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10 Cards in this Set
- Front
- Back
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A-183. What are the fast acting insulins?
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Insulin lispro, insulin aspart, insulin glulisine
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A-183. First line medication after a T2DM dx and its MOA?
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Metformin
Inhibit the absorption of glucose from gut, dec glucose output from liver, incr glucose uptake in adipose tissue and muscle |
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A-183. Rosiglitazone and pioglitazone MOA and have what ADRs?
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MOA: sensitize skeletal muscle and fat to insulin (increase receptors)
Cause edema, new onset of CHF, exacerbation of pre-existing CHF, hepatotoxin (monitor LFTs) |
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A-183. Name, MOA, contraindications of GLP-1 analouges?
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Exenatide and Liraglutide
Increase insulin release, decrease gastric emptying and inhibit glucagon release Contra: T1DM, renal failure, conditions that cause decr GI motility. Increased risk of pancreatitis |
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A-183. Defect and labs of Type I-V hyperlipidemias?
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1: lipoprotein lipase deficiency, abnormality or apo-CII defects - hi TGs, Chylos, and VLDL
2A: fucked up LDL receptors - hi LDL 2B: LDL hates their receptor - hi LDL and VLDL 3: Mutant apo E - hi chylos, VLDL, IDL, and LDL - decreased HDL 4: overprod of VLDL - low LDL and HDL 5: unknown - Hypercholes w/ low LDL and HDL |
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A-183. DOC for hyperTGs?
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Clofibrate
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A-183. Benefits of statins?
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1.) decr HmG-CoA Reductase
2.) Decreased ACE = decr BP 3.) Decreased aldosterone = decr NADPH oxidase and oxidative damage at atherosclerotic sites. |
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A-183. How fibric acid agents like Colfibrate, fenofibrate, and gemfibrozil work to low TGs, for which they are the DOC?
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Increase lipoprotien lipase activity thus decreasing chylos and VLDL by increasing tissue uptake of TGs
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A-183. What are the first and second generation sulfonylureas and their MOA?
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1st: Tolbutamide, Chlorpropamide, and Tolazamide
2nd: Glimepiride, Glyburide, Glipizide MOA: promote insulin release from beta-islet cells |
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A-183. What are the intermediate and long acting insulins?
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Intermediate: Lente
Long: Insulin glargine, insulin detemir, and protamine zinc insulin |
