Biochemistry
1 questionsWhat is the effect of moderate alcohol consumption on lipid profiles in dyslipidemia?
NEET-PG 2013 - Biochemistry NEET-PG Practice Questions and MCQs
Question 811: What is the effect of moderate alcohol consumption on lipid profiles in dyslipidemia?
- A. Decreased HDL levels
- B. Increased HDL levels (Correct Answer)
- C. Increased triglyceride levels
- D. Decreased LDL levels
Explanation: ***Increased HDL levels*** - Moderate alcohol consumption is known to **increase high-density lipoprotein (HDL) cholesterol levels**, which is often considered beneficial for cardiovascular health. - This effect is thought to be mediated by alcohol's influence on **hepatic lipoprotein metabolism**, leading to enhanced HDL production and reduced catabolism. *Decreased HDL levels* - This is incorrect, as multiple studies have consistently shown that **moderate alcohol consumption** tends to elevate, rather than decrease, HDL cholesterol. - Low HDL levels are associated with increased cardiovascular risk, making this effect an undesirable outcome that is not typical of moderate drinking. *Increased triglyceride levels* - While heavy or chronic alcohol consumption can lead to **increased triglyceride levels**, moderate intake typically has a neutral or only slightly elevated effect, if any, often overshadowed by the HDL increase. - Significant hypertriglyceridemia is a concern with **excessive alcohol use**, not usually with moderate consumption in healthy individuals. *Decreased LDL levels* - Moderate alcohol consumption generally has **little to no significant effect** on **low-density lipoprotein (LDL) cholesterol levels**, often referred to as "bad" cholesterol. - While HDL increases are observed, alcohol does not effectively lower LDL, which is a primary target in the management of dyslipidemia.
Forensic Medicine
1 questionsMinamata disease is caused by toxicity of:
NEET-PG 2013 - Forensic Medicine NEET-PG Practice Questions and MCQs
Question 811: Minamata disease is caused by toxicity of:
- A. Arsenic
- B. Antimony
- C. Lead
- D. Mercury (Correct Answer)
Explanation: ***Mercury (Correct Answer)*** - Minamata disease is a severe neurological syndrome caused by **mercury poisoning**, specifically from the consumption of fish and shellfish contaminated with **methylmercury**. - The disease was first identified in Minamata Bay, Japan, resulting from the release of industrial wastewater containing methylmercury. - **Clinical features** include: ataxia, dysarthria, constriction of visual fields, sensory disturbances, and in severe cases, convulsions and death. *Arsenic (Incorrect)* - **Arsenic poisoning** is associated with symptoms like **garlic breath**, skin lesions (hyperkeratosis, Raindrop pigmentation), and neurological damage, but it does not cause Minamata disease. - Exposure typically occurs through contaminated water or occupational settings. *Antimony (Incorrect)* - **Antimony toxicity** can manifest with symptoms such as nausea, vomiting, cardiac arrhythmias, and skin inflammation. - It is not linked to the distinct neurological syndrome known as Minamata disease. *Lead (Incorrect)* - **Lead toxicity** (plumbism) primarily affects the nervous system, kidneys, and hematopoietic system, leading to symptoms like **abdominal pain**, **wrist drop/foot drop**, and anemia. - While it causes neurological damage, it has a different clinical presentation and is not associated with Minamata disease.
Internal Medicine
4 questionsA diabetic patient presents with sensory involvement, tingling, numbness, ankle swelling, and absence of pain. What is the most likely diagnosis?
Which of the following is a sign of Bartter's syndrome?
Use of spironolactone in liver cirrhosis is
Metabolic change in severe vomiting is
NEET-PG 2013 - Internal Medicine NEET-PG Practice Questions and MCQs
Question 811: A diabetic patient presents with sensory involvement, tingling, numbness, ankle swelling, and absence of pain. What is the most likely diagnosis?
- A. Charcot's joint (Correct Answer)
- B. Gout
- C. Rheumatoid arthritis
- D. Ankylosing spondylitis
Explanation: ***Charcot's joint*** - This condition is characterized by **neuropathic arthropathy**, resulting from nerve damage (often due to **diabetes**), leading to sensory involvement, **numbness**, and **absence of pain** [1]. - The loss of protective sensation and repeated microtrauma contribute to joint destruction, often manifesting as **swelling** and deformity, particularly in the feet and ankles [1]. *Gout* - Gout typically presents with sudden, severe episodes of **pain**, redness, and swelling in a single joint, most commonly the **big toe**. - It is caused by **uric acid crystal deposition** and is not primarily associated with sensory deficits or chronic painless swelling. *Rheumatoid arthritis* - This is a **chronic autoimmune** inflammatory disease primarily affecting the **small joints** of the hands and feet symmetrically, causing pain, stiffness, and swelling. - It does not typically present with sensory neuropathy or painless joint destruction in the way described. *Ankylosing spondylitis* - This is a **chronic inflammatory disease** primarily affecting the **spine and sacroiliac joints**, causing progressive stiffness and pain that improves with activity. - It is not associated with peripheral joint neuropathy, numbness, or painless ankle swelling [1].
Question 812: Which of the following is a sign of Bartter's syndrome?
- A. High potassium levels
- B. Acidic blood
- C. Low potassium levels (Correct Answer)
- D. High sodium levels
Explanation: ***Low potassium levels*** * Bartter's syndrome is characterized by **renal salt wasting** and subsequent volume depletion, which activates the **renin-angiotensin-aldosterone system** [1]. * This leads to increased aldosterone levels, causing increased potassium secretion in the collecting ducts, resulting in **hypokalemia** [2]. *High potassium levels* * **Hyperkalemia** is not a feature of Bartter's syndrome; instead, it is marked by persistent potassium loss [1]. * Conditions causing hyperkalemia typically involve impaired renal potassium excretion or increased potassium release from cells. *Acidic blood* * Bartter's syndrome usually presents with **metabolic alkalosis** due to hydrogen ion loss in the urine, not acidic blood [2]. * Acidic blood (**acidemia**) would imply a state of respiratory or metabolic acidosis. *High sodium levels* * Bartter's syndrome primarily involves **renal salt wasting**, leading to **normal or low sodium levels** rather than high sodium levels. * High sodium levels (**hypernatremia**) are usually due to inadequate water intake or excessive water loss.
Question 813: Use of spironolactone in liver cirrhosis is
- A. Decrease edema (Correct Answer)
- B. May improve liver function indirectly
- C. May decrease afterload
- D. May decrease intravascular volume
Explanation: ***Decrease edema*** - Spironolactone is an **aldosterone antagonist** that blocks the effects of aldosterone, which is often elevated in liver cirrhosis. - By antagonizing aldosterone, spironolactone promotes **sodium and water excretion**, directly leading to a reduction in **ascites and peripheral edema** [1]. *May improve liver function indirectly* - While spironolactone manages complications of liver cirrhosis, it does **not directly improve liver function** or reverse liver damage. - Its primary role is in **symptom management**, particularly fluid retention, not in healing the underlying liver disease. *May decrease afterload* - Spironolactone's primary action is on the **kidneys** to promote diuresis; it is **not a vasodilator** and therefore does not directly decrease cardiac afterload. - Any effect on systemic vascular resistance would be minimal and secondary to volume changes rather than a direct vasodilatory property. *May decrease intravascular volume* - Spironolactone **decreases total body sodium and water**, leading to a reduction in extravascular fluid (edema and ascites) [1]. - While it decreases the total amount of fluid in the body, its main effect is on **extravascular volume**, and it's chosen over loop diuretics in cirrhosis to prevent **excessive intravascular depletion** which can worsen renal function.
Question 814: Metabolic change in severe vomiting is
- A. Metabolic alkalosis due to loss of gastric acid (Correct Answer)
- B. Respiratory alkalosis due to hyperventilation
- C. Hyperkalemia due to renal dysfunction
- D. Metabolic acidosis due to renal failure
Explanation: **Metabolic alkalosis due to loss of gastric acid** - Severe vomiting leads to the loss of **hydrochloric acid (HCl)** from the stomach, causing an increase in plasma bicarbonate and subsequently **metabolic alkalosis** [1], [3]. - This condition is often accompanied by **hypokalemia** due to renal compensation and increased aldosterone activity [1]. *Respiratory alkalosis due to hyperventilation* - **Hyperventilation** causes a decrease in arterial partial pressure of carbon dioxide (PaCO2), leading to **respiratory alkalosis** [2]. - While vomiting can sometimes cause mild hyperventilation due to discomfort, the primary metabolic derangement from severe vomiting is related to acid loss, not CO2 expulsion [4]. *Hyperkalemia due to renal dysfunction* - **Hyperkalemia** is an elevated potassium level, typically associated with **renal failure** or certain medications. - In severe vomiting, the loss of gastric fluid and subsequent fluid shifts tend to cause **hypokalemia** as the kidneys try to conserve hydrogen and excrete potassium [1]. *Metabolic acidosis due to renal failure* - **Metabolic acidosis** is characterized by a decrease in blood pH and bicarbonate, often caused by the accumulation of acids or loss of bicarbonate [3]. - **Renal failure** is a common cause of metabolic acidosis due to impaired acid excretion, which is not the primary issue in severe vomiting.
Pharmacology
2 questionsWhich of the following drugs is useful in acute attack of gout ?
What is the drug of choice for the treatment of kala-azar?
NEET-PG 2013 - Pharmacology NEET-PG Practice Questions and MCQs
Question 811: Which of the following drugs is useful in acute attack of gout ?
- A. Furosemide
- B. Sulfinpyrazone
- C. Allopurinol
- D. Piroxicam (Correct Answer)
Explanation: ***Piroxicam*** - **Piroxicam** is a **non-steroidal anti-inflammatory drug (NSAID)**, which are the first-line treatment for acute gout attacks. - NSAIDs work by inhibiting **prostaglandin synthesis**, thereby reducing inflammation and pain associated with the acute crystal-induced arthritis. *Furosemide* - **Furosemide** is a loop diuretic that can **raise uric acid levels** by increasing reabsorption in the renal tubules. - Therefore, it would exacerbate **gout** and is contraindicated during an acute attack. *Sulfinpyrazone* - **Sulfinpyrazone** is a **uricosuric agent** used for chronic gout management to increase uric acid excretion. - It is **not used for acute attacks** as it can precipitate or worsen an attack by mobilizing uric acid crystals. *Allopurinol* - **Allopurinol** is a **xanthine oxidase inhibitor** used for long-term management of hyperuricemia and chronic gout. - Starting allopurinol during an **acute attack** can worsen or prolong the attack by causing rapid changes in serum uric acid levels.
Question 812: What is the drug of choice for the treatment of kala-azar?
- A. Amphotericin B
- B. Quinine
- C. Paromomycin
- D. Liposomal Amphotericin B (Correct Answer)
Explanation: ***Liposomal Amphotericin B*** - It is currently considered the **drug of choice** for treating **visceral leishmaniasis (kala-azar)** due to its high efficacy and better tolerability profile compared to conventional amphotericin B. - The **liposomal formulation** allows for targeted delivery to macrophages, where *Leishmania* parasites reside, reducing systemic toxicity. *Amphotericin B* - While effective against *Leishmania*, conventional **Amphotericin B deoxycholate** is associated with significant **nephrotoxicity** and other severe side effects. - It is generally reserved for cases where liposomal amphotericin B is unavailable or as an alternative in specific clinical situations. *Quinine* - **Quinine** is an **antimalarial drug** primarily used for the treatment of *Plasmodium falciparum* malaria. - It has no significant efficacy against *Leishmania* species, which are the causative agents of kala-azar. *Paromomycin* - **Paromomycin** is an **aminoglycoside antibiotic** that can be used as an alternative treatment for visceral leishmaniasis, especially in combination therapies. - Although effective, it is generally not considered the first-line **drug of choice** globally, and its efficacy can vary by region.
Physiology
1 questionsResult of liquorice ingestion
NEET-PG 2013 - Physiology NEET-PG Practice Questions and MCQs
Question 811: Result of liquorice ingestion
- A. Hyperkalemic alkalosis
- B. Hypokalemic acidosis
- C. Hypernatremic acidosis
- D. Hypokalemic alkalosis (Correct Answer)
Explanation: ***Hypokalemic alkalosis*** - **Licorice** contains **glycyrrhizic acid**, which inhibits **11β-hydroxysteroid dehydrogenase** in the kidneys, preventing the conversion of cortisol to inactive cortisone. - This leads to increased cortisol acting on **mineralocorticoid receptors**, mimicking **aldosterone excess**, resulting in **sodium reabsorption**, **potassium excretion** (hypokalemia), and **hydrogen ion excretion** (metabolic alkalosis). *Hyperkalemic alkalosis* - This option is incorrect because licorice ingestion leads to **hypokalemia** due to increased potassium excretion, not hyperkalemia. - While it does cause alkalosis, the associated potassium imbalance is the opposite of this choice. *Hypokalemic acidosis* - This option is incorrect because licorice ingestion causes a **metabolic alkalosis** due to increased hydrogen ion excretion, not acidosis. - Although it correctly identifies hypokalemia, the acid-base disturbance is wrong. *Hypernatremic acidosis* - This option is incorrect as licorice ingestion initially causes **sodium and water retention** (which can lead to hypernatremia in severe cases, but is not the primary driver of the acid-base), but primarily leads to **metabolic alkalosis**, not acidosis. - The combination of hypernatremia and acidosis is not characteristic of licorice toxicity.
Psychiatry
1 questionsWhich of the following is not a typical symptom of Duchenne Muscular Dystrophy (DMD)?
NEET-PG 2013 - Psychiatry NEET-PG Practice Questions and MCQs
Question 811: Which of the following is not a typical symptom of Duchenne Muscular Dystrophy (DMD)?
- A. Muscle pseudo hypertrophy
- B. Muscle weakness
- C. Tenderness in muscles (Correct Answer)
- D. Cardiomyopathy
- E. Gower's sign
Explanation: ***Tenderness in muscles*** - **Muscle tenderness** and pain are **not typical primary symptoms** of Duchenne Muscular Dystrophy (DMD); the disease is characterized by progressive muscle weakness without significant pain. - While some discomfort might arise from muscle spasms or joint issues, widespread tenderness is characteristic of inflammatory conditions, not DMD. *Muscle pseudo hypertrophy* - **Pseudohypertrophy**, particularly in the calves, is a **hallmark sign** of DMD, caused by the replacement of muscle tissue with fat and connective tissue, making the muscles appear larger but weaker. - This symptom reflects the underlying muscle degeneration in DMD. *Muscle weakness* - **Progressive muscle weakness** is the defining characteristic of DMD, typically starting in the proximal muscles and leading to significant functional impairment. - This weakness is due to the lack of **dystrophin**, which is crucial for muscle fiber integrity. *Cardiomyopathy* - **Cardiomyopathy** is a **common and serious complication** of DMD, affecting nearly all patients by adolescence or early adulthood due to the absence of dystrophin in cardiac muscle. - It often manifests as **dilated cardiomyopathy**, contributing significantly to morbidity and mortality. *Gower's sign* - **Gower's sign** is a **classic clinical manifestation** of DMD, where the child uses their hands to "walk up" their legs when rising from the floor due to proximal muscle weakness. - This sign typically appears early in the disease course and is a key diagnostic indicator.