MLT GlobeASCP exam preparation (USA · MLS / MLT) – page 39
1200 practice MCQs for the ASCP medical laboratory exam. Level: Advanced.
Coarse, irregular red-purple dots (Maurer clefts) in red cells containing larger trophozoites are characteristic of:
Maurer clefts are membrane structures in red cells infected with P. falciparum. P. vivax shows fine Schüffner dots instead, and Babesia produces no stippling.
Which feature best separates a Howell-Jolly body from Pappenheimer bodies on a Wright-stained smear?
A Howell-Jolly body is usually one smooth, round, dark purple DNA remnant. Pappenheimer bodies are small, irregular granules in clusters and are the ones that stain with Prussian blue.
Pappenheimer bodies are most expected on the smear of a patient with:
Pappenheimer bodies are iron granules in red cells, seen when iron is poorly used, as in sideroblastic anemia, or after splenectomy. Iron-deficient cells have no excess iron to form them.
Brown-black granular pigment inside circulating monocytes and neutrophils in a febrile traveler most suggests:
Phagocytes ingest hemozoin, the digestion product of hemoglobin made by Plasmodium, and it appears as brown-black pigment. Toxic granulation is dark blue-purple and fine, not brown-black.
A patient has microcytosis and a raised RBC count. Which smear finding favors beta-thalassemia trait over iron deficiency?
Thalassemia trait often shows target cells and basophilic stippling with relatively uniform cells. Pencil (elongated) cells and a high RDW are more typical of iron deficiency.
Most people with common hereditary elliptocytosis have:
Most carriers of common hereditary elliptocytosis have elliptocytes on the smear but mild or no hemolysis. Severe forms (such as pyropoikilosis) are uncommon.
Irreversibly sickled cells in sickle cell disease stay sickled after reoxygenation mainly because:
Repeated sickling causes membrane loss, dehydration and skeletal damage, so the cell keeps its shape even when the polymer melts on reoxygenation. The cells still contain HbS.
A 70-year-old has a normal WBC, no lymphadenopathy, and 2.1 × 10^9/L monoclonal B cells with a CLL-type phenotype. The best classification is:
Clonal B cells below 5 × 10^9/L without lymphadenopathy, organomegaly or cytopenias define monoclonal B-cell lymphocytosis. CLL requires at least 5 × 10^9/L clonal B cells in blood.
A 60-year-old with rheumatoid arthritis has persistent neutropenia and increased large granular lymphocytes that are CD3+, CD8+, CD57+ with clonal TCR rearrangement. The likely diagnosis is:
T-LGL leukemia is a clonal CD8+/CD57+ disorder often linked to rheumatoid arthritis and neutropenia; STAT3 mutations are common. Proving clonality separates it from reactive LGL expansion.
A young adult has large 'hallmark' cells with horseshoe nuclei that are strongly CD30+ and ALK-positive. The typical genetic change is:
ALK-positive anaplastic large cell lymphoma usually carries t(2;5), fusing NPM1 with ALK; it has a relatively good prognosis in young patients. t(11;14) is mantle cell lymphoma.
Blasts are negative for myeloperoxidase and Sudan black B by cytochemistry but express CD13, CD33 and CD117 by flow cytometry, with no lymphoid markers. The best category is:
AML with minimal differentiation has fewer than 3% MPO-positive blasts on cytochemistry, so myeloid markers by flow are needed for diagnosis. Undifferentiated leukemia lacks lineage-specific markers.
Six years after alkylating-agent chemotherapy for breast cancer, a woman has pancytopenia, dysplasia and loss of chromosome 7. The best category is:
Alkylating agents typically cause myeloid neoplasms 5–10 years later with dysplasia and -5/-7 abnormalities. Topoisomerase II inhibitor–related cases appear sooner, often with KMT2A rearrangement.
A JAK2- and CALR-negative patient with essential thrombocythemia should next be tested for mutations in:
The three driver genes of ET and primary myelofibrosis are JAK2, CALR and MPL (exon 10, e.g., W515). BCR::ABL1 should be excluded by fusion testing, but kinase-domain sequencing is for TKI resistance.
Using WHO 5th edition criteria, which hemoglobin level in a man meets the major hemoglobin criterion for polycythemia vera?
WHO uses Hb >165 g/L in men and >160 g/L in women (or Hct >49%/48%). The older 185 g/L value was from earlier criteria and missed early disease.
A 2-year-old has splenomegaly, monocytes 3 × 10^9/L, raised hemoglobin F, circulating myeloid precursors and a PTPN11 mutation. No BCR::ABL1 is found. The likely diagnosis is:
JMML is a childhood myeloid neoplasm driven by RAS-pathway mutations (PTPN11, NRAS, KRAS, NF1, CBL), with monocytosis ≥1 × 10^9/L and often high HbF; WHO 5th edition places it among the myeloproliferative neoplasms (the ICC keeps it as MDS/MPN). CMML occurs in older adults.
An infant with delayed separation of the umbilical cord, severe infections without pus and persistent neutrophilia most likely lacks which molecule?
Leukocyte adhesion deficiency type I lacks CD18, so neutrophils cannot adhere and leave vessels, causing high blood neutrophil counts and no pus at sites of infection. CD55 loss is seen in PNH.
A child has fever, mouth ulcers and neutropenia that recur about every 21 days, with normal counts between episodes. The likely gene involved is:
Cyclic neutropenia is caused by ELANE (neutrophil elastase) mutations, giving neutrophil nadirs about every 3 weeks. LYST mutation causes Chédiak-Higashi syndrome.
On a CD45 versus side-scatter flow cytometry plot of marrow, where do myeloblasts usually lie?
Blasts have weaker CD45 than mature leukocytes and little granularity, so they sit in the 'blast gate'. Bright CD45 with low side scatter is the lymphocyte region; high side scatter marks granulocytes.
A patient on high-dose corticosteroids is most likely to show which pattern?
Corticosteroids release neutrophils and reduce their exit into tissues, while lymphocytes and eosinophils fall. Eosinophilia can be seen when cortisol is lacking, as in adrenal insufficiency.
On a poorly spread wedge smear, large cells such as monocytes and neutrophils tend to collect at the:
Large cells are pushed to the edges and tail during spreading, so counting only there overestimates them. A proper battlement or systematic pattern in the monolayer area reduces this bias.