Documente Academic
Documente Profesional
Documente Cultură
System
Contents
Page 5
Cardiovascular Anatomy
Pericardium
Page 7
Cardiac Muscle
Sarcomeres
Page 8
Arteries
Veins
Page 10
Page 11
Page 12
Page 14
Cardiac Cycle
Page 15
Heart Murmurs
Page 17
Blood Pressure
Definitions
Page 19
Electrocardiograms (ECG)
Cardiac Arrests
12 Lead ECG
Takotsubo Syndrome
Page 28
Page 29
Page 31
Page 33
Left-to-Right Shunts
Right-to-Left Shunts
Obstructive Lesions
Page 33
Page 36
Page 38
Page 40
Cardiomyopathy
Myocarditis
Page 41
Cardiovascular Drugs
Diuretics
-Blockers
Statins
Nitrates
Anti-arrhythmics
Nicorandil
Page 46
Page 47
Page 48
Hypertension (HTN)
Ischaemic Heart Disease (IHD) / Angina / Unstable Angina (UA) / NSTEMI / STEMI
Arrhythmias
Heart Failure
Hypercholesterolaemia
Page 51
Cardiovascular History
Page 51
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)
Parotid Gland
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
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
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.
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
Fat malabsorption can be due to pancreatic, hepatic and small intestinal mucosal reasons.
This leads to pale stools or steatorrhoea.
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
Oral vs. IV
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!
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
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
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.
Cirrhosis
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
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)
lab tests:
o
o
o
o
o
o
lfts
bilirubin
albumin
INR
FBC
Urine
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:
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
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.)
Antagonists:
Alosetron
o 5-HT3 antagonist
o Only given to women on a very restricted program.
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.
Associated with rice dishes. Acute onset 1-6h of nausea, abdominal pain and vomiting w/o
diarrhoea.
Campylobacter Spp.
Salmonellosis
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
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.
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
Risk Factors
Pathology
Steatosis (macrovesicular)
Alcoholic hepatitis (steatohepatitis)
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.
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
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
Treatment
For bleeding: endoscopic haemostasis
For acid suppression: h2 antagonist or PPI
Diverticular Disease
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.
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
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.
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.
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
Aetiology
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
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.
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
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.
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
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
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
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.
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.