DM 2 Flashcards

1
Q

dx of metabolic syndrome

A

≥ 102 cm abdominal obesity in Men

≥ 88 cm abdominal obestity in Women

Elevated triglycerides (≥ 150 mg/dL)

Low HDL (men < 40 mg/dL ; women < 50 mg/dL)

Elevated blood pressure (≥ 130/85 mmHg)

Elevated fasting glucose (≥ 100 mg/dL)

atleast 3 of the above

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2
Q

syndrome X

AKA

A

metabolic syndrome

OR

insulin resistance syndrome

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3
Q

metabolic syndrome definition

A

metabolic risk factors for BOTH diabetes & cardiovascular disease

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4
Q

metabolic syndrome has a higher prevalance with what 2 things

A

overweight

obesity

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5
Q

pharmacologic tx of metabolic syndrome

A

metformin

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6
Q

if you have prediabetes, how often should you monitor for T2DM?

A

annually

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7
Q

Prediabetes drug tx

A

metformin

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8
Q

what type of diabetes should you consider in children & adults dx in early adulthood?

A

monogenic dx in first 6 months of life

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9
Q

clinical px of monogenic diabetes

A

no diabetes associated antibodies

nonobese

no other metabolic features

stable, mild fasting hyperglycemia

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10
Q

impaired fasting glucose

A

hepatic insulin resistance

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11
Q

impaired glucose tolerance

A

muscle insulin resistance

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12
Q

what consists of prediabetes?

A

IGT or IFG or both

or

A1c of 5.7-6-4%

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13
Q

Main risk factors of T2DM

A

Prediabetes, metabolic syndrome, insulin resistance conditions (PCOS, AN)

Overweight

> 45 y/o

Immediate relative with T2DM

< 3 days/week physical activity

PMH gestational DM or given birth to baby weighing > 9 lbs

African American, Hispanic/Latino American, American Indian, Alaska Native

Genes/lifestyle/env/meds

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14
Q

what cells produce insulin?

A

Insulin produced by beta cells in the islets of Langerhans in the pancreas

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15
Q

what stimulates insulin production?

A

hyperglycemia

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16
Q

insulin causes glucose transport into which tissues?

A

Insulin causes glucose transport into adipose tissue and muscle

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17
Q

Physiology of fasting state

A

low insulin, high glucagon

+ glucagon further stimulates gluconeogenesis & glycogenolysis

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18
Q

Postprandial physiology

A

high insulin, low glucagon

+ carbohydrate storage

+ fat and protein synthesis

+ skeletal muscle uptake

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19
Q

Clinical Px of T2DM

A

usually asx

hyperglycemia (polyuria, polydipsia, nocturia, blurred vision, weight loss)

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20
Q

ADA Screening guidelines

A

All adults with BMI ≥ 25 + additional risk factor(s): q 3 years

Start at age 45 for everybody else

pts with prediabetes: annually

Women with GDM: q 3 years

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21
Q

T2DM USPSTF screening

A

Adults 40-70 y/o who are overweight/obese should be screened as a part of CV risk assessment q 3 years

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22
Q

T2DM Dx criteria if sx

A

Symptoms + random blood glucose ≥ 200 mg/dL

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23
Q

T2DM Dx criteria if asx

A

If asymptomatic:

FPG ≥ 126 mg/dL

2 hour glucose ≥ 200 mg/dL during OGTT

A1c ≥ 6.5%

Repeat on a different day

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24
Q

What are normal lab values of FPG, OGTT, A1c?

A

FPG < 100 mg/dL

2-hr glucose during OGTT < 140 mg/dL

A1c: <5.7

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25
Q

Pre-diabetic Dx criteria

A

IFG: FPG 100-125 mg/dL

IGT: 2-hr glucose during OGTT 140-199 mg/dL

A1c: 5.7 – 6.4%

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26
Q

What can cause falsely high levels of A1c?

A

Low cell turnover = falsely high levels

Iron, vitamin B12, or folate deficiency

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27
Q

What can cause falsely low levels of A1c?

A

High cell turnover = falsely low levels

Hemolytic anemia, treated iron/B12/folate deficiency, erythropoietin use`

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28
Q

Main mgmt goals for T2DM

A
  • Glycemic control
  • Monitoring/prevent micro/macrovascular complications
  • Patient education: Nutrition, Hypoglycemia, CV risk, vision, kidneys
  • Health maintenance
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29
Q

how do you approach a T2DM pt?

A

pt centered: active listening

multi-disciplinary:

  • Primary care
  • Specialty care: Podiatry, Ophthalmology, Mental health, Ob/gyn, Endocrine, Dieticians, Exercise specialists
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30
Q

How often do you monitor glycemic control in controlled T2DM pts?

A

2x/yr

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31
Q

How often do you manage glycemic control in T2DM pts with changes in therapy or those who are not meeting goals?

A

4x/yr

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32
Q

A1c goals for diff types of pts

A

Most patients < 7.0%

stringent goals: < 6.5%

Less stringent: < 8.0% if…

  • Hx severe hypoglycemia
  • Limited life expectancy
  • Older adults
  • Comorbid conditions
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33
Q

more often self monitoring of blood glucose in T1DM when…

A

titrating medications associated with hypoglycemia

Several times/wk – morning or before dinner

illness or changes in diet/exercise

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34
Q

Non-pharmacologic therapy options for T2DM

A
  • Diet
  • Physical activity
  • Weight reduction/management
  • Smoking cessation
  • Psychological interventions (diabetes distress)
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35
Q

most imp nutrition pearls

A
  • eat high fiber/nutrient dense foods (fruits & vegetables)
  • count carbs for bolus insulin
  • avoid carb sources high in protein
  • meditteranean diet = good
  • eat fatty fish and foods rich in long-chain n-3 fatty acids
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36
Q

dietary restrictions in T2DM

A

alcohol in moderation: (≤ 1/d women, ≤ 2/day men)

<2300mg/day Na

dec. nonnutritive sweeteners

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37
Q

Goals of pharmacologic tx

A

Inc. insulin availability

dec. sensitivity to insulin

Delay delivery and absorption of carbohydrates from the GI tract

Inc. urinary glucose excretion

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38
Q

A1c levels in regards to Rx

A

A1c > 7.5-8% at dx – start Rx

A1c < 7.5% at dx – 3-6 month trial of lifestyle modification (if highly motivated)

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39
Q

Initial pharmacologic therapy for T2DM pts

A

-Metformin

-Consider dual therapy

-Insulin may be considered

-Consider comorbidities (ASCVD, HF, CKD), hypoglycemia risk, impact on weight, cost, risk for side effects, patient preferences

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40
Q

Tx options

A
  • Metformin
  • Sulfonylureas
  • GLP-1 RA
  • (DPP-4)
  • (SGLT2) inhibitor
  • TZD
  • Meglitinides
  • Alpha-glucosidase inhibitor
  • Insulin
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41
Q

Decrease hepatic glucose output by inhibiting gluconeogenesis

Increases insulin-mediated glucose utilization in peripheral tissues (muscle, liver)

MOA of which drug?

A

Metformin (biguanide)

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42
Q

1st line tx of DM2

A

Metformin

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43
Q

A1c % drop w/Metformin

A

1-2% drop in A1c

44
Q

ADE/CI of metformin

A

GI side effects

Can reduce intestinal absorption of vitamin B12

Contraindicated with renal insufficiency, eGFR < 30 mL/min

IV contrast concerns

45
Q

weight neutral meds

A

Metformin

DPP-4 Inhibitors

alpha-glucosidase inhibitors

46
Q

which meds inc weight

A

TZD

Meglitinides

Insulin

sulfonylureas

47
Q

which meds dc weight

A

GLP-1 RA

SGLT2-I

48
Q

Stimulate insulin secretion from pancreatic beta cells

MOA of which drug?

A

sulfonylureas

  • Glipizide
  • Glyburide
  • Glimepiride
49
Q

ADE of sulfonylureas

A

risk of hypoglycemia

50
Q

A1c% drop of sulfonylureas

A

1-2%

51
Q

what is the incretin effect

A

oral glucose better stimulates insulin secretion than IV glucose secondary to GI peptides (GLP-1) released in response to a meal stimulating insulin synthesis and secretion

52
Q

stimulates glucose dependent insulin release from pancreatic islet cells

slows gastric emptying

inhibits post-meal glucagon release

MOA of what drug?

A

GLP-1 RA

53
Q

what special pt populations are you more likely to give a GLP-1 RA to?

A

pts w/ ASCVD

reduce risk of CKD progression and CV events

54
Q

what are the add-on therapies?

A

SGLT2-Inhibitor

TZD

DPP-4 Inhibitors

Meglitinides

55
Q

Possible improved CV outcomes with which GLP-1 RAs?

A

liraglutide

semaglutide

56
Q

A1c% drop w/GLP-1 RA

A

0.5-1% drop

57
Q

ADE of GLP-1 RA

A

GI: N/V/D

58
Q

which drug has the same MOA as GLP-1 RA (this is the reason you cannot give both drugs at once)

A

DPP-4 Inhibitors

59
Q

increase urinary glucose excretion leading to reduced blood glucose

MOA of which drug?

A

SGLT2 inhibitors

60
Q

in which pt populations should you use SGLT2 Inhibitors with?

A

pts w/ASCVD

high risk of HF or w/comorbid HF

Shown to reduce risk of CKD progression and CV events

61
Q

ADE of SGLT2 inhibitors

A

vulvovaginal candidiasis, UTIs

62
Q

SGLT2 % decrease in A1c?

A

0.5-0.7%

63
Q

Improve insulin action

Increase insulin sensitivity by acting on adipose, muscle, and liver to increase glucose utilization and decrease glucose production

MOA of which drug?

A

TZD

64
Q

ADEs of TZD

A

Fluid retention, HF, weight gain, bone fractures,

possible increase in MI (rosiglitazone)

possible increase in bladder cancer (pioglitazone)

65
Q

CIs of TZDs

A

symptomatic or class III-IV HF, bladder cancer, high fracture risk, liver disease

66
Q

Administered with meals to reduce postprandial hyperglycemia

Which drug?

A

Meglitinides

67
Q

ADE of meglitinides

A

risk of hypoglycemia

68
Q

% dec in A1c

A

0.5-1% decrease in A1c

69
Q

ADE of alpha-glucosidase inhibitors

A

flatulence and diarrhea

70
Q

% decrease in A1c of alpha-glucosidase inhibitors

A

0.5-0.8%

71
Q

types of insulin

A

Basal:

  • NPH (Humulin N, Novolin N)
  • Glargine (Lantus, Toujeo, Basaglar)
  • Detemir (Levemir)
  • Degludec (Tresiba)

Prandial

  • Short-acting: Regular (Humilin R, Novolin R)
  • Rapid-acting: lispro (Admelog, Humalog), aspart (Fiasp, Novolog), glulisine (Apidra)

Premixed combination of intermediate acting and short or rapid acting

72
Q

If A1C is above target despite recommended first-line treatment and ASCVD predominates, what should you give?

A

GLP-1 RA or SGLT-2 I

73
Q

If A1C is above target despite recommended first-line treatment and HF or CKD predominates, what should you give?

A

SGLT-2 I (1st choice)

or

GLP-1 RA

74
Q

examples of micro & macrovascular dz

A

Microvascular disease: Retinopathy, Nephropathy, Neuropathy

Macrovascular disease: Atherosclerosis (MI, PAD, CVA)

75
Q

Most common cause of blindness in adults aged 20-74

A

diabetic retinopathy

76
Q

what 4 things cause diabetic retinopathy

A

Macular edema

Hemorrhage from new vessels

Retinal detachment

Neovascular glaucoma

77
Q

Cotton wool spots

Intraretinal hemorrhages

Hard exudates

Microaneurysms

Occluded vessels

Dilated or tortuous vessels

Visual loss through macular edema

What type of diabetic retinopathy?

A

Nonproliferative diabetic retinopathy

78
Q

Neovascularization

Preretinal and vitreous hemorrhage

Fibrosis

Retinal detachment

Visual loss from bleeding, retinal detachment ischemia of macula

What type of diabetic retinopathy?

A

proliferative

79
Q
A

nonproliferative diabetic retinopathy: appearance of fundus

retinal hemorrhages

yellow lipid exudates

dull white cotton wool spots (nerve fiber layer infarcts)

80
Q
A

proliferative diabetic retinopathy showing neovascularization at the disc

81
Q
A

severe traction retinal detachment in proliferative Diabetic retinopathy

elevation & distortion of macula due to overgrowth and contraction of neovascular proliferations

82
Q
A

vitreous hemorrhage: appearance on fundus

arising from neovascularization

83
Q

clinical px of diabetic retinopathy

A

asx untul late stages

84
Q

diabetic retinopathy screening

A

Dilated and comprehensive eye exam

At the time of diagnosis in type 2

Within 5 years in type 1

Repeat annually

85
Q

diabetic retinopathy tx

A

Laser photocoagulation

Intravitreous injections of anti-vascular endothelial growth factor (ranibizumab)

86
Q

leading cause of ESRD

A

diabetic kidney dz

87
Q

diabetic kidney dz screening

A

Assess urinary albumin

Spot urinary albumin-to-creatinine ratio

  • Assess eGFR
  • At time of diagnosis in type 2
  • Within 5 years of diagnosis in type 1
  • In all patients with comorbid HTN
  • Repeat annually
88
Q

dx criteria for diabetic kidney dz

A
  • Moderately increased albuminuria (“microalbuminuria”)
  • 30-300 mg/day (normal < 30 mg/day)
  • > 300 mg/day = severely increased albuminuria (“macroalbuminuria”)
  • Requires 2 of 3 specimens abnormal over 3-6 months
89
Q

diabetic kidney dz tx

A

Consider SGLT2 inhibitor or GLP1 receptor agonist

ACE-I or ARB: if modest UACR elevation (30-299 mg/g Cr) & Strongly recommended for UACR ≥ 300 mg/g Cr and/or eGFR < 60

Protein intake: Nondialysis-dependent: 0.8 g/kg/d & Dialysis-dependent: > 0.8

•Refer for renal replacement treatment if eGFR < 30

90
Q

what is common in diabetic neuropathy?

A

foot ulcers & amputation

91
Q

diabetic neuropathy screening

A
  • Assess with history and either temperature or pinprick sensation and vibration sensation
  • Annual monofilament testing
  • At time of diagnosis for type 2
  • Within 5 years of diagnosis for type 1
  • Repeat annually
92
Q

diabetic neuropathy tx

A
  • First line Rx for neuropathic pain:pregabalin, duloxetine, or gabapentin
  • Foot self care education to all patients
  • Specialized therapeutic footwear for high-risk patients with severe neuropathy, foot deformities or history of amputation
93
Q

what does the annual comprehensive foot evaluation consist of

A

Skin inspection

Assess for foot deformities

Neurologic assessment (monofilament + pinprick or temperature or vibration)

Vascular assessment

94
Q

consider ABI/vascular referral for which sxs?

A

claudication or decreased or absent pedal pulses

95
Q

consider podiatry for which pts?

A

smokers or

hx of prior LE complications

loss of protective sensation

structural abnormalities

PAD

96
Q

goal BP for diabetics

A

High CV risk = < 130/80

Lower risk = < 140/90

97
Q

at what BP do you implement lifestyle interventions?

A

BP > 120/80

98
Q

at what BP do you implement dual therapy?

A

≥ 160/100

99
Q

Meds with demonstrated reduction of CV events

A

ACE-I

ARB

Thiazide diuretic

Dihydropyridine CCB

100
Q

ASCVD or 10-yr risk > 20%

OR

Multiple ASCVD risk factors

what tx?

A

high intensity statin therapy

101
Q

< 40 y/o with ASCVD risk factors

OR

40-75 and > 75 without ASCVD risk factors

what tx?

A

moderate intensity statin

102
Q

ASCVD and LDL ≥ 70 and on maximally tolerated statin

what tx?

A

additional LDL-lowering therapy (ezetimibe or PCSK9 inhibitor)

103
Q

Secondary prevention in patients with ASCVD

what tx?

A

aspirin 75-162 mg/d

104
Q

One year post ACS

what tx?

A

dual antiplatelet therapy with low dose aspirin and P2Y12 inhibitor

105
Q

Primary prevention with what if inc CV risk?

A

aspirin

106
Q
A