Module 4 – Gastrointestinal Disorders & Related Topics

Flashcards cover etiologies, pathophysiology, clinical manifestations, diagnostics, and treatments for GERD, gastritis, pancreatitis, IBD, liver disorders, metabolic disturbances, bowel elimination issues, diverticular disease, and pediatric fecal incontinence.

What cellular change occurs in the esophagus with chronic GERD exposure?

Squamous epithelium converts to glandular epithelium.

Name two common pharmacologic classes used to treat GERD.

H2-receptor blockers (e.g., famotidine/Pepcid) and proton-pump inhibitors (e.g., omeprazole/Prilosec).

Which serious malignancy is a complication of long-standing GERD?

Esophageal cancer.

List the three primary functions of the stomach.

Protection, digestion, and absorption (mainly water and alcohol).

How do prostaglandins protect the stomach lining?

They stimulate production of a protective mucus barrier.

Give two common irritants that precipitate acute gastritis.

Aspirin/NSAIDs and alcohol (others include microorganisms).

What makes the gastric mucosa more vulnerable in acute gastritis pathophysiology?

Inhibition or loss of the protective mucus layer.

State two potential severe complications of acute gastritis.

Hemorrhage and gastric perforation leading to shock.

Which lab findings help assess anemia in suspected acute gastritis?

Hemoglobin and hematocrit levels.

First-line management step for acute gastritis.

Removal of the gastric irritant.

Most common infectious agent in chronic gastritis.

Helicobacter pylori.

What symptom cluster defines dyspepsia in chronic gastritis?

Vague epigastric discomfort with nausea and heartburn.

Core drug class for eradicating H. pylori infection.

Antibiotics (often combined with acid suppressors).

Define pancreatitis.

Inflammation of the pancreas with autodigestion by pancreatic enzymes.

Two leading causes of acute pancreatitis.

Gallstone duct obstruction and excessive alcohol use.

Characteristic pain pattern in acute pancreatitis.

Sudden severe epigastric pain radiating to the back, progressing to a dull steady ache.

Primary pathophysiologic hallmark of chronic pancreatitis.

Progressive fibrosis and obstruction of pancreatic ducts causing loss of acinar function.

Most common etiology of chronic pancreatitis.

Chronic alcohol abuse (60–70%).

What two major diseases make up inflammatory bowel disease (IBD)?

Crohn disease and ulcerative colitis.

Describe the lesion pattern typical of Crohn disease.

Patchy transmural "skip lesions" that can affect any GI tract segment, commonly terminal ileum and ascending colon.

Name three classic Crohn disease manifestations.

Abdominal pain, non-bloody diarrhea, weight loss/malnutrition (others: fatigue, fever).

Which intestinal layers are primarily affected in ulcerative colitis?

Mucosal layer of the large intestine/colon.

Hallmark symptom of ulcerative colitis.

Diarrhea with rectal bleeding (bloody diarrhea).

Long-term complication risk increased by ulcerative colitis.

Colorectal cancer.

List four key functions of the liver.

Bile secretion, bilirubin metabolism, nutrient metabolism, detoxification (also blood storage, clotting factor synthesis, vitamin/mineral storage).

Visible clinical sign of excess bilirubin from liver damage.

Jaundice—yellow discoloration of skin and sclera.

Give three non-viral causes of hepatitis.

Alcoholic hepatitis, medication overdose (e.g., Tylenol), autoimmune causes.

Primary transmission route for Hepatitis A and E.

Fecal–oral via contaminated food, water, or person-to-person contact.

Which hepatitis viruses are commonly spread by blood and body fluids/needles?

Hepatitis B, C, and D.

Define the prodromal phase of viral hepatitis.

Flu-like symptoms (fatigue, malaise, low-grade fever, anorexia, headache) before jaundice onset.

What change occurs during the icteric phase of hepatitis?

Development of jaundice, dark urine, clay-colored stools, and tender enlarged liver.

State the body’s main chemical buffer pair regulating pH.

Bicarbonate (HCO3-) and hydrogen ions (H+).

Explain metabolic acidosis in simple terms.

Low pH with low bicarbonate due to loss of base or acid build-up (e.g., diarrhea, kidney failure).

Common clinical scenario causing metabolic alkalosis.

Excess loss of gastric acid through prolonged vomiting or diuretic therapy.

Outline the basic path of stool formation.

Nutrients absorbed in small intestine → waste enters large intestine → water reabsorbed, stool compacted → moves to rectum → expelled via anus.

Four categories of bowel-elimination disruption.

Motility, perfusion, patency, neurologic function.

Classic clinical triad of appendicitis.

Right lower quadrant pain, fever, nausea (plus rebound tenderness).

How does diarrhea differ from constipation in pathophysiology?

Diarrhea = ↑motility → ↓water reabsorption; Constipation = ↓motility → hard, dry stool.

Key dehydration risk associated with diarrhea.

Loss of water and electrolytes leading to imbalance.

Define diverticulosis.

Presence of multiple diverticula in the colon, usually asymptomatic.

What is diverticulitis?

Inflammation and possible infection of diverticula causing pain, fever, and complications.

Most common site for diverticular disease.

Sigmoid colon.

Typical pain location in diverticulitis.

Lower left quadrant of the abdomen.

Define functional fecal incontinence (encopresis).

Repeated passage of stool in inappropriate places by a child ≥4 years without organic disease.

Explain the pathophysiology linking constipation to functional fecal incontinence.

Chronic stool retention dilates colon, decreasing sensation to defecate, leading to overflow soiling.

Name two key components of treating functional fecal incontinence.

Establish regular toileting routine and increase dietary fiber/fluids.