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  1. 1. Nem’s Notes… Phase 2 Year 2GASTROENTEROLOGY 1 (page 1 of 4)Oropharynx & OesophagusOral Ulceration Causes: (a) Gastrointestinal Crohn’s Disease Ulcerative Colitis Coeliac Disease Lupus Erythematosus (systemic/discoid) Behçet’s Disease (b) Dermatalogical Lichen Planus Erythema Multiforme Dermatitis Herpetiformis (c) Viral HSV Coxsackie (d) Bacterial Syphilis TB (e) Trauma Poorly Fitting Dentures Harsh Brushing Sharp TeethDifferential 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) LeukoplakiaXerostomia 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 FailureOesophagitis Oesophagitis is inflammation of the oesophagus. Causes include: (a) Gastrooesophageal Reflux Disease (GORD) (b) Infection (c) Neoplastic Disease (d) Swallowed CorrosivesHiatus Hernia There are two type of hiatus hernia (a) Sliding (80%) (b) Rolling/Paraoesophageal (20%)more online at page 1 of 45
  2. 2. Nem’s Notes… Phase 2 Year 2GASTROENTEROLOGY 1 (page 2 of 4)Oropharynx & OesophagusGORD (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 HerniaMechanisms (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 refluxTreatment (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 mouthReflux & 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 specialisedOesophagus 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.more online at page 2 of 45
  3. 3. Nem’s Notes… Phase 2 Year 2GASTROENTEROLOGY 1 (page 3 of 4)Oropharynx & OesophagusDysphagia 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 RingsManagement 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 Carcinoma AdenocarcinomaEpidemiology 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 diseaseClinical (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 diseasePathway of (a) Ulcerative direct invasion of surrounding tissueSpread (b) Lymphatic spreadOesophageal Tumour NB Metastases rarely found on autopsyInvestigation (a) Barium SwallowOesophageal Tumour (b) Oesophagoscopy (c) CT Scan of thorax and abdomen (d) Endoscopic Ultrasoundmore online at page 3 of 45
  4. 4. Nem’s Notes… Phase 2 Year 2GASTROENTEROLOGY 1 (page 4 of 4)Oropharynx & OesophagusManagementOesophageal 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 Stent dilatation of the oesophagus Palliative Laser ablation Therapy Alcohol 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 patientsMotility (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) Endoscopymore online at page 4 of 45
  5. 5. Nem’s Notes… Phase 2 Year 2GASTROENTEROLOGY 2 (page 1 of 3)Stomach & DuodenumAcute 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 erosionsAetiology 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 failureComplications (a) Progression to chronic stateAcute Gastritis (b) Ulceration (c) HaemorrhageChronic 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 RefluxH. 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 DyspepsiaComplications (a) H. Pylori infection see above (b) Autoimmune pernicious anaemia (c) Chronic NSAIDs gastric erosion gastric ulcerPeptic 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) NSAIDsSite 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)more online at page 5 of 45
  6. 6. Nem’s Notes… Phase 2 Year 2 (ii) Infection causing metaplasia, inflammation and ulcerationGASTROENTEROLOGY 2 (page 2 of 3)Stomach & DuodenumComplications (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 Diffuse all over Epigastric Site of Pain Fits no recognisable pattern Points with one finger Frequency Daily for long periods Episodic Pain unaffected Food/Meals Exacerbates or helps pain Lasts all day Antacids No help Helps pain Nocturnal Pain Rare Common Waking Patient Vomiting No effect Relieves painInvestigations (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 disordersGastric Tumours of the stomach include:Carcinoma (a) Benign leiomyoma (b) Benign gastric polyps (c) Malignant carcinoma (d) Malignant lymphoma (e) Malignant stromal tumourEpidemiology 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 migrants More common in men Incidence rises after 50 yrs of agemore online at page 6 of 45
  7. 7. Nem’s Notes… Phase 2 Year 2GASTROENTEROLOGY 2 (page 3 of 3)Stomach & DuodenumRisk 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 polypsEarly 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 borderSpread (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)more online at page 7 of 45
  8. 8. Nem’s Notes… Phase 2 Year 2GASTROENTEROLOGY 3 (page 1 of 4)The Small IntestineCoeliac 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 factorsPathogenesis 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 propriaCauses of Subtotal (Flat) (a) Coeliac DiseaseVillous Atrophy (b) Dermatitis Herpetiformis (c) Zollinger-Ellison Syndrome (rare) (d) Hypogammaglobulinaemia (rare) Partial (Convoluted) (a) Tropical Sprue (b) GiardiasisClinical 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 biopsy is diagnostic for Coeliac Disease. (c) Anti-reticulin antibodies Antibodies also very sensitive but also present in other GI diseases such as Crohn’s. (d) Haematology Mild/moderate microcytic or macrocytic anaemia in 50% of casesmore online at page 8 of 45
  9. 9. Nem’s Notes… Phase 2 Year 2GASTROENTEROLOGY 3 (page 2 of 4)The Small IntestineTreatment 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) CarcinomaMalabsorption 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 DiseaseBacterial SEE Gastroenterology 6 (page 2 of 5)Overgrowth Causes of Bacterial Overgrowth Hypo/Achlorhydria Pernicious anaemia Partial gastrectomy Decreased Motility Scleroderma Diabetic autonomic neuropathy Structural Abnormality Gastric surgery (blind loops) Jejunal diverticulosis Enterocolic fistulae Strictures Impaired Immunity Hypogammaglobulinaemiamore online at page 9 of 45
  10. 10. Nem’s Notes… Phase 2 Year 2GASTROENTEROLOGY 3 (page 3 of 4)The Small IntestineIntestinal 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 syndromeWhipple’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.Tumours Benign Malignant Adenomas Adenocarcinomas Leiomyomas Carcinoid Tumours Lipomas Leiomyosarcoma Hamartomas Lymphomamore online at page 10 of 45
  11. 11. Nem’s Notes… Phase 2 Year 2GASTROENTEROLOGY 3 (page 4 of 4)The Small IntestineLymphoma 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 proximal bowel 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) ChemotherapyCarcinoid 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 resectionmore online at page 11 of 45
  12. 12. Nem’s Notes… Phase 2 Year 2GASTROENTEROLOGY 4 (page 1 of 5)Colon, Rectum & AnusDiverticular Diverticulosis Presence of diverticulaDisease Diverticulitis Inflammation of the diverticula Diverticular disease General term for disease involving diverticula Diverticula Protrusions of gut mucosa covered by peritoneum and present in 50% of patients over 50Epidemiology 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 lumenClinical (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 feverComplications (a) Perforation leading to generalised peritonitis(Diverticular Disease) (b) Fistula formation into bladder or vagina (c) Intestinal obstructionInvestigation (a) Blood test may show PMN leucocytosis(Diverticular Disease) (b) Spiral CT (c) Ultrasound (d) Flexible sigmoidoscopyTreatment (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 resectionColonic 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’ upper surface to the crypts. Lymphoid Polyps ?more online at page 12 of 45
  13. 13. Nem’s Notes… Phase 2 Year 2GASTROENTEROLOGY 4 (page 2 of 5)Colon, Rectum & AnusClinical 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) DysphasiaAdenoma-Carcinoma (a) Activation of OncogenesSequence (b) Loss or mutation of tumour suppressor genes (c) Defective genes of the DNA repair pathway (d) Genomic instabilityColorectal CarcinomaEpidemiology (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 usePathology (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 circulationDuke’s Staging(Colorectal Carcinoma) % of 5 yr Survival Stage Description Cases 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% Distant metatases or residual disease following D 25% <5% surgerymore online at page 13 of 45
  14. 14. Nem’s Notes… Phase 2 Year 2GASTROENTEROLOGY 4 (page 3 of 5)Colon, Rectum & AnusClinical (a) Altered bowel habitFeatures (b) Rectal bleeding(Colorectal Carcinoma) (c) Iron deficiency anaemia (d) Bowel obstruction (e) Weight lossManagement (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 patientsPrevention & (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 55Ischaemic Caused by insufficient or blocked blood supply to the mesenteric arteries or veinsColitisPathology (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 diseaseInvestigation (a) Sigmoidoscopy to rule out bleeding from diverticular disease or ulcerative colitis(Ischaemic Colitis) (b) Barium enema to see characteristic ‘thumb-printing’ on colon wallComplications (a) May develop strictures(Ischaemic Colitis) (b) May develop gangreneTreatment (a) Treatment of cardiovascular problems(Ischaemic Colitis) (b) Surgery if required to resect bowelmore online at page 14 of 45
  15. 15. Nem’s Notes… Phase 2 Year 2GASTROENTEROLOGY 4 (page 4 of 5)Colon, Rectum & AnusMegacolon & Megacolon refers to a number of different congenital and acquired conditions whereHirschsprung’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 helpMelanosis 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 stoolsFaecal Impaction Requires manual removal of faeces and care to prevent recurrencePruritis 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 timodineHaemorrhoids 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 st 1 degree Bleeding only nd 2 degree Prolapse at defaecation, but spontaneous return to anal canal rd 3 degree Prolapse and requires manual replacement th 4 degree Can’t be replacedAnal Fissures Anal fissures result in painful defaecation and minor rectal bleeding. They can be treated using local anaesthetic gels.more online at page 15 of 45
  16. 16. Nem’s Notes… Phase 2 Year 2GASTROENTEROLOGY 4 (page 5 of 5)Colon, Rectum & AnusAnal 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 unsatisfactorymore online at page 16 of 45
  17. 17. Nem’s Notes… Phase 2 Year 2GASTROENTEROLOGY 5 (page 1 of 2)Inflammatory Bowel DiseaseInflammatory There are two major forms of non-specific inflammatory bowel disease. These are:Bowel Disease (a) Crohn’s Disease (b) Ulcerative Colitis However, 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 patientsClinical (a) Terminal ileum, colon, perianal region (but may affect any part of GI tract)Features (b) Abdominal painCrohn’s Disease (c) Weight loss (d) DiarrhoeaIntestinal (a) MalabsorptionComplications (b) Nutritional defectsCrohn’s Disease (c) Bowel stenosis (d) Fistulaemore online at page 17 of 45
  18. 18. Nem’s Notes… Phase 2 Year 2GASTROENTEROLOGY 5 (page 2 of 2)Inflammatory Bowel DiseasePathology 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 depletionClinical (a) Rectum and descending colonFeatures (b) DiarrhoeaUlcerative Colitis (c) Urgency (d) Rectal bleedingIntestinal (a) Toxic megacolonComplications (b) Colorectal carcinomaCrohn’s DiseaseNatural 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 cholangitisDifferentials (a) Infection (bacterial, viral, protozoal) (b) Vascular disease (c) Drugs (d) IdiopathicInvestigations (a) Sigmoidoscopy (typical eryhtema and ulcerated surface) (b) Colonoscopy (c) Biopsy for histology (d) MRI or US (e) Barium studiesManagement (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 Diseasemore online at page 18 of 45
  19. 19. Nem’s Notes… Phase 2 Year 2GASTROENTEROLOGY 6 (page 1 of 5)Diarrhoea & GI Tract InfectionsTrue Diarrhoea Increase in stool weight > 300g/24hrs usually accompanied by increased frequency Patients and doctors often define diarrhoea in different ways. Other frequent uses of the word are for loose stools or increased frequency.Pathophysiology (a) Osmotic Diarrhoea The 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 Diarrhoea This 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 Motility Not 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) HyperthyroidCauses Chronic Acute (a) Inflammatory Bowel Disease (b) Parasitic/fungal infection (c) Malabsorption (a) Dietary Indiscretion (d) Gut resection (b) Infective Food poisoning (e) Drugs Viral gastroenteritis (f) Colonic neoplasia (c) Traveller’s Diarrhoea (g) Endocrine E. coli Panreatic tumour Giardia Medullary carcinoma Shigella Thyrotoxicosis Entamoeba histolytica Diabetic neuropathy (h) Faecal impaction in elderlyInvestigations 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) ERCPmore online at page 19 of 45
  20. 20. Nem’s Notes… Phase 2 Year 2GASTROENTEROLOGY 6 (page 2 of 5)Diarrhoea & GI Tract InfectionsMalabsorption 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 Hypoalbuminaemia Hypocalcaemia, vitamin D deficiency Hypomagnesaemia Phosphate, 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 casesmore online at page 20 of 45
  21. 21. Nem’s Notes… Phase 2 Year 2GASTROENTEROLOGY 6 (page 3 of 5)Diarrhoea & GI Tract InfectionsEscherichia 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 cases Prophylaxis to ETEC is with trimethoprim and doxycycline alongside good hygiene and well cooked food.Salmonella Salmonella can cause: (a) Gastroenteritis (S. enteritidis, S. typhimurium) Diarrhoea Malaise Nausea Headache (b) Typhoid fever (S. typhi) Insiduous onset of headache Increasing fever Cough, sore throat Initial 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/Amoxycillin Prophylaxis: (a) Good food hygiene (b) Annual vaccinationShigella 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 casesCampylobacter 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 severemore online at page 21 of 45
  22. 22. Nem’s Notes… Phase 2 Year 2GASTROENTEROLOGY 6 (page 4 of 5)Diarrhoea & GI Tract InfectionsYersinia 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 diarrhoea Management: (a) Stop antibiotics (b) Vancomycin/MetronizadoleClostridium Causes food poisoning due to spores in food which survive boiling.Perfringens Symptoms: (a) Watery diarrhoea (b) Cramping abdominal pain Investigation: Stool/food culture is diagnosticMycobacterium 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 yearsGiardiasis 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/MetronizadoleAmoebiasis 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/Tinidazolemore online at page 22 of 45
  23. 23. Nem’s Notes… Phase 2 Year 2GASTROENTEROLOGY 6 (page 5 of 5)Diarrhoea & GI Tract InfectionsCryptosporidiosis Usually caused by cryptosporidium parvum, a protozoan with a 7-10 day incubation causing: (a) Watery diarrhoea (b) Abdominal cramp Investigation: (a) Faecal microscopy for cysts Management: (a) Not necessary unless immuno-compromisedStrongyloides 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 larvae Management: (a) Ivermectin/AlbendazoleAIDS & 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.more online at page 23 of 45
  24. 24. Nem’s Notes… Phase 2 Year 2GASTROENTEROLOGY 7 (page 1 of 4)PancreasInvestigation (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) ArteriographyPancreatitis 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-surgery Idiopathic Trauma Drugs Metabolic InfectionMechanism Mechanism is unclear but activation of zymogen granules has been implicated, whichAcute Pancreatitis release proteases into the pancreas causing autodigestion.more online at page 24 of 45
  25. 25. Nem’s Notes… Phase 2 Year 2GASTROENTEROLOGY 7 (page 2 of 4)PancreasPathology (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 retroperitoneumComplicationsAcute Pancreatitis Systemic Pancreatic Gastrointestinal Shock/Renal Failure Abscess Upper GI bleed Hypoxia Pseudocyst Variceal haemorrhage Hyperglycaemia Pancreatic ascites Duodenal obstruction Hypocalcaemia Pleural effusion Obstructive jaundice Low serum albuminClinical (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 hypoxiaDifferentials (a) Perforated viscusAcute Pancreatitis (b) Acute cholecystitis (c) Myocardial InfarctionPrognosis 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 & lavageManagement (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 casesmore online at page 25 of 45
  26. 26. Nem’s Notes… Phase 2 Year 2GASTROENTEROLOGY 7 (page 3 of 4)PancreasCystic 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 testsTreatment (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 hepatomegalyDifferentials (a) All causes of painless jaundicePancreatic Carcinoma (b) All causes of upper abdominal painInvestigation (a) USSPancreatic Carcinoma (b) CT (c) Fine Needle Aspirate (FNA) or biopsy (d) ERCP for tumours at the head of the pancreasmore online at page 26 of 45
  27. 27. Nem’s Notes… Phase 2 Year 2GASTROENTEROLOGY 7 (page 4 of 4)PancreasNeuroendocrine 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, steatorrhoeamore online at page 27 of 45
  28. 28. Nem’s Notes… Phase 2 Year 2GASTROENTEROLOGY 8 (page 1 of 5)Liver 1FunctionsFunctional 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 Bilirubin Aminotransferases Alkaline Phosphatase (ALP) γ-glutamyl transferase Proteins/albuminImaging (a) USS (b) CT (c) MRI (d) MRCP (e) Abdominal X-Ray (f) Endoscopy (g) Endoscopic US (h) ERCPLiver 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 relativesmore online at page 28 of 45
  29. 29. Nem’s Notes… Phase 2 Year 2GASTROENTEROLOGY 8 (page 2 of 5)Liver 1Portal 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 liver branching 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 vein draining into the (f) Inferior Vena CavaCausesPortal Hypertension Prehepatic Intrahepatic Posthepatic Cirrhosis Alcoholic hepatitis Budd-Chiari syndrome Portal Vein Thrombosis Idiopathic Veno-occlusive disease SchistosomiasisConsequences 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 encephalopathyInvestigation (a) X-Ray (to detect varices)Portal Hypertension (b) Endoscopy (to detect varices) (c) USS (to detect splenomegaly or collateral vessels) (d) Portal venographyManagement (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)more online at page 29 of 45
  30. 30. Nem’s Notes… Phase 2 Year 2GASTROENTEROLOGY 8 (page 3 of 5)Liver 1Ascites 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 leakageCauses Common (a) Malignant DiseaseAscites (b) Cardiac Failure (c) Hepatic Cirrhosis Other (d) Hypoproteinaemia (e) Hepato-venous occlusion (f) Infection (g) Pancreatitis (h) Lymphatic obstructionClinical (a) Abdominal distensionFeatures (b) Shifting dullness on percussionAscites (c) Fluid thrill (d) Peripheral oedema (e) Pleural effusion at right baseInvestigation 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 ascitesManagement 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 shuntsmore online at page 30 of 45
  31. 31. Nem’s Notes… Phase 2 Year 2GASTROENTEROLOGY 8 (page 4 of 5)Liver 1Clinical (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 DiseaseClinical GradingHepatic Encephalopathy Grade Features Poor concentration, slurred speech, slow I mentation Drowsy but easily roused, occasionally II aggressive, lethargic Marked confusion, drosy, sleepy but responding III to pain and voice, gross disorientation Unconscious, unresponsive to voice, may or IV may not respond to painful stimuliInvestigation (a) Usually diagnosed clinicallyHepatic Encephalopathy (b) EEG – diffuse slowing of α wavesAcute 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) LeptospiraeClinical (a) Hepatic EncephalopathyFeatures (b) WeaknessAcute Liver Failure (c) Nausea, vomiting (d) JaundiceComplications (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 effectsmore online at page 31 of 45
  32. 32. Nem’s Notes… Phase 2 Year 2GASTROENTEROLOGY 8 (page 5 of 5)Liver 1Investigation (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) CXRChronic 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 abnormalitiesmore online at page 32 of 45
  33. 33. Nem’s Notes… Phase 2 Year 2GASTROENTEROLOGY 9 (page 1 of 2)Functional Bowel DisordersFunctional This is a general term covering two main syndromes:Bowel Disorder (a) Non-ulcer dyspepsia (b) Irritable bowel syndrome These 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 Diffuse all over Epigastric Site of Pain Fits no recognisable pattern Points with one finger Frequency Daily for long periods Episodic Pain unaffected Food/Meals Exacerbates or helps pain Lasts all day Antacids No help Helps pain Nocturnal Pain Rare Common Waking Patient Vomiting No effect Relieves painInvestigation (a) EndoscopyNon-Ulcer Dyspepsia (b) Barium studiesManagement (a) ReassuranceNon-Ulcer Dyspepsia (b) Antacids and H2-receptor antagonists probably have a placebo effect (c) Cisapride or Metoclopramide may helpmore online at page 33 of 45
  34. 34. Nem’s Notes… Phase 2 Year 2GASTROENTEROLOGY 9 (page 2 of 2)Functional Bowel DisordersIrritable 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 wellMechanism 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 presentInvestigation (a) May not be necessary – avoid over investigationIrritable Bowel (b) Rectal exam (c) Sigmoidoscopy (d) Barium studiesManagement (a) Discuss lifestyle and reassureIrritable Bowel (b) Reassurance of benign nature of disease (c) High fibre diet (d) Antispasmodics (e) Antidepressants therapy (f) Other therapymore online at page 34 of 45
  35. 35. Nem’s Notes… Phase 2 Year 2GASTROENTEROLOGY 10 (page 1 of 4)Liver 2Tumours 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 Tumours Malignant Benign Hepatocellular Carcinoma (HCC) Hepatic Adenoma Cholangiocarcinoma Haemangioma Angiosarcoma Focal Nodular Hyperplasia Hepatoblastoma Fibroma FibrosarcomaCarcinoma 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 vaccinationPathology 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 monthsInvestigation (a) USS shows large filling defectsCarcinoma (b) Serum α-fetoprotein (raised) (c) Ultrasound guided liver biopsy is diagnosticTreatment (a) Surgical resection sometimes possibleCarcinoma (b) Transplantation (c) Chemotherapy/Radiotherapy usually unhelpfulmore online at page 35 of 45