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Gastrointestinal System Pathophysiology

Explore GI anatomy, digestion mechanics, absorption processes, and pathophysiology of GI disorders.

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Overview

The gastrointestinal system processes food for nutrient absorption and eliminates waste. Understanding digestion, absorption mechanics, and common GI pathologies is essential for comprehensive nursing assessment. This guide covers normal GI physiology and disorders including GERD, peptic ulcers, inflammatory bowel disease, and hepatic dysfunction.

GI Tract Anatomy

Structural Organization

  • Pathway: mouth → esophagus → stomach → small intestine → colon → rectum → anus
  • Accessory organs: liver, gallbladder, pancreas
  • Wall layers: mucosa (epithelial), submucosa, muscularis, serosa

Stomach Function

  • Reservoir: fundus stores food
  • Mixing: body churns food into chyme
  • Secretion: HCl, pepsinogen, intrinsic factor, mucus
  • Digestion: pepsin initiates protein breakdown (10-15%)

Small Intestine (Absorption Site)

  • Structure: duodenum, jejunum, ileum (20+ feet length)
  • Villi and microvilli: 300-400× surface area increase
  • Absorption: monosaccharides, amino acids, fatty acids, vitamins, minerals
  • Special absorption: B12 (terminal ileum, requires intrinsic factor), iron (duodenum)

Colon & Liver Function

  • Colon: water reabsorption (8-10 L/day), electrolyte reabsorption, stool formation
  • Liver: bile production, protein synthesis, metabolic processing, detoxification
  • Gallbladder: bile storage and concentration
  • Pancreas: digestive enzymes (amylase, lipase, proteases), bicarbonate

Digestion & Absorption

Carbohydrate Digestion

  • Mouth: salivary amylase (10% digestion)
  • Small intestine: pancreatic amylase, brush border disaccharidases
  • Products: glucose, fructose, galactose
  • Absorption: active transport in duodenum/jejunum

Protein Digestion

  • Stomach: pepsin begins breakdown (10-15%)
  • Small intestine: pancreatic proteases, brush border peptidases
  • Products: amino acids, dipeptides, tripeptides
  • Absorption: active transport in duodenum/jejunum

Fat Digestion & Absorption

  • Pancreatic lipase: primary enzyme (90% fat digestion)
  • Bile salts: emulsification, micelle formation (essential)
  • Products: fatty acids, monoglycerides
  • Absorption: micelle transport, resynthesis into triglycerides, packaging as chylomicrons

Vitamin & Mineral Absorption

  • Water-soluble (B, C): absorbed throughout small intestine, excess excreted
  • Fat-soluble (A, D, E, K): require bile salts, stored in liver/adipose
  • Iron: duodenum (enhanced by vitamin C, inhibited by phytates)
  • B12: terminal ileum, requires intrinsic factor
  • Calcium: small intestine, vitamin D-dependent active transport

Common GI Disorders

GERD (Gastroesophageal Reflux Disease)

  • Pathophysiology: LES incompetence → acid reflux into esophagus
  • Causes: LES relaxation, ↑ intragastric pressure, delayed gastric emptying
  • Complications: esophagitis, Barrett's esophagus, stricture, aspiration
  • Management: lifestyle changes, antacids, H2-blockers, PPIs

Peptic Ulcer Disease

  • Causes: H. pylori (95% duodenal), NSAIDs (especially gastric), stress
  • Pathophysiology: mucosal damage from acid/pepsin, failed healing
  • Complications: bleeding (erosion into vessel), perforation, stenosis
  • Management: H. pylori eradication, PPI therapy, NSAID discontinuation

Inflammatory Bowel Disease

Crohn's Disease: full-thickness inflammation, skip lesions, any GI location, fistulas/strictures risk

Ulcerative Colitis: superficial inflammation, continuous, colon/rectum only, toxic megacolon risk

Pathophysiology: increased permeability, bacterial translocation, ↓ absorptive area, diarrhea

Malabsorption

  • Causes: luminal (inadequate digestion), mucosal (reduced surface/inflammation), post-mucosal (lymphatic obstruction)
  • Steatorrhea: fat malabsorption (pale, fatty stools)
  • Celiac Disease: gluten-triggered villous atrophy → surface area ↓, malabsorption
  • Lactose Intolerance: lactase deficiency → osmotic diarrhea, gas production

Liver Disease & Cirrhosis

  • Hepatitis: inflammation from viral, autoimmune, or alcoholic causes
  • Cirrhosis: end-stage liver disease, progressive fibrosis, hepatocyte necrosis
  • Consequences: ↓ synthetic function, ↓ detoxification, portal hypertension, ascites, encephalopathy
  • Variceal Bleeding: esophageal/gastric varices from portal hypertension

Pancreatitis & Biliary Disease

  • Acute Pancreatitis: autodigestion from premature enzyme activation
  • Chronic Pancreatitis: progressive inflammation/fibrosis, ↓ enzyme/hormone function
  • Cholecystitis: inflammation of gallbladder, stone in cystic duct
  • Choledocholithiasis: stone in common duct → obstructive jaundice

Clinical Assessment

Abdominal Symptoms

  • Dysphagia: difficulty swallowing (obstruction vs. motility)
  • Dyspepsia: upper abdominal discomfort, bloating, early satiety
  • Nausea/Vomiting: many causes, hematemesis = GI bleed
  • Diarrhea: osmotic, secretory, inflammatory, motility causes
  • Constipation: <3 stools/week, straining, hard stool

Physical Examination

  • Inspection: distention, scars, visible peristalsis
  • Auscultation: bowel sounds, bruits, quality
  • Palpation: tenderness, rebound, guarding, rigidity, masses
  • Percussion: tympany (gas), dullness (fluid/solid)
  • Signs: Murphy's (cholecystitis), McBurney's (appendicitis), Rovsing's

Diagnostic Tests

  • Labs: liver function tests, amylase/lipase, lipid panel, stool studies
  • Imaging: abdominal X-ray (obstruction, perforation), ultrasound, CT, ERCP
  • Endoscopy: visualizes esophagus/stomach/duodenum (upper), colon (lower)
  • Biopsy: inflammation assessment, H. pylori, malignancy

Study Questions

1. Explain the process of fat digestion and absorption, including the role of bile salts and the formation of chylomicrons.

2. Compare and contrast Crohn's disease and ulcerative colitis in terms of location, depth of involvement, complications, and clinical presentation.

3. Explain why a patient with celiac disease develops malabsorption despite having intact digestive enzymes.

4. A patient with cirrhosis develops ascites and hepatic encephalopathy. Explain the pathophysiological mechanisms of both complications.

5. Discuss the pathophysiology of lactose intolerance and why symptoms worsen with high lactose foods.

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