Anatomy
1 questionsT cells in lymph node are present in:
NEET-PG 2013 - Anatomy NEET-PG Practice Questions and MCQs
Question 611: 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.
Community Medicine
1 questionsWhat was the target reduction in child mortality rates set by the Millennium Development Goals (MDGs) between 1990 and 2015?
NEET-PG 2013 - Community Medicine NEET-PG Practice Questions and MCQs
Question 611: What was the target reduction in child mortality rates set by the Millennium Development Goals (MDGs) between 1990 and 2015?
- A. Half
- B. Two-thirds (Correct Answer)
- C. One-fourth
- D. One-third
Explanation: ***Two-thirds*** - The **Millennium Development Goal 4 (MDG 4)** specifically aimed to **reduce child mortality by two-thirds** among children under five years old between 1990 and 2015. - This target focused on improving maternal and child health outcomes globally. *Half* - Reducing child mortality by half was not the specific target set by MDG 4 for the 1990-2015 period. - While improvements were sought, the ambition was a more substantial reduction. *One-fourth* - A reduction of one-fourth would have been a significantly lower target than what was ultimately set and pursued by the MDGs. - The goals were designed to be ambitious yet achievable. *One-third* - Reducing child mortality by one-third falls short of the actual target established by the MDGs. - The international community aimed for a greater impact on child survival rates.
Microbiology
5 questionsWhich of the following is a superantigen ?
What is the primary use of the Hybridoma technique?
Cytolytic activity of membrane attack complex is modulated by ?
Which of the following statements about interleukin-1 is false?
All are true regarding the development of T-cells, except?
NEET-PG 2013 - Microbiology NEET-PG Practice Questions and MCQs
Question 611: Which of the following is a superantigen ?
- A. Cholera toxin
- B. Diphtheria toxin
- C. TSST (Correct Answer)
- D. Vero-cytoxin
Explanation: ***TSST*** - **Toxic Shock Syndrome Toxin-1 (TSST-1)** is a classic example of a superantigen produced by *Staphylococcus aureus*. - Superantigens **bind directly to MHC class II molecules and T-cell receptors (TCRs)** outside of the antigen-binding groove, leading to non-specific activation of a large percentage of T cells and a massive release of cytokines. *Cholera toxin* - **Cholera toxin** is an exotoxin produced by *Vibrio cholerae* that causes massive fluid secretion in the intestine by **activating adenylate cyclase** in enterocytes. - It functions by **ADP-ribosylating the Gs alpha subunit**, leading to constitutive activation of cyclic AMP production, but it is not a superantigen. *Diphtheria toxin* - **Diphtheria toxin**, produced by *Corynebacterium diphtheriae*, inhibits protein synthesis in eukaryotic cells by **ADP-ribosylating elongation factor-2 (EF-2)**. - This action leads to cell death and the characteristic pseudomembrane formation in diphtheria, but it does not act as a superantigen. *Vero-cytoxin* - **Vero-cytoxin** (also known as Shiga toxin or Shiga-like toxin) is produced by *E. coli* O157:H7 and other Shiga toxin-producing *E. coli* (STEC). - It inhibits protein synthesis by **cleaving ribosomal RNA**, primarily causing damage to intestinal cells and renal endothelial cells, but it is not a superantigen.
Question 612: What is the primary use of the Hybridoma technique?
- A. Monoclonal antibodies (Correct Answer)
- B. Antigen
- C. Specific antibodies
- D. Cytokines
Explanation: ***Monoclonal antibodies*** - The **hybridoma technique** is primarily used to produce **monoclonal antibodies (MAbs)**, which are highly specific antibodies derived from a single B-cell clone. - These antibodies recognize a **single epitope** on an antigen, providing exceptional specificity and uniformity. - The technique involves **fusing a B-lymphocyte** (antibody-producing cell) with a **myeloma cell** (immortal cancer cell) to create a hybridoma that continuously produces identical antibodies. - This is the **gold standard** for producing large quantities of identical, highly specific antibodies for diagnostic and therapeutic use. *Specific antibodies* - While monoclonal antibodies are indeed specific, this term is **too vague** and could refer to any antibody with specificity, including polyclonal antibodies. - **Polyclonal antibodies** are also specific but are produced through conventional immunization, not the hybridoma technique. - The defining characteristic of the hybridoma technique is that it produces **monoclonal** (single clone) antibodies, not just "specific" ones. *Antigen* - An **antigen** is a molecule that elicits an immune response and is used to immunize animals during antibody production. - However, antigens are the **input** for antibody production, not the **product** of the hybridoma technique. *Cytokines* - **Cytokines** are signaling molecules involved in immune cell communication and regulation. - They are not produced by the hybridoma technique, which is specifically designed for **antibody production**.
Question 613: Cytolytic activity of membrane attack complex is modulated by ?
- A. Factor I
- B. Factor B
- C. Factor S (vitronectin) (Correct Answer)
- D. Factor H
Explanation: ***Correct Option: Factor S (vitronectin)*** - Vitronectin (S-protein) is a **plasma protein** that directly modulates the **cytolytic activity of the membrane attack complex (MAC)**. - It binds to the **C5b-7 complex** in the fluid phase, preventing its insertion into target cell membranes and thereby blocking the formation of the complete, functional MAC. - By inhibiting membrane insertion of C5b-7, vitronectin prevents the subsequent binding of **C8 and C9**, which are essential for the cytolytic pore formation. - This is a **direct modulation** of MAC's cytolytic activity at the MAC assembly stage. *Incorrect Option: Factor H* - Factor H is a regulatory protein that controls the **alternative pathway** of complement activation by promoting degradation of **C3b**. - By degrading C3b, Factor H prevents formation of **C5 convertase**, thereby reducing downstream MAC formation. - However, Factor H acts **early in the complement cascade** and does not directly modulate the cytolytic activity of already-formed MAC components. - Its effect is on **preventing MAC formation**, not on modulating MAC's cytolytic function itself. *Incorrect Option: Factor I* - Factor I is a **serine protease** that cleaves and inactivates C3b and C4b, requiring cofactors like Factor H or C4bp. - Like Factor H, it regulates complement activation **upstream** of MAC formation. - It does not directly interact with or modulate the cytolytic activity of the MAC. *Incorrect Option: Factor B* - Factor B is a component of the **alternative pathway C3 convertase** (C3bBb). - It **promotes complement activation** rather than modulating MAC's cytolytic activity. - Factor B functions early in the cascade and has no direct role in regulating MAC function.
Question 614: Which of the following statements about interleukin-1 is false?
- A. IL-1 is an endogenous pyrogen.
- B. The primary source of IL-1 is the monocyte-macrophage system.
- C. IL-1 inhibits IL-2 production by T-cells. (Correct Answer)
- D. IL-1 promotes acute phase protein synthesis in the liver.
Explanation: ***IL-1 inhibits IL-2 production by T-cells*** - This statement is false because **IL-1** actually **enhances the production of IL-2** by T-cells, which is crucial for T-cell proliferation and immune response. - **IL-1 acts synergistically with IL-6 and TNF-α** to promote inflammation and immune cell activation, where IL-2 plays a key role. *The primary source of IL-1 is the monocyte-macrophage system* - This statement is true; **monocytes and macrophages** are the main producers of **IL-1α and IL-1β** upon activation by various stimuli. - Other cells, such as neutrophils, dendritic cells, and endothelial cells, can also produce IL-1, but monocytes and macrophages are the predominant source. *IL-1 is an endogenous pyrogen* - This statement is true; **IL-1** is a potent **endogenous pyrogen** that acts on the hypothalamus to induce fever, a hallmark of the acute phase response. - It triggers prostaglandin synthesis in the hypothalamus, leading to an elevation in the body's thermoregulatory set point. *IL-1 promotes acute phase protein synthesis in the liver* - This statement is true; **IL-1** is a key mediator that stimulates **hepatocytes** to produce **acute phase proteins**, such as C-reactive protein and serum amyloid A. - This hepatic response is part of the innate immune system's effort to control infection and inflammation.
Question 615: 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.
Pediatrics
1 questionsAt what age does clinically significant IgG production begin?
NEET-PG 2013 - Pediatrics NEET-PG Practice Questions and MCQs
Question 611: 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
2 questionsWhich anxiolytic acts through 5-HT1A receptor partial agonism without exhibiting significant anticonvulsant or muscle relaxant properties?
All of the following are adverse effects of nicotinic acid except:
NEET-PG 2013 - Pharmacology NEET-PG Practice Questions and MCQs
Question 611: Which anxiolytic acts through 5-HT1A receptor partial agonism without exhibiting significant anticonvulsant or muscle relaxant properties?
- A. Diazepam
- B. Zolpidem
- C. Phenobarbitone
- D. Buspirone (Correct Answer)
Explanation: ***Buspirone*** - **Buspirone** is a unique anxiolytic that primarily acts as a **partial agonist at 5-HT1A receptors**. - Unlike benzodiazepines, it lacks significant **anticonvulsant**, **muscle relaxant**, or **sedative-hypnotic properties** and does not lead to physical dependence or withdrawal. *Diazepam* - **Diazepam** is a **benzodiazepine** that acts by enhancing the effect of **GABA** at GABA-A receptors, leading to significant anxiolytic, sedative, muscle relaxant, and anticonvulsant effects. - It does not primarily act via **5-HT1A receptor partial agonism**. *Zolpidem* - **Zolpidem** is a **non-benzodiazepine hypnotic** that selectively binds to the **GABA-A receptor** subunit, primarily mediating sedative effects. - While it's used for insomnia, it doesn't primarily act as a **5-HT1A partial agonist** and is not typically used for its anxiolytic properties in the same way as buspirone. *Phenobarbitone* - **Phenobarbitone** is a **barbiturate** that acts by prolonging the opening of **chloride channels** associated with GABA-A receptors, leading to strong sedative, hypnotic, and anticonvulsant effects. - Its mechanism of action is distinct from **5-HT1A receptor partial agonism**, and it carries a high risk of dependence and overdose.
Question 612: All of the following are adverse effects of nicotinic acid except:
- A. Liver dysfunction
- B. Vasodilation
- C. Hyperpigmentation
- D. Pancreatitis (Correct Answer)
Explanation: ***Pancreatitis*** - **Pancreatitis** is not a commonly reported adverse effect of nicotinic acid (niacin) therapy. - While other gastrointestinal side effects like nausea and vomiting can occur, pancreatic inflammation is not characteristic. *Vasodilation* - **Cutaneous flushing** and **vasodilation** are very common adverse effects of nicotinic acid, mediated by prostaglandin release. - This effect can cause a sensation of warmth, redness, and itching, especially at the start of therapy. *Liver dysfunction* - **Liver dysfunction**, including elevated liver enzymes and rare cases of **hepatotoxicity**, can occur with high doses of nicotinic acid. - Regular monitoring of liver function tests is recommended for patients on niacin therapy. *Hyperpigmentation* - **Hyperpigmentation**, particularly **acanthosis nigricans**, is a known cutaneous side effect of nicotinic acid. - This typically presents as dark, velvety patches on the skin, especially in skin fold areas.