MLT GlobeDHA exam preparation (Dubai) – page 28
700 practice MCQs for the DHA medical laboratory exam. Level: Basic to intermediate.
A slim, non-pregnant 22-year-old has mild fasting hyperglycemia, negative islet autoantibodies, normal C-peptide, and diabetes in her mother and maternal grandfather. The most likely diagnosis is:
MODY is a monogenic, autosomal dominant form (e.g., GCK, HNF1A) with onset in young, often non-obese people, preserved C-peptide and no autoantibodies. LADA and type 1 are antibody-positive.
A patient with untreated iron deficiency anemia has an HbA1c of 6.6% (49 mmol/mol) but fasting glucose repeatedly near 95 mg/dL (5.3 mmol/L). The best explanation is:
Reduced red cell production in iron deficiency increases the average age of circulating cells, so they carry more glycated hemoglobin. HbA1c may fall after iron therapy. Shorter survival would lower HbA1c.
A patient with renal failure taking metformin has lactate 9 mmol/L (81 mg/dL), normal blood pressure and normal oxygen saturation. This is best classified as:
Type B lactic acidosis occurs without tissue hypoxia, for example from drugs such as metformin. Type A results from poor tissue oxygen delivery, such as shock or severe hypoxemia.
A patient with hypokalemia has a 24-hour urine potassium of 10 mmol/day. This most suggests potassium loss through the:
When potassium is lost outside the kidney, the kidney conserves it and urine K falls below about 20 mmol/day. Diuretics, mineralocorticoid excess and RTA all cause inappropriately high urine K.
A patient with profuse diarrhea has Na 138, Cl 115 and HCO3− 14 mmol/L. Which disorder is present?
Anion gap = 138 − (115 + 14) = 9 mmol/L, which is normal. Bicarbonate lost in stool is replaced by chloride, giving a hyperchloremic normal anion gap acidosis.
In the IFCC CK method (creatine phosphate + ADP → creatine + ATP), ATP is measured through hexokinase and G6PD coupled reactions. What is read?
ATP phosphorylates glucose (hexokinase); G6PD then oxidizes glucose-6-phosphate while reducing NADP+ to NADPH, so absorbance at 340 nm rises in proportion to CK activity.
By the Fourth Universal Definition, acute myocardial infarction requires a rise and/or fall of cardiac troponin with at least one value above the 99th percentile URL, plus:
Troponin changes alone define myocardial injury. Infarction also needs evidence of ischemia: symptoms, new ECG changes, imaging findings or a coronary thrombus.
After a crush injury, a patient has CK 45 000 U/L and red-brown urine. Dipstick blood is 3+ but urine microscopy shows no red cells, and the plasma is not pink. The urine pigment is most likely:
Myoglobin from damaged muscle is small, filtered quickly and gives a positive peroxidase (blood) reaction. Free hemoglobin would usually make the plasma pink; the very high CK points to rhabdomyolysis.
A non-drinker on long-term phenytoin has GGT 150 U/L with normal ALT, ALP and bilirubin. The most likely explanation is:
Phenytoin and other enzyme-inducing drugs increase hepatic GGT synthesis without liver damage, so an isolated GGT rise is common. Biliary obstruction would also raise ALP.
LD-1, the fastest-migrating lactate dehydrogenase isoenzyme, is composed of:
LD is a tetramer of H (heart) and M (muscle) subunits. LD-1 is H4, found in heart, red cells and kidney; LD-5 is M4, found in liver and skeletal muscle.
PCSK9 inhibitor drugs lower LDL cholesterol because PCSK9 normally:
PCSK9 binds the LDL receptor and directs it to lysosomes for destruction. Blocking PCSK9 leaves more receptors on liver cells to clear LDL. Gain-of-function PCSK9 mutations cause familial hypercholesterolemia.
Cholesteryl ester transfer protein (CETP) moves cholesteryl esters from HDL to:
CETP exchanges cholesteryl ester from HDL for triglyceride from VLDL and LDL. Low CETP activity is associated with high HDL cholesterol.
A jaundiced patient has a prolonged prothrombin time that corrects within 24–48 hours after parenteral vitamin K. This most suggests:
Without bile, fat-soluble vitamin K is poorly absorbed, but the liver can still make factors once vitamin K is given by injection. In cirrhosis the PT does not correct because synthesis is impaired.
The original MELD score, used to prioritize liver transplantation, is calculated from:
MELD uses serum bilirubin, INR and creatinine; later versions add sodium (MELD-Na) and albumin and sex (MELD 3.0). Albumin and ascites are parts of the Child–Pugh score.
Serum albumin is 2.8 g/dL (28 g/L) and ascitic fluid albumin is 1.2 g/dL (12 g/L), collected the same day. What is the serum–ascites albumin gradient (SAAG) and its meaning?
SAAG = 2.8 − 1.2 = 1.6 g/dL. A gradient of 1.1 g/dL (11 g/L) or more indicates portal hypertension, as in cirrhosis; a lower gradient suggests peritoneal causes.
A child with minimal change disease has highly selective proteinuria. The urine protein consists mainly of:
In selective glomerular proteinuria, only intermediate-size proteins such as albumin and transferrin pass the filter; large proteins like IgG are held back. Beta-2 microglobulin indicates tubular proteinuria.
A urine sample gives a negative protein dipstick but a positive sulfosalicylic acid test. This most suggests the presence of:
The dipstick protein pad reacts mainly with albumin, while sulfosalicylic acid precipitates all proteins, including Bence Jones light chains. Such a result calls for urine protein electrophoresis.
For cardiovascular risk assessment (AHA/CDC), which hs-CRP level indicates high risk in a person without acute illness?
hs-CRP below 1 mg/L is low risk, 1–3 mg/L average risk and above 3 mg/L high risk. Values above 10 mg/L suggest acute inflammation, and the test should be repeated later.
Newborn screening for many amino acid and fatty acid oxidation disorders from a single dried blood spot is performed by:
Tandem mass spectrometry measures many amino acids and acylcarnitines at once from one blood spot. The Guthrie test detected only phenylalanine and is now largely historical.
Blood for urea by the urease method was collected into an ammonium heparin tube. What effect is expected?
Urease methods measure ammonia released from urea, so ammonium ions from the anticoagulant add to the signal and falsely raise urea. Lithium heparin should be used instead.