GASTROINTESTINAL PATHOLOGY (Part 3) — Notes OmpathStudy

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 Ulcerati