Type 2 Diabetes Mellitus Flashcards Preview

Foundations III- Endocrine > Type 2 Diabetes Mellitus > Flashcards

Flashcards in Type 2 Diabetes Mellitus Deck (101)
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1
Q

How many diabetes cases are type 2?

A

> 90%

2
Q

Characteristics of DM type 2?

A

Characterized by hyperglycemia and varying degrees of insulin deficiency and resistance

Micro- and macrovascular complications

3
Q

What is impaired glucose tolerance?

A

during an OGTT, blood glucose values are between normal and overt diabetes (140-199 mg/dL)

4
Q

What glucose level is considered impaired fasting glucose?

A

fasting BS 100-125

5
Q

What is pre diabetes?

A

increased risk for DM

IGT or IFG or A1c of 5.7-6-4%

6
Q

% of ppl who have DM but are not diagnosed?

A

25-40%

7
Q

Risk factors for DM?

A

Genetic

Anthropometric factors (BMI, waist circumference)

Environmental/lifestyle factors

  • physical inactivity
  • smoking
  • diet
  • meds
8
Q

What drugs can impair glucose tolerance?

A

LOTS

Fluroquinolones

Thiazide diuretics *

glucocorticoids

oral contraceptives

9
Q

What comorbidities put pts at increased risk for development of DM?

A

Prediabetes

Gestational diabetes

CV disease (HF, MI, HTN)

Dyslipidemia

Hyperuricemia

PCOS

Metabolic syndrome

10
Q

Metabolic syndrome is also known as…

A

Insulin resistance syndrome or syndrome X

11
Q

Definition of metabolic syndrome?

A

Abdominal obesity
Measured by waist circumference
(≥ 102 cm (40 inches) in men
≥ 88 cm (35 inches) in women)

Triglycerides ≥ 150

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

Blood pressure ≥ 130/85 mmHg

FPG ≥ 100 mg/dL

12
Q

Metabolic syndrome increases with…

A

age

also higher prevalence with overweight/obese

13
Q

How common is metabolic syndrome?

A

22% in US

14
Q

Management goals for metabolic syndrome?

A

Treat underlying causes

Treat CVD risk factors

15
Q

What should be included in tx of metabolic syndrome?

A

aggressive lifestyle modification

weight reduction

increases physical activity

reduction of other risk factors

pharm options

16
Q

Weight loss goal for pts with metabolic syndrome?

A

Goal of 7-10% reduction in body weight within 1 year

17
Q

How much physical activity should you recommend for a patient with metabolic syndrome?

A

150 min/wk

18
Q

Where do we get blood glucose from?

A

diet

gluconeogenesis

glucogeneolysis of liver glycogen

19
Q

How is glucose regulated?

A

Glucose homeostasis requires hepatic glucose production to be balanced with peripheral glucose uptake and utilization

Insulin produced by beta cells –> causes glucose transport into adipose tissue and muscle

Glucagon produced by alpha cells –> stimulates glycogenolysis and gluconeogenesis

20
Q

What regulates insulin secretion?

A

glucose

also influenced by amino acids, ketones, various nutrients, GI peptides, & neurotransmitters

21
Q

Insulin/glucagon levels during fasting state?

during postprandial state?

A

low insulin, high glucagon

high insulin, low glucagon

22
Q

How does the body compensate when there is insulin resistance? What does this eventually lead to?

A

beta cells compensate by increasing insulin

–> impaired glucose tolerance (beta cells can’t keep up)

–> overt diabetes (fasting hyperglycemia, beta cell failure)

23
Q

Describe insulin resistance

A

decreased ability of insulin to act effectively on target tissues

impairs glucose utilization by insulin sensitive tissues

24
Q

Describe impaired insulin secretion

A

in response to insulin resistance insulin secretion is initially increased >

beta cell failure >

chronic hyperglycemia impairs islet func., >

reduced insulin secretion

25
Q

Why is there excessive hepatic glucose production in DM?

A

insulin resistance in the liver results in failure of hyperinsulinemia to suppress gluconeogenesis

26
Q

Why is there abn. fat metabolism in DM?

A

Insulin resistance in adipose tissue > increased liplysis and free fatty acid flux from adipocytes causing increased VLDL & TG synthesis in liver

lipid storage in liver > NAFLD and dyslipidemia

27
Q

Clinical presentation of DM?

A

Usually asymptomatic

Hyperglycemia on routine labs

Symptoms of hyperglycemia:

  • Polyuria
  • Polydipsia
  • Nocturia
  • Blurred vision
  • Weight loss
28
Q

ADA screening recommendation for DM?

A

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

Start at age 45 if no risk factors

Screen patients with prediabetes annually

Women with GDM should be screened q 3 years

29
Q

USPSTF screening recommendations for DM?

A

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

30
Q

Diagnostic criteria for DM?

A

sxs + random blood glucose > 200

If asxs

  • FPG >126
  • 2 hour glucose >200 during OGTT
  • A1C >6.5

repeat on different day

31
Q

Normal 2 hour glucose during OGTT? normal FPG?

A

<140mg/dL

<100

32
Q

IFG?

IGT?

A

100-125 mg/dl

2 hr glucose during OGTT between 140-199

33
Q

Glucated hemoglobin (A1c) correlates with?

what can effect this?

A

mean glucose concentration and DM complication

RBC turnover
-low cell turnover: false high
-high cell turnover: false low
Hemoglobinopathy, CKD

34
Q

What should you eval for in a DM pt?

A

Assess nutrition, weight, physical activity

Assess CV risk

Evaluate for diabetes related comps

Inquire about hypoglycemic episodes

35
Q

What labs should you check regularly in a DM pt?

A

A1c

Fasting lipids

Liver enyzmes

Urine albumin excretion

Serum creatinine

36
Q

What should be included in annual DM visit?

A

vitals

orthostatic BP

fundoscopic exam

thyroid palpation

skin exam

comprehensive foot exam

37
Q

What labs should you check annually in pt with DM?

A

A1c

lipid panel

LFTs

urine albumin-Cr ratio

TSH (type 1 DM)

+/- Vit B12

Serum K in pt on ACE/ARB or diuretics

38
Q

What is included in management of DM?

A

glycemic control: pharm/nonpharm

monitoring/prevent comps

Pt education

health maintenance

39
Q

What kind of pt education should you give to DM pt?

A

nutrition

hypoglucemia

CV risk

vision

kidneys

40
Q

Target A1c for DM?

A

individualized based on pt

most: <7.0%

more stringent

less stringent: hx severe hypoglycemia, limit life expectancy, older pts, comorbid conditions

41
Q

How freq. should you monitor A1c?

A

at least 2x/yr in controlled, quarterly in pts with changes in therapy or not meeting goals

42
Q

What else should be included in management for DM type 2?

A

self monitor blood glucose, more often when titrating medications assoc. with hypoglycemia

several times per wk

more freq. with illness/change in diet/exercise

43
Q

Nonpharm therapy for DM type 2?

A

diet

exercise

weight reduction

psychological interventions

diabetes education

44
Q

goals of pharm therapy for DM type 2?

A

Increase insulin availability

Improve sensitivity to insulin

Delay delivery and absorption of carbohydrates from the GI tract

Increase urinary glucose excretion

45
Q

A1c of …..at rx you should start Rx.

A1c of ….at dx, you can start with 3-6 months of lifestyle modifications

A

> 7.5-8%

<7.5

46
Q

Initial pharm therapy for DM type 2?

A

Metformin for most pts

Insulin is an alternative

47
Q

What are the classes of drugs that can be used for tx of DM type 2?

A

Metformin

Sulfonylureas

GLP-1 receptor agonist
Dipeptidyl peptidase-4 inhibitors (DPP-4)

Sodium-glucose co-transporter 2 (SGLT2) inhibitor

Thiazolidinediones (TZD)

Meglitinides

Alpha-glucosidase inhibitor

Insulin

48
Q

Drug class for Metformin? MOA?

A

Biguanide

Decrease hepatic glucose output by inhibiting gluconeogenesis

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

49
Q

1st line drug tx for DM?

A

METFORMIN

1-2% drop in A1c

weight neutral

50
Q

ADE of Metformin?

A

GI sxs

can reduce intestinal absorption of vit B12

51
Q

Contraindications for Metformin?

A

renal insufficiency

IV contrast concerns

52
Q

MOA of sulfonylureas? effect?

A

Stimulate insulin secretion from pancreatic beta cells

1-2% decrease in A1c

53
Q

ADEs of sulfonylureas?

A

risk of hypoglycemia

weight gain

54
Q

Examples of Sulfonylureas?

A

Glipizide (Glucotrol)

Glyburide (Diabeta, Glynase)

Glimepiride (Amaryl)

55
Q

MOA of GLP- 1 agonists?

A

GLP-1 stimulates glucose dependent insulin release from pancreatic islet cells

GLP-1 slows gastric emptying

GLP-1 inhibits post-meal glucagon release

56
Q

Incretin effect of GLP-1 agonists?

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

57
Q

How is GLP-1 agonist typically prescribed?

A

as an add on therapy (to Metformin)

0.5-1% drop in A1c

weight loss

58
Q

ADEs of GlP-1 agonists?

A

Possible improved cardiovascular outcomes with liraglutide and semaglutide

GI side effects: N/V/D (10-50%)

59
Q

Examples of GLP-1 agonists?

A

Exenatide (Bydureon, Byetta)

Liraglutide (Victoza)

Dulaglutide (Trulicity) etc.

60
Q

MOA of DPP-4 inhibitors ?

A

GLP-1 secreted in response to nutrients >

GLP-1 stimulates glucose dependent insulin release from pancreatic islet cells

GLP-1 slows gastric emptying

GLP-1 inhibits post-meal glucagon release

DPP-4 is an enzyme that deactivates GLP-1

61
Q

How is DPP-4 inhibitors usually prescribed? effect on weight?

A

usually add on therapy

0.5-.8 drop in A1c

weight neutral

62
Q

Examples of DPP-4 inhibitors?

A

Sitagliptan (Januvia)

Saxagliptin (Onglyza)

Linagliptin (Tradjenta)

Alogliptin (Nesina)

63
Q

MOA of SGLT2 inhibitor? effect on A1c?

A

SGLT2 inhibitors increase urinary glucose excretion leading to reduced blood glucose

0.5-0.7% decrease in A1c

usually add on therapy, Weight loss, reduced BP, possible reduced CV mortality

64
Q

ADEs of SGLT2 inhibitors?

A

vulvovaginal candidiasis, UTIs

65
Q

Examples of SGLT2 inhibitors?

A

Empagliflozin (Jardiance)
Canagliflozin (Invokana)
Dapagliflozin (Farxiga)

66
Q

MOA of TZDs?

A

Improve insulin action
Increase insulin

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

67
Q

effect of TZDs?

A

usually used as add on therapy

0.5-1.4% drop in A1c

68
Q

ADEs of TZDs?

A

Fluid retention, HF, weight gain, bone fractures, possible increase in MI (rosiglitazone), possible increase in bladder cancer (pioglitazone)

69
Q

Contraindications for TZDs?

A

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

70
Q

Examples of TZDs?

A

Pioglitazone (Actos)*preferred

Rosiglitazone (Avandia)

71
Q

MOA of Meglitinides? effect?

A

Stimulate insulin secretion from pancreatic beta cells

Add on therapy

0.5-1% decrease in A1c

72
Q

Admin of Meglitinides?

A

take with meals to reduce postprandial hyperglycemia

73
Q

ADEs of Meglitinides?

A

hypoglycemia

weight gain

74
Q

Examples of Meglitinides?

A

Nateglinide (Starlix)

Repaglinide (Prandin)

75
Q

MOA of alpha glucosidase Inhibitors?

A

decrease absorption of glucose

0.5-.8 % decrease

weight neutral

give with food

76
Q

ADEs of Alpha glucosidase inhibitors?

A

flatulence and diarrhea

77
Q

Examples of alpha glucosidase inhibitors?

A

Acarbose (Precose)

Miglitol (Glyset)

78
Q

Options for insulin therapy?

A

Basal therapy: NPH, Glargine, Detemir, Degludec

Intensive insulin therapy

79
Q

ADEs of insulin?

A

weight gain

hypoglycemia

80
Q

Examples of Prandial insulin?

A

Short-acting: Regular (Humilin R, Novolin R)

Rapid-acting: lispro (Admelog, Humalog), aspart (Fiasp, Novolog), glulisine (Apidra)

81
Q

When should you considered dual therapy for T2DM?

When should you considered combo injectable therapy?

A

if A1c grater than or equal to 9%?

A1c greater than or equal to 10%, blood glucose >300 or pt very sxs

82
Q

What are some microvascular diseases that may be complications of T2DM?

what about macrovascular diseases?

A

Retinopathy
Nephropathy
Neuropathy

Atherosclerosis (MI, CVA)

-these may be present at dx

83
Q

MCC of blindness in adults 20-74 yo?

A

diabetic retinopathy

Chronic hyperglycemia causes vascular changes leading to retinal injury and ischemia

84
Q

Why is there vision loss in diabetic retinopathy?

A

Macular edema

Hemorrhage from new vessels

Retinal detachment

Neovascular glaucoma

85
Q

Presentation of diabetic retinopathy?

A

asxs until late stages

86
Q

Screening for diabetic retinopathy?

A

dilated and comprehensive eye exam by ophtho or optometrist

at time of dx in type 2, within 5 yrs of type 1

repeat annually

87
Q

Treatment for diabetic retinopathy?

A

laser therapy- photocoagulation

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

Vitrectomy

88
Q

How can we prevent diabetic retinopathy?

A

glycemic control

control BP

89
Q

How can we screen for diabetic kidney disease?

A

assess urinary albumin

Assess eGFR

time of diagnosis in T2DM

Within 5 years of diagnosis in T1DM

In all patients with comorbid HTN
Repeat annually

90
Q

Dx for diabetic kidney disease?

A

mod increased albuminuria (mircoalbuminuria)

  • 30-300/day
  • > 300 = severe

requires 2 of 3 specimens abn. over 3-6 months

91
Q

Tx for diabetic kidney disease?

A

ACE/ARB

Protein Intake

  • Non dialysis: 0.8
  • dialysis: higher levels

refere for renal replacement tx

92
Q

How can we prevent diabetic kidney disease?

A

optimize glucose control

optimize BP control

93
Q

Presentation of diabetic neuropathy?

A

up to 50% asxs

foot ulcers and amputation common

dx of exclusion

94
Q

other risk factors for ulcers/amputations?

A

smoking

foot deformities

pre-ulcerative callus/corn

PAD

visual impairment

DKD

95
Q

Screening for diabetic neuropathy?

A

Assess with hx + temp/pinprick sensation/vibration sensation

annual monofilament testing

At time of dx of T2DM, within 5 yrs for T1DM

repeat annually

96
Q

How can we prevent diabetic neuropathy?

A

optimize glucose control

97
Q

Tx for diabetic neuropathy?

A

1st line: Pregabalin or Duloxetine

foot self care education

specialized footwear for high risk pts

98
Q

Foot care for diabetic neuropathy?

A

comprehensive foot eval annually

Consider ABI and/or vascular referral for symptoms of claudication or decreased or absent pedal pulses

Consider podiatry for smokers or hx of prior LE complications, loss of protective sensation, structural abnormalities, or PAD

99
Q

If a pt with DM and HTN has albuminuria, which kind of antihypertensive should they be placed on?

A

ACE or ARB

100
Q

Anti platelet recommendations for T2DM pts?

A

ASA as secondary prevention

Clopidogrel if ASA allergy

101
Q

Routine health maintenance in pts with T2DM?

A

flu vaccine annually

Pneumococcal vaccination

HBV to unvaccinated adults age 19-59

Update tetanus and diphtheria

Reproductive counseling

Indicated screenings