Cellular Physiology — MCQs

Cellular Physiology Indian Medical PG Practice Questions and MCQs

Question 291: Which cellular mechanism is predominantly affected by hyperkalemia?

A. Membrane depolarization (Correct Answer)
B. Membrane hyperpolarization
C. Intracellular protein synthesis
D. Cellular osmolarity

Explanation: ***Membrane depolarization*** - **Hyperkalemia** primarily causes the resting membrane potential to become less negative, moving it closer to the threshold for an action potential. - This initial depolarization can lead to **increased excitability** of nerve and muscle cells, followed by persistent depolarization that inactivates voltage-gated sodium channels, leading to inexcitability. *Membrane hyperpolarization* - **Hyperpolarization** means the membrane potential becomes more negative, moving further away from the threshold for an action potential. - This effect is typically associated with conditions like **hypokalemia**, where a lower extracellular potassium concentration makes it harder for cells to depolarize. *Intracellular protein synthesis* - **Intracellular protein synthesis** is a complex process involving ribosomes and various RNA molecules. - While electrolyte imbalances can indirectly affect cellular metabolism, **hyperkalemia** does not directly or predominantly impair protein synthesis as its primary mechanism of action. *Cellular osmolarity* - **Cellular osmolarity** is primarily regulated by major solutes like sodium, chloride, and impermeable organic molecules within the cell. - Although potassium is a key intracellular ion, changes in extracellular potassium concentration in **hyperkalemia** do not predominantly or directly alter overall cellular osmolarity to the extent seen with dysnatremias.

Question 292: How does the activation of phospholipase C by GPCRs affect intracellular calcium levels?

A. Activates adenylyl cyclase, increases cAMP
B. Produces IP3 and DAG, increases Ca2+ (Correct Answer)
C. Inhibits guanylyl cyclase, decreases cGMP
D. Activates phosphodiesterase, decreases cAMP

Explanation: ***Produces IP3 and DAG, increases Ca2+*** - Activation of **phospholipase C (PLC)** by GPCRs leads to the hydrolysis of **PIP2 (phosphatidylinositol 4,5-bisphosphate)** into two secondary messengers: **inositol triphosphate (IP3)** and **diacylglycerol (DAG)**. - **IP3** then binds to receptors on the **endoplasmic reticulum**, triggering the release of stored **calcium (Ca2+)** into the cytoplasm, thus increasing intracellular calcium levels. *Activates adenylyl cyclase, increases cAMP* - This describes the **Gαs pathway** of GPCR signaling, where the activated G protein stimulates **adenylyl cyclase** to convert ATP into **cyclic AMP (cAMP)**. - This pathway is distinct from the **Gαq pathway** which activates phospholipase C, and it primarily affects protein phosphorylation rather than direct calcium release. *Inhibits guanylyl cyclase, decreases cGMP* - This pathway involves **cGMP (cyclic GMP)**, which is typically produced by **guanylyl cyclase** and is often associated with nitric oxide signaling or specific GPCRs in photoreceptors. - It is not directly involved in the primary mechanism by which **PLC** activation influences intracellular calcium. *Activates phosphodiesterase, decreases cAMP* - This describes the action of the **Gαi pathway**, where activated G proteins can **inhibit adenylyl cyclase** or activate phosphodiesterases to break down **cAMP**. - While this pathway influences **cAMP levels**, it does not directly lead to the production of **IP3** and the release of **intracellular calcium** that is characteristic of PLC activation.

Question 293: Why is the S phase of the cell cycle MORE sensitive to radiation compared to the G1 phase?

A. Lower metabolic activity
B. Chromatin condensation state
C. Cell cycle checkpoint efficiency
D. Increased DNA replication activity (Correct Answer)

Explanation: ***Increased DNA replication activity*** - During the **S phase**, the cell is actively replicating its **DNA**, which makes it highly vulnerable to radiation damage. - The DNA strands are **unwound and exposed** at replication forks, creating single-stranded regions that are more susceptible to radiation-induced breaks and damage. - The active **DNA synthesis machinery** means any radiation-induced lesions can be directly incorporated into newly synthesized DNA strands, leading to mutations or chromosomal aberrations. - The presence of multiple **replication forks** throughout the genome provides numerous vulnerable targets for ionizing radiation. *Lower metabolic activity* - This is incorrect because **S phase** actually has *high metabolic activity* to support extensive DNA synthesis, nucleotide production, and histone synthesis. - Lower metabolic activity would not explain increased radiosensitivity; in fact, metabolically active phases tend to be more vulnerable to various insults. *Chromatin condensation state* - While chromatin is indeed **less condensed** in S phase (especially at replication origins), this is a contributing factor but not the primary reason for radiosensitivity. - The key issue is not just accessibility but the **active replication process itself**, where DNA damage can be propagated during synthesis. *Cell cycle checkpoint efficiency* - **Checkpoint efficiency** is a protective mechanism, not a cause of increased sensitivity. - S phase does have checkpoints (intra-S checkpoint), but their presence doesn't explain why this phase is inherently more vulnerable to radiation. - The increased sensitivity stems from the **biological vulnerability during active DNA replication**, independent of checkpoint function.

Question 294: Which of the following second messengers is involved in the pathway activated by beta-adrenergic receptors?

A. cAMP (Correct Answer)
B. cGMP
C. IP3
D. DAG

Explanation: ***Correct: cAMP*** - Beta-adrenergic receptors are **G-protein-coupled receptors (GPCRs)** that, when activated, stimulate **adenylyl cyclase** through a stimulatory G-protein (Gs). - Adenylyl cyclase then catalyzes the conversion of **ATP to cyclic AMP (cAMP)**, which acts as a second messenger in the cell. *Incorrect: cGMP* - **cGMP (cyclic guanosine monophosphate)** is typically associated with the signaling pathways of **nitric oxide** and **natriuretic peptides**, which activate guanylyl cyclase. - It is not directly produced as a second messenger in the classical beta-adrenergic receptor pathway. *Incorrect: IP3* - **IP3 (inositol trisphosphate)** is a second messenger produced by the cleavage of **PIP2 (phosphatidylinositol 4,5-bisphosphate)** by phospholipase C, often activated by **Gq-coupled receptors**. - This pathway leads to the release of **intracellular calcium**, distinct from the beta-adrenergic pathway. *Incorrect: DAG* - **DAG (diacylglycerol)** is also a product of **PIP2 cleavage by phospholipase C**, occurring simultaneously with IP3. - It is involved in activating **protein kinase C**, a pathway not directly linked to beta-adrenergic receptor activation.

Question 295: What is the primary second messenger that nitric oxide increases in target cells?

A. Soluble guanylate cyclase
B. cGMP (Correct Answer)
C. cAMP
D. Nitric oxide synthase

Explanation: ***cGMP*** - **Nitric oxide (NO)** directly activates **soluble guanylate cyclase**, an enzyme that catalyzes the conversion of **GTP to cGMP**. - **cGMP** then mediates most of the physiological effects of **NO**, such as **vasodilation** and **smooth muscle relaxation**. *cAMP* - **cAMP** is primarily activated by **adenylyl cyclase**, which is often coupled to G-protein coupled receptors that bind hormones like **epinephrine** or **glucagon**. - **Nitric oxide** does not directly increase **cAMP** levels; its signaling pathway involves a different nucleotide. *Nitric oxide synthase* - **Nitric oxide synthase (NOS)** is the **enzyme** responsible for synthesizing **nitric oxide** from L-arginine, not a second messenger itself. - It produces the signaling molecule, but does not transduce the signal within the target cell. *Soluble guanylate cyclase* - **Soluble guanylate cyclase (sGC)** is the **enzyme** that **nitric oxide** activates, leading to the production of **cGMP**. - While crucial to the pathway, **sGC** is an enzyme, not the second messenger itself; **cGMP** is the molecule that directly mediates downstream effects.

Question 296: Transport of ascorbic acid to the lens is done by:

A. Myoinositol
B. Choline
C. Taurine
D. SVCT2 (Sodium-dependent Vitamin C Transporter 2) (Correct Answer)

Explanation: ***SVCT2 (Sodium-dependent Vitamin C Transporter 2)*** - **SVCT2** is the primary transporter responsible for the uptake and accumulation of **ascorbic acid (vitamin C)** in various tissues, including the lens. - This transporter uses a **sodium-dependent mechanism** to actively move vitamin C into cells, maintaining its high concentration essential for antioxidant protection in the lens. *Myoinositol* - **Myoinositol** is a sugar alcohol that plays a role in cellular signaling and is a component of cell membranes. - It is transported into cells by specific inositol transporters, but it is **not involved in ascorbic acid transport**. *Choline* - **Choline** is an essential nutrient involved in neurotransmitter synthesis (**acetylcholine**) and membrane structure. - It has its own dedicated transport systems and is **not involved in the transport of ascorbic acid**. *Taurine* - **Taurine** is an amino acid derivative found in high concentrations in the eye, where it plays roles in osmoregulation and antioxidant defense. - It is transported by **taurine transporters** and is **not responsible for ascorbic acid transport**.

Question 297: All of the following cell types undergo cell division, EXCEPT:

A. Pericyte
B. Cardiac muscle cell (Correct Answer)
C. Smooth muscle cell
D. Satellite cell of skeletal muscle

Explanation: ***Cardiac muscle cell*** - **Cardiac muscle cells** are terminally differentiated and largely lose their ability to divide shortly after birth. - While some limited regenerative capacity exists, they do not undergo significant cell division for repair or growth in the adult heart. *Pericyte* - **Pericytes** are multipotent cells associated with capillaries and postcapillary venules and are involved in angiogenesis and tissue repair. - They can differentiate into **fibroblasts, smooth muscle cells, osteoblasts, and adipocytes**, and their proliferative capacity is crucial for these functions, especially after injury. *Smooth muscle cell* - **Smooth muscle cells** retain their ability to divide throughout life and can proliferate in response to injury or hormonal stimuli. - This proliferative capacity is important for the growth and repair of organs like the uterus and blood vessels, and can contribute to conditions like **atherosclerosis**. *Satellite cell of skeletal muscle* - **Satellite cells** are quiescent muscle stem cells located between the basal lamina and sarcolemma of muscle fibers. - Upon muscle injury, they become activated, proliferate, and differentiate into new muscle fibers, playing a critical role in **skeletal muscle regeneration** and repair.

Question 298: What is responsible for regeneration of liver cells?

A. TGF-beta
B. HGF (Correct Answer)
C. VEGF
D. IFN-γ

Explanation: **HGF** - **Hepatocyte growth factor (HGF)** is the primary growth factor responsible for stimulating hepatocyte proliferation and migration, playing a crucial role in **liver regeneration** after injury or resection. - It acts as a potent **mitogen** for hepatocytes, promoting their entry into the cell cycle and division. *VEGF* - **Vascular endothelial growth factor (VEGF)** is primarily involved in **angiogenesis**, the formation of new blood vessels. - While important for tissue repair, it does not directly stimulate the proliferation of liver cells themselves. *TGF-beta* - **Transforming growth factor-beta (TGF-β)** is generally considered an **inhibitor of cell proliferation** and a promoter of fibrosis in the liver. - It can suppress hepatocyte growth and promote the differentiation of stellate cells into myofibroblasts, leading to **scar formation**. *IFN-γ* - **Interferon-gamma (IFN-γ)** is a cytokine primarily involved in **immune responses** and has anti-proliferative and pro-apoptotic effects on various cell types. - It does not promote liver cell regeneration; instead, it can be involved in liver injury and fibrosis during chronic inflammation.

Question 299: Which of the following statements is false regarding intracellular receptors?

A. Act by regulating gene expression
B. Glucocorticoid receptors are a type of intracellular receptor.
C. They are the fastest acting receptors. (Correct Answer)
D. DNA contains hormone responsive elements.

Explanation: ***They are the fastest acting receptors.*** - Intracellular receptors regulate gene expression and protein synthesis, which is a **slow process** taking hours or days to manifest effects. - Receptors like **ligand-gated ion channels** are the fastest acting, producing effects within milliseconds due to direct ion flow. *Act by regulating gene expression* - Intracellular receptors, such as **steroid hormone receptors**, typically bind to their ligands within the cytoplasm or nucleus. - This binding leads to their translocation to the nucleus (if not already there), where they act as **transcription factors** to regulate gene expression. *Glucocorticoid receptors are a type of intracellular receptor.* - **Glucocorticoids** are **lipid-soluble hormones** that can readily cross the cell membrane. - They bind to specific intracellular receptors in the cytoplasm, forming a hormone-receptor complex that then translocates to the nucleus. *DNA contains hormone responsive elements.* - Once the activated intracellular hormone-receptor complex enters the nucleus, it binds to specific sequences on the DNA called **hormone responsive elements (HREs)**. - This binding initiates or represses the transcription of target genes, leading to changes in **protein synthesis**.

Question 300: What is the consequence of inhibiting Na⁺/K⁺ ATPase?

A. Decreased Na⁺ in the cell
B. Increased Ca²⁺ in the cell (Correct Answer)
C. Increased K⁺ in the cell
D. Increased Cl⁻ in the cell

Explanation: ***Increased Ca²⁺ in the cell*** - Inhibition of **Na⁺/K⁺ ATPase** leads to an increase in intracellular sodium, which in turn reduces the efficiency of the **Na⁺/Ca²⁺ exchanger**. - This impaired Na⁺/Ca²⁺ exchange results in **less calcium being expelled** from the cell, causing increased intracellular Ca²⁺. *Decreased Na⁺ in the cell* - The **Na⁺/K⁺ ATPase** actively pumps sodium out of the cell; inhibiting it would cause an **increase, not a decrease**, in intracellular Na⁺ concentration. - This option incorrectly states the direct effect of Na⁺/K⁺ ATPase inhibition on intracellular sodium levels. *Increased K⁺ in the cell* - The **Na⁺/K⁺ ATPase** actively pumps potassium into the cell; inhibiting it would lead to a **decrease, not an increase**, in intracellular K⁺ concentration. - This is because the pump is unable to transport extracellular K⁺ into the cell against its concentration gradient. *Increased Cl⁻ in the cell* - **Chloride ion (Cl⁻)** transport is generally managed by different channels and transporters, such as **Cl⁻ channels** or **Na⁺/K⁺/2Cl⁻ cotransporters**, and is not directly regulated by the Na⁺/K⁺ ATPase. - While changes in cell potential due to Na⁺/K⁺ ATPase inhibition might indirectly affect other ion movements, a direct and significant increase in intracellular Cl⁻ is not a primary consequence.

Practice by Chapter

Cell Membrane Structure and Function

Practice Questions

Membrane Transport Proteins

Practice Questions

Cellular Energetics and Metabolism

Practice Questions

Mitochondrial Function

Practice Questions

Cell Volume Regulation

Practice Questions

Cellular Responses to Stress

Practice Questions

Calcium Signaling

Practice Questions

Cell Cycle and Regulation

Practice Questions

Cellular Aging

Practice Questions

Apoptosis and Cell Death

Practice Questions

Want unlimited practice?

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

Start For Free