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ClinMed exam III > Type 2 DM > Flashcards

Type 2 DM Flashcards

1
Q

Do people with DM2 get DKA

A

no, endogenous insulin is enough to prevent DKA but not enough to prevent hypergylcemia

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2
Q

The most important environmental factor causing insulin resistance

A

obesity

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3
Q

What are the potential sources of DM2

A
  • dysregulation or deficiency on release of insulin by beta cells
  • inadequate or defective insulin receptors
  • production of inactive insulin or insulin that is destroyed before it can carry out its function
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4
Q

What percent of patients with DM2 are obsese

A

80%

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5
Q

DM2 is the leading cause of what in patients

A

end stage renal disease, non traumatic lower extremity amputations, adult blindeness

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6
Q

What do you need to make the diagnosis of DM2

A

ONE of the following

  • FPG >126
  • random blood glucose >200
  • A1c >6.5
  • glucose tolerance test >200
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7
Q

What is considered prediabetes

A

FPG: 100-125
glucose tolerance test: 140-199
-A1c of 5.7-6.4

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8
Q

What does prediabetes increase

A
  • risk of progression to DM2

- risk of cardiovascular disease

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9
Q

Directions to an oral glucose tolerance test

A
  • eat a diet with at least 150g card for three days prior
  • measure fasting glucose
  • drink 75-100mg of glucose
  • glucose is measured at certain time intervals
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10
Q

What is a normal oral glucose tolerance test

A

BG at 1 hour <184

BG at 2 hr <140

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11
Q

Risk factors for DM2

A
  • family hx
  • obesity
  • physical inactivity
  • hx of gestational DM or baby greater than 9 pounds
  • polycystic ovary syndrome
  • prediabetes
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12
Q

When should you screen for DM in normal everyday people

A

> 45 years old, every 3 years after if normal

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13
Q

What individuals should be screened for DM earlier

A
  • obese/sedentary
  • 1st degree relative with DM
  • high risk ethnicity
  • delivered baby >9 pounds
  • hypertensive
  • high cholesterol
  • hx of CVD or prediabetes
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14
Q

What are the high risk ethnic groups for diabetes

A
  • african american
  • latino
  • native american
  • asian
  • pacific islander
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15
Q

How does an individual with DM 2 usually present

A
  • polyuria
  • polydipsia
  • polyphagia
  • may have severe hyperosmolar
  • neuropathic complications
  • cardiovascular complications
  • chronic skin infections
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16
Q

What is acanthosis nigricans? what causes it

A

-dark discoloration of the skin casued by a defect in insulin receptor gene

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17
Q

What does acanthosis nigricans signify

A

extreme insulin resistance

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18
Q

What routine health maintenance should be done for a patient with DM2

A
  • monitor A1c
  • check urine microalbumin
  • podiatry referral
  • ophthalmology referral
  • self monitor of glucose levels
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19
Q

What is associated with improved outcomes from microvascular complications

A

every 1% drop in A1c

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20
Q

Drugs that lower glucose levels by improving insulin action

A
  • metformin (first line)

- TZDs

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21
Q

What drugs stimulate insulin secretion from beta cells

A
  • SUs (alternative first line)

- meglitinides

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22
Q

What drug slow intestinal absorption of glucose

A

alpha-glucosidase inhibitors

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23
Q

What drug mimic incretin effect or prolong incretin action

A

glucagon like peptides

24
Q

Mechanism of metformin

A

reduces hepatic gluconeogenesis and improves insulin sensitivity

25
Q

Contraindications of metformin

A

renal insufficiency, CrCl <30

26
Q

Side effect of metformin

A
  • low hypoglycemia risk

- lactic acidosis (rare)

27
Q

Mechanism of SUs

A

stimulate insulin release, reduce serum glucagon, increase insulin binding

28
Q

What are the 3 SUs

A
  • glyburide
  • glipizide
  • glimepiride
29
Q

What are the relative C/I of SUs

A

hepatic or renal insufficiency

increases hypoglycemia risk

30
Q

What are the side effects of SUs

A
  • weight gain

- hypoglycemia

31
Q

Mechanism of meglitinides

A

increase insulin secretion at beta cells

32
Q

What are the 2 meglitinides

A
  • repaglinide

- nateglinide

33
Q

C/I of meglitinides

A

nateglinide in renal dysfunction

34
Q

Mechanism of alpha-glucosidase inhibitors

A

inhibits alpha- glucosidase enzymes in the gut that digest dietary starch and sucrose, slow absorption of glucose

35
Q

What are the 2 alpha-glucosidase inhibitors

A
  • acarbose

- miglitol

36
Q

Side effects of alpha-glucosidase inhibitors

A

flatulence, diarrhea

37
Q

C/I of alpha-glucosidase inhibitors

A

caution in kidney insufficiency

38
Q

Mechanism of thiazolidinediones

A

sensitize peripheral tissues to insulin

39
Q

What are the 2 thiazolidinediones

A
  • rosiglitazone

- pioglitazone

40
Q

Side effects of thiazolidinediones

A
  • heart failure/edema
  • osteoperosis/fractures
  • bladder cancer
  • weight gain
41
Q

Mechanism of glucagon-like peptide-1 agonists

A

enhance glucose dependent insulin secretion, slow gastric emptying, reduce postprandial glucose

42
Q

What are the glucagon-like peptide-1 agonists

A
  • exenatide

- liraglutide

43
Q

How are GLP-1 receptor agonists administered

A

SQ injection

44
Q

Side effects of GLP-1 receptor agonists

A

nausea, vomiting, injection site reactions

45
Q

What is the black box warning on GLP-1 receptor agonists

A

causes medullary thyroid cancer in mice

46
Q

C/I for GLP-1 receptor agonists

A

personal or family hx of thyroid cancer

47
Q

What are the 4 DPP-4 agents

A
  • sitagliptin
  • saxagliptin
  • linagliptin
  • alogliptin
48
Q

When are DPP-4 inhibitors used as a monotherapy

A

patients that cant take metformin, SUs or TZDs

chronic kidney disease or high risk for hypoglycemia

49
Q

When do you add a second agent on to metformin

A

when A1c is not less than 7 withing three months of initial therapy

50
Q

What happens if A1c goal is not met while on two oral agents

A

add insulin

51
Q

What is HHNK

A

hyperglycemic condition resulting in hypovolemia and electrolyte abnormalities

52
Q

What can precipitate HHNK

A
  • major illness (MI,CVA,sepsis,pancreatitis)
  • drugs that affect carb metabolism (glucocorticoids, thiazides, “atypicals”)
  • compliance issues
53
Q

What is the clinical presentation of a hyperglycemic hyperosmolar state

A
  • polyuria
  • polydipsia
  • weight loss
  • lethargy
  • decreased skin turgor
  • dry mucous membranes
  • tachycardia
  • hypotension
54
Q

Lab abnormalities of HHS

A
  • hyperglycemia
  • hyperosmolality
  • pre renal azotemia
  • low potassium, magnesium and phosphate
55
Q

How do you treat HHS

A
  • IV insulin infusion
  • IV fluid
  • electrolyte monitoring and repletion (potassium, magnesium and phosphate)
56
Q

What are the microvascular complications of DM2

A
  • retinopathy
  • neuropathy
  • nephropathy
57
Q

What are the macrovascular complications of DM2

A
  • PVD, lover extremity ulcers, amputations

- CAD, MI

ClinMed exam III (7 decks)

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