GIT Flashcards
Meckel’s Diverticulum Features
Cause: incomplete involution of vitelline duct
Morphology: all layers of GIT present (can have heterotropic pancreatic or gastric tissue present)
*Rule of 2’s
Meckel Diverticulum Conditions
Hemorrhage and peptic ulcer, SBO, diverticulitis, perforation, fistula
Celiac Sprue
Morphology: villous atrophy (flattening of brush border and increased intraepithelial lymphocytes
Serology: anti-tTG Ab (and anti-gliadin Ab, anti-endomysial Ab)
HLA genotype: HLA DQ2 and DQ8
Tx: reversal of changes after gluten free diet
Meconium Ileus
Infant w/ CF, thick mucus at mid-terminal ileum causing SBO
*endogenous
Gallstone Ileus
Stone >2.5cm lodges in terminal ileum, usually through cholecystoduodenal fistula, causing SBO
*endogenous
Hirschsprung Dz
Cause: absence of ganglion cells in Meissen or Auerbach plexus
Localization: rectum always affected
Morphology: dilatation and hypertrophy of the portion proximal to the aganglionic segment (distal well-appearing part is the aganglionic part)
Achalasia complication (condition)?
Squamous cell ca of esophagus, aspiration pneumonia
Investigation: manometry to check LES pressure
Diffuse Adenocarcinoma of stomach
Familial: E-cadherin mutation
Morphology: signet ring cells, no glands
Course: mets to ovaries as Krukenberg’s tumor
Appearance: linitis plastica (leather bottle)
Intestinal Adenocarcinoma
Risk: H.pylori infection
Course: gastritis w/ intestinal metaplasia, then neoplastic cells forming glands
Macrovesicular Steatosis
Large droplet: single fat vacuole displaces nucleus to periphery
Small droplet: multiple fat vacuoles (ETOH, malnutrition)
Microvesicular Steatosis
Multiple fine vacuoles, nucleus is CENTRAL (acute fatty liver of pregnancy, Reye syndrome, drugs)
Mallory Bodies
Intermediate keratin filaments
Non-specific to ETOH hepatitis
Wilson’s Dz
Etiology: accumulation of Cu2+
Morphology: fatty liver, hepatitis
ROS: basal ganglia w/ Cu and Kayser-Fleischer rings in eyes
Labs: 👇🏽 serum ceruloplasmin
Autoimmune Hepatitis
Type 1: Anti-liver/kidney/microsomal (LKM) Ab, Anti-nuclear Ab (ANA), and Anti-smooth muscle Ab (ASMA)
Labs: high IgG
Primary Biliary Cholangitis
Pathogenesis: Anti-mitochondrial Ab
Morphology: granulomatous destruction of medium sized intrahepatic bile ducts *(florid duct lesion)