Allergic Reactions, Anaphylaxis, and Immunologic Emergencies - NREMT Paramedic Level

1. Which option best states when to repeat IM epinephrine in persistent anaphylaxis?

   Repeat every $5$–$15$ minutes if symptoms persist or worsen. This interval allows assessment of response while preventing delay in addressing persistent mediator effects and symptom progression.

2. Which mediator is most responsible for vasodilation and capillary leak in anaphylaxis?

   Histamine. Histamine binds to H1 receptors, promoting smooth muscle relaxation in blood vessels and increasing vascular permeability, which contributes to hypotension and edema.

3. What lower-airway finding is most consistent with bronchospasm from anaphylaxis?

   Wheezing with increased work of breathing. Bronchospasm leads to airway constriction, manifesting as wheezing and labored breathing due to mediator effects on bronchial smooth muscle.

4. Which option best defines biphasic anaphylaxis?

   Recurrence of symptoms after initial resolution without re-exposure. Biphasic reactions occur due to a secondary release of mediators, highlighting the need for prolonged observation after initial treatment.

5. What is the standard pediatric IM epinephrine dose for anaphylaxis using $1:1{,}000$?

   $0.01$ mg/kg IM, maximum $0.3$ mg per dose. Weight-based dosing ensures efficacy while minimizing side effects, with the cap preventing overdose in larger children.

6. What is the most common immunologic mechanism for classic anaphylaxis?

   IgE-mediated mast cell and basophil degranulation. This mechanism triggers the release of histamine and other mediators, leading to the rapid onset of symptoms characteristic of anaphylaxis.

7. What is the standard adult IM epinephrine dose for anaphylaxis using $1:1{,}000$?

   $0.3$–$0.5$ mg IM (=$0.3$–$0.5$ mL of $1$ mg/mL). This dose provides sufficient alpha and beta adrenergic stimulation to reverse hypotension and bronchospasm without excessive risk in adults.

8. Which diagnosis best fits isolated hives and itching with normal breathing and blood pressure?

   Mild allergic reaction (not anaphylaxis). Isolated cutaneous symptoms without systemic involvement indicate a localized reaction, not meeting criteria for anaphylaxis requiring aggressive intervention.

9. What is the primary physiologic effect of epinephrine that reverses anaphylactic shock?

   Alpha-1 vasoconstriction increasing SVR and reducing mucosal edema. Alpha-1 agonism constricts vessels to restore blood pressure and decreases edema by reducing vascular permeability in anaphylactic states.

10. What is the preferred initial fluid for hypotension from anaphylaxis, and why?

    Isotonic crystalloid bolus to treat relative hypovolemia from capillary leak. Crystalloids expand intravascular volume to counteract fluid shifts from increased permeability, supporting blood pressure in distributive shock.

11. Identify the correct immediate airway management priority in severe anaphylaxis with stridor.

    Early airway control with preparation for difficult airway and rapid deterioration. Stridor signals potential airway compromise, necessitating proactive management to secure the airway before edema worsens and complicates intubation.

12. What upper-airway finding is most concerning for impending obstruction in anaphylaxis?

    Stridor from laryngeal edema. Laryngeal edema causes upper airway narrowing, producing stridor as a sign of potential imminent airway compromise requiring immediate intervention.

13. Which adjunct medication treats bronchospasm in anaphylaxis but does not replace epinephrine?

    Inhaled albuterol. Albuterol provides targeted beta-2 agonism for bronchodilation but lacks the systemic effects needed to address hypotension or edema in anaphylaxis.

14. Choose the correct action: a patient on beta-blockers has refractory anaphylaxis after epinephrine.

    Administer glucagon per protocol for beta-blocker associated refractory anaphylaxis. Glucagon bypasses beta-receptor blockade to increase cyclic AMP, enhancing cardiac output and reversing refractory symptoms in such patients.

15. What is the typical time window for a biphasic anaphylactic reaction to occur?

    Within $1$–$72$ hours, most commonly within $8$–$12$ hours. This timeframe reflects the variable kinetics of mediator release and immune response reactivation without additional antigen exposure.

16. Which two medication classes are considered adjuncts for cutaneous symptoms in anaphylaxis?

    H1 antihistamines and corticosteroids (adjunctive, not first-line). These classes mitigate histamine effects and inflammation but act too slowly to serve as primary therapy for acute life-threatening symptoms.

17. What is the primary physiologic effect of epinephrine that improves bronchospasm?

    Beta-2 bronchodilation. Beta-2 receptor activation relaxes bronchial smooth muscle, alleviating airway constriction caused by anaphylactic mediators.

18. Which route and site are preferred for initial epinephrine in most anaphylaxis cases?

    Intramuscular injection into the lateral thigh (vastus lateralis). IM administration ensures rapid absorption and bioavailability, with the vastus lateralis providing optimal muscle mass for injection in emergencies.

19. Which diagnosis best fits hypotension after allergen exposure even if no hives are present?

    Anaphylaxis. Hypotension following exposure fulfills diagnostic criteria for anaphylaxis, as cardiovascular collapse can occur independently of dermatologic signs.

20. Which medication is first-line for anaphylaxis in the prehospital setting?

    Epinephrine. Epinephrine rapidly counteracts the effects of released mediators, stabilizing hemodynamics and relieving bronchospasm as the cornerstone of treatment.

21. Which two body systems involved strongly support anaphylaxis when symptoms are acute?

    Skin/mucosa plus respiratory or cardiovascular involvement. Involvement of these systems meets diagnostic criteria for anaphylaxis, as they signify widespread mediator effects beyond isolated cutaneous reactions.

22. What cardiovascular sign indicates distributive shock in anaphylaxis?

    Hypotension with tachycardia and weak pulses. Distributive shock in anaphylaxis arises from widespread vasodilation and capillary leak, resulting in compensatory tachycardia and diminished pulse quality.

23. What skin or mucosal findings are most characteristic of an allergic reaction or anaphylaxis?

    Urticaria, pruritus, flushing, angioedema. These manifestations result from histamine-induced vasodilation and increased vascular permeability in dermal and mucosal tissues.

24. Identify the key history elements that most strongly suggest anaphylaxis.

    Exposure + rapid onset + airway/breathing symptoms or hypotension. These elements indicate an IgE-mediated response with systemic involvement, differentiating anaphylaxis from localized allergic reactions.

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