B7.034 Ophthalmologic Diseases Overview Flashcards
etiologies of cataracts
process of aging -70% of people > 75 congenital -rubella infection genetic anomaly -Lowe syndrome, Wilsons secondary to various diseases, trauma, inflammation, radiation, meds (etc) -steroids and diabetes
basics of an eye exam
visual acuity pupillary response ocular motility slit lamp exam fundus exam
glare vision testing
shine light in eyes
in case of cataracts, this can worsen vision
types of cataracts
nuclear
cortical
posterior subcapsular
posterior
treatment of cataracts
cataract removal with/without intraocular lens implantation
phacoemulsification
posterior capsular opacification
most common “complication” of cataract surgery
-leftover cataract cells proliferate on back of lens
about 40% of patients require YAG laser capsulotomy to resolve
most common cause of acute glaucoma
angle closure
symptoms of angle closure glaucoma
pain blurred vision halos nausea/vomiting headache
signs of angle closure glaucoma
conjunctival injection fixed mid-dilated pupil "steamy" or edematous cornea elevated intraocular pressure history of hyperopia Asian race
why can hyperopia lead to angle closure glaucoma
smaller eye than average
structures more likely to be compressed
far sighted
treatment for angle closure glaucoma
IV Diamox
topical glaucoma meds
laser iridotomy (hole in iris to bypass usual channel that is closed off)
epidemiology of macular degeneration
leading cause of irreversible central vision loss among people 52 and up
symptoms of macular degeneration
metamorphopsia and decreased central vision (opposite of glaucoma, which tends to cause loss of peripheral vision first)
where is the macula
darkish spot 2 disc diameters from the optic nerve
high proportion of cones here
what is metamorphopsia
distortion of vision in addition to blurring
tested with grid to determine if it looks wavy
exam for macular degeneration
visual acuity
ophthalmoscopy
optical coherence tomography
fluorescein angiography
changes seen in macular degeneration
drusen
retinal pigment epithelium (RPE) changes
neovascular membrane
drusen
hyaline nodules in Bruch’s membrane, which separates RPE from inner choroidal vessels
RPE changes in macular degeneration
hyper and hypopigmentation
can occur with or without drusen
variable effect on vision
progression of macular degeneration
10-20% of eyes with AMD develop a neovascular membrane, which means a defect in Bruch’s membrane, leading to wet macular degeneration
worse prognostic factors in macular degeneration
larger membrane
closer to center of fovea
treatment of dry macular degeneration
ocular AREDS vitamins to slow progression
Amsler Grid testing to monitor progression to wet form
treatment of wet macular degeneration
intravitreal injections of anti-VEGF
-decreased swelling and abnormal blood vessels to get rid of fluid
diabetic eye changes
changes in refraction
-myopic shift (near sighted)
posterior subcapsular cataracts
retinopathy