Which of the following is a synthetic estrogen?
Which of the following medications does not interact with warfarin?
Which of the following antibiotics is known to cause bleeding due to its effect on blood clotting?
All are true regarding Sunitinib except which of the following?
Which of the following is not used as treatment for lymphatic filariasis -
What is the antidote for Ethylene Glycol?
Which of the following is the mechanism of action of tetanospasmin ?
What is the primary cardiotoxic effect of bupivacaine?
Which medication increases the efficacy of salmeterol when used together?
Desmopressin is preferred over vasopressin because it:
NEET-PG 2012 - Pharmacology NEET-PG Practice Questions and MCQs
Question 31: Which of the following is a synthetic estrogen?
- A. Estrone
- B. Estriol
- C. Estradiol
- D. Diethylstilbestrol (Correct Answer)
Explanation: ***Diethylstilbestrol*** - **Diethylstilbestrol (DES)** is a **synthetic non-steroidal estrogen** that was historically used as a medication, particularly to prevent miscarriage. - Its use was discontinued after being linked to various adverse effects, including **vaginal clear cell adenocarcinoma** in female offspring whose mothers took DES during pregnancy. *Estrone* - **Estrone** is one of the three major **naturally occurring endogenous estrogens** in humans. - It is the primary estrogen during **menopause** and is derived from androstenedione. *Estriol* - **Estriol** is another of the three major **naturally occurring estrogens**, predominantly produced during **pregnancy** by the placenta. - It is often used as a marker for fetal well-being. *Estradiol* - **Estradiol** is the **most potent and abundant naturally occurring estrogen** in women during their reproductive years. - It plays a crucial role in the development and maintenance of female reproductive tissues and secondary sexual characteristics.
Question 32: Which of the following medications does not interact with warfarin?
- A. Barbiturate
- B. Oral contraceptive
- C. Cephalosporins
- D. Benzodiazepines (Correct Answer)
Explanation: ***Benzodiazepines*** - **Benzodiazepines** are generally considered safe to use with warfarin as they are extensively metabolized in the liver, but they do not typically alter the **cytochrome P450 enzymes** responsible for warfarin metabolism. - They also do not interfere with **vitamin K recycling** or **platelet function**, which are key mechanisms through which other drugs interact with warfarin. *Barbiturate* - **Barbiturates** are **potent inducers of hepatic enzymes**, particularly CYP2C9, which is responsible for metabolizing warfarin. - This enzyme induction leads to **increased warfarin metabolism**, reducing its anticoagulant effect and necessitating higher warfarin doses. *Oral contraceptive* - **Oral contraceptives** can **reduce the anticoagulant effect of warfarin** by inducing clotting factors or inhibiting warfarin metabolism. - This interaction can increase the risk of **thromboembolic events** in patients on warfarin. *Cephalosporins* - Certain **cephalosporins**, especially those with a **methylthiotetrazole (MTT) side chain** (e.g., Cefamandole, Cefoperazone, Moxalactam), can **inhibit vitamin K epoxide reductase**. - This inhibition leads to a **decrease in vitamin K-dependent clotting factors**, thus potentiating the anticoagulant effect of warfarin and increasing bleeding risk.
Question 33: Which of the following antibiotics is known to cause bleeding due to its effect on blood clotting?
- A. Moxalactam (Correct Answer)
- B. Cefaloridine
- C. Cefazolin
- D. Ceftazidime
Explanation: Moxalactam - Moxalactam is a **third-generation cephalosporin** known to cause **hypoprothrombinemia** and platelet dysfunction, leading to an increased risk of bleeding. - This effect is due to its **N-methylthiotetrazole (NMTT) side chain**, which inhibits vitamin K-dependent clotting factor synthesis. Cefaloridine - This is a **first-generation cephalosporin** that does not have the NMTT side chain and is not commonly associated with significant bleeding risks. - Its primary adverse effect of concern is **nephrotoxicity** at high doses, rather than coagulopathy. Ceftazidime - Ceftazidime is a **third-generation cephalosporin** primarily used for *Pseudomonas aeruginosa* infections but does **not contain the NMTT side chain** responsible for bleeding complications. - While broad-spectrum, it generally has a favorable safety profile concerning coagulation. *Cefazolin* - Cefazolin is a **first-generation cephalosporin** [1] widely used for surgical prophylaxis and skin infections [1], and it does **not interfere with coagulation** pathways. - Its main side effects are typical for penicillin-related antibiotics, such as hypersensitivity reactions [1],[2].
Question 34: All are true regarding Sunitinib except which of the following?
- A. It inhibits tyrosine kinase receptors
- B. It is excreted primarily in urine (Correct Answer)
- C. It is used for the treatment of GIST
- D. It is used for renal cell carcinoma
Explanation: ***It is excreted primarily in urine*** - **Sunitinib** is predominantly metabolized in the **liver** by CYP3A4 and primarily excreted in the **feces**, not urine. - Its major active metabolite, N-desethyl sunitinib, is also primarily eliminated via the fecal route. *It inhibits tyrosine kinase receptors* - **Sunitinib** is a **multitargeted receptor tyrosine kinase (RTK) inhibitor**. - It blocks several RTKs involved in tumor growth, angiogenesis, and metastatic progression, such as **VEGFR, PDGFR, KIT, and FLT3**. *It is used for the treatment of GIST* - **Sunitinib** is approved for the treatment of **imatinib-refractory** or **imatinib-intolerant gastrointestinal stromal tumors (GIST)**. - Its mechanism in GIST involves inhibiting KIT and PDGFR, which are often mutated and constitutively active in this cancer. *It is used for renal cell carcinoma* - **Sunitinib** is a standard first-line treatment for **advanced renal cell carcinoma (RCC)**. - Its efficacy in RCC is primarily due to its inhibition of VEGFR, which targets the high vascularity characteristic of kidney tumors.
Question 35: Which of the following is not used as treatment for lymphatic filariasis -
- A. DEC
- B. Albendazole
- C. Ivermectin
- D. Praziquantel (Correct Answer)
Explanation: ***Praziquantel*** - **Praziquantel** is primarily an **anthelmintic drug** effective against **schistosomiasis** and **tapeworm infections**. - It does not have a significant role in the treatment of **lymphatic filariasis**. *Ivermectin* - **Ivermectin** is one of the **mainstays** of treatment for **lymphatic filariasis**, particularly in combination therapies. - It works by paralyzing and killing **microfilariae**, reducing their numbers in the bloodstream. *DEC* - **Diethylcarbamazine (DEC)** is a **highly effective antifilarial drug** used to kill both **microfilariae** and **adult worms** in lymphatic filariasis. - It is often used in mass drug administration programs and for individual treatment. *Albendazole* - **Albendazole** is an **anthelmintic drug** often used in combination with **Ivermectin** or **DEC** for the treatment of **lymphatic filariasis**. - It helps to kill **microfilariae** and has some macrofilaricidal effects, reducing the viability of adult worms.
Question 36: What is the antidote for Ethylene Glycol?
- A. Barbiturate
- B. Acetylcysteine
- C. Ferric chloride
- D. Fomepizole (Correct Answer)
Explanation: ***Fomepizole*** - **Fomepizole** is the primary and preferred antidote for ethylene glycol poisoning, as it competitively inhibits **alcohol dehydrogenase**, the enzyme responsible for metabolizing ethylene glycol into its toxic metabolites. - By blocking this enzyme, fomepizole prevents the formation of harmful compounds like **glycolic acid** and **oxalic acid**, which cause metabolic acidosis and kidney damage. - **Ethanol** is an alternative antidote that works by the same mechanism (competitive inhibition of alcohol dehydrogenase) and can be used when fomepizole is unavailable, though fomepizole is preferred due to better safety profile and easier dosing. *Barbiturate* - **Barbiturates** are a class of psychoactive drugs that act as central nervous system depressants, primarily used for sedation, anesthesia, and seizure control. - They have no role in neutralizing or metabolizing ethylene glycol or its toxic byproducts. *Acetylcysteine* - Acetylcysteine is an antidote primarily used for **acetaminophen (paracetamol) overdose**, where it replenishes glutathione stores and detoxifies its toxic metabolite, **NAPQI**. - It does not have any direct antidotal effect against ethylene glycol or its metabolites. *Ferric chloride* - **Ferric chloride** is a chemical compound used in various industrial processes, water treatment, and as a laboratory reagent. - It is highly corrosive and toxic if ingested, but it is not used as an antidote for any type of poisoning, including ethylene glycol.
Question 37: 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 38: What is the primary cardiotoxic effect of bupivacaine?
- A. Depressed pacemaker activity (Correct Answer)
- B. Toxic compound damaging myocardial cells
- C. Depressed neural control on heart
- D. Vascular thrombosis and Myocardial ischemia
Explanation: ***Depressed pacemaker activity*** - **Bupivacaine** is a potent **local anesthetic** that blocks voltage-gated **sodium channels** in myocardial cells with **high affinity** and **slow dissociation kinetics**. - This prolonged channel blockade leads to decreased cardiac excitability and **depressed automaticity** of pacemaker cells, particularly affecting the **SA node** and **His-Purkinje system**. - Results in slowing of the **heart rate**, **bradyarrhythmias**, **conduction blocks**, and potentially **ventricular arrhythmias** or **asystole**. - Bupivacaine is **more cardiotoxic** than other local anesthetics due to its **lipophilicity** and prolonged binding to cardiac sodium channels. *Toxic compound damaging myocardial cells* - While **bupivacaine** is cardiotoxic, its primary mechanism is not direct **cellular damage** through cytotoxic effects, oxidative stress, or cell membrane lysis. - The toxicity is predominantly due to **electrophysiological effects** on ion channels, interfering with normal cardiac conduction and contractility. *Depressed neural control on heart* - **Bupivacaine's** cardiotoxicity primarily affects the **myocardium directly** through sodium channel blockade, rather than indirectly through the **autonomic nervous system**. - Although high systemic concentrations can affect the **central nervous system** (causing seizures and CNS depression), the direct cardiac effects occur independently of neural influence. *Vascular thrombosis and Myocardial ischemia* - **Bupivacaine** cardiotoxicity does not typically involve formation of **thrombi** or mechanisms leading to **myocardial ischemia** through coronary artery occlusion. - Its effects are predominantly on the **electrical conduction system**, **myocardial contractility**, and **cardiac ion channels**, not the vascular supply to the heart.
Question 39: Which medication increases the efficacy of salmeterol when used together?
- A. Corticosteroid (Correct Answer)
- B. Theophylline
- C. Ipratropium
- D. Sodium cromoglycate
Explanation: ***Corticosteroid*** - **Corticosteroids** act synergistically with **beta-2 agonists** like salmeterol by increasing the number and sensitivity of beta-2 receptors on bronchial smooth muscle cells. - They also reduce inflammation, which contributes to airway hyperresponsiveness, thereby improving the overall efficacy of bronchodilators. *Theophylline* - **Theophylline** is a methylxanthine that causes bronchodilation through inhibition of phosphodiesterase, but it is not directly synergistic with **salmeterol** in potentiating its primary action. - While both treat airway obstruction, their mechanisms are distinct, and theophylline has a narrow therapeutic index with significant side effects. *Ipratropium* - **Ipratropium** is an **anticholinergic bronchodilator** that blocks muscarinic receptors, leading to bronchodilation. - Its mechanism of action is different from that of **salmeterol (a beta-2 agonist)**, and while they can be used together for additive bronchodilation, ipratropium does not directly increase the efficacy of salmeterol itself. *Sodium cromoglycate* - **Sodium cromoglycate** is a **mast cell stabilizer** that prevents the release of inflammatory mediators, primarily used for asthma prophylaxis. - It does not have direct bronchodilatory effects and does not enhance the bronchodilatory action of **salmeterol**.
Question 40: Desmopressin is preferred over vasopressin because it:
- A. Is more potent and has little vasoconstrictor activity (Correct Answer)
- B. Is more potent than vasopressin
- C. Has little vasoconstrictor activity
- D. Is more selective for V2 receptors than vasopressin
Explanation: **Is more potent and has little vasoconstrictor activity** - **Desmopressin** is a synthetic analog of **vasopressin** (ADH) that is modified to have much higher selectivity for **V2 receptors** in the renal collecting ducts, leading to potent **antidiuretic effects** [1], [3]. - This selective action results in significantly **reduced vasoconstrictor activity** (mediated by V1 receptors) compared to natural vasopressin, making it safer for clinical use to manage water balance without significant cardiovascular side effects [1], [3]. *Is more potent than vasopressin* - While desmopressin is indeed more potent in its **antidiuretic effect** due to increased affinity for **V2 receptors**, this option alone doesn't specify the critical advantage of *reduced vasoconstrictor activity* [3]. - Its superior potency alone doesn't fully explain its preference over vasopressin, as the **side-effect profile** is a major consideration. *Has little vasoconstrictor activity* - This statement is true and highlights a key advantage of desmopressin, but it omits the fact that **desmopressin is also more potent** in its desired antidiuretic effect compared to natural vasopressin [1]. - Both the **potency** and **reduced vasoconstrictor activity** contribute to its superior clinical profile [3]. *Is more selective for V2 receptors than vasopressin* - **Desmopressin's increased selectivity** for **V2 receptors** is the mechanistic basis for its preferred properties, leading to both greater antidiuretic potency and reduced vasoconstriction [1], [4]. - However, the option "Is more potent and has little vasoconstrictor activity" describes the *clinical consequences* of this selectivity, which are the direct reasons for its preferred use [2].