Anatomy
1 questionsWhich of the following statements about the great saphenous vein is true?
NEET-PG 2013 - Anatomy NEET-PG Practice Questions and MCQs
Question 251: Which of the following statements about the great saphenous vein is true?
- A. It begins at lateral end of dorsal venous arch
- B. It runs anterior to medial malleolus (Correct Answer)
- C. Terminates into popliteal vein
- D. It is accompanied by the sural nerve
Explanation: **It runs anterior to medial malleolus** - The **great saphenous vein** originates from the medial end of the **dorsal venous arch** of the foot and ascends anterior to the **medial malleolus** [1]. - This anatomical relationship makes it accessible for various clinical procedures, such as **venous cutdown** for rapid intravenous access [1]. *It begins at lateral end of dorsal venous arch* - The **great saphenous vein** actually begins at the **medial end** of the dorsal venous arch, not the lateral end [1]. - The **small saphenous vein** arises from the lateral end of the dorsal venous arch [1]. *It is accompanied by the sural nerve* - The **sural nerve** typically accompanies the **small saphenous vein**, not the great saphenous vein, in the posterior leg [1]. - The **saphenous nerve**, a branch of the femoral nerve, accompanies the great saphenous vein throughout its course in the leg. *Terminates into popliteal vein* - The **great saphenous vein** normally terminates by draining into the **femoral vein** in the femoral triangle, not the popliteal vein [1]. - The **small saphenous vein** is the one that typically drains into the popliteal vein [1].
Biochemistry
1 questionsWhat is the unit for a prolactin level of 20 in blood?
NEET-PG 2013 - Biochemistry NEET-PG Practice Questions and MCQs
Question 251: What is the unit for a prolactin level of 20 in blood?
- A. ng/ml (Correct Answer)
- B. mg/ml
- C. mg/l
- D. ng/l
Explanation: ***ng/ml*** - Prolactin levels in blood are typically measured in **nanograms per milliliter (ng/mL)**, reflecting the very small concentrations of hormones. - A value of 20 ng/mL falls within the typical reference range for prolactin. *mg/mL* - **Milligrams per milliliter (mg/mL)** is a unit used for much higher concentrations, more common for drugs or larger molecules, not hormones like prolactin. - If prolactin were measured in mg/mL, a value of 20 mg/mL would be an astronomically high and physiologically impossible level. *mg/L* - **Milligrams per liter (mg/L)** is also a unit for higher concentrations than those typically seen for hormones in blood. - 20 mg/L is equivalent to 20 µg/mL or 20,000 ng/mL, which would indicate severe hyperprolactinemia. *ng/L* - **Nanograms per liter (ng/L)** is a unit for extremely low concentrations. - A reading of 20 ng/L would be too low for normal physiological prolactin levels, as 1 ng/mL equals 1000 ng/L.
Obstetrics and Gynecology
2 questionsOvulation occurs how long after the LH surge peak?
Human sperm remains fertile for how many hours in a female genital tract ?
NEET-PG 2013 - Obstetrics and Gynecology NEET-PG Practice Questions and MCQs
Question 251: Ovulation occurs how long after the LH surge peak?
- A. 48-72 hours
- B. 72-96 hours
- C. 24-48 hours
- D. 12-24 hours (Correct Answer)
Explanation: ***12-24 hours*** - Ovulation, the release of a mature egg from the **ovary**, typically occurs within **12 to 24 hours after the peak of the luteinizing hormone (LH) surge**. - The LH surge itself usually lasts 24 to 48 hours and is a critical signal for the final maturation and release of the oocyte. *24-48 hours* - While the **LH surge** can last up to 48 hours, **ovulation** (the actual release of the egg) generally happens more rapidly, usually within 12-24 hours of the *peak* of this surge. - This timeframe is a common misconception, as it refers more to the duration of the surge rather than the precise timing of ovulation post-peak. *48-72 hours* - Ovulation rarely occurs this late after the peak of the **LH surge**; if it does, it suggests a potential delay or irregularity in the **ovulatory process**. - The window for successful fertilization is relatively narrow and aligns with the more immediate post-surge timing. *72-96 hours* - This time frame is significantly beyond the typical window for **ovulation** following the **LH surge**. - By this point, the egg would have either been released or the ovulatory event would have passed without the egg releasing.
Question 252: Human sperm remains fertile for how many hours in a female genital tract ?
- A. 6-8 hrs
- B. 12-24 hrs
- C. 24-48 hrs
- D. Up to 5 days (120 hrs) (Correct Answer)
Explanation: ***Up to 5 days (120 hrs)*** - **Sperm viability** within the female reproductive tract can extend up to **5 days (120 hours)** under optimal conditions. - This extended viability is crucial for fertility, as it allows for fertilization even if ovulation occurs several days after intercourse. *6-8 hrs* - This timeframe is significantly **too short** for typical human sperm viability in the female genital tract. - While some sperm may lose motility or viability relatively quickly, a substantial portion remains viable for much longer. *12-24 hrs* - This represents the average **lifespan of an ovum** (egg) after ovulation, not the typical viability of sperm. - Sperm generally survive longer than an unfertilized egg. *24-48 hrs* - This duration underestimates the maximum potential survival time of human sperm in the female reproductive tract. - While many sperm may be viable within this period, it does not represent the full potential for fertilization.
Pharmacology
3 questionsWhich beta-1 antagonist is used in congestive cardiac failure?
Which of the following is not a cardioselective beta blocker?
Which of the following is a second-generation beta blocker?
NEET-PG 2013 - Pharmacology NEET-PG Practice Questions and MCQs
Question 251: Which beta-1 antagonist is used in congestive cardiac failure?
- A. Atenolol
- B. Metoprolol (Correct Answer)
- C. Esmolol
- D. Bisoprolol
Explanation: ***Metoprolol*** - **Metoprolol succinate** (extended-release formulation) is a selective **beta-1 antagonist** proven to reduce mortality and hospitalizations in **chronic heart failure with reduced ejection fraction (HFrEF)**. - It works by **reducing heart rate, myocardial oxygen demand**, and preventing adverse cardiac remodeling through inhibition of chronic sympathetic activation. - Along with **bisoprolol and carvedilol**, it is one of the **three beta-blockers with proven mortality benefit** in heart failure trials. *Atenolol* - While atenolol is a selective beta-1 antagonist, it **lacks evidence for mortality benefit** in heart failure. - It has **high hydrophilicity** and renal elimination, leading to less favorable pharmacokinetics compared to metoprolol. - More commonly used for **hypertension and angina** rather than heart failure management. *Esmolol* - **Esmolol** is an ultra-short-acting selective beta-1 antagonist used for **acute control of heart rate** in perioperative and critical care settings. - Its **very short half-life (9 minutes)** makes it unsuitable for chronic management of heart failure. - Administered only **intravenously** and requires continuous infusion. *Bisoprolol* - While **bisoprolol is also approved** for heart failure and has proven mortality benefit (CIBIS-II trial), this question likely expects **metoprolol** as the answer given the historical context. - Both bisoprolol and metoprolol are acceptable answers, but **metoprolol** has been more widely studied and is more commonly cited in Indian medical exams. - Bisoprolol has **greater beta-1 selectivity** than metoprolol but similar clinical outcomes in heart failure.
Question 252: Which of the following is not a cardioselective beta blocker?
- A. Nebivolol
- B. Atenolol
- C. Betaxolol
- D. Oxprenolol (Correct Answer)
Explanation: ***Oxprenolol*** - **Oxprenolol** is a non-selective beta-blocker with **intrinsic sympathomimetic activity (ISA)**, meaning it blocks both β1 and β2 receptors and partially stimulates them. - Its non-selective action means it affects both the heart (β1) and other organs like the lungs (β2), making it less suitable for patients with respiratory conditions. *Nebivolol* - **Nebivolol** is a highly cardioselective beta-blocker that primarily blocks **β1 receptors** and also has **vasodilatory properties** due to nitric oxide release. - Its high selectivity translates to fewer β2-mediated side effects, such as bronchoconstriction. *Atenolol* - **Atenolol** is a **cardioselective beta-blocker** that predominantly blocks **β1 receptors** at therapeutic doses. - This selectivity makes it a common choice for cardiovascular conditions, reducing the risk of bronchospasm compared to non-selective agents. *Betaxolol* - **Betaxolol** is a **cardioselective beta-blocker** primarily used for the treatment of hypertension and glaucoma. - It selectively blocks **β1 adrenergic receptors**, minimizing effects on the lungs compared to non-selective beta-blockers.
Question 253: Which of the following is a second-generation beta blocker?
- A. Timolol
- B. Atenolol (Correct Answer)
- C. Nadolol
- D. Propranolol
Explanation: ***Atenolol*** - **Atenolol** is a **second-generation beta blocker** characterized by its **cardioselectivity**, meaning it primarily blocks beta-1 receptors in the heart. - This selectively reduces heart rate and contractility with fewer respiratory side effects compared to non-selective agents. *Propranolol* - **Propranolol** is a **first-generation non-selective beta blocker**, meaning it blocks both beta-1 and beta-2 adrenergic receptors. - Its non-selective action can cause significant bronchoconstriction, making it less suitable for patients with respiratory conditions. *Timolol* - **Timolol** is also a **first-generation non-selective beta blocker** commonly used in ophthalmic preparations for glaucoma. - It blocks both beta-1 and beta-2 receptors and does not possess the cardioselectivity of second-generation agents. *Nadolol* - **Nadolol** is another **first-generation non-selective beta blocker** with a long duration of action due to its extensive plasma half-life. - Like other first-generation agents, it lacks cardioselectivity and blocks both beta-1 and beta-2 receptors.
Physiology
3 questionsAfter injecting testosterone in a hypoandrogenic male, which of the following occurs ?
In the breast, lactiferous ducts are formed under the influence of which hormone?
What does spermiogenesis refer to?
NEET-PG 2013 - Physiology NEET-PG Practice Questions and MCQs
Question 251: After injecting testosterone in a hypoandrogenic male, which of the following occurs ?
- A. Decreased LH secretion
- B. Decreased FSH secretion (Correct Answer)
- C. Increased spermatogenesis
- D. None of the options
Explanation: ***Decreased FSH secretion*** - Exogenous testosterone administration leads to **negative feedback** on the hypothalamic-pituitary-gonadal axis, suppressing **GnRH** release, which in turn decreases both **LH** and **FSH** secretion. - FSH suppression is particularly clinically significant because it results in **inhibition of spermatogenesis**, which is a key consideration when using testosterone replacement therapy. - The decrease in FSH, combined with reduced **intratesticular testosterone** (due to LH suppression), impairs Sertoli cell function and sperm production. *Decreased LH secretion* - **This also occurs** with exogenous testosterone administration due to negative feedback on the hypothalamus and pituitary. - Testosterone primarily suppresses **LH** through direct negative feedback at the hypothalamic-pituitary level. - However, in the context of this question focusing on the consequences in a hypoandrogenic male receiving testosterone, the **FSH suppression** and its impact on spermatogenesis is the more clinically emphasized outcome. - **Note:** Both LH and FSH decrease; this question likely emphasizes FSH due to its role in fertility concerns with testosterone therapy. *Increased spermatogenesis* - This is **incorrect**. Exogenous testosterone actually **suppresses spermatogenesis** through multiple mechanisms: - Decreased **FSH** (essential for Sertoli cell function) - Decreased **intratesticular testosterone** concentration (despite high systemic levels) - The high local testosterone concentration within the seminiferous tubules (30-100x serum levels) cannot be achieved by systemic testosterone alone. *None of the options* - This is incorrect because exogenous testosterone administration clearly causes **suppression of gonadotropins** (both LH and FSH) through well-established negative feedback mechanisms.
Question 252: In the breast, lactiferous ducts are formed under the influence of which hormone?
- A. Progesterone
- B. LH
- C. FSH
- D. Estrogen (Correct Answer)
Explanation: ***Estrogen*** - **Estrogen** plays a primary role in the development and branching of the **lactiferous ducts** in the breast. - It stimulates the proliferation of ductal epithelial cells, contributing to the growth of the duct system. *Progesterone* - **Progesterone** is primarily responsible for the development of the **lobuloalveolar system** and secretory differentiation within the breast. - While essential for lactation, its main function is not duct formation but rather the maturation of secretory units. *LH* - **Luteinizing hormone (LH)** is crucial for ovulation and the formation of the **corpus luteum** in the ovaries. - It has no direct role in the structural development of the lactiferous ducts in the breast. *FSH* - **Follicle-stimulating hormone (FSH)** is essential for the growth and maturation of **ovarian follicles**. - It does not directly influence the formation or development of lactiferous ducts in the breast.
Question 253: What does spermiogenesis refer to?
- A. Formation of spermatozoa from spermatogonia
- B. Formation of spermatozoa from spermatids (Correct Answer)
- C. Formation of spermatids from spermatocytes
- D. Formation of secondary spermatocytes from primary spermatocytes
Explanation: ***Formation of spermatozoa from spermatids*** - **Spermiogenesis** is the final stage of spermatogenesis, involving the remarkable transformation of a round **spermatid** into a motile, mature **spermatozoon**. - This process includes crucial morphological changes such as the formation of the **acrosome**, condensation of the nucleus, development of the flagellum, and shedding of excess cytoplasm. *Formation of spermatozoa from spermatogonia* - This describes the entire process of **spermatogenesis**, which begins with **spermatogonia** and encompasses multiple stages including mitosis, meiosis, and spermiogenesis. - While it's the ultimate outcome, it doesn't specifically define the detailed transformation from spermatid to sperm. *Formation of spermatids from spermatocytes* - This stage refers to **meiosis II**, where **secondary spermatocytes** undergo division to produce **spermatids**. - Spermatids are precursors to spermatozoa and still require significant morphological changes to become mature sperm. *Formation of secondary spermatocytes from primary spermatocytes* - This describes **meiosis I**, where a **primary spermatocyte** divides to form two **secondary spermatocytes**. - This step reduces the chromosome number by half but doesn't involve the final morphological changes seen in spermiogenesis.