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Diabetes Pharmacology > Diabetes Pharmacology > Flashcards

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
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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
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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
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3
Q

Bromocriptine

A
  • dopamine receptor (D2) agonist

- can have modest effect on treating diabetes

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4
Q

Regular insulin

A
  • short acting
  • clinical use: DM1, DM2, GDM, DKA (IV), hyperkalemia (+glucose), stress hyperglycemia
  • toxicity: none
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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
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6
Q

Glargine

A
  • insulin, long acting
  • “peakless”
  • clinical use: DM1, DM2, GDM
  • basal glucose control
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7
Q

Detemir

A
  • insulin, long acting
  • clinical use: DM1, DM2, GDM
  • basal glucose control
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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)
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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
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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
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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
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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
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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
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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
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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
Q

Colesevalam

A
  • bile acid binding resin

- some treatment in DM type 2

26
Q

Pramlintide

A
  • amylin analog
  • decreases gastric emptying, decreases glucagon
  • inhibits glucagon production
  • treatment of type 1 and type 2 DM
  • toxicity: hypoglycemia, nausea, diarrhea
27
Q

Exenatide

A
  • 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
Q

Liraglutide

A
  • 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
Q

Linagliptin

A
  • 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
Q

Saxagliptin

A
  • 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
Q

Sitagliptin

A
  • 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

Diabetes Pharmacology (1 decks)

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