Injury, Inflammation, and Healing cards

Comprehensive vocabulary flashcards detailing mechanisms of cell injury, cell death, cellular adaptations, wound healing phases, inflammatory processes, and scar types based on lecture notes.

Apoptosis

Controlled or programmed cell death where the cell breaks into contained fragments without stimulating an inflammatory response or forming exudate.

Necrosis

Uncontrolled, irreversible cell death associated with membrane rupture, release of cell contents (exudates), and inflammation.

Coagulative Necrosis

Irreversible cell death where cell nuclei die but cell membranes remain intact causing cells to coalesce; common with ischemia in internal organs such as the heart, kidneys, or liver.

Liquefactive Necrosis

Irreversible cell death where cells and their contents are destroyed leaving pockets of liquid; most common in the brain and associated with wet gangrene or infection.

Caseous Necrosis

Irreversible cell death where cell membranes are destroyed and cellular contents become thick and cheesy, often walled off as a granuloma; most commonly associated with tuberculosis.

Fat Necrosis

Necrosis of fatty tissue characterized by white, chalky calcium deposits (soaps); occurs with acute pancreatitis or abdominal trauma.

Fibrinoid Necrosis

Necrosis of blood vessel walls in which plasma proteins and fibrin accumulate, causing vessel walls to become stiff; associated with high blood pressure.

Hyperplasia

Cellular adaptation characterized by an increase in the number of cells.

Hypertrophy

Cellular adaptation characterized by an increase in cell size.

Atrophy

Cellular adaptation characterized by a decrease in tissue or organ size and function.

Metaplasia

Cellular adaptation where one mature cell type is replaced by another mature cell type.

Dysplasia

Cellular alteration involving disordered growth with abnormal cellular appearance.

Neoplasia

Uncontrolled abnormal cellular proliferation resulting in new growth.

Aplasia

Absence or failure of development of an organ or tissue.

Hypoplasia

Underdevelopment of an organ or tissue due to a reduced number of cells.

Anaplasia

Loss of normal cellular differentiation.

Hemostasis

Initial phase of wound healing that begins immediately after injury to stop bleeding via vasoconstriction, platelet aggregation, and fibrin clot formation.

Inflammatory Phase

Wound healing phase focused on clearing debris, where neutrophils respond early ($24\text{--}48\,\text{hours}$) and macrophages continue phagocytosis ($72\,\text{hours}$ post-injury).

Proliferative Phase

Wound healing phase (also called epithelialization) that fills and closes tissue defects via angiogenesis, granulation tissue formation, collagen production by fibroblasts, and wound contraction.

Maturation/Remodeling Phase

Wound healing phase that reorganizes collagen and scar tissue to increase tensile strength, which may continue for $6\text{--}12\,\text{months}$ or longer.

Primary Intention

Wound healing type where clean wound edges are approximated or closed (e.g., surgical sutures), leading to faster healing, minimal scarring, and lower infection risk.

Secondary Intention

Wound healing type where edges remain open and healing occurs from the bottom upward via granulation and re-epithelialization; typical for large wounds or burns with significant tissue loss.

Tertiary Intention

Delayed primary wound healing where a wound at risk for complications is temporarily left open and closed once contamination or risk factors improve.

Recognition (Inflammatory Process)

First step of the inflammatory process where sentinel cells detect tissue damage, physiological stress, or microbial invasion.

Recruitment (Inflammatory Process)

Second step of the inflammatory process where chemical mediators like histamine trigger vasodilation and increased vascular permeability to recruit white blood cells and plasma proteins.

Removal (Inflammatory Process)

Third step of the inflammatory process where neutrophils and macrophages clear pathogens and cellular debris through phagocytosis via chemotaxis.

Repair/Reconstruction (Inflammatory Process)

Fourth step of the inflammatory process where fibroblasts move into the injured area to produce collagen and build a structural framework for new tissue.

Edema

Swelling caused by vasodilation and increased vascular permeability that allows fluid and plasma proteins to enter injured tissue.

Erythema

Redness of the skin or tissue resulting from increased blood flow bringing more red blood cells to an injured area.

Acute Inflammation

Short-duration inflammatory response to recent injury with pronounced signs and symptoms, generally leading to quicker healing with fewer residual deficits.

Chronic Inflammation

Long-duration inflammatory response persisting for weeks, months, or longer, which is more likely to contribute to scarring and impaired function.

Regeneration

Tissue replacement process where damaged cells are replaced by the same type of cells, fully restoring normal tissue structure and function.

Repair

Tissue replacement process where damaged tissue is replaced by scar tissue, which may not fully restore original tissue function.

Hypertrophic Scar

An abnormal scar that remains within the original boundaries of the wound.

Keloid

An abnormal scar that extends beyond the boundaries of the original wound.

Mechanotherapy

The application of mechanical stress or loading to trigger biological repair responses in tissues that would not occur without load.