Which tract is responsible for the loss of proprioception and fine touch?
Which of the following statements is true regarding the function of the spinocerebellar tract?
What happens to the concentration of inulin as fluid passes through the Proximal Convoluted Tubule (PCT)?
Gastric secretions are essential for absorption of -
Nonshivering thermogenesis in adults is due to:
Which of the following hormones does not mediate its action through cAMP?
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?
Salty taste is due to?
NEET-PG 2012 - Physiology NEET-PG Practice Questions and MCQs
Question 21: Which tract is responsible for the loss of proprioception and fine touch?
- A. Anterior spinothalamic tract
- B. Lateral spinothalamic tract
- C. Dorsal column (Correct Answer)
- D. Corticospinal tract
Explanation: ***Dorsal column*** - The **dorsal column-medial lemniscus pathway** is responsible for transmitting **fine touch**, **vibration**, and **proprioception** from the body to the cerebral cortex. - Damage to this tract (e.g., in **tabes dorsalis** or **vitamin B12 deficiency**) leads to a loss of these sensations. *Anterior spinothalamic tract* - This tract primarily conveys crude touch and pressure sensations. - While it carries tactile information, it does not transmit the fine discriminative touch or proprioception associated with the dorsal columns. *Lateral spinothalamic tract* - This pathway is responsible for transmitting **pain** and **temperature** sensations. - It does not play a role in proprioception or fine touch. *Corticospinal tract* - The **corticospinal tract** is a **motor pathway** responsible for voluntary movement. - It has no role in transmitting sensory information such as proprioception or fine touch.
Question 22: Which of the following statements is true regarding the function of the spinocerebellar tract?
- A. Smoothens and coordinates movements (Correct Answer)
- B. Involved in planning and programming motor activities
- C. Involved in maintaining equilibrium
- D. Facilitates learning through vestibulo-ocular reflex changes
Explanation: ***Smoothens and coordinates movements*** - The spinocerebellar tract provides the cerebellum with **unconscious proprioceptive information** from muscle spindles and Golgi tendon organs. - This information allows the cerebellum to compare intended movements with actual movements, thereby **smoothing and coordinating voluntary motor activity**. *Involved in planning and programming motor activities* - This function is primarily attributed to the **cerebral cortex** (e.g., premotor and supplementary motor areas) and the **basal ganglia**. - While the cerebellum is involved in motor learning and fine-tuning, the initial **planning and programming** of complex movements are cortical functions. *Involved in maintaining equilibrium* - Maintaining equilibrium and balance is primarily a function of the **vestibulocerebellum** (flocculonodular lobe), which receives input from the vestibular system. - While the spinocerebellum indirectly influences balance by coordinating limb movements, its direct role is less pronounced than that of the vestibulocerebellum. *Facilitates learning through vestibulo-ocular reflex changes* - This function is specific to the **vestibulocerebellum** and is crucial for adapting the vestibulo-ocular reflex (VOR) to maintain visual stability during head movements. - The spinocerebellar tract's primary role is proprioception for limb coordination, not VOR adaptation.
Question 23: What happens to the concentration of inulin as fluid passes through the Proximal Convoluted Tubule (PCT)?
- A. Concentration of inulin increases (Correct Answer)
- B. Concentration of urea remains constant
- C. Concentration of HCO3- increases
- D. Concentration of Na+ decreases
Explanation: ***Concentration of inulin increases*** - Inulin is **freely filtered** at the glomerulus and is neither reabsorbed nor secreted along the renal tubule, making it an excellent marker for **glomerular filtration rate (GFR)**. - As water is reabsorbed from the PCT, the volume of tubular fluid decreases, causing the concentration of **unreabsorbed solutes**, like inulin, to increase. *Concentration of urea remains constant* - Urea is **reabsorbed** along the tubule, though passively; its concentration typically **increases** initially in the PCT due to water reabsorption, but then decreases as some is reabsorbed. - The statement is incorrect because urea concentration changes significantly throughout the nephron, particularly increasing as water is reabsorbed and then decreasing with some reabsorption. *Concentration of HCO3- increases* - The majority (approximately 80-90%) of **bicarbonate (HCO3-)** is reabsorbed in the PCT, primarily through its conversion to CO2 within the tubular lumen and then back to HCO3- intracellularly. - Therefore, the concentration of HCO3- in the tubular fluid actually **decreases** significantly as fluid passes through the PCT. *Concentration of Na+ decreases* - **Sodium (Na+)** is actively reabsorbed along the entire nephron, with about 65-70% reabsorbed in the PCT. - While Na+ is reabsorbed, water follows passively, so its concentration in the tubular fluid remains relatively **iso-osmotic** with plasma, meaning its concentration does not significantly decrease as fluid passes through the PCT, remaining fairly constant.
Question 24: Gastric secretions are essential for absorption of -
- A. Cobalamin (Correct Answer)
- B. Fat
- C. Thiamine
- D. Folic acid
Explanation: ***Cobalamin*** - **Intrinsic factor**, secreted by gastric parietal cells, is crucial for the absorption of **vitamin B12 (cobalamin)** in the terminal ileum [1]. - Without sufficient intrinsic factor, **pernicious anemia** can develop due to impaired B12 absorption [2]. *Fat* - Fat digestion primarily occurs in the **small intestine** with the help of **bile salts** and **pancreatic lipases**. - While gastric lipase begins some fat digestion, it's not essential for overall fat absorption. *Thiamine* - **Thiamine (vitamin B1)** is absorbed in the jejunum and ileum, primarily via **active transport** and passive diffusion. - Gastric secretions do not play a direct, essential role in its absorption. *Folic acid* - **Folic acid** is absorbed in the **duodenum and jejunum** as monoglutamates after being deconjugated from polyglutamate forms. - This process is not directly dependent on gastric secretions [2].
Question 25: 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 26: Which of the following hormones does not mediate its action through cAMP?
- A. Glucagon
- B. Follicle stimulating hormone
- C. Estrogen (Correct Answer)
- D. Luteinizing hormone
Explanation: ***Estrogen*** - **Estrogen** is a **steroid hormone** that mediates its action by binding to intracellular receptors, forming a complex that directly influences gene transcription. - Steroid hormones, due to their **lipophilicity**, can cross the cell membrane and do not typically rely on cell surface receptors or second messengers like cAMP. *Glucagon* - **Glucagon** acts on a **G protein-coupled receptor (GPCR)**, specifically a Gs-coupled receptor, leading to the activation of adenylyl cyclase. - This activation increases the intracellular concentration of **cAMP**, which then activates protein kinase A to mediate its effects, primarily on glucose metabolism. *Follicle stimulating hormone* - **FSH** binds to a **GPCR** on target cells, activating the Gs protein pathway. - This activation stimulates **adenylyl cyclase** and increases intracellular **cAMP** levels, which are critical for its role in gamete development. *Luteinizing hormone* - **LH**, like FSH, binds to a cell surface **GPCR** that activates the Gs protein. - This leads to the stimulation of **adenylyl cyclase** and an increase in **cAMP**, mediating its effects on steroidogenesis and ovulation.
Question 27: 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 28: 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 29: 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 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.