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GIR Test 1 > B5.002 - Diabetes Mellitus Physiology > Flashcards

B5.002 - Diabetes Mellitus Physiology Flashcards

1
Q

what is DM

A

group of metabolic disorders that share a common feature of hyperglycemia

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2
Q

describe T1DM

A

destruction of beta cells - absolute insulin insufficiency
autoimmune
idiopathic
usually occurs at young age

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3
Q

describe T2DM

A

resistance to insulin and relative insulin insufficiency
classically called adult onselt
genetic and lifestyle factors

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4
Q

rank which ethnicities have the highest to lowest risk of DM

A 
hispanic F
non hispanic black F
hispanic M
non hispanic black M
non hispanic white F
non hispanic white M
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5
Q

90% of pts with newly diagnosed diabetes re what

A

overweight or obese

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6
Q

what is the most important stimulator of insulin secretion

A

glucose

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7
Q

what yields the best plasma insulin response, IV or oral insulin

A

oral, indicating alimentary mechanisms in addition to the arterial blood sugar concentration regulate insulin secretion

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8
Q

what are the core defects in T2DM

A

beta cell dysfunction

insulin resistance

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9
Q

more than 80% of pts progressing to T2DM are what

A

insulin resistant

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10
Q

what tissue is the major player in insulin resistance

A

skeletal muscle

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11
Q

describe the 2 major methods of glucose transport into skeletal muscle

A

insulin receptor is stimulated

muscle contraction

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12
Q

describe hepatic insulin resistance

A

NAFLD, ectopic lipids decrease sensitivity to insulin

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13
Q

what defines steatosis

A

> 5% of liver comprised of fat

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14
Q

hyerglycermia is linked to what

A

oxidative stress and CVD

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15
Q

insulin secretion is inversely related to what

A

insulin sensitivity

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16
Q

how are plasma glucose levels regulated

A

by alterations in insulin secretion relative to the underlying level of insulin sensitivity

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17
Q

what are measures of insulin sensitivity

A 
OGTT >200 = DM, >150 = IGT
Mixed meal tolerance test
continuous glucose monitors 
fasting lood glucose (100-125 elevated; >126 = DM)
HOMA >3 insuline resistance
hyerinsulinemic euglycemic clamp
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18
Q

fasting glucose levels

A

<100 normal
100-126 pre diabetic
>126 diabetic

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19
Q

OGTT levels

A

<140 normal
140-200 pre diabetic
>200 diabetic

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20
Q

what are IFG and IGT

A

IFG - impaired fasting glucose

IGT - impaired glucose tolerance

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21
Q

what is HbA1C

A

glucose chemically linked to Hb

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22
Q

excellent, good and bad HbA1C

A

4-6 excellent
7-8 good
9-14 action suggested

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23
Q

what are components leading to beta cell failure

A 
chronic hyperglycemia
glucotoxicity
lipotoxicity
oversecretion of insulin to compensate
high circulating free fatty acids
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24
Q

what are incretins

A

GLP-1, GIP

as much as 50% post prandial insulin release dependent on incretins

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25
describe how GLP-1 works
``` upon ingestion of food GLP-1 is secreted from L cell in the intestine this stimulates insulin secretion suppresses glucagon secretion slows gastric emptying reduces food intake increases B cell mass and maintains B cell function improves insulin sensitiviy enhances glucose disposal ```
26
describe GLP-1 levels in T2DM
they are lower either due to decreased production or increased production of DPP-4
27
cellular mediators of insulin secretion
``` gut peptides (GLP-1, GIP) glucose ```
28
biguanides MOA
activates AMP kinase | decreases hepatic glucose production
29
advantages of biguanides
extensive experience no hypoglycemia weight neutral low cost
30
disadvantages of biguanides
GI Lactic acidosis B12 deficiency
31
SU/Meglitinides MOA
closes KATP channels | increases insulin secretion
32
advantages of SU/Meglitinides
extensive experience decreased microvascular risk low cost
33
disadvantages of SU/meglitinides
hypoglycemia weight gain low durability
34
TZDs MAO
PPAR gamma activator | increased insulin sensitivity
35
advantages of TZDs
no hypoglycemia durability decreased TGs increased HDL
36
disadvantages of TZDs
weight gain edema/CHF bone fractures high cost
37
a-GIs MOA
inhibits alpha glucosidase | slows carbohydrate absorption
38
advantages of a-GIs
no hypoglycemia nonsystemic decreased post prandial glucose
39
disadvantages of a-GIs
GI dosing frequency modest decrease in a1c
40
DPP-4 inhibitors MOA
inhibits DPP-4 | increases GLP-1, GIP
41
advantages of DPP-4i
no hypoglycemia | well tolerated
42
disadvantages of DPP-4i
modest dec in a1c urticaria high cost
43
GLP-1 receptor agonist MOA
activates GLP-1 R increases insulin decreaes glucagon decreased gastric emptying increased satiety
44
advantages of GLP-1 RA
weight loss | no hypoglycemia
45
disadvantages of GLP-1RA
GI medullary ca injectable high cost
46
amylin mimetics MOA
activates amylin receptor decreasesd glucagon decreased gastric emptying increased satiety
47
advantages of amylin mimetics
weight loss | decreased PPG
48
disadvantages of amylin mimetics
``` GI modest dec in a1c injectable hypo w insulin dosing frequency high cost ```
49
bile acid sequestrants MOA
bind bile acid | dec. hepatic glucose production
50
advantages of bile acid sequestrants
no hypoglycemia nonsystemic dec post prandial glucose dec CVD events
51
disadvantages of bile acid sequestrants
GI modest dec in a1c dosing prequency high cost
52
dopamine 2 agonist MOA
activates DA receptor modulates hypothalamic control of metabolism increased insulin sensitivity
53
advantages fo dopamine 2 agonists
no hypoglycemia
54
disadvantages of dopamine 2 agonists
``` modest dec in a1c dizziness/syncope nausea fatigue high cost ```
55
do treatments stay constant over time?
no all get worse
56
what is the downside to using HbA1C as the measure of interest for treatment
it doesnt capture short term changes in glycemic control and dose not distinguish pre and post prandial conditions
57
what is the primary cause of T2D
inactivity
58
what volume of activity is needed to offset T2D?
>3500 steps/day
59
how does chronic exercise and weight loss affect DM
evidence of improved beta cell fxn
60
rank types of physical activity in order of best to worst at lowering a1c
aerobic resistance combined

GIR Test 1 (15 decks)

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