Type 1 vs. Type 2 Pathophysiology

Type 1 diabetes results from autoimmune destruction of pancreatic beta cells, causing absolute insulin deficiency; these patients require exogenous insulin for life and are prone to DKA due to complete lack of insulin. Type 2 diabetes involves insulin resistance with relative insulin deficiency, often linked to obesity, and can initially be managed with lifestyle changes and oral agents like metformin before insulin is needed; these patients are more prone to HHS than DKA because they retain some insulin production. A1C reflects average glucose over 2-3 months, with a goal generally under 7% for most adults.

Chronic Complications and Screening

Diabetic retinopathy requires annual dilated eye exams to catch changes before vision loss occurs. Diabetic nephropathy is screened with annual urine microalbumin testing, and ACE inhibitors are protective even without hypertension. Peripheral neuropathy causes loss of protective sensation, making daily foot inspection essential — teach patients to check feet with a mirror, never walk barefoot, wear well-fitting shoes, and see a podiatrist for nail care rather than self-trimming. Autonomic neuropathy can cause gastroparesis and silent MI, meaning chest pain may be absent even during cardiac events.

Sick-Day Rules and Glucose Monitoring

During illness, insulin needs typically increase due to stress hormones raising glucose, even if the patient is eating less — never stop insulin during illness. Teach patients to check blood glucose and ketones every 2-4 hours when sick, continue taking insulin, stay hydrated, and contact the provider if glucose exceeds 240 mg/dL with ketones present or if unable to keep fluids down. Metformin should be held before procedures using contrast dye due to lactic acidosis risk, and resumed only after renal function is confirmed stable 48 hours later.