Biochemistry
1 questionsWhich amino acid has two chiral centers?
NEET-PG 2013 - Biochemistry NEET-PG Practice Questions and MCQs
Question 401: Which amino acid has two chiral centers?
- A. Threonine (Correct Answer)
- B. Tyrosine
- C. Tryptophan
- D. Phenylalanine
Explanation: ***Threonine*** - Threonine is unique among the standard 20 amino acids because it possesses **two chiral centers**: one at the **alpha-carbon** and another at the **beta-carbon**. - The presence of two chiral centers means that threonine can exist as **four stereoisomers** (2^n, where n is the number of chiral centers). *Tryptophan* - Tryptophan has only **one chiral center**, which is the **alpha-carbon** bonded to the amino group, carboxyl group, hydrogen atom, and the side chain. - Its side chain, an **indole ring**, does not contain an additional chiral center. *Tyrosine* - Tyrosine, like most amino acids, possesses only **one chiral center** at its **alpha-carbon**. - The aromatic ring system (phenol group) in its side chain does not introduce another chiral center. *Phenylalanine* - Phenylalanine also has only **one chiral center** located at its **alpha-carbon**. - Its benzyl side chain, consisting of a methylene group and a benzene ring, is not chiral.
Internal Medicine
1 questionsChronic atrophy of adrenal gland will result in which hormone deficiency ?
NEET-PG 2013 - Internal Medicine NEET-PG Practice Questions and MCQs
Question 401: Chronic atrophy of adrenal gland will result in which hormone deficiency ?
- A. Aldosterone
- B. Dehydroepiandrosterone (DHEA)
- C. Epinephrine
- D. Cortisol (Correct Answer)
Explanation: ***Cortisol*** - **Chronic atrophy of the adrenal gland**, often seen in conditions like **Addison's disease** [1], primarily leads to a deficiency of **glucocorticoids**, the main one being cortisol [2]. - **Cortisol** is produced in the **zona fasciculata** of the adrenal cortex, which is highly susceptible to damage in atrophic conditions [2]. *Aldosterone* - While aldosterone is produced in the adrenal cortex (**zona glomerulosa**), its deficiency is more characteristic of primary adrenal insufficiency affecting the entire cortex, not necessarily solely from 'chronic atrophy' which can have varied pathophysiology [2]. - In some autoimmune forms of adrenal atrophy (Addison's disease), **aldosterone deficiency** can occur, but **cortisol deficiency** is a more universal and defining feature [1][3]. *Dehydroepiandrosterone (DHEA)* - **DHEA** is an adrenal androgen produced in the **zona reticularis** of the adrenal cortex [2]. Its deficiency is also common in adrenal atrophy. - However, **cortisol deficiency** generally has more immediate and life-threatening clinical consequences compared to DHEA deficiency. *Epinephrine* - Epinephrine is produced by the **adrenal medulla**, which is distinct from the adrenal cortex where atrophy typically occurs in conditions causing hormone deficiencies. - Therefore, **adrenal gland atrophy** primarily affecting the cortex would not lead to **epinephrine deficiency** as the medulla usually remains functional.
Obstetrics and Gynecology
1 questionsHuman 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 401: 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.
Physiology
7 questionsWhich of the following does not stimulate growth hormone (GH) release?
The primary oocyte remains arrested in which stage until ovulation?
Which of the following statements about thyroid hormone receptors is correct?
After injecting testosterone in a hypoandrogenic male, which of the following occurs ?
What is the half-life of the thyroid hormone triiodothyronine (T3)?
What is the effect of moderate exercise on cerebral blood flow?
Most common type of calcium channels of skeletal muscles is?
NEET-PG 2013 - Physiology NEET-PG Practice Questions and MCQs
Question 401: Which of the following does not stimulate growth hormone (GH) release?
- A. Exercise
- B. Free fatty acids (Correct Answer)
- C. Fasting
- D. Stress
Explanation: ***Free fatty acids*** - High levels of **free fatty acids** in the bloodstream inhibit growth hormone (GH) secretion. - This occurs through a **negative feedback loop** at the level of the hypothalamus and pituitary gland. *Fasting* - **Fasting** (especially prolonged) is a potent stimulus for GH release, helping to mobilize fat stores and maintain **glucose homeostasis**. - During fasting, ghrelin levels increase, which further promotes GH secretion. *Exercise* - **Physical exercise** is a well-known physiological stimulus for GH release, contributing to muscle growth and repair. - The intensity and duration of exercise can influence the magnitude of GH secretion. *Stress* - Various forms of **stress**, including physical (e.g., trauma, surgery) and psychological stress, stimulate GH release. - This response is mediated in part by the **sympathetic nervous system** and increased cortisol levels.
Question 402: The primary oocyte remains arrested in which stage until ovulation?
- A. Diplotene stage (Correct Answer)
- B. Pachytene stage
- C. Metaphase
- D. Telophase
Explanation: ***Diplotene stage*** - The primary oocyte enters **meiosis I** during fetal development but arrests in the **prophase I substage of diplotene**. - This arrest is maintained until **puberty** and **ovulation**, when hormonal surges trigger the completion of meiosis I. *Pachytene stage* - The **pachytene stage** of prophase I is when **crossing over** (recombination) occurs between homologous chromosomes. - While an important step in meiosis, it precedes the **diplotene arrest** point. *Metaphase* - **Metaphase** is a stage where chromosomes align at the metaphase plate, either in meiosis I or meiosis II. - The primary oocyte's arrest occurs much earlier, during **prophase I**, not metaphase. *Telophase* - **Telophase** is the final stage of mitosis or meiosis where chromosomes decondense and nuclear envelopes reform. - The oocyte's initial arrest point is in **prophase I**, long before telophase.
Question 403: Which of the following statements about thyroid hormone receptors is correct?
- A. They directly bind to thyrotropin-releasing hormone (TRH)
- B. They directly bind to thyroid-stimulating hormone (TSH)
- C. They cause nuclear transcription after binding with T4
- D. They are intracellular receptors that mediate gene transcription after binding with T3 or T4, but their primary action is through T3. (Correct Answer)
Explanation: ***They are intracellular receptors that mediate gene transcription after binding with T3 or T4, but their primary action is through T3.*** - **Thyroid hormone receptors** are indeed **intracellular** and act as **ligand-activated transcription factors**, regulating gene expression. - While both **T3** and **T4** can bind, **T3 (triiodothyronine)** is the more potent and active form, binding with much higher affinity to the receptors to exert its primary metabolic effects. *They directly bind to thyrotropin-releasing hormone (TRH)* - **TRH (thyrotropin-releasing hormone)** is produced by the hypothalamus and acts on the **pituitary gland** to stimulate TSH release, not directly on thyroid hormone receptors. - Thyroid hormone receptors bind to thyroid hormones (**T3 and T4**), not to the hypothalamic releasing hormones like TRH. *They directly bind to thyroid-stimulating hormone (TSH)* - **TSH (thyroid-stimulating hormone)** is produced by the pituitary gland and primarily acts on receptors located on the **thyroid gland cells** to stimulate thyroid hormone synthesis and release. - Thyroid hormone receptors are distinct from TSH receptors and bind to the hormones themselves (**T3/T4**), not the stimulating hormone TSH. *Causes nuclear transcription after binding with T4* - While **T4 (thyroxine)** can bind to thyroid hormone receptors, it is primarily a **prohormone**. - T4 is largely converted to the more active **T3** within target cells, and **T3** is the main mediator of nuclear transcription through these receptors.
Question 404: 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 405: What is the half-life of the thyroid hormone triiodothyronine (T3)?
- A. 8 hours
- B. 1 day (Correct Answer)
- C. 6 hours
- D. 10 days
Explanation: ***1 day*** - The **half-life of T3 (triiodothyronine)** is approximately **1 day (24 hours)**, making its biological effects relatively rapid compared to T4. - This shorter half-life contributes to its quicker onset and offset of action. *8 hours* - While reflecting a relatively short duration, **8 hours** is not the accepted half-life for T3. - This value is too short for T3, which has a more sustained biological effect. *6 hours* - A half-life of **6 hours** is too short for T3, which has a more sustained effect than such a rapid clearance would suggest. - This would imply a much faster metabolic turnover than observed clinically. *10 days* - **10 days** is longer than the actual **half-life of T4 (thyroxine)**, which is approximately **7 days**. - T4 serves as a prohormone and is more extensively protein-bound, contributing to its prolonged presence in circulation compared to T3.
Question 406: What is the effect of moderate exercise on cerebral blood flow?
- A. Decreases
- B. Initially decreases then increases
- C. Increases (Correct Answer)
- D. Does not change
Explanation: ***Increases*** - Moderate exercise leads to an **increase in systemic arterial pressure** and an increase in **cardiac output**, which often results in a moderate increase in cerebral blood flow. - This increase is also attributed to **vasodilation of cerebral arteries** in response to metabolic demands and changes in blood gas levels during exercise. *Decreases* - A decrease in cerebral blood flow is generally associated with conditions leading to **hypoperfusion** or **severe vasoconstriction**, which are not typical effects of moderate exercise. - While extreme exercise could potentially cause some transient vasoconstriction, moderate exercise typically has the opposite effect due to compensatory mechanisms. *Initially decreases then increases* - There is generally no physiological mechanism by which moderate exercise would cause an initial decrease in cerebral blood flow followed by an increase. - Cerebral autoregulation usually maintains a stable blood flow, and the overall trend with moderate exercise is an increase. *Does not change* - While **cerebral autoregulation** aims to keep cerebral blood flow stable over a range of blood pressures, moderate exercise often pushes parameters (like CO2 levels and systemic pressure) enough to cause a measurable, albeit modest, **increase in blood flow**. - The brain's metabolic demand also increases during exercise, necessitating an increased blood supply.
Question 407: Most common type of calcium channels of skeletal muscles is?
- A. N-type
- B. T-type
- C. R-type
- D. L-type (Correct Answer)
Explanation: ***L type*** - **L-type calcium channels**, also known as **dihydropyridine receptors (DHPRs)**, are the predominant type of calcium channel found in skeletal muscle. - In skeletal muscle, they serve as voltage sensors that **mechanically link** to ryanodine receptors (RyRs) on the sarcoplasmic reticulum to trigger calcium release without significant calcium influx from the extracellular space. *N-type* - **N-type calcium channels** are primarily found in **neurons** and play a crucial role in neurotransmitter release at synapses. - They are not the primary calcium channels involved in skeletal muscle excitation-contraction coupling. *T-type* - **T-type calcium channels** are low-voltage activated channels found in various excitable cells, including cardiac muscle and neurons, where they contribute to **pacemaker activity** and repetitive firing. - They are not the main calcium channels responsible for excitation-contraction coupling in skeletal muscle. *R-type* - **R-type calcium channels** are found in various neural cells and are involved in diverse functions, including **synaptic transmission**, but their precise physiological role is less clearly defined compared to other types. - These channels are not the primary calcium entry pathways in skeletal muscle and do not play a significant role in its contraction.