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endocrine > treatment of type 2 diabetes > Flashcards

treatment of type 2 diabetes Flashcards

1
Q

aims of management

A
  • treat symptoms
  • prevent microvascular complications
  • prevent cardiovascular complications
  • screen for complications early while treatable
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2
Q

diet changes

A
  • aim is to lose 5-10kg in one year
  • reduce refined sugar intake
  • reducing fat intake
  • increase fruit and veg intake
  • reducing salt
  • safe and sensible alcohol consumption
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3
Q

how low should glucose aim to be

A
  • low enough to stop symptoms

- prevent complications - HbA1c <7%

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4
Q

aim of HbA1c target for type 2

A

53mmol/mol (7%)

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5
Q

what are some insulin secretagogues

A
  • sulphonylureas
  • DPP4 inhibitors
  • GLP-1RA
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6
Q

what are some insulin sensitizers

A
  • metformin

- thiazolidinediones

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7
Q

molecular mechanism of metformin

A
  • inhibition of complex 1 of the mitochondrial respiratory chain
  • fall in cellular ATP
  • rise in ADP/ATP ratio
  • lowers hepatic glucose production
  • increases gut glucose utilisation and metabolism
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8
Q

where is metformins site of action

A
  • requires active transport by organic cation transporters

- these are present in the intestines, liver and kidneys

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9
Q

what is the usual dose of metformin

A

500mg bd

max dose 1g bd

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10
Q

side effects of metformin

A
  • GI intolerance
  • diarrhoea
  • bloating
  • abdo pain
  • dyspepsia
  • metallic taste in mouth
  • metformin associated lactic acidosis
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11
Q

what is done to reduce side effects of metformin

A

initiate slowly
-500mg od 1 week and increase by 500mg od per week

or use modified release formation

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12
Q

why does metformin associated lactic acidosis happen

A

metformin increases lactic acid production

  • lactate is normally cleared by the liver and kidneys
  • in acute kidney injury metformin is associated with greater risk of lactic acidosis
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13
Q

is metformin first line

A

yes

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14
Q

what are the 2nd generation sulphonylureas

A
  • gliclazide
  • glipizide
  • glimepiride
  • glibenclamide
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15
Q

mechanism of action of sulphonylureas

A
  • SUs bind to SUR1
  • closure of ATP sensitive K channels
  • rise in membrane potential triggers voltage gated calcium channel
  • calcium influx leads to insulin exocytosis
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16
Q

do sulphonylureas increase or decrease weight

A

increase

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17
Q

risk of sulphonylureas

A

hypoglycaemia

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18
Q

most common sulphonylurea in UK

A

gliclazide

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19
Q

who do we need to be cautious with when prescribing sulphonylureas

A
  • elderly

- where hypoglycaemia would be a risk (driving, working up ladders etc)

20
Q

what type of ligands are thiazolidinediones

A

PPARgamma

-results in switching on 100s on genes

21
Q

what does TZDs mainly have an effect on

A

adipose tissue

22
Q

what is TZDs effect on adipocytes

A
  • increase differentiation from pre-adipocytes to adipocytes
  • increased fat mass
  • lipid seal - FFA (free fatty acids) uptake removed fat from liver and muscle, reduces lipotoxicity
  • increases adiponectin which acts on liver to increase insulin sensitivity
  • net result is increased insulin sensitivity
23
Q

who are TZDs particularly potent in

A

obese women

24
Q

TZDs affect on blood pressure and weight

A

increase in weight

reduction in blood pressure

25
Q

what is the only available TZD called

A

Pioglitazone

26
Q

usual dose of Pioglitazone

A

15-30mg od

27
Q

side effects of TZDs

A
  • weight gain
  • fluid retention (doubles risk of cardiac failure)
  • fracture risk (fat accumulation in bone marrow and reduction in bone density)
28
Q

does Pioglitazone reduce cardiovascular risk

A

yes

29
Q

what are incretins

A

intestinal secretion of insulin

30
Q

what are the two incretin peptides

A

GIP from K cells

GLP-1 from L cells

31
Q

incretins mechanisms of action

A

increase in cAMP acts in many ways to increase release of insulin
-can only work when pathway is triggered by either glucose or sulphonylureas

32
Q

what do gliptins do (DPP4i)

A
  • inhibit breakdown of GLP-1 and GIP

- augment insulin secretion so are insulin secretagogues

33
Q

are DPP4i very potent?

A

no

-weak glucose lowering

34
Q

side effects of DPP4i

A

very minimal

-possible risk of pancreatitis

35
Q

what do GLP-1RA do

A
  • they are GLP-1 like molecules modified to avoid breakdown by DPP4
  • act directly on the GLP-1 receptor
  • promote insulin secretion in a glucose dependent mechanism
  • also lower glucagon
  • act on hypothalamus to reduce appetite
  • and intestines to reduce gastric emptying
36
Q

effect of GLP-1RA on weight and bp

A

lose weight
reduce bp
increase heart rate

37
Q

are GLP-1RA potent?

A

yes

38
Q

name two GLP-1RA

A

liraglutide and semaglutide

39
Q

side effects of GLP-1RA

A
  • nausea and vomiting

- small increase in gallstones

40
Q

how are GLP-1RA given

A

injection

-one is oral

41
Q

what do SGLT2 inhibitors do

A

increase renal glucose loss resulting in glucose reduction and weight loss

42
Q

what are the direct effects of SGLT2i

A

glucose loss results in osmotic diuresis

  • inhibition of SGLT2i reduces Na absorption
  • urate excretion is increased - reduction in plasma urate concentrations
  • renal protection
43
Q

indirect effects of SGLT2i

A
  • reduction in insulin and increase in glucagon
  • increase in FFA results in increase in ketone body production
  • cardiac benefit
  • BUT risk of ketosis and ketoacidosis
44
Q

what does SGLT2i glucose lowering effect rely on

A

renal glucose filtration

45
Q

name three commonly used SGLT2i’s

A
  • dapagliflozin
  • canagliflozin
  • empagliflozin
46
Q

side effects of SGLT2i

A
  • thrush
  • fournier gangrene
  • hypovolemia and hypotension
  • diabetic ketoacidosis
47
Q

do SGLT2i’s have a CV benefit

A

yes

endocrine (40 decks)

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