ophthalmology Flashcards
viral vs bacterial conjunctivitis - transmissible? itchy? adenopathy, vision?
viral –> not itchy, easiy transmissible, PREAURICULAR adenopathy, normal vision
bacterial –> itchy, poorly transmissible, no adenopathy, normal vision
red eye (opthalmologic emergencies) - types and presentation
- conjunctivitis: itchy eyes with discharge
- uveitis autoimmune disease
- glaucoma: pain
- abrasion: trauma
red eye (opthalmologic emergencies) - types and eye findings
- conjunctivitis: normal pupil
- uveitis: photophobia
- glaucoma: fixed midpoint pupil
- abrasion: like sand in the eye
red eye (opthalmologic emergencies) - types and most accurate test
- conjunctivitis: clinical diagnosis
- uveitis: slit lamp examination
- glaucoma: tonometry
- abrasion: fluorescein stain
red eye (opthalmologic emergencies) - types and best initial therapy
- conjunctivitis: topical antibiotics
- uveitis: topical steroids
- glaucoma: acetazolamide, mannitol, pilocarpine, laser trabeculoplasty
- abrasion: no specific therapy, patch not clearly beneficial
chronic glaucoma - presentation / diagnosed by / confirmed by (findings)
diagnosed by routine screening
confirmation with tonometry –> extremely elevated intraocular pressure
chronic glaucoma - drugs
- prostaglading analogues: latanoprost, travoprost, bimatoprost
- topical beta blockers: timolol, carteolol, metipranolol, betaxolol, levobunolol
- topical carboic anhydrase inh: dorzolamide, brinzolamide
- alpha-2 agonists: apraclonidine
- pilocarpine
- laser trabeuloplasty (if medical treatment fail)
chronic glaucoma - prostagladin analogues - drugs and purpose
latanoprost, travoprost, bimatoprost
increase outflow of aqueous humor (uveoscleral flow)
chronic glaucoma - topical beta blockers - drugs and purpose
timolol, carteolol, metipranolol, betaxolol, levobunolol
decrease synthesis by nonpigmented epithelium on ciliary body
chronic glaucoma - topical carboic anhydrase inh - drugs and purpose
dorzolamide, brinzolamide
decrease synthesis by nonpigmented epithelium on ciliary body
chronic glaucoma - alpha-2 agonists - drugs and purpose
apraclonidine
decrease synthesis by nonpigmented epithelium on ciliary body
chronic glaucoma - pilocarpine - drugs and purpose
pilocarpine
increase outflow of aqueous humor (trabecular ouflow bu cilliary body contraction)
epinephrine (a1 agonist on glaucoma)
decreases aqueous humor synthesis via vasoconstriction
acute angle-closure glaucoma - clinical presentation
- SUDDEN onset of an extremely painful
- red eye that s hard to palpation
- walking into a dark rook can precipitate pain because of pupillary dialation (SOS)
- steamy cornea
- non-reacting pupil
acute angle-closure glaucoma - diagnostic sign
the cup-to-disc ratio is greater than the normal 0.3
optic disc atrophy with charactersiting cupping (thinning of the outer rim of the optic nerve head vs normal
acute angle-closure glaucoma - the diagnosis is confirmed by
tonometry
acute angle-closure glaucoma - treat with (and why)
- IV acetazolamide
- IV mannitol: osmotic driving of fluid out of the eye
- Pilocarpie, beta-blockers and apracloinidine to constrict the pupil and enchance and enchance drainage)
- laser iridotomy
keratitis - definition / presentation
infection of the cornea
the eye may be very red, swollen and painful, but do not use steroids
hepres keratitis - never use …. (why)
steroids –> make it worse / increase the production of the virus
hepres keratitis - diagnosis
Fluorecein staining of the eye helps confirm the dendritic pattern seen on examination
hepres keratitis - treatment
oral acyclovir, famciclovir or valacyclovir
topical anthepretic treatment is trifluridine and
Cataracts - therapy
- no medical therapy
- surgically remove the lens and replace with a new intraocular lens. The lew lens may automatically have bifocal capability.
Cataracts - diagnosis
early Cataracts: ophthalmoscope or slit lamp exam
advanced: visible on examination
diabetic retinopathy - how to prevent / definition and types
- annual screening (before serious visual loss)
retinal damage due to chronic hyperclycemia:
1. prolferative
2. nonproliferative (or background)
nonprolferative vs proliferative diabetic retinopathy - treatment
nonprolif: blood glucose control
prolif: laser photocoagulation and VEGF inh(to control neovascularization, surgery
diabetic retinopathy - surgery
vitrectomy (remove the vitreous gel from the middle of the eye): to remove vitreal hemorrhage obstructing vision
diabetic retinopathy - most accurate test
flurescein angiography
retinal artery and vein occlusion - presentation
both conditions present with the sudden loss of monocular visual loss
retinal artery and vein occlusion - diagnosis
cannot diagnose without retinal examination
retinal examination - findings in retinal artery occlusion
the macula is described as “cherry red” because the retina is pale and macula is dark
retinal examination - findings in retinal vein occlusion
extravasation of blood into retina
retinal artery occlusion - treatment
- 100% O2
- ocular massage
- acetazolamide
- anterior chamber paracentiesis (decreased IOP)
- thrombolytics
- evaluate embolic source
retinal vein occlusion - treatment
ranibizumab (VEGF-A inh)
Retinal detachment - risks
- trauma of the eye
- extreme myopia that changes the shape of the eye
- diabetic retinopathy
ANYTHING THAT PULLS THE RETINA CAN DETACH IT
Retinal detachment - presentation
sudden onset of painless, unilateral loss of vision that is described as “A CURTAIN COMING DOWN”
Reattachemen of retina is attempted …
with a number of mechanical methods such as:
- surgery 2. laser 3. cryotherapy
- injection of an expansile gas that pushes the retina back up against the globe of the eye
The MCC of blindness in older person in the US
Macular degeneration
causes of Macular degeneration / diagnosis
unknown
diagnosed only by visualization of the retina
Macular degeneration - types
- atrophic (dry)
2. neovascular (wet)
Macular degeneration - characteristics of visual loss
- far more common in older patients
- bilateral
- Normal external appearance of the eye
- loss of central vision
Macular degeneration - atrophic dry vs neovascular regarding the progression and the severity (DESCRIBE)
neovascular is more rapid and more severe –> New vessels grow between the retina and the underlying Bruch membrane. The neovascular or wet type causes 90% of permanent blindness from macular desegregation
atrophic dry Macular degeneration - treatment
no proven effective therapy
neovascular or wet Macular degeneration - treatment
best initial: VEGF inh (ranibizumab, bevasizumab, aflibercept. Injected directly into the vitreous chamber every 4-8 wks.
neovascular or wet Macular degeneration - results of the treatment
- over 90% of patients will expereience a halt (stop) of progression
- 1/3 will have improvement in vision
