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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
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
DM

Medication classes
Secretagogues
- sulfonylureas
- meglitinides

Sensitizers
- biguanides
- thiazolidinediones

Alpha-glucosidase inhibitors

Peptide analogs
- incretin mimetics
- dpp-4 inhibitors
- amylin analogs
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)
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
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
DM

sensitizers - the drugs
biguanides
metformin (Glucophage)

thiazoladinediones (glitazones/TZDs)
rosiglitazone (Avandia)
pioglitazone (Actos)
DM

metformin - MOA / A1C
1. ↓ hepatic gluconeogenesis
2. improves glucose utilization
3. ↓ intestinal absorption of glucos

A1C reduction 1-2%
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
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)
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%
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
DM

TZDs - cautions/CIs
**edema** - Black Box for CHF

hepatotoxicity: LFTs qom for 12m. d/c if ALT > 3x ULN

decrease OC effectiveness
DM

alpha glucosidase inhibitors - the drugs
miglitol (Glyset)
acarbose (Precose/Glucobay)
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%
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
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
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)
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%
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
DM

exenitide - cautions/CI
- NOT GFR < 30
- NOT servere GI dz
- NOT DKA or type 1 DM
DM

sitagliptin (Januvia) - MOA/A1C
Inhibits degradation of GPP-4 & GIP→
1. ↑ insulin production
2. ↓ glucagon production
3. improved beta cell f(n)
DM

sitagliptin (Januvia) - clinical considerations
- combine w/met, TZDs

- minimal risk of hypoglycemia

- no effect on wt
DM

sitagliptin - cautions/CIs
adjust dose for renal insufficiency

Not in DKA or Tpye 1 DM
DM

- pramlintide (Symlin) - MOA/A1C
analog of endogenous amylin →
1. ↓ production of glucagon
2. slowing of gastric emptying
3. ↑ satiety and wt loss
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
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
DM

inhaled insulin (Exubera) - clinical consideration
provides prandia insulin coverage

pts need baseline spirometry, 6mo, then yearly

type 1 or 2
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
DM

Insulin - MOA/A1C
low levels - suppresses hepatic glucose production

higher levels - promotes glucose uptake by muscle tissue

A1C 2.5% or more
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®)
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)
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
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
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)
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)