Biochemistry
1 questionsWhich of the following is not an androgen?
NEET-PG 2013 - Biochemistry NEET-PG Practice Questions and MCQs
Question 401: Which of the following is not an androgen?
- A. 17α-hydroxyprogesterone (Correct Answer)
- B. Testosterone
- C. Dihydrotestosterone
- D. Androstenedione
Explanation: ***17α-hydroxyprogesterone*** - This is a **progesterone derivative** and an intermediate in the synthesis of androgens and corticosteroids, but it does **not possess significant androgenic activity** itself. - Its primary role is as a precursor, rather than a direct androgen. *Testosterone* - **Testosterone** is the **primary male sex hormone** and a potent androgen, responsible for the development of male secondary sexual characteristics. - It plays crucial roles in muscle mass, bone density, libido, and erythropoiesis. *Dihydrotestosterone* - **Dihydrotestosterone (DHT)** is a potent androgen, formed from testosterone by the enzyme 5α-reductase. - DHT is responsible for the development of external male genitalia during fetal development and contributes to prostate growth and male pattern baldness in adults. *Androstenedione* - **Androstenedione** is a **weak androgen** and an important **precursor hormone** in the biosynthesis of testosterone and estrogens. - It is produced in the adrenal glands and gonads, serving as an intermediate step in steroidogenesis.
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.
Pathology
3 questionsWhich of the following changes is NOT seen in atherosclerotic plaque at the time of rupture?
Which of the following cell types is classified as a labile cell?
Dystrophic calcification is seen in
NEET-PG 2013 - Pathology NEET-PG Practice Questions and MCQs
Question 401: Which of the following changes is NOT seen in atherosclerotic plaque at the time of rupture?
- A. Inflammatory cell infiltration
- B. Thick fibrous cap (Correct Answer)
- C. Cell debris
- D. Smooth muscle cell atrophy
Explanation: ***Smooth muscle cell hypertrophy*** - **Smooth muscle cell hypertrophy** is generally associated with stable plaques and does not typically occur in ruptured atherosclerotic plaques [2]. - At rupture, there is **loss of smooth muscle cells** and thinning of the fibrous cap, leading to plaque instability [2]. *Thin fibrosis cap* - A **thin fibrous cap** is a critical feature of vulnerable plaques, making them prone to rupture [2]. - It indicates a **weakened structure** that can no longer withstand the pressure of the underlying lipid core [2]. *Cell debris* - **Cell debris** is often found at the site of rupture, resulting from the necrosis of foam cells and smooth muscle cells. - This indicates **plaque instability** and contributes to the thrombus formation at the rupture site. *Multiple foam cap* - The presence of **multiple foam cells** reflectsing lipid accumulation in the plaque but does not contribute to the phenomenon of plaque rupture directly. - While foam cells are associated with rupture, a **foam cap** is not a recognized pathological finding at the time of rupture. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Cardiovascular Disease, pp. 271-272. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Cardiovascular Disease, pp. 268-270.
Question 402: Which of the following cell types is classified as a labile cell?
- A. Liver parenchymal cells
- B. Vascular smooth muscle cells
- C. Surface epithelium (Correct Answer)
- D. Neurons
Explanation: ***Surface epithelium*** - Surface epithelium is classified as **labile tissue**, meaning it undergoes constant regeneration due to its high turnover rate [1]. - Cells in this tissue are typically found in areas that experience frequent damage or abrasion, such as the skin and lining of the intestines. *Cardiac cell* - Cardiac cells are considered **permanent cells**, as they do not undergo significant regeneration after injury or damage. - Damage to cardiac cells typically leads to **fibrosis** rather than repair of the original tissue. *Liver parenchymal cell* - Liver parenchymal cells are categorized as **stable cells**, which can regenerate but do so under specific circumstances, such as injury. - They have a slower turnover rate compared to labile cells and do not constantly renew under normal conditions. *Vascular endothelial cells* - Vascular endothelial cells are considered **stable cells** as well, typically maintaining a stable population but capable of regeneration following injury. - They do not have the same rapid turnover and regeneration capability as labile cells do, especially under normal physiological conditions. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 113-115.
Question 403: Dystrophic calcification is seen in
- A. Vitamin A intoxication
- B. Atheromatous plaque (Correct Answer)
- C. Milk alkali syndrome
- D. Hyperparathyroidism
Explanation: ***Atheromatous plaque*** - Dystrophic calcification occurs in **local areas of tissue injury**, like atheromatous plaques, where necrotic debris provides a nidus for calcification [1]. - It's commonly observed in chronic **atherosclerosis**, leading to the deposition of calcium in the damaged arterial walls [1]. *Hyperparathyroidism* - Typically associated with **metastatic calcification** due to elevated calcium levels, not dystrophic calcification [2][3]. - It results in renal, pulmonary, or vascular calcifications rather than calcifications in previously damaged tissues [3]. *Milk alkali syndrome* - Involves **hypercalcemia** and can lead to calcifications, but they are primarily **metastatic** rather than dystrophic [2][3]. - The syndrome results from excess calcium intake and is associated with renal injury rather than tissue necrosis. *Vitamin A intoxication* - Can cause **hyperostosis** and **calcifications**, but these are diffuse and not primarily dystrophic in nature. - The calcifications in this condition do not stem from necrotic tissue but rather are due to toxicity effects on bone metabolism. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 506-507. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 134-135. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, pp. 76-77.
Physiology
5 questionsIntegration center of tonic labyrinthine reflex is?
In the breast, lactiferous ducts are formed under the influence of which hormone?
After injecting testosterone in a hypoandrogenic male, which of the following occurs ?
Which of the following statements about thyroid hormone receptors is correct?
The primary oocyte remains arrested in which stage until ovulation?
NEET-PG 2013 - Physiology NEET-PG Practice Questions and MCQs
Question 401: Integration center of tonic labyrinthine reflex is?
- A. Spinal cord
- B. Medulla (Correct Answer)
- C. Midbrain
- D. Cerebral cortex
Explanation: ***Medulla*** - The **tonic labyrinthine reflex** is a primitive reflex originating in the **vestibular system**, specifically the otolith organs, which respond to head position changes. - Its integration center lies in the **medulla oblongata**, a part of the brainstem responsible for essential involuntary functions. *Spinal cord* - The spinal cord integrates simpler reflexes like **stretch reflexes** and **withdrawal reflexes**. - It does not process the complex vestibular input required for the tonic labyrinthine reflex. *Midbrain* - The **midbrain** is involved in integrating reflexes related to visual and auditory stimuli, such as the **startle reflex** and **pupillary light reflex**. - It is superior to the primary integration center for the tonic labyrinthine reflex. *Cerebral cortex* - The **cerebral cortex** is responsible for higher cognitive functions, voluntary movements, and conscious sensation. - Reflexes like the tonic labyrinthine reflex are subcortical and operate without conscious control.
Question 402: 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 403: 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 404: 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 405: 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.