NEET-PG 2015 — Internal Medicine

Q: All are reversible causes of dementia except one.

Alzheimer's disease. ### Alzheimer's disease - Alzheimer's disease is the most common cause of **irreversible, progressive neurodegenerative dementia**, characterized by the accumulation of **amyloid plaques** and **neurofibrillary tangles**. - There is currently no cure for Alzheimer's disease, and treatments focus on symptom management rather than reversal. *Hypothyroidism* - **Severe or untreated hypothyroidism** can cause cognitive impairment and dementia-like symptoms, which are often reversible with **thyroid hormone replacement therapy**. - Symptoms like **memory loss**, **slowed thinking**, and confusion can improve significantly once **euthyroid state** is achieved. *Hydrocephalus* - **Normal pressure hydrocephalus (NPH)** can cause a triad of symptoms including **gait disturbance**, **urinary incontinence**, and **dementia**, which can be reversible with a **shunt placement** [1]. - The cognitive decline in NPH is due to increased intracranial pressure affecting brain function, and surgical intervention can alleviate this pressure [1]. *Meningoencephalitis* - **Inflammation of the brain and its surrounding membranes** due to infection can lead to cognitive dysfunction and dementia, which may be reversible with **appropriate antimicrobial or antiviral treatment** [1]. - Early and aggressive treatment of the underlying infection is crucial for potential recovery of cognitive function and prevention of permanent damage. [Practice more Internal Medicine PYQs on OnCourse]

Q: Absence of the intrahepatic bile ducts leads to which syndrome?

Alagille Syndrome. ***Alagille Syndrome*** - Characterized by the **absence of intrahepatic bile ducts**, leading to cholestasis and liver dysfunction. - Often associated with **cardiac defects** and **skeletal abnormalities**, as well as distinct **facial features**. *Von Meyenburg Complexes* - Refers to **bile duct hamartomas**, which are developmental abnormalities but do not lead to complete absence of ducts. - Typically discovered incidentally and are not associated with syndromic presentations like Alagille syndrome. *Caroli Disease* - Involves **dilated intrahepatic bile ducts** [1] and does not result in their absence; thus, it leads to **recurrent cholangitis**. - More associated with **cysts** and can lead to biliary complications rather than complete duct loss. *Polycystic Liver Disease* - Characterized by the presence of multiple **cysts** in the liver, but the intrahepatic bile ducts are typically present. - It is often associated with **kidney cysts** and systemic manifestations, not the absence of bile ducts. [Practice more Internal Medicine PYQs on OnCourse]

Q: Which of the following statements about Wilson's disease is true?

Low serum ceruloplasmin and high urinary copper. ***Low serum ceruloplasmin and high urinary copper*** - In **Wilson's disease**, there is a defect in **copper transport**, leading to impaired incorporation of copper into ceruloplasmin and reduced biliary excretion. - This results in **low serum ceruloplasmin** levels (since ceruloplasmin is the main copper-carrying protein in the blood) and **increased urinary copper excretion** as the body attempts to eliminate excess free copper. *Low serum ceruloplasmin and low urinary copper* - While **low serum ceruloplasmin** is characteristic, **low urinary copper** would indicate adequate copper elimination or a different condition, which is not the case for Wilson's disease. - Patients with Wilson's disease have **excess copper accumulation**, and increased urinary excretion is a compensatory mechanism [1]. *High serum ceruloplasmin and low urinary copper* - **High serum ceruloplasmin** is inconsistent with Wilson's disease, as ceruloplasmin levels are typically low due to the impaired copper binding. - **Low urinary copper** excretion would indicate normal or low total body copper, which contradicts the copper overload seen in Wilson's disease. *High serum ceruloplasmin and high urinary copper* - **High serum ceruloplasmin** would suggest normal or increased ceruloplasmin synthesis or release, which is contrary to the pathophysiology of Wilson's disease. - Although **high urinary copper** is a feature, it isn't accompanied by high ceruloplasmin in this condition, as ceruloplasmin is primarily involved in carrying copper in the blood rather than excreting excess copper [1]. [Practice more Internal Medicine PYQs on OnCourse]

Q: Which of the following is the MOST SIGNIFICANT modifiable predisposing factor for arterial thrombosis?

Cigarette smoking. ***Cigarette smoking*** - **Cigarette smoking** is a major modifiable risk factor for **atherosclerosis** and arterial thrombosis, primarily by promoting endothelial dysfunction, inflammation, and hypercoagulability. [1] - It damages the **endothelium**, leading to plaque formation and increasing the risk of **thrombotic events** such as myocardial infarction and stroke. [1] *Antiphospholipid syndrome* - This is an **autoimmune disorder** causing recurrent arterial and venous thromboses, but it is not a modifiable lifestyle factor. - While it dramatically increases thrombosis risk, therapeutic management focuses on anticoagulation rather than lifestyle modification. *Hyperlipidemia* - **Hyperlipidemia**, particularly elevated LDL cholesterol, is a significant risk factor for **atherosclerosis**, which can lead to thrombosis. [1] - However, while modifiable through diet and medication, its immediate thrombotic impact is often mediated through chronic plaque formation, whereas smoking has more direct prothrombotic effects on endothelium and platelet function. *Homocystinuria* - This is a rare, inherited **metabolic disorder** causing elevated homocysteine levels, leading to severe premature atherosclerosis and **thrombotic disease**. - It is a genetic condition and therefore not a modifiable risk factor in the same way as lifestyle choices. [Practice more Internal Medicine PYQs on OnCourse]

Q: What is the cause of perihepatic fibrosis in Fitz-Hugh-Curtis syndrome?

Pelvic Inflammatory Disease. ***Pelvic Inflammatory Disease*** - Fitz-Hugh-Curtis syndrome is a complication of **Pelvic Inflammatory Disease (PID)**, where infection spreads from the pelvic organs to the liver capsule [1]. - The inflammation leads to **perihepatic fibrosis** and adhesions, often described as "violin string" adhesions [1]. *Bile Duct Injury* - **Bile duct injury** can cause inflammation and fibrosis of the liver, but it typically affects the intrahepatic or extrahepatic bile ducts directly, rather than the liver capsule. - This condition is often associated with surgical procedures or gallstones, and not directly linked to PID. *Chronic Alcoholism* - **Chronic alcoholism** is a well-known cause of liver fibrosis and cirrhosis, but it specifically damages hepatocytes and leads to diffuse scarring of the liver parenchyma. - It does not primarily cause localized perihepatic fibrosis in the manner seen in Fitz-Hugh-Curtis syndrome. *Viral Hepatitis* - **Viral hepatitis** (e.g., Hepatitis B or C) causes diffuse inflammation and fibrosis throughout the liver, leading to cirrhosis over time. - It does not typically result in the characteristic localized perihepatic adhesions of Fitz-Hugh-Curtis syndrome, which is an ascendant infection. [Practice more Internal Medicine PYQs on OnCourse]

171 Previous Year Questions with Answers & Explanations

171

Questions

All are reversible causes of dementia except one.

Absence of the intrahepatic bile ducts leads to which syndrome?

Which of the following statements about Wilson's disease is true?

Which of the following is the MOST SIGNIFICANT modifiable predisposing factor for arterial thrombosis?

What is the cause of perihepatic fibrosis in Fitz-Hugh-Curtis syndrome?

Which of the following statements about Alport's syndrome is incorrect?

Which of the following is NOT a feature of facial nerve palsy?

In which portion of the esophagus do esophageal varices primarily occur?

Which of the following statements is false regarding the declaration of brain stem death in a hospital?

Q10

In which condition is Serum Amyloid Associated (SAA) protein most commonly found?

NEET-PG 2015 - Internal Medicine NEET-PG Practice Questions and MCQs

Question 1: All are reversible causes of dementia except one.

A. Alzheimer's disease (Correct Answer)
B. Hydrocephalus
C. Meningoencephalitis
D. Hypothyroidism

Explanation: ### Alzheimer's disease - Alzheimer's disease is the most common cause of **irreversible, progressive neurodegenerative dementia**, characterized by the accumulation of **amyloid plaques** and **neurofibrillary tangles**. - There is currently no cure for Alzheimer's disease, and treatments focus on symptom management rather than reversal. *Hypothyroidism* - **Severe or untreated hypothyroidism** can cause cognitive impairment and dementia-like symptoms, which are often reversible with **thyroid hormone replacement therapy**. - Symptoms like **memory loss**, **slowed thinking**, and confusion can improve significantly once **euthyroid state** is achieved. *Hydrocephalus* - **Normal pressure hydrocephalus (NPH)** can cause a triad of symptoms including **gait disturbance**, **urinary incontinence**, and **dementia**, which can be reversible with a **shunt placement** [1]. - The cognitive decline in NPH is due to increased intracranial pressure affecting brain function, and surgical intervention can alleviate this pressure [1]. *Meningoencephalitis* - **Inflammation of the brain and its surrounding membranes** due to infection can lead to cognitive dysfunction and dementia, which may be reversible with **appropriate antimicrobial or antiviral treatment** [1]. - Early and aggressive treatment of the underlying infection is crucial for potential recovery of cognitive function and prevention of permanent damage.

Question 2: Absence of the intrahepatic bile ducts leads to which syndrome?

A. Polycystic Liver Disease
B. Caroli Disease
C. Von Meyenburg Complexes
D. Alagille Syndrome (Correct Answer)

Explanation: ***Alagille Syndrome*** - Characterized by the **absence of intrahepatic bile ducts**, leading to cholestasis and liver dysfunction. - Often associated with **cardiac defects** and **skeletal abnormalities**, as well as distinct **facial features**. *Von Meyenburg Complexes* - Refers to **bile duct hamartomas**, which are developmental abnormalities but do not lead to complete absence of ducts. - Typically discovered incidentally and are not associated with syndromic presentations like Alagille syndrome. *Caroli Disease* - Involves **dilated intrahepatic bile ducts** [1] and does not result in their absence; thus, it leads to **recurrent cholangitis**. - More associated with **cysts** and can lead to biliary complications rather than complete duct loss. *Polycystic Liver Disease* - Characterized by the presence of multiple **cysts** in the liver, but the intrahepatic bile ducts are typically present. - It is often associated with **kidney cysts** and systemic manifestations, not the absence of bile ducts.

Question 3: Which of the following statements about Wilson's disease is true?

A. Low serum ceruloplasmin and low urinary copper
B. Low serum ceruloplasmin and high urinary copper (Correct Answer)
C. High serum ceruloplasmin and low urinary copper
D. High serum ceruloplasmin and high urinary copper

Explanation: ***Low serum ceruloplasmin and high urinary copper*** - In **Wilson's disease**, there is a defect in **copper transport**, leading to impaired incorporation of copper into ceruloplasmin and reduced biliary excretion. - This results in **low serum ceruloplasmin** levels (since ceruloplasmin is the main copper-carrying protein in the blood) and **increased urinary copper excretion** as the body attempts to eliminate excess free copper. *Low serum ceruloplasmin and low urinary copper* - While **low serum ceruloplasmin** is characteristic, **low urinary copper** would indicate adequate copper elimination or a different condition, which is not the case for Wilson's disease. - Patients with Wilson's disease have **excess copper accumulation**, and increased urinary excretion is a compensatory mechanism [1]. *High serum ceruloplasmin and low urinary copper* - **High serum ceruloplasmin** is inconsistent with Wilson's disease, as ceruloplasmin levels are typically low due to the impaired copper binding. - **Low urinary copper** excretion would indicate normal or low total body copper, which contradicts the copper overload seen in Wilson's disease. *High serum ceruloplasmin and high urinary copper* - **High serum ceruloplasmin** would suggest normal or increased ceruloplasmin synthesis or release, which is contrary to the pathophysiology of Wilson's disease. - Although **high urinary copper** is a feature, it isn't accompanied by high ceruloplasmin in this condition, as ceruloplasmin is primarily involved in carrying copper in the blood rather than excreting excess copper [1].

Question 4: Which of the following is the MOST SIGNIFICANT modifiable predisposing factor for arterial thrombosis?

A. Antiphospholipid syndrome
B. Hyperlipidemia
C. Cigarette smoking (Correct Answer)
D. Homocystinuria

Explanation: ***Cigarette smoking*** - **Cigarette smoking** is a major modifiable risk factor for **atherosclerosis** and arterial thrombosis, primarily by promoting endothelial dysfunction, inflammation, and hypercoagulability. [1] - It damages the **endothelium**, leading to plaque formation and increasing the risk of **thrombotic events** such as myocardial infarction and stroke. [1] *Antiphospholipid syndrome* - This is an **autoimmune disorder** causing recurrent arterial and venous thromboses, but it is not a modifiable lifestyle factor. - While it dramatically increases thrombosis risk, therapeutic management focuses on anticoagulation rather than lifestyle modification. *Hyperlipidemia* - **Hyperlipidemia**, particularly elevated LDL cholesterol, is a significant risk factor for **atherosclerosis**, which can lead to thrombosis. [1] - However, while modifiable through diet and medication, its immediate thrombotic impact is often mediated through chronic plaque formation, whereas smoking has more direct prothrombotic effects on endothelium and platelet function. *Homocystinuria* - This is a rare, inherited **metabolic disorder** causing elevated homocysteine levels, leading to severe premature atherosclerosis and **thrombotic disease**. - It is a genetic condition and therefore not a modifiable risk factor in the same way as lifestyle choices.

Question 5: What is the cause of perihepatic fibrosis in Fitz-Hugh-Curtis syndrome?

A. Bile Duct Injury
B. Chronic Alcoholism
C. Viral Hepatitis
D. Pelvic Inflammatory Disease (Correct Answer)

Explanation: ***Pelvic Inflammatory Disease*** - Fitz-Hugh-Curtis syndrome is a complication of **Pelvic Inflammatory Disease (PID)**, where infection spreads from the pelvic organs to the liver capsule [1]. - The inflammation leads to **perihepatic fibrosis** and adhesions, often described as "violin string" adhesions [1]. *Bile Duct Injury* - **Bile duct injury** can cause inflammation and fibrosis of the liver, but it typically affects the intrahepatic or extrahepatic bile ducts directly, rather than the liver capsule. - This condition is often associated with surgical procedures or gallstones, and not directly linked to PID. *Chronic Alcoholism* - **Chronic alcoholism** is a well-known cause of liver fibrosis and cirrhosis, but it specifically damages hepatocytes and leads to diffuse scarring of the liver parenchyma. - It does not primarily cause localized perihepatic fibrosis in the manner seen in Fitz-Hugh-Curtis syndrome. *Viral Hepatitis* - **Viral hepatitis** (e.g., Hepatitis B or C) causes diffuse inflammation and fibrosis throughout the liver, leading to cirrhosis over time. - It does not typically result in the characteristic localized perihepatic adhesions of Fitz-Hugh-Curtis syndrome, which is an ascendant infection.

Question 6: 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 7: Which of the following is NOT a feature of facial nerve palsy?

A. Loss of lacrimation
B. Facial muscle paralysis
C. Loss of taste sensation from posterior tongue (Correct Answer)
D. Loss of salivation

Explanation: Loss of taste sensation from posterior tongue - The **facial nerve (CN VII)** carries taste fibers from the **anterior two-thirds of the tongue** via the **chorda tympani**. - **Taste sensation** from the **posterior one-third of the tongue** is mediated by the **glossopharyngeal nerve (CN IX)**, so its loss would not be a feature of facial nerve palsy. *Loss of lacrimation* - The facial nerve provides **parasympathetic innervation** to the **lacrimal glands** via the **greater petrosal nerve**. - Damage to the facial nerve proximal to the geniculate ganglion can lead to **reduced tear production** on the affected side. [1] *Facial muscle paralysis* - The facial nerve is the primary motor nerve for the **muscles of facial expression**. [1] - Injury to this nerve results in varying degrees of **weakness or paralysis** of the facial muscles, leading to drooping and difficulty with facial movements. [1] *Loss of salivation* - The facial nerve carries **parasympathetic fibers** to the **submandibular** and **sublingual salivary glands** via the **chorda tympani**. - A lesion affecting the facial nerve can therefore impair **salivary gland function**, leading to reduced saliva production.

Question 8: In which portion of the esophagus do esophageal varices primarily occur?

A. All sites
B. Upper
C. Lower (Correct Answer)
D. Middle

Explanation: **Lower** - Esophageal varices are most commonly found in the **distal (lower) third of the esophagus** [1] because this is where the portal venous system (short gastric and left gastric veins) anastomoses with the systemic venous system (white esophageal veins draining into the azygous system) [1]. - Increased portal pressure (e.g., in **portal hypertension** due to liver cirrhosis) causes blood to back up into these collateral vessels, leading to their dilation and formation of varices, particularly prominent in the lower esophagus [1]. *Upper* - While some collateral circulation exists throughout the esophagus, varices are not predominantly found in the upper portion as the primary portosystemic anastomoses responsible for variceal formation are more distal. - Varices in the upper esophagus are less common and typically less clinically significant in terms of bleeding risk. *Middle* - The middle portion of the esophagus has some venous drainage, but it is not the primary site for the significant portosystemic collaterals that lead to the formation of large, high-risk varices. - Varices can extend into the middle esophagus, but their origin and highest concentration are usually in the lower third. *All sites* - While varices can technically be found at various points along the esophagus, stating "all sites" is inaccurate because they have a **marked predilection for the lower third** due to specific anatomical venous connections [1]. - The risk of rupture and bleeding is also highest in the larger varices found in the lower esophagus [1].

Question 9: Which of the following statements is false regarding the declaration of brain stem death in a hospital?

A. Presence of neurologist is not required
B. Drug overdose should be ruled out
C. All of the above (Correct Answer)
D. Patient must be in coma

Explanation: ***All of the above*** - This option indicates that all the preceding statements are false. Let's analyze why each individual statement is indeed false in the context of brain stem death declaration [1]. - This implies there is a misunderstanding regarding each aspect of brain stem death criteria, which often requires specific conditions like a neurologist's involvement (though not always strictly mandatory in all protocols), ruling out drug overdose, and the patient being in a coma. *Presence of neurologist is not required* - This statement is false because while it's not universally mandated that a neurologist be one of the two certifying doctors, one of them must be a **senior physician (consultant)** and both must be experienced in brain stem death diagnosis. - In many settings, especially for complex cases or where local protocols specify, a neurologist or neurosurgeon's involvement is highly recommended or required to confirm brain stem death. *Drug overdose should be ruled out* - This statement is false because the absence of drugs that could **mimic brain stem death (e.g., sedatives, muscle relaxants)** is a crucial precondition for testing [3]. - It is essential to ensure that the patient's neurological state is not confounded by reversible causes like drug intoxication before proceeding with brain stem death tests [3]. *Patient must be in coma* - This statement is false because while a patient declared brain stem dead will indeed be in a coma, the criteria for **brain stem death** specifically focus on the irreversible cessation of brainstem function [1], not merely a comatose state [2]. - A coma is a precondition for assessing brain stem death, but the declaration itself requires specific tests demonstrating the absence of **brainstem reflexes** [4] and **apnea** [3], confirming the permanent loss of brainstem activity.

Question 10: In which condition is Serum Amyloid Associated (SAA) protein most commonly found?

A. Alzheimer's disease
B. Malignant hypertension
C. Chronic inflammatory states (Correct Answer)
D. Chronic renal failure
E. Acute myocardial infarction

Explanation: ***Chronic inflammatory states*** [1][2] - Serum amyloid-associated protein is elevated in response to **chronic inflammation**, such as in rheumatic diseases and infections [1][2]. - It serves as a **biomarker** indicating systemic inflammation and is part of the **acute-phase response** [1]. *Chronic renal failure* - While renal failure can lead to amyloidosis, it is not a direct cause of serum amyloid-associated protein elevation. - **Renal impairment** is more associated with a decrease in clearance rather than production of amyloid proteins. *Alzheimer's disease* - Although amyloid plaques are a hallmark of Alzheimer's, they are related to **A-beta peptide**, not serum amyloid-associated protein. - Alzheimer's pathology primarily involves **neurodegeneration** rather than inflammatory response. *Malignant hypertension* - Malignant hypertension primarily affects the **vascular system** and does not directly involve the production of serum amyloid-associated protein. - It is characterized by end-organ damage, rather than a state of chronic inflammation. *Chronic inflammatory conditions like RA, TB & leprosy, osteomyelitis, ankylosing spondylitis, IBD, bronchiectasis, some tumors* [1][2] - While these conditions can be associated with systemic inflammation, they are too specific and do not comprehensively encompass the broader concept of **chronic inflammatory states**. - This option fails to highlight that serum amyloid-associated protein is a marker for **various chronic inflammatory states** beyond just those listed [1].