Diabetic Retinopathy Flashcards
Explain the pathology of microvascular complications.
Thickening of the capillary and arteriole basement membrane is the cardianl feature of microvascular complications.
The small vessels become progressively narrower and they will eventually become blocked.
This leads to ischaemia and tissue dysfunction.
The tissues that are damaged by hyperglycaemia are those that have high blood flow and cannot down-regulate glucose uptake.
Explain the formation of advanced glycation end products (AGE).
When some proteins are exposed to increased glucose the glucose will bind irreversibly and cause an advanced glycation end product called AGE.
Give an example of AGE.
HbA1c.
Consequences of formation of AGEs.
They cause tissue injury and inflammation via stimulation of pro-inflammatory factors, such as complement and cytokines.
Explain hyperglycaemia and the sorbitol-polyol pathway.
When there is excess glucose, the glucose is metabolised to sorbitol via the polyol pathway.
Issues with increased orbitol and fructose via the sorbitol-polyol pathway.
The accumulation of sorbitol and fructose causes changes in vascular permeability, cell proliferation and capillary structure.
Explain abnormal microvascular blood flow in hyperglycaemia.
Along with hypertension endothelial damage occurs and vasoconstrictors such as endothelins and thrombogenesis can lead to microvascular occlusions.
Growth factors and cytokines in diabetes.
Due to the increased expression of protein kinase C mitogenic cytokines and growth factors including TGF-beta, tumour necrosis factor and vascular endothelial growth factor (VEGF) are upregulated.
Explain the growth hormone-insulin-like growth factor axis in diabetes.
Reduction in portal insulin concentrations impairs the ability of growth hormone to generate IGF-1 in the liver.
This leads to growth hormone hypersecretion by the pituitary gland.
Which in its turn can cause microvascular complications.
What is the most common diagnosed diabetes-related complication?
Diabetic retinopathy
Affects around one third of all people with diabetes.
What are the earliest changes in the retina in diabetic retinopathy called?
Non-proliferative or background retinopathy.
What are the retinopathy grades of the peripheral retina?
Non-proliferative (R1)
Pre-proliferative (R2)
Proliferative (R3)
Advanced retinopathy
What is central retinopathy called?
Maculopathy
What retinal abnormalities can be seen in non-proliferative/background retinopathy (R1)?
Dot haemorrhages (microaneurysms)
Blot haemorrhages
Hard exudates (lipid deposits)
Expain dot aneurysms/haemorrhages.
Damage to the wall of small vessels causes microaneurysms within the retina.
Explain blot haemorrhages.
When the vessel walls are breached, superficial (blot) haemorrhages occur in the ganglion cell and outer plexiform layers.
Explain the hard exudates.
When the fluid is cleared into the retinal vessels from the blot haemorrhages, proteins and lipid deposits are left, they are seen as hard exudates.
They will eventually be removed by macrophages.
Explain cotton wool spots.
Micro-infarcts within the retina due to occluded vessels cause cotton wool spots.
It is actually a swelling of the retinal nerve fibres.
This leads to accumulation of axoplasmic debris.
Explain cytoid bodies.
The axoplasmic debris from the cotton wool spots are cleared by macrophages.
White dots will appear at the previous cotton wool spots which are called cytoid bodies.
Can the retinal abnormalities seen in R1 heal?
Yes, they can all heal.
What retinal abnormalities can be seen in pre-proliferative retinopathy (R2)?
Cotton-wool spots (infarcts)
Cytoid bodies
Venous beading/loops
Intraretinal microvascular abnormalities (IRMAs)
Multiple deep and round haemorrhages.
Refer to specialist
Explain venous beading and loops.
Damage to the walls of veins causes their calibre to vary. This is called venous beading.
Elongation also occurs due to the damage, causing elongation aka venous loops.