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Endo Week 3 > Diabetes Therapy > Flashcards

Diabetes Therapy Flashcards

1
Q

name the three sulfonyureas

A

glipizide
glyburide
glimepiride

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2
Q

name the two meglitinides

A

repagalinide

nateglinide

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3
Q

what is the MoA of sulfonyureas and meglitinides?

A

increase insulin secretion by binding the SUR channel and blocking K+ efflux and starting insuln secretion pathway

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4
Q

what can sulfonyureas and meglitinides cause?

A

hypoglycemia

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5
Q

what is drug class of glipizide, glyburide and glimepiride?

A

sulfonyureas

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6
Q

what is the main biguanide to know?

A

metformin

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7
Q

what is the MoA of metformin?

A

though to sensitize liver to glucose and deacrease gluconeogenesis

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8
Q

what are three SEs of metformin?

A

diarrhea, nausea and low B12

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9
Q

what is the main risk with metformin? what further increases this risk?

A

lactic acidosis…if patient has renal fialure

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10
Q

other thn glucose levels, what does metformin help with?

A

thought to decrease lipid levels and maybe even cause some weight loss

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11
Q

what molecule is it suspected that metformin activates in the liver?

A

AMPK

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12
Q

does metformin cause hypoglycemia?

A

NO

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13
Q

name the two thiazolidinediones

A

pioglitazone and rosiglitazone

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14
Q

what is the MoA of pioglitazone and rosiglitazone?

A

insulin sensitizer of muscle and adipose tissue

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15
Q

do pioglitazone and rosiglitazone cause hypoglycemi?

A

no

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16
Q

name the three SEs of pioglitazone and rosiglitazone?

A

edema and weight gain and fractures

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17
Q

what is main severe risks with pioglitazone and rosiglitazone?

A

CHF and liver toxicity

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18
Q

what cancer might there be increased risk with pioglitazone?

A

bladder cancer

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19
Q

what molecule on fat do pioglitazone and rosiglitazone activate? what does this do?

A

activate PPAR-gamma and this increases insulin sensitivity of the adipose cells and increases levels of adiponectin

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20
Q

name the two a glucosidase inhibitors

A

acarbose and miglitol

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21
Q

what is the MoA of miglitol and acarbose?

A

inhibit intestinal BB enzyme a glucosidases to delay absorption of glucose…lowering postprandial glucose

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22
Q

when do acarbose and miglitol have their main effects?

A

postprandial

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23
Q

what is the main SE with acarbose and miglitol?

A

bloating and Gi upset

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24
Q

what is the normal fxn of incretin GLP-1?

A

promotes satiety
stimulates glucose dependent insulin secretion
slows gastic emptying
inhibits glucagon release

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25
Q

name the two GLP-1 incretin analogues?

A

exenatide

liraglutide

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26
Q

what is the MoA of exenatide and liraglutide?

A

promotes satiety
stimulates glucose dependent insulin secretion
slows gastic emptying
inhibits glucagon release

27
Q

what are the SEs of exenatide and liraglutide?

A

nausea and pancreatitsi

28
Q

what is a sometimes desired SE of exenatide and liraglutide?

A

weight loss and satiety increase

29
Q

what is secreted with insulin from beta cells?

A

amylin

30
Q

what is role of amylin in body?

A

inhibit glucagon release
increase satiety
slow gastric emptying

31
Q

what is drug that can act as amylin in diabetes rx?

A

pramlinitide

32
Q

what is MOA of pramlinitide?

A

inhibit glucagon release

increase satiety and slow gastric emptying

33
Q

what is drawback of use of pramlinitide?

A

have to give injcn with every meal

34
Q

name the four SGLT2 inhibitors

A

canagliflozin
dapagliflozin
empagliflozin
ertugliflozin

35
Q

what is the ending of all the SGLT2 drugs?

A

gliflozin

36
Q

what is MoA of SGLT2 inhibitors?

A

inhibit the SGLT2 transporter in the PCT of the kidney so glucose secreted

37
Q

what is insulin therapy effect on liver?

A

increase glucose storage as glycogen

38
Q

what is insulin therapy effect on muscle?

A

increase glycogen and protein synthesis

39
Q

what is insulin therapy effect on fat??

A

increase TG storage

40
Q

what are the two subunits of human insulin?

A

alpha and beta chain

41
Q

what are the two modified human insulins?

A

regular insulin
and
NPH insulin

42
Q

regular insulin has what duration effect?

A

short acting insulin

43
Q

NPH insulin has what duration effect?

A

intermediate acting insulin

44
Q

short acting normal insulin lasts about how many hours?

A

6-8

45
Q

intermediate acting NPH insulin lasts about how long?

A

12-20 hours

46
Q

name the three insulin analogues that are rapid acting?

A

aspart
glulisine
lispro

47
Q

how quickly is peak effect of aspart, glulisine and lispro?

A

1 hr after administration

48
Q

what is mnemonic to remember the rapid acting insulins?

A

no LisproAaspartGlulisine

49
Q

name the two long acting insulins

A

detemir and glargine

50
Q

why are rapid acting insulins able to act so fast?

A

because they are monomers and wuickly absorbed

51
Q

what makes long acting insulins act longer?

A

they are hexamers and have to be broken down to monomers to act

52
Q

how long to long acting insulins act?

A

no real peak time…system for say 24 hrs

53
Q

when is peak of NPH?

A

4-10 hrs

54
Q

when is peak or normal insulin?

A

2-3 hrs

55
Q

when is peak of fast acting?

A

1 hr peak

56
Q

what is average insulin requirement in type 1 DM?

A

0.5-0.6U/Kg/day

57
Q

what is a normal insulin routine for type I DM?

A

regular insulin in AM and before dinner

intermediate insulin in AM and at dinner

58
Q

overnight glucose is controlled by what part of insulin dose?

A

prior nights intermediate acting insulin

59
Q

pre lunch glucose is controlled by what part of insulin dose?

A

morning short acting insulin

60
Q

pre supper glucose is controlled by what part of insulin dose?

A

morning intermediate acting dose

61
Q

bedtime glucose is controlled by what portion of the insulin dose?

A

supper short acting insulin

62
Q

what is a dermatologic manifestation of insulin use?

A

lipdystrophy where you can get lipohypertrophy around injxn sites

63
Q

what is lipoatrophy?

A

immune mediated with loss of fat at insulin injxn sites…this is very uncommon

Endo Week 3 (8 decks)

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