Long term complications of diabetes Flashcards
Why does it take a long time for microvascular complications to develop?
Most cells are able to reduce glucose transport in response to extracellular hyperglycaemia
- retinal endothelial cells, mesagial cells of glomerulus, schwann cells and peipheral nerve cells
Microvascular complications take years to develop
- rate before 5 years of T1DM, may be detected at presentation of T2DM
Consider microvascular complications of DM
State an epidemiological finding of retinopathy
What are the common pathological findings? Why are these so detrimental to the retinal microcirculation
Second commonest cause of blindess in those of working age (>4000 in England)
- Reason why risk of blindess is 10-20x higher in DM
- Reason for increased glaucoma and cataracts)
PATHOLOGICAL FINDINGS
- Loss of pericytes
- Basement membrane thickening
- Capillary closure
- Ischaemia leading to VEGF production and increased capillary permeability
The retinal microcirculation contains a low density of capillaries (little functional reserve, flow needs to respond to local needs, pericytes key to local regulation of flow)
Consider microvascular complications of DM
What are the clinical stages of retinopathy
- Non-proliferate (background, pre-proliferative)
- Proliferative
- Macular oedema (sight threatening, non-sight threatening)
Consider microvascular complications of DM
How is retinopathy treated?
What factors need to be controlled?
Laser treatment (pan retinal, focal)
Intra-vitreal anti VEGF Ab
Diabetic control important as BP control
Consider microvascular complications of DM
State an epidemiological fact regarding neuropathy
How can it be further subdivided?
(Try and give symptoms)
- Affects up to 50% of DM patients, 15% have painful neuropathy
- Peripheral neuropathy (hands and feet mainly)
- e.g. neuropathic ulcer, callus, charcot foot (swelling)
- Signs/ symptoms: numbness, tingling, burning, sharp pain, increased sensitivity to touch, muscle weakness, loss of reflexes/ balance/ coordination - Mononeuropathy: damage to a specific nerve in face, torso or leg. Common in older adults with sudden and painful onset. May cause difficulaty focusing, double vision, aching behind 1 eye, Bell’s palsy
- Autonomic neuropathy
Symptoms: Gastroparesis, postural hypotension, erectile dysfunction, gustation, sweating, diarrhoea - Nephropathy
Consider microvascular complications of DM
Nephropathy is the commonest cause of end-stage renal disease in the western world. How responsible is it for the deaths of T1 and T2 DM patients?
What are the pathological findings of it?
How are these specific to the renal microcirculation?
T1DM- 21%; T2DM- 11%
- Basement membrane thickening (loss of negative charge)
- Podocyte loss
- Glomerular sclerosis
- Mesangial expansion
Renal microcirculation contains fenestrated glomerular capillaries, basement membrance and many specialised podocytes which manitain the integrity of filteration barrier
Consider microvascular complications of DM
Outline the clinical stages of nephropathy
How would you treat?
NORMOALBUMINUREA - negative dipstick
MICROALBUMINUREA (20-200ug/min) - negative dipstick
ALBUMINUREA (>200ug/min)- positive dipstick, declining GFR
Important to keep BP controlled (and glucose but less once proteinurea)
- RAAS blockers preferred
- Associated with increased CVD risk
- Ultimately need a kidney replacement/ transplantation
Consider macrovascular complications of DM
How does the risk differ between those with T1 and those with T2 DM?
State 3 modifiable risk factors
How might macrovascular disorders present?
Dramatic increase in risk with DM
- Patients with T2DM have mutiple Rx factors, patients with T1DM have long disease duration
Modifiable risk factors: BP, lipids, smoking (glucose control)
Presentation depends upon vascular bed affected: angina/MI, stroke, PVD
- DM commonest cause of non-traumatic lower limb amputation due to PVD, neuropathy, impaired leucocyte function (= DIABETIC FOOT)
