Plabverse All

Anatomy
Vertebral levels
C3 • Hyoid bone
• Bifurcation of the common carotid artery
C4
• Thyroid cartilage
• Cricoid cartilage
C6 • Trachea begins (end of larynx)
• Esophagus begins (end of pharynx)
T1 • Sternoclavicular joint
• Superior angle of scapula
T2
• Suprasternal notch
• Thoracic plane or plane of Ludwig
• Sternal angle of louis
T4 • Arch of aorta
• Bifurcation of trachea (carina)
• Division between superior and inferior mediastinum
• Azygos vein drains into SVC
T8 • Inferior vena cava hiatus [I ate (8) 10 Eggs At 12]
T9 • Xiphisterna joint
T10 • Esophageal hiatus
T12 • Aorta hiatus
• Transpyloric plane = Addison’s plane (halfway between suprasternal (jugular) notch and SP)
• 9th costal cartilage
• Pylorus of stomach
• Fundus gallbladder (near the midclavicular line)
L1 • Neck of pancreas • Tip the 9th costal cartilage ⇋ GB fundus
• Conus medullaris (end of spinal cord)
• Superior mesenteric artery origin
• Hilum of kidneys (Lt → L1, Rt → L2)
• Duodenal jejunal flexure
• Renal veins
L2 • Thoracic duct begins
• Azygos and hemiazygos begin
L3 • Umbilicus, umbilical dermatome → T10
• Iliac crest (supracristal plane)
L4
• Bifurcation of abdominal aorta into left and right common iliac arteries
L5 • IVC formed (convergence of right and left common iliac veins)
S1 • Sacral promontory
• Posterior superior iliac spine

S2
• Dural sac ends
PLABverse - plabverse@yahoo.com 1
Anatomy
Clinchers for nerve supply
Anatomy
Anatomy
Anatomy
Anatomy
Muscles and n. supply of hand
Anatomy
Anatomy
Biliary tree
Ampulla of Vater = Hepatopancreatic ampulla at the 2nd part of the duodenum

- This
is where
celiac
trunk
stops
supplying the gut and the superior mesenteric artery takes over
Anatomy
Notes
• Flexor digitorum superficialis → Primary flexes MCP and proximal IP joints as well as thumb and wrist
• Organs in the retroperitoneal space → Pancreas, Duodenum, Aorta
• Posterior perforation of gastric ulcer will lead to accumulation of fluid in → Lesser sac, gastric contents and
pus will result in the formation of an abscess which will then pass into the peritoneal cavity through the
foramen of Winslow leading to generalized peritonitis
• Posterior perforation of pyloric and duodenal ulcer will result in accumulation in → Retroperitoneal space
• Deep tendon reflexes
- S1,2 – “buckle my shoe” → Achilles reflex
- L3,4 – “kick the door” → Knee reflex
- C5,6 – “pick up sticks” → Biceps reflex
- C6,7 – “straight up to heaven” → Triceps reflex
- L1,2 – “testicles move” → Cremasteric reflex
- S3,4 – “winks galore” → Anal reflex
• Remember, Superior oblique is the muscle used when reading
• 5th injury → Jaw deviation (at the same side)
• 12th injury → Tongue deviation (at the same side)
• 7th injury → Facial deviation (towards the opposite side)
• 10th injury → Uvular deviation (towards the opposite side)
• Lymph nodes drainage
- Skin (scrotum, valva, perineum) → Superficial inguinal LNs
- Drain all below umbilicus → Superficial inguinal LNs,
except Gonads and Lateral foot
- Gonads (testis, ovaries) → Para-aortic LNs
- Lateral foot → Popliteal LNs
- Deep lymphatics of lower leg, glans, clitoris → External
iliac LNs
- Tip of the tongue → Submental LNs
- Anterior 2/3 of the tongue → Submandibular LNs
- Posterior 1/3 of the tongue → Jugulo-omohyoid LNs
(deep cervical LNs)
- Posterior oropharynx → Jugular LNs (Deep cervical LNs)
Anatomy
• Ptosis + mydriasis + exophthalmos → Oculomotor
• Ptosis + miosis + enophthalmos → Horner $
• Chest drain:
- Should be inserted in the 5th intercostal space at the superior border of the lower rib and anterior to the
mid-axillary line
- Safe triangle: pectoralis major anteriorly, latissimus dorsi posteriorly, 5 th ICS inferiorly, base of axilla
superiorly
- Order of intercostal vessels going down (VAN): vein, artery, then nerve
• Inability to move the shoulder → Spinal accessory (CN11) injury → Test it by shrugging the shoulders
• Trigeminal → Mandibular branch → Inferior alveolar nerve → lower teeth + Chin & lower lib (via Mental N)
• Biceps tendon rupture:
- Proximal → Popeye muscle appearance + minimal loss function [Popeye still strong]
- Distal → Caused by flexion against resistance with elbow at a right angle + sudden sharp tearing
sensation + swollen elbow + weakness of flexion and supination
• Golfer’s elbow → Medial epicondylitis + all flexors to fingers and pronator injured (same as baseball players,
construction and plumber’s injury)
• Tennis elbow → Lateral epicondylitis + wrist extensors affected
• De Quervain’s disease → Pain under the foot of the thumb (same as Washer woman and Mummy thumb)
• Contralateral sensory loss/hemiplegia, dysphasia, homonymous hemianopia → Cerebral infarct
• Quadriplegia, locked-in $, vertigo, diplopia or other cranial nerve palsies → Brainstem infarct
• Only pontine hemorrhage has quadriplegia = locked in $
• Ataxic hemiparesis, pure motor loss, pure sensory loss, sensorimotor loss, dysarthria → Lacunar infarcts
• Pure motor loss + dysarthria → Lacunar infarct (posterior limb of internal capsule)
• Pure sensory loss → Lacunar infarct (thalamus)
• Sensor + motor involvement + loss of cortical function (aphasia, agnosia, neglect and visual field defects →
Cerebral infarcts
• Locked-in $ “pseudo coma” → patient is aware but cannot move or communicate verbally due to complete
paralysis of nearly all voluntary muscles in the body except for vertical eye movements and blinking
• Dysarthria → disorder of articulation and pronunciation
• Dysphasia → disorder of language (affects formulation of sentences and thoughts)
• Maxillary nerve carries sensory information from the following
- Lower eyelid
- Cheek
- Nares and upper lip
- Upper teeth and gums
- Nasal mucosa
- Palate
- Roof of the pharynx
- Maxillary, ethmoid and sphenoid sinuses and part of meninges
• Nerve roots and dermatomes
- C1, C2 → Neck flexion and neck extension
- C3 → Lateral neck flexion and diaphragm (C3,4,5). Dermatome → Clavicles
- C4 → Shrugging shoulders (via spinal accessory). Dermatome → Clavicles
- C5 → Movement of shoulders, raising of the arm and flexion of the elbow. Dermatome → Deltoid region
- C6 → External rotation (supination) of the arm, extension of the elbow and wrist and pronation of the
wrist. Dermatome → Lateral arm/forearm
- C7 → Wrist flexion and small muscles of the hand. Dermatome → Middle finger
Anatomy
- C8 → Finger extension, thumb abduction and thumb extension. Dermatome → Little finger
- T1 → Finger abduction and adduction
• Prepatellar bursa
- Frontal bursa of the knee joint. A superficial bursa with a thin synovial lining between skin and patella
- Occurs in housemaids “housemaid’s knee”. Commonly seen in people who kneel such as plumbers
- Common cause of swelling over the anterior inferior patella
- Symptoms: Redness, inability to flex the knee, pain and swelling is localized over site of bursa
- Relieved by rest
• Infrapatellar → inferior “clergyman/jumper’s knee”
• Suprapatellar → Superior to the knee cap
• Para → anterior
• Pes anserine → Infero-medial
• Cancer head of the pancreas = 2nd part of duodenum = CBD → jaundice due to obstruction
• Above the midpoint of inguinal ligament (ASIS-Pubic tubercle) by 2.5cm → Deep inguinal ring
• Mid inguinal point (ASIS-Pubic symphysis) = Femoral artery pulsation
• TIP → Tibial nerve, Inversion and Plantar flexion
• PED → Peroneal nerve, Eversion and Dorsiflexion
• Superior Quadrantanopia → Temporal lobe
• Inferior Quadrantanopia → Parietal lobe
• PITS – Parietal inferior, Temporal superior
• Long-term memory problems, language impairment and a change in sexual behavior → Temporal lobe
• Changes in personality and social behavior → Frontal lobe
• Visual field defects can be cause by lesion in Temporal, Parietal or Occipital lobes
• Glioma = brain or spinal cord tumor
• Venous drainage of medial ankle → Long/great saphenous vein
• Venous drainage of lateral ankle → Short saphenous vein
• Sensory supply of medial foot → Saphenous nerve
• Sensory supply of lateral foot → Sural nerve
• Foot drop → Common peroneal, Sciatic or Superficial peroneal n.
• Foot drop or loss of sensation between 1st and 2nd toes and pain on the dorsum of foot → Deep peroneal n.
• Deep peroneal n. (deep fibular n.) can be caused by overusing the anterior leg muscles, tight-fitting shoes
(ski boot $) or crossing legs for a long time
• Crutch palsy → Radial nerve compression against crutches
• Saturday night palsy → Radial nerve compression against a chair/operating table for a long time
• 5th ICS and anterior to the mid-axillary line → Chest drain insertion
• 5th ICS and medial to mid-clavicular line → Apex beat
• Dupuytren’s contracture
- Formation of thickened fibrous tissue within the palmar fascia
- The ring or 5th finger is permanently in a flexed position
- RF: family history, smoking, alcohol excess, DM and heavy manual work
- Managed by Fasciectomy
• Phrenic nerve (C3,4,5) → Diaphragm
• Hoarseness in lung cancer patients is due to RLN injury (branch of 10th)
• Injury to RLN: unilateral → HOV, bilateral → Aphonia
• Injury to the external (superior) laryngeal nerve → Changes to the voice pitch (Dysphonia)
• Indices = index finger
Anatomy
• Policies = thumb
• Digitiminimi = little finger
• All intrinsic muscles of the hand are innervated by the ulnar nerve except the thenar muscles (AFO) and
lateral two lumbricals → supplied by C8 and T1 via the median nerve
• If ulnar nerve injury occurs after a high lesion → Ulnar paradox → 4th and 5th fingers are in a fully extended
state
• Ulnar n. roots → C8, T1
• Median n. roots → C5, T1
• All cervical nerves emerge above their corresponding vertebrae except C8 emerge below the C7 vertebrae
(between C7 and T1)
• When requesting a cervical X-ray, lowest vertebrae that’s needed to be seen in a lateral film is C7/T1
Cardiology
Acute Myocardial Infarction
➢ Irreversible death of heart tissue, while Angina is chest pain due to ischemia but still heart tissue is alive
• Subendocardial (partial) infarct, 20-40m → Non-STEMI
• Transmural (whole wall thickness) infarct, 3-6h → STEMI
• Stable angina → relieved by rest/medications
• Unstable angina → doesn’t respond to rest/medications
Presentation
• Chest pain (central chest pain may not be the main symptom):
- Three quarters of patients present with characteristic central or epigastric chest pain radiating to the
arms, shoulders, neck, or jaw
- The pain is described as substernal pressure, squeezing, aching, burning, or even sharp pain
- Radiation to the left arm or neck is common
- Chest pain may be associated with diaphoresis (caused by increased sympathetic activity), nausea,
vomiting, dyspnea, fatigue and/or palpitations
- SOB: may be the patient's anginal equivalent or a symptom of heart failure
- Could be painless in DM (autonomic neuropathy) → Silent MI
Atypical presentations are common and tend to be seen in women, older men, people with diabetes and people from
ethnic minorities. Atypical symptoms include abdominal discomfort or jaw pain; elderly patients may present with
altered mental state
Investigation
• Troponin (increase within 3-12h, peaks at 24-48h and return to baseline over 5-14 days)
• CK-MB → return to baseline after 48-72h, specificity and sensitivity are not as high → useful to detect
reinfarction (10%)
Cardiac enzymes aren’t raised in unstable angina
Management of acute attack [MONA]

• Morphine IV
- To relieve pain
- Avoid intramuscular (IM) → absorption is unreliable and the injection site may bleed if the patient later
receives thrombolytic therapy
• Oxygen
- In signs of hypoxia, pulmonary edema or continuing myocardial ischemia
- If O2 saturation <94%
• Nitrates Management of Pulmonary edema
- Such as: GTN (sublingual/IV) to treat angina • MONA but replace the A with F (frusemide) → MONF
• Aspirin 300mg
- Should be given before arrival to the hospital
- Clopidogrel should also be given
Heparin or LMWH (enoxaparin sodium) should also be considered
Cardiology
Complications of MI
• Ventricular aneurysm
- When the cardiac muscle partially dies during a myocardial infarction, a layer of muscle may survive, and
being severely weakened, start to become an aneurysm (a balloon)
- 4-6 weeks post MI
- ECG → Persistent ST elevation and left ventricular failure
- CXR → Cardiomegaly with an abnormal bulge at the left heart border
- ECHO → Paradoxical movement of ventricular wall
- Thrombus may form within the aneurysm increasing the risk of a stroke
• Dressler’s syndrome
- 2ry autoimmune form of pericarditis that occur post MI
- 1 week-several months post MI
- Features: Fever, pleuritic pain, pericardial and pleural effusion
• Left bundle branch block (LBBB)

- Activation of the left ventricle of the heart is delayed, which causes the left ventricle to contract later than
the right ventricle
[WiLLiaM]
RBBB, QRS complex: [MaRRoW]
- ORS in V1 → looks like W Wide QRS + positive V1 → RBBB
• V1 → looks like M Wide QRS + negative V1 → LBBB
- QRS in V6 → looks like M • V6 → looks like W
Cardiology
Management of CHF [ABSD]
• 1st line → ACE-inhibitor and beta-blocker (e.g. Carvedilol)
- It’s better to start one drug at a time
- DM or signs of fluid overload → start with ACE-inhibitor
- Ejection fraction ≤40% → start with ACE-inhibitor
- Angina → start with beta-blocker
- When starting a beta-blocker, start low and go slow
• 2nd line → Spironolactone (especially when K+ <3.2 as it’s a K-sparing diuretic)
• Digoxin → Heart failure + Atrial Fibrillation
Management of STEMI
• If patient presents with symptom onset within 12 hours and PCI can be done within 120mins then withhold
fibrinolysis → perform PCI (percutaneous coronary intervention)
• If PCI is not available and cannot be delivered within 120mins → thrombolysis (Alteplase or streptokinase)
• Thrombolysis can only be done within 12 hours of symptom onset
Post myocardial infarction management / management of NSTEMI or unstable angina

1. Dual antiplatelet therapy: Aspirin + Clopidogrel (Plavix)
- Aspirin is continued life-long. Clopidogrel can be given for 1 year
2. Beta blockers
- As soon as they’re hemodynamically stable
- In people without heart failure → For 1 year after an MI
- In people with heart failure → Indefinitely
Once the patient is discharged, he can take a CAB or BAS
3. ACE inhibitor C – Clopidogrel
- As soon as they’re hemodynamically stable A – Aspirin
B – Beta-blocker
- If intolerant → ARB
A – ACE inhibitor
4. Statins S – Statin
- Atorvastatin 80 mg, used indefinitely
Angina
Vasospastic (Prinzmetal/variant) angina

- May or may not have atherosclerosis
- Ischemia is due to coronary artery vasospasm
Cardiology
DD of acute chest pain
• Widened mediastinum on CXR
Cardiology
Acute pericarditis
Features
• Chest pain is described as sharp, stabbing, central chest pain
• Radiates to the shoulders and upper arm
• Chest pain may be pleuritic and is often relieved by sitting forwards
• Worsened by inspiration, lying flat, cough, swallowing, or movement of the trunk
• Pericardial friction rub is pathognomonic - often a rub can be heard even when a pericardial effusion is
present)
• Other symptoms include non-productive cough and dyspnea
Causes
• Viral infections → Coxsackie
• Bacterial → Tuberculosis
• Uremia (causes 'fibrinous' pericarditis)
• Trauma
• Post-myocardial infarction, Dressler's syndrome → 2ry form of
pericarditis on top of cardiac injury
• Connective tissue disease
ECG changes
• Widespread 'saddle-shaped' ST elevation (Saddle-shaped meaning concavity directed upwards)
• PR segment depression
Acute Pericarditis Pericardial Effusion Cardiac Tamponade
Any cause of pericarditis but

Cause See above Any cause of pericarditis
especially trauma
• Central chest pain worse • Beck’s triad:

Clinical on inspiration or lying flat 1. Muffled heart sounds
• Dyspnea, raised JVP
Features ± relief by sitting forward. 2. Distended neck veins
• Pericardial friction rub 3. Hypotension
• CXR shows enlarged,

globular heart
• ECG → see above
Test • ECG shows low- voltage • Echo is diagnostic
• Troponin may be raised
QRS complexes and
alternating
Treatment NSAIDS Pericardiocentesis Urgent Pericardiocentesis
Cardiac tamponade → a life-threatening condition in which a pericardial effusion has developed so rapidly or has
become so large that it compresses the heart
Cardiology
Infective endocarditis
➢ Fever + new murmur = Endocarditis until proven otherwise
➢ Causative organisms: Staph aureus, in subacute IE → Strept viridians
Risk factors
• Valve replacement
• Recreational drug abuse and invasive vascular procedures
• Dentistry interventions
Presentation
• Along with fever, rigors, malaise and the new murmur (commonly MR), some patients may present with
congestive heart failure
Diagnosis [BE FIVE PM]
• 2 major criteria present
• 1 major + 2 minor
• 5 minor criteria
Management
• Antibiotics → Flucloxacillin + Benzylpenicillin + Gentamicin (Vancomycin with prosthetic valve)
• Surgery → Valve replacement
Major criteria [BE] Minor criteria [FIVE PM]
• Fever >38℃
• Immunological phenomena: AGN, Osler’s nodes,
Roth spots
• Vascular phenomena: major emboli, splinter hge,
• +ve blood culture
Janeway lesions
• +ve Echo → abscess formation, new valvular
• Echocardiographic evidence doesn’t meet major
regurgitation
criteria
• Predisposition: IV drug user or heart condition
• Microbiological evidence does not meet major
criteria
Splinter hemorrhage → hemorrhage under the nails

Janeway's lesion → painless macules
Osler's nodes → small painful tender
Roth’s spots → red retinal spots with pale white center
Cardiology
Differentiating murmurs
• Systolic
- Lesions above the level of the nipple → Ejection systolic
- Lesions below the level of the nipple → Pansystolic
• LEft sided murmurs louder with → Expiration

• RIght sided murmurs louder with → Inspiration
Cardiology
ECG arrythmias
Cardiology
Ventricular tachycardia
➢ More than 3 consecutive PVCs, HR 100-250 bpm → less filling → low cardiac output → hypotension and HF
➢ There’s lack of coordinated atrial contractions (loss of atrial click) → P wave may be present or absent. If
present, it has no relation to the QRS complex
• Sinus tachycardia: HR >100 bpm in a healthy individual

due to exercise/stress
• Premature ventricular contraction (PVC): a single beat
starts from the ventricles
• It’s impossible to see ventricular fibrillation in an awake

person
• Wide QRS + regular → VT

• Wide QRS + irregular → V-fib
• Narrow QRS + regular → SVT
• Narrow QRS + irregular → A-Fib
With pulse Without pulse
1. Hemodynamically stable
➢ Anti-arrhythmics [ALP]
o Amiodarone, lidocaine, procainamide
➢ Immediate electrical cardioversion
2. Hemodynamically unstable (defibrillation) is indicated
• Hypotension, chest pain, cardiac failure and
decreased conscious level
➢ Immediate electrical cardioversion
P and QRS dissociation + tachycardia → VT

P and QRS dissociation + bradycardia → 3rd degree heart block
A patient with VT → Ask yourself, does he have a pulse or not?

- No pulse → immediate electrical cardioversion
- If he has pulse → Is he stable or not? Stable? → ALP Not stable? → immediate electrical cardioversion
A patient with SVT → Ask yourself, Is he stable or not?
Cardiology
Supraventricular tachycardia
➢ Paroxysmal supraventricular tachycardia is manifested as an absolutely regular rhythm at a rate between 130
-220 beats/min
➢ In a YOUNG patient with recurrent palpitations, normal/slightly low BP, regular heart rate and NO
PREDISPOSITION TO HEART DISEASE → consider SVT
Acute management
If dynamically stable If unstable
1. Valsalva maneuver, carotid massage

2. Adenosine 6mg IV (if the patient is asthmatic →
• Chest pain, SOB, hypotension, fatigue, cold
verapamil instead)
extremities, decreased urine output, confusion or
- If unsuccessful → add another 12 mg IV
lost consciousness
- If still unsuccessful → give another 12
3. Electrical Cardioversion
➢ DC cardioversion
- If you’ve given 3 doses (30mg) of adenosine
with no improvement
Prevention
• Beta-blockers
• Radio-frequency ablation
Ventricular ectopic
➢ Caused by the premature discharge of a ventricular ectopic focus which produces an early and broad QRS
complex
➢ Maybe asymptomatic with palpitations, often described as skipped or missed beats
➢ Benign unless there’s an underlying heart disease → could lead to life-threating arrythmias
Causes
• IHD
• Cardiomyopathy
• Stress, alcohol, caffeine, medication, cocaine or amphetamines
• Occurs naturally
• Young patient with recurrent palpitations in the absence of heart disease → SVT
• Loss of consciousness → VF
• Middle-aged person with history of CHD → VT
• Missed beats, dyspnea, dizziness and never sustained in 2H → ectopic beats
Cardiology
Atrial fibrillation
➢ Atrial fibrillation is the most common arrythmia that develops in patients with dilated cardiomyopathy
➢ Dilated cardiomyopathy → Decreased ejection fraction + damaged myocardium (e.g. thinning of septal wall)
➢ History of ALCOHOLISM followed by palpitations, dizziness and syncope → arrythmias (atrial
fibrillation/flutter). This is known as “holiday heart syndrome”
➢ Atrial fibrillation leads to pulmonary edema due to the loss of atrial contribution to cardiac output
Features
• Dyspnea
• Palpitations Atrial flutter
• Syncope or dizziness - Abnormal focus in the atrium
- Transient stage between normal rhythm and AF
• Chest discomfort or pain - Absent P wave
• Stroke or TIA
• An irregularly irregular pulse
• Absent P wave
Atrial flutter Vs Atrial fibrillation
Cardiology
Atrial fibrillation management
Rate control Rhythm control
• Patient is unstable
• Patient is hemodynamically stable A- Electrical cardioversion under sedation
• 1st choice → beta-blockers or CCB (diltiazem B- Chemical cardioversion with amiodarone or
or verapamil) flecainide can be used [AF]
• Digoxin is used if there’s CHF • If symptoms >48h → risk of cardiac
• Thromboprophylaxis is also used thromboembolism when cardioverted → rate
control meds + LMWH
Persistent AF, lasts >7 days

Rate control Rhythm control
• >65
• Who are symptomatic
• Patient is stable and AF started >48h ago
• Who are younger
• Unsuitable for cardioversion
• Presenting for the first time with lone AF
- Long duration of AF (usually >12 months)
- History of multiple failed cardioversion
A patient with AF, you ask yourself

- Is he stable or not?
- Is he old or young?
Ventricular fibrillation
➢ VF means sudden death; blood pressure drops immediately to zero and so does the cardiac output
➢ Rate is up to 500 bpm → ventricles are unable to contract in a synchronized manner → immediate loss of
cardiac output
ECG findings
• Chaotic irregular deflections of varying amplitude
• No identifiable P waves
• Rate: 150-500 per minute
• There’s no specific pattern to the discharge
Cardiology
CHA2DS2VS (Secondary prevention after a stroke)
• Used to determine the most appropriate anticoagulation strategy for atrial fibrillation
• A score of 2 or more / men with a score of 1 → offer anticoagulation therapy
• <65 years old and no comorbidities → NO warfarin

• ≥65 years old + at least one comorbidity → Warfarin or DOAC (direct oral anticoagulants) such as apixaban,
edoxaban and rivaroxaban
Benefits of DOAC over warfarin

- Reduction of the risk factors of intracranial hemorrhage
- No INR monitoring
- Faster onset anticoagulation (2-4h)
• Warfarin may lead to intracranial hemorrhage
Disadvantages of DOAC and SAH → look out for headache
- No specific antidote
- Essential to be compliant
Stroke → syndrome of sudden onset focal neurological loss of presumed vascular origin lasting >24h
TIA → syndrome of sudden onset of focal neurological loss of presumed vascular origin lasting <24h
2ry prevention of a stroke or TIA

- Patient presented with AF → Warfarin or DOAC (stroke prophylaxis)
- Patient presented with disabling stroke and NO AF → defer anticoagulation treatment for 14 days from the
onset and start Aspirin 300mg for 2 weeks + Clopidogrel 75mg lifelong
- Consider carotid endarterectomy if internal carotid artery is stenosed ≥ 50% in men, ≥ 70% in women
Cardiology
Heart block
1st degree heart block • Prolonged PR interval > 0.2 seconds
• Mobitz type I AV block (Wenckebach block/phenomenon)

➢ Progressive prolongation of the PR interval with intermittent dropped beat
2nd degree heart block • Mobitz type II AV block
➢ Sudden drop of QRS WITHOUT prior PR changes
3rd degree (complete)

• P waves and QRS complexes have NO RELATION to each other
heart block
Management
• 1st degree and Mobitz I → no treatment, atropine could be given (Mobitz I)
• Mobitz II and 3rd degree → permanent pacemakers, atropine is contraindicated
P-R interval
- Represents the time it takes the impulse to move between atria and ventricles
- Normally 3-4 boxes
Cardiology
ECG interpretation
1. Rate
2. Regularity
3. P wave
4. PR interval
5. QRS duration
6. Determine the axis
7. Look at morphology
Rules of thumb to determine Cardiac Axis deviation on ECG

• Lead I → Left thumb while lead II → Right thumb
• Look at lead I and lead II
• A positive defalcation means and a negative deflection means
• If lead I and II are both positive → → Normal
• If lead I is positive and lead II is negative → LAD
• If lead I is negative and lead II is positive → RAD
LAD RAD Extreme RAD

Common • Right ventricular hypertrophy • Congenital heart disease
• Left ventricular hypertrophy • Thin, tall • Left ventricular aneurysm
• Left anterior fascicular block • Chronic lung disease
(hemiblock) • Pulmonary embolism
• Inferior myocardial infarction • Left posterior hemiblock
Less common • Lateral MI
• Obesity - Lateral wall of the left
• Wolff Parkinson white $ ventricle is supplied by the
left anterior descending
- Infarction will cause
deviation away from site of
infarction
Cardiology
ECG changes in myocardial infarction and coronary territories
Cardiology
Valvular heart diseases
Aortic stenosis • Elderly patient with exercise intolerance
or maybe asymptomatic
➢ The most common valvular heart disease in the UK
•Murmur is accentuated when sits upright
Causes
1. Degenerative sclerocalcific changes to valves → Most common, usually an elderly patient
2. Congenital bicuspid aortic valve → younger patients
Signs
• Ejection systolic murmur best heard at the 2nd right intercostal space, at the right sternal border which
radiates to the carotid arteries, louder with expiration (left-sided murmur)
Mitral regurgitation
➢ The 2nd most common heart valve disorder
➢ Due to ischemic papillary muscle dysfunction or partial rupture after myocardial infarction (days)
➢ Could be 2ry to rheumatic fever
➢ Commonly associated with inferior MI than anterior, usually seen 2-10 days post MI and the patient is
presented with pulmonary edema
Signs
• Left ventricular failure: dyspnea, orthopnea and paroxysmal nocturnal dyspnea
• With severe MR → right sided heart failure → edema and ascites
• Soft S1 and S2 pansystolic murmur at the 5th intercostal space, left midclavicular line (Apex) which radiates to
the axilla
Investigations
• ECG → broad/bifid P wave (P mitrale) indicating enlarged left atrium
• Echo → diagnostic
Mitral valve prolapse [MVP]

➢ Inheritable connective tissue disorder, may be associated with Marfan’s $, Ehlers Danlos $ and osteogenesis
imperfecta
➢ Most patients are asymptomatic
➢ Classic case → Slim young female with low blood pressure
Signs
• Mid-systolic click, best heard at the 5th intercostal space, left midclavicular line, followed by a mid or late-
systolic murmur with finding accentuated in the standing position
[MVP] in a basketball team
- Tall, thin with long arms → Marfan’s
- Has loose joints → Ehlers Danlos
- Shoots from the Middle of the court with great syspense and finishes with the ball entering the net
with a click → mid-systolic click
Cardiology
Mitral Stenosis [MS]
➢ Most commonly caused by → Rheumatic fever
➢ Mitral valve stenosis impedes left ventricular filling → increased blood volume in the left atrium → increased
left atrial pressure → blood is back to the lungs causing pulmonary congestion → 2ry pulmonary
vasoconstriction → pulmonary hypertension → becomes harder for the right ventricle to pump → right
ventricular failure
Signs
• Pulmonary congestion and edema → Dyspnea, orthopnea, paroxysmal nocturnal dyspnea
• Hepatomegaly, ascites, peripheral edema
• There may be hemoptysis (due to rupture of pulmonary vessels due to raised atrial pressure)
• Could lead to systemic embolism (due to stagnation of blood in an enlarged left atrium as a result from AF)
• Physical signs: Atrial fibrillation, Malar flush, pulmonary rales
• Loud S1
• Mid-diastolic murmur with an opening click (or a diastolic rumble, click represents the mitral valve opening),
best heard at the apex
[Michael Schumacher] he had an accident in the middle of his ski trip which he almost diad → Mid-diastolic murmur
ECG
• May show signs of right ventricular failure
• Atrial fibrillation
• P mitrale → bifid P wave
Chest x-ray
• Large left atrium → straightening of the left heart border
• Pulmonary hypertension, including Kerley B lines and increased vascular markings
Echocardiography
• Thickening of mitral valve leaflets
Aortic regurgitation
➢ Causes: RF, infective endocarditis, Marfan’s syndrome
Signs
• Early diastolic murmur, best heard at the left sternal edge (Erb’s point)
Pulmonary stenosis
Signs
• Ejection systolic murmur, best heard over the pulmonary area, radiates to the left shoulder or
infraclavicular region
Cardiology
Ventricular septal defect (VSD)
➢ Acyanotic congenital heart disease
➢ Left to right shunt Tricuspid atresia
Causes • Pansystolic murmur
• Presents at early week of life with poor feeding
• Congenital
• Cyanotic
• Acquired (post-MI)
Symptoms
• May present with severe heart failure in infancy, poor weight gain and frequent URTIs
• Could remain asymptomatic and be detected incidentally in later life
Signs
These depend on size and site:
A. Small holes
• Asymptomatic with normal feeding and weight gain
• May be detected accidently on routine examination
• Give louder murmurs
• Classically, a harsh pan-systolic murmur heard at the left sternal edge, with a systolic thrill, and a left
parasternal heave
B. Large holes
• Associated with signs of pulmonary hypertension
• These babies may develop a right to left shunt → cyanosis or Eisenmenger's syndrome (cyanosis +
pulmonary HTN + erythrocytosis)
Patent ductus arteriosus (PDA)

• Persistence of a normal fetal connection between the aorta and the pulmonary artery
• Very common in preterm babies and it also may close spontaneously
• May be asymptomatic or may cause apnea, bradycardia and increased oxygen requirements
• The continuous machinery murmur (rarely heard) → heard over the left infraclavicular area
• There may be a rough systolic murmur along the left sternal border
• Bounding peripheral pulses
• The diagnosis is confirmed by ECHO which not only allows the PDA to be visualized but also assesses the
hemodynamic significance of the PDA
• Prostaglandins → prevent closure of PDA
• Drugs that close the duct → Indomethacin or Ibuprofen
Cardiology
Most common cyanotic heart conditions (5Ts)
1. Tetralogy of Fallot (TOF)
2. Transposition of the great arteries (TGA)
3. Tricuspid atresia → pansystolic murmur + cyanosis is usually presented immediately after birth
4. Truncus arteriosus
5. Total anomalous pulmonary venous connection (TAPVC)
Tetralogy of Fallot (TOF)

➢ The most common cause of cyanotic congenital heart disease
➢ Typically presents at around 1-2 months, although may not be picked up until the baby is 6 months old
Four characteristic features
• VSD
• Right ventricular hypertrophy
• Pulmonary stenosis → ejection systolic murmur
• Overriding aorta
Other features
• Cyanosis
• Causes a right-to-left shunt
• Ejection systolic murmur due to pulmonary stenosis (the VSD does not usually cause a murmur)
• A right-sided aortic arch is seen in 25% of patients
• Chest x-ray → 'boot-shaped' heart
• ECG → right ventricular hypertrophy
Complications
• Pulmonary regurgitation (common after repair of pulmonary stenosis) → signs of right HF → pulmonary
valve replacement
Atrial myxoma
• Benign tumors, mostly in the left atrium and tend to grow on the wall
(septum)
• Sometimes tumor break off and fall into the bloodstream → brain, could
cause a stroke, lungs causing a pulmonary embolus
• Around 10% → inherited (familial myxomas)
• The symptoms occur due to obstruction of the mitral valve which result in
syncope and heart failure
Features
• Acts as Aortic stenosis on auscultation + prominent A-waves
• Platypnea → Dyspnea that’s relieved when lying down and worsens when sitting or standing
• Symptoms of hemodynamic obstruction, embolization, or constitutional symptoms such as fever, malaise,
tachycardia and tachypnoea
• Symptoms and signs of ischemia or infarction in the peripheries, due to embolization of adherent thrombus
• Atrial fibrillation
• Large myxomas may impair intracardiac blood flow, causing dyspnea, syncope or symptoms and signs of
congestive cardiac failure
• Echo: pedunculated heterogenous mass typically attached to the fossa ovalis
Cardiology
Hypertension
Step 1
• Age <55 or DM → ACE inhibitor (…pril) or ARBs (…sartan)
• Age >55 or Afro-Caribbean → CCB (Amlodipine, Diltiazem)
- If CCB isn’t suitable (e.g. intolerance or edema) or if there’s evidence of HF or a high risk of HF →
thiazide-like diuretic
Step 2 • if a patient >55 y/o is currently on Thiazides (Indapamide) →
assume he is intolerant to CCB and give ACE-inhibitors
• ACE-inhibitor + CCB
Step 2
• ACE-inhibitor + CCB + thiazide-like diuretic
Postural hypotension
• A drop in BP of more than 20 mmHg within 3 minutes of standing
• Should always be considered in old patient especially if on multiple medications and presents with dizziness
• May present with dizziness or sudden loss of consciousness after getting up from a chair with recovery
within minutes
• One of the most common causes of postural hypotension is dehydration → U&E should be requested
Diagnosis
• Blood pressure taken when lying down and standing up
Ruptured abdominal aortic aneurysm

• Severe sudden lower abdominal and back pain
• Tender pulsatile abdominal mass (lateral and superior to the umbilicus)
• Low BP
Investigation
• Stable → CT
• Unstable → US
Management
• Immediate IV fluids and Laparotomy
Digoxin toxicity
➢ Yellow halos are a clincher for digoxin toxicity
➢ Hypokalemia can lead to toxicity as K+ and digoxin bind to the same receptors → more digoxin binding →
increased intracellular calcium → increased cardiac contractility
Features [DIG]
• GIT symptoms are the most important → nausea, vomiting, diarrhea and anorexia
• Neurological and Eye [I] symptoms → blurred vision, yellow green vision (xanthopsia), hallucinations and
confusion
• Dysrhythmias → bradycardia, premature contractions, ventricular tachycardia and any other type of
arrythmia
Management
• Digibind (digoxin specific antibody fragments) • A serum digoxin can be ordered in patient
suspected of being intoxicated (history, etc.)
• Correct arrythmias
• Monitor potassium
Cardiology
Notes
• Symptomatic bradycardia
1. Atropine 0.5mg IV
2. Dopamine
3. Epinephrine
➢ Initial → ABCD
• Resuscitation guide for cardiac arrest
a. Call for help
b. Check for ABCD (if there’s no signs of life → call resuscitation team)
c. CPR 30:2
d. Defibrillation once we get help
• Drugs to be avoided in CHF, IHD, CKD
- NSAIDs → inhibit prostaglandins → afferent arteriole constriction → less filtration → lower urine output
→ fluid accumulation → heart failure worsens
- COX-2 inhibitors
• Thiazide diuretics increase the risk of gout → due to reduced clearance if uric acid
• Treatment of beta blocker overdose → Glucagon
• Antidote for warfarin → Vitamin K
• U wave → Hypokalemia
• J wave → Hypothermia
• A-waves → Atrial myxoma
• Delta waves → Wolff Parkinson White Syndrome (WPW $)
• Bifid/wide P wave → Left atrial enlargement (MR, MS)
• P mitrale (BROADER than 2 and a half small boxes) → Left atrial enlargement
• P pulmonale (taller than 2 and a half small boxes) → Right atrial enlargement
• ECG showing irregular/equivocal (ambiguous) rhythm, next investigation → ECHO
• ECG showing regular rhythm, next investigation → Holter ECG (24h ECG)
• Patients who have experienced episodes of syncope during or shortly after exertion → Exercise testing
• Investigations for Aortic dissection → Transesophageal Echo, CT, MRI
• Sinus sick syndrome → Alternating episodes of tachycardia, bradycardia, AF or flutter
• Polymorphic ventricular tachycardia = Torsades de pointes = Long Q-T syndrome = Spindle shaped ECG
- Prolonged Q-T interval
- Syncope and sudden death
- Exacerbated by exercise, stress, medications and electrolyte imbalance
- Treated with MgSO4
• Complications of MI
- Rupture and acute pericarditis – days → ECHO to diagnose
- Dressler’s – weeks
- Aneurysm – month (4-6 weeks)
• 85% are right-dominant → Right coronary artery, gives off the posterior descending artery (PDA), supplying
the inferior wall, ventricular septum and the posteromedial papillary muscle
- 15% left-dominant → left circumflex gives off the PDA
- Co-dominant if both give off the PDA
• Stokes Adam’s attack → sudden collapse into consciousness due to heart block
• Flushing after a syncopal attack is due to pumping of blood into the already dilated peripheral vessels due to
hypoxia
Cardiology
• Investigations following syncope
- Find witnesses → ask how the patient became unconscious, was there a seizure?
- ECG → to look for arrhythmias
- Blood pressure → supine and standing to look for postural hypotension
- Blood glucose → to exclude hypoglycemia (LOC + sweating + improves with glucose administration)
• Before commencing ACE-inhibitors → Check eGFR, if <30 → Avoid ACE-inhibitors and ARBs
• Decreased ejection fraction + damaged myocardium (e.g. thinning of septal wall) → Dilated cardiomyopathy
• Familial hypercholesterolemia
- Autosomal dominant
- Total cholesterol >7.5, LDL >5
- Family history of MI in a 1st degree relative <60 years (or a 2nd degree relative <50 years)
• Polygenic hypercholesterolemia is milder with total cholesterol >6.5, LDL >4
• Elevated LDL and triglyceride + decreased HDL → Mixed dyslipidemia
• Baseline assessment of Amiodarone
- TFTs, LFTs and U&E → every 6 months
- CXR and ECG → every 12 months
• Before using Amiodarone, initial assessment→ TFTs
• Before using lithium, initial assessment → Kidney function tests, then TFTs
• Anginal pain → last less than 30mins and is precepted by physical exertion/stress
• Decubitus angina → Anginal pain that occurs on lying down
• Patent foramen ovale is diagnosed by → Transesophageal ECHO (bubble ECHO)
• InnoSent/functional/physiologic murmur:
- ASymptomatic
- Soft lowing murmur, 1-2/6 intensity, acute illnesses (e.g. fever) can increase the intensity
- Systolic murmur
- Short
- Left Sternal edge
• SVC obstruction
- Commonly caused by compressing lung cancer or lymphoma
- C/P: shortness of breath (most common symptom), facial and upper body edema, facial plethora,
venous distension of the face and upper body, dysphagia, syncope and headache
- Initial investigation → X-ray: to diagnose lung cancer
- Appropriate investigation → CT with contrast: to assess collateral vessels and the extent of obstruction
- Managed by → Steroids (Dexamethasone), avoided in night as it disturbs sleep
- Histology should be obtained before starting steroids as it may alter the result
Emergency
Sepsis
➢ Life-threatening organ dysfunction caused by a dysregulated host response to infection
Questions to be asked when dealing with sepsis:

1. Is the patient acutely unwell or it there any clinical concern?
2. Does the total NEWS (National Early Warning Score) score 5 or more?
3. Is there a single NEWS score indicator of 3?
If any of the above questions were yes → then ask yourself, could this be an infection? If yes → look for RED FLAGS
• Systolic blood pressure <90 (or >40 mmHg fall from baseline)
• Heart rate >130 bpm
• O2 saturation <91% (<88% in COPD) Rigors: episodes of shaking or exaggerated shivering, caused
• RR >25 bpm mainly by:
1. Bacteremia (seen in biliary sepsis or pyelonephritis)
• Responds only to voice or pain/unresponsive
2. Malaria
• Lactate >2.0 mmol
• Urine output <0.5 ml/kg/h for ≥2h
If 1 or more RED FLAGS present → complete the SEPSIS SIX within 60 minutes
SEPSIS SIX → Take 3, Give 3
Take 3
Septic shock
- Blood cultures 1. Low BP unresponsive to IV fluids
- FBC, U&E, clotting, lactate 2. Requires Vasopressors to maintain a mean
- Start monitoring urine output arterial pressure ≥65 mmHg
3. Serum lactate ≥2
Give 3
Severe sepsis
- High flow O2 • Sepsis + organ hypoperfusion (hypoxemia,
- IV fluids oliguria, lactic acidosis or altered cerebral
- IV antibiotics function)
How’s organ dysfunction identified?

• At the bedside, organ dysfunction is identified by an increase in the SOFA score of 2 or more
1. RR ≥22
2. Altered mentation
3. Systolic blood pressure ≤100 mmHg
Emergency
Sepsis vs SIRS
Emergency
Acute upper GI bleeding

Blatchford score
- For the initial assessment, to determine who are at “low risk” and candidates for outpatient management:
• Urea <5-6 mmol/L
• Hemoglobin >130 g/L (men) or >120 g/L (women)
• Systolic blood pressure ≥110 mmHg
• Pulse <100 bpm
• Absence of melena, syncope, cardiac failure or liver disease
Rockall score
- Assessment for admission and early endoscopy
• Age ≥60 years (all patients >70 years should be admitted)
• Witnessed hematemesis or hematochezia (suspected continued bleeding)
• Hemodynamic disturbance (systolic blood pressure <100 mmHg, pulse ≥100 bpm)
• Liver disease or known varices
• Other significant comorbidity (cardiac disease, malignancy) should also lower the threshold for admission
Management for upper GI bleeding

• 1st → IV fluid + Terlipressin (ADH analogue)
• 2nd → Endoscopy + band ligation (in most patients who are unstable or with persistent bleeding)
• TIPS should be considered of bleeding from esophageal varices isn’t controlled by band ligation
- Always remember, upper GI bleeds are referred to the medical team not surgeons
- PPIs (omeprazole) should NOT be used prior to endoscopy
Post GIT bleeding due to Mallory-Weiss $

If patient is stable
• Discharge with advice
• Repeat FBC
• Observe his vitals
If hemodynamically unstable
• Resuscitation (maintain airway, high flow O2, IV fluid)
• Endoscopy immediately after resuscitation
Indications for Fresh frozen plasma (FFP)

• Replacement of isolated factor deficiency
• Platelet count <50 x109/L
• Reversal of warfarin effect
• Patient has clotting disorder (e.g. due to liver disease)
• Prolonged INR
Emergency
• Massive blood transfusion (>1 blood volume within several hours)
• Treatment of TTP
Hypovolemic shock
Early changes
• Hypovolemia → stretch receptors in the atria and baroreceptors in the aorta become activated →
vasomotor center triggers efferent output → increase in catecholamine → arteriolar constriction,
venoconstriction, tachycardia
Late changes
• Reduced GFR → secretion of Aldosterone and ADH → salt and water reabsorption → thirst center becomes
triggered
Emergency
Look for the heart rate and memorize the blood loss %
Stage 4: over 40% blood loss, 140bpm, marked hypotension

Stage 3: over 30% blood loss, >120bpm, hypotension
Stage 2: 15-30% blood loss, >100bpm, postural hypotension
Stage 1: normal
Stage 1-2 → IV fluids

Stage 3-4 → Blood transfusion, you might need to give IV fluid initially until the bloods arrive to prevent shock
Anaphylaxis features
➢ The speed of onset and severity vary with the nature and amount of the stimulus, but the onset is usually in
minutes/hours
Respiratory
• Swelling of lips, tongue, pharynx, and epiglottis → may lead to complete upper airway occlusion
• Lower airway involvement is similar to acute severe asthma e.g. dyspnea, wheeze, chest tightness, hypoxia,
and hypercapnia
Skin
• Pruritus, erythema, urticaria, and angio-edema (swelling of the deeper layers of the skin)
Cardiovascular
• Peripheral vasodilation and increased vascular permeability → plasma leakage from the circulation →
hypotension, and shock
Management
1. ABC
2. High-flow O2
3. Lay patient flat
4. Adrenaline (epinephrine) IM, in the anterolateral aspect of the middle third of the thigh
Emergency
- <6 years → .15ml 1 in 1,000
- 6-12 years → .3ml 1 in 1,000
- >12 years → .5ml 1 in 1,000
5. Hydrocortisone and chlorpheniramine (antihistamine)
Signs and symptoms of smoke inhalation injury

• Persistent cough
• Stridor
• Wheezing
• Black sputum (excessive exposure to soot)
• Use of accessory muscles of respiration
• Blistering or edema of the oropharynx
• Hypoxia or hypercapnia
Management
- Summon the anesthetic for intubation
- If airway is obstructed → Cricothyroidotomy
Choking and foreign body airway obstruction (FBAO) in infants

• In a seated position, support the infant in a head-downwards, prone position to let gravity aid removal of the
foreign body
• Perform five sharp blows with the heel of the hand to the middle of the back (between the shoulder blades)
• After five unsuccessful back blows, use chest thrusts: turn the infant into a supine position and deliver five
chest thrusts. These are similar to chest compressions for CPR, but sharper in nature and delivered at a
slower rate
• If respiratory distress → anesthetic removes the foreign body with Magill’s forceps under direct
laryngoscopy
<1y/o → Back blows then chest thrusts

>1y/o → Heimlich maneuver
Carbon dioxide poisoning
➢ Tasteless and odorless gas, may occur from car exhausts, fires, faulty gas heaters or painting products
Early features
• Headache malaise
• Nausea and vomiting
Severe toxicity
• “Pink” skin and mucosa
• Hyperpyrexia
• Arrythmia
• Coma with hyperventilation
Investigation
• Carboxyhemoglobin level (COHb)
Management
• Clear the airway
• Maintain ventilation with high concentration of O 2
• For a conscious patient → use a tight-fitting mask with an O2 reservoir, but if unconscious → intubate and
provide IPPV on 100% O2
Emergency
Indications for hyperbaric oxygen therapy (HBOT) -- NOPE
- COHb level >20%
- Loss of consciousness
- Neurological signs other than headache
- Myocardial ischemia/arrythmia diagnosed by ECG
- The patient is pregnant
Tricyclic antidepressant (TCA) overdose (Amitriptyline)

Features [3Cs → Convulsions, Coma, Cardiotoxicity]
• Dilated pupil
• Dry mouth, Dry flushed skin
• Dry urethra: Urinary retention
• Drowsiness and altered mental state leading to coma
• Decreased blood pressure
ECG monitoring is essential → Sinus tachycardia and signs of hyperkalemia
Broad complex tachycardia can occur which are life threatening
ABGs → Metabolic acidosis
Management
• ABCDE protocol
• If within 1h of ingestion and >4 mg/kg → activated charcoal
• IV fluid as bolus
• Sodium bicarbonate, if prolonged QRS >120ms or hypotension unresponsive to fluids (even if not acidotic)
Tricyclic antidepressant overdose →
Unilateral space occupying lesions such as tumors, hematomas or abscesses →
Opiate (heroin) overdose or a cerebrovascular accident affecting the brainstem →
Paracetamol overdose → Liver toxicity

Features
• Initially → Nausea, vomiting, pallor
• After 24h → Hepatic enzymes rise
• After 48h → Jaundice, an enlarged, tender liver
• Hypoglycemia, hypotension, encephalopathy, coagulopathy, coma may also occur
Management
• <24 tablets (>150mg), serum paracetamol is normal and no hepatic risk factors) → Refer to psychiatry
• >24 tablets or unknown amount / within 8h of ingesting → Admit to medical ward and measure
paracetamol level every 4h post-ingestion (calculated from the time of ingestion not the hospital visit)
• >8h or staged overdose, doubt over the time, increased plasma paracetamol (above the line on the
nomogram) → N-acetylcysteine
<1h → Charcoal
1-4 → Delay blood sample until 4h post-ingestion
>4h → Do serum PCM levels and give NAC if indicated
>8h → NAC immediately
150mg 24 tablets =
Emergency
Alcohol consumption reduces the effect, chronic alcohol drinking worsens the condition
Criteria for liver transplantation (paracetamol liver failure)
➢ Arterial pH <7.3, 24h after ingestion OR all of the following:
- PT >100s
- Creatinine >300
- Grade III or IV encephalopathy
Aspirin overdose
➢ Toxic to the brain → Encephalopathy
➢ Toxic to the brainstem → Hyperventilation
➢ Metabolic acidosis later on
Common drugs cause metabolic acidosis [I2A2 MD]
• Metformin
• Alcohol
• Isoniazid
• Iron
• Aspirin
• Digoxin
ACEIs and NSAIDs → Metabolic alkalosis
Benzodiazepine, organophosphates (active ingredient in insecticides) → Respiratory acidosis
Benzodiazepines over dose → [CRASH]

• C-Cognitive problems
• R-Respiratory depression → life threatening
• A-Anteretrograde amnesia → loss of ability to create new memory
• S-Sedation
• H-Hypotension
Heroin overdose → flu-like symptoms (e.g. runny nose, muscle aches), agitation, sweating and sleep disturbance
CT scan after a head injury
For adults who have sustained a head injury and have any of the following → perform CT head with 1h of the risk
factor being identified:
• GCS <13 on initial assessment in the emergency department
• GCS <15 at 2h after the injury on assessment in the emergency department
• Suspected open or depressed skull fracture
• Any sign of basal skull fracture (hemotympanum, panda eyes, CSF leakage from ear or nose, Battle’s sign →
can take several days to appear)
• Post-traumatic seizure
• Focal neurological deficit
• >1 episode of vomiting
For adults with any of the following who have experienced some loss of consciousness or amnesia since the injury →
perform CT head within 8h of the head injury
• Age 65 years or older
• Any history of bleeding or clotting disorders
• A patient on warfarin
Emergency
• Dangerous mechanism of injury (a pedestrian struck by a
motor vehicle, an occupant ejected from a motor vehicle or a
fall from height >1m or 5 stairs)
• >30 minutes retrograde amnesia of events immediately
before the head injury
Management for stabbed injury in the RUQ with

shock features and suspected liver injury
1. IV fluids
2. Call the surgeons
3. Cross match for packed RBCs
4. CT abdomen
5. Laparotomy
Indications for FAST

• BAT (blunt abdominal trauma)
• Stable penetrating injuries
• Assessment of intraperitoneal free fluid (2ry to perforation/hemorrhage
due to trauma)
Renal trauma
Features
• Severe loin or back pain
• Hypotension
• Macroscopic hematuria → due to tearing of blood vessels at the renal
pedicle or rupture of the ureter at the pelvi-ureteric junction
Investigations
• Most initial diagnostic tool → Urgent abdominal CT
• If CT is not available → IVU
Patients should be hemodynamically stable before performing CT
Parkland formula
• Used to count the fluids required after burns, this is calculated from the time of burn
• Fluid requirements = Body area burned (%) x Wt. (kg) x 4mL (use Hartmann’s)
• Give ½ of total requirement in 1st 8h, then give 2nd half over the next 16h
Types of burns or scalds (due to hot water/steam)

Superficial (epidermal) burns
• Red and painful but don’t blister
• Managed with → wound dressing, bandage and discharge
Partial thickness burn

Emergency
• Ranges from blistering to deep dermal burn
• The appearance is shiny and sensation is intact
• Capillary refill blanches
Full thickness burn

• Has a leathery or waxy appearance
• May be white, brown or black in color
• There are no blisters
• Sensation is lost so they don’t feel any pain
• There’s no capillary refill
Management
1. Analgesia
2. IV fluid if burn >15% in adults, >10% in children (disregard superficial burn)
3. Referring to a specialized burn service
- >3% of total body surface partial thickness burn
- Burns involving the face, hands, feet, genitalia, perineum or major joints
- All deep dermal and full thickness burns
- All burns associated with electrical shock or chemical burns
- All burns associated with no-accidental injury
- All burns with inhalation injury
Blisters should be left intact to reduce the risk of infection however large blisters (>1cm) can be de-roofed or
aspirated under aseptic techniques
A significant percentage of burns are due to child abuse; if the story doesn’t match or there’s a delay in presenting →
contact child protection and refer to the specialized burn service
You may check tetanus status and give tetanus toxoid if required
Emergency
CPR
<1 y/o, blow air through the nose and mouth

>1 y/o, nose pinched
For cardiac arrest → CAB (Compressions, Airway, Breathing)

For any non-cardiac arrest → ABC
Emergency
Flail chest
➢ A flail chest occurs as a result of a trauma to the chest, leading to at least 3 ribs becoming fractured or
broken, close together, with pieces of bone detaching from the chest wall
➢ These segments of bone start to move independently of the chest wall and in the opposite direction because
of lung pressure. The result is a “paradoxical respiration”
Causes
• Fall (for example, off a bicycle or a horse)
• Blunt trauma to the chest
• Car accident
Diagnosis
• Paradoxical respiration + shortness of breath + chest pain in a patient who has just had blunt chest trauma
raises the suspicion of a flail chest
• Diagnosis is usually clinical with the help of chest X-ray → rib fractures
Management
1. High flow oxygen
2. Analgesia → paracetamol / NSAIDS / Opiates / intercostal block / thoracic epidural (up to T4) + splinting of
injury
3. If worsening fatigue and RR → Intubation / mechanical ventilation
Diaphragmatic rupture (diaphragmatic injury or tear)

➢ It is usually secondary to blunt trauma due to a car accident where the seat belt compression causes a burst
injury directed to the diaphragm
➢ The pressure within the abdomen raises so quickly with a sudden blow to the abdomen causing a burst in
the diaphragm. It is commonly on the left side
Features
• Chest and abdominal pain
• Respiratory distress
• Diminished breath sounds on the side of the rupture
• Bowel sounds may be heard in the chest
Investigation
• Chest X-ray to diagnose diaphragmatic rupture is actually quite unreliable and has low sensitivity and low
specificity. However, there are specific signs detectable on X-ray which should raise suspicion:
- Raised left hemi diaphragm
- Air fluid levels in the chest may also be seen
- A nasogastric tube is seen curled into the chest → Pathognomonic but rare
• Thoracoabdominal CT scan is usually diagnostic
Emergency
Hemothorax
➢ Blood accumulates in the pleural cavity
Features
Similar to that seen in traumatic pneumothorax, except the following:
• Dullness to percussion over the affected lung
• Signs and symptoms of hypovolemia if massive hemothorax
Investigations
• Chest X-ray → increased shadowing on a supine X-ray, with no visible fluid level
Treatment
• Oxygen
• Insert 2 large venous cannula and send blood for cross matching
• Evacuation of blood may be necessary to prevent development of empyema; thus, chest tube is needed and
is often placed low. Usually the lung will expand and the bleeding will stop after a chest tube is inserted
• Surgery to stop the bleeding is seldom required. The lung is the usual the source of bleeding
Homogenous opacity = white = fluid or gas = Hemothorax or pleural effusion

In blunt trauma → could be both hemopneumothorax
Hemothorax Pneumothorax
• Usually sharp trauma (stabbing) • Usually blunt trauma

• Dullness to percussion • Hyperresonance over the affected lung
• JVP not raised • Raised JVP
• CXR → Homogenous opacity • CXR → Hyperlucency
Toxic shock syndrome

➢ Caused by Staphylococcus aureus typically manifests in otherwise healthy individuals with high fever,
accompanied by low blood pressure, malaise and confusion, which can rapidly progress to stupor, coma,
and multiple organ failure
➢ The characteristic rash → often seen early in the course of illness, resembles a sunburn, and can involve any
region of the body, including the lips, mouth, eyes, palms and soles
➢ In patients who survive the initial phase of the infection, the rash desquamates, or peels off
➢ High WBC and low platelets (platelet count < 100,000 / mm³)
Features
• Fever > 38.9 °C
• Hypotension: Systolic blood pressure < 90 mmHg
• Diffuse macular erythroderma
• Desquamation (especially of the palms and soles) 1–2 weeks after onset
Involvement of three or more organ systems
• Gastrointestinal (vomiting, diarrhea)
• Muscular: severe myalgia or creatine phosphokinase level elevation
• Mucous membrane hyperemia
• Kidney failure
• Liver inflammation
Emergency
Orbital blowout fracture
➢ Most common bone affected in an → Maxilla (orbital
floor)
➢ Followed by → Ethmoid (medial wall)
Signs of maxilla (orbital floor) fracture

• Periorbital ecchymosis
• Enophthalmos
• Diplopia, as inferior rectus is trapped preventing the eye
from going up → Upward gaze whenever the patient try
to look up
Hereditary angioedema (C1 esterase inhibitor deficiency)

• Rare genetic causing episodes of angioedema which includes life-threatening laryngeal edema
• Positive family history
• Onset from childhood of episodes of angioedema affecting the larynx
• Abdominal pain and vomiting
• Confirmed by → Low levels of C1-esterase inhibitor and complement studies during the acute episode
• Treated by → C1-INH (C1-esterase inhibitor) concentrate
Urethral injuries
• Often associated with pelvic fractures + perineal bruising + blood at the
external urethra
• Rectal examination → High-riding prostate or inability to palpate the
prostate imply urethral injury
• Retrograde urethrogram might be used to assess urethral injury
• Suprapubic catheterization is needed to empty the bladder
Compartment syndrome [5Ps]

➢ Often occurs after a traumatic injury such as a car crash
➢ Causes severe high blood pressure in the compartment which results in insufficient blood supply to muscles
and nerves
➢ If left untreated, it might lead to permanent muscle and nerve damage and can result in the loss of function
of the limb
➢ Managed by → Fasciotomy
Features
• Pain
• Pallor
• Paresthesia (feeling of numbness)
• Pulselessness
• Paralysis
- Acute limb ischemia is similar to Compartment $ except it develops gradually in the latter
Emergency
Notes
• In mixed acidosis, HCO3 is given when → pH <7 and HCO3 <10 mmol/L
• Commonest cause of mixed respiratory and metabolic acidosis → Cardiac arrest, patient is retaining carbon
dioxide as he’s not breathing and his kidneys aren’t perfusing due to low cardiac output, managed by →
Increase ventilation
• Sharp/aching pain, aggravated by movement such as deep inspiration, coughing or sneezing + tenderness on
the side of the sternum → Costochondritis
• Costochondritis + swelling over the affected joints of the anterior chest wall → Tietze’s $
• Autonomic nervous system responsible for “fight or flight” and VC of bl. Vessels → Sympathetic
• Autonomic nervous system responsible for “rest and digest” and VD of bl. Vessels → Parasympathetic
• A professional doing CPR for adults, compression with rescue breaths → 30:2
• A professional doing CPR for children, compression with rescue breaths → 15:2
• A layman doing CPR → 30:2
• Pressing depth in an infant should be → 4cm, Aim for rate → 100/min
• Mydriasis + nystagmus + tachycardia + hypotension → Carbamazepine toxicity
• Nausea, vomiting, diarrhea, abdominal pain, headache, dizziness, confusion, delirium, vision disturbance
(blurred or yellow vision) + cardiac abnormalities (VT, VF, heart block) → Digoxin toxicity
• Bradycardia, hypotension, hypothermia, hypoglycemia (especially in children) → Propranolol toxicity
• Hypotension, fever, frequent urination, muscle cramps and twitching → Thiazide toxicity
• Bleeding occurs at the time of surgery or immediately after an injury or an operation → 1ry hemorrhage →
Replace blood, if severe → return to theatre for adequate hemostasis
• Bleeding within the first 24h following trauma/surgery, usually caused by slipping of ligatures, dislodgement
of clots, patient warming up after surgery causing vasodilation, on top of normalization of blood pressure →
Reactionary hemorrhage → Replace blood and explore the wound
• Caused by necrosis of an area of blood vessel, related to previous repair and is often precipitated by wound
infection, it occurs 1-2 weeks post-op → 2ry hemorrhage → Admission and IV antibiotics
• Main concern in fracture femur → Blood loss into compartment, so initial action after ABCD → Thomas’s
splint
• RTA, trauma to left side of the chest + abdominal distension + falling blood pressure + rising pulse +
abdominal tenderness and diminished bowel sounds → Splenic fracture, initially → X-ray abdomen (loss of
left psoas shadow), confirmed by → CT abdomen
• Initial investigation for abdominal trauma in hemodynamically stable patient → CT
• Initial investigation for abdominal trauma in hemodynamically unstable patient → FAST
• FAST in splenic fracture → Free peritoneal fluids → Immediate laparotomy
• Stable patient with upper GI bleeding after excessive alcohol ingestion → Mallory-Weiss tear → Endoscopy
• An alcoholic seeking help to quit but lacks social support → Refer to social services
• If there’s any medical concerns → Admit
• Crackles at the lung could be due to → Pulmonary edema or infection
• Most common site for tearing in traumatic aortic rupture → Proximal descending aorta
• Calf swelling with a positive Homan’s sign (pain with ankle dorsiflexion) → DVT or Popliteal cyst ruptures
• Popliteal cyst ruptures → usually starts behind the knee (popliteal fossa)
• To differentiate between DVT and popliteal cyst rupture → US
• Asymptomatic swelling behind the knee that may cause discomfort → Baker’s cyst
• History of popping sound around the ankle with pain and decreased plantar flexion → Achilles Tendon
rupture
• DNR allows to withhold CPR not treatment
ENDOCRINOLOGY
Pituitary hormones
Control of gonadotropin secretion Adrenal hormones
RAAS
ENDOCRINOLOGY
Cortisol function
DM
Plasma glucose test Normal Prediabetes Diabetes
Random < 11.1 mmol/l NA ≥ 11.1 mmol/l
Fasting < 5.5 mmol/l 5.5 - 6.9 mmol/l ≥ 7 mmol/l
2-hour post prandial (OGTT) < 7.8 mmol/l 7.8 - 11 mmol/l ≥ 11.1 mmol/l
HbA1C < 42 mmol/mol (6%) 42-47 mmol/mol (6-6.4%) 48 mmol/mol (6.5%)
Diagnosing Type 2 Diabetes:

-Diabetes symptoms + 1 abnormal value -Two abnormal readings of FBG on two separate occasions
- Impaired glucose tolerance is FBG <7mmol/L & OGTT is 7.8-11mmol/L
- HbA1c is preferred in cases of uncertainty, fasting plasma OGTT test is no longer recommended for diagnosing DM.
glucose test is preferred in ESRD. However, it’s the gold standard for diagnosing gestational DM.
- Life style modification is advised if blood pressure is constantly above 140/90 or >130/80 with complications
- Treating DM with OHAs:

- Start with Metformin, HBA1c >58 → dual, still → triple
- With bad kidneys, don't use MS (Metformin, Sulphonylurea)
- With bad heart, don't use DG (DPP4 inhibitors, Glitazone)
- Weight Gain with GG (Glitazone, Gliclazide [SU]) / Loss with Metformin
- Risk of hypoglycemia & hyponatremia with Sulphonylurea (Gliclazide/Glibenclamide)
- G: bladder cancer, fractures / DDP4-inhibitors (Sitagliptin): pancreatitis
- Side effects of M: GI upset + lactic acidosis
- NICE recommends human NPH insulin (isophane, intermediate acting) taken at bed-time or twice daily
- Type 1 diabetes: patients always require insulin to control the blood sugar levels
- Management of hypertension in diabetic and non-diabetic patient
ENDOCRINOLOGY
- Management of the diabetic pre-op
- All OHAs: omit in the day of surgery except for PEM (pioglitazone, exenatide and metformin) taken as regular
- For drugs that are omitted: restart once eating and drinking
- Sliding scale is done by administering IV insulin, dextrose and saline to maintain glucose between 4-9 mmol/L
- Contraindications for Biguanide (metformin)

• eGFR < 30 ml/min
• severe infection Rule of 30 for biguanide:
• BMI > 30 ⟶ give biguanide
• shock
• eGFR < 30 ⟶ don’t
• hepatic insufficiency
With bad kidneys, use DDP4 inhibitors (Sitagliptin), if not there,
• alcohol addiction choose insulin.
Risk factor modification in DM

- Blood pressure
• target is < 140/80 mmHg (or < 130/80 mmHg if end-organ damage is present)
• ACE inhibitors are first-line → start immediately if there’s protein in urine
- Antiplatelets
• should not be offered unless a patient has existing cardiovascular disease
- Lipids
• patients with a 10-year cardiovascular risk > 10% (using QRISK2) or aged >85 should be offered a statin. The
first-line statin of choice is atorvastatin 20mg on
ENDOCRINOLOGY
Hypoglycemia:
- considered when blood glucose is < 4 mmol/L. However, cognitive function deteriorates when < 3 mmol/L
- Features of hypoglycemia: sweating, tachycardia, fatigue, confusion, reduced consciousness
Causes:
- alcohol
- drugs: insulin, Sulphonylurea, paracetamol excess, quinine, salicylate - Hypoglycemia is diagnosed by capillary
- Addison’s blood glucose & doesn’t have to be fasting
- liver failure
- insulinoma
Alpha and Beta receptors:
- Alpha blockers: Hypertension.

- Beta1 blockers: Heart problems. - Beta 2 agonists: Asthma
- 2ry hyperglycemia is seen in Cushing's, CF, pancreatitis, hemochromatosis, glucocorticoids
- Glucose level is measured in acromegaly as glucose may suppress growth hormone release
• D Dehydration, Delusion
• K Kussmaul breathing, Ketones
• A Acidosis, Abdominal pain, vomiting
- Precipitating factors in DKA

• Infection, missed insulin dose, CVD
- Diagnosis of DKA
• Hyperglycemia > 11 or known diabetic • ABG is used in DKA to determine the severity
• Acidosis (pH<7.3, HCO3<15)
• Ketonemia (>3 or urine dipstick ketones)
- Treating DKA
• Fluid replacement followed by Insulin administration
- Systolic BP <90 → 1L of 0.9% sodium chloride in 10-15 minutes
- Systolic BP >90 → 1L of 0.9% sodium chloride over 1h
- Administrating 0.9% sodium chloride over 6h in the acute management is NEVER the answer
• When glucose <12 → replace normal saline with 5% dextrose, Glucose <8 → 10% dextrose is used
• KCL for hypokalemia
ENDOCRINOLOGY
Adrenal insufficiency (1ry → Addison's disease)
➢ Autoimmune is the most common cause
Features
• tired, tanned (due to high ACTH), hypotensive (postural hypotension)
• diarrhea, vomiting, abdominal pain
Other causes of hypoadrenalism
Primary causes
• Tuberculosis → Common worldwide
• metastases (e.g. bronchial carcinoma)
• meningococcal septicemia (Waterhouse-Friderichsen syndrome)
• HIV
• antiphospholipid syndromes (a disorder of the immune system that causes an increased risk of blood clots)
Secondary causes
• pituitary disorders (e.g. tumors, irradiation, infiltration)
• Exogenous glucocorticoid therapy → Most common cause of 2ry adrenal insufficiency
Investigation
- The definite investigation is an ACTH stimulation test (short Synacthen test)
- Adrenal autoantibodies such as anti-21-hydroxylase may also be demonstrated
If an ACTH stimulation test is not readily available (e.g. in primary care) then sending a 9 am serum cortisol can be
useful:
• > 500 nmol/l makes Addison's very unlikely
• < 100 nmol/l is definitely abnormal
• 100-500 nmol/l should prompt an ACTH stimulation test to be performed
Management
• glucocorticoid and mineralocorticoid replacement therapy
• fludrocortisone for postural hypotension
Adrenal crisis
• Can be precipitated in patient with Addison’s by infection, trauma or surgery
• Steps to follow in management:
1. IV hydrocortisone → stimulates gluconeogenesis, absorbing sodium and excreting potassium
2. Normal saline infusion
3. Cardiac and electrolyte monitoring
4. Broad spectrum antibiotics if an infection is suspected
5. Hydrocortisone in 5% glucose via IV infusion
6. Weaning off of IV steroids and commencing on oral steroids
- In adrenal insufficiency (Addison's disease): All Hypo except hyperkalemia + metabolic acidosis
- Postural hypotension can be seen in Pheochromocytoma and Addison’s
- Postural hypotension and hyperpigmentation = Addison’s
- Polyuria and polydipsia in Conn’s are due to hypokalemia-induced nephrogenic diabetes insipidus
ENDOCRINOLOGY
Cushing's syndrome
- A clinical state caused by prolonged exposure to elevated levels of either endogenous or exogenous glucocorticoids
Causes can be divided into 2 groups:
• ACTH-dependent disease:
- excessive ACTH from the pituitary due to pituitary adenoma (Cushing’s disease) → BILATERAL adrenal
- ectopic ACTH-producing tumors (especially small cell lung cancer and carcinoid tumors)
• Non-ACTH- dependent:
• Excess steroid use would cause
- adrenal adenomas
premature fusion of the growth plate
- adrenal carcinomas
- excess glucocorticoid administration (iatrogenic) ⟶ This is the chief cause
Investigations: 1. Diagnose 2. Locate the cause
1. Outpatient tests 2. Inpatient tests
• 24-hour urinary free cortisol ⟶ for screening ACTH plasma levels:
• Overnight dexamethasone suppression test: • To differentiate between ACTH-dependent and non-
- this is the best initial test to diagnose dependent causes:
Cushing’s. - High ACTH: pituitary adenoma or ectopic
- Administration of low dose (1mg) of - Low ACTH: non-dependent
dexamethasone at midnight followed by • If ACTH is high ⟶ High dexamethasone suppression test
serum cortisol measurement at 9 a.m. - Pituitary adenoma: cortisol suppressed
- cortisol < 50 nmol/L makes Cushing’s unlikely - Ectopic: cortisol not suppressed
- The reason cortisol is suppressed in pituitary adenoma is because the adenoma is semi-autonomous. A low
dose dexamethasone will not suppress it but a high dose will. Whereas, ectopic ACTH producing tumors are
fully autonomous and will not respond to high dose dexamethasone suppression test
Facts about cortisol:
• cortisol is lipid-soluble (binding to CBG) and not water-soluble, only 5% free cortisol as a part of the circadian
rhythm. Free cortisol processed by the kidneys and are dumped in the urine
• cortisol increases blood pressure through:
1. increasing sensitivity of the peripheral blood vessels to catecholamines (epinephrine and
norepinephrine) which leads to VC
2. cortisol mimics mineralocorticoid activity therefore maintaining fluid
• cortisol increases blood glucose level so, insulin levels increase (insulin targets adipocytes in the center of the
body ⟶ activates lipoprotein lipase which helps adipocytes to accumulate more fat molecules ⟶ obesity)
• cortisol has a mineralocorticoid activity (aldosterone) → hypokalemia
- An insulin stress test is used to differentiate between true Cushing's and pseudo-Cushing's
Conn’s syndrome
• Hypertension associated with hypokalemia
• Refractory hypertension, e.g. despite antihypertensive drugs
• Hypertension occurring before the age of 40
• Hemoglobin can be increases due to polycythemia
Classic features include: • 1ry due to adrenal adenoma
- hypertension + hypokalemia • 2ry due to RAAS overactivity (due to renal artery stenosis,
- metabolic alkalosis nephrotic syndrome)
- headache and lethargy
Management
• Spironolactone (aldosterone antagonist) followed by adrenalectomy
ENDOCRINOLOGY
Causes of Hypocalcemia
• vitamin D deficiency (osteomalacia)
• CKD
• hyperparathyroidism, hyperphosphatemia, hypomagnesemia
Causes of Hypercalcemia
• 1ry hyperparathyroidism (commonest cause in non-hospitalized patients)
• Malignancy: breast cancer → bone metastasis, lung cancer (SCC), Multiple Myeloma (MC for hospitalized)
• Familial hypercalciuric hypercalcemia
• Immobilization
• Sarcoidosis
• Thyrotoxicosis
• Addison’s
• Thiazide
• dehydration
Hypercalcaemia (M, G, S, B + short QT) Hypocalcaemia (SPASMODIC + long QT)
Features Moans (abdominal pain, constipation) Spasm
Groans (lethargy, confusion, depression) Perioral paresthesia
Stones + DI (polyuria, polydipsia) Anxious
Bones (pain, fracture) Seizures
Short QT Muscle tone increased
Orientation impaired
Dermatitis
Impetigo
Chvostek's sign + Trousseau sign
Long QT (cardiomyopathy)
Rehydrate (saline) + bisphosphonate
Management Ca gluconate
(pamidronate, zoledronate)
- What to do when suspect hypercalcemia? [CALC]

1. Correct calcium level
2. Check albumin: ↑corrected calcium + ↑albumin + ↑urea = dehydration
3. Check alkaline phosphatase: ↑corrected calcium + ↑ALP = bony metastasis, sarcoidosis or thyrotoxicosis
4. Check serum calcitonin level: ↑corrected calcium + ↑serum calcitonin = B-cell lymphoma
- Magnesium is required for the production and release of parathyroid hormone, so hypomagnesaemia leads to 2ry
hypocalcaemia as a result from decreased PTH
- Vitamin D is essential for Ca and P absorption from the gut
- In renal patients (maybe as a complication of DM), the kidney is unable to get rid of phosphate; the phosphate
builds up and binds to calcium causing hypocalcaemia
- Pseudogout - Precepted by Hypothyroidism, Hyperparathyroidism, Hemochromatosis.

- Mainly in knee but can affect wrist, shoulder and ankle.
- There could be fever and raised WBCs
- Diagnosed by +ve birefringent crystals in synovial fluid.
ENDOCRINOLOGY
Thyroid diseases
Thyrotoxicosis Hypothyroidism
Most Graves' disease Hashimoto's thyroiditis

common • most common cause of • most common cause in the developed world
cause thyrotoxicosis • autoimmune disease, associated with vitiligo,
• as well as typically features of type 1 diabetes mellitus, Addison's or pernicious
thyrotoxicosis other features may be anemia
seen including thyroid eye disease • may cause transient thyrotoxicosis in the acute
→ lid retraction, lid lag on looking phase
downward (Von Graefe’s sign) • 5-10 times more common in women
exophthalmos, pain, diplopia,
• LR is affected → diplopia & upgaze
Other Subacute thyroiditis (de Quervain’s) ⇅ Riedel thyroiditis

causes • associated with a painful goiter (may • fibrous tissue replacing the normal
radiate to jaw) and raised ESR thyroid parenchyma
• usually followed by URTI • causes a painless goiter
• hyperthyroidism followed by hypothyroid
state before resolving to euthyroid Postpartum thyroiditis ⇅
• usually self-limiting → Propranolol to
control symptoms Drugs
• severe cases → Prednisolone • lithium
• amiodarone ⇅
Toxic multinodular goiter • interferons
• autonomously functioning thyroid nodules
that secrete excess thyroid hormones Iodine deficiency
• nuclear scintigraphy → patchy uptake • the most common cause of
hypothyroidism in the developing world
Drugs • goiter is present
• amiodarone
Feature Thyrotoxicosis Hypothyroidism

- Weight loss - Weight gain
General - Manic, restlessness - Lethargy
- Heat intolerance - Cold intolerance
- Palpitations, may even provoke arrhythmias
Cardiac - bradycardia
e.g. atrial fibrillation
- Increased sweating - Dry (anhidrosis), cold, yellowish skin

- Pretibial myxedema: erythematous, - Myxedema (e.g. hands, face)
Skin
edematous lesions above the lateral malleoli - Dry, coarse scalp hair, loss of lateral aspect of
- Thyroid acropachy: clubbing eyebrows
Gastrointestinal - Diarrhea - Constipation

- Menorrhagia and later oligomenorrhea or
Gynecological - Oligomenorrhea
amenorrhea
- Decreased deep tendon reflexes
Neurological - Anxiety, Tremor - Carpal tunnel syndrome
- Obstructive sleep apnea
ENDOCRINOLOGY
Thyroid function tests:
Diagnosis TSH Free T4 Notes
Thyrotoxicosis (e.g. Graves') Low High - Radioactive iodine uptake test is increased
Subacute thyroiditis (de - Radioactive iodine uptake test is decreased

Low High
Quervain’s) - Usually followed by URTI
Primary hypothyroidism
High Low
(e.g. Hashimoto's thyroiditis)
Secondary hypothyroidism Low Low
- Common in hospital inpatients. Changes are

Sick euthyroid syndrome Low Low reversible upon recovery from the systemic illness and
no treatment is usually needed
- This is a common finding and represents patients who

Subclinical hypothyroidism High Normal are 'on the way' to developing hypothyroidism but still
have normal thyroxine levels
- Patients who are poorly compliant may only take their

Poor compliance with thyroxine in the days before a routine blood test. The
High Normal
thyroxine thyroxine levels are hence normal but the TSH 'lags'
and reflects longer term low thyroxine levels
- TSH levels are more sensitive than T4 levels for monitoring patients with existing thyroid problems and are often
used to guide treatment
- A number of thyroid autoantibodies can be tested for (remember the majority of thyroid disorders are
autoimmune). The 3 main types are:
• Anti-thyroid peroxidase (anti-TPO) antibodies ➔ Hashimoto
• TSH receptor antibodies ➔ Graves
• Thyroglobulin antibodies
- There is significant overlap between the type of antibodies present and particular diseases, but generally
speaking TSH receptor antibodies are present in around 90-100% of patients with Graves' disease and anti-TPO
antibodies are seen in around 90% of patients with Hashimoto's thyroiditis.
Other tests include:

• nuclear scintigraphy; toxic multinodular goiter reveals patchy uptake
Treatment
- thyroxine is given in the form of levothyroxine to replace the underlying deficiency.
- Patients with thyrotoxicosis may be treated with:
• propranolol: this is often used at the time of diagnosis to control thyrotoxic symptoms such as tremor
• carbimazole: blocks thyroid peroxidase from coupling and iodinating the tyrosine residues on thyroglobulin
→ reducing thyroid hormone production. Agranulocytosis (severe leukopenia) is an important adverse effect
to be aware of
• radioiodine
ENDOCRINOLOGY
- Radioactive iodine in treatment of thyrotoxicosis: Iodine is essential for making thyroid hormones. The gland
will take up the radioactive iodine. The radiation can destroy thyroid tissue
- Drugs cause hypothyroidism: Antithyroid drugs (carbimazole, propylthiouracil), Amiodarone, Lithium, Iodine
Multiple endocrine neoplasia
- Congenital hypothyroidism:
• prolonged physiological jaundice
• goiter
• FTT, constipation
• Short stature
• Coarse features: protruding tongue, broad flat nose, widely set eyes
• Impaired mental functions
- 15% familial, usually screened for when the baby is 6-8 weeks old through TSH analysis
Pheochromocytoma
• Rare catecholamine secreting tumor
• Rule of 10% → 10% bilateral, 10% malignant, 10% extra-adrenal (MC site – organ of Zuckerkandl, adjacent to
the bifurcation of the aorta), 10% familial (may be associated with MEN type II, neurofibromatosis and von
Hippel-Lindau $), 10% not associated with hypertension
• PHeochromocytoma → Palpitations, Headaches, PHlushing
• Investigation → 24h collection of metanephrines
• Management → Surgery, but the patient must be stabilized first
- Alpha-blocker (phenoxybenzamine) → must be given before beta-blocker
- Beta-blocker (propranolol)
• Alpha and beta blockade are used to control blood pressure and prevent intraoperative hypertensive crisis
• Alpha blockade is given 7-10 days before operation to allow expansion of the blood volume, if beta blockade
started too soon, unopposed alpha stimulation can precipitate a hypertensive crisis
ENDOCRINOLOGY
Hyperkalemia (>5.5 mmol/L) Hypokalemia (<3.5 mmol/L)
Causes - Chronic renal failure
- Acute renal failure
- DKA
- K+ sparing diuretics (spironolactone),
- Diuretics (thiazide)
ACE inhibitors, ARBs
- Diarrhea, vomiting
- Metabolic acidosis (K+ ⇋ H+)
- Conn’s
- Addison's
- Villous adenoma
ECG - Tall tented T wave - Small inverted T wave
changes
- Small P wave - U wave [hypUkalemia]
- Wide QRS - Prolonged P-R interval
➢ Leading to a sinusoidal pattern and asystole - Non-specific ST depression
TTT - If K+ was low, a next step would
1. Stop the drugs be ordering magnesium level
2. ECG changes: IV calcium (low), ECG and cardiac
gluconate/chloride monitoring, as cardiac
3. Severe cases: Insulin and dextrose infusion arrhythmia is the most serious
4. Other methods: Ca resonium, loop common complications of
diuretics, dialysis (GFR>7.5) hypokalemia
• Once K+>6, the primary goal is to protect the heart by calcium • Insulin stimulates intracellular reuptake of K+
gluconate and glucose is given to prevent hypoglycemia
• Measuring serum K+ is more accurate than ECG • After Insulin and glucose infusion, blood
glucose is monitored after 15 mins, 30 mins and
• ACE inhibitors: ramipril, captopril then hourly for the next 6 hours due to fear of
• Mnemonic for ttt of hyperkalemia: C BIG K Soon Dial 75 late hypoglycemia
- Calcium Gluconate • it’s important to check K+ 30 mins afterwards
- Bicarbonate and if there’s good response, check U&E 1-2
- Insulin + Glucose (10 units of insulin & 50 ml of 50% glucose infusion IV over hours later
30 mins via a volumetric pump, lasts 1 hour)
Shifting K+ intracellularly doesn’t reduce total body K+, and after 2-
- Kayexalate (K+ binding resin)
6 hours, there’s an efflux of K+ back into the extracellular space
- Salbutamol (10-20 mg nebulized salbutamol, lasts for 2 hours)
resulting in serum levels as high or sometimes higher than at the
- Dialysis (GFR>7.5, patient is oligo or anuric)
outset. Therefore, any of these steps should be combined with
attempting to reduce total body K+. This can be done by:
• Avoiding medications that raise K+
• Promote urinary K+ loss
- IV fluid as long as the patient is not significantly
overload
- if well hydrated, consider starting on increasing the
dose of a loop diuretics (frusemide)
• Remove excess K+
- Ca resonium has a slow onset of action (at least 2-6
hours)
• Dialysis
- if hemodialysis is performed within 15-30 mins then
treatments to move K+ into cells are unlikely to be
helpful and may make K+ removal on dialysis more
difficult
• This is an example of a prominent U wave. A low T
wave followed by prominent U wave produces a “camel hump” effect
• As hypokalemia progresses to be more severe, the T wave decreases in amplitude and gets flattened or becomes
inverted. The U wave becomes more prominent, this may falsely be seen as a prolongation of the Q-T interval
ENDOCRINOLOGY
After fluid restriction in diabetes insipidus
FSH vs LH vs Oestradiol vs Prolactin
In post pill amenorrhea → All are normal (FSH & LH may be low), in Hypothalamic amenorrhea → All are low
Features of prolactinemia:
• Galactorrhea (uncommon in postmenopausal women)
• Menstrual abnormalities (amenorrhea, galactorrhea)
• Disturbed gonadal function in men (erectile function, decreased libido, gynecomastia, reduced fertility)
Causes of prolactinemia:
• pregnancy, stress, nipple suckling - Normal prolactin is < 400mU/L
• prolactinoma
• antipsychotic drugs (risperidone, haloperidol)
• hypothyroidism → raised TRH
• Hypothalamic disease (hemangioma, craniopharyngioma)
ENDOCRINOLOGY
Prolactinoma: a benign tumor (adenoma) of the pituitary gland that produces prolactin
Investigation
• Always exclude other causes of prolactinemia
• Serum prolactin < 2000mU/L → Microprolactinoma OR a non-functioning macroadenoma compressing the
pituitary stalk
• Serum prolactin > 4000mU/L → Macroprolactinoma→ may cause visual symptoms (bitemporal
hemianopia) due to compression of optic chiasm
• MRI
Management
• Drug treatment should always be tried first
• Cabergoline is more effective than bromocriptine with fewer side effects
• Microadenoma < 10mm: Cabergoline / bromocriptine only
• Macroadenoma > 10mm: Drugs + Trans-sphenoidal surgery
• Surgery is needed when failing to respond to medical treatments with persisting visual symptoms (uni- or
bitemporal hemianopia) or pressure effects
- MOA of dopamine agonists:

1. Suppress prolactin with normalization of gonadal functions and terminates galactorrhea
2. Shrink the tumor and restore other hormonal axes
3. Correct visual field defect by chiasmal decompression thus immediate surgical decompression is not
indicated
- Both Cs cause hypokalemia. Both are Cushing's and Conn's
- Small cell lung cancer causes: Hyponatremia due to SIADH + Hypokalemia (increased mineralocorticoid activity)
- Squamous cell lung cancer causes: Hypercalcemia due to PTH like action (Para-neoplastic phenomenon)
SIADH (increased blood volume) Diabetes Insipidus (polyuria)

Hyponatremia Hypernatremia
Low plasma osmolarity High plasma osmolarity
High urine osmolarity Low urine osmolarity
- SSRIs (e.g. fluoxetine) can cause SIADH
Management of SIADH
- Treat the cause and restrict fluid • Tumor in the diencephalon → DI
- If severe ➝ Salt + loop diuretics • Tumor in the cerebrum/cerebellum → SIADH
- Vaptans (Vasopressin receptor antagonist)

- Demeclocycline, used rarely
Diabetes insipidus
1. Cranial DI: due to low ADH → inability to concentrate urine → polyurea and polydipsia
- Could be due to metastasis to the Diencephalon (contains hypothalamus)
2. Nephrogenic DI: inability to concentrate urine due to resistance to ADH in the kidney
ENDOCRINOLOGY
Acromegaly:
In acromegaly there is excess growth hormone secondary to a pituitary adenoma in over 95% of cases. A minority of
cases are caused by ectopic GHRH or GH production by tumors e.g. pancreatic
Features
• coarse facial appearance, spade-like hands, increase in shoe size
• large tongue, prognathism, interdental spaces
• excessive sweating and oily skin
• features of pituitary tumor: hypopituitarism, headaches, bitemporal hemianopia
• raised prolactin in 1/3 of cases → galactorrhea
• 6% of patients have MEN-1
Investigations
• GH levels tend to vary during the day → unreliable and not recommended
• Best initial → Insulin like growth factor (IGF-1), used as screening and monitoring
• Most definitive → OGTT with serial growth hormone measurements
- normally, GH is usually suppressed with glucose
- in acromegaly, there is no suppression of growth hormone with glucose
• MRI may show a tumor. MRI scan is more sensitive than CT
Complications
• hypertension
• diabetes (>10%)
• cardiomyopathy
• colorectal cancer
Management:
• Trans-sphenoidal surgery
• Somatostatin analogue (GH-inhibiting hormone)
• Dopamine-agonists (cabergoline, bromocriptine)
• Pegvisomant
Osteomalacia
- normal bony tissue but decreased mineral content
Features
• Bone pain
• Fractures
• Muscle tenderness
• Proximal myopathy
Causes
• Vitamin D deficiency → Malabsorption, lack of sunlight and diet
• renal failure
• drug induced (anticonvulsants)
ENDOCRINOLOGY
Notes
• Electrolyte disturbance with vomiting: Hypokalemic metabolic alkalosis (losing HCL)
• Electrolyte disturbance with diarrhea: hypokalemic metabolic acidosis (losing bicarbonate)
• High alcohol consumption: >14 units per week (males), >7 units per week (females)
• UK guidelines → no more than 3 units per day, at least 2 days off every week
• 1 mmol/L = 18 mg/dl
• Increased glucose level (e.g. after dextrose infusion) → osmotic flow of water from ICF to ECF → hyponatremia
• All goiters grow diffuse except Hashimoto (diffuse and lobulated), while benign/malignant thyroid growths are
uninodular
• Always exclude hypoglycemia in patients with coma, altered behaviors, confusion or reduced consciousness
• Management of hypoglycemia (serum glucose <4mmol/L):
- Regular blood glucose monitoring should continue for 24-48h

- Glucose 50% IV is rarely given as it’s hypertonic and may damage veins
- Glucagon 1mg IM or SC is usually administered by ambulance crew or when IV access is difficult
- If hypoglycemia is induced by excess oral hypoglycemics or insulin overdose, maintenance glucose infusions
intravenously may be required for 24h or longer
• Thyroglossal cyst moves with protruding the tongue or swallowing, thyroid mass moves with swallowing only
• With Thyroglossal cyst, malignant nodules should be ruled out by FNAC (>1cm), but initially US for sizing
• Carbimazole is the 1st line in treating thyrotoxicosis, PTU has a small risk of liver injury
• Carbimazole is used once daily while PTU is used twice to three times daily
• PTU is preferred when:
- A woman trying to get pregnant or in the 1st trimester (Carbimazole → 2nd and 3rd trimesters)
- Thyroid crisis → as it prevents peripheral conversion of T4 to T3, while Carbimazole reduces production
which takes more time
• Other drugs to be used in thyroid storm
- Beta-blockers → for tachycardia and palpitations
- High dose steroids → blocks T4 to T3 conversion
- Iodine → to inhibit thyroid hormone release
ENDOCRINOLOGY
• Hypothyroidism + Addison’s = Schmidt’s $
• HTN is pheochromocytoma → Episodic/Paroxysmal
• HTN in hyperthyroidism → Systolic
• HTN in Conn’s → associated with hypokalemia
• Feature of GI upset + Hypotension = Adrenal insufficiency
• Pseudo Cushing → displays signs and symptoms of Cushing’s but the cause is idiopathic, could be due to
excessive alcohol consumption or COCP
• Autonomic neuropathy in Diabetes:
- Sweating
- Constipation
- Diarrhea
- Incontinence
- Postural hypotension
Treated with Metoclopramide or erythromycin
• Chvostek’s sign → facial muscles twitch in response to tapping over the parotid, revealing neuromuscular
excitability
• Trousseau’s sign → wrist flexes and the fingers are drawn together in response to occlusion of the brachial
artery (usually with a BP cuff above systolic BP for 3 minutes)
• Pheochromocytoma does NOT cause hypokalemia

• Refractory hypertension + hypokalemia → Conn’s
• Hypotension + Hyperkalemia → Addison’s
• Episodic hypertension + panic attack like symptoms → Pheochromocytoma
• In diagnosing DM, FBG is preferred over HbA1C as it’s much cheaper, HbA1C however is used in case of clinical
certainty and for monitoring
• Hyperpigmentation is seen in Addison’s and ACTH-dependent Cushing’s
• Levothyroxine and oral ferrous sulphate should NEVER be taken at the same time, Iron supplements interfere
with the absorption of levothyroxine and reduce its effectiveness so taking it at different times is appropriate
• HbA1C target is <48 mmol/mol
• MODY → Autosomal dominant, <25 years, mild hyperglycemia
• LADA → >30 years, a type of DM 1
• For terminally ill patients:
- After an episode of hypoglycemia → Reduce or discontinue insulin
- HbA1C target is up to 70mmol
- OHAs can be stopped at the very end of life if not tolerated
• Fluid restriction is performed to diagnose DI and to teat SIADH
• Before thyroid surgery, patient should be euthyroid to avoid thyroid storm
• In hyperemesis gravidarum, check TFTs as thyrotoxicosis can be the culprit
ENDOCRINOLOGY
• Treatment of DI:
- Central → Vasopressin
- Nephrogenic → Hydration
• Hyperkalemia
- Mild → 5.5 – 5.9
- Moderate → 6 – 6.4
- Severe → >6.5
• Regarding ECG in hyperkalemia
- ECG may be normal in severe cases
- The absence of ECG doesn’t mean there’s no need for treatment
- The presence of ECG changes means a need for urgent treatment
- The severity of ECG changes doesn’t always relate to the severity of hyperkalemia
- Measuring serum K+ is more accurate than ECG
• Intravenous fluids
• Symptoms are episodic in pheochromocytoma as catecholamines are short acting unlike the thyroid hormones
which are long-acting
• Gliclazide (SU) may be associated with hypoglycemic events, if the patient is experiencing hypoglycemic events
→ Gliclazide should be stopped
• High isolated ALP – B Bone, Biliary
- Bone → Bone metastasis, hyperparathyroidism, Paget’s disease, Osteomalacia
- Biliary → Cholestasis
- Pregnancy can also cause physiological increase in ALP
ENT
Otitis media with effusion
➢ Also known as glue ear, persistent build-up of fluid in the middle ear
➢ History of recurrent OM
➢ Issue stems from a dysfunction of the Eustachian tubes
Presentation
• Hearing diminished or lost (usually bilateral) → glue ear is the commonest cause of CHL in childhood
- Listening to the TV at excessively high volumes
- Needs things to be repeated
- Lack of concentration
- Withdrawal especially in school
• 2ry problems such as speech and language delay or behavioral problems
• Rarely complains of ear pain
• May have a prior history of infections (URTIs) or oversized adenoids
• Balance problems
• Peaks at 2 years of age
Signs (by otoscope)
• Retracted (more common) or bulging (less common) drum
• Dull, grey, or yellow tympanic membrane, there may be bubbles or a fluid level
Diagnosis
• Audiograms → conductive defects
• Tympanometry → assesses the ability of the eardrum to react to sound
Treatment
• <3 months → Reassure and review in 3 months
• >3 months → Surgery (insert grommets)
• If surgery is rejected → Hearing aids
- An important risk factor for OME is “parental smoking” → Always encourage parents of patients to stop smoking
- The light reflex (cone of light) is seen as a cone-shaped reflection in the anterior inferior quadrant of the TM
- Absence of the cone of light indicates distortion of the shape of the TM such as bulging due to an increase of
inner ear pressure seen in otitis media
ENT
Acute otitis media in children
➢ Acute inflammation of the middle ear and may be caused by bacteria or viruses
Features
• Rapid onset of pain (younger children may pull at the ear)
• Fever
Treatment of perforated OM
• Irritability
• Amoxicillin (5-days course)
• Coryza (rhinitis) • If penicillin-allergic → Erythromycin or clarithromycin
• Vomiting
• Often after a viral upper respiratory infection
• A red, yellow or cloudy tympanic membrane or bulging of the tympanic membrane
• An air-fluid level behind the tympanic membrane
• Discharge in the auditory canal secondary to perforation of the tympanic membrane
• Perforation of the eardrum often relieves pain. This is because bulging of the tympanic membrane causes
the pain
• Furuncles can be
found in diabetics or
low immunity
• Also called “boils”
• They’re infected hair
follicles
• MC organism →
Staph
• Red, hard, tender
• Self-limiting or
requires flucloxacillin
- Tenderness in movement of the tragus → Otitis externa

- If you’re treating otitis externa but suspect there may be a tympanic membrane perforation → aminoglycosides
ear drops are NOT the best choice as it’s toxic → use Ciprofloxacin drops
- Otitis externa with Pseudomonas (pus in the external canal) → topical gentamicin only or with topical
gentamicin with hydrocortisone (Gentisate HC)
ENT
Acoustic neuroma
➢ Also called “vestibular schwannomas”, accounts for 5% of intracranial tumors and 90% of cerebellopontine
angle
➢ Bilateral acoustic neuromas are seen in neurofibromatosis type II
Features
• Cranial nerve V → Absent corneal reflex
• Unilateral SNHL should be considered as caused by an
• Cranial nerve VII → Facial palsy acoustic neuroma until proven otherwise
• Cranial nerve VIII → SNHL, vertigo, tinnitus
Investigation
• MRI of the internal auditory meatus → to view the cerebellopontine angle
• MRI brain → for further evaluation
DVT = Deafness, Vertigo, Tinnitus

DVT + CN palsy = Acoustic neuroma
DVT + aural heaviness = Meniere’s disease
Meniere’s disease
Presentation
• Deafness, vertigo, tinnitus (DVT) + fullness in the ear (could be experienced with AN)
• Note: Vertigo → is usually the prominent symptom
• Episodes last minutes to hours
• MRI is normal
• Usually a female → male; 20-60 years old
• Typically, symptoms are unilateral but bilateral symptoms may develop after a number of years
Treatment
• Acute attacks → buccal or intramuscular prochlorperazine or cyclizine
• Admission is sometimes required
Vestibular schwannoma → high frequency SNHL, MRI is diagnostic, will have CN involvement
Meniere’s disease → low frequency SNHL
Otosclerosis → CHL + young age + patient reports better hearing in noisy places + precipitating factors like pregnancy
ENT
Otosclerosis
• Abnormal growth of bones of the middle ear preventing structures within the ear from working properly
• Most common cause of progressive deafness in young adults (CHL) (15-45 years)
• Tinnitus and vertigo
• Positive family history (50%) • Could be mixed hearing loss if cochlea is involved
• Usually bilateral (80%)
• Women + pregnant
Management
• Stapedectomy or stapedotomy, with the insertion of a prosthesis
• If surgery is rejected → Hearing aids
Peritonsillar abscess (Quinsy)

➢ Swelling of the soft palate and tissues lateral to the tonsils
➢ It’s a complication of acute tonsillitis
➢ Pus is trapped between the tonsillar capsule and the lateral pharyngeal wall
➢ Typically preceded by a sore throat for several days
Presentation
• Sore throat
• Dysphagia
• Pain localized to one side of the throat
• Peritonsillar bulge
• Uvular deviation (bulging tonsils push the uvula away from the affected side)
• Fever
• Trismus (difficulty opening the mouth)
• Fetor
• Drooling
• Altered voice quality (hot potato voice) due to pharyngeal edema and trismus
Management
• Antibiotics → IV benzylpenicillin
• Needle aspiration, incision and drainage
Tonsillar carcinoma → SCC, Lump in the neck

- RF: smoking, regular alcohol intake and HPV infection
- Direct spread often involves pharyngeal space and mandible
ENT
Hearing screening
➢ It’s offered to all babies within 4-5 weeks of birth
➢ Healthy born babies are normally given a hearing test before discharge otherwise it’ll be done during this
timeframe
2 types of tests
1. Automated otoacoustic emission (AOE)
- Soft-tipped earpiece is placed inside the ear to detect vibration of hair cells
2. Automated auditory brainstem response (AABR)
- Brain waves are measured by electrodes
- Can detect auditory neuropathy in children
Below 6 months → AOE or AABR

6 months – 18 months → Distraction test
2 years – 5 years → Conditioned response audiometry OR Speech discrimination
>5 years → Pure tone audiogram
Rinne’s and Weber’s
Rinne’s test
• A tuning fork is placed over the mastoid process until the sound is no longer heard, followed by repositioning
just over external acoustic meatus
• AC is normally better than BC → Positive Rinne's test (normal)
• If BC > AC, then the patient has conductive deafness → Negative Rinne’s test (Abnormal Rinne’s test)
Weber's test [CSSO]

• A tuning fork is placed in the middle of the forehead equidistant from the patient's ears. The patient is then
asked which side is loudest
• If sound is localized to the unaffected side → Unilateral SNHL
• If sound is localized to the affected side → Unilateral CHL
• SNHL = localized to the normal ear
Example
If Weber’s test localizes to the right side. It can either be right CHL or left SNHL, a Rinne’s test would be able to
confirm if it’s a right CHL
ENT
Candida vs LP vs Leukoplakia
Leukoplakia should be biopsied as it’s premalignant

Leukoplakia occurs primarily in HIV-positive individuals
For oral candidiasis → Nystatin suspension can be used
Leukoplakia may present with dysplasia of the vocal cords
- White patches over the vocal cord + hoarseness of voice
- Management → cessation of smoking and observation, as it might turn malignant
Difference between oral thrush (oral candidiasis) and Leukoplakia → Leukoplakia CANNOT be removed by rubbing
Ludwig’s angina
- Severe cellulitis involving the floor of the mouth
- Early, the floor of the mouth is raised and there’s difficulty swallowing saliva which might be drooling
- Usually following a dental infection
Dysphagia + Odynophagia + radiates to the back → Esophageal candidiasis, caused by candida albicans
ENT
Cholesteatoma
➢ Destructive and expanding growth consisting of keratinizing squamous epithelium in the middle ear and/or
mastoid process
➢ Uncommon abnormal collection of skin in the ear that left untreated can continue to grow and damage the
bones of the middle ear (ossicles)
➢ Small lesions → CHL, Large lesions → CHL + vertigo + headache + facial nerve palsy
Acquired
• Following repeated ear infections, they’re usually responsive to antibiotics
• Frequent painless otorrhea which may be foul-smelling
• Progressive, unilateral CHL
• TM perforation (90%) or retracted tympanum
• Otoscopy:
- Retraction pocket in attic or posterosuperior quadrant of TM
- Granular tissue
- White mass behind eardrum
- Purulent drainage
Congenital
• Present 6 months – 5 years, sometimes later in adulthood
• Often NO history of recurrent suppurative ear disease, previous ear surgery or TM perforation
• May be incidental finding on routine otoscopy of an asymptomatic child
• Otoscopy → Spherical pearly white mass behind intact membrane
Vestibular neuritis
➢ Inflammation of the vestibulocochlear nerve (CN VIII), but the etiology is thought to be a vestibular
neuropathy
Features
• Abrupt onset
• Recurrent vertigo (lasting hours-days)
• Unsteadiness, nausea and vomiting (feel as if the room is rotating)
• Symptoms are aggravated by head movement
• History of viral infection (runny nose, cough, fever)
Vestibular neuritis → commonly present with a history of viral infection + lasts hours-days
BPPV → lasts seconds
Labyrinthitis
- Vestibular nerve and labyrinth are affected
- Same as vestibular neuritis + Hearing loss (SNHL) ± tinnitus
Vertebrobasilar insufficiency (VBI)
- Very old male
- Most common cause → atherosclerosis
- RF: DM, HTN, smoking and dyslipidemia
ENT
Temporomandibular disorders (TMDs)
• A group of disorders affecting tempomandibular joint (TMJ), masticatory muscles and associated structures
• Associated with muscle overactivity which include bruxism (grinding of teeth)
• Symptoms → Facial pain, restricted jaw function and joint noise
• Pain is around the temporomandibular joint but is often referred to the head, neck and ear
• Managed by ice packs, NSAIDs, dental splits or Botox injections
Pleomorphic adenoma
• The most common tumor of the parotid gland
• They’re benign tumors which appear as a lump just behind the angle of mandible
• Benign with the capacity to turn malignant
Features
• Slow-growing and asymptomatic
• Firm
• Painless
• Mobile
Management
• Superficial parotidectomy or enucleation
- Tender and painful mass at the angle of the mandible, especially when eating → Parotiditis
- Mobile, soft, cystic and tender mass → Adenolymphoma (Warthin’s tumor)
- Mandibular and tonsillar tumors are NOT mobile
Sialadenitis
➢ Inflammation of salivary gland and may be acute or chronic, infective or autoimmune
Features
• Unilateral redness, swelling and pain
• May enlarge to reach a size of an orange
• Mild odynophagia, usually common before and during meals
• Fluctuation test positive if it’s filled with swelling
• Foul taste in the mouth
• Decreased mobility in the jaw
• Dry mouth, skin changes, weight loss, shortness of breath, keratitis, dental pain, skin changes and
lymphadenopathy
• Fever with rigors and chills along with malaise and generalized weakness as a result of septicemia
• In severe cases → pus can often be secreted from the duct by compressing the affected gland
• Duct orifice is reddened with reduced flow, there may be a visible or palpable stone
Acute sialadenitis
- Typically, present with erythema over the area, pain, tenderness on palpation and swelling
- Infection often occurs as a result of dehydration with overgrowth of oral flora (e.g. postoperative
dehydration)
- Purulent material may be observed
Chronic sialadenitis
- Less painful + gland enlargement (often following meals) WITHOUT erythema
- Associated with decreased salivary flow due to stones rather than dehydration
ENT
Nasal polyps
• Lesions arising from the nasal mucosa, occurring at any site in the nasal cavity or paranasal sinuses
• Nasal polyps tend to be bilateral
• Associated with → Asthma, Aspirin sensitivity (Samter’s triad)
Presentation [RAN]
• Rhinorrhea
• Anosmia (loss of smell)
• Nasal obstruction
Laryngeal cancer
Presentation
• Progressive hoarseness of voice → most common early symptom
• Later, Stridor, dysphagia and odynophagia
• If the pharynx is involved → Hemoptysis and ear pain • HPV → RF for tonsillar, oropharyngeal and
Risk factors laryngeal cancer
• Smoking → 1 st
• Occupational exposures (asbestos, formaldehyde, nickel, isopropyl alcohol and sulphuric acid mist)
• Insufficient fruit and vegetables intake
• HPV 16
Nasopharyngeal carcinoma
• Painless swelling or lump in the upper neck, often due to a swollen LN
• Nasal obstruction, epistaxis and otitis media from eustachian tube obstruction
• Unilateral CHL + tinnitus
• Other cranial nerves involvements
Risk factors EBV is associated with:
• Smoking, Alcohol • Hodgkin’s lymphoma
• Infection with EBV • Nasopharyngeal carcinoma
• South Asian, male
Nasopharyngeal carcinoma → Ear symptoms

Paranasal sinus tumors → Prominent ocular symptoms (e.g. epiphora, double vision)
Oropharyngeal cancer (tonsillar cancer)
- At the base of tongue, tonsils, soft palate and walls of the pharynx
- Associated with ear pain
- Often involves pharyngeal space and mandible
Malignant otitis externa
- An aggressive infection rather than a malignancy
- CHL + foul-smelling purulent otorrhea + facial nerve palsy
- Black skin around the ear
- RF: DM, weakened immune system
- Urgent refer to an ENT specialist is usually needed
ENT
Acute tonsillitis
Symptoms
• Sore throat
• Pain referred to the ear
Signs
• Throat is reddened
• Tonsils are swollen and may be coated or have white flecks of pus on them
• Fever
• Swollen regional LNs
• Examination shows intense erythema of tonsils and pharynx, yellow exudate and tender, enlarged anterior
cervical glands
3 or 4 of the Centor Criteria → Bacterial tonsillitis → Antibiotics (Penicillin V)

• Fever >38
• Tonsillar exudates
• No cough
• Tender anterior cervical
lymphadenopathy
Infectious mononucleosis
- Affects teenagers more often
- Very large purulent tonsils and long-
lasting lethargy
- Splenomegaly
Tonsillectomy
• Aim → Reducing the incidence if recurrent infections
• Indications → children with no other explanation for recurrent symptoms + frequency of symptoms
- >7 episodes per year for one year
- >5 episodes for 2 years
- >3 episodes for 3 years
• Complications
- Primary hemorrhage → may require a return to theatre
- Secondary hemorrhage → antibiotics and antiseptic mouthwashes
Otherwise, tonsillitis is treated with Analgesics (paracetamol and ibuprofen)

If tonsillitis + exudates + cervical lymphadenopathy + fever >38 → Antibiotics
ENT
Presbycusis
➢ Also known as age-related SNHL → most common cause of hearing impairment in elderly patients
➢ Etiology → degenerative changes in the inner ear (hair cells inside the cochlea)
Features
• Progressive high-frequency hearing loss
• Bilateral
• Usually occurs after age 50
• Difficulty understanding speech, especially in noisy environments
• Usually brought in by the family to clinics as the patient would not think his/her hearing is impaired
Management
• Hearing aids, to increase the high-frequency sound
The graph shows that hearing threshold level goes down as the frequency increases which is a feature seen in
presbycusis
Functional dysphonia
➢ Disturbance of voice in the absence of any structural abnormality of the larynx or any cord paralysis
➢ Diagnosed by exclusion
➢ There may be various interacting causes such as overuse of the voice, poor vocal technique and stress
➢ May occur after treatment of acute respiratory infection (if prior ttt of infection → Laryngitis)
Features
• Vocal fatigue (voice becoming worse with use) and laryngeal discomfort
Noise-induced hearing loss (NIHL)

• Hearing impairment resulting from exposure to loud sound
• Usually bilateral high frequency SNLH
- Acoustic trauma such as gun shooting or bomb explosion and barotrauma (such as sudden changes in pressure
like driving) → TM perforation → CHL
- Acoustic trauma → Sudden
- NIHL → Chronic
ENT
Management of ear wax buildup
1. Ear wax softeners
- Sodium bicarbonate, sodium chloride, olive oil can be used
- Prescribe for 2-3 days initially
2. If symptoms persist → Ear irrigation
3. If irrigation is unsuccessful
- Ear drops are advised for further 3-4 days and then return for further irrigation
- Instill water into the ear, after 15 mins → irrigate the ear
- Refer to ENT specialist
Management of epistaxis
1. Lean forward, open mouth, press soft nose for 10-15 minutes
2. Nasal cautery with silver nitrate
3. Nasal packing
After stopping the bleeding, if unstable → transfer to A&E
ENT
Notes
• An insect buzzing and stuck in the external ear → 2% Lidocaine, to kill it then remove it by Olive oil
• Soft objects, organic matter or seeds stuck in the ear → Suction with a small catheter
• Large clearly visible foreign bodies in adults or older children → Bayonet forceps
• Styrofoam or chewing gum → Acetone
• Superglue → Manual removal, in 1-2days after desquamation, or referral to the ENT specialist
• Batteries → Urgent ENT referral, removed within 24h
• Ear wax → Olive oil, to loosen the hard wax
• Any spherical object → Hook, can’t be grasped by forceps
• An intellectually-disabled patient with a foreign object in the ear → Removal under general anesthesia
• Indications for ENT referral:
- Uncooperative patient
- Requiring sedation
- Perforated ear drum
- An adhesive in contact with the eardrum
- Difficulty removing the foreign body
• Ear trauma with bleeding, tinnitus and CHL, possible nausea and vomiting initial investigation → Otoscopy
• RTA with bleeding and CSF leakage from the ear (a possible basilar fracture) → CT scan
• Small perforation the TM → Reassure
• Large perforation of the TM → Refer to a specialist
• Flamingo pink (Schwartz sign) → Otosclerosis
• Cartwheel appearance of the TM → Acute suppurative otitis media
• Chalky white patches on the TM → Tympanosclerosis
• Sudden vertigo + vomiting + preceding URTI → Labyrinthitis
• Difficulty hearing in noisy environment → Presbycusis
• Difficulty hearing in quiet environment → Otosclerosis
• Form of acute OM where vesicles develop on the TM, pain occurs suddenly and persists for 24h-48h, hearing
loss and fever suggest a bacterial origin → Myringitis
• Any salivary gland mass for more than 1 month → FNAC
• Paget’s disease + OI → Mixed hearing loss
• Headache worsens when bending forward + NO nausea or vomiting → Chronic sinusitis
• Headache worsens when bending forward + nausea, vomiting, photosensitivity → Migraine
• Swelling that moves up on swallowing → Goiter
• Moves up on swallowing and tongue protrusion → Thyroglossal cyst
• Fluctuant and transluminate → Cystic hygroma, a fluid-filled sac due to a blockage in the lymphatic system
• Pain at the cheeks preceded by URTIs + upper jaw pain/toothache → Maxillary sinusitis
• Same but pain at the nose bridge → Ethmoidal sinusitis
• Same but pain above the orbit → Frontal sinusitis
• Causes of SNHL:
- Acoustic neuroma
- Meniere’s disease
- Presbycusis → Bilateral
- Labyrinthitis
• Blunt trauma to the ear pinna with only redness → Oral analgesia
• Blunt trauma to the pinna with hematoma (bluish discoloration) → Incision and drainage + Oral antibiotics
• If left untreated, it will lead to → Cauliflower ear
GENERAL SURGERY
Inguinal hernia:
- Boundaries of Hesselbach's Triangle

• Medial: Rectus abdominis
• Lateral: Inferior epigastric vessels
• Inferior: Inguinal ligament
- Contents of the inguinal canal: Spermatic cord (round ligament) + Ilioinguinal nerve
- Direct inguinal hernia is medial to the inferior epigastric artery while indirect is lateral
- Inguinal hernias are ABOVE and medial to the pubic tubercle while femoral hernias are BELOW and lateral
- A small indirect inguinal hernia could be above and lateral to the PT
- Inguinal hernias has impulse on coughing
- Femoral hernias are usually irreducible (due to narrow femoral canal)

and cough impulse rarely detectable
- Only indirect inguinal hernias can extend into the scrotum
- Incarcerated: fixed to the wall, Strangulated: obstructed bl. supply
- Femoral hernia: (NAVY VAN)
- Groin hernias:
Direct inguinal hernia Indirect inguinal hernia Femoral hernia
Risk of
Low risk of strangulation Low risk of strangulation High risk of strangulation
strangulation
Age Seen in adults May occur in infants Seen in adults
Much more common in Much more common in

Gender More common in females
males males
GENERAL SURGERY
Breast anatomy
Breast cancer
• Invasive ductal carcinoma. This is the most common type of breast
cancer. been renamed 'No Special Type (NST)'. Other types are
classified as 'Special Type'
• Invasive lobular carcinoma
• Ductal carcinoma-in-situ (DCIS)
• Lobular carcinoma-in-situ (LCIS)
Predisposing factors
• BRCA1, BRCA2 genes - 40% lifetime risk of breast/ovarian cancer
• 1st degree relative premenopausal relative with breast cancer (e.g. mother)
• Nulliparity, 1st pregnancy > 30 years (twice risk of women having 1st child < 25 years)
• Early menarche, late menopause (risk increases with more menstrual cycles as breast undergoes division
and apoptosis, that increases the risk of genetic mutation and tumor formation)
• Combined hormone replacement therapy (relative risk increase * 1.023/year of use), COCP
• Past breast cancer
• Not breastfeeding Decreased risk
• Ionizing radiation • Early pregnancy
• Longer time breastfeeding
• p53 gene mutations
• Obesity
• Previous surgery for benign disease (more follow-up, scar hides lump)
Management
1) Surgery: Around two-thirds of tumors can be removed with a wide-local excision.
Mastectomy Wide Local Excision
• Multifocal tumor • Solitary lesion
• Central tumor • Peripheral tumor
• Large lesion in small breast • Small lesion in large breast
• DCIS > 4cm • DCIS < 4cm
2) Radiotherapy: to reduce recurrence.
3) Hormonal therapy: when tumor cells have hormone receptors, it blocks the effects of the hormones such as
estrogen. Tamoxifen in pre-menopausal, in post-menopausal, aromatase inhibitors such as anastrozole (side-
effects of tamoxifen include an increased risk of endometrial cancer, venous thromboembolism and menopausal symptoms)
4) Biological therapy: Trastuzumab, useful for HER-2 positive. Noting that it cannot be used in cardiac patients
5) Chemotherapy
GENERAL SURGERY
Histopathological findings in different breast lesions
Breast cancer (invasive intraductal) • Invasive ductal carcinoma extending to the epithelium
Paget’s disease of the breast • In situ carcinoma involving the nipple epidermis
• Well-circumscribed lump with clear margins and separate from the

Fibroadenoma surrounding fatty tissue, there’s overgrowth of fibrous and glandular
tissue
FibroadenoCIS • Fibrosis + epitheliosis with cystic formation
Fibrocystic changes of the breast • Cystic formation with mild epithelial hyperplasia in ducts
Core biopsy = tru-cut biopsy

Sentinel LN biopsy is done for staging
Breast cancer screening

• Women aged 50-70 years are offered mammogram every 3 years
• In high risk group, mammogram would be offered annually from ages 40-69
Triple assessment of the breast

1. Clinical
2. Radiology
- <35 → USG
- >35 → Mammogram
3. FNAC
- USG is used in young patients instead of mammogram due to increased tissue density which reduces sensitivity and
specificity of a mammography
- There’re four instances in which prophylactic mastectomy is advised:
1. Strong family history of breast cancer
2. Presence of gene mutations (BRCA1 or BRCA2)
3. Previous cancer in one breast
4. Biopsies showing lobular carcinoma in situ and\or atypical hyperplasia of the skin
- Remember, prophylactic bilateral mastectomies and prophylactic bilateral oophorectomies are offered in cases in
which patients has a strong family history and has genetic markers for the cancer
Axillary lymph node clearance

Indications
• SLNB
• Invasive breast cancer
Common complications
• Numbness around the scar and upper arm (can be permanent)
• Lymphoedema (localized fluid retention and tissue swelling caused by a compromised lymphatic system)
• Seroma (fluid collection at the site of operation)
• Frozen shoulders
GENERAL SURGERY
Breast disorders
Disorder Features
• < 30 years
Fibroadenoma • Often described as 'breast mice' as they are firm, discrete, non-
tender, highly mobile lumps
FibroadenoCIS (fibrocystic • Middle-aged women

disease) (Benign mammary • Lumpy breasts which may be painful
dysplasia) • Symptoms may worsen prior to menstruation
• Hard, irregular lump

Breast cancer
• There may be associated nipple inversion or skin tethering
• Chronic eczematous changes (itching – erythema – scales – blood

stained nipple discharge – inverted nipple)
Paget's disease of the breast
• Usually unilateral
• Diagnosed by punch biopsy
• Dilatation of the large breast ducts

• Most common around the menopause
• May present with a tender lump around the areola
Duct ectasia
• Green or brown nipple discharge
• Nipple retraction
• Associated with smoking
• Hyperplastic lesions rather than malignant or premalignant

Duct papilloma • Most common cause of blood-stained nipple discharge
• There could be skin changes
• More common in lactating women

Breast abscess • Unilateral, red, hot tender and fluctuant swelling
• May present with purulent nipple discharge
• More common in obese women

• May follow trivial or unnoticed trauma
Fat necrosis • Firm & solitary localized lump and usually painless
• Skin around the lump maybe red, bruised or dimpled
• Rare and may mimic breast cancer so further investigation is always
warranted
• Suggested by para-areolar discharge

• May follow abscess drainage or incision, there may be history of a
Ductal fistula spontaneous rupture of inflammatory mass preceding the fistula
• Managed by excision under antibiotic cover
• Recurrence is common
- Lipomas and sebaceous cysts may also develop around the breast tissue
- fibroadenoCIS is CYStic and CYClical
GENERAL SURGERY
Haemorrhoids
➢ Haemorrhoidal tissue is part of the normal anatomy which contributes to anal continence. These mucosal
vascular cushions are found in the left lateral, right posterior and right anterior portions of the anal canal (3
o'clock, 7'o'clock and 11 o'clock respectively). Haemorrhoids are said to exist when they become enlarged,
congested and symptomatic
Features
• Painless rectal bleeding → the most common symptom
• Pruritus
• Pain: intermittent and usually not significant unless piles are thrombosed
• Soiling may occur with third- or fourth-degree piles
Types Proctalgia fugax
External • Severe recurrent rectal shooting pain
• Originate below the dentate line (lower 1/3 of the anal canal) in the absence of any rectal disease
• Usually occurs at night, after bowl
• Prone to thrombosis, may be painful
action or following ejaculation
Internal • Anxiety is an associated feature
• Originate above the dentate line (upper 2/3)
• Do not generally cause pain
Grading of internal haemorrhoids:

Grade I Do not prolapse out of the anal canal
Grade II Prolapse on defecation but reduce spontaneously
Grade III Can be manually reduced
Grade IV Cannot be reduced
Management:
• Soften stools → increase dietary fiber and fluid intake
• To alleviate symptoms → topical local anesthetics and steroids may be used
• Outpatient treatments → rubber band ligation is superior to injection sclerotherapy
• Surgery → reserved for large symptomatic haemorrhoids which do not respond to outpatient treatments
• Newer treatments: Doppler guided hemorrhoidal artery ligation, stapled haemorrhoidopexy
Acutely thrombosed external haemorrhoids

• typically present with significant pain
• examination reveals a purplish, edematous, tender subcutaneous perianal mass
• if patient presents within 72 hours → referral should be considered for excision
• Otherwise patients can usually be managed conservatively with stool softeners, ice packs and analgesia
• Symptoms usually settle within 10 days
Anal fissure
• Exquisite pain with defecation FRESH blood streaks covering the stools
• The fear of pain is so intense they avoid bowel movements and get constipation
• They refuse PR exam → PR done under anesthesia
• Acute: <6 weeks, chronic > 6 weeks
- Anal fistula: if low-submucosal or simple → Lay open (fistulotomy), if complex/high (cross internal and external
sphincters) → Seton suture (ligation of fistula tract)
- Complex fistulas can NOT be laid open as it could result in fecal incontinence
GENERAL SURGERY
Pancreatic cancer
➢ 60% are adenocarcinoma that occurs at the head of the pancreas.
Risk factors
• Smoking
• Alcohol is an indirect RF as it causes chronic pancreatitis and liver cirrhosis
• Diabetes
• Chronic pancreatitis
Features
• Head: - Obstructive jaundice → Dark urine, pale stool, pruritis.
• Maybe painless although 70% are associated with epigastric or LUQ pain radiating to the back.
• Body or Tail: Epigastric or LUQ pain radiating to the back, relieved by sitting forward
• Both: Anorexia, weight loss or atypical weight loss
• Migratory thrombophlebitis (Trousseau sign): felt as small lumps under the skin
Investigations
• CA19-9 → non specific
• Transabdominal US
• CT
Management
• Whipple’s resection (Pancreaticoduodenectomy): considered when no metastasis.
- Side-effects → dumping syndrome (a group of symptoms, including weakness, abdominal discomfort, and
sometimes abnormally rapid bowel evacuation, occurring after meals in some patients who have
undergone gastric surgery) and peptic ulcer disease
• ERCP with stenting for palliation
Cholangiocarcinoma
➢ Rare cancer of the bile duct
Features
• Jaundice
• RUQ pain
• Weight loss
Bowel cancer screening

• Men and women aged 60-74 years old are sent a self-administered kit every 2 years
• Fecal immunological test (FIT) → self-administer kit that can be can be sent via the post
• One-off bowel scope test at 55 years
There are 3 screening programs in the UK → Breast, Ovarian and Bowel cancer
GENERAL SURGERY
Abdominal pain
Condition Characteristic exam feature
• Duodenal ulcers → more common than gastric ulcers, epigastric pain relieved by eating
Peptic ulcer disease • Gastric ulcers → epigastric pain worsened by eating
• Features of upper gastrointestinal hemorrhage may be seen (hematemesis, melena etc.)
• Pain initial in the central abdomen, then right iliac fossa

• Anorexia is common
Appendicitis • Tachycardia, low-grade pyrexia, tenderness in RIF
• McBurney sign → rebound tenderness at McBurney point
• Rovsing's sign → more pain in RIF than LIF when palpating LIF
• Usually due to gallstones or alcohol

• Severe epigastric pain
Acute pancreatitis • Vomiting is common
• Examination may reveal tenderness, ileus and low-grade fever
• Periumbilical discoloration (Cullen's sign) and flank discoloration (Grey-Turner's sign)
• RUQ radiates to the right shoulder or the back and interscapular region
• May be following a fatty meal. Slight misnomer as the pain may persist for hours
Biliary colic (4F) • Obstructive jaundice may cause pale stools and dark urine
• It is sometimes taught that patients are female, forties, fat and fair
• Managed as acute cholecystitis
• History of gallstones symptoms (see above)

• Continuous RUQ pain.
• Jaundice is NOT usually present with cholecystitis
• Fever, raised inflammatory markers and white cells
Acute cholecystitis • Murphy's sign positive (arrest of inspiration on palpation of the RUQ)
• US → thick-walled, shrunken gallbladder
• TTT → nil by mouth – analgesics (morphine) – IV fluids – antibiotics
• Surgery → Laparoscopic cholecystectomy is usually indicated if patient is fit, if
perforated GB → Open surgery
• Colicky pain typically in the LLQ

Diverticulitis
• Fever, raised inflammatory markers and white cells
• Severe central abdominal pain radiating to the back

Abdominal aortic • Presentation may be catastrophic (e.g. Sudden collapse) or sub-acute (persistent severe
aneurysm central abdominal pain with developing shock)
• Patients may have a history of cardiovascular disease
• History of malignancy/previous operations

Intestinal • Vomiting
obstruction • Not opened bowels recently
• 'Tinkling' bowel sounds
GENERAL SURGERY
Management of biliary colic (when stones occlude the cystic duct):
1. Analgesia
2. Nil by mouth
3. Rehydrate
4. Elective laparoscopic cholecystectomy is usually indicated
- Complications of tonsillectomy:
• Intraoperative
- 2ry hemorrhage is caused by necrosis of the blood vessels
- Hemorrhage → replace the loss related to a previous repair, often precipitated by wound
- Dental trauma infection. The best step is admission and IV antibiotics.
• Postoperative
- Reactive bleeding (during 24hours post-op) → explore + replace the loss
- 2ry bleeding (up to 7days post-op) → admission + IV antibiotics
- Temporary dysphagia.
Thyroglossal cyst:
• Asymptomatic fluid-filled midline neck mass below the level of hyoid bone
• Most often in children and adolescents
• Most common cause of midline masses in children → accounts for 75% of midline masses in children
How to diagnose?
1. US neck: to distinguish between solid and fluid-filled cyst → It can confirm the diagnosis
2. MRI & CT: when malignancy is suspected\Large cyst
3. Thyroid scan with tc-99m: to determine if there’s ectopic thyroid tissue
4. FNAC
- In elective/planned operations:
• Hb < 10 g/l → investigate and postpone
• Hb < 8 g/l → transfusion
- In emergency operations:
• Hb < 10 g/l → proceed
• Hb < 8 g/l → transfusion and stabilize before proceeding
- Post-op hypovolemia and oliguria can be caused by:

• Hemorrhage
• Adrenal cortex and posterior pituitary response to stress which release aldosterone and ADH respectively
- if the patient developed post-op hypotension and subsequent oliguria, it can be corrected by fluid challenge
- Fluid challenge:
• Rapid (up to 15 mins) administration of 500 ml crystalloid (normal saline/Hartmann’s)
• Immediate reassessment, if there’s still evidence of hypovolemia → administer a further bolus of 250-500 ml
of a crystalloid
- post-op oliguria:
• Normotensive → recheck the catheter
• Hypotensive = intra-abdominal bleeding → IV fluids
GENERAL SURGERY
Carpal tunnel syndrome is caused by compression of median nerve in the carpal tunnel
History
• pain/pins and needles in thumb, index, middle finger
• unusually the symptoms may 'ascend' proximally
• patient shakes his hand to obtain relief, classically at night
Examination
• weakness of thumb abduction (abductor pollicis brevis)
• wasting of thenar eminence (NOT hypothenar)
• Tinel's sign: tapping causes paresthesia De Quervain’s tenosynovitis
• Phalen's sign: flexion of wrist causes symptoms • Also called “Washerwoman sprain”, “Mummy
Causes thumb” or “Gamer’s Thumb”
• idiopathic • Caused by inflammation of the extensor pollicis
• pregnancy previs and the abductor pollicis longus due to
• edema e.g. heart failure repetitive stress injury
• lunate fracture • Commonly occurs at in women following
pregnancy due to the way in which the baby is
• rheumatoid arthritis
lifted and held
Electrophysiology
• motor + sensory: prolongation of the action potential
Treatment
• corticosteroid injection
• wrist splints at night
• surgical decompression (flexor retinaculum \ transverse carpal ligament \ anterior annular ligament)
After any GI surgery, there are 3 main concerns:

1. Anastomotic leaks are defined as ‘a leak of luminal contents from a surgical join between two hollow viscera’
• RF → immunosuppressed, corticosteroids, smoking, diabetes, peritoneal contamination, rectal anastomosis
• C/P → abdominal pain and fever, typically 5-7 days post-operatively
• Definitive investigation → CT with contrast
• Management → bowel rest (NBM), IV antibiotics and IV fluid. Minor leaks maybe managed through
observation and bowl rest alone with drainage if needed while exploratory laparotomy if a major leak
• Complication → peritonitis where there’s severe generalized abdominal pain with generalized guarding and
rigidity
2. Post-op bleeding
• reactive bleeding (during 24hours post-op) • Hot tip: if the patient present 10 days after bowel surgery
• 2ry bleeding (up to 7days post-op) with abdominal pain, it’s most likely anastomotic leak
3. Surgical site infection and subsequent sepsis
- Most common post-op complication is INFECTION
- It’s better to remove the catheter post-op in 24-48h using TWOC procedure. Reinsert again if
1) PVRVs is 300-500ml with discomfort, voiding problems or feeling of fullness 2) PVRVs >500ml
- PVRV is measure by ‘bladder scan’
GENERAL SURGERY
Perianal hematoma (external thrombosed

Perianal abscess
hematoma)
➢ Acute pain + Bluish/purple in color ➢ Red and tender + Throbbing pain (worsens when sitting
➢ tender peri-anal lump near the anal down).
verge ➢ Usually with low immunity/Diabetes/Crohn’s
➢ History of straining ➢ Can be associated with constipation
➢ TTT: ➢ TTT:
- Analgesics, stool softeners - Incision and drainage
- Incision and drainage - Antibiotics
- Antibiotic prophylaxis (IV) in colonic surgery should be given at the time of induction of anesthesia or within the
first 30 mins of the first excision:
• Cefuroxime: to cover gram -ve and +ve.

• Metronidazole: against anaerobic bacteria.
Esophageal atresia:
• Prenatal signs → Polyhydramnios, small stomach, absent fetal stomach bubble detected on US
• Postnatal signs → Cough, airway obstruction, secretions, blowing bubbles, distended abdomen, cyanosis,
aspiration. Inability to pass a catheter into the stomach → X-ray show it coiled in the esophagus
- Duodenal atresia: X-ray show double bubble sign (stomach & duodenum).
- Gastroschisis and exomphalos are two rare birth defects that cause a baby to be born with some of their internal
organs extending out of the body through a hole in the belly
exomphalos gastroschisis
hole in belly button hole next to belly button
intestines covered by protective sac intestines not covered by a protective sac
Gastric carcinoma
• C/P: non-specific as vomiting, tiredness, weight loss, abdominal pain and anemia
• RF: - Aging
- H. pylori infection
- Blood group A Enlarged right supraclavicular LNs:
- Gastric adenomatous polyp • Lung cancer
- Pernicious anemia • Esophageal cancer
- Smoking • Hodgkin’s lymphoma
- Diet: salty, spicy, nitrates

• Signs suggesting incurability:
- Troisier’s sign: enlarged left supraclavicular lymph nodes (Virchow’s LN)
- epigastric mass
- hepatomegaly
- jaundice
- ascites
GENERAL SURGERY
Pancoast tumor
- Tumor of the pulmonary apex, on top of the right or left lung
- Spreads to nearby tissues like ribs and vertebrae
- Most are NSCLC
Paralytic ileus: cessation of GI motility

• Causes:
- prolonged surgery, exposure and handling of the bowel
- peritonitis and abdominal trauma
- electrolyte disturbance
- Absent bowl movements + NO pain → Paralytic ileus
- anticholinergics and opiates - Exaggerated bowl sounds + pain → Mechanical obstruction
- immobilization
• Clinical picture:
- nausea, vomiting
- abdominal distension
- absent bowel sounds
• Imaging: Abdominal x-ray to show air/fluid filled loops of small and/or large bowel
• Management: (Drip & Suck)
- NG tube to empty the stomach from fluid & gas when the patient is nauseated or vomiting
- IV fluid
- Maintain electrolyte balance
- Reduce opiates and analgesia
- Encourage the patient to mobilize
- Lactulose or erythromycin can stimulate bowl movement
inflammation of the diverticulum, common in >50yrs and low fiber intake

• C/P: - All patients with diverticular disease who are
- Rapid onset of LIF pain and tenderness symptomatic or hemodynamically unstable require urgent
- Nausea and vomiting admission
- Bloating and constipation - Colonoscopy is contraindicated in acute diverticulitis
- Intussusception: pain is non-specific and intermittent
- Diarrhea
- Features of infection: fever, tachycardia, raised WBCs and high CRP (>50 mg/L)
- If perforated → guarding and rigidity
• Investigations: CT abdomen and pelvis
• Treatment:
- IV Antibiotics + IV Fluids
- Increase dietary fiber intake
• Complications: Massive rectal bleeding that requires admission.
- Diverticulum (plural diverticula): herniation of the large colon

- Diverticulosis: the presence of asymptomatic diverticula
- Diverticular disease: symptomatic diverticula - Hot tip: Diverticulitis is a left-side appendicitis
- Diverticulitis: inflammation of the diverticula
GENERAL SURGERY
Sigmoid volvulus: torsion of the colon around its mesenteric axis resulting in compromised blood flow and closed
loop obstruction
• Usually an elderly man with chronic constipation
• C/P: patient suddenly develops a classic picture of painful intestinal obstruction:
- abdominal distension
- vomiting (classically with no nausea?)
- pain
- absolute constipation
• Investigation: X-ray shows a coffee bean sign (omega sign)
• Management: rectal tube decompression, laparotomy and resection
Colorectal cancer
➢ Rt-sided colon cancer > Anemia, Lt-sided colon cancer > Obstructive symptoms
➢ Rt-sided colon cancer (cecum, ascending colon) tend to be exophytic so it rarely causes obstruction of feces
➢ Old + changing bowel habits + bleeding PR + single ulcer = Colorectal cancer until proven otherwise
➢ Diagnosed by colonoscopy with biopsy, barium enema, CT scan
- CEA is NOT for diagnosis however it’s useful for monitoring

- Anemia is not evident with left sided cancer because:
1. Bleeding is noticed as fresh blood with stool, cancer cecum is far away, it won’t be presented with fresh blood
2. Right colon is wider than left colon → obstruction is more prominent with the left side, let alone its exophytic
nature
- Krukenberg Tumor: bilateral ovarian malignancy due to metastasis from GIT cancer (most commonly gastric
carcinoma)
- Risk factors for colon cancer → 1- Age. 2- Family history. 3- Smoking.
GENERAL SURGERY
Pleomorphic adenoma (benign mixed tumor):
• most common salivary gland tumor
• Parotid > submandibular > sublingual
• Painless + slowly growing
• Firm, single, nodular mass and usually mobile
• Benign and can become malignant
• Treated by superficial parotidectomy or enucleation
Adenolymphoma
- mobile, soft, cystic mass and usually painless
(Warthin’s tumor)
- bilateral swelling of all salivary glands
Mikulicz’s disease
- welling of lacrimal glands resulting into narrowing of palpebral fissure
- pain especially when eating
Parotiditis
- fever, redness, swelling
- excessive sweating on cheeks when eating instead of salivation
Frey’s syndrome
- due to nerve damage as a parotid surgery complication
Common tumor markers:
Seminoma > LDH
- MRCP is an alternative to diagnostic ERCP for imaging the biliary tree and investigating biliary obstruction. A major
feature of MRCP is that it is not a therapeutic procedure, while in contrast ERCP is used for both diagnosis and
treatment.
- MRCP is used when US cannot detect CBD stones while the duct is dilated and/or LFT are abnormal.
Oropharyngeal carcinoma:
• Typical old patient, smoker
• Persistent sore throat
• A lump in the mouth or throat
• Referred otalgia
• Difficulty swallowing or moving mouth or jaw
• Unexplained weight loss
GENERAL SURGERY
Mesenteric ischemia vs Ischemic colitis
Mesenteric ischemia Ischemic colitis
• Embolic (in patients with AF) causing total loss of • Multifactorial (thrombotic event
blood supply to one segment of the bowel or hypoperfusion such as shock,
Etiology • decreased mesenteric arterial blood supply (in HF or MI) causing transient
patients with hypotension 2ry to myocardial interruption of blood supply
ischemia)
• sudden onset of abdominal pain • gradual onset (over hours)

• severity of the pain exceeds the physical signs • pain starts at the LIF
Clinical features • absent bowel sounds • moderate colicky pain and
• abdominal distension and tenderness tenderness with bloody diarrhea
• metabolic acidosis with high lactate
• resuscitate (O2), rehydrate and administer IV

analgesics and IV antibiotics • conservative
Management
• Urgent surgery to remove or bypass obstruction • surgical
• removal of necrotic bowel maybe required
Ramsay Hunt syndrome (herpes zoster oticus) is caused by the reactivation of the varicella zoster virus in the
geniculate ganglion of the facial nerve.
• Features
- Pain deep within the ear is often the first feature (often radiates to the ear pinna)
- facial nerve palsy
- vesicular rash around the ear
- other features include vertigo and tinnitus
• Management
- oral acyclovir and corticosteroids are usually given
Pain ladder:
1. Simple analgesics: aspirin, NSAIDs
2. Weak opioids: codeine, tramadol
3. Strong opioids: morphine, fentanyl, diamorphine, oxycodone
4. Nerve block epidural
- After myocardial infarction, elective surgery should not be performed for the next 6 months
- Blood pressure will be raised in any patient who’s in pain
- Superior laryngeal nerve injury → Dysphonia (inability to create high-pitched voices), they would have
monotonous voice
- Unilateral RLN injury → Hoarseness of voice
- Bilateral RLN injury → Aphonia and airway obstruction
- If the patient presents with a typical lipoma where the mass hasn’t been growing at all → Reassure
- If there’s a possible lipoma of liposarcoma and there’s uncertainty → US
- If the US shows features of a liposarcoma → MRI
- If there’s doubt of its diagnosis with imaging or if it’s interfering with the patient’s activities (e.g. difficulty sitting
back against a chair) → Removal by excision
Genetics
Genetic inheritance
Autosomal recessive Autosomal dominant X-linked dominant X-linked recessive
• 25% chance of • 50% chance of • 50% chance of • Male child has a 50%
inheritance if BOTH inheritance if ONE inheritance if of inheritance if
parents are carriers parent is a carrier MOTHER has the MOTHER is a carrier
disorder • Female child has 50%
Unaffected → 1:4 Unaffected → 1:2 • If FATHER has the chance to be a carrier
Affected → 1:4 Affected → 1:2 mutation, a female if MOTHER is a carrier
Carrier → 1:2 child has a 100% • X-linked recessive
chance while a male conditions don’t affect
25% chance to pass to a
child has 0% females to a
grandson
significant degree as
the other X-
chromosome is likely
If the affected parent is In X-linked diseases, sexes to be normal and can
Homozygous → 4:4 of offspring are usually compensate
If Heterozygous → 1:2 mentioned • Infected males don’t
live long enough to be
fathers → Mom is the
culprit
• Cystic fibrosis • Huntington • Fragile X syndrome • Hemophilia
• Sickle cell anemia • Neurofibromatosis • Duchenne muscular
• Thalassemia • PCKD atrophy
• Congenital adrenal • OI
hyperplasia
• Infantile PCKD
Approach
➢ Firstly, find out what is the disease? Then figure out its type
1. Autosomal recessive
• Usually both parents will have the faulty gene → Unaffected 1:4, Affected 1:4, Carrier 1:2
2. Autosomal dominant
• There’s no need to know the other partner genotype, as it’s enough to have one parent with the faulty
gene to have the disease → Unaffected 1:2
In X-linked → we need to know if the mother and the father are affected or not, also the effect on the offspring
3. X-linked dominant
a) MOTHER affected, FATHER affected → Unaffected 1:2, Affected 1:2
b) MOTHER unaffected, FATHER affected → 100% girls Affected, 0% boys Affected
Because the boy will always take his Y gene from his father, leaving the faulty X gene of the father behind and he’ll
receive his X gene from his mother who’s free of the disease
Girls will get one X gene from the father which is faulty, so all girls XX will have one gene X damaged
4. X-linked recessive
• Carrier MOTHER and unaffected father
- Affected boys 1:2, Unaffected boys 1:2
- Girls who become carrier 1:2
Genetics
Duchenne muscular dystrophy (DMD)
• A boy comes to the clinic by age 4-8 years
• Delayed motor milestones: walking at >18 months, can’t hold objects
• Inability to run – waddling gait
• Gower’s sign, proximal muscle weakness (rising from a sitting position)
• Pseudohypertrophy of calf muscles
• There may be respiratory or cardiac symptoms
• Elevated CK, AST, ALT
Diagnosis
• Initial → CK (extremely high since birth)
• Blood sample and muscle biopsy → genetic testing for dystrophin mutations → PCR
• Neuromuscular assessment → diagnose severity and determine management
• Genetic testing after a positive biopsy diagnosis of DMD is mandatory
Becker’s muscular dystrophy (BMD) → Big boys

- Less common than DMD, clinical course is milder
- Walking difficulties begin after the age of 16
Myotonic muscular dystrophy

- My testis (Testicular atrophy)
- My Ticker (Arrythmias)
- My Toupee (Frontal balding)
Huntington’s disease
➢ Autosomal-dominant inheritance with anticipation, progressive neurodegenerative disorder with a distinct
phenotype → enlargement of the frontal horns of the lateral ventricles
Presentation
• Typically, onset of symptoms at middle age
• Early signs may be personality change, self-neglect and clumsiness
• Incoordination
• Cognitive decline
• Behavioral difficulties
• Later → Chorea (dancing movements), dystonia, rigidity, dementia and athetosis (involuntary writing
movements)
Pedigree charts
Genetics
Klinefelter’s syndrome (XXY)
• Mental retardation (average IQ 85-90)
• Behavioral problems
• Long limbs (decreased upper: lower segment ratio)
• Tall and slim
• Hypogonadism
• Infertility
• Gynecomastia
Diagnosed by Chromosomal analysis
The most common indications for karyotyping → hypogonadism and infertility
Turner syndrome
[45XO]
- Xtra skin folds • Some turner syndrome patients can conceive with assisted
- Ovarian failure reproductive techniques
Other features
• Low set of ears
• Broad chest with widely spaced nipples and Webbed neck
• Peripheral edema, horseshoe shaped kidneys, aorta bicuspid
• No Barr body
Comparing the trisomies
Genetics
Patau’s Edward’s
Down’s
Ovarian cancer
➢ If high risk with no symptoms of ovarian cancer, next step is → Genetic counseling
Criteria of increased risk of ovarian cancer
• BRCA1 or BRCA2 mutations
• 1st degree relative who carries a gene mutation
• Two family members who are 1st degree relatives of each other have ovarian cancer
• One family member has both breast and ovarian cancer
High risk women should be offered genetic screening and counselling
Steps to investigate a patient with suspected ovarian cancer
1. CA 125
2. US pelvis and abdomen
3. CT pelvis and abdomen
4. MRI for pre-operative staging
5. Prophylactic salpingo-oophorectomy may be offered
Genetics
Chorionic Villus Sampling vs Non-invasive Prenatal Testing
CVS is done in late 1st trimester as the baby is still small and a placental sampling can be obtained
Amniocentesis is done in early 2nd trimester
Risk of fetal loss is 0.5-1%
Conditions which can be diagnosed with Amniocentesis
- NTD (raised AFP)
- Chromosomal disorders
- Inborn errors of metabolism
Genetics
Notes
• Diagnostic test to help diagnose genetic defects (e.g. Cystic fibrosis) prior to conception → Pre-implantation
genetic diagnosis (PGD)
• Chromosomal karyotyping can only be performed after conception
• Most enzymatic/metabolic diseases → Autosomal recessive
• Most structural diseases → Autosomal dominant
• Paternal inheritance by deletion of chromosome 15 → Prader Willi $
• Maternal inheritance of deletion of chromosome 15 → Angelman’s $ (happy puppet $)
• Double bubble sign = Duodenal atresia = Down’s syndrome
• Cardiac complications of Down’s syndrome → ASD, VSD
• Late complications of Down’s syndrome → Subfertility, learning difficulties, short stature, ALL, Alzheimer’s
• Microphthalmia → one eye or both are abnormally small
• Micrognathia → undersized jaw
• Edward $ → ROME
- Rocker bottom feet
- Overlapping fingers
- Micrognathia
- Ear (low set)
• Flat occiput → Down’s
• Prominent occiput → Edward’s
• Scalp defects → Patau
• Bloods in Down’s → low alpha-feto protein, hCG high, estriol low
• Most common US finding in Edward’s → Nuchal translucency thickness and absence or hypoplasia of the
nasal bone
• Infants with Edward’s don’t survive the first week of life, majority don’t survive longer than a year
• In chromosomal inheritance, each pregnancy is considered a new event so the probability is always the same
• Alport’s syndrome → X-linked mode of inheritance
• Familial hypercholesterolemia → Autosomal dominant
• VWD → Autosomal dominant
• Hereditary spherocytosis → Autosomal dominant
GIT
Achalasia
➢ Idiopathic loss of the normal neural structure of the lower esophageal sphincter resulting in inability to relax
Features
• Progressive dysphagia to both solid and fluids (more to fluids)
• Regurgitation (hours after eating)
• Weight loss
• There may be history of recurrent URTIs or aspiration pneumonia as a result from untreated achalasia that
leads to nocturnal inhalation of material lodged in the esophagus
• NO relationship with alcohol or tobacco use
Investigations Esophageal cancer
• dysphagia to solid first then liquids
• Barium swallow → (Sigmoid esophagus); dilation of the
• common in elderly with long history of
esophagus, which narrows into a “parrot’s beak” at the distal alcohol and tobacco use
end
• Manometric studies (most accurate) → increased tone of Schatzki ring
• Narrowing of the lower esophagus that
lower esophagus
leads to intermittent dysphagia but not
Management associated with pain, mainly to solids and
Dilation of the lower esophageal sphincter in old patients
• HELLER'S OPERATION (myotomy)
• Botulinum toxin injection, elderly not able to tolerate operations
Esophageal spasm (CCCC)

• Intermittent Chest pain and dysphagia, pain can be precipitated by
Cold liquids
• Pain can simulate that of MI, but it has no relation to exertion
• Relieved after ingestion of nitrates as they are smooth muscle
relaxants
Investigations
• Manometric study → High intensity and disorganized contractions
(most accurate)
• Barium meal → Corkscrew pattern
Treatment
• Ca channel blockers: nifedipine
Plummer Vinson $
➢ Middle-aged woman
➢ Dysphagia (painless/intermittent) + IDA + post cricoid esophageal web
Management
- Iron supplement
- Dilation of the web
Barret’s esophagus
• Occasional dysphagia
• Results from long history of GERD
• Replacement of Sq. epithelium to columnar epithelium
• Associated with esophageal adenocarcinoma
GIT
Dysphagia
• Dysphagia to both solids and liquids WITHOUT regurgitation

• Results from scarring due to:
- Acid reflux
Benign esophageal stricture
- Persistent GERD (retrosternal discomfort)
(peptic stricture)
- Ingestion of corrosives
- Drugs: Bisphosphonates (alendronate) – NSAIDs. So patients are
advised to lie down for 30min after administration
Esophageal carcinoma • Symptoms of cancer
Barrett's esophagus • A long hx of GERD, occasional dysphagia not persistent
• Hx of halitosis, regurgitation of stale food & a throat lump

Pharyngeal pouch (Zenker’s
• Barium swallow may show a residual pool of contrast within the pouch
diverticulum)
• Endoscopy should be AVOIDED in fear of perforation
Achalasia • Dysphagia + regurgitation

Ulcers and esophageal candidiasis • Painful dysphagia
Plummer Vinson $ • IDA + Esophageal web
- Bisphosphonates are used to treat osteoporosis but long-term use can cause esophagitis resulting in a stricture
Esophageal cancer
➢ Adenocarcinoma is more common
➢ Commonly occur in the lower third, Squamous cell type is less common and it affects the upper 2/3
➢ More likely to develop in patients with history of GERD or Barret’s
➢ Dysphagia to solid first then liquids + weight loss
Risk factors
• Smoking (RF for both but mainly for SCC)
• Alcohol
• GERD
• Barret’s
• Achalasia
• Plummer Vinson $
Diagnosis
• Upper GI endoscope and biopsy → 1st line
• Barium swallow
- Rat-tail appearance
- Apple-core appearance
- Shouldering
Treatment
• Operable → surgical resection, radiotherapy
• Inoperable (e.g. metastasis) → palliative esophageal Stent, Percutaneous endoscopic gastrostomy (PEG)
usually in stroke patients who are at risk of aspiration pneumonia or to decompress the stomach in cases of
gastric volvulus
GIT
Dyspepsia and H. Pylori
• < 55 with no red flags:
• > 55 with unexplained/persistent symptoms (not just alarm signs) ⟶ Endoscopy
➢ Red flags (ALARMS)

- Anemia
- Loss of weight - Serological tests have no value in confirming
- Anorexia successful eradication because antibodies persist
- Recent onset of progressive symptoms long after successful eradication, C-13 urea breath
test ensures successful eradication
- Masses, Melena or hematemesis
- Swallowing difficulty - If the patient is taking PPIs, stop it 14 days prior to
performing urea breath test or stool antigen test
➢ H. Pylori antibody testing - There must be a 28-day break after eradication

• Carbon-13 urea breath test with antibiotics prior to testing
• Stool antigen test
• Serum antibody testing
➢ H. Pylori eradication
- PPIs
- Clarithromycin
- Amoxicillin or metronidazole
GIT
Esophageal varices
➢ Dilated sub-mucosal veins in the lower 1/3 of the esophagus
➢ Often severe and life threatening
➢ History of chronic liver disease → portal hypertension → esophageal varices
Features
- Hematemesis (most commonly) and melena
- Signs of chronic liver disease
Investigations
• Endoscopy at early stage
Acute management of variceal bleeding
• Always with ABC
• Correct clotting: FFP, vitamin K
• Terlipressin (vasoactive agent) → should be offered to patients with suspected variceal bleeding at
presentation
• Antibiotic prophylaxis → reduces mortality in patients with acute upper GI bleeding in association with
chronic liver disease
• Endoscopic variceal band ligation → if it’s not available → emergency sclerotherapy
• Sengstaken-Blakemore tube if uncontrolled hemorrhage
• Transjugular Intrahepatic Portosystemic Shunt (TIPSS)
Prophylaxis of variceal hemorrhage
- Propranolol, given at discharge to reduce portal pressure in order to decrease the risk of repeat bleeding
Perforated peptic ulcer

➢ Sever sudden localized epigastric pain
➢ May worsen with coughing or moving
➢ May radiate to the shoulder tip
Examination
• Absent bowl sounds
• Shock
• Generalized peritonitis (fever, tachycardia,
abdominal guarding & rigidity)
Investigations
• Erect X-ray → free gas under the diaphragm
• CT scan
Management
• IV analgesics
• Antiemetic (e.g. metoclopramide 10mg)
• Resuscitate with IV 0.9% saline
• IV antibiotics
For bleeding peptic ulcer without perforation → Endoscopy, or IV PPIs if endoscopy isn’t available
GIT
IBD
Ulcerative Colitis → Lt Crohn’s disease → Rt
- Anywhere in the GIT mostly ileum & colon

- BD that forms ulcers in the colon and rectum only
- Extending to serosa
- Only affects mucosa and submucosa
Def. - Immune-related caused by pathogens
- Autoimmune
- Weight loss more prominent
- Bloody diarrhea is more prominent
- Steatorrhea
- Circumferential - Transmural/deep ulcers

- Continuous - Skip lesions (cobblestone
- Crypt abscesses appearance) on endoscopy
Diff. - 1ry sclerosing Cholangitis ➢ Peri-anal fistulas
➢ Kantor’s string sign
➢ Aphthous oral ulcers ➢ Rose thorn ulcers
- Pain in RLQ (ileum)

- Pain in LLQ (rectum)
Symptoms - LI: Diarrhea usually not bloody
- LI: Bloody diarrhea more common
- SI: Malabsorption
- Colonoscopy
- Barium enema (loss of haustration, drain pipe - Barium swallow
colon) - CT
Diagnosis
- CT \ MRI - Increased goblet cells + Granuloma on
- Decreased goblet cells on histology histology
- In children → P-ANCA positive
➢ Inducing remission
➢ Inducing remission
- 1st line (motions <4 times) → topical
- 1st line → prednisolone
aminosalicylates (e.g. rectal mesalazine)
- 2nd line → budesonide
- If not responding → oral mesalazine (5-
- 3rd line → mesalazine (5-ASA)
ASA)
- Still not responding or motions 5/day →
oral prednisolone • Add on treatment (not used as
monotherapy): azathioprine,
If severe colitis → IV steroids, Infliximab in mercaptopurine or methotrexate
children:
1. > 6 bowl movements
➢ Maintaining remission after surgery
2. Visible blood in large amount - 1st line → azathioprine,
3. Pyrexia > 37.8℃ mercaptopurine or 5-ASA
Treatment
4. Tachycardia
5. Anemic
6. ESR > 30
In severe cases, an abdominal X-ray would be
very appropriate in the setting to look for
features suggestive of toxic megacolon
➢ Maintaining remission
- Mesalazine
- If not well maintained → oral azathioprine
or mercaptopurine
GIT
Toxic megacolon
➢ IBD or infective colitis characterized by total or segmental non-obstructive colonic dilatation + systemic toxicity
Presentation
• Severe abdominal pain
• Marked toxicity (weakness, lethargy, confusion)
Investigation
• Abdominal X-ray
Treatment
• Admission to ITU, IV fluids
• IV steroid in case of IBD
• IV antibiotics in case of infectious cases
• Possible surgical resection (high risk of perforation and death)
• If rupture colon is suspected → Urgent laparotomy
Zollinger-Ellison $
➢ Gastrinoma (tumors found in pancreas or duodenum) → secretes gastrin → ↑ gastric acid → peptic ulcers at
usual sites, such as 2nd part of duodenum or jejunum
➢ Ulcers may occur after adequate surgery
Investigations
• Fasting gastrin levels
• Secretin stimulation test (gastrin goes up after secretin in
case of Gastrinoma)
ZES is suspected when
1. Multiple ulcers that are resistant to drugs
2. Associated with diarrhea + steatorrhea
3. Family history of peptic ulcers
Constipation management
➢ Hard stool → Stool softeners + high fiber (residue) diet
➢ Soft stool → Senna then lactulose
➢ Impacted stool → phosphate enema
➢ Constipation in pregnancy → Lactulose then Senna
Colorectal carcinoma
• Presents with a change in bowel habits, abdominal pain, anemia and weight loss
• Best diagnostic investigation → Colonoscopy
• Gold standard → Biopsy
• Alternatives → Barium enema and CT angiography
• CEA antigen is NOT used for diagnosis or staging but rather for monitoring relapses
GIT
Diarrhea
➢ 3 loose or watery stool /day
➢ Acute < 14 days → Microscopy, culture and sensitivity
➢ Chronic > 14 days → Colonoscopy
• Most common adenoma causing electrolytes disturbances → Villous adenoma
• Most common electrolyte imbalance in diarrhea → Hypokalemia
• Acid-base imbalance in diarrhea → Non-anion gap metabolic acidosis (due to loss of HCO3)
• Most common cause of bloody diarrhea → Campylobacter (a prodrome of headache, myalgia & fever)
• Second most common cause of bloody diarrhea → Shigella → Salmonella
• Diarrhea after camping → Giardia
• Most common cause of traveler diarrhea (in less than 72h) → E-coli
• Traveler diarrhea lasting >1 week and associated e’ steatorrhea and weight loss→ Giardia
• Most common cause of diarrhea in pediatrics → Viral (Rotavirus)
• Diarrhea followed by weakness and areflexia (Ascending paralysis) → GB$
• Diarrhea followed by renal impairment → HUS (hemolytic uremic syndrome)
• Bloody diarrhea followed by RUQ pain → Ameba > amoebic liver abscess
• Chronic bloody diarrhea in young male → IBD
• Diarrhea after long term antibiotics → Clostridium difficile
• MC Antibiotic causing clostridium difficile → Clindamycin, Cephalosporin, Co-amoxiclav
• TTT of clostridium difficile → Metronidazole (Vancomycin for severe cases/ failure to respond to metronidazole)
• Diarrhea after eggs or chicken → Salmonella → Ciprofloxacin
• Diarrhea/vomiting just hours after meal → Staph toxin
Overflow diarrhea
• Diarrhea in bed ridden with constipation → Fecal impaction • Severe constipation can cause fecal
• Main TTT of diarrhea → Fluid impaction and fecal fluid will flow around
the blockage
• TTT of traveler diarrhea → Fluid only • Common in bedridden elderly
• Can be due to opioid pain relievers →
• TTT of staph toxin → Fluid only
reduces GI motility
• TTT of shigella or campylobacter → Antibiotics
Fecal impaction
• TTT of ameba or giardia → Metronidazole ➢ Symptoms
- Dehydration, agitation, tachypnea
• 1st Inv of choice for acute diarrhea (<14 days) → Stool C&M ➢ Management
• HIV + watery diarrhea → Cryptosporidium parvum - Bisacodyl suppository
- Arachis oil retention enema
• HIV + bloody diarrhea → CMV - Phosphate enema
• Long standing diarrhea after recent travel:

1. Non-bloody / watery / steatorrhea → Giardiasis (1st → Stool microscopy, then stool PCR and ELISA)
2. Bloody → Campylobacter jejuni → Gram-negative curved bacilli → Erythromycin, alternatively → Clari/Azi,
if Macrolides are not tolerated → Ciprofloxacin
GIT
Celiac disease
➢ Caused by sensitivity to the protein gluten (exacerbated by consumption of wheat)
➢ Repeated exposure leads to villous atrophy which in turn causes malabsorption → buttock atrophy in
children
Signs and symptoms
• Diarrhea, chronic or intermittent
• Stinking stools, difficult to flush • One of the most common presentation of celiac
disease is Iron deficiency anemia (IDA).
• Steatorrhea
• May be associated with type 1 DM
• Persistent GI symptoms (bloating, nausea & vomiting) • Folate deficiency is more common than vitamin
• Fatigue B12 deficiency in celiac disease
• Recurrent abdominal pain, cramping and distension
• Sudden or unexpected weight loss
• Unexplained iron, folate or vitamin B12 deficiency anemia
• Any patient with confirmed celiac disease who
Complications
experience recurrence of the symptoms despite
• Osteoporosis gluten-free diet +/- weight loss ➝ Intestinal
• T-cell lymphoma of small intestine (rare) lymphoma until proven otherwise
• Dermatitis herpitiformis (presented as red raised patches,
often with blisters and severe itching, treated with Dapsone)
Investigations
1. Specific auto-antibodies
- TTG antibodies (IgA) → the first choice • Patients should not start gluten free diet until
- Endomysial antibody (IgA) diagnosis in confirmed
- Alpha-gliadin antibodies • If patients are already taking a gluten-free diet
2. Jejunal/duodenal biopsy (Still needed even if antibody test they should restart consuming gluten for at
least 6 weeks prior to testing
confirms the disease)
- Villous atrophy
- Crypt hyperplasia
- Increase in intraepithelial lymphocytes Differentiating tropical sprue from celiac disease:
1. Origin: infective in TS, autoimmune in CD
Management → Gluten-free diet
2. TS along with IDA will present with symptoms of other
vitamins deficiencies (Vit D, K, A). usually begins with
Pseudomembranous colitis acute diarrhea then progresses to chronic state and
malabsorption and steatorrhea
➢ Clostridium difficile is detected in stool, presented with 3. No dermatitis herpitiformis in tropical sprue
watery diarrhea (could be bloody), abdominal pain, 4. Biopsy: incomplete villous atrophy in TS while
complete in CD
raised WBCs and fever
Most common antibiotics that cause it
1. Clindamycin
2. Cephalosporin (2nd and 3rd gen)
3. Co-amoxiclav
4. Quinolones
5. Aminopenicillins (amoxicillin and ampicillin)
Management (only if symptomatic)
1. Stop the causative antibiotic
2. 1st line → Oral metronidazole
3. If severe/not responding → Oral vancomycin (to be absorbed in the gut)
GIT
Jaundice
1. Prehepatic
• ↑ Heme breakdown (e.g. hemolysis, G6PD deficiency, malaria) → ↑ unconjugated hyperbilirubinemia
2. Intrahepatic Gilbert’s $
• Inability to conjugate - Due to ↓UGT-1 which is the enzyme that
conjugate bilirubin with glucuronic acid
- Gilbert’s $ → ↑ unconjugated hyperbilirubinemia
- Jaundice is precipitated by: infection, illness,
- Crigler-Najjar $ physical exertion, stress or fasting
- liver disease Investigations
• Inability to excrete 1. Mildly raised bilirubin (<100) with
- Dubin-Johnson $ → ↑ conjugated hyperbilirubinemia normal LFTs
2. FBC → normal reticulocyte count
- PBC
3. Urine dipstick → normal
3. Post-hepatic/obstructive (surgical) • ↑ Reticulocyte count → Hemolysis

- Gallstones • Total bilirubin >100 → Crigler Najjar
- Cholangitis • Abnormal dipstick + Dark liver → Dubin-
Johnson (↑ conjugated)
Primary Biliary Cholangitis/Cirrhosis Primary Sclerosing Cholangitis

• Autoimmune, idiopathic • Autoimmune, idiopathic
• Associated with → Sjogren syndrome & RA • Fibrosis at some areas of bile ducts “beaded
• Pruritus, ↑ALP appearance”
• +ve AMA (ant-mitochondrial antibodies) • Associated with → IBD (especially UC)
• Treatment • Pruritus, ↑ALP
- Ursodeoxycholic acid • ERCP → the most specific
- Cholestyramine • Treatment:
- Ursodeoxycholic acid
- Cholestyramine
PBC – the M rule:

➢ IgM
➢ AMA
➢ Middle aged female • Investigations for cholecystitis → US – HIDA
• Only symptomatic Gallstones are treated with
elective cholecystectomy. However, CBD stones may
Ascending cholangitis need laparoscopic cholecystectomy regardless if
they’re symptomatic or not
• Due to ascending bacterial infection (E. coli) as a result • Choledocholithiasis (stones in CBD) → ERCP (both
of choledocholithiasis diagnostic & therapeutic)
• One complication of ERCP → Acute pancreatitis
• Charcot’s triad
• Cholangitis → inflammation of the bile ducts
- Fever
- RUQ pain
- Jaundice
• Confirmed by US gallbladder and biliary ducts
• Complications → Reynold’s triad = Charcot’s triad + hypotension + confusion
• Treatment → Emergency ERCP, rehydration & antibiotics
GIT
Autoimmune hepatitis (AIH)
➢ Chronic disease of unknown cause characterized by continuing hepatocellular inflammation and necrosis,
which tends to progress to cirrhosis. Often seen with autoimmune diseases (autoimmune thyroid disorder,
Addison’s or vitiligo)
➢ Middle-aged women
Features ➢ Deranged LFTs + 2ry amenorrhea → autoimmune hepatitis
• Fever, malaise • AST & ALT are usually elevated initially
• Rash, Polyarthritis • ALP is normal or slightly raised, > 2 folds suggests
another diagnosis
• Pulmonary infiltration, pleurisy
• Glomerulonephritis
• Liver enzymes are usually elevated
• Amenorrhea is common and disease tends to attenuate in pregnancy
Investigations
• ANA/SMA/LKM1 antibodies, raised IgG levels
• Liver biopsy → inflammation extending beyond limiting plate 'piecemeal necrosis', bridging necrosis
Management
• Steroids, other immunosuppressants e.g. azathioprine
• Liver transplantation
Acute fatty liver of pregnancy

Risk factors
• Pre-eclampsia
• First pregnancies
• Multiple pregnancies
Features
• Begins after 30 weeks of gestation, may also appear immediately after delivery
• Presents acutely with:
- Nausea, vomiting
- Abdominal pain
- Fever, headache
- Jaundice, pruritis
Investigations
• Elevated LFTs
• Raised bilirubin
• Hypoglycemia & ammonia
• Prolonged PT
• Liver biopsy → diagnostic
Management
• Treat hypoglycemia
• Correct clotting disorders
• N-acetylcysteine (NAC)
• Consider early delivery
AFL = HELLP + Hypoglycemia + Ammonia
GIT
Causes of elevated liver enzymes in postpartum period
➢ Pregnancy related liver diseases
• Obstetric cholestasis → severe pruritis due to high bile acids + x20 ALT
• Pre-eclampsia / Eclampsia
• HELLP syndrome
• Acute fatty liver of pregnancy
➢ Liver diseases unrelated to pregnancy
• Viral hepatitis
• Autoimmune liver disease
• Wilson’s
• Budd Chiari $
• Acute cholecystitis
• Drug-induced hepatotoxicity
Hemochromatosis
➢ Autosomal recessive condition in which increased intestinal absorption of iron causes iron accumulation in
tissues especially the liver which may lead to cirrhosis and HCC (hepatoma)
➢ Iron is accumulated mainly in peripheral hepatocytes and not in Kupffer cells, while in Hemosiderosis, iron is
accumulated in Kupffer cells and more in central rather than peripheral hepatocytes
Presentation
• Often asymptomatic until late stages • Hemochromatosis can lead to cardiomyopathy
• Symptoms usually start at 40-60 years old and it predisposes to HCC
• Initial symptoms are vague and non-specific
• Iron overload might cause symptoms of arthropathy and gynecomastia
• Maybe diagnosed accidentally following LFTs or abnormal serum ferritin
• Symptoms of advanced disease include a triad of:
1. Diabetes (bronze diabetes)
2. Hepatomegaly
3. Bronze pigmentation
• It may also include cardiac diseases (arrhythmias or cardiomyopathy) or neurological/psychiatric symptoms
GIT
Acute pancreatitis
➢ Main causes are gallstones and alcohol
GET SMASHED
• Gallstones
• Ethanol
• Trauma
• Steroids
• Mumps
• Alcohol, autoimmune
• Scorpion venom
• Hypertriglyceridemia, ↑Ca, hypothermia
• ERCP
• Drugs (azathioprine, mesalazine, Bendroflumethiazide, frusemide, didanosine, pentamidine, sodium
valproate)
Features
• Gradual or sudden severe epigastric pain or central abdominal pain (radiates to the back, relieved by sitting
forward)
• Vomiting is prominent
• Tachycardia
• Fever
• Jaundice
• Shock
• Rigid abdomen with local tenderness
• Periumbilical bruising (Cullen’s sign)
Investigations
1. Serum amylase: >1000U/mL (or around 3-fold upper limit of normal). However, lipase levels are more
sensitive and more specific but takes more time to rise following an attack (>24h)
2. CT with contrast
Treatment
• Fluid resuscitation, analgesia and nutritional support
• IV antibiotics (e.g. IV imipenem) after obtaining culture
• Laparoscopy → only when there’s infection or necrosis
Albumin
- Made is the Liver
- Its half-life is about 20 days so it’s a good parameter for chronic liver disease
- Its main function is to regulate the oncotic pressure of blood, it also binds to enzymes and hormones
- Shifts fluid into the intravascular compartment
- Produces only a transient effect but it’s useful in cases of intravascular fluid deficit and edema
- Also, useful to obtain diuresis in hypoalbuminemic patient
GIT
Chronic pancreatitis
Causes → alcohol, smoking, autoimmune
Features
• Epigastric pain
- Episodic with short periods of severe pain
- Pain free intervals are specific to chronic pancreatitis
- Radiates to the back
- Relieved by sitting forward
- Exacerbated by eating
• Steatorrhea
- Due to malabsorption of fats from the lack of pancreatic lipase secretion which results on weight loss
- Sometimes described as “loose, offensive stools which are difficult to flush”
• Diabetes
• Jaundice
- A late presentation due to obstruction of CBD
Investigations
1. Serum amylase/lipase
2. US
3. CT with contrast
- Gold standard
- Shows evidence of pancreatic calcification
Management
• Pain → Analgesia
• Steatorrhea or malabsorption → Pancreatic enzymes supplements and fat-soluble vitamins
• Diabetes → Oral hypoglycemics and insulin
Drug-induced hepatitis
• Drugs → Co-amoxiclav, flucloxacillin, steroids, Sulphonylurea
• Lab → Elevated bilirubin + massive increase in ALP and AST
• History of alcohol intake
Mediastinitis
• May occur after esophageal perforation (after endoscopy)
• Anterior mediastinitis → pain located in the substernal region
• Posterior mediastinitis → pain in the epigastric region with radiation to the interscapular region
• X-ray may show widened mediastinum or air in the mediastinum
GIT
Notes
• Alcoholic hepatitis → look for GGT in acute cases, AST is higher than ALT in chronic cases
• Hematogenous spread to the liver from the lungs is the most common route of metastasis
• TTF-1 is a protein seen by immunostaining which is used as a clinical marker of lung adenocarcinoma
• Gastroenteritis
- Very common in hospitals, especially with the spread of norovirus
- They present with acute onset of diarrhea (sometimes with vomiting) and abdominal pain
- Pain is usually central, could be epigastric
- Patients with gastroenteritis should be isolated and given a single side room until diarrhea resolves
• Dysentery → infection of the intestine that leads to severe diarrhea (blood + mucous) and abdominal pain
• Cancer head of pancreas → Courvoisier sign (painless obstructive jaundice with a palpable mass)
• Celiac disease is associated with lymphoma
• Ulcerative colitis and Crohn’s disease are associated with colon cancer
• In IBS → bloating, constipation alternating with diarrhea + NO blood in stool
• Fecal calprotectin → biochemical measurement of the protein calprotectin in the stool, if elevated → IBD, if
normal, suspect IBS
• Proctalgia fugax → Severe recurrent rectal pain in the absence of any organic disease, may occur at night,
after bowel actions or after ejaculation. Anxiety could be an associated feature
• If the patient has Ascites + bleeding → Terlipressin
• If the patient has Ascites without bleeding → Perform ascitic fluid aspiration, to detect Neutrophil count,
gram stain, culture and obtain protein level
• Raised neutrophil count >250 → Start antibiotic treatment
• Most accurate test would be a culture but it takes days
• Spontaneous bacterial peritonitis
- One of the complications of Ascites
- Includes abdominal pain, rebound tenderness, absent bowel sounds and fever
- Organism usually reaches the peritoneum via hematogenous spread
• Recurrent abdominal pain (often peri-umbilical) with episodic headache in a child with no abnormal finding
on examination and investigation, pain interferes with normal activities and associated with anorexia,
nausea, vomiting → Abdominal migraine → Reassure
Hematology
Iron-deficiency anemia
Etiology
• Blood loss from the gastrointestinal (GI) tract is the most common cause of iron-deficiency anemia in adult
men and postmenopausal women
• Blood loss due to menorrhagia is the most common cause of iron deficiency in premenopausal women
• In tropical countries, infestation of the gut may cause iron- deficiency anemia, especially with hookworm and
schistosomiasis
• Common causes of blood loss include:
Anemia of chronic disease
- Non-steroidal anti-inflammatory drug (NSAID) use e.g. Naproxen
- Decreased iron
- Colonic carcinoma - Decreased TIBC
- Gastric carcinoma - Raised ferritin
- Gastric or duodenal ulceration
• Dietary inadequacy
• Failure of iron absorption: Malabsorption conditions such as coeliac disease
• Excessive requirements for iron: Pregnancy
Features
• Angular stomatitis (can be seen in vit B12 deficiency as well)
• Koilonychia (spoon nails)
• PICA
Laboratory tests Hairy leukoplakia
• Low Hemoglobin • Irregular white patches on the side of the tongue
and occasionally anywhere on the tongue or in the
• Low Mean cell volume (MCV)
mouth
• Low Mean cell hemoglobin concentration (MCHC)
• Occurs primarily in HIV-positive individuals or in
• High Red cell distribution width (RDW) immunosuppression
• Low serum ferritin • Cannot be scraped off, benign and doesn’t require
• High Total iron-binding capacity (TIBC) treatment
Management
• Oral iron ⟶ Ferrous sulphate, ferrous gluconate (SE: black stool)
• Blood transfusion when:
- Hb <80 g/L
- Hb <90 g/L + known cardiovascular disease
A patient with RA on NSAIDs and methotrexate

• Low hg + low MCV ⟶ IDA due to GI bleeding from NSAIDs
• Low hg + high MCV ⟶ Folate deficiency from methotrexate
• Low hg + normal/low MCV ⟶ Anemia of chronic disease
Hematology
Vitamin B12 (Cobalamin) deficiency
➢ Found in meat, fish and dairy products but not in plants
• Folate ⟶ Fruits + Fegetables
➢ B12 binds to intrinsic factor in the stomach, and this complex is
• B12 ⟶ Beef + Bacon
absorbed in the terminal ileum
Causes Dude Is Just Feeling Ill Bro
• Pernicious anemia
➢ Dude Is ⟶ Duodenum, Iron
- Commonest cause ➢ Just Feeling ⟶ Jejunum, Folate
- Due to autoimmune gastric atrophy resulting in loss of intrinsic ➢ Ill Bro ⟶ Ileum, B12
factor production required for absorption if vitamin B12
- Usually associated with other autoimmune problems (e.g.
• Vitamin B1 (thiamine) deficiency in
vitiligo, hypothyroidism)
alcoholism → Werneck’s encephalopathy
• Chronic pancreatitis ⟶ inadequate absorption of Vit B12 • Folic acid is Vit B9
• Dietary (e.g. vegans)
• Following total gastrectomy, body stores of cobalamin only last a few years so depletion occurs after 1 to 2
years post-surgery
• Ileal disease ⟶ resection of the ileum, Crohn’s disease
• Malabsorption disorders ⟶ Celiac disease, tropical sprue
Features
• Symptoms of chronic anemia: fatigue, dyspnea on exertion
• Neurological symptoms (dementia, peripheral paresthesia and disturbances of position and vibration sense)
⟶ helps distinguish vit B12 deficiency from folate deficiency
• Can cause angular stomatitis, tongue is described as “beefy” or “fiery red and sore”
• If uncorrected ⟶ degeneration of the spinal cord and permanent ataxia
Hematological abnormalities
• Macrocytic anemia and the MCV is ⟶ seen in both B12 and folate deficiencies
• Hypersegmented neutrophils ⟶ seen in both B12 and folate deficiencies
• Homocysteine
- Deficiency of cobalamin results in elevation of plasma total homocysteine
- Not specific for cobalamin deficiency as it’s also elevated in folate deficiency
• Nucleated RBCs can be found in BM picture
Management
• Hydroxocobalamin IM
• Blood transfusion if:
- Symptoms of anemia + hemoglobin is <80 g/L
- Hemoglobin is <70 g/L in asymptomatic patient
Hematology
Folate Deficiency
Causes
• Dietary deficiency
- Malabsorption (e.g. coeliac disease, jejunal resection, inflammatory bowel disease).
- Poor intake
- Alcohol excess (also causes impaired utilization) • NSAIDs ⟶ IDA
• Antifolate drugs ⟶ Sulfasalazine, methotrexate • Methotrexate ⟶ Folate deficiency
Diagnosis •
• The hematological features are similar to B12 deficiency (macrocytic, megaloblastic anemia). Distinction is on
basis of demonstration of reduced red cell and serum folate. Vitamin B12 levels should be assessed at the
same time due to the close relationship in metabolism.
Management
• Folic acid 5 mg/d PO for 4 months
Note: It is important in a patient who is also deficient in both vitamin B12 and folic acid to treat the B12 deficiency
first to avoid precipitating subacute combined degeneration of the cord. Once the vitamin B12 levels are normal,
then start oral folic acid. [Treat B Before F]
Vitamin B12 Folate deficiency

• Neurological findings • No neurological findings
• Raised Methylmalonic acid • Normal Methylmalonic acid
Aplastic anemia
➢ Aplastic anemia is a rare, potentially life-threatening failure of hemopoiesis characterized by pancytopenia and
hypoplastic marrow (the marrow stops making cells), usually found in adolescents
Causes
• Most cases are autoimmune, triggered by drugs, viruses (e.g. parvovirus, hepatitis) or irradiation
Presentation
• Aplastic anemia can present abruptly or insidiously over, weeks to months
• Clinical manifestations are proportional to the peripheral-blood cytopenia and include:
- Symptoms of anemia (pallor, headache, palpitations, dyspnea, fatigue, or ankle edema) Note: Anemic
symptoms are usually less severe due to the chronic onset
- Symptoms of thrombocytopenia (skin or mucosal hemorrhage, visual disturbance due to retinal
hemorrhage, petechial rashes)
- Infection (a less common presentation) particularly upper and lower respiratory tracts, skin, mouth, and
peri-anal
- There is NO lymphadenopathy or hepatosplenomegaly (in the absence of infection)
Diagnostic tests
• Bone marrow is diagnostic ⟶ gross reduction in all hemopoietic tissue that’s replaced by fat tissue
• Blood film morphology is unremarkable ⟶ differentiates it from other types of leukemia
• At least TWO of the following must be present:
- Hemoglobin <10 g/dL • CML = Pancytopenia + Splenomegaly
9
- Platelet count < 50 x 10 /L • Aplastic anemia = Pancytopenia + Hypoplastic BM
with NO splenomegaly
- Neutrophil count <1.5 x 109/L
Hematology
Autoimmune hemolytic anemia
➢ A disease in which the red blood cells are destroyed prematurely. When hemoglobin within red blood cells is
broken down, heme is converted into bilirubin ⟶ jaundice
Types
• Warm antibody ⟶ IgG [Global Warming]
- Idiopathic
- Secondary to other autoimmune diseases e.g. SLE or lymphoproliferative diseases e.g. Lymphoma, CLL
• Cold antibody ⟶ IgM [it’s Cold in Moscow]
- Idiopathic
- MyCoplasma pneumoniae
- Infectious mononuCleosis
Warm antibody induced hemolysis

➢ Most cases are idiopathic with no underlying pathology
➢ Affects predominantly individuals >50 years of age
Clinical features
• Highly variable symptoms, asymptomatic or severely anemic
• Mild jaundice
• Splenomegaly
Diagnosis
• Anemia
• Spherocytes on peripheral blood film
• Increased reticulocytes
• Detect on direct Coombs test
Thalassemia
• α thalassemia major → is usually lethal in utero. It should be considered with hydrops fetalis (abnormal
accumulation of fluid in two or more fetal compartments, including ascites, pleural effusion, pericardial
effusion, and skin edema. It may also be associated with polyhydramnios and placental edema)
• β thalassemia major → Presents in infancy often includes FTT, vomiting feeds, sleepiness, stunted growth
and irritability. In severe, untreated cases there may be:
- Hepatosplenomegaly
- Bony deformities (frontal bossing). The extra medullary hemopoiesis occurs in response to anemia
- Marked pallor and slight to moderate jaundice
- Iron overload → endocrinopathy with diabetes, thyroid, adrenal and pituitary disorders
β-thalassemia carrier status is often confused with iron deficiency due to reduced MCV and MCH. But note that in
iron deficiency, serum ferritin and iron are low while in thalassemia they are usually high
Investigation
• Most confirmatory → Hb electrophoresis • Alpha thalassemia trait has mild anemia but
usually clinically asymptomatic
• Serum studies → increased serum iron
Management
• Lifelong blood transfusions are needed to maintain a hemoglobin level >9.5 g/dL (or >9.0 g/dL)
• Iron chelation to prevent overload syndrome (Oral deferiprone + deferoxamine SC twice weekly)
• A histocompatible marrow transplant can offer the chance of a cure
Hematology
Coombs tests
1. The direct Coombs test (DCT, also known as direct antiglobulin test or DAT)
2. The indirect Coombs test (also known as indirect antiglobulin test or IAT)
Direct Coombs test

• Used to test for autoimmune hemolytic anemia
Common examples of alloimmune hemolysis
1. Hemolytic disease of the newborn (also known as HDN or erythroblastosis fetalis)
2. Rh D hemolytic disease of the newborn (also known as Rh disease)
3. ABO hemolytic disease of the newborn
4. Alloimmune hemolytic transfusion reactions
Common examples of autoimmune hemolysis
- Cold agglutinin disease: Infectious mononucleosis
Drug-induced immune-mediated hemolysis In blood transfusion, we should test
• Cells of a giver
- Penicillin, Cephalosporins
• Serum of a receiver
Indirect Coombs test

• Used in prenatal testing of pregnant women (IgG antibodies) and in testing blood prior to a blood
transfusion
Hematology
Hematology
Glucose-6-phosphate dehydrogenase (G6PD) deficiency
➢ X-linked recessive and clinically important cause of oxidant hemolysis. It affects all races but is most common
in those of African, Asian or Mediterranean descent
➢ ↓ G6PD enzyme → ↓ glutathione → ↑ red cell susceptibility to oxidative stress
➢ Being X-linked → almost always male patient
➢ Most individuals with the G6PD defect are asymptomatic and unaware of their status
➢ Hemolysis occurs after exposure to oxidants or infection
➢ There are many drugs that can elicit hemolysis in patients with G6PD deficiency. One drug that you would
definitely need to look out for in the exam is → antimalarials (e.g. primaquine) and sulfa drugs
Presentation
• Most are asymptomatic
• May be a history of neonatal jaundice, severe enough to require exchange transfusion
• May have history of drug-induced hemolysis
• Gallstones are common
• Pallor from anemia
• During a crisis jaundice occurs
• Back or abdominal pain (usually occurs when >50% hemolysis occurs)
• Splenomegaly may occur
Diagnosis
• G6PD enzyme activity - is the definitive test
- Usually done 6 weeks after the episode as if done during hemolytic crisis could result in equivocal results
• Blood film
- In steady state (i.e. no hemolysis) the RBCs appear normal
- Heinz bodies is seen on blood film in drug-induced hemolysis
- Bite cells are also seen
Management
• Avoidance of precipitating drugs, and broad (fava) beans
• Blood transfusion in severe hemolysis
There are typically 4 ways the patient might present in PLAB. Below are the specifics:
Drug-induced hemolysis in G6PD deficiency
• Begins 1-3 days after ingestion of drug
• Anemia most severe 7-10 days after ingestion
• Associated with low back and abdominal pain
• Dark urine (black sometimes)
• Red cells develop Heinz body inclusions
• Hemolysis is typically self-limiting
Hemolysis due to infection and fever
• 1-2 days after onset of fever
• Mild anemia develops
• Commonly seen in pneumonic illnesses
Favism
• Hours/days after ingestion of fava beans (broad beans)
• Red/very dark urine
• Shock may develop and it may be fatal
Neonatal jaundice
• May develop kernicterus (possible permanent brain damage)
Hematology
IDIOPATHIC thrombocytopenic purpura (ITP)
➢ Children ⟶ preceded by URTI HUS → Hemolysis, Uremia, Stomach virus + thrombocytopenia
➢ Adults ⟶ no prior infection + insidious onset - Associated with E. coli → bloody diarrhea
Features - Microangiopathic hemolytic anemia (MAHA)
TTP → HUS + fever + neurological symptoms
• Purpura (non-raised, non-blanching)
- Usually in adults
• Mucosal bleeding → epistaxis & bleeding gums - Platelet count is much lower (around 35)
• Hemorrhage or menorrhagia - Inhibition of ADAMTS 13, which breaks down vWF
Investigation
• Isolated thrombocytopenia with otherwise normal blood count
Management
• Prednisone
• IVIG
• Emergency platelet transfusion ⟶ if life threatening hemorrhage (platelets <20x109/L)
Henoch-Schönlein purpura (HSP)

➢ IgA mediated vasculitis of childhood
➢ Usually preceded by URTI
Presentation → [PAAN]
1. Purpura (raised, non-blanching) over buttocks and extensor surfaces
2. Arthralgia (especially in the knees and ankles)
3. Abdominal pain • Complications → Intussusception
4. Nephropathy → microscopic hematuria
Diagnosis
• Mainly a clinical diagnosis
• Look for elevated ESR, IgA
• Raised creatinine; labs consistent with nephropathy
Treatment
• Self-limiting; conservative management
• NSAIDs for arthralgia → beware of choosing this option if patient has impaired renal involvement
• Corticosteroids → arthralgia + GI dysfunction
Von Willebrand disease

➢ Mucosal bleeding ⟶ Epistaxis, menorrhagia
➢ Autosomal dominant (type 3 is recessive but rare)
➢ Role of vWF:
- Facilitate platelet adhesion to endothelial cells
- Carrier
Investigation • Bleeding due to dental extraction is considered mucosal bleeding
• 2 words ⟶ 2 abnormalities
- Prolonged bleeding time
- Prolonged aPTT
• Factor 8 is reduced, Defective platelet aggregation with ristocetin
Management
• Tranexamic acid ⟶ for bleeding
• Desmopressin ⟶ raises vWF
• Factor 8 concentrate
Hematology
Hemophilia A and B
➢ Congenital bleeding disorders with low levels of factor 8 (hemophilia A, classical hemophilia) or factor 9
(hemophilia B, Christmas disease)
➢ Hemophilia A is more common (90%)
➢ X-linked inheritance → Males are typically affected
➢ Female carriers are rarely symptomatic
Clinical presentation
• Hemophilia A and B are clinically indistinguishable
• Symptoms depend on the factor level
• History of spontaneous deep bleeding into joints, especially the knees, ankles and elbows, without a history
of significant trauma. Spontaneous hemarthrosis are virtually pathognomonic
• Intramuscular hemorrhage may also occur. Spontaneous bleeding into arms, legs, or any site. The bleeding
may lead to nerve compression, or compartment syndrome
Investigations
• Activated partial thromboplastin time (APTT) is usually prolonged but can be normal in mild disease
• Factor VIII/IX assay → to diagnose
Hemophilia A-specific treatment

• Desmopressin → raises factor VIII levels, and may be sufficient to treat Hemophilia type A
• Major bleeds (e.g. hemarthrosis) → recombinant factor VIII
• Do not give IM injections when factor is low
Hemophilia B-specific treatment

• Recombinant factor IX is the treatment of choice
Note: Desmopressin has NO value in treatment of hemophilia B
Avoid NSAIDS and IM injections

- Questions may arise with this topic. In PLAB, in whichever scenario, avoid NSAIDS and IM injection as the
answer in Hemophilia. NSAIDs must not be used for the fear of gastrointestinal hemorrhage. If needed, give
opiates for pain relief and if given → IV or SC but NOT IM → will produce a large and painful hematoma
Disseminated intravascular coagulation (DIC)

➢ In DIC, the increased clotting activity uses up the platelets and clotting factors in the blood. As a result,
serious bleeding can occur. DIC can cause internal and external bleeding
Features
• Ecchymoses or spontaneous bleeding at venipuncture or at trauma site
• Bleeding from ears, nose, throat and GIT
• Petechiae, purpura
Diagnosis
• All are elevated except platelets and fibrinogen
Treatment
• Treat the cause
• FFP in severe bleeding
Hematology
• 2 words 2 abnormalities
• 1 word 1 abnormality
• 3 words 3 abnormalities
Hematology
Hereditary Spherocytosis
➢ Hereditary Spherocytosis is the most common inherited RBC membrane defect
➢ Characterized by hemolysis, spherocytic RBCs with increased osmotic fragility
➢ 75% are autosomal dominant
Clinical features
• Hemolytic anemia, jaundice (either from hemolysis or gallstones) and splenomegaly
• 20-30% are mild with an increased red cell turnover compensated with adequate replacement. They are
neither symptomatic nor anemic, but may have mild splenomegaly, slight reticulocytosis and minimal
spherocytes visible
• 60-70% of patients have moderate disease and half of these present in childhood with anemia
• Neonates with severe hereditary disease do not always present at birth with anemia, but hemoglobin may
fall dramatically over the first few weeks of life and may be severe enough to require exchange transfusion
• Occasional aplastic crises occur, e.g. with parvovirus B19 infection
Diagnosis
1. Blood film → spherocytes and increased reticulocytes
2. MCHC → elevated • Spherocytes can be found also in autoimmune hemolytic
3. Osmotic fragility test (diagnostic) → spherocytes anemias. To distinguish the two → a direct Coombs test
- Hereditary spherocytosis → negative
- This is not reliable until six months of age
- Autoimmune hemolytic anemias → positive
Management
• When you see parvovirus B19 in the exam, immediately
• Steroid therapy
think of sickle cell anemia or hereditary spherocytosis
- In patients with moderate disease with the diagnosis of aplastic crisis at hand
• Folate supplementation
• Splenectomy
- Eliminates anemia and hyperbilirubinemia and lowers the high reticulocyte number to nearly normal
levels
- Splenectomy is curative in most patients but increased recognition of the long-term risks of splenectomy
has led to re-evaluation of the role of splenectomy
- Mild cases do not usually require folate supplements or splenectomy
Complications
• Rapid hemolysis can be triggered by viral infections and produce jaundice, anemia and occasionally
abdominal pain and tender splenomegaly. Supportive treatment is usually all that is needed
• Aplastic crises (aplastic anemia). They are most commonly caused by infection with parvovirus B19 and
usually last 10-14 days. This can be life-threatening
Parvovirus and anemia

➢ Although most patients have a decrease of erythropoiesis (production of red blood cells) during parvovirus
infection, it is most dangerous in patients with sickle cell anemia or hereditary spherocytosis, as they are
heavily dependent on erythropoiesis due to the reduced lifespan of the red cells
Hereditary spherocytosis Autoimmune hemolytic anemia

- Spherocytes - Spherocytes
- +ve osmotic fragility test - +ve osmotic fragility test
- -ve direct comb test - +ve direct comb’s test
Hematology
Polycythemia rubra Vera (PRV)
➢ The most common form of primary polycythemia. It is a malignant proliferation of a clone derived from one
pluripotent marrow stem cell
- There is excess proliferation of RBCs, WBCs, and platelets, leading to hyperviscosity and thrombosis
- More commonly found in patients who are >60 years old
- A mutation in JAK2 is present in >90% → Diagnostic
Presentation
• It may be discovered accidently with no related symptoms or there may be nonspecific complaints of lethargy
and tiredness
• About a third present with features of thrombosis (stroke, myocardial infarction, deep vein thrombosis and
pulmonary embolism)
• Headaches, dizziness, sweating, and tinnitus
• Bleeding from gums or easy bruising is usually mild but gastrointestinal hemorrhage can be more severe. This
is secondary to abnormal platelet function
• Pruritus → worse after a hot shower or bath
• Splenomegaly → 75% of patients (OHCM says 60%) → left upper quadrant mass
• Hypertension is common → 30%
• Erythema, warmth, pain, and even sometimes infarction of the distal extremities. Burning sensation in
fingers and toes, are characteristic but not very common
• Facial plethora
• Gout from increased cell turnover
Investigation • There is usually an abnormally low serum erythropoietin
• Initial → EPO
- 1ry PRV → low erythropoietin, low ferritin (high demand)
- 2ry PRV → high erythropoietin → high RBCs count
• Definitive → JAK2 mutation screen
Management
• Venesection (phlebotomy), a surgical opening or puncture of a vein in order to withdraw blood
• Chemotherapy options include:
- <40 years of age → interferon
- >40 years of age → hydroxycarbamide (hydroxyurea)
• Low dose aspirin 75mg OD → To reduce thrombotic events
2ry polycythemia
• Chronic hypoxemia ⟶ increased production of erythropoietin by the kidneys ⟶ increased RBCs production
• Causes ⟶ living at high altitudes, smokers, patients with COPD
• Labs ⟶ High erythropoietin, normal WBCs and platelets
- The long-term hypoxia triggered an increased production of EP by the kidneys to stimulate the bone marrow to
produce more RBCs to transport O2 to the tissues
- If repeated hemoglobin is still high in 2 months, further investigations would be warranted
Red → PRV
Pale → CKD
Yellow → Liver failure
Hematology
Acute lymphoblastic leukemia (ALL)
Etiology
➢ Mostly unknown but there are several well-known associations with the development of acute leukemia that
are sometimes present. These include radiation exposure, chemotherapeutic agents, as well as some
retroviruses
➢ Commonest childhood leukemia. Peak age is 2-4 years old
➢ ALL and AML are indistinguishable clinically
Clinical Presentation
• Symptoms of pancytopenia even if the total white blood cell count is normal
- Low RBCs → Anemia, the most common presenting complaint
- Low platelets → Bleeding, petechiae, purpura or ecchymoses
- Low/ abnormal WBCs → Recurrent and severe infections (oral, throat, skin, perianal infections
commonly
- Splenomegaly (10-20%) → NOT a key feature
- ALL is more often associated with infiltration of other organs (liver, spleen, and lymph nodes and bone)
Diagnosis
• FBC [ALL are low] • When pancytopenia is in the options, it is
- Anemia → Hb may be below 5 g/L usually leukemia, or aplastic anemia
- WBCs → low, normal, or elevated • The Philadelphia chromosome occurs in
- Thrombocytopenia 15–30% (mostly adults) and is associated
with a poor prognosis
• Bone marrow biopsy → numerous blasts is diagnostic
Acute myeloid leukemia (AML)

➢ This neoplastic proliferation of blast cells is derived from marrow myeloid elements. It progresses rapidly
(death in about 2 months if untreated)
➢ Children or young adults may present with acute symptoms over a few days to a few weeks
➢ Most AML subtypes show >30% blasts of a myeloid lineage in the blood, bone marrow, or both
Presentation
• Anemia
• Thrombocytopenia → Bleeding. Thrombocytopenia often causes petechiae on the lower limbs. DIC may
aggravate the situation and cause larger lesions
• Low WBCs → Infection
• Gingivitis is common, with swollen, bleeding gums
• There can also be bone pain
• Hepatomegaly and splenomegaly (Left upper quadrant fullness and early satiety)
• Lymphadenopathy is less common
Investigations
• FBC
- High WBCs. However, it may also be normal or even low
- Depleted neutrophils and blast cells are seen in their place
• Bone marrow aspiration → >20% blasts in the peripheral blood is diagnostic
• Sudan black stain → Auer rods is diagnostic
• Flow cytometry (immunophenotyping) → to distinguish AML from ALL
Hematology
Hematology
Chronic lymphocytic leukemia (CLL)
➢ CLL often presents as an asymptomatic elevation of white cells found on routine investigations for other
health problems
➢ These patients are exclusively older >50 years old
When patients do have signs and symptoms, they are usually non-specific:
• Fatigue
• Lethargy
• Cervical lymphadenopathy
When should you suspect CLL?

• When an older patient has marked elevation in WBCs (manifesting as recurrent infections) with marked
lymphocytic predominance
• The marrow is often infiltrated with mature lymphocytes → “Smudge cells” are seen on smear
Hematology
Chronic myeloid leukemia (CML)
➢ CML is a clonal bone marrow stem cell disorder in which a proliferation of mature granulocytes (neutrophils,
eosinophils and basophils) and their precursors is found
➢ Mnemonic: CML ⟶ Crazy Massive Large Spleen ⟶ approaches the right iliac fossa (DD: Malaria ⟶ travel Hx)
CML typically progresses through three phases:

• Chronic phase
- The immune system is competent and patients are asymptomatic for prolonged periods - (typically 4-5
years) More than 90% of patients are diagnosed in the initial chronic phase
• Accelerated phase
- In about two thirds of patients, the chronic phase transforms into an accelerated phase characterized by
a moderate increase in blast cells, increasing anemia or thrombocytopenia
• Blast crisis or blastic phase
- After a variable amount of time (usually months) the accelerated phase progresses to acute blastic
transformation. Features of blastic phase include bone marrow or peripheral blasts ≥30%, severe
constitutional symptoms due to tumor burden (weight loss, fever, night sweats, bone pain), infection
and bleeding
Clinical Presentation
• Usually presents at age 40 to 50 years old (middle-age)
• 85-90% of patients are diagnosed in the chronic phase and in recent years about 40% of patients have been
diagnosed before any symptoms developed, with incidental abnormalities spotted on a blood test.
- Fatigue (due to anemia)
- Weight loss
- Night sweats
- Abdominal discomfort → from massive enlargement of spleen (this is common)
- Splenomegaly → Most common reaches right iliac fossa (Seen in >75%)
- Hepatomegaly
• Enlarged lymph nodes are rare and infection are
- Enlarged lymph nodes (rare)
uncommon because these white cells retain the
- Low grade fever majority of their function
- Gout due to rapid cell turnover • The main feature of the disease is an elevated white
blood cell count consisting predominantly of
Investigations at presentation neutrophils. Blasts are either absent or low in count
• The Philadelphia chromosome is present in more
• FBC
than 90% of patients with CML
- Leukocytosis is common (often >100 x 109/L)
- Differential shows granulocytes at all stages of development (increased numbers of neutrophils,
myelocytes, basophils, eosinophils)
- Platelets may be elevated, decreased or normal levels
- A mild-to-moderate, usually normochromic and normocytic, anemia is common
• Peripheral blood smear
- All stages of maturation seen
• Biochemistry
- U&Es are usually normal at presentation, LDH is usually raised, serum urate may be raised
• Bone marrow aspiration and biopsy
- To quantify the percentage of blasts and basophils, to assess the degree of fibrosis and to obtain
material for cytogenetic-molecular analyses
• Cytogenetics → Ph chromosome is diagnostic, found in about 90% of cases. (OHCM says > 80%). This can be
found on cytogenetic analysis of blood or bone marrow
Hematology
Classic features of Lymphoma
• Drenching night sweats, fever, weight loss
• Enlarged but asymptomatic lymph nodes, typically in the lower neck or supraclavicular region
• Occasionally, hepatomegaly or splenomegaly
Lymphoma (Hodgkin’s) TB
• Painless LNs • Painful LNs
• No cough • Cough
• No travel history • Travel history to endemic areas OR congested
environment/close contact
➢ Extrapulmonary TB ⟶ not always accompanied by

cough
Non-Hodgkin lymphoma
➢ Lymphomas WITHOUT Reed-Sternberg cells HIV-related lymphomas
➢ Most are derived from B-cell lines; diffuse large B-cell lymphoma 1. NHL
(DLBCL) is commonest 2. Burkitt’s lymphoma (form of NHL)
➢ Known as AIDS-related lymphoma

Presentation
• Painless, slowly progressive peripheral lymphadenopathy ⟶ most common
• Primary extra-nodal involvement and systemic symptoms (fatigue, weakness, fever, night sweats, weight
loss) are not common at presentation but are common in patients with advanced or end- stage disease
• Bone marrow is frequently involved and may be associated with pancytopenia - anemia, infection, bleeding
(platelets).
• NHL → spread involvement (neck & spleen)
• Hepatosplenomegaly
• HL → neck and mediastinum
• Constitutional symptoms are less common in
Hodgkin’s & indicates disseminated disease
Hodgkin's lymphoma
➢ Hodgkin's lymphoma is a malignant tumor of the lymphatic system that is characterized histologically by the
presence of multinucleated giant cells (Reed-Sternberg cells)
➢ Bimodal age distribution, one peak around 20-29 years while the other peak at 60 years
Presentation
• Enlarged but asymptomatic lymph node, typically in the lower neck or supraclavicular region. They are
painless, non-tender, ‘rubbery’ superficial lymph nodes. They also can be axillary or inguinal nodes
• Mediastinal masses are frequent and are sometimes discovered on a routine CXR
• B symptoms
Superior mediastinum mass → 5Ts
• Pruritus and lethargy • Thymus
• Hepatomegaly, splenomegaly, and superior vena cava syndrome (due • Thyroid
to an obstruction from mediastinal lymph node involvement causing • Thoracic aorta
features of a mass effect) • Terrible lymphoma
Diagnosis • Teratoma & germ cell tumors
• Lymph node excision biopsy if possible
Hodgkin’s Vs leukemias → Hodgkin’s has normal CBC as the problem is outside the bone marrow
Hematology
Multiple Myeloma
➢ A cancer of plasma cells resulting in their overproduction replacing the bone marrow as well as the
production of large quantities of functionless immunoglobulins → recurrent infections
Clinical Presentation [CRAB + recurrent infections]
• Bone disease → Bone pain is the most common clinical manifestation. This is most commonly in the back
and the ribs, secondary to pathologic fractures
• Renal failure
• Anemia (normocytic, normochromic) → may present with weakness, fatigue, and pallor
• HyperCalcaemia → may present with polyuria, polydipsia, and altered mental status
• Rarely, symptoms of a hyperviscosity syndrome such as blurry vision, and confusion, may occur.
Diagnosis
• Serum protein electrophoresis → markedly elevated monoclonal immunoglobulin
• Urine protein electrophoresis → Bence Jones' protein
• X-ray of the skeletal system and skull → punched out lytic lesion caused by the overproduction of osteoclast
activating factor from the plasma cells
• Hypercalcaemia from the destruction of bone
Note that the hypercalcemia is associated with normal alkaline phosphatase
• Bone marrow biopsy → plasma cells (>10%) is diagnostic
• Blood film → Rouleaux formation
Tumor lysis syndrome

➢ Severe metabolic disturbance following the rapid lysis of malignant cells a short while after chemotherapy,
radiotherapy, surgery or ablation procedures
Key features
• History of leukemia or NHL (Burkitt’s lymphoma)
• Chemotherapy
• AKI
• Blood results [UK Pc]
- Hyperuricemia → Gout
- Hyperkalemia (earliest sign) → Paresthesia, muscle weakness, arrythmia
- Hyperphosphatemia → AKI
- Hypocalcemia → SPASMODIC
Management → IV fluids
Cold haemagglutinin disease (CHAD)

➢ Describes syndrome associated with acrocyanosis in cold weather due to RBC agglutination in blood vessels
of skin. Caused by RBC antibody that reacts most strongly at temperatures below 32°C
➢ May be idiopathic or secondary to infection with Mycoplasma or EBV (infectious mononucleosis)
Clinical features
• Acrocyanosis (blue discoloration of extremities e.g. fingers, toes) in cold conditions
• Splenomegaly
Diagnosis
• Anemia
• Increased reticulocytes
• +ve direct Coombs test
Hematology
Warfarin and high INR management
• For major bleeds
1. Stop warfarin
• High INR → increased risk of bleeding
2. Administer IV or oral Vit K1 (phytomenadione)
3. Prothrombin complex concentration (factor 9 complex)
4. FFP
• INR >8 + minor/no bleeding → Stop warfarin, administer Vit K1
• INR (6-8) + minor/no bleeding → Stop warfarin, restart when INR <5
• INR (5-6) but more than 0.5 units above target range → Reduce the dose OR stop the warfarin, restart when
INR <5
• INR above target range but less than 5 → Reduce or omit one or two doses and measure INR in 2-3 days
Surgery and warfarin

➢ Warfarin should always be stopped temporarily 5 days before planned surgery in patients with intermediate
to high risk of thromboembolism
➢ Recent TIA or patients with mechanical cardiac valves, surgery can proceed once INR is <1.5
➢ Replace with Heparin “heparin bridging”
➢ Warfarin is usually resumed at the normal dose on the evening of surgery or the next day if hemostasis is
adequate
Superficial thrombophlebitis (superficial venous thrombosis)

➢ Thrombosis + inflammation of superficial veins most commonly in the great saphenous veins of the legs
➢ Most case DON’T require antibiotics as they are not infective
➢ US is needed (specifically with proximal long saphenous vein) → to exclude concurrent deep vein thrombus
Management
1. Symptoms reduction Cellulitis
- Pain → Oral/topical NSAIDs • Acute, painful, spreading infection of
- Swelling → Compression stockings + Leg elevation deeper dermis and SC tissue
• Starts with a break in the skin
2. Prevention of DVT and PE
(trauma or other infections) allowing
- With other risk factors of DVT → SC LMWH or Fondaparinux the bacteria to enter (Strept, Staph)
- NO other risk factors of DVT → LMWH
↑ effects of warfarin (↑INR) ⟶ [SICKFACES.COM] ↓ effects of warfarin (↓INR) → [CRPA GPs]

• Sodium valproate • Carbamazepine
• Isoniazid • Rifampin
• Clarithromycin, Cimetidine • Phenytoin
• Ketoconazole • Alcohol
• Fluconazole • Griseofulvin
• Alcohol (binge drinking) • Phenobarbital
• Chloramphenicol • Sulphonylurea
• Erythromycin
• Sulfonamides
• Ciprofloxacin
• Omeprazole
• Metronidazole
Hematology
Notes
• PT, aPTT, BT are normal ⟶ Thalassemia
• BT (mucosal bleeding), aPTT raised ⟶ VWD
• Only aPTT is prolonged ⟶ Hemophilia
• All elevated except for platelets and fibrinogen ⟶ DIC
• PT, platelets are low ⟶ ITP
• BT is prolonged ⟶ TTP
• Helmet cells ⟶ Schistocytes
• Blast cells ⟶ ALL, AML, CML (blastic crisis)
• Granulocytes without blast ⟶ CML (chronic phase)
• Smudge cells ⟶ CLL
• Plasma cells ⟶ MM
• Hypersegmented Neutropenia ⟶ B12 & Folate deficiency
• Target cells ⟶ IDA or Thalassemia
• Heinz bodies, Bite cells ⟶ G6PD
• Owl eyes or reed Sternberg ⟶ Hodgkin’s lymphoma
• Target INR for Thromboembolism/most cases ⟶ 2-3
• Target INR for patients with metallic valves ⟶ 3-4
• Low INR ⟶ Lesser bleeding, faster clotting
• High INR ⟶ More bleeding, slower clotting
• Bruising on the face or forearm ⟶ Non-accidental injuries
• Hip/shoulder joints ⟶ Accidental injuries
• HIV/autoimmune ⟶ NHL
• EBV ⟶ HL
• High LDH indicates → Tissue breakdown
• Severe anemia + low reticulocytes in sickle cell anemia → Parvovirus B19 is the culprit
• Severe anemia + high reticulocyte count in sickle cell anemia → Splenic sequestration crisis
• Vitamin K deficiency → prolonged aPPT + prolonged PT
• Von Willebrand disease→ prolonged aPPT + prolonged bleeding time
Infectious Disease
Notes
• Malaria prophylaxis doesn’t provide full protection against all subtypes of malarial parasites
• Two vaccines that HIV positive patients should not have (regardless of CD4 count) → BCG, Yellow fever
• A vaccine shouldn’t be given in HIV if above 5 years + CD4 <200 or less than 1 year old + <750 → MMR
• In AIDS (Stage 3 HIV), give ALL except → Live attenuated vaccines
• Post-exposure prophylaxis (PEP) to a person with HIV:
- If viral load <200 + antiretroviral therapy (ART) for >6m → REASSURE
- If ≥1000 copies → Prophylaxis for 28 days → Test again in 2m, then 3m
- If PEP is required → should be given IMMEDIATELY for 28 days
- DO NOT wait for serology (4th generation lab venous blood HIV test)
- PEP → 1st line: Truvada and Raltegravir
- PEP can be taken up to 72h post-exposure
• Tetanus vaccine:
- Is it high-risk wound? If yes → give IgG (regardless of the immunization status), if not → no IgG required
- What’s his immunization status? Fully immunized? → nothing needed, if incompletely immunized or
can’t remember → complete course of the vaccine
- As long as the patient is on schedule whether completed or not → discard the tetanus vaccine
- High risk wound → contaminated with soil, compound fracturs, wound containing foreign bodies,
wounds or burns with systematic sepsis
- Schedule: 2m, 3m, 4m, 3-5y, 13-18y
- Booster dose is given if they’ve completed their schedule and travelling to remote areas
- If a healthy individual had a tetanus booster within last 5 years → NO further booster is required
• URTI + Cervical lymphadenopathy → Infectious mononucleosis, until proven otherwise
• Bilateral/unilateral parotid enlargement with pain at the angle of the mouth→ Mumps
• Human herpes virus 4 (HH4) / EBV → Infectious mononucleosis
• Human herpes virus 8 (HH8) → Kaposi sarcoma
• CD4 count in AIDS
- 1500-700 → no infection
- 500 – 200 → Hairy leukoplakia and Thrush herpes
- 200-100 → P. jiroveci
- <100 → Cryptococcus, Cryptosporidium, Toxoplasmosis
- <50 → Leukoencephalitis CMV
• Chicken pox and Mumps are both self-limiting viral infections so NO need for antibiotics
• In chicken pox, antibiotics is ONLY used if there’s superimposed bacterial infection with vesicles and fever
- If there’s fever → Oral antibiotics
- If NO fever → Topical antibiotics
• Painful single ulcer + painful LNS → Chancroid, caused by → Hemophilus Ducreyi [you do cry with Ducreyi]
• Painless single ulcer + painless LNs → Chancre, caused by → 1ry Syphilis
• Multiple painful ulcers → HSV
• Neutropenic sepsis
- Temperature >38oC + Neutrophils <0.5x109/L
- Chemotherapy is the most common cause, can also be a result of BM transplant or Hodgkin’s lymphoma
- Antibiotics must be administered immediately, DO NOT wait for WBCs
- 1st line → Piperacillin + Tazobactam (Tazocin)
- If still febrile after 48h → Meropenem +/- vancomycin
- If still not responding after 4-6 days → Investigate for fungal infection, if positive → IV antifungal
Infectious Disease
• Active TB + productive cough → Statin for acid fast bacilli (AFB)
• Active TB + NON-productive cough → Bronchoalveolar lavage bronchoscopy / Gastric lavage
• Latent Tb or screening for contacts → Mantoux test
• History of travel to Africa + Dark urine only → Schistosomiasis Haematobium
• History of travel to Africa + Hepatomegaly only → Schistosomiasis Mansoni
• History of travel to Africa + Dark urine + Hepatomegaly → Malaria
• A drug for eradication of latent hypnozoites and prevent relapses in Malaria → Primaquine
- Screening for G6PD deficiency is essential before administering Primaquine because it can cause
hemolysis in G6PD deficient individuals
- It’s contraindicated in pregnancy and breastfeeding
- For Malaria prophylaxis in pregnancy → Mefloquine
• Chloroquine and proguanil are safe in pregnancy
• High fever + relative bradycardia + severe headache + crouching position → Faget sign → Typhoid fever
• Immunocompromised patients or patients on steroids with history of exposure to HSV should be tested for
Varicella Zoster antibodies REGARDLESS of history of chickenpox
• A person with active shingles can spread the virus when the rash is in the blister phase, a person is not
infectious before the blisters appear. Once the rash developed crusts, the person is no longer infectious
• Shingles is less contagious than chickenpox and the risk of a person with shingles spreading the virus is low if
the rash is covered
• All human bites should be treated with a 7-day course of Oral co-amoxiclav (PEP)
• If the patient has a penicillin allergy → Metronidazole + Doxycycline/erythromycin/clarithromycin
• Follow-up serology blood tests for Hep B, Hep C and HIV at 6 weeks, 12 weeks and 24 weeks are required
• Tonsils with white exudates → Infectious mononucleosis
• Tonsils with grey exudates → Diphtheria
• Infectious mononucleosis = Glandular fever = Kissing disease
• Monospot test = Heterophile Antibody test = Paul Bunnell test
• An antidepressant that is safe while breastfeeding → Sertraline
• Hepatitis B
- HBsAg +ve → Infection (acute or chronic)
- HBsAg +ve & HBeAg positive → Highly infectious
- Anti-HBs +ve alone → Recent vaccination
- Anti-HBc positive → Past infection
• John is infected with Hep B and he has started to Sag → HBsAg, the viruses are eager to spread (HBeAg)
• Amy is a Harvard Business School (anti-HBs) graduate, knows better and had her vaccinations
• After a needle stick during an operation
- For the patient → Test for HIV antibodies, HBsAg and Hep C antibodies
- For the surgeon → Test for HBsAg
- Surgeon should be offered a booster dose of Hep B if he can’t remember when the last booster dose
- If the patient is considered low-risk → No PEP needed
- The surgeon should return in 6 weeks for a full set of serology which now includes Hep C and HIV
antibodies → If this comes -ve and the patient’s initial blood test was also -ve → Discharge with no
further follow-up
- If patient didn’t provide samples → Test the surgeon immediately after the injury, at 6, 12, 24 weeks
• Rates of transmission following inoculation of blood through a hollow bore needle:
- 0.3% if the donor is HIV +ve
- 3% if the donor is Hepatitis C antibody +ve
- 30% if the donor is HBsAg +ve
Infectious Disease
• The mother is encouraged to continue breast feeding with all conditions except with → Maternal HIV
• Breastfeeding is encouraged with Hepatitis C unless mother has cracked or bleeding nipple
• Breastfeeding is encouraged with TB but infant should be immunized with BCG as soon as possible
• TB cannot spread from breast milk but can spread from respiratory droplets, however mothers are usually
not infectious after 2 weeks of TB treatment
• Most common cause of laryngitis → Common cold, overusing of vocal cords may also be the cause
• Edematous vocal cords lead to hoarseness of voice
• Positive Hepatitis C → HCV antibody reactive + HCV RNA detected
• Directly observed therapy (DOT) should be offered in patients with TB who:
- Have not adhered to treatment before
- Have a history of homelessness
- Have a history of drug or alcohol misuse
- Are currently in prison
- Are in denial of their diagnosis
- Have multidrug-resistant tuberculosis (MDR)
- Request the service
- Are too ill to administer the treatment themselves
• Patient with Gastroenteritis should not return to work/school until 48h have passed since the last episode of
diarrhea or vomiting
• If bacterial meningitis is suspected, local health protection team should be notified for any case with
potential public health implications, that’s done prior to lab confirmation
• A boy with chicken pox can return to the nursery once the rash has crusted over and 5 days have passed
from the onset of the rash
• Ramsey-Hunt syndrome (herpes zoster oticus)
- PURPLE → Pain (ear, face, mouth), Unsteady (vertigo, dizziness), Red Rash (vesicles on
ear/mouth/hairline), Palsy (VII), Loss of hearing, Exception (there’s not always a rash)
- RASH → Rapid Antiviral Steroid, Highlight (eye care)
• Laryngeal tuberculosis
- Hoarseness of voice + Dysphagia
- Features of TB (fever, weight loss, lethargy, lymphadenopathy)
• Investigations for syphilis
At the GP’s:
- Serology for syphilis → VDRL, TPHA or treponemal antibody absorption
- PCR → can only be carried out from a sample of the lesion or an infected LN
At the GUM:
- Dark field microscopy → can only be carried out from a sample of the lesion or an infected LN
Nephrology
Acute kidney injury (AKI)
➢ A reduction in renal function following an insult to the kidneys which occur over hours to days
Causes
➢ Prerenal ⟶ Ischemia ATN (acute tubular necrosis)
• Most common renal cause of AKI
• Hypovolemia secondary to diarrhea/vomiting
• Occurs after a prolonged ischemic event
• Renal artery stenosis (e.g. massive hemorrhage, hypotensive
➢ Intrinsic shock) with increased creatinine
• AGN • There may be a history of nephrotoxins
• Acute tubular necrosis (ATN) interstitial nephritis (allergic)
• Acute interstitial nephritis (AIN) ➢ Allergy + hematuria
• Rhabdomyolysis
• Tumor lysis syndrome (after killing large amount of tumor cells)
➢ Postrenal
• Kidney stone in ureter or bladder Drugs that are safe in AKI:
• Benign prostatic hyperplasia (BPH) - Paracetamol
- Warfarin
• External compression of the ureter
- Statins
Risk factors - Aspirin
• CKD - Clopidogrel
• Other organ failures - B-blockers
• Hx of AKI
• Nephrotoxic drugs (e.g. NSAIDs, aminoglycosides, ACE inhibitors & diuretics) ⟶ [DAMN]
• Usage of iodinated contrast in the past week
• >56 years old
Features
➢ Maybe asymptomatic until renal failure progresses
• Oliguria (<0.5 ml/kg/hour)
• Fluid over load ⟶ pulmonary and peripheral edema
• ↑ K+ ⟶ Arrythmias
• ↑ Urea & creatinine ⟶ pericarditis or encephalopathy
Chronic kidney disease (CKD)

➢ CKD results in decreased activity of 1-alpha
Symptoms hydroxylase which is responsible for the
• Usually asymptomatic, may be discovered by a chance conversion of 25-hydroxyvitamin D to its active
• Specific symptoms in severe CKD form 1,25-dihydroxyvitamin D (especially when
GFR is <30 mL/min) ⟶ low Ca absorption ⟶
- Peripheral edema
high parathyroid hormone
- Pruritis ➢ Findings in CKD
- Nausea, vomiting, fatigue • Small kidneys (<9cm)
- Sexual dysfunction • Anemia
Signs • Low Ca
• High PO4
• Skin pigmentation
• Pallor (due to anemia of chronic disease)
➢ The only definite sign of CKD is previous blood results showing high creatinine/low GFR
Management
• ACEI (e.g. Lisinopril) or ARB in all ethnic groups with CKD and HTN
- ACR (albumin creatinine ratio) ≥ 70
- ACR ≥ 30 + HTN • ACEIs are contraindicated in renal artery
stenosis and severe hyperkalemia
- ACR ≥ 3 + Diabetic
Nephrology
NephrOtic syndrome ⟶ loss of a lot of prOtein
➢ 1ry causes (80%)
• Children, young adults ⟶ Minimal change disease
• Elder adults ⟶ Membranous GN, minimal change nephropathy or Focal & segmental glomerulosclerosis
➢ 2ry causes
• SLE (comes 3rd as in the most common causes in adults)
• Hepatitis B & C, HIV
• DM, Amyloidosis ➢ A child with LL edema ⟶ order 24hr urine protein ⟶
Triad order serum albumin, if confirmed nephrotic $ ⟶
1. Proteinuria (≥3 gm/24hr) refer to a nephrologist
2. Hypoalbuminemia (≤ 30g/L) ➢ Definitive investigation is Renal biopsy
- Minimal change disease ⟶ fusion of podocytes
3. Edema (pre-orbital)
Complications
• Renal vein thrombosis (due to loss of anti-coagulation factors in urine e.g. Antithrombin III)
- Sudden left loin pain, hematuria & sudden swelling of the left testis
• Infections (due to loss of immunoglobulin proteins in urine)
• Na+ retention (due to 2ry hyperaldosteronism as a result of low renal perfusion)
• Hypercholesterolemia (due to non-specific increase in cholesterol synthesis)
Management
• Diet: Fluid restriction, low salt and sufficient protein
• Drugs: steroids (if resistance ⟶ cyclophosphamide) & diuretics
Nephritic syndrome ⟶ loss of a lot of blood

➢ Hematuria (microscopic or macroscopic) + red cell cast
➢ Proteinuria (++)
➢ Hypertension (mild) ➢ Goodpasture’s treated with plasmapheresis
➢ Low urine output (<300 ml/day) and immunosuppressants
Causes
• Post-streptococcal GN ⟶ appear after 1-2 weeks after URTIs
• IgA nephropathy (Berger’s disease) ⟶ appears after 1-2 days after URTIs
• Rabidly progressive glomerulonephritis
o Goodpasture’s $ (Anti-GBM antibodies)
o Vasculitis disorder: Wegener’s granulomatosis (C-ANCA), Churg Strauss disease (P-ANCA)
• Membranoproliferative GN
• Henoch-Schoenlein purpura ⟶ PAAN
ADPKD
Hematuria + HTN
- US
Goodpasture’s $
Hematuria + Hemoptysis - Anti-GBM antibodies
- Kidney or lung biopsy
Wegener’s granulomatosis
Hematuria + Hemoptysis + Nasal/sinus problems
- C-ANCA
Hematuria + Jaundice Alpha 1-antitrypsin deficiency
Nephrology
Post-streptococcal glomerulonephritis
➢ Typically occurs 1-2 weeks following URTI, impetigo, otitis media or cellulitis
➢ Caused by: group A beta-hemolytic Streptococcus (usually streptococcus pyogenes)
➢ Young children (below age 7) are most commonly affected
➢ Caused by immune complex (IgG, IgM and C3) deposition in the glomeruli
Features
➢ Nephritic $ + oliguria
➢ Tea-colored urine
Investigations
• Low C3
• Raised anti-streptolysin O titer ⟶ indicates recent streptococcal infection
• Renal biopsy ⟶ most accurate
o It shows subepithelial humps (IgG and C3 deposition)
Post-streptococcal glomerulonephritis IgA nephropathy (Berger’s disease)
- 1-2 weeks after URTIs - 1-2 days after URTIs (IgA ⟶ ASAP)
- Main symptom ⟶ Proteinuria - Main symptom ⟶ Hematuria
- Low C3 - Young males
Henoch-Schoenlein purpura
• Same pathology as IgA nephropathy and similar finding on renal biopsy
• However, it’s common among children
• A systemic disease that involves skin, connective tissue, scrotum, joints, GIT and kidneys
• Symptoms also include: abdominal pain, joint pain (knees) and rash
• Complication: intussusception
Orthostatic or isolated proteinuria

➢ Isolated proteinuria in otherwise healthy
• 1st step ⟶ Repeat the test individual ⟶ Repeat the dipstick analysis
• Still +ve ⟶ 24-urine collection or urine protein creatinine ratio ➢ False positive proteinuria:
• Recurrent ⟶ biopsy - Alkaline urine
- Exercise causes transient proteinuria
DD of small kidneys
- Hypertension
- Bilateral renal artery stenosis
- CKD
- Chronic pyelonephritis
Rule of thirds in Membranous Glomerulonephropathy

- 1/3 → Partial remission but still have the chronic disease
- 1/3 → Remission
- 1/3 → ESRD
Nephrology
Acute pyelonephritis
➢ Inflammation of the kidney and renal pelvis usually caused by ascending UTIs
➢ 80% of infections are due to E. coli
Risk factors
• Structural renal abnormalities, including vesicoureteral reflux (VUR)
• Calculi & urinary tract catheterization
• Stents
• Pregnancy ➢ Acute ⟶ Active infection (fever, loin pain, etc.)
➢ Chronic ⟶ Renal scarring (often asymptomatic,
• Diabetes renal failure symptoms)
• Neurogenic bladder
• Prostate enlargement
Presentation
Upper UTIs
• Rapid onset • 1st ⟶ Ciprofloxacin
• Unilateral/bilateral loin pain, suprapubic pain or back pain • 2nd ⟶ Co-amoxiclav
• Costovertebral tenderness may be present
Lower UTIs
• Fever & rigors • Trimethoprim
• Vomiting • Nitrofurantoin
• Accompanying symptoms of lower UTI
- Frequency, urgency
- Suprapubic pain
- Urethral burning on voiding
Investigations
➢ Urinalysis ⟶ look for blood, leukocyte esterase and nitrate Imaging is required with complicated pyelonephritis:
➢ Midstream specimen of urine (MSU) ⟶ for microscopy and - Persistent Fever more than 48h despite AB
culture - Recurrent episodes
- This should be done before starting empirical - Suspected stone
- Patients with DM and immunocompromised
antibiotics
Management
➢ Usually requires admission
➢ Antibiotics
- Start empirical antibiotic treatment whilst waiting for culture and sensitivity results
Non-pregnant women, men & people with indwelling • Ciprofloxacin 500mg twice daily for 7 days
catheters • Alternatively, co-amoxiclav for 14 days
• Co-amoxiclav as 1st line

Children
• Alternatively, cefixime
Pregnant women who don’t require admission • Cefalexin
Chronic pyelonephritis
Imaging
- Renal US ⟶ small kidneys with a thin cortex
- Intravenous pyelogram (IVP) ⟶ may show small kidneys, ureteric and caliceal dilatation/blunting with
cortical scarring
- Micturating cystourethrogram (MCUG) ⟶ to identify reflux
- Tc-99m (Tc-DMSA) ⟶ the most sensitive for demonstration of renal scar
Nephrology
Recurrent UTI
➢ Defined as >2 infections in the past 6 months or 3 within 12 months
➢ E. coli is the most common organism in all age groups
➢ There’s often an underlying functional or anatomical problem and infection will often not resolve until this
has been corrected
Causes
• Incomplete bladder emptying
• Renal or bladder stones
• Indwelling catheters
• Chronic bacterial prostatitis
• Vesicovaginal or colovesical fistula
• Bacteria within an obstructed or atrophic infected kidney
Presentation
• Dysuria
• Frequency
• Urgency
• Suprapubic pain or discomfort
• Cloudy foul-smelling urine
Investigations
• MSU microscopy and culture
• KUB X-ray → to detect radio-opaque renal calculi
• Renal and bladder US
- Looking for renal stones
- To determine the presence or absence of hydronephrosis
- To measure pre-void bladder volume (PVBV) and post-void residual urine volume (PVRV)
• Flexible cystoscopy, to identify abnormalities that may cause recurrence such as bladder stones, an
underlying bladder cancer which is rare, urethral or bladder neck stricture or fistula
Management
• Deal with the underlying cause
• Low-dose antibiotic prophylaxis ⟶ trimethoprim, nitrofurantoin or cefalexin
• If there’s residual urine present ⟶ optimize bladder emptying by intermittent catheterization
• Estrogen replacement in post-menopausal women ⟶ lack of estrogen in post-menopausal women cause loss
of vaginal lactobacilli and increased colonization by E. coli
Nephrology
Rhabdomyolysis
➢ It results from breakdown of skeletal muscle with the release of its contents
- Myoglobin & creatine kinase (CK)
- K+, P, urate
Causes Scenarios
- Elderly patient with hx of fall followed by long
- Sudden, severe crush injury
duration on the floor
- Status epilepticus - Mountain biker rescued from being trapped under
- Severe exertion heavy rocks for many hours
Complications - Trapped under a fallen wardrobe for several hours
- IV drug user found on floor not moving for a few
• AKI
days ⟶ tissue compression ⟶ muscle ischemia
• Hyperkalemia - Marathon runner who just completed a long-
Investigations distance run
- Best initial ⟶ Urinalysis (to look for hematuria)
DD
- Most important ⟶ ECG & K+ level
➢ Dermatomyositis
- Confirmed by ⟶ markedly elevated CK (>10,000 U/L) • Gottron’s papules (over the knuckles)
- Rabidly rising creatinine level • Heliotrope rash (around the eyelids)
Management
• Ca chloride/gluconate
- If there are ECG abnormalities from hyperkalemia
• IV fluid rehydration
- Priority to prevent AKI
- Decreases the duration of contact between the nephrotoxic myoglobin and the kidney tubule
• IV sodium bicarbonate
- To alkalinize urine to pH >6.5, to stabilize a less toxic form of myoglobin
- Alkalinizing the urine with bicarbonate may help prevent the precipitation of the pigment in the tubule
• Dialysis
- Only needed in severe cases
Autosomal dominant polycystic kidney disease (ADPKD)

➢ Gross hematuria following trauma is a classic presentation of ADPKD
➢ Sometimes present with kidney failure (usually in the fourth to sixth decade of life)
➢ May be asymptomatic on screening of family members
➢ Intracranial aneurysm is the most serious complication → leads to Subarachnoid hemorrhage
Features
- Flank pain
- Hematuria (micro & gross)
- UTIs and calculi
- Hypertension
- Bilateral kidney enlargement (maybe palpable)
Diagnosis
• US KUB
Treatment
• Nonspecific, treatment of hypertension
Nephrology
Hemolytic uremic syndrome (HUS)
➢ A triad of hemolytic anemia, uremia, stomach virus and thrombocytopenia
➢ Hemolytic anemia will be intravascular in nature with abnormal blood smear showing schistocytes, helmet
cells and fragmented red cells
➢ Mainly caused by E. coli. Occurs after eating undercooked contaminated meat
➢ Usually in young children, bloody diarrhea followed by renal impairment
Signs
HUS → Hemolysis, Uremia, Stomach virus + thrombocytopenia
- Abdominal pain
TTP = HUS + fever + neurological symptoms
- Bloody diarrhea • Usually in adults
- Signs of AKI • Platelet count is much lower (around 35)
Diagnosis
• Initially → E. coli serology, stool culture, urine analysis, FBC
• Renal US, to rule out damage
Management
- IV fluids, blood transfusion and dialysis if required
- DO NOT give antibiotics to those with possible HUS; this organism will release more toxins as it dies
- FFP is reserved for severe cases of HUS not associated with diarrhea
Host-versus-graft disease
1. Hyperacute – occurs within minutes
2. Accelerated – occurs within a few days → managed by IV methylprednisolone followed by high dose oral
prednisolone
3. Acute – occurs between 1-12 weeks
4. Chronic – a series of episodes of acute rejections over months that lead to a gradual loss of organ function
Management
- If the patient is anuric with severe hyperkalemia → Dialysis
- Definitive management → Renal transplant
Indications for dialysis (AEIOU)

• Acidosis
• Electrolyte imbalance (hyperkalemia)
• Ingesting toxins
• Overload (volume)
• Uremia (encephalopathy, pericarditis)
• Drug overdose (e.g. Aspirin, ethylene glycol, Lithium)
Contrast induced nephropathy

prevention
• Increasing fluid intake
• IV normal saline (12h pre- and 12h post-procedure)
• N-acetylcysteine (NAC)
• Stop metformin (if being taken)
Nephrology
Base access (+/- 2mmol/L)→ <-2 means acidosis, >+2 means alkalosis
Neurology
Stroke
Stroke → a syndrome of the sudden onset of focal neurological loss of presumed vascular origin lasting >24h
Transient ischemic attack (TIA) → a syndrome of the sudden onset of focal neurological loss of presumed vascular
origin lasting <24h
The posterior circulation

Presentation [DR DAN]
• Dizziness/vertigo, right hemianopia, nystagmus, ataxia, dysdiadochokinesia
• Usually sudden onset with possible further progression that takes place over hours
• May have underlying IHD, hypertension, carotid bruits, AF
Cerebellar lesion • Ophthalmoplegia or double vison → Brainstem

• Nystagmus → Cerebellum
Presentation [DAN SHIP]
• Dysdiadochokinesia, ataxia, nystagmus, slurred speech, intention tremor, hypotonia, past pointing
• Usually sudden onset with possible further progression that takes place over hours
• May have underlying IHD, carotid bruits, AF
• Strokes in the veRmis → tRuncal ataxia

Brainstem stroke • Strokes in the cerebellar lobes → limb ataxia
of the ipsilateral side
Presentation [ADD FOG]
• A-Ataxia
• D-Diplopia
• D-Dysarthria
Cerebellopontine angle stroke
• F-Facial numbness - CN 5,7,8
• O-Ophthalmoplegia - Cerebellum
• G-Gaze palsy
Diagnosis of acute stroke

• Non-contrast CT brain → initial investigation
• MRI brain → more sensitivity
Management of acute stroke

• Ischemic stroke → thrombolysis (alteplase) then, aspirin 300mg
- Cannot be started until a CT scan has excluded hemorrhage
- Thrombolysis is given only within 4.5h of onset of stroke, after 4.5h, it has no significance
• Maintain oxygen saturation, glucose control, blood pressure control
• Maintain nutrition and hydration
• Early mobilization
• If >4.5h has passed following a stroke or CT shows cerebral
infarction (which takes time to develop) → Aspirin
Post management stroke
• Aspirin 300mg + Clopidogrel 75mg
- Aspirin is given for 2 weeks immediately after an ischemic stroke is confirmed by brain imaging
- Clopidogrel is given daily long-term
- If clopidogrel is contraindicated/not-tolerated → dipyridamole + low dose insulin
• Ensure a statin has been offered
Neurology
Secondary prevention after a stroke or TIA
• Lower blood pressure
- Aim for 130/80
- DO NOT start controlling BP in the first 48h as this may cause extension of stroke
• Lower cholesterol
- Aim for 40% reduction in non-HDL cholesterol
- Statins can be taken lifelong after TIA or ischemic stroke → 80mg atorvastatin
• Antiplatelet and anticoagulation treatment
- Not recommended unless there’re clear indications
- If AF is present → Warfarin, Apixaban (Warfarin Target INR ranges 2.0-3.0)
- AF is absent → Clopidogrel 75mg daily lifelong, if intolerant → dipyridamole + low dose insulin
- Anticoagulants shouldn’t be started until CT has excluded hemorrhage and usually not until 14 days have
passed from the onset of an ischemic stroke
• Lifestyle advice
- Low salt diet
- Low cholesterol diet
- Weight loss
- Alcohol reduction
- Smoking cessation
Always consider “Carotid endarterectomy” as 2ry prevention in ischemic stroke

o Carotid duplex is used if internal carotid artery is stenosed (stenosis >50% in men, >70% in women)
o Should be done within 2 weeks of admission
Stroke
1. Cortical 2. Brainstem
- Focal involvement - Global involvement (whole side) → rule of 4s
Neurology
Rule of 4s
4 CNs in:
- Medulla
- Pons
- Above pons
4 CNs divide evenly into 12
- 3,4,6,12
- Motor nuclei are midline
Other CNs don’t divide into 12
- 5,7,8,9,10,11
- All are lateral
4 midline columns
- Motor pathway (corticospinal tract)
- Motor nucleus and nerve
- Medial longitudinal fasciculus (MLF)
- Medial lemniscus
4 lateral (side) columns
- Sympathetic pathway
- Spinothalamic
- Sensory nucleus of CN5
- Spinocerebellar pathway
Localizing lesions
• Medial vs. Lateral
- Which tract is affected?
• Medulla vs. Pons vs. Midbrain
- Which cranial nerves are affected?
Nerve Lesion
Olfactory CN1 • Not in the midbrain
Optic CN2 • Not in the midbrain
Oculomotor CN3 • Eye turned out and down (action of LR6 + SO4) + ptosis + mydriasis
Trochlear CN4 • Eye unable to look down when looking towards nose (affected SO)
Trigeminal CN5 • Ipsilateral facial sensory loss, afferent of corneal reflex
Abducent CN6 • Ipsilateral eye abduction weakness (affected LR)
Facial CN7 • Ipsilateral facial weakness/droop, efferent of corneal reflex
Auditory (vestibulocochlear) CN8 • Ipsilateral deafness or loss of balance
Glossopharyngeal CN9 • Ipsilateral pharyngeal sensory loss + impaired swallowing + loss of gag
Vagus CN10 • Ipsilateral palatal weakness (absent gag reflex) + vocal cord paralysis
Spinal Accessory CN11 • Ipsilateral shoulder weakness + affected head movement
Hypoglossal CN12 • Ipsilateral weakness of the tongue (towards the same side of the lesion)
Neurology
Midline structures (M)
Motor pathway (corticospinal tract) • Contralateral weakness
Motor nucleus and nerve • Ipsilateral CN motor loss (3,4,6,12)
MLF • Ipsilateral intranuclear ophthalmoplegia (INO)
Medial lemniscus • Loss contralateral proprioception/vibration
Side/Lateral structures (S)

Sympathetic pathway /chain • Ipsilateral Horner’s syndrome
Spinothalamic • Contralateral pain/temp sensory loss
Sensory nucleus of CN5 • Ipsilateral pain/temp loss in the face
Spinocerebellar pathway • Ipsilateral ataxia
Brainstem blood supply
Neurology
Vascular supply of the brain
• ACA – frontal and medial cerebrum
• MCA – lateral part of the hemisphere
• PCA – occipital lobe
• Basilar artery – cerebellum, brainstem, occipital
lobe
Middle cerebral artery occlusion

- Aphasia in the dominant hemisphere
- Neglect in the Non-dominant hemisphere (NN)
- Contralateral paralysis (face & arm)
- Contralateral sensory loss (face & arm)
- Gaze preference toward side of lesion
- Homonymous hemianopsia
All are contralateral except the gaze preference
Anterior cerebral artery occlusion

- Contralateral hemiparesis and sensory loss
Posterior cerebral artery occlusion

- Contralateral homonymous hemianopia with macular sparing
- Visual agnosia
Basilar artery occlusion

- Locked-in $ → body and most of the facial muscles are paralyzed but consciousness remains and the ability
to perform certain eye movements is preserved
Neurology
Bell’s palsy Be sure to exclude other causes of facial
weakness
Risk factors
- Lyme disease → Travel Hx + Borrelia
• Pregnancy antibodies and varicella zoster antibodies
• DM - Ramsay-Hunt $ → unilateral facial
Presentation weakness + ear pain + rash
- Brain tumors → MRI
• Unilateral facial weakness; facial droop
• Drooling
• Difficulty in eye closure
• Less common <15 years old
Treatment
• Within 72 hours onset → Prednisolone (also in pregnancy)
• If suspecting Ramsay-Hunt syndrome → Acyclovir
• Eye protection with eye patch
Which side of the face is affected by Bells’ palsy?

→ The right side (right CN7), he’s trying to smile and only his left facial muscles are
working
If the patient is able to close his eyes and raise his eyebrow on the affected side → UMNL, not Bell’s
Trigeminal neuralgia
Presentation
• Unilateral, shooting or stabbing electric shock-like facial pain
• Pain exacerbated with movement or touch especially in the jaw (CN V, 2nd and 3rd branch distribution)
• Abrupt in onset and termination
Diagnosis
• Clinical diagnosis
• MRI is routinely done to rule out other pathology (i.e. schwannoma, meningioma)
Treatment
• Medication then surgery
• Carbamazepine (Tegretol) >lamotrigine / phenytoin / gabapentin
• Surgical: microvascular decompression
Atypical facial pain

- Chronic dull aching pain, poorly localized but located in the maxilla
- Could be unilateral or bilateral
Herpes zoster ophthalmicus

- Reactivation of varicella zoster virus in the area supplied by the ophthalmic branch of the trigeminal nerve
- Features: vesicular rash around the eye, which may or may not involve the eye itself
Neurology
Types of traumatic brain injury
Epidural hematoma Subdural hematoma Subarachnoid hematoma
• Associated with skull fractures Chronic (2-3 weeks) • Aneurysm formation is the
and MMA injury • Usually elderly on most common etiology
• Usually a young athlete with an anticoagulation, high INR or • Sudden onset in the context of
injury to the side of the head alcoholic a ruptured cerebral aneurysm
• Features of increased ICP • History of falls or minor head but may be seen in association
• Immediate LOC then recovers injury with other injuries when a
spontaneously by lucid • Slow onset of symptoms patient has sustained a
intervals compared to epidural traumatic brain injury
• The patient will have a decline hematoma • Association with:
of mental function • Symptoms → progressive - PKD (Berry aneurysms)
• Lucid intervals (patient goes headache, confusion, nausea, - Ehlers Danlos $
back to doing what he was vomiting or gradually evolving - Hypertension
doing before, before falling neurological deficits - Alcohol consumption
unconscious again) • Hallmark → THUNDECLAP
Acute (3-7 days) HEADACHE, very severe
Investigation • Has lucid intervals → difficult to OCCIPITAL headache
• CT/MRI → Bi-convex differentiate • First headache in a long time in
• Patient is barely awake during a person who doesn’t usually
Management the lucid intervals suffer from headache, described
• Refer to a neurosurgeon • Think bigger trauma and sicker as the worst headache by the
• Burr hole over pterion (the patient patient
region where frontal, parietal, • Low GCS • Meningeal irritation (neck
temporal and sphenoid bone • Signs of increased ICP: stiffness, photophobia,
join together) to ensure that - Headache, nausea, vomiting vomiting)
bleeding escapes instead if - Confusion
expanding intracranially - Pupils doesn’t respond to Investigations
• Followed by craniotomy and light • CT brain without contrast
evacuation of hematoma - Decreased mental abilities • Lumbar puncture
- Confusion - Only done if CT is
If small volume hematoma with - Shallow breathing inconclusive + no
minimal midline shift and a good - Seizures contraindications
GCS without focal deficit → - Done after 12h from
managed conservatively (e.g. Investigations headache onset, to allow
Mannitol) + serial CT scans to • CT/MRI → Crescent-shaped breakdown of RBCs
monitor progress - CSF → bloody then
Management xanthochromic (bilirubin)
• Surgical evacuation
• Mannitol, can be given with After subarachnoid hemorrhage is
signs of ICP confirmed, its origin needs to be
determined → Cerebral
angiography or CT angiography
Neurology
Generalized vs partial seizures
Generalized seizures Partial seizures
• Loss of consciousness • May or may not have LOC depending if they’re
• Both halves of the body (right and left) are simple or complex
involved - Simple → conscious
- Complex → not conscious
Tonic → stiffness
Clonic → twitches
Tonic-clonic → stiffness + twitches
Myoclonic → conscious + less than 1s
Management Status epilepticus

Status epilepticus
• A seizure lasting >5 minutes OR not regaining consciousness in the interictal period (between seizures)
- Administer a maximum of 2 doses of the first line treatment

- In children → buccal midazolam is 1st line, if not available → rectal diazepam is used
- If seizures continue despite medications (>30min) → refer to the ICU for intubation
- For home treatment → Rectal diazepam or buccal midazolam
Neurology
Absence seizure
Presentation
• Child usually <10 years old
• Loss of awareness (“daydreaming”), stare blankly into space, will not respond to their surroundings
• Face often looks pale with a blank expression
• May be accompanied by upturning of eyes or eyelids may flutter
• They would still be able to maintain the balance and do not fall during the episode
• Will return to normal activities after seizure (unaware of the seizure) but may not perform well and feel tired
• Seizures start and finish abruptly
• Occasionally, head may fall down a little, or arms may shake once or twice
• No photosensitivity
• Maybe triggered by hyperventilation
Diagnosis
• EEG
• Check FBC, glucose levels, ECG, MRI for other underlying causes
Treatment
• If recurring → sodium valproate or ethosuximide
Epilepsy
- At least 2 unprovoked epileptic seizures occurring >24h apart
Epilepsy vs NEAD
- Patients with NEAD usually retain consciousness, if you elevated their arm above their face and drop it, the
patient would avoid hitting his face
- Video EEG is used to diagnose NEAD
- Tilt table testing is used to diagnose vasovagal episodes
Epilepsy and pregnancy

- Sodium valproate should NOT be used unless there’s no effective alternative
- Safest medications → Carbamazepine and Lamotrigine
- High dose (5mg) folic acid is recommended for at least 1 month periconceptually and throughout the first
trimester
- In established pregnancy, changes to alternate antiepileptic drug therapy should NOT be undertaken solely to
reduce teratogenic risk for 2 reasons:
1. Changing AEDs may precipitate seizures
2. Overlapping AEDs during the change exposes the fetus to effects of an additional antiepileptic drugs
- Once an unplanned pregnancy is discovered it is usually too late for changes to be made to the epilepsy
treatment regimen. The risk of harm to the mother and fetus from convulsive seizures outweighs the risk of
continued therapy
Neurology
Epilepsy vs Non-epileptic attack disorder (NEAD)
Neurology
Delirium
➢ It can be classified as a clinical syndrome involving acute brain dysfunction or failure where there’s
involvement of thought, perception and level of awareness
Precipitating factors
• Metabolic derangement
• Hypoxia
• Infection • Delirium → acute onset
• Dementia → chronic decline of mental functions
• Dehydration
• Schizophrenia → affects young people, diagnosed
• Aging after 6 months of having symptoms
• Constipation
• Medication (e.g. Benzodiazepines)
Presentation
• Acute onset
• Fluctuating levels of consciousness
• Disorientation, mood changes, paranoia
• Memory impairment
• Withdrawn or heightened arousal
Diagnosis
• Clinical assessment via DSM-V
• Consider radiological imaging to rule out organic pathology
Treatment:
• 1st line → De-escalation techniques • If the patient has Parkinson’s → Lorazepam
• If failed → Olanzapine or Haloperidol for 1 week
Normal pressure hydrocephalus

➢ A reversible cause of dementia seen in elderly, thought to be 2ry to reduced CSF absorption at the arachnoid
villi
Presentation
[GDU → grandpa in Arabic] – Hakim’s triad
• Gait abnormalities (may be similar to Parkinson’s disease) → Early
• Dementia
• Urinary incontinence → as the awareness of urine passage is absent
Investigation
• CT/MRI brain → enlarged lateral and third ventricles
• Lumbar infusion test (intrathecal infusion test)
Treatment
• CSF shunting: ventriculoperitoneal, ventriculo-pleural, or ventriculo-atrial
Neurology
Alzheimer
Alzheimer’s disease (3 A’s)
➢ The most common cause of Dementia • Apraxia (can’t move)
- Inability to carry out purposeful
Presentation
movements
• Elderly > 65 years • Aphasia (can’t speak)
• Early - Loss of ability to speak
- Memory loss (recent → distant) • Agnosia (can’t recognize)
- Difficulty finding words - Loss of ability to recognize
what objects are and do as well
• Followed by as people
- Progressive language deficits
- Inability to make decisions
- Confusion
• Late
- Disoriented
- Behavioral change
- Hallucinations
Diagnosis
• MRI brain → diffuse cortical atrophy
• Hexamethylprpyleneamine oxime (HMPAO) single-photon emission computed tomography (SPECT), to
differentiate Alzheimer from Pick’s disease and other pathology
• Mini-mental state exam (Folstein test), to assess the severity of cognitive dysfunctions and when to start
medication
Treatment
• Acetylcholinesterase inhibitors → 1st line, mild-moderate
- Donepezil [Dementia = Donepezil]
- Galantamine [Donna is galavanting near the river for a meme]
- Rivastigmine
• Memantine → 2nd line or in severe cases, contraindicated in depression
Alzheimer’s → memory changes before personality

Pick’s dementia (fronto-temporal dementia)
- Personality changes before memory
- Younger than Alzheimer’s (30-65y)
- Treated by Trazodone, SSRIs, if sexually disinhibited → Cimetidine or spironolactone
Lewy body dementia → Parkinson’s symptoms + hallucinations + fluctuating course of lucid intervals + sleep
disorders (REM sleep disorder, restless legs $)
Shy-Drager $ → Parkinson’s symptoms + autonomic symptoms (urine incontinence/retention, erectile dysfunction,
postural hypotension)
Vascular dementia → history of a cardiovascular event
Normal pressure hydrocephalus → GDU
Mini-mental state exam, used to indicate the presence of cognitive impairment

- 25-30/30 → normal
- 21-24/30 → mild
- 10-20/30 → moderate
- <10/30 → severe impairment
Neurology
Dementia, pseudodementia and grief response
Normal grief response → usually <6 months

Alzheimer’s patient doesn’t seek medical advice on his own, as he’s not aware of the condition
Neurology
Wernicke’s encephalopathy
➢ A neuropsychiatric disorder caused by thiamine (vit B1) deficiency and most commonly seen in alcoholics
and pregnant women, where there’s severe hyperemesis gravidarum
Wernicke’s encephalopathy Wernicke’s – Korsakoff $

Triad of: [congresswoman AOC] Addition of:
1. Ataxia 4. Amnesia
2. Ophthalmoplegia 5. Confabulation
3. Confusion - Production of fabricated memories without the
Treatment → Thiamine intention to deceive
Acamprosate + counselling for alcohol dependence
• Alcohol intoxication can lead to folate deficiency (low Hb, high MCV)
Alcohol withdrawal
Symptoms
• Anxiety, tremors, hyperactivity, sweating, nausea and retching
• Tachycardia, HTN and mild pyrexia
• Typically present about 8h after a significant fall in blood alcohol levels
• Symptoms peak on day 2 and, symptoms usually improves significantly by day 4 or 5
• If severe → delirium tremens which is characterized by hallucinations
• Alcoholic hallucinosis (can appear 12-24h after alcohol has stopped) → this includes visual, auditory or
tactile hallucinations
• Withdrawal seizures (generalized tonic-clonic seizures can appear 24-48h after alcohol has stopped)
Management
• Benzodiazepines
- Chlordiazepoxide or Diazepam
- If patient has withdrawal seizures or delirium termens → lorazepam/diazepam
• IV Pabrinex (thiamine) (vit B1)
- To prevent Wernicke’s encephalopathy [AOC]
• Disulfiram
- Used as a deterrent
- Patients should be aware that even small amounts of alcohol (in perfumes, food, mouthwashes) can
produce severe symptoms
- Used after 24h from the last alcoholic drink
• Acamprosate
- Reduces craving [AC is good for heating]
- Used after the patient has finished a planned withdrawal from alcohol
Antipsychotics (e.g. haloperidol or olanzapine) can be used in delirium tremens along with benzodiazepines not alone
DiSulfiram→ Deterrent that makes you Sick
aCamprosate → reduces Craving
Neurology
Meniere’s disease
Presentation
• Deafness, vertigo, tinnitus (DVT) + increased feeling of pressure in the ear
• Note: Vertigo → is usually the prominent symptom
• Episodes last minutes to hours
• MRI is normal
• Usually a female → male; 20-60 years old
• Typically, symptoms are unilateral but bilateral symptoms may develop after a number of years
Treatment
• Acute attacks → buccal or intramuscular prochlorperazine (-zine)
• Admission is sometimes required
Vestibular schwannoma → high frequency SNHL, MRI is diagnostic, will have CN involvement
Meniere’s disease → low frequency SNHL
Benign paroxysmal positional vertigo (BPPV)

➢ One of the most common causes of vertigo
➢ Characterized by sudden onset of vertigo triggered by a change in head position
Presentation
• Can be preceded by infections
• Vertigo on turning over in bed, lying down, or sitting up from supine position (described as room’s spinning)
• Each episode typically lasts 10-20 seconds
• There’s nausea during episodes • Vestibular neuritis → lasts hours-days
Diagnosis • BPPV → lasts seconds
• Hallpike's maneuver positive
Treatment
• Mostly spontaneous resolution with exacerbations
• Epley’s maneuver
- A repositioning technique used to reposition otoliths back into the utricles from the posterior
semicircular canals
Drop attacks
• Unexplained falls with no prodrome
• No loss of consciousness and rapid recovery
• Incidence increases with age
Causes
• Vertebrobasilar insufficiency (due to decreased blood flow in the posterior circulation of the brain)
• Weak legs (e.g. cauda equina $)
Stokes Adams → unconscious + abnormal ECG

Hypoglycemia → unconscious + sweating
Vasovagal syncope → young woman + unconscious + emotional stress/pain/excitement/prolonged standing,
reassure and tilt table training
Neurology
Comparison of headaches
Tension headache Migraine Cluster headache

• Unilateral → 60-70%
location • Bilateral • Strictly unilateral
• Bilateral
• Variable (sharp, burning

or throbbing)
• Focused on one eye
• Throbbing/pulsating
Pain character • Tightening/pressing/dull • Sudden onset and
• Gradual onset
resolution
• Triggered by: stress,
alcohol and exercise
Pain intesity • Mild-moderate • Moderate-severe • Very severe
• Photophopia
• Phonophopia • Ipsilateral autonomic
• Nausea features like:
• Vomiting - Red/watery eye
• Aura - Constricted pupil
Other - Headache begins before - Unilateral facial
• None
symptoms aura ends or within an swaeting
hour of the end - Drooping eyelid
- Lasts 5-60 mins - Rhinorrhea
- Visual symptoms • Recurrence affect the
(fortification spectra) same side
- Ipsilateral parasthesia
• Around 30 mins • 15mins-3h
Duration continuously, can be • 4-72h • May occur from 1 time
longer every 2-8 days
Patient • Prefers to sit in a dark, quiet • Restless and agitated

• Able to do daily activity
appearance room during an attack
• O2 100% for 10-20mins

• Aspirin • NSAIDs (aspirin, ibuprofen) • Subcut or nasal triptans
Management • NSAIDs • Triptan (oral) • Refers to a specialist if the
• Paracetamol 1st bout of attack as may
need neuroimaging
Prophylaxis • Acupuncture • Beta-blockers or topiramate • Verapamil
Cervical spondylosis
- Chronic cervical disc degeneration with disc herniation, calcification and osteophyteic outgrowths
- Early → Headach in the back of the head and pain in flexing neck
- Later → radiculopathies due to root compression in arms and hands
- Examination → decrease in neck mobility (ROM)
Neurology
Muscle syndromes
Motor neuron disease (MND)

➢ A condition where motor nerves become damaged and eventually stop working → muscle weakness
• The most common type, 8/10 MND patients

Amyotrophic lateral sclerosis (ALS) • Symptoms tend to start in the hands and feet
• Muscles tend to become stiff and weak at first
• 2/10 MND patients

Progressive bulbar palsy (PBP) • Muscles first affected: muscles for talking, chewing and swallowing
(the bulbar muscles)
Progressive muscular atrophy • Uncommon

(PMA) • Muscles of hands and feet are usually affected first but are not stiff
• Rare
Primary lateral sclerosis (PLS) • Muscles of leg are affected first
• Clumsiness in the hands and speech problems may develop
Amyotrophic lateral sclerosis (ALS)

Presentation
• Progressive weakness of bulbar (9,10,11,12), limb, thoracic and abdominal muscles
• Sensory, sexual and cognitive functions are intact
• Limb-onset ALS: starts in the hands or feet
• Bulbar-onset ALS: initial symptoms are difficulty speaking and swallowing
• Hoffman’s sign positive → indicates UMNL
Treatment
• MDT
• Neuroprotective medications → Riluzole
• Medications to treat respiratory symptoms, drooling, insomnia, fatigue and physiological symptoms
• Genetic testing and counseling for family
• For long-term feeding → Percutaneous endoscopic gastrostomy
Neurology
Guillain-Barre $
➢ A disorder causing demyelination of the peripheral nerves
➢ Usually preceded by infection (GI or respiratory infection) days-weeks prior
Presentation
• Weakness
- Ascending pattern of symmetric weakness
- Level of maximum severity of 2 weeks after initial onset
- Facial weakness, dysphagia or dysarthria
- In severe cases → respiratory failure
• Pain
- Neuropathic pain, particularly in the legs
• Hyporeflexia
• Sensory
- Paresthesia and sensory loss, starting in the lower extremities
Diagnosis
• CSF
- Albumin cytological dissociation → characteristic
- Increased protein level usually after 1st week
- Normal WBC
• Nerve conduction test → hallmark = focal conduction block
Treatment
• IVIG or plasma exchange
• If no response in 2 weeks → consider repeating IVIG course or plasma exchange
• Treat neuropathic pain with gabapentin
• Consider referral to ICU if respiratory depression detected → intubation and ventilation
Syringomyelia
• A rare condition where fluid-filled tubular cyst (syrinx) within the central, usually cervical spinal cord
• Symptoms and signs:
- Neuropathic pain in the upper limbs exacerbated by exertion or coughing
- Initially → Spinothalamic tract involvement → sensory loss of pain and temperature – may lead to
painless upper limb burns
- Corticospinal tract involvement → muscle weakness, starts in hands then forearms and shoulders
- Partial paralysis of the LL
- Loss of light touch, vibration and position senses in the feet
- Loss of tendon reflexes
Neurology
Syringobulbia
• Occurs when the syrinx extends into the brainstem
• Syringomyelia + involvement of CNs (facial palsies)
Myasthenia gravis
- Diplopia
- Drooping eyelids
- Dysphagia
- Dysarthria
- Dysphonia
Diagnosed by serum skeletal muscle nicotinic acetylcholine receptor antibody
Lambert-Eaton $
Presentation
• Young, female patients; mostly autoimmune
• Proximal weakness at the pelvic girdle / shoulder girdle
• Weakness improves with exercise as well as reflexes
• Cranial nerve involvement: dysphagia, dysarthria, ptosis, diplopia
• Associated with SCLC
Diagnosis
• EMG → decreased amplitude in CMAP after single supramaximal stimulus but increases after exercise
• Edrophonium test → may be positive but not as prominent as in myasthenia gravis
• Look for tumor → CT/MRI of chest, abdomen, pelvis + tumor markers
Treatment
• Treat tumor – first line
• Consider methylprednisolone and IVIG
Myasthenia gravis
- Has fatigue symptoms (e.g. walking → voice faded)
- Associated with thyrotoxicosis
- Intact reflexes
Lambert-Eaton $
- Muscle function improves with use
- Associated with SCLC
- Absent reflexes
SCLC
S → SIADH
C → Cushing $
L → Lambert-Eaton $
C → Central tumor treated with chemo
Bulbar palsy → LMNL, X, XI, XII nerve palsies, dysphagia, dysarthria, dysphonia (nasal speech) tongue fasciculations
Pseudobulbar → UMNL
Neurology
Multiple Sclerosis
➢ A demyelinating disease in which the insulating covers of central nerve cells in the brain and spinal cord are
damaged
➢ Mean age of onset → 30 years
➢ Most patients follow a relapsing-remitting course
➢ Optic neuritis + UMN features
1. Transverse myelitis
- Weakness, sensory symptoms
- Urinary urgency and retention
- Flexor spasms
- Spastic quadriparesis or paraparesis
2. Brainstem
- Ataxia
- Diplopia
- Dysarthria • MS → Autoimmune demyelination of CNS and spinal cord
- Facial numbness • GBS → immune mediated demyelination of peripheral nervous
- Ophthalmoplegia system triggered by an infection
- Gaze palsy
3. Cerebellum
- Ataxia
- Dysarthria
- Nystagmus
• PLAB 1 stem usually have some clue to optic neuritis. Optic neuritis is an acute, sometimes painful, reduction or
loss of vision in one eye and is a relatively common presenting symptom of MS
• Color vision may be impaired
• Also, depression is common
• Pattern is usually relapsing-remitting: symptoms evolve over days, plateau, then resolves over days/weeks
Diagnosis
• Mostly a clinical diagnosis
• MRI (definitive diagnostic test) → demyelination and/or lesions disseminated in time and place (i.e.
occurring at multiple sites)
• CSF → Oligoclonal bands • DO NOT give NSAIDs for neuropathic pain → it would mask the diagnosis
Treatment
• For relapses → IV or oral Methylprednisolone
• For disease modifying:
1. Dimethyl fumarate
2. Alemtuzumab and Natalizumab
3. Interferon-beta or Glatiramer (recommended by Oxford but not by NICE)
• Symptom control:
- Spasticity → baclofen or gabapentin
- Tremors → botulinum toxin
- Fatigue → amantadine
Neurology
Myofascial pain syndrome
• Chronic pain disorder characterized by regional muscle pain associated with restricted painful regions or
trigger points, pain is aching and deep in nature
• Occurs after a muscle has been contracted repetitively (e.g. a long car ride)
• Pain is relieved by changing position
• Mostly affected muscles: trapezius, levator scapula, infra-spinatus and scalenes
Essential tremors
Symptoms
• Distal symmetrical postural tremor of the upper limbs
• Initially transient. May progress to become persistent
• Amplitude of tremor may depend on physiological or emotional state
• May be seen to improve following alcohol ingestion
• Tremors persist even when the patient is distracted
• Absent at rest
Management
• Propranolol → 1st line
Psychogenic tremors → abrupt onset, spontaneous remission + stops when distracted + worsen when stressed
Parkinson’s tremors → “pin rolling” tremors present at rest + rigidity (cogwheel) + bradykinesia + postural inability
Cerebellar disease
- Intentional tremors, occur during voluntary active movements of an upper body, not present at rest
- Tremors would worsen when it approaches its target, usually include overshooting or undershooting the
target “dysmetria”
- Example: a patient would find difficulty due to his tremor when asked to touch his nose
Huntington’s chorea → typical dancing movement
Hemineglect
- A feature of parietal lobe lesion due to cerebral tumor • pH → parietal lobe, Hemineglect
• NN → Non-dominant hemisphere, Neglect
- Patient is inattentive to one half of his visual field
Neurofibromatosis
• Autosomal dominant → type 1 (Ch 17), type 2 (Ch 22), Schwannomatosis (benign nerve sheath tumor)
Neurology
Neurology
Cauda equina syndrome
•Compression of the cauda equina is a surgical emergency
•Symptoms of sciatica plus the following:
- Saddle paresthesia
- Urinary retention → urine accumulates until bladder is full → overflow incontinence
- Fecal incontinence
➢ Urgent MRI is required
➢ Once diagnosed → urgent surgical decompression, to prevent irreversible loss to the sphincter and motor
functions
Red flags for low back pain

- Age >50 years or <18 years
- Unexplained weight loss >10kg within 6 months
- Night pain or pain at rest
- Pain persists for >6 weeks
- Failure to improve with therapy
- History of cancer
- Urinary incontinence or retention
- Fecal incontinence
- Saddle anesthesia/paresthesia
- Progressive neurologic deficit
- Vertebral tenderness
Chemo MAN
- Vincristine SE → peripheral neuropathy, felt as numbness and tingling “glove-and-stock distribution” with
sensory loss and hypersensitivity and in some cases, motor and autonomic dysfunction
Neurology
Meningitis
Features
• Headache + Fever + Photophobia + Neck stiffness
• Cranial palsies: CN III, IV, VI, VII (eye movement & Facial n.)
Treatment
• Antibiotics → should be started before CT or LP whether it’s viral, bacterial or TB
- Prehospital setting → IV or IM Benzylpenicillin
- Hospital setting → IV cefotaxime or (IV ceftriaxone + IV vancomycin + IV ampicillin)
• If NO rash + NO signs of increased IOP → perform Lumbar Puncture
• If RASH → perform blood culture → Meningococcal septicemia (caused by Neisseria meningitides)
• If raised ICP → Mannitol
Bacterial Viral TB
Glucose low normal low
Protein high Normal or high high
White cells Mainly neutrophils Increased Neutrophils, then
lymphocytes lymphocytes
Nature Progresses rapidly + Less severe than Gradual
signs of septic shock bacterial
- Bacteria eats glucose and shits protein → TB or bacterial

- Lymphocytosis → Viral or TB → glucose will differ
- Meningitis cause by listeria (old age, history of air-conditioning) → Ampicillin/Amoxicillin + Gentamicin
- If hypersensitivity to penicillin → Chloramphenicol
- Prophylaxis to close contact → Oral Ciprofloxacin or Rifampicin
- TTT of Cryptococcal meningitis in HIV patients → Amphotericin B + flucytosine
- Complications of meningitis → Hearing loss → Hearing test should be performed after recovery
- Meningitis can lead to hearing loss in acute and severe cases, Otitis media can lead to Meningitis
- Complete recovery is the MOST LIKELY OUTCOME with a full treatment regimen
- Meningitis can lead to hyponatremia → Fluid restriction
Amaurosis fugax
• Sudden, transient, painless, unilateral vision loss; “black curtain coming down”
• It is indicative of retinal ischemia, usually associated with emboli or stenosis of the ipsilateral carotid artery
Presentation
• Duration: 5-15 minutes; resolves within < 24 hours
• Associated with stroke or transient ischemic attack (TIA) and its risk factors (i.e. hypertension,
atherosclerosis)
• Has an association with giant cell arteritis
Acute angle glaucoma

- Painful vision loss
- “halos” would be seen
Neurology
Cavernous sinus thrombosis
Presentation
• Headache – can be severe intensity
• Chemosis, edematous eyelids, proptosis, painful
ophthalmoplegia
• Fever
• Usually preceded by sinusitis
Diagnosis
• CT/MRI venography
Treatment
• Referral to neurosurgery
• Antibiotics
• Anticoagulation – heparin
• +/- Corticosteroids and surgical drainage
Restless leg syndrome (Willis-Ekbom $)

Features
• Urge to move (usually legs)
• Abnormal sensation, tingling or pain
• Tends to appear in the evening leading to sleep disturbance
• Worsen by pregnancy
• Relieved by moving
• Associated with Lewy Body Dementia
Investigations
• Serum iron → usually associated with IDA → if low serum ferritin is low, add iron supplementation despite
normal Hb
Management
• Avoid alcohol, smoking and caffeine along with exercise and good sleep hygiene
• Drugs needed in 20%:
- Dopamine agonist, as dopamine is responsible for regulating body movements
- Gabapentin
- Pregabalin
Cerebral abscess
Features
• Headache → most common symptoms and is often on the same side of abscess
• Fever
• Focal neurological deficit
• Cerebral abscess shows many of the features of brain
• Ear pain and discharge
tumors as both are space-occupying lesions
• Change in mental state
• Grand mal seizures
• Nausea, vomiting and neck stiffness
• Papilledema → due to cerebral edema
Investigation
• CT → radiolucent space-occupying lesion (ring enhancing lesion)
Neurology
Viral encephalitis
• Typically begins as flu-like illness with headache followed by rapid deterioration of severe symptoms
• Causative organisms: HSV, VZV
• CSF profile is similar to viral meningitis → lymphocytosis
Broca’s vs Wernicke’s aphasia

• Broca’s area (44,45) → frontal lobe, production of coherent speech
• Wernicke’s area → temporal lobe, speech comprehension + language development
• Both supplied by MCA, hence aphasia seen in MCA stroke
Broca’s (non-fluent aphasia) → Broken words

Wernicke’s (fluent aphasia) → What?
Clang association → rhyming speech with no meaning
Progressive supranuclear palsy

Features
• Axial rigidity (axial trunk and neck are more affected than the limbs)
• Falls (usually falls backwards while walking)
• Dysarthria
• Dysphagia
• Supranuclear gaze palsy affecting downgaze than upgaze → most distinctive feature
• Symptoms of frontal lobe dementia → unusual behaviors and personality changes
Investigation
• MRI
Downgaze affected → Progressive supranuclear palsy, rapidly more progressive than Parkinson’s
Upgaze affected → Idiopathic Parkinson’s
Neurology
UMNL vs LMNL
Neurology
Dermatomes
Neurology
C2 → posterior half of the skull
C3 → high turtleneck shirt
C4 → low-collar shirt
C5, C6 → thumb and index finger
C7 → middle finger and palm of the hand
C8 → ring and little finger
T4 → nipples
T5 → inframammary fold
T7 → xyphoid process
T10 → umbilicus
T12 → pubic bone region
L1 → groin and pelvic girdle
L2 → anterior thigh
L3, L4 → knee jerk reflex changes
L3 → inner thigh and distal anterior thigh
S1, S2 → ankle jerk reflex changes
L4 → inner shin and knee
L5 → outer shin and dorsum of the foot
S1 → posterior shin and lateral foot and small toe
S2, S3 → genitalia
Neurology
Notes
• [O, O, O, To Touch And Feel A Girl’s Vagina, Ah Heaven]
1. Olfactory
2. Optic
3. Oculomotor
4. Trochlear
5. Trigeminal
6. Abducent
7. Facial
8. Auditory/Vestibulocochlear
9. Glossopharyngeal
10. Vagus
11. Spinal Accessory
12. Hypoglossal
• Short term feeding → NG tube
• Long term feeding → Percutaneous endoscopic gastrostomy
• Dizzy when rolling in bed → Benign paroxysmal positional vertigo (BPPV)
• Light sensitivity during dizzy spells → Migraine
• First attack severe vertigo lasting hours + Vomiting + History of infection → Vestibular neuritis
• Light headed when getting up from bed → Orthostatic hypotension
• Epidural hematoma → MMA
• Subdural hematoma → Bridging veins
• Subarachnoid hematoma → Cerebral artery and berry aneurysm (circle of Willis)
• Most common artery involved in stroke → Middle cerebral artery (MCA)
• Na correction:
- From low to high, your pons will die → Osmotic demyelination $
- From high to low, your brain will blow → Cerebral edema/herniation
• Cytotoxic drug leads to cerebral edema → Isoniazid
• Cerebral edema + viral infection + liver toxicity + personality/awareness changes → Reye’s $
• Organic brain injury (MAC)
- Memory impairment
- Agitation
- Confusion
• PTSD → usually after 4 weeks + flashbacks + nightmares
• Infective neuropathy is associated with → Lyme disease
• Causes of Horner’s $:
- Lateral medullary $
- Pancost’s tumor
- Cervical syringomyelia
• Safest mode of contraception to be used in migraine with aura → IUD
• Best initial investigation in obstructive sleep apnea → Pulse oximetry
• Best definitive → Polysomnography (PSG)
• Best definitive investigation in narcolepsy → Multiple sleep latency test
• Medication to treat Parkinson’s → Levodopa + Cabergoline
• One of the more common side effects of levodopa → Hallucinations, it should always be started at a small
dose and increased according to the patient’s response
Neurology
• Controlled release preparations of levodopa are useful for nocturnal or early morning hypokinesia and
rigidity
• Medication to treat tremors and dystonia in Parkinson’s → Benzhexol
• Medication to treat psychosis in an old Parkinson’s patient → Lorazepam, lamotrigine
• Preferred symptomatic treatment in MG → Pyridostigmine
• Management of trigeminal neuralgia is the same as Epilepsy in pregnancy → Carbamazepine or Lamotrigine
• Mechanical lower back pain management → Increasing mobility + Analgesics
• Innervation of the voluntary muscles of the face (muscles of expression) → Facial n.
• Innervation of the involuntary muscles of the face and muscles of mastication and cornea → Trigeminal n.
• A disease characterized by motor weakness only (progressive dysphagia later) → ALS
• Motor weakness similar to ALS but with autoimmune panel + fatigue → Myasthenia gravis
• Initially with fatigue in the lower limbs → Polymyositis
• Poor DM control + Severe hip or leg pain for several days followed by muscle atrophy in the proximal leg,
thigh muscles are typically affected and is usually unilateral, patient may to be able to walk, it resolves
spontaneously over months → Diabetic amyotrophy
• Similar presentation to “Diabetic amyotrophy” + raised ESR → Vasculitis neuropathy
• Hx of infection + motor (ascending pattern weakness) + sensory + reflexes are all affected → GB$
• Motor + sensory + reflexes are affected but with typical loss of pain and temperature (spinothalamic tract
involvement) → Syringomyelia
• Disseminated in time and space (recurrent attacks at different locations) + optic neuritis → MS
• Initial management for pressure symptoms and edema due to space occupying lesion → IV dexamethasone
• A drug used for rapid decrease of ICP where GCS <8, history of head trauma or fixed unilateral or bilateral
pupils → Mannitol
• If GCS is 8 → Intubate (summon the anesthetic)
• Epilepsy, Low IQ, Adenoma Sebacium (acne like rash on the face) → Tuberous sclerosis [EPILOA]
• Port wine stain, seizure, paralysis on one side of the body and learning difficulties → Sturge weber $
• Young patient with hearing loss and multiple schwannomas → NF II
• Lateral medullary $ (Wallenberg $)
- Ipsilateral Horner’s $
- Ipsilateral loss of sensation of the face
- Contralateral loss of pain and temperature
• Shy-Drager $
- SHY person has erectile dysfunction and always wets his pants
- Often DRAGs his feet because of cerebellar ataxia
- DRops his blood pressure when he stands “postural hypotension”
• Contraindications for LP
- GCS <9, or dropped by 3 points
- Focal neurological finding
- Papilledema
- Unequal, dilated or poorly responsive pupils
- Bulging tense fontanelle
• Suspecting a stroke, initially → CT, definitive → MRI
• Suspecting hematoma → CT brain
• If there’re signs of meningeal irritation with migraine → perform CT brain to rule out SAH
• Long-term medication after a stroke → Clopidogrel 75mg
• Short-term medication after a stroke → Aspirin 300mg
Obstetrics & Gynecology
Amenorrhea
- Absence of menstruation. Pathological amenorrhea is the failure to menstruate for at least 6 months
- It can be divided into:
• 1ry amenorrhea ⟶ lack of menstruation before the age of 16 years or 14 in the absence of secondary
characteristic (the average age for menarche is 12-14 years old)
• 2ry amenorrhea⟶ cessation of menstrual cycles following established cycles
Etiology
• Hypothalamic amenorrhea Female athlete tirade:
- most common 1. 2ry amenorrhea
2. Osteoporosis
- usually due to low BMI or excessive exercise
3. Anorexia nervosa
- FSH, LH and prolactin are all low
• PCOS
• Hyperprolactinemia
• Premature ovarian failure (POI): raised FSH
• Anatomical problems • Asherman’s $ → adhesions of the endometrium
- usually results in 1ry amenorrhea often associated with dilatations and curettage
- vaginal examination to rule out imperforate hymen is of the intrauterine cavity
important • It results in infertility and they often experience
- pelvic US: to determine pelvic anatomy (Mullerian menstrual irregularities
agenesis)
- anatomical problems can also cause 2ry amenorrhea (Asherman’s syndrome)
• Thyroid problems (both hyper & hypo)
• Pregnancy
Short stature Turner Syndrome

Hirsutism, acne (androgen excess) PCOS, Hyperprolactinemia
Menopausal symptoms in women before 40s Premature ovarian failure
Eating disorder Anorexia nervosa
Galactorrhea hyperprolactinemia
Dysmenorrhea
1ry Dysmenorrhea 2ry Dysmenorrhea
Common etiologies:
- Endometriosis
no obvious organic cause
- Adenomyosis
- PID
Management: Management:
• NSAIDs such as Mefenamic acid (1st line) • Treat the underlying cause
• COCP (2nd line if the only symptom is pain)
• Mirena IUS
- Dysmenorrhea > Mefenamic acid (NSAIDs)

- Menorrhagia > Tranexamic acid (antifibrolytic → inhibits fibrinolysis)
Hematometra
- Accumulation of blood within the uterus, commonly caused by imperforate hymen or transverse vaginal septum
- 1ry amenorrhea and cyclical pain
Imperforate hymen → bluish bulging membrane visible at the introitus

Transverse vaginal septum → possible abdominal mass
Endometriosis
➢ Presence of endometrial-like tissue outside the uterine cavity. It's estrogen dependent, and therefore mostly
affects women during their reproductive years. If the ectopic endometrial tissue is within the myometrium
itself, it's called adenomyosis. Up to 10-12% of women have a degree of endometriosis
Features:
4 DYS- + CYClical pain
- Chronic pelvic pain (cyclic or constant)
• DYSmenorrhea
- Dysmenorrhea – pain often starts days before bleeding
• DYSpareunia
- Deep dyspareunia (indicates possible involvement of uterosacral ligaments)
• DYSuria
- Subfertility
• DYSchezia
Investigations:
• Laparoscopy is the gold-standard investigation
• TVUS (to diagnose & to exclude of an ovarian endometrioma) - Drug therapy does not seem to have a significant
Management: impact on fertility rates. However, laparoscopic
- NSAIDs (Mefenamic acid) excision and ablation of endometriotic ovarian
- COCP cysts may improve fertility
- Levonorgestrel IUS - It's acceptable to use COCP to treat pain without
Surgery: laparoscopic diagnosis as long as fertility isn't the
• Laparoscopic excision and ablation of endometrioid lesions issue
reduce associated pain
PID
➢ Infection and inflammation of the female pelvic organs including the uterus, fallopian tubes, ovaries and the
surrounding peritoneum. Most commonly caused by ascending infection from the endocervix
Causative organisms
• Chlamydia → most common cause
Cervicitis → is purely infection of the cervix not involving
• Neisseria gonorrhea
other pelvic organs
Risk factors • It presents with discharge, tender cervix (chandelier
• Age <25 sign) and dyspareunia but NO menstrual irregularities
• Previous STIs or lower abdominal pain
• If just Cervicitis – Chlamydia:
• New sexual partner or multiple partners
- Doxy 100mg twice a day for seven days (1st line)
• Uterine instrumentation - Azithromycin 1g s a single dose, followed by
• IUD 500mg once daily for 2 days
• Post-partum endometritis - If pregnant → Erythromycin
Features • If just Cervicitis – Neisseria gonorrhea:
- Ceftriaxone 1g IM as a single dose
• Lower abdominal pain
- Ciprofloxacin 500mg orally as a single dose if the
• Fever organism is susceptible to ciprofloxacin
• Deep dyspareunia (painful sexual intercourse)
• Dysuria and menstrual irregularities may occur • Pelvic abscess or tubo-ovarian abscesses are
possible complications of PID
• Vaginal or cervical discharge often purulent (NOT offensive)
• US is the diagnostic imaging method of choice
• Cervical excitation (tenderness) for acute pelvic pain in gynecology
• Abnormal vaginal bleeding (intermenstrual, postcoital) • Fitz-Hugh-Curtis $ → a complication of PID,
Complications usually presents with an acute onset of RUQ
pain (aggravated by breathing or coughing. Pain
• Infertility
may refer to right shoulder)
• Chronic pelvic pain • Endocervical swab → PID
• Ectopic pregnancy • USG → complications of PID
• In males → Acute epididymitis
Management
- Outpatient: IM Ceftriaxone + oral Doxycycline + oral Metronidazole for 14 days OR Ofloxacin + Metronidazole
- Inpatient: IV Ceftriaxone + IV Doxy + oral Metro for 14 days OR IV Ofloxacin + IV Metronidazole for 14 days
Chickenpox exposure in pregnancy
➢ Caused by primary infection with varicella zoster virus. Shingles is reactivation of dormant virus in dorsal
root ganglion. In pregnancy there is a risk to both the mother and also the fetus, a syndrome now termed as
fetal varicella syndrome
➢ The incubation period is 10-14 days but can be as long as 21 days
Fetal varicella syndrome (FVS)
• Risk of FVS following maternal varicella is 1% if occurred before 20 weeks, very few occur between 20-28
and none after 28 weeks
• Features include: skin scarring, eye defects (microphthalmia), limb hypoplasia, microcephaly and learning
disabilities
Other risks to the fetus
• Shingles in infancy: 1-2% risk if maternal exposure in the 2nd or 3rd trimester
• Severe neonatal varicella: if mother develops RASH between 5 days before or 2 days after birth there is a
risk of neonatal varicella, which may be fatal to the newborn child in around 20% of cases
Management of chickenpox exposure
1. Who gets checked for varicella antibodies?
- If the woman's immunity to chickenpox is unknown and if there is no previous history of chickenpox or
shingles
- Serum should be tested before administration of VZIG, 1. Pregnant exposed to chickenpox → check woman's
immunity (previous infection, varicella antibodies)
it takes 1-2 days or few hours if the serum is stored from
2. Not immunized → VZIG
an antenatal booking blood sample 3. Chickenpox rash develops (24h) → oral acyclovir
2. Who gets VZIG?
- If the pregnant woman is not immune to VZV and she has had a significant exposure, she should be offered
VZIG as soon as possible
- VZIG is effective when given up to 10 days after contact
- If the immune status is unknown, administration of VZIG can be delayed until serology results are available
- VZIG has NO significance once chickenpox has developed and should therefore NOT be used in pregnant
women who have developed a chickenpox rash
3. Who gets oral acyclovir?
- Oral acyclovir should be prescribed for pregnant women with chickenpox if they present within 24 hours of
the onset of the rash and if they are ≤ 20 weeks gestation
Chronic hypertension
- Hypertension that is present at the booking visit or before 20 weeks or if the woman is already on
antihypertensive medications
Gestational hypertension
- New hypertension presenting after 20 weeks without significant proteinuria
- Once developed → Refer for a same day assessment in the maternal unit
- If blood test come back at an acceptable level and she’s asymptomatic → she’s advised to measure blood
pressure four times daily and to come back if the BP >150/100 → Oral labetalol would be given
NHS guidelines for IV magnesium sulphate administration

- Women in a critical care setting who have severe hypertension or severe pre-eclampsia who have or
previously had an eclamptic fit
- Women with severe preeclampsia who are in a critical care setting if birth is planned within 24h
Pregnancy-induced hypertension
Degree of Mild Moderate Severe
hypertension (140/90 - 149/99 mmHg) (150/100 - 159/109 mmHg) (160/110 mmHg or higher)
Admit to hospital no no yes
Treat no Oral labetalol as first-line of Oral labetalol as first-line
treatment to keep: of treatment to keep:
• Diastolic pressure • Diastolic pressure
between 80-100 between 80-100
mmHg mmHg
• Systolic blood • Systolic blood
pressure < 150 mmHg pressure < 150 mmHg
Alternatives that are commonly used in pregnancy are Methyldopa, hydralazine and Nifedipine
Labetalol 100mg bd up to 600mg qds Avoid in asthma Breastfeeding- ok

Methyldopa 250mg bd up to 1 g tds Breastfeeding- ok
Nifedipine 10mg bd up to 30mg tds Breastfeeding- ok
Pre-eclampsia
➢ condition seen after 20 weeks gestation
➢ pregnancy-induced hypertension Symptoms (usually occur only with severe disease)
➢ Proteinuria (>0.3g /24 hours or dipstick ++ / +++) • Headache
• Visual disturbance (flashing lights)
Risk factors
• Epigastric or RUQ pain
• Extremes of both ages (over 40 – a teenager) • Rapid face edema
• First pregnancy Signs
• Multiple pregnancies • Hypertension
• DM type 1 and 2 • Proteinuria (>300 mg in 24 hours)
• Obesity • Hyperreflexia
• Chronic hypertension Treatment:
1. Lower the blood pressure (moderate hypertension)
• CKD
using oral labetalol
• Autoimmune disease (SLE, APS)
2. Delivery of placenta and baby
• Family history
• Pregnancy interval > 10 years
Eclampsia
➢ An obstetric emergency defined as tonic-clonic seizures in association with a diagnosis of pre-eclampsia
➢ 44% occur postnatally, seizure could happen before hypertension or proteinuria
Prevention and control of seizures
• Mg sulphate should be considered when there's risk of eclampsia. It's used to prevent seizures as well as
control it
• To control seizures, a loading dose of 4 g MgSO4 in 100 ml 0.9% normal saline is given by infusion pump over
5-10 minutes. This is followed by a further infusion of 1 g/hour maintained for 24 hours after the last seizure
• Recurrent seizures should be treated with either a further bolus of 2 g of MgSO4 or increase in the infusion
rate to 1.5 g or 2.0 g/hour
• Note that administering IV MgSO4 requires cardiac monitoring
In case of MgSO4 toxicity
• Confusion, loss of deep tendon reflex, respiratory depression and hypotension
• Stop MgSO4
• Use diazepam (a single dose because prolonged use is associated with maternal death) to stop the seizures
• Administer Ca gluconate (1g over 10 mins) as an antidote
Diagnosis Characteristics Treatment
• Itching
• Discharge: frothy yellow - greenish
• Ph: >4.5
Trichomoniasis
• Smelly Metronidazole
(Trichomonas vaginalis)
• Vulvar erythema
• Strawberry cervix
• Diagnosed by visualizing motile flagellates under microscope
• Itching
• Discharge: thin and offensive
Bacterial vaginosis Metronidazole
• Ph: >4.5
(overgrowth of
• Fishy smelly Clindamycin
Gardnerella vaginalis)
• +ve whiff (potassium hydroxide) test
• Presence of clue cells
• Itching
Vulvovaginal candidiasis • Discharge: thick, white and odorless with the consistency of
(candida albicans) cottage cheese → Yeast and hyphae with KOH 10% Clotrimazole
cAndidA → Acidic • Ph: 4-4.5
• Broad spectrum AB → kill vaginal normal flora → High risk
Bacterial vaginosis
• The commonest cause of vaginal discharge in the child bearing period, whilst BV is not a sexually-transmitted
infection, it's almost exclusive in sexually active women
• Amsel's criteria: 3 out of 4 is diagnostic IDK why I smell fish in the garden
1. Homogenous grey-white discharge

2. Characteristic fishy smell with KOH 10% added to the sample of discharge
3. Clue cells
4. pH> 4.5
➢ If TV, BV, Candida are suspected → High vaginal swap

➢ If Chlamydia or Gonorrhea → Endocervical swap
Lichen sclerosis
• Chronic inflammatory dermatosis that usually affects the skin of the anogenital region in women
• Presents with genital itching and white atrophic plaques
• Itching worse at night
• Dyspareunia and pain in case of erosions
Management
• Topical steroids
• Follow-up is important as long-standing untreated cases can turn malignant in 4%
➢ Vaginal thrush presents as a thick, white vaginal discharge (not tender)

➢ Lichen planus affects mucous membrane (mouth)
Placental abruption
➢ The premature separation of a normally seated placenta resulting in maternal hemorrhage or lost through
cervix
➢ Risk increases > 35 years old
Causes
• Two of the most common causes of Antepartum
1. Pre-eclampsia
hemorrhage are: placental abruption and placenta
2. Multiparity previa
3. Trauma • Other causes include local causes: vulva, vagina or
4. Maternal age cervix (polyp or carcinoma)
5. Cocaine • Pregnant woman usually has an US at 20 weeks to
show the location of the placenta
6. Smoking
• Single most important diagnostic in APH → US
Clinical features • Single best action in APH → CTG
• Constant sudden abdominal pain
• Tender and tense uterus (woody hard)
• Severe abruption can lead to hemorrhagic shock with acute
• Bleeding, which may be accompanied by pain
tubular necrosis from profound hypotension
• Fetal distress or fetal death (if CTG shows fetal • Disseminated intravascular coagulation (DIC) can result
distress → immediate delivery) from release of tissue thromboplastin into the circulation
• Maternal signs of hypovolemic shock if bleeding is from the disrupted placenta
• One should NOT look into at the extent of vaginal loss as an
severe
indicator of severity of abruption as maternal hemorrhage
Management may be much greater (If concealed behind the placenta)
• Resuscitation and delivery if presence of fetal
distress or maternal compromise
Placenta previa
• Placenta lying wholly or partly in the LUS
• The key clinical feature is painless bleeding after 24 weeks of
gestation
• For diagnosis → TVUS is preferred over abdominal US
• Digital vaginal examination should not be performed. However, a
speculum or a TV probe can be safely used in placenta previa
Risk factors
• Previous placenta previa
• Multiple pregnancies
Clinical features
• Non-tender uterus
• Lie and presentation may be abnormal
• Fetal heart usually normal
Vasa previa Placenta accreta

• Fetal vessels run over or in close • Less common than placenta previa
proximity to the cervical os and are seen commonly in the
• A triad of painless bleeding, presence of a uterine scar which
membrane rupture and fetal allows the placenta to attach to the
bradycardia. myometrium
Endometrial hyperplasia
• A para-malignant condition that can predispose to or be associated with endometrial carcinoma
• Characterized by overgrowth of endometrial cells and is caused by excess unopposed estrogen, endogenous
or exogenous, similar to endometrial carcinoma
Presentation
• Abnormal vaginal bleeding (intermenstrual, polymenorrhea or postmenopausal)
• Over 40 years old with irregular menstruations or in those with post-menopausal bleeding
Investigations
• TVUS
• Endometrial sampling
Management of EH without atypia
• Mirena IUD
• Continuous oral progestogen
Endometrial carcinoma
• Classically, PMB (could be presented as brown vaginal discharge)
Risk factors:
• DM, Obesity
• Nulliparity, Early menarche, Late menopause • The addition of progestogen to estrogen reduces the risk
• Unopposed estrogen (e.g. in HRT). Additional risk is eliminated if a progestogen is
• Tamoxifen given continuously
• PCOS
Investigations
• TVUS - 1st line of management – a normal endometrial thickness <4mm has a negative predictive value
• Hysteroscopy with endometrial biopsy – definitive diagnosis
Tamoxifen (↓Breast cancer ↑Endometrial carcinoma)

• A selective estrogen receptor modulator (SERM) used in the treatment of breast cancer
• Acts as an antagonist in breast tissue and acts as an agonist on the endometrium thus there is an increased
risk of endometrial cancer
• There may be rebound loss of bone
• There is also an increased risk of thromboembolism after tamoxifen is stopped,
• It prevents bone loss by acting as an estrogen receptor agonist bisphosphonates prevent that
SERMs are synthetic molecules. They have the ability to bind to estrogen receptors throughout the body and act as
estrogen agonists or antagonists depending upon the target organ:
- Tamoxifen is antagonist on breast, agonist on uterus and bones
- Raloxifene is antagonist on breast & uterus, agonist on bones
Ovarian cancer
Risk factors
COCP
1. Increasing age
• ↑Breast & cervical cancer
2. Family history, mutations in BRCA1 or BRCA2 • ↓ Ovarian, endometrial & colorectal
3. Many ovulations: early menarche, late menopause, nulliparity
Protective factors Risk for cervical cancer can be decreased by
• COCP (OCP=ovarian cancer protection) condoms by reducing the risk of HPV infection
• Pregnancy
Gestational trophoblastic disease (GTD)
➢ A spectrum of diseases caused by overgrowth of the placenta. It ranges from molar pregnancies to
malignant conditions such as choriocarcinoma
➢ If there is any evidence of persistence of GTD, the condition is referred as gestational trophoblastic
neoplasia (GTN)
Types
• Paramalignant – hydatidform mole
- Complete hydatidform mole (CHM) Hyperemesis gravidarum
- Partial hydatidform mole (PHM) • Pregnancy complication that is characterized by
severe nausea, vomiting, weight loss, and possibly
• Malignant – GTN dehydration
- Invasive mole • Symptoms begin between 6-8 weeks and peaks at 12
- Choriocarcinoma weeks
- Placental site trophoblastic tumor (PSTT) • Treated by cyclizine, promethazine
- Epithelioid trophoblastic tumor (ETT)

Features
• Hyperemesis gravidarum: due to excessive amounts of hCG
• Irregular 1st trimester (1-13 weeks) vaginal bleeding
• Uterus large for dates
• Vaginal passage of vesicles containing products of conception
• Serum hCG is excessively high with complete moles, but levels may be within the normal range for partial
moles
US findings of a complete mole

• Snowstorm appearance of mixed echogenicity, representing hydropic villi and intrauterine hemorrhage
• Large theca lutein cysts (bilateral cystic masses)
Management of hydatidform mole

• Surgical evacuation (suction curettage)
- Histological examination of products of conception is essential to confirm diagnosis
• Two-weekly serum and urine samples until hCG concentrations are normal
- Women should be advised not to conceive until hCG level has been normal and follow-up is complete as
pregnancy will raise serum hCG and we'll not know if it's due to the hydatidform mole or the pregnancy
• Barrier contraception
- Should be used until serum hCG is normal (oral contraception may also be used after molar evacuation,
before hCG returns to normal)
Management of GTN
• Chemotherapy
- If chemotherapy is started, women should wait a year from completion of their treatment before trying
to conceive
If the uterus is large for dates, then we have three options:

• Uterine fibroid
• Molar pregnancy
• Incorrect menstrual period
Multiple pregnancies like twin pregnancy
have similar presentation. However, in
multiple pregnancies the uterus is seen to be
larger in the 2nd trimester rather than the 1st
• The uterus cannot be felt per abdomen

until 12 weeks gestation
• By 16 weeks, its fundus lies half way
between the SP and the umbilicus
• The fundus is under ribs by 36 weeks
• At full term, the uterus lies a bit lower
than at 36 weeks, as the head descends
into the pelvis
• From 16 weeks the symphysis fundal
height (SFH) increases by 1 cm/week
• As a rule of thumb:
- 16-26 weeks: SFH = dates (in weeks)
- 26-36 weeks: SFH ± 2cm = dates
- 36 weeks – term: SFH ± 3cm = dates
Management of menorrhagia (NICE)

1. Mirena IUS
2. Tranexamic acid or Mefenamic acid or COCP
3. Norethisterone (15mg) daily from days 5-26 of the menstrual cycle or injected long-acting progestogens
Important combinations
• Tranexamic acid + Mefenamic acid (NSAID) if the patient has both menstrual bleeding and dysmenorrhea
• NSAIDs + COCP if dysmenorrhea is problematic
• DO NOT combine Tranexamic acid with COCP or Mirena
• For heavy menstruation that needs stopping rapidly → Oral Norethisterone (5mg 3/daily for 10 days)
• In secondary care, treatment include GnRH agonists
Fibroid
• Submucosal
- beneath the endometrium and bulge into the uterine cavity
• Intramural
- Within the muscular uterine wall
- Most common type
• Subserosal
- On the external surface of the uterus and project to the outside of the uterus
Clinical picture (1 of 3 patients)
• Menorrhagia, dysmenorrhea
• Abdominal pain, Low back pain
• Increased urinary frequency, constipation
Risk actors
• Increasing age (↓ by reaching menopause)
• Afro Caribbean
• Obese
Management
• If asymptomatic
- Follow-up annually to monitor size and
growth
• With menorrhagia
- Levonorgestrel-releasing IUS (Mirena) – provided uterine fibroid is not distorting the uterine cavity
- Tranexamic acid, NSAIDs or COCP
• With severe menorrhagia & fibroid > 3cm
- Ulipristal acetate up to 4 courses (each course is up to 3 months, usually used in pre-op treatment)
• Both myomectomy and uterine artery embolization can be

Surgical management
performed in patients who would like to preserve fertility
- Hysterectomy • Myomectomy is preferred, however increases the risk of
- Myomectomy uterine rupture
- Uterine artery embolization
- Endometrial ablation – only for submucosal fibroids < 3cm
Other medical management

- GnRH agonists → reduce the size of fibroids and are used prior to surgery to reduce perioperative blood
loss, surgery must take place as uterine fibroids would return to pretreatment size if GnRH agonist
stopped
Ectopic pregnancy
➢ Implantation of a fertilized ovum outside the uterus
• Any woman at a childbearing period attends
Features with pain MUST have a urine pregnancy test
• Lower abdominal pain → this is typically the first symptom performed
• Rupture ectopic pregnancies are life
• Vaginal bleeding
threatening
• History of recent amenorrhea → typically 6-8 weeks from
the start of last period as the baby is large enough to dilate the tubes
• Peritoneal bleeding can cause shoulder tip pain (in ruptured ectopic)
• PID → the most common cause
• Previous tubal pregnancy
• Previous induced abortion
• Previous ectopic pregnancy
• Copper IUD (rarely happens, but if the patient with IUD conceived it's most likely ectopic)
• Tubal ligation
Examination findings
• Always observe the blood pressure as a significant drop
• Abdominal tenderness in a suspected ectopic need to be quickly escalated
• Cervical excitation (cervical motion tenderness) due • B-hCG should be obtained to plan management:
to stretching of fallopian tubes - >1500 IU/L + no gestational sac = Ectopic
• Adnexal mass may be noticed → rarely noticed
Surgical management
• If hemodynamically stable → Laparoscopy (laparoscopic salpingectomy or salpingectomy)
• If unstable (BP<90/60, tachycardia, tachypnea) → laparotomy (open salpingectomy or salpingectomy)
Medical management
• Methotrexate would be first line for an ectopic pregnancy if it contains the criteria below:
- Not in significant pain
- Hemodynamically stable
- Adnexal mass smaller than 35mm with no fetal heart visible
- No intrauterine pregnancy
- Serum hCG less than 5000 IU/liter (ideally less than 1500 IU/liter)
- Able to return for follow-up
Infertility
Causes
Key counselling points
• Male factor 30% • Folic acid
• Unexplained 20% • Aim for BMI 20-25
• Advise regular sexual
• Ovulation failure 20% intercourse every 2 to 3 days
• Tubal damage 15% (highly suggestive with history of PID) • Smoking/drinking advice
• Other causes 15%
Investigations
• Semen analysis
• Mid-luteal progesterone 7 days prior to expected next period
Interpretation of serum progestogen

Level Interpretation
< 16 nmol/l Repeat, if consistently low → refer to specialist
16 - 30 nmol/l Repeat
> 30 nmol/l Indicates ovulation
FSH and LH should be measured if there is menstrual irregularity: High levels may suggest poor ovarian function
PCOS POI
• ↑LH • ↑LH and ↑FSH
• LH:FSH > 2 • FSH > 25 IU/I on two occasions > 4 weeks
apart is diagnostic
- Anti-Mullerian hormone can be used if there’s
diagnostic uncertainty
Hysterosalpingography
• Contrast media is being injected into the cervical canal that appears on real-time x-ray (fluoroscopy)
• It evaluates uterus and fallopian tubes to detect any blocking as a part of investigation for infertility
• If the fallopian tubes are patent, the contrast medium will fill the tubes and spill out into the abdominal
cavity
Complications
• Allergic reaction to the dye
• Infection (endometritis or salpingitis)
• Perforation of the uterus or fallopian tube → intra-abdominal bleeding → US as a 1st investigation,
laparoscopy (stable patients) or laparotomy
PCOS
➢ It comprises hyperandrogenism, oligomenorrhea/amenorrhea and polycystic ovaries on US (≥12 follicles)
➢ The commonest endocrine disorder in women of reproductive age
Symptoms
• Symptoms due to excess androgens → hirsutism, alopecia and acne
• Oligomenorrhea or amenorrhea
• Obesity
• Subfertility
Biochemical abnormalities
• Hyperandrogenism: elevated free androgen index (FAI) >5
• Hyperinsulinemia (due to insulin resistance) → acanthosis nigricans
• Increased LH (LH:FSH >2)
General management - 20% of women have an US suggestive of polycystic
• Weight loss ovaries but unless they fulfill the criteria of PCOS, they
Management for menstrual irregularities should NOT be treated
• Weight loss
• COCP, cyclical progestogen or Mirena IUD
Management of infertility
• Weight loss → the 1st initial management
• Clomiphene Citrate
• If Clomiphene Citrate fails, consider adding metformin, gonadotropins or consider laparoscopic ovarian
drilling
Regarding metformin
- Still used either combined with clomiphene citrate or alone, particularly in patients who are obese
- In order to improve insulin sensitivity and reduce hyperinsulinemia and subsequent hyperglycemia
Premature ovarian failure/insufficiency (POI)

➢ The onset of menopausal symptoms and elevated gonadotropin levels before 40 (around 1 of 100 women)
Causes
• Idiopathic → the most common cause • Early menopause is used to describe women who go
through their menopause between 40-45 years
• Chemotherapy → this can be temporary
• Treatment includes long-term HRT beyond menopause
• Radiation
• Autoimmune disease
• Perimenopausal: begins with the first, clinical, biological and
• Bilateral oophorectomy or surgical menopause
endocrinological features of approaching menopause (51y/o)
Presentation such as vasomotor symptoms and menstrual irregularities
• The most common presentation is amenorrhea • Menopause: 12 continuous months of amenorrhea
or oligomenorrhea (which may not necessarily • Diagnosis of menopause after the age of 45 years should be
based on symptoms and menstrual patterns, FSH levels tend to
be accompanied by hot flushes)
fluctuate in the perimenopausal period.
• Infertility
• Other features are similar to those of climacteric symptoms (in peri or post-menopausal): hot flashes, night
sweats, irritability, poor concentration, decreased sex drive, dyspareunia, vaginal dryness, palpitations
Investigations
• FSH level: > 25 IU/I on two occasions > 4 weeks apart are diagnostic
Management
• HRT until the average age of menopause (51 years)
Signs of labour
• Regular and painful uterine contractions Pregnancy is divided into trimesters:
• A show (shedding of mucus plug) • First trimester: week 1–13 - highest risk of miscarriage
• Rupture of the membranes (not always) • Second trimester: week 14–26
• Shortening and dilatation of the cervix • Third trimester: week 27–40
Stages of labour
Stage 1: from the onset of true labor to when the cervix is fully dilated
- It's divided into a latent and an active phase
• In a primigravida, stage 1 lasts typical 10-16 hours
1. Latent phase: begins with onset of regular
contractions and ends with the acceleration of cervical dilatation
2. Active phase: begins with cervical dilatation acceleration, usually at 3-4 cm of dilatation, ending with
complete cervical dilatation (10 cm)
Stage 2: from full dilatation of cervix until the delivery of the fetus
Stage 3: from delivery of fetus to when the placenta and membranes have been completely delivered
Poor progress in the 1st stage Management

• Oxytocin (syntocinon) will increase the
• Inefficient uterine activity (power → commonest cause) frequency and strength of contractions
• Malposition, malpresentation or large baby (passenger) • Amniotomy/AROM if the membrane is still
• Inadequate pelvis (passage) intact
Investigations for the viability of the fetus

- TVUS, heart rate is detected at 6 weeks
- CTG, useful after 32 weeks
Risks for shoulder dystocia

Management of shoulder dystocia
Pre-labour risk factors (HELPERR)
- Fetal macrosomia > 4.5 kg • Help
- Maternal BMI > 30 kg/m2 • Episiotomy
- DM • Legs (McRoberts)
• Pressure at suprapubic area
- Previous shoulder dystocia
• Enter
- Induction of labour • Remove the posterior arm
Intrapartum risk factors • Roll the patients to hands and knees
- Prolonged labour
- Oxytocin augmentation
Endometritis: most common cause of 2ry PPH
- Assisted vaginal delivery • Investigations
- High vaginal swap
Causes of primary PPH (4Ts) - Bloods including FBC and CRP
- TVUS
• Tone, abnormalities of uterine contraction • Treatment
• Tissue, retained products of conception - Co-amoxiclav
• Trauma (lacerations, incisions, uterine rupture)
• Thrombin, abnormalities in coagulation (DIC), associated with placental abruption
Uterine atony
➢ The most common cause of excessive PPH
Risk factors
• Rapid or protracted labour (slow cervical dilatation) → most common
• Chorioamnionitis
• Overdistended uterus (Macrosomic baby)
Clinical findings
- A soft uterus palpable above the umbilicus
Management
- Uterine massage → effective at stimulating endogenous oxytocin
- IV Oxytocin
Chorioamnionitis
➢ Acute inflammation of the fetal and chorion membranes typically due to an ascending bacterial infection
from vagina into the uterus in the setting of membrane rupture in pregnancy
Features
- Fever
- Abdominal pain, including contractions
- Maternal pyrexia and tachycardia (tachycardia often precedes pyrexia)
- Fetal tachycardia (normal FHR: 120-160 bpm)
- Uterine tenderness
- Foul odor of amniotic fluid
- Speculum shows offensive vaginal discharge (usually yellow/brown)
- Small for dates; due to amniotic fluid loss
Risk factors
• Prolonged ROM
• Chorioamnionitis → baby is still inside
• Prolonged labour • Endometritis → baby is out
• Multiple vaginal examinations
• Meconium-stained amniotic fluid
Endometritis (uterine infection)

➢ Most common cause of post-partum fever, could be a sequela to chorioamnionitis postpartum
➢ Most common cause of 2ry PPH
Risk factors
• Emergency cesarean section
• Endometritis is associated with CS while
• PROM retained product of conception is linked with
• Prolonged labour NSVD
• Multiple pelvic examinations • Endometritis → high vaginal swap
• Internal fetal monitoring
Signs and symptoms
• Fever (usually in proportion to the extent of infection)
• Foul smelling, profuse and bloody discharge
• Tender bulky uterus on abdominal examination
Management
• Antibiotics (Co-amoxiclav)
Rhesus -ve pregnancy
➢ If a Rh -ve mother delivers a Rh +ve child, a leak of fetal red blood cells may occur which causes anti-D IgG
antibodies to form in the mother
➢ In future pregnancies, these antibodies can cross the placenta and cause hemolysis in the fetus
Prevention of Rh sensitization
- Test for anti-D antibodies in all Rh -ve mothers at booking
- If Rh -ve and not previously sensitized, anti-D IgG at 28 weeks and 34 weeks gestation is given IM
- Anti-D is for prophylaxis only, once sensitization has occurred it's irreversible and Anti-D administration
would be pointless
Anti-rhesus (anti-D) IgG are given IM. It neutralizes any Rhesus D positive antigens which have entered mother's
blood. If the antigens have been neutralized, there will be no reason for mother to develop an immunity and produce
antibodies. She would remain non-sensitized
Anti D immunoglobulin should be given as soon as possible (but always within 72 hours of giving birth) in the
following situations:
- Delivery of a Rh +ve infant, whether live or stillborn
- Any termination of pregnancy or evacuation of retained products of conception (ERCP) after miscarriage
- Miscarriage if gestation > 12 weeks
- Ectopic pregnancy
- Blunt abdominal trauma
- External cephalic version (baby is turned from buttocks first → cephalic first)
- Antepartum hemorrhage, any vaginal bleeding over 12 weeks gestation
- Amniocentesis, chorionic villus sampling, fetal blood sampling
Affected fetus
If unborn:
- Edematous (hydrops fetalis, as liver devoted to RBC production thus albumin levels fall → more fluid
intracellularly)
- Fetal heart failure → treatment includes intrauterine blood transfusion
If born:
- Jaundice (due to buildup of excessive bilirubin from RBC breakdown)
- Anemia
- Hepatosplenomegaly
Treatment
• UV phototherapy
• Blood transfusion
• Exchange transfusion
Assessing the severity of fetal anemia
1. Assessing fetal middle cerebral artery on US: allows estimation of fetal hemoglobin
2. Fetal cord blood sampling, only indicated if the peak systolic velocity (PSV) of the MCA is abnormal
3. Kleihauer-Betke test is used to determine the required dose of anti-D IgG to inhibit the formation of Rh
antibodies in a Rh -ve mother to prevent Rh disease in future pregnancies with a Rh +ve fetus. It has no role
in women who are already sensitized
Hormonal replacement therapy (HRT)
Types
1. Estrogen-only HRT
- Used in women who had a hysterectomy or an IUS in situ
2. Sequential (cyclical) combined HRT
- Used in peri-menopausal women who are still menstruating or within 12 months of their last period
- Sequential combined HRT is where estrogen is taken every day, and progestogen is taken sequentially
(usually for the last 14 days of menstrual cycle) to induce bleed
- Patients often switch to Continuous combined HRT after 12 months
3. Continuous combined HRT
- Used in postmenopausal women (i.e. women who have had their last period > 12 months ago)
- Estrogen and progestogen are taken daily
- For women who still have uterus to prevent endometrial hyperplasia which could lead to endometrial
carcinoma if only an estrogen preparation is used
Indications
• Postmenopausal women with vasomotor symptoms (hot flushes and night sweats) should be treated by
hormonal replacement therapy (HRT) as a first line management for up to 5 years. Clonidine can be used
• For women with early menopause, they should be treated with HRT beyond the age of 51 years
• For women under 60 years who at risk of an osteoporotic fracture for whom non-estrogen treatments are
unsuitable
Contraception clinchers
• Young women, not sexually active (don't require contraception)
- Menorrhagia only → Tranexamic acid
- Menorrhagia and Dysmenorrhea → Mefenamic acid
- Menorrhagia/Dysmenorrhea/Metrorrhagia (irregular menses) → COCP
• Sexually active women (require contraception)
- Mirena IUD is the 1st line when:
1. Suffering from menorrhagia/dysmenorrhea
2. Those suffering from fibroids (which do not distort the uterine cavity)
3. Possible contraindications of COCP: obesity – smoking – history of thromboembolism
- Women with sickle cell disease and menorrhagia → IM Depo-Provera (SE → osteoporosis)
Mirena and Depo-Provera are NOT recommended for patients below 20 years
Under 20 years: POP, COCP and implants (Nexplanon)
Nexplanon implant
- Progesterone-only subdermal implant (inserted in the upper arm)
- Reliable and reversible form of contraception
- It must be removed after 3 years
Depo-Provera
- Progesterone-only IM injection once every 3 months
Pearl index: (per 100)
- Mirena → 0.2 → lowest failure rates
- COCP / POP → 0.3
- Female sterilization → 0.5
- Male condoms → 2
Emergency contraception
1. Copper IUD
- MOST EFFECTIVE form of emergency contraception
- Mechanism → inhibiting fertilization or implantation
- Should be inserted in 5 days of unprotected sexual intercourse (UPSI)
2. POP – Levonorgestrel
- Mechanism → inhibiting ovulation and implantation
- Should be used within 72h
3. Ulipristal Acetate (ellaOne)
- Mechanism → inhibition or delay of ovulation
- Should be taken within 5 days (120h) after intercourse
Post-partum contraception
- Breast feeding → COCP after 6 months
- Non breastfeeding → COCP after 6 weeks
- In both cases, during the period before they start using COCP, they can use condoms or POP
- IUS/IUCD → unless fitted within 48 hours of birth, delay until 28 days postpartum (as if inserted before
may risk uterine perforation)
➢ Menstrual periods return after 5-6 weeks after birth if the mother isn’t breast feeding. If the mother is
breastfeeding, the menstrual cycles usually return once breastfeeding is less often
➢ Women can become pregnant BEFORE their periods return because ovulation occurs prior to menstrual bleeds
➢ For women who aren’t breast feeding, contraception is started from 3 weeks after birth
➢ Menstrual cycles could return as early as 21 days postpartum in women who aren’t breastfeeding
➢ Irregular bleeding whilst on contraception is common, reassure and continue for 3 months before changing the
method of contraception
COCP are unlikely to be chosen for contraception

[Vitamins Make Boys Sleep Better Hours]
1. History of VTE (venous thromboembolism) or family hx → implants are used instead
2. Migraine with aura
3. BMI > 30 kg/m2
4. Smoker or ex-smoker
5. History of Breast cancer (it's okay to use with hx of breast cancer as long as there's no gene mutations)
6. Hypertension (even if adequately controlled)
How to manage lost IUD threads? • COCP might be necessary for the fear of ectopic
pregnancy; this could be the best immediate
1. Exclude pregnancy by performing a urine pregnancy test action/most appropriate next step
2. Request a pelvic US to look for IUD
- TVUS is preferred
- If there’s fear of perforation (acute abdomen) → TAUS
3. If IUD is not found on US, request an abdominal x-ray
Oral contraception interaction and hepatic enzyme inducers
• Women starting hepatic enzyme inducers should be advised to use a reliable contraceptive method which is
unaffected by the enzyme hepatic inducers → Depo-Provera or Mirena IUD
• Once stopping hepatic enzyme inducers, women are still advised to continue appropriate contraceptive
measures for another 4-8 weeks as enzyme activity does not return to normal until several weeks of stopping
hepatic enzyme inducers
Mnemonic for hepatic enzyme inducers CRPA GPs

- Carbamazepine
- Rifampicin
- Phenytoin
- Alcohol (chronic consumption)
- Griseofulvin
- Phenobarbitone
- Sulfonylurea
Uterine rupture
• Spontaneous tearing of the wall of the pregnant uterus with or without expulsion of the fetus that endangers
life of both mother and fetus
• Usually occur during labour but has been reported antenatally
Features
• Tenderness over previous uterine scars
• Fetal parts may be easily palpable
• To differentiate uterine rupture from placental
• Fetus not palpable on vaginal examination
abruption → no uterine contractions
• Vaginal bleeding may be evident
• Signs of maternal shock
• Fetal distress on CTG
Risk factors
• Previous C-section
• Excessive oxytocin stimulation
• Failure to recognize obstructed labour
Diagnosis
• Surgical exploration of the uterus and identifying the tear
Management
• Urgent laparotomy to deliver the fetus and repair the uterus
- Late fetal deceleration → fetal distress (due to placental insufficiency)

- Early deceleration → fetal head compression during contraction leading to increased vagal tone
- Variable deceleration → umbilical cord compression
HELLP syndrome
• A variant of severe pre-eclampsia which manifests with:
- Hemolysis (H)
- Elevated liver enzymes (EL)
- Low platelets (LP)
• Liver enzymes usually increase and platelets decrease before hemolysis occurs
• The syndrome is usually self-limiting, but permanent liver or renal damage may occur
• Note that eclampsia may co-exist
• 30% of patients develop HELLP symptoms within 48h postpartum
Signs and symptoms
• Epigastric or RUQ pain and tenderness Acute fatty liver of pregnancy (AFLP)
• Nausea and vomiting - Hypoglycemia (H)
• Tea-colored urine due to hemolysis (also causes high LDH) - Ammonia (A)
- Acidosis (A)
• Increased BP and other features of pre-eclampsia
Management
• Delivery
• Supportive and as for eclampsia (MgSO4 is indicated)
• Although platelet count is very low, platelet infusions are only required if bleeding or for surgery (<40)
Hyperemesis gravidarum
• Nausea and vomiting are common in early pregnancy, if severe or prolonged → hyperemesis gravidarum
• Symptoms usually begin between 6-8 weeks and peaks at 12 weeks and usually resolve at 20 weeks
Symptoms
• Nausea, Vomiting
• Food and fluid intolerance
• Lethargy
Signs
• Ketonuria
• Weight loss > 5%
• Tachycardia
• Signs of dehydration (decrease skin turgor – prolonged capillary refill – sunken eyes)
Management
1. IV fluids
2. Antiemetics
- 1st line: IM or oral cyclizine or promethazine → if it fails, prochlorperazine IM or orally
- 2nd line: IV Metoclopramide or Ondansetron
3. Steroids (a consultant decision)
4. Thiamine (vitamin B1) → to prevent Wernicke's encephalopathy which is due to vitamin B1 deficiency
CA125 should be performed if a woman – especially if aged 50 years old or over – has any of the following symptoms
on a regular basis:
• Bloating
• Loss of appetite
• Pelvic or abdominal pain
• Increased urinary urgency and/or frequency
Threatened miscarriage • Vaginal bleeding + fetal heart seen

• Cervical os is closed
• Dead fetus before 20 weeks without symptoms of expulsion (after 20
Missed miscarriage (delayed weeks → stillbirth)
miscarriage) • May or may not have vaginal bleeding
• Cervical os is closed
Inevitable miscarriage • Cervical os is open and bleeding
Incomplete miscarriage • Not all products of conception have been expelled
Complete miscarriage • Everything has been expelled
Pelvic congestion syndrome

• Caused by varicose veins in the lower abdomen, diagnosed by excluding other organic causes of dyspareunia
Features
1. Symptoms similar to premenstrual syndrome • Orgasm may help to alleviate the symptoms
2. Aggravated by standing
3. Non-organic dyspareunia
Anti-phospholipid syndrome
• The most important treatable cause of recurrent miscarriage
• A disorder of the immune system that causes an increased risk of DVT and recurrent miscarriage
• Women with recurrent miscarriage should be screened for APS (1st trimester→3 or more, 2nd→one or more)
• Investigated by Antiphospholipid antibodies
• Treated with Aspirin 75mg + Heparin
• Corticosteroids have no role in treatment
Parental Karyotyping is performed if cytogenic analysis performed on products of conception shows unbalanced
chromosomal abnormalities
Cysts under US
• PCOS → Multiple follicles/cysts
• Ovarian teratoma (Dermoid cyst) → Ice berg tip sign, flat-fluid level, dermoid mesh, echogenic tubercle
projecting into lumen of cyst
• Ovarian endometrioma (chocolate cyst) → Ground glass echoes
• Tubo-ovarian abscess → Multilocular, echogenic debris in pelvis
Ovarian torsion
• Presents with sudden onset of sharp, unilateral lower abdominal pain
• Often with nausea and vomiting
• Tender mobile mass
• The definitive diagnosis is often made in the theatre during a laparoscopy as ovarian torsion is difficult to
diagnose
Cervical screening
- Women aged 25-49 years are invited for a cervical screening every 3 years
- Women aged 50-64 are screened every 5 years
- Optimum time for a cervical smear is during mid-cycle (days 10-20 of a 28-day cycle) as most endocervical
cells can be collected then. It's also more challenging to obtain a smear while menstruating
Management based on results
• Negative → appropriate
• Inflammatory → repeat cervical swab in 6 months, take swabs for infection if severe inflammation
• Inadequate → repeat sample → if results still inadequate, consider colposcopy
• Borderline → perform HPV test → if positive, refer to colposcopy
• Mild dyskaryosis → perform HPV test → if positive, refer to colposcopy
• Moderate / severe dyskaryosis → refer to colposcopy for suspected cancer (two-week-wait)
- Endocervix → Columnar
Cervical ectropion - Ectocervix → Squamous
• When the columnar of the endocervix is displayed beyond the os. The stratified squamous epithelium that
normally lines the vaginal part of the cervix (ectocervix) is replaced by columnar epithelium, which has
migrated from the endocervix
• Cervix enlarges under the influence of estrogen (puberty, pregnancy or women on COCP)
• Very common and is seen as a red ring around the os
• Usually asymptomatic but occasionally present with post-coital bleeding or discharge (clear, watery and no
odor)
• NO cervical screening as there's no link to cervical cancer
Management
• If asymptomatic and NO bleeding after touch → Reassure
• If symptomatic → Cautery with silver nitrate, diathermy and
cryotherapy
• A cervical smear should be obtained prior to treatment
Cervical cerclage
➢ Cervical weakness is a recognized cause of 2nd trimester miscarriage
Criteria for the procedure
• A history of 2nd trimester miscarriage preceded by spontaneous rupture of membranes or painless cervical
dilatation
• A woman whom cervical length < 25mm with a history of large loop excision of the transformation zone
(LLETZ) procedure of the cervix
Risks of the procedure
• Infections
• Rupture of membranes
Folic acid dosage
• Usual dose is 0.4 mg/day until 12 weeks of gestation (the time it takes the fetus spine to develop)
• A dose of 5 mg/day until 12 weeks of gestation
- In a diabetic mother to reduce the risk of having a baby with neural tube defect
- BMI > 30
- Those taking antiepileptics
- History of NTD
• A dose of 5 mg/day for the entire pregnancy
- Thalassemia trait
- Sickle cell anemia
Hematological changes in pregnancy

Anemia in pregnancy [falls by 0.5g progressively]
• Plasma volume increases by 50% ⟶ Dilutional anemia
• 1st trimester: Hb <11 g/dl • Elevated erythropoietin increases the total red cell
mass
• 2nd & 3rd trimester: Hb <10.5 g/dl
• MCHC and MCV are unaffected
• Postpartum: Hb <10 g/dl
Management: Oral ferrous sulphate (if Hb <11g/dl) unless not tolerated
Vaccination in pregnancy (flue and sneeze vaccines)

1. For flu: Influenza vaccine
2. For whooping cough: Pertussis vaccine
- Best time for it is 20-32 weeks gestation
- Usually combined with DPT diphtheria, polio and tetanus
Routine blood tests performed at booking (ideally by 10 weeks)
- Hep B & HIV
- Syphilis screen
- Blood group and Rh status
- FBC & Haemoglobinopathies
Constipation in pregnancy
- 1st line is Lactulose
- 2nd line is Senna, used for short periods
Pain management during pregnancy

- As a junior doctor, Paracetamol is the ONLY analgesic to be prescribed
Antibiotics in pregnancy
Safe Unsafe
• Cefalexin (Cephalosporin) • Trimethoprim (T – Teratogenic, Term OK)
• Amoxicillin - Can lead to NTD
- If it should be used, folic acid 5mg should be given
Should be avoided if there's penicillin allergy, • Nitrofurantoin (N – Neonatal hemolysis, term Not OK)
avoid Co-amoxiclav as well - Shouldn't be used near term as it causes neonatal
hemolysis
• Ciprofloxacin
- Can cause arthropathy
Notes
• A transdermal approach of COCP has less risk of venous thromboembolism than oral route
• Smoking is not a contraindication for HRT use but can reduce the efficacy of orally administered estrogen
• A vaginal estrogen cream would be appropriate if the patients ONLY had symptoms of atrophic vaginitis:
1. Vaginal dryness
2. Atrophic changes within the urogenital tract (frequency, urgency, nocturia, incontinence and recurrent
infection
3. Dyspareunia, itching and burning
• If there’s additional systemic symptoms (hot flushes, night sweats) → HRT
• Endocervical swab has NO value in cervical screening
• Permanent cessation of menstruation for 12 consecutive months with no other obvious physiological or
pathological cause → Menopause (51)
• Cessation of menstruation >12 months along with climacteric symptoms → Perimenopause
• Amniotic fluid embolism can cause seizure post-delivery. However, it should occur within the first 30min
• 1ry amenorrhea + normal values → Absent uterus
• Turner syndrome and absent ovaries would have bloods with a low estradiol, high FSH and LH
• Patient in A&E with constant PID symptoms without discharge, best investigation → US, to exclude abscess
• Any pregnant woman with symptoms and/or signs suggestive of venous thromboembolism → LMWH
• An antibiotic that should be avoided in the 1st trimester → Trimethoprim
Ophthalmology
Acute angle closure glaucoma
➢ Also called acute glaucoma or narrow-angle glaucoma
➢ Obstructed anterior chamber angle → an impairment of aqueous outflow → rise in IOP
• Hypermetropia (farsightedness) Myopia is a Rf for:
• Pupillary dilatation • Cataract
• Retinal detachment
Presentation
• Open angle glaucoma
• Red, severely painful eye with a semi-dilated non-reacting pupil
• Headaches and decreased visual acuity are common
• Symptoms worsen with mydriasis (e.g. watching TV in a dark room, applying topical mydriatics)
• Colored haloes around lights may be seen by patients
• Palpation of the globe will reveal it to be hard
• Corneal edema results in dull or hazy cornea
• Systemic upset may be seen, such as nausea and vomiting and even abdominal pain
- The acute attack is usually unilateral; however, long-term management will be to both eyes
- ICP can lead to optic disc papilledema
Investigation
• Ocular tonometry → IOP >30 mmHg (normal IOP = 15-20)
Management
Medical
• Initial medical treatment typically involves all topical glaucoma medications that are not contra-indicated in
the patient, together with intravenous acetazolamide
• Topical agents include
- Beta-blockers - e.g. timolol, cautioned in asthma
- Steroids - prednisolone 15 every 15 minutes for an hour, then hourly
- Pilocarpine 1-2% → a miotic drug to constrict the pupil and open the angle
- Acetazolamide is given intravenously (500 mg over 10 minutes) and a further 250 mg slow-release tablet
after one hour
- Offer systemic analgesia ± antiemetics
• This should tide the patient over until they are able to be seen by a duty ophthalmologist who will assess the
situation at short intervals until the acute attack is broken
• These treatments may be repeated depending on the IOP response and a combination of these medications
will be given to the patient on discharge
• The patient will remain under close observation (e.g. daily clinic reviews or as an inpatient). Subsequent
treatment is aimed at specific mechanism of closure
Surgical
• Peripheral iridotomy (PI)
- This refers to (usually two) holes made in each iris with a laser
- This is to provide a free-flow transit passage for the aqueous
- Both eyes are treated, as the fellow eye will be predisposed to an AAC attack too
- This procedure can usually be carried out within a week of the acute attack, once corneal edema has
cleared enough to allow a good view of the iris
• Surgical iridectomy
- This is carried out where PI is not possible. It is a less favored option, as it is more invasive and therefore
more prone to complications
Ophthalmology
Anterior uveitis
➢ Also referred to as “iritis” or “iridocyclitis”. It is one of the important differentials of a red eye
Features
Acute anterior uveitis
• Progressive (over a few hours/days) unilateral, painful red eye
• Reduced visual acuity
• Photophobia
• Pupil → abnormal shape/size
- Small pupil, initially from iris spasm
- Later it may be irregular or dilate irregularly due to adhesions
between lens and iris
• Excess tear production
• Characteristic sign → cells in the aqueous humour seen on slit-lamp
- Aqueous humour is cloudy, giving the appearance of a 'flare'. This appears rather like a shaft of light
shining through a darkened, smoky room
- Anterior chamber flare is due to inflamed vessels leaking protein. Due to the cloudiness, as the slit-
lamp beam of light is shone through, the beam disperses hence the term flare
Chronic anterior uveitis

• Presents as recurrent episodes, with less acute symptoms
• Patients may find that one symptom predominates (this tends to be blurred vision)
• Most common cause of chronic anterior uveitis → Sarcoidosis
Associated conditions
• Ankylosing spondylitis • RA → Sclera
• AS → Uveitis
• Reactive arthritis
• IBD
Management
• Prednisolone eye drops → to reduce inflammation
• Cyclopentolate → to prevent adhesions between lens and iris by keep pupil dilated
- Intermediate uveitis = pars planitis = viritis

- Posterior uveitis = chorioretinitis
- Most common form of uveitis → Anterior uveitis
Ophthalmology
Central retinal vein occlusion (CRVO)
Causes
• Glaucoma • CRAO → No blood → Pale sclera
• Hypertension • CRVO → Blood obstructed → Hemorrhage
• Polycythemia
Presentation
• Similar to those with central retinal artery occlusion (CRAO) Hypertensive retinopathy
• Unilateral sudden loss of vision, may occur overnight - Asymptomatic, sudden, bilateral loss of vision
• NO pain, redness, or abnormality in pupillary dilation
Diagnosis
• Retinal hemorrhages → the main way of distinguishing venous obstruction from arterial obstruction
- You cannot have a hemorrhage in the retina if you don't have blood getting into the eye
• Fundoscopy
- Disk swelling, venous dilation, tortuosity, and retinal hemorrhages
(flame-shaped hemorrhages)
- Stormy sunset or tomato splash appearance
Treatment
• Immediate referral to an ophthalmologist and/or intra-vitreal steroids
Central retinal artery occlusion (CRAO)

➢ Occlusion before it branches out as it emerges from the optic nerve, resulting in almost complete hypoxia of
the inner retina
Presentation
• Unilateral, sudden painless visual loss
• In 94% of cases, vision is reduced to counting fingers (ophthalmic artery may also be affected)
• There may be a history of amaurosis fugax (amaurosis fugax precedes loss of vision in up to 10% of patients)
Examination
• An afferent pupil defect appears within seconds and may precede retinal changes by 1 hour
• Ophthalmoscopy
- White or pale retina
- Cherry red spot at the macula, supplied by choroid vessels
- Attenuation of the vessels, as blood backed up in retina
What is an afferent pupillary defect (absent direct response)?

- When the pupil won’t respond to light, but constricts to a beam in the other
eye (consensual response). Constriction to accommodation still occurs
Investigations
• Diagnosis is usually clinical and investigations are aimed at ruling out underlying diseases
• The most important cause to rule out is giant cell arteritis (10%) → visual loss is reversible
Management
• If the patient presents within 90-100 minutes of onset → firm ocular massage. The idea behind this is to try
to dislodge the obstruction
• This only works very occasionally and immediate referral is mandatory
Branch retinal artery occlusion (BRAO) → wedge-shaped pallor sparing the rest of the optic disc
Ophthalmology
Optic neuritis
➢ Inflammation of the optic nerve
Presentation
• Classically there is a triad of clinical features which are
- Reduced vision (of varying severity) → Usually unilateral. Progresses for less than 2 weeks and
spontaneously improves within 3 weeks
- Eye pain → Particularly on movement
- Impaired color vision → Initially loss of red color vision
• One of the most common cause of optic neuritis is multiple sclerosis → Seen especially in Caucasian
populations the stem would usually (but not always) include a female patient as multiple sclerosis is more
prevalent in the female gender
Examination
• Swollen optic disc
• Optic disc becomes pale later (4 to 6 weeks after onset)
• Relative afferent pupillary defect (RAPD) (Marcus Gunn pupil)
• Central scotoma may occur
RAPD
- When light is directed towards the unaffected eye, both pupils constrict
- When light is directed towards the affected eye, both pupils do NOT constrict (appear relatively dilated)
RAPD = damage to the whole optic nerve = mononuclear field loss
If NO RAPD = ONLY a part of optic nerve is affected = Central scotoma
Central scotoma → A blind spot in the middle of one’s vision
Ophthalmology
DM-related retinopathy
Background retinopathy (not proliferative) → [Painting as background]
• Microaneurysms (dots)
• Hemorrhage (blots)
• Hard exudates
Pre-proliferative retinopathy
• Addition of Cotton wool spots
Proliferative retinopathy
• Addition of new vessel formation (neovascularization)
• More serious. Progresses rapidly to blindness. Neovascularization may lead to vitreous hemorrhage
• Floaters in vision
• Laser photocoagulation is needed
Hypertensive retinopathy
➢ Most patients are asymptomatic
Chronic hypertension
• BP >140/90 mmHg
• Usually asymptomatic
• Fundoscopy
- Bilateral attenuation of arterial vessels (copper or silver wiring)
- Arteriovenous nipping/nicking (where arteries cross the veins)
- Eventually, hemorrhage and exudates
Malignant (accelerated) hypertension
• BP >180/110
• May have headache and decreased vision
• Fundoscopy
- Hard exudates, appear as (macular star), thin white streaks radiating around the macula
- Disc swelling
- Cotton wool spots
- Flame hemorrhage, also found in diabetic retinopathy and CRVO
- Arterial or venous occlusion
Ophthalmology
Amaurosis fugax
➢ Painless transient monocular visual loss (i.e. loss of vision in one eye that is not permanent)
➢ It is indicative of retinal ischemia, usually associated with emboli or stenosis of the ipsilateral carotid artery
➢ Resolves spontaneously (15-30 minutes)
Presentation
• Sudden, unilateral vision loss; “black curtain coming down”
• Duration: 5-15 minutes; resolves within < 24 hours
• Associated with stroke or transient ischemic attack (TIA) and its risk factors (i.e. HTN, atherosclerosis)
• Has an association with giant cell arteritis
• Curtains = CRAO (Amaurosis Fugax) or Retinal detachment
Retinal detachment
➢ Usually spontaneous, but it may result from trauma
➢ It occurs when the force that holds the retinal attachment fails which results in accumulation of fluid in the
subretinal spaces
➢ The two most common predisposing factors are extreme myopia and surgical extraction of cataracts,
proliferative retinopathy from diabetes, CRVO, and age-related macular degeneration
Presentation
• The classic symptom is → photopsia (flashing lights)
• A common presentation is unilateral blurry vision without pain or redness
• The patient may complain of seeing “floaters” as well as flashes at the periphery of vision
• Sometimes it is described as a "curtain coming down," as the retina falls off the sclera behind it
Detachment presents with 5 ‘F’s
- Floaters (tiny black dots)
- Flashes
- Field loss
- Fall in acuity
- Falling curtain
Diagnosis
• Direct ophthalmoscopy → grey, opaque and wrinkled retina, ballooning forward
Treatment
• Patients should lean their heads back to promote the chance that the retina will fall back into place
• The retina can be mechanically reattached to the sclera surgically, by laser photocoagulation, cryotherapy,
or by the injection of expansile gas into the vitreal cavity (gas will press the retina back into place)
• Scleral buckling, a "buckle," or belt, can be placed around the sclera to push the sclera forward so that it can
come into contact with the retina
Causes of sudden painless loss of vision

- Retinal detachment
- Vitreous hemorrhage
- CRVO
- CRAO
- Giant cell arteritis
Ophthalmology
Conjunctivitis
Management of bacterial conjunctivitis

• <7 days → cotton soaked in water to remove any sticky discharge
• >7 days → Topical antibiotics (Chloramphenicol drops)
Management of viral conjunctivitis

• Mostly caused by adenovirus → Reassure
• Artificial tears might be used
Acute dacryocystitis
➢ Acute inflammation of the lacrimal sac, often as a result of infection
Presentation
• Symptoms and signs are over the region of the lacrimal sac (but may spread to the nose and face with teeth
pain being experienced by some)
• Therefore, look just lateral and below the bridge of the nose for:
- Excess tears (epiphora)
- Pain
- Swelling and erythema at the inner canthus of the eye
Management
• Immediate antibiotic therapy may resolve the infection
- Children → Co-amoxiclav or Cefaclor
- Adults → Co-amoxiclav or Cefalexin
Oculomotor nerve palsy

Causes
• Diabetes
• PCA aneurysm → excluded by MRI, CT angiography
• Tumors, infarction, abscess or trauma
Features
• Initial sign → Fixed dilated pupil which doesn’t accommodate = O
• Ptosis
• Unopposed lateral rectus and SO → eye deviated down and outward
Ophthalmology
Cataract
➢ Clouding of the lens, Glare at night, Dazzle at light
➢ May cause gradual loss of vision (frequent changes of glasses), absent red reflex
➢ Children may present with squint, loss of binocular function or a white pupil
Risk factors
• Exposure to great amount of UV light (e.g. person from Australia who never wears glasses)
• Long term use of corticosteroids (e.g. an asthmatic patient on Oral steroids)
• Smoking, DM
• High myopia
• Eye trauma
Management
• Lens extraction
Herpes zoster ophthalmicus

➢ Reactivation of VZV in the area supplied by the ophthalmic division of the trigeminal nerve
Features
• Vesicular rash around the eye, may involve the eye itself
• Hutchinson’s sign → rash on the tip or side of the nose, indicates nasociliary involvement and is a strong
factor for ocular involvement
Management
• Oral antiviral
• Oral corticosteroids
• If ocular involvement → refer to a specialist
Complications
• Ocular → conjunctivitis, keratitis, episcleritis, anterior uveitis
• Ptosis
• Post-herpetic neuralgia, a chronic neuropathic pain that persists 3 months or more following an outbreak of
shingles, pain continues even after the eruption has resolved
Keratitis
- Inflammation of the cornea
- Herpes simplex keratitis → presents with a dendritic corneal ulcer
- Treated by topical acyclovir, steroid drops are contraindicated → flaring up and blindness
CMV Retinitis
• History of positive HIV, attends he clinic with visual deterioration
• Pizza retina
- Hemorrhages → tomato sauce
- Yellowish exudate → cheese
Presentation
• Decreased visual acuity, floaters, and loss of visual fields on one side
• Fundoscopy → yellow-white cloudy retinal lesions. Lesions may appear at the periphery of the fundus, but
they progress centrally
• On examination, multiple cotton wool spots can be seen
• Starts unilateral then bilateral
Ophthalmology
Ocular manifestations os rheumatoid arthritis (RA)
• Keratoconjunctivitis sicca → most common
• Episcleritis → erythema + pain (less severe than scleritis) • Ankylosing spondylitis → Iris
• Scleritis → erythema + pain • RA → Sclera [RAS]
• Iatrogenic steroid-induced cataract
Keratoconjunctivitis sicca
• Dry, itchy, gritty eye due to decreased lacrimation + sandy feeling under the eyes
• Can be found in RA or Sjogren $
• Schirmer’s test → <10mm
• Treated by artificial tears (Hypromellose, sodium chloride, sodium hyaluronate)
• Topical ciclosporin can be used
- Autoimmune diseases → Scleritis/episcleritis

- Seronegative arthropathies/Sarcoidosis/Syphilis/IBD → Anterior uveitis (iritis)
- Giant cell arteritis/MS → Optic nerve affected
Simple (primary) open angle glaucoma

Risk factors
• Old (>40 years) + black
• Myopia
Features
• Majority is asymptomatic
• Initially → Peripheral visual loss – nasal scotoma progressing to “tunnel vision”
• Other features → decreased visual acuity, optic disc cupping
- Myopia + Peripheral visual loss → Open-angle glaucoma
Retinitis pigmentosa
• Initially → night blindness
• Peripheral visual field loss
Subconjunctival hemorrhage
• Presents as a bloodshot eye
• Occurs due to a small bleed from one of the minor conjunctival vessels on the surface of the eye
• May be caused by HTN, straining (coughing or sneezing), trauma or spontaneously (with no apparent cause)
Management
• Trauma → CT
• HTN → BP monitoring
• Recurrent, patient is on anticoagulation → Check INR
• If no apparent cause → Reassure
Ophthalmology
Notes
• Colored halos → Closed angle glaucoma
• Glare at night → Cataract
• Flare → Iritis
• Floaters → Anterior Uveitis, retinal detachment, proliferative DM retinopathy, CMV retinitis
• Peripheral visual field loss → Open angle glaucoma
• Central scotoma → Optic neuritis
• Bilateral paracentral scotoma → Pituitary tumor compressing optic chiasma, may progress to arcuate,
double arcuate scotomas and eventually tunnel vision
• Bitemporal hemianopia → Pituitary tumor compressing optic chiasma
• Homonymous hemianopia → Optic tract lesions
• A child with acute onset of swelling, redness, increase warmth and tenderness of the eyelid with fever →
Periorbital cellulitis
• If it involves orbital signs such as gaze restriction, proptosis and pain on eye movements → Orbital cellulitis,
an emergency that requires → IV antibiotics, if CT confirms abscess → Drainage
• Hypermetropia = Farsightedness
• Myopia = Nearsightedness
• Degenerative corneal disease [Kill The Blue Parrot]
- Keratoconus, a cone-shaped cornea
- Terrien marginal degeneration, bilateral peripheral thinning of the cornea
- Band keratopathy, characterized by deposition of calcium
- Pellucid marginal degeneration, bilateral peripheral thinning of the cornea
• Central retinal artery is a branch of the ophthalmic which arises from the internal carotid artery
Orthopedics
Osteoarthritis
Features
• Monoarthritis
• Hip and knee are commonly affected, wrist and hand can be affected
• Joint pain that is exacerbated by exercise and relieved by rest (sometimes gives a history of pain worsening at
the end of the day)
• Bony deformity due to osteophytes. In fingers this presents as swelling:
- At the distal interphalangeal joints → Heberden's nodes
- At the proximal interphalangeal joints → Bouchard's nodes
Heberden → Distal interphalangeal joint (H-D) (High Definition)

Bouchard → Proximal interphalangeal joint (B-P) (Blue Picture)
Investigation
• X ray [LOSS]
- L → Loss of joint space
- O → Osteophytes
- S → Subchondral cysts
- S → Subchondral sclerosis
• DEXA scan
- T-score = -2.5
Management
• Exercise and physiotherapy
• Weight reduction
• Regular Paracetamol → 1st line
• Topical NSAIDs
• Oral NSAIDs (regular paracetamol and/or topical NSAIDs should be considered before oral NSAIDs)
• Joint surgery is the last option
T-score → describes the bone mineral density (BMD) at the site that’s being tested to that compared of a healthy
30-year-old
• -1 or higher → Normal
• -1 to -2.5 → Osteopenia
• -2.5 or lower (more than 2.5 standard deviation below the mean) → Osteoporosis / Osteoarthritis
Orthopedics
Fractures
• Injury to the extensor digitorum profundus tendon of the fingers at the distal IPJ
Mallet finger • Results from hyperflexion of an outstretched finger causing it to bend
• Splint is required in extension for 6-8 weeks
• Usually affects thumb, ring finger or little finger
Trigger finger
• Flexion is normal but beyond a certain range of motion, the patient would have
(stenosing
difficulty extending the flexed finger
tenosynovitis)
• Snap is frequently felt as the finger straightens out
• Avulsion of ulnar collateral ligament from the 1st metacarpal joint on the medial side
Gamekeeper/skier’s of the thumb due to forced abduction of the MCP
thumb • Thumb is lax, hyperextended and laterally deviated with weak pincer grip
• Incomplete injury → Thumb spica splint (4-6w), complete → Surgery then POP
• A condition where one or more fingers become permanently bent in a flexed position
Dupuytren’s
• Caused by alcoholic liver disease (cirrhosis), DM, thyroid problems and epilepsy
contracture
• Could be a family history
• Pain during thumb motion, swelling and pain at the base of thumb
• Due to entrapment tendinitis of the tendons contained within the dorsal compartment
at the wrist as a result of overusing of the wrist
• Also called “Washerwoman sprain”, “Mummy thumb” or “Gamer’s Thumb”
De Quervain’s
• Caused by inflammation of the extensor pollicis previs and the abductor pollicis
tenosynovitis
longus due to repetitive stress injury
• Commonly occurs in women following pregnancy due to the way in which the baby is
lifted and held
• Difficulty grasping or pinching
Gunstock deformity • Happens after supracondylar fracture of humerus malunites
• Leg appears shortened and extremely rotated laterally
Fracture neck femur • Typically, they would be unable to weight bear
(proximal) • Usually seen in an old patient secondary to osteoporosis
• There might be a history of fall or patient is having dementia and can’t remember
• Fall on an outstretched hand with forced dorsiflexion
• X-ray are usually negative but if repeated in 2 weeks become positive
• High rate of non-union
• Tender in anatomical snuff box and over scaphoid tubercle, pain on axial compression
Scaphoid fracture
of the thumb and on ulnar deviation of the pronated wrist or supination against
resistance (pain when holding the baby)
• If initial X-rays are negative → Cast and repeat X-ray in 2 weeks
• If fracture is seen after 2 weeks → Cast for another 4 weeks
• Most common fracture of childhood
• Peak incidence: 5-7 years
Supracondylar
• Mechanism: Hyperextension of the elbow in a child who falls on the hand with the
fracture of the
arm extended
humerus (most
• Posterior or posterolateral displacement of the distal part → Brachial artery
common humerus
compromised → absent radial pulse
fracture)
• Posteromedial displacement of the distal part → Radial n.
• Ant. Interosseous, median, radial or ulnar nerves injuries might occur
Orthopedics
• Axillary nerve, post circumflex artery injury
Humerus neck
• Deltoid affected → reduced abduction, numbness of upper arm below shoulder joint
fracture (proximal)
• Axillary artery injury is rare but possible → Low BP
Humerus shaft • Radial nerve, profunda brachii artery
fracture • Wrist drop, sensory loss of dorsum of the hand
• Fall on an outstretched hand, often in old osteoporotic women
• “Dinner fork” lesion, dorsal displacement of distal radius
• Compression of Median n. → numbness of the hand
• Analgesia, reduction, immobilization in a backslab POP and elevate with a sling
Colle’s fracture • Hematoma block using Lidocaine is usually performed for painless manipulation
[Colle with a fork] • Treatment
- Non-displaced → wrist slap
- Displaced → young (closed reduction and backslap), old (closed reduction & POP
below elbow)
- Intra-articular → open reduction and internal fixation
• Known as “reverse Colle’s fracture”
Smith’s fracture
• Fracture of distal radius + anterior displacement of the distal fragments
(inward)
• “garden spade deformity”
• When a child attains a fracture, it’s most always a greenstick injury
• Incomplete fracture of the long bones at the convex surface
Greenstick fracture
• Concave surface of the bone remains intact
• Usually occurs to a child who falls on an outstretched arm
Perthes disease
(Perthes-Calve- • Avascular necrosis of the femoral head, usually seen in children
Legg)
• LaTeral epicondylitis → wrist exTensors
• Caused by overuse and partial tear of the extensor digitorum
Tennis elbow • Activities involve repeated twisting of wrist (painting, shearing, racquet sports)
• Tenderness over the lateral epicondyle on forced dorsiflexion (extension) of the wrist
• Treated with painkillers, rest and cold compresses
GolFer’s elbow • Medial epicondylitis → wrist Flexors
Orthopedics
Atlas
Trigger finger
Orthopedics
Osteoporosis, Paget’s disease and Osteomalacia
Alkaline ph. is raised in Paget’s and MM

If associated with fractures → Alkaline ph. raised in MM only
Paget’s disease (Osteitis deformans)

➢ Increased bone turnover out of control
➢ Increased bone resorption and abnormal osteoclast activity → rapid increase in bone formation by
osteoblast
➢ The new bone structure is weaker, bulkier, less compact, more vascular → liable to pathological fracture
and deformity
➢ Paget's disease can affect any bone but is most common in the axial skeleton, long bones, and the skull. The
usual sites are the pelvis, lumbar spine, femur and tibia
Presentation
• Commonly asymptomatic and is discovered by the incidental finding of an elevated serum alkaline
phosphatase or characteristic abnormality on X-ray
• When symptoms occur, the most common complaints are bone pain and/or deformity
- Bone pain may be present anytime (at rest and on movement)
- Bone deformity includes sabre tibia (bowing of the tibia), kyphosis, and frontal bossing of the skull
• Other presentations include pathological fractures
• Deafness and tinnitus may be due to compression of CN8 (vestibulocochlear)
• High-output cardiac failure (due to increased blood flow through affected bone)
Investigations
• X-ray features of Paget's disease that include:
- A classical V-shaped pattern between healthy and diseased long bones known as 'the blade of grass'
lesion
- The 'cotton wool' pattern in the skull that is also characteristic (multifocal sclerotic patches)
• Serum calcium and parathyroid hormone levels are usually normal but immobilization may lead to
Hypercalcaemia
• Alkaline phosphatase is markedly raised
Note: Osteosarcoma is one of the complications thus Paget's needs to be monitored closely
Management
• Bisphosphonates (Alendronate)
- Multifocal sclerotic lesions → Paget’s

- Lytic lesions → Multiple myeloma, skeletal survey → “Punched out” lesions
- Serum paraprotein electrophoresis can be performed to diagnose MM
- A patient with Paget’s may notice his hat is getting smaller due to the sclerotic lesions
Orthopedics
Osteosarcoma
• Arises most often at the end of the bones where growth occurs (metaphysis)
• Most common 1ry bone cancer, affects half of children bone tumors (10-14 years)
• Males are commonly affected
• Most affected sites → Lower femur or upper tibia (60%), upper humerus (10%) and pelvis (10%)
• Intermittent, unilateral bone pain that’s worse at night
• X-ray → Sunburst lytic bone lesions
• Lab → raised Alkaline ph.
• May experience a sudden, unexplained fracture → due to sutural weakness of the affected bone
• Treatment → local excision, chemo
Ewing’s sarcoma
• Usually presents with systemic symptoms such as fever, weight loss and malaise
• Adolescents (5-15 years) are commonly affected
• Affects diaphysis (shaft)
• X-ray → lytic bone lesions + Onion skinning type pattern (due to bone destruction with overlying layers of
new bone)
Giant sell tumors / Osteoclastoma → epiphysis
Osteoid osteoma
• Benign bone tumor that develops in the long bones of the body such as the femur and tibia
• Pain is unrelated to activity and is relieved quickly by NSAIDS → characteristic for osteoid osteoma
• Pain usually worse at night
• Frequently affects children and young adults
• Usually < 1cm in diameter
Chondrosarcoma → pain, lump, popcorn calcification in middle-aged people
Orthopedics
Developmental dysplasia of the hip (DDH)
➢ Formerly referred to as congenital dislocation of the hip (CDH). DDH is now the preferred term to reflect that
DDH is an ongoing developmental process
➢ Defined simply as abnormal growth of the hip
➢ More common in the left hip
Risk factors
• Vaginal delivery of babies with breech presentation
• 80% of cases occur in girls
• [First, Fatty, Female, Family history, Foot deformity, Breech, Oligo]
Barlow test → attempts to dislocate an articulated femoral head [Barlow – Bad]
Ortolani test → attempts to relocate a dislocated femoral head
Investigation
• Ultrasound → confirmatory
Management
• <4-6 months → Pavlik harness
• Older children → Surgery
Slipped upper femoral epiphysis (SUFE)

- Limping. Obese, 13-year-old boy with knee pain
- Pain can be poorly localized, so it may be seen as hip, groin,
thigh or knee pain
- May present acutely od with a history of days or weeks
- Left side is more commonly affected
S – Shortness of limb
U – Unable to abduct
F – Flexed hip will rotate externally
E – External rotation of the hip
Osgood-Schlatter disease
- Inflammation (painful bump) of the patellar ligament at the tibial tuberosity, common in adolescent
Orthopedics
Comparing limps in children
<4.5 months → US
>4.5 months → X-ray
Acute hip pain + fever → Septic arthritis OR Transient synovitis

Kocher criteria for septic arthritis:
- Non-weight-bearing
• The higher the score the likelihood of septic arthritis
- Temp >38.5oC
- ESR >40mm/h
- WBCs >12.000 cells/mm3
Orthopedics
Knee injuries
Medial collateral ligament (MCL)

• Direct blow to the lateral side OR a twisting injury (outward)
• Often occurs along with meniscal tears
Lateral collateral ligament (LCL)

• Direct blow to the medial side of the knee OR a runner twisting
to the direction of the planted foot (twisting inwards)
Orthopedics
Anterior cruciate ligament
• Deceleration injury or when the athlete lands on the leg and quickly to the opposite direction
• ACL tears usually have a stem where the foot is fixed on the ground when a rotational force is applied which
is followed by a “pop” sound. They would complain that the knee “gives way”
• Followed by immediate swelling
Posterior cruciate ligament

• Hyperflexion injury or a fall onto a flexed knee or of the knee hits the dashboard of a car during a RTA
• Look for history of direct impact on the shin (especially the proximal tibia) when the knee is bent
Meniscal tears
• Twisting or pivoting, a popping sensation heard at time of injury
• Often associated with ACL injury, difference is swelling is delayed in meniscal tears
• Presents with a locked knee
Orthopedics
Sciatica
Positive femoral stretch test

- Positive if the patient experiences anterior thigh pain when prone with hip extension with maximal knee
flexion
- Indicates L2, L3, or L4 root pathology
Positive straight leg test

- Sciatic pain when the straight leg is at an angle of between 30 and 70 degrees
- Indicates herniated disc as a cause of pain
Orthopedics
Sling types
Broad arm sling (Used for 3-10 days)
• Should always be higher than the level of the elbow
• Applied in
- Injuries to the fingers, hand, wrist or distal forearm
- Support required above elbow POP splints/casts
High arm sling (used for 3-10 days)
• Same
Collar and cuff sling
• Applied in
- Fracture of clavicle or humerus
- Supracondylar fracture
- Radial head or neck fractures
Sprain injury
• Overstretch of the ligament
• Swelling, pain, limited range of movement after trauma
• High arm sling is used for 3 days
Management
- P: Protect
- R: Rest
- I: Ice
- C: Compression
- E: Elevation
Achilles tendon rupture

• History of a repetitive jumping motion or a burst of sudden activity
• A snap is heard (as if someone kicked his heal)
• Difficulty walking on tiptoes or plantar flexing against resistance
• Simmonds’s triad
- Affected leg rests in a more dorsiflexed position
- Palpable gap at the heel
- No plantar flexion on calf squeeze test
• Should be referred at the same day
• X-ray → to exclude calcaneal avulsion
• Prophylaxis of DVT may be offered
• Usually managed by casting and physiotherapy without surgical intervention
Orthopedics
Notes
• Causes of sciatica → Disc prolapse, Spondylarthritis, Spinal injury, Metastatic spinal cord compression or
cancer
• Management of neuropathic pain in disc prolapse → Amitriptyline (1st), gabapentin, pregabalin & duloxetine
• Safe painkiller in pregnancy → Paracetamol
• Compromise of Femoral artery → Hypotensive, absence of proximal and distal pulses
• Saphenous vein → there should be open wound
• Posterior tibial artery → Posterior compartment of leg and plantar of foot
• Dorsalis pedis → artery of foot
• Varum → A bottle of rum in between
• Valgum → Knees stick together like a gum
• Medial collateral ligament → Valgus stress test
• Lateral collateral ligament → Varus stress test
• Anterior cruciate ligament → Anterior drawer test, Lachman test
• Posterior cruciate ligament → Posterior drawer test
• Chondrosarcoma → pain, lump, popcorn calcification in middle-aged people
• Radial head = Big → Adult
• Radial neck = small → child
• Radial head/neck injury
- Swelling over lateral elbow
- Limited range of motion of elbow
- Pain is greatly increased with passive rotation of the elbow
- Tenderness at the radial tunnel
- Pain when fingers are extended against resistance
• Elbow fractures
- Radial neck, radial head, distal humerus fractures → fall onto an outstretched hand
- Intercondylar fracture → Direct blow to the elbow
- Condylar fracture → Direct blow to a flexed elbow
- Olecranon fractures → Pulling of triceps/brachioradialis (elderly), Direct blow to elbow (children)
• Fat embolism
- History of long bones (especially femur) or pelvic fracture
- Typically occurs between 24-72h
- Triad of: Hypoxemia, Neurological impairment and petechial rash (especially in axilla)
- Treatment is supportive as it resolves spontaneously
• Used in Osteoporosis to prevent osteoporotic fractures → Bisphosphonates (Alendronate)
• Common osteoporotic fractures are seen in hips, wrist (Colle’s) and compression fractures of vertebral
bodies
• Carpal tunnel $ [ID CRAMPS]
- I – Idiopathic
- D – DM
- C – Cushing’s $
- R – RA
- A – Amyloidosis and Acromegaly
- M – Menopause
- P – Pregnancy and Pill
- S – Sarcoidosis
Orthopedics
• Supraspinatus tendinitis
- Associated with shoulder impingement $
- History of repetitive overhead activities (sports like swimming, volleyball, tennis or badminton) or
carrying heavy objects
- Pain with overhead motion, often worse at night and can disturb sleep (particularly when lying on the
affected shoulder)
• Humerus injuries → [ARM]
- Proximal humerus → Axillary n.
- Shaft fracture → Radial n. → unable to dorsiflex (wrist drop)
- Distal humerus → Median n.
• Initial investigation for bone metastasis → Serum Ca
• Gold standard for bone metastasis → MRI (within 7 days if pain alone, if pain & neurological signs → 24h)
• If multiple bones are involved (e.g. spine and shoulder) → Bone scintigraphy (Radionuclide bone scan)
• Investigation to measure bone density in Osteoporosis to predict further fractures → DEXA scan
• Most common cause of bone metastasis in females → Breast cancer, then Lung cancer
• Most common cause of bone metastasis in males → Prostate cancer, then Lung cancer
• Most common sites for bone metastasis → Spine, then pelvis, ribs, skull and long bones
• Most commonly fractured bone in a vertiCAL fall → CALcaneus
• Calcaneus fracture is usually associated with spinal fractures and Foot X-ray is usually performed
• Stress fracture → Fatigue-induced fracture due to repetitive stress over time
• Bursitis → Tenderness and swelling localized to small area with pain on passive movement only felt in
certain direction
• Coxa vara → Deformity of the hip whereby the angle between the head and the shaft of the femur is
reduced to less than 120o (normally the angle = 130 o)
• Gold standard investigation for herniated disc → MRI
• Long-term steroid use + teeth loss → Osteoporosis
• Osteoporosis is usually clinically silent (doesn’t cause generalized skeletal pain) until a fracture occur
• Side effects of steroids
- Osteoporosis
- Hyperglycemia
- Peptic ulcer disease
- Cataract
• If there’s deformity after a fracture OR a neurovascular compromise, after ABCD, appropriate action would
be → Reduction with a sedative (IV midazolam)
• If the blood flow doesn’t return → Referral to vascular and orthopedic surgeons
• Treatment for Osteoporosis → Alendronate or risedronate
• Calcium supplements are only considered when calcium intake is inadequate (<700mg per day)
• Dupuytren’s contracture is due to formation of thickened fibrous tissue within the palmar fascia
Pediatrics
Obstructive sleep apnea syndrome in children
➢ It’s mainly due to enlarged tonsils and adenoids
Presentation
• Snoring - usually parents seek attention; many will just get better as they grow older
• Mouth breathing
• Witnessed apneic episodes → episodes of cessation of breathing
• Daytime sleepiness and somnolence are less important in children
• Sleep-deprived children tend to become hyperactive, with reduced attention and be labelled as difficult or
disruptive, or even ADHD. They may not be doing well at school due to poor concentration
• In adults → increased daytime somnolence + DM and HTN
Investigations
• Simple studies: pulse oximetry and overnight study of breathing patterns → initial investigation
• Overnight in-laboratory polysomnography (PSG) → the gold standard
Epworth sleepiness scale → a questionnaire to predict the likelihood the patient will fall asleep in certain conditions
Treatment
• Conservative → weight loss and reducing alcohol consumption
• Continuous positive airway pressure (CPAP)
• Rare cases require surgery to relieve pharyngeal obstruction (e.g. tonsillectomy, adenoidectomy or
tracheostomy)
Acute epiglottitis
• Caused by Hemophilus influenza type B
Features
Croup
• Rapid onset
• Barking cough, stridor, HOV and fever
• Fever • Cause by Para-influenza virus
• Stridor • X-ray → steeple sign
• Managed by oral dexamethasone
• Drooling of saliva • Emergency TTT → high flow O2 + nebulized adrenaline
• Difficulty speaking
• Muffling or changes in the voice
• X-ray → thumb sign “indicating an edematous and enlarged epiglottis and it suggests acute infectious
epiglottitis”
Management
- In acute attack → summon an anesthetist → intubation is required to avoid obstruction
Pediatrics
Childhood viral rashes
➢ Most children rashes present with similar flu-like symptoms such as a runny nose, cough, a high temperature
(38℃ or above), a sore throat, loss pf appetite and swollen neck glands
Roseola
• Sudden high temperature followed by non-itchy pink/red spots or patches after resolution of fever by 12-
24h on chest or legs and spreads to the rest of the body + Nagayama soft palate spots
• The most common rash of its kind under 2 years old
Parvovirus B19
• Bright red rash on both cheeks (slapped cheek syndrome) which may spread to the rest of the body
• Also called → Erythema infectiosum
• The rash can be itchy, especially on the soles of the feet
Measles
• Red-brown blotchy maculopapular rash on the head or neck (starts
behind the ear) and spreads to the rest of the body
• Tiny grey-white spots in the mouth (Koplik spots – not always but
diagnostic sign if occurs)
• Unwell child, usually fever >40℃
Hard K sound
- Koplik spots (before rash), white spot “grain of salts” on buccal mucosa
- Cough
- Conjunctivitis
- Coryza, inflammation of URT
Rubella
• Red/pink spotty rash which starts behind the ears and spreads to
the rest of the body
• Swollen LN
• Spots on the soft palate (Forchheimer spots)
• Very unlikely if had both doses of MMR vaccine
Hand, foot and mouth disease (HFMD)

• Commonly caused by Coxsackievirus A16 (CA16) and enterovirus 71 (EV71), very contagious among children
• Painful ulcers on the tongue or buccal mucosa and grey blisters in hands and feet
Management for all

- Paracetamol or ibuprofen
- Ensure adequate dehydration
- Fever and rashes will usually subside within a week
When to worry → Meningitis

• Non-blanching red pinpricks rashes which quickly spread turning into red or purple blotches
• Stiff neck, photosensitivity and uncontrollable fever
Pediatrics
Chickenpox
• Caused by VZV
• If the rash appears within a week of delivery or within 2 days after delivery, there’s a risk of neonatal
chickenpox. There’s transplacental transmission of virus but not antibody, as there is no time for IgG to
develop and the baby is at 30% risk of death from severe pneumonia or fulminant hepatitis → managed by
VZIG and Acyclovir
• If the mother’s onset of rash is >7 days before delivery or >7 days post-delivery → varicella zoster
immunoglobulin (VZIG) and isolation is not necessary for the neonate; just observation
Scarlet fever
Key points
• Commonest age → 2-8 years
• Caused by → group A streptococcus pyogenes
• Diagnosis is clinical
• Presents with sore throat, fever (usually >38.3℃) and a rash
• Rash → starts at torso 12-48h after fever and spreads to extremities, has a coarse texture like sandpaper
• Other features
- Strawberry tongue
- Cervical lymphadenopathy
- Tonsils covered with pal exudates with red macules on palate (Forchheimer spots)
• Treatment is with penicillin V for 10 days
Scarlet fever is the game os “S”
- Strept pyogenes
- Sore throat
- Strawberry tongue, tonsils could be coated with white exudates
- Sandpaper rash
- Spot le Forchheimer
- Servical lymphadenopathy
Kawasaki disease [RED + adenopathy]

➢ A febrile systemic vasculitis primarily affects children <5 years
➢ Coronary aneurysm is a potentially devastating complication
➢ Often misdiagnosed as a viral rash (exanthem) and sent home
Diagnosis [CRASH BURN]
• Fever >39℃ for more than 5 days + at least 4 of the following:
- Conjunctivitis
- Polymorphous rash
- Extremity changes: Erythema of palms and soles that later leads to desquamation
- Mucous membrane changes: Red, fissured lips, strawberry tongue
- Cervical lymphadenopathy
Management
• High dose aspirin → reduces risk of thrombosis
- Once fever subsides and inflammatory markers fall, low dose aspirin is given until ECHO is performed at
6 weeks to exclude aneurysm
• IVIG → if given within first 10 days, reduces the risk of coronary artery aneurysm
Pediatrics
Pyloric stenosis
Presentation Vomiting
• Pyloric stenosis → non-bilious, weeks after birth
• Age: 3-8 weeks • Duodenal atresia → bilious, hours after birth
• Projectile non-bilious vomiting
• Constipation is common due to reduced fluid intake
• Late signs: dehydration, malnutrition and jaundice
• Olive-sized abdominal mass (epigastric mass), may present at the right
side
• Visible peristalsis in the upper abdomen from left to right
• The child will feel hungry despite constant vomiting
Diagnosis
• Initial step/urgent investigation → serum K+, hypokalemia due to vomiting,
needs to be corrected immediately
• To diagnose → Abdominal US → hypertrophic pyloric muscle + target sign
Treatment
• Initially, correct dehydration and electrolyte imbalance (metabolic alkalosis) → IV fluid
• Then refer to a pediatric surgeon → Pyloromyotomy + NG tube
Gastro-esophageal reflux disease (GERD)

Presentation
• Age group: < 1 year, if it persists after 1 year old → hiatus hernia is possible
• Excessive and frequent episodes of regurgitation/vomiting after feeds
• Difficult to feed
• Failure to thrive
• Irritable and crying
Diagnosis
Investigations are not usually necessary unless severe. If warranted, they include
• Upper GI study with contrast – 1st line
• Upper GI endoscopy with biopsy
Treatment
• If breast-feeding → Breastfeeding assessment
• If formula-fed → take feeding history → increase feeding frequency and reduce amount per feed → use
thickened formula
• If no improvement → offer proton pump inhibitors (PPIs) or H2 receptor antagonists (H2RAs) and consider
enteral feeding
Duodenal atresia
- Presents at the 1st day of life
- Bilious vomiting WITHOUT abdominal distension
- Associated with Down’s $ and polyhydramnios
- X-ray and US → double bubble sign
Jejunal and ileal atresia
- Presents at the 1st day of life
- Bilious vomiting WITH abdominal distension
- X-ray → triple bubble appearance
Pediatrics
Malrotation and volvulus
Presentation
• Green, bilious vomiting
• Blood per rectum (painful)
• Sudden onset
• Age: neonates
Diagnosis
• Abdominal x-ray
- Coffee bean shape (Omega sign)
• Barium enema
Treatment
• ABCDE protocol
• Decompression with nasogastric tube
• Referral to pediatric surgery for laparotomy and
resection
Coffee bean shape → Malrotation and Volvulus

Double bubble sign → Duodenal atresia and midgut volvulus
Currant jelly stool + >6 months old → Intussusception
Meconium ileus → Cystic fibrosis
Meckel’s diverticulum
Presentation
• Mostly asymptomatic
• Age group: 2-3 years old; mostly male
• Painless rectal bleeding
• If obstruction → vomiting, abdominal pain
Diagnosis
• Radioisotope scan → initial
• Laparotomy
Treatment
➢ Surgical resection
Intussusception
Presentation
• TRIAD of: Abdominal pain, Currant jelly blood in stool, Sausage-shaped mass on palpation (often in RUQ)
• Child is crying persistently
• Drawing up of legs
[Jelly, Sausage, Doughnut]
• May be vomiting if severe
Diagnosis
• Abdominal US → may show doughnut or target sign
• Bowel enema → claw sign
Treatment
➢ Air enema reduction or laparotomy
Pediatrics
Necrotizing enterocolitis (NEC)
➢ Necrosis of intestinal mucosa (primarily colon) with possible perforation which can lead to pneumatosis
intestinalis, free air in the abdomen and portal venous gas
Presentation
• Premature > term infant
• Vomiting (feeding intolerance), decreased activity, varying temperature
• Abdominal distension, bloody stools
• Abdominal plain film → Air in the bowel wall
Diagnosis
• Bell’s criteria/staging system
• Abdominal x-ray (supine antero-posterior; lateral decubitus) → initial
• Blood work - include blood film, culture, coagulation, blood gas
Treatment
• Initial → stop feeds → NG tube free drainage with aspiration → antibiotics → fluids and electrolyte balance
• Antibiotics → penicillin + gentamicin + metronidazole
• If pneumoperitoneum (abnormal presence of air in the abdominal cavity)→ surgery
Biliary atresia
➢ It’s extremely important to diagnose it early as without intervention, chronic liver failure will develop which
usually leads to death before age 2 years
Presentation
• Jaundice + pale stools + dark urine
• Hepatomegaly → becomes palpable at 3-4 weeks after
biliary atresia
• Splenomegaly is not usually a feature unless presentation
is late
• Failure to thrive as a result of poor absorption
Diagnosis
• ↑ Conjugated bilirubin and abnormal liver function test
- CB >50% of total bilirubin
- GGT is usually high
• Abdominal US
• Cholangiogram
• Liver histology (obtained by percutaneous biopsy) → definitive diagnosis
Treatment
• Kasai procedure = Hepatopotoenterostomy
- High successful rate if presented early (<100 days)
- Small intestine is connected to the liver to drain the bile
• Liver transplant in late cases
Conjugated bilirubin
- Water soluble → passes in urine → Dark urine (in obstructive jaundice)
Unconjugated bilirubin
- Does NOT pass in urine → Pale urine
- Pass in stool → Yellow stool
Pediatrics
Lymphangioma
• Uncommon, hamartomatous, congenital malformations of the lymphatic system that involve the skin and
subcutaneous tissues
• It occurs as a result of sequestration or obstruction of developing lymph vessels in approximately 1 in 12,000
births
• Lymphangiomas can occur anywhere in the skin and the mucous membranes
• The most common sites → head and neck especially the posterior triangle of the neck
• The cysts are lined by endothelium and filled with lymph
• Occasionally unilocular cysts occur, but more often there are multiple cysts infiltrating the surrounding
structures and distorting the local anatomy
• The mass may be apparent at birth or may appear and enlarge rapidly in the early weeks or months of life as
lymph accumulates; most present by age 2 years. (90% of lymphangioma occur in children less than 2 years)
• Lymphangiomas are soft and nontender and when subjected to light test was brilliantly translucent
• They’re often partially compressible, a feature of lymphatic swellings
Brachial cyst
- Lateral neck mass that are NOT compressible, NOT/MAYBE translucent under light test and LESS common
Pediatrics
Neonatal jaundice
➢ <24h → pathological
- Neonatal jaundice within the first 24h of life should be taken seriously, it would require urgent
assessment within 2h according to NICE
- Investigations: bilirubin level, LFTs, FBC, blood film, blood group, Coomb’s test, G6PD levels and review
for sepsis
➢ >24h → physiological
➢ >2 weeks → pathological
Physiological jaundice
• Results from increased erythrocyte breakdown and immature liver function
• Presents at 2-3 days old, begin to disappear towards the end of the first week
• Bilirubin level doesn’t usually rise above 200 μmol/L and baby remains well
Early neonatal jaundice (onset <24h)

The most common pathological causes
• Hemolytic disease (e.g. RH incompatibility, ABO incompatibility, G6PD
of neonatal jaundice within 24h are:
deficiency and spherocytosis) • RH incompatibility
• Congenital infections such as toxoplasmosis, rubella, CMV, herpes • ABO incompatibility
simplex, syphilis or postnatal infections that develop into sepsis • G6PD deficiency
• Sepsis
• Crigler-Najjar $ or Dubin-Johnson $
• Gilbert’s $
Prolonged jaundice (lasting >14 days in term infants, >21 days in preterm)
• Congenital hypothyroidism → usually defined on routine neonatal biochemical screening (Guthrie test)
- Hypothyroidism impairs bilirubin conjugation, slows gut motility and impairs feeding leading to
hyperbilirubinemia
• Hypopitruitism
• Glactosemia
- Jaundice + vomiting + diarrhea + FTT + hepatomegaly + neurological symptoms
- No signs of obstructive jaundice
- ↑ unconjugated bilirubin (doesn’t pass in urine) → pale urine + yellow stool
• Breast milk jaundice
• Breastfeeding jaundice: resulted from insufficient milk intake
- Usually the baby is well
- Most common cause of prolonged unconjugated hyperbilirubinemia
- Jaundice resolves by six weeks, can continue for up to 4 months → Breastfeeding continues
• Gastrointistinal
- Biliary atresia → the most important diagnosis not to miss
- Neonatal hepatitis
Split bilirubin blood test

• ↑ Conjugated bilirubin → obstructive jaundice (biliary atresia)
• ↑ Unconjugated bilirubin → galactosemia, breast milk jaundice, congenital hypothyroidism, hemolysis
• Raised both → hepatitis
Pediatrics
Vesicoureteral reflux (VUR)
➢ Condition where urine flows retrograde from bladder into ureters/kidneys
Presentation
• Most children are asymptomatic
• Increases risk of urinary tract infection → Thus, symptoms of a UTI: Fever, Dysuria, Frequent urination, Lower
abdominal pain
Diagnosis
• Urinalysis, urine culture and sensitivity → initial investigation
• Renal ultrasound → initial investigation → might suggest the presence of VUR if ureteral dilatation is present
• Micturating cystourethrogram (MCUG)→ gold standard
• Technetium scan (DMSA) → for parenchymal damage (seen as cortical scars)
Treatment
• VUR grade I-IV → start with low dose antibiotics prophylaxis daily (i.e. trimethoprim or nitrofurantoin),
should be given prior to considering surgery
• Consider surgical reimplantation of the ureters
- Failed medical treatment
- Parenchymal damage
- Persistent renal reflux (grade IV/V)
- Breakthrough infection
- The International Reflux Study has found that children can be managed non-surgically with little risk of new or
increased renal scarring, provided they are maintained infection free
- Remember, the goal of treatment is to minimize infections, as it is infections that cause renal scarring and not the
vesicoureteral reflux. Thus, the importance of continuous antibiotic prophylaxis outweighs surgery in most cases
- Note that during early childhood, the kidneys are at higher risk of developing new scars. So, it is particularly
important to start parenteral antibiotic treatment for patients with vesicoureteral reflux before febrile
breakthrough infections
- For patients with frequent breakthrough infections, definitive surgical or endoscopic correction is preferred
- Surgical correction should also be considered in patients with persistent high-grade reflux (grades IV/V) or
abnormal renal parenchyma
Pediatrics
Pediatric urology scans [remember number 6]
If younger than 6 months:
• US during acute infection → if does NOT respond well to antibiotics within 48h
• US within 6 weeks → if responds well to antibiotics
• MCUG → if did NOT respond well to antibiotics during acute infection
• DMSA scan 4-6 months → if did NOT respond well to antibiotics during acute infection
US → good at determining anatomy, renal size, presence of most congenital anomalies

MCUG
- Gold standard for detecting vesicoureteral reflux
- Requires catheterization
- Radiation exposure
DMSA
- Gold standard for detecting renal scarring or damage to renal parenchyma
- Intravenous radioactive isotope is used
- Shouldn’t be done at time of infection as may get false results → 4-6 moths after infection
Types of UTIs
Straightforward UTI
• Responds well to treatment within
48h
Atypical UTI (any of the following)
• Failure to respond to treatment
within 48h
• Septicemia
• Raised creatinine
• Infection with non-E. coli species
Recurrent UTI (any of the following)
• ≥2 episodes + acute pyelonephritis
• ≥3 episodes + cystitis/lower UTI
Golden rules
- Below 6 months → US within 6 weeks if straightforward UTI → MCUG if US is abnormal
- Above 6 months → do NOT use US if straightforward UTI
- If atypical, ALWAYS use US during acute infection no matter the age
- Always perform DMSA after 4-6 months of any atypical or recurrent infection
- DMSA during an acute infection is always the wrong answer
- MCUG after 3 years old is always the wrong answer
Pediatrics
Febrile seizures
➢ Epileptic seizures + fever in the absence of an intracranial infection
Key points
• Usually between 6 months – 6 years with peak at 14-18 months
• Usually with a positive family history, 10% risk of developing febrile seizures if there a first degree relative
who has suffered from it
• Fever >39℃
• Typical generalized tonic-clonic seizure is seen
• Must determine the cause of fever and rule out meningitis → Blood and urine test → initial investigation
• Consider lumbar puncture only if meningitis is highly suspicious
Types
• Simple febrile seizures
- The most common type
- Characterized by a single generalized seizure lasting <15 minutes
• Complex febrile seizures
- Focal, prolonged or recurrent
Treatment
• Antipyretics (e.g. Paracetamol)
• Seizures lasting >5 minutes or frequent → managed with benzodiazepines (buccal midazolam)
- About 1 in 3 would have further episodes of febrile seizures (30-40% chance) before the age of 6
- About 1 in 3 who have further episodes would develop epilepsy (this means roughly about 10% of complex febrile
seizures would develop epilepsy)
Breath-holding spells (blue spells)

• Occur in young children due to stress
• They stop breathing for some time, may turn blue or have little jerks of the limbs
• After a period of time, they spontaneously start breathing, they become completely fine after an hour
• Management → Reassurance, put the child in a recovery position and check ferritin and treat iron deficiency
When a toddler cries after a minor injury, stops breathing and loses consciousness for a few seconds followed by
rapid recovery, you should be thinking of two conditions:
1. Blue breath holding spells
2. Reflex anoxic seizures also known as reflex asystolic syncope or white breath holding attacks
Reflex anoxic seizures don’t cause tongue biting
Pediatrics
Cystic fibrosis
➢ Autosomal recessive disorder which induces salt and chloride excretion into airways leading to increased
viscosity of secretions
Causative organisms
• In childhood and early teenage years
- Staph aureus → most common
- Hemophilus influenza
• In teens and adults
- Pseudomonas aeruginosa → most common
Clinical presentation
• Recurrent chest infections (Cough and chronic sputum production)
• Malabsorption, Leading to:
- Frequent, bulky, greasy stools (Steatorrhea)
- Failure to thrive
• Pancreas → increased incidence of DM
• Sweat test is 98% sensitive
• Delayed sexual development • Diagnosis of CF:
• Male infertility, female subfertility - Cl concentration >60 mmol/L
- Na concentration <Cl in 2 separate occasions
• Salty taste of skin • Prenatal US → echogenic bowel
• Short stature
• Meconium ileus (in neonatal period)
Diagnosis
• Primarily made during newborn screening (Guthrie test)
- All newborn infants in the UK are screened for cystic fibrosis using the heel-prick tests
- If positive → molecular genetic testing for CFTR gene and sweat test would follow
• If not picked up by the newborn screening and later on develops clinical manifestations of cystic fibrosis →
perform sweat test or genetic testing for CFTR gene
Management
• Often require an MDT approach
• Chest physiotherapy
- Techniques such as postural drainage is used to aid drainage
- Other techniques include chest percussion and positive expiratory-pressure device to aid dislodgement
and expectoration of the sputum
• Antibiotics → only in an acute exacerbation of the disease or as prophylaxis in childhood
- In children with cystic fibrosis, Prophylactic Floxacillin is prescribed up to 3-6 years of age
- If a mild exacerbation is present, antibiotics can be prescribed for 2 weeks
• Bronchodilators (beta-2 agonists)
• Diet
- High calorie
- High fat
- Pancreatic enzyme supplements
- Vitamins
Chest + GIT → Cystic fibrosis
Chest + Liver → Alpha-1 antitrypsin deficiency
Chest + Kidney → Goodpasture $
Kidney + Brain → Polycystic kidney
Liver + Brain → Wilson’s
Pediatrics
Wilson’s disease
➢ A genetic disorder characterized by excess copper storage in tissue
Presentation
• Kayser-Fleischer rings
• Liver dysfunction → deranged liver function tests, cirrhosis
• Neurological → ataxia, dysarthria, dystonia
• Behavioral → personality changes, decreased school performance
Investigation
• Serum ceruloplasmin is low (less than 0.1g/L) → initial test
• Deranged LFTs
• Measurement of hepatic parenchymal copper concentration
Treatment
• Lifelong penicillamine
• In acute liver failure or cirrhosis → liver transplant
Wolff-Parkinson-White syndrome (WPW)

➢ An extra electrical pathway between your atria and ventricles causes a rapid heartbeat
Presentation
• Child may be exercising with sudden onset of pallor, difficulty breathing and palpitation followed by
spontaneous recovery
• Otherwise asymptomatic child
• ECG → Delta waves, pre-excitation pattern, prolonged QRS, shortened PR
• Very dangerous drugs in WPW
- Verapamil (very)
- Digoxin (dangerous)
- Diltiazem (drugs)
Diagnosis
• ECG
• 24h Holter monitor
Treatment
• Catheter ablation → 1st line
• Medications → flecainide and propafenone
Tourette’s syndrome
Presentation
• Young (6-8 years old) mostly male
• Repetitive movements or gestures that are disruptive in the classroom or to people around the child (can be
motor or vocal) → Tics
• Jerks, blinks, sniffs, nods, spitting, stuttering, irrepressible explosive obscene verbal ejaculations, grunts,
and squeaks
Treatment
• Risperidone or haloperidol
• Behavioral therapy - Habit-reversal training
Pediatrics
DiGeorge $
• Deletion of chromosome 22.q11
• It causes absent thymus + fits + small parathyroid (decreased Ca) + anemia + lymphopenia + low level of GH +
low T-cell immunity
• The absent thymus shadow is pathognomonic
• Related to Velocardiofacial $ → characteristic face, multiple
anomalies (e.g. cleft palate, heart defects, cognitive
defects)
• Developmental delay, facial dysmorphism, palatal
dysfunction and feeding difficulties are seen in most infants
with this syndrome
CATCH-22
C → Cardiac abnormalities (interrupted aortic arch, truncus
arteriosus, TOF)
A → Abnormal facies
T → Thymic aplasia
C → Cleft palate
H → Hypocalcemia/Hypoparathyroidism
22 → deletion of chromosome 22.q11
Marfan’s syndrome
Features
• Tall and thin
• Long arms, legs, fingers and toes
• Arachnodactyly (long spidery fingers)
• Flexible joints
• Scoliosis
• Cardiovascular → Aortic dilatation or dissection, aortic regurgitation, mitral
valve prolapse (MVP), mitral regurgitation, abdominal aneurysm
• Lungs → pleural rupture causing spontaneous pneumothorax
• Eyes → lens dislocation, high myopia
Ehlers-Danlos syndrome
• Hyperextensible skin + joint hypermobility + tendency to bleed easily
Pediatrics
Prader Willi syndrome
➢ Chromosomal abnormality in chromosome 15 on the paternal side
Presentation
• Male with blonde hair, blue eyes
• Behavioral problems
• If uncontrolled feeding + obesity, the boy usually <6 years old
• Developmental delay
• As a neonate: hypotonia (floppy), sleepiness
Diagnosis
• Chromosomal analysis: abnormality of paternal chromosome 15
• Mostly clinical diagnosis
Treatment
• Referral to pediatric psychiatry for behavioral problems and developmental delay
Bs -15
Boy
Blue eyes
Behavioral polyphagia
BMI → obese
Tricyclic antidepressants overdose in pediatrics

Presentation
• Child ingesting an unknown bottle of medication
• Lethargy, drowsy
• +/- Coma or seizure
• ECG → widened QRS, peaked T waves (indication of hyperkalemia)
Diagnosis
• U&E
• Toxicology scan • In adults, signs of hypertension turning into
hypotension and ventricular dysrhythmias along
• ECG with signs of hyperkalemia (widened QRS)
• ABG
Treatment
• ABCDE protocol
• If within 1h of ingestion and >4 mg/kg → Activated charcoal
• Sodium bicarbonate
• Correct electrolytes if necessary
Pediatrics
Enuresis
• Enuresis is normal up to the age of 5 years
Primary enuresis
• Child aged 5 years or older who constantly wets the bed at night
• Daytime symptoms → urgency, frequency or daytime wetting
Management
Without daytime symptoms With daytime symptoms

• <5 years → Reassure • Refer all children above 24 months to secondary
• >5 years care on an enuresis clinic
- If bedwetting is infrequent (<2 times a week)
→ reassure Daytime symptoms below 2 years is normal
- If long-term treatment required → enuresis
alarm (1st line) + reward system
- If short-term control required (e.g. sleepovers)
→ Desmopressin
- If treatment has not responded to at least two
complete courses of treatment with either an
alarm or desmopressin → refer to secondary
care
Secondary enuresis
• Child of ANY age who has previously been dry at least 6 months and now wetting the bed consistently at
night
• With/without daytime symptoms
• Most common cause → emotional upset (one of the possible causes of emotional upset could be child
abuse)
• Other causes → UTIs, constipation or polyurea due to DM
• Investigations → blood culture for UTIs, if no treatable UTIs → refer to a pediatrician
Methods to obtain a urine sample

1. Clean catch sample (midstream)
2. Catheter or suprapubic aspiration
Pediatrics
Cow milk allergy
• IgE-mediated reactions → reaction is acute (nausea, vomiting, colicky pain) → a skin prick test or a blood
test for diagnosis
• Non-IgE-mediated reactions → delayed reaction (reflux, loose stools, not gaining weight) → exclude cow
milk from the diet and use a hypoallergenic formula such as extensively hydrolyzed formula and see if
there’s improvement
- Improvement is expected within 2 weeks
- If symptoms persist → swap to amino acid formula
Hypothyroidism in children
Presentation
• Difficulty feeding, little crying
• Not very responsive
• Hypotonia
• Dry mottled cold skin
• Prolonged neonatal jaundice
• On examination → enlarged posterior fontanelles (due to osseous immaturity)
• Other adult features of hypothyroidism
Diagnosis
• Neonatal screening for TSH and T4 serum/plasma → initial
• Radioisotope scan → definitive
• US neck
Treatment
• Levothyroxine oral until 2 years of age, after 2yrs, check TFTs and treat accordingly
Bronchiolitis
➢ An acute infectious disease of the lower respiratory tract that occurs primarily in the very young, most
commonly infants under the age of 2 years
➢ Respiratory syncytial virus (RSV) is the pathogen in 75-80% of cases
Features
• Breathing difficulties
• Cough
• Coryzal symptoms (including mild fever)
• Decreased feeding
• Apneas in the very young
• Wheeze or fine inspiratory crackles on auscultation
• Tachypnea or chest recession
Management
• Largely supportive involving humidified oxygen
• DO NOT use any other drugs
Pediatrics
Non-accidental injury (NAI)
Presentation
• Delayed time to medical presentation
• Usually brought by step-father or boyfriend
• Bruising
- Accidental → foreheads and chins for toddlers, knees and chins for children
- NAI → varying degrees and color variations of bruises or bruising at unusual sites, ankles are the most
common site of NAI in infants
• Fractures (old and new)
- Consider NAI with rib and spinal fractures
- Also fractures in infants that are independently mobile or long bone fractures in children less than 3
years old
Management
1. Admit to ward to manage pain and perform skeletal survey
2. Involve the safeguarding children team, as a junior doctor, you should inform the team first
3. Refer to social services
4. Treat any other underlying medical conditions
Don’t think of NAI but consider the other pathological disease that could result in:
• Bruising
- Henoch-Schoenlein purpura
- Hemophilia
- ITP
- Leukemia
• Fractures
- Osteogenesis imperfecta: would have other features such as blue sclera, dental abnormalities and brittle
bones (the type commonly involved with an explained fracture is type 1 which is autosomal dominant so
look for a family history too)
- Managed by IV bisphosphonates (pamidronate)
[OSTE]
Osteo → Bone fracture, Sclera blue, Teeth imperfections, Ears → hearing troubles
Head injuries
Presentation
• Child playing or in an athletic match
• Head/facial trauma
• Swelling, bruising on the face only
Diagnosis
• Facial X-ray → Initially, if fractures detected → CT head
• CT head → Definitive, if on arrival scan within 1h:
- The child has GCS< 14 or suffering from any neurological deficits
- Fall from height >3m
- Vomiting >3 times following trauma
Treatment
• Observation
• Analgesia for pain
Pediatrics
Sudden infant death syndrome (SIDS)
➢ Sudden death of a child under the age of one year during sleep with no apparent cause
➢ Diagnosed by exclusion of other possible causes
Prevention
• Avoid smoking near infants
• Put them to sleep on their backs (not their front or side)
• Avoid overheating by heavily wrapping infants
• Blankets should not be higher than their shoulders
• Infants should be placed with their feet at the foot of the cot
• Avoid bringing baby into the bed after consuming alcohol or sedatives
• Avoid sleeping with infant on sofa
• Avoid using pillow
• Use sheets and blankets rather than a duvet
Congenital adrenal hyperplasia

• Autosomal recessive disorder
• Comes in three forms: 21-hydroxylase, 11-hydroxylase or 3-beta hydroxysteroid dehydrogenase deficiency
• Female with classic form → ambiguous genitalia
• Males with classic form → hyperpigmentation, penile enlargement, aldosterone deficiency
• Males with salt-losing form: typically present at 7-14 days of life with vomiting, weight loss, lethargy,
dehydration, hyponatremia and hyperkalemia
21-hydroxylase deficiency
- The most common and is characterized by cortisol deficiency (with or without aldosterone deficiency) and
androgen excess
11-beta-hydroxylase deficiency
- The second most common and is characterized by aldosterone deficiency which causes salt-wasting in early
infancy and excess hypertension in childhood and adult life
Infant respiratory distress syndrome (IRDS)

➢ Caused by inadequate production of surfactant in the lungs, usually seen in premature infants
➢ It affects proximately one half of infants born at 28-32 weeks of gestation. rare after 32 weeks
Risk factors
• Premature delivery
• Infants delivered via cesarean section without maternal labour
• Maternal diabetes
Presentation
Respiratory distress very soon after birth:
- Tachypnea
- Expiratory grunting
- Subcostal and intercostal retractions
- Diminished breath sounds
- Cyanosis
- Nasal flaring
Investigation → Chest x-ray → Diffuse ground glass appearance
Pediatrics
Developmental milestones
Pediatrics
This figure is intersected at 4 different levels of the body which represent different time frames
• 3 months → Neck – Holds neck
• 6 moths → Body – Roles both direction
• 9 months → Knees – Crawling
• 12 months → Feet – Walks
For fine motor skills, remember this pattern:

• At 2 years → Draws a line + stacks 4 objects, 4 words
• At 3 years → Draws a circle + 8 objects
• At 4 years → Draws a cross and square + 12 objects
• At 5 years → Draws a triangle
• At 6 years → Draws a diamond
Below are certain negative indicators (things a child cannot do) by a certain age that you should recognize and refer
to a specialist community pediatric assessment:
• Unable to sit unsupported at 12 months
• Unable to walk by 18 months
• No meaningful speech at 18 months (at 15 months onwards, if unable to speak monosyllabic words and
difficulty understanding speech → consider arranging hearing test)
• Unable to formulate 2-3-word sentences by 30 months
• Unable to run by 2.5 years
• No smile at 8 weeks
• No eye contact at 5 months
• Unable to hold objects placed in hand by 5 months
• Unable to reach for objects by 6 months
Pediatrics
Weight for age
• Infants <12 months → Weight (kg) = (age in months + 9) / 2
• Children 1-5 years → Weight (kg) = 2 x (age in years + 5)
• Children 5-14 years → Weight (kg) = 4 x age in years
- Normal birth weight ranges between 2.5-4.5kg

- It’s usual for babies to lose between 5% and 10% of their birth weight a few days after the birth
- Very often mothers receive IV fluid to prevent dehydration, this can contribute to a slightly higher birth weight for
the neonate, fluids are lost over next hours-days which results in reduction of weight
- Following these few days of weight loss, there would be gradual weight gain
- By day 14, most babies would be above their birth weight
Dehydration in children step by step management

1. Estimate dehydration
- Mild → decreased urine output
- 5% dehydration → decreased urine output + dry mucous membranes
- 10% dehydration → decreased urine output + dry mucous membranes + sunken fontanelle
- >10% → decreased urine output + dry mucous membranes + sunken fontanelle + symptoms of shock
2. Calculate the preexisting deficit
- Amount of fluid to give in mL = % dehydration x weight (kg) x 10
3. Give maintenance plus ongoing losses for the first 24h
• 0.9% normal saline + 5% dextrose is usually used
- For the first 10kg → 100 ml/kg
as maintenance in children (excluding neonates)
- For the next 10kg → 50 ml/kg • Initial bolus → 0.9% normal saline
- For any weight after 20kg → 20 ml/kg
Red traffic (high risk) features

• Pale/mottled/ashen/blue skin
• NO response to social cues
• Appears “ill” in a healthcare professional
• Doesn’t wake, or if awaken (roused) → doesn’t stay awake
• Weak/high pitched/continuous cry
• Grunting (not flaring, flaring → yellow traffic-intermediate risk)
• Respiratory rate >60
• Moderate or severe chest indrawing (inward movement of the lower chest)
• Reduced skin turgor
• Prolonged capillary refill time >4 seconds
• Age <3 months + Fever ≥38
• Non-blanching rash
• Bulging fontanelle
• Neck stiffness
• Status epilepticus
• Focal seizure
• Focal neurological signs
Pediatrics
Constitutional delay in growth and puberty
➢ A temporary delay in the skeletal growth and thus height of a child with no physical abnormalities causing
the delay but the growth eventually resumes and the child would reach hist potential growth
➢ There’s usually a family history of similar growth pattern with delayed growth and delayed puberty with
normal height eventually
Investigations
• Determine bone age using X-ray of the left hand and wrist → to measure the gap between bones, as once
the gap between bones fuse there’s no more growth
Management
• Most cases DO NOT require treatment
• If delayed physical development or requested by the patient → a short course of sex steroids for 3-6 months
APGAR score
➢ A scoring system used to evaluate a newborn baby
➢ Done twice at 1 and 5 minutes after birth, maybe repeated at 10 minutes if scores remain low
➢ The 1-minute score determines how well the baby tolerated the birthing process. The 5-minute score tells the
health care provider how well the baby is doing outside the mother's womb
➢ Score 7-10 is normal
APGAR Sign 0 1 2
Appearance Bluish-gray or pale all Normal color (pink Normal color all over
(skin color) over body but bluish (hands and feet are
extremities) pink)
Pulse Absent <100 beats per >100 beats per

(heart rate) (no pulse) minute minute
Grimace Absent (no response Facial movement only Pulls away, sneezes,
("reflex irritability") to stimulation) (grimace) with coughs, or cries with
aggressive stimulation stimulation
Activity No movement, Some limb flexion Active, spontaneous

(muscle tone) "floppy" tone with little movement, movement, flexed
grasping for air arms and legs that
irregularly resist extension
Respiration Absent (no breathing) Slow or irregular Normal rate and

(breathing rate and breathing, weak cry effort, good cry
effort)
Pediatrics
Notes
• Strawberry tongue + Forchheimer spots → Scarlet fever
• Typical slapped cheek appearance → Provirus B19
• Sudden high fever + soft palate Nagayama spots → Roseola infantum
• Buccal (Koplik spots) → Measles
• Soft palate spots + swollen LN → Rubella
• Rash of palms and soles:
- Kawasaki disease
- Hand and foot disease
- 2ry syphilis
• Currant jelly blood in stool → Intussusception
• Currant jelly sputum → Klebsiella
• Strawberry tongue → Scarlet fever
• Strawberry vagina → Trichomonas vaginalis
• Group A Strept → Airway and skin infections
• Group A Strept pneumonia → Pneumonia
• Group A Strept pyogens → Scarlet fever
• Group B Strept (Strept aglactiae) → part of the normal flora of the gut and vagina → early-onset neonatal
infections [Group B–Birth canal]. Other organisms, E.coli and Listeria [GEL]
• Most common cause of gastroenteritis in children → Rotavirus
• Motor and verbal tics → Tourette $
• Impairment of social and behavioral skills → Asperger $
• Normal development for 2-3 years, followed by a loss of acquired motor, language and social skills between
3-4 years → Rett’s $
• Best way to deliver fluids in pediatrics with compromised peripheral venous access → Intraosseous access
• Lymph node that’s increasing in size and larger than 2cm → FBC and blood film
• US is used to examine lymph nodes if:
- Persistent beyond 6 weeks
- Isolated
- Larger than 2cm and increasing in size
• NG tube is diagnostic for esophageal atresia
• Causes of respiratory distress of an infant:
- IRDS
- Congenital pneumonia
- Transient tachypnea of the newborn
- Meconium aspiration syndrome → hours from birth, meconium may be aspirated before or at delivery,
may inhibit surfactant leading to pneumonitis, unlike IRDS incidence increases with gestational age (20%
after 42w), treated by O2 and antibiotics
- Pulmonary hemorrhage
- Milk aspiration
- Pulmonary air leaks (e.g. pneumothorax or pulmonary interstitial emphysema)
- Non-pulmonary conditions (e.g. congenital heart disease, sepsis or severe anemia)
• Most common cause of RD in term infants → Transient tachypnea of the newborn
- Caused by a delay in the resorption of lung liquid
- Risk factors include C-section
- Chest X-ray → fluid in the horizontal fissure - Managed by → O2
Pharmacology
Opioid equivalent doses
• Oral morphine has ½ the potency of oral oxycodone

- When converting from oral morphine to oxycodone → Use ½ the dose
• Oral morphine has the ½ the potency of injectable morphine
- When converting from oral morphine to injectable morphine → Use ½ the dose
• Oral morphine has the 1/3 the potency of injectable diamorphine
- When converting from oral morphine to injectable diamorphine → Divide the dose by 3
Oral morphine to oral Tramadol → X10

Oral morphine to oral Codeine → X10
Oral morphine to oral dihydrocodeine → X10
Chronic stable pain management (somatic)

1. Start with oral morphine
2. If pain still present → Oral Oxycodone
3. If there’s a problem with oral medication
- Pain is stable (e.g. stable cancer patient) → Transdermal fentanyl patch
- Pain isn’t stable (e.g. postoperative)→ IV Morphine
- Fentanyl patch is contraindicated with → Paralytic ileus or Night sweats
- With night sweats → remove fentanyl patch for 6-8h then add subcutaneous opioids
- Fentanyl takes around 36h to completely leave the system
- Amongst all opioids, codeine phosphate has the highest rate of side effects such as nausea, constipation and
confusion which young patients can often tolerate but not the elderly
- If conversion from codeine phosphate is required, offer → Buprenorphine patch, preferred over fentanyl patch
because the opioid conversion mismatch
- If buprenorphine patch isn’t available → Subcutaneous morphine
- Terminal patients with unstable pain on fentanyl patch → Keep the patch + add Subcutaneous morphine
- Please, differentiate between somatic and neuropathic pain

- Neuropathic pain (e.g. sciatica down the leg, perioral paresthesia)
Pharmacology
Neuroleptic malignant syndrome
• Rare but life-threatening reaction to anti-dopaminergic medications
- Neuroleptic (Metoclopramide) or antipsychotic drugs (haloperidol, clozapine)
• Onset is usually within a few weeks of starting the medication but can occur anytime
• Features → High fever, confusion, variable blood pressure, tachycardia, extra-pyramidal symptoms (rigidity
and tremors), dystonia, muscle weakness and stiffness
• Managed by → Stopping the drug, rapid cooling, dopaminergic agent (Bromocriptine)
Units of alcohol
- 1 unit → 1 spirit
- 2 unit → 1 pint of beer, 1 medium-sized glass of wine (175ml)
- 3 units → 1 pint of premium beer, 1 large-sized glass of wine (250ml), 1 pint of cider
- One unit = 10ml of pure alcohol, the amount of alcohol the average adult can process in 1h
- Units = Strength (ABV) x Volume (ml) ÷ 1000
- For example, a liter of Vodka contains 40 units
- High alcohol consumption: >14 units per week (males), >7 units per week (females)
- No more than 3 units per day, at least 2 days off every week
Pharmacology
Sexual side effects of antidepressants
- Haloperidol → blocks dopamine II receptors → Hyperprolactinemia → Erectile dysfunction and gynecomastia

- Fluoxetine → Anorgasmia (delayed ejaculation)
- Paroxetine → erectile dysfunction and vaginal dryness
Pharmacology
Notes
• First line treatment for neuropathic pain → Amitriptyline (TCAs), gabapentin (Lyrica), duloxetine or
pregabalin can be used
• TCAs (Amitriptyline or Oxybutynin) can cause dry eyes, urinary retention and increase the risk of falls in
elderly patients
• Polypharmacy → Elderly taking 5 or more medications
• For trigeminal neuralgia → Carbamazepine (Tegretol)
• If a skin condition was treated with an antibiotic cream with no resolve after a week → Change to antifungal
- Fucidin cream → Clotrimazole cream
• CCB → Peripheral edema, Gingival hypertrophy, Headache, Bradycardia, Dizziness
- Dihydropyridines (Amlodipine and Nifedipine) → VD
- Non-dihydropyridines (Verapamil and Diltiazem) → reduce vascular permeability and affect cardiac
contractility and causes → “Pedal edema”
• Thiazide → increased uric acid (Gout), Hyponatremia, Hypokalemia, Postural hypotension, ↑glucose, ↑Ca
• ACE-inhibitors
- A- Angioedema
- C- Cough → give ARBs instead
- E- Electrolyte imbalance (↑K+)
• Antihypertensive drugs that cause hyperkalemia
1. ACE-inhibitors →…. pril
2. ARBs → …. sartan
3. K+-sparing diuretics → Spironolactone (hyperkalemia, hyponatremia, gynecomastia)
• LOOP diuretics (furOOsemide) → HypOOnatremia, HypOOkalemia, HypOOcalcemia, GOOut
• Asthma drugs
- Salbutamol (beta II agonist) → Bronchodilatation → SE: Hypokalemia → Tremors
- Ipratropium bromide → Inhibits bronchoconstriction
- Theophylline → Bronchodilatation by relaxing bronchial smooth muscles
• Beta-agonists which are the treatment of asthma can cause → Tachycardia, while beta-blockers could
worsen the symptoms of asthma
• Bradycardia, hypotension, hypothermia, hypoglycemia (especially in children) → Propranolol toxicity
• Doxycycline should be administered with meals in order to avoid any side effects (nausea, vomiting and
esophageal irritation)
• The most common side effect of Warfarin → Intracranial hemorrhage, watch out for headache, could cause
GI bleeding, watch out for stomach pain
• 1ml = 10mg
• 1 mmol/L = 18 mg/dl
• Causes of gingival hyperplasia
- CCB
- Phenytoin
- Ciclosporin
- AML
• Somatic pain → Pain ladder
• Neuropathic pain → Amitriptyline, Gabapentin
• Muscle spasm → Baclofen, Diazepam
• Mechanism of N-acetylcysteine in treating Paracetamol toxicity → Protection from free radicals, by acting
like a precursor for glutathione synthesis increasing glutathione production and inactivate NAPQI
Pharmacology
• Mechanism of LMWH or UFH → Activation of Antithrombin III
• LMWH → Inhibits the conversion of prothrombin to thrombin by activation of antithrombin III
• UFH → Inhibits the conversion of prothrombin to thrombin + Blocks thrombin
• Warfarin → Inhibits vitamin K dependent factor synthesis
• Management of post-operative vomiting → IV Ondansetron, serotonin (5HT3) antagonist, oral routes
wouldn’t be beneficial as it would be vomited out almost immediately
• IV route is faster than oral route because → Hepatic first pass elimination
• Simvastatin should NOT be used with Clithromycin or Erythromycin as it can lead to → rhabdomyolysis and
AKI
• Common indications of spironolactone
- Ascites: patients with cirrhosis develop 2ry hyperaldosteronism
- Hypertension
- Heart failure
- Nephrotic syndrome
• Drugs that should be put down in patients with diarrhea and vomiting
- (D)iuretics → ↑Dehydration
- (A)CEIs → AKI
- (M)etformin → Lactic acidosis
- (N)SAIDs → AKI
• Methotrexate is a DMARD and is used to treat RA → SE: GI upset, angular stomatitis, anemia and Pulmonary
fibrosis - dyspnea, cough and fever
• Hydroxychloroquine is also a DMARD → SE: Visual loss → eye examination is mandatory every 6 months
• A drug used to help reduce craving and side effects of smoking cessation → Bupropion
• Pain ladder
1. Simple analgesics → Paracetamol, aspirin, NSAIDs
2. Weak opioids → Codeine, tramadol, dihydrocodeine
3. Strong opioids → Morphine, fentanyl patches, diamorphine, oxycodone
4. Nerve block epidural
• There’s no point of taking two opioids, if the patient is started on a strong opioid, the weaker one should be
stopped
• Liver metastasis may cause pain due to stretching of the liver capsule, treated with → NSAIDs or steroids
• Antiemetics
- Due to chemO/radiO → Ondansetron
- Due to ICP (e.g. brain tumors) → Cyclizine
- Bowel obstruction → Cyclizine
- Hyperemesis gravidarum → Cyclizine or promethazine
- Metabolic causes (Hormones) → Haloperidol, Levomepromazine
- BPPV → Prochlorperazine (severe → buccal, less severe → oral)
- With Parkinson’s → Levomepromazine
- Perforated peptic ulcer → Metoclopramide
• The dose of normal lease morphine for breakthrough pain should be 1/6 of the total 24-h morphine dose
- i.e. calculate total amount used by the patient daily, then calculate the breakthrough dose (1/6 the total)
• Anticipatory medications → given to patients “just in case” in end of life situations
- SC Morphine sulphate
- SC Midazolam
- SC Haloperidol
- SC Hyoscine
Pharmacology
• Catastrophic bleeding in a palliative patient → Midazolam + SC Morphine sulphate
• Treatment of central hiccups (e.g. stroke, trauma, SOL) → Chlorpromazine
• Treatment of peripheral hiccups (e.g. Vagus n. or phrenic n. irritation) → Metoclopramide
• Vagus irritation can be caused by gastric stasis and distension
• Phrenic irritation can be caused by liver metastasis
• Cancer-induced bone pain, 1st line → Radiotherapy, 2nd line → Bisphosphonates + NSAIDs
• Bone pain may worsen in the first few days of radiotherapy “pain flare”
• When the patient is seizing, it’s impossible to administer medications orally
• IV and IM routes cannot be administered at home
Psychiatry
Management of moderate depression
1. Prescribe an SSRI
2. If ineffective for at least 2-4 weeks → check adherence
3. Increase the dose
4. Change to a different SSRI
5. Try alternative class of antidepressant (atypical antidepressants → Mirtazapine)
- Antidepressants should usually show effect in 1-2 week, if no effect after 2-4 weeks → check adherence
- With good response to SSRIs → Continue for at least 6 months after remission as this reduces relapse
- Patients who had 2 or more depressive episodes in the recent past and who experienced significant functional
impairment during episodes → Continue for 2 years
- When stopping SSRIs, the dose should be reduced over a 4-week period
- If the patient stopped medications abruptly and experiencing delusions → Neuropsychiatric analysis
Hospital management for depression

1. Admission to the psychiatric ward
2. investigations
3. Treatment with SSRIs or SNRIs
4. Augmentation with lithium with CBT
5. If nothing works → ECT
Reasons for hospital admission

• Serious risk suicide
• Serious risk of harming others
• Significant self-neglect
• Severe depressive or psychotic symptoms
• Lack or breakdown of social support
• Initiation of Electroconvulsive therapy (ECT)
• Treatment-resistant depression (where inpatient monitoring may be helpful)
- High mood alone in the question (no mention of low mode at all) → Hypomania
- Low mode alone in the question (no mention of high mode at all) → Depression
- High mode and low mode (depression) (no matter time in between) → Bipolar
- High mode with hallucinations and delusions → Mania
- Mania and hypomania are distinguished by hallucinations and delusions in Mania
Risk factors for suicide

• Previous suicide attempts
• Previous self-harm
• Depression and other mental health problems
• Alcohol and drug abuse
• Low socio-economic status
Psychiatry
Bipolar affective disorder (Manic depression)
➢ Classically, periods of prolonged and profound depression alternate with periods of excessively elevated and
irritable mood, known as mania
Features
• Decreased need for sleep Cyclothymic disorder → milder form of bipolar lasting 2 years,
fluctuating from mild depressive and hypomanic symptoms
• Pressured speech
• Increased libido
• Reckless behavior without regard for consequences
• Grandiosity
• More talkative than usual
These symptoms of mania would alternate with depression
Treatment
• Mood stabilizers → Lithium- Despite problems with tolerability, lithium still remains the gold standard in the
treatment of bipolar affective disorder
Mood stabilizers (LCVL): Lithium, Carbamazepine, Valproic acid, Lamotrigine
Points about lithium

- Don NOT offer lithium to women who are planning a pregnancy or currently pregnant, unless antipsychotic
medication has not been effective
- If a woman taking lithium becomes pregnant consider stopping the drug gradually over 4 weeks
- If a woman continues taking lithium during pregnancy, check plasma lithium levels every 4 weeks, then
weekly from the 36th week and adjust the lithium dose to maintain plasma lithium levels at a therapeutic
dose
Tetralogy of lithium
- Ebstein anomaly of the heart
- Floppy baby $
- Thyroid abnormalities
Mania vs Hypomania
Psychiatry
Schizophrenia
1. Auditory hallucinations
• Third-person auditory hallucinations → voices are heard referring to the patient as ‘he’ or ‘she’, rather
than ‘you’
• Thought echo → an auditory hallucination in which the content is the individual’s current thoughts
- Hearing thoughts after being produced → Echo de la pensée
- Hearing thoughts at the same time or before as thought being produced → Gedankenlautwerden
• Voices commenting on the patient's behavior
2. Thought disorder
• Thought insertion → The delusional belief that thoughts are being placed in the patient’s head from
outside
• Thought withdrawal → The delusional belief that thoughts have been 'taken out' of his/her mind
• Thought broadcasting → The delusional belief that one’s thoughts are accessible directly to others
• Thought blocking → a sudden break in the chain of thought
3. Passivity phenomena
• Bodily sensations being controlled by external influence
4. Delusional perceptions
• A two-stage process where first a normal object is perceived then secondly there is a sudden intense
delusional insight into the object's meaning for the patient e.g. 'The traffic light is green therefore I am the
King'
Management
1. Antipsychotics
- 1st → olanzapine or risperidone
- If rapid tranquillization is needed → Diazepam
Tardive dyskinesia
- Continuous involuntary movements of the tongue and lower face
- Caused by long-term use of antipsychotic drugs
- Often reported by family members as patients are often unaware of these movements
Atypical antipsychotics have lower risk of TD:
1. Risperidone (tabs, injections) → better for incompliant patient (Depot, long-acting injections)
2. Olanzapine (tabs)
Tardive dyskinesia can be treated by → Tetrabenazine
o Drug-induced parkinsonism → 1 week after starting anti-psychotic

o Akathisia → 1 month after starting antipsychotics
o Tardive dyskinesia → months-years after starting antipsychotics
Paranoid personality disorder

• Hypersensitivity and an unforgiving attitude when insulted
• Unwarranted tendency to question the loyalty of friends
• Reluctance to confide in others
• Preoccupation with constitutional beliefs and hidden meaning
• Unwarranted tendency to perceive attacks on their character
Psychiatry
Postpartum blues vs Postnatal depression vs Postpartum psychosis
In postpartum depression, 1st line SSRI → Sertraline

Postpartum psychosis usually starts with postpartum depression
Postpartum psychosis = Puerperal psychosis
Psychiatry
Generalized anxiety disorder (GAD)
➢ ‘Excessive worry’ and feelings of apprehension about everyday events, with symptoms of muscle and psychic
tension, causing significant distress and functional impairment
Symptoms of GAD
• Restlessness
• Concentration difficulties or ‘mind going blank’
• Irritability
• Muscle tension
• Sleep disturbance • If symptoms on/off (attacks lasting 20-30min) →Panic attacks
• Palpitations/tachycardia • If continuous (for 6 months) → GAD
• Sweating
• Trembling or shaking
• Breathing difficulties as choking sensation
• Chest pain or discomfort
• Fear of losing control, ‘going crazy’, passing out or dying
GAD present most days for at least 6 months + 3 or more somatic symptoms
Management of GAD
• CBT or applied relaxation or drug treatment
• 1st line → Sertraline (SSRI)
• Alternative SSRIs → escitalopram or paroxetine
Panic disorders
➢ Several sudden onset episodes (>2 panic attacks)
➢ A panic attack peaks around 10min then gradually resolves over the next 20min
Features of panic attacks
• Palpitations, tremors, sweating, shaking, tachycardia and shortness of breath that develop rapidly
• Patient might feel he’s going to die from cardiac or respiratory problems
• Dizziness, circumoral paresthesia, carpopedal spasm
• Can occur with no obvious trigger and awaken the patient from sleep (nocturnal panic attacks)
- In a panic ATTACK, simple breathing exercises and reassurance is all what’s needed
- Numbness and circumoral paresthesia occur due to hyperventilation and wash of CO2 → respiratory alkalosis →
high pH enhances binding between Ca and protein → decreased ionized Ca
Management of panic disorder • When you’re panicking, avoid using
• CBT or applied relaxation or drug treatment FaceBook → Fluoxetine and
• 1 line → SSRIs (do NOT use fluoxetine)
st Benzodiazepine
• if SSRIs contraindicated or no response after 12 weeks → imipramine or clomipramine
• In an acute sitting → Beta-blockers and Rebreathing into paper bags
• DO NOT use benzodiazepine for panic attacks
Acute stress disorder

- Lasts hours-days
Psychiatry
Social anxiety disorder (Social phobia)
➢ Persistent fear and anxiety around people or in certain situations, sufferers fear being criticized. They tend
to worry excessively before, during and after the encounter
Anxiety-provoking situations
• Meeting people (especially strangers)
• Talking in meetings
• Talking to authority figures
• Eating or drinking while being observed
• Going to school
• Going shopping
• Being seen in public
There are two forms of the condition:
1. Generalized social anxiety which affects most, if not all areas of life. this is the more common type (70%)
2. Performance social anxiety which can be seen in certain situations such as public speaking
Agoraphobia → Fear of open places or being in situations escape might be difficult or help wouldn't be available if
things go wrong
- Public transport
- Shopping centers
- Leaving home
Autism spectrum disorders

➢ Can be recognized at any age
➢ Usually present in times of stress or sudden life change
Features
1. Severe difficulties communicating and forming relationships
2. Difficulties in language
3. Repetitive and obsessive behavior
Asperger $
- Autism spectrum disorder except language is normal + normal or high IQ
Psychiatry
Post-traumatic stress disorder (PTSD)
➢ Develops following a traumatic event, usually after 6 months since the event
Features
• Re-experiencing: Flashbacks, nightmares
• Avoidance: Avoiding people, situations or circumstances resembling or associated with the event
• Hyperarousal: Hypervigilance for threat, exaggerated startle response, sleep problems, irritability and
difficulty concentrating
• Emotional numbing: Lack of ability to experience feelings
• Depersonalization can be one of the symptoms
Management
• Trauma-focused cognitive behavioral therapy (TF-CBT) and eye movement desensitization and
reprocessing (EMDR) → first-line
• SSRI’s → second line. e.g. Paroxetine or Sertraline are licensed for PTSD
• Other unlicensed possibilities include: fluoxetine, citalopram, escitalopram, and fluvoxamine
If you find all these names of SSRI’s difficult to remember. Just remember these 3 → Paroxetine, sertraline, and
fluoxetine
Obsessive-compulsive disorder (OCD)

➢ Chronic condition, often associated with marked anxiety and depression, characterized by “obsession”
➢ Characterized by recurrent unreasonable obsessions concerning contamination, guilt, aggression and sex
➢ Compulsions are peculiar behaviors that reduces anxiety, commonly hand-washing, organizing, checking,
counting and praying
Management
• Low intensity CBT, including exposure and response prevention (ERP)
• If low intensity CBT is inadequate → more intensive CBT + SSRIs
• SSRIs → escitalopram, fluoxetine, sertraline or paroxetine
• If patient is suicidal or severely incapacitated → ECT
Psychiatry
Anorexia nervosa
➢ Most common cause of admissions to child and adolescent psychiatric wards. It is most commonly seen in
young women (13-17 years) in which there is marked distortion of body image, pathological desire for
thinness, and self-induced weight loss by a variety of methods
Features
• BMI <17.5kg/m2 or < 85% of that expected
• Rapid weight loss
• Self-induced weight loss → reduce food intake, vomiting, purging, excessive exercise
• Intense fear of being obese
• Disturbance of weight perception
• Endocrine disorders that cause amenorrhea, reduced sexual interest/impotence, raised GH levels, raised
cortisol, altered TFTs, abnormal insulin secretion
• Bradycardia
• Hypotension
• Fatigue
• Muscle weakness
• Intolerance to cold
Management
• BMI <15 OR rapid weight loss OR evidence of systemic failure (electrolyte disturbance as hypoglycemia or
bradycardia)
- Refer to eating disorder unit (EDU), medical unit (MU)
• Moderate (BMI 15-17.5) + NO evidence of systemic failure
- Refer to the local community mental health team or EDU if available
• Mild anorexia (BMI >17)
- Building a trusting relationship + self-help books and a food diary
If BP< 90/60 → Medical unit
Reasons for admission in a psychiatric illness
1. Lack of insight
2. Danger to self
3. Refusal of voluntary admission → mandatory admission under the mental health act
Bulimia nervosa
➢ Binge eating followed by compensatory weight loss behaviors (self-induced vomiting, fasting, intensive
exercise, abuse of medications such as laxatives, diuretics, thyroxine or amphetamines)
➢ They don’t usually have to be thin; some have BMI above 17.5 kg/m2
Examination
• Salivary glands (especially the parotid) may be swollen
• Russell’s sign may be present (calluses form on the back of the hand, caused by repeated abrasion against
teeth during inducement of vomiting)
• There may be erosion of dental enamel due to repeated vomiting
Psychiatry
Alcohol drinking questionnaires
AUDIT
A-Amnesia
U-Units
D-Doing less work
I-Injured yourself or others
T-Termination
CAGE
C-Cut down thoughts
A-Annoyed by friends or family asking you to cut down
G-Guilt or remorse after drinking
E-Eye opener drinker
Neuroleptic malignant $
➢ Rare but life-threatening reaction to anti-dopaminergic medications (e.g. clozapine, metoclopramide,
haloperidol)
➢ Onset is usually within a few weeks of starting the anti-dopaminergic medication but can occur at any time
Features
• High fever
• Confusion or alerted consciousness
• Variable blood pressure
• Extrapyramidal symptoms (e.g. Rigidity, tremors)
• Tachycardia
Management
• Stop offending medication
• Rapid cooling
• Dopaminergic agents → Bromocriptine
Serotonin syndrome
➢ Life threatening iatrogenic disorder that’s characterized by triad of autonomic, cognitive and somatic effects
➢ Precipitated shortly after use of SSRIs
Autonomic effects
• Pyrexia
• Tachycardia
• Nausea
• Diarrhea
Cognitive effects
• Confusion
• Agitation
• Hallucinations
Somatic effects
• Tremors
• Muscle spasms
Psychiatry
Cocaine overdose
• Arrhythmias
• Both tachycardia and bradycardia may occur
• Hypertension
• Seizures • Cocaine withdrawal → depression
• Mydriasis • Heroin withdrawal → increasing body secretions (sweating,
• Hypertonia runny nose), muscle aches, agitation, and sleep disturbance
• Hyperreflexia • Benzo withdrawal → features of a panic attack
• Agitation
• Psychosis
• Effects include necrosis of nasal septum
Heroin
• Intense pleasure and pain relief
• Relaxation, drowsiness and clumsiness
• Acute management of opiates (heroin) overdose → Naloxone IV
• Miosis • Chronic management/detoxification/addiction/withdrawal
• Confusion symptoms → Methadone
• Slurred and slow speech • Naloxone has a short half-life so coma and respiratory
depression often recur when naloxone wears off, observation is
• Slow breathing and heartbeat
essential and repeated doses might be needed
• Dry mouth
• Reduced appetite and vomiting - 2nd line in detoxification → Buprenorphine
• Decreased sex drive - 3rd line or for shorter detoxification period → Lofexidine
- Used as an adjuvant to prevent relapses → Naltrexone
- Naloxone has a short half-life → coma and respiratory
Ecstasy (MDMA) depression often recur after its effect wears off
• Uncontrolled body movements

• Dehydration or extreme thirst
• Hyperthermia
• HTN
• Insomnia
• Tachycardia
• Spots of color/floating colors/flashing colors when their eyes are open
• Increased RR
LSD (Lysergic acid diethylamide) • Visual hallucinations when eyes closed → LSD
• Visual hallucinations when eyes open → Ecstasy
• Mydriasis
• Flushing and sweating
• Diarrhea
• Paresthesia
• Hyperactive reflexes
• Delusions and hallucinations
• Intensified senses
• Smelling colors and seeing sound
• Testing things that aren’t there
Can be treated with benzodiazepines
Psychiatry
Lithium poisoning
Causes
• Therapeutic overdosage → common
• Drug interactions with either a diuretic or NSAIDs → common
• Deliberate self-harm (less common)
Mild
- Nausea
- Altered taste
- Diarrhea
- Blurred vision
- Polyuria
- Fine resting tremors
Moderate
- Increasing confusion
- Increased deep tendon reflexes
- Myoclonic twitches and jerks
- Increasing restlessness followed by stupor
Severe
- Coma
- Convulsions
- Cardiac arrythmias
- Cerebellar signs
With lithium
- Therapeutic dose → fine tremors
- OD → N, drowsiness & coarse tremors
Na Valproate
- Therapeutic dose → fine tremors
- OD → N, drowsiness but NO tremors
Before commencing on lithium After commencing on lithium
• Kidney function tests

• TFTs, thyroid disturbance can mimic mania or • Serum lithium every 3 months
depression • TFTs and renal function tests every 6 months
• ECG, BP, pulse, FBC, U&E and PT if sexually active
- Lithium should be checked a week after starting. Following that, lithium levels are checked every 3 months
- Lithium levels should also be checked 12h after taking the last lithium dose
Psychiatry
Notes
• Low mood, anhedonia, guilt, can’t concentrate (for at least 2 weeks) → Mild depression
• Mild depression + poor sleep + poor libido + easy fatigue → Moderate depression
• Moderate depression + suicidal thoughts → Severe depression
• Severe depression + hallucinations + delusions → Psychotic depression
• Increase in fatigue, appetite, weight and sleep with low mood but remains reactive, leaden paralysis (feeling
of heaviness in the limbs) may occur → Atypical depression
• Persistent depressive state, milder than MDD and persists more than 2 years → Dysthymia
• Milder form of bipolar lasting 2 years, fluctuating from mild depressive and hypomanic symptoms →
Cyclothymic disorder
• The individual is unable to cope with particular stress or major life event, they must occur within 1-3 months
of a particular psychosocial stressor, and shouldn’t persist longer than 6 months after the stressor is removed
→ Adjustment disorder
• Lack of interest in social relationships + tendency towards a solitary lifestyle → Schizoid personality disorder
• Mood swings, marked impulsivity, unstable relationships, fear of abandonment and inappropriate anger,
usually attention seekers and may have multiple self-inflicted scars → Borderline personality disorder
(Emotionally unstable personality disorder) (EUPD)
• Mild degree of mania where there’s elevated mood but no significant impairment of daily activities →
Hypomania
• Antihypertensive drugs when administered with lithium can cause psoriasis → ACEIs
• Antihypertensive drug causes hypokalemia + high lithium level → Thiazide diuretics
• Other causes of lithium toxicity → Metronidazole, Dehydration, renal failure
• Inability to resist impulses to deliberately start fires, in order to relieve tension or for instant gratification →
Pyromania
• Delusional belief that a famous person is secretly in love with them → Erotomania (De Clerambaut $)
• Impulsive urge to pull out one’s hair leading to noticeable hair loss → Trichotillomania
• Inability to refrain from stealing → Kleptomania
• False belief that significant remarks, events or objects in one’s environment have personal meaning or
significance (e.g. someone constantly gives him messages through the newspaper) → Delusion of reference
• Delusional belief that one’s life is being interfered in a harmful way → Persecutory delusion
• Fantastical beliefs that one’s famous, wealthy or powerful → Grandiose delusions
• False belief that one’s thoughts, feelings, impulses or behavior is being controlled → Delusion of control
• Delusional belief that patient died or the world has ended and nothing matter → Nihilistic delusions
• Nihilistic delusions + psychotic depression → Cotard’s $
• Feeling guilty or remorse with no valid reason, one believes they deserve punishment → Delusions of guilt
• When the person believes that different people are in fact a single person that changes appearances or in
disguise → Fregoli delusion (delusion of doubles)
• Patient believe that a person known to them has been replaced by a double → Capgras $
• Feigning physical or mental illness, most frequently in prison inmates, they produce “approximate answers”
or sometimes wrong however still hold some relevance to them → Ganser $ [Gangster]
• Perceptual distortions of the size and shape of objects and altered body images, they might feel their body is
expanding or getting smaller → Todd’s $
• Delusional jealousy, marked by suspecting a faithful partner of infidelity like cheating, adultery or having an
affair, patient may attempt monitoring his partner → Othello $
• Delusional parasitosis/infestation where they believe their skin/body is infected with parasites → Ekbom’s $
Psychiatry
• A situation where two people with a close relationship share a delusional belief, this arises as a result of a
psychotic illness in one individual, delusion resolves in the second person on separation, the first should be
assessed and treated → Folie à deux (madness of two)
• Persistent belief in the presence of an underlying serious disease (e.g. cancer or HIV), patient refuses to
accept reassurance or negative test results → Hypochondriasis (illness anxiety disorder)
• Multiple symptoms, multiple investigations, never reassured → Somatization disorder
• Feigning symptoms NOT for secondary gain but medical attention → Munchausen’s $ (factitious disorder)
• Feigning illness in a child to gain medical attention, a form of child abuse that subjects the child to
unnecessary medical procedures, hospitalization or treatments → Munchausen’s $ by proxy
• Feigning symptoms for secondary gain (e.g. for compensation, to avoid military service or to obtain an opiate
prescription) → Malingering
• Motor or sensory dysfunction which initially appears to have a neurological or other physical cause but is
later attributed to a psychological cause, patient doesn’t consciously feign the symptoms or seek material
gain. Memory loss, seizures, loss of speech and paralysis can occur → Conversion (dissociative) disorders
(functional neurological symptom disorder)
• Continuous antisocial or criminal acts and inability to conform to social rules, impulsivity, disregard for the
rights of others, aggressiveness and lack of remorse, they will typically be manipulative, deceitful and reckless
→ Antisocial Personality disorder (Antisocial behavioral disorder)
• A young patient <18y with similar features as Antisocial Personality disorder → Conduct disorder → Tx:
juvenile detention
• Young children with negative, defiant behavior WITHOUT serious violation of social norms, more common
with interaction with adults → Oppositional defiant disorder → Tx: parenting
• Inattention + hyperactivity + impulsiveness → Attention deficit hyperactivity disorder (ADHD)
• An incompliant patient in need for antipsychotics → Depot haloperidol
• An incompliant patient + tardive dyskinesia → Depot risperidone
• Pinpoint pupils, confusion, agitation and copious secretions → Organophosphate poisoning
• To avoid anxiety before a certain event → Beta-blocker
• If the patient is having an attack → Rebreathe into paper bags, if very severe → Benzodiazepines
• For long-time management and to prevent further attacks → CBT or SSRIs
• SSRIs are the first line medical management in → GAD, OCD, PTSD and Panic disorders
• In GAD, 1st line SSRIs → Sertraline
• In panic attacks → All except Fluoxetine
• In OCD → All except Citalopram
• Drugs that interact with SSRIs → NSAIDs, Aspirin, Heparin, Warfarin, Triptan [TWHAN]
• Preferred SSRIs with MI patients → Sertraline then, Citalopram
• Preferred SSRIs with no relevant medical history → Citalopram then, Fluoxetine
• Preferred SSRI in young kids → Fluoxetine
• For rapid tranquillization in an aggressive NOT-psychotic patient → oral lorazepam, then IM
• For rapid tranquillization in a psychotic patient → 1st Lorazepam IM, haloperidol IM
• For rapid tranquilization in a psychotic episode in elderly → Haloperidol IM
• 1st line for status epilepticus → IV Lorazepam
• Binge eating followed by compensatory weight loss behaviors → Bulimia nervosa
• Low weight, food restriction, fear of gaining weight and strong desire to be thin → Anorexia nervosa
• Ability to recognize one’s own mental illness (OCD, phobias)→ Insight
• A very fast and accelerated speech without a pause, hard to follow, cannot be interrupted, seen in mania →
Pressure of speech
• Thought and words leap from topic to another with frequent shifts abruptly → flight of ideas
Psychiatry
• Irrational fear of confined spaces → Claustrophobia
• Fear of spiders → Arachnophobia
• Fear of heights → Acrophobia
• Hallucinations hours after heavy drinking (12-24h) → Alcohol hallucinosis
• Hallucinations/tremors/disorientation/diaphoresis in a chronic alcoholic following a day of abstinence →
Delirium termens
• Transient false perception experienced when the person is on the verge of falling asleep → Hypnagogic
hallucinations [go to sleep]
• Transient false perception experienced while waking up → Hypnopompic hallucinations
• A psychotic feature of bipolar disorder where a person’s belief or action does not match their mood (e.g.
laughing at a funeral, believing to have superpowers while depressed) → Mood incongruence
• A psychotic feature of bipolar where the belief or action is consistent with the mood → Mood congruence
• Encourage women with a mental health problem to breastfeed unless they’re taking → Carbamazepine,
clozapine or lithium
• Everything is decreased + miosis → Heroin
• Everything is increased + mydriasis → Cocaine
• Colors when eyes open + increased thirst + uncontrolled body movements + hyperthermia, tachycardia,
tachypnea, insomnia → Ecstasy
• Colors when eyes closed + heightened senses + flushing, sweating → LSD
• Antidote for benzodiazepines (e.g. drowsiness after benzo) → Flumazenil
• Blood findings that support chronic alcoholism → High GGT, high MCV
• First line in delirium termens → Lorazepam, diazepam
• If de-escalation techniques failed in delirium → Olanzapine, haloperidol
• Antidepressants may precipitate mania and should be ceased if patients have manic episodes
Respiratory Medicine
Asthma
➢ Paroxysmal and reversible obstruction of the airways
➢ History of recurrent episodes of wheezes, chest tightness, breathlessness, and/or cough, particularly at
night/early morning
➢ Symptoms may be triggered by specific triggers (e.g. pollens, pets, cold air or perfumes)
➢ Symptoms may worsen after taking beta-blockers, aspirin or NSAIDs (BAN) ➝ Paracetamol is safe
➢ Evidence of variable airflow obstruction seen on tests such as peak expiratory flow measurement
Acute asthma
• Bronchospasm (smooth muscle spasm narrowing airways)
• Excessive production of secretions (plugging airways)
Risk factors
➢ A combination of genetic & environmental factors
- Personal history of atopy (genetic tendency to develop allergic diseases) such as eczema
- Family history of asthma or atopy
- Inner city environment
- Prematurity and low birth weight • SE of Atenolol ➝ wheezing
- Smoking • SE of Ramipril ➝ cough
- Maternal smoking
Presentation
• Cough
• SOB
• Wheezes
• Chest tightness
Mild attack Acute severe attack Life-threatening attack

o Slight tachypnea, tachycardia o Use of accessory muscles of o Silent chest (no wheeze at all)
o Classically, expiratory wheeze is respiration o Exhaustion
heard (widespread wheeze) o Inability to complete a sentence o Altered consciousness
in one breath o Cyanosis
o Intercostal retractions o Arrythmia
o hypotension
In children o Poor respiratory effort
• HR >125 (>5 years) or >140 (2-5 o PEF <33% best or predicted
years) o RR >26
• RR >30 or >40 o SpO2 <92%
o PaO2 <8 kPa
Normal PaCO2 (4.6-6 kPa)
Diagnosis
- Symptoms of asthma
- Pulmonary function tests (SPIROMETRY) ➝ Initial diagnostic tool ➝ Reversible obstructive pattern
- Day-to-day peak flow variability showing diurnal cycle ➝ Treatment monitoring and adjustment
- Post-dilator improvement of >12% in FEV1/FVC
- Unexplained peripheral blood eosinophilia
Long-term management
Asthma in adults Asthma in children
1. Low dose inhaled steroid (preventer) + SABA

1. Very low dose inhaled steroid (preventer) +
when needed (reliever)
SABA when needed (reliever)
2. Add LTRA (e.g. Montelukast)
2. >5 years ➝ LABA or LTRA // <5 years ➝ LTRA
3. Increase the dose of inhaled steroids OR add
3. Increase the dose of inhaled steroid
LABA (Salmeterol)
4. In severe cases ➝ SR Theophylline
4. In severe cases ➝ Short-term oral steroid
Management of acute exacerbation • Where diagnosis is uncertain but with

demonstration of airway obstruction
Immediate treatment [OSTHP]
(FEV1/FVC < 0.7), reversibility testing
1. Start O2 if saturation < 92%, aim for 94-98% and/or a trial of treatment are suggested
2. Salbutamol 5mg (or terbutaline 10mg) nebulized with O2 • Chest X-ray is not a routine assessment
but it’s useful for exclusion
3. IV Hydrocortisone 100mg OR oral prednisolone 40-50 mg
• Only benefit for IV hydrocortisone over
oral prednisolone if patient is vomiting or
If life threatening features present: [SIM] having severe dyspnea where they
cannot consume oral medication
1. Give salbutamol nebulizers every 15 minutes, or 10 mg continuously
• If immediate TTT is not working, add
2. Add in ipratropium 0.5mg to nebulizers ipratropium ➝ MgSO4 ➝ IV
3. Give single dose of MgSO4 (1.2-2g IV) over 20 minutes aminophylline + IV salbutamol (ICU)
• In children
If improving within 15-30 minutes [SP] - OSIPH
- IV Salbutamol or IV Aminophylline
1. Nebulized salbutamol every 4 hours - MgSO4 comes last
2. Prednisolone 40-50 mg PO OD for 5-7 day • SE of B2 agonist: palpitation, tachycardia
Exercise-induced asthma
➢ It’s a sign of poorly controlled asthma
➢ Choice of medication: Short acting beta 2 agonist (used before exercise)
➢ Review of the regimen including inhaled corticosteroids should be done
• Patients who are well controlled on inhaled corticosteroids but complains of exercise being the specific problem,
then consider ADDING either:
- Leukotriene receptor antagonist (LTRA) = Montelukast
- A long-acting beta 2 agonist (LABA) = Salmeterol
- Sodium cromoglicate
- An oral beta 2 agonist
- Theophylline
• This would be taken 2h before an exercise and will prevent symptoms for approximately 12h
COPD
➢ History of smoking and progressive dyspnea Chronic Bronchitis
➢ Evidence of irreversible airflow obstruction on spirometry • Productive cough (TABLESPOON of mucus)
that lasts for three months or more per year
- FEV1 < 80% predicted for at least two years
- FEV1/FVC < 0.7 (Post-dilator) • COPD is now the preferred term for patients
with airflow obstruction who were
➢ All spirometry findings are increased (TLC, RV) except for
previously diagnosed with chronic bronchitis
DLCO & VC or emphysema
Presentation
Asthma Vs COPD
• Cough + sputum production • Reversibility distinguishes asthma from
• Dyspnea COPD
• COPD is almost refractory to medication
• Low-grade fever (mostly afebrile)
• Almost all COPD patients do smoke or have
• Wheezes smoked in the past
Investigation • COPD tend to be in old age (>35 years)
• Raised hematocrit ➢ Asthma patients can develop COPD later in life

• Chest X-ray is not recommended but if ordered ➢ Venturi mask doesn’t create +ve pressure
unlike non-invasive ventilation
- Hyperinflated lung fields
- Flattened diaphragm
- Prominent posterior ribs markings (>7 posterior ribs seen)
- Small heart
- May see bullae
Management [APBOS ANIV]
• Antibiotics ➝ If sputum is purulent or clinical signs of pneumonia
• Prednisolone 30mg/day for 7-14 days
• Nebulized normal saline ➝ to clear out mucus
• Inhaled or nebulized bronchodilators
• Controlled O2 therapy 24% via Venturi face mask, with oximetry Maintain saturations between 88% and 92%
• IV aminophylline Beneficial if the patient is wheezy and has not improved with nebulizers alone
• Non-invasive ventilation ➝ RR> 30, pH< 7.34, falling PaO2 or rising PaCO2 despite medical treatment
Invasive mechanical ventilation

Indications
• Failed NIV
• Contraindicated NIV in scenarios such as: respiratory arrest, high aspiration risk or impaired mental status
Complications
Doxapram
• Pneumonia • A respiratory stimulant, given IV
• Barotrauma • Used to drive respiratory rate if
• Failure to wean to spontaneous ventilation >20 breaths/minute
• Been replaced by NIV
Pulmonary function test
• TLC: amount of air in the lungs after maximal inspiration
• RV: amount of air that remains in the lungs after maximal expiration
• VC: amount of air that is pushed out of the lungs after maximal inspiration
• FVC: amount of air pushed out of the lungs after forced maximal expiration
• FEV1: amount of air pushed out of the lungs in 1sec during maximal expiration
Obstructive lung disease Restrictive lung diseases
• COPD • Pulmonary fibrosis

• Asthma • Interstitial lung disease
• Cystic fibrosis • Other causes: obesity, deformities or
• Bronchiectasis neuromuscular disorders
➢ Obstructed airways ➝ patient struggles to breathe ➢ Restricted lung expansion ➝ decrease in the
out ➝ decreased FEV1 amount of air that lungs can hold ➝ decrease in VC
➢ Decrease FEV1 ➝ decreased FEV1/FVC ratio ➝ decreased FVC
➢ Restrictive lung disease ➝ decrease in lung
elasticity ➝ becomes harder to fore out air ➝
decreased FEV1
Long-term oxygen therapy (LTOT)
➢ Prescribed to patients with COPD and severe chronic hypoxemia
➢ Once started, it’s likely to be life-long
➢ Usually given over a minimum of 15h a day
➢ Add-ons to improve breathlessness → Prednisolone or Nebulized normal saline
Possible candidates
• Very severe airflow obstruction ➝ FEV1 < 30% predicted
• Polycythemia
• Cyanosis
• Peripheral swelling
• Raised JVP
• Oxygen saturation 92% or less on room air
Conditions for assessment
• Patient should be stable and >5 weeks have passed since last exacerbation of COPD
• On a fully optimized treatment for COPD
• 2 sets of ABG are taken 3 weeks apart to ensure the patient is sufficiently hypoxic
Indications
• pO2 <7.3 kPa
• pO2 = 7.3 kPa + one of the following
- 2ry polycythemia (raised hematocrit)
- Peripheral edema
- Pulmonary hypertension
Non-invasive ventilation
Indications
1. Acidosis (pH <7.35)
2. Rising PaCO2
3. Falling PaO2
4. PR >30
➢ All of these despite medical management (steroids, nebulized bronchodilators & standard O2 therapy) is an
indication of non-invasive ventilation
Pulmonary embolism
Risk factors
1. Surgery
2. Pregnancy (including the post-natal period) Pulmonary embolism is suspected with normal X-ray
3. Obesity & normal chest examination
4. COCP
5. History of prolonged immobility (such as airplane travel)
6. LL injury
7. Malignancy
8. Previous VTE (venous thromboembolism)
Presentation [non-specific]
Symptoms • Respiratory alkalosis + Hypoxia = PE
• Respiratory alkalosis + NO hypoxia = Panic attack
• Dyspnea
• Pleuritic chest pain or retrosternal chest pain
• Cough and hemoptysis
Signs
• Tachypnea, tachycardia
• Hypoxia, anxiety, restlessness, agitation and impaired consciousness
• Pyrexia
• Elevated JVP
• Gallop heart rhythm, a widely split-second heart sound, tricuspid regurgitant murmur
• Pleural rub
• Systemic hypotension and cardiogenic shock
Diagnosis
➢ CTPA (CT pulmonary angiogram) ➝ Gold standard
Management
➢ Immediate administration of LMWH once PE is suspected (even prior to CTPA)
Panic attacks
• Results in hyperventilation which causes a respiratory alkalosis
• There would be no metabolic compensation as panic attacks resolve rapidly
• We would not expect any metabolic compensation as it takes the kidneys days to conserve acid
• PaO2 would be normal
Pulmonary embolism in pregnancy
➢ Chest X-ray should be requested first before deciding whether a V/Q scan or CTPA should be done, in order to
exclude other pulmonary diseases such as pneumonia, pneumothorax or lobar collapse
- Abnormal X-ray + clinical suspension of PE ➝ CTPA
- Normal X-ray + clinical suspicion of PE ➝ V/Q scan
CTPA V/Q scan
• Lower risk of radiation to fetus

• Higher radiation to the mother ➝ High risk of • More risk of radiation to fetus ➝ High risk of
breast cancer for the mother childhood cancer
• Advantages: • Lower radiation to the mother
- Faster • Only used when:
- Easier to perform - Patient is allergic to the dye
- Reduced need for further imaging - Renal impairment
- In pregnancy if the initial X-ray is normal
- If CTPA is -ve ➝ NO further investigations
needed
*Note that the absolute risk of complications for both is very small
Two-level PE well’s score
[Can Not Treat If PE Help Me]
➢ >4 points ➝ PE likely

➢ ≤4 points ➝ PE not likely
Approach
• >4 ➝ Immediate CTPA • D-dimer may be elevated due to surgery
• ≤4 ➝ D-dimer test, if +ve ➝ Immediate CTPA

• If there’s a delay in getting the CTPA ➝ LMWH until the scan is performed
• If the patient has an allergy to contrast media or renal impairment ➝ V/Q scan should be used instead
Pneumonia
Pneumocystis carinii pneumonia (PCP) (Pneumocystis jiroveci pneumonia)
➢ HIV patient + desaturation on exercise while normal during rest
➢ HIV is an important risk factors especially if CD4 <200/mm3 ➝ should receive PCP prophylaxis (co-trimoxazole)
Features
• Exertional dyspnea • Think of flu-like symptoms in an immunocompromised patient
• Gradual onset of dry cough
• Fever
• HIV + dry cough ➝ PCP
• Tachypnea
• HIV + productive cough ➝ TB
• May be signs of AIDS (e.g. Thrush)
• Chest examination is typically normal
• Could present with Herpes labialis • Prophylaxis in HIV with Mycobacterium avium & CD4 <50 → Azithromycin
Investigation
• Sputum
• Bronchoscopy with bronchoalveolar lavage ➝ Diagnostic
Management
• Co-trimoxazole (trimethoprim-sulfa) in severe cases
• Atovaquone in mild to moderate cases
Legionnaires disease
➢ Caused by Legionella pneumophila • They often mention hints like travelling, hotel spas
➢ Acquired by droplet inhalation of contaminated water or hot tubs [millionaire]
➢ Severe, potentially fatal acute pneumonia
Features
• Flu-like symptoms
• Cough: dry ➝ productive
• Fever, diarrhea, vomiting, confusion, coma
Investigation
• Sputum ➝ Black currant jelly
• Chest X-ray ➝ Bi-basal consolidation • Chest X-ray should be arranged as a follow-up around 6
• Specific blood results: weeks after discharge
- Low sodium
- Lymphocytopenia (low WBCs)
- Low albumin
- Elevated Liver enzymes
Management
• Clarithromycin/Azithromycin +/- rifampicin or fluoroquinolone
- Clarithromycin + statin may lead ➝ rhabdomyolysis ➝ pause/decrease statins OR give Doxycycline
instead
- Clarithromycin + salbutamol can cause ➝ hypokalemia
Mycoplasma (atypical pneumonia)
Features
• Young adults (living in dorms)
• Dry cough
• No SOB
• Joint pain + rash (erythema multiform ➝ target lesions on the back of the hand)
• Low grade fever + flu-like symptoms
Chest X-ray ➝ perihilar shadowing + bilateral patchy consolidation
Management ➝ Erythromycin
Klebsiella
➢ Old / diabetic / alcoholic
Chest X-ray ➝ Cavitation (especially upper lobe)
Management ➝ Cefuroxime (Cephal.) (kephlex)
Aspiration pneumonia
• Commonest causative organisms ➝ Staph, Strept, H. influenza CURB = 0
CURB-65 ➝ risk factors for predicting mortality - Prescribe Amoxicillin
- If penicillin allergy Doxy or clarithromycin
• Confusion
CURB = 1 or 2
• Urea >7mmol/L (>19 mg/dl) - Dual amoxicillin + clarithromycin OR
• Respiratory rate ≥30/min monotherapy with Doxy
• BP < 90/60mmHg - Hospital admission for score 2
CURB = 3
• Age ≥ 65
- IV antibiotics
Score is also used in case of community acquired pneumonia
Pleural empyema
• A complication of pneumonia as well as invasive procedures of the thorax
• Pneumonia ➝ Parapneumonic effusion ➝ Pleural empyema
• Suspected when pneumonia does NOT improve with antibiotics
• Empyema usually starts in the lower lobe where sound would be absent
• Pneumonia and empyema share similar symptoms
Other features
• Swinging fever, night sweats
• Weight loss
• Chest pain
Investigation
• Pleural aspiration
• Blood and sputum culture
• HIV test
Management
• Chest drain, if:
- pH of the pleural aspirate is <7.2
- Effusion is causing respiratory compromise
Pneumothorax
Risk factors
➢ Smoking
Types
1. Primary spontaneous
- Occurs without apparent cause
- Most commonly in tall, athletic, thin men aged 20-40 years
- 90% unilateral (commonly at right side)
- Usually caused by rupture of a small subpleural blebs (collection of air < 2cm)
- Presented with dyspnea, chest pain, cough & tachypnea
- Ipsilateral decreased chest wall movement, hyper-resonant hemithorax to percussion
2. Secondary spontaneous
- Occurs in presence of existing lung pathology (e.g. Asthma, COPD)
3. Simple pneumothorax
- Non-expanding collection of air around the lung
4. Tension pneumothorax [one-way valve]
- Expanding collection of air around the lung
Investigation
➢ Chest X-ray ➝ Diagnostic
- Visible lung edge and absent lung markings peripherally
➢ ABG ➝ if patient is dyspneic, cyanosed or there’s an underlying condition
Tension pneumothorax
Hemothorax
Presentation • NO distended neck veins
• Acute respiratory distress • NO tracheal deviation
• Hypotension • Usually caused by stabbing injuries
• Raised JVP Management of 2ry spontaneous pneumothorax

• Tracheal deviation away from the pneumothorax side • >2 cm (50%) OR Hypoxic ➝ Chest drain
• Reduced air entry on affected side • <2 cm (50%) ➝ Cannula insertion
Management
1. Initial ➝ High flow O2
2. Insert large-bore cannula into 2nd intercostal space in midclavicular line (just above 3rd rib) on side of
pneumothorax – hiss sound is from the air escaping and confirms the diagnosis
3. Do NOT wait for chest X-ray if the patient is seriously compromised or cardiac arrest has occurred or if the
diagnosis is clinically certain
4. Air should be aspirated until the patient is less distressed, then insert a chest drain in mid-axillary line,
leaving the cannula in place until you’ve finished and the underwater seal is bubbling satisfactorily
5. Always perform a chest X-ray post chest drain insertion to ensure the drain is appropriately placed
➢ Engorged neck veins indicate high pressure in the right ventricle, seen in both tension pneumothorax and
cardiac tamponade
• Beck’s triad for cardiac tamponade

1. Engorged neck veins
2. Hypotension
3. Muffled heart sounds (Vs. reduced air entry and tracheal deviation in tension pneumothorax)
Causes of post-operative breathlessness

• Infection/atelectasis
- Occurs early (within hours)
- Common in smokers
• Pulmonary embolism
- Occurs early (within hours/days)
• Left ventricular failure (LVF) (fluid overload)
• Exacerbation of underlying disease such as COPD
• Tension pneumothorax
Atelectasis
➢ The collapse or closure of a lung resulting in reduced or absent gas exchange (Reduced air entry)
➢ History of smoking
Management
• Analgesia ➝ To encourage expectoration
• Atelectasis → Alveoli either deflated or filled
• Nebulized saline with alveolar fluid
• Chest physiotherapy • Pneumonia may happen in about 3 days if
• Deep breathing and coughing atelectasis is not resolved. If this happens, fever
• Postural drainage will persist and X-ray will show infiltrates
• Incentive spirometry
• If lung doesn’t re-inflate ➝ Bronchoscopy to suction out secretions
Bronchiectasis
➢ Irreversible dilatation of small and medium sized bronchi, with chronic airway inflammation destroying their
elastic and muscular structure
➢ It’s associated with chronic sputum production, chronic cough, recurrent acute chest infections and airflow
obstruction ➢ Bronchial obstruction and bronchopneumonia are
Etiology more likely to cause a focal bronchiectasis, whereas
• Infection ➝ Most common other causes are more likely to result in diffuse disease
- Childhood respiratory viral infections (e.g. measles, pertussis, influenza, respiratory syncytial virus)
- TB
- Bacterial pneumonia ➝ Look out for history of recurrent pneumonia
• Immunodeficiency
-HIV ➝ Serious, persistent or recurrent infections
• Connective tissue diseases
- RA
- Sjogren’s $
- Systemic sclerosis
- SLE
- Ehlers-Danlos $
- Marfan’s $
• Toxic insults
- Gastric aspiration
- Inhalation of toxic gases
• Congenital defects
- Cystic fibrosis ➝ Most important to exclude
Features
o Persistent cough with purulent COPIOUS/CUP sputum production (with specks of blood)
o Nonspecific respiratory symptoms including dyspnea, chest pain and hemoptysis. It may progress to
respiratory failure and cor pulmonale
o Coarse crackles (early inspiration and often in the lower zones) ➝ Most common finding
o Large airway rhonchi (low-pitched snore-like sounds)
o Wheezes
o Clubbing
Diagnosis
• Usually made clinically, with High-resolution computed tomography (HRCT) ➝ Gold standard
• A baseline chest X-ray should be done for all patients
- Mainly for exclusion
- Tramlines + hx of lung infection
- In advanced cases, it may show 1-2cm cysts
Management
Damaged lungs cannot be repaired, so the aim is to prevent or at least slow down any further deterioration
• Bronchodilators, chest physical therapy and postural drainage
• Cessation of smoking
• Immunization against influenza and pneumococcus
• Long-term oral antibiotics
- For patients having 3 or more exacerbations per year
- Patients with significant morbidity
Mesothelioma
➢ Malignant mesothelioma is a tumor of mesothelial cells that usually occurs in the pleura, rarely in peritoneum
➢ Associated with occupational exposures to asbestos (history of being a builder)
➢ Latent period between exposure and development of the tumor may be up to 45 years
➢ Deaths are reported to the coroner as it’s an industrial disease
Deaths reported to the coroner first:
Features
- Deaths due to (accidents, suicide,
• SOB, chest pain, weight loss ➝ Most common symptoms
violence, neglect, industrial disease)
• Finger clubbing - Sudden deaths within 24h after
• Recurrent pleural effusion admission
Signs of metastasis - Deaths of a person who hasn’t seen a
doctor with 14 days before death
• Lymphadenopathy - Unknown deaths
• Hepatomegaly - Deaths during a surgical operation or
• Bone pain and tenderness before recovery from anesthesia
- Deaths during police custody
• Abdominal pain or obstruction (peritoneal malignant mesothelioma)
Investigation
• Chest X-ray ➝ Pleural thickening or effusion
• Approximately 95% of all primary lung
• Thoracoscopy under local anesthetic: tumors are bronchial carcinomas
- Pleural fluid aspiration and cytological analysis ➝ very sensitive • 1ry bronchial carcinoma
- SCLC
Pleural biopsy ➝ Most definitive
-
- NSCLC
-
It also enables drainage of pleural fluid, and pleurodesis • Adenocarcinoma accounts for 39% of
• The diagnosis is often made post-mortem NSCLCs and is the most common
Management bronchial carcinoma associated with
asbestosis and is more common in non-
• Usually symptomatic
smokers, compared with other all types
• Cure is only possible with surgery for localized (stage I) • Investigation for central tumors ➝
Bronchoscopy + biopsy
Paraneoplastic syndromes
• When cancer-fighting antibodies (WBCs) mistakenly attack normal cells in the nervous system
• Often associated with SCLC
• SCLC ➝ Lambert-Eaton $ (proximal muscle weakness, depressed tendon reflexes & autonomic changes) +
Hyponatremia due to SIADH + Hypokalemia (increased mineralocorticoid activity)
• Sq. cell ➝ Hypercalcemia due to PTH like action
Extrinsic allergic alveolitis/Hypersensitivity pneumonitis

• Due to repeated inhalation of organic antigens in dusts (e.g. from dairy or grain products, animal dander and
protein and water reservoir vaporizers)
• Occupational risk: farmers, vets, bakers and people dealing with chemicals
• Chest X-ray ➝ Diffuse micronodular interstitial shadowing
• There are 3 forms of extrinsic allergic alveolitis
1. Acute
- Symptoms start 4-8h after exposure to the sensitizing antigen and resolve quickly, within days
- Flu-like illness with fever, chest tightness, dry cough, dyspnea
- Associated symptoms: malaise, chills, headache, generalized aches and pains. Sometimes wheezes
- Signs: fever, tachypnea and bi-basal fine respiratory crackles
2. Subacute
3. Chronic
Sarcoidosis
➢ A systemic disease of unknown cause
➢ Characterized histologically by the presence of non-specific non-caseating granulomas in the lungs and other
organs
Presentation
• Up to 50% are asymptomatic (discovered accidently by chest X-ray ➝ Hilar adenopathy)
• Involves almost any organ system but pulmonary is the most common
• Fever, Fatigue
• Skin: erythema nodosum
• Eyes: Uveitis
• Kidneys: Stones
• Lymphadenopathy
Heerfordt-Waldenstrom $ Lofgren $
- Parotid enlargement - Hilar adenopathy
- Uveitis - Erythema nodosum
- Fever - Arthritis
- Facial palsy
➢ Heerfordt tried a PUFF of steroid but did not HEAL

Investigation
• Chest X-ray ➝ Bilateral hilar lymphadenopathy
• Bloods
- Raised ACE (60% of patients, not specific but used to
follow the course of the disease)
- Abnormalities in LFTs (30% of patients)
- Hypercalcemia (due to increased circulation of vitamin
D produced by macrophages)
• Biopsy (definitive diagnosis) ➝ Non-caseating granulomas
- Can be from skin, LN, conjunctiva or lung
Treatment
• Steroids • Lung + kidney ➝ Goodpasture $
• Lung + GIT ➝ Cystic fibrosis
Pancoast tumor • Lung + eye ➝ Pancoast tumor
➢ A tumor of the pulmonary apex

➢ Defined primarily by its location situated on top of end of
either right or left lung
Presentation
• Ipsilateral invasion of cervical sympathetic plexus ➝ Horner’s $
(ptosis, myosis, anhidrosis + enophthalmos)
• Brachial plexus invasion ➝ Muscle wasting of the intrinsic
hand muscles and paresthesia in the medial side of the arm
along with shoulder and arm pain
• RLN compression ➝ HOV
Notes
• Patient works as a farmer or a baker ➝ Extrinsic allergic alveolitis/hypersensitivity pneumonitis

• Pt works at a pet shop ➝ [Ch]lamydiophilia pisittaci ➝ Rx with [Cl]arithromycin
• Pt was in anything starts with [H] like Hospital, hostel, hotel, hot tub ➝ Legionella
• Bilateral cavitation in the lung (for any reason) + pneumatoceles ➝ Staph
• Upper lobe cavitation on CXR ➝ Klebsiella ➝ Rx with Cephalosporin (Keflex)
• Bilateral Patchy consolidation, Myalgia + peri-hilar shadowing on CXR, dry cough, target lesions on back of the
hands (erythema multiform) ➝ Mycoplasma
• Lobar consolidation on CXR ➝ Strept (G +ve cocci) ➝ Most common cause of community-acquired
pneumonia
• Bi-basal consolidation ➝ Legionella
• Peri-hilar interstitial shadowing ➝ Carinii
• Diffuse micronodular interstitial shadowing ➝ Extrinsic allergic alveolitis
• Rusty-colored sputum ➝ Strept
• Currant jelly ➝ Klebsiella
• Green ➝ Pseudomonas
• Purulent ➝ Staph
• Pneumonia + neurological signs ➝ Legionella
• Fever + murmur + pneumonia ➝ Coxiella burentti
• Pneumonia + herpes labialis ➝ Strept or Carinii
• Reticular infiltrations + ground-glass appearance ➝ Viral/Atypical pneumonia (mycoplasma/legionella)
• Pneumatoceles ➝ Staph
• Asbestoses ➝ Mesothelioma
• Coal mining ➝ Coal worker’s pneumoconiosis (CWP) ➝ Progressive massive fibrosis
• Central lung cancers ➝ Sq. cell + Small cell
• Peripheral lung cancers ➝ Adenocarcinoma + Large cell
• Keratin pearls + intercellular bridges ➝ Sq. cell
• Oat cell + neuroendocrine involvement ➝ Small cell
• Glandular + mucin producing ➝ Adenocarcinoma
• Anaplastic + undifferentiated sheets/nests of polygonal/multinuclear cells ➝ Large cell
• Most common lung cancer in non-smokers ➝ Adenocarcinoma
• A lung cancer with a strong smoking history ➝ Sq. cell
• Hemithorax ➝ One side of the chest
• Erythema nodosum ➝ Sarcoidosis
• Erythema multiforme (target lesions at the back of the hand) ➝ Mycoplasma pneumonia
• Post-flu illness ➝ Staph
• Hyponatremia ➝ Legionella
• Terminal case with noisy breathing ➝ Terminal respiratory secretions (death rattle) ➝ Hyoscine SC
(Scopolamine) or Glycopyrronium
• Pleurodesis ➝ a procedure that uses medicine to adhere lungs to the chest wall
• Corticosteroid inhalers can lead to oral thrush → Spacers help steroids to get straight to the lungs as opposed
to the oral cavity
• Non-caseating granulomas → Sarcoidosis, Caseating granulomas → TB
Rheumatology
Ankylosing spondylitis
➢ An HLA-B27 associated spondyloarthropathy which primarily involves the axial skeleton (i.e. sacroiliitis and
spondylitis)
➢ It’s classified as a seronegative spondyloarthropathy, a group of diseases that are negative for rheumatoid
factor
➢ Common in patients with IBD
Features
• Young man (<30 years old) presenting with lower back
pain and stiffness
• Stiffness which is worse in the morning and improves
with exercise
• A strong association with HLA-B27
• There is often tenderness of the sacroiliac joints or a
limited range of spinal motion
Examination
• Schober's test
- A line is drawn 10 cm above and another line 5 cm
below the back dimples (dimples of Venus)
- The distance between the two lines should increase by more than 5 cm when the patient bends as far
forward as possible
Other important features
- Anterior uveitis (20-30%) → presents with an acutely painful red eye
and severe photophobia
- Aortic regurgitation
Investigations
• Plain x-ray of the sacroiliac joints → This is the most useful
investigation
- It would show evidence of sacroiliitis which is the earliest finding
- Later findings once there is significant chronic spine inflammation
include a “bamboo spine” and squaring of the vertebral bodies
• MRI → more sensitive in demonstrating sacroiliitis
• DO NOT use HLA-B27 to make the diagnosis as it is also positive in 10%
of normal patients
• Elevated ESR and CRP
• FBC → normochromic normocytic anemia
Management
- First line → NSAIDS
- Second line → Anti-TNF therapy
PEPSI
P → Pain lower back

E → Eye symptoms (anterior uveitis)
P → Progressive loss of special movements
S → Stiffness
I → IBD
Rheumatology
Gout
➢ A disease that affects middle-aged men and presents most commonly with acute Monoarthritis
➢ The metatarsophalangeal joint of the first toe is commonly affected (podagra), but other joints like the knee,
ankle, PIPs, or DIPs may be initially involved
➢ The first episode commonly occurs at night with severe joint pain waking the patient from sleep
➢ The joint rapidly becomes warm, red, and tender (it looks exactly like cellulitis). Without treatment the joint
pain goes away spontaneously in 2 weeks
➢ Certain events that precipitate gout sometimes precede the attack → a person has consumed excessive
amounts of alcohol or started taking diuretics such as thiazide diuretics (xipamide, metolazone, indapamide)
or furosemide → could be indirectly stated by mentioning a cardiac patient
➢ Gout can be associated with: PRV, CML, TL$, Psoriasis
Diagnosis
• Diagnosis is made by → Joint aspirate for microscopy → MSU crystals
• MSU crystals deposit → Tophi
• The serum uric acid during the acute attack may be normal or low and shouldn’t be measured until 4 weeks
after an acute attack → no value in the diagnosis of acute urate arthropathy
Treatment
• Acute management
- NSAIDs (naproxen) → 1st line unless the patient has asthma or renal insufficiency, often prescribed with
PPIs for gastric protection and in elderly
- Colchicine (SE → diarrhea and nausea), should be avoided in renal insufficiency as well
- Intra-articular steroid injection, could be given as tablets or IM, prescribed if asthma or renal insufficiency
• Chronic hypouricemic therapy
- Allopurinol should not be started until 2 weeks after an acute attack has settled as it may precipitate a
further attack if started too early, used to prevent recurrence not to treat
- NSAID or colchicine cover should be used when starting allopurinol
Drugs that precipitate gout [FACT] + Niacin

F → Furosemide
A → Alcohol
C → Cytotoxic drugs/cyclosporine
T → Thiazide
Pseudogout
➢ Usually involves larger joints (knees and ankles)
➢ There should be a history of hemochromatosis or hyperparathyroidism
Diagnosis
• Joint aspirate → calcium pyrophosphate (rhomboid crystals), +ve birefringence
Rheumatoid arthritis
Management
• Acute → NSAIDs (ibuprofen, naproxen), PPIs are used to prevent GI bleed
• Long-term → DMARDs (methotrexate, hydroxychloroquine, sulfasalazine)
Rheumatology
Septic arthritis
➢ The two most common organisms:
- Staphylococcus Aureus → Most common pathogen for septic arthritis overall
- Neisseria gonorrhoeae → Seen in young, sexually active adults
➢ Mode of infection:
- Hematogenous spread during transient bacteremia
- Through a skin lesion that penetrates the joint
- Local spread from a contiguous infected site
Knee is involved in more than 50% of cases
Risk factors
• Prior joint damage (rheumatoid arthritis, gout, osteoarthritis)
• Immunodeficiency states (HIV, corticosteroid use)
• Diabetes
Presentation
• Single swollen, red joint with pain on active or passive movement
• Restricted joint movement
• Fever and rigors ➢ Remember this triad of fever, pain and impaired range of motion
Investigations
• Aspiration of synovial fluid → Sent for gram staining, leukocyte count, microscopy and culture
• Blood cultures → Remember most cases of septic arthritis are due to hematogenous spread
Management
• Flucloxacillin for 4 to 6 weeks → IV antibiotics should be commenced before culture’s results
• If penicillin-allergic → Use clindamycin
• If gonococcal arthritis (NG) → Use cefotaxime or ceftriaxone
• If infection not responding to antibiotics → Perform repeated percutaneous aspiration
In general, intravenous antibiotics are used for 7 days until the swelling subsides and blood cultures become
negative. This is followed by a 4-week course of oral antibiotics
Reactive arthritis
➢ A form of seronegative spondyloarthritis clinically associated with back pain, migratory oligoarthritis
(affecting two to four joints during the first six months of disease) and extra-articular symptoms
➢ Typically follow a GI (campylobacter, salmonella, shigella) or urogenital infection (chlamydia trachomatis)
➢ The initial infection may be so mild it goes unnoticed
➢ Unlike septic arthritis, fever is not a typical feature however it can be seen
Features
• Young adults
• Develops 2-4 weeks after an initial infection which have been sexually acquired or gastrointestinal in origin
• Asymmetrical, especially lower extremity, oligoarhtritis in the major symptom (usually knees and ankles)
• Reiter triad [can’t see, can’t pee, can’t climb a tree]→ conjunctivitis/anterior uveitis + urethritis + arthritis
• Skin
- Circinate balanitis → painless vesicles on the coronal margin of the prepuce (foreskin)
- Keratoderma blennorrhagicum → waxy yellow/brown maculopapular rash seen on palms and soles
- Erythema nodosum → tender red nodules on the shins
Treatment
• NSAIDs
Rheumatology
Polymyositis
Features
• Muscle weakness involve the proximal muscles: lifting objects, combing hair, getting up from the chair
• Weakness usually symmetric and diffuse, involving the proximal muscles of the neck, shoulders, trunk, hips
and thighs. LL muscles tend to be clinically symptomatic first
• Fatigue, myalgia and muscle cramps
• Advanced cases: dyspnea and dysphagia
Investigation
• Raised CK
• Raised Aldolase level
• Autoantibodies: Anti-Jo-1 antibodies. Note that these are common in patients with polymyositis than in
patients with dermatomyositis
• Muscle biopsy can be diagnostic
Treatment
• Steroids
Polymyositis Polymyalgia rheumatica
• Stiffness not weakness

• Difficulty to raise hands above head
• Weakness of the proximal muscle + raised CK • Fever + weight loss
• Associated with breast/lung cancer • ESR> 30mm/h or CRP> 6mg/mL
• CK is NOT raised
• Associated with Temporal arteritis (TA)
Chronic fatigue syndrome (CFS) or Myalgic Encephalomyelitis (ME)

➢ Severe fatigue + unrelated to exertion or triggered by minimal activity + unrelieved by rest
➢ All tests are normal
➢ Sometimes the symptoms start with a viral infection and it keeps progressing
Features
• Persistent or recurrent fatigue
• Fatigue unexplained by other conditions
• Difficulty sleeping
• Muscle and joint pain at multi-sites without evidence of inflammation
• Painful lymph nodes without pathological enlargement
• Headaches
• Cognitive dysfunction (difficulty thinking, concentrating or finding words)
Rheumatology
Systemic lupus erythematous (SLE)
➢ Whenever patient has multi-system involvement + raised ESR + normal CRP → SLE
Features
• Remitting and relapsing illness
• Mouth ulcers → large, multiple and painful
• Lymphadenopathy
• Malar (butterfly) rash, sparing nasolabial folds
• Discoid rash: scaly, erythematous, well-demarcated rash in sun-exposed areas
• Photosensitivity
Most common drugs causing induced Lupus
• Arthralgia
• Hydralazine
• Raynaud’s phenomenon, occurs in 1/5 of the patients • Isoniazid
• Cardiovascular → pericarditis • Procainamide
• Respiratory → pleurisy, fibrosing alveolitis
• Renal → AGN, often asymptomatic and detected by proteinuria, hypertension or a raised serum urea and
creatinine
• Neuropsychiatric → anxiety and depression
Investigation
• FBC and ESR • Highly sensitive tests are used to screen (initial tests)
- Mild anemia while highly specific tests are used to diagnose
- Raised ESR
• Autoantibodies
- ANA → most sensitive (95%) but not diagnostic in the absence of clinical features
- Anti-dsDNA → highly specific (>99%), but less sensitive (70%)
- Anti-Smith → most specific (>99%), but even less sensitive (30%-40%)
- Anti-histone → drug-induced lupus ANA antibodies are often this type
- Rheumatoid factor → positive in 20%
• Complement levels (C3, C4) → low during active disease (formation of complexes leads to consumption of
complement)
SLE [SOAP BRAIN MD]

S → Serosis (pleuritis, pericarditis)
O → Oral ulcers
A → Arthritis
P → Photosensitivity
B → Blood (all are low; Anemia, Leukopenia, Thrombocytopenia)

R → Renal (AGN)
A → ANA
I → Immunological (Anti-dsDNA)
N → Neurological (psych, seizures)
M → Malar rash
D → Discoid rash
Rheumatology
Churg-Strauss Syndrome
➢ Also called “eosinophilic granulomatosis with polyangiitis” or “allergic granulomatosis”
➢ Rare diffuse vasculitis affecting coronary, pulmonary, cerebral, abdominal visceral and skin circulations
➢ The vasculitis affects small- and medium-sized arteries and veins and is associated with asthma
➢ The cardinal manifestations of Churg-Strauss syndrome are Asthma, Eosinophilia, and Lung involvement
Six criteria (4/6 is diagnostic)
• Asthma (wheezing, expiratory rhonchi)
• Eosinophilia of more than 10% in peripheral blood
• Pulmonary infiltrates (may be transient)
• Paranasal sinusitis
• Histological confirmation of vasculitis with extravascular eosinophils
• Mononeuritis multiplex (peripheral neuropathy)
Presentation
• Pulmonary → asthma
• Upper respiratory tract → allergic rhinitis, paranasal sinusitis, nasal polyposis
• Cardiac involvement is common → heart failure, myocarditis and myocardial infarction
• Skin → purpura, skin nodules
• Renal → glomerulonephritis
• Peripheral neuropathy → mononeuritis multiplex is the most frequent form
Investigations
• P-ANCA → +ve
• FBC → Eosinophilia and anemia
• Elevated ESR and CRP
• Elevated serum creatinine
• Increased serum IgE levels
• CXR → pulmonary opacities, transient pulmonary infiltrates, and bilateral multifocal consolidation
• High-resolution CT → Ground-glass attenuation
• Biopsy → small necrotizing granulomas, as well as necrotizing vasculitis (found especially in the lung)
Granulomatosis with polyangiitis (GPA) or Wegner’s granulomatosis

➢ Idiopathic small to medium vessel vasculitis
➢ Appears around middle-age
➢ A person bleeding from his nose, lungs and kidneys
Features
• URTIs
- Nosebleeds • Churg-Strauss → P-ANCA
- Nasal crusting • Granulomatosis with polyangiitis → C-ANCA
- Chronic sinusitis
• Lungs
- Hemoptysis
- Cough • Jaundice + hemoptysis → alpha 1 anti trypsin deficiency
• Hematuria + hemoptysis → good pasture syndrome
• Kidneys
• Hematuria + hemoptysis + nasal crusting + nosebleeds → GPA
- Hematuria
Investigation
• +ve C-ANCA
Rheumatology
Temporal arteritis (TA) or Giant cell arteritis (GCA)
➢ Vasculitis that affects the large arteries that supply the head, eyes and optic nerves
➢ New onset headache in any patient older than 50 years prompts consideration of this diagnosis, which if left
untreated may result in permanent vision loss
Features
• Headache → usually occurs in one or both temples
• Scalp tenderness, when comping hair
• Jaw claudication, pain when shewing
• Decreased/blurry vision, rarely sudden loss of vision
• Tongue numbness
+ Proximal stiffness (neck, arms, hips) due to polymyalgia rheumatica, a co-existing condition with TA
Investigation
• ESR → initial test
• Biopsy of the temporal arteries → Characteristic giant cells → confirmatory
Management
o Elevated ESR → Steroids (prednisolone) should be started immediately, before the biopsy is performed
o Add-on drugs
- Low-dose aspirin 75mg → reduces the rate of visual loss and strokes
- Bisphosphonates → reduces the risk of osteoporosis as a result of steroids especially in an elderly
female
Rheumatology
Sjogren’s $
➢ Autoimmune disorder affecting exocrine glands resulting in dry mucosal surfaces
➢ May be seen alone or in association with other autoimmune diseases (secondary) such as rheumatoid
arthritis, primary biliary cirrhosis or SLE
➢ As it progresses, it becomes a systemic disease involving major organs (lungs, kidneys, etc.) and may
eventually evolve into a lymphoproliferative disease → malignant lymphoma
➢ Much more common in females (9:1)
Features
• Dry eyes (keratoconjunctivitis sicca)
- Itchy eyes, sandy feeling under their eyes (because of decreased lacrimal production)
• Dry mouth
- Patients may complain of dysphagia
- Can cause altered sense of taste
- Dry throat can lead to hoarseness of voice
• Vaginal dryness
• Bilateral parotid enlargement
Investigation
• Schirmer’s test → decreased tear production
• Rose Bengal stain → corneal ulceration
• ANAs → +ve, especially anti-Ro (SSA) and anti-La (SSB) [ROLA has Sjogren’s S]
• Rheumatoid factor → +ve
Management
• There’s no cure
• Artificial tears may help with the dry eyes (Hypromellose)
• Pilocarpine can also be used to stimulate the tear production
Mikulicz’s syndrome
➢ Persistent swelling of lacrimal and parotid (or submandibular) glands due to lymphocytic infiltration
➢ When no specific cause is found → Mikulicz’s disease, if 2ry to diseases like sarcoidosis or tuberculosis →
Mikulicz’s $
➢ If associated with sarcoidosis → bilateral perihilar lymphadenopathy may be present due to sarcoidosis
Features
1. Symmetrical enlargement of ALL salivary glands
2. Narrowing of the palpebral fissures due to enlargement if the lacrimal glands
3. Dryness of the mouth
- Both Mikulicz and Lofgren can be associated with sarcoidosis. However, Lofgren $ is characterized by erythema
nodosum, arthritis and bilateral hilar lymphadenopathy
- Sarcoidosis → non-caseating granulomas on biopsy
- TB → Caseating granulomas
Rheumatology
Limited scleroderma vs Diffuse scleroderma
Limited scleroderma (CREST $) Diffuse scleroderma (systemic sclerosis)

Skin • Limited areas of skin are thick; usually • More areas are involved and thickened
just the fingers and/or face • Arms, legs and trunks are more affected
• Skin involvement doesn’t extend
above the elbow or above the knee
• NO trunk involvement
Onset • Slow • Rapid
Progression • Slow • Rapid
Length of skin • Raynaud’s phenomenon for many • Skin changes within 1 year of Raynaud’s
changes from years before any skin changes
Raynaud’s
phenomenon
Organ • Milder → less involvement • More severe → involvement of GIT, heart,

involvement • Lung involvement can be seen but lungs or kidneys
usually milder and less common
others CREST syndrome may be present • The skin can lose or gain pigment, making
areas of light or dark skin
• Calcinosis (Ca deposits)
• Raynaud’s phenomenon
• Esophageal dysmotility
• Sclerodactyly
• Telangiectasia (spider naevi)
Antibodies • Most have positive ANA • Most have positive ANA

• Antibodies to Scl-70 are usually • Anti-Scl-70 are usually positive (60%)
negative
Anti-Scl 70 is strongly associated with lung fibrosis
• Anti-centromere positive
and renal disease besides poor prognosis
Reynaud’s phenomenon
➢ Sudden episodes of pallor or cyanosis in response to cold or emotional stimuli
➢ Patients complain of cold sensitivity with other areas of skin affected (ears, nose and lower extremities)
➢ Attacks may begin in one or two fingers but typically involve all fingers and/or toes symmetrically and
bilaterally
➢ Could be secondary or associated with another disease (scleroderma)
- Vasoconstriction of blood vessels → Ischemia → pale

- Deoxygenation → blue
- After rewarming the hands, the blood flow will rebound (Reactive hyperemia) → red
Rheumatology
De Quervain’s tenosynovitis
• Also called “Washerwoman sprain”, “Mummy thumb” or “Gamer’s Thumb”
• Caused by inflammation of the extensor pollicis previs and the abductor pollicis longus due to repetitive
stress injury
• Commonly occurs at in women following pregnancy due to the way in which the baby is lifted and held
Urology
Prostate cancer
Risk factors ➢ PSA isn’t specific for prostate cancer but it’s
• Increasing age useful in follow-up & monitoring TTT
➢ Before PSA test, men should NOT have:
• Male, black Afro-Caribbean - An active UTI
• 1st degree relative with prostate cancer - Ejaculated in the past 48h
Presentation - Exercised vigorously in the past 48h
• Lower urinary tract symptoms (LUTS) are NOT specific for - Had a prostate biopsy in the last 6 weeks
prostate cancer
• LUTS include voiding or obstructing symptoms such as hesitancy, urgency, poor and/or intermittent stream,
straining, prolonged micturition, feeling of incomplete bladder emptying, dribbling
Investigation
• Initial → DRE (hard, irregular & nodular) + PSA Biopsy-related prostatitis
• Normal ⟶ E. coli
- ≥2 ng/ml at age 40-49 years
• Immunocompromised ⟶ Pseudomonas aeruginosa
- ≥3 ng/ml at age 50-69 years
- ≥5 ng/ml at age 70 years or older
• Definitive → Biopsy Leuprolide is a GnRH analog:
Management • If used in pulsatile fashion → agonist
➢ Leuprolide, used in a continuous manner • If used in a continuous fashion → antagonist
Local disease Locally invasive Metastatic
• Raised PSA on screening • Hematuria • Bone metastasis → hypercalcemia → thirst

• LUTS • Hematospermia • Bone pain or sciatica
• UTI • Obstruction of ureters, • Paraplegia 2ry to spinal cord compression
causing loin pain, anuria, • LN enlargement
symptoms of AKI or CKD • Lethargy (anemia, uremia)
• Weight loss
➢ KUB US
➢ MRI
Metastatic spinal cord compression

➢ An oncological emergency and an urgent MRI should be requested within 24h
➢ 20% of patients with spinal metastasis
Features
• Neurological symptoms like radicular pain, limb weakness, difficulty in walking, sensory loss or bladder or
bowel dysfunction
• Neurological signs of spinal cord or cauda equina compression
➢ DO NOT confuse between metastatic spinal cord compression and spinal • Spinal metastasis + symptoms of
metastasis. Spinal metastasis presents with pain in the thoracic or upper decompression → MRI
cervical spine, progressive lumbar spine pain or nocturnal spinal pain • Spinal metastasis WITHOUT symptoms
of compression→ Isotope scan
preventing sleep. Spinal metastasis isn’t considered emergency
➢ Most frequent sites for metastasis for prostate cancer are bone (by hematogenous spread) and lymph nodes of
the obturator fossa, internal, external and common iliac arteries and presacral regions
• Prostate cancer → Bone + LN
• Testicular cancer → LN + Lungs
Urology
Benign Prostatic Hyperplasia (BPH)
➢ An old male complaining of LUTS
➢ DRE reveals a large, firm and smooth prostate
Interstitial cystitis
Features
• Recurrent suprapubic pain
• Worsened by bladder filling
• Relieved by voiding but returns when bladder fills again
• LUTS: urine frequency, urgency & nocturia
• In women, symptoms are often worse during menstruation
Investigation
• Cystoscopy, to exclude bladder malignancy
- 10% have Hunner’s ulcers, they’re reddened mucosal areas
associated with small vessels radiating towards a central scar
- Glomerulations (petechial red areas)
Management
• 1st line
- Bladder training
- Pelvic floor relaxation techniques (avoid pelvic floor exercises)
- Avoid triggers like coffee, citrus fruits or smoking which can exacerbate symptoms
- Analgesics such as NSAIDs
• 2nd line
- Amitriptyline
- Oxybutynin
- Gabapentin
Pyogenic cystitis
- LUTS
- Fever
- Nitrates and leukocytes in urine
Bladder stones are rare in women
Urology
Bladder cancer
➢ Mostly transitional cell carcinoma ➢ Whenever you see painless, gross
hematuria in an elderly male, you should
➢ Presents with painless visible hematuria
immediately be thinking of cancer
Risk factors
• Smoking – the major cause
• Occupational exposure (industrial plants processing paint, dye (aniline), metal and petroleum products)
• Male
• Increasing age
Investigations of Hematuria
• After a UTI has been excluded or treated, all patients with persistent microscopic or macroscopic hematuria
require investigation of their upper tracts, bladder and urethra
- >40 + frank hematuria → Cystoscopy, CTU (CT-urography) & cytology

- >40 + non-visible hematuria OR <40 + hematuria (malignancy less likely) → CT-KUB for stones
- For renal and ureteric malignancy → CTU
• CTU is faster than US or IVU in detecting renal and ureteric tumors. However, it carries a higher radiation
dose and is more expensive. CTU also detects some bladder tumors, but may overcall bladder wall
hypertrophy as tumor and will miss flat CIS and urethral pathology so it cannot replace cystoscopy
Varicocele
➢ Abnormal enlargement of the testicular veins
➢ Incompetent valves of the internal spermatic veins lead to retrograde blood flow, vessel dilatation and
tortuosity of the pampiniform plexus
➢ > 80% on the left side, the left testicular vein opens at a right angle to the left renal vein
➢ 2ry varicocele can be caused by a kidney tumor (causing obstruction of the left testicular vein)
Features
• Classically described as a bag of worms
• Subfertility (due to elevated scrotal temperature
which affects spermatogenesis)
• Usually asymptomatic (rarely causes pain, if so →
scrotal heaviness)
• Swelling from varicocele may demonstrate cough
impulse like hernia and they also tend to
disappear when lying down (gravity allows
drainage of the pampiniform plexus)
Diagnosis
➢ Scrotal doppler US is diagnostic
Management
• Usually conservative → Reassure
• Surgery is occasionally considered if there’s
significant ongoing pain, debatable in managing
fertility
➢ Newly diagnosed varicocele over the age of 40 years is very suggestive of RCC
Urology
Testicular torsion
Key features Other investigations
• Severe sudden onset testicular pain • Color doppler US ⟶ reduced arterial blood
• Usually affects adolescents and young males (<20 years) flow in testicular artery
• Radionuclide scanning ⟶ decreased
• Possible history of trauma
radioisotope uptake
• Could be recurrent ⟶ testis twisting and then spontaneously
resolving ➢ If the clinical suspension is high, surgical
• On examination testis is tender and pain not eased by intervention should not be delayed for the
sake of further investigations
elevation
DD
- In testicular torsion ⟶ lifting the testis up over the • Mumps orchitis
symphysis increases pain - 70% unilateral
- In epididymitis ⟶ usually relieves pain - A week-history of parotitis
Management
➢ Urgent exploratory surgery (detorsion & orchidopexy) is needed to prevent ischemia of the testicle within 6h
Epididymo-orchitis
➢ An infection of the epididymis with or without an infection of the testes resulting in pain and swelling
➢ Most commonly caused by local spread of infections from the genital tract (e.g. chlamydia & gonorrhea)
where there’s a retrograde spread from the prostatic urethra and seminal vesicles
➢ It also could be caused by non-sexually transmitted organism causing UTI (e.g. E. coli)
Features
➢ Epididymo-orchitis in men VS. Salpingitis in women
• Unilateral scrotal pain and swelling
• Tenderness is usually localized to epididymis (may help distinguish from testicular torsion)
• Urethral discharge may be present, but urethritis is often asymptomatic
• Leukocytes & nitrates positive (e.g. E. coli)
• Fever and rigors in severe cases
• Tenderness may be relieved by elevating the scrotum
⟶ +ve Prehn’s sign
Management
➢ Antibiotics
Reiter’s syndrome [AUC]

1. Urethritis
2. Arthritis
3. Conjunctivitis
➢ Triggered by chlamydia infection, and usually in conjugation with HLA-B27
Urology
Testicular cancer
➢ Germ cell tumor mostly
1. Seminoma ⟶ the most common
2. Non-seminoma
➢ Usually present at earlier age (30-34 years old)
Risk factors
• Cryptorchidism (undescended testis), increases the risk 10 times higher ⟶ Orchidopexy at age 6 months
Features
• Painless lump in the body of the testis ⟶ the most common presentation
Diagnosis
• US is the 1st line ⟶ [This should be first line for any scrotal lump]
• CT ⟶ for staging
• Tumor markers ⟶ LDH (seminoma), B-HCG or AFP (non-seminoma)
Complications • No biopsy for testicular cancer for fear of
➢ 2ry spread to the para-aortic LN rather than the inguinal LN seeding
➢ Metastasis is rare, if happens ⟶ LNs, lungs • Enlarged scrotum ⟶ Hydrocele
• Enlarged testis ⟶ Testicular cancer
Epididymal cyst
➢ Derived from the collecting tubules of the epididymis and contains clear fluid
➢ They develop slowly, lie within the scrotum & often multiple (multiloculated)
➢ Most common cause of scrotal swelling seen in primary care
Features - Epididymal cyst ⟶ behind and above
• Painless - Hydrocele ⟶ anterior and below
• Lie behind and above the testis

➢ Epididymal cyst feels as a separate swelling
Diagnosis from testis. However, in hydrocele, testis feels
➢ US as a free-floating mass in scrotum
Management
• Usually supportive but surgical removal may be attempted for larger or symptomatic cysts
Urology
Nephrolithiasis
Risk factors
• Dehydration
• Hypercalcemia (either due to hyperparathyroidism or sarcoidosis -raised vitamin D produced by
macrophages-)
• ADPKD
• Gout ⟶ uric acid stones
• Loop diuretics ⟶ Ca excretion ⟶ hypercalciuria
Features
• Sudden onset flank pain, radiating to the loin/groin
• Nausea and vomiting • Renal colic + joint pain ⟶ uric acid stone
• Hematuria (painful) • Triad of gout = arthritis + nephrolithiasis + tophi
Types
• Ca oxalate ⟶ most common
• Uric acid (radiolucent)
• Struvite stone (staghorn stone) ⟶ alkaline urine (infection with urease producing bacteria, proteus &
klebsiella)
• Cysteine ⟶ a child with recurrent episodes of renal colic
Investigations
• Initial ⟶ X-ray
• If suspect a radio-lucent stone ⟶ US
• Most accurate ⟶ non-contrast CT
- It can also exclude other causes of acute abdomen (e.g. ruptured AAA)
Management
• <5 mm ⟶ manage conservatively by increasing fluid intake ➢ Ca stones ⟶ Thiazide diuretics
➢ Uric acid stones ⟶ K citrate
• 5-10 mm ⟶ medical therapy using CCB, analgesics and steroids
with increased fluid intake ➢ Besides increasing fluid intake, patient
• 10 mm – 2 cm ⟶ ESWL or uteroscopy (using dormia basket) can be treated with:
• >2 cm (large and complex stone) ⟶ percutaneous 1. Tamsulosin (relaxes the bladder
neck)
nephrolithotomy
2. Diclofenac (NSAID)
• Staghorn ⟶ surgery
An urgent percutaneous nephrostomy or uretic stent (JJ) may be needed

1. Infection + obstruction (fever, tender loin & pyuria)
2. Urosepsis (altered mental state, systolic blood pressure ≤ 100 mmHg, respiratory rate >22 breath/min)
3. Intractable pain or vomiting
4. Impending AKI (azotemia or elevated creatinine and BUN)
5. Obstruction in a solitary kidney
6. Bilateral obstructing stones
➢ For ureteral stones

- <5 mm → conservative
- >5 mm → CCB and Tamsulin, most pass in 48h, if not → ESWL or ureteroscope
- Larger stones, multiple or complex → percutaneous nephrolithotomy
Urology
Post-op ureteric injury
➢ May present in the first few days following surgery but it may also be delayed by weeks
➢ One of the most serious complications during gynecological & abdominal surgeries
➢ Ureter could be divided, ligated, angulated by a structure or damaged by a diathermy
Features
• Ileus (due to urine in the peritoneal cavity)
• Fever
• Flank pain (if the ureter has been ligated) ➢ Any investigation involving contrast media CANNOT
be given in case of impaired renal function
• Abdominal pain
• Abdominal distension
• Retroperitoneal urinoma (a collection of urine)
• Urinary leakage (vaginally or via abdominal wound)
Investigations
• Intravenous urography (IVU)
- Shows an obstructed ureter, extravasation of the dye from the site of injury or hydronephrosis
- The best imaging modality to evaluate the continuity of the ureter in cases of ureteral injury after an
operation
• Renal US
- Best non-invasive method to visualize the kidney
- Best when renal function is impaired
- Shows hydronephrosis or retroperitoneal urinomas. However, it CANNOT assess the ureteric continuity
• CT with contrast
• Retrograde urethrogram
Vesicovaginal fistula
➢ A continuous involuntary discharge of urine into the vaginal vault
➢ A possible complication after gynecological procedures (hysterectomy)
➢ A 3-swab test could identify a vesicovaginal fistula
- 3 gauze swaps placed into the vagina using a speculum (top, middle &bottom)
- Blue dye is inserted to the bladder by passing through a catheter
- Catheter is removed and the patient is asked to walk around for an hour without urinating
- Then, swabs are taken and evaluated for blue dye
Urology
Syphilis
➢ An STI caused by Treponema pallidum
➢ More common in homosexuals
➢ Acquired syphilis is characterized by primary, secondary and tertiary features
Incubation period
• Around 3 weeks • Single painless genital ulcer → Syphilis
Features • Single painful ulcer → Ducreyi
1. Primary features • Multiple painful ulcers → HSV
- Chancre, painless ulcer at the site of sexual contact
- Local non-tender lymphadenopathy
- In women, they’re found on the vulva, labia and can also be found on the cervix or within the anal canal
2. Secondary features
- Appears 6 weeks after beginning of the primary lesion but may overlap or not appear for several months
- Systemic symptoms: fever, lymphadenopathy, headache, malaise
- A generalized polymorphic rash often affect the palms, soles and face
- Papules enlarge into condylomata lata (pink or grey discs) in moist warm areas
3. Tertiary features
- Gummas (granulomatous lesions can occur in any organ but most commonly affect bone and skin)
- Cardiovascular syphilis → ascending aortic aneurysms, AR
- Neurological syphilis → tabes dorsalis, dementia
Investigations
• Visible ulcer or infected LN → (GP → PCR // GUM physician → Dark field microscopy)
• Healed ulcer → Serology (VDRL, TPHA or treponemal antibody absorption)
Management
➢ Benzathine penicillin + oral azithromycin
• Certain strains of Chlamydia can cause painless ulcer
+ lymphogranuloma venereum
DD of rash on palms and soles
• Classically found un Africa, India and Caribbean
1. 2ry Syphilis by Treponema pallidum • Outbreaks are possible in MSM
2. Hand, foot, mouth disease by Coxsackie virus
3. Rocky mountain spotted fever by rickettsia
Genital Herpes Simplex

➢ May be asymptomatic, or may remain dormant for months or even years
➢ When symptoms occur after infection, they tend to be severe
➢ It can be a chronic, lifelong infection
➢ Mostly caused by HSV-1 (most common cause of both orolabial and genital herpes)
Presentation
• Flu-like prodrome, followed by grouped vesicles/papules around genitals
• They burst and form shallow ulcers
• Dysuria is often present
Investigations
• NAAT (nucleic acid amplification test)
• PCR & viral culture
• Recurrent/atypical genital ulcers with -ve culture or PCR → Anti-HSV antibodies
Management
• Oral acyclovir
Urology
Genital warts
➢ Benign epithelial skin tumors commonly seen as cauliflower-like growths
➢ Most commonly caused by HPV 6 & 11
➢ Around 30% can resolve spontaneously
➢ Transmitted by sexual intercourse • HPV 16 & 18 are responsible for most cervical
cancers in the UK
➢ IP: 6 weeks to several months
Management
• Solitary, keratinized warts → Gardasil, protects against HPV 6,11, 16 & 18
• Multiple, non-keratinized → Podophyllotoxin
• Ablative (e.g. cryotherapy & excision under anesthesia)
TURP $
• Occurs when irrigation fluid enters the systemic circulation. It’s caused by venous destruction and
absorption of the irrigation fluid and it can be life threatening
• Characterized by dilutional hyponatremia
• Managed by fluid restriction
Purple urine bag $

• Resulted from co-existent UTI
• One of the most common causing bacteria is Providencia stuartii
• Managed by betadine lavage of the urethra and catheter change
Infected indwelling urinary catheter

- Action ⟶ Change the catheter
- If symptoms of UTI ⟶ Antibiotics
- Due to detrusor overactivity

Urge incontinence
- “when I have to go to the toilet, I really have to go”
/overactive bladder
- “sometimes urine passes before reaching the toilet”
(OAB)
Treatment → Bladder retraining, antimuscarinics (Oxybutynin, tolterodine or darifenacin)
- Leaking small amounts of urine when coughing or laughing
- Usually with a history of many vaginal deliveries as this would weaken the pelvic
Stress incontinence floor muscles
Treatment → Pelvic floor exercise, tension-free vaginal tape, retropubic mid-urethral tape
procedures, Duloxetine
Mixed incontinence - A mix of both stress and urge incontinence
- Involuntary release of urine from an overfull urinary bladder, often in the absence of
any urge to urinate
Overflow
- Occurs in patients who have blockage of the bladder outlet (BPH, prostate cancer or
incontinence
narrowing of the urethra) or when the muscle that expels urine from the bladder is
too weak to empty the bladder normally
- Opening between vagina and urethra
Urethrovaginal
- Continual leakage of urine from the vagina
fistula
- Vagina would have a foul smelling
Vascular Surgery
Peripheral artery disease (PAD)
➢ Occurs due to atherosclerosis causing stenosis of arteries
➢ Pain comes on walking and relieved by rest
Features
• Intermittent claudication which is cramping pain felt in the calf, thigh or buttock after walking
• Absent femoral, popliteal or foot pulses
• Rest pain in the more severe cases
• Ulcers and gangrene if the disease progresses
Risk factors
• HTN
• DM
• Smoking
• High cholesterol (1ry prevention → advice to exercise, 2ry prevention → atorvastatin)
Investigations
• Doppler US → 1st choice
- Used to measure the pressure at which detectable flow ceases using a compression cuff to determine
the ankle-brachial pressure index (ABPI)
• Color flow duplex US
- Assess stenosis of the vessel
• MR/CT angiography
- Used only if considering intervention
- Used to assess the extent and location of stenosis and quality of distal vessels
- MR/CT angiography has largely replaced digital subtraction angiography
Management
• Address risk factors for cardiovascular disease
• For 2ry prevention → Atorvastatin 80 mg
- Quit smoking
- Treat hypertension and high cholesterol
- Prescribe an antiplatelet to prevent progression and to reduce cardiovascular risk → 75mg Clopidogrel
(if not tolerated → aspirin)
• Encourage walking beyond the distance which pain occurs
• Naftidrofuryl oxalate, only if patient doesn’t want revascularization and if exercise fails to improve symptoms
• If severely affecting the patient’s life and disease is limited to a single arterial segment → percutaneous
transluminal angioplasty (PTA), a balloon is inflated in the narrowed segment
• If severely affecting the patient’s life and atheromatous disease is extensive but distal run-off is good (i.e.
distal arteries filled by collateral vessels) → surgical reconstruction (arterial reconstruction with a bypass
graft)
Thromboangiitis obliterans (Buerger’s disease)

• Usually young men (around 40 years) + smoking history
• It has a progressive nature compared to acute peripheral artery disease (PAD)
• Clinically, it presents with severe claudication and rest pain
• Ulcers could be present
• Treatment involves smoking cessation
Buerger’s disease → young + heavy smoker
PAD → old + atherosclerosis
Vascular Surgery
Acute limb ischemia
➢ Surgical emergency requiring revascularization within 4-8h to save the limb. It’s usually due to thrombosis in
situ, emboli or graft occlusion
➢ Emboli commonly arise from the heart (Atrial fibrillation, mural thrombus) or aneurysm
Features
• The 6 Ps of acute ischemia (pale, pulseless, paralyzed, • DVT doesn’t cause ischemia of the limb as DVT is
thrombosis of a vein and veins don’t supply
paraesthetic and perishingly cold) organs
• Pain in DVT is constant
• Acute limb ischemia is similar to Compartment $
Abdominal aortic aneurysm except it develops gradually in the latter
Etiology/risk factors
• Atheroma (severe atherosclerotic damage of the aortic wall)
• Family history
• Increasing age Commonest risk factor for the following conditions
• Hypertension, smoking • Abdominal aortic aneurysm → Atheroma
• Aortic dissection → Hypertension
• Syphilis
• Coarctation of the aorta → refractory HTN
• Ehler’s Danlos • Marfan’s $ → collagen abnormality
• Marfan’s syndrome • Ehler’s Danlos → elastin abnormality
Investigations
- US → unstable
- CT → stable
Ruptured aortic aneurysm

➢ Ruptured AAA should be considered in any patient with hypotension and atypical abdominal symptoms
Classical triad
1. Back/flank pain
2. Hypotension
3. Pulsatile abdominal mass
Management
➢ Immediate IV fluid to raise systolic blood pressure to 90 mmHg
• Minimum required BP for organ perfusion is preferred since increasing blood pressure increases the risk of
blood leakage
➢ Laparotomy
Coarctation of the aorta

➢ If COA presents late, it’s usually asymptomatic and the
diagnosis is usually suspected on examination, prompted
often by the presence of a murmur or refractory HTN
Clinical features of late COA
• Headache
• Nosebleeds (usually from high BP)
• BP is high in the arms and low in the legs
• LL muscle weakness, or cold feet due to poor blood supply
• Pulses distal to the obstruction are diminished and
delayed (e.g. femoral pulses are hard to feel, absent foot
pulses)
Vascular Surgery
Thoracic aortic dissection
➢ Occurs in poorly controlled hypertensive patients (>70% have a history of HTN)
➢ Episode resembles a myocardial infarction with sudden onset of very severe, tearing chest pain that
radiates to the back and may migrate down shortly after starting
➢ Unequal pulses in the upper extremities
➢ Paraplegia may occur due to decreased blood flow in spinal arteries
Risk factors
- Hypertension → most important
- Smoking and raised cholesterol • Blood pressure findings in aortic dissection can either be
- Marfan’s $, Ehlers-Danlos $ high (as HTN is a risk factor for aortic dissections), or low
(due to blood loss and cardiac tamponade)
Investigations
• X-ray → widened mediastinum
• ECG & cardiac markers → to rule out MI
• CT angiography (spiral) → Definitive diagnosis
• Trans-esophageal echo → appropriate in a hemodynamically unstable patient
Management
• Dissections of the ascending aorta → treated surgically
• Dissections of the descending aorta → treated medically with control of hypertension in the ICU
Stanford classification
Type A
• Ascending aorta (2/3 of cases)
• Surgical management, but blood pressure should be controlled to a target systolic of 100-120 mmHg whilst
awaiting intervention
Type B
• Descending aorta, distal to the left subclavian origin, 1/3 of cases
• Reduce blood pressure with intravenous labetalol
DeBakey classification
Type I
- Originates in ascending aorta – propagates to at least the aortic arch and possibly beyond it distally
Type II
- Originates in and is confined to the ascending aorta
Type III
- Originates in descending aorta – rarely extends proximally but will extend distally
Vascular Surgery
Femoral artery aneurysm
• Asymptomatic
• Discovered on routine examination accidently
• May experience a pulsating lump or swelling on thigh or radiating pain
• Rarely causes numbness in legs due to nerve compression
Femoral artery aneurysm → pulsatile

Femoral hernia → pulseless
Saphena varix → pulseless, saphenous vein dilatation at its junction with femoral vein in the groin, worm like bag
that subside on lying down and bulges with cough
Renovascular disease
➢ Defined as stenosis of the renal artery or one of its branches
➢ The two main causes are atherosclerosis and fibromuscular dysplasia
Signs
• BP resistant to treatment
• Worsening renal function after ACE-inhibitors/ARBs in bilateral renal artery stenosis
Tests
• Ultrasound: Renal size asymmetry (affected side is smaller), • When someone is started on ACE-inhibitors,
U&E are usually checked 7-10 days after
Disturbance in renal blood flow on Doppler US starting treatment, and at least annually
• CT/MR angiography are more sensitive
• Renal angiography is ‘gold standard’, but perform only after CT/MR angiography as it is invasive
Treatment
➢ Comprehensive antihypertensive regimens, transluminal angioplasty with/without stent replacement or
revascularization surgery
Inferior vena cava syndrome

➢ Symptoms resulting from the obstruction of the IVC
Causes
• Physical invasion (tumors, most commonly RCC)
• Compression (seen in pregnant women who lie in a supine position)
• Thrombosis (within the vein itself)
Symptoms
• Edema LL
• Tachycardia
Thoracic outlet syndrome

• Compression of the trunk of the brachial plexus, subclavian
artery or vein at the superior aperture of the chest
• It results in pain or numbness in the hand or forearm often
on the ulnar side
• It presents unilaterally
• It may lead to weak radial pulse, forearm cyanosis or
thenar muscles weakness
Vascular Surgery
Lower limb arteries
Claudication pain
• Aorto-iliac (common iliac) obstruction →Buttocks and thighs, associated with absent femoral pulses and male
impotence (Leriche’s $)
• External iliac → starts above the inguinal ligament
• Femoral artery → starts below the inguinal ligament
• Femoro-popliteal → below the knee
➢ Remember, symptoms of occlusion have to occur distal to the level of occlusion
Vascular Surgery
Notes
• Carotid artery stenosis → TIAs or thromboembolic stroke
• Atrial fibrillation → usually presented with major strokes, residual symptoms or leads to death
• Infantile form of COA is associated with PDA
• Distal embolization of atherosclerotic debris from Aneurysm → may lead to livedo reticularis of the feet
(mottled discoloration of the skin of the feet) → known as “Blue toe $”
• Complications of Marfan’s $
- Aortic sinuses dilatations (90%) → may lead to Aortic aneurysms
- Aortic dissection
- AR
- MVP (75%)
• Acute limb ischemia → 6Ps, Embolus, history of AF
• DVT → constant claudication pain
• Varicose veins → ugly legs
• Lymphedema
- Localized fluid retention and tissue swelling caused by a compromised lymphatic system
- Most common 2ry cause → Malignancy and cancer management, especially after regional LN dissection
- Upper limb infection (may be elicited by an insect bite) after TTT of breast cancer is a risk factor

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Anatomy

• Posterior superior iliac spine

Muscles and n. supply of hand

Ampulla of Vater = Hepatopancreatic ampulla at the 2nd part of the duodenum

Management of acute attack [MONA]

• Left bundle branch block (LBBB)

Post myocardial infarction management / management of NSTEMI or unstable angina

Vasospastic (Prinzmetal/variant) angina

• Widened mediastinum on CXR

Acute Pericarditis Pericardial Effusion Cardiac Tamponade

Any cause of pericarditis but

• Central chest pain worse • Beck’s triad:

• CXR shows enlarged,

Treatment NSAIDS Pericardiocentesis Urgent Pericardiocentesis

Major criteria [BE] Minor criteria [FIVE PM]

Splinter hemorrhage → hemorrhage under the nails

• LEft sided murmurs louder with → Expiration

• Sinus tachycardia: HR >100 bpm in a healthy individual

• It’s impossible to see ventricular fibrillation in an awake

• Wide QRS + regular → VT

With pulse Without pulse

P and QRS dissociation + tachycardia → VT

A patient with VT → Ask yourself, does he have a pulse or not?

1. Valsalva maneuver, carotid massage

Atrial flutter Vs Atrial fibrillation

Persistent AF, lasts >7 days

A patient with AF, you ask yourself

• <65 years old and no comorbidities → NO warfarin

Benefits of DOAC over warfarin

2ry prevention of a stroke or TIA

1st degree heart block • Prolonged PR interval > 0.2 seconds

• Mobitz type I AV block (Wenckebach block/phenomenon)

3rd degree (complete)

Rules of thumb to determine Cardiac Axis deviation on ECG

LAD RAD Extreme RAD

Mitral valve prolapse [MVP]

Patent ductus arteriosus (PDA)

Tetralogy of Fallot (TOF)

Ruptured abdominal aortic aneurysm

Questions to be asked when dealing with sepsis:

How’s organ dysfunction identified?

Acute upper GI bleeding

Management for upper GI bleeding

Post GIT bleeding due to Mallory-Weiss $

Indications for Fresh frozen plasma (FFP)

Stage 4: over 40% blood loss, 140bpm, marked hypotension

Stage 1-2 → IV fluids

Signs and symptoms of smoke inhalation injury

Choking and foreign body airway obstruction (FBAO) in infants

<1y/o → Back blows then chest thrusts

Tricyclic antidepressant (TCA) overdose (Amitriptyline)

Tricyclic antidepressant overdose →

Unilateral space occupying lesions such as tumors, hematomas or abscesses →

Opiate (heroin) overdose or a cerebrovascular accident affecting the brainstem →

Paracetamol overdose → Liver toxicity

Benzodiazepines over dose → [CRASH]

Management for stabbed injury in the RUQ with

Indications for FAST

Patients should be hemodynamically stable before performing CT

Types of burns or scalds (due to hot water/steam)

Partial thickness burn

Full thickness burn

<1 y/o, blow air through the nose and mouth

For cardiac arrest → CAB (Compressions, Airway, Breathing)