What is the caloric requirement for an adult male engaged in heavy physical work?
What is the SI unit of luminous intensity?
What is the most common mechanism responsible for causing arrhythmias in the heart?
Miracle fruit is used to change the taste from?
Testes are not palpable in
Osteoclasts have all of the following functions except -
The role of human placental lactogen is :
Antimullerian hormone is secreted by ?
What is the primary change in fetal circulation that occurs at birth?
Locking of the knee involves which of the following?
NEET-PG 2015 - Physiology NEET-PG Practice Questions and MCQs
Question 101: What is the caloric requirement for an adult male engaged in heavy physical work?
- A. 3500 kcal/d (Correct Answer)
- B. 2000 kcal/d
- C. 2500 kcal/d
- D. 3000 kcal/d
Explanation: ***3500 kcal/d*** - Adult males engaged in **heavy physical work** have significantly higher energy demands due to increased **metabolic expenditure**. - This level of caloric intake is necessary to support physical activity, maintain muscle mass, and prevent weight loss in individuals with demanding occupations. *2000 kcal/d* - This caloric intake is typically recommended for adult females who are **sedentary** or for adult males engaging in light activity, which is insufficient for heavy physical work. - It would likely lead to a **caloric deficit** and weight loss for an individual performing heavy labor. *2500 kcal/d* - This level of intake is more appropriate for moderately active adult males, but it would often be **insufficient** for those performing heavy physical work. - Individuals engaged in heavy labor require additional energy to fuel their intense activities to maintain **energy balance**. *3000 kcal/d* - While a higher intake, 3000 kcal/d might still be **borderline** or insufficient for an adult male engaged in very heavy or sustained physical work. - This value might be appropriate for moderately heavy work, but heavy work often necessitates an even higher **caloric intake** to meet energy demands.
Question 102: What is the SI unit of luminous intensity?
- A. Candela (Correct Answer)
- B. Lumen
- C. Lux
- D. Coulomb
Explanation: ***Candela*** - The **candela (cd)** is the **SI base unit** used to measure **luminous intensity**. - **Luminous intensity** quantifies the power emitted by a light source in a particular direction per unit solid angle. *Lumen* - The **lumen (lm)** is the **SI derived unit** for **luminous flux**, which measures the total perceived power of light. - It describes the total amount of visible light emitted by a source in all directions, not its intensity in a specific direction. *Lux* - The **lux (lx)** is the **SI derived unit** for **illuminance**, which measures how much luminous flux is spread over a given area. - It indicates the perceived brightness of a surface, rather than the intensity of the light source itself. *Coulomb* - The **coulomb (C)** is the **SI derived unit** for **electric charge**. - It is completely unrelated to light or luminous intensity.
Question 103: What is the most common mechanism responsible for causing arrhythmias in the heart?
- A. Re-entry (Correct Answer)
- B. Early after depolarization
- C. Late after depolarization
- D. Automaticity
Explanation: ***Re-entry*** - **Re-entry** is the most common mechanism for arrhythmias and involves a re-excitation of cardiac tissue due to a circulating electrical impulse. - This requires at least two pathways with differing conduction velocities and refractory periods, creating a path for the impulse to re-excite an area after its normal refractory period has ended. *Early after depolarization* - **Early afterdepolarizations (EADs)** occur during phase 2 or 3 of the action potential when repolarization is incomplete, often due to prolonged action potential duration. - They are typically associated with conditions like **long QT syndrome** and can trigger polymorphic ventricular tachycardia, but are less common than re-entry. *Late after depolarization* - **Late afterdepolarizations (DADs)** occur during phase 4 of the action potential, after repolarization is complete, due to excessive intracellular calcium. - They are often seen in conditions like **digoxin toxicity** or **catecholaminergic polymorphic ventricular tachycardia**, but are not the most prevalent mechanism. *Automaticity* - **Abnormal automaticity** refers to pacemaker activity arising in non-pacemaker cells or an acceleration of normal pacemaker activity. - While it can cause arrhythmias such as accelerated idioventricular rhythm, re-entry is far more frequently implicated in the etiology of clinical arrhythmias.
Question 104: Miracle fruit is used to change the taste from?
- A. Sour to Bitter
- B. Sour to Sweet (Correct Answer)
- C. Bitter to Sweet
- D. Salty to Sweet
Explanation: ***Sour to Sweet*** - The **miracle fruit** (Synsepalum dulcificum) contains a glycoprotein called **miraculin**. - Miraculin binds to taste receptors on the tongue and modifies their perception, making **sour foods taste sweet**. *Sour to Bitter* - The primary effect of miracle fruit is to convert **sour tastes into sweet tastes**, not bitter ones. - No known natural compound consistently changes sour perception to bitter. *Bitter to Sweet* - While miraculin makes sour foods sweet, it does not typically convert **bitter tastes into sweet sensations**. - Bitter taste perception involves different receptor pathways that are not significantly altered by miraculin. *Salty to Sweet* - Miracle fruit primarily targets **sour taste receptors**. - It does not have a significant effect on altering the perception of **salty tastes to sweet**.
Question 105: 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 106: Osteoclasts have all of the following functions except -
- A. Receptor for parathormone (Correct Answer)
- B. Ruffled border
- C. Bone resorption
- D. RANK ligand production
Explanation: ***Receptor for parathormone*** - **Osteoclasts** do not directly have receptors for **parathormone (PTH)**; instead, **osteoblasts** have PTH receptors. - When PTH binds to osteoblasts, they release factors (like **RANKL**) that stimulate osteoclast activity, thus indirectly regulating bone resorption. *Bone resorption* - **Osteoclasts** are specialized cells primarily responsible for **resorbing bone matrix**, a critical process in bone remodeling. - They secrete **acids and enzymes** to break down the mineral and organic components of bone. *Ruffled border* - The **ruffled border** is a characteristic morphological feature of active osteoclasts, representing a highly folded plasma membrane. - This specialized structure increases the surface area for the secretion of **protons and lysosomal enzymes** into the bone-resorbing compartment. *RANK ligand production* - **Osteoclasts** do not produce **RANK ligand (RANKL)**; rather, they have **RANK receptors** that bind to RANKL produced by **osteoblasts and stromal cells**. - The binding of RANKL to RANK is essential for the **differentiation, activation, and survival** of osteoclasts.
Question 107: The role of human placental lactogen is :
- A. Stimulate milk production
- B. Promotes growth of breast for lactation.
- C. Supports fetal growth and development. (Correct Answer)
- D. Provide fetal nutrition by antagonizing the action of insulin in maternal circulation, breakdown of fats and proteins and transport of fatty acids and amino acids from maternal to fetal circulation.
Explanation: ***Supports fetal growth and development.*** - Human placental lactogen (hPL) acts as a **growth hormone** for the fetus, primarily by altering maternal metabolism to favor fetal nutrient supply. - It increases **maternal insulin resistance**, leading to higher maternal glucose and free fatty acids, which are then shunted to the fetus, supporting its growth and development. *Stimulate milk production* - **Prolactin**, secreted by the anterior pituitary, is the primary hormone responsible for stimulating milk production (lactogenesis). - While hPL has some structural similarity to growth hormone and prolactin, its primary role is not to directly stimulate milk production during pregnancy; rather, it prepares the breasts. *Promotes growth of breast for lactation.* - hPL, along with **estrogen** and **progesterone**, contributes to the **mammary gland development** during pregnancy, preparing the breasts for lactation. - However, its direct role is more about **mammary gland proliferation and differentiation** rather than initiation of milk production. *Provide fetal nutrition by antagonizing the action of insulin in maternal circulation, breakdown of fats and proteins and transport of fatty acids and amino acids from maternal to fetal circulation.* - This is a highly detailed and largely accurate description of *how* hPL supports fetal growth and development, making it a mechanism rather than the primary, concise role. - It describes the metabolic changes induced by hPL, which ultimately lead to the **support of fetal growth and development**.
Question 108: 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 109: 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 110: Locking of the knee involves which of the following?
- A. Internal rotation of the tibia with the foot on the ground
- B. Contraction of the popliteus muscle
- C. Internal rotation of the femur with the foot on the ground (Correct Answer)
- D. External rotation of femur with the foot off the ground
Explanation: ***Internal rotation of the femur with the foot on the ground*** - When the foot is on the ground (closed kinematic chain), the **femur rotates internally on the tibia** during the end stages of knee extension. This creates a more stable, "locked" position of the knee. - This **terminal rotation of the femur** increases the contact area and tension in the cruciate ligaments, enhancing joint stability for weight-bearing. *Internal rotation of the tibia with the foot on the ground* - This describes the action of the **popliteus muscle** when "unlocking" the knee from full extension, not the locking mechanism itself. - With the foot on the ground, the tibia is fixed, and internal rotation would typically be a movement for unlocking, not locking. *Contraction of the popliteus muscle* - The **popliteus muscle** is primarily responsible for **unlocking the knee** from full extension, by causing internal rotation of the tibia (or external rotation of the femur). - Its contraction would lead to initial flexion of the knee, releasing the locked position, not establishing it. *External rotation of femur with the foot off the ground* - With the foot off the ground (open kinematic chain), **external rotation of the tibia** occurs during the final degrees of extension to lock the knee, not external rotation of the femur. - The locking mechanism requires specific relative rotation between femur and tibia; external rotation of the femur alone would not achieve the screw-home mechanism necessary for knee locking.