injury inflammation and healing

Reversible Cell Injury; Cell injury caused by mild, transient stimuli that allows the cell to return to a normal homeostatic state once the stimulus is removed.

Irreversible Cell Injury; Cell injury caused by severe, progressive stimuli that inevitably leads to cell death via necrosis or apoptosis.

Necrosis; A form of cell death resulting from irreversible injury, typically characterized by cell swelling, membrane rupture, and inflammation.

Apoptosis; Programmed cell death, a regulated process to eliminate damaged or unwanted cells without causing an inflammatory response.

Primary Hemostasis; The initial phase of hemostasis involving vasoconstriction, platelet activation by collagen, and the formation of a temporary platelet plug.

Secondary Hemostasis; The coagulation cascade triggered by tissue factor and collagen, leading to thrombin activation, fibrin formation, and a stable blood clot.

Fibrinolysis; The process of clot degradation and breakdown driven by the enzyme plasmin.

Arteriole Dilation; The expansion of arteriole diameter during acute inflammation, which increases blood flow and causes local redness (erythema) and heat.

Vascular Permeability; The widening of endothelial junctions during inflammation, allowing plasma proteins to leak into tissues and causing swelling (edema).

Margination; The accumulation and alignment of leukocytes (neutrophils) along the endothelial wall of blood vessels prior to emigration.

Diapedesis; The process by which leukocytes squeeze through widened endothelial cell junctions to exit blood vessels and enter injured tissue.

Chemotaxis; The directed migration of leukocytes along a chemical concentration gradient toward the source of injury or infection.

Acute Inflammatory Infiltrate; Immune cells that dominate early inflammation, primarily consisting of platelets and neutrophils.

Chronic Inflammatory Infiltrate; Immune cells that dominate persistent inflammation, primarily consisting of monocytes/macrophages, lymphocytes, and plasma cells.

Pro-inflammatory Mediators; Chemical signals (such as histamine, serotonin, bradykinin, C5a, and prostaglandins) that drive vasodilation, permeability, and leukocyte attraction.

Resolution; The ideal outcome of acute inflammation where injurious stimuli are cleared, inflammatory cells are removed, and normal tissue structure and function are restored.

Chronic Inflammation; A prolonged inflammatory response characterized by persistent injurious agents, recurrent acute cycles, mononuclear cell infiltration, angiogenesis, and progressive tissue injury/fibrosis.

Abscess; A localized collection of pus formed during acute inflammation that typically heals by scarring and fibrosis.

Fibrosis; The replacement of functional parenchymal tissue with a collagenous scar, leading to a permanent loss of function.

M1 Macrophage; A pro-inflammatory macrophage phenotype active during early coagulation/inflammation that secretes pro-inflammatory mediators.

M2 Macrophage; A pro-resolving macrophage phenotype active during the proliferation and remodeling phases that secretes resolving mediators to promote healing.

Inflammation Phase (Healing); The initial phase of tissue healing characterized by macrophage migration, antibacterial effects, vasodilation, and increased tissue oxygenation/temperature.

Proliferation Phase (Healing); The second phase of tissue healing characterized by angiogenesis, fibroblast migration/activation, myofibroblast creation, collagen deposition, and re-epithelialization.

Remodeling Phase (Healing); The final phase of tissue healing where collagen fibers reorganize, scars gain tensile strength, and the tissue regains functional capacity.

Myofibroblasts; Specialized fibroblasts active during the proliferation phase that are responsible for wound contraction and closing tissue gaps.

Angiogenesis; The formation of new blood vessels from pre-existing ones, driven by vascular endothelial cell migration during the proliferation phase.

Redness (Erythema); A local clinical sign of inflammation caused by increased blood flow via arteriole dilation.

Swelling (Edema); A local clinical sign of inflammation caused by the accumulation of fluid, plasma proteins, and immune cells in the interstitial space.

Pain (Inflammation); A clinical sign caused by the release of chemical mediators (like prostaglandins or bradykinin) that irritate local nerve endings.

Genetic Cell Injury; Cellular damage arising from chromosomal abnormalities or genetic mutations.

Acquired Cell Injury; Cellular damage arising from extrinsic factors, including hypoxia, chemical agents, physical agents, immune reactions, biological organisms, or nutritional imbalances.