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Anti & Hypoglycemics

USMLE Step 1

DrugMOA & ADRs
Dx w/ fasting serum glucose equal or > 126 mg/dL on 2 differ occasions
Dx w/ random serum glucose equal or > 200 mg/dL w/ sxs
Dx w/ PO glucose tolerance test serum glucose level equal or > 200 mg/dL 2 hrs after a 75 g PO glucose load
Metabolic syndrome approaching DM 2, but dont have criteria. dx is fasting serum glucose levels 100-125 mg/dL
Maintenance pre-prandial serum glucose levels 90-130 mg/dL
Maintenance post-prandial serum glucose levels < 180 mg/dL
Hb A1C glycated Hb from glucose binding to Hb & build up reflects the amt of glucose exposed to the 120 dy lifecycle. nml = < 0.6%, diabetic = maintain below 7% or lower.
Metformin MOA: 1st line 4 DM, biguanide - glucose absorption from gut, decrease output by liver, increase uptake in adipose & skeletal muscle; ADRs: must b stop prior giving IV contrast & dont use 48 hrs after, dont use 4 EtOHics, severe CHF, liver or renal failure
Acarbose MOA: alpha-glucosidase inhibitor = cant degrade carbs = less for absorption, good for post-prandial hyperglycemia; ADRs: flatulence (severe & disabiling)
Miglitol MOA: alpha-glucosidase inhibitor = cant degrade carbs = less for absorption, good for post-prandial hyperglycemia; ADRs: flatulence (severe & disabiling)
Rosiglitazone MOA: glitazone aka thiazolidinediones increase the # of insulin receptors & glucose transporters on skeletal muscle & adipose; ADRs: potential 2 cause edema, weight gain, new onset HF, & exacerbation of preexisting CHF, dont use in liver disease & do LFTs
Pioglitazone MOA: glitazone aka thiazolidinediones increase the # of insulin receptors & glucose transporters on skeletal muscle & adipose; ADRs: potential 2 cause edema, weight gain, new onset HF, & exacerbation of preexisting CHF, dont use in liver disease & do LFTs
Nateglinide MOA: meglitinide that are nonsulfonylurea insulin secretagogues cause release of insulin by beta-islet cells, ability to + doesnt decrease w/ time
Repaglinide MOA: meglitinide that are nonsulfonylurea insulin secretagogues cause release of insulin by beta-islet cells, ability to + doesnt decrease w/ time
1st generation sulfonulurea: Tolbutamide MOA: insulin release of beta cells by bind 2 specific receptors coupled 2 increase Ca entry & - K in, increase insulin sensitivity by increasing glucose uptake in fat & muscle cells-doesnt decrease over time; ADRs: MOA decreases over time w/ long term use
1st generation sulfonulurea: Chlorpropamide MOA: insulin release of beta cells by bind 2 specific receptors coupled 2 increase Ca entry & - K in, increase insulin sensitivity by increasing glucose uptake in fat & muscle cells-doesnt decrease over time; ADRs: MOA decreases over time w/ long term use
1st generation sulfonulurea: Acetohexamide MOA: insulin release of beta cells by bind 2 specific receptors coupled 2 increase Ca entry & - K in, increase insulin sensitivity by increasing glucose uptake in fat & muscle cells-doesnt decrease over time; ADRs: MOA decreases over time w/ long term use
1st generation sulfonulurea: Tolazamide MOA: insulin release of beta cells by bind 2 specific receptors coupled 2 increase Ca entry & - K in, increase insulin sensitivity by increasing glucose uptake in fat & muscle cells-doesnt decrease over time; ADRs: MOA decreases over time w/ long term use
2nd generation sulfonulurea: Glimepiride, potent @ low doses MOA: insulin release of beta cells by bind 2 specific receptors coupled 2 increase Ca entry & - K in, increase insulin sensitivity by increasing glucose uptake in fat & muscle cells-doesnt decrease over time; ADRs: MOA decreases over time w/ long term
2nd generation sulfonulurea: Glyburide, potent @ low doses MOA: insulin release of beta cells by bind 2 specific receptors coupled 2 increase Ca entry & - K in, increase insulin sensitivity by increasing glucose uptake in fat & muscle cells-doesnt decrease over time; ADRs: MOA decreases over time w/ long term use
2nd generation sulfonulurea: Glipizide, potent @ low doses MOA: insulin release of beta cells by bind 2 specific receptors coupled 2 increase Ca entry & - K in, increase insulin sensitivity by increasing glucose uptake in fat & muscle cells-doesnt decrease over time; ADRs: MOA decreases over time w/ long term use
Created by: jerrica_08
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