NEET-PG 2015 Practice Questions

Q: B cells are located in which region of lymph nodes?

Cortical follicles. ***Cortical follicles*** - **B cells** are predominantly found within the **cortical follicles** of lymph nodes, where they mature and become activated upon encountering antigens [2]. - These follicles can be primary (inactive) or secondary (active, containing **germinal centers** for B cell proliferation and differentiation). *Paracortical region* - The **paracortical region** is primarily occupied by **T cells** and is the site where T cells interact with antigen-presenting cells [1]. - While it's adjacent to B cell areas, it's not the primary location for B cells. *Medullary sinuses* - **Medullary sinuses** are channels in the medulla of the lymph node, containing macrophages and plasma cells, which are *differentiated B cells*. - They are not the primary residence for undifferentiated B cells. *Subcapsular region* - **Subcapsular region** is the space immediately beneath the capsule of the lymph node where lymph initially enters. - It contains macrophages and dendritic cells that sample antigens but is not a primary B cell zone.

Q: The process by which antigen-specific B lymphocytes are selected and activated to proliferate and produce antibodies is called:

Clonal selection. ***Clonal selection*** - **Clonal selection** is the fundamental process by which an antigen-specific B lymphocyte is **selected** when its B cell receptor (BCR) recognizes and binds to a matching antigen. - This binding triggers the B cell to become **activated**, **proliferate** (undergo clonal expansion), and **differentiate** into plasma cells that produce antibodies specific to that antigen. - This process is the cornerstone of **adaptive immunity**, ensuring that only B cells with receptors matching the encountered antigen are stimulated to respond. *Class switching* - **Class switching** (isotype switching) occurs AFTER clonal selection and activation. - It allows already-activated B cells to change the **antibody class** they produce (from IgM to IgG, IgA, or IgE) while maintaining the **same antigen specificity**. - This process modifies effector functions but does NOT involve the initial selection and activation of antigen-specific B cells. *Group switching* - This is not a recognized term in immunology. - It does not describe any standard process of B cell activation or antibody production. *Hybridisation* - **Hybridization** refers to the formation of double-stranded nucleic acids from complementary strands or the creation of hybrid cells (e.g., hybridomas for monoclonal antibody production). - It is not the physiological process by which B lymphocytes are selected and activated in response to antigen exposure.

Q: Subepithelial deposits in the kidney are primarily associated with which condition?

Post-Streptococcal Glomerulonephritis (PSGN). ***PSGN*** - Post-streptococcal glomerulonephritis (PSGN) is characterized by **subepithelial immune complex deposits** [1], typically after a streptococcal infection [1]. - It is associated with **hematuria**, **edema**, and elevated **anti-streptolysin O (ASO)** titers. *GPS* - Minimal change disease (often referred to as idiopathic nephrotic syndrome) does not primarily feature **subepithelial deposits** but rather **effacement of podocyte foot processes**. - Clinical presentation includes **nephrotic syndrome** symptoms, not glomerulonephritis like PSGN. *MPGN-1* - Membranoproliferative glomerulonephritis type 1 includes **subendothelial deposits** rather than subepithelial deposits associated with PSGN. - Symptoms often include **nephritic syndrome** and is commonly linked with conditions like **HCV infection**. *All* - While several conditions can show **deposits in kidney**, not all are characterized by **subepithelial deposits**, hence this option is inaccurate. - Each type of glomerular disease has specific types of deposits (immune complex vs. complement) associated with their pathophysiology. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 914-916.

Q: Which drug is not administered as a transdermal patch?

Morphine. ***Morphine*** - **Morphine** is generally not administered transdermally due to its **poor lipid solubility** [1] and **large molecular size**, which limit its ability to penetrate the skin effectively. - While experimental patches have been developed, they are **not widely available** or commonly used in clinical practice for systemic delivery. *Fentanyl* - **Fentanyl** is a potent opioid that is commonly administered via a **transdermal patch** for chronic pain management [2]. - Its **high lipid solubility** and small molecular size allow it to be effectively absorbed through the skin, providing sustained analgesia. *Clonidine* - **Clonidine** is an alpha-2 adrenergic agonist available as a **transdermal patch** for the treatment of **hypertension**. - The patch provides a **continuous and steady release** of the drug, leading to consistent blood pressure control. *Diclofenac* - **Diclofenac** is a non-steroidal anti-inflammatory drug (NSAID) available in **transdermal patch** formulations for topical pain relief. - These patches are used for localized pain conditions like **osteoarthritis** and provide targeted drug delivery with reduced systemic side effects.

Q: Volume of distribution of a drug is 500 ml and target concentration of drug in blood is 5 g/L. 20% of administered drug is reached to systemic circulation. What will be the loading dose of that drug -

12.5 gm. ***12.5 gm*** - The formula for loading dose (LD) is: LD = (Target Concentration × Volume of Distribution) / Bioavailability. - Given: Target Concentration = 5 g/L, Volume of Distribution = 500 mL = 0.5 L, Bioavailability = 20% = 0.2. - So, LD = (5 g/L × 0.5 L) / 0.2 = 2.5 g / 0.2 = **12.5 g**. *1 gm* - This value would be obtained if the target concentration was 2 g/L with 100% bioavailability, or if the calculation incorrectly handled the volume or bioavailability factor. - It does not account for the specified **bioavailability of 20%** or the given target concentration and volume of distribution. *5 gm* - This result would be obtained if the bioavailability was assumed to be 50% (LD = 2.5 g / 0.5 = 5 g), or if the volume of distribution was incorrectly used in the calculation. - This option does not correctly factor in the **20% bioavailability** of the administered drug. *25 gm* - This value would result from mistakes such as dividing by bioavailability of 10% instead of 20% (LD = 2.5 g / 0.1 = 25 g), or by multiplying bioavailability instead of dividing by it. - This answer significantly **overestimates** the required dose, which could lead to drug toxicity.

Q: Which of the following statements about glucocorticoids is true?

Glucocorticoids downregulate MHC class II expression.. ***Glucocorticoids downregulate MHC class II expression.*** - Glucocorticoids exert **immunosuppressive effects** by reducing the expression of **MHC class II molecules** on antigen-presenting cells. - This downregulation impairs the ability of antigen-presenting cells to activate **CD4+ T-helper cells**, thereby suppressing adaptive immune responses. *Glucocorticoids directly activate T-helper cells.* - Glucocorticoids do not directly activate T-helper cells; rather, they have an **inhibitory effect** on T-cell function and proliferation. - They tend to promote **T-cell apoptosis** and reduce cytokine production, thus dampening T-helper cell responses. *Glucocorticoids have no effect on immune cells.* - This statement is incorrect as glucocorticoids have profound and widespread **immunosuppressive and anti-inflammatory effects** on various immune cells. - They influence the function, proliferation, and survival of **lymphocytes, macrophages, and granulocytes**. *Glucocorticoids enhance the activity of cytotoxic T cells.* - Glucocorticoids generally **suppress immune responses**, including the activity of **cytotoxic T cells (CTLs)**, rather than enhancing it. - They tend to inhibit the production of **interleukins** necessary for CTL activation and proliferation.

Q: What is the mechanism of action of ticagrelor?

Reversible inhibition of ADP action. ***Reversible inhibition of ADP action*** - **Ticagrelor** is a **P2Y12 receptor antagonist** that works by preventing ADP from binding to its receptor on platelets [2]. - This binding is **reversible**, meaning ticagrelor can dissociate from the receptor, allowing for some recovery of platelet function over time [2]. *Irreversible inhibition of ADP action* - **Clopidogrel** and **prasugrel** are examples of **irreversible P2Y12 inhibitors**, forming a permanent bond with the receptor [2]. - Irreversible inhibition leads to a longer duration of platelet inhibition, as new platelets must be generated for function to return [2]. *Reversible inhibition of GPIIb/IIIa* - **GPIIb/IIIa inhibitors** like **eptifibatide** and **tirofiban** block the final common pathway of platelet aggregation by preventing fibrinogen binding [1]. - While their action is reversible, they target a *different* mechanism than ticagrelor. *Irreversible inhibition of GPIIb/IIIa* - **Abciximab** is a GPIIb/IIIa inhibitor that binds **irreversibly** (or with very slow dissociation) to the receptor [1]. - Unlike reversible GPIIb/IIIa inhibitors, abciximab is a monoclonal antibody with a prolonged antiplatelet effect [1]. - This is still an incorrect answer as ticagrelor targets the P2Y12 receptor, not GPIIb/IIIa.

Q: High volume of distribution is primarily determined by:

High lipid solubility. ***High lipid solubility***- Highly **lipid-soluble** drugs readily cross biological membranes and distribute extensively into tissues, including adipose tissue, CNS, and intracellular compartments, leading to a **high volume of distribution (Vd)** [1, 2].- This property allows the drug to move out of the bloodstream and into various body compartments, increasing the apparent volume in which the drug is dissolved [1].*High plasma protein binding*- **High plasma protein binding** generally **restricts** drug distribution to tissues because only the **unbound (free) fraction** can diffuse across capillary membranes into interstitial fluid and cells [1].- This typically leads to a **lower Vd**, as the drug is largely retained within the plasma compartment.*Elimination rate*- The **elimination rate** determines how quickly the drug is removed from the body, affecting the **duration of action** rather than the extent of distribution.- It influences drug concentration changes over time but does not directly determine the physical space (volume) into which the drug distributes.*Half-life of the drug*- The **half-life (t½)** is the time required for drug concentration to reduce by half, and it is **determined by** both Vd and clearance (t½ = 0.693 × Vd/CL).- Half-life is a **consequence** of Vd and clearance, not a primary determinant of how widely a drug distributes [3].

Q: What physiological mechanism is responsible for the increase in the duration of expiration?

Hering-Breuer reflex. ***Hering-Breuer reflex*** - The **Hering-Breuer reflex** is initiated by **stretch receptors in the bronchi and bronchioles** which are activated during lung inflation. - This reflex **inhibits inspiration** and **prolongs expiration**, preventing overinflation of the lungs. *J-reflex* - The **J-reflex** is stimulated by **juxtacapillary (J) receptors** in the alveolar walls, usually in response to pulmonary edema or congestion. - It typically causes **rapid, shallow breathing** and **bronchoconstriction**, not prolonged expiration. *Head's paradoxical reflex* - **Head's paradoxical reflex** (also known as the **inflation reflex** in newborns) involves an inspiratory effort triggered by lung inflation, often overcoming the Hering-Breuer reflex in specific conditions. - It tends to **increase respiratory rate** and depth, not prolong expiration. *Proprioceptors* - **Proprioceptors** are sensory receptors in muscles, tendons, and joints that provide information about body position and movement. - While they can influence respiration during exercise, they are not primarily responsible for directly **increasing the duration of expiration** as a reflex mechanism against overinflation.

Question 1

B cells are located in which region of lymph nodes?

Accepted Answer

Cortical follicles

Answer

Paracortical region

Answer

Subcapsular region

Answer

Medullary sinuses

Question 2

What is a key similarity between the processes of replication and transcription?

Accepted Answer

Involve phosphodiester bond formation with elongation occurring in the 5' - 3' direction.

Answer

Use RNA primers for initiation.

Answer

Use ribonucleotides as precursors.

Answer

Are semi-conservative events.

Question 3

The process by which antigen-specific B lymphocytes are selected and activated to proliferate and produce antibodies is called:

Accepted Answer

Clonal selection

Answer

Class switching

Answer

Group switching

Answer

Hybridisation

Question 4

Subepithelial deposits in the kidney are primarily associated with which condition?

Accepted Answer

Post-Streptococcal Glomerulonephritis (PSGN)

Answer

None of these conditions are associated with subepithelial deposits.

Answer

Membranoproliferative Glomerulonephritis (MPGN) Type I

Answer

Goodpasture's Syndrome (GPS)

Question 5

Which drug is not administered as a transdermal patch?

Accepted Answer

Morphine

Answer

Fentanyl

Answer

Clonidine

Answer

Diclofenac

Question 6

Volume of distribution of a drug is 500 ml and target concentration of drug in blood is 5 g/L. 20% of administered drug is reached to systemic circulation. What will be the loading dose of that drug -

Accepted Answer

12.5 gm

Answer

1 gm

Answer

5 gm

Answer

25 gm

Question 7

Which of the following statements about glucocorticoids is true?

Accepted Answer

Glucocorticoids downregulate MHC class II expression.

Answer

Glucocorticoids directly activate T-helper cells.

Answer

Glucocorticoids have no effect on immune cells.

Answer

Glucocorticoids enhance the activity of cytotoxic T cells.

Question 8

What is the mechanism of action of ticagrelor?

Accepted Answer

Reversible inhibition of ADP action

Answer

Irreversible inhibition of ADP action

Answer

Reversible inhibition of GPIIb/IIIa

Answer

Irreversible inhibition of GPIIb/IIIa

Question 9

High volume of distribution is primarily determined by:

Accepted Answer

High lipid solubility

Answer

High plasma protein binding

Answer

Elimination rate

Answer

Half-life of the drug

Question 10

What physiological mechanism is responsible for the increase in the duration of expiration?

Accepted Answer

Hering-Breuer reflex

Answer

J-reflex

Answer

Head's paradoxical reflex

Answer

Proprioceptors

NEET-PG 2015

Anatomy

Biochemistry

Microbiology

Pathology

Pharmacology

Physiology