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 is the preformed toxin involved in the mechanism of allergic rhinitis?
Paracusis willis is a feature of which condition?
What is the full form of ARIA?
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 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).
Question 9: Paracusis willis is a feature of which condition?
- A. Tympanosclerosis
- B. Otosclerosis (Correct Answer)
- C. Meniere's disease
- D. Presbyacusis
Explanation: **Explanation:** **Paracusis Willis** is a clinical phenomenon where a patient with hearing loss paradoxically hears better in a noisy environment than in a quiet one. **Why Otosclerosis is correct:** Otosclerosis is a condition characterized by the fixation of the stapes footplate, leading to **conductive hearing loss (CHL)**. In a noisy environment, normal-hearing individuals naturally raise their voice volume (the Lombard effect) to overcome background noise. A patient with Otosclerosis has a "conductive barrier" that filters out the low-frequency background noise, but because their inner ear and nerve function are intact, they can clearly perceive the loud, raised voices of others. This makes their hearing appear improved in noisy settings. **Why other options are incorrect:** * **Tympanosclerosis:** While this causes CHL due to hyalinization of the tympanic membrane, Paracusis Willis is classically described and most significantly associated with the stapes fixation found in Otosclerosis. * **Meniere’s Disease:** This is a sensory-neural hearing loss (SNHL) condition. Patients typically suffer from **loudness recruitment**, making noisy environments distressing rather than helpful. * **Presbyacusis:** This is age-related SNHL. These patients struggle significantly in noise due to poor speech discrimination and the loss of high-frequency clarity. **Clinical Pearls for NEET-PG:** * **Schwartz Sign:** A flamingo-pink flush seen on the promontory through the TM (indicates active otosclerosis/otospongiosis). * **Carhart’s Notch:** A characteristic dip in the bone conduction threshold at **2000 Hz**. * **Gelle’s Test:** Negative in Otosclerosis (indicates an immobile ossicular chain). * **Treatment of Choice:** Stapedotomy (using a Teflon piston).
Question 10: What is the full form of ARIA?
- A. Allergic rhinitis and its impact on asthma (Correct Answer)
- B. Allergic rhinitis induced asthma
- C. Antibody response in allergic rhinitis
- D. Antibody response in asthma
Explanation: **Explanation:** **1. Why Option A is Correct:** ARIA stands for **Allergic Rhinitis and its Impact on Asthma**. It is a global initiative launched by the World Health Organization (WHO) in 1999 (published in 2001) to provide evidence-based guidelines for the management of allergic rhinitis. The core medical concept behind ARIA is the **"United Airway Disease"** hypothesis, which posits that the upper and lower airways are a single functional unit. Inflammation in the nasal mucosa (allergic rhinitis) often coexists with and exacerbates inflammation in the bronchial tree (asthma). **2. Why Other Options are Incorrect:** * **Option B:** While allergic rhinitis is a major risk factor for developing asthma, ARIA is the name of the *guideline/initiative*, not a description of the pathophysiology of "induced" asthma. * **Options C & D:** These are distractors. While ARIA guidelines discuss IgE-mediated antibody responses, the acronym itself does not stand for "Antibody Response." **3. High-Yield Clinical Pearls for NEET-PG:** * **Classification:** ARIA replaced the old "seasonal/perennial" classification with a more clinical approach based on duration and severity: * **Intermittent:** Symptoms < 4 days/week OR < 4 consecutive weeks. * **Persistent:** Symptoms > 4 days/week AND > 4 consecutive weeks. * **Severity:** Categorized as **Mild** (normal sleep/daily activities) or **Moderate-Severe** (disturbed sleep/impairment of daily activities). * **Treatment Strategy:** Intranasal corticosteroids (INCS) are the first-line treatment for moderate-to-severe persistent rhinitis. * **The Link:** Approximately 80% of asthmatics have co-existing allergic rhinitis, and up to 40% of patients with allergic rhinitis have asthma. Treatment of the nose often improves asthma control.
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