AllergyImmunology Flashcards
(112 cards)
Late-phase reaction: Occurs _ to _ hours after acute phase and initial allergen exposure; symptoms are similar to acute-phase reaction and mirror the inflammation seen in asthma and chronic allergic rhinitis
4 to 12
Differences between mechanisms of anaphylaxis and acute phase reaction
elevated serum β-tryptase in anaphylaxis non–IgE-mediated factors include C3a and C5a
Diagnosis of anaphylaxis is supported by the measurement of elevated serum _ (usually peaks in the first _ hours)
tryptase, 2 hours
Anaphyaxis: Rx
epinephrine, first oxygen, antihistamines, corticosteroids, and β-agonists (
non–IgE-triggered process that clinically resembles anaphylaxis; causes include aspirin,NSAID, radiocontrast, and, rarely, opiates
Anaphylactoid reaction (is non-IgE mediated)
Prophylaxis: anaphylactoid reaction to radiocontrast
prednisone (50 mg, administered at 13 hours, 7 hours, and 1 hour before procedure) diphenhydramine (IM or PO) 1 hour before procedure
Heriditary angioedema(HAE-C1-INH): Dx, Rx
Clinical presentation + Absence or reduced level of C1-INH plus low C4 Synthetic androgens (e.g., danazol, stanazol) Purified C1-INH Kallikrein inhibitors
How doe synthetic androgens (danazol, stanazol) work in hereditary angioedema?
Induction of C1-inhibitor synthesis
Two types of heriditary angioedema?
HAE-C1-INH, HAE-FXII
Pathogenetic mechanisms: differences between HAE-C1-INH and HAE-FXII
HAE-C1-INH: low levels of C1-esterase HAE-FXII: Activation of kallikrein-bradykinin system
Acquired angioedema suggests:
malignancy - lymphoma, leukemia Low C1q levels distinguish this from hereditary form
Mechanism of allergic contact dermatitis
T cells activated, release interferon-γ Macrophages then activated
Allergic contact dermatitis: Dx method
Patch testing
Atopic dermatitis: mechanism, rx
1/3: skin barrier defect (filaggrin mutation) Inherited: elevated IgE, eosinophilia, IgE sensitization to antigens Topical steroids, Topical FK506, antistaph abx
FK506
Tacrolimus
Tacrolimus: Indxn
- Organ transplant - Atopic dermatitis - severe refractory uveitis after BMT - MCD - vitiligo - Kimura’s disease inhibis production of IL-2 thus decreasing development of T cell populations
Systemic diseases causing urticaria
- urticarial vasculitis - mastocytosis - SLE
Urticaria:Rx other than antihistamines
doxepin
Mechanism of penicillin allergy
Acting as hapten
Can aztreonam be given to a pen-allergic patient?
- cross-reactivity with cephalosporins is 6% to 30% - carbapenems cross-react with minor determinants PCN whereas monobactams (i.e., aztreonam) can be safely administered to PCN-allergic patients
Sulfonamide mediated allergy mechanism; which patients are prone to it?
T-Cell; HIV+
Recently identified genetic mutation (platelet-derived growth factor receptor alfa [FIP1L1-PDGFRA]) in some cases
Hypereosinophilic syndrome
Why do we need to notify the blood bank that a patient has IgG A deficiency?
If prior blood transfusion, patient will develop anti-IgG A antibodies which will react with transfused blood containing IgG A. Ie: blood bank should provide IgG A free blood
Samter’s triad
asthma, aspirin sensitivity, and nasal polyps
The first case of aspirin sensitivity in a patient with asthma was described in 1902, a few years after the introduction of aspirin into clinical use. In 1968, Samter and Beers described a