Hypersensitivity Reactions - Vocabulary Flashcards

Vocabulary flashcards covering the key concepts, mechanisms, classifications, diagnostics, and example diseases related to hypersensitivity reactions as presented in the lecture notes.

Hypersensitivity

An exaggerated or inappropriate immune response causing tissue injury and disease; triggered by self-antigens (autoimmunity), microbial antigens (post-infectious), or environmental antigens (allergens).

Autoimmunity

Immune response directed against self-antigens, leading to tissue injury.

Allergen

Environmental antigen that can trigger hypersensitivity in genetically predisposed individuals.

ACID mnemonic

A mnemonic to remember hypersensitivity types: A = Anaphylaxis (Type I), C = Cytotoxic-mediated (Type II), I = Immune complex-mediated (Type III), D = Delayed hypersensitivity (Type IV).

Type I hypersensitivity

Immediate hypersensitivity triggered by environmental antigens in predisposed individuals; IgE-mediated reaction with mast cell and basophil involvement.

Type I clinical manifestations

Food allergies, urticaria, anaphylaxis, allergic rhinitis, asthma, and atopic dermatitis.

Anaphylaxis

Severe systemic Type I hypersensitivity reaction that can be life-threatening.

IgE-mediated

Mechanism of Type I reactions in which IgE antibodies on mast cells and basophils release mediators causing symptoms.

Type II hypersensitivity

Antibody-mediated cytotoxic reactions where IgG or IgM target antigens on cell surfaces or tissues, causing cell damage.

Coombs test

Serologic test used to detect antibodies against red blood cells in antibody-mediated cytotoxic reactions (Type II).

ELISA test

Enzyme-linked immunosorbent assay used to detect specific antibodies; applied in Type II hypersensitivity evaluation.

Plasmapheresis

Procedure that removes antibodies from plasma to treat antibody-mediated diseases.

Intravenous Immunoglobulin (IVIG)

Infusion of pooled IgG used to modulate immune responses in antibody-mediated diseases.

Type II clinical diseases

Hemolytic anemia, Goodpasture’s syndrome, Graves’ disease (examples of antibody-mediated cytotoxicity).

Type III hypersensitivity

Immune complex–mediated reactions in which antigen–antibody complexes form in circulation, deposit in tissues (e.g., vessels, kidneys, joints), activate complement, and recruit neutrophils causing inflammation and tissue damage.

Immune complexes

Antigen–antibody aggregates that deposit in tissues and activate the complement system in Type III hypersensitivity.

Type III clinical examples

Systemic lupus erythematosus (SLE), serum sickness, immune complex–mediated glomerulonephritis.

Type III diagnostic tests

Evaluation includes checking complement levels and ANA, urinalysis, and biopsy to identify immune complex–mediated injury.

Type IV hypersensitivity

Delayed-type hypersensitivity; 48–72 hours after antigen exposure; mediated by sensitized T lymphocytes (CD4+ Th1 and CD8+ T cells) and macrophage activation.

Type IV clinical conditions

Contact dermatitis (poison ivy, nickel, latex), tuberculin skin test (Mantoux), granulomatous diseases (TB, sarcoidosis, Crohn’s), graft-versus-host disease (GVHD), autoimmune diabetes mellitus type 1.

Mantoux test

Tuberculin skin test used to detect delayed-type hypersensitivity to TB antigens.

Graft-versus-host disease (GVHD)

Donor immune cells attack recipient tissues in transplantation; a Type IV hypersensitivity reaction.

Delayed-type hypersensitivity mechanism

Mediated by T cells releasing cytokines that activate macrophages and cause inflammation; CD8+ cytotoxic T cells may kill targets in some variants.

Type I–IV summary framework

A quick framework: Type I = IgE-mediated; Type II = IgG/IgM cytotoxic; Type III = immune complex deposition; Type IV = T cell–mediated (delayed).