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85 Cards in this Set

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Hyperglycemia in DM may be caused by what 3 defects?
defect in:
1. insulin production
2. insulin action
3. combo of the two
Treatment goal of diabetes?
To achieve and maintain glycemic levels as close to the non-diabetic range as possible in order to prevent the development of complications of chronic diabetes.
Rapid-acting insulins?

Insulin aspart, lispro, and glulisine

2-4 hours
Regular insulin duration?
6-8 hours
Intermediate insulin?

NPH insulin (Lente if OTM)

16-24 hrs
Long-acting insulin?
insulin glargine, insulin detmir
Glargine duration?

Detmir duration?
glargine: 20-24 hrs

detmir: 6-24 hrs
How does insulin correct hyperglycemia?
1. promotes glucose uptake in muscle, liver, and adipose
2. inhibits hepatic glucose production (gluconeogenesis/glycogenolysis)
3. inhibits flow of gluconeogenic precursors from muscle/adipose to liver
4. inhibits secretion of counter-regulatory hormone glucagon
Why should sites of insulin injection be varied?
to avoid injection site lipodystrophy
Initial insulin dose?
0.2-0.6 units/kg/day in divided doses
How are insulin types usually divided up for a person in general?
50-75% of dose given as intermediate/long-acting insulin and remainder given as rapid-acting or short-acting insulin at meals.
Adverse reactions with insulin therapy?
1. headache
2. tachycardia
3. fatigue
4. mental confusion
5. injection site lipodystrophy
6. diaphoresis
7. hypersenstivity (less common w./ human insulin)
What drugs DECREASE hypoglycemic effects of insulin?
1. oral contraceptives
2. corticosteroids
3. diltiazem
4. niacin
5. epinephrine
6. thiazide diuretics
What drugs INCREASE hypoglycemic effects of insulin?
1. alcohol
2. alpha-blockers
3. beta-blockers
4. salicylates
5. sulfinpyrazone
6. tetracyclines
What does intensive/standard insulin therapy consist of?
1. a basal level of insulin to lower fasting glucose (daily or twice daily injections of long-acting insulin)

2. pre-meal boluses of a rapid or very rapid-acting insulin to control postprandial glucose elevations
Why give a type 1 diabetic intensive insulin therapy?
Significantly reduces risk of diabetes complications.
What two classes of drugs are insulin secretagogues?
1. Sulfonylureas
2. Meglitinides
What specific drugs are sulfonylureas?
1st generation:

2nd generation:
-Glimepiride (Amaryl)
-Glyburide (DiaBeta, Micronase)
-Glipizide (Glucotrol)
What specific drugs are meglitinides?
-Repaglinide (Prandin)
-Nateglinide (Starlix)
MOA of the sulfonyureas?
-sulfonylureas interact w/ SUR1 subunit of ATP-sensitive K+ channels (Kir6.2) on pancreatic beta cells --> inhibits channel activity --> cell deploarization triggers voltage-gated Ca++-channels to open --> influx of Ca++ and secretion of insulin
Sulfonylurea action on fasting and postprabdial sugars?
-primarily reduce fasting
-little effect on postprandial glucose
Who are sulfonylureas most effective in?
T2DM pts who have had diabetes for <10 years.
How do 2nd generation drugs differ from 1st generation drugs?
2nd gen are:
1. more potent
2. lower freq of hypoglycemia
3. fewer drug interactions
Adverse effects of sulfonylureas?
1. modest weight gain (~2 kg)
2. hypoglycemia - pts w/ impaired renal and/or hepatic function
What is the DOC for elderly pts or pts w/ chronic renal failure?
Glipizide - b/c it is metabolized in the liver and inactive metabolites are excreted in the urine
Why do sulfonylureas have many drug interactions? What are some specific ones?
They are highly protein bound: interact w/ salicylates, beta-blockers, warfarin, and phenylbutazone.
MOA of Meglitinides?
Meglitinides trigger insulin secretion by similar mechanism to sulfonylureas, but interact w/ different region of the SUR1 subunit of beta cell ATP-sensitive K+ channel.
Peak action and duration of Meglitinides?

How often should they be given?
peak: 1 hr
duration: 4 hrs

need to give 3 times daily
How do they alter fasting and postprandial glucose levels?
-primarily affect postprandial glucose

-likely beneficial in pts w/ barely elevated FPG but prominent postprandial hyperglycemia
By how much do Meglitinides decrease HbA1C?
by 1.0-1.5% points
What's the difference in effectiveness b/w nateglinide and repaglinide?
Nateglinide is less effective than repaglinide.

Repaglinide is as effective as sulfonylureas or metformin at lowering HbA1c.
Adverse effects of Meglitinides?
1. weight gain
2. hypoglycemia (less than w/ sulfonylureas)
C/Is of Meglitinides?
1. liver disease
2. pregnancy
What anti-diabetic drug is a biguanide?
**What is the 1st line therapy for type 2 diabetes?**
Metformin! (along w/ diet and exercise)
Primary action of Metformin?
Reduces hepatic glucose production (does not promote insulin production).
Likely MOA of Metformin?
activates AMP-dependent protein kinase (AMPK)
How does activation of AMPK by Metformin improve hyperglycemia?
1. promotes glucose uptake into muscle and adipose
2. inhibits hepatic glucose production, and hepatic cholesterol and TG biosynthesis
3. promotes FFA ocidation --> reduces FFA stores that contribute to insulin resistance
4. inhibits activity of inhibitors of insulin signaling pathway thereby enhancing insulin signaling and prevents insulin resistance
Metformin: time to peak plasma concentration and duration of action?
peak: 2 hrs
duration: 6 hrs
How dwell does Metformin improve FBG and HbA1c?
FBG: 20% decrease
HbA1c: ~1.5% decrease
Advantages of Metformin with regards to weight and hypoglycemia?
1. does NOT cause weight gain (promotes weight loss)
2. does NOT cause hypoglycemia
Advantages if Metformin over other oral hypoglycemic agents?
1. decreases frequency of MI
2. decreases diabetes-related death
3. decreases all-cause mortality in type-2 obese pts
Why does Metformin have beneficial effects on CD outcomes?
improves lipid profiles: dec TG and FFA, small dec in LDL, modest increase in HDL
Most common adverse effect w/ Metformin? How is it avoided?
GI tract problems - take w/ food
What can Metformin decrease the absorption of?
Decrease vitamin B12 absorption (folic acid) - rarely causes megaloblastic anemia.
Rare potentially fatal S/E of Metformin?

What drug showed increased frequency of this problem ans whas removed from the market?
Lactic acidosis (<1:100,000)- due to glucose metabolism in absence of adequate oxygen.

Phenformin was removed.
Contraindications of Metformin therapy?
1. pregnancy
2. impaired renal function (more susceptible to lactic acidosis)
3. elderly (>80 y/o)
4. Dicontinue in pts injected with iodinated contrast agents for radiographic studies. Restart 48 hrs later to avoid contrast-induced renal failure (use insulin during this time).
5. Conditions predisposing to lactic acidosis: CHF, impaired liver fxn/excessive EtOH consumption, shock/septicemia, serious acute illness or hypoxic condition
Metformin drug interactions?
Cimetidine - can increase Metformin by 60% --> hypoglycemia
What 2 drugs are Thiazolidinediones?
agonists of the peroxisome proliferator-activated receptor gamma (PPAR-gamma) transcription factor --> involved in regulation of many genes involved in insulin sensitivity
What does activation of PPAR-gamma result in? (2)
overall: promotes insulin sensitivity

adipose remodeling
TZD effects in FPG and PPG?
decreases FPG
Adverse effects of TZDs?
1. weight gain
2. fluid retention (peripheral edema) - occurs more w/ concurrent insulin use; due to increased Na+ reabsorption
C/Is for TZDs? (2)
1. liver dz
2. heart failure
What drugs are alpha-glucosidase inhibitors?
MOA of alpha-glucosidase inhibitors?
Reduce PPG by inhibiting rate of digestion of polysaccharides in small intestine (i.e. delays absorption of glucose).
Do alpha-glucosidase inhibitors cause hypoglycemia?
Why are alpha-glucosidase inhibitors not 1st line drugs?
less potent; poor tolerance due to S/Es
Why do patients stop taking alpha-glucosidase inhibitors?
GI problems (25-45%)
When should insulin be considered 1st line for T2DM?
HbA1c > 10%
FBG > 250
random BG > 300
When is insulin the preferred 2nd line for T2DM?
HbA1c > 8.5%
Who needs more insulin T1 or T2 diabetics?
T2 due to insulin resistance
What drug is an amylin homolog?
MOA: Pramlintide?
synthetic analog of amylin - helps control postprandial glucose
MOA of amylin/Pramlintide?
1. decreases postprandial glucagon levels
2. slows gastric emptying (T1 and T2)
3. increases satiety
How is Pramlintide used?
adjunct to insulin therapy in T1 and T2 diabetics

additive to insulin: decreases insulin dose by 50%

postprandial control
Positive S/E of Pramlintide?
weight loss
Adverse effects of Pramlintide? (one major one)
increases risk of severe hypoglycemia (need to reduce insulin dose by 50%!)

nausea, vomiting, anorexia, headache
Drug interactions w/ Pramlintide?
affect absorption of other orally admin drugs, thus need to take them 1 hr before or 2 hrs after
MOA of Exenatide?
GLP-1 analog
What is action of GLP-1?
produced by L-cells in small intestine

binds to GLP-1 receptor on pancreatic beta cells and causes insulin secretion
What is the Incretin Effect?
plasma insulin levels are higher in response to oral glucose compared to IV glucose --> indicates that factors produced in the GI tract influence insulin secretion
What is an alternative to starting insulin therapy in type 2 diabetic patients?
Action of Exanatide on BG levels?
reduces both PPG and FBG levels
What drugs for diabetes cause weight loss?
MOA: Sitagliptin?
inhibitor of DPP-IV, the peptidase that cleaves and inactivates GLP-1
Effect of Sitagliptin on BG?
decrease both FPG and PPG
What does the ADA recommend as DOC for new-onset T2DM?
Advantages of Metformin?
weight loss
no risk of hypoglycemia
beneficial effects on CV mortality
If T2DM is not controlled after 2-3 months of therapy w/ Metformin what do you do?

1. sulfonylurea
2. TZD
3. insulin (>8.5%)
When should a T2DM be switched to insulin?
if failure on combo of 2 oral agents, switch to 2X daily insulin plus metformin
What classes of anti-diabetic drugs lowers FPG only?
What classes of anti-diabetic drugs lowers PPG only?
alpha-glucosinase inhibitors
What class of anti-diabetic drugs lowers both FPG and PPG?
Which class of anti-diabetics has NO hypoglycemia risk?
alpha-glucosidase inhibitors