Pathophysiology Modules 3, 4, 5 & 7 Professor Loren

A comprehensive set of 100 vocabulary flashcards covering inflammation, immunity, infection, and cancer drawn from Modules 3, 4, 5, and 7 lecture notes.

Inflammation

The tissue response to injury characterized by redness, swelling, heat, pain, and loss of function.

First Line of Defense

Physical and chemical barriers such as skin and mucous membranes that prevent pathogen entry.

Second Line of Defense

The inflammatory response that activates when barriers are breached.

Third Line of Defense

The adaptive immune response that targets specific antigens and forms memory.

Acute Inflammation

Short-term inflammatory process lasting a few weeks, dominated by neutrophils with minimal scarring.

Chronic Inflammation

Prolonged inflammation (>6 months) involving monocytes, macrophages, and lymphocytes, often leading to fibrosis or granulomas.

Vascular Response

Phase of inflammation with vasodilation and increased capillary permeability to deliver blood, fluids, and cells to injury.

Cellular Response

Movement and action of leukocytes (e.g., mast cells, neutrophils, macrophages) at an injury site.

Mast Cell

‘First-responder’ immune cell that releases histamine to cause vasodilation during inflammation.

Neutrophil

Most abundant white blood cell and earliest phagocytic responder in acute inflammation.

Macrophage

Large, long-lived phagocyte derived from monocytes, prominent in chronic inflammation.

Chemotaxis

Directional movement of immune cells toward chemical signals at sites of injury or infection.

Cellular Adherence

Attachment of leukocytes to foreign material or endothelium, aiding phagocytosis.

Cellular Migration

Leukocyte movement through vessel walls to reach injured tissue.

Redness (Rubor)

Localized erythema caused by increased blood flow (vasodilation).

Heat (Calor)

Local warmth due to enhanced blood flow in inflamed tissue.

Swelling (Tumor)

Edema from fluid exudate accumulating in tissues during inflammation.

Pain (Dolor)

Sensation produced by tissue compression and inflammatory mediators stimulating nerves.

Loss of Function

Impaired movement or activity at an inflamed site from pain, swelling, or tissue damage.

Leukocytosis

Elevated white blood cell count (>10,000 cells/mm³) during inflammation or infection.

Erythrocyte Sedimentation Rate (ESR)

Blood test measuring RBC clumping; elevated values (>100 mm/h) indicate inflammation.

C-Reactive Protein (CRP)

Acute-phase plasma protein whose elevated level signals significant inflammatory disease.

Complement Activity

Blood test showing activation of the complement system; high early, decreases as factors are used.

Prothrombin Time

Coagulation test prolonged during inflammation, reflecting faster clotting tendency.

Fibrinogen

Clotting protein that rises in inflammation to promote hemostasis.

RICE Therapy

Non-pharmacologic treatment—Rest, Ice, Compression, Elevation—to reduce inflammation.

Aspirin

Drug that blocks arachidonic acid conversion to prostaglandins, reducing pain, fever, and inflammation.

NSAIDs

Non-steroidal anti-inflammatory drugs (e.g., ibuprofen) with actions similar to aspirin.

Glucocorticoids

Steroid medications that inhibit inflammatory mediators, reduce immune cell infiltration, and suppress immunity.

Healing and Tissue Repair

Three-phase process: inflammatory phase, proliferative phase, and remodeling phase restoring tissue integrity.

Primary Intention

Healing of clean, closed wounds where edges unite quickly with minimal scarring.

Secondary Intention

Healing of large, open wounds from the bottom up, slower with higher infection and scarring risk.

Infection (Healing Complication)

Invasion of a healing wound by microorganisms delaying repair.

Ulceration

Open sore resulting from poor perfusion that resists healing.

Dehiscence

Rupture or splitting of a wound due to deficient scar formation.

Keloid

Hypertrophic scar from excessive collagen, more common in darker skin.

Adhesion

Fibrous connection between serous cavities and nearby tissues that restricts movement.

Superficial Partial-Thickness Burn

First-degree burn damaging epidermis only; heals within a week without scarring.

Deep Partial-Thickness Burn

Second-degree burn penetrating dermis, causing blisters and potential scarring; heals in 2–4 weeks.

Full-Thickness Burn

Third-degree burn destroying epidermis, dermis, and possibly subcutaneous tissue with eschar formation.

Rule of Nines

Method for estimating burn surface area using body region percentages.

Hydrotherapy

Water-based wound cleansing technique used in burn care.

Debridement

Removal of dead or damaged tissue to promote wound healing.

Skin Grafting

Surgical placement of healthy skin to cover large burns or wounds.

Rheumatoid Arthritis (RA)

Chronic autoimmune inflammation of synovial membranes causing joint damage.

Pannus

Granulation tissue over inflamed synovium and cartilage that erodes joint surfaces in RA.

Cartilage Erosion

Destruction of joint cartilage due to nutrient deprivation and enzymes from pannus.

Fibrosis (RA)

Replacement of normal synovial tissue with collagen, reducing joint flexibility.

Ankylosis

Debilitating joint fixation resulting from fibrosis and bone fusion in RA.

Rheumatoid Factor

Autoantibody (usually IgG) often present in RA patients.

Antinuclear Antibodies (ANA)

Autoantibodies against nuclear components; elevated in autoimmune diseases like RA and SLE.

NSAIDs for RA

Drugs used to relieve pain and reduce inflammation in rheumatoid arthritis.

Immunosuppressants

Medications that dampen immune activity to control autoimmune diseases.

Adaptive Immunity

Specific, slower immune defense with memory provided by B and T lymphocytes.

Innate Immunity

Nonspecific, rapid defense mechanisms present at birth (e.g., skin, phagocytes).

T-Lymphocyte

White blood cell maturing in the thymus, central to cell-mediated immunity.

Cytotoxic T Cell (CD8+)

T-cell subtype that directly kills antigen-bearing cells.

Helper T Cell (CD4+)

T-cell that orchestrates immune responses by activating B cells and cytotoxic T cells.

Suppressor T Cell

Regulatory T-cell that down-modulates immune responses to prevent overactivity.

B-Lymphocyte

Bone-marrow-derived cell that differentiates into plasma cells producing antibodies.

Immunoglobulin (Ig)

Antibody molecule produced by plasma cells to bind specific antigens.

IgG

Most abundant antibody, provides long-term immunity and crosses the placenta.

IgM

First antibody produced in an immune response; excellent at agglutination.

IgA

Antibody found in mucosal secretions like saliva, tears, and breast milk.

IgE

Antibody that binds mast cells and mediates allergic type I hypersensitivity responses.

Natural Killer Cell

Innate lymphocyte that destroys virus-infected and tumor cells without prior sensitization.

Eosinophil

Granulocyte that combats parasitic infections and modulates allergic responses.

Basophil

Granulocyte that releases histamine and supports mast cells in allergic reactions.

Monocyte

Circulating precursor to macrophages that becomes phagocytic in tissues.

Active Immunity

Protection produced by an individual’s own immune system after antigen exposure or vaccination.

Passive Immunity

Temporary immunity transferred from another source, such as maternal antibodies or antibody therapy.

Type I Hypersensitivity

Immediate IgE-mediated allergic reaction involving mast cell degranulation.

Anaphylaxis

Severe, systemic type I hypersensitivity causing airway swelling and shock.

Type II Hypersensitivity

Antibody-mediated cytotoxic reaction against specific cells, e.g., transfusion reactions.

Type III Hypersensitivity

Immune complex-mediated reaction where antigen-antibody complexes deposit in tissues.

Type IV Hypersensitivity

Delayed, T-cell-mediated reaction such as contact dermatitis or TB skin test.

Systemic Lupus Erythematosus (SLE)

Chronic autoimmune type III hypersensitivity affecting multiple organ systems.

Butterfly Rash

Characteristic malar facial rash seen in many SLE patients.

Glomerulonephritis

Inflammation of kidney glomeruli, common renal manifestation of SLE.

DMARDs

Disease-modifying antirheumatic drugs that slow progression of inflammatory arthritis.

Infection

Tissue damage caused by invasion and multiplication of microorganisms.

Pathogen

Disease-producing microorganism that can harm host tissues.

Virulence

Degree of pathogenicity indicated by the microbe’s ability to cause severe disease.

Antigenicity

Pathogen’s ability to be recognized and provoke an immune response.

Coinfection

Simultaneous infection of a host with at least two different pathogens.

Superinfection

New infection arising during antimicrobial treatment of an existing infection.

Reservoir

Place where a pathogen lives and replicates, such as humans, animals, or water.

Portal of Entry

Pathway through which a pathogen enters the host (e.g., respiratory tract, broken skin).

Means of Transmission

Method by which a pathogen spreads (direct contact, airborne, fomites, etc.).

Incubation Period

Time from pathogen exposure to appearance of initial symptoms.

Prodrome

Onset of nonspecific symptoms preceding disease-specific manifestations.

Acute Clinical Illness

Phase with peak, disease-specific signs and symptoms.

Convalescence

Recovery stage when symptoms fade and tissue heals.

Septicemia

Systemic infection where pathogens multiply in the blood leading to sepsis.

Bacteremia

Presence of bacteria in the bloodstream, may progress to septicemia.

Neoplasm

Irreversible, abnormal cell mass (tumor) arising from uncontrolled proliferation.

Carcinogen

Agent (chemical, radiation, microbe) that initiates or promotes cancer development.

Benign Tumor

Non-invasive, localized neoplasm resembling tissue of origin and lacking metastasis.

Malignant Tumor

Invasive, rapidly proliferating cancer that can metastasize and lacks normal differentiation.

Tumor Staging (TNM)

Classification of cancer based on Tumor size, Node involvement, and Metastasis spread.