Microvascular complications Flashcards
What are the sites of microvascular complications
Retinal arteries
Glomerular arterioles
Vasa nervorum
What are examples of microvascular complications
Severity of hyperglycaemia Hypertension Genetic Hyperglycaemic memory Tissue damage through originally reversible and later irreversible alterations in proteins
What is the mechanism of glucose damage
Hyperglycaemia leads to oxidative stress leading to inflammatory signaling cascades that lead to local activation of proinflam cytokines leading to inflammation leading to nephropathy/retinopathy/neuropathy
What are hard exudates
When proteins come out of the vessels - yellow and lipid rich
What happens if you don’t treat background retinopathy
Cotton wool spots aka soft exudates appear, and this represents retinal ischaemia
What happens in proliferative retinopathy
There are visible new vessels on the disk or elsewhere in the retina
What is seen in background diabetic retinopathy
Hard exudates, microaneurysms and blot haemorrhages
What is maculopathy
When there are hard exudates near the macula
What is especially bad in maculopathy
It can threaten direct vision
What is the background management of diabetic retinopathy?
Improve control of blood glucose and warn patients that warning signs are present
What is the management for pre proliferative retinopathy
It suggests general ischaemia so if left alone, will grow new vessels. It needs pan retinal photocoagulation
What is the management for proliferative retinopathy
It can bleed so needs pan retinal photocoagulation
What is the management of diabetic maculopathy
Fire laser to the macula as there is only problem here - only need a grid of photocoagulation
What can happen in diabetic nephropathy if not treated early on?
Progressively increasing proteinuria and deteriorating kidney function
What is diabetic nephropathy associated with
Hypertension and classic histological features
What are glomerular changes in diabetic nephropathy
- mesangial expansion
- basement membrane thickening (v important- cells become rigid affecting kidney)
- glomerulosclerosis
How many patients with T1DM will get diabetic nephropathy?
20-40% after 30-40 years
How many patients with T2DM will get diabetic nephropathy?
Similar to T1DM: 20-40% after 30-40 years however the likelihood depends on different factors
What affects the likelihood of a patient with T2DM developing diabetic nephropathy?
Age at development of disease (may die from heart attack before even getting a problem with nephropathy)
Racial factors
Age at presentation
Loss due to cardiovascular morbidity
What are clinical features of diabetic nephropathy
- progressive proteinuria
- increased BP
- deranged renal function
What are the different proteinuria ranges for normal, microalbuminuric, assymptomatic, and nephrotic
Normal: <30mg/24hrs
Microalbuminuric: 30-300mg/24hrs
Assymptomatic: 300-3000mg/24hrs
Nephrotic: >3000mg/24hrs
What are strategies for intervention for diabetic nephropathy
Diabetic control
Blood pressure control
Inhibition of the activity of RAS system
Stop smoking
Why is albumin also measured as well as GFR to detect renal disease
Because GFR can stay the same when microalbumin can be detected to go up and this is an early sign of a problem with kidneys and therefore increases chance for intervention
What are the negative effects of angiotensin 2
Vasoactive effects Mediation of glomerular hyperfiltration Increased tubular uptake of proteins Induction of pro fibrotic cytokines Stimulation of glomerular and tubular growth Podocyte effects Induction of pro inflammatory cytokines Generation of ROS & NF-kB Stimulates fibroblast proliferation Up regulation of adhesion molecules on endothelial cells Up regulation of lipoprotein receptors
