Cellular Physiology Indian Medical PG Practice Questions and MCQs
Practice Indian Medical PG questions for Cellular Physiology. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Cellular Physiology Indian Medical PG Question 1: Reducing equivalents produced in glycolysis are transported from cytosol to mitochondria by ?
- A. Carnitine
- B. Creatine
- C. Malate-aspartate shuttle (Correct Answer)
- D. Glutamate shuttle
Cellular Physiology Explanation: ***Malate shuttle***
- The **malate-aspartate shuttle** is a primary mechanism for transporting **NADH reducing equivalents** from the cytosol to the mitochondrial matrix for **oxidative phosphorylation**.
- It involves a series of **enzymes and transporters** that indirectly move electrons from NADH by converting **oxaloacetate to malate** in the cytosol, which then enters the mitochondria.
*Carnitine*
- **Carnitine** is primarily involved in the transport of **long-chain fatty acids** into the mitochondrial matrix for **beta-oxidation**.
- It is not directly involved in the shuttle of NADH reducing equivalents generated during glycolysis.
*Creatine*
- **Creatine** and its phosphorylated form, **phosphocreatine**, are crucial for **energy buffering and transport** in tissues with high and fluctuating energy demands, like muscle and brain.
- The creatine-phosphocreatine shuttle facilitates the rapid regeneration of ATP, but it is not involved in transporting glycolytic reducing equivalents.
*Glutamate shuttle*
- While glutamate and aspartate are components of the **malate-aspartate shuttle**, there isn't a standalone "glutamate shuttle" for transporting glycolytic reducing equivalents.
- The **glutamate-aspartate transaminase** is an enzyme within the malate-aspartate shuttle, converting oxaloacetate to aspartate and alpha-ketoglutarate to glutamate from the matrix to the cytosol.
Cellular Physiology Indian Medical PG Question 2: Which one of the following conditions is caused by mutations in the gene that encodes the sodium-potassium-2-chloride cotransporter (NKCC2), and presents with sodium wasting, hypokalaemia, hypomagnesaemia and hypercalciuria?
- A. Bartter syndrome (Correct Answer)
- B. Fanconi syndrome
- C. Gitelman syndrome
- D. Alport syndrome
Cellular Physiology Explanation: ***Bartter syndrome***
- This syndrome is characterized by **loss-of-function mutations** in the **NKCC2 cotransporter** in the thick ascending limb of the loop of Henle, leading to impaired sodium and chloride reabsorption.
- The resulting electrolyte imbalances include **sodium wasting**, **hypokalemia**, **hypomagnesemia**, and **hypercalciuria**.
*Fanconi syndrome*
- This syndrome involves a generalized defect in the **proximal renal tubules**, leading to impaired reabsorption of multiple substances including glucose, amino acids, phosphate, and bicarbonate.
- It does not specifically involve a mutation in the NKCC2 cotransporter or present with the described electrolyte profile.
*Gitelman syndrome*
- This condition is caused by a mutation in the **thiazide-sensitive Na-Cl cotransporter (NCC)** in the distal convoluted tubule.
- While it shares some features like hypokalemia and hypomagnesemia, it is typically associated with **hypocalciuria**, not hypercalciuria, and a different genetic defect.
*Alport syndrome*
- This is a genetic disorder affecting type IV collagen, primarily impacting the **glomerular basement membrane**, leading to hematuria, proteinuria, and progressive renal failure.
- It is not associated with mutations in electrolyte transporters or the specific electrolyte abnormalities listed in the question.
Cellular Physiology Indian Medical PG Question 3: Which of the following is a late inward sodium channel blocker?
- A. Ranolazine (Correct Answer)
- B. Fasudil
- C. Ivabradine
- D. Trimetazidine
Cellular Physiology Explanation: ***Ranolazine***
- **Ranolazine** selectively inhibits the **late inward sodium current (I_Na)** in cardiac myocytes.
- By reducing this current, it helps to decrease intracellular **sodium and calcium overload**, thereby improving myocardial relaxation and reducing angina and ischemia.
*Ivabradine*
- **Ivabradine** is a selective **funny channel (If) inhibitor** in the sinoatrial node.
- It slows down the heart rate by reducing the rate of diastolic depolarization, primarily used for **chronic stable angina** and **heart failure**.
*Fasudil*
- **Fasudil** is a **rho-kinase inhibitor** used primarily in Japan and China for **cerebral vasospasm** following subarachnoid hemorrhage.
- It works by inhibiting the phosphorylation of myosin light chain, leading to **vasodilation**.
*Trimetazidine*
- **Trimetazidine** is an **anti-ischemic metabolic agent** that inhibits the enzyme 3-ketoacyl-CoA thiolase, shifting cardiac metabolism from fatty acid oxidation to glucose oxidation.
- This improves myocardial glucose utilization, which is more efficient in **ischemic conditions**, thereby reducing angina symptoms.
Cellular Physiology Indian Medical PG Question 4: What is the physiological condition in which the ratio of potassium permeability to sodium permeability (PK/PNa) is maximized?
- A. Depolarization
- B. Action Potential
- C. Resting Membrane Potential
- D. Hyperpolarization (Correct Answer)
Cellular Physiology Explanation: ***Hyperpolarization***
- During **hyperpolarization**, the membrane potential becomes more negative than the **resting membrane potential**, primarily due to the outflow of **potassium (K+)** ions or influx of **chloride (Cl-)** ions.
- This increased K+ efflux or Cl- influx signifies a state where potassium permeability is maximal relative to sodium permeability, making the membrane less excitable.
*Action Potential*
- An **action potential** involves a rapid **depolarization** phase due to a massive influx of **sodium (Na+)** ions, causing the PNa/PK ratio to be high, followed by repolarization where K+ efflux restores the resting potential.
- Therefore, during an action potential, the ratio of PK/PNa is at its lowest during the rising phase when sodium channels are open.
*Depolarization*
- **Depolarization** is characterized by a decrease in the absolute value of the membrane potential, making it less negative or even positive, primarily due to the influx of **sodium (Na+)** ions.
- During depolarization, the permeability to sodium is significantly higher than to potassium, thus the PK/PNa ratio is low.
*Resting Membrane Potential*
- At **resting membrane potential**, potassium permeability is already much higher than sodium permeability due to **leak potassium channels**, but it is not maximized to the extent seen during hyperpolarization.
- The resting potential is established by a balance of ion movements, primarily K+ efflux and limited Na+ influx, maintained by the **Na+/K+-ATPase pump**.
Cellular Physiology Indian Medical PG Question 5: In large neurons the nucleus can be found a large distance away from the terminal end of its axon. The body has a complex system of intracellular transporters that are able to carry essential proteins from the nucleus to the distal edge of the cell and back. Which of the following proteins are essential for this function?
- A. Kinesin, Troponin
- B. Myosin, Kinesin
- C. Actin, Dynein
- D. Dynein, Kinesin (Correct Answer)
- E. Glucose, Actin
Cellular Physiology Explanation: ***Dynein, Kinesin***
- **Kinesin** is primarily responsible for **anterograde transport** (from the cell body to the axon terminal) along microtubules, carrying vesicles and organelles.
- **Dynein** handles **retrograde transport** (from the axon terminal back to the cell body), essential for recycling components and signaling.
*Kinesin, Troponin*
- While **Kinesin** is involved in axonal transport, **Troponin** is a protein found in muscle tissue that regulates muscle contraction, not intracellular transport in neurons.
- Troponin binds **calcium ions** and influences the interaction between actin and myosin.
*Myosin, Kinesin*
- **Kinesin** is involved in microtubule-based transport, but **Myosin** is primarily associated with **actin filaments** for muscle contraction and intracellular movement, not long-distance axonal transport.
- Myosin functions as a **motor protein** that converts chemical energy in ATP into mechanical force.
*Actin, Dynein*
- **Dynein** is crucial for retrograde axonal transport, but **Actin** is a structural protein forming microfilaments that are involved in cell shape, motility, and some short-distance transport, not the major long-distance axonal transport mechanism.
- Actin filaments serve as tracks for **myosin motors**, primarily in the cell cortex.
*Glucose, Actin*
- **Glucose** is a sugar molecule, the primary energy source for cells, and not a transport protein.
- **Actin** forms microfilaments for cell structure and short-range movement, not long-distance axonal transport as described.
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