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NUTR 441 > Diabetes > Flashcards

Diabetes Flashcards

1
Q

what are central themes to diabetes management?

A

interdisciplinary team where person w/ diabetes is central to team, education focused on self management

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2
Q

definition of diabetes:

A

metabolic disorder characterized by presence of hyperglycemia due to defective insulin secretion and/or defective insulin action

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3
Q

long term complications of diabetes?

A

kidney, eye, nerves, heart, blood vessels

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4
Q

prevalence vs. incidence

A

existing vs. new cases

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5
Q

why increase in type 2?

A

excess food, obesity, sedentary, aging, indigenous, new immigrants with predisposition

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6
Q

primarily a result of pancreatic beta cell destruction and prone to ketoacidosis

A

type 1

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7
Q

ranges from predominant insulin resistance with relative insulin deficiency to a predominant secretory defect with insulin resistance

A

type 2

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8
Q

glucose intolerance with onset or first recognition during pregnancy

A

gestational diabetes mellitus

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9
Q

uncommon forms of diabetes:

A

pancreatitis, removal of pancreas, cystic fibrosis, excess glucocorticoids (acts opposite of insulin)

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10
Q

pathogenesis of type 1

A

autoimmune destruction of insulin producing beta cells in pancreas by CD4 and CD8 T cells and macrophages infiltrating the islets

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11
Q

insulin resistance caused by:

A

diminished tissue response to insulin(impaired signaling cuz postreceptor defects)

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12
Q

insulin secretion is a ____ defect

A

metabolic

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13
Q

what are primary effects of insulin on blood glucose?

A

act on liver release, act on muscles for uptake

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14
Q

fasting hyperglycemia caused by:

A

abnormally high hepatic gluc output due to hepatic resistance to insulin action

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15
Q

post prandial hyperglycemia caused by:

A

abnormal insulin secretion by beta cells in response to meal, too much liver production of glucose, defective gluc uptake by peripheral insulin-sensitive tissues (muscle)

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16
Q

how does chronic hyperglycemia exacerbate the situation?

A

decrease insulin secretion by beta cells, decrease tissue sensitivity to insulin

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17
Q

why is obesity major effect in causing insulin resistance?

A

hormones, cytokines, metabolic fuels (non esterified FFA) originate in adipocyte mass and interfere with insulin signaling (how it binds to receptor and initiates metabolic pathway)

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18
Q

factors that affect insulin production and release

A

increased blood glucose, increased blood amino acids, activation of autonomic nervous system (decreases insulin)

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19
Q

2 primary actions of insulin to lower BG:

A

^ transport and utilization of gluc to peripheral tissues, decrease gluconeogenesis and glycogen breakdown in liver

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20
Q

ketone body examples:

A

betahydroxybutyric acid, acetone, acetoacetic acid

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21
Q

type 1 DM symptoms:

A

hyperglycemia, glucosuria, polyuria, polydipsia, polyphagia

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22
Q

why type 2 less likely ketosis?

A

because adipose tissue is highest priority for sensitivity to insulin, meaning less lipolysis and fat oxidation

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23
Q

how to do OGTT

A

fasting plasma gluc, then glucose drink of 75g for adults (1.75 g/kg for kids), take plasma gluc measurements at intervals (120 minute important for diagnosis along with FPG)

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24
Q

diabetic post prandial features:

A

1) fasting value is high 2) peak is high 3) long time to normalize

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25
Q

how to diagnose diabetes?

A

FPG > 7 mmol/L or A1C > 6.5% or 2 h PG > 11.1 or random PG > 11.1–>must have 2nd repeat confirmatory lab test (preferably same except with RPG in asymptomatic person)

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26
Q

how to diagnose type one without needing confirm:

A

random PG > 11.1 and symptoms of diabetes

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27
Q

what are the 2 subsets of prediabetes?

A

impaired fasting glucose (FPG), impaired glucose tolerance (2 hr value on OGTT)

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28
Q

A1C of ____% considered prediabetes

A

6-6.4

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29
Q

what is normal FPG and 2 hr OGTT?

A

4-6; 5-7.7

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30
Q

goals of treatment for DM?

A

relieve symptoms, improve metabolism of glucose, prevent long term complications, assure adequate nutr status

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31
Q

venous blood vs. capillary blood

A

clinic vs. home monitoring

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32
Q

how long does it take for RBC to turn over?

A

4 months

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33
Q

when use ketone testing?

A

ill or BG high

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34
Q

glycemic targets individualized based on:

A

age, duration of diabetes, risk of severe hypoglycemia, frailty/function dependence and life expectency

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35
Q

what are the a1c targets <6.5 for?

A

<6.5 for adults with type 2 to reduce risk of retinopathy and CKD if at low risk of hypoglycemia

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36
Q

most adults with type 1/2 diabetes will have this A1c target:

A

<7

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37
Q

a1c target is higher for people who are:

A

functionally dependent, recurrent unawareness, limited life expectancy, frail elderly, dementia

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38
Q

to achieve a1c <7, preprandial PG should be ___ and 2 hour postprandial should be ____

A

4-7; 5-10

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39
Q

if a1c <7 not achieved despite targets, preprandial should be ____ and postprandial should be _____

A

4-5.5; 5-8

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40
Q

first line med

A

metformin

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41
Q

this class of drug enhances insulin sensitivity in liver and peripheral tissues (ie. improved response to insulin and reduced liver production of glucose)

A

biguanide (metformin in here)

42
Q

this class of drugs increases gluc dependent insulin release, slows gastric emptying

A

incretins (DPP-4 inhibitors, GLP-1 receptor agonists)

43
Q

this class of drugs prevents gluc reabsorption by kidney (enhances urinary gluc excretion)

A

SGLT-2 Inhibitors

44
Q

this class of drugs inhibits CHO absorption

A

alpha-glucosidase inhibitor (GI probs)

45
Q

this class of drugs stimulate endogenous insulin secretion

A

insulin secretagogues

46
Q

this class of drugs enhances insulin sensitivity in peripheral tissues and liver

A

thiazolidinedione

47
Q

these increase risk for hypoglycemia:

A

insulin, insulin secretagogues (meglitinide, sulfonylurea)

48
Q

subcutaneous injection by these 3 methods:

A

syringe, pen, insulin pump

49
Q

all types of insulin are human (recombinant) insulin either by being:

A

structurally similar to human insulin or structurally modified from human insulin (analogues)

50
Q

long or intermediate acting insulin that provides control of blood glucose in fasting state or between meals

A

basal insulin

51
Q

rapid/short acting insulin that controls the rise in blood glucose at meals and to correct hyperglycemia

A

bolus insulin

52
Q

when is insulin taken?

A

15-30min before meal, except 5 min with rapid acting and right at the start of the meal for the faster acting insulin aspart

53
Q

how does insulin pump therapy work?

A

uses rapid-acting insulin infused at a constant + a bolus of insulin that is adjusted prior to each meal based on BG and how much CHO they want to have that meal

54
Q

why is body composition factored in to figuring out how much insulin?

A

more adiposity need more insulin cuz more insulin resistance

55
Q

factors influencing amount of insulin administered

A

diet specific CHO, physical activity, constant blood glucose concentration monitoring, body comp, age and growth, other treatments, wt loss, own insulin production (type 2)

56
Q

times most likely have trouble with insulin?

A

as asleep, right before dinner

57
Q

examples of rapid acting:

A

humalog, novorapid, apidra

58
Q

onset, peak and duration of rapid acting?

A

10-15min; 60-90min; 3-5 hr

59
Q

onset, peak and duration of short acting?

A

30 min; 2-3hr; 6.5 hr

60
Q

onset, peak, duration of intermediate acting?

A

1-3hr; 5-8hr; up to 18hr

61
Q

onset, peak, and duration of long acting (levemir)?

A

1.5hr; none; 16-24 hr

62
Q

duration of basaglar/lantus (long acting)

A

24 hr+

63
Q

goals of nutr management:

A

1) maintain/improve quality of life and nutr health, 2) prevent and treat acute and long term complications and comorbidities

64
Q

which is more fixed: multiple injections or conventional regimen?

A

conventional regimen

matching vs consistency

65
Q

being consistent with cho and spreading over the day with Type 2 will prevent:

A

large glycemic excursions following meals

66
Q

type 2 often use a ___ or ____system

A

choice; exchange

67
Q

how to estimate energy requirements of new pt?

A

1) equations 2) energy intake (diet hx)

68
Q

% energy that should come from CHO in diabetes?

A

45-60%

69
Q

why is lower CHO diet not recommended usually?

A

ketoacidosis, could have higher protein and sat. fatty acids causing probs

70
Q

scale that ranks CHO rich foods by how much they raise BG compared to standard

A

glycemic index

71
Q

factors determining glycemic index

A

polymeric length, form of carb/starch, protein and fat, how you cook, ingested particle size

72
Q

benefits of replacing high GI with low GI

A

better Hb A1C, better blood lipid profile, reduce CRP (inflammation), reduce hypoglycemia, better post-prandial (less spike)

73
Q

fibre recommendations

A

25 g (women) 38 g (men); 21 and 30 for >51 years; at least 1/3 soluble; up to 30-50g fibre

74
Q

benefits of high fibre?

A

better post prandial BG, blood lipds, A1C, fasting BG, slow gastric emptying rate, reduce rate of absorption of CHO

75
Q

why limit sugar?

A

^ fasting TG, faster and higher spike of BG (only have less than 10% energy from sugar)

76
Q

protein should make up ___% of energy

A

15-20 (increased or maintained in nrg reduced)

77
Q

if have CKD, protein implications?

A

monitor plant sources for potassium, don’t exceed 0.8g/kg

78
Q

mediterranean style diet reduces ___ and improves ___

A

major CV events; glycemic control

79
Q

vegan / vegetarian improves:

A

body weight, glycemic control, blood lipids, reduce MI risk

80
Q

DASH improves:

A

glycemic control, LDL, reduce CV events

81
Q

diet pulses improve:

A

glycemic control, BW, systolic BP

82
Q

diet with fruit and veg improve:

A

glycemic control, reduce CV mortality

83
Q

diet with nuts improves:

A

glycemic control

84
Q

sweeteners that don’t increase blood sugar:

A

sugar alcohols, acesulfame potassium, aspartame, cyclamate, saccharin, sucralose (splenda), steviol glycosides (stevia)

85
Q

prob with sugar alcohols?

A

gas and bloating

86
Q

risks with alcohol?

A

mixed drinks, impair hepatic gluc release (^ hypoglycemia risk), when separated from meals, excess impairs judgement to take insulin properly and eat CHO, weight gain , increase blood pressure and TG, damage liver, inflame pancras, dehydrate, worsen eye disease

87
Q

___ doesn’t work when alcohol is in the body

A

glucagon

88
Q

why exercise beneficial?

A

^ insulin sensitivity, improves gluc tolerance, improves serum lipids, decreases risk for Cvd, assists wt loss

89
Q

CHO choice/exchange system best for:

A

client with diabetes not on insulin

90
Q

goal of beyond the basics:

A

allow pt maintain consistent diet pattern but also provide max variety in food choices

91
Q

2/3 of ppl in type 1 diabetes experience:

A

honeymoon period (short period of remission where some insulin produced in body)

92
Q

why need more insulin when ill?

A

secretion of counterregulatory hormones, pt sometimes believe can stop taking insulin cuz don’t feel like eating

93
Q

why sometimes insulin requirements decrease when ill?

A

vomiting, diarrhea, slow the absorption of food and drive down BG levels

94
Q

general guideline for illness

A

replace cho in mealplan with tolerable items, don’t be concerned about protein/fat comps, redistribute cho from meals and snacks to more frequent

95
Q

signs and symptoms of hypoglycemia due to:

A

epinephrine secreted in response to low BG (neurogenic); insufficient glucose for brain metabolism (neuroglycopenic)

96
Q

aim of pt education for hypoglycemia:

A

prevent, recognize early and treat promptly

97
Q

why not overtreat?

A

rebound hyperglycemia (somogyi effect), weight gain

98
Q

why somogyi effect?

A

epinephrine, glycogenolysis, gluconeogenesis

99
Q

complications of diabetes:

A

CHD, peripheral vascular disease, nephropathy, retinopathy, neuropathy

100
Q

cause of poor healing, occlusion of BVs and decrease circulation to periphery (feet and legs)

A

peripheral vascular disease

101
Q

neuropathy in pns:

A

pain, weakness, loss of peripheral sensations

102
Q

neuropathy in autonomic nervous system:

A

gastroparesis (delayed gastric emptying), abnormal eye control

NUTR 441 (14 decks)

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