Anatomy
1 questionsWhich type of glial cell is derived from mesodermal origin?
NEET-PG 2015 - Anatomy NEET-PG Practice Questions and MCQs
Question 361: 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
4 questionsWhich protein does the domain of plasminogen resemble?
Which 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 361: Which protein does the domain of plasminogen resemble?
- A. Fibrinogen (a clotting protein)
- B. LDL receptor (a lipid metabolism protein)
- C. Apolipoprotein (a) (a lipoprotein) (Correct Answer)
- D. Prothrombin (a coagulation protein)
Explanation: ***Apolipoprotein (a) (a lipoprotein)*** - **Plasminogen** and **apolipoprotein (a)** share structural homology, specifically due to the presence of **kringle domains**. - This structural similarity suggests a potential for apolipoprotein (a) to **interfere with plasminogen’s fibrinolytic activity**, contributing to **atherosclerosis**. *Fibrinogen (a clotting protein)* - While plasmin acts on fibrinogen (and its derivative fibrin), its domain structure does not **resemble fibrinogen**. - **Fibrinogen** is a large, multi-domain glycoprotein crucial for **clot formation**, distinct from plasminogen's primarily **kringle-rich structure**. *LDL receptor (a lipid metabolism protein)* - The **LDL receptor** is involved in **cholesterol uptake** by cells and has structural features like ligand-binding repeats and epidermal growth factor (EGF) repeats. - Its domain structure is **not similar to plasminogen**, which is characterized by **kringle domains** and a protease domain. *Prothrombin (a coagulation protein)* - **Prothrombin** is a precursor to thrombin, featuring **gla domains**, kringle-like domains (though structurally distinct from plasminogen's), and a serine protease domain. - While both are involved in coagulation/fibrinolysis, their **overall domain arrangements and specific kringle structures differ** significantly.
Question 362: 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 363: 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 364: 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
2 questionsInterleukin 2 is produced by
IFN-gamma is produced by
NEET-PG 2015 - Microbiology NEET-PG Practice Questions and MCQs
Question 361: Interleukin 2 is produced by
- A. T helper cells 1 (Correct Answer)
- B. T helper cells 2
- C. Natural killer cells
- D. Basophils
Explanation: ***T helper cells 1*** - **T helper 1 (Th1) cells** are a primary source of **interleukin-2 (IL-2)**, which is crucial for the proliferation and survival of T cells. - IL-2 acts as a **T-cell growth factor**, promoting the expansion of activated T cells, including cytotoxic T lymphocytes. *T helper cells 2* - **T helper 2 (Th2) cells** primarily produce cytokines like **IL-4, IL-5, IL-6, IL-10, and IL-13**, which are involved in humoral immunity and allergic responses. - While Th2 cells are important for immune responses, they are not major producers of IL-2. *Natural killer cells* - **Natural killer (NK) cells** are part of the innate immune system and produce cytokines such as **interferon-gamma (IFN-$\gamma$)** and **tumor necrosis factor-alpha (TNF-$\alpha$)**. - They are not a significant source of IL-2, which is primarily a T-cell derived growth factor. *Basophils* - **Basophils** are granulocytes involved in allergic reactions and anti-parasitic immunity, producing mediators like **histamine** and cytokines such as **IL-4** and **IL-13**. - Basophils do not produce IL-2; their role is distinct in the immune response compared to T cells.
Question 362: IFN-gamma is produced by
- A. Macrophages
- B. T-cells (Correct Answer)
- C. Neutrophils
- D. B-cells
Explanation: ***T-cells*** - **Interferon-gamma (IFN-γ)** is a crucial cytokine primarily produced by **activated T-lymphocytes**, especially **Th1 cells** and **cytotoxic T lymphocytes (CTLs)**. - Natural killer (NK) cells also produce **IFN-γ**, which plays a key role in **antiviral** and **antitumor immunity**, as well as in promoting **Type 1 immune responses**. *Macrophages* - While macrophages are **responsive to IFN-γ** (e.g., becoming activated), they are not the primary producers of this cytokine. - Macrophages primarily produce other cytokines such as **IL-1, IL-6, TNF-alpha**, and **IL-12** in response to infection or inflammation. *Neutrophils* - **Neutrophils** are key phagocytes in the innate immune system and are primarily involved in engulfing and killing pathogens. - They are not known to be a significant source of **IFN-γ** production; their main defensive mechanisms involve **phagocytosis**, **degranulation**, and **NETosis**. *B-cells* - **B-cells** are central to humoral immunity, specializing in **antibody production** and acting as **antigen-presenting cells**. - They generally do not produce **IFN-γ**; instead, their cytokine repertoire includes **IL-10**, **IL-6**, and **lymphotoxin**.
Pathology
1 questionsReversible change from one cell type to another is known as -
NEET-PG 2015 - Pathology NEET-PG Practice Questions and MCQs
Question 361: Reversible change from one cell type to another is known as -
- A. Hypertrophy
- B. Dysplasia
- C. Hyperplasia
- D. Metaplasia (Correct Answer)
Explanation: ***Metaplesia*** - Refers to the **reversible change** from one cell type to another in response to chronic irritation or damage [1][2]. - It often occurs as an adaptive response in **epithelial tissues**, such as in the respiratory tract in smokers [1][2]. *Hypertrophy* - Represents an **increase in cell size** rather than a change in cell type [2]. - It is often a response to increased functional demand, as seen in **cardiac muscle** in athletes. *Hyperplesia* - Refers to an **increase in cell number** within a tissue or organ, not a change in cell type [2]. - Common in conditions such as **benign prostatic hyperplasia** but does not involve differentiation into other cell types. *Dysplasia* - Indicates an **abnormal growth or development** of cells, leading to disordered morphology rather than a transformation into another cell type. - It is often a precursor to cancer but does not signify the reversible nature of metaplasia. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, p. 49. [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. 85-92.
Physiology
2 questionsChemotaxis is mediated by-
Interleukin responsible for Pyrexia is:
NEET-PG 2015 - Physiology NEET-PG Practice Questions and MCQs
Question 361: Chemotaxis is mediated by-
- A. Histamine
- B. Leukotriene C4 and C3a
- C. Bradykinin
- D. Leukotriene B4 and C5a (Correct Answer)
Explanation: ***Leukotriene B4 and C5a*** - Both **Leukotriene B4** [2] and **C5a** [1] are potent **chemoattractants** that guide the migration of neutrophils and other immune cells to sites of inflammation. - They are crucial in amplifying the **immune response**, particularly during acute inflammatory reactions. *Histamine* - Primarily involved in **vasodilation** and increased **vascular permeability**, rather than mediating chemotaxis. - Does not specifically attract immune cells to sites of injury or infection like leukotrienes do. *Bradykinin* - Mainly functions in **pain sensation** and promoting **vascular permeability**, not as a direct chemotactic agent. - It influences inflammation but does not effectively recruit immune cells to tissues. *Leukotriene C4 and C3a* - **Leukotriene C4** is involved in bronchoconstriction, while **C3a** [1] has roles in the complement system but is less potent than C5a in chemotaxis. - These mediators have different primary roles in inflammation, lacking the specificity of B4 and C5a for leukocyte attraction. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 99-100. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 95-96.
Question 362: Interleukin responsible for Pyrexia is:
- A. IL1 (Correct Answer)
- B. IL4
- C. IL3
- D. IL8
Explanation: ***IL1*** - **Interleukin-1 (IL-1)** is a primary **endogenous pyrogen**, directly acting on the thermoregulatory center in the hypothalamus to induce fever. - It stimulates the production of **prostaglandin E2 (PGE2)**, which then alters the hypothalamic set point, leading to increased body temperature. *IL3* - **Interleukin-3 (IL-3)** is a **hematopoietic growth factor** that primarily stimulates the proliferation and differentiation of hematopoietic stem cells. - Its main role is in the development of various blood cell lineages, not directly in inducing fever. *IL4* - **Interleukin-4 (IL-4)** is a key cytokine in **allergic reactions** and **Th2 immune responses**, promoting B cell activation and IgE production. - It does not directly cause pyrexia; its primary functions are related to humoral immunity and immune regulation. *IL8* - **Interleukin-8 (IL-8)**, also known as **CXCL8**, is a potent **chemotactic factor** for neutrophils and other immune cells. - Its main function is to recruit inflammatory cells to sites of infection or injury, not to induce fever directly.