What effect does morphine have on muscle tone?
Beta-blockers should be used with caution in patients with?
Antidepressant drug used in nocturnal enuresis is:
Which drug is not administered as a transdermal patch?
Which diuretic is known to cause the maximum potassium loss?
What is the primary mechanism of action of zonisamide?
Buprenorphine is a partial agonist at which opioid receptor?
Most common renal sequela of lithium toxicity is?
Which of the following drugs is not used in the treatment of akathisia?
Where is the benzodiazepine binding site located on GABA receptors?
NEET-PG 2015 - Pharmacology NEET-PG Practice Questions and MCQs
Question 31: What effect does morphine have on muscle tone?
- A. Increased muscle tone (Correct Answer)
- B. Respiratory stimulation
- C. Decreased muscle tone
- D. Mydriasis
Explanation: ***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.
Question 32: Beta-blockers should be used with caution in patients with?
- A. Hypertension
- B. CHF
- C. Conduction defect (Correct Answer)
- D. Glaucoma
Explanation: ***Conduction defect*** - Beta-blockers **slow heart rate** and **decrease AV nodal conduction**, which can worsen pre-existing conduction defects like **AV block** or **sick sinus syndrome**. - Their use can lead to **symptomatic bradycardia** or complete heart block in susceptible individuals. - This represents a **strong relative contraindication** requiring significant caution. *Hypertension* - Beta-blockers are a **first-line treatment for hypertension**, effectively lowering blood pressure by reducing cardiac output and renin release. - They are generally **well-tolerated** and beneficial in most hypertensive patients. *Glaucoma* - Topical beta-blockers, such as **timolol**, are a common treatment for open-angle glaucoma as they **reduce aqueous humor production**, thereby lowering intraocular pressure. - Systemic use of beta-blockers does not typically worsen glaucoma and may even offer some benefit. *CHF* - While certain beta-blockers (**carvedilol, metoprolol succinate, bisoprolol**) are now proven beneficial in **chronic heart failure with reduced ejection fraction (HFrEF)**, they do require careful use. - They must be **initiated at low doses and carefully titrated** to avoid acute decompensation, and are **contraindicated in acute decompensated heart failure**. - However, **conduction defects** represent a **stronger contraindication** where beta-blockers can cause life-threatening bradycardia or complete heart block, making it the best answer for conditions requiring the most caution.
Question 33: Antidepressant drug used in nocturnal enuresis is:
- A. Imipramine (Correct Answer)
- B. Fluoxetine
- C. Trazodone
- D. Sertraline
Explanation: ***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.
Question 34: Which drug is not administered as a transdermal patch?
- A. Morphine (Correct Answer)
- B. Fentanyl
- C. Clonidine
- D. Diclofenac
Explanation: ***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.
Question 35: Which diuretic is known to cause the maximum potassium loss?
- A. Spironolactone
- B. Furosemide (Correct Answer)
- C. Thiazide diuretics
- D. Acetazolamide
Explanation: ***Furosemide*** - Furosemide is a **loop diuretic** that inhibits the Na-K-2Cl cotransporter in the **thick ascending limb of the loop of Henle**, leading to significant excretion of sodium, chloride, potassium, and water. - Its potent diuresis and impact on potassium reabsorption result in a **high risk of hypokalemia**. *Thiazide* - Thiazide diuretics inhibit the **Na-Cl cotransporter** in the **distal convoluted tubule**, causing moderate sodium and water excretion, and some potassium loss. - While they can cause hypokalemia, their effect on potassium excretion is generally **less pronounced than loop diuretics**. *Acetazolamide* - Acetazolamide is a **carbonic anhydrase inhibitor** that acts primarily in the **proximal tubule**, inhibiting bicarbonate reabsorption and leading to increased excretion of bicarbonate, sodium, potassium, and water. - The potassium loss is due to increased delivery of sodium to the collecting duct, leading to enhanced potassium secretion, but it is typically **less severe than with loop diuretics**. *Spironolactone* - Spironolactone is a **potassium-sparing diuretic** that acts as an **aldosterone antagonist** in the collecting duct, inhibiting sodium reabsorption and potassium secretion. - Instead of causing potassium loss, spironolactone actually **conserves potassium** and can lead to hyperkalemia.
Question 36: What is the primary mechanism of action of zonisamide?
- A. GABA receptors
- B. Cl- channels
- C. Sodium channels (Correct Answer)
- D. T-type calcium channels
Explanation: ***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.
Question 37: Buprenorphine is a partial agonist at which opioid receptor?
- A. Mu (Correct Answer)
- B. Kappa
- C. Delta
- D. ORL-1
Explanation: ***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.
Question 38: Most common renal sequela of lithium toxicity is?
- A. Renal tubular acidosis
- B. Glycosuria
- C. MPGN
- D. Nephrogenic Diabetes Insipidus (Correct Answer)
Explanation: ***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.
Question 39: Which of the following drugs is not used in the treatment of akathisia?
- A. Benzodiazepine
- B. Propranolol
- C. Trihexyphenidyl
- D. Haloperidol (Correct Answer)
Explanation: ***Haloperidol*** - **Haloperidol** is a typical antipsychotic drug known to **cause** or worsen **akathisia**, rather than treat it. - Akathisia is an extrapyramidal symptom, and **first-generation antipsychotics** like haloperidol are frequent culprits due to their strong **D2 receptor blockade**. *Benzodiazepine* - **Benzodiazepines** like lorazepam or clonazepam are often used to treat akathisia due to their **sedative** and **anxiolytic** properties. - They act by enhancing **GABAergic transmission**, which can help calm the motor restlessness associated with akathisia. *Propranolol* - **Propranolol**, a **beta-blocker**, is a first-line treatment for akathisia, particularly effective for its objective motor symptoms. - It works by reducing **adrenergic activity**, which is thought to contribute to the motor restlessness. *Trihexyphenidyl* - **Trihexyphenidyl** is an **anticholinergic** agent primarily used to treat **parkinsonian-like extrapyramidal symptoms** (e.g., dystonia, pseudoparkinsonism). - While sometimes used for generalized EPS, it is **less effective** for the specific motor restlessness of akathisia compared to beta-blockers or benzodiazepines.
Question 40: Where is the benzodiazepine binding site located on GABA receptors?
- A. β-subunit
- B. δ-subunit
- C. γ-subunit (Correct Answer)
- D. α-subunit
Explanation: ***γ-subunit*** - The **benzodiazepine binding site** is located at the interface between the **α and γ subunits** of the GABA-A receptor, with the **γ-subunit (especially γ2) being essential** for benzodiazepine sensitivity. - The presence of the **γ2 subunit** is **mandatory** for benzodiazepine binding - receptors lacking this subunit are **insensitive to benzodiazepines**. - Benzodiazepines bind to this site and act as **positive allosteric modulators**, increasing the frequency of **chloride channel opening** in response to GABA. - This is the **standard answer** for NEET-PG and medical PG examinations in India. *α-subunit* - The **α-subunit** contributes to forming the benzodiazepine binding pocket at the α-γ interface. - Different **α-subunit isoforms** (α1, α2, α3, α5) determine the pharmacological profile and tissue distribution of benzodiazepine effects. - However, the **α-subunit alone** cannot bind benzodiazepines without the γ-subunit. *β-subunit* - The **β-subunit** contains the primary binding site for **GABA** itself. - It does not participate in benzodiazepine binding but is crucial for the receptor's overall function and GABAergic signaling. *δ-subunit* - The **δ-subunit** replaces the γ-subunit in certain GABA-A receptor subtypes that mediate **tonic inhibition**. - Receptors containing **δ-subunits** are **insensitive to benzodiazepines** but sensitive to neurosteroids and certain general anesthetics. - This is a key distinguishing feature between phasic (γ-containing) and tonic (δ-containing) GABA-A receptors.