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Foundations III Exam 2 Endocrine > DM Type 2 - Feirstein > Flashcards

DM Type 2 - Feirstein Flashcards

1
Q

What is DM characterized by?

A

Hyperglycemia

Insulin deficiency & resistance

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2
Q

What are RFs for DM?

A 
Genetic 
Anthropometric (BMI, waist)
Environmental/lifestyle
Age ≥ 45
Family hx
Obesity 
Inactivity 
Race
Smoking 
Diet 
Meds
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3
Q

What drugs can impair glucose tolerance or cause DM?

A

FQs
Thiazide
Glucocorticoids
OCPs

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4
Q

What is metabolic syndrome also known as?

A

Insulin resistance syndrome

Syndrome X

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5
Q

What are characteristics of metabolic syndrome?

A 
Abd obesity 
TG ≥ 150
Low HDL 
BP ≥ 130/85
FPG ≥ 100
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6
Q

How do you manage metabolic syndrome?

A
  • Treat underlying cause(s)
  • Treat CVD RFs
  • Lifestyle modification
  • Wt loss (7-10% within 1 yr)
  • Increase activity (150min/wk)
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7
Q

How can you treat metabolic syndrome pharmacologically?

A

Metformin

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8
Q

How do you reduce RFs for metabolic syndrome?

A
  • Stop smoking
  • Treat HTN
  • Lower cholesterol
  • Glycemic control
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9
Q

Describe: fasting state

A

Low insulin, high glucagon

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10
Q

Describe: postprandial

A

High insulin, low glucagon

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11
Q

What is the pathophysiology of DM?

A
  1. Insulin resistance: beta cells compensate by increasing insulin
  2. Impaired glucose tolerance: beta cells can no longer sustain hyperinsulinemic state
  3. Overt DM: beta cell failure
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12
Q

What is the clinical presentation of DM?

A
  • Usually asx
  • Hyperglycemia w/ sx:
    Polyuria
    Polydipsia
    Nocturia
    Blurred vision
    Wt loss
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13
Q

What are DM screening recommendations according to ADA?

A

BMI ≥ 25 + additional RFs q 3 yrs

Start at age 45 if no RFs

Screen prediabetics annually

Women w/ GDM q 3 years

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14
Q

What are DM screening recommendations according to USPSTF?

A

40-70yo overweight or obese q 3 yrs (as part of CV assessment)

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15
Q

What is the dx criteria for DM?

A

Sx + random blood glucose ≥ 200

If asx:
FPG ≥ 126
2hr glucose ≥ 200 (OGTT)
A1c ≥ 6.5%

*Repeat on different day

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16
Q

What is a normal FPG?

A

< 100

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17
Q

What is a normal OGTT?

A

< 140

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18
Q

What is a normal IFG?

A

100-125

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19
Q

What is a normal IGT?

A

140-199

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20
Q

What % of A1c increases one’s risk for developing DM?

A

5.7-6.4%

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21
Q

Describe: glycated hemoglobin (A1c)

A

Convenient

Correlates w/ mean glucose concentration & DM complications

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22
Q

What is A1c effected by?

A

RBC turnover

Also maybe: Hemoglobinopathy
CKD

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23
Q

What labs should you order for DM?

A
  • A1c (every 3-6mos)
  • Fasting lipids
  • Liver enzymes
  • Urine albumin excretion (annually)
  • Serum creatinine
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24
Q

When should diabetics have an eye, foot, & dental exam?

A

Annually!

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25
Q

Describe: glycemic control

A

Monitor 2x/yr in controlled & quarterly in uncontrolled

Most pt’s goal = < 7%

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26
Q

When would you consider less stringent goals for glycemic control?

A

Hx of severe hypoglycemia
Limited life expectancy
Older
Comorbid conditions

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27
Q

What are goals of pharmacologic therapy?

A

Increase insulin availability

Improve sensitivity to insulin

Delay delivery & absorption of carbs from GI tract

Increase urinary glucose excretion

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28
Q

When should you start pharmacologic therapy?

A

If A1c > 7.5-8% at dx

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29
Q

When can you try a 3-6 month trial of lifestyle modification?

A

A1c < 7.5%

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30
Q

What is initial pharmacological therapy for DM?

A

Metformin

Alternative = insulin

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31
Q

What is the MOA of metformin (biguanide)?

A

Inhibit gluconeogenesis –> decreased hepatic glucose output

Increase insulin mediated glucose in peripheral tissues

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32
Q

What are characteristics of metformin?

A
  • 1st line tx
  • 1-2% drop in A1c
  • Wt neutral
  • GI side effects
  • Can reduce absorption of B12
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33
Q

What are contraindications of metformin?

A

Renal insufficiency GFR<30

IV contrast concerns

34
Q

What is the MOA of sulfonylureas?

A

Stimulate insulin secretion from pancreatic beta cells

35
Q

What are characteristics of sulfonylureas?

A

1-2% decrease in A1c
Risk of hypoglycemia
Wt gain

36
Q

What are 3 examples of sulfonylureas?

A

Glipizide
Glyburide
Glimepiride

37
Q

What is the incretin effect?

A

Seen w/ GLP-1 agonists

Oral glucose better stimulates insulin secretion than IV glucose (secondary to GI peptides released)

38
Q

What is the MOA of GLP-1?

A

Stimulate insulin release from pancreatic islet cells

Slow gastric emptying

Inhibit post-meal glucagon release

39
Q

What are characteristics of GLP-1 agonists?

A

Add-on therapy
0.5-0.1% drop in A1c
Wt loss
N/V/D

40
Q

What do all of the GLP-1 agonist med names end w/?

A

“tide”

41
Q

Which 2 GLP-1 agonists show possible improved CV outcomes?

A

Liraglutide & semaglutide

42
Q

What is the MOA of DPP-4?

A

Deactivates GLP-1

43
Q

What are characteristics of DPP-4 inhibitors?

A

Add-on therapy
0.5-0.8% drop in A1c
Wt neutral

44
Q

What do the DPP-4 inhibitor med names end w/?

A

“gliptan” or “gliptin”

45
Q

What is the MOA of SGLT2 inhibitors?

A

Increase urinary glucose excretion –> reduced blood glucose

46
Q

What are characteristics of SGLT2 inhibitors?

A

0.5-0.7% decrease in A1c

Add-on therapy

Wt loss

Decreased BP & CV mortality

47
Q

What are the ADEs of SGLT2 inhibitors?

A

Vulvovaginal candidiasis

UTIs

48
Q

What do SGLT2 inhibitor med names end w/?

A

“agliflozin”

49
Q

What is the MOA of TZDs?

A

Improve insulin action

Increase insulin sensitivity by acting on adipose, muscle, & liver to increase glucose utilization & decrease produciton

50
Q

What are characteristics of TZDs?

A

Add-on therapy

0.5-1.4% drop in A1c

51
Q

What are ADEs of TZDs?

A 
Fluid retention 
HA
Wt gain 
Bone fx
Increase in MI &amp; bladder CA
52
Q

What are 4 contraindications of TZDs?

A

Symptomatic or class III-IV HF

Bladder CA

High fx risk

Liver disease

53
Q

What do the TZD med names end w/?

A

“glitazone”

54
Q

How are meglitinides & alpha-glucosidase inhibitors administered?

A

w/ meals to reduce postprandial hyperglycemia

55
Q

What is the MOA of meglitinides?

A

Stimulate insulin secretion from beta cells

56
Q

What are characteristics of meglitinides?

A

0.5-1% decrease in A1c
Add-on therapy
Risk of hypoglycemia
Wt gain

57
Q

What do the meglitinide med names end w/?

A

“glinide”

58
Q

What is the MOA of alpha-glucosidase inhibitors?

A

Decrease glucose absorption

59
Q

What are characteristics of alpha-glucosidase inhibitors?

A

Add-on therapy
0.5-0.8% decrease in A1c
Wt neutral
Flatulence & diarrhea

60
Q

What are 2 examples of alpha-glucosidase inhibitors?

A

Acarbose

Miglitol

61
Q

What are options for insulin?

A

Basal

Prandial (short or rapid)

Premixed combo of intermediate acting & short or rapid acting

62
Q

What are 4 categories of basal therapy?

A

NPH
Glargine
Detemir
Degludec

63
Q

What are complications of DM?

A

Microvascular disease:
Retinopathy, nephropathy, neuropathy

Macrovascular disease:
Atherosclerosis

*MAY BE PRESENT AT DX!

64
Q

Describe: diabetic retinopathy

A

Chronic hyperglycemia –> vascular changes –> retinal injury/ischemia

65
Q

Diabetic retinopathy involves vision loss due to….

A

Macular edema
Hemorrhage
Retinal detachment
Neovascular glaucoma

66
Q

What are nonproliferative signs of diabetic retinopathy?

A
  • Cotton wool spots
  • Intraretinal hemorrhage
  • Hard exudates
  • Microanerurysms
  • Occluded vessels
  • Dilated/tortuous vessels
  • Visual loss through macular edema
67
Q

What are proliferative signs of diabetic retinopathy?

A
  • Neovascularization
  • Preretinal & vitreous hemorrhage
  • Fibrosis
  • Retinal detachment
  • Visual loss from bleeding, retinal detachment
68
Q

What is the clinical presentation of diabetic retinopathy?

A

Asx until later stages

69
Q

What are screening recommendations for diabetic retinopathy?

A

At time of dx in type 2

Within 5 yrs in type 1

Repeat annually

70
Q

How do you treat diabetic retinopathy?

A

Laser

Intravitreous injections of growth factor

Vitrectomy

71
Q

How do you prevent diabetic retinopathy and nephropathy?

A

Glycemic & BP control

72
Q

What are screening recommendations for diabetic kidney disease?

A

Assess urinary albumin & GFR

At time of dx in type 2
Within 5 yrs of dx in type 1
In all pts w/ HTN

Repeat annually

73
Q

What is the dx criteria for diabetic kidney disease?

A

Moderately increased albuminuria

Requires 2-3 specimens abnormal over 3-6 mos

74
Q

How do you tx diabetic kidney disease?

A

ACE-I or ARB

Protein intake

Refer for renal replacement if GFR < 30

75
Q

What are screening recommendations for diabetic neuropathy?

A

Assess w/ hx & temp or pinprick/vibration sensation

Annual monofilament test

At time of dx for type 2
Within 5 yrs of dx for type 1

Repeat annually

76
Q

How do you treat diabetic neuropathy?

A

Pregabalin or duloxetine

Foot care

77
Q

How often should foot care be performed?

A

At least annually

Consider ABI &/or vascular referral (claudication or decreased/absent pulses)

78
Q

When should you consider podiatry referral?

A 
Smokers 
Hx of LE complications
Loss of protective sensation
Structural abnormalities 
PAD
79
Q

Macrovascular disease: Considerations

A

HTN
Lipids
Smoking hx
Antiplatelets

80
Q

When should you use ASA?

A

As secondary prevention in those w/ diabetics & hx of ASCVD

Dual anti platelet therapy for 1 year after ACS

81
Q

How do you treat ASCVD?

A

ACE-I or ARB

Foundations III Exam 2 Endocrine (2 decks)

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