Microvascular Complications of Diabetes Mellitus Flashcards
State the three main sites of microvascular complications.
- Retinal arteries (retinopathy)
- Glomerular arterioles (nephropathy)
- Vasa vasorum (neuropathy)- tiny blood vessels that supply nerves
What factors correlate with risk of microvascular and macrovascular complications?
- Glycaemic control (HbA1c)
- Hypertension
- Hyperglycaemic memory - poor diabetes control even briefly will give an increased risk
- Genetics
- Tissue damage - through originally reversible and later irreversible alterations in proteins
Describe the mechanism of glucose damage to blood vessels.
Hyperglycaemia leads to oxidative stress and hypoxia
This triggers an inflammatory cascade, which leads to damage
What instrument is used to look into the eye?
Fundoscope
Where is the optic disc relative to the macula on the back of the eye?
The optic disc is nasal to the macula
What are the 4 types of diabetic retinopathy?
- Background
- Pre-proliferative
- Proliferative
- Maculopathy
What three features do you see in background diabetic retinopathy?
- Hard exudates
- Microaneurysms - small blood vessels bulge
- Blot haemorrhages - blots of blood
What are hard exudates caused by?
Leakage of lipid contents makes the back of the eye look a cheesy colour
Describe pre-proliferative diabetic retinopathy.
Soft exudates (cotton wool spots)
What do soft exudates indicate?
Retinal ischaemia
Describe proliferative diabetic retinopathy.
Involves the formation of visible new vessels (in response to retinal ischaemia) on disc or elsewhere in retina
The new vessels are generally more fragile and can bleed at any time
Describe maculopathy.
Presence of hard exudates in the macula
This is the same disease as background diabetic retinopathy, it’s just that the hard exudates are in the macula
This can threaten direct vision
What are the steps taken in managing background diabetic retinopathy?
Improve blood glucose control
What is the treatment for pre-proliferative and proliferative diabetic retinopathy?
-suggests general ischaemia so to stop it progressing
need Pan-retinal photocoagulation (laser to retina)
Describe the treatment of maculopathy.
You need a grid of photocoagulation in the affected area (aim to limit damage to the macula so you don’t do pan-retinal photo coagulation)
State some histological glomerular features of diabetic nephropathy.
- Mesangial expansion
- Basement membrane thickening
- Glomerulosclerosis (hardening of the capillaries)
- if there is no retinopathy, any CKD cannot be due to diabetes, these come together
In diabetic nephropathy you get over production of matrix. What can this be caused by?
Effects of prolonged exposure to high glucose or glycosylated proteins
A rise in pressure within the glomerular capillaries
Angiotensin II
State 3 clinical features of diabetic nephropathy.
- Hypertension
- Progressively increasing proteinuria
- Progressively deteriorating kidney function
What is the normal range for proteinuria?
< 30 mg/24hr
Why do patients with diabetic nephropathy get oedematous?
Increased proteinuria means that they are losing albumin through their urine
This decreases serum albumin hence decreases the osmotic potential of the plasma so less fluid is drawn back into the circulation
Describe some strategies for intervention of patients with diabetic nephropathy.
- Improve blood glucose control
- the lower the Hb1ac, the lower the microvascular complications - Blood pressure control
- control of blood pressure will slow down the deterioration of kidney function - Inhibition of the activity of the renin-angiotensin system
- Stopping smoking
What effect does angiotensin II have on endothelial cells?
It makes endothelial cells more rigid
Where is renin produced?
Juxtaglomerular apparatus
What can stimulate renin release?
Low renal perfusion (i.e. low blood pressure)
