What is the most common mechanism responsible for causing arrhythmias in the heart?
Miracle fruit is used to change the taste from?
What is the average survival time of a person without food and water under normal conditions?
What is the caloric requirement for an adult male engaged in heavy physical work?
The role of human placental lactogen is :
Antimullerian hormone is secreted by ?
Testes are not palpable in
Osteoclasts have all of the following functions except -
Locking of the knee involves which of the following?
During pregnancy, the increased size of the pituitary gland is primarily due to the enlargement of which hormone-secreting cells?
NEET-PG 2015 - Physiology NEET-PG Practice Questions and MCQs
Question 101: 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 102: 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 103: What is the average survival time of a person without food and water under normal conditions?
- A. 10 to 12 days
- B. 3 to 5 days (Correct Answer)
- C. 1 to 3 days
- D. 5 to 10 days
Explanation: ***3 to 5 days*** - When deprived of **both food and water**, the human body can typically survive for **3 to 5 days** under normal conditions. - **Water is the critical limiting factor** - while the body can tolerate food deprivation for weeks, lack of water becomes life-threatening within days. - Water is essential for cellular metabolism, temperature regulation, waste elimination, and cardiovascular function. *1 to 3 days* - This represents the **absolute minimum survival time** without water, particularly under harsh environmental conditions (heat, physical exertion, humidity). - However, under normal/average conditions, most individuals can survive slightly longer than this range. *10 to 12 days* - This duration is **not possible** without water, even with optimal conditions. - This timeframe is more consistent with survival **without food but WITH water**, which can extend to 3-4 weeks or more. *5 to 10 days* - While exceptional cases might approach 5-7 days without water in cool, resting conditions with low metabolic demands, **10 days is physiologically implausible**. - Severe dehydration typically causes death by day 5-7 maximum, with most succumbing earlier.
Question 104: 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 105: 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 106: 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 107: 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 108: 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 109: 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.
Question 110: During pregnancy, the increased size of the pituitary gland is primarily due to the enlargement of which hormone-secreting cells?
- A. Growth hormone
- B. Prolactin (Correct Answer)
- C. ACTH
- D. TSH
Explanation: ***Prolactin*** - During pregnancy, the number and size of **lactotrophs**, the cells that secrete prolactin, increase significantly due to high **estrogen** levels. - This **hyperplasia** and **hypertrophy** of lactotrophs contribute to the overall enlargement of the pituitary gland, preparing it for lactation. *Growth hormone* - While growth hormone is important, there isn't a primary enlargement of **somatotrophs** (GH-secreting cells) in the pituitary during pregnancy. - Furthermore, most circulating GH during pregnancy is **placental growth hormone**, rather than pituitary-derived. *ACTH* - Adrenocorticotropic hormone (ACTH) is secreted by **corticotrophs**, and these cells do not undergo prominent hypertrophy or hyperplasia during normal pregnancy. - While cortisol levels increase, this is largely due to factors other than increased pituitary ACTH cell size. *TSH* - Thyroid-stimulating hormone (TSH) is secreted by **thyrotrophs**, which do not notably enlarge during pregnancy. - Thyroid gland activity increases during pregnancy, but this is mediated by **hCG** and other mechanisms, not pituitary thyrotroph growth.