ASCP exam preparation (USA · MLS / MLT) – page 25
1200 practice MCQs for the ASCP medical laboratory exam. Level: Advanced.
In capillary zone electrophoresis of serum, separated proteins are usually detected by:
Capillary systems pass proteins through a detector that reads UV absorbance of peptide bonds, so no gel staining is needed. Staining and densitometry apply to agarose gel electrophoresis.
A 70-year-old with blurred vision, bleeding gums and a large IgM monoclonal protein most likely has:
An IgM monoclonal protein with hyperviscosity symptoms (visual changes, mucosal bleeding) is typical of Waldenström macroglobulinemia (lymphoplasmacytic lymphoma). MGUS has a small M-protein without symptoms.
Why is creatinine calibration traceable to isotope dilution mass spectrometry (IDMS) important?
Current eGFR equations such as CKD-EPI were derived using IDMS-traceable creatinine, so non-standardised results give biased eGFR. Calibration cannot correct biological factors such as muscle mass or tubular secretion.
A patient with upper gastrointestinal bleeding has serum urea (BUN) 20 mmol/L (56 mg/dL) and creatinine 110 µmol/L (1.2 mg/dL). The high BUN/creatinine ratio is best explained by:
Blood in the upper GI tract is digested and absorbed as protein, increasing urea production, so BUN rises more than creatinine (ratio well above 20:1). Liver failure and low protein intake lower urea.
In the urease–glutamate dehydrogenase method for urea, the reaction is followed by measuring:
Urease produces ammonia, which GLDH uses with 2-oxoglutarate and NADH; NADH oxidation is seen as falling absorbance at 340 nm. Conductivity-based urea methods exist, but the coupled GLDH method is read at 340 nm.
An elderly woman with very low muscle mass after amputation has serum creatinine 50 µmol/L (0.57 mg/dL). Which test gives a more reliable GFR estimate?
Low muscle mass lowers creatinine production, so creatinine-based eGFR overestimates GFR. KDIGO suggests confirming with cystatin C (combined equation) in such cases.
Serum creatinine is a relatively late marker of reduced kidney function because:
Because of the hyperbolic relationship between creatinine and GFR, and some tubular secretion, creatinine may remain 'normal' until substantial GFR loss. Creatinine is not reabsorbed.
A drug level is 40 mg/L at 08:00 and 10 mg/L at 16:00, with no dose in between. The half-life is:
40 to 20 is one half-life and 20 to 10 is a second, so two half-lives took 8 hours. Each half-life is therefore 4 hours.
A patient on lithium has a very high result with no signs of toxicity. The sample was collected in a green-top tube. The most likely cause is:
Lithium heparin tubes add lithium to the sample and falsely raise the result. Lithium should be measured in serum or a lithium-free tube, about 12 hours after the last dose.
A patient with low albumin has toxic signs while the total phenytoin level is within range. The best next test is:
Phenytoin is about 90% protein-bound; with low albumin or uremia the free, active fraction rises. Free phenytoin reflects the true effect better than total.
A patient has a high anion gap acidosis, a raised osmolal gap and many calcium oxalate crystals in the urine. The most likely poison is:
Ethylene glycol is metabolized to oxalic acid, which forms calcium oxalate crystals and can damage the kidneys. Methanol causes visual damage but not oxalate crystals.
A farm worker has miosis, sweating and excess salivation after pesticide exposure. Which lab result supports organophosphate poisoning?
Organophosphates inhibit acetylcholinesterase; low RBC cholinesterase (and serum pseudocholinesterase) activity supports the diagnosis.
A patient has flushing and diarrhea. A 24-hour urine 5-HIAA is raised. This supports:
5-HIAA is the main metabolite of serotonin, which carcinoid tumors make in excess. Foods such as bananas and walnuts can falsely raise it.
A 45-year-old man has fatigue and bronze skin. Fasting transferrin saturation is 78% and ferritin is very high. The next test is:
High transferrin saturation with high ferritin suggests hereditary hemochromatosis, most often HFE C282Y homozygosity. Genetic testing is the usual next step.
Serum iron is 60 µg/dL (10.7 µmol/L) and TIBC is 400 µg/dL (71.6 µmol/L). The transferrin saturation is:
Transferrin saturation = serum iron ÷ TIBC × 100 = 60 ÷ 400 × 100 = 15%. A value below about 16–20% supports iron-deficient erythropoiesis.
Why are serum iron samples ideally collected in the morning after fasting?
Serum iron is usually highest in the morning and varies widely during the day; recent intake or supplements also raise it. Standard timing makes results easier to interpret.
Hydrodynamic focusing in a hematology analyzer is used to:
A sheath fluid narrows the sample stream so cells pass in single file through the center of the aperture or laser beam, reducing coincidence and edge-path errors. Lysis of red cells is done by a separate reagent.
The WBC count is 20.0 × 10^9/L and 25 nucleated red cells are seen per 100 white cells on the differential. What is the corrected WBC count?
Corrected WBC = WBC × 100 ÷ (100 + nRBC) = 20.0 × 100 ÷ 125 = 16.0 × 10^9/L. 15.0 is obtained by wrongly subtracting 25% of the count.
A patient with severe microcytosis and many red cell fragments has an impedance platelet count higher than the smear estimate. The platelet histogram does not return to baseline near 20 fL. The cause is:
Microcytes and schistocytes fall into the platelet size range, raising the count and lifting the upper end of the histogram. Platelet clumps and giant platelets lower the platelet count instead.
Blood diluted 1:20 is counted in a hemacytometer (depth 0.1 mm). A total of 200 white cells are counted in 4 large squares (4 mm²). What is the WBC count?
Cells/µL = count × dilution ÷ (area × depth) = 200 × 20 ÷ (4 × 0.1) = 10,000/µL, which is 10.0 × 10^9/L. 5.0 results from wrongly using an area of 8 mm² instead of 4 mm².