D

GI System Module 4

Stomach: Functions and Gastritis

  • Functions of the stomach: organ of protection, digestion, and absorption (primarily absorbing water and alcohol).
  • Stomach acid forms a first line of defense by destroying many microorganisms and harmful substances on contact.
  • During digestion, foods and liquids are mixed with gastric secretions, which are composed of: mucus, acid, enzymes, hormones, and intrinsic factor (IF).
  • Gastric glands are lined by specialized epithelial cells that secrete these substances.
  • Epithelial cells form tight connections; this tight junction is an important source of protection from the corrosive effects of gastric acid.
  • Prostaglandins play a key role in maintaining gastric mucosal integrity by stimulating a protective mucus barrier.

Acute Gastritis: Pathophysiology, Manifestations, and Management

  • Inflammation of the gastric mucosa most often caused by irritants such as aspirin, alcohol, or certain microorganisms.
  • Typically acute and reversible when the causative agent is removed.
  • Clinical manifestations (vary with severity):
    • Mild to severe abdominal pain
    • Indigestion (heartburn)
    • Loss of appetite
    • Nausea, vomiting, hiccups
    • Hematemesis (vomiting blood) can occur, which may lead to anemia

Chronic Gastritis and Helicobacter pylori

  • H. pylori is a Gram-negative bacterium transmitted person-to-person via infected saliva and stool.
  • Infection process:
    • Ingested bacteria multiply on epithelial surface cells and mucus barrier.
    • H. pylori produces enzymes that neutralize gastric acid, allowing survival.
    • Produces toxins that can destroy gastric mucosa.
    • As infection becomes chronic, macrophages and T/B lymphocytes infiltrate to clear bacteria.
    • Epithelial cells and mucous glands may atrophy; mucosal lining becomes thin and gastric acid production/secretion is impaired.
  • Treatment: Proton Pump Inhibitors (PPIs) reduce gastric acid production and promote mucosal healing.

Chronic Gastritis: Autoimmune Type

  • Autoantibodies directed against gastric parietal cells or intrinsic factor.
  • Pathophysiology:
    • Parietal cells secrete hydrochloric acid (HCl). Autoantibodies impair acid secretion.
    • Intrinsic factor is necessary for vitamin B12 absorption in the intestine; antibodies against intrinsic factor impair B12 absorption.
    • Chronic autoimmune inflammation allows T cells to infiltrate the gastric mucosa, destroying epithelial cells and causing gastric atrophy.
  • Pernicious anemia may be the first clue indicating chronic autoimmune gastritis.

Pancreas: Structure and Function

  • The pancreas is both an endocrine and exocrine gland located in the upper posterior abdomen on the patient’s left side.
  • Endocrine pancreas ≈ 20% of the gland; produces insulin.
  • Exocrine pancreas ≈ 80% of the gland; produces and secretes digestive enzymes essential for carbohydrate, fat, and protein metabolism.

Acute Pancreatitis: Pathophysiology and Clinical Features

  • Pathophysiology: injury to acinar cells, pancreatic ducts, or protective digestive feedback mechanisms in the exocrine pancreas.
  • Common causes: ductal obstruction by gallstones; excessive alcohol use.
  • Clinical manifestations:
    • Upper abdominal pain of sudden onset, increasing in intensity, often radiating to the back (dull, steady ache).
    • Nausea, vomiting, anorexia, and/or diarrhea.
  • Treatment: aggressive IV hydration in the first 24 hours.

Chronic Pancreatitis

  • Definition: ongoing inflammatory process with irreversible cellular and tissue changes in the pancreas.
  • Most common cause: chronic alcohol abuse ≈ 60\% \text{ to } 70\%.
  • Other causes: autoimmune, hereditary.
  • Clinical manifestations: often severe intermittent abdominal pain (mid or upper right-sided, radiating to the back) lasting several hours at unpredictable intervals.
  • Disease development typically begins months to years before symptom onset.

Inflammatory Bowel Disease (IBD)

  • Main conditions covered: Crohn's disease and Ulcerative Colitis (UC).

Crohn's Disease

  • Definition: chronic inflammatory disease of the small intestine (most often), colon, or both; recurrent with remissions and exacerbations.
  • Cobblestone appearance: granulomas (granulomatous inflammation) with skip lesions.
  • Clinical manifestations: severe diarrhea and anemia.
  • Symptoms depend on location of affected areas:
    • Abdominal cramping and pain, typically in the right lower quadrant, may be relieved with defecation.
    • Non-bloody diarrhea (usually watery).
    • Indications of inflammation: fever, weight loss, fatigue.
  • Diagnosis: direct visualization with endoscopy (sigmoidoscopy) or radiographs showing cobblestone mucosa with alternating inflamed and unaffected areas.

Ulcerative Colitis (UC)

  • Location: exclusively in the large intestine; does not affect other GI tract regions.
  • Pattern: typically begins in the distal rectum and extends proximally up the descending colon.
  • Mucosa: erythematous and granular; hemorrhagic lesions in intestinal glands can become abscesses.
  • Clinical manifestations: diarrhea, often with rectal bleeding.
  • Diagnostic criteria: endoscopy shows mucosal erythema.

Chapter 5: Hepatitis (Overview and Types)

  • Viral hepatitis refers to inflammation of the liver caused by viral infection.
  • Types: A, B, C, D, E.
  • Transmission routes:
    • Fecal–oral contact (leading to acute hepatitis typically).
    • Blood and body fluids (risk of chronic disease).

Hepatitis A

  • Transmission: fecal-oral route.
  • Clinical course: recovery usually uneventful; very contagious.
  • Prevention: vaccine.
    • First dose: 12\text{-}23\ \text{months of age}.
    • Second dose: 6\text{-}18\ \text{months after the first dose}.

Hepatitis B

  • Transmission: blood, sexual contact, sharing needles, pregnancy/delivery.
  • Outcomes: most people clear the virus and develop immunity; a small percentage become carriers.
  • Risks: carriers can infect others even when asymptomatic; high risk for cirrhosis and liver cancer.
  • Prevention: vaccine.
    • First dose: within 24\ \text{hours} of birth.
    • Second dose: 1\text{-}2\ \text{months} of age.
    • Third dose: 6\text{-}18\ \text{months} of age.

Hepatitis C

  • Transmission: blood, sexual contact, perinatal.
  • Significance: leading cause of end-stage liver disease.
  • Course: HCV typically does not clear and progresses to chronic illness—cirrhosis and liver cancer.
  • Prevention: avoidance of risk behaviors.

Appendicitis

  • Cause: obstruction by trapped fecal material in the appendix.
  • Pathophysiology: obstruction triggers inflammatory response, followed by infection.
  • Treatment: surgical removal of the appendix once obstruction is identified.
  • If untreated and rupture occurs: bacteria spill into peritoneal cavity, leading to peritonitis and septic shock; reduced perfusion to all organ systems, especially the GI tract.

Diverticular Disease

  • Characterized by decreased motility, obstruction, and impaired perfusion.
  • Diverticulum: small sac or pouch along the wall of the colon, most often in the ascending colon.
  • Diverticulosis: presence of diverticula (more than one).
  • Diverticulitis: fecal matter caught in diverticula may promote inflammation.
  • Pathophysiology: chronic constipation is linked to diverticular disease; slow bowel movement increases and prolongs pressure on colon walls, leading to structural changes.
  • Clinical manifestations: pain, most commonly in the left lower quadrant (sigmoid colon).
  • Treatment: colostomy may be required temporarily until healing, after which re-anastomosis may be performed.

Peritonitis

  • Definition: life-threatening, acute inflammation and infection of the peritoneum and lining of the abdominal cavity.
  • Common causes: bacteria entering the peritoneum via perforation (e.g., from appendicitis or diverticulitis), penetrating wounds, or bowel obstruction.
  • Classic manifestation: abdominal rigidity due to peritoneal inflammation (involuntary muscle guarding).