GASTROENTEROLOGY

Nem’s Notes… Phase 2 Year 2

GASTROENTEROLOGY 1 (page 1 of 4) Oropharynx & Oesophagus

Oral Ulceration Causes: (a) Gastrointestinal Crohn’s DiseaseUlcerative ColitisCoeliac DiseaseLupus Erythematosus (systemic/discoid)Behçet’s Disease

(b) Dermatalogical Lichen PlanusErythema MultiformeDermatitis Herpetiformis

(c) Viral HSVCoxsackie

(d) Bacterial SyphilisTB

(e) Trauma Poorly Fitting DenturesHarsh BrushingSharp Teeth

Differential The differential diagnosis for white patches in the mouth is:Diagnosis (a) Ulceration (apthous)

(b) Neoplastic Lesion(c) Candida (Oral lichen planus/thrush)(d) Systemic Lupus Erythematosus (SLE)(e) Leukoplakia

Xerostomia Xerostomia is due to decreased salivation causing a dry mouth. Causes include:(a) Sjörgen’s Syndrome(b) Drugs (anti-Parkinson’s, antihistamine, lithium, antidepressants)(c) Radiotherapy(d) Psychogenic Causes(e) Dehydration, Shock, Renal Failure

Oesophagitis Oesophagitis is inflammation of the oesophagus. Causes include:(a) Gastrooesophageal Reflux Disease (GORD)(b) Infection(c) Neoplastic Disease(d) Swallowed Corrosives

Hiatus Hernia There are two type of hiatus hernia

(a) Sliding (80%) (b) Rolling/Paraoesophageal (20%)

Diaphragm

Stomac h s lidesthrough diaphragm

Diaphragm

Herniated s ac trappednex t to oes ophagus

more online at http://homepage.virgin.net/nemonique.sam/noteindx.htm page 1 of 44

http://homepage.virgin.net/nemonique.sam/noteindx.htm



GORD (a) Smoking (f) ObesityRisk Factors (b) Alcohol (g) Tight clothes

(c) Dietary Fat (h) Big Meals(d) Coffee (i) Surgery in Achalasia(e) Pregnancy (j) Hiatus Hernia

Mechanisms (a) Low resting lower oesophageal sphincter (LOS) tone which does notof GORD increase on lying flat (as is normal)

(b) LOS tone does not increase due to raised intraabdominal pressure (eg pregnancy or tight clothing)

(c) Decreased peristalsis resulting in decreased acid clearance. Exacerbated by hiatus hernia which traps acid in the hernial sac.

(d) Decreased oesophageal mucosal resistance to acid(e) Hiatus hernia preventing the ‘pinchcock’ mechanism of diaphragm(f) Delayed gastric emptying increasing chance of reflux

Treatment (a) Drugs Magnesium Trisilicateof GORD Alginate containing antacids (Gaviscon)

H2 receptor antagonists (Ranitidine/Cimetidine)Proton Pump inhibitors (Omeprazole)Prokinetic agents (Cisapride)

(b) Helicobacter Pylori Eradication (H. pylori can cause increased acid secretion in some patients)

(c) Surgery Hernia Repair (Laparoscopically)Anti-reflux Surgery (Fundoplication)

Effect of (a) Heartburn due to stimulation of hypersensitive oesophageal mucosa by acid/heatOesophagitis (b) Haematemesis, Iron deficiency anaemia from blood loss.

(c) Regurgitation of food and acis into the mouth

Reflux & There is a poor correlation between the degree of oesophagitis and heartburn due toOesophagitis acid reflux, although oesophagitis is caused by irritation of the oesophagus.

Barrett’s Barrett’s oesophagus is defined as oesophagus containing > 3cm of specialised Oesophagus columnar epitheilum extending up into the lower oesophageal mucosa. For this

reason it is also known as columnar-lined oesophagus. It is usually due to long standing acid reflux, and is premalignant for adenocarcinoma ( Risk x40). Loss of the p53 tumour suppressor gene may be important.

Heartburn Heartburn is a burning retrosternal pain anywhere between the epigastrium to the throat, characteristically worsening on stooping, lying, hot drinks and relieved by antacids. The differential diagnosis is MI or IHD.

Reflux Reflux is a normal event occurring when gastric contents make contact with the lower oesophageal mucosa. It causes symptoms when the anti-reflux mechanisms fail to reduce acid contact time. This can cause heartburn, oesophagitis, barrett’s oesophagus, but may be asymptomatic until an episode of haematemesis or chronic anaemia.





Dysphagia Dysphagia is defined as difficulty swallowing. Causes include:(a) Disease of Mouth & Tongue (eg tonsillitis)(b) Neuromuscular Disorders (pharyngeal disorders, myasthenia gravis)(c) Oesophageal Motility Disorders (achalasia, scleroderma, DM)(d) Extrinsic Pressure (mediastinal glands, goitre, enlarged left atrium)(e) Intrinsic Lesion (foreign body, stricture)(f) Lower Oesophageal Rings

Management of (a) Drug treatment (see above)Reflux Disease (b) Decrease intraabdominal pressure (lose weight, braces instead of belts)

(c) Smaller low fat meals and no food <3hrs before bed(d) Regular endoscopic surveillance for Barrett’s(e) Multiple biopsies for detection of dysplasia(f) Oesophageal resection or Laser ablation if abnormalities found.

Oesophageal (a) Benign LeiomyomaTumours Squamous Papilloma

(b) Malignant Squamous CarcinomaAdenocarcinoma

Epidemiology High incidence in China, parts of Africa and Caspian regions of Iran.Oesophageal Tumour In UK oesophageal carcinoma has an incidence of 5-10 per 100,000 .

It represents 2.2% of all malignant disease in the UK.

Risk Factors (a) MaleOesophageal Tumour (b) Heavy alcohol intake

(c) Heavy smoking(d) Plummer-Vinson syndrome(e) Achalasia(f) Coeliac disease

Clinical (a) Progressive and unrelenting dysphagia (first solids then liquids)Appearance (b) Weight loss secondary to dysphagiaOesophageal Tumour (c) Anorexia secondary to dysphagia

(d) Cough and aspiration of saliva into lungs (due to dysphagia)(e) Lymphadenopathy in metastatic disease

Pathway of (a) Ulcerative direct invasion of surrounding tissueSpread (b) Lymphatic spreadOesophageal Tumour NB Metastases rarely found on autopsy

Investigation (a) Barium SwallowOesophageal Tumour (b) Oesophagoscopy

(c) CT Scan of thorax and abdomen(d) Endoscopic Ultrasound





ManagementOesophageal Tumour

Treatment Indication

Surgery When tumour has not infiltrated beyond oesophageal wall

Radiotherapy Squamous Carcinoma of upper two-thirds of the oesophagus

Chemotherapy Often in combination with radiotherapy

Palliative Therapy

Stent dilatation of the oesophagusLaser ablationAlcohol injection

Overall 10% 5 yr survival; with treatment a 80% 5 yr survival is possible.

Achalasia Achalasia is a motility disorder involving aperistalsis of the oesophagus and failure of the LOS to relax, resulting in difficulty swallowing. Most cases are idiopathic. Often degenerative lesions are found in the vagus. NO neurones are more affected than cholinergic neurones causing lack of relaxation of the LOS. Two thirds of patients have autoantibody against dopamine carrying protein.

Treatment (a) Endoscopic dilatation of the LOSAchalasia (b) Endoscopic injection of botulinum toxin into the LOS

(c) Heller’s operation (laparoscopically) to divide muscle at lower end of oesophagus(d) Nifedipine (20mg sublingually) in older patients

Motility (a) Systemic Sclerosis (replacement of smooth muscle by fibrous tissue)Disorders (b) Diffuse Oesophageal Spasm

Symptoms: (a) Atypical or non-cardiac chest pain due to lodged food.(b) Dysphagia is common(c) Regurgitation of food(d) Aspiration pneumonia secondary to (c)

Investigations of (a) Barium swallowthe Oesophagus (b) Chest X-Ray

(c) Ultrasonography(d) CT Imaging of thorax/abdomen(e) MRI Imaging(f) Radionucleotide Imaging (detecting GORD)(g) Endoscopy




GASTROENTEROLOGY 2 (page 1 of 3) Stomach & Duodenum

Acute Gastritis In acute gastritis there is an acute inflammatory infiltrate, predominantly of neutrophils, which invade the superficial gastric mucosa. There are various forms including:

(a) Acute erosive gastritis due to multiple small erosions(b) Acute gastic ulceration due to multiple larger, less superficial erosions

Aetiology of (a) Drugs NSAIDs esp aspirinAcute Gastritis (b) Alcohol

(c) Infection (CMV, HSV)(d) Stress(e) Secondary to burns (Curling ulcers)(f) Trauma, Shock, Renal failure

Complications (a) Progression to chronic stateAcute Gastritis (b) Ulceration

(c) Haemorrhage

Chronic Chronic active gastritis consists of infiltration of the lamina propria with lymphocytesGastritis plasma cells leading to atrophy of the mucosa and fibrosis.

Causes (a) Helicobacter Pylori (main cause)Chronic Gastritis (b) Autoimmune (Pernicious anaemia – B12 malabsorption)

(c) Chronic Ingestion of NSAIDs/Aspirin(d) Biliary Reflux

H. Pylori Helicobacter Pylori initially causes acute gastritis leadin to chronic disease.Infection Infection causes: (a) Gastroduodenal Disease (duodenal ulcer)

(b) Intestinal Metaplasia (gastric cancer)(c) Non-ulcer Dyspepsia

Complications (a) H. Pylori infection see above(b) Autoimmune pernicious anaemia(c) Chronic NSAIDs gastric erosion

gastric ulcer

Peptic Ulcer A break in the superficial epithelial cells penetrating down to the muscularis mucosa. Ulcers can be either acute or chronic.

Acute caused by: (a) acute gastritis(b) complication of severe stress response(c) hyperacidity

Chronic causes: (a) H pylori infection(b) NSAIDs

Site of Ulcers (a) Duodenum (mostly in duodenal cap)(b) Stomach (mostly lesser curve)

Pathogenesis (a) Gastric (i) Destruction/loss of integrity of mucous barrier (reflux of bile)Peptic Ulcer (ii) Increased acid secretion (not so important)

(b) Duodenal (i) Increased acid production (due to H pylori)(ii) Infection causing metaplasia, inflammation and ulceration





Complications (a) Perforation (spillage of gastric contents leading to peritonitis)Peptic Ulcer (b) Penetration (ulcer erodes into adjacent organ eg liver or pancreas)

(c) Haemorrhage (from eroded vessels)(d) Pyloric Stenosis (obstruction due to oedema/scarring of ulcer)

Non-Ulcer Non-ulcer dyspepsia is a common condition where the patient presents withDyspepsia dyspepsia and other ulcer like symptoms but where investigation fails to find an ulcer.

Symptoms are mainly stress related and include:(a) Indigestion(b) Wind(c) Nausea(d) Early satiety(e) Heartburn

Functional dyspepsia can be differentiated from peptic ulcer using the following table

Functional Dyspepsia Peptic Ulceration

Site of PainDiffuse all overFits no recognisable pattern

EpigastricPoints with one finger

Frequency Daily for long periods Episodic

Food/MealsPain unaffectedLasts all day

Exacerbates or helps pain

Antacids No help Helps pain

Nocturnal Pain Waking Patient

Rare Common

Vomiting No effect Relieves pain

Investigations (a) EndoscopyNon-Ulcer Dyspepsia (b) Ultrasound (to detect gallstones)

(c) Detailed History (to detect psychogenic causes)

Management (a) Explanation & ReassuranceNon-Ulcer Dyspepsia (b) Encourage patient to stop smoking and drinking alcohol

(c) Drugs (antacids/prokinetics)(d) Counselling for stress (eg marriage/divorce, financial/employment difficulties)(e) Formal psychotherapy for major chronic psychological disorders

Gastric Tumours of the stomach include:Carcinoma (a) Benign leiomyoma

(b) Benign gastric polyps(c) Malignant carcinoma(d) Malignant lymphoma(e) Malignant stromal tumour

Epidemiology In the UK gastric carcinoma causes 12/13 deaths per 100,000Gastric Carcinoma More common in China, Japan, S America

Uncommon in USA even in Japanese migrantsMore common in menIncidence rises after 50 yrs of age





Risk Factors (a) SmokingGastric Carcinoma (b) Alcohol

(c) H pylori(d) Dietary factors (high salted, pickled, smoked food, low vitamin A and C)(e) Autoimmune gastritis (pernicious anaemia)(f) Adenomatous gastric polyps

Early Gastric Most gastric cancers are quite advanced at time of initial diagnosis and only 45% ofCancer cases can be operated on. This accounts for the poor prognosis of gastric cancers.

Thus early diagnosis of symptoms is extremely important.

Gastric cancers can be classed as either:(a) Early confined to mucosa or submucosa (90% 5yr survival)(b) Late extending into muscle coats of stomach (10-15% 5yr survival)Classification is independent of lymph node involvement.

Appearance Endoscopically visible as slightly elevated plaque or shallow depression.Gastric Carcinoma (a) Intestinal Carcinoma glandular formation of mucous secreting

cells with well demarcated ‘pushing’ border(b) Diffuse Carcinoma chains of single cells with less well demarcated

border

Spread (a) Direct (pancreas, transverse colon, liver, spleen)Gastric Carcinoma (b) Lymphatic (nodes of the left and right gastric arteries)

(c) Blood (via portal vein metastasising to the liver)




GASTROENTEROLOGY 3 (page 1 of 4) The Small Intestine

Coeliac Disease (also called Gluten-sensitive Enteropathy).

Epidemiology (a) Common in Europe 1 in 1500 (UK) 1 in 300 (Ireland)(Coeliac Disease) (b) Rare in Black Africans

(c) Increased incidence (10-15%) in first-degree relatives(d) Increased incidence (30%) in monozygotic twins(e) Linked to specific HLA types (90% have HLA DQ2)

Therefore a mixture of genetic and environmental factors

Pathogenesis Uncertain pathogenesis and may be due to a variety of possible factors such as:(Coeliac Disease) (a) Toxicity of α-Gliadin (a peptide product of gluten)

(b) Immunogenetic factors (due to high incidence with specific HLA types)(c) Environmental factors (possibly a viral infection)

Pathology Affects the mucosa of the proximal small bowel, but decreasing in severity from(Coeliac Disease) jejunum to ileum (since the gluten is broken down to smaller non-toxic fragments).

(a) Absence of villi at the mucosal surface(b) Elongated crypts(c) Chronic inflammatory cells found in lamina propria

Causes of Subtotal (Flat) (a) Coeliac DiseaseVillous Atrophy (b) Dermatitis Herpetiformis

(c) Zollinger-Ellison Syndrome (rare)(d) Hypogammaglobulinaemia (rare)

Partial (Convoluted) (a) Tropical Sprue(b) Giardiasis

Clinical Coeliac disease can present at any age. Symptoms are very variable & non-specific:Features (a) Tiredness and malaise(Coeliac Disease) (b) Diarrhoea or Steatorrhoea

(c) Abdominal discomfort or pain(d) Weight Loss(e) Intermittent Mouth Ulcers(f) Intermittent Stomatitis

Rare complications might include tetany, osteomalacia, gross malnutrition with peripheral oedema.

Increased incidence of atopy and autoimmune disease such as thyroid disease and IDDM. Other associated diseases are inflammatory bowel disease, chronic liver disease.

There are usually few physical signs and are related to anaemia and malnutrition.

Investigation (a) Endomysial antibodies (IgA) Antibodies very specific and sensitive to coeliac(Coeliac Disease) disease and is carried out using

immunoflouresence on monkey oesophagus for transglutamase antigen.

(b) Jejunal biopsy The mucosal appearance of the biopsyis diagnostic for Coeliac Disease.

(c) Anti-reticulin antibodies Antibodies also very sensitive but also present inother GI diseases such as Crohn’s.

(d) Haematology Mild/moderate microcytic or macrocytic anaemiain 50% of cases





Treatment The removal of gluten from diet results in rapid clinical and morphological(Coeliac Disease) improvement in patients with Coeliac Disease.

Complications (a) Intestinal lymphoma(Coeliac Disease) (b) Ulcerative jejunitis

(c) Carcinoma

Malabsorption Malabsorption is the reduced absorption of food due to either:(a) intraluminal maldigestion (deficiency of enzymes)(b) mucosal malabsorption (due to decreased surface area)(c) postmucosal lymphatic obstruction (prevents uptake due to lymphatic blockage)

SEE Gastroenterology 6 (page 2 of 5)

Protein Losing Excessive loss of protein into the gut lumen sufficient to cause hypoproteinaemiaEnteropathy

Causes: (a) With mucosal erosions/ulcerations(i) Crohn’s Disease(ii) Ulcerative Colitis(iii) Oesophageal, Gastric, Colonic Ulcer(iv) Lymphoma(v) Radiation Damage

(b) Without mucosal erosions/ulcerations(i) Ménétrier’s Disease(ii) Bacterial Overgrowth(iii) Coeliac Disease(iv) Tropical Sprue(v) Eosinophilic gastroenteritis(vi) SLE

(c) With lymphatic obstruction(i) Intestinal lymphangiectasia(ii) Constrictive pericarditis(iii) Lymphoma(iv) Whipple’s Disease

Bacterial SEE Gastroenterology 6 (page 2 of 5)Overgrowth

Causes of Bacterial OvergrowthHypo/Achlorhydria Pernicious anaemia

Partial gastrectomyDecreased Motility Scleroderma

Diabetic autonomic neuropathyStructural Abnormality Gastric surgery (blind loops)

Jejunal diverticulosisEnterocolic fistulaeStrictures

Impaired Immunity Hypogammaglobulinaemia





Intestinal Effects: (a) 30-50% resection can be toleratedResection (b) Gastric hypersecretion

(c) Gallstones(d) Decreased fat absorption(e) Hyperplasia/hypertrophy of bowel (adaptation)(f) Increased bile salt synthesis (due to decreased absorption)(g) Pernicious anaemia (decreased B12 absorption)(h) Short gut syndrome

Investigation: (a) SBFT(b) B12 measurement(c) Bile salt measurement(d) Fat absorption tests

Treatment: (a) B12 replacement(b) Low fat diet for steatorrhoea(c) Cholestyramine or aluminium hydroxide for diarrhoea(d) Parenteral nutrition in short gut syndrome

Whipple’s This is a rare disease usually affecting males who present with steatorrhoea, weightDisease loss, abdominal pain and fever.

Villi are stunted and contain periodic acid-Schiff (PAS) positive macrophages (diagnostic). On electron microscopy bacilli can be seen within the macrophages.Treatment is with penicillin, tetracycline and sulphonamides.

Radiation Radiation over 50 Gy will damage the intestine (usually the ileum and rectum due toEnteritis pelvic irradiation). Symptoms of diarrhoea and abdominal pain usually improve within

6 weeks. Chronic radiation enteritis is diagnosed if symptoms persist for longer than 3 months.

There is muscle atrophy, ischaemic ulceration & obstruction due to fibrosed strictures.Malabsorption and bacterial overgrowth can occur. Treatment is symptomatic.

Meckel’s Most common abnormality of the GI tract affecting 2-3% of the population where aDiverticulum diverticulum projects from the wall of the ileum. It is usually asymptomatic but 50%

contain mucosa which secrete hydrochloric acid. Peptic ulceration and bleeding can occur. Acute inflammation may also occur which is indistinguishable from appendicitis. Treatment is surgical removal.

Amyloid Systemic amyloidosis may cause amyloid deposits in the GI tract. Deposits in the small intestine result in diarrhoea.

Connective Disorders of the connective tissue can affect the GI tract. Systemic sclerosis mostTissue commonly affects the oesophagus although occasionally the small bowel and colon. It

is frequently asymptomatic but diarrhoea and steatorrhoea may occur due to bacterial overgrowth secondary to decreased motility, dilatation and presence of diverticulae. Rheumatoid arthritis and SLE may also cause GI problems.

TumoursBenign MalignantAdenomasLeiomyomasLipomasHamartomas

AdenocarcinomasCarcinoid TumoursLeiomyosarcomaLymphoma

GASTROENTEROLOGY 3 (page 4 of 4)




The Small Intestine

Lymphoma Predisposing Factors: (a) Coeliac Disease(b) Crohn’s Disease(c) Immunoproliferative Small Intestine Disease

Pathological Features: (a) Most frequently found in ileum(b) Most common is B-cell derived lymphoma (from MALT)(c) Annular or polypoid masses(d) T-cell lymphomas are ulcerated plaques or proximalbowel strictures

Clinical Features: (a) Abdominal pain(b) Diarrhoea(c) Anorexia(d) Weight loss(e) Anaemia(f) May have a palpable mass

Investigation: (a) SBFT(b) USS(c) CT

Treatment: (a) Surgery(b) Radiotherapy(c) Chemotherapy

Carcinoid Pathological Features: (a) Originate from enterochromaffin cells of intestineTumour (b) Common sites are appendix, terminal ileum and rectum

Clinical Features: (a) Small bowel obstruction(b) Intestinal ischaemia(c) Hepatic metastases (pain, hepatomegaly, jaundice)(d) Flushing/wheezing(e) Diarrhoea(f) Cardiac involvement(g) Facial telangiectasia

Investigation: (a) USS

Treatment: (a) Octreotide relieves flushing and diarrhoea(b) Surgical resection




GASTROENTEROLOGY 4 (page 1 of 5) Colon, Rectum & Anus

Diverticular Diverticulosis Presence of diverticulaDisease Diverticulitis Inflammation of the diverticula

Diverticular disease General term for disease involving diverticulaDiverticula Protrusions of gut mucosa covered by peritoneum and

present in 50% of patients over 50

Epidemiology Found more commonly in populations with low intake of dietary fibre. This may be due(Diverticular Disease) to small volume stools which require higher intraabdominal pressure for propulsion

and may lead to herniation of mucosa. Female preponderance.

Pathology (a) Protrusions of mucosa covered by peritoneum(Diverticular Disease) (b) Hypertrophy of circular muscle

(c) Inflammation can result from impaction of faecaliths(d) Repeated inflammation leads to narrowing or obstruction of the lumen

Clinical (a) Usually asymptomatic (90% cases)Features (b) May be associated with constipation or spasm(Diverticular Disease) (c) Colicky pain in left iliac fossa

(d) Can produce rectal bleeding(e) Acute cases present with severe pain and fever

Complications (a) Perforation leading to generalised peritonitis(Diverticular Disease) (b) Fistula formation into bladder or vagina

(c) Intestinal obstruction

Investigation (a) Blood test may show PMN leucocytosis(Diverticular Disease) (b) Spiral CT

(c) Ultrasound(d) Flexible sigmoidoscopy

Treatment (a) Asymptomatic cases require no treatment(Diverticular Disease) (b) Acute cases treated with cephalosporin & metronidazole as outpatient

(c) Emergent cases may require surgery and bowel resection

Colonic Polyps Colonic polyps are protrusions above the colon epithelium and may be epithelial or mesenchymal.

Histology Harmartomatous Polyps Large, stalked.(Colonic Polyps) Inflammatory Polyps Involve granulation due to excess regeneration during

inflammatory bowel disease.Neoplastic Polyps Can be either tubular or villous. Tubular polyps are small

(<10mm diameter), have numerous crypts, mucous-secreting epithelium and are stalked. Villous polyps have elongated villi with columnar epithelium.

Hyperplastic Polyps Elongated crypts without dysplasia and a ‘serrated’ uppersurface to the crypts.

Lymphoid Polyps ?





Clinical Features Most polyps are asymptomatic and found when patients are investigated for(Colonic Polyps) other GI tract disorders, such as pain, altered bowel habit, bleeding

haemorrhoids etc.

Extraintestinal (a) Subcutaneous epidermoid cystsFeatures (b) Lipomas(Colonic Polyps) (c) Benign osteomas (esp skull and angle of mandible)

(d) Desmoid tumours(e) Dental abnormalities(f) Congenital hypertrophy of retinal pigment epithelium (CHRPE)

Risk Factors (a) Large size (>2cm)for Malignancy (b) Multiple polyps(Colonic Polyps) (c) Villous architecture

(d) Dysphasia

Adenoma-Carcinoma (a) Activation of OncogenesSequence (b) Loss or mutation of tumour suppressor genes

(c) Defective genes of the DNA repair pathway(d) Genomic instability

Colorectal Carcinoma

Epidemiology (a) Rare in the underdeveloped world(Colorectal Carcinoma) (b) Common in Western populations (60 per 100,000 UK)

(c) Increasing incidence with increasing age (esp >50)

Risk Factors Non-Dietary Factors Dietary Factors(Colorectal Carcinoma) (a) Colorectal adenomas (a) High red meat & saturated fat

(b) Chronic extensive ulcerative colitis (b) Low fibre intake(c) Acromegaly (c) Low fruit/veg intake(d) Pelvic radiotherapy (d) Low calcium/folic acid intake(e) Obesity and sedentary lifestyle(f) Alcohol and tobacco use

Pathology (a) Arise from an adenomatous polyp(Colorectal Carcinoma) (b) >50% in rectosigmoid region

(c) Lymphatic invasion common at presentation(d) Metatases to liver through systemic/portal circulation

Duke’s Staging(Colorectal Carcinoma)

Stage Description% of

Cases5 yr Survival

Rate

A Tumour confined to bowel wall 10% 90-100%

B Beyond bowel wall but no metatases 35% 65-75%

C Involving lymph nodes 30% 30-40%

DDistant metatases or residual disease following surgery

25% <5%





Colon, Rectum & Anus

Clinical (a) Altered bowel habitFeatures (b) Rectal bleeding(Colorectal Carcinoma) (c) Iron deficiency anaemia

(d) Bowel obstruction(e) Weight loss

Management (a) Surgical removal of tumour by resection(Colorectal Carcinoma) (b) Adjuvant chemotherapy for stage C colon cancer patients

(c) Combination radiotherapy for stage C rectal cancer patients

Prevention & (a) Healthcare agencies advocate low-fat, high-fibre dietScreening (b) Endoscopic screening with polyp removal for families with FAP (Familial(Colorectal Carcinoma) Adenomous Polyposis) and HNPCC (Hereditary Non Polyposis Colon Cancer)

(c) Possible flexible sigmoidoscopy at age 55

Ischaemic Caused by insufficient or blocked blood supply to the mesenteric arteries or veinsColitis

Pathology (a) Anoxic or hypoxic injury depending on adequacy of collateral supply(Ischaemic Colitis) (b) Cell death due to calcium ion movement through damaged membranes

(c) Free radical damage on reperfusion with oxygen (in non-occlusive cases)

Causes (a) Occlusive (i) Superior mesenteric embolus/thrombosis(Ischaemic Colitis) (ii) Mesenteric vein thrombosis

(b) Non-occlusive (i) Systemic hypotension(ii) Vasoconstriction(iii) Viscosity disturbances(iv) Arterial narrowing(v) Pharmacological effects (eg digitalis, cocaine)

Clinical (a) Sudden Abdominal painFeatures (b) Passage of bright red blood with or without diarrhoea(Ischaemic Colitis) (c) Distended abdomen

(d) Signs of shock(e) Signs of cardiovascular disease

Investigation (a) Sigmoidoscopy to rule out bleeding from diverticular disease or ulcerative colitis(Ischaemic Colitis) (b) Barium enema to see characteristic ‘thumb-printing’ on colon wall

Complications (a) May develop strictures(Ischaemic Colitis) (b) May develop gangrene

Treatment (a) Treatment of cardiovascular problems(Ischaemic Colitis) (b) Surgery if required to resect bowel





Megacolon & Megacolon refers to a number of different congenital and acquired conditions where Hirschsprung’s the colon is dilated.Disease Presents in first years of life when an aganglionic segment of the rectum gives rise to

constipation and subacute obstruction.Anticholinesterase is increased. Failure of relaxation of the internal sphincter can be treated successfully with surgery.Treatment of megacolon is similar to constipation, but saline wash-outs and manual removal of faeces is sometimes required.

Solitary Rectal Features (a) Bowel IrregularityUlcer (b) Rectal bleeding with the passage of mucous

(c) Mainly due to excess straining at stool

Management (a) Rectal exam(b) Sigmoidoscopy reveals redness/ulcer 10com from rectal margin(c) Histology is diagnostic – non-specific inflammatory changes(d) Treatment is unsatisfactory. Local steroids may help

Melanosis Coli &Pigmentation of mucosa (melanosis coli) caused by surreptitious laxative ingestionLaxative Abuse Commonly seen in young females with anorexia or bulemia.

(a) Diarrhoea of high volumes (1 litre per day)(b) Pigmented mucosa(c) Histological rectal biopsy shows pigment-laden macrophages(d) Phenolphthalein laxatives detected by NaOH poured onto stools

Faecal Impaction Requires manual removal of faeces and care to prevent recurrence

Pruritis Ani Causes (a) Soiling of perianal skin(b) Local anal lesions eg infection of haemorrhoids(c) Hydrocortisone creams

Management (a) Hygiene – weak local steroids mixed with antiseptic eg timodine

Haemorrhoids Haemorrhoids are varicosities resulting from the dilatation of internal haemorrhoidal venous plexus and require no treatment if minor. Otherwise treated with topical emollients and high fibre diet.

Classification Symptom

1st degree Bleeding only

2nd degree Prolapse at defaecation, but spontaneous return to anal canal

3rd degree Prolapse and requires manual replacement

4th degree Can’t be replaced

Anal Fissures Anal fissures result in painful defaecation and minor rectal bleeding. They can be treated using local anaesthetic gels.





Anal Abscess Perianal abscesses develop between internal and external sphincters. They usually& Fistulae result from infection. Crohn’s is sometimes responsible. Symptoms include:

(a) Extreme perianal pain(b) Fever(c) Discharge of pus

Spontaneous rupture may lead to fistulae. Abscesses are treated by surgical drainage and fistulae are laid open with car to avoid damage to the anal sphincters.

Faecal Causes (a) Faecal impaction with overflow diarrhoeaIncontinence (b) Anorectal (i) rectal prolapse

(ii) anal stricture(iii) haemorroidectomy(iv) anal dilatation(v) rectal carcinoma

(c) Post childbirth damage to pelvic floor innervation(d) Neurological disorders (i) spinal trauma to S2-4

(ii) spina bifida(iii) multiple sclerosis

(e) Senile dementia(f) Congenital abnormalities of anus/rectum(g) Impalement injuries(h) Diabetes mellitus with autonomic involvement

Management Treatment for underlying causes is often unsatisfactory




GASTROENTEROLOGY 5 (page 1 of 2) Inflammatory Bowel Disease

Inflammatory There are two major forms of non-specific inflammatory bowel disease. These are:Bowel Disease (a) Crohn’s Disease

(b) Ulcerative ColitisHowever, since their aetiology is unknown, they may in fact be manifestations of the same disease.

Epidemiology (a) Crohn’s Disease Incidence: 5-8 per 100,000 (and rising)Prevalence: 50-60 per 100,000

(b) Ulcerative Colitis Incidence: 6-15 per 100,000 (relatively stable)Prevalence: 80-120 per 100,000

Both conditions are more common in the West, although have a worldwide distribution suggesting combined environmental and genetic aspects to the conditions.

Pathogenesis (a) Familial – Both conditions are more common in relatives of patients, than in the general population. Crohn’s also has a high monozygotic twin concordance.(b) Genetic – There are no HLA markers but HLA-B27 is increased in patients with inflammatory bowel disease.(c) Diet – There is little evidence of a dietary factor, although Crohn’s has been linked to patients with high dietary sugar intake.(d) Smoking – Patients with Crohn’s are more likely to be smokers whilst those with Ulcerative Colitis are more likely to be non-smokers or ex-smokers.(e) Infection – Possible infective agent theory behind Crohn’s, but no bacterium, virus or parasite has been identified as being definitely linked. However two agents have been investigated: (i) Measle’s virus; (ii) Mycobacterium.(f) Multifocal gastrointestinal infarction due to granulomatous angiitis has been suggested as a primary event in Crohn’s.(g) Inducible nitric oxide synthase (iNOS) is expressed after activation by mediators. It produces NO in acute colitis and could damage host cells.

Pathology Crohn’s Disease may affect the whole bowel, but more commonly the small bowel.Crohn’s Disease Macroscopic: (a) Affected parts of small bowel have thick wall and narrow lumen

(b) Deep ulcers and fissures found in the mucosa(c) Fistulae and abscesses may be found in the colon(d) ‘Cobblestone’ appearance due to mucosal damage

Microscopic: (a) Transmural inflammation (through all layers of mucosa)(b) Increased chronic inflammatory cells(c) Lymphoid hyperplasia(d) Granulomas in 50% of patients

Clinical (a) Terminal ileum, colon, perianal region (but may affect any part of GI tract)Features (b) Abdominal painCrohn’s Disease (c) Weight loss

(d) Diarrhoea

Intestinal (a) MalabsorptionComplications (b) Nutritional defectsCrohn’s Disease (c) Bowel stenosis

(d) Fistulae




GASTROENTEROLOGY 5 (page 2 of 2) Inflammatory Bowel Disease

Pathology Ulcerative Colitis affects only the colon and rectum.Ulcerative Colitis Macroscopic: (a) Superficial inflammation

(b) Reddened, inflamed, easily bleeding mucosa(c) Ulceration and inflammatory polyps in severe cases

Microscopic: (a) Chronic inflammatory cells in lamina propria(b) Crypt abscesses(c) Goblet cell depletion

Clinical (a) Rectum and descending colonFeatures (b) DiarrhoeaUlcerative Colitis (c) Urgency

(d) Rectal bleeding

Intestinal (a) Toxic megacolonComplications (b) Colorectal carcinomaCrohn’s Disease

Natural History Inflammatory Bowel Disease is a relapsing disease. Without treatment patients will experience at least one exacerbation episode a year. 10-15% of those with ulcerative colitis, and 50% of those with Crohn’s, will require surgical resection.

Systemic (a) Eyes ConjunctivitisComplications Scleritis

Uvetis(b) Joints Monoarticular arthritis

Ankylosing spondylitis(c) Skin Erythema nodosum

Pyoderma gangrenosum(d) Biliary tree Sclerosing cholangitis

Differentials (a) Infection (bacterial, viral, protozoal)(b) Vascular disease(c) Drugs(d) Idiopathic

Investigations (a) Sigmoidoscopy (typical eryhtema and ulcerated surface)(b) Colonoscopy(c) Biopsy for histology(d) MRI or US(e) Barium studies

Management (a) Prednisolone for acute episodes(b) 5-amino salicyclates for mild relapses and prevention(c) Topical treatment(d) Surgery (can cure ulcerative colitis)

There is no cure for Crohn’s Disease




GASTROENTEROLOGY 6 (page 1 of 5) Diarrhoea & GI Tract Infections

True Diarrhoea Increase in stool weight > 300g/24hrs usually accompanied by increased frequencyPatients and doctors often define diarrhoea in different ways. Other frequent uses of the word are for loose stools or increased frequency.

Pathophysiology (a) Osmotic DiarrhoeaThe gut mucosa acts as a semipermeable membrane allowing fluid to enter the gut if there are large quantities of hypertonic substances in the lumen The diarrhoea usually stops after stopping eating.

(i) Ingestion of unabsorbable purgative or substance(ii) Malabsorption(iii) Specific absorptive defect

(b) Secretory DiarrhoeaThis mechanism is due to seretion of electrolytes and fluid into the gut as well as decreased absorption. The diarrhoea does not stop when the patient stops eating.

(i) Enterotoxin (cholera, E. coli)(ii) Hormones (vasoactive intestinal peptide)(iii) Bile acids/fatty acids in colon after ileal resection(iv) Some laxatives

(c) Inflammatory Diarrhoea (Mucosal Destruction)Damage to intestinal mucosal cells leads to loss of fluid and blood into the lumen. In addition there is defective absorption of fluid and electrolytes.

(i) Infection (dysentery due to shigella)(ii) Inflammatory bowel disease (ulcerative colitis)

(d) Abnormal MotilityNot a true diarrhoea since it is usually due to increased frequency rather than volume or weight. It is due to abnormal upper gut motility.

(i) Diabetes(ii) Post-vagotomy(iii) Hyperthyroid

CausesChronic Acute(a) Inflammatory Bowel Disease(b) Parasitic/fungal infection(c) Malabsorption(d) Gut resection(e) Drugs(f) Colonic neoplasia(g) EndocrinePanreatic tumourMedullary carcinomaThyrotoxicosisDiabetic neuropathy

(h) Faecal impaction in elderly

(a) Dietary Indiscretion(b) InfectiveFood poisoningViral gastroenteritis

(c) Traveller’s DiarrhoeaE. coliGiardiaShigellaEntamoeba histolytica

Investigations Investigation is only required if the diarrhoea has lasted for more than 1 week. In chronic diarrhoea investigation is always required. The basic repertoire of tests include: (a) Stool culture and exam (cysts, parasites)

(b) Sigmoidoscopy(c) Rectal biopsy(d) Small bowel follow through (SBFT)(e) VIP(f) ERCP





Malabsorption Malabsorption is the decreased absorption of food from the gut leading to clinical symptoms and can be caused by the following mechanisms:

(a) Intraluminal maldigestion due to deficiency of bile or pancreatic enzymes leading to inadequate solubilisation and hydrolysis.(b) Mucosal malabsorption due to small bowel resection or small intestine epithelial damage causing decreased surface area for absorption.(c) Postmucosal Lymphatic Obstruction which prevents uptake and transport of absorbed lipids into the lymphatic vessels. The increased pressure causes leakage back into the intestinal lumen.

Effects of (a) General LethargyMalabsorption Depression

Anaemia (Fe, folate, B12 deficiency)Poor wound healing (vitamin C, protein, zinc deficiency)Purpura/Bruising (vitamin C, K deficiency)

(b) Mouth Angular stomatitis (Fe, folate, B12 deficiency)

(c) Limbs Peripheral neuropathy (B12 deficiency)Peripheral oedema (hypoalbuminaemia)Paraesthesia, tetany (Ca, Mg deficiency)

(d) Bone Osteomalacia, rickets (vitamin D, Ca deficiency)

(e) Muscle Wasting (protein deficiency)Proximal myopathy (vitamin D)

Investigation (a) Haematology Microcytic anaemia (Iron deficiency)Macrocytic anaemia (Folate, B12 deficiency)Increased Prothrombin Time (vitamin K deficiency)

(b) Biochemistry HypoalbuminaemiaHypocalcaemia, vitamin D deficiencyHypomagnesaemiaPhosphate, zinc deficiency

(c) 14C-trolein breath test (increased fat)(d) Duodenal biopsy, aspirate(e) Barium studies(f) Pancreatic function tests(g) Imaging (CT/MRI)

Small Bowel Normal upper intestine organisms never exceed 103/ml. In bacterial overgrowth theBacterial normal mechanisms controlling organisms in the mouth fail and there may beOvergrowth 108-1010/ml. Caused by: (a) decreased acid

(b) decreased motility(c) structural abnormalities(d) decreased immunity

Symptoms include: (a) Watery diarrhoea +/- steatorrhoea(b) B12 deficiency anaemia(c) Symptoms of underlying GI problems

Investigations include: (a) FBC(b) Barium follow through(c) Endoscopic duodenal biopsy

Management (a) Treat underlying cause(b) Tetracycline/Metronizadole/Ciprofloxacin(c) B12 supplements IM in chronic cases





Escherichia E. Coli is one of the organisms which can cause Traveller’s Diarrhoea. ClinicalColi features include: (a) Diarrhoea

(b) Vomiting(c) Abdominal cramps/pain(d) Fever

Enterotoxigenic E. Coli (ETEC) produces toxins and acts on cAMP to secrete water and electrolytes into the lumen.Management: (a) Oral fluids and electrolytes

(b) Ciprofloxacin in severe casesProphylaxis to ETEC is with trimethoprim and doxycycline alongside good hygiene and well cooked food.

Salmonella Salmonella can cause:(a) Gastroenteritis (S. enteritidis, S. typhimurium)

DiarrhoeaMalaiseNauseaHeadache

(b) Typhoid fever (S. typhi)Insiduous onset of headacheIncreasing feverCough, sore throatInitial constipation leading to diarrhoea

Investigations: (a) FBC/Blood culture (leucopenia, positive culture)(b) Widal test (serum agglutins to O and H antigens)

Management: (a) Ciprofloxacin/Chloramphenocol/Cotrimoxazole/AmoxycillinProphylaxis: (a) Good food hygiene

(b) Annual vaccination

Shigella Gram negative bacteria usually causing disease in children under 5 yrs.Symptoms: (a) Acute fever

(b) Malaise symptoms increasing in severity(c) Abdominal pain(d) Watery diarrhoea

Investigation: (a) Sigmoidoscopy (inflamed mucosa and ulcers)(b) Stool culture is diagnostic

Treatment: (a) Symptomatic treatment(b) Antibiotics in severe cases

Campylobacter Gram negative bacteria causing the following symptoms:(a) Acute diarrhoea +/- blood(b) Asymptomatic carriers in children(c) Fever(d) Headache(e) Severe cramping abdominal pain

Investigation: (a) Sigmoidoscopy (shows acute colitis)(b) Stool microscopy is diagnostic(c) Blood/stool culture

Management: (a) Usually self-limiting in 5-7 days(b) Antibiotics if severe





Yersinia Causes enterocolitis which presents with the following symptoms:Enterocolitica (a) Fever

(b) Diarrhoea(c) Severe abdominal pain(d) Arthritis

Usually self-limiting and no treatment is needed unless severe.

Clostridium Gram positive bacteria which causes pseudomembranous colitis. It is usually hospital-Difficile acquired and becomes established when colonic bacterial flora are disrupted by

antibiotic treatment. It produces endotoxins and causes mucosal inflammation and ulceration and, if severe, an adherent ‘pseudomembrane’ (fibrin, debris, polymorphs).Symptoms: (a) Insidious onset of lower abdominal pain

(b) Profuse watery diarrhoeaManagement: (a) Stop antibiotics

(b) Vancomycin/Metronizadole

Clostridium Causes food poisoning due to spores in food which survive boiling.Perfringens Symptoms: (a) Watery diarrhoea

(b) Cramping abdominal painInvestigation: Stool/food culture is diagnostic

Mycobacterium Droplet infection of M. tuberculosis causes TB and tuberculous peritonitis. SymptomsTuberculosis include: (a) Insidious onset of fever

(b) Anorexia(c) Weight loss(d) Abdominal pain(e) Ascites

Investigation: (a) Peritoneal fluid exam/culture(b) Tubercle biopsy (laparoscopically)

Management: (a) Chemotherapy for 18 months – 2 years

Giardiasis Usually ingested in contaminated water in tropical regions. Incubation of 1-3 weeks.Symptoms: (a) Diarrhoea/Steathorrhoea

(b) Abdominal pain(c) Weakness(d) Anorexia(e) Nausea/Vomiting

Investigation: (a) Malabsorption of xylose, B12

(b) Lactose intolerance(c) Sigmoidoscopy (partial villous atrophy)(d) Stool exam for cysts

Management: (a) Tinidazole/Metronizadole

Amoebiasis Commonly caused by entamoeba histolytica which is ingested in food contaminated with human faeces. The organism causes amoebic ulceration. Symptoms are chronic including: (a) Abdominal pain

(b) Alternating diarrhoea/constipation(c) Mucous in stool

Investigation: (a) Naked eye stool exam for organisms(b) Sigmoidoscopy shows ulcers and scraping examined

Management: (a) Metronizadole/Tinidazole





Cryptosporidiosis Usually caused by cryptosporidium parvum, a protozoan with a 7-10 day incubation causing: (a) Watery diarrhoea

(b) Abdominal crampInvestigation: (a) Faecal microscopy for cystsManagement: (a) Not necessary unless immuno-compromised

Strongyloides This is a nematode parasite found in the tropics, sub-tropics and Far East. The worm burrows into the skin causing initial dermatalogical symptoms and then into the gut mucosa inducing inflammation and malabsorption.Symptoms: (a) Abdominal pain

(b) Diarrhoea(c) Steatorrhoea(d) Weight loss

Investigation: (a) Faecal microscopy will show motile larvaeManagement: (a) Ivermectin/Albendazole

AIDS & GIT Weight loss and diarrhoea are extremely common in HIV infection. Wasting is usuallyProblems due to systemic effects causing anorexia. ‘HIV enteropathy’ is a syndrome of

diarrhoea, malabsorption and weight loss where there is no other pathology. This is probably due to infection of white cells in the gut mucosa by the HIV virus.




GASTROENTEROLOGY 7 (page 1 of 4) Pancreas

Investigation (a) Serum amylase (raised in acute disease)Exocrine Function (b) Serum lipase (raised in acute disease)

(c) Duodenal enzymes (chronic disease)(d) PABA test (pancreatic insufficiency)(e) Fat absorption tests (faecal fat, 14C-triolein breath test)

Imaging (a) Conventional USS (gallstones, fluid collection)(b) Endoscopic USS (small pancreatic tumours, small bile duct stones)(c) Laparascopic USS(d) Helical CT(e) MRI(f) MRCP (magnetic resonance cholangio-pancreatography)(g) ERCP(h) Arteriography

Pancreatitis Pancreatitis can be classified as either:(a) Acute In acute pancreatitis there may be isolated or recurrent attacks with

the pancreas returning to normal after the attack.(b) Chronic In chronic pancreatitis there will be continuing inflammation,

irreversible structural changes and eventual loss of endocrine and exocrine function.

Causes Common (90%) RareAcute Pancreatitis Gallstones Post-ERCP

Alcohol Post-surgeryIdiopathic Trauma

DrugsMetabolicInfection

Mechanism Mechanism is unclear but activation of zymogen granules has been implicated, whichAcute Pancreatitis release proteases into the pancreas causing autodigestion.

Defec tive intracellular transport &secretion of pancreatic zym ogens

P ancreatic duc t obs truc tioneg galls tones , tum ours

Reflux of infec ted bile or duodenalcontents into pancreatic duc t

Hypers tim ulation of pancreaseg alcohol, fat

P ROE NZY M ES

A CTIV ATE D P ROTE OLY TICE NZY M ES





Pathology (a) Acute oedematous pancreatitis Interstitial inflammation and oedema with peri-Acute Pancreatitis pancreatic fat necrosis but sparing acinar cells

(b) Necrotising pancreatitis As above but with destruction of acinar cells(c) Acute haemorhagic pancreatitis Bleeding into the pancreas and retroperitoneum

ComplicationsAcute Pancreatitis

Systemic Pancreatic GastrointestinalShock/Renal FailureHypoxiaHyperglycaemiaHypocalcaemiaLow serum albumin

AbscessPseudocystPancreatic ascitesPleural effusion

Upper GI bleedVariceal haemorrhageDuodenal obstructionObstructive jaundice

Clinical (a) Severe upper abdo pain radiating to back building over 15-60 minsFeatures (b) Nausea/vomitingAcute Pancreatitis (c) Marked epigastric tenderness (initially without guarding or rebound tenderness)

(d) Severe cases may cause hypovolaemic shock and hypoxia

Differentials (a) Perforated viscusAcute Pancreatitis (b) Acute cholecystitis

(c) Myocardial Infarction

Prognosis Overall mortality is 10% in acute pancreatitis. Mortality is at least 50% in necrotisingAcute Pancreatitis pancreatitis or pancreatic abscess. Mortality is nearer 100% when there are multiple

complications. The following are bad prognostic indicators in the first 48hrs.

Age >55 urea >16 mmol l-1

WBC >15 x 109/l albumin <30 g l-1

Blood Glucose >10 mmol l-1 aminotransferases >200 Ul-1

Pa02 <8.0 kPa calcium <2 mmol l-1

LDH >600 U l-1

The right hand column are serological tests. LDH is lactate dehydrogenase.

Investigation (a) Serum amylase (x5 normal suggests pancreatitis)Acute Pancreatitis (b) USS

(c) Contrast enhanced dynamic CT(d) MRI(e) Peritoneal aspiration & lavage

Management (a) Analgesia (usually pethidine)Acute Pancreatitis (b) Fluids/electrolytes to correct hypovolaemia

(c) Intensive care if in shock/respiratory failure(d) Parenteral IV nutrition(e) ERCP for gallstones(f) Surgery in complicated cases





Cystic Fibrosis Cystic fibrosis is an inherited autosomal recessive disorder due to a defective epithelial membrane chloride channel gene (CFTR). This causes cystic dilatation of ducts and fibrosis.

Complications (a) Pancreatic insufficiency leading to steatorrhoeaCystic Fibrosis (b) Meconium ileus (mucous obstruction of intestine)

(c) Peptic ulcer(d) Hepatobiliary disease (usually cholesterol stones)(e) Malnutrition due to anorexia and malabsorption secondary to (a)

Diagnosis (a) Sweat testing (high Na2+ concentration > 60 mmol l-1)Cystic Fibrosis (b) Immunoreactive trypsin assay

(c) Genetic studies(d) Pancreatic function tests

Treatment (a) Pancreatic supplements (high dose pancreatin)Cystic Fibrosis (b) Increased calorie intake (150% recommended daily intake with vit supplements)

(c) Treatment of respiratory problems (antibiotics, transplantation)

Carcinoma of Carcinoma of the pancreas has an prevalence of around 10-15 per 100,000 in thePancreas West. The prevalence is greatest in those over 70 (100 per 100,000). Men are twice

as likely to be affected as women. There is a link to smoking and high cholesterol.

Pathology 90% are adenocarcinomas arising from the pancreatic ducts. They metastasise to thePancreatic Carcinoma lymph nodes early. 70% of tumours are in the head of the pancreas and spread to

local organs such as the duodenum, liver and spleen.

Clinical Head or Ampulla of Vater (a) Painless obstructive jaundiceFeatures (b) Abdominal painPancreatic Carcinoma (c) Anorexia and weight loss

Body or Tail of Pancreas (a) Abdominal pain (dull, boring, radiating to back)(b) Anorexia and weight loss

There is a palpable mass in 20% of cases and all will eventually have hepatomegaly

Differentials (a) All causes of painless jaundicePancreatic Carcinoma (b) All causes of upper abdominal pain

Investigation (a) USSPancreatic Carcinoma (b) CT

(c) Fine Needle Aspirate (FNA) or biopsy(d) ERCP for tumours at the head of the pancreas





Neuroendocrine These arise from neuroendocrine tissue in the pancreas. The majority are non-Tumours secretory, metastasise late and grow slowly. Other tumours secrete hormones which

affects the clinical presentation. The tumour can be single but are usually multifocal.

Tumour Hormone Effect

Gastrinoma Gastrin Peptic ulcer, steatorrhoea

Insulinoma Insulin Recurrent hypoglycaemia

VIPoma VIP Watery diarrhoea, hypokalaemia

Glucagonoma Glucagon DM, necrolytic migratory erythema

Somatostatinoma Somatostatin DM, steatorrhoea




GASTROENTEROLOGY 8 (page 1 of 5) Liver 1

FunctionsNutrie nt M e ta bolismCarbohydratesP roteinsLipids

S tora geIronCopperV itam ins A , D, B 12

Ex cre tionB ile S altsB ilirubin

P rote in S ynthe sisA lbum inCoagulation Fac torsCom plem ent Fac torsHaptoglobinCaeruloplasm inTrans ferrinP rotease Inhibitors

Live r

G a llb la dde r

Functional The functional unit of the liver is the hepatic acinus. Blood arrives in the acinus via theAnatomy portal triad (portal vein, hepatic artery, bile duct). The zone closest to the vein and

artery is zone 1 and is well oxygenated. The zone furthest away is zone 3 and relatively hypoxic. This allows the liver to perform different functions in different physiological zones. Blood is then drained into the hepatic veins. Bile flows in the opposite direction to the blood draining from the liver into the bile duct and to the gallbladder.

Liver Function (a) FBCTests (b) Coagulation Tests

(c) Biochemistry BilirubinAminotransferasesAlkaline Phosphatase (ALP)γ-glutamyl transferaseProteins/albumin

Imaging (a) USS(b) CT(c) MRI(d) MRCP(e) Abdominal X-Ray(f) Endoscopy(g) Endoscopic US(h) ERCP

Liver Biopsy Liver biopsy is indicated for the following:(a) Unexplained hepatomegaly(b) Some cases of jaundice(c) Persistent abnormal liver biochemistry(d) Acute/chronic hepatitis(e) Cirrhosis(f) Infiltration(g) Tumour(h) Screening relatives





Liver 1

Portal Portal hypertension occurs when there is a prolonged elevation of portal venousHypertension pressure (normally 2-5 mmHg). Clinical features are usually due to pressure greater

than 12 mmHg.

Normal blood flows into the (a) Portal vein into the liverbranching into the (b) Portal venules (pre-sinusoidal)branching into the (c) Hepatic capillaries (sinusoidal)draining into the (d) Hepatic venules (post-sinusoidal)draining into the (e) Hepatic veindraining into the (f) Inferior Vena Cava

CausesPortal Hypertension

Prehepatic Intrahepatic Posthepatic

Portal Vein Thrombosis

CirrhosisAlcoholic hepatitisIdiopathicSchistosomiasis

Budd-Chiari syndromeVeno-occlusive disease

Consequences The increased resistance in the portal vein leads to the development of collateralPortal Hypertension vessels allowing the direct return of blood to the systemic circulation. This occurs

particularly in the oesophagus, stomach and rectum.

Complications (a) Variceal bleedingPortal Hypertension (b) Congestive gastropathy

(c) Hypersplenism(d) Ascites(e) Renal failure(f) Hepatic encephalopathy

Investigation (a) X-Ray (to detect varices)Portal Hypertension (b) Endoscopy (to detect varices)

(c) USS (to detect splenomegaly or collateral vessels)(d) Portal venography

Management (a) Blood & Plasma (to restore circulation)Acute Variceal Bleeding (b) Endoscopy (to confirm diagnosis)

(c) Injection sclerotherapy(d) Variceal banding(e) Balloon tamponade(f) Vasoconstriction (Octreotide/Vasopressin)(g) Transjugular intrahepatic shunt (TIPS)(h) Emergency surgery (transection & ligation of oesophagus)

Prevention of (a) Long term sclerotherapyRecurrence (b) Long term variceal bandingAcute Variceal Bleeding (c) β-adrenoreceptor blockade (decreasing heart rate with propranolol)

(d) Surgery (TIPS, transection/ligation)





Liver 1

Ascites Ascites is the presence of fluid within the peritoneal cavity. Several factors are involved including:(a) Sodium and water retention(b) Portal hypertension leading to increased lymph production(c) Low serum albumin due to decreased hepatic function leading to decreased plasma oncotic pressure preventing vascular leakage

Causes Common (a) Malignant DiseaseAscites (b) Cardiac Failure

(c) Hepatic CirrhosisOther (d) Hypoproteinaemia

(e) Hepato-venous occlusion(f) Infection(g) Pancreatitis(h) Lymphatic obstruction

Clinical (a) Abdominal distensionFeatures (b) Shifting dullness on percussionAscites (c) Fluid thrill

(d) Peripheral oedema(e) Pleural effusion at right base

Investigation A diagnostic aspiration of 10-20 ml of fluid should be obtained and the following testsAscites performed: (a) Cell count (neutrophils > 250 cells suggests bacterial peritonitis)

(b) Gram stain/culture(c) Protein (<11 gl-1 suggests transudate, otherwise exudate)(d) Cytology for malignancy(e) Amylase to exclude pancreatic ascites

Management The main aim is to reduce sodium intake and increase sodium excretion to allowAscites reabsorption and mobilisation of ascitic fluid.

(a) Sodium restriction (40 mmol/day)(b) Water restriction (0.5-1.0 l/day)(c) Diuretic drugs (spironolactone/frusemide)(d) Paracentesis (3-5 l/day)(e) Shunts (LeVeen into veins of neck/TIPS)

Hepatic This is a neuropsychiatric syndrome secondary to liver disease. It is generallyEncephalopathy considered to be due to abnormal brain biochemistry. There are a number of

precipitating factors including:(a) Uraemia(b) Drugs(c) GI bleeding(d) Excess dietary protein(e) Constipation(f) Paracentesis (of volumes > 3-5 l/day)(g) Hypokalaemia(h) Infection(i) Trauma/surgery(j) Portasystemic shunts





Clinical (a) Change of intellect/emotion/personality/consciousnessFeatures (b) Later apathy, poor concentration, confusion, disorientation, slurred speech, comaHepatic Encephalopathy (c) Convulsion

(d) Asterixis(e) Fetor hepaticus (sweet, musty odour to breath)

Differentials (a) Subdural HaematomaHepatic Encephalopathy (b) Drug/alcohol intoxication

(c) Delirium tremens(d) Wernicke’s Encephalopathy(e) Primary psychiatric disorders(f) Hypoglycaemia(g) Neurological Wilson’s Disease

Clinical GradingHepatic Encephalopathy

Grade Features

IPoor concentration, slurred speech, slow mentation

IIDrowsy but easily roused, occasionally aggressive, lethargic

IIIMarked confusion, drosy, sleepy but responding to pain and voice, gross disorientation

IVUnconscious, unresponsive to voice, may or may not respond to painful stimuli

Investigation (a) Usually diagnosed clinicallyHepatic Encephalopathy (b) EEG – diffuse slowing of α waves

Acute Liver Acute liver failure can be caused by a number of things including:Failure (a) Virus (Hep A, B, D)

(b) Drugs (paracetamol, halothane, aspirin, antituberculous drugs)(c) Poisons (amanite phalloides, carbon tetrachloride)(d) Miscellaneous (Wilson’s disease, shock, cardiac failure)(e) Leptospirae

Clinical (a) Hepatic EncephalopathyFeatures (b) WeaknessAcute Liver Failure (c) Nausea, vomiting

(d) Jaundice

Complications (a) EncephalopathyAcute Liver Failure (b) Cerebral oedema

(c) Respiratory failure(d) Hypotension(e) Hypothermia(f) Infection(g) Bleeding(h) Pancreatitis(i) Renal failure(j) Metabolic effects





Investigation (a) Toxicology screen of blood/urineAcute Liver Failure (b) IgM anti-Hbs

(c) IgM anti-HAV(d) Anti-HEV, CMV, HSV, EBV(e) Caeruloplasmin, serum copper, urinary copper(f) Autoantibodies(g) Doppler US of liver and heaptic veins(h) CXR

Chronic Liver Chronic liver failure develops when liver function can no longer maintain normalFailure physiological conditions. The term ‘hepatic decompensation’ is used when chronic

liver failure occurs and may be precipitated by a number of events including infection or variceal haemorrhage.

It is a syndrome characterised by clinical and laboratory features including:(a) Hepatic encephalopathy(b) Jaundice(c) Hypoalbuminaemia(d) Coagulation abnormalities




GASTROENTEROLOGY 9 (page 1 of 2) Functional Bowel Disorders

Functional This is a general term covering two main syndromes:Bowel Disorder (a) Non-ulcer dyspepsia

(b) Irritable bowel syndromeThese syndromes are extremely common and frequently overlap in pathology. They make up 60-80% of the patients presenting in GI clinic. There is a very strong psychological link to functional bowel disorders.

Non-Ulcer Symptoms are mainly stress related and include:Dyspepsia (a) Indigestion

(b) Wind(c) Nausea(d) Early satiety(e) Heartburn

No ulcer can be found.

Functional dyspepsia can be differentiated from peptic ulcer using the following table

Functional Dyspepsia Peptic Ulceration

Site of PainDiffuse all overFits no recognisable pattern

EpigastricPoints with one finger

Frequency Daily for long periods Episodic

Food/MealsPain unaffectedLasts all day

Exacerbates or helps pain

Antacids No help Helps pain

Nocturnal Pain Waking Patient

Rare Common

Vomiting No effect Relieves pain

Investigation (a) EndoscopyNon-Ulcer Dyspepsia (b) Barium studies

Management (a) ReassuranceNon-Ulcer Dyspepsia (b) Antacids and H2-receptor antagonists probably have a placebo effect

(c) Cisapride or Metoclopramide may help




GASTROENTEROLOGY 9 (page 2 of 2) Functional Bowel Disorders

Irritable Bowel The clinical features of irritable bowel syndrome include:Syndrome (a) Pain in left iliac fossa relieved by defecation or wind

(b) Constipation or diarrhoea(c) Frequent small volume stools(d) Abdominal distension and bloating(e) Recurrent episodes with long symptom free periods(f) Patient generally looks well

Mechanism The pathophysiology is extremely variable from patient to patient. MotilityIrritable Bowel abnormalities are sometimes found but psychological factors are extremely important.

Stress often exacerbates symptoms and depression may be present

Investigation (a) May not be necessary – avoid over investigationIrritable Bowel (b) Rectal exam

(c) Sigmoidoscopy(d) Barium studies

Management (a) Discuss lifestyle and reassureIrritable Bowel (b) Reassurance of benign nature of disease

(c) High fibre diet(d) Antispasmodics(e) Antidepressants therapy(f) Other therapy





Tumours Tumours of the liver can either be: (a) primary arising in the liver(b) secondary metastasising from elsewhere

Secondary tumours are abut 50 times commoner than primary tumours.

Primary TumoursMalignant BenignHepatocellular Carcinoma (HCC)CholangiocarcinomaAngiosarcomaHepatoblastomaFibrosarcoma

Hepatic AdenomaHaemangiomaFocal Nodular HyperplasiaFibroma

Carcinoma HCC is rare in the west (1-2 per 100,000 per year). Common in Africa and SE Asia.Cholangiocarcinoma is rare comprising about 10% of hepatic malignancy. it is most common between the ages of 50 and 70 yrs.

Risk Factors (a) Carriers of HBV/HCVCarcinoma (b) Cirrhosis

(c) Male sex(d) Aflatoxin (fungus found in groundnut)(e) OC Pill

Prevention is by widspread HBV vaccination

Pathology The tumour is either single or occurs in multiple nodules. Histologically the tumourCarcinoma contains cells resembling heaptocytes. The tumour may metastasise via the hepatic

portal vein to lymph node, bones and lungs.

Clinical Usually presents below the age of 50 with rapid onset in cirrhotic patientsFeatures (a) Weight lossCarcinoma (b) Anorexia

(c) Fever(d) Aching right hypochondrium(e) Ascites(f) Hepatomegaly

In cholangiocarcinoma a jaundice is also seen.

Prognosis: survival is not usually more than 6 months

Investigation (a) USS shows large filling defectsCarcinoma (b) Serum α-fetoprotein (raised)

(c) Ultrasound guided liver biopsy is diagnostic

Treatment (a) Surgical resection sometimes possibleCarcinoma (b) Transplantation

(c) Chemotherapy/Radiotherapy usually unhelpful





Wilson’s Wilson’s Disease is due to accumulation of copper in the body, particularly the liver.Disease Dietary copper is usually absorbed from the stomach and upper small intestine and

transported in the liver loosely bound to albumin. It is incorporated into caeruloplasmin which is a glycoprotein synthesized in the liver and secreted in the blood. Copper is normally excreted in the bile. Dysfunction of the enzymes involved in transport of copper causes Wilson’s Disease.

Genetics Wilson’s is an autosomal recessive disorder within a copper transporting ATPase. TheWilson’s Disease problem is due to failure of biliary excretion of copper and the consequential

accumulation in the body.

Clinical Hepatic Non-HepaticFeatures Acute hepatitis Kayser-Fleischer rings in corneaWilson’s Disease Fulminant hepatic failure Tremor

Chronic hepatitis DysarthriaCirrhosis Involuntary movement

Dementia

Pathology (a) Hepatic damage varies from chronic hepatitis to macronodular cirrhosisWilson’s Disease (b) Periportal distribution of copper stain

(c) Basal ganglia show damage & cavitation(d) Kidneys show tubular degradation(e) Bones show erosions

Investigations (a) Serum copper and caeruloplasmin decreased (but can be normal)Wilson’s Disease (b) Urinary copper increased

(c) Liver biopsy(d) Haemolysis and anaemia

Treatment Lifetime treatment with penicillamine to chelate copper. Dose dependent on urinaryWilson’s Disease copper monitoring. Siblings and children should be screened and treatment given for

copper accumulation even if asymptomatic.

Haemo- Haemochromatosis is the primary accumulation of iron in the body due to a geneticchromatosis defect causing excess iron absorption leading to fibrosis of various organs, including

the liver, and eventual organ failure.Haemosiderosis is a secondary overload of iron and can be distinguished from haemochromatosis by MRI which shows pancreatic destruction in haemochromatosis, but is spared in haemosiderosis.

(Normal iron metabolism discussed in Blood & Lymph 2)

Genetics Haemochromatosis is an autosomal recessive disorder with a prevalence inHaemochromatosis caucasians of 1/400 affected homozygotes and 1/10 heterozygous carriers. There is

an association with HLA-A3.





Clinical Less clinical manifestation in women due to physiological blood loss and lower iron.Features Most cases present in the 5th decade.Haemochromatosis (a) Bronze skin pigmentation

(b) Hepatomegaly(c) Diabetes Mellitus(d) Hypogonadism (secondary to pituitary dysfunction)(e) Heart failure and arrythmias(f) Liver iron deposition and fibrosis(g) Liver cirrhosis (late feature)

Pathology Total body iron of 20-40g (normal is 2-4g). Liver and pancreas show 50-100 timesHaemochromatosis normal iron level. Iron is initially deposited in the periportal hepatocytes and then later

distributed to the rest of the liver.

Investigation (a) Raised serum ironHaemochromatosis (b) Raised serum ferritin

(c) Liver biochemistry normal(d) Liver biopsy(e) MRI

Treatment (a) VenesectionHaemochromatosis (b) Chelation therapy (desferrioxamine)

(c) Screening of family members

α1-Antitrypsin α1-AT is aglycoprotein which inhibits the proteolytic enzyme neutrophil elastase.Deficiency 1/10 North Europeans carry a deficiency gene. The abnormal protein is produced and

not secreted causing liver accumulation. This results in low plasma levels ofα1-antitrypsin.

Clinical (a) Cirrhosis in 10-15% (usually > 50 yrs)Features (b) Respiratory Problems in 75% (eg emphysema)α1-Antitrypsin Deficiency (c) Chronic hepatitis

(d) Cholestatic jaundice in neonates(e) Hepatocellular Carcinoma (HCC) (late feature)

Investigation Serum α1-antitrypsin decreased (10% of normal in homozygotes)α1-Antitrypsin Deficiency

Treatment No treatment other than for the complications of liver disease. Transplantation is aα1-Antitrypsin Deficiency possibility. Patients should be encouraged to stop smoking to prevent emphysema.

Liver Infection Infection of the liver can cause:(a) Pyogenic abscess (E. coli, streptococcus faecalis, vulgaris, aureus)(b) Amoebic abscess (entamoeba histolytica)(c) Schistosomiasis (schistosoma mansoni, schistosoma japonicum)(d) Hydatid Disease (echinococcus granulosus)

Routes of (a) Intra-abdominal sepsis (eg appendicitis)Infection (b) Portal venous system

(c) Trauma/surgery





Liver Abscess Liver abscess can be either: (a) Bacterial(b) Amoebic

The clinical presentation is variable and can include the following features:(a) Fever(b) Rigors(c) Weight loss(d) Vomiting(e) Abdominal pain(f) Jaundice

Treatment (a) Aspiration of abscess under ultrasoundLiver Abscess (b) Broad-spectrum antibiotics

Liver Disease (a) Viral hepatitis (B, C, D)in AIDS (b) Neoplasia (Kaposi’s sarcoma, non-Hodgkin’s lymphoma)

(c) Opportunistic infection (mycobacterium tuberculosis, cryptococcus, candida)(d) Drug hypertoxicity(e) Sclerosing cholangitis

SchistosomiasisThe bacterial ova reach the liver via the venous system obstructing the portal branches. The pathology involves granuloma, fibrosis and inflammation (but no cirrhosis). Clinically there is hepatosplenomegaly and presinusoidal portal hypertension. Investigation shows increased alkaline phosphatase and ova in the stool. Treatment is with praziquantel.

Veno-occlusive This involves widespread occlusion of the central hepatic veins often due to toxins inDisease certain teas, but also chemotherapy or body irradiation before bone marrow

transplantation. Clinical features include: (a) Acute abdominal pain(b) Nausea and vomiting(c) Tender hepatomegaly(d) Ascites

Budd-Chiari This syndrome is due to obstruction of venous outflow of the liver due to occlusion ofSyndrome the hepatic vein.

Causes: (a) Idiopathic (~50%)(b) Hypercoaguability (eg polycythaemia vera)(c) OC Pill(d) Leukaemia(e) Tumours(f) Radiotherapy(g) Trauma

The clinical features are similar to those of veno-occlusive disease.

Venous Outflow Hepatic venous outflow obstruction can occur in:Obstruction (a) Small hepatic veins

(b) Large hepatic veins(c) Inferior vena cava(d) Heart

Cardiac Hepatic damage due to congestion is present in cardiac failure from any cause butDisease particularly: (a) Acute hepatitis following MI or decompensation

(b) Ascites due to cardiac failure





Acute Acute hepatitis can be caused by a number of things including:Hepatitis (a) Viral (Hep A, B, C, E, (D), EBV, CMV, Yellow Fever)

(b) Non-viral (toxoplasma gondii, leptospira icterohaemorrhagiae)(c) Drugs (paracetamol, halothane)(d) Alcohol(e) Poison (mushroom, aflatoxin, carbon tetrachloride)(f) Other (pregnancy, circulatory insufficiency)

Viral Hepatitis

HAV HBV HCV HDV HEV

VirusGroup Enterovirus Hepadna Flavivirus Incomplete Calcivirus

Genetics RNA DNA RNA RNA RNASize 27nm 42nm 30-38nm 35nm 27nm

Spread

Faecal Blood Uncommon Saliva ? ?Sexual Uncommon Uncommon ?Vertical Uncommon

Incubation 2-4 weeks 4-20 weeks 2-26 weeks 6-9 weeks 3-8 weeksChronic Infection No 5-10% 50%

Hepatitis A Most common viral hepatitis worldwide. Poor sanitation and hygiene cause epidemics.

Clinical Features: (a) Fever(b) Lethargy(c) Jaundice

Diagnosis: (a) IgM anti-HAV(b) Alkaline phosphatase increased(c) Alanine transferase increased(d) Bilirubin increased

Prevention: (a) Immunisation by inactivated vaccine

Treatment: (a) No specific treatment

Hepatitis B 2000 million people affected with 300 million carriers worldwide. UK and USA have lower prevalence of carriers than Africa, Far and Middle East. Risk factors include multiple sexual partners and IV drug use.

Clinical Features: (a) Same as HAV(b) Chronic (asymptomatic) hepatitis(c) Cirrhosis (also ascites, variceal haemorrhage, encephalopathy)

Natural History: (a) 30% die of cirrhosis(b) Hepatocellular carcinoma(c) HBe antigen negative virus may emerge

Diagnosis: (a) Markers for HBV(b) ALT increased

Prevention: (a) Passive and active immunisation

Treatment: (a) No specific treatment





Hepatitis C Rates of infection in healthy blood donors is 0.02% in Europe, 6% in Africa, 19% in Egypt. Transfusion before the screening of donor’s blood is a major risk factor.

Clinical Features: (a) Mild flu-like symptoms(b) Jaundice(c) May present with chronic liver disease years after infection(d) Extrahepatic manifestations (arthritis, aplastic anaemia)

Natural History: (a) Progresses over 15-50 years to cirrhosis in 20-30% of cases(b) 2-3% die of hepatocellular carcinoma per year

Diagnosis: (a) Anti-HCV(b) HCV-RNA positive

Prevention: None

Treatment: (a) Interferon-α plus ribavarin for 6-12 months

Hepatitis D Can only be acquired by patients with pre-existing HBV infection

Clinical Features: (a) Severe hepatitis if HBV and HDV infect together(b) Progressive disease if HDV superimposed on HBV

Diagnosis: (a) IgM anti-HDV(b) IgM anti-HBc antigen

Prevention: (a) None

Treatment: (a) None

Hepatitis E Epidemics seen in developing countries

Clinical Features: (a) Mild hepatitis (more severe in pregnancy)(b) Frequently cholestatic(c) Mortality from fulminant hepatic failure

Diagnosis: (a) ELISA for IgG and IgM anti-HEV (unreliable)

Prevention: (a) Good sanitation and hygiene

Treatment: (a) Conservative

Hepatitis G Hepatitis G is a parenterally transmitted flavivirus (also GBV-C). It replicates to a minor degree in the liver, but the main site is unknown. It rarely causes mild hepatitis but usually causes chronic disease. No treatment is needed.





Alcoholic Liver Epidemiology (a) Causes 12% of male and 3% of female deaths.Disease (b) Causes 27% of medical and 20% of psychiatric admissions.

(c) There is strong evidence for a genetic component to the disease and its aetiology.

Pathology (a) Fatty change in liver cells (especially zone 3).(b) Acute hepatitis (with Mallory’s hyalin)(c) Architectural damage (eg portal fibrosis, cirrhosis)

Clinical Features (a) Can have few or mild symptoms (diagnosed histologically)(b) Jaundice(c) Ascites(d) Abdominal Pain(e) Fever(f) Hepatomegaly

Diagnosis (a) Elevated MCV(b) High serum gamma-glutamyl transferase(c) Fat in liver histology(d) High serum bilirubin(e) High serum AST and ALT(f) High ALP(g) Increased PT

Treatment (a) Encourage patient to stop drinking(b) Diazepam or chlormethiazole for delirium tremens(c) Bed rest(d) Protein and vitamin supplements

Cirrhosis Liver cirrhosis is a condition in which the liver responds to injury or death of some of its cells by producing interlacing strands of fibrous tissue between which are nodules of regenerating cells.

Causes (a) Hepatitis B, C or D(b) Alcohol(c) Biliary cirrhosis(d) Primary sclerosing cholangitis(e) Haemochromatosis(f) Wilson’s Disease(g) α-antitrypsin deficiency

Complications (a) Portal hypertension(b) GI haemorrhage(c) Ascites(d) Encephalopathy(e) Renal failure(f) Hepatocellular carcinoma

Investigation (a) Liver function tests(b) Liver biochemistry(c) Serum electrolytes(d) Imaging(e) Liver biopsy (if PT is not too long)

Management (a) US scan and α-fetoprotein every 6 months to check for HCC





Chronic Biliary Causes Common (a) GallstonesDisease (b) Infections

(c) Strictures (benign or malignant)Rare (a) Primary biliary cirrhosis

(b) Sclerosing cholangitis(c) Drugs(d) Congenital (biliary atresia, fibropolycystic disease)

Clincal Features (a) Abdominal Pain(b) Jaundice(c) Dark urine, pale stools(d) Itching(e) Nausea and vomiting(f) Fevers and rigors(g) Hepatomegaly(h) Weight loss(i) Skin pigmentation(j) Xanthomas, xanthalasmas

Biochemistry (a) Increased bilirubin(b) Increased alk phosp(c) Increased transaminases(d) Increased cholesterol(e) Increased prothrombin time(f) Normal albumin

Imaging (a) Abdo X-Ray(b) USS(c) CT(d) MRI(e) ERCP(f) Percutaneous transhepatic cholangiography (PTC)




GASTROENTEROLOGY 12 (page 1 of 2) Gall Bladder & Biliary Tract

Gallstones Gallstones occur in the gallbladder or biliary tract and can be composed of either:(a) Cholesterol (more common in industrialised countries)(b) Bile Pigment (more common in developing countries)

Epidemiology In the UK gallstones occur in 7% of males and 15% of females between 18 and 65.Gallstones There is an overall prevalence of 11%

Common in N America, Europe, AustraliaLess common in India, Far East, Africa

Pathogenesis (a) Cholesterol Cholesterol is held in solution in bile by bile acids and phospholipidGallstones which form micelles and vesicles. Due to either excess cholesterol

or deficiency of bile salts, bile becomes supersaturated or lithogenic. Cholesterol becomes crystallized out of the lithogenic bile by other factors which are poorly defined.

(b) Bile Pigment Brown pigment stones contain cholesterol, calcium salts of fattyacids and calcium bilirubinate. They form due to stasis or infection of the common bile duct and are due to precipitation of deconjugated bilirubin with calcium. They mainly form in the common bile duct. Commonly associated with parasitic infection of the biliary tract.

Black pigment stones contain calcium salts of bilirubin which can be caused by haemolysis in chronic haemolytic disease. Other pathogenic mechanisms are unclear. They mainly form in the gallbladder.

Risk Factors (a) Increasing age (e) High saturated fat dietCholesterol Gallstones (b) Female > Male (f) OC Pill & other drugs

(c) Obesity (g) Diabetes(d) Rapid weight loss (h) Liver cirrhosis

Complications (a) Acute cholecystitis due to prolonged occlusion of the cystic ductGallstones (b) Chronic cholecystitis

(c) Biliary colic due to migration of gallstones to the common bile duct(d) Pancreatitis(e) Gallstone ileus due to the fistula allowing migration of stone to gut(f) Carcinoma of the gallbladder

Management (a) No treatment if asymptomaticGallstones (b) Cholesystectomy (open/laparascopic)

(c) Bile acids (chenodeoxycholic/urodeoxycholic acid) (non-calcified stones only; 10%)(d) Lithotripsy (shock-wave treatment)

Acute Gallstones occur in 90% of cases of acute cholecystitis. Obstruction of the neck of theCholecystitis gallbladder or cystic duct occurs due to an impacted stone. This causes inflammation

which can be mild (causing slight abdominal pain and a palpable gallbladder) or severe (causing localised peritonitis and acute pain).

Clinical (a) Severe, continuous, increasing, epigastric or right hypochondrial painFeatures (b) Mild jaundice in 20%Acute Cholecystitis (c) Fever

(d) Murphy’s sign (pain worse on inspiration causing shallow breathing)(e) Guarding & rebound tenderness




GASTROENTEROLOGY 12 (page 2 of 2) Gall Bladder & Biliary Tract

Investigations (a) FBC/Blood Film moderate leucocytosisAcute Cholecystitis (b) Biochem slightly raised bilirubin, alkaline phosphatase, aminotranserases

(c) USS sonographic Murphy’s sign, gallbladder wall thickening, distension, sludge(d) Iodida Scintiscan blockage of cystic duct(e) X-Ray gallstones in 10%; excludes lower lobe pneumonia

Differentials (a) Perforated peptic ulcerAcute Cholecystitis (b) Retrocaecal appendicitis

(c) Acute pancreatitis(d) Right basal pneumonia(e) Myocardial Infarction

Management (a) Bed rest, opiate analgesia, antibiotics (amoxycillin/cephalosporin)Acute Cholecystitis (b) Cholecystectomy

Chronic This is due to chronic inflammation of the gallbladder as a consequence of gallstones.Cholecystitis Pathology Inflammation of gallbladder

Shrunken gallbladder on USS/radiologyClinical Features Vague symtpoms including recurrent indigestion, right abdominal

pain/distension often at night and following a heavy mealInvestigation Same as for acute cholecystitisDifferential Functional bowel diseaseManagement Same as for acute cholecystitis

Common Bile 10-15% of gallstones occur in the common bile duct due to migration from theDuct Stones & gallbladder. Primary bile duct stones may develop within the bile duct due to anCholangitis accumulation of biliary sludge. Cholangitis is a bacterial infection of the bile duct

secondary to bile duct abnormality.

Clinical (a) May be asymptomaticFeatures (b) Abdominal pain (epigastric, right hypochondrium)

(c) Fever(d) Jaundice(e) Rigor (in cholangitis)

Investigation (a) LFTs (cholestatic pattern/bilirubinaemia)(b) FBC/Blood film (leucocytosis)(c) USS (dilated intra/extra-hepatic ducts, gallstones)(d) ERCP

Differentials (a) Gallstones(b) Tumours of gallbladder/bile duct(c) Biliary motor disorders(d) Cholesterolosis(e) Adenomyomatosis of gallbladder

Management (a) Analgesia(b) IV fluids(c) Broad-spectrum antibiotics(d) Surgical/endoscopic stone removal

Haemobilia This can occur as a result of hepatic trauma (occasionally tumour). Blood enters the biliary tree and produces a cholestatic jaundice or GI bleeding



GASTROENTEROLOGY

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