Final Exam Flashcards Preview

Oc Dz 3 > Final Exam > Flashcards

Flashcards in Final Exam Deck (321):
1

Cystoid Macular Edema

Accumulation of fluid in Henle's fiber layer with cyst like spaces.

2

What is CME called if there are no cyst

clinically significant macular edema. Often seen in diabetic maculopathy.

3

CME subjective

blurred vision, metamorphosis, washed out vision

4

What conditions cause CME

DR, Vein occlusion, post surgery (cataracts, glaucoma, retinal detachment), uveitis, RP. Post DR. OU.

5

Signs of CME

Loss of foveal depression, thickening of fovea, foveal folds.

6

FA of CME

Increase in vascular permeability, accumulation of dye in OPL of retina, Radial arrangement of fingers in henley (causes a petaloid pattern)

7

Tx of CME

Topical NSAIDs (voltaren qid) or topical steroid (prednisolone acetate qid) for 1 month and taper. If doesn't work Consider oral NSAIDS (indomethacin) or oral steroid (prednisone) or oral acetazolamide (diamox). Can also do steroid injection. Can also do vitrectomy.

8

Epiretinal Membrane

Cellular proliferation along the internal limiting membrane and retinal surface. Epirretinal membrane looks like wrinkled cellophane.

9

What causes epiretinal membrane

Most are idiopathic. Can be due to prior retinal surgery, intraocular inflammation, vitreous hemorrhage, trauma, cryotherapy.

10

Epidemiology of epiretinal membrane

increases in incidence with age

11

Symptoms of Epiretinal membrane

asymptomatic, decreased vision, metamorphosis, micropsia, monocular diplopia.

12

Epiretinal membrane signs

Normal or decreased acuity. Abnormal ambler grid. BV are tortuous by stretched from the disc. Retinal folds or striae.

13

Epiretinal membrane Tx

Tx rarely needed. Vitrectomy and membrane peel in patients with reduced acuity (

14

What does chloroquine and hydroxychloroquine treat.

(used to treat malaria, arthritis, and SLE)

15

Signs of toxic retinopathy from chloroquine and hydroxychlorquine

small scotoma, supernormal EOG, abnormal photostress test, decreased color vision, VA typically affected later. Abnormal macular pigmentation (bulls eye)

16

What dosage of chlorine and hydroxyqhloroquine will cause toxic maculopthy?

chloroquine > 250-300 mg/d. Hydroxychloroquine >700-750 mg/d

17

How to scan patient taking hydroxychlorquine or chloroquine?

DFE, OCT, 10-2 threshold VF, and autofluroscene as baseline. Should be seen every 6 m.

18

Toxic maculopathy caused by Thioridazine

Used to treat psychotic patients. Can produce decreased vision, night vision problems, ring scotomas, brown discoloration of vision. Will have granular pigment-normally mid peripheral and then coalesces into large areas of pigmentation.

19

Toxic Retinopathy caused by Tamoxifen.

Tamoxifen used to treat breast cancer. Results in decreased vision, refractive yellow-white spots thought the posterior pole. Can also be seen with drug user as they dilute drugs with it.

20

Choroidal Folds

Folds of the choroid and the overlying structures. Due to flattening of the posterior pole-->acquired hyperopia as the retina is pushed anterior to the plan of focus.

21

Choroidal Folds causes

idiopathic, hyperopia, choroidal tumor, CNM, optic disc swelling, orbital tumors, hypotony, orbital and scleral inflammation.

22

Choroidal folds symptoms

asymptomatic, blurry vision, metamorphsia.

23

Choroidal folds FA

Will see alternating hypo and hyper fluorescent lines. Hypo=RPE troughs. Hyper=RPE peaks.

24

Mgmt of choroidal folds

Usually idiopathic. Diagnosis of exclusion.

25

How much ocular volume does vitreous compromise?

75%

26

What percent H20 is vitreous?

99

27

Vitreous attachments

Lens attachments (Weiger's adhesion), vitreous base (pars plans), Optic disc margin, Macular area

28

Which vitreous attachment is weakest

Macular

29

What vitreous attachment is strongest

vitreous base (pars plans and peripheral retina)

30

Vitreous degenerations

Liquefaction occurs over time. Syneresis=shrinking with inward collapse of vitreous also occurs. Increases in myopes. Creates Lacunae (liquid spots)

31

Examination of the viterous

Must dilate.

32

Unusually findings in vitreous

cells, blood, pigment, PVD.

33

Asteroid Hyalosis (benson's disease)

90% unilateral. Calcium. Reflective yellow shite spheres-gold. Commonly asymptomatic. Associated with Diabetes, HTN, vascular disease.

34

Synchysis Scintillans (cholosterolosis bulbi)

Bilateral and rare. Free floating flat crystals of cholesterol. Associated with severe eye disease.

35

Non-pigmented cells (white) in viterous

Inflammatory cells. May be fine, course, or snowball.

36

Staffer's Sign

Pigmented cells (red brown) in vitreous. Occurs with retinal tear or detachment.

37

Intraviterous hemorrhages

Ruptured vessel bleeds through break in hyaloid membrane. Associated with DR, Retinal breaks without RD, rhegmatogenous RD, RVO. Slow reabosrption

38

Retroviterous hemorrhage

Blood trapped between retina and hyaloid membrane. Associated with trauma, DR, retinal breaks without RD, RD, RVO. Shifts with eye movement. Boats and blobs.

39

PVD

Hyaloid membrane is pushed forward due to liquification.

40

PVD symptoms

Floaters, photopsia, blurry vision, possible metamorphosis, possible red hue of vision.

41

Signs with PVD

Weiss Ring, Possible hemorrhage, may be able to see collapsed posterior limiting layer of the vitreous,

42

Epiretinal membrane and PVD

Associated with PVD. 75% of eyes with PVD. May result in macular edema or full thickness macular hole.

43

How to dx Macular hole

Stratus OCT.

44

Categories of vitreous detachments

complete PVD with collapse, complete PVD without collapse, incomplete PVD with collapse, anterior vitreous detachment.

45

Retinal involvement with PVD

Breaks usually at posterior base. PVD found in 80% of patients with retinal tears. Retinal tears with PVD occurs in 10%.

46

Mgmt of PVD

DFE with scleral depression (normally retinal detachment will occur 6 weeks after PVD), Advise, RTC 1-2 weeks then 1 month later, retinal referral if break noted.

47

Persistent Hyperplatic Primary Viterous (PHPV)

Failure of primary vitreous to regress, unilateral, full term gestation with no oxygen supplementation.

48

Anterior PHPV

Mild to severe lens involvement with minimal posterior pole changes. Mgmt with surgery

49

Posterior PHPV

Vitreous membrane and vitreoretinal adhesion, peripapilallary RPE changes, pale hypo plastic disc. Mgmt-monior.

50

Congenital hereditary retinoschisis

Retinal splits at NFL. Bilateral. X-linked. Inferotemporal 50% with a veil membrane that does NOT run to ora. Macular involvement 98%. RD 25%, vitreous hemorrhage 40%.

51

How to diff. congenital hereditary retinoschisis from RD

Will not move or bounce around at all. Retinal with move with RD. Will have an absolute field defect (with RD can have normal field as cells still firing)

52

Iatrogenic Viterous changes

PVD (from surgeries), vitrectomy (removal of vitreous for RD surgery), vitreal prolapse (herniation of vitreous through breaks/holes), literal hemorrhage (break during surgery)

53

Peripheral retina

zone from the equator to the ora errata. 3DD in width.

54

Landmarks in peripheral retina

vortex vein, long posterior ciliary nerves, short posterior ciliary nerves, ora serrated, pars plans, vitreous base

55

Cystoid degeneration

Present in almost everyone. Retinoschisis association. Found in peripheral retina

56

Chrotioretinal degeneration

Found in peripheral retina. AKA pigmentary degeneration. Very common

57

Paving stone degeneration

Found in peripheral retina. AKA cobblestone degeneration. 27% population and in myopes more. Inferior temporal retina more common.

58

Reticular pigmentary degeneration

Peripheral retina findings. Bone spicule like RPE mottling. Elder patients.

59

Equatorial drusen

AKA peripheral druse. Not involving macula=benign

60

Snowflake degneration

inherited condiiton. Don't worry about. Peripheral retina.

61

Lattice degneration

Thin areas of the retina. IN mid periphery. Holes often form. Education on RD

62

Pigmented lattice degeneration

Thin areas of the retina but with pigmentation.

63

Snail track degeneration

lattice variation in a snail track line. Risk of RD.

64

White without Pressure

Usually benign.Seen temporal in most eyes and bilateral. Vitreous liquefaction. Retinal holes/breaks can occur.

65

Vitreoretinal adhesion

No tear-watch. Tear-refer.

66

How to best view peripheral retina

Scleral indentation

67

What is the distance from ora to equator?

1/5 the entire retina

68

Where is paving stone degeneration normally found

Inferior nasal

69

Where is lattice normally found

superior.

70

Enclosed oral bay

Entrapment of pars plans around the areas of ora. More common in nasal. Not important. DDX with depression and will not lift with dynamic movement of the tissue.

71

What color are holes in the retina?

Red

72

Meridional Fold

Whiter, slightly elevated compared to the retina. Involve all neural layers. 1/2-4 DD. Vessels course over them. Most commonly aligned with processes.

73

Incidence of Meridional Folds

25% of eyes. Bilateral in 50%. M>F. Usually only one fold but multiple in 27%. Congenital but can increase in size with age.

74

Location of Meridional Folds

Superior nasal. Perpendicular to ora. Radially oriented folds of redundant retinal tissue

75

Meridional Complex

Meridional folds that covers both bay and process.

76

Associated findings with meridional folds

Vitro-retinal tags at end of folds. Can also find holes at posterior end possible and this can lead to retinal detachment (especially temporally). Holes even more common in meridional complex.

77

Management of meridional folds

Scleral depression to check for holes. Follow every 3 months for RD if hole or tag. If risky use cryopexy.

78

Cystoid Degeneration

Tiny bubble appearance next to ora beneath vitreous base. Salt and pepper appearance. Thickened retinal tissue. Slightly opaque. Can be difficult to distinguish from WWP.

79

Cystoid degeneration location

Superior temporal retina. Bilateral and symmetrical. May go all the way to the equator. .

80

Incidence of cystoid degeneration

Common in children over age of 8 but progresses with age.

81

Where does the cystoid degeneration occur

Cystoid spaces occur between retinal layers (outer plexiform layer)

82

Cystoid degeneration associations

Retinoschisis. With time can extend between inner and outer limiting membrane.

83

Cystoid Degeneration Managment

No tx. If hole found in tissue, very little chance of RD. Holes usually within vitreous base so no traction-tugging is from a broad base and not pulling on that hole and fluid in the retina goes into cyst spaces.

84

White without pressure description

Usually parallel to ora. Milky white/opalecent. Scleral depression increases whiteness. Present without pressure. Posterior margin is irregular, yet sharp. Flat.

85

White with pressure

Only can see it when pressing on retina with pressure

86

White without pressure incidence

32% of eyes. Increases with age. More commonly seen in more deeply pigmented race.

87

White without pressure location

Between ora and equator. Can extend to posterior pole. Inferior nasal least common. Can increase with age.

88

What causes white without pressure?

Unknown cause but two theories. Increased reflectivity of photoreceptor outer segment or manifestation of peripheral vitreous traction.

89

White without pressure tx

No significant associated findings. No management unless vitreous degeneration, nearby lattice degeneration, or history of large retinal tear in other eye.

90

Pavingstone degeneration description

appears as multiple round punched out lesions. Yellow white in appearance because seeing sclera. Discrete margins often with pigment. Can see large choroidal vessels at base. Excavated and not elevated.

91

Paving stone degeneration incidence

22% of eyes. Increases with age

92

Paving stone degeneration location

80% in inferotemporal quadrant. usually between ora and equator.

93

Cause for paving stone degeneration

Infarcts in choriocapillaries. Inner retinal layers and vitreous are not affected. There is thinning in outer retina.

94

Tx for paving stone degeneration

Sometimes coalesce to yield scallops of pigment. No associated findings. Only need to document.

95

Reticular Senile Pigmentary Degeneration Description

Pigment clumping

96

Reticular Senile pigmentary degeneration incidence

18% of population. Bilateral in almost all cases

97

Reticular Senile Pigmentary degeneration location

Can be anywhere but possibly more apparent nasal. Can extend to equator.

98

What is reticular senile pigment degeneration often seen as?

RP. Will not have no VF defects or night blindness though

99

What causes reticular senile pigment degeneration

Loss of pigment granules from some RPE cells with increase in others. Pigment may be deposited near retinal venules

100

Clinical course of reticular senile pigmentary degeneration

Increases with age. No associated findings. No management necessary.

101

Vitreoretinal Tufts Description

Discrete white to gray irregular clumps on retinal surface. Elevated. Granular appearing. Can be surrounded by cystoid.

102

Vitreoretinal Tufts incidence

Non cystic tufts seen in 72% of population. Bilateral 50% of the time

103

Vitreoretinal Tufts location

Most common nasal. usually located just posterior to ora in vitreous base

104

What are vitreoretinal tufts

Small masses of cells of degenerated retina or proliferated glial cells. Retina is intact with a tuft.

105

Clinical course of vitreoretinal tufts

Remain stationary in size and number.

106

Vitreoretinal tufts associated findings

firm attachments between retina and vitreous can cause retinal breaks.

107

Management of vitreoretinal tufts

Make sure there are no holes at base. If hole present watch q3m then q6m. If risks are present consider treating holes with cryopexy.

108

Risks with vitreoretinal tufts

If have any of these send out. Complains of flashing lights, pigment in vitreous, RD in fellow eye.

109

Lattice Degeneration

Well circumscribed oval or elliptical lesion. Criss-cross pattern of white lines in classic (only 6-9%). Well demarcated area of retinal degeneration that has a dull, rough appearance. Blood vessels that cross the lesion give it the name. Fairly normal retina is always present between lattice degeneration and the ora serrata. May have pigmented borders.

110

Where does lattice tend to occur?

Superior.

111

What is lattice if it goes right against the ora?

It is cystoid degeneration

112

What are we worried about with lattice degeneration?

A hole forming in the lattice. We are concerned about the posterior leading border of the lattice. Nothing will prevent it from heading straight down to the macula.

113

Incidence of lattice degeneration

8-11% population. 42% there are atrophic holes. Bilateral 50% of the time.

114

Location of lattice

between periphery and equator. 5-7 and 11-1. If near equator tend to be radial and follow blood vessel.

115

What is lattice degeneration

Pigmented cavity in center due to atrophic retinal thinning. Lines are blood vessels with thickened walls. Continues with normal vessels outside of lesion. Will have virtual tent with form attachment on border. Vitreous liquification above lesion.

116

Clinical course of lattice degeneration

Becomes visible in teens and increases with age. Associated with RD, holes, overlying vitreous liquification, fine white specks in lesion.

117

Lattice degeneration Mgmt

Follow regularly. Consider laser prophylaxis if holes. Consider tx with risk. Tx needed if history of rd in other eye. Holes increase chance of RD if PVD or cataract removal.

118

Snail Track Degeneration

Glistening white area in the retina. Usually found between equator and ora. 80% within 2 DD anterior to equator. Most frequently temporal.

119

Associated conditions with snail track degeneration

As with lattice can result in retinal breaks or holes. Normally RD only occur in a very small amount

120

Tx for snail track degeneration

With large holes may condition retionoplexy

121

Atrophic retinal hole description

Look pinker or refer then surrounding tissue. Round and discrete cut out

122

Where are atrophic retinal holes found

all quadrants

123

What causes atrophic retinal holes

atrophic retinal thinning.

124

Are atrophic retinal holes associated with RD

very rarely. No virtual attachment to them

125

Mgmt for atrophic retinal hole

Consider laser tx if in periphery with traction or risk.

126

Retinal horseshoe tear Description

Elevated flap of light colored retinal tissue in V shape. Tears may be round, linear, or horseshoe shaped depending on characteristics of retina and vitreous.

127

Incidence of retinal horseshoe tear

6.4% of retinal breaks

128

Location of retinal horseshoe tear

Superior more often.

129

Who has a higher chance of horseshoe tears?

Myopes.

130

What causes Retinal horseshoe tear

degeneration of inner retinal layers, overlying vireos degeneration, and traction. Often trauma induced tear. One end attached to vitreous tuft. Lattice on flap quite common.

131

Management of Retinal horseshoe tear

Due to vitreous attachment and the flap it leads to RD more often. Always refer for treatment.

132

Are smaller are larger retinal horseshoes more scary?

Smaller indicates it has been there longer so less of a scary situation.

133

Operculate tears

Retinal hole with flap of tissue completely torn off.

134

Who is operculated tears found most commonly in?

Older people because of their association with PVD.

135

Where are operculated tears found?

between ora and equator. Most often superior but any quadrant is possible.

136

How are percolated tears caused?

Most often trauma

137

Are percolated tears correlated with RD?

No. Very rarely cause.

138

MGMT of percolated hole

Tx if high myopia, aphasia, extensive degeneration, or family history of RD.

139

What will be seen with RD

Top with decrease as fluid can now drain out, photpsia, shafer's sign.

140

RD description

Separation of neurosensory retina from the RPE. White folds of retinal tissue, masks choroid detail, tissue moves with eye movement.

141

RD VF

Will only have a relative scotoma or normal. Photoreceptors are still functioning.

142

When will you see a pigmented demarcation line with RD?

If stable for 3 m.

143

Symptoms of a RD

Initially related to vitreous traction on retina. Light flashes due to pulling and floaters that appear.

144

RD epidemiology

Can be any age. Myopes >6, Aphakes have high risk 1 year after surgery.

145

What condition can result in an exudative retinal detachment?

best's disease

146

RD cause

Fluid accumulates between RPE and sensory retina

147

Rhegmatogenous RD

Full thickness break. Atrophic holes and tractional tears allow vitreous into the sub-retinal space and leading to separation of sensory retina from RPE. (the retina is not intact).

148

What condition cause rhegmatogenous RD

high myopia, lattice, family history, PVD, trauma, RRD in fellow eye, Marfan's syndrome, stickler's syndrome.

149

Tractional RD

Pre-retinal. Chronic traction of the inner surface via neovascularization and scarring (The retina is intact)

150

What causes traction RD

DR. VOS. Proliferative diabetic retinopathy, retinopathy of prematurity, vein occlusion, ocular ischemic syndrome, proliferative sickle cell retinopathy.

151

Exudative RD

Sub-retinal. Leakage of fluid into the sub retinal space from damage to RPE or choroidal blood vessels (the retina is intact)

152

Causes of exudative RD

Vascular conditions, inflammatory conditions, neoplasia conditions, and congenital anomalies. CNVM conditions (CH BALA)-chroidal rupture, histoplasmosis, best's, angled streaks, lacquer cracks, wet-amd

153

What condition has an increased prevalence of lattice and RD?

transillumination defects associated with PSD.

154

RRD symptoms

flashes of light, floaters or recent onset or many, curtain, loss or blurring of vision.

155

Subclinicical RRD

A retinal break with surrounding sub retinal fluid extending at least 1DD from the break but no more than 2DD posterior to the equator.

156

Types of RRD

1. subclinical 2. retinal break without detachment (both can lead to clinical) 3. Clinical

157

Types of Clinical RRD

Macula off, macular on and not likely to detach, macula on and likely to detach

158

Do RRD progress normally?

No most do not. The distance of the detachment from the fovea was the only risk factor for foveal detachment.

159

Management for RD

Silicone oil, scleral buckle, laster photocoagulation, aspiration of sub retinal fluid, pneumatic retinopathy (gas bubbles), primary vitrectomy.

160

What else does scleral buckle cause?

Myopic shift.

161

Retinoschisis Description

Fluid filled and cyst like, relatively immobile, blanches when depressed, see choroidal detail, sheathed vessel possible, honeycomb appearance of the outer wall possible, absolute scotoma.

162

Where is retinoschsis most commonly found?

bilateral inferior temporal. Next is superior temporal.

163

Retinoschsis incidence

3.7% patients. Increasing with age and hyperopia. F>M

164

Pathophysiology of retinoschsis

Retinal splitting between inner plexiform and outer nuclear layers. Inner layer is stretched and thinned. No demarcation line expected.

165

Clinical course of retinoschsis

Progress very slowly. Associated with holes in inner or outer layers. Very low potential for RD

166

MGMT of retinoschsis

DDX from RD. If within 25 degrees of temporal arcades FU q6m. Laser only if macular area in danger of inner and outer holes present.

167

CHRPE vs. Nevus

Deeper and will leave with red free.

168

How many Nevus convert to melanoma?

1/9,000

169

Risk factors for cancerous nevus acronym

To find small ocular melanoma using helpful hints daly

170

Risk factos for cancerous nevus

Thickness: >2 mm
Fluid: Subretinal
Symptoms: phopsia, Vision loss
Orange Pigment overlying lesion
Margin touch ONH
Ultrasound hollowness
Halo absesnse
Druse absence.

171

How to monitor nvus

No features initially monitored twice yearly and followed up annually. 1/2 features should be monitored every 4-6m. Nevi with 3+ should be evaluated at an experienced center for management alternatives and possible treatment .

172

Where does a primary choroidal melanoma tend to metastasize to?

Liver. Won't survive this. This is death. Less common sites are skin and lung.

173

CHRPE

Unifocal or multifocal. Unifocal CHRPE results in pigmented, flat, round lesions with distinct margins. No change in color with depression. Stable in size but their color may change. Full or partial hypo pigmentation ring seen around the lesion.

174

What finding is diagnostic for CHRPE

Halo

175

Where are CHRPEs normally found

Most occur in temporal funds.

176

Multifocal CHRPE

AKA bear tracks. Presence of a number of small CHRPE lesions. Associated with gardner's syndrome.

177

Avulsed vitreous base

Vitreous base will appear as floating white strip and can be twisted

178

What causes avulsed vitreous base

Due to blunt trauma. Vitreous base has been pulled away from ora.

179

Who is avulsed vitreous base most common in

young

180

Where is avulsed vitreous base found

usually superior nasal.

181

Clinical course with avulsed vitreous base

No changes. Associated with vitreous hemorrhages or RD

182

MGMT of avulsed vitreous base

No treatment unless RD.

183

Oral Pearls

Usually appear as white glistening round object on dark background. Can be pigmented. Only seen with scleral depressing.

184

Incidence of oral pearls

20% of eyes

185

Location of oral pearls

On pars plana

186

Cause of oral pearls

Druse like structures beneath dentate processes may be large and lose their pigment epithelial covering.

187

MGMT of oral pearls

Benign incidental finding. No associated findings/risks.

188

Pars Plana Cysts

Looks like blisters. Increased with scleral depression.

189

Pars Plana cysts incidence

7% population. Increases with age. Acquired and not congenital. More commonly found with RD and posterior uveitis.

190

Location of pars plans cysts

Most likely temporal.

191

Cause of pars plans cysts

separation of non pigmented and pigmented epithelium.

192

Tx for pars plana cysts

no mgmt

193

Neoplams

New or abnormal growth. Growth is uncontrolled and progressive

194

Melanoma

Tumor made up of melanin pigmented cells. Mestatic.

195

Hamartoma

benign tumor like nodule. Composed of cells and tissue that don't normally occur in that tissue.

196

Blastoma

Neoplasm composed of embryonic cells of the tissue/organ

197

Carcinoma

Cancer that begins in the skin or in tissues that line or cover the body organs.

198

Enhanced depth imaging OCT

Allows you to image deeper into the retina.

199

Choroidal Nevus

Benign choroidal neoplasm. Increased pigment in choroid. Typically flat or minimally elevated. May see overlying druse. May have serous retinal detachment over nevus. Probably present at birth and grows maximally during prepubertal years (rare to grow after that)

200

How many people have a choroidal nevus

30%

201

Choroidal Nevus and malignancy

Can convert. When under 2DD 95% are benign. Document and follow up.

202

A choroidal lesion will _______ with a red free filter

disappear

203

A choroidal lesion will _____ with an infrared filter on

enhance

204

What does drusen over nevus indicate?

Long standing

205

What size should a benign nevus be

2-5 DD

206

How often to follow up with a nevus?

Biannual

207

When to suspect malignancy

5 DD +, elevation, druse that is more orange, may see feeder vessels.

208

What additional tests to do with nevus that may be malignant?

ultrasound, FAs, photo documentation, P32.

209

What is the most common adult primary intraocular malignant tumor

malignant choroidal nevus

210

What population very rarely gets malignant choroidal melanoma

African americans

211

Circumscribed malignant choroidal melanoma

More common, better prognosis. Highly elevated, grayish-green, mottled with brown, black, orange. Associated with serous RD, VH, and proptosis.

212

Diffuse malignant choroidal melanoma

Less common, worse prognosis. Horizontal growth pattern, poorly defined edges.

213

Ocular findings associated with malignant choroidal melanoma

Hard exudates, serous detachment of the retina, choroidal folds, sub retinal and intraretinal hem, literal hem, secondary glaucoma, cataracts, anterior and/or posterior uveitis.

214

Sx of Malignant choroid melanoma

May be asymp. May have reduced VA, may or may not have VF defect, photopisa/floaters.

215

Secondary Malignant choroidal melanoma common causes

Males-lung, liver cancer. Females-breast.

216

Primary lesions are often _____, while secondary are often____

unilateral, bilateral.

217

Performing transillumination of sclera for lesion

Pigmented lesions will not transmit the light. Non pigmented will transmit the light.

218

Diagnosing malignant choroid melanoma

Serial retinal photographs (monitor change), FA, B-scan, P32 uptake.

219

B-Scan and malignant choroidal melanoma

B-scan ultrasonography will show the mass. Retinal detachment can often occur over the melanoma and hide it. B-scan will reveal it.

220

P32 test

Perform on large tumors. The uptake of P in malignant cells is greater than in normal cells.

221

Enucleation for choroidal malignant melanoma

Perform on large tumors with functional vision loss or growth around ONH. Fit prosthesis 5-12 weeks later.

222

Radioactive plaques

Option for malignant choroidal melanoma. Gamma radiation. Plaque stitched to tissue for several days. Can cause retinopathy, cataracts, and vitreous hem.

223

Transpupillary thermotherapy

Diode laser delivering radiation through the pupil. Most effective at tumor apex

224

Combination TTT/Plaque

Sandwich therapy for malignant choroidal melanoma

225

Which malignant choroidal melanoma lesions would you must observe

Small tumors (less than 3 mm thick and 10 mm in diameter) Have low metastatic potential.

226

Local resection

Lots of complications. Not a good choice

227

Heavy charged particle irradiation

External beam. Proton bean irradiation. Uses cyclotron generated heavy ions. Can be used on large tumors. Limited availability.

228

Systemic problems with malignant choroidal melanoma

Can spread to other organs. Males-lung, liver. Females-breast cancer.

229

A bening nevus will _____ with FA

Hypofluoresce

230

A malignant nevus will ____ with FA

Hyper

231

Monosomy 3

Only one chromosome 3. Poor prognosis. Testing for choroidal melanoma

232

Class 1 melanoma

Two chromosome 3 copies, low metastasis risk

233

Class 2 melanoma

Only one chromosome 3, high metastasis risk.

234

BAP1

BRCA-Associated Protein 1 mutation or inactivation. BRCA is breast cancer. Also associated with lung cancer from asbestos. Often found in choroidal tumors with a higher risk of metastasis.

235

Choroidal Osteomas

Acquired, slow-growing intrachoroidal calcification near ONH. Benign but has potential for growth. Bone-like tumor.

236

What percent of choroidal stemmas are unilateral

75%

237

What does a choroidal osteoma look like?

Yellow white to orange red lesion with scalloped edges

238

Choroidal ostema on A vs B scan

A=reflective B=elevated

239

Tx for choroidal ostema

Monitor. Prognosis variable and unpredictable. Can cause vision loss.

240

Ciliary Body Malignant Melanoma

May involve pigment or non pig. epithelium or storm. Hard to see and normally detected once big enough to grow into pupil.

241

How to detect CB malignant melanoma

Pressure on lens may breast secondary irregular astigmatism, corectopia, anterior dislocation of lens, focal opacity of th lens, focal dilation of episcleral vessels, glaucoma, RD. Erosion of iris root and forward extension of tumor into the anterior chamber. Erosion of the sclera with extension of the tumor outward. Anterior uveitis.

242

Tx for CB malignant melanoma

Enucleation (if large and spread to anterior choroid). Sector reaction for small to medium.

243

Melanocytoma

ONH tumors.

244

Melanocytoma characteristics

Dark black, elevated mass on the ON. Usually found in darker skin. Unilateral. Growth may occur over 5-20 years. May spread off the disc.

245

How much of ON is normally involved in a melanocytoma?

Usually 50% of less of the ON is involved. Usually the inferior part.

246

____ have no vision reduction with melanocytoma

75%

247

TX for melanocytoma

None. Photodocument/VF. Routine follow up.

248

Mestatic Carcinoma of the choroid

Secondary Tumor. The eyes may be one of the first sites of malignant spread.

249

Primary tumor that travels to the eyes are common from where

lung breast, kidneys, GI.

250

Mestatic carcinomas of the choroid description

Can occur anywhere but common in posterior pole. Flat or slight elevation, placoid lesions. Creamy-white to yellow to gray.

251

Metastatic carcinoma of the choroid objective

multifocal or solitary. Grows faster than malignant melanoma. Surface has characteristic mottled pigment clumping. Extensive exudative RD. Pain may be associated.

252

Prognosis with me static carcinoma of the choroid

Prognosis is poor. enucleation is more conservative. chemotherapy, irradiation, photocoagulation, cryotherapy, irradiation, sector excision may be used.

253

Metastatic carcinoma of optic nerve

Very rare to have direct metastasis to ON.

254

Metastatic carcinoma of ON symptoms

loss of VAs

255

Mestatic carcinoma signs

swollen nerve her, yellowish tumor above the normal ON. Venous tortuosity or CVO

256

Prognosis with metastatic carcinoma

Mean survival 10 month

257

TX for metastatic carcinoma

Irradiation/chemo

258

When to enucleate with metastatic carcinoma?

If pain from secondary uveitis or intractable glaucoma is severe

259

Leukemia

Infiltration of retina, choroid, and ON. Infiltration into ON displaces normal neurons and causes Vision loss. Occurs in terminal stage of disease. Survival rate less than 12 m.

260

TX for leukemia

Irradiation may delay or abort the n. destruction

261

what is the most common primary ocular tumor in childhood

retinoblastoma

262

Retinoblastoma

Malignant, congenital intraocular tumor. Mostly dx by age 4. (1/4) bilateral and (3/4) unilateral.

263

Origin of retinoblastoma

Undifferentiated retinal neural tissue. Present at birth and develops during first 2 years.

264

Average number of tumors with retinoblastoma

Average of 5. Metastasis by blood stream. Mortality in 18%

265

Genetics with retinoblastoma

AD, high penetrance. 6% of all cases. Most are sporadic in origin. 25% can be passed on. Should do genetic counseling.

266

Subjective retinoblastoma

white pupil, leukocoria (2/3 present in this way) Poor VA, infant may rub eyes

267

Retinoblastoma Signs

No pigment, dull chalky white lesion. High calcium content so reflective on ultrasound. Hyper fluoresce during FA.

268

TX for Retinoblastoma

Enucleation (large tumors), photocoagulation (small) Brachytherapy, irradiation (medium to large), cryotherapy (small peripheral tumors)

269

Embryonic Medulooepithelioma

CB equivalent to retinoblastoma. Involves non-pigmented layer. Unilateral most common.

270

Presenting signs with embryonic medulloepithelioma

Usually leukocoria. Usually in first decade of life.

271

Signs with medulloepithelioma

Poor vision. May have pain

272

Objective with medulloepithlioma

white mass in pupil, may find corresponding mass in the iris and/or anterior chamber.

273

TX with medulloepithelioma

Sector extraction, many times too late to enculeate.

274

Adult medulloepithelioma

A carcinoma. Multiple white to gray fluffy mass of inner surface of ciliary body. usually associated with trauma to the eye or post inflammation.

275

Prognosis with adult medulloepithelioma

Growth rate is slow. Locally invasive. Sector if small. Enculcleate if large.

276

CHRPE

Are of enlarged RPE cells.

277

Prevalence of CHRPE

1.2-4.4%

278

CHRPE objective

single or multiple presentations. Dark gray in color. Well demarcated. Flat but may have an area of hypo pigmentation surrounding (halo Nevi). Area may show a scotoma.

279

What is multiple CHRPE called

bear track or animal track

280

Will CHRPE disappear with red free?

NO

281

Tx with CHRPE

Document, monitor changes. Follow up with routine eye exam.

282

CHRPE and FAP

CHRPE connected to familial adenomatous polyposis. FAP is AD disorder. 4 or more lesions is specific.

283

What causes Retinal pigment epithelial hyperplasia

Occurs due to insults or trauma to retina, chorioretinal inflammations, scars, or choroidal neovascarulization. Occurs by invasion of RPE into sensory retina.

284

Tx of Retinal Pigment epithelial Hyperplasia

Non-progressive if underlying cause not active. Treat the cause and monitor for change.

285

Retinal Pigment epithelial Hyperplasia appearance

Appears as a jet black irregular pigment. Size and shape varies.

286

Cerebroretnnal Angiomatosis (von Hipple-Lindau dz)

Predisposes pt to benign and malignant tumors. Angiomatosis of retina, CNS, and visceral organs. Vascular tumors.

287

Inheritance with Cerebroretnnal angiomatosis

AD with variable expression.

288

Onset of cerebroretinal angiomatosis

30s, No racial or sexual predilection.

289

Ocular manifestation with cerebroretnnal angiomatosis

Tumors start slow and enlarge. Tumors in vessels and arteries. More common in mid-peripheral retina but may be found anywhere in the ONH.

290

How many of patients with cerebroretnnal angiomatosis have ocular manifestations?

25%

291

How often is cerebroretnnal angiomatosis bilateral

50%

292

Ocular complications with cerebroretnnal angiomatosis

As the tumor enlarges it tend to leak hemorrhages and hard exudates. Can cause secondary glaucoma and RD.

293

Ocular tx for cerebroretnnal angiomatosis

Depends on location and size. Irradiation, photocoagulation, cryotherapy.

294

Systemic tx for cerebroretnnal angiomatosis

annual physical, renal analysis, MRI/CT q3 years.

295

Encephalotrigeminal Angiomatosis (Sturge weber)

Intracranial angioma, facial angioma, and choroidal angioma. Usually ipsilateral and present at birth. Inheritance pattern unclear and no sexual or racial predilection.

296

Cutaneous angioma with enchephalotrigeminal angiomatosis

Nevus flammeus or port wine stain. Present at birth.

297

Intracranial lesion with encephalotrigeminal angiomatosis

Can have epileptic seizes or VF defects, etc.

298

Choroidal Angioma

With encephalotrigeminal angiomatosis. A choroidal hemangioma. Can be localized or diffuse.

299

Localized choroidal angioma

Occurs with storage-weber. Yellow to red orange lesion. Elevated circular area. May cause serous retinal detachment

300

Diffuse choroidal angioma

More common in storage-weber. Entire funds is deep red. Might miss unless compare to other eye.

301

Other ocular manifestations with encephalotrigeminal angiomatosis

Primary concern is congenital glaucoma, 30% develop glaucoma. Heterochromia iridis. Conj. vessels show dilation and are tortuous.

302

Dx of encephalotrigeminal angiomatosis

Ultrasound shows choroidal thickening but no excavation or orbital involvement. FA shows the large choroidal vessels.

303

TX for encephalotrigmeinal angiomatosis

control seizures, tx for glaucoma, PDT for choroidal hemangioma, photocoagulation for RD.

304

Arteriovenous malformations

Not a true phacomatoses. Involves the retina and CNS with A/V malformations (dilated and tortuous retinal arteries and veins). Embryonic origin.

305

Ocular manifestations with arteriovenous malformations

Usually unilateral. Enlarged tortuous and frequently more vessels. May involve single vessel, one area, a single quadrant, or the entire fundus.. Arteries and v are similar in appearance. May project forward from the retina. Large lesions can cause hemes. Normally asymp.

306

Systemic manifestations of Arteriovenous malformation

lesions in brain. May cause epilepsy.

307

Tx for arteriovenous malformation

Congenital has no progression. Retinal AVMs (especially if continuous with ON) referred for neurological consult.

308

Tuberous Sclerosis (bourneville's dz) epidemiology

No race or gender preference. Auto dominant. 50% new mutations.

309

Sebaceous Adenoma (pringle's Dz)

cutaneous manifestation of tub. sclerosis. Angiofibroma. Begins about age 5. Pale pink, usually around the nose and lip area. Lesions vary in size. Highly vascularized red papular.

310

Achromatic nevi

Cutaneous manifestation of tub. sclerosis. Congenital white patches. Hypo pigment. Usually on trunk or limbs.

311

Shagreen patch

tub. sclerosis cuatnous manifestation. Diffuse fibrous thickening of the skin. This lesion has an elevated orange peel appearance. May find small fibroma at the fingernail side.

312

Ocular manifestation of tub. sclerosis

Small tumors on conj, hypo pigmentation iris spots, may see retinal lesion (Astrocytoma)

313

Astrocytoma with tub. sclerosis

50% of those with t.s. usually unilateral but bilateral (15%). Astrocytoma arising from inner layers of retina.May be white or multiple. Gray-white. usually located on the post. pole near the ON. Can be found anywhere. Raised and nodular (mulberry). Druse of ONH associated. Slow growth. May break off and mestasisize.

314

SE with astrocytoma

VF defect.

315

Tx for astrocytoma

tx symptoms. Refer if papilledema.

316

Neurofibromatosis (von Recklinghausens disease)

Congenital but may not be seen until late childhood. Autosomal dominant with varied expression.

317

Neurofibromatosis cutaneous manifestations

Appearance of Cafe spots. Hyper pigmentation areas. 6 or more think this disease. Plexiform neurofibromas-subcutanous tumors that are diffuse. Fibroma molluscum-skin tumor appear as small subcutaneous nodules over the entire body.

318

Systemic manifestations with Neurofibromatosis

CNS: multiple tumors in brain. Bone: abnormal spinal and skull Visceral: can include neurofibroma of all organs
Ocular: neurofibromas can be found in the ocular tissue.

319

Ocular manifestation in Neurofibromatosis

Partial to complete ptosis of the lid. Produces S shaped lids. Proptosis due to tumor (may be pulsating due to absence of sphenoid). Creators heterochromia. Can be tumors in conj, cornea, and iris. Can also have retinal and choroidal tumors but are more rare.

320

Associated conditions with Neurofibromatosis

Congenital, unilateral glaucoma is associated.

321

Tx for Neurofibromatosis

Surgical removal of the tumors. Prognosis is variable. Optic n. gliomas may respond to irradiation.