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2 Endocrine > Type 2 Diabetes Drugs > Flashcards

Type 2 Diabetes Drugs Flashcards

1
Q

what does an insulin sensitiser mean?

A

deceases insulin resistance

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2
Q

what T2 drugs are insulin sensitisers

A

thiazolidinediones

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3
Q

what T2 drugs increase secretion of insulin?

A

SURs
incretin mimetics
glinides
DPP-4 inhibitors

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4
Q

what T2 drugs do not involve insulin control?

A

alpha glucosidase

SGLT-2

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5
Q

what do SGLT2 inhibitors do?

A

enhance glucose excretion by kidney

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6
Q

what do alpha glucosidase drugs do?

A

slow glucose absorption from GI tract

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7
Q

when is glucose phosphorylated to g6p?

A

just after it is diffused into the cell by GLUT-2

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8
Q

how is the membrane depolarised for insulin secretion?

A

ATP from glycolysis closed KATP channels

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9
Q

what is the structure of a KATP channel?

A

octomer containing 6 KIR6.2) receptors in the middle and 4 SUR1 receptors on the outside

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10
Q

what do the SUR1 subunits in the KATP channel do?

A

regulate the channel’s activity

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11
Q

is the KATP channel opened or closed when extracellular glucose is low?

A

opened

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12
Q

what opens the KATP channel?

A

ADP binding to SUR1 subunits only

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13
Q

what do SURs do?

A

bind to SUR1

close the channel = depolarisation and insulin release

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14
Q

why do SURs require functioning beta cells in order to work?

A

cause pancreatic beta cell insulin secretion

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15
Q

what kind of drug is gliclazide?

A

SUR

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16
Q

what kind of drug is glibenclamide?

A

SUR

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17
Q

how long does it take for an SUR to cause peak insulin release?

A

1-2hrs

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18
Q

who is most likely to get hypoglycaemic from SURs?

A

elderly

reduced hepatic/renal function patients

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19
Q

when would an SUR be first line?

A

if pt is intolerant of metformin

if they have weight loss

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20
Q

why do you get weight gain with insulin secreting drugs?

A

insulin is anabolic
increase appetite
less urine loss of glucose

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21
Q

what onset do glinides have?

A

glinides

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22
Q

do glinides cause hypoglycaemia like SURs?

A

no

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23
Q

what drugs can glinides be used with?

A

metformin

thiazolidinediones

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24
Q

what are the 2 types of enteroendocrine cells and where are they located?

A

L cells- ileum

K cells- duodenum

25
Q

what stimulates release of GLP-1 and GIP?

A

ingestion of food

26
Q

what does GIP stand for?

A

glucose dependent insulinotropic peptide

27
Q

what to GLP-1 and G1P do?

A

BOTH enhance insulin release from beta cells to enhance glucose uptake

GLP-1 ONLY decreases glucagon release from alpha cells

28
Q

main role of DPP-4 inhibitors?

A

restore incretin by terminating DPP-4 which inhibits GLP-1 and GIP

29
Q

how should DPP-4 inhibitors be used?

A

combo with SU or metformin

30
Q

if it says “gliptin” in the name, what drug class should it belong to?

A

DPP-4 inhibitors

31
Q

what drug mimics the action of GLP-1?

A

incretin analogues

32
Q

do incretin analgogues cause weight loss?

A

yes

33
Q

can incretin analogues cause hypos?

A

no

34
Q

what drug can stop postprandial glucose spikes?

A

alpha glucosidase inhibitors

35
Q

why can alpha glucosidase inhibitors stop postprandial glucose spikes?

A

stops the enzyme that breaks down starch and disaccharides into absorbable glucsoe

36
Q

side effect of alpha glucosidase inhibitors?

A

GI upset

37
Q

what kind of drug is metformin

A

biguanide

38
Q

how does metformin work?

A

reduces gluconeogenesis
reduces carb absorption
increases glucose uptake by skeletal muscle
increases fatty acid oxidation

39
Q

can metformin cause hypos?

A

no

40
Q

side effects of metformin?

A

GI upset

lactic acidosis

41
Q

main action of TZDs?

A

PPAR (a transcription factor coding insulin signalling proteins) gamma agonists

42
Q

can TZDs cause hypos?

A

no

43
Q

can TZDs cause weight gain?

A

yes

44
Q

only TZD used in UK?

A

pioglitazone

45
Q

what other drugs can pioglitazone be used in combo with?

A

metformin

SUs

46
Q

what part of the kidney do SGLT2 inhibitors work?

A

proximal tubule of kidney

47
Q

what is the main aim of SGLT2 inhibitors?

A

cause glycosuria to get it out

48
Q

why is the closing of KATP channels called depolarisation?

A

the ATP is changing the membrane potential of the cell from negative to more positive

49
Q

what should you do if a patient’s HbA1C is >2% over target? why?

A

give insulin as most oral agents only decrease HbA1C by 1-2%

50
Q

what BMI would make you think the T2D problem is insulin deficiency rather than insulin resistance?

A

<30

51
Q

which T2D drug causes increased incidence of bladder cancer?

A

TZDs

52
Q

maximum dose of metformin available?

A

1g tds (3g per day)

53
Q

another word for DPP4 agonists?

A

gliptin

54
Q

what is the no.1 drug to use in patients who still have a high HbA1C + are obese but are on metformin and SUR?

A

GLP-1

55
Q

no.1 drug to use in a patient with a BMI of 27 who isnt responding to metformin or SUR?

A

insulin

56
Q

when could you use DPP4 agonists instead of SURs?

A

don’t have co-morbid renal disease

57
Q

essential information to give a patient hen they commence a SUR?

A

hypo symptoms

58
Q

if a patient is getting recurrent hypos from an SUR, do you decrease dose or change drug?

A

decrease dose

59
Q

target HbA1C values in pregnancy?

A

43mmol/mol

2 Endocrine (35 decks)

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