CDN Practice Questions (2026) — Free Sample Questions with Answers

Answer: B

Dialyze the patient at any station after universal precautions and a bleach wipe-down: Standard precautions alone are not enough for HBsAg-positive patients in hemodialysis; CDC adds isolation and dedicated equipment.

Dialyze the patient in a separate isolation room with a dedicated machine, supplies and staff: Correct. CDC recommends an isolation room with dedicated machine, equipment, instruments and supplies; staff caring for this patient should not care for HBV-susceptible patients during the same shift.

Reuse the patient's dialyzer only after reprocessing it with the other patients' dialyzers: CDC advises against dialyzer reuse for HBsAg-positive patients.

Dialyze the patient next to other patients whose anti-HBs titers are not yet known: Patients of unknown or susceptible status are at highest risk and should not be grouped with an HBsAg-positive patient.

HBsAg-positive HD patients: isolation room, dedicated machine and supplies, no dialyzer reuse, staff not shared with susceptible patients that shift; vaccinate susceptible patients and staff.

Answer: C

Rapid fluid removal causes cerebral hypoperfusion; prevent it by setting UF to zero: Hypotension can cause symptoms, but the classic first-treatment syndrome with very high BUN is osmotic, not caused by UF volume.

A dialysate sodium that is too high causes thirst and edema; prevent it with low-sodium bath: High dialysate sodium causes thirst and weight gain, not this neurological picture; low-sodium baths may make cerebral edema worse.

Urea leaves the blood faster than the brain, so water shifts in; use a short, gentle first run: Correct. Dialysis disequilibrium results from a blood–brain osmotic gradient causing cerebral edema; prevent it with short, low-efficiency first treatments (lower blood flow, smaller dialyzer).

A reaction to ethylene oxide in the dialyzer causes these signs; prevent it by pre-rinsing: Type A dialyzer reactions happen within minutes of starting and cause anaphylactoid signs, not symptoms at the end of treatment.

Disequilibrium syndrome: highest risk with very high BUN and first treatments; prevent with gradual urea reduction (short, low-blood-flow, small-dialyzer sessions, sometimes on consecutive days).

Answer: C

30%; it does not meet the minimum of 65%: 30% is the post/pre ratio (24/80), not the reduction. URR = (pre − post) / pre.

56%; it does not meet the minimum of 65%: This is a calculation error; (80 − 24) = 56 must be divided by 80, not read as a percentage.

70%; it meets the minimum of 65%: Correct. URR = (80 − 24) ÷ 80 = 0.70, or 70%, which is above the commonly cited minimum URR of 65% (about spKt/V 1.2).

76%; it meets the minimum of 65%: Rounding or arithmetic error; (80 − 24) ÷ 80 = 70%.

URR = (pre-BUN − post-BUN) ÷ pre-BUN × 100. Minimum adequacy for thrice-weekly HD: URR ≥ 65% or spKt/V ≥ 1.2 (KDOQI target spKt/V 1.4).

Answer: C

A parathyroid adenoma producing PTH independent of calcium, as in primary disease: Primary hyperparathyroidism usually causes high calcium with low phosphorus, the opposite of this pattern.

Excess vitamin D activation by the failing kidneys, which raises PTH directly: Failing kidneys produce less calcitriol (1,25-dihydroxyvitamin D), and less calcitriol leads to more PTH, not the other way around.

Phosphate retention, low calcitriol and high FGF-23 stimulating the parathyroid glands: Correct. Secondary hyperparathyroidism in CKD comes from phosphate retention, reduced calcitriol, a tendency to hypocalcemia and rising FGF-23, which together drive parathyroid hyperplasia.

Aluminum toxicity from water treatment, which stimulates parathyroid hormone release: Aluminum toxicity is linked to adynamic bone disease with low or normal PTH and is rare with modern water treatment.

CKD-MBD: high phosphorus + low calcitriol + low calcium + high FGF-23 → secondary hyperparathyroidism; manage with diet, binders, vitamin D analogs and calcimimetics.

Answer: A

Assess regularly for kidney recovery and avoid intradialytic hypotension and excess ultrafiltration: Correct. The goal in AKI is recovery: monitor urine output and pre-dialysis chemistries, adjust or space treatments as function returns, and avoid hypotension that could cause further kidney injury.

Place a permanent arteriovenous fistula right away, as for any ESRD patient starting dialysis: Permanent access planning is usually deferred while recovery is possible; access is chosen with the nephrologist based on prognosis.

Use the same fixed thrice-weekly prescription as ESRD patients until a year has passed: AKI prescriptions are reassessed often; a fixed long-term schedule ignores the potential for recovery.

Begin transplant evaluation and waitlisting at the first outpatient treatment: Transplant referral is for irreversible kidney failure, not for AKI that may still recover.

AKI in the outpatient unit: dialysis is a bridge to recovery; track residual function, prevent hypotension, avoid nephrotoxins, and reassess the need for dialysis often.

Answer: C

Aluminum toxicity; testing water conductivity before each shift: Aluminum causes chronic encephalopathy and bone disease over months, not acute hemolysis on one shift; conductivity monitors dialysate, not chlorine.

Pyrogenic reaction; culturing the water monthly for bacteria: Pyrogenic reactions cause fever and chills; monthly cultures would not detect an acute chlorine breakthrough.

Hemolysis from chloramine breakthrough; testing total chlorine before each shift: Correct. Chloramine that passes exhausted carbon oxidizes hemoglobin and causes hemolysis and methemoglobinemia; total chlorine must be tested after the carbon (worker) tank before each patient shift.

Fluoride intoxication; checking water hardness at the softener daily: Fluoride toxicity is rare and causes pruritus and arrhythmias; softener hardness tests do not detect chlorine.

Carbon tanks remove chlorine and chloramine; test total chlorine (limit about 0.1 mg/L) after the worker tank before each shift. Breakthrough → hemolysis, anemia, methemoglobinemia.