Vascular complications of DM Flashcards

(41 cards)

1
Q

what are the microvascular complications of diabetes mellitus?

A

retinopathy
nephropathy
neuropathy

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2
Q

what are the macrovascular complications of diabetes mellitus?

A

cerebrovascular disease
ischaemic heart disease
peripheral vascular disease

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3
Q

Is extent of hyperglycaemia (as judged by HbA1c) associated with the risk of developing microvascular complications?
What is the target HbA1c to reduce risk of microvascular complications?
Name another factor that increases this risk

A

Yes, strongly
53mmol/mol (<7%)
Clear relationship between rising systolic BP and risk of MI and microvascular complications in people with T1DM and T2DM

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4
Q

what are the other risk factors (besides HbA1c) for complications of diabetes?

A

Hyperlipidaemia
Duration of diabetes
Hyperglycaemic memory – inadequate glucose control early on can result in higher risk of complications LATER, even if HbA1c improved
Smoking – endothelial dysfunction
Genetic factors – some people develop complications despite reasonable glycaemic control

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5
Q

Mechanism of damage of hyperglycemia leading to microvascular complications

A

Increased formation of mitochondrial superoxide free radicals in the endothelium
Generation of glycated plasma proteins to form advanced glycation end products (AGEs)
Activation of inflammatory pathways
Damaged endothelium results in
‘Leaky’ capillaries
Ischaemia

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6
Q

COmplications of diabetic retinopathy

A

Main cause of
visual loss in people with diabetes
blindness in people of working age

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7
Q

how do we aim to detect retinopathy?
What is the aim of this?
How is this acheived in the UK

A

through screening as early stages are asymptomatic
Aim of screening - to detect retinopathy EARLY when it can be treated before it causes visual disturbance / loss
Annual retinal screening in the UK for all diabetes patients

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8
Q

describe the appearance of a normal retina

A

optic disk bright spot visible
thin veins semi visible
macula densa visible

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9
Q

describe background retinopathy?

A

hard exudates (cheese colour, lipid)
microaneuyrsms (dots)
blot haemorrhages
enhanced blood vessels

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10
Q

describe pre proliferative retinopathy

A

Cotton wool spots also called soft exudates
Represent retinal ischaemia
More extensive haemorrhage

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11
Q

describe proliferative retinopathy

A

new vessels visible (on disc or elsewhere in retina)

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12
Q

describe maculopathy retinopathy

A

Hard exudates / oedema near the macula
Same disease as background, but happens to be near macula
This can threaten vision

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13
Q

General treatments to reduce risk of retinopathy

A

Improve HbA1c, stop smoking, lipid lowering,
good blood pressure control <130/80 mmHg

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14
Q

how do you treat background retinopathy?

A

you can’t.
annual surveillance
lifestyle changes

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15
Q

how do you treat pre proliferative retinopathy

A

If left alone will progress to new vessel growth
So, early pan-retinal photocoagulation

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16
Q

how do you treat proliferative retinopathy?

A

panretinal photocoagulation

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17
Q

how do you treat diabetic maculopathy?

A

Oedema: anti-VEGF injections directly into eye
grid photocoagulation

18
Q

what are the risks of panretinal photocoagulation?

A

loss of some peripheral vision due to burns

19
Q

Why is treating diabetic nephropathy improtant?

A

Associated with progression to end-stage renal failure requiring haemodialysis (healthcare burden)
Associated with increased risk of cardiovascular events

20
Q

how do you diagnose diabetic nephropathy?

A

urinalysis (microalbuminuria >2.5mg/mmol proteinuria (ACR>30mg/mmol), nephrotic range (>3000mg/24hr))
increased blood pressure
eGFR (deranged)

21
Q

what is the mechanism of diabetic nephropathy?

A

hypertension & hyperglycaemia–>glomerular hypertension–>progressive proteinuria (urine ACR)–> glomerular &interstitial fibrosis
glomerular filtration rate decline (eGFR)
renal failure
Advanced: peripheral oedema

22
Q

What receptors does angiotensin II bind to?
Name2 classes of antihypertensives. What does each block?

A

Angiotensin II acts via angiotensin receptors
ACE inhibitors (ACEi) are antihypertensives which block ACE
Angiotensin receptor blockers (ARBs) are antihypertensives which block angiotensin receptors ((on adrenal cortex and vasculature))

23
Q

Benefits of blocking RAAS with an ACEi/ ARB?
when are antihypertensive treatments prescribed?
Is it beneficial to have both an ACEi/ARB simultaneously

A

Blocking RAAS with an ACE inhibitor (‘-pril) or angiotensin 2 receptor blocker (ARB, ‘-sartan’) reduces blood pressure & progression of diabetic nephropathy
All diabetes patients with microalbuminuria/proteinuria should have an ACEi/ARB even if normotensive
No benefit to having both ACEi/ARB simultaneously

24
Q

how is nephropathy managed?

A

Aim for tighter glycaemic control
ACEi/ARB even if normotensive as soon as patient has microalbuminuria
Reduce BP (aim <130/80 mmHg) usually through ACEi or A2RB
Stop smoking
Start an SGLT-2 inhibitor if T2DM?

25
What is the most common cause of neuropathy/ lower limb amputation?
Diabetes mellitus is the most common cause of neuropathy and therefore lower limb amputation
26
when does diabetic neuropathy occur?
when vasa nervorum get blocked (blood vessels supplying nerves)
27
what are the risk factors of diabetic neuropathy?
age duration of diabetes poor glycaemic control height (longer nerves in lower limbs of tall people) smoking prescence of diabetic retinopathy
28
where is most common for diabetic neuropathy to show?
Longest nerves supply feet – so more common in feet Commonly glove & stocking distribution – peripheral neuropathy
29
Is diabetic nephropathy painful? What is the danger of diabetic nephropathy?
Can be painful Danger is that patients will not sense an injury to the foot (eg. stepping on a nail)
30
what is included in annual foot checks?
inspection for foot deformity, ulceration assess sensation (monofilament, ankle jerks) assess foot pulses (dorsalis pedis, posterior tibial)
31
when is the risk of ulceration highest?
- reduced sensation to feet (peripheral neuropathy) - poor vascular supply to feet (peripheral vascular disease)
32
Management of peripheral neuropathy without ulceration
1. Regular inspection of feet by affected individual 2. Good footwear 3. Avoid barefoot walking Podiatry and chiropody if needed
33
what is the management of peripheral neuropathy with ulceration?
multidisciplinary diabetes foot clinic offloading revascularisation if concomitant PVD antibiotics if infected orthotic footwear amputation if needed
34
presentation of mononeuropathy
usually sudden motor loss (foot drop, wrist drop) cranial nerve palsy - double vision due to 3rd nerve palsy
35
what is autonomic neuropathy?
damage to sympathetic & parasympathetic nerves innervating GI tract, bladder, CV system
36
GI effects of autonomic neuropathy
delayed gastric emptying which can lead to nausea and vomiting (makes prandial short acting insulin hard) constipation/nocturnal diarrhoea
37
how is the CV system affected by autonomic neuropathy?
postural hypertension (collapsing on standing, can be disabling) cardiac autonomic supply causing sudden cardiac death
38
What effect does treatment targeted to hyperglycemia alone have on risk of macrovascular complications? What does this mean?
Treatment targeted to hyperglycaemia alone has minor effect on increased risk of cardiovascular disease Prevention of macrovascular disease requires aggressive management of multiple risk factors
39
what are the non-modifiable risk factors for macrovascular complications of DM?
age sex birth weight FH/genetics
40
what are the modifiable risk factors for macrovascular complications of DM?
dyslipidaemia hypertension diabetes mellitus smoking central obesity
41
how is CV risk in DM managed?
Smoking status – support to quit Blood pressure < 140/80 mmHg, < 130/80 mmHg if microvascular complication (NB often needs multiple agents) Lipid profile – total chol <4, LDL <2 Weight – discuss lifestyle intervention +/- pharmacological treatments Annual urine microalbuminuria screen – risk factor for cardiovascular disease.