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Product Modules > OADs, GLP-1, Amylinomimetics > Flashcards

OADs, GLP-1, Amylinomimetics Flashcards

1
Q

How many generations of SU are there?

A

3

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2
Q

What 2 agents are included in the meglitinide class?

A
  1. repaglinide (Prandin) - approved 1997
  2. nateglinide (Starlix) - approved 2000
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3
Q

What combinations may SUs be used with?

A
  • as monotherapy
  • combined with metformin
  • combined with insulin (glimepiride)
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4
Q

What treatment regimens can the meglitinides be used with?

A
  • indicated for monotherapy
  • combined with metformin
  • combined with TZD
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5
Q

True or False: both the ADA and AACEA recommend SUs as a first-line treatment.

A

False, both recommend SU as a second or third line agent.

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6
Q

According to AACE, who is the candidate for monotherapy?

A

7.5% A1c or lower

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7
Q

According to AACE, who is a candidate for dual therapy?

A

patients with A1Cs 7.6-9.0%

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8
Q

What is the MOA of an SU?

A
  • SUs bind to SURs (SU Receptors) at the beta-cell potassium channels
  • this closes the channel and blocks K+ ions from leaving the cell
  • the membrane becomes depolarized and calcium channels open
  • Ca2+ ions enter the cell and triggers the release of insulin
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9
Q

What is the only first generation SU still in use?

A

chlorpropamide

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10
Q

Second-generation SUs bind _____ tightly to proteins and are better able to penetrate cellular membranes. This makes them less likely to interact with other meds.

A

less

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11
Q

How is glimepiride different from second generation SUs?

A
  • it binds to a different part of the SUR
  • binds less tightly to the SUR
  • binds more quickly to the SUR (2-3 times faster)
  • separates from the SUR more quickly (8-9 times faster)
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12
Q

How often is glimepiride dosed?

A

once daily with first main meal

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13
Q

What is the brand name of glimepiride?

A

Amaryl

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14
Q

In general, SU monotherapy can be expected to lower A1C by _______%.

A

1.0-1.5%

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15
Q

What are the limitations of SU therapy?

A
  • hypoglycemia
  • elimination through kidneys puts patients with decreased kidney function at greater risk of hypoglycemia
  • Weight gain
  • Some studies suggest that SUs may cause beta cell death.
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16
Q

SUs are contraindicated in patients with __________________.

A

diabetic ketoacidosis.

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17
Q

When does ADA recommend use of meglitinides?

A

they may be used in place of SUs, particularly in patients with irregular meal schedules or how develop late postprandial hypoglycemia on SUs

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18
Q

When does AACE recommend use of meglitinides?

A
  • only for patients with A1C levels between 6.5-7.5% as one of the last alternatives for the second component of dual therapy OR
  • as a third medication in triple therapy
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19
Q

What is the MOA of meglitinides?

A
  • stimulate rapid, short-lived pancreatic secretion of insulin
  • bind to a different site within the SUR on pancreatic beta cells and for a shorter time than SUs
  • the mechanism of insulin release is otherwise the same as SU
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20
Q

Is insulin release triggered by meglitinides glucose dependent?

A

Yes and it diminishes at low glucose concentrations.

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21
Q

When taken before a meal, how long is the insulin-releasing effect of the meglitinides?

A

about 3 hours

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22
Q

What is an advantage of Prandin (repaglinide)?

A

It is rapidly and completely absorbed and eliminated.

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23
Q

When do peak plasma levels of Prandin occur?

A

within 1 hour of dosing

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24
Q

A dose of nateglinide (Starlix) stimulates pancreatic insulin secretion within ___ minutes of dosing.

A

20 minutes

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25
Q

Prandin is metabolized exclusively in the ________, so a decrease in ________ function will ___________ its half-life and possibly cause hypoglycemia.

A

liver, liver, increase

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26
Q

What are the primary benefits of meglitinides?

A
  • rapid onset
  • short duration
  • reduced hypoglycemia risk compared with some SUs
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27
Q

What is the average A1C reduction of Prandin?

A

1.5%

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28
Q

Which meglitinide causes the greatest A1C reduction?

A

Prandin has a greater effect on A1C than Starlix (1.5% vs. 0.5%).

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29
Q

What are the limitations of meglitinides?

A
  • dosing frequency (up to 30 minutes before each meal)
  • weight gain
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30
Q

Metformin may be used in patients ___ years old or older and extended release metformin may be used in patients ___ years old or older.

A

10, 17

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31
Q

According to the PIs of these drugs, metformin can be used in combination with what other agents?

A
  1. TZDs
  2. meglitinides
  3. exenatide
  4. liraglutide
  5. acarbose
32
Q

Both metformin and extended release metformin may be used in combination with SU or insulin in patients ___ years old or older.

A

17

33
Q

What is the branded name of metformin?

A

Glucophage

34
Q

What treatment regimen(s) are the TZDs indicated with?

A
  • as monotherapy
  • combination with an SU
  • combination with metformin
  • with insulin (pioglitazone only)
35
Q

How does metformin affect glucose control?

A
  • decreases the amount of glucose produced by the liver (impacts FPG)
  • to a lesser degree it improveds cellular glucose uptake and utilization
36
Q

On average, metformin lowers A1C values by how much?

A

1.5%

37
Q

True or False: metformin appears to have a favorable effect on serum lipids.

A

True.

38
Q

What is the maximum daily dose of immediate-release metformin and extended release metformin, respectively?

A
  • Glucophage: 2550 mg
  • Glucophage XR: 2000 mg
39
Q

How often is XR metformin dosed compared to IR metformin?

A

XR metformin can be dosed once daily while IR metformin is dosed 2-3 times per day

40
Q

What are the contraindications for metformin?

A
  1. renal disease or dysfunction (plasma creatinine => 1.5 mg/dL in men or =>1.4 mg/dL in women, or abnormal creatinine clearance)
  2. hypersensitivity
  3. acute or chronic metabolic acidosis
41
Q

Who else should not use metformin besides those it is contraindicated for?

A
  • patients undergoing radiologic studies with iodinated contrast materials
  • CHF requiring drug treatment
  • liver disease
  • patients who are hypoxemic, dehydrated, or septic
42
Q

What is the greatest danger associated with metformin?

A

Lactic Acidosis

43
Q

True or False: since metformin is excreted unchanged through the urine, if a patient has kidney impairment, the drug may accumulate in the blood and produce acidosis.

A

True

44
Q

How often should metformin users have their kidney function checked?

A
  • before beginning therapy
  • at least once a year after starting therapy
  • more regularly if older or if kidney dysfunction is anticipated
45
Q

Why should patients who drink alcohol excessively or have liver disease not take metformin?

A

Both conditions can create lactic acidosis.

46
Q

What are the common side effects of metformin?

A
  • Diarrhea
  • Nausea and Vomiting
  • Flatulence
47
Q

What is the main effect of the TZDs?

A
  • increase the sensitivity of muscle, fat, and liver tissue to insulin
48
Q

How do the TZDs work?

A

by improving the insulin sensitivity of peripheral tissues (muscle and fat cells) and the liver when the drug is bound to them

49
Q

What do TZDs bind to to initiate their MOA?

A

peroxisome proliferator-activated receptor-gamma (PPARy)

50
Q

Which TZD is indicated for use with insulin?

A

pioglitazone (Actos)

51
Q

What are the primary advantages of TZDs?

A
  • efficacy
  • low risk of hypoglycemia
  • lipid improvements
  • simplified dosing
52
Q

What is the average A1C reduction with TZDs?

A

0.5% - 1.4%

53
Q

How often is Avandia dosed?

A

once or twice daily

54
Q

How often is Actos dosed?

A

once daily

55
Q

What are the limitations associated with TZDs?

A
  • edema and weight gain
  • heart failure (has boxed warning)
  • urinary bladder tumors (Actos)
  • bone fractures in women
  • liver toxicity (should be monitored)
56
Q

Addition of Victoza to metformin, SU, insulin detemir, and/or TZD therapy has been shown to reduce A1C by _______%.

A

0.5-1.5%

57
Q

What was the mean weight loss in the 52-week Victoza monotherapy trial in the 1.2 mg arm and 1.8 arm, respectively?

A
  • 1.2 mg arm: 2.1 kg (4.6 lb)
  • 1.8 mg arm: 2.5 kg (5.5 lb)
58
Q

Where does ADA place DPP-4 inhibitos in the treatment spectrum?

A

as 2nd or 3rd line combination therapy

59
Q

Where does AACE position the use of DPP4 inhibitors?

A

as monotherapy after metformin and in dual and triple therapy

60
Q

Sitagliptin lowers A1C levels by __% to __% from baseline.

A

0.7%-0.8%

61
Q

AGI stands for what?

A

Alpha-Glucosidase Inhibitors

62
Q

What is the indication for AGIs?

A
  • for use in monotherapy as an adjunct to diet
  • The PI for acarbose reports clinical efficacy when used in combination with SU, metformin, or insulin
  • Miglitol is indicated for monotherapy or in combination with SU
63
Q

True or False: AGIs will be most effective in combination with other glucose lowering agents due to their distinct MOA.

A

True.

64
Q

How do AGIs work?

A

They slow intestinal absorption of carbohydrates, and thus blunt the sharp postprandial rise in blood glucose.

65
Q

What is the detailed MOA of the AGIs?

A
  • they bind to and competitively inhibit the 2 types of enzymes - alpha-amylases and alpha-glucosidases - responsible for the breakdown of carbs in the small intestine
  • this inhibition prolongs carbohydrate absorption, and thus blunts postprandial glucose spikes
66
Q

What are the 2 types of enzymes that AGIs inhibit?

A
  1. Alpha-amylases
  2. Alpha-glucosidases
67
Q

What are the main benefits of AGI therapy?

A
  • not associated with hypoglycemia or weight gain in monotherapy
  • only about 2% of acarbose is absorbed into the bloodstream, which reduces the possibility of drug interactions in the blood
68
Q

What is the average A1C reduction of the AGIs?

A

0.5%-0.8%

69
Q

What are the limitations with AGI therapy?

A
  • modest efficacy
  • dosing (at each meal)
  • GI adverse events
  • expensive
70
Q

What are the common AEs associated with AGIs?

A
  • bloating
  • abdominal pain
  • diarrhea
  • flatulence
71
Q

What are the predominant AGIs and their brand name?

A
  • acarbose: Precose
  • miglitol: Glyset
72
Q

Which AGI may elevate liver enzymes?

A

acarbose (Precose)

73
Q

True or False: Pramlintide can only be used in patients with type 1 diabetes.

A

False. Pramlintide can be used in patients with both type 1 and type 2 diabetes who are taking mealtime insulin.

74
Q

When starting therapy with pramlintide, patients should reduce their insulin dose by ___% to reduce the risk of hypoglycemia.

A

50%

75
Q

The average A1C reduction of pramlintide is how much?

A

0.5% - 0.7%

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