Lecture 11: Glucose Regulation Part 2

Lecture 11: Glucose Regulation Part 2 Overall Diabetes Overview! 1) Type 1 Diabetes · insulin deficiency due to destruction of beta cells (autoimmune or genetic) · Tx: Insulin, beta cell transplant 2) Type 2 Diabetes · relative insulin deficiency, insulin resistance often due to lifestyle (obesity) or genetics · Tx: weight loss, diet, exercise, antidiabetic drugs & insulin if none of that works 3) Type 3 Diabetes · induced by pancreatic disease · Tx: insulin (DM 1 protocol) until recovery (if not full recovery maybe DM2) -> also antidiabetic drugs 4) Type 4 Diabetes · gestational diabetes from pregnancy hormones that cause insulin resistance ↳ should return back to normal after baby is born, if not then DM2 Tx protocol ↳ glucose checks done at 24 weeks (OGTT test) · Tx: diet and/or insulin until delivery Beta Cell Transplant · Another treatment choice for DM 1 · beta cell transplant + immunosuppressant drugs (eg. Tacrolimus -> T-cell suppression) ↳ challenges: donor numbers, chronic immunosuppression (risk of infection) · 2-3 infusions of islet cells required (over time) Hypoglycemia Protocol "15-15 rule" · give l5g of glucose and reassess in 15 minutes · S&S: blood glucose < 4mmol/L · conscious or unconscious? ↳ PO or IV fluids & IM Antidiabetic Agents: 1. Biguinides 2. Incretin Enhancers (GLP-1 agonist) 3. Sulphonylureas 4. SGLT2 Inhibitors 1) Biguinides · MOA: decreases glucose absorption, increases glucose tissue uptake, and decreased glucogenesis (liver, inhibit AMPK enzyme) · drug: Metformin (Glucophage), PO - -glutide suffix 2) Incretin Enhancers (GLP-1 agonists) · MOA: binds GLP-1 receptors (beta cell) & stimulates satiety -> decreased appetite and GI glucose uptake (Stops producing glucagon) · drugs: Dulaglutide (Trulicity, SC), Semaglutide (ozempic, Rybelsus, SC) ↳ ozempic was used for weight loss so they created Wegovy so diabetics could still have their meds - 3) Sulphonylureas · MOA: increases beta cell synthesis (risk of hypoglycemia) ↳ stimulates the release of insulin from beta cells and increases sensitivity of insulin receptors on target cells · drug: Glyburide (Diabeta) u s e 4) SGLT2 Inhibitors · MOA: increases renal glucose excretion ↳ uptake of glucose into cells is unchanged still so may still experience fatigue · drug: Sanagliflozin (Invokana) a i Hyperosmolar Hyperglycemic State (HHS) · instead of DKA, DM2 may develop HHS · HHS has similar symptomology to DKA, but the body has just enough insulin to prevent the high ketones found in DKA · risk factors: infection, poor BG control · main symptom: dehydration! ↳ affects LOC, due to hyperosmolality (320 mmol/L) & hyperglycemia (32 mmol/L) · Tx: rehydrate, recover potassium, Tx underlying cause Keto Diet is Not Great · its a low carb diet that relies on fat intake (fatty acids) · because fats are main energy source, metabolism leads to high Ketones ↳ ketoacidosis · Tests: cholesterol, triglycerides, LDL, HDL, liver enzymes, GFR, CBC, BG, lactate · Risks: CAD risk, liver stress, Kidney stress, GI stress, low glucose to CNS CBC = info on WBC & hemoglobin DIC panel = info on coagulation and clotting END OF 216A