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NRE-1 JUNE 2025

SOLVED PAPER
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NRE-1 JUNE
SOLVED PAPER MD(USA), FCSP-1, MD/MS-1

NRE-1 June 2025 SOLVED Paper

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MD(USA), FCSP-1, MD/MS-1

Question:
Which of the following is the most common causative agent in urinary tract infection (UTI)?

A. E. coli
B. Klebsiella pneumoniae
C. Proteus mirabilis
D. Staphylococcus

Correct Answer: A. E. coli

Why correct:
E. coli is the most common organism causing UTIs (up to 90% of community-acquired cases). Its
fimbriae enhance adhesion to the uroepithelium.

Why others are incorrect:

B. Klebsiella – Less common; associated with nosocomial UTIs.

C. Proteus – Seen in complicated UTIs; associated with stone formation.

D. Staphylococcus saprophyticus – Seen in young, sexually active women, but less frequent
than E. coli.

99. First-line treatment for stable SVT

Question:
25-year-old lady presents in emergency department with complains of palpitations and dizziness. Her
radial pulse is very fast and blood pressure is 110/70. Her ECG shows regular narrow complex
tachycardia. Which of the following is the first line treatment for this condition?

A. Defibrillation
B. Diltiazem
C. Metoprolol
D. Vagal maneuver

Correct Answer: D. Vagal maneuver

Why correct:
SVT – Key Diagnostic Approach (Short Table)

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Step Key Point
1. Clinical Clue Sudden palpitations, regular rapid HR
2. Stability Assess BP, mental status (unstable = cardiovert)
3. ECG Regular narrow QRS, HR 150–250 bpm, no clear P waves
4. Response Test Vagal maneuver or adenosine → diagnostic + therap

Hemodynamically stable Hemodynamically unstable

1. Vagal maneuvers (Valsalva, carotid massage) 1. Synchronized cardioversion
2. Adenosine (if vagal fails)
3. Alternatives: Beta-blocker or CCB

Vagal maneuvers (e.g., Valsalva, carotid massage) are the first-line treatment for stable
supraventricular tachycardia (SVT). They increase vagal tone and slow AV node conduction.

Why others are incorrect:

A. Defibrillation – Used in unstable or pulseless patients.

B. Diltiazem, C. Metoprolol – Used after vagal maneuvers fail; second-line pharmacologic

options.

100. Best test to diagnose gestational diabetes

Question:
What is the most appropriate test to diagnose gestational diabetes?

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A. HbA1c
B. Glucose tolerance test
C. Fasting blood sugar
D. Random blood sugar

Correct Answer: B. Glucose tolerance test

The oral glucose tolerance test (OGTT) is the gold standard for diagnosing gestational diabetes,
performed at 24–28 weeks.

Why others are incorrect:

A. HbA1c – Not reliable in pregnancy due to altered RBC turnover.

C. Fasting/Random glucose – Can be used for screening but not definitive.

101. Most common dyslipidemia pattern in T2DM

Question:
Which of the following is the most common lipid abnormality in type 2 diabetes?

A. High LDL, Low TGs, Low HDL

B. Low LDL, High TGs, Low HDL
C. High LDL, High TGs, Low HDL
D. High LDL, High TGs, High HDL

Correct Answer: C. High LDL, High TGs, Low HDL

Patients with type 2 diabetes mellitus (T2DM) often exhibit an atherogenic lipid profile,
characterized by:

↑ LDL (often small, dense particles – more atherogenic)

↑ Triglycerides (due to insulin resistance)

↓ HDL (reduced reverse cholesterol transport

This dyslipidemia increases the risk of cardiovascular disease, a major complication of T2DM.

Why others are incorrect:

Options A, B, D – Do not reflect the classic triad of diabetic dyslipidemia.

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Question:
A patient was diagnosed with acute inflammatory demyelinating neuropathy 1 week after he recovered
from an acute gastroenteritis infection. He was admitted with mild sensory symptoms which were
getting worse with progressive weakness that first began in his lower limbs. He was finding hard to
breathe and move his upper limbs as well. Which of the following treatments would you recommend?

Correct Answer: C. IV immunoglobulin

Why correct:
IVIG is first-line therapy for Guillain-Barré syndrome (GBS) along with
plasmapheresis. Both reduce autoantibody-mediated nerve damage.
Key Diagnostic Markers

Topic High-Yield Points

Cause Autoimmune demyelination of peripheral nerves
Trigger Post-infection (especially Campylobacter jejuni)
Symptoms Ascending symmetric weakness, areflexia, paresthesias
Complications Respiratory failure, autonomic instability
Diagnosis Clinical + CSF (↑ protein, normal WBC) + NCS/EMG
CSF finding Albuminocytologic dissociation
Treatment IVIG or plasmapheresis (no steroids)
Monitoring Vital capacity → <20 mL/kg = intubation

Test Finding
CSF (LP) ↑ Protein, normal WBC
Nerve studies Demyelination (slowed conduction)
Clinical exam Ascending weakness + areflexia

Why others are incorrect:

A & D. Steroids – Not effective in GBS.

B. Antibiotics – Unnecessary unless active infection is present.

103. Best investigation for myasthenia gravis

Question:
A 32 years old woman complaining of 6 months history of dysphagia and nasal regurgitation, which is
worse during evening. She also reports intermittent drooping of her left eyelid and diplopia when she
gets tired. Neurological examination reveals partial left ptosis and diplopia but no ophthalmoplegia.
She also has mild cough. What will be the most appropriate investigation in this case?

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A. Acetylcholine receptor antibodies
B. Barium swallow
C. CT brain
D. Tumor markers

Correct Answer: A. Acetylcholine receptor antibodies

Why correct:
These antibodies are positive in ~85% of generalized myasthenia gravis and confirm the diagnosis.

Category Key Points

Cause Autoantibodies against acetylcholine receptors at the neuromuscular junction
Fluctuating weakness (worsens with use), ptosis, diplopia, dysphagia, dysarthria, normal
Symptoms
reflexes and sensation
AChR antibodies (most sensitive), edrophonium (Tensilon) test, CT chest to rule out
Diagnosis
thymoma
Pyridostigmine (first-line), steroids, azathioprine, IVIG or , thymectomy if thymoma or
Treatment
generalized MG

Why others are incorrect:

B. Barium swallow – May assess dysphagia but doesn't confirm MG.

C. CT brain – Not helpful without CNS signs.

D. Tumor markers – Not relevant for diagnosis.

A woman came with collapse and vomiting preceded by occipital headache of acute onset. After 8
hours she was conscious and alert with photophobia and mild neck stiffness, CT scan brain was
carried out which came out to be normal. Which one of the following investigations would yield the
diagnosis?
A. CT scan brain with contrast
B. MRI brain
C. CSF examination by LP after 12 hours
D. Cerebral angiography

Correct Answer: C. CSF examination by LP after 12 hours

Why correct:
If non-contrast CT is negative but suspicion of SAH remains, LP after 12 hours is done to detect
xanthochromia, confirming SAH.

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Aspect Details
Cause Ruptured berry aneurysm (e.g., anterior communicating artery), trauma
Risk factors Hypertension, smoking, polycystic kidney disease, Ehlers-Danlos syndrome
Classic symptom Sudden, severe "thunderclap" headache ("worst headache of life")
Other signs Nuchal rigidity, photophobia, vomiting, loss of consciousness
Diagnosis Approach
Step Action
1st test Non-contrast CT head – best initial test
If CT is negative Do lumbar puncture (after 12 hrs) → look for xanthochromia
Confirm aneurysm CT angiography or cerebral angiography
Treatment
Goal Management
Prevent rebleed Surgical clipping or endovascular coiling
Prevent vasospasm Nimodipine (DHP calcium channel blocker)

Why others are incorrect:

A. CT with contrast – Not sensitive for early blood.

B. MRI – May miss early SAH.

D. Angiography – Identifies aneurysm but not diagnostic in acute setting

Question:
Which one of the following is used in the emergency treatment of organophosphate poisoning?

A. Atropine
B. Naloxone
C. Flumazenil
D. Pralidoxime

Correct Answer: A. Atropine

Organophosphate Poisoning – USMLE High-Yield Table

Aspect Key Points
Cause Inhibits acetylcholinesterase → ↑ ACh
Source Pesticides, insecticides
DUMBBELSS: Diarrhea, Urination, Miosis, Bradycardia, Bronchorrhea, Emesis,
Symptoms
Lacrimation, Salivation, Sweating; + muscle weakness, seizures
Diagnosis Clinical; ↓ cholinesterase activity (if tested)

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Aspect Key Points
Atropine (muscarinic), Pralidoxime (reactivates AChE), benzodiazepines (seizures),
Treatment
airway support
Pralidoxime (2-PAM) is also used but only after atropine, to regenerate acetylcholinesterase.

Tips

Atropine treats muscarinic symptoms (e.g., bronchorrhea, bradycardia)

Pralidoxime reverses both muscarinic + nicotinic effects (must be given early)

Miosis + bradycardia + diarrhea + muscle weakness = think organophosphate

Naloxone – opioid overdose.

Flumazenil – benzodiazepine reversal.

Which one of the following drugs is most appropriate to treat a patient with anaphylactic shock?

A. Dobutamine
B. Epinephrine
C. Norepinephrine
D. Phenylephrine

Correct Answer: B. Epinephrine

First-line treatment. Acts on α1 (vasoconstriction) and β2 (bronchodilation).

Norepinephrine – preferred in septic shock.

Dobutamine – used in cardiogenic shock.

Phenylephrine – α-agonist; not adequate for anaphylaxis.

Question:
Which one of the following types of epinephrine receptors is responsible for bronchodilation and
is commonly targeted in the management of asthma?

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A. Alpha-1 receptor
B. Alpha-2 receptor
C. Beta-1 receptor
D. Beta-2 receptor

Correct Answer: D. Beta-2 receptor

β2 stimulation = bronchodilation, key for asthma/anaphylaxis.

Beta-1 – increases heart rate and contractility.

Alpha-1 – vasoconstriction.

Alpha-2 – feedback inhibition of norepinephrine release

Question:
A known diabetic developed dyskinesia and akathisia after receiving an injection for gastroenteritis.
Which one of the following drugs is most likely responsible?

A. Ondansetron
B. Domperidone
C. Metoclopramide
D. Erythromycin

Correct Answer: C. Metoclopramide

Metoclopramide is a dopamine antagonist; can cause extrapyramidal symptoms like akathisia

and dystonia.

Extrapyramidal symptoms are drug-induced movement disorders caused by dopamine (D₂)

blockade in the nigrostriatal pathway, most commonly due to antipsychotics or antiemetics (e.g.,
metoclopramide).

Types of EPS (with timing)

EPS Type Description Onset
Acute dystonia Sustained muscle spasms (e.g., torticollis, oculogyric crisis) Hours to days
Akathisia Restlessness, urge to move Days to weeks
Parkinsonism Tremor, rigidity, bradykinesia Weeks to months
Tardive dyskinesia Involuntary facial/tongue movements (chronic) Months to years

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Domperidone is less likely to cross the BBB.

Ondansetron – 5-HT3 blocker, not linked to movement disorders.

Erythromycin – prokinetic via motilin receptor, not dopaminergic.

Question:
Which one of the following diuretics is used as an emergency management in a head injury patient
with increased intracranial pressure (ICP)?

A. Acetazolamide
B. Furosemide
C. Mannitol
D. Torsemide

Correct Answer: C. Mannitol

Mannitol is an osmotic diuretic used acutely to reduce intracranial pressure.

Acetazolamide – used for chronic ICP (e.g., pseudotumor cerebri).

Furosemide – adjunct, not first-line for ICP.

Torsemide – similar to furosemide.

Question:
Which one of the following is the therapeutic indication of Dextromethorphan?

A. Analgesic
B. Antihistaminic
C. Antitussive
D. Expectorant

Correct Answer: C. Antitussive

Dextromethorphan – Quick Facts

Aspect Key Points

Use Antitussive (cough suppressant) – NMDA receptor antagonist
Mechanism Suppresses cough reflex in medulla; structurally related to opioids
Side effects High doses → CNS effects: euphoria, hallucinations, dissociation ("robotripping")
Toxicity Serotonin syndrome if combined with SSRIs
Abuse potential Recreational use common in teens,abusive potential

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Dextromethorphan = antitussive + NMDA blocker → dissociation + serotonin risk at high dos

Question:
After committing suicide, the revolver remained firmly grasped in the hand of a person. What is the
name of this phenomenon?

A. Instantaneous rigor
B. Rigor mortis
C. Secondary relaxation
D. Primary rigidity

Correct Answer: A. Instantaneous rigor

• Instantaneous rigor refers to immediate stiffening of the body at the moment of

death, instead of the usual gradual onset of rigor mortis.

Also called cadaveric spasm; seen in sudden death with intense emotion or activity
(e.g., suicide with revolver in hand).
Instantaneous Rigor vs Rigor Mortis – Key Differences (USMLE Table)
Feature Instantaneous Rigor Rigor Mortis
Onset Immediately at the moment of death Begins after 2–4 hours postmortem
Sudden, violent death → rapid ATP
Cause Natural ATP depletion post-death
depletion
All deaths (normal postmortem
Associated with Lightning strike, seizures, electrocution
process)
Progression Generalized stiffness immediately Head → toe over 12 hours
Duration Transient Lasts up to 24–36 hours
Forensic
Suggests sudden/violent death Helps estimate time since death
relevance

Rigor mortis – generalized, sets in after 1–2 hours.

Secondary relaxation – occurs after rigor ends.

Primary rigidity – not a standard forensic term.

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