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Gastrointestinal

System

Contents

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Cardiovascular Anatomy

Pericardium

Left/Right Atrium and Left/Right Ventricle

Atrioventricular and Semilunar Valves

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Cardiac Muscle

Sarcomeres

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Histology of Blood Vessels

Arteries

Veins

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Histology of Heart Muscle (Mitral Valve)

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Cholesterol and Lipoproteins Review

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Electrical and Contractile Function

Pacemaker/Contractile Cell Action Potentials

Intrinsic Conduction Network

Extrinsic/Neural Control of the Heart

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Cardiac Cycle

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Heart Murmurs

Normal Heart Sounds

Systolic and Diastolic Murmurs

S3 and S4 Heart Sounds

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Blood Pressure

Definitions

Regulation of CO / HR / Blood Flow / BP

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Electrocardiograms (ECG)

Supraventricular Arrhythmias / Ventricular Arrhythmias

Pulseless Electrical Activity (PEA)

Cardiac Arrests

Atrioventricular (AV) Heart Blocks

12 Lead ECG

Myocardial Infarctions / Acute Coronary Syndrome

Takotsubo Syndrome

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Atrial Fibrillation (AF)

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Hypertensive Heart Disease

Primary / Secondary HTN

Pulmonary HTN / Cor Pulmonale

Benign / Accelerated Nephrosclerosis

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Peripheral Vascular Disease

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Congenital Heart Disease

Left-to-Right Shunts

Right-to-Left Shunts

Obstructive Lesions

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Valvular Heart Disease

Degenerative Valve Disease

Non-Bacterial Thrombotic Endocarditis (NBTE)

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Ischaemic Heart Disease

Acute Coronary Syndrome (ACS)

Myocardial Infarction (MI)

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Congestive Heart Failure (CHF)

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Cardiomyopathy

Dilated / Hypertrophic / Restricted Cardiomyopathy (DCM / HCM / RCM)

Myocarditis

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Cardiovascular Drugs

Diuretics

Angiotensin Converting Enzyme Inhibitor (ACEI)

Angiotensin II Receptor Blocker (ARB)

Calcium Channel Blocker (CCB)

-Blockers

Statins

Nitrates

Anti-arrhythmics

Thrombolytics / Anticoagulants / Anti-platelets

Nicorandil

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Triple Whammy Drug Interactions

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Vaughan Williams Classification of Antiarrhythmic Agents

Sodium Channel Blockers / -Blockers / Anti-Arrhythmics / CCBs

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Pharmacological Guidelines for Management of VCD

Hypertension (HTN)

Ischaemic Heart Disease (IHD) / Angina / Unstable Angina (UA) / NSTEMI / STEMI

Arrhythmias

Heart Failure

Hypercholesterolaemia

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Cardiovascular History

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Cardiovascular Physical Examination

Histology of the Gastrointestinal Tract


Classification of Epithelia
Squamous: When the width of the cell is greater than the height
Cuboidal: When the width, depth and height are approximately the same
Columnar: When the height exceeds the width.
Pseudo-stratified: Epithelium appears stratified although some of the cells do not reach the free
surface
Transitional: Epithelium (urothelium) lines lower urinary tract (urinary bladder, ureters and superior
urethra + gland ducts of the prostate). It is a stratified epithelium which allows it to distend.

Functions of Epithelia
Secretion: Eg. Columnar epithelium stomach and gastric glands
Absorption: Eg. Columnar epithelium in gut and proximal convoluted tubules in the kidney
Transport: of materials along surface by cilia or across the epithelium to and from the connective
tissue
Protection: As in stratified squamous epithelium of skin or transitional epithelium of urinary bladder
Receptor function: To receive and interpret external stimuli as in taste buds, olfactory epithelium
and the retina of the eye.

Oral Cavity
Hard Palate: Consists of keratinised and parakeratinised stratified squamous epithelium
Lining Mucosa: Eg. Lips, cheek, floor of mouth and inferior surface of tongue is non-keratinised.
Stratum basale (resting on basal lamina)
Stratum spinosum
Stratum superficiale (surface layer of mucosa)
Tongue: Muscular organ with both intrinsic and extrinsic muscles. Dorsum of the tongue is divided
by the sulcus terminalis.
Multiple lingual papillae cover the surface:
Filiform (like lines on the surface)
Fungiform (like mushrooms on the surface)
Foliate (like gills on the side)
Circumvallate (like toadstools at the back in a V shape)

Salivary Glands: Paired parotid,


submandibular and sublingual glands
Parotid gland is completely serous (watery)
Parotid duct enters at the upper 2nd molar
Submandibular glad is completely mucinous
Sublingual gland is a mixture of mucous and serous fluid being produced.

Parotid Gland

Structure of the Gastrointestinal Tract


The major layers include:
Mucosa

Submucosa

Oesophagus:
Consists of non-keratinised stratified squamous
epithelium
Glads are present to lubricate the oesophagus
The mucosa and submucosa are thrown into large
folds that extend the length of the oesophagus.
These allow for expansion during the passage of
large bolus.

Muscularis externa
Serosa (visceral peritoneum)

Stomach:
Gastric Pits:
o The muscous cells at the base, or neck of
each pit actively divide replacing superficial
cells that are shed into the chime.
These release a mucus gel layer to
protect the stomach.
o Also contain chief cells (release pepsin) and
parietal cells (HCl and intrinsic factor for B12
digestion)

Small Intestine:
Principal site of digestion and absorption
Duodenum:
o Contains brunners glands which help to identify the duodenum
Jejunum:
o Most absorption takes place here
o Note the plica are arrange perpendicular to the lumen
Ileum:
o Plica are still apparent here, however they disappear in the distal ileum.
o Note the presence of lymphoid tissue (L) aggregated in nodules called Peyers
patches.

Large Intestine:
Principal function is reabsorption of electrolytes and water and elimination of undigested food
and waste..
Muscularis externa exhibits thickened band known as teniae coli.
There are no villi or plica present, however the large intestine exhibits sacculations (bunching)
known as haustrations.

Rectum:
Transition exists between simple columnar epithelium of the intestinal mucosa and stratified
squamous epithelium.
Also note the disappearance of the muscularis mucosae, replaced by the internal anal

sphincter.

Pancreas
Exocrine Component: synthesises and secretes enzymes into the duodenum to assist in fat
breakdown (acinar cells characteristic acidophilic zymogen granules in the cytoplasm)
Endocrine Component: Synthesises and secretes insulin and glucagon into the blood (islets
of Langerhans). It appears scattered throughout the pancreas and is pale compared to the
rest of the organ. 3 Types of Cells:
Alpha 15-20% make Glucagon
Beta 70% make insulin
Delta 5-10% make somatostatin

Liver
Characteristic Spoke-Wheel formation
hexagonal cross section
Typical liver lobule has 6 portal areas, or hepatic
triads, one at each corner of the lobule.
The central veins ultimately merge to form the
hepatic vein, which then empties into the inferior
vena cava.

Gallbladder
Hollow, pear-shaped organ that stores and
concentrates bile prior to its excretion into the
small intestine.
The gallbladder has two major functions:
o Bile storage
o Bile modification
Bile is secreted continuously, but it is released into the duodenum only under the stimulation
of CCK

If bile becomes too concentrated, crystals of insoluble


minerals and salts begin to appear (cholelithiasis)
If these are large and severe, the gallbladder may be
surgically removed in a procedure called a
cholecystectomy.

Embryology of the GIT

Basic Overview of Embryology


Day 1 7: Ferilisation
Week 1 8: Progression from a single cell to establishing organs embryogenesis
Week 9 delivery: Foetal period (total 38 weeks)
Week 3: trilaminar germ disc is formed
Epiblast cells form all three embryonic layers:
Ectoderm:
o CNS, PNS, sensory epithelium of ears, eye, nose, skin, glands, enamel
Mesoderm:
o Vascular system, urogenital system (except bladder), spleen, skeleton
Endoderm:
o GIT, respiratory tract, bladder, thyroid, parathyroids, liver, pancreas, tympanic cavity,
auditory tube.
Note: mesoderm differentiates into a visceral and parietal mesoderm. The lateral mesoderm
and endoderm go on to form the gut.

Formation of the Gastrointestinal Tract


As a result of folding, part of the yolk sac is incorporated into
the primitive gut.
Endoderm forms the epithelial lining of the digestive tract
and gives rise to specialised cells (hepatocytes, pancreas,
etc.)

Mesentery
Ventral mesentery is derived from the septum transversum
(mesoderm septum formed by the folding of the embryo.
Growth of the liver divides this into the lesser omentum and
falciform ligament
Oesophagus normalities form around the same time as lung
buds begin to form.

Atresia / Fistula
Oesophageal atresia results in
accumulation of fluid in the
amniotic sac

Stomach
Appears as a dilation of the
foregut.
Due to rotation and differering
growth rates, the stomach forms
its shape and the omental bursa

Liver and Gallbladder


Liver appears as an endodermal epithelium outgrowth at week 3.
The bud proliferates and penetrates the septum transversum (plate between the pericardial
cavity and stalk of the yolk sac)
The outpouching between the liver and foregut narrows to form the bile duct
o Further outpouching of this duct gives rise to the gallbladder.

Pancreas
Formed from the uniting of the ventral and dorsal buds
After rotation, the ventral bud lies below the dorsal bud.
Further development fuses the two parts together with uniting of
the pancreatic ducts.
An annular pancreas can occur when the ventral pancreas splits
and forms a ring.

Caecum and Appendix


The loops rotate 270 degrees in total, causing
the caecum to move from the upper right
quadrant to the right iliac fossa.
A small bud appears on the caecum the
primate appendix.
Note: malrotation can occur, where the colon
does not rotate properly, forming a volvulus.

Hindgut
Hindgut forms the distal third of the transverse colon, the descending colon, the sigmoid, the
rectum and the upper part of the anal canal.
The cloaca is an endoderm lined cavity, covered ventrally
by ectoderm this forms the cloacal membrane
At the 7th week, the membrane ruptures, creating the
anal opening.
The urorectal septum separates the allantois from the
hindgut

Failure to Thrive:
Chronic Disease and Diarrhoea

Influences on Growth

Nutrition
Absorption of food
Metabolism of food fat, protein and carbohydrates
Energy utilisation and chronic disease
Hormones growth hormone, steroids, thyroid hormone, insulin
Diarrhoea

Fats and Diet

Fat malabsorption can be due to pancreatic, hepatic and small intestinal mucosal reasons.
This leads to pale stools or steatorrhoea.

Breast Feeding Benefits


More Fat and CHO than formula hence about 10% more calorie dense and breast fed infants
grow more quickly.
Lower protein and may lower/defer incidence of allergies in childhood
Omega-3 fats help with CNS development may enhance IQ
IgA antibodies that help infants recover from gastroenteritis and respiratory infection.
Bonding and helps mothers return to pre-pregnancy weight.
Is free and is hygienic.

Infant Feeding
6 Months: Introduction of solids
12 Months: Family food introduced
No cows milk until 12 months
Maximum 500ml/day cows milk at any age

Failure to Thrive
< 3rd centile or crossing two percentile chart lines
Organic causes:
o Malabsorption coeliac disease
o Increase energy utilisation chronic infection, cardiac failure
Non-organic causes

neglect

Detection:
Weight centile low relative to length and head circumference centile
Crossing centiles
Appear physically malnourished poor fat and muscle stores, loose skin folds in groin and
axilla.

Gastrointestinal Disease
Acute vs. Chronic Diarrhoea (more than 4 loose motions a day for > 2 weeks)
Infectious diarrhoea
o Commonest worldwide cause of morbidity and mortality in children < 5 yrs old.
Villous atrophy / partial villous atrophy
o Coeliac disease
o CMPI
o Giardia

Dehydration
Moderate vs Severe Dehydration
Moderate
5-10% dehydrated
Sunken eyes
Definite loss of skin tugor
Tachycardia
Reduced urine output

Severe
10%+
Moderate plus hypotension
Poor peripheral perfusion
Poor peripheral perfusion
No urine output

Differential Diagnosis
Causes of serious bacterial infection
o UTI
o Bacteraemia
o Pneumonia
o Meningitis
Acute Surgical Causes:
o Appendicitis
o Intussusception (inversion of one portion of the intestine within another
o Acute obstruction
o Torsion of the testis
o Inguinal hernia
o Reflux
o Pyloric stenosis

Gastroenteritis Causes
Rotavirus:
Less than 10% of cases since introduction of the vaccine
33% of patients will have fevers of 39C
Illness last 3-7 days
Most clinically significant infections occur in the 3-36month age group
Norovirus:
Responsible for more than 50% of non-bacterial gastroenteritis
Milder than rotovirus
Lasts 1-2 days

Spread by fecal oral route

Oral vs. IV

Oral works faster than IV


o In mild-moderate dehydration at 2hours (better rehydrated on oral)

Clinical Aspects of Liver Disease

Liver Tests
AST:
Aspartate aminotransferase
Liver, heart, skeletal muscle, kidney, brain
ALT:
Alanine aminotransferase
Primarily in the liver
GGT:
Gamma-Glutamyl Transpeptidase
In hepatobiliary system, kidneys, pancreas, intestine and prostate
ALP:
Alkaline Phosphatase
In liver, bone, placenta and intestine

Patterns of Abnormalities

Hepatocellular / Hepatic
AST, ALT > GGT, ALP
Cholestatic / Infiltrative
GGT, ALP > AST, ALT
Can be mixed!

Real Liver Function Tests

Bilirubin
o End product of heme
o Elevated in jaundice from all causes
Albumin
o Synthesised by liver; half-life 14-20days
o Levels influenced by non-hepatic factors
o Indicator of severity of chronic liver disease (CLD)
Prothrombin time / INR
o Dependent on hepatic synthesis of clotting factors and uptake of Vit K
o Shorter half-life than albumin
o Earlier indicator of severe liver injury than albumin

Causes of Elevated Liver Function Tests


Viral Hepatitis
Drug reactions / toxicity
Alcoholic liver disease
Biliary disease
o Stones
o Malignancy
Hepatic infiltration
Haemochromatosis
Others
Hepatitis A
RNA virus
Transmission: Faecal-oral

Incubation 4wks
Causes: Acute icteric (jaundiced) illness, rarely fulminant (sudden and severe)
Anti-HAV IgM , elevated ALT, AST
o Anti-HAV IgM recent infection
o Anti-HAV IgG past infection and immunity
Progression to chronicity NONE
Symptoms:
o Prodromal illness including RUQ pain
o Jaundice 1-4weeks
o Palpable liver in 70% and spleen in 20%
Drugs
Paracetamol direct toxicity
Antibiotics flucloxacillin, augmentin
Anticonvulsants phenytoin, carbamazepine
NSAIDs
Amiodarone
Allopurinol (Anti-gout)
Isoniazid (anti-tb)
Zidovudine (anti-retroviral)
Biliary Obstruction:
Gallstones
Strictures
Cholangiocarcinoma
Pancreatic cancer
^ bilirubin, GGT, ALP

Causes of Chronic Liver Disease

Alcoholic liver disease


Hepatitis B
Hepatitis C
Haemochromatosis
Non-alcoholic fatty liver disease / non-alcoholic steatohepatitis

Hepatitis B

DNA virus
Transmission: blood borne, sexual, vertical (mother -> child), saliva
Incubation 1- 4 months, may be asymptomatic
Acute icteric illness, 1% become fulminant
Diagnosis:
o Acute infection HbsAg and anti-HBc IgM
o Recovery anti-HBc IgG and anti-HBs IgM
o Chronic infection HBsAG, anti-HBc IgG
IF ACTIVE: also have HBV DNA pos
Progression to chronicity
o Adults <5%
o Infants 90%
Symptoms:
o Cirrhosis, liver failure, hepatocellular cancer
Treatment:
o Acute supportive
o Chronic:
Pegylated interferon
Antivirals (entecavir, tenofovir)
Prevention:
o Vaccination
o Immune globulin

Hepatitis C
RNA virus
Common ~ 1% population
Transmission blood borne, vertical
Incubation 6-8wks, often asymptomatic
Anti-HCV, HCV RNA N or elevated ALT, AST
Progression to chronicity: 70%
Symptoms:
o Cirrhosis, liver failure, hepatocellular cancer
Treatment:
o Pegylated interferon, ribavirin.

Chronic Liver Disease


Symptoms:
o Lethargy, pruritus, RUQ
discomfort
Progresses to cirrhosis over years
decades
Eventually develops complications
o Decompensated cirrhosis
Liver transplantation for decompensated
disease

Mild jaundice: serum


bilirubin 51 mol/l
Physical Signs:
Spider naevi
Leuconychia (white nails)
Palmar erythema
Scratch marks, bruising
Oedema
Scleral or generalised jaundice
Hepato- and splenomegaly
asterixis

Cirrhosis

Diffuse process with fibrosis and nodule formation


Follows ongoing inflammation and hepatocellular necrosis
And be micronodular or macronodular

Complications:
o Portal HTN
o Ascites (inc. oedema)
o Hepatorenal syndrome
o Hepatic dysfunction
o Hepatic encephalopathy
o Hepatocellular carcinoma

Portal Hypertension
Obstruction of portal circulation results in development of a collateral circulation
Oesophageal and gastric (fundal) varices
These correlate with severity of liver disease
40% of compensated cirrhosis patients will show varices
85% of decompensated cirrhosis patients will show varices

Ascites
Portal hypertension splanchinic dilatation decreased effective arterial blood volume
vasoconstrictor and antinatruiretic factors secondary hyperaldosteronism sodium and
water retention increased lymph production
Ascites develops in 30% of cirrhotics over 5 years.
Once it develops, 5 yr survival = 30-40%
Management:
o Salt restriction
o Diuretics
Spironolactone and possibly addition of frusemide

Spontaneous Bacterial Peritonitis


Bacterial translocation from intestinal lumen to lymph nodes with bacteraemia and ascetic
infection.
Prevalence 10-30% of hospitalised patients
In-hospital mortality 20%
Median survival after episode is 9 months
Symptoms:
o Pain, vomiting
o Fever, hepatic encephalopathy
Management:
o Ascetic tap for diagnosis
o Antibiotics (triple therapy ciprofloxacin, ampicillim, metronidazole), and albumin for
acute episode
o Prophylaxis reduces recurrence

Hepatobiliary Disorders and Clinical Approach


to Jaundice

Bilirubin Metabolism
Haemoglobin released from destruction of RBCs
In the liver: haemoglobin haeme biliverdin bilirubin bilirubin glucuronide
urobillinogens fecal excretion

Pathophysiology of Jaundice
Arises
o
o
o
o

in 4 different ways:
Increased bilirubin load
Disturbance in uptake and transport
Defects in conjugation
Failure of excretion

Prehepatic:
o Haemolysis
Hepatocelluar (hepatitis)
o Acute
o Chronic
Cholestatic
o Undilated ducts (intrahepatic)
o Dilated ducts (obstructive)

Differential Diagnosis of Jaundice


Acute:
o
o
o
o
o
o

Viral hepatitis: A, B, C, E or EBV, CMV, HSV


Drug reactions
Alcoholic hepatitis
Immune: autoimmune hepatitis
Other toxins
Biliary disease
Gall stones
Malignancy
o Pregnancy related
o Hepatic infiltration
Chronic:
o Chronic cholestasis
o Biliary disease
PBC (primary biliary cirrhosis)
PSC (primary sclerosis cholangitis)
Biliary strictures
o cirrhosis

Clinical Approach to Jaundice

lab tests:

o
o
o
o
o
o

lfts
bilirubin
albumin
INR
FBC
Urine

Introduction to Abdominal Imaging

Abdominal X-Ray
3 films: supine, erect and CXR
o CXR to check for air under diaphragm, or lung pathology that might cause abdominal
symptoms.

Method of looking:
Follow the densities black to white
Gas first, then fat, soft tissue, calcifications, bones, metal
Soft tissues liver, spleen, kidneys.
Note: small bowel obstruction: small bowel >3cm = dilated
o Causes:
Adhesions,
Herniae
Nalignancy
Intraperitoneal inflammation
Gallstone ileus
Crohns disease
Large bowel obstruction:
o Causes:
Carcinoma
Volvulus
Diverticulitis
Colonic pseudo-obstruction
Herniae
Faecal impaction

Calcifications:

Fluoroscopic Studies Barium Meal and Enema

Barium
o Suspension of inert powder particles
o High density good images
o Viscosity can use double contrast
o AE: dries out in lumen constipation or obstruction
Barium Enema:

Volvulus

Abdominal Ultrasound
Most organs are quite accessible except if covered by gas
filled bowel.
Focal tenderness can be quite well judged.
Dynamic and interactive element of study
No radiation especially important in paediatrics.
Used to view:
o Liver parenchyma,
hepatic and portal veins
o Gallbladder and bile duct
o Pancreas and duct
o Spleen
o Kidneys
o Aorta
o Bladder
o ascites

PET Scan

Alcohol Abuse

National Guidelines
No more than 2 standard drinks on any day
No more than 4 standard drinks on a single occasion
Standard drink:
o 10 grams of pure alcohol

Alcohol Treatment
Pharmacological Methods of Detoxification
Benzodiazepines are the drugs of choice in managing alcohol withdrawal as they:
o Alleviate many withdrawal symptoms
o Are effective in preventing development of complex withdrawal features when given
early
o Have a wide margin of safety
o Have a low likelihood of cross-dependence
Naltrexone:
o Opioid receptor antagonist
o Used in both alcohol and opioid dependence
Topiramate:
o
Anti-epileptic drug which also assists in alcohol dependence
Ondansetron:
o A serotonin antagonist, it may also be used in alcohol dependence
Post-Detoxification:
Rehab centres
Alcoholics Anonymous

Pharmacology of Lower
Gastrointestinal Tract

Overview of the Small Intestine


Functions:
Digestion and absorption
Defence against antigen entry
Pathophysiology:
Malabsorption:
o Coeliac disease
Bleeding / Ulceration:
o Duodenal ulcer (Tx of PPI, H2 antagonist)
Structure:
Extends from duodenum to ileum
SA increased by mucosal folds.
Innervation:
o Parasympathetic cholinergic (muscarinic and nicotinic receptors)
o Sympathetic, adrenergic (alpha and beta receptors)

Large Intestine (Colon)


Functions:
Stores waste
Reclaims water, maintains water balance and absorbs some vitamins and electrolytes.
Defence against antigen entry
Pathophysiology:
Malabsorption:
o Diarrhoea
o Inflammatory bowel diseases
Ulcerative colitis
Crohns disease
May affect from mouth to anus
Pseudomembranous colitis
o Irritable bowel diseases
Diverticulitis
o Diarrhoea
o Constipation
Megacolon

Antidiarrhoeal Agents
Antiperistaltic Agents:
Opiods such as codeine
Inhibit gastric motility and peristalsis
o Diphenoxylate
o Loperamide
Adsorbents:
Kaolin
o Acts as an adsorbant agent
o May prevent absorption of other drugs

Laxatives
Step 1:
o Exercise,
o Fluid intake
o Increased fibre
Step 2:
o Bulk forming laxatives
Psyllium hydrophilic mucilloid (Metamucil)
Ispaghula husk
Step 3:
o Stool softeners
Coloxyl
Step 4:
o Osmotic laxatives
Sorbitol
Magnesium sulphate
Lactulose
Onset is dose dependant 2-6hrs
Watch for griping, wind.
Step 5:
o Stimulants
Sennoside granules
Senna
Bisacodyl
Step 6:
o Suppositories / enemas
Suppositories glycerine, bisacodyl
Enemas microlax
Step 7:
o Colonic lavage
Golytely
Glyo-prep
Involves surgery
Step 8:
o Manual evacuation
o Surgical deimpactation

Antispasmodics
Hyoscine, hyoscyamine, atropine, propantheline
o Eg. Travacalm
All are anticholinergic
o Cause antimuscarinic side-effects (dry mouth, constipation, etc.)

Serotonin (5-HT) Modulators in the Intestine


Serotonin stimulates gut motility so agonists help constipation, while antagonists can help
diarrhoea predominant IBS.
Agonists:
Tegaserod
o Selective 5-HT4 agonist for constipation
SSRIs
o Would believe this would help with constipation predominant IBS

Antagonists:
Alosetron
o 5-HT3 antagonist
o Only given to women on a very restricted program.

Motility Stimulants / Prokinetic Agents


Metoclopramide, domperidone, erythromycin
MOA:
o Accelerate gut transit time
o Absorption of concomitant drugs may be affected
o Causes diarrhoea
Examples: metoclopramide (maxolon)
Class: Dopamine antagonist with cholinergic activity
MOA: enhances motility from the oesophagus through to the small bowel AND decreased
relaxation of the upper stomach and increases antral contraction
Indications: Nausea and vomiting, IBS, GORD
AE: Hirsutism, drowsiness, confusion (elderly)

Pathologies of the GIT

Oesophageal Cancer
The most common malignant tumour in the proximal 2/3 of the oesophagus is squamous cell
carcinoma; adenocarcinoma is the most common in the distal 1/3. Symptoms are progressive
dysphagia and weight loss. Diagnosis is by endoscopy, followed by CT and endoscopic
ultrasound for staging. Treatment varies with stage and generally includes surgery with or
without chemotherapy and radiation. Long-term survival is poor except for those with local
disease.

Food Intoxication: Staphylococcus Aureus


Associated with foods rich in protein salt and sugar (ham, creamy cakes, salads with
mayonnaise). It induces diarrhoea and vimiting 1-6h after ingestion.

Food Intoxication: Bacillus Cereus

Associated with rice dishes. Acute onset 1-6h of nausea, abdominal pain and vomiting w/o
diarrhoea.

Campylobacter Spp.

Most common cause of diarrhoea in developed countries. C. jejuni most common.

Salmonellosis

Second most common cause of diarrhoea in developed countries. Trasmitted via


contaminated foods; especially poultry, eggs, meats and dairy products.

Enteric Fevers: Typhoid and Paratyphoid

Caused by Salmonella typhi and S. paratyphi. Incubation period 10-14 days, early symptoms
of fever, headache, dry cough, abdominal discomfort (diarrhoea or constipation), fever
increases if untreated. Around 3% of patients become chronic carriers.

Rotavirus

Causes severe watery diarrhoea lasting 4-7days. Major cause of gastroenteritis in infants and
children.

Noroviruses

Often food borne; common in older children and adults. Usually presents as acute-onset
vomiting, watery non-bloody diarrhoea with abdominal cramps and nausea. It is highly
infections and can spread rapidly in confined areas (aged care, cruise liners, etc.)

Giardia Intestinalis

Epidemic in developed countries and endemic in developing countries. Faecal-oral


transmission in day-care setting most common. Many cases asymptomatic.

Cholelithiasis

Cholelithiasis is the presence of one of more calculi (gallstones) in the gallbladder. It affects
approximately 30% of the population, and is more common in females. It is generally
asymptomatic, with the most common symptom being biliary colic; gallstones do not cause
dyspepsia or fatty food intolerance. More serious complications include cholecystitis; biliary
tract obstruction (stones in the bile ducts or choledocholithiasis), sometimes with infection
(cholangitis); and gallstone pancreatitis. Diagnosis is usually by ultrasonography. If
cholelithiasis causes sypmtoms or complications, cholecystectomy is necessary.

Acute Cholecystitis

Acute cholecystitis is inflammation of the gallbladder that develops over hours, usually
because a gallstone obstructs the cystic duct. Symptoms include right upper quadrant pain
and tenderness, sometimes accompanied by fever, chills nausea and vomiting. Abdominal
ultrasonography detects the gallstone and sometimes the associated inflammation.
Treatment usually involves antibiotics and cholecystectomy.

Bile Duct Obstruction (Cholestasis)


Extrahepatic or Intrahepatic
Extrahepatic:
Obstructs the flow of bile within the ducts or secondary to external compression
Gallstones are the most common cause
Other causes are inflammation of surrounding structions, malignancy infection or biliary
cirrhosis.
Intrahepatic:
Cholestasis generally occurs at the level of the hepatocyte or biliary canalicular membrane.
Causes include hepatocellular disease (viral hepatitis, drug induced hepatitis), cirrhosis and
alcoholic liver disease.
Excretion is the rate limiting step and is usually impaired to the greatest extent.
o As a result, conjugated bilirubin predominates in the serum.
o Raised conjugated bilirubin and raised ALP

Meckels Diverticulum
Meckels diverticulum is a congenital sacculation of the distal ileum
occurring in 2-3% of people. It is usually located with 100cm of the
ileocec al valve and often contains heterotopic gastric tissue,
pancreatic tissue or both. Symptoms are uncommon but include
bleeding, bowel obstruction and inflammation. Diagnosis is difficult
and often involves radionuclide scanning and barium studies.
Treatment is surgical resection.

Intussusception
An intussusception is a medical condition in which a part of the intestine has invaginated into
another section of intestine, similar to the way in which the parts of a collapsible telescope
slide into one another. It causes intestinal obstruction and sometimes intestinal ischaemia. It
generally occurs between ages 3months and 3 years. 65% of cases are before age 1.

Acute Appendicitis

Obstruction of the appendix lumen is


the primary cause of appendicitis.
Obstruction of the lumen leads to
distension of the appendix due to
accumulated fluid. Ineffective
lympatic and venous drainage allows
bacterial invasion of the appendix
wall and, in advanced cases,
perforation and spillage of pus into
the peritoneal cavity.

Alcoholic Liver Disease

Alcohol abusers often have disorders that occur in this sequence:


Fatty liver (in >90%)
Alcoholic hepatitis (in 10-35%)
Cirrhosis (in 10-20%)
Hepatocellular carcinoma may also develop, especially in association with iron accumulation.

Risk Factors

Quantity and duration of alcohol use


(>8years)
Sex - women

Pathology

Steatosis (macrovesicular)
Alcoholic hepatitis (steatohepatitis)

Signs and Symptoms

Genetic and metabolic traits


Nutritional status

Fibrosis
Cirrhosis (micronodular)

Symptoms usually become apparent in patients in their 30s-40s, with more severe problems
appearing about a decade later.
Fatty Liver is often asymptomatic. In 1/3 of patients, the liver is enlarged and smooth, but it
is not usually tender.
Alcoholic hepatitis ranges from mild and reversible to life threatening. Most patients with
moderate disease are undernourished and present with fatigue, fever, jaundice, right upper
quadrant pain, tender hepatomegaly, and sometimes a hepatic bruit. About 40% deteriorate
soon after hospitalisation, with consequences ranging from mild (eg. Increasing jaundice) to
severe (eg. Ascites, portal-systemic encephalopathy, variceal bleeding, liver failure with
hypoglycaemia, coagulopathy). Other manifestations of cirrhosis may be present.
Cirrhosis, if compensated, may be asymptomatic. The liver is unusually small; when the liver
is enlarged fatty liver or hepatoma should be considered.
Symptoms range from those of alcoholic hepatitis to the complications of end-stage liver
disease, such as portal hypertension (often with oesophageal varices and upper GI bleeding),
splenomegaly, ascites and portal-systemic encephalopathy. Portal hypertension may lead to
intrapulmonary arteriovenous shunting with hypoxemia (hepatopulmonary syndrome), which
can cause cyanosis and nail clubbing. Acute renal failure secondary to progressively

decreasing renal blood flow may develop. Hepatocellular carcinoma develops in 10-15% of
patients with alcoholic cirrhosis.

Diagnosis
Confirmed history of alcohol use
Liver function tests and CBC
Sometimes liver biopsy
Acohol is suspected as the cause of liver disease in any patient who chronically consumes
excess alcohol. History should be confirmed by family members.
There is no specific test for alcoholic liver disease, however liver function tests (PT; serum
bilirubin, aminotransferase, and albumin levels) and FBC are done to change for severity of
liver damage or anaemia.

Treatment

Abstinence
Supportive care AA, etc.
Corticosteroids and enteral nutrition for severe alcoholic hepatitis
Sometimes liver transplant

Gastro-Oesophageal Reflux
Disease (GORD)

Incompetence of the lower oesophageal sphincter allows reflux of gastric contents into the
oesophagus, causing burning pain. Prolonged reflux may lead to oesophagitis, stricture and
rarely metaplasia or cancer. Diagnosis is clinical, sometimes with endoscopy, with or without
acid testing. Treatment involves lifestyle modification, acid suppression using PPIs and
sometimes surgical repair.

Epidemiology
GORD is common, occurring in 30-40% of adults. It also occurs frequently in infants, typically
beginning at birth

Aetiology
The prescence of reflux implies lower oesophageal sphincter (LOS) incompetence, which may
result from a generalised loss of intrinsic sphincter tone or from recurrent inappropriate
transient relaxations. Treansient LES relaxations are triggered by gastrict distention or
subthreshold pharyngeal stimulation
Factors contributing to reflux include weight gain, fatty foods, caffeinated or carbonated
beverages, alcohol, tobacco smoking and drugs. Drugs that lower LOS pressure include
anticholinergics, antihistamines, TCAs and CCBs.
Complications:
GORD may lead to oesphagitis, peptic oesophageal ulcer, oesophageal stricture, barretts
oesophagus and oesophageal adenocarcinoma. Factors that contribute to the development of
oesophagitis include the caustic nature of the reflux, the inability to clear the reflux from the
oesophagus and the volume of gastric contents.

Signs and Symptoms

The most prominent symptom of GORD is heartburn, with or without regurgitation of gastric
contents into the mouth. Infants present with vomiting, irritability, anorexia and sometimes
symptoms of chronic aspiration.
Oesophagitis may cause odynophagia (a dysphagia in which swallowing causes pain) and
even oesphageal haemorrhage, which is usually occult, but can be massive. Peptic stricture
causes a gradually progressive dysphagia for solid foods. Peptic oesophageal ulcers cause the
same pain as gastric or duodenal ulcers, but the pain is usually localised to the xiphoid or
high substernal region. They generally heal slowly, tend to recur and usually leave a stricture
on healing.

Diagnosis
Clinical diagnosis
Endoscopy for those not responding to emperic treatment
A detailed history points to the diagnosis. Patients with typical symptoms of gORD may be
given a trial of therapy. Patients who do not improve or have long-standing symptoms or
symptoms of complications, should be studied. Endoscopy with cytologic washings and biopsy
of abnormal areas, is the test of choice. Endoscopic biopsy is the only test that consistently
detects the columnar musocsal changes of barretts oesophagus.

Treatment
Head of bed elevated
Coffee, alcohol, fats and smoking avoided
PPIs
Management of uncomplicated GORD consists of elevating the head of the bed about 15cm
and avoiding the following: eating within 2-3h of bedtime, strong stimulants of acid secretion
(coffee and alcohol), certain drugs (eg. Anticholinergics), specific foods and smoking.

Omeprazole or oesomeprazole may be given before breakfast or in some cases bid, and can
be continued long-term.

Gastritis

Gastritis is inflammation of the gastric mucosa caused by any of several


conditions, including infection (helicobacter pylori), drugs (NSAIDs, alcohol),
stress, and autoimmune phenomena (atrophic gastritis). Many cases are
asymptomatic, but dyspepsia (indigestion) and GI bleeding sometimes occur.
Diagnosis is by endoscopy. Treatment is directed at the cause but often
includes acid suppression and, for H. pylori, antibiotics.

Aetiology

Acute:
Aspirin and other NSAIDs
Alcohol, cigarette smoking
Stress, burns, surgery
Trauma: NG tube
Chemotherapy, irradiation
Infection: salmonellosis, CMV,

Chronic:
Helicobacter pylori: most common
cause
Autoimmune: pernicious anaemia
Crohns disease
Bile reflux

Signs and Symptoms


Can be asymptomatic, or present with dyspepsia, nausea or vomiting. Often, the first sign is
haematemesis or melena.

Treatment
For bleeding: endoscopic haemostasis
For acid suppression: h2 antagonist or PPI

Peptic Ulcer caused by H. Pylori

A peptic ulcer is an erosion in a segment of the GI mucosa, typically in the


stomach or first few cm of the duodenum. Nearly all ulcers are caused by
helicobacter pylori infection or NSAID use. Symptoms typically include
burning epigastric pain that is often relieved by food. Diagnosis is by
endoscopy and testing for H. pylori. Treatment involves acid suppression,
eradication of H. pylori (if present), and avoidance of NSAIDs.
Treatment
Eradication of H. pylori
Acid suppressive drugs
Antibiotics plus a PPI are the mainstay of treatment for a H. pylori infection. Triple therapy is
recommended with:
Oral omeprazole (PPI)
Clarithromycin
Amoxicillin (or metronidazole)

Diverticular Disease

Diverticula are saclike mucosal out-pouchings that protrude from a tubular


structure. True diverticular contain all layers of the parent structure; while
false or pseudodiverticula are mucosal prjections through the muscular later.
Esophageal and meckels diverticula are true diverticula. Colonic diverticula
are pseudodiverticula; they cause symptoms by trapping faeces and being
inflamed or infected, bleeding or rupturing. This passage focuses on
diverticulitis.
Diverticulitis is inflammation of a diverticulum, which can result in phlegmon
(spreading, diffuse inflammation with formation of exudate or pus) of the

bowel wall, peritonitis, perforation, fistula, or abscess. The primary symptom


is abdominal pain. Diagnosis is by CT. Treatment is with antibiotics
(ciprofloxacin, cephalosporin and metronidazole) and occasionally surgery.

Aetiology
Diverticulitis occurs when a micro or macro perforation develops in a diverticulum, releasing
intestinal bacteria. The resultant inflammation remains localised in 75% of patients. The
remaining 25% may develop abscess, free intraperitoneal perforation, bowel obstruction or
fistulas.
Occurs in people > 35years old and increases with age.

Signs and Symptoms


Diverticulitis usually manifests with pain or tenderness in the lower left quadrant of the
abdomen and fever. Peritoneal signs (eg. Rebound or guarding) may be present, especially if
there is abscesses or perforation. Fistulas may manifest as pneumaturia, feculent vaginal
discharge or a cutaneous or myofascial infection of the abdominal wall, perneum or upper leg.
Patients with bowel obstruction have nausea, vomiting and abdominal distention.

Diagnosis
Abdominal CT
Colonoscopy after resolution
Clinical suspicion is high in patients with known diverticulosis. However because other
disorders can have similar symptoms (appendicitis, colon or avarian cancer), testing is
required. Abdominal CT with oral and IV contrast is preferred, although findings in about 10%
of patients cannot be distinguished from colon cancer. Colonoscopy after resolution of the
acute infection, is necessary for definitive diagnosis.

Treatment
Liquid diet, oral antibiotics for mild disease
IV antibiotics, npo for more severe disease
CT-guided percutaneous drainage of abscess
Sometimes surgery
A patient who is not very ill is treated at home with rest, a liquid diet and oral antibiotics
(ciprofloxacin, metronidazole and amoxicillin). Symptoms usually subside rapidly.
Patients with more severe symptoms should be hospitalised, as should patients taking
prednisone (who are at higher risk of perforation and general peritonitis). Treatment is bed
rest, npo, IV fluids and IV antibiotics.
Surgery involves resection of the affect colon and this is indicated for patients with free
perforation or general peritonitis.

Coeliac Disease

Coeliac disease is an immunologically mediated disease in genetically


susceptible people caused by intolerance to gluten, resulting in mucosal
inflammation and villous atrophy, which causes malabsorption. Smptoms

usually include diarrhoea and abdominal discomfort. Diagnosis is by smallbowel biopsies showing characterisitic though not specific pathologic
changines of villous atrophy that resolve with a strict gluten-free diet.

Epidemiology
Affects 10-20% of first degree relatives. Female to male ratio is 2:1. Onset is generally in
childhood although can vary drastically.

Aetiology
Coeliac disease is a hereditary disorder causes by sensitivity to the gliadin fraction of gluten,
a protein found in wheat, rye and barley. In a genetically susceptible person, T cells are
activated and cause an inflammatory response which causes characteristic mucosal villous
atrophy in the small bowel.

Signs and Symptoms


The clinical presentation varies, from asymptomatic to significant GI symptoms.
It can manifest in infancy and childhood after introduction to cereals. The child has FTT,
apathy, anorexia, pallor. Abdominal distention and muscle wasting. Stools are soft, bulky,
clay-coloured and offensive.
In adults, lassitude, weakness and anorexia are most common. Steatorrhoea ranges from
mild, to severe.

Diagnosis
Serologic markers
Small-bowel biopsy
The diagnosis is suspected clinically and by laboratory abnormalities suggestive of
malabsorption. Family incidence is a valuable clue. Celiac disease should be strongly
considered in a patient with iron deficiency, without obvious GI bleeding.
Confirmation requires a small-bowel biopsy from the second portion of the duodenum.
Findings include lack-of, or shortening of villi, increased intraepithelial cells, and crypt
hyperplasia. However, such findings can also occur in tropical sprue, severe intestinal
bacterial overgrowth, eosinophilic enteritis, lactose introlerance and lymphoma.
Because biopsy is not specific, serologic markers can aid diagnosis. Anti-tissue
transglutaminase (AGA) and anti-endomysial antibody (EMA) tests are >90% sensitive and
specific.

Treatment
Gluten-free diet
Supplements to replace any serious deficiencies
On a gluten free diet, symptoms improve in as fast as 1-2 weeks.
If a patient responds poorly to gluten withdrawal, either the diagnosis is wrong, or the disease
has become refractory, in which case corticosteroids, DMARDs or MAbs (eg. Infliximab TNF
inhibitor) may be used.

Irritable Bowel Syndrome

Irritable bowel syndrome (IBS) is characterised by abdominal discomfort or


pain that is accompanied by at least two of the following: relief by defecation,
change in frequency of stool or change in consistency of stool. The cause is
unknown and the pathophysiology is incompletely understood. Diagnosis is
clinical. Treatment is symptomatic, consisting of dietary management and
drugs, including anticholinergics and agents active at serotonin receptors.
Aetiology
The cause is unknown. It is believed to be a combination of psychosocial and physiological
factors.

Signs and Symptoms


IBS tends to begin in the teens and 20s, causing bouts of symptoms that recur at irregular
periods. Onset in late adult life is less common but not rare. Symptoms are often triggered by
food, particularly fats, or by stress.
Patients have abdominal discomfort, which varies considerably but is often located in the
lower quadrant, steady or cramping in nature and relieved by defacation. In addition,
abdominal discomfort is temporally associated with alterations in stool frequency (increase in
diarrhoea and decreased in constipation) and consistency (loose or lumpy and hard).
Although bowel patterns are relatively consistent in most patients, it is not unusual for
patients to alternate between constipation and diarrhoea. Patients may also have symptoms
of abnormal stool passage (straining, urgency, tenesmus), pass mucus or complain of bloating
or abdominal distension. Many patients also have symptoms of dyspepsia.

Diagnosis
Clinical evaluation with Rome criteria
Screening for organic causes with basic laboratory tests and sigmoidoscopy or colonoscopy.
Patients with red flag findings must have other tests (rectal blood, weight loss, fever)
Diagnosis is based on characteristic bowel patterns, time and character of pain, and exclusion
of other disease processes through physical examination and routine diagnostic tests. The
rome criteria are at least 2 of the following: relief after defecation, change in stool frequency
or change in stool consistency.

Treatment
Support and understanding
Normal diet, avoiding gas-producing and diarrhoea-producing foods
Increased fiber intake for constipation
Anticholinergic drugs (hyoscine, propantheline) or serotonin receptor agonists
Loperamide for diarrhoea
Possibly TCAs
Anticholinergic drugs may be used for their anti-spasmodic effects.
Serotonin agonists may be of bene to stimulate motility and alleviate constipation.
Loperamide may be used for diarrhoea.

Crohns Disease

Crohns disease is a chronic transmural inflammatory disease that usually


affects the distal ileum and colon but may occur in any part of the GI tract.
Symptoms include diarrhoea and abdominal pain. Abscesses, internal and
external fistulas and bowel obstruction may arise. Extraintestinal symptoms,
particularly arthritis may occur. Diagnosis is by colonoscopy and barium
contrast studies. Treatment is with 5-ASA, corticosteroids,
immunomodulators, anticytokines, antibiotics and often surgery.
Epidemiology

Occurs in 1-6 per 100,000 people.

Aetiology

There is no known cause of Crohns disease, however it is believed to be autoimmune.


Crohns disease begins with crypt inflammation and abscesses, which progress to tiny focal
ulcers. These lesions may then develop into deep longitudinal and transverse ulcerswith
invtervening mucosal oedema, creating a characteristic cobblestoned appearance to the
bowel.
Inflammation spreads transmurally, leading to lymphedema and thickening of bowel wall and
mesentery. This extensive inflammation may result in hypertrophy of various structures and
possible strictures, leading to obstruction. Abscesses are common and fistulas often penetrate
into adjoining structures, including other loops of bowel, the bladder or psoas muscle. Fistulas
may even extend to the skin of the anterior abdomen or flanks.
Segments of diseased bowel are sharply demarcated from adjacent normal bowel (skip
areas). About 35% of Crohns disease cases involve the ileum alone; 45% the ileum and
colon; and about 20% involve the colon alone, most of which (unlike ulcerative colitis) spares
the rectum.

Signs and Symptoms


The most common initial manifestation is chronic diarrhoea with abdominal pain, fever,
anorexia and weight loss. The abdomen is tender and a mass or fullness may be palpable.
Gross rectal bleeding isunusual except in isolated colonic disease, which may manifest
similarly to UC.
About 33% of patients will have perianal disease (especially fistulas and fissures), which is
sometimes the most prominent or initial complaint.
Chronic disease causes a variety of systemic symptoms, including fever, weight loss,
undernutrition and extraintestinal manifestations.

Diagnosis
Barium x-rays of the stomach, small bowel, and colon
Abdominal CT
Sometimes MR enterography, upper endoscopy and/or colonoscopy
Crohns disease should be suspected in a patient with inflammatory or obstructive symptoms
or in a patient without prominent GI symptoms but with perianal fistulas or abscesses or with
otherwise unexplained arthritis, fever, anaemia or stunted growth.

Differentiation from UC may be an issue in the 20% of cases in which Crohns disease is
confined to the colon; however as treatment is similar, this is only important in the case of
surgery.
If initial presentation is less acute, an upper GI series is preferred over CT. These imaging
studies are virtually diagnostic if they show characteristic strictures or fistulas with
accompanying separation of bowel loops. Barium enema x-ray may be used if symptoms
seem predominatly colonic (eg. Diarrhoea) and may show reflux of barium into the terminal
ileum with irregularity, nodularity, stiffness, wall thickening and a narrowed lumen.

Treatment
Loperamide (Imodium) or antispasmodics (atropine, dicycloverine) for relief
5-ASA or antibiotics
Other drugs depending on symptoms and severity
Sometimes surgery
Fistulas:
Fistulas are treated initially with metronidazole (antibiotic) and ciprofloxacin (quinone). If no
response in 3-4 weeks, may receive an immunomodulator.
Surgery:
Even though about 70% of patients will require an operation, it is done reluctantly. Resection
of the involved bowel may ameliorate symptoms but does not cure the disease. There is also
a very high relapse rate of >70% at 1 year.

5-Aminosalycylic acid:
Examples: olsalazine, sulphasalazine
Class: anti-inflammatory (GI)
MOA: breaks down into 5-ASA and sulfapyridine which has anti-inflammatory and free radical
scavenging effects.
Indications: Ulcerative colitis and Crohns disease
AE: GIT, skin, malaise
Immunosuppressants
Examples: azathioprine, methotrexate, infliximab, ciclosporin
Class: Immunosuppressant - DMARD
MOA: inhibits purine synthesis
Indications: refractory Crohns disease, transplant rejection, rheumatoid arthritis
AE: myelosuppression

Ulcerative Colitis

Ulcerative colitis (UC) is a chronic inflammatory and ulcerative disease arising in the colonic
mucosa, characterised most often by bloody diarrhoea. Extraintestinal symptoms include,
anorexia, fatigue, arthritis. Long-term risk of colon cancer is high. Diagnosis is by
colonoscopy. Treatment is with 5-aminosalicylic acid, corticosteroids, immunomodulators,
anticytokines, antibiotics and occasionally surgery.

Epidemiology

2 10 per 100000 people.

Aetiology

It has an unknown cause. It begins in the rectum and may remain localised (ulcerative
proctitis) or extends proximally, sometimes involving the entire colon.
The inflammation caused by US affects the mucosa and submucosa and there is a sharp
border between normal and affected tissue. In early cases the mucous membrane is
erythematous, finely granular, and friable, with loss of the normal vascular pattern, and often
with scattered haemorrhagic areas.
Islands of normal or hyperplastic inflammatory mucosa (pseudopolyps) project above areas of
ulcerated mucosa.

Signs and Symptoms


Bloody diarrhoea of varied intensy and duration is interspersed with asymptomatic intervals.
Usally an attack begins insidiously, with increased udgency to defecate, mild lower abdominal
cramps, and blood and mucus in the stools. Some cases develop aftre an infection.
If confined to the rectosigmoid, stolls may be normal or hard and dry. If more proximal, stools
become looser and the patient may have >10 bowel movements per day, often with severe
cramps and distressing rectal tenesmus.
Systemic signs and symptoms, more common with extensive UC, include malaise, fever,
anaemia, anorexia and weight loss. Extraintestinal manifestations (joint and skin
complications) are most common when sstemic symptoms are present.

Diagnosis
Stool cultures and microscopy (to exclude infection eg. Clostridium difficile)
Sigmoidoscopy with biopsy
The diagnosis is suggested by typical symptoms and signs, particularly when accompanied by
extraintestinal manifestations or a hitory of previous similar attacks. UC should be
differentiated from Crohns Disease, and from other causes of acute colitis.
Sigmoidoscopy should be done; it allows visual confirmation of colitis and permits direct
sampling of stool or mucus for culture and microscopic evaluation, as well as biopsy of
affected areas. Visual inspection and biopsies may be nondiagnostic (because of much
overlap between different types of collitis), however can tell apart infectious colitis from
Crohns colitis.

Treatment

Loperamide (Imodium antidiarrhoeal) and dietary management for symptom relief


5-aminosalicylic acid (5-ASA)
Corticosteroids and other drugs depending on symptoms and severity
Loperamide may be given bid to qid for mild diarrhoea, to higher oral doses for more intense
diarrhoea.

5-ASA is given once or bid via enemas or suppositories.


In moderate or extensive disease, oral 5-ASA may be given in addition to the enemas. Also,
corticosteroids and immunomodulators may be indicated.
In the case of severe disease, patients will have to be hospitalised and placed on IV
corticosteroids.
In 1/3rd of patients, surgery will be necessary which will involve a total proctocolectomy. This
will return life expectancy and QoL to normal.

Colorectal Cancer

Colorectal cancer (CRC) is extremely common. Symptoms include blood in the stool or
changes in bowel habits. Screening is with fecal occult blood testing. Diagnosis is by
colonoscopy. Treatment is surgical resection and chemotherapy for nodal involvement.

Epidemiology

CRC accounts for more new cases than any anatomic site except the lung. Incidence begins to
rise at age 40 and peaks at age 60-75. Overall, 70% of cases occur in the rectum and
sigmoid, and 95% are adenocarcinomas. Colon cancer is more common among women; rectal
cancer is more common among men.

Aetiology

CRC most often occurs as transformation within adenomatous polyps. About 80% of cases are
sporadic, and 20% have an inheritable component. Predisposing factors include chronic
ulcerative colitis and granulomatous colitis; the risk of CRC increases with the duration of
these disorders.

Signs and Symptoms

Colorectal adenocarcinoma grows slowly and a long interval elapses before it is large enough
to cause symptoms. Symptoms depend on lesion location, type, extent and complications.

The right colon has a large caliber and a thin wall so obstruction is usually very late. Bleeding
is usually occult (seen in faeces generally microscopically). Fatigue and weakness caused by
severe anaemia may by the only complaints. Tumours sometimes grow large enough to be
palpable through the abdominal wall before other symptoms appear.
The left colon has a smaller lumen, the faeces are semi-solid and cancer tends to encircle the
bowel, causing alternating constipation and increased stoll frequency or diarrhoea. Partial
obstruction with colicky abdominal pain or complete obsturction may be the initial
manifestation. The stool may be streaked or mixed with blood. Some patients present with
symptoms of perforation, usually walled off (focal pain and tenderness), or rarely diffuse
peritonitis.
In rectal cancer, the most common initial symptom is bleeding with defecation. Whenever
rectal bleeding occurs, even with obvious haemorrhoids or known diverticular disease,
coexisting cancer must be ruled out. Tenesmus or a sensation of incomplete evacuation may
be present. Pain is common with perirectal involvement.

Diagnosis
Colonoscopy
Screening Tests:
For average-risk patients, FOB testing should be done annually after the age of 50, with
flexible sigmoidoscopy every 5 years.
Diagnostic Tests:
Patients with positive FOB tests require colonoscopy, as do those with lesions seen on
sigmoidoscopy or imaging study. All lesions should be completely removed for histologic

examination. If a lesion is sessile (attached directly to the wall) or not removable at


colonoscopy, surgical excision should be strongly considered.
Once cancer is diagnosed, patients should have an abdominal CT, chest x-ray and routine
laboratory tests to seek metastatic disease and anaemia and to evaluate overall condition.

Prognosis

Prognosis depends greatly on stage. The 10 yr survival rate for cancer limited to the mucosa
approaches 90%; with extension through the bowel wall 70-80%; with positive lymph nodes
30-50%; and with metastatic disease, <20%.

Treatment

Surgical resection, sometimes combined with chemotherapy, radiation or both.

Surgery for cure can be attempted in the 70% of patients presenting without metastatic
disease. It consists of wide resection and its regional lymphatic drainage with reanastomosis
of bowel segments.
Chemotherapy (5-flurouracil usually) improves survival by 10-30% in colon cancer patients
with positive lymph nodes.
In the case of palliation, median survival is 7 months.

Myasthenia Gravis

Myasthenia gravis involves episodic muscle weakness and easy fatigability


caused by autoantibody and cell-mediated destruction of acetylcholine
receptors. It is more common among young women but may occur in men or
women at any age. Symptoms worsen with muscle activity and lessen with
rest. Diagnosis is by measurement of serum acetylcholine receptor (AChR)
antibody levels, electromyography and sometimes IV edrophonium challenge,
which briefly lessens the weakness. Treatment includes anticholinesterase
drugs, immunosuppressants, corticosteroids, plasma exchange, IV immune
globin, and possibly thymectomy.
Epidemiology

Myasthenia gravis most commonly affects young women aged 20 40 yrs.

Aetiology

It results from an autoimmune attack on the post synaptic Ach receptors, which disrupts
neuromuscular transmission. The trigger is unknown, but the disorder is associated with
abnormalities of the thymus, autoimmune hyperthyroidism and other autoimmune disorders.
65% of patients will have thymic hyperplasia, and 10% have a thymoma.
Uncommon forms:
Ocular myasthenia gravis (15% of cases) involves only extraocular muscles.

Signs and Symptoms


The most common symptoms are ptosis, diplopia and muscle weakness after using the
affected muscle. Occular muscles are affected initially in 40% of patients and eventually 85%.
Handgrip may alternate between weak and normal. Neck muscles may become weak. If
generalised myasthenia gravis is going to develop after ocular symptoms, it usually does so
within the first 3 years.
Myasthenic Crisis may develop in 15-20% of patients over a lifetime. It is a severe
generalised quadriparesis or life-threatening respiratory muscle weakness. It is often due to a
supervening infection that reactivates the immune system.

Diagnosis
Bedside tests
AChR antibody levels, electromyography or both.
The traditional anticholinesterase test, done at the bedside by using the short-acting (<5 min)
drug edrophonium, is positive in most patients who have myasthenia with overt weakness. It
should only be done in patients with obvious ptosis or ophthalmoparesis; as these deficits
must be clearly apparent to clearly see the improvement to normal strength. To perform the
test, fatigue the muscles, give 2mg of edrophonium. If no adverse event occurs, give another
8mg. Rapid (<2min) improvement should be seen for a positive test result.
Following this, a serum AChR antibody level test should be performed to confirm the
diagnosis. These antibodies are present in 80%-90% of pts with generalised, but only 50%
with the ocular form.

After confirmation of diagnosis, a x-ray of the thorax should be performed to check for a
thymoma.