MLT GlobeASCP exam preparation (USA · MLS / MLT) – page 26
1200 practice MCQs for the ASCP medical laboratory exam. Level: Advanced.
On a CD45 versus side scatter plot for acute leukemia immunophenotyping, blasts typically appear as:
Blasts express less CD45 than mature leukocytes and have few granules, so they fall in the dim CD45, low-SSC 'blast gate'. Bright CD45 with low SSC is the position of mature lymphocytes.
A man of African descent has an acute hemolytic episode after an infection. His G6PD activity measured during the episode is normal. The best action is to:
During hemolysis the oldest, most deficient cells are destroyed and young cells with higher G6PD activity dominate, giving a false normal result. A repeat test next day would still be affected by the reticulocytosis.
A 5-year-old passes dark red urine after a viral illness and cold exposure. An antibody binds red cells in the cold and causes lysis when warmed to 37°C. This is:
PCH is caused by a biphasic IgG anti-P antibody that binds in the cold and fixes complement, causing lysis on warming; it is typical in children after viral infections. PNH is an acquired stem cell defect, not antibody-mediated.
A woman has fever, confusion, severe thrombocytopenia and many schistocytes. PT and aPTT are normal. Which test best confirms the suspected diagnosis?
This picture suggests thrombotic thrombocytopenic purpura, which is confirmed by severely reduced ADAMTS13 activity (usually below 10%). The DAT is useful for immune hemolysis but is negative in TTP.
A positive sickle solubility test must be followed by hemoglobin electrophoresis or HPLC mainly because the solubility test:
Both HbAS and HbSS (and HbSC) give turbidity, so the amount and type of each hemoglobin must be measured to make the diagnosis. The test works in adults; its weakness is in infants, not adults.
Infants with beta-thalassemia major usually appear normal at birth and become anemic after about 6 months because:
At birth HbF (alpha2 gamma2) is the main hemoglobin and does not need beta chains; when gamma production falls, the beta chain defect appears. Alpha chains are already made from fetal life, so they do not start after birth.
An untransfused 2-year-old has severe microcytic anemia. HPLC shows HbF 95%, HbA2 5% and no HbA. The most likely diagnosis is:
With no beta chains produced, HbA is absent and HbF forms most of the hemoglobin, with severe anemia. HPFH gives high HbF but little or no anemia and normal red cell indices.
A woman has MCV 72 fL, normal ferritin, and normal HbA2 and HbF on HPLC. Which test is most appropriate to confirm the likely cause?
Alpha-thalassemia trait does not raise HbA2 or HbF in adults, so it is confirmed by molecular methods such as gap-PCR. Repeating HbA2 will not detect an alpha-gene deletion.
For routine coagulation testing, centrifugation should produce platelet-poor plasma with a platelet count below:
CLSI requires platelet-poor plasma <10 × 10^9/L. Residual platelets release phospholipid and PF4, which can shorten clotting times and neutralize heparin.
A capped, citrated sample from a patient not on heparin is kept at room temperature. Per CLSI, the aPTT should be tested within:
CLSI allows 4 hours for aPTT (1 hour if the patient is on unfractionated heparin). PT samples are stable for up to 24 hours.
A patient's PT is 26 s, the geometric mean normal PT is 13 s and the thromboplastin ISI is 1.2. The INR is about:
INR = (PT/MNPT)^ISI = (26/13)^1.2 = 2^1.2 ≈ 2.3. Forgetting the ISI exponent gives 2.0.
PT and aPTT are both prolonged, thrombin time is normal and both correct with 1:1 normal plasma. Which deficiency best fits?
A common pathway factor (X, V or II) prolongs both PT and aPTT but not the TT. Low fibrinogen would prolong the TT as well.
In the Bethesda assay, one Bethesda unit is the amount of inhibitor that:
One BU destroys half of the factor VIII activity of an equal volume of normal plasma after 2 hours' incubation at 37 °C. Titers guide treatment choices.
A woman of Ashkenazi Jewish descent bleeds after dental extraction. aPTT is prolonged, PT normal, and it corrects on mixing. The most likely deficiency is:
Factor XI deficiency (hemophilia C) is autosomal, affects both sexes and is common in Ashkenazi Jews. Factor VIII and IX deficiencies are X-linked and rare in women.
When interpreting borderline-low VWF antigen, which factor normally gives lower VWF levels?
People with blood group O have about 25–30% lower VWF levels. Pregnancy, stress, exercise and inflammation raise VWF and can mask mild vWD.
For monitoring unfractionated heparin by anti-Xa activity, the commonly used therapeutic range is:
The widely used therapeutic range for UFH is 0.3–0.7 anti-Xa IU/mL. Higher ranges apply to peak LMWH levels, not UFH.
Plasma levels of rivaroxaban or apixaban are best measured by:
Direct Xa inhibitors are quantified with drug-specific calibrated anti-Xa assays. The thrombin time is unaffected by Xa inhibitors.
The main physiologic inhibitor of tissue plasminogen activator is:
PAI-1 inhibits tPA and urokinase. Alpha-2-antiplasmin inhibits plasmin itself, not the activator.
According to the cell-based model of coagulation, the initiation phase begins when:
Initiation occurs on tissue factor–bearing cells, where TF–VIIa activates factors IX and X and makes a small amount of thrombin. Factor XII is not needed for in vivo hemostasis.
A patient with an MYH9 disorder has many giant platelets. On an impedance counter the platelet count is most likely to be:
Impedance counters exclude particles above the platelet size window, so giant platelets are missed or counted as RBCs. Optical, fluorescent or CD61-based counts and smear review are better.