MLT GlobeASCP exam preparation (USA · MLS / MLT) – page 57
1200 practice MCQs for the ASCP medical laboratory exam. Level: Advanced.
Serum electrophoresis of a healthy adult shows the albumin band split into two equal peaks; other fractions are normal. The most likely explanation is:
Bisalbuminemia is a double albumin band caused by a genetic variant with different charge, and is usually of no clinical importance. It can rarely be acquired, for example with high-dose beta-lactam drugs.
A patient with known kappa light chain myeloma has a free kappa result far lower than expected, but it rises greatly when the sample is re-run at a higher dilution. The cause is:
In immunonephelometry, very high antigen saturates the antibody and forms fewer large complexes, giving falsely low results. Dilution restores the correct antigen–antibody ratio.
A patient starts trimethoprim. Serum creatinine rises by 15% but measured GFR by iohexol clearance is unchanged and cystatin C is stable. The most likely explanation is:
Trimethoprim (like cimetidine) blocks tubular creatinine secretion, raising serum creatinine without true loss of GFR. Stable cystatin C and measured GFR argue against real kidney injury.
Oliguric patient: urine Na 10 mmol/L, plasma Na 140 mmol/L, urine creatinine 8000 µmol/L, plasma creatinine 200 µmol/L. What is the fractional excretion of sodium (FENa)?
FENa = (UNa × PCr)/(PNa × UCr) × 100 = (10 × 200)/(140 × 8000) × 100 = 0.18%. A value below 1% shows avid sodium retention, typical of prerenal azotemia; ATN usually gives above 2%.
A patient with oliguria has been given furosemide. Which index is more reliable than FENa to separate prerenal azotemia from tubular injury?
Loop diuretics increase sodium excretion and falsely raise FENa. Urea handling is less affected, so a fractional excretion of urea below about 35% still suggests prerenal azotemia.
A child is 120 cm tall with serum creatinine 0.6 mg/dL (53 µmol/L). Using the bedside Schwartz equation (eGFR = 0.413 × height in cm ÷ creatinine in mg/dL), the eGFR is about:
0.413 × 120 = 49.6; 49.6 ÷ 0.6 = 82.6, about 83 mL/min/1.73 m². Forgetting to divide by creatinine gives about 50, a common error.
A patient started on carbamazepine has good levels at week 1, but at week 4 the level is lower on the same dose with good adherence. The most likely reason is:
Carbamazepine induces the CYP3A4 enzymes that metabolize it, so clearance increases over the first few weeks and levels fall. Doses often need adjusting after this autoinduction.
Current consensus guidelines for serious MRSA infections recommend vancomycin dosing be guided by:
The 2020 ASHP/IDSA/SIDP guideline moved from trough-only monitoring to AUC-guided dosing, targeting AUC/MIC 400–600 (MIC 1 mg/L). This balances efficacy and nephrotoxicity better than trough targets.
A patient has a raised osmolal gap, ketones in blood and urine, normal glucose and no metabolic acidosis. Which ingestion is most likely?
Isopropanol is metabolized to acetone, a ketone that is not an acid, so ketosis and a raised osmolal gap occur without acidosis. Methanol and ethylene glycol produce organic acids and a high anion gap.
After digoxin-specific antibody Fab fragments are given for toxicity, total serum digoxin by immunoassay rises greatly. The best explanation is:
Fab fragments pull digoxin from tissue into plasma, where it is tightly bound and inactive. Total immunoassay results become misleading, so free (ultrafiltrate) digoxin is measured if needed.
A patient being tested for a neuroendocrine tumor has a raised chromogranin A. Which medication is a well-known cause of a false-positive result?
Proton pump inhibitors cause high gastrin, which stimulates enterochromaffin-like cells to release chromogranin A. The drug is usually stopped for a period before testing when safe.
Serum transferrin is 2.4 g/L. Using TIBC (µmol/L) ≈ transferrin (g/L) × 25, the estimated TIBC is about:
Each transferrin molecule binds two iron atoms, giving the factor of about 25. 2.4 × 25 = 60 µmol/L (about 335 µg/dL). Using 12.5 would give only the transferrin molar value, not binding capacity.
ICSH recommends K2EDTA rather than liquid K3EDTA for blood counts mainly because K3EDTA:
Liquid K3EDTA dilutes the blood by about 1–2% and causes more red cell shrinkage, lowering MCV and Hct. Spray-dried K2EDTA avoids dilution.
Hb Lepore is formed by:
Unequal crossing over joins the start of the delta gene to the end of the beta gene. The delta-beta hybrid chain is made poorly, giving a beta-thalassemia phenotype. Beta-26 glutamic acid to lysine is HbE.
On alkaline (pH 8.4–8.6) hemoglobin electrophoresis, which hemoglobin moves farthest toward the anode?
HbH (β4) and Hb Bart's (γ4) carry a stronger negative charge and run ahead of HbA. HbS and HbC are more positive and move more slowly, with HbC closest to the origin.
A woman with microcytosis has ferritin 5 µg/L (5 ng/mL) and HbA2 3.0% on HPLC. Several relatives have beta-thalassemia trait. The best interpretation is:
Severe iron deficiency reduces HbA2 synthesis and can mask beta-thalassemia trait, so HbA2 should be rechecked once iron is replaced. A normal value in an iron-deficient patient does not exclude the trait.
A child given ceftriaxone develops sudden severe intravascular hemolysis with hemoglobinuria. The DAT is positive with anti-C3. The mechanism is best described as:
Ceftriaxone-dependent antibodies bind only when the drug is present, activating complement and causing brisk intravascular lysis with C3 on the cells. Hapten-type (penicillin) reactions are IgG-mediated and extravascular.
A patient on rivaroxaban is tested for lupus anticoagulant. A positive dRVVT result should be interpreted with caution because:
The dRVVT activates factor X directly, so anti-Xa DOACs prolong it and can mimic lupus anticoagulant. Testing is best done when the drug is absent or removed.
Unlike the other coagulation factors, factor VIII is produced mainly by:
Factor VIII is made mainly by liver sinusoidal endothelial cells (and other endothelium), not hepatocytes. This is one reason factor VIII is normal or high in liver disease while hepatocyte-made factors fall.
A patient receives 4 × 10^11 platelets. Body surface area is 2.0 m². Pre-count is 10 × 10^9/L and the 1-hour post-count is 30 × 10^9/L. The corrected count increment (CCI) is:
CCI = increment (per µL) × BSA ÷ platelets transfused (×10^11) = 20 000 × 2.0 ÷ 4 = 10 000. A 1-hour CCI above 7500 indicates an adequate response.