MLT GlobeChemistry: Enzymes & cardiac markers – page 7
132 Chemistry MCQs on Enzymes & cardiac markers with answers and explanations.
A patient with stage 5 chronic kidney disease has chest discomfort. hs-cTnT is 40 ng/L (99th percentile 14 ng/L) at 0 h and 41 ng/L at 3 h. The best interpretation is:
Acute MI needs a rising and/or falling troponin pattern with clinical evidence of ischemia. A stable value above the 99th percentile indicates chronic myocardial injury, common in CKD.
An asymptomatic patient has troponin I 600 ng/L with a normal ECG. The same sample gives <5 ng/L on another manufacturer's assay. The most likely cause is:
Large disagreement between immunoassays in a clinically unlikely setting suggests interfering antibodies (heterophile or macro-troponin). Blocking reagents or dilution studies can confirm this.
A heart failure patient is started on sacubitril/valsartan. Which natriuretic peptide test is preferred for monitoring?
Sacubitril inhibits neprilysin, which breaks down BNP, so BNP rises from the drug itself. NT-proBNP is not a neprilysin substrate and better reflects cardiac status.
A patient has persistently raised serum amylase, normal lipase, and a low amylase-to-creatinine clearance ratio. No abdominal pain. The most likely cause is:
Macroamylase is amylase bound to immunoglobulin; it is too large to be filtered, so serum amylase stays high while urine amylase is low. Lipase is normal and there is no pancreatic disease.
Which additives are needed in lipase reagents so that the assay is specific and fully active for pancreatic lipase?
Pancreatic lipase needs colipase and bile salts to act at the oil–water interface; bile salts also inhibit other esterases. P5P is a cofactor for aminotransferases.
A patient has prolonged apnea after succinylcholine. Serum cholinesterase is low and the dibucaine number is 20%. This suggests:
Dibucaine inhibits normal pseudocholinesterase by about 80%; a dibucaine number near 20% indicates the homozygous atypical variant, which cannot break down succinylcholine efficiently.
An uncompetitive inhibitor binds only to the enzyme–substrate complex. What is its effect on the kinetic constants?
By removing ES complex, an uncompetitive inhibitor lowers Vmax and also lowers apparent Km, giving parallel lines on a Lineweaver–Burk plot. Km rising with Vmax unchanged is competitive inhibition.
An NADH-linked assay gives ΔA/min of 0.050 at 340 nm. Total volume 1.0 mL, sample 0.05 mL, light path 1 cm, NADH molar absorptivity 6220 L·mol⁻¹·cm⁻¹. What is the enzyme activity?
U/L = (ΔA/min × total volume × 10⁶) ÷ (ε × path × sample volume) = (0.050 × 1.0 × 10⁶) ÷ (6220 × 1 × 0.05) = 50 000 ÷ 311 ≈ 161 U/L.
An elderly woman without chest pain has CK-MB by immunoinhibition of 60 U/L with total CK 90 U/L. CK-MB mass by immunoassay is normal. The most likely cause is:
Immunoinhibition treats all non-M activity as MB, so CK-BB in a macro-complex gives a falsely high CK-MB, often a large share of total CK. A mass assay using MB-specific antibodies is not affected.
A person of blood group O who is a secretor has a mildly raised ALP after a fatty meal; a fasting repeat sample is normal. The extra ALP most likely came from:
Intestinal ALP enters the blood after fatty meals, especially in group O and B secretors. For this reason ALP is best measured on a fasting sample.
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.
During recovery from acute viral hepatitis, ALT stays raised longer than AST mainly because:
ALT has a half-life of about 47 hours compared with about 17 hours for AST, so AST falls faster once liver cell damage stops.