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Question 1
What is the primary mechanism of penicillin-induced anaphylaxis?
A) IgG-mediated cytotoxicity
B) IgE-mediated histamine release
C) Complement activation
D) T-cell mediated reaction
Rationale:
Penicillin anaphylaxis is a classic example of an immediate Type I
hypersensitivity reaction, where IgE antibodies specific to penicillin bind to
mast cells and basophils. Upon re-exposure, cross-linking of these antibodies
triggers histamine and other mediator release, leading to symptoms such as
hypotension, bronchospasm, and urticaria. IgG and T-cell-mediated reactions
are involved in delayed or less severe forms of hypersensitivity, not
anaphylaxis.
Question 2
Which immune cells are primarily responsible for the release of histamine
in IgE-mediated penicillin allergy?
A) Neutrophils
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B) B lymphocytes
C) Mast cells
D) CD8+ T cells
Rationale:
Mast cells are key effector cells in IgE-mediated hypersensitivity reactions,
including penicillin anaphylaxis. When penicillin binds to IgE on the mast cell
surface, it causes degranulation and the release of histamine, leukotrienes,
and other inflammatory mediators. This process results in vasodilation,
bronchoconstriction, and other allergic symptoms.
Question 3
A delayed maculopapular rash from amoxicillin in the absence of systemic
symptoms is typically mediated by which immune mechanism?
A) IgE
B) IgG
C) Complement
D) T cells
Rationale:
Delayed rashes (especially in the context of viral infections) are usually T-cell
mediated Type IV hypersensitivity reactions. These reactions occur days
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after drug exposure and are not typically life-threatening. They differ from
immediate IgE-mediated reactions, which occur within minutes to hours.
Question 4
Which HLA allele has been associated with an increased risk of penicillin
hypersensitivity in some populations?
A) HLA-B57:01
B) HLA-A02:01
C) HLA-DRB1*10:01
D) HLA-DQ2
Rationale:
Although genetic links to penicillin allergy are still under investigation, HLA-
DRB1*10:01 has been identified in some studies as potentially associated with
increased risk of penicillin-induced hypersensitivity, especially in certain
ethnic populations. This allele may influence antigen presentation pathways
that promote immune activation. Other alleles like HLA-B*57:01 are more
classically linked to hypersensitivity to other drugs like abacavir.
Question 5