Allergy and Immunology Flashcards

A 28-year-old woman develops urticaria, angioedema, bronchospasm, and hypotension within 15 minutes of receiving amoxicillin. Which of the following is the MOST critical immediate intervention?

Answer: Epinephrine 0.3–0.5 mg IM into the anterolateral thigh

Epinephrine IM is the drug of choice for anaphylaxis and must be given immediately — it is the only agent that addresses the life-threatening cardiovascular and respiratory components. Antihistamines and corticosteroids are adjuncts and are never substitutes for epinephrine. Albuterol addresses bronchospasm but not the systemic reaction. Delay in epinephrine administration is the leading cause of anaphylaxis fatality.

A 35-year-old man develops angioedema of the lip and tongue 2 weeks after starting lisinopril for hypertension. He has no urticaria and no prior allergic history. Which mechanism best explains this reaction?

Answer: Bradykinin accumulation due to ACE inhibition

ACE inhibitor-induced angioedema is bradykinin-mediated, not IgE or histamine-mediated. ACE normally degrades bradykinin; inhibition leads to bradykinin accumulation causing vascular leakage. This explains why it does not respond to antihistamines or steroids. Hereditary angioedema involves C1 esterase inhibitor deficiency but is not drug-induced. Direct histamine release is not the mechanism for lisinopril.

A 6-month-old boy has had recurrent pneumonia caused by Pneumocystis jirovecii, oral candidiasis, and failure to thrive since birth. On examination, no lymph nodes are palpable. CBC shows lymphopenia. Which immunodeficiency is most likely?

Answer: Severe combined immunodeficiency (SCID)

SCID presents in infancy with both T and B cell deficiency, causing susceptibility to bacterial, viral, and opportunistic infections (including PCP and Candida). XLA presents later after maternal antibody wanes and predominantly affects B cells, causing bacterial infections. CVID presents in young adults. DiGeorge involves T cell deficiency from thymic aplasia but B cells are intact.

A 25-year-old woman develops a diffuse maculopapular rash 10 days after starting ampicillin for mononucleosis. She denies prior penicillin allergy. What is the correct interpretation of this reaction?

Answer: This is a non-allergic ampicillin rash associated with EBV infection, not a true penicillin allergy

Ampicillin given during active EBV (mononucleosis) infection causes a nonallergic maculopapular rash in up to 80–100% of patients — this is not an IgE-mediated drug allergy. Mislabeling this as penicillin allergy leads to unnecessary avoidance of an important antibiotic class. The rash is immune-complex-mediated and specific to the EBV-ampicillin interaction.

A 32-year-old woman has recurrent episodes of angioedema without urticaria, triggered by stress and minor trauma, with no identifiable allergen. Her C4 level is consistently low. C1 esterase inhibitor (C1-INH) level and function are markedly reduced. Family history reveals her father had similar episodes. What is the most likely diagnosis?

Answer: Hereditary angioedema (HAE) type I

HAE type I is caused by autosomal dominant deficiency of C1 esterase inhibitor (low levels and function), leading to bradykinin-mediated angioedema without urticaria. Attacks are triggered by stress/trauma. Low C4 is a reliable screening marker. ACE inhibitor angioedema occurs in patients on that drug. Acquired HAE is associated with lymphoproliferative disease and presents in older patients without family history.

A 45-year-old man with recurrent sinopulmonary infections since age 25 is found to have serum IgG of 280 mg/dL (normal 700–1600), IgA of 15 mg/dL, and IgM of 40 mg/dL. He has normal T cell counts but markedly reduced B cell numbers. What is the most appropriate long-term management?

Answer: Intravenous immunoglobulin (IVIG) replacement therapy

Common variable immunodeficiency (CVID) is characterized by low IgG, IgA, and IgM with normal T cells and recurrent bacterial infections in adults. The mainstay of treatment is IVIG (or SCIG) replacement to prevent infections. TMP-SMX prophylaxis is used for PCP in T cell deficiencies, not antibody deficiencies. BMT is reserved for SCID. Interferon-gamma is used for chronic granulomatous disease.