What effect does morphine have on muscle tone?
Which of the following is the most characteristic sexual side effect of SSRIs?
Most common renal sequela of lithium toxicity is?
Which drug is not administered as a transdermal patch?
Antidepressant drug used in nocturnal enuresis is:
What is the primary mechanism of action of zonisamide?
Buprenorphine is a partial agonist at which opioid receptor?
Beta-blockers should be used with caution in patients with?
Which statement best describes first-order kinetics in pharmacokinetics?
Alkaline diuresis in drug poisoning is not done in?
NEET-PG 2015 - Pharmacology NEET-PG Practice Questions and MCQs
Question 71: 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 72: Which of the following is the most characteristic sexual side effect of SSRIs?
- A. Retrograde ejaculation
- B. Erectile dysfunction
- C. Delayed ejaculation (Correct Answer)
- D. Anxiety
Explanation: ***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.
Question 73: 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 74: 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 75: 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 76: 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 77: 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 78: 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 79: Which statement best describes first-order kinetics in pharmacokinetics?
- A. Absorption of the drug is independent of the serum concentration
- B. Elimination of the drug is proportional to the serum concentration (Correct Answer)
- C. Absorption of the drug is proportional to the serum concentration
- D. Elimination of the drug is independent of the serum concentration
Explanation: ***Elimination of the drug is proportional to the serum concentration*** - In **first-order kinetics**, a **constant fraction** (or percentage) of the drug is eliminated per unit of time. - This means that as the **serum drug concentration** increases, the absolute amount of drug eliminated per unit time also increases proportionally. *Absorption of the drug is independent of the serum concentration* - Drug absorption is generally driven by factors like **concentration gradient**, surface area, and blood flow, and while it can be influenced by drug concentration, this statement does not define first-order kinetics of *elimination*. - This statement is not the primary characteristic distinguishing first-order from zero-order kinetics regarding drug disposition. *Elimination of the drug is independent of the serum concentration.* - This describes **zero-order kinetics**, where a **constant amount** of drug is eliminated per unit of time, regardless of the serum concentration. - In zero-order kinetics, the elimination rate becomes saturated, so the elimination process cannot keep up with higher drug concentrations. *Absorption of the drug is proportional to the serum concentration* - While drug absorption can be proportional to the concentration (especially through passive diffusion), first-order kinetics specifically refers to the **elimination phase** of pharmacokinetics. - The rate of absorption can be a complex process and is not the defining characteristic for distinguishing first-order from zero-order *elimination*.
Question 80: Alkaline diuresis in drug poisoning is not done in?
- A. Aspirin
- B. Morphine (Correct Answer)
- C. Phenobarbitone
- D. Methotrexate
Explanation: ***Morphine*** - **Morphine** is an **alkaline drug**, so its elimination is actually enhanced by **acidification of the urine**, not alkalinization. - Alkaline diuresis would decrease the ionization of morphine in the renal tubules, leading to **increased reabsorption** and reduced excretion. *Aspirin* - **Aspirin (acetylsalicylic acid)** is an **acidic drug**, and **alkaline diuresis** is effective in increasing its excretion by trapping the ionized form in the renal tubules. - This process prevents reabsorption and promotes clearance, which is a standard treatment for aspirin overdose. *Methotrexate* - **Methotrexate** is a **weak organic acid**, and **alkaline diuresis** is crucial in reducing its toxicity, especially in high-dose therapy. - By increasing urine pH, the renal elimination of methotrexate is significantly enhanced, preventing kidney damage and systemic accumulation. *Phenobarbitone* - **Phenobarbitone** is a **weak acid**, and **alkaline diuresis** is a well-established method to increase its renal excretion in cases of overdose. - Alkalinization of the urine promotes the ionization of phenobarbitone, reducing its reabsorption by the renal tubules and accelerating its elimination.