General Physiology — MCQs

General Physiology Indian Medical PG Practice Questions and MCQs

Question 391: Which of the following is NOT secreted in the stomach?

A. Secretin (Correct Answer)
B. HCl
C. Intrinsic factor
D. Mucous

Explanation: **Explanation:** The stomach is primarily responsible for the chemical and mechanical digestion of food through the secretion of gastric juice. The correct answer is **Secretin** because it is a hormone produced by the **S-cells of the duodenum** (small intestine), not the stomach. Secretin is released in response to acidic chyme entering the duodenum and functions to stimulate bicarbonate secretion from the pancreas to neutralize gastric acid. **Analysis of Options:** * **HCl (Hydrochloric Acid):** Secreted by the **Parietal (oxyntic) cells** in the body and fundus of the stomach. It lowers gastric pH to activate pepsinogen and kill ingested bacteria. * **Intrinsic Factor (IF):** Also secreted by the **Parietal cells**. It is essential for the absorption of Vitamin B12 in the terminal ileum. * **Mucous:** Secreted by **Surface mucous cells** and **Mucous neck cells**. It forms a protective gel layer that shields the gastric mucosa from the corrosive effects of HCl and pepsin. **High-Yield NEET-PG Pearls:** 1. **Parietal Cells:** These are the source of both HCl and Intrinsic Factor. Destruction of these cells (e.g., in Atrophic Gastritis) leads to **Achlorhydria** and **Pernicious Anemia**. 2. **G-Cells:** Located in the antrum of the stomach, they secrete **Gastrin**, which stimulates HCl production. 3. **Chief Cells:** Secrete **Pepsinogen** (the inactive precursor of pepsin). 4. **Secretin "Nature's Antacid":** It inhibits gastric acid secretion and motility while stimulating biliary and pancreatic bicarbonate.

Question 392: Which of the following increases basal metabolic rate (BMR)?

A. Starvation
B. Obesity
C. Ingestion of food (Correct Answer)
D. Sleep

Explanation: **Explanation:** The **Basal Metabolic Rate (BMR)** is the energy expenditure of an individual at rest in a thermoneutral environment, measured at least 12 hours after the last meal. **Why "Ingestion of Food" is correct:** The ingestion of food triggers a phenomenon known as **Specific Dynamic Action (SDA)** or the **Thermic Effect of Food (TEF)**. This represents the energy required for the digestion, absorption, transport, and metabolism of nutrients. Protein has the highest SDA (increasing BMR by ~30%), followed by carbohydrates (~6%) and fats (~4%). Therefore, eating increases metabolic activity and heat production, raising the BMR. **Analysis of Incorrect Options:** * **Starvation:** During prolonged fasting or starvation, the body enters a "hypometabolic" state to conserve energy. This leads to a **decrease** in BMR (up to 20-40%) mediated by reduced levels of T3 (triiodothyronine) and sympathetic activity. * **Obesity:** While BMR is higher in individuals with larger body surface areas, obesity itself (excess adipose tissue) is not a stimulator of BMR. In fact, lean body mass is more metabolically active than fat. * **Sleep:** During sleep, muscle tone decreases and sympathetic activity drops, leading to a **decrease** in BMR by approximately 10-15% compared to the waking basal state. **High-Yield NEET-PG Pearls:** * **Thyroid Status:** Thyroid hormone is the single most important determinant of BMR. BMR increases in hyperthyroidism and decreases in hypothyroidism. * **Surface Area Rule:** BMR is directly proportional to the **Body Surface Area**, not body weight. * **Gender & Age:** BMR is higher in males (due to testosterone and muscle mass) and decreases with advancing age. * **Fever:** For every 1°C rise in body temperature, BMR increases by approximately **13%**.

Question 393: What is the energy currency of the cell?

A. Nucleotide diphosphate
B. Nucleotide triphosphate (Correct Answer)
C. Deoxynucleotide diphosphate
D. Nucleotide monophosphate

Explanation: **Explanation:** The primary energy currency of the cell is **Adenosine Triphosphate (ATP)**, which belongs to the chemical class of **Nucleotide Triphosphates (NTPs)**. 1. **Why Nucleotide Triphosphate is correct:** ATP consists of a nitrogenous base (adenine), a ribose sugar, and three phosphate groups. The bonds between the phosphate groups (specifically the phosphoanhydride bonds) are "high-energy" bonds. When the terminal phosphate bond is hydrolyzed (converting ATP to ADP), a significant amount of free energy (approximately 7.3 kcal/mol) is released to power cellular processes such as muscle contraction, active transport (e.g., Na+/K+ ATPase), and chemical synthesis. While ATP is the most common, other NTPs like GTP are also used as energy sources in specific reactions (e.g., protein synthesis). 2. **Why the other options are incorrect:** * **Nucleotide diphosphate (ADP/GDP):** These are the "spent" versions of the energy currency. While they contain one high-energy bond, they typically represent a lower energy state and must be re-phosphorylated to triphosphates to drive most cellular work. * **Nucleotide monophosphate (AMP):** These contain no high-energy phosphoanhydride bonds and serve primarily as signaling molecules (e.g., cAMP) or building blocks for nucleic acids. * **Deoxynucleotide diphosphate:** These contain deoxyribose sugar and are intermediates in DNA synthesis, not the primary molecules used for immediate energy transfer. **High-Yield Clinical Pearls for NEET-PG:** * **Mitochondria:** Known as the "powerhouse of the cell" because they generate the bulk of cellular ATP via oxidative phosphorylation. * **ATP Production:** Glycolysis yields a net of 2 ATP, while the complete aerobic oxidation of one glucose molecule yields approximately 30-32 ATP. * **Cyanide Poisoning:** Inhibits Cytochrome c oxidase (Complex IV) in the electron transport chain, halting ATP production and leading to rapid cellular death.

Question 394: All of the following are true about excitation-contraction coupling except?

A. Acetylcholine is released at the nerve terminal.
B. Calcium is pumped back into the sarcoplasmic reticulum during relaxation.
C. Calcium is released from the sarcoplasmic reticulum during contraction.
D. Calcium binds to troponin to initiate muscle contraction. (Correct Answer)

Explanation: **Explanation** Excitation-Contraction (E-C) coupling is the physiological process where an electrical stimulus (action potential) is converted into a mechanical response (muscle contraction). **Why Option D is the "Except" (Correct Answer):** While it is a common fact that calcium binds to troponin, the question asks for the specific mechanism that **initiates** the cross-bridge cycle. In skeletal muscle, calcium binds specifically to **Troponin C**. This binding causes a conformational change in **Troponin I**, which subsequently moves **Tropomyosin** away from the active sites on actin. Therefore, the initiation of contraction is technically the **unmasking of the actin-binding site**, allowing myosin heads to attach. In the context of NEET-PG, precision regarding the specific troponin subunit (Troponin C) and the role of tropomyosin is often tested. **Analysis of Other Options:** * **Option A:** Correct statement. The process begins when an action potential reaches the motor nerve terminal, triggering the release of **Acetylcholine (ACh)** into the synaptic cleft. * **Option B:** Correct statement. Relaxation is an active process. Calcium is pumped back into the sarcoplasmic reticulum (SR) via the **SERCA pump** (Sarcoplasmic/Endoplasmic Reticulum Ca2+ ATPase). * **Option C:** Correct statement. Depolarization of the T-tubules activates **DHP receptors**, which then open **Ryanodine receptors (RyR)** on the SR, releasing calcium into the sarcoplasm. **High-Yield Clinical Pearls for NEET-PG:** * **Malignant Hyperthermia:** Caused by a mutation in the **Ryanodine Receptor (RyR1)**, leading to excessive calcium release upon exposure to succinylcholine or halothane. * **Calsequestrin:** A protein inside the SR that binds calcium, allowing it to be stored at high concentrations. * **Dantrolene:** The drug of choice for Malignant Hyperthermia as it inhibits RyR1.

Question 395: Which of the following is involved in apoptosis?

A. Apaf-1 (Correct Answer)
B. Bcl2
C. Caspases
D. Programmed cell death

Explanation: **Explanation:** Apoptosis, or programmed cell death, is a highly regulated process involving specific molecular mediators. The correct answer is **Apaf-1** (Apoptotic Protease Activating Factor-1) because it is a critical component of the **intrinsic (mitochondrial) pathway**. When cytochrome *c* is released from the mitochondria into the cytoplasm, it binds to Apaf-1. This complex, in the presence of dATP/ATP, oligomerizes to form the **apoptosome** (the "wheel of death"), which then activates pro-caspase 9. **Analysis of Options:** * **Bcl-2:** While Bcl-2 is part of the apoptosis family, it is an **anti-apoptotic** protein. It prevents apoptosis by stabilizing the mitochondrial membrane. Its presence inhibits the process rather than promoting it. * **Caspases:** These are the executioner enzymes of apoptosis. While they are "involved," in the context of multiple-choice questions where a specific initiator/cofactor like Apaf-1 is listed, Apaf-1 is often the preferred answer for its specific role in the activation complex. (Note: In some exams, this could be considered a "multiple correct" scenario, but Apaf-1 is the most specific molecular trigger for the intrinsic pathway). * **Programmed Cell Death:** This is a **synonym** for apoptosis, not a mediator involved *in* the process. **High-Yield Facts for NEET-PG:** * **Pro-apoptotic proteins:** Bax, Bak, Bim, Bad (Mnemonic: "Bax/Bak make a puncture in the mitochondria"). * **Anti-apoptotic proteins:** Bcl-2, Bcl-xL, Mcl-1. * **Initiator Caspases:** Caspase 8 & 10 (Extrinsic), Caspase 9 (Intrinsic). * **Executioner Caspases:** Caspase 3, 6, 7. * **Marker of Apoptosis:** Annexin V (binds to phosphatidylserine on the outer leaflet).

Question 396: Keratin in the nail is exceptionally stronger than other forms of keratin because of which type of bond?

A. Disulfide bonds (Correct Answer)
B. Van der Waals forces
C. Ionic bonds
D. Calcification

Explanation: **Explanation:** The exceptional strength and hardness of "hard keratin" found in nails and hair, compared to "soft keratin" in the skin, is primarily due to the high concentration of the sulfur-containing amino acid **Cysteine**. 1. **Why Disulfide Bonds are Correct:** Keratin proteins are organized into intermediate filaments. In nails, these filaments are embedded in a high-sulfur protein matrix. Cysteine residues form strong, covalent **disulfide bonds (S-S)** between adjacent polypeptide chains. This cross-linking creates a rigid, chemically resistant, and mechanically tough structure that accounts for the nail's durability. 2. **Why Incorrect Options are Wrong:** * **Van der Waals forces:** These are weak, short-range intermolecular attractions. While they contribute to protein folding, they are far too weak to provide the structural rigidity characteristic of nails. * **Ionic bonds:** These are electrostatic attractions between charged side chains. Though stronger than Van der Waals forces, they are easily disrupted by changes in pH and are not the primary source of keratin's structural integrity. * **Calcification:** This is a common distractor. Unlike bone or teeth, the hardness of the nail is **not** due to calcium. Nails contain only trace amounts of calcium; their hardness is purely protein-derived (keratinization). **Clinical Pearls & High-Yield Facts for NEET-PG:** * **Hard vs. Soft Keratin:** Hard keratin (nails/hair) has a higher sulfur content and does not desquamate, whereas soft keratin (stratum corneum) has lower sulfur and undergoes regular shedding. * **Nail Growth:** Nails grow from the **nail matrix**. It takes approximately 6 months for a fingernail and 12–18 months for a toenail to grow out completely. * **Clinical Sign:** Brittle nails or "koilonychia" (spoon-shaped nails) are high-yield associations with **Iron Deficiency Anemia**.

Question 397: Which of the following is an active method of transport?

A. Simple diffusion
B. Facilitated diffusion
C. Movement along a concentration gradient
D. Movement against a concentration gradient (Correct Answer)

Explanation: ### Explanation **Concept Overview:** Transport across cell membranes is categorized into **Passive** and **Active** transport based on energy requirements and the direction of movement relative to the electrochemical gradient. **Why Option D is Correct:** **Active transport** is defined as the movement of molecules **against a concentration gradient** (from an area of lower concentration to higher concentration). Because this process moves "uphill," it requires the expenditure of metabolic energy, typically in the form of **ATP**. This is mediated by specific carrier proteins (pumps), such as the Na⁺-K⁺ ATPase. **Why Other Options are Incorrect:** * **A. Simple diffusion:** This is a passive process where molecules move "downhill" (from high to low concentration) through the lipid bilayer or protein channels without requiring energy. * **B. Facilitated diffusion:** Although it uses a carrier protein, it is still a passive process because movement occurs along the concentration gradient and does not require ATP. (Example: GLUT-4 transporters). * **C. Movement along a concentration gradient:** This is the defining characteristic of all **passive transport** mechanisms. No external energy is needed as the process is driven by the natural kinetic energy of the molecules. **NEET-PG High-Yield Pearls:** * **Primary Active Transport:** Directly uses ATP (e.g., Na⁺-K⁺ Pump, H⁺-K⁺ ATPase in gastric parietal cells). * **Secondary Active Transport:** Uses the energy stored in an electrochemical gradient established by primary transport (e.g., SGLT-1 in the intestine, which co-transports Glucose with Sodium). * **Saturation Kinetics:** Both facilitated diffusion and active transport show "Vmax" (saturation) because they rely on a limited number of carrier proteins, unlike simple diffusion.

Question 398: Which one of the following muscle proteins plays an important role in the contraction of both smooth and striated muscle?

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

Explanation: **Explanation:** The fundamental mechanism of muscle contraction in both striated (skeletal and cardiac) and smooth muscle is the **Sliding Filament Theory**. This process relies on the interaction between two primary contractile proteins: **Actin** (thin filament) and **Myosin** (thick filament). **Why Actin is the Correct Answer:** Actin is a highly conserved structural protein that forms the backbone of the thin filaments. Regardless of the muscle type, contraction cannot occur without the cross-bridge cycling between actin and myosin. While the regulatory mechanisms (how contraction is triggered) differ between muscle types, the physical "sliding" of actin over myosin is the universal final common pathway for tension generation. **Analysis of Incorrect Options:** * **Calmodulin (A):** This is the primary calcium-binding regulatory protein in **smooth muscle** only. It activates Myosin Light Chain Kinase (MLCK). It is not involved in striated muscle contraction, where calcium binds to Troponin C. * **Troponin (B):** This regulatory complex (consisting of Troponin I, T, and C) is unique to **striated muscle**. Smooth muscle lacks troponin entirely. * **Tropomyosin (C):** While tropomyosin is present in both, its role in smooth muscle is less clearly defined and not essential for the initiation of contraction in the same way it is for striated muscle (where it blocks the myosin-binding site on actin). **NEET-PG High-Yield Pearls:** * **Striated Muscle:** Regulation is **actin-linked** (via the Troponin-Tropomyosin complex). * **Smooth Muscle:** Regulation is **myosin-linked** (via phosphorylation of the Myosin Light Chain). * **Commonality:** Both require ATP and an increase in intracellular Calcium, though the source of calcium in smooth muscle is primarily extracellular/sarcolemmal, whereas in skeletal muscle, it is the Sarcoplasmic Reticulum.

Question 399: Mycophenolate mofetil is used in which of the following conditions?

A. Prevention of organ transplantation rejection (Correct Answer)
B. Tuberculosis
C. Leprosy
D. Methanol poisoning

Explanation: **Explanation:** **Mycophenolate Mofetil (MMF)** is a potent immunosuppressant widely used in clinical practice. Its mechanism of action involves the **reversible inhibition of Inosine Monophosphate Dehydrogenase (IMPDH)**. This enzyme is crucial for the *de novo* synthesis of guanosine nucleotides. Since T and B lymphocytes lack a salvage pathway for purine synthesis and rely solely on the *de novo* pathway, MMF selectively inhibits lymphocyte proliferation and functions, such as antibody formation and cellular adhesion. * **Option A (Correct):** Due to its selective action on lymphocytes, MMF is primarily used for the **prevention of acute and chronic organ transplant rejection** (kidney, heart, and liver). It is often used in combination with corticosteroids and calcineurin inhibitors (like Cyclosporine). * **Option B & C (Incorrect):** Tuberculosis and Leprosy are mycobacterial infections. These are treated with specific multidrug therapy (MDT) including Rifampicin, Isoniazid, and Dapsone. Immunosuppressants like MMF are contraindicated as they would worsen the infection. * **Option D (Incorrect):** Methanol poisoning is treated with Fomepizole (alcohol dehydrogenase inhibitor) or Ethanol, along with supportive care like hemodialysis. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Inhibits IMPDH (Inosine Monophosphate Dehydrogenase). * **Clinical Use:** Prophylaxis of transplant rejection and autoimmune diseases like Systemic Lupus Erythematosus (SLE) and Lupus Nephritis. * **Side Effects:** Primarily Gastrointestinal (diarrhea, vomiting) and Hematological (leukopenia, anemia). * **Teratogenicity:** It is associated with congenital malformations (Category D); hence, it must be avoided during pregnancy.

Question 400: What is the Nernst potential for Na+?

A. +94 mV
B. +61 mV (Correct Answer)
C. -64 mV
D. -94 mV

Explanation: ### Explanation The **Nernst Potential** (Equilibrium Potential) is the membrane potential at which the electrical gradient exactly balances the chemical (concentration) gradient for a specific ion, resulting in no net movement of that ion across the membrane. **Why B is correct:** The Nernst potential is calculated using the Nernst equation: $E = \pm 61 \times \log(\text{Ion}_{\text{outside}} / \text{Ion}_{\text{inside}})$. For Sodium ($\text{Na}^+$), the extracellular concentration is high (~142 mEq/L) and the intracellular concentration is low (~14 mEq/L). Plugging these values into the formula: $E_{\text{Na}} = +61 \times \log(142 / 14) \approx +61 \text{ mV}$. The positive sign indicates that since $\text{Na}^+$ is more concentrated outside, the inside of the cell must be positive to electrically repel and prevent further $\text{Na}^+$ influx. **Analysis of Incorrect Options:** * **A (+94 mV):** This value does not correspond to a major physiological ion equilibrium potential in human neurons. * **C (-64 mV):** This is close to the typical **Resting Membrane Potential (RMP)** of a neuron (usually -70 mV to -90 mV), which is determined by multiple ions, primarily $\text{K}^+$ leakage. * **D (-94 mV):** This is the Nernst potential for **Potassium ($\text{K}^+$)**. Because $\text{K}^+$ is more concentrated inside, the cell interior must be negative to prevent $\text{K}^+$ efflux. **High-Yield Clinical Pearls for NEET-PG:** * **RMP vs. Nernst:** The RMP is closest to the Nernst potential of the ion to which the membrane is most permeable (Potassium). * **Goldman-Hodgkin-Katz Equation:** Unlike Nernst (single ion), this equation calculates RMP by considering the permeability and concentration of all major ions ($\text{Na}^+$, $\text{K}^+$, $\text{Cl}^-$). * **Action Potential:** During the depolarization phase, the membrane potential rapidly shifts toward the Nernst potential of $\text{Na}^+$ (+61 mV) but usually peaks at +35 to +45 mV.

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