FNP: Type 2 Diabetes

Duloxetine is a serotonin-norepinephrine reuptake inhibitor that effectively treats both depression and neuropathic pain. Its pharmacodynamic profile involves the inhibition of both serotonin and norepinephrine reuptake. This dual action modulates descending pain pathways in the spinal cord, which rely heavily on norepinephrine and serotonin to suppress incoming pain signals. Option D correctly identifies this mechanism. Option A is incorrect because duloxetine lacks significant dopamine reuptake inhibition. Options B and C are incorrect because duloxetine does not primarily act on histamine or glutamate to relieve pain, and pain modulation by this class of medications occurs primarily via descending inhibitory pathways rather than ascending tracts.

Proper sick day management dictates that patients with type 1 diabetes should never stop their basal insulin, even if they are vomiting or unable to eat solid foods. Illness and infection trigger counter-regulatory hormones that increase insulin resistance and hepatic glucose production, raising the risk for diabetic ketoacidosis. Option B is correct because continuing the basal dose provides the necessary background insulin to suppress ketogenesis. Option A is dangerous and directly leads to ketoacidosis. Option C is incorrect because doubling the basal dose without a specific sliding scale or continuous monitoring risks severe delayed hypoglycemia once the illness resolves. Option D is inappropriate because rapid-acting insulin is meant for prandial coverage or acute correction, not for maintaining stable background metabolic control over twenty-four hours.

Mild hyperkalemia up to 5.5 mEq/L is common when treating diabetic nephropathy with an ACE inhibitor. Because the renal protective benefits of the drug are crucial and the creatinine is stable, the best initial approach is to implement a low-potassium diet rather than stopping the medication. Option A is incorrect because stopping the drug deprives the patient of essential proteinuria reduction, and 5.2 mEq/L is not acutely life-threatening. Option C is incorrect because while a thiazide might lower potassium, it lacks the specific renoprotective effects needed for diabetic nephropathy. Option D is a massive overreaction, as mild asymptomatic hyperkalemia in the outpatient setting does not require inpatient cardiac monitoring.

When a patient experiences recurrent hypoglycemia without a clear precipitating cause, the basal insulin dose should be decreased by 10-20%. Option A is correct because reducing the 24-unit dose by 4 units (approximately 15-20%) safely mitigates the hypoglycemia risk, which is particularly dangerous in CKD due to delayed insulin clearance. Option B is incorrect because "feeding the insulin" with extra carbohydrates promotes weight gain and erratic glycemic control. Option C is incorrect because a 10-unit drop is nearly a 40% reduction, which is too drastic and risks rebound hyperglycemia. Option D is incorrect because sulfonylureas carry a high risk of severe, prolonged hypoglycemia, especially in older adults with reduced renal function.

The anterior lower leg is an area with notoriously poor vascular supply, a problem significantly compounded in diabetic patients. Creating a full-thickness defect in this area carries a high risk of poor healing and secondary infection. Therefore, a shave biopsy is the safest choice for a raised nodule, as it remains superficial and preserves the deeper dermal vascular plexus, allowing for faster secondary intention healing. Option A is incorrect because leaving a deep punch biopsy open on a diabetic leg almost guarantees a chronic ulcer. Option C is incorrect because a wide excisional biopsy creates an unnecessarily large full-thickness defect for an initial diagnosis. Option D is incorrect because even with sutures, full-thickness punch defects on the lower legs of diabetics frequently experience dehiscence and delayed healing due to high skin tension and poor perfusion.