Ophthalmology Flashcards
Anatomy of the eye
Sclera white layer, goes all around and finishes at cornea
Iris is coloured, anterior chamber in front
Cornea is dome at the front (only bit covering the pupil)
Blood retinal barrier with tight junctions, so immune priveleged
Muscles of the eye and their innervation
Rectus muscles
- superior/inferior/lateral/medial
- superior and inferior tend to draw in medially
- medial, superior and inferior rectus - occulomotor nerve III
- lateral recuts - abducens nerve VI
Oblique
- superior/inferior
- allow rolling of eye when head to one side
- superior - down and out, intortion - trochlear nerve IV
- inferior - up and in, extortion - occulomotor nerve III
Light -> eye -> brain
Eye sees upside down image, visual cortex needs to convert
Need clear media to get light into retina - cornea, lens and vitreous fluid (so no blood supply to cornea, need nutrients from tears)
Light refracted at tear/air interface
Further refined at cornea through pupil by lens
Retina converts light signals to brain messages - by photoreceptors and supporting cells
Need muscles to align and coordinate
Need structures to protect and maintain (sclera, fascia, conjunctiva, lids)
Emmetropia
Myopia
Hypermetropia
Emmetropia = normal refraction Myopia = short sighted, eye too long Hypermetropia = long sighted, eye too short
Cataracts
‘A cataract is any congenital or acquired opacity in the lens capsule or substance, irrespective of effect on vision’
- but practically, ignore unless symptomatic
Can affect nucleus of lens, cortex of lens or back surface of lens
Presents - blurred vision worse on distance, glare, gradual onset, painless, monocular diplopia (double vision if just one eye)
Causes of cataracts
Mostly AGE - 70% of 70+yos
(lens made of multiple layers which are added to through life, accumulation of layers/metabolites -> opacity)
Also
- diabetes (glucose in aqueous humour, overhydrate lens, swell)
- trauma (direct penetrating/concussion/infrared)
- drug induced (steroids/chlorpromazine/gold)
- congenital (genetic/chromosomal/prenatal infection/metabolic/skeletal)
Cataracts surgery
Most common operation in UK
(may do both eyes in order to keep balance of short/long sightedness)
Involves removal of lens from capsule and replace with biometric artificial lens
Age related macular degeneration symptoms
Damage to retinal pigment epithelium (waste management zone)
Major cause of blindness
Symptoms
- loss of central vision
- metamorphosia (distortions in straight lines)
- change to colour vision
Age related macular degeneration - dry/wet
Dry form (atrophic)
- Atrophy of retinal pigment epithelium and cells immediately under and over it
- 90% of cases
- Progressive decline in vision over time, more metamorphopsia
- ‘Drusen’ - intracellular deposits
Wet form (exudative)
- Growth of underlying choroidal vessels, resulting in a neovascular membrane - new vessels leak and cause bleeds and fluid accumulation
- More acute and debilitating vision loss, more big spots knocked out due to haemorrhage
- 10% of cases
Risk factors and treatment for ARMD
Eye conditions- ARM, hypermetropia HTN, (not diabetes) Genetics Lifestyle Nutrition Anti-oxidants, obesity
Treat - anti-VGEF (vascular endothelial growth factor) injections, maybe monthly, to reduce existing vessels and stop new ones forming
+ glasses, low vision clinic, counselling (driving), support groups
Diabetic retinopathy and vasculopathy
Hyperglycaemia causes glycosylation of tissue proteins, small vessels disease
- Small vessel occlusion
- Increased permeability
- Neovascularisation following ischaemic tissue drive to compensate
See cotton wool spots
+ micro-aneurysms, exudates, oedema
+ retinal detachment in end stage disease
Should have yearly screening in T2DM (won’t necessarily get early symptoms but need early management)
Vascular occlusions
Sudden painless loss of vision, manifestation of underlying systemic disease
Arterial occlusion
- embolisation usually, or arteritis
- severity according to location
- cherry red spot over fovea (macula lost blood supply, fovea preserved)
- address underlying disease
Venous occlusion
- thrombosis in vessel lumen
- usually older age (if young consider SLE/myeloma etc)
- ‘clogged up’ looking retina with oedema and diffuse haemorrhage
- need anti-VGEF and laser
Hypertensive retinopathy
- only in very badly managed HTN (rare now)
- vasospastic reaction, then arteriosclerotic response
- macular star exudate, disc swelling, haemorrhage, exudate, cotton wool sports
- treat by managing HTN
Retinopathy of prematurity
Relative hypoxia intrauterine for retinal growth, so when premature birth into hyperoxic conditions, halts vascular growth
Eye continues to grow, so peripheral area of hypoxia, then compensatory pathological neovascularisation (fragile and leaky)
Risk of retinal detachment
Need laser therapy, or if severe then vitrectomy
Conjunctivitis
Mild-moderate pain, no vision loss
Can stain to see if corneal involvement
Bacterial or viral (very rarely fungal/amoebic)
Bacterial
- purulent, gunky
- unilateral
- staphylococcus/streptococcus
- broad spectrum topical abx (or oral if need be)
Viral
- less purulent/irritant, watery discharge
- bilateral
- much more contagious
- adenovirus/herpes simples/herpes zoster
- will go in 5 days ish (eye drops may help dry eye)
Keratitis
If involvement of cornea also (redness in sclera/conjunctiva, oedema around eye and discharge is just secondary)
More acute presentation in 24-48h
More painful, impacting vision earlier
May see fluid level of pus inside eye = hypopyon
Bacterial
- more acute, clearly demarcated lesion in cornea
- contact lens use associated
Viral
- more in older population
- herpes simples, herpes zoster, adenovirus
Fungal rare unless immunosupressed, or rotting vegetable contact with eye
Acanthamoeba if left contact lens in for several weeks, very agressive
Uveitis
Triad with reactive arthritis/spondyloarthropathies and urethritis (can’t see, can’t pee, can’t climb a tree) - Reiter’s Syndrome
Anterior uvea is inflamed (ciliary body and iris itself) becomes sticky and causes posterior synichae (so drags pupil as it dilates)
- deep boring pain
- photophobia
- decreased vision
- limbal injection (inflammation)
- see flare and cells floating in anterior chamber
- may get hypopyon
Need topical steroids, mydriatics. Systemic steroids/immunosupressant if very aggressive
Episcleritis
Common, self-limiting, frequently recurrent
Occasionally with underlying systemic disorder
- mild discomfort
- epiphora (watering)
- unilateral redness
Scleritis
Sectoral red eye (only one part) - cellular infiltration of entire thickness of sclera
Rarer than episcleritis, more serious
Systemic associations, maybe secondary to corneal ulcers/infections, may be post ocular surgery
- extremely painful, waking patient at night - deep boring
Acute angle closure glaucoma
Very high pressure, very painful (compression on optic nerve)
- acute unbearable pain (hard to locate?)
- haloes in vision, rings around lights
- reduced vision
- red eye
- corneal oedema
- fixed dilated pupil
Why?
- predisposed shallow anterior chamber (short eye, east asian)
- lens swelling from cataract
- feels funny for a while, then added strain (reading in low light), forces into closed angle then positive feedback to maintain
(chronic wide angle is when drainage interrupted but angle open)
Treat medically - acetazolamide + B blockers, pilocarpine - or surgically - laser iridotomy
Blepharitis
Infection of lid margins by staph bacteria + overproduction of sebum
- chronic ocular irritation
- watery red eye
- crusting and scaling of lash line
Malposition of lid
Entropion
- turning inwards of lid margin
- upper or lower eyelid
- corneal abrasions caused by lashes
- caused by age, conjunctival scarring, acute spastic
Ectropion
- turning outwards of lid margin
- lower eyelid
- exposed conjunctiva become inflamed, scarred, keratinised
- caused by age, conjunctival scarring, facial nerve palsy, large lower lid tumours
Topical steroids in red eye
NO
Can potentiate infection, need proper diagnosis
Don’t give as a GP
Ischaemic optic neuropathy
Optic nerve damaged if posterior ciliary arteries occluded by inflammation or arteriosclerosis
Pale swollen disc on fundoscopy
In temporal arteritis/GCA, with malaise, jaw claudication, tender scalp/temporal arteries
Central retinal artery occlusion
Dramatic vision loss in seconds
Afferent pupillary defect associated
Retina appears white, with cherry red spot at macula
May go with signs of atherosclerosis (often thromboembolic)
If occlusion longer than an hour, likely optic nerve will atrophy and cause blindness
Vitreous haemorrhage
Common in diabetics, bleeding disorders, retinal detachment, central retinal vein/branch vein occlusions
Expect spontaneous resorption by 3 months
Primary glaucoma
Primary open angle - chronic, blockage of trabecular meshwork
Primary angle closure - pupillary block, fluid builds in posterior chamber, iris pushed forward and angle narrows
- pain
- reduced vision, esp in centre
- nausea and vomiting maybe
(tend to be in long-sighted)
Secondary glaucoma
Traumatic - acute or chronic
Pseudoexfoliative - deposition of exfoliation material in anterior segment, drainage blockage
Neovascular glaucoma - new vessels over angle of iris, blockage of angle (secondary to diabetic retinopathy or central vein occlusion)
Normal tension glaucoma
Normal eye pressure, and yet structural and functional changes to nerve
- Optic neuropathy
- Open angle
- Absence of raised IOP
But treatment still tends to be lowering the pressure in the eye to below normal
Ocular hypertension
Higher than normal eye pressure, but no damage to optic nerve
(So not glaucoma - nerve normal, optic fields normal)
Normal is 11-21mmHg
Treat by decreasing eye pressure
- By drops
- By laser treatment
- By surgery
Eye assessment
Pachymetry - corneal thickness (IOP influencer)
Gonioscopy - iridocorneal angle, goniolens over slit lamp
Tonometry - to measure IOP, touch eye to indent and see pressure. Blue light and fluorescence, aligning semi circles.
Visual fields - temporal blind spot normal
Fundoscopy - to see optic disc - cup:disc ratio of 0.3-4 is normal, increased cup size = glaucoma
Eye drops
Decrease aqueous production
- Beta blockers (beware side effects) (timolol)
- Alpha agonists (brimonidine)
- Carbonic anhydrase inhibitors (acetazolamide)
Increase aqueous drainage
- Prostaglandin analogues (latanaprost - first line)
- Alpha agonists (brimonidine)
- Muscarinic stimulants (not used anymore as give headaches)
Can get combinations
Laser treatments
Peripheral iridotomy
- For closed angle glaucoma (to relieve fluid drainage)
Argon laser trabeculoplasty
- For open angle glaucoma
If failure of medications
Eye surgery
Last line after medical + laser management!
Goniotomy
- To open the abnormal angle
- Only for congenital, not adult glaucoma
Trabeculotomy
- To open Schlemm’s canal
- Only for congenital, not adult glaucoma
Trabiculetomy
- For adult and congenital glaucoma
- Drainage uncontrolled in trabeculotomy, pressure may drop too much. Need to put in a kind of valve with a flap in sclera
