DM pharm Flashcards
rapidly acting insulins
lispro
aspart
glulisine
short acting insulins
regular insulin
intermediate acting insulins
NPH and NPL
ultra-long actin insulins
glargine
detemir
sulfonylureas
glipizide
glyburide
glimepiride
non-sulfonylurea insulin releasers
repaglinide
nateglinide
alpha glucosidase inhibitors
acarbose
miglitol
TZDs
rosiglitazone
pioglitazone
adjuncts
exenatide
sitagliptin
saxagliptin
regulation of insuline secretion
glut 2 transports glucose into beta cells -> high ATP -> opens ATP sensitive KCh -> depolarizes membrane -> opens CaChs -> insulin release
degradation of insuline
primarily liver
kidney
t1/2= 5-15min
recommended hA1C
6.5-7%
Dx of DM
classic signs and symptoms
FBG >126
random glucose >200
failure of oral glucose tolerance test
typical insulin regimen
30 U/day
2/3 before breakfast (2/3 NPH 1/3 regular)
1/3in evening (1/3 regular before dinner, 2/3 NPH at bed)
metformin
first line
antihyperglycemic
does not cause hypoglycemia
metformin affects
- increases action of insulin
- increases glycolysis
- increases glucose uptake and utilization by mm
- decreases gluconeogenesis and hepatic glucose output
- decreases GI absorption of glucose
advantages of metformin
no hypoglycemia
no weight gain
favorable lipid profile
adverse effects of metformin
GI: anorexia, nausea, diarrhea, abdominal discomfort
lactic acidosis
complications of metformin induced lactic acidosis
renal or hepatic insufficiency
CV disease
second generation sulfonylureas
glipizide
glyburide
third generation sulfonylureas
glimeperide
MOA sulfonylureas
bind ATP sensitive KCh -> continuously open -> Ca influx -> insulin secretion
indirectly increase insulin sensitivity
adverse effects of sulfonylureas
weight gain and hypoglycemia
glimerperide advantages
less weight gain then 2nd gen
doses once daily PO
glimerperide CI
sulfa allergy pregnancy type I DM ketoacidosis renal failure hepatic failure major surgery
glipizide
dose 1-2x/day PO
inactive metabolites
no CIs
glyburide
freater incidence of hypoglycemia
use with caution
non-sulfonylurea secretagogues
same MOA as sulfonylureas, but have different binding site
short half-life
rapid action
can be taken right before meal
alpha-glucosidase inhibitors
not very popular b/c block glucose absorption -> more gut bacteria digestion -> serious gas
can also cause hypoglycemia
GLP-1 agonists
peptide hormone cleaved from pro-glucagon precursor
secreted by intestinal L cells
highly resistant to DPP-4 degredation
actions of GLP-1 agonists
glucose dependent enhancement of insulin secretion
inhibition of glucagon secretion
appetite suppression and satiety induction
reduce gastric emptying
possible stimulation of islet cell growth
Decrease HbA1c
decrease postprandial glucose
weight loss
little hypoglycemia
GLP-1 combos
with metformin, TZDs, and/or sulfonylurea
NOT with insulin
must be injected
DDP-4 inhibitors
prevents break down of GLP-1 and GIP
oral
cannot be combined with insulin
actions of DDP-4 inhibiots
increase insulin secretion decrease glucagon decrease hepatic glucose production increase peripheral glucose uptake and utilization little hypoglycemia
pramlintide
synthetic analog of amylin
4th line drug
used with DMI or II when already on insulin
cannot be dosed with insulin and must be injected
TZDs MOA
insulin sensitizers act as steroid hormone -> PPAR-gamma RXR R complex decrease insulin resistance decrease hepatic glucose output increase glucose uptake
risks of TZDs
very controversial
risk of MI with rosiglitazone
risk of bladder CA with pioglitazone
SGLT2 inhibitors
-flozin
PO 1/day for DMII
used in combo
SGLT2 inhibitors MOA
SGLT2 is membrane protein expressed in kidney and inhibition of this protein blocks glucose reabsorption
