diabetes Flashcards
medication classes for type 2 diabetes
biguanides
sulfonylureas
meglitinides(non-sulfonylurea secretagogues)
alpha-glucosidase inhibitors
thiazolidinediones (TZDs) aka Glitazones
dipeptidyl peptidase-4 (DPP-4) inhibitors
**insulin may be given in conjunction with any drug from each class above
metformin MOA
inhibits glucose production by the liver & decreases insulin resistance
sulfonylureas & meglitinides MOA
increase secretion of insulin
keep the ion channels open longer to continue the trigger for insulin release
alpha-glucosidase inhibitors MOA
delay absorption of glucose by the intestine
thiazolidinediones (glitazones)
decrease insulin resistance
change gene expression so that GLUT receptors are more effecient
-can cause CHF
dipeptidyl peptidase-4 (DPP-4)
promote the release of insulin from the pancreas after eating a meal
-slow down enzyme release
switch from oral diabetic medication to insulin when…
- acute infx
- in-patient surgery requiring NPO
- pregnancy
- for tighter glucose control
- to avoid developing macrosomia
biguanides
metformin
-decreases hepatic glucose production, enhances insulin sensitivity in skeletal muscle
Metformin/ Glucophage
biguanide
for type II diabetics
MOA- decreases hepatic production of glucose
-similar effficacy as sulfonylureas by slight reduction in pts’s fasting glucose, non-fasting glucose, & HA1C
-may cause modest wt loss
SE- cramping & nausea, reduced by using slow release forms of the drug, metallic taste, LACTIC ACIDOSIS(mb fatal)
-DO NOT USE IN RENAL INSUFFICIENCY PT’s- monitor creatinine lvls in pts
-inc. risk of B12 def.- supplementation w/B-complex should be standard practice
metformin dosing
- 500, 850, 100 mg tabs
- generally dosed BID
- usu daily dose 1500-200mg
extended release
- 500 & 750mg
- QD
- 1500-2000mg daily
brand names- glucophage, fortamet- more expensive
sulfonylureas MOA
stimulate intact beta cells to release more insulin
- interacts with ATP-sensitive K channels in the beta cell membrane- blocks them= increased calcium release= more insulin release
- hypoglycemia is possible SE- particularly in pts with impaired renal or hepatic funx
- wt gain MC SE
- genreally ineffective after 5-10 yrs use d/t decline of beta cell funx
- AVOID IN PT’s W/SULFA ALLERGY
meglitinides
AKA- non-sulfonylurea secretagogues
stimulate beta cells to release insulin
-bind to ATP-sensitive K channels= inc insulin release
-wt gain, hypoglycemia
-for combined use with metformin or drugs from glitazone class- avoid combining with sulfonylureas
-rapidly absorbed in GI- blood lvls peak in 30-60 min- rapidly cleared
-taken 3-4 times /day- not taken if a meal is missed
-Nateglinide/ starlix- less effective
-repaglinide/ prandin- equal to sulfonylureas
thiazolidinediones(TZD’s)/ glitazones
TZDs/ Glitazones
MOA- improve insulin sensitivity in skeletal muscle cells, fat cells, liver cells, decrease hepatic glucose production
-dosed QD, may take 6-14 wks to achieve full effect
-approved for use as montherapy, or combined with metformin or a sulfonylurea
-INC RISK OF CHF
-red bone density, inc fracture, wt gain- 5-10 lbs
specific examples of TZD’s/glitazones
Rosiglitazone/ avandia
pioglitazone/ ACTOS
-both can be used as monotherapy or concurrent with Metformin or sulfonylurea
-only ACTOS approved for concurrent use with insulin
-test liver funx before tx, then retest at 1 & 3 months for any rise in ALT
troglitazone/rezulin- lethal SE & removed from market
Alpha-glucosidase inhibitors
MOA- inhibit the alpha-glucosidase enzymes that line the brush border of SI- interfere with hydrolysis of CHO- delays absorp. of glucose & monosaccharides
-must be TAKEN WITH MEALS!
SE- from unabsorbed CHO(osmotic, fermentation)- abd pn, diarrhea, flatulence
-hypoglycemia with these drugs must be treated with glucose, not sucrose
-CI in pts w/GI dz- IBS, colonic ulceration, intestinal obstruction