Anatomy
2 questionsB cells are located in which region of lymph nodes?
Which type of glial cell is derived from mesodermal origin?
NEET-PG 2015 - Anatomy NEET-PG Practice Questions and MCQs
Question 371: B cells are located in which region of lymph nodes?
- A. Paracortical region
- B. Cortical follicles (Correct Answer)
- C. Subcapsular region
- D. Medullary sinuses
Explanation: ***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.
Question 372: Which type of glial cell is derived from mesodermal origin?
- A. Macroglial cells
- B. Microglial cells (Correct Answer)
- C. Oligodendrocytes
- D. Ependymal cells
Explanation: ***Microglial cells*** - **Microglial cells** are unique among glial cells as they originate from **mesoderm**, specifically from **monocyte/macrophage precursors** in the bone marrow [1]. - They function as the **immune cells of the central nervous system (CNS)**, scavenging for plaques, damaged neurons, and infectious agents [1]. *Macroglial cells* - This is a broad category that includes **astrocytes, oligodendrocytes, and ependymal cells**, all of which are derived from **neuroectoderm**, not mesoderm [1]. - They perform various supportive roles but are distinct in origin from microglial cells [1]. *Oligodendrocytes* - **Oligodendrocytes** are derived from **neuroectoderm** and are responsible for forming the **myelin sheath** around axons in the CNS [2]. - Myelination is crucial for rapid and efficient nerve impulse conduction. *Ependymal cells* - **Ependymal cells** are derived from **neuroectoderm** and line the **ventricles of the brain** and the **central canal of the spinal cord**. - They play a role in the production and circulation of **cerebrospinal fluid (CSF)**.
Biochemistry
3 questionsWhich of the following statements about Niemann-Pick disease is false?
How many molecules of Acetyl CoA are produced from β-oxidation of palmitic acid?
What primarily forms the core of chylomicrons?
NEET-PG 2015 - Biochemistry NEET-PG Practice Questions and MCQs
Question 371: Which of the following statements about Niemann-Pick disease is false?
- A. Due to deficiency of sphingomyelinase.
- B. CNS symptoms are present in type A.
- C. Type B Niemann-Pick disease is characterized by severe neurological symptoms. (Correct Answer)
- D. Histiocytes show PAS positive inclusions, and Type A is more severe.
Explanation: ***Type B Niemann-Pick disease is characterized by severe neurological symptoms.*** - This statement is **false** because **Type B Niemann-Pick disease** generally presents with **visceral involvement** (e.g., hepatosplenomegaly, lung disease) with **minimal to no neurological symptoms**. - **Severe neurological symptoms** are characteristic of **Type A Niemann-Pick disease**, which involves widespread CNS degeneration and a more rapidly progressive course. *Due to deficiency of sphingomyelinase.* - This statement is **true**. - Niemann-Pick disease (Types A and B) is caused by a deficiency of the enzyme **acid sphingomyelinase**, leading to the accumulation of sphingomyelin within lysosomes, particularly in macrophages. *CNS symptoms are present in type A.* - This statement is **true**. - **Type A Niemann-Pick disease** is the most severe form and is characterized by significant **neurodegeneration** in addition to visceral involvement. - Patients typically present with **developmental regression**, **ataxia**, and **spasticity** due to extensive sphingomyelin deposition in the central nervous system. *Histiocytes show PAS positive inclusions, and Type A is more severe.* - This statement is **true**. - The characteristic "foam cells" (lipid-laden macrophages/histiocytes) found in tissues of Niemann-Pick patients stain positive with **periodic acid–Schiff (PAS)** due to accumulated sphingomyelin. - **Type A Niemann-Pick disease** is indeed the most severe form, with a rapidly progressive course and early fatality, usually by early childhood.
Question 372: How many molecules of Acetyl CoA are produced from β-oxidation of palmitic acid?
- A. 3 acetyl CoA
- B. 16 Acetyl CoA
- C. 6 acetyl CoA
- D. 8 acetyl CoA (Correct Answer)
Explanation: ***8 acetyl CoA*** - Palmitic acid is a **16-carbon saturated fatty acid (C16:0)**. During β-oxidation, each cycle cleaves two carbons as **acetyl CoA**. - The formula for acetyl CoA produced is **n/2**, where n = number of carbons. For palmitic acid: 16/2 = **8 acetyl CoA molecules**. - Alternatively: Palmitic acid undergoes **7 cycles of β-oxidation** [(n/2) - 1 = 7], each producing 1 acetyl CoA (7 total), plus the final 2-carbon fragment forming the 8th acetyl CoA. *3 acetyl CoA* - This number is too low for a 16-carbon fatty acid. **Short-chain fatty acids** would produce fewer acetyl CoA molecules. - This value corresponds to β-oxidation of a **6-carbon fatty acid** (hexanoic acid), not palmitic acid. *6 acetyl CoA* - This number is also too low for a 16-carbon fatty acid. - This quantity would be produced from a **12-carbon fatty acid** (lauric acid), not palmitic acid. *16 Acetyl CoA* - This number is too high and would incorrectly imply that each carbon forms an acetyl CoA independently. - Sixteen acetyl CoA molecules would be produced from a **32-carbon fatty acid**, which is extremely rare in biological systems.
Question 373: What primarily forms the core of chylomicrons?
- A. Triglycerides and Cholesterol together
- B. Triglycerides (Correct Answer)
- C. Free fatty acids
- D. Triglyceride, Cholesterol and Phospholipids
Explanation: ***Triglycerides*** - Chylomicrons are primarily responsible for transporting **dietary triglycerides** from the intestines to other tissues. - Their large core, composed mainly of **triglycerides**, allows efficient transport of these hydrophobic molecules. *Triglycerides and Cholesterol together* - While **cholesterol** is present in chylomicrons, it is less abundant than **triglycerides** and primarily exists as **cholesterol esters** in the core. - The core is not an equal mixture; **triglycerides** overwhelmingly dominate the volume. *Free fatty acids* - **Free fatty acids** are transported in the blood primarily bound to **albumin**, not within the core of chylomicrons. - Chylomicrons typically carry **esterified fatty acids** as part of triglycerides. *Triglyceride, Cholesterol and Phospholipids* - **Phospholipids** form the outer monolayer of the chylomicron, along with apoproteins, making them **amphipathic**. - They do not constitute a core component but rather the **surface interface** with the aqueous environment.
Microbiology
1 questionsIn the context of immune response, which of the following cell types does not express MHC class II molecules?
NEET-PG 2015 - Microbiology NEET-PG Practice Questions and MCQs
Question 371: In the context of immune response, which of the following cell types does not express MHC class II molecules?
- A. Cortical macrophages
- B. Neutrophils
- C. Medullary macrophages
- D. NK cells (Correct Answer)
Explanation: ***NK cells*** - **Natural Killer (NK) cells)** are innate lymphocytes that do **NOT express MHC class II molecules** under any circumstances. - NK cells use alternative recognition mechanisms (KIRs, activating receptors) to detect target cells, primarily recognizing the **absence of MHC class I** or stress-induced ligands. - They function in innate immunity without antigen presentation capability. - **This is the best answer** as NK cells never express MHC class II, making them distinctly different from professional APCs. *Cortical macrophages* - **Cortical macrophages** in lymphoid organs are professional **antigen-presenting cells (APCs)** that constitutively express **MHC class II molecules**. - They present processed antigens to CD4+ T helper cells, playing a crucial role in initiating adaptive immune responses. *Medullary macrophages* - **Medullary macrophages** are also professional APCs that constitutively express **MHC class II molecules**. - They participate in antigen presentation and immune surveillance within the medullary regions of lymphoid tissues. *Neutrophils* - Neutrophils are granulocytes that **typically do not constitutively express MHC class II molecules** in their resting state. - However, under certain inflammatory conditions with prolonged stimulation (IFN-γ, GM-CSF), neutrophils can be induced to express low levels of MHC class II. - While neutrophils generally lack MHC class II, **NK cells are the more definitive answer** as they never express MHC class II under any physiological or pathological conditions.
Pathology
3 questionsPost-streptococcal glomerulonephritis (PSGN) is an example of which type of hypersensitivity?
What is the initial event in serum sickness?
Which protein is defective in dilated cardiomyopathy?
NEET-PG 2015 - Pathology NEET-PG Practice Questions and MCQs
Question 371: Post-streptococcal glomerulonephritis (PSGN) is an example of which type of hypersensitivity?
- A. Type -1 hypersensitivity
- B. Type -2 hypersensitivity
- C. Type -3 hypersensitivity (Correct Answer)
- D. Type -4 hypersensitivity
Explanation: ***Type -3 hypersensitivity*** - Post-streptococcal glomerulonephritis (PSGN) is caused by **immune complex deposition**, a hallmark of type III hypersensitivity reactions [1][2][3]. - It involves the formation of **antigen-antibody complexes** following a streptococcal infection, leading to inflammation in the kidneys [1][2]. *Type -1 hypersensitivity* - Characterized by **IgE-mediated** reactions, such as allergies and anaphylaxis, which do not apply to PSGN. - It typically involves **mast cells** and histamine release, notably absent in PSGN cases. *Type -4 hypersensitivity* - Involves **T-cell mediated** responses and is related to delayed-type reactions, not applicable to PSGN. - Common examples include **contact dermatitis** and graft-versus-host disease, differing fundamentally from PSGN's mechanism. *Type -2 hypersensitivity* - Characterized by **antibody-mediated cytotoxicity**, such as in hemolytic anemia, unrelated to immune complexes in PSGN. - Typically involves direct damage to cells, contrasting with the immune complex mechanism observed in PSGN [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 214-215. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 910-915. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 215-216.
Question 372: What is the initial event in serum sickness?
- A. It is associated with hypocomplementemia.
- B. It is a type III hypersensitivity reaction.
- C. It occurs due to exposure to heterologous antigens. (Correct Answer)
- D. It can lead to leukocytoclastic vasculitis.
Explanation: ***Can lead to leukocytoclastic vasculitis*** - Serum sickness is characterized by the formation of **immune complexes**, which can trigger **leukocytoclastic vasculitis** affecting the blood vessels [1][2]. - Symptoms can include **rash, fever, and arthralgia**, typically occurring 1-3 weeks after exposure to the offending antigen [2]. *Can occur due to homologous antigen* - Serum sickness is usually a reaction to **heterologous** antigens, such as those from animal serum, not **homologous** ones. - Homologous antigens do not typically elicit the immune response seen in serum sickness; hence, this statement is incorrect. *Type 2 hypersensitivity* - Serum sickness is classified as a **Type III hypersensitivity** reaction due to the immune complex formation, not Type II [1]. - Type II is characterized by antibody-mediated destruction of **target cells**, which does not apply here. *Hypercomplementemia* - Serum sickness is associated with **hypocomplementemia** due to complement consumption from immune complex formation, not hypercomplementemia. - This can lead to **decreased complement levels** during the response, making this statement incorrect. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 214-216. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 172-173.
Question 373: Which protein is defective in dilated cardiomyopathy?
- A. Tropomyosin
- B. Myosin
- C. Troponin
- D. Dystrophin (Correct Answer)
Explanation: ***Dystrophin*** - **Dystrophin** is a crucial protein in the **muscle cell membrane** that anchors the cytoskeleton to the extracellular matrix. - Defects in dystrophin lead to sarcolemmal fragility, causing muscle damage and can result in **dilated cardiomyopathy**, especially in conditions like **Duchenne muscular dystrophy** [1]. *Myosin* - **Myosin** is a fundamental **motor protein** involved in muscle contraction, forming the thick filaments. - While mutations in myosin can cause various cardiac conditions, like hypertrophic cardiomyopathy, direct primary defects in myosin are not typically identified as the cause of dilated cardiomyopathy [2]. *Troponin* - **Troponin** is a protein complex that regulates muscle contraction by controlling the interaction between actin and myosin, particularly in response to calcium. - Although troponins are vital for cardiac function and are released during myocardial injury, their primary defect is not typically implicated in the etiology of dilated cardiomyopathy [2]. *Tropomyosin* - **Tropomyosin** is a protein that winds around actin filaments and, along with troponin, regulates the binding of myosin to actin. - While essential for muscle contraction, direct defects in tropomyosin are not a common genetic cause of dilated cardiomyopathy. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Peripheral Nerves and Skeletal Muscles, pp. 1244-1245. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, p. 574.
Surgery
1 questionsWhich solid organ is considered to have the lowest risk of rejection during transplantation?
NEET-PG 2015 - Surgery NEET-PG Practice Questions and MCQs
Question 371: Which solid organ is considered to have the lowest risk of rejection during transplantation?
- A. Pancreas
- B. Kidney
- C. Heart
- D. Liver (Correct Answer)
Explanation: ***Liver*** - The liver has a unique immunologic environment, often referred to as **immunologic privilege**, which contributes to its lower rates of rejection compared to other transplanted solid organs. - It produces various **immunosuppressive factors** and has a high capacity for regeneration and repair, adapting more readily to the recipient's immune system. - The liver's **dual blood supply** (hepatic artery and portal vein) and tolerogenic properties make it the most immunologically privileged solid organ. *Pancreas* - **Pancreas transplantation** carries a high risk of rejection, with rejection rates significantly higher than liver transplantation. - Pancreatic tissue is highly **immunogenic** due to its endocrine and exocrine functions, requiring aggressive immunosuppression. - Often transplanted with kidney in diabetic patients, and rejection episodes are common. *Kidney* - Kidney transplantation is common, but it carries a significant risk of both **acute and chronic rejection**, requiring lifelong immunosuppression. - The kidney expresses various **MHC antigens** that are readily recognized by the recipient's immune system, making it more immunogenic than the liver. *Heart* - **Heart transplantation** is associated with a high risk of rejection due to the rich vascularity and immunogenicity of cardiac tissue. - It often requires aggressive immunosuppressive regimens to prevent both **acute cellular rejection** and **antibody-mediated rejection**.