SCFHS exam preparation (Saudi Arabia) – page 22
749 practice MCQs for the SCFHS medical laboratory exam. Level: Intermediate.
Methotrexate levels are monitored after high-dose therapy mainly to decide:
Delayed methotrexate clearance leads to severe toxicity; timed levels guide how much and how long leucovorin (folinic acid) is given.
A patient with rheumatoid arthritis has anemia. Which iron profile is most typical?
Inflammation raises hepcidin, trapping iron in stores: serum iron falls, TIBC is low or normal, and ferritin is normal or high. High TIBC with low ferritin fits iron deficiency.
Hepcidin controls body iron by:
Hepcidin binds ferroportin and causes its breakdown, reducing iron absorption from the gut and release from macrophages. Raised hepcidin in inflammation explains the low serum iron of chronic disease.
An EDTA sample hemolyzed during collection is analyzed. Which pattern is expected?
Lysed cells are not counted, lowering RBC and calculated Hct, but the released hemoglobin is still measured, so MCH and MCHC rise falsely. Hemoglobin itself is not reduced.
A lavender (EDTA) tube is filled with only a small amount of blood. The microhematocrit is likely to be:
Excess EDTA makes the sample hypertonic, water leaves the red cells and they pack more closely, lowering the spun hematocrit. Swelling occurs with delayed testing, not excess EDTA.
A laboratory runs a high-count sample three times followed by a low-count sample three times. The purpose is to check:
Carryover is the contamination of a sample by the one before it; comparing the first and third low-sample results against the high sample estimates it. Linearity is checked with serial dilutions across the reportable range.
In the fluorescent spot screening test for G6PD deficiency, a deficient sample is recognised because the spot:
Normal G6PD converts NADP to NADPH, which fluoresces under long-wave UV light; deficient samples produce little NADPH and show no fluorescence. Turbidity is the endpoint of the sickle solubility test, not the G6PD screen.
A urine sediment from a patient with chronic intravascular hemolysis is stained with Prussian blue. Blue granules in tubular cells indicate:
Filtered hemoglobin is taken up by renal tubular cells and stored as hemosiderin, which stains blue with Prussian blue; cells shed into urine show this a few days after hemolysis starts. Myoglobin does not form Prussian blue-positive granules in tubular cells.
Which direct antiglobulin test (DAT) pattern is most typical of warm autoimmune hemolytic anemia?
Warm AIHA is usually caused by IgG autoantibodies that react at 37°C, sometimes with complement fixation, and cells are removed in the spleen. A C3-only pattern is typical of cold agglutinin disease.
Both DIC and TTP show schistocytes and thrombocytopenia. Which result best supports TTP rather than DIC?
In TTP, platelet-rich microthrombi form without major consumption of clotting factors, so PT, aPTT and fibrinogen stay near normal. Prolonged clotting times and low fibrinogen point to DIC.
Which specimen condition can give a FALSE POSITIVE sickle solubility test?
Lipemia or very high plasma proteins make the solution turbid even without HbS. Severe anemia, recent transfusion and deteriorated reagent tend to cause false negatives, not false positives.
An adult has normal blood counts. HPLC shows HbA 58%, HbS 38%, HbA2 3.0% and HbF 1%. The most likely diagnosis is:
In sickle cell trait HbA is greater than HbS, with HbS usually 35–40% and normal indices. In sickle-beta+ thalassemia HbS exceeds HbA and the cells are microcytic.
A newborn screening result by HPLC is reported as 'FS' (HbF and HbS present, no HbA). The best interpretation is:
Absence of HbA with HbS present suggests HbSS or sickle-beta0 thalassemia, which must be confirmed on a repeat sample. Sickle cell trait in a newborn gives an 'FAS' pattern, with HbA present.
A child has severe mucosal bleeding and hemarthroses, undetectable VWF antigen and factor VIII activity of 3%. This is:
Type 3 vWD has virtually absent VWF, so factor VIII loses its carrier and falls very low. Type 2N has low factor VIII but normal VWF antigen.
A patient needs very high heparin doses but the aPTT barely changes. Antithrombin activity is 40%. The best explanation is:
Heparin works by accelerating antithrombin; low antithrombin reduces its effect. Lupus anticoagulant would prolong the baseline aPTT rather than blunt heparin response.
A negative D-dimer result in an outpatient with low clinical probability of DVT is useful because:
D-dimer is sensitive but not specific; a negative result with low pretest probability safely excludes VTE. Positive results occur in many conditions.
The prothrombin G20210A variant increases thrombosis risk mainly by:
This 3' untranslated region variant increases prothrombin mRNA stability and plasma prothrombin level. It does not change the structure of thrombin.
A PT sample is strongly icteric and lipemic, and the photo-optical analyzer gives an error. The best next step is:
High bilirubin and lipids interfere with light-based clot detection; mechanical (viscosity-based) systems are not affected. Diluting would change factor levels.
A boy has eczema, recurrent infections and thrombocytopenia with abnormally small platelets. The most likely diagnosis is:
Wiskott-Aldrich syndrome is X-linked, with microthrombocytes (low MPV), eczema and immunodeficiency. Bernard-Soulier and May-Hegglin show giant platelets.
A child with hereditary spherocytosis suddenly becomes very pale after a febrile illness, and the reticulocyte count falls to almost zero. The most likely cause is:
Parvovirus B19 infects erythroid progenitors (via the P antigen) and stops red cell production for about a week. In patients with shortened red cell survival this causes a transient aplastic crisis.