NEET-PG 2012 - Internal Medicine Practice Questions

Q: Which of the following is a characteristic feature of primary Sjogren's syndrome?

Enlargement of salivary glands. ***Enlargement of salivary glands*** - **Sjögren's syndrome** is characterized by chronic inflammation of **exocrine glands**, leading to swelling and dysfunction, most notably in the **parotid** and **submandibular glands**. - This glandular enlargement often presents as recurrent or persistent **bilateral swelling** of the major salivary glands. *Can occur in children* - While possible, Sjögren's syndrome is predominantly a disease of **adults**, with incidence peaking in individuals between **40 and 60 years old**. - **Juvenile Sjögren's syndrome** is rare and typically presents with more variable symptoms, making it less of a characteristic feature of the primary disease in the general population. *Increased complement C4 is associated with thymoma* - **Increased complement C4** levels are generally not associated with Sjögren's syndrome; instead, **hypocomplementemia** (low C4) can be seen in some patients, indicating immune complex activity. - **Thymoma** is primarily linked to **myasthenia gravis** and other paraneoplastic syndromes, not a direct or characteristic association with Sjögren's syndrome or C4 levels in this context. *Can be associated with rheumatoid arthritis* - Sjögren's syndrome can be classified as **primary** (occurring alone) or **secondary** (occurring in conjunction with another autoimmune disease). - Its association with **rheumatoid arthritis** defines **secondary Sjögren's syndrome**, meaning it's not a characteristic feature of the *primary* form of the disease itself.

Q: What is the first symptom of leprosy?

Decreased pain. Decreased pain - Leprosy primarily targets Schwann cells in peripheral nerves, leading to sensory loss [1]. - The sensation of pain is typically affected earliest, often presenting as areas of numbness [1]. Decreased vibration & position sense - These sensations are typically carried by larger myelinated fibers, which tend to be affected later in the disease progression of leprosy. - While eventually involved, they are not usually the first symptom of sensory loss. Decreased temperature - Temperature sensation is also an early modality affected in leprosy, as it's carried by small, unmyelinated or thinly myelinated fibers [1]. - However, pain is often cited as the very first sensory loss, even preceding temperature changes in some cases. Decreased light touch - Light touch sensation is generally an early loss, similar to pain and temperature, due to damage to nerve fibers in the skin. - But, when distinguishing the absolute first symptom, pain perception often shows impairment even before light touch in affected areas.

Q: Migraine is due to

Cortical spreading depression. ***Cortical spreading depression*** - The current understanding is that **cortical spreading depression (CSD)** is the initiating event in migraine with aura, characterized by a wave of neuronal and glial depolarization that spreads across the cerebral cortex, leading to a temporary shutdown of neuronal activity [1]. - CSD is thought to activate the **trigeminal nerve**, subsequently causing the release of inflammatory neuropeptides and contributing to the pain phase [1]. *Dilatation of cranial blood vessels* - While **vasodilation of intracranial and extracranial blood vessels** does occur during the headache phase of migraine, it is now considered a *consequence* of the initial neurological events rather than the primary cause [1]. - This vasodilation contributes to the throbbing sensation of migraine pain but does not explain the aura or the initiation of the attack. *Constriction of cranial blood vessels* - **Vasoconstriction** was previously thought to be the cause of the migraine aura, but this theory has largely been disproven. - While some temporary constriction may precede CSD, it is not the primary mechanism behind the migraine attack. *Inflammation of the meninges* - While **neurogenic inflammation** of the meninges, involving the release of inflammatory mediators like **calcitonin gene-related peptide (CGRP)**, does play a role in sensitizing the trigeminal system and contributing to migraine pain, it is a downstream effect. - It is not the initial trigger for a migraine attack but rather part of the pain pathway activated by events like CSD.

Q: In which condition is paradoxical splitting of the second heart sound observed?

Left Bundle Branch Block (LBBB). ***Left Bundle Branch Block (LBBB)*** - In LBBB, the **left ventricle** depolarizes and contracts *after* the right ventricle, causing the **aortic valve (A2)** to close *after* the **pulmonic valve (P2)** [1]. - During inspiration, right ventricular ejection time is prolonged, which further delays P2. However, in LBBB, A2 is already delayed, and the inspiratory delay of P2 can bring P2 closer to A2, or even cause them to merge, making the splitting *less wide* or *disappear* on inspiration, which is paradoxical. *Right Bundle Branch Block (RBBB)* - RBBB causes a **delay in right ventricular depolarization**, leading to a **delayed P2** (pulmonic valve closure). - This typically results in **wide and fixed splitting of S2**, where the splitting persists during expiration and widens further with inspiration, which is not paradoxical. *Ventricular Septal Defect (VSD)* - A VSD can cause a **loud holosystolic murmur** and may lead to increased pulmonary blood flow. - While it can affect the timing of heart sounds, it does not typically cause paradoxical splitting of S2. *Atrial Septal Defect (ASD)* - An ASD causes a **left-to-right shunt**, leading to chronic volume overload of the right ventricle and increased pulmonary blood flow. - This often results in a **widely fixed splitting of S2**, where the split between A2 and P2 is constant regardless of respiration, which is different from paradoxical splitting.

Q: Which of the following electrolyte imbalances is least likely to be observed in Chronic Renal Failure (CRF)?

Hypercalcemia. ***Hypercalcemia*** - In **chronic renal failure (CRF)**, the kidneys' inability to activate vitamin D leads to impaired calcium absorption and **hypocalcemia** [1], [2]. - Additionally, the kidneys fail to excrete phosphate, leading to **hyperphosphatemia**, which further exacerbates hypocalcemia by forming calcium-phosphate precipitates [1]. *Hyperkalemia* - **Hyperkalemia** is a common and serious complication of CRF due to the kidneys' impaired ability to excrete **potassium**. - This is exacerbated by conditions like **metabolic acidosis** and certain medications. *Hyperphosphatemia* - In CRF, the kidneys are unable to adequately excrete **phosphate**, leading to an accumulation of **phosphate** in the blood [1]. - This condition directly contributes to **secondary hyperparathyroidism** and bone disease [1], [2]. *Hypocalcemia* - **Hypocalcemia** is very common in CRF, primarily due to decreased production of **calcitriol (active vitamin D)** by the failing kidneys [2]. - Reduced calcitriol leads to lower intestinal **calcium absorption** and impaired bone mineralization [1].

Q: What is the best treatment for anemia in patients with Chronic Renal Failure (CRF)?

Erythropoietin Stimulating Agents. ***Erythropoietin Stimulating Agents*** - **Erythropoietin Stimulating Agents (ESAs)** are the cornerstone of anemia treatment in CRF because the primary cause of anemia in these patients is inadequate production of **endogenous erythropoietin** by the damaged kidneys [1]. - ESAs stimulate the bone marrow to produce red blood cells, effectively reversing the anemia and improving symptoms like fatigue and exercise intolerance [1]. *Oral Iron Therapy* - While **iron deficiency** often coexists with **anemia of chronic disease** in CRF patients, oral iron alone is usually insufficient to correct the anemia; it only addresses the iron component. - Many CRF patients have **functional iron deficiency** due to chronic inflammation, which impairs iron utilization, making oral iron less effective even with adequate stores. *Blood transfusion* - **Blood transfusions** provide a rapid increase in hemoglobin but are not the preferred long-term treatment for anemia in CRF due to risks of **iron overload**, **alloreactions**, and potential sensitization, which can complicate future transplantation. - Transfusions are typically reserved for acute, severe anemia or specific circumstances where ESAs are ineffective or contraindicated. *Androgenic Steroids* - **Androgenic steroids** can stimulate erythropoiesis, but their use is limited due to significant side effects such as **hepatotoxicity**, **virilization**, and **cardiac complications**, making them a less favorable option compared to ESAs. - They are considered a secondary or tertiary option, often in patients unresponsive to primary treatments or when other options are exhausted.

Q: An adult hypertensive male presented with sudden onset severe headache and vomiting. On examination, there is marked neck rigidity and no focal neurological deficit was found. The symptoms are most likely due to:

Subarachnoid hemorrhage. ***Subarachnoid hemorrhage*** - The sudden onset of a **"thunderclap" headache**, vomiting, and **neck rigidity** in a hypertensive patient are classic signs of subarachnoid hemorrhage [1]. - The absence of focal neurological deficits is common, as the bleeding is often in the subarachnoid space rather than directly in brain tissue. *Intracerebral hemorrhage* - While it can cause sudden headache and vomiting, an **intracerebral hemorrhage** would typically present with **focal neurological deficits** corresponding to the affected brain region. - Neck rigidity is less common unless there's significant mass effect or ventricular involvement. *Cerebral ischemia* - **Cerebral ischemia** (e.g., ischemic stroke) usually manifests with **focal neurological deficits** (e.g., weakness, aphasia), often without a severe headache or neck rigidity [2]. - Headache, if present, is usually less severe and not described as "thunderclap." *Bacterial meningitis* - **Bacterial meningitis** presents with headache, fever, and neck rigidity [1], but the onset is typically **gradual** over hours to days, not sudden. - While vomiting can occur, the acute, thunderclap nature linked to hypertension points away from infection as the primary cause.

Q: What is the most characteristic cerebrospinal fluid (CSF) finding in viral meningitis?

Lymphocytic pleocytosis in CSF. ***Lymphocytic pleocytosis in CSF*** - **Lymphocytic pleocytosis**, meaning an increase in lymphocytes in the CSF, is the hallmark of **viral meningitis**, reflecting the immune response to the viral pathogen. [1] - While other CSF parameters can be altered, the presence of predominantly lymphocytes is the most reliable distinguishing feature from bacterial meningitis. [1] *WBC count typically less than 1000/mL* - This statement is generally true for viral meningitis, as the **WBC count** is usually lower than in bacterial meningitis. - However, it is not the *most characteristic* finding because bacterial meningitis can sometimes present with a WBC count under 1000/mL, especially early in the disease, and the *predominance* of lymphocytes is more specific to viral infection. *Glucose levels normal or slightly decreased* - **Normal glucose levels** are typical in viral meningitis, but they can be slightly decreased in a minority of cases. - This finding is not as characteristic as lymphocytic pleocytosis because significantly decreased glucose levels are more indicative of **bacterial or fungal meningitis**. *Protein levels normal or slightly increased* - **Protein levels** in viral meningitis are often normal or mildly elevated, usually not exceeding **100-150 mg/dL**. - While consistent with viral meningitis, this finding is less specific than lymphocytic pleocytosis, as protein levels can also be elevated in other conditions, including early bacterial meningitis.

Q: Which of the following statements is MOST accurate regarding herpes encephalitis?

The temporal lobe is commonly involved.. ***The temporal lobe is commonly involved.*** - **Herpes simplex encephalitis (HSE)** characteristically targets the **temporal lobes** [1] and **orbitofrontal cortex**, leading to specific neurological deficits. - This predilection for the temporal lobes often results in symptoms such as **aphasia**, **seizures**, and **memory disturbances** [1]. *Focal neurological symptoms are common.* - While focal neurological symptoms such as **aphasia**, **hemiparesis**, and **seizures** are indeed common in HSE [1], this statement is less specific than the involvement of the temporal lobe. - The **localization** of the infection to the temporal lobes explains why these focal symptoms are so prevalent [1]. *MRI is a key diagnostic tool.* - **MRI findings**, particularly **T2-weighted** and **FLAIR sequences**, showing **edema** and **hemorrhage** in the temporal lobes and insular cortex, are highly suggestive of HSE. - However, the most definitive diagnostic tool remains the detection of **HSV DNA** in the **cerebrospinal fluid (CSF)** via **PCR**. *EEG findings are nonspecific and not diagnostic.* - **EEG** in HSE often shows **periodic lateralizing epileptiform discharges (PLEDs)** or **focal slowing** primarily over the temporal lobes, which are highly suggestive, although not entirely diagnostic on their own. - These findings can help guide further investigation and support a clinical diagnosis in conjunction with other tests.

Q: Esophageal manometry is useful in diagnosing all of the following conditions EXCEPT:

Malignancy (not typically diagnosed with this test). ***Malignancy (not typically diagnosed with this test)*** - **Esophageal manometry** evaluates the **motor function** of the esophagus, measuring pressure changes during swallowing. - **Malignancy**, such as esophageal cancer, is primarily diagnosed with **endoscopy with biopsy** and imaging studies, not by assessing motility. *Achalasia (a motility disorder)* - **Esophageal manometry** is the **gold standard** for diagnosing achalasia, characterized by **absent peristalsis** in the esophageal body and **incomplete relaxation of the lower esophageal sphincter (LES)** [1]. - High-resolution manometry shows elevated **integrated relaxation pressure (IRP)** and often pan-esophageal pressurization. *Diffuse esophageal spasm (a motility disorder)* - This condition is also diagnosed by **esophageal manometry**, which reveals simultaneous, **non-peristaltic contractions** of high amplitude, often interspersed with normal peristalsis [1]. - It may also show **premature contractions** and **multiple rapid swallows** triggering spasm. *Assessment of esophageal motility prior to surgery for GERD* - **Manometry** is routinely performed before **anti-reflux surgery (e.g., Nissen fundoplication)** to rule out underlying esophageal motility disorders that could complicate surgery or worsen symptoms post-operatively [1]. - Identifying conditions like **achalasia** or **scleroderma** would contraindicate a standard fundoplication, as dysphagia could worsen [1].

Question 1

Which of the following is a characteristic feature of primary Sjogren's syndrome?

Accepted Answer

Enlargement of salivary glands

Answer

Can occur in children

Answer

Increased complement C4 is associated with thymoma

Answer

Can be associated with rheumatoid arthritis

Question 2

What is the first symptom of leprosy?

Accepted Answer

Decreased pain

Answer

Decreased vibration & position sense

Answer

Decreased temperature

Answer

Decreased light touch

Question 3

Migraine is due to

Accepted Answer

Cortical spreading depression

Answer

Dilatation of cranial blood vessels

Answer

Constriction of cranial blood vessels

Answer

Inflammation of the meninges

Question 4

In which condition is paradoxical splitting of the second heart sound observed?

Accepted Answer

Left Bundle Branch Block (LBBB)

Answer

Right Bundle Branch Block (RBBB)

Answer

Ventricular Septal Defect (VSD)

Answer

Atrial Septal Defect (ASD)

Question 5

Which of the following electrolyte imbalances is least likely to be observed in Chronic Renal Failure (CRF)?

Accepted Answer

Hypercalcemia

Answer

Hyperkalemia

Answer

Hyperphosphatemia

Answer

Hypocalcemia

Question 6

What is the best treatment for anemia in patients with Chronic Renal Failure (CRF)?

Accepted Answer

Erythropoietin Stimulating Agents

Answer

Oral Iron Therapy

Answer

Blood transfusion

Answer

Androgenic Steroids

Question 7

An adult hypertensive male presented with sudden onset severe headache and vomiting. On examination, there is marked neck rigidity and no focal neurological deficit was found. The symptoms are most likely due to:

Accepted Answer

Subarachnoid hemorrhage

Answer

Intracerebral hemorrhage

Answer

Cerebral ischemia

Answer

Bacterial meningitis

Question 8

What is the most characteristic cerebrospinal fluid (CSF) finding in viral meningitis?

Accepted Answer

Lymphocytic pleocytosis in CSF

Answer

WBC count typically less than 1000/mL

Answer

Glucose levels normal or slightly decreased

Answer

Protein levels normal or slightly increased

Question 9

Which of the following statements is MOST accurate regarding herpes encephalitis?

Accepted Answer

The temporal lobe is commonly involved.

Answer

Focal neurological symptoms are common.

Answer

EEG findings are nonspecific and not diagnostic.

Answer

MRI is a key diagnostic tool.

Question 10

Esophageal manometry is useful in diagnosing all of the following conditions EXCEPT:

Accepted Answer

Malignancy (not typically diagnosed with this test)

Answer

Achalasia (a motility disorder)

Answer

Diffuse esophageal spasm (a motility disorder)

Answer

Assessment of esophageal motility prior to surgery for GERD

NEET-PG 2012 — Internal Medicine