MLT GlobeChemistry: Carbohydrates & diabetes – page 5
121 Chemistry MCQs on Carbohydrates & diabetes with answers and explanations.
A patient with sickle cell disease needs monitoring of glycemic control. Which test is a suitable alternative to HbA1c?
Fructosamine measures glycated serum proteins (mainly albumin) and is not affected by red cell survival or Hb variants. C-peptide measures insulin secretion, not glycemic control.
HbA1c is formed by the non-enzymatic attachment of glucose to:
HbA1c is defined as hemoglobin with glucose bound as a stable ketoamine to the N-terminal valine of the beta chain. Glycated albumin is measured as fructosamine.
A laboratory reports HbA1c in IFCC units. Which value corresponds to the ADA diabetes cut-off of 6.5%?
6.5% (NGSP/DCCT) equals 48 mmol/mol (IFCC). 39 mmol/mol equals 5.7%, the lower limit of prediabetes.
The nitroprusside reaction used in urine ketone strips reacts mainly with:
Nitroprusside reacts strongly with acetoacetate, weakly with acetone (if glycine is present), and not at all with beta-hydroxybutyrate. Lactate is not a ketone body.
An elderly type 2 diabetic has glucose 980 mg/dL (54 mmol/L), serum osmolality 350 mOsm/kg, pH 7.36, bicarbonate 23 mmol/L and trace ketones. This is most consistent with:
Very high glucose and osmolality with near-normal pH and bicarbonate and minimal ketones define HHS. DKA would show acidosis (pH below 7.30, low bicarbonate) and marked ketonemia.
A non-diabetic nurse has glucose 38 mg/dL (2.1 mmol/L), very high insulin and very low C-peptide. The most likely cause is:
Pharmaceutical insulin contains no C-peptide and suppresses the patient's own secretion, so insulin is high and C-peptide low. Insulinoma and sulfonylureas raise both insulin and C-peptide.
Which antibodies support a diagnosis of autoimmune (type 1) diabetes?
Antibodies to GAD65, IA-2 (tyrosine phosphatase), ZnT8 and insulin mark beta-cell autoimmunity. Anti-TPO antibodies indicate autoimmune thyroid disease.
Albuminuria in a diabetic patient is confirmed when the urine albumin-to-creatinine ratio is at least:
Moderately increased albuminuria is ACR 30–299 mg/g, confirmed in at least 2 of 3 samples over 3–6 months because of day-to-day variation. One random sample is not enough.
According to ADA, level 2 (clinically significant) hypoglycemia is a glucose below:
Level 1 is below 70 mg/dL (3.9 mmol/L); level 2 is below 54 mg/dL (3.0 mmol/L); level 3 is defined by severe altered mental status, not a number.
A neonate with a hematocrit of 70% has a point-of-care meter glucose that is much lower than the laboratory plasma glucose. Most likely cause?
Many glucose meters read falsely low at high hematocrit, because less plasma reaches the strip. Glycolysis in the laboratory tube would make the laboratory value lower, not higher.
In a person with normal kidneys, glucose usually appears in the urine when plasma glucose exceeds about:
The renal threshold for glucose is about 160–180 mg/dL (9–10 mmol/L); above this the tubular reabsorption capacity is exceeded and glycosuria occurs.
A non-pregnant adult has a 75 g OGTT: fasting glucose 92 mg/dL (5.1 mmol/L) and 2-hour glucose 165 mg/dL (9.2 mmol/L). By ADA criteria this is:
A 2-hour value of 140–199 mg/dL (7.8–11.0 mmol/L) defines impaired glucose tolerance (prediabetes). The fasting value is below 100 mg/dL, so it is not impaired fasting glucose.
A breastfed 2-week-old with vomiting, jaundice and poor weight gain has a positive copper-reduction urine test but a negative glucose oxidase dipstick. Which enzyme is most likely deficient?
Classic galactosemia (GALT deficiency) causes galactose accumulation after milk feeding. Galactose is a reducing sugar detected by copper reduction but not by the glucose-specific glucose oxidase strip.
Calculate HOMA-IR for fasting glucose 5.0 mmol/L and fasting insulin 18 µU/mL. [HOMA-IR = glucose (mmol/L) × insulin (µU/mL) ÷ 22.5]
HOMA-IR = 5.0 × 18 ÷ 22.5 = 90 ÷ 22.5 = 4.0. Higher values indicate greater insulin resistance; cut-offs vary between populations.
A patient with diabetic ketoacidosis has Na 135, K 5.0, Cl 95 and HCO3 8 mmol/L. What is the anion gap, calculated as Na − (Cl + HCO3)?
135 − (95 + 8) = 32 mmol/L, a high anion gap caused by unmeasured ketoacid anions. 37 would be the result if potassium were wrongly added.
A peritoneal dialysis patient using icodextrin has a meter glucose of 250 mg/dL, while laboratory hexokinase glucose is 95 mg/dL. The meter most likely uses:
Icodextrin is metabolized to maltose. GDH-PQQ enzymes are not glucose-specific and react with maltose, giving dangerously high false readings. Glucose oxidase is specific for glucose.
In the enzymatic β-hydroxybutyrate assay, β-hydroxybutyrate dehydrogenase converts β-hydroxybutyrate to acetoacetate. What is measured?
The reaction uses NAD+ as coenzyme, so NADH is produced and the absorbance at 340 nm rises in proportion to β-hydroxybutyrate. Nitroprusside does not react with β-hydroxybutyrate.
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.
Why is C-peptide, rather than insulin, used to assess the body's own insulin secretion in a patient treated with insulin injections?
C-peptide is released in equal amounts with insulin from proinsulin, but commercial insulin lacks it, so C-peptide reflects endogenous secretion only. It is cleared by the kidney and rises in renal failure.
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.