Alkaline diuresis in drug poisoning is not done in?
Which of the following pairs are considered physiological antagonists in pharmacology?
Which of the following drug combinations demonstrates receptor level antagonism?
Which of the following is not a common side effect of clonidine?
Which of the following is a lipid insoluble beta-blocker?
Which of the following is an example of topical administration producing only local effects (not systemic)?
Which of the following statements represents the most clinically significant aspect of drug metabolism?
Which of the following are CYP3A inhibitors?
Beta-blockers should be used with caution in patients with?
Which antimuscarinic drug is used in overactive bladder?
NEET-PG 2015 - Pharmacology NEET-PG Practice Questions and MCQs
Question 11: 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.
Question 12: Which of the following pairs are considered physiological antagonists in pharmacology?
- A. Adrenaline and Isoprenaline
- B. Isoprenaline and Propranolol
- C. Histamine and Adrenaline (Correct Answer)
- D. All of the options
Explanation: ***Histamine and Adrenaline*** - **Physiological antagonism** occurs when two drugs produce opposite effects by acting on different receptors or pathways. - **Histamine** causes bronchoconstriction and vasodilation, while **adrenaline** causes bronchodilation and vasoconstriction, counteracting each other's effects through different mechanisms. *Adrenaline and Isoprenaline* - Both **adrenaline** and **isoprenaline** are **adrenergic agonists** that produce similar physiological effects, primarily through beta-adrenergic receptor activation. - They are not physiological antagonists but rather have **synergistic** or similar pharmacological actions. *Isoprenaline and Propranolol* - **Isoprenaline** is a **beta-adrenergic agonist**, while **propranolol** is a **beta-adrenergic antagonist**. - This is an example of **pharmacological antagonism (receptor antagonism)**, where one drug blocks the effect of another at the same receptor site, rather than physiological antagonism.
Question 13: Which of the following drug combinations demonstrates receptor level antagonism?
- A. Histamine and Adrenaline
- B. Isoprenaline (agonist) and Propranolol (antagonist) (Correct Answer)
- C. Adrenaline and Isoprenaline
- D. None of the options
Explanation: ***Isoprenaline (agonist) and Propranolol (antagonist)*** - **Propranolol** is a **beta-adrenergic receptor antagonist**, meaning it binds to and blocks beta-adrenergic receptors. - **Isoprenaline** is a **beta-adrenergic receptor agonist**, meaning it activates these same receptors. Their combined action demonstrates **receptor-level antagonism** as propranolol prevents isoprenaline from binding and eliciting its effect. *Histamine and Adrenaline* - This combination illustrates **physiological antagonism**, where two drugs produce opposite effects through different mechanisms and different receptors. - **Adrenaline** causes bronchodilation and vasoconstriction via adrenergic receptors, counteracting the effects of **histamine** (e.g., bronchoconstriction, vasodilation) which acts on histamine receptors. *Adrenaline and Isoprenaline* - Both **adrenaline** and **isoprenaline** are **agonists** of adrenergic receptors, specifically beta-adrenergic receptors. - They would produce similar effects (e.g., increased heart rate, bronchodilation) rather than opposing each other at the receptor level. *None of the options* - This is incorrect because **Isoprenaline and Propranolol** is a valid example of receptor-level antagonism, making this option unnecessary.
Question 14: Which of the following is not a common side effect of clonidine?
- A. Xerostomia
- B. Sedation
- C. Diarrhea (Correct Answer)
- D. Impotency
Explanation: ***Diarrhea*** - **Clonidine** commonly causes **constipation**, not diarrhea, due to its **alpha-2 adrenergic agonist** effects, which decrease gastrointestinal motility. - Diarrhea is not typically associated with clonidine's mechanism of action or adverse effect profile. *Xerostomia* - **Xerostomia** (dry mouth) is a very common side effect of **clonidine** occurring in up to 40% of patients. - This results from **alpha-2 agonist** activity that reduces sympathetic stimulation of salivary gland secretions. - This symptom can significantly impact patient compliance and quality of life. *Sedation* - **Sedation** is a frequent side effect of **clonidine**, particularly when initiating treatment or increasing dosage, because it acts as an **alpha-2 agonist** in the central nervous system, reducing sympathetic outflow and promoting drowsiness. - Patients are often advised to avoid driving or operating heavy machinery until they know how the medication affects them. *Impotency* - **Impotency** or **erectile dysfunction** is a recognized and common sexual side effect of **clonidine**, which can interfere with quality of life and adherence to treatment for hypertension. - This effect is related to the drug's impact on the autonomic nervous system and vascular tone through central alpha-2 agonism.
Question 15: Which of the following is a lipid insoluble beta-blocker?
- A. Timolol
- B. Carvedilol
- C. Pindolol
- D. Celiprolol (Correct Answer)
Explanation: ***Celiprolol*** - **Celiprolol** is a **hydrophilic** (lipid-insoluble) beta-blocker, meaning it has low lipid solubility and does not readily cross the blood-brain barrier. - This property reduces the likelihood of **CNS side effects** such as nightmares and insomnia. *Timolol* - **Timolol** is a **lipophilic** (lipid-soluble) beta-blocker, allowing it to penetrate the central nervous system. - Its high lipid solubility contributes to a higher incidence of **CNS side effects**. *Carvedilol* - **Carvedilol** is a **lipophilic** mixed alpha and beta-blocker, which means it can cross the blood-brain barrier. - This can lead to central nervous system effects, although its primary clinical use is in heart failure and hypertension. *Pindolol* - **Pindolol** is a **lipophilic** beta-blocker with intrinsic sympathomimetic activity (ISA). - Its lipid solubility allows it to enter the brain, potentially causing **CNS-related side effects**.
Question 16: Which of the following is an example of topical administration producing only local effects (not systemic)?
- A. Topical corticosteroid cream (Correct Answer)
- B. Sublingual nitroglycerin
- C. Transdermal patch
- D. Rectal diazepam
Explanation: ***Topical corticosteroid cream*** - When applied to the skin for conditions like dermatitis, topical corticosteroids primarily exert their effects at the site of application, reducing **local inflammation** and itching. - While systemic absorption can occur with potent steroids over large areas, typical use aims for **localized action** without significant systemic effects. *Sublingual nitroglycerin* - This route is designed for **rapid systemic absorption** through the oral mucosa, bypassing first-pass metabolism to quickly treat angina. - The goal is a **widespread vasodilatory effect** throughout the body, not a local one within the mouth. *Transdermal patch* - Transdermal patches, such as those for nicotine or fentanyl, are specifically designed to deliver medication **systemically** through the skin into the bloodstream over a prolonged period. - They provide a **sustained release** and systemic therapeutic effect throughout the body. *Rectal diazepam* - Administered rectally, diazepam is absorbed into the systemic circulation to produce **CNS effects** such as sedation, anxiolysis, or anticonvulsant activity. - Although the administration is local, the intended clinical effect is **systemic** and widespread throughout the body.
Question 17: Which of the following statements represents the most clinically significant aspect of drug metabolism?
- A. Most common enzyme involved is CYP 3A4/5 (Correct Answer)
- B. Glucuronidation is a phase II reaction
- C. Reduction is a phase I reaction
- D. Cytochrome P450 is involved in phase I reactions
Explanation: ***Most common enzyme involved is Cyp 3A4/5*** - CYP3A4/5 is the **most abundant and clinically significant** cytochrome P450 enzyme, responsible for metabolizing approximately **50% of all clinically used drugs**. - Its widespread involvement means variations in its activity (due to **genetics, drug interactions, or disease**) have a major impact on drug efficacy and toxicity. *Glucuronidation is a phase II reaction* - While correct that glucuronidation is a **Phase II metabolic reaction**, this statement describes a biochemical classification rather than a clinically significant aspect compared to the involvement of CYP3A4/5. - Phase II reactions generally involve **conjugation** to increase water solubility and facilitate excretion, but they do not collectively account for as many drug interactions as CYP3A4/5 alone. *Reduction is a phase I reaction* - This statement is factually correct as **reduction** is indeed a **Phase I metabolic reaction**. - However, it represents a generic classification of a metabolic pathway and doesn't highlight the specific clinical importance or prevalence of a particular enzyme or reaction in drug metabolism. *Cytochrome P450 is involved in phase I reactions* - This is true; the **cytochrome P450 system** is the primary enzyme system for **Phase I metabolism**, which introduces or exposes polar groups to make drugs more reactive. - While fundamentally important, this statement is too broad; it does not specify the most clinically significant *aspect* or *enzyme* within the P450 system compared to directly identifying CYP3A4/5.
Question 18: Which of the following are CYP3A inhibitors?
- A. Ritonavir
- B. Amiodarone
- C. Verapamil
- D. Both a and c (Correct Answer)
Explanation: ***Both a and c (Ritonavir and Verapamil)*** - **Ritonavir** is a **potent CYP3A4 inhibitor**, one of the strongest known, commonly used as a pharmacokinetic booster for other protease inhibitors to increase their bioavailability - **Verapamil** is a **calcium channel blocker** that acts as a **moderate CYP3A4 inhibitor**, leading to clinically significant drug interactions requiring dose adjustments - Both drugs have **clinically relevant and well-established** CYP3A4 inhibitory effects *Ritonavir alone* - While correct that Ritonavir is a potent CYP3A4 inhibitor, this option is incomplete as it excludes Verapamil - Ritonavir's inhibitory effect is so strong that it can increase plasma concentrations of co-administered CYP3A4 substrates by several-fold *Amiodarone* - Amiodarone is primarily a **potent inhibitor of CYP2C9, CYP2D6, and P-glycoprotein** - While it does have **weak to moderate CYP3A4 inhibitory activity**, this effect is **less clinically significant** compared to its effects on other CYP enzymes - In the context of clinically important CYP3A4 inhibitors, Ritonavir and Verapamil are more relevant examples *Verapamil alone* - While correct that Verapamil is a CYP3A4 inhibitor, this option is incomplete as it excludes Ritonavir - Verapamil can increase plasma concentrations of drugs like simvastatin, cyclosporine, and other CYP3A4 substrates
Question 19: 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 20: Which antimuscarinic drug is used in overactive bladder?
- A. Trospium (Correct Answer)
- B. Atropine
- C. Tropicamide
- D. Pirenzepine
Explanation: ***Trospium*** - **Trospium** is a quaternary ammonium compound that acts as an **antimuscarinic agent** primarily used to treat **overactive bladder (OAB)**. - Its **polar nature** limits its ability to cross the blood-brain barrier, reducing central nervous system side effects common with other antimuscarinics. *Tropicamide* - **Tropicamide** is an **antimuscarinic** agent primarily used as a **mydriatic** (to dilate pupils) and **cycloplegic** (to paralyze the ciliary muscle) for ophthalmic examinations. - It has a short duration of action, making it unsuitable for chronic conditions like overactive bladder. *Atropine* - **Atropine** is a non-selective **muscarinic antagonist** with a wide range of uses, including bradycardia, organophosphate poisoning, and ophthalmic procedures. - While it has antimuscarinic effects on the bladder, its systemic side effects (e.g., dry mouth, blurred vision, tachycardia) limit its use for overactive bladder. *Pirenzepine* - **Pirenzepine** is a selective **M1 muscarinic antagonist** primarily used to treat **peptic ulcers** by reducing gastric acid secretion. - Its selectivity for M1 receptors means it has limited efficacy for relieving bladder symptoms, which are primarily mediated by M2 and M3 receptors.