What is the fixed length of a myosin filament?
Which of the following statements about lung compliance is NOT true?
What is the normal range of interstitial pressure?
ANP acts at which site?
Which of the following is most important in sodium and water retention ?
What is the effect of acetylcholine on the Lower Esophageal Sphincter (LES)?
Diurnal variation of ACTH depends on ?
Nonshivering thermogenesis in adults is due to:
Which of the following is NOT a location where multi-unit smooth muscle is present?
Salty taste is due to?
NEET-PG 2012 - Physiology NEET-PG Practice Questions and MCQs
Question 21: What is the fixed length of a myosin filament?
- A. 0.16 nm
- B. 1.6 micrometers (Correct Answer)
- C. 16 nm
- D. 1.6 mm
Explanation: ***1.6 micrometers*** - Myosin filaments, also known as **thick filaments**, are integral components of muscle contraction and have a characteristic fixed length. This length is precisely **1.6 micrometers** in mammalian skeletal muscle. - This consistent length is crucial for the **sliding filament model** of muscle contraction, ensuring proper overlap with actin filaments and efficient force generation. *0.16 nm* - This value is significantly too small; **nanometers (nm)** are typically used for atomic or molecular distances, not for entire protein filaments like myosin. - A myosin filament is composed of hundreds of myosin molecules, making its overall length much larger than a fraction of a nanometer. *16 nm* - While nanometers are used for molecular structures, 16 nm is still too small for a myosin filament. The entire filament is roughly **100 times larger** than this value. - This dimension might be more appropriate for the diameter of a single myosin molecule's head region, but not the entire filament's length. *1.6 mm* - This value is significantly too large; **millimeters (mm)** are visible to the naked eye and represent macroscopic objects. - Muscle filaments are microscopic structures, and a length of 1.6 mm would imply they are many times longer than an entire muscle cell.
Question 22: Which of the following statements about lung compliance is NOT true?
- A. Measured by intrapleural pressure at different lung volumes. (Correct Answer)
- B. Decreased at the height of inspiration.
- C. Increased in emphysema.
- D. Increased by surfactant.
Explanation: ***Measured by intrapleural pressure at different lung volumes.*** - Lung compliance is measured by the **change in lung volume (ΔV)** divided by the **change in transpulmonary pressure (ΔP)**, which is the difference between alveolar and intrapleural pressure. - While intrapleural pressure is a component of transpulmonary pressure, compliance is not measured solely by intrapleural pressure at different lung volumes. *Increased in emphysema.* - This statement is **true**. Emphysema involves the destruction of **elastic fibers** in the lung tissue. - Loss of elastic recoil leads to an **increase in compliance**, meaning the lungs are easier to distend but collapse more readily. *Decreased at the height of inspiration.* - This statement is **true**. At high lung volumes (height of inspiration), the **elastic limit** of the lung tissue is approached. - The lungs become **stiffer** and less compliant, requiring a greater pressure change for a given volume change. *Increased by surfactant.* - This statement is **true**. Surfactant reduces **surface tension** in the alveoli. - By lowering surface tension, surfactant prevents alveolar collapse and **increases overall lung compliance**, making it easier to inflate the lungs.
Question 23: What is the normal range of interstitial pressure?
- A. -3 to 0 mmHg
- B. -5 to 0 mmHg (Correct Answer)
- C. 0 to 5 mmHg
- D. 5 to 10 mmHg
Explanation: ***-5 to 0 mmHg*** - The interstitial fluid is normally under a **slight negative pressure**, typically ranging from **-5 to 0 mmHg** - This negative pressure helps pull fluid from the capillaries into the interstitial space and facilitates **lymphatic drainage** - Maintained by continuous drainage of fluid and proteins by the **lymphatic system** - This range is the commonly accepted value in standard physiology references for Indian medical exams *-3 to 0 mmHg* - While this range acknowledges the typically **negative nature** of interstitial pressure, it represents a slightly narrower range - Some sources cite this as the average range, but **-5 to 0 mmHg** is the more commonly accepted standard range - Not the most precise or widely cited range for exam purposes *0 to 5 mmHg* - This range suggests a **positive interstitial pressure**, which is generally **abnormal** - Indicates **edema formation** due to excess fluid accumulation in the interstitial space - Positive pressure impairs fluid reabsorption and lymphatic drainage - Represents pathological fluid dynamics *5 to 10 mmHg* - Represents significant **positive interstitial pressure** leading to severe **interstitial edema** - Markedly impairs tissue function and fluid exchange - Indicates pathological conditions where capillary filtration far exceeds lymphatic drainage capacity - Associated with severe edematous states
Question 24: ANP acts at which site?
- A. Glomerulus
- B. Loop of Henle
- C. PCT
- D. Collecting duct (Correct Answer)
Explanation: ***Collecting duct*** - Atrial Natriuretic Peptide (**ANP**) exerts its primary effect on the **collecting duct** by inhibiting sodium reabsorption, leading to increased sodium and water excretion (natriuresis and diuresis). - This action helps to reduce blood volume and blood pressure in conditions like **hypervolemia**. *Glomerulus* - While ANP does cause **afferent arteriolar dilation** and **efferent arteriolar constriction**, increasing **glomerular filtration rate** (GFR), its direct tubular action is most prominent in the collecting duct. - The primary function of the glomerulus is **filtration**, influenced by many factors including pressure, but it is not the main site of ANP's direct tubular reabsorptive effects. *Loop of Henle* - The loop of Henle is responsible for establishing the **medullary osmotic gradient** and reabsorbing a significant amount of sodium and water. - ANP has minor effects on the loop of Henle, but its most impactful reabsorptive modulation occurs downstream in the collecting duct. *PCT* - The **proximal convoluted tubule (PCT)** is where the bulk of reabsorption of filtered substances (e.g., glucose, amino acids, most sodium and water) occurs. - ANP has very little direct influence on the reabsorptive processes of the PCT.
Question 25: Which of the following is most important in sodium and water retention ?
- A. Renin angiotensin system (Correct Answer)
- B. ANP
- C. BNP
- D. Vasopressin
Explanation: ***Renin angiotensin system*** - The **renin-angiotensin-aldosterone system (RAAS)** is the most important mechanism for **both sodium AND water retention**, which is what the question specifically asks about. - **Aldosterone** directly promotes **sodium reabsorption** in the principal cells of the collecting duct by increasing apical ENaC channels and basolateral Na-K-ATPase pumps. - **Angiotensin II** stimulates sodium reabsorption in the proximal tubule and also stimulates ADH release, contributing to water retention. - When sodium is retained, **water follows passively** due to the osmotic gradient, resulting in effective volume expansion. - RAAS is the primary system activated in states of volume depletion and is most important for combined sodium and water retention. *Vasopressin* - **Vasopressin (ADH)** primarily controls **water retention only** by increasing aquaporin-2 channels in the collecting duct. - While crucial for water balance, it has minimal direct effect on sodium reabsorption. - It causes retention of **free water**, which can actually dilute plasma sodium concentration. - ADH is the answer if the question asked about water retention alone, but not for combined sodium and water retention. *ANP* - **Atrial natriuretic peptide (ANP)** promotes **sodium and water excretion** (natriuresis and diuresis). - Released in response to atrial stretch from volume expansion. - Acts to *oppose* retention mechanisms, making it incorrect for this question. *BNP* - **Brain natriuretic peptide (BNP)** similarly promotes **natriuresis and diuresis**. - Released from ventricular myocytes in response to volume overload. - Like ANP, it acts to *excrete* sodium and water, not retain them.
Question 26: What is the effect of acetylcholine on the Lower Esophageal Sphincter (LES)?
- A. Causes contraction (Correct Answer)
- B. Causes relaxation
- C. No effect on LES
- D. Contraction followed by relaxation
Explanation: ***Correct Option: Causes contraction*** - Acetylcholine acts on **M3 muscarinic receptors** on LES smooth muscle cells to cause **contraction** - This is part of the **excitatory cholinergic pathway** that maintains LES tone and prevents gastroesophageal reflux - Acetylcholine is released from **excitatory motor neurons** in the myenteric plexus *Incorrect: Causes relaxation* - LES relaxation during swallowing is mediated by **nitric oxide (NO)** and **vasoactive intestinal peptide (VIP)**, NOT acetylcholine - These inhibitory neurotransmitters are released from separate **inhibitory motor neurons** - The relaxation response during swallowing is due to activation of the inhibitory pathway, which suppresses cholinergic tone *Incorrect: No effect on LES* - Acetylcholine has a significant effect on the LES - It is one of the key neurotransmitters maintaining basal LES tone - Loss of cholinergic input can lead to decreased LES pressure *Incorrect: Contraction followed by relaxation* - Acetylcholine itself causes only contraction - The swallowing reflex involves coordinated activation of inhibitory (NO/VIP) and suppression of excitatory (acetylcholine) pathways - The sequence of events is neural, not a biphasic response to acetylcholine alone
Question 27: Diurnal variation of ACTH depends on ?
- A. Suprachiasmatic nucleus (Correct Answer)
- B. Supraoptic nucleus
- C. Ventrolateral nucleus
- D. Thalamus
Explanation: ***Suprachiasmatic nucleus*** - The **suprachiasmatic nucleus (SCN)** acts as the body's **master circadian clock**, synchronizing various physiological rhythms, including the **diurnal variation of ACTH** secretion. - It receives light input from the **retina** and projects to other brain regions to regulate the timing of hormone release. *Supraoptic nucleus* - The **supraoptic nucleus (SON)** is primarily involved in the production of **vasopressin (ADH)** and **oxytocin**, which are released by the posterior pituitary. - It does not directly control the diurnal rhythm of ACTH. *Ventrolateral nucleus* - The **ventrolateral preoptic area (VLPO)** is a key region for **sleep regulation**, promoting sleep by inhibiting wake-promoting neurotransmitters. - While it contributes to sleep-wake cycles, it is not the primary regulator of ACTH's diurnal variation. *Thalamus* - The **thalamus** is a major relay center for sensory information and plays a role in consciousness, sleep, and alertness. - It does not directly control the **circadian rhythm of ACTH secretion**.
Question 28: Nonshivering thermogenesis in adults is due to:
- A. Muscle metabolism
- B. Thyroid hormone
- C. Noradrenaline
- D. Brown fat between the shoulders (Correct Answer)
Explanation: ***Brown fat between the shoulders*** - In adults, the primary **effector tissue** for **non-shivering thermogenesis** is **brown adipose tissue (BAT)**, with major depots located between the shoulders, around the neck, and along the spine. - **BAT** contains specialized mitochondria with **uncoupling protein 1 (UCP1)** that uncouples oxidative phosphorylation, generating heat instead of ATP. - This is the tissue where non-shivering thermogenesis actually occurs, making it the direct answer to what non-shivering thermogenesis is "due to." *Noradrenaline* - **Noradrenaline** is the key neurotransmitter that **activates brown fat** via **β3-adrenergic receptors** to initiate non-shivering thermogenesis. - While noradrenaline is the **trigger/stimulus**, the actual heat production occurs in brown adipose tissue. - Noradrenaline itself does not produce heat directly; it acts as the signal that activates the thermogenic machinery in BAT. *Thyroid hormone* - **Thyroid hormone** increases **basal metabolic rate** and can potentiate the thermogenic response by upregulating UCP1 expression in brown fat. - Its role is **permissive and long-term** rather than being the immediate effector of acute non-shivering thermogenesis. - It modulates overall cellular metabolism but is not the primary mechanism for rapid heat generation in cold exposure. *Muscle metabolism* - **Muscle contraction** during shivering generates heat through increased ATP hydrolysis, which is **shivering thermogenesis**. - **Non-shivering thermogenesis** specifically refers to heat production **without muscle contraction**, making muscle metabolism the mechanism for shivering, not non-shivering, thermogenesis.
Question 29: Which of the following is NOT a location where multi-unit smooth muscle is present?
- A. Blood vessels
- B. Iris
- C. Gut (Correct Answer)
- D. Ciliary muscle
Explanation: ***Gut*** - The gut primarily contains **unitary (single-unit) smooth muscle**, characterized by cells connected by **gap junctions** that allow for synchronized contractions (e.g., peristalsis). - This type of smooth muscle exhibits **spontaneous rhythmic contractions** due to pacemaker cells, and its activity is modulated by neural and hormonal inputs rather than requiring individual innervation of each cell. - Multi-unit smooth muscle is **NOT present** in the gut. *Blood vessels* - Many larger blood vessels (e.g., large arteries) contain **multi-unit smooth muscle**, which allows for **fine, graded control** over vascular tone and blood flow. - Each muscle cell is typically **innervated individually**, enabling precise regulation of contraction strength. *Iris* - The iris contains **multi-unit smooth muscle** (e.g., sphincter pupillae and dilator pupillae muscles) which control pupil size. - These muscles require **individual innervation** to allow for very fine and precise movements in response to light intensity changes. *Ciliary muscle* - The ciliary muscle of the eye contains **multi-unit smooth muscle**, which controls the shape of the lens for accommodation (focusing). - These muscle fibers are **individually innervated** to allow precise control of lens curvature for near and far vision.
Question 30: Salty taste is due to?
- A. Sodium ion channels (Correct Answer)
- B. Calcium ion channels
- C. G-protein coupled receptors
- D. Proton channels
Explanation: ***Sodium ion channels*** - The sensation of **salty taste** is primarily mediated by the direct influx of **sodium ions (Na+)** into taste receptor cells. - This influx leads to **depolarization** of the cell membrane, triggering neurotransmitter release and signaling to the brain. *Calcium ion channels* - While calcium ions are crucial for various cellular processes, including **neurotransmitter release**, they are not the primary initiators of the salty taste transduction pathway. - Calcium channels are more directly involved in the sensation of **umami** and **sweet tastes**, often via G-protein coupled receptors. *G-protein coupled receptors* - **G-protein coupled receptors (GPCRs)** are responsible for the transduction of **sweet, bitter, and umami tastes**. - They are not involved in the direct detection of **saline compounds**, which operate through ion channels. *Proton channels* - **Proton channels (H+)** are primarily involved in the sensation of **sour taste**. - The influx of protons causes intracellular acidification, leading to cell depolarization.