Antimullerian hormone is secreted by ?
What is the primary change in fetal circulation that occurs at birth?
Testes are not palpable in
Gamma waves of REM sleep are associated with?
Which type of pain is characterized by unknown etiology?
Which of the following is not true about sleep -
Most recently identified taste sensation is?
Vibration sense is detected by ?
Stress induced hyperglycemia is mediated through which hormone:
NEET-PG 2015 - Physiology NEET-PG Practice Questions and MCQs
Question 111: Antimullerian hormone is secreted by ?
- A. Theca cells
- B. Leydig cells
- C. Both Sertoli cells and granulosa cells (Correct Answer)
- D. None of the above
Explanation: ***Both Sertoli cells and granulosa cells*** - **Antimullerian hormone (AMH)** is produced by **Sertoli cells in males** and **granulosa cells in females** - In **males**: Sertoli cells secrete AMH during fetal development to cause **regression of Müllerian ducts** (which would otherwise develop into uterus, fallopian tubes, and upper vagina) - In **females**: Granulosa cells of developing ovarian follicles secrete AMH, which serves as a **marker of ovarian reserve** and inhibits excessive follicle recruitment - This is the only option that correctly identifies both cell types that produce AMH *Theca cells* - Theca cells are found in ovarian follicles and produce **androgens** (androstenedione and testosterone), not AMH - These androgens are converted to estrogens by granulosa cells via aromatase enzyme - Theca cells do not produce antimullerian hormone *Leydig cells* - Leydig cells are located in the **testes** and produce **testosterone** - They do not produce antimullerian hormone - Only Sertoli cells (not Leydig cells) produce AMH in males *None of the above* - This is incorrect because AMH is indeed produced by specific cell types: **Sertoli cells in males** and **granulosa cells in females**
Question 112: What is the primary change in fetal circulation that occurs at birth?
- A. Closure of the ductus venosus
- B. Increased activity of the right ventricle
- C. Closure of the foramen ovale (Correct Answer)
- D. Closure of the patent ductus arteriosus
Explanation: ***Closure of the foramen ovale*** - The **foramen ovale** undergoes functional closure within minutes of birth, making it the **primary immediate circulatory change** - At birth, the first breath causes **dramatic decrease in pulmonary vascular resistance** and **increased pulmonary blood flow**, which raises **left atrial pressure** - Simultaneously, umbilical cord clamping **increases systemic vascular resistance** and **decreases right atrial pressure** (loss of placental return) - This **pressure gradient reversal** (left atrial pressure > right atrial pressure) causes the **septum primum** to be pushed against the **septum secundum**, achieving functional closure - This immediately separates the systemic and pulmonary circulations, which is the **most critical primary change** in transitioning from fetal to neonatal circulation *Closure of the patent ductus arteriosus* - The **ductus arteriosus** undergoes **functional closure over 10-15 hours** after birth, followed by **anatomical closure over 2-3 weeks** - Closure occurs due to increased arterial oxygen tension and decreased prostaglandin E2 levels, causing smooth muscle constriction - While important, this is a **secondary change** that occurs more gradually compared to the immediate foramen ovale closure *Closure of the ductus venosus* - The **ductus venosus** closes functionally within 3-7 days as umbilical venous flow ceases - This redirects portal blood through the liver but does not directly impact the critical pulmonary-systemic circulation separation *Increased activity of the right ventricle* - After birth, the **left ventricle** becomes dominant as it pumps against higher systemic vascular resistance - The right ventricle actually experiences **decreased afterload** due to falling pulmonary vascular resistance - This is a consequence of, not the primary change in, the circulatory transition
Question 113: Testes are not palpable in
- A. SRY deletion (Correct Answer)
- B. DAX 1 deletion
- C. WNT- 4 gene mutation
- D. RSPO-1 gene mutation
Explanation: ***SRY deletion*** - **SRY (Sex-determining Region Y) gene** is the master regulator of male sex determination on the Y chromosome; its deletion in 46,XY individuals results in **Swyer syndrome** (pure gonadal dysgenesis). - Without functional SRY, **testes fail to develop entirely**, and the gonads remain as non-functional **streak gonads** rather than differentiating into either testes or ovaries. - Result: **No palpable testes** because testicular tissue never forms; individuals develop female external genitalia despite XY karyotype. *DAX1 deletion* - DAX1 (NR0B1) normally **antagonizes testicular development** and supports adrenal/gonadal development. - **Deletion of DAX1** would actually **reduce anti-testis effects**, allowing testicular development to proceed more readily if SRY is present. - DAX1 **duplications** (not deletions) can impair male development; deletions cause **adrenal hypoplasia congenita** but do not prevent testicular formation. *WNT-4 gene mutation* - **WNT4** promotes **ovarian development** and opposes male differentiation pathways in normal female development. - **Loss-of-function mutations** in WNT4 do not prevent testicular development in 46,XY individuals where SRY is present and functional. - WNT4 overexpression (not loss-of-function mutation) could theoretically interfere with male development, but standard WNT4 mutations do not cause absent testes. *RSPO-1 gene mutation* - **RSPO1** (R-spondin 1) enhances **Wnt/β-catenin signaling** and supports ovarian differentiation; primarily relevant in 46,XX sex development. - Loss-of-function mutations in RSPO1 lead to **46,XX testicular/ovotesticular DSD**, where testicular tissue develops inappropriately in XX individuals. - In 46,XY individuals with functional SRY, RSPO1 mutations would **not prevent testicular development**, so testes would be palpable.
Question 114: Gamma waves of REM sleep are associated with?
- A. Dream consciousness and memory consolidation
- B. Deep subconscious processing
- C. Non-REM sleep
- D. Subconscious processing (Correct Answer)
Explanation: ***Subconscious processing*** - **Gamma waves (30-100 Hz)** during **REM sleep** represent high-frequency neural oscillations associated with **complex cognitive processing** occurring below the level of conscious awareness. - These waves reflect **integration of neural activity** across different brain regions, facilitating information processing and neural plasticity during sleep. - The term encompasses the underlying **neural mechanisms** that support dream generation and memory consolidation processes. *Dream consciousness and memory consolidation* - While **gamma waves** do correlate with dreaming and memory processes during **REM sleep**, these represent the **experiential and functional outcomes** rather than the primary neurophysiological association. - Dream consciousness is a **manifestation** of the underlying subconscious processing, not the direct association with gamma wave activity itself. *Deep subconscious processing* - The term "deep subconscious" is **non-specific** and lacks precise neurophysiological definition in the context of gamma wave activity. - While directionally correct, this option uses imprecise terminology compared to the more accurate "subconscious processing." *Non-REM sleep* - **Gamma waves** are characteristic of **waking states** and **REM sleep**, not non-REM sleep stages. - **Non-REM sleep** (stages N1, N2, N3) is dominated by **slower wave activity** including theta waves (stage N1), sleep spindles and K-complexes (stage N2), and delta waves (stage N3/deep sleep).
Question 115: Which type of pain is characterized by unknown etiology?
- A. Nociceptive pain
- B. Neuropathic pain
- C. Idiopathic pain (Correct Answer)
- D. Inflammatory pain
Explanation: ***Idiopathic pain*** - This term refers to pain where the **underlying cause** or pathology cannot be identified, despite thorough investigation. - It signifies that the **etiology is unknown**, fitting the description in the question directly. *Nociceptive pain* - This type of pain arises from the activation of **nociceptors** due to actual or threatened tissue damage. - Its etiology is typically clear, involving an injury, inflammation, or mechanical stress. *Neuropathic pain* - This pain results from damage or disease affecting the **somatosensory nervous system**. - The etiology is known to be nerve damage or dysfunction, not an unknown origin. *Inflammatory pain* - This pain is driven by the inflammatory process, involving the release of **pro-inflammatory mediators** at the site of tissue injury or infection. - The cause is directly linked to inflammation, making its etiology known.
Question 116: Which of the following is not true about sleep -
- A. Dreams come in REM sleep
- B. REM sleep comes earlier than NREM sleep (Correct Answer)
- C. REM sleep is also called paradoxical sleep
- D. Sleep walking comes in NREM sleep
Explanation: ***REM sleep comes earlier than NREM sleep*** - This statement is **incorrect** because the sleep cycle typically begins with **NREM (non-rapid eye movement) sleep**, specifically NREM stage 1, before progressing to NREM stages 2 and 3, and then finally entering REM sleep. - NREM sleep accounts for about **75% of total sleep time** and occurs prior to REM sleep in a typical nocturnal sleep episode. *Dreams come in REM sleep* - This statement is **true** as **vivid, memorable dreams** are most commonly associated with **REM sleep**. - During REM sleep, brain activity significantly increases, mimicking the awake state, which facilitates complex dream formation. *REM sleep is also called paradoxical sleep* - This statement is **true** because **REM sleep** is characterized by **high brain activity** (similar to wakefulness) and rapid eye movements, yet the body experiences **muscle atonia**, leading to a state of profound relaxation. - This paradoxical combination of an active brain and a paralyzed body gives it the name **paradoxical sleep**. *Sleep walking comes in NREM sleep* - This statement is **true** as **sleepwalking (somnambulism)** typically occurs during **slow-wave sleep**, which is **NREM stage 3 (deep sleep)**. - During this stage, arousal thresholds are very high, and complex motor behaviors can occur while the individual remains in a sleep state.
Question 117: Most recently identified taste sensation is?
- A. Sour
- B. Bitter
- C. Umami (Correct Answer)
- D. Sweet
Explanation: ***Umami*** - **Umami** is the most recently identified **fifth basic taste**, often described as a savory or meaty taste. - Its discovery and recognition as a distinct taste sensation occurred in the **early 20th century** by Kikunae Ikeda, who isolated glutamate from kombu. *Sour* - The sensation of **sourness** is one of the traditionally recognized basic tastes, identified much earlier than umami. - It is typically associated with **acids**, such as those found in lemons or vinegar. *Bitter* - **Bitterness** is another long-standing basic taste that serves an important protective function, often signaling potential toxins. - It is one of the earliest tastes understood and recognized, with receptors for a wide range of bitter compounds. *Sweet* - **Sweetness** is a fundamental and ancient taste, universally recognized as pleasurable and indicating energy-rich foods. - The perception of sweet taste, primarily from sugars, has been understood for centuries.
Question 118: Vibration sense is detected by ?
- A. Superficial receptors
- B. Free nerve endings
- C. Nociceptors
- D. Deep receptors (Correct Answer)
Explanation: ***Deep receptors*** - **Vibration sense** is primarily mediated by **Pacinian corpuscles** and **Meissner's corpuscles**, which are considered deep receptors. - **Pacinian corpuscles** are located in the **deep dermis** and **subcutaneous tissue** and are highly sensitive to **high-frequency vibration** (200-300 Hz). - **Meissner's corpuscles** in dermal papillae detect **lower frequency vibration** and are rapidly adapting mechanoreceptors. *Superficial receptors* - **Superficial receptors** like **Merkel cells** primarily detect **sustained touch** and **pressure**, providing information about texture. - While they contribute to tactile sensation, they are **slowly adapting** and not specialized for rapidly oscillating stimuli like vibration. *Free nerve endings* - **Free nerve endings** are unmyelinated or lightly myelinated nerve terminals that detect **pain**, **temperature**, and **crude touch**. - They are not specialized mechanoreceptors and lack the structural organization needed to transduce vibratory stimuli. *Nociceptors* - **Nociceptors** are specialized sensory receptors that detect **noxious (harmful) stimuli** and mediate the sensation of **pain**. - They respond to extreme temperatures, intense mechanical stress, or chemical irritants, not to non-painful vibration.
Question 119: Stress induced hyperglycemia is mediated through which hormone:
- A. Cortisol (Correct Answer)
- B. Epinephrine
- C. Insulin
- D. Growth hormone
Explanation: ***Cortisol*** - **Cortisol** is the **primary mediator** of stress-induced hyperglycemia among the counter-regulatory hormones - It promotes **gluconeogenesis** (formation of new glucose from amino acids and glycerol) in the liver - Stimulates **protein catabolism** in muscles, providing substrates for gluconeogenesis - Induces **insulin resistance** in peripheral tissues, reducing glucose uptake - Released as part of the **HPA axis response** to stress, with sustained elevation during prolonged stress - This is the **correct answer** for stress-induced hyperglycemia mediation *Epinephrine* - **Epinephrine** (adrenaline) is a potent hyperglycemic hormone but acts as an **acute, immediate response** to stress - Rapidly increases blood glucose through **glycogenolysis** (breakdown of glycogen) in liver and muscles - Stimulates **gluconeogenesis** and inhibits insulin secretion - Effects are **rapid but short-lived**, making it more of an emergency response rather than the sustained mediator - Works synergistically with cortisol but is not the primary sustained mediator *Growth hormone* - **Growth hormone** does contribute to hyperglycemia through **anti-insulin effects** and promoting lipolysis - Its hyperglycemic effects are **slower and less pronounced** compared to cortisol and epinephrine - Plays a role in **chronic stress** but is not the primary acute mediator - More important for **long-term metabolic adaptation** rather than immediate stress response *Insulin* - **Insulin** is a **glucose-lowering hormone** that facilitates glucose uptake into cells - During stress, insulin secretion is **suppressed** and tissues become **insulin-resistant** due to counter-regulatory hormones - It does **not mediate** stress-induced hyperglycemia; rather, its action is **opposed** by stress hormones - Decreased insulin action contributes to hyperglycemia but insulin itself is not the mediator