Management of Anaphylaxis — MCQs
Drug of choice for beta antagonist toxicity is?
A cardiovascular parameter helpful in diagnosis of anaphylaxis during anaesthesia:
A 3-year-old is diagnosed with severe acute asthma exacerbation. Which medication is given first?
In the treatment of shock, why is dobutamine preferred over dopamine?
Which of the following is NOT typically administered during an anaphylactic reaction?
What is the best and most effective drug to control convulsions in toxicity cases?
A 70-year-old man was administered penicillin intravenously. Within 5 minutes, he developed generalized urticaria, swelling of lips, hypotension, and bronchospasm. What is the first choice of treatment?
What is the principal action of ammonia in syncope?
A 70-year-old man was administered penicillin intravenously. Within 5 minutes, he developed generalized urticaria, swelling of lips, hypotension, and bronchospasm. What is the first choice of treatment?
A patient develops facial puffiness, rash, hypotension, and breathing difficulty after the administration of antibiotics. What is the immediate treatment?
Management of Anaphylaxis Indian Medical PG Practice Questions and MCQs
Question 1: Drug of choice for beta antagonist toxicity is?
- A. Adrenaline
- B. Glucagon (Correct Answer)
- C. ACE inhibitors
- D. Dopamine
Explanation: ***Glucagon*** - **Glucagon** is the drug of choice for **beta-blocker overdose** because it bypasses the beta-adrenergic receptors and directly activates **adenylate cyclase** to increase intracellular cAMP [1]. - This action leads to increased heart rate and myocardial contractility, counteracting the cardiac depression caused by beta-blockers [1]. *Adrenaline* - **Adrenaline** (epinephrine) is a beta-agonist, but its effects are blunted in severe **beta-blocker overdose** due to **competitive antagonism** at beta receptors. - While it can be used for its alpha-agonist effects to increase blood pressure, its efficacy in reversing profound bradycardia and myocardial depression may be limited. *ACE inhibitors* - **ACE inhibitors** are used in the management of hypertension and heart failure, primarily by reducing **angiotensin II** formation and inhibiting **bradykinin** degradation. - They have no direct role in reversing the immediate cardiovascular effects of **beta-antagonist toxicity**. *Dopamine* - **Dopamine** is a **catecholamine** with dose-dependent effects, including positive inotropy and chronotropy at higher doses, but it relies on **adrenergic receptor activation**. - Its effects can be attenuated in **beta-blocker overdose**, similar to adrenaline, making it less effective than glucagon as first-line therapy.
Question 2: A cardiovascular parameter helpful in diagnosis of anaphylaxis during anaesthesia:
- A. Bradycardia
- B. Dysrhythmia
- C. Increased peripheral vascular resistance
- D. Hypotension (Correct Answer)
Explanation: ***Hypotension*** - **Hypotension** is a hallmark cardiovascular sign of anaphylaxis, occurring due to widespread **vasodilation** and increased vascular permeability. - This symptom is often profound and unresponsive to initial fluid resuscitation due to the ongoing systemic release of inflammatory mediators. *Bradycardia* - While bradycardia can occur in some rare cases of anaphylaxis (e.g., **vasovagal response**), **tachycardia** is the more common cardiac response due to compensatory mechanisms. - It is not a primary or consistent indicator of anaphylaxis, making it less helpful for diagnosis in this context. *Dysrhythmia* - **Dysrhythmias** can occur during anaphylaxis due to myocardial ischemia or electrolyte imbalances, but they are not a direct or consistent diagnostic feature. - Their presence often reflects severe compromise or co-existing conditions rather than being a primary anaphylactic sign. *Increased peripheral vascular resistance* - Anaphylaxis is characterized by a significant **decrease in peripheral vascular resistance** due to mast cell and basophil degranulation releasing vasodilatory mediators like histamine. - Therefore, an increase in peripheral vascular resistance would contradict the pathophysiology of anaphylaxis.
Question 3: 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 4: In the treatment of shock, why is dobutamine preferred over dopamine?
- A. It causes fewer arrhythmias.
- B. It causes less renal vasodilation.
- C. It causes less coronary vasoconstriction.
- D. All the above. (Correct Answer)
Explanation: **Explanation:** Dobutamine is often preferred over Dopamine in specific shock scenarios (particularly cardiogenic shock) due to its more favorable pharmacological profile and lower side-effect burden. **1. Why the Correct Answer (D) is Right:** * **Fewer Arrhythmias (Option A):** While both are inotropes, Dopamine significantly increases endogenous norepinephrine release. This, combined with its strong $\beta_1$ and $\alpha$ effects at higher doses, makes it more **arrhythmogenic** than Dobutamine. * **Less Renal Vasodilation (Option B):** This is a comparative pharmacological fact. While low-dose Dopamine acts on $D_1$ receptors to cause renal vasodilation, Dobutamine lacks this specific dopaminergic activity. In the context of the question, the absence of this "distracting" vasodilator effect allows for more predictable hemodynamic management in heart failure. * **Less Coronary Vasoconstriction (Option C):** At higher doses, Dopamine stimulates $\alpha_1$ receptors, leading to systemic and **coronary vasoconstriction**, which increases myocardial oxygen demand and can worsen ischemia. Dobutamine has mild $\beta_2$ activity which promotes vasodilation, reducing afterload and improving coronary perfusion. **2. Clinical Pearls for NEET-PG:** * **Mechanism:** Dobutamine is a relatively selective **$\beta_1$ agonist** (Inotrope > Chronotrope). * **Drug of Choice:** Dobutamine is the preferred inotrope for **Cardiogenic Shock** and is used in **Stress Echocardiography**. * **The "Dopamine Myth":** Modern trials (like the SOAP II trial) have shown that Dopamine is associated with higher mortality and more arrhythmic events compared to Norepinephrine/Dobutamine, leading to its declining use in clinical practice. * **Side Effect:** The most common side effect of Dobutamine is tachycardia.
Question 5: Which of the following is NOT typically administered during an anaphylactic reaction?
- A. Epinephrine
- B. Antihistamine
- C. Blood transfusion (Correct Answer)
- D. Beta-adrenergic agonists
Explanation: Anaphylaxis is a severe, life-threatening Type I hypersensitivity reaction characterized by systemic vasodilation, increased capillary permeability, and bronchospasm [1]. The management focuses on reversing these physiological derangements. **Why Blood Transfusion is the correct answer:** Blood transfusion is **not** a treatment for anaphylaxis. In fact, blood products are a common *cause* of anaphylactic reactions (IgA deficiency-mediated). Anaphylaxis results in **distributive shock** (fluid shifting from vessels to tissues), not hemorrhagic shock. The appropriate fluid resuscitation involves rapid infusion of **Isotonic Crystalloids** (Normal Saline) to restore intravascular volume, not blood. **Why the other options are incorrect:** * **Epinephrine (Adrenaline):** The **drug of choice**. Its $\alpha_1$ agonist effect causes vasoconstriction (reducing edema and hypotension), while $\beta_2$ effects cause bronchodilation and inhibit further mast cell degranulation [1]. * **Antihistamines (H1 & H2 blockers):** Used as **adjuvant therapy** to manage cutaneous symptoms like urticaria and itching. They do not treat airway obstruction or hypotension. * **Beta-adrenergic agonists (e.g., Salbutamol):** Administered via nebulization to treat refractory bronchospasm that does not fully respond to epinephrine. **High-Yield Clinical Pearls for NEET-PG:** * **Route of Epinephrine:** Always **Intramuscular (IM)** in the anterolateral thigh (1:1000 concentration). Dose: 0.5 mg in adults; 0.01 mg/kg in children. * **Biphasic Reaction:** Symptoms can recur 1–72 hours after initial resolution; hence, patients must be observed. * **Refractory Cases:** If a patient is on **Beta-blockers** and unresponsive to epinephrine, the antidote/alternative is **Glucagon**.
Question 6: What is the best and most effective drug to control convulsions in toxicity cases?
- A. Phenobarbitone
- B. Phenytoin
- C. Diazepam (Correct Answer)
- D. Carbamazepine
Explanation: **Explanation:** The correct answer is **Diazepam (Option C)**. **Why Diazepam is the Drug of Choice:** In the context of acute toxicity (poisoning) or drug-induced seizures, the primary goal is rapid termination of seizure activity to prevent hyperthermia, rhabdomyolysis, and metabolic acidosis. **Benzodiazepines (BZDs)** like Diazepam are the first-line agents because they act rapidly by enhancing GABA-mediated inhibition via the $GABA_A$ receptor. Diazepam is highly lipid-soluble, allowing it to cross the blood-brain barrier almost immediately after intravenous administration, making it the most effective "rescue" drug in emergency toxicology. **Analysis of Incorrect Options:** * **Phenytoin (Option B):** It is generally **ineffective** for toxin-induced seizures (e.g., theophylline, isoniazid, or cocaine toxicity). It has a slow onset of action and does not act on the GABAergic pathways typically disrupted by toxins. * **Phenobarbitone (Option A):** While effective as a second-line agent, it causes significant respiratory depression and sedation. It is usually reserved for seizures refractory to benzodiazepines. * **Carbamazepine (Option D):** This is a maintenance antiepileptic drug for focal seizures. It has no role in emergency seizure control and can actually worsen seizures in certain toxicities (e.g., tricyclic antidepressant overdose). **High-Yield Clinical Pearls for NEET-PG:** * **First-line for Status Epilepticus:** Lorazepam (due to longer duration of action in the brain) or Diazepam. * **Specific Antidote Exception:** For **Isoniazid (INH)** induced convulsions, the specific treatment is **Intravenous Pyridoxine (Vitamin B6)**, though Diazepam is used adjunctively. * **Avoid Phenytoin** in seizures caused by local anesthetic toxicity or TCA overdose as it may exacerbate cardiac arrhythmias.
Question 7: A 70-year-old man was administered penicillin intravenously. Within 5 minutes, he developed generalized urticaria, swelling of lips, hypotension, and bronchospasm. What is the first choice of treatment?
- A. Chlorpheniramine injection
- B. Epinephrine injection (Correct Answer)
- C. High dose hydrocortisone tablet
- D. Nebulized salbutamol
Explanation: ### Explanation **Correct Answer: B. Epinephrine injection** The patient is presenting with **Anaphylaxis**, a life-threatening Type I hypersensitivity reaction characterized by multi-system involvement (skin, respiratory, and cardiovascular). **Epinephrine (Adrenaline)** is the drug of choice and must be administered immediately. **Why Epinephrine is the First Choice:** Epinephrine acts as a **physiological antagonist** to histamine and other mediators. Its mechanism of action addresses all life-threatening components of anaphylaxis: * **$\alpha_1$ agonism:** Causes vasoconstriction, which increases peripheral vascular resistance to treat hypotension and reduces mucosal edema (laryngeal edema). * **$\beta_1$ agonism:** Increases cardiac contractility and heart rate (positive inotropic and chronotropic effects). * **$\beta_2$ agonism:** Causes potent bronchodilation and inhibits further mediator release from mast cells and basophils. **Why Other Options are Incorrect:** * **A. Chlorpheniramine:** This is an H1-antihistamine. While it helps with urticaria and itching, it is too slow-acting and does not treat life-threatening airway obstruction or shock. * **C. Hydrocortisone:** Corticosteroids have a delayed onset of action (4–6 hours). They are used to prevent "biphasic reactions" (delayed recurrence of symptoms) but are never the primary treatment for acute anaphylaxis. * **D. Nebulized Salbutamol:** This treats bronchospasm but does not address laryngeal edema or circulatory collapse. It is only an adjunct therapy. **High-Yield Clinical Pearls for NEET-PG:** * **Route of Choice:** Intramuscular (IM) in the anterolateral thigh (vastus lateralis) is preferred over SC or IV in the initial setting due to rapid absorption and safety. * **Dose/Concentration:** 0.5 mg (0.5 ml of **1:1000** solution) IM for adults. * **Mechanism:** Physiological antagonism (different receptor, opposite action). * **Drug of Choice for Anaphylactic Shock:** Epinephrine. * **Drug of Choice for Acute Bronchial Asthma:** Salbutamol (Selective $\beta_2$ agonist).
Question 8: What is the principal action of ammonia in syncope?
- A. Vasomotor stimulant
- B. Respiratory stimulant (Correct Answer)
- C. Vagal stimulant
- D. Inhibitor of vasomotor tone
Explanation: **Explanation:** The correct answer is **B. Respiratory stimulant.** **Mechanism of Action:** Ammonia (often administered as "smelling salts" or aromatic spirits of ammonia) acts as a **reflex respiratory stimulant**. When inhaled, the pungent ammonia gas causes acute irritation of the sensory nerve endings (primarily the trigeminal nerve) in the nasal mucosa and upper respiratory tract. This irritation triggers a rapid, reflex stimulation of the **medullary respiratory center**, leading to an increased rate and depth of breathing. This surge in ventilation helps increase oxygenation and can facilitate the restoration of consciousness in patients experiencing vasovagal syncope. **Analysis of Incorrect Options:** * **A & D (Vasomotor stimulant/Inhibitor):** While the sympathetic surge following the irritation may cause a transient rise in blood pressure, ammonia does not have a direct or primary pharmacological action on the vasomotor center or vascular smooth muscle. * **C (Vagal stimulant):** Vagal stimulation would cause bradycardia and a further drop in blood pressure, which would worsen syncope. Ammonia aims to counteract the overactive vagal tone seen in common fainting. **NEET-PG High-Yield Pearls:** * **Clinical Use:** Ammonia is used for "simple fainting" (vasovagal syncope) but is contraindicated if a head, neck, or back injury is suspected, as the reflex "jerking" of the head away from the inhalant could worsen spinal injuries. * **Classification:** It is categorized as a **reflex stimulant** (acting via peripheral irritation) rather than a direct stimulant (like Caffeine or Theophylline which act directly on the CNS). * **Differential:** Do not confuse this with the treatment of hepatic encephalopathy, where the goal is to *lower* systemic ammonia levels.
Question 9: A 70-year-old man was administered penicillin intravenously. Within 5 minutes, he developed generalized urticaria, swelling of lips, hypotension, and bronchospasm. What is the first choice of treatment?
- A. Chlorpheniramine injection
- B. Epinephrine injection (Correct Answer)
- C. High dose hydrocortisone tablet
- D. Nebulized salbutamol
Explanation: ### Explanation The patient is presenting with **Anaphylaxis**, a Type I hypersensitivity reaction characterized by multisystem involvement (skin, respiratory, and cardiovascular). In this emergency, **Epinephrine (Adrenaline)** is the drug of choice and the first-line treatment. **Why Epinephrine is the Correct Choice:** Epinephrine acts as a **physiological antagonist** to histamine and other mediators released during anaphylaxis. It works through multiple receptors: * **$\alpha_1$ receptors:** Cause vasoconstriction, which increases blood pressure and reduces mucosal edema (laryngeal edema). * **$\beta_1$ receptors:** Increase cardiac output (positive inotropic and chronotropic effects). * **$\beta_2$ receptors:** Cause potent bronchodilation and inhibit further mediator release from mast cells and basophils. **Analysis of Incorrect Options:** * **A. Chlorpheniramine:** An H1-antihistamine. It helps with urticaria and itching but does not treat life-threatening hypotension or airway obstruction. It has a slow onset of action. * **C. Hydrocortisone:** Corticosteroids take 4–6 hours to work. They are used to prevent "biphasic reactions" (delayed recurrence) but are never the primary treatment for acute anaphylaxis. * **D. Nebulized Salbutamol:** While it helps with bronchospasm, it does not address laryngeal edema or circulatory collapse (hypotension). **High-Yield Clinical Pearls for NEET-PG:** * **Route of Choice:** Intramuscular (IM) in the anterolateral thigh (vastus lateralis) is preferred over SC or IV in initial management due to rapid absorption and safety. * **Dose:** 0.5 mg (1:1000 concentration) for adults; 0.01 mg/kg for children. * **Mechanism:** Physiological antagonism (different receptors, opposite effects). * **Drug of choice for Anaphylactic Shock:** Epinephrine. * **Drug of choice for Cardiogenic Shock:** Dobutamine. * **Drug of choice for Septic Shock:** Norepinephrine.
Question 10: A patient develops facial puffiness, rash, hypotension, and breathing difficulty after the administration of antibiotics. What is the immediate treatment?
- A. 0.5 ml of adrenaline IM (1:1000 dilution) (Correct Answer)
- B. 1 ml of adrenaline IV (1:10,000 dilution)
- C. 1 ml of adrenaline IV (1:10,000 dilution)
- D. 0.5 ml of adrenaline IV (1:1000 dilution)
Explanation: ### Explanation **Diagnosis:** The patient is presenting with **Anaphylaxis**, a Type I hypersensitivity reaction characterized by angioedema (facial puffiness), urticaria (rash), bronchospasm (breathing difficulty), and distributive shock (hypotension). **Why Option A is Correct:** Adrenaline (Epinephrine) is the drug of choice for anaphylaxis. It acts as a physiological antagonist to histamine. Its **α1-agonist** effects increase peripheral vascular resistance to treat hypotension, while its **β2-agonist** effects cause bronchodilation and inhibit further mast cell degranulation. * **Route:** The **Intramuscular (IM)** route in the anterolateral thigh is preferred because it achieves peak plasma concentrations faster and has a superior safety profile compared to the IV route. * **Dose/Dilution:** The standard adult dose is **0.5 mg (0.5 ml)** of a **1:1000** concentration. **Why Other Options are Incorrect:** * **Options B & C:** IV adrenaline (1:10,000) is reserved for patients with profound hypotension or cardiac arrest who have failed to respond to multiple IM injections. Giving IV adrenaline as a first-line treatment in a conscious patient carries a high risk of fatal arrhythmias and severe hypertension. * **Option D:** Giving a **1:1000** dilution via the **IV route** is a critical medical error. This concentration is ten times more potent than the standard IV preparation and can cause immediate myocardial infarction or intracranial hemorrhage. **High-Yield Clinical Pearls for NEET-PG:** * **Site of Injection:** Vastus lateralis (lateral thigh) is preferred over the deltoid due to better absorption. * **Pediatric Dose:** 0.01 mg/kg (up to 0.3 mg) of 1:1000 IM. * **Second-line drugs:** Hydrocortisone and Pheniramine are used to prevent "biphasic reactions" but are **never** the first-line treatment. * **Glucagon:** The drug of choice for anaphylaxis in patients taking **Beta-blockers** who are refractory to adrenaline.
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