Dry Mouth in a Cancer Survivor with Diabetes

Correct answer: D. His radiation therapy

• A. Incorrect — this is a strong contributor. Multiple agents with even modest anticholinergic activity summate, and cumulative anticholinergic burden is a well-recognized cause of dry mouth.
• B. Incorrect — this is a strong contributor. Hyperglycemia causes osmotic diuresis and dehydration, and diabetic autonomic neuropathy impairs the parasympathetic drive to the salivary glands.
• C. Incorrect — this is a strong contributor. Tricyclic antidepressants have potent antimuscarinic activity and are among the most reliably xerostomic drugs in clinical use.
• D. Correct — this is the least likely cause. Radiation damages salivary tissue only when the glands lie within the treatment field. His radiation was directed at the pelvis, anatomically remote from the parotid, submandibular, and sublingual glands, so it has no bearing on his salivary function.

Note: When head and neck radiation is the cause, the pattern is different: a dose above roughly 26 Gy to the parotid produces largely irreversible hypofunction, whereas drug-induced xerostomia typically improves if the agent can be changed.

Correct answer: B. Increased cellular resistance to insulin

• A. Incorrect. Autoimmune destruction of beta cells defines type 1 diabetes, which typically presents in childhood or adolescence with absolute insulin deficiency and a tendency to ketoacidosis.
• B. Correct. Type 2 diabetes begins with peripheral insulin resistance in muscle, liver, and adipose tissue. The pancreas compensates with hyperinsulinemia, and hyperglycemia emerges only when beta cell output can no longer keep pace with the demand.
• C. Incorrect. An insulinoma secretes excess insulin and causes hypoglycemia, the opposite metabolic problem.
• D. Incorrect. Cortisol excess describes Cushing syndrome, which can produce secondary hyperglycemia but is a distinct endocrine disorder with its own characteristic physical findings.

Correct answer: D. 3 months

• A. Incorrect. A two-week window is what fructosamine measures, reflecting glycated serum proteins with a much shorter turnover.
• B. Incorrect. Twelve months is far beyond the lifespan of any circulating cell used for glycemic monitoring.
• C. Incorrect. Six months exceeds red cell lifespan. No single glycemic marker covers that period.
• D. Correct. The measurement reflects the lifespan of the erythrocyte, roughly 120 days, so it captures average glycemia over the preceding 2 to 3 months. The most recent weeks are weighted somewhat more heavily than the earliest.

Note: Interpretation thresholds: below 5.7% is normal, 5.7 to 6.4% indicates prediabetes, 6.5% or above is diagnostic of diabetes, and below 7% is the general treatment target. His 8.4% represents poor control, and above 8% elective surgical procedures warrant caution and medical consultation.

Correct answer: A. Glycated hemoglobin

• A. Correct. Glucose binds non-enzymatically and irreversibly to the N-terminal valine of the hemoglobin beta chain. The proportion of hemoglobin so modified rises in direct relation to ambient glucose concentration over the life of the cell.
• B. Incorrect. C-peptide is released in equimolar amounts with endogenous insulin and is used to assess residual beta cell function, not glycemic control.
• C. Incorrect. Fructosamine measures glycated serum proteins, chiefly albumin, over a 2 to 3 week window. It is useful when hemoglobin A1c is unreliable, such as in hemoglobinopathies.
• D. Incorrect. Fasting plasma glucose is a single point-in-time measurement taken after an overnight fast. It says nothing about long-term control.