Diabetes Flashcards

1
Q

What does diabetes show in urine?

A

sugar and high blood sugar

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2
Q

When does diabetes develop

A

when insulin production or use is inadequate

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3
Q

Besides type I and II what are two other types of diabetes?

A

gestational

secondary

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4
Q

What percentage of people in US have diabetes?

A

9.3% or 28.9 million

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5
Q

Symptoms of diabetes

A
  • increased urine
  • increased thirst
  • unexplained weight loss
  • fatigue
  • blurred vision
  • sores that don’t heal
  • increased hunger
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6
Q

What are the three ways you can diagnosis diabetes?

A
  • A1C test (Hemoglobin A1c, HbA1c, glycohemoglobin test)
  • fasting plasma glucose test (FPG)
  • oral glucose tolerance test
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7
Q

What percent would your A1C level be if you had diabetes?

A

6.5 and above

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8
Q

What percent would your A1C level be if you had pre diabetes?

A

5.7 - 6.4

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9
Q

What is a normal A1C?

A

about 5

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10
Q

What would your FPG be in diabetes?

A

126 or above

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11
Q

What would your FPG be in pre diabetes?

A

100 - 125

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12
Q

What would a normal FPG be?

A

99 or below

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13
Q

What would a diabetic oral glucose tolerance test be?

A

200 or above

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14
Q

What would a pre diabetes oral glucose tolerance test be?

A

140 - 199

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15
Q

What would a normal oral glucose tolerance test be?

A

139 or below

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16
Q

Which is more sensitive FPG or oral glucose tolerance test?

A

Oral glucose tolerance test

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17
Q

When is an oral glucose tolerance test given?

A

Fasting 8 - 12h

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18
Q

When is a baseline level drawn for an oral glucose tolerance test?

A

0 hour

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19
Q

Oral glucose tolerance test

A
  • given measured dose of glucose

- blood drawn at various time points

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20
Q

What is the glucose dose based on in US?

A

based on body weight

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21
Q

What type of diabetes is the most common?

A

type II

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22
Q

What percent of people with diabetes have type II?

A

90-95%

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23
Q

When does type II diabetes occur?

A

any age, but mostly older age and obesity

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24
Q

Characteristics of T2D

A
  • hyperglycemia
  • hypertriglyceridemia
  • ketoacidosis NOT common
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25
Insulin levels in T2D
normal or elevated
26
What is T2D often preceded by?
obesity
27
Insulin levels in T2D vs obese with no diabetes
not as high as obese with no diabetes
28
What can cause T2D?
IR | impaired B-cell function
29
Risk factors of T2D
- family history - 45 and older - race - overweight, not active - history of gestational - impaired glucose tolerance (pre diabetes)
30
When does someone with pre diabetes develop T2D?
10 years
31
Gestational diabetes
- during pregnancy | - can cause complications for mother and baby
32
Link between obesity and T2D
- obese are hyperinsulinemic - response to insulin diminished - elevated FFAs --> cause IR - Increase in TNFa, resisting - decrease in adiponectin
33
What is the percentage of those with T2D that are obese?
80%
34
Factors predisposing obese individuals to T2D
- lipid toxicity - adipose inflammation - altered adipokine secretion - genetic factors
35
Insulin and glucose
improves glucose uptake in muscles and adipose tissue
36
Insulin and gluconeogenesis
Suppresses
37
Insulin and glycogen
promotes storage in liver and adipose tissue
38
Insulin and FAs
promotes synthesis in liver and adipose tissue
39
Insulin and fat storage
Improves in adipose
40
Insulin and protein
suppresses breakdown in muscles
41
What drug targets the liver and gluconeogenesis?
biguanides
42
What drug targets the pancreas and stimulate insulin release?
Sulfonylureas
43
What drug targets the gut and improves insulin secretion?
GLP-1R
44
What drug inhibits glucose reabsorption by kidneys?
SGLT2 inhibitors
45
What does adipose tissue release on demand?
FFA
46
What is adipose tissue responsive to?
insulin
47
What does adipose tissue secrete?
- adipokins - cytokines - growth factors
48
Adipose tissue inflammation and T2D target
- inflammatory mediators released from obese AT - chronic low grade inflammation risk factor - TNFa impairs insulin signaling
49
What are some anti-inflammatory drugs used to treat T2D?
- salsalates - PPAR gamma agonists - Interleukin 1 receptor antagonist
50
Strengths of bariatric surgery
- effective in achieving weight loss - reduction in co-morbidities - enhanced survival
51
Weaknesses of bariatric surgery
- preoperative mortality - surgical complications - frequent need for reoperation
52
When does T1D usually appear?
Childhood or in teens
53
Insulin and T1D
secretion is very low
54
T1D and cells
- defective B-cell function due to autoantibodies
55
Characteristics of T1D
- hyperglycemia - hypertriglyceridemia - severe ketoacidosis
56
Hyperglycemia
- inability of tissues to take up glucose | - accelerated hepatic gluconeogenesis
57
Hypertriglyceridemia
- Increased VLDL production - chylomicron accumulation - low LPL activity
58
Ketoacidosis
- Increased AT lipolysis | - accelerated hepatic FA oxidation
59
Management of T1D
- insulin therapy - islet cell transplantation - dietary and lifestyle modification
60
Complications of insulin therapy
- hypoglycemia - insulin allergy - immune insulin resistance - lipodystrophy at injection site
61
Which type of diabetes is insulin deficiency?
T1D
62
Which type of diabetes is insulin resistance?
T2D
63
Long term complications of diabetes
- stroke - heart disease - HTN - vascular disease - foot problems - eye disease - renal disease - neuropathy
64
Biochemical mechanisms of diabetes complications
- advanced glycation end products - sorbitol pathway - oxidized LDL - oxidative stress
65
Polyol pathway
- conversion of glucose to sorbitol
66
What enzyme is used in the Polyol pathway?
aldose reductase
67
When is the polyol pathway activated?
if large amounts of glucose are present
68
What does an increased sorbitol accumulation lead to?
increased oxidative stress
69
What can polyol pathway cause?
glycation of cellular proteins impairing their function
70
What is the clinical significance of the polyol pathway?
Diabetic complications