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Pharm Diabeetus

QuestionAnswer
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