Diabetes Pharmacology Flashcards
0
Q
Aspart
A
- insulin, rapid acting
- bind insulin receptor (tyrosine kinase activity)
- liver: increase glucose stored as glycogen
- muscle: increase glycogen, protein synthesis, K+ uptake
- fat: increase TG storage
- clinical use: DM1, DM2, GDM (postprandial glucose control)
- toxicity: hypoglycemia, rare hypersensitivity rxn
1
Q
Lispro
A
- insulin, rapid acting
- bind insulin receptor (tyrosine kinase activity)
- liver: increase glucose stored as glycogen
- muscle: increase glycogen, protein synthesis, K+ uptake
- fat: increase TG storage
- clinical use: DM1, DM2, GDM (postprandial glucose control)
- toxicity: hypoglycemia, rare hypersensitivity rxn
2
Q
Glulisine
A
- insulin, rapid acting
- bind insulin receptor (tyrosine kinase activity)
- liver: increase glucose stored as glycogen
- muscle: increase glycogen, protein synthesis, K+ uptake
- fat: increase TG storage
- clinical use: DM1, DM2, GDM (postprandial glucose control)
- toxicity: hypoglycemia, rare hypersensitivity rxn
3
Q
Bromocriptine
A
- dopamine receptor (D2) agonist
- can have modest effect on treating diabetes
4
Q
Regular insulin
A
- short acting
- clinical use: DM1, DM2, GDM, DKA (IV), hyperkalemia (+glucose), stress hyperglycemia
- toxicity: none
5
Q
NPH
A
- insulin, intermediate acting
- combination of insulin (neg. charged) and protamine (pos. charged) such that neither is present in uncomplexed form
- action is highly unpredictable and clinical use is waning
- clinical use: DM1, DM2, GDM
6
Q
Glargine
A
- insulin, long acting
- “peakless”
- clinical use: DM1, DM2, GDM
- basal glucose control
7
Q
Detemir
A
- insulin, long acting
- clinical use: DM1, DM2, GDM
- basal glucose control
8
Q
Metformin
A
- decreases hepatic glucose output
- decreases fasting glucose
- decreases hepatic insulin resistance
- targets the liver
- decreases gluconeogenesis, increases glycolysis, increases peripheral glucose uptake (insulin sensitivity)
- DOES NOT increase insulin release
- clinical use: PO, first-line therapy in DM2; can be used in pts w/o islet fxn
- toxicity: GI upset; most serious adverse effect is lactic acidosis (thus contraindicated in renal failure)
9
Q
Tolbutamide
A
- first generation sulfonylureas
- seretogogue
- close K+ channel in beta-cell membrane, so cell depolarizes and triggers insulin release via influx of Ca2+
- clinical use: stimulate release of endogenous insulin in DM2; require some islet fxn, so useless in DM1
- chronic (weeks) therapy decreases glucagon in circulation
- toxicity: risk of hypoglycemia increases in renal failure
- first generation toxicity: disulfiram-like effects
- second generation toxicity: hypoglycemia
10
Q
Chlorpropamide
A
- first generation sulfonylureas
- seretogogue
- close K+ channel in beta-cell membrane, so cell depolarizes and triggers insulin release via influx of Ca2+
- clinical use: stimulate release of endogenous insulin in DM2; require some islet fxn, so useless in DM1
- chronic (weeks) therapy decreases glucagon in circulation
- toxicity: risk of hypoglycemia increases in renal failure
- first generation toxicity: disulfiram-like effects
- second generation toxicity: hypoglycemia
11
Q
Glyburide
A
- second generation sulfonylureas
- seretogogue
- close K+ channel in beta-cell membrane, so cell depolarizes and triggers insulin release via influx of Ca2+
- clinical use: stimulate release of endogenous insulin in DM2; require some islet fxn, so useless in DM1
- chronic (weeks) therapy decreases glucagon in circulation
- toxicity: risk of hypoglycemia increases in renal failure
- first generation toxicity: disulfiram-like effects
- second generation toxicity: hypoglycemia
12
Q
Glimepiride
A
- second generation sulfonylureas
- seretogogue
- close K+ channel in beta-cell membrane, so cell depolarizes and triggers insulin release via influx of Ca2+
- clinical use: stimulate release of endogenous insulin in DM2; require some islet fxn, so useless in DM1
- chronic (weeks) therapy decreases glucagon in circulation
- toxicity: risk of hypoglycemia increases in renal failure
- first generation toxicity: disulfiram-like effects
- second generation toxicity: hypoglycemia
13
Q
Glipizide
A
- second generation sulfonylureas
- seretogogue
- close K+ channel in beta-cell membrane, so cell depolarizes and triggers insulin release via influx of Ca2+
- clinical use: stimulate release of endogenous insulin in DM2; require some islet fxn, so useless in DM1
- chronic (weeks) therapy decreases glucagon in circulation
- toxicity: risk of hypoglycemia increases in renal failure
- first generation toxicity: disulfiram-like effects
- second generation toxicity: hypoglycemia
14
Q
Meglitinide
A
- second generation sulfonylureas
- seretogogue
- close K+ channel in beta-cell membrane, so cell depolarizes and triggers insulin release via influx of Ca2+
- clinical use: stimulate release of endogenous insulin in DM2; require some islet fxn, so useless in DM1
- chronic (weeks) therapy decreases glucagon in circulation
- toxicity: risk of hypoglycemia increases in renal failure
- first generation toxicity: disulfiram-like effects
- second generation toxicity: hypoglycemia
15
Q
Nateglinide
A
- seretogogogue
- D-phenylalanine derivative
- quick onset, short duration
- hypoglycemic episodes unlikely, but causes weight gain
- inactivated by liver; use with caution in pts with liver disease
- safe for pts with very reduced renal fxn
17
Q
Rosiglitazone
A
- glitazones/thiazolidinediones
- increases insulin sensitivity in peripheral tissue (adipose tissue is the primary target)
- binds to PPAR-gamma nuclear transcription regulator
- genes activated by PPAR-gamma regulate fatty acid storage and glucose metabolism… activation of PPAR-gamma increases insulin sensitivity and levels of adiponectin
- used as monotherapy in DM2 or combined with above agents
- toxicity: weight gain, edema, hepatotoxicity, heart failure
18
Q
Meglitinides (repaglinide)
A
- newer secretologues
- structurally unrelated to sulfonylureas, but with same primary fxn
- rapid absorption and short half-life… fast and brief stimulation of insulin secretion
- indicated to reduce postprandial hyperglycemia
19
Q
Acarbose
A
- alpha-glucosidase inhibitor
- inhibit intestinal brush-border alpha-glucosidases
- delayed sugar hydrolysis and glucose absorption leads to decreased postprandial hyperglycemia
- clinical use: used as monotherapy in DM2 or in combination with above agents
- toxicity: GI disturbances
20
Q
Miglitol
A
- alpha-glucosidase inhibitor
- inhibit intestinal brush-border alpha-glucosidases
- delayed sugar hydrolysis and glucose absorption leads to decreased postprandial hyperglycemia
- clinical use: used as monotherapy in DM2 or in combination with above agents
- toxicity: GI disturbances
- miglitol is a simple sugar analog
21
Q
Canagliflozin
A
- kidney sodium-glucose transporter 2 (SGLT2) inhibitor
- reduce reabsorption of glucose and increase secretion
- can cause orthostatic hypotension due to osmotic diuresis
22
Q
Dapagliflozin
A
- kidney sodium-glucose transporter 2 (SGLT2) inhibitor
- reduce reabsorption of glucose and increase secretion
- can cause orthostatic hypotension due to osmotic diuresis
23
Q
Empagliflozin
A
- kidney sodium-glucose transporter 2 (SGLT2) inhibitor
- reduce reabsorption of glucose and increase secretion
- can cause orthostatic hypotension due to osmotic diuresis
24
Q
Pioglitazone
A
- glitazones/thiazolidinediones
- increases insulin sensitivity in peripheral tissue (adipose tissue is the primary target)
- binds to PPAR-gamma nuclear transcription regulator
- genes activated by PPAR-gamma regulate fatty acid storage and glucose metabolism… activation of PPAR-gamma increases insulin sensitivity and levels of adiponectin
- used as monotherapy in DM2 or combined with above agents
- toxicity: weight gain, edema, hepatotoxicity, heart failure
25
Colesevalam
- bile acid binding resin
| - some treatment in DM type 2
26
Pramlintide
- amylin analog
- decreases gastric emptying, decreases glucagon
- inhibits glucagon production
- treatment of type 1 and type 2 DM
- toxicity: hypoglycemia, nausea, diarrhea
27
Exenatide
- GLP-1 analog
- GLP-1 is an incretin (GI hormone that is released after meals and stimulates insulin secretion)
- glucagon receptor agonist
- increases insulin and decreases glucagon release
- potentiates insulin secretion, suppresses glucagon secretion, slows gastric motility
- stimulates glucose dependent insulin secretion
- treatment of type 2 diabetes
- toxicity: nausea, vomiting, pancreatitis
28
Liraglutide
- GLP-1 analog
- GLP-1 is an incretin (GI hormone that is released after meals and stimulates insulin secretion)
- glucagon receptor agonist
- increases insulin and decreases glucagon release
- potentiates insulin secretion, suppresses glucagon secretion, slows gastric motility
- stimulates glucose dependent insulin secretion
- treatment of type 2 diabetes
- toxicity: nausea, vomiting, pancreatitis
29
Linagliptin
- DPP-4 inhibitor
- DDP-4 blocks GLP-1
- increases insulin secretion and decreases glucagon release
- increases incretins GLP-1 and GLP (glucose-dependent insulinotropic peptide)
- treatment for DM2
- toxicity: mild urinary or respiratory infections
30
Saxagliptin
- DPP-4 inhibitor
- DDP-4 blocks GLP-1
- increases insulin secretion and decreases glucagon release
- increases incretins GLP-1 and GLP (glucose-dependent insulinotropic peptide)
- treatment for DM2
- toxicity: mild urinary or respiratory infections
31
Sitagliptin
- DPP-4 inhibitor
- DDP-4 blocks GLP-1
- increases insulin secretion and decreases glucagon release
- increases incretins GLP-1 and GLP (glucose-dependent insulinotropic peptide)
- treatment for DM2
- toxicity: mild urinary or respiratory infections
