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Endocrinology 2 > Micro and Macrovascular Complications > Flashcards

Micro and Macrovascular Complications Flashcards

1
Q

What are microvascular and macrovascular complications?

A

Micro: Nephropathy, neuropathy, retinopathy
Macro: Cerebravascular disease, Ischaemic Heart Disease, Peripheral vascular disease

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2
Q

What is 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 is 53mmol/L.

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3
Q

How does blood pressure contribute to 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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4
Q

What are 5 factors related to the development of microvascular complications?

A
  1. Duration of diabetes
  2. Smoking – endothelial dysfunction
  3. Genetic factors – some people develop complications despite reasonable glycaemic control
  4. Hyperlipidaemia
  5. Hyperglycaemic memory – inadequate glucose control early on can result in higher risk of complications LATER, even if HbA1c improved.
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5
Q

Describe the mechanism of damage

A

Hyperglycaemia and hyperlipidaemia lead to increased formation of mitochondrial superoxide free radicals in the endothelium. Leads to generation of glycated plasma proteins to form advanced glycation end products (AGEs). This leads to activation of inflammatory pathways. Endothelium then damaged leading to leaky capillaries and ischaemia.

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6
Q

Why is diabetic retinopathy screened for?

A

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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7
Q

What are the features of background retinopathy?

A 
Hard exudates (cheese colour, lipid)
Microaneurysms (“dots”)
Blot haemorrhages
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8
Q

What are features of pre-proliferative retinopathy?

A

Cotton wool spots also called soft exudates. Haemorrhages. Represent retinal ischaemia.

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9
Q

What is a feature of proliferative retinopathy?

A

Visible new vessels

On disc or elsewhere in retina

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10
Q

What are features of 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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11
Q

What are general treatment principles for retinopathies and specific for background retinopathy?

A

General: Good HbA1c, BP control, lipid lowering, stop smoking
Specific: Annual surveillance

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12
Q

How is pre-proliferative ret., prolif ret and maculopathy treated?

A

Pre-prolif: Can lead to development of new vessels so early panretinal photocoagulation
Prolif: panretinal photocoagulation
Maculopathy:
Oedema: Anti-VEGF injections directly into the eye (VEGF: vascular endothelial growth factor)
Grid photocoagulation

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13
Q

What is panretinal photocoagulation?

A

Thermal burns created on the retina causing tissue coagulation and overall improving oxygenation, reducing the hypoxia induced by capillary non-perfusion.

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14
Q

Why is diabetic nephropathy important?

A

Associated with progression to end-stage renal failure requiring haemodialysis. Is a healthcare burden and associated with increased risk of cardiovascular events.

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15
Q

How is nephropathy diagnosed?

A

Progressive proteinuria (urine albumin:creatinine ratio - ACR)
Increased blood pressure
Deranged renal function (eGFR)
Advanced: peripheral oedema

Microalbuminuria of >2.5mg/mmol is diagnosis
Proteinuria = ACR > 30mg/mmol
Nephrotic Range > 3000mg/24hr

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16
Q

Describe the mechanism of diabetic nephropathy

A

Hyperglycaemia and hypertension cause glomerular hypertension. Leads to proteinuria and then glomerular + interstitial fibrosis. GFR declines and finally leads to renal failure.

17
Q

How do hypertensives work?

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.

18
Q

What is the link between diabetic nephropathy and the renin-angiotensin system?

A

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.

19
Q

How is diabetic nephropathy managed?

A
  1. Tighter glycaemic control
  2. ACEi/ARB even if normotensive as soon as patient has microalbuminuria
  3. Reduce BP (aim <130/80 mmHg)
  4. Stop smoking
  5. Start an SGLT-2 inhibitor if T2DM?
20
Q

What is diabetic neuropathy?

A

Small vessels supplying nerves are called vasa nervorum. Neuropathy results when vasa nervorum get blocked.

21
Q

What are risk factors for diabetic neuropathy?

A
  • Age
  • Duration of diabetes
  • Poor glycaemic control
  • Height (longer nerves in lower limbs of tall people)
  • Smoking
  • Presence of diabetic retinopathy
22
Q

What are features of diabetic neuropathy?

A

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)

23
Q

What happens in the annual foot check for those with diabetes?

A
  • Look for foot deformity, ulceration
  • Assess sensation (monofilament, ankle jerks)
  • Assess foot pulses (dorsalis pedis and posterior tibial)
24
Q

Who has a risk of foot ulceration?

A

Those with:

  • reduced sensation to feet (peripheral neuropathy)
  • poor vascular supply to feet (peripheral vascular disease)
25
Q

How is peripheral neuropathy managed?

A
  1. Regular inspection of feet by affected individual
  2. Good footwear
  3. Avoid barefoot walking
  4. Podiatry and chiropody if needed
26
Q

How is peripheral neuropathy with ulceration managed?

A
  1. Multidisciplinary diabetes foot clinic
  2. Offloading
  3. Revascularisation if concomitant PVD
  4. Antibiotics if infected
  5. Orthotic footwear
  6. Amputation if all else fails
27
Q

What is mononeuropathy?

A

Usually, sudden motor loss eg wrist drop, foot drop. Cranial nerve palsy - double vision due to 3rd (oculomotor) nerve palsy.

28
Q

What is autonomic neuropathy?

A

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

29
Q

What are the symptoms when autonomic neuropathy affects the GI tract?

A
  • Delayed gastric emptying: nausea and vomiting (can make prandial short-acting insulin challenging)
  • Constipation / nocturnal diarrhoea
30
Q

What are the symptoms when autonomic neuropathy affects the cardiovascular system?

A
  • Postural hypotension: can be disabling - collapsing on standing.
  • Cardiac autonomic supply: sudden cardiac death
31
Q

What does treatment of macrovascular complications need to include?

A

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.

32
Q

What are the modifiable and non-modifiable risk factors for risk factors for macrovascular disease?

A

Non-modifiable: Age, Sex, Birth weight and FH/Genes

Modifiable: Dyslipidaemia, Hypertension, Smoking, Diabetes mellitus and Central obesity

33
Q

How can cardiovascular risk be managed with T2 DM?

A

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

Endocrinology 2 (11 decks)

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