Chapter 38: Agents to Control Blood Glucose Levels

Glucose homeostasis is maintained primarily by the pancreatic hormones insulin (released by beta cells in response to high glucose and incretins like glucagon-like polypeptide-1 (GLP-1), promoting cellular glucose uptake and energy storage) and glucagon (released by alpha cells in response to low glucose, mobilizing liver glycogen). The regulatory balance is further influenced by adiponectin (which increases insulin sensitivity), endocannabinoid receptors (which promote energy gain and insulin resistance), and various stress hormones, which can exacerbate instability, leading to states of hyperglycemia (elevated blood glucose levels leading to fatigue, polyphagia, polydipsia, and glycosuria) or hypoglycemia (blood sugar 70 mg/dL or lower). Diagnosis relies on markers like fasting blood glucose and glycosylated hemoglobin (HbA1c), which provides a 3-month average of glucose exposure. Treatment protocols emphasize diet and exercise as foundational, supplemented by drugs categorized based on their mechanism of action. Insulin replacement therapy, the definitive treatment for Type 1 DM and severe Type 2 DM, is administered parenterally via various preparations (e.g., rapid-acting, long-acting, inhaled), requiring precise dosing, site rotation, and strict management during stress, pregnancy, and lactation. For Type 2 DM, oral and injectable non-insulin agents are used, including sulfonylureas, which stimulate insulin release from functioning beta cells; the biguanide metformin, often the first-line therapy, which decreases hepatic glucose output and increases glucose uptake; thiazolidinediones, which reduce insulin resistance but carry a Black Box Warning for increased heart failure risk; alpha-glucosidase inhibitors, which delay glucose absorption; and newer classes like dipeptidyl peptidase-4 (DPP-4) inhibitors (which prolong GLP-1 effects) and GLP-1 receptor agonists (which increase insulin secretion and promote satiety), noting the latter's risk for thyroid C-cell tumors. The newest class, sodium–glucose cotransporter-2 (SGLT-2) inhibitors (e.g., canagliflozin), block renal glucose reabsorption, resulting in glucose excretion and risk of dehydration or urinary tract infections. If glucose levels drop dangerously low, glucose-elevating agents like parenteral glucagon or oral diazoxide are utilized to restore normoglycemia quickly by accelerating glycogen breakdown in the liver. Nursing care is crucial, focusing on continuous blood glucose monitoring, comprehensive patient education regarding proper administration techniques (including disposal of sharps), recognizing adverse effects, managing drug interactions (e.g., beta-blockers masking hypoglycemia signs), and adjusting therapy across the lifespan. Special characteristics are unable to be transferred to youtube.