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brs (phase 1b) > (endo) microvascular and macrovascular complications of diabetes mellitus > Flashcards

(endo) microvascular and macrovascular complications of diabetes mellitus Flashcards

1
Q

define microvascular (complications of diabetes)

A

long-term complications that affect small blood vessels

e.g. neuropathy, nephropathy, retinopathy

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2
Q

define macrovascular (complications of diabetes)

A

long-term complications that affect large blood vessels

e.g. cerebrovascular disease, ischaemic heart disease, peripheral vascular disease

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3
Q

what increases the risk of developing microvascular complications of diabetes?

A

1) extent of hyperglycaemia i.e. HbA1c levels

2) rising systolic BP and risk of MI

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4
Q

what are the target HbA1c levels to reduce the risk of microvascular complications?

A

53 mmol/mol

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5
Q

how do increasing HbA1c levels affect microvascular complications of diabetes?

A

= increase risk of microvascular complication in the following order

1) retinopathy
2) nephropathy
3) neuropathy
4) microalbuminuria

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6
Q

prevention of microvascular complications in diabetes requires reduction in which two parameters mainly?

A

1) HbA1c

2) blood pressure

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7
Q

besides HbA1c and BP, which factors increase the risk of developing microvascular complications?

A

1) (longer) duration of diabetes
2) smoking
3) genetic factors
4) hyperlipidaemia
5) hyperglycaemic memory

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8
Q

explain the link between duration of diabetes and risk of developing microvascular complications

A

the longer a patient has had diabetes + associated hyperglycaemia, the more likely they are to develop microvascular complications

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9
Q

explain the link between hyperlipidaemia and risk of developing microvascular complications

A

the greater the levels of hyperlipidaemia, the greater the risk of developing microvascular complications of diabetes

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10
Q

explain the link between smoking and risk of developing microvascular complications

A

smoking causes endothelial dysfunction

= increased risk of microvascular complications

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11
Q

explain the link between genetic factors and risk of developing microvascular complications

A

some individuals may be genetically prone to developing microvascular complications despite having reasonable glycaemic control

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12
Q

what is hyperglycaemic memory?

A

the idea that individuals with a period of past poor glycaemic control may have caused irreversible damage in such a way that increases the risk of complications

(despite the chance that the patients may NOW have good glycaemic control)

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13
Q

explain the link between hyperglycaemic memory and risk of developing microvascular complications

A

inadequate glucose control in the past can result in a higher risk of complications, even if HbA1c is improved now

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14
Q

how does hyperglycaemic memory come about?

A

periods of hyperglycaemia (poorly controlled)
= can cause epigenetic modifications
= increase the risk of complications

(does not matter if HbA1c is improved/better controlled now)

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15
Q

briefly explain the mechanism of damage in terms of microvascular complications

A

hyperglycaemia + hyperlipidaemia
= oxidative stress
= increased formation of mitochondrial superoxide free radicals in the endothelium
= activation of inflammatory signalling cascade
= inflammation + endothelial damage

= leaky capillaries, ischaemia (+ retinopathy, nephropathy, neuropathy)

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16
Q

why are the effects of persistent hyperglycaemia long-lasting?

A

poorly-controlled persistent hyperglycaemia causes long-lasting epigenetic modifications
= persistent expression of pro-inflammatory genes
= even if HbA1c is better controlled now, there is always an increased risk of complications

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17
Q

what is diabetic retinopathy?

A

a microvascular complication of diabetes that causes damage to the vessels supplying the retina

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18
Q

what is diabetic retinopathy the main cause of?

A
  • visual loss in people w diabetes

- blindness in people of working age

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19
Q

why is annual retinal screening essential in people with diabetes?

A

patients are usually asymptomatic in the early stages of diabetic retinopathy

= SO, screening is essential to identify + treat it early while treatment is still possible and before visual loss/blindness

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20
Q

what are the possible stages of diabetic retinopathy?

A
  • background retinopathy
  • pre-proliferative retinopathy
  • proliferative retinopathy
  • maculopathy
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21
Q

what are the characteristic features of background retinopathy?

A
  • hard exudates (cheese colour, as a result of lipid leakage)
  • microaneurysms
  • blot haemorrhages
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22
Q

why do hard exudates form in background retinopathy?

A

inflammation of the vessels supplying the retina
= leads to leaky capillaries
= lipid leakage

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23
Q

what are the characteristic features of pre-proliferative retinopathy?

A
  • soft exudates (i.e. cotton wool spots)

= form due to retinal ischaemia

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24
Q

what occurs in pre-proliferative retinopathy that leads to the formation of soft exudates?

A

retinal ischaemia

due to endothelial dysfunction as a result of inflammation of the retinal capillaries

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25
Q

what are the characteristic features of proliferative retinopathy?

A
  • formation of new blood vessels (visible)
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26
Q

why does angiogenesis occur in proliferative retinopathy?

A 
inflammation of the retinal capillaries
= endothelial dysfunction
= retinal ischaemia
= hypoxia
= compensatory angiogenesis
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27
Q

what is the implication of angiogenesis in proliferative retinopathy?

A

the new vessels that form in the retina as part of the compensatory angiogenesis are very weak + friable

= prone to rupture
= increased risk of haemorrhages

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28
Q

what are the characteristic features of maculopathy?

A
  • hard exudates (cheese colour, lipid leakage, oedema)
  • blot haemorrhages, microaneurysms

= same disease as background retinopathy BUT happens to be near the macula
= threatens vision

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29
Q

why is maculopathy particularly dangerous?

A

= same disease as background retinopathy w hard exudates, oedema and haemorrhages BUT happens to be near the macula
= site of CENTRAL VISION
= so, maculopathy threatens vision

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30
Q

how is background retinopathy treated?

A

1) improve HbA1c + lipid levels, stop smoking
2) good blood pressure control of < 130/80 mmHg
3) CONTINUED ANNUAL SURVEILLANCE

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31
Q

how is pre-proliferative retinopathy treated?

A

1) improve HbA1c + lipid levels, stop smoking
2) good blood pressure control of < 130/80 mmHg
3) EARLY PANRETINAL PHOTOCOAGULATION

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32
Q

why is panretinal photocoagulation commonly done for patients with pre-proliferative retinopathy?

A

to prevent progression onto proliferative retinopathy

i.e. formation of new, friable blood vessels

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33
Q

how is proliferative retinopathy treated?

A

1) improve HbA1c + lipid levels, stop smoking
2) good blood pressure control of < 130/80 mmHg
3) PANRETINAL PHOTOCOAGULATION

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34
Q

how is diabetic maculopathy treated?

A

1) improve HbA1c + lipid levels, stop smoking
2) good blood pressure control of < 130/80 mmHg
3) anti-VEGF injections for oedema
4) GRID PHOTOCOAGULATION

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35
Q

why are anti-VEGF used to treat diabetic maculopathy?

A

in diabetic maculopathy, fluid build-up + swelling in the retina (oedema)

= so anti-VEGF reduce the thickening of the macula and improve vision

36
Q

what is panretinal photocoagulation?

A

the preferred form of treatment for proliferative retinopathy

= wherein a laser is used to burn through the layers of the retina to prevent the formation of new blood vessels
= reducing the risk of haemorrhages

37
Q

why is diabetic nephropathy important?

A
  • associated with progression to end-stage renal failure requiring haemodialysis
  • associated with an increased risk of cardiovascular events

= healthcare burden

38
Q

which parameter is measured to assess renal function in patients w diabetes?

A

ACR (urine albumin-creatinine ratio)

39
Q

what is the earliest hallmark of diabetic kidney disease?

A

microalbuminuria

i.e. >2.5mg/mmol loss of protein

40
Q

what are the features of more advanced diabetic kidney disease?

A
  • increased blood pressure (i.e. hypertension)
  • deranged renal function (eGFR)

very advanced:
- peripheral oedema (due to fluid imbalance)

41
Q

list the progressive stages of protein loss in diabetic nephropathy

A

1) microalbuminuria (>2.5 mg/mmol)
2) proteinuria (>30 mg/mmol)
3) nephrotic syndrome (>3000mg/24hr) = extremely rare

42
Q

what are the parameters for microalbuminuria in diabetic nephropathy?

A

ACR of >2.5mg/mmol

43
Q

what are the parameters for proteinuria in diabetic nephropathy?

A

ACR of >30mg/mmol

44
Q

what are the parameters for nephrotic syndrome in diabetic nephropathy?

A

proteinuria greater than 3000mg/24 hours

= extremely rare but very large amounts of protein are lost in the urine

45
Q

explain the mechanism of diabetic nephropathy briefly

A 
hypertension + hyperglycaemia
= glomerular hypertension
= endothelial damage
= proteinuria
= glomerular/interstitial fibrosis
= GFR declines
= renal failure
46
Q

briefly summarise the RAAS system

A
  • angiotensinogen (produced in the liver) is converted into angiotensin I by renin (released from the renal JGA)
  • angiotensin I is converted into angiotensin II by ACE (produced in the liver)
  • angiotensin II then acts on the zona glomerulosa of the adrenal cortex to stimulate aldosterone production
47
Q

what are ACE inhibitors?

A

anti-hypertensives that inhibit the lung enzyme, ACE and prevent conversion of angiotensin I into angiotensin II

= reducing aldosterone production
= reducing hypertension

48
Q

briefly summarise how ARBs work

A

ARB = angiotensin receptor blocker

49
Q

how are people at risk of diabetic nephropathy most commonly managed?

A
  • block RAAS with
    1) ACE inhibitor (-pril)
    2) ARB (-sartan)

= reduces blood pressure + progression of diabetic nephropathy

50
Q

what measure must be taken to manage patients with diabetes that have microalbuminuria/proteinuria?

A

must be either on an ACEi/ARB even if normotensive
= as a precautionary measure

(no benefit to simultaneous intake)

51
Q

in patients w diabetes, what is microalbuminuria a risk factor for?

A

development of cardiovascular disease

people w microalbuminuria = increased risk of stroke, MI etc

52
Q

list the ways in which diabetic nephropathy is managed

A
  • aim for tighter glycaemic control
  • reduce BP to < 130/80
  • start ACEi/ARB if microalbuminuria (even if normotensive)
  • stop smoking

(- start SGLT-2 inhibitor if T2DM?)

53
Q

what is diabetic neuropathy and how does it occur?

A

the blood vessels supplying the nerves are termed the vasa vasorum

when the vasa vasorum are damaged as a result of diabetes, nerve functioning can consequently be impaired
= neuropathy

54
Q

what can diabetic neuropathy lead to?

A

lower limb amputation

diabetes mellitus is the most common cause of neuropathy which can lead to LLA

55
Q

what are the wider implications of diabetic neuropathy?

A

impaired nerve function

= lack of pain sensation + lack of wound sensation

56
Q

what are the risk factors of diabetic neuropathy?

A
  • age
  • smoking
  • height
  • duration of diabetes
  • poor glycaemic control
  • presence of diabetic retinopathy
57
Q

how is the duration of diabetes a risk factor for diabetic neuropathy?

A

the longer the patient has had diabetes, the greater the time they have been exposed to hyperglycaemia

= greater potential for more damage

58
Q

how is height a risk factor for diabetic neuropathy?

A

in the limbs of tall people, there are longer nerves
= more prone to damage
= greater/wider implications if they are damaged

59
Q

how is diabetic retinopathy a risk factor for diabetic neuropathy?

A

the presence of microvascular disease somewhere in the body increases the risk of the same elsewhere in the body

60
Q

what regions of the body are most commonly affected by diabetic neuropathy?

A

1) glove + stocking distribution = most commonly, peripheral neuropathy
2) longest nerves affected (i.e. the ones that supply the feet)

61
Q

explain why diabetic neuropathy is commonly painful

A

damage to the blood vessels supplying nerves
= impaired nerve function
= lack of pain/wound sensation
= more prone to not realising when they are injured
= greater scope for infection

(+ reduced healing ability due to poor/impaired blood supply to the region)

62
Q

why are patients w diabetes at risk of foot ulceration?

A

1) reduced sensation to feet (due to peripheral neuropathy)

2) reduced healing due to poor vascular supply (peripheral vascular disease)

63
Q

how is the risk of diabetic foot reduced?

A

all people w diabetes = annual foot check

64
Q

what does the annual foot check for people w diabetes consist of?

A
  • look for foot deformity/ulceration
  • assess sensation (monofilament, ankle jerks)
  • assess foot pulses (dorsalis pedis, posterior tibial)
65
Q

why do people w diabetes have poor healing rates for wounds?

A

poor vascular supply due to damage to the blood vessels

= reduced ability to heal wounds

66
Q

how is peripheral neuropathy managed?

A
  • regular inspection of feet by affected individuals
  • good footwear
  • avoid barefoot walking
67
Q

how is peripheral neuropathy with ulceration managed?

A
  • MDT foot clinic
  • revascularisation (if PVD)
  • orthotic footwear
  • antibiotics
  • amputation, if all else fails
68
Q

why are flip flops & socks risky for people who may develop diabetic foot disease?

A

1) flip flops = open-toed so increased risk fo damage + debris
2) socks = increased risk of blister formation

69
Q

define mononeuropathy

A

when damage occurs to a single nerve

= that can cause individual pain, numbness or sudden loss of movement (e.g. wrist/foot frop)

70
Q

give an example of a mononeuropathy

A

oculomotor nerve palsy (i.e. 3rd nerve palsy)

= cranial nerve palsy that can cause diplopia

71
Q

what is autonomic neuropathy?

A

damage to sympathetic and parasympathetic nerves innervating GI tract, bladder, cardiovascular system

72
Q

what are the implications of autonomic neuropathy on the GI tract?

A
  • delayed gastric emptying
  • vomiting + nausea (can make post-prandial short-acting insulin a problem)
  • constipation/nocturnal diarrhoea
73
Q

what are the implications of autonomic neuropathy on the cardiovascular system?

A
  • postural hypertension (can be disabling i.e. collapsing on standing)
  • cardiac autonomic supply impaired = sudden cardiac death
74
Q

list the possible macrovascular complications of diabetes

A
  • ischaemic heart disease
  • peripheral vascular disease
  • cerebrovascular disease
75
Q

how is macrovascular disease prevented and why?

A

need to target and aggressively manage MULTIPLE risk factors

76
Q

why is it inefficient to target only hyperglycaemia when managing macrovascular complications?

A

targeting only hyperglycaemia = minor effect of increased cardiovascular

= so to target the CVR as effectively as possible, = need to address multiple risk factors

77
Q

how does the presence of T1DM affect CVR?

A

the presence of T1DM increases cardiovascular risk + mortality

78
Q

what are the non-modifiable risk factors for macrovascular complications in diabetes?

A
  • age
  • sex
  • birth weight
  • family history/genetics
79
Q

what are the modifiable risk factors for macrovascular complications in diabetes?

A
  • diabetes mellitus
  • hypertension
  • dyslipidaemia
  • smoking
  • central obesity
80
Q

list five ways in which cardiovascular risk is managed in diabetes mellitus

A

1) reduce/control blood pressure
2) control lipid profile

3) weight loss
4) stop smoking

5) annual urine microalbuminuria screen

81
Q

what is the desired blood pressure in patients w diabetes?

A

normally <140/80 mmHg

but if MICROVASCULAR complications in patient then <130/80 mmHg

82
Q

what is the desired lipid profile in patients w diabetes?

A

total cholesterol < 4

LDL < 2

83
Q

how is weight managed in patients w diabetes?

A
  • lifestyle interventions

- pharmacogloical interventions

84
Q

why is an annual urine microalbuminuria screen recommended for patient w diabetes?

A

microalbuminuria is a risk factor for cardiovascular disease

85
Q

what is the biggest risk associated with neuropathy?

A

risk of foot ulceration with peripheral neuropathy

86
Q

what is the biggest risk associated with nephropathy?

A

associated w cardiovascular risk

microalbuminuria

brs (phase 1b) (71 decks)

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