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1533 Cards in this Set
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New COURSE: Ocular Disease II
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New lecture: 2 Opt 631 - Corneal Degen Fall 2009
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what is the difference between corneal dysgenesis, dystrophy, and degenerations
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Dysgenesis: tend to be congenital. may be hereditary. Dystrophy: happens later in life. generally hereditary. typically central cornea. Degeneration: no developmental or hereditary pattern. usually start in peripheral cornea. happens later in life.
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name and describe the two main types of corneal degenerations
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involutional: more benign conditions age-related conditions: Pinguecula, Limble girdle of Vogt, Arcus, Hassal-Henle bodies, Crocodile (mosaic) shagreen non-involutional: related to local and systemic conditions: Pterygium, Amyloid degeneration, Band keratopathy, Salzmann’s nodular, Terrien’s marginal, Pellucid marginal
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what does involutional mean
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The retrogressive change in vital processes after their functions have been fulfilled, such as the change that follows the menopause. 4. A backward change.
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what is the most common corneal degeneration that you will see in clinic
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arcus (senilis) (50% by age 50, 100% by age 80)
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what is arcus
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cholesterol deposits in the anterior stroma of the cornea
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is arcus unilateral or bilateral
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bilateral
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what does arcus look like
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1-2 mm white band in the mid-periphery of the cornea
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when should you be suspicious if you see arcus and of what
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if the pt is under 40. suspicious of cardiovascular disease (hypercholesterimia etc.)
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what test should you do if you find arcus on a pt under 40
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blood pressure. -refer if no medical exam in past 2 yrs.
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describe the progression of arcus
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usually start inferior and superior and fills in 360 degrees.
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what is the name of the condition with two thin white lines at 3 and 6 o'clock
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limbal girdle of vogt
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is limbal girdle of vogt unilateral or bilateral
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bilateral
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whta is limbal girdle of vogt
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Narrow band of white crystalline-like opacity in nasal and temporal limbus area Degeneration of collagen fibers; Not vascularized
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name and describe the two types of limbal girdle of vogt and any conditions associated with them
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Type I -- associated with early band keratopathy - see clear zone between limbus and opacity line Type II -- simply peripheral corneal finding - no clear zone
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describe the management of limbal girdle of vogt
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none tx necessary. tx for band keratopathy if present.
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what is this
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dellen
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what is a dellen
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Focal, peripheral thinning near limbus
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is the epithelium intact in a dellen
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May occupy up to 1/2 of corneal thickness but epithelium is intact
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what causes a dellen
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secondary to dessication, poor wetting
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describe the management of dellen
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lubrication, theraputic SCL
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what are the normal type of corneal gutota called
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hassal-henle bodies
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what are hassal-henle bodies
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Small, round thickenings of Descemet's membrane with overlying endothelial displacement they are peripheral corneal guttata
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are hassal-henle bodies in central or peripheral cornea
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peripheral
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what is the main DDX for hassall-henle bodies
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fuch's dystrophy
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what is the tx for hassall-henle bodies
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none necessary.
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what is the name of the condition with the kissing bird topography
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pellucid marginal degeneration
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what is pellucid marginal degeneration a variation of
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keratoconus
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how does the area of corneal steepening compare in pellucid marginal degeneration and keratoconus
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pellucid: inferior keratoconus: central
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is pellucid marginal degeneration unilateral or bilateral
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bilateral, but asymetrical
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what corneal complication can result from pellucid marginal degeneration and what is it
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hydrops. where the stretched descemet's membrane breaks and aqueous floods into the stroma causing massive corneal edema
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is hydrops painful
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yes
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what is this
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Terrien's marginal degeration
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describe 2 subjective symptoms that a pt with terrien's marginal degeration will complain of
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pain and decreased VA
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is terrien's marginal degeneration more common in men or women
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75% males
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is terrien's marginal degeneration usually unilateral or bilateral
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bilateral but asymmetric
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descirbe the pathophysiology of terrien's marginal degeneration
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Marginal stromal thinning, opacification and superficial neovascularization Begins as marginal opacification, usually superionasally (may look like arcus) Central edge may have a yellow border of lipid
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what can happen as a result of trauma with a pt with terrien's marginal degeration
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minor trauma can cause corneal rupture
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describe the management of terrien's marginal degeneration
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you need to refer this to corneal specialist. my tx with steroids for pain, keratoplasty often indicated.
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what is this
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(marginal) furrow degeneration
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is furrow degeneration unilateral or bilateral
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bilateral
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what is furrow degeneration
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corneal thinning usually seen in or adgacent to arcus. no neovascularization.
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is the epithelium intact in furrow degeration
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yes
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is furrow degeneration associated with any other conditions
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yes. Ring ulcer seen with acute rheumatoid arthritis, systemic lupus erythematous, leukemia, polyarteritis nodosa, tuberculosis
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describe the management of furrow degeneration
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treat the underlysing systemic cause
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what is this
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mooren's ulcer
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is mooren's ulcer more common in males or females
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males
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describe the two types of mooren's ulcer
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2 types:
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describe the progression of mooren's ulcer
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3 - 12 month course, with remissions.
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what is mooren's ulcer
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autoimmune reaction. Begins with marginal infiltrate (WBC)à chronic, serpiginous limbal ulceration
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is a pt with mooren's ulcer suseptable to trauma
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mild trauma may perforate globe. cornea can thin to 200 microns.
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describe the management of mooren's ulcer? are they able to have a corneal transplant
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you need to refer this to a corneal specialist. there is too much of a chance of perforation. they are not able to have a corneal transplant because the area they would need to place the graft onto is the thinned part of the cornea in this condition.
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how is mooren's ulcer different from terrien's marginal degeneration
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they are pretty similar. they differ in their geographical presentation. terrien's usually begins superonasally.
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what is this
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Posterior Crocodile Shagreen
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is posterior crocodile shagreen unilateral or bialteral
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bilateral
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what causes posterior crocodile shagreen
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changes in the appearence of descemet's that forms the lines in this condition
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describe the management of posterior corcodile shagreen
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no tx necessary. totally benign condition.
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what is this
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anyloid degeneration
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what is anyloid degeneration
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gellatenous blobs on the cornea. Degeneration in the area of Bowman's and epithelium. Secondary to long standing disease (i.e. trachoma, glaucoma (not usually), uveitis, bullous keratopathy)
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describe the appearence of amyloid degeneration
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Fleshy mass; Creates nodular surface Salmon pink to yellow-white Cornea may be vascularized
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when do you see amyloid degeneration
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with uncontrolled, long-standing ocular disease. typically we will treat primary cause before it gets to this stage.
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are there any treatments for amyloid degeneration
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prevention, keratectomy (with golf club spud), corneal transplant.
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what is the ring left from a foriegn body called
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coat's white ring
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what condition is this
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band keratopathy
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what is band keratopathy
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Calcium deposits within the interpalpebral fissure White to yellow deposits at Bowman's and anterior stroma
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is band keratopathy a primary or a secondary disorder
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secondary May be secondary to ocular inflammation or systemic diseases: Chronic anterior uveitis, prolonged glaucoma, phthisis bulbi Hypercalcemia conditions: sarcoid, Vit D toxicity, hyperparathyroid, metastatic carcinoma of the bones Many other causes including autoimmune: gout, lupus, JRA
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describe the managment of band keratopathy
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treat the primary cause. you would refer this out; tx include: chelating agents (EDTA), keratectomy, lamellar keratoplasty, phototheraputic keratectomy, corneal transplant.
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what condition is this
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bullous keratopathy
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describe the pathophysiology of bullous keratopathy
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fluid accumulates and the epithelium lifts off the basement membrane Caused by long term, prolonged corneal edema Bubbling of the cornea, break down and reform; Eventually scar
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what is the main DDX for bullous keratopathy
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fuch's dystrophy
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describe the management of bullous keratopathy
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1. antiedema tx 2. therapeutic CLs
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name a common hyperosmotic
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muro 128
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what condition is this
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salzmann's nodular degeneration
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is salzmann's nodular degeneration more common in males or females
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females
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is salzmann's nodular degeneration usually unilateral or bilateral
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bilateral
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what are of the cornea is salzmann's nodular degeneration usually found
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mid-periphery
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is salzmann's nodular degeneration associated with any other conditions
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Related to previous inflammations -- esp. Phlyctenular disease
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what are the two ocular conditions related to vitamine A deficiency
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xerophthalmia and keratomalacia
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what is keratomalacia
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vit. A deficiency in which the cornea becomes desiccated at first and then softens, at which stage it is associated with infiltration, pannus, necrosis, opacification and the eye becomes blind. there is also a lack of reaction to inflammation leading to a destruction of the eye if infection occurs.
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what is xerophthalmia
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extreme dryness of the conjunctiva and cornea due to a failure of the secretory activity of the mucin-secreting goblet cells of the conjunctiva. keratinization of the epithelium
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what does the term neurotrophic mean
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there is a desensativity of the corneal nerves
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what is the number one cause of blindness of children world wide
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vitamine A deficiency
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bitot's spot
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foamy patch found on the bulbar conjunctive near the limbus in xerophthalmia and due to vit. A deficiency.
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what is this
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Kruckenberg's spindle
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what is kruckenberg's spindle
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Vertical spindle shaped pigment deposition on posterior cornea Inferior 1/3 to 1/2
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what does kruckenberg's spindle suggest
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old uveitis or pigment dispersion syndrome (glaucoma)
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why is kruckenberg's spindle verticle
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because of the convection current of the aqueous.
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describe the convection current in the aqueous
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aqueous moves up towards the body and downward toward the cornea because heat from our body is warmer than air.
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what extra test should you do if you see kruckenberg's spindle
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iris transillumination
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how long does a kruckenberg's spindle last
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months to years
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what condition is this
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vortex keratopathy
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what part and level of the cornea does vortex keratopathy occur
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epithelium just below the pupil
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what does vortex keratopathy look like
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Greyish or golden epithelial deposits
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what medical condition is assoiated with vortex keratopathy? what medications are associated with vortex keratopathy (4)?
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Fabry disease drugs, including but not limited to: Amiodarone Hydroxychloroquine Indomethacin Tamoxifen
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if you see vortex keratopathy what do you need to do if you can not rule out medications as the cause?
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you need to send them out for glactosidase A deficiency testing (fabry disease). this is a case where you can save a pts life from detecting this condition.
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if you see vortex keratopathy and the pt tells you that they are taking plaquenil (hydroxychloroquine) what do you need to do
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look at the macula (OCT, fields, amsler, high plus, etc.). if they are taking high enough doses to cause vortex keratopathy there will likely be changes to the macula and if you detect them you could save their sight.
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what is this
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arlt's triangle
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describe the pathophysiology of arlt's triangle
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WBCs that have deposited on the endothelium
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what does arlt's triangle indicate
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Pathognomonic for old uveitis
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what is this
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brawny cornea
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brawny cornea is kind of academic. you don't actually see it very often
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describe the pathophysiology of brawny cornea
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usually insult to the limbal area causes pigmented cells from the limbal area to migrate into the cornea. -in recurrent corneal erosion, the stem cells that come to replace the epithelium that has sloughed off bring pigmented cells in with them.
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what is the ferric deposition around a filtration bleb called
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Ferry's ring
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what should you do if you see a ferry's ring
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nothing, no pathologic indication.
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what is this
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fleisher's ring
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what does a fleisher's ring indicate
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Pathognomonic for keratoconus. not many other conditions cause fleisher's ring.
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what is a fleisher's ring
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Orangish in color Ferric deposition at the base of keratoconic cone
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what is the best way to see a fleisher's ring
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cobalt blue light without fluorescein. the iron is picked up as a black line.
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what is goar's line
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horizontal brownish line. basically a horizontal kruckenberg's spindle. indicates pigmentary glaucoma.
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what is this
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hemosiderosis (complete)
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what is hemosiderosis
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intracorneal or posterior corneal surface blood stain
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what can cause hemosiderosis
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hyphema
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what is the orange-brown line at the area of the junction of the upper lid
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hudson-stahli line.
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does a hudson-stahli line occur more frequently in males or females
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males
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at what layer of the cornea does a hudson-stahli line occur
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deposition at bowman's
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what is this
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kaiser-fleischer ring
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what is a kaiser-fleischer ring and what is the best way to see it
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copper deposition in anterior chamber angle
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what layer of the cornea does a kaiser-fleischer ring occur
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posterior surface
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if you see kaiser-fleischer ring in a young person what should you suspect
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Wilson's hepaticolenticular disease
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what are these
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keratic precipitates
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what are keratic precipitates
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WBCs on the endothelial surface of the cornea. indicate uveitis or trauma.
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what is keratomelanocytosis
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Pigmented spokes radiating out into the cornea from the limbus. not pathologic.
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what is this
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sampaolesi's line
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what is sampaolesi's line
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pigment granules deposited at schwalbe's line
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what does sampaolesi's line suggest
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pigmentary glaucoma
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what is the ferric deposition at the edge of a pterygium called
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stocker's line
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is iridocorneal endothelial symdrome (ICE syndrome) usually unilateral or bilateral
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unilateral
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is iridocorneal endothelial syndrome more common in males or females
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females
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what are the three condition that make up the iridocorneal endothelial syndrome
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Chandler syndrome Cogan-Reese syndrome Progressive Iris Atrophy
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what is the mechanism of iridocorneal endothelial syndrome and what condition is it likely to cause
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The common link between the three forms is an abnormal corneal endothelium The endothelium can proliferate and migrate into the angle and onto the iris surface The migration into the angle can cause synechial angle closure leading to glaucoma
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New lecture: 3 Opt 631 - Corneal Dysgen Ant Stromal Dyst Cone 2009
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name 4 corneal dysgeneses that impact the size or curvature of the cornea
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Cornea Plana Microcornea Megalocornea Keratoglobus
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picture in question
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what condition is this
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cornea plana
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what type of lens do you put on the keratometer to extend the range for a flat cornea
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minus lens
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what is cornea plana
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a severe decrease in corneal curvature
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what does the limbus and the AC look like in cornea plana
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Limbal landmarks often obscured Shallow anterior chamber
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what ocular disease is associated with cornea plana
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angle closure glaucoma
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is cornea plana associated with any other conditions
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Usually associated with other anterior segment abnormalities i.e. microcornea, sclerocornea, iris coloboma, congenital cataracts
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what quadrant does an iris coloboma usually occur
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inferior or inferionasal
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what is HVID
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horizontal visable iris diameter
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what is microcornea
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small adult cornea. less than 10 mm
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are there any conditions that can occur secondary to microcornea
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risk of glaucoma due to AC crowding
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what type of refractive error is most commonly associated with microcornea
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hyperopia because cornea is flatter than usual
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at what age does the cornea reach near adult size
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Cornea nearly adult size by age 3 - 4 yrs
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what is the normal corneal size of a neonate
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9-10 mm
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is megalocornea or microcornea more common
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megalocornea
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what is megalocornea
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large cornea. greater than 13 mm
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is megalocornea a hereditary disorder
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yes
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describe the progression of megalocornea
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non-progressive
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what type of refractive error is associated with megalocornea
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myopia
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what do you need to DDX with megalocornea
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congenital glaucoma
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what condition is this
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keratoglobus
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what is keratoglobus
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thinning of the entire cornea. especially in the periphery.
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how common is keratoglobus
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extremely rare. both Pat and Dr. Yudkovitch have only seen one in their career.
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is keratoblobus unilateral or bilateral
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bilateral
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what condition is this
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posterior keratoconus
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what is posterior keratoconus
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thinning of the cornea on the back surface only
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what are two cilically observable diagnostic signs of posterior keratoconus
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thinning of the back surface of the cornea (see with optic section) variable degrees of central stromal hazing and scarring
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is posterior keratoconus usually unilateral or bilateral
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unilateral
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how common is posterior keratoconus
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extremely rare
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what is peter's anamoly
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a rare, congenital naomaly of the anterior segment of the eye. it is characterized by a central corneal opacity, usually accompanied by the adhesion of strands of iris tissue to the margins of the opacity, thinning of the stroma and attenuation or abscence of descemet's membrane.
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are there any other ocular conditions associated with peter's anamoly
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Possible anterior segment abnormalities: microcornea, microphthalmos, coloboma, iris dysgenesis
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name the three anterior chamber cleavage syndromes
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Posterior Embryotoxon Axenfeld’s Anomaly or Syndrome Rieger’s Anomaly or Syndrome
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what is the order of structures you see from posterior to anterior on gonioscopy
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cilary body, scleral spur, trabecular meshwork, schwalbe's line
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is posterior embryotoxon common or uncommon
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relatively common
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what condition is this
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posterior embryotoxon
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wht is posterior embryotoxon
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Anterior displacement of Schwalbe’s line
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what area on the corena is posterior embryotoxin found
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Ring may be partial or complete Usually the greatest at 3 - 9 position
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what is the best way to see posterior embryotoxin
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Can be seen with slit lamp, but best seen with gonioscopy
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are there any other ocular conditions associated with posterior embryotoxon
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Monitor IOP's annually. Glaucoma risk is low if this is all that is present -not a serious condition
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what condition is this
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axenfeld's anomaly or syndrome
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what is axednfeld's anomaly
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Posterior Embryotoxin PLUS iris strands that run across AC and attach to Schwalbe’s line
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are there any ocular conditions that occur secondary to axenfeld's anomaly
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May see iris abnormalities (i.e. corectopia) Increased risk of glaucoma: 20-50%
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what position usually has the thinnest angle on gonioscopy? where is the widest angle?
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thinnest superior. widest inferior.
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on gonioscopy consider starting by viewing the inferior angle becuase you will be albe to see the most structures there becase the angle is the widest there. it is most narrow in the superior quadrant.
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what is the differnece between axenfeld's anomaly and axenfeld's syndrome
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Anomaly VS syndrome Anomaly: IOPs normal Syndrome: elevated IOPs (glaucoma)
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what is rieger's anomaly or syndrome
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All of Axenfeld’s PLUS iris hypoplasia
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name three ocular conditions associated with rieger's anomaly or syndrome
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Corectopia: pupil distortion May see corneal defects or strabismus Increased risk of glaucoma: 50-70%
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what is the difference between rieger's anomaly and rieger's syndrome
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Anomaly VS syndrome Anomaly: involves only the eye Syndrome: involves systemic findings as well primarily facial: hypoplasia esp. maxillary (missing teeth...) other systemic findings involve the hands, spine, feet, heart, and hearing
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most corneal dystrophies are what type of inheritance pattern
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autosomal dominant
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are most corneal dystrophies associated with other systemic or ocular diseases
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no
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describe the onset of most corneal dystrophies
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onset early in life with variable progression. usually observed by second decade.
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are most corneal dystrophies unilateral or bilateral
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bilateral; may or may not be symmetrical
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describe the progression of most corneal dystrophies
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slow
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do most corneal dystrophies tend to be central or pheripheral
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central
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most corneal dystrophies involve _______ layer(s) of the cornea
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a single layer
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name two epithelial layer corneal dystrophies
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Epithelial Basement Membrane Dystrophy (EBMD) Meesman’s Juvenile Epithelial Dystrophy
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what are the three diagnostic pattern you see on the cornea of pts with EBMD
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map, dot, fingerprints
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what is another name for epithelial basement membrane dystrophy
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map-dot-fingerprint dystrophy
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what time of day to pts tend to have symptoms associated with EBMD and why
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morning because when them open there eyes in the morning they tear away epithelium
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describe the severity of EBMD
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may present mild, moderate, or severe Mild:
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what type of view is best to see objective signs of EBMD
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retroillumination of the slit lamp with high magnification
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what causes negative staining
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humps on the eipthelium where the stain doesn't get to
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what is this
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map patternn on the cornea from EBMD
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what is this
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dot pattern in EBMD
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what other condition looks like dot pattern in EBMD
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eipthelial ingrowth after LASIK surgery (which needs to be refered right away)
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describe the appearence of a dot pattern from EBMD
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Discrete grayish to clear “spots” Round, ameboid or comma shaped May be clustered Size: usually = 1 mm Often seen with maps
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describe the appearence of a fingerprint pattern associated with EBMD
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Larger patterns centrally Swirled refractile lines- like a fingerprint May originate out of a single point -- mares tail Clear to gray
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what is the common common complication of EBMD
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spontaneous epithelial erosion
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what should you tell the pt before rxing hypertonic solution
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they will sting quite a bit
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what can you do to reduce the sting of a hypertonic drop
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refrigerate it
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how do you want to fit a bandage CL for EBMD
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steep to vault the cornea
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why is lid hygiene importnat for pts with EBMD
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to prevent infection in compromised cornea.
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what is the condition where you puncture the cornea to treat recurrent corneal erosion called
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anterior stromal puncture
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name three surgical proceedures to treat recurrent corneal erosion
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anterior stomal puncture, lamellar keratectomy, phototherapeutic keratectomy
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describe the progression of EBMD
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goes through remissions and exacerbations
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why are hypertonics used to tx recurrent corneal erosion
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the cornea becomes swollen because of the missing epithelium
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describe the prognosis for EBMD
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Prognosis: Guarded Most retain good vision - usually no less than 20/50 Patient Education: **No cure** and recurrent nature of condition
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what condition is this
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meesman's juvenile epithelial dystrophy
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what is meesman's juvenile epithelial dystrophy
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Intraepithelial cysts or vesicles
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what is the best way to see meesman's juvenile epithelial dystrophy
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indirect retoillumination off the fundus (red reflex)
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what do the cysts in meesman's juvenile epithelial dystorphy look like and how can you tell the difference.
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corneal guttata. guttata are on the endothelium and meesman's cysts are in the epithelium
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what is the age of onset for meesman's juvenile epithelial dystrophy
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1 to 2 years
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what region of the cornea (not layer) do the cysts from meesman's juvenile epithelial dystrophy occur
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entire cornea, extends to the limbus. usually dystrophies are more central, but this is an exception that extends all the way to the limbus.
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describe the prognosis for meesman's juvenile epithelial dystorphy
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excellent. acuity reduction is usually slight. may have epithelial erosions after age 40.
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what condition is this
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reis-buckler's dystrophy
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what does reis-bucler's dystrophy look like
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Gray-white irregular opaque pattern in Bowman's layer Creates a mottled or ‘fish-net’ pattern that may project into the epithelium
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are there any complications from reis-buckler's dystrophy
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Painful RCE. Causes anterior stromal opacification Usually by age 20 to 30 VA's drop
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describe the prognosis associated with reis-buckler's dystrophy
|
guraded. acuity usually begins to drop by age 20 to 30.
|
|
what condition is this
|
anterior mosaic dystrophy
|
|
how does anterior mosaic dystrophy and posterior crocodile shagreen differ
|
anterior mosaic dystrophy is kind of like posterior crocadile shagreen but shagreen is more peripheral and mosaic is more central. mosaic may be a variation of crocadile shagreen.
|
|
how is vision impacted by anterior mosaic dystrophy
|
Vision usually not affected
|
|
name three common anterior stromal dystrophies
|
Granular dystrophy Lattice dystrophy Crystalline dystrophy
|
|
what condition is this
|
granular dystrophy
|
|
what do we think is the pathophysiology for granular dystrophy
|
thought to be due to changes in the keratocytes in the cornea. they tend to coalesce and form larger granules.
|
|
how does granular dystrophy affect vision
|
VA's gradually drop (usually no worse then 20/200) by age 60
|
|
what does granular dystrophy look like
|
Round, oval, discrete white spots
|
|
what is the age of onset typically for granular dystophy
|
usually before age 10
|
|
granular dystrophy has a pretty disticnt clinical appearance. you probably will be able to diagnose based on appearance.
|
|
|
what condition is this
|
lattice dystrophy
|
|
what does lattice dystrophy (of the cornea) look like
|
Anterior stromal refractile lines May see dots, flakes, and stellate opacities between the lines
|
|
describe the prognosis associated with lattice dystrophy (of the cornea)
|
guarded
|
|
are there any complications associated with lattice dystrophy (of the cornea)
|
recurrent corneal erosion
|
|
what condition is this
|
cystalline dystrophy
|
|
what is cyrstalline dystrophy
|
crystals form a ring in the central cornea
|
|
what does crystalline dystrophy look like
|
Crystals are white to yellow, may be polychromic. they form a ring in the central cornea.
|
|
are there any conditions associated with crystalline dystrophy
|
Patients usually develop corneal arcus (dense) by age 30 to 40 Associated with hypercholesterolemia xanthelasma
|
|
name two bowman's layer dystrophies
|
Reis-Buckler’s Dystrophy Anterior Mosaic Dystrophy
|
|
xanthelasma
|
a cutaneous deposition of lipid material that appears in the skin of the eyelids, most commonly near the inner canthi. it appears as a yellowish, slightly elevated area. it is a benign and chronic condition that occurs primarily in the elderly. it may be associated with raised blood cholesterol, high-density lipoprotein and triglyceride levels, leading to heart disease or diabetes.
|
|
describe the management of crystalline dystrophy
|
referral for cardiovascular work up. routine follow up.
|
|
what condition is this
|
macular dystrophy
|
|
what is macular dystrophy
|
entire Stroma invaded by mucopolysaccharide material
|
|
describe the age of onset for macular dystrophy
|
Diffuse corneal clouding by age 5 to 9
|
|
describe the visual prognosis associated with macular dystrophy
|
VA's drop substantially by age 30
|
|
what type of inheritance pattern is seen with macular dystrophy
|
usually corneal dystrophies are AD, but macular dystrophy is autosomal recessive
|
|
what area of the cornea is affected by macular dystrophy (not layer)
|
Extends to the periphery (whole cornea)
|
|
are there any complications associated with macular dystrophy
|
corneal guttata formation
|
|
what is the normal corneal thickness of an average person
|
545 microns
|
|
what is the prevalence of keratoconus (number)
|
1 in 2,000 persons
|
|
what do we think is the mechanism for keratoconus
|
we don't know, but might be : enzyme induction leading to cell toxicity à keratocyte aptosis à secondary stromal thinning and corneal ectasia
|
|
describe the progression of keratoconus
|
Slow, insidious refractive changes and the reduction of BVA Usually starts age 15 to 25 Progressive for 5 to 6 years Tends to stabilize ( may destabilize 10 to 15 years later)
|
|
name 7 clinically observable diagnostic signs of keratoconus
|
1. oil drop retinal reflex (edge of the cone seen over red reflex) 2. munson's sign 3. corneal thinning 4. fleischer's ring 5. vogt's striae 6. anterior stromal scarring 7. hydrops
|
|
if you can't get a pt down to 20/20 how can you tell clinically if it is due to irregular astigmatism
|
place a RGP on the eye and see if then can get down to 20/20
|
|
what are the top three reasons for penetrating keratoplasty
|
1. pseudophakic corneal edema 2. endothelial corneal dystophies 3. ectasias/thinning disorders
|
|
what is this
|
oil droplet reflex seen in keratoconus
|
|
what is this
|
vogt's striae
|
|
what are the IC3D Classification for Corneal Dystrophies
|
new classification system based on how well defined a disorder is
|
|
name three common endotheilial dystrophies
|
Fuch’s endothelial dystrophy Congenital Hereditary dystrophy Posterior Polymorphous dystrophy
|
|
what is the age of onset for fuch's endothelial dystrophy
|
starts age 20-30 symptomatic usually age 40-60
|
|
is fuch's endothelial dystrophy more common in males or females
|
females
|
|
what layers of the cornea are affected by fuch's dystrophy
|
problem is with the endothelium, but results in changes to all layers of the cornea.
|
|
what is another name for guttata and what layer of the cornea do they occur in
|
descemet's warts. accumulation posterior to and sometimes in descemet's membrane
|
|
what is the name of guttata found in the periphery
|
hasell-henle bodies
|
|
how does fuch's endothelial dystrophy affect the corneal thickness
|
increases. usually greater than 600 microns.
|
|
what is this
|
corneal guttata
|
|
why is it important to take pachymetry in the center of the cornea
|
because the corneal thickness increases as you go from the center towards the limbus. so you need to take this measurement at the center cornea to be able to compare it to norms.
|
|
what is the mechanism of vision loss in fuch's endothelial dystrophy
|
Endothelial cells overlying the guttata enlarge and are functionally disrupted. Disrupts the pump mechanism (endothelium pumps water out of the cornea). Causes edema of stroma and ultimately epithelium. Stromal edema: Striae, thickening Epithelial edema varies: Epithelial microcysts Wet ground glass-like Bullae formation
|
|
name 4 signs and symptoms of fuch's endothelial dystrophy
|
1. VA loss in late stages 2. photophobia and glare 3. edema (causing fluctuating VA) 4. pain from bullae rupture
|
|
if you have an older pt who is not getting clear vision through the phoropter, and you suspect it is due to an ocular surface issue, try putting a lubricating drop in their eye and see if that improves their vision.
|
|
|
describe 4 treatment options for fuch's endothelial dystrophy
|
1. hypertonic solution 2. hair dryer (for the edema; hot air drys out the tear film, which causes fluid to be drawn out of the eye) 3. therapeutic SCL (to reduce pain if they have bullae rupture) 4. penetrating keratoplasty
|
|
what is the name of the condition that is like fuch's endothelial dystrophy
|
congenital hereditary endothelial dystrophy
|
|
what is congential hereditary endothelial dystrophy
|
similar appearance to Fuch’s but early onset Rare or absent endothelial cells Increased thickness of corneal mass (2-3X's; you can have a cornea over 1,000 micrometers) Diffuse edema - ground-glass like stromal and epithelial Thickening of Descemet's
|
|
name and describe the two forms of cengenital hereditary endothelial dystrophy
|
Recessive form -- has nystagmus – congenital Dominant form -- no nystagmus – onset 1st to 2nd decade
|
|
describe the visual outcome of cengenital hereditary endothelial dystrophy
|
VA's drop, level depends upon edema Can lead to blindness - epithelial cause
|
|
what condition is this
|
posterior polymorphous dystrophy
|
|
what is posterior polymorphous dystrophy
|
the endothelium displays “epithelial characteristics”.
|
|
describe the visual outcome associated with posterior polymorphous dystrophy
|
pretty benign
|
|
describe 4 clinically observable signs associated with posterior polymorphous dystrophy
|
1. vesicular pattern on the back of the cornea 2. band-like pattern (thickening of descemet's membrane) 3. peripheral anterior synechiae 4. corectopia
|
|
what is this type of appearance called
|
ground-glass appearance
|
|
describe the management of posterior polymorphous dystrophy
|
none required unless there are complications. just monitor. Vesicles on epithelium may rupture à bullae Treatment: Artificial tears Hypertonic saline drops/ointment (5% NaCl) Temporary bandage therapeutic soft contact lens Recurrent corneal erosion treatment Secondary glaucoma treatment (synechae)
|
|
|
|
|
is there a heriditary component to posterior polymorphous dystrophy
|
yes, AD
|
|
with the epithelial dystrophies what clinical tests do you need to be concerned about doing
|
tonometry or gonioscopy because their epithelium is compromised and you dont' want to remove a bunch of the epithelium
|
|
is posterior polymorphous dystrophy associated with any other conditions
|
Alpert's syndrome, keratoconus
|
|
what is this
|
pannus
|
|
what is corneal pannus
|
Superficial vascular invasion with fibrous tissue bed Usually chronic result of inflammatory response
|
|
causes of pannus:
|
Rosacea, Staphylococcal hypersensitivity Tight CL fit/CL overwear Phlyctenule Chlamydia (trachoma/inclusion conjunctivitis) Superior limbic keratoconjunctivitis (micropannus only) Vernal/allergic keratoconjunctivitis Herpes simplex virus Chemical burn, trauma
|
|
what is the differnece between corneal neovascuarization and corneal pannus
|
you won't see the haze and the stromal infiltration with neovascularization. pannus is more white and leukoric in appearance.
|
|
what are two of the major causes of interstitial keratitis
|
syphilis and herpes simplex
|
|
describe the management and follow up associated with corneal pannus
|
Treatment Treat underlying cause Discontinue/reduce CL wear Document size and extent Topical vasoconstrictors may reduce redness Follow-up 1-2 weeks if progressing; 3mo-1yr when stable Monitor once stable Refer to corneal specialist if affects VA/central
|
|
what is it important to DDX a pterygium with
|
a conjunctival tumor
|
|
can a pterygium affect refractive error
|
can induce irregular astigmatism
|
|
|
1. protection (sunglasses) 2. artifical tears and or ointments 3. topical vasoconstrictors 4. topical steroid 5. surgical removal (likely to come back)
|
|
what do you need to remember to do if you rx a steroid for pterygium or any other condition
|
take IOP and follow up, checking the IOP
|
|
what is this
|
interstitial keratitis
|
|
what is interstitial keratitis
|
keratitis involving the stroma. it is characterized by deep vascularization of the cornea and is often associated with iridocyclitis.
|
|
is interstitial keratitis usually unilateral or bilateral
|
usually unilateral; may become bilateral
|
|
describe the timing of an interstitial infection caused by a systemic infection
|
Acute ocular infection can occur 5 to 15 years after systemic infection Congenital ocular form can present at age 15
|
|
causes of interstitial keratitis:
|
Congenital syphillis usu. affects both eyes Acquired syphillis unilateral, often sectoral Tuberculosis unilateral, often sectoral Cogan’s syndrome vertigo, tinnitus/hearing loss, vasculitis (e.g. polyarteritis nodosa) Leprosy Herpes simplex virus (HSV) Lyme disease (Borellia bordoferi)
|
|
describe the triad of corneal findings associated with interstitial keratitis
|
Stromal infiltration Stromal haze and edema towards center of cornea Stromal thinning Most apparent in chronic forms; posterior thinning Neovascularization Usually superior 180 degree and deep stroma No blood (“ghost vessels”) in chronic, inactive form
|
|
what is hutchenson's triad
|
in congenital syphilis Notched incisor teeth Deafness (Cogan’s syndrome) Interstitial keratitis
|
|
what is a saddle nose bridge
|
finding in congenital syphilis along with hutchenson's triad
|
|
|
picture in question
|
|
New lecture: 5 Bacterial Keratitis & ulcers 2009 Vault
|
|
|
basal layer of the epithelium is responsible for mitosis. basement membreane is below basal layer.
|
|
|
why does damage to the cornea cause scarring
|
bowmann's layer can not regenerate, so damage causes scarring.
|
|
in what layer of the cornea is the greatest concentration of nerves
|
anterior stroma
|
|
name five cuases of superificial punctate keratitis (SPK)
|
1. dry eye 2. contacts 3. blepharitis 4. baceterial conjunctivitis 5. allergic conjunctivitis
|
|
what is the best way to see superifical punctate keratitis
|
you probably won't be able to see this with white light on slit lamp. the best way is the fluorescein and cobalt blue filter
|
|
what is superficial punctate keratitis
|
Describes superficial punctate corneal epithelial disruption
|
|
what are the two forms of superficial punctate keratopathy
|
Punctate Epithelial Erosion (PEE) Punctate Epithelial Keratopathy (PEK)
|
|
what is punctate epithelial erosion (PEE)
|
Focal areas of epithelial disruption or lesion Slightly depressed Stain well with NaFl, rose bengal and lissamine green
|
|
can you see punctate epithelial keratophthy without any stain
|
yes
|
|
what is punctate epithelial keratopathy
|
Grayish white opacities in the epithelium. Accumulation of epithelial cells that are surrounded by a focal inflammatory infiltrate
|
|
what is the difference between the strict definition and how we use superficial punctate keratopathy clinically
|
Commonly used to refer generally to superficial punctate epithelial disruptions of multiple etiologies Clinically, often used interchangeably with PEE
|
|
describe 4 subjective complaints that a pt with SPK will come in with
|
FB sensation Redness Tearing Photophobia
|
|
what is the difference between confluent and focal SPK
|
confluent: localized area of SPK focal: localized area of SPK where punctate lesions coalesce to form a larger epithelial defect
|
|
name three common pathogens that cuase superficial keratitis
|
Staphylococcus Streptococcus Haemophilus
|
|
is staphylococcus gram positive or negative
|
gram positive cocci
|
|
name two common staphylococcus organisms
|
staph. aureus and staph. epidermidis (part of normal flora, but can also be pathogenic)
|
|
what is the most common ocular pathogen in pts of all ages
|
staphylococcus aureus
|
|
why does staph cause punctate epithelial defects
|
exotoxins from bacteria
|
|
what are the two main causes of phylectenule
|
staphylococcus infection and TB
|
|
what are collarettes (blepharitis)
|
debris and protein build-up at the base of the lashes.
|
|
are there any ocular side effect to aminoglycosides
|
yes, toxic to the cornea. they are still good drugs, but don't be suprised if you start to see some staining after useing for a while.
|
|
what is the minimum amount of times you should rx an antibiotic per day? what is the minimum length of time you should rx an antibiotic for?
|
QID, otherwise you will develop resitance. there are some exceptions, vigamox for example. -continue therapy for at least a week (7-14 days) for prevent resistance.
|
|
what drug is less effective due to many resistant strains and what drug class is it.
|
sulfacetamide (a sulfonamide)
|
|
what is important to remember to tell a pt who is using artifical tears that you rx a topical medication
|
wait between artifical tear use and medication use because the artifical tears will wash out the medication. need to be at least 3 or 4 minuets apart.
|
|
is streptococcus gram positive or negative
|
gram positive cocci
|
|
what is important to remember if you rx an ointment
|
it will make them blurry. usually used at night.
|
|
name two clinically observable signs that indicate streptococcus as the organism behind an ocular infection
|
pseudomembranes and petechial hemorrhages. -petechial hemorrhages also associated with heamophilus infection
|
|
what group of medications is thought to be ineffected against streptococcus infection
|
aminoglycosides (tobramicin and gentamycin)
|
|
Aminoglycosides Fluroquinolones QID to q2-3h Depending on severity & drug used Treatment duration: 7-14 days Exception: Polytrim q3h
|
|
|
are contact lens related complications infectious or inflammatory
|
can be either.
|
|
what can a corneal ulcer look like in it's early stages
|
corneal infiltrate
|
|
are corneal infiltrates or corneal ulcers more common
|
corneal infiltrates are far more common
|
|
what is another name for corneal infiltrates
|
corneal infiltrative events (CIE)
|
|
what type of reaction is a corneal infiltrate
|
not infectious. antigen-antibody reaction (hypersensativity reaction); can be due to hypoxia (CL wearers).
|
|
what causes negative staining
|
elevation on the cornea.
|
|
there may be sectoral hyperemia of the conjectiva in the area adjacent to a corneal infiltrate.
|
|
|
what type of staining do corneal infiltrates cause
|
positive and/or negative (positive is less common and usually smaller than the area of the lesion)
|
|
what do you need to remember with regards to the timing of a fluorescein stain
|
you need to wait a few minuets to see staining. you will miss staining if you look at it right away and don't recheck it after a few minuets.
|
|
is it possible to see old epithelial infiltrates
|
if the epithelial infiltrate involves the stroma it will leave scarring, which you will be able to see.
|
|
is haemophilus gram positive or gram negative
|
gram negative
|
|
corneal infiltrates are frequently associated with chronic conjunctivitis due to blepharitis
|
|
|
what type of medication do you use to tx corneal infiltrate
|
steroid. antibiotic if it is due to chronic infection.
|
|
what do you need to be sure of before you tx a corneal infiltrate with steroid
|
you need to be absolutely sure that it is not infectious in origin. -if there is a break in the epithelium you can use a steroid/antibiotic combo as prophylaxis
|
|
what is the difference between tobradex and zylet clinically
|
dexamethasone has more of a tendancy to increase IOP, but tobradex there is a big difference in price.
|
|
list five ways you can differentiate between a corneal ulcer and a corneal infiltrate
|
ulcer: pain moderate to severe, always have an epithelial defect, discharge, usually have an anterior chamber reaction, can be anywhere but tend toward center infiltrate: mild pain, if there is an epithelial defect it is usually smaller than the lesion, no discharge, no anterior chamber reaction, can be anywhere but tend to be peripheral P: Pain E: Epithelial defects D: Discharge A: Anterior Chamber reaction L: Location
|
|
will a corneal ulcer leave a scar
|
yes, by definition a corneal ulcer involves the stroma. tell them up front, so they don't think that scarring is from poor treatment
|
|
what are the top 2 causes of corneal ulcer in adults
|
1. contact len overwear 2. trauma
|
|
describe the appearance of a corneal ulcer
|
Epithelial edges are usually distinct with an indistinct underlying stromal border. Corneal edema surrounds area involved.
|
|
describe the progression of corneal ulcer
|
TREAT QUICKLY and AGGRESIVLY!! The cornea may scar or perforate Leading to permanent vision loss!!!
|
|
what is a very common organism that cuases a corneal ulcer in CL wearers
|
pseudomonas
|
|
name 5 signs and symptoms that a pt with a corneal ulcer will come complaining of
|
1. decreased VA 2. photophobia 3. pain 4. redness 5. purulent discharge
|
|
is pseudomonas gram positive or gram negative
|
negative
|
|
how quickly can a pseudomonas infection perforate the cornea
|
24 to 48 hours
|
|
describe the tx of corneal ulcer
|
Broad spectrum antibiotics should be used initially until the organism is identified Three main strategies: Monotherapy with fluoroquinolones Combination therapy with fortified cefazolin and fortified tobramycin Combination therapy with fluoroquinolones and fortified antibiotics Monotherapy: Loading dose: 1gtt every minute for 5 minutes, then 2gtts q15mins x 6 hours, then 2gtts q30mins x 18hours, then 2gtts q1h x 24 hours, then 1gt q4h x 12 days, then at the discretion of the treating doctor Cipro ung qhs (treatment is around the clock) -continue use of antibiotics for 1 week after resolution of ulcer Homatropine 5% bid or tid to relieve ciliary spasms and prevent synechiae formation as well as decreased pt discomfort sub-conj. injection or hospitalization if compliance may be an issue
|
|
what are the three fluroquinolones FDA approved for corneal ulcer
|
1. ciprofloxacin 2. ofloxacin 3. levofloxacin -zymar and vigamox are often used off lable
|
|
New lecture: 6 Fungal_and_Amoebic_Keratitis_2009
|
|
|
what is the name of a fungal infection of the cornea
|
keratomycosis
|
|
name thre predisposing facotrs for fungal infection
|
1. trauma (especially with vegtable matter) 2. immunosupression 3. steroid use
|
|
what are the four most common fungi with ocular involvement in the US
|
fillamentous: fusarium, aspergillus, cephalosporium non-fillamentous (unicellular yeast): candida
|
|
Fusarium keratitis outbreak 2006
|
1.
|
|
where is candida found that most other fungi are not
|
all four common ocular pathogens are found ubiquitously on plants and in soil. candida is also found in inanimate objects, food, hospital environments
|
|
which of the four common fungi with ocular involvement in the US is the most virulent
|
fusarium
|
|
describe the pain associated with fungal infection of the eye
|
often less than expected from the clinical picture
|
|
describe the subjective symptoms associated with fungal eye infection
|
similar to bacterial ulcer: Pain (can start as FB sensation)
|
|
describe the onset of fungal eye infection
|
Patient reports SXs no sooner than 5 days after injury, more often from 10 days to 3 weeks ((this is because it takes some time for fungus to grow than bacteria)
|
|
name 5 clinically observable objective signs associated with fungal corneal infection
|
1. stromal grey-white opacity with elevation -epithelium likely intact 2. feathery margins (less distinct than bacterial ulcer) 3. sattellite lesions surrounding primary lesion 4. possible endothelial plaque 5. hypopion
|
|
what is the main DDX for fungal corneal infection
|
bacterial corneal ulcer
|
|
what additional testing do you need to do if you have a corneal ulcer
|
culture
|
|
describe the tx of fungal corneal ulcer
|
48 hours to several weeks ((is how long it takes to grow a culture; you need to treat sooner than this though. Remember that bacterial ulcer is more common. If you treat as a bacterial infection this infection will continue to get worse. This is your clue that your diagnosis is wrong) Filamentous infection
|
|
what is acanthamoeba
|
Ubiquitous protozoans found in water, soil, air, dust
|
|
acanthamoeba are very resistant to chlorine and are found in all kinds of bodies of water. acanthamoeba is usually found in healthy people not immunocompromised people like fungal infections
|
|
|
Acanthamoeba outbreak 2007
|
1.
|
|
subjective symptoms of acanthamoeba
|
Unilateral red eye C.
|
|
what is the most important diagnositc symptoms of achanthamoeba
|
Waxing and waning of symptoms ((very important symptom; months to years)
|
|
describe the early and late clinically observable objective signs of acanthamoeba
|
Early
|
|
why is acanthamoeba often co-infected with bacteria
|
acanthamoeba feed on bacteria
|
|
describe two tests used to diagnose acanthamoeba
|
lab tests, confocal microscopy (HRT)
|
|
how do you tx acanthamoeba
|
refer to corneal specalist! no consensus on how to treat. know the dosage though: Dosage
|
|
New lecture: 1 Anterior_Uveitis_2009
|
|
|
uveal tract is the middle vascular layer of the eye. it includes the uvea the ciliary body and the iris. the primary function of the uveal tract is to provide nutrition to the eye.
|
|
|
what is uveitis
|
an inflammation of any combination of the structures of the uvea.
|
|
what is uveitis that involves the iris only called
|
iritis
|
|
what is uveitis that involves the iris and the biliary body called
|
iridocyclitis
|
|
what is uveitis that involves the ciliary body or pars plana area called (3)
|
cyclitis (pars planitis, peripheral uveitis)
|
|
what is uveitis that involves the iris and the choroid called
|
iridochoroiditis
|
|
where do you see cells in iritis
|
anterior chamber but not anterior vitreous
|
|
where do you see cells with iridocyclitis
|
in the anterior chamber and/or the anterior vitreous
|
|
what is the difference between anterior, posterior and intermediate uveitis
|
1. Anterior = inflammation of iris or ciliary body or both
|
|
where do you see cells in posterior uveitis
|
in the posterior vitreous
|
|
what are the names of the chronic and the acute forms of uveitis
|
gramulomatous uveitis is usually choronic and non-granulomatous is usually acute.
|
|
what are keratic precipitates
|
inflammatory cells that deposit on the endothelium of the cornea.
|
|
describe the etiology of uveitis
|
|
|
what types of keratic precipitates do you see with granulomatous and non-granulomatous uveitis
|
granulomatous: mutton fat KPs non-granulomatous: fine KPs
|
|
are iris nodules associated with granulomatous or non-granulomatous uveitis
|
granulomatous
|
|
is anterior or posterior uveitis more common
|
Anterior uveitis more common than posterior
|
|
describe the age of onset of uveitis
|
peak prevalence 20-50 years old. rarely makes first appearance in old age.
|
|
racial, sexual and geographical predilection of uveitis:
|
Sexual predilection (depends on specific condition)
|
|
what is the most common cause of anterior uveitis
|
idiopathic
|
|
in cases of idiopathic uveitis there is a very strong associate with what gene
|
HLA B27
|
|
describe 6 subjective symptoms that a pt with ACUTE anterior uveitis will come in complaining of
|
Classic SXs
|
|
describe 6 subjective symptoms that a pt with CHRONIC uveitis will come in complaining of
|
Chronic anterior uveitis - may be asymptomatic
|
|
photophobia is a very strong indicator of uveitis
|
|
|
how does acute and chronic uveitis differ in their response to treatment
|
acute: will usually respond to topical drops alone chronic: will usually need topical drops as well as oral meds
|
|
are acute or chronic cases of uveitis more likely to recur
|
chronic
|
|
is acute or chornic uveitis more commonly associated with systemic disease
|
chronic
|
|
does acute and chronic uveitis tend to be unilateral or bilateral
|
acute: unilateral chronic: bilateral
|
|
name 13 clinically observable signs of uveitis
|
1. reduced, painful accommodation (why cyclopligics help) 2. VA possibly reduced 3. circumcorneal (perilimbal) flush 4. corneal edema 5. keratic precipitates 6. AC cells/flare 7. hypopion 8. plasmoid aqueous 9. posterior synechiae 10. iris atrophy (tranillumination defect) 11. iris nodules 12. anisocoria/sluggish pupil (usually the affected eye will be miotic due to prostaglandid release) 13. IOP usually reduced in the affected eye (possibly raised)
|
|
what type of cataracts tend to form from steroid use
|
posterior sub-capsular
|
|
name and describe the two types of iris nodules seen in uveitis
|
a. Busacca
|
|
what is flare
|
protein leaking from the iris and ciliary body
|
|
what are the guidelines for grading cells and flare
|
|
|
cycloplegics will help reduce the pain in uveitis quite a bit; but you need to educate them bc they are already experiencing photophobia and dilating them will make it worse.
|
|
|
what is the difference betwee fine and mutton fat keratic precipitates
|
Fine - whitish/grey fibrin adherent to corneal endothelium
|
|
how long do keratic precipitates take to dissapear
|
months. they may never completely resolve.
|
|
what is circumcorneal (perilimbal) flush
|
a ring of dilated blood vessels around the limbus
|
|
how do the symptoms that a pt will experience differen between chronic and acute uveitis
|
acute: moderate to severe chronic: mild to moderate
|
|
how can you differentiate clinically between keratitis and uveitis
|
pain from keratitis will go away with proparocaine. if it is uveitis it will not.
|
|
if a pt has photophobia that you suspect is from uveitis, you will usually tx with cycloplegics even if you can't see any cells and flare
|
|
|
what are the standard concentrations of tropicamide and phenylephrine
|
tropicamide 1%; phenylephrine 2.5%
|
|
what is the duration of dilation for the following drops: atropine, cyclopentolate, homatropine, phenylephrine, scopolamine, tropicamide
|
atropine: 7-14 days cyclopentolate: 6-12 hours homatropine: 18-24 hours phenylephrine: 4-8 hours scopolamine: 5-7 days tropicamide: 3-6 hours
|
|
what types of medicatinos do you use to tx uveitis (3)
|
cycloplegics, steroids, NSAIDS
|
|
if a pt has an allergy to ________ you should be cautious about using acetazolamide (diamox)
|
sulfa drugs
|
|
|
|
|
why does dilation reduce the likelihood of synechia
|
because the iris is anatomically closest to the lens at the pupilary boarder. if we enlarge the size of the pupil we increase the distance between the iris and the lens.
|
|
what should you do in a uveitis case if synechia has already started to form
|
dilate the eye anyway. if you rip the iris free it's not going to hurt that much, and you need to prevent synechia to preserve vision. your risk of not treating is greater than if you do dilate.
|
|
what do you do if you need to cycloplege a pt with uveitis, but they have narrow angles.
|
ask them if they have ever been dilated before and if there were any problems. if they have then go ahead and dilate because you need to prevent synechia.
|
|
lab test for uveitis: think if the testing is going to change how you treat the condition.
|
|
|
what sex and age range do you expect to see ankylosing spondylitis
|
males 20s and 30s
|
|
what is ankylosing spondylitis
|
chronic form of arthritis
|
|
what test is indicated for all young males with anterior uveitis
|
sacroiliac x-ray (ankylosing spondylitis)
|
|
what is the major subjective symptom associated with ankylosing spondylitis
|
back pain (50% are asymptomatic!)
|
|
what is another name for reiter's syndrome
|
reactive arthritis
|
|
what is reactive arthritis
|
= triad of nongonococcal urethritis, polyarthritis & acute
|
|
what should you be suspicious of if you see an acute conjunctivitis with anterior uveitis
|
reactive arthritis (reiter's syndrom)
|
|
describe the demographic associated with reactive arthritis`
|
males, 20s to 40s
|
|
describe the tx of reactive arthritis
|
Oral tetracycline 250 mg QID x 10 d. ((thought to be clymidial in cause) -treat uveitis as usual
|
|
describe the age of onset and sexual prediliction of juvenile chronic arthritis
|
arthritis by 15 YO or younger, but onset is typically 1 – 4 YO
|
|
what condition that we deal with is associated with still's disease
|
juvenile chronic arthritis
|
|
what is still's ocular triad
|
iridocyclitis, band keatopathy and cataract
|
|
steroids can retard growth in children
|
|
|
what is sarcoidosis
|
multisystem granulomatous disease of unknown etiology which can affect
|
|
what percent of pts with sarcoidosis will have ocular complications
|
20-50%
|
|
describe the demographic associated with sarcoidosis
|
most common is younger african american females
|
|
what type of uveitis is common with sarcoidosis
|
granulomatous
|
|
|
|
|
|
|
|
what is "candle wax dripping"
|
yellow exudate that forms around the blood vessel in retinal vasculitis
|
|
what percent of sarcoidosis pts will have an abnormal chest x-ray
|
80%
|
|
what is tuberculosis
|
granulomatous infection of Mycobacterium tuberculosis; generally
|
|
what percent of pts with tuberculosis will have ocular involvement
|
most pts with TB do not have ocular involvement; only 1-2%
|
|
what is the most common cause of phlyctenular keratoconjunctivits
|
staph infection. could also be due to tuberculosis, but TB is rare.
|
|
what test do you need to do if you suspect TB
|
PPD
|
|
name three drugs used to tx tuberculosis
|
Isoniazid (INH) - drug of choice
|
|
what ocular condition can result from tertiary syphilis
|
argyl-robertson pupil
|
|
name and describe the stages of syphilis
|
Primary – painless ulcer (chancre) Secondary – skin rash (palms, soles, trunk) Tertiary – neurosyphilis
|
|
is ocular complication common or rare with syphilis
|
relatively rare
|
|
what is the "salt and pepper fundus"
|
the appearance of the ocular fundus characterized by a stippling of dark pigmented spots and yellow-red spots of atrophy, as is found in congenital syphilis and other conditions.
|
|
what is hutchinson's triad and what disease is it associated with
|
IK (interstitial keratitis), notched incisors, deafness associated with syphilis
|
|
which of the tests for syphilis are positive only during acitve disease and which are positive throughout the lifetime of the pt
|
VDRL or RPR positive ((during active phase of disease)
|
|
what is the most common cause of chorioretinitis
|
toxoplasmosis
|
|
describe your view of the fundus in a pt with chorioretinitis
|
"headlights in the fog" the more you turn up your illumination the more it will reflect off the inflammatory cells in the vitrial chamber and you won’t be able to see
|
|
you can contract toxoplasmosis from (3):
|
1. animal feces 2. drinking unhomogenized milk 3. eating raw beef
|
|
name 4 antitoxoplasmic drugs
|
Antitoxoplasmic agents
|
|
common cuses of uveitis:
|
ankylosing spondylitis, reiter's syndrome (reactive arthritis), juvenile chronic arthritis, sarcoidosis, tuberculosis, syphilis, many others.
|
|
THE TOP TWELVE REALLY USEFUL LABORATORY TESTS FOR UVEITIS – Dr. Brooks Allredge 12.
|
Human leukocyte antigen (HLA): expensive; reveals conditions that are generally
|
|
New lecture: 2 Epi_Scleritis 2009
|
|
|
when the episclera is inflammed, what other structure is also inflammed
|
conjunctiva
|
|
describe the prognosis associated with episcleritis
|
benign and self limitating
|
|
what are the two types of episcleritis
|
simple 80% nodular 20%
|
|
is simple episcleritis usually unilateral or bilateral
|
unilateral 70% of the time
|
|
is simple episcleritis acute or chronic
|
acute onset of signs and symptoms
|
|
is simple episcleritis diffuse or localized
|
localized
|
|
describe the subjective symptoms that a pt with simple episcleritis will come in complaining of (2)
|
1)
|
|
is VA affected by simple episcleritis
|
no
|
|
is simple episcleritis recurrent
|
yes
|
|
name 4 objective signs and symptoms that are either present or absent that help diagnos simple episcleritis
|
1. sectoral hyperemia (can be diffuse) and inflammation (wedge with apex towards limbus (hard to see clinically)) 2. engorged blood vessels (BUT MAINTAIN THEIR NORMAL ARCHITECTURE) 3. usually no anterior chamber response 4. lacrimation
|
|
what is a good way to differentiate between scleritis and episcleritis based on the appearance of the blood vessels
|
in epicleritis the blood vessels maintain their normal architecture. in scleritis they do not necessarily maintain their normal architecture.
|
|
what is the most common cause of simple episcleritis
|
idiopathic (70%)
|
|
30% of simple episcleritis is associated with systemic disease:
|
Collagen vascular disease
|
|
|
picture
|
|
|
picture
|
|
if you see a pt that you think has episcleritis or scleritis you need to look at their eye out of the slit lamp in normal room illumination and look for a bluish color of the sclera. what does this tell you?
|
it tells you that there is thinning of the sclera, as seen in scleritis. it looks blue because thinning allows you to start to see the choroid.
|
|
if you have a pt that you suspect scleritis or episcleritis, what do you need to consider before you dilate the pt
|
phenylephrine will blanch the blood vessels, and make it so you can't see them to differentially diagnose what layer of the sclera the engorged blood vessels are in.
|
|
you can take a q-tip and move around the blood vessels to see which layer of the sclera hyperemic vessels are in (ddx scleritis and episcleritis). use a topical anesthetic.
|
|
|
how can you DDX episcleritis and scleritis with pharmaceuticals
|
DDX with phenylephrine 2.5% ((phenylephrine will blanch the conjunctival vessels, partial blanching of episcleral vessels, and none of the sclera vessels). so you can tell what layer of the eye the engorged blood vessels are in.
|
|
describe the progression of episcleritis
|
most will resolve in 1.5 to 3 weeks whether you treat it or not.
|
|
describe the tx of simple episcleritis
|
Mild cases
|
|
what is the follow up schedule for a pt with episcleritis
|
RTC q 2 - 3 weeks
|
|
what percent of episcleritis is simple and what percent is nodular
|
simple 80% nodular 20%
|
|
how do the symptoms compare in nodular episcleritis to simple episcleritis
|
in nodular form symptoms are more intense
|
|
is nodular episcleritis recurrent
|
less likely to recur than simple form
|
|
describe the clinically observable signs of nodular episcleritis
|
Nodule formation usually in the center of sectorial
|
|
how does the nodule help you differentiate between nodular episcleritis and scleritis
|
((nodule is movable in episcleritis, not the case for scleritis) -episcleritis usually has only one nodule, in scleritis it is possible to have multiple nodules.
|
|
how do you differentiate between nodular episcleritis and pingueculitis
|
history. pts with pinguecula know that they are there and they have been there for a long time. episcleritis is acute.
|
|
describe the tx and the follow up for nodular episcleritis
|
tx and follow up same as for moderate-severe cases of simple episcleritis. -nodular form takes longer to resolve than simple form though.
|
|
can recurrent cases of episcleritis switch between the simple and nocular form
|
yes
|
|
can episcleritis progress to scleritis
|
no
|
|
how does episcleritis and scleritis compare in how common they are
|
episcleritis is common, scleritis is rare.
|
|
what tissues are inflammed in scleritis
|
sclera, episclera, and overlying conjunctiva
|
|
what percent of the time is scleritis associated with systemic disease
|
50%
|
|
name the five types of scleritis
|
1. diffuse anterior scleritis 2. nodular anterior scleritis 3. necrotizing anterior scleritis with inflammation 4. necrotizing anterior scleritis without inflammation (scleromalacia perforans) 5. posterior scleritis
|
|
what is the most common form of scleritis
|
diffuse anterior scleritis (40-80% of cases)
|
|
can the diffuse form of scleritis progress to the nodular form
|
typically does not
|
|
what is the most serious type of scleritis
|
necrotizing anterior scleritis with inflammation
|
|
what is the systemic prognosis for a pt with necrotizing anterior scleritis with inflammation
|
high mortality rate due to other systemic factors
|
|
how does the color of the slcera change with nectotizing anterior scleritis with inflammation
|
sclera becomes more blue because it is more transparent and you are seeing choroid. -look for this outside the slit lamp in normal room illumination
|
|
what form of scleritis is called scleromalacia perforans
|
necrotizing anterior scleritis without inflammation
|
|
describe the subjective symptoms experienced by a pts with scleromalacia perforans
|
almost no symptoms
|
|
in what systemic condition do you see scleromalacia perforans
|
seen almost exclusively in pts with long-standing rheumatoid arthritis
|
|
name four objective retinal findings that are associated with posterior scleritis
|
1. exudative RD 2. disc swelling 3. retinal hemorrhage 4. choroidal folds
|
|
describe the onset for scleritis
|
gradual onset
|
|
how does scleritis affect vision
|
indisious decrease in VA
|
|
describe the pain associated with scleritis
|
1. severe, boring pain which may radiate to forehead, brow or jaw
|
|
name 4 clinically observable objective signs of scleritis
|
1. inflammation of scleral, episcleral, and conjunctival blood vessels -commonly diffuse (may be sectoral) 2. blue sclera 3. scleral nodules 4. corneal changes (sclerokeratitis: peripheral thinning, deep stromal and endothelial disruption) 4. anterior uveitis
|
|
Causes of scleritis: 1.*
|
CT disease
|
|
in what condition are subconjunctival steroids contraindicated
|
scleritis because of the risk of scleral thinning/perforation at the injection site
|
|
with herpes simplex you can not use pain as an indicator of progress in your tx because the corneal nerves are destroyed. but in scleritis you can use a decrease in the amount of pain as an indicator of improvement.
|
|
|
New lecture: 3 Retinal Overview 2009
|
|
|
vista mind: things that could cause problems in the retina Vascular, vitamin deficiency
|
EX.
|
|
New lecture: 4 Lens Abnormalities 2009
|
|
|
what types of materials make up the cyrstalline lens
|
65% water, 35% protein
|
|
proteins in the lens:
|
Crystallines a, b, g -insoluble crystallines increase with age
|
|
what type of metabolism is the main type in the crystalline lens
|
mainly anaerobic
|
|
from what part of the lens does the lens develop
|
from surface ectoderm
|
|
what are the zones of the lens
|
- most evident after age 45 years Outer capsule Subcapsular clear zone Cortex Nucleus (outer adult, middle infantile, central fetal) Suture lines surround fetal nucleus (“Y” sutures)
|
|
what is the one part of the human body that continues to grow from birth until death
|
cyrstalline lens
|
|
why does an adult cyrstalline lens appear brighter and less clear than a child's
|
because light passing through it scatters because of the irregular fibers
|
|
what type of tissue is the lens capsule
|
basement membrane of lens epithelium
|
|
in what part of the lens is epithlium present
|
only anteriorly. creates a orange peel appearance.
|
|
how many cell layers thick is the lens epithelium
|
1
|
|
|
picture
|
|
how much power does the cyrstalline lens have unaccommodated
|
15 D
|
|
how big is the cyrstalline lens at birth? what age does it reach adult size? how big is that?
|
7 to 7.5mm diameter at birth 9 to 9.5mm diameter at age 2 yrs 9.6 +/- 0.4mm diameter as adult
|
|
how thick (anterior to posterior) is the averge adult lens
|
4.2 +/- 0.5 mm
|
|
what is it called when you are born without a cyrstalline lens
|
congenital aphakia
|
|
name and describe the two types of congenital aphakia
|
Congenital Primary Aphakia No lens induction of surface ectoderm Complete aplasia of anterior of eye Congenital Secondary Aphakia Lens resorbed/expelled in utero
|
|
how does congenital aphakia affect vision (3)
|
severely reduced VA, nystagmus, amplyopia
|
|
why are CLs preferred in congenital aphakia
|
CLs can reduce nystagmus due to tactile feedback. also, they have an extremely high power.
|
|
why is a IOL typically not done in cases of congenital aphakia
|
usually the lens capsule is gone, which means that they would need an anterior chamber IOL. anterior chamber IOLs come with more complications. also, they eye is growing in early age, which means that the would need to replace the IOL if they put it in before the eye had stopped growing.
|
|
what is it called when you have an abnormally small crystalline lens diameter
|
microphakia
|
|
how does microphakia affect VA
|
severely reduced VA
|
|
is IOL usually done for microphakia? why or why not?
|
not usually. small lens capsule makes IOL implantation difficult.
|
|
name three systemic conditions associated with microspherophakia
|
1. weill-marchesani syndrome 2. marfan's syndrome 3. peter's anomaly
|
|
what type of refractive error is most commonly associated with microspherophakia and why
|
severe myopia. due to the rounder shape of the lens
|
|
what is microspherophakia
|
a congenital, usually bilateral, condition in which the crystalline lens is smaller than normal and spherical in shape.
|
|
what orientation do lens colobomas usually occur
|
infero-nasal
|
|
how does lens coloboma affect vision
|
reduced VAs, irregular astigmatism, accommodative dysfunction
|
|
if lens coloboma is present, iris, choroid, retina and optic nerve coloboma is also likely present.
|
|
|
what condition is this
|
posterior lenticonus
|
|
what is posterior lenticonus
|
Circumscribed round or oval bulge at posterior axial zone of lens
|
|
how common is posterior lenticonus
|
very rare. Dr. yudkovitch has only seen 1.
|
|
what is the age of onset for posterior lenticonus
|
develops in infancy or early childhood
|
|
describe the progression of posterior lenticonus
|
The bulge increases in size with age The lens cortex may become opaque
|
|
what is anterior lenticonus and what disease is it associated with
|
bulging on the anterior surface of the cyrstalline lens. associated with alport's syndrome
|
|
what is alport's syndrome
|
congenital glomerulonephritis associated with deafness and a decrease in large thrombocytes
|
|
name 2 ocular conditions associated with alport's syndrome
|
anterior lenticonus, posterior polymourphous dystrophy
|
|
what is lentiglobus
|
more general hemispherical deformity of the lens than. the bulging is more spherical, instead of conical as in lenticonus.
|
|
what is the name of the condition where the lens is shifted from its normal postion (luxated)
|
ectopia lentis
|
|
what is the difference between a luxated lens and a subluxated lens
|
luxated: completely dislocated form pupillary space subluxated: partially dislocated from pupillary space.
|
|
what should you be sure to look for if you see a displaced lens
|
any mass that may be causing the displacement
|
|
what is the name of the drug that can melt the zonules
|
alpha-chymotrypsin
|
|
what is marfan syndrome. and what is the most severe complication you are worried about.
|
a hereditary disorder of connective tissue, bones, and muscles (hypoplasia of the medsodermal layer). associated with atopia lentis and microspherophakia. -major concern is aneurysm of the aorta. they shold have their heart checked.
|
|
what is the systemic triad seen in marfan syndrome
|
1. cardiac anomalies 2. skeletal anomalies 3. muscluar underdevelopment (leads to high incidence of hernias)
|
|
what is the name of the term for long spider-like fingers (as seen in marfan syndrome)
|
arachnodactyly
|
|
what percent of the time is there lens subluxation with marfan syndrome? what direction is the subluxation?
|
80% of cases. upward subluxation.
|
|
name 6 objective ocular findings associated with marfan syndrome
|
0. ectopia lentis 1. angle anomaly (75%, dense iris processes, thick trabecular sheets) 2. retinal detachment (from lattice degeneration) 3. hypoplasia of dilator muscle in the iris 4. flat cornea 5. axial mypoia
|
|
which dilating drop would work best on a pt with marfan syndrome and why
|
tropicamide (not phenylephrine). because the dilator muscle of the iris doesn't work well.
|
|
what is weill-marchesani syndrome
|
rare systemic connective tissue disorder; dystrophia mesodermalis hypERplasia. short stubby fingers (bradydactyly), mental handicap.
|
|
what is the age of onset of weill-marchiesani syndrome
|
teens to early 20s
|
|
name three objective ocular findings associated with weill-marchiesani syndrome
|
1. microspherophakia 2. lens dislocation 3. angle anomaly
|
|
what direction is the subluxation of the lens in weill-marchiesani syndrome
|
downward lens subluxation
|
|
what is homocystinuria
|
an inheritied disease that results in excess homocystine. which can result in systemic complications, cardiovascular problems for example.
|
|
what is the primary ocular complication associated with homocystinuria
|
ectopia lentis
|
|
what is ehlers-danlos syndrome
|
collagen disorder from dygroxylysine defect. hyperelastic skin, joint, aneurysms, hernias. associated with ocular findings.
|
|
what ocular findings are associated with ehlers-danlos syndrome (4)
|
angioid streaks, keratoconus, blue sclera, subluxed lens.
|
|
what condition is this
|
pseudoexfoliation
|
|
under what conditions do you normally see pseudoexfoliation
|
in the slit lamp when the pt is dilated.
|
|
what is true exfoliation
|
people who blow glass, for example, and are exposed to a lot of heat, will develop an exfoliation of the lens exfoliaiton: the shedding or casting off of a body surface.
|
|
what pseudoexfoliation
|
Secretion of grey-white fibrillogranular material off the iris, ciliary body, zonules, and lens epithelium Thought to be secondary to abnormal basement membrane produced by aging epithelial cells Constant rubbing by iris when pupil constricts and dilates frees pseudoexfoliative flakes off anterior lens capsule surface Results in “bulls-eye” appearance of clear ring surrounding central untouched “disc” Weak zonules and iris sphincter muscle atrophy
|
|
is pseudoexfoliation usually unilateral or bilateral
|
often unilateral or asymmetric bilateral presentation
|
|
describe 5 clinically observable objective signs associated with pseudoexfoliation
|
1. bullseye pattern on the lens 2. flake material/pigment in anterior chamber angle 3. pupillary ruf atrophy "moth eaten" 4. iris transillumiation defects 5. krukenberg spindle/corneal endothelial pigment
|
|
what should be your first view on gonioscopy
|
inferior, because that is where a lot of stuff deposits on the eye.
|
|
what ethnicity is pseudoexfoliation most common in
|
northern europeans
|
|
describe the management of pseudoexfoliation
|
1. tx secondary glaucoma 2. lens extraction
|
|
IOP spikes from pseudoexfoliation can come and go, so it is possible that you would miss them on exam
|
|
|
what is the name of the cataract formed due to acute angle closure glaucoma
|
glaukomflecken
|
|
what part of the lens do claukomflecken usually form
|
anterior, subcapsular, or capsular
|
|
is glaukomflecken permanent
|
may resolve if IOP treated promptly
|
|
do benign congenital cataracts usually affect vision
|
no
|
|
types of benign congenital cataracts (6):
|
Anterior polar May have associated persistent pupillary memb. Posterior polar May have associated Mittendorf’s dot Cortical, Nuclear Single or multiple Lamellar Usually surrounds fetal or nuclear zones Coronary At nuclear-cortical junction Subcapsular Anterior or posterior
|
|
how do you differentiate between a mittendorf's dot and a cataract
|
you use an optic section on the posterior surface of the lens and look for a little dot or bump popping out. if you don't see a dot or bump, then the opacity is on the inside of the lens and is a cataract. -mittendorf's dot is outside the lens, cataract is inside the lens
|
|
if you see a cataract at all, even a benign congenital one, you need to tell the pt, because if you don't, another doctor will and they will think that you missed it.
|
|
|
cataracts related to diabetes (2 types):
|
Senile (age related) cataract Occurs earlier/progresses more rapidly in a diabetic patient versus a non-diabetic patient True diabetic cataract Osmotic over-hydration of lens Bilateral white punctate or ‘snowflake’ anterior or posterior opacities May mature in a few days
|
|
what is the condition called where the body cannot utilize galactose metabolically
|
galactosemia
|
|
what food is very high in galactose
|
milk -need to eliminate milk from diet in pts with galactoseemia
|
|
what type of cataract forms in galactosemia
|
oil droplet
|
|
oil droplet cataract indicating galactosemia is something you should be looking for in a pediatric exam. because it would be very beneficial to the infant to have this condition discovered early.
|
|
|
what is galactokinase deficiency
|
unable to metabolize galactose
|
|
how does galactokinase deficiency compare to galactosemia
|
pts with galactokinase deficiency are relatively healthy; pt with galactosemia are not.
|
|
what type of ocular signs form in pts with galactokinase deficiency
|
lamellar cataracts
|
|
what is mannosidosis
|
alpha-mannosidase deficiency. mannose-rich oligosaccharide accumulation in the body.
|
|
what ocular sign occurs in pts with mannosidosis
|
posterior subcapsular cataracts
|
|
what is Lowe's syndrome (oculocerebrorenal syndrome)
|
Amino acid metabolism error Mental handicap, dwarfism, osteomalaica, frontal prominence, muscular hypotonia
|
|
what ocular sign is associated with Lowe's syndrome (2)
|
microphakia. congenital glaucoma in 50%.
|
|
what type of cataracts are associated with hypocalcemic syndromes
|
Multicolored crystals/discrete white flecks in lens Seldom progress to maturity
|
|
what type of cataracts are associated with myotonic dystrophy
|
Subcapsular and cortical polychromatic glistening granules (‘blue-dot’ cataract) à PSC ? total -can be a diagnostic sign of the disease, but usually found in advanced disease
|
|
what is the most common cause of congenital cataracts
|
rubella
|
|
what is rubella
|
a mild, febrile, highly infectious viral disease historically common in childhood prior to the advent of an effective vaccine
|
|
what are the classic signs associated with rubella
|
Sensorineuronal deafness Cataracts 15% of cases virus latent in the lens Heart defect Microcephaly Severe mental retardation
|
|
remeber that congenital cataracts have to be removed to prevent amblyopia
|
|
|
what is cytomegalovirus
|
an opportunistic disease seen in HIV/AIDS
|
|
why is uveitis associated with cataract
|
From long-term anterior or posterior chamber inflammation From topical and/or oral steroid use to treat uveitis
|
|
hereditary fundus dystrophies associated with cataract (3)
|
retinitis pigmentosa, gyrate dystrophy, leber's congenital amaurosis
|
|
what is a glass-blower's cataract
|
Infrared radiation Capsular splitting and peeling True exfoliation of lens capsule
|
|
what is arc flash
|
aka actinic keratopathy or solar keratopathy UV light reflected off snow/ice/water/sand or arc welding or tanning bed without proper eye protection Painful corneal epithelial/conj sloughing/inflammation not related to glass-blower's cataract
|
|
can cataracts form from topical or systemic steroids
|
both
|
|
what type of cataracts tend to form from steroid use
|
Classic posterior subcapsular cataracts form Eventually anterior subcapsular cataracts also form
|
|
are cataracts from steroid use reversable
|
regression may occur if drug stopped/reduced
|
|
|
picture
|
|
drugs that can cause cataract formation (4)
|
1. chlorpromazine 2. amiodarone 3. psoralen (psoriasis and vitiligo) 4. gold salts (rheumatoid arthritis)
|
|
New lecture: 5 Cataracts 2009
|
|
|
what are epicapsular stars
|
Small light brown or tan (despite iris color) dots or star-shaped deposits on anterior lens capsule
|
|
epicapsular stars may be single or multiple, unilateral or bilateral. does not affect vision, no associated symptoms.
|
|
|
what is this
|
vossius ring
|
|
what is a vossius ring
|
Imprint deposition of melanocytes from pupillary border of the iris due to contusion
|
|
is vossius ring permanent
|
usually fades with time, but some pigment may remin permanently
|
|
what other ocular complication should you watch out for if you see a vossius ring
|
traumatic cataract
|
|
three causes for capsular pigment dusting (lens)
|
1. pigment dispersion syndrome 2. pseudoexfoliation 3. ocular trauma
|
|
what else should you look at if you see capsular pigent dusting on the lens (3)
|
1. corneal endothelial pigment 2. pigment dusting in the angle 3. retroillumination defect of the iris
|
|
in what quadrant of the lens do you find a mittendorf's dot most commonly
|
nasal or inferonasal
|
|
what are the three general types of age-related cataracts
|
1. nuclear 2. cortical 3. subcapsular
|
|
what the the most common type of cataract you will see
|
nuclear
|
|
what is a nuclear cataract
|
Diffuse sclerosis (yellowing) of nuclear area
|
|
what wavelength is reduced in neclear cataracts
|
blue wavelengths. that is why older ladies have blue hair and don't realize it.
|
|
what do you need to do to see a nuclear cataract
|
Lens may look clear upon retroillumination ((need an angled beam to see it)
|
|
what is rubeosis (in the lens)
|
advanced form of nuclear cataract
|
|
what is a cortical cataract
|
|
|
describe the progression of cortical cataracts
|
start in the periphery and move centrally
|
|
what quadrant of the lens do cortical cataracts tend to start in
|
inferior-nasal area
|
|
what is the best way to see a posterior subcapsular cataract
|
retroillumination (red reflex)
|
|
what is the most visually debilitating of the three major types of cataracts
|
posterior subcapsular because it is right on the visual axis
|
|
is anterior or posterior subcapsular cataract more common
|
posterior
|
|
describe the etiology of anterior subcapsular cataract
|
Rarely in senile form Usually secondary to external or systemic etiology Highly elevated IOP (glaukomfleken) Wilson’s disease Miotic therapy (i.e. pilocarpine) Amiodarone administration
|
|
usually senile nuclear sclerosis appears before posterior subcapsular cataract.
|
|
|
what is the most common pre-senile cause of posterior subcapsular cataracts
|
steroid use
|
|
what is the best way to see a posterior subcapsular cataract
|
retroillumination (red reflex) with the direct ophthalmoscoe (not slit lamp)
|
|
describe the age of onset of lamellar cataracts
|
almost invariably congenital
|
|
what are lamellar cataracts
|
Involve lamella of fetal or nuclear zones Radial spoke-like opacities (riders) Frequently surround the cataract
|
|
describe the LOCS grading system for cataracts
|
LOCS Grading Intervals (1989): Nuclear color (NC)
|
|
how do cataracts affect contrast sensativity
|
a lot. they could still have 20/20 vision, but severely reduced contrast sensativity. -pelli-robson chart is most clinically applicable techinque
|
|
name and describe the classification of cataract maturity
|
Immature (Mild) Also termed ‘presurgical’ cataract Lens retroillumination may appear clear Moderate May be ‘presurgical’ or ‘surgical’ Some opacification seen on retroilluminaton Mature Cortex is totally opaque; ‘surgical’ Posterior pole views are difficult Hypermature Water leaks out of lens ‘surgical’ Lens is slightly smaller with wrinkled capsule
|
|
what is this
|
morgagnian cataract
|
|
what is a morgagnian cataract
|
total liquifaction of the cortex of the lens, which causes the nucleus to sink inferiorly
|
|
what ocular condition can occur secondary to a morgagnian cataract
|
phacolytic glaucoma. if the lens capsule breaks.
|
|
what are the categories of cataract based on age of onset
|
congenital, infantile, juvenile, adult, senile
|
|
is a unilateral or a bilateral congenital cataract a worse prognosis
|
unilateral is actually a worse prognosis because of the potential of developing amblyopia.
|
|
what are the surgical indications for congenital cataract
|
bilateral advanced cataract, unilateral cataract.
|
|
if you rx contact lenses for an infant with no crystaline lens, you need a commitment on the part of the parents.
|
|
|
what is the VA cutoff for insurance to cover cataract surgery
|
20/40 or worse at this point
|
|
how is the power of the IOL calculated in cataract surgery
|
by using Ks and axial length.
|
|
what are the two types of IOL implantations based on their location
|
posterior chamber IOL and anterior chamber IOL
|
|
when is an anterior chamber IOL done
|
Used if posterior capsular rupture Also used if complete lens extraction performed
|
|
describe the risks associated with anterior chamber IOLs (3)
|
More risks: uveitis, corneal endothelial decompensation, chronic cystoid macular edema (CME)
|
|
what is the name for the current proceedure for cataract removal
|
extracapsular cataract extraction and phacoemulsification.
|
|
what are the names for the two parts of an IOL
|
optic, and haptic
|
|
cataract pts may require an asymmetric add power if unilateral and they sill have accommodative ability
|
|
|
what test is a must before referral for cataract surgery
|
potential acuity
|
|
name three tests that test for potential acuity
|
Potential Acuity Meter Super Pinhole Laser Interferometry
|
|
under what conditions should the potential acuity meter (PAM) test be done and why
|
this test is best done while the pt is dilated. the test works by projecting around the cataract.
|
|
how does the laser interformeter work
|
Laser light waves pass through opacities to superimpose on retina, creating a grating pattern Grating width can be changed, thus changing visual acuity demand Can therefore determine potential retinal acuity May be more effective than PAM or Super Pinhole with denser cataract opacities
|
|
what is the difference between disability glare and discomfort glare
|
disability glare reduced visual acuity, discomfort glare is just uncomfortable
|
|
New lecture: 6 Cataract Comgt 2009
|
|
|
what is the most common refractive error change associate with cataract formation
|
myopic. not always the case, but usually.
|
|
with cataracts is the best refraction or the pinhole better acuity
|
commonly the pinhole will proved better acuity because you are reducing light scatter. you might want to do the pinhole over their refraction.
|
|
think about treating lid disease before sending a pt in for eye surgery to reduce the risk of infection.
|
|
|
if you have a pt with uveitis you might want to tx the uveitis before sending them in for cataract surgery, because the surgery will tend to cause inflammation to increase.
|
|
|
high hyperopes are at a greater risk for cataract surgery because smaller eyes are harder to work on. <20 mm axial length.
|
|
|
name one pharmaceutical contraindication to cataract surgery
|
flomax
|
|
tearing is normal after cataract surgery, but not excessive. if excessive you need to consider that there might be a leak.
|
|
|
pain is associated with ocular hypertension and ocular hypotension
|
|
|
New lecture: Glaucoma Classification Fall 09 Vault
|
|
|
what is glaucoma
|
A group of ocular diseases of the optic nerve involving loss of retinal ganglion cells with progressive optic neuropathy.
|
|
how many types of glaucoma are there
|
about 60
|
|
what is a primary glaucoma
|
not associated with any other apparent ocular or systemic disorder
|
|
what is primary open-angle glaucoma
|
Aqueous outflow is reduced on submicroscopic and or biomechanical level. The angle is usually open!!
|
|
what is secondary glaucoma
|
Caused by a variety of ocular and/or systemic disorders: Causes decrease in aqueous outflow leading to either: Open or closed angle glaucoma
|
|
what are developmental glaucomas
|
due to abnormalities in the anterior chamber angle. abnormalities during gestation
|
|
what is the most common form of adult glaucoma
|
open angle glaucoma
|
|
what is the order of structures seen on gonioscopy from posterior to anterior
|
ciliary body, scleral spur, trabecular meshwork, schwalbe's line
|
|
what is closed angle glaucoma
|
aqueous flow is obstructed by the root of the iris
|
|
what condition is pigmentary glaucoma associated with
|
secondary to pigmentary dispersion syndrome
|
|
what is the pathophysiology of pigmentary glaucom
|
Liberation of pigment from the iris pigment epithelium, due to an abnormality in the IPE, and its deposition on anterior segment structures (trabecular meshwork, corneal endothelium, lens). deposition on the TM clogs the aqueous outflow. back of the iris rubs on the lens during normal miosis and mydryasis, liberating pigment. -trabecular endothelial cells are unable to adequately phagocytize the excess pigment.
|
|
what is a pupillary block
|
a blockage of the normal flow of aqueous humor from the posterior to the anterior chamber of the eye. it may be caused by a posterior annular synechia or other cuases.
|
|
what is the difference between pigmentary dispersion syndrome and pigmentary glaucoma
|
pigmentary glaucoma is pigmentary dispersion syndrome with optic nerve head damage.
|
|
what percent of pts with pigmentary dispersion syndrome will develop pigmentary glaucoma
|
30-50%
|
|
what is reverse pupil block
|
1. increased resistance to flow of aqueous humor through the pupil from the anterior chamber to the posterior chamber, leading to posterior bowing of the peripheral iris against the zonules; a possible mechanism for pigmentary glaucoma.
|
|
what is iris bombe
|
1. increased resistance to flow of aqueous humor through the pupil from the anterior chamber to the posterior chamber, leading to posterior bowing of the peripheral iris against the zonules; a possible mechanism for pigmentary glaucoma.
|
|
what is the age of onset of pigmentary dispersion syndrome/pigmentary glaucoma
|
younger. age 20-50.
|
|
what ethnicity is pigmentary glaucoma most common in
|
caucasians. unusual in african americans or asians.
|
|
is the conversion from pigmentary dispersion syndrome to pigmentary glaucoma more common in men or women
|
Sex predilection: PDS is equal in men and women. PG is More common in men
|
|
is there a genetic component to pigmentary glaucoma
|
yes. AD.
|
|
what type of refractive error is associated with pigmentary glaucoma and why
|
Approx 90% of pts with PDS have MYOPIA. PDS more prevalent in patients with deeper anterior chamber angles. Patients with higher myopia and deeper angles develop PDS at an earlier age and have a more difficult clinical course.
|
|
is pigmentary glaucoma usually unilateral or bilateral
|
most commonly bilateral, though often asymmetrical
|
|
what three clinical signs indicate pigmentary glaucoma
|
1. krukenberg spindle 2. iris transillumination defects 3. pigment deposition on the trabecular meshwork
|
|
what is the best way to see krukenberg spindle
|
indirect illumination.
|
|
what is krukenberg spindle
|
vertical accumulation of pigment on the central corneal endothelium
|
|
what is the name for a pigmented line found anterior to schwalbe's line on gonioscopy
|
sampaolesi's line
|
|
what shape of the iris is common to find on gonioscopy in pts with pigmentary glaucoma
|
mid-peripheral concavity
|
|
are there any activities associated with pigment liberation in pigmentary glaucoma
|
strenuous exercise, dilation. these may be accompanied by IOP spike and clinical symptoms associated (HA, pain, halos etc.)
|
|
what is the difference between pseudoexfoliative glaucoma and pseudoexfoliation syndrome
|
Pseudoexfoliative syndrome PXE Anterior segment changes without increased intraocular pressures and/or glaucomatous visual fields and optic nerve changes Pseudoexfoliative Glaucoma PXG Anterior segment changes with increased intraocular pressures and/or glaucomatous visual fields and optic nerve changes
|
|
what is pseudoexfoliative glaucoma
|
Characterized by flakes of granular material at the pupillary margin of the iris and throughout the inner surface of the anterior chamber.
|
|
other names for pseudoexfoliative glaucoma
|
Glaucoma capsulare, glaucoma senilis, basement membrane exfoliation syndrome, and senile exfoliation syndrome to name a few.
|
|
describe the pathophysiology of pseudoexfoliative glaucoma
|
Fibrilogranular material of a protein nature Is possibly secondary to disturbances in the biosynthesis of basement membranes Exact origin is uncertain material is released when the back of the iris near the pupil rubs the roughened surface of the lens. material moves into the aqueous humor and is carried to the trabecular meshwork
|
|
you need to dilate in order to see pseudoexfoliative glaucoma.
|
|
|
not all pts with pseudoexfoliative syndrome go on to develop pseudoexfoliative glaucoma
|
|
|
describe the age of onset of pseudoexfoliative glaucoma
|
onset most commonly between 60 and 80 year old. rarely seen before age 50
|
|
prevalance of pseudoexfoliative glaucoma varies a lot by ethnicity and location
|
|
|
are men or women with pseudoexfoliative syndrome more likely to develop pseudoexfoliative glaucoma
|
men
|
|
is pseudoexfoliative glaucoma usually unilateral or bilateral
|
usually starts unilateral, but becomes biateral in most cases.
|
|
what percent of people with pseudoexfoliative syndrome will develop pseudoexfoliative glaucoma
|
15%. a higher percent develop high IOPs, but no ONH damage.
|
|
describe 6 clinically observable objective signs indicating pseudoexfoliative glaucoma
|
1. bull's eye pattern of the lens 2. lens subluxation more common (10-15%) 3. cataract 4. iris transillumination defects (moth eaten) 5. krukenberg's spindle (pigment) 6. increased pigment at the angle (sampaolesi's line possible)
|
|
how can you differentiate pseudoexfoliative glaucoma from pigmentary glaucoma
|
1. with pigmentary the iris tranillumination defects tend to be mid-peripheral; with pseudoexfoliative iris transillumination defects tend to be at the pupillary boarder "moth eaten" 2. pseudoexfoliative associated with narrow angles; pigmentary more commonly associated with deep angles.
|
|
what is neovascular glaucoma
|
A condition associated with IOP elevation due to synechial angle closure resulting from fibrovascular membrane formation obstructing aqueous outflow.
|
|
describe the pathophysiology associated with neovascular glaucoma
|
Hypoxic retina produces an angiogenic factor that stimulates a neovascular response. New blood vessels on the iris NVI (neovasculerization of the iris) or RI (rubeosis iridies) Angiogenic factor = vascular endothelial growth factor (VEGF)
|
|
early detection in neovascular glaucoma is crucial. it is also very hard to see; you need to use high magnification.
|
|
|
name four major conditions that can cause neovascular glaucoma
|
1. central retinal vein occlusion (36%) (number 1 cause of unilateral neovascular glaucoma) 2. diabetic retinopathy (32%) (number 1 cause of bilateral neovascular glaucoma) 3. central retinal artery occlusion (18%) 4. carotid artery disease (13%)
|
|
what is the earliest sign of neovascular glaucoma
|
small dilated vessels at the pupillary margin
|
|
describe the mechanism of progression of neovascular glaucoma
|
neo progresses from the pupillary margin toward the angle. neovascularization of the angle in the absence of pupillary involvement may occur. in the late phase you get a fibrovascular membrane in the anterior chamber, which contracts producing peripheral anterior synechia (starts in one quadrant and can progress to 360 degrees).
|
|
if the trabecular meshwork starts to turn red, it means that you are pushing to hard with the goino lens.
|
|
|
describe 4 clinically observable objective signs associated with neovascular glaucoma
|
1. neovascularization 2. cells and flare as vascular proliferation develops 3. hyphema 4. peripheral anterior synechia
|
|
describe the mechanism for peripheral antrior synechia in neovascular glaucoma
|
neovascular membrane forms, which can contract and pull the iris forming anterior synechia
|
|
in ligher pigmented irides it is possible for the normal iris vasculature to look like neovascularization of the iris
|
|
|
describe four mechanisms for angle closure glaucoma
|
Iris (pupilary block) Ciliary body (plateau iris) Lens (phacomorphic glaucoma) Posterior to the lens (malignant glaucoma)
|
|
what is primary angle closure glaucoma with pupil block
|
adherence between the back of the iris and the front of the lens that prevents aqueous from passing forward to the anterior chamber.
|
|
posterior synechia can result in iris bombe, causing angle closure glaucoma
|
|
|
how soon after dilation is angle closure likely to happen
|
a couple hours. becuase angle closure glaucoma is most likely to happen when the pupil is mid-dilated.
|
|
list 8 signs and symptoms associated with acute angle closure.
|
1. severe pain 2. blurred vision/halos around lights 3. fixed mid-dilated pupil 4. corneal edema 5. IOP >40 6. nausea/vomiting 7. severe HA 8. shallow AC
|
|
what is plateau iris
|
an anatomical anomaly in which the iris lies in a plane rather than bluging anteriorly. this is due to the fact that the root of the iris is inserted more anteriorly in to the ciliary body than usual. on dilation of the pupil the peripheral iris expands against the trabecular meshwork and can predispose the eye to angle closure glaucoma.
|
|
Primary Angle closure glaucoma: With or without pupillary block can be a slow progressive process. Chronic progressive angle closure glaucoma this is more common than acute angle closure
|
|
|
what is phacomorphic glaucoma
|
due to lens swelling leading to shallower anterior chamber.
|
|
what type of glaucoma is phacomorphic glaucoma
|
secondary angle closure glaucoma
|
|
what type of glaucoma is malignant glaucoma
|
secondary angle closure glaucoma
|
|
what is malignant glaucoma
|
Posterior misdirection of aqueous into the vitreous. Increases post seg pressure. Angle closure due to posterior forces pushing the lens-iris diaphragm forward.
|
|
how common is malignant glaucoma
|
very rare. Dr. Dina Erickson has never seen one.
|
|
New COURSE: Ocular Disease III
|
|
|
New lecture: 1 Glaucoma Risk Factors, Signs and Visual Field 2010 (study this one)
|
|
|
where does glaucoma rank in terms of causing blindness in the US
|
3rd (macular degeneration and diabetes are number 1 and 2)
|
|
what race is more prone to developing glaucoma
|
african american
|
|
is blood pressure related to eye pressure
|
no, but hypertension is a risk factor for glaucoma
|
|
systemic diseases linked to glaucoma
|
1. diabetes 2. hypertension/hyperlipidemia 3. systemic vascular disease
|
|
are smoking and drinking a risk factor for glaucoma
|
yes
|
|
list 6 ocular risk factors for glaucoma
|
1. IOP 2. ONH characteristics 3. angle abnormalities 4. corneal thinkness 5. myopia 6. visual field defects
|
|
what is the name of the test that measures corneal thickness
|
pachymetry
|
|
OHTS: ocular hypertension treatment study
|
|
|
what are the most common subjective symptoms at the time of diagnosis for POAG
|
almost every POAG pt is asymptomatic at the time of diagnosis
|
|
how does glaucoma affect VA
|
usually not affected unless the papillomacular bundle of the NFL is affected in advanced cases
|
|
is there an RAPD in glaucoma
|
not usually, only if it is asymmetrical.
|
|
describe the onset of traumatic glaucoma
|
can be years after innitial injury. (related to angle recession)
|
|
what types of glaucoma are related to krukenberg's spindle
|
pigmentary glaucoma, pseudoexfoliative glaucoma
|
|
is there pain assoicated with glaucoma
|
only actue glacoma with extremely high IOP. most glaucoma is painless.
|
|
if you see neovascularization of the iris you need to refer to a retinal specialist
|
|
|
what is the normal range for IOP
|
10-21 mmHg (average is 16)
|
|
why time of day is IOP highest
|
early morning is highest
|
|
how does glaucoma influence diurnal variation
|
much greater diurnal variation than normal
|
|
greater than ____ difference in IOP between the two eyes is suspicious
|
2 mmHg
|
|
what percent of people with primary open angle glaucoma have IOP less than 22 mmHg at the time of diagnosis
|
50%
|
|
there is no normal pressure. the higher the IOP the greater the risk of developing glaucoma.
|
|
|
what IOP is high enough to treat based on IOP alone
|
30 mmHg -you should definately check corneal thickness though
|
|
corneal curvature can distort the mires and give you a false goldmann IOP reading
|
|
|
how can exophthalmos affect IOP
|
artifically high because of pressure behind the eye pushing the eye forward.
|
|
what is the instrument that a pt can take home and measure IOP at home called
|
proview
|
|
how does corneal thickness impact IOP
|
Thin corneas underestimate IOP Thick corneas overestimate IOP
|
|
how does LASIK impact IOP and why
|
falsely lowers IOP because the cornea is thinner
|
|
what type of corneal thickness is a risk factor for glaucoma
|
thin cornea: < 555 microns higher risk* > 588 microns lower risk*
|
|
what is normal corneal thickness
|
550 microns (545 precisely)
|
|
corneal disease/surgery can affect central corneal thickness: fuch's endothelial dystrophy, keratoconus, LASIK
|
|
|
what things do you need to record when doing gonioscopy
|
1. iris approach 2. most posterior structure visible 3. amount of pigment 4. angle recession present or not 5. any abnormalities
|
|
what are the types of iris approaches as seen on gonioscopy
|
flat, bowed, plateau, concave
|
|
what is angle recession and iridodialysis
|
the angle has been pulled by something (traumatic or otherwise) the iris root is pulled away from the ciliary body. iridodialysis is where the iris is completely seperated from the ciliary body and there is a tear there.
|
|
in what quadrant are you most likely to see pigment on gonioscopy and why
|
inferior because of gravity
|
|
what is sampolisi's line
|
a line of pigment deposited on schwalbe's line
|
|
what is this
|
angle recession
|
|
what is the mechanism for angle recession glaucoma
|
scarring that results from the tearing of the iris root blocks the trabecular meshwork.
|
|
how does direct ophthalmoscopy tend to influance CD ration
|
tends to underestimate because you are monocular and not getting a 3D view.
|
|
progressive thinning of the neural rim is pathonogmonic for glaucom
|
|
|
what structure determines the ONH size
|
scleral canal
|
|
how many nerve fibers are there in the optic nerve
|
1.2 million (every 90 minuets we lose one of them)
|
|
what is the range of normal ONH sizes
|
1.33-2.66 mm
|
|
how does ONH size relate to CD
|
usually the bigger the nerve head the larger the CD
|
|
do myopes or hyperopes usually have large optic nerve heads
|
myopes
|
|
what are two ways to measure the size of the ONH
|
use the reticule in the slit lamp, or estimate how many blood vessel widths it is.
|
|
if you estimate ONH size by blood vessel width what is normal, large and small
|
12 blood vessel widths is normal, 15 is large, 9 is small
|
|
nwhat do you need to look at before you look at CD
|
ONH size
|
|
another trick for estimating ONH size
|
use the small circle on a welch-allen or a keeler ophthalmoscope and if the ONH is just smaller than the circle it is a normal sized nerve head
|
|
at what CD do you start getting suspicious of glaucoma (if all else is normal)
|
0.6
|
|
when writing the CD does the horizontal or the vertical ratio come first
|
horizontal over vertical (H/V)
|
|
if you have a deep cup, what do you expect to see at the base of the cup
|
lamina cribosa (laminar dots)
|
|
what type of elongation is a risk factor for glaucoma
|
vertical elongation of CD is a risk factor for glaucoma. -glaucoma usually affects the inferior rim first
|
|
what is the ISN'T rule
|
the normal ONH should be thickest inferiorly and thinnest temporally.
|
|
temporal part of the cup may look more pale than the rest of the disc, but this is normal.
|
|
|
name 9 optic nerve head signs that would indicate glaucoma
|
1. CD over .6 2. difference in CD between the two eyes 3. vertical elongation of the CD 4. pallor 5. temporal rim <1/8 DD 6. progressive thinning of rim tissue 7. "bean pot" appearance 8. "bayoneting" of vasculature over rim 9. laminar dots
|
|
there are many many things that can mimic glaucoma
|
|
|
YOU CAN HAVE NORMAL-LOOKING NERVES AND HAVE GLAUCOMA! YOU CAN ALSO HAVE GLAUCOMATOUS CUPPING AND NO FIELD LOSS!
|
|
|
BIO is a great way to look at the nerve fiber layer
|
|
|
look for NFL defects in glaucoma
|
|
|
how does the fundus appear when you have nerve fiber damage form glaucoma
|
the blood vessels appear more bright and sharp and crisp because they are in the ganglion cell layer and there is no NFL covering them
|
|
what is it called when the blood vessels are more bright and sharp and crisp because of NFL atrophy
|
bearing of the circumlinear vessels
|
|
what are the circumlinear blood vessels
|
-circumlinear vessels are the ones that eminate from the disc
|
|
rarely you can have arteroirlar pulsation with very high IOP
|
|
|
name 4 objective retinal signs that indicate glaucoma (ONH changes only 1)
|
1. optic disc changes 2. NFL defects 3. collateral/shunt vessel formation 4. DRANCE HEMORRHAGE
|
|
what location do you usually see drance (splinter) hemorrhages in
|
interior-temporal to the disc
|
|
what is the best way to see a splinter hemorrhage
|
use the red-free filter
|
|
name four conditions other than glaucoma that can cause drance (splinter) hemorrhage
|
AION, pipillitis, HTN, DM
|
|
what is a "bean pot" cup
|
rim becomes undermined
|
|
what is the only subjective test for glaucoma
|
visual fields
|
|
what does higher decibels on a visual field indicate? what about apostilbs?
|
higher decibels equals more sevsitive. decible are inverse to apostilbs (amount of brightness)
|
|
how many degrees does a 30-2 visual field cover
|
60 degrees.
|
|
what is usually the first sign of glaucoma
|
paracentral scotomas between 5 and 20 degrees of fixation
|
|
describe the progression of visual field loss assoicated with glaucoma
|
paracentral scotomas, arcuate scotoma, double arcuate scotoma, temporal wedge defect (nasal fibers are finally affected), overall field constriction, overall field depression.
|
|
what is the most important indicator on a visual field printout
|
pattern deviation plot
|
|
what is the mean deviation of a visual field
|
the average elevation or depression of the overal field compred to normal for their age. they add up all the points on the field and average them.
|
|
what is the pattern standard deviation of a visual field
|
the irregularity of the overal field from the normal
|
|
what is the short-term fluctuation (SF) of a visual field
|
measures consistancy or responses twice at 10 pre-selected points
|
|
what is the corrected pattern standard deviation (CPSD) of a visual field
|
measures intra-test variability of field shape to reference while taking consistency into account
|
|
what factors do the total deviation and pattern deviation take into account on a visual field
|
total deviation does not taking into consideration age, and media opacification. but pattern deviation does.
|
|
glaucoma hemifield test is not 100% reliable
|
|
|
the only thing that is consistant about a glaucomatous visual field is that it will be inconsistant
|
|
|
what is FASTPAC
|
speeds up visual field exam by using age-reference statistics
|
|
blue on yellow perimetry is though to pick up glaucomatous visual field changes earlier by 3-4 year
|
|
|
what is SITA-standard/fast
|
threshold adjustment to speed test without data compromise
|
|
why is FDT supposed to pick up glaucomatous changes earlier
|
we think that the magnocellular ganglion cells die first in glacoma, and the FDT attempts to isolate them due to flicker of target.
|
|
scanning laser ophthalmoscopy that looks at the nerve fiber thickness
|
HRT, RTA (retinal thickness analyzer), GDx, OCT,
|
|
New lecture: 2 Glaucoma Treatment Slides 2010 (study this one)
|
|
|
describe the progression of treatment types in the US
|
Medical (Pharmacologic) Laser Treatment (Laser Trabeculoplasty) Surgery (Filtration/Bleb/Trabeculectomy)
|
|
describe the active and passive forms of aqueous secretion from the ciliary body
|
Non-pigmented ciliary epithelium (active) ((enzyme: carbonic anhydrase) Ultrafiltration & diffusion (passive)
|
|
describe the two pathways of aqueous outflow from the eye
|
Trabecular meshwork à Schlemm’s ? Veins Uveoscleral outflow ? CB ? SC Space ? Sclera
|
|
describe the three theories as to why the ONH fibers die in glaucoma
|
Direct Mechanical Theory Ocular pressure blocks axoplasmic flow Ischemic Theory Ocular pressure blocks circulation to nerve Apoptosis “Programmed cell death”, mediators involved Genetic predisposition
|
|
describe the main categroies of anti-glaucoma drus and whether they decrease aqueous production or increase aqueous outflow
|
Reduce Aqueous Production Beta-blockers, Alpha-2 agonists, CAIs Increase Aqueous Outflow Miotics, adrenergic/Alpha-2 agonists, prostaglandins/prostamides, docosanoids(?)
|
|
name 5 carbonic anhydrase inhibitors
|
Dorzolamide
|
|
what tissues have beta 1 adronergic receptors and which have beta 2
|
Beta 1 Heart muscle Tachycardia, increased cardiac output when stimulated Beta 2 Bronchial muscle Bronchial dilation when stimulated
|
|
name 5 topical beta-blockers
|
Timolol Betaxolol Levobunolol Metipranolol Carteolol
|
|
which is the only topcial beta-blocker that is beta-1 selective
|
Betaxolol is the only Beta-1 selective Beta-blocker
|
|
what is the trade name for timoptic
|
timoptic
|
|
what is the trade name for timolol that comes in a gel
|
timoptic XE
|
|
what is the trade name for betaxolol
|
betoptic
|
|
what is the difference between betoptic and Betoptic S
|
Betoptic is a solution; Betoptic S is a suspension
|
|
how many times a day do you take timolol, betaxolol, levobunolol, metipranolol, and carteolol
|
|
|
why would you need to chose a beta-1 selective beta blocker
|
(betaxolol) for asthmatics
|
|
what is the trade name for levobunolol
|
betagan
|
|
what is the trade name for metipranolol
|
optipranolol
|
|
what is the trade name for carteolol
|
ocupress
|
|
which beta blocker stings the least
|
carteolol
|
|
how much do beta-blocker usually reduce IOP by
|
20-30%
|
|
beta-blocker side effects: CNS depression, fatigue, decreased libido, headaches, hallucinations (rare), dizziness Ocular sting/burn, blurred vision, SPK Heart Bradycardia, arrhythmia, palpitation, CHF Lungs Bronchospasm, short of breath, respiratory failure Hematological Aggravate lipid levels, mask hypoglycemia
|
|
|
what should you have the pt do while taking beta blocker
|
punctal occlude to reduce systemic absorption
|
|
what do you need to check before you start a pt on beta-blockers and while they are on them
|
Always check blood pressure, pulse, and respiratory status before initiating B-blocker
|
|
who should you avoid using beta blockers on if possible
|
Avoid if possible with asthmatics, COPD, bradycardia/CHF and DM/chol patients
|
|
are beta blockers additive to other drugs in terms of their IOP reducing capabilities
|
Insert your new answer text hereBeta-blockers additive to almost every other glaucoma medication ((beta blocker and a carbonic anhydrase inhibitor could reduce up to 50% then)
|
|
Oral beta-blockers (eg: atenolol) used for HTN may also reduce IOP (30%) as beneficial side-effect
|
|
|
what is the mechanism for the reduction of IOP with carbonic anhydrase inhibitors
|
Inhibits carbonic anhydrase enzyme in ciliary epithelium from producing aqueous
|
|
how much do carbonic anhydrase inhibitors reduce IOP by
|
15-20 percent
|
|
are carbonic anhydrase inhibitors used by themselves or in conjunction with other IOP lowering drugs
|
rarely used by themselves
|
|
name two topical carbonic anhydrase inhibitors
|
Dorzolamide Brinzolamide
|
|
what is the trade name for dorzolamide
|
trusopt
|
|
what is cosopt
|
dorzolamide and tomolol maleate
|
|
what is the dosage for dorzolamide
|
TID
|
|
what is the trade name for brinzolamide
|
azopt
|
|
does dorzolamide or brinzolamide sting less
|
brinzolamide stings less
|
|
name three systemic carbonic anhydrase inhibitors
|
acetazolamide (diamox), methazolamide, dichlorphenamide
|
|
what are systemic carbonic anhydrase inhibitors used for
|
emergency use if you need to lower IOP while the pt is in your chair. side effects make them too risky for long-term use.
|
|
name three adrenergic agonists
|
Dipivefrin
|
|
name two cholinergic agonists (miotics)
|
Pilocarpine
|
|
name three prostaglandins
|
Latanoprost
|
|
name four hyperosmotics
|
Glycerol – Isosorbide (the next two are only used if the pt is hospitalized) Mannitol – -Urea
|
|
what is the trade name for dpipvefrin
|
propine
|
|
what is dipivefrin
|
Prodrug – converts to epinephrine
|
|
how much does dipivefrin lower IOP by
|
15 to 20%. pupil dilation with initial IOP elevation.
|
|
what is the trade name for apraclonidine
|
Iopidine
|
|
what is apraclonidine used for
|
angle closure glaucoma. up to 40% drop.
|
|
what is the trade name for brimonidine
|
alphagan
|
|
how much does brimonidine lower IOP by
|
25 to 30%
|
|
what is combigan
|
combo drug with brimonidine and timolol
|
|
what drug is pilocarpine not effective with
|
latanoprost
|
|
what is the trade name for latanoprost
|
xalatan
|
|
by what mechanism does latanoprost incrase aqueous outflow
|
incrases uveoscleral outflow
|
|
by how much does latanoprost lower IOP
|
30 to 35%
|
|
what drug is lattice and what are the side effects
|
irreversable iris darkening and lash thickening
|
|
by how much does travaprost lower IOP
|
30%
|
|
what is the trade name for bimatoprost
|
lumigan
|
|
lumigan probably lowers IOP more than other prostaglandins
|
|
|
when are hyperosmotics indicated for glaucoma
|
acute angle closure
|
|
you wouldn't want to use glycerol on a diabetic because it is sugar water, but you could use isosorbide
|
|
|
when would you use a steroid to tx glaucoma
|
Steroids may reduce IOP in certain inflammatory glaucoma conditions ((TM is inflammed and outflow is blocked)
|
|
|
picture (click on picture to make it bigger)
|
|
glaucoma tx: consider monocular trial to start so you will have a control to see how your tx is working.
|
|
|
minimum follow up for glaucoma is 3 months
|
|
|
New lecture: 3 ONHstu6332010
|
a
|
|
Describe the shape of a normal optic disc and the shape of a normal cup
|
Generally disc has a slightly oval shape (V > H) Cup is nearly circular although may be slightly oval. If it is oval, in normals, it is most commonly elongated horizontally.
|
|
With a malinserted disc which side is most commonly raised and which side is most commonly depressed
|
Usually raised nasal side and depressed temporal margin
|
|
How does a malinserted disc affect vision
|
usually no visual effect
|
|
What is the congenital condition called where the disc is rotated from 90 degrees but remains in the plane of the retina.
|
a tilted disc
|
|
What is the congenital condition called where the disc is shifted so that one meridian (usually the horizontal) is no longer in the plane of the retina.
|
malinserted disc
|
|
how can you differentiate a congenital retinal condition from an acquired retinal condition based on laterality
|
congenital retinal conditions are ofted bilateral and look identical between the two eyes. acquired retinal conditions often look different between the two eyes.
|
|
Which direction is a tilted disc usually displaced
|
so that the elongated meridian is pointing in a supero-nasal and infero-temporal direction.
|
|
Name 7 diagnostic findings that indicate there is a tilted disc
|
1. disc is tilted so that vertical axis is not at 90 degrees 2. choroidal crescent (usually in the infero-nasal quadrant of the retina) 3. hypopigmentation of infero-nasal quadrant 4. moderate oblique astigmatism 5. bilateral 6. bitemporal defect that crosses the midline 7. situs inversus of retinal blood vessels
|
|
How do you differentiate the bi-temporal visual field defect caused by a tilted disc from one caused by a neurological defect
|
if it is cause by a tilted disc then it will not respect the vertical midline.
|
|
What side of the disc are normal choroidal and scleral crescents usually found
|
temporal
|
|
Describe the physiology of a choroidal crescent
|
either neural retina, or neural retina and the RPE does not extend all the way to (or is pulled away from) the disc, exposing either the RPE or the choroid
|
|
describe the physiology of a scleral crescent
|
neural retina, the RPE, and the choroid all fail to extent all the way to (or are pulled away from) the disc, exposing the sclera.
|
|
What should you look for if you see a choroidal or a scleral crescent
|
anything that might be pulling the retina away from the disc. For example, myopia, retinopothy of prematurity
|
|
do hyperopes or myopes tend to have less distinct disc margins and why
|
hyperopes, because there is the same amount of nerve fibers covering a smaller amount of the ONH
|
|
When you see myelinated fibers on the retina is it typically unilateral or bilateral
|
unilateral
|
|
if you see myelinated fibers on the retina how would you expect this to affect VAs
|
usually no effect on VA
|
|
how do you differentiate between myelination and cotton wool spots base on apperience (3 points)
|
Cotton wool spots are typically more yellow, smaller and less striated than myelation
|
|
look up physiology of drusen
|
|
|
is ONH drusen usually unilateral or bilateral
|
bilateral over 70 percent of the time
|
|
how does ONH drusen tend to affect blood vessel apperance
|
blood vessels branch prematurly
|
|
Does ONH drusen tend to become more or less obvious with age
|
more
|
|
name two negative affects that can be caused by ONH drusen and their mechanisms
|
visual field loss and circumpapillary hemorrhaging leading to choroidal neovascularization due to the drusen blocking axoplasmic flow and blood supply respectively.
|
|
Describe the management of ONH drusen
|
there is no treatment. monitor for field loss and development of neovascularization.
|
|
Papilledema
|
Papilledema reserved for bilateral swelling due to increased intracranial pressure
|
|
describe five visably observable findings you can see with papilledema
|
blurry margins, hyperemia, intra-retinal hemorrhages, cotton wool spots, loss of spontaneous venous pulsation.
|
|
how can you induce spontaneous venous pulsation clinically if you don't see it on a normal patient
|
put a slight amount of pressure on the globe which will raise the pressure of the IOP higher than the pressure inside the vein in between heart beats.
|
|
what is the average optic nerve head size vertically and horizontally
|
1.88 mm vertically and 1.77 mm horizontally
|
|
how far from the ONH is the macula
|
2-2.5 disc diameters
|
|
should you includ a scleral ring as part of the C/D measurement
|
no
|
|
What is the physiological cuase of ONH hypoplasia
|
Congenital defect due to failure of ganglion cells to develop
|
|
is ONH hypoplasia unilateral or bilateral
|
can be either
|
|
describe three visually observable signs you tend to see with optic nerve head hypoplasia
|
small ONH, double ring sign, tortuous blood vessels.
|
|
double ring sign
|
typically seen in ONH hypoplasia: a yellow zone that forms a ring around the ONH. The surrounding zone approximates the size of the ONH if it were normal in its development. The edge of the ourter zone is formed by the junction of the sclera and the lamina cribosa.
|
|
what types of visual consequences can you expect with ONH hypoplasia.
|
Decreased VA (normal to light perception) VF loss Defective color vision APD if unilateral Strabismus ((in unilateral cases) Nystagmus (especially in bilateral cases)
|
|
What is your main concern is you see bilateral optic nerve head hypoplasia
|
there is an increased risk of associated systemic disorders
|
|
what condition is often mistakenly diagnosed, when the true disorder is ONH hypoplasia
|
if it is mistakenly diagnosed as amblyopia they could be sent for amblyopia/strabismis treatment, which would be a waste of time if it was really ONH hypoplasia
|
|
describe the management for OHN hypoplasia
|
visual prognosis is unresponsive to threapy. the main concern is any associated systemic abnormalities. the likelihood of other systemic abnormalities goes up if it is bilateral. any child with bilateral ONH hypoplasia should be sent out for evaluation of pituitary function because of the potential consequences of developing without sufficinet growth hormone could easily be avoided with exogenous growth hormone.
|
|
name two of the common systemic anomolies you often find with ONH hypoplasia
|
pituitary disfunction and De Morsier Syndrome
|
|
what is De Morsier's syndrome
|
thinning of the optic nerves and chiasm, absence of the septum pellucidum, and agenesis of the corpus callosum. Systemic anomoly associated with ONH hypoplasia.
|
|
in what portion of the disc does an ONH coloboma usually occur
|
inferior
|
|
how does the size of the ONH of a disc with a coloboma compair to the size of one without a coloboma
|
the disc of an ONH with a coloboma will be larger than a normal disc
|
|
are ONH colobomas usually unilateral or bilateral
|
can be either unilateral or bilateral
|
|
how is vision impacted from a ONH coloboma
|
VA is variable (but can be reduced to light perception). visual field loss is common and often pretty dramatic.
|
|
are ONH colobomas associated with retinal detachment
|
there is a strong association btwn ONH colobomas and non-rhegmatongenous RDs that occur early in life (2nd or 3rd decade).
|
|
are there systemic findings associate with ONH coloboma
|
yes: CHARGE: coloboma, heart dz, atresia choanae, retarded growth, genital hypoplasia, ear abnormalities.
|
|
describe the anatomical changes that take place in morning glory disc anomoly
|
funnel shapped excavation of the posterior globe.
|
|
in morning glory disc anomoly how does the size of the disc compair to a normal disc
|
morning glory disc anomoly has a larger than normal disc size.
|
|
describe the apperance of the blood vessels exiting the disc in morning glory disc anomoly (3 points)
|
vessels are often hidden by white glial tissue. they appear straighter than normal. they may appear more numerous than usual, but this is because many bifricate before leaving the disc.
|
|
is morning glory disc anomoly usually unilateral or bilateral
|
usually unilateral
|
|
how is vision impacted by morning glory disc anomoly
|
VA is variable from barely reduced to hand motion
|
|
name two systemic findings associated with morning glory disc anomoly
|
hypertelorism and transsphenoidal encephalocele
|
|
is morning glory disc anomoly associated with retinal detachment? What percent?
|
there is a strong association with non-rhegmatogenous RD. about 30%
|
|
describe the management of morning glory disc anomoly
|
education and evaluation for any retinal detachment. because of the risk of RD contact sports should be avoided and protective eyewear prescribed. also refer for evaluation of potential systemic conditions that may be associated with the condition.
|
|
describe the pigment changes associated with an ONH pit
|
Peripapillary RPE disturbance common if not central pit
|
|
is the disc size of a nerve with an ONH pit larger or smaller than one without
|
If unilateral, ONH larger on side with pit ((almost always)
|
|
in what portion of the disc is a pit most commonly found
|
usually temporally, often inferiorly
|
|
describe the anatomical mechanism of an ONH pit
|
Histologically, a pit consists of dysplastic retina that has herniated posteriorly through a defect in the lamina cribrosa
|
|
are ONH pits usually unilateral or bilateral. what percent of the time.
|
unilateral 85% of the time
|
|
how does an ONH pit affect vision
|
The most common visual field defects are enlargement of the blind spot with connected paracentral arcuate scotoma (60-70%) [86]. Visual acuity usually is not affected by the pit
|
|
how does the location of an ONH pit affect the liklihood of developing a retinal detachment
|
if the pit is central, they are much less likely to develop a retinal detachment
|
|
is ONH pit typically associated with other systemic anomolies
|
no
|
|
describe the management of ONH pits (3 steps)
|
1. educate pt of chances of developing retinal detachment. 2. educate on avoidance of head trauma and protective eyewear. 3. amsler grid to monitor retinal detachment of macular area.
|
|
are optic nerve head pits associated with any other systemic anomolies
|
no
|
|
if you have a larger than average ONH due to physiological variation, would you expect a larger or smaller than normal C/D ratio
|
larger
|
|
at what difference in C/D between an individuals two eyes would you start to be concerned
|
0.2 or greater asymmetry in absence of different optic disc sizes or anisometropia is highly suspicious
|
|
how does the color of the ONH vary with location in the disc
|
the temporal side is more pale and the nasal side is more pink
|
|
how does the color of the ONH vary with sized of the disc
|
small disc is pinker than a larger disc
|
|
what is ONH pallor and what causes it
|
Absence of expected rim tissue color (pale) Due to atrophy of nerve axons Pallor implies pathology. Don’t use it for ONHs that are pale due to normal physiological variation. Can be total or segmental
|
|
what clinical sign indicates ONH atrophy
|
pallor
|
|
name three common mechanisms that cause ONH pallor
|
Often secondary to intracranial lesion, inflammation or trauma
|
|
describe the ISN'T rule
|
a way to remember how the ONH is supposed to look. it should be thickest inferiorly and thinnest temporally.
|
|
what is one way to differentiate btwn vessels that are congenitally tortuous from those that are acquired
|
If congenitally tortuous should involve both arteries and veins
|
|
what is the most common position of the disc for vessels to exit
|
Superior nasal most common position of exit
|
|
what is a splinter or drance hemorrhage
|
Flame-shaped hemorrhage just off optic nerve head
|
|
name four major causes of a drance hemorrhage
|
Commonly associated with glaucoma Also caused by PVD, Resolving BRVO, NPDR
|
|
what is a peripapillary vascular loop
|
twisted blood vessels
|
|
are retinal detachments associated with ONH pits. what percent of the time
|
yes: 45%, mean age is 30 years old
|
|
New lecture: 4 DDxOpticNeuropst2010
|
a
|
|
optic neuropathy
|
Pathological injury to the optic nerves or the blood supply to them
|
|
name three common optic neuropathies
|
Glaucoma is most common Optic neuritis (often associated with MS) Anterior ischemic optic neuropathy
|
|
name five clinically observable findings you can see with optic neuropathy
|
Decreased VA Decreased color vision Visual field defect RAPD in unilateral or asymmetric cases Optic disc edema or atrophy
|
|
how do you differentiate between different optic neuropathies
|
In most cases, appearance of nerve does not help differentiate Must use epidemiology information as well as associated signs and symptoms
|
|
name two conditions that are uncommon causes of optic neuropathies, but are so common in the population that you should always consider them as a cause of optic neuropathy
|
diabetes and high blood pressure
|
|
optic neuritis vs. papillitis vs. retrobulbar optic neuritis
|
Optic neuritis: inflammation of the optic nerve, which can occur anywhere along its course from the ganglion cells in the retina to the symapse of these cell fibers in the LGN. Papillitis: if the inflammation is restructed to the optic nerve head the condition is called papillitis. Retrobulbar optic neuritis: if inflammation is limited to the orbital portion of the nerve it is retrobulbar optic neuritis.
|
|
what is the syn. for papillitis
|
anterior optic neuritis
|
|
list of causative agents of optic neuropathy:
|
MS Bacteria Syphilis, Lyme dz, Meningitis, Whipple’s dz Viruses Adenovirus, Rubella, Herpes zoster, Mumps, HIV Protozoa Toxoplasmosis Fungi
|
|
what is the most frequent cause of optic neuritis
|
MS is by far the most common cause of optic neuritis
|
|
describe 5 clinical ocular findings commonly associated with a typical optic neuritis
|
1. acute unilateral visual acuity or visual field (central scotoma) loss 2. RAPD 3. periocular pain with eye movement 4. reduced contrast sensativity 5. swollen ONH
|
|
how quick is the onset of VA loss due to a typical optic neuritis
|
1 to 10 days
|
|
describe the patient demographic most commonly associated with typical optic neuritis
|
Usually young adult; female > male
|
|
what percent of the time do you have periocular pain on eye movement with typical optic neuritis
|
Periocular pain with eye movement (90%) ((this is significant pain with EOMs; you won’t have to ask the pt to tell you if it hurts when they follow the bead)
|
|
what percent of the time do you have swollen ONHs in a patient with optic neuritis
|
Normal (65%) or swollen (35%) ONH
|
|
what percent of the time does vision loss, due to typical optic neuritis, return to near normal and how long does this take
|
Eventual visual improvement to near normal over weeks (90%)
|
|
what test would be best for diagnosis of MS
|
MRI of brain to look for lesions consistent with MS
|
|
in what percent of cases of MS is optic neuritis the presenting sign
|
35%
|
|
in what percent of patient who have had a single episode of optic neuritis is MS diagnosed within 15 years
|
>50%
|
|
based on the results from the optic neuritis treatment trial what are the pros and cons of treating optic neuritis with IV methylprednisolone, oral prednisone, or not treating it at all.
|
Intravenous group Quickest recovery for all visual measures No long term VA benefit (6-12 months virtually =) ((same as in other treatments after 6-12 months) Reduced rate CDMS within 2 years but very close at 4 years Prednisone group No advantage for visual measures Increased risk of new ON attacks compared to other 2 groups -third group was placebo
|
|
management of optic neuritis
|
|
|
describe the visual prognosis for optic neuritis
|
most return to normal or near normal VA, but there will usually be permanently compromised constrast sensitivity, percieved as a washing out by the pt.
|
|
what is the name of the optic neuropathy that causes an altitudinal visual field defect
|
anterior ischemic optic neuropathy
|
|
describe six clinical observable ocular findings commonly associated with anterior ischemic optic neuropathy
|
1)Acute unilateral loss of vision (Usually painless (90%)) 2)Often altitudinal VF loss, but can have other patterns 3) pallor 4) ONH swelling 5) splenter hemorrhages 6) RAPD
|
|
how quickly does vision loss from anterior ischemic optic neuropathy occur
|
onset hours to days
|
|
over what age do you expect to see anterior ischemic optic neuropathy
|
50
|
|
describe the appearence of the ONH in anterior ischemic optic neuropathy (3 points)
|
Pallid ONH edema in sector with or without peripapillary hemes
|
|
are there any premonitory signs or symptoms that occur with anterior ischemic optic neuropathy
|
No premonitory symptoms but may have disc edema as early sign
|
|
describe the prognosis for anterior ischemic optic neuropathy
|
poor; vision loss is usually permanent and may have continuing loss
|
|
what is a "disk at risk" and what is it a risk factor for
|
it is a relatively small optic nerve head with an absent to small physiological cup, an abnormal branching pattern of the central retinal blood vessels and a lush of nerve fiber layer elevating the disc margins. it is a risk factor for anterior ischemic optic neuropathy.
|
|
what is the name of the condition that can potentially result in death that is associated with arteritic anterior ischemic optic neuropathy
|
giant cell arteritis
|
|
describe the etiology of anterior ischemic optic neuropathy
|
ischemic infarction of the anterior optic nerve due to occlusion of the posterior ciliary circulation just behind the lamina cribosa
|
|
what is the difference between arteritic and non-arteritic anterior ischemic optic neuropathy
|
non-arteritic is from a non-inflammatory cause. the process associated with development is thought to be secondary to an alteration of the blood supply to the optic nerve or as a result of toxic alteration of the metabolism of the neurons. arteritic is caused by inflammation of the elastic tissue in the media and adventitia of the arterial walls, leading to occlusion.
|
|
what is the most common cause of arteritic anterior ischemic optic neuropathy
|
giant cell arteritis
|
|
if anterior ischemic optic neuropathy is not treated, what are the chances that the vision loss will spread to the other eye with in one week
|
70%
|
|
what systemic outcome are we most concerned with giant cell arteritis
|
stroke and death
|
|
name five signs and symptoms you should check for if you are concerned that a pt has giant cell arteritis
|
HAs, scalp tenderness, jaw claudication, fever/malaise etc. Check for decreased temporal artery pulse with tenderness
|
|
name three tests you would want to do if you suspected giant cell arteritis
|
westergren erythrocyte sedimentation rate (elevated, not even close to normal), c-reactive protein, temporal artery biopsy
|
|
is a temporal artery biopsy 100% accurate for diagnosis of giant cell arteritis
|
if biopsy is negative you still have to be suspicious because you can have areas of normal artery and areas of diseased artery and they may have just biopsied a normal area of the artery.
|
|
describe the managment of arteritic anterior ischemic optic neuropathy (5 steps)
|
1. Educate the pt on seriousness of potential systemic causes, and potential to spread to the fellow eye 2. emergency neuro-ophthalmology or neurology consultation for immediate institution of steroid therapy 3. STAT Westergren erythrocyte sedimentation rate 4. temporal artery biopsy within 1 week 5. refer to neuro-ophthalmology or neurology
|
|
is arteritic anterior ischemic optic neuropathy typically unilateral or bilateral
|
usually starts unilateral with a 70% chance of spreading to the fellow eye whithin 1 week if not treated
|
|
describe four cilincal findings commonly associated with optic disc edema with macular star
|
Peripapillary and macular exudate Swelling of ONH Vitreous cells APD if unilateral
|
|
what age range do you tend to see optic disc edema with macular star
|
young children to adult
|
|
does optic disc edema with macular star tend to be unilateral or bilateral (how much of the time)
|
Unilateral in 66%
|
|
how does optic disc edema with macular star affect vision
|
Variable VA (20/20 to LP) Dyschromatopsia
|
|
with optic disc edema with macular star does the disc edema and the macular star appear simultaneously
|
-macular star can appear up to two weeks after optic disc edema
|
|
what is the most common cause of optic disc edema with macular star
|
Most cases are idiopathic Possibly due to viral infection Hepatitis B, H. Simplex, H. Zoster, Epstein-Barr, Influenza Other common causes
|
|
describe the type of visual loss and the type of progression associated with compressive optic neuropathy
|
Painless, progressive, gradual loss of VA, VF and color vision
|
|
how does compressive optic neuropathy affect the nerve head
|
ONH edema and atrophy
|
|
list two causes of compressive optic neuropathy
|
Intracranial or intraorbital tumors Thyroid ophthalmopathy
|
|
is toxic optic neuropathy usually unilateral or bilateral
|
bilateral
|
|
describe the progression of vision loss associated with toxic neuropathy
|
symmetric, slowly progressive vision loss
|
|
what type of visual field defect do you tend to see with toxic or nutritional optic neuropathy
|
bilateral central or cecocentral scotomas
|
|
name five common causes of toxic or nutritional optic neuropathy
|
Ethambutol (TB drug)
|
|
describe the patient demographic most commonly associated with Leber's heriditary optic neuropathy
|
90% are males between ages of 18 -30
|
|
describe the progression of VA loss associated with Leber's heriditary optic neuropathy
|
Rapid, painless and unremitting VA loss. VA quickly reduced to the 20/200 level where it stabilizes.
|
|
what type of visual field loss is most commonly associated with Leber's heriditary optic neuropathy
|
Central or cecocentral VF loss NFL loss in papillomacular bundle
|
|
is Leber's heridiatary optic neuropathy usually unilateral or bilateral
|
Sequential bilateral involvement (2nd eye weeks to months later)
|
|
what is the mechanism that causes Leber's heriditary optic neuropathy
|
Mitochondrial DNA mutation
|
|
does Leber's heriditary optic neuropathy have any systemic conditions associated with it
|
Usually isolated but may have Cardiac conduction defects (heart block or WPW syndrome) Dystonia
|
|
describe three clinically observable findings associated with Lebers heriditary optic neuropathy
|
pseudoedema of the peripapillary nerve fibre layer, retinal telangiectasias and increased vascular tortuosity
|
|
what type of test is done to diagnose Leber's heriditary optic neuropathy
|
there is a specific genetic test
|
|
describe the management of Leber's heriditary optic neuropathy (4 setps)
|
1. Education of visual prognosis 2. genetic counseling 3. potential cardiac anomolies should be investigated in both the affected patient and in the carrier mother and sisters 4. low vision aids
|
|
papilledema
|
Reserved for bilateral swelling secondary to increased intracranial pressure
|
|
what is the most common cause of papilledema
|
Idiopathic intracranial hypertension (pseudotumor cerebri)
|
|
what condition is important to rule out as a cause of papilledema
|
Mass lesions must be ruled out Less likely but possible causes: trauma, meningitis/encephalitis, subarachnoid hemorrhage
|
|
describe the management associated with papilledema (1 steps)
|
1. immediate consulation with neurology or neuro-ophthalmology to determine the underlying cause (potentially life threatening)
|
|
What do you need to DDX papilledema with
|
pseudopapilledema
|
|
what will happen (to the eye) if papilledema is left untreated
|
optic atrophy
|
|
why is it important to find the underlying cause of papilledema
|
because, if left untreated could result in death
|
|
what is pseudopapilledema
|
burried drusen of the ONH. not a benign condition
|
|
what do you need to DDX papilledema with
|
pseudopapilledema
|
|
describe 6 subjective symptoms associated with idiopathic intracranial hypertension
|
Headache (75 - 80%) ((often severe) TVO ((transient visual obscurations (72%) Decreased acuity (68%) ((20/30 to 20/40) Intracranial noises (pulsatile tinnitus) 58% Photopsia (54%) Diplopia in (36%) - CN VI palsy
|
|
what percent of cases of idiopathic intracranial hypertension will have papilledema
|
Papilledema in almost 100% of cases
|
|
describe the follow up time frame on a patient with papilledema and what tests you would do at the follow up
|
Follow q 1 m until papilledema has regressed Perform VA, RAPD testing, VF, Stereo ONH evaluation
|
|
New lecture: 5 OPT 633 - Hematologic and Systemic 2010
|
a
|
|
What is a complete blood count (CBC)
|
a test panel (group of tests) requested by a doctor or other medical professional that gives information about the cells in a patient's blood
|
|
what are the three main types of cells found in blood
|
leukocytes, erythrocytes, and thrombocytes (platlets)
|
|
Red Blood Cell Count (RBCC)
|
Number of RBCs x 106/ml of blood
|
|
what is the hemoglobin concentration
|
Hemoglobin concentration measurement is among the most commonly performed blood tests, usually as part of a complete blood count. Results are reported in g/L, g/dL or mol/L.
|
|
what is the hematocrit level
|
is the proportion of blood volume that is occupied by red blood cells
|
|
what is the White blood cell count (WBCC)
|
Number of white cells x 103/ml
|
|
what is a White blood cell differential (WBC diff)
|
Percent of the five types of white blood cells in the blood:
|
|
what are the 5 types of white blood cells found in blood
|
Neutrophils Eosinophils Basophils Lymphocytes Monocytes
|
|
what types of white blood cells are most elevated in bacterial infection
|
Neutrophils
|
|
what types of white blood cells are most elevated with allergies or paracytic infections
|
Eosinophils
|
|
what types of white blood cells are most elevated with viral infections
|
Lymphocytes
|
|
in what layer of the retina do flame shapped hemorrhages occur
|
nerve fiber layer
|
|
in what layer of the retina do dot/blot hemorrhages occur
|
inner nuclear and plexiform layers
|
|
anemia
|
Reduction in the total number of red blood cells Or reduction in the quantity of hemoglobin
|
|
list three common systemic signs and symptoms associated with anemia
|
Results in pallor ((of skin), weakness, lethargy and dyspnea
|
|
describe the mechanism that causes elevated intracrainial pressure to result in retinal anemia
|
optic nerves are part of the brain, when there is increased pressure in the brain the optic nerve swells and blocks blood vessels in the optic nerve, causing anemia in the retina.
|
|
can you tell the cause of retinal anemia based on appearence
|
Can't differentially diagnosis based on observations made by an ophthalmoscope All cause similar type of ocular changes
|
|
what is the most common cause of anemia in the US
|
iron deficiency
|
|
what percent of women and pregnant woment have iron deficiency anemia
|
20% of women and 50% of pregnant women have iron deficiency anemia (only 2% of adult men)
|
|
is it common to see retinal changes with iron deficiency anemia
|
Typically no retinal changes unless very severe
|
|
what is the treatment for iron deficiency anemia
|
Treatment - iron supplements
|
|
what is the mechanism that causes pernicious anemia
|
Small intestinal tract failure to absorb vitamin B12 due to lack of intrinsic factor: In pernicious anemia, an autoimmune disease, auto-antibodies directed against intrinsic factor or parietal cells themselves lead to an intrinsic factor deficiency, malabsorption of vitamin B12
|
|
what is the treatment for pernicious anemia and is it efficacious
|
Sublingual or parenteral (injected) vitamin supplements Usually respond well Oral (ingested) B12 supplements are not typically absorbed as well through the small intestine wall
|
|
what is hemolytic anemia
|
Anemia as the result of the destruction of red blood cells
|
|
how long do red blood cells live in a normal healthy person
|
RBC survives avg. 90 to 120 days
|
|
where are old RBCs absorbed and new RBCs produced in the body
|
Spleen removes old and damaged RBCs from blood Production of new RBCs in the bone marrow
|
|
what substance is released when red blood cells are broken down
|
Bilirubin
|
|
what condition results from an excess of bilirubin in the blood
|
jaundice
|
|
describe the mechanism that causes aplastic anemia
|
Bone marrow damage à inefficiency to make enough RBCs
|
|
list of medications that cause aplastic anemia
|
Medications Tolbutamide (Orinase) – insulin secretion drug Methimazole (Tapazole) – inhibits thyroxine Phenylbutazone (Butazolidin) – NSAID, arthritis Tx Gold compounds – autoimmune anti-inflammatory Trimethadione (Tridione) – epileptic anticonvulsant Lindane (Kwell) – insecticide for head lice/mites Chloramphenicol (Chloromycetin) Acetazolamide (Diamox) ((long-term use) Methazolamide (Neptazane)
|
|
what clinically observable ocular signs should you look for with pts who are taking drugs that are known to cause aplastic anemia
|
Watch for conjunctiva and/or retinal hemorrhages in patients known to be on these medications to diagnosis early and improve the prognosis.
|
|
what ethnicity has the highest occurance of sickle cell anemia
|
African Americans - 10%
|
|
what type of inheratince pattern do you see with sickle cell anemia
|
Gene is recessive
|
|
what is the mechanism for sickle cell anemia causing ischemia
|
sickled RBCs accumulate and occlude vessels
|
|
describe the retinal changes you tend to see from sickle cell anemia
|
venous tortuosity, shunt vessels (arteriovenous anastomoses), "sea fan" neovascularizatioin
|
|
what is the function of erythropoietin in the body
|
A cytokine made by the kidneys that stimulates the proliferation of red blood cells.
|
|
what is primary and secondary polycythemia
|
Primary polycythemia Bone marrow abnormally over-produces all types of blood cells (RBC, WBC, platelets) Secondary polycythemia Kidney overproduces erythropoietin (hematopoietin) hormone causing an increased production of erythrocytes
|
|
is polycythemia vera a name for primary or secondary polycythemia
|
primary
|
|
describe the mechanism for the vascular damage caused by polycythemia
|
Hyperviscosity of blood Viscosity may be 4+ times normal Occlusion of blood vessels
|
|
what is the typical age of onset of polycythemia
|
Most in middle to elderly age
|
|
describe three systemic signs associated with polycythemia
|
Red complexion ((not pallor) Hypertension Hemorrhages in the skin and mucous membranes
|
|
describe 3 clinically observable ocular signs associated with polycythemia
|
-dilated tortous retinal vessels -Deep or superficial retinal hemorrhages -Retinal vein occlusion -May see visible emboli – result in amaurosis fugax (monocular blindness)
|
|
leukemia
|
Neoplastic proliferation of WBC's in bone marrow (cancer)
|
|
what percent of pts with leukemia have some observable ocular finding associated with the condition
|
50 to 70% have some ocular finding
|
|
name 6 clinically observable ocular signs associated with Leukemia
|
venous dilation and tortuosity, retinal hemorrhages, cotton wool spots, pre-retinal hemorrhages, perivascular infiltration (w/ WBCs), infiltration of the ONH
|
|
what is waldenstrom's macroglobulinemia
|
Cancer involving increased IgM fraction of plasma 1500 cases diagnosed per year, accounting for approximately 2% of hematologic malignancies
|
|
what is lipemia retinalis
|
A condition in which retinal vessels appear reddish white (pink) or white; found in cases of extreme hyperlipidemia
|
|
what is behcet's disease
|
A rare, multisystem, chronic, recurrent form of vasculitis, marked by ulceration of the mouth and genitalia and by uveitis.
|
|
what is sarcoidosis
|
A chronic multisystem inflammatory disease of unknown etiology, characterized by noncaseating (hard) granulomas
|
|
what two organs does sarcoidosis have the biggest impact on
|
lungs and the lymph glands (forms granulomas)
|
|
what demographic is sarcoid most common in
|
Incidence african americans Women more than men 20 to 40 years of age
|
|
name three of the most common presenting systemic signs and symptoms associated with sarcoidosis
|
Persistent dry cough Fatigue Shortness of breath
|
|
name two diagnositc tests that help with the diagnosis of sarcoidosis
|
chest x-ray (looking for hilar lymphademopathy), ACE
|
|
name 6 clinically observable ocular signs associated with sarcoidosis
|
Enlargement of lacrimal gland Granulomatous anterior uveitis Vitritis or string of pearls vitreous opacities Periphlebitis with candle-wax drippings Retinal vein occlusions, hemorrhages Optic nerve granulomas causing a swollen ONH
|
|
what does an S-shaped upper lid indicate
|
Enlargement of the lacrimal gland
|
|
describe the progression of sarcoidosis
|
remissions and exacerbations
|
|
describe the ocular management of sarcoidosis
|
Manage dry eye Watch for cataracts from uveitis and steroid use Control anterior uveitis Watch for secondary glaucoma
|
|
at what age do people typically develop systemic lupus erythematosus
|
Adults 20-40 years of age
|
|
what ethnicities are prone to developing systemic lupus erythematosus
|
African, American Indian, and Asian greater than Caucasian
|
|
name four systemic symptoms associated with systemic lupus erythematosus
|
Malar rash over the cheeks Discoid rash - red, raised patches Oral ulcers usually painless Arthritis involving two or more peripheral joints
|
|
New lecture: 6 HereditRetDisease (study this one)
|
a
|
|
what is one way you can differentiate between heriditary retinal disease and acquired retinal disease
|
the retina in pathology like diabetic retinopathy or inflammatory disease will almost never be perfectly symmetrical. In hereditary retinal disease the two retinas will often look the same.
|
|
what kind of heriditary retinal disease does it indicate if you have photosensativity (rod or cone disease)
|
disorder affecting cones
|
|
name the four most common heridiatry retinal disorders affecting the rods
|
-retinitis pigmentosa -leber's congenital amaurosis -Oguchi's -congenital stationary night blindness
|
|
name the three most common heridiatry retinal disorders affecting the cones
|
-stargart's -best's -achromatopsia
|
|
what is the most common heridiatary retinal disorder
|
retinitis pigmentosa
|
|
does RP only affect the rods, the cones, or both
|
Common end result is loss of rods with secondary involvement of cones
|
|
what type of inheritance pattern do you see with retinitis pigmentosa
|
Many variants Including AD, AR, X-linked
|
|
which inheritance pattern of RP is the most common
|
Autosomal Recessive:
|
|
which inheritance pattern of RP is the most visually devistating
|
Autosomal Recessive:
|
|
describe the progression of the autosomal recessive form of RP
|
Night vision and peripheral field loss in early childhood, central vision loss by adulthood
|
|
which inheritance pattern or RP has the least visually devistating outcome
|
Autosomal Dominant
|
|
describe the progression of the autosomal dominant form or RP
|
Least severe form with central vision intact until 40’s or 50’s
|
|
is RP typically associated with other systemic abnormalities
|
30-40% of cases are part of a systemic syndrome
|
|
describe 5 clinically observable ocular findings associated with RP
|
Arterial attenuation (sometimes the earliest sign) Waxy looking optic nerve pallor (atrophy) Classic bone spicule pigmentary pattern Begins in mid-periphery Corresponding visual field loss (ring scotoma) Cataracts (PSC) develop in 50% of cases ((treating cataract can help improve central acuity) Macular edema in late stages
|
|
what type of field loss do you typically find with RP
|
ring scotoma
|
|
what test will show signs of RP well before there are any clinically observable changes to the retina
|
Scotopic ERG will usually be abnormal before retinal signs are present Often necessary for firm diagnosis in early stages of disease Results can help determine the RP type and therefore prognosis
|
|
what is retinitis sine pigmento
|
No clinically recognizable pigmentary changes May be just presentation early in disease
|
|
what is usher's syndrome
|
Congenital sensorineural hearing loss and RP Accounts for 50% of deaf-blind individuals
|
|
describe the treatment options for RP (6)
|
No direct treatment…yet. Nutrient supplements (primarily Vit.A palmitate) have demonstrated some slowing in progression Short-wavelength blocking tints May help with photosensitivity May slow progression Cataract removal may improve VA’s Treatment of CME Low Vision management is difficult Refer to Commission for the Blind for orientation and mobility
|
|
what is Leber's congenital amaurosis
|
Similar to RP except congenital (or very early onset),
|
|
describe the diagnostic clues associated with Leber's congenital amaurosis
|
Visually unresponsive baby with nystagmus Retina may look normal at first, many variations on fundus appearance ERG shows severely diminished or absent rod and cone responses Molecular genetic testing is critical
|
|
is there any treatment for Leber's congenital amaurosis
|
Gene Therapy Trials for LCA are happening now
|
|
whatis the difference between sensory and motor congenital nystagmus
|
Sensory (Afferent): Secondary to disease disrupting the foveal pathway early in life Motor (efferent): Due to primary abnormality in the ocular-motor system
|
|
what is congenital stationary night blindness
|
Night Blindness is primary symptom Mild acuity reduction (usually 20/30 - 20/60) Normal retina
|
|
what is Oguchi's disease
|
Variant of CSNB found in Japanese populations Yellow-gray retina color reversed by 2-3 hrs of dark adaptation
|
|
how do cone-rod dystrophies differ from rod-con dystrophies in their progressive involovment of rods and cones
|
Both Rod and Cone function affected ((fairly equally) early in disease rod-cone dystrophies (like RP) tend to affet the rods first and then the cones later on in the disease process
|
|
what is gyrate atrophy
|
circular patches of chorioretinal atrophy in the periphery, which increase in number and become confluent and form a scalloped border. atrophy spreads peripherally and centrally, with relative sparing of the fovea.
|
|
describe the visual impact of gyrate dystrophy
|
poor; legal blindness by the fourth to seventh decade
|
|
is there any treatment for gyrate atrophy
|
Treatment: B6 supplements, diet low in protein (low arginine, precursor of ornithine) slows, may halt progression
|
|
what type of inheritance pattern is seen with choroideremia
|
X-linked, Affects Males only
|
|
describe the clinically observable diagnostic signs associated with choroideremia
|
Diffuse RPE mottling is early sign then large patches of RPE and choroidal atrophy in mid-periphery leaving bare sclera Corresponding peripheral field loss Central field lost in 40’s to 60’s Scotopic ERG becomes non-recordable
|
|
what is the most common heriditary macular dystrophy
|
stargardt's macular dystrophy
|
|
what is the typical age of onset of stargardt's
|
Usual Onset 8 - 16 yrs with poor acuity
|
|
with stargardt's do you have acuity loss or visible macular changes first
|
Acuity loss may precede observable macular changes Macular changes very subtle at first
|
|
describe the changes to the macula that take place with stargatdt's
|
Foveal Light Reflex lost as mottling appears Beaten Bronze appearance at end stage Yellow pisciform (fishy) flecks in surrounding posterior pole vary in timing and appearance
|
|
at what age and at what level do acuities stabalize with stargardt's
|
Usually stabilizes by early 20’s with acuities in 20/200 - 20/400 range
|
|
what is fundus flavimaculatus
|
Variant of Stargardt’s Pisciform lesions are primary presentation Macular disease and acuity loss develops later (40’s - 50’s)
|
|
what is another name for vitelliform dystrophy
|
best's disease
|
|
with Best's disease, do you have changes in acuity or visible changes to the retina first
|
opposite of stargardt’s: you can have a large lesion with little VA change
|
|
describe the progression of Best's disease
|
4 - 10 yrs: Vitelliform Stage: Yellow spots coalesce into “Egg Yolk” macula appearance VA still near normal (opposite of Stargardt’s in terms of the relationship of appearance to VAs) Teens - 20’s: Vitelliruptive Stage: Lesion breaks up in to “scrambled egg” VA drops to 20/200 range
|
|
what is another name for rod monochromatism
|
achromatopsia
|
|
what is achromatopsia
|
Congenital Absence of Cone Function
|
|
what is the inheritance pattern associated with achromatopsia
|
autosomal recessive
|
|
describe four clinically observable signs and symptoms associated with achromatopsia
|
Photophobia (Rods Bleach Quickly in bright light) Nystagmus Poor VA (20/200 range) No Color Vision
|
|
what type of tint is usually best to use for a rod monochromat
|
Red tint is often the best
|
|
describe the most common appearence of the macula of a person with progressive cone dystrophy
|
Bull’s Eye macular lesion
|
|
describe the visual outcome you would expect for a person with progressive cone dystrophy
|
Reduced VA to 20/60 - 20/200 range by teens
|
|
what is the age of onset you would expect for a person with central areolar choroidal dystrophy
|
Later onset, usually after 40
|
|
describe the visual outcome you would expect for a person with central areolar choroidal dystrophy
|
Loss of central vision with acuity dropping below 20/200
|
|
name the two forms of albinism and the difference between the two
|
Oculocutaneous: pigment is lacking in the eyes, skin and hair Ocular Albinism: only the eyes lack pigment
|
|
why do individuals with albinism have limited binocularity
|
Anomalous wiring at the chiasm limits binocularity
|
|
name six clinically observable ocular signs associated with albanism
|
Amelanosis of iris and retina (iris transillumination defect) photophobia Foveal hypoplasia Nystagmus (and ability to dampen) Strabismus and impaired BV Astigmatism
|
|
why are CLs a good option for pts with nystagmus
|
contact lenses are a good option for pts with nystagmus. It minimizes swim and will provide mechanical feedback to allow the pt to control nystagmus
|
|
New lecture: 7 AMD Dx I DE 10 Vault
|
a
|
|
what is the most common cause of vision loss in the elderly in the developed world
|
age-related macular degeneration (AMD)
|
|
is AMD a genetic or environmental disease process
|
both
|
|
what layers of the eye does AMD primarily affect
|
photorecepters, RPE, Bruch's mem brane, Choriocapillaris
|
|
what are the chances of developing AMD if you are over the age of 75
|
30%
|
|
are males of females more likely to develop AMD
|
females
|
|
is AMD more common in caucasians or african americans
|
caucasians
|
|
by how much does it increase your risk of developing AMD if you have a primary relative with AMD
|
2.4 times
|
|
name four modiiable risk factors for AMD
|
smoking, short wavelength light, obesity, macular pigment density (zexanthene and leuteine)
|
|
what gives the macula a yellowish color
|
xanthophyll carotenoid pigments lutein and zeaxanthin
|
|
does the RPE have stronger adhesions with the retina or with Bruch's membrane
|
Strong adhesion to Bruch’s membrane Weaker adhesions to sensory retina
|
|
between what layers of the retina is the subretinal space located
|
between the sensory retina and the RPE
|
|
what specific layer of the retina is drusen found in
|
inner portion of bruch's membrane between the basement membrane of the RPE (part of bruch's membrane) and the inner collagenous layer of bruch's membrane.
|
|
what layer of the retina produces the material that forms drusen
|
RPE
|
|
name 5 clinically observable retinal signs associated with AMD
|
1) Drusen and lipofusin 2) RPE hyper or hypo-pigmentation 3) pigment epithelial detachment 4) geographic atrophy 5) choroidal neovascularization
|
|
how does the appearence of flourscene angiography change in AMD with areas of RPE pigment clumping vs. areas of hypopigmentation
|
HypOflourescences in areas of pigment clumping HypeRflourescences in areas of hypopigmentation
|
|
what is lipofuscin
|
undigestable pigment granules that are a product of lipid oxidation and accumulate in cells with age
|
|
how does lipofuscin affect the RPE
|
damages the RPE, resulting in RPE atrophy and drusen
|
|
does retinal drusen tend to appear unilatterally or bilatterally
|
bilaterally, and often symmetrical
|
|
what area of the retina does drusen tend to accumulate
|
around the macula and ONH
|
|
what is drusen made of
|
exact composition is controversial. extracellular material, components include: proteins, vitronectin, amyloid, inflammatory components, immunological products
|
|
what are the 4 types of drusen
|
1) small hard drusen 2) large soft drusen 3) familial drusen 4) calcific drusen
|
|
how big is small hard drusen
|
less than 63 microns (half a the diameter of a vein)
|
|
how big is large soft drusen
|
larger than 63 microns (half a vein diameter)
|
|
how does hard and soft drusen compair in their apperence
|
hard: small, discrete, yellow, well defined borders, round soft: larger, fluffier, pale yellow, indistinct borders, can vary in shape
|
|
is hard drusen associated with diffuse or focal RPE dysfunction. what about soft
|
hard: focal RPE dysfunction soft: diffuse RPE dysfunction
|
|
can hard drusen turn into soft. can soft drusen turn into hard
|
hard drusen may break down and become soft. soft drusen can not turn into hard.
|
|
why is soft drusen associated with pigment epithelial detachment
|
large soft drusen may coalesce and create a PED
|
|
which type of drusen has the poorest prognosis
|
large soft drusen
|
|
what is familial drusen
|
inherited condition (AD), drusen caused by metabolic defect in RPE
|
|
at what age do you tend to see familial drusen
|
20-30s
|
|
what is calcific drusen
|
long standing drusen that has calcified, leaving multifocal patches of atrophy and calcium deposits. Can be seen in hard or soft drusen.
|
|
is pigment epithelial detachment common in AMD? why?
|
yes; drusen loosen adherence between RPE basement membrane and inner collagenous portion of bruch's membrane.
|
|
what are the layers of bruch's membrane from inner to outer
|
basement membrane of the RPE inner collagenous zone elastic zone outer collagenous zone basement membrane of the choriocapillaris
|
|
what does a PED look like
|
sharp borders, dome shaped, round or oval elevations of the RPE
|
|
what can a pigment epithelial detachment turn into
|
can collapse, causing RPE or geographic atrophy
|
|
what visual consequences can result from PED (2)
|
reduced VA and metaporphopsia
|
|
what are the two types of AMD
|
exudative (wet, neovascular) and non-exudative (dry, atrophic, non-neovascular)
|
|
which type of AMD is most common
|
non-exudative (dry) 75-90% of AMD pts
|
|
is there choroidal neovascularization in the non-exudative form of AMD
|
no
|
|
is it common for dry AMD to reduce vision to legal blindness
|
no
|
|
name three clinically observable retinal findings you see with dry AMD
|
hyper/hypopigment of the RPE, geographich atrophy
|
|
what percent of pts with dry AMD progress to wet AMD
|
10-20%
|
|
what percent of legal blindness caused by AMD is from the wet form
|
75%
|
|
is the presence of hard drusen sufficient to make the diagnosis of AMD? what about soft drusen?
|
presence of hard drusen is not sufficient to make the diagnosis of AMD. the presence of soft drusen IS sufficient to make the diagnosis of AMD.
|
|
what form of AMD can have soft drusen
|
either (dry or wet)
|
|
name nine clinical tests that would be good to do on an AMD pt
|
stereoscopic retinal exam color fundus photography amsler grid photostress test color vision testing central 10 automated perimetry OCT preferential hyperacuity perimetry FA
|
|
what does the photostress test tell us about the cause of VA loss
|
helps differentiate btwn macular and optic nerve problems
|
|
what do the think is the pathophysiology of AMD
|
light causes generation of free radicals which damage the molecules within the retina
|
|
how do we think we can prophylactically reduce the changes of developing AMD
|
AREDS (age-related eye disease study) antioxidants help prevent free-radical formation
|
|
what is the group of people who you would not want to rx one of the vitamins in the AREDS formulation and what was that vitamin and why
|
don't use beata-carotene (form of vitamin A) with people who smoke or who have smoked in the last 5-10 years because of an increased risk of developing lung cancer
|
|
what can a pt do to help control/prevent AMD (5)
|
UV protection, diet (high in lutein and zexanthene), antioxidant supplimentation (check w/ primary care for interactions), exercise and HTN control, QUIT SMOKING
|
|
how often should you schedule follow up visits with AMD patients
|
minimal RPE changes: 1 year as RPE worsens: every 6 months high risk: 4-6 months
|
|
New lecture: 8 AMD Advanced Dx part II Vault
|
a
|
|
what are hard exudates
|
discrete white yellow lipid deposits and macrophages in the posterior pole. associated with DR, HTN retinopathy, coat's disease, choroidal neovascularization. -indicates that there has been edema. macrophages are there to reabsorb the lipid deposits, but they may never become entirely reabsorbed
|
|
how do you differentiate between hard exudates and drusen (4)
|
1) hard exudates are more anterior (between the inner plexiform and inner nuclear layers (drusen is between the RPE basement membrane and the inner collagenous layer of bruch's membrane)) 2) hard exudates may have a distinct pattern (ring pattern, clumps or stellate pattern depending on cause) 3) hard exudates are lipids and have a waxy yellow (glistening) appearance 4) hard exudates may have accompanying signs of disease process (hemes and cotton wool spots)
|
|
are cotton wool spots deep or superficial in the retina
|
superifical (NFL edema)
|
|
describe the appearence of cotton wool spots
|
white to yellowish (more white), fluffy w/ indistinct boarders
|
|
cotton wool spots, drusen or hard exudates?
|
drusen
|
|
cotton wool spots, drusen or hard exudates?
|
cotton wool spots
|
|
cotton wool spots, drusen or hard exudates?
|
hard exudates
|
|
cotton wool spots, drusen or hard exudates?
|
drusen
|
|
do you tend to see choroidal neovascularization in the atrophic regions of the retina in AMD
|
CNV will usually not occur within atrophic zone (bc the choriocapillaris is not working in this area) 20% of eyes may develop CNV at the margins of the atrophy
|
|
picture of geographic atrophy
|
|
|
what blood vessels become apparent that weren't before in areas of geographic atrophy in AMD
|
choroidal blood vessels are visable on ophthalmoscopy
|
|
what is foveal sparing in geographic atrophy associated with AMD
|
the fovea contains leutein and zeaxanthine pigments with keep atrophy from affecting this region. you will have a large area of atrophy surrounding an island of foveal sparing. pt can have advanced atrophy and come in with 20/25 vision because of foveal sparing. eventually atrophic area will engulf macula.
|
|
is there currently any treatment for dry AMD
|
no effective treatment at this time; studies currently being done
|
|
is there currently treatment for wet AMD
|
yes
|
|
what percent of adults over the age of 43 have wet AMD
|
1.2%
|
|
what do you need to have in order to classify AMD as wet
|
neovascularization
|
|
describe the process of choroidal neovascularization
|
new blood vessels grow through breaks in bruch's membrane. new blood vessels leak, creating sub-RPE/sub-retinal hemorrhage, which can result in RPE or sensory retinal detachment
|
|
what test should you do if you suspect development of choroidal neovascularization in a pt with AMD
|
STAT flourescene angoigraphy (can't always see it on ophthalmoscopy)
|
|
what ophthalmoscopic findings would make you suspicious that AMD is turing into the wet form (4)
|
any elevation (detatchment), exudates (blood vessel leakage), ANY hemorrhage in the absence of diabetes/HTN, grey-green membrane -note any change in their vision (VA or other) would be highly suspicious because many CNVs can not be seen on ophthalmoscopy -educate dry AMD pts to come in if they notice ANY changes in their vision
|
|
what is the best way to see slight elevations associated with the development of wet AMD
|
contact fundus lens in the center of your gonio lens
|
|
what is the MOST important factor in preventiing vision loss from AMD that is progressing from the dry to the wet form
|
early detection; you need to educate dry AMD pts to come in if they see ANY changes in their vision
|
|
if you see hard exudates in a pt with AMD what does this tell you
|
there is likely choroidal neovascularization (exudates are lipids excreated by damaged blood vessels) (hard exudates are not drusen)
|
|
what is preferential hyperacuity perimetry (PHP)
|
central visual field test that is specifically designed to monitor progression of AMD from the dry to the wet form
|
|
name the three types of choroidal neovascular membranes seen on flourescene angiography
|
classic, minimally classic, and occult CNVM
|
|
what is a classic choroidal neovascular membrane
|
well defined membrane with distinct borders
|
|
what percent of patients with choriodal neovascular membrane have the classic type of membrane
|
13%
|
|
what is an occult choroidal neovascular membrane
|
poorly defined boarders
|
|
what is a minimally classic choroidal neovascular membrane
|
has parts that appear classic and parts that appear occult
|
|
what does a detachment of the RPE look like
|
sharply circumscribed, dome-shaped elevation at the posterior pole of varying size. sub-RPE fluid may be clear or turbid
|
|
name 5 consequences that can result if choroidal neovascularization is left untreated
|
1) hemorrhagic RPE detachment 2) hemorrhagic sensory retina detachment 3) vitreous hemorrhage (blood breaks through sensory retina) 4) disciform scarring (subretinal scarring) 5) massive exudation
|
|
New lecture: 9 AMD Tx DE 10 Vault
|
a
|
|
what are the three catagories of therapies currently available to treat wet AMD
|
laser photocoagulation photodynamic therapy vascular endothelial growth factors (VEGF)
|
|
what is the goal of photocoagulation therapy for wet AMD
|
prevent further deterioration
|
|
what test needs to be done before a surgen can perform photocoagulation therapy
|
flourescene angiography (not more than 72 hours old to localize CNV)
|
|
how does the final VA after photocoagulation for wet AMD relate to the proximity of the choroidal neovacularization (CNV) to the macula
|
the closer to the macula the worse the final visual acuity (VA).
|
|
Photocoagulation therapy for wet AMD: there is likely to be reduced VA following the surgery, but the goal is to prevent future vision loss. the improvement of final VA with photocoagulation therapy over non-treatment depends quite a bit on the location and size of the CNV; in some cases there can be little or no benefit. Recurrence of CNV is fairly common as well.
|
|
|
what is the name of the drug used in photodynamic threapy
|
verteporfin (visudyne)
|
|
describe the process of photodynamic therapy
|
IV injection of verteportin, which targets new leaky blood vessels. then they use a laser directed at verteporfin, which destroys new blood vessels.
|
|
what type of CNV is photodynamic therapy FDA approved to treat
|
classic CNV
|
|
what is the VA loss at 2 years with and without photodynamic therapy following treatment of wet AMD
|
-2.3 lines with therapy; -4.5 lines without therapy. (TAP study) -reduces vision loss by about half
|
|
name two side effect associated with photodynamic therapy
|
infusion pain and photosensativity
|
|
how much does photodynamic therapy cost
|
about $3,000 per treatment. 5-6 treatments in the first 2 years often needed to stop leakage.
|
|
what is anti-VEGF (vascular endothelial growth factor) therapy
|
VEGF is a hormone that stimulates growth of new blood vessels. anti-VEGF inhibits this hormone.
|
|
what are the names of the three anti-VEGF drugs used for treatment of wet AMD
|
1) macugen 2) lucentis 3) avastin (not currently FDA approved for the eye)
|
|
Second dummy question
|
Second dummy answer
|
|
what type of CNV is macugen approved for
|
all types
|
|
about how often do you have injections of macugen to treat wet AMD
|
every 6 weeks (no recommended long term duration)
|
|
are there any known systemic side effect to macugen
|
none
|
|
are there any ocular complications associated with macugen instillation
|
enophthalmitis, traumatic cataracts, RD (all less than 1.5%)
|
|
does macugen slow progression of vision loss associated with wet-AMD or improve vision
|
only delays progression of vision loss
|
|
how much does treatment with macugen cost
|
$1,500 per injection. injections every 6 weeks
|
|
how often is Lucentis injected
|
every 4 weeks
|
|
does treatment of wet-AMD cause a slowing of vision loss or an improvement in vision
|
pts can actually have vision improvements!
|
|
how much does it cost per year for pts to be on lucentis
|
$2,000 per injection, one injection per month. $24,000 per year.
|
|
are there any systemic side effects associated with lucentis
|
cerebrovascular accident (stroke), BUT it was not statistically significant.
|
|
what is avastin FDA approved for
|
treatment of colon cancer; used off label for AMD
|
|
how much does avastin cost
|
$60 per injection; injections every 1 month. same company makes lucentis and avastin, so they don't want to do the studies to aprove avastin for tx of AMD because it is way less expensive.
|
|
New lecture: 10 Macular Post Pole 2010
|
a
|
|
what is central serous retinopathy (central serous chorioretinopathy, central serous choroidopathy)
|
small break in the RPE leads to a serous retinal detachment under the macula
|
|
what causes central serous retinopathy
|
idiopathic (unknown)
|
|
what age and demographic do you expect to see central serous retinopathy in
|
males between the ages of 20 and 45; type A personality (dealing with stress)
|
|
describe the visual changes you expect to see with central serous retinopathy
|
1. fairly sudden onset of blurred vision in one eye (modestly reduced) 2. relative scotoma 3. metamorphopsia 4. micropsia (because cones are spread out)
|
|
what type of refractive change would you expect to see with central serous retinopathy
|
often correctable to 20/20 with a weak plus lens (because swelling shortens axial length)
|
|
what is the best way to see central serous retinopathy
|
often won't be able to see with direct scope or high plus, but can see with fundus photography. may also be able to see with BIO. this is because you are getting a larger field of view and you can see the subtle edges more easily when you can see the entire lesion. -also, you may be able to better see the lesion with your red-free filter
|
|
what type of filter is really good to see macular problems with
|
red-free
|
|
OCT image of central serous retinopathy
|
|
|
describe the sequence of patterns you see on FA with central serous retinopathy
|
1. early dot 2. smoke stack 3. umbrella or mushroom smoke stack - mushroom is diagnostic for central serous (but is possible it will not have these)
|
|
describe the prognosis and long-term outcomes of central serous retinopathy (2)
|
1. 80-90% have spontaneous resolution in 1-6 months 2. mild metamorphopsia that may remain much longer (1 or more years)
|
|
what are the chances of reoccurance with central serous retinopathy
|
40% develop recurrent attacks
|
|
name three comorbidities that may present with central serous retinopathy
|
RPE atrophy, cystoid maculopathy, or choroidal nerovascularization
|
|
describe the treatment associated with central serous retinopathy
|
no treatment required. laser treatment done in rare cases. triamcinalone and anti-VEGF being explored.
|
|
what gender and age range are macular holes more frequently found
|
women 3:1 -older 60-80
|
|
what type of vision do you expect to result from a macular hole
|
20/200 to 20/400
|
|
describe the common mechanism for macular holes
|
posterior hyaloid is often attached to the macula. as vitreous ages it becomes more liquid and the posterior hyaloid moves forward. this creates traction on the macula and can pull a piece free
|
|
what is the piece of macula pulled free in a macular hole called
|
operculum
|
|
what material is often present on the retina at the site of a macular hole
|
drusen (yellow lipid deposits)
|
|
what is the Watzke-Allen test
|
test for macular hole -narrow slit lamp beam. move the beam back and forth over the pts macula as you look at it with high plus. ask the pt if they see the beam split into two and then come back together or become distorted in the middle. if they see a distortion in the beam, that means there's a potential emminant macular hole or that there's macular changes. if they see the beam split into two, that means that there if a full thinkness hole.
|
|
desccribe the stages of macular hole
|
1. premacular hole (impending hole): foveal detachment absent surface of retina and surface of vitreous make an X because vitrious is pulling on retina. more of a cyst. 2. there is a tear in the retina, but it is not completely detached 3. full thickness hole, operculum present 4. full thickness hole with vitreal detachment (presence of Weis ring)
|
|
what is the treatment for macular holes
|
stage one holes: no treatment; spontaneous hole closure can occur full-thickness holes: vitrectomy, membrane peel, gas injection (only if less than 1.5 years)
|
|
what are they doing to the retina when they do a vitrectomy, membrane peel and gas injection for treatment of a retinal hole? what kind of VA do you expect after treatment? how old can the hole be?
|
they are not able to reattach the operculum. they simply pull the edges of the macular hole together and seal them there. -20/50 or 20/60 acuity post surgery (an improvement from 20/200) -holes need to be less than 1 to 1.5 years
|
|
if they do a gas bubble treatment for a macular hole how long does the pts have to sit with there head facing down
|
couple weeks
|
|
beyond what refractive error is there in increased risk of developing retinal detachment
|
6 D myopia
|
|
1 mm of axial length corresponds to how many doipters of refractive error
|
3 D
|
|
what is myopic degeneration
|
in high myopia the retina and the choroid can atrophy around the edge of the disc.
|
|
what are fuch's spots
|
a round or elliptical, pigmented spot, usually located in the macular or paramacular area. it occurs in patients who have pathological myopia. it is due to lacquer cracks (breaks in bruch's membrane) and to the development of a choroidal neovascular membrane followed my subretinal hemorrhage which has changed color and has become pigmented. pt may notice photopsia, but eventually causes a loss of vision with central scotoma.
|
|
what is a posterior staphyloma
|
posterior bulging of the retina usually due to high myopia
|
|
name 7 clinically observable retinal findings associated with high myopia
|
myopic crescent, fuch's spot, lacquer cracks, posterior staphyloma, chorioretinal atrophy, subretinal hemorrhage (leads to fuch's spot), retinal detachment
|
|
how often should you have high myopes RTC
|
every 1 year to look for changes.
|
|
if you have a high myope, put like a diopter less than you got on the refraction in a trial frame and see if they can still get 20/20; because high myopes like to suck up minus in the phoropter
|
|
|
what are angioid streaks
|
degeneration of bruch's membrane of the choroid characterized by brown or reeeish lines or streaks in the fundus of the eye.
|
|
are angioid streaks usually unilateral or bilateral
|
bilateral
|
|
angioid streaks are very gragile and are liable to rupture in cases of ocular trauma
|
|
|
what is the etiology of angioid streaks
|
idiopathic or associated with disease (50%): Pseudoxanthoma elasticum Paget’s disease Sickle cell disease Thalassemia Ehlers-Danlos Syndrome Optic disc drusen Retinitis pigmentosa
|
|
name two ways that angioid streaks can affect vision
|
decreased VA, metamorphopsia (if choroidal neovascularization)
|
|
describe the management of angioid streaks (3 steps)
|
1. treat any neovascularization (similar to AMD) 2. treat any underlyaing medical conditions 3. Rx polycarbonate (because of how fragile the retina is)
|
|
what is cystoid macular edema
|
edema and cyst formation of the macuylar area of the retina.
|
|
in what layer of the retina does cystoid macular edema develop
|
Henle's fiber layer of the macula
|
|
what is clinically significant macular edema
|
asked Dr. Y
|
|
name two ways that cystoid macular edema could impact vision
|
blurred vision, metamorphopsia
|
|
describe the pattern that tends to form on flourescene angiography in cases of cystoid macular edema
|
Radial arrangement of fibers in Henle’s fiber layer causes dye to take on a flower-petal pattern (petalloid)
|
|
describe the treatment of cystoid macular edema
|
Topical nonsteroidal anti-inflammatory drops (Voltaren or Acular qid) and/or topical steroid drops (prednisolone acetate 1% qid) for 1 month and then taper slowly If no response consider oral NSAIDS (indomethacin) or oral steroid (prednisone) and/or oral acetazolamide (Diamox) If no response, consider sub-Tenon’s steroid injection (triamcinolone) If vitreous is present to the wound and vision is < 20/80, consider YAG laser vitreolysis or perform vitrectomy
|
|
what is another name for macular pucker
|
epiretinal membrane
|
|
what is an epiretinal membrane
|
cellular proliferation along the internal limiting membrane. contraction of the membrane causes retinal surface to become wrinkled.
|
|
what is the most common cause of epiretinal membrane
|
idiopathic
|
|
name four ways epiretinal membranes can affect vision
|
could be asymptomatic -decreased VA, metamorphopsia, macropsia, monocular diplopia
|
|
describe the treatment of epiretinal membrane
|
Treatment rarely required Vitrectomy and membrane peel in patients with reduced acuity (< 20/60) or intractable symptoms Prognosis Good; 75% of patients have improvement in symptoms and acuity after surgery
|
|
what conditions is chloroquine used to treat
|
malaria, rheumatoid arthritis and systemic lupus erythematosus
|
|
what pattern do you tend to see on the retina with toxicity due to chloroquine use
|
bull's eye maculopathy
|
|
what types of conditions is thioridazine used to treat
|
psychotic conditions
|
|
what types of retinal signs do you tend to see from thioridazine toxicity
|
pigment granularity; usually midperipheral first, then progresses
|
|
what is talc
|
used to dilute drugs used by IV drug abusers
|
|
what type of retinal signs do you tend to see from talc retinopathy
|
refractile yellow deposits near or in retinal arterioles
|
|
at what level in the retina are talc deposits located
|
very anterior, they are on top of the blood vessels
|
|
what is the most concerning cause of choroidal folds
|
Causes Idiopathic Hyperopia Choroidal tumor or detachment CNM Optic disc swelling Orbital tumors ((most concerning cause!) Hypotony Orbital and scleral inflammation
|
|
what causes choroidal folds
|
flattening of the psterior pole
|
|
name two visual symptoms pts might have from choroidal folds
|
blurry vision, metamorphopsia
|
|
describe the appearence of choroidal folds
|
alternating dark and light yellowish streaks
|
|
describe the management of choroidal folds
|
need to determine cause (rule out tumor etc). usually idiopathic, diagnosis of exclusion.
|
|
New lecture: 11-a Retinal Vascular Disease Intro 2010
|
a
|
|
name 5 types of hemorrhages you can see behind the iris
|
Pre-retinal (boat shaped), flame shaped, dot/blot, subretinal/subpigment epithelial, vitreous
|
|
what structure ruptures in a pre-retinal hemorrhage
|
internal limiting membrane
|
|
how does a pre-retinal hemorrhage affect vision
|
creates scotomas
|
|
does a pre-retinal hemorrhage move pt movement
|
moves with gravity
|
|
how does the apperance of a pre-retinal hemorrhage change as it is being absorbed
|
change to red to yellow to white
|
|
from which capillary bed do flame shaped hemorrhages occur
|
superifical capilary bed
|
|
in what level of the retina do dot/blot hemorrhages occur
|
Inner nuclear layer, outer plexiform layer (deep capilary bed)
|
|
what is the cause of sub-retinal/sub-pigment epithelial hemorrhages
|
secondary to choroidal neovascular membranes. can be from deep retinal hemorrhages.
|
|
how does the color of a sub-retinal and a sub-pigment epithelial hemorrage compare
|
subretinal: dark red sub RPE: grey green
|
|
how does a vitreous hemorrhage affect your ability to see the retina
|
will blur view of post. pole near the heme
|
|
what are the two forms of vitreous hemorrhage
|
retrovitreous and intravitreous
|
|
name two causes of vitreous hemorrhage
|
secondary to rupture of neovascular net, or development of a retinal tear associated with a vitreous detachment
|
|
what must precede hard exudates
|
edema
|
|
in what part of the retina do you expect to find cotton wool spots (CWSs)
|
usually within 3 DD of the ONH
|
|
how do you determine if tortuosity is congenital based on symmetry
|
congenital: involves all quadrents (symmetrical OU) acquired: sectoral involvement (also, previously documented as normal)
|
|
what is the difference between collateral and shunt vessels
|
Collaterals: new vessels that give A-A or V-V communications, making up for a compromised or obstructed vessel
|
|
what is intraretinal microvascular abnormalities (IRMA)
|
looks like neo, but doesn't leak with FA. eventually develops into neo.
|
|
why do you have hypofluorescence at the macula on FA
|
because RPE is dense
|
|
what are the three phases of FA and at what time intervals do they occur
|
choroidal flush (within seconds of injection) arterial-venous phase (6-8 seconds) late phase (5-10 min.)
|
|
Pharmacokinetics of penicillins
|
Most are eliminated via active tubular secretion except Nafcillin . Ampicillin undergoes enterohepatic circulation but is excreted by the kidney. Benzathine penicillin G repository form (t1/2: 2 weeks)
|
|
New lecture: 11 Retinal Vascular Disease 2010 (study this one)
|
a
|
|
what are the two most common retinal vascular disease seen
|
1. diabetic retinopathy 2. branch retinal vein occlusion (BRVO)
|
|
is BRVO usually unilateral or bilateral
|
95% unilateral
|
|
name and describe the three categories of BRVO
|
Major = involves 5+ DD of retina Primary = involves 2-5 DD of retina Secondary = involves <2 DD of retina
|
|
is BRVO associated with any other disorders
|
Strong association with systemic disease
|
|
why is glaucoma assciated with a risk of BRVO
|
because the high IOP puts extra pressure on the all ready thin walled vein. this is why anti-glaucoma meds are part of the tx for BRVO.
|
|
describe the VA loss associated with BRVO
|
sudden, unilateral, painless VA loss over a period of 24-48 hours. some describe it as blur.
|
|
why is metamorphopsia associated with BRVO
|
because it can cause macular edema
|
|
name 6 clinically observable retinal signs associated with BRVO
|
1. dilated tortuous veins 2, 3. retinal hemes and CWSs in a wedge shape radiating from an A-V crossing 4. macular edema 5. lipid infiltrates near occlusion site (hard exudates) 6. collaterals
|
|
why do BRVO tend to occur in an superotemporal A-V crossing
|
because there are more A-V crossings in that quadrant
|
|
how does the location of a BRVO affect the changes of developing macular edema and why
|
there is a higher chance of developing macular edema if it is superotemporal. because gravity causes the fluid to move toward the macula if it is in this quadrant
|
|
what is Bonnet's sign
|
a prodromal sign indicating there may be a BRVO in the future. it is a small splinter hemorrhage at an A-V (artery-vein) crossing
|
|
what is the difference between an ischemic and a non-ischemic BRVO
|
Non-ischemic (perfused, < 5 DD) or ischemic (nonperfused, > 5DD)
|
|
what is a retinal finding that indicates that there has been edema in that area of the retina in the past
|
hard exudates indicates there has been edema
|
|
name five complications associated with BRVO
|
chronic macular edema, neovascularization, vitreous hemorrhage (from rupture of neovascular net), neovascular glaucoma, retinal detachment
|
|
how does BRVO lead to retinal detachment
|
neovascularization: new blood vessels have glial tissue associated with them. glial tissue is fibrotic. as it grows together, fibrosis can cause traction on the retina.
|
|
why do you need to do gonioscopy on a pt with a BRVO
|
because BRVO can cause neovascularization, which can lead to neovascularization of the angle and neovascular glaucoma
|
|
management of BRVO
|
often will resolve on its own. need to determine underlying cause.
|
|
is CRVO (central retinal vein occlusion) usually unilateral or bilateral
|
unually unilateral
|
|
what can cause CRVO in younger pts (under 50)
|
estrogen-containing preparations (birth control pills)
|
|
what is the most common cause of CRVO in pts over 50 years old
|
HTN (hypertension) about 60%
|
|
is glaucoma associated with CRVO
|
yes
|
|
describe the VA loss associated with CRVO
|
sudden, unilateral, painless vision loss
|
|
what could cause the pt pain 90 days after a CRVO or BRVO
|
neovascularization that causes neovascular glaucoma (3 month glaucoma)
|
|
what happens to the foveal light reflex (FLR) if there is macular edema
|
FLR will dissapear. if you think you see macular edema and there is a FLR, you are not seeing macular edema. -compare it to the macular in the other eye if you are not sure
|
|
name 5 clinically observable retinal signs associated with CRVO
|
1. diffuse retinal hemorrhages in ALL quadrants (BRVO usually only one) 2. cotton wool spots (CWSs) 3. swollen optic nerve head 4. neo of the disc, retina, or iris 5. macular edema -possible APE
|
|
what condition is associated with the "blood and thunder" appearence of the retina
|
CRVO
|
|
how do you differentiate between diabetic retinopathy and CRVO
|
history; there appearence may look very similar. CRVO will be sudden, painless, unilateral vision loss.
|
|
|
|
|
what is the difference between ischemic and non-ischemic CRVO and what kind of VA do you have with each type
|
non-ischemic: an incomplete CRVO. retina doesn't look as bad. VAs 20/20-20/200 depending on macular edema. ischemic: complete CRVO (total blockage). extensive retinal hemorrhaging. VAs 20/400 to light perception.
|
|
describe the prognosis for ischemic and non-ischemic CRVO
|
non-ischemic is fair. ischemic is poor regardless of tx.
|
|
how often does neovascularization occur in CRVO
|
20% of all CRVO and 60% of the ischemic type -high risk of developing neovascular glaucoma
|
|
if you see neovascularization on the iris where else should you expect neovascularization
|
on the retina
|
|
what is the main cause of branch retinal artery occlusion (BRAO)
|
embolism
|
|
name for materials that can cause an embolism
|
1. cholesterol (hollenhorst plaque) 2. calcifications 3. platelet-fibrin (arterosclerosis) 4. septic (bacterial endocarditis)
|
|
what is a septic embolism
|
A septic embolism is a type of embolism that is infected with bacteria, resulting in the formation of pus. These may become dangerous if dislodged from their original location
|
|
is CRAO usually unilateral or bilateral
|
usually unilateral
|
|
which is more common, CRAO or BRAO? how about CRVO or BRVO?
|
CRAO is more common than BRAO BRVO is more common then CRVO
|
|
describe the vision loss associated with BRAO
|
sudden, unilateral, painless loss of part of the visual field
|
|
name 4 clinically observable retinal signs associated with BRAO
|
1. focal or wedge shaped area of retinal whitening 2. narrowing of arteries 3. possible cotton wool spots 4. may see emboli
|
|
what quadrant is most likely to be affected by a BRAO
|
superotemporal
|
|
what is a hollenhorst plaque
|
orange-yellow spots, usually found at branching sites of retinal arterioles. they are due to necrosis and ulceration of atheromatous, cholesterin-containing emboli in the carotid arteries which discharge into the circulation
|
|
describe the management of BRAO
|
tx is controversial because there is a really good prognosis if it is a BRAO. the problem is that it is hard to tell if it is branch or central arterty occlusion, so you have to tx as if it were the worse of the two (CRAO) to be safe. 1. digital massage (to move emboli from blockage site) 2. paracentesis (only if you think it is CRAO) 3. anti-glaucoma meds
|
|
describe the prognosis for BRAO
|
good. 90% reach 20/40.
|
|
describe the prognosis for central retinal artery occlusion (CRAO)
|
most have severe perminate vision loss (counting fingers to light perception) -life expectancy is decreased as well after a CRAO
|
|
the reason we treat BRAO so agressively is because we are usually not sure if it is branch or central artery occlusion and CRAO is so severe.
|
|
|
name 6 clinically observable retinal findings associated with CRAO
|
1. narrowing of the arteries 2. superficial whitening of the post. pole 3. cherry red spot of the macula 4. APD 5. Boxcarring of veins 6. neovascularization
|
|
describe the tx of CRAO
|
1. digital massage 2. paracentesis is an option 3. carbonic anhydrase inhibitors PO 4. topical beta blockers 5. consider admission to hospital
|
|
how often do you have the pts back for follow-ups and what are you looking for
|
Q1-4 weeks, looking for neovascularization
|
|
describe the overall health prognosis associated with CRAO
|
poor; CRAO is caused by systemic vasculopathy
|
|
what are the ranges of blood pressure for normal, pre-HTN, stange 1 and stage 2 HTN
|
a. Normal
|
|
name 6 observable retinal signs associated with chronic hypertensive retinopathy
|
1. A-V crossing changes (A-V nicking) 2. narrowing of arterioles (tortuous veins) 3. arteriosclerosis (copper/silver wiring) 4. cotton wool spots (CWSs) 5. flame hemorrhages 6. macroaneurysms
|
|
name 5 clinically observable retinal signs associated with acute hypertensive retinopathy
|
1. exudates (macular star configuration) 2. retinal edema 3. CWSs 4. flame hemorrhages 5. swelling of the ONH (hallmark)
|
|
what is the "copper wire" and "silver wire" appearance and what does it indicate
|
arteries resemble a copper wire as they become infiltrated with lipid deposits and eventually as silver wire as the deposits increase and the whole thickness of the artery appears as a bright white reflex. -retinal signs of arteriosclerosis
|
|
what other disease do the signs of hypertensive retinopathy look like
|
diabetic retinopathy
|
|
if you see signs of hypertension in just one eye, what should you suspect
|
a problems with one side of the carotid artery
|
|
what are two other terms for venous beading
|
boxcarring, saushaging
|
|
if you see sign of hypertensive retinopathy you need to check blood pressure.
|
|
|
it is important to call the 911 people when you need them. if a pt comes in with chest pains or trouble breathing you need to call 911. -if their blood pressure is too high they could stoke out
|
|
|
describe the prognosis for hypertensive retinopathy
|
usually pretty good
|
|
what systemic condition is retinal vaso-occlusive disease associated with
|
cerebrovascualr disease (stroke)
|
|
which cerebrovascular diseases are most commonly associated with ocular signs (2)
|
1. cerebral thromboembolism 2. cerebral embolism
|
|
name three symptoms associated with TIA
|
1. sudden numbness or weakness of face, arm, or leg on one side of the body 2. temporary loss of speech 3. temporary dimness or loss of vision in only one eye (amaurosis fugax)
|
|
describe the systemic prognosis associated with ocular ischemic syndrome (OIS)
|
poor, due to underlying etiology (40% will be dead within 5 years)
|
|
what is the cause of OIS
|
usually carotid artery disease (stenosis of 90% or more). other causes: HTN, diabetes, giant cell arteritis
|
|
is ocular ischemic syndrome usually in men or women? is it usually unilateral or bilateral
|
usually in men, usually unilateral
|
|
what symptom does OIS have that most other DDXs don't have that can help you diagnose (4)
|
-pain in 40%. most other differential diagnosis are painless. -uveitis that makes its first presentation in old age -mid-peripheral hemorrhages -unilateral
|
|
name 7 signs and symptoms associated with ocular ischemic syndrome
|
1. mild loss of vision (20/20 to light perception) 2. pain 40% 3. TIA up to 90% 4. red eye 5. mid-peripheral hemorrhages (good diagnostic sign) 6. neovascularization of the iris 66% 7. uveitis (secondary to neo of iris)
|
|
if the pt passes out from gonio do you need to call 911
|
no, just a vasovagal response.
|
|
what are you looking for on follow-up for a pt wil ocular ischemic syndrome
|
neovascularization
|
|
describe the visual prognosis associated with OIS
|
60% will have counting fingers vision on 1 year follow-up
|
|
describe the pathogenesis of retinopathy of prematurity
|
nasal retinal vessels reach the ora at 8 mo. gestation. temporal retinal vessels reach ora after birth. pre-mature infants are put in high oxygen environments, which inhibits the growth of those temporal retinal blood vessels. when they return to a normal oxygen environment it stimulates neovascularization. the neovascularization occurs with a fibrotic framework (fibrotic scaffolding), which can over time contract and case traction on the retina.
|
|
how do you manage retinopathy of prematurity
|
monitor frequently and refer to retina if there is vasoproliferation
|
|
describe the prognosis of retinopathy of prematurity
|
good; spontaneous regression of signs in 80-90%
|
|
New lecture: 12 Diabetic Retinopathy 2010
|
a
|
|
AOA CLINICAL PRACTICE GUIDELINES FOR DIABETES: http://www.aoa.org/documents/CPG-3.pdf -they provide clinical practice guidelines for almost any disease
|
|
|
what percent of diabetic pts are type 1
|
5-10%
|
|
type II diabetes was prevously known as non-insulid dependant diabetis melitus, but many of these pts end up on insulin, so that term is not really used any more. just called type II. -now when the term insulin-dependant is used, it is independant of type, just indicates whether they use insulin or not
|
|
|
what age group in diabetes increasing in
|
children and teens
|
|
what are the fasting and non-fasting numbers for the plasma glucose test that are considered to be indicative of diabetes. what about the oral glucose tolerance test
|
fasting: 126 or higher non-fasting: 200 or higher oral-GTT: 200 or higher
|
|
what is a glucose tolerance test
|
A glucose tolerance test is a medical test in which glucose is given and blood samples taken afterward to determine how quickly it is cleared from the blood
|
|
how is the length of time a person has had diabetes related to their level or diabet retinopathy
|
the longer you have the disease the more likely you are to have diabetic retinopathy and the more severe it will be Type 1: 5 years
|
|
8% of pre-diabetic have diabetic retinopathy. you don't even have to be diagnosed with diabetes to have retinal changes associated witht the disease
|
|
|
what ethnicities have a high prevelance of diabetes
|
african americans 1.7X, hispanic 2.0X, asian/pacific island 2.0X, native americans 2.8X (figures relative to caucasian)
|
|
how can diabetes affect vision (4)?
|
1. color vision defect (tritan) 2. refractive error changes (can be dramatic) 3. accommodative dysfunction 4. visual field defects
|
|
does refractive error tend to become more myopic or hyperopic from diabetes? why?
|
more myopic. the sugar will cause the lens to swell. -remember thought that if the pt is returning to nomal from a diabetic induce refractive error change, that this will be in the opposite direction.
|
|
name three systemic symptoms associated with diabetes
|
polyphagia, polydypsia, polyuria
|
|
name 10 ways that diabetes can affect the eyes (retinal changes only 1)
|
1. diplopia (neuropathies involving 3rd, 4th, or 6th cranial nerve) 2. sluggish pupil reflexes (dilate poorly and slowly; use more dilating drops) 3. conjunctival microaneurysms 4. dry eye (very common) 5. cornea: reduced sensativity (careful of CL wearers), reduced wound-healing ability 6. iris: neovascularization 7. lens: higher prevalence of cataracts 8. vitreous: hemorrhages 9. retinal changes 10. optic nerve: ischemic optic neuropathy, link to glaucoma
|
|
name 6 test outside your normal routine that you might want to do for a diabetic pt
|
1. color vision 2. contrast sensitivity 3. fundus photography 4. gonioscopy 5. macular function 6. blood pressure
|
|
what is NVE (neovascularization elsewhere)
|
neo that is not at the disc or the iris. anywhere else.
|
|
name 9 pertinant negatives you need to check for and record on a diabetic eye exam and their abbreviations
|
1. NVI (neo of the iris) 2. H/MA (hemes/microaneurysms) 3. VB (venous beading) 4. IRMA (intraretinal microvascular abnormalities) 5. NVD (neo of the disc) 6. NVE (neo elsewhere) 7. HE (hard exudates) 8. CWS (cotton wool spots) 9. CSME (clinically significant macular edema)
|
|
describe the pathophysiology for diabet retinopathy
|
vessels become damaged and leak (supporting glial cells (pericytes) are reduced) (capilary walls are weakened and ballon out (microaneursym)). the retina becomes ischemic. vessel proliferation can occur.
|
|
what is the difference between proliferative and non-proliferative diabetic retinopathy
|
proliferative has neovascularization
|
|
can microaneurysms leak
|
yes
|
|
microaneurysms are tiny; you will have a really hard time seeing them. they look like dot hemorrhages; if you can see it clearly, it is probably a dot hemorrhage.
|
|
|
what type of hemorrhage are dot/blot/flame hemorrhages
|
intraretinal hemorrhages
|
|
what do hard exudates indicate
|
that there has been edema in the retin a some point in the past. the are lipids that have excaped from the blood vessels and then macrophages come to engulf them. the leave a demarking border of where the edema has been (like a ring around the bath tub)
|
|
what causes cotton wool spots
|
hypoxia
|
|
where in the retina do you tend to see cotton wool spots in diabetic retinopathy
|
within 3 DD of the ONH -usually not on the retina
|
|
what IRMA
|
intraretinal microvascular abnormalities. collateral route of circulation. form where there is hypoxia.
|
|
can IRMA turn into neovascularization
|
yes; it is a germination bed for neovascularization elsewhere.
|
|
what is the best way to look for venous beading on ophthalmoscopy
|
pick a major vessel and follow it out from the disc as far as you can. -flourescene in a really good way to see it.
|
|
what is venous beading
|
areas of vascular sludging or slowing of blook. look like beads.
|
|
diabetic retinopathy grading: http://eyephoto.ophth.wisc.edu/ResearchAreas/Diabetes/DiabStds.htm
|
|
|
how do you define minimal NPDR (non-prolifative diabetic retinopathy)
|
rare microaneuuysm
|
|
how do you define mild NPDR
|
at least one microaneurysm and one of the following: retinal hemorrhage or hard exudate.
|
|
describe the management of mild NPDR
|
1. monitor with Amsler grid 2. RTC 6-12 months 3. report findings to PCP/diabetologist
|
|
what are the chances that a person with mild NPDR will develop proliferative diabetic retinopathy (PDR) within one year
|
5%
|
|
how do you define moderate NPDR
|
(heme or microaneurysm > standard photo) OR (soft exudates, venous beading or IRMA)
|
|
describe the management of moderate NPDR (4)
|
1. monitor with Amsler grid 2. report findings to PCP/diabetologist 3. RTC 3-6 months 4. retinal consult if IRMA
|
|
what are the chances that a pt with moderate NPDR will develop PDR within 1 year
|
12-27%
|
|
how do you define severe NPDR
|
-4-2-1 rule: any of the following -heme/microcaneurysm > standard photo in all FOUR quadrants -venous beading definately present in at least TWO quadrants -IRMA > standard photo in at least ONE quadrant
|
|
describe the management for severe NPDR (3)
|
1. retinal consult for FA 2. report findings to PCP/diabetologist 3. RTC 3 months
|
|
what are the chances that a pt with severe NPDR will develop PDR within 1 year
|
52%
|
|
how close to the disc is NVD (neo of the disc)
|
right at the disc, or with-in 1-2 DD
|
|
what is NVE and where does it come from
|
neo elsewhere (not the iris or the disc). usually along the major arcades, come from IRMA.
|
|
why is fibrous proliferation an indication of proliferative diabetic retinopathy
|
neovascular blood vessels are accompanied by a fibrotic membrane. this is an attempt of the glial cells to provide a supportive network for the neovascular blood vessels.
|
|
why is diabetic retinopathy associated with retina detachment
|
because the fibrotic proliferation by the glial cells that acompany neovascularization, to provide a supportive network, can contract and cause traction on the retina.
|
|
in what stages of diabetic retinopathy do you find clinically significant macular edema (CSME)
|
any stage
|
|
what is the difference between diabetic macular edema (DME) and clinically significant macular edema (CSME)
|
DME: within 1 DD of the macula CSMD: threatens or involves the macula
|
|
what ways can you tell clinically that there is macular edema
|
there will be a loss of foveal light reflex (FLR). also, the macula will look darker than usual. -hard exudates less than 500 microns, or 1/3 DD from the center of the macula (hard exudates are diognostic)
|
|
edema shows up really well on OCT. hemorrhages and microaneurysms are hard to see with OCT though.
|
|
|
which form of diabetic retinopathy is pan-retinal photocoagulation most helpful for
|
proliferative diabetic retinopathy
|
|
does controling you blood glucose levels reduce your chances of developing diebetic retinopathy
|
yes; diabetes control and complications trial (DCCT) clearly showed that control of blood glucose levels substantially decreased the risk of DR onset in type 1 pts and can slow the progression of DR in those who have alread developed it. (UKPDS study showed the same for type 2)
|
|
how soon do you need to refer pts with diabetic retinopathy
|
Refer within 2-4 weeks Macular edema PDR or very severe NPDR Refer within 24-48 hours High risk PDR Vitreous heme
|
|
do intravitreal injections of steroids help with the symptoms from diabetic retinopathy
|
the literature suggests that it does
|
|
New lecture: 13 Vitreous and Peripheral Retina 2010 (study this one)
|
a
|
|
where does a posterior vitreous detatchment (PVD) usually occur
|
around the optic disc (weiss ring)
|
|
what is the difference betwee vitreous liquefaction and syneresis
|
liquefaction is the collapse of the mollecular framework resulting in decreased viscosity. syneresis is the shrinkage and inward collapse of the vitreous
|
|
what are lacunae
|
little pocket of fluid that you can see in the vitreous. they can enlarge and coalesce
|
|
you need to look at the vitreous with the slit lamp when the eye is dilated. look to the side of the light rather than directly where the light is shining. the contact fundus lens is really good to see the vitreous attachment with the retina
|
Third dummy answer
|
|
is asteroid hyalosis usually unilateral or bilateral
|
90% unilateral
|
|
is there an associate between asteroid hyalosis and any systemic conditions
|
yes. diabetes, HTN, vascular disease
|
|
what is synchysis scintillans
|
a very rare condition of freely floating crystals of cholesterol in the vitreous. it is associated with severe eye disease.
|
|
name 4 things you might see in the vitreous
|
1. asteroid hyalosis 2. synchysis scintillans 3. non-pigmented (white) cells (inflammatory) 4. pigmented cells (red-brown) (Shaffer'sign)
|
|
what is shafer's sign
|
red-brown pigmented cell that can be observable in the vitreous. can indicate retinal tear or detachment
|
|
name a pertinant negative for a retinal detachment suspect
|
Shafer's sign
|
|
name three subjective symptoms associated with posterior vitreal detachment (PVD)
|
1. sudden onset of floaters 2. photopsia 3. metamorphopsia
|
|
is a vitrectomy typically done for pts with PVD? why or why not?
|
no, because of the possibility of retinal detachment
|
|
why does an epiretinal membrane form from posterior vitreal detachment
|
because, as the vitreous detaches from the retina, it can cause a small tear. glial cells on the internal limiting membrane can proliferate to repair the tear. they can then contract causing the epiretinal membrane
|
|
what percent of the time do you tend to see epiretinal membrane form after a PVD
|
75%
|
|
name 4 clinically observable signs associated with PVD
|
1. weiss ring 2. possible hemorrhage 3. epiretinal membrane 4. macular edema or hole
|
|
what might you observe on high plus that would make you suspect epiretinal membrane
|
if you see retinal sheen or foveal light reflex on an older patient that you would no longer expect to see one.
|
|
what is the tx for epiretinal membrane
|
epiretinal membrane peel -has to be severe enough to make the surgery worth the risk.
|
|
what are the kinds of vitreous detachments
|
a)
|
|
how do you tell clinically if there is collapse of the vitreous
|
you look in the slit lamp for the floating white strands in the vitreous that move up and down through the entire extent of the pupil. if there is a collapse of the vitreous you wil not see these strands in the superior part of the pupil
|
|
what percent of pts with PVD will have an associated retinal tear
|
10-15%
|
|
what proceedure do you need to do on pts with a PVD
|
BIO w/ scleral depression.
|
|
what is it called when the primary vitreous fails to regress completely
|
Persistent hyperplastic primary vitreous (PHPV)
|
|
New lecture: 14 PeripheralretinaST2010
|
a
|
|
can scleral indentation cause a retinal detachment
|
no, rubbing your eyes puts more pressure on the globe than scleral indentation. there is a very minimal risk of RD; the greater risk is of you causing a corneal abrasion.
|
|
scleral indentation with BIO is usually binocular. if you do it with a 3 mirror lens this will give you your best view and will allow you to see binocularly
|
Second dummy answer
|
|
what part of the retina is considered to be the peripheral retina
|
between the equator and the ora
|
|
how can you tell where the equator is on BIO
|
the vortex veins are pretty much mark the equator
|
|
what part of the retina do you find the short ciliary nerves
|
superior and inferior. somewhere between 10 and 2 and corresponding inferior positions. -used to deliniate nasal and temporal retina
|
|
what part of the retina do you find the long ciliary nerves
|
along the horizontal meridian (at about 3 and 9 o'clock) -they can be used to deliniate superior and inferior retina
|
|
how does the appearence of the ora differ between nasal and temporal sides
|
nasal ora is more notched. temporal ora is more smooth.
|
|
what is a common name for a vertex vein
|
mop (because it looks like a string mop)
|
|
what is common to see around vortex veins and why does this occur? is this of concern?
|
pigment. during development as the vortex vein gets pushed through the layers of the retina it brings some RPE cells with it. it is of no concern what so ever to see pigment around a vortex vein -also commonly seen around short ciliary nerves
|
|
what do we think is the mechanism for white without pressure
|
retinal sheen caused by the interface between the retina and the vitreous causes reflectinos.
|
|
what is this
|
ciliary nerve
|
|
what is the pigmented patch between 2 and 5 o'clock
|
ora serrota
|
|
how can you tell if you are seeing ora during BIO
|
(it is common to mistake a shadow from the iris as ora). the blood vessels start to change course and start to run parallel to the ora as you reach the ora
|
|
how can you tell if something on the retina is a hole
|
retinal holes are always red
|
|
how can you tell the difference between an enclosed oral bay and a retinal hole
|
both can appear red. when you do scleral indentation an oral bay will be attached to the retina, and a hole will not be fixed down (flap)
|
|
describe the appearence of the vitreous base if you are able to see it on BIO
|
it will either be very light or very dark. light because of a sheen causing reflections, dark if vitreous is tugging on the retina (which causes RPE hyperplasia)
|
|
what can cause RPE hyperplasia
|
anytime the vitreous is tugging on the retina
|
|
what is cystoid degeneration
|
Tiny bubble appearance next to ora beneath vitreous base Salt and pepper appearance at ora
|
|
what is cystoid degeneration of the peripheral retina difficult to distinguish with
|
whit without pressure
|
|
what is the difference between white with and without pressure
|
without pressure means appearence is there without scleral indentation. with pressure means that it appears when you do scleral indentation.
|