Summary This section covers high-yield gastrointestinal pathology topics not included in previous parts (Parts 1 & 2), focusing on the oesophagus, stomach, and
Summary This section covers high-yield gastrointestinal pathology topics not included in previous parts (Parts 1 & 2), focusing on the oesophagus, stomach, and intestines. It addresses critical conditions such as oesophageal varices, Mallory-Weiss tears, various acute peptic ulcers, malabsorption syndromes like lactase deficiency and abetalipoproteinaemia, inflammatory conditions including Irritable Bowel Syndrome (IBS) and microscopic colitis, Graft-Versus-Host Disease (GI manifestations), environmental enteropathy, and sigmoid diverticulitis. Key Points Oesophageal varices: Develop in 90% of cirrhotic patients, ~50% die from first bleed; alcoholic cirrhosis is the most common cause, schistosomiasis is second worldwide. Mallory-Weiss: Superficial tear at the gastroesophageal junction (GEJ); associated with alcohol and vomiting; heals spontaneously. Boerhaave: Transmural oesophageal tear leading to mediastinitis; catastrophic. Inlet patch: Ectopic gastric mucosa in the upper third of the oesophagus; usually asymptomatic. Stress ulcers: Associated with shock/sepsis; typically found in the stomach with a brown-black base, sharply demarcated, and no scarring. Curling ulcers: Linked to severe burns or trauma; located in the proximal duodenum. Cushing ulcers: Related to intracranial disease, involving vagal stimulation; carry a high risk of perforation. Oesophageal SCC: 6 times more common in African Americans; upper third spreads to cervical nodes, middle to mediastinal nodes, lower to gastric nodes. Lactase deficiency: Acquired type is most common, prevalent in Native Americans, African Americans, and Chinese populations; causes osmotic diarrhoea; biopsy is typically normal. Abetalipoproteinaemia: Caused by a mutation in microsomal triglyceride transfer protein; leads to lipid vacuoles visible with oil red O stain; results in acanthocytes and fat-soluble vitamin deficiency. IBS: No structural abnormality found grossly or microscopically; typically manifests between 20–40 years with a significant female predominance; affects 5–10% of the population in developed countries. Microscopic colitis: Diagnosis requires biopsy despite normal endoscopic findings; collagenous type shows a dense subepithelial collagen layer; lymphocytic type shows a greater increase in intraepithelial lymphocytes (IELs). GvHD (GI): Occurs after allogeneic haematopoietic stem cell transplantation; characterized by epithelial apoptosis, particularly of crypt cells, and manifests as watery diarrhoea. Environmental enteropathy: Affects 150 million children in developing countries; histologically resembles severe coeliac disease (villous atrophy); no accepted diagnostic criteria or proven treatment. Sigmoid diverticulitis: Common in Western populations over age 60; often linked to low-fibre diets; perforation is the most severe complication. Detailed Notes FROM PART 1 — OESOPHAGUS AND STOMACH Oesophageal Varices Pathogenesis: Portal hypertension → collateral channels → portal blood shunts into caval system → subepithelial and submucosal venous plexuses in distal oesophagus enlarge = varices. Develop in 90% of cirrhotic patients ; most common cause = alcoholic liver disease . Worldwide: hepatic schistosomiasis = second most common cause. Morphology: Tortuous dilated veins in submucosa of distal oesophagus and proximal stomach. Collapse when no blood flow. Overlying mucosa intact OR ulcerated/necrotic if rupture occurred. Clinical features: Often asymptomatic until rupture. Rupture → massive haematemesis → medical emergency. ~50% die from first bleeding episode (haemorrhage OR hepatic coma from protein load + hypovolaemic shock). Among survivors: additional haemorrhage in 50% — each potentially fatal. 50% of deaths in advanced cirrhosis result from variceal rupture. Mallory-Weiss Tears and Boerhaave Syndrome Mallory-Weiss Tears Most common oesophageal lacerations. Associated with severe retching or vomiting — classic setting: acute alcohol intoxication. Mechanism: Reflex relaxation of gastroesophageal musculature fails during prolonged vomiting → refluxing gastric contents overwhelm gastric inlet → oesophageal wall tears. Morphology: Roughly linear, longitudinally oriented. Cross gastroesophageal junction . Superficial — do NOT require surgery; heal rapidly and completely. Presentation: Haematemesis . Boerhaave Syndrome Transmural oesophageal tears → mediastinitis . Same causative factors as Mallory-Weiss but more severe. Rare but catastrophic — life-threatening surgical emergency. Key distinction: Mallory-Weiss = superficial/mucosal; Boerhaave = transmural + mediastinitis. Ectopia (Inlet Patch) Most frequent site of ectopic gastric mucosa = upper third of oesophagus = "inlet patch" ; usually asymptomatic. Acid from ectopic mucosa → dysphagia, oesophagitis, Barrett oesophagus, or adenocarcinoma. Gastric heterotopia in small bowel/colon → occult blood loss from peptic ulceration of adjacent mucosa. Stress, Curling, and Cushing Ulcers Acute Peptic Ulceration — Three Types: Type Location Associated Condition :---------------- :------------------------------- :-------------------------------------------------- Stress ulcers Stomach Shock, sepsis, severe trauma Curling ulcers Proximal duodenum Severe burns or trauma Cushing ulcers Stomach, duodenum, or oesophagus Intracranial disease; high incidence of perforation Pathogenesis: NSAID-induced: COX inhibition → no prostaglandins → lost bicarbonate + lost vascular perfusion. Intracranial injury: direct vagal stimulation → gastric acid hypersecretion. Critically ill: systemic acidosis lowers mucosal intracellular pH; hypoxia from splanchnic vasoconstriction. Morphology: Rounded, 100-fold between countries; highest in Iran, central China, Hong Kong, Argentina, Brazil, South Africa . Lymph node spread by location: Upper third → cervical lymph nodes . Middle third → mediastinal, paratracheal, tracheobronchial nodes. Lower third → gastric and coeliac nodes . Rich submucosal lymphatic network → circumferential and longitudinal spread; intramural tumour nodules several centimetres from principal mass. FROM PART 2 — INTESTINES Lactase (Disaccharidase) Deficiency Type Features :------------- :------------------------------------------------------------------------------------------------------------------------------------------------------------------- Congenital Autosomal recessive; mutation in lactase gene; rare; explosive diarrhoea + abdominal distention after milk; resolves when milk removed Acquired Most common; downregulation of lactase gene expression; most common in Native Americans, African Americans, Chinese ; sometimes triggered by enteric viral/bacterial infections Disaccharidases located in apical brush border membrane of villous absorptive epithelial cells. Biopsies generally unremarkable — defect is biochemical, not structural. Osmotic diarrhoea — abates with fasting. Abetalipoproteinaemia Autosomal recessive ; mutation in microsomal triglyceride transfer protein → enterocytes cannot export lipoproteins and free fatty acids. Monoglycerides and triglycerides accumulate within epithelial cells → lipid vacuoles visible on light microscopy; highlighted by oil red O stain (especially after fatty meal). Manifests in infancy : failure to thrive, diarrhoea, steatorrhoea. Failure to absorb essential fatty acids → deficiencies of fat-soluble vitamins (A, D, E, K) . Lipid defects in plasma membranes → acanthocytic red cells (spur cells) in peripheral blood. Classic example of transepithelial transport defect causing malabsorption. Irritable Bowel Syndrome (IBS) Chronic and relapsing abdominal pain, bloating, changes in bowel habits (diarrhoea and/or constipation). Pathogenesis poorly defined: psychologic stressors, diet, abnormal GI motility. No gross or microscopic abnormalities in most patients — diagnosis based entirely on clinical symptoms . Manifests between 20–40 years ; significant female predominance . Prevalence in developed countries: 5–10