Type 2 DM Flashcards
around 1995 there were only ____ classes of drugs besides insulin: _____ and _______. now there are about __ with more on the horizon
1995: 2: metformin and sulfonyureas
now: 9
certain companies are now classifying the “cure” for DM as an A1C < ___ for __ years …. however the real cure may be a possibility for the future
<6.4 for 2 years
NOT IN NOTES, HADLEY MADE A POINT OF IN LECTURE
Txt: increases in insulin should be by ____ at a time
5%
At what age and frequency are average people (no obesity of complications) checked for DM ? and if there are risk factors (aka preDM or suspiscion of preDM)?..
45 years old, every 3 years.
risk factors? every 1 year
what must you have before you can actually Dx someone with type 2 DM?
two abnormal test results
can use the same sample for two separate tests, so that you dont have to re-stick pt
what are way to test for DM?
fasting blood glucose (FBG)
glucose tolerance test
A1C
for those with preDM, _________ can reduce risk of developing typ 2DM by ____. The goal is to get __% loss of INITIAL body weight.
intensive behavioral interventions, dec. by 50%
want 7% dec initial body weight
alcohol for DM pts?
yes its ok! (if moderate)
< 1/day for women
<2 /day for men
what do we use to check for glycemic target?
assessment of glycemic control: use A1C (not FBG or glucose tolerance)
if were testing for glycemic control and they have good control, we will then re-test ____ time a year. if not good control then re-test ____ a year.
good control: 2x year
not good control:4x year
DM txt: sliding scale or no?
NO SLIDING SCALE
general approach to DM treatment
- diet, exercise, pt education
- metformin to start
- maybe add on other meds
- txt comorbid conditions
- (consider txt pre-DM with meds, diet/exercise)
the average decrease in A1C from drugs? but a higher starting A1C means what?
1%
higher starting A1C, usually >1% decrease from drugs (higher starting A1C = bigger response to drugs)
first line oral antiDM drug? what is the starting dose?
biguanides (metformin)
starting dose: 500mg at night for two weeks
why dont you want to increase metformin dosage too quickly?
people will become intolerant (bad GI ADRs more likely)
metformin: restrictions of txt with specific GFR levels, what about if the pt is going to receive contrast for imaging?
cant have if GFR <30
dose adjust GFR 30 to 45 (no current kidney failure: therapy initiated at half initial dose, if GFR falls into this range DURING therapy: drop dose by half)
must stop before having IV contrast
when dosing for metformin, always use _____.
feedback- A1C levels
metformin max dose. why is this good to know?
2500 mg/day
max out on metformin THEN try something else
ADR of alpha glucosidase inhibitors?
GI issues- flatulence/diarrhea, fecal incontinence
which anti-DM drugs have a first phase insulin response? which dont? this first phase is good but with what risk? …
first phase: meglitinides and incretins
(insulin and amylin as well)
(produce insulin at the time of the meal to counter that initial glucose spike.. but leads to hypoglycemia risk if no carbs are in the meal)
no first phase: sulfonyureas
which anti-DM drug increases sensitivity?
TZDs (“glitazones”)
the remaining “ok” TZD/glitazone without CVD risk and beneficial effects on lipids
pioglitazone
which type of anti-DM drug is byetta(exantide)?
what are two major added benefits of it?
incretin: aka GLP1 agonist or “mimic”
weight loss, decreased CVD risk (moderately)
do incretins increase pancreatitis risk?
according to hadley, no, DM is what increases the risk
amylin has what added benefit (same as GLP1s)
weight loss
which anti-DM drug decreass CVD and CHF risk and lowers BP?
SGLT2 inhibitors
GLP-1 vs DPPIV drug administration
GLP 1- subQ
DPP IV- oral
which anti-DM drug decreases insulin resistance?
SGLT-2 inhibitors (do so while paradoxically increasing glucagon and endogenous glucose production)
the impact on cardiovascular outcomes is positive with this drug..
SGLT2-Is (empagliflozin specifically)
drug considerations for txt: start ____ and go _____ to minimize ADRs. especially with _____ and _____.
start _____ early.
what is always an option?
start low and go slow
Alpha glucosidase-Is and lipase inhibitors (drugs for weight loss)
-start combo therapy early
-insulin is ALWAYS an option to get sugars down
for DM txt STRATEGIES, always consider ____ ____ ____.
global cardiovascular risk
we see DM treatments that provide good lab outcomes (aka______) but dont consider what?
- good lab values aka “surrogate endpoints”
- good outcomes that matter to the pt ( quality of life, risks etc)
why do we want to minimize insulin use?
can increase CVD risk
Txt that affect the Mechanisms of DM ______ are high priority targets
earlier in the cascade
- (obesity, insulin resistance and reduced gut peptide function are the root of DM, these should be addressed FIRST)
what two drug options will be look to add-on for decreased CVD risk
liraglutide (a GLP-1)
any SGLT2
what two drug classes would be good add-ons to decrease renal risk?
GLPs and SGLT2s
if there is no risk for renal or CVD, what three things will we take into consideration when deciding on an add-on drug for DM?
weight loss/minimize weight gain (any except sulfonyurea)
minimize hypoGlycemia risk (SGLT2 or GLP1)
cost (Sulfonyurea) or TZD)
what to do if a pt has hypoglycemia from med?
oral glucose, wait 15min, then give more if it hasnt come up
what two drugs can cause weight gain ?
sulfonyureas and insulin
what txt method is best for type 1 DM?
basal-bolus
do we take someone off metformin?
no (unless their GFR<30)
..only add-on (again… no sliding scale)
what to monitor if someones on metformin?
B12 levels
high TriGs? what is the txt strategy?
lifestyle and glycemic control! almost never txt with meds just for this… unless its really bad.
what to do for DM retinopathy? different approach for type 1 and type 2?
optimize BP and sugar control
type 2: assume its been going on a while.. txt right away
type 1: maybe txt 5 years from Dx
for older Pts… err on the side of _____
hyperglycemia.. targets should be slightly higher for their A1C b/c its worse for them to by hypoglycemic than hyperglycemic
in Type 2 DM glucagon is ____ likely due to what?
elevated inappropriately
- dysregulation of gut peptide interactions
- ->drives hepatic glucose output despite high serum glucose levels
Kidney works hard to reclaim glucose in the _______, even when blood glucose is high, but cannot keep up with amounts over _____
ultrafiltrate
150 mg/dL
why do we treat DM?
acute symptoms and longterm complications
hyperglycemia in type 1 vs type 2
type 1: DKA
type 2: HHNK (no ketones, much higher glucose >600mg/dL)
why do we want a SLOW correction of HHNK?
prevent brain swelling from rehydration of brain cells
why is insulin “not essential” for HHNK?
dont really need it for txt (focus on rehydration) PLUS it can cause worse hypoKalemia
what is insulin resistance?
hyperinsulemia (high insulin levels) with insulin resistance to maintain glucose levels
(path is broken somewhere between where the insulin binds on target cell and where glucose is supposed to come into target cells)
how can you tell someone has DM when looking at first and second phase response ?
1st: normal person will have insulin spike from glucose spike (from meal) . DM will not have insulin spike (decreased spike)
2nd: somewhat equal DM and non DM
impaired fasting glucose vs type 2 DM (in regards to insulin resistance, production and fasting plasma glucose? )
IFG: insulin resistance just outweighs insulin production, fasting plasma glucose low
DM type 2: insulin resistance HIGH, insulin production LOW (drops), fasting plasma glucose higher.
dont just treat sugar levels, treat ______
insulin resistance! supranormal insulin levels are harmful!
most sensitive detector to indicate when complications will start from DM: lab and symptom?
FPG >126
Retinopathy
UKPDS: txt _____ for microvascular problems, ______ for macrovascular problems
insulin- micro
metformin- macro
what meds do you have to monitor A1C levels for?
those with hypoglycemia risk (ex/ yes insulin , dont need to for metformin)
