What is the name of the mumps vaccine?
Which of the following statements about dopamine is false?
As per RNTCP guidelines, Multi drug resistance (MDR) TB is defined as resistance to:
All are true regarding Sunitinib except which of the following?
What is the primary reason for using a combination of four drugs in Anti-Koch's Treatment (AKT) for tuberculosis?
Which of the following drugs acts directly to induce an erection without the need for sexual stimulation?
Which of the following is not a selective serotonin reuptake inhibitor?
What is the primary cardiotoxic effect of bupivacaine?
Which of the following medications does not interact with warfarin?
Which of the following is a synthetic estrogen?
NEET-PG 2012 - Pharmacology NEET-PG Practice Questions and MCQs
Question 21: What is the name of the mumps vaccine?
- A. Jeryl Lynn (Correct Answer)
- B. Moraten
- C. Edmonston-Zagreb
- D. Schwarz
Explanation: ***Jeryl Lynn*** - The **Jeryl Lynn strain** is a widely used and highly effective **live attenuated mumps vaccine virus** found in many combined MMR (measles, mumps, rubella) vaccines. - It was developed by **Maurice Hilleman** and is known for its **low reactogenicity** and good safety profile. *Edmonston-Zagreb* - The **Edmonston-Zagreb strain** is a specific type of **live attenuated measles vaccine virus**, not mumps. - It is used in some combinations of the **MMR vaccine** but is distinct from the mumps component. *Schwarz* - The **Schwarz strain** is another variant of **live attenuated measles vaccine virus**, primarily distinguished by its passage history. - Like Edmonston-Zagreb, it targets **measles prevention** and is not used for mumps. *Moraten* - The **Moraten strain** is a specific **live attenuated measles vaccine virus** that is derived from the **Edmonston B strain**. - It is one of the most common measles vaccine strains, also used in **MMR vaccines**, but it does not protect against mumps.
Question 22: 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 23: As per RNTCP guidelines, Multi drug resistance (MDR) TB is defined as resistance to:
- A. Rifampicin
- B. Rifampicin, isoniazid and ethambutol
- C. None of the above
- D. Rifampicin and isoniazid (Correct Answer)
Explanation: ***Rifampicin and isoniazid*** - According to **RNTCP guidelines** (now NTEP), **MDR-TB** is specifically defined as tuberculosis that is resistant to at least both **rifampicin** and **isoniazid**. - These two drugs are the **most potent first-line anti-TB medications**, and resistance to both significantly complicates treatment. *Rifampicin* - While resistance to **rifampicin alone** is a serious concern, it is classified as **rifampicin-resistant TB (RR-TB)**, not full **MDR-TB**. - **MDR-TB** requires resistance to at least two key first-line drugs. *Rifampicin, isoniazid and ethambutol* - Resistance to **rifampicin**, **isoniazid**, and **ethambutol** would be a form of **MDR-TB** (as it includes resistance to rifampicin and isoniazid), but it is a more extensive form of resistance. - The minimum definition of **MDR-TB** focuses on the two most crucial first-line drugs. *None of the above* - This option is incorrect because there is a specific definition for **MDR-TB** that aligns with one of the provided choices. - The guidelines clearly define **MDR-TB** based on resistance to specific drugs.
Question 24: 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 25: What is the primary reason for using a combination of four drugs in Anti-Koch's Treatment (AKT) for tuberculosis?
- A. To decrease the risk of resistance due to mutation. (Correct Answer)
- B. To decrease the risk of resistance due to conjugation.
- C. To enhance overall treatment efficacy.
- D. To simplify treatment.
Explanation: ***To decrease the risk of resistance due to mutation*** - **Tuberculosis bacteria** can spontaneously develop resistance to a single drug through **random genetic mutations**. - Using multiple drugs simultaneously significantly reduces the probability that a bacterium will spontaneously develop resistance to **all drugs** in the regimen. - This is the **primary rationale** for multi-drug therapy in TB, as emphasized by WHO guidelines. *To decrease the risk of resistance due to conjugation* - **Conjugation** is a mechanism of horizontal gene transfer in bacteria, primarily involving the transfer of plasmids. - While important for antibiotic resistance in some bacteria, it is **not the primary mechanism** of resistance development in *Mycobacterium tuberculosis*. - TB resistance develops mainly through **chromosomal mutations**, not plasmid transfer. *To enhance overall treatment efficacy* - While multi-drug regimens do enhance treatment efficacy by targeting different bacterial populations (actively dividing, slow-growing, dormant), this is a **consequence** of the multi-drug approach. - The **primary reason** for using four drugs specifically is to prevent the emergence of **drug-resistant mutants**. - Enhanced efficacy is achieved *because* resistance is prevented, making this a secondary benefit. *To simplify treatment* - A four-drug regimen actually makes treatment more **complex** due to multiple pills, potential drug interactions, and increased side effects. - The complexity is a necessary trade-off for **resistance prevention** and treatment success.
Question 26: 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 27: Which of the following is not a selective serotonin reuptake inhibitor?
- A. Buspirone (Correct Answer)
- B. Citalopram
- C. Fluoxetine
- D. Fluvoxamine
Explanation: ***Buspirone*** - **Buspirone** is an anxiolytic that primarily acts as a **serotonin 5-HT1A receptor partial agonist**, not an SSRI. - It does not significantly affect the reuptake of serotonin, distinguishing it from SSRIs. *Fluoxetine* - **Fluoxetine** is a well-known and widely used **SSRI**. - It works by selectively inhibiting the reuptake of serotonin, thereby increasing its concentration in the synaptic cleft. *Fluvoxamine* - **Fluvoxamine** is another antidepressant classified as an **SSRI**. - It is often used for the treatment of **obsessive-compulsive disorder (OCD)** due to its strong serotonin reuptake inhibition. *Citalopram* - **Citalopram** is an **SSRI** frequently prescribed for depression and anxiety disorders. - Its mechanism involves potent and selective inhibition of **serotonin reuptake**.
Question 28: 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 29: 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 30: 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.