Cell Injury, Adaptation, and Inflammation

Flashcards generated from lecture notes on cell injury, adaptation, and inflammation.

Cellular Adaptation

Alterations in cell size, number, phenotype, metabolic activity, or function in response to changes in their environment.

Types of Cellular Adaptations

Atrophy, hypertrophy, hyperplasia, metaplasia

Atrophy

Decrease in cell size due to loss of cell substance

Hypertrophy

Increase in cell size

Hyperplasia

Increase in cell number

Metaplasia

Reversible change in which one adult cell type is replaced by another adult cell type

Outcomes of Cell Injury

Reversible cell injury resolves if the stressor is removed; irreversible injury leads to cell death (apoptosis or necrosis).

Active vs. Passive Processes

Active processes require cellular energy input, while passive processes do not.

Cellular Adaptations: Active or Passive?

Cellular adaptations are active processes because they involve cellular remodeling and require the cell to expend energy to change its structure, size, number, or type.

Insufficient Adaptation

If adaptation is insufficient, cells may undergo cell injury, leading to necrosis or apoptosis.

Atrophy Examples

Physiological: Atrophy of hormone-sensitive tissues after menopause. Pathophysiological: Disuse atrophy due to immobility.

Hypertrophy Examples

Physiological: Uterine hypertrophy during pregnancy. Pathophysiological: Cardiac hypertrophy due to increased workload.

Hyperplasia Examples

Physiological: Epithelial cell hyperplasia during pregnancy. Pathophysiological: Benign prostatic hyperplasia.

Metaplasia Examples

Physiological: Not applicable. Pathophysiological: Metaplasia of conductive respiratory epithelium in smokers or Barrett's esophagus in GERD.

Labile, Stable, and Permanent Tissues

Labile tissues continuously divide (e.g., bone marrow, epithelia); stable tissues divide when stimulated (e.g., hepatocytes); permanent tissues have limited regenerative capacity (e.g., neurons, cardiomyocytes).

Mechanisms of Cellular Injury

Ischemia, free radical damage, physical agents, disruption of calcium homeostasis, and infectious agents

Types of Cell Death

Apoptosis (active) and Necrosis (passive)

Apoptosis vs. Necrosis

Apoptosis is programmed cell death; necrosis is accidental cell death due to injury.

Cellular Changes in Apoptosis vs. Necrosis

Apoptosis shrinks the cell, keeps the membrane intact, and does not induce inflammation. Necrosis swells the cell, ruptures the membrane, and induces inflammation.

Autophagy

Cell eating itself, breaks down dysfunctional components, mechanism for cellular remodeling, coping when cells under stress

Types of Necrosis

Coagulative, liquefactive, caseous, and fat necrosis

Coagulative Necrosis

Firm grey appearance due to protein degradation; caused by ischemia.

Liquefactive Necrosis

Liquefaction of dead tissue by enzymes; often seen in the brain.

Caseous Necrosis

Cheeselike appearance; mix of coagulative and liquefactive necrosis; seen in tuberculosis.

Fat Necrosis

Lipase breakdown of lipids, forming calcium deposits; occurs in the pancreas

Types of Gangrene

Dry, wet, gas gangrene

Dry Gangrene

Caused by ischemia, coagulative necrosis, dry sunken blackened tissue.

Gas Gangrene

Caused by bacterial infection, anaerobic, produce gas within tissue.

Key Vascular Changes in Acute Inflammation

Vasodilation and increased vascular permeability.

Cellular Response in Inflammation

Attraction and action of white blood cells (WBCs) at the inflammation site.

Chemotaxis

Chemotaxis is the process by which inflammatory cells are attracted to the inflammatory site by chemical signals.

Neutrophils

Neutrophils are phagocytic cells that engulf foreign particles. They are the primary cell type in acute inflammation and are present in pus.

Monocytes

Monocytes arrive later than neutrophils and mature into macrophages before contributing to the inflammatory response.

Macrophages

Macrophages are phagocytic and coordinate the immune response. Activated macrophages can damage host cells but also promote repair.

Inflammatory Mediators

Histamine, prostaglandins, leukotrienes, platelet-activating factor, cytokines, and bradykinin.

Role of Histamine

Histamine causes vasodilation by acting on vascular smooth muscle and increases vascular permeability.

Five Cardinal Signs of Inflammation

Heat (calor), redness (rubor), swelling (tumor), pain (dolor), and loss of function (functio laesa).

Cells Involved in Inflammation

Mast cells, neutrophils, monocytes/macrophages, lymphocytes, eosinophils, and platelets.

Key Mediators/Cytokines in Inflammation

IL-1, TNF-alpha, chemokines

Possible Outcomes of Acute Inflammation

Complete resolution, healing with scarring or fibrosis, or progress to chronic inflammation.

Cellular Differences: Acute vs. Chronic Inflammation

Neutrophils are predominant in acute inflammation, while macrophages and lymphocytes are characteristic of chronic inflammation.

Granulomas

Granulomas are small lesions formed in granulomatous inflammation, consisting of macrophages, lymphocytes, and a surrounding connective tissue layer.

Wound Healing Stages

Inflammation, proliferation, and remodeling.

Resolution, Regeneration, and Organization

Resolution restores tissue to its original state; regeneration replaces damaged tissue with the same type of tissue; organization/fibrosis replaces damaged tissue with collagen fibers (scar formation).

Scar Formation

Damaged tissue is replaced by collagen fibers, forming a scar.

Systemic Response of Inflammation

Fever, loss of appetite, malaise, increased acute phase proteins, neutrophilia,. eosinophilia

Classification of Thermal Burns

Based on depth of burn and percentage of body surface affected.

Consequences of Severe Thermal Burns

Hypovolemic shock, systemic inflammatory response syndrome (SIRS), circulatory shock.