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Endorine > Type 2 Diabetes > Flashcards

Type 2 Diabetes Flashcards

1
Q

What is the modern T2D diagnostic criteria?

A
  • Fasting plasma glucose >=126mg/dl on two separate occasions
  • Random glucose >200mg/dl with classic symptoms
  • 2 hr postprandial glucose >=200mg/dl after consuming 75g carbs (ie oral glucose tolerance test)
  • HbA1c>=6.5
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2
Q

What is HbA1c?

A

Reflects the average plasma glucose level over the past 2-3 mo. Non enzymatic glycosylation of Hb amnio acid residues

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3
Q

What is type 2 diabetes?

A

May range from predominantly insulin resistance with relative insulin deficiency to a predominantly secretory defect with insulin resistance. Result of multiple defects.

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4
Q

What is a major contributor to the dev of insulin resistance?

A

Obesity

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5
Q

When does progression to type 2 diabetes occur?

A

When B cells are no longer able to secrete sufficient insulin to overcome insulin resistance. Before that it is “prediabetes”

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6
Q

What two hormones regulate normal glucose homeostasis?

A

Insulin and glucagon

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7
Q

When is glucagon secreted

A

Fasting state, gluconeo and glycogenolysis–>inc blood glucose levels

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8
Q

What causes hyperglycemia?

A

Insulin resistance at the tissue level causes reduced glucose uptake into fat and muscle. This, in combo with excess glucose output by the liver, causes hyperglycemia

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9
Q

Inherited insulin resistant conditions are…

A

RARE

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10
Q

What environmental factors worsen insulin resistance?

A
  • Smoking
  • Aging
  • Obesity
  • In-activity
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11
Q

What is glucotoxicity

A

Toxic effect of sustained hyperglycemia that causes worsening of insulin resistance in skeletal muscle, liver, and also worsens secretory defects in the pancreas

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12
Q

What do high levels of free fatty acids do

A

Also increase insulin resistance

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13
Q

Why do beta cells fail?

A

More insulin resistance=more demand on beta cells=start to fail because can’t keep up with demand

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14
Q

Visceral fat

A

More associated with insulin sensitivity than ‘pear shape’

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15
Q

Describe the adipocyte dysfunction and ectopic lipid deposition model for insulin resistance

A

Overnutrition can overwhelm adipose ability to store fat and keep it from having toxic effects

XS free FAs travel in portal system and get despised in the liver and skeletal muscle where they interfere with insulin

Can’t store fat safely in adipose tissue..

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16
Q

What is the initial response to insulin resistance?

A

Hyperinsulinemia and islet hypertrophy

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17
Q

What is the long term response to insulin resistance?

A

There is a progressive decrease in pancreatic function, beta cells eventually fail, leading to diabetes

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18
Q

What types of toxicity induce beta cell dysfxn

A

Lipotoxicity and glucotoxicity

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19
Q

What is the sign of beta cell failure?

A

Loss of first phase insulin response (initial burst of insulin normally shuts down hepatic glucose production). This causes postmeal glucose to start rising

-In type II second phase must now deal with cab load and liver glucose that is pouring out

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20
Q

What is pre-diabetes?

A

HbA1c: =5.7%

Fasting glucose: =100mg/dl (impaired fasting glucose)

Oral glucose tolerance test (OGTT): =140mg/dl (impaired glucose tolerance)

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21
Q

What % US adults age 20+ have prediabetes

A

35%

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22
Q

How long do dev type 2?

A

10 yrs

23
Q

How much does prediabetes inc risk for CV events?

A

50%

24
Q

What helps with prediabets?

A

modeset lifestyle modifications can lower to normal levels of glucose

25
Q

What is necessary to dev type 2?

A
  1. Insulin resistance

2. Beta cell failure

26
Q

?What are the secretory defects in T2DM>?

A
  1. Reduced insulin

2. Increased glucagon

27
Q

What does glucagon do?

A

Major contributor to hepatic glucose output

28
Q

What are incretins?

A

Modulators of postprandial glycemia

29
Q

What causes inc insulin secretion? Oral or IV? Why?

A

ORAL due to incretins being released from the intestines in response to food ingestion.

30
Q

What are the incretins we learned?

A

These stimulate insulin secretion in the presence of glucose:

GLP-1: More potent, works on alpha cells, suppressing glucagon–>suppressing hepatic glucose production. Promotes satiety. Increases insulin secretion, slows gastric emptying (attenutes postprandial glycemia)–>levels are dec in type 2, but fxn remains intact

GIP: les spotent

31
Q

What is the incretin effect? How does it affect type 2?

A

Difference in insulin sec when glucose is given intravenously vs orally. This effect is markedly reduced in ppl with type 2

32
Q

?What are the classic symptoms of T2D

A

Polyuria
Polydipsia
Polyphagia
Unexplained wt loss

33
Q

What are the non specific symptoms of T2D?

A 
Fatigue
Blurry vision
Dry mouth
Dry or itchy skin
Poor wound healing
34
Q

What are some complications of T2D?

A

25%: retinopathy
9%: neuropathy
8%: nephropathy

at time of diag

35
Q

List some poss physical exam findings with T2D

A

Obesity, hypertension, skin findings (acanthosis nigricans), fundoscopic changes, changes in feet, genitourinary infections

36
Q

What are some risk factors for T2D?

A

Obesity, race, metabolic factors, lifestyle factors, genetics, hx of gestational diabetes, intrauterine effects, microbiome effects

37
Q

What is the general lifetime risk of dev T2D?

A

7%

38
Q

What BMI recommends screening for T2D?

A

> 25

39
Q

What reduces incidence of microvascular (retinopathy, nephropathy) complications of T2D?

A

Lower HA1c

40
Q

What were the results of lowering glucose late in course of disease?

A

Intensive glucose lowering in the course of disease only wekaly affects outcomes

-Small reduction in CV events, no effect on mortality, large inc in hypoglycemic episodes

41
Q

Explain “metabolic memory”

A

Tells us we need to intervene early to have an effect because microvascular effects persisted even when A1c normalized when treated early

42
Q

When do we do aggressive treatment?

A

-Early intensive treatment
-Older pts: long-standing diabetes in whom complications have already dev, can cause harm
-

43
Q

What is the A1c goal for nonpreg individuals

A

<6.5% if early

44
Q

What is the A1c goal for severe individuals

A

<8%

45
Q

What are the treatment strategies?

A

1st lifestyle mods, then oral, then insulin

46
Q

What drug is recommended for prevention in pts with prediabetes?

A

Metformin

47
Q

What are lifestyle interventions affect on CV outcomes?

A

NONE! No dif in mortality

48
Q

What is an efective surgery for T2D?

A

gastric bypass (weight loss–>lower remission rates

49
Q

Bariatric surgery

A

-Diabetes remission occurs almost immediately after surgery and before weight loss begins
-benefit to surgery in overall mortality
-

50
Q

Describe T2D genetic componetn

A

Has a large genetic component that is highly influenced by environment

51
Q

What causes T2D?

A

Insulin resistance and dysfxn of endocrine pancreas

52
Q

Prediabetes includes:

A

Impaired fasting glucose
Impaired glucose tolerance
Elevated HbA1c

53
Q

List the 4 ways to diagnose T2D

A
  1. FPG>126mg/dl
  2. HbA1c >=6.5%
  3. 2 hours plasma glucose >200mg/dl after 75gm carbs
  4. Random plasma glucose >200 mg/dl with symptoms

Endorine (24 decks)

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