Introduction to Pathology Quiz

Introduction to Pathology

• Pathology studies changes in cells, tissues, and organs linked to diseases.
• Essential for disease understanding, diagnosis, progression tracking, and treatment development.
• Requires identification of morphological, molecular, and biochemical changes, examined via gross and microscopic methods.

Cellular Responses Overview

• Cells must adapt to maintain homeostasis when faced with environmental changes.
• Adaptation enables cells to survive by achieving a new steady state.
• Cell injury occurs when the adaptive capacity is exceeded or when exposure to harmful stimuli occurs.

Classifications of Injurious Stimuli

• Hypoxia and Ischemia: Results in oxygen deficiency, reduced nutrient flow, and waste accumulation.
• Toxins: Includes air pollutants, drugs, and various chemical agents affecting cell function.
• Infectious Agents: Bacteria, viruses, parasites, and fungi can cause cellular disturbances.
• Immunologic Reactions: Autoimmune responses can injure tissues through excessive inflammation.
• Genetic Abnormalities: Mutations can lead to malfunctioning proteins and cellular damage.
• Nutritional Imbalances: Deficiencies or excesses in nutrients disrupt normal cellular functions.
• Physical Agents: Trauma or extreme environmental changes lead to potential injury.
• Aging: Senescence contributes to the decline in cellular function over time.

Cell Injury Sequence

• Injury initiates a sequence of reversible changes: swelling of cells and organelles, membrane blebbing, loss of ribosome attachment on the endoplasmic reticulum, chromatin clumping, and myelin figure formation.

Cell Death

• Two main types based on severity of the injurious stimulus:
  • Necrosis: Results from severe disturbances leading to uncontrolled cell death.
  • Apoptosis: A controlled process for removing dysfunctional or old cells.

Morphological Differences between Necrosis and Apoptosis

• Necrosis: Cells are enlarged, nucleus undergoes fragmentation, plasma membrane is disrupted, and inflammation is frequent.
• Apoptosis: Cell size is reduced, nuclear content is fragmented, plasma membrane remains intact, and no inflammation occurs.

Necrosis Types

• Coagulative Necrosis: Preservation of tissue architecture; common in solid organ infarcts.
• Liquefactive Necrosis: Occurs due to bacterial infections leading to tissue liquefaction.
• Gangrenous Necrosis: Combination of coagulative and liquefactive necroses, associated with limb ischemia followed by infection.
• Caseous Necrosis: Characteristic of tuberculosis infection, appears cheese-like microscopically.
• Fat Necrosis: Caused by the release of pancreatic enzymes leading to fat degradation.
• Fibrinoid Necrosis: Associated with immune-mediated vascular injury, resulting in an amorphous pink appearance in blood vessel walls.

Diagnostic Markers for Necrosis

• Specific proteins leak into the bloodstream indicating cellular damage:
  • Cardiac markers: Creatine kinase, troponin for heart injury.
  • Liver injury markers: Alkaline phosphatase, transaminases (ALT, AST) for liver health assessment.

Apoptosis Mechanisms

• Apoptosis plays a critical role in normal cellular turnover and physiological changes without causing inflammation.
• Two major pathways: intrinsic (mitochondrial) and extrinsic pathways.

Other Cell Death Pathways

• Necroptosis: Resembles necrosis but is triggered by cellular signals typical of apoptosis.
• Pyroptosis: Inflammatory form of apoptosis linked with fever response.
• Autophagy: Cellular response to nutrient deprivation involving lysosomal degradation of cellular components.

Injury Mechanisms

• Responses to injury depend on the type, duration, and severity of the stimulus.
• Hypoxia and Ischemia: Major causes of cell injury; ATP production is oxygen-dependent.
• Ischemia-Reperfusion Injury: Restoring blood flow can cause stress from reactive oxygen species and inflammation.
• Oxidative Stress: Excess reactive oxygen species produced by mitochondria and leukocytes can damage cells.
• Toxins: Can be direct-acting or prodrugs activated within cells and can lead to cell injury.

Cellular Adaptations

• Adaptations are reversible and may involve:
  • Hypertrophy: Increase in cell size, often due to heightened functional demand (e.g., muscle growth).
  • Hyperplasia: Increase in cell number in tissues with replication capability (e.g., liver regeneration).
  • Atrophy: Decrease in cell size from loss of substance, often due to reduced workload or aging.
  • Metaplasia: Change in cell type, often due to stress; can predispose to malignancy.

Intracellular Accumulations

• Abnormal accumulation of substances can occur due to metabolic disturbances, protein misfolding, enzyme deficiencies, or inability to process ingested particles.

Pathologic Calcification

• Involves deposits of calcium salts in tissues, categorized into:
  • Dystrophic Calcification: Normal metabolism with deposits in damaged tissues (e.g., atherosclerosis).
  • Metastatic Calcification: Occurs in normal tissues in the context of hypercalcemia due to increased parathyroid hormone or vitamin D disorders.