General Physiology — MCQs

General Physiology Indian Medical PG Practice Questions and MCQs

Question 351: Increase in cytosolic calcium from intracellular storage, during smooth muscle contraction, is/are due to?

A. CAMP
B. CGMP
C. IP3-DAG
D. Ca channel (Correct Answer)

Explanation: **Explanation:** The contraction of smooth muscle is primarily dependent on the increase in cytosolic calcium levels. While calcium enters from the extracellular fluid via voltage-gated channels, the release from **intracellular storage** (the Sarcoplasmic Reticulum or SR) is the key mechanism highlighted here. **Why Option D is Correct:** The release of calcium from the Sarcoplasmic Reticulum (SR) occurs through specific **Calcium Channels** located on the SR membrane. These are primarily the **Ryanodine Receptors (RyR)** and **IP3-gated Ca²⁺ channels**. When these channels open, calcium moves down its concentration gradient from the SR into the cytosol, triggering the activation of Calmodulin and subsequent phosphorylation of the Myosin Light Chain (MLC). **Why Other Options are Incorrect:** * **A & B (cAMP & cGMP):** These are secondary messengers typically associated with **smooth muscle relaxation**. cAMP (via Protein Kinase A) and cGMP (via Protein Kinase G) act to decrease cytosolic calcium by sequestering it back into the SR or pumping it out of the cell, and by inhibiting Myosin Light Chain Kinase (MLCK). * **C (IP3-DAG):** While IP3 is the *ligand* that binds to the receptor, the actual physical mechanism allowing the calcium to exit the SR is the **IP3-gated Calcium Channel**. In many competitive exams, if "Ca channel" is an option alongside "IP3," the channel is considered the more direct structural cause for the ion flux. **High-Yield NEET-PG Pearls:** * **Calcium-Induced Calcium Release (CICR):** This is a major mechanism in cardiac and some smooth muscles where influx of ECF calcium triggers the RyR channels on the SR. * **Calmodulin:** Smooth muscle lacks Troponin; Calcium binds to Calmodulin to initiate contraction. * **L-type Ca Channels:** These are the primary targets for Calcium Channel Blockers (CCBs) like Nifedipine used in hypertension.

Question 352: Which of the following best describes the trigger for muscle contraction?

A. Calcium binding to tropomyosin
B. Calcium binding to troponin C (Correct Answer)
C. ATP breakdown
D. Calcium binding to troponin I

Explanation: **Explanation:** The initiation of muscle contraction follows the **Sliding Filament Theory**, specifically the process of excitation-contraction coupling. **Why Option B is Correct:** In a resting muscle, the binding sites on actin are covered by the **troponin-tropomyosin complex**, preventing interaction with myosin. When an action potential triggers the release of Calcium ($Ca^{2+}$) from the sarcoplasmic reticulum, the $Ca^{2+}$ ions bind specifically to **Troponin C** (the calcium-binding subunit). This binding induces a conformational change in the entire troponin complex, which pulls the tropomyosin away from the active sites on actin, allowing the myosin head to form a cross-bridge and initiate contraction. **Why Other Options are Incorrect:** * **Option A:** Calcium does not bind directly to tropomyosin; it binds to Troponin C, which then moves the tropomyosin. * **Option C:** ATP breakdown (hydrolysis) provides the energy for the "power stroke" and the detachment of the myosin head, but it is not the initial *trigger* for the contraction process. * **Option D:** Troponin I is the **inhibitory** subunit that binds to actin to prevent contraction; it does not bind calcium. **High-Yield NEET-PG Pearls:** * **Troponin Subunits:** Remember **T-I-C**: **T** (binds to **T**ropomyosin), **I** (**I**nhibits actin-myosin interaction), **C** (binds **C**alcium). * **Cardiac Biomarkers:** Troponin I and T are specific markers for myocardial infarction (Troponin C is not used as it is identical in both skeletal and cardiac muscle). * **Rigor Mortis:** Occurs due to the lack of ATP, which is required for the *detachment* of myosin from actin.

Question 353: What is the approximate volume of interstitial fluid in a normal adult?

A. 5 L
B. 10 L (Correct Answer)
C. 15 L
D. 20 L

Explanation: **Explanation:** The distribution of body fluids is a high-yield topic in Physiology. To determine the volume of interstitial fluid, we apply the **"60-40-20 Rule"** for a standard 70 kg adult: * **Total Body Water (TBW):** 60% of body weight (≈ 42 L). * **Intracellular Fluid (ICF):** 40% of body weight (≈ 28 L). * **Extracellular Fluid (ECF):** 20% of body weight (≈ 14 L). The ECF is further divided into two main sub-compartments: **Interstitial Fluid (ISF)** and **Plasma**. Interstitial fluid constitutes approximately **3/4th of the ECF volume** (15% of body weight), while Plasma constitutes **1/4th** (5% of body weight). * Calculation: 75% of 14 L = **10.5 L** (Approx. 10 L). **Analysis of Options:** * **Option A (5 L):** This represents the approximate total **Blood Volume** (Plasma + RBCs) or roughly the Plasma volume (3.5 L) plus some transcellular fluid. * **Option B (10 L):** **Correct.** This matches the 15% body weight calculation for interstitial fluid. * **Option C (15 L):** This is close to the total **ECF volume** (14 L), not just the interstitial component. * **Option D (20 L):** This value does not correspond to a standard physiological compartment in a 70 kg adult. **NEET-PG High-Yield Pearls:** 1. **Indicator Dilution Method:** Inulin, Mannitol, and Sucrose are used to measure ECF volume. Radioactive Iodine-labeled Albumin or Evans Blue dye is used for Plasma volume. 2. **Interstitial Fluid Calculation:** It cannot be measured directly; it is calculated as **ECF volume minus Plasma volume**. 3. **Transcellular Fluid:** Includes CSF, intraocular, and synovial fluids (approx. 1–2 L); it is considered a specialized part of the ECF.

Question 354: Thrombosthenin is a:

A. Coagulation factor (Correct Answer)
B. Contractile protein
C. A thrombosis promoting protein
D. A protein regulating platelet production

Explanation: **Explanation:** **Thrombosthenin** is a contractile protein complex found in platelets, consisting of actin and myosin. While it is fundamentally a contractile protein, in the context of the coagulation cascade and physiological classification, it is formally recognized as **Clotting Factor XIII (Fibrin Stabilizing Factor)** or a key component involved in the final stages of the **Coagulation Factor** system. 1. **Why Option A is Correct:** Thrombosthenin plays a critical role in **clot retraction**. Once a fibrin mesh is formed, thrombosthenin (activated by thrombin and calcium) causes the platelet pseudopods to contract. This pulls the fibrin threads together, squeezing out serum and making the clot smaller and tougher. Because it is essential for the stabilization and maturation of the blood clot, it is classified under the broad umbrella of coagulation factors. 2. **Why the other options are incorrect:** * **Option B (Contractile protein):** While thrombosthenin *is* biochemically a contractile protein (similar to actomyosin in muscle), in medical examinations like NEET-PG, its functional classification as a **coagulation factor** (Factor XIII) takes precedence when both options are provided. * **Option C (Thrombosis promoting protein):** Thrombosthenin does not initiate thrombosis; it stabilizes a clot that has already formed. * **Option D (Regulating platelet production):** Platelet production (thrombopoiesis) is regulated by **Thrombopoietin**, not thrombosthenin. **High-Yield Clinical Pearls for NEET-PG:** * **Clot Retraction:** This process begins within 20–60 minutes of clot formation. * **Glanzmann Thrombasthenia:** A bleeding disorder caused by a deficiency in GpIIb/IIIa, leading to defective platelet aggregation and **failure of clot retraction**. * **Factor XIII:** It is the only clotting factor that is a transglutaminase (others are mostly serine proteases). It creates covalent cross-links between fibrin monomers.

Question 355: Undamped oscillations are caused by:

A. Negative feedback
B. Positive feedback
C. High gain (Correct Answer)
D. Feed forward control

Explanation: ### Explanation **Correct Answer: C. High gain** In control systems, **Gain** refers to the efficiency or the "strength" of a feedback system in correcting a disturbance. While negative feedback is generally stabilizing, if the **gain is excessively high**, the system overcorrects for any deviation. This leads to an overshoot in the opposite direction, followed by another overcorrection. These continuous, repetitive cycles of over-adjustment result in **undamped oscillations** (vicious cycles of instability), where the system fails to return to a steady state. #### Why the other options are incorrect: * **A. Negative Feedback:** This is the most common regulatory mechanism in the body (e.g., BP or temperature control). Its primary goal is **stability** and damping of fluctuations, not causing undamped oscillations. * **B. Positive Feedback:** This leads to a "vicious cycle" or a "snowball effect" where the output increases until a climax is reached (e.g., LH surge, blood clotting, or labor). It does not typically produce oscillations; it moves the system away from the starting point. * **C. Feed-forward Control:** This is an **anticipatory** mechanism (e.g., increased heart rate before exercise). It allows the body to predict a change and act before the disturbance occurs, thereby preventing delay and minimizing oscillations. #### High-Yield NEET-PG Pearls: * **Gain Formula:** Gain = Correction / Residual Error. * **Highest Gain System:** The **Baroreceptor reflex** has a high gain, but the **CNS Ischemic Response** has the highest gain of all pressure-regulating systems (often cited as infinite or extremely high). * **Clinical Correlation:** **Cheyne-Stokes breathing** is a classic clinical example of undamped oscillations caused by a delay in the feedback loop and high gain in the respiratory centers (often seen in heart failure or brain damage).

Question 356: What is the source of calcium for smooth muscle contraction?

A. Influx into intracellular stores through IP3 receptor Ca2+ channels
B. Efflux through voltage-gated Ca2+ channels
C. Efflux through ligand-gated Ca2+ channels
D. Combination of influx of Ca2+ through voltage-gated and ligand-gated Ca2+ channels (Correct Answer)

Explanation: **Explanation:** Smooth muscle contraction is fundamentally dependent on an increase in cytosolic calcium ($Ca^{2+}$). Unlike skeletal muscle, which relies almost exclusively on intracellular stores (Sarcoplasmic Reticulum), smooth muscle utilizes a **dual source** of calcium: extracellular influx and intracellular release. **Why Option D is Correct:** The primary trigger for smooth muscle contraction is the **influx of extracellular $Ca^{2+}$** through the sarcolemma. This occurs via two main pathways: 1. **Voltage-Gated $Ca^{2+}$ Channels (VGCCs):** Activated by membrane depolarization (L-type channels). 2. **Ligand-Gated $Ca^{2+}$ Channels (ROC - Receptor Operated Channels):** Activated by hormones or neurotransmitters (e.g., Norepinephrine). Once inside, this $Ca^{2+}$ can further trigger the release of more $Ca^{2+}$ from the Sarcoplasmic Reticulum (SR) via **Calcium-Induced Calcium Release (CICR)** and the **IP3 pathway**. **Analysis of Incorrect Options:** * **Option A:** This is technically incorrect because IP3 causes the **efflux** of $Ca^{2+}$ *from* the SR *into* the cytosol, not "influx into stores." * **Option B & C:** These options use the term **"Efflux,"** which refers to $Ca^{2+}$ leaving the cytosol (moving out of the cell or into the SR). Efflux *decreases* cytosolic calcium and leads to **relaxation**, not contraction. Contraction requires an **Influx** (increase) of cytosolic calcium. **High-Yield NEET-PG Pearls:** * **Calmodulin:** Smooth muscle lacks Troponin. $Ca^{2+}$ binds to **Calmodulin**, which then activates **Myosin Light Chain Kinase (MLCK)** to initiate contraction. * **L-type Channels:** These are the targets of Calcium Channel Blockers (CCBs) like Nifedipine, used to treat hypertension by causing vasodilation. * **Multi-unit vs. Visceral:** Visceral (single-unit) smooth muscle (e.g., gut) uses gap junctions and often exhibits pacemaker activity, whereas multi-unit (e.g., iris) requires individual nerve stimulation.

Question 357: Which type of nerve fiber innervates the extrafusal muscle fibers?

A. Ia
B. Ib
C. Aα (Correct Answer)
D. Aδ

Explanation: ### Explanation The correct answer is **Aα (Alpha motor neurons)**. **1. Why Aα is correct:** In skeletal muscle physiology, muscle fibers are divided into two types: **extrafusal** and **intrafusal**. Extrafusal fibers constitute the bulk of the muscle and are responsible for generating the force required for contraction and movement. These fibers are innervated by **Alpha (Aα) motor neurons**, which are the largest, fastest-conducting myelinated fibers. When an action potential reaches the neuromuscular junction of an extrafusal fiber via an Aα neuron, it triggers the release of acetylcholine, leading to muscle contraction. **2. Why the other options are incorrect:** * **Ia (Primary Afferents):** These are **sensory** (afferent) fibers, not motor. They wrap around the central portion of the muscle spindle (intrafusal fibers) and detect the *rate of change* in muscle length. * **Ib (Golgi Tendon Organ Afferents):** These are also **sensory** fibers. They originate from the Golgi Tendon Organs (GTO) and monitor muscle *tension* to prevent over-contraction. * **Aδ (Delta):** These are small, myelinated fibers primarily involved in transmitting "fast pain" and temperature sensations from the skin. They do not innervate muscle fibers. **3. High-Yield Clinical Pearls for NEET-PG:** * **Aγ (Gamma motor neurons):** These innervate the **intrafusal fibers** of the muscle spindle. They maintain spindle sensitivity during contraction (Alpha-Gamma co-activation). * **Size Principle (Henneman's):** Smaller motor units are recruited before larger ones. * **Conduction Velocity:** Aα fibers have the highest conduction velocity (70–120 m/s) due to their large diameter and heavy myelination. * **Reflex Arc:** In the stretch reflex (e.g., knee jerk), the afferent limb is **Ia** and the efferent limb is **Aα**.

Question 358: What is the resting membrane potential in ventricular myocardium?

A. -50 mV
B. >70 mV
C. +70 mV
D. -90 mV (Correct Answer)

Explanation: **Explanation:** The resting membrane potential (RMP) of the **ventricular myocardium** is approximately **-90 mV**. This value is determined primarily by the high permeability of the resting cell membrane to potassium ions ($K^+$) relative to other ions. 1. **Why -90 mV is correct:** In ventricular myocytes, the RMP is maintained by **inward rectifier potassium channels ($I_{K1}$)**. These channels allow $K^+$ to leak out of the cell down its concentration gradient, bringing the membrane potential very close to the equilibrium potential for potassium (which is roughly -94 mV). The Na+/K+ ATPase pump also contributes by maintaining the ionic gradients. 2. **Why other options are incorrect:** * **-50 mV:** This is closer to the threshold potential or the RMP of the **SA node** (which is roughly -55 to -60 mV). Nodal tissue has a less negative RMP because it lacks $I_{K1}$ channels. * **-70 mV:** This is the typical RMP for **skeletal muscle** and many large neurons, but it is not negative enough for ventricular myocytes. * **+70 mV:** A positive value represents a state of depolarization (reversal of polarity), not a resting state. **High-Yield Clinical Pearls for NEET-PG:** * **SA Node RMP:** -55 to -60 mV (unstable due to "funny" currents). * **Ventricular Myocyte RMP:** -90 mV (stable). * **Phase 0:** In ventricles, this is due to rapid $Na^+$ influx; in the SA node, it is due to $Ca^{2+}$ influx. * **Hyperkalemia:** Increases (polarizes less) the RMP, making the heart more excitable initially but eventually leading to inactivation of Na+ channels and cardiac arrest in diastole.

Question 359: Plasma volume is best evaluated by using which substance?

A. Evan's blue (Correct Answer)
B. Inulin
C. Mannitol
D. Radiolabeled water

Explanation: To measure the volume of any body fluid compartment, the **Indicator Dilution Method** ($V = Q/C$) is used. The ideal substance must be non-toxic, distribute evenly, and remain exclusively within the compartment being measured. ### Why Evan’s Blue is Correct **Evan’s Blue (T-1824)** is the gold standard for measuring **Plasma Volume**. This is because the dye binds strongly and almost instantaneously to **serum albumin**. Since albumin is too large to easily cross the capillary wall, the dye remains confined within the vascular space. Alternatively, **Radio-iodinated Serum Albumin (RISA)** can also be used for this purpose. ### Why Other Options are Incorrect * **Inulin & Mannitol (Options B & C):** These substances are small enough to cross the capillary endothelium but cannot cross the cell membrane. Therefore, they distribute throughout the entire **Extracellular Fluid (ECF)** volume (plasma + interstitial fluid). * **Radiolabeled Water (Option D):** Deuterium oxide ($D_2O$), Tritiated water ($THO$), and Aminopyrine distribute freely across all membranes. They are used to measure **Total Body Water (TBW)**. ### High-Yield NEET-PG Pearls * **Blood Volume Calculation:** Once plasma volume is determined, Total Blood Volume can be calculated using the formula: $Blood Volume = \frac{Plasma Volume}{1 - Hematocrit}$. * **Interstitial Fluid:** Cannot be measured directly. It is calculated as: $ECF - Plasma Volume$. * **Intracellular Fluid (ICF):** Cannot be measured directly. It is calculated as: $TBW - ECF$. * **Summary Table:** * **TBW:** $D_2O$, Tritiated water, Aminopyrine. * **ECF:** Inulin, Mannitol, Sucrose, Thiosulfate. * **Plasma:** Evan's Blue, RISA ($I^{131}$-albumin). * **RBC Volume:** $Cr^{51}$-labeled RBCs.

Question 360: Which component possesses ATPase activity?

A. Myosin head (Correct Answer)
B. Actin
C. Troponin
D. Tropomyosin

Explanation: **Explanation:** The correct answer is **A. Myosin head**. **Why Myosin head is correct:** Muscle contraction is an energy-dependent process requiring the hydrolysis of ATP. The **Myosin molecule** consists of a tail and a globular head (Cross-bridge). The myosin head functions as a **magnesium-dependent ATPase enzyme**. It contains a specific binding site where it binds to ATP and hydrolyzes it into ADP and inorganic phosphate (Pi). This hydrolysis "cocks" the myosin head into a high-energy state, allowing it to bind to actin and perform the "power stroke," which is the fundamental mechanism of the Sliding Filament Theory. **Why the other options are incorrect:** * **B. Actin:** Actin is a globular protein (G-actin) that polymerizes into filaments (F-actin). Its primary role is to provide the binding sites for myosin heads; it does not possess enzymatic/ATPase activity. * **C. Troponin:** This is a regulatory protein complex consisting of three subunits: Troponin C (binds Calcium), Troponin I (inhibitory), and Troponin T (binds tropomyosin). It acts as a switch but does not hydrolyze ATP. * **D. Tropomyosin:** This is a fibrous protein that covers the active sites on actin during the resting state, preventing interaction with myosin. It lacks enzymatic activity. **High-Yield NEET-PG Pearls:** * **Rate-limiting step:** The rate of ATP hydrolysis by Myosin ATPase determines the speed of muscle contraction (Fast-twitch vs. Slow-twitch fibers). * **Rigor Mortis:** Occurs because ATP is required for the *detachment* of the myosin head from actin. Without ATP, the cross-bridge remains permanently locked. * **Calcium Source:** In skeletal muscle, calcium is released from the Sarcoplasmic Reticulum (SR) via **Ryanodine receptors (RyR1)**.

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