NEET-PG 2018 - Physiology PYQs Practice Questions

Q: Which of the following is endogenous pyrogen?

PG E2. ***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. [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: 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: Endothelin primarily acts through which type of receptors?

Endothelin receptor type A (ETA). ***Endothelin receptor type A (ETA)*** - **ETA receptors** are primarily responsible for the **vasoconstrictive effects** of endothelin-1 in various tissues, leading to increased vascular tone and blood pressure. - Activation of **ETA receptors** on vascular smooth muscle cells mediates signaling pathways that result in **smooth muscle contraction**. *Endothelin receptor type B (ETB)* - **ETB receptors** have dual roles, mediating both **vasoconstriction** (via smooth muscle ETB) and **vasodilation** (via endothelial ETB, stimulating nitric oxide and prostacyclin release). - They also play a significant role in **clearance of endothelin-1** from circulation. *General receptor type (GPCRs)* - While **endothelin receptors (ETA and ETB)** are indeed **G protein-coupled receptors (GPCRs)**, "General receptor type (GPCRs)" is too broad and not the most specific answer for how endothelin *primarily acts*. - Endothelin's specific effects are mediated through its dedicated subtypes of GPCRs, not the general class. *Calcium receptors* - **Calcium receptors** (e.g., calcium-sensing receptors) are involved in sensing extracellular calcium levels and regulating calcium homeostasis. - Endothelin's mechanism involves **intracellular calcium mobilization** *after* receptor activation, but it does not act *through* calcium receptors. [Practice more Physiology PYQs on OnCourse]

Question 1

Which of the following is endogenous pyrogen?

Accepted Answer

PG E2

Answer

PG D2

Answer

PGF2 alpha

Answer

PG I2

Question 2

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

Accepted Answer

No exchange of O2 and CO2 occurs.

Answer

Partial pressure of O2 becomes negligible.

Answer

Partial pressure of CO2 becomes negligible.

Answer

Partial pressures of both CO2 and O2 remain normal.

Question 3

What is the physiological response of the kidney during shock?

Accepted Answer

Renal blood flow decreases

Answer

GFR decreases

Answer

Perfusion of kidney decreases

Answer

Afferent arteriole resistance increases

Question 4

In hypovolemic shock there is -

Accepted Answer

Decreased cardiac output

Answer

Efferent arteriolar constriction

Answer

Increased blood flow to kidney

Answer

Afferent arteriolar constriction

Question 5

Endothelin primarily acts through which type of receptors?

Accepted Answer

Endothelin receptor type A (ETA)

Answer

Calcium receptors

Answer

General receptor type (GPCRs)

Answer

Endothelin receptor type B (ETB)

Question 6

Insulin-like growth factor is secreted by:

Accepted Answer

Liver

Answer

Pituitary gland

Answer

Pancreas

Answer

Adrenal glands

Question 7

Nude mice are not resistant to xenografts due to absence of

Accepted Answer

T cell

Answer

B cell

Answer

Absence of both B and T cells

Answer

Presence of both B and T cells

Question 8

Glucose is absorbed in the intestine by?

Accepted Answer

Secondary active transport

Answer

Facilitated diffusion

Answer

Simple diffusion

Answer

Primary active transport

Question 9

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

Accepted Answer

Calcium

Answer

Potassium

Answer

Sodium

Answer

Magnesium

Question 10

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

Accepted Answer

Actin

Answer

Dynein

Answer

Kinesin

Answer

Myosin

NEET-PG 2018 — Physiology