Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
108 Cards in this Set
- Front
- Back
|
name the 6 classes of diabetes meds |
Insulin sensitizers alpha glucosidase inhibitors insulin secretegogues amylinomimetics (pramlintide) sodium-glucose co-transporter 2 (SGCT 2)inhibitor Insulin |
|
|
what are the 2 insulin sensitizers? |
Biguarides (Metformin) Thiazolinidediondes (TZDs)/Glitazones |
|
|
both of these drugs do not cause __________ _______ |
insulin release |
|
|
what is the generic name for Biguanide? |
Metformin |
|
|
what does Metformin target? |
insulin sensitizer |
|
|
MOA of Metformin? |
primary: ↓ hepatic glucose output by inhibiting hepatic gluconeogenesis
↓ intestinal glucose absorption (SI)
↑ glucose uptake |
|
|
metformin primarily reduces the ___________ goal |
FBG |
|
|
what effect does Metformin not have? so what is it rarely assoc. w/? |
does not promote insulin secretion so very rarely assoc. w/ HYPOGLYCEMIA |
|
|
what's the pharmacokinetics of metformin? |
does not bind to serum proteins and is not metabolized so excreted through the urine rapidly |
|
|
What are SE of metformin? |
DIARRHEA NAUSEA metallic taste |
|
|
long term use of metformin may interefere w/ ______ so cause __________ anemia
|
B12 absorption so cause megablastic anemia |
|
|
what are the benefits to metformin? |
weight neutral no hypoglycemia positive lipid effects (↑ HDL, ↓ TG, ↓ LDL)→ results in 4-6 weeks |
|
|
CI of metformin? |
renal insufficiency ( Cr >1.5 in men, >1.4 in women) acute CHF shock acute MI septicemia lactic acidosis- rare (CHF, dehydration, excessive ETOH intake, sepsis, hepatic/renal impairment) |
|
|
when should metformin be held? |
48 hrs prior to any contrast media like contrast CT → acute kidney failure |
|
|
name 2 examples of TZDs |
pioglitazone rosiglitazone |
|
|
what's the MOA of TZDs? |
insulin sensitizer ↑ glucose uptake ↑ adipocyte production ↓ glucose metabolism
possible B cell preservation |
|
|
what are SE of TZDS |
weight gain fluid retention→ CHF (rosiglitazone) ↑ risk of MI (rosiglitazone) HA anemia fxs bladder CA (pioglitazone) hepatic failure |
|
|
how is TZD metabolized? |
metabolism by P450 (pioglitazone) 99% hepatic metabolism |
|
|
what are benefits of TZDs? |
↑ HDL ↓ TG (Pioglitazone) no hypoglycemia use in RENAL INSUFFICIENCY once daily dosing |
|
|
CI of TZDs? |
class III and IV HF |
|
|
what's a precaution that must be taken? |
premenapausal/anovulatory females: result in resumption of ovulation→ ↑ risk of PG |
|
|
Pioglitazone (Actos)- be aware of the risk to ______ |
bladder cancer |
|
|
when using rosiglitazone (Avandia), it ↑ the risk of ______ |
MI, CHF |
|
|
name the 2 alpha glucosidase inhibitors |
acarbose miglitol |
|
|
what is the MOA for alpha glucosidase inhibitors |
prevents the breakdown of complex carbohydrates into glucose |
|
|
what does goal does it target? |
↓ post-prandial BG |
|
|
what does goal does it target? |
GI tract |
|
|
SE of alpha glucosidase inhibitors? |
FLATULENCE cramping diarrhea
occurs more as more complex carbs pass into the colon for digestion |
|
|
CI of alpha glucosidase inhibitors? |
IBD obstruction ulceration |
|
|
benefits of alpha glucosidase inhibitors |
↓ TG weight neutral no hypoglycemia |
|
|
disadvantages of alpha glucosidase inhibitors |
less effective to ↓ A1C TID dosing poorly tolerated GI adverse effects USE ONLY SIMPLE SUGAR (GLUCOSE) TO TX HYPOGYLCEMIA |
|
|
name the types of insulin secretagogue |
sulfonylurea Meglitinides GLP-1 Agonists DPP-4 Inhibitors |
|
|
what's the MOA of sulfonylurea |
-stim. B-cells to release insulin -reduce serum glucagon levels -↑ binding of insulin to target receptors and tissues
|
|
|
what goal does it target? |
↓ fasting and post-prandial BG (mixed effect) |
|
|
how is it metabolized? |
bind to serum albumin and metabolized by the liver |
|
|
SE of sulfonylurea |
HYPOGLYCEMIA weight gain rash photosensitivity |
|
|
what are the benefits of sulfonylurea |
works quickly (within hrs) high initial response rate |
|
|
disadvantage of sulfonylurea |
hypogylcemia weight gain eventual treatment failure |
|
|
1st generation sulfonylurea drugs are ______ and _______ |
tolbutamide (orinase) chlorpropamide |
|
|
why don't we use 1st generation anymore? |
disulfiram reaction: flushing w/ ingestion of ETOH |
|
|
2nd generation of sulfonylurea are _____, ______, _____ |
glyburide glipizide glimepiride |
|
|
what are the benefits of 2nd gen? |
last about 24 hrs fewer drug interactions |
|
|
which 2nd gen drug has the least amount of risk for hypogylcemia? why? what else can it be used in? |
Glipizide inactive metabolite so can be used in kidney dysfunction |
|
|
Meglitinides is what type of drug? what does it act on? |
insulin secretagogue
binds to ATP-dependent K cell on b cells to open calcium channels to increase insulin secretion |
|
|
what target goal does it reduce? |
↓ postprandial BG |
|
|
how is it metabolized? |
liver- bound to albumin |
|
|
what are SE of meglitinides? |
hypoglycemia ( weight gain ( |
|
|
what are benefits of meglitinides |
rapid onset of action less hypogylcemia and weight gain compared to sulfonylurea |
|
|
what are disadvantages of meglitinides |
hypogylcemia weight gain eventual treatment failure TID dosing |
|
|
which of the following drugs acts by decreasing the amount of glucose produced by the liver?
sulfonylurea meglitinides biguanides alpha-glucosidase inhibitors |
biguanides (Metformin) |
|
|
type 2 diabetics have a ↓ secretion of _______ |
GLP-1 |
|
|
incretin hormone GLP-1 does what 4 functions? |
↑ insulin ↓ glucagon secretion ↓ gastric emptying ↓ appetite ↑ glucose uptake/storage ↑ cardiac function |
|
|
what's the problem w/ GLP-1? |
rapidly deactivated by DPP-IV |
|
|
2 pharmacologic methods to increase GLP-1 are: |
long acting GLP-1 receptor agonist DPP-IV inhibitors |
|
|
name some examples of GLP-1 agonist |
exenatide exenatide ER liraglutide albiglutide dulaglutide |
|
|
what GLP1 agonist primarily targets postprandial glucose reduction |
exenatide |
|
|
what GLP1 agonist primarily targets ↓ FBG |
liraglutide |
|
|
what are SE of GLP1 agonist? |
GI- nausea, indigestion, belching HA dizziness WARNINGS OF POSSIBLE PANCREATITIS, THYROID TUMORS (done in animal studies) weight loss |
|
|
what are the benefits of GLP1 agonist? |
no hypoglycemia weight reduction possible potential for improved beta-cell mass/function possible CV protective actions |
|
|
what are disadvantages of GLP1 agonist? |
GI side effects (n/V) possible acute pancreatitis C-cell hyperplasia/medullary thyroid tumors in animals |
|
|
what's the dosing of each? |
Exenatide: short duration requiring frequent injection within a hr before 1st and last meal of the day
Liraglutide: once daily dosing, dosed independent of meals
Exenatide ER: once weekly form of exenatide for 24 hr coverage
Albiglutide and Dulagutide: once weekly dosing |
|
|
name some examples of Dipeptidyl peptidase-4 inhibitors (DPP-4 inhibitors) |
sitagliptin linagliptin saxagliptin alogliptin |
|
|
what's the MOA of DPP-4 inhibitors |
degrades incretins prolongs action of incretins to inhibit glucagon release ↑ insulin secretion ↓ gastric emptying to ↓ blood glucose levels |
|
|
what does it primarily reduce? |
postprandial glucose |
|
|
benefits to DPP-4 inhibitors |
very well-tolerated half-life is 15 min no hypoglycemia weight neutral once daily dosing |
|
|
SE of DPP-4 inhibitors |
HA nausea skin reactions nasopharyngitis or URI pancreatitis- rare skin reactions- rare |
|
|
disadvantages of DPP-4 inhibitors |
modest A1c lowering weight neutral |
|
|
what's the only drug that has been prescribed for type I and type 2 DM? |
amlyinomimetic: pramlintide |
|
|
Pramlintide is what type of drug? |
Amylinomimetic |
|
|
what is amylin? |
it's co-secreted w/ insulin by pancreatic beta cells in response to food so there is a deficit in diabetes |
|
|
MOA of amylinomimetic |
↓ glucagon secretion ↓ rate of gastric emptying ↑ satiety |
|
|
what does amylinomimetic target? |
↓ postprandial glucose levels |
|
|
how is amylinomimetic metabolized? |
primarily renal metabolism |
|
|
SE of amylinomimetics |
N/V hypogylcemia when given w/ insulin (meal time insulin dose must be reduced by 50% at initiation of pramlintide) |
|
|
benefits of amylinomimetics |
weight loss ↓ total dose of insulin used |
|
|
disadvantages of amylinomimetics |
requires 3 additional injections per day CAN'T BE MIXED W/ INSULIN
↓ rate and extent of absorption of drugs that require rapid absorption: pain relievers, antibiotics, oral contraceptives→ need separate admin. by at least 1 hr |
|
|
Pramlintide and exenatide both primarily ↓ post prandial BG. which additional activity does exenatide have that pramlintide lacks? |
ability to cause a glucose dependent increase in insulin secretion
they both ↓ glucagon secretion, ↑ satiety, ↓ rate of post-meal carbohydrate absorption |
|
|
name some examples of SGLT2 inhibitors |
canagliflozin dapagliflozin empagliflozin |
|
|
what's the MOA of SGLT2 inhibitors |
blocks reabsorption of filtered glucose in kidneys→ leads to glucosuria, improved gylcemic control |
|
|
SE of SGLT2 inhibitors |
repeated urinary infections VUVOVAGINAL CANDIDIASIS BALANITIS/BALANOPOSTHITIS ↑ Hct ↓ BP hyperkalemia ↑ LDL |
|
|
Benefits of SGLT2 inhibitors |
insulin-independent action caloric loss low hypogylcemia weight loss CAN BE USED REGARDLESS OF DIABETES DURATION |
|
|
CI of SGLT 2 inhibitors |
severe renal impairment (GFR <30) |
|
|
Invokana is what type of drug? |
SGLT2 inhibitor |
|
|
what are the most common SE of Invokana? |
vaginal yeast infection and UTI diuretic effect so orthostatic hypotension dizziness and fainting common in the first 3 months of therapy |
|
|
drug combo that is not good is |
metformin + Nateglinide + glipizide |
|
|
in the pipeline: glucokinase activators glucagon receptor antagonists sirtuin activators |
Glucokinase activators: increase prod. of insulin suppress hepatic glucose production
Sirtuin activators: anti-aging effect red-wine |
|
|
which patients need insulin? |
type 1 diabetics type 2 diabetics: sx PG or planning PG intolerant or have CI to oral anti-diabetic drugs (OADs) |
|
|
you may initiate insulin at any point in T2DM spectrum at: |
HbA1c >7.5% despite use of 2 or 3 OADs
HbA1c >9% despite previous T2 DM pharamacological therapy
HbA1C >9% + symptoms in newly diagnosed T2 DM |
|
|
what are advantages to insulin? |
-↑ glucose uptake by adipose tissue and muscles -suppress hepatic glucose release -ability to lower glucose is limitless -most clinically effective tx to lower blood glucose |
|
|
what are disadvantages to insulin? |
-hypoglycemia -weight gain -reluctance from patient -reluctance from providers |
|
|
what are S/S of hypogylcemia |
-shaking -fast heartbeat -sweating -anxious -dizziness -hunger -impaired vision -weakness/fatigue -HA -irritable |
|
|
the inhaled human insulin that recently came out is called _______ |
Afrezza |
|
|
when do you use Afrezza? who can use it? |
rapid-acting, pre-meal time insulin for type 1 and type 2 DM |
|
|
what's the onset for Afrezza and how long is the duration? |
onset- 12-15 min duration- 28-39 min |
|
|
before initiating Afrezza, all pts need _________ to identify potential lung dz |
spirometry (FEV1) |
|
|
CI of Afrezza? |
chronic lung dz- acute bronchospasm observed in pts w/ asthma and COPD |
|
|
take caution when taking Afrezza in what 2 kinds of patients? |
-pts who have recently stopped smoking -may cause a decline in pulmonary function over time (consider discontinuation when FEV1 decline is >20%) |
|
|
what are your rapid acting insulin drugs? onset, peak, duration? |
Lispro (humalog) aspart (novolog) Glulisine (Apidra)
onset- <0.25 hrs peak- 0.5-25 hrs duration- 3-5 hrs
**estimation- check PPT for specific times** |
|
|
what are your short acting insulin drugs? onset, peak, duration? |
regular insulin (Novolin R or humulin R) onset- 0.5-1 hr peak- 2-3 hrs duration- 3-6 hrs
**estimation- check PPT for specific times** |
|
|
what are your intermediate acting insulin drugs? what's the onset, peak, and duration? |
NPH onset- 2-4 hrs peak- 4-10 hrs duration- 10-16 hrs
**estimation- check PPT for specific times** |
|
|
what are your long acting insulin drugs? onset, peak, duration? |
Gargline (lantus) Detemr (Levemir) DEGLUDEC
onset- 2-4 hrs peak- rel. flat duration- 20-24 hr
**estimation- check PPT for specific times** |
|
|
what is the onset, peak, and duration of Degludec? |
onset- 0.5-1.5 peak- rel. flat duration- 36-40 hrs |
|
|
use insulin analogs or regular insulin? |
insulin analogs |
|
|
when do you want to consider giving a low glucose threshold suspend pump? |
pts w/ frequent nighttime hypogylcemia and/or hypoglycemia unawareness, |
|
|
what are goals in managing a hospitalized diabetic patient? |
-avoid hypogylcemia -avoid severe hypergylcemia -avoid volume depletion -avoid electrolyte abnormalities -ensure adequate nutrition |
|
|
what is the blood glucose goal for a critically ill patient? how is it administered? |
140-180
IV insulin |
|
|
in a non-critical ill patient, what are the BGL goals for premeal and random? how is it administered |
premeal <140 random <180
subcutaneous insulin |
|
|
specific CI to DM treatments SU TZD Metformin |
SU: MI TZD: LV dysfunction (CHF) Metformin: renal impaired and using radiocontrast dye |
