Immunology
Showing 39 of 39 topics
  A
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            ACE‑I angioedema is bradykinin‑mediated; stop ACE‑I permanently. Airway protection is paramount; icatibant or C1‑INH may help in severe cases; avoid ACE‑I/possibly caution with ARB.
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            Non-histaminergic swelling (often lips/tongue) typically within months to years of ACEi use. Prioritize airway management; epinephrine/antihistamines/steroids may have limited effect. Consider icatibant or C1-INH in severe cases; avoid ACEi permanently.
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            Differentiate histaminergic from bradykinin‑mediated angioedema; identify triggers/medications; avoid unnecessary broad testing in acute urticaria.
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            Rule out anaphylaxis; treat with non sedating H1 antihistamines, consider short steroid burst for severe cases, and identify triggers.
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            Suspect allergic contact dermatitis with well‑demarcated, patterned eczema. Patch testing identifies allergens; avoidance is primary therapy.
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            Treating allergic rhinitis improves asthma control. Combine intranasal steroids/antihistamines, environmental control, and consider allergen immunotherapy in sensitized patients with symptoms.
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            Skin prick testing and serum specific IgE support diagnosis but must match clinical history; avoid testing large panels without pre‑test probability. Consider component‑resolved diagnostics for select foods/venoms.
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            Multi-system allergic reaction: give IM epinephrine in lateral thigh immediately; support airway and breathing; add adjuncts and observe for biphasic reactions; prescribe auto-injector and action plan.
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            Immediate intramuscular epinephrine in the lateral thigh is first line; add oxygen, IV fluids, and adjuncts; observe for biphasic reactions and discharge with auto injector and education.
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            Treat rapidly with IM epinephrine in the lateral thigh; repeat every 5–15 min as needed. Add oxygen, IV fluids, H1/H2 blockers, and corticosteroids as adjuncts; observe for biphasic reactions and prescribe an epinephrine auto‑injector with an action plan.
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            Acute, life-threatening allergic reaction with airway, breathing, or circulatory compromise. Give IM epinephrine 0.3–0.5 mg (1 mg/mL) in the lateral thigh immediately and repeat every 5–15 minutes as needed. Position patient supine, provide high-flow oxygen and IV fluids; add adjuncts after epinephrine.
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            Anaphylaxis is a rapid, systemic hypersensitivity reaction. Inject IM epinephrine in the anterolateral thigh promptly; repeat every 5–15 min as needed. Position patient supine with legs elevated, give high-flow oxygen, IV fluids, H1/H2 blockers, bronchodilators, and steroids as adjuncts; observe for biphasic reactions.
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            Life-threatening systemic reaction: diagnose clinically; give IM epinephrine 0.3–0.5 mg (1 mg/mL) in the mid-outer thigh immediately; repeat every 5–15 min as needed; airway and fluids; observe for biphasic reactions.
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            Immediate IM epinephrine in the mid‑anterolateral thigh is first‑line; support airway/breathing/circulation, identify trigger, and arrange observation with autoinjector and action plan at discharge.
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            Triad of asthma, nasal polyps, and sensitivity to cyclooxygenase 1 inhibitors; treat acute bronchospasm and rhinosinusitis, avoid culprit NSAIDs, and consider desensitization and leukotriene pathway therapy.
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            Triad of asthma, nasal polyps, and respiratory reactions to NSAIDs. Manage with avoidance, optimal asthma/CRS control, and consider aspirin desensitization; biologics may help.
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            Emollients and trigger control are foundational; step‑up with topical steroids/calcineurin inhibitors, phototherapy, and systemic agents (dupilumab, JAK inhibitors) for moderate–severe disease.
B
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            Cross reactivity is largely driven by side chains; many cephalosporins and carbapenems can be used safely with appropriate assessment and testing.
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            Swelling from ACE inhibitor use or hereditary angioedema does not respond to epinephrine or antihistamines; secure airway early and give targeted therapies such as C1 inhibitor, icatibant, or ecallantide when indicated.
C
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            CRSwNP is a Type 2‑skewed disease; treat with high‑volume saline rinses, intranasal steroids (sprays or irrigations with steroid), short steroid bursts for flares, ESS for refractory disease, and biologics for severe cases.
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            Begin with daily non sedating H1 antihistamine, increase dose stepwise, add omalizumab for refractory disease, and consider cyclosporine under specialist care.
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            Treat with high‑dose second‑generation H1 antihistamines, then omalizumab, then cyclosporine for refractory cases; avoid chronic steroids.
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            CVID features low IgG with low IgA and/or IgM and impaired vaccine responses, causing recurrent sinopulmonary infections and autoimmunity. Treat with Ig replacement and targeted management of complications.
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            Treat acute reactions as anaphylaxis when present; future imaging may use alternative agents and premedication regimens, recognizing that risk reduction is incomplete.
E
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            Chronic, immune‑mediated esophageal disease. Diagnose with symptoms and ≥15 eos/hpf on biopsy; treat with high‑dose PPI, swallowed topical steroids, and/or empiric elimination diet; dilate strictures.
F
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            After food triggered anaphylaxis or suspected IgE mediated reaction, provide auto injector prescription, avoidance counseling, label reading education, and allergy referral.
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            OIT increases threshold to accidental exposures in select patients. Requires daily dosing, adherence, and management of adverse events including anaphylaxis and EoE risk.
H
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            Treat stings with rapid epinephrine for systemic reactions, remove stinger, and refer for venom immunotherapy which markedly reduces risk of future systemic reactions.
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            Venom immunotherapy (VIT) prevents life‑threatening anaphylaxis in patients with systemic sting reactions. Diagnose with history + testing; continue carry of autoinjector.
L
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            Ensure latex‑free environments for sensitized patients and healthcare workers. Identify cross‑reactive foods (banana, avocado, kiwi) and manage perioperative exposure risks.
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            Identify immediate hypersensitivity with contact or airborne exposure; avoid latex products, provide epinephrine for systemic reactions, and ensure latex free environments.
P
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            Use practical red flags to identify children at risk of PID and start an initial lab panel; refer early to Immunology for definitive testing and management.
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            Most patients labeled 'penicillin allergic' are tolerant. Use risk stratification to guide direct oral amoxicillin challenge vs skin testing, especially in stewardship programs and pre‑op clinics.
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            Most penicillin allergy labels are inaccurate; risk stratify by history, use direct oral challenge for low risk patients, skin test when indicated, and update records.
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            Inducible urticarias (cold, cholinergic, delayed pressure, dermographism, heat, solar) are diagnosed with provocation testing; management centers on trigger avoidance and high‑dose second‑generation antihistamines.
R
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            Adult PID work‑up starts with CBC with differential, quantitative immunoglobulins, specific antibody titers (pre/post immunization), and HIV testing; tailor further testing to pattern of infections.
S
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            Most are asymptomatic; some have recurrent infections, autoimmunity, or celiac disease. No routine Ig replacement; manage infections, vaccinate, and use washed/IgA‑depleted blood if anti‑IgA antibodies present.
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            Phenotype severe asthma (Type 2 high vs low) to select biologics (omalizumab, mepolizumab/benralizumab, dupilumab, tezepelumab). Optimize inhaled therapy and adherence first.
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            Recognize and manage severe cutaneous adverse reactions (SJS/TEN, DRESS). Stop culprit drugs immediately, provide supportive care (burn unit for TEN), and consult dermatology/immunology early.
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