Chapter 5 – Inflammation and Healing

Vocabulary flashcards covering key terms, mediators, healing types, drugs, exudates, and burn classifications from Chapter 5 on inflammation and healing.

Inflammation

A protective, nonspecific response of vascularized tissue to injury or infection, characterized by redness, heat, swelling, pain, and loss of function.

First Line of Defense

Nonspecific mechanical and chemical barriers such as intact skin, mucous membranes, tears, and gastric juices that prevent pathogen entry.

Second Line of Defense

Nonspecific internal mechanisms—including phagocytosis and the inflammatory response—that act once pathogens enter the body.

Third Line of Defense

Specific immune response involving production of antibodies and cell-mediated immunity against particular antigens.

Phagocytosis

Engulfment and digestion of microorganisms, debris, or foreign particles by neutrophils, macrophages, or other phagocytes.

Interferon

Small proteins released by virus-infected cells that protect uninfected cells by inhibiting viral replication.

Immune Response

Specific defense involving recognition of antigens and activation of B-cells (humoral) or T-cells (cell-mediated).

Hydrostatic Pressure

The blood pressure-derived force that pushes water, electrolytes, oxygen, and nutrients out of capillaries at the arterial end.

Osmotic Pressure

Pulling force generated mainly by plasma proteins that draws fluid, carbon dioxide, and wastes back into capillaries at the venous end.

Histamine

Chemical mediator from mast-cell granules causing immediate vasodilation and increased capillary permeability.

Cytokines

Interleukins or lymphokines released by T-cells and macrophages that induce fever, leukocytosis, and chemotaxis.

Leukotrienes

Arachidonic-acid derivatives that cause later-phase vasodilation, increased permeability, and chemotaxis.

Prostaglandins (PGs)

Arachidonic-acid metabolites producing vasodilation, pain, fever, and potentiation of histamine effects.

Kinins (e.g., Bradykinin)

Plasma proteins that trigger vasodilation, increased permeability, pain, and chemotaxis when activated.

Complement System

Cascade of plasma proteins that promotes vasodilation, permeability, chemotaxis, and histamine release.

Platelet-Activating Factor (PAF)

Mediator from platelet membranes that activates neutrophils and enhances platelet aggregation.

Serous Exudate

Watery, low-protein fluid containing some WBCs, typical of mild inflammation or burns.

Fibrinous Exudate

Thick, sticky fluid rich in fibrin and cells, increasing the risk of scar formation.

Purulent Exudate

Thick, yellow-green pus containing many leukocytes, debris, and microbes; may form an abscess.

Hemorrhagic Exudate

Exudate containing blood due to vessel damage at the inflammatory site.

Pyrexia

Mild fever caused by pyrogens resetting the hypothalamic thermostat during extensive inflammation.

Leukocytosis

Increase in circulating white blood cells, especially neutrophils, during acute inflammation.

Erythrocyte Sedimentation Rate (ESR)

Blood test measuring how fast RBCs settle; elevated rates indicate increased plasma proteins and inflammation.

C-Reactive Protein (CRP)

Acute-phase protein not normally present but appearing 24–48 h after tissue damage or acute inflammation.

Granuloma

Small mass of macrophages and fibrous tissue that forms around foreign material in chronic inflammation.

Regeneration

Healing process in which damaged tissue is replaced by identical functional cells.

Resolution

Minimal tissue damage with complete recovery of original structure and function.

Replacement

Healing in which functional tissue is replaced by fibrous scar tissue, resulting in loss of function.

Healing by First Intention

Union of clean, closely approximated wound edges producing minimal scarring.

Healing by Second Intention

Wound healing with large gaps, extensive granulation tissue, and a larger residual scar.

Contracture

Permanent tightening of scar tissue that restricts joint movement or flexibility.

Adhesion

Band of scar tissue joining two normally separate surfaces after injury or surgery.

Hypertrophic Scar

Excessive fibrous tissue overgrowth forming raised, firm ridges or keloids.

RICE Therapy

Standard acute-injury management: Rest, Ice, Compression, Elevation to reduce inflammation.

Acetylsalicylic Acid (ASA)

Aspirin; anti-inflammatory, analgesic, antipyretic drug that inhibits prostaglandin synthesis but may cause GI irritation and delayed clotting.

Acetaminophen

Analgesic and antipyretic drug lacking significant anti-inflammatory action.

Nonsteroidal Anti-Inflammatory Drugs (NSAIDs)

Drugs such as ibuprofen that provide anti-inflammatory, analgesic, and antipyretic effects by inhibiting COX enzymes.

Glucocorticoids

Steroidal drugs that decrease capillary permeability, reduce leukocytes, and suppress immune responses but have many adverse effects.

Hypermetabolism

Elevated metabolic rate occurring during burn healing that increases nutritional demands.

Superficial Partial-Thickness (First-Degree) Burn

Burn involving epidermis with redness and minimal blistering.

Deep Partial-Thickness (Second-Degree) Burn

Burn involving epidermis and part of dermis, characterized by blister formation.

Full-Thickness (Third/Fourth-Degree) Burn

Burn destroying all skin layers and possibly underlying tissues; requires grafting.

Rule of Nines

Method to estimate total body surface area (TBSA) burned by assigning percentage values to body regions.

Interferon

(duplicate removed)

Skeletal Muscle Spasm

Protective, painful contraction of muscles surrounding an inflamed area.

Chemotaxis

Directed migration of leukocytes toward higher concentrations of chemical mediators at an injury site.