Cellular Physiology — MCQs

Cellular Physiology Indian Medical PG Practice Questions and MCQs

Question 181: Which of the following is NOT a cell adhesion protein?

A. Anchorin (Correct Answer)
B. Integrin
C. Selectins
D. Cadherin

Explanation: **Explanation:** Cell adhesion molecules (CAMs) are specialized transmembrane proteins that facilitate cell-to-cell and cell-to-matrix interactions. They are categorized into four major families: Integrins, Cadherins, Selectins, and the Immunoglobulin superfamily. **Why Anchorin is the correct answer:** **Anchorin** (specifically Anchorin CII, also known as Annexin V) is not a cell adhesion protein. It is a collagen-binding protein found on the surface of chondrocytes that interacts with Type II collagen. While it mediates binding to the extracellular matrix, it lacks the structural characteristics and classification of the primary CAM families. In some contexts, "Ankyrin" (a similar-sounding protein) is also a common distractor; Ankyrin is a peripheral membrane protein that links the cytoskeleton to integral membrane proteins, not an adhesion molecule itself. **Analysis of incorrect options:** * **Integrins:** These are heterodimeric receptors (alpha and beta subunits) that primarily mediate **cell-matrix** adhesion (e.g., binding to fibronectin or laminin) and link the ECM to the actin cytoskeleton. * **Selectins:** These are calcium-dependent glycoproteins that mediate **transient** cell-cell adhesion. They are crucial for the "rolling" phase of leukocyte extravasation. * **Cadherins:** These are calcium-dependent homophilic adhesion molecules (e.g., E-cadherin) that maintain structural integrity by forming **adherens junctions** and desmosomes. **High-Yield Clinical Pearls for NEET-PG:** * **Pemphigus Vulgaris:** Antibodies against **Desmoglein** (a Cadherin) lead to loss of cell-cell adhesion (acantholysis). * **LAD Type 1:** Caused by a deficiency of **Integrins** (CD18), leading to impaired leukocyte adhesion and delayed umbilical cord separation. * **LAD Type 2:** Caused by a defect in **Selectin** ligands (Sialyl-Lewis X). * **Cancer Metastasis:** Often involves the "downregulation" of **E-cadherin**, allowing tumor cells to detach and migrate.

Question 182: Which of the following causes an increase in intracellular cAMP?

A. Somatostatin
B. Beta receptor activation (Correct Answer)
C. Alpha receptor activation
D. Acetylcholine

Explanation: ### Explanation The concentration of intracellular cyclic Adenosine Monophosphate (cAMP) is regulated by the **G-protein coupled receptor (GPCR)** signaling pathway. **1. Why Beta receptor activation is correct:** Beta-adrenergic receptors ($\beta_1, \beta_2, \beta_3$) are coupled to **Gs (stimulatory) proteins**. When a ligand (like epinephrine) binds, the Gs alpha subunit activates the enzyme **Adenylate Cyclase**, which catalyzes the conversion of ATP into **cAMP**. Increased cAMP then activates Protein Kinase A (PKA) to mediate cellular effects like increased heart rate or bronchodilation. **2. Why the other options are incorrect:** * **Somatostatin:** Acts via **Gi (inhibitory) proteins**. Activation of Gi inhibits Adenylate Cyclase, leading to a **decrease** in intracellular cAMP levels. * **Alpha receptor activation:** * $\alpha_2$ receptors are coupled to **Gi**, which **decreases** cAMP. * $\alpha_1$ receptors are coupled to **Gq**, which activates Phospholipase C (PLC) to increase $IP_3/DAG$ and Calcium, not cAMP. * **Acetylcholine:** * At **$M_2$ receptors** (heart), it acts via **Gi** to **decrease** cAMP. * At **$M_1/M_3$ receptors**, it acts via **Gq** ($IP_3/DAG$ pathway). **Clinical Pearls for NEET-PG:** * **Gs-coupled (Increase cAMP):** Beta receptors, Glucagon, TSH, ACTH, PTH, Vasopressin ($V_2$). * **Gi-coupled (Decrease cAMP):** $\alpha_2$, $M_2$, Somatostatin, Dopamine ($D_2$). * **Gq-coupled ($IP_3/DAG$):** $\alpha_1$, $M_1$, $M_3$, Vasopressin ($V_1$), Oxytocin. * **Phosphodiesterase (PDE) inhibitors** (e.g., Theophylline, Sildenafil) increase cAMP/cGMP by preventing their breakdown.

Question 183: Which one of the following does NOT primarily involve the action of K+ channels?

A. Hypoxic Pulmonary Vasoconstriction
B. Insulin secretion by Sulfonylurea
C. Carotid body discharge with reduced O2
D. Dantrolene in the treatment of Malignant Hyperthermia (Correct Answer)

Explanation: **Explanation:** The correct answer is **Dantrolene in the treatment of Malignant Hyperthermia**, as its mechanism of action involves Calcium (Ca²⁺) signaling rather than Potassium (K⁺) channels. **1. Why Option D is Correct:** Malignant Hyperthermia is caused by a mutation in the **Ryanodine Receptor (RyR1)** in the sarcoplasmic reticulum of skeletal muscle. This leads to excessive Ca²⁺ release, causing sustained muscle contraction and hypermetabolism. **Dantrolene** acts by binding to the RyR1 receptor, inhibiting the release of Ca²⁺. It has no direct primary action on K⁺ channels. **2. Why the other options are incorrect:** * **Hypoxic Pulmonary Vasoconstriction (HPV):** Hypoxia inhibits **Voltage-gated K⁺ channels** in pulmonary artery smooth muscle cells. This leads to depolarization, opening of L-type Ca²⁺ channels, and subsequent vasoconstriction to shunt blood to better-ventilated areas. * **Insulin secretion by Sulfonylureas:** Sulfonylureas bind to the SUR1 subunit of **ATP-sensitive K⁺ (Kₐₜₚ) channels** in pancreatic beta cells, closing them. This causes depolarization, Ca²⁺ influx, and insulin exocytosis. * **Carotid body discharge:** In response to low PO₂, **O₂-sensitive K⁺ channels** in Type I (glomus) cells close. The resulting depolarization triggers neurotransmitter release, stimulating the glossopharyngeal nerve to increase ventilation. **Clinical Pearls for NEET-PG:** * **Malignant Hyperthermia triggers:** Volatile anesthetics (e.g., Halothane) and Succinylcholine. * **Kₐₜₚ Channels:** These are the "metabolic sensors" of the cell; they close when the ATP/ADP ratio increases. * **Dantrolene** is also used in **Neuroleptic Malignant Syndrome (NMS)**, though its primary indication remains Malignant Hyperthermia.

Question 184: Increase in cytosolic calcium from intracellular storage during smooth muscle contraction is due to?

A. Cyclic adenosine monophosphate (cAMP)
B. Cyclic guanosine monophosphate (cGMP)
C. Cyclic cytidine monophosphate (cCMP)
D. Inositol trisphosphate (IP3) and diacylglycerol (DAG) (Correct Answer)

Explanation: **Explanation:** The correct answer is **D. Inositol trisphosphate (IP3) and diacylglycerol (DAG)**. In smooth muscle, contraction is initiated by an increase in cytosolic calcium ($Ca^{2+}$). While some calcium enters via voltage-gated channels, a significant portion is released from the **Sarcoplasmic Reticulum (SR)**—the primary intracellular storage site. This process is mediated by the **Gq-protein coupled receptor (GPCR) pathway**: 1. A ligand (e.g., Norepinephrine, Acetylcholine) binds to a Gq-coupled receptor. 2. This activates **Phospholipase C (PLC)**, which cleaves membrane-bound PIP2 into **IP3** and **DAG**. 3. **IP3** binds to specific IP3-gated calcium release channels on the SR membrane, triggering the efflux of $Ca^{2+}$ into the cytosol. 4. **DAG** activates Protein Kinase C (PKC), which further modulates contractile proteins. **Why the other options are incorrect:** * **A. cAMP:** Generally promotes **smooth muscle relaxation** (e.g., via $\beta_2$ receptors) by inhibiting Myosin Light Chain Kinase (MLCK) and stimulating calcium sequestration back into the SR. * **B. cGMP:** Acts as a second messenger for Nitric Oxide (NO) and Atrial Natriuretic Peptide (ANP). It causes **vasodilation/relaxation** by activating Protein Kinase G (PKG), which dephosphorylates Myosin Light Chains. * **C. cCMP:** This is a minor signaling molecule and does not play a primary role in the standard excitation-contraction coupling of smooth muscle. **High-Yield NEET-PG Pearls:** * **Calmodulin:** Unlike skeletal muscle (which uses Troponin C), smooth muscle $Ca^{2+}$ binds to **Calmodulin** to activate MLCK. * **L-type Calcium Channels:** These are the targets of Calcium Channel Blockers (CCBs) like Nifedipine. * **Pharmacomechanical Coupling:** The ability of IP3 to cause contraction without a change in membrane potential is a unique feature of smooth muscle.

Question 185: Which of the following steps is known as the gateway to the cell cycle?

A. G0 to G1 transition (Correct Answer)
B. G1 to S transition
C. S to G2 transition
D. G2 to M transition

Explanation: ### Explanation The cell cycle is a highly regulated process that determines whether a cell remains quiescent or undergoes division. **Why G0 to G1 is the Correct Answer:** The **G0 to G1 transition** is known as the **"Gateway to the Cell Cycle"** because it represents the point where a quiescent (resting) cell re-enters the active proliferative state. Cells in G0 are metabolically active but are not dividing. The transition into G1 is triggered by external stimuli such as **growth factors** and mitogens. Once a cell moves from G0 into G1, it has officially committed to leaving its resting state to prepare for DNA synthesis. **Analysis of Incorrect Options:** * **G1 to S transition:** This is known as the **Restriction Point (R-point)** or the "Point of No Return." Once a cell passes this stage, it is committed to DNA replication regardless of whether growth factors are removed. While critical, it is a checkpoint *within* the cycle, not the gateway *into* it. * **S to G2 transition:** This stage involves the completion of DNA replication and the beginning of protein synthesis for mitosis. It is a progression phase, not a regulatory gateway. * **G2 to M transition:** This is the final major checkpoint where the cell ensures DNA is fully replicated and undamaged before entering mitosis (M phase), regulated primarily by **Cyclin B-CDK1** (Maturation Promoting Factor). **NEET-PG High-Yield Pearls:** * **G0 Phase:** Also called the quiescent stage. Neurons and skeletal muscle cells stay in G0 permanently (permanent cells), while hepatocytes are stable cells that can re-enter G1 when stimulated. * **Cyclin-CDK Complexes:** The G1/S transition is regulated by **Cyclin D-CDK4/6**, while the G2/M transition is regulated by **Cyclin B-CDK1**. * **p53 Protein:** Known as the "Guardian of the Genome," it primarily acts at the G1/S checkpoint to arrest the cycle if DNA damage is detected.

Question 186: What is the important function of cytosolic cytochrome C?

A. Apoptosis (Correct Answer)
B. Cell necrosis
C. Electron transport chain
D. Cell division

Explanation: ### Explanation **Correct Answer: A. Apoptosis** Cytochrome C is a peripheral membrane protein typically located in the inner mitochondrial membrane. Its presence in the **cytosol** is a hallmark of the **intrinsic (mitochondrial) pathway of apoptosis**. When a cell undergoes stress (DNA damage, oxidative stress, or withdrawal of growth factors), the pro-apoptotic proteins **BAX and BAK** create pores in the mitochondrial outer membrane. This leads to the leakage of Cytochrome C into the cytosol. Once in the cytosol, Cytochrome C binds to **Apaf-1** (Apoptotic protease activating factor-1) and ATP to form a wheel-like complex called the **Apoptosome**. This complex activates **Caspase-9**, triggering a proteolytic cascade that leads to programmed cell death. **Why other options are incorrect:** * **B. Cell Necrosis:** Necrosis is an uncontrolled, accidental cell death characterized by cell swelling and membrane rupture. It is not mediated by the specific Cytochrome C/Caspase pathway. * **C. Electron Transport Chain (ETC):** While Cytochrome C is vital for the ETC (shuttling electrons between Complex III and IV), this function occurs strictly **within the mitochondria**, not the cytosol. The question specifically asks for the *cytosolic* function. * **D. Cell Division:** Cytochrome C has no direct regulatory role in mitosis or the cell cycle. **High-Yield Clinical Pearls for NEET-PG:** * **The "Point of No Return":** The release of Cytochrome C into the cytosol is considered the irreversible step in the intrinsic pathway of apoptosis. * **Bcl-2 Family:** Remember that **Bcl-2 and Bcl-xL** are anti-apoptotic (they prevent Cytochrome C release), while **BAX and BAK** are pro-apoptotic. * **Caspase Cascade:** Intrinsic pathway = Caspase **9**; Extrinsic (Death Receptor) pathway = Caspase **8**. Both converge on executioner Caspases **3 and 6**.

Question 187: During which phase of the cell cycle does DNA synthesis occur?

A. G1
B. G2
C. S (Correct Answer)
D. M

Explanation: **Explanation:** The cell cycle is a highly regulated sequence of events leading to cell division. The correct answer is **S phase (Synthesis phase)**. **Why S Phase is Correct:** The S phase is the specific period during interphase when **DNA replication** occurs. During this phase, the DNA content of the cell doubles (from 2n to 4n), ensuring that each daughter cell receives a complete set of chromosomes. This process involves the unwinding of the double helix and the synthesis of new complementary strands by DNA polymerase. **Analysis of Incorrect Options:** * **G1 (Gap 1):** This is the pre-synthetic phase. The cell grows in size and synthesizes RNA and proteins required for DNA replication, but the DNA content remains constant. * **G2 (Gap 2):** This is the post-synthetic phase. The cell prepares for mitosis by synthesizing tubulin for spindle fibers and checking for DNA errors. DNA synthesis has already been completed. * **M (Mitosis):** This is the actual phase of nuclear and cytoplasmic division. Chromosomes are distributed to daughter cells, but no new DNA is synthesized here. **High-Yield NEET-PG Pearls:** 1. **Duration:** The S phase typically lasts about 8–10 hours in human cells, making it a significant portion of the cell cycle. 2. **Centrioles:** In addition to DNA, the **centrioles** also replicate during the S phase in the cytoplasm. 3. **G0 Phase:** Cells that cease dividing (like neurons or mature muscle cells) exit the cycle at G1 to enter a quiescent state called G0. 4. **Regulation:** The transition from G1 to S is the most critical checkpoint (Restriction point), regulated by **Cyclin D-CDK4/6** complexes.

Question 188: Which factor favors transport across a cell membrane?

A. Polar substance
B. High concentration gradient (Correct Answer)
C. Thick membrane
D. Large particle size

Explanation: ### Explanation The transport of substances across a cell membrane is governed primarily by **Fick’s Law of Diffusion**. This law states that the rate of net diffusion is directly proportional to the concentration gradient, the surface area of the membrane, and the lipid solubility of the substance, while being inversely proportional to the membrane thickness and molecular weight. **1. Why "High concentration gradient" is correct:** Diffusion is a passive process driven by the potential energy difference between two points. A **high concentration gradient** (the difference in solute concentration between the intracellular and extracellular fluid) provides a stronger driving force, thereby increasing the rate of transport across the membrane. **2. Why the other options are incorrect:** * **Polar substance:** The cell membrane is a lipid bilayer with a hydrophobic core. Polar (water-soluble) substances have low lipid solubility and cannot easily cross the membrane without specific transport proteins. Non-polar (lipid-soluble) substances cross more easily. * **Thick membrane:** According to Fick’s Law, the rate of diffusion is inversely proportional to the distance (thickness). A thicker membrane increases the resistance, thereby slowing down transport. * **Large particle size:** Smaller molecules diffuse more rapidly than larger ones. Large particles often require specialized mechanisms like facilitated diffusion or vesicular transport (endocytosis/exocytosis). **High-Yield Clinical Pearls for NEET-PG:** * **Fick’s Law Formula:** $J = -DA (ΔC/ΔX)$ (where $J$ is flux, $D$ is diffusion coefficient, $A$ is area, and $ΔC/ΔX$ is the concentration gradient over distance). * **Permeability:** Lipid solubility is the most important determinant of the diffusion coefficient for a substance. * **Clinical Correlation:** In **Pulmonary Edema** or **Interstitial Lung Disease**, the "thickness" of the respiratory membrane increases, which decreases the diffusion of oxygen, leading to hypoxemia.

Question 189: Which of the following ions is least diffusible?

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

Explanation: **Explanation:** The diffusibility of an ion across a cell membrane depends on its **permeability**, which is determined by the presence of specific leak channels and the size of the ion’s **hydration shell**. **1. Why Na+ is the correct answer:** Although the sodium ion ($Na^+$) is physically smaller than the potassium ion ($K^+$), it has a much higher **charge density**. This causes it to attract a larger shell of water molecules (hydration shell). This large hydrated radius, combined with a **very low density of sodium leak channels** in the resting membrane, makes $Na^+$ the least diffusible among the options. In a resting state, the membrane is roughly 50–100 times less permeable to $Na^+$ than to $K^+$. **2. Analysis of Incorrect Options:** * **K+ (Potassium):** The resting cell membrane is highly permeable to $K^+$ due to the abundance of **K+ leak channels**. It is the most diffusible cation and is the primary determinant of the Resting Membrane Potential (RMP). * **Cl- (Chloride):** Many cells have high permeability to $Cl^-$, and it can diffuse relatively easily through specific channels to follow electrochemical gradients. * **Urea:** Urea is a small, uncharged polar molecule. While it is slower than water, it can cross the lipid bilayer via simple diffusion or through specialized transporters (UT-A), making it significantly more diffusible than the charged $Na^+$ ion. **High-Yield Clinical Pearls for NEET-PG:** * **Relative Permeability:** $K^+ > Cl^- > Na^+$. * **Gibbs-Donnan Effect:** Large intracellular anions (proteins) are non-diffusible, leading to the unequal distribution of diffusible ions. * **RMP Calculation:** The **Goldman-Hodgkin-Katz equation** is used instead of the Nernst equation when considering the permeability of multiple ions ($K^+$, $Na^+$, and $Cl^-$). * **Hydration Rule:** Smaller ions (like $Na^+$) have larger hydration shells than larger ions (like $K^+$), making the hydrated $Na^+$ physically bulkier.

Question 190: Which molecule is most permeable to a pure phospholipid bilayer?

A. O2 (Correct Answer)
B. Na+
C. H2O
D. Cl-

Explanation: **Explanation:** The permeability of a molecule through a pure phospholipid bilayer is determined by its **size, charge, and lipid solubility (hydrophobicity)**. The cell membrane is a semi-permeable lipid barrier that favors the passage of non-polar, uncharged substances. **1. Why O2 is Correct:** Oxygen (O2) is a small, non-polar, and highly lipid-soluble gas. According to **Fick’s Law of Diffusion**, such molecules can dissolve directly into the hydrophobic fatty acid tails of the phospholipid bilayer and diffuse rapidly. Other gases like CO2 and N2 follow the same principle. **2. Why the others are Incorrect:** * **Na+ and Cl- (Options B & D):** These are small ions, but they carry a **net charge**. Charged particles are surrounded by a hydration shell and are strongly repelled by the hydrophobic core of the membrane. They require specific transmembrane proteins (channels or pumps) to cross. * **H2O (Option C):** Water is a small, uncharged molecule, but it is **polar**. While it can leak through the membrane slowly via simple diffusion, its permeability is significantly lower than that of dissolved gases. In physiological systems, water primarily moves through specialized channels called **Aquaporins**. **High-Yield Facts for NEET-PG:** * **Permeability Hierarchy:** Hydrophobic molecules (O2, CO2, Steroids) > Small uncharged polar molecules (H2O, Urea) > Large uncharged polar molecules (Glucose) > Ions (Na+, K+, Cl-). * **Lipid Solubility:** This is the single most important factor determining the rate of simple diffusion (measured by the oil-water partition coefficient). * **Clinical Pearl:** General anesthetics (like Halothane) work on the principle of high lipid solubility (Meyer-Overton theory) to cross the blood-brain barrier and cell membranes rapidly.

Practice by Chapter

Cell Membrane Structure and Function

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Membrane Transport Proteins

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Cellular Energetics and Metabolism

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Mitochondrial Function

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Cell Volume Regulation

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Cellular Responses to Stress

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Calcium Signaling

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Cell Cycle and Regulation

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Cellular Aging

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Apoptosis and Cell Death

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