Biochemistry
1 questionsWhat is the approximate half-life of albumin in the human body?
NEET-PG 2013 - Biochemistry NEET-PG Practice Questions and MCQs
Question 271: What is the approximate half-life of albumin in the human body?
- A. 30 days
- B. 20 days (Correct Answer)
- C. 3 days
- D. 7 days
Explanation: ***20 days*** - The **half-life of albumin** in the human body is approximately **20 days**, reflecting the time it takes for half of the circulating albumin to be catabolized or excreted. - This relatively long half-life means that changes in albumin levels, such as those due to malnutrition or liver disease, may take several weeks to become evident. *3 days* - A half-life of 3 days is too short for albumin, which is a major, long-lasting plasma protein. - Proteins with such a short half-life typically include more rapidly turnover proteins or small peptides. *7 days* - A half-life of 7 days is also too short for albumin, which plays a critical role in maintaining plasma oncotic pressure and transporting various substances. - While some proteins have a 7-day half-life, albumin's is considerably longer. *30 days* - A half-life of 30 days is longer than the typical half-life of albumin. - While some proteins may have half-lives in this range, 20 days is the more commonly accepted value for albumin.
Internal Medicine
2 questionsWhat is the most common location of gastrinoma?
What is the primary condition associated with positive anti-dsDNA antibodies?
NEET-PG 2013 - Internal Medicine NEET-PG Practice Questions and MCQs
Question 271: What is the most common location of gastrinoma?
- A. Pancreas
- B. Duodenum (Correct Answer)
- C. Jejunum
- D. Gall bladder
Explanation: ***Duodenum*** - The **duodenum** is the most common site for gastrinomas, accounting for over **half of all cases**, particularly in sporadic gastrinoma and Zollinger-Ellison syndrome. - These tumors are often **small** and **multiple** in the duodenum, making them challenging to locate. *Pancreas* - Pancreatic gastrinomas are also common, representing approximately **25-40% of cases**, but are less frequent than duodenal gastrinomas. - Pancreatic gastrinomas tend to be **larger** and more amenable to surgical resection when compared to duodenal gastrinomas. *Jejunum* - Gastrinomas found in the jejunum are **rare**, accounting for only a small percentage of cases. - The small intestine distal to the duodenum is an **uncommon site** for primary gastrinoma formation. *Gall bladder* - The **gallbladder** is not a typical location for gastrinoma development. - Gastrinomas are neuroendocrine tumors that arise from **gastrin-producing cells**, which are not found in the gallbladder.
Question 272: What is the primary condition associated with positive anti-dsDNA antibodies?
- A. RA
- B. SLE (Correct Answer)
- C. Scleroderma
- D. PAN
Explanation: ***SLE*** - **Anti-dsDNA antibodies** are a highly specific marker for **Systemic Lupus Erythematosus (SLE)** and are included in its diagnostic criteria [1]. - The levels of **anti-dsDNA antibodies** can also correlate with disease activity, particularly in cases of **lupus nephritis** [1]. *RA* - **Rheumatoid Arthritis (RA)** is primarily associated with **rheumatoid factor (RF)** and **anti-citrullinated protein antibodies (ACPA)** or **anti-CCP antibodies**. - While ANA (antinuclear antibodies) can be positive in RA, **anti-dsDNA antibodies** are not a characteristic serological marker [1]. *Scleroderma* - **Scleroderma**, or systemic sclerosis, is characterized by specific antibodies such as **anti-Scl-70 (topoisomerase I)**, **anti-centromere antibodies**, and **anti-RNA polymerase III antibodies**, depending on the subtype. - **Anti-dsDNA antibodies** are not typically found in scleroderma and do not play a role in its diagnosis [1]. *PAN* - **Polyarteritis Nodosa (PAN)** is a **necrotizing vasculitis** of medium-sized arteries and is not associated with **anti-dsDNA antibodies**. - PAN is generally considered an **ANCA-negative vasculitis**, and its diagnosis relies more on clinical features, angiography, and biopsy findings.
Pathology
4 questionsDystrophic calcification is seen in
Which of the following changes is NOT seen in atherosclerotic plaque at the time of rupture?
The MOST COMMON cause of concentric hypertrophy of left ventricle is?
What is the sequence of events in acute inflammation?
NEET-PG 2013 - Pathology NEET-PG Practice Questions and MCQs
Question 271: Dystrophic calcification is seen in
- A. Vitamin A intoxication
- B. Atheromatous plaque (Correct Answer)
- C. Milk alkali syndrome
- D. Hyperparathyroidism
Explanation: ***Atheromatous plaque*** - Dystrophic calcification occurs in **local areas of tissue injury**, like atheromatous plaques, where necrotic debris provides a nidus for calcification [1]. - It's commonly observed in chronic **atherosclerosis**, leading to the deposition of calcium in the damaged arterial walls [1]. *Hyperparathyroidism* - Typically associated with **metastatic calcification** due to elevated calcium levels, not dystrophic calcification [2][3]. - It results in renal, pulmonary, or vascular calcifications rather than calcifications in previously damaged tissues [3]. *Milk alkali syndrome* - Involves **hypercalcemia** and can lead to calcifications, but they are primarily **metastatic** rather than dystrophic [2][3]. - The syndrome results from excess calcium intake and is associated with renal injury rather than tissue necrosis. *Vitamin A intoxication* - Can cause **hyperostosis** and **calcifications**, but these are diffuse and not primarily dystrophic in nature. - The calcifications in this condition do not stem from necrotic tissue but rather are due to toxicity effects on bone metabolism. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 506-507. [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. 134-135. [3] 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. 76-77.
Question 272: Which of the following changes is NOT seen in atherosclerotic plaque at the time of rupture?
- A. Inflammatory cell infiltration
- B. Thick fibrous cap (Correct Answer)
- C. Cell debris
- D. Smooth muscle cell atrophy
Explanation: ***Smooth muscle cell hypertrophy*** - **Smooth muscle cell hypertrophy** is generally associated with stable plaques and does not typically occur in ruptured atherosclerotic plaques [2]. - At rupture, there is **loss of smooth muscle cells** and thinning of the fibrous cap, leading to plaque instability [2]. *Thin fibrosis cap* - A **thin fibrous cap** is a critical feature of vulnerable plaques, making them prone to rupture [2]. - It indicates a **weakened structure** that can no longer withstand the pressure of the underlying lipid core [2]. *Cell debris* - **Cell debris** is often found at the site of rupture, resulting from the necrosis of foam cells and smooth muscle cells. - This indicates **plaque instability** and contributes to the thrombus formation at the rupture site. *Multiple foam cap* - The presence of **multiple foam cells** reflectsing lipid accumulation in the plaque but does not contribute to the phenomenon of plaque rupture directly. - While foam cells are associated with rupture, a **foam cap** is not a recognized pathological finding at the time of rupture. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Cardiovascular Disease, pp. 271-272. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Cardiovascular Disease, pp. 268-270.
Question 273: The MOST COMMON cause of concentric hypertrophy of left ventricle is?
- A. Hypertension (Correct Answer)
- B. Aortic stenosis
- C. Mitral stenosis
- D. Aortic regurgitation
Explanation: ***Hypertension*** - Chronic **hypertension** is the most common cause of **pressure overload** on the left ventricle, leading to concentric hypertrophy [1]. - In response to the increased afterload, the ventricular wall thickens uniformly inward, reducing the chamber size while maintaining normal wall stress [2]. - Due to its high prevalence (30-40% of adults), hypertension is epidemiologically the most frequent cause of concentric LVH [1]. *Aortic stenosis* - While **aortic stenosis** is the classic pathological cause of **pressure overload** and concentric hypertrophy [2], **hypertension** is more prevalent in the population. - Aortic stenosis causes fixed outflow obstruction, leading to significant pressure work for the left ventricle. - This is the second most common cause but occurs in only 2-5% of elderly patients. *Mitral stenosis* - **Mitral stenosis** primarily causes pressure overload on the **left atrium** and **pulmonary circulation**, not the left ventricle. - It doesn't typically lead to **left ventricular hypertrophy** directly; instead, it causes left atrial enlargement and right ventricular hypertrophy. *Aortic regurgitation* - **Aortic regurgitation** results in **volume overload** of the left ventricle due to blood flowing back into the chamber during diastole. - This typically leads to **eccentric hypertrophy**, where the chamber dilates and the wall thickens proportionally, rather than concentric hypertrophy [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 560-562. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, p. 536.
Question 274: What is the sequence of events in acute inflammation?
- A. Transient vasoconstriction - Stasis - Vasodilatation - Increased permeability
- B. Transient vasoconstriction - Vasodilatation - Increased permeability - Stasis (Correct Answer)
- C. Transient vasoconstriction - Vasodilatation - Stasis - Increased permeability
- D. Vasodilatation - Stasis - Transient vasoconstriction - Increased permeability
Explanation: ***Transient vasoconstriction → Vasodilatation → Increased permeability → Stasis*** - This sequence accurately reflects the **initial phase** of acute inflammation where **vasoconstriction** briefly occurs for tissue protection, followed by **vasodilatation** that enhances blood flow [3]. - **Increased permeability** allows plasma proteins to exit the bloodstream, crucial for inflammatory responses [1], while **stasis** occurs as blood flow slows, facilitating leukocyte adhesion [2]. *Transient vasoconstriction → Stasis → Vasodilatation → Increased permeability* - This option incorrectly places **stasis** before **vasodilatation**, as stasis occurs only after blood flow has increased. - **Vasodilatation** is essential for increased blood flow, which precedes stasis, making this sequence incorrect. *Transient vasoconstriction → Vasodilatation → Stasis → Increased permeability* - Although it includes **vasodilatation** and **transient vasoconstriction**, it incorrectly suggests that **stasis** occurs before the increase in vascular permeability. - **Increased permeability** is a critical event after vasodilatation [1], thus this order is not accurate. *Vasodilatation → Stasis → Transient vasoconstriction → Increased permeability* - This sequence is incorrect as it starts with **vasodilatation**, neglecting the initial protective phase of **transient vasoconstriction**. - **Transient vasoconstriction** is the first event, making this option inaccurate as it misrepresents the order of events in acute inflammation. **References:** [1] 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. 187-188. [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. 186-187. [3] 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. 185-186.
Physiology
3 questionsBy what percentage can cardiac output increase in a healthy adult during intense physical activity compared to resting levels?
P wave is due to:
Which of the following does not stimulate growth hormone (GH) release?
NEET-PG 2013 - Physiology NEET-PG Practice Questions and MCQs
Question 271: By what percentage can cardiac output increase in a healthy adult during intense physical activity compared to resting levels?
- A. 300 - 400 % (Correct Answer)
- B. 0 - 50 %
- C. 50 - 100 %
- D. 100 - 200 %
Explanation: ***300 - 400 %*** - In a healthy adult, **cardiac output** can increase remarkably during intense physical activity. - The heart can increase its output by **3 to 4 times** (or 300-400%) above resting levels during peak exertion. - At rest, cardiac output is approximately **5 L/min**, but during maximal exercise, it can reach **20-25 L/min** in well-conditioned individuals. - This represents the heart's **reserve capacity** to meet increased metabolic demands during exercise. *0 - 50 %* - This range represents a very **limited increase** in cardiac output and would be indicative of significant underlying cardiac impairment or **heart failure**. - A healthy individual would experience a much greater increase in cardiac output during intense activity than this small percentage. *50 - 100 %* - This range also suggests a **suboptimal cardiac response** for a healthy adult undergoing intense physical activity. - While some increase is present, it does not reflect the full capacity of a healthy cardiovascular system to adapt to extreme demands. *100 - 200 %* - While a 100-200% increase is substantial, it still **underestimates the maximal capacity** achievable in a healthy, well-conditioned individual during intense physical exertion. - The heart has a greater capacity for increasing its output to meet metabolic demands during peak exercise.
Question 272: P wave is due to:
- A. Atrial depolarization (Correct Answer)
- B. Atrial repolarization
- C. Ventricular depolarization
- D. Ventricular repolarization
Explanation: **Atrial depolarization** - The **P wave** on an electrocardiogram (ECG) represents the electrical activity associated with the **depolarization of the atria**. - This depolarization leads to **atrial contraction**, pushing blood into the ventricles. *Atrial repolarization* - **Atrial repolarization** also occurs but is usually hidden within the **QRS complex** and thus not separately visible as a distinct wave on a standard ECG. - While it's an electrical event, it does not produce the P wave. *Ventricular depolarization* - **Ventricular depolarization** is represented by the **QRS complex** on an ECG. - This electrical activity leads to **ventricular contraction**, pumping blood out of the heart. *Ventricular repolarization* - **Ventricular repolarization** is represented by the **T wave** on an ECG. - This process allows the ventricles to relax and refill with blood.
Question 273: Which of the following does not stimulate growth hormone (GH) release?
- A. Exercise
- B. Free fatty acids (Correct Answer)
- C. Fasting
- D. Stress
Explanation: ***Free fatty acids*** - High levels of **free fatty acids** in the bloodstream inhibit growth hormone (GH) secretion. - This occurs through a **negative feedback loop** at the level of the hypothalamus and pituitary gland. *Fasting* - **Fasting** (especially prolonged) is a potent stimulus for GH release, helping to mobilize fat stores and maintain **glucose homeostasis**. - During fasting, ghrelin levels increase, which further promotes GH secretion. *Exercise* - **Physical exercise** is a well-known physiological stimulus for GH release, contributing to muscle growth and repair. - The intensity and duration of exercise can influence the magnitude of GH secretion. *Stress* - Various forms of **stress**, including physical (e.g., trauma, surgery) and psychological stress, stimulate GH release. - This response is mediated in part by the **sympathetic nervous system** and increased cortisol levels.