Anaphylaxis Management — MCQs
First line therapy in anaphylactic shock is:
A 3-year-old is diagnosed with severe acute asthma exacerbation. Which medication is given first?
A person presents with recurrent swelling on the face and lips due to emotional stress. The likely cause is?
What is the dose of adrenaline given to a child with cardiac arrest?
Which is the best investigation to confirm diagnosis of anaphylaxis?
Which of the following is false regarding transfusion-associated anaphylactic reactions?
Which of the following are early mediators of allergic rhinitis?
Which of the following preformed toxins is involved in the mechanism of allergic rhinitis?
A 29-year-old non-smoker man presents with sneezing, post-nasal drip, eye-watering, and an itch of his posterior pharynx. These symptoms tend to be worse in the spring and summer and have been bothering him since mid-April. His past medical history is remarkable only for mild asthma induced by being outdoors. He takes no regular medications but does take diphenhydramine on occasion. What is the most appropriate diagnostic test at this time?
Which of the following is the preformed toxin involved in the mechanism of allergic rhinitis?
Anaphylaxis Management Indian Medical PG Practice Questions and MCQs
Question 1: First line therapy in anaphylactic shock is:
- A. Epinephrine .5 ml of 1:1000 IM (Correct Answer)
- B. Atropine 3 mg intravenously
- C. Adenosine 12 mg intravenously
- D. Epinephrine 1 ml of 1:10000 intravenously
Explanation: ***Epinephrine .5 ml of 1:1000 IM*** - **Epinephrine** is the **first-line treatment** for anaphylaxis due to its alpha-1 agonist effects (vasoconstriction, which increases blood pressure) and beta-2 agonist effects (bronchodilation, which improves breathing). [1] - The recommended dose and concentration for intramuscular administration in adults is **0.3-0.5 mg (0.3-0.5 mL of 1:1000 solution) IM**, repeated every 5-15 minutes as needed. *Atropine 3 mg intravenously* - **Atropine** is an anticholinergic medication used to treat **bradycardia** or organophosphate poisoning, not anaphylaxis. [4] - It does not address the widespread vasaodilation or bronchoconstriction seen in anaphylactic shock. *Adenosine 12 mg intravenously* - **Adenosine** is an antiarrhythmic drug primarily used to convert **supraventricular tachycardia (SVT)** to normal sinus rhythm. [3] - It has no role in the management of anaphylactic shock. *Epinephrine 1 ml of 1:10000 intravenously* - While epinephrine is the correct drug, **intravenous administration** of epinephrine 1:10,000 is typically reserved for **cardiac arrest** [2] or in cases of severe, refractory anaphylaxis under expert care, and carries a higher risk of adverse effects. - The initial and preferred route for anaphylaxis is **intramuscular**, as it provides rapid absorption with lower risks compared to IM administration.
Question 2: A 3-year-old is diagnosed with severe acute asthma exacerbation. Which medication is given first?
- A. Inhaled ipratropium
- B. IV corticosteroids
- C. Nebulized salbutamol (Correct Answer)
- D. IV magnesium sulfate
Explanation: ***Nebulized salbutamol*** - **Salbutamol** (albuterol) is a **short-acting beta-2 agonist (SABA)** which provides rapid bronchodilation by relaxing smooth muscles in the airways. - It is the **first-line treatment** for acute asthma exacerbations due to its quick onset of action and effectiveness in relieving bronchospasm. *Inhaled ipratropium* - **Ipratropium**, an anticholinergic, is often added to bronchodilators like salbutamol in **severe exacerbations** but is not the primary initial bronchodilator. - It works by blocking muscarinic receptors, causing **bronchodilation**, but its onset of action is slower than salbutamol. *IV corticosteroids* - **Corticosteroids** reduce airway inflammation and are crucial for preventing relapse and shortening recovery in severe asthma, but their **onset of action is delayed** (several hours). - They are typically administered after initial bronchodilation with SABAs and are not the first medication given for immediate symptom relief. *IV magnesium sulfate* - **Magnesium sulfate** is a smooth muscle relaxant that can be used in **severe, life-threatening asthma exacerbations** that are refractory to standard therapy. - It is considered a **second or third-line treatment** rather than an initial intervention for immediate bronchodilation.
Question 3: A person presents with recurrent swelling on the face and lips due to emotional stress. The likely cause is?
- A. C1 esterase inhibitor deficiency (Correct Answer)
- B. Allergy
- C. Anaphylaxis
- D. ACE inhibitor-induced angioedema
Explanation: C1 esterase inhibitor deficiency - This condition presents with recurrent episodes of angioedema (swelling of face, lips, airway, or gastrointestinal tract) that are often triggered by stress, trauma, or medical procedures. - The deficiency leads to unregulated activation of the complement and kallikrein-kinin pathways, resulting in excessive bradykinin production which causes increased vascular permeability and swelling. Allergy - Allergic reactions typically involve hives (urticaria) and itching, which are usually absent in C1 esterase inhibitor deficiency. - Allergic angioedema is often mediated by histamine and resolves with antihistamines or epinephrine, which are ineffective in C1 esterase inhibitor deficiency [2]. Anaphylaxis - Anaphylaxis is a severe, life-threatening allergic reaction that includes symptoms such as respiratory distress, hypotension, and generalized urticaria, in addition to angioedema [2]. - While angioedema can be a feature, the constellation of symptoms and the common triggers differ significantly from C1 esterase inhibitor deficiency [2]. ACE inhibitor-induced angioedema - This type of angioedema is a known side effect of ACE inhibitor medications and usually occurs after beginning the medication [1]. - It is also caused by increased bradykinin levels but is directly linked to the drug's action, not an underlying genetic deficiency, and typically resolves upon discontinuation of the medication.
Question 4: What is the dose of adrenaline given to a child with cardiac arrest?
- A. 0.1 ml/kg of 1:10000 solution (Correct Answer)
- B. 0.1 ml/kg of 1:1000 solution
- C. 0.01 ml/kg of 1:1000 solution
- D. 0.01 ml/kg of 1:10000 solution
Explanation: ***0.1 ml/kg of 1:10000 solution*** - The recommended dose of **adrenaline** (epinephrine) for **pediatric cardiac arrest** is **0.01 mg/kg IV/IO**, which translates to **0.1 ml/kg of a 1:10,000 solution** (0.1 mg/ml). - This is the **standard concentration** recommended by **AHA PALS guidelines** and international resuscitation protocols for intravenous/intraosseous administration during cardiac arrest. - The 1:10,000 dilution provides the correct dose in an appropriate volume that is safe for rapid IV/IO bolus administration. *0.01 ml/kg of 1:10000 solution* - This volume would deliver only **0.001 mg/kg**, which is a **ten-fold underdose** of adrenaline. - This insufficient dose would fail to achieve the necessary **vasoconstrictive** and **inotropic effects** required during cardiopulmonary resuscitation. *0.01 ml/kg of 1:1000 solution* - While this delivers the correct dose (0.01 mg/kg), the **1:1000 concentration** (1 mg/ml) is typically reserved for **intramuscular** or **subcutaneous** administration (e.g., anaphylaxis). - Using 1:1000 solution IV/IO requires extreme caution due to the high concentration and risk of **dosing errors**; standard resuscitation protocols specify 1:10,000 for IV/IO use. *0.1 ml/kg of 1:1000 solution* - This represents a **ten-fold overdose** (0.1 mg/kg) of adrenaline. - Such an excessive dose can cause severe adverse effects including **severe tachyarrhythmias**, profound hypertension, **myocardial ischemia**, and increased myocardial oxygen demand, which are dangerous during cardiac arrest.
Question 5: Which is the best investigation to confirm diagnosis of anaphylaxis?
- A. IgA levels
- B. Serum tryptase (Correct Answer)
- C. IgD levels
- D. Serum precipitins
Explanation: ***Serum tryptase*** - **Serum tryptase** is released from activated mast cells and is a reliable biomarker for confirming anaphylaxis, particularly when measured within 1-3 hours of symptom onset. - Elevated levels help differentiate anaphylaxis from other conditions with similar symptoms, especially when the clinical picture is ambiguous. *IgA levels* - **IgA levels** are relevant in diagnosing conditions like selective IgA deficiency or celiac disease, but they do not play a direct role in confirming acute anaphylaxis. - They reflect long-term immune status rather than immediate hypersensitivity reactions. *IgD levels* - **IgD levels** have no established role in the diagnosis or confirmation of anaphylaxis. - Their physiological function is not fully understood, but they are not used as biomarkers for acute allergic reactions. *Serum precipitins* - **Serum precipitins** are antibodies detected in various hypersensitivity reactions, especially to inhaled antigens, and are not specific for anaphylaxis [1]. - They are primarily associated with conditions like hypersensitivity pneumonitis, reflecting different immunological mechanisms [1].
Question 6: Which of the following is false regarding transfusion-associated anaphylactic reactions?
- A. Different from allergy
- B. Epinephrine is the drug of choice
- C. Washed blood products prevent it
- D. Seen in IgG deficient individuals (Correct Answer)
Explanation: ***Seen in IgG deficient individuals*** - Transfusion-associated **anaphylactic reactions** are most commonly seen in **IgA-deficient individuals** who develop **anti-IgA antibodies** and receive blood products containing IgA. - Anaphylaxis occurs when these pre-formed IgA antibodies react with donor IgA, leading to mast cell degranulation and severe allergic symptoms. *Different from allergy* - Transfusion-associated **anaphylactic reactions** are a severe form of allergic reaction, often distinguished by their **rapid onset** and life-threatening nature [1]. - While all allergies involve an immune response to an allergen, anaphylaxis represents the most extreme systemic manifestation. *Epinephrine is the drug of choice* - **Epinephrine** is indeed the **first-line treatment** for acute anaphylaxis, regardless of its cause, including transfusion-associated reactions [2]. - It acts rapidly to counteract the systemic effects of histamine and other mediators by acting on α and β adrenergic receptors [3]. *Washed blood products prevent it* - **Washing blood products** (e.g., packed red blood cells or platelets) is an effective strategy to **remove plasma proteins**, including IgA. - This is particularly crucial for patients with a known **IgA deficiency and anti-IgA antibodies** to prevent severe anaphylactic reactions.
Question 7: Which of the following are early mediators of allergic rhinitis?
- A. Leukotrienes
- B. Interleukin-4
- C. Interleukin-5
- D. Platelet-activating factor and bradykinin (Correct Answer)
Explanation: ### Explanation Allergic rhinitis is a Type I hypersensitivity reaction occurring in two distinct phases: the **Early Phase** (within minutes) and the **Late Phase** (4–8 hours later). **Why Option D is Correct:** The early phase is triggered when an allergen cross-links IgE antibodies on the surface of **mast cells**, leading to immediate degranulation. This releases **pre-formed mediators** and rapidly synthesized lipid mediators. * **Histamine** is the primary mediator. * **Platelet-activating factor (PAF), Bradykinin, and Prostaglandin D2** are also released during this immediate window, causing vasodilation, increased vascular permeability (edema), and stimulation of sensory nerves (itching/sneezing). **Why Other Options are Incorrect:** * **A. Leukotrienes:** While Cysteinyl Leukotrienes (CysLTs) are produced during the early phase, they are most characteristic of the transition to and maintenance of the **Late Phase** response, contributing significantly to prolonged nasal congestion. * **B & C. Interleukin-4 and Interleukin-5:** These are **cytokines** produced by Th2 lymphocytes. They are involved in the **Late Phase** response. IL-4 promotes IgE isotype switching, while IL-5 is the primary factor for **eosinophil** recruitment and activation. **NEET-PG High-Yield Pearls:** 1. **Early Phase (Minutes):** Mediated by Mast cells. Key symptoms: Sneezing, itching, rhinorrhea. Key mediator: Histamine. 2. **Late Phase (Hours):** Mediated by Eosinophils, Basophils, and Th2 cells. Key symptom: Nasal congestion. 3. **Gold Standard Diagnosis:** Skin Prick Test (detects specific IgE). 4. **Pharmacology Link:** Antihistamines work best on early-phase symptoms (itch/sneeze), while Intranasal Steroids are the most effective treatment for late-phase symptoms (congestion) because they inhibit cytokine release.
Question 8: Which of the following preformed toxins is involved in the mechanism of allergic rhinitis?
- A. Histamine (Correct Answer)
- B. Leukotriene
- C. TXA2
- D. PGD2
Explanation: Allergic rhinitis is a **Type I Hypersensitivity reaction** mediated by IgE antibodies. When an allergen cross-links IgE on the surface of mast cells, it triggers **degranulation**, releasing two types of chemical mediators: **Preformed mediators** (stored in granules) and **Newly synthesized mediators** (produced after activation). ### Why Histamine is Correct **Histamine** is the primary **preformed mediator** stored in the granules of mast cells and basophils. Upon degranulation, it is released immediately (within minutes), causing the "Early Phase" symptoms of allergic rhinitis: vasodilation, increased capillary permeability (edema/nasal block), and stimulation of sensory nerves (itching/sneezing). ### Why Other Options are Incorrect * **Leukotrienes (B):** These are **newly synthesized** mediators derived from arachidonic acid via the lipoxygenase pathway. While potent (causing mucus secretion and congestion), they are produced *after* mast cell activation and are not pre-stored. * **TXA2 (Thromboxane A2) (C):** This is a product of the cyclooxygenase pathway primarily involved in platelet aggregation and vasoconstriction; it plays a minimal role in the pathophysiology of allergic rhinitis. * **PGD2 (Prostaglandin D2) (D):** Like leukotrienes, PGD2 is a **newly synthesized** mediator produced via the cyclooxygenase pathway. It contributes to late-phase inflammation but is not preformed. ### NEET-PG High-Yield Pearls * **Early Phase Response:** Mediated by **Histamine** (Preformed). Occurs within minutes. * **Late Phase Response:** Mediated by **Leukotrienes, PGD2, and Cytokines**. Occurs 4–8 hours later; characterized by eosinophil infiltration. * **Drug of Choice:** Intranasal corticosteroids are the most effective maintenance therapy for allergic rhinitis. * **Gold Standard Test:** Skin Prick Test (SPT) is used to identify specific allergens.
Question 9: A 29-year-old non-smoker man presents with sneezing, post-nasal drip, eye-watering, and an itch of his posterior pharynx. These symptoms tend to be worse in the spring and summer and have been bothering him since mid-April. His past medical history is remarkable only for mild asthma induced by being outdoors. He takes no regular medications but does take diphenhydramine on occasion. What is the most appropriate diagnostic test at this time?
- A. Blood radioallergosorbent test
- B. None, the diagnosis is based solely on the history and physical examination (Correct Answer)
- C. Intradermal testing
- D. Serum protein electrophoresis
Explanation: **Explanation:** The patient presents with classic symptoms of **Allergic Rhinitis (AR)**: paroxysmal sneezing, post-nasal drip, ocular symptoms (watering), and palatal itching. The seasonal pattern (spring/summer) and comorbid mild asthma strongly suggest **Seasonal Allergic Rhinitis**. **1. Why Option B is Correct:** In clinical practice, the diagnosis of Allergic Rhinitis is primarily **clinical**, based on a characteristic history and physical examination (e.g., pale/bluish nasal mucosa, turbinate hypertrophy). Diagnostic testing is **not mandatory** for initial management. Testing (like Skin Prick Tests) is typically reserved for patients who do not respond to empirical therapy (intranasal corticosteroids/antihistamines) or those being considered for allergen-specific immunotherapy. **2. Why Other Options are Incorrect:** * **Option A (RAST):** This measures allergen-specific IgE in the blood. While useful if skin testing is contraindicated (e.g., severe eczema or antihistamine use), it is more expensive and less sensitive than skin testing. It is not the first-line diagnostic step. * **Option C (Intradermal testing):** This is more sensitive but less specific than the Skin Prick Test (SPT). It carries a higher risk of systemic anaphylaxis and is generally used only if SPT is negative despite a strong clinical suspicion. * **Option D (Serum protein electrophoresis):** This is used to diagnose plasma cell dyscrasias (like Multiple Myeloma) and has no role in the diagnosis of allergy. **Clinical Pearls for NEET-PG:** * **First-line treatment for AR:** Intranasal Corticosteroids (e.g., Fluticasone). * **Allergic Shiners:** Dark circles under eyes due to venous congestion. * **Allergic Salute:** Upward rubbing of the nose leading to a **transverse nasal crease**. * **Gold Standard for identifying allergens:** Skin Prick Test (SPT). * **Definitive/Disease-modifying treatment:** Immunotherapy (SIT/SLIT).
Question 10: Which of the following is the preformed toxin involved in the mechanism of allergic rhinitis?
- A. Histamine (Correct Answer)
- B. Leukotriene
- C. TXA2
- D. PGD2
Explanation: ### Explanation The pathophysiology of Allergic Rhinitis is a **Type I Hypersensitivity reaction** mediated by IgE. When an allergen cross-links IgE antibodies on the surface of mast cells, it triggers **degranulation**, leading to the release of two types of inflammatory mediators: **1. Why Histamine is Correct:** Histamine is a **preformed mediator** stored in the granules of mast cells and basophils. Upon activation, it is released immediately (within minutes), causing the "Early Phase" response characterized by sneezing, itching, and rhinorrhea. Because it is synthesized and stored *before* the allergic trigger occurs, it is classified as a preformed toxin/mediator. **2. Why the Other Options are Incorrect:** * **Leukotrienes (B), TXA2 (C), and PGD2 (D):** These are **newly synthesized mediators** (lipid-derived). They are not stored in granules but are produced *de novo* from arachidonic acid via the cyclooxygenase (COX) or lipoxygenase (LOX) pathways only after the mast cell is activated. These mediators typically contribute to the "Late Phase" response, leading to nasal congestion and sustained inflammation. ### NEET-PG High-Yield Pearls: * **Early Phase (Minutes):** Primarily mediated by **Histamine**. Clinical features: Sneezing, itching, watery rhinorrhea. * **Late Phase (4–8 hours):** Mediated by **Leukotrienes (LTC4, LTD4, LTE4)**, Cytokines, and PGD2. Clinical feature: Nasal congestion (due to cellular infiltration, mainly eosinophils). * **Gold Standard Investigation:** Skin Prick Test (detects specific IgE). * **Drug of Choice:** Intranasal Corticosteroids (act on both early and late phases). * **Mast Cell Stabilizer:** Sodium Cromoglycate (prevents degranulation; used prophylactically).
Want unlimited practice?
Get full access to all questions, explanations, and performance tracking.
Start For Free