Midterm 2 pt. 2 Flashcards

1
Q

if pancreatic beta cells have decreased sensitivity to incretins,

A

decreased insulin secretion

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2
Q

if pancreatic alpha cells remain sensitive to GIP,

A

increased glucagon secretion

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3
Q

in type II DM, there are

A

altered levels of GLP-1 and GIP and response at tissues

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4
Q

in type II DM, the liver

A

still takes up glucose in high capacity (because it has GLUT2, insulin independent)

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5
Q

in the type II DM, insulin is a _________________

A

relative deficiency (not enough to compensate for high levels of blood glucoss

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6
Q

synonym for pre-diabetes is

A

impaired glucose tolerance

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7
Q

for pre-diabetics, progression of type II DM

A

is NOT inevitable (can be delayed w/ body wt loss)

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8
Q

healthy fasting blood glucose number/range

A

below 100 mg/dL

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9
Q

diabetes fasting blood glucose number/range

A

126 mg/dL

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10
Q

healthy A1C number/range

A

<5.5%

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11
Q

diabetic A1C number/range

A

> 6.5%

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12
Q

healthy result from 2 hr oral glucose

A

below 140 mg/dL

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13
Q

diabetes result from 2 hr oral glucose

A

200 mg/dL

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14
Q

type II DM is associated

A

with obesity, but can also occur in lean people

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15
Q

type 1 DM etiology

A

autoimmune destruction of beta cells

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16
Q

three signs and symptoms of uncontrolled DM

A

polyuria
polydipsia
polyphagia

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17
Q

polyuria is characterized by

A

presence of glucose in urine

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18
Q

polydipsia is characterized by

A

increased thirst

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19
Q

polyphagia is characterized by

A

hunger

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20
Q

signs and symptoms of type I DM

A

wt loss, nausea/vomiting, diabetic ketoacidosis

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21
Q

decreased intracellular glucose results

A

polyphagia

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22
Q

when the threshold of renal glucose is exceeded

A

polyuria, leads to polydipsia

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23
Q

how is fat metabolism affected by insulin deficiency for type I DM

A

decreased TG synthesis, increased lipolysis

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24
Q

in type I diabetes, we use _______________ as an energy source

A

fatty acids, increased risk of ketoacidosis

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25
Q

what is the GLUT4 pathway?

A

PI3K - AKT

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26
Q

long term consequences of insulin deficiency and hyperglycemia

A

macrovascular and microvascular

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27
Q

macrovascular complications include

A

CVD, atherosclerosis, HTN

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28
Q

microvascular complications include

A

nephropathy, retinopathy, neuropathy

29
Q

nephropathy refers to

A

the end stage renal disease

30
Q

retinopathy refers to

31
Q

neuropathy refers to

A

peripheral neuropathy/foot problems

32
Q

HbA1C reflects

A

average blood glucose over the past 3 mo

33
Q

diabetes control and complications trial

A

study of type 1 DM, intensive treatment vs conventional treatment, intensive treatment lowered blood glycemia more, better glucose control = fewer complications

34
Q

10 yrs after the diabetes control and complications trial,

A

there were still decreases in CVD risk

35
Q

A1C treatment goal

A

below 7%, but should be individualized

36
Q

ABCs and of DM management

A

A (average blood glucose/HbA1C)
B (blood pressure)
C (cholesterol)

37
Q

diabetes prevention program

A

compared lifestyle with metformin, lifestyle decreased much more

38
Q

nutritional requirements of people with DM are

A

similar to those of a general healthy population

39
Q

no insulin or hypoglycemic meds leads to

A

CHO is spread throughout the day

40
Q

how does diabetes affect protein metabolism

A

increased blood amino acids + muscle wasting

41
Q

what pathway is responsible for bringing GLUT4 to membrane?

42
Q

what are long-term complications of hyperglycemia?

A

macrovascular (CVD, atherosclerosis, HTN) and microvascular (retino-, neuro-, nephropathy)

43
Q

advanced glycosylation end products

A

accumulation of intermediate products of glycolysis

44
Q

glycated hemoglobin is an example of

A

hemoglobin is an example of
an advanced glycosylation end product

45
Q

risk of diabetes concentrations increases with

A

average blood glucose concentrations

46
Q

primary prevention goal in diabetes prevention is to

A

prevent diabetes

47
Q

secondary prevention in diabetes prevention is to

A

prevent complications from diabetes

48
Q

tertiary prevention in diabetes prevention is to

A

prevent death from diabetes

49
Q

for diabetes, is MNT clinically and cost effective?

50
Q

the american diabetes assocation

A

does not have an “ADA” diet, no 1 diet for diabetics

51
Q

basic CHO counting is

A

adding up total CHO regardless of source

52
Q

advanced CHO counting

A

matches insulin to CHO

53
Q

advanced CHO counting uses

A

insulin to CHO ratio (ICR) and corrective factor (CF)

54
Q

advanced CHO counting is useful for

A

patients with an insulin pump or who take multiple shots a day

55
Q

taking oral hypoglycemic meds leads to

A

daily CHO is spread throughout the day, monitor blood sugar closely because some meds cause hypoglycemia

56
Q

when on a fixed/daily dose of insulin,

A

need consistent timing and CHO content of meals

57
Q

kcal for normal wt

A

30 kcal/kg body wt

58
Q

kcal for overwt/obese

A

20-24 kcal/kg body wt

59
Q

CHO kcal

60
Q

protein kcal

61
Q

fat kcal

62
Q

limit CHO at breakfast to

63
Q

what eating pattern has robust evidence for type 1 DM?

A

none, low-carb has preliminary evidence of benefit

64
Q

what eating pattern has robust evidence for type 2 DM?

A

low-carb and mediterranean have highest evidence

65
Q

mediterranean diet vs. low fat in type 2 DM development

A

mediterranean has lower risk

66
Q

what has the most overall evidence for improving glycemia?

67
Q

glycemic index refers to the

A

quantity and rate which different CHO foods influence blood glucose response

68
Q

in individuals with pre-DM, 7-10% wt loss

A

is shown to prevent/delay type 2 DM

69
Q

in individuals with type 2 DM, 5% wt loss

A

achieves clinical benefits