Emergency Pharmacology — MCQs

Emergency Pharmacology Indian Medical PG Practice Questions and MCQs

Question 61: What is the primary treatment approach for organophosphate poisoning?

A. Activated charcoal
B. Sodium bicarbonate
C. Atropine and pralidoxime (Correct Answer)
D. Dialysis

Explanation: ***Atropine and pralidoxime*** - **Atropine** is primarily used to block the muscarinic effects of **acetylcholine** excess, such as **bradycardia**, **bronchospasm**, and excessive secretions. - **Pralidoxime** (2-PAM) is an **acetylcholinesterase reactivator** that can reverse both muscarinic and nicotinic effects by detaching the organophosphate from the enzyme. *Activated charcoal* - While generally used for decontamination in many poisonings, **activated charcoal** is primarily effective in the early stages (within 1-2 hours) after ingestion for substances that undergo enterohepatic recirculation. - Its role in moderate to severe **organophosphate poisoning** is limited once systemic absorption has occurred. *Sodium bicarbonate* - **Sodium bicarbonate** is primarily used to treat **metabolic acidosis** or to alkalinize urine in certain drug overdoses to enhance excretion. - It does not directly counteract the pharmacological effects of **organophosphate poisoning**. *Dialysis* - **Dialysis** is a procedure used to remove toxins from the blood in cases of **renal failure** or poisoning by substances with specific characteristics (e.g., low molecular weight, low protein binding). - Most **organophosphates** are not effectively removed by dialysis due to their lipid solubility and rapid distribution into tissues.

Question 62: In organophosphate (OP) poisoning, which treatment is prioritized?

A. Atropine (Correct Answer)
B. Activated charcoal
C. Gastric lavage
D. Pralidoxime (2-PAM)

Explanation: ***Atropine*** - **Atropine** is the **FIRST-LINE and priority treatment** for organophosphate (OP) poisoning. - It competitively blocks **muscarinic receptors**, rapidly reversing life-threatening symptoms: **bronchospasm**, **bronchorrhea**, **bradycardia**, **salivation**, and **miosis**. - Administered in **high and repeated doses** until **atropinization** is achieved (dry skin, tachycardia, mydriasis). - **Critical for immediate stabilization** and can be life-saving within minutes of administration. *Pralidoxime (2-PAM)* - **Pralidoxime** is an important **adjunctive therapy** given after or alongside atropine. - It is a **cholinesterase reactivator** that detaches organophosphate from acetylcholinesterase, restoring enzyme function. - Most effective when given **early** (within 24-48 hours) before **aging** of the enzyme-organophosphate complex occurs. - Addresses **nicotinic effects** (muscle weakness, fasciculations) that atropine does not treat, but is not the priority in acute management. *Activated charcoal* - Can be used for **gastrointestinal decontamination** if ingestion occurred within 1-2 hours. - **Not a priority** compared to specific antidotes, and effectiveness is limited by rapid absorption of organophosphates. *Gastric lavage* - Involves flushing the stomach to remove ingested toxins. - **Rarely recommended** in modern practice due to risk of complications (aspiration, esophageal perforation). - Not appropriate in OP poisoning unless the patient is intubated and lavage can be performed safely within 1 hour of ingestion.

Question 63: Which drug is used to treat cyanide poisoning by converting cyanide to a less toxic compound?

A. Pralidoxime
B. Atropine
C. Sodium thiosulfate (Correct Answer)
D. Deferoxamine

Explanation: ***Sodium thiosulfate*** - **Sodium thiosulfate** acts as a sulfur donor, which allows the enzyme **rhodanase** to convert **cyanide** into the less toxic compound **thiocyanate**. - This reaction aids in the detoxification and subsequent excretion of cyanide from the body. *Pralidoxime* - **Pralidoxime** is primarily used to treat poisoning by **organophosphates** by reactivating **acetylcholinesterase**. - It has no direct role in the detoxification pathway of cyanide. *Atropine* - **Atropine** is an anticholinergic agent used to counteract the muscarinic effects of **organophosphate poisoning**. - It does not have any mechanism of action that deactivates or converts cyanide. *Deferoxamine* - **Deferoxamine** is a **chelating agent** primarily used to treat **iron overload** or **iron poisoning**. - It binds to iron to form a stable complex that can be excreted, and has no efficacy in cyanide poisoning.

Question 64: In anaphylaxis, adrenaline is the drug of choice. What is its mechanism of action in this emergency?

A. Activate histamine receptors
B. Block muscarinic receptors
C. Stimulate adrenergic receptors (Correct Answer)
D. Inhibit prostaglandin synthesis

Explanation: ***Stimulate adrenergic receptors*** - **Adrenaline (epinephrine)** is a potent agonist of **alpha-1, beta-1, and beta-2 adrenergic receptors**, leading to widespread physiological effects that counteract anaphylaxis. - By stimulating these receptors, adrenaline causes **vasoconstriction** (alpha-1), increases **heart rate and contractility** (beta-1), and induces **bronchodilation** (beta-2). - These combined actions rapidly reverse the life-threatening manifestations of anaphylaxis: **hypotension, bronchospasm, and angioedema**. *Activate histamine receptors* - Histamine is a primary mediator released during anaphylaxis, causing vasodilation, increased vascular permeability, and bronchoconstriction. - Adrenaline does not activate histamine receptors; rather, it **antagonizes the effects of histamine** through its adrenergic actions. *Block muscarinic receptors* - Blocking muscarinic receptors would lead to effects like bronchodilation and increased heart rate, similar to some effects of adrenaline. - However, adrenaline primarily acts on **adrenergic receptors**, not muscarinic receptors, and its broader effects in anaphylaxis are not due to muscarinic blockade. *Inhibit prostaglandin synthesis* - Inhibition of prostaglandin synthesis is the primary mechanism of action for **NSAIDs** (Non-Steroidal Anti-Inflammatory Drugs). - While prostaglandins can play a role in inflammatory responses, they are not the primary target for acute management of anaphylaxis, and adrenaline does not act through this mechanism.

Question 65: A young man presents with pinpoint pupils and respiratory depression after ingesting an unknown substance. Which substance is likely responsible?

A. Opioids (Correct Answer)
B. Alcohol
C. Benzodiazepines
D. Amphetamines

Explanation: ***Opioids*** - **Pinpoint pupils** (miosis) and **respiratory depression** are hallmark signs of opioid intoxication due to their action on mu-opioid receptors in the central nervous system. - Opioids also commonly induce **CNS depression**, leading to decreased consciousness and reduced respiratory drive. *Alcohol* - While alcohol can cause **respiratory depression** at high doses, it typically causes **dilated pupils** (mydriasis) rather than pinpoint pupils. - Alcohol intoxication is also characterized by **ataxia**, **slurred speech**, and **nystagmus**. *Benzodiazepines* - Benzodiazepines primarily cause **CNS depression** and can lead to **respiratory depression**, especially when combined with other depressants like alcohol. - However, they generally do **not cause pinpoint pupils**; pupils are usually normal or slightly dilated. *Amphetamines* - Amphetamine overdose leads to a **sympathomimetic toxidrome**, characterized by **mydriasis** (dilated pupils), **tachycardia**, **hypertension**, and **agitation**. - They cause **respiratory stimulation** initially, not depression, although severe cases can lead to respiratory compromise due to seizures or hyperthermia.

Question 66: Which drug is used to counteract opioid overdose because of its high affinity for opioid receptors?

A. Naloxone (Correct Answer)
B. Buprenorphine
C. Methadone
D. Naltrexone

Explanation: ***Naloxone*** - **Naloxone** is an **opioid antagonist** with a high affinity for opioid receptors, making it effective in rapidly reversing the effects of an opioid overdose [1]. - Its mechanism of action involves competitively binding to and blocking opioid receptors, thereby displacing opioids and reversing respiratory depression and other overdose symptoms [3]. *Naltrexone* - **Naltrexone** is also an **opioid antagonist**, but it has a longer duration of action and is primarily used for preventing relapse in opioid-dependent individuals and treating alcohol dependence [1][3]. - While it blocks opioid effects, its slower onset and longer action make it less suitable for emergency overdose reversal compared to naloxone. *Buprenorphine* - **Buprenorphine** is a **partial opioid agonist**, meaning it produces some opioid effects while also blocking other opioids from binding to receptors [4]. - It is used in medication-assisted treatment for opioid use disorder to reduce cravings and withdrawal symptoms, but it is not used to reverse an acute opioid overdose. *Methadone* - **Methadone** is a **long-acting full opioid agonist** used primarily for pain management and in medication-assisted treatment for opioid use disorder [2]. - It significantly occupies opioid receptors and can prevent other opioids from having an effect, but it is an opioid itself and would exacerbate, not reverse, an opioid overdose [2].

Question 67: What is the recommended dose of diphtheria antitoxin for adults?

A. 1000 to 2000 IU
B. 20000 to 50000 IU (Correct Answer)
C. 10000 to 20000 IU
D. None of the options

Explanation: ***20000 to 50000 IU*** - For adults with **diphtheria**, the recommended dose of **diphtheria antitoxin (DAT)** in the range of 20,000 to 50,000 IU is appropriate for **pharyngeal or laryngeal diphtheria** of moderate severity (typically disease present for 48-72 hours). - This dosage aims to neutralize the **diphtheria toxin** circulating in the bloodstream and prevent further tissue damage. - **Note:** More severe or extensive disease (>3 days duration or with bull neck) may require higher doses (80,000-120,000 IU). *1000 to 2000 IU* - This dosage is **too low** for therapeutic treatment of diphtheria in adults. - Such a low dose would be insufficient to neutralize the substantial amount of **toxin** produced during an active infection, regardless of disease severity. *10000 to 20000 IU* - This dose is **suboptimal** for most forms of diphtheria in adults. - Even for **mild cutaneous diphtheria**, doses typically start at 20,000 IU or higher. - For respiratory diphtheria, this range would be inadequate to effectively counteract the toxin. *None of the options* - This is incorrect because **20,000 to 50,000 IU** is a recognized and recommended range for diphtheria antitoxin in adult treatment of moderate pharyngeal/laryngeal disease. - Diphtheria antitoxin is a crucial and **specific treatment** for diphtheria, and evidence-based dosage ranges exist based on disease severity and location.

Question 68: Gastric lavage is not contraindicated after ingestion of which of the following substances?

A. H2SO4
B. Nitric acid
C. Carbolic acid
D. Paracetamol overdose (Correct Answer)

Explanation: ***Paracetamol overdose*** - Gastric lavage is a recognized method for early removal of **unabsorbed paracetamol** from the stomach, especially if performed within the first hour of ingestion. - It helps reduce the total body burden of the drug, thus theoretically minimizing the risk of **hepatotoxicity**. *H2SO4* - Ingestion of strong acids like **sulfuric acid** (H2SO4) causes corrosive injury to the esophagus and stomach. - Lavage could lead to further **perforation** of damaged tissues or aspiration of the acid. *Carbolic acid* - **Carbolic acid** (phenol) is a corrosive substance that can cause severe chemical burns to the mucous membranes. - Gastric lavage is contraindicated due to the risk of **esophageal perforation** and potential for further absorption. *Nitric acid* - Similar to other strong acids, **nitric acid** causes significant corrosive damage upon ingestion. - Performing gastric lavage in such cases increases the risk of **perforation, bleeding**, and aspiration, intensifying the injury.

Question 69: What is the typical initial dose of diazepam when starting treatment for alcohol withdrawal symptoms?

A. 80 mg
B. 20 mg (Correct Answer)
C. 40 mg
D. 50 mg

Explanation: ***20 mg*** - The typical initial dose of diazepam for alcohol withdrawal is **10-20 mg orally**, with 20 mg being the standard starting dose for **moderate to severe withdrawal symptoms**. - This dosing is based on **CIWA-Ar (Clinical Institute Withdrawal Assessment for Alcohol) protocol**, the most widely used symptom-triggered regimen for alcohol withdrawal management. - The dose can be **repeated every 1-2 hours** based on symptom severity (tremors, anxiety, agitation, autonomic hyperactivity) to prevent progression to **seizures or delirium tremens**. - This approach balances efficacy with safety, minimizing risks of over-sedation and respiratory depression. *40 mg* - An initial dose of **40 mg** is above standard evidence-based protocols and not routinely recommended as a starting dose. - While some severe cases may eventually require cumulative doses in this range over several hours, starting with 40 mg carries **unnecessary risk of over-sedation** and is not consistent with **CIWA-Ar or other established guidelines**. - Standard practice is to start lower (10-20 mg) and titrate upward based on clinical response. *50 mg* - An initial dose of **50 mg** is excessive and well above recommended starting doses, significantly increasing the risk of **respiratory depression, hypotension, and over-sedation**. - Such high doses would require intensive monitoring and are not part of standard initial management protocols. *80 mg* - An initial dose of **80 mg of diazepam** is dangerously high and carries severe risk of **over-sedation, respiratory arrest, and cardiovascular collapse**. - This dose far exceeds any standard initial dosing protocol and would only be considered as a **cumulative dose over many hours** in refractory cases under intensive care monitoring, never as an initial single dose.

Question 70: Which of the following statements about epinephrine is false?

A. It improves coronary perfusion pressure and myocardial blood flow
B. Routine use of high dose epinephrine during resuscitation is indicated (Correct Answer)
C. Has potent alpha and beta stimulating properties
D. Increases cerebral blood flow during CPR

Explanation: ***Routine use of high dose epinephrine during resuscitation is indicated*** - Current **ACLS guidelines** do not recommend routine use of high-dose epinephrine during cardiac arrest resuscitation. - While epinephrine is crucial during cardiac arrest, higher doses have not shown improved survival and may increase the risk of **post-resuscitation myocardial dysfunction**. *Has potent alpha and beta stimulating properties* - Epinephrine is a potent **vasoconstrictor** (alpha-1 agonism) and **bronchodilator** with positive inotropic and chronotropic effects (beta-1 and beta-2 agonism). - Its diverse receptor activity makes it effective in treating conditions like **anaphylaxis** and cardiac arrest. *It improves coronary perfusion pressure and myocardial blood flow* - Through its **alpha-1 adrenergic effects**, epinephrine causes peripheral vasoconstriction, increasing **diastolic blood pressure** and thus improving coronary perfusion pressure. - This enhanced perfusion is critical for maintaining myocardial oxygen supply during cardiac arrest. *Increases cerebral blood flow during CPR* - The alpha-adrenergic effects of epinephrine lead to **increased peripheral vascular resistance**, which elevates global perfusion pressure during CPR. - This rise in pressure helps to improve **cerebral blood flow** and oxygen delivery to the brain, which is vital for neurological outcomes.

Practice by Chapter

Management of Anaphylaxis

Practice Questions

Drugs in Cardiac Arrest

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Status Epilepticus Management

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Acute Stroke Therapeutics

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Toxicological Emergencies

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Antidotes in Emergency Medicine

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Pain Management in Emergency

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Sedation and Paralysis in Emergency

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Drugs in Traumatic Emergencies

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Thrombolysis in Emergency Settings

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