NEET-PG 2013 - Pharmacology Practice Questions

Q: Botulinum toxin acts on

Synapse. ***Synapse*** - **Botulinum toxin** acts by inhibiting the release of **acetylcholine** at the **neuromuscular junction**, which is a type of synapse. - This blockade of neurotransmitter release at the **presynaptic terminal** prevents muscle contraction, leading to paralysis. *Smooth muscle of intestine* - While botulinum toxin can affect smooth muscle indirectly by paralyzing the motor nerves innervating them, its primary site of action is the **synapse** itself, not directly on the muscle fibers. - The toxin primarily targets the nerve endings, rather than the mechanical contractility of the muscle cell. *Central nervous system* - **Botulinum toxin** does not readily cross the **blood-brain barrier**, meaning its primary effects are peripheral. - Its therapeutic and toxic effects are localized to the **peripheral nervous system** and neuromuscular junctions. *Sensory nerves* - **Botulinum toxin** specifically targets **motor nerve endings** to inhibit acetylcholine release, leading to muscle paralysis. - It does not directly affect the function of **sensory nerve transmission** or pain perception in the same way.

Q: Which class of drugs does botulinum toxin mimic in its action?

Anticholinergics. ***Anticholinergics*** - **Botulinum toxin** inhibits the release of **acetylcholine** from **presynaptic nerve terminals** [2] by preventing vesicle fusion, leading to muscle paralysis [1]. - While the **mechanism differs** (botulinum acts presynaptically, anticholinergics act postsynaptically at receptors), the **functional outcome** is similar: reduced cholinergic neurotransmission. - In terms of **clinical effect** at the neuromuscular junction, both reduce acetylcholine's action, making anticholinergics the closest functional parallel among the given options. *Cholinergics* - **Cholinergics** enhance acetylcholine activity, either by increasing its release, mimicking its effects at receptors, or inhibiting its breakdown. - This is the **opposite** of botulinum toxin's action, which reduces acetylcholine's impact. *Adrenergics* - **Adrenergics** stimulate the **sympathetic nervous system** via **adrenergic receptors** (α and β receptors). - They act on **norepinephrine/epinephrine pathways**, not the cholinergic system where botulinum toxin acts. *Antiadrenergic* - **Antiadrenergic drugs** block **adrenergic receptors** or inhibit sympathetic activity. - These are unrelated to botulinum toxin's effect on **cholinergic neuromuscular transmission**.

Q: Botulinum toxin type B is used in which disease?

Cervical dystonia. ***Cervical dystonia*** * **Botulinum toxin type B (Myobloc/NeuroBloc)** is specifically approved for the treatment of **cervical dystonia**, which involves involuntary contractions of neck muscles. * It works by blocking the release of **acetylcholine** at the neuromuscular junction, leading to muscle relaxation. *Strabismus* * **Botulinum toxin type A (Botox, Dysport, Xeomin)** is the preferred and most commonly used form for treating **strabismus** by temporarily weakening specific extraocular muscles. * Type B is generally not indicated for strabismus due to differences in potency and duration of action. *Blepharospasm* * **Botulinum toxin type A** (e.g., Botox) is the primary treatment for **blepharospasm**, an involuntary forceful closure of the eyelids. * While both types inhibit acetylcholine release, type A has a more established and concentrated use in treating localized muscle spasms like blepharospasm. *Glabellar lines* * **Botulinum toxin type A** is widely used for cosmetic applications such as reducing **glabellar lines** (frown lines between the eyebrows). * Its efficacy and safety for cosmetic indications are well-established, making type A the standard choice over type B.

Q: Which one of the following agents has been associated with hemorrhagic stroke?

Phenylpropanolamine. ***Phenylpropanolamine*** - **Phenylpropanolamine (PPA)** is a sympathomimetic agent that was formerly used as a nasal decongestant and anorectic. - Its use has been linked to an increased risk of **hemorrhagic stroke**, particularly in young women, due to its **vasoconstrictive effects** and potential to cause a sudden, severe rise in blood pressure. *Terfenadine* - **Terfenadine** is a second-generation antihistamine that was voluntarily withdrawn from the market due to its association with severe **cardiac arrhythmias (QT prolongation and Torsades de Pointes)**, not hemorrhagic stroke. - It works by blocking H1 histamine receptors but also had effects on cardiac potassium channels. *Quinidine* - **Quinidine** is an antiarrhythmic drug (Class Ia) primarily used to treat supraventricular and ventricular arrhythmias. - Its main side effects include **gastrointestinal disturbances**, **cinchonism**, and the risk of **QT prolongation** leading to Torsades de Pointes; it is not typically associated with hemorrhagic stroke. *Fenfluramine* - **Fenfluramine** was an anorectic drug used in the treatment of obesity, often in combination with phentermine. - It was withdrawn from the market due to its association with **pulmonary hypertension** and **cardiac valvulopathy**, not hemorrhagic stroke.

Q: Which of the following drugs can cause thyroid dysfunction?

Amiodarone. ***Amiodarone*** - **Amiodarone** is known to cause both **hypothyroidism** and **hyperthyroidism** due to its high iodine content and direct toxic effects on the thyroid gland. - Its effects can persist for months after discontinuation due to its **long half-life** and accumulation in tissues. *Ampicillin* - **Ampicillin** is an antibiotic that generally does not directly affect thyroid function. - Its primary mechanism of action involves inhibiting **bacterial cell wall synthesis**, with no known significant endocrine side effects. *Ibutilide* - **Ibutilide** is an antiarrhythmic drug used for recent-onset atrial fibrillation or flutter. - It works by blocking potassium channels and has no recognized association with thyroid dysfunction. *Acyclovir* - **Acyclovir** is an antiviral medication used to treat herpes virus infections. - Its mechanism of action involves inhibiting viral DNA replication and it is not known to impact thyroid hormone synthesis or metabolism.

Q: Which of the following drugs has not been withdrawn from the Indian market for safety reasons?

Cotrimoxazole. ### Cotrimoxazole - Cotrimoxazole, a combination of **trimethoprim and sulfamethoxazole**, remains a widely used and available antibiotic in India [1], [2]. - It treats various bacterial infections, including **urinary tract infections** and respiratory infections, and has not been withdrawn for safety reasons [1]. ### Gatifloxacin - **Gatifloxacin** was withdrawn from the Indian market due to concerns about **severe glycemic disturbances**, including both hypo- and hyperglycemia. - These side effects posed significant risks, especially in patients with diabetes or those predisposed to blood sugar fluctuations. ### Rofecoxib - **Rofecoxib**, an NSAID, was withdrawn globally, including from India, due to an increased risk of **cardiovascular events** such as heart attack and stroke. - Its selective inhibition of COX-2 was found to disturb the balance of prostaglandins, leading to adverse cardiovascular outcomes. ### Phenformin - **Phenformin**, an oral antidiabetic drug, was withdrawn from the Indian market due to its association with a high incidence of **lactic acidosis**, a severe and often fatal metabolic complication. - This serious side effect made its risk-benefit profile unacceptable for continued use.

Q: What is the initial loading dose of chloroquine base for treating uncomplicated malaria in children?

10 mg/kg (maximum 600 mg). ***10 mg/kg (maximum 600 mg)*** - The standard **initial loading dose** of chloroquine base for uncomplicated malaria in children is **10 mg/kg body weight**, with a maximum cap of **600 mg** to prevent toxicity. - This is followed by **5 mg/kg** at 6 hours, 24 hours, and 48 hours (total course of 25 mg/kg over 3 days). - This represents **WHO-recommended** weight-based dosing for pediatric malaria treatment. *5 mg/kg* - **5 mg/kg** is the dose for the **subsequent doses** (at 6, 24, and 48 hours after the initial dose), not the initial loading dose. - The initial dose must be higher (10 mg/kg) to rapidly achieve therapeutic blood levels. *15 mg/kg* - **15 mg/kg** exceeds the recommended initial dose and increases the risk of **chloroquine toxicity**. - Chloroquine has a narrow therapeutic index, and overdosing can cause serious **cardiovascular** (arrhythmias, hypotension) and **neurological** effects (seizures, visual disturbances). *25 mg/kg* - **25 mg/kg** represents the **total cumulative dose** over the entire 3-day treatment course, not the initial single dose. - Giving this amount as a single dose would result in severe toxicity and is contraindicated.

Q: Drug for prophylaxis of malaria in chloroquine resistant P.falciparum ?

Mefloquine. ***Mefloquine*** - **Mefloquine** is a well-established and effective drug for prophylaxis against **chloroquine-resistant Plasmodium falciparum**. - It is often used in regions with high chloroquine resistance, although it can have significant neuropsychiatric side effects. *Quinine* - **Quinine** is primarily used for the *treatment* of severe or complicated malaria, especially in cases of multidrug resistance. - It is not typically recommended for malaria **prophylaxis** due to its relatively short half-life and potential for side effects with chronic use. *Halofantrine* - **Halofantrine** is an *antimalarial treatment* drug, not a prophylactic agent. - Its use is limited due to potential for **cardiotoxicity** (QT prolongation) and poor bioavailability. *Artesunate* - **Artesunate** is an **artemisinin derivative** and a potent antimalarial drug used for the *treatment* of acute malaria, particularly severe cases. - It has a very short half-life and is not suitable for **prophylaxis**.

Q: An Englishman travels to a place which is resistant to chloroquine and mefloquine. What should he take as prophylaxis?

Atovaquone-proguanil. ***Atovaquone-proguanil*** - This combination, known as **Malarone**, is the most appropriate prophylactic agent for areas with **multi-drug resistant malaria**, including resistance to chloroquine and mefloquine [1], [2]. - It targets multiple stages of the parasite life cycle, providing excellent protection and is generally well-tolerated with specific **WHO and CDC recommendations** for chloroquine and mefloquine resistant areas [1], [3]. *Primaquine* - **Primaquine** is primarily used for **causal prophylaxis** against *P. vivax* and *P. ovale* to prevent relapse, not as primary prophylaxis [2]. - It is not typically recommended as the primary prophylactic agent in areas with **chloroquine and mefloquine resistance** and requires **G6PD testing** due to risk of hemolysis [1]. *Proguanil* - While proguanil is used for malaria prophylaxis, **proguanil alone** is not effective enough for prophylaxis in areas with multi-drug resistant malaria. - It is typically used in **combination with atovaquone** rather than as monotherapy for effective protection [3]. *Doxycycline* - **Doxycycline** is also an effective prophylactic agent for areas with **chloroquine and mefloquine-resistant malaria** and is commonly recommended [1], [2]. - While effective, it can cause **photosensitivity** and **gastrointestinal upset**, making atovaquone-proguanil the preferred first-line choice.

Q: Which of the following is NOT a side effect of digitalis?

Vasodilatation. **Vasodilatation** - **Digitalis**, primarily digoxin, is known for its **positive inotropic effect**, increasing myocardial contractility, and for its **vasoconstrictive properties** at higher doses due to sympathetic activation and direct smooth muscle effects, not vasodilatation. - While it can indirectly improve cardiac output and thus tissue perfusion, its direct vascular effects do not typically include widespread vasodilatation. *Ventricular tachycardia* - **Digitalis toxicity** can lead to various arrhythmias, including **ventricular tachycardia**, which is a potentially life-threatening side effect. - This occurs due to increased automaticity and delayed afterdepolarizations in ventricular myocytes. *Nausea and vomiting* - **Gastrointestinal symptoms** such as **nausea and vomiting** are common early signs of digitalis toxicity. - These effects are thought to be mediated by the drug's action on the chemoreceptor trigger zone in the brainstem. *Ventricular Bigeminy* - **Ventricular bigeminy**, characterized by alternating normal and premature ventricular beats, is another classic manifestation of **digitalis toxicity**. - This arrhythmia results from enhanced automaticity and altered conduction properties in the ventricles.

Question 1

Botulinum toxin acts on

Accepted Answer

Synapse

Answer

Smooth muscle of intestine

Answer

Central nervous system

Answer

Sensory nerves

Question 2

Which class of drugs does botulinum toxin mimic in its action?

Accepted Answer

Anticholinergics

Answer

Adrenergics

Answer

Antiadrenergic

Answer

Cholinergics

Question 3

Botulinum toxin type B is used in which disease?

Accepted Answer

Cervical dystonia

Answer

Blepharospasm

Answer

Strabismus

Answer

Glabellar lines

Question 4

Which one of the following agents has been associated with hemorrhagic stroke?

Accepted Answer

Phenylpropanolamine

Answer

Terfenadine

Answer

Quinidine

Answer

Fenfluramine

Question 5

Which of the following drugs can cause thyroid dysfunction?

Accepted Answer

Amiodarone

Answer

Ampicillin

Answer

Ibutilide

Answer

Acyclovir

Question 6

Which of the following drugs has not been withdrawn from the Indian market for safety reasons?

Accepted Answer

Cotrimoxazole

Answer

Gatifloxacin

Answer

Phenformin

Answer

Rofecoxib

Question 7

What is the initial loading dose of chloroquine base for treating uncomplicated malaria in children?

Accepted Answer

10 mg/kg (maximum 600 mg)

Answer

5 mg/kg

Answer

15 mg/kg

Answer

25 mg/kg

Question 8

Drug for prophylaxis of malaria in chloroquine resistant P.falciparum ?

Accepted Answer

Mefloquine

Answer

Quinine

Answer

Halofantrine

Answer

Artesunate

Question 9

An Englishman travels to a place which is resistant to chloroquine and mefloquine. What should he take as prophylaxis?

Accepted Answer

Atovaquone-proguanil

Answer

Primaquine

Answer

Doxycycline

Answer

Proguanil

Question 10

Which of the following is NOT a side effect of digitalis?

Accepted Answer

Vasodilatation

Answer

Nausea and vomiting

Answer

Ventricular Bigeminy

Answer

Ventricular tachycardia

NEET-PG 2013 — Pharmacology