Pharmacology
9 questionsWhich diuretic is most likely to cause hyponatremia by impairing free water excretion?
Which ACE inhibitor is safe in renal failure?
Which sympathomimetic drug is primarily known to increase heart rate?
Which of the following agents requires the MOST caution when combined with spironolactone due to increased risk of hyperkalemia:
At which receptor is the primary action of antipsychotic medications required?
What is the primary mechanism of action of opioids in pain management?
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?
NEET-PG 2015 - Pharmacology NEET-PG Practice Questions and MCQs
Question 471: Which diuretic is most likely to cause hyponatremia by impairing free water excretion?
- A. Loop diuretics
- B. Acetazolamide
- C. Amiloride
- D. Thiazide diuretics (Correct Answer)
Explanation: ***Thiazide diuretics*** - **Thiazide diuretics** inhibit the **Na-Cl cotransporter in the distal convoluted tubule (DCT)**, impairing the kidney's ability to dilute urine and excrete free water - This impaired urinary dilution leads to **water retention relative to sodium**, resulting in **dilutional hyponatremia** - **Most common in elderly patients**, those on low-salt diets, or with pre-existing volume depletion - **Mechanism**: By blocking sodium reabsorption in the DCT (a key site for urinary dilution), thiazides prevent the generation of free water, leading to hyponatremia when water intake continues *Loop diuretics* - **Loop diuretics** inhibit the **Na-K-2Cl cotransporter in the thick ascending limb of Henle**, causing significant diuresis - They impair the medullary concentration gradient, **enhancing free water excretion** - **Less likely to cause hyponatremia** compared to thiazides because they promote rather than impair free water clearance - When hyponatremia occurs with loop diuretics, it's usually due to concurrent SIADH or excessive free water intake *Acetazolamide* - **Acetazolamide** is a **carbonic anhydrase inhibitor** acting primarily on the **proximal tubule** - Causes **bicarbonate and sodium excretion**, leading to mild diuresis - Main side effect is **metabolic acidosis** (type 2 RTA) - **Does not significantly impair free water excretion**, making hyponatremia uncommon *Amiloride* - **Amiloride** is a **potassium-sparing diuretic** that blocks **epithelial sodium channels (ENaC) in the collecting duct** - Weak diuretic effect, primarily used to prevent potassium loss - **Does not impair urinary dilution mechanisms**, so hyponatremia is rare - Main concern is **hyperkalemia**, especially with ACE inhibitors or in renal insufficiency
Question 472: Which ACE inhibitor is safe in renal failure?
- A. Captopril
- B. Enalapril
- C. None of the options
- D. Benazepril (Correct Answer)
Explanation: ***Benazepril*** - Among the listed ACE inhibitors, benazepril has the **most favorable excretion profile** in renal failure with approximately **50% renal and 50% hepatic elimination** (dual excretion pathway). - This balanced elimination reduces the risk of drug accumulation compared to predominantly renally excreted ACE inhibitors. - While dose adjustment may still be needed in **severe renal impairment**, benazepril is considered the **safest option among those listed** for patients with renal dysfunction. - **Note:** Fosinopril (not listed here) has true 50/50 dual elimination and requires no dose adjustment in renal failure, making it the ideal choice in clinical practice. *Captopril* - This ACE inhibitor undergoes predominantly **renal excretion (95%)** as unchanged drug and metabolites. - Requires significant **dose reduction** in renal failure to prevent accumulation and adverse effects including **hyperkalemia** and **hypotension**. - Less safe than benazepril in renal impairment due to heavy dependence on renal elimination. *Enalapril* - Enalapril is a prodrug converted to **enalaprilat**, with approximately **90% renal excretion**. - Dose adjustment is mandatory based on **creatinine clearance** in patients with renal failure. - Higher risk of accumulation and toxicity compared to dual-elimination ACE inhibitors like benazepril.
Question 473: Which sympathomimetic drug is primarily known to increase heart rate?
- A. Isoprenaline (Correct Answer)
- B. Phenylephrine
- C. Noradrenaline
- D. Adrenaline
Explanation: ***Isoprenaline*** - **Isoprenaline** (isoproterenol) is a non-selective beta-adrenergic agonist, with a strong affinity for **β1 and β2 receptors** [1]. - Its activation of **β1 receptors** in the heart leads to a significant increase in **heart rate (positive chronotropy)** and contractility (positive inotropy) [1]. - It is the **most potent chronotropic agent** among sympathomimetics and is primarily known for increasing heart rate [2]. *Phenylephrine* - **Phenylephrine** is a selective **α1 adrenergic agonist** that causes vasoconstriction [4]. - It increases blood pressure but typically causes **reflex bradycardia** (decreased heart rate) due to baroreceptor activation. - Does NOT directly increase heart rate. *Noradrenaline* - **Noradrenaline** (norepinephrine) primarily acts on **α1 receptors** causing vasoconstriction, and to a lesser extent on **β1 receptors** [3]. - While it can stimulate β1 receptors, its predominant effect is to increase **mean arterial pressure** through vasoconstriction, often causing **reflex bradycardia** [3]. *Adrenaline* - **Adrenaline** (epinephrine) acts on **α1, β1, and β2 receptors** [4]. While it does increase heart rate via **β1 receptor** stimulation, it also causes significant **vasoconstriction** (via α1) and **vasodilation** (via β2). - Its cardiovascular effects are more complex and dose-dependent compared to isoprenaline's specific chronotropic action.
Question 474: Which of the following agents requires the MOST caution when combined with spironolactone due to increased risk of hyperkalemia:
- A. ACE inhibitors (Correct Answer)
- B. Beta-blockers
- C. Amlodipine
- D. Chlorothiazide
Explanation: ***ACE inhibitors*** - Spironolactone is a **potassium-sparing diuretic** that increases potassium levels by blocking aldosterone's effects in the collecting duct [1]. - **ACE inhibitors** also decrease aldosterone production [2], leading to reduced potassium excretion and a significant risk of **severe hyperkalemia** when combined with spironolactone [1, 2].*Beta-blockers* - While beta-blockers can cause a slight increase in plasma potassium by inhibiting cellular potassium uptake, this effect is generally modest and does not pose a major hyperkalemia risk when co-administered with spironolactone. - Their primary interaction concerns blood pressure and heart rate, not direct potassium handling.*Amlodipine* - Amlodipine is a **calcium channel blocker** that primarily causes vasodilation and does not significantly alter potassium balance. - Therefore, it does not substantially increase the risk of hyperkalemia when used concurrently with spironolactone.*Chlorothiazide* - Chlorothiazide is a **thiazide diuretic** that promotes potassium excretion, leading to a risk of hypokalemia. - When combined with spironolactone, a potassium-sparing diuretic, these agents can **partially offset each other's effects** on potassium balance, potentially reducing the risk of hyperkalemia compared to ACE inhibitors.
Question 475: At which receptor is the primary action of antipsychotic medications required?
- A. M, muscarinic
- B. 5HT4 serotonergic
- C. D1 dopaminergic
- D. D2 dopaminergic (Correct Answer)
Explanation: ***D2 dopaminergic*** - The **antipsychotic effects** of typical (first-generation) antipsychotics are primarily mediated through **D2 receptor blockade** [1]. - Blocking D2 receptors in the **mesolimbic pathway** helps reduce positive symptoms of psychosis like hallucinations and delusions [2]. *M, muscarinic* - **Muscarinic receptor blockade** is a common adverse effect of some antipsychotics, leading to anticholinergic side effects such as **dry mouth** and **blurred vision**, rather than their primary therapeutic action. - This action does not directly contribute to the antipsychotic effect. *D1 dopaminergic* - While D1 receptors are involved in dopamine signaling, they are **not the primary target** for the antipsychotic action of most drugs [1]. - Some atypical antipsychotics may affect D1 receptors, but it's secondary to their D2 antagonism and serotonin modulation. *5HT4 serotonergic* - **Serotonin receptors (5HT)**, particularly 5HT2A, are important targets for atypical (second-generation) antipsychotics. - However, 5HT4 receptors are **not a primary target** for the antipsychotic effects, and 5HT2A blockade modulates dopamine release, which is still connected to the D2 hypothesis.
Question 476: What is the primary mechanism of action of opioids in pain management?
- A. Inhibition of cyclooxygenase (COX) enzymes
- B. Activation of opioid receptors in the spinal cord only
- C. Activation of opioid receptors in the brain only
- D. Activation of opioid receptors at both spinal and supraspinal levels (Correct Answer)
Explanation: ***Activation of opioid receptors at both spinal and supraspinal levels*** - Opioids primarily exert their analgesic effects by binding to and activating **mu (μ), delta (δ), and kappa (κ) opioid receptors** located throughout the central nervous system, including the brain and spinal cord. - Activation of these receptors modulates **pain perception**, emotional responses to pain, and descending pain inhibitory pathways. *Inhibition of cyclooxygenase (COX) enzymes* - This is the primary mechanism of action for **Non-Steroidal Anti-Inflammatory Drugs (NSAIDs)**, not opioids. - NSAIDs reduce pain, inflammation, and fever by blocking the synthesis of **prostaglandins**. *Activation of opioid receptors in the spinal cord only* - While opioids do activate receptors in the spinal cord to inhibit **pain transmission**, their action is not confined to this area. - Significant **supraspinal analgesic effects** contribute to their overall pain-relieving properties, affecting higher brain centers involved in pain processing. *Activation of opioid receptors in the brain only* - Opioids act on opioid receptors in the brain to modulate pain perception and emotional aspects of pain, but they also have crucial effects at the **spinal cord level**. - Their action at the spinal cord level helps to prevent pain signals from reaching the brain, making **both levels crucial** for their comprehensive pain management.
Question 477: 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 478: 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 479: 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.
Psychiatry
1 questionsWhich of the following is NOT a known side effect of lithium?
NEET-PG 2015 - Psychiatry NEET-PG Practice Questions and MCQs
Question 471: Which of the following is NOT a known side effect of lithium?
- A. Polyuria
- B. Nephropathy
- C. Ebstein's anomaly
- D. Hyperthyroidism (Correct Answer)
Explanation: ***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.