Opthalmology Flashcards
State 4 RFs for cataracts
- age- affects 50% of those over age 65
- smoking
- diabetes
- systemic corticosteroids
- eye trauma, female, uveitis, UV exposure, poor nutrition, alcohol are smaler RFs
- retinitis pigmentosa lol- pt in 20s w/ night vision loss, feild defect, fhx and black peripheries on fundoscopy (google it)
- Downs
Describe the pathophys of catartacts in adult and what may cause in a child?
- There is deposition of new crystallin lens fibres with age, old ones are not removed
- New deposition disruption of the carefully composed structure leading to protein aggregation and so clouding and light scattering
- 2nd factor= accumulation of yellow- brown pigement making reading more difficult as affects contrast
- Paediatric cataracts may be caused by galactosaemia, genetic, TORCH infection, diabetes, traumatic or post radiotherapy
Describe the clinical features of cataracts
- gradual painless loss of vision- not improved by viewing through pinhole
- haloes around lights and problems watching tv
- problems recognising faces and diplopia in one eye
- defects in red reflex
- lens appears brown or white when bright white light shone on eye
- pupillary reactions normal
How is cataracts managed?
- extracapsular lens extraction or phacoemulsification (lens liquidied with USS probe and then aspirated before replacing it with artificial lens)
- decision to treat depends on affect on QoL an risk vs benefit rather than specific acuity
State 4 early complications of cataracts surgery
- poor vision (inadequate correction of refractive error or pre- exisitng eye condition)
- capsular rupture with vitreous loss- endopathalmitis risk
- protruding or broken sutures
- trauma to iris
- wound gape or iris prolapse
- anterior chamber haemorrhage
- vitreous or choroidal haemorrhage
State 4 late complications of cataracts surgery
- posterior chamber opacification: vision can usually be restored with laser capsulotomy
- cystoid macular odema
- uveitis
- retinal detachment
- open or closed angle glaucoma
- ARMD
- dysphotopsias: unwanted optic phenomena due to light artefacts reflecting off IOL
What is primary open angle glaucoma
Progressive, chronic condition characteristed by:
- Adult onset
- Intraocular pressure >21mmHg- however 20-52% have normal tension glaucoma
- Open iridocorneal angle- flow is simply reduced through the trabecular meshwork
- Glaucomatous optic neuropathy
- Visual field loss compatible with nerve fibre damage
- Absence of underlying cause
- Usually bilateral but asymmetrical
Give 4 RFs for primary open angle glaucoma
- age (rare before 40)
- fhx
- afrocarribean
- ocular htn
- myopia, retinal disease diabetes, systemic htn
describe the clinical features of primary open angle glaucoma
- Most asymptomatic as vision loss is initially to peripheral vision so when they notice it is too late and damage is permenant
- May be picked up on checking IOP and part of visual fields by optician or by GP looking at optic disc
- Gonioscopy is used to measure angle between cornea and iris
- Corneal thickness needs to be done as will increase IOP reading falsely
- Goldmann tonometry is used to measure IOP- usually raised (9-21 is normal)
- Optic disc exam- increase in cup size in relation to disc ( ratio >0.7)
- Loss of peripheral visual fields (measure with perimetry)
How is primary open angle glaucoma managed?
- topical beta blocker (timolol) or prostaglandin analogue (latanoprost) 1st to reduce IOP
- miotics and sympathmiometics can also be used
- laser and surgical management if 2 of these fail (selective laser trabeculoplasty)
- Even if IOP isnt raised they’re still given medication to lower it
What can cause angle closure glaucoma?
- insidious/ primary
- hypermetropia
- lens bulging forward as a result of swelling eg blood(hyphaema), blood vessels (diabetic eye disease) or protein (hypertensive uveitis)
describe the clinical features of acute angle closure glaucoma
- severe rapidly progressive pain in and around the eye
- blurred vision/ visual loss
- marked red eye- reddest around cornea
- pupil fixed and dilated, sometimes hazy cornea
- hard globe (press with eye lids closed and will be hard and tender)
- IOP raised (often 50s or more)
- N+V common
- attacks often start when something dilates pupil
- coloured haloes around lights (subacute attacks)
How should acute angle closure glaucoma be managed?
- give all glaucoma meds that arnt contraindicated (timolol, lantoprost, pilocarpine, maxidex etc)
- IV acetazolamide (500mg over 10 mins) and lay supine
- if no response in 1 hr and U&E normal give hyperosmotics such as mannitol
- If this fails or U&E abnormal, iridoplasty can be done
- systemic analgesia and antiemetics
- laser peripheral iridotomy within a few weeks of the attack, sometimes lensectomy
- top steroids often given bc eye becomes inflammed
- pilocarpine drops often given to constrict the pupil and help unblock the drainage
Give 3 complications of acute angle closure glaucoma
- permanent visual loss
- repetition of attacks
- attack in other eye
- central retinal vein or artery occlusion
Describe and explain the 5 retinal findings in diabetic retinopathy
- Microvascular occlusion causes retinal ischaemia and leds to AV shunts and NEOVASCULARISATION .
- Leakage results in intraretinal haemorrhages and MACULAR ODEMA
- MICROANEURYSMS: physical weakening of capillary walls which predispose them to leakages
- HARD EXCUDATES precipitates of lipoproteins leaking from retinal blood vessels
- HAEMORRHAGES: rupture of weakened capillaries, appearing as small dots/ larger blots or flame haemorrhages that track along nerve- fibre budles in superficial retinal layers
- COTTON WOOL SPOTS- axonal debris build up due to poor axonal metabolism at margin of ischaemic infarcts
Describe the grading of diabetic retinopathy
- Non proliferative (MILD (<2 microaneurysm) MOD (mciroa + intraretinal haemorrhages +/- cotton wool spots, venous bleeds) SEVERE/ PRE-PROLIFERATIVE (number of change in number of quadrants)
- Proliferative (non high risk (no changes within 1 diameter of optic disc) and high risk (large new vessels on disc or everywhere, retinal detachment or pre retinal haemorrhage)
Describe the grading of diabetic maculopathy
- focal or diffuse macular odema
- ischaemic maculopathy (normal but reduced acuity and ischaemia seen on fluorescein angiography)
- clinically significant macular odema: thickening or hard exudates which are of certain size/ distance from the fovea
Describe the clinical features of diabetic eye disease
- Painless gradual reduction in central vision
- Haemorrhages result in sudden onset dark painless floaters which may resolve over several days
- Severe haemorrhages result in painless visual loss
- Spots within the red reflex suggest vitreous haemorrhage
How is diabetic retinopathy managed?
- laser photocoagulation treatment if neovascularisation to induce regression and also helps reduce central macula thickening
- diabetes, BP, lipid control
- sometimes vitrectomy after preretinal/intravitreal bleeds
How is diabetic maculopathy managed?
- anti VEGF injections
- intravitreal triacinolone (steroid) injections
give 4 complications of diabetic eye disease
- macular ischaemia
- vitreous haemorrhage
- retinal detachment
- glaucoma
Describe the pathophys of dry and wet ARMD
Dry: soft drusen in macula + atropy of retinal pigment epithelium causing gradual vision loss
Wet: new blood vessels grow in choriocapillaries under the retina, they lead to haemorrhage and scarring, progression varies from 3 months to 3 yrs. end point is scar formation known as disciform macular degeneration
Describe the clinical features of ARMD
- painless deterioration in central vision (esp near vision) in person age >55
- loss of contrast sensitivity
- size or colour of objects appear differnt in each eye
- flashing or flickering lights and glare
- In wet ARMD straight lines appear crooked or wavey (due to macula odema) and visual deterioration is much quicker, often get profound sudden loss, flashers and floaters in event of a bleed
- yellow deposits called drusen seen in macula area on opthalmoscop
How is ARMD diagnosed?
Ocular coherence tomography (OCT), fluorescein angiography if wet ARMD suspected