MLT GlobeSCFHS exam preparation (Saudi Arabia) – page 37
749 practice MCQs for the SCFHS medical laboratory exam. Level: Intermediate.
A patient with severe abdominal pain has CT evidence of acute pancreatitis, grossly lipemic serum (triglycerides 4000 mg/dL, 45 mmol/L) and a normal amylase. The best explanation is:
In hypertriglyceridemia-induced pancreatitis, lipemic serum can suppress measured amylase. Diagnosis rests on imaging and lipase, and diluting or clearing the sample helps.
ALT is 400 U/L (upper limit 40) and ALP is 240 U/L (upper limit 120). Using R = (ALT ÷ ALT ULN) ÷ (ALP ÷ ALP ULN), the liver injury pattern is:
ALT is 10 × ULN and ALP is 2 × ULN, so R = 10 ÷ 2 = 5, a hepatocellular pattern. The R ratio is widely used to classify drug-induced liver injury.
A patient with stage 4 chronic kidney disease and no evidence of plasma cell disease has a serum free kappa/lambda ratio of 2.1. The best interpretation is:
Kappa is cleared faster by the kidney than dimeric lambda, so in renal failure both rise and the ratio increases. A renal reference range of about 0.37–3.1 is used instead of 0.26–1.65.
A woman heterozygous for a G6PD-deficient allele has a normal G6PD screening test. The best explanation is:
Random X-inactivation (lyonization) makes heterozygous women mosaics; the normal cell population can give a normal screen, so quantitative or cytochemical testing may be needed. The G6PD gene is on the X chromosome.
A 17-year-old has DAT-negative hemolytic anemia, raised liver enzymes and a new tremor. Which test is most useful next?
Wilson disease can present with acute hemolysis when copper is released from the liver, along with liver and neurological signs. Low ceruloplasmin supports the diagnosis; lead causes stippling and anemia but not this combination.
A hemophilia A patient on emicizumab prophylaxis has a very short aPTT. Why is a one-stage aPTT-based factor VIII assay unreliable?
Emicizumab is a bispecific antibody that bridges factors IXa and X, acting like VIIIa and strongly shortening the aPTT. Chromogenic assays using bovine reagents are used to measure the patient's own factor VIII.
A patient with AL amyloidosis has an isolated low factor X with prolonged PT and aPTT, and no inhibitor. The mechanism is:
Amyloid fibrils bind factor X and remove it from the circulation, a known acquired factor X deficiency. Vitamin K deficiency lowers II, VII, IX and X together.
A patient with lifelong bleeding has low factor VIII (15%) but normal VWF antigen and ristocetin cofactor. Father and mother both have mild symptoms. Which test best separates type 2N vWD from mild hemophilia A?
Type 2N VWF cannot bind and protect factor VIII, so VIII is low despite normal VWF levels; the VWF:FVIIIB assay shows this. Its autosomal pattern also differs from X-linked hemophilia.
A thromboelastography (TEG) tracing from a bleeding surgical patient shows a normal R time but a very low maximum amplitude (MA). This mainly suggests:
R time reflects time to initial fibrin (clotting factors, heparin effect), while MA reflects clot strength, which depends mainly on platelets and fibrinogen. Heparin prolongs the R time.
A young man has microcytic anemia with ring sideroblasts in the marrow. His maternal uncle had the same disorder, and his Hb improves with pyridoxine. Which enzyme is most likely defective?
X-linked sideroblastic anemia is caused by ALAS2 mutations; pyridoxal phosphate is its cofactor, so some cases respond to pyridoxine. Ferrochelatase defects cause erythropoietic protoporphyria.
An adult has chorea, raised creatine kinase, normal plasma lipids and normal Kell antigens. The smear shows many acanthocytes. The most likely diagnosis is:
Neuroacanthocytosis syndromes combine movement disorders, muscle damage and acanthocytes with normal lipids. Normal Kell antigens argue against McLeod syndrome, and normal lipids argue against abetalipoproteinemia.
During a hemolytic crisis in G6PD deficiency, the smear shows cells whose hemoglobin is pulled to one side, leaving a clear membrane 'bubble' at the edge. These are called:
Oxidant damage causes hemoglobin to retract from part of the membrane, creating a clear blister-like area; these cells are called blister cells or hemighosts. Stomatocytes have a slit-like central pallor instead.
A CML patient responding well to imatinib shows rising BCR::ABL1 levels. Kinase domain sequencing finds T315I. What does this mean?
The T315I 'gatekeeper' mutation blocks binding of imatinib, dasatinib, nilotinib and bosutinib; ponatinib or asciminib are options. A higher imatinib dose does not overcome this mutation.
Circulating Sézary cells in a patient with erythroderma typically show which immunophenotype?
Sézary cells are mature helper T cells (CD4+) that commonly lose CD7 and CD26, which helps count them by flow cytometry. CD8+/CD57+ fits T-cell large granular lymphocytic leukemia.
A paraffin ribbon curves to one side during sectioning on a rotary microtome. The most likely cause is:
When the upper and lower block edges are not parallel (or the block is wedge-shaped), one side of each section is longer and the ribbon curves. Trimming the edges parallel corrects it.
A patient with rapidly progressive diffuse skin thickening develops sudden hypertension and acute kidney injury. Which autoantibody carries the highest risk for this complication?
Anti-RNA polymerase III is linked to diffuse cutaneous systemic sclerosis and scleroderma renal crisis. Anti-centromere is associated with limited cutaneous disease and a lower risk of renal crisis.
An infant has severe combined immunodeficiency with absent T cells but normal B-cell numbers. A defect in the receptor for which cytokine, essential for early T-cell development, is a known cause?
IL-7 signalling through IL-7Rα is required for thymocyte development; its loss causes T-negative, B-positive, NK-positive SCID. IL-5 acts on eosinophils.
A naive T cell binds its specific peptide–MHC complex on a cell that lacks B7 costimulatory molecules. The most likely outcome is:
Signal 1 without signal 2 makes the T cell anergic, a mechanism of peripheral tolerance. Clonal expansion needs both signals; class switching is a B-cell event.
Class switch recombination and somatic hypermutation in activated B cells both require:
AID deaminates cytidine in switch and variable-region DNA, starting both processes in germinal centres. RAG enzymes act earlier, during V(D)J recombination.
Which immunoglobulin classes lack a hinge region and instead have an extra heavy-chain constant domain (CH4)?
μ and ε heavy chains have four constant domains and no true hinge. IgG, IgA and IgD have three constant domains plus a flexible hinge.