oral hypoglycemic agents Flashcards
what is the MOA for a sulfonylurea?
act at pancreatic beta cells to simulate release of insulin
T/F sulfs can cause hypoglycemia
TRUE
they have the HIGHEST incidence
Which drug class has high failure rates?
sulfonylureas
20% primary failures
10-15% secondary failures
which drug class should you avoid in patients with sulfa allergy?
sulfonylureas.
some that are allergic to sulfa ABX are OK though.
which drug has a high risk of hypoglycemia in renal failure patients
sulfonylureas.
because there are active and inactive metabolites
which is the safest sulf to use in renal dysfunction?
which is the worst?
gylpizide is safest
glyburide & chlorpropamide is worst - one your CC is less than 50, your risk of fluid retention and hypoglycemia increases dramatically
T/F Sulfonylureas may cause fetal hypoglycemia
TRUE
T/F Although hypoglycemia with sulfs is less frequent than with insulin, it is often more prolonged and more dangerous
TRUE
It can require prolonged infusions of glucose-containing solutions
sulfonylureas should be avoided in patients with liver disease, except ______
acetohexamide
____ are contraindicated in patients with hypoglycemia unawareness
Sulfonylureas
remember bc they have the greatest risk of hypoglycemia!
what is the shortest acting and least potent sulf?
tolbutamide (orinase)
also has the fewest side effects
most of the hypoglycemic action of acetohexamide is due to
its principle metabolite
what is the longest acting sulf
chlopropamide (diabeinese)
may approach 72h.
what sulf is associated with disulfiram-like reactions
chlopropamide (diabeinese)
what sulf is associated with severe hyponatremia? why?
chlopropamide (diabeinese)
when you have large glucose molecules floating around in the blood, it changes the osmolarity and in response to that, your body will start pulling water out of cells and into the blood stream - an osmotic type movement of water - body tries to combat the increase in osmolarity , causing a dilatational hyponatremia.
If you can treat the hyperglycemia, the sodium will correct itself.
what drugs are alpha-glucosidase inhibitors?
acarbose (precose)
miglitol (glyset)
alphas = acar + mig
whats the MOA of alpha-glucosidase inhibitors? (acar/mig)
think: alphas—absorption (inhibit)
decrease intestinal hydrolysis of complex carbs
inhibits the enzyme that breaks down complex carbs. you can’t absorb them, just eliminate them. so less glucose in the blood stream,.
whats the MOA of meglitinides
increase insulin secretion from islet cells (like sulfonylureas)
T/F Meglitinides have a faster onset and shorter duration than sulfs
TRUE
which drugs are meglitinides
RepaGLINIDE (Prandin)
NateGLINIDE (starlix)
meglitINIDES = repGLINIDE and NateGLINIDE
T/F Meglitinides are active whether glucose is present or not
FALSE - only active in the presence of glucose.
this decreases the risk of prolonged hypoglycemic episodes
meglitinies cause you to ___ weight
gain
the #1 med for new onset type!! diabetes that requires medication =
metformin
what class is metformin
bigauanides
bc metformin is the big dog
T/F Metformin has a high risk of hypoglycemia
FALSE - it decreases BG concentrations with only a very low risk of hypoglycemia - almost neutral when it comes to hypoglycemic events
what is the MOA of metformin? 3 points
- decreases hepatic glucose production (reduces gluconeogenesis)
- reduces glucose absorption from the intestine
- increases insulin sensitivity
why can someone who’s on metformin get off of their sulfonylurea?
because metformin reduces glucose absorption from the SI so you don’t need the sulf to increase beta islet insulin release
which drug produces satisfactory results in 50% of the sulf failures
metformin
whats the BB warning with metformin?
lactic acidosis
n/v, inc RR, HR, abd pain, shock
how long before surgery should metformin be d/c’d?
48h
whats the best way to prevent lactic acidosis
hydration
hold metformin ___h prior to and after IV contrast because of
48, nephrotoxicity
whats the package insert for metformin say
that withholding food/fluids during surgery may increase the risk for volume depletion, hOt, renal impairment.. so temporarily d/c metformin while patients have restricted food and fluid intake.
metformin is contraindicated if GFR is
30
do not initiate or re-evaulate patents with GFR
45
metformin is contradicted in patents aged >__
80
metformin has high rates of ____ upset
GI
new recommendations for metformin are based on ___ NOT ___ and ____
GFR..
not gender and cr
T/F metformin is contraindicated in CHF and hepatic impairment
TRUE
which drugs are thiazolidinediones
rosiglitaZONE and pioglitaZONE
Thia is in the ZONE
which drug class is esp effective in the obese
TZD’s
whats the MOA of TZD’s
decrease hepatic glucose output and decrease insulin resistance
so TZD’s stop the liver and stop resistance
which drug class cause hepatotoxicity
TZD’s
think: they work in the liver decreasing hepatic glucose output
which drug class has a bizarre risk of bone fx
TZD’s
TZDs cause weight ___
gain
T/F: higher rates of CV deaths and MI’s in patients that take TZD’s
TRUE - avandia (ros)
aVan = cV death
TZD’s have Three Terrible side effects like:
hepatotoxic, peripheral edema, CHF exacerbations
DPP-4 inhibitor drugs =
gliptins
sitagliptin (Januvia)
Saxagliptin (onglyza)
linagliptin (tradjenta)
alogliptin
DPP4 MOA
- increases pancreatic insulin secretion
- limits glucagon secretion
- slows gastric emptying
- promotes satiety
glucagon-like peptide.. when you eat, it is released.. tells you youre full and not to eat anymore and also kick starts a couple of processes to prep for glucose load.. pancreas/liver. so DPP4 is dipeptidyl peptidase and that reduces the breakdown of GLP1. so it lasts longer and continues to stimulate satiety
so it is working at different places where your glucagon like peptide normally works, to inc the amt of it.. to then limit glucagon sectretion, increase insulin secretion, slow gastric emptying , making you feel full
revise this card…..
which drugs basically cause a forced gastroparesis
DDP4 inhibitors - the gliptins
DPP4 inhibitors have 4 really bad side effects that were discovered post-marketing =
pancreatitis, angioedema, Stevens johnsons, anaphylaxis `
which drugs have infection risk
DDP4 inhibitors - the gliptins
risk of URI + UTI’s
which 2 drug classes fall under incretin mimetics
GLP-1 analogs & amylin analogs
how do GLP1 analogs work
prolong gastric emptying, reduce post-prandial glucagon secretion
think: DPP4 inhibitors work like this too bc they reduce the breakdown of GLP1
which drugs are GLP1 analogs?
the TIDES
exanatide (byetta, bydureon)
liraglutide (victoza)
albiglutide (tandem)
dulaglutida (trulicity)
avoid which GLP1 analog in renal failure
exanatide (byetta)
BYEpass Byetta in RF
avoid which GLP1 analog in thyroid carcinoma
liraglutide (victoza)
vicotza is NOT a victory in thyroid cancer
how do amylin analogs work?
they increase insulin secretion, slow gastric emptying, increase beta cell growth, central appetite suppression
which drug is an amylin analog
pramlinide (symlin)
slimy like the gila monster
whats the BB warning with Amylin
hypoglycemia (esp type1)
which drugs are SLGT2 inhibitors
the gliflozin’s
canagliflozin (invokana)
dapagliflozin (farxiga)
empagliflozin (jardiance)
gliFLOZIN’s get the glucose FLO goin
how do SLGT2 inhibitors work
increase urinary glucose excretion.
make you pee it out.
within the kidneys there is a sodium and glucose transporter and by inhibiting this, we are now holding on to less glucose, we are peeing more out.
think STG = sodium glucose transporter
SLGT2 inhibitors are contraindicated with
crcl <30
ESRD
HD
since SLGT2’s increase urinary glucose excretion, what side effects are you thinking of
s/e r/t fluid shifts so hOtn
UTI (d/t extra glucose in urinary tract)
toe amputations (bc of the dehydration/fluid shifts/PVD)
