Anatomy
1 questionsT cells in lymph node are present in:
NEET-PG 2013 - Anatomy NEET-PG Practice Questions and MCQs
Question 581: 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
8 questionsWhich of the following is a saccharolytic species of Clostridium?
Which staining method is specifically used for the detection of mycoplasma?
All are non-sporing anaerobes of medical importance except which of the following?
All are true regarding the development of T-cells, except?
Rosette formation with sheep RBCs (SRBCs) indicates functioning of -
Cytolytic activity of membrane attack complex is modulated by ?
Which of the following statements about interleukin-1 is false?
Which of the following is a superantigen ?
NEET-PG 2013 - Microbiology NEET-PG Practice Questions and MCQs
Question 581: Which of the following is a saccharolytic species of Clostridium?
- A. Clostridium tetani
- B. Clostridium septicum (Correct Answer)
- C. Clostridium cochlearium
- D. None of the options
Explanation: ***Clostridium septicum*** - *Clostridium septicum* is a **saccharolytic** species, meaning it ferments carbohydrates to produce gas, which contributes to the rapid tissue destruction seen in **gas gangrene**. - Its ability to rapidly consume sugars in tissues fuels its invasive growth and toxin production, which is characteristic of its pathogenic mechanism. *Clostridium tetani* - *Clostridium tetani* is a **proteolytic** species, primarily deriving its energy from **protein degradation**. - It does not ferment carbohydrates, and its pathogenicity is mainly due to the production of **tetanospasmin**, a neurotoxin. *Clostridium cochlearium* - *Clostridium cochlearium* is a **proteolytic** species that metabolizes proteins and amino acids. - It is not known for significant saccharolytic activity and is typically found in environments rich in protein. *None of the options* - This option is incorrect because *Clostridium septicum* is indeed a saccharolytic species, as detailed above.
Question 582: Which staining method is specifically used for the detection of mycoplasma?
- A. Dienes method (Correct Answer)
- B. Fontana method
- C. Lavaditi method
- D. No applicable method
Explanation: ***Dienes method*** - The **Dienes staining method** is a specialized procedure used specifically to identify **Mycoplasma colonies** grown on agar medium. - It works by staining the characteristic **fried-egg appearance** of Mycoplasma colonies. *Fontana method* - The Fontana method is a **silver impregnation stain** used primarily for the visualization of **spirochetes**, such as *Treponema pallidum*. - It is not suitable for detecting Mycoplasma due to their distinct cellular structure and size differences compared to spirochetes. *Lavaditi method* - The Lavaditi method is another type of **silver stain** developed for the detection of **spirochetes** in tissue sections. - Similar to the Fontana method, it is not appropriate for the identification of Mycoplasma. *No applicable method* - This statement is incorrect as the **Dienes method** is, in fact, specifically applicable and widely used for the detection and identification of Mycoplasma colonies. - There are established microbiological techniques for identifying Mycoplasma.
Question 583: All are non-sporing anaerobes of medical importance except which of the following?
- A. Bacteroides
- B. Fusobacterium
- C. Clostridia (Correct Answer)
- D. Actinomyces
Explanation: ***Clostridia*** - This genus is characterized by its ability to form **spores**, which are highly resistant structures allowing survival in adverse conditions. - Examples include *Clostridium difficile*, *Clostridium tetani*, and *Clostridium botulinum*, all of which are important human pathogens. *Actinomyces* - *Actinomyces* are **non-sporing, Gram-positive, anaerobic rods** that cause chronic, granulomatous infections, often forming sinus tracts. - They are known for producing characteristic **"sulfur granules"** in pus. *Bacteroides* - *Bacteroides* are **non-sporing, Gram-negative, anaerobic rods** that are a major component of the normal human gut flora. - They are frequently involved in **intra-abdominal infections** and abscess formation. *Fusobacterium* - *Fusobacterium* species are **non-sporing, Gram-negative, fusiform-shaped anaerobic rods**. - They are common in the **oral cavity** and can cause infections such as Vincent's angina and Lemierre's syndrome.
Question 584: 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 585: 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.
Question 586: 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 587: 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 588: 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.
Pediatrics
1 questionsAt what age does clinically significant IgG production begin?
NEET-PG 2013 - Pediatrics NEET-PG Practice Questions and MCQs
Question 581: 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.