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year 2 > diabetic drugs > Flashcards

diabetic drugs Flashcards

1
Q

what 2 types of diabetic drugs have an insulin independent action

A

alpha-glucosidase inhibitors

SGLT2 inhibitors

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2
Q

sulfonylureas act by displacing the binding of ___ from the ___ subunit therefore closing the ____ channel which causes ____

A

sulfonylureas work by displacing the binding of ADP-Mg2+ from the SUR1 subunit therefore closing the K-ATP channel which causes the release of insulin

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3
Q

what effect on the blood sugar do sulfonylureas have

A

decrease fasting and postprandial blood glucose

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4
Q

give an example of a short acting sulfonylurea

A

Tolbutamide

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5
Q

give 3 examples of a long acting sulfonylurea

which is ok for use in pregnancy in MODY

A

Glibenclamide

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6
Q

do sulfonylureas reduce micro or macrovascular complications

A

micro

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7
Q

are sulfonylureas orally active? are they well tolerated?

A

yes and yes

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8
Q

do sulfonylureas cause weight loss

A

no - undesirable weight gain

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9
Q

sulfonylureas will work in patients who no longer have a functioning mass of B-cells
true or false

A

false - require a functioning mass of beta cells

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10
Q

is there a risk of hypo with sulfonylureas?

A

yes

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11
Q

when should LA sulfonylureas be avoided?

A

CKD
elderly
pregnancy

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12
Q

when are sulfonylureas used first line

A

if metformin intolerant or if weight loss

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13
Q

what is the diabetic treatment ladder

A

metformin
+ sulfonylurea
+ TZD

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14
Q

when would a TZD be used 2nd line with metformin instead of a sulfonylurea

A

if hypo was a concern

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15
Q

when would a DPP4 inhibitor be used 2nd line with metformin instead of a sulfonylurea

A

if weight gain was a concern

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16
Q

when would a DPP4 inhibitor be used instead of a TZD 3rd line

A

if weight gain was a concern

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17
Q

when would a GLP-1 be used 3rd line instead of a TZD

A

if BMI > 30

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18
Q

when would insulin be used in diabetes? - last line

A

osmotic symptoms / rising HbA1c

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19
Q

what kind of drugs are repaglinide and nateglinide

A

glinides

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20
Q

how do glinides work?

A

they act similarly to sulfonylureas although their action is augmented by glycaemia - they lack the sulfonylurea moiety - bind at a distinct benzoamido site to close the Katp channel causing insulin to be released

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21
Q

are glinides orally active

A

yes

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22
Q

what is more likely to cause a hypo: glinide or sulfonylurea

A

sulfonylurea

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23
Q

are glinides safe to use in CKD

A

yes - mainly hepatic metabolism

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24
Q

what is the effect of glinides on blood glucose levels

A

reduce post prandial blood glucose - promote insulin secretion in response to meals

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25
Q

what is the action of glinides like with regard to time

A

rapid onset (30-60 mins) and offset (4 hours) kinetics

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26
Q

are glinides safe to use in pregnancy

A

no

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27
Q

are glinides safe to use in breast feeding

A

no

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28
Q

are glinides safe to use in hepatic impairment

A

no

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29
Q

when can glinides be used

A

in conjunction with metformin and TZDs

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30
Q

what kind of drug is sitagliptin

A

DPP4 inhibitor / gliptin

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31
Q

DDP4 inhibitors (competitively/non-competitively) inhibit the action of DPP4 and so (shorten/prolong) the action of __ and __

A

competitively inhibit

prolong action of GLP-1 and GIP

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32
Q

are DPP4 inhibitors effective in a patient with no preservation of insulin secretion

A

no

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33
Q

when are DPP4 inhibitors used

A

in combination with sulfonylurea or metformin

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34
Q

can DDP4 inhibitors be used as a monotherapy

A

yes

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35
Q

is sitagliptin orally active

A

yes

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36
Q

does sitagliptin cause weight gain?

A

no - weight neutral

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37
Q

does sitagliptin cause hypo?

A

not when used as a monotherapy

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38
Q

what is a side effect of sitagliptin

A

nausea

39
Q

what kind of drugs are extenatide and liraglutide

A

incretin analogues

40
Q

what peptides do incretin analogues mimic the action of

A

GLP-1

41
Q

what is more potent - DPP4 inhibitors or incretin analogues

A

incretin analogues

42
Q

incretin analogues bind as (antagonists/agonists) to the GLP-1 GPCR

A

agonists

43
Q

what does the binding of the incretin analogue to the GLP-1 GPCR cause

A

increase in intracellular cAMP concentration in pancreatic beta cells to stimulate insulin secretion/expression

44
Q

give 3 additional effects of incretin analogues

A

suppress glucagon secretion
slow gastric emptying
decrease appetite (hypothalamic cation)

45
Q

are incretin analogues orally active

A

no - SC admin

46
Q

do incretin analogues cause weight gain

A

no - modest weight loss

47
Q

do incretin analogues cause hypo

A

no

48
Q

what are some side effects of incretin analogues

A

nausea

rarely pancreatitis

49
Q

what kind of drugs are miglitol, voglibose and acarbose

A

alpha-glucosidase inhibitors

50
Q

what is alpha-glucosidase

A

brush border enzyme that breaks down dietary CHO (start and disaccharides) to absorbable glucose

51
Q

when are alpha-glucosidase inhibitors taken

A

with meals

52
Q

what is the effect of alpha-glucosidase inhibitors

A

delay absorption of glucose thus reduce post prandial increase in blood glucose

53
Q

when are alpha-glucosidase inhibitors used

A

in T2DM poorly controlled by diet and other drugs (infrequently)

54
Q

what are some side effects of alpha-glucosidase inhibitors

A 
flatulence
loose stools
diarrhoea
abdominal pain
bloating
55
Q

do alpha-glucosidase inhibitors cause hypo

A

no

56
Q

what kind of drug is metformin

A

biguanide

57
Q

biguandies increase (secretion of/sensitivity to) insulin

A

increase sensitivity to insulin

58
Q

biguandies (increase/decrease) hepatic gluconeogenesis by stimulating _____

A

biguanides decrease hepatic gluconeogenesis by stimulating AMP-activated protein kinase

59
Q

biguandies (increase/decrease) glucose and fatty acid uptake and utilisation by skeletal muscle by increasing insulin secretion

A

biguandies increase glucose and fatty acid uptake and utilisation by skeletal muscle by increasing insulin secretion

60
Q

do biguandies have an effect on CHO absoprtion?

A

yes - reduce CHO absorption

61
Q

biguandies increase/decrease fatty acid oxidation

A

biguandies increase fatty acid oxidation

62
Q

when is metformin used

A

1st line in T2DM irrespective to obesity

63
Q

do biguandies reduce microvascular complications

A

yes

64
Q

how is metformin administered

A

orally

65
Q

does metformin cause hypo

A

no

66
Q

metformin is weight neutral

true/false

A

false - weight loss

67
Q

metformin is used as a monotherapy only

true/flase

A

false

can be combined with other drugs

68
Q

can metformin be used in pregnancy

A

yes

69
Q

when is metformin contraindicated

A

severe renal/hepatic dysfunction

70
Q

what are 2 side effects of metformin

A 
GI upset (nausea, diarrhoea, anorexia, abdominal pain)
lactic acidosis - excessive alcohol consumption, severe renal/cardiac/liver failure
71
Q

at what GFR should metformin be stopped

and why?

A

GFR < 30

tissue hypoxia

72
Q

at what GFR should metformin be halfed

A

GFR 30-45

73
Q

metformin starts at a certain dose and remains as that

true or false

A

false

start low and increase slowly

74
Q

what kind of drug is pioglitazone

A

thiazolidinediones/glitazones

75
Q

why are ciglitazone and troglitazone no longer used

A

serious hepatotoxicity - not with pioglitazone

76
Q

when are TZDs used

A

in combination with either metformin or a sulfonylurea

77
Q

how do TZDs affect the secretion of insulin

A

they dont

they decrease insulin resistance at target tissues

78
Q

how do TZDs work?

A

they act as exogenous agonists of the nuclear receptor PPAR-Y which associates with RXR (retinoid receptor X)

79
Q

where is PPAR-Y found

A

largely confined to adipocytes

80
Q

what does the activated PPARY-RXR complex do

A

acts as a transcription factor that binds to DNA to promote the expression of genes encoding several proteins involved in insulin signalling and lipid metabolism

81
Q

what is the time of onset of action of TZDs

A

delayed

82
Q

increasing gene transcription does what to the uptake of glucose and fatty acids

A

increases

83
Q

do TZDs decrease microvascular complications

A

no

reduce MACROvascular comps

84
Q

what is the effect of TZDs on heart problems

A

decrease risk of MI but worsen heart failure

85
Q

do TZDs cause hypo

A

no

86
Q

give 4 other benefits of using TZDs

A
  • promote fatty acid uptake and storage in adipocytes rather than in skeletal muscle and liver
  • reduce hepatic glucose output
  • enhances peripheral glucose uptake
  • improves microalbuminuria
87
Q

do TZDs cause weight loss

A

no - weight gain

88
Q

why do TZDs cause fluid retention

A

promote Na+ reabsorption by the kidney

89
Q

what increases in incidence in the use of TZDs

A

fractures

90
Q

what kind of drugs are dapagliflozin, canagliflozin, ampagliflozin

A

SGLT2 inhibitors

91
Q

how do SGLT2 inhibitors work

A

they selectively block the reabsorption of glucose by SGLT2 in the proximal tubule of the kidney - enhance renal secretion of glucose

92
Q

what are 2 bad side effects of SGLT2 inhibitors and why do they happen

A

UTI and thrush

due to glucosuria

93
Q

do SGLT2 inhibitors cause weight gain

A

no - weight loss

94
Q

do SGLT2 inhibitors cause hypo

A

little risk

year 2 (19 decks)

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