Creatine kinase is elevated in MI after
Which of the following statements about Alport's syndrome is incorrect?
Which of the following statements about hypercalcemia in sarcoidosis is false?
What is the complete classic triad of findings that defines Young's syndrome?
Chronic atrophy of adrenal gland will result in which hormone deficiency ?
Which of the following statements about HIV associated nephropathy (HIVAN) is incorrect?
Cerebellar damage causes all of the following except?
Most common cause of death in SLE in children
What is the drug of choice for bleeding oesophageal varices?
Which of the following characteristics can be used to differentiate the rash of chickenpox from the rash of smallpox?
NEET-PG 2013 - Internal Medicine NEET-PG Practice Questions and MCQs
Question 31: Creatine kinase is elevated in MI after
- A. 4-8 hours
- B. >24 hours
- C. 12-24 hours
- D. 2-4 hours (Correct Answer)
Explanation: ***2-4 hours*** - **Creatine kinase (CK)** levels typically begin to rise within **2-4 hours** after the onset of myocardial infarction. - This early elevation makes CK an effective, though non-specific, marker for **acute MI** in the initial stages [1]. *4-8 hours* - While CK levels may continue to rise during this period, the initial measurable elevation usually occurs earlier, within **2-4 hours**. - A significant elevation at 4-8 hours would indicate that the myocardial event occurred at least several hours prior. *12-24 hours* - Creatine kinase levels typically peak much earlier, between **12-24 hours**, rather than just beginning to elevate at this time. - By this time, other more specific markers like **troponins** would also be significantly elevated and are often preferred for diagnosis [1], [2]. *>24 hours* - Beyond 24 hours, CK levels usually start to decline, making it less useful for the initial detection of an acute MI that began many hours earlier. - For events occurring over 24 hours ago, a positive CK would indicate that the event had happened, but it's not the first time it would be elevated.
Question 32: Which of the following statements about Alport's syndrome is incorrect?
- A. Nerve deafness
- B. Glomerulonephritis
- C. Autosomal dominant (Correct Answer)
- D. X-linked
Explanation: ***Autosomal dominant*** - While there are rare autosomal dominant forms, the most common and classic presentation of **Alport's syndrome is X-linked recessive**, affecting males more severely. - This statement is incorrect because it implies that autosomal dominant inheritance is the primary or typical mode, which is not true for the majority of cases. *Nerve deafness* - **Sensorineural hearing loss**, particularly for high frequencies, is a common and characteristic extra-renal manifestation of Alport's syndrome. - This symptom typically progresses with age and is a key diagnostic feature. *Glomerulonephritis* - **Progressive glomerulonephritis** is the hallmark renal feature of Alport's syndrome, leading to hematuria, proteinuria, and eventually end-stage renal disease. - It is caused by mutations in collagen type IV genes, which disrupt the integrity of the glomerular basement membrane. *X-linked* - The majority of Alport's syndrome cases (about 85%) are **X-linked recessive**, caused by mutations in the *COL4A5* gene located on the X chromosome. - This explains why males are more severely affected and typically present with earlier onset and more rapid progression of renal disease.
Question 33: Which of the following statements about hypercalcemia in sarcoidosis is false?
- A. PTHrP level is increased
- B. Parathormone level is increased (Correct Answer)
- C. Oral steroids are useful
- D. Calcitriol level is increased
Explanation: ***Parathormone level is increased*** - In **sarcoidosis-associated hypercalcemia**, the parathormone (PTH) level is typically **low or suppressed**. [1] - This is because the hypercalcemia is due to **extra-renal 1-$\alpha$ hydroxylation** of 25-hydroxyvitamin D to 1,25-dihydroxyvitamin D (calcitriol) by macrophages in granulomas, not primary hyperparathyroidism. [1] *PTHrP level is increased* - This statement is **false** for sarcoidosis. Elevated **parathyroid hormone-related peptide (PTHrP)** is a common cause of hypercalcemia in **malignancy**, particularly squamous cell carcinomas, but not in sarcoidosis. - Hypercalcemia in sarcoidosis is **PTH-independent** and not mediated by PTHrP. [1] *Oral steroids are useful* - This statement is **true**. **Corticosteroids** (like oral prednisone) are effective in treating hypercalcemia in sarcoidosis. - They work by **inhibiting the activity of 1-$\alpha$ hydroxylase** in alveolar macrophages and reducing intestinal calcium absorption. *Calcitriol level is increased* - This statement is **true**. In sarcoidosis, activated **macrophages within granulomas** aberrantly express **1-$\alpha$ hydroxylase**. [1] - This leads to the **extra-renal synthesis of calcitriol** (1,25-dihydroxyvitamin D), which increases intestinal calcium absorption and bone resorption, causing hypercalcemia. [1]
Question 34: 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 35: Chronic atrophy of adrenal gland will result in which hormone deficiency ?
- A. Aldosterone
- B. Dehydroepiandrosterone (DHEA)
- C. Epinephrine
- D. Cortisol (Correct Answer)
Explanation: ***Cortisol*** - **Chronic atrophy of the adrenal gland**, often seen in conditions like **Addison's disease** [1], primarily leads to a deficiency of **glucocorticoids**, the main one being cortisol [2]. - **Cortisol** is produced in the **zona fasciculata** of the adrenal cortex, which is highly susceptible to damage in atrophic conditions [2]. *Aldosterone* - While aldosterone is produced in the adrenal cortex (**zona glomerulosa**), its deficiency is more characteristic of primary adrenal insufficiency affecting the entire cortex, not necessarily solely from 'chronic atrophy' which can have varied pathophysiology [2]. - In some autoimmune forms of adrenal atrophy (Addison's disease), **aldosterone deficiency** can occur, but **cortisol deficiency** is a more universal and defining feature [1][3]. *Dehydroepiandrosterone (DHEA)* - **DHEA** is an adrenal androgen produced in the **zona reticularis** of the adrenal cortex [2]. Its deficiency is also common in adrenal atrophy. - However, **cortisol deficiency** generally has more immediate and life-threatening clinical consequences compared to DHEA deficiency. *Epinephrine* - Epinephrine is produced by the **adrenal medulla**, which is distinct from the adrenal cortex where atrophy typically occurs in conditions causing hormone deficiencies. - Therefore, **adrenal gland atrophy** primarily affecting the cortex would not lead to **epinephrine deficiency** as the medulla usually remains functional.
Question 36: 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 37: Cerebellar damage causes all of the following except?
- A. Ataxia
- B. Past-pointing
- C. Dysmetria
- D. Hypertonia (Correct Answer)
Explanation: ***Hypertonia*** - Cerebellar lesions typically lead to **hypotonia**, a decrease in muscle tone, rather than hypertonia [1]. - Hypertonia, or increased muscle tone, is more commonly associated with lesions of the **upper motor neurons** or **basal ganglia** [2]. *Dysmetria* - **Dysmetria** is a common sign of cerebellar damage, characterized by an inability to accurately control the **range, direction, and force** of muscle movements [1]. - This leads to overshooting or undershooting a target during voluntary movements. *Ataxia* - **Ataxia**, particularly truncal or appendicular ataxia, is a cardinal symptom of cerebellar dysfunction [3]. - It refers to a lack of **voluntary coordination** of muscle movements, leading to an unsteady gait and impaired balance [3]. *Past-pointing* - **Past-pointing** is a form of dysmetria where a patient consistently points or reaches **beyond their target** [1]. - It is a specific sign that indicates a deficit in the cerebellum's ability to modulate and refine motor commands.
Question 38: 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 39: What is the drug of choice for bleeding oesophageal varices?
- A. Ethanolamine oleate
- B. Octreotide (Correct Answer)
- C. Propanolol
- D. Phytonadione
Explanation: ***Octreotide*** - **Octreotide** is an analogue of **somatostatin** that reduces splanchnic blood flow and portal pressure, thereby decreasing bleeding from esophageal varices. - It is often used in the acute management of **bleeding esophageal varices** due to its rapid onset of action and favorable safety profile. *Ethanolamine oleate* - **Ethanolamine oleate** is a **sclerosing agent** used for endoscopic sclerotherapy of esophageal varices, not typically as the initial drug of choice for acute bleeding [1]. - It acts by causing inflammation and fibrosis of the varices, which can be effective but carries risks such as **esophageal ulceration** or perforation. *Propranolol* - **Propranolol** is a **non-selective beta-blocker** used for the prophylactic prevention of variceal bleeding, not for acute management of active bleeding. - It works by reducing portal venous pressure by decreasing cardiac output and splanchnic vasoconstriction. *Phytonadione* - **Phytonadione** (vitamin K1) is used to reverse **coumarin anticoagulant effects** or to treat **vitamin K deficiency**, which can contribute to bleeding but is not a direct treatment for variceal bleeding itself. - It helps in the synthesis of **coagulation factors II, VII, IX, and X**, thereby improving clotting.
Question 40: Which of the following characteristics can be used to differentiate the rash of chickenpox from the rash of smallpox?
- A. Deep-seated
- B. Pleomorphic (Correct Answer)
- C. Centrifugal
- D. Multilocular
Explanation: ***Pleomorphic*** - The rash of **chickenpox** is **pleomorphic**, meaning lesions at various stages of development (macules, papules, vesicles, scabs) are present simultaneously in the same body area. - In contrast, a **smallpox** rash is **monomorphic**, with all lesions in a given area appearing at the same stage of development. *Centrifugal* - A **centrifugal distribution** (lesions more concentrated on the face and extremities) is characteristic of **smallpox**. - **Chickenpox** typically has a **centripetal distribution**, with lesions more concentrated on the trunk. *Deep-seated* - **Smallpox** lesions are described as **deep-seated** and feel like "shot under the skin," often associated with significant scarring. - **Chickenpox** lesions are superficial and less likely to cause scarring unless secondarily infected. *Multilocular* - **Smallpox** vesicles and pustules are typically **multilocular**, meaning they have internal septations and do not collapse when punctured. - **Chickenpox** vesicles are unilocular, appearing as a single compartment, and collapse when punctured.