Gynaecomastia is caused by which drug?
Which of the following is not commonly recognized as a hepatotoxic drug?
Botulinum toxin acts on
Which class of drugs does botulinum toxin mimic in its action?
Botulinum toxin type B is used in which disease?
Which of the following drugs can cause thyroid dysfunction?
Which of the following drugs has not been withdrawn from the Indian market for safety reasons?
Which vaccine is associated with a risk of encephalopathy?
What is the appropriate diluent for the BCG vaccine?
What is the initial loading dose of chloroquine base for treating uncomplicated malaria in children?
NEET-PG 2013 - Pharmacology NEET-PG Practice Questions and MCQs
Question 51: Gynaecomastia is caused by which drug?
- A. Spironolactone (Correct Answer)
- B. Rifampicin
- C. Thiazide
- D. Propranolol
Explanation: ***Spironolactone*** - Spironolactone is a **well-established cause of gynaecomastia**, occurring in 5-10% of patients in a dose-dependent manner. - It acts as an **anti-androgen** by blocking androgen receptors and inhibiting testosterone synthesis, thereby increasing the estrogen to androgen ratio. - It is a **potassium-sparing diuretic** and aldosterone antagonist, commonly used in heart failure, hypertension, and conditions requiring androgen blockade. *Rifampicin* - Rifampicin is an **antibiotic** primarily used to treat tuberculosis and acts as a **strong inducer of cytochrome P450 enzymes**. - While rare hormonal effects have been reported, it is **not a recognized common cause** of gynaecomastia. - Main side effects include hepatotoxicity, orange discoloration of bodily fluids, and drug interactions. *Thiazide* - Thiazide diuretics work by inhibiting the **sodium-chloride cotransporter** in the distal convoluted tubule. - They are **not commonly associated** with gynaecomastia; typical side effects include hypokalemia, hyponatremia, and hyperglycemia. *Propranolol* - Propranolol is a **non-selective beta-blocker** used for hypertension, angina, arrhythmias, and anxiety. - While beta-blockers have rarely been implicated, propranolol is **not a well-established cause** of gynaecomastia compared to spironolactone. - Common side effects include bradycardia, fatigue, and bronchospasm.
Question 52: Which of the following is not commonly recognized as a hepatotoxic drug?
- A. Chlorpropamide
- B. Allopurinol
- C. Streptomycin (Correct Answer)
- D. Halothane
Explanation: ***Streptomycin*** - Streptomycin is primarily associated with **ototoxicity** (vestibular and cochlear damage) and **nephrotoxicity** (kidney damage), not significant hepatotoxicity. - While most drugs can theoretically cause liver injury, streptomycin is not frequently cited as a major hepatotoxin in clinical practice. *Chlorpropamide* - This **sulfonylurea oral hypoglycemic agent** can cause a range of liver injuries, from asymptomatic enzyme elevations to severe **cholestatic hepatitis** or hepatocellular damage. - Its hepatotoxic potential is well-documented, leading to its decreased use compared to newer antidiabetic agents. *Allopurinol* - Allopurinol, used to treat **gout** and hyperuricemia, is known to cause a variety of adverse effects, including **hypersensitivity reactions** that can involve the liver. - It can lead to **hepatocellular injury**, cholestasis, or mixed liver damage, sometimes as part of a severe drug reaction with eosinophilia and systemic symptoms (**DRESS syndrome**). *Halothane* - Halothane is a potent **halogenated inhalational anesthetic** historically associated with a rare but severe form of idiosyncratic liver injury known as **halothane hepatitis**. - This condition involves **massive hepatic necrosis** and has a high mortality rate, leading to its eventual replacement by newer anesthetics.
Question 53: Botulinum toxin acts on
- A. Synapse (Correct Answer)
- B. Smooth muscle of intestine
- C. Central nervous system
- D. Sensory nerves
Explanation: ***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.
Question 54: Which class of drugs does botulinum toxin mimic in its action?
- A. Adrenergics
- B. Antiadrenergic
- C. Cholinergics
- D. Anticholinergics (Correct Answer)
Explanation: ***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**.
Question 55: Botulinum toxin type B is used in which disease?
- A. Cervical dystonia (Correct Answer)
- B. Blepharospasm
- C. Strabismus
- D. Glabellar lines
Explanation: ***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.
Question 56: Which of the following drugs can cause thyroid dysfunction?
- A. Amiodarone (Correct Answer)
- B. Ampicillin
- C. Ibutilide
- D. Acyclovir
Explanation: ***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.
Question 57: Which of the following drugs has not been withdrawn from the Indian market for safety reasons?
- A. Gatifloxacin
- B. Cotrimoxazole (Correct Answer)
- C. Phenformin
- D. Rofecoxib
Explanation: ### 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.
Question 58: Which vaccine is associated with a risk of encephalopathy?
- A. OPV
- B. Rubella
- C. Measles (Correct Answer)
- D. BCG
Explanation: ***Measles*** - Among the options provided, **measles vaccine** has been reported to have a very rare association with **post-vaccination encephalitis/encephalopathy** (approximately 1 per million doses). - **Important note:** The **pertussis vaccine (particularly whole-cell DTP)** is the vaccine most classically associated with encephalopathy risk, but it is not among the options here. - The risk of encephalopathy from the measles vaccine is significantly lower than the risk from natural measles infection itself. - Modern measles vaccines are highly purified and safer than earlier formulations. *OPV* - **Oral Polio Vaccine (OPV)** is associated with **vaccine-associated paralytic poliomyelitis (VAPP)**, not encephalopathy. - VAPP occurs at a rate of approximately 1 case per 2.4 million doses due to reversion of the attenuated virus to a neurovirulent form. - Manifests as flaccid paralysis, not encephalopathy. *Rubella* - **Rubella vaccine** (component of MMR) is very safe with no significant association with encephalopathy. - Rare adverse effects include transient arthralgia (especially in adult women), mild rash, or lymphadenopathy. - Severe neurological complications are extremely rare. *BCG* - **Bacillus Calmette-Guérin (BCG) vaccine** protects against tuberculosis and is not associated with encephalopathy. - Common adverse effects are local reactions: induration, ulceration, scarring, and rarely lymphadenitis. - Disseminated BCG infection can occur in immunocompromised individuals but is distinct from encephalopathy.
Question 59: What is the appropriate diluent for the BCG vaccine?
- A. Sterile normal saline
- B. Sterile distilled water (Correct Answer)
- C. Sterile dextrose solution
- D. Colloid solutions
Explanation: ***Sterile distilled water*** - **Sterile distilled water** is the recommended diluent for the **BCG vaccine** to ensure proper reconstitution and antigen stability. - Using the correct diluent is critical for maintaining the **efficacy** and safety of the vaccine. *Sterile normal saline* - **Sterile normal saline** (0.9% NaCl) can be used as a diluent for some vaccines, but it is **not appropriate for BCG** as it can negatively impact vaccine viability. - The **salt concentration** in saline can affect the live attenuated organisms in the BCG vaccine. *Sterile dextrose solution* - **Dextrose solutions** are generally avoided as vaccine diluents due to their potential to support **bacterial growth** or alter vaccine stability. - They are primarily used for **intravenous fluid administration** and not for vaccine reconstitution. *Colloid solutions* - **Colloid solutions** like albumin or dextran are never used as vaccine diluents as they can interfere with the **vaccine antigens** and cause adverse reactions. - These solutions are typically used for **plasma volume expansion** and have no role in vaccine preparation.
Question 60: What is the initial loading dose of chloroquine base for treating uncomplicated malaria in children?
- A. 5 mg/kg
- B. 10 mg/kg (maximum 600 mg) (Correct Answer)
- C. 15 mg/kg
- D. 25 mg/kg
Explanation: ***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.