Systemic Disease In The Eye, and Retinal vascular disease Flashcards
Pathogenesis of thyroid eye disease?
Thought to be due to autoimmune response directed against TSH receptors and a T cell mediated response. There is GAG deposition behind the eye with production by fibroblasts stimulated by cytokine relapse from T cells e.g. TNF and IL-1 with a hyper osmotic shift causing oedema of both the orbital fat and extra ocular muscles.
Can occur in hyper/hypo/euthyroid patients, possibly presenting alongside other features of thyroid disease or before any other manifestations of thyroid disease present or even may be the only presentation of thyroid disease.
Can radioiodine be used in treating a patient with thyroid eye disease?
Only if inactive (fibrotic) phase of this disease otherwise the eye disease is worsened by radioiodine treatment.
Features suggesting optic neuropathy in thyroid eye disease?
Visual blurring Loss of visual acuity Visual field defects Impaired colour perception Relative afferent pupillary defect (RAPD)
Due to periorbital swelling, what might thyroid eye disease be initially misdiagnosed as?
Allergic conjunctivitis
But this will lack the reduced eye movements, lid retraction and blurred vision seen with TED.
Who should fully assess ocular movement and visual fields in a patient with suspected thyroid eye disease?
Orthoptist
How can the degree of proptosis in thyroid eye disease be measured and what is usually characteristic of the proptosis in thyroid eye disease?
Using a hertel exophthalmometer
Bilateral proptosis, in contrast to unilateral proptosis expected with a retrobulbar tumour.
General points to consider in managing thyroid eye disease?
MDT approach with endocrinologist and ophthalmologist and GP to refer early if identify sight threatening eye complications
Smoking cessation
Achieving and maintaining euthyroid state
Ocular lubricants if corneal exposure
Sleep propped up and avoid dusty conditions
Most commonly used medical therapy for moderate to severe active thyroid eye disease?
Corticosteroids, IV likely more effective
Rituximab may be given to steroid resistant patients
With sight threatening disease, need urgent orbital decompression surgery and IV steroids.
Poor prognostic factors in TED?
Male gender Older age at onset Smoker Diabetes Rapid progression at onset Longer duration of active disease Drop in visual acuity during active phase
How is hypertensive retinopathy linked to central vein of the retina occlusion, and how does the latter present on fundoscopy?
Grade 2 hypertensive retinopathy involves nipping of the venues at arterio-venous crossings, which is thought to be the pathology behind central vein of the retina occlusion.
Px: widespread haemorrhages over the retina, and hard exudates visible assoc. with grade 4 hypertensive retinopathy.
what 2 changes happen to the retinal capillary microcirculation to cause retinal vascular disease?
retinal capillary occlusion and leakage
retinal vascular leakage results in what?
retinal oedema due to fluid leakage from damaged vessels
haemorrhages due to blood leakage from damaged vessels
hard yellow exudates-result of lipid, lipoprotein and lipid-containing macrophage leakage, exudates have well defined margins.
retinal vascular occlusion results in what?
ISCHAEMIA:
cotton wool spots (soft exudates)-fluffy white focal lesions with indistinct margins, occurring at margins of an ischaemic retinal infarct due to axoplasmic flow obstruction and build up of axonal debris-scatters light causing white appearance, in nerve fibre layer of retina. readily seen close to optic disc due to thick nerve fibre layer here.
new blood vessel formation, including irregular retinal veins-vasogenic factors e.g. VEGF released from ischaemic retina, promoting new abnormal vessel growth, along with fibrous tissue onto retinal surface and forwards onto the vitreous. intravitreal vessels formed more permeable than normal, so leak dye in retinal fluorescein angiography. also abnormally located predisposing them to break and bleed.
what diseases affect the ocular circulation?
diabetic retinopathy hypertensive retinopathy central retinal artery occlusion branch retinal artery occlusion central retinal vein occlusion branch retinal vein occlusion retinopathy of prematurity sickle cell retinopathy abnormal retinal b.vessels
where do new blood vessels form due to ischaemia in diabetic retinopathy?
optic disc
elsewhere on the retina
iris-rubeosis iridis*
how does the prevalence of diabetic retinopathy differ between patients with type 1 and those with type 2 diabetes?
type 1: lower prevalence compared to type 2 within 1st 5 yrs of disease (17% vs. 30%), but after 15 yrs prevalence is greater in type 1 DM than in type 2 (97% vs. 78%)
so diabetic retinopathy more likely to be found at presentation in type 2 DM, but greater prevalence in type 1 DM after 15 years of the disease.
triggers to retinal capillary damage in diabetic retinopathy?
hyperglycaemia
HTN
pathogenesis of microvascular occlusion in diabetic retinopathy?
capillary non-perfusion (patchy closure of capillary network), leads to retinal ischaemia, causing development of AV shunts-opening up of pre-existing vessels?, and resulting in release of VEGFs stimulating neovascularisation on the optic disc, elsewhere on the retina and on the iris-proliferative retinopathy and rubeosis iridis.
factors thought to be important in diabetic retinopathy development?
duration of diabetes
poor glycaemic control
HTN
hyperlipidaemia
nephropathy-protein loss in urine, causes decreased oncotic pressure and increased capillary leakage in retina
pregnancy-known can accelerate retinopathy-this is especially in those with poor glycaemic control during preg, at conception or postpartum, if severe baseline retinopathy, if DM has been present for a long time, if HTN and even if rapid improvement of diabetic control so be wary of too rapid a decrease in HbA1c increasing microvascular changes.
less consistent association with smoking, alcohol, obesity and lack of physical activity.
ocular diseases associated with DM?
retinopathy
cataract-increased frequency and earlier age of onset of age related cataract, and a rare ‘snowflake’ cataract in youth
glaucoma-rubeotic glaucoma, ?link with chronic simple glaucoma
EO muscle palsies due to microvascular disease of 3rd, 4th and 6th cranial nerves.
features of diabetic maculopathy?
this may coexist with other stages of diabetic retinopathy
hard exudates and haemorrhages within macular region, and/or evidence of retinal oedema, and/or evidence of retinal ischaemia.
Vision is reduced
SIGHT-THREATENING
what visual problems associated with advancement of proliferative diabetic retinopathy?
vitreal haemorrhage- can often be resorbed allowing vision to resolve but each bleed leads to vitreal fibrosis, causing the retina to contract inwards-vtireo-retinal traction, which can lead to the neuroretina being pulled from its overlying pigment epithelium-retinal detachment-irreversible visual damage, may complain of shade over their vision. can be repaired with vitrectomy?
iris new b.vessel formation-rubeosis iridis-can precipitate acute angle closure glaucoma-rubeotic glaucoma-new b.vessel growth in angle of anterior chamber causing fibrosis and closure.
treatment threshold for diabetic maculopathy?
clinically significant macula oedema-may be thickening of the retina and hard exudates found within specific distance of fovea.
assessment is with slit lamp examination, but haemorrhages over macula with fundoscopy is an important finding.
