Pathophysiology of the Gastrointestinal Tract

Vocabulary flashcards covering major terms and concepts from Module 4: Pathophysiology of the Gastrointestinal Tract.

Gastroesophageal Reflux Disease (GERD)

Backward flow of hydrochloric acid from the stomach into the lower esophagus causing chronic inflammation and heartburn.

Metaplasia

Protective change of esophageal squamous epithelium to columnar epithelium in chronic GERD; increases cancer risk.

Peptic Ulcer Disease (PUD)

Erosive lesions penetrating the muscularis mucosae of the stomach or duodenum.

Duodenal ulcer

Most common PUD; pain relieved by eating; strongly linked to NSAIDs and H. pylori.

Gastric ulcer

Less common but more lethal PUD; pain worsens with eating; often linked to NSAIDs or malignancy.

Gastritis

Inflammation of the gastric mucosa that may be acute or chronic.

Acute gastritis

Sudden gastric inflammation from irritants (alcohol, NSAIDs) leading to pain, N/V, and possible hemorrhage.

Chronic gastritis (H. pylori)

Long-term gastric inflammation caused by H. pylori infection; raises gastric cancer risk.

Helicobacter pylori

Gram-negative bacterium that neutralizes acid, releases toxins, and causes chronic gastritis and ulcers.

Autoimmune gastritis

Chronic gastric inflammation with antibodies against intrinsic factor, impairing vitamin B12 absorption.

Pernicious anemia

Vitamin B12 deficiency anemia due to lack of intrinsic factor from autoimmune gastritis; causes fatigue and pallor.

Bile secretion (liver)

Liver function that emulsifies fats to aid digestion and absorption.

Bilirubin metabolism

Liver process that breaks down heme from old RBCs for excretion.

Portal hypertension

Elevated pressure in portal vein from cirrhosis-induced scarring, leading to varices and ascites.

Ascites

Fluid accumulation in peritoneal cavity due to low albumin production in cirrhosis.

Esophageal varices

Engorged esophageal veins from portal hypertension; prone to life-threatening bleeding.

Pancreatitis

Inflammation of the pancreas caused by autodigestion from pancreatic enzymes.

Acute pancreatitis

Sudden pancreatic inflammation typically from gallstones or alcohol; severe epigastric pain radiating to back.

Chronic pancreatitis

Progressive pancreatic fibrosis (often alcohol-related) causing intermittent pain, steatorrhea, and weight loss.

Steatorrhea

Fatty, pale, foul-smelling stools caused by fat malabsorption (e.g., chronic pancreatitis, Crohn’s).

Duodenum

Proximal first section of the small intestine where most chemical digestion occurs.

Jejunum

Middle portion of the small intestine specialized for nutrient absorption.

Ileum

Distal small intestine segment that absorbs vitamin B12 and bile salts.

Cecum

First part of the large intestine receiving chyme through the ileocecal valve.

Ileocecal valve

Sphincter between ileum and cecum regulating flow of intestinal contents into colon.

Peristalsis

Coordinated muscular contractions that propel contents through the GI tract.

Functional fecal incontinence

Repetitive inappropriate stool passage in children ≥4 without anatomical defects, often linked to constipation.

Intestinal obstruction

Partial or complete blockage of intestinal lumen by tumors, adhesions, or impaction causing distention and pain.

Diverticulitis

Inflamed infected diverticula in distal colon causing LLQ pain, fever, and perforation risk.

Inflammatory Bowel Disease (IBD)

Chronic immune-mediated inflammation of GI tract, mainly Crohn’s disease and ulcerative colitis.

Crohn’s disease

IBD affecting any GI site, commonly ileum and ascending colon, with transmural skip lesions and malabsorption.

Skip lesions

Patchy segments of inflamed bowel separated by normal tissue, typical of Crohn’s disease.

Ulcerative colitis

IBD limited to colon mucosa beginning in rectum, producing continuous lesions and bloody diarrhea.

Pseudopolyps

Islands of regenerating mucosa amid ulcerations seen in ulcerative colitis.

Colorectal cancer

Most common GI malignancy; usually arises from adenomatous polyps and presents with occult bleeding.

Anion gap

Calculated difference between measured cations and anions in serum used to detect metabolic acidosis.

Plasma buffer system

Immediate chemical buffering of blood pH via bicarbonate, phosphate, and proteins.

Respiratory buffer system

Minute-to-minute pH regulation by altering CO₂ exhalation through respiratory rate changes.

Renal buffer system

Hours-to-days pH control by kidneys generating, reabsorbing, or excreting bicarbonate and hydrogen ions.

Arterial blood gas (ABG)

Blood test measuring pH, PaCO₂, and HCO₃⁻ to assess acid-base status.

Normal pH range

Physiologic arterial blood pH of 7.35 – 7.45.

Normal PaCO₂ range

Arterial carbon dioxide pressure of 35 – 45 mm Hg.

Normal HCO₃⁻ range

Arterial bicarbonate concentration of 22 – 28 mEq/L.

Metabolic acidosis

Acid-base disorder with low HCO₃⁻ or excess H⁺; pH <7.35 and HCO₃⁻ <22.

Metabolic alkalosis

Acid-base disorder with high HCO₃⁻ or loss of H⁺; pH >7.45 and HCO₃⁻ >28.

Hyperkalemia

Elevated serum potassium often accompanying metabolic acidosis as H⁺ shifts drive K⁺ out of cells.

Hypokalemia

Low serum potassium frequently associated with metabolic alkalosis and excessive GI losses.

Melena

Black tarry stools signifying upper GI bleeding, common in PUD.