Endo - Diabetes microvascular complications Flashcards
(37 cards)
State the three main sites of microvascular complications?
- Retinal arteries (Retinopathy)
- Glomerular arteries (nephropathy)
- Vasa vasorum (neuropathy)
What factors correlate with risk of microvascular and macrovascular complications?
- Glycaemic control (HbA1c)
- Hypertension
Describe the mechanism of glucose damage to blood vessels?
- Hyperglycaemia leads to oxidative stress and hypoxia
- This triggers an inflammatory cascade which causes damage
What instrument is used to look into the eye?
A fundoscope
Where is the optic disc relative to the macula on the back of the eye?
The optic disc is nasal to the macula - more medial
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
- Blot haemorrhages
What are hard exudates caused by?
Leakage of lipid contents
Describe pre-proliferative diabetic retinopathy?
- Soft exudates
- Some haemorrhages
What do soft exudates indicate?
Retinal ischaemia
Describe proliferative diabetic retinopathy?
- Involves formation of new vessels (in response to retinal ischaemia)
- New vessels are fragile and can bleed at any time
Describe maculopathy?
- Presence of hard exudates on the macula
- Same as background diabetic retinopathy just with hard exudates on the macula
- Threatens 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?
Pan-retinal photocoagulation:
Slows the growth of new blood vessels by laser burning the retina
Describe the treatment for maculopathy?
A grid of photocoagulation in the affected area - limit to area affected to prevent pan-retinal photocoagulation
State some histological features of diabetic nephropathy
- Mesangial expansion
- Basement membrane thickening
- Glomerulosclerosis (hardening of capillaries)
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
- Progressive proteinuria
- Increased blood pressure
- Deranged renal function
What is the normal range for proteinuria?
< 30mg/24hr
Why do patients with diabetic nephropathy get oedematous?
- Increased proteinuria means 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 levels
- Blood pressure control
- Inhibition of the activity of the renin-angiotensin system
- Smoking cessation
What effect does angiotensin II have on endothelial cells?
It makes endotheial cells more rigid
Where is renin produced?
Juxtaglomerular apparatus
What can stimulate renin release?
Low renal perfusion (Low blood pressure)