Allergy & Immunology: Anaphilaxis and Allergic Reactions Flashcards
ACE INHIBITORS
Angioedema is a rare and serious adverse effect of ACE inhibitor therapy. ACE inhibition increases bradykinin levels,
which increase vascular permeability and lead to angioedema. Symptoms include tongue, lips, or eyelid swelling and,
less frequently, laryngeal edema and difficulty breathing. ACE inhibitors should be discontinued in affected patients.
ANAPHYLAXIS
Anaphylactic shock is characterized by vasodilatation, increased vascular permeability, and bronchoconstriction. Epinephrine counteracts these physiological mechanisms and is the drug of choice for the treatment of anaphylaxis. [1366]
Wheal-and-flare lesions usually result from allergic (type I hypersensitivity) reactions. On initial exposure, an allergen
(eg, insect venom) promotes antibody class switching to IgE. Subsequent exposure promotes cross-linking of IgE on
basophils and mast cells, resulting in degranulation and release of multiple vasoactive mediators, including histamine.
[556]
Anaphylaxis (type 1 hypersensitivity) can quickly lead to respiratory compromise (eg, bronchospasm, oropharyngeal edema) and distributive shock. The most common autopsy findings include upper airway edema, hyperinflation of the lungs from airway obstruction, and cerebral edema from hypoxia. [20720]
In anaphylaxis, allergen exposure triggers widespread IgE-mediated release of inflammatory chemical mediators (eg, histamine, prostaglandin, leukotrienes). These chemical mediators cause peripheral vasodilation and increase vascular permeability, leading to hypotension. [20767]
Anaphylaxis is a type 1 (immediate) hypersensitivity reaction involving IgE-mediated mast cell and basophil
degranulation. Epinephrine is the primary treatment for anaphylaxis because it decreases further mast cell release of
inflammatory mediators and counteracts existing systemic inflammatory effects (eg, shock, bronchoconstriction).
[21470]
Anaphylaxis is an IgE-mediated response to an allergen that results in the release of histamine by mast cells and basophils. Histamine causes widespread physiologic effects, including vasodilation and increased vascular permeability (eg, hypotension), increased catecholamine secretion (eg, tachycardia), and bronchoconstriction (eg, wheezing). [20715]
Anaphylaxis is the result of widespread mast cell and basophil degranulation and the release of preformed inflammatory mediators, including histamine and tryptase. Tryptase is relatively specific to mast cells and can be used as a marker for mast cell activation. [2068]
The high-affinity IgE receptor (FcεRI) is found on the surface of mast cells and basophils and normally binds the Fc portion of circulating IgE antibodies. Cross-linking of multiple membrane-bound IgE antibodies by a multivalent antigen results in aggregation of the FcεRI receptors, causing degranulation and the release of preformed mediators (eg, histamine, tryptase) that initiate an allergic response. [2069]
ANGIOEDEMA
Angioedema can be hereditary (autosomal dominant) or acquired (associated with angiotensin-converting enzyme [ACE] inhibitor treatment). In hereditary angioedema, low C1 esterase inhibitor activity leads to increases in bradykinin activity. ACE inhibitors should not be used in these patients. [1612]
C1 inhibitor (C1INH) deficiency causes increased cleavage of C2 and C4 and results in inappropriate activation of the complement cascade. C1INH also blocks kallikrein-induced conversion of kininogen to bradykinin, a potent vasodilator associated with angioedema. [11667]
Hereditary angioedema is characterized by recurrent episodes of cutaneous and/or mucosal swelling due to C1 inhibitor deficiency. C4 levels are low due to uninhibited cleavage of C4 by excess activated C1. [20747]
ANTIHISTAMINES
First-generation antihistamines can cause significant side effects due to blockade of cholinergic, alpha-adrenergic,
and serotonergic pathways. They should be avoided in older patients with cognitive or functional impairments.
DRUG ALLERGY
Red man syndrome (RMS) is the most common adverse reaction to vancomycin. It occurs due to rapid vancomycin infusion, which leads to the direct activation of mast cells and the subsequent release of vasoactive
mediators. Patients develop flushing, pruritus, and an erythematous rash on the upper torso, face, and neck within minutes of initiation. Because RMS is not a true allergic reaction (not IgE mediated), vancomycin can be restarted at a slower rate of infusion once symptoms resolve. [19115]
IMMUNIZATIONS
Vaccine reactogenicity is a local (eg, warmth, swelling, edema) and systemic (eg, fatigue, fever, headache) inflammatory reaction to the vaccine due to the innate immune response. It is primarily caused by pattern recognition receptors present on the surface of macrophages and mast cells, which identify the antigen and release inflammatory cytokines (eg, IL-1, IL-6)
OPIOIDS
Opioids (eg, morphine) can generate a pseudoallergic response by directly activating mast cells to stimulate degranulation, releasing histamine and other vasoactive mediators. This nonimmunologic reaction can cause itching, urticarial rash, wheezing, hypotension, and tachycardia that closely mimic true IgE-mediated type 1
hypersensitivity. However, true IgE-mediated allergic reaction is rare with opioids.
RHINITIS
Glucocorticoids inhibit transcription of proinflammatory mediators and promote apoptosis of eosinophils, T cells, and monocytes.
SERUM SICKNESS
Serum sickness is an immune complex–mediated type III hypersensitivity reaction that typically forms 5-14 days after exposure to foreign proteins in an antitoxin, antivenom, monoclonal antibody, or vaccine. Patients typically develop fever, urticarial rash, and arthralgia that resolve spontaneously over days as the immune complexes are cleared by the mononuclear phagocyte system
SYNCOPE
Vasovagal syncope is a known complication of vaccine administration, particularly in adolescents. It typically involves a prodrome and can be differentiated from anaphylaxis based on skin findings (pallor vs urticaria), absence of respiratory symptoms (eg, upper airway edema, bronchospasm), and presence of bradycardia (vs tachycardia)
