What is the SI unit of luminous intensity?
What is the intensity in decibel of normal conversation in humans?
Miracle fruit is used to change the taste from?
What is the most common mechanism responsible for causing arrhythmias in the heart?
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?
Cardiac output in pregnancy shows significant increase from which week of gestation
Oxygen consumption increases in pregnancy by
Testes are not palpable in
Osteoclasts have all of the following functions except -
NEET-PG 2015 - Physiology NEET-PG Practice Questions and MCQs
Question 101: 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 102: What is the intensity in decibel of normal conversation in humans?
- A. 30dB
- B. 60dB (Correct Answer)
- C. 90dB
- D. 150dB
Explanation: ***60dB*** - The sound intensity of **normal human conversation** is typically around **60 decibels (dB)**. - This level is considered **moderate** and is comfortably audible without causing discomfort or hearing damage. *30dB* - A sound intensity of **30dB** is characteristic of a **quiet whisper** or a **soft rustle of leaves**. - This level is much **quieter** than a normal conversation and would require closer proximity to be clearly heard. *90dB* - **90dB** represents a significantly **louder sound**, comparable to that of a **lawnmower** or a **heavy truck** passing by. - Prolonged exposure to sounds at this intensity can start to cause **hearing damage**. *150dB* - **150dB** is an **extremely loud** and potentially **painful** sound level, similar to a **jet engine at takeoff** or a **firecracker** exploding nearby. - Exposure to sounds this intense can cause **immediate and permanent hearing loss**.
Question 103: 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 104: 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 105: 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 106: 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.
Question 107: Cardiac output in pregnancy shows significant increase from which week of gestation
- A. 25 weeks
- B. 35 weeks
- C. 5 weeks
- D. 15 weeks (Correct Answer)
Explanation: ***15 weeks*** - Cardiac output shows a **significant and clinically measurable increase around 10-15 weeks of gestation**, which continues to rise, peaking between **20-28 weeks**. - This rise is primarily due to an increase in both **stroke volume** (increased by 25-30%) and **heart rate** (increased by 10-15 bpm) to meet the metabolic demands of the growing fetus and placenta. - By 15 weeks, cardiac output has typically increased by approximately **20-30% above pre-pregnancy levels**. *5 weeks* - While cardiac output does begin to rise very early in pregnancy (as early as 5-8 weeks), the increase at this stage is **subtle and not yet significant**. - At 5 weeks, the **placental circulation is still in early development**, and the hemodynamic changes are just beginning. - The question asks about **significant increase**, which is not yet established at 5 weeks. *25 weeks* - By 25 weeks, cardiac output has already completed its major rise and is at or near its **peak levels** (40-50% above baseline). - The **significant increase had already occurred** much earlier, around 10-15 weeks. - This timing represents the plateau phase rather than the initial significant increase. *35 weeks* - At 35 weeks, cardiac output remains elevated at near-peak levels but the **major increase happened much earlier** in pregnancy. - By this gestational age, the cardiovascular system has been adapted for months. - There may be minor positional variations (e.g., aortocaval compression in supine position) but no new significant increase occurs.
Question 108: Oxygen consumption increases in pregnancy by
- A. 10%
- B. 20% (Correct Answer)
- C. 30%
- D. 40%
Explanation: ***20%*** - During **pregnancy**, the maternal **metabolic rate increases** to support fetal growth and the physiological changes occurring in the mother's body. - This increased metabolic demand leads to a **rise in oxygen consumption** by approximately 20% compared to the non-pregnant state. *10%* - A 10% increase is an **underestimation** of the physiological change in oxygen consumption during pregnancy. - The demands of supporting a growing fetus and increased maternal tissue mass require a more substantial metabolic adjustment. *30%* - While oxygen consumption does increase significantly, a 30% rise is generally considered an **overestimation** of the average increase. - The typical physiological adaptation usually falls within the 15-25% range. *40%* - A 40% increase in oxygen consumption would represent an **extreme physiological demand** that is not typically observed during an uncomplicated pregnancy. - Such a drastic increase might indicate underlying pathology rather than normal adaptation.
Question 109: 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 110: 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.