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
how to diagnose diabetes?
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)
26
how to diagnose type one without needing confirm:
random PG > 11.1 and symptoms of diabetes
27
what are the 2 subsets of prediabetes?
impaired fasting glucose (FPG), impaired glucose tolerance (2 hr value on OGTT)
28
A1C of ____% considered prediabetes
6-6.4
29
what is normal FPG and 2 hr OGTT?
4-6; 5-7.7
30
goals of treatment for DM?
relieve symptoms, improve metabolism of glucose, prevent long term complications, assure adequate nutr status
31
venous blood vs. capillary blood
clinic vs. home monitoring
32
how long does it take for RBC to turn over?
4 months
33
when use ketone testing?
ill or BG high
34
glycemic targets individualized based on:
age, duration of diabetes, risk of severe hypoglycemia, frailty/function dependence and life expectency
35
what are the a1c targets <6.5 for?
<6.5 for adults with type 2 to reduce risk of retinopathy and CKD if at low risk of hypoglycemia
36
most adults with type 1/2 diabetes will have this A1c target:
<7
37
a1c target is higher for people who are:
functionally dependent, recurrent unawareness, limited life expectancy, frail elderly, dementia
38
to achieve a1c <7, preprandial PG should be ___ and 2 hour postprandial should be ____
4-7; 5-10
39
if a1c <7 not achieved despite targets, preprandial should be ____ and postprandial should be _____
4-5.5; 5-8
40
first line med
metformin
41
this class of drug enhances insulin sensitivity in liver and peripheral tissues (ie. improved response to insulin and reduced liver production of glucose)
biguanide (metformin in here)
42
this class of drugs increases gluc dependent insulin release, slows gastric emptying
incretins (DPP-4 inhibitors, GLP-1 receptor agonists)
43
this class of drugs prevents gluc reabsorption by kidney (enhances urinary gluc excretion)
SGLT-2 Inhibitors
44
this class of drugs inhibits CHO absorption
alpha-glucosidase inhibitor (GI probs)
45
this class of drugs stimulate endogenous insulin secretion
insulin secretagogues
46
this class of drugs enhances insulin sensitivity in peripheral tissues and liver
thiazolidinedione
47
these increase risk for hypoglycemia:
insulin, insulin secretagogues (meglitinide, sulfonylurea)
48
subcutaneous injection by these 3 methods:
syringe, pen, insulin pump
49
all types of insulin are human (recombinant) insulin either by being:
structurally similar to human insulin or structurally modified from human insulin (analogues)
50
long or intermediate acting insulin that provides control of blood glucose in fasting state or between meals
basal insulin
51
rapid/short acting insulin that controls the rise in blood glucose at meals and to correct hyperglycemia
bolus insulin
52
when is insulin taken?
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
how does insulin pump therapy work?
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
why is body composition factored in to figuring out how much insulin?
more adiposity need more insulin cuz more insulin resistance
55
factors influencing amount of insulin administered
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
times most likely have trouble with insulin?
as asleep, right before dinner
57
examples of rapid acting:
humalog, novorapid, apidra
58
onset, peak and duration of rapid acting?
10-15min; 60-90min; 3-5 hr
59
onset, peak and duration of short acting?
30 min; 2-3hr; 6.5 hr
60
onset, peak, duration of intermediate acting?
1-3hr; 5-8hr; up to 18hr
61
onset, peak, and duration of long acting (levemir)?
1.5hr; none; 16-24 hr
62
duration of basaglar/lantus (long acting)
24 hr+
63
goals of nutr management:
1) maintain/improve quality of life and nutr health, 2) prevent and treat acute and long term complications and comorbidities
64
which is more fixed: multiple injections or conventional regimen?
conventional regimen | matching vs consistency
65
being consistent with cho and spreading over the day with Type 2 will prevent:
large glycemic excursions following meals
66
type 2 often use a ___ or ____system
choice; exchange
67
how to estimate energy requirements of new pt?
1) equations 2) energy intake (diet hx)
68
% energy that should come from CHO in diabetes?
45-60%
69
why is lower CHO diet not recommended usually?
ketoacidosis, could have higher protein and sat. fatty acids causing probs
70
scale that ranks CHO rich foods by how much they raise BG compared to standard
glycemic index
71
factors determining glycemic index
polymeric length, form of carb/starch, protein and fat, how you cook, ingested particle size
72
benefits of replacing high GI with low GI
better Hb A1C, better blood lipid profile, reduce CRP (inflammation), reduce hypoglycemia, better post-prandial (less spike)
73
fibre recommendations
25 g (women) 38 g (men); 21 and 30 for >51 years; at least 1/3 soluble; up to 30-50g fibre
74
benefits of high fibre?
better post prandial BG, blood lipds, A1C, fasting BG, slow gastric emptying rate, reduce rate of absorption of CHO
75
why limit sugar?
^ fasting TG, faster and higher spike of BG (only have less than 10% energy from sugar)
76
protein should make up ___% of energy
15-20 (increased or maintained in nrg reduced)
77
if have CKD, protein implications?
monitor plant sources for potassium, don't exceed 0.8g/kg
78
mediterranean style diet reduces ___ and improves ___
major CV events; glycemic control
79
vegan / vegetarian improves:
body weight, glycemic control, blood lipids, reduce MI risk
80
DASH improves:
glycemic control, LDL, reduce CV events
81
diet pulses improve:
glycemic control, BW, systolic BP
82
diet with fruit and veg improve:
glycemic control, reduce CV mortality
83
diet with nuts improves:
glycemic control
84
sweeteners that don't increase blood sugar:
sugar alcohols, acesulfame potassium, aspartame, cyclamate, saccharin, sucralose (splenda), steviol glycosides (stevia)
85
prob with sugar alcohols?
gas and bloating
86
risks with alcohol?
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
___ doesn't work when alcohol is in the body
glucagon
88
why exercise beneficial?
^ insulin sensitivity, improves gluc tolerance, improves serum lipids, decreases risk for Cvd, assists wt loss
89
CHO choice/exchange system best for:
client with diabetes not on insulin
90
goal of beyond the basics:
allow pt maintain consistent diet pattern but also provide max variety in food choices
91
2/3 of ppl in type 1 diabetes experience:
honeymoon period (short period of remission where some insulin produced in body)
92
why need more insulin when ill?
secretion of counterregulatory hormones, pt sometimes believe can stop taking insulin cuz don't feel like eating
93
why sometimes insulin requirements decrease when ill?
vomiting, diarrhea, slow the absorption of food and drive down BG levels
94
general guideline for illness
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
signs and symptoms of hypoglycemia due to:
epinephrine secreted in response to low BG (neurogenic); insufficient glucose for brain metabolism (neuroglycopenic)
96
aim of pt education for hypoglycemia:
prevent, recognize early and treat promptly
97
why not overtreat?
rebound hyperglycemia (somogyi effect), weight gain
98
why somogyi effect?
epinephrine, glycogenolysis, gluconeogenesis
99
complications of diabetes:
CHD, peripheral vascular disease, nephropathy, retinopathy, neuropathy
100
cause of poor healing, occlusion of BVs and decrease circulation to periphery (feet and legs)
peripheral vascular disease
101
neuropathy in pns:
pain, weakness, loss of peripheral sensations
102
neuropathy in autonomic nervous system:
gastroparesis (delayed gastric emptying), abnormal eye control