NEET-PG 2019 — Physiology

Q: Which of the following is the MOST CHARACTERISTIC metabolic feature of type 1 diabetes mellitus?

Increased lipolysis. ***Increased lipolysis*** - Due to **absolute insulin deficiency** in type 1 diabetes, the body cannot properly utilize glucose, leading to a shift toward **fat metabolism** for energy. - This results in increased breakdown of **triglycerides** into **fatty acids** and **glycerol**, which are then converted to **ketone bodies** in the liver. - **Ketoacidosis** resulting from increased lipolysis is the most **characteristic and distinguishing** metabolic feature of type 1 diabetes, differentiating it from type 2 diabetes. *Decreased glucose uptake* - Decreased glucose uptake by insulin-sensitive tissues (muscle and adipose tissue) is the **primary metabolic defect** in type 1 diabetes due to the absolute lack of insulin. - While this is fundamental to the pathophysiology, it occurs in **both type 1 and type 2 diabetes**, making it less characteristic of type 1 specifically. *Increased hepatic glucose output* - Increased hepatic glucose output (via gluconeogenesis and glycogenolysis) is a prominent feature due to loss of insulin's suppressive effects on the liver. - However, this also occurs in **type 2 diabetes** and is not as distinctive as the dramatic shift to lipolysis and ketone production seen in type 1. *Increased protein catabolism* - While protein catabolism is increased in type 1 diabetes, contributing to **muscle wasting** and providing substrates for gluconeogenesis, it is a less immediate and less specific feature. - The metabolic shift to **lipolysis and ketogenesis** is more rapid, more clinically significant, and more characteristic of the type 1 diabetic state. [Practice more Physiology PYQs on OnCourse]

Q: Vasopressin acts through which aquaporin channels in the collecting duct?

Aquaporin 2. ***Aquaporin 2*** - Vasopressin (ADH) stimulates the insertion of **Aquaporin 2 (AQP2)** channels into the apical membrane of collecting duct cells, increasing water reabsorption. - This process is crucial for the kidney's ability to concentrate urine and maintain **water balance**. *Aquaporin 1* - **Aquaporin 1 (AQP1)** is predominantly found in the proximal tubules and descending limb of the loop of Henle, where **constitutive water reabsorption** occurs, independent of vasopressin. - It plays a role in bulk water reabsorption rather than regulated fine-tuning. *Aquaporin 3* - **Aquaporin 3 (AQP3)** is located on the **basolateral membrane** of collecting duct cells, facilitating the exit of water from the cell into the interstitial fluid. - While essential for water movement, its insertion into the membrane is **not directly regulated by vasopressin** in the same way as AQP2. *Aquaporin 4* - **Aquaporin 4 (AQP4)** is also found on the **basolateral membrane** of collecting duct cells and in other tissues like the brain. - Similar to AQP3, it allows water to leave the cell but is not the primary target for vasopressin-mediated regulation of water permeability. [Practice more Physiology PYQs on OnCourse]

Q: With increase in age, which of the following statements about lung function is true?

Pulmonary compliance increases. ***Pulmonary compliance increases*** - With **increasing age**, there is a loss of **elastic recoil** in the lungs due to changes in elastin and collagen fibers, leading to an increase in **pulmonary compliance**. - This increased compliance means the lungs become less stiff and easier to inflate, but also less able to recoil and expel air effectively. - The **net effect** of aging is increased compliance, as the loss of elastic fibers is the predominant change in normal aging. *Residual volume decreases* - **Residual volume (RV)** actually **increases** with age. This is because the loss of elastic recoil makes it harder to fully exhale, causing more air to remain in the lungs after a maximal exhalation. - An increased residual volume contributes to an overall rise in **functional residual capacity** and total lung capacity in older adults. *Mucociliary clearance increases* - **Mucociliary clearance** generally **decreases** with age. This is due to a reduction in the number and function of cilia, as well as changes in mucus quality. - Impaired mucociliary clearance makes older individuals more susceptible to respiratory infections and difficulties in clearing secretions. *Fibrosis of the interstitium decreases* - The **fibrosis of the interstitium** can **increase** with age in some individuals. However, in normal aging (without pathological conditions), the predominant change is loss of elastic recoil rather than significant fibrotic changes. - When present, increased interstitial fibrosis would make the lungs stiffer, but this is not the primary age-related change in healthy individuals. [Practice more Physiology PYQs on OnCourse]

Q: Tubuloglomerular feedback control is useful for which one of the following?

GFR. ***GFR*** - **Tubuloglomerular feedback (TGF)** is a critical autoregulatory mechanism that maintains a relatively constant **glomerular filtration rate (GFR)** despite fluctuations in arterial blood pressure. - The **macula densa** cells at the end of the thick ascending limb of the loop of Henle sense the **volume** and **sodium chloride concentration** of the tubular fluid and release paracrine factors to adjust afferent arteriolar resistance. *Plasma sodium* - While TGF senses the **sodium chloride concentration** in the filtrate, its primary role is to regulate GFR, not directly control systemic plasma sodium levels. - Plasma sodium is primarily regulated by hormones like **ADH** and **aldosterone**, which influence water reabsorption and sodium excretion. *Plasma volume* - **Plasma volume** is regulated predominantly by hormonal mechanisms (e.g., **renin-angiotensin-aldosterone system**, **ADH**, **ANP**) and control over overall sodium and water balance, rather than by the acute, intrinsic GFR regulation of TGF. - Changes in plasma volume can indirectly affect GFR, but TGF is not the direct control mechanism for plasma volume itself. *Determining tubular secretion* - **Tubular secretion** is the process by which solutes are actively transported from the peritubular capillaries into the tubular lumen. - TGF influences **glomerular filtration**, not directly the rates of tubular secretion, which are regulated by specific transport proteins and physiological needs. [Practice more Physiology PYQs on OnCourse]

Q: What is the effect of the Bainbridge reflex?

Increased heart rate. ***Increased heart rate*** - The **Bainbridge reflex** produces an increase in heart rate (tachycardia). - This reflex is triggered by an increase in **venous return** and **atrial distension**, which stimulates stretch receptors in the atria, leading to increased heart rate. - The reflex helps prevent venous pooling and maintains efficient cardiac function. *Bradycardia* - **Bradycardia** (slow heart rate) is the opposite effect of the Bainbridge reflex. - Other reflexes like the **baroreceptor reflex** can cause bradycardia when arterial pressure increases. *Increased cardiac output* - While increased heart rate can contribute to **increased cardiac output**, this is a secondary consequence, not the primary effect of the reflex. - Cardiac output = Heart rate × Stroke volume, so the direct effect is on heart rate. *Decreased venous return* - The Bainbridge reflex does not cause decreased venous return. - Instead, the reflex is **triggered by increased** venous return and responds by increasing heart rate to accommodate the increased blood flow. [Practice more Physiology PYQs on OnCourse]

13 Previous Year Questions with Answers & Explanations

Questions

Which of the following is the MOST CHARACTERISTIC metabolic feature of type 1 diabetes mellitus?

Vasopressin acts through which aquaporin channels in the collecting duct?

With increase in age, which of the following statements about lung function is true?

Tubuloglomerular feedback control is useful for which one of the following?

What is the effect of the Bainbridge reflex?

Functional residual capacity (FRC) is defined as the volume of air remaining in the lungs at which specific moment in the respiratory cycle?

In forceful expiration, which of the following neurons gets fired?

What is the PRIMARY mechanism by which Interleukin-1 (IL-1) induces fever?

Achondroplasia shows which type of inheritance?

Q10

All are true about Decerebrate posture except:-

NEET-PG 2019 - Physiology NEET-PG Practice Questions and MCQs

Question 1: Which of the following is the MOST CHARACTERISTIC metabolic feature of type 1 diabetes mellitus?

A. Increased protein catabolism
B. Increased hepatic glucose output
C. Increased lipolysis (Correct Answer)
D. Decreased glucose uptake

Explanation: ***Increased lipolysis*** - Due to **absolute insulin deficiency** in type 1 diabetes, the body cannot properly utilize glucose, leading to a shift toward **fat metabolism** for energy. - This results in increased breakdown of **triglycerides** into **fatty acids** and **glycerol**, which are then converted to **ketone bodies** in the liver. - **Ketoacidosis** resulting from increased lipolysis is the most **characteristic and distinguishing** metabolic feature of type 1 diabetes, differentiating it from type 2 diabetes. *Decreased glucose uptake* - Decreased glucose uptake by insulin-sensitive tissues (muscle and adipose tissue) is the **primary metabolic defect** in type 1 diabetes due to the absolute lack of insulin. - While this is fundamental to the pathophysiology, it occurs in **both type 1 and type 2 diabetes**, making it less characteristic of type 1 specifically. *Increased hepatic glucose output* - Increased hepatic glucose output (via gluconeogenesis and glycogenolysis) is a prominent feature due to loss of insulin's suppressive effects on the liver. - However, this also occurs in **type 2 diabetes** and is not as distinctive as the dramatic shift to lipolysis and ketone production seen in type 1. *Increased protein catabolism* - While protein catabolism is increased in type 1 diabetes, contributing to **muscle wasting** and providing substrates for gluconeogenesis, it is a less immediate and less specific feature. - The metabolic shift to **lipolysis and ketogenesis** is more rapid, more clinically significant, and more characteristic of the type 1 diabetic state.

Question 2: Vasopressin acts through which aquaporin channels in the collecting duct?

A. Aquaporin 1
B. Aquaporin 2 (Correct Answer)
C. Aquaporin 4
D. Aquaporin 3

Explanation: ***Aquaporin 2*** - Vasopressin (ADH) stimulates the insertion of **Aquaporin 2 (AQP2)** channels into the apical membrane of collecting duct cells, increasing water reabsorption. - This process is crucial for the kidney's ability to concentrate urine and maintain **water balance**. *Aquaporin 1* - **Aquaporin 1 (AQP1)** is predominantly found in the proximal tubules and descending limb of the loop of Henle, where **constitutive water reabsorption** occurs, independent of vasopressin. - It plays a role in bulk water reabsorption rather than regulated fine-tuning. *Aquaporin 3* - **Aquaporin 3 (AQP3)** is located on the **basolateral membrane** of collecting duct cells, facilitating the exit of water from the cell into the interstitial fluid. - While essential for water movement, its insertion into the membrane is **not directly regulated by vasopressin** in the same way as AQP2. *Aquaporin 4* - **Aquaporin 4 (AQP4)** is also found on the **basolateral membrane** of collecting duct cells and in other tissues like the brain. - Similar to AQP3, it allows water to leave the cell but is not the primary target for vasopressin-mediated regulation of water permeability.

Question 3: With increase in age, which of the following statements about lung function is true?

A. Fibrosis of the interstitium decreases
B. Residual volume decreases
C. Mucociliary clearance increases
D. Pulmonary compliance increases (Correct Answer)

Explanation: ***Pulmonary compliance increases*** - With **increasing age**, there is a loss of **elastic recoil** in the lungs due to changes in elastin and collagen fibers, leading to an increase in **pulmonary compliance**. - This increased compliance means the lungs become less stiff and easier to inflate, but also less able to recoil and expel air effectively. - The **net effect** of aging is increased compliance, as the loss of elastic fibers is the predominant change in normal aging. *Residual volume decreases* - **Residual volume (RV)** actually **increases** with age. This is because the loss of elastic recoil makes it harder to fully exhale, causing more air to remain in the lungs after a maximal exhalation. - An increased residual volume contributes to an overall rise in **functional residual capacity** and total lung capacity in older adults. *Mucociliary clearance increases* - **Mucociliary clearance** generally **decreases** with age. This is due to a reduction in the number and function of cilia, as well as changes in mucus quality. - Impaired mucociliary clearance makes older individuals more susceptible to respiratory infections and difficulties in clearing secretions. *Fibrosis of the interstitium decreases* - The **fibrosis of the interstitium** can **increase** with age in some individuals. However, in normal aging (without pathological conditions), the predominant change is loss of elastic recoil rather than significant fibrotic changes. - When present, increased interstitial fibrosis would make the lungs stiffer, but this is not the primary age-related change in healthy individuals.

Question 4: Tubuloglomerular feedback control is useful for which one of the following?

A. GFR (Correct Answer)
B. Plasma sodium
C. Plasma volume
D. Determining tubular secretion

Explanation: ***GFR*** - **Tubuloglomerular feedback (TGF)** is a critical autoregulatory mechanism that maintains a relatively constant **glomerular filtration rate (GFR)** despite fluctuations in arterial blood pressure. - The **macula densa** cells at the end of the thick ascending limb of the loop of Henle sense the **volume** and **sodium chloride concentration** of the tubular fluid and release paracrine factors to adjust afferent arteriolar resistance. *Plasma sodium* - While TGF senses the **sodium chloride concentration** in the filtrate, its primary role is to regulate GFR, not directly control systemic plasma sodium levels. - Plasma sodium is primarily regulated by hormones like **ADH** and **aldosterone**, which influence water reabsorption and sodium excretion. *Plasma volume* - **Plasma volume** is regulated predominantly by hormonal mechanisms (e.g., **renin-angiotensin-aldosterone system**, **ADH**, **ANP**) and control over overall sodium and water balance, rather than by the acute, intrinsic GFR regulation of TGF. - Changes in plasma volume can indirectly affect GFR, but TGF is not the direct control mechanism for plasma volume itself. *Determining tubular secretion* - **Tubular secretion** is the process by which solutes are actively transported from the peritubular capillaries into the tubular lumen. - TGF influences **glomerular filtration**, not directly the rates of tubular secretion, which are regulated by specific transport proteins and physiological needs.

Question 5: What is the effect of the Bainbridge reflex?

A. Bradycardia
B. Increased cardiac output
C. Decreased venous return
D. Increased heart rate (Correct Answer)

Explanation: ***Increased heart rate*** - The **Bainbridge reflex** produces an increase in heart rate (tachycardia). - This reflex is triggered by an increase in **venous return** and **atrial distension**, which stimulates stretch receptors in the atria, leading to increased heart rate. - The reflex helps prevent venous pooling and maintains efficient cardiac function. *Bradycardia* - **Bradycardia** (slow heart rate) is the opposite effect of the Bainbridge reflex. - Other reflexes like the **baroreceptor reflex** can cause bradycardia when arterial pressure increases. *Increased cardiac output* - While increased heart rate can contribute to **increased cardiac output**, this is a secondary consequence, not the primary effect of the reflex. - Cardiac output = Heart rate × Stroke volume, so the direct effect is on heart rate. *Decreased venous return* - The Bainbridge reflex does not cause decreased venous return. - Instead, the reflex is **triggered by increased** venous return and responds by increasing heart rate to accommodate the increased blood flow.

Question 6: Functional residual capacity (FRC) is defined as the volume of air remaining in the lungs at which specific moment in the respiratory cycle?

A. During active expiration
B. After normal expiration (Correct Answer)
C. At peak inspiration
D. During active inspiration

Explanation: ***After normal expiration*** - **Functional residual capacity (FRC)** is the volume of air remaining in the lungs at the end of a **normal, passive expiration**. - It represents the sum of the **expiratory reserve volume (ERV)** and the **residual volume (RV)**. *During active expiration* - **Active expiration** involves the use of accessory muscles to force more air out of the lungs than during normal expiration. - This process would result in a lung volume less than FRC, closer to the **residual volume**. *At peak inspiration* - **Peak inspiration** represents the total lung capacity (TLC), which is the maximum volume of air the lungs can hold after a maximal inspiratory effort. - This is the largest lung volume, significantly greater than FRC. *During active inspiration* - **Active inspiration** is the process of inhaling air, which increases lung volume. - FRC is a static volume measured at the end of expiration, not during the dynamic process of inhaling.

Question 7: In forceful expiration, which of the following neurons gets fired?

A. VRG (Correct Answer)
B. DRG
C. Pneumotaxic centre
D. Chemoreceptors

Explanation: ***VRG*** - The **ventral respiratory group (VRG)** contains both inspiratory and expiratory neurons, and it is primarily involved in controlling the muscles necessary for **forceful breathing**. - During forceful expiration, the expiratory neurons in the VRG become active, stimulating accessory muscles of expiration like the **internal intercostals** and **abdominal muscles**. *DRG* - The **dorsal respiratory group (DRG)** primarily contains inspiratory neurons and is fundamental for **normal, quiet breathing**. - Its activity leads to contraction of the diaphragm and external intercostals, and it is largely inactive during quiet expiration, which is a passive process. *Pneumotaxic centre* - The **pneumotaxic center** (or pontine respiratory group) helps to fine-tune breathing patterns by **inhibiting inspiration**, thereby limiting the duration of inhalation. - It influences the rate and depth of breathing but does not directly activate muscles for forceful expiration. *Chemoreceptors* - **Chemoreceptors** (central and peripheral) monitor blood levels of **carbon dioxide (PCO2)**, **oxygen (PO2)**, and **pH**, and they send signals to the respiratory centers to adjust breathing accordingly. - While they regulate the overall respiratory drive, they do not directly fire to initiate forceful expiration; rather, they modulate the activity of the respiratory groups in the brainstem.

Question 8: What is the PRIMARY mechanism by which Interleukin-1 (IL-1) induces fever?

A. Stimulates antibody production
B. Inhibits inflammation
C. Endogenous pyrogen (Correct Answer)
D. Activates complement cascade

Explanation: ***Endogenous pyrogen*** - **IL-1** is a potent **endogenous pyrogen** that acts directly on the **hypothalamus**, the body's thermoregulatory center. - It stimulates the production of **prostaglandin E2 (PGE2)** in the hypothalamus, which then resets the body's thermoregulatory set point to a higher temperature, leading to fever. *Stimulates antibody production* - While IL-1 can have broader immune functions and can influence B cell activity, its **primary role in fever** production is not through antibody stimulation. - Antibody production is a function of **B lymphocytes** and is primarily driven by antigen presentation and T cell help. *Inhibits inflammation* - **IL-1** is a key **pro-inflammatory cytokine** that promotes inflammation, rather than inhibiting it. - It induces the expression of various adhesion molecules and inflammatory mediators, contributing to the inflammatory response. *Activates complement cascade* - The **complement cascade** is a part of the innate immune system, typically activated by **antigen-antibody complexes** (classical pathway) or **microbial surfaces** (alternative and lectin pathways). - While IL-1 plays a role in overall immune responses, its direct mechanism for inducing fever does not primarily involve activating the complement system.

Question 9: Achondroplasia shows which type of inheritance?

A. X-linked dominant (XLD)
B. Autosomal recessive inheritance
C. Autosomal dominant inheritance (Correct Answer)
D. X-linked recessive (XLR)

Explanation: ***Autosomal dominant inheritance*** - Achondroplasia is caused by a **mutation in the FGFR3 gene**, which is located on an **autosomal chromosome** (chromosome 4). - The disease manifests with only **one copy of the mutated gene**, hence it follows an autosomal dominant pattern. *X-linked dominant (XLD)* - X-linked dominant disorders are caused by mutations on the **X chromosome** and typically affect females more severely or frequently than males. - Achondroplasia does not show sex-linked inheritance patterns, as its causative gene is on an autosome. *Autosomal recessive inheritance* - Autosomal recessive disorders require **two copies of the mutated gene** (one from each parent) for the disease to manifest. - Achondroplasia can occur with only one copy of the mutated gene, distinguishing it from recessive inheritance. *X-linked recessive (XLR)* - X-linked recessive disorders primarily affect **males** and are carried by females, who are usually asymptomatic carriers. - The inheritance pattern of achondroplasia is independent of sex, ruling out X-linked recessive inheritance.

Question 10: All are true about Decerebrate posture except:-

A. Exaggerated gamma motor neuron discharge
B. Flexion of upper extremity and extension of lower extremity (Correct Answer)
C. Extension of both upper and lower extremity
D. Reticulo spinal tract is also involved

Explanation: ***Flexion of upper extremity and extension of lower extremity*** - This description corresponds to **decorticate rigidity**, not decerebrate rigidity. - In decorticate rigidity, there is **flexion** of the **upper extremities** and **extension** of the **lower extremities**, indicating a lesion above the red nucleus. *Exaggerated gamma motor neuron discharge* - Decerebrate rigidity is characterized by an **increase in muscle tone** due to disinhibition of extensor muscles, which is mediated by increased **gamma motor neuron activity**. - This increased discharge leads to potentiation of the **stretch reflex**, contributing to the rigidity. *Extension of both upper and lower extremity* - **Decerebrate posture** is defined by **extension of all four limbs** (both upper and lower extremities). - This posture results from a lesion in the brainstem **below the red nucleus** but above the vestibular nuclei, causing disinhibition of the pontine reticular formation and vestibular nuclei, which primarily excite extensor muscles. *Reticulo spinal tract is also involved* - The **reticulospinal tracts** (both pontine and medullary) play a crucial role in regulating muscle tone and posture. - In decerebrate rigidity, the **pontine reticulospinal tract** is overactive due to loss of cortical inhibition, leading to **increased extensor tone**.