CIS chp. 14 Exam 3 concepts

These flashcards cover key concepts, mechanisms, clinical manifestations, and testing related to hypersensitivity reactions.

Hypersensitivity

An exaggerated or inappropriate immune response that causes tissue injury and pathology rather than protection.

Type 1 Hypersensitivity

Mediated by IgE, involving mast cells and basophils, associated with environmental allergens; reaction occurs within approximately 30 minutes.

Type 2 Hypersensitivity

Cytotoxic hypersensitivity mediated by IgG or IgM, involves complement activation, with RBCs as antigen triggers; takes hours for reaction.

Type 3 Hypersensitivity

Immune complex hypersensitivity mediated by IgG and IgM, involves complement fixation, with soluble antigen-antibody complexes as triggers; reaction timing is 4 to 8 hours.

Type 4 Hypersensitivity

Delayed cell-mediated hypersensitivity mediated by T lymphocytes, not involving complement, triggered by intracellular microbes and allergens; reaction occurs between 48 to 72 hours.

Clinical Manifestation of Type 1

Allergic rhinitis, asthma, anaphylaxis, food allergies, and urticaria.

Clinical Manifestation of Type 2

Hemolytic disease of the newborn (HDN), autoimmune hemolytic anemia, Goodpasture syndrome, myasthenia gravis.

Clinical Manifestation of Type 3

Systemic lupus erythematosus (SLE), rheumatoid arthritis, serum sickness, arthus reaction.

Clinical Manifestation of Type 4

Contact dermatitis (poison ivy, nickel), tuberculin skin test, granulomatous infections (TB, sarcoidosis), hypersensitivity pneumonitis.

Mechanism of Type 1 Hypersensitivity

Allergen cross-links IgE on mast cells causing release of histamine, leading to vasodilation and smooth muscle contraction.

Mechanism of Type 2 Hypersensitivity

Antibodies (IgG/IgM) bind to cell-bound antigens causing complement activation, opsonization, and cell lysis.

Mechanism of Type 3 Hypersensitivity

Immune complexes deposit in tissues causing complement activation, recruiting neutrophils that lead to inflammation and tissue damage.

Mechanism of Type 4 Hypersensitivity

Sensitized T cells recognize antigen in context of MHC, leading to cytokine release and macrophage recruitment.

Skin Testing for Type 1 Hypersensitivity

Involves pricking small amounts of an allergen onto the skin and assessing the wheal-and-flare reaction after 15-20 minutes.

Advantages of Skin Testing

Rapid, cheap, and highly sensitive method for diagnosing various allergic reactions.

Limitations of Skin Testing

Risk of systemic reaction, requirement for antihistamines before testing, unreliable in severe eczema or dermatographism.

Total IgE Testing

Measures overall allergic status through immunoassays, does not specify types of allergies.

Allergen-specific IgE Testing

Detects IgE to individual allergens, useful when skin testing is contraindicated.

Hemolytic Disease of the Newborn (HDN)

Occurs when an Rh-negative mother carries an Rh-positive fetus, leading to maternal immune response and fetal RBC destruction.

Direct Coombs Test (DAT)

Detects IgG or complement bound to RBCs in vivo; used for autoimmune hemolytic anemia and transfusion reactions.

Indirect Coombs Test (IAT)

Detects unbound antibodies in serum that may react with RBCs in vitro; used for crossmatching and antibody screening.

Cold Agglutinins Testing

Involves incubating patient serum with type O RBCs at 4°C to test for cold autoantibodies; agglutination indicates a positive result.

Clinical Associations of Positive Cold Agglutinins

can be associated with infections such as Mycoplasma pneumoniae and infectious mononucleosis, as well as certain lymphoproliferative disorders like lymphomas

Skin Testing for Delayed Hypersensitivity

Antigen is injected and read after 2 days; used for TB diagnosis, contact dermatitis, and cellular immunity evaluation.