What is the primary clinical feature of Henoch-Schonlein purpura?
Interstitial nephritis is common with
Use of spironolactone in liver cirrhosis is
Which of the following is a sign of Bartter's syndrome?
A diabetic patient presents with sensory involvement, tingling, numbness, ankle swelling, and absence of pain. What is the most likely diagnosis?
Genitourinary complication of ulcerative colitis
In Wilson's disease, copper deposition primarily occurs in which part of the brain?
What is the volume of blood loss associated with Class III hemorrhagic shock?
Which of the following is a complication of total parenteral nutrition?
Prepyloric or channel ulcer in the stomach is termed as:
NEET-PG 2013 - Internal Medicine NEET-PG Practice Questions and MCQs
Question 121: What is the primary clinical feature of Henoch-Schonlein purpura?
- A. Abdominal pain due to vasculitis
- B. Joint pain associated with the condition
- C. Kidney involvement in the disease
- D. Skin rash characterized by palpable purpura (Correct Answer)
Explanation: ***Skin rash characterized by palpable purpura*** - **Palpable purpura** is the hallmark cutaneous manifestation of **Henoch-Schonlein purpura (HSP)**, a small-vessel vasculitis [1]. - This rash typically appears on the **lower extremities and buttocks**, reflecting the deposition of IgA in vessel walls [1]. *Abdominal pain due to vasculitis* - While **abdominal pain** is a common feature of HSP due to gastrointestinal vasculitis, it is not considered the primary clinical feature [1]. - Gastrointestinal involvement can manifest with pain, bleeding, and intussusception, but the **skin rash** is more consistently present and diagnostic. *Joint pain associated with the condition* - **Arthralgia** or **arthritis** (joint pain) is seen in a significant number of HSP patients, particularly in the knees and ankles. - However, it is a secondary manifestation, and not the **defining primary sign** of the disease. *Kidney involvement in the disease* - **Renal involvement**, presenting as hematuria and proteinuria, occurs in about one-third of HSP cases and can lead to serious long-term complications. - Despite its significance for prognosis, **kidney disease** is a later and not universally present feature, making the rash the most critical initial diagnostic clue.
Question 122: Interstitial nephritis is common with
- A. Black water fever
- B. Rhabdomyolysis
- C. Tumor lysis syndrome
- D. Nonsteroidal anti-inflammatory drugs (NSAIDs) (Correct Answer)
Explanation: ***Nonsteroidal anti-inflammatory drugs (NSAIDs)*** - **NSAIDs** are a known cause of **acute interstitial nephritis** (AIN), an inflammatory condition affecting the tubules and interstitium of the kidney [1]. - This adverse reaction often manifests as **fever**, **rash**, **eosinophilia**, and **acute kidney injury**, typically 7-10 days after drug exposure. *Black water fever* - **Blackwater fever** is a severe complication of **malaria**, characterized by massive hemolysis leading to **hemoglobinuria**, which darkens the urine. - It primarily causes **acute kidney injury** through **acute tubular necrosis** due to hemoglobin precipitation in the renal tubules, not interstitial nephritis. *Rhabdomyolysis* - **Rhabdomyolysis** involves the breakdown of muscle tissue, releasing myoglobin into the bloodstream, which is toxic to the kidneys. [1] - This condition leads to **acute kidney injury** predominantly through **acute tubular necrosis** due to myoglobin casts obstructing tubules and direct toxicity, not interstitial inflammation. *Tumor lysis syndrome* - **Tumor lysis syndrome** occurs when large numbers of cancer cells are rapidly destroyed, releasing intracellular contents like potassium, phosphate, and nucleic acids. - The high concentration of **uric acid** and **phosphate** in the renal tubules leads to crystal formation, causing **acute kidney injury** primarily through **acute uric acid nephropathy** and **phosphate nephropathy**, rather than interstitial nephritis [1].
Question 123: 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 124: 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 125: 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 126: Genitourinary complication of ulcerative colitis
- A. Urinary calculi (Correct Answer)
- B. Pyelonephritis
- C. Urethritis
- D. Cystitis
Explanation: ***Urinary calculi*** - Patients with ulcerative colitis are at an increased risk of developing **urinary calculi** due to several factors, including chronic dehydration, malabsorption of fats leading to increased oxalate absorption (enteric hyperoxaluria), and altered urine composition. - The inflammatory process and potential for surgical interventions (e.g., colectomy with ileostomy) can further predispose individuals to kidney stone formation. *Cystitis* - While cystitis (bladder inflammation) can occur in the general population, it is not considered a specific or significantly elevated genitourinary complication directly linked to the pathogenesis of ulcerative colitis itself. - It results primarily from bacterial infection, and there is no direct evidence suggesting UC patients have a higher intrinsic risk compared to the general population. *Pyelonephritis* - Pyelonephritis (kidney infection) is not a direct or common complication of ulcerative colitis. - It is typically caused by bacterial ascent from the lower urinary tract and is not specifically promoted by the inflammatory processes or metabolic changes associated with UC. *Urethritis* - Urethritis (inflammation of the urethra) is primarily associated with sexually transmitted infections or irritation and is not a recognized genitourinary complication directly caused by ulcerative colitis. - There is no increased incidence of urethritis in UC patients compared to the general population.
Question 127: In Wilson's disease, copper deposition primarily occurs in which part of the brain?
- A. Basal ganglia (Correct Answer)
- B. Cerebellum
- C. Pons
- D. Medulla
Explanation: ***Basal ganglia*** - The **basal ganglia**, particularly the **putamen** and **globus pallidus**, are the most common sites for copper deposition in the brain in Wilson's disease [1]. - This deposition leads to **neurological symptoms** such as dystonia [2], tremor, and dysarthria. *Pons* - While copper can accumulate in various brain regions, the **pons** is not a primary or characteristic site of significant copper deposition. - Neurological symptoms associated with pontine damage are not typical presenting features of Wilson's disease. *Cerebellum* - The **cerebellum** can show some copper accumulation in advanced stages, but it is not the primary site. - Cerebellar signs like **ataxia** can occur in Wilson's disease, but usually secondary to more widespread pathology rather than primary cerebellar copper deposition. *Medulla* - The **medulla oblongata** is generally spared from significant copper deposition in Wilson's disease. - Involvement of the medulla would typically manifest with severe autonomic or brainstem dysfunction, which is not a hallmark of early Wilson's disease.
Question 128: What is the volume of blood loss associated with Class III hemorrhagic shock?
- A. 750 - 1500 ml
- B. 1500 - 2000 ml (Correct Answer)
- C. > 2000 ml
- D. < 750 ml
Explanation: ***1500 - 2000 ml*** - **Class III hemorrhagic shock** is characterized by a significant loss of blood volume, typically ranging from **30-40%** of total blood volume. - For an average adult, this translates to an estimated **1500-2000 ml** of blood loss, leading to marked physiological compromise. *750 - 1500 ml* - This range of blood loss corresponds to **Class II hemorrhagic shock**, where physiological changes are moderate, but compensatory mechanisms are still largely effective. - Patients in Class II shock typically present with **tachycardia** and a slight decrease in pulse pressure but generally normal blood pressure. *> 2000 ml* - A blood loss exceeding **2000 ml** (or >40% of total blood volume) is indicative of **Class IV hemorrhagic shock**, the most severe category. - This level of blood loss results in pronounced **hypotension**, severe tachycardia, and often requires immediate massive transfusion to prevent irreversible organ damage. *< 750 ml* - This range represents **Class I hemorrhagic shock**, which involves a minimal blood loss of up to 15% of total blood volume. - Patients in Class I shock typically show **minimal to no clinical signs of shock**, as compensatory mechanisms are highly effective in maintaining vital signs.
Question 129: Which of the following is a complication of total parenteral nutrition?
- A. Hyperglycemia (Correct Answer)
- B. Hyperkalemia
- C. Hyperglycemia and Hyperkalemia
- D. Hyperosmolar dehydration
Explanation: ***Hyperglycemia*** - Total parenteral nutrition (TPN) solutions contain a high concentration of **dextrose** (glucose), which can lead to elevated blood glucose levels, especially in patients with pre-existing metabolic issues or high infusion rates. - The sudden and continuous infusion of carbohydrates can overwhelm the body's **insulin response**, resulting in hyperglycemia [3]. *Hyperkalemia* - **Hypokalemia**, rather than hyperkalemia, is a more common electrolyte disturbance associated with TPN due to intracellular shifts of potassium with glucose metabolism [2]. - While TPN solutions do contain potassium, hyperkalemia is generally rare unless there is significant renal impairment or excessive potassium supplementation. *Hyperglycemia and Hyperkalemia* - While **hyperglycemia** is a common complication, **hyperkalemia** is not; in fact, hypokalemia is a more frequent concern linked to the significant glucose load in TPN. - This option incorrectly pairs a common complication with one that is rare and generally only seen in specific circumstances. *Hyperosmolar dehydration* - This condition, also known as **hyperosmolar hyperglycemic state (HHS)**, is a severe complication that can arise from uncontrolled hyperglycemia, where high glucose levels lead to osmotic diuresis and severe dehydration [1]. - While hyperglycemia is a precursor to hyperosmolar dehydration, the direct complication of TPN administration itself is the hyperglycemia.
Question 130: Prepyloric or channel ulcer in the stomach is termed as:
- A. Type 3 (Correct Answer)
- B. Type 1
- C. Type 4
- D. Type 2
Explanation: ***Type 3*** - **Type 3 ulcers** are located in the **prepyloric region** or within the **pyloric channel** of the stomach. - They are often associated with **duodenal ulcers** and are characterized by **normal to high acid secretion**. *Type 1* - **Type 1 ulcers** are typically found in the **lesser curvature of the stomach body**, not the prepyloric region. - These ulcers are usually associated with **low or normal acid secretion** and are often linked to *H. pylori* infection. *Type 2* - **Type 2 ulcers** involve both a **gastric ulcer** (usually in the body) and an **active or healed duodenal ulcer**. - They are associated with **normal to high acid secretion**, but the location is not exclusively prepyloric. *Type 4* - **Type 4 ulcers** are located high on the **lesser curvature near the gastroesophageal junction**. - They are associated with **low acid secretion** and are sometimes termed **juxta-esophageal ulcers**.