Anatomy
1 questionsWhich type of glial cell is derived from mesodermal origin?
NEET-PG 2015 - Anatomy NEET-PG Practice Questions and MCQs
Question 341: 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 questionsHow many molecules of Acetyl CoA are produced from β-oxidation of palmitic acid?
What primarily forms the core of chylomicrons?
Which of the following is an example of an antiapoptotic gene?
NEET-PG 2015 - Biochemistry NEET-PG Practice Questions and MCQs
Question 341: 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 342: 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.
Question 343: Which of the following is an example of an antiapoptotic gene?
- A. FLIP (Correct Answer)
- B. P53
- C. BAX
- D. BIM
Explanation: ***FLIP*** - **FLIP** is an **antiapoptotic gene** that inhibits the activation of caspase-8, thereby blocking the extrinsic apoptotic pathway. - It acts as an **FLICE-inhibitory protein**, preventing the formation of the death-inducing signaling complex (DISC) or its downstream activation. *P53* - **P53** is a **tumor suppressor gene** that promotes apoptosis in response to DNA damage or cellular stress. - It is a **pro-apoptotic gene**, orchestrating cell cycle arrest and apoptosis to prevent the propagation of damaged cells. *BAX* - **BAX** is a **pro-apoptotic gene** belonging to the Bcl-2 family, which promotes the release of cytochrome c from mitochondria. - This release initiates the **intrinsic apoptotic pathway**, leading to caspase activation and cell death. *BIM* - **BIM** is a **pro-apoptotic gene** of the Bcl-2 family, acting as a sensitizer for apoptosis by binding to and inhibiting anti-apoptotic Bcl-2 family proteins. - Its activation leads to the **neutralization of survival factors**, thereby promoting mitochondrial outer membrane permeabilization and apoptosis.
Microbiology
1 questionsIFN-gamma is produced by
NEET-PG 2015 - Microbiology NEET-PG Practice Questions and MCQs
Question 341: 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
3 questionsHyaline degeneration is found in -
During cell death, myelin figures are derived from which of the following?
Which of the following is not an apoptotic gene?
NEET-PG 2015 - Pathology NEET-PG Practice Questions and MCQs
Question 341: Hyaline degeneration is found in -
- A. Alzheimer's disease
- B. Alcoholic liver disease (Correct Answer)
- C. Acute myocardial infarction
- D. Acute appendicitis
Explanation: ***Alcoholic liver disease*** - **Mallory bodies**, a form of hyaline degeneration, are characteristic histologic findings in hepatocytes in alcoholic liver disease. - They represent aggregates of **intermediate filaments** and other proteins, indicating severe hepatocellular damage. *Acute myocardial infarction* - Characterized by **coagulative necrosis** of cardiac myocytes due to ischemia, not hyaline degeneration. - Inflammation and subsequent repair with **fibrosis** are key features. *Alzheimer's disease* - Defined by the presence of **senile plaques** (amyloid-beta deposits) and **neurofibrillary tangles** (hyperphosphorylated tau protein). - These are specific protein aggregates, distinct from hyaline degeneration of cellular components. *Acute appendicitis* - Involves acute inflammation of the appendix, leading to **neutrophilic infiltration** and often **fibrinopurulent exudate**. - There is no characteristic hyaline degeneration associated with this inflammatory process.
Question 342: During cell death, myelin figures are derived from which of the following?
- A. Cell membrane (lipid bilayer) (Correct Answer)
- B. Cytoplasmic components
- C. Mitochondrial structures
- D. Nuclear membrane
Explanation: ***Cell membrane (lipid bilayer)*** - **Myelin figures** are whorled phospholipid masses formed during cell injury and death from the breakdown of **cellular membranes**, particularly the plasma membrane and **endoplasmic reticulum**. - These structures represent damaged membrane lipids (phospholipids) that undergo structural rearrangement into concentric lamellar (layered) configurations resembling myelin. - The term "cell membrane" encompasses both the plasma membrane and lipid-rich intracellular membranes, making this the most accurate answer among the options provided. - They are a characteristic morphologic feature of **irreversible cell injury** and can be seen with electron microscopy. *Cytoplasmic components* - While cytoplasmic proteins and organelles do degrade during cell death, they do not form the organized **phospholipid structures** characteristic of myelin figures. - Cytoplasmic breakdown produces different morphologic changes such as cytoplasmic eosinophilia and loss of ribosomes. *Mitochondrial structures* - Mitochondria have their own membranes that are damaged during cell death (leading to release of cytochrome c and other apoptotic factors). - However, mitochondrial membranes are not the primary source of **myelin figures**, which predominantly arise from ER and plasma membranes. *Nuclear membrane* - The nuclear envelope does fragment during cell death, contributing to nuclear changes like **karyopyknosis, karyorrhexis, and karyolysis**. - While technically a membrane structure, the nuclear envelope is not the primary source of myelin figures, which are mainly derived from the more abundant plasma and ER membranes.
Question 343: Which of the following is not an apoptotic gene?
- A. Mcl-1
- B. Bax
- C. P53
- D. n-myc (oncogene) (Correct Answer)
Explanation: ***n-myc*** - **n-myc** is primarily known for its role in **cell proliferation and differentiation**, not specifically associated with apoptosis [2]. - It is an **oncogene** that can contribute to tumorigenesis, but does not directly regulate apoptotic pathways [3]. *P53* - **P53** is a well-known **tumor suppressor gene** that plays a crucial role in inducing apoptosis in response to DNA damage [1]. - Activation of P53 leads to the transcription of genes that promote cell death, thus it is definitely an apoptotic gene [1]. *Bax* - **Bax** is a pro-apoptotic member of the **Bcl-2 family**, promoting apoptosis by facilitating mitochondrial outer membrane permeabilization [4,5]. - It plays a direct role in the apoptotic pathway, making it an important apoptotic gene [5]. *Mcl-1* - **Mcl-1** is an anti-apoptotic member of the **Bcl-2 family**, which helps prevent apoptosis by inhibiting pro-apoptotic factors [2,3]. - Its function is to **promote cell survival**, not apoptosis, but it is still classified as part of the apoptotic regulatory network [3]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 303-304. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, p. 310. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 310-311. [4] 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, pp. 65-67. [5] 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. 80-81.
Physiology
2 questionsTetany in muscle occurs in spite of normal serum Ca2+ level. Which ion is responsible?
Which of the following receptors is stimulated by sustained pressure?
NEET-PG 2015 - Physiology NEET-PG Practice Questions and MCQs
Question 341: Tetany in muscle occurs in spite of normal serum Ca2+ level. Which ion is responsible?
- A. Mg2+
- B. K+
- C. Na+
- D. Ionized Ca2+ (Correct Answer)
Explanation: ***Ionized Ca2+*** - While total serum calcium might be normal, **tetany** is specifically caused by a decrease in the concentration of **ionized (free) calcium** in the extracellular fluid. - Ionized calcium is the physiologically active form of calcium responsible for neuromuscular excitability. *Mg2+* - **Hypomagnesemia** can exacerbate hypocalcemia and contribute to tetany, but it is not the primary ion directly responsible for tetany when **total serum calcium is normal**. - A deficiency in Mg2+ can impair the release of **parathyroid hormone** and reduce target organ responsiveness to PTH. *K+* - Abnormalities in **potassium levels** (hypokalemia or hyperkalemia) primarily affect cardiac and muscular excitability, leading to arrhythmias or muscle weakness/paralysis. - While electrolyte imbalances are interconnected, changes in potassium are not the direct cause of tetany due to calcium's role. *Na+* - **Sodium ions** are crucial for nerve impulse transmission and muscle contraction by establishing the resting membrane potential and initiating action potentials. - However, direct changes in sodium concentration do not typically cause tetany; rather, they can lead to neurological symptoms like seizures (hyponatremia) or altered mental status (hypernatremia).
Question 342: Which of the following receptors is stimulated by sustained pressure?
- A. Ruffini's end organ (Correct Answer)
- B. Merkel's disc
- C. Hair cells
- D. Meissner Corpuscles
Explanation: ***Ruffini's end organ*** - These are **slowly adapting mechanoreceptors** located deep in the dermis and subcutaneous tissue. - They are responsible for detecting **sustained pressure**, stretch, and position sense. *Merkel's disc* - These are **slowly adapting mechanoreceptors** found in the basal epidermis. - They are crucial for sensing **light touch** and **two-point discrimination**. *Hair cells* - These are **mechanoreceptors** primarily found in the inner ear, responsible for hearing and balance. - They are not involved in the perception of somatosensory stimuli like pressure on the skin. *Meissner Corpuscles* - These are **rapidly adapting mechanoreceptors** located in the dermal papillae, close to the skin surface. - They are primarily involved in detecting **light touch** and **discriminative touch**, especially changes in texture.