patho. ch 2 (Mechanisms of Self‑Defence)

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107 Terms

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Innate immunity

Natural/native defense; first and second lines of defense

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First line

Physical barriers (skin, mucous membranes, cilia) and chemical barriers (lysozymes, low pH, antimicrobial secretions, normal flora)

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Second line

Innate immune cellular responses (NK cells, phagocytes, fever, inflammation)

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NK cells

Natural killer lymphocytes; kill infected/tumor cells without prior sensitization

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Phagocytes

Engulf and digest debris and microbes (macrophages, neutrophils, monocytes)

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Inflammation

First response to injury; vascular tissue reaction to harmful stimuli

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Goals of inflammation

Prevent/limit damage, control response, initiate adaptive immunity, start healing

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Vasodilation

Increases vascular permeability and leakage during inflammation

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Margination

WBCs align along vessel walls during inflammation

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Diapedesis

WBC migration through vessel wall into tissues

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Chemotaxis

Directed migration of WBCs toward chemical signals at injury site

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Opsonization

Coating target cells with antibodies or complement (C3b) to enhance phagocytosis

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Mast cells

Tissue basophils; key activators of inflammation, release histamine and mediators

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Histamine

Vasoactive amine causing vasodilation and permeability increase

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Prostaglandins

Lipid mediators from arachidonic acid; induce pain; inhibited by NSAIDs

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Leukotrienes

Lipid mediators similar to histamine, promote inflammation

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Platelet activating factor

Increases vascular permeability + platelet activation

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Endothelium

Lining of blood vessels; regulates inflammation and allows leukocyte movement

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Platelets

Cell fragments from megakaryocytes; central to clotting and inflammation

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Plasma protein systems

Complement, coagulation, and kinin systems

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Complement system

Circulating proteins activated by antibodies, lectins, or microbes; form membrane attack complex (MAC)

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Classical pathway

Complement activation via antibodies (C1 → C3, C5)

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Lectin pathway

Complement activation by mannose‑binding lectin binding sugars on microbes

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Alternative pathway

Complement activation directly by microbial surfaces (factors B, D, properdin)

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C3a

Anaphylatoxin; triggers mast cell degranulation

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C3b

Opsonin; enhances phagocytosis and activates C5

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C5a

Potent chemotactic factor + anaphylatoxin

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C5b

Part of MAC; directly lyses bacteria

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Membrane attack complex (MAC)

C5b, C6, C7, C8, C9 proteins that lyse bacteria

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Coagulation system

Forms fibrin mesh to stop bleeding, trap microbes, and provide framework for healing

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Extrinsic pathway

Triggered by tissue factor and factor VII; tested with PT/INR

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Intrinsic pathway

Triggered by contact (factor XII); tested with PTT

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Common pathway

Both intrinsic and extrinsic converge at factor X → thrombin → fibrin

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Kinin system

Produces bradykinin; roles in vasodilation, pain, permeability, smooth muscle contraction

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Bradykinin

Primary kinin; causes vasodilation, pain, permeability, smooth muscle contraction, chemotaxis

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Cytokines

Small proteins secreted by immune cells; primary inflammatory mediators

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Chemokines

Small cytokines; guide migration of leukocytes (traffic cops of inflammation)

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Interleukins

Cytokines produced by macrophages/lymphocytes in response to infection

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IL‑1

Pro‑inflammatory cytokine; fever (endogenous pyrogen), neutrophil proliferation, chemotaxis

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IL‑10

Anti‑inflammatory cytokine; suppresses lymphocyte and macrophage activity

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Interferons

Cytokines that interfere with viral infections; produced by infected cells

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IFN alpha/beta

Type I interferons; induce antiviral proteins, protect neighboring cells

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IFN gamma

Type II interferon; produced by lymphocytes; activates macrophages

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TNF‑alpha

Tumor necrosis factor; produced by macrophages, induces fever, apoptosis, cachexia, thrombosis

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Types of inflammation

Acute (neutrophil‑dominant) vs chronic (lymphocyte/macrophage‑dominant)

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Acute inflammation

Rapid onset, lasts

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2 weeks, neutrophil infiltration

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Chronic inflammation

Longer duration, lymphocytes/macrophages/fibroblasts; granuloma formation possible

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Exudate

Fluid leakage in inflammation; types include serous, fibrinous, purulent, hemorrhagic

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Serous exudate

Watery; early inflammation

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Fibrinous exudate

Thick, clotted; advanced inflammation

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Purulent exudate

Pus; bacterial infection

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Hemorrhagic exudate

Bloody; indicates bleeding

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Granuloma

Organized collection of macrophages (epithelioid + giant cells) walling off chronic infection (e.g., TB)

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Langerhans giant cell

Large multinucleated macrophage in granulomas

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Wound healing

Process of repair after injury; requires blood supply + connective tissue

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Phases of wound healing

Inflammation (1‑2 days), proliferation (3‑4 days, angiogenesis + fibroblasts + re‑epithelialization), remodeling (weeks‑years, collagen remodeling + wound contraction)

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Primary intention

Healing with minimal tissue loss (e.g., surgical wounds); clean scar

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Secondary intention

Healing with large tissue loss; slower, broad scar (e.g., burns, ulcers)

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Dysfunctional healing

Poor healing due to bleeding, hypovolemia, infection, poor inflammatory response

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Deficient scar

Weak tissue, wound rupture, infection risk

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Excessive scar

Keloid or hypertrophic scar from excess collagen

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Impaired epithelialization

Poor re‑growth due to steroids, hypoxemia, malnutrition

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Contractures

Excessive wound contraction → restricted joint movement

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Conditions impairing wound healing

Diabetes mellitus, stress, age extremes, hypoxemia, obesity, alcoholism, poor nutrition, smoking, steroids, chemotherapy

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Neonates and healing

Immature immune system, poor neutrophil chemotaxis, complement deficiency → high sepsis risk

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Elderly and healing

Decreased innate immune function, chronic illnesses, polypharmacy, poor regenerative ability

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Adaptive immunity

3rd line of defense; long‑term, specific, inducible

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Components of adaptive immunity

Humoral (B cells, antibodies) and cellular (T cells)

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Active immunity

Exposure or vaccination; long‑lasting

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Passive immunity

Pre‑formed antibodies (Ig transfer); short‑term

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Antigen presenting cells (APCs)

Dendritic cells, macrophages; process/present antigens to lymphocytes

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Major histocompatibility complex (MHC)

Proteins presenting antigen fragments to T cells

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MHC I

Presents to CD8 cytotoxic T cells

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MHC II

Presents to CD4 helper T cells

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B cells

Differentiate into plasma cells that produce antibodies

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T helper cells (CD4)

Coordinate immune response; TH1 for cell‑mediated, TH2 for antibody‑mediated

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Cytotoxic T cells (CD8)

Kill infected or cancerous cells directly

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Regulatory T cells

Suppress immune response, maintain tolerance

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Antibodies (immunoglobulins)

Proteins produced by plasma cells; variable Fab region binds antigens, constant Fc region mediates function

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IgG

Most abundant, crosses placenta, secondary immune response

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IgM

Pentamer, first produced in primary response

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IgA

Found in secretions (saliva, tears, breast milk)

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IgD

On B cells, initiates activation

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IgE

Allergy, parasitic defense

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Primary immune response

First exposure; slower, mediated by IgM

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Secondary immune response

Subsequent exposure; faster, stronger; IgG dominant

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Immune aging

Decreased T cell activity, antibody response, memory B cells; ↑autoantibodies and immune complexes

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Primary immunodeficiency

Genetic; recurrent infections; includes B cell, T cell, combined, complement, phagocyte defects

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Secondary immunodeficiency

Acquired; from illness, drugs, malnutrition, stress, trauma, viral infection (e.g., AIDS)

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DiGeorge syndrome

Thymic aplasia → T cell deficiency

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SCID

Severe combined immunodeficiency; defective T and B cells

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Wiskott‑Aldrich syndrome

X‑linked; low IgM; recurrent infections and bleeding

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C3 deficiency

Severe complement deficiency; recurrent infections

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Hypersensitivity

Exaggerated immune response → host damage

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Type I hypersensitivity

IgE‑mediated, immediate (allergy, anaphylaxis, asthma)

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Type II hypersensitivity

Tissue‑specific; antibodies destroy cells (Grave’s disease, hemolytic anemia)

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Type III hypersensitivity

Immune complex‑mediated; complexes deposit in tissues (SLE, serum sickness, post‑strep GN)

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Type IV hypersensitivity

Delayed T‑cell‑mediated (TB, contact dermatitis, graft rejection)

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Autoimmunity

Immune system attacks self antigens (e.g., rheumatoid arthritis, SLE)