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What is hypersensitivity?
An exaggerated or inappropriate immune response causing tissue damage or death.
Who classified the types of hypersensitivity?
Coombs and Gell.
What are the four types of hypersensitivity?
Type I (immediate), Type II (antibody-dependent), Type III (immune complex-mediated), and Type IV (cell-mediated).
What mediates Type I hypersensitivity?
IgE antibodies binding to mast cells and basophils.
Name common examples of Type I hypersensitivity.
Allergic asthma, hay fever, anaphylaxis, and urticaria (hives).
What are the three phases of a Type I reaction?
Sensitization phase, reaction phase, and effector phase.
What triggers mast cell degranulation in Type I hypersensitivity?
Cross-linking of IgE bound to allergens on mast cells.
What are treatments for Type I hypersensitivity?
Epinephrine, antihistamines, corticosteroids, and allergen avoidance.
What antibodies mediate Type II hypersensitivity?
IgG and IgM.
How does complement activation contribute to Type II reactions?
It leads to cell lysis or opsonization for phagocytosis
Name three examples of Type II hypersensitivity.
Hemolytic anemia, granulocytopenia, and thrombocytopenia.
What is antibody-dependent cell-mediated cytotoxicity (ADCC)?
Destruction of IgG-coated target cells by NK cells or macrophages.
What diagnostic test can confirm Type II hypersensitivity?
Detection of tissue-specific antibodies and complement deposition via immunofluorescence
What mediates Type III hypersensitivity?
Soluble antigen-antibody immune complexes
What role does complement play in Type III hypersensitivity?
It attracts neutrophils, which release lysosomal enzymes causing tissue damage.
Give examples of diseases caused by Type III hypersensitivity.
Serum sickness, systemic lupus erythematosus (SLE), and Arthus reaction.
What is the Arthus reaction?
A localized immune complex-mediated inflammatory reaction caused by antigen-antibody deposition.
Why do neutrophils fail to clear immune complexes in Type III hypersensitivity?
Large immune complexes are difficult to phagocytose, leading to degranulation and tissue damage.
What mediates Type IV hypersensitivity?
T lymphocytes, especially CD4+ and CD8+ cells.
Why is Type IV hypersensitivity called delayed hypersensitivity?
It develops 24–72 hours after antigen exposure.
What are two types of Type IV hypersensitivity?
Contact hypersensitivity and tuberculin-type hypersensitivit
What are common causes of contact hypersensitivity?
Poison ivy, nickel, and certain drugs like sulfonamides.
What does a positive tuberculin skin test indicate?
Previous exposure to Mycobacterium tuberculosis, not necessarily active disease.
How do immune complexes in Type III hypersensitivity cause tissue damage?
By activating complement, leading to inflammation and neutrophil-mediated damage.
What causes mast cell degranulation in Type I hypersensitivity?
Increased intracellular calcium triggered by IgE cross-linking.
What is the main effector cell in Type IV hypersensitivity?
Macrophages activated by T cells.
What distinguishes Type II from Type IIMacrophages activated by T cells.I hypersensitivity?
Type II targets cell surfaces, while Type III involves soluble immune complexes deposited in tissues.
What role do cytokines play in Type IV hypersensitivity?
They recruit and activate macrophages and other inflammatory cells.
What are the symptoms of anaphylaxis in Type I hypersensitivity?
Airway obstruction, hypotension, urticaria, and possible death.
How does serum sickness manifest in Type III hypersensitivity?
Fever, rash, joint pain, and kidney damage due to immune complex deposition.
What skin changes occur in contact dermatitis (Type IV)?
0Erythema, eczema, and necrosis within 12–48 hours.
What causes hemolytic anemia in Type II hypersensitivity?
Antibodies binding to red blood cells, leading to complement-mediated lysis.
How is Type I hypersensitivity managed?
With epinephrine, antihistamines, corticosteroids, and environmental interventions.
What is the treatment for immune complex diseases?
Immunosuppressive drugs and removal of the antigen.
Why is corticosteroid therapy useful in hypersensitivity?
It suppresses inflammation by inhibiting cytokine production.
How are contact hypersensitivities diagnosed?
Through patch testing to identify allergens.
What precautions should be taken for individuals prone to anaphylaxis?
Carrying an epinephrine auto-injector and avoiding known allergens.
What diagnostic test is used for Type IV hypersensitivity?
Tuberculin skin test.
What is a key diagnostic feature of Type II hypersensitivity?
Detection of autoantibodies and complement deposition in tissues.
How is the wheal-and-flare reaction related to Type I hypersensitivity?
It is a hallmark of allergic reactions, caused by vasodilation and increased vascular permeability.
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