Ophthalmologic Disorders

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jknell
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194910
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Ophthalmologic Disorders
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2013-01-25 00:59:47
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MBB II
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  1. 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
  2. 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
  3. 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
  4. 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
  5. 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
  6. 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
  7. 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
  8. 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)
  9. 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
  10. 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
  11. 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
  12. 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
  13. 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
  14. 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
  15. 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
  16. 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)
  17. 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
  18. 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)
  19. 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
  20. 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
  21. 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
  22. 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
  23. 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)
  24. 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
  25. 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
  26. 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
  27. 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
  28. 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
  29. Astimgatism
    • Presentation:
    • -visual image distorted

    • Pathophysiology:
    • -deviated cornea shape

    • Treatment:
    • -refractive therapy
  30. 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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