < 50x109/L
pre-eclampsia – when severe = HELLP syndrome
immune thrombocytopenia
SLE
- Maternal mortality
o 1:10.000 in Aus.
o causes
Primary pulmonary HT – 50% die during pregnancy or puerperium
Severe pre-eclampsia and eclampsia
PE
Postpartum hemorrhage
Amniotic fluid embolism
Anesthetic accidents
- IUGR
o viscera least affected is the brain
o can be
Asymmetric
MC- AC is affected
due to placental dysfunction
Biparietal head diameter (BPD) is last one to be affected
Symmetric
more rare
causes
- intrauterine infections
- other intrauterine abnormalities
All parameters are reduced, BPD is reduced alongwith others
- Premature delivery
o causes
increased uterine size
macrosomia
polyhydroamnios
multiple pregnancy
shortened cervix < 1.5 cm
open cervix especially if:
internal OS is open
108
Lochia rubra (or cruenta) is the 1st discharge, red in color because of
large amount of blood it contains.
- It typically lasts no longer than 3 to 5 days after birth.
Lochia serosa is the term for lochia which has thinned and turned
brownish or pink in color. It contains serous exudate, erythrocytes,
leukocytes and cervical mucus.
- This stage continues until around the 10th day after delivery.
Lochia alba (or purulenta) is the name for lochia once it has turned
whitish or yellowish-white. It contains fewer red blood cells and is
mainly made up of leukocytes, epithelial cells, cholesterol, fat & mucus.
- It typically lasts from 2nd through 3rd to 6th week after delivery
- Puerperial fever/ sepsis (1 to 10th day after delivery)
o > 38OC
o > 24 hrs
o causes
3 Bs
Birth canal – endometritis (MC, 75%, with high grade fever)
- post-partum endometritis or pyrexia (fever, tender uterus, foul
smelling lochia):
Ampicilin (or amoxycylin) and metronidazole
if not improving add Gentamycin
Breast - mastits
Bladder – UTI
+ DVT
MC
UTI – E.coli
breast inf – Staph. aureus
wound inf. – if C-section
less common
Genital – endometritis – strepto.
DVT?
o Dx
U/S: bulky uterus
inspection of lower tract for infected tears or lacerations
MSU for microscopy, culture, sensitivity
vaginal swab
signs of mastitis
o Rx
1 - init. empirical: penicilin + metronidazole + gentamycin
after result, adjust for sensitivity
- After birth - http://en.wikipedia.org/wiki/Fetal_circulation
o Umbilical vein closes and becomes ligamentum teres
o Closure of ductus venosus
o Lateral umbilical artery becomes lateral umbilical ligament
o Ductus arteriosus is closing due to increased local PG
o increased venous return from the lungs causes pressure to increase in the left atrium,
which closes the foramen ovale flap valve
111
o MC cranio-facial malformation
o causes
Benzodiazepine
Antiepileptics - carbamazepine
Amphetamines
Rubella
Genetic factors
Kalman syndrome
Smoking
Alcohol
- Alcohol abuse:
o from 80 g alcohol/ day => Fetal alcoholic syndrome
Microcephaly
Mental retardation
Poor muscle tone
short palpebral fissure
long and smooth philtrum
underweight till puberty
short stature
septal defect
facial hypoplasia
joint deformities
low IQ
attention deficit
forebrain malformation
- Cocaine abuse:
o IUGR
o Placenta abruption
o Premature labour
o Intraventricular hemorrhage
o Developmental delay
o Stillbirth
o Teratogenic effect not proven
- fetal malformations can be assoc. with umbilical cord vessel anomalies
o Normal – 2 arteries & 1 vein (3 vessels cord)
o MC anomaly assoc. with fetal malformation = only 2 vessels in cord
1 artery + 1 vein – baby can survive
otherwise – stillbirth in 1st trimester
Antenatal care
o 1st antenatal checkup
Confirm pregnancy
FBE
Blood group, Rh, Coomb’s test
Blood sugar level
Random
Fasting
MSU, urine analysis, electrolytes
114
LFT
Infections
Rubella
Hep. B
HIV
Syphillis - VDRL
CMV
- consider Varicella, Hep. C
o Hb electrophoresis – Thalassemia
o for Gestational DM
Screening test is Glucose challenge test (non-fasting) at 26-28 wks (not OGTT)
Normal = 8
> 8 is abnormal -> then do OGTT (fasting)
- also do OGTT if high risk: Previous Hx of gestational DM, DM,
family Hx of DM or Gestational DM, Hx of macrosomia, PCOS,
Glycosuria.
Insulin requirements
↑ in last trimester
↓ immediately after delivery
Fetal hypoglycemia
should be checked @ 4 hrs after delivery or after second feeding,
whatever comes first
o International travel/ flight
after 28 wks – Better to avoid
after 36 wks – Prohibited
o Pregnancy + cardiac disease
never give ergometrine
don’t put in lithotomy position
watch for fluid balance
o VSD in pregnancy
if only VSD – can go for vaginal delivery
if VSD + transverse lie – C-section
o ≥ 42 wks (41 wks + 6 days) = Postdated pregnancy
Induction and C/S then
U/S – check amniotic fluid index – N > 5
CTG – if CTG abnormal, do pH test (fetal scalp)
Meconium stained indicates fetal distress
We have to do CTG before Dx of fetal distress
pH < 7.2 = fetal hypoxia
- have to check cord prolapse too
o after ROM – check for cord prolapse
o C/S in
Breech presentation
Fetal distress
Labour progress is slow
Labour:
Contractions:
115
< 30 weeks: small localized contractions every 1 min + higher amplitude contraction every 30-30 min
after 30 weeks: more intense (Braxton Hicks contractions)
after 36 weeks: increasing progressively until labour starts
labour starts: 1 contraction every 10 min, lasts 20 sec
late labour: 2-4 contractions every 10 min (1 every 2-4 min), last 40-90 sec
contractions still occur for 48 hrs after delivery with decreased frequency
Cervix dilatation:
anytime after 34 weeks, but usually later (especially in primigravida)
dilatation of min. 1 cm/h during labor
Onset of labour: dilatation of cervix more than 2 cm + painful contractions at least every 10 min with
increasing frequency
Duration of labor: 6 (multipara) – 9 (nullipara) hrs (90% within 12 – multiparae to 16 – nulliparae – hrs)
Stage I – till complete cervical dilatation (10 cm); only passive uterine contractions
- has a:
o passive phase
o active phase – from cervix dilated 3-4 cm to fully dilated; cervix dilates faster,
contractions become more painful
Stage II – till birth: passive uterine contractions + active abdominal contractions
- if it lasts more than 2 hrs -> vacuum extraction or forceps
Stage III: placenta expulsion: 15-30 min after birth of baby. Wait 2-3 min after birth before clamping the
umbilical cord
- Labour
o epidural – up to 7 cm dilatation
o monitoring of fetal well being
uncomplicated labor – intermittent auscultation (stethoscope with Doppler)
complication - CTG
o There are 3 signs of onset of labor:
A bloody show
passage of a small amount of blood or blood-tinged mucus through
vagina near the end of pregnancy
It can occur just before labor or in early labor as the cervix changes
shape, freeing mucus and blood that occupied the cervical glands or
cervical OS
Rupture of membranes (waters breaking)
Onset of contractions
o 1st stage
116
starts when
cervix is at least 2 cm dilated
contr. become painful and regular, at progressively shorter intervals (3-
5 min), and lasting > 1 min
Duration
average 8.25 hrs in nulliparae, 5.5 hrs in multipare
Phases
a. latent: onset -> 4 cm dilat.
b. active: 4 cm -> 10 cm dilat.
- 1 cm/ hr dilatation
Pulse, temp., BP every 2 hrs
monitor contr.
monitor FHR every 15 min
PV exam every 4 hrs
if ROM – check for cord prolapse
every woman should receive Syntometrine (ergometrine + oxytocin), to
promote contr.
minimize bleeding (16 x less)
nd
o 2 stage – begins when cervix is fully dilated
duration
< 45 min – multiparous (average 15 min)
< 2 hrs – nulliparous (average 1 hr)
> 2 hrs – can be:
- 1. Obstructed labor - very low chance woman will deliver
naturally
if on epidural (no urge to push) we can wait up to 3 hrs
causes:
Pelvic swellings: Ovarian tumors, fibroids,
ectopic pelvic kidney, very distended urinary
bladder
o (not cystocele or rectocele – are soft,
can easily be pushed out of the way)
Cephalopelvic disproportion
Large baby: DM, hydrops fetalis, etc.
Postterm pregnancy
MCQ: MC finding = 4 cm of head is palpable in abd.,
although bony head is at ischial spines on pelvic
assessment.
Rx
if good contr. -> assisted delivery
o Forceps
more traumatic for mother not
for baby
↑in vaginal tears
↑need for episiotomy
o Vacuum extraction
more traumatic for baby
117
118
Erb's Palsy - Paralysis of arm caused by injury to upper group of arm's main nerves,
specifically if upper trunk C5-C6 is severed - loss of sensation in arm, paralysis and atrophy of
deltoid, biceps & brachialis muscles. Position of limb under such condition is characteristic:
arm hangs by side and is rotated medially; forearm is extended and pronated. Arm can’t be
raised from side. All power of flexion of elbow is lost as is also supination of forearm.
Resulting biceps damage is main cause of this classic physical position commonly called
"waiter's tip." Risk factors – breech presentation, shoulder dystocia
- 2. Inefficient or incoordinated labor
Feature on PV examination Obstructed labor Inefficient/ incoordinate labor
Moulding of fetal head ++ Usually none
Caput formation on fetal head ++ ±
Cervical oedema Anterior lip oedema Usually none
Fetal tachycardia ++ and progressive +
Station of fetal head – relation Just at or above ischial Can be above or below ischial
of lowest part to ischial spines spines spines
Amount of head palpable above > 2 finger breadths Usually < 1 finger breadth
pelvic brim when lower point of (most important feature)
head is at ischial spines
monitor FHR every 5 min
if FHR falls < 100 + for > 2 min => PV (cord prolapse?)
monitor contr. – normal: 60-90 seconds every 2-4 min
if not good give oxytocin
o 3rd stage:
duration
15 min in both nullipara and multipara (90%)
If placenta still not delivered after 15 min
- encourage contraction by rubbing uterine fundus
- no effect => manual removal
MC SE = Uterine inversion
o total duration of labor:
9.5 hrs in nullipara
6 hrs in multipara
o Cardinal movements of labor:
engagement
descent
flexion
first 3 occur simultaneously
internal rotation
119
extension
external rotation
expulsion
o sign of progress of labor
incr. strength, duration and frequency of uterine contraction
descent of fetal head into pelvis
rotation of fetal head (occipito-transverse to occipito-anterior) on abd.
palpation
best sign of progress – progressive increase in cervical dilatation (1cm/hr)
with effacement (shortening) of the cervix
rotation of fetal head (occipito-transverse to occipito-anterior) on pelvic exam.
descent of head within and through the pelvis
above spines -> spines level -> below spines -> coccyx -> vulva
- Induction of labor
o indic.
Prolonged pregnancy > 42 weeks
Hypertensive disorders in pregnancy
Pregn. induced HTN
Pre-eclampsia
Eclampsia
PROM
Intrauterine fetal death (IUD)
IUGR
Antepartum hemor.
Isoimunisation
ABO incompat.
Rh incompat.---Hydrops fetalis
o CI
absolute
Cephalopelvic disproportion
Placenta praevia
Vasa praevia
Fetal distress
previous classical C-section (not low segmental)
invasive cervical CA
cord presentation
some abnormal presentations
- Breech pres.
complete – ok (bent knee)
frank – ok (knee extended)
incomplete – NOT OK (with feet down)
o when to start: when cervix is ready/ favorable -> assesed with Bishop score
1. Cervix dilatation
2. Cervix length
3. Cervix consistency
4. Cervix position
5. Head station (in raport to ischial spines)
120
0 1 2 3
Dilatation (cm) <1 2 3 >4
Length (cm) >4 3 2 <1
Consistency Firm Mild Soft
Position Post. Ant. Central
Head station -3 -2 -1 >0
score 0-4 – cervix not ready for induction (very high risk to fail induction)
score at least 5 to start induction (with amniotomy)
o Procedure:
start with intravaginal PG gel
PG E2 – Dynoprostone – for alive baby
PG F2 alpha – Dynoprost
- indic.
dead fetus
missed abortion
termination of pregnancy
evac. of hydatidiform mole
wait until cervix will be ready (if no fetal distress) with Bishop score ≥ 5
then do amniotomy
SE
- cord prolapse
- inf.
after amniotomy, deliver within 5-8 hrs
after amniotomy, use oxytocin infusion (drips) to promote contr.
then proceed with normal delivery
Preterm premature rupture of membranes: rupture of membranes before 37 wks
Premature rupture of membranes: rupture of membranes after 37 wks without onset of labor.
Position of baby: important after 28 wks
Lie:
- longitudinal (99%)
- cephalic – 95%
- breech – 4%
- oblique
- transversal
Presentation:
- Cephalic – 95%
- Vertex – head flexed, occiput leads
- Face - head extended, face leads
- Brow – head slightly extended (between vertex and face)
- Breech (buttocks down) – 3.5%
- Shoulder – 0.5%
- Malpresentations
o Breech presentation
15% at 30 weeks, but only 3% at birth
↑ risk for fetus
- due to
121
intracranial hemor.
asphyxia
fractues of humerus, femur or clavicle
- preterm and late post term babies – mortality 12%
- term babies – mortality 1%
Types
- with extended legs (frank) – 65-70%
- with flexed legs (complete)- NVD can be attempted
- footling (incomplete) – one foot comes first (rare)
Rx
if still breech pres. at 37 wks, attempt cephalic version - easier if the baby has
flexed legs
Ext. cephalic version @ 36 wks or end of 37 week + tocolytic
CI
Cephalopelvic disproportion
Placenta praevia
Multiple pregnancies
Antepartum bleeding
Hx of uterine scar, HTN, bad obstetric Hx
PE
Hx of unstable lie
Small for date baby
absolute indic.
shoulder presentation
face presentation
Risk of cord prolapse: first do PV to exclude cord prolapse
- Rx
if the cord is still puslating, push the presenting part
and cord as far in as possible (MCQ).
place mother in knee – chest position
urgent delivery
C-section – preferred
Vaginal delivery with forceps or vacuum
extraction avoiding cord pressure
- C-section – preferred, with decr. perinatal mortality (from 1.15% to 0.6%)
- normal delivery can also be used
baby with normal size
complete breech or extended legs
eyebrow presentation
head flexed
CPD excluded
labor onset spontaneously
e.g. if unexpected breech presentation with full cervical dilatation with
insufic. time to organize a C-section
o Transverse or oblique presentation
may convert to a longitudinal one later on
122
Dx – 1st - U/S to rule out placenta previa (this is what might be causing the baby
to have this presentation, prevents him from having a cephalic presentation)
Mx
- at 36 weeks – Cephalic version
- > 36 weeks: wait for normal labor
if beyond 37 wks (term) best Mx is C-Section
- Malpositions
o types
Occipito-posterior – MC
11 cm (vs. 9.5 for normal position)
assoc. with poor quality uterine contraction
- if this is excluded – Cephalopelvic disproportion
incoordinate uterine action -> ↑ intrauterine pressure -> incr. fetal
distress (MCQ).
- CTG is recommended for monitoring
- even more common when oxytocin and epidural were used
in this case CTG is mandatory
slow labor
- Rx
labor can be stimulated with
amniotomy
oxytocin
epidural is often necessary
C-section may be necessary in case of obstructed
labour or fetal distress
occipito-transverse
(occipito-ant. = N)
face
brow
o Rx
if no other problems – vaginal delivery in most of them (especially in occipito-
post. and occipito-transverse)
exception: Face – vaginal delivery may be impossible => C-section
C-section – in prolonged labor with maternal exhaustion, obstructed labor, CPD,
fetal distress, selected primigravida, face and brow (only in nulliparous not
multiparous) presentation .
Post partum depression occurs in 30% of women in first 6-12months postpartum
Post partum Blues occur during first 2 weeks after delivery.
- Anesthesia
o Epidural:
Anaesthetist conducting an epidural places catheter in the mid-lumbar, or lower
back region of spine.
In adults, spinal cord terminates around the level of disc between L1 and L2 (in
neonates it extends to L3 but can reach as low as L4), below which lies a bundle
of nerves known as cauda equina ("horse's tail"). Hence, lumbar epidurals carry
a very low risk of injuring the spinal cord.
123
o at 1 and 5 min
0 1 2
Appearance/ color Absolutely blue Centrally pink, Pink
peripherally blue
Pulse/ heart rate Absent < 100 > 100
Grimace/ response to No response Some facial grimace Cries
stimulation (place
suction catheter in
nose of child)
Activity/ muscle tone Floppy, flaccid & Some flexion Good active
hypotonic limbs movement
Respiration effort Absent Gasping, irregular & slow Normal good crying
Good > 7
How ready is this child =
heart rate
resp. effort
irritability
tone
colour
low score at 1 and 5 min => child needs resuscitation
causes
significant hypoxia
perinatal asphyxia
Apgar score
The test is generally done at 1 and 5 min after birth and may be repeated later if score is and
remains low.
- Scores 3 and below are generally regarded as critically low.
- 4 to 6 fairly low
- 7 to 10 generally normal.
A low score @ 1min indicates neonate requires medical attention[3] but is not necessarily an
indication that there will be long-term problems, particularly if there is an improvement @
5min. If Apgar score remains below 3 at later times such as 10, 15, or 30 minutes, there is a risk
that child will suffer longer-term neurological damage.
Gynecology - OK
Breast pathology
- Mastalgia:
o 30-50 yrs (MC 35-45 yrs)
o Causes:
MC – Cyclical mastalgia
Pregnancy
Caffeine
Breast CA
risk is < 10%
e.g. mastitis carcinomatosa – red and hot breast, during lactation
Fibroadenoma
Mastitis
125
Drugs
OCP
HRT – Diffuse bilateral pain
- Rx – ↓ estrogen dose
Theophylline
o Types
diffuse, bilateral and cyclical = Cyclical mastalgia
30-50 (35) yrs
hormonal basis
causes
- MC = benign mammary dysplasia (fibroadenosis, chronic
mastitis, cystic hyperplasia, fibrocystic breast dis.)
30-50 yrs
Dx
mammogram – if diffuse lumpiness > 40 yrs
o shows calcifications
U/S
biopsy
Mx
large cysts - aspiration
Sx
- pain in breasts (mid-cycle till end of period) & feeling of lumpy
breasts
pain extend down inner aspect of upper arm
- possible - straw-like or green grey discharge from the nipple
- breasts diffusely nodular or lumpy
Rx – Murtagh 969
- Mild
reassurance
rule out fear of CA in patient
analgesic (paracetamol)
lifestyle advice
low fat, eliminate caffeine
wear good quality, comfortable bra
lose weight
- Moderate
Mefenamic acid (NSAID - inh. of PG synthesis)
add Vit B1, Vit B6
(Primrose oil – contains an essential fatty acid - Awad)
- No response
Danazol (progestogen = modified testosterone –
inhibits ovarian synthesis of estrogen)
norethisterone – progestogen
Diffuse, bilat. non-cyclical mastalgia
poorly understood
causes (may be)
- duct ectasis
126
- periductal mastitis
Rx
- much more difficult to treat
- exclude caffeine & lose weight
- Vit B1, Vit B6
- norethisterone – progestogen
Unilateral difuse non-cyclical
Mastitis – cellulits of interlobular connective tissue
- in lactating women with
cracked nipple
poor milk drainage
- causes
bact
MC cause – Staph. aureus (coagulase-positive)
o Rx
Flucloxacilin
Erythromycin
E. coli
Candida – after A/B
severe breast pain (hot knife, hot shooting
pains)
- Sx
a sore lump at first
then red tender area
fever
- Cx – Breast abscess
if persisting > 48 hrs + area of tense induration
develops
Rx
surgical drainage (under GA) or aspiration with
a large bore needle (under LA)
A/B
- Rx
Breast feeding should continue from both sides (milk
production not affected)
empty the breast well
flucloxacilin
or cephalexin
for candida – fluconazole
or nystatin
localised
Costochondritis (Tietze’s syndrome)
- constochondral junction becomes strained in persistent cough
- palpable swelling about 4 cm from sternal edge (enlargement of
costochondral cartilage)
- initiated or aggravated by deep breathing and coughing
- Self-limiting – may take a few mths
127
o Carcinoma – 22%
o Cysts – 10%
40-50 yrs, painful solid lumps.
associated with mammary dysplasia
regress after menopause
Dx
for breast cyst – 1st test is always U/S!
mammography
FNAC
MCQ: 45 yrs, painful solid lump in the breast – breast cyst (tense)
rapid growth – pain
o Breast abscess - 2%
o Duct ectasia
Looks like CA
A whole breast quadrant is indurated and tender
Green toothpaste-like nipple discharge
Dx – widespread linear and globular calcifications on mammography
Rx - Surgery
o Duct papilloma
Benign-----not premalignant
Bloody discharge
Rx – excision of duct and affected breast segment
o Lactation cyst (Galactocele)
Rx - Aspiration
o Paget’s syndrome of nipple
o Fat necrosis (traumatic)
after large bruise or trauma (e.g. protracted breast feeding)
with skin and nipple retraction
looks like CA
it usually disappears
Dx – excision biopsy
- Breast CA
o MC CA in women
o Lifetime risk: 1 in 11 women in Aus.
1 in 11 women will develop CA by age 75 – max around 60 yrs
o 1 in 25 women die of breast CA
o incidence rises with age and incr. in higher socioeconomic class
o Types:
MC - non-invasive: intraductal CA
invasive
invasive duct CA – 90%
lobular CA
o risk factors
Sex -100 x MC in women
Caucasian race
low in Asian countries
Age:
129
solid lumps
FNAC: 90-95% accuracy – better than mammography
indications for biopsy or excision of lump:
cyst fluid is blood stained
lump dn’t dissapear completely with aspiration
swelling recurs within 1 mth
- unsure/suspicion of CA: core biopsy -> histology (can Dx CA) –
radiologists do this under U/S guidance
FNAC can’t distinguish between CA in situ & invasive!
core biopsy can do that
tumor markers
estr. receptors – in 2/3 of breast CA
- good prognostic factor
progesterone receptors
o Staging
Manchester
I - Confined to breast
II - Confined to breast + palpable mobile axillary lymph nodes
III - Skin changes (fixation, cutaneous ulcers, peau d’orange) + fixed
axillary nodes, supraclavicular nodal involvement
IV - Distant metastasis
o Rx
workflow (dr. Gaya)
a. for younger women - wide local excision (quadrantectomy), with a 1
cm margin
- “sentinel node” procedure to detect if first node draining from
the breast (sentinel node) is involved
single most powerful predictor of subsequent
metastases and death = lymph node involvment
radiopharmaceutical injected at nuclear medicine
centre a day before surgery + on the day of surgery we
inject some blue dye close to the nipple:
we remove sentinel node during surgery, send it
to pathology & check it
o if not affected, we don’t remove lymph
nodes
o if affected, we remove all nodes
(axillary disection)
if more nodes are involved, we
do chemotherapy
- plus Radiotherapy – otherwise 40% chance of recurrence
indications
tumor > 5 cm
axillary node involvement > 3 nodes
positive of close tumor margins
132
COCP
Barrier methods
condoms
- < 5 pregnancies/ 100 women/ yr
diaphragms
IUD (can be inserted any time within first 12 days of start of menstrual bleeding)
with
- copper – affect sperm motility and transport
- progest. (Mirena – with levonorgestrel)
96-99% pregnancy protection
Post-partum
- 6 wks after vaginal delivery
- 12 wks after C-section
CI
- absolute
pregnancy
active PID
undiagnosed abnormal genital tract bleeding
previous ectopic pregnancy
severe uterine cavity distortion
- in nulliparous women?
Cx
risk of infection
bleeding
Side Effects:
- risk of ectopic pregnancy 10x > than with COC
- if pregnancy occurs, 40-50% risk of abortion or intraut. sepsis in
2nd trimester
- incr. risk of PID in 1st 30 days after insertion -> prophylactic
doxycycline (especially if having multiple sexual partners)
- extrusion, perforation and translocation of uterus
- may incr. bleeding for 2-3 mths, then disappears
if it persists, remove IUD
– Mirena reduces or stops bleeding
- lower abd. cramp-like pains
Spermicidal agents
adjuvants
when used alone < 10 pregnancies per 100 women/ yrs
Rhythm
coitus interruptus
calendar method
- facts
ovulation occurs always 14 days before her period
(luteal phase is always 14 days)
sperm survival is up to 6 days
ovulated egg can be fertilized during 24-36 hrs following
ovulation
135
- method
keep track of length of cycles: e.g. between 26-29 days
=> ovulation between day 12-15
safe periods -
up to 12-6 (how much sperm survives) =1st 6dys
after day 15 + 2 (how much time ovum can be
fertilized) = day 17
unsafe from day 6 to 17
Basal body temp.
- 2-3 days after ovulation, body temp.↑0.3o C for the rest of cycle
(over temp. of previous 6 days) -> safe from 2 dys after rise of
temp. (4-5 dys after ovulation) until next period.
- + calendar method for safe period at the beginning of her cycle
Billing method
- fertile mucus – clear, watery, stringy, incr. in amount, feels
lubricative
on ovulation – highest secretion
ovum survives for 2 days + 1-2 days extra for
safety => safe = 4 days after maximal mucus
secretion (spinbarkiet phenomenon)
(ovulation) MCQ
then abrupt change to non fertile mucus
- not fertile mucus – more whitish, thick, sticky
- failure rate: 1-2 (average 3) / 100 women/ yrs
Lactational amenorrhoea - Awad
- during breastfeeding
- < 1% risk of pregnancy (90% safety – Awad)
- conditions
exclusive breastfeeding
< 6 months
mother didn’t get her period yet
+ Progest. Only Pill (POP) (main action is thickening of cervical mucus)
mini-pill
- not as efficacious as OCP bc it doesn’t inhibit ovulation (but
almost same) and are taken regularly for 28 days of cycle (no
inactive pills).
- pregnancy rate 3/ 100 women/ yr
- contains
lovenorgestrel 30 µgms/ day
norethisterone
- Side Effects (only few)
cycle irregularity (oligomenorrhea, irregular bleeding
or amenorrhea) and weight gain
reduces cycle to < 25 days
- Indications
> 45 yrs
smokers > 35 yrs
136
- Essure procedure
introduction of microinsert in tubes-> occulsion of tubes
+ Yasmin contraceptive pills (Awad)
can also help for wt. loss
decr. fluid retention
decr. acne formation, decr. greasy skin
- Post-partum contraception
o C.I. - OCPs or NUVA ring – combined estr. or prog. (estr. would suppress lactation)
o can give any progesteron
- Combined Oral Contraceptive Pills: (act on hypothalamus MCQ)
o inhibits hypothalamic and pitutary function => Anovulation
o risk of pregnancy: 1-3 ideally (2-6 in practice)/ 100 women/yr
o OCP – safe to be used for 10 yrs, up to the age of 50 yrs
o contain
estr – MC ethinyl estradiol (20-30ug)
prog.– MC levonorgestrel
o types
microgynon 30 – first line
microgynon 50 – indic:
in epileptics and other enzyme inductors
if with microgynon 30 she has breakthrough bleeding that doesn’t
resolve in time
for control of menorrhagia
failure of microgynon 30
o Woman > 35 yrs
smoker -> mini-pill (POP)
non-smoker -> mono-phasic OCPs
o Advantages
effective Rx for most menstrual cycle disorders
primary dysmenorrhoea & menorrhagia
↓ Fe-deficiency anemia
↓ benign breast dis.
↓ Ovarian cysts
50% ↓ in PID
↓incidence of ovarian, endometrial and colorectal CA.
does NOT protect from cervical CA (slightly ↑ probably due to ↑ sexual
activity)
+ decr. sebacous disorders
+ decr. thyroid disorders
+ decr. endometriosis, fibroids?
o SE
Thromboembolic dis.
Venous:
- DVT
PE
- rarely mesenteric, hepatic and kidney thrombosis
Arterial:
138
- MI
- stroke
thrombotic
hemorrhagic
- rarely retinal and mesenteric thrombosis
CAs
possible incr. In
- Cervical CA {Breast CA minimal (has no effect latest research
shows)}
protective in
- endometrial, ovarian and colorectal CA
OCP are not recommended with any antihypertensives. Condoms can be used.
Migraine – Rx: discontinue COC and give POP
depression – Rx: decr. or change the progest.
Acne – Rx: ↑ estr. dose (estr. will clean acne)
Breast feeding, DM and smoking >35 yrs: POP
Chloasma – Rx: POP
Amenorrhoea – Rx: incr. estr. and decr. progest.
PCOS: An OCP containing ethinyl estrsadiol + cyproterone acetate
Excessive fluid retention: ethinyl estrsadiol + drospirenone
Dysmenorrhoea or menorrhagia – Rx: increase progest.
Breakthrough bleeding
20% at beginning
3% after 3-6 mths
- Rx - keep using OCPs at same day, every day at same time
if persists after 3 mths, ↑ dose or change to different
type
early to mid cycle bleeding – ↑ estr. –
Microgynon 50
late cycle – incr. prog. or change type
Breast problems
fullness/ tenderness: decr. estr.
mastalgia: decr. progest.
Libido loss: incr. estr.
Weight gain
constant – decr. or change progest.
cyclic – decr. estr.
nausea, vomiting – decr./change/stop estrogen
post-pill amenorrhoea
delayed onset of ovulation after stopping OCPs (Usually periods resumes 2–3
days after stopping tablets).
50% - after 2 weeks
90% - after 6 weeks
1% - hasn’t occurred after 12 mths
HTN? (blue book 3.201)
stop OCP, use a different contraception method & reassess in 3 months
- HT will usually settle
139
o Special interactions:
warfarin and oral hypoglycemics doses have to be adjusted
if using warfarin – STOP OCPs (warfarin is more important)?
High doses of Vit. C, griseofulvin, rifampicin, anticonvulsants (except Sod.
valproate) interact with COCs. Phenobarbitone, phenytoin, primidone,
carbamazepine, oxacarbezepine, topiramate all are enzyme inducing anti-
epileptics. If we have to use these drugs along with hormonal contraceptive
methods either ↑ dose of estrogen in pill or use mirena or barrier method.
Following anti-epileptic drugs are non inducers and don’t effect efficacy of
hormonal contraceptives. Valproic acid, gabapentin, levetricetam , pregabalin,
vogabatrin.
if using A/B or if vomiting/ diarrhea: they might inh. the effect of OCPs -> use
another contraceptive method beside OCPs (condoms)
o Contraindications:
Absolute – Murtagh 961
1
- Pregnancy
- First 2 wks post-partum/ post abortion – there’s still bleeding
happening and OCPs would increase risk of clots, thrombosis
2
- Thrombembolic Hx
DVT
PE
Thrombophilia
- Coronary artery disease
- Cerebrovascular history
- Migraine
3 Estrogen dependant tumors
- Breast
- Cervix
- Ovarian
- Uterus
4
- Active liver diseases
- Polycythemia vera
Relative
heavy smoking/ smoker > 35 yrs old (prescribe POP)
diagnosed abnormal vaginal bleeding
HTN
DM
hyperlipidemia
long term immobilisation
complicated valvular heart disease
breast feeding – mini-pill (progest)
4 wks before surgery and 2 wks after
gall blader or liver dis.
Chloasma (prescribe POP)
140
cardiac disease
o Protective for:
Bowel CA but not for ovarian CA
Cardiac dis.
Alzhimer dis.
if given from time of menopause
- decline in cognitive fc. (= early manifestation of Alzhimer)
- BUT
doesn’t decr. the rate of progression of Alzheimer
doesn’t make advanced Alzhimer less severe
if started at 60-65 yrs, incidence of Alzheimer is ↑
o SE
Premenstrual syndrome
Nausea and breast disorders
Bleeding problems
↑ risk of Breast CA
after 5 yrs of combined estrogen + progesteron
after 7.2 yrs of estrogen only
↑risk of stroke!
o CI
estr.-dep. CAs (Estrogen containing HRT is CI in Breast CA)
Breast CA
- Rx just Biphosphonates to prevent osteoporosis
Endometrial CA
recurrent thrombembolism
Hx of coronary artery disease
uncontrolled HT
undiagnosed vaginal bleeding
active liver disease
active SLE
otosclerosis
acute intermittent porphyria
smoking?
o Rx
with uterus present, no CI
first 2 yrs after LMP
- Best choice: Cyclical HRT: Continous daily estr. + cyclical
progest.(MPA) (12 dys/ mth)
need to add progesteron (min. 12 dys/ cycle) to protect
uterus.
usually causes predictable periods, generally
comencing 2 days after progesteron course was
completed.
can cause breakthrough bleeding -> is she can’t tolerate
it -> continuous estr. + progest.
2 yrs after LMP – Continuous HRT: continuous estr. + progest (MPA).
143
other SERMs
- Tamoxifen
- Clomiphene
Calcitriol = Vit. D metabolite
if using this, don’t use Ca
Good dietary intake of Ca
800 mg/ day premenopause
1000 - 1500 mg/day postmenopause
- 1.5 glass of milk = 1.5 g Ca = enough/ day in osteoporosis (Calin)
Ca supplementation is poorly absorbed after menopause => inefficient in
preventing bone loss, even when combined with vit. D, unless estrogen
suplementation is given. Ca citrate is better absorbed than carbonate.
o Prevention:
Menopause – patches of HRT, for 2-3 yrs
increased dietary intake of Ca
incr. exercise
decr. smoking, alcohol, coffee
monitor with regular bone density scans
Amenorrhoea
- Primary amenorrhoea
o types
Sexually infantile
Short stature and non functioning ovaries (streak gonads)
- Turner syndrome – 45X0
gonadal dysfunc. – infertility, lack of breast develop.
Non functioning ovaries, uterus and vagina normal
web neck (cystic hygroma)
wide carrying angle, widely spaced nipples
low ear insertion & low hairline
vision and hearing problems
lymphedema, chromatin negative buccal smear
coarctation of aorta, bicuspid aortic valve
horseshoe kidney
- hypothyroidism
Normal stature
- Kalman Syndrome – hypothalamo-hypogonadism
deficit of GnRH => lack of FSH and LH
anosmia, hyposmia
optic problems: color blindness or optic atrophy
cleft palate
- true gonadal agenesis
Masculinized
Congenital adrenal hyperplasia
- 95% due to 21-hydroxylase defic. - AR
normal male genitalia , ambiguous female genitalia /
enlarged clitoris
baby vomits, decr. Na, K incr. – salt-wasting
146
PCOS
PCOS POF Ovarian resistant syndr. Menopause
FSH slightly ↑ or normal Very incr. Incr. Incr.
LH Very incr. Very incr. Incr. Increase
(LH:FSH = 2:1/3:1)
Estr. N Decr. Incr. Decr.
Testosterone Incr.-->
(free, DHEA) Hirsutism
U/S > 10 cysts <10 cysts 3-4 cysts
o Sx
irreg. cycles (anovulatory), oligo- or amenorrhoea, infertility
obesity
hirsutism, acne
± DM
o MC cause of anovulatory infertility
o causes
insulin resistance
incr. androgens (LH and FSH)
o risk of endometrial hyperplasia -> endomet. CA (unopposed estrogen)
o Dx.
Very high LH (LH > FSH, LH:FSH = 2:1/3:1) – normally FSH > LH
148
estr. N
↑ Androstendione (testosterone)
± insulin incr., blood sugar level incr.
sex hormone binding globulin decr.
transvaginal U/S
if thickness > 5 mm
- hysteroscopy + biopsy
if thickness < 5 mm – CA very unlikely
Rostterdam Dx criteria – at least 2 of the following:
1. Oligo- or amenorrhoea
2. Signs of hyperandrogenism:
- Clinical: Acne, hirsutism, deepening of voice, clitoromegaly
- Labs.: ↑ Testosterone & DHEA
3. U/S ≥ 10 (12) cysts in any of ovaries or both (at the periphery)
o Rx
lifestyle modification
Metformin – Best Rx
OCP
↓ Cyst formation, acne & testosterone
for hirsutism
wax
laser
wants to get pregnant: metformin and clomiphene have equal efficacy, but:
BMI > 25 – Metformin
BMI normal – Clomiphene
Blue book p. 527 says:
- 1. Metformin &
- 2. Clomiphene but both are equally effective
- 3. Laparoscopic ovarian drilling, IVF, gonadotrophin therapy –
when 1. and 2. have failed
PCOS with normal prolactin:
Rx – Clomiphene citrate
- SERM
- stimulates pituitary gland to produce more (mainly FSH) & LH =>
ovulation and superovulation
- effects
Excessive estrogen
fluid retention, breast enlargement
hot flushes (vasomotor sympt.)
o cold and warm feeling on face, neck
and upper thorax
dev. of more than 1 follicle and release of
more than 1 ovum => multiple pregnancy (5-
10% risk)
inadequate ovulation (corpus luteum dysfc.)
enlarged ovaries with multiple cysts, pain and
↑risk of torsion
149
Physiological - DUB
- ovulatory (regular cycle)
- anovulatory cycles (irregular cycle)
MCQ: MC cause of menorrhagia (irregular cycles)
suddenly occuring in a 45 yrs old woman, previously
OK (disorder of ovulation)
Iatrogenic
hormonal – HRT
non-hormonal – IUD
anticoagulants
- Uterine fibroids: (Regular cycle + enlarged uterus)
o encapsulated uterine smooth muscle fiber tumors (leiomyoma – pl. is leiomyomata)
o types
intramural - MC
submucosal (in muscle beneath the endometrium) – MC to cause menorrahgia
subserosal (underneath the peritoneal surface of uterus)
intrauterine – pedunculated causes continuous bleeding
o Estrpgen dependat decrease by menopause
o in fertile women, especially in obese women
o Sx
totally asympt or
menorrhagia
dysmenorrhea, pelvic discomfort (if big)
dysuria, constipation, back pain
if pedunculated – torsion
infertility
calcification
in pregnancy
red degeneration of fibroid
- mostly in 2nd trimester of pregnancy
- low grade fever, severe abd. pain, local tenderness, guarding
- but no shock (no blood loss)
- Dx diff. with
torsion of ovarian cyst
placental abruption
appendicitis (if right sided)
effects of pregnancy on fibroid:
- incr. in size
- softens
effects of fibroid on baby:
- incr. risk of miscarriage
- premature labor
- malposition
- post-partum hemorrhage – lack of contraction
- may prevent vaginal labour (if big and located near internal OS)
o Dx
U/S
151
o types:
extension of squamous CA spread from cervix - MC
metastatic adenoCA from endometrium
primary invasive squamous cell CA of vagina
clear cell CA following diethylstilbestrol Rx
CA of the urethra, Bartholin gland, Gartner duct
- Cyclical (recurrent) vulvitis
o MC cause – Candida
o exacerbates premenstrually
o Sx – chronic vulvar itch, burning, swelling, dyspareunia, aggravated with systemic A/C
with or without discharge
o Dx
low vaginal swab
o Rx
topical antifungal: Imidazole, Nystatin
oral antifungal: Ketokonazol, fluconazol, itroconazole
severe itching – C/S
Pregnancy – Nystatin pessaries
- Sebaceous cysts – in labia majora
Endometriosis & adenomyosis
- Endometriosis
o 10% incidence.
o Ectopically loca ted endometrial tissue responds to sex hormones.
locations:
MC - ovary (60%), uterosacral ligament (60%)
28% - cul de sac of Douglas
15% - broad ligament
15% - bladder
12% - rectum
7% - sigmoid colon
5% - round ligament
2% - appendix
o Puberty to menopause: Peak 25-35 yrs.
o MC in nulliparous women and resolves with pregnancy
o CLINICAL FEATURES:
most patients are asymptomatic
Dx made when a laparoscopy is done to investigate infertility
pain
Secondary dysmenorrhoea.
- painful period
- pain usually starts before period and continues through the
period, then ↓
Acute pain with rupture of endometrioma.
Dyspareunia
Non-specific pelvic pain or dyscomfort, low back pain
pain at urination and or defecation
abnormal bleeding
161
Menorrhagia
Premenstrual spotting
irregular spotting
Infertility
diarrhoea/ constipation, bloating
(almost) never undergoes malignant change
o DIAGNOSIS:
The most suggestive sign is tenderness, mass or nodularity in the pouch
of Douglas or uterosacral ligaments. MCQ
cervical excitation (motion tenderness)
1st exam. – U/S
rule out: ovarian cysts, fibroids, etc.
Gold stand. of Dx: direct visual inspection at laparoscopy or laparotomy
o Rx
Analgesics.
MEDICAL:
1. OCP: once daily for 6 mnths
2. Progestogens
3. GnRH analogues (treatment of choice)
4. Danazol
SURGICAL:
indic
- if medical Rx fails
- causing infertility
- if significant impact on patient’s life
Laser or microsurgery
- removal of tissue
- endometrial ablation or electrodiathermy excision
- hysterectomy
- Adenomyosis:
o invasion of the myometrum by the basal endometrium of the uterine cav., with ectopic
glandular tissue (adenomyotic glands) found in the muscle
o 35-50 yrs
o not MC in nulliparous (diff. from endometriosis)
o Sx
dysmenorrhoea
menorrhagia
dyspareunia
slightly enlarged (bulky) and tender uterus
o Dx
D&C not helpful
core biopsy of myometrum
removed uterine specimen (after hysterectomy)
o Rx
if severe sympt. -> hysterectomy (adenomyotic glands repond poorly to
hormonal suppression)
162
color Doppler
o Rx
laparotomy and surgical correction
- Ovarian CA – M 998
o often Dx late (not many Sx), usually an incidental finding
o > 45 yrs, peak 60-65 yrs
o risk factors
nulliparity
age
family Hx
hereditary breast - ovarian CA syndrome – BRCA1, BRCA2
o protective factors
pregnancies
OCP (they suppress/ shut down ovaries)
o Sx
non-specific: lower abd. pain or discomfort, bloating, constipation, pelvic
heaviness, urine frequency, dysuria, vaginal bleeding, menstr. dysfc.
(dyspareunia, dysmenorrhoea)
ascites
adnexal mass on physical or bi-manual exam.
any ovarian enlargement detected after menopause must be
considered malignant until proven otherwise!
large adnexal mass developed in a postmenopausal woman – e.g. 60
yrs (+vaginal bleeding) – MC cause = Ovarian CA (Ovarian cysts or
benign tumors are unusual at this age)
o Dx
1. Pelvic Doppler U/S
No FNAC – risk of spreading the CA!
2. tumor markers:
CA-125 – most specific
- (still not very specific) also ↑ in follicular cyst & endometriosis
AFP
Beta HCG
CEA
o Dx and Sx
3. urgent referal to gynecologist: excision (Oophorectomy)
- CA metastases in ovaries (blue book p. 531) – only 5% of the CA in the ovaries
o in Aus. MC from colon CA -----Colonoscopy is advised for screening
o in underdev. countries – MC from breast CA
o in Japan (with a very high incidence of stomach CA) – MC from stomach CA
(Krukenburg tumor in both ovaries)
Endometrial CA
o Risk factors
Anovulatory cycles
Old age
Obesity
nulliparity
164
late menopause
DM
PCOS
NOT - smoking
o Dx
U/S
if thickness > 5 mm
- hysteroscopy + biopsy
if thickness < 5 mm – CA very unlikely
Cervical CA
o risk factors
all women who were sexually active
higher risk
Early age at 1st intercourse
Multiple partners or partner who had multiple partners
Smoking
OCP
Radiotherapy
Diethylstilbestrol (DES)
HPV – especially with high risk strains (16, 18)
- 4 of 5 women get HPV after they start sexual life, most clear
infection in 1-2 yrs
- condoms give limited protection from transmitting disease
o Prevention
Vaccine = Gardasil – for types 6, 11, 16, 18
6, 11 – anogenital warts
16, 18 - cervical cancer
also prevents some vulval and vaginal cancers
admin. 0, 1-2 mths, 4-6 mths IM
Girls – any age (9-26 yrs)
- in school free, then they have to buy it
Boys – 9-15 yrs, safe but not proven to be effective
useful until 26 yrs
not in pregnant women
- always do a pregnancy test first
S.E. - mild fever, allergy
useful in existing warts
after admin., continue with PAP smears as usually
o Screening
PAP smears (cellular level) – every 2 yrs until 70 yrs
if (LSIL CIN I) -> repeat PAP in 12 mths
- -> if normal -> repeat in 12 mths
-> if normal -> normal screening every 2 yrs
- if LSIL CIN I-> colposcopy + biopsy (tisular level – how deep and
extensive is the lesion)
-> if LSIL -> ablation
165
cryo
laser
sugical
if HSIL (CIN II or CIN III) -> Colposcopy + biopsy
- if HSIL -> ablation
cryo
laser
sugical
- if invasive -> Cone biopsy
SE
bleeding
cervix incompetence
cervix stenosis
premature labor in future
PROM
in Pregnancy – cone biopsy and vaginal delivery are CI
IF LSIL – follow same 12 months protocol
If HSIL-- first Colposcopy then
< 20 wks – termination of pregnancy + Rx the CA
> 20 wks – discuss with mother:
o terminate pregnancy
o continue but risk of advanced CA
best to wait till 36 wks, then C-
Section (vaginal delivery is CI)
o Stages
I – limited to cervix
II
IIa – upper 2/3 of vagina
IIb – upper 2/3 of vagina + parameters
III – lower vagina
IV
IVa - bladder and rectum
IVb – distant metastases
o Rx
I – Cervical conization
II – Radiation + chemotherapy
III, IV – radiation + chemotherapy
Uterovaginal (genital) prolapse
o 50% of parous women
o Risk factors/ causes
multiparity – after long 2nd stage labor
obesity
old women at menopause/ post-menopausal – decr. estr. -> decr. collagen
strenght -> weak vaginal muscles
delivering large baby
smoking
o types:
166
o
vaginal hernia, which occurs when small intestine (small bowel) descends into
lower pelvic cavity and pushes at the top of vagina, creating a bulge.
Enteroceles MC occur in women who have hysterectomy done
Rx – Surgery
- Rectocele:
o
If muscles of posterior wall of vagina are damaged, rectum will begin pressing
into vagina. This is called a rectocele.
167
FSH, LH
testosterone
o Rx
Inj. with FSH – if sperm analysis isn’t very bad (can improve it)
Regular IVF - if sperm analysis isn’t very bad (5-20 mill/ml)
if very bad – 2%/ cycle treated success rate
IVF with ICSI – if severe Oilgospermia
20% per cycle treated success rate
o MCQ
no fructose = no sperm coming from testicles
0-3 ml – coming from prostate
- Female infertility
o Dx
Ovulating?
Patency of tubes?
Cervical factor?
Post-coital test – 2 hrs after check:
- spermatozoids
- cervix – mucus consistency
- IVF
o indic.
Male
Oligospermia (5-20 mill/ml)
Presence of sperm AB
Female
endometriosis
damaged or absent fallopian tubes
unexplained infertility
- ICSI (Intracytoplasmic sperm injection)
o indication
severe oligospermia or azoospermia (<5mill/ml)
failure of IVF
- Fertility treatment – Monash IVF
o infertility rate – 15%
o cause of infertility
1/3 woman
1/3 man
1/3 man and woman
o Safety Net – out of 7500 you get 5000 back
o in Vivo:
Ovulation induction – Clomiphene (only if FSH not raised)
Intrauterine insemination (IUI) – 2000 AUD
10% success rate
risk of multiple pregnancies
o in Vitro:
IVF – try this first
no good sperm
172
donor program
- donor types
Known
Unknown =altruistic – when child becomes 18 has the
right to find who is biological mother/ father
- for
Sperm
Ovum
Method: Put sperm and ovum together for (short insemination protocol)
2 or 16 hrs (long)
Intra Cytoplasmic Sperm Injection – if IVF failed or we need to do testicular
aspiration, go for this one
low sperm count
inject sperm
o Overall success rate is 90% in 3 attempts.
Orthopedics - OK
Trauma and fractures
General stuff
- MC causes of post-traumatic arterial thrombosis
o 1. fracture of femur
o knee dislocation
o hip fracture
- MC cause of artery injury – posterior knee dislocation (Popliteal A.)
- nerves that regenerate most after traumatic laceration:
o Digital N.
o Sural N.
- after visit to chiropractor = dissection of vertebral artery: neck pain, facial hemisensory loss,
ataxia
- Compartment syndrome – haematoma within a fascia, compressing on close structues
(nerves, arteries, etc.)
o Sx – e.g. leg swollen, post. tibial pulse not felt, pain on moving toes
o Rx - fasciotomy
- MVA
o thoracolumbar pain – transport in supine position on a flat surface
o with blood in urethra -> retrograde urethrogram
o main cause of death after MVA - disruption of great vessels, hypoperfusion and shock
- Compound/ open fracture – first step = debridement
- internal organ rupture in trauma
o MC source of air under diaphragm = ruptured intestine
o blow in the abdomen – Organ least often to rupture = Stomach
o MC organ injured in abd. trauma – Spleen 45%
2 – Liver: 40%
- Splenic rupture
o Mx
Stable pat.
U/S and CT scan
isolated splenic rapture
173
conservative Rx
- if it fails -> splenectomy
hT -> splenectomy
other organs are affected -> splenectomy
- Greenstick fracture
o Hx of trauma
o usually occur most often during infancy and childhood when one's bones are soft
o Because a child's bones are much more pliable than adult bone, an incomplete, or
'greenstick,' fracture may occur. A "greenstick fracture" means that one side of bone is
broken and one side is bent; therefore it is classified as an incomplete break.
o The name for a greenstick fracture comes from the analogy of breaking a young, fresh
tree branch. The broken branch snaps on one side (the outer side of the bend), while the
inner side is bent and still in continuity.
o Rx: Most often greenstick fracture must be bent back into the proper position (called a
"reduction") and then casted for about 6 weeks. Greenstick fractures can take a long
time to heal because they tend to occur in the middle and slower growing parts of bone.
- Stress fractures
o normal bone but repeated stresses/ injury on it
diff. from
pathol. fractures
acute traumatic fractures
o Athletes, soldiers
o locations
MC – neck and shaft of 2nd metatarsal bone----March troopers
Spinal vertebra in cricket players
Neck of 1st rib in COPD (coughing)
neck of fibula and proximal tibia in runners
perpendicular fracture starts from the cortical in -> advances till it
becomes transversal
Rx – rest!
o Sx – pain worse on weight bearing, point tenderness
o Dx
1. X Rray – Usually normal
2. Nuclear bone scan – ↑uptake at the point of fracture
o Mx
rest
healing takes 6-8 wks
walking boots
- Insufficiency fractures
o anorexia
o women from Middle East all covered (insuf. Vit. D)
- Flail chest
o 3 or more ribs broken
o Sx
Paradoxical resp. -> gas exchanage impaired -> resp. distress
o Rx
174
-
External Auditive Conduct laceration with bony debris in the canal
Haemotympanum
175
o
o Longitudinal Fractures
70-90% of temporal bone fractures
Extending to EAC, ME, ET, & foramen lacerum
Presentation: bleeding from EAC, CHL, CSF otorrhea, facial paralysis
o Transverse Fractures
20-30% of temporal bone fractures, usually more severe occipital bone injury
Presentation: hemotympanum, CSF rhinorrhea, SNHL, facial paralysis in 50% of
cases
o Treatment
Stabilize for other neurologic & life-threatening injuries
Observation
Antibiotic coverage
Surgery for persistent Tympanic Membrane perforation – paper patch
myringoplasty or standard tympanoplasty
CHL – hemotympanum resolves in 3-4 weeks with no sequaelae
Facial paralysis – facial nerve decompression & exploration
CSF leak – head elevation, stool softeners, acetazolamide (to decrease CSF
production), placement of a lumbar drain, repair of CSF leak
fracture of the base of skull – CSF leak
- don’t touch the nose (use orogastric tube)
- AB prophylaxis to prevent meningitis
- Orbital floor (blow-out) fractures
o Fracture of the orbital floor caused by blunt, non-penetrating force
o Direct blunt trauma to the globe causes ↑ intraorbital pressure, causing thin bones of
the orbit to “blow out”
o Inferior orbital wall is most commonly involved
o Ocular globe is protected by the orbital fat
o Forced duction testing is done to evaluate possible muscle/ nerve entrapment
o Inferior oblique muscle is tested, other muscles tested if necessary
o Plain films (tear drop sign on Water’s view)
176
o
o CT scan
Clinical features
Enophthalmos MC sign
• Swelling of cheek
• Circumocular haematoma
• Subconjunctival haemorrhage
• Palpable step in infraorbital margin
• Flat malar eminence when viewed from above
• Paraesthesia/diplopia due to infraorbital nerve injury
o • Loss of function (i.e. difficulty opening mouth
o Indications for surgical repair of orbital floor (blow-out) fracture
Rapid onset of intraorbital bleeding & decreased visual acuity
Entrapment (diplopia)
Enophthalmos
o infraorbital nerve entrapment -> diplopia with restricted upward gaze
- Zygomatic fracture
o enophtalmos
Arm
- Lateral epicondylitis = Tennis elbow = Source of extensor tendons (M 714)
On examination the elbow looks normal, and flexion and extension are painless
o pain on pressing on lateral epicondyle
o pronated forearm inc pain (MCQ) + extended wrist (MCQ)-> pain
o resisting extension of wrist -> pain
o Rx
Dumbell exercise with palm facing down
RICE (rest, ice, compression, elevation)
C/S local inj. (1-2)
- Medial epicondylitis = Golf elbow = Source of flexor tendons
o pain on pressing on medial epicondyl
o resisting flexion of wrist -> pain
o Rx
Dumbell exercise with palm facing up
RICE (rest, ice, compression, elevation)
Brace below elbow
C/S local inj. (1-2)
- De Quervain tenosynovitis = Washerwoman’s sprain– M 689
177
Splinting
C/S infiltration
Surgery
- Injuries to the wrist and hand
o Colle’s fracture
Fracture of distal radius usually within 2.5 cm of wrist.
MC of wrist fractures.
Elderly women with osteoporosis
Fall on outstretched hand
Dorsal angulation and dorsal displacement of the distal radial fragment or
radial displacement.
CLINICAL FEATURES:
Swelling, ecchymosis & tenderness.
‘Dinner fork’ deformity.
ASSESS neurovascular status: Acute carpal tunnel syndrome.
Common association
- Ulna
- Scaphoid
- Radial or ulnar styloid fracture
X-Ray: distal fragment is:
Dorsally displaced with dorsal comminution
Dorsally tilted fragment with apex or fracture volar
Supinated
Radially deviated
Shortened
Cx
1. Stiffness of wrist and fingers (MCQ)
- + Most frequent LATE complication of a Colle’s facture in an
elderly woman
2. Osteoarthritic changes
3. Malunion
4. Non-union – Rx: internal fixation
5. Delayed union
MANAGEMENT:
Colles’ backslab: Permit full elbow flexion & thumb movements
extends from below elbow to metacarpal heads (thumb not included)
- include thumb if associated scaphoid fracture
Types:
- Undisplaced or minimally displaced (stable):
Colle’s backslab
No manipulation (reduction)
7-10 days
- Displaced, angulated fractures with radial deviation :
Reduction (Bier’s block = regional nerve block for all the
wrist and hand fractures using a blood pressure cough
on the arm + injection with anestetic in hand).
Circumferential plaster cast for 6-8 wks
179
-
The wrist should be (like holding an apple – Awad):
Fully pronated
Radially deviated
Partially dorsiflexed
Thumb held in mid-abduction
- displacement > 2 mm and or angulation – open reduction &
fixation
COMPLICATIONS:
Non union.
Avascular necrosis of proximal half of bone.
- circulation (sama as for femoral head)
central to periphearl – usually closes
periphearal to center – from the capsule (main one)
Osteoarthritis.
o MALLET FINGER:
Injury to extensor digitorum tendon at DIP joint
It results from hyperflexion of extensor digitorum tendon.
Sx
Full passive but incomplete active extension at DIP joint
TREATMENT:
Mallet splint for 6-8 wks.
Elevate hand
Analgesics
181
- Injuries to elbow
o Pulled elbow - Subluxation of radial head
Children 2-6 years.
Axial traction applied to an extended arm.
The radial head is subluxed out of annular ligament.
CLINICAL FEATURES:
Anxious child
Local pain
Loss of use of arm, particularly supination
Elbow semi-flexed and pronated on examination.
There is no neurovascular compromise
Motor activity is normal
X RAY:
Only to exclude a fracture if extensive swelling.
Reduction is not successful after two or 3 attempts.
MANAGEMENT:
Reduction
- Apply pressure to the region of the radial head with one hand.
- Apply axial compression at the wrist.
- Supinate the forearm.
- Gently flex the elbow with other hand.
supination + force flexion of elbow while holding the
thumb over radial head, to feel it move into position, in
the anular ligament-> moves into position
No immobilization is required.
- Injuries to shoulder & upper arm
o Acromioclavicular dislocation
Fall on to the apex of shoulder with arm held in adduction
types
Subluxation: Causes local tenderness to palpation with minimal
deformity.
Full dislocation: Prominent outer end of clavicle (step deformity)
CLINICAL FEATURES:
Local tenderness and swelling.
Palpable step between distal clavicle and acromion.
Pain with adduction.
Assess the clavicle and scapula for associated fractures.
DIAGNOSIS:
X Ray: Apparent on stress view. Patient holding a weight in each hand,
compare the shoulders.
TREATMENT:
Minor: Ice, oral analgesics sling immobilization, daily range of motion
exercises.
Complete: Same initial treatment, refer to Orthopedic team for possible
operative intervention.
o Glenohumeral joint dislocation
182
ANTERIOR DISLOCATION - MC
Caused by forced abduction and external rotation of shoulder
Young adults from sports, traffic crashes or elderly from a fall.
It tends to become recurrent.
CLINICAL FEATURES:
- ‘Squared off’ shoulder: arm held in slight abduction & external
rotation.
- Loss of deltoid contour (MCQ)
- Humeral head can be palpated anteriorly
- Loss of internal rotation
- Pt can’t rise arm above head (but can move his head to that
position)
most specific – can’t scratch in interscapular region
with his hand
- All shoulder movements are painful.
ASSOCIATED WITH (These result in recurrent dislocations)
- Hill-Sachs lesion: Flattening or a wedge-shaped defect in
posterolateral aspect of humeral head.
- Bankart lesion – after the first dislocation: Avulsion of capsule
when shoulder dislocates. Occurs in 85% of all anterior shoulder
dislocations.
COMPLICATIONS:
- Look for complications before any attempt of manipulation
- Axillary N damage:
Check sensation over lateral deltoid (police patch)
check motor function with isometric contractions of
deltoid muscle – Murtagh 1394
- Posterior cord of brachial plexus.
- Axillary artery damage.
- Fracture of the upper humerus.
DIAGNOSIS:
- X Ray: Always to rule out associated humeral head fracture
Mercedes Benz sign on lateral oblique view – normal
humeral head displaced anterior or posterior
ant dislocation – humeral head under coracoid
process of scapula
post dislocation – humeral head over coracoid
process of scapula
- Humeral head is displaced anteromedially with loss of contact
with glenoid fossa
TREATMENT:
- Pain relief: Morphine 2.5-5 mg IV
- Conscious sedation with fentanyl (analgesic) and midazolam
(sedative, muscle relaxant)
or fentanyl and propofol (used currently)
- Perform the reduction:
Kocher’s manoeuvre
183
Hippocratic method
Jay: straight arm, pull forward (in axul bratului) +
upward (flexion) + abduction + supination
- Sling
- Test again for neurovascular damage
- X Ray to confirm reduction
o Fractures of upper humerus
location:
Greater tuberosity
Lesser tuberosity
Surgical neck of humerus
Supracondylar
Usually in elderly patients
CLINICAL FEATURES:
Localized pain.
Loss of movements.
Swelling and tenderness.
COMPLICATIONS:
Dislocation of humeral head.
Complete distraction of the humeral head from the shaft.
Axillary N damage -> anaesthesia over lateral deltoid & loss of deltoid
movement.
Axillary (circumflex) vessel damage.
in supracondylar fracture (just above epicondyles)
- Sx – huge hematoma
- Cx = Brachial A. injury => Volkmann's ischemic contracture
Permanent flexion contracture of hand at wrist,
resulting in a claw-like deformity of hand and fingers.
It is more common in children. Passive extension of
fingers is restricted and painful. On examination fingers
are white or blue, cold and Radial pulse is absent.
It’s caused by obstruction of brachial artery near elbow
results from acute ischaemia/ necrosis of
muscle fibres of flexor group of muscles of
forearm, specially flexor digitorum profundus
and flexor pollicis longus which become fibrotic
and short.
Causes:
Any fracture at elbow or upper arm may lead
to Volkmann's ischemic contracture but
commonly caused by supracondylar fracture of
humerus.
improper use of a tourniquet
improper use of a plaster cast – too tight
compartment syndrome.
Rx
surgery to fix the damaged tissues
184
Leg
- Dislocation of hip
o Occurs in violent trauma such as:
Traffic crash.
knee strikes dashboard w/ thigh abducted
Blow from back while in squatting position
Fall from height.
Direct fall on hip.
o location
The MC is posterior dislocation (85%)
The posterior capsular ligaments are weaker than anterior
Central and anterior dislocation are rare
o CLINICAL FEATURES:
The hip is held slightly flexed
Adducted
Internally rotated
externally rotated – for anterior dislocation (rotation is more specific in
determining whether anterior or posterior dislocation)
o DIAGNOSIS:
X Ray of pelvis, hip and shaft of femur in all cases.
o Cx:
Avascular necrosis of fem. head: ↑dramatically after 6 hrs of hip dislocation
Assess L5 & S1 of ankle: Sensation over medial side of ankle (L5) and lateral
border of foot (S1).
Sciatic nerve neuropraxia: 15%
o MANAGEMENT:
185
children
- do nothing till 8 yrs
- refer if inter medial malleloar space > 8 cm
Genu varum (bowed legs)
where is my horse?
stress test
children
- up to 3 yrs normal
- Mx
reassurance
3 yrs – observe
refer if intercondylar dist. > 6 cm
Genu recurvatum
o Cruciate ligament
Ant (ACL) – MC than post.
Soccer player accident – MC = Injury to anterior cruciate ligament
Knee giving way
tests
- Ant drawer test – with knee at 90 degrees (> 10 degree pathol.)
- Lachmann’s test – with knee at 15-20 degrees (> 5 mm pathol.)
- Pivot shift test
Post (PCL)
tests
- post drawer test
- post. sac test?
o Meniscus – in twisting movts.
Medial
more frequent (75%) than lateral
most common knee injury
Sx
- giving away sensation
- locking of joint – MC cause of locking
Knee locking in flexion
lateral
tests
Apply grind/ distraction test
McMurray test
- Knee pain – frequent in hip problems, with knee joint being normal
- Fractures of patella
o Usually by direct trauma:
Traffic crash
Fall
Indirect force from violent quadriceps contraction
o CLINICAL FEATURES:
Acute knee pain.
Swelling and bruising.
Loss of function, especially inability to extend knee.
187
o DIAGNOSIS:
1st: X Ray of both knees.
Confusion may arise from congenital bipartite or tripartite patella but
these are BILATERAL.
Consider CT scan when a suspected fracture is not seen on X-ray.
o MANAGEMENT:
Refer immediately: Distracted or comminuted fractures.
Stable: Aspiration of haemarthrosis.
Place the leg in a padded plaster cylinder from the thigh to the ankle.
Refer to fracture clinic.
- Flat feet (pes plano valgus)
o painless, asympt.
o refer if painful, stiff
o majority: Physiological
o by 6th birthday: 80% resolve
Bone pathology
- Osteosarcoma
o primary – in adolescents: knee (in the metaphysis)
o sec. – metastases to lungs
o Sx
Pain + swelling
Stress fractures
o Dx
X Ray typical:
Sunburst appearance
Codman’s triangle – due to periosteal elevation
+ new bone formation
o Rx
surgery
chemotherapy
- Paget’s disease of bone
o Normal bone replaced by new soft (medullary) bone:
Osteoclastic activity then osteoblastic activity
o 10% at 90 yrs
o Sx
Male 2:1
95% asymptomatic
Dx. during X Ray or incr. ALP level
Bone pain, joint pain, stiffness and waddling gait,
MC bones affected: pelvis, femur, skull
his hat don’t fit him anymore!
deafness
hyperdynamic circ. -> heart failure (hight output cardiac fail)
o Dx
Marked incr. of ALP (asympt. incr. of ALP)
Normal Ca and Phosphate
X Ray – dense, expanded bone (bigger, thicker bone)
188
X Ray features
- larger bone/ bony extension
- thickened cortex
- coarse/ thicker trabeculation
Metastases of prostate CA and transitional cell CA of bladder =
Osteosclerotic -> have to be excluded (Do PSA)
o Cx
Fractures
Cardiac failure – in bones more AV shunts, bypassing capillaries (more input
blood coming back to heart => High output cardiac failure)
Osteogenic sarcoma – rarely
Deafness----Cranial nerve involvement
Deformities
o Rx
1. Bisphosphonates
SE – Oesophagitis (don’t go to sleep right after taking it)
Neurology - OK
- Cranial nerves
o Only 1st and 2nd pair emerge from cerebrum; remaining 10 pairs emerge from brainstem.
-
Sensory,
Name Motor Origin Nuclei Function
or Both
Cranial nerve zero olfactory trigone, New research indicates CN 0 may
(CN0 is not medial olfactory play a role in detection of
0 Sensory
traditionally gyrus, and lamina pheromones. Linked to olfactory
recognized.)[1] terminalis system in human embryos[4]
Acute mastoiditis
Malignant otitis externa
Acute suppurative otitis media
Tuberculosis
Lyme disease
AI+DS
Infectious mononucleosis
Influenza
Encephalitis
Sarcoidosis
o NEOPLASIA
Cholesteatoma
Carcinoma (primary or metastatic)
Acoustic neuroma
Meningioma
Facial Neuroma
Ossifying hemangioma
Glomus jugulare or tympanicum
Schwannoma of lower cranial nerves
Benign and malignant parotid tumors
Leukemia
Hemangioblastoma
Histiocytosis
Rhabdomyosarcoma
o METABOLIC/ SYSTEMIC
Diabetes mellitus
Hyperthyroidism/hypothyroidism
Pregnancy
Autoimmune disorders
o NEUROLOGIC
Guillain-Barre’ syndrome
Multiple sclerosis
Millard-Gubler syndrome
- Bell’s palsy – idiopathic
o MC cause of acute facial paralysis (70% of cases)
o LMN
o Can occur in any age group, prevalent in 3rd decade of life
o Recurrent paralysis in 10-12% of cases, more often on contralateral side
o Positive family history in 14% of cases
o Association - Type I Herpes virus (HSV-1)
Viral infection induces an inflammatory response resulting in neural edema and
vascular compromise of facial nerve
o Sx
paralysis of all facial muscles, including frontalis (MCQ)
can’t close eye (NOT PTOSIS – Horner)
mouth pulled to opposite direction and up when opening it
unilat. loss of taste (ant 2/3rd of tongue)
o isolated, with no other sympt. (e.g. dysphagia – brainstem infarct)
192
o Treatment is controversial
o Treatment options:
Steroid therapy (Prednisolone) – always, 7 days
artificial tears (can’t blink or close eyes)
surgical decompression – if steriods dn’t help
antivirals – sometimes
-
- Herpes zoster oticus – Ramsay Hunt syndrome
o Vesicular eruptions on ear or ear canal (crusts) + ipsilateral facial paralysis
o Other symptoms:
o Nerve degeneration is more progressive and severe than Bell’s palsy!
o Prognosis for recovery is worse!
o Treatment:
antivirals – within first 72 hrs.
steroids
pain management – very painful
- Trigeminal neuralgia
o males > 40 yrs
o paroxystic burning pain in the maxillary and mandibulary region (nerve V distribution)
no Ophtalmic N involv.
o lasts seconds – 1-2 min
o recurs many times during day and night
o triggered by
touching of skin of affected area
washing
shaving
eating
talking
o Unilateral
2nd mandibular division of Vth nerve
3rd maxillar division of Vth nerve
o cause
local pressure on nerve root entry zone by tortuous pulsatile dilated small
vessels – 75%
MS
neurosyphillis
tumor in posterior fossa
o Rx
193
Carbamazepine
(amytriptiline)
Phenytoin
Gabapentin
Surgery
- Postherpetic neuralgia
o Unilateral or bilateral
o Ophtalmic area involved
o Rx
Amytriptiline – Murtagh, we used to be told to select this
Carbamazepine – less SE
Gabapentin
Nerve traumatic pathology
- Hand
o Brachial plexus C5-T1 - http://en.wikipedia.org/wiki/Brachial_plexus
Axillary nerve
Deltoid muscle
Small area of overlying skin – “police patch”
Musculocutaneous nerve
Biceps brachii
Radial nerve C5-C8 (goes more towards back of arm-forarm-hand)
all extensors: triceps = elbow extension, wrist extension
- Injury
above elbow: dropped elbow and wrist (can’t extend)
elbow level: dropped wrist (can’t extend)
- Rotation of thumb (thumb up – antenna, 90 degrees to Palm, in
same plane as palm) – Alena
Post. interosseous n. (branch of radial n.) – extension of finger lost but
hand extension intact
Median nerve C6-T1
Motor – grasp (hand) and flexors + thenar muscles (under thumb)
tests
- above elbow (cubital fossa)
Clasping test (Ochsner’s test) – can’t flex index finger
on affected side when asked to clasp hands firmly
together.
- below elbow (wrist)
Pen touch test – can’t do flexion of thumb, 90o
perpendicular on palm’s plane
injury -> median claw affecting fingers 2-3
opposition (adduction OK) of thumb to index finger (OK – O –
Opposition) alena
Ulnar nerve C8-T1
Ulnar paradox: higher the lesion, less sever the injury
- high – flexor digitorum profundus paralized => less severe “Claw
hand” affecting fingers 4-5
194
- low – flexor digitorum not paralized => more severe “Claw hand”
affecting fingers 4-5
can’t adduct (opposition) thumb (can’t hold a piece of paper between
thumb & index finger = Froment’s sign)
all small muscles of hand except thenar: interosseus + hypothenar
(under fingers 2-5) (sparing thenar muscles) + abduction and adduction
of fingers (spread fingers) – alena
C8
Loss of sensation of ring finger, may be extending to little finger
Weakness of extensors of wrist.
T1 (both Ulnar & Median N)
all small muscles of hand, including thenar and hypothenar eminences
including all fingers (1-5)
- diff. from medial or ulnar injury
difficulty of precision grip and opposition of thumb to fingers,
weakness spreading and bringing together fingers
in time – claw hand
o Sensory
Palm
3 ½ median (fingers 1-3.5)
1 ½ ulnar (fingers 3.5-5)
Dorsum
3 ½ radial (fingers 1-3.5)
1 ½ ulnar (fingers 3.5-5)
o Erb's Palsy - Paralysis of arm caused by injury to upper group of arm's main n,
specifically upper trunk C5-C6 is severed- loss of sensation in arm, paralysis and
atrophy of Deltoid, Biceps and Brachialis muscles. The position of limb, under such
conditions is characteristic: arm hangs by side and is rotated medially; forearm is
extended and pronated. The arm can’t be raised from side; all power of flexion of
elbow is lost, as is also supination of forearm. The resulting “Biceps” damage is main
cause of this classic physical position commonly called "Waiter's tip."
Risk factors – breech presentation, Shoulder dystocia due to macrosomia
materanal or gestational DM.
o Klumpke palsy- Paralysis involving muscles of forearm and hand, resulting from a
lower brachial plexus injury (C8-T1 severed)- affects principally intrinsic muscles of
hand and flexors of wrist and fingers".± dilators of iris and elevators of eyelid (both of
which may be seen in case of associated Horner's Syndrome). The classic presentation
of Klumpke's palsy is “Claw Hand” where forearm is supinated, wrist and fingers are
hyperextended. If Horner syndrome is present there is miosis (constriction of pupils) in
affected eye (Complete claw).
195
o
Syringomyelia
o
- Leg – Murtagh 714, Blue book 190-191
o Sciatic N, coming from sacral (or lumbosacral) plexus – branches above popliteal fossa
into: Common peroneal and tibial N
PED: P = Common Peroneal n (at front of leg) damaged => E = Eversion, D =
Dorsiflexion
L5-S1
Complic. of lithotomy position -> compression of common peroneal n
branches:
- deep peroneal N – dorsiflexors: tibialis ant., extensor hallucis
longus, extensor digitorum longus, fibularis brevis
- superf. peroneal N – eversion muscles: fibularis longus, fibularis
brevis
- L4-L5-S1-S2
Muscles supplied by P:
- Extensor hallucis longus
- Extensor digitorum longus
- Tibialis anterior
- Peroneus brevis
- Short head of biceps femoris
TIP: T= Tibial n (at back of leg) damaged => I= Inversion, P= Plantar flexion
L4-L5
SEDIP => Sciatic n damaged (peroneal n and tibial n are branches)
Power loss Reflex Sensory loss
C5 Abduction of arm Biceps
C6 Elbow flexion, extension of wrist Biceps
C7 Elbow extension Triceps
C8 Hand grip
T1 Finger spread (abduction / adduction of fingers)
L3 Extension of knee Knee jerk Ant. Aspect of thigh
L4 Inversion of foot Knee jerk Medial aspect of ankle
L5 Dorsiflexion of great toe Dorsum of foot
S1 Plantar flexion & eversion Ankle Plantar Lateral aspect of ankle
- Nerve roots asked in MCQs – Oxford p. 457
o Biceps jerk: C5-C6 (Erb’s palsy)
o Triceps jerk: C7
o Hip flexion L1-L2
196
Upper limb: Biceps reflex C5/C6 · Brachioradialis reflex C6 · Extensor digitorum reflex
Tendon reflexes C6/C7 · Triceps reflex C7/C8
Lower limb: Patellar reflex L2-L4 · Ankle jerk reflex S1/S2 · Plantar reflex L5-S2
- Corneal reflex
o V – afferent
o VII – efferent
- Gag reflex
o Glossopharyngeal IX - afferent –
197
o Vagus X – efferent
- Oculocephalic reflex (doll’s reflex) – Brainstem integrity
Motor neurone lesions and back pain
o types:
UMN LMN
Weakness Yes Yes
Power Decr. Decr.
Muscle Wasting Absent/mild Marked
Tone Incr. (spasticity) Absent or decr. (flaccid)
Fasciculations No May be present
Reflexes Brisk Absent or diminished
UMN – above anterior horn cell: cerebral cortex, internal capsule, brain stem,
spinal cord (stroke, tumors, MS, etc.)
LMN – lesion from anterior horn cell = spinal reflex arc (peripheral neuropathy,
Bell’s palsy, GBS, motor neuron dis., poliomyelitis, etc.)
o Motor neuron dis. (MND)
progressive neuromusc. disorder due to death of motor neurons in brain, brain
stem and spinal cord.
no sensory loss (MCQ)
no sphincter involvment
cause
5-10% inherited AD
rest – sporadic
types
amyotrophic lateral sclerosis (ALS)
- LMN muscle atrophy + UMN hyper-reflexia (progressive
spasticity)
progressive muscle atrophy
progressive bulbar and pseudobulbar palsy
Sx
Triad: LMN + fasciculations (in hands – wasting of all muscles) and UMN
signs (hyper reflexia in legs)
weakness or muscle wasting
difficulty with swallowing, speech
fasciculations & cramps
Dx
clinical
neurophysiological tests
no Rx
incurable – death in 3-5 yrs from respiratory failure/ aspiration pneumonia
- Back pain:
Without neurological sympt. With neurological sympt.
1. Muscular spasm 1. Disc prolapse – compress on nerve roots
After heavy weight lifting Limited neurol sympt. = sensory abnormality (no motor) –
Diffuse tenderness numbness, shooting pain in leg
2. Vertebral crush/ collapse 2. Cauda equina syndrome (L1-5, S1-5)
198
Old lady with osteoporosis Urinary retention (> 500 ml after urination) Saddle shape
Point tenderness paresthesia (numbness in groin area) +↓ anal tone (ask
patient to squeeze + do you feel my finger in your anus?)
LMN only
3. Spinal canal stenosis 3. Spinal cord compression
Pain relieved by trunk flexion Urinary & fecal retention/ incontinence
LMN + UMN
- Examples:
Spinal cord compression/ lesion:
MCQ: Pain in mid-thoracic region & spastic paraparesis progressing over last 2
mths.
Sx
Above lesion - normal
At the level of lesion - ipsilateral LMN signs
below lesion – ipsilateral UMN signs + ipsilateral loss of position
- this is after a few wks; initially we have flaccid motor paralysis +
loss of all sensory modalities
contralat. sensory loss, temperature and pain
+ spinal root pain, precedes weakness
Rx
Acute – high dose steroids to lower edema!
o Cauda equina syndr. – Murtagh p.37
pain at back of thigh and legs, shooting to leg
saddle anesthesia (numbness of inner buttocks, perineum and upper medial
thigh), back of legs, soles of feet,
bowel and bladder involvement (urinary retention)
weakness of legs and feet
atrophy of calves
Rx – Surgical decompression
o Spinal canal stenosis – neurogenic claudication: Murtagh p. 710
pain in buttocks related to walking, relived by trunk flexion or rest
pain relieved when going up hill and amplified when extending spinal column
(going down hill)
Dx diff from vascular claudication = pain relieved at rest or going down
hill
Bowel/ bladder involvement
Tremor
o Types
Resting – Parkinsonism
Action or postural
Benign Essential tremor (MCQ)
- AD in 50% of cases
- can be present in Parkinson
- Sx
Triad: tremor with little disability + normal gait +
family Hx
tremor
199
cogwheel ridigity
slow and shuffling gait with flexed trunk and short steps
no arm swing
bradykinesia
slowness to start movements
micrographia
↓ blinking
slow monotonous speech
progressive forward flexion of trunk
poor balance – suspect Parkinson in a fractured hip
constipation (common)
congnitive impairment – due to:
progressive Parkinson-associated dementia in 30-40% usually after 10
yrs
Alzhimer
medication
normal reflexes
o Dx
clinical!
Dx. diff.
Parkinsonism – doesn’t respond to levodopa
Lewy bodies in the neurons – pathognomonic
o Rx
1. drugs:
types:
- Dopaminergic
Levodopa – best drug, baseline and gold standard of Rx
initiate Rx ASAP
start low: 100 mg/day
↑if needed:Max. tolerated dose = 450-600
mg/day
+ Carbidopa or Benserazide – with onset of disability
(motor disturbances)
improves rigidity, dyskinesia, gait disorder but not
tremors
- Dopamine agonists
Bromocriptine
SE - severe psychiatric disturbances -> not in
elderly with confusion or dementia
Pergolide – assoc. in Rx for levodopa “on-off”
phenomenon
SE - severe psychiatric disturbances -> not in
elderly with confusion or dementia
Cabergoline
- Anticholinergic – for tremor (in young people)
benztropine
benzhexol
201
- COMT inhibitors
entacapone – levodopa potentiation
- others
amantadine
selegiline
approach:
- Mild (minimal disability)
levodopa + carbidopa or
selegiline (can be use as first line monotherapy)
amantadine
- Moderate (disabled but independent)
levodopa
+ dopamin agonist: pergolide or bromocriptine or
cabergoline
- Severe (disabled, dependent on others)
levodopa + pergolide or cabergoline
+ entacapone
Long term problems – after 3-5 yrs of Rx with levodopa
- Dyskinesia: Choreiform, involuntary flickering movt. of mouth
(lips, tongue), face, eyelids, cheeks, limbs, trunk – 80-100% of
patients.
Rx: ↓ Levodopa and carbidopa + add pergolide or
cabergoline
- end of dose failure (effect lasts for only 2-3 hrs)
Rx:
Add entacapone
dosages closer together
- “on-off” phenomenon (sudden inability to move – recovery in 30-
90 min)
Rx:
Apomorphine (+ domperidone to prevent
vomiting) for off phase
add pergolide
- early morning dystonia (clawing of toes)
Rx – slow release levodopa
- nocturnal akinesia
Rx – slow release levodopa
- sundown effect: pts often go psychotic as sun goes down
2. Surgery:
Alleviates only tremor and rigidity
Does not prevent progression to bradykinesia, dysarthria and dementia
types:
- Pallidotomy
- Stereotactic thalamotomy
indic:
- tremor or rigidity not responding to drugs
202
-
types:
Partial (non-convulsive, no loss of consciousness)
- Simple
e.g. Jacksonian march: starts from a part of body and
moves to other area of body
- Complex
with impaired (altered or cloudy but not lost)
consciousness
e.g. temporal lobe epilepsy – with olfactory
hallucinations.
Generalized (convulsive, with loss of consciousness)
- Grand-mal (tonic – clonic)
Sx
usually last 1-2 min
loss of consciousness
tonico-clonic contractions: This is a generalized
seizure with varying phases of muscular rigidity
(tonic) followed by jerking of muscles of body
for several minutes (clonic).
tongue-biting
incontinence
post-ictal confusion
Dx diff with functional or pseudo-seizures = means of
coping with stress (exams, etc.)
Atypical: no loss of consciousness, no tongue-
biting, no incontinence, etc.
Nocturnal epilepsy – Involuntary vocalisation
followed by grand-mal.
blood on pillow & enuresis noticed in morning
- Petit-mal (absence) Consciousness is impaired only briefly (few
seconds). Pt often remains upright and gives a normal appearance
or seems to be staring into space. Absence seizures occur more
often in children.
203
> 10 min
multiple convulsions during 1 episode (complex)
family Hx of epilepsy
o prognosis – excellent
o Mx
reassurance
control temperature - Paracetamol
> 10 min -> rectal diazepam (0.2-0.4-0.5 mg/kg)
if seizures during examination: Observe -> if not improving in 5-10 min -
> rectal diazepam
Oral or nasal midazolam 0.3-0.5 mg/ kg
recurrance > 30-40%
30% in first 24 hrs
- Infantile spasm = Sallam attacks = West syndrome = hypsarrythmia (high amplitude irregular
EEG waves) (M 588)
o funny turns (flexion/ bending forward of trunk and extended limbs)
o first year of life
o assoc. with HSP and intussusception
o Dx: Increased CRH – (corticotrope releasing hormone)
o Rx
ACTH (lowers CRH) – best
- Tourette syndrome (boys)
o Multiple motor tics & 1 or more vocal tics that are recurrent many times a day for > 1 yr
o starts with motor tics
o echolalia
o coprolalia (10% only)
o 3-8 (4-15) yrs
o any stress may exacerbate it
o Rx
1. Clonidine
2. Resperidone
3. Haloperidol
electrode on brain?
- Habitual tics
o Sx
recurrent tics > 1yr
NO echolalia, coprolalia
Syncope
o Transient loss of consciousness.
Associated with blurred vision, dizziness, sweating and loss of postural tone,
followed by spontaneous full recovery results from ↓ cerebral perfusion.
o Causes vary from benign to imminently life threatening.
Dx diff.
Vaso-vagal: with prodrome – vomiting
- syncope after going to bathroom or post-op (pain), change of
position
posture change by standing
206
Neurological:
- Subarachnoid haemorrhage.
- Vertebrobasilar insufficiency. – in posterior circular problems
(vertebrobasilar), less from anterior (cerebral) circ.
Postural (orthostatic) hypotension:
- Diabetes, hypoadrenalism (Addison’s).
- Parkinson’s disease and autonomic failure.
- Drugs: antihypertensives, diuretics, nitrates.
- Cough, micturition or defecation syncope.
- Hypoglycemia (relative).
o DIAGNOSIS:
Priority: Blood glucose test strip and ECG.
Send blood for FBC, U&Es, cardiac biomarkers, pregnancy test, CXR and CT scan.
o TREATMENT:
Underlying condition.
TIA
o Cerebral circ. Oxford 452
o Origin
80% carotid origin
20% vertebrobasilar
o Episodes of sudden transient focal neurological deficit lasting for less than 24 hrs (usually
less than 10 min).
o 12% of patients have a stroke by 1 month (often within 1-7 days).
o types
Anterior
usually carotid artery or middle cerebral artery
Posterior
Vertebral, PICA, basilar
o CAUSES:
Embolic:
Cardiac: Post MI, AF, mitral stenosis, valve prosthesis.
Extracranial vessels: Carotid stenosis, narrowed vertebral artery.
Reduced cerebral perfusion:
Hypotension: Hypovolemia, drugs or cardiac arrhythmia.
Hypertension: Hypertensive encephalopathy.
Hypercoagulable states: Protein C, S or antithrombin III deficiency.
Vasculitis: TA, SLE, PAN.
Lack of nutrients:
Anemia
Hypoglycemia
o CLINICAL FEATURES:
Anterior - Carotid artery dysfunction – unilateral sympt.
Hemiparesis.
Hemianesthesia.
Homonymous hemianopia.
Dysphasia.
208
Dysarthria.
Amaurosis fugax (Transitory monocular blindness).
Posterior - Vertebrobasilar territory dysfunction:
Bilateral limb paresis.
Crossed sensory symptoms.
Diplopia
Bilateral blurred vision
3rd cranial N palsy due to Posterior communicating artery aneurysm
(MCQ)
Bilateral cortical blindness
homonymous hemianopia?
Nystagmus
Ataxia
Vertigo
Cranial nerve paralysis (e.g. IX, X, etc.)
Memory loss
PICA – lateral medullary syndrome, due to injury to lateral part of
medulla oblongata
- vertigo
- nystagmus
- ataxia
- Horner
- dissociated sensory loss (affecting face and limbs – MCQ: Blue
Book p. 401)
dorsal colum medial leminiscus fibers: Ipsilateral
sensory fibres in posterior columns (for touch,
vibration, posture) – they only cross at pons level ->
from there up all the fibres from other side are
together) + contralateral anterior and lateral column
spinothalamic fibres (pain + temperature) – they cross
at spinal cord level)
Corticospinal tract – Motor (UMN)
o 80% of fibres cross at medulla
oblongata level--- lateral corticospinal
o 20 % don’t cross--anterior corticospinal
o DIAGNOSIS:
Glucose test strip.
FBC, ESR, coagulation profile, blood sugar, LFT, electrolytes and lipid profile.
ECG and CXR.
URGENT CT BRAIN to differentiate
hemorrhage from
infarction and to look for structural non-vascular lesion.
CT aspect:
- Infarction – black
- Hemorrhage – white
- Calcification – very white
209
-
- SUBDURAL HAEMATOMA:
o Neurosurgical emergency if mass effect.
o MC (20-40%) venous bleeding, slow deterioration.
o in elderly people
o Between dura matter and arachnoid membrane.
o Imaging: Sickle shaped collection of blood. It will NOT cross the mid-line
-
212
- SAH
o massive pain (worse pain ever)
o Diffuse layering of blood below arachnoid membrane.
o Does not cause mass effect, predisposes to vasospasm.
o PICA aneurysms: Intraventricular haemorrhage.
o
o Causes
Head injury.
Ruptured aneurysm.
in polycystic kidney dis. - AD
HTN.
Coarctation of aorta, anticoagulants
AV malformation.
Coagulopathy or vasculitis.
o Sx
Sudden, severe ‘worst headache ever’
Lethargy, nausea, vomiting, meningism
A 3rd N (Oculomotor) palsy suggests bleeding from posterior communicating
artery aneurysm.
o DIAGNOSIS:
Arrange a CT scan urgently to confirm diagnosis (99% caught - Amit)
Lumbar puncture (1%): If CT scan is negative or unavailable (Xanthochromia =
blood in CSF)
o MANAGEMENT:
O2
Prevent main Cx = Vasospasm
Nimodipine (if BP is stable) – to prevent vasospasm & Subsequent
ischemic stroke!!
3 H therapy:
- control HTN
- hypervolemia – overload patient
- hemodilution – thin blood
Refer to neurosurgical unit.
Lorazepam 0.07mg/kg, diazepam 0.2mg/kg or midazolam 0.1mg/kg for seizures
or severe agitation.
Paracetamol 500 mg and Codeine phosphate 8 mg two tablets orally.
Meningitis
o CAUSES:
213
Meningococcus
Streptococcus pneumoniae.
Listeria monocytogenes (infants under 3 months, adults over 55 yrs,
immunosuppression)
Viruses.
Cryptococcus neoformans.
TB
o CLINICAL FEATURES:
Prodromal malaise.
Generalized headache
Fever, vomiting
TRIAD: fever + vomiting + headache
Altered mental status with irritability and drowsiness (lethargy).
Confusion, coma.
Photophobia.
Neck stiffness ----- Sign of meningial irritation – (also in SAH)
Localized cranial nerve palsies or seizures may occur
o Always consider meningitis in:
Confused elderly.
Sick neonate.
Generalized convulsive status epilepticus.
Coma of unknown cause.
o Meningococeal septicemia
early signs
Muscle pain: Legs.
Abnormal skin colour: Pallor or mottling.
Cold hands and feet.
Rigors, vomiting, headache.
late signs
Petechial rash (non-blanching).
Impaired consciousness.
Meningism.
o DIAGNOSIS:
Blood cultures
CT scan: If focal neurological signs, especially if signs of incr. ICP
LP: If there are no focal neurological signs and no ↑ICP (CI if ↑ ICP is
suspected) – to confirm diagnosis.
CSF findings (table – Jay’s notes)
- Bacterial meningitis: WBC - neutrophils incr. (85%), protein
incr. (1 – normal 0.15-0.4), Glucose decr.
- Viral – lymphocytes incr., normal glucose
- TB – Lymphocytes incr., Glucose decr.
- GBS - Prot. incr., cells normal (WBC are not incr. – 90%,
mononuclear cells incr. – 10%)
o Rx
O2 and fluids.
Ceftriaxone (3rd generation) 2 g IV
214
Sumatriptan 6mg SC
Dihydroergotamine 1 mg IM
Lignocaine
Bridging Rx
often needed while preventive Rx is commenced
C/S to produce rapid suppresion of attacks (within 24-48 hrs)
- Prednisolone oral 50 mg OD for 7-10 dys then taper over 3 wks
may recur when steroids are tapered so preventive drug must be
initiated in parallel
Preventive Rx
Verapamil 160 mg orally daily or
Methylsergide 1 mg orally daily or
Lithium 250 mg orally twice
Raised ICP
o signs of raised ICP
deteriorating/ LOC
deteriorating resp. pattern
HTN with bradycardia
progressive headache, worse when waking up in morning
ataxia & vomiting
lateralizing signs (cranial n. paralysis) – tentorial herniation
3rd n. palsy
- superior eyelid drop = ptosis
- dilated pupils = mydriasis
- diplopia - eye looking “down and out”
4th n. palsy
- diplopia in downward gaze
6th n. palsy (lateral rectus m.)
- diplopia – on lateral gaze
9th n.
- taste absent on post. 1/3rd of tongue
- Absent gag reflex on side of lesion
Seizures
Papilloedema – late sign
usually benign
seizures for 3 years, then suddenly worsening (hemiparesis, etc.)
more common
o Glioblastoma multiforme – much faster
seizures + hemiparesis at the same time
MC malignant and most aggressive tumor
adults
o Astrocytoma - less aggressive
o oligodendroglioma
o ependymoma
Coma and confusion
- Glasgow Coma Scale (GCS)
o Eye 4
1 - No response to pain
2 – Opens eye to pain
3 – Opens eyes to verbal command
4 – Spontaneous eye opening
o Mouth (Verbal command) 5
1 None
2 – Incomprehensive speech
3 – Inapropriate speech (rudeness, responds with something unrelated to the Q)
4 – Confused conversation (doesn’t know where he is)
5 - Oriented
o Hand (motor) 6
1 No response
2 (abnormal) extension response to pain (decerebrated – extended neck,
extended and internally rotated arms, extended legs)
3 (abnormal) flexion response to pain (decorticated – mummy position: flexed
arms, extended legs)
4 Withdrawing to pain
5 Localizes pain
6 Obeys commands
o Values
GCS ≥ 13 -- Mild
GCS 9-12 -- Moderate
GCS ≤ 8 -- Severe
Intubate
GCS > 8 – Nasogastric (avoid in base of skull fractures) or orogastric tube
- Coma
o GCS ≤ 8
o Types
Metabolic.: Reactive pupils + low GCS
causes: METABOLIC
- major organ failure
- electrolyte or endocrine disorder
- toxins or temperature (hypothermia)
- acid disorder
218
- base disorder
- O2 - hypoxia
- lactate
- insulin or inf.
- cardiac output decr.
Primary CNS problem: Unreactive pupils + low GCS
- Coma of unknown cause:
o give TONG
Thiamine (B1)
O2
Naloxone
Glucose
- Head injury
o Cushing’s Triad – in advanced states of incr. ICP (brain herniation is imminent!)
irregular resp. (resp. depression)
Bradycardia
HT (incr. systolic, decr. diastolic)
o level of consciousness – Most important
- Confusion
o Postop. confusion and disorientation = Acute delirium
causes
MC = hypoxia
- due to:
atelectasis
analgesics
anesthetic from surgery
Mx/ Dx – Pulse Oximetry
o Other causes
Sepsis
MC cause of confusion in elderly – UTI
Alcohol withdrawal
hyponatraemia, hypoglycemia
arrhythmias
hypotension
o Confused elderly person
Investigation
Urine microscopy
Blood culture
FBE+ ESR
Blood glucose
Urea, creat. and elctrolytes
Ca and PO4
TFT
LFT
serum B12 and folic acid
ECG, troponin
Chest X-ray
219
CT brain
Syphilis serology
ABG
- Brain lobes function.
o Parietal
types
Dominant
- simple arithmetical calculations (acalculia)
- writing (agraphia)
- right/ left orientation + touch his right ear with his left hand (left-
right disorientation)
- name his fingers (finger agnosia)
Non-dom.
- recognize digits and letters written in his palm (=graphestesia)
- copy an object that is drawn: house, flower, clock, 2 pentagons
that are overlapping (constructional apraxia)
- recognize shape of objects – astrognosis, tactile agnosia
o Temporal lobe
Memory
Short term – first affected in Alzheimer
Long term
o Frontal lobe
Grasp reflex
Verbal fluency – say 7-15 words that start with a certain letter
Interpretation of proverbs
Similarities and differences between objects, people, etc.
Motor sequencing: fist-edge-palm - 5 times
o Occipital lobe
Visual field – examination
- Horner syndrome:
o Due to lesion or compression of one side of the cervical or thoracic sympathetic chain,
which generates symptoms on the ipsilateral side of the body.
o symptoms:
Triad:
Miosis
Partial (palpebral) ptosis
Loss of hemifacial sweating
(PAMELa): Ptosis, Anhydrosis, Miosis, Enophthalmos & Loss of ciliospinal reflex
o causes:
1. Tumors - often bronchogenic carcinoma (Pancoast tumor) of apex of lung
T1 compression: affects small muscles of hand (can’t oppose thumb
against other fingers) + sensitivity affected on inner arm (above elbow)
2. PICA
Syringomyelia
Cluster headache - combination termed Horton's headache [6]
Trauma - base of neck, usually blunt trauma, sometimes surgery.
Aortic aneurysm, thoracic
220
o degen. of the posterior (dorsal) column of the spinal cord, which carry information that
help maintain a person's sense of position (proprioception), vibration, and discriminative
touch. Triad: Unsteadiness of gait + urin. Retention + lightining pains.
o Sympt. start after decades
o Rx
Penicillin
- GB Syndrome
o Acute inflam. neuropathy (autoimmune) (AB destroy the myelin) of peripheral nerves,
Triggered by an infection
URTI
dig. – Campylobacter
o inquire about SLE, HIV, Vaccination
o Sx
Progressive ascending bilat. paralysis: Legs -> Arm –> Face
Hypo- to areflexia
Cranial n. palsies – bulbar lesions (I, II and VIII are never affected)
Paresthesias, sensory nerve loss
Dysautonomia
Tachycardia/ bradycardia
hT/ HT
Urinary retention
o Dx
Immune stimmulus should be detected
Monospot test - EBV
Cold agglutinins
- CMV
- HIV
1. to confirm - CSF
Protein ↑
Cells normal
- WBC are not incr. – 90%
- Mononuclear cells incr. – 10%
2. Nerve conduction studies
+ EMG
o Mx
Monitor resp. fc. with Forced Vital Capacity
if FVC < 1 L -> assisted resp. (risk of resp. failure) – 30%
Physiotherapy
prevent contractures of the muscles
plasmapheresis
IV gamaglob. -> ↓the recovery time
Steroids are NOT beneficial
- Botulism – flaccid type of paralysis, descending
- Myasthenia gravis
o autoimmune dis. which affects muscle strength
o assoc. with
thymic tumours
222
- Sydenham chorea
o in Rheumatic fever + SLE
o invol. dancing moments, patient is very emotional, hypotonia
rapid, uncoordinated jerking movements affecting primarily face, hands & feet
- Huntington’s disease
o AD – mutation on chromosome 4
o causes neuronal loss in frontal lobes and other parts of brain
o movement disorder (Chorea) + behaviour changes + dementia
o progression in generation - earlier onset of disease in descendents
- CT brain
o indications
loss of consciousness (LOC)
post traumatic amnesia
vomiting or raised ICP
focal neurol. sign
otorrhea, rhinorhea
fits, seizures
penetrating wounds
on warfarin
o careful in children -> incr. risk of brain tumor
- MRI – only for spine or posterior cranial fossa (brain)
- acute disseminated encephalomyelitis or postinfectious encephalomyelitis, a demyelinating
disease of brain and spinal cord, possibly triggered by vaccination or viral infection
- Cerebral palsy
o Static, non-progressive
Hypoxia -> ischemic injury -> hypoxia disappears, injury stops progressing
o cause
80% antenatal cause
Maternal inf. – chorioamnionitis
Congenital inf. – TORCH
Prematurity - periventricularmalacia
10% intrapartum cause (birth asphyxia)
10% postpartum cause (asphyxia, meningitis, etc.)
o Sx
problem in muscle tone (usually spasticity – biplegia MC in preterm,
quadriplegia in term), posture, movement (can’t walk properly)
epilepsy – 30%
intellectual disability
impaired vision
impaired hearing
Dermatology - OK
o Description
general outlook of patient
location and pattern of lesions
morphology of lesions
well defined/ poorly defined
mono/poly morphous
224
- Acyclovir
- Silver nitrate
Oral acyclovir, famcyclovir, etc.
- only within 72 hrs of rash
- 5 days
- doesn’t cure but shortens the episode
Analgesia
- topical – lignocaine, povidone iodine
Ice packs
Wear loose clothing
Cx
Postherpetic neuralgia
- Rx - amytriptiline
o if recurrent HSV, do HIV testing
- HIV – Murtagh 259
o least risk of inf. = hemophiliacs
o after travel to Thailand
o Stages:
Primary HIV inf. = Erythematous maculopapular rash all over body
Mononucleosis-like inf., with Splenomegaly and lymphadenopathy
MCQ: fever and generalized rash erythematous maculopapular, all over
the body, mainly face and trunk, non itchy, no Hx of allergy or drugs, in
30 yr old man, fashion consultant, onset 2 days ago, splenomegaly,
lymphadenopathy. In sexual rship with another man for 2 yrs, without
condoms.
Chronic HIV inf.
2 wks – 20 yrs.
chronic diarrhoea, axillary & inguinal lymphadenopathy, failure to
thrive
AIDS
o HIV antibody testing should not be performed routinely on pts but only after obtaining
their informed consent and after pretest counselling
o Dx
Screening – ELISA:
Positive - repeat in 12 wks
Unprotected intercourse + negative – repeat in 12 wks
Confirmation – Western blot (ELISA can be positive in EBV inf.)
evaluate with: Viral load + CD4
o Cx
CMV retinitis
Pneumocysitis carinii pneumonia
Candida inf. (Esophagitis)
cryptosporidiosis – diarrhoea
Cryptococcus neoformans = fungs opportunistic inf. in immunsuppressed (HIV,
kidney transplant, TB), complicated with cryptococcal meningitis
CSF findings – like in viral meningitis
- Rx – Amphotericin B IV
227
o Mx
CD4 < 200 - prophylaxis
- Scabies (scabie, riie)
o elderly in retirement places, homeless
o Mite - Sarcoptes scabiei
o Erythematous papular rash, intensely itchy -> scratch marks
o itch worse at night or when the body is worm (after shower)
o wrists, hands and web spaces (between fingers), male genitalia, elbows, feet, axilla,
ankles, nipples
o Norwegian scabies – crusted form, with millions of mites
nursing homes
AIDS
o transm.
skin to skin
clothes, bed sheets
sexual contact
o MCQ: itchy rash on skin of 19 yr woman
o Dx
clinical
confirmed: Scrapings seen under microscopy
o Mx
Permethrin cream 5% or
Benzyl benzoate 25% emulsion
apply all over body for whole night, wash in morning
avoid hot bath or scrubbing body
treat everybody in house
wash the clothing and bedding in hot water and expose to sun
- MCQ: Pt wid scabies treated wid permethrin. After 1 month symp again developed. What next tt
option ?
a) repeat permethrin
b) corticosteroids
- Re treat the patient again after 1-2 weeks
- Prolonged itching after scabies is normal and usually requires NO ttt or cortisone
- Head lice (paduchi)
o Pediculus humanus capitis
o white spots in hair
unlike dandruff, the white spots can’t be brushed off
o Rx
Pyrethrins foam/ shampoo
Permethrin
- Fleas (purici)
o itchy erythematous maculopapular lesions, grouped in clusters
o on arms, forearms, leg, waist
- Bed bugs
o 3 or more bites along superficial blood vessels – maculopapular red lesions
o extremely itchy
228
- exanthematous dis.
DISEASE INCUBATION PRODROME RASH OTHER FEATURES &
PERIOD INFECTIVITY
(DAYS)
Chickenpox 10-20 None Macules, papules, Infective until vesicles are crusted
(Varicella) vesicles & pustules of over
different ages
Measles 9-14 Cold, cough, Red, confluent, Koplik’s spots, may be quite ill
Paramyxovirus conjunctivitis maculopapular
Rubella 14-21 None Discrete ink, Occipital & preauricular
(German maculopapular lymphadenopathy. High fever.
measles or 3 Fetal abnormality
day measles)
rash (exanthem) on face which spreads to trunk, limbs and usually fades after 3
days (known as 3-day measles). The facial rash usually clears as it spreads to
other parts of the body. The rash of German measles is typically pink or light
red. The rash causes itching and often lasts for about 3 days.
Other symptoms include low grade fever, swollen glands (sub occipital &
posterior cervical lymphadenopathy), joint pains, headache and conjunctivitis.
if mother is infected within first 20 wks of pregnancy, child may be born with
congenital rubella syndrome, which entails a range of serious incurable illnesses.
o Infectious mononucleosis (kissing disease, glandular fever) - from Epstein Barr Virus
Sx (MCQ 2077 p70)
Triad = Sore throat + fever + lymphadenopathy
Maculopapular rash – 5%
- but 90-100% of pts have prescribed ampicillin or amoxycillin,
develop an extensive rash, with a purplish tinge!!
Sore throat, pharyngitis (MC), tonsilitis, petechiae of palate. MCQ
fever, fatigue, weight loss, malaise, loss of appetite.
lymphadenopathy
Splenomegaly – 50%
Hepatitis, jaundice, hepatomegaly – 5-10 %
Hemolysis
Resembles acute HIV, CMV and toxoplasmosis inf.
Dx
FBE: lymphocytosis (50%) with > 10% atypical lymphocytes (incr. in
bands – immature lymphocytes) (atypical lymphocytes are incr.)
Confirmed by Monospot or Paul-Bunnell test (for heterophil AB): Only
positive in 70% in first wk. That why repeated.
- False pos. in hepatitis, Hodgkin’s lymphoma, acute leukemia
EBV IgM – better than Paul-Bunnell test – Murtagh 805
Cx
Splenic rupture (feels faint, collapses)
Chronic fatigue syndrome (myalgic encephalomyelitis, chronic Epstein-
Barr syndrome, chronic neuromuscular viral syndrome)
- > 6 months
- extreme exhaustion, headache, muscle ache, poor concentration
and memory, hypersomnia, arthralgia, tender swollen lymph
glands, subjective feeling of fever, sore throat
Rx
rest, reassurance, psychological support
Rx
Bed rest
Symptomatic treatment.
o Viral exanthema (4th syndrome, Duke’s dis.)
caused by various viruses (enterov.)
rubella-like rash, confined to the trunk
no. of skin rashes:
- Measles
- Scarlet fever
230
> 4 yrs :
if EBV – no A/B
if GAS
- if GAS:
Penicillin
if allergic, erythromycin
- Scarlet fever (Scarlatina)
o children, aboriginals (Strepto. inf. in general)
o GA Strepto. pyogenes which produces erythrogenic toxin (exotoxin)
o Sx
prodromal sympt.: fever, sore throat, malaise, then
rash appears on 2nd day, sand-paper like under touch, blanches on pressure,
spares face, palms and soles
is worse in skin folds. These Pastia lines (where rash runs together in
armpits and groin) appear and can persist after rash is gone.
Circumoral pallor
Strawberry tongue
recovers in 5 days – fine desquam. on recovery
o Dx
PR interval can be prolonged -> may be evolving towards rheumatic fever
o Cx
Rheumatic fever
GN
Erythema nodosum
o Rx
Phenoxymethylpenicillin 250-500 mg orally q.d.s. for 10 days
- Rheumatic fever
o after a Streptococcus group A (S. pyogenes) inf.: tonsilitis, scarlet fever
o indigenous population
o Sx
acute onset with fever, joint pains, malaise
flitting arthralgia mainly in leg (knees, ankles) and arms (elbows, wrists)
one joint settles as the other one gets affected
o Dx
2 or more major Jones criteria
1 major + 2 or more minor Jones criteria
Major criteria:
polyarthritis
carditis
- MC affected = mitral valve
- can lead to congestive heart failure
Sydenham’s chorea
subcut. nodules
erythema marginatum
Minor criteria
arthralgia
ECG – prolonged PR interval
234
bald head
including lips (lower)
BCC and melanoma rarely on lip
- neck
- + oral cavity, tongue, tonsil, genitalia
more keratotic and more scaly
MCQ: lesion on lip of 35 yrs son (SCC)
Squamous - upper layer of skin
although they metastasise to lymph nodes, there is no evidence that
prophylactic lymph node dissection is beneficial
initially firm thickening of skin --> hard nodules --> ulcerate!
Premalignant lesions
- Solar keratosis = Actinic keratosis JM1365
mildest lesion caused by exposure to sun
with atypical cells
on areas most exposed to sun
back of hands – very common
involves epidermis and dermis
scaly lesion with hyperemic basis that bleed easily with
trauma
Auzpitz sign – bleeding when scratching it
Rx
Cryotherapy – liquid nitrogen
Excision
if left untreated, 15-20% progress to SCC
- Burns - burn scars
- Chronic ulcers
- Leucoplakia
with dysplasia
non-smoker
white patch, hard to take off
- Bowen’s dis. = SCC in situ (slow growing intra-epidermal CA)
scaly red plaque with clearly defined margins
not much related to solar damage
lower legs of females
Rx
Depth
- in situ – Bowen
- invasive
Rx (Q 18 block 2 bridging course) MCQ
- Surgical excision in depth and laterally.
4-5 mm margin if diameter < 1 cm
> 5 (10) mm margin if diameter > 1 cm
BCC (not causing keratin scaling MCQ)
MC skin CA in Aus.
80% males
236
- SCC (only in sun exposed areas)= BCC in both exposed and non
exposed areas.
- ear
outer helix – SCC
inner helix - BCC
o Melanotic
Malignant melanoma
MCQ: pigment mole on trunk of a 30 yr old woman; dark spot was there
for many year (many born with it) but in last few months spot has
become darker
mainly in elderly
slow growing intra-epidermal
mainly on sun exposed area
Rx - excision
- Superficial spreading
MC type – 70%
with strking color variation
multiple or unusual colors – poorer prognosis
grows horizontally (not vertical)
Rx - excision
- Nodular – 20% (called so bc its elevated and looks nodular)
vertical spread but no radial growth
easy to misdiagnose (DD pigmented BCC)
but variable colors, irregular borders
blueberry appearance
most dangerous
EFG mnemonic:
elevated
firm
growing for more than 1 month
- Acral lentiginous – 2.5%
MC in palms and soles and distal phalanges
poor progn.
MC in dark skinned people
macule -> then a nodule surrounded by a pigmented
halo
- Amelanocytic
skin colored
poor progn. – diagn. too late
can involve lymph nodes – satellite nodules = late sign
Metastases
- lungs
- liver
- brain
- small bowel -> can cause intussusception
Dx
- ABCDE
asymmetry
border is irregular
color – blue-black +/or variety of colors
diameter – when 1st seen usually at least 7 mm in diam
elevation – indicates invasion
Rx
- Suspicious lesion MCQ
local excision biopsy – 2-3 mm till mid fat layer –> send
to histopathol.
if malignant melanoma:
239
o Rx
excision + biopsy, because it looks a lot like SCC (to exclude SCC)
o Seborrheic keratosis (senile wart) --- Benign (JM 1364)
o waxy texure, painted on appearance
o very superficial, epidermis only
o like a sultana pressed on the skin
o usually multiple
o can be raised (stucco – on lower legs) or plaque like lesion with waxy texture
o hemosiderin causes brownish spots on it
o Rx
excision – only if asked for, for cosmetic lesions
- Molluscum contagiosum – on whole body (JM 1363)
o Self limiting, Pox Virus
o Single or multiple lesions: vesicular papules with central umbilication.
on any part of body
o Kissing lesion: Spread to areas of skin contact, e.g., from chest wall to upper arm.
o No systemic symptoms
Advice to parents
• Give the child a shower instead of a bath (the child can spread the virus to other parts of the body).
• Don’t share baths.
• Wash and dry bath toys after use.
• After showers/baths/swimming, dry areas with molluscum last and don’t share/re-use towels.
• Wash hands after touching molluscum.
• Don’t exclude children from school or playing together. MCQ
• If swimming (Avoid swimming in public pool MCQ) , reasonable precautions include
covering the lesions with waterproof tape and having personal kick-boards.
o Mx
Difficult to treat
Reassurance: will resolve within 1 year with no scarring (MCQ)
Pin pricking – if only a few lesions
Cryotherapy – variable success
- Skin infection after trauma
o Staph. Aureus not Strep pyogenes (MCQ)
o Clostridium perfringes
o Pseudomonas aeruginosa - anaerobes
- Longstanding subcutaneous swelling
o Lipoma – diagn. diff. with epidermoid cyst
common benign tumor of mature fat cells in the subcut. tissue
Sx
soft, well defined, lobulated, painless, rubbery in consistency, freely
mobile
- except trunk and back – attached to skin
may be one/ many
any site – MC limbs (arm) and trunk
family Hx.
pain + tender = angiolipoma
Sx
241
reassurance (benign)
removal – for cosmetic reasons
- recurrance is common if incompletely removed
o Ganglion (cyst)
wrist
deeply placed subcutaneous lump around joints or tendon sheets
more proeminent on tendon contraction or joint movement.
do not communicate with adjacent joint (only to one they are located on)
Rx
Aspiration – if cystic
o Bursae
cystic sacs between skin and underlying bony prominences
inf. => bursitis (e.g. olecranon)
o Epidermoid (Sebaceous, Keratinous) cyst (JM 1360)
any age, any site
MC – back
traumatic origin
filled with a fatty, white, semi-solid material called sebum
sometimes associated with hereditary syndrome – e.g. Gardner Syndrome
when infected = Cock’s peculiar tumor (on head)
resemble SCC
central punctum with keratin – attached to skin
Rx
No inf.
- enucleation
inf.
- incision + drainage
- Dermoid cyst = congenital inclusion cyst
o true hamartomatous cyst
o in ovaries, cranium, spine
o thin wall cyst
o with fatty material and occasionally hair, even teeth
o at any age
o on face, around the eyes – attached to underlying periosteum
o Rx – excision
- Warts (over growth of skin) JM 1361
o caused by HPV
o types:
common warts – HPV 2, 4
fingers, elbows, knees
plane warts – along scratch lines
filiform warts – face, neck
digitate warts - scalp
plantar warts – HPV 1, 2, 3, 4
anogenital warts – HPV 6, 11
Condyloma accuminata (MCQ Rx in pregnancy)
- Rx Podophyllotoxin if fails… Cryotherapy, laser, electrocautry
242
C/S
chloral hydrate
iodides or bromides
Lithium
Antiepileptics – e.g. Phenytoin
Quinine
OCP
o Response to any Rx occurs after 2 months or later
o types
Mild and moderate
Rx
- Basic regeimn – 3 months, then review
Benzoyl peroxide – in morning +
Tretinoin or isotretinoin cream at night (causes
photosensitivity)
only specialist can prescribe it
causes atrophy of sebaceous glands
teratogenic –> do a pregnancy test first!
- alternative Rx/ if recalcitrant
topical clindamycin
topical erythromycin
Inflammatory acne (moderate to severe papulopustular) – min. 4 mths (std. 6
mths)
Rx
- Oral tetracyclin or doxycyclin
- Erythromycin
Severe (nodular/ cystic) or non-responsive
Rx
- Oral isotretinoin
- Spironolactone – antiandrogenic effect
- Dapsone – antibact. (leprosy), anti-malleric, antiinflam.
- OCP – second line
o additional advice
usually not assoc. with food
if it does (e.g. chocolate) –> avoid that food
avoid oily and creamy cosmetics
avoid picking and squeezing blackheads
UV/ sun light helps
- Rosacea (JM 1326)
o unknown etiology
o middle aged women
o acneiform lesions on forehead, cheeks, nose, chin - with papules, pustules & erythema
o flushing and blushing precedes the rash
o telangiectasia, erythema
o photosensitivity, hypertrophy of soft tissue on nose
o improved by OCP
o worsened by topical C/S
247
o Rx
1 – Tetracyclin
1 - Erythromycin
- Dermatitis herpetiformis
o Herpes simplex-like vesicles, erupt at dermatoepidermal junction
o Extremely itchy
o Mainly over extensor surfaces of elbows, knees, trunk, shoulders
o MC assoc. with coeliac disease
o Skin biopsy is diagnostic
o Rx
gluten-free diet
dapsone 100 mg/ day
- Lichen planus (JM 1305)
o Idiopathic inflam. condition found on flexor surface of wrist and hand
o occasionaly triggered by drugs or Hep. C infection
o can affect skin, hair, nails, oral and genital mucosa
o Violaceous polygonal flat topped papules that show lacy white lines (Wickham’s striae)
o can form ulcers
o risk of malignant transformation of oral l.p. needs to be considered, especially in
patients with chronic ulcers and Hx of tobacco use
o Mx
skin eruptions resolve in 6-9 mths, but leave discolored marks and no scarring
moderately potent topical C/S ointment
if not improved, oral prednisolon
- Lichen simplex chronicus: Fibrosis and thickening of skin due to excessive itching caused by
eczema, seborrhic dermatitis, psoriasis and dermatitis a process called lichenificaton.
- Lichen sclerosus (JM 1163)
o Premalignant for SCC of vulva
o Reticular white (sclerotic) lesion in vagina or genital area causing irritation, pruritis,
o Mx
must do biopsy
if no SCC is Dx – still life long surveillance.
- Nappy rash
o MC cause: simple irritant dermatitis
o itchy – fungus
o non itchy – seborrheic dermatitis
Common causes Uncommon causes Rare causes
Irritant - MC Staph. inf. Tinea
Candidiasis Strep. inf Gluteal granuloma
Seborrheic dermatitis Herpes simples Zinc deficiency
Psoriasis
Atopic dermatitis
o irritant nappy rash
loss of epidermal barrier fc. due to overhydration and exposure to fecal
enzymes
later becomes colonized by candida
o Mx
248
o These yeasts are normally found on the human skin and only become troublesome under
certain circumstances, such as a warm and humid environment
o Rx
selenium sulphide
clotrimazole, ketoconazole
- Portwine stain
o cavernous haemangiomas
o can have vasc. malformation = Sturge – Weber syndr.
Rx – laser therapy
trigeminal n. affected
- Erythema marginatum – rheumatic fever
- Erythema nodosum (M 259, fig. 30.1)
o acute inflam. immunol. reaction
o resolves in 2-3 wks, with discoloration but no scarring
o tender, bright, red, raised subcut. nodule on shin (usually bilat.) below knee
o can be seen in:
Sarcoidosis
Dx – chest X-ray
IBD - Crohn
autoimmune dis. – SLE, rheumatoid arthritis, Behcet’s syndrome
inf.: strepto., viral, TB, leprosy, fungus, toxoplasmosis
drug induced – sulphonamide, OCP, tetracyclines, bromides
TB
lepromatosus leprosy
Mycoplasma pn.
lymphoma, leukemia
idiopathic
o Rx
bed rest
RICE and NSAIDS
Prednisolone
- Erythema multiforme (JM 1341)
o very serious condition – can evolve to a Stevens–Johnson syndrome
o mild to severe forms
o causes
HSV
mycoplasma
drugs
Sulphonamides
Trimetoprim
Allopurinol
NSAIDs
anticonvulsants: phenytoin, lemotrigin
nifedipin?
o macules, papules, wheals, vesicles (hands, feet, face, mouth) – lesions with raised edges
and central scar (target appearance)
round to oval triphasic iris-like lesions known as target lesions
250
fungal inf.
…
o types
Areata (Patchy, non scaly) – one or more discrete circular areas of hair loss
can occur anywhere on body (not just on head)
triad: patch of complete hair loss + clean scalp + exclamation-mark
hairs
Totalis – involves whole scalp
Universalis – involves eyebrows and eyelids as well
o triggers
severe febrile illness
severe emotional stress
o Dx
FBE – Hb, thyroid, iron, zinc
biopsy of scalp
examine hair under microscope
exclamation mark sign
pull hair sign
examine nail – psoriasis
where else in body is hair loss: eyebrow, chest, etc.
o Rx
aim: regrowth of hair + pyschological support
initial – potent topical C/S Betamethasone 0.5% – 1 – 2 times/ day
small lesion – intralesional C/S
triamcinolone acetonide
oral C/S if topical failed
topical dithranol
topical minoxidil
adjuvant
topical immunotherapy
UV radiation (PUVA)
drugs – each used for 3-6 months before switching to another one
o prognostic
33% chance of complete regrowth within 6 mths
50% chance of complete regrowth within 1 yr
80% chance the cured people will relapse
- 4 conditions that can be confused with alopecia:
o Tinea capitis
scaly! (not clean skin as in alopecia)
o Trichotillomania
they don’t have clear patches of hair loss, but patches with short/ long hair
Hx of stressor (in family)
o Lichen planus – causes permanent scarring of scalp
o Discoid cutaneous lupus – causes permanent scarring of the scalp
- any hairy lesion on skin = benign until proven otherwise
Nail problems
- Ingrowing toe nail/ onychocryptosis:
253
no edema
less granulation tissue
loss of hair
ABI (Ankle brachial index) < 0.5-0.8
Hx of arterial disease, smoking, DM
o Rx
we need patient’s compliance
promote clean granulation tissue
appropriate cleansing and dressing
avoid antiseptics and soaps
just wash with NS
use intrasite gel and Benzoyl peroxide
occlusive bandages with Zinc oxide
in infection or cellulitis - A/B
compression banding is mainstay of Rx
from base of toe (toe not included) to just below knee
depending on ABI
- ABI < 0.8 – caution
mild compression for 0.6-0.8
Bed rest, elevation above heart level
RICE:
Rest Ice Compression Elevation
encourage early mobilization and good nutrition
if edema elevate leg + diuretics
ulcers will not heal in edema
treat varicose veins
Unna`s boots - compression stockings + unna`s paste = 15% Zinc oxide
o + Metabolic Ulcer
DM – (Neuropathic) = Trophic ulcer
Due to diabetic neuropathy causing loss of sensation which follows an
injury of which pt is unaware.
Deep punched out lesions over pressure points.
MC site – ball of foot under 1st metatarsal head. Sometimes heel may
also be affected.
Ulcers may extend to bones and joints.
Prone to secondary infections.
Rx
- control diabetics.
- infection with appropriate antibiotics.
(IV Flucloxacillin + IV Gentamycin + IV Metranidazole)
- Sensory loss: Gloves and stockings
- Dx to confirm cause – Arterial Doppler
o + Pyoderma gangrenosum
deep ulcers, usually on legs in IBS, RA, multiple myeloma, etc.
oral C/S as Rx of choice in pyoderma gangrenosum (skin manif. in ulcerative
colitis)
o Infections. – Smelly discharge
256
Mantoux test:
delayed hypersensitivity test
- evaluated after 72 hrs
< 5 mm = negative
- do vaccination!
5-10 mm = past vaccination
> 10 mm = positive
- evidence of inf.
active
inactive – latent TB
chest X Ray
if productive cough
sputum – acid-fast bacili
- stain – Ziehl Nielson
- culture
TB specific – interferon gama release assay
bronchoscopy and biopsy can be considered
pleural effusion – with monocytes
o Mx
only by specialist! (not by GP)
notifiable dis. -> Dept. of Human Services
contact tracing by Dept. of Human Services
bacterial confirmation and drug susceptibility testing first – only then will be
Rx
no isolation!
o Rx
Active TB (RIPE)
4 drugs (rifampicin, isoniazid, pyrazinamide, ethambutol) for 2 mths
then 2 drugs (rifampicin and isoniazid) for 4 mths
- total 6 mths
Latent TB (Mantoux positive, no sympt., no X Ray features)
when active TB is excluded: isoniazid mono-therapy for 6-9 mths
treat only specific groups:
- recent TB converters (Mantoux test neg., recently – within last 2
yrs - became pos.)
- children, adolescents
- close contact with patient smear-TB positive
- patient with HIV, DM uncontrolled, CRF, Ch liver Failure
- overseas trained people (immigrants)
Pregnant (IRE)
start Rx ASAP
- pyrazinamide not recommended
- isoniazid, rifampicin, ethambutol – 9months
don’t cross placenta
no teratogenic effect
minimal conc. in milk – breast feeding is NOT CI
Isoniazid resistant TB
258
Traveller’s disease
- Traveller’s diarrhoea (after visiting developing countries)
o 1. E. coli – 12-72 hrs
o 2. campylobacter – 2-5 days
o 3. yersinia & pseudomonas aer.
o Giardia – 1-4 weeks
- Travaller’s dis. (Alena)
o travelling to an area with sleeping sickness – Rx – give him vaccine
o after travel
Sympt. within 2 wks in most diseases
Sympt. > 2 wks -> only HIV
o if GIT symptoms
Dx
1 - stool microscopy
2 - stool culture
o Traveller’s diarrhea:
Acute (not persistent)
E. coli - MC
6-12 hrs after food intake
lasts for 2-3 days
watery stool ± vomiting
Mx
- Rehydration in mild cases
- A/B only in moderate and severe cases
Norfloxacin, ciprofloxacin, azithromycin
Persistent diarrhoea
Giardiasis (symptoms 3-25 days after infection)
- no mucous, no blood, no fever
- Mx - metronidazol
Amoebiasis
- mucus and blood
- Mx - metronidazol
Typhoid fever
Salmonella typhi
incub 3-21 days
spread: Feco –oral Route
Sx
- Triad: stepladder fever (gradually increases over 4 days) + abd.
pain + bradycardia
- insidious onset, headache, dry cough, fever, abd. pain, pea-soup
diarrhoea or constipation
- high fever with relative bradycardia (usually fever causes
tahycardia)
- abd. pain, splenomegaly
- rose spots on trunk (40%) – late sympt.
- CNS signs: confusion, lethargy, coma, meningism = Toxic state
- Dx
260
viral disease
more common in US
o Immunisations
Compulsory
Yellow fever
Menigococcus
Voluntary
Hep. A, B, E
Typhoid
Cholera
Japanese B encephalitis
- triad: febrile illness + vomiting + stupor
Rabies
Typhus
Plague
- Zoonoses
o Brucellosis (undulant fever, Malta fever)
from cattle
Triad: malaise + headache + undullant fever
Cx – chronic fatigue syndrome
o Q fever – Coxiella Burnetti (MCQ 3174 P285)
in cattle (and sheep) handlers and farmers
abattoir workers
Triad: fever + headache + prostration
sudden onset with fever, rigors, myalgia
pneumonia, hepatitis, endocarditis – sometimes
Dx - Serum antibody level (MCQ )
Rx – Doxycycline
Vaccine
o Leptospirosis:
in abatoir workers, veterinarians, sewage workers, farmers
Sx
Triad: abrupt fever + headache + conjunctivitis
undulant fever?
abrupt headache
severe myalgia
jaundice
petechial rash on skin
liver and spleen enlarged
- HIV
o chronic diarrhoea, axillary and inguinal lymphadenopathy, failure to thrive
- Diarrhoea
o hyponatremic – can cause seizures but less often
o hypernatremic – with less dehydration but more often seizures
Other infectious diseases
- Ischaemic colitis
263
o in elderly
o Perfusion problems e.g. after thrombosis
- Gas gangrene (is an emergency)
o also known as "Clostridial myonecrosis"
o bacterial infection that produces gas within tissues in gangrene.
o deadly form of gangrene usually caused by Clostridium perfringes bacteria.
o sudden onset of pain + swelling in contaminated wound + brown exudate + dusky
decoloration of skin + gas in tissue on palpation and X Ray + toxemia + shock & circ.
failure
o Dx
initial Dx is based on patient’s Sx and exam. findings
finding bubbles in muscle tissue on X Ray increases suspicion
exam. of secretion from wound swab under microscope may reveal Clostridium
culture from swab will confirm it
o Rx
Wound debridement
A/B
Hyperbaric O2
Anticlostridium immunglobulins
- Meningococcal septicemia
o Rx
GP
Benzyl penicillin -> send to tertiary hospital
- Blood cultures -> ceftriaxone
ED
Ceftriaxone
Cefotaxine
o Prophylaxis
Rifampicine – in close contacts of patient
- Hemolytic uremic syndrome vs. DIC
o Cause: after camping + E. coli for both
o DIC: Bleeding from venopuncture sites, hematuria, incr. bruising
o HUS: Hemolysis (low Hb), kidney involv. (high urea, high creat.), unconj. bilirubin incr.,
pallor, hematuria, hemoglobinuria, incr. in uric acid.
- Tetanus – Murtagh 1384
o DPT – 3 shots required: 1st and 2nd 4wks apart and 3rd after 12 months
Time since vaccination Type of wound Tetanus toxoid Tetanus immunoglobulin
Hx of 3 or more doses of tetanus toxoid (or DPT)
< 5 yrs All wounds No No
5-10 yrs Clean minor wounds No No
All other wounds Yes No
> 10 yrs All wounds Yes No
Uncertain vaccination Hx, not vaccinated or < 3 doses of tetanus toxoid (or DPT)
Clean minor wounds Yes No
All other wounds (+ A/B) Yes Yes
264
- Trachoma:
o MC inf. cause of blindness in aboriginals
o direct transm.
o Chlamydia trachomatis
o 5 stages: FISTO
1. follicles > 5
2. inflam.
3. scarring
4. trichiasis (inversion or eversion of eyelashes)
5. opacity of cornea
o Mx: SAFE
Surgery
A/B
Non-pregnant woman, child – Azythromycin
Pregnant woman, child < 6 kg – Erythromycin or Roxythromycin
Facial cleanliness
Environmental upgrade: sanitation, hygiene
Hematology - OK
Leukemias
- Multiple myeloma (MM)
o cancer of plasma cells, a type of WBC normally responsible for production of antibodies.
o elderly – 60 yrs
o Sx
Triad: weakness + back pain + weight loss
CRAB: calcium incr., renal failure, anemia, bone lesions
Osteoporosis, back pain (> 80%), bone pain and tenderness
↑ pathological bone fractures (MCQ)
weakness, tiredness and recurrent inf.
CRF
hyperviscos. syndrome – clots in brain, dementia, etc.
o Dx
Normocytic anemia
Next examination: Protein electrophoresis in serum and urine -> ↑ level of
abnormal globulins
Serum – M (monoclonal protein) spike in IgG zone
Urine - Bence-Jones protein (composed of free light chains)
ALP is normal, unless fractures present
very high ESR
↑ Ca, normal phosphate
Best examination: Bone marrow aspiration to confirm Dx: increased plasma
cells, replacing bone marrow
X Ray: “Punched out osteoclastic lesions on skull.”
o Rx
Chemotherapy
Medial survival = 3 yrs
- Leukemias
ALL AML CLL CML
265
o Cx
Thrombosis, due to blood thickening: MI, stroke, DVT, Budd-Chiari syndrome
o Dx criteria
Major criteria
incr. red cell mass
- Man 36ml/ kg
- Woman 32 ml/ kg
SaO2 92%
Splenomegaly – 60% - most characteristic
Minor
Platelets > 400,000
WBC > 1200
leucocyte Al PO4 > 1000 ?
serum B12 > 900 micrograms/ ml ?
unbound B12 > 2200
o Rx
Venesection
- Ig stuff
o Ig that crosses placenta = IgG
o Ig related to Grave’s disease = IgG
Coagulation problems
INR, PT (extrinsic APTT (intrinsic & common Platelets Bleeding time
pathway) pathways)
DIC Incr. Incr. Decr. Incr.
Heparin Incr. Incr. N N
Warfarin, Vit. K def. Incr. Incr. N N
Hemophillia A N Incr. N N
Von Willebrand N Incr. N Incr.
Thrombocytopenia N N Decr. Incr.
HSP (vasculitis) N N N N
- DIC
o Sx
Bleeding from venopuncture sites, hematuria, ↑bruising
o Dx
↓Platelets & fibrinogen
incr. D-dimer = incr. fibrin degradation products
+ schizocytes = fragmented RBCs
o Rx
fresh frozen plasma
IV heparin – to stop clotting in peripheral vessels
- Bleeding problems
o Haemophilia – X-linked recessive (only in boys)
A
Fact. VIII deficiency, more common
Sx
268
- cocaine abuse
- chronic rhinitis, chronic sinusitis
- ulcers in nasal cav.
- perforation of nasal septum
- nasal polyps
Bleeding disorders: von Willebrand dis., etc.
- Thrombophilia – Murtagh 1367
o primary tendency to coagulopathy
o types
inherited
fact. V Leiden gene mutation
prot. C deffic.
prot. S deffic.
prothrombin gene mutation
antithrombin deffic.
acquired
anti-phospholip. AB
lupus anticoagulant
incr. homocystein
o thrombophilia screening – all the factors above:
fact. V Leiden
prot. C
prot. S
prothrombin
antithrombin
antiphosphopholipid AB
lupus anticoag.
homocystein
+ anthrombin C AB?
+ antiocardiolipin AB?
o indic. for investig.
recurrent thrombosis
venous thromboembolism < 40 yrs
arterial thrombosis < 30
skin necrosis on warfarin
recurrent fetal loss
familial thromboembolism
o MCQ:
daugther asking for OCP, mother had DVT
woman with DVT wants to get pregnant
-> do thrombophilia screen
Anemia
- Iron studies – Murtagh table p. 146
o 1. Serum iron
o 2. Transferrin (major iron carrying protein in blood)
Transferrin conc. = TIBC (total iron-binding capacity)
Level rises in iron deficiency
272
Phototherapy or exchange
transfusion – if kernicterus +
folic acid to prevent
megaloblastic crisis
Splenectomy
Hereditary eliptocytosis
Thalassemia: microcytic hypochromic anemia
Sickle cell anemia
Defic. of G6PD
o X- linked recessive – in boys only
o African (Sudanese), Mediteranean,
Asian
o causes episodic H. anemia due to ↓
capac. of RBC to deal with oxidative
stress; precip. by
inf.
antioxidant drugs:
Sulphonamides, antimalarial,
nitrofurantoin, Vit. C Vit. K,
traditional medicine, high dose
aspirin, naphthalene,
cotrimoxazole
broad b eans (favism)
o Neonatal jaundice
o Dx
Beutler fluorescent spot test
Heinz bodies (bill cell) –
Denatured Hb within RBC
Peripheral smear: Bite cells
sometimes with spherocytes
o no Rx
defic. of pyruvate kinase
Acquired
ABO/ Rh immunis.
Drug toxicity
o A/B: antimalarials, sulphamethoxazole
o Anti-inflammatory
o Penicillin, methyldopa
Infections:
o Mycoplasma
o malaria
DIC
Auto immune:
o cause
Idiopathic - 50%
Non-Hodgkin lymphomas
SLE
278
o action
cold agglutinin dis. - IgM
act at body temp. – Ig G -
autoimmune hemol. anemia
o Dx – direct Coomb’s test +
3. Anemia of chronic disease and malignancy
- enough iron, but intercellular iron transport within bone marrow
is suppressed in inflam. => erythropoiesis is suppressed
- MCQ: boy who looks pale and has chronic diarrhea.
4. Chronic kidney disease – defic. of erythropoietin
- Rx – adm. of erythropoietin
5. Endocrine disorders: hypothyroidism (can be macrocytic as well)
- with bradycardia, fatigue, constipation, lymphocytosis
6. Bone marrow replacement
- metast.
- myelofibrosis
- ALL, AML, CML, CLL, lymphoma
- Aplastic anemia
o destruction of hematopoesis and bone marrow stem cells
o pancytopenia + hypocellularity in bone marrow
o types
Congenital – Fanconi
Acquired
idiopathic – MC
immune
post-viral inf.
- Parvovirus B19
- HBV
- Epstein-Barr
- HIV
o Sx
no splenomegaly
no hepatomegaly
no lymphadenopathy
o Rx
supportive
RBCs, platelets transfusion
A/B
immunosuppresion – if immune cause
Bone marrow transplant
Digestive system - OK
Jaundice and other biliary problems
- Murtagh – table P 622
- Bilirubin metabolism: MCQ 2079 P 71
o Old erythrocytes -> destroyed in spleen -> heme is converted to unconjugated billirubin-
> sent to liver -> conjugated bilirubin -> eliminated through bile -> some is metabolized
in large intestine to urobilinogen (-> stercobilinogen -> stercobilin, gives feces brown
279
color) -> some of urobilinogen is reabsorbed and eliminated through urine (along with
an oxidized version, urobilin).
o Pathology:
liver problems + biliary obstruction = some of conjugated bilirubin leaks out
from hepatocytes in blood and is excreted in urine as bilirubin -> dark urine.
Hemolytic anemia - ↑ unconjugated bilirubin in blood -> ↑urobilinogen in urine
high ratio of unconjugated to conjugated bilirubin in serum.
Hemolytic Hepatic Obstructive
Function test Pre-hepatic Jaundice Hepatic Jaundice Post-hepatic Jaundice
Total bilirubin Normal/ Increased Increased
Conjugated bilirubin Increased ↑
Unconjugated bilirubin Increased Normal/ Increased Normal
Urobilinogen Normal/ Increased Decreased/ Negative
Normal Dark (urobilinogen + Dark (conjugated bilirubin)
Urine Color
(urobilinogen) conjugated bilirubin) Absence of urobilinogen
Stool Color Normal Pale
Alkaline phosphatase
Increased
levels
Normal
Alanine & Aspartate
Increased
transferase levels
Conjugated Bilirubin in Urine Absent Present
- Jaundice
o Blirubin > 17 µmol/L
o Clinical jaundice > 50 µmol/ L
- Hyperbilirubinemia:
o Unconjugated
Hemolytic jaundice (Prehepatic) – starts after 4-6 mths
Spherocytosis
G6PD deficit, (X linked recessive), Dx by Heinz bodies
Drugs – Methyldopa, penicillin
Sickle cell anemia
- Dickle cell crisis
sickle cells get plucked inside capillaries & cause infarcts
precip. by
infection
cold weather
hypoxia
dehydration
acidosis
surgery
types:
Vaso-occlusive
Splenic sequestration
o => infarction
280
- rifampicin
radiographic agent
Crigler Najjar syndrome --- AR (very rare)
types
- I
Uridine diphospho- glucuronyl transferase absent
unconj. bilir. > 340 µmol/ L -> kernicterus, unless
treated
Rx
Phenobarbital doesn’t help
Phototherapy, exchange transfusion, etc.
- II
UDP-G decr.
Unconj. bilirubin < 340 µmol/L
Rx
Phenobarbital helps
Hypothyroidism
Rx - thyroxine
ABO/ Rh hemolysis
Breast milk jaundice
Physiological
o Conjugated
familial disorders
Rotor syndrome—AR - rare
- non-itching jaundice
- liver cells are not pigmented
- no Rx is required
Dubin Johnson syndrome---- AR
- inability of hepatocytes to secrete conjugated bilirubin into bile
- liver is pigmented black
- no Rx is required
Hepatitis
both direct and indirect bilir. ↑
FTT, dark urine, pale stools
drug induced
Chlorpromazine
OCP
Primary biliary sclerosis
Biliary atresia
after first week
stools are white
AST/ ALT incr.
chronic cholestatic jaundice
Neonatal sepsis
Galactosemia
Postop. jaundice
Intraductal problems/ Obstructive Jaundice
282
Rx
- Bed rest
- < 1.5 L of fluids/ day
measure body wt. daily
- Spironolactone 100 mg (up to 400 mg)/ day
add furosemide if response is inadequate
- Paracentesis + albumin infusion
Bilateral parotid gland enlargement
Pigmentation of skin
telangiectasis
palmar erythema
easy bruising
spider naevi
muscle wasting
testicular atrophy
gynecomastia
asterixis (hepatic flap)
lymphadenopathy
NO peripheral neuropathy
o Dx
Smooth muscle autoantibodies
o poor prognosis factors – Child-Pugh classif. of severity
1. Encephalopathy resistant to Rx
2. Ascitis resitant to Rx
3. ↑ bilirubin
4. Low serum albumin
5. Incr. INR
o Cx
Portal HTN
portal pressure gradient (difference in pressure bw portal and hepatic
veins) of 5 mm Hg or greater
types
- Prehepatic
portal vein thrombosis
congenital atresia
- Intrahepatic.
congenit. fibrosis
Primary biliary stenosis -> primary biliary cirrhosis
Hemochromatosis
other infiltrates:
Sarcoidosis
Wilson’s dis.
chronic viral inf. – HBV, HCV, HDV
Alcohol
- Posthepatic
Budd-Chiari = hepatic v thrombosis (or
thrombophlebitis)
288
Pancreatic pathology
- Acute pancreatitis
o past Hx of gall stones, alcoholism
o previous attacks
o risk factors: GET SMASHED
Gall stones
Ethanol
Trauma
Steroids
Mumps
Autoimmune
Scorpion, snake bites
Hypercalcemia, hyperlipidemia, hypertriglyceridemia, hypothermia
ERCP, emboli
Drugs (azathioprine), duodenal ulcers
o Sx
first sympt = severe and constant pain in epigastrium region, radiating to back
pain may be partly relieved by sitting up and leaning forwards.
nausea and vomiting
fever, tachycardia, pale, sweating, anxious (shock)
reduced or absent bowel sounds, abd. distension
Cullen sign – periumbilical echymosis (discoloration)
Bluish discoloration in the loins (Grey Turner’s sign): Uncommon and develops
after several days.
o Dx
I - FBE
Amylase – early, at least 3x > normal level
- Inaccurate ↑ in people with hyperlipidemia!
Serum lipase – most reliable
if jaundice, high bilirubin, severe pancreatitis, suspicion of stone
II = ERCP – Dx and Rx
MRCP – more acurate, non invasive
if no jaundice, mild pancreatitis
II = abd CT - best
- if stone => do III. ERCP
U/S to identify Gall stones
X Ray
exclude intraperit. gas as a result of visceral perforation
- usually normal or showing ileus
exclude basal pneumonia
LFT
CRP incr., leucocytosis
glucose incr., Ca decr.
o Rx
Admission
hydration:
needle-by-mouth (nothing by mouth) = iv fluids
290
analgezics – morphine
antiemetics – Metoclopramide, Prochlorperazine
Ca gluconate (if Ca decr.) – slow IV
o mortality > 20%
o Complic
early
shock
acute renal failure
severe dehydration => renal failure (hypovolemia)
DIC
sepsis
hypocalcemia, hyperglycemia
resp. problems
- atelectasis
- pneumonia
- pleural effusion
late
Pseudocyst
- no epithelial lining: Wall = granulation tissue-> fibroid wall
- complic. of acute or chronic pancreatitis
- doesn’t move with resp. (retroperit.)
- Size of cyst
< 6 cm – small, usually asympt., will resolve on its own
> 6 cm – large, symptomatic, can cause gastric outlet
obstr. or compression of bile ducts
Palpable, painful
Mx – if stomach obstr. or bile ducts drainage,
even if < 6 weeks, do drainage into stomach,
duodenum or jejunum
o laparoscopic or laparotomy (depending
on size and surgeon)
- Age of cyst
< 6 wks – fragile wall (only granulation tissue), can
break
Mx – wait, will probably disappear on its own
> 6 wks – mature, with fibroid capsule, stronger,
resistant wall
Mx – no matter the size, do drainage
- Dx
best investig: CT scan
abscess
pressure on surrounding organs (if inflamed) obstruct.
hemorrhage/ rupture
Portal V thrombosis
- Chronic pancreatitis
o MC assoc. with alcoholism
o Sx
291
pain
o Dx
amylase is N or slightly incr.
some have calcification
o if associated DM -> Rx with low doses of insulin
- Dilatation of gall/ bile ducts
o Dx
first – USG
ERCP - best
MRCP – even better – if available
- Pancreatic CA
o head of pancreas
men
Sx
Triad: anorexia + wt. loss + jaundice ± epigastric pain
distended gall bladder, which moves with respiration
jaundice, pale stools, dark urine (Obstr. jaundice)
Wt. loss
Dx
U/S: distended intra and extrahepatic bile ducts
- pancr. duct might be dilated as well
Urine: conj. bilirubin, no urobilinogen.
Blood: AST/ALT moderately elevated, incr. total and conj. bilirubin, incr.
ALP
Abdominal pain
o Pancreatitis – Hx of alcoholism or biliary stones
fever + epigastric pain + radiating to back
no abd. signs except for
Cullen sign
Gray Turner sign
o Hemorroids – small amounts of painless rectal bleeding
o Anal fissure – small amounts of painFULL rectal bleeding
o Rectal CA – tenesmus + rectal bleeding + alternate bowel habits + wt. loss
o pregnant woman with lower abd pain
I trim – ectopic
II trim – ovarian torsion/ twisted ovarian cyst
III trim – red degeneration of fibroid
o a few wks Hx of postprandial pain = Mesenteric ischemia
Acute mesenteric ischemia Chronic mesenteric ischemia
Hx of atherosclerosis/ AF (irregular pulse)/ digoxin After eating -> abd. pain
Acute abd. pain + tenderness + no bowel sounds
Blood stained stool
o Acute mesenteric ischemia = acute abd. pain + tenderness + irregular pulse + no
bowel sounds = Mesenteric infarction (Afshan)
CAUSES:
Mesenteric arterial embolism (often associated with AF).
292
o Peptic stricture
lower 3rd of esoph.
Cx of reflux oesophagitis
rare today with current treatments
Dx
Barium swallow
Endoscopy
Rx
dilate stricture
treat reflux
o Globus hystericus = lump in the throat
o Pharyngeal pouch (Zenker’s diverticulum)
post. pharyngeal diverticulum, pushing the esophagus
elderly
Sx
dysphagia, food regurgitation, gurgling in neck
coughing immediately after eating (food regurgitated in airways)
halitosis
no pain
o Esophageal diverticulum
usually sec. to an underlying motility problems -> sympt. due to primary pbm
hiatal hernia
o Achalasia
Failure of relaxation of lower oesophageal sphincter + ↑muscle tone
women, 30-40 yrs
Sx
dysphagia for liquids and solids organic, mechanical causes usually have
dysphagia only for solids!)
- if severe: has more difficulty in swallowing liquids than solids
- usually not progressive!
wt. loss
regurgitation
- at night
- when lying down
chest pain, hiccups, aspir. pneumonia
Dx
1. Plain X Ray
- air-fluid level behind heart
- absence of gastric air bubble
2. Barium swallow
- distended esoph. - S-shaped + narrowing of contarst in barium
swallow = “rat-tail” (not charact.) + fluid level
3. Manometry - high tension at lower end of esophagus
4. Endoscopy – exclude CA
Cx
Stricture
295
Esophageal CA
Rx
Botox inj. – Short term relief
Drugs:
- Nitrates—relaxes lower esoph. sphincter
- Ca channel blockers
Pneumatic dilatation – may recur
Laparoscopic cardiomyotomy (Heller’s myotomy) – the best
o Esophageal CA
Barrett’s esophagus = Premalignant lesion for adeno CA of esoph. = metaplasia
with columnar-lined epithelium in lower 3rd of esophagus + ulcer inside +
stricture (blue book MCQ 3.106) P 250
due to prolonged reflux
types
SCC CA
Adeno CA
Sx
Triad: fatigue + gradual dysphagia + wt. loss
severe dysphagia at beginning of meal + painful swallowing + severe
wt. loss
- gradual (increasing) dysphagia initially for solids, then for liquids
dysphagia + hoarseness of voice = Esoph. CA
Dx
Barium swallow – apple core
Endoscopy: narrowing of esophagus + ulcer
- + Biopsy
if initially negative (especially with premalignant
lesion), repeat (MCQ)
Upper GI hemorrhage
o Mortality: 5-10% related to age over 60 years, comorbid disease, shock and
coagulopathy.
o CAUSES:
Peptic ulceration: Over 40% of cases.
1. Duodenal Ulcer.
Gastric Ulcer (less common).
Gastric erosions or gastritis.
Post-alcohol.
Drug-induced (Salicylates, NSAIDs, steroids).
Mallory-Weiss tear (partial esophageal tear following vomiting or retching).
bouts of protracted vomiting or cough -> blood
- tear of mucosa at gastroesophagal junction
- self limiting
- Dx – esophagoscopy
2. Bleeding esophageal or gastric varices associated with portal HTN
MC in alcoholic cirrhosis
Reflux esophagitis.
Others: Gastric neoplasm, coagulation disorders.
296
o PRESENTATIONS:
Hematemesis:
Fresh red blood.
Altered blood ‘coffee grounds’.
Melaena.
Collapse and shock.
Syncope and postural hypotension.
Hematochezia (bright red rectal bleeding).
Signs of CLD: Jaundice, bruising, palmar erythema, clubbing, gynecomastia,
spider naevi, hepatomegaly and encephalopathy.
Signs of portal HTN: Splenomegaly and ascites.
o MANAGEMENT: General
High-dose oxygen.
Fluid replacement.
Cross-matched blood if patient is shocked or bleeding is continuing.
Disease specific:
Peptic ulcer: PPI
- Omeprazole 40-80mg IV followed by and infusion at 8 mg/h.
Varices: Octreotide 50µg IV(↓portal vessel pressures in bleeding varices)
Urgent endoscopy: to differentiate the cause of bleeding +
allow injection therapy or banding for varices.
adrenaline injection in ulcer’s edges
Sangstaken-Blackmore tube
with 2 balloons
after being introduced and inflated, it has to be checked every 2 hrs
- did it stop bleeding?
- prevent mucosal ischemia
- Stomach CA
o Risc factors
gastric resection > 25 yrs before (CA on gastric stump)
↑age (> 40 yrs)
smoking
blood group A
atrophic gastritis
o Male 3:1
o Metastases
left supraclavicular node
ovary – Krukenberg tumor
liver
o Sx
Triad: anorexia + dyspepsia + wt. loss
o Rx - Gastrectomy
Cx
Dumping syndrome
- types
Early
297
- failed Rx after 1 yr
- complic.
uncontrollable bleeding
perforation
pyloric stenosis
- suspicion of malignity in GU
- recurrent ulcer after previous surgery
- + elderly – tolerate less well the blood loss
types
- GU
partial gastrectomy +
Billroth I (gastroduodenostomy)
Billroth II (gastrojejunostomy)
- DU
Vagotomy
truncal
highly selective
- Apendicitis
o CLINICAL FEATURES:
Anorexia, nausea, vomiting, diarrhoea or constipation.
Low-grade pyrexia.
Localized abdominal pain: Epigatrium, periumbilical region, RIF.
Tenderness and guarding in RIF.
Rectal examination: To help diagnose a retrocecal or pelvic appendix.
o Typical march of symptoms (J.B Murphy):
Prodromal mild bowel upset.
Development of abdominal pain, which progressively worsens.
Anorexia (key word), nausea, vomiting.
Moderate (not high) fever.
Signs of focal peritonitis over inflammed appendix.
o DIAGNOSIS:
Physical examination: Abdominal auscultation, palpation, percussion.
FBC and Urinalysis: Leukocytosis, rule out UTI.
Pregnancy test: Female adolescents.
USG: Female (doubt and no peritonitis).
CT: For doubtful cases only.
o MANAGEMENT:
Normal saline infusion.
Give gentamicin 5 mg/kg IV, ampicillin 1 g IV and metronidazole 500 mg IV if
rupture is suspected with peritonitis.
Refer to Surgical team.
- Meckel’s diverticulum: (MC presentation is asymptomatic anomaly noted during surgery for
another cause)
o most frequent malformation of gastrointestinal tract
o rule of 2s
2% population
2 inches in length
300
2% are symptomatic
usually discovered during abd. surgery for a different problem
2 feet from ileo-cecal valve (distal ileum)
age group – 2 yrs
male:female = 2:1
2 types of ectopic tissue:
gastric
pancreatic
o Sx
painless rectal bleeding (not mixed with feces), malena or blood loss anemia
acute/ chronic bleeding
umbilicus fistula
o Dx – Tc99m pertechnetate scan, laparotomy
o Cx
intestinal obstruction
o Rx – surgical resection
- Diverticular disorder (large bleeding not accompanied by fecal mater)
o 90% in descending colon
o due to lack of fibres
o over 40 yrs
o 1/3 people > 60 yrs
o Sx
usually asympt. = diverticulosis
sometimes - irregular bowel habits, constipation
diverticulits – sympt. (< 10% of people with diverticulosis)
This follows inflammation of one or more colonic diverticulae.
LOWER abdominal pain radiating to left iliac fossa + tenderness in LIF
can occur anywhere (e.g. small bowel)
Bloody diarrhea
Sometimes with sudden PROFUSE rectal bleeding (without feces).
Sx
- triad: acute pain + left-sided irradiation + fever
- Low-grade fever.
- Abdominal tenderness in LIF
- pain increased with walking and change of position
- Guarding on LIF with a palpable mass.
Complications:
- Perforation.
- Paracolic abscess
- Severe bleeding (elderly).
- Fistula formation (Colovesical fistula + vagina, small bowel).
MCQ 2045 P128.
- Bowel obstruction.
DIAGNOSIS
- Request an erect CXR if perforation is suspected.
- USG, CT scan – detect fistula or perforation
- Sigmoidscopy
301
Rx
- Commence an IV infusion to treat dehydration or shock.
- Analgesia.
- Antibiotics: Gentamicin, ampicillin and metronidazole.
- Refer to surgical team.
- Profuse rectal bleeding
o diverticular Disease
o angiodysplasia
o ulcerated CA
o IBD
o ischemic colitis
Inflammatory bowel disease (IBD)
Ulcerative colitis Crohn (terminal ileitis) disease
Main Sx Long history of bouts of diarrhea + blood Triad: colicky abd. pain + diarrhoea +
in young adult (15-40 yrs) fever Recurrent diarrhea (with blood
May present as a fulminating attack. and mucus in stools) in a young person
(20-40 yrs) + abd. Pain.
Fever, tachycardia and hypotension. Malaise, wt. Loss. May present acutely
Risk factors: family Hx, previous attacks, with obstruction, perforation or RIF
low-fibre diet pain. CAN MIMIC acute appendicitis.
Site Colon only (begins in rectum, continues All GIT, mouth to anus (terminal ileus),
proximally) lead pipe deformity repeated perianal lesions (abscesses,
fistulas), mouth ulcers – caused from
granulomas (granulomas in Crohn - non-
caseating - and TB - caseating)
½ ileocolic, ¼ - small bowel only, ¼-
colon only
Rectal Rectum always involved Lump in right iliac fossa + rectal changes
(e.g. fistula)
Systemic Wt. loss, fever, lethargy are UNCOMMON Wt. loss, fever, lethargy, etc.
Sx
Lesions The whole colon involvemt but superficial Skip lesions but affecting whole width
mucosal only of intestinal wall. Fine granular mucosa
FBE ESR Incr.
Dx Extensive mucosal ulceration may leave X Ray: Free air associated with
normal mucosal islands (pseudo-polyps) perforation may be seen.
visible on plain film. Stenotic regions are best visualized with
Dilation of the transverse colon > 6 cm Ba follow-through studies or on
indicates presence of toxic megacolon. colonoscopy.
Sigmoidoscopy: granular red proctitis, Sigmoidscopy: Cobblestone appearance
with contact bleeding (patchy mucosal edema) Aphthous
1st Step: Stool culture - exclude a ulceration
gastrointest. Infection Colonoscopy – Dx diff. with UC
CA Colon CA more often, > 7 yrs (colon CA more rare)
100 x incr. risk for adenoCA in affected
portion (terminal ileum)
Extrainte Arthritis, ankylosing spondylitis, sclerosing Arthritis, ankylosing spondylitis,
302
o
o DIAGNOSIS:
Send blood for FBC.
Urea and electrolytes.
Lipase.
Amylase.
Blood sugar levels.
Request erect and supine abdominal X Rays and look for following features:
- SMALL BOWEL OBSTRUCTION - LARGE BOWEL OBSTRUCTION
304
Not USG
o Duke’s classif.
Stage Extension 5 yr survival
A Mucosa and submucosa 90%
B Muscularis or serosa 75-85%
C Regional lymph nodes 30-40%
D Distant metastases <5%
Duke A – 75% detected with FOB
o Rx
Duke A, B – surgery
pancolectomy
paucy surgery
C,D – surgery + radiation
- Peutz-Jehgers – AD = hereditary intestinal polyposis syndr.
o dev. of benign hamartomatous polyps in the GIT -> strong tendency to dev. CA in
multiple sites (breast, liver, pancreas, etc.), while the polyps don’t have malignant
tendency
o lowest malignant potential (2%) for colon CA
may undergo malignant transf. into adenocarcinoma
o hyperpigmented (black) macules on the lips and oral mucosa
- Tumors in small bowel – predom. benign
o types
Adenocarcinoma
100 x incr. risk in Crohn in the affected portion (distal ileum)
Lymphomas
terminal ileum
proximal jejunum – assoc. with celiac dis.
Carcinoids
Familial adenomatous polyposis
incr. risk of duodenal and small bowel carcinoma
Peutz-Jehgers – hamartomas, may undergo malignant transf. into
adenocarcinoma
- Adenoma with incr. malignant potential (benign tum. of colon)
o villous
o > 2 cm
o multiple
o with dysplasia
- benign villous adenoma
o Sx - clear discharge
o Cx - causing marked electrolyte imbalance = depletion syndrome - prerenal azotemia,
hyponatremia, hypokalemia
Anal pathology
- anal anatomy:
o lower ½ of the anal canal – sensitive, painful
o upper ½ of the anal canal – where the hemorrhoids start from
separated by the dentate line
- Anal fissure
308
40%
slow growth
better prognosis: stage 1 - 98% 5 year survival rate
90% diagnosed at stage I
lymphatic spread
- -> retroperit. lymphnodes -> mediastinal -> left cervical with
worst prognosis (eval. with CT)
tumor markers - normal
- purple book: raised in a large proportion of seminomas?
sensitive to radiotherapy
non-sensitive to chemotherapy
non-seminoma (teratoma)
60%
rapid growth
poorer prognosis: stage 1 - 75% survival at 5 yrs
60% Dx at stage I
tumor markers – markedly incr.
- 1 - alfa fetoprot.
- 2 - beta HCG
blood stream metastases to liver and lungs
- + lymph. nodes involv.
sensitive to chemotherapy
o staging
I – only testis
orchidectomy
II – paraaortic lymphnodes involved (below diaphragm)
orchidectomy + lymphnode resection
III – lymphnodes above the diaphragm
radiotherapy or chemotherapy
IV - lungs, liver metastases
radiotherapy or chemotherapy
o Dx
1. USG
2. tumor markers:
alfa fetoprot.
beta HCG
- Alpha-fetoprotein (AFP, a-fetoprotein)
In adults, levels over 500 nanograms/milliliter of AFP
are seen in only three situations: Hepatocellular
carcinoma, Germ cell tumors, and metastatic cancer in
the liver originating from other primary tumors
elsewhere.
- Beta HCG (human chorionic gonadotrophin)
raised in testicular cancer
- Carcinoembryonic antigen (CEA)
serum from individuals with colorectal carcinoma,
gastric carcinoma, pancreatic carcinoma, lung
311
Dx
- U/S
- no aspiration (can spread the CA)
in children
types
- Bilat – usually disappears at 1 yr
- Unilat – tense
Might persist after 1 yr -> 90% will resolve by 18 mths
> 2 yrs -> refer for surgical intervention.
o Cryptorhidism:
2-4% at full term
20% in premature babies
1% at 1 yr
2/3 are in superf. inguinal pouch – can be palpated
types
Undescended
Retractile – can be manipulated into the scrotum
Ectopic – 5%
Ascending
risk for
1. Torsion
2. Testic. CA (seminoma) – 5-10 x incr. risk
testic. dysplasia
infertility
most assoc. with indirect inguinal hernia??
- Hernias – Murtagh 1081
o types
Inguinal
Direct
- men
- doesn’t go to scrotum
- doesn’t usually strangulate (least often)
- through the post. wall of the inguinal canal, above the inguinal
ligament, above and lateral to pubic tubercle.
Indirect
- at external inguinal ring, above and medial to pubic tubercle
- cough impulse +ve
- pain referring to testicle
- disappears when lying down, usually reducible
but can strangulate
- if inguinoscrotal -> you can’t get above swelling (continues
toward abd.)
- Dx – Clinical!
Femoral
below the inguinal ligament, below and lateral to pubic tubercle
female, after multiple pregnancies or wt. loss
often irreducible
315
X Ray
Endoscopy
Manometry
- Rx
Antisecretory drugs
PPI
H2 receptor blockers
if severe sympt. – surgery: Nissen fundoplication
prophylactic AB least needed in fundoplication
o Rx
surgical repair
conservative
truss to control a small inguinal hernia, with a perineal band to control
slipping
in
- asympt. patients
- associated medical conditions, with significant operative risk
o Sx
Obstruction – w/o any previous abd surgery -> hernias:
I - femoral
II - indirect inguinal
III - direct inguinal
(Obstruction – w/ previous abd surgery
adhesions!!)
Renal, urinary and male pathology - OK
- Renal function.
o Plasma urea & creatinine
o Most accurate tests: eGFR (new standard) or creatinine clearance test
- Renal failure
o CRF
Def. = GFR < 60 ml/min/1.73m2 for ≥ mths w/ or w/o evidency of kidney dis.
causes
MC – DM
HT
GN
- MC with IgA nephropathy
Analgesic nephropathy
Polycystic kidney dis.
Reflux nephropathy
Gout
Drugs:
- Aminoglycosides: Gentamicin, etc.
- Vancomycin
- Tetracyclines
- Cephalosporins - some
- NSAIDs, COX-2 inhibitors
- ACE inh. and AIIRA antagonists
317
- Lithium
Stages – 1-5, based on eGFR
1. > 90 (Normal)
2. 60-89 – mild
3. 30-59 – moderate
4. 15-29 – severe
5. < 15 – end-stage kidney failure -> requires dialysis or transplantation
Sx
triad: a/n/v + fatigue + sallow (yellow-brown) skin
anorexia/ nausea/ vomiting
tiredness, lethargy
polyuria with less concentrated urine (can’t concentrate urine)
normocytic anemia
- due to defic. of erythropoietin
Rx – erythropoietin
Mx
restrict protein in sympts. of uremia (vomiting, etc.)
low sodium and potassium
best way to measure day to day fluid balance = Wt.
dialysis
- hemodialysis – 2/3
- peritoneal dialysis – 22%
kidney transplant
o Acute renal failure: ARF
Triad: extreme malaise + anorexia/ nausea/ vomiting + confusion ± oliguria
types – by the cause:
Prerenal – ischemic
Postrenal - obstruction
Kidney (intrinsic)
- GN
- Acute tubular necrosis: ATN- MC cause
Death of tubular cells that form the tubules that
transport urine to the ureters.
Tubular cells continually replace themselves and if the
cause of ATN is removed then recovery is likely. ATN
presents with ARF and is one of the MC causes of ARF.
ATN is classified as a "renal" (i.e. not pre-renal or post-
renal) cause of ARF.
Classification
Toxic ATN occurs when the tubular cells are
exposed to a toxic substance (nephrotoxic ATN).
o can be caused by free Hb or myoglobin,
by medication such as antibiotics and
cytostatic drugs, or by intoxication
(ethylene glycol, "anti-freeze",
poisons, organic solvents, heavy
metals)
318
4. systemic vasculitis
II. Nehprotic syndrome: edema + hypoalbuminemia +proteinuria
1-4 yrs
Sx
- triad: proteinuria + generalised edema + waxy pallor
- proteinuria + dysmorphic hematuria + RBC casts = glomerular
origin
- proteinuria > 3g/ 24 hrs
- generalized gravitational edema (anasarca), ascites, periorbital
puffness
- hypoalbuminemia < 25g/L
- normal BP, No hematuria
causes
- 1/3: systemic kidney dis. (DM, HBV, malaria, etc.)
- 2/3 (90%): idiopathic nephrotic syndrome
Dx: kidney biopsy
Minimal change dis. – MC (85%)
o modest if any hematuria
o responds to C/S!
focal segmental glomerular sclerosis - FSGS =
GN (10-15%)
o frequent in HIV
o = GN
HT
significant hematuria
RBC casts
o no response to prednisolone!
Mx – renal biopsy to conform
the type of lesion
membranous nephropathy
o hyaline, granulous casts in urine
membranoprolif. GN
Rx
- C/S - prednisolone
-> if they fail -> renal biopsy:
MC
o minimal change nephritis/dis. in
children or
o membranous glomerulonephritis in
adults?
CA?
III. asympt.
- Proteinuria
o N: < 100 mg/ 24 hrs
o Pathol. > 300 mg/ 24 hrs (> 150 mg/ 24 hrs in adults)
> 1 g/ 24 hrs – serious problem
≤ 1 g re-examine
322
orthostatic
fever
…
o causes
orthostatic
5-10%
adolescents
usually self-limiting
- can foreshadow serious kidney dis.
DM – Diabetic microalbuminuria
first sign of DM nepropathy = Kimmelstiel-Wilson lesion (diabetic
glomerulosclerosis)
- UTI
o types
sterile pyuria
asympt. bacteriuria
treated only
- if recurrent in pregnancy
- if recurrent after sexual intercourse
acute cystitis
dysuria, urinary frequency
acute pyelonephritis
loin pain, fever, rigors, nausea, vomiting
dysuria, urinary frequency
urethral syndrome
dysuria and frequency, but nothing in the cultures
e.g. interstitial cystitis
- continuous pain relieved briefly by bladder emptying
- small hemorrhages on distension of the bladder
o Dx
(MCQ recalls: urine sample
0-12 mths: suprapub. (SPA)
1-3 yrs: catheter
> 3 yrs: MSU
URINE COLLECTION:
> 3-4 yrs
- Midstream specimen (MSU)
- Catheter specimen (CSU)
in women with failed MSU
< 3-4 yrs
- Suprapubic aspirate collection (SPA): Any growth indicates
infection.
Urinary dipstick test: Only a screening test for UTI.
leucocytes
nitrites - bacteria
- but not in all the inf. nitrites are present!! (e.g. some Gram-pos.
cocci don’t produce nitrites)
323
Microscopic exam.
> 5-10 WBCs/ HPF
- = > 5-10 x 106 WBC/ L
> 8000 WBC/mL in phase-contrast microscopy
Culture
MC: E. coli + Staph. saprophyticus > 90%
> 105/ ml (108/ L) in fresh MSU
o Rx
Acute cystitis:
AB - TG (Alena)
- 1 – Trimethoprim – not in pregnancy
- 2 – Amoxiclave – also in pregnancy
- 3 – Cefalexin – Drug of choice in pregnancy
- 4 – Nitrofurantoin – also in pregnancy
duration of Rx
- 5 days in women
10 days if known urinary tract abnormality
MSU – 3 wks later
+ make the urine alkaline with sodium citrotartrate
- 14 days in men
+ investigate underlying abnormalities, e.g. prostatitis
Acute pyelonephritis
same AB – use for 10 days
ciprofloxacin – if resistance
severe inf. + septicemia: Amoxycillin + Gentamicin – 14 days
in recurrent UTIs after coitus (in women)
Rx
- A/B before or after each coitus
trimethoprim
nitrofurantoin
- prophylactic coitus-time A/B: as effective as continuous Rx
Pyelonephritis in pregnancy and puerperium
2% of women
when unilat., MC on right side
anorexia, nausea, vomiting
cause - due to dilatation and slower emptying of the urinary tract, due
to high progest. in pregnancy
MC agent is E.coli
Pregnancy
Cephalexin 500 mg orally 12 hrls for 10 days – class A
amoxy + clavulanate (500 + 125 mg) 12 hourly for 10 days
- class B in pregnancy (some teratogenicity)
nitrofurantoin 50 mg orally 6 hourly for 10 days– class A
Children
Sx
- Non-specific: fever, irritability, poor feeding and vomiting.
324
horshoe kidney
polycystic kidney
bilat. large kidneys, with multiple cysts
Sx
- renal pain
- hematuria
- UTI
- progressive renal impairment
hydronephrosis
o trauma of kidney
- 1 kidney smaller than the other
o causes
normal
hypofc. kidney
o Dx. diff
Doppler U/S – blood flow
renal isotope scan – renal fc.
- Urinary retention
o acute – BPH
painful
o chronic
painless
- Acute urinary retention
o PREDISPOSING FACTORS:
Prostatic hypertrophy.
Urethral stricture.
Bladder neck obstruction by fecal loading or pelvic mass
Pelvic neoplasm.
Anticholinergic drugs.
Pregnancy.
Local painful conditions such as genital herpes.
Neurogenic: Multiple sclerosis.
o often precipitated by extreme cold or alcohol
o CLINICAL FEATURES:
Enlarged bladder is easily palpable.
Dull to percussion.
Painful.
o Dx
Rectal examination:
assess perineal sensation.
empty any fecal impaction
Examine leg reflexes in all patients. – neurol. cause?
catheterisation to relieve obstruction
if drug induced -> drug withdrawal + catheterisation for 48 h
give a trial of prazosin -> if it works, use it as a long term Rx for BPH
- Urinary ret. in women
o causes
329
spinal tumor
fibroid
vaginal herpes
enlarged retroverted uterus
NOT - HPV
- Urinary schistosomiasis (bilharziasis)
o small trematode flat worm – Schistosoma sp.
o endemic in Egypt
o UTI (cystitis) + terminal haematuria in a male patient from Egypt
+ haemospermia
o primary inf. transm. from water - “swimmer’s itch”
o worms live in vesical veins or intestinal veins
o chronic hepatitis, fibrosis, cirrhosis
o Dx - urine microscopy
o Rx - praziquantel
Male pathology
- ED – Murtagh 1120
o causes
psychosocial – young
elderly
DM
hyperlip.
- Premature ejaculation
o persistent or recurrent ejaculation before, on or shortly after penetration
time from penetration to ejaculation < 2 min
o MC male sexual dysfc.
o MC cause = performance anxiety
o can be
primary – since beginning of sexual life
sec. – developed later
o Rx
short term
topical anesthetics
- lignocaine 2.5% + pilocaine 2.5% cream to glans penis ½ hr
before intercourse
long term
SSRI (fluoxetine, sertraline, paroxetine) + clomipramine => relieve
anxiety
- 3-5 hrs before intercourse
squeeze technique no longer advised
- Balanitis
o inflam. of glans penis + foreskin
o MC – candida
o children – wet nappies
o adults – immunocompromised people, DM
o Sx
saline bath
330
topical C/S
topical nystatin
topical myconazol
- balanitis xerotic obliterans
o thickening of the foreskin + skin pallor
o Sx
topical C/S
circumcision
- Prostate CA
o 80% at 80 yrs
o risk factors
1. age > 75 yrs
2. relative Dx with prostate CA < 60 yrs – most important!
family Hx is responsible for 5-10% of cases
o MC CA in men
o structure
central/ transitional -> BPH
periph. -> CA
peripheral -> doesn’t usually give urinary sympt. (like BPH or prostatitis -
central)
o metastases
lymphatic -> pelvic nodes (not groin)
blood
Osteosclerotic mets in the bones: Pelvis, spine
o CA that doesn’t metastasize to brain = Prostate
o Sx
obstruction
acute retention
back pain
hematuria, uremia – 5%
o Dx
screening – controversial
PR
- signs of CA:
Hard lump
Asymmetry/ irregular
Induration
Loss of median sulcus
PSA:
can be elevated without cancer (e.g. BPH, exercise, infection,
instrumentation, recent ejaculation)
must be tested with DRE is prostate specific, not prostate cancer specific
No PSA testing over age 70
- > 10 ng/ mL suggestive of prostate CA
> 20 – most probably advanced CA with mets
- 4-10- prostatitis, benign hypertrophy
- Normal < 4
331
1. urethral catheter
2. suprapubic drainage if 1 fails
drugs
alpha blocking drugs (inh. contr. of muscle in bladder neck and urethra)
- phenoxybenzamine
- prazosin
- terazosin
5-alpha-reductase inhibitors (reduce prostatic volume)
- finasteride
surgery
indic.
- renal failure
- upper tract dil.
- retention
- bladder stones
methods:
- TURP
Cx
retrograde ejaculation - MC
ED – 5%
- laser ablation
- transurethral incision of prostate (TUIP) – for small glands
- open prostatectomy – less used these days (<1%)
- Prostatitis
o Sx:
triad: dysuria + fever + perineal pain
PR: very tender prostate, swollen, firm
o Rx:
Amoxycillin + gentamicin
Electrolytes, ABG, dehydration, burns - OK
- Electrolyte disorders
o K
Normal: 3.5-5 mmol/l
usually intracellular
hyperkalemia
MC electrolyte disorder associated with cardiac arrest.
CAUSES:
- ↑ K intake: banana, low fat milk, beans, sweat potato.
- Increased production – when cellular membranes are ruptured!
e.g. Rhabdomyolisis, burns, ischemia, hemolysis.
- ↓ renal excretion: Acute and chronic renal failure, Addison’s
disease, hypoaldosteronism, drugs (K⁺ sparing diure cs –
Spironolactone, amiloride; ACE inhibitors and AIIRA, NSAIDs).
- Transcellular compartmental shift: acidosis, hyperglycemia, low
insulin, digoxin poisoning, β blockers
Drugs:
Digoxin
334
Indomethacin
IV Benzyl penicillin (contains K)!
Sx
- Weakness, ascending paralysis, loss of deep tendon reflexes and
respiratory failure
types:
- MILD: 5-6 mmol/L
- MODERATE: 6-7 mmol/L
- SEVERE: more than 7 mmol/L - ECG changes:
(5.5-6.5mmol/L) Tall, peaked T waves.
(6.5-7.5 mmol/l) Prolonged PR interval with flattened P
waves.
ST segment depression.
(7-8 mmol/L) - QRS widening, absent P waves and
sinusoidal wave pattern.
VT, VF, PEA and (> 8 mmol/L) asystole
- MANAGEMENT:
SEVERE:
Immediate cardioprotection: 10% Ca gluconate
Other therapies to shift K into cells, and
eliminate potassium from body (IV insluin &
loop diuretics)
MODERATE:
Shift K intracellularly with 10% dextrose 500 ml
IV/ glucose ē 25 units of insulin over 20 min
8.4% Sod bicarbonate 20 ml IV over 5 min
Salbutamol 5-10 mg nebulized
+ cation exchanging enema while waiting for
dialysis
MILD:
Remove potassium from the body with:
o Furosemide 40-80 mg IV
o Potassium-exchange resin orally or
enema
Hypokalemia
↑ incidence of cardiac arrhythmias esp. if pre-existing heart disease.
CAUSES:
- Inadequate intake of K, e.g. Alcoholism, Starvation.
- Abnormal GIT losses: Vomiting, diarrhoea, laxative abuse
- Abnormal renal losses: Cushing syndrome, ectopic ACTH
production, hyperaldosteronism, diuretics and steroids.
- Compartmental shift: Metabolic alkalosis, insulin.
types
- normal - Potassium levels less than 3.5 mmol/L
- SEVERE: L.
CLINICAL FEATURES:
- muscle weakness, fatigue, leg cramps and constipation.
335
Hyponatraemia
Serum sodium level < 130 mmol/L
Clinical Features: The more rapid the fall the greater the symptoms:
- >125 mmol/L: usually asymptomatic.
- 115-125 mmol/L: lethargy, weakness, ataxia and vomiting.
- <115 mmol/L: confusion, headache, convulsions and coma.
- PSEUDOHYPONATREMIA - Associated with hyperglycaemia,
(hyper osmolar hyponatremia) hyperlipidemia, hyperproteinemia, azotemia.
- Zinc deficiency
o after prolonged IV fluid admin.
337
Gelatins (3.5%)
no serious SE
very common in use
2 hr of plasma expanding properties
Hydroxyethyl starch – very good but also very expensive
6%, 10%
no complic
4 hr of plasma expanding properties
best solution in severe hypovolemia
Albumin – 5%, 25%
hypoalbuminemia: burns, malignancies, cirrosis, ascitis, etc.
o Blood components
RBC (packed cells)
indic. when volume replacement is not the issue
- e.g. Hb = 6.0
FFP
indic. in warfarin toxicity, advanced liver disease (causing
coagulopathy), antithrombin III deficiency
Platelet concentrates
the only ones that can be stored at room temp.
can also be stored as powder
but usually a solution
indic. – thrombocytopenia
Cryoprecipitate – contain fact. VIII , XIII, von Willebrand factor & fibrinogen
indic. – Von Willebrand dis., hemophilia
- Blood transfusion
o 1 unit = 450 ml
o before – compatib. test
ABO -> blood group
Rh typing -> test with Anti-D AB, (RH + or -)
cross matching – check other AB
AB screening for other diseases (HBV, etc.)
o Cx
Allergic reaction: itching, shivering, rigors, rash, anaphylactic shock
hemolytic reaction:
acute
- ABO incompat.
MC cause – human error
intravascular hemolysis: hemoglobinuria (acute RF)
delayed
- Rh incompat.
extravascular hemolysis
Dx – Coombs test
inf.
HCV
HIV
CMV – MC inf. in organ transplant
341
Epstein Barr v.
metab.
hyperkalemia (cellular destruction)
hypocalcemia
acid-base abnormalities
coag. problems
dilutional coagulopathy – dilutional thrombocytopenia
e.g. in massive blood transfusion: > 5 l in 24 hrs
- dilutional coagulopathy – dilutional thrombocytopenia
- DIC
hypothermia
immune suppression
tissue hypoxia
- Blood loss
o 5-10% body can compensate
o > 20% - body can’t compensate anymore
o 30% = clinical shock (loss of 1.5-2l)
- Dehydration assessment – see printout from Afshan
o most specific indicator = lethargic and irritable (nervous system affected)
o water content by age group
12 wks fetus – 90 % water, 55% is extracel. fluid
newborn – 80%, 40 % extracel.
12 mths – 60%, 25% extracel.
adult – 60%, 20% extracel.
o clinical classif.
mild
moderate
severe
% of body wt. loss Clinical
Mild 4 Dry mucosa
(70 kg man lost 3 L) (<5) Thirst
HTN, tachycardia
capil. refil > 2 sec (N < 2 sec)
Decr. skin turgor
Moderate 5-8 adults Dry mucosa, firm dry tongue, sunken eyes, decr.
(lost 4-6 L) 4-6% children skin turgor
Have to admit him! (5-10) capil. refil > 2 sec
Tachycardia
Oliguria (<0.5 ml / kg / hr)
(Normal 1 ml / kg / hr)
Orthostatic HTN
(keep the pt standing 5 min – systolic BP drops >
15-20 mm) Depreesed fontanelle in Child
Severe 8-10 Dry mucosa
(lost 7 L) > 7% children Thirst
(>10) capil. refil > 2 sec
Decr. skin turgor
342
Tachycardia
Oliguria (<0.5 ml/ kg/ hr)
(Normal 1 ml/ kg/ hr)
hT
Cardiovasc. collapse
- Dehydration - Afshan
o Mild < 5%
no clinical signs, only thirst
(deficit: 50 ml/ kg)
o Moderate 5-9%
loss of skin turgor
sunken eyes
dry mucous membranes
no tears
depressed fontanelle in children
o Severe ≥ 10%
circ. failure, shock
hT
tachycardia
cold and clammy skin
oliguria (< 0.5 ml/ kg/ hr)
capil. refil > 2 sec (N < 2 sec)
lethargy or irritability
(deficit: 100ml/ kg)
- I. Hypovolemia
o e.g. 1: 1 yr old child, 10 kg,10% dehydration and shock
o e.g. 2: 20 yrs old man, 50 kg, 7% loss
o I. Maintenance/ongoing losses: (replacement of fluid)
Infant, child < 5 yrs (Maria, Afshan)
0-3 mths: 120 ml/kg/24h
4-12 mths: 100 ml/kg/24h
>12 mths: 80 ml/kg/24h
e.g.1: 100 x 10 = 1000 ml / 24 hrs for the child
(Amit- by body weight
- first 10 kg: 100 ml/ kg/ 24 hrs
- 11-20 kg: 75 ml/ kg/ 24 hrs
- > 20 kg: 50 ml/ kg/ 24 hrs
- e.g.1: 100 x 10 = 1000 ml/ 24 hrs) = Maintenance fluid
Adult, child > 5 yrs (Amit, Maria)
- In eg, 2 of an adult of 50 kg.
- first 10 kg: 100 ml/ kg/ 24 hrs = 1000ml
- 10-20 kg: 50 ml/kg/24 hrs = 500ml
- > 20 kg: 20 ml/ kg/ 24 hrs = 600ml
- e.g. 2: 1000 + 500 + 600 = 2100 ml/ 24 hrs = Maintenance fluid
o II. Estimation of volume deficit (fluid loss due to dehydration)
5%
5-10%
343
> 10%
o % Dehydration x body weight in kg x 10 in ml
e.g. 1: 10 % x 10 kg x 10 = 1000 ml/ 24 hrs child
e.g.2: deficit: 50 x 7 x 10 = 3500 ml/ 24 hrs man
o e.g. 1: total fluid to give: 1000 + 1000 = 2 L
o e.g.2: total fluid to give: 2100 + 3500 = 5600 ml
o steps:
I. if severe dehydration with shock:
initial bolus – 20 ml/ kg of NS
if still in shock, repeat with another 20 ml/ kg of NS
- e.g.1: 20 x 10 = 200 ml bolus, repeated one more time if needed
- e.g.2: 20 x 50 = 1000 ml bolus
II. give half of the amount in the first 8 hrs (Amit)
e.g.1: 2000/ 2 =1000 – 200 bolus = 800 ml
e.g.2: 5600/ 2 = 2800 – 1000 bolus = 1800 ml
III. Give the rest in remaining 16 hrs
e.g.1: 1000 ml
e.g.2: 2800 ml
(II. Afshan - give more in the first 6 hrs
100 ml/kg in infants
- 100 x 10 = 1 L in the first 6 hrs – 200 ml bolus = 800 ml after the
initial bolus in the first 6 hrs
50 ml/kg in adults
III. give the rest in the remaining 18 hrs
2L – 200 ml bolus – 800 ml = 1 L in the remaining 18 hrs of the first day )
- II. Intraop. fluid management - Amit
o 4-2-1 formula
e.g. 50 kg patient
up to 10 kg body wt. 4ml/kg/hr = 40
10-20 kg 2 ml/kg/hr = 20
20-50 kg 1 ml/kg/hr = 30
- total 90 ml/hr
- III. post-op rehydration (especially in abd. surgery)
o always 3 L daily requirements for adult
2 L NS + 1 L dextrose
o + losses, divided between normal saline and dextrose, based on the patient (he doesn’t
eat -> give more dextrose, etc.)
o + 70-90 ml of K
e.g. blood loss of 2L + hypokalemia -> 3L normal saline + 2L 5% dextrose + 100
ml K
- IV. Burns
o rehydration: 2-4 ml / kg / % burned in the first 24 h + maintenance fluids
50% in the first 8 hrs
50 % in the other 16 hrs
using ½ Hartman solution (with K+) and ½ NS
o minimum required urine output: 0.5-1 ml / kg /h
min. 40-50 ml/h = 1000 ml/24hrs
344
o Rule of 9s
head & neck 9%
arm 9% (4.5% each)
leg 18% (9% each leg)
trunk
front - 18%
back - 18%
perineum 1%
o MC common cause of death: renal failure – in first 2-3 days
then death from inf. (after first 3-5 days)
shock in major burn in first day (M 1381)
o indication for intubation
horseness of voice
stridor
coughing black materials
facial swelling
nasal hair burned (singed)
resp. distress
- Fluid replacement - Amit
o urgent – intravasc. fluid resuscitation (bolus) – only in severe cases
hypovolemic shock or severe dehydr.
0.9% NS - 20 ml / kg IV ASAP stat run (bolus)
- e.g. 50 kg pacient = 1L
vasodilatory shock: sepsis, anaphylaxis, spinal shock
0.9% NS - 20 ml / kg IV ASAP stat run (bolus)
cardiogenic shock
0.9% NS - 10 ml / kg IV ASAP stat run (bolus)
moderate dehydr., without shock
0.9% NS - 10 ml / kg IV ASAP stat run (bolus)
minimum volume resusc.
titrate perfusion in order to maintain a systolic BP of min. 90 /60)
e.g. ectopic pregnancy, penetrating chest wounds, rupture of aortic
aneurysm
Respiratory/ lung pathology - OK
Lung volumes
- These values vary with the age and height of the person; the values that follow are for a 70 kg
(154 lb), average-sized adult male [2]:
Physiologic = 155 The anatomic dead space plus the alveolar dead
dead volume ml space.
- The tidal volume, vital capacity, inspiratory capacity and expiratory reserve volume can be
measured directly with a spirometer. Determination of residual volume can be done by
radiographic planemetry, body plethysmography, closed circuit dilution and nitrogen washout.
- These are basic elements of a ventilatory pulmonary func. test. Results (in particular FEV1/FVC
and FRC) can be used to distinguish between restrictive & obstructive pulmonary diseases:
diseases but flow rates are impeded 0.6, Emphysema can ↓ratio to 0.7
- 0.4)
Lung Abscess
o MC - staph.
o Sx
sputum with foul odour
pleuritic chest pain
tachyc., tachypneic
bronchial breath
crepitations
fever > 38.5o C
o Dx
X Ray: small cavity with fluid level
best investig: CT chest
Bronchoscopy
o Rx
O2, strong analgezic
postural drainage, tapping
IV A/B:
Clindamycin (active on anaerobs; SE – Pseudomembranous colitis) +
Cephalosp. (ceftriaxone)
Cephalosp. + flucloxacillin
Bronchitis
o Acute - sore throat, runny nose, persistent cough especially at night and in the morning,
small amount of yellow sputum
Rx
Amoxycillin
Doxycycline
o Chronic - persistent cough especially at night and in the morning, large amount of
yellow sputum
o Dx
X Ray
- Sputum types – Murtagh p. 446
- Fibrosing alveolytis – all pulmonary parameters decreased
- Idiopathic pulmonary fibrosis-IPF
o Hx of shortness of breath and cough
o clubbing with coarse crackles in both lung bases
Sleep apnoea
o types
Obstructive:
decr. airway size
- Obesity
- Tonsillar hypertrophy
- Macroglossia
upper airway muscle hypotonia
- Alcohol
347
nasal obstruction
Central:
Neurological (sleep center affected)
o Dx
Sleep study (somnography)
bad when interferring with REM sleep
o Mx – Step ladder
1. lifestyle
wt. loss
2. drugs
stop sedatives
use nasal decongestives
3. C-PAP mask
4. Surgery
5. Mandibular implants (splint)
6. Amytriptilline
- chest findings – Murtagh 529
Dx Trachea Chest wall Percussion Breath Vocal Abnormal
movt. sounds fremitus sounds
(↑ in
consolid.
& fibrosis)
N Middle Equal Resonant Vesicular N None
expansion
Lung fibrosis Middle Decr. bilat. Resonant Vesicular Incr. Fine
(generalised) crackles
Pneumonia/ CA Middle Decr. Dull Bronchial Incr. Fine late
consolidation unilat. inspiratory
(CA: No fever, crackles
no crackles)
Lung collapse Towards Decr. Dull Absent or Absent or None
collapse unilat. decr. decr.
Pleural effusion opposite Decr. Stony dull Absent or Absent or None
side unilat. decr. decr.
Pneumothorax opposite Decr. Hyperresonant Absent or Absent or None
side unilat. decr. decr.
Emphysema Middle Decr. bilat. Resonant to Vesicular Decr. ± crackles
hyperresonant & wheezing
from chronic
bronchitis
Asthma Middle Decr. bilat. Resonant Vesicular ē N or decr. Expiratory
prolonged wheezes
expiration
eformoterol
- Adrenaline – sc, im or iv
Anticholinergic medications:
- ipratropium bromide
Methylxanthines: – limited use due to side effects and limited efficacy
- theophylline - Oral
- aminophylline – Injection
Anti-IgE agents:
- Omalizumab
- Mauzumab
Antiinflammatory - Long term control
Glucocorticoids are the most effective treatment available for long
term control. (Best preventer)
- inhaled
fluticasone (Best preventer)
beclomethasone
budesonide
ciclesonide (single daily dose)
- Oral – for exacerbations
prednisolone
Mast cell stabilizers – inhaled; adverse effects are uncommon!
- sodium cromglycate
- nedocromil sodium
Leukotriene antagonist – chewable tablets
- montelukast
- zafirlukast
o routes of delivery
<3 yrs - metered dose inhalation (MDI) + small volume spacer + face mask
3-5 yrs - MDI + small volume spacer
5-8 yrs – MDI + large volume spacer
> 8 yrs – MDI
o Sx - patterns in children – Murtagh 1280
Mild - infrequent, episodic type
not severe
attacks > 6-8 wks apart
Mx
- SABA: Salbutamol, Terbutaline – when required
Moderate - frequent episodic
attacks < 6 wks apart (4-6 wks)
attacks more severe
Mx:
- SABA during attack
- Montelukast or cromolyn or
- inhaled Corticosteroids = ICS
beclomethasone
fluticasone
ciclesonide
351
budesonide
Severe - persistent asthma
attacks on most of the days
nocturnal attack > 1/ week
multiple ED admissions
Mx:
- SABA in attack
- ICS
- consider LABA (salmeterol, eformeterol)
- if needed:
theophylline
ipratropium bromide
oral prednisolone
Status asthmaticus:
Rx
- O2
- hydration
- salbutamol
- Corticosteroids oral or IV
Mx of attack
monitoring of attack:
- FEV1/ FVC
- PEFR
hydration!
O2
- when do you intubate:
after other Rx have failed
blood gases are affected
Inhaled Salbutamol + Oral C/S
- wait 20 min and assess
if 2nd attack or sympt. persist -> repeat inhaled
Salbutamol
if 3rd attack or sympt. persist -> repeat inhaled
Salbutamol
o if sympt. persist other drugs:
Theophylline
Ipratropium bromide
Oral prednisolone
IV C/S
Moderate/ severe asthma attack in children
- a. Salbutamol puffs with spacer + prednisolone
1 puff/ 4 breaths
how many puffs
6 puffs < 6 yrs
o + 2 puffs ipratropium if severe attack
12 puffs > 6 yrs
o + 4 puffs ipratropium if severe attack
352
then
20 min later – repeat
20 min later – salbutamol (repeat)
o if still not better -> ICU
- or continuous nebulised salbutamol via mask
Salbutamol with nebulizer + O2 (nebulizer better than
spacer)
Salbutamol 2.5 mg < 6 yrs
Salbutamol 5 mg > 6 yrs
- b. O2 through nebuliser
- c. IV infusion of salbutamol + hydrocortison
- d. Adrenaline IM
Criteria for sending the child home
- off salbutamol > 4 hrs
- off the O2 for > 24 hrs
- eating/ drinking normally
- no sign of resp. distress
exercise-induced asthma:
1-2 puffs of Salbutamol before exercise (last for 1-2 hrs)
antihistamine – not in children, except in severe asthma
poor outcome if severe attacks requiring intubation
COPD
o Dx
FEV1/ FEV
<70% after bronchodilator
< 80% predicted
o Rx
stop smoking
drugs
SABA
LABA
Ipratroprium bromide
Corticosterioids: COPD – only 10% respond to steroids
- Inhal.
- P.O.
A/B – in infection
Β blockers in associated CV problems
- decr. the need of home O2
- decr. the exacerbations
Steroids and salmeterol (LABA) improve quality of life
O2
if SaO2 < 92%
correct O2 admin in COPD:
- low flow 2-3 L
- prolonged > 15 hrs/ day
- low percent (conc.) 30-40%
353
CO2 narcosis
- if Rx with too much O2 => CO2 retention => resp. depression
-> anxiety
-> progress to confusion: flapping tremors (asterixis)
O2 – best factor for incr. long term prognosis
o sign of poorest prognosis in bronchospasm = high PaCO2
o MCQ: emphysema, V1-4 ST segm depression, normal axis, right bundle block: RV
Hypertrophy with right bundle block
o MCQ: COPD with incr. JVP, edema, decr. O2, incr. CO2, why advise for a home O2 therapy
system? because hypoxia is the cause of his heart failure
Pulmonary Embolism
- Acute pulmonary edema (APO)
o cause: MI, etc.
o Sx – dyspnea, etc.
o Rx
O2
CPAP, PEEP
nitrates (GTN)
morphine
diuretics
- PE – my p.41
o predispoz. factors (same as for DVT):
contraception – OCP
obesity
surgery or immobilisation or long flights
thrombophilia
trauma
varicose veins
malignancy
pregnancy
prev. episode of DVT or PE
family Hx in first degree relative
o Sx
Small PE: Sudden dyspnoea, pleuritic pain and pleural rub, and possibly
haemoptysis, with few physical signs
Major PE: Dyspnoea, chest pain and light-headedness or collapse/ syncope,
followed by recovery.
Look for cyanosis, tachycardia, hypotension, raised JVP and loud delayed
pulmonary 2nd sound (due to pulmonary HT)
o Dx
FIRST: X-Ray: Mainly to exclude pneumonia, pneumothorax.
SECOND & Best: CT Pulmonary angiogram (CTPA).
THIRD - if CTPA unavailable or CI (e.g. renal failure – no contrast): Ventilation-
Perfusion isotope lung scan (V/Q scan)
V/Q ratio (ventil/ perfusion)- isotope scanning ē Technetium Tc-99m
Excludes pulmonary
Normal No perfusion deficit
thromboembolism
Low probability Perfusion deficit with matched ventilation deficit Non diagnostic
V/Q ratio measurement used to assess the efficiency and adequacy of matching of two variables:
"V" - ventilation - the air which reaches the lungs
"Q" - perfusion - the blood which reaches the lungs
- A lower V/Q ratio (with respect to expected value for a particular lung area in a defined position)
impairs pulmonary gas exchange and is a cause of low arterial partial pressure of O 2 (paO2).
Excretion of CO2 is also impaired but a rise in paCO2 is very uncommon because this leads to
respiratory stimulation and the resultant increase in alveolar ventilation returns paCO 2 to within
the normal range. These abnormal phenomena are usually seen in chronic bronchitis, asthma
and acute pulmonary edema.
- A high V/Q ratio increases paO2 and decreases paCO2. This finding is typically associated with
pulmonary embolism (where blood circulation is impaired by an embolus), but can also be
observed in COPD as a maladaptive ventilatory overwork of the undamaged lung parenchyma.
nd
a. Needle aspiration -> observe Needle aspiration 2 ICS
-> didn’t resolve, repeast medioclavicular line.Then
aspiration -> still didn’t resolve, replace with chest tube under
chest tube water seal (5th ICS mid-axillary
b. chest tube for drainage or anterior axillary line)
Sx: Hyperresonance, decreased vocal resonance on auscultation, shift of trachea to opposite site
Rx
Sympt – treat
Asympt < 2 cm – Observe
> 2 cm treat
> 15% loss of lung volume - Treat
- Needle aspiration
o Tension pneumothorax
o Spontaneous pneumothorax
- Chest tube
o Tension pneumothorax – after doing needle aspir.
o Sec. spontaneous pneumothorax
o Most traumatic pneumothoraxes
o Malignant pleural effusion
o Hemopneumothorax
o Empyema
Dx: Not done in emergency
Chest X Ray in expiration
- Pneumohemothorax
o If not urgent – do chest tube directly, without doing the needle first.
Pleural pathology
- Pleural effusion
o Sx
Dullness on percution
o Dx
Pleural fluid contains
Mononuclear cells predominantly = TB
Transudate vs. exudate
- Criteria for exudate:
Ratio of pleural fluid protein to serum protein > 0.5
Ratio of pleural fluid LDH and serum LDH > 0.6
Pleural fluid LDH > 0.6 or 2/3 times the normal upper
limit for serum.
Lung CA
o 2nd MC CA in Australia after non-melanoma skin CA
o Most lethal CA in Aus.
o Prognosis at 5 yrs – 12-14%
o Risk factors
Smoking
Silicosis, working in a mine
Asbestos
o Relationship with smoking:
356
smoker
squamous
small cell
non-smoker
adenocarcinoma – MC in non-smokers
o Sx
Triad: malaise + wt. loss + cough
Hemoptisis
Superior vena cava compression syndrome
Jugular veins proeminent, subcut veins on upper chest dilated.
Paraneoplastic phenomena
Squamous cell carcinoma
- Parathyroid hormone-related peptide (PTHrP) - hypercalcemia
Sx - fatigue,
Small cell carcinoma
- SIADH – Hyponatremia (120mm/l or less) bc of ↑ total body
water----Hypo-osmolar hyponatremia.
- Ectopic ACTH secretion – Cushing syndrome: Moon face buffalo
hump, central obesity, striae and bruising ↑ secretion of
melanocyte secreting horomone (MSH) -> ↑ Pigmentation of
mucosal membranes and skin. Hypokalemic alkalosis bc of
excess glucocorticoid and muscle weakness.
Pancoast tumor/ Hornor syndrome:
+ compression on T1
- all small muscles of hand, including thenar and hypothenar
eminences
- difficulty of precision grip and opposition of thumb to fingers,
weakness spreading and bringing together the fingers
- in time – claw hand
o types
Small cell (SCLC) - 15-20%
Rx
- Chemotherapy
- Radiotherapy - palliative
Non-small cell (NSCLC)
Squamous – 20-30%
Adenocarcinoma – 20-30%
Large cell carcinoma – 20-30%
Rx
- surgery
- chemotherapy
- radiotherapy - palliative
o Dx
sometimes incidental finding at chest X Ray
Bronchoscopy and biopsy (if close to a bronchi)
Mesothelioma:
o Risk factors
357
o Mx
take blood cultures, then
start ASAP empiric Rx with:
Benzyl penicillin + Flucloxacilin + Gentamicin x IV
- HOCM
o family Hx of father who died early – usually AD
o Sx
exertional syncope
collapse during physical effort (plays football) due to arrythmia
ejection systolic murmur (same as aortic stenosis) non radiating
non radiating & exacerbation with Valsalva manouver = HOCM
o Dx
1 – Echocardiography – every 5 yrs
LVH
Subaortic septal hypertrophy -> pushes valve -> similar to Aortic Stenos
o Rx
No digoxin (can ↓ ejection fraction)
- JVP – internal jugular vein
o raised if > 4 cm
o Components:
a wave – atrial systole
c wave – closure of tricuspid valve (not normally visible)
x descent – ventricular systole
v wave – atrial filling against a closed tricuspid valve
y descent – opening of the tricuspid valve
o Pathology:
raised JVP with normal waveform: Right heart failure, fluid overload
raised JVP with absent pulsation: SVC obstruction
large a wave – Pulmonary hypertension, Pulmonary stenosis
cannon a wave – right atrium contracts against a closed tricuspid valve -
complete heart block
absent a wave – atrial fibrillation
large v wave – tricuspid regurgitation
high plateau of JVP with deep x and y descents – constrictive pericarditis
absent JVP – reduced circulatory volume
o Positive abdomino-jugular reflux sign – rise in JVP presistent after 15-60 sec of abdominal
compression = right ventricular failure
- Cardiac tamponade
o Sx
Beck triad
hypotension
muffled heart sounds
increased JVP, distended neck veins
Pulsus paradoxus: exaggeration of normal phyisiological resp. variation in BP
(fall in BP of > 10 mm Hg during inspiration)
o Dx
X Ray
359
e.g. AF
- CI in bradycardia
5. + Spironolactone
- careful when combining with ACE inh. (risk of hyperkalemia)
6. + consider vasodil.
7. + consider transplant
o highest risk for non-cardiac operation: heart failure (> Hx of of DVT or MI)
o 50% will die in 5 yrs
Cardiac arrhythmias
- Arrhythmias
o causes:
I - Medications: Side effect.
II - Exclude myocardial ischemia from ACS as a priority.
III - Electrolyte disturbances: Hyperkalemia.
Hypoxia
Hypovolemia
Thyroid disease
Septicemia
o types:
Bradycardia < 60
can be:
- SINUS
Rx
Bolus of atropine 0.5-0.6 mg IV
o Repeat if it persists (up to 3 mg IV)
if pt conscious: Consider insertion of a
temporary transvenous pacemaker (2nd or
complete heart block)
- JUNCTIONAL
- AV BLOCK = Prolongation of PR interval to > 200 ms
First degree: Benign
PR > 0.2 s (5 small boxes)
Rx
o none, unless sympt.
Second degree:
types:
o Mobitz I (Wenckebach Phenomon)
– Progressive prolongation of PR
interval then drop of a QRS complex
AV node is blocked
Rx - none
o Mobitz II
intermittently nonconducted P
waves not preceded by PR
prolongation and not followed
by PR shortening.
361
- Atrioventricular blocks
o Grade I – PR extended > 0.20 sec - digitalis
o Grade II – PR extended and certain SA impulses are missed (do not make it to ventricles)
Mobitz type I (Wenkebach) – digitalis
Mobits type II – usually not from digitalis
o Grade III – complete AV block, ventricles contracting at lower rate than atria
- Atrioventricular dissociation
o Ventricles contracting at a higher rate than atria (unlike AV block Grade III)
Tachycardia
Broad-complex: (VT, VF, SVT with block)
VT
Broad QRS
> 300/ min, regular, usually post MI
Rx
o Pulseless VT or unconscious, unstable:
Give a synchronized DC shock 120-150 J
and repeat up to 3 times.
o with pulse, conscious, stable:
Amiodarone 300 mg IV over 20-60 min
followed by an infusion of amiodarone
900 mg over 24 hours.
VF
no QRS complex
Rx
o cardioversion
adrenalin
CPR
362
MI
- Coronary ischemic syndr.
o stable angina
o acute coronary syndrome (ACS)
STEMI
NSTEACS
NSTEMI
unstable angina
- AMI
o STEMI
365
if coronary block is not relieved, MI will progress over next 6-12 hrs (4 hrs =
window period)
main goal of Rx is reperfusion
causes of new systolic murmur post MI
V septal rupture
papillary muscle rupture
papillary muscle dysfc. in ant. MI
func. mitral regurgitation sec. to LV dil.
pericardial friction rub, limited to systole
Dx
First step in management: ECG within 10 minutes of patient arrival.
- ECG: ST elevation in two or more contiguous leads:
Inferior MI: II, III, aVF
Anterior MI
anteroseptal – V1-V3
anterolateral – V3-V4
Lateral: I, aVL, V5-V6
Posterior: Mirror-image ST depression V1-V4
Repeat ECG after 5-10 min if non-dx ECG.
- repeat ECG every 2-3 hours
Send blood for laboratories: Cardiac biomarkers.
- Second step = Troponin I or T
normal < 0.02
rise after 4-6 hours after symptom onset.
Repeat in 6-8 hours if normal.
Indicate myonecrosis.
Remains elevated for 5-14 days (not useful for re-
infarction).
More sensitive for myocardium than CK-MB.
can also be elevated in CRF – due to renal destruction
Dx diff with CRF:
o do also CK – not elevated in CRF
o if troponin is gradually increasing – MI
constantly increased = CRF
- + CK-MB, CK.
If troponin is unavailable.
rise after 4 hrs
not specific for myocard infarction
CK-MB is more specific than total CK
Returns to normal within 72 hrs
May be used to confirm re-infarction
366
-
complic.
LVF: pulm. congestion
- Rx: diuretics
- O2
- morphine
- digoxin is CI – ↑force of contr. -> risk of rupture
cardiogenic shock – 90% mortality
- Rx – dopamine, dobutamine
aseptic pericarditis (Dressler syndrome)
- Rx
NSAIDS, paracetamol, aspirin
C/S
Mx
I. MONA
367
absolute
o Intracerebral or subarachnoid hemrhg.
o Intracranial neoplasm ever.
o Stroke in previous 6 months.
o Active GI bleeding in last month.
o Major surgery or trauma in previous 3
wks
o Known bleeding diathesis.
o CRP > 10
o Aortic dissection
first rule out aortic disection
before giving thrombolysis ->
can kill a patient with aortic
dissection
relative
o Oral anticoagulant therapy
o Pregnancy within 1 week post-partum.
o Central line.
o Refractory hypertension.
o Infective endocarditis.
o Severe hepatic or renal disease.
indic.
ST elevation > 1 mm in limb leads
ST elevation > 2 mm in chest leads
new LBBB
post MI-ST depression in V2-V3-> ask for V7-V9
after 12 hrs, thrombolysis is still considered if:
persistent pain
preservation of R waves in infarct-related ECG
leads (not replaced by pathological Q wave)
major complic. – cardiogenic shock
- Antiplatelets
Aspirin 300 mg
Clopidogrel 300 mg
-Heparin.
III. After reperfusion
- Antiplatelet agents
- Cardioselective β blockers – increase the survival (MCQ)
Atenolol
Metoprolol
- ACE inh. – within 24-48 hrs after MI
- Statin therapy – regardless of cholesterol level
- + Warfarin
drugs that ↓mortality in MI
1. β blockers
2. ACE inh. (if no renal failure)
3. aspirin
369
4. statins
- Neha:
o cardiac chest pain
MONA -> hospital: ECG, Trop
No pain Hx of pain at rest or repetitive
pain or prolonged pain
No ECG/ enzyme changes Low risk Intermed. risk
ECG /enzyme changes High risk High risk
o Mx
Low risk -> stress test
Intermed -> reassess patient, repeat ECG and
troponins in 8 hrs -> if any risk factors
(↑cholesterol, fam. Hx, etc.) -> heparin SC
High risk -> coronary angiography (PCI)
if refractory pain – IV GTN (rare)
o NSTEMI
Dx
ECG: Within 10 min of patient arrival:
- ST depression
- T-wave inversion or flattening
- Non-specific or transient changes
- Normal
Rise in troponin and CK-MB
types – Afshan’s diagram for ACS
high risk:
- > 10 min or elevation of troponins
intermed. (>48 hrs)
low risk – same as for stable angina (pain only on exertion)
Mx
MONA
NO THROMBOLYSIS
Heparin: LMW heparin such as enoxaparin 1mg/ kg or UF heparin 5000
units IV as a bolus followed by an infusion of 1000 units/ h.
- Angina
o types
Stable (effort angina)
ST depression
Unstable – due to unstable plaque
smaller rise in cardiac biomarkers, normal ECGs, normal stress test
special types
- nocturnal a.
- decubitus a.
- variant a. or Prinzmetal a. (spasm a.)
ST elevated
don’t give β blockers!
o Rx
acute
370
GTN subling.
isosorbide dinitrate subling.
nifedipine capsules – suck or chew
chronic
Aspirin 150 mg daily
- or clopidogrel
Nitrates
- GTN
- Isosorbide mononitrate
β Blockers
- Atenolol
- Metoprolol
Ca Channel blockers
- Nifedipine
- Amlodipine
- Felodipine
- Diltiazem
- Verapamil
- Recurrent pain in ACS
o consider IV nitrate infusion
o maximize dose of β blocker
o consider Amlodipine or Nifedipine
o if high risk pain (persistent)
GP IIb/IIIa (strong antiplatelets): abciximab
transfer patient for PCI
- Coronary artery bypass grafting indic. (otherwise – angioplasty)
o triple vessel disease: all 3 arteries > 50%
left anterior descending (LAD)
left circumflex a.
right coronary artery
o 2 vessel disease + DM
o main one – left anterior descending > 50%
ECG
o Normal impulse conduction
Sinoatrial node (right atrium) – 60-100 beats/ min
AV junction – delay, so A can contract before V (including atrial kick at the end
of A contr.)
AV node – 40-60 pacemaker
Bundle of His
Bundle branches (left and right)
Purkinje fibers
Ventricular cells – 20-45 beats/ min
o Small square=0.04sec, large square=0.2 sec
o ECG interpretation: RRAHIM
Rate
Rhythm
371
Axis
Hypertrophy
Interval
MI and miscellaneous
o 1. Calculate rate:
Vertical bar every 15 large squares
I. count 30 large squares (6 sec) – count the no. of R waves in those squares,
multiply by 10 -> in regular and irregular rhythms
II. look for R wave falling on a line, then see where the next R wave falls – in
regular rhythms only
300 - next line in large square (300:1)
150 – next line … (300:2)
100 (300:3)
75 (300:4)
60 (300:5)
50 (300:6)
…
III. 300/ no. of large squares between 2 QRS complexes – in regular rhythms
o 2. determine Rhythm (RR intervals are regular?):
Regular
regularly irregular
irregularly irregular – AF
o 3. Assess P waves – do they exist? are they followed by QRS? are they all same in size
and shape?
MAT = Multifocal atrial tachycardia ≥ 3 P waves, each different, in same ECG
o 4. Determine PR interval – beginning of P to beginning of R
o 5. Determine QRS duration
o 6. QT interval – beginning of Q to end of T (T= terminal)
o Components
P waves = Atrial depolarization (contraction) - best appreciated in lead II
Present
absent - AF
relationship to QRS complexes (no rship. = AV block)
PR interval: 0.12-0.2 (3-5 boxes)
QRS complexes = Ventricular depolarization = 0.04-0.12 (1-3 boxes)
narrow (supraventric)
widened (> 0.12 s) (ventric.)
ST segment
T waves = Ventricular repolarization
Elevated
depressed
inverted (ischemia)
U wave = after repolarization
o Leads
I, II, III – Limb leads
aVR (right arm), aVL (left arm), aVF (feet) = Augmented limb leads
V1-V6 = Chest leads (V1 = right -> V6 = left)
372
V1-V2 = medial
V2-V3 = septum
V4-V6 = lateral
Rhythm strip = longer strip of II
o Problems
Sinus bradycardia
Sinus tachycardia
1 extra atrial focus firing = Normal sinus rhythm with PAC-Premature atrial contc
1 extra ventricular focus = PVC
wide and bizarre QRS (slower conduction of impulse from ectopic foci)
can be
- Uniform. arises from single focus
Bigeminism (normal QRS, ectpioc beat after 2 normal
QRS)
trigeminism ectpioc beat after 3 normal QRS
couplet: normal PVC PVC – 2 consecutive ectopic beats
triplet: normal PVC PVC PVC- 3 consecutive ectopics
-
- Polymorphic: arises from multiple foci
Multiple extra atrial foci firing = A Fib
1. absent Ps
2. irregularly irregular rhythm
3. narrow (normal) QRS
Multiple extra foci in V = V Fib
1. absent Ps
373
PE – S1Q3T3
- I – Deep S
- III – Deep Q and T wave inversion (positive)
Hypokaleima:
ST depression, T wave inversion. Prol onged QT, Elevation of U wave
Hyperkalemia
Tall tended T wave, Shortened QT interval, Wide QRS, Prolonged PR
interval, P flattens then disappears
Digoxin: ST depression, T wave inversion, Shortened QT interval,
Prolonged PR.
Vascular pathology - OK
- Surgery indication
o Carotid occlusion
> 70% carotid occlusion
60-70% - grey area
surgery in DM, elderly, hyperlip., recurrent TIP
< 60%
Rx – aspirin low dose
o > 50% coronary artery occlusion
- Angiodysplasia > 55 yrs
o AV malformation in intestine
o in ceceum + right colon
o Sx
multiple episodes of profuse rectal bleeding
assoc. with CREST syndrome
o Rx
surgical resection
Arterial pathology
- Vasculary problems/ surgery
o Arterial
Risk factors
smoking
DM
HTN
hypercholesterolemia
family Hx
AF
Acute/ sudden onset = “cold white leg” – very painful
causes:
- thrombosis
- embolism
- traumatic contusion
MC site – common femoral artery
Sx
377
stop smoking
keep legs warm and dry
proper care of foot
aspirin
if ABI < 0.3 -> refer for urgent surgery
o endarterectomy or bypass grafting
- Resting pain: Constant severe burning pain in forefoot at rest
During night time
Pain in the forefoot, toes, heels
Relieving factor: hanging the foot out of bed
Emergency condition => refer to surgeon immediately
indic. for vascular surgeon – Murtagh 719
o unstable claudic. of recent onset,
deteriorating
o severe claudic. – unable to maintain a
normal life
o rest pain
o tissue loss – ulcers, heel’s cracks, dry
gangrenous patches, inf.
Venous pathology
- Varicose veins
o predisposing factors
family Hx.
female
pregnancy
multiparity
previous DVT
extrinsic venous compression – intraabd. tumors, etc.
occupation – dentist, etc.
diet – low in fibre
o Rx
High-fibre diet
supportive stockings or tights
Surgery
Sclerotherapy
- for small, isolated veins
Surgical ligation and stripping
- DVT
o risk factors
Family Hx
Hx of previous thrombo-embolism
Thrombophilia
Drugs: OCP, HRT, tamoxifen
> 40 yrs
Varicose veins
significant illness: heart failure, CA
Malignancy (in idiopathic DVT)
379
Recent surgery
Major/ orthopedic surgery
Immobility
Long flights
Pregnancy/ puerperium
Obesity
Dehydration
o Recurrent DVT – pancr. CA
o Unilat. sudden onset of DVT – Ovarian CA
o Sx
“Hot blue leg” = Acute venous obstruction
painful, tender
edema
o Dx
Gold standard = Doppler U/S
contrast venography – if U/S doubtful
D-dimer – to exclude DVT when doubtful (if negative)
don’t do Hoffman sign (plantar dorsiflexion causes pain) since it might
mobilise the thrombus
o Cx
PE
20%
- of these 30% will be fatal
varicose veins => venous ulcer
o Rx
heparin, then
warfarin
3-6 mths
we need to treat at least for 3 mths (with warfarin)
do not give aspirin
mobilisation
compression stockings
- Thrombophlebitis
o Red cord-like vein, tender on palpation
o Usually in superficial varicose veins
o Migratory superficial thrombophlebitis = Pancreatic CA
o Rx
early mobilisation
bed rest
compression with uniform pressure over the vein
prevent propagation of thrombus
limb elevation
NSAIDs
Aortic pathology
- Coarctation of aorta
o narrowing of distal ductus arteriosus and subclavian artery
o male 2:1
380
o Sx
asympt. always
headache, epistaxis, claudication, cold legs
BP difference between upper and lower limbs
weak delayed pulse in legs
mid to late systolic murmur over aortic area
infraclavicular murmur
o Rx
surgical resection of the narrowed portion – if HTN
angioplasty
- widened mediastinum + systolic murmur – can be:
o aortic aneurysm
leaking aneurysm
Sx
- severe abd. pain
- moderate abd. rigidity
- shock
- if leaked posteriorily -> pain radiates to back and down into
genitalia
- intense lower back pain
ruptured aneurysm
Sx
- lower abd. pain, generalised
o Aortic dissection – with shock, chest pain, etc.
- Aortic abdominal aneurysm
o risk factors
Marfan syndrome
o Sx
pulsating palpable mass in abd
abd pain, back pain
o Cx
Rupture
Sudden abdominal pain.
Radiating to back or groin.
Syncope, collapse or unexplained shock.
Feel for a tender mass with expansible pulsation on examination.
Classic triad:
- Abdominal or back pain
- shock
- pulsatile or tender abdominal mass in men over 45 years.
Dx
- Perform a rapid bedside USG to confirm presence of abdominal
aneurysm.
- X Ray – midline opacity with calcified border
Dx diff. with chronic pancreatitis – calcifications like a
chain (2 parallel lines)
- CT scan
381
Rx
- High-flow O2 by face mask.
- Slow IV infusion: avoid giving massive fluid replacement, as this
leads to coagulopathy, hypothermia, ↑ bleeding.
- Refer urgently to vascular surgical team.
o Rx
< 5 cm – observe, elective surgery
> 5 cm – urgent surgery
no matter what size + symptoms = urgent surgery
method: stenting
- Aortic dissection
o PREDISPOSED BY:
HTN
pre-existing aortic aneurysm
Marfan syndrome
inflam. vasculitides (temporal arteritis, syphilitic aortitis, Takayasu arteritis)
Bicuspid aortic valve.
Coarctation
Iatrogenic trauma.
o Sx
Abrupt onset with sudden pain.
Sharp or tearing pain, radiating to back
Retrosternal, interscapular or lower in back, migratory, severe, resistant to
opiates
Unequal radial artery pulses ± decr. or absent pulses at femoral arteries
Difference of BP in arms.
Diastolic murmur if Aortic Regurgitation occurred.
o Dx
1. investig. of choice = contrast CT
2. if renal fc. is abnormal -> transesophageal U/S
X Ray – wide mediastinum
o Rx
Morphine
β blocker – relaxes muscles of aorta, decr. the extension of dissection
or Ca channel blockers – if β blockers are CI
+ sod. nitroprusside – vasodil.
Surgery – stent graft for type A (MCQ)
o Cx.
MI – dissection before origin of coronary arteries will cause MI
(inferior) MI with wide mediastinum
- Dx: transoesophageal U/S
if aortic dissection, don’t give thrombolysis (can kill the
person) and don’t give aspirin (gets worse with aspirin)
Aortic incompetence (regurgitation) – diastolic murmur
Cardiac tamponade
Pleural effusion
Intestinal ischemia
382
actions:
increases water reabsorption
increases Na and Cl reabsorption
increases K elimination
increases Ca elimination
modified:
increase in Hyperaldosteronism
- Sx
weakness (hypokalemia)
polyuria, polydypsia
HTN
- Primary (hyporeninemic)hyperaldosteronism (MCQ 2022, P52)
causes:
Bilateral adrenal hyperplasia (90%)
Adrenal adenoma – Conn’s syndrome
Adrenal CA
Diagnostic:
low renin: If there is primary
hyperaldosteronism, decreased renin (and
subsequent decreased angiotensin II) will not
lead to a decrease in aldosterone levels (a very
helpful clinical tool in diagnosis of primary
hyperaldosteronism)
o Usually, renin levels are suppressed,
leading to a very low renin-aldosterone
ratio (< 0.0005)
hypertension
hypokalemia (normal Na and Cl)
Rx
Spironolactone
resection of adrenal adenoma
ACE inh. do not help (aldosterone works
outside the renin-angiotensinogen system)
- Secondary (hyper reninemic) hyperaldosteronism
causes
a juxtaglomerular cell tumor (renin producing
tumor) leads to increased aldosterone, as the
body's aldosterone production is normally
regulated by renin levels.
renal artery stenosis in which the reduced
blood supply across the juxtaglomerular
apparatus stimulates the production of renin
diagnostic
high renin
hypertension
hypokalemia (normal Na and Cl)
decreased in Addison’s disease.
384
Antagonists:
Spironolactone, eplerenone – competitive antagonist for aldosterone’s
receptors
o ADH (vasopressin) – synthesized by pituitary gland
increases water reabsortion (main effect)
ADH secretion is increased when body osmolality increases (more
concentrated blood; ADH reabsorbs more water, to dilute the blood) =>
more concentrated urine
ADH defficiency leads to hypernatremia (more water than Na is lost)
increases reabsorption of urea
increases Na and Cl reabsorption
↑ peripheral vascular resistance and thus increases arterial BP
- High blood pressure
o Measurement
Sphygmomanometer – use 3 sizes:
types
o child
o adult
o large adult (obese)
rules:
o cuff’s
Width
40% of arm circumference (Murtagh)
cover 2/3rd of arm (not more) – AMC
o children - cuff width should cover 75%
of arm (Murtagh)
cuffs that are too wide underestimate BP, cuffs
that are too narrow overestimate it (AMC)
Length
at least double the arm circumference
(Murtagh)
bladder length should not completely encircle the limb
(but only 80%) - AMC
bladder width is half the length of bladder- AMC
o types of drugs used
1. Diuretics
Thiazides
o actions:
↑Na and Cl excretion (inhibiting reabsorption of Na+
and Cl- ions from distal convoluted tubules in kidneys by
blocking the thiazide-sensitive Na+- Cl- symporter)
↑ K+ excretion
↑ serum uric acid
o side effects
hypokalemia, hyponatraemia (SIADH), loss of Mg
hyperuricemia
hyperglycaemia
385
Felodipine
o Non dihydropyridine
Verapamil
Diltiazem
4. ACE inhibitors & AIIRA (Angiotensin II receptor antagonist, more selective
than ACE inhibitors, do not produce cough)
actions
o vasodilation
o ↓ aldosterone (diuresis)
indications:
o Hypertension
o Heart failure
o Peripheral vascular disease
o Diabetes
o Cardioprotective after a heart attack
side effects
o dry cough
o disturbance in taste (dysgeusia)
o rash
o hyperkalemia
o first dose hypotension
o angioedema
contraindications
o bilateral renal artery stenosis, precaution in CRF
o pregnancy
o hyperkalemia, avoid K sparing diuretics
o hypersensitivity to ACE inhibitors
examples:
o ACE inhibitors
captopril
enalapril
lisinopril
o AIIRA
irbesartan
losartan
5. Central-acting agents
actions
o α 2 agonists - stimulate α 2 receptors in brain, which decreases
cardiac output and peripheral vascular resistance, lowering BP.
indications:
o Hypertension – in asthma, pregnancy
side effects
o sedation
o dry mouth
o constipation
o impotance
contraindications
388
DM, dyslipidemia
ACEI/ AIIRA
Ca channel blockers
o Verapamil, diltiazem
o Nifedipine, felodipine
coronary heart dis. (MI/ Ischemia)
β blockers
Nifedipine, felodipine
congestive heart failure
diuretic
ACE inh./ AIIRA
- Cx in HTN
o HTN retinopathy – stages:
I – Silver lining (silver wiring)-(Narrowing + ↑ reflectivity of vessels walls).
II – Arterial & venous nipping (crossing over)
III
flame-shaped micro hemorrhages
soft exudate (cotton wool)
IV - Papilledema
o HTN ENCEPHALOPATHY
Acute and malignant hypertensive crisis.
Severe HTN (diastolic > 140 mmHg).
very high BP (systolic > 200)
Severe headache, confusion, vomiting and blurred vision.
Focal neurological signs, seizures and coma may develop later.
Fundoscopy: retinal hemorrhages, exudates and papilledema. (Grade IV
changes)
DIAGNOSIS:
ECG and CXR
Examine a MSU for proteinuria and send it for microscopy to look for
evidence of renal disease, with casts or abnormal urinary RBC ( > 70%
dysmorphic)
MANAGEMENT:
Aim for O2 of 94%
Aim to initially reduce main arterial pressure gradually by 25% or aim for
a diastolic BP of 100-110 within first 24 hours.
Use Oral treatment with Labetalol 100 mg, Atenolol 100 mg or long
acting Nifedipine 20-30 mg.
Dyslipidemia
- Hyperlipidemia
o risk factors for
Coronary artery dis.
↑ LDL and ↓HDL
LDLC/ HDL > 4
Pancreatitis
TG > 10 mmol/L
o Goal:
391
Nicotinic acid (Niacin, Vit. B3) – lowers cholesterol, increases HDL, lowers TG
Probucol – lowers cholesterol absorption
Estrogen – in postmenopausal women
Omega-3 fatty acids in fish oil– lowers TG and cholesterol (VLDL)
o usage:
Elevated LDL Cholesterol:
statin + ezetimibe
statin + resin
Elevated TG:
fibrates
or nicotinic acid, n-3 fatty acids
+ decr. alcohol
Mixed (CT and TG elevated):
if TG < 4 – statin
if TG > 4 – fibrate
- Familial hypercholesterolemia – Xanthoma (Yellowish plaque) on Achilles
- Familial combined hyperlidpidaemia – Xanthelasma ( yellowish plaque on superior & inferior
eyelid )
Rheumatology - OK
- Arthritis disorders:
o Simple analgezics – aspirin, paracetamol
o NSAID, Cyclo-oxygenase-2 (COX-2) specific inhibitors
o Disease-modifying agents
Rheumatoid arthritis
sulphasalazine
hydroxychloroquine
gold
D-penicillamine
methotrexate
cyclosporin
cyclophosphamide
azathioprine
leflunomide
biological DMARDS
fish oil – omega 3
Systemic lupus erythematosus
hydroxychloroquine
azathioprine
Spondylarthropathies
sulphasalazine
methotrexate
Osteoarthritis
glucosamine
chondroitin
o Disease-suppresant agents
corticosteroids
o Intra-articular injections
393
corticosteroids
hylan (hyaluronic acid)
o Surgery
synovectomy
joint replacement
arthrodesis
- Gout
o men
o symptoms:
arthritis
monoarthritis 90%
- metatarso-phalangeal 75%
- other toes
- ankles
- knees
tophi – in ears, elbow, big toes, fingers, Achilles tendon
renal calculi
high fever, fatigue
o risk factors:
alcohol
diuretic (thiazides)
β blockers (?)
niacin, aspirin, cyclosporin
fructose sweetened drinks
meat, seafood (purine-rich)
o precipitate an acute attack of gout in a susceptible individual
alcohol
surgery
starvation
drugs
thiazides
frusemide
probenecid
aspirin
sulphonylpyrazone
o Dx
monosodium urate crystals in synovial fluid or in tophus with strong negative
birefringence in polarized light microscopy
hyperuricemia – 70%
X Ray – punched out erosions at joints margins
o Rx of attacks
1. Indomethacin (or other NSAIDs) 50 mg until symptoms abate (3-5 days),
then taper to 25 mg until cessation of attack
2. Colchicine
SE – diarrhoea
3. C/S intra-articular
ACTH in difficult cases
394
antiendomysial AB
o Anti-thyroid microsomal AB - Hashimoto
o ANCA – antineutrophil cytoplasmic AB
c-ANCA – Wegner granulomatosis
p-ANCA – microscopic polyangitis, Churg-Strauss syndrome, Goodpasture?
o Anti-GBM – Goodpasture
o Anti acetycholine receptors AB – Myasthenia Gravis
o Anti smooth-muscle – Chronic active hepatitis
- Reiter vs. Behcet
Reiter (reactive arthritis) Behcet
Gender Men 10:1 Men 2:1
HLA HLA B27 HLA B51
Triad Triad: non-specific urethritis + conjunctivitis A rare immune mediated
(± iritis) + arthritis vasculitis (small arterioles) of
(similar, but w/o ocular and mucocutanous multiple organs
lesions = reactive arthrits)
Ulcers Painless ulcers Traid of oral, genital (scrotal,
labial ulcers) ulcers + Uveitis
Vision Conjunctivitis Uveitis, retinitis (severe pain
problems in eye,↓ eye vision)
Long term Rare Inevitable – prompt referral
ocular disability required!
Arthritis – long Frequent – 50% Rare (knees)
term Spondylitis, sacroilitis common + knees, ankle,
involvement toes polyarthritis
Cause After an acute inf. with specific venereal or Genetic, race
dysenteric organisms: Multiorgan dis. (vasculitis)
SARA (Shigella), CARA (Chlamydia)
Rx NSAIDs C/S, Immunosupressants
- Uveitis – always part of connective tissue/ autoimmune dis. (not inf. dis.)
o causes
Behcet’s disease
Reiter’s syndrome
Ankylosing spondylitis
IBS
Psoriasis
SLE
(Sarcoidosis, Juvenile RA)
o Rx – treat underlying condition
- Connective tissue disorders
o WHEN TO SUSPECT?
Middle aged person.
Female: More common.
Multisystemic involvement.
Skin lesions + arthritis + other features
- SLE
o MC connective tissue disorder.
396
ANA antibodies
Skin biopsy
- Vasculitis
o Inflammation and necrosis of blood vessels resulting in ischemia and infarction.
o Any organ system can be involved.
o Keys to diagnosis: Clinical suspicion, laboratories are not specific, biopsy will confirm.
Small vessel Medium vessel Large vessel
o Rx
Immunoglobulin IgG – 3-5 days + most imp to reduce aneurysms (MCQ)
high doses of aspirin – risk of thrombosis
If coronary artery disease: Anti-thrombotic therapy.
NO C/S!!!
- Temporal arteritis
o Untreated can lead to blindness: 20-25%
o Commonly associated with Polymyalgia Rheumatica: 30% of pts.
o Peak onset: Over 50 yrs.
o MC in females.
o > 60% neurol. sequelae
o Sx
Triad = fatigue + headache + jaw claudication
Unilateral Temporal headaches and scalp tenderness.
Sudden, painless loss of vision.
Tongue and jaw claudication.
Symptoms of polymyalgia rheumatica if present.
o DIAGNOSIS:
Clinical Diagnosis.
first test - Dramatically increased ESR.
Increased CRP.
Best test - Temporal artery biopsy: Confirms diagnosis.
o TREATMENT:
High dose of prednisolone until symptoms resolve (1mg/ kg)
IV – if visual symptoms present
PO – if no visual sympt.
Immunosuppressant drugs if refractory (?).
- Polymyalgia rheumatica (MCQ 2123 P 86)
o 30% association with temporal arteritis
o may be associated with carpal tunnel syndrome
o F:M=2:1, > 50yrs
o inflammatory condition of muscles: pain or stiffness usually in neck, shoulders and hips.
o Most PMR sufferers wake up in morning with pain in their muscles which are tender on
palpation.
o Sx
triad: malaise + painful shoulder girdle + morning stiffness > 20 yrs
pain and early morning stiffness (no weakness – but blue book MCQ 3.068
says: with proximal weakness) in proximal muscles or shoulder and pelvic
girdle, symmetrical
Painful restriction of movement of shoulders and hips.
O/E: Painful and tender muscles but no weakness or atrophy.
weight loss, malaise, anorexia, fever, tiredness
depression
o DIAGNOSIS: Requires:
Age > 50 yrs.
More than 2 affected muscle groups: Neck, hip and shoulder girdles, thighs.
At least 2 wks duration
401
EMG
Anti Jo-1, Anti MI-2 AB
best - Muscle biopsy
o TREATMENT:
Physical therapy
Assessment of organ involvement
High dose of C/S
Immunosuppressive agents
Immunoglobulin IV
Malignancy surveillance (Ovarian, stomach, prostate, BCC, SCC increased)
- Sjogren’s syndrome:
o Chronic inflammatory disorder.
o CD4/ CD8 cell mediated infiltration and destruction of salivary and lacrimal glands.
o Pt’s with Sjogren’s syndrome are at higher risk of non-Hodgkin’s lymphoma.
o MC assoc. with RA
o CLINICAL FEATURES:
Dry mouth: Difficulty swallowing food without drinking, carries, erythema of
oral mucosa.
Bilateral swelling of salivary glands (parotids, submand.)
Ocular: Burning, dry, painful eye relieved by tears, foreign body sensation,
blepharitis.
o DIAGNOSIS:
Autoantibodies: Anti-Ro, Anti-La, RF
Salivary flow measurements
Salivary gland biopsy (MCQ)
Schirmer test – shows ↓ lacrimal production
o TREATMENT:
Good dental hygiene.
Artificial tears
Hydroxychloroquine, C/S, immunosuppressants for severe systemic
involvement
- Rheumatoid arthritis
o affects multiple joints, most commonly small joints of hands, feet and cervical spine,
symmetrically but larger joints like the shoulder and knee can also be involved.
o AB attack synovium – initially joint space is wider, then becomes narrow (not use it as an
X Ray criterion)
then attack the bone (osteopenia, erosion)
o attacks synovium everywhere => symmetrical
o Sx
Synovitis can lead to tethering of tissue with loss of movement and erosion of
joint surface causing deformity and loss of function
Morning stiffness
affects tendons and ligaments => Ulnar deviation of hands (Subluxation of
joints)
Rx – fixation with metal rod in straight position (arthrodesis)
Rheumatoid nodules – often subcut. usually found over bony prominences/
pressure points, such as olecranon, calcaneal tuberosity, metacarpophalangeal
joint or other areas that sustain repeated mechanical stress.
403
Nodules are associated with a +ive RF titer and severe erosive arthritis
fatigue, malaise
carpal tunnel syndrome
o lab:
Rheumatoid factor – if negative, seronegative arthritis – 15% of patients
anti-citrullinated protein antibodies (ACPAs). Like RF, these tests are positive in
only a proportion (67%) of all RA cases but are rarely positive if RA is not
present, giving it a specificity of around 95%.
anti-CCP AB (cyclic citrullinated peptide) test and the Anti-MCV assay
(antibodies against mutated citrullinated Vimentin)
RF and anti-CCP present = Worst prognosis
ESR and CRP are elevated
o diagnostic - American College of Rheumatology has defined (1987) the following criteria
for classification of RA - at least 4 criteria have to be met for classification as RA
Morning stiffness of >1 hr most mornings for at least 6 wks.
Arthritis and soft-tissue swelling of > 3 of 14 joints/ joint groups, present for at
least 6 wks
Arthritis of hand joints, present for at least 6 wks
Symmetrical arthritis, present for at least 6 wks
Subcutaneous nodules at specific places
RF at a level above 95th percentile
Radiological changes suggestive of joint erosion
o Murtagh 355 – DD of various arthritis types
o Rx
Splintage
Exercise
Bed rest
drugs
Aspirin, paracetamol, fish oils
C/S
Methotrexate
+ sulfasalazine
+ hydrochloroquine
RA Osteoarthritis Gout
Primary joints MCP, PIP, wrist First MCP of thumb,DIP DIP
Symmetrical Cervical, lumbar spine, hips & knees joints
Heberden’s nodes on DIP Absent Frequently present
joint (osteophytes) +
Bouchard’s nodes (PIP
joint) less common
Joints Soft, warm, tender Hard and bony
Stiffness Worse after If present, worse after effort
resting (morning (evening stiffness)
stiffnes)
RF Positive Negative
anti-CCP AB Positive Negative
ESR and CRP ↑ Normal
404
o young men
o sacroiliac joints and spine – pain and stiffness
o also hips, shoulders, knees, ankles
o Morning stiffness
o Iridocyclitis, Uveitis
o Dx: XRAY of Sacro-iliac joint, investigation of choice.
o Rx
Exercise
NSAIDs
Infliximab
- Psoriatic arthritis:
o Fingers and toes - DIP involvement
o Sacroilitis – like in Akylosing spondylitis
o RF neg.
- Goodpasture’s syndrome
o Hemoptysis + hematuria
o sore throat, cough, runny nose
o anti-GBM AB
o Dx
Anti-glomerular basement membrane (anti-GBM) from lungs and kidneys
p-ANCA?
o Rx
C/S
Immunosupressants
- Wegener granulomatosis
o Triads:
Physiopathol: URT granuloma + fleeting pulmonary shadows (nodules) + GN
Sympt: Malaise + URTs (rhinits, sinusitis), LRTs (wheeze, cough).
o 40-50 yrs
o Sx
LRT + URT sympt.
Polyarthritis
Eye involv. – Orbital mass
Oral ulcers
GN 75%
o Dx
C XRay: Multiple nodes (rubbery pulmonary masses) and cavitations
c-ANCA (Antineutrophil cytoplasm AB)
Dx confirmed by open lung biopsy
o Rx
Cyclophosphamide
Fatal w/o Rx!
- Takayasu’s arteritis – (Pulseless disease)
o Young Japanese females
o Large vessel vasculitis
affects arch of aorta and other major arteries
o Sx
406
o Dx
CK
urine
Blood
Myoglobin
o Rx – Supportive
- Myoglobinuria/ hemoglobinuria (not hematuria) – no RBCs on microscopy.
Endocrinology - OK
- Insulinoma
o incr. insulin, proinsulin and C-peptide levels
o hypoglycemia improved by eating
o U/S – pancr. tumor
- Paraneoplastic syndromes
o in CAs of lung, liver, stomach
o Sx
hypercalcemia
hypokalemia
hypoglycemia
etc.
o e.g.
Squamous cell carcinoma
Hypercalcemia – production of parathyroid hormone-related peptide
(PTHrP)
- Sx - fatigue, constipation, polyuria, confusion, coma
Small cell carcinoma
SIADH – hyponatremia (less than 120mmol/L) with hypervolemia.
Ectopic ACTH secr. – (Cushing syndrome) Stimulates melanocytes -> ↑
skin and mucosal pigmentation.
o Dx diff. with carcinoid syndr. –> here Sx appear long before the local growth and metast.
Carcinoid syndrome
Symptoms sec to carcinoid tum. (which can occur anywhere in GIT +
lung).
- MC in appendix, ileum, rectum, caecum, lungs
due to incr. production of serotonin metabolyte: 5-HIAA
flushing of the skin, wheezing, bronhoconstr., diarrhoea, abd. pain, hT,
right side of heart affected (tricuspid valve dis. syndrome - prolif. of
myocytes on the valve)
Dx
- urine 5HIAA
- chromograffin test
Rx
- octretide
- tumor resection
Bouts of flushed face
- w/ diarrhoea – Carcinoid syndr. – Dx. 5-HIAA
- w/o diarrhoea – Phaeochromocytoma
- Acromegaly
408
o Sx
Triad: Nasal problems + fitting problems (rings, shoes, etc.) + incr. sweating
excessive growth of hands, tissues (nose, lips, face), feet, jaw and tongue
Weakness, sweating, headaches
Amenorrhoea, loss of libido
Sleep apnoea
Glycosuria
o Dx
Measurement of GH levels after glucose challenge test (OGTT)
hyperglycemia inhibits release of growth hormone in normal people
Insuline-like growth factor 1 (IGF-1) – Key test
Hyperprolactinemia
o causes
Physiol. –Pregnancy, breast-feeding, intercourse, sleeping, stress
tumors
Prolactinoma = prolactin-producing tumor in anterior pituitary gland
- very high levels of prolactin (especially in macroadenomas)
Pituitary adenoma - tum. that compress stock of pituitary gland (releases
dopamin which inhibits release of hormones from Anterior pituitary - FSH,
LH, ACTH, Prolactin - or Posterior - Vassopresin, Oxytocin)
Hypothyroidism, PCOS, POF – through -ve feedback, stimulate pituitary gland
sarcoidosis
renal failure
cirrhosis
silicosis
breast trauma
breast herpes zoster
drugs
drugs that inhibit dopamine
- typical antipsychotics (haloperidol) and some atypical
antipsychotics (risperidone, amisulpride)
fluoxetine (SSRI)
metoclopramide
ranitidine
estrogen (HRT) – MC cause
methyldopa
Ca channel blockers
estrogen
- (drugs causing gynecomastia:
- digoxin
- isoniazide
- spironolactone, steroids
- cimetidine
- omeprazole
- metyhldopa, marijuana
- estrogen
- + calcium antagonists, amiodarone, TCAs
409
sweating
palpitations
angina can occur
Bouts of flushed face
o w/o diarrhea - Phaeocromocytoma
o w/diarrhea- carcinoid syndr. – Dx. 5-
HIAA
- Dx
24 hrs urinary free catecholamines – incr.
o Cortex (CSR)
Produces:
Glucocorticoids (Cortisone, Corticosterone)
Mineralocorticoids - Aldosterone
Androgens – Testosterone
diseases
Addison’s disease – deficit of glucocorticoids and mineralocorticoids
- causes
TB in adrenal glands
Amyloidosis
Autoimmune destruction
Adrenoleukodystrophy
- Symptoms:
triad: fatigue + a/n/v + abd. pain + skin discoloration
orthostatic hypotension– which doesn’t respond to NS
fatigue, malaise
hyperpigmentation on knuckles, creases of palms,
elbows and scars, oral mucosa, gums
hyponatremia and hyperkalemia - deficit of
aldosterone
hypoglycemia
metabolic acidosis
hypercalcemia
Addisonian crisis:
Symptoms aggravated after infection, sudden
steroid withdrawl or adrenal hemorrahge
can be lethal if untreated
Rx – Hydrocortisone IV
- Dx
confirm:
cortisol
ACTH
- Rx - hydrocortison
Cushing’s syndrome
- causes:
taking glucocorticoid drugs
Cushing’s disease – adenoma of pituitary gland that
produces too much ACTH (pituitary Cushing).
411
Thyroid pathology
- Murtagh – P 221 – table for Sx
Hypothyroidism Hyperthyroidism
Risk factors Autoimmune dis. (Hashimoto) Graves’
Down’s Excessive thyroxine
Turner’s Hot nodules
Rx: Radioiodine, Amiodarone, Lithium Amiodarone – less frequently
Thyroid surgery Inf. (De Quervain’s subacute
Postpartum (Sheehan’s syndrome) thyroiditis)
S/s General Tiredness, lethargy, cold intolerance Anxiety, agitation, restlessness,
heat intolerance
Psychiatric Depression, psychosis Psychosis
MSK Weakness, decr. reflexes, myalgia, carpal Weakness, incr. reflexes, clonus,
tunnel syndrome proximal myopathy, fine tremor
pain in shoulders due to calcific
tendinitis -> adhesive capsulitus
Skin Dry, cold, coarse Warm skin, moist or sweaty
Myxedema (non-gravity dependant)
Thin hair, brittle
Face Puffy Exophtalmos, lid lag
Cardiovasc. Bradycardia, AMI, cardiomyopathy, Tachycardia, heart failure, AF, HTN
cardiomegaly (Systolic) wide pulse pressure
412
TSH T4 T3 Rx
Primary hypothyroid. Incr. Decr. Decr. Thyroxine:
Non-vasc. Pt: Start with 50 µg/day
Vasc. patient, > 65: do ECG (address any
vasc. problems first), then start 25
µg/day (thyroxine can cause an Acute
Cor. Synd.) Test TSH, T4 every 4-6 wks
until you reach desired level: if needed
↑ in increments of 25 µg. Then 1-2
times after 6 mths. Then yearly. In
pregnacy: check at least every trimester
Sec./ central hypothyr. N or Decr. N or ↓ Inx MRI
(hypothalamus) decr.
Hyperthyr. Decr. Incr. Incr. 1. β blockers (for tachycardia & palpit.)
2. First try Propylthiouracyl (PTU) or
Carbimazole (in pregnancy)
3. Radio iodine (before surgery)
4. Surgery
5. in subacute thyroiditis: symptomatic
Sick euthyroid N or a N or a N or a Only symptomatic (self-limited)
(post-op. – response to bit bit bit
stress: cortisol ↑ ≥ decr. decr. decr.
TSH, T3, T4 just a bit ↓
but with symptoms
- thyroid problems
o Sx
dysphagia
painful in inflamation – Hashimoto
complete – anaplastic carcinoma
stridor – requires urgent surgery
o Dx
blood hormones: T1, T3, TSH, calcitonin, Ca
U/S
FNAC
thyroiditis?
nodules
thyroid scintigraphy - scan
diffusely increased activ.
- Graves dis.
diffusely decreased activ.
- subacute thyroiditis
413
- silent thyroiditis
- post-partum thyroiditis
diffusely heterogenous activity
- toxic multinodular goitre
focally increased activity
- hyperfc. adenoma
o thyroglossal cyst
o thyroid cyst
Dx – U/S
o nodules
single – benign
multinodular goitre – benign
less likely to be malignant than a single nodule
a multinodular goiter is with hyperthyr.?
Toxic nodule
Dx
- Localized increased uptake of radioiodine
Cold nodule
Dx
- Localized decreased uptake of radioiodine
- CA?
o Thyrotoxycosis
types
Primary = Grave’s disease
- autoimmune
- Sx
Diffuse goitre
Exopthalmia, lid lag
- Dx
Diffusely increased uptake of radioiodine
Secondary
- hot nodule
- De Quervain’s subacute thyroiditis
post. inf. – Viral, URTI
initially hyperthyr., then hypothyr.!
Sx
fever
enlarged painful thyroid
tender lump or swollen goitre
Dx
diffusely decr/ no uptake of radioiodine
incr. T3 and T4, decr. TSH
no AB
o Dx diff from Graves
Rx
Propranolol
Paracetamol
414
Self-resolving
Sx
triad: anxiety + wt. loss + weakness
amenorrhoea (everything else incr.)
Rx
Antithyroid drugs (thyrostatics) - inhibit production of thyroid hormones:
carbimazole, methimazole, propylthiouracil
β-blockers: propranolol, metroprolol
Radioactive iodine therapy ( I131)
Surgery
o Thyroid crisis (thyroid storm)
An emergency life threatening condition caused by sudden rise in thyroid
hormones. Sx precip. by surgery or inf. in undiagnosed patient.
Rx
emmergency admission!
antithyroid drugs
C/S
anti-heart failure and antiarrhythmic drugs
o Hyperthyroidism in pregnancy
dangerous for baby
Premature delivery
IUGR
Fetal death
Malformations
Rx
medical
- Propylthiouracil
passes less to baby
risk of hypothyroidism in mother
check level of T4 in mother regularly
- Carbimazole – if propylthyouracil doesn’t work
long acting thyroid stimulator -> protector? detect
status of baby
if not working -> surgery
radioactive Rx is prohibited!
o Hypothyroidism
Sx
Triad: tiredness + husky voice + cold intoleration
Menorrahagia (everything else decr.)
Rx
Thyroxin – monitor TSH levels:
- check every month, till stable
check every 2-3 months, till stable
check every 2-3 yrs
o Hashimoto’s thyroiditis
autoimmune
415
o contralateral Horner?
o cavernous sinus pathology
o intraorbital pathology
- Stridor post-thyroidectomy (due to haematoma) -> open wound/ all (superficial/ deep)
sutures in ward
Hyperparathyroidism
Ca PO4 ALP PTH
Multiple myeloma Incr. Incr. or N N N
Paget’s dis. N N Very very incr. N
Primary hyperparathyr. Incr. Decr. Slightly incr. or N Very very incr.
Osteoporosis N N N N
Osteomalacia (↓bone density) Decr. Decr. N N
Malignancy Incr. Incr. Incr. N
CRF Decr. Incr. Incr. or N N
o Types
Primary
Parathyroid adenoma ↑ PTH ↑ Ca
Secondary
↓ Ca ↑ PTH
o MC cause of isolated (asymptomatic) hypercalcemia
o Sx
Moans – muscle aching
abd. groans – abd. pain, gastroesoph. reflux, constipation
Stones - Renal
Bones – pain, back pain
Psychic overtones - fatigue, depression
o Dx
PTH very incr.
DM
- Murtagh – 194 – Dx + 1320 Rx + Jay’s notes
- Sx
o Polyuria + polydipsia + Wt. loss
o Lethargy
o Neuropathy
diabetic foot ulcer is MC cause of prolonged hospital stay in DM
if DM is properly controlled, amputation can be reduced by 50%
if untreated, 1/3 of DM patients will have amputation due to DM neuropathy
with presence of normal pedal pulse, dev. of foot ulcer is unlikely
types:
MCQ: burning pains in feet, pins and needles in fingers and toes,
weakness and unsteadiness of legs, distal wasting and weakness in all
limbs, glove and stocking sensory loss of all modalities, areflexia.
1. Sensory polyneuropathy – Bilateral peripheral symmetrical (glove
& stocking distribution) ē numbness, tingling, pain often worse at night
- Rx
Paracetamol/ aspirin
417
Gabapentin
TCA
2. Moneneuritis - cranial nerve neuropathy
- III, IV
- difficult to Rx – C/S
3. Amyotrophy – asymetrical motor neuropathy
- a. Painful wasting of quadriceps (lumbosacral radiculopathy)
Dx – EMG
- b. focal neuritis – pain & tingling of anterior surface of thighs
Rx - Immunglobulins
4. Autonomic neuropathy
- heart – Orthostatic hypotension, tahycardia
- GIT – Gastroparesis (bloating, early satiety)
usually slower GIT movement => bacterial overwgrowth
=> diarrhoea
- Urine retention
- ED
Rx
Amytryptilline
o HbA1C < 6.5% normal
control in last 3 months
o Childhood DM
Polyuria, Polydypsia, wt. loss (despite polyphagia)
Rx
- insulin: 2 divided doses
- 0.5 unit/kg/day - honeymoon period (first 2 weeks after Dx)
- 1 unit/kg/day – older child
- 1.5 unit/kg/day adolescent
2/3 in the morning + 1/3 in the evening
2/3 long / intermed. + 1/3 short acting
Dx – blood sugar
o Rx
types of drugs
o Insulin
o Oral hypoglycemic agents
Insulin secretagogues
sulfonylureas: glipizide, gliclazide, glibenclamide,
tolbutamide, chlorpropamide
(me)glitinides: repaglinide
Insulin sensitisers
Biguanides: metformin
Glitazones: pioglitazone, rosiglitazone
alpha-glucosidase inhibitors - slow the digestion of starch in the
small intestine, so that glucose from the starch of a meal enters
the bloodstream more slowly, and can be matched more
effectively by an impaired insulin response or sensitivity
acarbose
418
Peptide analogs
incretin mimetics
o GLP analogs: exenatide
DPP-4 inhibitors
o vildagliptin
Amylin analogs
approach
type II
- start with lifestyle changes – 2-3 month trial
- if not controlled, then start Metformin – incr. dose to max.
- then add Gliclazide – incr. dose
- then add Acarbose – incr. dose
- then insulin
type I
- insulin
ultra-short: Lispro
short acting: neutral
intermediate acting: Isophane, Protophane
- Cx
o 1. Hypoglycemia
glucose < 3 mmol/L
Sx - sweating, anxiety, hunger, palpitations, confusion, drowsiness, seizures,
coma
types
Mild-moderate = conscious patient
- Oral food containing glucose (20-25 g glucose)
Severe = unconscious or delirious
- 20-30 ml of 50% glucose/ dextrose IV (hospital) in cubital fossa
(not in hand – high glucose concentration could cause
thrombosis of small veins) or
1 ml glucagon IM (at home, in ambulances)
- in kids – 10% glucose (50% could cause complic.?)
- neonatal hypoglycemia
5ml/ kg 10% dextrose IV over 5 min
then 100 ml/kg/day IV infusion
- at home – apply instaglucose – rub gel on gums
o 2. DKA (Diabetic Ketoacidosis)
Hyperglycemia + dehydration + ketonuria +hyperosmolality+ high anion gap
Ketonuria = production of ketone bodies is a normal response to a shortage of
glucose, meant to provide an alternate source of fuel from fatty acids.
causes
- in DM – especially type 1
- in significant dehydration and electrolyte loss (e.g. massive
vomiting)
- in starvation
MCQ: K+ shifts to extracel space K+ in blood is incr., but total body K+ (intra
+ extracel) is low (due to renal loss)
419
carotid body tumor
carotid aneurysm
lateral thyroid tumor (metastases)
Post neck triangle
developmental remnants
- Cystic hygroma
-
can be huge
soft, transilluminated
May be macrocystic or microcystic
MRI is gold standard for radiologic evaluation
- Bronchial sinuses and cysts
Pancoast tumor (from lung apex)
cervical rib
Midline
thyroid nodule
Thyroglossal duct cyst:
- Midline lesion anywhere from foramen cecum and thyroid gland
- May contain ectopic thyroid tissue
- May contain all functioning thyroid
- Ultrasound, thyroid scans
- moves with protrusion of tongue + moves with swallowing
- Rx
Surgical excision - Sistrunk procedure
422
o
dermoid cyst – beneath the chin
midline cervical lymph node swelling
anywhere/ widespread
sebaceous cyst
lipoma
submandibular
salivary gland tumor
cervical actinomycosis
sternocleidomastoid tumor
ENT - OK
- uvula is shy (away from the lesion) and the tongue is bold (towards the lesion)
Laryngeal pathology
- Laryngitis
o acute
hoarseness
loss of voice
o chronic
due to
smoking
- active
- passive (in barmaids, etc.)
voice abuse
- Laryngeal CA
o Hx of chronic laryngitis and smoking
o might be preceeded by leukoplakia
o hoarseness of voice + lump (cervical l. node) + sore throat + cough + stridor + earache
o Rx
Radiotherapy, laser therapy
Laryngectomy.
- Laryngomalacia
o MC cause of stridor in infants
Usually presents as inspiratory stridor within first 6 months of life.
o 90% of pts will have spontaneous resolution of symptoms usually by 12 mths of age (18
mths – 2 years).
10% require surgery.
423
Play audiometry
o 6 years +
Modified play audiometry
o 8 years +
Standard adult audiometry
1. Rinne test - Place a vibrating tuning fork (512 or 256 Hz) initially on mastoid process until sound
is no longer heard, tuning fork is then immediately placed just outside ear. Normally, sound is
audible at ear. It’s a test of outer and middle ear.
2. Weber test - A vibrating tuning fork (either 256 or 512 Hz) is placed in middle of forehead, chin,
head equidistant from patient's ears. Pt. is asked to report in which ear sound is heard louder.
a. A patient with a unilateral conductive hearing loss would hear tuning fork loudest in
affected ear (because conduction problem masks ambient noise of room, whilst well-
functioning inner ear picks up sound)
b. A patient with a unilateral sensorineural hearing loss would hear sound louder in normal
ear (because affected ear is less effective at picking up sound even if it is transmitted
directly by conduction into inner ear.)
Normal ear, air conduction (AC) is better than bone conduction (BC) AC > BC = + Rinne
In conductive hearing loss, bone conduction is better than air AC < BC = - Rinne
In sensorineural hearing loss, BC and AC are both equally depreciated,
AC > BC = + Rinne
maintaining relative difference of bone and air conductions
MCQ 2012, P 49
Conductive hearing loss
Criteria Sensorineural hearing loss
(weird behavior!)
Anatomical Inner ear, cranial nerve VIII or central processing Middle ear (ossicular chain), tympanic
Site centers membrane or outer ear
Hearing Loss
o Degrees
normal: 0-20 dB (20 = soft speaking voice)
mild: loss of 20-40 dB (40 = normal speaking voice)
moderate: 40-70 (70 = shout)
severe: 70-90 dB
profound: > 90 dB
425
o MC causes
Impacted cerumen (wax)
Serious otitis media
Otitis externa
Children – congenital deafness
Elderly - presbyacusis
o Types
Conductive Hearing Loss
acquired or congenital, caused by blockage or damage in outer or middle
ear. Bone conduction is normal.
A conductive hearing loss leads to a loss of loudness and can often be
helped by medical or surgical treatment.
Causes:
- Blockage of ear canal by impacted wax or foreign objects
- Otitis externa
- Middle ear infection (glue ear)
- Perforated eardrum (due to infection or trauma)
- Otosclerosis
- Partial or complete closure of ear canal.
Sensorineural Hearing Loss
acquired or congenital and is caused by damage to or malfunction of
cochlea (sensory part) or hearing nerve (neural part).
leads to a loss of loudness as well as a lack of clarity. Quantity & quality
of sound are affected and sometimes may limit benefit of a hearing aid.
Causes:
- Presbyacusis - Ageing process (MCQ 2064 P66)
bilat. high frequency (s, f, th) progressive hearing loss
- excessive noise exposure (occupational and traffic noise)
- meningitis and Meniere's disease
- viruses, such as mumps and measles
- Ototoxic drugs
- head injuries
Mixed Hearing Loss
Mixed hearing loss results when there is a problem in both conductive
pathway (in outer or middle ear) and in nerve pathway (inner ear).
An example of a mixed hearing loss is a conductive loss due to a middle-
ear infection combined with a sensorineural loss due to damage
associated with ageing.
o Rx
Hearing aid – in conductive hearing loss
Cochlear implant - effective if implanted early
children > 2 yrs
adults
- Otosclerosis (MCQ 2099 P78) 3022 P 214
o Disease of bone surrounding middle ear and is MC cause of CHL in adults with a normal
tympanic membrane.
o Normal middle ear bone is replaced by vascular, spongy bone that becomes sclerotic
426
-
427
o
o 2/3rd of children have at least one episode by age of 3 yrs, 90% by school entry
o 2 cardinal features
Inflammation & effusion
o Clinical Features:
Earache, pulling of ear, reduced hearing, irritability, anorexia, lethargy
Fever, vomiting – bacterial -> A/B
o EXAMINATION:
Usual middle ear landmarks are not well seen.
Tymp membrane is dull and opaque with loss of light reflex and may be
bulging, yellow-grey colour
Fluid level might be seen
On pneumatic otoscopy TM mobility is reduced
May have associated signs of URTI
o CAUSES:
Streptococcus pneumonie 35-40%
H. Influenzae 25-30%
Viral: 25%
Moraxella catarrhalis 15-20%
least common – Staph.
Do not accept otitis media as sole diagnosis in a sick febrile young child
without elimination of a more serious cause
Meningitis – frequently assoc. with otitis media
o Rx
try to avoid using A/B
never use A/B in children, except for this!
> 1 yr old, mildly unwell, immuncompetent
just observation for 12-24 h, analgezia, no A/B
if symptoms not resolving or severely ill (Vomiting, fever---Bacterial)
- First line = Amoxycillin
- still not resolving after 48 hrs
2. Cefaclor or
Amoxycillin + clavulanic acid – if resistance is
suspected
< 1 yr, moderate/ severe, immuncompromised
- amoxycillin
- still not resolving after 48 hrs
amoxycillin + clavulanic acid
o Complications:
Effusion – 70%
428
- Cholesteatomas are expanding lesions of the temporal bone
composed of a stratified squamous outer epithelial lining and a
desquamated keratin centre
- Clinically defined as an abnormal extension of skin into middle
ear and mastoid air cell spaces
- The point of entrance of skin into middle ear is reliably
identifiable on otoscopic examination
- Otoscopy is the most reliable and sensitive means of diagnosing
a cholesteatoma
Signs of an unsafe perforation on otoscopy:
Superior and or posterior edge of tympanic
membrane perforation
Perforation involving fibrous edge or annulus
of tympanic membrane
Associated granulation tissue
White mass within middle ear seen through
perforation
Bone erosion
Dizziness (a condition of faint, wekness and unsteady gait)
o can be with
Central cause – brain, cerebellum
acoustic neuroma
MS
head injury
vertebrobasilary insuf.
Peripheral cause – inner ear
Meniere
Benign Paroxysmal Positional Vertigo
Vestibular neuritis/ labyrinthitis
o causes:
COMMON
Benign Paroxysmal Positional Vertigo
Vestibular neuritis/ labyrinthitis (unilateral peripheral vestibulopathy)
Meniere’s syndrome
Vestibular migraine
Psychogenic
Idiopathic
LESS COMMON
430
Acoustic neuroma
Vertebro-basilar transient ischaemic attack/stroke
Multiple sclerosis
Posterior fossa tumours
Arnold-Chiari malformations
Autoimmune inner ear disease
Perilymph fistula/semicircular canal dehiscence
Invasive middle/inner ear disease (e.g. otomastoiditis, tumours,
cholesteatoma)
Bilateral peripheral vestibulopathy (if asymmetric)
o Diagnostic Triads (J.Murtagh)
only vertigo caused by movement = BPPV
Acute vertigo + nausea + vomiting = Vestibular neuronitis
(acute vertigo + nausea + vomiting) + hearing loss ± tinnitus = Acute
labyrinthitis (similar symptoms to Meniere). Symptoms upto days.
Vertigo + vomiting + tinnitus + SNHL = Meniere’s syndrome
(unilateral) Tinnitus + SNHL + unsteady gait = Acoustic neuroma
- duration of common causes of vertigo
Seconds Benign positional vertigo
Minutes Vertibrobasillar insuf., migraine
Hours Meniere’s disease
Days Vestibular neuritis, labyrinthine infarcts
o 4 common causes
1. Benign paroxysmal positional vertigo (BPPV)
MC of vertigo seen by otolaryngologists (20-40% of pts with peripheral
vestibular disease)
Affects all ages.
Approximately 50% of people > 70y have experienced at least 1 episode
Symptoms & signs are brought about by changes in head position, in
relation to gravity, 5-10 sec later, lasts 10-60 sec.
May be associated with closed head injury, infections, surgery and
prolonged bed rest.
Pathophysiology:
- Otoconia become dislodged and pass through endolymphatic
space of vestibule into one of the semicircular canals.
Pathognomonic sign:
- nystagmus towards affected ear on doing a Dix-Hallpike test
Treatment:
- Epley repositioning maneuver
- Brandt-Darrof exercises
2. Vestibular neuronitis – M 508
20-40 yrs
only vestibular portion of VIII N is affected, unilateral & no hearing loss
- if both vestibular and auditory portions (hearing loss) are
affected = labyrinthitis
2nd MC disorder affecting labyrinth
431
-
- Vertigo, fullness in ear (due to distension labyrinthitis)
- Tinnitus
- Nausea and vomiting
- hearing better in noisy environment MCQ
- Deafness (progressive) – sensorineural hearing loss
- + nystagmus during attack
Treatment:
- Vestibular sedative, antiemetic for acute episodes
Prochlorperazine
urea crystals in orange juice
Diazepam
Betahistine
- Low salt diet ± diuretic for maintenance treatment
- Meniett device
- Intra-tympanic gentamycin or surgery for refractive cases
4. Acoustic neuroma = Vestibular schwannoma
tumor of Schwann cells on 8th cranial n.
slow growing –> brain has time to adjust => less vertigo
78% of all cerebellopontine angle tumors
0.8% to 2.7% of population: 0.7 to 1 per 100,000
433
Symptoms:
- Unilateral progressive SNHL 85% (handbook 401 )
- Sudden hearing loss 15%
- Tinnitus 56%
- Vertigo 19%
- absence of corneal reflex
- Facial paresthesia from 5th cranial N irritation.
- (7th 9th 10th and 11th N involvement) - Diplopia, facial weakness
and hypoaesthesia, Cerebellar ataxia (Unsteadiness of gait) MCQ.
Treatment:
- Observation
50-55% show little or no growth in 1-3 years
less than 0.2mm/ year
Repeat MRI to monitor growth
- Surgical resection
Translabyrinthine, middle fossa or suboccipital
retrosigmoid approaches
Stereotactic radiosurgery (gamma knife)
- Vertigo + Nystagmus + Horner Syndrome = Cerebellar lesi on = PICA (MCQ)
- Nystagmus: (Dancing eyes) involuntary rapid eye moevemts, can be horizontal, vertical or
rotatory.
o VOR: Head movement (vestibular stimulation) in one direction stimulates eye movement
in opposite direction. Important in reading as head constantly moves a little.
o Physiological = Part of vestibulo-oculo reflex (VOR)
tested with caloric reflex test (VIII N nucleaus)
Syringing of ears with warm water: eyes will turn towards the
contralat. ear + horizontal nystagmus towards the ipsilateral ear
with cold water – opposite effect
o Pathological
caused by lesions of
Inner ear
VIII nerve
Brainstem
Cerebellum
Cortex
434
Ophtalmology - OK
-
o normal left eye fundus
- Dx
o vision
6/4
6/5
6/6
6/60
…
count fingers at 6 m
count fingers at 1 m
see fingers?
perception of light
o Optic disc - nasal
clear contour
o Retinal vessels
narrower arteries
wider veins
o Macula – temporal
no blood vessels in the middle
darker in color
- Cranial nerves for eye muscles
o III
MR
SR
IR
IO
levator palpebral superioris
palsy:
Ptosis + fixed (non reactive) dilated pupil + down & out eye
- DM or any ischemic problem – pupil normal (peripheral fibres
will still get supplied, here are ones for the pupil)
causes
- DM (diplopia with normal pupil) or other ischemic problems
- cavernous sinus lesions
- sup. orbital fissure
435
o IV
SO
Palsy: diplopia on downward (vertical) and lateral gaze
Diabetic ocular neuropathy: Vertical binocular diplopia with normal pupil (MCQ
3023 P 214)
o VI
L.R
Palsy: divergent squint on lateral gaze
- Diplopia
o Monocular – persists after occluding 1 eye
causes: in same eye!
early cataract
dislocated lens
severe astigmatism
psychogenic/ functional
Rx – not urgent
o Binocular – (doesn’t persist when ocluding 1 eye)
REFER URGENTLY!!
causes: in higher nerve centres
ocular nerve palsy – III, IV, VI
- CVA or TIA
- tumor
- aneurysm
- DM ocular neuropathy
- arthritis
- head injury
- migraine (ophtalmic) - transient
blow out fractures (MCQ)
concussion
MS – recurrent diplopia
myasthenia gravis
hyperthyroidism
- Blocked naso-lacrimal duct
o repeated inf.
o usually self-corrected between 6-12 mths
o Rx
repeated bathing with normal saline
massage over lacrimal sac
local A/B for inf.
refer – probing of lacrimal sac, if
severe blockage or
if not self-corrected by 12 mths
o Cx
Dacryocystitis – inf. of lacrimal sac sec. to obstruction
Rx
Systemic A/B – Flucloxacillin
Drainage
436
septicemia
neonatal conj. (+ chlamydia)
Rx
o IV cephalosporins or penicillin
o topical sulfacetamide
Chlamydia
brick red follicular conj. with stringy mucus
discharge
types
o neonatal
o young patient with venereal inf.
o isolated Aboriginal people with
trachoma
MC cause of blindness in world
recurrent & untreated => lid
scarring & inturned lashes
(endtropion) ē corneal
ulceration & visual loss
Dx
o swabs for culture and PCR
Rx
o local sulfacetamide eye drops
o systemic
neonates – Erythromycin
children > 6 kg: Azithromycin
- Dx
clinical
swab
- Rx
severe cases - cloramphenicol eye drops
milder cases
saline irrigation
antiseptic – propamidine isothionate
Viral
- MC assoc. with an URTI
- highly contagious –> good hygiene
- Hx of infected contacts
- resolves in 3 wks
- caused by adenovirus
- Cx – sec. bact. inf.
- preauric. Lymph node
- Rx —cool compress and topical lubricants (artificial tear
preparations), naphazoline (e.g. Albalon), vasoconstrictors (e.g.
phenylephrine) or saline bathing.
C/S are CI
Non-infectious
from welding (actinic)
438
Allergic
types
- assoc. with hay fever
Rx
topical antihistam.
topical sodium cromoglycate
topical C/S
- contact hypersensitivity
assoc. with topical opthalmic drugs (A/B) contact lens
sol., cosmetics, etc.
Rx
remove cause
naphazoline
topical C/S
- Episcleritis
o no discharge
o no watering
o N vision
o self-limiting
o Rx
topicl and oral C/S
- Scleritis – assoc. with autoimmune dis. FIGURE 51.1 JM P 577
o painful loss of vision
o urgent referral
- Uveitis
o acute
anterior uveitis = iritis and iridocyclitis
Sx
- photophobia
- iris is sticky and sticks to lens => adhesion => constricted/
irregular pupils
- blurred vision, floaters in field of vision
causes
- 80% isolated
- 20% Reiter, ankylosing sponditlytis, Crohn, IBS, psoriasis
(seronegative arthropaties), SLE – HLA B27
Rx
- referral
- pupil dil. with atropine
- topical C/S
- systemic C/S
frequently recurrs after Rx
post. uveitis = choroiditis
o chronic
Sx
pupil is bound to the lens by synechiae and distorted
Cx – loss of vision due to:
439
glaucoma
cataract
- Refractive errors
o Presbyopia
> 45 yrs
o Myopia
image formed IN FRONT of the retina (long eye or steep cornea)
Rx – concave lenses
Cx in high myopia
retinal detach.
macular degen.
glaucoma
o Hypermetropia
image formed BEHIND retina (long eye or steep cornea)
Rx – convex lenses
Cx – closed angle glaucoma
o astigmatism
causes – conical cornea (keratoconus – e.g. Down)
o pinhole test – 1 mm hole
corrects any refractive error
if not => not just a refraction error!
Cx – Closed angle glaucoma.
- Acute visual loss
o flashers and floaters
causes
constant – less of a concern
- age
440
- myopia
- eye surgery
fresh onset = concern
- retinal detachment
o Retinal detachment
types
Posterior vitrous degen. and detachment – in everybody
- sudden onset of floaters
- flashing lights = Traction on retina
- Rx – Urgent referral
some people – pathol. detachment
- causes
trauma
high myopia (thin retina)
previous surgery (e.g. cataract)
DM retinopathy
- Sx
no pain
more dangerous if affecting macula
sudden onset of: (the 4 Fs)
flashes
floaters (spots, dots, cobwebs)
field loss
fall in visual acuity
o Partial
o Total – if macula detached
then suddenly irreversible blindness.
“a curtain came down over the eye”
if revers. = carotid stenosis and embolism
- Dx
Opththalmoscopy: detached retinal fold as a large grey
shadow in the vitreous cav.
- Mx
transport to the hospital ASAP!
can’t transport by air
tilt head back and cover eye
keep pressure on the detached retina
o Upper curtain (MC) – lower
detachment – keep head up.
441
Sx
Acute painless loss of vision (usually profound) with sudden onset.
- “curtain descending over one eye.”
- Irreversible.
Waxy, swollen, pale retina, thin arteries.
chilly red spot in macula – init. still vascularization but then same color
as the rest of retina.
Rx
lower intraocular pressure (glaucoma medication)
inhale CO2 (paper bag).
poor prognostic, unless treated within 30 min.
o Central retinal vein occlusion (CRVO)
442
Embolic occlusion of central retinal artery Due to blood clot in central retinal vein
Sudden Gradual (hours/ days)
Painless loss of vision Painless loss of vision
Unilateral Unilateral Often hypertensive
Mx: Mx:
Exclude GCA & TIA Elective referral to ophthalmologist within
Refer ophthalmologist 1 wk
Ocular massage Screen for HTN, DM &
Acetazolamide oral – reduce IOP Hypercholesterolemia
o Ischemic optic neuropathy – irrevers.
Temporal arteritis:
sudden and often bilat. occlusion of the short ciliary aa. supplying the
optic nerve.
Sx
- revers. loss of vision, then can lead to irreversible
- sudden loss of central vision
unilat., can rapidly become bilat.
- assoc. temporal headache, temporal aa. tender, thickened and
nonpulsatile.
Dx
- ESR (> 40), CRP (sometimes ESR can be normal, then we do CRP)
- FBE (Hb – anemia; gives you higher ESR)
- temporal a. biopsy – confirm Dx
Rx – Predisolone for 18-24 mths
- IV if patient has transitory loss of vision
- after 10 days of Rx – changes biopsy result (modif. have
disappeared)
o Optic (retrobulbar) neuritis Most Common Dif Dx = MS (MCQ)
neurosyphilis
toxins
woman, 20-40 yrs
443
Sx
retrooc. discomfort with eye movement
central field loss (central scotoma)
- or peripheral circumferential blindness
Dx: Visual evoked potentials (VEPs) are an important means of evaluating
patients with suspected optic neuritis. They may be abnormal even when MRI of
the optic nerve is normal
optic disk swollen, then atrophic, then disc pallor
Rx
IV C/S
most pts recover spontaneously but are left with diminished acuity
o Migraine:
zigzag lines and lights
multicolored flashing lights
unilat. or bilat. field deficit
self-resolution within a few hrs
o Hysteria
bilat. loss of vision, with tunnel vision
o Vitreous haemorrhage
assoc. with
trauma
DM retinopathy
tumor
retinal detachment
Sx
sudden onset of floaters
loss of vision
Dx
clots of blood that move with the vitreous (black swirling cloud)
Mx
urgent referral – exclude retinal detach.
may resolve spontaneously
surgical vitrectomy for persistent haemorr.
o Closed angle glaucoma (see below)
- Chronic loss of vision
o in children = Amblyopia = ↓visual acuity due to abnormal visual experience in early
childhood
strabismus
444
cataracts
refractive errors
retinoblastoma
o Glaucoma (Optic n is slowly damaged bc of ↑ IOP)
Dx for incr. intraoc. pressure
Cup: Disc
- N ≤ 30%
- if > 30% = raised intraocular pressure
Tonometry
- Normal 10-22 mm Hg
incr. – can go up to 55-60
Acute angle closure glaucoma: (Acute painful Red eye) 3024,P 215
acute -> acute loss of vision
- ciliary flush (hyperemia)
- Common in middle aged or elderly hypermetropes.
- Narrowed anterior chamber.
- Precipitated by pupillary dilation – in the evening, (peripheral iris
blocks aqueduct outflow and an abrupt rise in intraocuolar pressure)
- Sx – similar with migraine without aura, but with visual Sx –
diagn diff.!
Severe throbbing pain.
Headache.
Nausea and vomiting.
Weakness.
Visual changes:
Vision is ↓ with HALOES around lights/ objects.
The cornea is HAZY/edematous.
Fixed and DILATED oval pupil.
corneal or scleral injection
On palpation: eye feels firm/ stony hard.
- MANAGEMENT:
Ocular emergency.
Urgent referral to the Ophthalmology team.
1. Miotic drops (Pilocarpine every 5 min for up to 1 hr).
2. Acetazolamide (carbonic anhydrase inhibitor) 500
mg slowly IV then 250 mg orally t.d.s. – diuretic
3. Peripheral iridotomy – perforation in the iris to
evacuate the liquid
Antiemetic such as metoclopramide 10 mg IV and
analgesia such as morphine 2.5 mg.
- DM
- HTN
Screening
- > 40 yrs – every 2-5 yrs
- if family Hx – start from 30 yrs, every 2 yrs
Sx
- Progressive painless loss of vision (tunnel vision) + cupping of
optic disc + raised intracranial pressure.
also in
retinitis pigmentosa
hysteria
central vision is N
Rx – for life!
- drugs
β blockers: timolol, betaxolol
acetazolamide (diuretic)
pilocarpine - parasympathomimetic alkaloid
latanoprost - PG analogue
dipivefrine – prodrug of epinephrine, converted to
epinephrine in the eye
- surgery or laser therapy – if drugs failed
o Cataract
cause
age – everybody > 80 yrs have opacities
DM
trauma
C/S
UV light
uveitis
Sx
blurring of vision in bright light
Dx
diminished red reflex
change in appearance of lens
Rx
lens extraction + intraoc. lens implant
- CI:
Intraoc. inflammation
Severe DM retinopathy
Px – UV sunglasses
Cx
Hypopyon (puss in ant. chamber of eye)
446
-
- causes
in case of endophtalmitis after
penetrating injuries
surgery
cataract
- urgent referral!
- Rx
avoid movt.
avoid smoking/ alcohol
don’t give heparin
bed rest 5 days
sedative
check daily
if floaters / flashes -> emmergency!
bleeding 2nd, 3rd, 4th day?
o Retinitis pigmentosa
displacement of melanin-containing cells from pigment epithelium into more
superficial parts of retina
Sx
night blindness in childhood
tunnel vision
blind by adolescence/ middle age
Dx
patches of dark pigment especially at the periphery
o Macular degeneration
447
causes/ risk factors
age related
high myopia
types
acute – exudative
chronic – pigmentary (slow onset)
drusen (neovasc. membranes which develop under the retina of the macular
area and leek fluid or bleed ) + visual loss
Sx
central visual loss
- acute – sudden fading of central vision
- eventually central vision is completely lost
distorted images = macular degen.!
- lines of the words bend / seem wavy while reading
Dx
screening: using a grid pattern (Amsler chart)
- shows distorted lines
- cannot see the central dot
-
ophthalmoscopy – white exudates, haemorrhage in the retina
fluorescein angiography
can be
wet – acute?
- hemorrh., fluid leaks in macula
- Rx
laser photocoagulation
inj. inside the eye – vascular growth factor inhibitor =
new Rx
stabiliz.
1/3 improve
dry – chronic?
- “worn-out jumper”
- Rx
448
nutritional supplements
antiox. – Vit. A, C, E + Zn
- corneal disorders
o Keratoconjunctivitis sicca - “dry eyes”
causes
ageing, menopause
systemic dis.
- RA
- SLE
- Sjogren
drugs
- Beta blockers
Rx
artificial tears – hypromellose, polyvinyl alcohol
o Keratitis
causes
UV light (“arc eye”)
herpes simplex
herpes zoster ophthalmicus
superficial punctate keratitis
- in various conditions:
e.g. UV light exposure = flash burns
microbiol keratitis
- risk factors
contact lenses – MC with pseudomonas
corneal trauma or surgery
post-herpetic corneal lesion
etc.
Cx
perforation and blindness
Rx
urgent referral!
topical A/B – ciprofloxacin oint.
o Abrasion/ ulceration
causes
trauma
contact lenses
fingernails
UV burns
dendritic ulcer
- primary herpes simplex I inf.
can also cause follicular conjunctivitis
- Dx
stain with fluorescein
- Rx
Acyclovir
atropine – prevent reflex spasm of the pupil
449
Dx
slit lamp and fluorescein staining
Rx
chloramphenicol oint.
eye pad
- Pterygium
o
o fleshy overgrowh of the conjunctiva onto the nasal side of the cornea
o in dry, dusty, windy areas
o Rx
surgical excision
- Pinguecula
-
o yellowish elevated nodular growth of the cornea
o Rx
surgery – if uncomfortable
- corneal ulcer with hypopyon - emmergency
o rheumatoid arthritis
o contact lenses abuse
- Blepharitis
o inflam. of lid margins
o freq. assoc. with seborrhoeic and atopic dermatitis and rosacea
o types
seborrhoeic
staphylococcus
assoc. with rosacea
o Rx
eyelid hygiene – mainstay of Rx
topical C/S
topical A/B
tetracycline
chloramphenicol
- Stye (hordeolum ext.) – inflam. external glands (2026, P 54)
450
o
o Acute abscess of eye lash follicle
o Staph. aureus
o Red tender swelling of lid margin, usually on medial side
o Rx
Hot compress
Lash epilation
Chloramphenicol oint.
- Chalazion (Internal hordeolum, Meibomian cyst)
o
o Granuloma of the Meibomian glands (embedded in tarsal plates)
o Inflammed tender irritant lump in the eyelid
o Chronic – Chalazion
o Rx
Hot compress
Chloramphenicol oint.
If large and uncomfortable -> surgery – incision and curretage under LA
- Herpes zoster ophtalmicus (Shingles)
o Ophtalmic distribution of V nerve (trigeminal)
o Respects the midline!
o Ocular problems: conjunctivitis, uveitis, keratitis, glaucoma
o Rx
Topical acyclovir
Systemic acyclovir – Oral, IV
- Penetrating eye injury
o not a lot of pain
o do not give pain killers – Morphine, etc. – can cause vomiting, making things worse
small dose + antiemetic (metoclopramide)
o no local anestetic eye drops – can be retinotoxic
o don’t put bandage (pressure), just a shield or cone
o urgent referral!
if delay – give systemic A/B
- Ectropion – rolling outward of the eye lid
451
o cause
age – involution
facial nerve palsy
o Rx – lubricant Rx
- Entropion – rolled inward
o irritation of the cornea
o Rx – attach eyelid to the cheek
- Lid tumor
o BCC 90 %, SCC 9 %, other 1%
o with loss of eye lashes (madarosis) – serious!
- Subluxated lens
o
o Marfan syndrome
o trauma
- MRI – don’t do if metalic foreign body in the eye (magnetic)
- burn
o acid – injury just on the spot
o alkaline – injury keeps evolving
wash with excess water for 30 min
- Leukoria- White eye reflex
-
- Retinoblastoma!, Toxocariasis, Retrolental fibroplasias, Coat’s diease
- Retinopathy
o typical
Cotton wool (intra-retinal infarcts) - DM
Flame shaped haemor., AV nicking - HTN
o DM
Non-proliferative
Related to ischaemia of blood vessels and include:
452
Proliferative: Changes in blood vessels in response to ischaemia to retina.
- New vessel formation.
- Vitreal hemorrhage.
- Retinal detachment.
can leak, rupture with hemorrhge in vitreous, healing with fibrosis,
retractional retinal detachment
- Rx - Panretinal argon laser photocoagulation
o HTN
Grade 1: ‘Silver wiring’ of arteries only.
Grade 2: Grade 1 plus arteriovenous nipping or nicking.
Grade 3: Grade 2 plus flame shaped hemorrhages and cotton wool exudates
(soft or hard).
Grade 4: Grade 3 plus papilledema.
deposits around macula – cartwheel
- Papiloedema – bilat. disc edema due to ↑intracranian pressure
o vs. disc edema
- Lymph drainage
o Preauricular -> submandibular nodes
- Hyperemia
o Ciliary – close to the centre – central (eye) origin
o Conjunctival – peripheral
453
- Visual field problems – M 837 + Jay’s notes
o Retrobulbar neuritis -> circumferential blindness
o Optic nerve affected -> complete loss of vision in that eye
o Partial lesion of chiasma (perichiasmal area) -> unilat. nasal hemianopia
o Optic chiasma lesion -> Bitemp. Hemianopia (or bitemporal upper field blindness)
cause - pituitary adenoma (MCQ)
macroadenoma of pituitary gland
- init. upper bitemp. hemianopia
- then complete bitemp. hemianopia
o Homonymous hemianopia (e.g. left temporal and right nasal hemianopia)
Optic tract
Optic radiation
Visual cortex (occital lobe)
o Quadrantanopia (same side quarter in both eyes – e.g. left in both eyes)
Sup. quadrants – temporal lobe
Inf. quadrants – parietal lobe
Emergency medicine - OK
- Emmergency situations >- Rapid primary survey = assess ABCD (disability) E (exposure)
o 1. Airway
Secure airway
454
response
A
B
C
CPR
o how:
30 compress. : 2 breaths
chest depression: 4-5 cm
rate of compressions: 100/min
o most important sign of successful
resuscitation: Pupillary light reflex OK
o how long to continue CPR: as long as
you can, till specialized team has
arrived (usually max. 45-50 min)
o if cardioversion is not available, IV
adrenalin should be given every 3 min.
Disability
neurological signs
Defibrillation
o use it right away if available
o for a witnessed cardiac arrest, using a
manual defibrillator:
give 3 consecutive shocks in
first defibrillation attempt
further shocks –> single shock
o 1st shock: 200 J Biphasic (before 360 J
monophasic – no longer used)
o continue CPR for 2 min
o 2nd shock:200 J Biphasic-> max. 3shocks
o Shockable rhythms:
Unstable VT
VF
o Non-shockable rhythms:
Asystole (no pulse)
Pulseless electricl activity (PEA)
Advanced life support (specialized team has arrived)
- continue CPR
- in shockable rhythms (VT/ VF) - defibrillate again
- non-shockable rhythms – drugs only
- drugs
Adrenalin 1 mg IV or intracardiac repeat every 3 min
during defibrillation
Atropine 1-3 mg
in asystole or severe bradycardia
Amiodarone – 300 mg bolus
in VT or VF
Mg – muscle relaxation, etc.
457
tender lymphadenopathy
o Cx
greatest danger: Resp. obstruction and failure
neurological – Ptosis
hematological (anticoag.) – affects clotting
+don’t rely on abdominal sympt.!
+ cardiology
+ nephrology
o Mx
1st aid: firm bandage, starting from distal to proximal + splint 2 limbs together
if on buttocks – no bandage but do not move
not too tight, no turniquet, no ice.
make window in bandage to do the swab (don’t displace the bandage)
No sympt. – no treat.
observe patient for 12 hrs, then release
no helicopter/ air transportation
Sympt. – Antivenom + antihistamine + C/S (to avoid Serum sickness – if it
happens, use adrenaline)
Venom detection kit: Take swab (if scratch marks) or use fresh urine and
detect type of snake.
- Monovalent antivenom preferred (e.g. specific for tiger snake)
over polyvalent (since it can cause anaphylaxia).
- if we can’t detect the type of snake -> polyvalent.
- Dilute antivenom 1: 10 in NS, prolonged 30 min. infusion
- Air transportation
o CI in:
Snake bite
Retinal detachment
- Spider bite
o Only one spider is life-threatening – Sydney funnel-web spider (Murtagh 1346)
Sx
Muscle fasiculation, salivation and lacrimation, piloerection, dyspnea,
neurological symptoms.
Mx – like for snake bites
Resuscitation
Specific antivenom
o Red-back spider and black widow spider can also cause envenomation
rarely fatal, more serious in the young, frail, elderly
Mx
Antihistamine
Antivenom x IM
o Rest – life support
Mx
Apply ice pack
No bandage
CA metastases - OK
- Murtagh p. 242-243
461
- 1. Lymph Nodes
o Supraclav. nodes
Right – 1. Breast (women), lung (men)
also lung (Pancoast tumor)
Left – Gastric (small percentage of gastric – to right as well) – Troisier’s sign
also lung (Pancoast tumor)
- by location/ destination
o Metastases in brain (same as lungs)
Breast
Lung
colon
lymphoma
kidney
melanoma
prostate
o
o Metastases in the lungs (same as brain)
1. breast – MC - Murtagh
2. lung
3. colon
4. (MC at MCQ course) kidney – cannon ball
5. testis
melanoma
+ thyroid – cannon ball
o Metastases in bone – all are osteolytics, except for prostate CA (osteosclerotic)
from
Breast – MC (Murtagh) mixed
462
lungs
liver
brain
small bowel
o Testicular CA metastasizes to
lungs
liver
o Prostate CA metastasizes to
bones: pelvis, spine
brain
- Malignant ascitis
o source
Ovary - MC
Uterus
Colorectal
Stomach
Liver
o can be associated with:
nodules on PR
hepatic bruit
supraclavicular lymph nodes
absent ankle edema
Genetic diseases - OK
- inheritance patterns – Murtagh 167
o AD – Anatomical/ morphol. defects = 50% of all MCQ (male or female) inherit the dis.
Familial adenomatous polyposis (FAP)
Huntington’s disease
Von Willebrand
Neurofibromatosis
Marfan’s syndrome
Triad: tall stature + dislocated lens and myopia + coarctation of aorta
tall and thin
long fingers
mitral v. prolapse
Gilbert’s disease
Tuberous sclerosis
Hereditary spherocytosis
Achondroplasia
Noonan’s syndrome
Acute intermittent porphyria
o AR – enzymes = 25% Cystic Fibrosis, 50% unaffected, 25% carrier, if both mother and
father are carrying the dis.
Cystic fibrosis
β thalassemia
Hemochromatosis
Wilson’s disease
Phenylketonuria
464
- moderate analgezic
- moderate antipyretic
- anti-inflammatory
side effects:
- affects stomach (ulcers, stomach bleeding)
- has an antiplatelet effect (by inhibiting production of
thromboxane, which under normal circumstances binds platelet
molecules together)
Dosage:
- 600 mg 4 hourly (max. 4 g / day)
o NSAIDs – it takes 10 days for them to achieve maximal effectiveness (recommend
intermitent 14 day courses). Most NSAIDs act as nonselective inhibitors of enzyme
cyclooxygenase (COX), inhibiting both (COX-1) & (COX-2) isoenzymes. COX catalyzes
formation of prostaglandins and thromboxane from arachidonic acid. Prostaglandins act
as messenger molecules in process of inflammation.
types by chemical structure
Propionic acid derivatives
- Ibuprofen – short half-life
- Naproxen
long half-life – in bony metastases in cancer
- Fenoprofen
- Ketoprofen
- Flurbiprofen
- Oxaprozin
Acetic acid derivatives
- Indomethacin – short half-life
- Sulindac
long half-life – in bony metastases in cancer
- Etodolac
- Diclofenac – short half-life
Enolic acid (Oxicam) derivatives
- Piroxicam - non-selective cox inhibitor - analgesic antipyretic
long half-life – in bony metastases in cancer
- Meloxicam - preferential inhibitor of COX-2 over COX-1
- Tenoxicam
long half-life – in bony metastases in cancer
- Droxicam
- Lornoxicam
- Isoxicam
Fenamic acid derivatives
- Mefenamic acid
- Meclofenamic acid
- Flufenamic acid
- Tolfenamic acid
Selective COX-2 inhibitors = coxibs – don’t have G. intestinal side effects
of COX-1 inhibitors, but they can cause CV problems (high BP,
thrombosis – fatal MI & stroke), kidney problems
466
transdermal
epidural
efficacy similar to morphine but with fewer side effects
(10 mg morphine SC = 150 micrograms fentanyl SC)
- hydromorphone – 5 - 7 times more potent than morphine
high risk of dependence
- tramadol – atypical, with opiod and non-opiod features
more and more popular
analgesia without sedation or respiratory
depression
low abuse/ dependence
- buprenorphine
limited use, in opioid dependence
- pentazocine – not recommended
- diamorphine = heroin
side effects:
nausea, vomiting
constipation
respiratory depression
dysphoria
tolerance/ physical dependence/ psychological dependence
o Combined analgesics: Paracetamol/ aspirine + opioid (codeine)
not recommended – rather prescribed separately
o Methoxyflurane – inhalatory – in emergencies, roadside accidents (ambulance)
o in neuropathic pain:
Tricyclic antidepressant (TCA) – Amitryptilin – 1st choice in diabetic neuropathy
Antiepileptics:
Carbamazepine - trigeminal neuralgia
Gabapentin – newer - diabetic neuropathy (2 nd choice after TCAs), post-
herpetic neuralgia)
o by age:
Children
Paracetamol
Aspirin – not used < 18 years – risk of Reye’s syndrome (fatty liver,
encephalopathy)
Opioids
- Oral
- Parenteral
bolus – IM, IV, SC
continuous infusion – IV, SC
Elderly – more sensitive, lower doses
- Psychogenic pain
o Periumbilical
o during the day
o not referred
o exclude from Hx: constipation, UTI, dairy product allergy
o Hx – emotional changes in family
468
o Rx
enough dietary fibre and fluids to have normal transit
family meeting to support the child (do not punish the child)
Radiology - OK
- X Ray
o Abdomen
Erect/ supine
Chest – pneumonia in lower lung lobes, can cause abd. pain
Bowel obstruction
location
- Small bowel – center
- Large bowel – periphery
folds
- Small – continuous from side to side---valvulae coniventi
- Large – can’t see whole fold--Haustration
size
- Small – 3 cm
- Large – 6 cm
Cecum – 9 cm
Sigmoid volvulus
inverted U, pointing up and right (distended sigmoid loop)
- bed-ridden elderly people, chronic constipation -> stretching ->
twisting
- young paralyzed people, bed-ridden
Cecal volvulus – small bowel obstruction
Emphysematous cholecystitis – air in the wall of gall bladder
Gas in the liver
Biliary tracts
Portal vein
Hydatic cyst – multilocular, with multiple daugther cysts inside a big cyst
Cyst vs. abscess – abscess might have air inside
U/S can’t see through air – e.g. Retrocecal apendix
o Fractures
cortical disruption
Colles - post. dislocation of distal fragm. compared to the proximal fragment
Pathological fracture (malignancy) = Fracture through lucency
- CT Brain
o Bleeding
Intra-axial bleeding – inside brain
Extra-axial bleeding – outside brain
SAH
- cause
Aneurysm, trauma, anticoagulation
AV malformation
Surgery – immediate effect
Radiotherapy - after 12 months they scar;
during these 12 months they can still bleed
469
- Dx
CT scan
75% show up on CT scan
25% - small amount of bleeding not seen on CT
o do a lumbar puncture
to locate aneurysm or AV malformation
contrast angiogram
U/S through fontanelle – till 12 (max. 18) mths
CT angiogram
MRI angiogram
Subdural hematoma
- elderly
- Multiple minor trauma
- Sx – confused
- Venous
- Sickle-shape (crescent) concavo-convex
- With dark areas inside (chronic, acute on chronic hemorrhage)
- can cause midline shift (if large)
Extradural
- young
- major trauma
- Sx – headache
- arterial (middle meningeal)
- biconvex
- can cause midline shift (if large)
Scalp hematoma after head injury
- Rx – with no loss of consciousness -> observe them for 4hrs., then
discharge them
Blood = white
would be at the botton of the pic/ bottom of the ventricles as the
patient is in supine position (heavier than CSF)
o Stroke
cause
Emboli
- if multiple vessels obstructed, MC with emboli (2 emboli coming
from a proximal source)
e.g.
Elderly – AF
o Dx U/S – clot in a heart chamber
Young
o HOCM
o Mitral valve dis.
o DVT + patent foramen ovale -> could
cause an emboli to brain
Thrombus
types
Ischemic
470
Folic acid
Vit. C and Ca
- Edema
o Pitting – pressing with finger leaves an indentation that persists for some time
cardiac
hepatic
renal
DVT/ varicose veins/ thrombophlebitis
o Non-pitting oedema
Lymphoedema
lymphatic obstruction – do abdmino-pelvic CT to look for tumors
check for DVT - Doppler U/S??
Myxedema
- Hereditary angioedema – bouts of abd. pain and facial edema
o Dx – C1 esterase inhibitor
- Autonomic nervous system
o Sympathetic
originate from thoracolumbar region of spinal cord (levels T1 - L2, specifically) -
"thoracolumbar outflow"
o Parasympathetic
arise from CNS with the:
III, VII, IX and X cranial nerves
S2, S3, and S4 spinal nerves
"craniosacral outflow"
- CNS membranes and spaces
o Epidural (or peridural) space – just in spine
o Dura mater
o Subdural space – virtual, becomes real in cases of haemorrage (subdural hematoma)
o Arachnoid
o Subarachnoid space – contains CSF
hemorrhage from aneurysms
o Pia mater
- Types of tissues
o epithelium is classified as a primary body tissue - cells which line the cavities and surfaces
of structures throughout the body. It is also the type of tissue of which many glands are
formed. Epithelium lines both the outside (skin) and the inside cavities and lumen of
bodies.
o connective tissue
o muscle tissue
o nervous tissue.
- Marital disruption – single most powerful sociodemographic predictor of stress-related dis.
- greatest predictor of cardiovasc. dis. and DM = low educational level
- prevention
o primary – prevent the disease from occurring
o secondary – stop or delay the progression of dis.
screening and early detection of dis.
472
o 18.5-24.9 = normal
o 25-29.9 = overweight
Rx – lifestyle changes
o 30-34.9 = Grade 1 obesity
Rx - Supervised lifestyle changes
o 35-39.9 = Grade 2 obesity
Rx
Supervised lifestyle changes
Medical Rx:
- local
bulking agents – methycellulose
lipase inh. - xenical
- central
decr. hunger – amphetamines derivates: Phentermine,
diethylpropion
incr. satiety – SSRI
o ≥ 40 = Grade 3 (morbid) obesity
Rx – as above +
consider Gastric banding
- SaO2 < 92% - give O2
o in COPD – cut off value = 88%
- Adrenergic receptors
Receptor Agonist
Location / Action Mechanism Agonists Antagonists
type potency order
Smooth muscle. In blood
vessels the principal effect is
vasoconstriction. Blood (Alpha
vessels with α1 receptors are blockers)
Gq:
present in the skin and GI phenoxyben
α1: phospholipa noradrenaline
noradrenaline≥ system, and during the fight- zamine
ADRA1A, se C (PLC) phenylephrine
adrenaline >> or-flight response phentolami
ADRA1B, activated, methoxamine
isoprenaline vasoconstriction results in ↓ ne
ADRA1D IP3 and Cirazoline
blood flow to these organs. prazosin
calcium up
This accounts for an tamsulosin
individual's skin appearing terazosin
pale when frightened. In GI
tract, effect is relaxation.
Gi:
clonidine (Alpha
α2: adrenaline > adenylate
Pre- and postsynaptic nerve lofexidine blockers)
ADRA2A, noradrenaline cyclase
terminals. Mediates synaptic xylazine yohimbine
ADRA2B, >> inactivated,
transmission. Tizanidine rauwolscine
ADRA2C isoprenaline cAMP
Guanfacine idazoxan
down
isoprenaline > Heart and cerebral cortex. In Gs: noradrenaline (Beta
β 1:
noradrenaline heart, agonists enhance adenylate isoprenaline blockers)
ADRB1
> adrenaline myocardial contractility and cyclase dobutamine metoprolol
475
- in delusions - Haloperidol
- hypoxia - O2 40%
- C/S?
o 10 days + fever + mucous diarrhea = Pelvic abscess
without fever: resolved paralytic ileus
o Serosanguinous discharge = Wound dehiscence (rupture)
Surgical emergency: Rx – return to OT: wound toilet and resuturing
in first 10 days after op.
Wound dehiscence = Paralytic ileus (MC cause)
MC with Vertical incisions
o Pulmonary emb. with pulmonary infarction – Chest pain, hemoptysis, pleural friction
rub on 10th day Post-op
o Postop. confusion and disorientation = Acute delirium
causes
Hypoxia – MC, due to:
- Atelectasis
- Analgesics
- Anesthetic from surgery
- Lifestyle changes
o SNAP
Smoking
Nutrition
Alcohol
Physical exercise
Psychiatry - OK
Main pathology
Defense mechanisms (MCQ 2071 p146)
- types: http://en.wikipedia.org/wiki/Defence_mechanism
o I. Pathological
2. Denial = Avoid to become aware of some painful aspect of reality, you’re
not ready to accept it
e.g. patient doesn’t accept that he has cancer (“no, you are lying”)
Rx – don’t confront him, just give him time to accept it (unless he’s
dealing with a life-threatening situation)
3. Splitting = external objects are divided into “all good” or “all bad”
e.g. patient doesn’t talk to any nurse because doctors are better than
nurses; morning stuff is better than evening stuff
mainly in borderline personalities.
Resistance refers to the conscious and informed decision of a patient not
to change behaviour or comply with treatment. e.g, refuses for ECT
o II. Immature – MC in adolescents, often also in adults
o Blocking, regression, somatisation, introjections, projections are examples of immature
defense mechanism (MCQ)
o
1. Projection=projecting your own vicious thoughts/ feelings onto someone else
477
e.g. husband is cheating on wife -> tells her “I think you are cheating on
me”
5. Somatisation = Phsychic derivatives are converted into bodily symptoms
e.g. you think of an exam and you develop symptoms (e.g. diarrhoea)
o III. Neurotic – in adults
6. Displacement = An emotion or drive is shifted to another that resembles
original in some aspect.
e.g. stressed from work/ boss, get home, take it on your partner/ family/ pet.
7. Intellectualization = excessive use of intelectual processes to avoid affective
expression (mood) but emotions are missing in the talks/ arguments.
e.g. patient finds out he has cancer, he researches it, he talks about it like
in a speech, with no emotion
8. Rationalization = rational explanations are used to justify unacceptable
attitudes or behaviour (blame game)
e.g. blaming something else for your mistakes
9. Isolation = Separation of an idea from the emotional effect that
accompanies it
e.g. when seeing body of her dead son, mother is very cold and detached
11. Repression: Ideas or emotions which the person finds painful or
unacceptable are forced out of consciousness and are forgotten.
10 Suppresion: Suppression refers to conscious or 'semi-conscious' decision of
an emotionally mature, healthy adult to postpone dealing with conflict ideas.
e.g., in interview a pt avoids discussion of certain topics
12. Reaction formation: Unacceptable impulse is transformed to its opposite
e.g. we are afraid of an exam, but when asked we tend to say “I’m fine”
Choosing medicine as a career solely to treat other’s illness as a defence
against ones own death or illness anxieties.
Pyromanic becomes firefighter
13. Regression = you don’t behave according to your age (but like a younger
person) MC in males
e.g. after sister born a boy (6yrs) start sucking his thumb & wetting
bed. MCQ 2071 p146
after his parents’ divorce, a 7 yrs old boy starts to wet his bed again
14. Jealousy: A normal human emotion.
15. Compensation or counter dependancy: a form of denial where
individuals respond to limits being recommended by taking more work,
responsibilities or becoming more energetic.
Example, CHF patient who has been told by doctors to remain in home
and not to do exercise recently attends aerobic classes and do 2 km
jogging every day
Acting out: a dramtic or sometimes aggressive behaviour that occurs under
stress/ anxiety eg. throwing tantrums, shouting and yelling.
o IV. Normal, healthy, mature
14. Sublimation = impulse gratification has been achieved but the aim or
object has been changed from unacceptable to acceptable.
the most mature one
478
DIFFERENTIAL DIAGNOSIS:
o Panic attack secondary to a medical
condition.
o Panic attack secondary to medications.
o Caffeine intox. – no chest tightness
o Other anxiety disorders: Panic attack
are unexpected. The fear is of having an
attack, not of a specific situation.
TREATMENT:
o CBT/ Relaxation, training or
desensitization.
o SSRI, Benzodiazepines or TCAs.
long term – between attacks
1. Breathe in paper bags or relaxation
techniques
2. SSRIs
3. TCAs
2. Phobic disorders
- irrational fear focused on certain things (not generalized like in
the generalized anxiety) disorder
- with insight – the person recognizes that the fear is irrational and
out of proportion with the real danger
- resistance is usually minimal and unsuccessful
- types:
Agora phobia – fear of the market, public, busses or
confined places, far from home, you cannot run away
from there
untreated may culminate in a panic attack
Social phobia – talking / eating / socializing with
people; ok 1 on 1, but not with a larger group of people
(public speaking, "stage fright," urinating in public
restrooms)
may be a predisposing factor for alcoholism
(alcohol is anxiolytic)
Specific phobias
Fear of spiders, snakes, illness, contamination,
etc.
- Rx
1. CBT:
systematic desensitization
assertive thinking
2. SSRI
in social phobia (stage fear):
Beta blockers (control the physiological comp.)
3. OCD
- Recurrent and obtrusive false thoughts (Obsession) with insight,
they know it’s wrong but can’t help it + repeated action
482
2. group therapy
3. SSRI
for nightmares: zopiclone, zolpidem (non-benzos
anxiolytics)
5. Generalized anxiety disorder – anxious about everything
- mild, > 6 mths
- charact. = anticipatory feelings, especially in the morning (things
will go wrong today) + physical sympt.
- difficulty falling asleep (thinking about what happened during
the day) and then walking up during the night.
- women
- Rx
1. CBT
2. SSRI
6. Adjustment (reactive) disorder
an acute reaction to overwhelming stress (minor stress like accident) at
any age, who have no underlying mental disorder.
Rx
all antidepressents: SSRI, SNRI, TCA
Benzodiapines – with a clear time limit (otherwise – addicted)
CBT
- Relaxtion + gradual exposure to trigger
o II. Somatoform disorder (MTB3 477)
Physical sympt. with no medical explanation
transform psychological emotions to physical problems, without being
able to connect the 2.
types:
1. Somatisation disorder – Classical form - never seen
- Young women (starts < 30 yrs)
- 8 or more complaints:
4 of pain
2 GI
1 Neurol.
1 Sexual
- + atypical forms – with less complaints
- Rx
CBT
keep rescheduling their appts., don’t confront
2. Conversion disorder
- MC in women
- Psychological symoptoms (stress) convert into physical symptoms
(paralysis or blindess).
- e.g. husband had MI => woman can’t move her legs, but on
physical examination reflexes are normal and she can sit up.
- Woman fell from horse and complains of paralysis of leg.
- Rx
CBT – comforting
484
usually low IQ. Pyromania is not the diagnosis if the motive is personal
gain (i.e., insurance money) or to show anger, which differentiates
this from conduct disorder.
4. Trichotillomania
pull their hair out when stressed
Life change (parents separated, new father, etc.)
Some also eat their hair => Bezoars of hair causing intestinal obstruction
with unequal areas of balding and hair shafts of different lengths.
Dx diff – KOH preparation to exclude a fungal infection
o V. Adjustment disorder
an acute reaction to overwhelming stress (minor stress like accident) at any
age, who have no underlying mental disorder.
inability or maladaptive reaction to an identifiable stressful life event like:
divorce, family crisis, failing exams, etc.
Sx must occur within 3 mths of event and shouldn’t persist longer than 6 mths
females
genetic comp.
Sx = Variety of disturbances at home or work, like: rage, shame, guilt, anxiety,
depression
o VI. Delusionals disorder (A fixed false belief)
just delusions – non-bizarre, initially seem reasonable, but upon investig. no
foundation is found for them
no insight
personality doesn’t desintegrate, well inserted in society
types
Paranoid disorder (MC)
- subtype – pathological jealousy
- can occur as a psychological reaction to deafness
tinnitus may produce or aggravate auditory
hallucinations
Erotomanic – they believe a celebrity is in love with them
can be dangerous – if their delusion refers to another person
e.g. pathological jealousy, Othello`s syndrome, attracted to a celebrity
could kill the person they fantasize about
Rx very difficult, don’t usually respond to antypsychotics
early detection is very important
o VII. Eating disorders –
o Anorexia nervosa – feeling fat (MTB 480) feeling fat, overvalued idea of body image –
even tough they are skin on bone
90% women- a young female who is underweight.
11-21 yrs -MC
Risk factor Athlete (MCQ)
Sx
- stop eating
subtype/ some patients – binge eating (like in bulimia)
- Heavy exercise – this keeps them healthy for a long time!
486
disorganized behaviour
psychomotor disturbance
- agitation
- retardation – catatonic
saccidic eye movement – when asked to follow an object with their eyes,
they do it in steps
Negative sympt.
Lack of motivation
Blunted affect/ emotional blunting
Poverty of speech (Alogia ---- Inability to speak)
Anhedonia- lack of interest in pleasureable activities.
Social withdrawal
o types:
Paranoid
Disorganized – bizarre
Catatonic
psychomotor disturbance (agitation or retardation)
catalepsy - keep their body in weird positions for a long time, e.g. with
the head above the pillow
- diff. from cataplexy – sudden loss of muscle tone + temporary
episodes of paralysis
part of the narcolepsy syndrome
o Rx
Typical (conventional) antipsychotics – not used very much; very few used
these days (5-6 out of 25-30) due to SE
Dopamine receptor antagonists, most effective for +ve features of
Schizo.
- dopamine hypothesis in schizophrenia: positive features in Sch.
are due to overactivity of dopaminergic pathways
e.g.
- Haloperidol – tablet, inj long or short acting
- Droperidol – PO only
- Chlorpromazine , Thioridizine, fluphenazine
- trifluperazine
- flupenentixole – inj long acting
- zuclupentixol – inj long acting
SE (MTB 3 463 table)
- Extrapyramidal
1. Acute dystonia – within hrs to days of Rx
young males at higher risk
severe sustained painful agonizing spastic
contr. of axial muscles: around the eyes
(oculogyric crisis – eyes rolled up and open –
“the look-ups”), tongue (protrudes to 1 side),
spasm of the masticatory muscles (trismus),
neck (torticolis), dysarthria, dysphonia,
dysphagia.
491
avoided in elderly
Block histamine => sedation, Wt. gain
Block α receptors => hypotension
Atypical antipsychotics good for both positive and negative symptoms of
schizophrenia. Typical only for positive symptoms.
o act on 3 tracts in the brain:
1. tuberoinfundibular tract -> decr. dopamin -> incr. prolactin
2. nigrostriatal tract
important in Parkinson: dopamine goes down, acethycholine goes up
cause extrapyramidal effects.
3. meso-limbic tract -> Clozapine works only here => no endocr. effects (1), no
extrapyr. effects (3)
but not a first line drug (but as the 3rd line of attack, after 2 drug failure),
due to the life-threatening risk of agranulocytosis
- I choice in psychosis = Risperidone (causes least sedation)
- II – e.g. Olanzapine
- III – Clozapine = indic. no. 1
also indicated in tardive dyskinesia = indic no. 2
SE:
Hypersalivation, drooling of saliva
Wt. gain
Diabetogenic
leucopenia or agranulocytosis – 1% of pts.
o 85% in the first 9 months
o FBC once a week
o Check FBC for neutropenia in any pt
presenting with fever, sore throat or
other infection.
CI
myeloprolif. disorders
severe CNS depression
previous Hx of leucopenia or agranulocytosis
o types:
Typical = pure D2-antagonists
Butyrophenones
- Haloperidol – the only one available IV
e.g. ED – pacient with agitation
1 – lorazepam (other benzodiapines)
2 – haloperidol – available IV
- Droperidol – p.o. only
Phenothiazine
- chlorpromazine
Atypical
D2-5HT2 (serotonin)
- Risperidone
D2-D4-5HT2
- Clozapine
494
(3-5 days) pregnancy have fallen abruptly during preg. have fallen abruptly
Due to hormonal Mother doesn’t want the baby to be Mother has psychotic sympt.:
changes. Mother a sad/ unhappy like her – she thinks life believes or hears voices telling
bit sad/ depressed is not worth living her that the baby is evil/ devil
and she must kill him. They may
also harm themselves.
Baby is at risk!
(Purple book)
- 1 in 500 births
- MC in primiparous women, Hx of major psychiatric illness or family Hx of
major psychiatric history.
- clinical pictures: organic, affective (MC – predom. with manic disorders)
and schizophrenic
- abrupt onset with insomnia, followed by confusion, fluctuating agitation
and labile mood.
Recurrence in future pregnancies – as high as 20%
Also risk of relapse of mood disorder independant of future pregnancies.
Rx – just family Rx: Rx:
support - antidpressants in milder forms - antipsychotics (Olanzapine)
- ECT in severe depression - if not responding early -> ECT
type - Psychogenic depression = Depression (predom.) with psychotic elements
Rx – ECT
Rx
Antidepressants
- 1. TCA – not used so much anymore
e.g.
Amitriptyline
Nortriptyline
Imipramine
Clomipramine
dophiepin
Paroxetine
Citalopram
Escitalopram, Sertraline
Fluvoxamine
- 3. SNRI (serotonin-norepinephrine reuptake inhibitor)
e.g.
Venlafaxine
duloxetine
Mirtazapine – not commonly used (Samir
Ibrahim = part of a SSRI subgroup - serotonin
agonists)
o heavy sedation, crazy stimulation of
appetite -> wt. gain
o takes effect very fast compared with
the other drugs
Venlavaxan
Desvenlavaxan
SE for SSRI and SNRI
headache, nausea (serotonin surge)
drowsiness, sedation, lack of sleep
impotence (10-35%) – become depressed over
this
SNRI – more cholinergic side effects
- 4. MAOI – not used today
SE - food with tyramine (cheese reaction) – surge in
catecolamines – HTN emmergency -> crisis (can cause
death).
pts had to avoid 50% of the the food items
subtype: RIMA (reversable inhibitor of MAO)
just 1 drug – moclobemide
weak antidepressant, but used when SSRIs
cause ED
SE – same as SSRI
o but no ED!!
- 5. Lithium – mood stabilizer
SE
fibrosis of thyroid -> hypothyroidism (check
every 3 mths)
renal failure (check every 3 mths)
- 6. Dopaminergic
wilberton (Zyben) – used only for cessation of smoking
very expensive
not used in Aus. for depression
- if stopping antidepressive medication, do it gradually over 2 wks
ECT (MCQ 2146 P 94)
- treatment of choice if pt has suicidal ideation
- consent from pt. is required
500
work on
- norepinephrine, serotonin, dopamine receptors (block their
reuptake) -> increase in the brain
- alpha receptors
- muscarinic rec.
- histamine
e.g.
- Imipramine
- Clomipramine – OCD, premature ejaculation (MCQ)
- Amitryptiline – Diabetic neuropathy, chronic back pain, post
herpetic neuralgia.
2. MAOI – MAO breaks down norepinephrine, serotonin, dopamine; MAOI
causes incr. in norepinephrine, serotonin, dopamine
e.g. Tranycypromine, selegiline, phenelzine.
Can’t have cheese, red wine, chocolate, sausages – (all foods containing
high tyramine) => HTN crisis: headaches, nose bleeds, palpitations
3. SSRI – only work on serotonin (hence the name SSRI)
1,2,3 have the same efficiency, but SSRI preferred due to less SE
- Fluoxetine (Prozac) 1st indic. in adolescents ē major depression
- paroxetine (Aropax)
- sertraline (Zoloft)
- citalopram
- escitalopram
4. Newer antidepressants (Atypicals)
Trazodone - used if insomnia is a major problem (highly sedating)
Buproprion - least sexual dysfc.
- also used in quiting smoking
acts on dopamine, which is responsible for causing
craving and hunger, (CI in pts with eating disorder)
o General SE
Sedation (antihistaminic effect) – less with SSRIs
HTN and tachycardia – more with TCAs
anticholinergic – more with TCAs
cardiac problems – only with TCAs (hypokalemia, prolongation of QT interval -
> risk for torsade de pointes)
decreases the seizure threshold--> should be stopped before ECT
↑depending on the washout period: 2-3 days in SSRI, 2-3 weeks TCA
if anxious, non-benzodiazepine anxiolitic = zolpidem (because BD also
decr. the seizure threshold)
Sexual dysfc. (ED, ejaculatory dysfc.) – more with SSRIs, less with escitalopram
MCQ: nausea, vomiting, diarrhea, abdominal pain – SSRIs (especially
sertraline) switch to another SSRI
o TCA intoxication:
SE
Anticholinergic (dry mouth, constipation, urinary retention & sedation)
Cardiotoxic: Cardiac arrythmias, prolongation of QT interval
Overdose Rx:
504
-
- washout periods
From To Washout period
Short acting SSRI Short acting SSRI Nil
505
- Schizoaffective disorder
- Adjustment disorder
admin.
- 750-1000 mg P O in 2-3 divided doses
incr. by max. 250-500 mg/ day
- plasma level
maintain at start 0.8-1.4 mmol/L
chronic users 0.6-0.8 mmol/ L
very narrow therapeutic range – keep blood level at
0.6-1 (< 0.6 not effective, > 1.2 toxic, > 1.6 fatal)
- monitor every 1-3 months!
- Pregnancy: Stop in 1st trimester (Ebstein’s anomaly in babies) Use
ECT for 1st trimester manic episodes, Use lamotrigene in 2 nd and
3rd trimester.
CI - in kidney disease
SE
- Acne and wt gain MC problems (MCQ)
- nausea, vomiting, diarrhoea
- metallic taste
- headache
- afects the cardiac conduction
- hypothyroidism (used in hyperthyr.)
- Polyuria – nephrogenic diabetes insipidus
- kidney failure (very small risk)
test thyroid and kidney evey 2-3 months
toxicity
- sympt. – indic. to decr. the dose
fine tremor
apathy, lethargy, slurred speech
muscle weakness
ataxia, anorexia, nausea
muscle fasciculations
choreoathetosis, convulsions, coma, death
- for pt - important not to get:
Dehydrated
Hyponatraemic
-> both incr. lithium toxicity (by ↑ renal
reabsorbtion)
- Rx
stop drug
dialysis
indic.
o Convulsions, coma
o Lithium > 4 mmol/L
o in renal failure
2. Valproic acid (sodium valproate)
Indic.
507
o MMSE < 24
o 1 in 10 over 65 years.
o 1 in 5 over 80 years.
o CAUSES:
Degenerative cerebral diseases:
Alzheimer’s disease: 60%
Dementia of frontal type: (up to 10%)
Dementia with Lewy bodies: (up to 10%)
Vascular: 15% (after stroke) – is reversible
Alcohol excess: (5%)
o Forgetfullness and loss of cognitive functio.
o Dx of exclusion – after excluding organic causes
o Types
1. ALZHEIMER’S DISEASE:
Insidious onset (Prgressive dementia of degenerative cause).
Initial forgetfulness.
- Forgets: I time, then II place, then III person (faces)
Progresses to severe memory loss.
Dx at autopsy – post mortem
2. FRONTAL LOBE DEMENTIAS:
Young age
Personality changes (rudeness).
Alteration of behaviour including social dysfunction (running naked,
cursing, masturbatingh in front of nursing station (MCQ) hypersexual –
inhibitions from frontal lobe are erased).
Progressive aphasia.
3. LEWY BODIES:
Visual hallucinations and fluctuating confusion.
Spontaneous motor parkinsonism.
Fluctuation in the mental state.
4. VASCULAR (Multi infarct, stroke):
Sudden onset.
Focal neurological signs
Hx of HTN or stroke
o Differential diagnosis: Depression which is termed pseudodementia.
DEMENTIA PSEUDO
DEMENTIA
o incidence – 3%
- Creutzfeld-Jacobs disease
o Mad-cow disease
o spongiform disease of brain
o rapidly progressive mental deterioration + myoclonus
o Death within 1 year of symptom onset
Behavioral emmergencies
o Situations where pts show behaviour that potentially “put them or other people at risk
of physical harm”.
o Requires immediate intervention.
o The criteria for defining behavioural emergencies are vague.
o WORKING DEFINITION:
Refusal to cooperate
Intense staring
Motor restlessness
Purposeless movements
Affective lability
Loud speech
Irritability
Intimidating behaviour
Aggression to property
Signs of imminent intentional or unintentional self-harm
Demeaning or hostile verbal behaviour
o DIAGNOSIS: May be unknown or provisional:
1. Medical disorders: Usually associated with delirium
2. Substance intoxication or withdrawal with or without delirium
3. Psychiatric disorders – after ruling out 1 and 2
Schizophrenia
Mania
Psychotic depression
Personality disorder
Post-traumatic stress disorder
o LEGAL AND PROFESIONAL OBLIGATIONS:
Treatment without consent is conducted under relevant mental health act.
Those treating an acutely disturbed person in such an emergency will need to be
aware of the provisions of relevant legislation and be satisfied that the person
meets criteria for involuntary treatment.
When situation is too dangerous for medical personnel to intervene (weapons
are involved or there is a high likelihood of extreme violence) emergency
personnel such as security staff or police will be required to disarm and restrain
pt.
o Rx
INITIAL STEPS IN MANAGEMENT:
In approaching the patient, care should be taken to ensure the safety of
yourself, other patients and staff, and of the patient.
Measures that can reduce the risk of harm include:
- Room with two exits.
511
- Delirium:
o Confusion + hypo or hyperactive behaviour
o Usually affects elderly people admitted to hospital.
o 10% to 15% are delirious on arrival.
o 5% to 40% will develop delirium while inpatients.
o Pts with dementia are at particular risk.
o Children and the seriously ill are also more likely to develop delirium.
o Impaired cognitive function (especially in orientation and memory) and reduced ability to
focus, sustain or shift attention.
o Psychomotor changes:
Agitation or withdrawal.
Drowsiness.
Illusions, hallucinations, delusions.
o Symptoms develop over hrs to days.
o CAUSES:
Infection: especially systemic but also pulmonary, urinary or ear infections.
Toxicity due to drugs: especially anticholinergic drugs or narcotic analgesics.
Withdrawal from sedative drugs or alcohol: This should be suspected when
tremors, sweating and visual hallucinations are present.
o DD
Mania.
Schizophrenia.
Dementia: especially dementia with Lewy-bodies.
o PREVENTION is most important
Adequate hydration and nutrition.
Adequate pain relief.
Promotion of sleep.
Correction of visual and hearing impairments.
Avoidance of restraints.
Provision of lighting appropriate to the time of day.
Close involvement of family members.
o MANAGEMENT:
Identification.
Treatment of its underlying cause.
The delirious pt must be nursed in a setting where they can be observed at all
times, because behaviour may be unpredictable.
UTI (MC cause of confusion in elderly)
FBE – U & E, Blood sugar
X Ray
o Rx
Frequently no medication will be needed.
If delusions or hallucinations are causing distress or if behavioural disturbance
threatens pt's treatment or care or is causing significant threat to others, then
use Haloperidol 1-5 mg orally.
If oral administration is impossible: Haloperidol 2.5-5 mg IM.
If significant extrapyramidal adverse effects:
- Benztropine 1 to 2 mg orally.
- Benzhexol 2 mg orally.
513
- Avoid chlorpromazine.
Child psychiatry
- ADHD
o Boys 6:1
o 5 % of school age children
o in 60% no complete recovery
o can’t be Dx < 4 yrs
o Age: 7 yrs, going to school
o Dx. of exclusion
o Dx diff. with autism
o Family Hx
o Very common
o Sx
very easily distracted – can only focus for 1 min to the TV
usually only picked up in school (not noticed by parents)
attention + behavior: attention deffict +
with hyperkinesis ADHD
- non-goal directed behav. (he doesn’t want to achieve something
specific)
- can’t help it
without hyperkinesis ADD
impulsiveness and hyperactivity
inattention
hyperactivity, impulsiveness
o Dx
first exclude other causes
Always need to check vision, hearing, lead level first
Exclude outside causes for the child’s behavior: e.g. if his parents
divorced, etc. – talk to both parents (MCQ)
Psychometric assessment– exclude intellectual impairment & learning
disorders
2 situations – home and school
obtain behavioral rating scales from both
sympt. present for at least 6 mths, causing significant functional impairement
o Dx diff. with conduct disorder – were antisocial during childood
Angry child
Abused by parents – friends
is goal directed + full of anger
o Mx
Refer to child phychiatryst
Confirm from family/ home or school
exclude social causes, social disruption
Speech therapist
Involve teacher
Audiometry
Drugs:
Dexamphetamine
514
Methylphenidaze (ritalin)
Autism ADHD
Before 36 mths < 7 yrs, (5 % of school going children)
No family Hx. Family Hx – Boy inherited from father
Criteria: 2 situations – home and school
Autistic spectrum 3 specific issues: Impulsiveness + overactivity + loss of
1. Verbal problems concentration
2. Non-verbal communication and
no social interaction (hugging, etc.)
3. Fixation/ specific focus on
something (e.g. he likes dinosaurs) &
doesn’t like when his life is changing
Asperger – only 2 and 3
Any sex Boys
Rx - Refer to child psychiatrist Ask for school report
Dexamphetamine –> ↓hyperactivity
o Autism
Autistic spectrum disorder – many subtypes
e.g. Asperger syndrome – very mild form of autism
- many will have an almost normal life
- sedentary, isolated life
- avoid eye contact
- normal speech
- some are very good in mathematics
- communication through language is preserved
Autism Asperger
Boys 4:1 Boys 8:1
Onset before 3 yrs (30 mths) after a period of normal development
Low IQ Normal or high IQ
No social interaction, use of 2 word phrases only Can speak, normal speech, likes friends
Lack joint attention: Fascination with things
No eye contact. No pointing No eye contact
Lack of pretend play (feeding doll)
Lack of social interest (no peekaboo)
Lack of social play (plays alone)
Lack of communication (verbal, non-verbal) communication is preserved
Lack of peer-rship
Lack of spontaneous seeking
Stereotype repetitive behav.
Don’t like change in routine Rigid to routine
Assoc. with: tuberous sclerosis, epilepsy,
rubella, tourette syndr.
No Rx. Need regular check-ups (don’t complain Rx: behav. therapy, individual assessment,
even when sick or in pain) speech therapists
used to be called childhood schizophrenia
25% develop epilepsy during adolescence
515
o Sx
recent onsef of irritability, angry outbursts, anxiety symptoms or depression
then memory problems and confusional episodes.
memory disturbance
short term memory only is affected
long term/ autobiographic memory is preserved
episodic confusion
hallucinations
paranoid ideation
insomnia
psychomotor seizures
history: recent onset of irritability, anger outbursts, anxiety or depression ->
then memory and confusional problems (MCQ).
o Rx
C/S
plasma exchange
immunomodulation
cyclophosphamide
- hypnagogic hallucinations – vivid dreamlike hallucinations occuring at the onset of sleep
- REM sleep disorder – acting out (yelling, punching, etc.) of dreams that are vivid and intense
Ekbom syndrome
o types
1 - they believe they have an insect/ worm on their body
2 - restless legs syndrome
middle-aged, elderly
up to 10% of population
familial Hx – AD with variable penetrance
precip. factors
- anemia
- hypothyroidism
- renal failure
- DM
Sx
- irresistible urge to move legs, “tingling, burning and crawling” of
the skin, from thighs to feet
- occurs when sitting down or lying in bed
- worse during the evening and at night before sleep
- relieved by walking
- typically pt complaints of limb discomfort at rest and then urge to
move the affected part, relieved by walking.
Rx
- mild
lifestyle changes – good sleep hygiene (bed just for
sleeping: no reading, TV, etc.)
Levodopa
Benserazide
Dopamine agonists – amantadine, selegilin
518
- Illusion - there is something there, but incorrectly interpreted (interpreting string as a snake)
o diff. from hallucination (there’s nothing there)
- types of thoughts
o Overvalued idea – quantitatively different from reality
in anorexia nervosa, morbid jealousy, hypochondriasis, querulous paranoia,
body image disturbance
o Delusion – qualitatively different from reality (fixed false belief)
o Phobia – with excessive arousal or anxiety in presence of the trigger, with minimal
resistance to it
o obsession – recognized by the patient as senseless and irrational and is resisted by him
rumination – more complex obsessional thoughts, which are repetitive,
intrusive, unwanted and upsetting
- reassurance should only be offerred when the pt’s concerns have been fully understood and
investigated
- Vaginismus
o Spasm of perineal musculature of the lower 1/3 of vagina
o Young women of high socioeconomic standard
o can be caused by:
a sexual trauma (rape, childhood sexual abuse) or very strict upbringing (sex =
sin)
scarring following episiotomy
o can be assoc. with a phobic anxiety of anticipating vaginal intercourse, e.g. in the
presence of an inexperienced partner
- Diogenes – people who like to collect garbage or have a dirty life style.
- Charles Bonnet - Visual hallucinations due to organic reasons in blind or partilly sighted elders
o if organic reason (occipital or ocular disease) is resolved, the hallucinations will go away
- Cotard syndrome – they believe they have lost body parts, blood, their soul, they are dead or
never born.
- Folie-a-deux
o rare
o one psychotic sympt. is transm. from one person to another (sympt. manifest only when
they are together)
- amygdala – in the temporal lobe, regulates affects
o regulates limbic system
- corpus calossum – responsible for sexual dimorphysm
- cingulate gyrus – part of limbic system, involved in emotion formation, processing, learning and
memory
- Transient global amnesia < 8 hrs
o loss of both recent and biographical memory
o in vertebro-basilar insufficiency
- which psychiatric dis. is increasing in incidence = Dementia (incr. ageing population)
- Paraphilias
o unusual sexual preferences, “perverts”
o types:
1. Exhibitionism – Recurrent urge to expose oneself to strangers
2. Fetishism – use/ collection of non-living objects (e.g. bras, etc.) usually assoc.
with the human body
3. Pedophilia – Recurrent urge or arousal towards pre-pubescents (children)
519
Legal age for sex, including abortion and OCP – 16 yrs (South Aus. and
Tasmania – 17)
> 16 yrs – OK to prescribe OCPs or perform abortion at her request/ with
only her consent.
14-16 Gillick test (or the stem will tell me that she lives alone, she is
mature, etc.) – asses whether:
- Mature minor – treat as a 16 yrs old
lives independently of her parents + is mature and
understands the potential risks and complications of
the required medical procedure.
e.g. pregnant girl, 14 yrs, asking for abortion – blue
book 573
if she is mature (Gillick test)
and if it was by consent
o OK
even if > 2 yrs between her and
her boyfriend
even though it’s illegal, she is
under 16 yrs
- Immature minor – treat as a kid and request her parents’
consent.
< 14 yrs - request her parent’s consent.
- mom wants her mentally retarded girl to have an hysterectomy
o we can’t do that (we refuse) – the girl is entitled to have her uterus (human rights)
o mom can make a request to the child health court (?)
she will probably be refused
- mentally retarded girl - contraception
o under institutional care – OCP
o alone – contact guardianship court
- consent form checked by
o HMO
o nurse
o anesthetist
o surgeon – he is the only one legally responsible
- adopted children have the right to be informed they were adopted
o but this remains the decision of their parents at least until the child is 18 yrs old
- consent in incompetent patients (e.g. elderly demented people)
o 1. advance directive from the patient
The first source of guidance for doctors on the treatment to be offered to an
incompetent patient is the patient’s own advance directive given BEFORE he or
she became incompetent.
This may state whether pt wishes to have particular treatment or to refuse it.
o 2. Surrogate decision maker appointed by the patient (Health attorney, medical agent
or enduring guardian).
If a patient is incompetent and has not previously consented to treatment or
refuse it, a person appointed in advance by the patient may have authority to
decide on the patient’s behalf.
521
Most Australian jurisdictions now have legislation enabling patients who are
over the age of 18, while competent, to appoint someone else to make
medical decisions for them if they later become incompetent.
o 3. Guardian appointed by a board, tribunal or court.
If a patient is not competent (and, in jurisdictions that have legislation allowing
people to make advance directive or to appoint their own substitute decision
maker, has not done so), it may be necessary for a substitute decision maker to
be appointed by a guardianship body.
A guardianship body will not intervene by appointing a guardian unless that is
NECESSARY.
IF THE PERSON’S RELATIVES ARE CARING FOR THE PERSON
SATISFACTORILY, IT IS GENERALLY CONSIDERED THAT THERE IS NO
NEED FOR A GUARDIAN.
If, however, there is a dispute between family members about the
person’s care, a formally appointed guardian may be needed to make or
review decision about the person.
o 4. The bottom line: Relatives and carers.
If there is no person who has been formally appointed as a surrogate decision
maker, either by the patient or by a guardianship body, a relative or carer may
be able to consent.
This Acts set out a hierarchy of people to decide the ‘person responsible’
including relatives and carers, for consenting to treatment (different
depending on state).
e.g. Victoria:
1. A person appointed by the patient under the Medical
Treatment Act.
2. A person appointed by the Victorian Civil and Administrative
Tribunal to male decisions in relation to the proposed
treatment.
3. A person appointed under a guardianship order with power to
make such decisions.
4. An enduring guardian appointed by the patient while
competent.
5. A person appointed by the patient with power to make such
decisions.
6. The patient’s spouse of domestic partner.
7. The patient’s primary carer.
8. The patient’s nearest relative.
Prevalence Incidence
New vaccine introduced Decr. Decr.
Disease that kills patients Decr. Constant
Drug that cures a disease Decr. Constant
Drug that doesn’t cure the dis. but extends life Incr. Constant
- Sensitivity & Specificity
Disease present Disease absent
Test pos. A = true positive B = false positive
Test neg. C = false negative D = true negative
o Prevalence: A+C/ (A+B+C+D) = Incidence x Duration
o Accuracy: A+D/A+B+C+D
o Sensitivity – Ability to detect true positives
Sensitivity = A/(A + C) = (true pos./total pos.) = TP/ TP + FN
not related to prevalence
o Specificity – Ability to detect true negatives
Specificity = D/(B + D)= (true neg./ total neg.) = TN/ TN + FP
not related to prevalence
o Positive predictive value – Proportion of true +ves identified in a defined population.
PPV = A/(A + B) = (true pos./ total population)
PPV = TP/TP+FP or (sensitivity x prevalence)/(sensitivity x prevalence) + (1 –
specificity) x (1 – prevalence)
computation of sensitivity, specificity and prevalence
When prevalence is low = PPV ↓ and NPV increases. (MCQ 3339 P 352) test
loses PPV when prevalence is low.
Sensitivity and specificity are inversely related.
o An ideal test would be 100% sensitive and 100% specific. No test can attain this ideal. In
screening population one needs a highly sensitive test for screening.
o Negative predictive value – Proportion of true -ves identified in a defined population =
TN/TN+FN
NPV = D/(C + D) = (true neg./ total p opulation)
Computation of sensitivity, specificity and prevalence.
- All these above 4 formulas have A& D always up
- Odd Ratio: AD/ BC
- Number need to teat: is the no of pts required to be treated to prevent bad oucome. NNT =
1/incidence = 1/Absolute risk reduction.
- Absolute risk reduction: Incidene in unexposed – Incidence in exposed.
- Reliability how well a test performs when repeated 2nd time and or by 2nd tester (test-retest
reliability) and how well test items correlate with each other. It is not affected by prevalence
- Likelihood ratio: an explnation for Likelihd ratio what it means. e.g If LR + = 9 for a test say ELISA,
then it means that likelihood of ELISA test to be positive in HIV pts is 9 times more than not
having HIV.
- LR + = Sensitivity/ 1-Specificity
- LR - = 1- Sensitivity/ Specificity
- Case fatality rate: total no of deaths/ total no of diseased.
- Standard Deviation.
o Mean BP + 2 std. deviation = Systolic (CI)
o Mean BP – 2 std. deviation = Diastolic
523
Normal values
Australia: (Murtagh – p. 148)
Adult Male:
17-50 years 1-10 mm/h
> 50 years 2-15 mm/h
Adult Woman:
17-50 years 3-12 mm/h
> 50 years 5-20 mm/h
> 100 mg/L 80% sensitivity and 88% specificity for bacterial infection
10-40 mg/L 69% & sensitivity and 54% specificity for viral infection
Renal fuction
Creatinine: 0.04 – 0.1 mmol/L
Urea: 3-8 mmol/L
eGFR > 60 ml/min/1.72 m2
Normal urinary output = Normal 1 ml/ kg/ hr.
Hematology
Red cells 4.5-6 x 1012/ L male, 4-5.5 female
Reticulocytes 0.5 – 2 % (1%) (immature cells in circulation)
Leucocytes 4.5-11 x 109/ L
Platelets 150-400 x 109/ L
Neutrophils 2-7.5 x 109 / L
Eosinophils 0.2-0.4 x 109 / L (<0.44)
Lymphocytes 1-4 x 109 / L (<4.5)
Monocytes 0.2-0.8 x 109 / L (<0.8)
Basophils ?
Coagulation Profile:
Bleeding time 2-8 min
Fibriongen
Prothrombin time – (12-15) seconds
Prothorombin international normalized ratio (INR) 1-1.2
526
- The prothrombin time is the time it takes plasma to clot after addition of tissue factor
(obtained from animals). It measures quality of extrinsic pathway (as well as the common
pathway) of coagulation.
- The speed of extrinsic pathway is greatly affected by levels of factor VII in body. Factor VII
has a short half-life & its synthesis requires Vit. K.
- The prothrombin time can be prolonged as a result of deficiencies in vit. K, which can be
caused by warfarin, malabsorption, or lack of intestinal colonization by bacteria (such as in
newborns). In addition, poor factor VII synthesis (due to liver disease) or increased
consumption (in disseminated intravascular coagulation) may prolong the PT.
- A high INR such as INR = 5 there is a high chance of bleeding, if INR = 0.5 there is a high
chance of having a clot. Normal range for a healthy person is 0.9–1.3 and for people on
warfarin therapy, 2.0–3.0, although target INR may be higher in particular situations, such
as for those with a mechanical heart valve, or bridging warfarin with a LMW heparin (such as
enoxaparin) perioperatively.
SaO2 98%
Lipids:
Total Plasma cholesterol: < 4 mmol/L
Triglycerides: < 1.5 mmol/L (Use mono or PUFA, marine Omega 3 (fish oil) and fibrates as Rx)
HDL cholesterol > 1mmol/L (Gemfibrozil and nicotinic acid increases HDL)
LDL cholesterol < 2.5 mmol/L (Simvastatin and Ezetimibe as Rx to lower). Ezetimbe decreases
cholesterol absorption.
Predictors of effects of obesity on health: Waist to Hip ratio (MCQ) and Waist circumference and these
are less accurate than BMI alone
528
Trachoma prophylaxis:
a. Contacts of cases identified through community screening:
Active trachoma community prevalence in 5-9 year old Aboriginal and Torres Strait Islander children:
i. ≥ 20%: Treat all people > 3kg living in households with children <15 years of age.
ii. ≥ 5 to < 20% and there is no obvious clustering of cases: Treat all people > 3kg living in households
with children <15 years of age.
iii. ≥ 5 to < 20% and cases are obviously clustered within several households and health staff can easily
identify all household contacts of cases: Single-dose azithromycin to all people > 3kg living in households
with an active trachoma case.
iv. < 5%: Treat all people > 3kg living in households with an active trachoma case.
regardless of any of these measures. The somatostatin analogue octreotide, given before meals, has
been shown to be useful in some individuals and the long-acting preparation may also be
useful. However, this treatment can lead to the development of gallstones and it does not help the
diarrhoea from which many patients with dumping also suffer. Revisional surgery may be occasionally
required. In patients with a gastroenterostomy, the drainage may be taken down or, in
the case of a pyloroplasty, repaired. Alternatively, antrectomy with Roux-en-Y reconstruction is often
effective, although the procedure is of greater magnitude; following gastrectomy, it is the
revisional procedure of choice.
#Late dumping syndrome :
This is reactive hypoglycaemia. The carbohydrate load in the
small bowel causes a rise in the plasma glucose level, which, in
turn, causes insulin levels to rise, causing a secondary hypoglycaemia.
This can be easily demonstrated by serial measurements
of blood glucose in a patient following a test meal. The treatment
is essentially the same as for early dumping. Octreotide is very
effective in dealing with this problem.