In Wilson's disease, copper deposition primarily occurs in which part of the brain?
Genitourinary complication of ulcerative colitis
A 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
The common cause of subarachnoid hemorrhage is:
Which of the following is not a recognized complication of chronic pancreatitis?
Impotence is a feature of which of the following:
All of the following are features of Obstructive jaundice except:
NEET-PG 2013 - Internal Medicine NEET-PG Practice Questions and MCQs
Question 111: 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 112: 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 113: 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 114: 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 115: 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 116: 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.
Question 117: The common cause of subarachnoid hemorrhage is:
- A. Arterio-venous malformation
- B. Cavernous angioma
- C. Aneurysm (Correct Answer)
- D. Hypertension
Explanation: ***Aneurysm*** - Aneurysms, particularly **saccular** or **berry aneurysms**, are the most frequent cause of **spontaneous subarachnoid hemorrhage (SAH)**, accounting for about 80-85% of cases [2]. - The sudden rupture of an intracranial aneurysm leads to blood spilling into the **subarachnoid space**, causing characteristic symptoms like a "thunderclap headache" [1]. *Arterio-venous malformation* - While AV malformations (AVMs) can cause SAH, they are a less common cause than aneurysms, accounting for approximately 5-10% of cases. - AVMs are abnormal direct connections between arteries and veins that bypass the capillary system and can rupture, leading to SAH or intraparenchymal hemorrhage. *Cavernous angioma* - Cavernous angiomas are abnormal clusters of dilated, thin-walled capillaries that can lead to hemorrhage, but they primarily cause **intraparenchymal hemorrhage** rather than SAH. - They are much less likely to result in diffuse bleeding into the subarachnoid space compared to ruptured aneurysms. *Hypertension* - Hypertension is a significant risk factor for the formation and rupture of aneurysms [1], but it is not a direct cause of SAH itself in the same way an aneurysm rupture is. - While uncontrolled hypertension is often associated with **intracerebral hemorrhage** (bleeding within the brain tissue), its direct role in causing SAH is usually secondary to an underlying vascular abnormality like an aneurysm.
Question 118: Which of the following is not a recognized complication of chronic pancreatitis?
- A. Renal artery thrombosis (Correct Answer)
- B. Pancreatic pseudocyst
- C. Splenic vein thrombosis
- D. Pancreatic fistula
Explanation: ***Renal artery thrombosis*** - **Renal artery thrombosis** is generally associated with conditions like **atherosclerosis**, atrial fibrillation, or vasculitis, not directly with chronic pancreatitis. - While chronic pancreatitis can lead to systemic complications, direct renal arterial clotting is an atypical and **uncommon sequela**. *Pancreatic pseudocyst* - **Pancreatic pseudocysts** are common complications of chronic pancreatitis, occurring when fluid collections around the pancreas become walled off by fibrous tissue [1]. - They can cause pain, obstruction, and even rupture if left untreated [2]. *Splenic vein thrombosis* - **Splenic vein thrombosis** can result from inflammation and compression of the splenic vein by the diseased pancreatic tissue in chronic pancreatitis [1]. - This can lead to **splenomegaly** and **gastric varices** due to increased pressure in the portal system. *Pancreatic fistula* - A **pancreatic fistula** occurs when pancreatic fluid leaks from the gland, often forming a connection to another organ or the skin [2]. - This is a well-recognized complication of both acute and chronic pancreatitis, usually due to ductal disruption.
Question 119: Impotence is a feature of which of the following:
- A. Poliomyelitis
- B. Amyotrophic lateral sclerosis
- C. Meningitis
- D. Multiple sclerosis (Correct Answer)
Explanation: ***Multiple sclerosis*** - **Erectile dysfunction** (impotence) is a common symptom in men with multiple sclerosis, often resulting from **demyelination** in nerve pathways controlling sexual function [1], [2]. - MS can affect various neurological functions, leading to problems with **autonomic nervous system** control, sensation, and motor coordination, all of which can impact sexual health. *Poliomyelitis* - Poliomyelitis primarily affects the **anterior horn cells** of the spinal cord, leading to acute **flaccid paralysis** of muscles. - While it can cause muscle weakness and atrophy, it is not typically associated with chronic impotence or sexual dysfunction as a primary feature. *Amyotrophic lateral sclerosis* - ALS is a progressive neurodegenerative disease affecting **motor neurons**, leading to muscle weakness, atrophy, and spasticity. - It primarily impacts voluntary muscle movement and does not directly cause impotence, although the physical limitations and psychological stress can indirectly affect sexual function. *Meningitis* - Meningitis is an inflammation of the **meninges** (membranes surrounding the brain and spinal cord) caused by infection. - Its symptoms include headache, fever, and neck stiffness, and while severe cases can lead to neurological complications, impotence is not a typical direct consequence.
Question 120: All of the following are features of Obstructive jaundice except:
- A. Clay colour stools
- B. Pruritis
- C. Normal alkaline phosphatase (Correct Answer)
- D. Elevated serum aminotransferases level
Explanation: ***Normal alkaline phosphatase*** - In obstructive jaundice, alkaline phosphatase is typically **elevated** due to bile duct obstruction [2]. - A **normal level** suggests that the jaundice may not be of obstructive origin. *Pruritis* - Often seen in obstructive jaundice due to **bile salts** accumulating in the bloodstream, leading to itching. - It is a common symptom associated with **cholestasis**. *Mildly elevated serum aminotransferases level* - In obstructive jaundice, serum aminotransferases are usually elevated, though may be mildly in early cases [1]. - This reflects liver involvement, which is consistent with biliary obstruction [2]. *Clay colour stools* - Clay-colored stools arise from the absence of **bile** in the intestines, indicative of obstruction [3]. - This is a direct result of blockage in the bile duct system affecting stool pigmentation [3].