Inflammation, Tissue Repair, and Wound Healing

Vocabulary flashcards covering key terms and definitions from the lecture notes.

Inflammation

The body's response to injury intended to eliminate the cause, remove damaged tissue, and generate new tissue.

Rubor

Redness produced by vasodilation and increased blood flow at the inflamed site.

Tumor

Swelling resulting from edema and fluid accumulation in injured tissue.

Calor

Heat generated by increased blood flow to the affected area.

Dolor

Pain caused by inflammatory mediators and tissue stretching.

Functio laesa

Loss of function at the site of inflammation.

Inflammatory reaction

Protective responses including inflammation, immune response, and tissue repair.

Granulomatous inflammation

Inflammation associated with foreign bodies or certain microbes (eg, TB, syphilis, sarcoidosis, deep fungal infections, brucellosis).

Immediate transient response

Vascular change occurring with minor injury; brief duration.

Immediate sustained response

Prolonged vascular change with more serious injury, lasting days and damaging local vessels.

Delayed hemodynamic response

Increase in capillary permeability beginning 4–24 hours after injury.

Acute inflammation

Inflammation marked by recruitment of phagocytic leukocytes to the injury site; includes granulocytes and monocytes.

Granulocytes

White blood cells consisting of neutrophils, eosinophils, and basophils.

Neutrophils

Most abundant granulocytes; key players in the acute inflammatory response.

Eosinophils

Granulocytes involved in parasitic infections and allergic responses.

Basophils

Granulocytes involved in inflammatory and allergic responses.

Monocytes

Largest white blood cells that differentiate into macrophages in tissue.

Margination

Leukocytes move to and line the endothelium in preparation for adhesion.

Adhesion

Leukocytes binding to endothelium via adhesion molecules.

Transmigration

Leukocytes crossing the endothelium into tissue.

Chemotaxis

Movement of leukocytes toward chemotactic signals at the injury site.

Activation and phagocytosis

Leukocytes recognizing, engulfing, and killing microbes intracellularly.

Adhesion molecules

Molecules that mediate leukocyte adhesion (selectins, integrins, immunoglobulins).

Selectins

Adhesion molecules that mediate initial leukocyte rolling on endothelium.

Integrins

Adhesion molecules enabling firm adhesion and transmigration.

Immunoglobulin (as adhesion molecule)

Immunoglobulin family molecules aiding leukocyte-endothelium adhesion.

Histamine

Primary mediator causing endothelial retraction and increased vascular permeability.

Cytokines

Mediators regulating immune responses and leukocyte recruitment.

Arachidonic acid metabolites

Eicosanoids derived from arachidonic acid; include prostaglandins and leukotrienes (and related omega-3 effects).

Prostaglandins

Eicosanoids that modulate vasodilation, pain, and edema.

Leukotrienes

Eicosanoids promoting chemotaxis and vascular permeability.

Omega-3 polyunsaturated fatty acids

Fatty acids that influence inflammation and eicosanoid production.

Platelet-activating factor

Phospholipid mediator that activates platelets and leukocytes.

Plasma proteins

Proteins involved in inflammation, including components of complement and coagulation.

Serous exudates

Watery, protein-poor fluids from plasma leakage at inflammation site.

Hemorrhagic exudates

Exudates with red blood cells due to vessel damage.

Membranous or pseudomembranous exudates

Exudates on mucous membranes composed of necrotic cells in fibropurulent material.

Purulent or suppurative exudates

Exudates containing pus—degraded neutrophils, proteins, and tissue debris.

Fibrinous exudates

Exudates rich in fibrinogen forming a thick, sticky mesh.

Acute phase response

Systemic inflammatory changes such as leukocytosis, fever, and potential sepsis.

Leukocytosis

Increase in white blood cell count during acute inflammation.

Leukopenia

Decrease in white blood cell count (less common in acute inflammation).

Chronic inflammation

Long-lasting inflammation with mononuclear cell infiltration and fibroblast proliferation.

Parenchymal

Tissues containing the functioning cells of an organ.

Stromal

Supporting connective tissues, vessels, ECM, and nerves of an organ.

Labile cells

Cells that continuously divide and replace destroyed cells.

Stable cells

Cells that normally stop dividing after growth; can re-enter division after injury.

Permanent/Fixed cells

Cells that do not undergo mitotic division.

Granulation tissue

New vascularized connective tissue formed during wound healing.

Fibrogenesis

Formation of fibrous tissue during repair.

Scar formation

Deposition of ECM and collagen to replace damaged tissue.

Wound healing

Process to fill the injury gap and restore structural continuity.

Primary healing

Healing of a small, clean wound with minimal tissue loss.

Secondary healing

Healing of large or contaminated wounds with greater tissue loss.

Extracellular matrix (ECM)

Network of proteins and carbohydrates providing structural support.

Fibrous structural proteins

Collagen and elastin that give strength and elasticity.

Proteoglycans and hyaluronic acid

Water-rich ECM components providing resilience and lubrication.

Adhesive glycoproteins

Fibronectin and laminin connecting matrix to cells.

Basement membrane

Thin sheet surrounding epithelial, endothelial, and smooth muscle cells.

Interstitial matrix

ECM found between cells in connective tissue and around vessels.

Wound healing stages

Inflammatory phase, proliferative phase, remodeling phase.

Angiogenesis

Formation of new blood vessels during tissue repair.

Capillary sprout

Early growth of new capillaries during angiogenesis.

Migration of endothelial cells

Endothelial cells move toward angiogenic signals.

Proliferation of endothelial cells

Endothelial cells divide to form new vessels behind the leading edge.

Pericytes

Cells that stabilize capillaries and small vessels during angiogenesis.

Smooth muscle cells

Cells forming vessel walls in larger vessels during remodeling.

Emigration and proliferation of fibroblasts

Fibroblasts move into the wound and multiply during scar formation.

Deposition of the ECM

Fibroblasts lay down extracellular matrix components in repair.

Factors regulating healing

Mediators, growth factors, ECM-cell interactions, nutrition, blood flow, infection, age.

Diabetes mellitus

Condition that slows wound healing due to vascular and immune impairment.

Peripheral artery disease

Reduced blood flow impairing wound healing.

Venous insufficiency

Poor venous return that delays wound healing.

Braden Q Scale

Assessment tool for risk of pressure ulcers in neonates and children.

Neonates and children wound healing

Immature immune system, high metabolic needs, Braden Q Scale used.

Older adults wound healing

Aging skin and comorbidities increase risk of chronic wounds.