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36 Cards in this Set
- Front
- Back
DM
Treatment Principles and Goals Glycemic control BP Lipids |
-A1C < 7% (<6% may reduce complications at the cost of increased risk of hypoglycemia)
-Preprandial plasma glucose - 90-130 -peak postprandial plasma glu - < 180 -BP < 130/80 -LDL < 100 -Triglycerides < 150 -HDL > 40 |
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DM
Prevention of complications |
-smoking cessation
-ASA TX -secondary prevention in all -primary prevention if >40 or have RF -immunizations -influenze -lifetime pneumococcal -foot care - daily self annual MD -skin inspection daily -eye: annual dilated eye |
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DM
Medication classes |
Secretagogues
- sulfonylureas - meglitinides Sensitizers - biguanides - thiazolidinediones Alpha-glucosidase inhibitors Peptide analogs - incretin mimetics - dpp-4 inhibitors - amylin analogs |
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DM
secratagogues - the drugs |
SULFONYLUREAS
First-generation agents o tolbutamide (Orinase) o acetohexamide (Dymelor) o tolazamide (Tolinase) o chlorpropamide (Diabinese) Second-generation agents o glipizide (Glucotrol) o glyburide (Diabeta, Micronase, Glynase) o glimepiride (Amaryl) o gliclazide (Diamicron) MEGLITINIDES - repaglinide (Prandin) - nateglinide (Starlix) |
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DM
secratagogues MOA and Clinical consideration |
Both
- ↑ insulin secretion from pancreas - cause wt gain - s/e hypoglucemia (sul > meg) - not in pregnancy or breastfeeding sulfonylureas - "LA - secratagogue" - 1-2% A1C ↓ - before meals QD/BID meglitinides "SA - secratagogue" - 0.5-2% A1C ↓ - before every meal |
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DM
Secratagogues Cautions/CIs |
- caution w/↓ renal/hep f(n) & elderly
- safe with metformin or glitazones **disulfiram (Antabuse)-like reaction with EtOH use** - following ↑ risk for hypoglycemia: - anticoagulants, tricyclics - fluconazole, digoxin - gemfibrozil, sulfonamides - CId in pts with: - severe infection - DKA - surgery or trauma |
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DM
sensitizers - the drugs |
biguanides
metformin (Glucophage) thiazoladinediones (glitazones/TZDs) rosiglitazone (Avandia) pioglitazone (Actos) |
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DM
metformin - MOA / A1C |
1. ↓ hepatic gluconeogenesis
2. improves glucose utilization 3. ↓ intestinal absorption of glucos A1C reduction 1-2% |
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DM
metformin - clinical consideration |
1. first choice in new dx of DM
2. ↓ weight a tad 3. favorable on trigs, LDL, HDL 4. GI sx: - take w/food - dose low and increase slowly 5. may take 8 weeks to see effects 6. may be best choice for HF pts |
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DM
metformin - cautions/CIs |
1. ↑risk of lactic acidosis (↑ risk for la)
- aMI, CHF exacerbation - severe respiratory dz 2. CIs - SCr>1.4 F, 1.5 M - hepatic dysf(n) - excessive EtOH use (>2/d or binge) |
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DM
TZDs - MOA / A1C |
agonist of PPARγ (a nuclear regulatory protein) → production of insulin-depen
enzymes that ultimately leads to 1. ↑ insulin sensitivity and therefore better use of glucose by the cells 2. ↓ hepatic glucose output A1C reduction of 1-2% |
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DM
TZDs - clinical consideration |
1. low risk of hypoglycemia
2. 5kg wt gain 3. favorable for Trigs, HDL 4. unfavorable for LDL 5. may take 16 wks to see effects |
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DM
TZDs - cautions/CIs |
**edema** - Black Box for CHF
hepatotoxicity: LFTs qom for 12m. d/c if ALT > 3x ULN decrease OC effectiveness |
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DM
alpha glucosidase inhibitors - the drugs |
miglitol (Glyset)
acarbose (Precose/Glucobay) |
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DM
alpha glucosidase inhibitors MOA, A1C |
delay digestion of carbs from a meal into simple sugars and their absorption in small Intestine
reduce A1C by 0.5 to 1% |
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DM
alpha glucosidase inhibitors clinical considerations/CIs |
main target tx on postprandial hyperglycemia
GI sx: flatulence and bloating limit use in united states but not Europe counsel pt to ↓ intake of simple sugars Avoid in pts w/GI disorders and SCr > 2 |
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DM
Peptide analogs - the theory/players |
Incretins are insulin secretagogues
Two incretins: - Glucagon-like peptide-1 (GLP-1) - Gastric inhibitory peptide (GIP) Dipeptidyl peptidase-4 (DPP-4) - rapidly inactivates GLP-1 and GIP |
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DM
Peptide analogs - the drugs - incretin mimetics - dpp-4 inhibitors - amylin analogs |
Incretin mimetics
- exenitide (Byetta) - GLP-1 agonist DPP-4 inhibitors - sitagliptin (Januvia) Amylin analogs - pramlintide (Symlin) |
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DM
exenitide (Byetta) - MOA/A1C |
GLP-1 agonist binding →
1. ↑ insulin production 2. ↓ glucagon production 3. slowing gastric emptying 4. ↑ satiety and wt loss 5. improved beta cell f(n) reduces A1C by 0.5 - 1% |
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DM
exenitide - clinical considerations |
- dose limiting s/e = naseua (50%)
- pts must ↓ meals size and CHO intake prior to use - dose 10-15 min before 2 largest meals - not indicated to combine w/insulin - most effective for post-prandial glucos elevations |
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DM
exenitide - cautions/CI |
- NOT GFR < 30
- NOT servere GI dz - NOT DKA or type 1 DM |
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DM
sitagliptin (Januvia) - MOA/A1C |
Inhibits degradation of GPP-4 & GIP→
1. ↑ insulin production 2. ↓ glucagon production 3. improved beta cell f(n) |
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DM
sitagliptin (Januvia) - clinical considerations |
- combine w/met, TZDs
- minimal risk of hypoglycemia - no effect on wt |
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DM
sitagliptin - cautions/CIs |
adjust dose for renal insufficiency
Not in DKA or Tpye 1 DM |
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DM
- pramlintide (Symlin) - MOA/A1C |
analog of endogenous amylin →
1. ↓ production of glucagon 2. slowing of gastric emptying 3. ↑ satiety and wt loss |
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DM
pramlinitde (Symlin) - clinical considerations |
can use in combo w/insulin in DM 1 & 2
due to sig risk of hypoglycemia, when used w/insulin, prandial insulin dose should be ↓d by 50% DLs/e is naseua |
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DM
pramlintide (Symlin) - cautions/CIs |
do NOT use in following:
1. severe GI dz 2. poor adherence w/current insulin 3. recurrent severe hypoglycemia 4. A1C<9% 5. hypoglycemia unawareness |
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DM
inhaled insulin (Exubera) - clinical consideration |
provides prandia insulin coverage
pts need baseline spirometry, 6mo, then yearly type 1 or 2 |
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DM
inhaled insuline (Exubera) - cautions/CIs |
Not inpts with lung dz (COPD, Asthma..)
Not in active smokers or quit < 6mo - insulin exposure incs by 2-5 fold |
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DM
Insulin - MOA/A1C |
low levels - suppresses hepatic glucose production
higher levels - promotes glucose uptake by muscle tissue A1C 2.5% or more |
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DM
Insulin - rapid-acting - onset - time of peak - duration - names |
-onset: 10-30 min
-peak: 30-90 min -duration: 3-5 hours Insulin lispro (Humalog®) Insulin aspart (NovoLog®) Insulin glulisine (Apidra®) |
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Insulin - short-acting
- onset - time of peak - duration - names |
-onset: 30 min
-peak: 2.5 -5 hours -duration: 4 -12 hours Insulin regular (Humulin® R, Novolin® R) |
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Insulin - intermediate-acting
- onset - time of peak - duration - names |
-onset: 1-2 hours
-peak: 4-12 -duration: 18-24 Insulin NPH (isophane suspension) (Humulin® N, Novolin® N) Human Lente |
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Insulin - intermediate- to LA (Basal)
- onset - time of peak - duration - names |
-onset: 3-4
-peak: 3-14 -duration: 6-23 Insulin detemir (Levemir®) Human Lente |
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Insulin - long-acting (Basal)
- onset - time of peak - duration - names |
-onset: 3-4
-peak: no pronounced peak (glargine) -duration: > 24h Insulin glargine (Lantus®) human ultra lente (not basal-simply LA) |
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Insulin - combinations
- onset - time of peak - duration - names |
-onset: 10 - 30 min
-peak: 2 -12 h -duration: 18 -24 Insulin aspart protamine suspension and insulin aspart (Novolog® Mix 70/30) Insulin lispro protamine and insulin lispro (Humalog® Mix 75/25™) Insulin NPH suspension and insulin regular solution (Novolin® 70/30) |