NEET-PG 2018 — Physiology

Q: In hypovolemic shock there is -

Decreased cardiac output. ***Decreased cardiac output*** - **Hypovolemic shock** is fundamentally defined by **decreased circulating blood volume**, which leads to **decreased venous return** to the heart. - According to the **Frank-Starling mechanism**, decreased venous return leads to **decreased preload**, which results in **decreased stroke volume** and consequently **decreased cardiac output**. - This is the **primary hemodynamic characteristic** of hypovolemic shock and is present in ALL cases. - Decreased cardiac output triggers all the compensatory mechanisms seen in hypovolemic shock, including sympathetic activation and RAAS activation. *Afferent arteriolar constriction* - While afferent arteriolar constriction does occur in hypovolemic shock due to **sympathetic activation**, it is a **compensatory response** rather than the primary feature. - The predominant effect at the kidney level is actually a combination of both afferent and efferent arteriolar changes. - This occurs secondary to the decreased cardiac output. *Efferent arteriolar constriction* - **Efferent arteriolar constriction** is mediated primarily by **angiotensin II** and is actually MORE prominent than afferent constriction. - This helps **maintain glomerular filtration rate (GFR)** despite reduced renal blood flow by increasing glomerular hydrostatic pressure. - However, this is also a compensatory response, not the primary feature of hypovolemic shock. *Increased blood flow to kidney* - This is incorrect as hypovolemic shock causes **decreased renal blood flow**. - Blood is redistributed away from the kidneys to vital organs like the heart and brain through compensatory vasoconstriction. [Practice more Physiology PYQs on OnCourse]

Q: What happens to gas exchange when the Va/Q ratio approaches infinity?

No exchange of O2 and CO2 occurs.. ***No exchange of O2 and CO2 occurs.*** - When the **Va/Q ratio approaches infinity**, it signifies a scenario of **ventilation without perfusion** (Q approaches zero). - This represents **alveolar dead space** - despite adequate ventilation, there is **no blood flow** to participate in gas exchange. - Therefore, **no O2 enters the blood** and **no CO2 leaves the blood**, making this the most accurate description of what happens to gas exchange. *Partial pressure of O2 becomes negligible.* - This statement is incorrect because with **no blood flow** (Q = 0), the alveolar air retains high O2 partial pressure. - O2 is being delivered via ventilation but not removed by blood, so **alveolar PO2** would approach that of **inspired air (~150 mmHg)**, not become negligible. *Partial pressure of CO2 becomes negligible.* - While this statement is technically true (alveolar PCO2 would approach zero/inspired air levels), it doesn't directly answer what happens to **gas exchange**. - With no blood flowing through the alveolus, no **CO2 from venous blood** can reach the alveolus to be excreted. - However, the question asks about **gas exchange** itself, not just partial pressures, making the first option more comprehensive. *Partial pressures of both CO2 and O2 remain normal.* - This statement is incorrect as the **Va/Q mismatch** significantly alters the partial pressures of both gases. - In infinite Va/Q scenario (dead space ventilation), **alveolar PO2 would be high** (approaching inspired air ~150 mmHg) and **alveolar PCO2 would be low** (approaching zero). [Practice more Physiology PYQs on OnCourse]

Q: What is the physiological response of the kidney during shock?

Renal blood flow decreases. ***Renal blood flow decreases*** - During shock, the **primary and most fundamental** physiological change affecting the kidney is a marked **reduction in renal blood flow (RBF)**. - Shock triggers intense **sympathetic activation** and **renin-angiotensin system (RAS) activation**, causing preferential **vasoconstriction** of renal vessels to redirect blood to vital organs (brain, heart). - RBF can drop to as low as **20-30% of normal** in severe shock, making this the hallmark renal response. - This reduction in RBF is the **upstream event** that triggers all other renal changes during shock. *Perfusion of kidney decreases* - While technically correct, "decreased perfusion" is **essentially synonymous** with decreased blood flow in this context. - The term "renal blood flow" is the **standard physiological terminology** used in medical literature to describe this phenomenon, making it the more precise answer. *Afferent arteriole resistance increases* - This is a **mechanism** by which RBF decreases, not the overall response itself. - Increased afferent arteriolar resistance is **secondary** to sympathetic activation and angiotensin II effects during shock. - It describes the "how" rather than the "what" of the kidney's response. *GFR decreases* - GFR reduction is a **consequence** of decreased RBF and increased afferent arteriolar resistance. - While clinically important (oliguria/acute kidney injury), it's a **downstream effect** rather than the primary physiological response. - The relationship: ↓RBF → ↓Glomerular hydrostatic pressure → ↓GFR [Practice more Physiology PYQs on OnCourse]

Q: Nude mice are not resistant to xenografts due to absence of

T cell. ***T cell*** - Nude mice have a **congenital athymia**, meaning they lack a functional **thymus**. - The thymus is essential for the maturation and development of **T lymphocytes**, making these mice severely **T-cell deficient**. - Without functional T cells, nude mice cannot reject **xenografts** (tissue transplanted from a different species). *B cell* - While nude mice have impaired T-cell function, their **B-cell development and function remain largely intact**. - B cells develop in the **bone marrow** and do not require the thymus for maturation. - B cells alone are insufficient to reject xenografts, as this requires cell-mediated immunity. *Absence of both B and T cells* - This statement is incorrect because nude mice **do possess B cells**, even if their T-cell immunity is severely compromised. - The primary defect is in the **thymus**, affecting T-cell maturation, not B cells. - Complete absence of both would describe **SCID mice**, not nude mice. *Presence of both B and T cells* - This is incorrect as nude mice clearly have a **severe deficiency in T cells** due to athymia. - Their inability to reject xenografts is directly linked to this lack of functional T-cell immunity. - If both were present and functional, the mice would reject xenografts normally. [Practice more Physiology PYQs on OnCourse]

Q: Insulin-like growth factor is secreted by:

Liver. ***Liver*** - The **liver** is the primary site of **insulin-like growth factor 1 (IGF-1)** production in response to **growth hormone (GH)** stimulation. - IGF-1 mediates many of the growth-promoting effects of GH, affecting various tissues throughout the body. *Pituitary gland* - The **pituitary gland** secretes **growth hormone (GH)**, which then stimulates the liver to produce IGF-1, but it does not directly secrete IGF-1. - Its role is upstream in the GH-IGF-1 axis, initiating the signaling cascade. *Pancreas* - The **pancreas** is primarily known for secreting **insulin** and **glucagon**, which regulate blood glucose levels. - It does not produce significant amounts of IGF-1. *Adrenal glands* - The **adrenal glands** produce hormones like **cortisol**, **aldosterone**, and **androgens**. - They are not involved in the direct secretion of IGF-1. [Practice more Physiology PYQs on OnCourse]

13 Previous Year Questions with Answers & Explanations

Questions

In hypovolemic shock there is -

What happens to gas exchange when the Va/Q ratio approaches infinity?

What is the physiological response of the kidney during shock?

Nude mice are not resistant to xenografts due to absence of

Insulin-like growth factor is secreted by:

Which of the following is endogenous pyrogen?

Glucose is absorbed in the intestine by?

In a child with suspected tetany, the following test is performed. Identify the sign?

Which ion plays a role in the process shown below? (Recent NEET Pattern 2018)

Q10

Which of the following is not a component of the process shown in the image?

NEET-PG 2018 - Physiology NEET-PG Practice Questions and MCQs

Question 1: In hypovolemic shock there is -

A. Efferent arteriolar constriction
B. Increased blood flow to kidney
C. Decreased cardiac output (Correct Answer)
D. Afferent arteriolar constriction

Explanation: ***Decreased cardiac output*** - **Hypovolemic shock** is fundamentally defined by **decreased circulating blood volume**, which leads to **decreased venous return** to the heart. - According to the **Frank-Starling mechanism**, decreased venous return leads to **decreased preload**, which results in **decreased stroke volume** and consequently **decreased cardiac output**. - This is the **primary hemodynamic characteristic** of hypovolemic shock and is present in ALL cases. - Decreased cardiac output triggers all the compensatory mechanisms seen in hypovolemic shock, including sympathetic activation and RAAS activation. *Afferent arteriolar constriction* - While afferent arteriolar constriction does occur in hypovolemic shock due to **sympathetic activation**, it is a **compensatory response** rather than the primary feature. - The predominant effect at the kidney level is actually a combination of both afferent and efferent arteriolar changes. - This occurs secondary to the decreased cardiac output. *Efferent arteriolar constriction* - **Efferent arteriolar constriction** is mediated primarily by **angiotensin II** and is actually MORE prominent than afferent constriction. - This helps **maintain glomerular filtration rate (GFR)** despite reduced renal blood flow by increasing glomerular hydrostatic pressure. - However, this is also a compensatory response, not the primary feature of hypovolemic shock. *Increased blood flow to kidney* - This is incorrect as hypovolemic shock causes **decreased renal blood flow**. - Blood is redistributed away from the kidneys to vital organs like the heart and brain through compensatory vasoconstriction.

Question 2: What happens to gas exchange when the Va/Q ratio approaches infinity?

A. Partial pressure of O2 becomes negligible.
B. No exchange of O2 and CO2 occurs. (Correct Answer)
C. Partial pressure of CO2 becomes negligible.
D. Partial pressures of both CO2 and O2 remain normal.

Explanation: ***No exchange of O2 and CO2 occurs.*** - When the **Va/Q ratio approaches infinity**, it signifies a scenario of **ventilation without perfusion** (Q approaches zero). - This represents **alveolar dead space** - despite adequate ventilation, there is **no blood flow** to participate in gas exchange. - Therefore, **no O2 enters the blood** and **no CO2 leaves the blood**, making this the most accurate description of what happens to gas exchange. *Partial pressure of O2 becomes negligible.* - This statement is incorrect because with **no blood flow** (Q = 0), the alveolar air retains high O2 partial pressure. - O2 is being delivered via ventilation but not removed by blood, so **alveolar PO2** would approach that of **inspired air (~150 mmHg)**, not become negligible. *Partial pressure of CO2 becomes negligible.* - While this statement is technically true (alveolar PCO2 would approach zero/inspired air levels), it doesn't directly answer what happens to **gas exchange**. - With no blood flowing through the alveolus, no **CO2 from venous blood** can reach the alveolus to be excreted. - However, the question asks about **gas exchange** itself, not just partial pressures, making the first option more comprehensive. *Partial pressures of both CO2 and O2 remain normal.* - This statement is incorrect as the **Va/Q mismatch** significantly alters the partial pressures of both gases. - In infinite Va/Q scenario (dead space ventilation), **alveolar PO2 would be high** (approaching inspired air ~150 mmHg) and **alveolar PCO2 would be low** (approaching zero).

Question 3: What is the physiological response of the kidney during shock?

A. GFR decreases
B. Perfusion of kidney decreases
C. Afferent arteriole resistance increases
D. Renal blood flow decreases (Correct Answer)

Explanation: ***Renal blood flow decreases*** - During shock, the **primary and most fundamental** physiological change affecting the kidney is a marked **reduction in renal blood flow (RBF)**. - Shock triggers intense **sympathetic activation** and **renin-angiotensin system (RAS) activation**, causing preferential **vasoconstriction** of renal vessels to redirect blood to vital organs (brain, heart). - RBF can drop to as low as **20-30% of normal** in severe shock, making this the hallmark renal response. - This reduction in RBF is the **upstream event** that triggers all other renal changes during shock. *Perfusion of kidney decreases* - While technically correct, "decreased perfusion" is **essentially synonymous** with decreased blood flow in this context. - The term "renal blood flow" is the **standard physiological terminology** used in medical literature to describe this phenomenon, making it the more precise answer. *Afferent arteriole resistance increases* - This is a **mechanism** by which RBF decreases, not the overall response itself. - Increased afferent arteriolar resistance is **secondary** to sympathetic activation and angiotensin II effects during shock. - It describes the "how" rather than the "what" of the kidney's response. *GFR decreases* - GFR reduction is a **consequence** of decreased RBF and increased afferent arteriolar resistance. - While clinically important (oliguria/acute kidney injury), it's a **downstream effect** rather than the primary physiological response. - The relationship: ↓RBF → ↓Glomerular hydrostatic pressure → ↓GFR

Question 4: Nude mice are not resistant to xenografts due to absence of

A. B cell
B. T cell (Correct Answer)
C. Absence of both B and T cells
D. Presence of both B and T cells

Explanation: ***T cell*** - Nude mice have a **congenital athymia**, meaning they lack a functional **thymus**. - The thymus is essential for the maturation and development of **T lymphocytes**, making these mice severely **T-cell deficient**. - Without functional T cells, nude mice cannot reject **xenografts** (tissue transplanted from a different species). *B cell* - While nude mice have impaired T-cell function, their **B-cell development and function remain largely intact**. - B cells develop in the **bone marrow** and do not require the thymus for maturation. - B cells alone are insufficient to reject xenografts, as this requires cell-mediated immunity. *Absence of both B and T cells* - This statement is incorrect because nude mice **do possess B cells**, even if their T-cell immunity is severely compromised. - The primary defect is in the **thymus**, affecting T-cell maturation, not B cells. - Complete absence of both would describe **SCID mice**, not nude mice. *Presence of both B and T cells* - This is incorrect as nude mice clearly have a **severe deficiency in T cells** due to athymia. - Their inability to reject xenografts is directly linked to this lack of functional T-cell immunity. - If both were present and functional, the mice would reject xenografts normally.

Question 5: Insulin-like growth factor is secreted by:

A. Liver (Correct Answer)
B. Pituitary gland
C. Pancreas
D. Adrenal glands

Explanation: ***Liver*** - The **liver** is the primary site of **insulin-like growth factor 1 (IGF-1)** production in response to **growth hormone (GH)** stimulation. - IGF-1 mediates many of the growth-promoting effects of GH, affecting various tissues throughout the body. *Pituitary gland* - The **pituitary gland** secretes **growth hormone (GH)**, which then stimulates the liver to produce IGF-1, but it does not directly secrete IGF-1. - Its role is upstream in the GH-IGF-1 axis, initiating the signaling cascade. *Pancreas* - The **pancreas** is primarily known for secreting **insulin** and **glucagon**, which regulate blood glucose levels. - It does not produce significant amounts of IGF-1. *Adrenal glands* - The **adrenal glands** produce hormones like **cortisol**, **aldosterone**, and **androgens**. - They are not involved in the direct secretion of IGF-1.

Question 6: Which of the following is endogenous pyrogen?

A. PG E2 (Correct Answer)
B. PG D2
C. PGF2 alpha
D. PG I2

Explanation: ***PG E2*** - **Prostaglandin E2 (PGE2)** is considered the **endogenous mediator of fever** in the context of this question (NEET-PG 2018). - **Mechanism:** PGE2 acts on the **preoptic area of the hypothalamus** to raise the body's temperature set point, leading to fever. - **Production pathway:** Endogenous pyrogens like **IL-1, IL-6, and TNF-α** stimulate **cyclooxygenase-2 (COX-2)** in hypothalamic endothelial cells → **PGE2 synthesis** → binds to EP3 receptors → raises set point. - **Clinical relevance:** This is why **antipyretics** (aspirin, paracetamol, NSAIDs) work by inhibiting COX enzymes, thereby reducing PGE2 production. - **Terminology note:** Strictly speaking, cytokines (IL-1, IL-6, TNF-α) are the true "endogenous pyrogens," while PGE2 is the "final common mediator" - but for exam purposes, PGE2 is accepted as the endogenous pyrogenic mediator. *PG D2* - **Prostaglandin D2 (PGD2)** is primarily involved in **allergic reactions**, **sleep regulation**, and modulating immune responses. - Main roles include **bronchoconstriction** in asthma, **vasodilation**, and mast cell activation. - It does **not** act as a fever mediator in the hypothalamus. *PGF2 alpha* - **Prostaglandin F2 alpha (PGF2α)** functions primarily in **reproductive physiology**. - Causes **uterine contractions** (labor induction), **luteolysis** (corpus luteum regression), and **bronchoconstriction**. - It has **no direct role** in fever generation or thermoregulation. *PG I2* - **Prostacyclin (PGI2)** is a potent **vasodilator** and **inhibitor of platelet aggregation**. - Produced by vascular endothelium, it has **anti-thrombotic** and **anti-inflammatory** properties. - It does **not** function as a pyrogenic mediator and may actually have **antipyretic effects** in some contexts.

Question 7: Glucose is absorbed in the intestine by?

A. Facilitated diffusion
B. Simple diffusion
C. Secondary active transport (Correct Answer)
D. Primary active transport

Explanation: ***Secondary active transport*** - Glucose absorption in the intestine primarily occurs via the **SGLT1 (sodium-glucose cotransporter 1)** protein. - SGLT1 uses the **electrochemical gradient of sodium** (established by Na+/K+-ATPase) to co-transport glucose against its concentration gradient, classifying it as secondary active transport. *Facilitated diffusion* - While **facilitated diffusion** by GLUT2 transporters is involved in glucose exit from the intestinal cells into the bloodstream, it's not the primary mechanism for uptake from the lumen. - This process does not require direct energy expenditure, but relies on a **concentration gradient**. *Simple diffusion* - **Simple diffusion** involves the movement of substances directly across the membrane, down their concentration gradient, without the help of transport proteins. - Glucose is a **hydrophilic molecule** and too large to pass through the lipid bilayer by simple diffusion. *Primary active transport* - **Primary active transport** directly uses ATP hydrolysis to move substances against their concentration gradient (e.g., Na+/K+-ATPase). - While essential for maintaining the sodium gradient, it is not the direct mechanism for glucose uptake from the intestinal lumen.

Question 8: In a child with suspected tetany, the following test is performed. Identify the sign?

A. Chvostek sign
B. Allen sign
C. Trousseau sign (Correct Answer)
D. Turner sign

Explanation: ***Trousseau sign*** - The image depicts a blood pressure cuff inflated on the arm, leading to **carpopedal spasm** in the hand, which is characteristic of the **Trousseau sign**. - This sign is indicative of **latent tetany** and is often seen in conditions causing **hypocalcemia**. *Chvostek sign* - The Chvostek sign involves a **facial muscle twitch** elicited by tapping the facial nerve anterior to the ear. - This sign is also associated with hypocalcemia but differs clinically from the presentation in the image. *Allen sign* - The Allen test (not "sign") is performed to assess the **patency of the ulnar and radial arteries** before arterial puncture or cannulation. - It involves digitally compressing both arteries and observing the return of color to the hand after releasing one artery, which is unrelated to the image. *Turner sign* - The Turner sign refers to **flank ecchymosis** (bruising) and is a physical finding associated with **hemorrhagic pancreatitis**. - This sign indicates retroperitoneal bleeding, which is not represented by the image or related to tetany.

Question 9: Which ion plays a role in the process shown below? (Recent NEET Pattern 2018)

A. Potassium
B. Sodium
C. Magnesium
D. Calcium (Correct Answer)

Explanation: ***Calcium*** - **Calcium ions (Ca2+)** are the primary trigger for **exocytosis**, binding to **synaptotagmin** proteins on synaptic vesicles to initiate membrane fusion. - Ca2+ influx activates the **SNARE complex** formation, allowing vesicles to fuse with the plasma membrane and release neurotransmitters or other cellular contents. *Potassium* - **Potassium ions (K+)** are primarily responsible for maintaining the **resting membrane potential** and **repolarization** during action potentials. - While essential for neuronal function, K+ does not directly trigger **vesicle fusion** or exocytosis processes. *Sodium* - **Sodium ions (Na+)** are crucial for **action potential depolarization** and maintaining **electrochemical gradients** across cell membranes. - Na+ influx initiates nerve impulses but does not serve as the direct trigger for **vesicle release** during exocytosis. *Magnesium* - **Magnesium ions (Mg2+)** function as essential **cofactors** for numerous enzymes and play roles in **ATP metabolism** and **protein synthesis**. - Although Mg2+ can modulate some cellular processes, it is not the primary ion responsible for triggering **exocytotic release**.

Question 10: Which of the following is not a component of the process shown in the image?

A. Dynein
B. Kinesin
C. Myosin
D. Actin (Correct Answer)

Explanation: ***Actin*** - The image depicts **microtubule-based transport** involving motor proteins (dynein and kinesin) moving cargo along microtubules. - **Actin filaments** are a completely separate cytoskeletal system and are NOT components of the microtubule-based process shown. - This is the most fundamental distinction - actin vs. microtubule cytoskeletal systems. *Dynein* - **Dynein** is clearly shown in the image, transporting **retrograde cargo** toward the minus end of the microtubule. - It is a key motor protein for minus-end directed movement along microtubules. *Kinesin* - **Kinesin** is depicted in the image, transporting **anterograde cargo** toward the plus end of the microtubule. - It is the primary motor protein for plus-end directed movement along microtubules. *Myosin* - While **myosin** typically works with actin filaments rather than microtubules, it belongs to the same functional category as dynein and kinesin (motor proteins). - Some myosin isoforms can even associate with microtubule-based processes in specific contexts. - **Actin** is the better answer as it represents a completely different cytoskeletal system, whereas myosin is still a motor protein like the others listed.