Ophthalmology yr4.txt

• inferior orbital wall - maxillary bone
• blow out fracture

• ethmoid bone
• infection in paranasal sinus can get through tiny holes in ethmoid and to orbit

• optic nerve
• ophthalmic artery with its sympathetic nerves

• conjunctiva
• cornea
• sclera

• anterior: iris, ciliary body
• posterior: choroid
• other name: uveal layer - black grape - choroid is very vascular

retina

• anterior chamber
• posterior chamber
• vitreous chamber

• dilator pupillae: radial configuration - sympathetic
• sphincter pupillage: on the papillary margin - circular motion contracts

• choroid is between retina and sclera
• function: provide O2 and nutrients to outer layers of retina (RPE)

transparent

• 1. epithelium
• 2. Bowman's
• 3. stroma
• 4. Descemet's membrane
• 5. endothelium

• get corneal oedema
• endothelium is an active layer - function is to pump WATER OUT OF CORNEA
• so if waters stays - lose its transparency

• HSV1 and 2 lesion to epithelium of cornea
• treat: antiviral eg aciclovir topical/systemic

• pain
• photosensitivity
• reduced VA
• discharge
• circumcorneal injection

• pseudomonas (anaerobic)
• rapidly destructive

topical steroids

fluorescine dye - goes into epithelium

• 1. aqueous humour production: 2ul/min
• 2. accommodation: from CB - suspensory ligaments hold the lens to fit its position. if ligaments fail, get a dislocated lens

becomes more round and fat - looking near

• with ageing the CB loses its ability to contract so cant look near (accommodate) as well
• so need reading glasses

• inner neurosensory layer
• outer retinal pigmented epithelium

3 OD diameters temporal to the OD and a bit inferior

• optical coherence tomography
• use to detect detachment - fluid between the RPE and NS retina ie intraretinal fluid

• floaters and flashes
• with age the vitreous gel liquefies - vitreous syneresis
• floaters: collagen fibres in vitreous stick together to make cobweb shapes - black FLOATERS - where vitreous collapses and casts shadow on retina
• these forcibly detach the posterior virtual surface from the retina
• the traction forces applied to the retina create FLASHES

myopic

• most are self limiting, become less noticeable
• only few develop retinal tear

risk of retinal tear and detachment if notice sudden shower of floaters or new flashing lights

• spontaenous PVD
• trauma

• upper temporal part
• u shaped

• vitreous can enter the space between the retina (NS) and RPE
• causing a rhegmatogenous retinal detachment
• myopes are at high risk of this type of RD

• flashing light (photopsia)
• floaters
• then gradual blurring or LOSS OF VISION -
• painless

• 1. argon laser retinopexy in the area around the tear - to make strong adhesions between the retina and RPE
• 2. cryotherapy - if tear in extreme periphery and difficult to approach with laser

• 1. rhegmatogenous RD: from PVD - lqd between retina and RPE
• 2. tractional RD: in proliferative diabetic retinopathy - fibrous or vascular membranes growing abnormally in the vitreous can contract and pull retina away from RPE
• 3. exudative RD: inflammatory or neoplastic condition can lead to serous exudate form leaky bld vessels beneath retina

when look at white background (snow / ceiling)

• 1. external approach: scleral buckle - silicone band presses the etina and enforces the RPE to attach to the retina
• 2. internal approach: laparoscopic vitrectomy - mainly used nowadays. remove vitreous and source of traction that caused RD then inject gas into eyeball to make retina stick to RPE (or silicone oil - but very heavy and need to remove)

• macula on - as able to repair
• macula off - too late :(

• acute PVD
• trauma
• previous eye surgery
• FH
• myopia

• myopia: longer
• hypermetropia: shorter

• opacity of lens
• when fluid gathers between lens fibres

• reduced VA
• glare in sunshine - due to scattering of light rays
• blurred vision
• difficulty reading and watching tv
• cant recognise faces
• gradual PAINLESS loss of vision
• diplopia in one eye

• age
• UV light
• DM
• uveitis
• trauma
• myopia
• myotonic dystrophy
• atopic dermatitis
• steroids

• anterior subcapsular
• posterior subcapsular
• cortical - see in periphery of eye
• nuclear

dislocated lens: suspensory ligaments degenerate so lens falls down

superior subluxation of the lens

inferior subluxations of the lens

• negative lens to weaken the high power of the eyeball
• biconcave

• positive lens to weaken the high power of the eyeball
• biconvex

wont need reading glasses over 40yo as they wont get presbyopia

phaecoemulsification: use US to emulsify nucleus and take out of the capsule, without breaking the capsule and suspensory lieges

• local anaesthetic drops - awake but feel nothing in eye
• 1. corneal incision
• 2. capsulorrhexis: make incision into anterior capsule (5-6mm)
• 3. hydrodissection: blunt needle between the capsule and cortex - inject water and detach the cortex from capsule so easy to suck out cortex
• 4. phaecoemulsification: US to nucleus - it is very hard so need to break it into 4 pieces
• 5. remove remaining cortex
• 6. implant IOL - artifical lens. haptics stabilise lens into capsule
• 7. put pad/shield over eye to protect it from accidental rubbing after op

• no threshold of VA
• depends upon impact of cataract on QOL

• 1. improve vision
• 2. prevent glaucoma. the natural lens grows in life with age which increases pressure on anterior chamber, may get glaucoma

• 1. worse vision: 1%
• 2. blind 0.1%
• 3. inflammation
• 4. bleeding
• 5. endophthalmitis
• 6. PC rupture or dropped nucleus or IOL into vitreous
• 7. retinal detachment
• 8. posterior capsule opacification - long term complication - individual cells remain, multiply and migrate to the posterior capsule. treat with YAG laser capsulotomy
• 9. crystoid macular oedema: esp in DM or uveitis

unable to lie flat

gram positive strep or staph

• pain
• reduced VA
• vision gets progressively worse
• red eye
• hazy cornea

• vitreous aqueous tap
• intravitreal antibiotics

optic neuropathy which may result in progressive visual field loss

10-21mmHg

golman tonometer

>21mmHg

• produced: CB
• goes through pupil
• drainage: to iridocorneal angle of anterior chamber - trabecular meshwork - canal of schlemm - episcleral veins

<0.5

• aqueous humour has access to the angle
• BUT there is RESISTANCE in the trabecular meshwork

• aqueous humour has NO ACCESS TO THE ANGLE - cannot enter the pupil as the iris is bowed and touching the lens
• so aq hum stuck in posterior chamber
• EMERGENCY!!!!!

• 1st: BB monotherapy eg timolol, MOA: reduces production of AH
• 2nd: PG analogue monotherapy eg latanoprost MOA: increase uveoscleral outflow of AH
• 3rd: combination therapy
• 4th: alpha 2 agonist eg brimonide MOA both reduce AH production and increase trabecular outflow
• CAinhibitor eg acetozolamide, MOA: reduces production of AH
• cholinergics eg pilocarpine: contract CB so miosis and so increased outflow

peripheral, nasal step

• COPD, asthma
• heart block
• bradycardia

• laser treatment: selective laser treatment trabeculoplasty - laser spots increase the intratrabecular space and increase outflow of AH
• surgeli: trabeculectomy +/- mitomicin (antimetabolite) to prevent fibroplast prolif and scar tissue closing the hole made! this operation creates an alternative route for AH flow.

• asymptomatic
• halos due to corneal oedema
• reduced vision
• peripheral loss of vision: arcuate scotoma
• optic nerve cupping
• disc haemorrhages

• FH
• blacks

• SVCO
• cavernous sinus thrombosis
• Sturge Weber syndrome - large haemangioma in the face
• all increase the pressure in the episcleral veins

• hypermetropia
• shallow AC

• acute PAINFUL red eye
• loss of vision
• N&V
• pupil: fixed, semi dilated - vertical oval
• corneal oedema

• 1. iv acetozolamide (diamox) or mannitol
• 2. topical BB, PG, CAI, alpha 2 agonist (brimonidine), cholinergics
• 3. topical steroids to reduce inflammation

• bilateral YAG laser peripheral iridotomy
• this makes a hole in the iris to create

ARMD

• distortion
• loss of central vision

• dry: drusen deposited on RPE - slow distortion and reduced vision
• wet: new bld vessels - choroidal neovascularisation, vessels leak/bleed get SUDDEN (not slow) distortion of vision

dry

• dry: untreatable but get them to self test using an Amsler grid - if get lines of distortion then go to A&E as may have some wet ARMD which can treat
• wet: anti VEGF

see haemorhage in retina

• same as atherosclerotic disease because happens where the hardened, calcified arteries press on the veins
• Age, BP, DM
• also blood dyscrasias

• non ischaemic: see blot haemorrhage
• ischaemic: more CWS

VEGF secreted so get neovascularisation which are abnormal vessels - they get replaced with fibrous tissue and contract and can cause tractional detachment

• new vessels forming in the iris
• called rubeotic glaucoma

• sudden onset
• reduced vision
• VF defect
• blurred vision - whole retina

superior VF defect

• cherry red spot in fovea - which is the choroidal circulation underneath
• oedema in CRAO - as retina not perfused so becomes oedematous and opaque

• in GCA - may affect ophthalmic artery
• in that case no cherry red spot because the choroidal circulation is also affected (as supplied by ophthalmic artery)

GCA

sudden painless loss of vision - amourosis fugal

• RAPD
• cherry red spot
• if TIA - then contralateral CNS signs