MLT GlobeQCHP exam preparation (Qatar) – page 28
749 practice MCQs for the QCHP medical laboratory exam. Level: Intermediate.
In the CK-MB immunoinhibition method, antibody to the M subunit is added and the remaining activity is multiplied by 2. Why?
Anti-M blocks CK-MM completely and the M half of CK-MB. The activity left is the B subunit of CK-MB (assuming no CK-BB), so doubling gives CK-MB activity.
CK activity falls in stored serum as its sulfhydryl groups oxidize. Which reagent component restores this activity?
N-acetylcysteine is a thiol reagent that reduces oxidized sulfhydryl groups and reactivates CK. Diadenosine pentaphosphate inhibits adenylate kinase; pyridoxal phosphate is the cofactor for aminotransferases.
Amylase measured on EDTA plasma gives a falsely low result because amylase requires:
Amylase is a calcium-containing metalloenzyme (also activated by chloride). EDTA and citrate chelate calcium and inhibit it, so serum or heparin plasma should be used.
A farmer has miosis, heavy salivation and bradycardia after pesticide spraying. Which result supports organophosphate poisoning?
Organophosphates irreversibly inhibit acetylcholinesterase (and serum butyrylcholinesterase), so acetylcholine accumulates. Red cell AChE best reflects inhibition at nerve synapses.
A 6-year-old has recurrent pancreatitis, eruptive xanthomas and triglycerides of 3000 mg/dL (34 mmol/L). Refrigerated plasma shows a creamy layer over a clear infranatant. The most likely defect is:
Familial chylomicronemia is caused by loss of lipoprotein lipase (or its activator apo C-II), so chylomicrons cannot be cleared. The clear infranatant shows VLDL is not raised, unlike type V.
Serum triglycerides are 177 mg/dL. Using 1 mmol/L = 88.5 mg/dL, what is the result in SI units?
177 ÷ 88.5 = 2.0 mmol/L. Dividing by 38.67 (the cholesterol factor) gives the wrong answer of 4.6 mmol/L.
Total cholesterol is 5.8 mmol/L, HDL cholesterol 1.1 mmol/L and measured LDL cholesterol 3.6 mmol/L. What is the remnant cholesterol (TC − HDL − LDL)?
5.8 − 1.1 − 3.6 = 1.1 mmol/L, the cholesterol carried in triglyceride-rich lipoproteins (VLDL, IDL, remnants). 4.7 mmol/L is the non-HDL cholesterol.
A child has unconjugated bilirubin of 12 mg/dL (205 µmol/L) that falls by more than 25% on phenobarbital treatment. Liver enzymes are normal. The most likely diagnosis is:
Type II (Arias syndrome) has some UGT1A1 activity that phenobarbital can induce, lowering bilirubin. Type I has no activity and does not respond. Dubin–Johnson and Rotor cause conjugated hyperbilirubinemia.
About 80% of the bilirubin produced each day comes from:
An adult produces about 250–350 mg (4–6 mmol) bilirubin daily, mostly from senescent red cells destroyed by macrophages. The rest comes from ineffective erythropoiesis and other heme proteins.
A patient with fulminant liver failure becomes hypoglycemic. The main cause is:
The liver maintains fasting glucose through glycogenolysis and gluconeogenesis. Massive hepatocyte loss removes both; reduced hepatic insulin clearance adds to the problem. Glucose must be checked often.
A newborn screening test shows high blood phenylalanine. The classic form of this disorder is caused by deficiency of:
Classic phenylketonuria is phenylalanine hydroxylase deficiency, which blocks conversion of phenylalanine to tyrosine. Tyrosinase deficiency causes albinism.
An adult's urine turns black on standing; he also has dark ear cartilage and early arthritis. Which substance accumulates?
Alkaptonuria is a homogentisate 1,2-dioxygenase deficiency. Homogentisic acid oxidizes to a black pigment in urine and deposits in connective tissue (ochronosis).
According to KDIGO, which change in serum creatinine meets the definition of acute kidney injury?
KDIGO defines AKI as a rise of ≥0.3 mg/dL (≥26.5 µmol/L) within 48 hours, or ≥1.5 times baseline within 7 days, or low urine output. A single value above range does not define AKI.
A lab finds some therapeutic drug levels are lower in gel separator tubes than in plain red-top tubes held for the same time. The best explanation is:
Some lipophilic drugs (e.g. certain anticonvulsants and tricyclic antidepressants) can be absorbed into the gel, especially with long contact. Many labs therefore use plain tubes for TDM.
Why is a hemolyzed sample unsuitable for neuron-specific enolase (NSE) measurement in small cell lung cancer?
NSE is present in erythrocytes and platelets, so hemolysis or delayed separation releases it and falsely raises results. Samples should be separated promptly and not hemolyzed.
A patient with thalassemia receives regular transfusions. Roughly how much iron does each unit of red cells add to body stores?
Each unit of red cells contains about 200–250 mg of iron, and the body has no active way to excrete it. Repeated transfusion therefore leads to iron overload needing chelation.
A patient took an oral iron tablet 2 hours before a blood sample for iron studies. What is the expected effect?
Absorbed iron raises serum iron and transferrin saturation for several hours. Iron supplements should be stopped at least 24 hours before testing. Ferritin does not change rapidly.
A patient's MCV was 88 fL yesterday and is 104 fL today, with no transfusion and normal other parameters in the run. The first thing to investigate is:
MCV changes very slowly because red cells live about 120 days, so a large sudden change fails the delta check and suggests a mislabeled or wrong-patient sample. Nutritional causes cannot change MCV in one day.
In the osmotic fragility test, red cells are placed in graded saline solutions, and the amount of lysis in each tube is measured by:
After incubation and centrifugation, released hemoglobin is read at about 540 nm and expressed as a percentage of full lysis in water. The curve shifts right when fragility is increased.
A 2-year-old with HbSS suddenly becomes pale, with a rapidly enlarging spleen, Hb falling from 8.0 to 4.0 g/dL (80 to 40 g/L) and a high reticulocyte count. This is most likely:
Sudden pooling of sickled cells in a still-functioning spleen causes rapid anemia with splenic enlargement while the marrow keeps responding. In an aplastic crisis the reticulocyte count falls to near zero and the spleen does not enlarge.