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PMCOL 344 > Diabetes-2 > Flashcards

Diabetes-2 Flashcards

1
Q

how can you describe insulin release

A

biphasic

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2
Q

what does it mean that insulin release is biphasic (what are the phases)

A

2 phases, first is a spike and it descends a bit then second is more rounded increase then down again

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3
Q

what happens in T2DM with biphasic release

A

the first phase is missing, the second phase is normal

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4
Q

what happens in T1DM with biphasic release

A

both phases absent, its just a straight line of insulin release (being none)

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5
Q

what happens to ions in insulin secreting cells with low plasma glucose

A

K+ exits the cells, making the inside more negative

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6
Q

what happens to ions in insulin secreting cells with high plasma glucose

A

block K+ leaving, Ca++ enters and insulin release

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7
Q

what does adding glucose do to membrane from beta cells

A

increases depolarization, so more insulin secretion

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8
Q

what is the mechanism of action of sulfonylureas

A

inhibit SUR1 , part of the K ATP channels (inhibiting the channel causes insulin release)

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9
Q

what is Kir6.2

A

pore forming subunit to allow K+ to pass through

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10
Q

what does ATP do to Kir6.2

A

inhibits it

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11
Q

what is the mechanism of diazoxide - what does this cause

A

binds to SUR1 to open channel (reduces insulin secretion)

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12
Q

what disease state do you use diazoxide for

A

hypoglycemia

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13
Q

what is a drug we use to inhibit insulin release

A

diazoxide

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14
Q

what do anabolic hormones do

A

uptake and store glucose (as polymer glycogen), amino acids and fats, inhibits catabolism

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15
Q

is insulin anabolic or catabolic

A

anabolic

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16
Q

what does insulin do to the liver

A

inhibits glycogenolysis and gluconeogenesis, stimulates glycogen synthesis, increases lipogenesis —> increases glycogen and triglyceride stores

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17
Q

what does insulin do to the muscle

A

increase glucose uptake by GLUT4 and stimulates glycogen synthesis —> increase glycogen stores

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18
Q

what does insulin do to the adipose tissue

A

increase glucose uptake by GLUT4, stimulates glycerol and fatty acid synthesis (end products of glucose metabolism) —> increase glycogen and triglyceride stores

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19
Q

which tissues get increase TG with insulin

A

liver and adipose

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20
Q

which tissues get increase glycogen with insulin

A

adipose, muscle and liver

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21
Q

which tissues get both increased glycogen and TG stores with insulin

A

adipose and liver

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22
Q

which tissues only get increased glycogen stores with insulin

A

muscle

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23
Q

what kind of receptors does insulin bind to (what mechanism)

A

tyrosine kinase linked receptors

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24
Q

what subunits are in the tyrosine kinase linked receptors that insulin bind to

A

2alpha and 2beta

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25
Q

what happens when insulin binds to its receptors

A

dimerization and auto phosphorylation on tyrosine residues

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26
Q

what happens when there is dimerization and auto phosphorylation on tyrosine residues

A

phosphorylation of insulin receptor substrate (IRS) proteins

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27
Q

what do IRS (insulin receptor substrate) proteins do

A

interact with -SH2 domain

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28
Q

what does insulin do to glycogen fat and protein formation

A

increase

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29
Q

what does insulin do to glucose uptake

A

increase

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30
Q

what does insulin do to glucose utilization

A

increase

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31
Q

what does insulin do to formation of glucose from glycogen fat and protein

A

decrease

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32
Q

what does insulin do to growth

A

increase

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33
Q

what does insulin do to gene expression

A

increase

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34
Q

what does insulin do to blood glucose

A

decrease

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35
Q

what kind of molecule is glucagon

A

peptide hormone

36
Q

where is glucagon produced

A

alpha cells and in GI tract

37
Q

is glucagon the fight or flight or rest and digest

A

fight or flight

38
Q

is insulin the fight or flight or rest and digest

A

rest and digest

39
Q

what stimulates glucagon secretion (3)

A

amino acids, low plasma glucose, sympathetic activation (beta adrenoceptors)

40
Q

what inhibits glucagon secretion (2)

A

somatostatin, high glucose

41
Q

what does glucagon do to plasma glucose

A

increases

42
Q

what does glucagon do to fat

A

causes breakdown for more energy

43
Q

what does glucagon do to protein

A

breakdown for more energy

44
Q

what does glucagon do to glycogenolysis

A

increase

45
Q

what does glucagon do to gluconeogenesis

A

increase

46
Q

what does glucagon do to glycogen synthesis

A

decrease

47
Q

what does glucagon do to glucose oxidation

A

decrease

48
Q

what does glucagon do to lipolysis

A

increase

49
Q

what does glucagon do to fatty acid oxidation

A

increase

50
Q

when do you use glucagon therapeutically

A

when hypoglycemic and acute heart failure caused by beta blockers

51
Q

what are the mechanisms similar to of glucagon

A

beta adrenoceptor mediated actions of adrenaline (cAMP)

52
Q

why can glucagon be used in acute heart failure caused by beta blockers

A

because it has similar actions to beta adrenoceptor mediated actions of adrenaline (cAMP), it can help icnrease cardiac output

53
Q

what is amylin structure

A

a 37aa peptide

54
Q

when is amylin secreted

A

co-secreted with insulin

55
Q

is amylin affected in DM

A

yes, it is absent or reduced

56
Q

what are 3 things that amylin does

A

inhibits glucagon secretion, delays gastric emptying, acts as satiety agent

57
Q

who may amylin replacement be good for

A

DM to improve glycemic control

58
Q

what may be bad with amylin replacement therapy

A

it tends to aggregate and form amyloid fibres, which plays a part in beta cell destruction in T2DM

59
Q

what is a synthetic amylin analogue

A

pramlintide

60
Q

what is pramlintide

A

synthetic amylin analogue with improved bioavailability

61
Q

what are incretins

A

peptides released from gut

62
Q

what are 2 examples of incretins

A

GLP-1 and GIP

63
Q

what is GIP

A

glucagon-like insulinotropic peptide

64
Q

what is GLP-1

A

glucagon-like peptide 1

65
Q

when are incretins released

A

in response to ingestion of food

66
Q

what stimulates the first peak in insulin release + how

A

incretins via cAMP production

67
Q

what are 2 main things that incretins cause

A

stimulate first insulin peak and inhibit glucagon secretion

68
Q

what is DPP-4 / what does it do

A

terminates the actions of incretins (breaks down GLP-1 and GIP)

69
Q

are incretins affected with T2DM + how

A

yes, loss of incretin effects

70
Q

what is diabetes mellitus

A

chronic metabolic disorder characterized by high blood glucose

71
Q

what causes hyperglycemia in DM

A

uncontrolled hepatic output and reduced uptake of glucose by skeletal muscle with reduced glycogen synthesis

72
Q

why do you drink a lot more in DM

A

glucose in urine which causes osmotic diuresis, then dehydration

73
Q

what % of people have type1DM that have DM

A

10%

74
Q

what are 2 main causes of T1DM

A

immune mediated or idiopathic

75
Q

what happens in T1DM

A

destruction of beta cells means that pancreas no longer produces insulin, or very little (more than %destruction causes hyperglycemia)

76
Q

what happens in T2DM

A

body does not produce or respond properly to insulin (insulin resistant)

77
Q

what is gestational diabetes

A

insufficient insulin secretion and lack of responsiveness during pregnancy, increased chance of both mother and fetus getting DM later

78
Q

what are 2 examples of genetic defects that cause cause types of DM

A

defects in beta cell function (like K ATP mess up)

defects in insulin action (like receptor defects)

79
Q

what is an example of a disease that can cause DM

A

pancreatic disease (like CF or pancreatitis)

80
Q

can drugs cause DM

A

yes

81
Q

can viruses cause DM

A

yes

82
Q

what is HbA1c + what is the role

A

glycolated hemoglobin, a measure of average glucose concentrations to which Hb has been exposed over last 3 months

83
Q

what is a good tool to diagnose DM

A

check HbA1c

84
Q

what is a healthy fasting plasma glucose level in mmol/L

A

3.89-5.5

85
Q

what is a diabetes fasting plasma glucose level in mmol/L

A

7+

PMCOL 344 (27 decks)

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