Station 5 Flashcards
(285 cards)
Signs of optic atrophy
- RAPD (constricts when shine light to normal pupil, dilates when shine light on abnormal pupil)
Signs of causes
- Cupping of disc: glaucoma
- Retinitis pigmentosa
- Central retinal artery occlusion: cherry red macula + milky fundus
- Foster-Kennedy syndrome (frontal tumour): optic atrophy in one eye = tumour compression; papilloedema in other eye = raised ICP)
Causes of absent red reflex
Red reflex = reflection of light from back of eye
Absent = opacity in ocular media (cornea, lens, aqueous and vitreous humour)
- Cataract
- Vitreous haemorrhage
Acronym for which lobe corresponds to which quadrantopia
PITS
- Parietal inferior
- Temporal superior
An important cause of absent pupillary response
- Glass eye!
Causes of sudden vision loss
Will always be vascular or trauma
- Vitreous haemorrhage
- Retinal artery occlusion
- Retinal vein occlusion
- Haemorrhagic (‘wet’) age-related macular degeneration
- Stroke
Causes of altitudinal visual field defect (upper/lower visual field loss)
- Branch retinal artery occlusion
- Anterior ischaemic optic neuropathy
Causes of vitreous haemorrhage
Bleeding into vitreous (clear jelly between retina and lens)
- Diabetic retinopathy = most common
- Trauma
- Retinal detachment
Features of vitreous haemorrhage
- Sudden vision loss
- Cobwebs in vision
- Absent red reflex
- Photopsia (bright lights in peripheral vision)
Pathogenesis of diabetic retinopathy
- Vascular occlusion –> VEGF release –> new vessels
Diabetic retinopathy and pregnancy
- Progresses rapidly in pregnancy
- Diabetic pregnant ladies need to be reviewed once a trimester for retinopathy
Stages of diabetic retinopathy
Mild/moderate non-proliferative = background retinopathy:
- Microaneurysms (dots)
- Blot haemorrhages
Severe/very severe non-proliferative = pre-proliferative
- Cotton wool spots (infarcts)
- Venous dilation/beading
- Intraretinal microvascular abnormalities (IRMA) = branching/dilation of existing vessels in retina
Proliferative retinopathy
- New vessels
Treatment for diabetic retinopathy
- Mild/moderate: annual Diabetic Retinopathy Screening Service
- Pre-proliferative/maculopathy: Ophthalm referral within 3months
- Proliferate: Ophthalm referral within 2weeks
- Pan-retinal photocoagulation (lasers applied to 4 quadrants of retina)
- Do as many sessions until new vessels start to regress
- Side effects: reduced night vision/visual field loss
Pathogenesis of diabetic maculopathy
- Oedema from leaking capillaries
- And/or ischaemia due to capillary loss
Features of diabetic maculopathy
- Central vision loss (due to macular oedema)
Indications for laser treatment in diabetic maculopathy
- Retinal thickening within 500μm of fovea (centre of macula)
- Exudates within 500 μm of the fovea, if associated with adjacent retina thickening
- Retinal thickening >1 disc area, any part of which is within 1 disc diameter of the fovea
(won’t be expected to detect retinal thickening in exam!)
Features and inheritance mode of retinitis pigmentosa
- Age 10-30, symptoms progress over years–> registered blind by 40s
- Night vision loss
- Peripheral vision loss
- Severe: central vision and colour vision loss
Can be many different modes of inheritance so ask for family history (usually autosomal recessive)
Loss of peripheral vision vs loss of central vision
Peripheral vision loss
- Retinitis pigmentosa (constricted fields)
- Glaucoma (constricted)
- Laser photocoagulation (constricted)
- Ischaemic optic neuropathy (unilateral)
- Stroke (homonymous)
Central vision loss
- Diabetic maculopathy
- Age-related macular degeneration
- Optic neuropathy (demyelinating/nutritional)
- Cataract
Syndromes associated with retinitis pigmentosa
- Usher syndrome: sensorineural deafness = most common
- Alport Syndrome: abnormal glomerular basement membrane–> nephrotic syndrome (defect in collagen)
- Kearns–Sayre syndrome (mitochondrial disease): progressive ophthalmoplegia, cardiac conduction defect (PACEMAKER)
- Refsum disease (excess phytanic acid): scaly skin, cerebellar ataxia, peripheral neuropathy, cardiomyopathy
Investigations for retinitis pigmentosa
- Automated perimetry (visual fields)
- Electroretinogram: reduced amplitude
- Optical coherence tomography: retinal atrophy
- Genetic analysis: especially X-linked recessive
Management of retinitis pigmentosa
- Mainly supportive: register as blind to get benefits/reduced TFL costs
- Luxturna = gene therapy for biallelic RPE65 mutations
- Vitamin A may slow progression
Mitochondrial inheritance comes from which parent
- Mother as all mitochondrial in embryo come from the egg
Features of optic atrophy
- PAINLESS loss of central vision
- RAPD
- 3rd nerve palsy (inflammatory/compressive affects CNIII)
- INO if MS
- Speed of progression depends on cause
Causes of optic atrophy
Sudden = ischaemic
- Embolic
- Giant Cell Arteritis!!
Subacute = demyelination
- MS
- Neuromyelitis optica
Gradual
- Compressive tumour: optic nerve glioma, frontal meningioma (at anterior cranial fossa), pituitary macroadenoma (compresses optic chiasm)
- Nutritional: B12, alcohol
Investigations for optic atrophy
- Visual-evoked potentials: assess optic nerve function and differentiate from retinal disease (evoked potentials will be delayed and reduced amplitude)
- Automated perimetry
- CT brain + orbits with contrast