Ophthalmology Flashcards
P Uvea=
iris + ciliary body + choroid
Production and flow of aqueous humour
Produced by posterior ciliary body, travels through pupil to anterior chamber. Trabeculum and Cansl of Schlemm take back to venous system.
Maintain 10-21mmHg normal pressure on the eye
Differentials for painful loss of vision
GCA, unveitis, keratitis, conjunctivitis, acute angle glaucoma
Differentials for painless loss of vision
Retinal detachment, vitreous haemorrhage, retinal artery occlusion, anterior ischemic optic neuropathy
Red flags for visual loss
Headache (do an ESR if over 50)
Eye movements painful (optic neuritis)
Lights or flashes preceding visual loss (retinal detachment)
“like a curtain descending” (amaurosis fungax, preceding peripheral vision loss)
Poorly controlled DM (virtuous haemorrhage)
Central retinal artery occlusion appearance on fundoscop
Pale retina, macula has cherry red spot. Attenuated blood vessels.
Sudden painless loss of vision, fundoscopy shows many flame haemorrhages in all quadrants: Diagnosis?
Central retinal vein occlusion
Risks for retinal detachment
pathological myopia
Trauma
Previous retinal detachment
Intraocular surgery
Unilateral swelling of optic disc differentials
NIGHT TIC
Neuritis
Infectious
Granulomatous
Hereditary
Toxic
Traumatic
Infiltrative
Compressive
Papilloedema differentials
=see bilateral swelling of optic disc specifically due to raised ICP
Space occupying lesion
Idiopathic intracranial hypertension
Obstructive hydrocephalus
Venous sinus thrombosis
Differentials for gradual loss of vision
glaucoma
AMD
cataracts
Diabetic and hypertensive retinopathy
open angle glaucoma
increased resistance to aqueous outflow leads to slow and Insidious rise in intraocular pressure. May have decreased visual fields and acuity.
Fingins: High IOP
Incteased cup to disc ratio
Scotoma, peripheral field loss, Central sparing
Management of open angle glaucoma
Prostaglandin analogues (reduce aqueous humor production)
Beta blockers
Acute angle glaucoma
Lens pushes against iris, closed angle blocks aqueous drainage. Acute rise in intraocular pressure -> red, painful eye, photophobia, N&V, red haloes
Cloudy cornea and middilated sluggish pupils
Risks for acute angle glaucoma
Hypermetropia
DM
Trauma
Indian ethnicity
Management of acute angle glaucoma
Urgently reduce IOP: IV acetazolamide, pilocarpine and beta blocker
Then laser iridotomy
Age-related macular degeneration fundoscopy
Yellow spots around macular = drusen, dry AMD, build up of deposits between retinal pigment epithelium and Brooke’s membrane
If haemorrhagic look = wet AMD
Symptoms of AMD
Metamorphopsia, blurred vision, Central scotoma, visual fluctuation
Most common cause of irreversible visual loss on developed world
Risk factors for AMD
Age
Smoking
Cardiovascular disease
Cataract surgery
Caucasian ethnicity
Family history
Cataracts presentation
clouding of lens in different layers, leads to gradual painless loss of vision, glare
Stage I Keith Wagener classification of hypertensive retinopathy
Arteriolar narrowing and tortuosity. Incr light reflex - silver wiring
Stage II Keith Wagener classification of hypertensive retinopathy
Arterio-venous nipping
Stage III Keith Wagener classification of hypertensive retinopathy
Cotton wool exudates
Flame and blot haemorrhages
Stage IV Keith Wagener classification of hypertensive retinopathy
Papilloedema
Fearures of anterior uveitis
Acute onset
Ocular discomfort and pain (may incr w use)
Pupil may be small and possibly irregular due to sphincter muscle contraction
Photophobia
Lacrimation
Red eye
Blurred vision
Ciliary flush (ring of red spreading out)
Hypopyon (pus and inflammatory cells in anterior chamber, often visible fluid level)
Visual acuity initially normal but becomes impaired
Anterior uveitis associations
Ankylosing spondylitis
Reactive arthritis
IBD
Behcet’s disease
Sarcoidosis
Management of anterior uveitis
Cycloplegics to dilate pupil, eg atropine
Steroid eye drops
Pathophysiology of diabetic retinopathy
Hyperglycemia leads to increased retinal blood flow, abnormal metabolism in vessel walls. Therefore there is damage to the endothelial cells and pericytes, so increased vascular permeability and formation of exudates; retinal ischaemia and so neovascularisation; pericyte dysfunction and so micrpaneurysms
Mild non proliferative diabetic retinopathy
1+ microaneurysm
Moderate non proliferative diabetic retinopathy
Microaneurysms, blot haemorrhages, hard exudates, cotton wool spots, venous beading/looping
Severe non proliferative diabetic retinopathy
Blot hemorrhages and microaneirysms in four quadrants
Venous bleedijg in at least 2 quadrants
Intraretinal microvasculature abnormal in at least 1 quadrant
Proliferative diabetic retinopathy
Retinal neovascularisarion (may lead to vitreous haemorrhage)
Fibrous tissue anterior to retinal disc
More common in DM 1
30% blind in 5 years
Maculopathy
Located in the macula so any pathology is more serious
Hard exudates and other background change
Check visual acuity
More common in DM2
Management of non proliferative diabetic retinopathy
Optimize glycaemic control
Control BP
Control hypelipidaemia
Regular ophthalmology review
If severe consider panretinal laser photocoagulation
Management of proliferative diabetic retinopathy
Optimize glycaemic control
Control BP
Control hypelipidaemia
Regular ophthalmology review
Panretinal lazer photocoagulatiom
VEGF inhibitor
Pilocarpine in acute angle glaucoma
Direct parasympathomimetic
Increases vitreous outflow
Timolol in acute angle glaucoma
Beta Blocker
Decreases aqueous humor production
Apraclonidine in acute angle glaucoma
Alpha2 agonist
Blepharitis
Inflammation of eyelid margins, causes red eye
Entropion and ectropion
EN= inturned eyelids
EC= outturned eyelids
