Medicine β Nephrology, NMC MBBS licence examination syllabus (Nepal Medical Council).
Kidney disease β NMC-style practice questions
Practice questions written for this chapter. These are not past NMC papers.
π About these questions: These are practice questions written to test the reasoning in this chapter. They are NOT reproduced from any past Nepal Medical Council examination, and no verified past NMC questions were supplied for this chapter.
Level 1β2 β recall and understanding
Q1. Which urinary finding is characteristic of acute
tubular necrosis?
A. Red cell casts
B. Muddy brown granular casts
C. Bland sediment with low urinary sodium
D. White cell casts only
ANSWER: B β muddy brown granular casts.
Why: sloughed tubular epithelial cells form these casts in
ATN.
A: red cell casts indicate glomerulonephritis.
C: describes pre-renal azotaemia.
LEARNING POINT: the urine sediment separates the intrinsic
causes from the pre-renal ones.
Q2. In hyperkalaemia, intravenous calcium gluconate acts by:
A. Lowering serum potassium rapidly
B. Stabilising the cardiac membrane without lowering
potassium
C. Increasing renal potassium excretion
D. Shifting potassium into cells
ANSWER: B β membrane stabilisation.
Why: calcium antagonises the effect of potassium on the
myocardium, protecting against arrhythmia. It does not alter
the potassium level at all.
D: that is insulin with glucose, or salbutamol.
LEARNING POINT: stabilise, shift, remove β three separate
jobs, three separate drugs.
Level 3β4 β application and clinical reasoning
Q3. An 82-year-old on ramipril and furosemide develops
gastroenteritis and takes ibuprofen. Creatinine rises
from 90 to 300. The mechanism is:
A. Direct nephrotoxicity of ibuprofen alone
B. Loss of both afferent dilation and efferent
constriction during hypovolaemia
C. Obstruction
D. Glomerulonephritis
ANSWER: B.
Why: the NSAID blocks prostaglandin-mediated afferent
dilation, the ACE inhibitor blocks angiotensin-mediated
efferent constriction, and the diuretic plus diarrhoea
depletes volume. All three renal defences are disabled at
once.
LEARNING POINT: none of these drugs is wrong alone. The
combination during dehydration is the problem.
Q4. An anuric patient with KβΊ 7.2 receives calcium and
insulinβdextrose; potassium falls to 5.5. The next
step is:
A. No further action β the problem is treated
B. Arrange definitive removal (dialysis or a binder)
C. Give further insulin only
D. Start a loop diuretic
ANSWER: B β arrange removal.
Why: insulin shifts potassium into cells but removes none
from the body. In an anuric patient there is no excretory
route, so it will rise again.
D: diuretics are ineffective in an anuric patient.
LEARNING POINT: shifting buys time; it does not solve the
problem.
Q5. A 78-year-old with a poor urinary stream has creatinine
460 and a distended, dull suprapubic abdomen. The most
appropriate immediate action is:
A. Fluid challenge
B. Bladder scan and urethral catheterisation
C. Urgent dialysis
D. Renal biopsy
ANSWER: B β bladder scan and catheterise.
Why: this is post-renal AKI from retention. Relieving the
obstruction is immediate, cheap and definitive, and every
hour of delay costs nephrons.
A: could worsen an already overloaded patient.
LEARNING POINT: exclude obstruction EARLY, and anticipate
post-obstructive diuresis afterwards.
Level 5 β exception-based
Q6. A patient with proteinuric CKD starts an ACE inhibitor.
Creatinine rises from 145 to 162 at two weeks, potassium
4.8, blood pressure improved. The correct action is:
A. Stop the ACE inhibitor immediately
B. Continue and recheck β a small rise is expected
C. Halve the dose and add an NSAID
D. Refer for urgent dialysis
ANSWER: B β continue and recheck.
Why: ACE inhibitors reduce intraglomerular pressure by
dilating the efferent arteriole. That produces a small,
expected creatinine rise and IS the mechanism of long-term
renal protection.
A: discards the benefit for an anticipated effect.
A large or progressive rise would be different, and raises
the question of renal artery stenosis.
LEARNING POINT: distinguish the intended effect from a
warning sign.
Q7. A frail 84-year-old woman weighing 42 kg has a
creatinine of 96 Β΅mol/L. This most likely indicates:
A. Entirely normal renal function
B. Possibly significant impairment, because creatinine
depends on muscle mass
C. Acute kidney injury
D. Laboratory error
ANSWER: B.
Why: creatinine is generated from muscle. In a small,
sarcopenic patient, a value within the reference range can
correspond to substantially reduced filtration.
A: the assumption this question targets.
LEARNING POINT: interpret creatinine against the patient in
front of you, and use eGFR with the same caution.
Syllabus points
Recall and understanding questions
Application and clinical reasoning questions
Exception-based questions
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