Anatomy
1 questionsT cells in lymph node are present in:
NEET-PG 2013 - Anatomy NEET-PG Practice Questions and MCQs
Question 641: T cells in lymph node are present in:
- A. Paracortical area (Correct Answer)
- B. Mantle layer
- C. Medullary cords
- D. Cortical follicles
Explanation: ***Paracortical area*** - The **paracortical area** contains a high concentration of **T cells**, particularly activated T cells in response to antigenic stimulation [1]. - It plays a crucial role in **immune responses**, bridging the cortex and medulla of the lymph node [1]. *Mantle layer* - The **mantle layer** surrounds the follicles and primarily consists of **B cells**, not T cells. - It is involved in the initial immune response but does not contain a significant number of T lymphocytes. *Medullary cords* - **Medullary cords** mainly contain **plasma cells** and macrophages, with very few T cells present. - Their primary function is the secretion of antibodies rather than T cell activation or response. *Cortical follicles* - **Cortical follicles** are primarily sites for **B cell activation and proliferation**. - While they may have some T cells at their periphery, the majority of T cells are located in the paracortical area.
Microbiology
3 questionsWhich of the following bacteria is known to exhibit antigenic variation?
All are true regarding the development of T-cells, except?
Rosette formation with sheep RBCs (SRBCs) indicates functioning of -
NEET-PG 2013 - Microbiology NEET-PG Practice Questions and MCQs
Question 641: Which of the following bacteria is known to exhibit antigenic variation?
- A. Yersinia
- B. Bordetella
- C. Brucella
- D. Borrelia (Correct Answer)
Explanation: ***Borrelia*** - *Borrelia* species, particularly *Borrelia burgdorferi* (causing **Lyme disease**), are known for extensive **antigenic variation** of their outer surface proteins (Osps), especially OspC. - This variation helps the bacteria evade the host's immune response, contributing to persistent infection. *Yersinia* - While *Yersinia* species produce various virulence factors, including proteins that interfere with immune cell function, they are not primarily known for the type of rapid and extensive **antigenic variation**seen in *Borrelia*. - Their immune evasion strategies often involve modifying host cell signaling pathways and resisting phagocytosis. *Bordetella* - *Bordetella pertussis*, causative agent of **whooping cough**, varies its expression of adhesins and toxins through **phase variation**, which is a form of phenotypic switching. - However, this is distinct from the frequent and sequential changes in surface antigens (antigenic variation) observed in *Borrelia*. *Brucella* - *Brucella* species are **intracellular pathogens** that primarily evade the immune system by surviving and replicating within host cells. - They do not typically engage in significant **antigenic variation** of their surface components as a primary immune evasion mechanism.
Question 642: All are true regarding the development of T-cells, except?
- A. T-cells are formed in bone marrow
- B. In lymph nodes, T-cells are found in paracortical area
- C. Maturation of T-cells take place in thymus
- D. T-cells are located in mantle layer of spleen (Correct Answer)
Explanation: ***T-cells are located in mantle layer of spleen*** - The **mantle layer** (or marginal zone) of the spleen is primarily associated with **B-lymphocytes**, which are involved in antibody production. - While T-cells are present in the spleen, they are predominantly found in the **periarteriolar lymphoid sheath (PALS)**, which is part of the white pulp, rather than the mantle layer. *T-cells are formed in bone marrow* - **Hematopoietic stem cells** in the **bone marrow** are the progenitors of all blood cells, including lymphocytes. - These stem cells differentiate into **lymphoid stem cells**, which then travel to the thymus to become T-cells. *Maturation of T-cells take place in thymus* - **T-cell precursors** migrate from the bone marrow to the **thymus**, where they undergo a complex process of differentiation and selection. - In the thymus, T-cells acquire their **T-cell receptors (TCRs)** and undergo positive and negative selection to ensure they are self-MHC restricted and tolerant to self-antigens. *In lymph nodes, T-cells are found in paracortical area* - The **paracortical area** (or paracortex) of the lymph node is the **T-cell zone**, rich in T-lymphocytes and dendritic cells. - This region is crucial for the interaction between T-cells and antigen-presenting cells, initiating adaptive immune responses.
Question 643: Rosette formation with sheep RBCs (SRBCs) indicates functioning of -
- A. T-cells (Correct Answer)
- B. B-cells
- C. Neutrophils
- D. Monocytes
Explanation: ***T-cells*** - **T-cells** possess specific receptors, like **CD2** on their surface, that can bind to ligands on sheep red blood cells (SRBCs). - This binding leads to the formation of characteristic **rosettes**, where SRBCs cluster around the T-lymphocytes, indicating functional T-cells. *B-cells* - **B-cells** primarily function in **humoral immunity** by producing antibodies and do not typically form rosettes with sheep RBCs. - While B-cells have surface receptors, they are not CD2 and thus do not facilitate this specific type of rosette formation. *Neutrophils* - **Neutrophils** are **phagocytic cells** involved in innate immunity, primarily combating bacterial and fungal infections. - They lack the specific surface receptors (like CD2) required to form rosettes with sheep RBCs. *Monocytes* - **Monocytes** are precursors to macrophages and dendritic cells, involved in phagocytosis and antigen presentation. - They do not possess the necessary surface markers to form rosettes with sheep RBCs.
Pediatrics
1 questionsAt what age does clinically significant IgG production begin?
NEET-PG 2013 - Pediatrics NEET-PG Practice Questions and MCQs
Question 641: At what age does clinically significant IgG production begin?
- A. Around 6 months (Correct Answer)
- B. Around 1 year
- C. Around 2 years
- D. Around 3 years
Explanation: ***Around 6 months*** - Maternal IgG levels, which provide **passive immunity**, decrease significantly by 3-6 months of age. - Infants begin to produce their own **clinically significant** levels of IgG around this time, coinciding with the "physiologic nadir" of IgG. *Around 1 year* - While IgG production continues to mature, significant production has already begun by 6 months to replace declining maternal antibodies. - By 1 year, the immune system is more robust, but the initial critical transition occurs earlier. *Around 2 years* - By this age, children generally have a robust adaptive immune response, and the period of vulnerability due to low IgG has passed. - This option is too late for the beginning of clinically significant IgG production. *Around 3 years* - This age is far past the point where children start producing their own significant levels of IgG. - The immune system is well-developed by 3 years, and initial IgG production started much earlier.
Pharmacology
5 questionsWhich of the following statements about sitagliptin is false?
What is a potential risk associated with the use of thiazolidinediones in the treatment of type 2 diabetes?
What conditions is Metformin primarily used to treat?
Which of the antithyroid drugs inhibits iodine trapping?
Which of the following is the longest acting glucocorticoid?
NEET-PG 2013 - Pharmacology NEET-PG Practice Questions and MCQs
Question 641: Which of the following statements about sitagliptin is false?
- A. Used in type II diabetes mellitus
- B. Cannot be used orally (Correct Answer)
- C. Used in combination with other oral hypoglycemic agents
- D. All of the above statements are true
Explanation: ***Cannot be used orally*** - This statement is **false** because **sitagliptin** is an **oral medication** approved for the treatment of type 2 diabetes mellitus. - As a **DPP-4 inhibitor**, it is designed to be taken by mouth to increase incretin hormone levels. *Used in type II diabetes mellitus* - This statement is **true** as **sitagliptin** is a commonly prescribed **oral antidiabetic drug** for the management of type 2 diabetes. - It works by inhibiting the enzyme **dipeptidyl peptidase-4 (DPP-4)**, which increases levels of **GLP-1** and **GIP** to enhance insulin secretion and reduce glucagon secretion. *Used in combination with other oral hypoglycemic agents* - This statement is **true** as **sitagliptin** is often used as **add-on therapy** with other oral hypoglycemic agents like **metformin** or a **sulfonylurea** when monotherapy is insufficient. - This combination approach helps achieve better glycemic control by targeting different mechanisms of action. *All of the above statements are true* - This statement is **false** because the first statement "Cannot be used orally" is incorrect. - Since sitagliptin is indeed an oral medication, not all the above statements are true, making this option incorrect.
Question 642: What is a potential risk associated with the use of thiazolidinediones in the treatment of type 2 diabetes?
- A. Heart failure (Correct Answer)
- B. Pulmonary fibrosis
- C. Myocarditis
- D. Renal dysfunction
Explanation: ***Heart failure*** - Thiazolidinediones (TZDs), such as **pioglitazone** and **rosiglitazone**, can cause **fluid retention** and **volume expansion**, which may precipitate or worsen congestive heart failure. - This risk is higher in patients with pre-existing cardiac conditions and is a significant concern for these drugs. *Pulmonary fibrosis* - **Pulmonary fibrosis** is not a known or common adverse effect associated with thiazolidinedione use. - This condition is typically linked to certain other medications (e.g., **amiodarone**, **methotrexate**) or systemic diseases. *Myocarditis* - **Myocarditis**, inflammation of the heart muscle, is not a recognized side effect of thiazolidinediones. - Myocarditis is more commonly caused by viral infections, autoimmune diseases, or hypersensitivity reactions to certain drugs, but not TZDs. *Renal dysfunction* - While TZDs can cause fluid retention, they do not directly cause **renal dysfunction** or damage the kidneys. - In fact, some studies suggest they may have renoprotective effects due to reduced proteinuria, although fluid balance needs careful monitoring in patients with impaired renal function.
Question 643: What conditions is Metformin primarily used to treat?
- A. Only Type 2 Diabetes
- B. Only Polycystic Ovary Syndrome (PCOS)
- C. Both Type 2 Diabetes and Polycystic Ovary Syndrome (PCOS) (Correct Answer)
- D. Pregnancy Induced Hypertension
Explanation: ***Both Type 2 Diabetes and Polycystic Ovary Syndrome (PCOS)*** - **Metformin** is a first-line treatment for **Type 2 Diabetes** due to its ability to decrease hepatic glucose production and improve insulin sensitivity [1], [2]. - It is also commonly used off-label for **PCOS** to improve insulin resistance, ovulation, and reduce androgen levels. *Only Type 2 Diabetes* - While Metformin is a cornerstone for **Type 2 Diabetes** treatment, stating "only" is incorrect as it has other significant therapeutic uses [2]. - Its benefits extend beyond diabetes management, particularly in conditions involving **insulin resistance**. *Only Polycystic Ovary Syndrome (PCOS)* - Metformin is used in **PCOS**, but it is not the sole condition it treats, and its primary indication remains **Type 2 Diabetes** [2]. - This option incorrectly limits its application to just one condition, overlooking its major role in diabetes. *Pregnancy Induced Hypertension* - **Metformin** is not indicated for the treatment of **pregnancy-induced hypertension** (gestational hypertension). - Treatment for pregnancy-induced hypertension typically involves medications like **labetalol**, **methyldopa**, or **nifedipine**, with delivery being the definitive management for severe cases.
Question 644: Which of the antithyroid drugs inhibits iodine trapping?
- A. Radioactive iodine
- B. Iodides
- C. Thiocyanates (Correct Answer)
- D. Methimazole
Explanation: ***Thiocyanates*** - **Thiocyanates** are competitive inhibitors of the **sodium-iodide symporter (NIS)**, which is responsible for actively transporting iodide into thyroid follicular cells (iodine trapping) [1]. - By blocking NIS, thiocyanates prevent the thyroid gland from accumulating iodide, thereby inhibiting thyroid hormone synthesis [1]. *Radioactive iodine* - **Radioactive iodine (RAI)** primarily works by being taken up by thyroid cells and emitting **beta particles**, which destroy the thyroid tissue [3]. - It does not inhibit iodine trapping, but rather uses the trapping mechanism to concentrate in the thyroid and exert its destructive effect [3]. *Iodides* - **Iodides** (e.g., Lugol's solution) paradoxically inhibit organification and hormone release from the thyroid gland, an effect known as the **Wolff-Chaikoff effect** [2]. - They also decrease the vascularity and size of the thyroid gland, making them useful in preparing patients for thyroidectomy, but do not directly inhibit iodine trapping [2]. *Methimazole* - **Methimazole** is a **thionamide** drug that primarily inhibits the enzyme **thyroid peroxidase**. - This prevents the **organification of iodide** (incorporation of iodine into tyrosine residues) and the **coupling of iodotyrosines** (forming T3 and T4), not the initial trapping of iodine.
Question 645: Which of the following is the longest acting glucocorticoid?
- A. Prednisone
- B. Prednisolone
- C. Cortisone
- D. Dexamethasone (Correct Answer)
Explanation: ***Correct: Dexamethasone*** - **Dexamethasone** is a long-acting glucocorticoid with a **biological half-life of 36–72 hours**, making it the longest acting among the options provided - Its prolonged action is due to its **high affinity for the glucocorticoid receptor** and relatively slow metabolism - Provides sustained anti-inflammatory and immunosuppressive effects *Incorrect: Prednisone* - **Prednisone** is an intermediate-acting glucocorticoid with a biological half-life of 12-36 hours - Requires metabolism in the liver to its active form, prednisolone - Duration of action is significantly shorter than dexamethasone *Incorrect: Prednisolone* - **Prednisolone** is the active form of prednisone, with a similar intermediate duration of action (12-36 hours) - Primarily used when liver conversion of prednisone is impaired - Does not possess the extended duration of action characteristic of dexamethasone *Incorrect: Cortisone* - **Cortisone** is a short-acting glucocorticoid with a biological half-life of 8-12 hours - It is a prodrug that needs to be converted to **hydrocortisone** (cortisol) in the liver to become active - Has the shortest duration among all options