Emergency Pharmacology — MCQs

Emergency Pharmacology Indian Medical PG Practice Questions and MCQs

Question 41: All of the following statements about pralidoxime in organophosphate poisoning are true except:-

A. It does not cross blood brain barrier
B. It should be started after 24 hours of poisoning (Correct Answer)
C. Reactivates the AChE enzyme
D. It is given intravenously

Explanation: ***It should be started after 24 hours of poisoning*** - **Pralidoxime (2-PAM)** is most effective when administered **early** in organophosphate poisoning, ideally within minutes to a few hours of exposure. - Delaying administration beyond **24-48 hours** significantly reduces its efficacy because the bond between the organophosphate and **acetylcholinesterase (AChE)** becomes **irreversible** (a process called "aging"). *It does not cross blood brain barrier* - **Pralidoxime** is a **quaternary ammonium compound**, which makes it highly polar and unable to readily cross the **blood-brain barrier**. - Therefore, it primarily reactivates **acetylcholinesterase** in the **peripheral nervous system** but has limited effect on central nervous system symptoms. *Reactivates the AChE enzyme* - **Pralidoxime** works by **reactivating the acetylcholinesterase enzyme** that has been inhibited by organophosphates. - It does this by binding to the organophosphate molecule, thereby freeing the active site of the **AChE enzyme** to metabolize **acetylcholine** again. *It is given intravenously* - **Pralidoxime** is typically administered via **intravenous (IV) infusion** to achieve rapid and sustained therapeutic concentrations. - Due to its poor oral absorption, oral administration is not a suitable route for treating acute organophosphate poisoning.

Question 42: Which of these is the best for management of methanol poisoning?

A. Fomepizole (Correct Answer)
B. Naltrexone
C. Disulfiram
D. Acamprosate

Explanation: ***Fomepizole*** - **Fomepizole** is a competitive inhibitor of **alcohol dehydrogenase**, the enzyme responsible for metabolizing methanol into toxic metabolites like formic acid. - By inhibiting this enzyme, it prevents the formation of these toxic metabolites, thereby reducing organ damage and metabolic acidosis in methanol poisoning. *Naltrexone* - **Naltrexone** is an **opioid receptor antagonist** used in the treatment of alcohol and opioid dependence. - It does not have any direct action on the metabolism of methanol or its toxic byproducts. *Disulfiram* - **Disulfiram** inhibits **aldehyde dehydrogenase**, leading to an unpleasant reaction when alcohol is consumed (flushing, nausea, vomiting). - It is used for alcohol cessation and has no role in the management of methanol poisoning. *Acamprosate* - **Acamprosate** is a medication used to reduce alcohol cravings in individuals recovering from alcohol dependence, possibly by modulating **glutamate neurotransmission**. - It does not directly affect the metabolism of methanol or mitigate its toxic effects.

Question 43: Drug used for treatment of scorpion sting is -

A. Adrenaline
B. Morphine
C. Prazosin (Correct Answer)
D. Captopril

Explanation: ***Prazosin*** - **Prazosin**, an alpha-1 blocker, is the drug of choice for treating **scorpion sting envenomation** due to its ability to counteract the systemic effects like hypertension and myocardial dysfunction. - It works by blocking the effects of excessive catecholamine release caused by the scorpion venom, thereby reducing **vasoconstriction** and improving peripheral circulation. *Adrenaline* - **Adrenaline (epinephrine)** is primarily used in cases of **anaphylaxis** or severe allergic reactions, which are not the typical primary concern in scorpion stings. - Its **vasoconstrictive** and **chronotropic** effects could worsen the cardiovascular complications already present due to scorpion venom. *Morphine* - **Morphine** is a potent **analgesic** used to relieve severe pain. While pain is a symptom of scorpion sting, it does not address the underlying **cardiovascular and systemic effects**. - It can also cause **respiratory depression**, which might complicate the management, especially in severe envenomation. *Captopril* - **Captopril** is an **ACE inhibitor** used primarily for **hypertension** and **heart failure**. - It is not the drug of choice for acute management of scorpion stings as it modulates the **renin-angiotensin system**, which is not the primary mechanism to counteract the venom's effects.

Question 44: According to traditional teaching, dopamine is preferred over dobutamine in treatment of renal shock because:

A. Increased cardiac output
B. Peripheral vasoconstriction
C. Prolonged action
D. Renal vasodilatory effect (Correct Answer)

Explanation: ***Renal vasodilatory effect*** - In traditional teaching, low-dose **dopamine** was thought to selectively stimulate **D1 dopamine receptors** in the kidneys, leading to **renal vasodilation** and improved renal blood flow. - This effect was believed to be beneficial in preventing or treating **acute kidney injury (AKI)** in the context of shock, thus making it a preferred agent for "renal shock." *Increased cardiac output* - While dopamine can increase **cardiac output** through beta-1 agonism at intermediate doses, dobutamine is generally considered a more potent inotropic agent for this purpose. - The primary reason for preferring dopamine in renal shock was not its inotropic effect but its purported renal-specific action. *Peripheral vasoconstriction* - At higher doses, dopamine stimulates **alpha-1 adrenergic receptors**, leading to **peripheral vasoconstriction**, which can increase **systemic vascular resistance (SVR)** and blood pressure. - This generalized vasoconstrictive effect is typically avoided in renal shock if the goal is to improve renal perfusion, as it can potentially compromise renal blood flow. *Prolonged action* - Neither dopamine nor dobutamine has a particularly **prolonged action**; both are typically administered via continuous infusion due to their short half-lives. - The duration of action was not the primary factor in preferring dopamine for renal shock.

Question 45: 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 46: Which is not used in status epilepticus?

A. Lorazepam
B. Phenytoin
C. Phenobarbitone
D. Metformin (Correct Answer)

Explanation: ***Metformin*** - **Metformin** is an **oral hypoglycemic agent** used to treat **type 2 diabetes mellitus** and has no role in the management of seizures or status epilepticus. - Its primary mechanism involves decreasing **hepatic glucose production** and improving **insulin sensitivity**. *Lorazepam* - **Lorazepam** is a first-line treatment for **status epilepticus** due to its rapid onset of action and efficacy in terminating seizures. - It enhances the effect of **GABA** (gamma-aminobutyric acid) at the GABA-A receptor, leading to neuronal hyperpolarization and reduced excitability. *Phenytoin* - **Phenytoin** is a common second-line agent used in status epilepticus, administered after benzodiazepines, to maintain seizure control. - It works by blocking **voltage-gated sodium channels**, thereby stabilizing neuronal membranes and preventing repetitive firing. *Phenobarbitone* - **Phenobarbitone** (phenobarbital) is an effective antiepileptic drug, often considered as a second or third-line agent in status epilepticus, especially when other treatments fail. - It acts primarily by enhancing the activity of **GABA** at the GABA-A receptor, similar to benzodiazepines, but with a longer duration of action.

Question 47: Which of the following drugs is not used for the treatment of hyperkalemia?

A. Sodium bicarbonate
B. Salbutamol
C. Calcium gluconate
D. Magnesium sulphate (Correct Answer)

Explanation: ***Magnesium sulphate*** - **Magnesium sulphate** is primarily used to treat conditions like **hypomagnesemia**, eclampsia, and certain arrhythmias, but it does not directly lower serum potassium levels. - While magnesium can affect potassium channels indirectly, it is not a recommended treatment for **hyperkalemia**. *Sodium bicarbonate* - **Sodium bicarbonate** promotes an intracellular shift of potassium by increasing blood pH, which activates the **Na+/H+ antiporter** on cell membranes, exchanging H+ out and Na+ in. - This influx of Na+ then activates the **Na+/K+ ATPase pump**, moving Na+ out of the cell and K+ into the cell. *Salbutamol* - **Salbutamol**, a **beta-2 adrenergic agonist**, stimulates the **Na+/K+ ATPase pump**, causing a shift of potassium from the **extracellular** to the **intracellular** space. - It is often administered via nebulization for **hyperkalemia** treatment, particularly in patients without renal failure. *Calcium gluconate* - **Calcium gluconate** does not lower serum potassium levels, but it **stabilizes the cardiac membrane** by increasing the action potential threshold, thereby protecting the heart from the adverse effects of hyperkalemia. - It is typically the **first-line emergency treatment** for severe hyperkalemia, especially with ECG changes, to prevent arrhythmias.

Question 48: The safe intramuscular dose of adrenaline for anaphylaxis in a patient with compromised cardiac condition is:

A. 0.02 mg
B. 0.4 mg
C. 0.04 mg
D. 0.2 mg (Correct Answer)

Explanation: ***0.2 mg*** - For patients with **compromised cardiac conditions** experiencing anaphylaxis, a slightly reduced initial IM dose of **0.2 mg** (compared to the standard 0.3-0.5 mg) may be considered to minimize cardiovascular stress. - This dose provides adequate **bronchodilation** and **vasopressor** effect while reducing the risk of **tachyarrhythmias**, **myocardial ischemia**, or severe **hypertension**. - The dose can be repeated every 5-15 minutes if needed based on clinical response. *0.02 mg* - This dose is far too low for **intramuscular administration** in anaphylaxis and would be **therapeutically inadequate**. - Doses this small (0.01-0.05 mg) are only used for **slow IV push** in specific contexts like refractory hypotension, not for anaphylaxis treatment. *0.04 mg* - This dose is also **subtherapeutic** for IM administration in anaphylaxis. - Such a low dose would fail to reverse the life-threatening manifestations of anaphylaxis including **bronchospasm**, **laryngeal edema**, and **cardiovascular collapse**. *0.4 mg* - This is within the **standard dosing range** (0.3-0.5 mg IM) for anaphylaxis in patients with healthy hearts. - While not contraindicated in cardiac patients, a slightly lower dose like **0.2 mg** is often preferred initially to allow for careful monitoring and dose titration based on response and tolerance.

Question 49: Dose of Human Rabies Immunoglobulin (HRIG) is:

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

Explanation: ***20 IU/kg*** - The standard dose for **Human Rabies Immunoglobulin (HRIG)** is **20 IU/kg** of body weight, administered once. - This dose is critical for providing immediate passive immunity by neutralizing the rabies virus at the wound site. *30 IU/kg* - This dosage is higher than the recommended standard for HRIG and is not typically used. - Administering an unnecessarily high dose could potentially lead to more adverse effects without additional benefit. *40 IU/kg* - This dosage is double the recommended amount and is significantly higher than necessary. - Overdosing immunoglobulin can increase the risk of adverse reactions and is not supported by guidelines for rabies post-exposure prophylaxis. *10 IU/kg* - This dosage is below the recommended amount and would be insufficient to provide effective passive immunity against the rabies virus. - Underdosing could compromise the protective effect, leaving the patient vulnerable to disease progression.

Question 50: Succinylcholine when given for endotracheal intubation causes all of the following EXCEPT –

A. Prolonged apnea
B. Hypokalemia in paraplegic patient (Correct Answer)
C. Raised intraocular pressure
D. Bradycardia

Explanation: ***Hypokalemia in paraplegic patient*** - Succinylcholine is a **depolarizing neuromuscular blocker** that can cause a significant efflux of **potassium from cells**, leading to **transient hyperkalemia**, particularly in patients with muscle denervation (e.g., paraplegia, burns, crush injuries). - Therefore, it causes **hyperkalemia**, not hypokalemia, in predisposed patients. *Prolonged apnea* - **Prolonged apnea** can occur if a patient has atypical pseudocholinesterase, leading to a delayed metabolism of succinylcholine. - This enzyme deficiency causes **succinylcholine to remain active** for a longer duration, resulting in extended paralysis and respiratory depression. *Raised intraocular pressure* - Succinylcholine causes **contraction of extraocular muscles**, leading to an increase in **intraocular pressure**. - This effect is a concern in patients with **open globe injuries** or acute **narrow-angle glaucoma**. *Bradycardia* - Succinylcholine can stimulate **muscarinic receptors** at the sinoatrial node, leading to a **decrease in heart rate** (bradycardia). - This effect is more common with **repeated doses** or in **pediatric patients**.

Practice by Chapter

Management of Anaphylaxis

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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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