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Hordeolum
- Epidemiology:
- -risk factors = seasonal changes, make up, contacts, stress
- Presentation:
- -swelling of upper or lower eyelid
- -pain
- -red
- -inflammed
- Pathophysiology:
- -acute infection of meibomian (oil) glands of the eye
- -due to stasis of oil in the gland
- Treatment:
- -lid hygeine
- -warm compress
- -Abx
- -I and D if doesn't respond to conservative
- Complications:
- -rule out neoplasm (loss of eye lashes, multiple recurrences, discoloration)
- -may lead to preseptal cellulitis or orbital cellulitis
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Chalazion
- Presentation:
- -swelling of upper or lower eyelid
- -NO sign of infection
- Pathophysiology:
- -sterile, chronic granulomatous infection
- Treatment:
- -lid hygiene
- -warm compress
- -I and D
- -rule out neoplasm
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Conjuctivitis
- Epidemiology:
- -viral is most common and most contagious
- -bacterial is spread by fomites
- -trachoma is spread by flies
- -inclusion spread by oral sex
- Presentation:
- -foreign body sensation
- -itching or burning
- -sensitivity to light
- -blurring but not loss of vision
- -redness (hyperemia)
- -tearing
- -exudate
- ***if there is pain then the cornea is involved (keratoconjuntivitis)
- Pathophysiology:
- 1. Viral
- -one eye followed by the other in 3-5d
- -may be preceded by URI
- 2. Bacterial
- -mucopurulent discharge
- -not as contagious
- 3. C. trachomatis
- -common cause of vision loss - 3rd world
- -bilateral redness, irritation, discharge
- -can lead to conjunctival scarring
- 4. Inclusion Conjunctivitis
- -chlamydia infection due to a different bug
- -seen in patients with genital chlamydia
- Treatment:
- -hygiene (hand washing)
- -often self-limiting
- -Abx
- -systemic tx for gonorrhea and chlamydia
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Pterygium
- Epidemiology:
- -risk factor = UV light exposure
- Presentation:
- -asymptomatic at the border of cornea and conjunctiva
- -may be inflammed
- -vision loss if block pupil
- Pathophysiology:
- -submucosal growth of fibrovascular connective tissue
- -typically benign
- Treatment:
- -prevention
- -lubrication
- -topical anti-inflammatory
- -surgical excision
- Complications:
- -may block vision or disrupt tear film
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Subconjunctival Hemorrhage
- Epidemiology:
- -more common in elderly or pts on blood thinners
- Presentation:
- -bright red patch of blood on the sclera
- -typically asymptomatic
- Pathophysiology:
- -can occur without clear cause
- -may be due to sudden P increase (cough)
- -rupture of the small conjunctival vessels that bleed into the subconjunctival space
- -blood is broken down by MPs
- Treatment:
- -resolution in one to several weeks
- -reassurance and education
- -lubrication
- -evaluate for coagulopathy
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Corneal Abrasion
- Epidemiology:
- -main risk factor = contact lenses
- Presentation:
- -pain
- -redness
- -tearing
- -photosensitivity
- -blurred or hazy vision
- -discharge
- -foreign body sensation
- Pathophysiology:
- -loss of outer epithelial cell layer over the cornea
- -usually caused by trauma
- -little inflammation
- Treatment:
- -Abx
- -steroids
- -oral doxy and Vit C for corneal integrity
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Corneal Ulcer
- Pathophysiology:
- -pain
- -redness
- -tearing
- -photosensitivity
- -blurred or hazy vision
- -discharge
- -foreign body sensation
- Pathophysiology:
- -erosion of the epithelial and stromal layer over the cornea
- -most often caused by infection
- 1. Bacterial: staph, strep, mycobacterium, pseudomonas (highly associated with contacts!)
- 2. Fungal: Corticosteroid drop users, agricultural workers
- 3. Viral: usually herpes
- Treatment:
- -Anti-microbial therapy
- -oral doxy and vit C
- -steroids
- Complications:
- -may lead to perforation of the cornea and loss of eye
- -corneal opacification, corneal melting, corneal necrosis
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Uveitis
- Presentation:
- -inflammation of uvea (choroid, ciliary body, iris)
- 1. If includes the iris
- -pain
- -light sensitive
- -decreased vision
- 2. Includes only posterior portion
- -floaters
- -blurred vision
- -loss of field or acuity
- Pathophysiology:
- 1. Autoimmune
- 2. Toxoplasmosis
- 3. Syphilis
- 4. Sympathetic ophthalmia (trauma induces exposure of immune system to eye antigens --> attack the other eye)
- 5. Malignancy
- Treatment:
- -steroids
- -cycloplegic (reduces risk of scarring)
- -tx underlying disorder
- Complications:
- -scarring of retina or optic nerve (blindness)
- -scarring of iris (glaucoma)
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Episcleritis
- Epidemiology:
- -relatively common
- -1/3 associated with local or systemic disorder
- Presentation:
- -localized patch of redness
- -minimal pain
- -no vision change
- -no discharge
- Pathophysiology:
- -inflammation of episclera (thin layer of vascularized connective tissue that lies btwn the sclera and conjunctiva)
- -cause unknown
- Treatment:
- -resolves w/in 2 weeks --> observation
- -NSAIDs or steroids
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Cataracts
- Epidemiology:
- -age related cataract is one of the most common causes of blindness in the developing world
- Presentation:
- -progressive vision loss over years
- -increasing glare
- -decreased vision in bright settings
- -often bilateral
- -opacity of lens
- -unable to see fundus on exam
- Pathophysiology:
- -nuclear sclerosis: lens epithelial cells divide throughout life
- -cataract consists of proteins aggregating within the lens that reduce transparency
- -could be central (myopic shift like DM)
- Treatment:
- -refraction
- -surgery
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Vitreous Floaters
- Epidemiology:
- -most ppl have at some point
- -almost always benign
- Presentation:
- -transparent webs, strings etc floating in vision
- Pathophysiology:
- -normally the vitreous is transparent (made of collagen fiber matrix and hyaluronic acid gel)
- -condensations within the vitreous are mildly opaque
- -probably persist for life but only noted sometimes due to cerebral adaptation
- Treatment:
- -reassurance and education
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Vitreous Detachment
- Presentation:
- -increased number and size of floaters
- -photopsia
- Pathophysiology:
- -vitreous contracts with age
- -transient stimulation of the retina produces photopsia
- Treatment:
- -reassurance and education
- Complications:
- -vitreous hemorrhage
- -retinal detachment
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Vitreous Hemorrhage
- Epidemiology:
- -caused by: untreated severe diabetic retinopathy, traumatic vitreous detachment, intracranial hemorrhage
- Presentation:
- -painless vision loss
- -"blacking out" of vision
- -seeing "shadows"
- -floaters
- -boat shaped area of blood
- Pathophysiology:
- -diabetic neovascularization leads to small, poorly developed blood vessels that may grown into the vitreous
- -these vessels are easily torn
- Treatment:
- -observation
- -surgery
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Retinal Detachment
- Presentation:
- -floaters
- -photopsia
- -painless vision loss ("dark curtain")
- Pathophysiology:
- -separation of sensory retina (photoreceptors and inner tissue layer) from underlying retinal pigmented epithelium
- 1. Rhegmatogenous
- -most common type
- -usually preceded by vitreous detachment
- -full thickness break in sensory retina with passage of liquid vitreous into subretinal space
- 2. Tractional:
- -most commonly due to diabetic proliferative retinopathy
- -retina actively pulled away by membranes
- 3. Exudative:
- -diseases of retinal pigmented epithelium and choroid
- -accumulation of fluid beneath sensory retina
- Treatment:
- -location and type dependent
- -tx underlying etiology
- -typically an emergency
- -laser or cryotherapy to create adhesion
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Age-Related Macular Degeneration
- Epidemiology:
- -leading cause of irreversible vision loss in developed world
- -pts > 55 years
- -genetic susceptibility
- -Risk factors: female, white, smoking
- Presentation:
- -slowly progressive bilateral vision loss
- -central vision distorted first (scotoma)
- -dry: drusen in macular region
- -wet: neovascularization
- Pathophysiology:
- 1. Dry: drusen are made of ECM material that results from degeneration of retinal pigmented epithelial cells
- 2. Wet: choroidal neovascularization that can leak blood and impair retinal fxn
- Diagnosis:
- -fluorescein angiography
- Treatment:
- -Dry: vitamins and antioxidants
- -Wet: VEGF antagonists
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Diabetic Retinopathy
- Epidemiology:
- -DM1: 3-5 years after presentation, higher rate of progression to proliferative
- -DM2: may have at the time of diagnosis
- -one of leading causes in the west
- Presentation:
- -vision loss (already indicates significant progression)
- -cotton wool spots
- -flame shaped hemorrhages
- Pathophysiology:
- -progressive microangiopathy
- 1. Non-proliferative
- -microaneurysms can rupture --> intraretinal hemorrhage
- -venous beading
- -cotton wool spots
- -macular edema (blindness)
- 2. Proliferative
- -progressive retinal ischemia stimulates VEGF
- -formation of fragile blood vessels
- -vessels leak serum proteins and bleed
- -may grow over the optic disc and retina
- Treatment:
- -control glucose, BP and lipids
- -stop smoking
- -pan-retinal laser photocoagulation
- -anti-VEGF agents
- Complications:
- -neovascular glaucoma (vessels grow into iris and anterior chamber causing increased IOP)
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Hypertensive Retinopathy
- Epidemiology:
- -increased in patients with systemic HTN
- Presentation:
- -usually asymptomatic
- -"copper wire", "silver wire" appearance
- -A-V nicking
- -cotton wool spots
- Pathophysiology:
- -arteriolosclerosis of retinal vessels
- Treatment:
- -tx HTN and other risk factors
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Central Retinal Artery Occlusion
- Epidemiology:
- -same risk factors as cerebrovascular disease
- -temporal arteritis
- Presentation:
- -sudden onset of painless severe vision loss in one eye
- -precursor: amaurosis fugax
- -central sparing in 25%
- -afferent pupillary defect
- -decreased vessels
- -retina appears opaque
- -"cherry red spot" (thinner retina over macula)
- Pathophysiology:
- -atherothrombotic disease
- -emboli from cardiac mural thrombi
- -emboli from ulcerated plaques of carotid
- -vasculitis (temporal arteritis)
- -irreversible damage after 90 minutes
- Treatment:
- -decrease intraocular pressure
- -ocular massage
- -paracentesis
- -thrombolytics (controversial)
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Branch Retinal Artery Occlusion
- Epidemiology:
- -better prognosis than CRAO
- Presentation:
- -often asymptomatic
- -may present with sudden onset impaired vision
- -Hollenhorst plaques (fragments of atherosclerotic material)
- Pathophysiology:
- -branch occlusion with infarction of corresponding segment of retina
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Central Retinal Vein Occlusion
- Epidemiology:
- -risk factors = HTN, DM, vasculitides, hyperviscosity, smoking
- Presentation:
- -sudden onset of unilateral painless vision loss
- -blood and thunder appearance
- Pathophysiology:
- -occlusion leads to congestion of the venous blood in the intraretinal space
- -vision compromised by fluid and blood
- 1. Nonischemic: better visual potential
- 2. Ischemic: poor visual potential, leads to neovascularization
- Treatment:
- -anti-VEGF agents
- -pan-retinal laser photocoagulation
- Complications:
- -neovascular glaucoma
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Primary Open Angle Glaucoma
- Epidemiology:
- -acquired optic neuropathy
- -one of the leading causes of blindness
- Presentation:
- -slowly progressive peripheral vision loss
- -painless
- -enlarged cup to disc ratio
- -elevated intraocular pressure
- Pathophysiology:
- -increased intraocular pressure damages the optic nerve leading to thinning of the retinal nerve fiber layer
- --> compensatory enlargement of the optic cup
- Treatment:
- -enhance outflow of aqueous humor: PG analogs (first line)
- -reduce production of aqueous humor: beta blocker, CAI, alpha agonist
- -Muscarinic agonist
- -Cholinesterase inhibitors
- -laser trabeculoplasty
- -glaucoma drainage surgery
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Acute Closed Angle Glaucoma
- Presentation:
- -acute
- -painful
- -pro-inflammatory (red)
- -nausea and vomiting
- -enlarged cup to disc ratio
- -elevated intraocular pressure
- Pathophysiology:
- -attack often precipitated by pupillary dilation in ppl with shallow anterior chamber
- -transient contact of iris with anterior surface of the lens obstructs outflow of aqueous humor
- --> iris bombe (iris bulges forward)
- -iris blocks anterior chamber angle and prevent outflow into trabecular meshwork
- Treatment:
- -Enhance outflow of aqueous humor (alpha agonist, miotics, topical steroids)
- -reduce production of aqueous humor (beta blocker, CAI, mannitol)
- -laser peripheral iridotomy (permanent connection btwn anterior and posterior chambers)
- -preventive laser peripheral iridotomy on the other eye
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Anterior Ischemic Optic Neuropathy
- Presentation:
- -sudden onset painless vision loss in one eye
- -visual obscurations
- -swelling of optic disc
- -flame-shaped hemorrhages
- Pathophysiology:
- 1. Temporal arteritis
- -vasculitic inflammation of short ciliary arteries
- 2. Cerebrovascular type
- -same nonarteritic processes that cause cerebrovascular disease in posterior ciliary arteries
- -segmental or complete infarction of the portion of the optic nerve that lies just deep to the surface layer of the optic disc
- -develop optic atrophy
- Treatment:
- -steroids (can save vision)
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Retinopathy of Prematurity
- Epidemiology:
- -disorder in some premature infants
- Pathophysiology:
- -retinal vascularization occurs right before birth
- -premature infants may have incomplete vasculature of their retina
- -if baby is exposed to high level of O2 the immature vessels can constrict and lead to retinal ischemia
- -ischemia leads to upregulated VEGF and neovascularization
- Treatment:
- -Laser
- -anti-VEGF
- -surgery to repair strabismus and retina
- Complications:
- -retinal detachment
- -macular dragging
- -vitreous hemorrhage
- -strabismus
- -premanent vision loss
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Retinitis Pigmentosa
- Epidemiology:
- -hereditary retinal degeneration
- Presentation:
- -chronic onset of painless bilateral vision loss
- -impaired night vision
- -delayed recovery from glare
- -progressive loss of peripheral vision
- -deposits of black pigment in the shape of "bone corpuscles"
- -pale optic discs due to optic atrophy
- Pathophysiology:
- -autosomal recessive, autosomal dominant, X-linked
- -mutations in the genes that regulate the function of photoreceptor cells or the retinal pigment epithelium
- -rods affected more than cones
- Treatment:
- -supportive
- -genetic counseling
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Chorioretinitis
- Presentation:
- -painless or painful vision loss of one or both eyes
- Pathophysiology:
- -inflammation of the choroid (uveitis) and the retina
- -caused by a host of infectious, autoimmune, neoplastic and idiopathic disorders
- -commonly caused by toxoplasmosis
- Complications:
- -retinal damage
- -loss of vision
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Myopia
- Epidemiology:
- -most commonly presents during teens
- -related to family history
- Presentation:
- -loss of visual acuity
- -near sighted-distant objects blurry
- Pathophysiology:
- -eyeball too long for refractory system
- Treatment:
- -refractive therapy
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Hyperopia
- Epidemiology:
- -most commonly presents during teens
- Presentation:
- -loss of visual acuity
- -far sighted
- -near vision poor
- Pathophysiology:
- -eyeball too short for refractory system
- -near vision poor due to less accommodation
- Treatment:
- -refractive therapy
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Astimgatism
- Presentation:
- -visual image distorted
- Pathophysiology:
- -deviated cornea shape
- Treatment:
- -refractive therapy
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Presbyopia
- Presentation:
- -near objects appear blurry
- Pathophysiology:
- -lens gradually loses its normal elasticity, leading to gradual increase of the near point
- Treatment:
- -refractive therapy
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