NEET-PG 2025 - Internal Medicine Practice Questions

Q: A patient is on salbutamol and ipratropium but continues to have nocturnal exacerbations of asthma. What is the next step?

Laba plus inhalation steroids. ***Laba plus inhalation steroids*** - In a patient with persistent symptoms (nocturnal exacerbations) despite using a SABA (**salbutamol**) and a SAMA (**ipratropium**), the next step is to initiate or step up therapy by adding a long-term controller medication, which is typically a combination of **Inhaled Corticosteroids (ICS)** and a **Long-Acting Beta-Agonist (LABA)** [1]. - This combination is crucial for controlling airway inflammation and providing prolonged bronchodilation, effectively managing nocturnal symptoms [1], [2]. *Oral corticosteroids* - **Oral corticosteroids** are reserved for acute, severe exacerbations, short courses for bridging, or in cases of very severe asthma refractory to high-dose inhaled therapy [3]. - They are not the standard next step for managing persistent nocturnal symptoms in a patient previously stable on SABA/SAMA. *Montelukast* - **Montelukast** (a leukotriene receptor antagonist) is generally considered a less potent controller than the ICS/LABA combination and is often used as an add-on therapy or for specific phenotypes like aspirin-exacerbated respiratory disease (AERD). - Its efficacy in independently controlling moderate-to-severe persistent asthma, characterized by nocturnal symptoms, is lower than that of ICS/LABA [2]. *Increase the dose of salbutamol* - **Salbutamol** is a **Short-Acting Beta-Agonist (SABA)**, used primarily as a reliever for acute symptoms, not as a long-term controller [2], [4]. - Increasing its dose or frequency significantly suggests reliance on relief medication, which indicates poorly controlled asthma and can increase the risk of adverse cardiac side effects like **tachycardia**.

Q: A 25-year-old sewage worker presents with fever for 1 week and weakness for 1 day. Laboratory evaluation reveals elevated bilirubin and decreased urine output. Conjunctival redness? What is the most likely diagnosis?

Weil's disease. ***Weil's disease*** - The clinical triad of fever, **jaundice (elevated bilirubin)**, and **acute kidney injury (decreased urine output)**, particularly in an individual with exposure to contaminated water (**sewage worker**), is the classical presentation of the severe form of leptospirosis, also known as Weil's disease [1]. - **Conjunctival suffusion/redness** without inflammation or discharge is a pathognomonic physical sign highly suggestive of Weil's disease, caused by the spirochete **Leptospira interrogans** [1], [2]. *Brucellosis* - Usually presents with an undulating fever, night sweats, and localized infection in the bones (**spondylitis**) or reticuloendothelial system; it is often linked to consumption of **unpasteurized dairy**. - While mild hepatic involvement can occur, it rarely causes the severe combination of **acute renal failure** and deep jaundice seen in this patient. *Enteric fever* - Characterized by a gradually rising fever, **relative bradycardia**, and often features a dry cough, abdominal discomfort, and sometimes **rose spots**. [2] - Severe organ damage like acute kidney injury and profound jaundice simultaneously is unusual in typhoid fever, and **conjunctival suffusion** is not a feature. *Acute Viral Hepatitis* - Presents with fever, malaise, and eventually **jaundice (elevated bilirubin)**; the primary pathology is hepatocyte necrosis. [2] - It typically does not cause simultaneous severe **acute renal failure** and the specific finding of **conjunctival suffusion**, which are hallmarks of Weil's disease.

Q: The pedigree diagram of a family is shown below. Affected individuals present with progressive external ophthalmoplegia, pigmentary retinopathy, and cardiac conduction defects. Based on the pedigree and clinical features, what is the most likely diagnosis?

Kearns-Sayre Syndrome. ***Kearns-Sayre Syndrome*** * Kearns-Sayre Syndrome (KSS) is a **mitochondrial disorder** caused by large-scale deletions in **mtDNA** (mtDNA deletion syndrome). * The classic triad of KSS is **progressive external ophthalmoplegia (PEO)**, **pigmentary retinopathy**, and onset before age 20, often associated with **cardiac conduction defects** and cerebellar ataxia, matching the clinical presentation. *Duchenne Muscular Dystrophy* * DMD is an **X-linked recessive** disorder, which would show mother-to-son transmission, but not father-to-son transmission. The pedigree shows affected males having affected children (both male and female), inconsistent with X-linked inheritance. * The primary features are **progressive proximal muscle weakness** and Gower's sign, not the characteristic ophthalmoplegia, retinopathy, and heart block of KSS. *Friedreich Ataxia* * Friedreich ataxia is an **autosomal recessive** disorder, which would typically skip generations and mainly present in siblings of unaffected parents. This is inconsistent with the clear mother-to-child transmission seen in the pedigree. * The key features are **ataxia**, **dysarthria**, and **loss of vibratory sense**, not primarily ophthalmoplegia and pigmentary retinopathy. *Myotonic Dystrophy* * Myotonic dystrophy (DM1) is an **autosomal dominant** disorder, consistent with the vertical transmission, but the genetic defect is an **unstable trinucleotide repeat (CTG)**. While it can involve **cardiac conduction defects**, the primary clinical feature is **myotonia** (inability to quickly relax muscles) and facial weakness. * The absence of myotonia and the distinct presentation of PEO and pigmentary retinopathy make KSS a better fit than myotonic dystrophy.

Q: Patient came with severe headache and seizures. Sodium on admission was 98 meq/L. We have started correction with 3 % saline and now after 24 hours of infusion sodium is 110 meq/L. Patient develops mutism and altered sensorium. Which investigation will you perform now?

MRI Head. ***MRI Head*** - A rapid correction of **severe chronic hyponatremia** (from 98 to 110 mEq/L in 24 hours, exceeding the recommended limit of 8-10 mEq/L) puts the patient at very high risk for **Osmotic Demyelination Syndrome (ODS)** (previously Central Pontine Myelinolysis). [1] - The new onset of **mutism** and **altered sensorium** are classic, late symptoms of ODS, necessitating an **MRI head** to visualize characteristic **pontine** (and sometimes extrapontine) lesions. *LP for CSF biochemistry* - LP is primarily indicated for diagnosing infections or inflammatory conditions of the CNS, which is less likely given the clear history of electrolyte imbalance and complication following rapid correction. - While CSF analysis can reveal demyelination products, an **MRI** is the definitive, non-invasive imaging modality for diagnosing ODS. *Brainstem evoked potentials* - Brainstem auditory evoked potentials (BAEP) primarily assess the **integrity of the auditory pathways** through the brainstem. [2] - While ODS affects the brainstem, BAEP is not the standard or most sensitive first-line investigation for confirming demyelinating lesions in the pons. *EEG* - EEG measures the electrical activity of the cerebral cortex and is primarily useful for localizing seizure foci or assessing the severity of encephalopathy. [2] - The symptoms (mutism, altered sensorium) point strongly to a structural brainstem lesion (ODS), which is best confirmed by **MRI head**, not EEG.

Q: A 68-year-old male with a history of COPD presents to the emergency room with severe dyspnea and altered mental status. An arterial blood gas (ABG) is drawn with the following results: pH: 7.28 PaCO2: 60 mmHg HCO3-: 28 mEq/L Na+: 142 mEq/L Cl-: 100 mEq/L Based on these results, what is the calculated anion gap?

B. 14 mEq/L. ***14 mEq/L*** - The **anion gap (AG)** is calculated using the formula: $\text{AG} = [\text{Na}^+] - ([\text{Cl}^-] + [\text{HCO}_3^-])$. [1] - Plugging in the patient's values: $142 - (100 + 28) = 142 - 128 = **14 \text{ mEq/L}**$. *10 mEq/L* - This value is below the calculated 14 mEq/L and would be considered low if the normal range upper limit is 12, suggesting a calculation error. [1] - An anion gap of 10 mEq/L is typically a normal value, but it is not the mathematically correct result based on the patient's **serum electrolyte** values. *18 mEq/L* - Obtaining this value would imply that $[\text{Cl}^-] + [\text{HCO}_3^-]$ equaled 124 mEq/L ($142 - 18$), which is incorrect as the sum is **128 mEq/L**. - An anion gap of 18 mEq/L indicates a **High Anion Gap Metabolic Acidosis (HAGMA)**, which is metabolically possible but mathematically inconsistent with the provided electrolyte numbers. [1] *24 mEq/L* - This value is significantly higher than 14 mEq/L and would suggest a severe uncompensated **HAGMA** (e.g., severe ketoacidosis or lactic acidosis). [1] - The calculation based on the given **plasma concentrations** of sodium, chloride, and bicarbonate simply does not support this result.

Q: Based on the image provided, what is the most appropriate confirmatory investigation?

Manometry. ***Manometry*** - Esophageal manometry is the **gold standard** (confirmatory test) for achalasia, as it directly evaluates the motility and pressure patterns of the esophagus. - It definitively demonstrates the two key pathognomonic findings: **absent esophageal peristalsis** and **incomplete relaxation of the lower esophageal sphincter (LES)**. *pH monitoring* - This test is used primarily to diagnose **Gastroesophageal Reflux Disease (GERD)** by quantifying abnormal acid exposure in the distal esophagus. - It is not relevant for confirming achalasia, which is a **motor disorder** causing functional obstruction, not acid reflux. *Upper GI Endoscopy* - Endoscopy is crucial for **ruling out secondary achalasia** (pseudoachalasia), caused by underlying conditions like malignancy, which can structurally mimic the radiologic findings. - Although mandatory in evaluation, it does not confirm the **functional motor deficit** (aperistalsis and failed relaxation) required for definitive diagnosis of primary achalasia. *Barium swallow study* - The image provided is a Barium swallow study, which serves as the **initial screening tool** for achalasia by showing the classic **"bird-beak" appearance** of the distal esophagus. - While suggestive, this radiological study reports morphology and transit, but **manometry** is required to confirm the associated physiological defect (abnormal pressures and motility).

Q: A patient presents with palpitations and an irregularly irregular pulse. He presents within 2 hours of symptom onset, and has no history of diabetes or other comorbidities. What is the most appropriate initial management?

Cardioversion. ***Cardioversion*** - Since the patient presented within **<12 hours** of symptom onset (paroxysmal AF) and is hemodynamically stable, particularly without comorbidities, urgent rhythm control via **cardioversion (electrical or pharmacological)** is the optimal management to restore sinus rhythm [1]. - The very early presentation (within 2 hours) and the absence of significant comorbidities suggest a good chance for maintenance of sinus rhythm without immediate concern for complex thrombus formation. *TEE for starting anticoagulation* - **Transesophageal echocardiography (TEE)** is performed to rule out left atrial appendage thrombus before cardioversion if the duration of AF is **unknown or >48 hours**, or if anticoagulation has been inadequate (less than 3 weeks). - In this case, since the onset is clearly 48 hours** ago. - For new-onset AF with a short duration, **rhythm control** (cardioversion) is preferred [1]. *Wait and watch* - **Wait and watch** is inappropriate as **atrial fibrillation (AF)** is associated with a high risk of systemic embolization and stroke, necessitating prompt management (either rhythm or rate control). - Immediate intervention is required to prevent complications and potentially restore sinus rhythm, especially given the very early presentation.

Q: A patient presents with sudden onset aphasia and right sided arm weakness for past 4 hours. Which of the following investigations will be done to determine etiology of this case presentation?

Transesophageal echocardiography. ***Transesophageal echocardiography*** - The patient presents with **sudden onset focal neurological deficits** (aphasia and hemiparesis), highly suggestive of an acute stroke, likely ischemic [2]. - TEE is superior to TTE for visualizing potential **cardiac sources of embolism**, such as intracardiac thrombi (especially in the left atrial appendage), patent foramen ovale (PFO), or aortic arch plaques, which are common etiologies in cryptogenic stroke [1], [4]. *Transthoracic echocardiography* - TTE is the initial, non-invasive cardiac evaluation but may miss smaller defects or clots, particularly in the **left atrial appendage** or smaller PFOs, due to poor resolution. - While useful for overall cardiac function, it has **lower sensitivity** than TEE for detecting specific high-risk embolic sources. *Carotid doppler* - This test assesses **carotid artery stenosis**, which is a common cause of ipsilateral stroke [1]. - It primarily determines large vessel disease in the neck, but the clinical presentation (sudden onset) and age may also suggest a **cardioembolic source** warranting cardiac investigation. *MRI brain* - MRI brain is the standard imaging modality used to **confirm the stroke** (especially DWI in the acute stage) and localize the lesion [1], [3]. - However, it determines the **consequence of the stroke** (location and extent of damage) rather than the underlying **etiology** (the source of the embolus or infarct), which is the focus of this question [1], [4].

Q: A patient presents with salt wasting, craving, hyperkalemia, metabolic acidosis, and skin pigmentation. What is the most likely diagnosis?

Addison's disease. ***Addison's disease*** - The features (salt wasting, hyperkalemia, metabolic acidosis, and skin pigmentation) are hallmarks of **primary adrenal insufficiency** (Addison's disease) [1], [2]. - **Skin pigmentation** (due to increased ACTH/MSH) and **salt wasting** (due to cortisol and aldosterone deficiency) are key differentiating points [2]. *Cushing's syndrome* - This condition is caused by **excess glucocorticoids** and typically presents with central obesity, moon facies, hypertension, and hypokalemia [3]. - It is characterized by **fluid retention** and suppressed ACTH (in secondary/tertiary causes), entirely opposite to the salt wasting seen here [3]. *Conn's syndrome* - Conn's syndrome is **primary hyperaldosteronism**, leading to sodium retention, **hypertension**, **hypokalemia**, and metabolic alkalosis [1]. - The presentation includes **hypokalemia** and **alkalosis**, which directly contradict the hyperkalemia and acidosis noted in the patient. *Pheochromocytoma* - This is a catecholamine-secreting tumor leading to episodic or sustained **hypertension**, palpitations, headaches, and sweating. - It primarily affects the cardiovascular system and does not cause the **salt wasting** or **hyperkalemia** profile seen in this patient.

Question 1

A patient is on salbutamol and ipratropium but continues to have nocturnal exacerbations of asthma. What is the next step?

Accepted Answer

Laba plus inhalation steroids

Answer

Montelukast

Answer

Increase the dose of salbutamol

Answer

Oral corticosteroids

Question 2

A 25-year-old sewage worker presents with fever for 1 week and weakness for 1 day. Laboratory evaluation reveals elevated bilirubin and decreased urine output. Conjunctival redness? What is the most likely diagnosis?

Accepted Answer

Weil's disease

Answer

Enteric fever

Answer

Acute Viral Hepatitis

Answer

Brucellosis

Question 3

The pedigree diagram of a family is shown below. Affected individuals present with progressive external ophthalmoplegia, pigmentary retinopathy, and cardiac conduction defects. Based on the pedigree and clinical features, what is the most likely diagnosis?

Accepted Answer

Kearns-Sayre Syndrome

Answer

Duchenne Muscular Dystrophy

Answer

Friedreich Ataxia

Answer

Myotonic Dystrophy

Question 4

Patient came with severe headache and seizures. Sodium on admission was 98 meq/L. We have started correction with 3 % saline and now after 24 hours of infusion sodium is 110 meq/L. Patient develops mutism and altered sensorium. Which investigation will you perform now?

Accepted Answer

MRI Head

Answer

LP for CSF biochemistry

Answer

EEG

Answer

Brainstem evoked potentials

Question 5

A 30-year-old man with 6 month past history of PND and SOB. On examination, JVP is elevated with irregularly irregular pulse and tender hepatomegaly and MDM. past medical history of ARF. Which of the following is not seen in this patient?

Accepted Answer

Presystolic accentuation of mid-diastolic murmur is hallmark feature

Answer

Right heart failure

Answer

Absent a wave in JVP

Answer

Patient has increased risk of embolic stroke

Question 6

A 68-year-old male with a history of COPD presents to the emergency room with severe dyspnea and altered mental status. An arterial blood gas (ABG) is drawn with the following results:
pH: 7.28
PaCO2: 60 mmHg
HCO3-: 28 mEq/L
Na+: 142 mEq/L
Cl-: 100 mEq/L
Based on these results, what is the calculated anion gap?

Accepted Answer

B. 14 mEq/L

Answer

A. 10 mEq/L

Answer

D. 24 mEq/L

Answer

C. 18 mEq/L

Question 7

Based on the image provided, what is the most appropriate confirmatory investigation?

Accepted Answer

Manometry

Answer

Barium swallow study

Answer

Upper GI Endoscopy

Answer

pH monitoring

Question 8

A patient presents with palpitations and an irregularly irregular pulse. He presents within 2 hours of symptom onset, and has no history of diabetes or other comorbidities. What is the most appropriate initial management?

Accepted Answer

Cardioversion

Answer

Control ventricular rate with verapamil

Answer

TEE for starting anticoagulation

Answer

Wait and watch

Question 9

A patient presents with sudden onset aphasia and right sided arm weakness for past 4 hours. Which of the following investigations will be done to determine etiology of this case presentation?

Accepted Answer

Transesophageal echocardiography

Answer

Transthoracic echocardiography

Answer

MRI brain

Answer

Carotid doppler

Question 10

A patient presents with salt wasting, craving, hyperkalemia, metabolic acidosis, and skin pigmentation. What is the most likely diagnosis?

Accepted Answer

Addison's disease

Answer

Pheochromocytoma

Answer

Cushing's syndrome

Answer

Conn's syndrome

NEET-PG 2025 — Internal Medicine