Gastroenterology Revision Article ✅

🍽️ Gastroenterology is easiest to revise by anatomical level: oesophagus, stomach, small bowel, colon, rectum/anus, pancreas, liver and biliary tree. For exams and ward work, always connect the symptom to the mechanism: dysphagia = swallowing/obstruction, vomiting = gastric or CNS/metabolic trigger, diarrhoea = water/electrolyte malabsorption or inflammation, jaundice = bilirubin handling problem, and GI bleeding = mucosal/vascular/variceal source.

✅ 1. Core GI Anatomy and Physiology

🧃 1.1 Digestion and Absorption

• Mouth: mechanical breakdown and salivary amylase begins carbohydrate digestion.
• Stomach: acid, pepsin and churning begin protein digestion; intrinsic factor enables vitamin B12 absorption later in terminal ileum.
• Duodenum: receives bile and pancreatic enzymes; major site for iron and calcium absorption.
• Jejunum: main site of nutrient absorption, especially carbohydrates, amino acids and many vitamins.
• Terminal ileum: absorbs bile salts and vitamin B12; affected in Crohn’s disease.
• Colon: absorbs water and electrolytes; bacterial fermentation produces short-chain fatty acids.

🧬 1.2 Liver Functions

• Synthetic: albumin, clotting factors, complement proteins and transport proteins.
• Metabolic: glucose storage/release, lipid metabolism, amino acid metabolism.
• Detoxification: alcohol, drugs, ammonia conversion to urea.
• Bile production: excretion of bilirubin, cholesterol and bile acids.
• Immune: Kupffer cells clear bacteria and endotoxin from portal blood.

🧠 Exam pearl: In liver disease, bilirubin reflects excretion/conjugation, albumin and INR reflect synthetic function, and platelets can fall from portal hypertension and hypersplenism.

🩺 2. Key Gastrointestinal Symptoms

🧃 2.1 Dysphagia

• Oropharyngeal dysphagia: difficulty initiating swallow, coughing/choking, nasal regurgitation; think stroke, Parkinson’s, neuromuscular disease.
• Oesophageal dysphagia: food sticks after swallowing; solids only suggests mechanical obstruction; solids and liquids suggests motility disorder.
• Progressive dysphagia with weight loss is cancer until proven otherwise.
• Intermittent dysphagia with rings/webs may suggest Schatzki ring or eosinophilic oesophagitis.
• Regurgitation of undigested food plus halitosis may suggest pharyngeal pouch.

🔥 2.2 Dyspepsia and Reflux Symptoms

• Dyspepsia is upper abdominal discomfort, early satiety, bloating, nausea or epigastric pain.
• GORD causes heartburn and acid regurgitation due to reflux of gastric contents into the oesophagus.
• Alarm features: dysphagia, weight loss, persistent vomiting, GI bleeding, anaemia, abdominal mass.
• Medication causes include NSAIDs, bisphosphonates, steroids, calcium channel blockers and antiplatelets.
• Consider cardiac causes if pain is exertional, crushing, associated with dyspnoea or cardiovascular risk factors.

🚽 2.3 Diarrhoea

• Acute diarrhoea: commonly infective, toxin-mediated, medication-related or inflammatory.
• Chronic diarrhoea: IBS, IBD, coeliac disease, bile acid diarrhoea, pancreatic insufficiency, microscopic colitis, cancer.
• Inflammatory diarrhoea: blood, mucus, fever, raised CRP/faecal calprotectin.
• Osmotic diarrhoea improves with fasting; secretory diarrhoea often continues despite fasting.
• Steatorrhoea: bulky, pale, offensive, floating stools; think fat malabsorption or pancreatic insufficiency.

🩸 2.4 GI Bleeding

• Haematemesis: vomiting blood; usually upper GI source.
• Melaena: black tarry stool; usually upper GI bleed but can occur from right colon bleeding.
• Haematochezia: fresh red rectal bleeding; usually lower GI but can occur in massive upper GI bleeding.
• Occult bleeding: iron deficiency anaemia, positive FIT or unexplained microcytosis.
• Always assess haemodynamic stability first: pulse, BP, postural drop, shock, lactate, Hb trend.

🧪 3. GI Investigations

🩸 3.1 Blood Tests

• FBC: anaemia, infection, thrombocytopenia from portal hypertension.
• U&E: dehydration, AKI, electrolyte disturbance from vomiting/diarrhoea.
• LFTs: hepatocellular, cholestatic or mixed pattern.
• CRP/ESR: inflammation, infection, IBD activity; can be normal in some disease.
• Coagulation/INR: important in liver synthetic failure and active bleeding.
• Amylase/lipase: pancreatitis; lipase is more specific and remains elevated longer.

🧫 3.2 Stool Tests

• Stool culture/PCR: acute infectious diarrhoea, travel, outbreaks, severe illness.
• C. difficile toxin/PCR: after antibiotics, hospitalisation or healthcare exposure.
• Faecal calprotectin: neutrophil-derived marker supporting intestinal inflammation; useful to distinguish IBD from IBS in appropriate patients.
• FIT: detects occult blood and helps colorectal cancer risk stratification in symptomatic patients.
• Faecal elastase: low in pancreatic exocrine insufficiency.

📷 3.3 Endoscopy and Imaging

• OGD: oesophagus, stomach and duodenum; used for dysphagia, upper GI bleeding, dyspepsia alarm features, varices.
• Colonoscopy: colon and terminal ileum; used for bleeding, IBD, cancer, chronic diarrhoea.
• Flexible sigmoidoscopy: left-sided colonic assessment; useful in suspected distal colitis.
• Ultrasound: gallstones, biliary dilatation, liver morphology, ascites.
• CT abdomen/pelvis: obstruction, perforation, malignancy, pancreatitis complications, diverticulitis.
• MRCP: non-invasive biliary and pancreatic duct imaging.
• ERCP: therapeutic biliary intervention; carries pancreatitis risk.

🔥 4. GORD, Dyspepsia and Peptic Ulcer Disease

🔥 4.1 GORD

• GORD occurs when reflux of gastric contents causes troublesome symptoms or oesophageal inflammation.
• Symptoms: heartburn, acid regurgitation, sour taste, cough, hoarseness, chest discomfort.
• Risk factors: obesity, pregnancy, hiatus hernia, smoking, alcohol, large meals, lying flat after eating.
• Complications: erosive oesophagitis, strictures, Barrett’s oesophagus, aspiration, dental erosion.
• Management: weight loss if overweight, avoid late meals, raise head of bed, review triggers, PPI trial.

🦠 4.2 H. pylori and Peptic Ulcer Disease

• H. pylori causes chronic gastritis and increases risk of duodenal ulcer, gastric ulcer and gastric cancer.
• NSAIDs and antiplatelets increase ulcer and bleeding risk by impairing prostaglandin-mediated mucosal protection.
• Duodenal ulcer pain often improves with food; gastric ulcer pain may worsen with food - but this is not reliable enough to diagnose.
• Test for H. pylori using urea breath test, stool antigen or biopsy-based tests.
• Stop PPI before testing where possible because PPIs can cause false-negative results.
• Eradication usually requires PPI plus two antibiotics according to local resistance guidance.

🚩 4.3 Upper GI Alarm Features

• Dysphagia.
• Unintentional weight loss.
• Persistent vomiting.
• Haematemesis or melaena.
• Iron deficiency anaemia.
• Palpable abdominal mass.
• New dyspepsia in an older patient or concerning clinical context.

🚽 5. Irritable Bowel Syndrome

IBS is a disorder of gut-brain interaction causing recurrent abdominal pain associated with altered bowel habit. It is not “imaginary”: visceral hypersensitivity, altered motility, microbiome changes, immune activation and psychosocial stress can all contribute.

• Symptoms: abdominal pain, bloating, altered stool frequency/form, urgency, incomplete evacuation, mucus.
• Subtypes: IBS-D, IBS-C, IBS-M and unclassified.
• Red flags are not IBS: rectal bleeding, nocturnal symptoms, weight loss, anaemia, fever, family history of colorectal/ovarian cancer, abnormal inflammatory markers.
• Initial tests often include FBC, CRP/ESR, coeliac serology and faecal calprotectin in younger patients with diarrhoea.
• Management: explanation, reassurance, dietary review, soluble fibre, low FODMAP diet with dietitian support, antispasmodics, laxatives or loperamide depending on subtype.
• Psychological therapies may help refractory IBS, especially when pain and gut-brain symptoms dominate.

🧠 Exam pearl: IBS should not cause rectal bleeding, anaemia or raised faecal calprotectin. Those features should push you towards IBD, cancer, infection or another organic diagnosis.

🧬 6. Inflammatory Bowel Disease

🔥 6.1 Ulcerative Colitis

• UC is continuous mucosal inflammation starting in the rectum and extending proximally.
• Symptoms: bloody diarrhoea, urgency, tenesmus, mucus, abdominal pain, fatigue.
• Extent: proctitis, left-sided colitis, extensive colitis/pancolitis.
• Complications: toxic megacolon, colorectal cancer, severe bleeding, primary sclerosing cholangitis.
• Histology: crypt abscesses, mucosal inflammation, no granulomas usually.
• Management: 5-ASA for induction/maintenance in mild disease; steroids for flares; immunomodulators/biologics/small molecules for refractory or moderate-severe disease.

🧱 6.2 Crohn’s Disease

• Crohn’s is transmural, patchy inflammation that can affect mouth to anus, commonly terminal ileum and colon.
• Symptoms: abdominal pain, chronic diarrhoea, weight loss, fatigue, fever, perianal disease.
• Complications: strictures, fistulae, abscesses, obstruction, malabsorption, B12 deficiency.
• Histology: transmural inflammation and non-caseating granulomas may be seen.
• Smoking worsens Crohn’s disease and increases relapse/surgery risk.
• Management: steroids for induction, immunomodulators/biologics for maintenance in selected patients; surgery for complications but not curative.

🚨 6.3 Acute Severe Ulcerative Colitis

• Medical emergency: ≥6 bloody stools/day plus systemic toxicity.
• Assess stool frequency, pulse, temperature, Hb, CRP, albumin, electrolytes and abdominal X-ray if severe.
• Exclude infection including C. difficile.
• Treat with IV corticosteroids, VTE prophylaxis, fluids/electrolyte correction and close monitoring.
• Rescue therapy: infliximab or ciclosporin if poor steroid response.
• Early colorectal surgical review is essential; colectomy can be life-saving.

🌾 7. Coeliac Disease and Malabsorption

• Coeliac disease is immune-mediated small bowel enteropathy triggered by gluten in genetically susceptible people.
• Symptoms: diarrhoea, bloating, weight loss, fatigue, mouth ulcers, infertility, osteoporosis, dermatitis herpetiformis.
• Bloods: iron deficiency, folate deficiency, low vitamin D, abnormal LFTs.
• Test: tissue transglutaminase IgA plus total IgA while the patient is still eating gluten.
• Diagnosis may require duodenal biopsy showing villous atrophy and crypt hyperplasia.
• Management: lifelong gluten-free diet, dietitian input, correct deficiencies, monitor bone health.

⚠️ Do not start a gluten-free diet before testing if coeliac disease is suspected, because serology and biopsy can become falsely negative.

🧱 8. Diverticular Disease and Colorectal Cancer

🧱 8.1 Diverticular Disease

• Diverticulosis: presence of colonic diverticula, often asymptomatic.
• Diverticular disease: symptomatic diverticulosis with pain/bloating/change in bowel habit.
• Diverticulitis: inflammation/infection causing left iliac fossa pain, fever, raised inflammatory markers.
• Complications: abscess, perforation, fistula, obstruction, stricture, bleeding.
• CT abdomen/pelvis confirms complicated diverticulitis and guides drainage/surgery decisions.

🎗️ 8.2 Colorectal Cancer

• Symptoms: change in bowel habit, rectal bleeding, iron deficiency anaemia, abdominal pain, weight loss, tenesmus.
• Right-sided cancers often present with iron deficiency anaemia and occult bleeding.
• Left-sided cancers more often cause altered bowel habit, visible bleeding or obstruction.
• Risk factors: age, family history, Lynch syndrome, FAP, IBD, obesity, smoking, alcohol, processed meat.
• Investigations: FIT in symptomatic pathways, colonoscopy with biopsy, CT staging, CEA for monitoring.
• Management: surgery, chemotherapy, radiotherapy depending on site and stage.

🧫 9. Gastroenteritis and Infectious Diarrhoea

• Common pathogens: norovirus, Campylobacter, Salmonella, Shigella, E. coli, Giardia, Cryptosporidium.
• Food poisoning with rapid vomiting suggests preformed toxin such as Staphylococcus aureus or Bacillus cereus.
• Bloody diarrhoea suggests invasive bacterial infection, IBD or ischaemic colitis.
• Assess dehydration, sepsis, immunosuppression, recent antibiotics, travel, outbreak risk and food history.
• Most cases need fluids and safety-netting rather than antibiotics.
• Send stool sample if severe, bloody, prolonged, immunocompromised, travel-related, public health concern or hospital-acquired.

🦠 9.1 C. difficile Infection

• Risk factors: antibiotics, older age, hospitalisation, care home, PPI use, immunosuppression.
• Symptoms: watery diarrhoea, abdominal pain, fever, leukocytosis; severe disease can cause toxic megacolon.
• Management: stop unnecessary antibiotics/PPIs, isolate, oral vancomycin or fidaxomicin according to severity/local guidance.
• Avoid antimotility drugs in suspected severe infective colitis.

🟡 10. Jaundice and Cholestasis

🟡 10.1 Types of Jaundice

• Dark urine suggests conjugated bilirubin, because it is water soluble.
• Pale stools and itch suggest cholestasis with reduced bile pigment reaching the gut.
• Painless progressive jaundice with weight loss suggests pancreaticobiliary malignancy.
• Fever, jaundice and right upper quadrant pain suggests cholangitis.

🚨 10.2 Acute Cholangitis

• Ascending bacterial infection of an obstructed biliary tree.
• Charcot triad: fever, jaundice, right upper quadrant pain.
• Reynolds pentad: Charcot triad plus hypotension and confusion - severe sepsis.
• Management: ABCDE, blood cultures, IV antibiotics, fluids, analgesia, urgent biliary decompression usually by ERCP.

🪨 11. Gallstones and Biliary Colic

• Gallstones are common and often asymptomatic.
• Biliary colic: episodic right upper quadrant/epigastric pain, often after fatty meals, due to transient cystic duct obstruction.
• Acute cholecystitis: persistent pain, fever, Murphy’s sign, raised inflammatory markers.
• Choledocholithiasis: common bile duct stones causing jaundice, cholestatic LFTs and biliary dilatation.
• Gallstone pancreatitis: epigastric pain radiating to back with raised lipase/amylase.
• Management ranges from analgesia and elective cholecystectomy to urgent antibiotics/drainage/ERCP depending on complication.

🔥 12. Pancreatitis

🔥 12.1 Acute Pancreatitis

• Common causes: gallstones and alcohol; also ERCP, hypertriglyceridaemia, hypercalcaemia, drugs, trauma and malignancy.
• Symptoms: severe epigastric pain radiating to the back, nausea and vomiting.
• Diagnosis: typical pain plus lipase/amylase elevated, and/or imaging evidence.
• Early management: aggressive supportive care, fluids, analgesia, antiemetics, oxygen if needed, treat cause.
• Complications: necrosis, pseudocyst, infected necrosis, ARDS, AKI, hypocalcaemia, shock.
• Severity assessment: clinical deterioration, organ failure, inflammatory markers and imaging findings.

🧈 12.2 Chronic Pancreatitis

• Usually due to chronic alcohol exposure, smoking, genetic causes, autoimmune pancreatitis or obstructive disease.
• Symptoms: chronic epigastric pain, steatorrhoea, weight loss, diabetes.
• Pathology: irreversible fibrosis and loss of exocrine/endocrine pancreatic function.
• Management: alcohol/smoking cessation, analgesia, pancreatic enzyme replacement, fat-soluble vitamin support, diabetes management.

🍺 13. Alcohol-Related Liver Disease and MASLD/NAFLD

🍺 13.1 Alcohol-Related Liver Disease

• Spectrum: fatty liver, alcoholic hepatitis, fibrosis and cirrhosis.
• Alcoholic hepatitis: jaundice, fever, tender hepatomegaly, raised bilirubin, AST often greater than ALT but usually not extremely high.
• Management: alcohol cessation, nutritional support, thiamine, manage withdrawal, specialist assessment for severe alcoholic hepatitis.
• Long-term abstinence is the most important intervention.

⚖️ 13.2 MASLD / NAFLD

• Linked to insulin resistance, obesity, type 2 diabetes, dyslipidaemia and metabolic syndrome.
• Can progress from steatosis to steatohepatitis, fibrosis, cirrhosis and hepatocellular carcinoma.
• ALT may be mildly raised but normal LFTs do not exclude significant fibrosis.
• Risk stratification uses non-invasive fibrosis scores and tests such as FIB-4, ELF, transient elastography depending on pathway.
• Management: weight loss, exercise, diabetes/lipid optimisation, alcohol reduction and cardiovascular risk management.

🧱 14. Cirrhosis and Portal Hypertension

Cirrhosis is advanced hepatic fibrosis with regenerative nodules, causing distorted liver architecture, portal hypertension and reduced liver function. Patients may remain compensated for years before decompensation occurs.

🔍 14.1 Clinical Features

• Compensated cirrhosis: often asymptomatic or fatigue, abnormal LFTs, thrombocytopenia.
• Decompensation: ascites, variceal bleeding, jaundice, hepatic encephalopathy, spontaneous bacterial peritonitis.
• Signs: spider naevi, palmar erythema, gynaecomastia, testicular atrophy, bruising, muscle wasting, hepatosplenomegaly, ascites.
• Portal hypertension causes splenomegaly, thrombocytopenia, varices and ascites.

💧 14.2 Ascites

• New ascites should be sampled with diagnostic paracentesis.
• SAAG helps distinguish portal hypertensive from non-portal causes.
• Management: salt restriction, spironolactone ± furosemide, therapeutic paracentesis with albumin for large-volume drainage.
• Refractory ascites may require TIPS or transplant assessment.

🦠 14.3 Spontaneous Bacterial Peritonitis

• Suspect in cirrhosis with ascites plus fever, abdominal pain, encephalopathy, renal dysfunction or unexplained deterioration.
• Ascitic neutrophils ≥250 cells/mm³ supports diagnosis.
• Treat promptly with antibiotics according to local guidance plus albumin in selected high-risk patients.
• Secondary prophylaxis is usually required after an episode.

🧠 14.4 Hepatic Encephalopathy

• Neuropsychiatric syndrome from liver failure/portosystemic shunting; ammonia contributes but level does not perfectly match severity.
• Triggers: infection, GI bleed, constipation, dehydration, sedatives, electrolyte disturbance, renal failure.
• Features: sleep reversal, confusion, asterixis, drowsiness, coma.
• Management: treat trigger, lactulose titrated to soft stools, rifaximin in recurrent episodes, avoid sedatives where possible.

🧠 Exam pearl: In cirrhosis, any deterioration is infection until proven otherwise - check cultures, urine, chest, ascitic tap and consider SBP early.

🩸 15. Upper GI Bleeding and Varices

🩸 15.1 Initial Approach

• ABCDE assessment, high-flow oxygen if needed, two large-bore cannulas, bloods, group and save/crossmatch.
• Assess shock and comorbidity; use risk tools such as Glasgow-Blatchford score.
• Resuscitate with blood products as clinically indicated; correct coagulopathy only when appropriate and guided by senior advice.
• Urgent endoscopy after stabilisation; immediate senior involvement if unstable.

🔥 15.2 Non-Variceal Bleeding

• Common causes: peptic ulcer disease, erosive gastritis/oesophagitis, Mallory-Weiss tear, malignancy, angiodysplasia.
• Endoscopic therapy may include injection, clips, thermal therapy or haemostatic spray.
• PPI therapy is used after endoscopic haemostasis for high-risk ulcer bleeding.

🧱 15.3 Variceal Bleeding

• Occurs from portal hypertension, usually in cirrhosis.
• Management: resuscitation, IV antibiotics, vasoactive therapy such as terlipressin, urgent endoscopy with band ligation.
• Balloon tamponade or oesophageal stent may be bridge therapy in uncontrolled bleeding.
• Secondary prevention: non-selective beta-blocker and repeat banding, with TIPS for selected high-risk/refractory cases.

🚨 16. Acute Abdomen and GI Emergencies

🧱 16.1 Bowel Obstruction

• Small bowel obstruction: colicky pain, vomiting, distension, constipation; adhesions and hernias common.
• Large bowel obstruction: distension, absolute constipation, later vomiting; cancer and volvulus important causes.
• Management: nil by mouth, IV fluids, NG tube if vomiting/distended, analgesia, CT imaging, surgical review.
• Red flags: peritonism, fever, tachycardia, metabolic acidosis, raised lactate, strangulated hernia.

🕳️ 16.2 Perforation and Peritonitis

• Features: sudden severe pain, rigid abdomen, guarding, shock, shoulder tip pain if diaphragmatic irritation.
• CXR/CT may show free air under diaphragm.
• Management: resuscitation, broad-spectrum antibiotics, urgent surgery.

🩸 16.3 Mesenteric Ischaemia

• Pain out of proportion to examination is the classic early clue.
• Risk factors: AF, atherosclerosis, low-flow states, vasculitis, thrombophilia.
• Late signs: peritonitis, bloody diarrhoea, shock, lactic acidosis.
• Requires urgent CT angiography and vascular/surgical input.

🧬 16.4 Toxic Megacolon

• Severe colonic dilatation with systemic toxicity, classically from UC, infection or C. difficile.
• Features: abdominal distension, pain, fever, tachycardia, shock, reduced bowel sounds.
• Avoid antimotility drugs and colonoscopy if severe.
• Management: resuscitation, IV steroids if IBD-related, antibiotics if infection suspected, urgent surgical review.

📚 17. OSCE / Exam Pearls

• Progressive dysphagia plus weight loss is malignancy until proven otherwise.
• IBS should not cause rectal bleeding, anaemia, fever or nocturnal diarrhoea.
• UC is continuous from the rectum; Crohn’s is patchy and transmural.
• Do not test for coeliac disease after starting a gluten-free diet unless gluten has been reintroduced.
• Right-sided colon cancer often presents with iron deficiency anaemia.
• Painless jaundice and weight loss suggests pancreaticobiliary malignancy.
• Charcot triad = fever, jaundice and right upper quadrant pain.
• New ascites in cirrhosis needs diagnostic tap.
• Any cirrhotic patient with deterioration needs infection/SBP considered.
• Massive GI bleeding is an ABC emergency before it is an endoscopy problem.

📌 18. Quick Differentials Table

📚 References

• NICE. Gastro-oesophageal reflux disease and dyspepsia in adults: investigation and management. CG184.
• NICE. Irritable bowel syndrome in adults: diagnosis and management. CG61.
• NICE. Crohn’s disease: management. NG129.
• NICE. Ulcerative colitis: management. NG130.
• NICE. Cirrhosis in over 16s: assessment and management. NG50.
• British Society of Gastroenterology guidance should be checked for specialist pathways such as IBD biologics, endoscopy surveillance and variceal management.

⚠️ Disclaimer

This article is for medical education and exam revision. Clinical decisions should follow current local guidelines, antimicrobial policies, endoscopy pathways, formularies, senior advice and national guidance. Gastroenterology presentations can deteriorate quickly, especially GI bleeding, cholangitis, acute liver failure, severe colitis and bowel ischaemia.