NEET-PG 2013 - Internal Medicine Practice Questions

Q: What is the most common cause of lobar consolidation?

Streptococcus. ***Streptococcus*** - **_Streptococcus pneumoniae_** is the **most common bacterial cause** of community-acquired pneumonia, frequently leading to lobar consolidation. [1] - It often presents with classic symptoms such as **sudden onset of fever**, productive cough with **rusty sputum**, and pleuritic chest pain. [1] *Mycoplasma* - **_Mycoplasma pneumoniae_** typically causes **"walking pneumonia"**, characterized by a more indolent course and often presents with **interstitial infiltrates** rather than dense lobar consolidation. - Though common, it is a less frequent cause of true lobar consolidation compared to _Streptococcus pneumoniae_. *Chlamydia* - **_Chlamydia pneumoniae_** causes atypical pneumonia, similar to _Mycoplasma_, presenting with less severe symptoms and **patchy infiltrates** or **interstitial patterns** rather than lobar consolidation. - It is a common cause of **atypical pneumonia** but not the leading cause of lobar consolidation. *Legionella* - **_Legionella pneumophila_** can cause severe pneumonia with consolidation, but it is **less common overall** than pneumococcal pneumonia. [1] - **Legionnaires' disease** is often associated with exposure to contaminated water sources and may present with **gastrointestinal and neurological symptoms** in addition to respiratory manifestations.

Q: In head injury, unilateral dilatation of the pupil is seen due to?

Oculomotor nerve compression. 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].

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: Impotence is a feature of which of the following:

Multiple sclerosis. ***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.

Q: In inflammatory myopathy, which group of muscles is not affected

Ocular. ***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.

Q: What is the best immediate management strategy for a patient experiencing respiratory alkalosis due to anxiety-induced hyperventilation?

Rebreathing in paper bag. ***Rebreathing in paper bag*** - This helps to **increase the inspired CO2 concentration**, thereby correcting the hypocapnia (low CO2) caused by hyperventilation. - It's a simple, non-invasive method to raise arterial PCO2 and normalize blood pH in acute respiratory alkalosis. *IPPV* - **Intermittent positive pressure ventilation (IPPV)** would further reduce CO2 by assisting ventilation and is typically used for respiratory *acidosis* or failure [1]. - This intervention would worsen the patient's respiratory alkalosis rather than alleviating it. *Normal saline* - **Normal saline** administration is primarily used for volume expansion or to correct electrolyte imbalances; it does not directly address respiratory alkalosis. - It would not correct the underlying issue of excessive CO2 exhalation. *Acetazolamide* - **Acetazolamide** is a carbonic anhydrase inhibitor that reduces bicarbonate reabsorption and is used to treat metabolic alkalosis or as a diuretic. - It would not be an immediate or appropriate solution for acute respiratory alkalosis and might even worsen the acid-base balance if used improperly.

Q: This patient came to the casualty with palpitations. His ECG has been shown below. What is your diagnosis?

Supraventricular tachycardia. ***Supraventricular tachycardia*** - The ECG shows a **narrow QRS complex tachycardia** (QRS < 0.12 seconds) with a **regular rhythm** and a **rapid ventricular rate** of 150-250 bpm, which is characteristic of SVT. The P waves may be hidden within the QRS or T waves. - While specific findings for SVT types (e.g., AVNRT, AVRT) aren't detailed without more specific ECG leads or maneuvers, the overall morphology points to a supraventricular origin. *Ventricular tachycardia* - **Ventricular tachycardia** is characterized by a **wide QRS complex** (> 0.12 seconds) tachycardia, which is not seen in the provided ECG. - It often presents with **AV dissociation** (P waves dissociated from QRS complexes) and fusion beats, which are absent here. *A-V dissociation* - **AV dissociation** refers to the atria and ventricles beating independently, which can be seen in VT or complete heart block. - It is a specific ECG finding and not a primary diagnosis, especially in the context of a narrow complex tachycardia like the one shown. *Sinus tachycardia* - **Sinus tachycardia** also presents with a narrow QRS complex but is characterized by a **normal P wave morphology** preceding each QRS complex with a rate typically not exceeding 150 bpm in an adult. - The rate in the given ECG is significantly higher, and distinct P waves are likely not preceding every QRS complex, ruling out sinus tachycardia.

Q: What is the recommended rate of correction for sodium deficit in patients with chronic hyponatremia?

0.5 mmol/hour. ***0.5 mmol/hour*** [1] - This rate of correction is recommended to avoid **osmotic demyelination syndrome (ODS)**, also known as central pontine myelinolysis [1]. - The aim is to correct the sodium deficit gradually, with a maximum increase not exceeding **8-10 mmol/L in any 24-hour period** [1]. *1 mmol/hour* - This rate is generally considered too rapid for chronic hyponatremia and increases the risk of **osmotic demyelination syndrome**. - While acceptable in some acute severe cases, it is typically avoided in chronic settings where the brain has adapted to lower osmolality. *1.5 mmol/hour* - This rate would lead to an even faster correction of sodium, significantly elevating the risk of **osmotic demyelination syndrome**. - It would result in a correction of 36 mmol/L over 24 hours, far exceeding the recommended daily limit of 8-10 mmol/L. *2.0 mmol/hour* - Such a rapid correction rate is highly dangerous and almost guarantees the development of **osmotic demyelination syndrome**. - This aggressive correction would lead to severe brain injury due to rapid osmotic shifts.

Q: A 40-year-old male patient presents to the Emergency department with central chest pain for 2 hours. The ECG shows ST segment depression and cardiac troponins are elevated. The patient has a positive history of previous PCI 3 months back. He is administered Aspirin, Clopidogrel, Nitrates, and LMWH in the Emergency Department and shifted to the coronary care unit. What is the best recommended course of further action?

Early Revascularization with PCI. ***Early Revascularization with PCI*** - The patient presents with **NSTEMI** (ST depression, elevated troponins) and is already on antiplatelet and anticoagulant therapy. **Early revascularization** (ideally within 24 hours for high-risk NSTEMI) is indicated to restore blood flow and prevent further myocardial damage [1]. - Given the patient's history of prior **PCI** and the current NSTEMI presentation, this suggests possible **in-stent restenosis** or progression of coronary artery disease, making revascularization crucial. *Continue conservative management and monitoring of cardiac enzymes and ECG* - While initial conservative management with medications is appropriate, simply continuing monitoring without definitive intervention is insufficient for a **high-risk NSTEMI** patient. - The elevated troponins and ST depression indicate ongoing myocardial injury that requires active management beyond just observation [1]. *Continue conservative management and plan for outpatient follow-up* - This approach is entirely inappropriate for a patient presenting with an **acute coronary syndrome (NSTEMI)**. - Outpatient follow-up is for stable conditions, not for an ongoing cardiac event that requires urgent hospital-based intervention. *Immediate Revascularization with Coronary Angiography* - **Immediate revascularization** (within 90 minutes) is primarily indicated for **STEMI** (ST elevation myocardial infarction). - While coronary angiography will precede PCI, the term "immediate" in this context usually refers to the urgency seen in STEMI; NSTEMI typically warrants "early" rather than "immediate" intervention (within 12-24 hours for high-risk patients like this one) [1].

Q: Which of the following is not a feature of distal renal tubular acidosis

Hyperkalemia. ***Hyperkalemia*** - **Distal renal tubular acidosis (dRTA)** is characterized by impaired acid excretion, leading to metabolic acidosis. The impaired excretion of acid is often accompanied by impaired potassium secretion, resulting in **hypokalemia**, not hyperkalemia. - While hyperkalemia is a feature of **type 4 RTA**, which is characterized by hypoaldosteronism or renal tubular unresponsiveness to aldosterone, it is not a feature of **distal RTA (type 1)**. [1] *Normal anion gap* - **Distal RTA** is a form of **normal anion gap metabolic acidosis**, also known as **hyperchloremic metabolic acidosis**. [1] - The anion gap is calculated as [Na+] - ([Cl-] + [HCO3-]), and in dRTA, the bicarbonate loss is compensated by an increase in chloride, maintaining a normal anion gap. *Renal hypercalciuria* - **Distal RTA** is associated with **impaired acid excretion**, which leads to chronic metabolic acidosis. - This **acidosis** promotes the dissolution of bone, releasing calcium, and decreases tubular reabsorption of calcium, resulting in **hypercalciuria**. *Alkaline urine* - In **distal RTA**, the distal tubule is unable to acidify the urine due to a defect in hydrogen ion secretion. - This leads to a persistent **urine pH > 5.5** (typically alkaline or inappropriately normal) despite systemic acidosis, making it a key diagnostic feature. [1]

Question 1

What is the most common cause of lobar consolidation?

Accepted Answer

Streptococcus

Answer

Mycoplasma

Answer

Chlamydia

Answer

Legionella

Question 2

In head injury, unilateral dilatation of the pupil is seen due to?

Accepted Answer

Oculomotor nerve compression

Answer

Ophthalmic N. compression

Answer

Trigeminal N. compression

Answer

None of the options

Question 3

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 4

Impotence is a feature of which of the following:

Accepted Answer

Multiple sclerosis

Answer

Poliomyelitis

Answer

Amyotrophic lateral sclerosis

Answer

Meningitis

Question 5

In inflammatory myopathy, which group of muscles is not affected

Accepted Answer

Ocular

Answer

Facial

Answer

Proximal muscles of limb

Answer

Distal muscles of limb

Question 6

What is the best immediate management strategy for a patient experiencing respiratory alkalosis due to anxiety-induced hyperventilation?

Accepted Answer

Rebreathing in paper bag

Answer

IPPV

Answer

Normal saline

Answer

Acetazolamide

Question 7

This patient came to the casualty with palpitations. His ECG has been shown below. What is your diagnosis?

Accepted Answer

Supraventricular tachycardia

Answer

Ventricular tachycardia

Answer

A-V dissociation

Answer

Sinus tachycardia

Question 8

What is the recommended rate of correction for sodium deficit in patients with chronic hyponatremia?

Accepted Answer

0.5 mmol/hour

Answer

1 mmol/hour

Answer

1.5 mmol/hour

Answer

2.0 mmol/hour

Question 9

A 40-year-old male patient presents to the Emergency department with central chest pain for 2 hours. The ECG shows ST segment depression and cardiac troponins are elevated. The patient has a positive history of previous PCI 3 months back. He is administered Aspirin, Clopidogrel, Nitrates, and LMWH in the Emergency Department and shifted to the coronary care unit. What is the best recommended course of further action?

Accepted Answer

Early Revascularization with PCI

Answer

Continue conservative management and monitoring of cardiac enzymes and ECG

Answer

Continue conservative management and plan for outpatient follow-up

Answer

Immediate Revascularization with Coronary Angiography

Question 10

Which of the following is not a feature of distal renal tubular acidosis

Accepted Answer

Hyperkalemia

Answer

Renal hypercalciuria

Answer

Normal anion gap

Answer

Alkaline urine

NEET-PG 2013 — Internal Medicine