Opthal conditions Flashcards
OPEN ANGLE GLAUCOMA PATHOPHYS
i) what is glaucoma? what is it caused by?
ii) where is the anterior chamber of the eye found? where is the posterior chamber found? what are they filled with and what does this do?
iii) what produces aqueous humour? where does it flow after this? (2) where does it exit tthe eye?
iv) what is normal intraocular pressure? what is the pressure created by?
v) what happens to pressure of aqueous humour in open angle glaucoma? what is this due to?
vi) what happens to the iris in acute angle closure glaucoma? how quick does this need to be treated?
i) glaucoma = optic nerve damaged
caused by a signif rise in intraocular pressure due to blockage of aq humour trying to escape eye
ii) ant chamber - between the cornea and iris
post chamber - between lens and iris
both ant and post are filled with aq humour that supplies nutrients to the cornea
iii) aq humour produced by the cililary body
aq then flows from cil body around the lens and under the iris > anterior chamber > trabecular network into canal of schlemm where it exits the eye
iv) normal pressure - 10-21mmHg created by resistance to flow through trabecular network into canal of schlemm
v) OAG - there is a gradual increase in resistance through the trabecular network > harder for aq hum to flow through the meshwork and exit the eye
pressure builds up slowly > chronic onset glauu
vi) in acute angle closure glaucoma - iris bulges forward and seals off the trabecular meshwork therefore aq cant drain away > build up pressure > opthal emergency
OPEN ANGLE GLAUCOMA
i) what is the optic cup? what does increased pressure in the eye cause to the optic disk? what is classed as abnormal in relation to the optic cup?
ii) name three RF
iii) who is OAG usually dx by? what type of vision is usually affected first? what can happen eventually? name three other ways that it may present?
iv) name two ways intra ocular pressure can be measured? what does each involve? which is gold standard?
i) optic cup is a small indent in the optic disk (shoulld be less than half the size)
increased pressure causes the indent to be larger = cupping (>0.5 size of optic disc is abnormal)
ii) RF - increasing age, FH, black ethnic origin, nearsightedness (myopia)
iii) asymp for a long time due to gradual bup of pressure > dx by routine screening with optometrist
affects peripheral vision first > gradual closure of periph vision until tunnel vision is seen
can also px with fluctuating pain, headache, blurred vision and halos appearing around lights
iv) measure intraoc pressure with non contact telemetry (shoots puff of air at cornea and measure corneal response) - less accurate
goldmaann applanation tonometry - mount device on slit lamp > contacts cornea and applies diff pressures to accurate measure pressure = gold standard
DX/MX OF OPEN ANGLE GLAUCOMA
i) what can be used to check intra occ pressure? what can be used to check for optic disc cupping/optic nerve health?
ii) what can be assessed to check for periph visual loss?
iii) what does mx aim to do? when is tx usually started? what is given first line?
iv) how does first line tx work? name two SEs? name three other tx options
v) what is a trabeculectomy? when is it offered? what does it do?
i) goldmann applanation tonometry to check pressure
fundoscopy to check optic disk cupping and optic nerve health
ii) visual field assessment to check for periph vision loss
iii) mx aims to reduce extraocular pressure
start tx at pressure of 24+
first line - prostaglandin analogue eye drops eg latanaprost
iv) latanaprost - increase uveoscleral outflow (SE are increased eyelash growth and eyelid/iris pigmentation)
other tx (all reduced aq prod) - beta blockers - reduce prod of aq
Ca inhibitors - dorzolamide - reduce prod aw
symapthomimetics eg brimonidine - reduced from of aq and increaase outflow
v) trabeculectomy - used if eye drops are ineffective
creates a new channel from ant chanber through the sclera to under the conjunctiva > causes a bleb where aq drains > reabs into general circ
ACUTE ANGLE CLOSURE GLAUCOMA (CLOSED ANGLE)
i) what happens? what does this lead to? which area is particularly affected? how quick does it need be treated?
ii) name four RF? name three medications that can ppt it
iii) name four ways it my px? is the patient systemically unwell?
iv) name five things that may be seen on exam? will the pupil be dilated or constricted?
i) iris bulges forward and seals off trabecular meshwork of the ant chamber > aq cant draain away > build up of pressure in the eye
partic bup in post chamber > pressure behind iris which worsens it
opthal emergency
ii) RF - inc age, females, FH, chinese/east asian, shallow anterior chamber
adrenergic medications (NAA), anti cholinergics (oxybutinin), tricyclics (amitryp)
iii) px - generally unwell, severe painful red eye, blurred vision, halos around lights, headache, N+V
iv) O/E - red eye, teary, hazy cornea, decreased visual acuity, dilated pupil, fixed pupil size, firm eyeball on palpation
CLOSED ANGLE GLAUCOMA MX
i) what should be done immed? if waiting: how should pt be positioned? what eyedrops can be given? what can be given orally? name two other things that can be given?
ii) how do the eye drops work? (2) how does the oral medication work?
iii) name four things that can be done in secondary care to help reduce the pressure?
iv) what is definitive tx? what does it involve?
i) refer to opthalmology
lie pt on back without a pillow
pilocarpine eye drips, acetazolamide orally and analgesia/anti emetic
ii) eye drops - acts on muscarinic Rs in sphincter muscles > pupil contriction (miotic agent) also causes cilliary muscle contraction
acetazolamide is a carbonic anhydrase inhibitor - reduces aq humour production
iii) pilocarpine, acetazolamide, hyperosmotic agents eg glycerol, timolol bb, dorzolamide
iv) definitive - laser iridotomy
laser to make a whole in iris to allow aq to flow out from post > ant chamber
relieves pressure and allows drainage
AGE RELATED MACULAR DEGEN
i) what happens? what is it the most common cause of? what is they key finding?
ii) what type are 90% of cases? which type has a worse prognosis?
iii) how many layers does the macula have? what is in each layer
iv) name two features common to both types?
i) degeneration of macula > vision deterioration = most common cause of blindness
key finding is drusen = yellow deposits of proteins and lipids between retinal pig ep aand bruchs membrane - seen in both weight aand dry
ii) 90% are dry, wet has worse prognosis
iii) four layer - bottom - choroid (bv), bruchs membrane, retinal pig epithelium, photoreceptors
iv) common features = large numbers of drusen, atrophy of retinal pig ep, degen of photoreceptors
AGE RELATED MAC DEGEN
i) what occurs in wet AMD? what leads to more rapid loss in vision? which signalling molecule facilitates this?
ii) name four RFs? name three key ways it can present?
iii) which type presents more acutely? how long does it take for full vision loss? is it uni or bilat?
iv) name four things found on exam?
v) what type of examination can be used to dx? what does optical coherence tomography show? what does fluorescein angiograaphy show?
i) wet AMD - new vessel dev growing from choroid layer into the retina > vessels can leak fluid > oedema > rapid loss of vision
facil by VEGF
ii) age, smoking, white/chinese, FH, CV history
px with gradual worsening central visual loss, reduced visul acuity, crooked/wavy appearnce to straight lines
iii) wet presents more actute - loss of vision over days > full loss over 2-3 yrs and often becomes billateral
iv) reduced vis acuity on snelllen chart, scotoma, amsler grid test to look at straight line distorition, fundoscopy = drusen
v) slit lamp biopmicroscopic fundus exam to dx
OCT = cross sec view of layers of retina > dx wet AMD
FA = give contrast and photograph retina to look at blood supply - see oedema and neovasc
used second line to dx wet AMD if OCT doesnt dx
MX OF AMD
i) what does mx of dry AMD focus on? name three things that can be done?
ii) what is tx mainstay for wet AMD? how are they admin? how odten?
iii) how quickly does the above tx need to be started to be effective?
i) lifestyle measures that slow progress eg avoid smoking, control BP and vitamin supp
ii) VEGF inhibitors - injected directly into vitreous chamber once a month
iii) start within 3 months to be beneficial
DIABETIC RETINOPATHY
i) what happens? what causes it? name three things that increased vasc permeability leads to?
ii) what causes microaneurysms? what is venous beading? what causes fluffy white patches to form? what are they called?
iii) what are intra retinal microvasc abnorms?
iv) which two broad categories can it be split into? what does this depend on? what type of exam allows this classification?
i) bv in retina damaged by prolonged exposure to high blood sugar levels > progressive deterioration of retinal health
damaged retinal small vessels/endo cells > inc vasc perm > leakage from bv, blot haemmorhage, hard exudate formation (lipid)
ii) damage to bv waall > micro aneurysm (weakness in wall causes small bulges)
venous beading - walls of veins are no longer straight - string of beads
damage to nerve fibres > fluffy patches = cotton wool spots
iii) IRMA = dilated and tortuous caps in retina
iv) split into non prolif and prolif depending on whether new bv have developed
classification based on fundus examination
DIABETIC RETINOPATHY DX AND MX
i) what are the three types of non prolif?
ii) what two things charac prolif?
iii) what two things charac diabetic maculopathy?
iv) name five complications
v) name three ways to manage
i) mild - microaneurysms
mod - MA, blot haemm, hard exudate, cotton wool spot, venous bleed
severe - BH, IMRA
ii) neovasc and vitreous haemmorhage
iii) macular oedemaa, isch maculopathy
iv) retinal detach, vitreous haemm, rebeosis iridic (new bv in iris), optic neuropathy, cataracts
v) mx with laser photocoag, anti VEGF (ranibizumab, becacizumab), vitreoretinal surgery if severe
HYPERTENSIVE RETINOPATHY
i) what is it? what can it be due to? (2)
ii) what is silver/copper wiring? what is arteriovenous nipping? what causes cotton wool spots? what causes hard exudate?
iii) what causes retinal haemm? what causes papilloedema
iv) which classification is used?
v) how is it managed?
draw changes seen in the eye
i) damage to small bv of retina due to systemic HTN
due to years of chronic HTN or quick develop in response to malignant HTN
ii) silver wiring - walls of arterioles become thick and sclerosed > inc refelc of light
AV nipping - arterioles cause compress of veins where they cross > due to sclerosis and hardnening
CW spots - due to isch and infarction in retina > damage to nerve fibres
hard exudate - caused by damaged vessels leaking lipids into retina
iii) retinal haem - damaged vessels rupturing
papiloedema - caused by isch to optic nerve > optic nerve swelling > blurring of disc margins
iv) keith wagner classification - four stages (stage 4 is papillloedema)
v) mx - control BP and other RFs eg smoking and blood lipid levels
CATARACTS
i) what happens? how is visual acuity affected?
ii) what is the role of the lens? what holds it in in place? what contracts and relaxes to focus the lens? does it have a blood supply?
iii) how are congenital cataracts screened for? name five RFs?
iv) does it present symm or asymm? name three other presenting features? what is the key examination sign for cataracts?
v) name a way they may be managed? whaat is endophtlamitis? how is it treated?
i) when the lens in the eye becomes cloudy and opaque
reduces visual acuity by reducing the amount of light that enters the eye
ii) the lens focuses light coming into the eye onto the retina > held by suspensory ligaments which are attached to ciliary body which contracts and relaxes to focus lens
doesnt have a blood supp as nourished by surrounding fluid
iii) congen - red reflex during neonate exam
RFs - inc age, smoking, alcohol, diabetes, steroid use, hypocalc
iv) usually asymmetrical with slow reduced vision, progressive blurring, change in colour vision (see more brown/yellow)
starbursts appear around lights partic at night
key exam - loss of red reflex
v) may need no intervention
surgery > drill and break lens, remove and implant an artificial lens
endopthalmitis - serious complication of cataract surgery - inflam of inner contents of eye caused by infection
tx with intravitreal abx (may lead to visual loss)
FEATURES OF EYE DISEASE
i) what causes general reduc in visual acuity and starbursts around lights?
ii) what causes peripheral vision loss with halos around lights?
iii) what causes central loss of vision with crooked/wavy appearance to straight lines
i) cataracts
ii) glaucoma
iii) macular degeneration
PUPILS
i) which muscles in the iris cause pupil constric? what ANS branch are they stim by? which NT is used? which CN fires?
ii) which branch of ANS stim pupil dilation? which NT is used?
iii) what can cause adhesions in the iris? what can misshape the pupil into vertical oval?
iv) name four causes of a dilated pupil (mydriasis)
v) name four causes of a constricted pupil? (miosis)
i) circular muscles in iris > constriction (PNS and Ach) - CN III
ii) dilator muscles stim by symp NS, adrenaline
iii) anterior uveitis > adhesions
acute angle closure glaucoma > vertical oval
iv) dilated - CN III palsy, raised ICP, congenital, trauma, stimulants eg cocaine, anticholinergics, holmes-adie syndrome
v) constricted - horners, cluster headache, opiates, nicotine, pilocarpine
THIRD NERVE PALSY
i) name three characs of a third nerve palsy? what does it supply? how does the eye appear? ii) why does it also cause a ptosis? name two vascular causes of CNIII palsy?
iii) what does CNIII palsy with sparing of pupil suggest? name three causes
iv) what is a full CN III palsy caused by? what is it aka? name three causes
i) ptosis, dilated non reactive pupil (CN III cont psym fibres), divergent strabismus (squint - down and out)
supplies all extraocular muscles except lat rectus and sub oblique
ii) ptosis due to also suppluing levator palp superioris > lifts upper eyelid
vascular - cav sinus thrombosis and PCA aneurysm (travels through cav sinus and close to PCA)
iii) sparing pupil suggest microvasc cause as psym fibres are spared - diabetes, HTN, isch
iv) full - compression of the nerve inc psym fibres = surgical third due to physical compression
causes - idiopathic, tumour, trauma, cav sinus thrombosis, PCA aneurysm, raised ICP
HORNERS SYNDROME
i) what is the horners syndrome triad? name another symptom they may have? are light and accomodation reflexes affected?
ii) what ANS branch is damaged? how can the location of the horners syndrome be determined?
iii) what are the four S of central lesions (sentral) what are the four Ts (torso - pre gang), what aare the four Cs (cervical - post gang)
iv) what is congenital horners assoc with?
v) what can be used to test for horners? how does this work? what can alternatively be used?
i) horners > ptosis, miosis and anhidrosis (loss of sweating)
may also have enopthalmos (sunken eye)
light and accom reflex not affected
ii) damage to symp fibres
determine location by anhidrosis
central lesion - anhidrosis of arm/trunk/face
pre gang lesion - anhidrosis of face
post gang dont case anhidrosis
iii) central - stroke, MS, swelling (tumour), Syst in Sp cord (syringomyelia)
pre gang - tumour (pancoast), trauma, thyroidectomy, top rib (extra rib growing above first rib)
post gang - carotid aneurysm, CA dissection, cav sinus thrombosis, cluster headache
iv) congential assoc with heterochromia (diff coloured iris on aff side)
v) test with cocaine eye drops > stop NA reuptake which normally causes dilation (horners - no NA rel so no diff to eye)
alt use adrenaline eye drip - wont dilate a normal pupil but will dilate a horners pupil
EYELID DISORDERS
i) what is blepharitis? what sensation is felt in the eyes? which glands are implicated? what can it lead to? what relives symptoms?
ii) what are hordeolum externum and hordeolum internum? which one tend to be deeper and more painful? how are they treated? what cana be considered?
iii) what is a chalazion? how does it px? how is it treated? (2)
iv) what is an entropion? what does it result in? what is intial and definitive mx?
v) what is ectropion? what can it result in? what can be used to treat? what do most cases require?
i) blepharitis is inflamm of eyelid margins > gritty, itchy, dry
dysfunc of meibomian glands that secrete oil onto eye surfce
can leaad to stye and chalazion
treat with lubricating eye drops
ii) HE and HI are types of stye
internum are deeper and more painfil
treat with hot compress and analgesia
consider topical abx eg chloramphenicol if assoc with conjunc or persis
iii) chalazion - meibomian gland becomes blocked and swells > swelling is eyelid not tender
tx with hot compress and analgesia or topical abx if acute inflam
iv) entropion - eyelid turns inwards with lashes against > pain and corneal damage/ulceration
initial - tape down eyelid to prevent turning inwaards
definitive - surgical intervention
v) ectropion - eyelid turns outwards and inner aspect is exposed
cna result in exposure keratopathy
mild maay need tx, can give regular lubricating eyedrips
more signfic may need surgery
EYE CELLULITIS
i) what is periorbital cellulitis? how does it present? (3) what must it be differen from? how is this done?
ii) how is periorbital treated? what can it progress to in vulnerable patients?
iii) what is orbital cellulitis? what does it involve?
iv) what key features differentiate the two types? (4)
v) how quick does oribital cell need to be tx? how is it tx? when may surgery be needed?
i) POC - eyelid and skin infection in front of orbital sepptum
px with swelling, redness, hot skin around eyelids and eye
differen from orbital cellulitis (life threat) do this with a CT scan
ii) tx with systemic abx
can dev into orbitaal in vuln - may be admitted
iii) OC - infection around eyeball that involves tissue behind orbital septum
iv) key features - pain on eye move, reduce eye move, chnge in vision, abnormal pupil reaction, forward movement of eyeball (proptosis)
v) emergency - admit and IV abx
may need surgical drain of an abscess forms
CONJUNCTIVITIS
i) what is it? what are the three main types?
ii) name four ways it can px? does it cause pain/photophobia/reduced visual acuity?
iii) how does bacterial px? how does viral px?
iv) name three DDs for painless red eye, name four DDs for painful red eye?
v) how long does it usually take to resolve? what advice should be given? what medical tx can be considered?
vi) what do patients <1m need?
i) inflammation of conjunctiva - thin layer of tissue that covers inside of eyelids and sclera
bacterial/viral/allergic
ii) px uni or bilat, red eye, blood shot, itchy/gritty, discharge from eye
doesnt cause pain, PP, reduced acuity
iii) bacterial - purulent discharge and inflamed conjunctiva (worse in AM, starts in one eye and spreads > contagious)
viral - presents with clear discharge, assoc with ccough, sore throat, may have preauricular LNs, contagious
iv) painless - conjunctivitis, episcleritis, subconjunc haemm
painful - glaucoma, ant uveitis, scelritis, corneal abrsaions, keratitis, foreign body, trauma
v) usually resolves in 1-2 weeks no tx
good hygiene, clean eyes with cooled boiled water and cotton wool
bac can give abx drops - chloramphenicol, fusidic acid
vi) <1m - urgent opthal review as neonate conjunctivitis caan be assoc with gonococcal infection > loss of sight and pneumonia
ANTERIOR UVEITIS
i) what is it? what three things does the uvea involve? what does each do?
ii) what happens? name three cells involved? what is it usually caused by? what do inflammatory cells in the ant chamber cause in vision? what is the difference between acute and chronic?
iii) what gene is acute assoc with? name three conditons that chronic is assoc with?
iv) do symptoms start uni or bilat? how do they occur?
v) name six symptoms? what is a hypopyon? why may patients have abnormally shaped pupils?
i) inflammation of anterior part of uvea - iris, cil body and choroid (layer bet retina and sclera)
ii) inflammation and imm cells in ant chamber of eye - infiltration by neutrophils, lymphos and MPs > usually caused by autoimmune
inflam cells in ant chamber > floaters in vision
chronic has more granulomatous inflam
iii) acute = HLA B27
chronic - sarcoid, syphilis, lyme disease, TB, herpes
iv) symptoms are unilateral and start spontaneously
v) symptoms - dull/aching/painful eye, reduced vis acuity, floaters/flashers, miosis (cons pupil), photophobia due to cil musc spasm, excess lacrimation
hypopyon = collec of WBC in aant chamber seen as yellow fluid settled infront of iris = fluid level
aborm shaped pupuls due to posterior synechiae (adhesions) that pull the iris into abnormal shapes
MX OF ANTERIOR UVEITIS
i) what can be given first line?
ii) what do cycloplegic mydriatic medications do? what receptor do they act on? how does this help?
iii) name three other tx that may be given
i) steroids = oral, topical or IV
ii) cycloplegic = paralysing cilliary muscles
mydriatic = dilates pupils
antimuscarinics that block action of iris sphincter muscles and ciliary body > dilate pupil and reduce pain aassoc with ciliary spasm
iii) immsupps, laser, cryotherapy
EPISCLERITIS
i) what is it? where is the episclera? who does it most commonly occur in?
ii) what is it often assoc with? is it caused by infection?
iii) is it painful? where does it occur? is there discharge? name two other symptoms
iv) how long does it usually take to resolve? what can be given to tx symptoms? (3)
v) which eye drops can be added to differen from scleritis? what is seen in epi?
i) self limiting inflam of the episclera - outermost layer of the sclera under the conjunctiva
occ in middle aged adults
ii) assoc with inflam disorders eg RA and IBD
not caused by infection
iii) not usually painful, no discharge
occ in segments of the eye (not diffuse) usually lateral sclera
dilated episcleral vessels, watering of eye
iv) usually resolves in 1-4 weeks
lubricating eye drops, analgesia, cold compress, safety net
NSAIDs if severe
v) pheylephrine eye drops - if epi then redness disappears as vessels as superficial
SCLERITIS
i) what does it involve? what type of conditions are assoc with 50% of cases? name some
ii) how quickly do symptoms usually appear? name five px features?
iii) what should be done first? name three tx that may be given?
iv) what is the most severe type? how may these patients present? wht can it lead
i) inflammation of full thickeness of sclera
assoc with inflammatory conditions eg RA, SLE, IBD, sarcoid
ii) acute onset, 50% are bilat
severe pain, pain on movement, photophobia, eye watering, reduced vis acuity, abnormal pupil reac to light
iii) same day refer to opthal
oral NSAIDs first line, steroids, immsupp
CORNEAL ABRASIONS
i) what are they and what do they result in? name three causes
ii) what bug may be present if caused by contact lens use? what is an important DD to consider?
iii) name four ways it can px? how is it diagnosed?
iv) where may mild/uncomplicated abrasions be managed? name four ways to manage
v) what must be done immediately for chemical abrasions? how quickly do uncomplicated abrasions heal?
i) scratches/damage to cornea > red painful eye
caused by contacts, foreign body, fingernail, eyelash, entropion
ii) pseudomonas
consider herpes keratitis > tx with antiviral eyedrops
iii) px with painful, red eye, foreign body sensation watery, blurred vision, photophobia
dx with fluorescein eye drops - collect in abrasion and highlight it
iv) mild can be mx in primary care
remove foreign body, simple analgesia, lubricating eye drips, abx eyedrips eg chlorampenicol, fu 24 hours later
v) immed irrigate for 20-30 mins > urgent opthal refer
uncomplicated usually heal over 2-3 days
