Gastrointestinal Pathology Lecture Notes

Gastroesophageal Reflux Disease (GERD)

• Definition / Core Idea

  • Movement of acidic gastric contents into the esophagus → chemical injury of esophageal epithelium.

• Pathophysiology

  • Repeated acid exposure triggers metaplasia: squamous epithelium → glandular/columnar epithelium ("Barrett‐type" change).

  • Persistent inflammation (esophagitis) accompanies cellular conversion.

• Potential Sequelae

  • Esophageal ulcers.

  • \text{Adenocarcinoma of the esophagus} – malignant transformation in metaplastic tissue.

• Clinical Manifestations

  • Epigastric pain / heartburn.

  • Burning substernal chest sensation.

  • Belching.

  • Nausea.

  • Regurgitation of sour/bitter gastric fluid.

  • Persistent bitter taste in mouth.

  • Day-time (often described as "7-day") cough not explained by respiratory illness.

Gastritis

General Definition

• Inflammation of gastric mucosa → impaired stomach function.

Acute Gastritis

• Definition – Rapid‐onset inflammation due to recent exposure to gastric irritants; reversible once the insult is removed.

• Key Irritants: aspirin & other NSAIDs, alcohol, corrosive/irritating foods, microorganisms, stress.

• Pathophysiology

  • Irritants inhibit production of protective mucus and bicarbonate.

  • Acid and pepsin become unopposed → erythema → erosions → possible perforation.

  • Superficial epithelial necrosis; may extend to submucosa if severe.

• Clinical Manifestations

  • Mild → severe epigastric/abdominal pain.

  • Indigestion (dyspepsia).

  • Loss of appetite (anorexia).

  • Nausea / vomiting.

  • Hiccups (vagal irritation).

Chronic Gastritis

• Definition – Ongoing, unrelenting mucosal injury (months–years) from chronic infection or autoimmunity.

• Etiologic Highlight – \text{Helicobacter pylori (H.\ pylori)} infection; less commonly autoimmune attack on parietal cells/intrinsic factor.

• Pathophysiology

  • \text{H.\ pylori} transmitted by infected saliva & stool.

  • Bacterial urease & cytotoxins → mucosal destruction → chronic inflammation.

  • ↓/dysregulated gastric acid production; progressive mucosal & glandular atrophy.

  • Autoimmune variant: antibodies against parietal cells → loss of \text{IF} → vitamin B_{12} malabsorption → pernicious anemia.

• Clinical Manifestations

  • Dyspepsia.

  • Anorexia / early satiety.

  • Vomiting.

  • Iron‐deficiency or pernicious anemia.

  • May be completely asymptomatic.

Pancreatitis

Core Definition

• Inflammatory destruction of pancreas by prematurely activated pancreatic enzymes (\"auto-digestion\").

Acute Pancreatitis

• Trigger – Sudden injury to acinar cells or duct obstruction → enzyme activation in situ.

• Common Causes

  • Gallstone obstruction of pancreatic duct.

  • Heavy alcohol intake (also major chronic cause).

• Clinical Manifestations

  • Nausea & vomiting.

  • Anorexia.

  • Diaphoresis (profuse sweating).

  • Sudden, severe upper abdominal pain: dull/steady, intensifies, radiates to back.

  • Systemic/secondary effects:

  • Jaundice if common bile duct fully blocked.

  • Abdominal bloating / distention.

  • Clay-colored stools (lack of bile pigments).

  • Hiccups, fever, tachycardia.

Chronic Pancreatitis

• Definition – Long-standing inflammation with irreversible parenchymal destruction & fibrosis.

• Pathophysiology Highlights

  • Alcohol → protein plugs & enzyme precipitates → duct obstruction.

  • Ischemia due to vascular compromise ↓ blood flow.

  • Progressive acinar atrophy & fibrosis → exocrine failure.

  • Destruction of islet cells → insulin loss → \text{Type IIIc (pancreatogenic) diabetes}.

  • Oxidative stress & possible autoimmune mechanisms accelerate damage.

• Clinical Manifestations

  • Severe, intermittent abdominal pain.

  • Chronic diarrhea.

  • Steatorrhea (greasy, bulky, foul-smelling stools).

  • Progressive weight loss despite normal intake.

Inflammatory Bowel Disease (IBD)

• Umbrella term for chronic, immune-mediated inflammation anywhere from mouth → anus.

Crohn Disease

• Definition – Transmural, granulomatous inflammation; primarily terminal ileum, ascending colon, but can affect any GI segment.

• Pathophysiology

  • Characteristic "skip lesions" – patchy inflammatory segments separated by normal bowel.

  • Involves all layers → deep ulcers, fissures, fistulas.

  • Increased capillary permeability & vascular congestion → edema; chronic cycle → fibrosis & strictures → bowel obstruction.

  • Malabsorption due to mucosal damage & shortened bowel.

• Clinical Manifestations

  • Crampy abdominal pain.

  • Chronic, non-bloody diarrhea.

  • Malnutrition & weight loss.

  • Occult (hidden) blood in stool.

  • Low-grade fever.

  • Fatigue.

  • "Skip lesions" visible on CT/MRI, barium studies, or endoscopy.

Ulcerative Colitis

• Definition – Continuous superficial inflammation limited to COLON (almost always begins in rectum, extends proximally).

• Pathophysiology

  • Involves mucosa & submucosa only.

  • Hemorrhagic erosions → micro-abscesses.

  • Continuous ulcerations (no skip areas).

  • Long-term: epithelial atrophy, pseudopolyps, risk for perforation, toxic megacolon, massive bleeding.

• Clinical Manifestations

  • Bloody (often mucus-rich) diarrhea.

  • Rectal bleeding / urgency.

  • Colicky abdominal pain.

  • Fever.

  • Weakness, fatigue.

  • Anemia from chronic blood loss.

Viral Hepatitis

• Definition – Viral-mediated inflammation of liver → hepatocyte necrosis.

• Transmission Pathways

  • Fecal-oral (enteric) or parenteral (blood/body fluids).

• Types & Routes

  • \text{Hepatitis A} (HAV) – Fecal-oral; person-to-person, contaminated food/water. → Typically acute, self-limited.

  • \text{Hepatitis B} (HBV) – Blood, sexual fluids, perinatal (mother → infant). → Frequently becomes chronic.

  • \text{Hepatitis C} (HCV) – Primarily blood (shared needles, transfusions). → Highest rate of chronicity.

• Clinical Course / Manifestations

  1. Prodromal phase – Fatigue, anorexia, low-grade fever, malaise.

  2. Icteric phase – Jaundice, hepatomegaly, RUQ tenderness, dark urine, clay-colored stools.

  3. Convalescent / Recovery – Gradual symptom resolution; hepatomegaly may persist.

  • Additional physical sign – Yellowing of sclera (scleral icterus).

Cross-Links & Clinical Pearls

• Metaplasia → Dysplasia → Cancer: GERD-induced metaplastic changes (Barrett esophagus) underscore how chronic inflammation can precipitate malignancy – same caution for chronic gastritis & ulcerative colitis (colorectal carcinoma risk).

• Pain Radiation Patterns: Pancreatic pain classically radiates to the back, helping distinguish it from gastric or biliary pain during differential diagnosis.

• Steatorrhea vs. Clay-colored Stool:

  • Steatorrhea (fatty, oily) indicates malabsorption/pancreatic insufficiency.

  • Clay colored stool reflects lack of bile pigment passage (biliary obstruction or severe hepatitis).

• Autoimmune Overlap: Chronic gastritis (pernicious anemia) & IBD patients often share other autoimmune conditions (e.g., thyroiditis, primary sclerosing cholangitis) – monitor accordingly.

• Public Health: Hepatitis A outbreaks are strongly linked to inadequate sanitation; vaccination prevents spread. Needle-exchange programs & antiviral screening curtail HBV/HCV.

Quick-Reference Equations / Numbers

• None explicitly provided in transcript; key biological agents expressed in LaTeX for clarity (e.g., \text{H.\ pylori}, \text{HBV}).

Ethical & Practical Implications

• Over-prescription of NSAIDs (a modifiable risk factor for acute gastritis) raises ethical duty to balance pain control vs. GI safety.

• Alcohol education programs double as pancreatitis prevention strategies.

• Vaccination (HAV, HBV) is both an individual and community responsibility, directly reducing hepatic disease burden.