Which of the following is the mechanism of action of tetanospasmin ?
Which antibiotic is Actinomycosis sensitive to?
Which of the following best describes a Type B adverse drug reaction?
Which of the following statements about dopamine is false?
Which of the following is a centrally acting antihypertensive drug?
Which of the following statements about Conivaptan is correct?
Which of the following potassium-sparing diuretics was the first to be shown to reduce cardiac mortality in chronic heart failure patients?
Which medication is commonly used in heart failure that also has aldosterone antagonistic properties?
Which of the following drugs acts directly to induce an erection without the need for sexual stimulation?
Which of the following is not an alpha-blocker?
NEET-PG 2012 - Pharmacology NEET-PG Practice Questions and MCQs
Question 41: Which of the following is the mechanism of action of tetanospasmin ?
- A. Inhibition of release of GABA and glycine (Correct Answer)
- B. Inhibition of Ach release from synapse
- C. Inhibition of protein synthesis
- D. Activation of adenylyl cyclase
Explanation: ***Inhibition of release of GABA and glycine*** - **Tetanospasmin** is a potent neurotoxin produced by *Clostridium tetani* that acts by blocking the release of inhibitory neurotransmitters, specifically **GABA (gamma-aminobutyric acid)** and **glycine**, from presynaptic terminals in the spinal cord and brainstem. - This inhibition leads to **uncontrolled muscle spasms**, rigidity, and convulsions, characteristic of tetanus, due to the lack of inhibitory signals to motor neurons. *Inhibition of Ach release from synapse* - This mechanism is characteristic of **botulinum toxin** (produced by *Clostridium botulinum*), not tetanospasmin. - Botulinum toxin inhibits the release of **acetylcholine (ACh)** at the neuromuscular junction, leading to flaccid paralysis. *Inhibition of protein synthesis* - This mechanism is associated with toxins like **diphtheria toxin** and **exotoxin A** from *Pseudomonas aeruginosa*. - These toxins inactivate elongation factor-2 (EF-2), thereby blocking protein synthesis and causing cell death. *Activation of adenylyl cyclase* - Toxins such as **cholera toxin** and **pertussis toxin** act by activating adenylyl cyclase, leading to an increase in intracellular cAMP levels. - This mechanism causes effects like severe diarrhea in cholera and respiratory symptoms in whooping cough.
Question 42: Which antibiotic is Actinomycosis sensitive to?
- A. Streptomycin
- B. Nystatin
- C. Doxycycline
- D. Penicillin (Correct Answer)
Explanation: ***Penicillin*** - **Penicillin** is the **antibiotic of choice** for treating Actinomycosis due to the organism's high sensitivity. - Treatment typically involves a **long course** of high-dose penicillin for several months. *Streptomycin* - **Streptomycin** is an **aminoglycoside antibiotic** primarily used for **tuberculosis** and some gram-negative bacterial infections. - It is **not effective** against Actinomyces species. *Nystatin* - **Nystatin** is an **antifungal medication** used to treat **yeast infections**, particularly Candida. - It has **no antibacterial activity** and thus no role in treating Actinomycosis. *Doxycycline* - While **doxycycline** can be used as an **alternative** in patients allergic to penicillin, it is **not the primary choice**. - Its effectiveness is generally less pronounced than penicillin, and it's reserved for second-line treatment.
Question 43: Which of the following best describes a Type B adverse drug reaction?
- A. Augmented effect of drug
- B. Effect seen on chronic use of drug
- C. Delayed effect of drug
- D. Unpredictable bizarre reaction (Correct Answer)
Explanation: ***Unpredictable bizarre reaction*** - Type B reactions are **unpredictable**, **bizarre**, and not directly related to the drug's known pharmacological actions. - They often involve **immunological reactions** or genetic predispositions, such as allergies or idiosyncratic responses. *Augmented effect of drug* - This describes a **Type A** adverse drug reaction, which is predictable and results from an **exaggerated pharmacological effect** of the drug. - It is typically dose-dependent and can be managed by adjusting the dosage. *Effect seen on chronic use of drug* - This description can apply to several types of adverse reactions, but it commonly relates to **Type C (chronic) reactions**, where effects occur only after prolonged exposure. - These reactions might be due to **cumulative toxicity** or adaptive changes in the body. *Delayed effect of drug* - This aligns with **Type D (delayed) adverse drug reactions**, which manifest long after the drug exposure has ended or after a period of latency. - Examples include **carcinogenesis** or teratogenesis, occurring months or years later.
Question 44: Which of the following statements about dopamine is false?
- A. Improves renal perfusion
- B. Causes Vasoconstriction
- C. Causes increase in GI Ischemia (Correct Answer)
- D. Positive ionotropic
Explanation: ***Causes increase in GI Ischemia*** (FALSE Statement) - This statement is **incorrect and misleading** as dopamine does not primarily "cause increase in GI ischemia" - While dopamine at **higher doses** can cause **splanchnic vasoconstriction** via alpha-1 receptors, this is not characterized as "causing GI ischemia" in standard pharmacology - GI ischemia is a potential adverse effect in susceptible patients, but not a primary pharmacological effect or standard clinical description of dopamine *Positive inotropic* (TRUE Statement) - Dopamine is a **catecholamine** with dose-dependent effects; at **moderate doses (5-10 mcg/kg/min)**, it stimulates **beta-1 adrenergic receptors** in the heart - This beta-1 stimulation leads to increased **myocardial contractility** and **heart rate**, thus exerting a **positive inotropic effect** - This is a well-established therapeutic effect of dopamine *Improves renal perfusion* (TRUE Statement) - At **low doses (0.5-3 mcg/kg/min)**, dopamine selectively activates **dopamine-1 (D1) receptors** in the renal vasculature - This activation causes **renal vasodilation**, leading to increased **renal blood flow**, improved **glomerular filtration rate**, and enhanced **sodium excretion** - This "renal dose" effect is a classic pharmacological property of dopamine *Causes Vasoconstriction* (TRUE Statement) - At **high doses (>10 mcg/kg/min)**, dopamine primarily stimulates **alpha-1 adrenergic receptors** - This leads to generalized **vasoconstriction**, increasing **systemic vascular resistance** and **blood pressure** - This dose-dependent alpha effect is well-documented
Question 45: Which of the following is a centrally acting antihypertensive drug?
- A. Phenoxybenzamine
- B. Propranolol
- C. Prazosin
- D. Methyldopa (Correct Answer)
Explanation: ***Methyldopa*** - **Methyldopa** is a **prodrug** that is converted to **alpha-methylnorepinephrine** in the brain, which then stimulates **alpha-2 adrenergic receptors** in the brainstem. - This stimulation reduces **sympathetic outflow** from the central nervous system, leading to decreased heart rate, stroke volume, and peripheral vascular resistance, thus lowering blood pressure. *Phenoxybenzamine* - **Phenoxybenzamine** is an **alpha-1 and alpha-2 adrenergic receptor antagonist** (non-selective alpha blocker) that primarily acts peripherally. - It causes **vasodilation** by blocking alpha-1 receptors on smooth muscle, which reduces peripheral vascular resistance. *Propranolol* - **Propranolol** is a **non-selective beta-blocker** that primarily acts on peripheral beta-adrenergic receptors. - It reduces heart rate and cardiac output by blocking **beta-1 receptors** in the heart and can also affect beta-2 receptors in the lungs and vasculature. *Prazosin* - **Prazosin** is a **selective alpha-1 adrenergic receptor antagonist** that acts primarily on peripheral blood vessels. - It causes **vasodilation** in both arteries and veins by blocking alpha-1 receptors, which reduces both preload and afterload, lowering blood pressure.
Question 46: Which of the following statements about Conivaptan is correct?
- A. It is a vasopressin antagonist. (Correct Answer)
- B. It selectively acts on V2 receptors.
- C. It is administered orally.
- D. All of the options.
Explanation: ***It is a vasopressin antagonist.*** * **Conivaptan** is a non-peptide, dual **vasopressin V1A and V2 receptor antagonist**, meaning it blocks the action of vasopressin. * By blocking vasopressin, it promotes **aquaresis** (excretion of solute-free water), which is beneficial in conditions like **hyponatremia**. * *It selectively acts on V2 receptors.* * **Conivaptan** is a **dual antagonist**, blocking both **V1A and V2 receptors**, not just V2. * **Tolvaptan**, in contrast, is a selective **V2 receptor antagonist**. * *It is administered orally.* * **Conivaptan** is typically administered intravenously, particularly in hospital settings for acute hyponatremia. * **Tolvaptan** is the orally administered vasopressin antagonist. * *All of the options.* * Since Conivaptan is not selectively acting on V2 receptors and is not administered orally, this option is incorrect.
Question 47: Which of the following potassium-sparing diuretics was the first to be shown to reduce cardiac mortality in chronic heart failure patients?
- A. Spironolactone (Correct Answer)
- B. Amiloride
- C. Triamterene
- D. Eplerenone
Explanation: ***Spironolactone*** - **Spironolactone** was the first potassium-sparing diuretic shown to reduce **cardiac mortality** in patients with **chronic heart failure** in the **RALES trial** (Randomized Aldactone Evaluation Study). - Its beneficial effects in heart failure are primarily attributed to its **aldosterone receptor antagonist** properties, which counteract the harmful effects of aldosterone on the myocardium and vasculature, rather than just its diuretic effect. *Amiloride* - **Amiloride** is a potassium-sparing diuretic that works by directly inhibiting **epithelial sodium channels (ENaC)** in the collecting duct. - While it helps in potassium conservation, it has not been shown to significantly reduce cardiac mortality in chronic heart failure patients in clinical trials. *Triamterene* - **Triamterene** is another potassium-sparing diuretic that also directly inhibits **ENaC** in the collecting duct, similar to amiloride. - Like amiloride, it is used to prevent hypokalemia but lacks evidence for significant **cardiac mortality reduction** in chronic heart failure. *Eplerenone* - **Eplerenone** is a selective **aldosterone receptor antagonist**, similar to spironolactone, with fewer hormonal side effects. - While it has been shown to reduce **cardiac mortality** in chronic heart failure (e.g., in the EMPHASIS-HF trial), it was introduced later than spironolactone and was not the *first* to demonstrate this benefit.
Question 48: Which medication is commonly used in heart failure that also has aldosterone antagonistic properties?
- A. Carvedilol
- B. Spironolactone (Correct Answer)
- C. Abiraterone
- D. Sacubitril/Valsartan
Explanation: ***Spironolactone*** - **Spironolactone** is a **potassium-sparing diuretic** that acts as a **competitive antagonist of aldosterone** receptors, primarily in the collecting ducts of the kidneys. - This action leads to increased excretion of sodium and water, and retention of potassium, which is beneficial in **heart failure** by reducing fluid overload and mitigating the detrimental effects of aldosterone on cardiac remodeling. *Carvedilol* - **Carvedilol** is a **beta-blocker** with additional **alpha-1 blocking** properties, commonly used in heart failure to reduce heart rate, blood pressure, and myocardial oxygen demand. - It does not possess significant aldosterone antagonistic properties. *Sacubitril/Valsartan* - **Sacubitril/Valsartan** is an **angiotensin receptor-neprilysin inhibitor (ARNI)**. Valsartan is an **angiotensin receptor blocker (ARB)**, and sacubitril inhibits neprilysin, an enzyme that degrades natriuretic peptides. - While it modulates the **renin-angiotensin-aldosterone system (RAAS)** and is highly effective in heart failure, it does not directly antagonize aldosterone receptors. *Abiraterone* - **Abiraterone** is an **androgen-biosynthesis inhibitor** used in the treatment of **prostate cancer**. - Its primary mechanism involves inhibiting **CYP17**, an enzyme critical for androgen production, and it has no role in the management of heart failure or aldosterone antagonism.
Question 49: Which of the following drugs acts directly to induce an erection without the need for sexual stimulation?
- A. Sildenafil
- B. Tadalafil
- C. Alprostadil (Correct Answer)
- D. Testosterone
Explanation: ***Alprostadil***- **Alprostadil** is a **prostaglandin E1** analog that can directly induce vasodilation in the penile arteries, leading to an erection without sexual stimulation [1].- It is typically administered via **intracavernosal injection** or as a **urethral suppository**.*Sildenafil*- **Sildenafil** is a **PDE5 inhibitor** that works by enhancing the effects of **nitric oxide**, which is released in response to sexual stimulation [2, 3].- It requires **sexual arousal** to be effective, as it doesn't directly initiate the erectile process [2, 3].*Tadalafil*- Similar to sildenafil, **tadalafil** is also a **PDE5 inhibitor** that works by increasing cGMP levels and promoting smooth muscle relaxation [2, 3].- Its action is dependent on the release of **nitric oxide** triggered by sexual stimulation [2, 3].*Testosterone*- **Testosterone** is a hormone involved in sex drive and overall erectile function over time, but it does not directly or acutely induce an erection.- Its primary role in erectile dysfunction is in cases of **hypogonadism**, and it requires sexual stimulation for its effects on erection.
Question 50: Which of the following is not an alpha-blocker?
- A. Atenolol (Correct Answer)
- B. Indoramine
- C. Idazoxan
- D. Prazosin
Explanation: ***Atenolol*** - Atenolol is a **selective beta-1 adrenergic receptor blocker**, primarily used to treat hypertension, angina, and certain arrhythmias. - Its mechanism of action involves **blocking the effects of adrenaline** on the heart, leading to decreased heart rate and blood pressure, rather than affecting alpha receptors. *Indoramine* - Indoramine is an **alpha-1 adrenergic receptor blocker** used historically for hypertension. - It specifically **antagonizes alpha-1 receptors** in vascular smooth muscle, causing vasodilation. *Idazoxan* - Idazoxan is an **alpha-2 adrenergic receptor antagonist**, primarily used in research contexts. - It **blocks presynaptic alpha-2 receptors**, which can lead to an increase in norepinephrine release. *Prazosin* - Prazosin is a well-known **alpha-1 adrenergic receptor blocker** used to treat hypertension and benign prostatic hyperplasia (BPH). - It causes **vasodilation** by relaxing vascular smooth muscle, thus lowering blood pressure.