Pathophysiology Unit 2 | Chapter 9 (Porth 5th Edition) Flashcards
Acute Inflammation
A short-duration inflammatory response (minutes to days) characterized by vascular changes, neutrophil infiltration, and exudate formation to eliminate pathogens and initiate healing.
Chronic Inflammation
Prolonged inflammation (weeks to years) involving lymphocytes, macrophages, fibrosis, and tissue necrosis, often due to persistent irritants or unresolved acute inflammation.
Cardinal Signs of Inflammation
Rubor (redness), tumor (swelling), calor (heat), dolor (pain), and functio laesa (loss of function) at the injury site.
Vascular Stage of Acute Inflammation
Initial phase marked by vasoconstriction followed by vasodilation, increased permeability, and exudation of protein-rich fluid, causing edema.
Cellular Stage of Acute Inflammation
Phase involving leukocyte margination, adhesion, transmigration, chemotaxis, and phagocytosis to clear pathogens.
Neutrophils
Primary phagocytic cells in acute inflammation; arrive early (within 90 minutes) and perform microbial killing via enzymes and reactive oxygen species.
Macrophages
Long-lived phagocytes in chronic inflammation; secrete cytokines, growth factors, and mediate tissue repair.
Mast Cells
Release histamine and other mediators (e.g., TNF-α, leukotrienes) to initiate vasodilation and vascular permeability.
Histamine
Preformed mediator from mast cells causing vasodilation and increased vascular permeability via H1 receptors.
Arachidonic Acid Metabolites
Prostaglandins and leukotrienes derived from cell membranes; regulate inflammation, pain, and bronchoconstriction.
Prostaglandins
Cyclooxygenase pathway products that induce vasodilation, fever, and pain; targeted by NSAIDs.
Leukotrienes
Lipoxygenase pathway products causing bronchoconstriction (e.g., SRS-A in asthma) and increased vascular permeability.
Platelet-Activating Factor (PAF)
Lipid mediator inducing platelet aggregation, neutrophil activation, and bronchoconstriction.
Complement System
Plasma proteins enhancing inflammation via opsonization, chemotaxis (C5a), and membrane attack complex (MAC) formation.
Cytokines
Proteins (e.g., TNF-α, IL-1, IL-6) coordinating local and systemic inflammatory responses, including fever and acute-phase proteins.
Chemokines
Chemotactic cytokines directing leukocyte migration to injury sites (e.g., IL-8).
Granulomatous Inflammation
Chronic inflammation with epithelioid macrophages forming granulomas to wall off indigestible agents (e.g., TB, foreign bodies).
Acute-Phase Response
Systemic effects of inflammation including fever, leukocytosis, and increased CRP, fibrinogen, and ESR.
CRP (C-Reactive Protein)
Acute-phase protein produced by the liver; binds pathogens for complement activation and serves as an inflammation biomarker.
Leukocytosis
Elevated white blood cell count (>10,000/µL), often neutrophilia in bacterial infections or lymphocytosis in viral infections.
Tissue Regeneration
Replacement of damaged cells with identical functional cells; possible in labile (e.g., skin) and stable (e.g., liver) cells.
Fibrous Tissue Repair
Healing via scar formation (collagen deposition) when regeneration is impossible, as in permanent cells (e.g., cardiac muscle).
Granulation Tissue
Temporary tissue during repair containing fibroblasts, new capillaries, and inflammatory cells; forms the foundation for scarring.
Primary Intention Healing
Wound closure with minimal tissue loss (e.g., surgical incision), involving rapid re-epithelialization and minimal scarring.
Secondary Intention Healing
Healing of large wounds with significant tissue loss; involves extensive granulation tissue, contraction, and noticeable scarring.
Inflammatory Phase of Wound Healing
Initial phase (0-3 days) involving hemostasis, neutrophil recruitment, and macrophage-mediated debridement.
Proliferative Phase of Wound Healing
Phase (3-21 days) marked by fibroblast activity, collagen synthesis, angiogenesis, and epithelialization.
Remodeling Phase of Wound Healing
Final phase (3 weeks to years) involving collagen cross-linking, scar maturation, and increased tensile strength.
Keloid
Excessive collagen deposition forming raised, tumor-like scars beyond wound margins, common in genetically predisposed individuals.
Factors Impeding Wound Healing
Malnutrition, ischemia, infection, foreign bodies, diabetes, corticosteroids, and advanced age.
Labile Cells
Continuously dividing cells (e.g., skin, GI epithelium) capable of regeneration.
Stable Cells
Quiescent cells (e.g., hepatocytes) that proliferate after injury.
Permanent Cells
Non-dividing cells (e.g., neurons, cardiac muscle) replaced by scar tissue after damage.
Opsonization
Coating pathogens with antibodies or complement (e.g., C3b) to enhance phagocyte recognition.
Chemotaxis
Directed migration of leukocytes toward chemical gradients (e.g., C5a, bacterial peptides).
Exudate Types
Serous (watery), hemorrhagic (bloody), fibrinous (fibrin-rich), purulent (pus-containing), and membranous (necrotic debris).
Abscess
Localized collection of pus walled off by fibroblasts and collagen, requiring drainage for resolution.
Systemic Inflammatory Response Syndrome (SIRS)
Life-threatening systemic inflammation with vasodilation, shock, and organ failure due to cytokine storm.
Angiogenesis
Formation of new blood vessels from pre-existing vasculature, critical for granulation tissue development.
Braden Q Scale
Tool assessing pressure ulcer risk in children based on mobility, nutrition, and tissue perfusion.
