Diabetes Flashcards

1
Q

Characteristics of adults who should be screened for diabetes?

A

Adults:

  • BMI ≥ 25 (Asian Am ≥23) + ≥1 risk factor
  • Prediabetes Dx
  • ≥ 45yo
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2
Q

Characteristics of children who should be screened for diabetes?

A

overweight + ≥ 2 additional risk factors

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3
Q

Criteria for prediabetes diagnosis

A

Any one of:

  • FPG 100-125 mg/dL
  • 2hr PG 140-199mg/dL after 75g OGTT
  • HbA1c 5.7-6.4%
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4
Q

Criteria for diabetes diagnosis

A

Any one of*

  • FPG ≥ 126
  • 2hr PG ≥ 200 after 76g OGTT
  • Random PG ≥200 + classic Sx hyperglycemia

*repeat test to confirm unless unequivocal hyperglycemia

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5
Q

Sx Hypoglycemia

A

• Confusion • Diaphoresis • Tachycardia • Nausea • Tremulousness • Weakness • Coma • Seizures

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6
Q

BBs and hypoglycemia

A

BBs can match Sx e.g., tachycardia & tremors

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7
Q

Significance of hypoglycemic events

A

1+ severe hypoglycemic events = more likely to die in next 5yrs

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8
Q

Studies that showed evidence for tight glycemic control

A

DCCT

EDIC

UKPDS

ADVANCE

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9
Q

DCCT

A

Diabetes Control & Complications Trial

• check BG, intensive insulin, diet + exercise, monthly visits → reduced diabetic retinopathy nephropathy, neuropathy

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10
Q

EDIC

A

Epidemiology of Diabetes Interventions & Complications

10 more years w/DCCT Ptsl→ reduced CVD, nonfatal MI, stroke, death from CV cause

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11
Q

UKPDS

A

UK Prospective Diabetes Study 10 yr RCT

  • diet alone vs intensive Tx w/insulin & sulfonylurea +/- metformin if needed
    • tight BP control w/ACEi, BB, or CCB

GC & BP control → reduced microvascular complications metformin significantly reduced risk MI & stroke

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12
Q

ADVANCE

A

Action in Diabetes & Vascular Disease: Preterax & Diamicron Modified Release Controlled Evaluation

  • Perindopril + indapimide reduced mortality compared to placebo
  • HbA1c <6.5% no change in mortality
  • 6yr f/u study confirmed initial findings
  • HbA1c target reduced progression to ESRD
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13
Q

Recommended Goal HbA1c (ADA)

A

6.0-6.5% in selected pts

<7% most adult pts

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14
Q

HbA1c Treatment goals Advanced Age (ADA)

A
  • Usual goals if pt functional, cognitively intact, significant life expectancy
  • May consider lower, e.g., <8% if above criteria not met
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15
Q

HbA1c Treatment goals Pediatric

A

<7.5% pediatric patients w/DMI

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16
Q

When should HbA1c Treatment goals be more liberal? (ADA)

A

More liberal goals if - episodes of severe hypoglycemia / hypoglycemia unawareness - complex comorbid conditions, limited life expectancy (3-5years before benefits of tight glyc control seen. Focus on BP or lipids instead)

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17
Q

General guidelines for non-pharm therapy? (ADA)

A
  • Medical nutrition therapy
    • Wt loss if overweight (≥ 7%)
    • Whole grains & fibers
    • reduced sat & trans fats, sugary bevs, sodium
    • etoh in moderation
  • 150 min/week moderate intensity aerobic
  • resistance training 2x week unless C/I’d
  • Separate recs for pedi, e.g., ~ 1 hr daily
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18
Q

Guidelines for non-pharm therapy in advanced age? (ADA)

A
  • Symptomatic hyper/hypoglycemia should always be prevented / treated
  • Lifestyle & metformin comparable in younger, but older pts shown to have no benefit from metformin but significant benefit from lifestyle modification (Caspersen et al., 2012)
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19
Q

2015 ADA guidelines emphasize…

A

individualized Tx plan: patient preference, comorbidities

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20
Q

Guidelines for DMI pharm therapy in adults (ADA)

A

Insulin (basal, bolus, correction regimen, continuous infusion or pump)

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21
Q

Guidelines for DMII pharm therapy in adults (ADA)

A
  • first line: metformin unless C/I’d
  • +/- insulin if symptomatic and/or markedly elevated A1c or glucose
  • Add second PO drug, GLP-1 agonist, or insulin if goal A1c not achieved w/max tolerated dose after 3 mths
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22
Q

Guidelines for DMI pharm therapy in kids (ADA)

A

Insulin (basal, bolus, correction regimen, continuous infusion or pump)

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23
Q

Guidelines for DMII pharm therapy in kids (ADA)

A

10-18yo w/random BG ≥ 250mg/dL, HbA1c >9%, or w/ketoacidosis: same as DMI

10-18yo w/o above features: Glucophage (metformin)

Always w/lifestyle modifications

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24
Q

Sulfonylureas: indication

A

DMII

Need some β cell function

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25
Q

Sulfonylureas: MOA/PK

A
  • Binds to ATP dependent K+ channel in β cell.
  • Closes channel which depolarizes cell
  • Altered resting membrane potential opens Ca++ channel.
  • Ca++ influx leads to insulin secretion
  • Net effect: stimulate insulin release through β cells
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26
Q

Sulfonylureas: ADRs

A
  • Weight gain (increased glc)
  • Hypoglycemia
  • Rare CV deaths (may be increased w/glimepiride)
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27
Q

Sulfonylureas: Relative Efficacy

A

reduced A1c 1-2%

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28
Q

Sulfonylureas: special considerations

A
  • increased glycogen, fat, protein formation
  • may → β cell burnout
  • avoid in sulfa allergy
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29
Q

Sulfonylureas: drug names

A

Diabinese (chlorpropamide)

Diabeta (glyburide)

Glucotrol (glipizide)

Amaryl (glimepiride)

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30
Q

Diabinese (chlorpropamide): Dose, peak, duration

A
  • 250-750 mg/day
  • Peak: 3-6h
  • Duration: 24h

(sulfonylurea)

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31
Q

Diabinese (chlorpropamide): important considerations

A
  • reduce dose in renal impairment
  • CYP2C9 substrate
  • active metabolite – can accumulate
  • high risk d/t unpredictable PKs, longer acting
  • rarely used

(sulfonylurea)

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32
Q

Diabeta (glyburide): Dose, peak, duration

A
  • 2.5 – 20mg/day micronized: 1.25 – 12mg/day
  • Peak: 2-4h
  • Duration: ≤ 24h

(sulfonylurea)

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33
Q

Diabeta (glyburide): important considerations

A
  • Caution in renal impairment
  • CYP2C9 substrate
  • risk d/t longer acting

(sulfonylurea)

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34
Q

Diabeta (glyburide): GDM

A

not as good as insulin or metformin in GDM (insulin recommended (sulfonylurea)

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35
Q

Glucotrol (glipizide): Dose, peak, duration

A
  • 5-20 mg/day
  • Peak: 1-3h
  • Duration: 12-24h

(sulfonylurea)

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36
Q

Glucotrol (glipizide): important considerations

A
  • CYP2C9 substrate
  • recommended

(sulfonylurea)

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37
Q

Amaryl (glimepiride): Dose, peak, duration

A
  • -5 mg/day
  • Peak: 2-3h
  • Duration: 24h

(sulfonylurea)

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38
Q

Amaryl (glimepiride) important considerations

A
  • CYP2C9 substrate
  • recommended

(sulfonylurea)

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39
Q

Which sulfonylurea is safe in elderly?

A

Amaryl (glimepiride)

no active renal metabolite = safe in elderly

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40
Q

Which sulfonylureas are recommended?

A

Amaryl (glimepiride)

Glucotrol (glipizide):

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41
Q

Meglinitides: typical dosing

A

Typically 2-3x/day

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42
Q

Meglinitides: agents

A

Prandin (repaglinide)

Starlix (nateglinide)

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43
Q

Meglinitides: MOA

A

Stimulate insulin release through β cells

Quick peak, short duration compared to sulfonylureas

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44
Q

Meglinitides: ADRs

A

Weight gain

hypoglycemia

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45
Q

Meglinitides: hypoglycemia risk

A

Important counseling: Skip a meal, skip a dose to avoid hypoglycemia

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46
Q

Meglinitides: relative efficacy

A

Reduces A1c A1c 1-1.5%

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47
Q

Meglinitides: important considerations

A

increase glycogen, fat, protein formation

Most effective for postprandial hyperglycemia

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48
Q

Prandin (repaglinide): dose, peak, duration

A
  • 0.5-4mg ac
  • Peak: 1h
  • Duration: 4-6h

(Meglinitide)

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49
Q

Prandin (repaglinide): metabolism

A

CYP3A4 substrate

(Meglinitide)

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50
Q

Starlix (nateglinide): dose, peak, duration

A
  • 60-120mg ac
  • Peak: 1h
  • Duration: 4h

*no dose titration required!

(Meglinitide)

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51
Q

Starlix (nateglinide): metabolism

A

CYP2C9 & CYP3A4 substrate

(Meglinitide)

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52
Q

Meglinitides - hepatic or renal impairment

A

no adjustment

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53
Q

Biguanides: agents

A

Glucophage (metformin)

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54
Q

Glucophage (metformin): Dose

A

1000-3000mg QD divided into 2 doses or as ER formulation

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55
Q

Glucophage (metformin): renal / hepatic impairment

A

AVOID in renal impairment (men SCr >1.5mg/dL, women SCr >1.4mg/dL) (Biguanide)

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56
Q

Glucophage (metformin): MOA/PK

A
  • Reduce A1c 1-1.5%
  • hepatic gluconeogenesis
  • Increase insulin sensitivity – often insulin resistance is the problem & not lack of insulin (Biguanide)
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57
Q

Glucophage (metformin) ADRs

A

GI distress, vit B12 deficiency, lactic acidosis (Biguanide)

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58
Q

Glucophage (metformin) hypoglycemia

A

No! except in combo w/other agents (Biguanide)

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59
Q

Glucophage (metformin) relative efficacy

A

Reduce A1c 1-2%

(Biguanide)

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60
Q

Glucophage (metformin): how to minimize GI effects

A

Minimize GI SEs via slow titration -start low, go slow!

(Biguanide)

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61
Q

Glucophage (metformin): when to avoid

A

Avoid in renal impairment, dehydration, CHF, or recent contrast dye administration

(Biguanide)

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62
Q

Glucophage (metformin): weight

A

weight neutral

(Biguanide)

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63
Q

Glucophage (metformin): GDM

A

GDM: did better than insulin for weight gain, but earlier births, etc. Insulin still rec’d.

(Biguanide)

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64
Q

THIAZOLIDINEDIONES: Agents

A

Actos (pioglitazone)

Avandia (rosiglitazone)

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65
Q

Actos (pioglitazone): dose

A

15-45mg PO QD

(thiazolidinediones)

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66
Q

Actos (pioglitazone): renal or hepatic impairment

A

AVOID in hepatic impairment (thiazolidinediones)

67
Q

Actos (pioglitazone): MOA

A

Increase peripheral insulin sensitivity by activating PPAR gamma

PPAR gamma influences the production of gene products involved in glc and lipid metabolism. Abundant in renal collecting tubules

(thiazolidinediones)

68
Q

Actos (pioglitazone): ADRs

A

Edema, anemia, HF, weight gain, increase bone fractures in women

(thiazolidinediones)

69
Q

THIAZOLIDINEDIONES: hypoglycemia?

A

No!

70
Q

Actos (pioglitazone): relative efficacy

A

reduce A1c 1-1.5%

(thiazolidinediones)

71
Q

Actos (pioglitazone): β cell function

A

May preserve β cell function

(thiazolidinediones)

72
Q

Actos (pioglitazone): avoid in…

A

Avoid in CHF (edema), hepatic impairment

(thiazolidinediones)

73
Q

Avandia (rosiglitazone): special considerations

A

Associated w/increased risk MI

Only available through REMS program for pts w/o other options including Actos

Well studied in pedi. Controversy over whether FDA overreacted

74
Q

What are DPP-4 Inhibitors?

A

Dipeptidyl Peptidase-4 Inhibitors

75
Q

DPP-4 Inhibitors MOA

A

Increase glucose-dependent insulin release, suppress glucagon secretion

76
Q

DPP-4 Inhibitors: ADRs

A

Rhinitis, HA, URIs, rare angioedema, pancreatitis

77
Q

DPP-4 Inhibitors: hypoglycemia?

A

No!

78
Q

DPP-4 Inhibitors: relative efficacy

A

decrease A1c 0.6-0.8%

79
Q

DPP-4 Inhibitors: β cell function

A

May preserve β cell function

80
Q

DPP-4 Inhibitors vs sulfonylureas

A

more $ than sulfonylureas

81
Q

DPP-4 Inhibitors: agents

A

Januvia (sitagliptin)

Onglyza (saxagliptin)

Tradjenta (linagliptin)

82
Q

DPP-4 Inhibitors: special considerations

A
  • ø combine w/meglinitide or sulfonylurea as both act on β cell.
    • All can combine w/metformin
83
Q

Januvia (sitagliptin): dose & peak

A

100mg QD

Peak: 1-4h

(DPP-4 Inhibitor)

84
Q

Onglyza (saxagliptin): dose & peak

A
  • 2.5-5mg QD
  • Peak: 2h

(DPP-4 Inhibitor)

85
Q

Tradjenta (linagliptin): dose & peak

A
  • 5mg QD
  • Peak: 1.5h

(DPP-4 Inhibitor)

86
Q

Januvia (sitagliptin): hepatic & renal impairment

A

reduce in renal impairment

(DPP-4 Inhibitor)

87
Q

Onglyza (saxagliptin): when to reduce dose

A

reduce in renal impairment

reduce w/strong CYP3A4/5 inhibitors

(DPP-4 Inhibitor)

88
Q

Tradjenta (linagliptin): hepatic & renal impairment

A

no adjustments!

(DPP-4 Inhibitor)

89
Q

Onglyza (saxagliptin): special considerations/ADR

A
  • ? association w/HF
90
Q

SGLT-2 Inhibitors: Agents

A

Invokana (canagliflozin)

Farxiga (dapagliflozin)

Jardiance (empagliflozin)

91
Q

SGLT-2 Inhibitors: Hepatic & renal dose adjustment?

A

AVOID in ESRD

92
Q

SGLT-2 Inhibitors: MOA

A

Unique mechanism Inhibits sodium-glucose-transporter (SGLT)-2 which is responsible for ~90% of glc resorption in the kidney

Results in glucosuria

93
Q

SGLT-2 Inhibitors: ADRs

A

Hypotension, fungal infections, thirst, nausea, constipation, polyuria, increased LDL-C

94
Q

SGLT-2 Inhibitors: hypoglycemia?

A

No!

95
Q

SGLT-2 Inhibitors: relative efficacy?

A

Reduce A1c 0.7-1%

96
Q

SGLT-2 Inhibitors: weight

A

• May cause weight loss

97
Q

SGLT-2 Inhibitors: BP

A

• Beneficial effects on BP

98
Q

SGLT-2 Inhibitors: Avoid in…

A

• Avoid in ESRD, volume-depleted pts

99
Q

Invokana (canagliflozin): dosing

A

100-300mg QD

Reduce in renal impairment

(SGLT-2 Inhibitor)

100
Q

Farxiga (dapagliflozin): dosing

A

5-10mg QD

Reduce in renal impairment

(SGLT-2 Inhibitor)

101
Q

Jardiance (empagliflozin): dosing

A

1—25mg QD

AVOID in renal impairment

(SGLT-2 Inhibitor)

102
Q

(GLP-1) MIMETICS: stands for

A

GLUCAGON-LIKE POLYPEPTIDE-1 MIMETICS

103
Q

GLP-1 Mimetics: Agents

A

Byetta (exanatide)

Victoza (Liraglutide)

Tanzeum (albiglutide)

Trulicity (dulaglutide)

104
Q

GLP-1 Mimetics: MOA

A

Stimulates insulin release in presence of glucose, suppresses glucagon release, slows gastric emptying, early satiety

105
Q

GLP-1 Mimetics: ADRs

A

N/V/D, HA, rare necrotizing pancreatitis Some believe wt loss d/t emesis and diarrhea

106
Q

GLP-1 Mimetics: hypoglycemia?

A

No! Except in combo w/sulfonylureas

107
Q

GLP-1 Mimetics: relative efficacy?

A

A1c ~1%

108
Q

GLP-1 Mimetics: formulation

A

• Only available as injection

109
Q

GLP-1 Mimetics: advantages

A
  • Weight loss (Victoza – also for chronic weight loss)
  • May preserve β cell function
110
Q

GLP-1 Mimetics: Avoid in…

A

Avoid in DMI, severe GI problems, DKA, FH or personal history medullary cancer or multiple endocrine neoplasm type 2

111
Q

Byetta (exanatide): dosing

A
  • 5-10mcg SQ BID
  • ER: 2mg SQ weekly
  • Peak: 2h

(GLP-1 Mimetics)

112
Q

Victoza (Liraglutide)

A
  • 0.6-1.8mg SQ QD
  • Peak: 8-12h

(GLP-1 Mimetics)

113
Q

Tanzeum (albiglutide)

A
  • 30mcg SQ weely, may increase to 50mcg weekly
  • Peak: 3-5days

(GLP-1 Mimetics)

114
Q

Trulicity (dulaglutide)

A
  • 0.75 mg SQ weekly, may increase to 1.5mg SQ weekly
  • Peak: 24-72h

(GLP-1 Mimetics)

115
Q

AMYLINOMIMETICS: agents

A

Symlin (pramlinide)

116
Q

Symlin (pramlinide): dosing

A
  • DMI: 15-60mcg
  • DMII: 60-120mcg SQ ac

(amylinomimetic)

117
Q

Symlin (pramlinide): MOA

A

Binds w/amylin receptors which suppresses glucagon release, slows gastric emptying, early satiety

(amylinomimetic)

118
Q

Symlin (pramlinide): ADRs

A

Weight loss, nausea, anorexia

(amylinomimetic)

119
Q

Symlin (pramlinide): Hypoglycemia

A

Yes!

(amylinomimetic)

120
Q

Symlin (pramlinide): Relative Efficacy

A

Reduces A1c 0.4-0.6% - marginal

(amylinomimetic)

121
Q

Symlin (pramlinide): special considerations

A

Nausea is significant barrier to adherence

(amylinomimetic)

122
Q

Insulin: major effects in liver

A
  • Inhibits glycogenolysis, formation of keto acids;
  • Promotes storage of glc as glycogen;
  • increases TG and VLDL synthesis
123
Q

Insulin: major effects in fat

A

increased TG storage, inhibits intracellular lipase

124
Q

Insulin: major effects in muscle

A

increased glycogen synthesis, increased glc transport

125
Q

Graphical representation: onset, peak, duration of rapid, regular, NPH, detemir and glargine

A
  • Far left: ultra rapid acting – mimics what insulin would do w/high carb meal
  • Regular: short but not as rapid as Rapids. Inject before eat to coincide w/peak in bg
  • NPH: used to be used often as basal regimen. Delayed peak and prolonged lower peak. Maybe time around big breakfast, big dinner, w/effects between
  • Long acting: detemir – little peak, tapers off. Usually BID, but QD for some
  • Glargine: QD – low peak and stays
126
Q

Types of insulin

A

Rapid: Novolog (aspart), Humalog (lispro), Apidra (glulisine)

Short: Regular

Intermediate: NPH

Long: Levemir (detimir), Lantus (glargine)

127
Q

Insulin: MOA

A

Small endogenous protein normally present at low levels throughout the day interspersed w/increased levels following stimuli such as glc. See effects on liver, fat, muscle.

128
Q

Insulin​: ADRs

A

Weight gain

Hypokalemia

Hypoglycemia

Rare hypersensitivity reactions

129
Q

Insulin: relative efficacy

A

Most effective!

130
Q

Insulin: administration

A

All subQ except regular can be IV

Do not mix long-acting w/other agents

131
Q

Insulin: analogs vs human

A
  • Insulin analogs (glargine, detemir, lispro, aspart)
  • human insulin (NPH, regular)
132
Q

Insulin: regimens

A

Various regimens: Sliding scale, Single nightly dose, Basal-bolus-correction

Sliding scales associated w/more hypo/hyperglycemia

133
Q

Rapid acting Insulin: P, O, D

A

Onset: 10-15min

Peak: 1-2h

Duration: 3-5h

Novolog (aspart)

Humalog (lispro)

Apidra (glulisine)

134
Q

Intermediate-acting Insulin: P, O, D

A

Onset: 1-3h

Peak: 4-10h

Duration: 10-18h

NPH

135
Q

Short acting Insulin: P, O. D

A

Onset: 30-60min

Peak: 2-4h

Duration: 4-8h

Regular

136
Q

Long acting insulin: P, O, D

A

Levemir (detimir)

  • Onset: 2-3h
  • Peak: none
  • Duration: 24h

Lantus (glargine)

  • Onset: 1h
  • Peak: none
  • Duration: 24h
137
Q

Afrezza: what is it?

A

Rapid acting inhaled insulin

Regular human insulin

138
Q

Afrezza: dosing

A

AC or w/in 20min after starting a meal

(inhaled insulin)

139
Q

Afrezza: ADRs

A

Similar to other insulins

May cause acute bronchospasm in chronic lung dz

(inhaled insulin)

140
Q

Afrezza: drug interactions

A

Albuterol increases absorption

141
Q

Afrezza: avoid in…

A

Avoid in pts w/chronic lung dz (e.g., asthma, copd), active lung cancer, who smoke, or at high risk of DKA

(inhaled insulin)

142
Q

Afrezza: monitoring & special considerations

A

Monitor for lung dz – spirometry, FEV1 at baseline, 6mths, then annually

Expensive and difficult to store/use

143
Q

Diabetes in advanced age: more likely than nondiabetic to have….

A

Depression, cognitive impairment, urinary incontinence, injurious falls, persistent pain, HTN, coronary heart disease, stroke, functional disability, premature death

Multiple comorbidities, polypharmacy, limited financial resources

144
Q

Diabetes & advanced age: short acting vs long acting agents

A

Shorter acting agents preferred: avoid glyburide, chlorpropamide d/t hypoglycemia

also why sliding scales should be avoided

145
Q

Diabetes & advanced age: considerations for visual impairment

A
  • ~30% ≥65yo have diabetic retinopathy, can lead to blindness
  • Increased risk cataracts
  • may increase risk primary open-angle glaucoma in women
  • –> consider insulin pen to deliver – they can hear click
146
Q

Diabetes & advanced age: cognitive decline - risks

A
  • 25% using insulin in UK showed CI
  • increased risk dementia, alzheimers, vascular dementia
  • may impair self-care, assess social network
  • assess cognitive status regularly
147
Q

Diabetes & advanced age: cognitive decline & pharm mgmt

A

5yr observational study:

  • metformin may reduce dementia risk by up to 50%
  • Sulfonylureas, thiazolidenidiones, insulin may increase risk

good insulin control can help prevent cognitive decline

148
Q

Diabetes & advanced age: interventions to address polypharmacy

A
  • List indication of each med, consider including in Rx instructions
  • Simplify med regimens and use tools e.g., pill boxes if possible

Increased risk adverse events w/each added medencourage maintained med list!

149
Q

Diabetes & advanced age: hypoglycemia considerations. Insulin vs other agents

A
  • Increased risk d/t comorbidities e.g., CKD, polypharmacy, CI
  • Insulin is most effective in reducing A1c. Adding insulin to SU is more effective w/less hypoglycemia than increasing SU dose
  • Severe hypoglycemia 2x more likely w/insulin than SU in pts ≥65yo
  • Insulin analogs (glargine, detemir, lispro, aspart) preferred over human insulin (NPH, regular)
  • Basal-bolus regimens w/strict carb counting or difficult dose adjustments not appropriate for some
150
Q

Diabetes meds that should be reduced in renal impairment

A
  • Diabinese (chlorpropamide) - sulfonylurea
  • Januvia (sitagliptin) and Onglyza (saxagliptin) - DPP-4is
  • Invokana (canagliflozin) & Forxiga (dapagliflozin) - SGLT-2is
151
Q

Diabetes meds that should be avoided in renal impairment

A
  • Glucophage (metformin) - biguanide
  • Precose (acarbose) & Glyset (miglitol) - Alpha-glucosidase inhibitors
  • Jardiance (empagliflozin) - SGLT-2i
152
Q

Diabetes meds that should be used w/caution in renal impairment​

A

Diabeta (glyburide) - sulfonylurea

153
Q

Diabetes meds that should be avoided in ESRD (besides those already mentioned for renal impairment)

A

all SGLT-2is

  • Invokana (canagliflozin)
  • Forxiga (dapagliflozin)
  • Jardiance (empagliflozin)
154
Q

Diabetes meds that should be avoided in hepatic impairment

A
  • precose (acarbose) & Glyset (miglitol) - alpha-glucosidase inhibitors
  • Actos (pioglitazone) - thiazolidinedione
155
Q

ALPHA-GLUCOSIDASE INHIBITORS: agents

A

Precose (acarbose)

Glyset (miglitol)

156
Q

ALPHA-GLUCOSIDASE INHIBITORS: MOA

A

Slows carb absorption from gut by inhibiting alpha-glucosidases

decrease postprandial hyperglycemia, insulin-sparing

157
Q

ALPHA-GLUCOSIDASE INHIBITORS: hepatic / renal

A

AVOID in renal or hepatic impairment

Precose (acarbose)

Glyset (miglitol)

158
Q

ALPHA-GLUCOSIDASE INHIBITORS: ADRs

A

GI Distress (will not go away)

Precose (acarbose)

Glyset (miglitol)

159
Q

ALPHA-GLUCOSIDASE INHIBITORS: hypoglycemia?

A

No!

Precose (acarbose)

Glyset (miglitol)

160
Q

ALPHA-GLUCOSIDASE INHIBITORS: relative efficacy

A

reduces A1c 0.5%

Precose (acarbose)

Glyset (miglitol)

161
Q

ALPHA-GLUCOSIDASE INHIBITORS​: weight gain

A

Weight neutral

Precose (acarbose)

Glyset (miglitol)

162
Q

ALPHA-GLUCOSIDASE INHIBITORS: what if patient skips a meal?

A

Skip a meal, skip a dose – but not b/c will bottom out. B/c would be pointless

Precose (acarbose)​

Glyset (miglitol)

163
Q

ALPHA-GLUCOSIDASE INHIBITORS: avoid in…

A

Avoid in renal or hepatic impairment, IBD

Precose (acarbose)

Glyset (miglitol)

164
Q

ALPHA-GLUCOSIDASE INHIBITORS: dietary consideration

A

Eat similar carbs each meal if possible

Precose (acarbose)​

Glyset (miglitol)