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Inflammation
localized immune response to injury or infection
Acute inflammation
rapid, short-lived response featuring redness, heat, swelling, pain, and loss of function
Vasodilation
widening of blood vessels increasing blood flow to affected area
Increased vascular permeability
allows plasma proteins and leukocytes to migrate from circulation into tissue
Exudate
protein-rich fluid and immune cells that leak out of blood vessels
Transudate
low-protein fluid caused by imbalanced hydrostatic/osmotic pressures
Margination
movement of leukocytes toward vessel walls
Diapedesis
passage of leukocytes through blood vessel walls into tissues
Chemotaxis
directional movement of leukocytes toward chemical signals at injury site
Neutrophils
first responders to inflammation, phagocytose pathogens and debris
Macrophages
phagocytic cells that clear debris, coordinate repair and immunity
Inflammatory mediators
molecules (e.g., histamine, prostaglandins, cytokines) that regulate inflammatory response
Histamine
mediator from mast cells causing vasodilation and vascular permeability
Prostaglandins
lipid mediators involved in pain, fever, and vasodilation
Cytokines
signaling proteins (e.g., IL‑1, TNF) that regulate immune and inflammatory responses
Fever
elevated body temperature induced by pyrogens acting on hypothalamus
Chronic inflammation
prolonged inflammation featuring tissue destruction and fibrosis
Granuloma
organized cluster of macrophages (often with lymphocytes) in chronic inflammation
Fibrosis
formation of scar tissue through collagen deposition by fibroblasts
Resolution
restoration of normal tissue structure and function after injury
Regeneration
replacement of lost cells with identical tissue
Scar formation
deposition of collagen in wound, replacing normal structures
Wound healing phases
hemostasis → inflammation → proliferation → remodeling
Primary intention
wound edges approximated, minimal tissue loss and scarring
Secondary intention
wound heals with significant tissue loss and granulation, more scarring required.