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Endocrinology > Pharmacology of drugs for T2DM > Flashcards

Pharmacology of drugs for T2DM Flashcards

1
Q

how do SGLT2 inhibitors work?

A

cause a decrease in the absorption of glucose in the so that it is excreted in the urine

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2
Q

what do SUs bind to?

A

SUR1

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3
Q

what do SUs cause the SUR1 to do & what does this cause?

A

close the cannel causing depolarisation & insulin release

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4
Q

what aspect of SUs mechanism of action could be the cause of their negative die effects?

A

the fact that insulin is released independent of plasma glucose concentration meaning there is a loss in the link between glucose & insulin secretion

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5
Q

give some examples of SUs

A

tolbutamide
glibenclamide
glipizide

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6
Q

how do SUs appear to act?

A

by displacing the binding of ADP-Mg2+f from the SUR1 subunit, closing the channel

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7
Q

which of the SUs are more potent and longer acting?

A

glibenclamide

glipazide

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8
Q

what adverse effect are the more potent & longer acting SUs more likely to cause?

A

episodes of hypoglycaemia

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9
Q

when are SUs 1st line?

A

in patients who are intolerant to metformin or who are not overweight

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10
Q

which other drugs can SUs be used in conjunction with?

A

metformin

thiazolidinediones

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11
Q

what can SUs cause that would be undesirable in diabetics?

A

weight gain

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12
Q

how do glinides work?

A

bind to SUR1 to close the Katp channel & trigger insulin release

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13
Q

give some examples of glinides

A

repaglinide

nateglinide

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14
Q

what is the benefit of glinides?

A

have rapid onset/offset kinetics so are less likely to cause hypos than SUs

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15
Q

when are glands taken?

A

before meals to reduce postprandial rise in blood glucose

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16
Q

which drugs can glinides be used in conjunction with?

A

metformin

thiazolidinediones

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17
Q

GIP

A

gastric inhibitory peptide

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18
Q

what do both GLP-1 & GIP do?

A

enhance insulin release from pancreatic beta cells & delay gastric emptying meaning enhanced glucose uptake & utilisation

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19
Q

what does GLP-1 do that GIP doesn’t do?

A

decreases glucagon release from pancreatic alpha cells so decreased glucose production

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20
Q

what stimulates the release of GLP-1 & GIP?

A

ingestion of food

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21
Q

GLP-1

A

glucagon like 1

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22
Q

where are GLP-1 & GIP released from?

A

enteroendocrine cells in the small intestine (L cells & K cells)

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23
Q

where are L cells found?

A

ileum & colon

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24
Q

where are K cells found?

A

jejunum/duodenum

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25
Q

which cells release GLP-1?

A

L cells

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26
Q

which cells release GIP?

A

K cells

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27
Q

how do incretin analogues work?

A

mimic the action of GLP-1 but are longer lasting

28
Q

give an example of an incretin analogue

A

extenatide

29
Q

how does extenatide work?

A

binds to GPCR GLP-1 receptor that increase intracellular cAMP concentration

30
Q

what physiological effects does extenatide have?

A

increases insulin secretion
suppresses glucagon secretion
sloes gastric emptying
decreases appetite

31
Q

what does extenatide do to the body?

A

causes modest weight loss & reduces hepatic fat accumulation

32
Q

how is extenatide administered & how often?

A

subcutaneously twice daily

33
Q

what side effects could extenatide cause?

A

nausea
hypoglycaemia
rarely pancreatitis

34
Q

name a longer acting incretin analogue suitable for once daily subcutaneous administration

A

liraglutide

35
Q

which ensyme rapidly terminates the actions of GLP-1 & GIP?

A

enzyme dipeptidyl peptidase-4 (DPP-4)

36
Q

what do DPP-4/gliptins do?

A

competitively inhibit DPP-4 prolonging the actions of GLP-1 & GIP

37
Q

what other drug classes are gliptins usually used in combination with?

A

thiazolidinediones

metformin

38
Q

name some gliptins

A

sitagliptin
saxigliptin
vildagliptin

39
Q

how is sitagliptin administered & how often?

A

orally once daily

40
Q

what is alpha-glucosidase & what does it do?

A

a brush border enzyme that breaks down start & disaccharides to absorbable glucose

41
Q

what do alpha-glucosidase inhibitors do?

A

delay absorption of glucose thus reducing postprandial increase in blood glucose

42
Q

when are alpha-glucosidase inhibitors used?

A

in T2DM patients inadequately controlled by life style measures or other drugs

43
Q

where do adverse affects of alpha-glucosidase inhibitors occur?

A

in the GI tract:

flatulence, loose stools, diarrhoea, abdominal pain, bloating

44
Q

what adverse effect do alpha-glucosidase inhibitors pose no risk of?

A

hypoglycaemia

45
Q

what type of drug is metformin?

A

biguanide

46
Q

how does metformin work?

A

reduces hepatic gluconeogenesis by stimulating AMP-activated protein kinase

47
Q

which drug is first line in the treatment of T2DM in obese patients?

A

metformin

48
Q

what does metformin do to the body?

A

increases glucose uptake & utilisation by skeletal muscle (increases insulin signalling)
reduces carbohydrate absorption
increases fatty access oxidation

49
Q

how is metformin administered?

A

orally

50
Q

what desirable affects does metformin have?

A

prevents hypoglycaemia but doesn’t cause hypos
causes weight loss
may be combined with other agents

51
Q

what adverse affects an metformin cause?

A 
GI upsets (diarrhoea, nausea, anorexia)
rarely lactic acidosis due to the reduction in gluconeogenesis
52
Q

what do thiazolidinediones/glitazones (TZDs) do?

A

enhance the action of insulin at target tissues which reduces the amount of insulin required to maintain a given blood level of glucose

53
Q

how do TZDs work?

A

act as exogenous agonists of the nuclear receptor PPAR-gamma which associated with retinoid receptor X (RXR)

54
Q

what does an activated PRARgamma-RXR complex act as?

A

a transcription factor that binds to DNA to promote the expression of genes encoding several proteins involved in insulin signalling

55
Q

what other proteins are involved in insulin signalling?

A

lipoprotein lipase
fatty acid transport protein
GLUT4

56
Q

what are the desirable effects of TZD?

A

promote fatty acid uptake & storage in adipocytes rather than muscles & liver
reduced hepatic glucose output

57
Q

what are the adverse effects of TZDs?

A

weight gain
fluid retention
increased incidence of bone fractures

58
Q

name the only TZD currently used & why?

A

pioglitazone doesn’t cause hepatotoxicity

59
Q

what other drugs can pioglitazone be used in combination with?

A

metformin or SUs

60
Q

SGLT2

A

sodium-glucose contratransporter-2

61
Q

how do SGLT2 inhibitors work?

A

act to selectively block the reabsorption of glucose by SGLT2 in the proximal tubule of the kidney nephron to deliberately cause glucosuria

62
Q

glucosuria

A

glucose in urine, usually there is none found

63
Q

what are the desirable effects of SGLT2 inhibitors?

A 
cause decrease in blood glucose with little risk of hypos 
calorific loss (weight loss)
64
Q

name the currently licensed SGLT2 inhibitor

A

dapagliflozin

65
Q

what is the adverse effects of SGLT2?

A

glucosuria provides enhanced breeding ground for bacteria & fungi, increasing the incidence of lower UTIs

Endocrinology (23 decks)

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