General Physiology — MCQs

General Physiology Indian Medical PG Practice Questions and MCQs

Question 321: Dye studies were completed on a healthy man of average build to determine the distribution of water in his body. Which range is most likely to represent the percentage of his lean body mass that is intracellular water?

A. 5% to 6%
B. 18% to 20%
C. 40% to 50% (Correct Answer)
D. 60% to 70%

Explanation: ### Explanation **Concept Overview:** Total Body Water (TBW) accounts for approximately **60% of the total body weight** in a healthy adult male. This water is distributed into two primary compartments: 1. **Intracellular Fluid (ICF):** Comprises 2/3 (approx. 40%) of total body weight. 2. **Extracellular Fluid (ECF):** Comprises 1/3 (approx. 20%) of total body weight. **Why Option C is Correct:** The question asks for the percentage of **lean body mass** that is **intracellular water**. Since ICF makes up roughly 40% of the total body weight, the range **40% to 50%** is the most accurate representation. In a standard 70 kg man, ICF is about 28 liters (40% of 70). **Analysis of Incorrect Options:** * **Option A (5% to 6%):** This represents the **Plasma volume**, which is a sub-compartment of the ECF (approx. 1/4th of ECF). * **Option B (18% to 20%):** This represents the **Extracellular Fluid (ECF)** volume, not the intracellular volume. * **Option D (60% to 70%):** This represents the **Total Body Water (TBW)** percentage, not the specific intracellular fraction. **High-Yield NEET-PG Pearls:** * **The 60-40-20 Rule:** TBW is 60%, ICF is 40%, and ECF is 20% of body weight. * **Dye Dilution Method (Indicator Dilution Principle):** * **TBW** is measured using Tritiated water ($^3H_2O$), Deuterium oxide ($D_2O$), or Aminopyrine. * **ECF** is measured using Inulin (Gold Standard), Mannitol, or Thiosulfate. * **Plasma Volume** is measured using Evans Blue (T-1824) or Radio-iodinated Albumin ($^{131}I$-Albumin). * **ICF** cannot be measured directly; it is calculated as **TBW – ECF**. * **Variation:** TBW is lower in females and the elderly due to a higher percentage of adipose tissue (fat is hydrophobic). In infants, TBW is highest (approx. 75%).

Question 322: The difference between total cations and total anions is termed as what?

A. Cation gap
B. Anion gap (Correct Answer)
C. Equivalent concentration
D. Molar concentration

Explanation: **Explanation:** The **Anion Gap (AG)** is a clinical calculation used to identify the cause of metabolic acidosis. According to the principle of **electroneutrality**, the total number of positive charges (cations) must equal the total number of negative charges (anions) in the serum. However, in routine clinical practice, we only measure the most common electrolytes. The Anion Gap represents the "unmeasured anions" (such as phosphates, sulfates, organic acids, and albumin) that are not accounted for when subtracting the measured anions (Chloride and Bicarbonate) from the measured cation (Sodium). * **Formula:** $AG = [Na^+] - ([Cl^-] + [HCO_3^-])$ * **Normal Range:** 8–12 mEq/L. **Analysis of Incorrect Options:** * **A. Cation gap:** This is a distractor term. In clinical medicine, we focus on the "gap" created by unmeasured anions, as unmeasured cations (like $K^+$, $Ca^{2+}$, and $Mg^{2+}$) are present in much smaller concentrations. * **C. Equivalent concentration:** This refers to the concentration of a substance based on its valence (mEq/L), representing its chemical combining power rather than the difference between ions. * **D. Molar concentration:** This is the number of moles of a solute per liter of solution (mol/L), describing the amount of substance regardless of its electrical charge. **Clinical Pearls for NEET-PG:** 1. **High Anion Gap Metabolic Acidosis (HAGMA):** Caused by the addition of acid (e.g., Diabetic Ketoacidosis, Lactic Acidosis, Salicylate poisoning, Methanol, or Uremia). Remember the mnemonic **MUDPILES**. 2. **Normal Anion Gap Metabolic Acidosis (NAGMA):** Also called hyperchloremic acidosis; caused by loss of $HCO_3^-$ (e.g., Diarrhea, Renal Tubular Acidosis). 3. **Albumin Correction:** Since albumin is the major unmeasured anion, for every 1 g/dL decrease in serum albumin, the "normal" anion gap decreases by approximately 2.5 mEq/L.

Question 323: Which tissue is most susceptible to hypoxia?

A. Muscle
B. Neurons (Correct Answer)
C. Hepatocytes
D. Myocytes

Explanation: **Explanation:** The susceptibility of a tissue to hypoxia is directly proportional to its metabolic rate and its dependence on continuous aerobic respiration. **Why Neurons are the Correct Answer:** Neurons have the highest metabolic demand in the body and possess virtually no stores of glycogen or oxygen. They rely exclusively on a continuous supply of glucose and oxygen to maintain the Na+/K+ ATPase pump, which preserves membrane potential. Irreversible damage to cortical neurons occurs within just **3–5 minutes** of total oxygen deprivation. This makes the brain the most hypoxia-sensitive organ. **Analysis of Incorrect Options:** * **A & D. Muscle/Myocytes:** Skeletal muscle is highly resistant to hypoxia because it contains significant stores of glycogen and myoglobin (which stores oxygen). It can also switch to anaerobic glycolysis for extended periods. Cardiac myocytes are more sensitive than skeletal muscle but can still survive hypoxia for approximately 20–30 minutes before irreversible necrosis (infarction) occurs. * **C. Hepatocytes:** While metabolically active, hepatocytes have better regenerative capacity and can tolerate hypoxia longer than neurons (typically up to 1–2 hours) due to different enzymatic pathways and glycogen stores. **NEET-PG High-Yield Pearls:** 1. **Hierarchy of Sensitivity:** Neurons > Cardiac Myocytes > Hepatocytes > Skeletal Muscle > Connective Tissue/Skin. 2. **Selective Vulnerability:** Within the brain, the most sensitive areas to hypoxia are the **Pyramidal cells of the Hippocampus (Sommer’s sector)** and the **Purkinje cells of the Cerebellum**. 3. **Critical Threshold:** The brain consumes roughly 20% of the body's total oxygen despite being only 2% of body weight.

Question 324: Delayed afterdepolarizations are typically associated with which of the following?

A. Increased intracellular calcium
B. Excessive catecholamines
C. Digitalis toxicity
D. All of the above (Correct Answer)

Explanation: **Explanation:** **Delayed Afterdepolarizations (DADs)** are abnormal oscillations in membrane potential that occur shortly after the completion of repolarization (Phase 4). The fundamental mechanism behind DADs is **Intracellular Calcium Overload**. 1. **Mechanism (Why DADs occur):** When intracellular calcium levels are excessively high, the **Sodium-Calcium Exchanger (NCX)** is activated to pump one $Ca^{2+}$ ion out of the cell in exchange for three $Na^{+}$ ions moving in. This net influx of positive charge creates a "transient inward current" ($I_{ti}$), which causes a sub-threshold depolarization. If this depolarization reaches the threshold, it triggers an ectopic action potential (triggered activity). 2. **Analysis of Options:** * **Increased Intracellular Calcium:** This is the direct physiological trigger for DADs. * **Digitalis Toxicity:** Digoxin inhibits the $Na^{+}-K^{+}$ ATPase pump, leading to increased intracellular $Na^{+}$, which subsequently reverses or slows the NCX, causing a massive buildup of intracellular $Ca^{2+}$. This is the classic cause of DAD-mediated arrhythmias. * **Excessive Catecholamines:** High levels of catecholamines (e.g., in stress or exercise) stimulate $\beta_1$ receptors, increasing cAMP and activating Protein Kinase A. This leads to increased calcium entry via L-type channels and increased calcium release from the Sarcoplasmic Reticulum, predisposing the heart to DADs. **High-Yield Clinical Pearls for NEET-PG:** * **DADs vs. EADs:** Early Afterdepolarizations (EADs) occur during Phase 2 or 3 and are associated with **Long QT Syndrome**. DADs occur during Phase 4 and are associated with **Digoxin toxicity** and **CPVT** (Catecholaminergic Polymorphic Ventricular Tachycardia). * **Triggered Activity:** DADs are the primary mechanism for arrhythmias seen in hypercalcemia and reperfusion therapy.

Question 325: What is the receptor for Brain-Derived Neurotrophic Factor (BDNF)?

A. TRK A
B. TRK B (Correct Answer)
C. TRK C
D. TRK D

Explanation: ### Explanation **Neurotrophins** are a family of proteins essential for the survival, development, and function of neurons. They exert their effects by binding to specific high-affinity **Tropomyosin Receptor Kinases (TRK)**, which are transmembrane tyrosine kinase receptors. #### Why TRK B is Correct: **BDNF (Brain-Derived Neurotrophic Factor)** specifically binds with high affinity to **TRK B**. Upon binding, it triggers intracellular signaling pathways (like MAPK and PI3K) that promote neuronal plasticity, long-term potentiation (LTP) in the hippocampus, and the survival of dopaminergic and serotonergic neurons. #### Analysis of Incorrect Options: * **TRK A:** This is the primary receptor for **Nerve Growth Factor (NGF)**. It is crucial for the survival of sympathetic and sensory neurons. * **TRK C:** This is the primary receptor for **Neurotrophin-3 (NT-3)**. It plays a vital role in the development of proprioceptive neurons. * **TRK D:** This is a **distractor**. While there are various isoforms and related receptors, the primary neurotrophin receptors are categorized as A, B, and C. #### High-Yield Clinical Pearls for NEET-PG: 1. **The "Universal" Receptor:** All neurotrophins (NGF, BDNF, NT-3, NT-4/5) bind to the **p75 neurotrophin receptor (p75NTR)** with low affinity. While TRK receptors promote survival, p75NTR can sometimes initiate apoptosis. 2. **BDNF & Memory:** BDNF is a key mediator of **synaptic plasticity**; decreased levels are associated with Alzheimer’s disease and depression. 3. **NT-3 Versatility:** While NT-3 primarily binds to TRK C, it is unique because it can also activate TRK A and TRK B to a lesser extent. 4. **NT-4/5:** These also bind to **TRK B**, similar to BDNF.

Question 326: Which is the most potent pain-producing neurotransmitter?

A. Acetylcholine
B. Substance P
C. Bradykinin (Correct Answer)
D. Histamine

Explanation: ### Explanation **Correct Option: C. Bradykinin** Bradykinin is considered the **most potent pain-producing chemical** (algesic agent) known. It is a nonapeptide released during tissue injury and inflammation. It acts by directly stimulating **nociceptors** (pain receptors) and sensitizing them to other stimuli (hyperalgesia). It functions via G-protein coupled receptors (B1 and B2), triggering the release of prostaglandins, which further amplifies the pain signal. **Analysis of Incorrect Options:** * **A. Acetylcholine:** While it can stimulate free nerve endings, it is primarily a neurotransmitter at the neuromuscular junction and in the autonomic nervous system. It is not a primary or potent mediator of clinical pain. * **B. Substance P:** Often confused with the "most potent" agent, Substance P is a neuropeptide released from the central terminals of primary afferent fibers in the spinal cord. Its primary role is **pain transmission** and "neurogenic inflammation" (vasodilation and edema), rather than being the most potent direct stimulator of peripheral nociceptors. * **D. Histamine:** Released from mast cells during inflammation, histamine primarily causes itching (pruritus) and vasodilation. While it can contribute to pain, its potency is significantly lower than that of Bradykinin. **NEET-PG High-Yield Pearls:** * **Triple Response of Lewis:** Mediated by Histamine (Flush, Flare, and Wheal). * **Pain Fibers:** **A-delta** (Fast pain, myelinated, glutamate) vs. **C-fibers** (Slow pain, unmyelinated, Substance P). * **Glutamate:** The major excitatory neurotransmitter for fast pain in the dorsal horn. * **Enkephalins/Endorphins:** Endogenous opioids that inhibit pain by suppressing Substance P release.

Question 327: Resting membrane potential is mainly due to:

A. Na+
B. K+ (Correct Answer)
C. Cl-
D. Mg++

Explanation: **Explanation:** The **Resting Membrane Potential (RMP)** is primarily determined by the equilibrium potential of the ion to which the cell membrane is most permeable at rest. **Why K+ is the correct answer:** At rest, the cell membrane is significantly more permeable to **Potassium (K+)** than to any other ion (about 50–100 times more permeable than to Na+). This is due to the presence of **non-gated K+ leak channels**, which allow K+ to diffuse out of the cell down its concentration gradient. As K+ leaves, it carries positive charges out, leaving behind immobile anions, thus creating a negative potential inside the cell. The RMP of a typical neuron (-70 mV) or muscle fiber (-90 mV) sits very close to the **Nernst equilibrium potential of K+ (-94 mV)**. **Why other options are incorrect:** * **Na+:** The membrane has very low permeability to Sodium at rest. Na+ influx is primarily responsible for the **depolarization** phase of the action potential, not the RMP. * **Cl-:** While Chloride contributes to the RMP in some cells (like skeletal muscle), its overall influence is secondary to K+ in most excitable tissues. * **Mg++:** Magnesium is an intracellular cation that acts as a cofactor for enzymes (like Na+-K+ ATPase) but does not directly contribute to the generation of the RMP. **High-Yield Facts for NEET-PG:** 1. **Goldman-Hodgkin-Katz (GHK) Equation:** Used to calculate RMP by considering the permeability and concentration gradients of all ions (Na+, K+, and Cl-). 2. **Na+-K+ ATPase Pump:** It is **electrogenic** (pumps 3 Na+ out for 2 K+ in). While it maintains the concentration gradients, it directly contributes only about -5 to -10 mV to the RMP. 3. **Gibbs-Donnan Effect:** Refers to the presence of non-diffusible intracellular proteins that contribute to the negative internal charge.

Question 328: What is the effect on the resting membrane potential when the extracellular concentration of potassium is decreased?

A. Increased magnitude of RMP
B. Increased negativity of the RMP (Correct Answer)
C. Decreased magnitude of RMP
D. Decreased negativity of the RMP

Explanation: ### Explanation The Resting Membrane Potential (RMP) is primarily determined by the concentration gradient of potassium ions ($K^+$) across the cell membrane, as the membrane is highly permeable to $K^+$ at rest. This relationship is governed by the **Nernst Equation**. **1. Why the correct answer is right:** When the extracellular concentration of potassium ($[K^+]_{out}$) decreases (Hypokalemia), the concentration gradient between the inside and outside of the cell increases. According to the laws of diffusion, more $K^+$ ions will leak out of the cell down their chemical gradient. As positively charged potassium ions leave the cell, the interior becomes more negative relative to the exterior. This process is called **hyperpolarization**, which manifests as an **increased negativity of the RMP** (e.g., moving from -70 mV to -90 mV). **2. Why the incorrect options are wrong:** * **Options C & D:** Decreased magnitude or decreased negativity (depolarization) occurs when extracellular potassium increases (**Hyperkalemia**). In hyperkalemia, the gradient is reduced, less $K^+$ leaves the cell, and the RMP becomes less negative (closer to zero). * **Option A:** While "increased magnitude" is technically synonymous with becoming more negative, in medical physiology exams, "increased negativity" is the more precise descriptive term for hyperpolarization. However, in many contexts, A and B could be seen as similar; B is the most specific physiological description. **3. Clinical Pearls for NEET-PG:** * **Hypokalemia:** Leads to hyperpolarization, making it harder for cells (like neurons and muscle) to reach the threshold potential. This results in **muscle weakness and paralysis**. * **ECG in Hypokalemia:** Look for flattened T-waves, prominent **U-waves**, and ST-segment depression. * **Na+/K+ ATPase:** Maintains the steady-state concentrations by pumping 3 $Na^+$ out and 2 $K^+$ in, contributing slightly to the electronegativity of the RMP.

Question 329: A sudden increase in total peripheral resistance has all of the following effects EXCEPT:

A. Increase the diastolic blood pressure
B. Reduce the stroke volume
C. Increase the mean arterial blood pressure
D. Increase cardiac output (Correct Answer)

Explanation: **Explanation:** The correct answer is **D. Increase cardiac output**. **1. Why Option D is correct:** Total Peripheral Resistance (TPR) is the resistance against which the left ventricle must pump to eject blood (Afterload). According to the formula **Cardiac Output (CO) = Stroke Volume × Heart Rate**, and the relationship where **CO = Mean Arterial Pressure / TPR**, an increase in TPR leads to an increase in afterload. This increased resistance makes it harder for the heart to eject blood, leading to a decrease in stroke volume and, consequently, a **decrease (or no change) in cardiac output**, but certainly not an increase. **2. Why the other options are incorrect:** * **Option A (Increase diastolic BP):** Diastolic blood pressure is primarily determined by TPR. When resistance increases, the rate at which blood leaves the arterial system during diastole decreases, maintaining a higher pressure. * **Option B (Reduce stroke volume):** As TPR (afterload) increases, the velocity of muscle fiber shortening decreases, and the end-systolic volume increases. This results in a lower stroke volume. * **Option C (Increase mean arterial BP):** Mean Arterial Pressure (MAP) is directly proportional to TPR (MAP = CO × TPR). Therefore, a sudden rise in resistance will cause a corresponding rise in MAP. **Clinical Pearls for NEET-PG:** * **Afterload:** Think of TPR as the "Afterload." High afterload decreases stroke volume (inverse relationship). * **Preload:** Determined by venous return; increases stroke volume via the Frank-Starling mechanism. * **Pulse Pressure:** Primarily determined by stroke volume and arterial compliance, whereas **Diastolic BP** is primarily determined by TPR.

Question 330: Which of the following substances moves most rapidly across a cell membrane?

A. Carbon dioxide (Correct Answer)
B. Water
C. Glucose
D. Urea

Explanation: **Explanation:** The movement of substances across a cell membrane is primarily governed by the **lipid solubility** and the **size** of the molecule. The cell membrane is a phospholipid bilayer; therefore, lipid-soluble (hydrophobic) substances can dissolve directly into the membrane and diffuse rapidly via simple diffusion. **1. Why Carbon Dioxide (CO₂) is Correct:** CO₂ is a small, non-polar, and highly **lipid-soluble** gas. According to Fick’s Law of Diffusion, lipid solubility is a major determinant of the diffusion coefficient. CO₂ is approximately 20 times more soluble than Oxygen (O₂), allowing it to pass through the lipid bilayer almost instantaneously without the need for channels or carriers. **2. Why the other options are incorrect:** * **Water (B):** Although water molecules are small, they are highly **polar** (insoluble in lipids). They move through the membrane via specialized channels called **aquaporins**. While this process is fast, it is not as rapid as the direct lipid diffusion of CO₂. * **Glucose (C):** Glucose is a large, polar molecule. It is completely lipid-insoluble and requires **facilitated diffusion** via specific carrier proteins (GLUT transporters), making its transport significantly slower. * **Urea (D):** Urea is a small, polar molecule. While it can permeate the membrane, its lipid solubility is much lower than that of dissolved gases, resulting in a slower rate of diffusion compared to CO₂. **High-Yield NEET-PG Pearls:** * **Permeability Order:** Hydrophobic molecules (O₂, CO₂, N₂, Steroids) > Small uncharged polar molecules (H₂O, Urea) > Large uncharged polar molecules (Glucose) > Ions (Na⁺, K⁺). * **Clinical Correlation:** The high solubility of CO₂ is the reason why, in respiratory failure, CO₂ retention (hypercapnia) often occurs later than hypoxia; CO₂ diffuses across the alveolar-capillary membrane much more efficiently than O₂.

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