Ocular Disease I, Ii & Iii

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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

Front 5

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.

Front 6

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

Front 9

what does arcus look like

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1-2 mm white band in the mid-periphery of the cornea

Front 10

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.)

Front 11

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.

Front 12

describe the progression of arcus

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usually start inferior and superior and fills in 360 degrees.

Front 13

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

Front 15

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

Front 16

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

Front 17

describe the management of limbal girdle of vogt

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none tx necessary. tx for band keratopathy if present.

Front 18

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

Front 20

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

Front 22

describe the management of dellen

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lubrication, theraputic SCL

Front 23

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.

Front 28

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

Front 30

how does the area of corneal steepening compare in pellucid marginal degeneration and keratoconus

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pellucid: inferior keratoconus: central

Front 31

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

Front 40

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

Front 46

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

Front 57

what causes posterior crocodile shagreen

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changes in the appearence of descemet's that forms the lines in this condition

Front 58

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)

Front 61

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

Front 73

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

Front 79

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)

Front 88

why is kruckenberg's spindle verticle

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because of the convection current of the aqueous.

Front 89

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.

Front 90

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

Front 95

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

Front 96

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.

Front 97

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

Front 103

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.

Front 104

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

Front 118

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

Front 119

what layer of the cornea does a kaiser-fleischer ring occur

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posterior surface

Front 120

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

Front 128

is iridocorneal endothelial symdrome (ICE syndrome) usually unilateral or bilateral

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unilateral

Front 129

is iridocorneal endothelial syndrome more common in males or females

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females

Front 130

what are the three condition that make up the iridocorneal endothelial syndrome

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Chandler syndrome Cogan-Reese syndrome Progressive Iris Atrophy

Front 131

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

Front 132

New lecture: 3 Opt 631 - Corneal Dysgen Ant Stromal Dyst Cone 2009

Front 133

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

Front 138

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

Front 141

what quadrant does an iris coloboma usually occur

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inferior or inferionasal

Front 142

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

Front 144

are there any conditions that can occur secondary to microcornea

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risk of glaucoma due to AC crowding

Front 145

what type of refractive error is most commonly associated with microcornea

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hyperopia because cornea is flatter than usual

Front 146

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

Front 152

what type of refractive error is associated with megalocornea

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myopia

Front 153

what do you need to DDX with megalocornea

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congenital glaucoma

Front 154

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.

Front 156

how common is keratoglobus

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extremely rare. both Pat and Dr. Yudkovitch have only seen one in their career.

Front 157

is keratoblobus unilateral or bilateral

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bilateral

Front 158

what condition is this

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posterior keratoconus

Front 159

what is posterior keratoconus

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thinning of the cornea on the back surface only

Front 160

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

Front 161

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

Front 163

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.

Front 164

are there any other ocular conditions associated with peter's anamoly

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Possible anterior segment abnormalities: microcornea, microphthalmos, coloboma, iris dysgenesis

Front 165

name the three anterior chamber cleavage syndromes

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Posterior Embryotoxon Axenfeld’s Anomaly or Syndrome Rieger’s Anomaly or Syndrome

Front 166

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

Front 167

is posterior embryotoxon common or uncommon

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relatively common

Front 168

what condition is this

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posterior embryotoxon

Front 169

wht is posterior embryotoxon

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Anterior displacement of Schwalbe’s line

Front 170

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

Front 171

what is the best way to see posterior embryotoxin

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Can be seen with slit lamp, but best seen with gonioscopy

Front 172

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

Front 173

what condition is this

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axenfeld's anomaly or syndrome

Front 174

what is axednfeld's anomaly

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Posterior Embryotoxin PLUS iris strands that run across AC and attach to Schwalbe’s line

Front 175

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%

Front 176

what position usually has the thinnest angle on gonioscopy? where is the widest angle?

Back 176

thinnest superior. widest inferior.

Front 177

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.

Front 178

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)

Front 179

what is rieger's anomaly or syndrome

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All of Axenfeld’s PLUS iris hypoplasia

Front 180

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%

Front 181

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

Front 182

most corneal dystrophies are what type of inheritance pattern

Back 182

autosomal dominant

Front 183

are most corneal dystrophies associated with other systemic or ocular diseases

Back 183

no

Front 184

describe the onset of most corneal dystrophies

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onset early in life with variable progression. usually observed by second decade.

Front 185

are most corneal dystrophies unilateral or bilateral

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bilateral; may or may not be symmetrical

Front 186

describe the progression of most corneal dystrophies

Back 186

slow

Front 187

do most corneal dystrophies tend to be central or pheripheral

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central

Front 188

most corneal dystrophies involve _______ layer(s) of the cornea

Back 188

a single layer

Front 189

name two epithelial layer corneal dystrophies

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Epithelial Basement Membrane Dystrophy (EBMD) Meesman’s Juvenile Epithelial Dystrophy

Front 190

what are the three diagnostic pattern you see on the cornea of pts with EBMD

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map, dot, fingerprints

Front 191

what is another name for epithelial basement membrane dystrophy

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map-dot-fingerprint dystrophy

Front 192

what time of day to pts tend to have symptoms associated with EBMD and why

Back 192

morning because when them open there eyes in the morning they tear away epithelium

Front 193

describe the severity of EBMD

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may present mild, moderate, or severe Mild:

Front 194

what type of view is best to see objective signs of EBMD

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retroillumination of the slit lamp with high magnification

Front 195

what causes negative staining

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humps on the eipthelium where the stain doesn't get to

Front 196

what is this

Back 196

map patternn on the cornea from EBMD

Front 197

what is this

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dot pattern in EBMD

Front 198

what other condition looks like dot pattern in EBMD

Back 198

eipthelial ingrowth after LASIK surgery (which needs to be refered right away)

Front 199

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

Front 200

describe the appearence of a fingerprint pattern associated with EBMD

Back 200

Larger patterns centrally Swirled refractile lines- like a fingerprint May originate out of a single point -- mares tail Clear to gray

Front 201

what is the common common complication of EBMD

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spontaneous epithelial erosion

Front 202

what should you tell the pt before rxing hypertonic solution

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they will sting quite a bit

Front 203

what can you do to reduce the sting of a hypertonic drop

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refrigerate it

Front 204

how do you want to fit a bandage CL for EBMD

Back 204

steep to vault the cornea

Front 205

why is lid hygiene importnat for pts with EBMD

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to prevent infection in compromised cornea.

Front 206

what is the condition where you puncture the cornea to treat recurrent corneal erosion called

Back 206

anterior stromal puncture

Front 207

name three surgical proceedures to treat recurrent corneal erosion

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anterior stomal puncture, lamellar keratectomy, phototherapeutic keratectomy

Front 208

describe the progression of EBMD

Back 208

goes through remissions and exacerbations

Front 209

why are hypertonics used to tx recurrent corneal erosion

Back 209

the cornea becomes swollen because of the missing epithelium

Front 210

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

Front 211

what condition is this

Back 211

meesman's juvenile epithelial dystrophy

Front 212

what is meesman's juvenile epithelial dystrophy

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Intraepithelial cysts or vesicles

Front 213

what is the best way to see meesman's juvenile epithelial dystrophy

Back 213

indirect retoillumination off the fundus (red reflex)

Front 214

what do the cysts in meesman's juvenile epithelial dystorphy look like and how can you tell the difference.

Back 214

corneal guttata. guttata are on the endothelium and meesman's cysts are in the epithelium

Front 215

what is the age of onset for meesman's juvenile epithelial dystrophy

Back 215

1 to 2 years

Front 216

what region of the cornea (not layer) do the cysts from meesman's juvenile epithelial dystrophy occur

Back 216

entire cornea, extends to the limbus. usually dystrophies are more central, but this is an exception that extends all the way to the limbus.

Front 217

describe the prognosis for meesman's juvenile epithelial dystorphy

Back 217

excellent. acuity reduction is usually slight. may have epithelial erosions after age 40.

Front 218

what condition is this

Back 218

reis-buckler's dystrophy

Front 219

what does reis-bucler's dystrophy look like

Back 219

Gray-white irregular opaque pattern in Bowman's layer Creates a mottled or ‘fish-net’ pattern that may project into the epithelium

Front 220

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

Front 221

describe the prognosis associated with reis-buckler's dystrophy

Back 221

guraded. acuity usually begins to drop by age 20 to 30.

Front 222

what condition is this

Back 222

anterior mosaic dystrophy

Front 223

how does anterior mosaic dystrophy and posterior crocodile shagreen differ

Back 223

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.

Front 224

how is vision impacted by anterior mosaic dystrophy

Back 224

Vision usually not affected

Front 225

name three common anterior stromal dystrophies

Back 225

Granular dystrophy Lattice dystrophy Crystalline dystrophy

Front 226

what condition is this

Back 226

granular dystrophy

Front 227

what do we think is the pathophysiology for granular dystrophy

Back 227

thought to be due to changes in the keratocytes in the cornea. they tend to coalesce and form larger granules.

Front 228

how does granular dystrophy affect vision

Back 228

VA's gradually drop (usually no worse then 20/200) by age 60

Front 229

what does granular dystrophy look like

Back 229

Round, oval, discrete white spots

Front 230

what is the age of onset typically for granular dystophy

Back 230

usually before age 10

Front 231

granular dystrophy has a pretty disticnt clinical appearance. you probably will be able to diagnose based on appearance.

Front 232

what condition is this

Back 232

lattice dystrophy

Front 233

what does lattice dystrophy (of the cornea) look like

Back 233

Anterior stromal refractile lines May see dots, flakes, and stellate opacities between the lines

Front 234

describe the prognosis associated with lattice dystrophy (of the cornea)

Back 234

guarded

Front 235

are there any complications associated with lattice dystrophy (of the cornea)

Back 235

recurrent corneal erosion

Front 236

what condition is this

Back 236

cystalline dystrophy

Front 237

what is cyrstalline dystrophy

Back 237

crystals form a ring in the central cornea

Front 238

what does crystalline dystrophy look like

Back 238

Crystals are white to yellow, may be polychromic. they form a ring in the central cornea.

Front 239

are there any conditions associated with crystalline dystrophy

Back 239

Patients usually develop corneal arcus (dense) by age 30 to 40 Associated with hypercholesterolemia xanthelasma

Front 240

name two bowman's layer dystrophies

Back 240

Reis-Buckler’s Dystrophy Anterior Mosaic Dystrophy

Front 241

xanthelasma

Back 241

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.

Front 242

describe the management of crystalline dystrophy

Back 242

referral for cardiovascular work up. routine follow up.

Front 243

what condition is this

Back 243

macular dystrophy

Front 244

what is macular dystrophy

Back 244

entire Stroma invaded by mucopolysaccharide material

Front 245

describe the age of onset for macular dystrophy

Back 245

Diffuse corneal clouding by age 5 to 9

Front 246

describe the visual prognosis associated with macular dystrophy

Back 246

VA's drop substantially by age 30

Front 247

what type of inheritance pattern is seen with macular dystrophy

Back 247

usually corneal dystrophies are AD, but macular dystrophy is autosomal recessive

Front 248

what area of the cornea is affected by macular dystrophy (not layer)

Back 248

Extends to the periphery (whole cornea)

Front 249

are there any complications associated with macular dystrophy

Back 249

corneal guttata formation

Front 250

what is the normal corneal thickness of an average person

Back 250

545 microns

Front 251

what is the prevalence of keratoconus (number)

Back 251

1 in 2,000 persons

Front 252

what do we think is the mechanism for keratoconus

Back 252

we don't know, but might be : enzyme induction leading to cell toxicity à keratocyte aptosis à secondary stromal thinning and corneal ectasia

Front 253

describe the progression of keratoconus

Back 253

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)

Front 254

name 7 clinically observable diagnostic signs of keratoconus

Back 254

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

Front 255

if you can't get a pt down to 20/20 how can you tell clinically if it is due to irregular astigmatism

Back 255

place a RGP on the eye and see if then can get down to 20/20

Front 256

what are the top three reasons for penetrating keratoplasty

Back 256

1. pseudophakic corneal edema 2. endothelial corneal dystophies 3. ectasias/thinning disorders

Front 257

what is this

Back 257

oil droplet reflex seen in keratoconus

Front 258

what is this

Back 258

vogt's striae

Front 259

what are the IC3D Classification for Corneal Dystrophies

Back 259

new classification system based on how well defined a disorder is

Front 260

name three common endotheilial dystrophies

Back 260

Fuch’s endothelial dystrophy Congenital Hereditary dystrophy Posterior Polymorphous dystrophy

Front 261

what is the age of onset for fuch's endothelial dystrophy

Back 261

starts age 20-30 symptomatic usually age 40-60

Front 262

is fuch's endothelial dystrophy more common in males or females

Back 262

females

Front 263

what layers of the cornea are affected by fuch's dystrophy

Back 263

problem is with the endothelium, but results in changes to all layers of the cornea.

Front 264

what is another name for guttata and what layer of the cornea do they occur in

Back 264

descemet's warts. accumulation posterior to and sometimes in descemet's membrane

Front 265

what is the name of guttata found in the periphery

Back 265

hasell-henle bodies

Front 266

how does fuch's endothelial dystrophy affect the corneal thickness

Back 266

increases. usually greater than 600 microns.

Front 267

what is this

Back 267

corneal guttata

Front 268

why is it important to take pachymetry in the center of the cornea

Back 268

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.

Front 269

what is the mechanism of vision loss in fuch's endothelial dystrophy

Back 269

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

Front 270

name 4 signs and symptoms of fuch's endothelial dystrophy

Back 270

1. VA loss in late stages 2. photophobia and glare 3. edema (causing fluctuating VA) 4. pain from bullae rupture

Front 271

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.

Front 272

describe 4 treatment options for fuch's endothelial dystrophy

Back 272

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

Front 273

what is the name of the condition that is like fuch's endothelial dystrophy

Back 273

congenital hereditary endothelial dystrophy

Front 274

what is congential hereditary endothelial dystrophy

Back 274

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

Front 275

name and describe the two forms of cengenital hereditary endothelial dystrophy

Back 275

Recessive form -- has nystagmus – congenital Dominant form -- no nystagmus – onset 1st to 2nd decade

Front 276

describe the visual outcome of cengenital hereditary endothelial dystrophy

Back 276

VA's drop, level depends upon edema Can lead to blindness - epithelial cause

Front 277

what condition is this

Back 277

posterior polymorphous dystrophy

Front 278

what is posterior polymorphous dystrophy

Back 278

the endothelium displays “epithelial characteristics”.

Front 279

describe the visual outcome associated with posterior polymorphous dystrophy

Back 279

pretty benign

Front 280

describe 4 clinically observable signs associated with posterior polymorphous dystrophy

Back 280

1. vesicular pattern on the back of the cornea 2. band-like pattern (thickening of descemet's membrane) 3. peripheral anterior synechiae 4. corectopia

Front 281

what is this type of appearance called

Back 281

ground-glass appearance

Front 282

describe the management of posterior polymorphous dystrophy

Back 282

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)

Front 284

is there a heriditary component to posterior polymorphous dystrophy

Back 284

yes, AD

Front 285

with the epithelial dystrophies what clinical tests do you need to be concerned about doing

Back 285

tonometry or gonioscopy because their epithelium is compromised and you dont' want to remove a bunch of the epithelium

Front 286

is posterior polymorphous dystrophy associated with any other conditions

Back 286

Alpert's syndrome, keratoconus

Front 287

what is this

Back 287

pannus

Front 288

what is corneal pannus

Back 288

Superficial vascular invasion with fibrous tissue bed Usually chronic result of inflammatory response

Front 289

causes of pannus:

Back 289

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

Front 290

what is the differnece between corneal neovascuarization and corneal pannus

Back 290

you won't see the haze and the stromal infiltration with neovascularization. pannus is more white and leukoric in appearance.

Front 291

what are two of the major causes of interstitial keratitis

Back 291

syphilis and herpes simplex

Front 292

describe the management and follow up associated with corneal pannus

Back 292

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

Front 293

what is it important to DDX a pterygium with

Back 293

a conjunctival tumor

Front 294

can a pterygium affect refractive error

Back 294

can induce irregular astigmatism

Back 295

1. protection (sunglasses) 2. artifical tears and or ointments 3. topical vasoconstrictors 4. topical steroid 5. surgical removal (likely to come back)

Front 296

what do you need to remember to do if you rx a steroid for pterygium or any other condition

Back 296

take IOP and follow up, checking the IOP

Front 297

what is this

Back 297

interstitial keratitis

Front 298

what is interstitial keratitis

Back 298

keratitis involving the stroma. it is characterized by deep vascularization of the cornea and is often associated with iridocyclitis.

Front 299

is interstitial keratitis usually unilateral or bilateral

Back 299

usually unilateral; may become bilateral

Front 300

describe the timing of an interstitial infection caused by a systemic infection

Back 300

Acute ocular infection can occur 5 to 15 years after systemic infection Congenital ocular form can present at age 15

Front 301

causes of interstitial keratitis:

Back 301

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)

Front 302

describe the triad of corneal findings associated with interstitial keratitis

Back 302

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

Front 303

what is hutchenson's triad

Back 303

in congenital syphilis Notched incisor teeth Deafness (Cogan’s syndrome) Interstitial keratitis

Front 304

what is a saddle nose bridge

Back 304

finding in congenital syphilis along with hutchenson's triad

Back 305

picture in question

Front 306

New lecture: 5 Bacterial Keratitis & ulcers 2009 Vault

Front 307

basal layer of the epithelium is responsible for mitosis. basement membreane is below basal layer.

Front 308

why does damage to the cornea cause scarring

Back 308

bowmann's layer can not regenerate, so damage causes scarring.

Front 309

in what layer of the cornea is the greatest concentration of nerves

Back 309

anterior stroma

Front 310

name five cuases of superificial punctate keratitis (SPK)

Back 310

1. dry eye 2. contacts 3. blepharitis 4. baceterial conjunctivitis 5. allergic conjunctivitis

Front 311

what is the best way to see superifical punctate keratitis

Back 311

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

Front 312

what is superficial punctate keratitis

Back 312

Describes superficial punctate corneal epithelial disruption

Front 313

what are the two forms of superficial punctate keratopathy

Back 313

Punctate Epithelial Erosion (PEE) Punctate Epithelial Keratopathy (PEK)

Front 314

what is punctate epithelial erosion (PEE)

Back 314

Focal areas of epithelial disruption or lesion Slightly depressed Stain well with NaFl, rose bengal and lissamine green

Front 315

can you see punctate epithelial keratophthy without any stain

Back 315

yes

Front 316

what is punctate epithelial keratopathy

Back 316

Grayish white opacities in the epithelium. Accumulation of epithelial cells that are surrounded by a focal inflammatory infiltrate

Front 317

what is the difference between the strict definition and how we use superficial punctate keratopathy clinically

Back 317

Commonly used to refer generally to superficial punctate epithelial disruptions of multiple etiologies Clinically, often used interchangeably with PEE

Front 318

describe 4 subjective complaints that a pt with SPK will come in with

Back 318

FB sensation Redness Tearing Photophobia

Front 319

what is the difference between confluent and focal SPK

Back 319

confluent: localized area of SPK focal: localized area of SPK where punctate lesions coalesce to form a larger epithelial defect

Front 320

name three common pathogens that cuase superficial keratitis

Back 320

Staphylococcus Streptococcus Haemophilus

Front 321

is staphylococcus gram positive or negative

Back 321

gram positive cocci

Front 322

name two common staphylococcus organisms

Back 322

staph. aureus and staph. epidermidis (part of normal flora, but can also be pathogenic)

Front 323

what is the most common ocular pathogen in pts of all ages

Back 323

staphylococcus aureus

Front 324

why does staph cause punctate epithelial defects

Back 324

exotoxins from bacteria

Front 325

what are the two main causes of phylectenule

Back 325

staphylococcus infection and TB

Front 326

what are collarettes (blepharitis)

Back 326

debris and protein build-up at the base of the lashes.

Front 327

are there any ocular side effect to aminoglycosides

Back 327

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.

Front 328

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?

Back 328

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.

Front 329

what drug is less effective due to many resistant strains and what drug class is it.

Back 329

sulfacetamide (a sulfonamide)

Front 330

what is important to remember to tell a pt who is using artifical tears that you rx a topical medication

Back 330

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.

Front 331

is streptococcus gram positive or negative

Back 331

gram positive cocci

Front 332

what is important to remember if you rx an ointment

Back 332

it will make them blurry. usually used at night.

Front 333

name two clinically observable signs that indicate streptococcus as the organism behind an ocular infection

Back 333

pseudomembranes and petechial hemorrhages. -petechial hemorrhages also associated with heamophilus infection

Front 334

what group of medications is thought to be ineffected against streptococcus infection

Back 334

aminoglycosides (tobramicin and gentamycin)

Front 335

Aminoglycosides Fluroquinolones QID to q2-3h Depending on severity & drug used Treatment duration: 7-14 days Exception: Polytrim q3h

Front 336

are contact lens related complications infectious or inflammatory

Back 336

can be either.

Front 337

what can a corneal ulcer look like in it's early stages

Back 337

corneal infiltrate

Front 338

are corneal infiltrates or corneal ulcers more common

Back 338

corneal infiltrates are far more common

Front 339

what is another name for corneal infiltrates

Back 339

corneal infiltrative events (CIE)

Front 340

what type of reaction is a corneal infiltrate

Back 340

not infectious. antigen-antibody reaction (hypersensativity reaction); can be due to hypoxia (CL wearers).

Front 341

what causes negative staining

Back 341

elevation on the cornea.

Front 342

there may be sectoral hyperemia of the conjectiva in the area adjacent to a corneal infiltrate.

Front 343

what type of staining do corneal infiltrates cause

Back 343

positive and/or negative (positive is less common and usually smaller than the area of the lesion)

Front 344

what do you need to remember with regards to the timing of a fluorescein stain

Back 344

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.

Front 345

is it possible to see old epithelial infiltrates

Back 345

if the epithelial infiltrate involves the stroma it will leave scarring, which you will be able to see.

Front 346

is haemophilus gram positive or gram negative

Back 346

gram negative

Front 347

corneal infiltrates are frequently associated with chronic conjunctivitis due to blepharitis

Front 348

what type of medication do you use to tx corneal infiltrate

Back 348

steroid. antibiotic if it is due to chronic infection.

Front 349

what do you need to be sure of before you tx a corneal infiltrate with steroid

Back 349

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

Front 350

what is the difference between tobradex and zylet clinically

Back 350

dexamethasone has more of a tendancy to increase IOP, but tobradex there is a big difference in price.

Front 351

list five ways you can differentiate between a corneal ulcer and a corneal infiltrate

Back 351

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

Front 352

will a corneal ulcer leave a scar

Back 352

yes, by definition a corneal ulcer involves the stroma. tell them up front, so they don't think that scarring is from poor treatment

Front 353

what are the top 2 causes of corneal ulcer in adults

Back 353

1. contact len overwear 2. trauma

Front 354

describe the appearance of a corneal ulcer

Back 354

Epithelial edges are usually distinct with an indistinct underlying stromal border. Corneal edema surrounds area involved.

Front 355

describe the progression of corneal ulcer

Back 355

TREAT QUICKLY and AGGRESIVLY!! The cornea may scar or perforate Leading to permanent vision loss!!!

Front 356

what is a very common organism that cuases a corneal ulcer in CL wearers

Back 356

pseudomonas

Front 357

name 5 signs and symptoms that a pt with a corneal ulcer will come complaining of

Back 357

1. decreased VA 2. photophobia 3. pain 4. redness 5. purulent discharge

Front 358

is pseudomonas gram positive or gram negative

Back 358

negative

Front 359

how quickly can a pseudomonas infection perforate the cornea

Back 359

24 to 48 hours

Front 360

describe the tx of corneal ulcer

Back 360

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

Front 361

what are the three fluroquinolones FDA approved for corneal ulcer

Back 361

1. ciprofloxacin 2. ofloxacin 3. levofloxacin -zymar and vigamox are often used off lable

Front 362

New lecture: 6 Fungal_and_Amoebic_Keratitis_2009

Front 363

what is the name of a fungal infection of the cornea

Back 363

keratomycosis

Front 364

name thre predisposing facotrs for fungal infection

Back 364

1. trauma (especially with vegtable matter) 2. immunosupression 3. steroid use

Front 365

what are the four most common fungi with ocular involvement in the US

Back 365

fillamentous: fusarium, aspergillus, cephalosporium non-fillamentous (unicellular yeast): candida

Front 366

Fusarium keratitis outbreak 2006

Back 366

1.

Front 367

where is candida found that most other fungi are not

Back 367

all four common ocular pathogens are found ubiquitously on plants and in soil. candida is also found in inanimate objects, food, hospital environments

Front 368

which of the four common fungi with ocular involvement in the US is the most virulent

Back 368

fusarium

Front 369

describe the pain associated with fungal infection of the eye

Back 369

often less than expected from the clinical picture

Front 370

describe the subjective symptoms associated with fungal eye infection

Back 370

similar to bacterial ulcer: Pain (can start as FB sensation)

Front 371

describe the onset of fungal eye infection

Back 371

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)

Front 372

name 5 clinically observable objective signs associated with fungal corneal infection

Back 372

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

Front 373

what is the main DDX for fungal corneal infection

Back 373

bacterial corneal ulcer

Front 374

what additional testing do you need to do if you have a corneal ulcer

Back 374

culture

Front 375

describe the tx of fungal corneal ulcer

Back 375

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

Front 376

what is acanthamoeba

Back 376

Ubiquitous protozoans found in water, soil, air, dust

Front 377

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

Front 378

Acanthamoeba outbreak 2007

Back 378

1.

Front 379

subjective symptoms of acanthamoeba

Back 379

Unilateral red eye C.

Front 380

what is the most important diagnositc symptoms of achanthamoeba

Back 380

Waxing and waning of symptoms ((very important symptom; months to years)

Front 381

describe the early and late clinically observable objective signs of acanthamoeba

Back 381

Early

Front 382

why is acanthamoeba often co-infected with bacteria

Back 382

acanthamoeba feed on bacteria

Front 383

describe two tests used to diagnose acanthamoeba

Back 383

lab tests, confocal microscopy (HRT)

Front 384

how do you tx acanthamoeba

Back 384

refer to corneal specalist! no consensus on how to treat. know the dosage though: Dosage

Front 385

New lecture: 1 Anterior_Uveitis_2009

Front 386

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.

Front 387

what is uveitis

Back 387

an inflammation of any combination of the structures of the uvea.

Front 388

what is uveitis that involves the iris only called

Back 388

iritis

Front 389

what is uveitis that involves the iris and the biliary body called

Back 389

iridocyclitis

Front 390

what is uveitis that involves the ciliary body or pars plana area called (3)

Back 390

cyclitis (pars planitis, peripheral uveitis)

Front 391

what is uveitis that involves the iris and the choroid called

Back 391

iridochoroiditis

Front 392

where do you see cells in iritis

Back 392

anterior chamber but not anterior vitreous

Front 393

where do you see cells with iridocyclitis

Back 393

in the anterior chamber and/or the anterior vitreous

Front 394

what is the difference between anterior, posterior and intermediate uveitis

Back 394

1. Anterior = inflammation of iris or ciliary body or both

Front 395

where do you see cells in posterior uveitis

Back 395

in the posterior vitreous

Front 396

what are the names of the chronic and the acute forms of uveitis

Back 396

gramulomatous uveitis is usually choronic and non-granulomatous is usually acute.

Front 397

what are keratic precipitates

Back 397

inflammatory cells that deposit on the endothelium of the cornea.

Front 398

describe the etiology of uveitis

Front 399

what types of keratic precipitates do you see with granulomatous and non-granulomatous uveitis

Back 399

granulomatous: mutton fat KPs non-granulomatous: fine KPs

Front 400

are iris nodules associated with granulomatous or non-granulomatous uveitis

Back 400

granulomatous

Front 401

is anterior or posterior uveitis more common

Back 401

Anterior uveitis more common than posterior

Front 402

describe the age of onset of uveitis

Back 402

peak prevalence 20-50 years old. rarely makes first appearance in old age.

Front 403

racial, sexual and geographical predilection of uveitis:

Back 403

Sexual predilection (depends on specific condition)

Front 404

what is the most common cause of anterior uveitis

Back 404

idiopathic

Front 405

in cases of idiopathic uveitis there is a very strong associate with what gene

Back 405

HLA B27

Front 406

describe 6 subjective symptoms that a pt with ACUTE anterior uveitis will come in complaining of

Back 406

Classic SXs

Front 407

describe 6 subjective symptoms that a pt with CHRONIC uveitis will come in complaining of

Back 407

Chronic anterior uveitis - may be asymptomatic

Front 408

photophobia is a very strong indicator of uveitis

Front 409

how does acute and chronic uveitis differ in their response to treatment

Back 409

acute: will usually respond to topical drops alone chronic: will usually need topical drops as well as oral meds

Front 410

are acute or chronic cases of uveitis more likely to recur

Back 410

chronic

Front 411

is acute or chornic uveitis more commonly associated with systemic disease

Back 411

chronic

Front 412

does acute and chronic uveitis tend to be unilateral or bilateral

Back 412

acute: unilateral chronic: bilateral

Front 413

name 13 clinically observable signs of uveitis

Back 413

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)

Front 414

what type of cataracts tend to form from steroid use

Back 414

posterior sub-capsular

Front 415

name and describe the two types of iris nodules seen in uveitis

Back 415

a. Busacca

Front 416

what is flare

Back 416

protein leaking from the iris and ciliary body

Front 417

what are the guidelines for grading cells and flare

Front 418

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.

Front 419

what is the difference betwee fine and mutton fat keratic precipitates

Back 419

Fine - whitish/grey fibrin adherent to corneal endothelium

Front 420

how long do keratic precipitates take to dissapear

Back 420

months. they may never completely resolve.

Front 421

what is circumcorneal (perilimbal) flush

Back 421

a ring of dilated blood vessels around the limbus

Front 422

how do the symptoms that a pt will experience differen between chronic and acute uveitis

Back 422

acute: moderate to severe chronic: mild to moderate

Front 423

how can you differentiate clinically between keratitis and uveitis

Back 423

pain from keratitis will go away with proparocaine. if it is uveitis it will not.

Front 424

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

Front 425

what are the standard concentrations of tropicamide and phenylephrine

Back 425

tropicamide 1%; phenylephrine 2.5%

Front 426

what is the duration of dilation for the following drops: atropine, cyclopentolate, homatropine, phenylephrine, scopolamine, tropicamide

Back 426

atropine: 7-14 days cyclopentolate: 6-12 hours homatropine: 18-24 hours phenylephrine: 4-8 hours scopolamine: 5-7 days tropicamide: 3-6 hours

Front 427

what types of medicatinos do you use to tx uveitis (3)

Back 427

cycloplegics, steroids, NSAIDS

Front 428

if a pt has an allergy to ________ you should be cautious about using acetazolamide (diamox)

Back 428

sulfa drugs

Front 430

why does dilation reduce the likelihood of synechia

Back 430

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.

Front 431

what should you do in a uveitis case if synechia has already started to form

Back 431

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.

Front 432

what do you do if you need to cycloplege a pt with uveitis, but they have narrow angles.

Back 432

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.

Front 433

lab test for uveitis: think if the testing is going to change how you treat the condition.

Front 434

what sex and age range do you expect to see ankylosing spondylitis

Back 434

males 20s and 30s

Front 435

what is ankylosing spondylitis

Back 435

chronic form of arthritis

Front 436

what test is indicated for all young males with anterior uveitis

Back 436

sacroiliac x-ray (ankylosing spondylitis)

Front 437

what is the major subjective symptom associated with ankylosing spondylitis

Back 437

back pain (50% are asymptomatic!)

Front 438

what is another name for reiter's syndrome

Back 438

reactive arthritis

Front 439

what is reactive arthritis

Back 439

= triad of nongonococcal urethritis, polyarthritis & acute

Front 440

what should you be suspicious of if you see an acute conjunctivitis with anterior uveitis

Back 440

reactive arthritis (reiter's syndrom)

Front 441

describe the demographic associated with reactive arthritis`

Back 441

males, 20s to 40s

Front 442

describe the tx of reactive arthritis

Back 442

Oral tetracycline 250 mg QID x 10 d. ((thought to be clymidial in cause) -treat uveitis as usual

Front 443

describe the age of onset and sexual prediliction of juvenile chronic arthritis

Back 443

arthritis by 15 YO or younger, but onset is typically 1 – 4 YO

Front 444

what condition that we deal with is associated with still's disease

Back 444

juvenile chronic arthritis

Front 445

what is still's ocular triad

Back 445

iridocyclitis, band keatopathy and cataract

Front 446

steroids can retard growth in children

Front 447

what is sarcoidosis

Back 447

multisystem granulomatous disease of unknown etiology which can affect

Front 448

what percent of pts with sarcoidosis will have ocular complications

Back 448

20-50%

Front 449

describe the demographic associated with sarcoidosis

Back 449

most common is younger african american females

Front 450

what type of uveitis is common with sarcoidosis

Back 450

granulomatous

Front 453

what is "candle wax dripping"

Back 453

yellow exudate that forms around the blood vessel in retinal vasculitis

Front 454

what percent of sarcoidosis pts will have an abnormal chest x-ray

Back 454

80%

Front 455

what is tuberculosis

Back 455

granulomatous infection of Mycobacterium tuberculosis; generally

Front 456

what percent of pts with tuberculosis will have ocular involvement

Back 456

most pts with TB do not have ocular involvement; only 1-2%

Front 457

what is the most common cause of phlyctenular keratoconjunctivits

Back 457

staph infection. could also be due to tuberculosis, but TB is rare.

Front 458

what test do you need to do if you suspect TB

Back 458

PPD

Front 459

name three drugs used to tx tuberculosis

Back 459

Isoniazid (INH) - drug of choice

Front 460

what ocular condition can result from tertiary syphilis

Back 460

argyl-robertson pupil

Front 461

name and describe the stages of syphilis

Back 461

Primary – painless ulcer (chancre) Secondary – skin rash (palms, soles, trunk) Tertiary – neurosyphilis

Front 462

is ocular complication common or rare with syphilis

Back 462

relatively rare

Front 463

what is the "salt and pepper fundus"

Back 463

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.

Front 464

what is hutchinson's triad and what disease is it associated with

Back 464

IK (interstitial keratitis), notched incisors, deafness associated with syphilis

Front 465

which of the tests for syphilis are positive only during acitve disease and which are positive throughout the lifetime of the pt

Back 465

VDRL or RPR positive ((during active phase of disease)

Front 466

what is the most common cause of chorioretinitis

Back 466

toxoplasmosis

Front 467

describe your view of the fundus in a pt with chorioretinitis

Back 467

"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

Front 468

you can contract toxoplasmosis from (3):

Back 468

1. animal feces 2. drinking unhomogenized milk 3. eating raw beef

Front 469

name 4 antitoxoplasmic drugs

Back 469

Antitoxoplasmic agents

Front 470

common cuses of uveitis:

Back 470

ankylosing spondylitis, reiter's syndrome (reactive arthritis), juvenile chronic arthritis, sarcoidosis, tuberculosis, syphilis, many others.

Front 471

THE TOP TWELVE REALLY USEFUL LABORATORY TESTS FOR UVEITIS – Dr. Brooks Allredge 12.

Back 471

Human leukocyte antigen (HLA): expensive; reveals conditions that are generally

Front 472

New lecture: 2 Epi_Scleritis 2009

Front 473

when the episclera is inflammed, what other structure is also inflammed

Back 473

conjunctiva

Front 474

describe the prognosis associated with episcleritis

Back 474

benign and self limitating

Front 475

what are the two types of episcleritis

Back 475

simple 80% nodular 20%

Front 476

is simple episcleritis usually unilateral or bilateral

Back 476

unilateral 70% of the time

Front 477

is simple episcleritis acute or chronic

Back 477

acute onset of signs and symptoms

Front 478

is simple episcleritis diffuse or localized

Back 478

localized

Front 479

describe the subjective symptoms that a pt with simple episcleritis will come in complaining of (2)

Back 479

1)

Front 480

is VA affected by simple episcleritis

Back 480

no

Front 481

is simple episcleritis recurrent

Back 481

yes

Front 482

name 4 objective signs and symptoms that are either present or absent that help diagnos simple episcleritis

Back 482

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

Front 483

what is a good way to differentiate between scleritis and episcleritis based on the appearance of the blood vessels

Back 483

in epicleritis the blood vessels maintain their normal architecture. in scleritis they do not necessarily maintain their normal architecture.

Front 484

what is the most common cause of simple episcleritis

Back 484

idiopathic (70%)

Front 485

30% of simple episcleritis is associated with systemic disease:

Back 485

Collagen vascular disease

Back 486

picture

Back 487

picture

Front 488

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?

Back 488

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.

Front 489

if you have a pt that you suspect scleritis or episcleritis, what do you need to consider before you dilate the pt

Back 489

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.

Front 490

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.

Front 491

how can you DDX episcleritis and scleritis with pharmaceuticals

Back 491

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.

Front 492

describe the progression of episcleritis

Back 492

most will resolve in 1.5 to 3 weeks whether you treat it or not.

Front 493

describe the tx of simple episcleritis

Back 493

Mild cases

Front 494

what is the follow up schedule for a pt with episcleritis

Back 494

RTC q 2 - 3 weeks

Front 495

what percent of episcleritis is simple and what percent is nodular

Back 495

simple 80% nodular 20%

Front 496

how do the symptoms compare in nodular episcleritis to simple episcleritis

Back 496

in nodular form symptoms are more intense

Front 497

is nodular episcleritis recurrent

Back 497

less likely to recur than simple form

Front 498

describe the clinically observable signs of nodular episcleritis

Back 498

Nodule formation usually in the center of sectorial

Front 499

how does the nodule help you differentiate between nodular episcleritis and scleritis

Back 499

((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.

Front 500

how do you differentiate between nodular episcleritis and pingueculitis

Back 500

history. pts with pinguecula know that they are there and they have been there for a long time. episcleritis is acute.

Front 501

describe the tx and the follow up for nodular episcleritis

Back 501

tx and follow up same as for moderate-severe cases of simple episcleritis. -nodular form takes longer to resolve than simple form though.

Front 502

can recurrent cases of episcleritis switch between the simple and nocular form

Back 502

yes

Front 503

can episcleritis progress to scleritis

Back 503

no

Front 504

how does episcleritis and scleritis compare in how common they are

Back 504

episcleritis is common, scleritis is rare.

Front 505

what tissues are inflammed in scleritis

Back 505

sclera, episclera, and overlying conjunctiva

Front 506

what percent of the time is scleritis associated with systemic disease

Back 506

50%

Front 507

name the five types of scleritis

Back 507

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

Front 508

what is the most common form of scleritis

Back 508

diffuse anterior scleritis (40-80% of cases)

Front 509

can the diffuse form of scleritis progress to the nodular form

Back 509

typically does not

Front 510

what is the most serious type of scleritis

Back 510

necrotizing anterior scleritis with inflammation

Front 511

what is the systemic prognosis for a pt with necrotizing anterior scleritis with inflammation

Back 511

high mortality rate due to other systemic factors

Front 512

how does the color of the slcera change with nectotizing anterior scleritis with inflammation

Back 512

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

Front 513

what form of scleritis is called scleromalacia perforans

Back 513

necrotizing anterior scleritis without inflammation

Front 514

describe the subjective symptoms experienced by a pts with scleromalacia perforans

Back 514

almost no symptoms

Front 515

in what systemic condition do you see scleromalacia perforans

Back 515

seen almost exclusively in pts with long-standing rheumatoid arthritis

Front 516

name four objective retinal findings that are associated with posterior scleritis

Back 516

1. exudative RD 2. disc swelling 3. retinal hemorrhage 4. choroidal folds

Front 517

describe the onset for scleritis

Back 517

gradual onset

Front 518

how does scleritis affect vision

Back 518

indisious decrease in VA

Front 519

describe the pain associated with scleritis

Back 519

1. severe, boring pain which may radiate to forehead, brow or jaw

Front 520

name 4 clinically observable objective signs of scleritis

Back 520

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

Front 521

Causes of scleritis: 1.*

Back 521

CT disease

Front 522

in what condition are subconjunctival steroids contraindicated

Back 522

scleritis because of the risk of scleral thinning/perforation at the injection site

Front 523

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.

Front 524

New lecture: 3 Retinal Overview 2009

Front 525

vista mind: things that could cause problems in the retina Vascular, vitamin deficiency

Back 525

EX.

Front 526

New lecture: 4 Lens Abnormalities 2009

Front 527

what types of materials make up the cyrstalline lens

Back 527

65% water, 35% protein

Front 528

proteins in the lens:

Back 528

Crystallines a, b, g -insoluble crystallines increase with age

Front 529

what type of metabolism is the main type in the crystalline lens

Back 529

mainly anaerobic

Front 530

from what part of the lens does the lens develop

Back 530

from surface ectoderm

Front 531

what are the zones of the lens

Back 531

- 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)

Front 532

what is the one part of the human body that continues to grow from birth until death

Back 532

cyrstalline lens

Front 533

why does an adult cyrstalline lens appear brighter and less clear than a child's

Back 533

because light passing through it scatters because of the irregular fibers

Front 534

what type of tissue is the lens capsule

Back 534

basement membrane of lens epithelium

Front 535

in what part of the lens is epithlium present

Back 535

only anteriorly. creates a orange peel appearance.

Front 536

how many cell layers thick is the lens epithelium

Back 536

1

Back 537

picture

Front 538

how much power does the cyrstalline lens have unaccommodated

Back 538

15 D

Front 539

how big is the cyrstalline lens at birth? what age does it reach adult size? how big is that?

Back 539

7 to 7.5mm diameter at birth 9 to 9.5mm diameter at age 2 yrs 9.6 +/- 0.4mm diameter as adult

Front 540

how thick (anterior to posterior) is the averge adult lens

Back 540

4.2 +/- 0.5 mm

Front 541

what is it called when you are born without a cyrstalline lens

Back 541

congenital aphakia

Front 542

name and describe the two types of congenital aphakia

Back 542

Congenital Primary Aphakia No lens induction of surface ectoderm Complete aplasia of anterior of eye Congenital Secondary Aphakia Lens resorbed/expelled in utero

Front 543

how does congenital aphakia affect vision (3)

Back 543

severely reduced VA, nystagmus, amplyopia

Front 544

why are CLs preferred in congenital aphakia

Back 544

CLs can reduce nystagmus due to tactile feedback. also, they have an extremely high power.

Front 545

why is a IOL typically not done in cases of congenital aphakia

Back 545

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.

Front 546

what is it called when you have an abnormally small crystalline lens diameter

Back 546

microphakia

Front 547

how does microphakia affect VA

Back 547

severely reduced VA

Front 548

is IOL usually done for microphakia? why or why not?

Back 548

not usually. small lens capsule makes IOL implantation difficult.

Front 549

name three systemic conditions associated with microspherophakia

Back 549

1. weill-marchesani syndrome 2. marfan's syndrome 3. peter's anomaly

Front 550

what type of refractive error is most commonly associated with microspherophakia and why

Back 550

severe myopia. due to the rounder shape of the lens

Front 551

what is microspherophakia

Back 551

a congenital, usually bilateral, condition in which the crystalline lens is smaller than normal and spherical in shape.

Front 552

what orientation do lens colobomas usually occur

Back 552

infero-nasal

Front 553

how does lens coloboma affect vision

Back 553

reduced VAs, irregular astigmatism, accommodative dysfunction

Front 554

if lens coloboma is present, iris, choroid, retina and optic nerve coloboma is also likely present.

Front 555

what condition is this

Back 555

posterior lenticonus

Front 556

what is posterior lenticonus

Back 556

Circumscribed round or oval bulge at posterior axial zone of lens

Front 557

how common is posterior lenticonus

Back 557

very rare. Dr. yudkovitch has only seen 1.

Front 558

what is the age of onset for posterior lenticonus

Back 558

develops in infancy or early childhood

Front 559

describe the progression of posterior lenticonus

Back 559

The bulge increases in size with age The lens cortex may become opaque

Front 560

what is anterior lenticonus and what disease is it associated with

Back 560

bulging on the anterior surface of the cyrstalline lens. associated with alport's syndrome

Front 561

what is alport's syndrome

Back 561

congenital glomerulonephritis associated with deafness and a decrease in large thrombocytes

Front 562

name 2 ocular conditions associated with alport's syndrome

Back 562

anterior lenticonus, posterior polymourphous dystrophy

Front 563

what is lentiglobus

Back 563

more general hemispherical deformity of the lens than. the bulging is more spherical, instead of conical as in lenticonus.

Front 564

what is the name of the condition where the lens is shifted from its normal postion (luxated)

Back 564

ectopia lentis

Front 565

what is the difference between a luxated lens and a subluxated lens

Back 565

luxated: completely dislocated form pupillary space subluxated: partially dislocated from pupillary space.

Front 566

what should you be sure to look for if you see a displaced lens

Back 566

any mass that may be causing the displacement

Front 567

what is the name of the drug that can melt the zonules

Back 567

alpha-chymotrypsin

Front 568

what is marfan syndrome. and what is the most severe complication you are worried about.

Back 568

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.

Front 569

what is the systemic triad seen in marfan syndrome

Back 569

1. cardiac anomalies 2. skeletal anomalies 3. muscluar underdevelopment (leads to high incidence of hernias)

Front 570

what is the name of the term for long spider-like fingers (as seen in marfan syndrome)

Back 570

arachnodactyly

Front 571

what percent of the time is there lens subluxation with marfan syndrome? what direction is the subluxation?

Back 571

80% of cases. upward subluxation.

Front 572

name 6 objective ocular findings associated with marfan syndrome

Back 572

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

Front 573

which dilating drop would work best on a pt with marfan syndrome and why

Back 573

tropicamide (not phenylephrine). because the dilator muscle of the iris doesn't work well.

Front 574

what is weill-marchesani syndrome

Back 574

rare systemic connective tissue disorder; dystrophia mesodermalis hypERplasia. short stubby fingers (bradydactyly), mental handicap.

Front 575

what is the age of onset of weill-marchiesani syndrome

Back 575

teens to early 20s

Front 576

name three objective ocular findings associated with weill-marchiesani syndrome

Back 576

1. microspherophakia 2. lens dislocation 3. angle anomaly

Front 577

what direction is the subluxation of the lens in weill-marchiesani syndrome

Back 577

downward lens subluxation

Front 578

what is homocystinuria

Back 578

an inheritied disease that results in excess homocystine. which can result in systemic complications, cardiovascular problems for example.

Front 579

what is the primary ocular complication associated with homocystinuria

Back 579

ectopia lentis

Front 580

what is ehlers-danlos syndrome

Back 580

collagen disorder from dygroxylysine defect. hyperelastic skin, joint, aneurysms, hernias. associated with ocular findings.

Front 581

what ocular findings are associated with ehlers-danlos syndrome (4)

Back 581

angioid streaks, keratoconus, blue sclera, subluxed lens.

Front 582

what condition is this

Back 582

pseudoexfoliation

Front 583

under what conditions do you normally see pseudoexfoliation

Back 583

in the slit lamp when the pt is dilated.

Front 584

what is true exfoliation

Back 584

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.

Front 585

what pseudoexfoliation

Back 585

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

Front 586

is pseudoexfoliation usually unilateral or bilateral

Back 586

often unilateral or asymmetric bilateral presentation

Front 587

describe 5 clinically observable objective signs associated with pseudoexfoliation

Back 587

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

Front 588

what should be your first view on gonioscopy

Back 588

inferior, because that is where a lot of stuff deposits on the eye.

Front 589

what ethnicity is pseudoexfoliation most common in

Back 589

northern europeans

Front 590

describe the management of pseudoexfoliation

Back 590

1. tx secondary glaucoma 2. lens extraction

Front 591

IOP spikes from pseudoexfoliation can come and go, so it is possible that you would miss them on exam

Front 592

what is the name of the cataract formed due to acute angle closure glaucoma

Back 592

glaukomflecken

Front 593

what part of the lens do claukomflecken usually form

Back 593

anterior, subcapsular, or capsular

Front 594

is glaukomflecken permanent

Back 594

may resolve if IOP treated promptly

Front 595

do benign congenital cataracts usually affect vision

Back 595

no

Front 596

types of benign congenital cataracts (6):

Back 596

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

Front 597

how do you differentiate between a mittendorf's dot and a cataract

Back 597

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

Front 598

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.

Front 599

cataracts related to diabetes (2 types):

Back 599

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

Front 600

what is the condition called where the body cannot utilize galactose metabolically

Back 600

galactosemia

Front 601

what food is very high in galactose

Back 601

milk -need to eliminate milk from diet in pts with galactoseemia

Front 602

what type of cataract forms in galactosemia

Back 602

oil droplet

Front 603

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.

Front 604

what is galactokinase deficiency

Back 604

unable to metabolize galactose

Front 605

how does galactokinase deficiency compare to galactosemia

Back 605

pts with galactokinase deficiency are relatively healthy; pt with galactosemia are not.

Front 606

what type of ocular signs form in pts with galactokinase deficiency

Back 606

lamellar cataracts

Front 607

what is mannosidosis

Back 607

alpha-mannosidase deficiency. mannose-rich oligosaccharide accumulation in the body.

Front 608

what ocular sign occurs in pts with mannosidosis

Back 608

posterior subcapsular cataracts

Front 609

what is Lowe's syndrome (oculocerebrorenal syndrome)

Back 609

Amino acid metabolism error Mental handicap, dwarfism, osteomalaica, frontal prominence, muscular hypotonia

Front 610

what ocular sign is associated with Lowe's syndrome (2)

Back 610

microphakia. congenital glaucoma in 50%.

Front 611

what type of cataracts are associated with hypocalcemic syndromes

Back 611

Multicolored crystals/discrete white flecks in lens Seldom progress to maturity

Front 612

what type of cataracts are associated with myotonic dystrophy

Back 612

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

Front 613

what is the most common cause of congenital cataracts

Back 613

rubella

Front 614

what is rubella

Back 614

a mild, febrile, highly infectious viral disease historically common in childhood prior to the advent of an effective vaccine

Front 615

what are the classic signs associated with rubella

Back 615

Sensorineuronal deafness Cataracts 15% of cases virus latent in the lens Heart defect Microcephaly Severe mental retardation

Front 616

remeber that congenital cataracts have to be removed to prevent amblyopia

Front 617

what is cytomegalovirus

Back 617

an opportunistic disease seen in HIV/AIDS

Front 618

why is uveitis associated with cataract

Back 618

From long-term anterior or posterior chamber inflammation From topical and/or oral steroid use to treat uveitis

Front 619

hereditary fundus dystrophies associated with cataract (3)

Back 619

retinitis pigmentosa, gyrate dystrophy, leber's congenital amaurosis

Front 620

what is a glass-blower's cataract

Back 620

Infrared radiation Capsular splitting and peeling True exfoliation of lens capsule

Front 621

what is arc flash

Back 621

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

Front 622

can cataracts form from topical or systemic steroids

Back 622

both

Front 623

what type of cataracts tend to form from steroid use

Back 623

Classic posterior subcapsular cataracts form Eventually anterior subcapsular cataracts also form

Front 624

are cataracts from steroid use reversable

Back 624

regression may occur if drug stopped/reduced

Back 625

picture

Front 626

drugs that can cause cataract formation (4)

Back 626

1. chlorpromazine 2. amiodarone 3. psoralen (psoriasis and vitiligo) 4. gold salts (rheumatoid arthritis)

Front 627

New lecture: 5 Cataracts 2009

Front 628

what are epicapsular stars

Back 628

Small light brown or tan (despite iris color) dots or star-shaped deposits on anterior lens capsule

Front 629

epicapsular stars may be single or multiple, unilateral or bilateral. does not affect vision, no associated symptoms.

Front 630

what is this

Back 630

vossius ring

Front 631

what is a vossius ring

Back 631

Imprint deposition of melanocytes from pupillary border of the iris due to contusion

Front 632

is vossius ring permanent

Back 632

usually fades with time, but some pigment may remin permanently

Front 633

what other ocular complication should you watch out for if you see a vossius ring

Back 633

traumatic cataract

Front 634

three causes for capsular pigment dusting (lens)

Back 634

1. pigment dispersion syndrome 2. pseudoexfoliation 3. ocular trauma

Front 635

what else should you look at if you see capsular pigent dusting on the lens (3)

Back 635

1. corneal endothelial pigment 2. pigment dusting in the angle 3. retroillumination defect of the iris

Front 636

in what quadrant of the lens do you find a mittendorf's dot most commonly

Back 636

nasal or inferonasal

Front 637

what are the three general types of age-related cataracts

Back 637

1. nuclear 2. cortical 3. subcapsular

Front 638

what the the most common type of cataract you will see

Back 638

nuclear

Front 639

what is a nuclear cataract

Back 639

Diffuse sclerosis (yellowing) of nuclear area

Front 640

what wavelength is reduced in neclear cataracts

Back 640

blue wavelengths. that is why older ladies have blue hair and don't realize it.

Front 641

what do you need to do to see a nuclear cataract

Back 641

Lens may look clear upon retroillumination ((need an angled beam to see it)

Front 642

what is rubeosis (in the lens)

Back 642

advanced form of nuclear cataract

Front 643

what is a cortical cataract

Front 644

describe the progression of cortical cataracts

Back 644

start in the periphery and move centrally

Front 645

what quadrant of the lens do cortical cataracts tend to start in

Back 645

inferior-nasal area

Front 646

what is the best way to see a posterior subcapsular cataract

Back 646

retroillumination (red reflex)

Front 647

what is the most visually debilitating of the three major types of cataracts

Back 647

posterior subcapsular because it is right on the visual axis

Front 648

is anterior or posterior subcapsular cataract more common

Back 648

posterior

Front 649

describe the etiology of anterior subcapsular cataract

Back 649

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

Front 650

usually senile nuclear sclerosis appears before posterior subcapsular cataract.

Front 651

what is the most common pre-senile cause of posterior subcapsular cataracts

Back 651

steroid use

Front 652

what is the best way to see a posterior subcapsular cataract

Back 652

retroillumination (red reflex) with the direct ophthalmoscoe (not slit lamp)

Front 653

describe the age of onset of lamellar cataracts

Back 653

almost invariably congenital

Front 654

what are lamellar cataracts

Back 654

Involve lamella of fetal or nuclear zones Radial spoke-like opacities (riders) Frequently surround the cataract

Front 655

describe the LOCS grading system for cataracts

Back 655

LOCS Grading Intervals (1989): Nuclear color (NC)

Front 656

how do cataracts affect contrast sensativity

Back 656

a lot. they could still have 20/20 vision, but severely reduced contrast sensativity. -pelli-robson chart is most clinically applicable techinque

Front 657

name and describe the classification of cataract maturity

Back 657

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

Front 658

what is this

Back 658

morgagnian cataract

Front 659

what is a morgagnian cataract

Back 659

total liquifaction of the cortex of the lens, which causes the nucleus to sink inferiorly

Front 660

what ocular condition can occur secondary to a morgagnian cataract

Back 660

phacolytic glaucoma. if the lens capsule breaks.

Front 661

what are the categories of cataract based on age of onset

Back 661

congenital, infantile, juvenile, adult, senile

Front 662

is a unilateral or a bilateral congenital cataract a worse prognosis

Back 662

unilateral is actually a worse prognosis because of the potential of developing amblyopia.

Front 663

what are the surgical indications for congenital cataract

Back 663

bilateral advanced cataract, unilateral cataract.

Front 664

if you rx contact lenses for an infant with no crystaline lens, you need a commitment on the part of the parents.

Front 665

what is the VA cutoff for insurance to cover cataract surgery

Back 665

20/40 or worse at this point

Front 666

how is the power of the IOL calculated in cataract surgery

Back 666

by using Ks and axial length.

Front 667

what are the two types of IOL implantations based on their location

Back 667

posterior chamber IOL and anterior chamber IOL

Front 668

when is an anterior chamber IOL done

Back 668

Used if posterior capsular rupture Also used if complete lens extraction performed

Front 669

describe the risks associated with anterior chamber IOLs (3)

Back 669

More risks: uveitis, corneal endothelial decompensation, chronic cystoid macular edema (CME)

Front 670

what is the name for the current proceedure for cataract removal

Back 670

extracapsular cataract extraction and phacoemulsification.

Front 671

what are the names for the two parts of an IOL

Back 671

optic, and haptic

Front 672

cataract pts may require an asymmetric add power if unilateral and they sill have accommodative ability

Front 673

what test is a must before referral for cataract surgery

Back 673

potential acuity

Front 674

name three tests that test for potential acuity

Back 674

Potential Acuity Meter Super Pinhole Laser Interferometry

Front 675

under what conditions should the potential acuity meter (PAM) test be done and why

Back 675

this test is best done while the pt is dilated. the test works by projecting around the cataract.

Front 676

how does the laser interformeter work

Back 676

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

Front 677

what is the difference between disability glare and discomfort glare

Back 677

disability glare reduced visual acuity, discomfort glare is just uncomfortable

Front 678

New lecture: 6 Cataract Comgt 2009

Front 679

what is the most common refractive error change associate with cataract formation

Back 679

myopic. not always the case, but usually.

Front 680

with cataracts is the best refraction or the pinhole better acuity

Back 680

commonly the pinhole will proved better acuity because you are reducing light scatter. you might want to do the pinhole over their refraction.

Front 681

think about treating lid disease before sending a pt in for eye surgery to reduce the risk of infection.

Front 682

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.

Front 683

high hyperopes are at a greater risk for cataract surgery because smaller eyes are harder to work on. <20 mm axial length.

Front 684

name one pharmaceutical contraindication to cataract surgery

Back 684

flomax

Front 685

tearing is normal after cataract surgery, but not excessive. if excessive you need to consider that there might be a leak.

Front 686

pain is associated with ocular hypertension and ocular hypotension

Front 687

New lecture: Glaucoma Classification Fall 09 Vault

Front 688

what is glaucoma

Back 688

A group of ocular diseases of the optic nerve involving loss of retinal ganglion cells with progressive optic neuropathy.

Front 689

how many types of glaucoma are there

Back 689

about 60

Front 690

what is a primary glaucoma

Back 690

not associated with any other apparent ocular or systemic disorder

Front 691

what is primary open-angle glaucoma

Back 691

Aqueous outflow is reduced on submicroscopic and or biomechanical level. The angle is usually open!!

Front 692

what is secondary glaucoma

Back 692

Caused by a variety of ocular and/or systemic disorders: Causes decrease in aqueous outflow leading to either: Open or closed angle glaucoma

Front 693

what are developmental glaucomas

Back 693

due to abnormalities in the anterior chamber angle. abnormalities during gestation

Front 694

what is the most common form of adult glaucoma

Back 694

open angle glaucoma

Front 695

what is the order of structures seen on gonioscopy from posterior to anterior

Back 695

ciliary body, scleral spur, trabecular meshwork, schwalbe's line

Front 696

what is closed angle glaucoma

Back 696

aqueous flow is obstructed by the root of the iris

Front 697

what condition is pigmentary glaucoma associated with

Back 697

secondary to pigmentary dispersion syndrome

Front 698

what is the pathophysiology of pigmentary glaucom

Back 698

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.

Front 699

what is a pupillary block

Back 699

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.

Front 700

what is the difference between pigmentary dispersion syndrome and pigmentary glaucoma

Back 700

pigmentary glaucoma is pigmentary dispersion syndrome with optic nerve head damage.

Front 701

what percent of pts with pigmentary dispersion syndrome will develop pigmentary glaucoma

Back 701

30-50%

Front 702

what is reverse pupil block

Back 702

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.

Front 703

what is iris bombe

Back 703

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.

Front 704

what is the age of onset of pigmentary dispersion syndrome/pigmentary glaucoma

Back 704

younger. age 20-50.

Front 705

what ethnicity is pigmentary glaucoma most common in

Back 705

caucasians. unusual in african americans or asians.

Front 706

is the conversion from pigmentary dispersion syndrome to pigmentary glaucoma more common in men or women

Back 706

Sex predilection: PDS is equal in men and women. PG is More common in men

Front 707

is there a genetic component to pigmentary glaucoma

Back 707

yes. AD.

Front 708

what type of refractive error is associated with pigmentary glaucoma and why

Back 708

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.

Front 709

is pigmentary glaucoma usually unilateral or bilateral

Back 709

most commonly bilateral, though often asymmetrical

Front 710

what three clinical signs indicate pigmentary glaucoma

Back 710

1. krukenberg spindle 2. iris transillumination defects 3. pigment deposition on the trabecular meshwork

Front 711

what is the best way to see krukenberg spindle

Back 711

indirect illumination.

Front 712

what is krukenberg spindle

Back 712

vertical accumulation of pigment on the central corneal endothelium

Front 713

what is the name for a pigmented line found anterior to schwalbe's line on gonioscopy

Back 713

sampaolesi's line

Front 714

what shape of the iris is common to find on gonioscopy in pts with pigmentary glaucoma

Back 714

mid-peripheral concavity

Front 715

are there any activities associated with pigment liberation in pigmentary glaucoma

Back 715

strenuous exercise, dilation. these may be accompanied by IOP spike and clinical symptoms associated (HA, pain, halos etc.)

Front 716

what is the difference between pseudoexfoliative glaucoma and pseudoexfoliation syndrome

Back 716

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

Front 717

what is pseudoexfoliative glaucoma

Back 717

Characterized by flakes of granular material at the pupillary margin of the iris and throughout the inner surface of the anterior chamber.

Front 718

other names for pseudoexfoliative glaucoma

Back 718

Glaucoma capsulare, glaucoma senilis, basement membrane exfoliation syndrome, and senile exfoliation syndrome to name a few.

Front 719

describe the pathophysiology of pseudoexfoliative glaucoma

Back 719

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

Front 720

you need to dilate in order to see pseudoexfoliative glaucoma.

Front 721

not all pts with pseudoexfoliative syndrome go on to develop pseudoexfoliative glaucoma

Front 722

describe the age of onset of pseudoexfoliative glaucoma

Back 722

onset most commonly between 60 and 80 year old. rarely seen before age 50

Front 723

prevalance of pseudoexfoliative glaucoma varies a lot by ethnicity and location

Front 724

are men or women with pseudoexfoliative syndrome more likely to develop pseudoexfoliative glaucoma

Back 724

men

Front 725

is pseudoexfoliative glaucoma usually unilateral or bilateral

Back 725

usually starts unilateral, but becomes biateral in most cases.

Front 726

what percent of people with pseudoexfoliative syndrome will develop pseudoexfoliative glaucoma

Back 726

15%. a higher percent develop high IOPs, but no ONH damage.

Front 727

describe 6 clinically observable objective signs indicating pseudoexfoliative glaucoma

Back 727

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)

Front 728

how can you differentiate pseudoexfoliative glaucoma from pigmentary glaucoma

Back 728

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.

Front 729

what is neovascular glaucoma

Back 729

A condition associated with IOP elevation due to synechial angle closure resulting from fibrovascular membrane formation obstructing aqueous outflow.

Front 730

describe the pathophysiology associated with neovascular glaucoma

Back 730

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)

Front 731

early detection in neovascular glaucoma is crucial. it is also very hard to see; you need to use high magnification.

Front 732

name four major conditions that can cause neovascular glaucoma

Back 732

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%)

Front 733

what is the earliest sign of neovascular glaucoma

Back 733

small dilated vessels at the pupillary margin

Front 734

describe the mechanism of progression of neovascular glaucoma

Back 734

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).

Front 735

if the trabecular meshwork starts to turn red, it means that you are pushing to hard with the goino lens.

Front 736

describe 4 clinically observable objective signs associated with neovascular glaucoma

Back 736

1. neovascularization 2. cells and flare as vascular proliferation develops 3. hyphema 4. peripheral anterior synechia

Front 737

describe the mechanism for peripheral antrior synechia in neovascular glaucoma

Back 737

neovascular membrane forms, which can contract and pull the iris forming anterior synechia

Front 738

in ligher pigmented irides it is possible for the normal iris vasculature to look like neovascularization of the iris

Front 739

describe four mechanisms for angle closure glaucoma

Back 739

Iris (pupilary block) Ciliary body (plateau iris) Lens (phacomorphic glaucoma) Posterior to the lens (malignant glaucoma)

Front 740

what is primary angle closure glaucoma with pupil block

Back 740

adherence between the back of the iris and the front of the lens that prevents aqueous from passing forward to the anterior chamber.

Front 741

posterior synechia can result in iris bombe, causing angle closure glaucoma

Front 742

how soon after dilation is angle closure likely to happen

Back 742

a couple hours. becuase angle closure glaucoma is most likely to happen when the pupil is mid-dilated.

Front 743

list 8 signs and symptoms associated with acute angle closure.

Back 743

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

Front 744

what is plateau iris

Back 744

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.

Front 745

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

Front 746

what is phacomorphic glaucoma

Back 746

due to lens swelling leading to shallower anterior chamber.

Front 747

what type of glaucoma is phacomorphic glaucoma

Back 747

secondary angle closure glaucoma

Front 748

what type of glaucoma is malignant glaucoma

Back 748

secondary angle closure glaucoma

Front 749

what is malignant glaucoma

Back 749

Posterior misdirection of aqueous into the vitreous. Increases post seg pressure. Angle closure due to posterior forces pushing the lens-iris diaphragm forward.

Front 750

how common is malignant glaucoma

Back 750

very rare. Dr. Dina Erickson has never seen one.

Front 751

New COURSE: Ocular Disease III

Front 752

New lecture: 1 Glaucoma Risk Factors, Signs and Visual Field 2010 (study this one)

Front 753

where does glaucoma rank in terms of causing blindness in the US

Back 753

3rd (macular degeneration and diabetes are number 1 and 2)

Front 754

what race is more prone to developing glaucoma

Back 754

african american

Front 755

is blood pressure related to eye pressure

Back 755

no, but hypertension is a risk factor for glaucoma

Front 756

systemic diseases linked to glaucoma

Back 756

1. diabetes 2. hypertension/hyperlipidemia 3. systemic vascular disease

Front 757

are smoking and drinking a risk factor for glaucoma

Back 757

yes

Front 758

list 6 ocular risk factors for glaucoma

Back 758

1. IOP 2. ONH characteristics 3. angle abnormalities 4. corneal thinkness 5. myopia 6. visual field defects

Front 759

what is the name of the test that measures corneal thickness

Back 759

pachymetry

Front 760

OHTS: ocular hypertension treatment study

Front 761

what are the most common subjective symptoms at the time of diagnosis for POAG

Back 761

almost every POAG pt is asymptomatic at the time of diagnosis

Front 762

how does glaucoma affect VA

Back 762

usually not affected unless the papillomacular bundle of the NFL is affected in advanced cases

Front 763

is there an RAPD in glaucoma

Back 763

not usually, only if it is asymmetrical.

Front 764

describe the onset of traumatic glaucoma

Back 764

can be years after innitial injury. (related to angle recession)

Front 765

what types of glaucoma are related to krukenberg's spindle

Back 765

pigmentary glaucoma, pseudoexfoliative glaucoma

Front 766

is there pain assoicated with glaucoma

Back 766

only actue glacoma with extremely high IOP. most glaucoma is painless.

Front 767

if you see neovascularization of the iris you need to refer to a retinal specialist

Front 768

what is the normal range for IOP

Back 768

10-21 mmHg (average is 16)

Front 769

why time of day is IOP highest

Back 769

early morning is highest

Front 770

how does glaucoma influence diurnal variation

Back 770

much greater diurnal variation than normal

Front 771

greater than ____ difference in IOP between the two eyes is suspicious

Back 771

2 mmHg

Front 772

what percent of people with primary open angle glaucoma have IOP less than 22 mmHg at the time of diagnosis

Back 772

50%

Front 773

there is no normal pressure. the higher the IOP the greater the risk of developing glaucoma.

Front 774

what IOP is high enough to treat based on IOP alone

Back 774

30 mmHg -you should definately check corneal thickness though

Front 775

corneal curvature can distort the mires and give you a false goldmann IOP reading

Front 776

how can exophthalmos affect IOP

Back 776

artifically high because of pressure behind the eye pushing the eye forward.

Front 777

what is the instrument that a pt can take home and measure IOP at home called

Back 777

proview

Front 778

how does corneal thickness impact IOP

Back 778

Thin corneas underestimate IOP Thick corneas overestimate IOP

Front 779

how does LASIK impact IOP and why

Back 779

falsely lowers IOP because the cornea is thinner

Front 780

what type of corneal thickness is a risk factor for glaucoma

Back 780

thin cornea: < 555 microns higher risk* > 588 microns lower risk*

Front 781

what is normal corneal thickness

Back 781

550 microns (545 precisely)

Front 782

corneal disease/surgery can affect central corneal thickness: fuch's endothelial dystrophy, keratoconus, LASIK

Front 783

what things do you need to record when doing gonioscopy

Back 783

1. iris approach 2. most posterior structure visible 3. amount of pigment 4. angle recession present or not 5. any abnormalities

Front 784

what are the types of iris approaches as seen on gonioscopy

Back 784

flat, bowed, plateau, concave

Front 785

what is angle recession and iridodialysis

Back 785

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.

Front 786

in what quadrant are you most likely to see pigment on gonioscopy and why

Back 786

inferior because of gravity

Front 787

what is sampolisi's line

Back 787

a line of pigment deposited on schwalbe's line

Front 788

what is this

Back 788

angle recession

Front 789

what is the mechanism for angle recession glaucoma

Back 789

scarring that results from the tearing of the iris root blocks the trabecular meshwork.

Front 790

how does direct ophthalmoscopy tend to influance CD ration

Back 790

tends to underestimate because you are monocular and not getting a 3D view.

Front 791

progressive thinning of the neural rim is pathonogmonic for glaucom

Front 792

what structure determines the ONH size

Back 792

scleral canal

Front 793

how many nerve fibers are there in the optic nerve

Back 793

1.2 million (every 90 minuets we lose one of them)

Front 794

what is the range of normal ONH sizes

Back 794

1.33-2.66 mm

Front 795

how does ONH size relate to CD

Back 795

usually the bigger the nerve head the larger the CD

Front 796

do myopes or hyperopes usually have large optic nerve heads

Back 796

myopes

Front 797

what are two ways to measure the size of the ONH

Back 797

use the reticule in the slit lamp, or estimate how many blood vessel widths it is.

Front 798

if you estimate ONH size by blood vessel width what is normal, large and small

Back 798

12 blood vessel widths is normal, 15 is large, 9 is small

Front 799

nwhat do you need to look at before you look at CD

Back 799

ONH size

Front 800

another trick for estimating ONH size

Back 800

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

Front 801

at what CD do you start getting suspicious of glaucoma (if all else is normal)

Back 801

0.6

Front 802

when writing the CD does the horizontal or the vertical ratio come first

Back 802

horizontal over vertical (H/V)

Front 803

if you have a deep cup, what do you expect to see at the base of the cup

Back 803

lamina cribosa (laminar dots)

Front 804

what type of elongation is a risk factor for glaucoma

Back 804

vertical elongation of CD is a risk factor for glaucoma. -glaucoma usually affects the inferior rim first

Front 805

what is the ISN'T rule

Back 805

the normal ONH should be thickest inferiorly and thinnest temporally.

Front 806

temporal part of the cup may look more pale than the rest of the disc, but this is normal.

Front 807

name 9 optic nerve head signs that would indicate glaucoma

Back 807

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

Front 808

there are many many things that can mimic glaucoma

Front 809

YOU CAN HAVE NORMAL-LOOKING NERVES AND HAVE GLAUCOMA! YOU CAN ALSO HAVE GLAUCOMATOUS CUPPING AND NO FIELD LOSS!

Front 810

BIO is a great way to look at the nerve fiber layer

Front 811

look for NFL defects in glaucoma

Front 812

how does the fundus appear when you have nerve fiber damage form glaucoma

Back 812

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

Front 813

what is it called when the blood vessels are more bright and sharp and crisp because of NFL atrophy

Back 813

bearing of the circumlinear vessels

Front 814

what are the circumlinear blood vessels

Back 814

-circumlinear vessels are the ones that eminate from the disc

Front 815

rarely you can have arteroirlar pulsation with very high IOP

Front 816

name 4 objective retinal signs that indicate glaucoma (ONH changes only 1)

Back 816

1. optic disc changes 2. NFL defects 3. collateral/shunt vessel formation 4. DRANCE HEMORRHAGE

Front 817

what location do you usually see drance (splinter) hemorrhages in

Back 817

interior-temporal to the disc

Front 818

what is the best way to see a splinter hemorrhage

Back 818

use the red-free filter

Front 819

name four conditions other than glaucoma that can cause drance (splinter) hemorrhage

Back 819

AION, pipillitis, HTN, DM

Front 820

what is a "bean pot" cup

Back 820

rim becomes undermined

Front 821

what is the only subjective test for glaucoma

Back 821

visual fields

Front 822

what does higher decibels on a visual field indicate? what about apostilbs?

Back 822

higher decibels equals more sevsitive. decible are inverse to apostilbs (amount of brightness)

Front 823

how many degrees does a 30-2 visual field cover

Back 823

60 degrees.

Front 824

what is usually the first sign of glaucoma

Back 824

paracentral scotomas between 5 and 20 degrees of fixation

Front 825

describe the progression of visual field loss assoicated with glaucoma

Back 825

paracentral scotomas, arcuate scotoma, double arcuate scotoma, temporal wedge defect (nasal fibers are finally affected), overall field constriction, overall field depression.

Front 826

what is the most important indicator on a visual field printout

Back 826

pattern deviation plot

Front 827

what is the mean deviation of a visual field

Back 827

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.

Front 828

what is the pattern standard deviation of a visual field

Back 828

the irregularity of the overal field from the normal

Front 829

what is the short-term fluctuation (SF) of a visual field

Back 829

measures consistancy or responses twice at 10 pre-selected points

Front 830

what is the corrected pattern standard deviation (CPSD) of a visual field

Back 830

measures intra-test variability of field shape to reference while taking consistency into account

Front 831

what factors do the total deviation and pattern deviation take into account on a visual field

Back 831

total deviation does not taking into consideration age, and media opacification. but pattern deviation does.

Front 832

glaucoma hemifield test is not 100% reliable

Front 833

the only thing that is consistant about a glaucomatous visual field is that it will be inconsistant

Front 834

what is FASTPAC

Back 834

speeds up visual field exam by using age-reference statistics

Front 835

blue on yellow perimetry is though to pick up glaucomatous visual field changes earlier by 3-4 year

Front 836

what is SITA-standard/fast

Back 836

threshold adjustment to speed test without data compromise

Front 837

why is FDT supposed to pick up glaucomatous changes earlier

Back 837

we think that the magnocellular ganglion cells die first in glacoma, and the FDT attempts to isolate them due to flicker of target.

Front 838

scanning laser ophthalmoscopy that looks at the nerve fiber thickness

Back 838

HRT, RTA (retinal thickness analyzer), GDx, OCT,

Front 839

New lecture: 2 Glaucoma Treatment Slides 2010 (study this one)

Front 840

describe the progression of treatment types in the US

Back 840

Medical (Pharmacologic) Laser Treatment (Laser Trabeculoplasty) Surgery (Filtration/Bleb/Trabeculectomy)

Front 841

describe the active and passive forms of aqueous secretion from the ciliary body

Back 841

Non-pigmented ciliary epithelium (active) ((enzyme: carbonic anhydrase) Ultrafiltration & diffusion (passive)

Front 842

describe the two pathways of aqueous outflow from the eye

Back 842

Trabecular meshwork à Schlemm’s ? Veins Uveoscleral outflow ? CB ? SC Space ? Sclera

Front 843

describe the three theories as to why the ONH fibers die in glaucoma

Back 843

Direct Mechanical Theory Ocular pressure blocks axoplasmic flow Ischemic Theory Ocular pressure blocks circulation to nerve Apoptosis “Programmed cell death”, mediators involved Genetic predisposition

Front 844

describe the main categroies of anti-glaucoma drus and whether they decrease aqueous production or increase aqueous outflow

Back 844

Reduce Aqueous Production Beta-blockers, Alpha-2 agonists, CAIs Increase Aqueous Outflow Miotics, adrenergic/Alpha-2 agonists, prostaglandins/prostamides, docosanoids(?)

Front 845

name 5 carbonic anhydrase inhibitors

Back 845

Dorzolamide

Front 846

what tissues have beta 1 adronergic receptors and which have beta 2

Back 846

Beta 1 Heart muscle Tachycardia, increased cardiac output when stimulated Beta 2 Bronchial muscle Bronchial dilation when stimulated

Front 847

name 5 topical beta-blockers

Back 847

Timolol Betaxolol Levobunolol Metipranolol Carteolol

Front 848

which is the only topcial beta-blocker that is beta-1 selective

Back 848

Betaxolol is the only Beta-1 selective Beta-blocker

Front 849

what is the trade name for timoptic

Back 849

timoptic

Front 850

what is the trade name for timolol that comes in a gel

Back 850

timoptic XE

Front 851

what is the trade name for betaxolol

Back 851

betoptic

Front 852

what is the difference between betoptic and Betoptic S

Back 852

Betoptic is a solution; Betoptic S is a suspension

Front 853

how many times a day do you take timolol, betaxolol, levobunolol, metipranolol, and carteolol

Front 854

why would you need to chose a beta-1 selective beta blocker

Back 854

(betaxolol) for asthmatics

Front 855

what is the trade name for levobunolol

Back 855

betagan

Front 856

what is the trade name for metipranolol

Back 856

optipranolol

Front 857

what is the trade name for carteolol

Back 857

ocupress

Front 858

which beta blocker stings the least

Back 858

carteolol

Front 859

how much do beta-blocker usually reduce IOP by

Back 859

20-30%

Front 860

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

Front 861

what should you have the pt do while taking beta blocker

Back 861

punctal occlude to reduce systemic absorption

Front 862

what do you need to check before you start a pt on beta-blockers and while they are on them

Back 862

Always check blood pressure, pulse, and respiratory status before initiating B-blocker

Front 863

who should you avoid using beta blockers on if possible

Back 863

Avoid if possible with asthmatics, COPD, bradycardia/CHF and DM/chol patients

Front 864

are beta blockers additive to other drugs in terms of their IOP reducing capabilities

Back 864

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)

Front 865

Oral beta-blockers (eg: atenolol) used for HTN may also reduce IOP (30%) as beneficial side-effect

Front 866

what is the mechanism for the reduction of IOP with carbonic anhydrase inhibitors

Back 866

Inhibits carbonic anhydrase enzyme in ciliary epithelium from producing aqueous

Front 867

how much do carbonic anhydrase inhibitors reduce IOP by

Back 867

15-20 percent

Front 868

are carbonic anhydrase inhibitors used by themselves or in conjunction with other IOP lowering drugs

Back 868

rarely used by themselves

Front 869

name two topical carbonic anhydrase inhibitors

Back 869

Dorzolamide Brinzolamide

Front 870

what is the trade name for dorzolamide

Back 870

trusopt

Front 871

what is cosopt

Back 871

dorzolamide and tomolol maleate

Front 872

what is the dosage for dorzolamide

Back 872

TID

Front 873

what is the trade name for brinzolamide

Back 873

azopt

Front 874

does dorzolamide or brinzolamide sting less

Back 874

brinzolamide stings less

Front 875

name three systemic carbonic anhydrase inhibitors

Back 875

acetazolamide (diamox), methazolamide, dichlorphenamide

Front 876

what are systemic carbonic anhydrase inhibitors used for

Back 876

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.

Front 877

name three adrenergic agonists

Back 877

Dipivefrin

Front 878

name two cholinergic agonists (miotics)

Back 878

Pilocarpine

Front 879

name three prostaglandins

Back 879

Latanoprost

Front 880

name four hyperosmotics

Back 880

Glycerol – Isosorbide (the next two are only used if the pt is hospitalized) Mannitol – -Urea

Front 881

what is the trade name for dpipvefrin

Back 881

propine

Front 882

what is dipivefrin

Back 882

Prodrug – converts to epinephrine

Front 883

how much does dipivefrin lower IOP by

Back 883

15 to 20%. pupil dilation with initial IOP elevation.

Front 884

what is the trade name for apraclonidine

Back 884

Iopidine

Front 885

what is apraclonidine used for

Back 885

angle closure glaucoma. up to 40% drop.

Front 886

what is the trade name for brimonidine

Back 886

alphagan

Front 887

how much does brimonidine lower IOP by

Back 887

25 to 30%

Front 888

what is combigan

Back 888

combo drug with brimonidine and timolol

Front 889

what drug is pilocarpine not effective with

Back 889

latanoprost

Front 890

what is the trade name for latanoprost

Back 890

xalatan

Front 891

by what mechanism does latanoprost incrase aqueous outflow

Back 891

incrases uveoscleral outflow

Front 892

by how much does latanoprost lower IOP

Back 892

30 to 35%

Front 893

what drug is lattice and what are the side effects

Back 893

irreversable iris darkening and lash thickening

Front 894

by how much does travaprost lower IOP

Back 894

30%

Front 895

what is the trade name for bimatoprost

Back 895

lumigan

Front 896

lumigan probably lowers IOP more than other prostaglandins

Front 897

when are hyperosmotics indicated for glaucoma

Back 897

acute angle closure

Front 898

you wouldn't want to use glycerol on a diabetic because it is sugar water, but you could use isosorbide

Front 899

when would you use a steroid to tx glaucoma

Back 899

Steroids may reduce IOP in certain inflammatory glaucoma conditions ((TM is inflammed and outflow is blocked)

Back 900

picture (click on picture to make it bigger)

Front 901

glaucoma tx: consider monocular trial to start so you will have a control to see how your tx is working.

Front 902

minimum follow up for glaucoma is 3 months

Front 903

New lecture: 3 ONHstu6332010

Back 903

a

Front 904

Describe the shape of a normal optic disc and the shape of a normal cup

Back 904

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.

Front 905

With a malinserted disc which side is most commonly raised and which side is most commonly depressed

Back 905

Usually raised nasal side and depressed temporal margin

Front 906

How does a malinserted disc affect vision

Back 906

usually no visual effect

Front 907

What is the congenital condition called where the disc is rotated from 90 degrees but remains in the plane of the retina.

Back 907

a tilted disc

Front 908

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.

Back 908

malinserted disc

Front 909

how can you differentiate a congenital retinal condition from an acquired retinal condition based on laterality

Back 909

congenital retinal conditions are ofted bilateral and look identical between the two eyes. acquired retinal conditions often look different between the two eyes.

Front 910

Which direction is a tilted disc usually displaced

Back 910

so that the elongated meridian is pointing in a supero-nasal and infero-temporal direction.

Front 911

Name 7 diagnostic findings that indicate there is a tilted disc

Back 911

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

Front 912

How do you differentiate the bi-temporal visual field defect caused by a tilted disc from one caused by a neurological defect

Back 912

if it is cause by a tilted disc then it will not respect the vertical midline.

Front 913

What side of the disc are normal choroidal and scleral crescents usually found

Back 913

temporal

Front 914

Describe the physiology of a choroidal crescent

Back 914

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

Front 915

describe the physiology of a scleral crescent

Back 915

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.

Front 916

What should you look for if you see a choroidal or a scleral crescent

Back 916

anything that might be pulling the retina away from the disc. For example, myopia, retinopothy of prematurity

Front 917

do hyperopes or myopes tend to have less distinct disc margins and why

Back 917

hyperopes, because there is the same amount of nerve fibers covering a smaller amount of the ONH

Front 918

When you see myelinated fibers on the retina is it typically unilateral or bilateral

Back 918

unilateral

Front 919

if you see myelinated fibers on the retina how would you expect this to affect VAs

Back 919

usually no effect on VA

Front 920

how do you differentiate between myelination and cotton wool spots base on apperience (3 points)

Back 920

Cotton wool spots are typically more yellow, smaller and less striated than myelation

Front 921

look up physiology of drusen

Front 922

is ONH drusen usually unilateral or bilateral

Back 922

bilateral over 70 percent of the time

Front 923

how does ONH drusen tend to affect blood vessel apperance

Back 923

blood vessels branch prematurly

Front 924

Does ONH drusen tend to become more or less obvious with age

Back 924

more

Front 925

name two negative affects that can be caused by ONH drusen and their mechanisms

Back 925

visual field loss and circumpapillary hemorrhaging leading to choroidal neovascularization due to the drusen blocking axoplasmic flow and blood supply respectively.

Front 926

Describe the management of ONH drusen

Back 926

there is no treatment. monitor for field loss and development of neovascularization.

Front 927

Papilledema

Back 927

Papilledema reserved for bilateral swelling due to increased intracranial pressure

Front 928

describe five visably observable findings you can see with papilledema

Back 928

blurry margins, hyperemia, intra-retinal hemorrhages, cotton wool spots, loss of spontaneous venous pulsation.

Front 929

how can you induce spontaneous venous pulsation clinically if you don't see it on a normal patient

Back 929

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.

Front 930

what is the average optic nerve head size vertically and horizontally

Back 930

1.88 mm vertically and 1.77 mm horizontally

Front 931

how far from the ONH is the macula

Back 931

2-2.5 disc diameters

Front 932

should you includ a scleral ring as part of the C/D measurement

Back 932

no

Front 933

What is the physiological cuase of ONH hypoplasia

Back 933

Congenital defect due to failure of ganglion cells to develop

Front 934

is ONH hypoplasia unilateral or bilateral

Back 934

can be either

Front 935

describe three visually observable signs you tend to see with optic nerve head hypoplasia

Back 935

small ONH, double ring sign, tortuous blood vessels.

Front 936

double ring sign

Back 936

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.

Front 937

what types of visual consequences can you expect with ONH hypoplasia.

Back 937

Decreased VA (normal to light perception) VF loss Defective color vision APD if unilateral Strabismus ((in unilateral cases) Nystagmus (especially in bilateral cases)

Front 938

What is your main concern is you see bilateral optic nerve head hypoplasia

Back 938

there is an increased risk of associated systemic disorders

Front 939

what condition is often mistakenly diagnosed, when the true disorder is ONH hypoplasia

Back 939

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

Front 940

describe the management for OHN hypoplasia

Back 940

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.

Front 941

name two of the common systemic anomolies you often find with ONH hypoplasia

Back 941

pituitary disfunction and De Morsier Syndrome

Front 942

what is De Morsier's syndrome

Back 942

thinning of the optic nerves and chiasm, absence of the septum pellucidum, and agenesis of the corpus callosum. Systemic anomoly associated with ONH hypoplasia.

Front 943

in what portion of the disc does an ONH coloboma usually occur

Back 943

inferior

Front 944

how does the size of the ONH of a disc with a coloboma compair to the size of one without a coloboma

Back 944

the disc of an ONH with a coloboma will be larger than a normal disc

Front 945

are ONH colobomas usually unilateral or bilateral

Back 945

can be either unilateral or bilateral

Front 946

how is vision impacted from a ONH coloboma

Back 946

VA is variable (but can be reduced to light perception). visual field loss is common and often pretty dramatic.

Front 947

are ONH colobomas associated with retinal detachment

Back 947

there is a strong association btwn ONH colobomas and non-rhegmatongenous RDs that occur early in life (2nd or 3rd decade).

Front 948

are there systemic findings associate with ONH coloboma

Back 948

yes: CHARGE: coloboma, heart dz, atresia choanae, retarded growth, genital hypoplasia, ear abnormalities.

Front 949

describe the anatomical changes that take place in morning glory disc anomoly

Back 949

funnel shapped excavation of the posterior globe.

Front 950

in morning glory disc anomoly how does the size of the disc compair to a normal disc

Back 950

morning glory disc anomoly has a larger than normal disc size.

Front 951

describe the apperance of the blood vessels exiting the disc in morning glory disc anomoly (3 points)

Back 951

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.

Front 952

is morning glory disc anomoly usually unilateral or bilateral

Back 952

usually unilateral

Front 953

how is vision impacted by morning glory disc anomoly

Back 953

VA is variable from barely reduced to hand motion

Front 954

name two systemic findings associated with morning glory disc anomoly

Back 954

hypertelorism and transsphenoidal encephalocele

Front 955

is morning glory disc anomoly associated with retinal detachment? What percent?

Back 955

there is a strong association with non-rhegmatogenous RD. about 30%

Front 956

describe the management of morning glory disc anomoly

Back 956

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.

Front 957

describe the pigment changes associated with an ONH pit

Back 957

Peripapillary RPE disturbance common if not central pit

Front 958

is the disc size of a nerve with an ONH pit larger or smaller than one without

Back 958

If unilateral, ONH larger on side with pit ((almost always)

Front 959

in what portion of the disc is a pit most commonly found

Back 959

usually temporally, often inferiorly

Front 960

describe the anatomical mechanism of an ONH pit

Back 960

Histologically, a pit consists of dysplastic retina that has herniated posteriorly through a defect in the lamina cribrosa

Front 961

are ONH pits usually unilateral or bilateral. what percent of the time.

Back 961

unilateral 85% of the time

Front 962

how does an ONH pit affect vision

Back 962

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

Front 963

how does the location of an ONH pit affect the liklihood of developing a retinal detachment

Back 963

if the pit is central, they are much less likely to develop a retinal detachment

Front 964

is ONH pit typically associated with other systemic anomolies

Back 964

no

Front 965

describe the management of ONH pits (3 steps)

Back 965

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.

Front 966

are optic nerve head pits associated with any other systemic anomolies

Back 966

no

Front 967

if you have a larger than average ONH due to physiological variation, would you expect a larger or smaller than normal C/D ratio

Back 967

larger

Front 968

at what difference in C/D between an individuals two eyes would you start to be concerned

Back 968

0.2 or greater asymmetry in absence of different optic disc sizes or anisometropia is highly suspicious

Front 969

how does the color of the ONH vary with location in the disc

Back 969

the temporal side is more pale and the nasal side is more pink

Front 970

how does the color of the ONH vary with sized of the disc

Back 970

small disc is pinker than a larger disc

Front 971

what is ONH pallor and what causes it

Back 971

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

Front 972

what clinical sign indicates ONH atrophy

Back 972

pallor

Front 973

name three common mechanisms that cause ONH pallor

Back 973

Often secondary to intracranial lesion, inflammation or trauma

Front 974

describe the ISN'T rule

Back 974

a way to remember how the ONH is supposed to look. it should be thickest inferiorly and thinnest temporally.

Front 975

what is one way to differentiate btwn vessels that are congenitally tortuous from those that are acquired

Back 975

If congenitally tortuous should involve both arteries and veins

Front 976

what is the most common position of the disc for vessels to exit

Back 976

Superior nasal most common position of exit

Front 977

what is a splinter or drance hemorrhage

Back 977

Flame-shaped hemorrhage just off optic nerve head

Front 978

name four major causes of a drance hemorrhage

Back 978

Commonly associated with glaucoma Also caused by PVD, Resolving BRVO, NPDR

Front 979

what is a peripapillary vascular loop

Back 979

twisted blood vessels

Front 980

are retinal detachments associated with ONH pits. what percent of the time

Back 980

yes: 45%, mean age is 30 years old

Front 981

New lecture: 4 DDxOpticNeuropst2010

Back 981

a

Front 982

optic neuropathy

Back 982

Pathological injury to the optic nerves or the blood supply to them

Front 983

name three common optic neuropathies

Back 983

Glaucoma is most common Optic neuritis (often associated with MS) Anterior ischemic optic neuropathy

Front 984

name five clinically observable findings you can see with optic neuropathy

Back 984

Decreased VA Decreased color vision Visual field defect RAPD in unilateral or asymmetric cases Optic disc edema or atrophy

Front 985

how do you differentiate between different optic neuropathies

Back 985

In most cases, appearance of nerve does not help differentiate Must use epidemiology information as well as associated signs and symptoms

Front 986

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

Back 986

diabetes and high blood pressure

Front 987

optic neuritis vs. papillitis vs. retrobulbar optic neuritis

Back 987

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.

Front 988

what is the syn. for papillitis

Back 988

anterior optic neuritis

Front 989

list of causative agents of optic neuropathy:

Back 989

MS Bacteria Syphilis, Lyme dz, Meningitis, Whipple’s dz Viruses Adenovirus, Rubella, Herpes zoster, Mumps, HIV Protozoa Toxoplasmosis Fungi

Front 990

what is the most frequent cause of optic neuritis

Back 990

MS is by far the most common cause of optic neuritis

Front 991

describe 5 clinical ocular findings commonly associated with a typical optic neuritis

Back 991

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

Front 992

how quick is the onset of VA loss due to a typical optic neuritis

Back 992

1 to 10 days

Front 993

describe the patient demographic most commonly associated with typical optic neuritis

Back 993

Usually young adult; female > male

Front 994

what percent of the time do you have periocular pain on eye movement with typical optic neuritis

Back 994

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)

Front 995

what percent of the time do you have swollen ONHs in a patient with optic neuritis

Back 995

Normal (65%) or swollen (35%) ONH

Front 996

what percent of the time does vision loss, due to typical optic neuritis, return to near normal and how long does this take

Back 996

Eventual visual improvement to near normal over weeks (90%)

Front 997

what test would be best for diagnosis of MS

Back 997

MRI of brain to look for lesions consistent with MS

Front 998

in what percent of cases of MS is optic neuritis the presenting sign

Back 998

35%

Front 999

in what percent of patient who have had a single episode of optic neuritis is MS diagnosed within 15 years

Back 999

>50%

Front 1000

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.

Back 1000

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

Front 1001

management of optic neuritis

Front 1002

describe the visual prognosis for optic neuritis

Back 1002

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.

Front 1003

what is the name of the optic neuropathy that causes an altitudinal visual field defect

Back 1003

anterior ischemic optic neuropathy

Front 1004

describe six clinical observable ocular findings commonly associated with anterior ischemic optic neuropathy

Back 1004

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

Front 1005

how quickly does vision loss from anterior ischemic optic neuropathy occur

Back 1005

onset hours to days

Front 1006

over what age do you expect to see anterior ischemic optic neuropathy

Back 1006

50

Front 1007

describe the appearence of the ONH in anterior ischemic optic neuropathy (3 points)

Back 1007

Pallid ONH edema in sector with or without peripapillary hemes

Front 1008

are there any premonitory signs or symptoms that occur with anterior ischemic optic neuropathy

Back 1008

No premonitory symptoms but may have disc edema as early sign

Front 1009

describe the prognosis for anterior ischemic optic neuropathy

Back 1009

poor; vision loss is usually permanent and may have continuing loss

Front 1010

what is a "disk at risk" and what is it a risk factor for

Back 1010

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.

Front 1011

what is the name of the condition that can potentially result in death that is associated with arteritic anterior ischemic optic neuropathy

Back 1011

giant cell arteritis

Front 1012

describe the etiology of anterior ischemic optic neuropathy

Back 1012

ischemic infarction of the anterior optic nerve due to occlusion of the posterior ciliary circulation just behind the lamina cribosa

Front 1013

what is the difference between arteritic and non-arteritic anterior ischemic optic neuropathy

Back 1013

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.

Front 1014

what is the most common cause of arteritic anterior ischemic optic neuropathy

Back 1014

giant cell arteritis

Front 1015

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

Back 1015

70%

Front 1016

what systemic outcome are we most concerned with giant cell arteritis

Back 1016

stroke and death

Front 1017

name five signs and symptoms you should check for if you are concerned that a pt has giant cell arteritis

Back 1017

HAs, scalp tenderness, jaw claudication, fever/malaise etc. Check for decreased temporal artery pulse with tenderness

Front 1018

name three tests you would want to do if you suspected giant cell arteritis

Back 1018

westergren erythrocyte sedimentation rate (elevated, not even close to normal), c-reactive protein, temporal artery biopsy

Front 1019

is a temporal artery biopsy 100% accurate for diagnosis of giant cell arteritis

Back 1019

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.

Front 1020

describe the managment of arteritic anterior ischemic optic neuropathy (5 steps)

Back 1020

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

Front 1021

is arteritic anterior ischemic optic neuropathy typically unilateral or bilateral

Back 1021

usually starts unilateral with a 70% chance of spreading to the fellow eye whithin 1 week if not treated

Front 1022

describe four cilincal findings commonly associated with optic disc edema with macular star

Back 1022

Peripapillary and macular exudate Swelling of ONH Vitreous cells APD if unilateral

Front 1023

what age range do you tend to see optic disc edema with macular star

Back 1023

young children to adult

Front 1024

does optic disc edema with macular star tend to be unilateral or bilateral (how much of the time)

Back 1024

Unilateral in 66%

Front 1025

how does optic disc edema with macular star affect vision

Back 1025

Variable VA (20/20 to LP) Dyschromatopsia

Front 1026

with optic disc edema with macular star does the disc edema and the macular star appear simultaneously

Back 1026

-macular star can appear up to two weeks after optic disc edema

Front 1027

what is the most common cause of optic disc edema with macular star

Back 1027

Most cases are idiopathic Possibly due to viral infection Hepatitis B, H. Simplex, H. Zoster, Epstein-Barr, Influenza Other common causes

Front 1028

describe the type of visual loss and the type of progression associated with compressive optic neuropathy

Back 1028

Painless, progressive, gradual loss of VA, VF and color vision

Front 1029

how does compressive optic neuropathy affect the nerve head

Back 1029

ONH edema and atrophy

Front 1030

list two causes of compressive optic neuropathy

Back 1030

Intracranial or intraorbital tumors Thyroid ophthalmopathy

Front 1031

is toxic optic neuropathy usually unilateral or bilateral

Back 1031

bilateral

Front 1032

describe the progression of vision loss associated with toxic neuropathy

Back 1032

symmetric, slowly progressive vision loss

Front 1033

what type of visual field defect do you tend to see with toxic or nutritional optic neuropathy

Back 1033

bilateral central or cecocentral scotomas

Front 1034

name five common causes of toxic or nutritional optic neuropathy

Back 1034

Ethambutol (TB drug)

Front 1035

describe the patient demographic most commonly associated with Leber's heriditary optic neuropathy

Back 1035

90% are males between ages of 18 -30

Front 1036

describe the progression of VA loss associated with Leber's heriditary optic neuropathy

Back 1036

Rapid, painless and unremitting VA loss. VA quickly reduced to the 20/200 level where it stabilizes.

Front 1037

what type of visual field loss is most commonly associated with Leber's heriditary optic neuropathy

Back 1037

Central or cecocentral VF loss NFL loss in papillomacular bundle

Front 1038

is Leber's heridiatary optic neuropathy usually unilateral or bilateral

Back 1038

Sequential bilateral involvement (2nd eye weeks to months later)

Front 1039

what is the mechanism that causes Leber's heriditary optic neuropathy

Back 1039

Mitochondrial DNA mutation

Front 1040

does Leber's heriditary optic neuropathy have any systemic conditions associated with it

Back 1040

Usually isolated but may have Cardiac conduction defects (heart block or WPW syndrome) Dystonia

Front 1041

describe three clinically observable findings associated with Lebers heriditary optic neuropathy

Back 1041

pseudoedema of the peripapillary nerve fibre layer, retinal telangiectasias and increased vascular tortuosity

Front 1042

what type of test is done to diagnose Leber's heriditary optic neuropathy

Back 1042

there is a specific genetic test

Front 1043

describe the management of Leber's heriditary optic neuropathy (4 setps)

Back 1043

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

Front 1044

papilledema

Back 1044

Reserved for bilateral swelling secondary to increased intracranial pressure

Front 1045

what is the most common cause of papilledema

Back 1045

Idiopathic intracranial hypertension (pseudotumor cerebri)

Front 1046

what condition is important to rule out as a cause of papilledema

Back 1046

Mass lesions must be ruled out Less likely but possible causes: trauma, meningitis/encephalitis, subarachnoid hemorrhage

Front 1047

describe the management associated with papilledema (1 steps)

Back 1047

1. immediate consulation with neurology or neuro-ophthalmology to determine the underlying cause (potentially life threatening)

Front 1048

What do you need to DDX papilledema with

Back 1048

pseudopapilledema

Front 1049

what will happen (to the eye) if papilledema is left untreated

Back 1049

optic atrophy

Front 1050

why is it important to find the underlying cause of papilledema

Back 1050

because, if left untreated could result in death

Front 1051

what is pseudopapilledema

Back 1051

burried drusen of the ONH. not a benign condition

Front 1052

what do you need to DDX papilledema with

Back 1052

pseudopapilledema

Front 1053

describe 6 subjective symptoms associated with idiopathic intracranial hypertension

Back 1053

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

Front 1054

what percent of cases of idiopathic intracranial hypertension will have papilledema

Back 1054

Papilledema in almost 100% of cases

Front 1055

describe the follow up time frame on a patient with papilledema and what tests you would do at the follow up

Back 1055

Follow q 1 m until papilledema has regressed Perform VA, RAPD testing, VF, Stereo ONH evaluation

Front 1056

New lecture: 5 OPT 633 - Hematologic and Systemic 2010

Back 1056

a

Front 1057

What is a complete blood count (CBC)

Back 1057

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

Front 1058

what are the three main types of cells found in blood

Back 1058

leukocytes, erythrocytes, and thrombocytes (platlets)

Front 1059

Red Blood Cell Count (RBCC)

Back 1059

Number of RBCs x 106/ml of blood

Front 1060

what is the hemoglobin concentration

Back 1060

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.

Front 1061

what is the hematocrit level

Back 1061

is the proportion of blood volume that is occupied by red blood cells

Front 1062

what is the White blood cell count (WBCC)

Back 1062

Number of white cells x 103/ml

Front 1063

what is a White blood cell differential (WBC diff)

Back 1063

Percent of the five types of white blood cells in the blood:

Front 1064

what are the 5 types of white blood cells found in blood

Back 1064

Neutrophils Eosinophils Basophils Lymphocytes Monocytes

Front 1065

what types of white blood cells are most elevated in bacterial infection

Back 1065

Neutrophils

Front 1066

what types of white blood cells are most elevated with allergies or paracytic infections

Back 1066

Eosinophils

Front 1067

what types of white blood cells are most elevated with viral infections

Back 1067

Lymphocytes

Front 1068

in what layer of the retina do flame shapped hemorrhages occur

Back 1068

nerve fiber layer

Front 1069

in what layer of the retina do dot/blot hemorrhages occur

Back 1069

inner nuclear and plexiform layers

Front 1070

anemia

Back 1070

Reduction in the total number of red blood cells Or reduction in the quantity of hemoglobin

Front 1071

list three common systemic signs and symptoms associated with anemia

Back 1071

Results in pallor ((of skin), weakness, lethargy and dyspnea

Front 1072

describe the mechanism that causes elevated intracrainial pressure to result in retinal anemia

Back 1072

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.

Front 1073

can you tell the cause of retinal anemia based on appearence

Back 1073

Can't differentially diagnosis based on observations made by an ophthalmoscope All cause similar type of ocular changes

Front 1074

what is the most common cause of anemia in the US

Back 1074

iron deficiency

Front 1075

what percent of women and pregnant woment have iron deficiency anemia

Back 1075

20% of women and 50% of pregnant women have iron deficiency anemia (only 2% of adult men)

Front 1076

is it common to see retinal changes with iron deficiency anemia

Back 1076

Typically no retinal changes unless very severe

Front 1077

what is the treatment for iron deficiency anemia

Back 1077

Treatment - iron supplements

Front 1078

what is the mechanism that causes pernicious anemia

Back 1078

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

Front 1079

what is the treatment for pernicious anemia and is it efficacious

Back 1079

Sublingual or parenteral (injected) vitamin supplements Usually respond well Oral (ingested) B12 supplements are not typically absorbed as well through the small intestine wall

Front 1080

what is hemolytic anemia

Back 1080

Anemia as the result of the destruction of red blood cells

Front 1081

how long do red blood cells live in a normal healthy person

Back 1081

RBC survives avg. 90 to 120 days

Front 1082

where are old RBCs absorbed and new RBCs produced in the body

Back 1082

Spleen removes old and damaged RBCs from blood Production of new RBCs in the bone marrow

Front 1083

what substance is released when red blood cells are broken down

Back 1083

Bilirubin

Front 1084

what condition results from an excess of bilirubin in the blood

Back 1084

jaundice

Front 1085

describe the mechanism that causes aplastic anemia

Back 1085

Bone marrow damage à inefficiency to make enough RBCs

Front 1086

list of medications that cause aplastic anemia

Back 1086

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)

Front 1087

what clinically observable ocular signs should you look for with pts who are taking drugs that are known to cause aplastic anemia

Back 1087

Watch for conjunctiva and/or retinal hemorrhages in patients known to be on these medications to diagnosis early and improve the prognosis.

Front 1088

what ethnicity has the highest occurance of sickle cell anemia

Back 1088

African Americans - 10%

Front 1089

what type of inheratince pattern do you see with sickle cell anemia

Back 1089

Gene is recessive

Front 1090

what is the mechanism for sickle cell anemia causing ischemia

Back 1090

sickled RBCs accumulate and occlude vessels

Front 1091

describe the retinal changes you tend to see from sickle cell anemia

Back 1091

venous tortuosity, shunt vessels (arteriovenous anastomoses), "sea fan" neovascularizatioin

Front 1092

what is the function of erythropoietin in the body

Back 1092

A cytokine made by the kidneys that stimulates the proliferation of red blood cells.

Front 1093

what is primary and secondary polycythemia

Back 1093

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

Front 1094

is polycythemia vera a name for primary or secondary polycythemia

Back 1094

primary

Front 1095

describe the mechanism for the vascular damage caused by polycythemia

Back 1095

Hyperviscosity of blood Viscosity may be 4+ times normal Occlusion of blood vessels

Front 1096

what is the typical age of onset of polycythemia

Back 1096

Most in middle to elderly age

Front 1097

describe three systemic signs associated with polycythemia

Back 1097

Red complexion ((not pallor) Hypertension Hemorrhages in the skin and mucous membranes

Front 1098

describe 3 clinically observable ocular signs associated with polycythemia

Back 1098

-dilated tortous retinal vessels -Deep or superficial retinal hemorrhages -Retinal vein occlusion -May see visible emboli – result in amaurosis fugax (monocular blindness)

Front 1099

leukemia

Back 1099

Neoplastic proliferation of WBC's in bone marrow (cancer)

Front 1100

what percent of pts with leukemia have some observable ocular finding associated with the condition

Back 1100

50 to 70% have some ocular finding

Front 1101

name 6 clinically observable ocular signs associated with Leukemia

Back 1101

venous dilation and tortuosity, retinal hemorrhages, cotton wool spots, pre-retinal hemorrhages, perivascular infiltration (w/ WBCs), infiltration of the ONH

Front 1102

what is waldenstrom's macroglobulinemia

Back 1102

Cancer involving increased IgM fraction of plasma 1500 cases diagnosed per year, accounting for approximately 2% of hematologic malignancies

Front 1103

what is lipemia retinalis

Back 1103

A condition in which retinal vessels appear reddish white (pink) or white; found in cases of extreme hyperlipidemia

Front 1104

what is behcet's disease

Back 1104

A rare, multisystem, chronic, recurrent form of vasculitis, marked by ulceration of the mouth and genitalia and by uveitis.

Front 1105

what is sarcoidosis

Back 1105

A chronic multisystem inflammatory disease of unknown etiology, characterized by noncaseating (hard) granulomas

Front 1106

what two organs does sarcoidosis have the biggest impact on

Back 1106

lungs and the lymph glands (forms granulomas)

Front 1107

what demographic is sarcoid most common in

Back 1107

Incidence african americans Women more than men 20 to 40 years of age

Front 1108

name three of the most common presenting systemic signs and symptoms associated with sarcoidosis

Back 1108

Persistent dry cough Fatigue Shortness of breath

Front 1109

name two diagnositc tests that help with the diagnosis of sarcoidosis

Back 1109

chest x-ray (looking for hilar lymphademopathy), ACE

Front 1110

name 6 clinically observable ocular signs associated with sarcoidosis

Back 1110

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

Front 1111

what does an S-shaped upper lid indicate

Back 1111

Enlargement of the lacrimal gland

Front 1112

describe the progression of sarcoidosis

Back 1112

remissions and exacerbations

Front 1113

describe the ocular management of sarcoidosis

Back 1113

Manage dry eye Watch for cataracts from uveitis and steroid use Control anterior uveitis Watch for secondary glaucoma

Front 1114

at what age do people typically develop systemic lupus erythematosus

Back 1114

Adults 20-40 years of age

Front 1115

what ethnicities are prone to developing systemic lupus erythematosus

Back 1115

African, American Indian, and Asian greater than Caucasian

Front 1116

name four systemic symptoms associated with systemic lupus erythematosus

Back 1116

Malar rash over the cheeks Discoid rash - red, raised patches Oral ulcers usually painless Arthritis involving two or more peripheral joints

Front 1117

New lecture: 6 HereditRetDisease (study this one)

Back 1117

a

Front 1118

what is one way you can differentiate between heriditary retinal disease and acquired retinal disease

Back 1118

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.

Front 1119

what kind of heriditary retinal disease does it indicate if you have photosensativity (rod or cone disease)

Back 1119

disorder affecting cones

Front 1120

name the four most common heridiatry retinal disorders affecting the rods

Back 1120

-retinitis pigmentosa -leber's congenital amaurosis -Oguchi's -congenital stationary night blindness

Front 1121

name the three most common heridiatry retinal disorders affecting the cones

Back 1121

-stargart's -best's -achromatopsia

Front 1122

what is the most common heridiatary retinal disorder

Back 1122

retinitis pigmentosa

Front 1123

does RP only affect the rods, the cones, or both

Back 1123

Common end result is loss of rods with secondary involvement of cones

Front 1124

what type of inheritance pattern do you see with retinitis pigmentosa

Back 1124

Many variants Including AD, AR, X-linked

Front 1125

which inheritance pattern of RP is the most common

Back 1125

Autosomal Recessive:

Front 1126

which inheritance pattern of RP is the most visually devistating

Back 1126

Autosomal Recessive:

Front 1127

describe the progression of the autosomal recessive form of RP

Back 1127

Night vision and peripheral field loss in early childhood, central vision loss by adulthood

Front 1128

which inheritance pattern or RP has the least visually devistating outcome

Back 1128

Autosomal Dominant

Front 1129

describe the progression of the autosomal dominant form or RP

Back 1129

Least severe form with central vision intact until 40’s or 50’s

Front 1130

is RP typically associated with other systemic abnormalities

Back 1130

30-40% of cases are part of a systemic syndrome

Front 1131

describe 5 clinically observable ocular findings associated with RP

Back 1131

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

Front 1132

what type of field loss do you typically find with RP

Back 1132

ring scotoma

Front 1133

what test will show signs of RP well before there are any clinically observable changes to the retina

Back 1133

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

Front 1134

what is retinitis sine pigmento

Back 1134

No clinically recognizable pigmentary changes May be just presentation early in disease

Front 1135

what is usher's syndrome

Back 1135

Congenital sensorineural hearing loss and RP Accounts for 50% of deaf-blind individuals

Front 1136

describe the treatment options for RP (6)

Back 1136

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

Front 1137

what is Leber's congenital amaurosis

Back 1137

Similar to RP except congenital (or very early onset),

Front 1138

describe the diagnostic clues associated with Leber's congenital amaurosis

Back 1138

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

Front 1139

is there any treatment for Leber's congenital amaurosis

Back 1139

Gene Therapy Trials for LCA are happening now

Front 1140

whatis the difference between sensory and motor congenital nystagmus

Back 1140

Sensory (Afferent): Secondary to disease disrupting the foveal pathway early in life Motor (efferent): Due to primary abnormality in the ocular-motor system

Front 1141

what is congenital stationary night blindness

Back 1141

Night Blindness is primary symptom Mild acuity reduction (usually 20/30 - 20/60) Normal retina

Front 1142

what is Oguchi's disease

Back 1142

Variant of CSNB found in Japanese populations Yellow-gray retina color reversed by 2-3 hrs of dark adaptation

Front 1143

how do cone-rod dystrophies differ from rod-con dystrophies in their progressive involovment of rods and cones

Back 1143

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

Front 1144

what is gyrate atrophy

Back 1144

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.

Front 1145

describe the visual impact of gyrate dystrophy

Back 1145

poor; legal blindness by the fourth to seventh decade

Front 1146

is there any treatment for gyrate atrophy

Back 1146

Treatment: B6 supplements, diet low in protein (low arginine, precursor of ornithine) slows, may halt progression

Front 1147

what type of inheritance pattern is seen with choroideremia

Back 1147

X-linked, Affects Males only

Front 1148

describe the clinically observable diagnostic signs associated with choroideremia

Back 1148

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

Front 1149

what is the most common heriditary macular dystrophy

Back 1149

stargardt's macular dystrophy

Front 1150

what is the typical age of onset of stargardt's

Back 1150

Usual Onset 8 - 16 yrs with poor acuity

Front 1151

with stargardt's do you have acuity loss or visible macular changes first

Back 1151

Acuity loss may precede observable macular changes Macular changes very subtle at first

Front 1152

describe the changes to the macula that take place with stargatdt's

Back 1152

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

Front 1153

at what age and at what level do acuities stabalize with stargardt's

Back 1153

Usually stabilizes by early 20’s with acuities in 20/200 - 20/400 range

Front 1154

what is fundus flavimaculatus

Back 1154

Variant of Stargardt’s Pisciform lesions are primary presentation Macular disease and acuity loss develops later (40’s - 50’s)

Front 1155

what is another name for vitelliform dystrophy

Back 1155

best's disease

Front 1156

with Best's disease, do you have changes in acuity or visible changes to the retina first

Back 1156

opposite of stargardt’s: you can have a large lesion with little VA change

Front 1157

describe the progression of Best's disease

Back 1157

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

Front 1158

what is another name for rod monochromatism

Back 1158

achromatopsia

Front 1159

what is achromatopsia

Back 1159

Congenital Absence of Cone Function

Front 1160

what is the inheritance pattern associated with achromatopsia

Back 1160

autosomal recessive

Front 1161

describe four clinically observable signs and symptoms associated with achromatopsia

Back 1161

Photophobia (Rods Bleach Quickly in bright light) Nystagmus Poor VA (20/200 range) No Color Vision

Front 1162

what type of tint is usually best to use for a rod monochromat

Back 1162

Red tint is often the best

Front 1163

describe the most common appearence of the macula of a person with progressive cone dystrophy

Back 1163

Bull’s Eye macular lesion

Front 1164

describe the visual outcome you would expect for a person with progressive cone dystrophy

Back 1164

Reduced VA to 20/60 - 20/200 range by teens

Front 1165

what is the age of onset you would expect for a person with central areolar choroidal dystrophy

Back 1165

Later onset, usually after 40

Front 1166

describe the visual outcome you would expect for a person with central areolar choroidal dystrophy

Back 1166

Loss of central vision with acuity dropping below 20/200

Front 1167

name the two forms of albinism and the difference between the two

Back 1167

Oculocutaneous: pigment is lacking in the eyes, skin and hair Ocular Albinism: only the eyes lack pigment

Front 1168

why do individuals with albinism have limited binocularity

Back 1168

Anomalous wiring at the chiasm limits binocularity

Front 1169

name six clinically observable ocular signs associated with albanism

Back 1169

Amelanosis of iris and retina (iris transillumination defect) photophobia Foveal hypoplasia Nystagmus (and ability to dampen) Strabismus and impaired BV Astigmatism

Front 1170

why are CLs a good option for pts with nystagmus

Back 1170

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

Front 1171

New lecture: 7 AMD Dx I DE 10 Vault

Back 1171

a

Front 1172

what is the most common cause of vision loss in the elderly in the developed world

Back 1172

age-related macular degeneration (AMD)

Front 1173

is AMD a genetic or environmental disease process

Back 1173

both

Front 1174

what layers of the eye does AMD primarily affect

Back 1174

photorecepters, RPE, Bruch's mem brane, Choriocapillaris

Front 1175

what are the chances of developing AMD if you are over the age of 75

Back 1175

30%

Front 1176

are males of females more likely to develop AMD

Back 1176

females

Front 1177

is AMD more common in caucasians or african americans

Back 1177

caucasians

Front 1178

by how much does it increase your risk of developing AMD if you have a primary relative with AMD

Back 1178

2.4 times

Front 1179

name four modiiable risk factors for AMD

Back 1179

smoking, short wavelength light, obesity, macular pigment density (zexanthene and leuteine)

Front 1180

what gives the macula a yellowish color

Back 1180

xanthophyll carotenoid pigments lutein and zeaxanthin

Front 1181

does the RPE have stronger adhesions with the retina or with Bruch's membrane

Back 1181

Strong adhesion to Bruch’s membrane Weaker adhesions to sensory retina

Front 1182

between what layers of the retina is the subretinal space located

Back 1182

between the sensory retina and the RPE

Front 1183

what specific layer of the retina is drusen found in

Back 1183

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.

Front 1184

what layer of the retina produces the material that forms drusen

Back 1184

RPE

Front 1185

name 5 clinically observable retinal signs associated with AMD

Back 1185

1) Drusen and lipofusin 2) RPE hyper or hypo-pigmentation 3) pigment epithelial detachment 4) geographic atrophy 5) choroidal neovascularization

Front 1186

how does the appearence of flourscene angiography change in AMD with areas of RPE pigment clumping vs. areas of hypopigmentation

Back 1186

HypOflourescences in areas of pigment clumping HypeRflourescences in areas of hypopigmentation

Front 1187

what is lipofuscin

Back 1187

undigestable pigment granules that are a product of lipid oxidation and accumulate in cells with age

Front 1188

how does lipofuscin affect the RPE

Back 1188

damages the RPE, resulting in RPE atrophy and drusen

Front 1189

does retinal drusen tend to appear unilatterally or bilatterally

Back 1189

bilaterally, and often symmetrical

Front 1190

what area of the retina does drusen tend to accumulate

Back 1190

around the macula and ONH

Front 1191

what is drusen made of

Back 1191

exact composition is controversial. extracellular material, components include: proteins, vitronectin, amyloid, inflammatory components, immunological products

Front 1192

what are the 4 types of drusen

Back 1192

1) small hard drusen 2) large soft drusen 3) familial drusen 4) calcific drusen

Front 1193

how big is small hard drusen

Back 1193

less than 63 microns (half a the diameter of a vein)

Front 1194

how big is large soft drusen

Back 1194

larger than 63 microns (half a vein diameter)

Front 1195

how does hard and soft drusen compair in their apperence

Back 1195

hard: small, discrete, yellow, well defined borders, round soft: larger, fluffier, pale yellow, indistinct borders, can vary in shape

Front 1196

is hard drusen associated with diffuse or focal RPE dysfunction. what about soft

Back 1196

hard: focal RPE dysfunction soft: diffuse RPE dysfunction

Front 1197

can hard drusen turn into soft. can soft drusen turn into hard

Back 1197

hard drusen may break down and become soft. soft drusen can not turn into hard.

Front 1198

why is soft drusen associated with pigment epithelial detachment

Back 1198

large soft drusen may coalesce and create a PED

Front 1199

which type of drusen has the poorest prognosis

Back 1199

large soft drusen

Front 1200

what is familial drusen

Back 1200

inherited condition (AD), drusen caused by metabolic defect in RPE

Front 1201

at what age do you tend to see familial drusen

Back 1201

20-30s

Front 1202

what is calcific drusen

Back 1202

long standing drusen that has calcified, leaving multifocal patches of atrophy and calcium deposits. Can be seen in hard or soft drusen.

Front 1203

is pigment epithelial detachment common in AMD? why?

Back 1203

yes; drusen loosen adherence between RPE basement membrane and inner collagenous portion of bruch's membrane.

Front 1204

what are the layers of bruch's membrane from inner to outer

Back 1204

basement membrane of the RPE inner collagenous zone elastic zone outer collagenous zone basement membrane of the choriocapillaris

Front 1205

what does a PED look like

Back 1205

sharp borders, dome shaped, round or oval elevations of the RPE

Front 1206

what can a pigment epithelial detachment turn into

Back 1206

can collapse, causing RPE or geographic atrophy

Front 1207

what visual consequences can result from PED (2)

Back 1207

reduced VA and metaporphopsia

Front 1208

what are the two types of AMD

Back 1208

exudative (wet, neovascular) and non-exudative (dry, atrophic, non-neovascular)

Front 1209

which type of AMD is most common

Back 1209

non-exudative (dry) 75-90% of AMD pts

Front 1210

is there choroidal neovascularization in the non-exudative form of AMD

Back 1210

no

Front 1211

is it common for dry AMD to reduce vision to legal blindness

Back 1211

no

Front 1212

name three clinically observable retinal findings you see with dry AMD

Back 1212

hyper/hypopigment of the RPE, geographich atrophy

Front 1213

what percent of pts with dry AMD progress to wet AMD

Back 1213

10-20%

Front 1214

what percent of legal blindness caused by AMD is from the wet form

Back 1214

75%

Front 1215

is the presence of hard drusen sufficient to make the diagnosis of AMD? what about soft drusen?

Back 1215

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.

Front 1216

what form of AMD can have soft drusen

Back 1216

either (dry or wet)

Front 1217

name nine clinical tests that would be good to do on an AMD pt

Back 1217

stereoscopic retinal exam color fundus photography amsler grid photostress test color vision testing central 10 automated perimetry OCT preferential hyperacuity perimetry FA

Front 1218

what does the photostress test tell us about the cause of VA loss

Back 1218

helps differentiate btwn macular and optic nerve problems

Front 1219

what do the think is the pathophysiology of AMD

Back 1219

light causes generation of free radicals which damage the molecules within the retina

Front 1220

how do we think we can prophylactically reduce the changes of developing AMD

Back 1220

AREDS (age-related eye disease study) antioxidants help prevent free-radical formation

Front 1221

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

Back 1221

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

Front 1222

what can a pt do to help control/prevent AMD (5)

Back 1222

UV protection, diet (high in lutein and zexanthene), antioxidant supplimentation (check w/ primary care for interactions), exercise and HTN control, QUIT SMOKING

Front 1223

how often should you schedule follow up visits with AMD patients

Back 1223

minimal RPE changes: 1 year as RPE worsens: every 6 months high risk: 4-6 months

Front 1224

New lecture: 8 AMD Advanced Dx part II Vault

Back 1224

a

Front 1225

what are hard exudates

Back 1225

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

Front 1226

how do you differentiate between hard exudates and drusen (4)

Back 1226

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)

Front 1227

are cotton wool spots deep or superficial in the retina

Back 1227

superifical (NFL edema)

Front 1228

describe the appearence of cotton wool spots

Back 1228

white to yellowish (more white), fluffy w/ indistinct boarders

Front 1229

cotton wool spots, drusen or hard exudates?

Back 1229

drusen

Front 1230

cotton wool spots, drusen or hard exudates?

Back 1230

cotton wool spots

Front 1231

cotton wool spots, drusen or hard exudates?

Back 1231

hard exudates

Front 1232

cotton wool spots, drusen or hard exudates?

Back 1232

drusen

Front 1233

do you tend to see choroidal neovascularization in the atrophic regions of the retina in AMD

Back 1233

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

Front 1234

picture of geographic atrophy

Front 1235

what blood vessels become apparent that weren't before in areas of geographic atrophy in AMD

Back 1235

choroidal blood vessels are visable on ophthalmoscopy

Front 1236

what is foveal sparing in geographic atrophy associated with AMD

Back 1236

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.

Front 1237

is there currently any treatment for dry AMD

Back 1237

no effective treatment at this time; studies currently being done

Front 1238

is there currently treatment for wet AMD

Back 1238

yes

Front 1239

what percent of adults over the age of 43 have wet AMD

Back 1239

1.2%

Front 1240

what do you need to have in order to classify AMD as wet

Back 1240

neovascularization

Front 1241

describe the process of choroidal neovascularization

Back 1241

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

Front 1242

what test should you do if you suspect development of choroidal neovascularization in a pt with AMD

Back 1242

STAT flourescene angoigraphy (can't always see it on ophthalmoscopy)

Front 1243

what ophthalmoscopic findings would make you suspicious that AMD is turing into the wet form (4)

Back 1243

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

Front 1244

what is the best way to see slight elevations associated with the development of wet AMD

Back 1244

contact fundus lens in the center of your gonio lens

Front 1245

what is the MOST important factor in preventiing vision loss from AMD that is progressing from the dry to the wet form

Back 1245

early detection; you need to educate dry AMD pts to come in if they see ANY changes in their vision

Front 1246

if you see hard exudates in a pt with AMD what does this tell you

Back 1246

there is likely choroidal neovascularization (exudates are lipids excreated by damaged blood vessels) (hard exudates are not drusen)

Front 1247

what is preferential hyperacuity perimetry (PHP)

Back 1247

central visual field test that is specifically designed to monitor progression of AMD from the dry to the wet form

Front 1248

name the three types of choroidal neovascular membranes seen on flourescene angiography

Back 1248

classic, minimally classic, and occult CNVM

Front 1249

what is a classic choroidal neovascular membrane

Back 1249

well defined membrane with distinct borders

Front 1250

what percent of patients with choriodal neovascular membrane have the classic type of membrane

Back 1250

13%

Front 1251

what is an occult choroidal neovascular membrane

Back 1251

poorly defined boarders

Front 1252

what is a minimally classic choroidal neovascular membrane

Back 1252

has parts that appear classic and parts that appear occult

Front 1253

what does a detachment of the RPE look like

Back 1253

sharply circumscribed, dome-shaped elevation at the posterior pole of varying size. sub-RPE fluid may be clear or turbid

Front 1254

name 5 consequences that can result if choroidal neovascularization is left untreated

Back 1254

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

Front 1255

New lecture: 9 AMD Tx DE 10 Vault

Back 1255

a

Front 1256

what are the three catagories of therapies currently available to treat wet AMD

Back 1256

laser photocoagulation photodynamic therapy vascular endothelial growth factors (VEGF)

Front 1257

what is the goal of photocoagulation therapy for wet AMD

Back 1257

prevent further deterioration

Front 1258

what test needs to be done before a surgen can perform photocoagulation therapy

Back 1258

flourescene angiography (not more than 72 hours old to localize CNV)

Front 1259

how does the final VA after photocoagulation for wet AMD relate to the proximity of the choroidal neovacularization (CNV) to the macula

Back 1259

the closer to the macula the worse the final visual acuity (VA).

Front 1260

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.

Front 1261

what is the name of the drug used in photodynamic threapy

Back 1261

verteporfin (visudyne)

Front 1262

describe the process of photodynamic therapy

Back 1262

IV injection of verteportin, which targets new leaky blood vessels. then they use a laser directed at verteporfin, which destroys new blood vessels.

Front 1263

what type of CNV is photodynamic therapy FDA approved to treat

Back 1263

classic CNV

Front 1264

what is the VA loss at 2 years with and without photodynamic therapy following treatment of wet AMD

Back 1264

-2.3 lines with therapy; -4.5 lines without therapy. (TAP study) -reduces vision loss by about half

Front 1265

name two side effect associated with photodynamic therapy

Back 1265

infusion pain and photosensativity

Front 1266

how much does photodynamic therapy cost

Back 1266

about $3,000 per treatment. 5-6 treatments in the first 2 years often needed to stop leakage.

Front 1267

what is anti-VEGF (vascular endothelial growth factor) therapy

Back 1267

VEGF is a hormone that stimulates growth of new blood vessels. anti-VEGF inhibits this hormone.

Front 1268

what are the names of the three anti-VEGF drugs used for treatment of wet AMD

Back 1268

1) macugen 2) lucentis 3) avastin (not currently FDA approved for the eye)

Front 1269

Second dummy question

Back 1269

Second dummy answer

Front 1270

what type of CNV is macugen approved for

Back 1270

all types

Front 1271

about how often do you have injections of macugen to treat wet AMD

Back 1271

every 6 weeks (no recommended long term duration)

Front 1272

are there any known systemic side effect to macugen

Back 1272

none

Front 1273

are there any ocular complications associated with macugen instillation

Back 1273

enophthalmitis, traumatic cataracts, RD (all less than 1.5%)

Front 1274

does macugen slow progression of vision loss associated with wet-AMD or improve vision

Back 1274

only delays progression of vision loss

Front 1275

how much does treatment with macugen cost

Back 1275

$1,500 per injection. injections every 6 weeks

Front 1276

how often is Lucentis injected

Back 1276

every 4 weeks

Front 1277

does treatment of wet-AMD cause a slowing of vision loss or an improvement in vision

Back 1277

pts can actually have vision improvements!

Front 1278

how much does it cost per year for pts to be on lucentis

Back 1278

$2,000 per injection, one injection per month. $24,000 per year.

Front 1279

are there any systemic side effects associated with lucentis

Back 1279

cerebrovascular accident (stroke), BUT it was not statistically significant.

Front 1280

what is avastin FDA approved for

Back 1280

treatment of colon cancer; used off label for AMD

Front 1281

how much does avastin cost

Back 1281

$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.

Front 1282

New lecture: 10 Macular Post Pole 2010

Back 1282

a

Front 1283

what is central serous retinopathy (central serous chorioretinopathy, central serous choroidopathy)

Back 1283

small break in the RPE leads to a serous retinal detachment under the macula

Front 1284

what causes central serous retinopathy

Back 1284

idiopathic (unknown)

Front 1285

what age and demographic do you expect to see central serous retinopathy in

Back 1285

males between the ages of 20 and 45; type A personality (dealing with stress)

Front 1286

describe the visual changes you expect to see with central serous retinopathy

Back 1286

1. fairly sudden onset of blurred vision in one eye (modestly reduced) 2. relative scotoma 3. metamorphopsia 4. micropsia (because cones are spread out)

Front 1287

what type of refractive change would you expect to see with central serous retinopathy

Back 1287

often correctable to 20/20 with a weak plus lens (because swelling shortens axial length)

Front 1288

what is the best way to see central serous retinopathy

Back 1288

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

Front 1289

what type of filter is really good to see macular problems with

Back 1289

red-free

Front 1290

OCT image of central serous retinopathy

Front 1291

describe the sequence of patterns you see on FA with central serous retinopathy

Back 1291

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)

Front 1292

describe the prognosis and long-term outcomes of central serous retinopathy (2)

Back 1292

1. 80-90% have spontaneous resolution in 1-6 months 2. mild metamorphopsia that may remain much longer (1 or more years)

Front 1293

what are the chances of reoccurance with central serous retinopathy

Back 1293

40% develop recurrent attacks

Front 1294

name three comorbidities that may present with central serous retinopathy

Back 1294

RPE atrophy, cystoid maculopathy, or choroidal nerovascularization

Front 1295

describe the treatment associated with central serous retinopathy

Back 1295

no treatment required. laser treatment done in rare cases. triamcinalone and anti-VEGF being explored.

Front 1296

what gender and age range are macular holes more frequently found

Back 1296

women 3:1 -older 60-80

Front 1297

what type of vision do you expect to result from a macular hole

Back 1297

20/200 to 20/400

Front 1298

describe the common mechanism for macular holes

Back 1298

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

Front 1299

what is the piece of macula pulled free in a macular hole called

Back 1299

operculum

Front 1300

what material is often present on the retina at the site of a macular hole

Back 1300

drusen (yellow lipid deposits)

Front 1301

what is the Watzke-Allen test

Back 1301

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.

Front 1302

desccribe the stages of macular hole

Back 1302

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)

Front 1303

what is the treatment for macular holes

Back 1303

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)

Front 1304

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?

Back 1304

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

Front 1305

if they do a gas bubble treatment for a macular hole how long does the pts have to sit with there head facing down

Back 1305

couple weeks

Front 1306

beyond what refractive error is there in increased risk of developing retinal detachment

Back 1306

6 D myopia

Front 1307

1 mm of axial length corresponds to how many doipters of refractive error

Back 1307

3 D

Front 1308

what is myopic degeneration

Back 1308

in high myopia the retina and the choroid can atrophy around the edge of the disc.

Front 1309

what are fuch's spots

Back 1309

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.

Front 1310

what is a posterior staphyloma

Back 1310

posterior bulging of the retina usually due to high myopia

Front 1311

name 7 clinically observable retinal findings associated with high myopia

Back 1311

myopic crescent, fuch's spot, lacquer cracks, posterior staphyloma, chorioretinal atrophy, subretinal hemorrhage (leads to fuch's spot), retinal detachment

Front 1312

how often should you have high myopes RTC

Back 1312

every 1 year to look for changes.

Front 1313

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

Front 1314

what are angioid streaks

Back 1314

degeneration of bruch's membrane of the choroid characterized by brown or reeeish lines or streaks in the fundus of the eye.

Front 1315

are angioid streaks usually unilateral or bilateral

Back 1315

bilateral

Front 1316

angioid streaks are very gragile and are liable to rupture in cases of ocular trauma

Front 1317

what is the etiology of angioid streaks

Back 1317

idiopathic or associated with disease (50%): Pseudoxanthoma elasticum Paget’s disease Sickle cell disease Thalassemia Ehlers-Danlos Syndrome Optic disc drusen Retinitis pigmentosa

Front 1318

name two ways that angioid streaks can affect vision

Back 1318

decreased VA, metamorphopsia (if choroidal neovascularization)

Front 1319

describe the management of angioid streaks (3 steps)

Back 1319

1. treat any neovascularization (similar to AMD) 2. treat any underlyaing medical conditions 3. Rx polycarbonate (because of how fragile the retina is)

Front 1320

what is cystoid macular edema

Back 1320

edema and cyst formation of the macuylar area of the retina.

Front 1321

in what layer of the retina does cystoid macular edema develop

Back 1321

Henle's fiber layer of the macula

Front 1322

what is clinically significant macular edema

Back 1322

asked Dr. Y

Front 1323

name two ways that cystoid macular edema could impact vision

Back 1323

blurred vision, metamorphopsia

Front 1324

describe the pattern that tends to form on flourescene angiography in cases of cystoid macular edema

Back 1324

Radial arrangement of fibers in Henle’s fiber layer causes dye to take on a flower-petal pattern (petalloid)

Front 1325

describe the treatment of cystoid macular edema

Back 1325

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

Front 1326

what is another name for macular pucker

Back 1326

epiretinal membrane

Front 1327

what is an epiretinal membrane

Back 1327

cellular proliferation along the internal limiting membrane. contraction of the membrane causes retinal surface to become wrinkled.

Front 1328

what is the most common cause of epiretinal membrane

Back 1328

idiopathic

Front 1329

name four ways epiretinal membranes can affect vision

Back 1329

could be asymptomatic -decreased VA, metamorphopsia, macropsia, monocular diplopia

Front 1330

describe the treatment of epiretinal membrane

Back 1330

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

Front 1331

what conditions is chloroquine used to treat

Back 1331

malaria, rheumatoid arthritis and systemic lupus erythematosus

Front 1332

what pattern do you tend to see on the retina with toxicity due to chloroquine use

Back 1332

bull's eye maculopathy

Front 1333

what types of conditions is thioridazine used to treat

Back 1333

psychotic conditions

Front 1334

what types of retinal signs do you tend to see from thioridazine toxicity

Back 1334

pigment granularity; usually midperipheral first, then progresses

Front 1335

what is talc

Back 1335

used to dilute drugs used by IV drug abusers

Front 1336

what type of retinal signs do you tend to see from talc retinopathy

Back 1336

refractile yellow deposits near or in retinal arterioles

Front 1337

at what level in the retina are talc deposits located

Back 1337

very anterior, they are on top of the blood vessels

Front 1338

what is the most concerning cause of choroidal folds

Back 1338

Causes Idiopathic Hyperopia Choroidal tumor or detachment CNM Optic disc swelling Orbital tumors ((most concerning cause!) Hypotony Orbital and scleral inflammation

Front 1339

what causes choroidal folds

Back 1339

flattening of the psterior pole

Front 1340

name two visual symptoms pts might have from choroidal folds

Back 1340

blurry vision, metamorphopsia

Front 1341

describe the appearence of choroidal folds

Back 1341

alternating dark and light yellowish streaks

Front 1342

describe the management of choroidal folds

Back 1342

need to determine cause (rule out tumor etc). usually idiopathic, diagnosis of exclusion.

Front 1343

New lecture: 11-a Retinal Vascular Disease Intro 2010

Back 1343

a

Front 1344

name 5 types of hemorrhages you can see behind the iris

Back 1344

Pre-retinal (boat shaped), flame shaped, dot/blot, subretinal/subpigment epithelial, vitreous

Front 1345

what structure ruptures in a pre-retinal hemorrhage

Back 1345

internal limiting membrane

Front 1346

how does a pre-retinal hemorrhage affect vision

Back 1346

creates scotomas

Front 1347

does a pre-retinal hemorrhage move pt movement

Back 1347

moves with gravity

Front 1348

how does the apperance of a pre-retinal hemorrhage change as it is being absorbed

Back 1348

change to red to yellow to white

Front 1349

from which capillary bed do flame shaped hemorrhages occur

Back 1349

superifical capilary bed

Front 1350

in what level of the retina do dot/blot hemorrhages occur

Back 1350

Inner nuclear layer, outer plexiform layer (deep capilary bed)

Front 1351

what is the cause of sub-retinal/sub-pigment epithelial hemorrhages

Back 1351

secondary to choroidal neovascular membranes. can be from deep retinal hemorrhages.

Front 1352

how does the color of a sub-retinal and a sub-pigment epithelial hemorrage compare

Back 1352

subretinal: dark red sub RPE: grey green

Front 1353

how does a vitreous hemorrhage affect your ability to see the retina

Back 1353

will blur view of post. pole near the heme

Front 1354

what are the two forms of vitreous hemorrhage

Back 1354

retrovitreous and intravitreous

Front 1355

name two causes of vitreous hemorrhage

Back 1355

secondary to rupture of neovascular net, or development of a retinal tear associated with a vitreous detachment

Front 1356

what must precede hard exudates

Back 1356

edema

Front 1357

in what part of the retina do you expect to find cotton wool spots (CWSs)

Back 1357

usually within 3 DD of the ONH

Front 1358

how do you determine if tortuosity is congenital based on symmetry

Back 1358

congenital: involves all quadrents (symmetrical OU) acquired: sectoral involvement (also, previously documented as normal)

Front 1359

what is the difference between collateral and shunt vessels

Back 1359

Collaterals: new vessels that give A-A or V-V communications, making up for a compromised or obstructed vessel

Front 1360

what is intraretinal microvascular abnormalities (IRMA)

Back 1360

looks like neo, but doesn't leak with FA. eventually develops into neo.

Front 1361

why do you have hypofluorescence at the macula on FA

Back 1361

because RPE is dense

Front 1362

what are the three phases of FA and at what time intervals do they occur

Back 1362

choroidal flush (within seconds of injection) arterial-venous phase (6-8 seconds) late phase (5-10 min.)

Front 1363

Pharmacokinetics of penicillins

Back 1363

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)

Front 1364

New lecture: 11 Retinal Vascular Disease 2010 (study this one)

Back 1364

a

Front 1365

what are the two most common retinal vascular disease seen

Back 1365

1. diabetic retinopathy 2. branch retinal vein occlusion (BRVO)

Front 1366

is BRVO usually unilateral or bilateral

Back 1366

95% unilateral

Front 1367

name and describe the three categories of BRVO

Back 1367

Major = involves 5+ DD of retina Primary = involves 2-5 DD of retina Secondary = involves <2 DD of retina

Front 1368

is BRVO associated with any other disorders

Back 1368

Strong association with systemic disease

Front 1369

why is glaucoma assciated with a risk of BRVO

Back 1369

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.

Front 1370

describe the VA loss associated with BRVO

Back 1370

sudden, unilateral, painless VA loss over a period of 24-48 hours. some describe it as blur.

Front 1371

why is metamorphopsia associated with BRVO

Back 1371

because it can cause macular edema

Front 1372

name 6 clinically observable retinal signs associated with BRVO

Back 1372

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

Front 1373

why do BRVO tend to occur in an superotemporal A-V crossing

Back 1373

because there are more A-V crossings in that quadrant

Front 1374

how does the location of a BRVO affect the changes of developing macular edema and why

Back 1374

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

Front 1375

what is Bonnet's sign

Back 1375

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

Front 1376

what is the difference between an ischemic and a non-ischemic BRVO

Back 1376

Non-ischemic (perfused, < 5 DD) or ischemic (nonperfused, > 5DD)

Front 1377

what is a retinal finding that indicates that there has been edema in that area of the retina in the past

Back 1377

hard exudates indicates there has been edema

Front 1378

name five complications associated with BRVO

Back 1378

chronic macular edema, neovascularization, vitreous hemorrhage (from rupture of neovascular net), neovascular glaucoma, retinal detachment

Front 1379

how does BRVO lead to retinal detachment

Back 1379

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.

Front 1380

why do you need to do gonioscopy on a pt with a BRVO

Back 1380

because BRVO can cause neovascularization, which can lead to neovascularization of the angle and neovascular glaucoma

Front 1381

management of BRVO

Back 1381

often will resolve on its own. need to determine underlying cause.

Front 1382

is CRVO (central retinal vein occlusion) usually unilateral or bilateral

Back 1382

unually unilateral

Front 1383

what can cause CRVO in younger pts (under 50)

Back 1383

estrogen-containing preparations (birth control pills)

Front 1384

what is the most common cause of CRVO in pts over 50 years old

Back 1384

HTN (hypertension) about 60%

Front 1385

is glaucoma associated with CRVO

Back 1385

yes

Front 1386

describe the VA loss associated with CRVO

Back 1386

sudden, unilateral, painless vision loss

Front 1387

what could cause the pt pain 90 days after a CRVO or BRVO

Back 1387

neovascularization that causes neovascular glaucoma (3 month glaucoma)

Front 1388

what happens to the foveal light reflex (FLR) if there is macular edema

Back 1388

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

Front 1389

name 5 clinically observable retinal signs associated with CRVO

Back 1389

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

Front 1390

what condition is associated with the "blood and thunder" appearence of the retina

Back 1390

CRVO

Front 1391

how do you differentiate between diabetic retinopathy and CRVO

Back 1391

history; there appearence may look very similar. CRVO will be sudden, painless, unilateral vision loss.

Front 1393

what is the difference between ischemic and non-ischemic CRVO and what kind of VA do you have with each type

Back 1393

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.

Front 1394

describe the prognosis for ischemic and non-ischemic CRVO

Back 1394

non-ischemic is fair. ischemic is poor regardless of tx.

Front 1395

how often does neovascularization occur in CRVO

Back 1395

20% of all CRVO and 60% of the ischemic type -high risk of developing neovascular glaucoma

Front 1396

if you see neovascularization on the iris where else should you expect neovascularization

Back 1396

on the retina

Front 1397

what is the main cause of branch retinal artery occlusion (BRAO)

Back 1397

embolism

Front 1398

name for materials that can cause an embolism

Back 1398

1. cholesterol (hollenhorst plaque) 2. calcifications 3. platelet-fibrin (arterosclerosis) 4. septic (bacterial endocarditis)

Front 1399

what is a septic embolism

Back 1399

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

Front 1400

is CRAO usually unilateral or bilateral

Back 1400

usually unilateral

Front 1401

which is more common, CRAO or BRAO? how about CRVO or BRVO?

Back 1401

CRAO is more common than BRAO BRVO is more common then CRVO

Front 1402

describe the vision loss associated with BRAO

Back 1402

sudden, unilateral, painless loss of part of the visual field

Front 1403

name 4 clinically observable retinal signs associated with BRAO

Back 1403

1. focal or wedge shaped area of retinal whitening 2. narrowing of arteries 3. possible cotton wool spots 4. may see emboli

Front 1404

what quadrant is most likely to be affected by a BRAO

Back 1404

superotemporal

Front 1405

what is a hollenhorst plaque

Back 1405

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

Front 1406

describe the management of BRAO

Back 1406

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

Front 1407

describe the prognosis for BRAO

Back 1407

good. 90% reach 20/40.

Front 1408

describe the prognosis for central retinal artery occlusion (CRAO)

Back 1408

most have severe perminate vision loss (counting fingers to light perception) -life expectancy is decreased as well after a CRAO

Front 1409

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.

Front 1410

name 6 clinically observable retinal findings associated with CRAO

Back 1410

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

Front 1411

describe the tx of CRAO

Back 1411

1. digital massage 2. paracentesis is an option 3. carbonic anhydrase inhibitors PO 4. topical beta blockers 5. consider admission to hospital

Front 1412

how often do you have the pts back for follow-ups and what are you looking for

Back 1412

Q1-4 weeks, looking for neovascularization

Front 1413

describe the overall health prognosis associated with CRAO

Back 1413

poor; CRAO is caused by systemic vasculopathy

Front 1414

what are the ranges of blood pressure for normal, pre-HTN, stange 1 and stage 2 HTN

Back 1414

a. Normal

Front 1415

name 6 observable retinal signs associated with chronic hypertensive retinopathy

Back 1415

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

Front 1416

name 5 clinically observable retinal signs associated with acute hypertensive retinopathy

Back 1416

1. exudates (macular star configuration) 2. retinal edema 3. CWSs 4. flame hemorrhages 5. swelling of the ONH (hallmark)

Front 1417

what is the "copper wire" and "silver wire" appearance and what does it indicate

Back 1417

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

Front 1418

what other disease do the signs of hypertensive retinopathy look like

Back 1418

diabetic retinopathy

Front 1419

if you see signs of hypertension in just one eye, what should you suspect

Back 1419

a problems with one side of the carotid artery

Front 1420

what are two other terms for venous beading

Back 1420

boxcarring, saushaging

Front 1421

if you see sign of hypertensive retinopathy you need to check blood pressure.

Front 1422

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

Front 1423

describe the prognosis for hypertensive retinopathy

Back 1423

usually pretty good

Front 1424

what systemic condition is retinal vaso-occlusive disease associated with

Back 1424

cerebrovascualr disease (stroke)

Front 1425

which cerebrovascular diseases are most commonly associated with ocular signs (2)

Back 1425

1. cerebral thromboembolism 2. cerebral embolism

Front 1426

name three symptoms associated with TIA

Back 1426

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)

Front 1427

describe the systemic prognosis associated with ocular ischemic syndrome (OIS)

Back 1427

poor, due to underlying etiology (40% will be dead within 5 years)

Front 1428

what is the cause of OIS

Back 1428

usually carotid artery disease (stenosis of 90% or more). other causes: HTN, diabetes, giant cell arteritis

Front 1429

is ocular ischemic syndrome usually in men or women? is it usually unilateral or bilateral

Back 1429

usually in men, usually unilateral

Front 1430

what symptom does OIS have that most other DDXs don't have that can help you diagnose (4)

Back 1430

-pain in 40%. most other differential diagnosis are painless. -uveitis that makes its first presentation in old age -mid-peripheral hemorrhages -unilateral

Front 1431

name 7 signs and symptoms associated with ocular ischemic syndrome

Back 1431

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)

Front 1432

if the pt passes out from gonio do you need to call 911

Back 1432

no, just a vasovagal response.

Front 1433

what are you looking for on follow-up for a pt wil ocular ischemic syndrome

Back 1433

neovascularization

Front 1434

describe the visual prognosis associated with OIS

Back 1434

60% will have counting fingers vision on 1 year follow-up

Front 1435

describe the pathogenesis of retinopathy of prematurity

Back 1435

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.

Front 1436

how do you manage retinopathy of prematurity

Back 1436

monitor frequently and refer to retina if there is vasoproliferation

Front 1437

describe the prognosis of retinopathy of prematurity

Back 1437

good; spontaneous regression of signs in 80-90%

Front 1438

New lecture: 12 Diabetic Retinopathy 2010

Back 1438

a

Front 1439

AOA CLINICAL PRACTICE GUIDELINES FOR DIABETES: http://www.aoa.org/documents/CPG-3.pdf -they provide clinical practice guidelines for almost any disease

Front 1440

what percent of diabetic pts are type 1

Back 1440

5-10%

Front 1441

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

Front 1442

what age group in diabetes increasing in

Back 1442

children and teens

Front 1443

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

Back 1443

fasting: 126 or higher non-fasting: 200 or higher oral-GTT: 200 or higher

Front 1444

what is a glucose tolerance test

Back 1444

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

Front 1445

how is the length of time a person has had diabetes related to their level or diabet retinopathy

Back 1445

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

Front 1446

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

Front 1447

what ethnicities have a high prevelance of diabetes

Back 1447

african americans 1.7X, hispanic 2.0X, asian/pacific island 2.0X, native americans 2.8X (figures relative to caucasian)

Front 1448

how can diabetes affect vision (4)?

Back 1448

1. color vision defect (tritan) 2. refractive error changes (can be dramatic) 3. accommodative dysfunction 4. visual field defects

Front 1449

does refractive error tend to become more myopic or hyperopic from diabetes? why?

Back 1449

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.

Front 1450

name three systemic symptoms associated with diabetes

Back 1450

polyphagia, polydypsia, polyuria

Front 1451

name 10 ways that diabetes can affect the eyes (retinal changes only 1)

Back 1451

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

Front 1452

name 6 test outside your normal routine that you might want to do for a diabetic pt

Back 1452

1. color vision 2. contrast sensitivity 3. fundus photography 4. gonioscopy 5. macular function 6. blood pressure

Front 1453

what is NVE (neovascularization elsewhere)

Back 1453

neo that is not at the disc or the iris. anywhere else.

Front 1454

name 9 pertinant negatives you need to check for and record on a diabetic eye exam and their abbreviations

Back 1454

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)

Front 1455

describe the pathophysiology for diabet retinopathy

Back 1455

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.

Front 1456

what is the difference between proliferative and non-proliferative diabetic retinopathy

Back 1456

proliferative has neovascularization

Front 1457

can microaneurysms leak

Back 1457

yes

Front 1458

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.

Front 1459

what type of hemorrhage are dot/blot/flame hemorrhages

Back 1459

intraretinal hemorrhages

Front 1460

what do hard exudates indicate

Back 1460

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)

Front 1461

what causes cotton wool spots

Back 1461

hypoxia

Front 1462

where in the retina do you tend to see cotton wool spots in diabetic retinopathy

Back 1462

within 3 DD of the ONH -usually not on the retina

Front 1463

what IRMA

Back 1463

intraretinal microvascular abnormalities. collateral route of circulation. form where there is hypoxia.

Front 1464

can IRMA turn into neovascularization

Back 1464

yes; it is a germination bed for neovascularization elsewhere.

Front 1465

what is the best way to look for venous beading on ophthalmoscopy

Back 1465

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.

Front 1466

what is venous beading

Back 1466

areas of vascular sludging or slowing of blook. look like beads.

Front 1467

diabetic retinopathy grading: http://eyephoto.ophth.wisc.edu/ResearchAreas/Diabetes/DiabStds.htm

Front 1468

how do you define minimal NPDR (non-prolifative diabetic retinopathy)

Back 1468

rare microaneuuysm

Front 1469

how do you define mild NPDR

Back 1469

at least one microaneurysm and one of the following: retinal hemorrhage or hard exudate.

Front 1470

describe the management of mild NPDR

Back 1470

1. monitor with Amsler grid 2. RTC 6-12 months 3. report findings to PCP/diabetologist

Front 1471

what are the chances that a person with mild NPDR will develop proliferative diabetic retinopathy (PDR) within one year

Back 1471

5%

Front 1472

how do you define moderate NPDR

Back 1472

(heme or microaneurysm > standard photo) OR (soft exudates, venous beading or IRMA)

Front 1473

describe the management of moderate NPDR (4)

Back 1473

1. monitor with Amsler grid 2. report findings to PCP/diabetologist 3. RTC 3-6 months 4. retinal consult if IRMA

Front 1474

what are the chances that a pt with moderate NPDR will develop PDR within 1 year

Back 1474

12-27%

Front 1475

how do you define severe NPDR

Back 1475

-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

Front 1476

describe the management for severe NPDR (3)

Back 1476

1. retinal consult for FA 2. report findings to PCP/diabetologist 3. RTC 3 months

Front 1477

what are the chances that a pt with severe NPDR will develop PDR within 1 year

Back 1477

52%

Front 1478

how close to the disc is NVD (neo of the disc)

Back 1478

right at the disc, or with-in 1-2 DD

Front 1479

what is NVE and where does it come from

Back 1479

neo elsewhere (not the iris or the disc). usually along the major arcades, come from IRMA.

Front 1480

why is fibrous proliferation an indication of proliferative diabetic retinopathy

Back 1480

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.

Front 1481

why is diabetic retinopathy associated with retina detachment

Back 1481

because the fibrotic proliferation by the glial cells that acompany neovascularization, to provide a supportive network, can contract and cause traction on the retina.

Front 1482

in what stages of diabetic retinopathy do you find clinically significant macular edema (CSME)

Back 1482

any stage

Front 1483

what is the difference between diabetic macular edema (DME) and clinically significant macular edema (CSME)

Back 1483

DME: within 1 DD of the macula CSMD: threatens or involves the macula

Front 1484

what ways can you tell clinically that there is macular edema

Back 1484

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)

Front 1485

edema shows up really well on OCT. hemorrhages and microaneurysms are hard to see with OCT though.

Front 1486

which form of diabetic retinopathy is pan-retinal photocoagulation most helpful for

Back 1486

proliferative diabetic retinopathy

Front 1487

does controling you blood glucose levels reduce your chances of developing diebetic retinopathy

Back 1487

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)

Front 1488

how soon do you need to refer pts with diabetic retinopathy

Back 1488

Refer within 2-4 weeks Macular edema PDR or very severe NPDR Refer within 24-48 hours High risk PDR Vitreous heme

Front 1489

do intravitreal injections of steroids help with the symptoms from diabetic retinopathy

Back 1489

the literature suggests that it does

Front 1490

New lecture: 13 Vitreous and Peripheral Retina 2010 (study this one)

Back 1490

a

Front 1491

where does a posterior vitreous detatchment (PVD) usually occur

Back 1491

around the optic disc (weiss ring)

Front 1492

what is the difference betwee vitreous liquefaction and syneresis

Back 1492

liquefaction is the collapse of the mollecular framework resulting in decreased viscosity. syneresis is the shrinkage and inward collapse of the vitreous

Front 1493

what are lacunae

Back 1493

little pocket of fluid that you can see in the vitreous. they can enlarge and coalesce

Front 1494

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

Back 1494

Third dummy answer

Front 1495

is asteroid hyalosis usually unilateral or bilateral

Back 1495

90% unilateral

Front 1496

is there an associate between asteroid hyalosis and any systemic conditions

Back 1496

yes. diabetes, HTN, vascular disease

Front 1497

what is synchysis scintillans

Back 1497

a very rare condition of freely floating crystals of cholesterol in the vitreous. it is associated with severe eye disease.

Front 1498

name 4 things you might see in the vitreous

Back 1498

1. asteroid hyalosis 2. synchysis scintillans 3. non-pigmented (white) cells (inflammatory) 4. pigmented cells (red-brown) (Shaffer'sign)

Front 1499

what is shafer's sign

Back 1499

red-brown pigmented cell that can be observable in the vitreous. can indicate retinal tear or detachment

Front 1500

name a pertinant negative for a retinal detachment suspect

Back 1500

Shafer's sign

Front 1501

name three subjective symptoms associated with posterior vitreal detachment (PVD)

Back 1501

1. sudden onset of floaters 2. photopsia 3. metamorphopsia

Front 1502

is a vitrectomy typically done for pts with PVD? why or why not?

Back 1502

no, because of the possibility of retinal detachment

Front 1503

why does an epiretinal membrane form from posterior vitreal detachment

Back 1503

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

Front 1504

what percent of the time do you tend to see epiretinal membrane form after a PVD

Back 1504

75%

Front 1505

name 4 clinically observable signs associated with PVD

Back 1505

1. weiss ring 2. possible hemorrhage 3. epiretinal membrane 4. macular edema or hole

Front 1506

what might you observe on high plus that would make you suspect epiretinal membrane

Back 1506

if you see retinal sheen or foveal light reflex on an older patient that you would no longer expect to see one.

Front 1507

what is the tx for epiretinal membrane

Back 1507

epiretinal membrane peel -has to be severe enough to make the surgery worth the risk.

Front 1508

what are the kinds of vitreous detachments

Back 1508

a)

Front 1509

how do you tell clinically if there is collapse of the vitreous

Back 1509

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

Front 1510

what percent of pts with PVD will have an associated retinal tear

Back 1510

10-15%

Front 1511

what proceedure do you need to do on pts with a PVD

Back 1511

BIO w/ scleral depression.

Front 1512

what is it called when the primary vitreous fails to regress completely

Back 1512

Persistent hyperplastic primary vitreous (PHPV)

Front 1513

New lecture: 14 PeripheralretinaST2010

Back 1513

a

Front 1514

can scleral indentation cause a retinal detachment

Back 1514

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.

Front 1515

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

Back 1515

Second dummy answer

Front 1516

what part of the retina is considered to be the peripheral retina

Back 1516

between the equator and the ora

Front 1517

how can you tell where the equator is on BIO

Back 1517

the vortex veins are pretty much mark the equator

Front 1518

what part of the retina do you find the short ciliary nerves

Back 1518

superior and inferior. somewhere between 10 and 2 and corresponding inferior positions. -used to deliniate nasal and temporal retina

Front 1519

what part of the retina do you find the long ciliary nerves

Back 1519

along the horizontal meridian (at about 3 and 9 o'clock) -they can be used to deliniate superior and inferior retina

Front 1520

how does the appearence of the ora differ between nasal and temporal sides

Back 1520

nasal ora is more notched. temporal ora is more smooth.

Front 1521

what is a common name for a vertex vein

Back 1521

mop (because it looks like a string mop)

Front 1522

what is common to see around vortex veins and why does this occur? is this of concern?

Back 1522

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

Front 1523

what do we think is the mechanism for white without pressure

Back 1523

retinal sheen caused by the interface between the retina and the vitreous causes reflectinos.

Front 1524

what is this

Back 1524

ciliary nerve

Front 1525

what is the pigmented patch between 2 and 5 o'clock

Back 1525

ora serrota

Front 1526

how can you tell if you are seeing ora during BIO

Back 1526

(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

Front 1527

how can you tell if something on the retina is a hole

Back 1527

retinal holes are always red

Front 1528

how can you tell the difference between an enclosed oral bay and a retinal hole

Back 1528

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)

Front 1529

describe the appearence of the vitreous base if you are able to see it on BIO

Back 1529

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)

Front 1530

what can cause RPE hyperplasia

Back 1530

anytime the vitreous is tugging on the retina

Front 1531

what is cystoid degeneration

Back 1531

Tiny bubble appearance next to ora beneath vitreous base Salt and pepper appearance at ora

Front 1532

what is cystoid degeneration of the peripheral retina difficult to distinguish with

Back 1532

whit without pressure

Front 1533

what is the difference between white with and without pressure

Back 1533

without pressure means appearence is there without scleral indentation. with pressure means that it appears when you do scleral indentation.