GASTROINTESTINAL PATHOLOGY (Part 3)

## 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