Diabetes Path Flashcards

1
Q

diabetes is the ________ leading cause of death

A

seventh

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2
Q

prevalence of diabetes in ethnicity

A

most to least

  • American Indian/Alaska Native
  • black
  • Hispanic
  • white
  • Asian
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3
Q

risk factors for type 1

A

genetic predisposition or autoimmune trigger

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4
Q

risk factors for type 2

A

family history, overweight/obesity, sedentary lifestyle, race/ethnicity, American, previous pre-diabetes, gestational diabetes or baby <9lbs, hypertension, decreased HDL, increased TG, PCOS, vascular disease

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5
Q

parts of proinsulin

A

A chain, B chain, C-peptide

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6
Q

what creates active insulin

A

C-peptide cleavage

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7
Q

C-peptide and insulin are

A

stored and co-secreted from secretory granules

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8
Q

beta cells secrete

A

islet amyloid polypeptide (IAPP) or amylin

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9
Q

amylin

A

further helps insulin release

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10
Q

beta cell - fasting

A

cell membrane remains mostly polarized allowing very little calcium influx, incretin hormone levels are low

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11
Q

fasting insulin

A

small basal amount of insulin is released to maintain euglycemia and glucose supply to muscle, fat, and liver

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12
Q

is there always insulin being released?

A

yes, unless your beta cells don’t work

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13
Q

fasting glucose is at it’s highest or lowest level?

A

lowest

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14
Q

beta cell - fed

A

extracellular glucose concentrations increase; incretin hormone levels/binding increase

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15
Q

food intake causes

A

an increase of glucose concentration

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16
Q

glucose is transported into the beta cell by

A

GLUT2 - which is not insulin dependent

17
Q

glucose under goes glycolysis which yields

A

pyruvate - pyruvate enters the mitochondria yielding ATP

18
Q

increase in ATP causes

A

closure of ATP-dependent K+ channels

19
Q

K+ channel closure causes

A

depolarization of the cell

20
Q

Depolarization allows for

A

opening of calcium channels and calcium influx occurs

21
Q

increase intracellular calcium causes

A

migration of insulin secretory granules to the cell membrane and release of insulin

22
Q

after insulin is secreted, how much is destroyed by the liver?

A

half

23
Q

what happens to the remaining insulin

A

enters circulation and is able to bind to the receptor

24
Q

insulin binding to receptor causes a cascade of reactions

A

1) expression of GLUT4 transporters
2) GLUT4 is expressed on the surface of the cell in response to insulin binding to its receptor
3) this causes the cell to take up glucose

25
Q

fasting glucose homeostasis

A

decrease insulin which increases glucagon which increases glucose production which decreases uptake by fat/muscle and increases lipolysis

26
Q

fed glucose homeostasis

A

increases insulin which decreases glucagon which decreases glucose production which increases uptake by fat/muscle and increases lipolysis

27
Q

in glucose homeostasis there is a balance between

A

hepatic production and peripheral uptake/utilization

28
Q

overall fasting glucose homeostasis

A

undergo gluconeogenesis in the liver, undergo lipolysis to help generate more glucose

29
Q

overall fed glucose homeostasis

A

decrease glucagon as insulin goes up, stops stimulating liver to produce insulin, and increase uptake of fat

30
Q

Type 1 DM has

A

islet cell antibodies and activated lymphocytes in islets/lymph/circ

31
Q

T cells proliferate when

A

exposed to islet protein (presence of cytokines in protein)

32
Q

autoimmune targets

A

insulin, glutamic acid decarboxylase, Tyr phosphate, phogrin

33
Q

stages of type 2

A

normal, insulin resistance (hyperinsulinemia), impaired glucose tolerance (postprandial), type 2 diabetes mellitus (fasting)

34
Q

role of genetics in type 2

A

increased risk if present in single parent, genetic risk is polygenic, environment clouds the picture

35
Q

genetic predisposition of type 2

A

insulin signaling and obesity/fat distribution

36
Q

beta cell dysfunction precedes hyperglycemia by

A

10+ years

37
Q

primary cause of beta cell dysfunction is

A

poor metabolic environment

38
Q

glucotoxicity

A

oxidative metabolism of glucose leads to production of reactive oxygen species, which are normally quickly detoxified