General Physiology Practice Questions

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

Ca++ entry. ### 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.

Q: 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?

Electrotonic potential. ### 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).

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

Gonadotropin-Releasing Hormone (GnRH). **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).

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

Cl-. **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.

Q: What is the main component of the thin filament?

Actin. **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.

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

GABAA receptor. **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).

Question 1

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

Accepted Answer

Ca++ entry

Answer

K+ entry

Answer

Na+ entry towards the end of repolarization

Answer

Cl- efflux

Question 2

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?

Accepted Answer

Electrotonic potential

Answer

Action potential

Answer

Local potential

Answer

Resting potential

Question 3

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

Accepted Answer

Plasma membrane of human erythrocyte

Answer

Inner mitochondrial membrane

Answer

Myelin

Answer

Sarcoplasmic reticulum

Question 4

What is the predominant determinant of the amplitude of the action potential?

Accepted Answer

Equilibrium potential of Cl-

Answer

Equilibrium potential of Na+

Answer

Equilibrium potential of K+

Answer

Equilibrium potential of HCO3-

Question 5

Mitochondria possess which type of DNA?

Accepted Answer

Double-stranded circular DNA

Answer

Plasmid DNA

Answer

Circular DNA

Answer

Single-stranded DNA

Question 6

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

Accepted Answer

Gonadotropin-Releasing Hormone (GnRH)

Answer

Follicle-Stimulating Hormone (FSH)

Answer

Inhibin

Answer

Thyroid-Stimulating Hormone (TSH)

Question 7

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

Accepted Answer

Cl-

Answer

K+

Answer

Na+

Answer

Ca+

Question 8

What is the main component of the thin filament?

Accepted Answer

Actin

Answer

Myosin

Answer

Tropomyosin

Answer

Dystrophin

Question 9

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

Accepted Answer

Generating a lower intravascular than tissue hydrostatic pressure

Answer

Contracting and forcing lymph into larger lymphatics

Answer

Opening and closing one-way valves in the lymph vessels

Answer

Lowering the colloid osmotic pressure inside the lymph vessel

Question 10

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

Accepted Answer

GABAA receptor

Answer

VIP receptor

Answer

Norepinephrine receptor

Answer

GABAB receptor

General Physiology — MCQs

General Physiology — MCQs

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