Anatomy
1 questionsWhich type of glial cell is derived from mesodermal origin?
NEET-PG 2015 - Anatomy NEET-PG Practice Questions and MCQs
Question 401: 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
2 questionsHow 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 401: 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 402: 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.
Internal Medicine
2 questionsWhich of the following statements about sickle cell disease is true?
Which of the following is not a feature of Poststreptococcal Glomerulonephritis (PSGN)?
NEET-PG 2015 - Internal Medicine NEET-PG Practice Questions and MCQs
Question 401: Which of the following statements about sickle cell disease is true?
- A. Sickling is completely reversible with oxygenation, making it clinically insignificant.
- B. Sickling leads to a significant increase in overall MCHC levels in the blood.
- C. Fetal hemoglobin inhibits sickling. (Correct Answer)
- D. Sickling occurs exclusively in the homozygous state and never in the heterozygous state.
Explanation: ***Sickling is reversible with oxygenation*** - When oxygen tension is restored, hemoglobin S can re-hydrate and revert to its normal shape, reducing sickling. - This reversible process is essential for managing episodes of vaso-occlusive crisis in sickle cell disease. *Fetal hemoglobin facilitates Sickling* - Fetal hemoglobin (HbF) actually inhibits sickling by stabilizing the erythrocyte shape and reducing the proportion of hemoglobin S [1]. - Individuals with higher levels of HbF experience fewer sickling-related complications [1]. *Sickling occurs both in heterozygous and homozygous state* - Sickling primarily occurs in the homozygous state (HbSS); heterozygotes (HbAS) usually do not experience significant sickling effects [1]. - Heterozygous individuals may have a selective advantage against malaria, but they are not prone to sickle cell crises. *Sickling Leads to decreased MCHC* - Sickling does not directly lead to decreased mean corpuscular hemoglobin concentration (MCHC); MCHC is typically normal in sickle cell patients. - In fact, sickle cell disease often results in hemolysis and can lead to increased MCHC in some cases.
Question 402: Which of the following is not a feature of Poststreptococcal Glomerulonephritis (PSGN)?
- A. HTN
- B. Increased urea
- C. Increased creatinine
- D. Normal C3 level (Correct Answer)
Explanation: ***Normal C3 level*** - In Post-streptococcal glomerulonephritis (PSGN), **C3 levels are typically decreased** due to complement consumption during the inflammatory process. [1] - A **normal C3 level** would not be consistent with PSGN, as it suggests no significant complement activation. *Increased urea* - Increased urea can occur due to **impaired renal function**, which is common in PSGN due to glomerular inflammation. [1] - It's a typical finding reflecting the kidneys' inability to excrete waste products properly. *HTN* - Hypertension is frequently associated with PSGN due to **volume overload** and activation of the renin-angiotensin system. [1] [2] - It is a common clinical feature that results from increased fluid retention. *Increased creatinine* - Increased creatinine levels indicate **renal impairment**, which is characteristic of PSGN as kidney function is affected during this condition. [1] - This finding highlights the reduction in glomerular filtration rate (GFR), typical in glomerulonephritis. [2]
Pathology
4 questionsConcentric hypertrophy of left ventricle is seen in -
Which of the following statements is true regarding the Duffy Fy(a-b-) blood group?
What is a distinguishing feature of reticulocytes?
Irregular scarred kidney with pelvic dilatation is seen with?
NEET-PG 2015 - Pathology NEET-PG Practice Questions and MCQs
Question 401: Concentric hypertrophy of left ventricle is seen in -
- A. Congenital aortic stenosis due to bicuspid aortic valve (Correct Answer)
- B. Mitral Stenosis
- C. Aortic Regurgitation
- D. Hypertrophic Obstructive Cardiomyopathy
Explanation: ***Congenital aortic stenosis due to bicuspid aortic valve*** - **Aortic stenosis** creates a **pressure overload** on the left ventricle, leading to a compensatory increase in myocardial wall thickness without significant chamber dilation, which is the classic example of **concentric hypertrophy** [1]. - A **bicuspid aortic valve** is a common congenital anomaly that causes aortic stenosis and thus concentric left ventricular hypertrophy [2]. - This represents **acquired concentric hypertrophy** due to hemodynamic stress. *Mitral Stenosis* - **Mitral stenosis** primarily causes a pressure overload on the **left atrium**, leading to left atrial enlargement [3]. - While it can indirectly affect the left ventricle, it typically does not cause **concentric left ventricular hypertrophy** itself. *Aortic Regurgitation* - **Aortic regurgitation** leads to a **volume overload** on the left ventricle as blood flows back into the ventricle during diastole. - This typically results in **eccentric hypertrophy**, where both the ventricular wall thickness and chamber size increase significantly (dilated ventricle with increased mass) [1]. *Hypertrophic Obstructive Cardiomyopathy* - **Hypertrophic obstructive cardiomyopathy (HOCM)** is a **primary genetic myocardial disease** characterized by **asymmetric septal hypertrophy** rather than uniform concentric hypertrophy. - While HOCM involves significant myocardial hypertrophy, it represents a distinct pathophysiologic entity with **asymmetric distribution** (predominantly septal), not the classic concentric pattern seen with pressure overload states. - The hypertrophy in HOCM is **intrinsic (genetic)** rather than **adaptive (hemodynamic)** like in aortic stenosis. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, p. 536. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 562-563. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 533-534.
Question 402: Which of the following statements is true regarding the Duffy Fy(a-b-) blood group?
- A. lacks H- antigen
- B. lacks A-antigen
- C. All of the options
- D. lacks Fy(b) antigen (Correct Answer)
Explanation: ***lacks Fy(b) antigen*** - The **Duffy Fy(a-b-)** phenotype indicates absence of both Fy<sup>a</sup> and Fy<sup>b</sup> antigens on red blood cells. - Since the phenotype is **Fy(a-b-)**, it definitively lacks the **Fy<sup>b</sup> antigen** (indicated by the "b-" notation). - This phenotype is common in people of **African descent** and confers natural **resistance to Plasmodium vivax malaria**, as these antigens serve as receptors for the parasite to enter RBCs. *lacks H- antigen* - The **H antigen** belongs to the **H/h blood group system** and is a precursor to A and B antigens in the ABO system. - The absence of H antigen (Bombay phenotype - Oh) is completely **unrelated to the Duffy blood group system**. - Duffy antigens are on the **DARC (Duffy Antigen Receptor for Chemokines)** protein, distinct from the H antigen. *lacks A-antigen* - The **A antigen** is part of the **ABO blood group system** and defines blood types A and AB. - The Duffy blood group system is **genetically and structurally independent** from the ABO system. - Having Fy(a-b-) phenotype does not affect A antigen expression. *All of the options* - This is incorrect because the Duffy Fy(a-b-) phenotype **specifically refers only to the absence of Duffy antigens** (Fy<sup>a</sup> and Fy<sup>b</sup>). - It has **no relationship** with A, B, or H antigens, which belong to different blood group systems controlled by different genes on different chromosomes.
Question 403: What is a distinguishing feature of reticulocytes?
- A. Slightly larger in size than RBCs
- B. Presence of residual RNA and ribosomes (Correct Answer)
- C. Mature in bone marrow
- D. Constitute approximately 1% of the red cells
Explanation: ***Presence of residual RNA and ribosomes*** - This is the **defining and most distinguishing feature** of reticulocytes that differentiates them from mature red blood cells. - Reticulocytes contain residual **ribosomal RNA** and other organelles that are lost when they mature into erythrocytes. - This residual RNA forms a **reticular (network-like) pattern** when stained with supravital stains like **new methylene blue** or **brilliant cresyl blue**, which is the basis for their name and identification. - The presence of RNA allows for **reticulocyte counting**, an important marker of bone marrow erythropoietic activity. *Slightly larger in size than RBCs* - While reticulocytes may be slightly larger (polychromatophilic appearance), size variation is **not specific** and overlaps significantly with mature RBCs. - Size is not a reliable distinguishing feature and is not used for identification or counting. *Mature in bone marrow* - Reticulocytes are **released from the bone marrow** as immature red cells and complete their maturation in the **peripheral circulation** over 24-48 hours. - They do not fully mature in the bone marrow; their presence in peripheral blood is normal. *Constitute approximately 1% of the red cells* - Normal reticulocyte count is **0.5-2%** (or approximately 1%) of total red blood cells in healthy adults. - This is a **population characteristic** indicating normal erythropoietic activity, not a distinguishing cellular feature.
Question 404: Irregular scarred kidney with pelvic dilatation is seen with?
- A. Chronic pyelonephritis (Correct Answer)
- B. Polycystic kidney
- C. Renal artery stenosis
- D. Tuberculosis of kidney
Explanation: ***Chronic pyelonephritis*** - Characterized by irregular scarring of the kidney and often leads to **pelvic dilatation** due to recurrent infections and obstruction [1]. - The damage from inflammation results in **cortical scarring** and can affect kidney function significantly over time [1]. *Renal artery stenosis* - Typically presents with **hypertension** and may lead to ischemic atrophy, but does not cause significant **pelvic dilatation**. - The kidney appears small and often asymmetric, but not typically irregular and scarred. *Tuberculosis of kidney* - Can cause damage to the kidney, but usually leads to **caseating granulomas** and can cause abscesses, not specifically irregular scarring with pelvic dilation. - Often presents with systemic symptoms such as fever and night sweats, along with hematuria. *Polycystic kidney* - Characterized by multiple cysts in both kidneys leading to enlarged kidneys, but does not typically present as **irregularly scarred kidneys**. - Usually associated with **hemodynamic issues** and hypertension but not pelvic dilatation in the sense of scarring or fibrosis. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 937-939.
Surgery
1 questionsAmount of blood loss in Stage I of hemorrhagic shock is -
NEET-PG 2015 - Surgery NEET-PG Practice Questions and MCQs
Question 401: 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.