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
Contraindications of metformin
renal insufficiency, CrCl <30
26
Side effect of metformin
- low hypoglycemia risk | - lactic acidosis (rare)
27
Mechanism of SUs
stimulate insulin release, reduce serum glucagon, increase insulin binding
28
What are the 3 SUs
- glyburide - glipizide - glimepiride
29
What are the relative C/I of SUs
hepatic or renal insufficiency | increases hypoglycemia risk
30
What are the side effects of SUs
- weight gain | - hypoglycemia
31
Mechanism of meglitinides
increase insulin secretion at beta cells
32
What are the 2 meglitinides
- repaglinide | - nateglinide
33
C/I of meglitinides
nateglinide in renal dysfunction
34
Mechanism of alpha-glucosidase inhibitors
inhibits alpha- glucosidase enzymes in the gut that digest dietary starch and sucrose, slow absorption of glucose
35
What are the 2 alpha-glucosidase inhibitors
- acarbose | - miglitol
36
Side effects of alpha-glucosidase inhibitors
flatulence, diarrhea
37
C/I of alpha-glucosidase inhibitors
caution in kidney insufficiency
38
Mechanism of thiazolidinediones
sensitize peripheral tissues to insulin
39
What are the 2 thiazolidinediones
- rosiglitazone | - pioglitazone
40
Side effects of thiazolidinediones
- heart failure/edema - osteoperosis/fractures - bladder cancer - weight gain
41
Mechanism of glucagon-like peptide-1 agonists
enhance glucose dependent insulin secretion, slow gastric emptying, reduce postprandial glucose
42
What are the glucagon-like peptide-1 agonists
- exenatide | - liraglutide
43
How are GLP-1 receptor agonists administered
SQ injection
44
Side effects of GLP-1 receptor agonists
nausea, vomiting, injection site reactions
45
What is the black box warning on GLP-1 receptor agonists
causes medullary thyroid cancer in mice
46
C/I for GLP-1 receptor agonists
personal or family hx of thyroid cancer
47
What are the 4 DPP-4 agents
- sitagliptin - saxagliptin - linagliptin - alogliptin
48
When are DPP-4 inhibitors used as a monotherapy
patients that cant take metformin, SUs or TZDs | chronic kidney disease or high risk for hypoglycemia
49
When do you add a second agent on to metformin
when A1c is not less than 7 withing three months of initial therapy
50
What happens if A1c goal is not met while on two oral agents
add insulin
51
What is HHNK
hyperglycemic condition resulting in hypovolemia and electrolyte abnormalities
52
What can precipitate HHNK
- major illness (MI,CVA,sepsis,pancreatitis) - drugs that affect carb metabolism (glucocorticoids, thiazides, "atypicals") - compliance issues
53
What is the clinical presentation of a hyperglycemic hyperosmolar state
- polyuria - polydipsia - weight loss - lethargy - decreased skin turgor - dry mucous membranes - tachycardia - hypotension
54
Lab abnormalities of HHS
- hyperglycemia - hyperosmolality - pre renal azotemia - low potassium, magnesium and phosphate
55
How do you treat HHS
- IV insulin infusion - IV fluid - electrolyte monitoring and repletion (potassium, magnesium and phosphate)
56
What are the microvascular complications of DM2
- retinopathy - neuropathy - nephropathy
57
What are the macrovascular complications of DM2
- PVD, lover extremity ulcers, amputations | - CAD, MI