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Oc Dz 3 > Final Exam > Flashcards

Final Exam Flashcards

1
Q

Cystoid Macular Edema

A

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

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2
Q

What is CME called if there are no cyst

A

clinically significant macular edema. Often seen in diabetic maculopathy.

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3
Q

CME subjective

A

blurred vision, metamorphosis, washed out vision

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4
Q

What conditions cause CME

A

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

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5
Q

Signs of CME

A

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

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6
Q

FA of CME

A

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

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7
Q

Tx of CME

A

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.

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8
Q

Epiretinal Membrane

A

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

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9
Q

What causes epiretinal membrane

A

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

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10
Q

Epidemiology of epiretinal membrane

A

increases in incidence with age

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11
Q

Symptoms of Epiretinal membrane

A

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

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12
Q

Epiretinal membrane signs

A

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

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13
Q

Epiretinal membrane Tx

A

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

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14
Q

What does chloroquine and hydroxychloroquine treat.

A

(used to treat malaria, arthritis, and SLE)

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15
Q

Signs of toxic retinopathy from chloroquine and hydroxychlorquine

A

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

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16
Q

What dosage of chlorine and hydroxyqhloroquine will cause toxic maculopthy?

A

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

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17
Q

How to scan patient taking hydroxychlorquine or chloroquine?

A

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

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18
Q

Toxic maculopathy caused by Thioridazine

A

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.

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19
Q

Toxic Retinopathy caused by Tamoxifen.

A

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.

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20
Q

Choroidal Folds

A

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.

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21
Q

Choroidal Folds causes

A

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

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22
Q

Choroidal folds symptoms

A

asymptomatic, blurry vision, metamorphsia.

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23
Q

Choroidal folds FA

A

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

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24
Q

Mgmt of choroidal folds

A

Usually idiopathic. Diagnosis of exclusion.

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25
Q

How much ocular volume does vitreous compromise?

A

75%

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26
Q

What percent H20 is vitreous?

A

99

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27
Q

Vitreous attachments

A

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

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28
Q

Which vitreous attachment is weakest

A

Macular

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29
Q

What vitreous attachment is strongest

A

vitreous base (pars plans and peripheral retina)

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30
Q

Vitreous degenerations

A

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

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31
Q

Examination of the viterous

A

Must dilate.

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32
Q

Unusually findings in vitreous

A

cells, blood, pigment, PVD.

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33
Q

Asteroid Hyalosis (benson’s disease)

A

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

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34
Q

Synchysis Scintillans (cholosterolosis bulbi)

A

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

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35
Q

Non-pigmented cells (white) in viterous

A

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

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36
Q

Staffer’s Sign

A

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

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37
Q

Intraviterous hemorrhages

A

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

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38
Q

Retroviterous hemorrhage

A

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

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39
Q

PVD

A

Hyaloid membrane is pushed forward due to liquification.

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40
Q

PVD symptoms

A

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

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41
Q

Signs with PVD

A

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

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42
Q

Epiretinal membrane and PVD

A

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

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43
Q

How to dx Macular hole

A

Stratus OCT.

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44
Q

Categories of vitreous detachments

A

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

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45
Q

Retinal involvement with PVD

A

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

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46
Q

Mgmt of PVD

A

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.

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47
Q

Persistent Hyperplatic Primary Viterous (PHPV)

A

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

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48
Q

Anterior PHPV

A

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

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49
Q

Posterior PHPV

A

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

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50
Q

Congenital hereditary retinoschisis

A

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%.

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51
Q

How to diff. congenital hereditary retinoschisis from RD

A

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)

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52
Q

Iatrogenic Viterous changes

A

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

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53
Q

Peripheral retina

A

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

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54
Q

Landmarks in peripheral retina

A

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

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55
Q

Cystoid degeneration

A

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

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56
Q

Chrotioretinal degeneration

A

Found in peripheral retina. AKA pigmentary degeneration. Very common

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57
Q

Paving stone degeneration

A

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

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58
Q

Reticular pigmentary degeneration

A

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

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59
Q

Equatorial drusen

A

AKA peripheral druse. Not involving macula=benign

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60
Q

Snowflake degneration

A

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

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61
Q

Lattice degneration

A

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

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62
Q

Pigmented lattice degeneration

A

Thin areas of the retina but with pigmentation.

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63
Q

Snail track degeneration

A

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

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64
Q

White without Pressure

A

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

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65
Q

Vitreoretinal adhesion

A

No tear-watch. Tear-refer.

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66
Q

How to best view peripheral retina

A

Scleral indentation

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67
Q

What is the distance from ora to equator?

A

1/5 the entire retina

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68
Q

Where is paving stone degeneration normally found

A

Inferior nasal

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69
Q

Where is lattice normally found

A

superior.

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70
Q

Enclosed oral bay

A

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.

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71
Q

What color are holes in the retina?

A

Red

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72
Q

Meridional Fold

A

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

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73
Q

Incidence of Meridional Folds

A

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

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74
Q

Location of Meridional Folds

A

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

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75
Q

Meridional Complex

A

Meridional folds that covers both bay and process.

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76
Q

Associated findings with meridional folds

A

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.

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77
Q

Management of meridional folds

A

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

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78
Q

Cystoid Degeneration

A

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.

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79
Q

Cystoid degeneration location

A

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

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80
Q

Incidence of cystoid degeneration

A

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

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81
Q

Where does the cystoid degeneration occur

A

Cystoid spaces occur between retinal layers (outer plexiform layer)

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82
Q

Cystoid degeneration associations

A

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

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83
Q

Cystoid Degeneration Managment

A

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.

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84
Q

White without pressure description

A

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

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85
Q

White with pressure

A

Only can see it when pressing on retina with pressure

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86
Q

White without pressure incidence

A

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

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87
Q

White without pressure location

A

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

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88
Q

What causes white without pressure?

A

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

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89
Q

White without pressure tx

A

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

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90
Q

Pavingstone degeneration description

A

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.

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91
Q

Paving stone degeneration incidence

A

22% of eyes. Increases with age

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92
Q

Paving stone degeneration location

A

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

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93
Q

Cause for paving stone degeneration

A

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

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94
Q

Tx for paving stone degeneration

A

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

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95
Q

Reticular Senile Pigmentary Degeneration Description

A

Pigment clumping

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96
Q

Reticular Senile pigmentary degeneration incidence

A

18% of population. Bilateral in almost all cases

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97
Q

Reticular Senile Pigmentary degeneration location

A

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

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98
Q

What is reticular senile pigment degeneration often seen as?

A

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

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99
Q

What causes reticular senile pigment degeneration

A

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

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100
Q

Clinical course of reticular senile pigmentary degeneration

A

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

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101
Q

Vitreoretinal Tufts Description

A

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

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102
Q

Vitreoretinal Tufts incidence

A

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

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103
Q

Vitreoretinal Tufts location

A

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

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104
Q

What are vitreoretinal tufts

A

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

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105
Q

Clinical course of vitreoretinal tufts

A

Remain stationary in size and number.

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106
Q

Vitreoretinal tufts associated findings

A

firm attachments between retina and vitreous can cause retinal breaks.

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107
Q

Management of vitreoretinal tufts

A

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

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108
Q

Risks with vitreoretinal tufts

A

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

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109
Q

Lattice Degeneration

A

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.

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110
Q

Where does lattice tend to occur?

A

Superior.

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111
Q

What is lattice if it goes right against the ora?

A

It is cystoid degeneration

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112
Q

What are we worried about with lattice degeneration?

A

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.

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113
Q

Incidence of lattice degeneration

A

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

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114
Q

Location of lattice

A

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

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115
Q

What is lattice degeneration

A

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.

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116
Q

Clinical course of lattice degeneration

A

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

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117
Q

Lattice degeneration Mgmt

A

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.

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118
Q

Snail Track Degeneration

A

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

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119
Q

Associated conditions with snail track degeneration

A

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

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120
Q

Tx for snail track degeneration

A

With large holes may condition retionoplexy

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121
Q

Atrophic retinal hole description

A

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

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122
Q

Where are atrophic retinal holes found

A

all quadrants

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123
Q

What causes atrophic retinal holes

A

atrophic retinal thinning.

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124
Q

Are atrophic retinal holes associated with RD

A

very rarely. No virtual attachment to them

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125
Q

Mgmt for atrophic retinal hole

A

Consider laser tx if in periphery with traction or risk.

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126
Q

Retinal horseshoe tear Description

A

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.

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127
Q

Incidence of retinal horseshoe tear

A

6.4% of retinal breaks

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128
Q

Location of retinal horseshoe tear

A

Superior more often.

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129
Q

Who has a higher chance of horseshoe tears?

A

Myopes.

130
Q

What causes Retinal horseshoe tear

A

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
Q

Management of Retinal horseshoe tear

A

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

132
Q

Are smaller are larger retinal horseshoes more scary?

A

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

133
Q

Operculate tears

A

Retinal hole with flap of tissue completely torn off.

134
Q

Who is operculated tears found most commonly in?

A

Older people because of their association with PVD.

135
Q

Where are operculated tears found?

A

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

136
Q

How are percolated tears caused?

A

Most often trauma

137
Q

Are percolated tears correlated with RD?

A

No. Very rarely cause.

138
Q

MGMT of percolated hole

A

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

139
Q

What will be seen with RD

A

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

140
Q

RD description

A

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

141
Q

RD VF

A

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

142
Q

When will you see a pigmented demarcation line with RD?

A

If stable for 3 m.

143
Q

Symptoms of a RD

A

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

144
Q

RD epidemiology

A

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

145
Q

What condition can result in an exudative retinal detachment?

A

best’s disease

146
Q

RD cause

A

Fluid accumulates between RPE and sensory retina

147
Q

Rhegmatogenous RD

A

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
Q

What condition cause rhegmatogenous RD

A

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

149
Q

Tractional RD

A

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

150
Q

What causes traction RD

A

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

151
Q

Exudative RD

A

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

152
Q

Causes of exudative RD

A

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
Q

What condition has an increased prevalence of lattice and RD?

A

transillumination defects associated with PSD.

154
Q

RRD symptoms

A

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

155
Q

Subclinicical RRD

A

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
Q

Types of RRD

A
  1. subclinical 2. retinal break without detachment (both can lead to clinical) 3. Clinical
157
Q

Types of Clinical RRD

A

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

158
Q

Do RRD progress normally?

A

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

159
Q

Management for RD

A

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

160
Q

What else does scleral buckle cause?

A

Myopic shift.

161
Q

Retinoschisis Description

A

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
Q

Where is retinoschsis most commonly found?

A

bilateral inferior temporal. Next is superior temporal.

163
Q

Retinoschsis incidence

A

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

164
Q

Pathophysiology of retinoschsis

A

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

165
Q

Clinical course of retinoschsis

A

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

166
Q

MGMT of retinoschsis

A

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
Q

CHRPE vs. Nevus

A

Deeper and will leave with red free.

168
Q

How many Nevus convert to melanoma?

A

1/9,000

169
Q

Risk factors for cancerous nevus acronym

A

To find small ocular melanoma using helpful hints daly

170
Q

Risk factos for cancerous nevus

A 
Thickness: >2 mm
Fluid: Subretinal
Symptoms: phopsia, Vision loss
Orange Pigment overlying lesion
Margin touch ONH
Ultrasound hollowness
Halo absesnse
Druse absence.
171
Q

How to monitor nvus

A

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
Q

Where does a primary choroidal melanoma tend to metastasize to?

A

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

173
Q

CHRPE

A

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
Q

What finding is diagnostic for CHRPE

A

Halo

175
Q

Where are CHRPEs normally found

A

Most occur in temporal funds.

176
Q

Multifocal CHRPE

A

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

177
Q

Avulsed vitreous base

A

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

178
Q

What causes avulsed vitreous base

A

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

179
Q

Who is avulsed vitreous base most common in

A

young

180
Q

Where is avulsed vitreous base found

A

usually superior nasal.

181
Q

Clinical course with avulsed vitreous base

A

No changes. Associated with vitreous hemorrhages or RD

182
Q

MGMT of avulsed vitreous base

A

No treatment unless RD.

183
Q

Oral Pearls

A

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

184
Q

Incidence of oral pearls

A

20% of eyes

185
Q

Location of oral pearls

A

On pars plana

186
Q

Cause of oral pearls

A

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

187
Q

MGMT of oral pearls

A

Benign incidental finding. No associated findings/risks.

188
Q

Pars Plana Cysts

A

Looks like blisters. Increased with scleral depression.

189
Q

Pars Plana cysts incidence

A

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

190
Q

Location of pars plans cysts

A

Most likely temporal.

191
Q

Cause of pars plans cysts

A

separation of non pigmented and pigmented epithelium.

192
Q

Tx for pars plana cysts

A

no mgmt

193
Q

Neoplams

A

New or abnormal growth. Growth is uncontrolled and progressive

194
Q

Melanoma

A

Tumor made up of melanin pigmented cells. Mestatic.

195
Q

Hamartoma

A

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

196
Q

Blastoma

A

Neoplasm composed of embryonic cells of the tissue/organ

197
Q

Carcinoma

A

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

198
Q

Enhanced depth imaging OCT

A

Allows you to image deeper into the retina.

199
Q

Choroidal Nevus

A

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
Q

How many people have a choroidal nevus

A

30%

201
Q

Choroidal Nevus and malignancy

A

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

202
Q

A choroidal lesion will _______ with a red free filter

A

disappear

203
Q

A choroidal lesion will _____ with an infrared filter on

A

enhance

204
Q

What does drusen over nevus indicate?

A

Long standing

205
Q

What size should a benign nevus be

A

2-5 DD

206
Q

How often to follow up with a nevus?

A

Biannual

207
Q

When to suspect malignancy

A

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

208
Q

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

A

ultrasound, FAs, photo documentation, P32.

209
Q

What is the most common adult primary intraocular malignant tumor

A

malignant choroidal nevus

210
Q

What population very rarely gets malignant choroidal melanoma

A

African americans

211
Q

Circumscribed malignant choroidal melanoma

A

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

212
Q

Diffuse malignant choroidal melanoma

A

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

213
Q

Ocular findings associated with malignant choroidal melanoma

A

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
Q

Sx of Malignant choroid melanoma

A

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

215
Q

Secondary Malignant choroidal melanoma common causes

A

Males-lung, liver cancer. Females-breast.

216
Q

Primary lesions are often _____, while secondary are often____

A

unilateral, bilateral.

217
Q

Performing transillumination of sclera for lesion

A

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

218
Q

Diagnosing malignant choroid melanoma

A

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

219
Q

B-Scan and malignant choroidal melanoma

A

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

220
Q

P32 test

A

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

221
Q

Enucleation for choroidal malignant melanoma

A

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

222
Q

Radioactive plaques

A

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

223
Q

Transpupillary thermotherapy

A

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

224
Q

Combination TTT/Plaque

A

Sandwich therapy for malignant choroidal melanoma

225
Q

Which malignant choroidal melanoma lesions would you must observe

A

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

226
Q

Local resection

A

Lots of complications. Not a good choice

227
Q

Heavy charged particle irradiation

A

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

228
Q

Systemic problems with malignant choroidal melanoma

A

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

229
Q

A bening nevus will _____ with FA

A

Hypofluoresce

230
Q

A malignant nevus will ____ with FA

A

Hyper

231
Q

Monosomy 3

A

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

232
Q

Class 1 melanoma

A

Two chromosome 3 copies, low metastasis risk

233
Q

Class 2 melanoma

A

Only one chromosome 3, high metastasis risk.

234
Q

BAP1

A

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
Q

Choroidal Osteomas

A

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

236
Q

What percent of choroidal stemmas are unilateral

A

75%

237
Q

What does a choroidal osteoma look like?

A

Yellow white to orange red lesion with scalloped edges

238
Q

Choroidal ostema on A vs B scan

A

A=reflective B=elevated

239
Q

Tx for choroidal ostema

A

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

240
Q

Ciliary Body Malignant Melanoma

A

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

241
Q

How to detect CB malignant melanoma

A

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
Q

Tx for CB malignant melanoma

A

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

243
Q

Melanocytoma

A

ONH tumors.

244
Q

Melanocytoma characteristics

A

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
Q

How much of ON is normally involved in a melanocytoma?

A

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

246
Q

____ have no vision reduction with melanocytoma

A

75%

247
Q

TX for melanocytoma

A

None. Photodocument/VF. Routine follow up.

248
Q

Mestatic Carcinoma of the choroid

A

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

249
Q

Primary tumor that travels to the eyes are common from where

A

lung breast, kidneys, GI.

250
Q

Mestatic carcinomas of the choroid description

A

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

251
Q

Metastatic carcinoma of the choroid objective

A

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

252
Q

Prognosis with me static carcinoma of the choroid

A

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

253
Q

Metastatic carcinoma of optic nerve

A

Very rare to have direct metastasis to ON.

254
Q

Metastatic carcinoma of ON symptoms

A

loss of VAs

255
Q

Mestatic carcinoma signs

A

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

256
Q

Prognosis with metastatic carcinoma

A

Mean survival 10 month

257
Q

TX for metastatic carcinoma

A

Irradiation/chemo

258
Q

When to enucleate with metastatic carcinoma?

A

If pain from secondary uveitis or intractable glaucoma is severe

259
Q

Leukemia

A

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
Q

TX for leukemia

A

Irradiation may delay or abort the n. destruction

261
Q

what is the most common primary ocular tumor in childhood

A

retinoblastoma

262
Q

Retinoblastoma

A

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

263
Q

Origin of retinoblastoma

A

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

264
Q

Average number of tumors with retinoblastoma

A

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

265
Q

Genetics with retinoblastoma

A

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

266
Q

Subjective retinoblastoma

A

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

267
Q

Retinoblastoma Signs

A

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

268
Q

TX for Retinoblastoma

A

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

269
Q

Embryonic Medulooepithelioma

A

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

270
Q

Presenting signs with embryonic medulloepithelioma

A

Usually leukocoria. Usually in first decade of life.

271
Q

Signs with medulloepithelioma

A

Poor vision. May have pain

272
Q

Objective with medulloepithlioma

A

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

273
Q

TX with medulloepithelioma

A

Sector extraction, many times too late to enculeate.

274
Q

Adult medulloepithelioma

A

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
Q

Prognosis with adult medulloepithelioma

A

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

276
Q

CHRPE

A

Are of enlarged RPE cells.

277
Q

Prevalence of CHRPE

A

1.2-4.4%

278
Q

CHRPE objective

A

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
Q

What is multiple CHRPE called

A

bear track or animal track

280
Q

Will CHRPE disappear with red free?

A

NO

281
Q

Tx with CHRPE

A

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

282
Q

CHRPE and FAP

A

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

283
Q

What causes Retinal pigment epithelial hyperplasia

A

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

284
Q

Tx of Retinal Pigment epithelial Hyperplasia

A

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

285
Q

Retinal Pigment epithelial Hyperplasia appearance

A

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

286
Q

Cerebroretnnal Angiomatosis (von Hipple-Lindau dz)

A

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

287
Q

Inheritance with Cerebroretnnal angiomatosis

A

AD with variable expression.

288
Q

Onset of cerebroretinal angiomatosis

A

30s, No racial or sexual predilection.

289
Q

Ocular manifestation with cerebroretnnal angiomatosis

A

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
Q

How many of patients with cerebroretnnal angiomatosis have ocular manifestations?

A

25%

291
Q

How often is cerebroretnnal angiomatosis bilateral

A

50%

292
Q

Ocular complications with cerebroretnnal angiomatosis

A

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

293
Q

Ocular tx for cerebroretnnal angiomatosis

A

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

294
Q

Systemic tx for cerebroretnnal angiomatosis

A

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

295
Q

Encephalotrigeminal Angiomatosis (Sturge weber)

A

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

296
Q

Cutaneous angioma with enchephalotrigeminal angiomatosis

A

Nevus flammeus or port wine stain. Present at birth.

297
Q

Intracranial lesion with encephalotrigeminal angiomatosis

A

Can have epileptic seizes or VF defects, etc.

298
Q

Choroidal Angioma

A

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

299
Q

Localized choroidal angioma

A

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

300
Q

Diffuse choroidal angioma

A

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

301
Q

Other ocular manifestations with encephalotrigeminal angiomatosis

A

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

302
Q

Dx of encephalotrigeminal angiomatosis

A

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

303
Q

TX for encephalotrigmeinal angiomatosis

A

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

304
Q

Arteriovenous malformations

A

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

305
Q

Ocular manifestations with arteriovenous malformations

A

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
Q

Systemic manifestations of Arteriovenous malformation

A

lesions in brain. May cause epilepsy.

307
Q

Tx for arteriovenous malformation

A

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

308
Q

Tuberous Sclerosis (bourneville’s dz) epidemiology

A

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

309
Q

Sebaceous Adenoma (pringle’s Dz)

A

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
Q

Achromatic nevi

A

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

311
Q

Shagreen patch

A

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
Q

Ocular manifestation of tub. sclerosis

A

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

313
Q

Astrocytoma with tub. sclerosis

A

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
Q

SE with astrocytoma

A

VF defect.

315
Q

Tx for astrocytoma

A

tx symptoms. Refer if papilledema.

316
Q

Neurofibromatosis (von Recklinghausens disease)

A

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

317
Q

Neurofibromatosis cutaneous manifestations

A

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
Q

Systemic manifestations with Neurofibromatosis

A

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
Q

Ocular manifestation in Neurofibromatosis

A

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
Q

Associated conditions with Neurofibromatosis

A

Congenital, unilateral glaucoma is associated.

321
Q

Tx for Neurofibromatosis

A

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

Oc Dz 3 (3 decks)

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