NEET-PG 2025 - Physiology PYQs Practice Questions

Q: Effect of pulmonary embolism on graph of V/Q?

Increased V/Q ratio approaching infinity (dead space). ***Increased V/Q ratio approaching infinity (dead space)*** - In pulmonary embolism, an embolus obstructs a pulmonary artery, leading to a significant reduction or complete cessation of **perfusion (Q)** to the downstream lung tissue, while **ventilation (V)** remains unaffected. - This creates a V/Q mismatch where the ratio V/Q becomes very high, approaching infinity. This ventilated but unperfused lung region is known as **physiological dead space**. *Decreased V/Q ratio approaching zero* - A decreased V/Q ratio occurs when ventilation is impaired relative to perfusion (V<Q), a condition known as a **shunt**. - This is characteristic of conditions like **pneumonia**, **pulmonary edema**, or **atelectasis**, where alveoli are filled with fluid or collapsed but still receive blood flow. *Normal V/Q ratio* - Pulmonary embolism is a classic cause of a severe **V/Q mismatch**, specifically creating high V/Q units; therefore, the ratio in the affected area is not normal. - A normal V/Q ratio (approximately 0.8) implies well-matched ventilation and perfusion, which is the state PE directly disrupts. *Increased perfusion (Q) and decreased ventilation (V)* - This describes the opposite of what occurs in pulmonary embolism, where the primary problem is a **decrease in perfusion (Q)** due to the arterial blockage. - Increased perfusion with decreased ventilation would result in a **low V/Q ratio (shunt)**, not the high V/Q dead space seen in PE. [Practice more Physiology PYQs on OnCourse]

Q: In a woman with a regular 28-day menstrual cycle, which of the following best describes the typical hormonal profile during days 21 to 25 of the cycle?

High estrogen, high progesterone. ***High estrogen, high progesterone*** - Days 21 to 25 fall within the **mid-to-late luteal phase** of a 28-day cycle, which is dominated by the corpus luteum. - The corpus luteum secretes large amounts of **progesterone** (peak luteal levels) and **moderate-to-high levels of estrogen** (secondary luteal peak). - Both hormones exert **negative feedback** on the hypothalamus and pituitary, leading to suppressed **LH and FSH** levels. - This combination of high progesterone with moderately elevated estrogen is characteristic of a functional corpus luteum during the mid-luteal phase. *Low estrogen, high progesterone, low LH and FSH* - While **LH and FSH** are correctly low due to negative feedback, and **progesterone** is high, describing estrogen as "low" is inaccurate for days 21–25. - During the mid-luteal phase, the corpus luteum produces a **secondary estrogen peak** that is moderate-to-high, not low. - Low estrogen would only occur if the corpus luteum had already regressed, which happens closer to menstruation (days 26–28). *Low estrogen, high progesterone, high LH and FSH* - High levels of **LH and FSH** occur only during the **LH surge** around day 14 (ovulation) or during the **menstrual/early follicular phase** when steroid hormones are low. - The combination of **high progesterone** and **high gonadotropins** does not occur normally in the menstrual cycle, as progesterone and estrogen suppress LH and FSH through negative feedback. *Low estrogen, low progesterone, low LH and FSH* - This hormonal profile is characteristic of the **late follicular phase** before the LH surge, or the very end of the luteal phase when the corpus luteum regresses. - During days 21–25, the **corpus luteum** is still fully functional, maintaining high levels of **progesterone** and moderate-to-high levels of **estrogen**. [Practice more Physiology PYQs on OnCourse]

Q: A woman is diagnosed with a pituitary microadenoma and has elevated serum prolactin levels. She presents with secondary amenorrhea and infertility. What is the most likely mechanism by which hyperprolactinemia causes these symptoms?

Decreased GnRH secretion from the hypothalamus. ***Decreased GnRH secretion from the hypothalamus*** - High levels of prolactin directly inhibit the pulsatile release of **Gonadotropin-Releasing Hormone (GnRH)** from the hypothalamus. - This inhibition leads to decreased pituitary secretion of **Luteinizing Hormone (LH)** and Follicle-Stimulating Hormone (FSH), causing **hypogonadotropic hypogonadism**, resulting in anovulation, amenorrhea, and infertility. *Antagonism of estrogen receptors* - Prolactin primarily exerts its reproductive effects centrally on the **hypothalamic-pituitary axis**, not by acting as a peripheral antagonist of estrogen receptors. - The resulting symptoms are due to **low estrogen production** secondary to inhibited gonadotropins, not receptor blockade. *Increased pulsatile FSH secretion* - Hyperprolactinemia actually causes **decreased** and non-pulsatile secretion of FSH and LH, rather than an increase. - If FSH were increased, it would stimulate follicular development and likely lead to ovarian hyperfunction, which is the opposite of the clinical presentation. *Increased LH secretion from the pituitary* - Prolactin actively inhibits LH release, causing **low plasma LH** levels and disrupting the mid-cycle LH surge necessary for ovulation. - The resulting state is one of inadequate follicular stimulation and anovulation, causing infertility and oligomenorrhea/amenorrhea. [Practice more Physiology PYQs on OnCourse]

Q: A man is climbing a mountain for trekking. Based on his physiological response to the high altitude, what is the most likely primary acid-base abnormality in his blood?

Respiratory alkalosis. ***Respiratory alkalosis*** - Exposure to **high altitude** causes decreased ambient partial pressure of oxygen (PO₂), leading to **hypoxemia**. - The physiological response to hypoxemia is reflex **hyperventilation** mediated by peripheral chemoreceptors, which blows off excessive **carbon dioxide (CO₂)**, causing decreased PaCO₂ and consequently elevated blood pH (alkalosis). - This is the **primary and immediate** acid-base abnormality at high altitude. *Metabolic acidosis* - This condition occurs due to the accumulation of **non-volatile acids** (e.g., lactic acid, ketoacids) or loss of bicarbonate. - While the kidney eventually compensates for the respiratory alkalosis by excreting bicarbonate (leading to compensatory **metabolic acidosis**), this is the **secondary, not the primary**, abnormality. *Metabolic alkalosis* - This abnormality is typically caused by loss of acid (e.g., severe vomiting, gastric suction) or excessive administration of alkali. - It is not related to the immediate respiratory compensatory response to **high-altitude hypoxemia**. *Respiratory acidosis* - This is caused by **hypoventilation** or impaired alveolar ventilation, leading to retention of **CO₂** and decreased pH. - At high altitude, the body actively **hyperventilates** to improve oxygen uptake, making respiratory acidosis the opposite of the expected primary response. [Practice more Physiology PYQs on OnCourse]

Q: Hyperpigmentation in Addison's disease is due to increased secretion of:

B. ACTH. ***ACTH*** - In **primary adrenal insufficiency** (Addison's disease), low cortisol production results in loss of negative feedback to the pituitary gland, leading to massively increased secretion of **ACTH** (Adrenocorticotropic Hormone) [1]. - ACTH is synthesized from the precursor molecule **Pro-opiomelanocortin (POMC)**. Cleavage of POMC also generates Melanocyte-Stimulating Hormone (MSH) (or ACTH itself acts like MSH), which stimulates melanocytes, causing **hyperpigmentation** [1]. *Cortisol* - Cortisol levels are **low** in Addison's disease because of adrenal gland destruction, which is the underlying pathological issue [2]. - Cortisol is a glucocorticoid and its primary role is metabolic; it does not directly stimulate **melanogenesis**. *Aldosterone* - Aldosterone, a mineralocorticoid, is also deficient in primary Addison's disease, leading to **salt-wasting** and electrolyte disturbances (hyponatremia, hyperkalemia) [2]. - Aldosterone's synthesis pathway is distinct from that of the pituitary hormone ACTH and therefore does not influence **skin pigmentation**. *Renin* - Renin levels are often **elevated** in Addison's disease due to hypovolemia and hypotension resulting from aldosterone deficiency (activation of the **Renin-Angiotensin-Aldosterone System**) [3]. - Renin is an enzyme secreted by the kidney and has no direct mechanism or shared precursor pathway related to stimulating **melanocytes**. [Practice more Physiology PYQs on OnCourse]

Question 1

Effect of pulmonary embolism on graph of V/Q?

Accepted Answer

Increased V/Q ratio approaching infinity (dead space)

Answer

Decreased V/Q ratio approaching zero

Answer

Normal V/Q ratio

Answer

Increased perfusion (Q) and decreased ventilation (V)

Question 2

In a woman with a regular 28-day menstrual cycle, which of the following best describes the typical hormonal profile during days 21 to 25 of the cycle?

Accepted Answer

High estrogen, high progesterone

Answer

Low estrogen, high progesterone, high LH and FSH

Answer

Low estrogen, low progesterone, low LH and FSH

Answer

Low estrogen, high progesterone, low LH and FSH

Question 3

A woman is diagnosed with a pituitary microadenoma and has elevated serum prolactin levels. She presents with secondary amenorrhea and infertility. What is the most likely mechanism by which hyperprolactinemia causes these symptoms?

Accepted Answer

Decreased GnRH secretion from the hypothalamus

Answer

Increased LH secretion from the pituitary

Answer

Antagonism of estrogen receptors

Answer

Increased pulsatile FSH secretion

Question 4

A man is climbing a mountain for trekking. Based on his physiological response to the high altitude, what is the most likely primary acid-base abnormality in his blood?

Accepted Answer

Respiratory alkalosis

Answer

Metabolic acidosis

Answer

Respiratory acidosis

Answer

Metabolic alkalosis

Question 5

Hyperpigmentation in Addison's disease is due to increased secretion of:

Accepted Answer

B. ACTH

Answer

C. Aldosterone

Answer

D. Renin

Answer

A. Cortisol

NEET-PG 2025 — Physiology