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Therapeutics > Diabetes Drugs > Flashcards

Diabetes Drugs Flashcards

1
Q

what drug class is metformin and what organs does it target?

A

Biguanide

Targets: liver, muscle, adipose tissue

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2
Q

what is metformin’s MOA?

A

decreases hepatic glucose production and increases insulin sensitivity

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3
Q

metformins A1C lowering?

A

1-2%

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4
Q

when is metformins maximum therapeutic effect?

A

within 2 weeks

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5
Q

what glucose does metformin effect? (FPG or PPG)

A

FPG & PPG (FPG > PPG)

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6
Q

what are the adrs of metformin?

A
  • low hypoglycemia
  • vit B12 deficiency (high dose & chronic use) (REQUIRES PERIODIC TESTING)
  • weight neutral or loss (frail elders)
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7
Q

what are some symptoms of vitamin B12 deficiency and who is at risk?

A
  • cognitive impairment or paresthesias (tingling or numbness)
  • people at risk: elderly, vegetarians, use of chronic PPIs
  • if pt has tingling or numbness could also be diabetic peripheral neuropathy
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8
Q

metformin dosing?

A

titrate over 4 wks to minimize GI effects (start low and go slow)

  • week 1: start 500mg daily
  • week 2: incr to 500mg BID
  • week 3: incr to 500mg in AM and 1000mg in PM
  • week4: incr to 1000mg BID (maximum clinical dose)
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9
Q

if GI effects are bothersome with metformin, what do you do?

A

do slower titration, lower doses, and or d/c

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10
Q

what form of metformin do you consider to minimize GI effects?

A

extended-release (ER) formulation

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11
Q

metformin dose adjustments in renal disease

A
  • Metformin is C/I if eGFR < 30

- do NOT initiate if eGFR ≥ 30-45

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12
Q

if patient is already on metformin:

  • eGFR ≥ 45-60
  • eGFR ≥ 30-45
A
  • eGFR ≥ 45-60 -> continue use, but monitor renal fxn routinely
  • eGFR ≥ 30-45 -> weigh the pros and cons of continued use (routine renal fxn monitoring & consider dose reduction of 50%)
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13
Q

what does metformin reduce in obese its?

A

CV death

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14
Q

what drug class are glyburide, glipizide, & glimeperide?

A

Sulfonylurea

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15
Q

Sulfonylurea drugs

A

glyburide, glipizide, & glimeperide

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16
Q

what organs do sulfonylurea’s target?

A

pancreas

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17
Q

mechanism of sulfonylurea’s?

A

enhance insulin secretion of beta cells (independent of glucose load)

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18
Q

what is the A1c lowering effect of sulfonylurea’s?

A

1-2%

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19
Q

what do sulfonylurea’s require to work?

A

requires functioning beta-cells
*CHECK DISEASE DURATION!
(diabetes for 20-30 years probably won’t have good beta-cell fxn)

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20
Q

what glucose do sulfonylurea’s effect? (FPG or PPG)

A

FPG

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21
Q

when is sulfonylureas max therapeutic effects?

A

max therapeutic effects at 50% max daily dose

-avoid high doses to avoid hypoglycemia

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22
Q

what sulfonylurea should you avoid the use of?

A

Glyburide
-it’s long acting, so has a higher risk of hypoglycemia
(try glipizide or glimeperide)

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23
Q

sulfonylurea adrs?

A
  • HIGH hypoglycemia risk (b/c stimulates pancreas to secrete insulin)
  • limited durability - usually good for 6 months with high secondary failure thereafter
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24
Q

sulfonylurea dosing (max daily dose & max therapeutic dose)?

A

Glyburide:

  • MDD = 10mg BID
  • Max therapeutic dose = 5mg BID

Glipizide:

  • MDD = 20mg BID
  • Max therapeutic dose = 10mg BID

Glimeperide:

  • MDD = 8mg daily
  • Max therapeutic dose = 4mg daily
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25
Q

what drug class are repaglinide and nateglinide?

A

glinides

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26
Q

glinide drugs

A

repaglinide and nateglinide

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27
Q

what organs do the glinides target?

A

pancreas

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28
Q

Glinides MOA?

A

Enhance insulin secretion of B cells (independent of glucose load)
*same as Sulfonylurea

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29
Q

what is the A1c lowering effect of glinides?

A

0.5-1.5%

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30
Q

what do glinides require to work?

A

functioning beta-cells
(check disease duration)
*same as sulfonylurea

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31
Q

what glucose do glinides effect? (FPG or PPG)

A

PPG

vs SU effect FPG

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32
Q

glinide dosing

A
  • multiple daily doses
  • take before meals

*not in ADA algorithm

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33
Q

glinide adrs?

A
  • less hypoglycemia than SU

- short duration, rapid onset

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34
Q

what drugs are in thiazolidinediones (TZDs) class?

A
  • Pioglitazone

- Rosilglitazone

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35
Q

Pioglitazone & Rosilglitazone are in what drug class?

A

TZDs

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36
Q

what organs do TZDs target?

A

liver, muscle, adipose tissue

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37
Q

TZD MOA?

A

activate PPAR in muscle, liver, fat -> increase glucose transporter expression

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38
Q

what is TZD A1c lowering effect?

A

0.5-1.4%

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39
Q

what glucose do TZDs effect? (FPG or PPG)

A

FPG

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40
Q

TZDs are ___ sensitizers

A

TZDs are insulin sensitizers

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41
Q

when are the max therapeutic effects for TZDs seen?

why is titrating to max dose not recommended?

A

8-12 weeks (counsel pts)

-titrating to max dose (45 mg/d) is NOT recommended b/c of side effects (edema, weight gain)

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42
Q

TZD adrs?

A
  • low hypoglycemia risk
  • Pioglitazone: edema, weight gain (5-10kg), bone fracture, bladder cancer, macula edema
  • Rosilglitazone: was associated with CV risk and MI death
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43
Q

TZDs have good what and maintain what?

A

A1c durability

-maintain A1c lowering effect

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44
Q

Alpha-glucosidase inhibitor drugs?

A
  • Acarbose

- Miglitol

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45
Q

Arcarbose & Miglitol are in what drug class?

A

Alpha-glucosidase inhibitor

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46
Q

Alpha-glucosidase inhibitor MOA?

A

inhibit enzymes in small intestine that digest carbs -> delay carb absorption & inhibit breakdown of dietary carbohydrates

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47
Q

what organs do Alpha-glucosidase inhibitor target?

A

GIT (small intestine)

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48
Q

A1c lowering effect of Alpha-glucosidase inhibitor?

A

0.5-0.8%

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49
Q

what glucose do Alpha-glucosidase inhibitor effect? (FPG or PPG)

A

effect PPG

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50
Q

when are Alpha-glucosidase inhibitor most effective?

A

most effective if diet contains large amounts of CHO

-watch for diet changes/low CHO diets

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51
Q

Alpha-glucosidase inhibitor dosing?

A

requires multiple daily doses

  • must be present in gut to exert its effects
  • max therapeutic effects are 1 hour after eating
  • take 30-60min before eating, so in gut before eating
  • not in ADA algorithm
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52
Q

Alpha-glucosidase inhibitor and titrating

A

tirate over 4-8 weeks to minimize GI side effects

-poor tolerability -> not used often clinically

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53
Q

Alpha-glucosidase inhibitor adrs?

A
  • FLATULENCE
  • bloating
  • poorly tolerated
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54
Q

what drugs are in DPP-4 inhibitor class?

A
  • sitagliptin
  • saxagliptin
  • linagliptin
  • alogliptin
55
Q

Sitagliptin, saxagliptin, linagliptin, alogliptin are in what drug class?

A

DPP-4 inhibitors

56
Q

DPP-4 inhibitors MOA

A

(sitagliptin, saxagliptin, linagliptin, alogliptin)

  • Inhibit enzyme responsible for breakdown of GLP-1
  • GLP-1 promotes insulin secretion (dependent on glucose)
57
Q

what is the A1c lowering effect of DPP-4 inhibitors?

A

(sitagliptin, saxagliptin, linagliptin, alogliptin)

  1. 5-0.8%
    - modestly effective at lowering A1c b/c T2DM pas already have less endogenous GLP-1 hormone
58
Q

what glucose do DPP-4 inhibitors effect? (FPG or PPG)

A

(sitagliptin, saxagliptin, linagliptin, alogliptin)

effect PPG

59
Q

DPP-4 inhibitor max therapeutic effects are when?

A

(sitagliptin, saxagliptin, linagliptin, alogliptin)

-max therapeutic effects within 2 weeks

60
Q

DPP-4 inhibitor adrs?

A

(sitagliptin, saxagliptin, linagliptin, alogliptin)

  • weight neutral
  • well-tolerated
  • low hypoglycemia risk
61
Q

DPP-4 inhibitor dosing

A

may need to reduce dose of SU if given in combination

-b/c SU’s also help to stimulate insulin secretion

62
Q

what drugs are in SGLT-2 inhibitor class?

A
  • canagliflozin
  • empagliflozin
  • dapagliflozin
63
Q

canagliflozin, empagliflozin, dapagliflozin are in what drug class?

A

SGLT-2 inhibitors

64
Q

what organ DPP-4 inhibitors target?

A

(sitagliptin, saxagliptin, linagliptin, alogliptin)

-target GIT

65
Q

what organ do SGLT-2 inhibitors target?

A

(canagliflozin, empagliflozin, dapagliflozin)

-target kidneys

66
Q

SGLT-2 inhibitors MOA

A

(canagliflozin, empagliflozin, dapagliflozin)

  • inhibit SGLT-2 in kidney, increase urinary glucose excretion
  • SGLT-2 normally reabsorbs glucose in kidney
67
Q

what is the A1c lowering effect of SGLT-2 inhibitors?

A

(canagliflozin, empagliflozin, dapagliflozin)

0.5-0.8%

68
Q

can you use SGLT-2 inhibitors at any point in disease?

A

(canagliflozin, empagliflozin, dapagliflozin)

YES! they are useful for all durations of diabetes (but are expensive)
-not dependent on beta cell for efficacy

69
Q

what glucose do SGLT-2 inhibitors effect? (FPG or PPG)

A

(canagliflozin, empagliflozin, dapagliflozin)

effect FPG

70
Q

SGLT-2 inhibitors adrs?

A

(canagliflozin, empagliflozin, dapagliflozin)

  • weight loss (b/c peeing out sugars)
  • low risk of hypoglycemia
  • UTI risk & genital infections
  • decreased BP (check for volume depletion & routinely monitor BP)
  • risk of amputations
  • acute kidney injury (AKI)
71
Q

what do you need to routinely monitor for SGLT-2 inhibitors?

A

(canagliflozin, empagliflozin, dapagliflozin)

-routinely monitor BP & check for volume depletion b/c decreases BP

72
Q

if a pt has a hx of recurrent UTIs, can you give them SGLT-2 inhibitors?

A

probably wouldn’t want to b/c one of their adrs is increased risk of UTIs

73
Q

what drug class is colesevelam in?

A

bile acid sequesterant

74
Q

what organs does colesevelam effect?

A

GIT, liver?

75
Q

colesevelam A1c lowering effect?

A

0.3-0.5%

76
Q

colesevelam adrs & DDIs?

A
  • bad GI (poorly tolerated)
  • no weight effect
  • lowers LDL but may incr TG

DDIs: warfarin, levo, phenytoin, digoxin, fat vitamins - A, D, E, K
(take interacting meds 4 hours prior to administering colesevelam)

*not in ADA algorithm

77
Q

when do you take interacting meds when also taking colesevelam?

what are the interacting meds?

A

take interacting meds 4 hours prior to administering colesevelam

Interacting meds are: warren, levo, phenytoin, digoxin, fat vitamins - A, D, E, K

78
Q

what drug class is bromocriptine in?

A

dopa agonist

79
Q

what drug is a dopa agonist?

A

bromocriptine

80
Q

what organs does bromocriptine target?

A

brain, muscle, adipose?

81
Q

bromocriptine A1c lowering effect?

A

0.1-0.4%

82
Q

bromocriptine adrs?

A
  • N/V
  • HA, dizziness

*not in ADA algorithm

83
Q

what drugs are in GLP-1 agonist class?

A
  • exenatide
  • liraglutide
  • abiglitide
  • dulaglitide
  • liexenitide
84
Q

exenatide, liraglutide, abiglitide, dulaglitide, liexenitide are in what drug class?

A

GLP-1 agonists

85
Q

what organs do the GLP-1 agonists target?

A

(exenatide, liraglutide, abiglitide, dulaglitide, liexenitide)

-GIT, brain, liver, pancreas (beta-cells)

86
Q

GLP-1 agonists MOA?

A

(exenatide, liraglutide, abiglitide, dulaglitide, liexenitide)

  • enhance glucose dependent insulin secretion
  • slow gastric emptying
  • increase satiety
  • suppress post-prandial glucagon release
  • suppress hepatic glucose production
87
Q

what is the A1c lowering effect of GLP-1 agonists?

A

(exenatide, liraglutide, abiglitide, dulaglitide, liexenitide)

0.5-1.6%

88
Q

what glucose do the GLP-1 agonists effect?

A

(exenatide, liraglutide, abiglitide, dulaglitide, liexenitide)

short-acting effect PPG more
long-acting effect FPG more

89
Q

GLP-1 agonists adrs?

A

(exenatide, liraglutide, abiglitide, dulaglitide, liexenitide)

  • weight loss of ~2-4kg over 12 wks
  • low hypoglycemia risk
90
Q

what are GLP-1 agonists approved to be used with?

A

(exenatide, liraglutide, abiglitide, dulaglitide, liexenitide)

most are approved to be used with basal insulin
-no approval for use with prandial insulin

91
Q

administration of GLP-1 agonists?

A

injectables only

-not good for needle phobia

92
Q

exenatide dosing

A

(GLP-1 agonist)

daily: BID, short-acting (PPG coverage)
weekly: long-acting & extended release

93
Q

liraglutide dosing

A

(GLP-1 agonist)

daily: long-acting (FPG > PPG coverage)

94
Q

lixisenatide dosing

A

(GLP-1 agonist)

daily: short-acting (PPG coverage)

95
Q

dulaglutide dosing

A

weekly: long-acting (FPG)

96
Q

albiglutide dosing

A

weekly: long-acting (FPG)

97
Q

which GLP-1 agonists are good for patients that are non-adherent?

A
  • exenatide ER
  • dulaglutide
  • albiglutide

weekly dosing & long acting

98
Q

what drug is in the amylin analogue class?

A

pramlintide

99
Q

pramlintide is in what drug class?

A

amylin analogue

100
Q

amylin analogue MOA?

A

(pramlintide)

  • slows gastric emptying
  • increases satiety
  • suppresses post-prandial glucagon release
  • suppresses hepatic glucose production
101
Q

amylin analogue A1c lowering effect?

A

(pramlintide)

0.5-1%

102
Q

what organs does the amylin analogue effect?

A

(pramlintide)

-GIT, liver, brain

103
Q

what glucose does the amylin analogue effect? (FPG or PPG)

A

(pramlintide)

-effects PPG

104
Q

what MUST the amylin analogue be used with?

A

(pramlintide)

must be used with intensive insulin regimens (basal-bolus)

105
Q

amylin analogue dosing?

A

(pramlintide)

-reduce dose of bolus insulin by 50% to avoid hypoglycemia
(risk is higher in T1DM vs T2DM b/c T2 is insulin resistant and T1 is insulin sensitive)

  • requires multiple daily doses
  • not in ADA algorithm
106
Q

what does amylin analogue work to complement?

A

(pramlintide)

-works to complement the action of insulin

107
Q

amylin analogue adrs?

A
  • injection
  • expensive
  • high risk of hypoglycemia if don’t reduce dose of bolus insulin by 50%
108
Q

when do you intensify regimen?

A
  • every 3 months until glycemic goals are met

- start at low doses and titrate until max doses or max tolerated doses are reached before intensifying

109
Q

what medication is usually kept on board even when transitioning over to insulin therapy?

A

metformin is usually kept on board to reduce weight gain from insulin

110
Q

what combinations of drugs should you avoid?

A

SU + glinide
-duplicate MOA (increased risk of hypoglycemia, increased beta-cell “burnout”

GLP-1 + DPP-4 inhibitor

  • some overlap w/MOA
  • GLP-1 agonist does everything a DPP-4 inhibitor does (and more) and is more eficacious
111
Q

what drugs should you consider using in patients with CVD?

A
  • liraglutide
  • empagliflozin
  • canagliflozin
  • metformin (obese patients)
112
Q

what drugs should you consider avoiding or use with caution in patients with CVD?

A
  • saxagliptin/alogliptin (incr hospitalizations for HF)
  • TZDs (increased risk of HF)
  • SU? (conflicting data)
113
Q

what medications need to be avoided or dose reduced in renal disease?

A
  • metformin
  • SUs (especially glyburide)
  • DPP-4 inhibitors (except linagliptin)
  • exenatide, exenatide ER
  • SGLT-2 inhibitors
114
Q

canaglifozin dosing

  • usual dose
  • renal dosing
  • other renal notes
A

Usual dose: 100 or 300mg daily

Renal dosing: eGFR 45-59 give 100mg daily
-AVOID if eGFR < 45

Renal notes: AKI reported (requiring dialysis)
-monitor for: edema, decreased urine production

115
Q

empagliflozin dosing

  • usual dose
  • renal dosing
  • other renal notes
A

Usual dose: 10 or 25mg daily

Renal dosing: AVOID if eGFR < 45

Renal notes: reduction in AKI

116
Q

dapagliflozin dosing

  • usual dose
  • renal dosing
  • other renal notes
A

Usual dose: 5 ot 10 mg daily

Renal dosing: AVOID if eGFR < 60

Renal notes: AKI reported (requiring dialysis)
-monitor for: edema, decreased urine production

117
Q

when should you avoid the use of canaglifozin in terms of eGFR?

A

avoid if eGFR < 45

118
Q

when should you avoid the use of empagliflozin in terms of eGFR?

A

avoid if eGFR < 45

119
Q

when should you avoid the use of dapagliflozin in terms of eGFR?

A

avoid if eGFR < 60

120
Q

what medications have the highest risk of hypoglycemia (monotherapy)?

A
  • insulin
  • SUs
  • glinides (less than SUs)
  • amylin analogue
121
Q

how do you reduce the risk of hypoglycemia when using insulin?

A

use rapid & long or ultra-long acting analogues

122
Q

how do you reduce the risk of hypoglycemia when using SUs?

A

take with food

*avoid glyburide!

123
Q

how do you reduce the risk of hypoglycemia when using glinides?

A

take with food

124
Q

how do you reduce the risk of hypoglycemia when using amylin analogue?

A

reduce dose of bolus insulin by 50%

125
Q

what increases when anti diabetic drugs are used in combo?

A

risk of hypoglycemia increases when any of the anti diabetic drugs are used in combo

  • Monitor!
  • consider dose reduction if needed
126
Q

is age a C/I for use of any anti diabetic agent?

A

no

127
Q

if older in age, what should you watch for/monitor/be careful of?

A
  • watch for agents that cause hypoglycemia
  • monitor renal function
  • be careful of medications that can cause weight loss
128
Q

what medications cause weight loss?

A
  • GLP-1 agonists
  • Amylin analogue
  • SGLT-2 inhibitors
129
Q

what medications are weight neutral?

A
  • metformin
  • DPP-4 inhibitors
  • alpha-glucosidase inhibitors
130
Q

what medications cause weight gain?

A
  • TZDs
  • SUs
  • Glinides
  • Insulin
131
Q

what medications come in generic form?

A
  • metformin
  • SUs
  • glinides
  • TZDs
  • AGIs

insulin glargine U-100 (Basaglar is not “generic”, but is a lot cheaper than Lantus

132
Q

what medications come in brand form?

A
  • DPP-4 inhibitors
  • SGLT-2 inhibitors
  • GLP-1 agonists
  • Amylin analogue
  • Insulin (basal, bolus, inhaled)
133
Q

what medications are SQ injectables?

A
  • GLP-1 agonists
  • Amylin analogue
  • Insulin (Basal, bolus)

all others are oral

Therapeutics (6 decks)

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