Microvascular and Macrovascular complications Flashcards

1
Q

What are examples of microvascular complications

A

Retinopathy

Nephropathy

Neuropathy

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2
Q

What are examples of macrovascular complications

A

Cerebrovascular disease

Ischaemic heart disease

Peripheral vascular disease

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3
Q

Explain the relationship of risk with rising HbA1c

A

Extent of hyperglycaemia (as judged by HbA1c) is strongly associated with the risk of developing microvascular complications

Target HbA1c to reduce risk of microvascular complications
= 53 mmol/mol (<7%)

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4
Q

How does hypertension increase complication risk

A

Clear relationship between rising systolic BP and risk of MI and microvascular complications in people with T1DM and T2DM

Therefore, prevention of complications requires reduction in HbA1c and BP control

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5
Q

What other factors are related to the development of microvascular complications

A

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

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6
Q

Describe the mechanism of damage

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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7
Q

Explain diabetic retinopathy

A

Main cause of
-visual loss in people with diabetes
-blindness in people of working age
The early stages of retinopathy are all asymptomatic, therefore screening is needed
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

What does a normal retina look like?

A

Optic disk (Bright white)

Macula - central, high resolution, colour vision (darker yellow)

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9
Q

What is background retinopathy?

A

Haemorrhages
Microaneurysms - red dots
Hard exudates (cheese colour, lipid)

Endothelial damage, leaking blood vessels

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10
Q

What is pre-proliferative retinopathy

A

Cotton wool spots aka Soft exudates, Represent retinal ischaemia

Haemorrhage

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11
Q

What is proliferative retinopathy

A

Visible new vessels
On disc or elsewhere in retina

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12
Q

What is maculopathy

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

How do you treat retinopathy and maculopathy?

A

Improve HbA1c, stop smoking, lipid lowering

good blood pressure control <130/80 mmHg

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14
Q

What to do for background retinopathy?

A

Continued annual surveillance

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15
Q

What to do for pre-proliferative retinopathy

A

If left alone will progress to new vessel growth

So, early panretinal photocoagulation

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16
Q

What to do for proliferative retinopathy

A

Panretinal photocoagulation

17
Q

What to do for diabetic maculopathy

A

Oedema: Anti-VEGF injections directly into the eye (VEGF: vascular endothelial growth factor)
Grid photocoagulation

18
Q

Why is diabetic nephropathy important

A

Associated with progression to end-stage renal failure requiring haemodialysis

Healthcare burden

Associated with increased risk of cardiovascular events

19
Q

What is pan-retinal photocoagulation?

A

Blast vessels with laser to stop them form bleeding or forming

Reduces peripheral vision

20
Q

How to diagnose diabetic nephropathy?

A

Progressive proteinuria (urine albumin:creatinine ratio - ACR)

Increased blood pressure

Deranged renal function (eGFR)

Advanced: peripheral oedema

21
Q

What test results indicate diabetic nephropathy

A

Microalbuminuria
>2.5 mg/mmol = early sign

Proteinuria = ACR > 30mg/mmol

Nephrotic Range > 3000mg/24hr

22
Q

What is the mechanism of diabetic nephropathy

A

Diabetes leads to hyperglycaemia / hypertension
This leads to glomerular hypertension
Leads to proteinuria
Leads to glomerular and interstitial fluids
Leads to glomerular filtration rate decline
Leads to renal failure

23
Q

Describe the renin-angiotensin system

A

Renin from the kidney converts angiotensinogen to angiotensin I
ACE converts angiotensin I to angiotensin II
Angiotensin II promotes release of aldosterone from adrenal cortex (zona glomerulosa) and vasoconstrictor

Very active in those with diabetic nephropathy

Angiotensin II acts via angiotensin receptors
ACE inhibitors (ACEi) are antihypertensives which block ACE
Angiotensin receptor blockers (ARBs) are antihypertensives which block angiotensin receptors

Blocking RAS 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

What is microalbuminuria a risk factor for?

A

Cardiovascular disease

25
How to manage diabetic nephropathy
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?
26
What is diabetic neuropathy
Diabetes mellitus is the most common cause of neuropathy and therefore lower limb amputation Small vessels supplying nerves are called vasa nervorum Neuropathy results when vasa nervorum get blocked Longest nerves supply feet – so more common in feet Commonly glove & stocking distribution – peripheral neuropathy Can be painful Danger is that patients will not sense an injury to the foot (eg. stepping on a nail)
27
What are the risk factors for diabetic neuropathy
-Age - Duration of diabetes - Poor glycaemic control - Height (longer nerves in lower limbs of tall people) - Smoking - Presence of diabetic retinopathy
28
Why do patients with diabetes needs an annual foot check
- Look for foot deformity, ulceration - Assess sensation (monofilament, ankle jerks) - Assess foot pulses (dorsalis pedis and posterior tibial)
29
Which patients are more at risk of foot ulceration
- reduced sensation to feet (peripheral neuropathy) - poor vascular supply to feet (peripheral vascular disease)
30
How to manage diabetic food disease
Peripheral neuropathy 1. Regular inspection of feet by affected individual 2. Good footwear 3. Avoid barefoot walking Podiatry and chiropody if needed Peripheral neuropathy with ulceration: Multidisciplinary diabetes foot clinic Offloading Revascularisation if concomitant PVD Antibiotics if infected Orthotic footwear Amputation if all else fails
31
What is a mononeuropathy
Usually, sudden motor loss eg wrist drop, foot drop Cranial nerve palsy double vision due to 3rd (oculomotor) nerve palsy 3rd nerve palsy Eye looks DOWN & OUT
32
What is autonomic neuropathy and what do patients present with?
Damage to sympathetic and parasympathetic nerves innervating GI tract, bladder, cardiovascular system GI tract - Delayed gastric emptying: nausea and vomiting (can make prandial short-acting insulin challenging) - Constipation / nocturnal diarrhoea Cardiovascular - Postural hypotension: can be disabling - collapsing on standing. - Cardiac autonomic supply: sudden cardiac death
33
What are the non modifiable risk factors for macrovascular disease
Age Sex Birth weight FH/Genes
34
What are the modifiable risk factors for macrovascular disease
Dyslipidaemia Hypertension Smoking Diabetes mellitus Central obesity
35
How to manage cardiovascular risk in Dm
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