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26 Cards in this Set
- Front
- Back
Rapid acting insulin
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Lispro
Aspart |
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Short-acting insulin
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Regular Insulin
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Intermediate and long-acting insulin
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Intermediate insulin = NPH
Long acting insulin = Glargine Long acting insulin = Detemir |
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Insulin toxicity
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Hypoglycemia
Hypersensitivity reaction (very rare) |
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Insulin Clinical use
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Type 1 Dm
Type 2 Dm Gestational Diabetes Life-threatening Hyperkalemia Stress-induced hyperglycemia |
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Insulin action on muscle
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Protein synthesis and icnresed glycogen. Also Increase K+ uptake
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Sulfonylureas - First Generation - list them
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Tolbutamide
Chlorpropamide |
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Sulfonyureas - 2nd Generation - list them
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The "Gly/Glis"
Glyburide Glymepiride Glipizide |
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Glitazones/Thiazolidinediones - List them
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Proglitazone
Rosiglizatones |
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Alpha Glucosidase inhibitors
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Acarbose
Miglitol |
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Pramlintide belongs to what drug class?
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Mimetics
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GLP-1 Analogs - name them
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Exenatide
Analog - "example"=Examplatide(sounds similar) |
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Pramlintide : Action, use and toxicity
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Action : Decrease glucagon
Clinical Use : Type 2 DM Toxicities : Hypoglycemia, Nause, Diarrhea |
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Exentaide : Action, use and toxicity
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Action : Increase in insulin, Decresae in glucagon release
Use : Type 2 DM Toxicity : Nausea, vomiting, pancreatitis(site of action) |
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Alpha glucosidase inhibitors - Clinical use / toxicity
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Clinical Use - Monotherapy in Type 2 DM or with combo therapy
Toxicity = GI disturbances (works there) |
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Metformin Action :
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Exact mechanism unknown.
Decreased gluconeogenesis Increased Glycolysis Increased peripheral glucose uptake (increased insulin sensitivity) |
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Glitazones mechanism
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"Glitters"(binds) peripheral tissues and increases their sensitivity to insulin. Binds to PPAR-gamma nuclear transcription regulator.
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Glitazones Clinical use? Toxicity?
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Monotherapy or combotherapy for Type 2 DM.
Toxicity : Weight gain Edema (can lead to weight gain) Hepatotoxicity Heart Failure |
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Alpha Glucosidase inhibitors - Action
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Inhibits intestinal alpha glucosidase inhibitors on brush border cells.
Delayed sugar hydrolysis and glucose absorption leads to decreaseed postprandial hyperglycemia |
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Alpha glucosidase inhibitors - Clinical use / toxicity
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Clinical Use - Monotherapy in Type 2 DM or with combo therapy
Toxicity = GI disturbances (works there) |
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Metformin Action :
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Exact mechanism unknown.
Decreased gluconeogenesis Increased Glycolysis Increased peripheral glucose uptake (increased insulin sensitivity) |
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Metformin Clinical Use and Toxicity
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Use : ORAL . First line treatment for type 2 DM.
Can be used in patients without Islet funciton Toxicity : Worst effect is lactic acidosis (contraindicated in Renal Failure Patients) |
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Metformin contraindicated in?
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Renal failure patients (b/c of lactic acidosis side effect)
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Sulfonylurea Action:
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Close K+ channel in beta cell pancreas membrane leading to depolarization which triggers Ca2+ influx leading to insulin release.
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Sulfonylurea Use?
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Use : Stimulate release of ENDOGENOUS insulin in type 2 DM. Useless in Type 1 DM (no endocrine pancreas fxn)
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Sulfonylurea Toxicity:
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First generation : Disulfiram-like effects
Second generation : Hypoglycemia |