click below
click below
Normal Size Small Size show me how
Endo pancreas pharm
Disorders & Tumors of the Endocrine Pancrease Pharmacology
| Question | Answer |
|---|---|
| Management of severe hypoglycemia related to high insulin levels from insulinoma (pancreatic islet cell adenoma) | Rapid restoration of blood glucose to prevent brain damage (I.V. concentrated solution of Dextrose); Maintain normal blood glucose (lower Dextrose concentration); Discover and reverse cause of increased insulin (drugs, resection of tumor); Follow-up |
| Reactive hypoglycemia | Person has inherited or acquired insulin resistance; When they eat carbs their body has exaggerated insulin secretion; This leads to hypoglycemia and adrenergic response |
| Management of Reactive Hypoglycemia | Diet-decrease carb challenge; Alpha-glucosidase inhibitors (inhibit the breakdown of carbs, thus they can't be absorved); Parenteral glucagon (Increase hepatic glucose release); Insulin secretion antagonists |
| Symptoms/Findings of gastrinoma/Zollinger-Ellison Syndrome | Prominent gastric folds and multiple ulcers in upper G.I., and diarrhea due to gastrin secreting tumor in the pancreas. Could be part of MEN-1 and have symptoms indicative of parathyroid or pitiutary tumors as well. |
| Treatment for Gastrinoma | Surgical resection & proton pump inhibitors (PPIs) to treat excessive acid production. Lansoprazole (Prevacid), Omeprazole (Prilosec), Esomeprazole Magnesium (Nexium), etc. |
| Treatment of DKA: Immediate Action | Insulin replacement w/ ultra-rapid or fast-acting insulin, and fluid & sodium replacement with isotonic saline. After plasma glucose and ketone bodies decrease add 5% glucose (prevent hypoglycemia) & hypotonic saline |
| Treatment of DKA: Non-immediate Action | Reduction of blood pH and restoration of bicarbonate; Potassium replacement |
| Treatment goals for Metabolic Syndrome | Decrease risk factors, which are: Truncal Obesity (Diet & Exercise), Increased TGs, Increased LDL, Hypertension, Increased fasting glucose |
| Metabolic Syndrome: Lipid Therapy | Decrease LDL with statins, or bile acid sequestrants, Ezetmibe, or fibrates; Increase HDL with Niacin or Fibrates; Decrease VLDL-TG with diet and/or statins, or fibrates. |
| Statins MOA | Inhibit HMG-CoA reductase, the rate-limiting enzyme needed to form cholesterol |
| Niacin MOA | Reduce hepatic LDL & VLDL production, inhibit lipolysis, decrease TG esterifiction, increase lipoprotein lipase activity, participate in tissue respiration oxidation-reduction reactions |
| Fibrates MOA | Inhibit TG synthesis and stimulate catabolism of TG-rich lipoproteins. |
| Metabolic Syndrome: Antihypertensive Therapy | Thiazide diuretics, but since it may cause loss of K+ then may need combination of thiazide-spironalactone (aldosterone antagonist), K+ supplement, combine with K-sparing diuretic (Amiloride). Also ACE inhibitors, ARBs, Ca-channel blockers, beta blockers |
| Metabolic Syndrome: Antithrombotic Therapy | Counteract prothrombotic state by using aspirin (aspirin + Dipyridamole is better), Clopidogrel, aspirin + Clopidogrel (increased bleeding though). Counteract procoagulant state with warfarin, or LMWH, or Heparin. |
| Dipyridamole | An antiplatelet drug that inhibits platelet adhesion, and dilates coronary arteries. |
| Clopidogrel | An antiplatelet drug that inhibits ADR-induced platelet aggregation. ADR=adrenaline/epinephrine |