MLT GlobeASCP exam preparation (USA · MLS / MLT) – page 27
1200 practice MCQs for the ASCP medical laboratory exam. Level: Advanced.
A 35-year-old has confusion, fever, platelets 18 × 10^9/L and many schistocytes. Which laboratory result confirms the most likely diagnosis?
Severe ADAMTS13 deficiency (<10%) confirms TTP, usually from an autoantibody. Unprocessed large VWF multimers then form platelet thrombi.
A patient on unfractionated heparin has a platelet fall from 260 to 110 × 10^9/L on day 7 and a new DVT. While HIT testing is pending, the right approach is:
HIT is prothrombotic; all heparin (including LMWH, which cross-reacts) must stop and a non-heparin anticoagulant such as argatroban started. Platelet transfusion is avoided.
The antibodies causing heparin-induced thrombocytopenia are directed against:
HIT antibodies (mainly IgG) bind PF4–heparin complexes, then activate platelets via FcγRIIa. GPIIb/IIIa is the usual target in ITP.
A patient on clopidogrel is most likely to show reduced platelet aggregation with:
Clopidogrel irreversibly blocks the P2Y12 ADP receptor. Arachidonic acid response is mainly affected by aspirin.
Platelet dense (delta) granules store:
Dense granules contain ADP, ATP, serotonin, calcium and pyrophosphate. Fibrinogen, VWF and PF4 are alpha-granule proteins.
Why does a single aspirin dose affect platelet function for about a week?
Aspirin acetylates COX-1 irreversibly; anucleate platelets cannot synthesize new enzyme, so the effect lasts their lifespan (7–10 days). The drug itself is cleared within hours.
A patient develops sudden severe thrombocytopenia a week after starting quinine; counts recover after stopping it. The mechanism is:
Quinine causes drug-dependent antibodies that bind platelet GPs (often GPIb or GPIIb/IIIa) only when the drug is present. Recovery occurs after the drug is cleared.
Which handling practice is correct for platelet aggregation samples?
Platelet function samples are citrated, kept at room temperature and tested within 4 hours. Cold, pneumatic tube transport and EDTA activate or impair platelets.
A reticulocyte count is 6% and the hematocrit is 20%. Using a normal hematocrit of 45%, what is the corrected reticulocyte count?
Corrected retic = observed retic × (patient Hct ÷ normal Hct) = 6 × 20/45 = 2.7%. The correction removes the false rise caused by fewer circulating red cells.
The reticulocyte count is 2% and the RBC count is 3.0 × 10^12/L. What is the absolute reticulocyte count?
Absolute retic = retic fraction × RBC = 0.02 × 3.0 × 10^12/L = 0.06 × 10^12/L = 60 × 10^9/L. The absolute value avoids the error caused by anemia in percentage results.
Neutrophil hypersegmentation is usually defined as:
Normally neutrophils have 2–5 lobes, with few five-lobed cells. More than 5% five-lobed cells or even one six-lobed cell is hypersegmentation, an early sign of megaloblastic anemia.
A patient with chronic alcohol use has MCV 106 fL with round macrocytes and target cells, no hypersegmented neutrophils and normal B12 and folate. This is best described as:
Alcohol and liver disease cause macrocytosis with round (not oval) macrocytes and target cells due to membrane lipid change. Absent hypersegmentation and normal vitamins argue against megaloblastic anemia.
Thin, red-violet ring or figure-of-eight structures in red cells of a patient with megaloblastic anemia are:
Cabot rings are thought to be remnants of the mitotic spindle and occur in severe megaloblastic anemia and lead poisoning. Howell-Jolly bodies are round DNA dots, not rings.
A smear made from an EDTA sample left overnight shows evenly spread red cells with many short, regular projections. The cells look normal in a fresh wet preparation. This is most likely:
Crenated cells (echinocytes) commonly form in vitro from prolonged storage, alkaline glass or slow drying, and disappear in fresh wet mounts. Acanthocytes in spur cell anemia or abetalipoproteinemia are present in vivo and persist in wet preparations.
Red cells on a smear show sharp-edged, bright refractile areas that change with the fine focus. The stain methanol was left uncovered in humid air. These are most likely:
Water in the fixative or stain produces refractile, sharply outlined areas that shine when focusing, unlike true inclusions. Pappenheimer bodies are small dark granules that do not glisten.
An inclusion on top of a red cell has a clear halo around it and lies in a slightly different focal plane. It is most likely:
A platelet lying on a red cell often has a surrounding halo and a different focal plane, and may show granules. True inclusions lie within the cell in the same plane as the hemoglobin.
In a person with sickle cell trait who is well, the peripheral smear usually shows:
HbS below about 40% does not polymerize under normal oxygen levels, so sickle cells are not seen in trait. Irreversibly sickled cells are a feature of sickle cell disease.
Infected red cells are enlarged and contain fine pink-red stippling (Schüffner dots) with amoeboid trophozoites. The most likely species is:
P. vivax prefers reticulocytes, so infected cells are enlarged, and they show Schüffner dots. P. malariae infects older cells, which stay normal-sized, and forms band trophozoites.
A jaundiced group O mother's group A newborn has a weakly positive DAT. The smear most likely shows:
In ABO hemolytic disease of the newborn, IgG anti-A partly removes membrane in the spleen, producing microspherocytes. Target cells are not a feature of immune hemolysis.
AML showing monocytic and granulocytic blasts plus abnormal eosinophils with large purple-violet granules is associated with:
inv(16)/t(16;16) gives myelomonocytic AML with abnormal eosinophils and carries a favorable prognosis. t(15;17) is APL with hypergranular promyelocytes.