Chronic Vascular Complications Flashcards

1
Q

What are the vascular complications of diabetes

A

Retinopathy, nephropathy, neuropathy

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2
Q

What are the microvascular complications

A

Diabetic retinopathy, nephropathy, neuropathy, amputation

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3
Q

What are the macrovascular complications

A

CHD, ischaemic stroke, congestive heart failure

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4
Q

How long does it take for the manifestation of vascular complications of diabetes to occur

A

5-10 years

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5
Q

How does glucose alter angiogenesis in retinopathy

A

Protective angiogenesis altered due to high glucose. New blood vessel formation in the retina are abnormal - more fragile and delicate. More prone to bleeding. Can get retinal detachment

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6
Q

What is the pathogenesis of retinopathy

A

Hyperglycaemia and chronic inflammation leads to local inflammation -> elevated levels of vascular endothelial GF -> angiogenesis with elevated vascular permeability -> haemorrhage. Vascular damage leads to macular oedema -> visual loss

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7
Q

What occurs in the pre-proliferative phase of retinopathy

A

Basement membrane thickening
Micro-aneurysm formation (microvessel dilatation secondary to peripheral loss of pericytes -> venous statis -> focal proliferation of capillary endothelial cells)
Micro-aneurysm complication: in vessel permeabiltiy with accumulation of exudate and haemorrhage due to rapture
Vascular occlusions: ischaemic lesion with alteration of normal vessel permeability - cotton wool spots = small infarct within the nervous fibre layer)

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8
Q

What occurs in the proliferative phase of retinopathy

A

New vessel formation anterior to the retina on its inner surface within vitreous
Traction of new vessels with haemorrhages formation
Retinal detachment

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9
Q

What is diabetic nephropathy a major cause of

A

End stage renal failure (stage IV)
Microalbuminuria/proteinuria
Increase risk of CVD

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10
Q

How does the RAAS system work in diabetes

A

RAAS over-activated. Drives oxidative stress, inflammation and hypoxia
AGII key effector molecules driving vasoconstriction, increase in aldosterone, efferent constriction, PT reabsorption

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11
Q

What drugs are first line in hypertensive treatments

A

ACE inhibitors and angiotensin receptor blockers

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12
Q

How is GFR affected by diabetes

A

Progressive fibrosis drive by cytokine, GFR starts to fall
More proteinuria occurs
As proteinuria occurs - px has lost 505 of renal function

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13
Q

What are the severe debilities in neuropathy

A

Neuropathic pain, autonomic failure, contribution to diabetic foot ulceration

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14
Q

What are the generalised sensory neuropathies

A

Painful: distal, burning pain at night. Parastheisa/hyperasthesia
Painless: asymptomatic sensory loss, impaired light touch/vibration/temperature
Absent reflexes
Autonomic dysregulation - warm skin, bounding pulses

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15
Q

What are the autonomic neuropathies

A

CV: resting tachycardia, postural hypertension, risk of cardiac arrhythmias/sudden death
GI: gastroparesis, autnomic diarrhoeas
Genitourinary: bladder dysfunction, erectile dysfunction

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16
Q

What is the screening procedure of diabetes

A
Urine tests: ACR over 3 mg/mmol sign of nephropathy
BP
eGFR
Cholesterol
Smoking status
Retinal photography
Foot check
Done at least once a year
17
Q

How can risks be reduced for diabetes

A
Glycaemic control: new insulins, new oral agents, CBG testing
BP control
ACE inhibitors/SGLT2 antagonist 
Cholesterol control
Smoking cessation