Help
Options
Didn't know it?
click below
click below
Knew it?
click below
click below
Don't Know
Remaining cards (0)
Know
retry
shuffle
restart
0:00
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
PDA 1 Diabetes Drugs
Diabetes Drug Mechanisms
| Question | Answer |
|---|---|
| intermediate/long-acting | basal insulin |
| rapid and short-acting | bolus insulin |
| replace proline at B28 with aspartic acid residue | insulin aspart (bolus) |
| proline at B28 and lysine at B29 are reversed | insulin lispro (bolus) |
| protamine-insulin (bolus) complex; disassociates after cleavage making it intermediate acting | netral protamine hagedorn (NPH) (basal) |
| add fatty acid moiety to LysB29; increases self-aggregation and reversible albumin binding | insulin detemir (basal) |
| two arginine residues added to C terminus of B chain + asparagine at A21 is replaced with glycine - exists as a hexamer in solution at pH 4, dissociates at pH 7 (provides prolonged predictable absorption fro SC injection) PEAKLESS ABSORPTION | glargine (basal insulin) |
| imitates increase of ATP - inhibits K efflux channel: (increase of intracellular ATP results in inhibition of K+ efflux protein channel; results in depolarization & activation of the Ca channel, which results in exocytosis of insulin granules into blood) | sulfonylureas |
| imitates increase of ATP - inhibits K efflux channel: (increase of intracellular ATP results in inhibition of K+ efflux protein channel; results in depolarization & activation of the Ca channel, which results in exocytosis of insulin granules into blood) | K+ channel modulators |
| mimic the insulin pathway! (AMPK is naturally activated when cellular ATP stores are reduced - AMPK phosphorylates AS160 in a manner similar to Akt/PKB (a part of the insulin receptor pathway!)) | AMPK agonists |
| increases activity of AMPK - mech unknown (not direct activation) | metformin (an AMPK agonist) |
| substrate for PPAR gamma (which is a group of nuclear receptors responsible for the regulation of genes involved in glucose and lipid metabolism) --> when these drugs bind to PPAR g, results in activation of AMPK | thiazolidinediones (PPAR gamma agonists) |
| binds to GLP-1 receptors in the pancreas and hypothalamus resulting in: 1) stimulation of insulin secretion 2) inhibition of glucagon release 3) delay of stomach emptying - reduces food intake b/c you think you're full | GLP-1 receptor agonists |
| inhibits DPP-4 so that GLP-1 (normal substrate for it) does not bind --> increases GLP-1 conc causing: 1) stimulation of insulin secretion 2) inhibition of glucagon release 3) delay of stomach emptying - reduces food intake b/c you think you're full | DPP-4 inhibitors |
| work in brush border of small intestine! these drugs stop a-glucosidase from breaking down starches, dextrin, and disaccharides into sugars that can be absorbed: 1) slow absorption of carbs from GI tract 2) increase release of GLP-1 | alpha-glucosidase inhibitors |
| mimic actions of amylin! (amylin is a 37 AA peptide produced by the B cells of the pancreas) actions: 1) reduced glucagon release 2) delayed gastric emptying 3) satiety (hunger satisfaction) --> plasma glucose levels reduced | amylin receptor agonists |
| small AA peptide with sequence similar to that of amylin | pramlintide |
| lower plasma glucose - mech unknown but could be: 1) good at binding fat, bile acid, and glucose in plasma OR 2) act as a nuclear receptor signaling molecule | bile acid binding resins |
| released by the pancreas naturally in response to low blood sugar - bind with Gs-protein coupled receptor (results in synthesis of cAMP) stimulates production of glucose by: 1) gluconeogenesis 2) glycogen breakdown | glucagon |
| interacts with the K+ channel on the pancreatic B cells results: 1) prevents closing of channel 2) prolongs open time of channel --> prevents release of insulin | diazoxide |
Created by:
astephens5
Popular Pharmacology sets