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PMCOL 344 > diabetes-3 > Flashcards

diabetes-3 Flashcards

1
Q

what is T1DM

A

chronic disorder resulting from autoimmune destruction of beta cells

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2
Q

what relates to the complications of hyperglycemia

A

the degree and length of duration

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3
Q

what part of the body is most vulnerable to hyperglycemia

A

capillary endothelium

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4
Q

what are 3 alterations to cell metabolism that happen in T1DM

A
  • imbalance glucose and FA oxidation
  • ER stress, accumulation lipids, NADPH depletion
  • increased free radicals
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5
Q

what causes glycosuria

A

overcome renal glucose resorption

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6
Q

what can happen to protein metabolism in T1DM

A

it is dysfunctional, leads to protein wasting

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7
Q

what is ketoacidosis

A

limited ability to take up glucose and subsequent lack of glycogen stores means that fats converted to acetyl-CoA to acetoacetate, beta hydroxybutyeate and acetone

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8
Q

what are the goals in T1DM treatment

A

tight regulation of plasma glucose to alleviate symptoms related to hyperglycemia and prevent chronic complications

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9
Q

what are 2 main regiments in T1DM

A

regular monitoring of glucose and insulin replacement therapy

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10
Q

what is used in insulin replacement therapy

A

human recombinant insulin

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11
Q

can you give insulin orally and why

A

no, destroyed in GI tract

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12
Q

what is the half life of insulin

A

10 mins

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13
Q

what are 2 major differences when it comes to injected insulin and normal human made

A
  • absorption kinetics do not reproduce rapid rise and fall of endogenous insulin in response to food
  • enters peripheral rather than portal circulation so may alter effects on hepatic metabolic processes
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14
Q

what are the 2 main preparations of insulin

A

soluble and protamine NPH insulin

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15
Q

what is soluble insulin route and timing

A

rapid acting, short duration of action, IV or IM

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16
Q

what is protamine NPH insulin

A

insulin complexed with zine and protamine, relatively insoluble crystals injected as a suspension

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17
Q

what is protamine NPH insulin route and timing

A

IM or SC, slower absorption and longer duration of action (once or twice a day)

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18
Q

what are 2 types of insulin analogues

A

insulin lispro and glargine

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19
Q

what is insulin lispro structure

A

lysine and proline residues at position 28 and 29 switched (on B chain)

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20
Q

what is duration of insulin lispro and why

A

reduces tendency of molecules to self associate, so act rapidly for shorter time, inject immediately before eating

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21
Q

what is insulin glargine structure

A

asparagine substituted for glycine at position 21 on A chain and B chain, lengthened by adding 2 arginines

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22
Q

what is the duration of insulin glardine and why

A

long acting, reduced solubility at pH7.4 so precipitates in sub-cutaneous tissue and slowerly released (mimic basal release)

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23
Q

which insulin is made to mimic basal release

A

insulin glargine

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24
Q

which insulin is made to mimic rapid release

A

insulin lispro

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25
what are some side effects of insulin
hypoglycemia, can cause brain damage and sudden cardiac death
26
what characterizes T2DM
insulin resistance and insulin deficiency
27
what happens to glucagon in T2DM
increased levels
28
what happens to GLP-1 in T2DM
reduced levels/ actions
29
what does insulin resistance do to liver
inadequate suppression of glucose output after meals
30
what does insulin resistance do to glucose utilization and uptake
decrease
31
what does insulin resistance do to lipolysis and fatty acid release
increase
32
what usually happens with insulin receptor activation
tyrosine phosphorylation
33
what happens with tyrosine phosphorylation
P13K/Akt activation, GLUT4 translocaction
34
why may obesity be linked to T2DM
because lipid accumulation leads to PKC activation (DAG elevated by increased free fatty acid), phosphorylation of insulin receptor, inhibits normal receptor signalling, inflammatory
35
what are the goals in the treatment of T2DM
improve beta cell function and sensitivity to insulin to alleviate symptoms and prevent chronic complications
36
what are the 3 main groups of drugs for T2DM
insulin sensitizers, drugs targeting beta-cell dysfunction, incretin based therapies
37
what are 2 drugs used as insulin sensitizers
metformin and thiazoladinediones
38
what are 1 drug used as drugs targeting beta-cell dysfunction (drug and class)
sulfonylureas, glibenclamide
39
what are 2 drugs used as incretin based therapies
exenatide and sitagliptin
40
generally, what do metformin and thiazoladinediones do
insulin sensitizers
41
generally, what do sulfonylureas, glibenclamide do
drugs used as drugs targeting beta-cell dysfunction
42
generally, what does exenatide do
GLP-1 mimetic
43
generally, what does sitagliptin do
DDP-4 inhibitor
44
how do you ingest metformin
oral
45
how do you ingest thiazoladinediones
oral
46
what drug class is thiazoladinediones
glitazone
47
what are 2 main effects of metformin
decrease glucose output, increase glucose uptake due to increase GLUT4 expression
48
how does metformin increase glucose uptake
increased GLUT4 expression
49
what is the mechanism of action of metformin
activates AMPK, which enhances insulin sensitivity
50
what does AMPK activation lead to
decrease glucose output, increase glucose uptake due to increase GLUT4 expression
51
what does metformin do to glucose output
decrease
52
what does metformin do to glucose uptake
increase
53
what is the mechanism of action of thiazoladinediones
activates PPAR gamma ligands
54
what happens once PPAR gamma ligands are activated
they alter transcription of enzymes involved in metabolism and proteins involved in insulin response
55
what do thiazoladinediones do to liver
decrease glucose output
56
what do thiazoladinediones do to muscle
increase glucose uptake
57
what do metformin do to liver
decrease glucose output
58
what do metformin do to muscle
increase glucose uptake due to increase GLUT4 expression
59
what 2 things can thiazoladinediones do (besides the PPAR gamma)
increase transcription of lipoprotein lipase (LPL) and GLUT-4
60
what can thiazoladinediones do to weight + how
cause weight gain, differentiation of adipocytes, increased lipogenesis, reduced leptin
61
what can thiazoladinediones do to blood pressure + how
lower, vasodilation
62
what do sulfonylureas and gibenclamide come from
antibiotic derivaties
63
what is the mechanism of action of sulfonylureas and gibenclamide
block pancreatic B-cell KATP channel by binding to SUR subunit, depolarization, increased, calcium channels, then release of insulin
64
does sulfonylureas insulin secretion depend on glucose levels
no
65
which kind of people would sulfonylureas not work for
patients that dont have beta cell function
66
how is sulfonylureas often prescribed
with metformin or glitazones
67
what kind of side effects come with sulfonylureas and why
cardiovascular cause there are KATP channels in the heart
68
what are a couple of drug interactions with sulfonylureas
NSAIDS, alcohol, MAO inhibitors, antibiotics
69
why does sulfonylureas have drug interactions
competition for metabolizing enzymes, interference with plasma protein binding or excretion
70
what % of secreted insulin in healthy individuals are caused by incretins
50%
71
what are 2 examples of incretins
GLP-1 and GIP
72
what is the mechanism of incretins
bind to GPCR, Gs, cAMP
73
what does cAMP do to beta cells
- phosphorylate SUR1 to inhibit KATP - inhibit delayed rectifier Kv channel - cells depolarize longer - mobilize Ca++ From intracellular stores - increase ATP (more KATP inhibition)
74
what does ATP to do KATP channel
inhibit
75
what does SUR1 phosphorylation cause
inhibition of KATP channels
76
what does incretins do to glucagon
inhibit secretion
77
what does incretins do to appetite
decrease
78
what does incretins do to gastric emptying
slow - feel full longer, slows sugar absorption
79
how is exenatide administered
sc in sustained release capsules
80
what is exenatide
synthetic GLP-1
81
what makes exenatide special
it is not broken down by DPP-4
82
what does DPP-4 do
breaks down GLP-1 and other incretins (serine protease)
83
what drugs is exenatide used with
sulfonylureas (synergism) and metformin (additive)
84
what is the duration of exenatide and why
longer, 12-14 hours so take twice daily | because it is not broken down by DPP-4
85
what is sitagliptin
DPP-4 inhibitor
86
what is the half life of sitagliptin
about 2 mins
87
what is the absorption of sitagliptin
less than 25% leaves the gut, 40-50% degraded in liver, 10-15% reaches systemic circulation
88
what is the mechanism of sitagliptin
prevents breakdown of endogenous incretins, so potentiates actions of GLP-1
89
why does barely any sitagliptin get into the systemic circulation
not much leaves the gut and lots of it degraded in liver
90
what does alpha-glucosidase do
releases glucose from more complex carbohydrates in intestine (like starch)
91
what does alpha-glucosidase blocker do
slows absorption of glucose, prevents initial glucose spike
92
what is another thing that alpha-glucosidase inhibitors do
increase GLP-1 secretion
93
what are some side effects of alpha-glucosidase inhibitors
fart, weight loss, diarrhea
94
what do a majority of T2DM patients require at some point + why
exogenous insulin because beta cell function declines
95
what is first line therapy
metformin + sitagliptin is smart to add

PMCOL 344 (27 decks)

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