Pathophysiology Exam #5 Overview

Pathophysiology Exam #5 Master Document

• This document covers everything needed for the 5th Pathophysiology Exam.
• Content may be subject to change based on the released exam blueprint.
• The document's key is used to differentiate different levels of importance for the exam.
• Green: Big topic (similar to orange if a subtopic).
• Blue: Subtopic.
• Yellow: Vocabulary and important concepts within subtopics; helps separate ideas. Subtopics under yellow are now bigger than blue, but smaller than green.
• Orange: Same as yellow, but with more detailed content.
• Red: Specific examples; likely not all that important.

GI Disorders

• Inflammation:
  • Gastritis: Stomach inflammation.
  • Pancreatitis: Pancreas inflammation.
  • Inflammatory Bowel Disease (Crohn's and Ulcerative Colitis): Chronic inflammation increases cancer risk. Tissue changes also increase cancer risk.
• Inflammation/Infection:
  • Hepatitis: Viral liver inflammation.
• Stomach:
  • Functions:
    • Protection: Stomach acids destroy harmful substances. Prostaglandins protect the gastric mucosa. Gastric mucosa is highly vascular, dependent on blood flow for function. Alteration of blood flow causes gastritis.
    • Digestion: Food and liquids mix with gastric secretions (mucus, acid, enzymes, hormones, intrinsic factor) in the stomach lining. Absorption mostly involves water and alcohol.
• Acute Gastritis: Inflammation of the stomach lining (gastric mucosa) that resolves when the cause is removed.
  • Causes: Aspirin, alcohol, certain microorganisms.

Acute Pancreatitis

• Causes:
  • Duct blockage by gallstones.
  • Excessive alcohol use.
• Symptoms:
  • Sudden upper abdominal pain, radiating to the back.
  • Nausea, vomiting, anorexia, diarrhea.
• Patho:
  • Injury triggers blockage of enzymatic pathways.
  • Spills secretory enzymes → Inflammation .
  • Response leads to increased vascular permeability, edema, hemorrhage, necrosis, granuloma formation, and abscess formation.
• Chronic Pancreatitis:
  • Characterized by irreversible damage and tissue changes.
  • Causes: Chronic alcohol use (most common), autoimmune disease, cystic fibrosis, and unknown causes.

Inflammatory Bowel Disease

• Chronic Inflammatory Processes:
• Can Occur Anywhere Along The GI Tract
• Most Commonly Of Small And Large Intestine
• MORE COMMON IN DEVELOPING COUNTRIES
• INCREASED RISK FOR PEOPLE IN COLDER CLIMATES AND URBAN AREAS.
• Small Intestine
• Digestion and Absorption:
• Primary Roles: Digestion and absorption through villi. Absorption happens in the intestinal mucosa. Processes include vitamin absorption, mineral absorption, fat absorption, carbohydrate absorption, protein absorption, water absorption, and electrolyte absorption (Na+ and K+).
• Large Intestine:
• Absorbs water and electrolytes (No villi).

Crohn's Disease

• Patchy Inflammation: Inflammation skips segments.
• Chronic Inflammation: Occurs in patchy segments (skip lesions).
• Increased Permeability: Inflammation begins in the mucosa and submucosa; increases permeability and vascularity leading to edema and fibrosis.
• Patho:
  • Macrophages, plasma cells, and lymphocytes are released.
  • Inflammation leads to granuloma formation.
• Location: Submucosal layers of the small intestine and ascending colon are the most common locations.

Ulcerative Colitis

• Non-Patchy Inflammation: Doesn't skip segments.
• Begins in the Rectum: Extends up the descending colon.
• Invades the Superficial Mucosa: Causes friability and causes bleeding.

Liver Disorders

• Liver Roles:
  • Bile secretion involved in fat emulsification and absorption.
  • Detoxification (removes toxins from the body).
  • Bilirubin metabolism (breaks down red blood cells into heme and globin). Heme is then broken down into amino acids.
  • Blood storage.
  • Clotting factor synthesis.
  • Nutrient metabolism
  • Mineral and vitamin storage.
• LIVER IS ENCAPSULATED BY THE GLISSON CAPSULE.

Hepatitis (Viral)

• Transmission varies by type (fecal-oral or infected blood/body fluids).
• Incubation period and carrier states vary per type.
  • Hepatitis A: Fecal-oral transmission, 1-2 months incubation period, no carrier state, and vaccine available.
  • Hepatitis B: Contacted with infected blood , 2-3 months incubation period, carrier state possible, vaccine available.
  • Hepatitis C: Contacted with infected blood, 2-3 months incubation period, carrier state possible, no vaccine.
  • Hepatitis D: Contacted with infected blood, 2-3 months incubation period, carrier state possible, no vaccine.
  • Hepatitis E: Fecal-oral transmission, 1-2 months incubation period, no carrier state, no vaccine.

Chronic Renal Failure

• Patho:
• Sodium and water balance is affected.
• Potassium balance is affected.
• There is an elimination of nitrogenous wastes.
• Erythropoietin production is affected.
• Acid-base balance issues occur.
• Activation and elimination of Vitamin D is affected.
• Phosphate elimination and hypocalcemia are potential complications.
• Possible complications result in skeletal issues, gastrointestinal disorders, neurologic issues, and sexual dysfunction.