Emergency Pharmacology — MCQs

A female patient presents to the emergency department with severe restlessness, palpitations, and tremors. She is a known case of bronchial asthma. On examination, the neck looks swollen. Blood pressure is elevated, and tachycardia is noted. ECG shows atrial fibrillation. Which of the following drugs is used for immediate management in this patient?

Q76

What is the recommended dose of diphtheria antitoxin for severe cases of diphtheria?

Q77

What is the drug of choice (DOC) for a scorpion sting bite?

Q78

What is the progestogen of choice in emergency contraception?

Q79

What is the drug of choice (DOC) for an acute attack of Hereditary Angioedema?

Q80

What is the best method for treating methanol poisoning?

Emergency Pharmacology Indian Medical PG Practice Questions and MCQs

Question 71: Oximes are ineffective in which of the following poisonings?

A. Dhatura poisoning
B. Carbamate poisoning
C. Amanita phylloides poisoning (Correct Answer)
D. Organophosphate poisoning

Explanation: ***Amanita phalloides poisoning*** - **Amanita phalloides** (Death Cap mushroom) poisoning causes **hepatotoxicity** and **nephrotoxicity** due to amatoxins and phallotoxins. - The mechanism is **completely unrelated to cholinergic pathways** - toxins inhibit RNA polymerase II causing cellular damage. - **Oximes are completely ineffective** as they only reactivate acetylcholinesterase and have no role against non-cholinergic toxins. - This is the **best answer** as oximes have absolutely no therapeutic role in this poisoning. *Organophosphate poisoning* - **Organophosphates** irreversibly inhibit **acetylcholinesterase**, leading to cholinergic crisis. - **Oximes (pralidoxime/2-PAM) are highly effective** - they reactivate the phosphorylated acetylcholinesterase and are standard treatment alongside atropine. - Must be given early (within 24-48 hours) before "aging" of the enzyme-inhibitor complex occurs. *Carbamate poisoning* - **Carbamates** cause **reversible** inhibition of acetylcholinesterase with spontaneous reactivation. - **Oximes are generally not recommended** as the enzyme reactivates spontaneously and oximes may worsen toxicity in some carbamate poisonings (especially carbaryl). - Atropine alone is usually sufficient treatment. *Dhatura poisoning* - **Dhatura** contains **anticholinergic** alkaloids (atropine, scopolamine, hyoscyamine). - While oximes are ineffective here (anticholinergic not cholinergic toxidrome), this poisoning still involves the cholinergic system. - Treatment is physostigmine (cholinesterase inhibitor), not oximes which work on cholinergic excess, not cholinergic blockade.

Question 72: Maximum dose of rTPA in acute ischaemic stroke is

A. 60 mg
B. 90 mg (Correct Answer)
C. 100 mg
D. 120 mg

Explanation: ***90 mg*** - The standard dose of **recombinant tissue plasminogen activator (rTPA)**, also known as **alteplase**, for acute ischemic stroke is **0.9 mg/kg** with a maximum dose of 90 mg. - This dose is given as a 10% bolus over 1 minute, followed by the remaining 90% infused over 60 minutes. *60 mg* - A 60 mg dose would be suboptimal for most adult patients, as it falls significantly below the recommended 0.9 mg/kg standard dosing, potentially leading to **insufficient thrombolysis**. - While a maximum of 90 mg is set, a 60 mg dose is not typically the target dose unless the patient's weight is exceptionally low, which is not stated here. *100 mg* - A 100 mg dose **exceeds the maximum recommended dose** of 90 mg for rTPA in acute ischemic stroke, regardless of the patient's weight. - Administering a dose higher than 90 mg increases the risk of **intracranial hemorrhage** and other bleeding complications without providing additional therapeutic benefit. *120 mg* - A 120 mg dose is significantly **higher than the maximum recommended dose** for rTPA in acute ischemic stroke (90 mg). - Such an excessive dose would greatly increase the risk of serious adverse events, particularly **symptomatic intracranial hemorrhage**, and is not medically indicated.

Question 73: Dose of rabies immunoglobulin for post-exposure prophylaxis?

A. 40 IU/kg
B. 10 IU/kg
C. 20 IU/kg (Correct Answer)
D. 30 IU/kg

Explanation: ***20 IU/kg*** - The recommended dose for **rabies immunoglobulin (RIG)** for post-exposure prophylaxis is **20 IU/kg** of body weight. - This dose is crucial for providing immediate passive immunity primarily by infiltrating around the wound, while the active immune response to the vaccine develops. *10 IU/kg* - This dose is **insufficient** to provide adequate passive immunity against rabies after exposure. - Using a lower dose could compromise the effectiveness of post-exposure prophylaxis. *30 IU/kg* - Administering **30 IU/kg** is a higher dose than recommended and does not provide additional benefit. - Such an excessive dose could lead to **unnecessary cost and potential side effects**, without improving protection. *40 IU/kg* - This dose is **significantly higher** than the recommended amount for rabies immunoglobulin. - Overdosing can lead to side effects and is **wasteful of resources**, particularly with a biologic product like RIG.

Question 74: A patient comes to the casualty with organophosphate poisoning. He was started on atropine infusion and pralidoxime. After 2 hours, the patient had a sudden rise in temperature. What is the most likely cause of the fever?

A. Side effect of pralidoxime.
B. Result of organophosphate poisoning.
C. Unrelated or unknown cause.
D. Fever due to atropine toxicity. (Correct Answer)

Explanation: ***Fever due to atropine toxicity.*** - **Atropine** blocks muscarinic receptors, leading to inhibition of **sweat glands** and subsequent rise in body temperature (hyperthermia), especially with high doses or prolonged infusion. - Given the patient is receiving an **atropine infusion** and developed fever, **atropine toxicity** is a primary concern. *Side effect of pralidoxime.* - While pralidoxime can cause side effects like dizziness, blurred vision, or tachycardia, **fever is not a typical side effect** of pralidoxime. - Pralidoxime works by **regenerating acetylcholinesterase** [2, 3] and does not directly interfere with thermoregulation in a way that would cause fever. *Result of organophosphate poisoning.* - **Organophosphate poisoning** typically causes **hypothermia** due to excessive cholinergic stimulation leading to peripheral vasodilation and increased sweating [1]. - **Fever** is not a direct result of the acute phase of organophosphate poisoning itself, but rather a complication of treatment or other factors. *Unrelated or unknown cause.* - While possible, it's less likely to be "unrelated or unknown" when a clear pharmacological explanation (**atropine toxicity**) exists for fever in the context of the patient's treatment. - It would be important to first rule out known causes related to the ongoing treatment before attributing it to an unknown cause.

Question 75: A female patient presents to the emergency department with severe restlessness, palpitations, and tremors. She is a known case of bronchial asthma. On examination, the neck looks swollen. Blood pressure is elevated, and tachycardia is noted. ECG shows atrial fibrillation. Which of the following drugs is used for immediate management in this patient?

A. Esmolol (Correct Answer)
B. Diltiazem
C. Propranolol
D. Propylthiouracil

Explanation: ***Esmolol*** - The patient presents with **thyroid storm** (severe restlessness, palpitations, tremors, swollen neck, elevated BP, tachycardia, atrial fibrillation), which is a **life-threatening endocrine emergency** requiring immediate intervention. - **Beta-blockers are first-line therapy** for thyroid storm as they: (1) control cardiovascular manifestations, (2) block peripheral effects of thyroid hormones, and (3) inhibit peripheral conversion of T4 to T3. - **Esmolol** is the **optimal choice** in this asthmatic patient because it is a **cardioselective β1-blocker** with an **ultra-short half-life (9 minutes)**, allowing rapid titration and immediate discontinuation if bronchospasm occurs. - Its cardioselectivity minimizes (though does not eliminate) the risk of bronchospasm, and close monitoring makes it safer than avoiding beta-blockade entirely in this life-threatening condition. *Propranolol* - **Propranolol** is highly effective in thyroid storm and is traditionally considered first-line therapy. - However, it is a **non-selective beta-blocker** that blocks both β1 (cardiac) and β2 (bronchial) receptors, making it **relatively contraindicated in asthma** due to significant risk of severe bronchospasm. - In this patient with known asthma, esmolol is preferred over propranolol. *Diltiazem* - **Diltiazem** is a **calcium channel blocker** useful for rate control in atrial fibrillation and is safe in asthmatic patients. - However, in **thyroid storm**, it does NOT address the underlying pathophysiology: it does not block peripheral thyroid hormone effects or inhibit T4 to T3 conversion. - While it may control heart rate, **beta-blockade is essential** for managing the acute thyroid storm crisis, making diltiazem inadequate as monotherapy for immediate management. *Propylthiouracil* - **Propylthiouracil (PTU)** is an **antithyroid drug** that inhibits thyroid hormone synthesis and blocks peripheral conversion of T4 to T3. - While PTU is crucial in treating the **underlying hyperthyroidism** in thyroid storm, it has a **delayed onset of action** (hours to days) and does not provide immediate relief of acute cardiovascular manifestations. - It must be combined with beta-blockers for comprehensive thyroid storm management.

Question 76: What is the recommended dose of diphtheria antitoxin for severe cases of diphtheria?

A. 20,000 to 40,000 IU
B. 60,000 to 80,000 IU
C. 40,000 to 60,000 IU
D. 80,000 to 120,000 IU (Correct Answer)

Explanation: ***80,000 to 120,000 IU*** - For **severe cases** of diphtheria, especially those with extensive pseudomembrane formation (involving larynx, extensive pharyngeal/tonsillar involvement, or "bull neck" appearance) or systemic toxicity, a high dose of **diphtheria antitoxin (DAT)** ranging from **80,000 to 120,000 IU** is recommended. - This high dose is necessary to neutralize the large amount of circulating toxin and prevent life-threatening complications such as **myocarditis**, **neuropathy**, and **respiratory obstruction**. - The antitoxin should be administered as early as possible, ideally after a **test dose** to check for hypersensitivity [1], and is given **intravenously** for rapid effect in severe cases. *20,000 to 40,000 IU* - This dose range is typically reserved for **mild cases** of pharyngeal or tonsillar diphtheria without extensive membrane formation or systemic involvement. - Administering this dose in a severe case would be **insufficient** to neutralize the toxin load, potentially leading to fatal complications. *40,000 to 60,000 IU* - This is the recommended range for **moderate cases** of nasopharyngeal or more extensive pharyngeal diphtheria. - While higher than mild case dosing, it remains inadequate for severe presentations with extensive membrane or systemic toxicity. *60,000 to 80,000 IU* - This intermediate dose might be considered for **moderately severe cases**, but falls short of the recommended dosing for truly severe diphtheria. - Severe cases with laryngeal involvement, bull neck, or signs of toxemia require higher doses to ensure adequate toxin neutralization.

Question 77: What is the drug of choice (DOC) for a scorpion sting bite?

A. EDTA
B. Neostigmine
C. N-acetylcysteine
D. Prazosin (Correct Answer)

Explanation: ***Prazosin*** - **Prazosin** is an **alpha-1 adrenergic antagonist** that effectively counteracts the symptoms of scorpion envenomation, particularly **autonomic hyperactivity** like hypertension and tachycardia. - It works by blocking the effects of norepinephrine released by the scorpion venom, helping to stabilize vital signs and reduce cardiovascular complications. *EDTA* - **EDTA (ethylenediaminetetraacetic acid)** is a **chelating agent** primarily used to treat **heavy metal poisoning**, such as lead or mercury. - It binds to metal ions, forming a stable complex that can then be excreted from the body; it has no role in scorpion envenomation. *Neostigmine* - **Neostigmine** is an **acetylcholinesterase inhibitor** used to treat conditions like myasthenia gravis or to reverse the effects of neuromuscular blocking agents. - It increases acetylcholine levels at the neuromuscular junction; it is not indicated for the management of scorpion stings. *N-acetylcysteine* - **N-acetylcysteine (NAC)** is primarily used as an **antidote for acetaminophen overdose** and as a mucolytic agent in respiratory conditions. - It replenishes glutathione stores, helping to detoxify harmful metabolites; it has no direct role in treating scorpion venom effects.

Question 78: What is the progestogen of choice in emergency contraception?

A. Norethisterone
B. Medroxyprogesterone
C. Oxytocin
D. Levonorgestrel (Correct Answer)

Explanation: ***Correct Option: Levonorgestrel*** - **Levonorgestrel** is the **progestogen of choice** for **emergency contraception** (Plan B, morning-after pill) - It works by **inhibiting or delaying ovulation**, preventing fertilization - Also alters **cervical mucus** to prevent sperm penetration and may affect endometrial receptivity - WHO-recommended as **single dose (1.5 mg)** or two doses (0.75 mg each, 12 hours apart) - Most effective when taken **within 72 hours** of unprotected intercourse, preferably within 24 hours *Incorrect Option: Norethisterone* - **Norethisterone** is a progestogen used in **oral contraceptive pills** and for managing gynecological conditions (menorrhagia, endometriosis, dysmenorrhea) - While it has progestational effects, it is **not the first-line choice** for emergency contraception - Less effective than levonorgestrel for post-coital contraception *Incorrect Option: Medroxyprogesterone* - **Medroxyprogesterone acetate** is used as a **long-acting depot contraceptive** (Depo-Provera injection every 3 months) - Also used for hormone replacement therapy and treating endometrial hyperplasia - **Not suitable for emergency contraception** due to its formulation and mechanism of action *Incorrect Option: Oxytocin* - **Oxytocin** is a posterior pituitary hormone that causes **uterine contractions** during labor and **milk ejection** during breastfeeding - It has **no role in contraception** or preventing pregnancy - Used therapeutically for labor induction, postpartum hemorrhage prevention, and augmentation of labor

Question 79: What is the drug of choice (DOC) for an acute attack of Hereditary Angioedema?

A. Danazol
B. Icatibant
C. Methylprednisolone
D. C1 inhibitor concentrate (Correct Answer)

Explanation: ***C1 inhibitor concentrate*** - **C1 esterase inhibitor (C1-INH)** concentrate is the **first-line therapy** for acute hereditary angioedema (HAE) attacks. - It directly replaces the deficient C1-INH protein, which helps to regulate the **bradykinin pathway** and prevent further swelling. *Danazol* - **Danazol** is an attenuated androgen used for **long-term prophylaxis** of HAE to increase C1-INH levels, not for acute attacks. - Its onset of action is too slow to effectively treat an acute and potentially life-threatening angioedema episode. *Icatibant* - **Icatibant** is a **bradykinin B2 receptor antagonist** that can be used for acute HAE attacks, typically when C1-INH concentrate is unavailable or ineffective. - While effective, C1-INH concentrate is generally considered the drug of choice due to its direct replacement of the deficient protein. *Methylprednisolone* - **Methylprednisolone** (a corticosteroid) is **ineffective** in treating acute HAE attacks because it does not target the underlying bradykinin-mediated pathophysiology. - HAE swelling is not mediated by mast cells or histamine release, making corticosteroids and antihistamines unhelpful.

Question 80: What is the best method for treating methanol poisoning?

A. Calcium gluconate
B. BAL
C. Fomepizole (Correct Answer)
D. Deferoxamine

Explanation: ***Fomepizole*** - **Fomepizole** (Antizol) is a potent inhibitor of **alcohol dehydrogenase**, the enzyme responsible for metabolizing methanol into toxic metabolites like formic acid [1]. - By inhibiting this enzyme, fomepizole prevents the formation of these harmful metabolites, thus halting the progression of methanol toxicity and reducing mortality [1]. - It is the **gold standard** antidote for methanol poisoning. *Calcium gluconate* - **Calcium gluconate** is primarily used to treat **hypocalcemia** and magnesium toxicity. - It has no role in the direct treatment or detoxification of methanol poisoning. *Deferoxamine* - **Deferoxamine** is a **chelating agent** used to treat **iron toxicity** by binding to iron and facilitating its excretion [3]. - It is not effective for methanol poisoning as it does not interact with methanol or its toxic metabolites. *BAL* - **BAL** (British Anti-Lewisite, dimercaprol) is a chelating agent primarily used for poisoning by **heavy metals** such as arsenic, mercury, and gold [2]. - It has no therapeutic role in methanol poisoning, which involves a different toxicological mechanism.

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