Gradual Visual Loss Flashcards
how does dry ARMD present
gradual vision loss
bilateral central vision loss with maintenance of peripheral vision
o/e atrophic macula
can dry ARMD be treated
no treatment only prevention helps
visual aids and register as blind
what is a cataract
opacification of the lens
state the causes of cataract
congenital - must be treated within 4 weeks of birth
age
metabolic - diabetes and hypertension
smoking and alcohol
describe the vision loss seen in cataract
gradual vision loss - difficulty reading signs and recognising faces
what is seen with a cataract on examination
loss of red reflex
opaque lens
how is cataract treated
phaecoemulsification + intraocular lens implant
what are the complications of cataract surgery
glaucoma
anterior uveitis
retinal detachment
endophthalmitis
what is glaucoma
group of disorders leading to progressive optic nerve damage and visual loss
raised IOP is a feature but not diagnostic
list the triad of changes that occur in glaucoma
visual field defect
raised IOP
optic disc cupping
how does raised IOP arise
backflow of aqueous humour in the anterior chamber of the eye damaging retinal fibres in the optic disc
what is the normal range for intraocular pressure
10-22mmHg
what are the visual field defects seen in glaucoma
defect starts in the periphery causing crescent shape
central vision and acuity is maintained until late stages of disease
what is optic disc cupping
optic disc is the pale part of disc where there are no neurones, the optic disc increases in size in glaucoma due to damage of the nerve fibres and the size of the cup increases
what is the normal ratio of the optic disc
0.4-0.7
anything >0.7 is suggestive of glaucoma
how does chronic closed angle glaucoma present
asymptomatic therefore needs picked up through screening
visual field defect, raised IOP and optic disc cupping are observed
what is the outline of management of glaucoma
aim to reduce production of aqueous humour or increase the drainage of it
what drugs are used to treat glaucoma
topical prostaglandins
topical beta-blockers and alpha agonists
carbonic anhydrase inhibitors such as acetazolamide
acute angle closure glaucoma is an emergency true/false
true
what is the pathophysiology of acute angle closure glaucoma
rapid build up of IOP, iris is pushed against the trabecular meshwork blocking AH flow out of the anterior chamber
how does acute glaucoma present
sudden painful vision loss
blurred vision
haloes around light
headache, nausea and vomiting
what are the examination findings of acute glaucoma
hazy cornea
hard tense eye
fix mid-dilated pupil
how is glaucoma investigated
slit lamp
genioscopy to assess anterior chamber
how is acute glaucoma treated
IV acetazolamide first line to reduce IOP
trabeculectomy can be carried out once IOP has reduced
which factors within diabetes increase risk of developing diabetic retinopathy
pregnancy
long duration of disease
poor glycaemic control
how does retinopathy develop within diabetes
glycosylation of proteins leads to formation of microaneurysms and reduces oxygen transport causing ischaemia
ischaemia congests vessels causing neovascularisation leading to leakage and haemorrhage
outline the retinal changes seen in diabetic retinopathy
hard exudates - lipoprotein
cotton wool spots
dot blot and flame haemorrhages
what is the difference between non-proliferative and proliferative retinopathy
non-proliferative does not have neovascularisation of vessels yet, less severe forms
what are the features of maculopathy seen in retinopathy
macular oedema
blot haemorrhages
hard exudates
how is retinopathy managed
cannot reverse changes only prevent further damage through tighter glycaemic control
outline the stage of retinopathy and the screening time for each
R0 no retinopathy - 12 month R1 mild - 12 months R2 background - 6 months R3 referable - refer to oph R4 proliferative - refer to oph
