NEET-PG 2015 - Pharmacology Practice Questions

Q: What effect does morphine have on muscle tone?

Increased muscle tone. ***Increased muscle tone*** - Morphine **increases skeletal muscle tone** and can cause muscle rigidity, particularly with rapid IV administration (truncal rigidity). - It significantly increases **smooth muscle tone** in various organs including the sphincter of Oddi (causing biliary colic), bladder sphincter (causing urinary retention), and GI tract (causing constipation). - This increased tone in sphincters and smooth muscle is a well-documented effect mediated through **opioid receptor activation**. *Bradycardia (not increased heart rate)* - Morphine typically causes **bradycardia** (decreased heart rate) due to vagal stimulation and central effects, not tachycardia. - Increased heart rate would be atypical and not a primary pharmacological effect of morphine. *Miosis (not mydriasis)* - Morphine characteristically causes **miosis** (pinpoint pupils) due to stimulation of the Edinger-Westphal nucleus of the oculomotor nerve. - Mydriasis (dilated pupils) is seen with anticholinergics or sympathomimetics, not opioids. *Respiratory depression (not stimulation)* - Morphine causes **respiratory depression**, not stimulation, by reducing the responsiveness of brainstem respiratory centers to CO2. - This is one of the most dangerous adverse effects and the primary cause of death in opioid overdose.

Q: Which of the following is the most characteristic sexual side effect of SSRIs?

Delayed ejaculation. ***Delayed ejaculation*** - **Delayed ejaculation** is a common and characteristic sexual side effect of SSRIs due to their impact on serotonin pathways involved in sexual response. - This effect can lead to significant distress and non-adherence to treatment, and often requires dose adjustment or switching to an alternative antidepressant. *Erectile dysfunction* - While **erectile dysfunction** can occur with SSRIs, it is a less specific and less consistently reported sexual side effect compared to ejaculatory dysfunction. - Many factors, including underlying mood disorder and comorbidities, can contribute to erectile dysfunction, making it less characteristic of SSRI use alone. *Retrograde ejaculation* - **Retrograde ejaculation** is a condition where semen enters the bladder during orgasm, and while it can be a side effect of some medications (e.g., alpha-blockers), it is not a hallmark sexual side effect of SSRIs. - SSRIs primarily affect the process of emission and expulsion, leading more commonly to delayed or absent ejaculation rather than retrograde flow. *Anxiety* - **Anxiety** is generally a *primary symptom* of the conditions SSRIs are prescribed to treat, such as depression or anxiety disorders, not a sexual side effect of the medication itself. - Although SSRIs can initially cause or worsen anxiety in some patients before therapeutic effects are seen, this is a systemic side effect, not a sexual one.

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

Hyperthyroidism. ***Hyperthyroidism*** - Lithium commonly causes **hypothyroidism** by interfering with thyroid hormone synthesis and release, not hyperthyroidism. - Patients on lithium often require **thyroid function monitoring** and may need thyroid hormone supplementation. *Polyuria* - **Nephrogenic diabetes insipidus**, characterized by polyuria and polydipsia, is a common side effect of lithium. - Lithium interferes with the kidney's ability to respond to **vasopressin (ADH)**, leading to increased water excretion. *Nephropathy* - Chronic lithium use can lead to **interstitial nephropathy**, characterized by a reduction in glomerular filtration rate. - Long-term monitoring of **renal function** is crucial for patients on lithium therapy. *Ebstein's anomaly* - While not a general "side effect" in adults, **Ebstein's anomaly** is a congenital heart defect associated with lithium exposure during the first trimester of pregnancy. - It involves displacement of the **tricuspid valve leaflets** into the right ventricle.

Q: Most common renal sequela of lithium toxicity is?

Nephrogenic Diabetes Insipidus. ***Nephrogenic Diabetes Insipidus*** - **Lithium** interferes with the action of **ADH** on the renal tubules, specifically at the **collecting ducts**, leading to an inability to concentrate urine. - This results in **polyuria** (excessive urination) and **polydipsia** (excessive thirst), characteristic symptoms of **nephrogenic diabetes insipidus**. *Renal tubular acidosis* - While lithium can affect tubular function, **renal tubular acidosis** is less common than nephrogenic diabetes insipidus. - RTA involves impaired acid excretion or bicarbonate reabsorption, leading to **metabolic acidosis**. *Glycosuria* - **Glycosuria** (glucose in urine) is primarily associated with **diabetes mellitus** or other conditions affecting glucose reabsorption in the proximal tubule. - Lithium toxicity does not typically cause glycosuria. *MPGN* - **Membranoproliferative glomerulonephritis (MPGN)** is a type of glomerular injury characterized by specific changes in the glomerulus. - MPGN is not directly caused by **lithium toxicity**; lithium primarily affects tubular function rather than glomerular structure.

Q: Which drug is not administered as a transdermal patch?

Morphine. ***Morphine*** - **Morphine** is generally not administered transdermally due to its **poor lipid solubility** [1] and **large molecular size**, which limit its ability to penetrate the skin effectively. - While experimental patches have been developed, they are **not widely available** or commonly used in clinical practice for systemic delivery. *Fentanyl* - **Fentanyl** is a potent opioid that is commonly administered via a **transdermal patch** for chronic pain management [2]. - Its **high lipid solubility** and small molecular size allow it to be effectively absorbed through the skin, providing sustained analgesia. *Clonidine* - **Clonidine** is an alpha-2 adrenergic agonist available as a **transdermal patch** for the treatment of **hypertension**. - The patch provides a **continuous and steady release** of the drug, leading to consistent blood pressure control. *Diclofenac* - **Diclofenac** is a non-steroidal anti-inflammatory drug (NSAID) available in **transdermal patch** formulations for topical pain relief. - These patches are used for localized pain conditions like **osteoarthritis** and provide targeted drug delivery with reduced systemic side effects.

Q: Antidepressant drug used in nocturnal enuresis is:

Imipramine. ***Imipramine*** - **Imipramine**, a **tricyclic antidepressant (TCA)**, is frequently used off-label for **nocturnal enuresis** in children [1]. - Its mechanism of action in enuresis is thought to involve a combination of anticholinergic effects (which relax the bladder detrusor muscle) and central nervous system effects (which may increase bladder capacity and arousal from sleep) [1]. *Fluoxetine* - **Fluoxetine** is a **selective serotonin reuptake inhibitor (SSRI)** and is primarily used for depression, anxiety disorders, and OCD [2]. - It is not indicated for the treatment of nocturnal enuresis and does not have the same bladder-relaxing or arousal-modulating properties as imipramine in this context. *Trazodone* - **Trazodone** is a **serotonin antagonist and reuptake inhibitor (SARI)**, commonly prescribed for depression and insomnia due to its prominent sedative effects. - It is not used for nocturnal enuresis and its mechanism of action does not confer benefits for bladder control. *Sertraline* - **Sertraline** is another **selective serotonin reuptake inhibitor (SSRI)** used for a wide range of psychiatric conditions, including depression, anxiety, and panic disorder [2]. - Like fluoxetine, it is not an appropriate treatment for nocturnal enuresis and lacks the specific known effects beneficial for this condition.

Q: What is the primary mechanism of action of zonisamide?

Sodium channels. ***Sodium channels (Correct Answer)*** - Zonisamide's primary mechanism involves **blocking voltage-sensitive sodium channels**, which stabilizes neuronal membranes and inhibits repetitive neuronal firing. - This action helps to prevent the propagation of **seizure activity** in the brain. *GABA receptors* - While zonisamide has some weak effects on GABA, it is not its **primary mechanism of action** for antiepileptic efficacy. - Drugs like **benzodiazepines** and **barbiturates** primarily act by enhancing GABAergic transmission. *T-type calcium channels* - Zonisamide also blocks T-type calcium channels, contributing to its broad-spectrum antiepileptic activity, but this is a **secondary mechanism** compared to its sodium channel blockade. - **Ethosuximide** is a classic example of a drug primarily acting on T-type calcium channels, especially for absence seizures. *Cl- channels* - Zonisamide does not primarily act on **chloride channels**; these are often modulated by GABA receptors. - Drugs that act directly on chloride channels are not typically used as **antiepileptics** in the same way.

Q: Buprenorphine is a partial agonist at which opioid receptor?

Mu. ***Mu*** - Buprenorphine primarily acts as a **partial agonist** at the **mu opioid receptor**, providing analgesic effects with a ceiling effect on respiratory depression. - Its partial agonism at the mu receptor contributes to its lower potential for respiratory depression and overdose compared to full mu agonists. *Kappa* - While buprenorphine has some antagonist activity at the kappa receptor, its primary therapeutic action is not at this receptor. - **Kappa receptor agonists** like pentazocine can produce dysphoria and psychotomimetic effects. *Delta* - The delta opioid receptor is involved in analgesia and emotional responses, but buprenorphine has very low affinity and activity at this receptor. - **Delta receptor agonists** are not widely used clinically due to limited efficacy and side effects. *ORL-1* - The ORL-1 (Opioid Receptor-like 1) receptor, also known as the nociceptin receptor, is distinct from classical opioid receptors. - Buprenorphine has **no significant activity** at the ORL-1 receptor, which primarily mediates pain, anxiety, and learning.

Q: Which class of antihypertensive drugs is known to cause erectile dysfunction?

Beta-blockers. ***Beta-blockers*** - **Beta-blockers** are the antihypertensive class most commonly associated with **erectile dysfunction** - Mechanism: Reduced cardiac output, decreased peripheral blood flow, central nervous system effects reducing libido, and blockade of β2-mediated vasodilation - **Non-selective beta-blockers** (propranolol, nadolol) have higher incidence of ED compared to selective β1-blockers (metoprolol, atenolol) - Newer vasodilating beta-blockers (nebivolol, carvedilol) have lower risk of sexual dysfunction *Calcium channel blockers* - Generally have **neutral or minimal effect** on erectile function - May even improve ED in some patients due to **vasodilatory properties** - Side effects include peripheral edema and headache, but not sexual dysfunction *ACE inhibitors* - Associated with **lower risk of erectile dysfunction** compared to other antihypertensives - May have neutral or even protective effects on sexual function - Preferred choice for hypertensive patients with existing sexual dysfunction concerns - Common side effects: dry cough and angioedema (not related to sexual function) *AT1 receptor antagonists* - **ARBs have neutral to potentially beneficial effects** on sexual function - Considered an excellent alternative for patients experiencing sexual side effects with other antihypertensive medications - Some studies suggest they may improve erectile function in hypertensive patients

Q: Which non-selective beta-blocker has sympathomimetic activity?

Pindolol. ***Pindolol*** - **Pindolol** is a **non-selective beta-blocker** that exhibits **intrinsic sympathomimetic activity (ISA)**, meaning it acts as a partial agonist at beta-adrenergic receptors. - Due to ISA, it causes less reduction in resting heart rate and cardiac output compared to beta-blockers without ISA. *Acebutalol* - **Acebutalol** is a **beta-1 selective blocker** (cardioselective) that possesses **intrinsic sympathomimetic activity (ISA)**. - While it has ISA, it is not a non-selective beta-blocker, making it an incorrect answer for this question. *Nadolol* - **Nadolol** is a **non-selective beta-blocker** that does **not** have intrinsic sympathomimetic activity (ISA). - It primarily acts as a pure antagonist at both beta-1 and beta-2 adrenergic receptors. *Metoprolol* - **Metoprolol** is a **beta-1 selective blocker** (cardioselective) and does **not** possess intrinsic sympathomimetic activity (ISA). - Its primary action is blockade of cardiac beta-1 receptors.

Question 1

What effect does morphine have on muscle tone?

Accepted Answer

Increased muscle tone

Answer

Respiratory stimulation

Answer

Decreased muscle tone

Answer

Mydriasis

Question 2

Which of the following is the most characteristic sexual side effect of SSRIs?

Accepted Answer

Delayed ejaculation

Answer

Retrograde ejaculation

Answer

Erectile dysfunction

Answer

Anxiety

Question 3

Which of the following is NOT a known side effect of lithium?

Accepted Answer

Hyperthyroidism

Answer

Polyuria

Answer

Nephropathy

Answer

Ebstein's anomaly

Question 4

Most common renal sequela of lithium toxicity is?

Accepted Answer

Nephrogenic Diabetes Insipidus

Answer

Renal tubular acidosis

Answer

Glycosuria

Answer

MPGN

Question 5

Which drug is not administered as a transdermal patch?

Accepted Answer

Morphine

Answer

Fentanyl

Answer

Clonidine

Answer

Diclofenac

Question 6

Antidepressant drug used in nocturnal enuresis is:

Accepted Answer

Imipramine

Answer

Fluoxetine

Answer

Trazodone

Answer

Sertraline

Question 7

What is the primary mechanism of action of zonisamide?

Accepted Answer

Sodium channels

Answer

GABA receptors

Answer

Cl- channels

Answer

T-type calcium channels

Question 8

Buprenorphine is a partial agonist at which opioid receptor?

Accepted Answer

Mu

Answer

Kappa

Answer

Delta

Answer

ORL-1

Question 9

Which class of antihypertensive drugs is known to cause erectile dysfunction?

Accepted Answer

Beta-blockers

Answer

Calcium channel blocker

Answer

ACE inhibitors

Answer

AT1 receptor antagonists

Question 10

Which non-selective beta-blocker has sympathomimetic activity?

Accepted Answer

Pindolol

Answer

Nadolol

Answer

Acebutalol

Answer

Metoprolol

NEET-PG 2015 — Pharmacology