Eye Disorders Flashcards
mutations in various genes cause damage to the RPE which leads to reduced ability of the RPE to remove shed rod and cone outer segments causing loss of rods and eventual loss of cones
attributed to over 100 mutations
Autosomal dominant, autosomal recessive, or X-linked
Incidence 1/4000
Retinitis pigmentosum (RP)
Neural retina detaches from the RPE cells and the rods and cones begin to starve
Patients suddenly see a lot of floaters and can see flashes of light or what seems like a veil interfering with their vision
If not repositioned quickly, the rods and cones die and fibroblast like cells grow over the RPE
Lasers are used to reattach the retina
Retinal detachment
most frequent cause of blindness in people over 65
yellow pigment (drusen) accumulates in and around the macula and interferes with vision
no treatment, disease progresses from dry form (non-vascular) to wet form (vascular)
most likely autoimmune and made worse by smoking, hypertension, and obesity
age related macular degeneration (AMD)
25% of 60 year olds and 65% of 80 year olds are affected
vitreous liquefies in the center of the eye and eventually flows towards the back of the eye and the posterior wall of the vitreous pulls away from the retina
puts the retina at risk of detachment
Weiss’ ring is the name given to the residue of the vitreous that floats in the posterior chamber
posterior vitreous detachment (PVD)
caused by blockage of aqueous outflow via Schlemm’s Canal
results in elevated intraocular pressure and loss of visual function due to loss of rods adn cones within specific visual fields
Glaucoma
corneal cloudiness and blindness due to mutations in genes that mediate corneal homeostasis
Corneal Dystrophies
accumulation of damaged proteins in the lens is followed by denaturation of proteins and loss of lens clarity
corrected surgically, lens proteins are removed and an artificial intraocular lens is implanted within the lens capsule
Cataracts
defects in either the volume of tears produced or in the composition of the tears produced
Allows corneal epithelial denudation to occur which then allows bacteria to adhere and infections to occur
Scarring from infections can interfere with vision
more common in women and incidence increases after menopause
Dry Eye
loss of visual acuity
dyschromatopsia (loss of color vision, typical of optic nerve deficit)
visual field defect
deficit in contrast sensitivity
relative afferent pupillary defect (RAPD)
normal or abnormal optic disc
abnormal visual evoked potential (VEP)
consequences of optic nerve neuropathy
optic disc edema caused by increased intracranial pressure
results from accumulation of axoplasmic elements in the optic nerve from an increase in ICP
mechanical distortion and vascular factors contribute because of the increased ICP at lamina cribrosa
clinical features: elevation of optic disc, blurring of optic margins obscuration of retinal vessels hyperemia and dilation of the capillary net retinal venous dilation peripapillary hemorrhages retinal choroidal folds macular edema
Papilledema
hyperemic ON, dilation of capillary net, telangiectasias of surface and radial peripapillary vessels, flame heme, peripapillary NFL, grayish white margins, obscure retinal vessels, disc edge, absence of venous pulsations (VP)
grade I: C-shaped halo with a temporal gap
grade II: halo becomes circumferential
grade III: loss of major vessels as the leave the disc
grade IV: loss of major vessels on the disc
grade V: partial or total obscuration of all vessels on the disc
acute papilledema
gliosis of peripapillary NFL, grayish opacification, more membranous, vascular sheathing
optociliary shunt vessels from preexisting venous channels on disc surface that dilate in response to chronic retinal vein obstruction from elevated ICP
refractile bodies of the disc – chronic lipid exudation, smaller than drusen and noncalcified
chronic papilledema
optic disc edema in the absence of increased ICP
blurred disc margins located deep to retina blood vessels (vessels are clear and visible as they cross disc margins)
causes: optic nerve drusen crowded disc astrocyte hamartoma optic disc hypoplasia optic disc coloboma
pseudopapilledema
headache, nausea, vomiting
more common in females in third decade
associated with obesity, pregnancy, vitamin A excess, tetracyclines (think acne treatment), nalidixic acid, cyclosporine, OCP use, corticosteroids, superior venous thrombosis
transient visual obscurations (loss of vision for a few seconds on certain movements)
diplopia due to CN VI palsy
increased blind spot
pulsatile tinnitus
dizziness
increased opening pressure (>200mmHg) on lumbar puncture and normal CSF composition
no other causes of ICP can be identified (mass, vascular lesion, structural lesion) – R/O with MRI
there are signs of increased ICP but papilledema is not necessary for diagnosis
there is an absence of neurological signs except for CN VI palsy
Neuroimaging: Empty sella 25%,
Flattening of globe, Enlarged optic nerves, Protrusion/enhancement of optic nerve head, Increased tortuosity of optic nerve
Mechanism of increased ICP is unknown
Absorption of CSF across arachnoid granulation into dural venous sinuses is impaired
Associated with cerebral venous obstruction, dural AV malformation, systemic vasculitis (decreased outflow, increased ICP)
Magnetic resonance venogram (MRV) is used to r/o thrombosis of cerebral venous sinuses in atypical presentations (male, nonobese, suspected coagulopathy)
Follow-up work-up with visual acuity, color, visual field testing
Management:
Acetazolamide (Diamox) – risk of tingling in extremities and kidney stones
Furosemide if intolerant to acetazolamide
Corticosteroids (controversial)
Weight loss
With intractable headaches and progressive visual fields deficits on max meds – surgical interventions
Optic nerve sheath fenestration with progressive vision loss
CSF diversion procedure with headaches, CN VI palsy, papilledema
Lumboperitoneal or ventriculoperitoneal shunt
Morbid obesity: gastric bypass
Prognosis:
Better prognosis with better visual acuity
Gradual improvement with treatment but not necessarily recovery
Significant vision loss at presentation suggests higher risk
Worse prognosis: female, black race, HTN, anemia, younger age, severe obesity, severe papilledema
idiopathic intracranial hypertension (IIH)
opacity of the crystalline lens
age related or secondary to an insult – inflammation, trauma, drugs
multiple types: cortical, nuclear sclerosis, posterior subcapsular, white mature, traumatic, congenital
leading cause of reversible blindness worldwide
decreased vision, glare, inability to perform activities of daily living, trouble with small print reading
treatment:
glasses to correct refractive error
surgery - now use extracapsular technique in which the capsule is opened (capsulorhexis), the lens is broken down and aspirated (phacoemulsification), and an artificial lens is inserted
complications are uncommon but sight threatening
no medical prevention available
Catract
elevated intraocular pressure due to functional obstruction of trabecular meshwork
optic nerve cupping (loss of retinal NFL leads to increase in cup in center of nerve)
visual field defects (usually arcs in peripheral visual field, advances without treatment)
increases with age and is asymptomatic
reduce intraocular pressure with topical eye drops, laser treatment to trabecular meshwork, or surgery
primary open angle glaucoma
common – associated with ASA, warfarin, straining (increased intrathoracic pressure)
especially common in the elderly
appears serious but is not
small about of blood is layered between the conjunctive and sclera
resolves with time, no treatment needed
subconjunctival hemorrhage
most common cause of pink eye
redness, watery discharge, foreign body sensation, blurry vision
adenovirus, HSV, MMR
follicles, pre-auricular LAD, conjunctival membranes, corneal sub-epithelial infiltrates
counsel patient, will get worse over 4-7 days and lasts 2-3 weeks; highly contagious, hand washing is important
viral conjunctivitis
less common cause of pink eye
purulent discharge, redness, discomfort
papillae, chemosis
staph, pneumococcus, Moraxella, Haemophilus, gonococci (hyperacute), chlamydia
culture if not responding to empiric treatment, severe, or recurrent
treat with polytrim or fluoroquinolone drops
H. flu – systemic antibiotics
Neisseria – IM/IV antibiotics
bacterial conjunctivitis
Yellow flat or raised lesion in palpebral conjunctiva that does not involve the cornea
nasal or temporal actinic changes
redness, irritation
elastoid degeneration of conjunctiva from UV light exposure
treat with lubrication, anti-inflammatories, no surgical intervention required
Pingueculum
wing shaped fibrovascular growth extending to the cornea resulting from UV light exposure
can grow over the visual axis or cause significant astigmatism
decreased vision, redness, irritation
treat with lubrication, topical NSAIDs, topical steroids, surgery (excision with conjunctival autograft or amniotic membrane)
Pterygium
inflammation of the episclera
causes: idiopathic, infectious, rosacea, thyroid dysfunction
redness, discomfort (moderate), no discharge
sectoral or diffuse redness
phenylephrine test shows blanching
cotton tipped applicator test shows mobile redness
if recurrent: ANA, RF, ESR, uric acid, RPR, FT-ABS, ANCA work-up
treatment: time, oral NSAIDs, topical steroids
episcleritis
inflammation of the sclera
severe pain (tender to touch), acute red eye, recurrent symptoms
inflammation of scleral vessels – no blanching with phenylephrine or movement with cotton tipped applicator test
scleral edema or thinning
subtypes: diffuse anterior, nodular anterior, necrotizing with inflammation, necrotizing without inflammation, posterior
etiology: RA, ANCA-associated, PAN, reactive arthritis, IBD, herpes zoster, syphilis, TB, gout
treatment: systemic steroids or immunosuppressants
scleritis
leukoplakic or grey-white gelatinous lesion, usually at the limbus
middle age – elderly
unilateral, unifocal
dysplasia, carcinoma in situ, can become invasive
treatment: complete excision with cryotherapy at the margins
conjunctival intraepithelial neoplasm (CIN)
