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RB Y2 Endocrine - 1 Diabetes > Management of T2DM > Flashcards

Management of T2DM Flashcards

1
Q

describe the insulin curve and the purpose of management

A

T2DM can be described as falling off the curve - aim to get one back on

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2
Q

what are the ideal treatment aims for T2DM

A

alleviate hyperglycaemic symptoms and improve glycaemic control

minimise hypoglycaemia

minimise weight gain/cause weight loss

reduce micro and macro vascular complications

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3
Q

what benefit has maintaining a lower HbA1c been show to have

A

reduce risk of microvascular endpoints, MI, cataract extraction, retinopathy and albuminuria

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4
Q

HbA1c targets

A

48 mmol/L in younger patients

53 mmol/L in others

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5
Q

what does HbA1c relate to

A

mean glucose level over past 8 weeks

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6
Q

when would one consider less tight HbA1c control

A

if patient is at risk of hypoglycaemia

eg elderly patients prone to falls

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7
Q

what can the failure to reach glycaemic targets be influenced by

A

youner, female, obese

not at BP or lipid targets

more complex glucose lowering therapies - several drugs

poor adherence to meds and lifestyle

reluctance to intensify treatment

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8
Q

outline of T2DM treatment

A

information

diet and lifestyle

weight target

exercise target

metformin

statin

ACE

review (foot care)

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9
Q

what is the foundation of treatment

A

diet, exercise and education

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10
Q

is it better to add on drugs or increase the dose of a drug

A

far better to add on - efficacy can be decreased at higher dosages

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11
Q

SIGN guidelines for pharmacological treatment

A

metformin

sulphonylurea

TZD (eg Pioglitazone) or DDP-4 or SGLT2

insulin

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12
Q

outline the criteria to add on a second drug from metformin

A

HbA1c ≥53 mmol/L 16 weeks later

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13
Q

when is sulphonyurea first line

A
  • intolerance to Metformin or contraindications (renal failure etc)
  • patients with osmotic symptoms - quicker onest of action
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14
Q

outline the criteria to add a drug on from sulphonylurea

A

HbA1c ≥57 mmol/L 6 months later

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15
Q

what type of drug is Metformin

A

Biguanide

insulin sensitiser

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16
Q

what is Metformin derived from

A

guanidine

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17
Q

describe how Metformin must be started

A

gradually increased (from around 500mg to 1000mg BD)

otherwise the patient will have diarrhoea and vomiting

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18
Q

Metformin mechanism

A

decrease hepatic gluconeogenesis and increase peripheral glucose uptake

suppress appetite- of particular use in overweight patients

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19
Q

is hypoglycaemia a risk in Metformin treatment

A

not in monotherapy

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20
Q

does Metformin have an effect on complications

A

reduce micro and macro complications

  • reduce triglycerides and LDL
  • minor reduction in BP
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21
Q

what is metformin also used to treat

A

PCOS and NAFLD

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22
Q

is Metformin safe in pregnancy

A

yes

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23
Q

GI adverse effects of Metformin

A

nausea, vomiting, anorexia, abdominal pain, taste disturbance

up to 25% patients

this is why start low and go slow

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24
Q

when should Metformin be avoided

A
  • renal impairement - significant risk of lactic acidosis as adequate renal function is required to excrete Metformin
    • do not give if eGFR <30ml/min
  • also have caution in patients with pre-existing risk eg acute heart failure, sepsis, acute MI, respiratory failure, hypotension
  • temporarily withhold if IV contrast being used eg angiography or CT scan
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25
Q

other adverse affects of Metformin

A

interference with vitamin B12 and folic acid absorption

liver failure - discontinue use if there is advanced cirrhosis/liver failure.

rash

renal toxicity

26
Q

what eGFR values indicate that Metformin should be stopped due to renal toxicity

A

eGFR <30 ml/min or serum creatinine >150

half dose if eGFR 30/45 ml/min

27
Q

what should happen to Metformin dose if IV contrast eg angiography/CT scan being usd

A

temporarily withheld

28
Q

Sulphonylurea examples

A

2nd generation - Glicazide, Glibenclamide, Glimeparide

29
Q

patients with which symptoms are recommended a sulphonylurea as first line

A

those with osmotic symptoms

30
Q

which generation of Sulphonylurea drugs are used

A

2nd generation

31
Q

Sulphonylurea mechanism of action

A

Mimic the action of ATP on KATP to depolarize ß cells, and stimulate insulin release.

32
Q

does Sulphonylurea prevent complications

A

only microvascular ones

33
Q

effects of Sulphonylureas

A

hyperglycaemia management:

  • redice HbA1c by about 15-20 mmol/L by increasing insulin secretion
  • reduces glucose more rapidly than insulin sensitisers
34
Q

what decreases glucose levels faster? insulin sensitisers or Sulphonylurea

A

Sulphonylurea

35
Q

adverse effects of Sulphonylureas

A

weight gain

hypoglycaemia - take particular care in the frail/elderly, alcohol excess or liver disease

GI upset, headache

36
Q

what stage in the path is Sulphonylurea

A

2nd as an add on to metformin

1st in underweight T2DM / if intolerant to Metformin

37
Q

when should Sulphonylureas be avoided

A

severe renal or hepatic failure

38
Q

what is the only available TZD

A

Pioglitazone

39
Q

TZD onset

A

slow onset, maximum effect is after 1-2 months of treatment

40
Q

TZD mechanism of action

A
  • PPARgactivator. They are lipophilic so readily enter cells and bind to PPARg, which is anuclear receptorfound predominantly inadipose tissue, but also skeletal muscle and liver. It is combined with RXR.
  • PPARg causes differentiation of adipocytes (weight gain), increased lipogenesis and enhances uptake of fatty acids and glucose. It also promotes Sodium ion reabsorption in renal collecting ducts (fluid retention).
  • TZDs cause PPARg-RXR to bind to DNA, promoting transcription of several genes that are important in insulin signalling.
41
Q

LPL

A

hydrolyses the breakdown of lipids found in lipoproteins (eg chylomicrons and VLDL) into fatty acids and glycerol

LPL deficiency is assoicated with hypertriglyercidaemia

42
Q

effects of TZD

A

hyperglycaemia managment: reduces bA1c by about 15-20 mmol/L by increasing insulin sensitivity

43
Q

adverse effects of TZD

A
  • Weight gain is almost inevitable
    • Due to increased deposition of subcutaneous (not visceral) fat and fluid retention
    • 1-4kg usually stabilising in 6-12 months
  • Hypoglycaemia
    • Usually not if used without a SU
  • Heart failure
    • Fluid retention results in doubling risk
  • Avoid in over 65s
  • Doesn’t prevent micro or macro vascular complications
  • Risk of fracture with chronic use and hepatotoxicity (regular LFTs)
44
Q

do TZDs prevent complications

A

neither micro nor macro

45
Q

incretin pathway

A
  • group of metabolic hormones that stimulate a decrease in blood glucose levels
  • are secreted after eating and augment the secretion of insulin from pancreatic ß cells
  • also inhibit glucagon release from alpha cells of islet of Langerhans
  • Drugs acting on this are used in combination with metformin/sulphonylurea/pioglitazone in patients who have not achieved adequate glycaemic control with these drugs alone/in combination.
46
Q

incretin hormone life

A

very short half life

GIP (from K cells) and GLP-1(from L cells) are rapidly inactivated by the enzyme DPP4 and then are cleared by the kidney

47
Q

GLP-1 analogues

A
  • Exenatide – BD - subcutaenously
  • Exendin – once weekly
  • Liraglutide – OD
  • Lixisenatide – OD

These mimic the action of GLP-1, but are longer lasting

48
Q

benefits of GLP analogues

A
  • Lowers blood glucose after a meal by increasing insulin secretion, suppressing glucagon secretion and slowing gastric emptying
    • Promote insulin secretion from pancreas without hypoglycaemia – increase insulin in a glucosensitive manner
  • Reduces food intake (by an effect on satiety), hence causing weight loss
49
Q

cons of GLP analogues

A

injectable

nausea

pancreatitis/pancreatic cancer?

50
Q

DPP4 inhibitors

A

orally active

less potent that GLP

these competitively inhibit DDP4, prolonging the actions of GLP-1 and GLP,

51
Q

DPP4 inhibitors name

A
  • gliptins
52
Q

DPP4 inhibitors effect on glucose

A

dont reduce HbA1c that much - useful in the elderly

no hypos

53
Q

DPP4 inhibtors effect on weight

A

neutral

54
Q

do GLP inhibitors or DPP4 inhibitors have a lower incidence of hypos

A

DPP4 lower incidence - less potent drugs

55
Q

SGLT2 inhibitors name

A

-agliflozin

56
Q

SGLT2 inhibitors mechanism of action

A
  • Glucose reabsorption occurs in the proximal tubule, normally 100% of glucose is reabsorbed. It crosses the apical membrane by a secondary active transporter (SGLT1 and 2 - Sodium), and then crosses the basolateral membrane down its concentration gradient by facilitated diffusion
  • 90% through SGLT2
  • SGLT2 inhibitors decrease the uptake of glucose by about one quarter, all this comes out in the urine.
57
Q

which patients are SGLT2 inhibitors good for

A

CV risk - reduce CV events, death and hospitalization for heart failure

also beneficial for most renal outcomes

58
Q
A
59
Q

which drugs have a risk of hypos

A

sulphonylureas

60
Q

side effects of SGLT2 inhibitors

A
  • These can cause weight loss: calorific loss and mild osmotic diuresis
  • However, loss of glucose in the urine can increase risk of thrush and UTI.

RB Y2 Endocrine - 1 Diabetes (16 decks)

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