Healing & Tissue Repair Vocabulary

Comprehensive vocabulary flashcards covering healing, tissue repair, wound healing phases, mechanisms of inflammation resolution, and related pathology concepts.

Resolution (Acute Inflammation Outcome)

The outcome of acute inflammation characterized by a complete return of tissue to normal structure and function following minimal damage.

Abscess

A localized collection of pus (purulent exudate) within a tissue, formed as an outcome of sustained or continuous tissue damage.

Labile Cells

Cells that continuously proliferate under normal conditions to replace damaged or lost tissue, such as surface epithelia and hematopoietic cells of the bone marrow.

Stable Cells

Quiescent cells that normally have a low rate of division but can proliferate in response to growth factors or injury, including liver, kidney, and pancreas parenchymal cells, endothelial cells, fibroblasts, and smooth muscle cells.

Permanent Cells

Terminally differentiated non-proliferative cells, such as neurons and cardiac muscle cells, whose injury is irreversible and usually results in scar formation.

Regeneration

The process of tissue repair occurring via the proliferation of surviving mature differentiated cells or stem cells that retain the capacity to replace lost mature tissue cells.

Scar Formation

A repair process that patches tissue by laying down fibrous connective tissue (collagen) when regeneration alone cannot repair the damage.

Acute Renal Tubular Necrosis

A condition caused by aminoglycoside antibiotics resulting in detachment and necrosis of tubular epithelial cells; complete regeneration occurs only if the supporting basement membrane remains intact.

Hemostatic Plug

A temporary plug composed of platelets formed within minutes after injury to stop bleeding and provide a scaffold for fibrin deposition.

Granulation Tissue

A soft, pink, granular connective tissue formed during repair, characterized histologically by proliferating fibroblasts, delicate thin-walled capillaries (angiogenesis), and loose extracellular matrix with mononuclear inflammatory cells.

M1 Macrophages

Classically activated macrophages involved in the early inflammatory phase that function in microbial killing and removal of dead tissue.

M2 Macrophages

Alternatively activated macrophages key to tissue repair that clear dead tissue, secrete growth factors (PDGF, FGF-2, TGF-beta), stimulate fibroblast proliferation, and promote collagen deposition.

Angiogenesis

The development of new blood vessels sprouting from pre-existing vessels, initiated by nitric oxide-induced vasodilation and VEGF-induced permeability.

VEGF (Vascular Endothelial Growth Factor)

A key growth factor that induces increased vascular permeability and stimulates endothelial cell migration and proliferation during angiogenesis.

TGF-beta (Transforming Growth Factor-Beta)

The most important cytokine involved in stimulating fibroblast proliferation, collagen synthesis, and ECM protein deposition during scar formation.

Myofibroblasts

Differentiated fibroblasts that acquire smooth muscle cell features and contribute to the contraction of the scar over time.

Matrix Metalloproteinases (MMPs)

A family of enzymes responsible for degrading collagens and other extracellular matrix components during tissue remodeling.

TIMPs (Tissue Inhibitors of Metalloproteinases)

Specific protein inhibitors that control matrix metalloproteinases (MMPs) to balance ECM synthesis and degradation during connective tissue remodeling.

Vasospasm

The immediate constriction of blood vessels following tissue injury to reduce local blood flow as part of hemostasis.

Primary Intention Healing

The healing of clean, non-septic surgical wounds with closely apposed edges, resulting in minimal fibrosis, little visible scar, and tensile strength comparable to normal skin.

Secondary Intention Healing

The healing of wounds with non-apposed edges (e.g., large ulcers), characterized by disorganized connective tissue, formation of abundant granulation tissue, weak tensile strength, and hairless scarred tissue.

Proud Flesh

Exuberant, cauliflower-like proliferation of granulation tissue (hypertrophic scar) occurring most commonly in skin wounds on the distal limbs of horses, preventing epithelial coverage.

Keloid

Large, bulging, raised, irregular scars caused by excessive collagen deposition (rather than excessive granulation tissue); common in humans but lacking significance in animals.

Scirrhous Reaction

Extensive wound contraction mediated by myofibroblasts following severe thermal/chemical burns or large-surface abrasions, causing skin immobility, tension, deformation, and pain.

Scurvy (Vitamin C Deficiency)

A nutritional deficiency in species requiring dietary vitamin C that decreases collagen hydroxyproline synthesis, impairing collagen formation and wound healing.

Osteogenesis Imperfecta

A genetic collagen disorder characterized by defective type I collagen production, leading to abnormal extracellular matrix deposition.

Ehlers-Danlos Syndrome

A genetic disorder affecting collagen synthesis, cross-linking, hydroxylation, or post-translational processing, resulting in delayed wound healing.

Exudate

A protein-rich extravascular fluid with cellular debris accumulated in tissues or body cavities during inflammation, resulting from increased vascular permeability.

Hemoconcentration

An intravascular change caused by the loss of protein-rich fluid from blood vessels during acute inflammation, leading to increased blood viscosity and slower circulation (stasis).

Leukocyte Extravasation Sequence

The step-by-step sequence of leukocyte movement during inflammation: Margination -> Rolling -> Adhesion -> Transmigration.

Selectins

Adhesion molecules on endothelial cells and leukocytes that specifically mediate the initial capture and rolling of leukocytes along the vessel wall.

Integrins

Cell surface receptors on leukocytes that mediate firm leukocyte adhesion to the vascular endothelium prior to transmigration.

Leukocyte Adhesion Deficiency (LAD) Type I

An inherited disorder caused by a defect in $\beta_2$ integrins, leading to impaired firm adhesion and transmigration of leukocytes.

Myeloperoxidase (MPO)

A lysosomal enzyme in neutrophils that converts hydrogen peroxide ($H_2O_2$) and chloride ($Cl^-$) into hypochlorous acid ($HOCl$), a potent antimicrobial compound.

Eosinophil

A specialized leukocyte particularly associated with defending against parasitic infections and mediating allergic reactions.

Serous Inflammation

A pattern of acute inflammation characterized by a thin, watery, relatively cell-poor fluid exudate derived from serum or mesothelial secretions.

Purulent (Suppurative) Inflammation

An inflammatory exudate rich in pus, composed of neutrophils, necrotic cellular debris, and edema fluid.

Phlegmon

An acute, diffuse, spreading suppurative inflammation that extends unconfined through connective tissue planes.

Pleural Empyema

The accumulation of purulent exudate (pus) within the pleural cavity.

Pyemia

A severe condition involving hematogenous spread of pyogenic bacteria resulting in multiple secondary abscesses in organs like the lungs, liver, and kidneys.

Th1 Cells

A subset of T-helper cells that produce interferon-gamma ($IFN-\gamma$) and promote classical macrophage activation (M1 phenotype).

IL-17 (Interleukin-17)

A cytokine produced by Th17 cells that stimulates chemokine production and recruits neutrophils to sites of inflammation.

IL-5 (Interleukin-5)

A cytokine produced by Th2 cells that plays a key role in the activation and recruitment of eosinophils.

Stratum Basale

The innermost basal layer of the epidermis containing progenitor cells that proliferate and migrate to re-epithelialize skin wounds.

Desmoplasia / Fibroplasia

The growth of fibrous or connective tissue stroma generated during the proliferation phase of wound healing to restore tissue integrity.

Adnexal Structures

Skin appendages including hair follicles, sebaceous glands, and sweat glands, which are typically lost at the site of deep dermal wound healing or secondary intention scars.

Hyperglycosylation of Proteins

A pathological mechanism in Diabetes Mellitus that alters vascular wall integrity, impairs wound healing, and predisposes to diabetic ulcers.

Postcapillary Venules

The principal microvascular site where increased vascular permeability and endothelial cell retraction occur during acute inflammation.

Transient Vasoconstriction

The earliest vascular response in acute inflammation, occurring transiently within seconds after injury before vasodilation begins.

Cachexia

Severe muscle wasting and weight loss seen in chronic illness or cancer, creating a negative energy balance and amino acid deficit that impairs ECM protein synthesis and wound healing.