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PHAR 152 > Diabetes - Part 4 > Flashcards

Diabetes - Part 4 Flashcards

1
Q

What does core management consist of for T2DM?

A

Self-management
Lifestyle modifications
Pharmacotherapy

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2
Q

What is the MOA of Metformin?

A

Decrease hepatic glucose production
Can also enhance sensitivity to insulin
Increases glucose utilization via action in the gut

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3
Q

What is the dosing for Metformin?

A

Start slow: initiate at 250-500mg OD
Titrate up by 500mg weekly if no GI side effects
Desired usual dose: 850-1000mg BID
Max dose: 850 TID
Adjust in renal failure

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4
Q

What is the efficacy for Metformin?

A

Decrease A1C 1-1.5% (up to 2% with A1C of 9%
Also decreases TG and LDL 8-15%, and slightly increases HDL by 2%

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5
Q

What drug interactions does Metformin have?

A

Cimetidine: increases Metformin levels by 60%
Dolutegravir: can increase Metformin concentration
Alcohol: potentiates Metformin effect on lactate metabolism; enhanced hypoglycemia effect
Contrast media: hold for 48 hours after imaging

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6
Q

What are the adverse effects of Metformin?

A

Common: GI
Less common: metallic taste, vit B12 deficiency with long term use
Very low risk of hypo when used as monotherapy
Weight neutral to modest weight loss

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7
Q

What precautions should be taken for Metformin?

A

Watching for lactic acidosis
If someone has reduced eGFR there will be reduced elimination and therefore a concern for accumulation of lactate

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8
Q

What is the dosing of Metformin for renal impairment?

A

Decrease dose if ClCr <60ml/min
EGFR 45-59: 1500mg/d (divided doses)
EGFR 30-44: 1000mg/d (divided doses)
CI when eGFR < 30ml/min

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9
Q

What are the risk factors for lactic acidosis?

A

History of lactic acidosis
Severe liver disease
Alcohol abuse
Radiologic procedures
Acute illness
Server dehydration

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10
Q

What is the MOA of sulfonylureas(SUs)?

A

They enhance the secretion of insulin by binding to SU receptors on the beta cells of the pancreas
This leads to closing of K+ channels and opening of calcium channels which stimulates insulin secretion
They stimulate both basal and meal-stimulated insulin release

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11
Q

What are the SUs?

A

2nd gen: glyburide, gliclazide, glimepiride

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12
Q

What is the dosing for glyburide?

A

5-20mg/d (OD or BID)
Usual dose is 5mg BID; may increase to 10 BID
CI in eGFR < 60ml/min

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13
Q

What is the dosing for gliclazide?

A

80-160mg (80mg OD or 80mg BID)
Gliclazide MR 30-120mg OD
Caution in eGRF 30-60ml/min
CI in eGFR <30ml/min

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14
Q

Which SUs are on the formulary?

A

Glyburide and gliclazide MR

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15
Q

Directions for SUs:

A

Take with food
Take in am
Start at lower doses and increase pm

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16
Q

What is the efficacy of SUs?

A

Decrease A1C 1-1.5% (up to 2% in elevated A1C)
Effective at 1/2 max dose
May get a better response if initiated early in diagnosis; long-term durability is poor
Must dose adjust in renal impairment

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17
Q

What are the adverse effects of SUs?

A

Hypoglycemia (2-30%)
- higher incidence with glyburide > glimepiride > gliclazide
Weight gain (~2kg)
Less frequent: nausea, skin reaction

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18
Q

What are the precautions for SUs?

A

Pregnancy/breast-feeding (would only use glyburide)
CI in severe hepatic and renal impairment
Hold in acute illness

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19
Q

What are drug interactions do SUs have?

A

Sulfonamides, salicylates, warfarin
Alcohol
Cimetidine, clarithromycin, fluconazole, NSAIDs, beta-blockers, MAOIs
These drugs may increase risk of hypo
~
Phenytoin
Rifampin
Colesevelam
These drugs may lessen effect and increase blood sugar

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20
Q

What is the meglitinide drug?

A

Repaglinide

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21
Q

What is the MOA of repaglinide?

A

Binds to a side adjacent to the SU receptor, resulting in stimulation of the secretion of insulin from the pancreas
Similar to SUs but have faster onset and shorter D of A
Peak levels within 1 hour

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22
Q

What is the efficacy of repaglinide?

A

Decrease A1C 1-1.5%
Works primarily to decrease PPG: is intended to be taken before meals or improve early phase meal-induces insulin secretion

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23
Q

What is the dosing for repaglinide?

A

A1C <8%: initiate at 0.5mg before each meal + titrate up
A1C >8%: initiate at 1-2mg before each meal + titrate up
Max dose: 4mg before each meal (16mg/d)
Start at a low dose and titrate up every 1-2 weeks until target BG achieved
Needs to be administered right before a meal

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24
Q

What are the adverse effects of repaglinide?

A

Hypoglycemia (more so when combined with other agents)
Weight gain (~0.3-1kg)

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25
Q

What are the precaution for repaglinide?

A

Metabolized in the liver. Clearance significantly reduced in hepatic impairment.
Precaution worn moderate hepatic impairment and CI with severe liver disease.
Use caution if eGFR <30ml/min

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26
Q

What drug interactions does repaglinide have?

A

Increased repaglinide with:
- 3A4 inhibitors (cyclosporine, clarithromycin, grapefruit, azoles)
- 2C8 (gemfibrozil, clopidogrel; these are CI)
Decreased repaglinide with 3A4 inducers (carbamazepine, rifampin)

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27
Q

What is the alpha-glucosidase inhibitors?

A

Acarbose

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28
Q

What is the MOA of Acarbose?

A

Alpha-glucosidase enzymes in the small intestine are responsible for the breakdown of polysaccharides into absorbable glucose.
Acarbose inhibits these enzymes, hence there is a delay in the rate of digestion of CHOs and glucose absorption
NET EFFECT IS REDUCTION OF PPG LEVELS

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29
Q

What is the efficacy of Acarbose?

A

Decrease A1C 0.5-0.8% (less then the others)
Does not affect body weight or lipids

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30
Q

What is the dosing for Acarbose?

A

Initial: 25-50mg OD titrate up every couple of weeks to 50mg TID
Max dose of 100mg TID
Take with the first bite of each main meal

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31
Q

What are the adverse effects of Acarbose?

A

GI: flatulence (40-80%), diarrhea (30%), bloating, abdominal pain
May elevate ALT
Hypoglycemia
Weight neutral

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32
Q

What drug interactions does Acarbose have?

A

Digestive enzyme preparations
May decrease digoxin effect

33
Q

What are the precautions for Acarbose?

A

Those with IBD or GI conditions
CI if eGFR < 25ml/min and severe liver disease

34
Q

What are the thiazolidinediones?

A

Rosiglitazone and pioglitazone

35
Q

What is the MOA of thiazolidinediones?

A

Bind to PPAR-y receptors which are primarily found in adipose tissue
Activation alters genes that influence glucose and lipid metabolism
ENHANCE INSULIN SENSITIVITY AT MUSCLE, LIVER AND FAT TISSUE
- decreases insulin resistance
Insulin sensitizers

36
Q

What is the efficacy of thiazolidinediones?

A

Decrease A1C by 1-1.5%

37
Q

What is the dosing for Rosiglitazone?

A

Initiate at 2-4mg OD; may increase to 4mg BID or 8mg OD (greater effects seen BID)
Larger people will generally require larger doses
Have delayed onset: wait 4-8 weeks for dose adjustments

38
Q

What is the dosing for pioglitazone?

A

Initiate at 15mg OD; titrate up to 30-45mg OD
Larger people will generally require larger doses
Have delayed onset: wait 4-8 weeks for dose adjustments

39
Q

What are the precautions for thiazolidinediones?

A

Caution in eGFR <60ml/min
Mainly metabolized by liver: use with caution or use an alternative in severe liver disease

40
Q

What must you have tried to get a thiazolidinedione in SK?

A

They are both EDS so must have tried a SU and Metformin first

41
Q

What are the drug interactions for thiazolidinediones?

A

Metabolized by CYP 2C8:
- increased effects with inhibitors (gemfibrizol, TMP)
- decreased effects with inducers (rifampicin)

42
Q

What are the adverse effects of thiazolidinediones?

A

Peripheral edema(~5%); combined with insulin (~15%)
New-onset/worsening of HF
Weight gain (2.5-8.8kg; dose related)
Increase distal fractures in post menopausal women
CI in heart failure

43
Q

T or F: TZDs are good fro CV safety

A

False. They are controversial

44
Q

What are the incretin-based therapies?

A

GLP-1 receptor agonists
DPP-4 inhibitors

45
Q

What does activation of the GLP-1 receptor result in?

A

Potent inhibition of gastric emptying
Potent inhibition of glucagon secretion
Reduction of food intake and body weight

46
Q

What is the MOA of DPP-4 inhibitors?

A

Block the enzyme DPP-4 which rapidly hydrolysis incretins, thus enhancing the action of endogenous incretins
As a result they increase insulin release and decrease glucagon in a dose dependent manner

47
Q

What is the efficacy of DPP-4 inhibitors?

A

Decrease A1C by ~0.7% (ranges, but typically < 1%)
Work quickly - can see effects within a couple weeks

48
Q

How can you get a DPP-4 inhibitor?

A

Uncontrolled after Metformin and a SU

49
Q

What are the generic DPP-4 inhibitors?

A

Sitagliptin & saxagliptin

50
Q

What is the dosing for DPP4 inhibitors?

A

Sitagliptin 100mg OD
Saxagliptin 5mg OD
Linagliptin 5mg OD
Alogliptin 25mg OD

51
Q

How should DPP4 doses be adjusted for renal dosing?

A

Sitagliptin: eGFR 30-44 50mg OD, eGFR<30 25mg OD
Saxagliptin: eFGR 30-44 2.5mg OD, eGFR<30 2.5mg OD with caution(avoid in ESRD, dialysis)
Linagliptin: no dose adjustment
Alogliptin: eGFR 30-44 12.5mg OD, eGFR<30 6.25mg OD

52
Q

What are the adverse effects of DPP4i?

A

Overall, well tolerated medications
No hypo on their own
Weight neutral

More common: headache, nasopharyngitis, URTI
Less common: hypersensitivity reactions, joint pain, pancreatitis

53
Q

What are the drug interactions of DPP4i?

A

Increase risk of hypo when combined with SU or insulin
Avoid with GLP1RA: similar MOA and increased risk of pancreatitis

54
Q

Are DPP4i cardioprotective?

A

No but they are CV safe

55
Q

What is the cost for GLP1RAs?

A

> $200/month

56
Q

What is semaglutide (ozempic)?

A

A GLP1RA

57
Q

Which GLP1RAs are covered under SK formulary?

A

Lixisenatide and semaglutide

58
Q

When can someone get semaglutide?

A

For treatment of T2 when combined with Metformin and a SU when control is not adequate with a SU and Metformin

59
Q

When can someone get lixisenatide?

A

For treatment of T2 combined with a basal insulin when control is not adequate with a SU and Metformin

60
Q

What is the MOA of GLP1RA?

A

Stimulate insulin secretion in a glucose-dependent manner; decrease glucagon, slow gastric emptying, increase satiety

61
Q

What is the dosing for exenatide?

A

Short acting
5ug BID sc x 1 month, then 10ug BID
Within 60 minutes prior to am and pm meals (meals must be at least 6 hours apart)

62
Q

What is the dosing for lixisenatide?

A

Short acting
10ug od sc x 14 days, them 20ug OD
- take within 1 hour prior to the first main meal of the day

63
Q

What is the dosing for liraglutide?

A

Long acting - can take at anytime
0.6mg OD x 1 week, then 1.2mg to 1.8mg daily

64
Q

What is the dosing for exenatide?

A

2mg sc q week

65
Q

What is the dosing for dulaglutide?

A

0.75mg sc weekly; can increase to 1.5mg q week

66
Q

What is the dosing for semaglutide?

A

0.25mg sc weekly; increase to 0.5mg after 4 weeks then 1mg

67
Q

If you miss a weekly dose for a long acting GLP1RA how long do you have to retake it?

A

Admitted ASAP if at least 3 days until next dose (dulaglutide and exenatide) and if at least 5 days for semaglutide

68
Q

What is the dosing for oral semaglutide?

A

Start with 3mg OD for 30 days
Increase to 7mg OD for at least 30 days
May increase to 14mg OD

69
Q

How is oral semaglutide to be taken?

A

Take on empty stomach after waking up
Take with a sip of water (<120ml)
Wait at least 30 minutes before eating, drinking, or taking other oral medications

70
Q

What do you do if you miss a dose of oral semaglutide?

A

Skip and take the next day

71
Q

Which GLP1RA should you take caution with when eGFR < 15?

A

Dulaglutide
Liraglutide
Semaglutide SC

72
Q

When should caution be taken with semaglutide po?

A

When eGFR <30

73
Q

Which GLP1RAs are not recommended for eGFR<30 and caution in 30-50?

A

Exenatide QW and exenatide
Lixisenatide just not recommended for eGFR<30

74
Q

What is the efficacy of GLP1RAs?

A

Decrease A1C by about 1-1.5%
Benefits are dose dependent
Long acting GLPs are more potent then short acting
Modest decrease in BP(within 3 weeks)

75
Q

Short acting GLPs have more effect on _____ and long acting have more effect on ____.

A

PPG, FPG

76
Q

What are the common adverse effects of GLP1RAs?

A

GI: N/V/D(up to 40%); especially nausea (20-50%)
Less common: injection site reactions, increased HR
Rare: acute gallstone disease, retinopathy, acute pancreatitis??

77
Q

What are the affects on weight for GLP1RAs?

A

Cause wight loss - on average ~3kg

78
Q

What is the affect on hypoglycemia for GLP1RAs?

A

Low risk of hypo

79
Q

What drug interactions doo GLP1RAs have?

A

Since they decrease gastric emptying they need to be spaced out more then an hour from drugs that require rapid GI absorption:
- oral contraceptives
- antibiotics
- narrow TI drugs
- increase levothyroxine by 33%

PHAR 152 (10 decks)

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