NEET-PG 2013 - Internal Medicine Practice Questions

Q: A 68-year-old patient presents with sudden onset of right-sided weakness and slurred speech. The symptoms completely resolve within 30 minutes with no residual neurological deficits. This clinical presentation is most consistent with:

Transient Ischemic Attack (TIA). ***Transient Ischemic Attack (TIA)*** - A TIA is characterized by **transient neurological dysfunction caused by focal brain, spinal cord, or retinal ischemia**, without acute infarction [1]. - The key diagnostic feature here is the **complete resolution of symptoms within a short period** (30 minutes) with no residual deficits, fitting the definition of TIA [1]. *Subarachnoid hemorrhage* - This typically presents with a **sudden, severe headache** (often described as "thunderclap"), stiff neck, and altered mental status. - While it can cause sudden neurological deficits, these symptoms usually **do not resolve completely within minutes**, and often lead to persistent deficits or life-threatening complications. *Intracerebral hemorrhage* - An intracerebral hemorrhage involves **bleeding directly into the brain tissue**, leading to sudden onset of neurological deficits that **progress over time** [2]. - The symptoms are generally **severe and persistent**, and would not resolve completely within 30 minutes. *Ischemic stroke* - An ischemic stroke is caused by a **blockage of blood flow to the brain**, resulting in brain tissue damage (infarction) and persistent neurological deficits [2]. - While initial symptoms can be similar to a TIA [3], an ischemic stroke by definition involves **permanent damage and lasting deficits**, unlike what is described in the patient's presentation.

Q: Pea soup diarrhea is seen in -

Typhoid. ***Typhoid*** - **Pea soup diarrhea** is a classic symptom of **typhoid fever**, caused by *Salmonella Typhi* [1]. - This characteristic stool is a greenish-yellow watery diarrhea due to inflammation and ulceration of the Peyer's patches in the small intestine [1]. *Cholera* - Characterized by **rice-water stools**, which are profuse, watery, and often contain flecks of mucus, resembling water in which rice has been rinsed [2]. - This type of diarrhea is due to the potent **cholera toxin** causing massive fluid and electrolyte secretion [2]. *Yersinosis* - Causes diarrhea that can range from watery to bloody, often associated with severe **abdominal pain** mimicking appendicitis. - While it can cause enterocolitis, the stool consistency is not typically described as "pea soup" like in typhoid. *Hepatitis* - Hepatitis primarily affects the **liver** and typically does **not cause diarrhea** as a prominent symptom. - Common symptoms include jaundice, dark urine, and pale stools due to impaired bilirubin metabolism.

Q: Which of the following is not a treatment option for hypercalcemia?

Strontium. ***Strontium*** - **Strontium ranelate** is primarily used in the treatment of **osteoporosis** to promote bone formation and inhibit bone resorption. - It does not have a recognized role in the acute or long-term management of **hypercalcemia** and could potentially worsen it due to its bone-targeting effects if not carefully managed. *Steroids* - **Glucocorticoids** are effective in treating hypercalcemia associated with **granulomatous diseases** (e.g., sarcoidosis) and certain malignancies (e.g., multiple myeloma) by reducing calcitriol production or tumor burden. - They decrease intestinal calcium absorption and increase renal calcium excretion in conditions where 1,25-dihydroxyvitamin D is elevated. *Bisphosphonates* - **Bisphosphonates** (e.g., zoledronic acid, pamidronate) are potent inhibitors of **osteoclast-mediated bone resorption** and are a cornerstone in the treatment of moderate to severe hypercalcemia, especially due to malignancy. [1] - They are administered intravenously and act by inducing osteoclast apoptosis, thereby reducing the release of calcium from bone. [1] *Phosphate* - **Intravenous phosphate** can be used in severe, resistant hypercalcemia, as it promotes calcium deposition into bone and soft tissues, and forms insoluble calcium-phosphate complexes, thus lowering serum calcium. - Its use is limited due to risks of **ectopic calcification**, renal failure, and hypotension, and it is usually reserved for life-threatening situations where other treatments have failed.

Q: Which of the following is commonly seen in Polycythemia Vera?

Thrombosis. ***Spontaneous severe infection*** - In Polycythemia Vera, there is usually an **increased red blood cell mass** leading to complications like thrombosis, rather than a predisposition to severe infections. - Severe infections are not a typical feature, as the condition usually maintains **functional immunity** despite hyperviscosity. *Thrombosis* - Individuals with Polycythemia Vera have increased blood viscosity that results in a higher risk of **thrombosis**, which is a common complication [1]. - Events like **deep vein thrombosis (DVT)** or **cerebral venous sinus thrombosis** are often observed due to altered hemodynamics. *Hyperuricemia* - Hyperuricemia occurs due to increased cell turnover and breakdown of red cells in Polycythemia Vera, leading to elevated **uric acid levels** [1]. - Patients may experience **gout attacks** as a consequence of this elevated uric acid [1]. *Prone for acute leukemia* - While there is an increased risk of transformation to myeloid neoplasms, the risk for **acute leukemia** is not directly attributed to Polycythemia Vera in most cases. - It is more related to myelofibrosis or secondary conditions developing over time rather than a direct association.

Q: What is the expected Transtubular Potassium Gradient (TTKG) in a patient with hypokalemia due to extrarenal losses?

< 3-4. ***< 3-4*** - A **Transtubular Potassium Gradient (TTKG)** of less than 3-4 indicates appropriate renal potassium conservation in response to hypokalemia. - This suggests that the hypokalemia is likely due to **extrarenal losses**, such as gastrointestinal losses (diarrhea, vomiting) or inadequate dietary intake, as the kidneys are working to retain potassium. *3-4* - A TTKG value in this range is typically considered indeterminate but could still point towards appropriate renal conservation if other clinical signs of extrarenal losses are present. - However, it does not as strongly confirm appropriate renal conservation as a value clearly below 3. *> 4-5* - A TTKG greater than 4-5 suggests **inappropriate renal potassium excretion** for a patient with hypokalemia. - This would indicate that the kidneys are complicit in the potassium loss, pointing towards renal causes of hypokalemia, such as **mineralocorticoid excess** or **diuretic use**. *> 5-6* - A TTKG greater than 5-6 strongly indicates significant **renal potassium wasting**. - This would be seen in conditions where the kidneys are actively secreting potassium despite hypokalemia, thereby contributing to the low potassium levels rather than conserving it.

Q: What is the primary cause of Waterhouse-Friderichsen syndrome?

Adrenal hemorrhage after meningococcal infection. ***Adrenal hemorrhage after meningococcal infection*** - **Waterhouse-Friderichsen syndrome** is characterized by **massive, bilateral adrenal hemorrhage**, leading to acute adrenal insufficiency [1]. - It is most commonly associated with overwhelming **meningococcal sepsis**, particularly due to *Neisseria meningitidis* [1]. *Adrenal hemorrhage post malignancy* - While malignancies can cause adrenal hemorrhage, it is not the primary cause of **Waterhouse-Friderichsen syndrome**. - This syndrome is specifically linked to severe **bacterial sepsis**, not typically cancer-related adrenal bleeding [1]. *Congenital adrenal deficiency* - **Congenital adrenal hyperplasia (CAH)** involves genetic defects affecting cortisol synthesis, leading to chronic adrenal insufficiency. - It does not involve acute **adrenal hemorrhage** as seen in Waterhouse-Friderichsen syndrome. *Adrenal hemorrhage after corticosteroid withdrawal* - Abrupt withdrawal of corticosteroids can precipitate an **adrenal crisis** due to suppression of the hypothalamic-pituitary-adrenal (HPA) axis [2]. - However, it does not typically cause the characteristic **massive adrenal hemorrhage** seen in Waterhouse-Friderichsen syndrome [2].

Q: A 25 year old female presents with generalized restriction of eye movement in all direction, intermittent ptosis, proximal muscle weakness and fatigability.Which is the MOST useful test in making the diagnosis?

Edrophonium test. ***Edrophonium test*** - The **Edrophonium test** (Tensilon test) is highly useful for diagnosing **myasthenia gravis** due to its rapid onset and short duration of action. - In a patient with suspected myasthenia gravis, such as this one presenting with **generalized restriction of eye movement**, **intermittent ptosis**, and **fatigable proximal muscle weakness**, the administration of edrophonium will lead to a temporary but significant improvement in muscle strength. It works by inhibiting the breakdown of acetylcholine, thereby increasing its availability at the neuromuscular junction [1]. *CPK* - **Creatine phosphokinase (CPK)** levels are typically normal in myasthenia gravis, as it is a disorder of the **neuromuscular junction**, not a primary muscle disease. - Elevated CPK levels usually indicate muscle damage, seen in conditions like **myositis** or **muscular dystrophies**, which are not suggested by the patient's symptoms. *EMG* - **Electromyography (EMG)**, specifically **repetitive nerve stimulation (RNS)** or **single-fiber EMG (SFEMG)**, can show characteristic decremental responses or increased jitter/blocking in myasthenia gravis [2], but it is less direct and often more invasive than the Edrophonium test for initial diagnostic confirmation. - While supportive, it is generally considered a secondary diagnostic tool after a strong clinical suspicion and is not the *most useful* initial test compared to the rapid symptomatic improvement seen with edrophonium. *Muscle biopsy* - A **muscle biopsy** is generally not useful in diagnosing myasthenia gravis as the muscle tissue itself is structurally normal. - This diagnostic tool is reserved for primary **muscle disorders** like muscular dystrophies or inflammatory myopathies, which would show characteristic histological changes.

Q: Subclavian steal syndrome is

Reversal of blood flow in the ipsilateral vertebral artery. ***Reversal of blood flow in the ipsilateral vertebral artery*** - Subclavian steal syndrome occurs due to a **proximal stenosis** or **occlusion of the subclavian artery**. - This causes blood to be "stolen" from the **ipsilateral vertebral artery**, flowing retrograde to supply the arm and thereby reducing blood flow to the brainstem. *Reversal of blood flow in the contralateral carotid artery* - The carotid arteries supply blood to the brain directly and are typically not directly involved in thesteal phenomenon in this specific syndrome. - Reversal of flow in the carotid artery would indicate a much more severe and different pathology, not characteristic of subclavian steal. *Reversal of blood flow in the contralateral vertebral artery* - The steal phenomenon specifically involves the vertebral artery on the **same side (ipsilateral)** as the subclavian artery obstruction. - The contralateral vertebral artery would typically continue to supply blood to the brain without a reversed flow in this syndrome. *B/L reversal of blood flow in vertebral arteries* - Subclavian steal syndrome is generally a **unilateral phenomenon**, affecting the vertebral artery ipsilateral to the subclavian artery stenosis. - Bilateral reversal would imply bilateral subclavian artery obstruction or other severe cerebrovascular disease, which is not the definition of subclavian steal syndrome itself.

Q: Isolated painful third nerve palsy is a feature of aneurysms of:

Aneurysm of the posterior communicating artery. ***Aneurysm of the posterior communicating artery*** - An aneurysm of the **posterior communicating artery (PCOM)** can compress the ipsilateral **oculomotor nerve (CN III)** as it exits the brainstem. - This compression typically affects the **superficial parasympathetic fibers** first, leading to a **dilated pupil** (mydriasis) along with ophthalmoplegia and ptosis, making the third nerve palsy "painful" and "isolated" without other focal neurological deficits. *Aneurysm of the anterior communicating artery* - Aneurysms of the **anterior communicating artery (ACoM)** are more commonly associated with **subarachnoid hemorrhage** and can cause **visual field defects** or **frontal lobe dysfunction**, but generally not isolated CN III palsy. - While rupture can lead to various neurological deficits, isolated painful third nerve palsy due to ACoM aneurysm is atypical. *Aneurysm of the vertebrobasillary artery* - Aneurysms in the **vertebrobasillar system** typically present with symptoms related to **brainstem compression** or ischemia, such as cranial nerve palsies beyond the third nerve, ataxia, or motor/sensory deficits. - Isolated third nerve palsy is an uncommon presentation for vertebrobasilar aneurysms compared to PCOM aneurysms. *Aneurysm of the ophthalmic artery* - **Ophthalmic artery aneurysms** are usually **intraorbital** and can cause **visual loss** due to direct compression of the **optic nerve (CN II)** or orbital structures. - They are less likely to cause isolated painful third nerve palsy, as the third nerve's course is generally not directly compromised by ophthalmic artery aneurysms.

Q: In Wilson's disease, copper deposition primarily occurs in which part of the brain?

Basal ganglia. ***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 1

A 68-year-old patient presents with sudden onset of right-sided weakness and slurred speech. The symptoms completely resolve within 30 minutes with no residual neurological deficits. This clinical presentation is most consistent with:

Accepted Answer

Transient Ischemic Attack (TIA)

Answer

Subarachnoid hemorrhage

Answer

Intracerebral hemorrhage

Answer

Ischemic stroke

Question 2

Pea soup diarrhea is seen in -

Accepted Answer

Typhoid

Answer

Cholera

Answer

Yersinosis

Answer

Hepatitis

Question 3

Which of the following is not a treatment option for hypercalcemia?

Accepted Answer

Strontium

Answer

Bisphosphonates

Answer

Steroids

Answer

Phosphate

Question 4

Which of the following is commonly seen in Polycythemia Vera?

Accepted Answer

Thrombosis

Answer

Hyperuricemia

Answer

Prone for acute leukemia

Answer

Spontaneous severe infection

Question 5

What is the expected Transtubular Potassium Gradient (TTKG) in a patient with hypokalemia due to extrarenal losses?

Accepted Answer

< 3-4

Answer

3-4

Answer

> 4-5

Answer

> 5-6

Question 6

What is the primary cause of Waterhouse-Friderichsen syndrome?

Accepted Answer

Adrenal hemorrhage after meningococcal infection

Answer

Adrenal hemorrhage post malignancy

Answer

Adrenal hemorrhage after corticosteroid withdrawal

Answer

Congenital adrenal deficiency

Question 7

A 25 year old female presents with generalized restriction of eye movement in all direction, intermittent ptosis, proximal muscle weakness and fatigability.Which is the MOST useful test in making the diagnosis?

Accepted Answer

Edrophonium test

Answer

CPK

Answer

EMG

Answer

Muscle biopsy

Question 8

Subclavian steal syndrome is

Accepted Answer

Reversal of blood flow in the ipsilateral vertebral artery

Answer

Reversal of blood flow in the contralateral carotid artery

Answer

Reversal of blood flow in the contralateral vertebral artery

Answer

B/L reversal of blood flow in vertebral arteries

Question 9

Isolated painful third nerve palsy is a feature of aneurysms of:

Accepted Answer

Aneurysm of the posterior communicating artery

Answer

Aneurysm of the anterior communicating artery

Answer

Aneurysm of the vertebrobasillary artery

Answer

Aneurysm of the ophthalmic artery

Question 10

In Wilson's disease, copper deposition primarily occurs in which part of the brain?

Accepted Answer

Basal ganglia

Answer

Cerebellum

Answer

Pons

Answer

Medulla

NEET-PG 2013 — Internal Medicine