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Pharm Diabeetus
| Question | Answer |
|---|---|
| Metabolic Actions of Insulin: glucose metabolism | facilitates entry of glucose into muscle, adipocytes, stimulate liver to store glucose in glycogen form |
| Metabolic Actions of Insulin: Lipid Metabolism | promotes synthesis of fatty acids in liver, inhibits breakdown of fat in adipose tissue |
| Metabolic Actions of Insulin: protein metabolism | promotes glucose oxidation (glycolysis) in muscle = increased pyruvate =, increased amino acids, increased protein synthesis |
| Type 1 Diabetes | - 5-10% of all cases (~1 million Americans) - insulin dependent Diabetes Mellitus - Juvenile onset DM - Primary defect is destruction of pancreatic beta cells (autoimmune process) - Insulin levels are low in early stage and absent in later stages |
| Type 2 Diabetes: | - most prevalent form of diabetes (~19 million Americans) - non insulin dependent DM - adult onset DM - obesity is usually present - insulin resistance and inappropriate insulin secretion - insulin levels: low (deficiency), normal or high (resistanc |
| Symptoms of Diabetes Mellitus: | - hyperglycemia - polyuria - polydipsia - polyphagia - weight loss |
| 5 ways to treat diabetes mellitus | 1) dietary measure 2) Insulin Replacement 3) Oral hypoglycemic for DM2 4) Injectable hypoglycemic drugs 5) Glucagon for insulin overdose |
| target glucose level before meals | 90-130 |
| target glucose level at bedtime | 100-140 |
| target glycosylated hemoglobin | 7% |
| Diabeteic Ketoacidosis | Less utilization of glucose causes increase in fat metabolism= increased fatty acids. Fatty acid oxidation causes formation of ketones, which causes ketoacidosis (vomiting, shock, coma, death) |
| how does shock occur in DKA? | insulin deficiency leads to hyperglycemia, which leads to glycosuris, which causes osmotic diuresis, which causes water loss and dehydration, which leads to concentrated blood and shock. |
| treatment of Diabetic ketoacidosis | insulin replacement and electrolyte replacement |
| Short Duration, Rapid Acting Insulin (MOA) | onset <30 minutes, duration <4 hours); administered 15 min before meals to control postprandial rise in blood glucose |
| Short Duration, Rapid Acting Insulin (drugs) | Insulin Lispro (Humalog), Insulin Aspart (NovoLog) Insulin glulisine (Apidra) |
| Short Duration, slower acting insulin (MOA) | onset 15-60 min, duration <8hours. Administered 30 minutes before meals to control postprandial hyperglycemia |
| Short Duration, slower acting insulin (drug) | Regular Insulin (Humulin R, Novolin R), natural insulin |
| intermediate Duration insulin (MOA) | onset 1-2 hours, duration <12-24 hours. Administered 2x daily (basic glycemic control) |
| intermediate Duration insulin (drugs) | Neutral Protamine Hagedorn (NPH) insulin, Insulin Detemir (Levemir) |
| Long duration insulin (MOA) | onset 70 min, duration 24 hours, administered once daily at bedtime |
| Long duration insulin (drugs) | Insulin glargine (Lantus) |
| Adverse Effects of Insulin Treatment | hypoglycemia, lipodystrophies (deposition of fat at sites of injection), allergic reactions |
| 4 classes of oral hypoglycemics | insulin secretagogues, insulin sensitizers, agents that delay intestinal carbohydrate absorption, Glp-1 enhancers |
| Insulin Sectretagogues- MOA | stimulate insulin release from pancreatic islets (only works in DM2) |
| Insulin secretagogues -drugs | 1) Sulfonylureas 2) Meglitinides |
| Sufonylureas | 1st gen: Tolbutamide (Orinase) 2nd gen: Glipizide (Glucotrol), Glyburide (Micronase), GLynase (Amaryl) |
| Meglitinides | Repaglinide (Prandin), Nateglinide (Starlix) |
| Insulin Sensitizers - MOA | lowers insulin resistance, increases muscle and adipose tissues sensitivity to insulin, increases glucose uptake by muscle and adipocytes, decreases blood glucose (insulin must be present to be effective) |
| Insulin Sensitizers - drug classes | Biguanides and Glitazones |
| Biguanides | Metformin (may reduce B12 absorption, lactic acidosis) |
| Glitazones | Pioglitazone and Rosiglitazone (cause fluid retnetion and increased risk of CVD b/c of increased HDL/LDL/TG) |
| Agents that Delay intestinal Carbohydrate Absorption -MOA | lowers the rise of blood glucose levels after meal |
| Agents that Delay intestinal Carbohydrate Absorption- drugs | alpha-glucosidase inhibitors- Acarbose (Precose), Miglitol (Glyset) |
| Glp-1 enhancers- Drug class | Dipeptidyl Peptidase 4 inhibitors |
| Dipeptidyl Peptidase 4 inhibitors -MOA | inhibit DPP-4 (enzyme that degrades Glp-1). Increase action of Glp-1 (a peptide hormone that reduces postprandial levels of glucose by delaying gastric emptying) |
| Dipeptidyl Peptidase 4 inhibitors -Drugs | Sitagliptin, Saxagliptin, Lingagliptin |
| adverse effects of Glp-1 enhancers/Dipeptidyl Peptidase 4 inhibitors | Cv (edema), hypoglycemia, bone fractures |
| 2 new injectable hypoglycemic drugs | Pramilintide (Symlin) and Exenatide (Byetta) and Liraglutide (Victoza) |
| - Pramilintide (Symlin) | o Synthetic analogue of amylin (Amylin is a peptide hormone produced in the pancreas and released with insulin → reduces postprandial levels of glucose by delaying gastric emptying) o Indicated as a supplement to mealtime insulin in DM type 1 and 2 |
| - Exenatide (Byetta), Liraglutide (Victoza) | o Synthetic analogues of GLP-1, a peptide hormone in the incretin family → reduces postprandial levels of glucose by delaying gastric emptying |
Created by:
alexadianna
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