Biochemistry
2 questionsWhat is the main enzyme involved in glycogen breakdown (glycogenolysis)?
Which organelle produces and destroys H2O2?
NEET-PG 2013 - Biochemistry NEET-PG Practice Questions and MCQs
Question 391: What is the main enzyme involved in glycogen breakdown (glycogenolysis)?
- A. Glycogen phosphorylase (Correct Answer)
- B. Glycogen synthase
- C. Glucose-6-phosphatase
- D. Hexokinase
Explanation: ***Glycogen phosphorylase*** - This is the **rate-limiting and primary enzyme** for **glycogenolysis**, the breakdown of glycogen into glucose units. - It cleaves **α-1,4-glycosidic bonds** in glycogen, releasing **glucose-1-phosphate** units. - Regulated by both **allosteric mechanisms** and **hormonal control** (epinephrine, glucagon). - Works until it reaches 4 glucose residues from a branch point, where debranching enzyme takes over. *Glycogen synthase* - This is the main enzyme for **glycogenesis** (glycogen synthesis), not breakdown. - It catalyzes formation of α-1,4-glycosidic bonds to build glycogen chains. - This is the opposite direction of metabolism from what the question asks about. *Glucose-6-phosphatase* - This enzyme is involved in **gluconeogenesis** and the final step of converting **glucose-6-phosphate to free glucose**. - It is NOT directly involved in glycogen breakdown itself, but rather in the subsequent conversion pathway. - Found primarily in **liver and kidney** to release free glucose into blood. *Hexokinase* - This enzyme phosphorylates free glucose to **glucose-6-phosphate** (opposite direction). - It is involved in **glucose utilization**, not glycogen breakdown. - It traps glucose inside cells for metabolism or glycogen synthesis.
Question 392: Which organelle produces and destroys H2O2?
- A. Peroxisome (Correct Answer)
- B. Lysosome
- C. Golgi body
- D. Ribosome
Explanation: ***Peroxisome*** - **Peroxisomes** are organelles that both produce and break down **hydrogen peroxide (H2O2)** during metabolic processes. - They contain **oxidases** (such as D-amino acid oxidase and urate oxidase) that produce H2O2 as a byproduct during oxidation reactions. - They also contain the enzyme **catalase** that converts H2O2 into water and oxygen, protecting the cell from oxidative damage. - This dual function makes peroxisomes unique in H2O2 metabolism. *Lysosome* - **Lysosomes** are responsible for breaking down waste materials and cellular debris through **hydrolytic enzymes**. - They are primarily involved in **cellular digestion** and waste removal, not H2O2 metabolism. *Golgi body* - The **Golgi apparatus** modifies, sorts, and packages proteins and lipids for secretion or delivery to other organelles. - It is crucial for **protein trafficking** and glycosylation, but does not produce or destroy H2O2. *Ribosome* - **Ribosomes** are responsible for **protein synthesis** (translation) based on genetic information carried by mRNA. - They are involved in the assembly of amino acids into proteins, not the metabolism of hydrogen peroxide.
Internal Medicine
3 questionsWhat is the complete classic triad of findings that defines Young's syndrome?
Most common cause of death in SLE in children
Which of the following statements about HIV associated nephropathy (HIVAN) is incorrect?
NEET-PG 2013 - Internal Medicine NEET-PG Practice Questions and MCQs
Question 391: What is the complete classic triad of findings that defines Young's syndrome?
- A. Azoospermia, bronchiectasis, and chronic sinusitis (Correct Answer)
- B. Oligospermia, bronchiectasis, and chronic sinusitis
- C. Azoospermia, asthma, and chronic rhinitis
- D. Azoospermia, chronic bronchitis, and nasal polyps
Explanation: ***Azoospermia, bronchiectasis, and chronic sinusitis*** - Young's syndrome is characterized by the triad of **azoospermia** (due to obstructive epididymal dysfunction), **bronchiectasis**, and **chronic sinusitis** [1]. - This syndrome primarily affects **middle-aged men** and is often mistaken for cystic fibrosis due to similar respiratory symptoms. *Azoospermia, asthma, and chronic rhinitis* - This option incorrectly lists **asthma** and **chronic rhinitis** instead of bronchiectasis and chronic sinusitis. - While respiratory symptoms are part of Young's syndrome, specifically **bronchiectasis** and **sinusitis** are key [1]. *Oligospermia, bronchiectasis, and chronic sinusitis* - This option is incorrect because Young's syndrome is defined by **azoospermia** (complete absence of sperm), not just **oligospermia** (low sperm count). - The obstructive nature of the epididymal dysfunction in Young's syndrome leads to a complete lack of sperm. *Azoospermia, chronic bronchitis, and nasal polyps* - This option incorrectly identifies **chronic bronchitis** and **nasal polyps** as part of the classic triad. - The correct respiratory components are **bronchiectasis** and **chronic sinusitis**, which signify persistent inflammation and structural lung changes rather than simply bronchitis.
Question 392: Most common cause of death in SLE in children
- A. Libman sacks endocarditis
- B. Lupus cerebritis
- C. Lupus nephritis
- D. Anemia and infections (Correct Answer)
Explanation: ***Anemia and infections*** - **Infections** are a leading cause of death in pediatric SLE patients, often due to immunosuppression from the disease itself or its treatment. Although pediatric Systemic Lupus Erythematosus (SLE) is not a primary immune deficiency, the susceptibility to encapsulated bacteria and recurrent infections seen in primary B- and T-lymphocyte deficiencies mirrors the infection risks managed in these patients [1]. - **Anemia** can contribute to overall morbidity and mortality, although it is less directly a cause of death than severe infections or organ failure. *Lupus nephritis* - While **lupus nephritis** is a common and severe manifestation of SLE in children and a major cause of morbidity, particularly long-term kidney failure, it is not the most frequent immediate cause of death. - Advancements in treatment for nephritis have improved prognosis, shifting the leading cause of mortality to other factors. *Lupus cerebritis* - **Lupus cerebritis** (neuropsychiatric SLE) can be life-threatening, causing seizures, stroke, or psychosis, but it is less common as the primary cause of death compared to infections. - Its presence usually indicates severe disease requiring intensive treatment, but not the most common direct cause of death. *Libman sacks endocarditis* - **Libman-Sacks endocarditis** involves sterile vegetations on heart valves and is a known complication of SLE, but it rarely causes acute mortality in children. - It is more often associated with chronic complications like valvular dysfunction or a source of emboli rather than being the most common cause of death.
Question 393: Which of the following statements about HIV associated nephropathy (HIVAN) is incorrect?
- A. HIVAN is characterized by proteinuria.
- B. HIVAN is associated with shrunken kidneys. (Correct Answer)
- C. HIVAN typically develops when CD4 count is less than 200.
- D. About 15% of cases show mesangial proliferation.
Explanation: ***Shrunken kidneys*** - In HIV-associated nephropathy, kidneys typically appear **enlarged** due to hyperplasia of podocytes and other glomerular changes. - **Shrunken kidneys** are not a characteristic feature, making this statement incorrect. *Develops when CD4<200* - HIV-associated nephropathy often arises when CD4 counts drop **below 200 cells/mm³**, indicating severe immunosuppression. - This is a common threshold for the occurrence of opportunistic infections and kidney issues in HIV patients. *15% cases show mesengial proliferation* - **Mesangial proliferation** can occur in about **15% to 30%** of cases of HIV-associated nephropathy, which aligns with the typical histological findings. - Incorrect assumptions might stem from misunderstanding the varying morphologies associated with HIV nephropathy. *Proteinuria* - **Proteinuria** is a common clinical feature of HIV-associated nephropathy, with the condition often presenting with significant protein loss in the urine. - The nephropathy especially results in **nephrotic syndrome**, characterized by high levels of proteinuria.
Pathology
5 questionsAmyloidosis is associated with all of the following conditions except?
Which of the following is a sign of reversible injury in alcoholic liver disease?
Caseous necrosis is seen in -
Dystrophic calcification is seen in
Which of the following cell types is classified as a labile cell?
NEET-PG 2013 - Pathology NEET-PG Practice Questions and MCQs
Question 391: Amyloidosis is associated with all of the following conditions except?
- A. Chronic bronchitis (Correct Answer)
- B. Osteomyelitis
- C. Bronchiectasis
- D. Tuberculosis
Explanation: ***Chronic bronchitis*** - Chronic bronchitis is primarily characterized by **inflammation of the airways** and **excess mucus production**, not typically associated with amyloidosis [1]. - Amyloidosis more commonly relates to chronic inflammatory states but does not directly result from the long-term exposure seen in chronic bronchitis [1]. *Tuberculosis* - Tuberculosis can lead to chronic inflammation, which may precipitate **secondary amyloidosis** due to persistent infection [1]. - It often causes systemic effects, including weight loss and fever, which can result in **amyloid deposition** [1]. *Osteomyelitis* - Osteomyelitis, as a chronic bone infection, can trigger an inflammatory response leading to **secondary amyloidosis** [1]. - The ongoing inflammation can result in the accumulation of amyloid proteins in the bone and surrounding tissues [1]. *Bronchiectasis* - Bronchiectasis often results from persistent lung infections leading to chronic inflammation, which can cause **amyloid deposition** [1,3]. - It is associated with recurrent lung infections and can lead to systemic complications, including amyloidosis [1,3]. **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. 135-136. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 269-270.
Question 392: Which of the following is a sign of reversible injury in alcoholic liver disease?
- A. Cytoplasmic vacuole (Correct Answer)
- B. Pyknosis (nuclear shrinkage)
- C. Loss of cell membrane integrity
- D. Nuclear karyolysis (nuclear dissolution)
Explanation: ***Cytoplasmic vacuole*** - The presence of **cytoplasmic vacuoles** in liver cells indicates fatty change, which is a **reversible injury** in alcoholic liver disease [1][2]. - This injury allows the liver to recover if **alcohol consumption** is ceased, highlighting its reversible nature [1]. *Nuclear karyolysis* - **Nuclear karyolysis** signifies severe cellular damage and necrosis, indicating an irreversible process [2]. - This feature involves the dissolution of the nucleus, which does not align with reversible injury. *Loss of cell membrane* - Loss of the **cell membrane** indicates irreversible damage, leading to cell death rather than a reversible condition [2]. - This change is associated with significant cellular impairment, contrary to the concept of recovery. *Pyknosis* - **Pyknosis**, the condensation of chromatin in the nucleus, suggests irreversible cellular injury and impending necrosis [2]. - It is often a precursor to cell death and is not indicative of reversible damage in liver pathology. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Liver and Gallbladder, pp. 848-850. [2] 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. 51-53.
Question 393: Caseous necrosis is seen in -
- A. Tuberculosis (Correct Answer)
- B. CMV infection
- C. Treponemal infection
- D. Staphylococcal infection
Explanation: ***Tuberculosis*** - **Caseous necrosis** is the **pathognomonic** and **most characteristic** form of necrosis seen in **tuberculosis (TB)** caused by *Mycobacterium tuberculosis* [1]. - It appears as a **cheesy, friable, granular material** in the center of **tuberculous granulomas** (tubercles) [1], [2]. - The unique **lipid-rich cell wall** of *M. tuberculosis* combined with the host's **type IV hypersensitivity reaction** results in this distinctive pattern of tissue destruction [2]. - This is a **classic histopathological hallmark** of TB and is essential for diagnosis [2]. *Treponemal infection* - **Syphilis**, caused by *Treponema pallidum*, causes **gummatous necrosis**, NOT caseous necrosis [3]. - Gummas have a **rubbery consistency** and different histological appearance compared to the cheesy, friable caseous necrosis. - While syphilis produces granulomatous inflammation, the necrosis pattern is distinctly different from TB [3]. *CMV infection* - **Cytomegalovirus (CMV)** infection typically causes **coagulative necrosis** with **cytopathic effects** (enlarged cells with intranuclear and intracytoplasmic inclusions - "owl's eye" appearance) [3]. - Does NOT produce caseous necrosis. *Staphylococcal infection* - **Staphylococcal infections** (e.g., *Staphylococcus aureus*) cause **liquefactive necrosis** leading to **abscess formation** [3]. - Dead cells are enzymatically digested into **liquid pus**, completely different from the solid, cheesy appearance of caseous necrosis. **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. 55. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 383-384. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, p. 360.
Question 394: 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 395: Which of the following cell types is classified as a labile cell?
- A. Liver parenchymal cells
- B. Vascular smooth muscle cells
- C. Surface epithelium (Correct Answer)
- D. Neurons
Explanation: ***Surface epithelium*** - Surface epithelium is classified as **labile tissue**, meaning it undergoes constant regeneration due to its high turnover rate [1]. - Cells in this tissue are typically found in areas that experience frequent damage or abrasion, such as the skin and lining of the intestines. *Cardiac cell* - Cardiac cells are considered **permanent cells**, as they do not undergo significant regeneration after injury or damage. - Damage to cardiac cells typically leads to **fibrosis** rather than repair of the original tissue. *Liver parenchymal cell* - Liver parenchymal cells are categorized as **stable cells**, which can regenerate but do so under specific circumstances, such as injury. - They have a slower turnover rate compared to labile cells and do not constantly renew under normal conditions. *Vascular endothelial cells* - Vascular endothelial cells are considered **stable cells** as well, typically maintaining a stable population but capable of regeneration following injury. - They do not have the same rapid turnover and regeneration capability as labile cells do, especially under normal physiological conditions. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 113-115.