L18 - Long term Diabetic Complications Flashcards
Microvascular complications (3)
Retinopathy
Nephropathy
Neuropathy
Macrovascular complications (3)
IHD
CVD
PVD
Mechanism of microvascular complications
Most cells are able to reduce glucose transport in response to extracellular hyperglycaemia
Cells involved in microvascular complications
Retinal endothelial cells
Mesangial cells of glomerulus
Schwann cells and peripheral nerve cells
These 3 types of cells cannot control how much glucose is transported into the cell
How many years can it take for microvascular complications to arise?
Many years
Rare before 5 years of type 1
May be detected at presentation of type 2
Retinopathy prevalence and risk
Second commonest cause of blindness in those of working age
4000+ in England blind from diabetic retinopathy
Risk of blindness increased 10-20 fold by DM
Glaucoma and cataract increased
What is retinopathy?
Destruction of the retinal cells
The retinal microcirculation
Low density of capillaries
- little functional reserve
- flow needs to respond to local needs
- pericytes key to local regulation of flow
Pathological findings of diabetic retinopathy
Loss of pericytes
Basement membrane thickening
Capillary closure
Ischaemia
- VEGF production
- Increased capillary permeability
Clinical stages of retinopathy
Non-proliferative
- background
- pre-proliferative
Proliferative
Muscular oedema
- sight threatening
- non sight threatening
What is important to control in diabetic retinopathy?
Diabetic control
Blood pressure control
Treatments available for diabetic retinopathy
Laser treatment
- pan retinal
- focal
Intra-vitreal anti VEGF Ab
Prevalence of Neuropathy
Affects up to 50% of diabetic patients
15% have painful neuropathy (cf 5% non-diabetic population)
Types of neuropathy
Peripheral neuropathy
Mononeuropathy
Autonomic neuropathy
(Entrapment neuropathy increased)
Peripheral neuropathy
Affects hands and feet - numbness
Features of peripheral neuropathy
Neuropathic ulcer
Callus
Charcot foot
Mononeuropathy definition
Only a single nerve is damaged
e.g. only one eye affected
Autonomic neuropathy
Gastroparesis
Postural hypotension
Erectile dysfunction
Gustatory sweating
Diarrhoea
Nephropathy prevalence
Commonest cause of ESRD in Western world
Accounts for deaths of 21% of type 1 and 11% of type 2 patients
The renal microcirculation
Fenestrated glomerular capillaries
Basement membrane
Highly specialised podocytes
Pathological findings of diabetic nephropathy
Basement membrane thickening
-loss of negative charge
Podocyte loss
-loss of integrity of filtration barrier
Glomerular sclerosis
Mesangial expansion
Clinical stages of diabetic nephropathy
Normoalbuminuria
-dipstick negative
Microalbuminuria (20-200ug/min or 30-300mg/24hrs)
-dipstick negative
Albuminuria (>200ug/min or >300mg/24hrs)
- dipstick positive
- declining GFR
Diabetic nephropathy
BP control important
Blockers of RAS system preferred
Glucose control important but less so once overt proteinuria
Associated with increased CVD risk
Ultimately renal replacement/transplantation
Microvascular disease
Dramatic increase in risk with diabetes
Patients with type 2 diabetes have multiple RFs
Patients with type 1 diabetes have long disease duration
Presentation depends upon vascular bed affected
- angina/MI
- stroke
- PVD
