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205 Cards in this Set

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Where are the places where the vitreous is firmly attached (4)?

Weakly attached (3)?
vitreous base, optic nerve head, along areas of chorioretinal scarring, along the edges of lattice degeneration

macula, along retinal blood vessels, vitreoretinal tufts
When encountering a recent onset PVD, carefully evaluate the peripheral retina. An acute PVD has a _____ likelihood of having a retinal tear at initial presentation
15%
If there are no retinal defects seen (after a PVD), repeat examination in ________.

When encountering an acute PVD with vitreous or pre-retinal hemorrhage, but no discernible break (examining with Goldmann fundus lens, non-contact lens, and scleral depression), re-examine every ______ for ____. If no break is seen, re-examine at regular intervals until ______________ (what happens)?
6 weeks

2 weeks for 6 weeks; hemorrhage clears
When encountering a recent onset PVD and a retinal tractional break is seen associated with the PVD, refer for therapeutic treatment, as the risk of detachment is ___.
52%
Most floaters in patients under the age of 50 are due to __________.
benign vitreous syneresis.
PVD typically presents as what?
a singular large floater.
_______________ represents thinning of all 10 retinal layers due to dropout of peripheral retinal capillaries and resulting ischemia with subsequent retinal collapse and glial fibrosis.
lattice degeneration
Lattice degeneration typically has an appearance of a white lattice-type of degeneration representing ______ filling the degenerated lumen of the larger capillaries. A classic appearance is _____ degeneration, where it appears as a discrete fibrotic trail across the retina. Fibrotic appearance occurs in 12% of cases.

What is present in 80-90% of cases?
glial cells; "snail-track"

RPE hyperplasia (pigmentation due to the RPE thinking the retinal thinning=damage)
Lattice nearly always runs _______ around the eye.
circumferentially
Retinal degeneration (lattice and atrophic holes) causes secondary effects on the vitreous. What overlies the lesion? What is present along the edges?
• Vitreous liquefaction (hyaluronic acid) overlying lattice lesion. Develops lacunae.
• Increased vitreoretinal adhesion along edges of lattice lesion
Approximately _____ of all rhegmatogenous retinal detachments are caused by holes in lattice. Less than _____ of atrophic holes in lattice progress to retinal detachment.

In contrast to atrophic holes within lattice degeneration, the risk of retinal detachment occurring from a tear along the edge of lattice is much higher (____%).
30%; 2%

37%
T or F: The only instances where lattice lesions are treated prophylactically is if the patient previously had a retinal detachment from lattice degeneration in the fellow eye, or possibly if there is lattice in the eye of a monocular patient. Lattice lesions alone and those with atrophic holes are not treated. Tears along the border of lattice lesions are treated.
T
• Base of a flap tear is always toward_____ and apex of flap points towards _____.
• Mechanical forces pulling on the retina produce symptoms. The same forces that pull on the retina and cause symptoms exert force to further pull the retina off of the RPE. Traction may avulse flap, releasing traction and creating _____.
vitreous base; posterior pole; operculum
Subclinical retinal detachment can occur with flap tear or any other break. Subclinical detachment is defined as retinal detachment (or subretinal fluid) extending beyond ____ from the edge of the break, but not progressing more than ____ posterior to the equator. The presence of subretinal fluid is ominous as the retina has begun to detach.
1DD; 2DD
T or F: Symptomatic flap tears need prophylactic therapy. Asymptomatic flap tears with subclinical retinal detachment (fluid) and asymptomatic flap tear without fluid likely does not need treatment.
F!!! Asymptomatic flap tears with subclinical retinal detachment (fluid) NEED PROPHYLAXIS!
A patient comes into your office for a routine exam. They said several months ago they saw some flashes but they have stopped since then. You dilate and find a flap tear. Does this patient need prophylactic treatment?
No--> If a symptomatic retinal break stops being symptomatic for a period of several months, then it is considered to be asymptomatic and thus safer. (An asymptomatic flap tear without fluid likely does not need treatment.)
Asymptomatic operculated breaks without fluid DO/DO NOT need treatment. Symptomatic operculated breaks and those with sub-retinal fluid (either symptomatic or asymptomatic) DO/DO NOT need prophylactic treatment.
do not; do
_________: The splitting of the retina into an inner and outer layer.
• Results from the coalescence of ____________ of the peripheral retina.
retinoschisis; microcystoid degeneration
Where do Gunn dots show up?
Retinoschisis
Retinoschisis: 72% are in the ______quadrant while 28% are _________. It does not (seem to) occur anywhere else. Bilaterality in 82% of cases.
inferotemporal; superotemporal
T or F: The risk of detachment in retinoschisis with double layer holes is .25-1.4% which is ten times higher than risk of detachment in eyes with schisis without breaks.
T (w/out= .024%)
BOTH STILL LOW!!!
T or F: all symptomatic breaks must be treated
T
What's the most significant risk factor for progression (in phakic eyes) regarding retinal breaks?
The presence of photopsia in phakic eyes is the most significant risk factor for progression
T or F: : there is no difference in progression rate for a superiorly or inferiorly located retinal break.
T (BUT THERE IS MORE TROUBLE WITH SUPERIOR RETINAL DETACHMENTS DUE TO GRAVITATIONAL EFFECTS)
T or F: We treat ALL breaks associated with hemorrhage and of recent origin.
T
What's the most common management for a retinal detachment?
Scleral buckling procedure
T or F: prophylactic treatment are 99.9% successful in preventing detachment.
FF! 95-98%...untreated, many breaks have a better prognosis
Treat or don't treat? (Retinal breaks):
1. Any symptomatic break
2. • Lattice degeneration (without a history of lattice-related RD)
3. • Asymptomatic operculated breaks without fluid
4. • Retinoschisis (unless macula is threatened)
5. Any break with an associated subclinical detachment (fluid)
6 Any break associated with trauma
7. Any break with vitreous hemorrhage
1 tx
2 no tx
3 no tx
4 no tx
5 tx
6 tx
7 tx
Increased deposition of drusen is associated with RPE __________ and ________.

Drusen do alter Bruch's membrane and can lead to ________________________________.
thinning and atrophy.; choroidal neovascularization.
T or F: RPE atrophy increases the risk of wet AMD
F! atrophy= poor perfusion which can't support neo
Clinical Pearl: _________ is the most significant modifiable risk factor for AMD.
smoking
Hard drusen typically ____ AMD and soft drusen typically ___ AMD.
dry; wet
What people should take the AREDS supplement of antioxidants plus zinc for their AMD?
Those with extensive intermediate sized drusen, at least one large drusen, or non-central geographic atrophy in one or both eyes or those with advanced AMD or vision loss due to AMD in one eye and without contraindications such as smoking.
We use ____ laser for the juxtafoveal net and ________ laser for the extrafoveal net.
krypton; argon
What is Verteporfin (Visudyne) used for? What is it?
Photodynamic therapy: It is a light activated drug used to treat wet AMD...the tissues of the macula collect it and a laser activates it causing CNVM thrombosis
T or F: Photodynamic therapy is generally accepted as a good stand-alone treatment for wet AMD
F! likely to be used in conjuction with other tx's
Clinical Pearl: __________ are being investigated and used for edema secondary to vascular occlusions, diabetes, cystoid macular lesions, and wet age related macular degeneration. This promises to be a significant advancement in the treatment of maculopathies secondary to edema.
Intravitreal injections of steroids
What are the top four causes of CNVM?
1- mad degen
2- idiopathic
3- degenerative myopia
4- ocular histoplasmosis syndrome
What condition is due to the breakdown of RPE cells allowing seepage to occur into the sensory retina AND is believed to occur secondary to vasomotor instability or sympathetic nervous excitation?
central serous chorioretinopathy
T or F: an RPE detachment can commonly occur simultaneously to a retinal detachment in CSC
T
What is CSC highly associated with?
all kinds of STEROID use
CSC most often affects what gender? What ages?
male 10:1
20-50 (mid 30s)
What condition presents with decreased VA, metamorphopsia and hyperopic shift?
CSC (lifted PRs still viable-->hyperopic shift)
What characteristic does the Fluorescein angiogram have with central serous chorioretinopathy?
smokestack appearance with 1 or 2 well demarcated cavities
T or F: Treatment options for CSC are observation and direct photocoagulation to leaking areas in severe cases....nothing else.
T (NO STEROIDS/NO ANTI-VEGF)
There are two kinds of RPE detachment: ______ and ______.

Which one usually indicates CNVM?
serous; hemorrhagic

hemorrhagic (with serous: if no CNVM: observe)
With RPE detachment, ___% have concurrent sensory retinal detachment.
90
CP: T or F: RPE detachment and CSC typically occur simultaneously
T
CP: Always consider _____________________ in cases of mild paramacular hemorrhaging. Too often, this condition is overlooked and the findings are ascribed to diabetic retinopathy (even if the pt doesn't have diabetes!)
idiopathic juxtafoveal retinal telangiectasia
30% over 55 who develop RPE detachments will have what?
CNVM
CME occurs almost always from what?
leaking perifoveal capillaries
CME has a ___ appearance on FA.
petalloid
What is Irvine-Gass syndrome?
CME s/p complicated intracapsular cataract extraction (CP)
What is the prognosis for CME s/p cataract extraction?
GOOD: 50% spontaneously recover in 6 mos
T or F: Topical steroids are a good treatment for CME.
T (QID in notes...)
Vitreomacular traction syndrome can lead to what 3 things?
CME, epiretinal membrane or macular hole
___% progress from a stage 1->2 macular hole.

___% progress from a stage2-->3 macular hole.
50; 70
If you don't have an OCT, how can you tell if a macular hole is lamellar or full thickness?
VA: 20/80= lamellar
20/200= full
T or F: a patient with a stage 1 macular hole has a greater chance of it progressing if the fellow eye has RPE defects.
T
What's the most effective surgical tx for a full thickness macular hole?
vitrectomy to remove traction at hole edge and either gas or silicone oil tamponade
CP: small, symmetrical foveal cysts should be investigated for history of ______?
sun gazing (solar retinopathy)
After several days, this condition will have a reddish spot with pigment halo, which progresses to red lamellar foveal depression.
solar retinopathy (may progress to hole)
What is caused by VMT and is a break in the ILM with retinal glial cells proliferating on the surface?
epiretinal membrane
What is the treatment for epiretinal membrane? How bad does the VA have to be before you do the tx?
Vitrectomy with membrane peeling if vision is worse than 20/70
T or F: epiretinal membranes do not usually have acuity less than 20/200
T...only 5%
T or F: The best way to diagnose VMT is with OCT.
T
Pars plana vitrectomy and epimacular vitreous cortex aspiration is "today's management" for what conditon?
VMT and impending macular hole (when the VMT is bad enough to warrant surgery)
________ injections are a new/future therapy for VMT and macular holes.

The MIVI-TRUST study tested this injection vs. placebo and:
1. ___% had resolution of VMT
2. ___% had complete closure of macular holes
Microplasmin injections (Ocriplasmin)

1. 30%
2. 40%
_________: thrombolytic agent that targets adherence of vitreous to macula--> liquifies vitreous--> lysis between vitreous cortex and ILM.
Microplasmin injection (Ocriplasmin)
T or F: a healthy diet, physical activity and not smoking are good recommendations for those at risk for AMD, but the odds that the patient will develop AMD are the same.
F!!! 71% lower odds!
During the first AREDS study, what were the 5 constituents that were tested?

During the AREDS report 22-23, what 3 things were introduced?
Vit C, Vit E, Beta carotene, Zinc and Copper.

Lutein, Zeaxanthine, Omega's
T or F: according to AREDS research group report 22, high intake of lutein and zeaxanthine was independently assoc with decreased likelihood of progression towards ANY AMD stage.
T
T or F: AREDS 2 assessed Lutein, Zeaxanthine, and Omega-3s on patients with stage 3-4 AMD and also increased the amounts of Beta carotene and zinc in the original formula.
F!!! last part is false...they took out beta carotene and decreased zinc levels.
What were the results of the CATT study?
Avastin was equally effective as Lucentis for wet AMD (about 30% improvement in VA and over 90% avoided further vision loss)

Also, there might be more side effects with Avastin, but it could be due to casual finding or the pharmacy's fault
The VIEW study was to see if _____ was effective in treating _____ compared to ______.

Was is effective?
VEGF trap (Eylea); wet AMD; Lucentis

Yes (that's all I know...)
For diabetic macular edema, what is the only FDA approved treatment? What study is it based on?
Laser (Argon laser--focal photocoagulation of CSME); ETDRS (early tx of diabetic ret study)
T or F: only recommend the AREDS formulation for moderate to severe AMD.
T (that's what she said in class)
Diabetic Retinopathy clinical research network: Which has greater benefits with acceptable safety profile for the tx of DME: laser or intravitreal triamcinolone acetonide (2mg vs. 4mg)?
better efficacy on retinal thickness/VA improvement with LASER (laser still standard of care)
Retisert, Medidur, and Ozurdex are _____ that are being evaluated for use in diabetic macular edema.
steroid implants (may increase efficacy)
Match the study with the results (for diabetic retinopathy):
Studies: RIDE/RISE, RESOLVE, READ-2, Da Vinci phase 2

1. combo therapy of lucentis + laser showed less re-injection needed (and better than laser alone)
2. pts treated with anti-VEGF has fewer long-term DR complication/progression vs. sham
3. the anti-VEGF group had better VA gain: Ranibizumab for Edema of the Macula in Diabetes phase 2
4. VEGF trap had better visual improvement than laser
1. RESOLVE
2. RIDE/RISE
3. READ-2
4. Da Vinci
According to the SCORE study (steroids vs. standard of care), what was the better tx for:
1. CRVO?
2. BRVO?
1. intravitreal steroid (1mg)
2. grid photocoagulation (b/c there was no different with the steroid and the steroid caused more side effects)

these are for the edema causing decreased vision...
___________ is the first FDA approved steroid implant to treat macular edema assoc with vein occlusion.
Ozurdex
T or F: VEGF trap is a future tx option for vein occlusion
T (also advanced AMD and diabetic ret)
T or F: the BRAVO and CRUISE studies concluded that Lucentis injections were better than placebo for improving VA over 12 months
T (the sham group couldnt catch up to Lucentis group at 12 month mark...)
What new technology is a form of wide-filed retinal imaging and takes panoramic images of the central and peripheral fundus?
OPTOS
T or F: digital system - NIDEK is a digital stereo camera that is good for taking pics of the macula, optic nerve and for glaucoma.
T
Fundus autoflourescence uses the principle that _____ flouresces within the RPE cells.
lipofuscin (and atrophy hypoflouresces)
Detection of _____ AMD is important due to capability of progressing to wet AMD.
imtermediate (so genetic testing is good to test probability that the pt will develop advanced amd)
MPOD "Quantifeye"- HFP:

Measures amounts of ____ and ____ in the macula. These are ____ in the subclass _____. They filter ___ light and quench ___ ___.
lutein and zeaxanthine; carotenoids; xanthophylls; blue; free radicals
MPOD "Quantifeye"- HFP:

HFP measures ____ of light by Macular pigments.

_________= optical density

There will be a need for higher/lower intensity of the test stimulus (white/green) required centrally due to attenuation of blue light by MP.
absorbance;

absorbance of MP;

higher
MPOD = ?

What's the average MPOD value?
log (intensity required centrally/intensity required peripherally)

.25-.45
T or F: you would not due MPOD-HFP on an eye with advanced macular disease.
T (too late at this point...this test is to see the pigment available to prevent the condition from getting this far)

also, wouldnt do for an eye with cataract (they wont see flicker)
___________________- is a good test for monitoring dry AMD since early detection influences treatement outcomes
preferential hyperacuity perimetry
PHP is a _______ test that evaluates the central _____ degrees. (TQ)
functional; 14
Drug toxicity is ______ and ________ dependent.
dose; duration
_____ and _____ are anti-malarial and anti-inflammatory drugs as well as anti-rheumatic drugs that can cause ocular toxicity.
1. Which is more toxic?
2. whats the mechanism of causing toxicity?
Plaquenil (HCQ) and Aralen (CQ);
1. Aralen
2. They are melanotropic drugs: RPE holds drug for prolonged time even after d/c...accumulation of toxic products causes photoreceptor damage
What are the two ocular toxicities (the names of them...one anterior seg one posterior seg) that are caused by Plaquenil/Aralen?
Corneal verticillata (Vortex keratopathy) and Bull's eye maculopathy (also see this with cone dystrophy...)
For Plaquenil:

1. a daily dose of > ____ mg/kg is toxic.
2. a person with more/less fat could be given overdosage of med
3. duration of use over ___ years increases risk of toxicity
4. age over ___ years old increases risk
1. 6.5
2. more (so it should be based on HEIGHT not weight)
3. 5
4. 60

also, renal or retinal impairment can increase risk of toxicity
Plaquenil drug toxicity: New 2011 Screening procedures:

1. Baseline exam --> ____.
2. ____ visual field (identifies functional loss
3. fundus __________
4. ________ ____ (loss of IS/OS junction or thinned ONL)
5. fundus _________ (loss of this= RPE damage...degree of loss correlates with vision)
6. ________- will show a paracentral ERG depression
1. DFE
2. 10-2 (2 deg within macula)
3. photography
4. SPECTRAL domain OCT
5. autofluorescence
6. mfERG
T or F: with patients on Plaquenil, low/high risk patients need yearly screenings and those with probable/clear toxicity need to be monitored every 3 months.
T (for those with toxicity, we need to co-manage with PCP/rheumatologist to discuss discontinuing the med)
Why does VA decrease with Tamoxifen use?

What shows up in the macula?
secondary to foveal cysts

white crystalline macular deposits
_______, a high cholesterol medication, can lead to what?
Niacin; cystoid macular edema (resolves when d/c)
________, used for MS, hepatitis and other viral diseases, can lead to CWS near the optic nerve, hemorrhaging and macular edema.
Interferon
Commotio retinae is an example of coup or contrecoup traumatic retinopathy?
contrecoup
What traumatic retinopathy can be confused with white without pressure (looks white/opaque)?

What's the VA?

What's the best tx?
commotio retinae

20/20-400 depending on maular involvement

benign neglect (these pts have good prognosis)
_______: preretinal or subretinal hemorrhage usually from subarachnoid hemorrhage (ruptured cerebral aneurysm).

When is this an emergency?

CP: Where are the hemorrhages? What testing must be done if this is an emergency?
Terson's syndrome

If seen in conjunction with head trauma...and/or patient is complaining of a severe headache

peripapillary; immediate radiological scans
__________: preretinal hemorrhages arising from sudden increase in internal pressure thru exertion or strangling.

Are these self-limiting or need tx?
valsalva hemorrhages

self-limiting...no tx...follow up closely if the patient has sickle cell/a hemoglobinopathy
__________: seen in crush injuries (head/chest trauma).

What's the VA?

What color are the patches?
Purtscher's retinopathy

severe vision loss (20/200- CF) (pts left with patchy retinal dysfunction)

white (could represent extensive microinfarct--Purtscher flecken-- or leukocytic infiltration or fat embolization from bone marrow)
What inheritance pattern is the most common with the best prognosis? Which has the worst prognosis?
AD; X-linked
T or F: Multifocal ERG is a more non-specific test while Flash ERG is more specific (targets macular/cone disorders)
F! other way around
Which test (Flash ERG, Multifocal ERG, EOG):
1. is helpful for patients with rod-cone disease when rod response is already clearly abnormal or extinguished but need to monitor cone progression

2. mostly used to confirm Best's disease.
1. mfERG
2. EOG
The Arden ratio (light peak/dark trough) is used for what testing procedure?

What does it indicate?
EOG (2:1 is normal...less than 1.7:1 is abnormal)

disease of the RPE
If the ERG and mfERG are normal but the VEP is abnormal, where is the problem isolated?
the optic nerve
What's the most common hereditary dystrophy?

What's the most common macular dystrophy?

What's the second most common macular dystrophy?
retinitis pigmentosa

stargardt's macular dystrophy

Best's vitelliform macular dystrophy
What are the two systemic associations (that we have to know for the test) associated with Retinitis pigmentosa and what do they consist of?
USHER'S SYNDROME: RP WITH HEARING LOSS

Bardet-Biedl syndrome: RP with obesity, retardation, polydactyly, hypogenitalism and renal disease
Retinitis pigmentosa:
1. what is lost first: rods or cones?
2. WHAT IS THE CLASSIC TRIAD?
3. What diagnostic tests (2) are needed for this disease and what do they show?
1. rods
2. Arteriolar attenuation, waxy (yellow) pallor of the optic nerve, and retinal bone-spicule pigmentation due to pigmentation in the vascular walls...early on it is seen as SALT AND PEPPER fundus due to diffuse de-pigmentation of the RPE
3. VF: ring scotoma 360 degrees and ERG: ABNORMAL DARK ADAPTATION, decrease A or B amplitude and increase latency of scotopic responses (As disease progresses, abnormal cone response will occur)
T or F: the prognosis for retinitis pigmentosa is poor
T (most pts have poor acuity and are legally blind by 50)
What are three nutritional supplements that can be recommended for retinitis pigmentosa?

What other tx is there?
Vit A palmitate, DHA (omega 3), and Lutein (for non-smokers)

NO REAL GOOD TX; hearing test, treat assoc conditions (CME, PSC), low vision referral/counseling
What condition has: abnormal color vision, arteriolar attenuation, disc pallor, and bone spiculing within the macula?
inverse atypical retinitis pigmentosa
What condition has punctate whitish-yellow spots outside of the posterior pole with autosomal recessive inheritance and is PROGRESSIVE?
Retinitis puntuate albescens (advanced cases demonstrate classic RP appearance)
What condition is a form of congenital stationary night blindness and may be confused with retinitis pigmentosa but doesn't progress? (has small white spots in midperiphery with non-progressive congenital night blindness)
Fundus albipunctatus
What congenital dystrophy has the classic bulls-eye maculopathy later in the progression of the disease?
Cone dystrophy
What congenital dystrophy will have an abnormal ERG with reduced or absent photopic and cone response with normal scotopic response (late stage will have abnormal scotopic if rods become involved)
Cone dystrophy
Best's vitelliform macular dystrophy has what inheritance pattern?

What does the Vitelliform stage consist of?

What's the best diagnostic test to do?

What's the prognosis?
autosomal dominant

elevated "egg yolk" macular lesion

EOG (low Arden ratio 1.1-1.5)

Ultimately poor (need to watch for development of CNVM)
What condition has an oval macular lesion with a beaten bronze appearance (mottling of fovea) and possibly yellowish flecks around the posterior pole?
Stargardt's macular dystrophy
For stargardt's macular dystrophy:
1. what does the FA look like?
2. what does the mfERG show?
3. what does the flash ERG show?
4. what is the underlying cause of disease?
1. dark, silent choroid
2. abnormal even in the early stages
3. normal unless late stage
4. enzymatic defect within RPE-->enlarged RPE with lipofuscin-> retinal atrophy/thinning
Fundus flavimaculatus is a variant of STargardt's but without the what?
maculopathy (good prognosis)
What choroidal dystrophy is:
1. AD?
2. X-linked?
1. central areolar dystrophy
2. choroideremia
What choroidal dystrophy has hyperornithemia?

What's the tx?
Gyrate atrophy

B6 (puridoxine)
The primary retinal telangiectasias has _____ predilection and _____ presentation.
male; unilateral
Idiopathic macular telangiectasia:
1. group 1: unilateral or bilateral? males, females, or no difference? easily visible telangiectasias or occult? exudates or no exudates?
2. group 2? same questions as above
1. unilateral; 90% males; easily visible (temporal to the fovea); exudates
2. bilateral (98%); males and females in middle age; occult; no exudates
What condition is known for right angle venules?
Group 2 idiopathic macular telangiectasia
Always consider _____ if pt presents with idiopathic parafoveal edema or dot/blot hemorrhages especially if there is no hx of ischemic vascular disease.
idiopathic macular telangiectasia
What does the classic OCT look like in group 2 idiopathic macular telangiectasia? (TQ)
draped ILM (superficial retina) over a cystic change (may look like ERM but vessels won't be misdirected here!)
CP: Consider _____ testing in pts with parafoveal hemorrhaging or leakage. If these diseases are not present, then __________ is the likely cause
vascular (HTN, DM); telangiectasia
When do you treat idiopathic macular telangiectasia and with what?
Observe: typically for type 2 non-proliferative or early type 1

Laser photocoag: for progressive or moderate type 1 with vision loss

Anti-VEGF: tx edema assoc with type 1 or for proliferative stage type 2
Leber's miliary aneurysm is most likely a variant of ________ but affect only one quadrant (_______) in the mid-periphery. It has a ____ predilection with _____ presentation.
Coat's disease; superior temporal; male; unilateral

(has later onset than Coat's and has no exudation/leakage unlike Coat's)
Coat's disease has a ____ predilection and ____ presentation. It presents with mild to massive aneurysmal _____ along with hemorrhage and edema.

A _____ RD can develop as well as ____ glaucoma.
male; unilateral; EXUDATES; serous (exudative); neovascular
When determining if there is a CNVM, look for a _________(color) lesion, _____, and signs of _____.
gray-green; fluid; leakage (retinal thickening, edema, detachments, hemorrhage)
What 3 locations can CNVM be in?
subfoveal, juxtafoveal, extrafoveal
Type 1 CNVM is ___ the RPE (commonly observed in ___ pts)

Type 2 CNVM is ___ the RPE and observed in ____ and ____ patients
below; AMD

above; myopic degeneration and histoplasmosis
What dye is better to use for a fluorescien angiography to detect CNVM?
indocyanine green (ICG) imaging-- better penetrates deep layers
CP: Suspected/actual CNVM is an ocular urgency or emergency?

When should the patient get a FA?
emergency--- they can grow 10-20 microns per day

72 hours
What vasculopathy was originally thought to be prevalent in middle-aged black women? (now is known to be 50-70s with predilection for pigmented races)?
Polypoidal choroidal vasculopathy (CNV variant)
What condition presents as aneurysmal structures at the termination of a network of dilated inner choroidal veins AND gives recurrent hemorrhagic/exudative detachments of the retinal pigment epithelium?

What does the diagnosis require?
Polypoidal choroidal vasculopathy

Indocyanine green angiography (you can see the polyps under the RPE!)
According to the EVERST study, what treatment is showing promise for polypoidal choroidal vasculopathy?
PDT + anti-VEGF drugs
_______ is pathological new vessels that initiate from the intra-retinal capillaries invading superficial and subretinal/choroidal space.

It is unilateral/bilateral affecting younger/elderly indivduals.
retinal angiomatous proliferation (RAPP-CNV variant)

bilateral; elderly
T or F: to differentiate retinal angiomatous proliferation from wet AMD, you need to look for drusen. RAPP won't have drusen.
T
What diagnostic test is used for RAPP?
Indocyanine green angiography
What's the difference between ERM and choroidal folds in terms of how they look?
ERM radiates from the macula[ choroidal folds are horizontal foldings often across the macula...they also produce alternating dark and light yellowish streaks in the posterior pole
T or F: tumors can cause epiretinal membrane
F! choroidal folds might appear like ERM...but choroidal folds is the answer
What condition do Laquer cracks and Fuch's spots occur? What are they?
degenerative myopia

laquer cracks: breaks in bruch's membrane with accompanying choroidal atrophy (increased risk for CNVM)

fuch's spots: RPE hyperplasia overlying CNVM
T or F: the CNVM in degenerative myopia is generally not treated
T...spontaneously involutes and doesn't grow significantly
____ ____ are breaks in Bruch's membrane that appear similar to blood vessels.

What is the systemic assoc that occurs most often with this condition?
angoid streaks

pseudoxanthoma elasticum (80-90% of the 50% who have systemic assoc...) groinblad-standberg syndrome
What's the most common intraocular tumor?
choroidal nevi (BENIGN)
T or F: choroidal nevi is common in children
F: Rare
T or F: overlying drusen or orange pigment is normal for choroidal nevi
T (macrophages containing lipofuscin from disrupted RPE)
CP: while ____ mm is considered the upper limit in size of benign choroidal nevi, they can be (rarely) larger. They won't, however, exceed ___mm in thickness.
5; 2
Oculocutaneous albinism can be tyrosinase+ or -. Which one has better vision?

In ocular albinism, ____ are deficient in number.
tyrosinase + (hermasky-pudlak syndrome is a subtype assoc with abnormal bleeding patterns)

melanosomes (chediak-higashi syndrome is a subtype assoc with poor bacterial resistance and lymphoma like condition)
CP: What's the main cause of visual difficulty in albinism? What is the other hallmark of true albinism?
macular hypopigmentation; nystagmus
T or F: oculocutaneous albinism is autosomal recessive only
T (ocular can be this or x-linked)
T or F: high oxygen concentrations (like in an incubator) shunts normal maturation of BVs
T
T or F: with retinopathy of prematurity, you need to monitor any infant under 2lbs 2oz for retinal detachment every day for 14 weeks.
F...every 2 weeks for 14 weeks, then every 1-2 months, then 6-12 months.
What is the inheritance pattern of familial exudative vitreoretinopathy? Is it unilateral or bilateral?

What is the treatment if a patient develops neo?
AD; bilateral

panretinal photocoag
CP: In pts with an ectopic macula, dragged retinal vessels, peripheral vitreoretinopathy with incomplete peripheral retinal vascularization yet no Hx of premature birth or low birth weight, what's the dx?
FEVR (familial exudative vitreoretinopathy)
CP: Consider what two conditions when encountering peripheral exudation?
FEVR and Coat's disease
What are the main causes (2) of blurred vision with posterior uveitis?
CME and vitritis
T or F: pain and photophobia are not complaints with posterior uveitis
T
___________= old inflammatory exudates that accumulate on vessels in posterior uveitis
vascular sheathing (candle wax dripping)
Who does pars planitis usually happen to? Unilateral or bilateral?

TQ: What condition is it strongly assoc with? What testing would you need to test for this?
young, healthy patients; bilateral (85%)

multiple sclerosis (and Crohn's); MRI for MS
CP: What is the #1 cause of pediatric vitreous hemorrhage?
pars planitis
When encountering a PVD in a young patient, what are you looking for?
vitreal cells and other signs of pars planitis
PVD, snowballs, snow banks and periphlebitis are signs of what?
pars planitis
What is the medical (not surgical) tx for pars planitis (that need tx)?
Systemic steroids (preferably) for several months
What is the #1 cause of posterior uveitis?

What is the #1 cause of focal chorioretinitis?
Toxoplasmosis for both
What posterior uveitis is caused by:

1. an obligate intracellular protozoean parasite
2. a fungus in soil
3. a parasitic nematode (round worm)
1. toxoplasmosis
2. histoplasmosis
3. toxocariasis
Quick: HEADLIGHTS IN A FOG?!!
toxoplasmosis (fuzzy white lesion with overlying vitritis)
If you give a patient oral sulfadiazine with pyrimethamine for toxoplasmosis, what else do you have to give them? Why?
folic acid supplementation: pyr is a folic acid inhibitor
What is the treatment that would most likely be given TODAY for toxoplasmosis?
Bactrim DS (trimethoprim/sulfamethoxazole) BID x 4-6 weeks

(or Bactrim BID and Bactrim DS QD?)
T or F: all patients with toxoplasmosis need treatment with Bactrim (or another appropriate drug)
F! it's often simply monitored if not affecting vision and immune system is healthy
When encountering active toxoplasmosis, especially in a young patient, strongly consider what testing?
HIV (immunosuppression can cause you to acquire this/have recurrent episodes)
Chorioretinal scarring in the absence of trauma= ?
toxoplasmosis
T or F: you can treat toxoplasmosis with prednisone 40mg QD if the patient is allergic to Bactrim
F!!! need to have at least one other appropriate tx in order to use a steroid
What is this: granuloma on retina, ONH or macula (white, elevated, about 1 DD) as well as vitritis with vitreal strand to the optic nerve?
toxocariasis
T or F; toxoplasmosis is assoc with cats and toxocariasis is assoc with puppies
T
What is this: peripapillary choroidal scarring with peripheral atrophic spots/scars (punched out lesions)
ocular histoplasmosis syndrome
CP: treatment for histoplasmosis is not directed towards the cause of histo but to the _____________.
neovascular maculopathy (krypton laser for juxtafoveal neo, PDT, anti-VEGF)
CP: Ocular histoplasmosis syndrome can look exactly like multifocal choroidopathy with one exception: _______________.
OHS never causes cells to appear in the vitreous bc it is purely a choroiditis
What gender/race does sarcoidosis occur more often in?

What are 3 things that can diagnose sarcoidosis?
Females/A.A.

Chest x-ray: hilar adenopathy
angiotensin converting enzyme
gallium scan (gallium uptake only in sarcoidosis)

(conj.biopsy or biopsy of skin granulomas)
What is this found in: granulomatous anterior uveitis (mutton fat KPs) and posterior synechiae as well as periphlebitis (candlewax drippings) and vitritis
Sarcoidosis
CP: ____ should be high on your list of differntial diagnoses when encountering retinal periphlebitis (HE SAID TWO CONDITIONS)
sarcoidosis and syphilis (also found in toxoplasmosis, pars planitis, Eales' disease)
What is this: vascular occlusion secondary to posterior segment inflammation (this should be all you need...)
Eales' disease
Who does Eales' disease effect? (gender/age/health)

25% also have __________.

There's a high association to ________ sensitivity.
Healthy, young males 20-30s

hearing/balance difficulties

tuberculoprotein
CP: two key features of Eales' are _____ and _____.

CP: Eales' disease targets who?
venous periphlebitis and venous obstruction

healthy young males
CP: Suspect ____ in cases of posterior seg neo, vitreous hemorrhage, tractional detachment in young, healthy males with no hx of diabetes.
Eales' disease
CP: Suspect ____ when encountering perivascular scarring
Eales'
CP: Whenever you see retinal periphlebitis, vasculitis, or candlewax drippings, immediately think of what two things?
sarcoidosis and syphilis
What three conditions have a viral prodrome (in this lecture)?
Vogt-Kyanagi-Harada syndrome and two white dot syndromes: APMPPE and multiple effervescent white dot syndrome
CP: __________ is characterized by granulomatous panuveitis ssoc with serous retinal detachments, optic disc edema, neurologic abnormalities and skin pigmentary changes.
Vogt-Koyanagi-Harada syndrome
White dot syndromes:

1. which does NOT occur in young patients?

2. which does NOT have a preference towards females?

3. which is the only one with a poor prognosis?
1. birdshot retinochoroidopathy

2. APMPPE

3. birdshot (due to chronicity)
Which white dot syndrome:

1. has HLA B27 assoc?
2. has HLA A29 assoc?
1. birdshot
2. APMPEE
White white dot syndrome has yellow-white placoid lesions (cream colored--may be gray) with an overlying vitritis?
APMPEE
What white dot syndrome has early hypofluorescence due to blockage then late staining (hyperfluor) on FA?
APMPEE
Which white dot syndrome is unilateral?

(hint: old lesions manifest as tiny orange dots in the fovea: macular granularity)
multiple effervescent white dot syndrome
What differentiates multifocal choroiditis (pseudo-histoplasmosis) from true histo?
THIS HAS VITRITIS (vitreous cells); true histo doesn't

also, this likely doesn't have peripapillary scarring