Term
| Type I Diabetes is ____ onset and is insulin____. While Type II is ____ onset and is insulin-_____ |
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Definition
| childhood onset and insulin dependent; adulthood and insulin independent. Most Diabetics (80-90%) are |
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Term
| What is the treatment of Type I? Type II? generally |
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Definition
| Type I- insulin replacement. Type II- lifestyle change, drugs that influence insulin secretion or sensitivity, and end stage insulin replacement |
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Term
| When do Type II Diabetics receive insulin therapy? |
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Definition
|
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Term
| What does an insulin curve look like after infusing glucose? |
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Definition
| rapid increase in insulin secretion |
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Term
| What does an insulin curve look like in a Type I Diabetic folloiwng glucose infusion? |
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Definition
|
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Term
| What does an insulin curve look like in a Type II diabetic following glucose infusion? |
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Definition
| delayed, blunted insulin release |
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Term
| What is the original form of natural insulin? What is it made of? |
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Definition
| Proinsulin, made of an A and B chain, connected by an intervening C chain |
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Term
| How is Proinsulin modified? |
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Definition
| C-peptide is cleaved and the A chain and B chain are connected by 2 disulfide bridges. |
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Term
| Native insulin has what propensity? |
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Definition
| to form crystals/aggregate in the presence of Zinc |
|
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Term
| what is the effect of insulin forming aggregates in the presence of Zinc? |
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Definition
|
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Term
| What are the 3 rapidly acting insulins? |
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Definition
| lispro, aspart, glulisine |
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Term
| What are the rapidly acting insulins formulated with? |
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Definition
|
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Term
| When are the rapidly acting insulins injected? |
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Definition
| 5-15 minutes beofre each mean and even after a meal. |
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Term
| The rapidly acting insulins are more effective in decreasing ____ and less likely to cause ____ |
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Definition
| postprandial hyperglycemia; nocturnal hypoglycemia |
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Term
| What is the short acting insulin? |
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Definition
|
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Term
| What are the intermediate acting insulins? |
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Definition
| NPH insulin and Lente Insulin |
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Term
| WHat is NPH Insulin complexed with? Lente Insulin? |
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Definition
|
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Term
| What are the 2 long acting insuling? |
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Definition
| Ultralente and Glargine insulin |
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Term
| WHy is Glargine Insulin long-acting? |
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Definition
| it is soluble at pH 4, but forms microprecipitate at pH 7.4, delaying absorption form Subcutaneous site. |
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Term
| What is Intense insulin therapy? and when is it used |
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Definition
| inject with ultra-short acting before meals, longer acting at night, acheiving HbA1C of 7% and mean blood glucose of 150 mg/dL; Type I Diabetics are strongly encouraged to use Intense Therapy |
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Term
| What is Standard Insulin Therapy? and when is it used? |
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Definition
| 2 injections per day, two intermediate acting, achieves HbA1C of 8-9%; and a mean blood glucose of 225 mg/dL. used for Type II Diabetics in advanced disease when lifestyle change isnt good enough. |
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Term
| What is the structure of the Insulin Receptor? |
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Definition
| 4 subunits: 2 alpha and 2 beta, linked to a tyrosine kinase |
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Term
| How are the metabolic effects of the Insulin receptor mediated? |
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Definition
| IRS proteins 1-4, which mediates PI3 Kinase, leading to protein synthesis and glycogen synthesis. |
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Term
| How are mitogenic effects of Insulin receptor mediated? |
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Definition
| MAP Kinase leads to Mitogenesis. |
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Term
| Insulin is a ____ hormone. |
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Definition
| STORAGE: it promotes storage of glycogen, protein, and triglycerides; inhibits glycogenolysis and gluconeogenesis |
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Term
| What are some complications of Insulin therapy? |
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Definition
| Hypoglycemia, tachycardia, sweating, confusion, coma; S.Cutaneous fat hypertrophy at the site of injection (rotate injxn site), immune insulin resistance due to Ab production |
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|
Term
| with increased disease severity of Type II Diabetses |
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Definition
| what happens to endogenous iNsulin?,decreases |
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Term
| How does Glucose cause insulin release in a Beta cell? |
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Definition
| Enters the beta cell, ATP is generated from glucose metabolism. ATP closes the K+ channel, which depolarizes the cell, allowing Ca2+ entry, which allows fusion and exocytosis of Insulin. |
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Term
| How do Sulfonylurea drugs cause insulin release? |
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Definition
| They mimic the action of Glucose, by blocking the K+ channels, depolarizing the membrane, allowing for Ca2+ entry and exocytosis of insulin. |
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Term
| What drug also works like the Sulfonylureas? |
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Definition
|
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Term
| What are the Sulfonylureas? |
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Definition
| Glipizide, Glyburide, and Glimepiride; Replaglinide works the same way |
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Term
| What is the main side effect of Sulfonylureas? |
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Definition
|
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Term
| What are side effects of Sulfonylureas? |
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Definition
| nausea, Hypersensitivity Reactions, Pruritis, Alcohol-induced flush, anemia. |
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Term
| Which of the Sulfonylureas has the lowest incidence of Hypoglycemia? |
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Definition
|
|
Term
| what does the term "euglycemic" refer to? |
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Definition
|
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Term
| What is Metformin commonly used with? |
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Definition
|
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Term
| What is the target of Metformin? |
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Definition
| AMP-activated protein kinase |
|
|
Term
| what are the side effects of Metformin? |
|
Definition
| severe GI side effects; anorexia, vomiting, diarrhea, lactic acidosis |
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Term
| what is the MOA of Acarbose? |
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Definition
| alpha-glucosidase inhibitor; inhibits the abosrption of starch and complex sugar |
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Term
| When is Acarbose taken and what is its effect? |
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Definition
| taken before meals; the post-prandial rise of glucose is blunted |
|
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Term
| what are the side effects of Acarbose? |
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Definition
| flatulence, cramping, diarrhea due to passage of unabsorbed starches and complex sugars |
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Term
| What are the 2 Glitazones? |
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Definition
| Rosiglitazone and Pioglitazone |
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Term
| What is the MOA of Glitazones? |
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Definition
| They activate PPAR gamma, which activates insulin-responsive genes, affecting carbohydrage and lipid metabolism. |
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Term
| What is carefully monitored with administration of Glitazones? |
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Definition
| liver function because liver damage resulted in a Glitazone being removed from the market |
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Term
|
Definition
| They are substances released druing meals that stimulate insulin secretin and depress glucagon secretion. They are GLP-1 and 2 and are degraded by DPP4 |
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Term
| What are the two GLP-1 Agonists? |
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Definition
|
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Term
| What is the MOA of GLP-1 agonists? |
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Definition
| increase insulin secretion, decrease glucagon secretion |
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Term
| How are GLP-1 agonists given? |
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Definition
|
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Term
| What are the DPP-4 inhibitors? |
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Definition
|
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Term
| What is the MOA of DPP-4 inhibitors? |
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Definition
| increase insulin by inhibiting the breakdown of GLP-1/incretins |
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Term
| How are DPP-4 inhibitors given? |
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Definition
|
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Term
| DO sulfonylureas lose efficacy over time? |
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Definition
|
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Term
| What is Metformin and what class is it? |
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Definition
|
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Term
| WHere are insulin injections given to be more rapidly absorbed? |
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Definition
|
|
Term
| How does skin perfusion/exercise affect insulin injection absorpiton? |
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Definition
| exercise increases absorption. |
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|
Term
| A. With continued therapy |
|
Definition
| sulfonylureas such as glyburide |
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