In head injury, unilateral dilatation of the pupil is seen due to?
Which of the following conditions is associated with ectopia lentis?
What is the primary brain region associated with ocular bobbing?
The common cause of subarachnoid hemorrhage is:
Extraintestinal manifestations of Inflammatory bowel disease include all of the following, Except:
Which of the following is NOT an indication for a liver biopsy?
Which of the following is a common finding in patients with Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH)?
Which of the following conditions is associated with megaloblastic anemia?
In inflammatory myopathy, which group of muscles is not affected
Which of the following is a feature of tumor lysis syndrome?
NEET-PG 2013 - Internal Medicine NEET-PG Practice Questions and MCQs
Question 121: In head injury, unilateral dilatation of the pupil is seen due to?
- A. Ophthalmic N. compression
- B. Trigeminal N. compression
- C. Oculomotor nerve compression (Correct Answer)
- D. None of the options
Explanation: Oculomotor nerve compression - Unilateral pupillary dilation, often referred to as a **blown pupil**, is a classic sign of **oculomotor nerve (CN III) compression** due to increased intracranial pressure, typically from a **herniating uncus** [1]. - The parasympathetic fibers responsible for pupillary constriction run on the superficial aspect of the oculomotor nerve and are thus vulnerable to extrinsic compression [1], [2]. *Ophthalmic N. compression* - The **ophthalmic nerve (CN V1)** is a sensory nerve responsible for sensation to the forehead, scalp, upper eyelid, and cornea, not pupillary control. - Compression of this nerve would cause **sensory deficits** in its distribution and potentially abolish the **corneal reflex**, but not pupillary dilation. *Trigeminal N. compression* - The **trigeminal nerve (CN V)** is primarily responsible for sensation to the face and motor control of the muscles of mastication. - Compression would lead to **facial numbness or pain** and **weakness in chewing**, with no direct impact on pupillary size. *None of the options* - This option is incorrect because oculomotor nerve compression is a well-established cause of unilateral pupillary dilation in head injuries [1].
Question 122: Which of the following conditions is associated with ectopia lentis?
- A. Homocystinuria (Correct Answer)
- B. Alport syndrome
- C. Lowe syndrome
- D. Sulphite oxidase deficiency
Explanation: ***Homocystinuria*** - **Ectopia lentis** (lens dislocation) is a common and characteristic ocular manifestation of homocystinuria. - The lens typically dislocates **downward and inward**, differentiating it from Marfan syndrome. *Alport syndrome* - Characterized by **glomerulonephritis**, **sensorineural hearing loss**, and ocular abnormalities. - Ocular manifestations include **anterior lenticonus** (which can be mistaken for ectopia lentis in some descriptions), posterior polymorphous corneal dystrophy, and retinal flecks, but not classic ectopia lentis. *Lowe syndrome* - Also known as oculocerebrorenal syndrome of Lowe, it primarily affects the **eyes, brain, and kidneys**. - Ocular features include **congenital cataracts** and glaucoma, but not ectopia lentis. *Sulphite oxidase deficiency* - This is a rare metabolic disorder affecting the metabolism of sulfur-containing amino acids, leading to severe neurological symptoms. - While it can manifest with **cataracts** and **lens subluxation** in some cases, ectopia lentis is more characteristically associated with homocystinuria, and the overall clinical picture of sulphite oxidase deficiency is dominated by severe neurological impairment.
Question 123: What is the primary brain region associated with ocular bobbing?
- A. Midbrain
- B. Pons (Correct Answer)
- C. Medulla
- D. Cerebral cortex
Explanation: Pons - **Ocular bobbing** is a characteristic eye movement disorder strongly associated with **pontine lesions**, particularly infarctions or hemorrhages affecting the tegmentum. - The pons contains critical connections for vertical gaze control within the **brainstem**, and damage here disrupts these pathways [1]. *Midbrain* - While important for eye movements, particularly **vertical gaze centers**, injuries to the midbrain typically cause disorders like Parinaud syndrome (upgaze palsy), not classic ocular bobbing. - Midbrain lesions might cause other types of nystagmus or gaze palsies but not generally the rapid downward and slow upward movement seen in bobbing. *Medulla* - The medulla primarily controls vital functions like breathing and heart rate, as well as some ocular reflexes, but is less directly involved in the generation of sustained vertical eye movements. - Damage to the medulla is more likely to cause effects like **nystagmus** (e.g., downbeat nystagmus in some cases) or other brainstem signs, rather than ocular bobbing. *Cerebral cortex* - The cerebral cortex is responsible for voluntary eye movements and integration of visual information, but it does not directly generate or control the brainstem reflexes associated with ocular bobbing [1]. - Lesions in the cortex would typically manifest as **gaze preference**, apraxia, or other higher-level visual processing deficits, not involuntary brainstem driven eye movements like bobbing.
Question 124: 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 125: Extraintestinal manifestations of Inflammatory bowel disease include all of the following, Except:
- A. Sclerosing cholangitis
- B. Skin nodules
- C. Osteoarthritis (Correct Answer)
- D. Uveitis
Explanation: ***Osteoarthritis*** - **Osteoarthritis** is a **degenerative joint disease** caused by wear and tear on cartilage, and it is **not** an extraintestinal manifestation of IBD [3]. - While patients with IBD can develop osteoarthritis, it does not share the same **pathophysiological link** to the inflammatory process of IBD as other extraintestinal manifestations. *Uveitis* - **Uveitis** is an inflammation of the **uvea** (middle layer of the eye) and is a well-recognized ocular extraintestinal manifestation of IBD [2]. - It can cause eye pain, redness, and blurred vision, and its severity may correlate with IBD disease activity. *Sclerosing cholangitis* - **Primary sclerosing cholangitis (PSC)** is a chronic cholestatic liver disease characterized by inflammation and fibrosis of the **bile ducts**, and it is strongly associated with **ulcerative colitis** [1]. - It often progresses to **cirrhosis** and liver failure and is a significant extraintestinal manifestation. *Skin nodules* - **Erythema nodosum** and **pyoderma gangrenosum** are common cutaneous extraintestinal manifestations of IBD, often presenting as **painful red nodules** or ulcers on the skin [2]. - These skin conditions are thought to be immune-mediated and often parallel the activity of the underlying inflammatory bowel disease.
Question 126: Which of the following is NOT an indication for a liver biopsy?
- A. Amoebic hepatitis (Correct Answer)
- B. Chronic hepatitis B and C
- C. Autoimmune hepatitis
- D. Wilson's disease
Explanation: ***Amoebic hepatitis*** - Liver biopsy is **not routinely indicated** for amoebic hepatitis as diagnosis is typically made through clinical history and serological tests. - The condition is usually managed with **medications** rather than requiring invasive procedures like a biopsy. *Wilson's disease* - Liver biopsy is important for assessing **copper accumulation** in Wilson's disease, establishing a diagnosis. - It may also provide information regarding the extent of **hepatocellular damage**. *Chronic hepatitis B and C* - In chronic hepatitis B and C, liver biopsy is crucial to evaluate the **degree of fibrosis** and hepatic inflammation. - It assists in determining the need for **antiviral therapy** and prognostication. *Autoimmune hepatitis* - Liver biopsy helps confirm the diagnosis of autoimmune hepatitis and assess the **severity of liver damage**. [1] - It also aids in monitoring the response to **immunosuppressive therapy**. [1] **Note on technique:** Percutaneous liver biopsy requires specific conditions for safety, such as cooperative patients and adequate coagulation profiles. [2]
Question 127: Which of the following is a common finding in patients with Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH)?
- A. Ascites
- B. Normal BP (Correct Answer)
- C. Generalized edema
- D. Dry mucous membrane
Explanation: ***Normal BP*** - In SIADH, patients are typically **euvolemic** due to the primary issue being water retention rather than salt retention or frank dehydration [2]. - While hyponatremia occurs, the body's compensatory mechanisms usually prevent significant changes in blood pressure, maintaining it within the **normal range**. *Generalized edema* - Generalized edema is uncommon in SIADH because the excessive water retention is initially within the **intravascular compartment**, and the body attempts to excrete the additional volume of water [1]. - Although the patient is effectively retaining water, the osmolality is low, leading to fluid shifts rather than overt edema unless severe, protracted fluid overload occurs. *Ascites* - **Ascites**, which is the accumulation of fluid in the peritoneal cavity, is not a characteristic feature of SIADH [2]. - Ascites is more commonly associated with conditions like **liver cirrhosis**, heart failure, or malignancy. *Dry mucous membrane* - **Dry mucous membranes** are a sign of dehydration and fluid volume deficit. - In contrast, SIADH involves **fluid overload** (though euvolemic), making dry mucous membranes an unlikely finding [2].
Question 128: Which of the following conditions is associated with megaloblastic anemia?
- A. Pernicious anemia (Correct Answer)
- B. Iron deficiency anemia
- C. Intestinal lymphatic ectasia
- D. Chronic kidney disease
Explanation: a and b - Megaloblastic anemia is commonly associated with **vitamin B12** [1] and **folate deficiencies** [2], which can occur due to various causes. - Conditions leading to malabsorption (such as those related to the gastrointestinal tract) contribute significantly to megaloblastic anemia [1, 2]. *ileal resection* - Ileal resection can indeed lead to **malabsorption** of vitamin B12 [1], particularly if the distal ileum is removed. - However, it is important to note that megaloblastic anemia specifically reflects a broader range of potential deficiencies, thus it is not an exclusive answer. *Crohn's disease* - Crohn's disease can cause **malabsorption** and result in vitamin B12 deficiency but is not a direct cause of megaloblastic anemia on its own. - The anemia may occur due to complications like **ileo-pouch anastomosis** rather than the disease itself. *Intestinal lymphatic ectasia* - This condition leads to **protein-losing enteropathy**, potentially causing deficiencies but not specifically leading to megaloblastic anemia. - The anemia associated with this condition is typically due to **hypoalbuminemia** and not a result of any vitamin deficiency directly.
Question 129: In inflammatory myopathy, which group of muscles is not affected
- A. Facial
- B. Proximal muscles of limb
- C. Ocular (Correct Answer)
- D. Distal muscles of limb
Explanation: ***Ocular*** - The **extraocular muscles** responsible for eye movement are generally spared in typical inflammatory myopathies, distinguishing them from other neuromuscular disorders. - Inflammatory myopathies primarily affect **skeletal muscles**, but **ocular muscles** have unique immunological and physiological properties that often protect them. *Facial* - While less commonly affected early in the disease, some inflammatory myopathies, particularly **dermatomyositis**, can eventually involve **facial muscles**, leading to weakness. - Involvement of **facial muscles** can manifest as difficulty with smiling, whistling, or closing the eyelids. *Proximal muscles of limb* - Inflammatory myopathies characteristically cause **proximal muscle weakness**, affecting muscles of the **shoulders, hips, and thighs** [1]. - This weakness often presents as difficulty climbing stairs, getting up from a chair, or lifting objects overhead [1]. *Distal muscles of limb* - While less common than proximal involvement, **distal muscle weakness** (affecting hands and feet) can occur in some subsets of inflammatory myopathies, such as **inclusion body myositis**. - This can lead to difficulties with fine motor tasks or foot drop.
Question 130: Which of the following is a feature of tumor lysis syndrome?
- A. Metabolic alkalosis (a rise in blood pH)
- B. Hypokalemia (a decrease in blood potassium levels)
- C. Hypocalcemia (a decrease in blood calcium levels) (Correct Answer)
- D. Hypophosphatemia (a decrease in blood phosphate levels)
Explanation: ***Hypocalcemia (a decrease in blood calcium levels)*** - **Hypocalcemia** in tumor lysis syndrome results from the precipitation of calcium with excessive phosphate released from lysed tumor cells. - The elevated phosphate levels bind to calcium, forming **calcium phosphate crystals** that can deposit in tissues, further lowering serum calcium. *Metabolic alkalosis (a rise in blood pH)* - Tumor lysis syndrome typically leads to **metabolic acidosis**, not alkalosis, due to the release of acidic intracellular metabolites like uric acid and phosphate. - The accumulation of these acidic compounds overwhelms the body's buffering systems, decreasing blood pH. *Hypokalemia (a decrease in blood potassium levels)* - Tumor lysis syndrome is characterized by **hyperkalemia**, an increase in blood potassium, as potassium is a major intracellular cation released during cell lysis. - The rapid breakdown of numerous tumor cells dumps vast amounts of intracellular potassium into the bloodstream. *Hypophosphatemia (a decrease in blood phosphate levels)* - Tumor lysis syndrome causes **hyperphosphatemia**, an elevation in blood phosphate levels, because phosphate is abundantly present within tumor cells and is released upon their destruction. - This excessive release of intracellular phosphate is a hallmark biochemical feature of the syndrome.