diabetes in practice Flashcards

1
Q

When is treatment started?

A

HbA1c levels rise to 48 mmol/mol on lifestyle interventions

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2
Q

metformin dose

A

500mg od with meals
titrated up after 7 days
max 2g daily

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3
Q

s/e of metformin

A

GI side effects - transient

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4
Q

When should metformin be avoided?

A

eGFR < 30 ml/min/1.73 m cubed

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5
Q

What can happen if metformin is given when eGFR is < 30?

A

lactic acidosis

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6
Q

When is the 1st intensification done?

A

if HbAc1 rises to 58 mmol/mol

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7
Q

What drugs can be given with metformin for the 1st intensification?

A

DPP 4i
pioglitazone
sulfonylurea
SGLT 2i

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8
Q

example of sulfonlyurea

A

gliclazide

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9
Q

another name for DPP4i

A

giliptin

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10
Q

example of a giliptin

A

sitagliptin

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11
Q

another name for SGLT 2 inhibitor

A

gilflozins

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12
Q

example of SGLT 2 inhibitor

A

dapagliflozin

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13
Q

aim for 1st intensification of treatment

A

HbA1c 53 mmol/mol

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14
Q

When is a 2nd intensification of treatment given?

A

HbA1c levels rise to 58 mmol/mol

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15
Q

drug combinations for 2nd intensification (metformin)

A
- metformin and:
SU + DPP 4i
SU + pioglitazone
SU + SGLT2i
pioglitazone + SGLT 2i
  • insulin based treatment
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16
Q

What can be given if triple therapy is not effective/tolerated/contraindicated?

A

combination therapy with metformin, SU and a GLP 1

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17
Q

example of a GLP 1

A

exenatide

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18
Q

When is exenatide considered?

A
  1. BMI > 35 in patients of European decent and there are problems associated with high weight/obesity
  2. BMI < 35 and insulin is unacceptable because of occupational implications or weight loss would benefit other comorbidities
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19
Q

aim for triple therapy

A

53 mmol/mol

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20
Q

treatment if metformin is c/i or not tolerated

A

monotherapy:

  • DPP 4i
  • SU
  • pioglitazone
  • SGLT 2i
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21
Q

aim for monotherapy where metformin is c/i

A

48 mmol/mol for DPP 4i, pioglitazone and SGLT 2i

53 mmol/mol for sulphonylurea

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22
Q

1st intensification for non-metformin treatment

A

DPP 4i + pioglitazone
DPP 4i + SU
piolgitazone + SU

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23
Q

aim for 1st intensification?

A

53 mmol/mol

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24
Q

2nd intensification for non-metformin treatment

A

insulin based treatment

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25
Q

aim for insulin based treatment (2nd intensification)?

A

53 mmol/mol

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26
Q

What random plasma glucose levels indicates hyperglycaemia?

A

> 11 mmol/L

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27
Q

characteristic features of hyperglycaemia in children/young people

A

polyuria
polydipsia
weight loss
excessive tiredness

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28
Q

characteristic features of hyperglycaemia in adults

A
(polyuria, polydipsia, weight loss, excessive tiredness)
ketosis
< 50 yrs
BMI < 25 kg/m squared
Hx/FHx of autoimmune disease
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29
Q

plasma glucose optimal targets

A
  • 5-7 mmol/L on waking (fasting)
  • 4-7 mmol/L before meals and during the day
  • 5-9 mmol/L 90 mins after meals
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30
Q

How often are HbA1c tests carried out?

A

every 3-6 months

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31
Q

What is the natural profile of insulin?

A
  1. basal - steady, low level of background insulin

2. bolus - meal time, increased secretion in response to glucose absorbed from food/drink

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32
Q

4 types of insulin

A
  1. animal insulin
  2. human insulin (recombinant DNA technology)
  3. insulin analogues (modified human insulin to have an extended duration of action/faster absorption)
  4. biosimilars
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33
Q

3 insulin regimens

A
  1. 1/2/3 injections per day
  2. MDI (multiple daily injections)
  3. CSII (continuous subcutaneous insulin infusion)
34
Q

What type of insulin is used when giving 2/3 insulin injections per day?

A
  • rapid or short acting insulin
  • mixed with intermediate acting insulin
  • can be premixed/self mixed
35
Q

MDI regimen?

A
  • rapid or short acting insulin before meals
    AND
  • one or more separate daily injections of intermediate/long acting insulin analogue
36
Q

CSII (continuous subcutaneous insulin infusion)

A

portable electromechanical pump that can give basal infusion and individual bolus doses when required

37
Q

What is the first line insulin regimen?

A

basal-bolus insulin regimen

38
Q

What types of insulin are in the basal-bolus regimen?

A

long acting twice daily
and
rapid acting insulin before meals

39
Q

Glucose levels for hypoglycaemia?

A

< 3.5 mmol/L

40
Q

less serious signs of hypoglycaemia

A
hunger
anxiety/irritability
palpitations
sweating
tingling lips
41
Q

medium signs of hypoglycaemia

A
weakness
leathargy
visual disturbances
confusion
behavioural changes
42
Q

serious signs of hypoglycaemia

A

convulsions
loss of consciousness
coma

43
Q

management of hypoglycaemia

A

10-20g fast acting carbohydrate

- recheck blood glucose levels after 10-15 mins (no response, repeat carbs)

44
Q

hypoglycaemia treatment if person is unconscious and can’t swallow

A

IM glucagon

1mg adults

45
Q

What is fasting plasma glucose levels that indicates DM?

A

> 7 mmol/mol

46
Q

HbA1c recommendations for patient on a drug not associated with hypoglycaemia and on a drug assocoated with hypoglycaemia?

A

48 mmol/mol

53 mmol/mo, (drug associated with hypoglycaemia

47
Q

sulphonylurea (glicazide) dose

A
initially 40 - 80mg od
increased if necessary to 160mg od
dose taken with breakfast
> 160mg given in divided doses
max dose 320mg
48
Q

s/e and risks associated with sulphonylurea

A

can cause weight gain

risk of hypoglycaemia - increased risk in renal/hepatic impairment

49
Q

pioglitazone dose

A

15 - 30mg OD

max 45mg OD

50
Q

risks with pioglitazone

A

increased incidence of HF (don’t Rx in HF)
increased incidence of bladder cancer
increased fracture risk

51
Q

Gliptins (DPP4i - sitagliptin)

A
  • reduced dose in renal impairment
  • can help with weight loss
  • reduced appetite
  • increased incidence of pancreatitis
52
Q

Warning/risks with SGLT 2 inhibitors (gliflozins)?

A
  • increased risk of DKA
  • restrictions with renal impairment
  • increased UTI risk (increased glucose excretion in the urine)
53
Q

diabetic complications

A

cardiovascular risk (BP, lipids, anti-thrombotic therapy)
kidney damage
eye damage
nerve damage

54
Q

BP targets for T2DM already on hypertensive meds U80?

A

below 140/90 mmHg

55
Q

BP targets for T2DM already on hypertensive meds

OVER 80?

A

below 150/90 mmHg

56
Q

BP treatment

A
  1. lifestyle advice
  2. ACEI/ARB
  3. CCB/diuretic (thiazide)
  4. diuretic/CCB
  5. alpha blocker/BB/K sparing diuretic
57
Q

lipids treatment

A

statin - atorvastatin 20mg

58
Q

antithrombotic therapy

A

aspirin 75mg daily

NOT unless there’s established risk of CVD

59
Q

How to identify kidney damage?

A
  • first-pass morning urine specimen to estimate albumin:creatinine ratio (ACR)
  • measure serum creatinine
  • calculate eGFR
60
Q

How is kidney damage confirmed?

A

2 or more raised ACR results:
>2.5 mg/mmol (men)
> 3.5 mg/mmol (women)

61
Q

treatment for kidney damage

A

ACEI/ARB titrated to full dose

62
Q

What is periodontis?

A

chronic inflammatory disease caused by bacterial infection of the supporting tissues surrounding the teeth

63
Q

What OTC treatments should diabetics avoid?

A

systemic decongestants

- pseudoephedrine (Benadryl), phenylephedrine (Sudafed)

64
Q

Why should systemic decongestants be avoided?

A

unwanted sympathomimetic effects (CV risk, inc BP)

65
Q

What could diarrhoea be a sign of in diabetics?

A
  • side effect of meds (metformin titrated too quickly)

- autonomic nervous system damage

66
Q

Can topical decongestants be used in diabetics?

A

yes

short term use only

67
Q

example of topical decongestant that should be used with caution/short time in diabetics

A

xylometazoline (Otrivine)

68
Q

If a diabetic patient has an infection what should be questioned?

A

their blood glucose control

69
Q

If a patient NOT diagnosed with diabetes has a topical infection (throat) what should be questioned?

A

questioned about symptoms of hyperglycaemia (polyuria, thirst, weight loss)

70
Q

Diabetic patient with cystitis/thrush

A

cannot be treated OTC
can be a sign of worsening diabetes
infections can cause diabetics to become hyperglycaemic

71
Q

3 signs of DKA

A

ketosis
hyperglycaemia
acidaemia

72
Q

What is increased in DKA?

A

counter regulatory hormones

  • glucagon
  • cotrisol
  • growth hormone
  • catecholamines
73
Q

What is enhanced in DKA?

A

gluconeogenesis

glycogenolysis

74
Q

What does DKA cause?

A

severe hyperglycaemia

75
Q

What causes ketogenesis (production of ketones) in DKA?

A

increased lipolysis and metabolism of free fatty acids

76
Q

diagnosis of DKA

A

ketonaemia > 3mmol/L or ketonuria
blood glucose > 11 mmol/L (or knowm DM)
bicarbonate < 15 mmol/L
venous pH < 7.3

77
Q

diagnosis of DKA

A

ketonaemia > 3mmol/L or ketonuria
blood glucose > 11 mmol/L (or knowm DM)
bicarbonate < 15 mmol/L
venous pH < 7.3

78
Q

symptoms of DKA

A
polyuria
polydipsia
weight loss
vomiting/diarrhoea
abdominal pain
lethargy/confusion
fruity smell of acetone on breath
acidotic breathing (deep sighing)
dehydration
shock - tachycardia, hypotension, decreased consciousness, reduced urine output
79
Q

management of DKA

A
  • fluid replacement (correct hypotension, osmotic diuresis, electrolyte disturbance)
  • insulin (0.1 units/kg)
  • IV glucose (avoid hypoglycaemia, usually when glucose < 14 mmol/L, continue until normal eating/drinking)
79
Q

management of DKA

A
  • fluid replacement (correct hypotension, osmotic diuresis, electrolyte disturbance)
  • insulin (0.1 units/kg)
  • IV glucose (avoid hypoglycaemia, usually when glucose < 14 mmol/L, continue until normal eating/drinking)
80
Q

When to start a statin after QRISK3 assessment?

A

if the risk is > 10%