Anatomy
1 questionsType of collagen found in space of Disse in liver is -
NEET-PG 2013 - Anatomy NEET-PG Practice Questions and MCQs
Question 321: Type of collagen found in space of Disse in liver is -
- A. Collagen I & II
- B. Collagen III & IV (Correct Answer)
- C. Collagen II
- D. Collagen II & V
Explanation: ***Collagen III & IV*** - The **space of Disse** in the liver contains a delicate extracellular matrix predominantly composed of **collagen type III (reticular fibers)**, which provides structural support, and **collagen type IV**, a major component of basement membranes. - This specific collagen composition is crucial for regulating the exchange of solutes between **sinusoidal blood** and **hepatocytes**, as well as for the functional integrity of the liver [1]. *Collagen I & II* - **Collagen type I** is the most abundant collagen in the human body, found in connective tissues like **bone, skin, tendons, and ligaments**, but is not primary in the space of Disse. - **Collagen type II** is characteristic of **hyaline cartilage** and vitreous humor, and is not a significant component of the liver's extracellular matrix in the space of Disse. *Collagen II* - As mentioned, **collagen type II** is primarily found in **cartilage** and vitreous humor, which are distinct from the architectural requirements of the liver sinusoidal space. - Its presence in the space of Disse would not provide the necessary structural flexibility and support for the metabolic functions of the liver. *Collagen II & V* - While **collagen type V** is a minor fibrillar collagen that associates with collagen type I in many tissues, it is not a primary component of the space of Disse. - **Collagen type II** is, again, largely confined to cartilaginous structures, making this an unlikely combination for the liver microenvironment.
Biochemistry
2 questionsWhat is the main enzyme involved in glycogen breakdown (glycogenolysis)?
Which protein hormone is often referred to as the 'guardian angel against obesity' due to its role in regulating metabolism?
NEET-PG 2013 - Biochemistry NEET-PG Practice Questions and MCQs
Question 321: 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 322: Which protein hormone is often referred to as the 'guardian angel against obesity' due to its role in regulating metabolism?
- A. Adiponectin (Correct Answer)
- B. Fibronectin
- C. High-Density Lipoprotein (HDL)
- D. Insulin
Explanation: ***Adiponectin*** - **Adiponectin** is a hormone secreted by **adipose tissue** that plays a crucial role in regulating glucose and fatty acid metabolism, increasing **insulin sensitivity**, and decreasing inflammation. - Its levels are inversely correlated with body fat percentage; individuals with obesity tend to have lower adiponectin levels, leading to its nickname as the 'guardian angel against obesity'. *Fibronectin* - **Fibronectin** is a glycoprotein involved in cell adhesion, growth, migration, and differentiation, and is a key component of the **extracellular matrix**. - It does not primarily function in metabolic regulation or body weight control, unlike adiponectin. *High-Density Lipoprotein (HDL)* - **HDL** is a type of lipoprotein that transports cholesterol from peripheral tissues back to the liver, a process known as **reverse cholesterol transport**. - While beneficial for cardiovascular health, HDL is a lipid-carrying particle, not a protein hormone, and its primary role is not in metabolic regulation or direct obesity prevention. *Insulin* - **Insulin** is a peptide hormone produced by the pancreas that regulates carbohydrate and fat metabolism, primarily by facilitating glucose uptake from the blood into cells. - While essential for metabolism, high levels of insulin in the context of insulin resistance can contribute to obesity, rather than act against it.
Internal Medicine
4 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?
What is the most appropriate initial management for paralysis resulting from organophosphorus poisoning?
NEET-PG 2013 - Internal Medicine NEET-PG Practice Questions and MCQs
Question 321: 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 322: 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 323: 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.
Question 324: What is the most appropriate initial management for paralysis resulting from organophosphorus poisoning?
- A. Supportive care, including respiratory support (Correct Answer)
- B. Atropine to counteract muscarinic symptoms
- C. Oximes to reactivate acetylcholinesterase
- D. No specific antidote
Explanation: **Supportive care, including respiratory support** * **Paralysis** in organophosphorus poisoning (OPP) is often due to **nicotinic effects** at the neuromuscular junction, leading to respiratory muscle weakness and failure [2]. * **Respiratory support** through mechanical ventilation is crucial to maintain oxygenation and prevent complications while awaiting the effects of antidotal therapy [1], [2]. * *Atropine to counteract muscarinic symptoms* * **Atropine** primarily blocks **muscarinic receptors**, effectively treating symptoms like bradycardia, bronchorrhea, and miosis [2]. * It does **not reverse the nicotinic effects** responsible for muscle paralysis and respiratory failure. * *Oximes to reactivate acetylcholinesterase* * **Oximes (e.g., pralidoxime)** reactivate **acetylcholinesterase**, thereby addressing the underlying cause of acetylcholine accumulation [2]. * They are most effective if given **early** before irreversible aging of the enzyme occurs, but their effect on established paralysis can be limited without concurrent respiratory support [2]. * *No specific antidote* * This statement is incorrect; **atropine** and **oximes** are specific antidotes for organophosphorus poisoning [2]. * While these antidotes are vital, initial management prioritizing **airway and breathing support** is paramount due to the life-threatening respiratory paralysis [1].
Pathology
2 questionsWhich of the following cell types is classified as a labile cell?
Which of the following changes is NOT seen in atherosclerotic plaque at the time of rupture?
NEET-PG 2013 - Pathology NEET-PG Practice Questions and MCQs
Question 321: 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.
Question 322: 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.
Pharmacology
1 questionsMuscarinic cholinergic receptors are seen at all sites, except?
NEET-PG 2013 - Pharmacology NEET-PG Practice Questions and MCQs
Question 321: Muscarinic cholinergic receptors are seen at all sites, except?
- A. Stomach
- B. CNS
- C. Glands
- D. Neuromuscular junction (Correct Answer)
Explanation: ***Neuromuscular junction*** - The **neuromuscular junction** primarily contains **nicotinic cholinergic receptors**, not muscarinic receptors. - Activation of these nicotinic receptors by acetylcholine causes muscle contraction. *Stomach* - The stomach contains **muscarinic M3 receptors** which mediate gastric acid secretion and smooth muscle contraction. - Activation by acetylcholine via the vagus nerve promotes digestion. *CNS* - The **central nervous system** has various subtypes of **muscarinic receptors (M1-M5)** distributed throughout, playing roles in learning, memory, and motor control. - These receptors modulate neuronal excitability and neurotransmitter release. *Glands* - Most exocrine glands (e.g., salivary, lacrimal, sweat glands) are richly supplied with **muscarinic receptors**, primarily **M3**. - Activation leads to increased glandular secretion.