Diabetes Meds
About this set
Created by:
nyashy on December 8, 2009
Subjects:
endocrine system, pharmacology
Log in to favorite or report as inappropriate.
Order by
44 terms
Terms | Definitions |
|---|---|
 What is the HgA1c target in diabetes? | <7% |
| What is the BP target in diabetes | < 130/80 |
| What is the LDL-C target in diabetes | <100 mg/dL |
| What is the HDL-C target in diabetes | >40 mg/dL |
| What is the TG target in diabetes | <150 mg/dL |
| The three organs to target | 1. Pancreas 2. Liver 3. Muscle |
| What are the effects of weight loss in type 2 diabetics? | 1.decrease fasting plasma glucose 2. decrease hepatic liver content 3. decreased rate of glucose production 4. increase in insulin suppression of hepatic glucose production |
| What are the effect of exercise in type 2 diabetes and why? | Increase in insulin stimulated muscle glycogen synthesis. Exercise decreases the ATP/ADP ratio which then stimulates AMPkinase which in turn increases the transport of GLUT4 to the surface of muscle cells thus allowing glucose into the cell |
| True/False: type 2 diabetics may have normal or high levels of insulin, but truly they have too little insulin for their insulin resistance | True |
| Sulfonylureas (example glyburide) | act on the beta cell in the pancreas and inhibit the ATP-regulated K+ channels which facilitate beta cell depolarization and the secretion of insulin |
| Glyburide (sulfonylurea) therapy increases insulin secretion and decreases plasma glucose: true/false | true |
| Pros of sulfonylurea treatment | 1. Moderate HgA1c lowering of about 1-2% 2. Long track record of use in treating diabetics |
| Cons of sulfonylurea treatment | 1. Risk of hypoglycemia 2. Hyperinsulinemia and weight gain 3. Long term failure in 30% of patients |
| What are incretins? | 1. Hormones 2. Originate in GI tract 3. Released during nutrient absorption (are glucose dependent) 4. Augment insulin secretion usually by acting on beta cells 5. Some incretins also decrease glucagon synthesis |
| True/False: incretin effects are diminished in type 2 diabetes | True |
| What is an example of an incretin | GLP-1 |
| Where is GLP-1 produced? | In the L cells of the GI tract |
| How is GLP-1 inactivated | Over 50% of GLP-1 is inactivated in 1 minute by the ubiquitous plasma protease dipeptidyl peptidase-4 which cleaves N terminal dipeptides |
| GLP-1 | 1. Glucagon-like peptide 2. Increases insulin secretion and decreases glucagon secretion in a glucose-dependent manner 3. Is rapidly inactivated by DPP-4 |
| Exendin | A GLP-1 analogue isolated from gila monsters |
| Exenatide's (exendin's) effect on body weight? | Decreases (may be related to the drug-induced nausea) |
| Cons of exendin (exenatide) | nausea (dose related), high costs, injectable |
| Pros of using exenatide | 1. no risk of hypoglycemia 2. moderate reduction in HgA1c 3. associated with significant weight loss 4. preserves beta cell function |
| What is the logic behind targeting DPP-4 for type 2 diabetes control? | Most of secreted GLP-1 and most of circulating GLP-1 is degraded by DPP-4; ergo, decrease DPP-4, you concomittantly increase GLP-1 and thus increase insulin secretion when it is needed |
| DPP-4 | a serine protease widely distributed in the body that inactivates GLP-1 and GIP |
| Pros of using DPP-4 inhibitors? | 1. Safe 2. No hypoglycemia like sulfonylurea drugs 3. Can be used with metformin or TZDs |
| Cons of DPP-4 inhibitors? | Modest reductions in HgA1c when used as monotherapy |
| Metformin | Inhibits hepatic glucose production |
| Pros of metformin therapy | 1. No hypoglycemia 2 Weight neutral or weight reducing 3. Only agent that acts on gluconeogenesis by liver 4. Cheap 5. moderate reductions (1-2%) in HgA1c |
| Cons of metformin therapy | GI toxicity (abdominal pain, diarrhea), cannot be used in people with renal insufficiency or hepatic dysfunction |
| What happens if metformin is used on people with renal insufficiency or hepatic dysfunction? | Rare lactic acidosis (this makes sense as the reduced clearance of metformin will result in high plasma levels and complete inhibition of gluconeogenesis and thus a need to switch to anaerobic glycolysis and lactate buildup) |
| Thiazolidinediones (TZDs) | do not affect insulin secretion but instead enhance the action of insulin at target tissues |
| Name two Thiazolidinediones | (look for the suffix "glitazone") Pioglitazone HCL and Rosiglitazonae maleate |
| Mechanism of action of thiazolidinediones | agonists for the nuclear hormone receptor peroxisome proliferator activated receptor-gamma (PPARgamma). PPAR-gamma functions as a heterodimer with the retinoid X receptor to activate the transcription of some gene. PPAR-gamma is expressed primarily in adipose tissue and is involved in adipose tissue differentiation which causes adipose cells to accumulate triglycerides. This has indirect effects on the insulin sensitivities of muscle and liver by removing free fatty acids from liver and muscle (thus redistributing the fat). |
| Cons of TZD | weight gain, slow onset of action, edema/chf, increased bone fracture risk, costs |
| Pros of TZD | no hypoglycemia because it does not target insulin secretion, only insulin sensitizer available, moderate reductions inHgA1c (1-2%), beta cell preservation |
| Contraindications of TZD | congestive heart failure, hepatic dysfunction |
| Alpha-glucosidase inhibitors | (nickname= starch blockers) |
| Mechanism of action of alpha-glucosidase inhibitors | Carbohydrate analogues that bind 1,000 times more acidly than dietary carbohydrates to intestinal brush border alpha-glucosidase enzymes. Glucosidases- maltase, isomaltase, sucrase, and glucoamylase- aid absorption by cleaving complex carbohydrates to yield glucose. By reversibly inhibiting these enzymes, alpha-glucosidase inhibitors increase the time required for absorption of carbs like starch, dextrin, and disaccharides. The drugs thus increase the postprandial peak in blood sugar when taken with meals- they are not effective for controlling fasting hyperglycemia |
| Pros of alpha-glucosidase inhibitor | good safety profile, no hypoglycemia, weight neutral |
| Cons of alpha-glucosidase inhibitor | mild reduction in HgA1c (0.5-1%), GI side effects (gas, cramping), frequent dosing, costs |
| Examples of alpha-glucosidase inhibitors | Acarbose, miglitol |
| Pramlintide | Pramlintide is an analogue of amylin, a small peptide hormone that is released into the bloodstream by the β-cells of the pancreas along with insulin, after a meal. Like insulin, amylin is deficient in individuals with diabetes. By augmenting endogenous amylin, pramlintide aids in the absorption of glucose by slowing gastric emptying, and inhibiting inappropriate secretion of glucagon |
| Cons of pramlintide | Injections, GI, cost |
First Time Here?
Welcome to Quizlet, a fun, free place to study. Try these flashcards, find others to study, or make your own.