NEET-PG 2015 - Internal Medicine Practice Questions

Q: Major contribution to cachexia with advanced cancer?

Tumor-necrosis-factor (TNF). ***Tumor-necrosis-factor (TNF)*** - **Tumor necrosis factor (TNF-α)** is a prominent cytokine involved in the pathogenesis of cancer cachexia, leading to muscle wasting and weight loss [1]. - It induces inflammation, increases **catabolism**, and reduces anabolism, contributing significantly to the metabolic dysfunction seen in cancer patients [1]. *Histamine* - **Histamine** is primarily known for its role in allergic reactions and inflammatory responses, but it is not a major direct driver of cachexia. - While it can be released in various inflammatory conditions, its direct contribution to the severe muscle wasting and metabolic changes of cachexia is limited compared to other cytokines. *Interferon* - **Interferons (IFNs)** are cytokines typically associated with antiviral responses and immune modulation, which can have diverse effects on metabolism. - While some interferons can indirectly contribute to systemic inflammation and fatigue, they are not considered a primary or major direct mediator of muscle catabolism and fat loss characteristic of cancer cachexia. *Clathrin* - **Clathrin** is a protein involved in the formation of clathrin-coated vesicles, essential for **endocytosis** and intracellular trafficking. - It has no direct role in the systemic metabolic dysregulation or muscle wasting associated with cancer cachexia.

Q: Which of the following is NOT a common cause of acute renal failure?

Chronic kidney disease due to analgesic nephropathy. Chronic kidney disease due to analgesic nephropathy - This is a cause of chronic kidney disease, characterized by gradual, irreversible kidney damage over a long period due to prolonged use of certain analgesics. [1] - It does not present as an acute, sudden decline in kidney function, which is the hallmark of acute renal failure. [1] Acute pyelonephritis - Severe cases of acute pyelonephritis (kidney infection) can lead to acute kidney injury due to sepsis, inflammation, and potential obstruction. [1] - The systemic inflammatory response and direct tissue damage can impair kidney function rapidly. [1] Acute kidney injury from snakebite - Snake envenomation can cause acute kidney injury through various mechanisms, including hemolysis, rhabdomyolysis, direct nephrotoxicity, and systemic hypotension. - These effects can lead to rapid and severe kidney damage. Acute kidney injury due to rhabdomyolysis - Rhabdomyolysis involves the breakdown of skeletal muscle tissue, releasing large amounts of myoglobin into the bloodstream. [1] - Myoglobin is toxic to the renal tubules, leading to acute tubular necrosis and rapid onset of acute kidney injury. [1]

Q: Thrombocythemia is characterized by an elevated platelet count.

Elevated platelet count. Elevated platelet count - Thrombocythemia is a condition specifically defined by an abnormally high number of platelets (thrombocytes) in the blood [2]. - This elevated count can lead to issues with both bleeding and clotting [2]. Low platelets - Low platelets, also known as thrombocytopenia, is the opposite of thrombocythemia [1]. - This condition is associated with an increased risk of bleeding [1]. Neutrophilia - Neutrophilia refers to an elevated count of neutrophils, a type of white blood cell, which is typically seen in bacterial infections. - It does not directly describe the platelet count. Monocytosis - Monocytosis indicates an increase in monocytes, another type of white blood cell, often seen in chronic infections or inflammatory conditions. - This term is unrelated to platelet levels.

Q: Which of the following is the common cause of respiratory failure type 2 ?

Chronic bronchitis exacerbation. ***Chronic bronchitis exacerbation*** - **Chronic bronchitis** is a common cause of **Type 2 respiratory failure**, characterized by **hypercapnia** (elevated CO2) due to impaired alveolar ventilation [1]. - An exacerbation worsens **airflow obstruction** and leads to increased work of breathing and CO2 retention [1]. *Acute attack asthma* - While severe asthma can cause respiratory failure, it typically presents initially as **Type 1 (hypoxemic)**, with severe bronchospasm and V/Q mismatch [2]. - **Hypercapnia** in asthma is a sign of **severe, impending respiratory collapse** rather than the primary cause of respiratory failure. *ARDS* - **Acute Respiratory Distress Syndrome (ARDS)** is a classic cause of **Type 1 (hypoxemic) respiratory failure**, characterized by widespread inflammation and fluid accumulation in the lungs [2]. - ARDS primarily involves impaired oxygenation rather than CO2 elimination issues, unless it progresses to severe stages with significant muscle fatigue. *Pneumonia* - **Pneumonia** predominantly causes **Type 1 (hypoxemic) respiratory failure** due to consolidation and V/Q mismatch in affected lung areas, leading to impaired oxygen diffusion [2]. - While severe, widespread pneumonia can eventually lead to ventilatory failure, its initial and primary impact is on oxygenation.

Q: Buboes form is which stage of LGV?

Secondary. ***Secondary*** - Buboes, which are swollen, painful lymph nodes, are a hallmark of the **secondary stage** of **Lymphogranuloma Venereum (LGV)** [1]. - This stage typically develops weeks after the initial infection, following the unnoticed or transient primary lesion. *Primary* - The primary stage of LGV is characterized by a **small, painless papule or ulcer** at the site of inoculation, which often goes unnoticed. - **Buboes are not formed** during this initial, often asymptomatic, phase. *Tertiary* - The tertiary stage of LGV involves **chronic inflammation** and **tissue destruction**, leading to complications like **genital elephantiasis**, rectal strictures, and fistulas. - While there is chronic lymphedema, the acute, painful buboes are characteristic of the secondary stage, not this late, destructive phase. *Latent* - The concept of a latent stage is not typically used to describe the progression of LGV in the same way as other infections like syphilis. - LGV progresses through distinct symptomatic primary, secondary, and potentially tertiary stages without a prolonged asymptomatic latency period between symptom presentations.

Q: Most common complication of diphtheria is -

Myocarditis. ***Myocarditis*** - Diphtheria toxin can directly damage myocardial cells, leading to inflammation and dysfunction of the heart muscle, making **myocarditis** the most common and serious complication. - This can result in **heart failure**, arrhythmias, and even death, highlighting its significance in diphtheria. *Pneumonia* - While respiratory complications can occur in diphtheria, **pneumonia** is not the most common or life-threatening complication associated with the diphtheria toxin itself. - Secondary bacterial infections might lead to pneumonia, but it is not a direct toxic effect like myocarditis. *Meningitis* - **Meningitis**, an inflammation of the membranes surrounding the brain and spinal cord, is an extremely rare complication of diphtheria. - Diphtheria primarily affects the upper respiratory tract and heart [1], with neurological complications typically manifesting as neuropathies rather than meningitis. *Endocarditis* - Although diphtheria can cause cardiac complications, **endocarditis** (inflammation of the heart's inner lining, including the valves) is not a common complication. - Myocarditis, due to the direct toxic effect on heart muscle, is far more prevalent than endocarditis in diphtheria.

Q: What is the recommended postprandial capillary glucose level (in mg/dl) for adequate diabetes control?

< 180 mg/dl. ***< 180 mg/dl*** - This is the **recommended target** for postprandial (1-2 hours after a meal) capillary glucose levels in most non-pregnant adults with diabetes to achieve **adequate glycemic control** [1], [2]. - Maintaining levels below 180 mg/dl helps to minimize the risk of **long-term microvascular and macrovascular complications**. *< 100 mg/dl* - While this is an ideal fasting glucose level, it is generally **too low for postprandial glucose**, and attempting to maintain such levels might increase the risk of **hypoglycemia** in many patients with diabetes [1]. - This target is more appropriate for **fasting or pre-meal glucose** goals. *< 140 mg/dl* - This is a **more stringent target** that may be appropriate for some individuals with diabetes, particularly those who are carefully managed and at low risk of hypoglycemia. - However, for the general population with diabetes, **< 180 mg/dl is the more commonly accepted and achievable goal** for postprandial readings [2]. *< 200 mg/dl* - A postprandial glucose level of < 200 mg/dl is considered **good control** in some contexts, but it's often a **less strict target** than < 180 mg/dl for optimal long-term management. - While better than uncontrolled high levels, consistently approaching 200 mg/dl may still contribute to **increased risk of complications** over time compared to tighter control.

Q: What is the recommended regimen for post-exposure prophylaxis for HIV?

Tenofovir disoproxil fumarate + Emtricitabine + Dolutegravir for 28 days. ***Tenofovir disoproxil fumarate + Emtricitabine + Dolutegravir for 28 days*** - This is the **current first-line recommended regimen** for **HIV post-exposure prophylaxis (PEP)** according to WHO (2021), CDC, and Indian NACO guidelines. - It includes two **nucleoside reverse transcriptase inhibitors (NRTIs)** and an **integrase strand transfer inhibitor (INSTI)**. - **Dolutegravir** is preferred over Raltegravir due to **superior efficacy, better tolerability, higher barrier to resistance, once-daily dosing**, and fewer drug interactions. - The duration of **28 days** is crucial for effective PEP to cover the window period for potential HIV integration and replication. *Tenofovir disoproxil fumarate + Emtricitabine + Raltegravir for 28 days* - This was the **previous standard PEP regimen** and is still an acceptable alternative if Dolutegravir is contraindicated or unavailable. - Raltegravir requires **twice-daily dosing** compared to Dolutegravir's once-daily regimen, which may affect adherence. - The 28-day duration is correct, but Raltegravir is no longer the first-line INSTI choice in current guidelines. *Single dose Tenofovir + Emtricitabine + Raltegravir* - A **single dose** of these medications is insufficient for **post-exposure prophylaxis (PEP)** as HIV replication needs to be suppressed over an extended period to prevent seroconversion. - PEP typically requires a **28-day course** to be effective. *Zidovudine + Lamivudine + Lopinavir/ritonavir for 28 days* - While this is an older, effective **antiretroviral regimen**, it is **not the preferred first-line PEP regimen** due to a higher incidence of side effects, particularly with zidovudine (anemia, nausea). - Modern guidelines favor regimens with **Tenofovir/Emtricitabine + Dolutegravir** due to better tolerability and superior efficacy.

Q: Most common cause of Addison's Disease in India is:

Tuberculosis. ***Tuberculosis*** - In India, **tuberculosis** is the most common cause of **Addison's disease** due to the high prevalence of TB infections. - Adrenal involvement in TB can lead to gradual destruction of the adrenal cortex, resulting in **adrenal insufficiency**. *Autoimmune* - **Autoimmune adrenalitis** is the leading cause of Addison's disease in developed Western countries. - It involves the destruction of adrenal cortical cells by the body's own immune system, often associated with other autoimmune conditions. *Malignancy* - **Malignancy**, particularly metastatic cancer to the adrenals, can cause adrenal insufficiency but is a less common primary cause of Addison's disease overall. - While possible, it is not the most prevalent cause in India compared to infectious etiologies. *HIV* - **HIV infection** can lead to adrenal dysfunction, but it's typically through opportunistic infections like CMV, cryptococcosis, or direct HIV effects, rather than being the direct cause of widespread adrenal destruction. - It increases the risk of adrenal insufficiency but is not the most common etiology in India for Addison's disease.

Q: In a patient with COPD, what is the best management option?

Quit smoking. ***Quit smoking*** - **Smoking cessation** is the single most effective intervention for slowing the progression of **COPD** and improving lung function [1]. - It reduces exacerbation rates and improves overall mortality, making it the cornerstone of management [1]. *Bronchodilators* - **Bronchodilators** (e.g., beta-agonists, anticholinergics) are crucial for symptomatic relief by opening airways, but they do not alter the disease progression [1]. - While essential for managing symptoms, they are not the "best" in terms of modifying the disease course. *Low flow oxygen* - **Oxygen therapy** is indicated for patients with **severe hypoxemia** (PaO2 < 55 mmHg or SaO2 < 88%) to improve survival and quality of life [2]. - It is a supportive treatment for advanced disease and does not prevent or slow the progression of COPD itself. *Mucolytics* - **Mucolytics** may be used in some patients with COPD and chronic productive cough to reduce sputum viscosity and improve clearance. - Their benefit is primarily symptomatic, and they do not have a significant impact on disease progression or mortality.

Question 1

Major contribution to cachexia with advanced cancer?

Accepted Answer

Tumor-necrosis-factor (TNF)

Answer

Histamine

Answer

Interferon

Answer

Clathrin

Question 2

Which of the following is NOT a common cause of acute renal failure?

Accepted Answer

Chronic kidney disease due to analgesic nephropathy

Answer

Acute pyelonephritis

Answer

Acute kidney injury from snakebite

Answer

Acute kidney injury due to rhabdomyolysis

Question 3

Thrombocythemia is characterized by an elevated platelet count.

Accepted Answer

Elevated platelet count

Answer

Low platelets

Answer

Neutrophilia

Answer

Monocytosis

Question 4

Which of the following is the common cause of respiratory failure type 2 ?

Accepted Answer

Chronic bronchitis exacerbation

Answer

Acute attack asthma

Answer

ARDS

Answer

Pneumonia

Question 5

Buboes form is which stage of LGV?

Accepted Answer

Secondary

Answer

Tertiary

Answer

Latent

Answer

Primary

Question 6

Most common complication of diphtheria is -

Accepted Answer

Myocarditis

Answer

Pneumonia

Answer

Meningitis

Answer

Endocarditis

Question 7

What is the recommended postprandial capillary glucose level (in mg/dl) for adequate diabetes control?

Accepted Answer

< 180 mg/dl

Answer

< 200 mg/dl

Answer

< 100 mg/dl

Answer

< 140 mg/dl

Question 8

What is the recommended regimen for post-exposure prophylaxis for HIV?

Accepted Answer

Tenofovir disoproxil fumarate + Emtricitabine + Dolutegravir for 28 days

Answer

Zidovudine + Lamivudine + Lopinavir/ritonavir for 28 days

Answer

Tenofovir disoproxil fumarate + Emtricitabine + Raltegravir for 28 days

Answer

Single dose Tenofovir + Emtricitabine + Raltegravir

Question 9

Most common cause of Addison's Disease in India is:

Accepted Answer

Tuberculosis

Answer

Autoimmune

Answer

HIV

Answer

Malignancy

Question 10

In a patient with COPD, what is the best management option?

Accepted Answer

Quit smoking

Answer

Bronchodilators

Answer

Low flow oxygen

Answer

Mucolytics

NEET-PG 2015 — Internal Medicine