Pathogenesis: chronic hyperglycaemia glycosylation of
protein/basement membrane.
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Pathogenesis: chronic hyperglycaemia glycosylation of
protein/basement membrane loss of pericytes
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Pathogenesis: chronic hyperglycaemia glycosylation of
protein/basement membrane loss of pericytes reduced O 2 transport
tissue hypoxia
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Pathogenesis: chronic hyperglycaemia glycosylation of
protein/basement membrane loss of pericytes reduced O 2 transport
tissue hypoxia Microaneurysms
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Pathogenesis: chronic hyperglycaemia glycosylation of
protein/basement membrane loss of pericytes reduced O 2 transport
tissue hypoxia vaso-formative factors produced (TGF- &
VEGF)
Slide 15
Pathogenesis: chronic hyperglycaemia glycosylation of
protein/basement membrane loss of pericytes reduced O 2 transport
tissue hypoxia vaso-formative factors produced (TGF- & VEGF)
Neo-vascularisation
Slide 16
Pathogenesis: chronic hyperglycaemia glycosylation of
protein/basement membrane loss of pericytes reduced O 2 transport
tissue hypoxia vaso-formative factors produced (TGF- & VEGF)
Neo-vascularisation Haemorrhage / Scarring
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1.Haemorrhage
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2.Scaring
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new vessels new vessels grow on posterior vitreous face grow on
disc (NVD) grow in the periphery (NVE) grow on iris if ischaemia is
severe (NVI)
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(NVE)
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(NVD)
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( rubeosis iridis )
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The natural history of neovascularisation note lack of laser
treatment scars
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The natural history of neovascularisation note lack of laser
treatment scars
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The natural history of neovascularisation note lack of laser
treatment scars
Classification 1: retinopathy No retinopathy mild moderate
Severe Very severe proliferative retinopathy non-proliferative
retinopathy
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Classification 1: retinopathy No retinopathy mild moderate
Severe Very severe proliferative retinopathy non-proliferative
retinopathy laser observe / re-screen
Signs of non proliferative retinopathy microaneurysms / dot +
blot haemorrhages hard exudate cotton wool patches abnormalities of
venous calibre Intra-retinal microvascular abnormailities
(IRMA)
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mild non proliferative retinopathy microaneurysms +/or very
small blots only
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moderate non proliferative retinopathy microaneurysms dot +
blot haemorrhages venous calibre changes in only 1 quadrant
(1/4)
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severe non proliferative retinopathy Microaneurysms plus: >
4 per quadrant of dot + blot haemorrhages > 2 quadrants of
venous tortuosity/looping > 1 quadrant of IRMA 4,2,1 rule
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Very severe non proliferative retinopathy 2 of 4,2,1 rule
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Proliferative retinopathy New vessels disc (NVD) New vessels
elsewhere (NVE) Treated if you see laser scars; untreated if no
laser
Management of DR Medical Surgical laser laser vitrectomy
vitrectomy
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Risk factors Duration of diabetes HBP Hyperglycemia Smoking
Hyperlipidemia Pregnancy Weight Type 1 diabetes
Slide 54
Panretinal and macular photocoagulation were established as the
gold standard of treatment, supported by the data of the (ETDRS)
and the (DRS).
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A number of molecular mechanisms connect hyperglycemia to the
vascular damage,: protein kinase C (PKC), vascular endothelial
growth factor (VEGF).
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Percent of diabetic patients with retinopathy according to
duration of disease in patients under the age of 30 years who were
treated with insulin (primarily type 1 diabetes) and patients over
the age of 30 years who were not treated with insulin (primarily
type 2 diabetes). Retinopathy increased over time in both groups,
affecting virtually all patients with type 1 diabetes by 20 years.
The increased incidence in type 2 diabetes at three years is a
probable reflection of the difficulty in determining the time of
onset of that disease. Data from Klein, R, Klein, BE, Moss, SE, et
al, Arch Ophthalmol 1984; 102:520,527.
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Risk of sustained progression of retinopathy in patients with
type 1 diabetes according to the mean glycosylated hemoglobin
values at six-month intervals (green line). Better glycemic control
was associated with a lesser rate of progressive retinopathy. The
red lines represent the 95 percent confidence intervals. Data from
The Diabetes Control and Complications Trial Research Group, N Engl
J Med 1993; 329:977.
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Cumulative incidence of progressive retinopathy in patients
with type 1 diabetes and very mild to moderate nonproliferative
retinopathy who were treated with either conventional (dashed line)
or intensive (solid line) insulin therapy for nine years. There was
an increasing benefit of intensive therapy over time, although
intensive therapy was associated with transient worsening in the
first year (p