General Physiology — MCQs

General Physiology Indian Medical PG Practice Questions and MCQs

Question 261: The pre-depolarization phase of the SA node Action potential is due to?

A. K+ entry
B. Ca++ entry (Correct Answer)
C. Na+ entry towards the end of repolarization
D. Cl- efflux

Explanation: ### Explanation The SA node acts as the primary pacemaker of the heart because it exhibits **automaticity**, characterized by a slow, spontaneous depolarization known as the **pacemaker potential** (Phase 4). **Why Option B is Correct:** The pre-depolarization (pacemaker potential) occurs in two stages. While the initial phase is triggered by the "funny" sodium current ($I_f$), the **late stage of pre-depolarization** is specifically driven by the opening of **T-type (Transient) Calcium channels**. These channels allow $Ca^{2+}$ entry, pushing the membrane potential toward the threshold. Once the threshold is reached, **L-type (Long-lasting) Calcium channels** open, causing the actual depolarization (Phase 0). Therefore, $Ca^{2+}$ entry is the critical ion movement leading up to the action potential. **Why Other Options are Incorrect:** * **Option A:** $K^+$ entry would cause hyperpolarization, not depolarization. In the SA node, $K^+$ **efflux** is responsible for repolarization (Phase 3). * **Option C:** While $Na^+$ entry via $I_f$ channels starts the pacemaker potential, the question specifically targets the phase leading into the upstroke. In many competitive exams, the influx of Calcium is highlighted as the definitive trigger for reaching the threshold in nodal tissue. * **Option D:** $Cl^-$ efflux is not a significant contributor to the pacemaker potential in cardiac physiology. ### High-Yield Clinical Pearls for NEET-PG: * **Phase 0 in SA Node:** Driven by $Ca^{2+}$ influx (unlike ventricular muscle, which uses $Na^+$). * **Funny Current ($I_f$):** Activated by hyperpolarization; it is the target of the drug **Ivabradine**, used in chronic heart failure to reduce heart rate. * **Autonomic Control:** Acetylcholine increases $K^+$ conductance (hyperpolarization), slowing the heart rate, while Norepinephrine increases $Ca^{2+}$ and $I_f$ conductance, increasing the heart rate.

Question 262: After the application of a stimulus, a change in neuronal membrane potential occurs without the opening of gated ion channels. What is this change in membrane potential called?

A. Action potential
B. Local potential
C. Electrotonic potential (Correct Answer)
D. Resting potential

Explanation: ### Explanation The correct answer is **Electrotonic potential**. **1. Why Electrotonic Potential is Correct:** Electrotonic potentials (also known as passive potentials) are non-propagated local changes in membrane potential that occur due to the **passive physical properties** of the cell membrane. Unlike action potentials or graded local potentials, they do **not** involve the opening or closing of voltage-gated or ligand-gated ion channels. Instead, they result from the direct spread of electrical current through the membrane’s capacitance and resistance. These potentials are characterized by being **decremental** (fading with distance) and **graded** (proportional to stimulus intensity). **2. Why the Other Options are Incorrect:** * **Action Potential:** This is an "all-or-none" phenomenon that **requires** the opening of voltage-gated sodium and potassium channels once the threshold is reached. * **Local Potential (Graded Potential):** While similar to electrotonic potentials in being localized, local potentials (like EPSPs or receptor potentials) typically involve the opening of **ligand-gated or mechanical ion channels**. * **Resting Potential:** This is the static membrane potential (usually -70mV to -90mV) maintained when the neuron is not being stimulated, primarily by K+ leak channels and the Na+/K+ ATPase pump. **3. High-Yield NEET-PG Pearls:** * **Length Constant ($\lambda$):** The distance at which an electrotonic potential falls to 37% of its original value. Higher membrane resistance and lower internal resistance increase the length constant. * **Time Constant ($\tau$):** The time taken for the potential to reach 63% of its final value. * **Clinical Significance:** Electrotonic spread is crucial for **summation** (temporal and spatial) at the axon hillock. In myelinated neurons, the current spreads electrotonically between the Nodes of Ranvier (Saltatory conduction).

Question 263: A protein to lipid ratio on a weight basis of 1:1 is present in the membrane of which organelle?

A. Inner mitochondrial membrane
B. Myelin
C. Plasma membrane of human erythrocyte (Correct Answer)
D. Sarcoplasmic reticulum

Explanation: **Explanation:** The composition of biological membranes varies significantly depending on the specific function of the cell or organelle. The ratio of proteins to lipids is a reflection of the metabolic activity occurring within that membrane. **1. Why the Correct Answer is Right:** The **plasma membrane of a human erythrocyte (RBC)** contains approximately **52% protein, 40% lipid, and 8% carbohydrate** by weight. This results in a protein-to-lipid ratio of roughly **1:1** (or 1.2:1). This balance allows the RBC to maintain structural integrity while hosting essential transport proteins (like Band 3 and Glycophorin) and cytoskeletal anchors (like Spectrin) necessary for its unique biconcave shape and deformability. **2. Analysis of Incorrect Options:** * **Inner Mitochondrial Membrane:** This membrane is the site of the electron transport chain and is metabolically "heavy." It has the highest protein content (approx. **75-80%**), resulting in a ratio of **3:1**. * **Myelin:** Myelin acts as an electrical insulator for axons. To perform this function, it is rich in lipids (approx. 80%) and poor in proteins (approx. 20%), resulting in a ratio of **1:4**. * **Sarcoplasmic Reticulum:** This membrane is specialized for calcium sequestration and contains a very high density of calcium-ATPase pumps, typically resulting in a protein-to-lipid ratio higher than 1:1 (often closer to 2:1). **High-Yield Facts for NEET-PG:** * **Metabolic Rule:** The more metabolically active a membrane, the higher its protein content. * **Carbohydrates:** Always located on the **outer surface** of the plasma membrane (forming the glycocalyx); they are never found on the inner (cytosolic) leaflet. * **Cholesterol:** Present in plasma membranes but notably **absent** or very low in the inner mitochondrial membrane. * **Major RBC Proteins:** **Band 3** (Anion exchanger) and **Spectrin** (main peripheral protein maintaining shape). Defects in Spectrin lead to Hereditary Spherocytosis.

Question 264: What is the predominant determinant of the amplitude of the action potential?

A. Equilibrium potential of Na+
B. Equilibrium potential of K+
C. Equilibrium potential of Cl- (Correct Answer)
D. Equilibrium potential of HCO3-

Explanation: **Explanation:** The amplitude of an action potential is primarily determined by the **electrochemical gradient** of the ion responsible for the depolarization phase. In most excitable tissues (neurons and skeletal muscle), this is the sodium ion (Na+). **Why Option A is the Correct Concept (Note on Question Discrepancy):** In standard physiological teaching, the **Equilibrium Potential of Na+ ($E_{Na}$)** is the predominant determinant of action potential amplitude. During the rising phase, voltage-gated Na+ channels open, and the membrane potential moves toward the $E_{Na}$ (approx. +60 mV). The closer the peak of the action potential gets to $E_{Na}$, the greater the amplitude. *Note: If your source marks **Option C (Cl-)** as correct, it likely refers to specific inhibitory postsynaptic potentials (IPSPs) or specialized non-neuronal cells where chloride flux dominates. However, for a standard Action Potential, **Na+** is the gold standard answer.* **Analysis of Incorrect Options:** * **Equilibrium potential of K+ ($E_K$):** This primarily determines the **Resting Membrane Potential (RMP)** and the hyperpolarization phase, not the peak amplitude. * **Equilibrium potential of Cl-:** While Cl- influences the RMP and inhibitory signaling (via GABA receptors), it does not typically determine the depolarization amplitude of a standard action potential. * **Equilibrium potential of $HCO_3$-:** Bicarbonate ions play a role in pH buffering and some specialized neuronal signaling but are not primary determinants of action potential magnitude. **High-Yield NEET-PG Pearls:** 1. **Nernst Equation:** Used to calculate the equilibrium potential for a single ion. 2. **Goldman-Hodgkin-Katz Equation:** Determines the RMP by considering the permeability of all major ions (K+, Na+, Cl-). 3. **Tetrodotoxin (TTX):** Blocks voltage-gated Na+ channels, abolishing the action potential amplitude. 4. **Hypokalemia:** Lowers the RMP (makes it more negative), making it harder to reach the threshold for an action potential.

Question 265: Mitochondria possess which type of DNA?

A. Plasmid DNA
B. Circular DNA
C. Single-stranded DNA
D. Double-stranded circular DNA (Correct Answer)

Explanation: **Explanation:** Mitochondria are unique organelles often referred to as the "powerhouse of the cell." According to the **Endosymbiotic Theory**, mitochondria originated from ancient prokaryotes (proteobacteria) that entered into a symbiotic relationship with eukaryotic cells. Consequently, they possess their own independent genome, known as **mtDNA**. **Why Option D is correct:** Mitochondrial DNA (mtDNA) is a **double-stranded circular molecule**, closely resembling the genomic structure of bacteria. In humans, it consists of approximately 16,569 base pairs encoding 37 genes (13 proteins for the electron transport chain, 22 tRNAs, and 2 rRNAs). **Analysis of Incorrect Options:** * **A. Plasmid DNA:** While plasmids are circular DNA found in bacteria, they are extrachromosomal elements distinct from the primary bacterial genome. mtDNA represents the primary genome of the organelle. * **B. Circular DNA:** This is partially correct but incomplete. mtDNA is specifically double-stranded; "circular DNA" alone does not specify the strandedness. * **C. Single-stranded DNA:** mtDNA is double-stranded. Single-stranded DNA is typically found only in certain viruses (e.g., Parvovirus). **High-Yield Clinical Pearls for NEET-PG:** * **Maternal Inheritance:** Mitochondria are inherited exclusively from the mother (the sperm's mitochondria are tagged with ubiquitin and degraded in the zygote). * **Heteroplasmy:** This refers to the presence of a mixture of more than one type of organellar genome (normal and mutated mtDNA) within a single cell. This explains the variable clinical severity in mitochondrial diseases. * **High Mutation Rate:** mtDNA lacks histones and has limited repair mechanisms, making it 10 times more prone to mutations than nuclear DNA. * **Mitochondrial Diseases:** Common examples include **LHON** (Leber’s Hereditary Optic Neuropathy) and **MELAS** (Mitochondrial Encephalopathy, Lactic Acidosis, and Stroke-like episodes).

Question 266: Phospholipase C acts as a secondary messenger for which of the following hormones?

A. Follicle-Stimulating Hormone (FSH)
B. Inhibin
C. Thyroid-Stimulating Hormone (TSH)
D. Gonadotropin-Releasing Hormone (GnRH) (Correct Answer)

Explanation: **Explanation:** The correct answer is **Gonadotropin-Releasing Hormone (GnRH)**. Hormones act via specific signal transduction pathways. GnRH binds to G-protein coupled receptors (GPCRs) linked to the **Gq protein**. This activates the enzyme **Phospholipase C (PLC)**, which cleaves phosphatidylinositol 4,5-bisphosphate (PIP2) into two secondary messengers: **Inositol triphosphate (IP3)** and **Diacylglycerol (DAG)**. IP3 triggers the release of calcium from the endoplasmic reticulum, while DAG activates Protein Kinase C (PKC), leading to the secretion of LH and FSH. **Analysis of Incorrect Options:** * **FSH and TSH:** These are glycoprotein hormones that act via the **Gs protein-cAMP pathway**. Binding to their receptors activates Adenylyl Cyclase, which increases intracellular cAMP levels. * **Inhibin:** This is a member of the TGF-β superfamily. It acts through **Serine/Threonine kinase receptors** and the **SMAD** signaling pathway, rather than the PLC or cAMP systems. **High-Yield Clinical Pearls for NEET-PG:** * **Gq-PLC Pathway Mnemonic:** Remember **"GOAT HAG"** for hormones using the PLC/IP3 pathway: **G**nRH, **O**xytocin, **A**DH (V1 receptor), **T**RH, **H**istamine (H1), **A**ngiotensin II, and **G**astrin. * **Pulsatility:** GnRH must be secreted in a pulsatile manner to maintain receptor sensitivity. Continuous administration leads to "downregulation" of receptors, a principle used clinically in treating prostate cancer and endometriosis (GnRH analogues). * **V1 vs. V2:** ADH uses the PLC pathway for vasoconstriction (V1 receptor) but the cAMP pathway for water reabsorption in the kidney (V2 receptor).

Question 267: The resting membrane potential (RMP) of a nerve cell is equal to the equilibrium potential of which ion?

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

Explanation: **Explanation:** The Resting Membrane Potential (RMP) of a cell is determined by the permeability of the membrane to specific ions and their respective concentration gradients. **Why Cl- is the Correct Answer:** In many neurons, chloride ions ($Cl^-$) are **passively distributed** across the cell membrane. This means there is no active transport mechanism (like a pump) moving chloride against its gradient. Consequently, $Cl^-$ shifts across the membrane until it reaches an equilibrium where the electrical gradient perfectly balances the chemical gradient. Therefore, the equilibrium potential ($E_{Cl}$) often aligns exactly with the RMP (typically -70 mV to -90 mV). **Analysis of Incorrect Options:** * **K+ (Potassium):** While the RMP is *closest* to the equilibrium potential of $K^+$ (approx. -94 mV) because the membrane is highly permeable to it, they are not equal. The slight influx of $Na^+$ prevents the RMP from reaching the full $E_K$. * **Na+ (Sodium):** The equilibrium potential for $Na^+$ is positive (approx. +60 mV). At rest, the membrane has very low permeability to $Na^+$, so the RMP stays far from this value. * **Ca2+ (Calcium):** Similar to sodium, $Ca^{2+}$ has a positive equilibrium potential and very low resting permeability; it does not determine the RMP. **High-Yield Clinical Pearls for NEET-PG:** * **Goldman-Hodgkin-Katz Equation:** This equation calculates the RMP by considering the permeability and concentration of all major ions ($Na^+$, $K^+$, $Cl^-$). * **Nernst Equation:** Used to calculate the equilibrium potential for a *single* ion. * **The Na+-K+ ATPase Pump:** This is "electrogenic" and contributes about -5 to -10 mV directly to the RMP, but its primary role is maintaining the concentration gradients that allow the RMP to exist. * **Key Concept:** If an ion is distributed purely passively, its equilibrium potential **must** equal the RMP.

Question 268: What is the main component of the thin filament?

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

Explanation: **Explanation:** The sarcomere, the functional unit of skeletal muscle, is composed of thick and thin filaments. The **thin filament** is primarily composed of three proteins: **Actin**, Tropomyosin, and Troponin. 1. **Why Actin is correct:** **G-actin (globular actin)** polymerizes to form **F-actin (filamentous actin)**, which serves as the structural backbone of the thin filament. Two strands of F-actin twist into a double helix. It contains the specific binding sites for myosin heads during the cross-bridge cycle. Because it forms the primary structural mass of the filament, it is considered the "main" component. 2. **Why other options are incorrect:** * **Myosin:** This is the primary component of the **thick filament**. It is a motor protein with a head (ATPase activity) and a tail. * **Tropomyosin:** While present in the thin filament, it is a regulatory protein. It wraps around the actin helix to cover the myosin-binding sites during rest. * **Dystrophin:** This is a structural protein located just beneath the sarcolemma. It links the actin cytoskeleton to the extracellular matrix; it is not a component of the thin filament itself. **High-Yield Clinical Pearls for NEET-PG:** * **Troponin Complex:** Consists of **Troponin T** (binds to tropomyosin), **Troponin I** (inhibits actin-myosin binding), and **Troponin C** (binds Calcium). * **Duchenne Muscular Dystrophy (DMD):** Caused by a mutation/absence of the **Dystrophin** protein, leading to muscle fiber fragility. * **Z-line:** Defines the boundaries of a sarcomere; actin filaments are anchored here by **α-actinin**. * **H-zone:** The central part of the thick filament where there is no actin overlap.

Question 269: What is the first step for lymphatic vessels to remove excess fluid from interstitial tissue spaces?

A. Generating a lower intravascular than tissue hydrostatic pressure (Correct Answer)
B. Contracting and forcing lymph into larger lymphatics
C. Opening and closing one-way valves in the lymph vessels
D. Lowering the colloid osmotic pressure inside the lymph vessel

Explanation: ### Explanation **Correct Answer: A. Generating a lower intravascular than tissue hydrostatic pressure** The movement of fluid from the interstitium into the lymphatic system follows the basic laws of bulk flow driven by a **pressure gradient**. For fluid to enter the initial lymphatic capillaries, the **interstitial fluid pressure must be higher than the intraluminal (intravascular) pressure** of the lymphatic vessel. The initial lymphatics are composed of endothelial cells attached to surrounding connective tissue by **anchoring filaments**. When excess fluid accumulates in the tissue, it causes the tissue to swell, pulling on these anchoring filaments. This physical pull holds the lymphatic vessel open, maintaining a very low internal pressure (often slightly negative or near zero). This creates a pressure gradient that "sucks" or pushes the interstitial fluid into the lymphatic capillary through the gaps between endothelial cells. **Why other options are incorrect:** * **Option B:** Contraction of lymphatic segments (lymphangions) occurs *after* the fluid has already entered the vessel to propel it forward; it is not the "first step" of entry. * **Option C:** One-way valves (semilunar valves) prevent backflow within the larger vessels, but they do not initiate the primary movement of fluid from the tissue into the capillary. * **Option D:** Colloid osmotic pressure (oncotic pressure) inside lymphatics is actually relatively high because lymph contains proteins. Lowering it would technically decrease the osmotic pull into the vessel, which is counterproductive to fluid removal. **High-Yield NEET-PG Pearls:** * **Anchoring Filaments:** These are unique to initial lymphatics and prevent the collapse of vessels during high interstitial pressure. * **Lymphatic Pump:** Once inside, lymph is moved by the "intrinsic pump" (myogenic contraction of smooth muscle) and "extrinsic pump" (skeletal muscle contraction and respiratory movements). * **Edema Safety Factor:** The lymphatic system can increase its flow rate by up to **20-fold** to prevent edema when interstitial pressure rises. * **Protein Transport:** The lymphatic system is the *only* route by which high-molecular-weight proteins can be removed from interstitial spaces.

Question 270: Which of the following is a ligand-gated ionic channel?

A. VIP receptor
B. GABAA receptor (Correct Answer)
C. Norepinephrine receptor
D. GABAB receptor

Explanation: **Explanation:** The core concept tested here is the classification of membrane receptors into **Ionotropic** (ligand-gated ion channels) and **Metabotropic** (G-protein coupled receptors). **Why GABAA is correct:** The **GABA$_A$ receptor** is a classic example of an **ionotropic receptor**. It is a pentameric transmembrane protein that functions as a **ligand-gated chloride (Cl⁻) channel**. When GABA binds to it, the channel opens, allowing chloride ions to enter the cell, causing hyperpolarization and resulting in fast inhibitory postsynaptic potentials (IPSPs). **Why the other options are incorrect:** * **GABA$_B$ receptor:** Unlike GABA$_A$, this is a **metabotropic receptor** (GPCR). It acts via G-proteins to either open K⁺ channels or close Ca²⁺ channels, mediating slow, prolonged inhibition. * **VIP receptor:** Receptors for Vasoactive Intestinal Peptide (VIP) are **G-protein coupled receptors** (typically linked to the Gs-adenylyl cyclase pathway). * **Norepinephrine receptor:** All adrenergic receptors ($\alpha$ and $\beta$) are **GPCRs**. They act through second messengers like cAMP or IP$_3$/DAG, not by direct gating of an ion channel. **High-Yield Clinical Pearls for NEET-PG:** * **GABA$_A$ Pharmacology:** This receptor is the target for **Benzodiazepines** (increase frequency of channel opening) and **Barbiturates** (increase duration of channel opening). * **Other Ionotropic Receptors:** Nicotinic ACh receptors, NMDA, AMPA, Kainate (Glutamate), and 5-HT$_3$ (Serotonin) receptors. * **Mnemonic:** All 5-HT receptors are GPCRs **except 5-HT$_3$** (Ionotropic). All GABA receptors are GPCRs **except GABA$_A$** (Ionotropic).

Practice by Chapter

Cell Structure and Function

Practice Questions

Membrane Transport Mechanisms

Practice Questions

Bioelectric Phenomena

Practice Questions

Homeostasis and Feedback Mechanisms

Practice Questions

Body Fluid Compartments

Practice Questions

Signal Transduction Mechanisms

Practice Questions

Cell-to-Cell Communication

Practice Questions

Principles of Physiological Measurement

Practice Questions

Osmosis and Osmotic Pressure

Practice Questions

Physiological Adaptation Mechanisms

Practice Questions

Want unlimited practice?

Get full access to all questions, explanations, and performance tracking.

Start For Free