Anatomy
1 questionsWhich type of glial cell is derived from mesodermal origin?
NEET-PG 2015 - Anatomy NEET-PG Practice Questions and MCQs
Question 301: 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
1 questionsWhich of the following is a positive acute phase protein that enhances the acute phase response?
NEET-PG 2015 - Biochemistry NEET-PG Practice Questions and MCQs
Question 301: Which of the following is a positive acute phase protein that enhances the acute phase response?
- A. Fibrinogen (Correct Answer)
- B. Transferrin
- C. Albumin
- D. Prealbumin
Explanation: ***Fibrinogen*** - **Fibrinogen** is a key **positive acute phase protein** whose concentration increases significantly during inflammation - Its elevation contributes to the acute phase response by promoting **blood clotting** and influencing **erythrocyte sedimentation rate (ESR)** - Along with C-reactive protein (CRP), haptoglobin, and serum amyloid A, fibrinogen is among the major positive acute phase reactants *Transferrin* - **Transferrin** is a **negative acute phase protein**, meaning its concentration decreases during inflammation - This reduction is part of the body's iron-sequestration strategy to limit iron availability for invading pathogens - The decrease in transferrin helps restrict bacterial growth by reducing available iron *Albumin* - **Albumin** is a prominent **negative acute phase protein**, with its concentration decreasing during acute inflammation due to redistribution and reduced synthesis - It plays a vital role in maintaining **oncotic pressure** and transporting various substances - Its decline reflects the severity of inflammation and is used as a marker of the acute phase response *Prealbumin* - **Prealbumin** (also known as transthyretin) is a **negative acute phase protein** and a sensitive marker of nutritional status - Its rapid decline during inflammation makes it a useful indicator, as its synthesis is quickly reduced - It has a short half-life (2-3 days), making it more sensitive to acute changes than albumin
Microbiology
1 questionsInterleukin 2 is produced by
NEET-PG 2015 - Microbiology NEET-PG Practice Questions and MCQs
Question 301: 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.
Pathology
3 questionsWhich of the following is derived from fibroblast cells?
Which substance plays a significant role in the tumor metastasis cascade?
Rolling of leucocytes on endothelial cells is mediated by which of the following?
NEET-PG 2015 - Pathology NEET-PG Practice Questions and MCQs
Question 301: Which of the following is derived from fibroblast cells?
- A. MMP2
- B. Collagen (Correct Answer)
- C. Angiopoietin
- D. TGF-β
Explanation: ***Collagen*** - Collagen is a structural protein that is predominantly produced by **fibroblast cells** in the extracellular matrix [1][2]. - It provides tensile strength and structural support to various tissues, playing a crucial role in wound healing and tissue repair [2]. *TGF-13* - Transforming Growth Factor-beta 1 (TGF-β1) is primarily produced by **immune cells** and is involved in cell growth and differentiation, not primarily by fibroblasts. - It plays a role in **fibrosis** and inflammation, but is not directly synthesized by fibroblast cells themselves. *MMP2* - Matrix Metalloproteinase-2 (MMP-2) is produced by various cell types, including **endothelial and epithelial cells**, but not predominantly by fibroblasts. - It is involved in the degradation of **extracellular matrix** components rather than being a product of fibroblast synthesis. *Angiopoietin* - Angiopoietin is primarily secreted by **endothelial cells** and plays a significant role in blood vessel formation and maturation. - It is not derived from fibroblast cells and is unrelated to their primary function of producing the extracellular matrix. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. With Illustrations By, pp. 31-32. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. With Illustrations By, pp. 34-35.
Question 302: Which substance plays a significant role in the tumor metastasis cascade?
- A. TNF-alpha
- B. CD99
- C. NM23
- D. MMP-2 (Matrix Metalloproteinase-2) (Correct Answer)
Explanation: ***Collagenase IV*** - Collagenase IV is involved in the **degradation of extracellular matrix**, facilitating tumor invasion and metastasis [1,2]. - It plays a crucial role in breaking down **type IV collagen**, a major component of the **basement membrane**, allowing cancer cells to migrate [2]. *TNF-alpha* - While TNF-alpha is a cytokine that can promote **tumor growth**, it is not directly involved in the **metastatic cascade** like collagenase IV [3,4]. - It primarily functions in **inflammation** and immune response, affecting tumor microenvironment rather than directly facilitating invasion. *NM23* - NM23 is noted for its potential role as a **tumor suppressor**, and lower levels are associated with metastasis. - However, it does not play a direct role in the *metastatic cascade* itself [3,4], as it primarily influences **tumor progression** rather than matrix degradation. *CD99* - CD99 is a cell adhesion molecule implicated in **cell migration**, but it is not a significant factor in the **enzymatic breakdown** of tissue during metastasis [1,2]. - Its expression has more to do with **cell adhesion characteristics**, rather than directly promoting invasive capabilities. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 315-316. [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. 232-233. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 314-315. [4] 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. 233-234.
Question 303: Rolling of leucocytes on endothelial cells is mediated by which of the following?
- A. ICAM-1
- B. Integrin
- C. IL-8
- D. P-selectin (Correct Answer)
Explanation: ***P- selectin*** - P-selectin is a **cell adhesion molecule** crucial for the **rolling** of leukocytes on endothelial cells during the inflammatory response [1]. - It is expressed on activated endothelial cells and binds to **sialylated carbohydrates** on leukocytes, facilitating their transient adhesion [1]. *IL-8* - IL-8 is a **chemokine** that primarily acts as a chemotactic factor for neutrophils rather than mediating rolling on endothelium. - While it attracts leukocytes to sites of inflammation, it does not play a role in the initial contact or rolling process. *ICAM-1* - ICAM-1 is an **intercellular adhesion molecule** that facilitates **firm adhesion** rather than rolling of leukocytes. - It primarily interacts with **integrins** on leukocytes to stabilize their adhesion after rolling has occurred. *(3, integrin* - Integrins play a significant role in **firm adhesion** and not the rolling phase, interacting with receptors like ICAM-1. - The binding of integrins to their ligands occurs after leukocytes have initially rolled on the endothelium. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 87.
Pediatrics
1 questionsWhat is the typical lifespan of neonatal red blood cells (RBCs)?
NEET-PG 2015 - Pediatrics NEET-PG Practice Questions and MCQs
Question 301: What is the typical lifespan of neonatal red blood cells (RBCs)?
- A. 120-150 days
- B. 150-200 days
- C. 60-90 days (Correct Answer)
- D. 90-120 days
Explanation: ***60-90 days*** - The typical lifespan of **neonatal red blood cells (RBCs)** is **60-90 days**, which is **shorter than adult RBCs** (120 days). - This reduced lifespan is due to **increased membrane fragility**, **higher metabolic rate**, and **immature enzyme systems** in neonatal erythrocytes. - Neonatal RBCs contain more **fetal hemoglobin (HbF)** and have structural differences that contribute to their shorter survival. - This shorter lifespan contributes to the **physiological anemia of infancy** seen in the first few months of life. *90-120 days* - This range represents the typical lifespan of **adult RBCs**, not neonatal RBCs. - Neonatal RBCs have a **demonstrably shorter lifespan** compared to adult erythrocytes. - Confusing adult and neonatal RBC lifespans is a common error in clinical practice. *120-150 days* - This range is **longer than even adult RBC lifespan** (typically 120 days). - This would be **highly atypical** for any normal erythrocyte population. *150-200 days* - This represents an **abnormally prolonged** RBC lifespan not seen in normal physiology. - Such extended survival would suggest **pathological conditions** affecting RBC destruction or measurement error.
Physiology
2 questionsInterleukin responsible for Pyrexia is:
Chemotaxis is mediated by-
NEET-PG 2015 - Physiology NEET-PG Practice Questions and MCQs
Question 301: 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.
Question 302: 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.
Surgery
1 questionsAmount of blood loss in Stage I of hemorrhagic shock is -
NEET-PG 2015 - Surgery NEET-PG Practice Questions and MCQs
Question 301: Amount of blood loss in Stage I of hemorrhagic shock is -
- A. <10%
- B. <30%
- C. <15% (Correct Answer)
- D. <40%
Explanation: ***<15%*** - Stage I (Class I) hemorrhagic shock is characterized by **minimal blood loss of up to 15%** of total blood volume (up to 750 mL in a 70 kg adult). - This is the **universally accepted ATLS definition** for Class I hemorrhage. - At this level, compensatory mechanisms maintain normal vital signs with minimal clinical manifestations. - Patients typically show minimal or no symptoms, with possible mild tachycardia only. *<10%* - While this amount falls within Stage I, it represents only a **portion of the Stage I range** and is not the complete definition. - Stage I actually extends up to 15%, making this option incomplete. *<30%* - This range encompasses **both Stage I (up to 15%) and Stage II (15-30%)** hemorrhagic shock. - Stage II manifests with tachycardia (>100 bpm), tachypnea, and decreased pulse pressure, but blood pressure remains normal. - This is too broad to specifically define Stage I. *<40%* - This range covers **Stage I, II, and III** hemorrhagic shock. - Stage III (30-40% loss) presents with significant hypotension, marked tachycardia (>120 bpm), altered mental status, and decreased urine output. - This is far beyond the compensated Stage I definition.