Friedman posterior segment Flashcards

1
Q

DDx causes of exudative RD

A

V: HTN, glomerulonephritis, eclampsia/pre-eclampsia
I: uveitis (VKH, SO, pars planitis, posterior scleritis)
T:
A:
M: hypoTH
I: CSR, Coat’s
N: retinal capillary hemangioma/VHL, choroidal hemangioma, choroidal malignant melanoma

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2
Q

Characteristics of exudative RD

A
>located inferiorly
>display shifting fluid
>smooth appearance
>chronic exudative RD can lead to NVG
>important to perform depressed exam and R/O RRD

In contrast, traction RDs are usually taut and immobile with a CONCAVE surface that does not extend to the ora serrata

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3
Q

Work-up for Exudative RD

A

FA: evalute tumor (intrinsic vasculature, feeder vessels) and vascular abnormalities
ICG: superior to FA to show intrinsic vascularity, hot spots, wash-out phenomenon for tumors*

B-scan: confirm shifting fluid, evaluate choroidal thickness, evaluate for masses
A-scan: evaluate internal reflectivity if mass is found

OCT: verify thickened choroid using enhanced depth imaging techniques in uveitic conditions, image SRF and/or CME

Rarely necessary: orbital imaging

*Wash-out phenomenon: rapid increase in hyperfluorescence, which peaks around 3 to 4 min. In the late phases of the ICG angiogram, a “washout” effect with reduction of the initial hyperfluorescence is observed secondary to the outflow of dye from the hemangioma

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4
Q

Choroidal hemangioma Rx

A

Individualized, based on:
> extent of Sx
>loss of vision
>potential for visual recovery

Aim: induce tumor atrophy with SRF resolution and reduce foveal distortion without destroying retinal function (NOT to obliterate the tumor)

Rx: laser photocoagulation (moderately intense, white reaction on tumor surface to eliminate serous exudation)
cryotherapy
PDT with verteporfin (visudyne) using standard treatment parameters
transpupillary thermotherapy
I-125 plaque brachytherapy
low-dose XRT

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5
Q

Choroidal hemangioma Px

A

visual loss can be progressive/irreversible if fovea involved in chronic cases
Poor VA results 2/2 fluid resolution from chronic macular edema/photoreceptor loss

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6
Q

Serous RD over macula DDx

A

CSR (central serous chorioretinopathy)
inflammatory choroidal disorders (VKH syndrome)
uveal effusion syndrome
ON pit (no leakage)
choroidal tumor
vitelliform macular detachment
PED from other causes including CNV (+leakage)

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7
Q

Serous RD over macula work-up

A

OCT: characterize features present along with the obvious SRF
>checking for macular schisis or ON excavations seen with an ON pit
>thickened choroid seen in VKH, CSR and uveal effusion syndrome or the characteristic OCT appearance of vitelliform lesions

FA: useful to R/O CNV and to visualize the early hyperF with late pooling of a PED and the SRF

If both of these tests fail, ICG can show hyperF with late staining in CSC, vascularity with tumors, and R/O CNV

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8
Q

CSR Rx

A

observation initially since most cases resolve spontaneously over 6 weeks
laser Rx or verteporfin (Visudyne) ocular PDT can be considered for pts who require more rapid visual recovery 2/2:
> occupational reasons
>poor vision in fellow eye 2/2 CSC
>no resolution of fluid after several months
>recurrent episodes with poor vision
>severe forms of CSC

Rx reduces the duration of Sx but does not affect the final visual acuity. Experimental use of oral rifampin and mifepristone (RU486) has been suggested in chronic/bilateral cases.

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9
Q

ARN DDx

A
ARN
PORN
syphilis
CMV
toxoplasmosis
sclopteria
lymphoma
sarcoidosis
amnioglycoside toxicity
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10
Q

ARN exam findings

A

possibly:
granulomatous anterior uveitis
vitritis
retinal vasculitis

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11
Q

Lab tests for ARN

A

PCR tap for HZV, HSV, CMV
blodo testing for HZV and HSV type 1 and 2 IgG and IgM
immunocompetent (ARN)/immunocompromised (PORN)

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12
Q

ARN Rx

A

systemic IV acyclovir until resolution of retinitis then PO for 1-2 months.

Atlernatively if lesions are more peripheral then use PO therapy with valacycovir instead of IV therapy
Ganciclovir is alternative

Important to follow BUN and creatinine for nephrotoxicity

Both PO and topical steroids can be started s/p patient begins to respond to prevent inflammatory complications

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13
Q

ARN complications

A

high risk of RRD 2/2 holes/tears 2/2 retinal necrosis

important to observe fellow eye

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14
Q

Chronic vitritis DDx

A

V
I: infections/noninfectious uvetitis - birdshot chrioretinopathy, pars planitis, toxoplasmosis, syphilis, sarcoidosis, multifocal choroiditis, APMPPE, Behcets, TB, ARN
T
A
M
I
N: primary intraocular lymphoma (diffuse large B-cell non-hodgkin’s lymphoma)

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15
Q

chronic vitritis work-up

A

R/O uveitis: CBC, ESR, ACE, HLAB27 and 51, ANA, VDRL or RPR, FTA-ABS/MHA-TP

MRI to evaluate CNS involvement with LP for CNS cytology

If negative: Dx PPV: undilute vitreous biopsy (1 cc) should be sent for cytology, flow-cytometry analysis for B and T cell markers, kappa/lamda light chains

Measure: IL6 and IL10 (high IL10 to IL6 ratio is suggestive of intraocular lymphoma)

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16
Q

Intraocular lymphoma Rx

A

Intravitreal MTX and rituximab and orbital radiation if no CNS involvement (however majority of pts - [60-80% within 29 months] - develop CNS involvment) so usually Rx with blood-brain barrier disruption and high-dose systemic MTx

Poor Px if brain involvement

Need to complete metastatic survey (chest/abdomen) and bone marrow biopsy

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17
Q

Granulomatous uveitis DDx

A

V
I: Syphilis, TB, leprosy, brucellosis, toxoplasmosis, P. Acnes endophthalmitis, fungal infection (cryptococcus, aspergillus), HIV
T
A
M
I: sarcoidosis, VKH, SO, phacoanaphylactic rxn
N

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18
Q

Granulomatous uveitis findings

A
Ciliary injection
AC cell and flare
hypopyon
iris nodules
rubeosis
synchiae
increased/decreased IOP
Cataract 
Pars planitis
ON hyperemia
chorioretinitis
periphlebitis
CME
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19
Q

Granulomatous uveitis work-up in pt with negative history/ROS/exam

A
CBC with differential
ESR
VDRL or RPR with FTA-ABS or MHA-TO
ELISA or indirect immunofluorescence assay (IFA) for toxoplasma IgM and IgG
ACE, lysozyme

+/- the following: ANA, RF, ELISA for LYme (IgM and IgG), HIV antibody test, CXR or CT (for TB/sarcoidosis), sarcroiliac radiographs and urinalysis

+/- HLA typing (HLA-A29 for birdshot)
if vasculitis present (ANCA)
Raji cell and C1q binding assays for ciruclating immune complexes (SLE, systemic vasculitides)
C3, C4, total complement (SLE, cryoglobulinemia, glomerulonephritis)
soluble IL-2 receptor

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20
Q

Toxoplasmosis chorioretinitis Rx

A

topical steroids and cycloplegics for anterior inflammation
Systemic steroids added for posterior pole lesions or those with intense inflammation

Small peripheral lesions: observe since they often heal spontaneously esp in immunocompetent pts

Rx with antibiotics if:
>Decreased vision
>moderate/severe vitreous inflammation or lesions that threaten the macular, papillomacular bundle, or ON

Rx with 4-6 wks with Abx to kill tachyzoites in the retina (Rx does not affect cysts) - Rx with Bactrim (TMP-SUF)
For aggressive lesions or posterior pole lesions - use triple therapy:
primethamine (daraprim)
folinic acid (leucovorin)
and one of the following:
>sulfadiazine
>clindamycin
>clarithromycin
>azithromycin
>Atovoquone
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21
Q

IOFB classification

A

Inert (do not require removal) - glass, plastic, sand, stone, ceramic, gold, platinum, silver, aluminium

Reactive (cause inflammation/toxicity and must be removed) - copper (>= 85% severe endophthalmitis,

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22
Q

Chalcosis findings

A

mild intraocular inflammation
copper deposition in the anterior lens capsule (sunflower cataract) and DM (Kayser-Fleischer ring)
retinal degeneration

Iris may become green and the pupil sluggishly reactive to light

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23
Q

Siderosis findings

A
iris heterochromia (Hyperchromic on involved side)
Mid-dilated minimally reactive pupil
lens discoloration (brown-orange dots from iron deposition in lens epithelium, generalized yellowing from involved cortex)
vitritis
pigmentary RPE degenration
vessel sclerosis
retinal thinning
atrophy
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24
Q

DDx for causes of cotton wool spots

A

MCC = DM and HTN

V: ischemic (RVO, ocular ischemic syndrome, severe anemia, pre-eclapmisa, carotid artery obstruction)
embolic (carotid embolic, cardiac emboli, deep venous emboli, WBC emboli - Purtcher’s retinopathy)

Blood disease (aplastic anemia, dysprotenimiea, perniciious anemia vitamin B12 deficiency),

Hyperviscosity syndromes (multiple myeloma, Waldenstrom macroglobulinemia), hypercoagualibity syndromes (factor V Leiden, prothrombin 20210A, hyperhomocysteinemia, protein C/S deficiency, antithrombin 3 deficiency, dysfibrinogenemia, factor 13 deficiency)

I:HIV, RMSF, Cat-scratch fever (b. henselae), toxoplasmosis, subacute bacterial endocarditis, leptospirossis, onchocerciasis

T: severe chest compression/long bone fractures, foreign bodies, amniotif fluid embolization
traumatic nerve fiber layer laceration (in which case CWS will not resolve)

Toxic (interferon, MTX), radiation induced
A: immune-mediated (SLE, sarcoidosis, dermatomysosis, scleroderma, cryogloublinemia)
M
I: ERM traction
N: neoplastic (lymphoma, leukemia, mtz carcinoma, Hodgkin’s dz)

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25
Q

cotton wool spot work-up

A

CBC with diff, platelet count
HgA1c
ANA
HIV antibody test

+/- cardiac valvular dz, carotid stenosis, Deep venous source of emboli

CWS resolve spontaneously in 1-2 months

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26
Q

Macular hole DDx

A

macular hole
psuedohole (Appearance of hole w/ steep walls
Caused by vascular tortuosity around macula)

lamellar hole Thin layer of retina lifted w/ walls “bulging out”; Maybe precursor or resolved macular hole

CME, ERM
solar retinopathy (usually bilateral)
CSR, wet AMD

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27
Q

Macular hole work-up

A

Clinical test?
Watzke-allen test (absolute scotoma in the hole)

Stages (antiquated)?
Stage 1: 1A (pseudocyst); 1B (outer layer loss)
50% spontaneously resolve (no surgery)

Stage 2: Full-thickness hole 400um + elevated rim

Stage 4: Hole with PVD

New grading system?
Small 400um

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28
Q

Risk factors for macular hole

A

CME, VMT, trauma, post-surgical, post-laser Rx and post-inflammatory disroders

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29
Q

Rx for macular holes:

A

Jetrea (if 250um) + ILMP (if >400um)

PPV Treatment success?
92% closure ; 50% if re-op
short-acting gas (SF6 or 10% C3F8)
ILMP (↑ closure) if >400um
Face down (3 days; ↑ closure if >400um)
Treatment for traumatic MH? 
Observation (no traction; spontaneous closure ~2 mo)
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30
Q

Px for macular holes

A

Good for recent onset & smaller diameter holes, as well as patients with good pre-operative visual acuity

Px: poor for holes > 1 year and > 400 um wide.

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31
Q

PVD exam

A
retinal tear (10-15% of PVDs) and RRD esp when pigmented anterior vitreous cells are present
VH (seen in 7.5% of PVDs) from a torn vessel during vitreous separation (70% of a retinal tear)

Repeat DFE in 4-6 weeks

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32
Q

Risk factors for retinal tears

A
Age
history of RD in fellow eye (15%)
high myopia/axial length (7%)
FH
lattice degeneration
trauma, cataract surgery (1% s/p ICCE, 0.1% s/p ECCE with intact posterior capsule)
DM
YAG for PCO
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33
Q

DDx for inflammatory disorders

A

white dot syndromes (birdshot, MEWDS, APMPPE)
pars planitis
PIC
sarcoidosis

infectious: TB, syphilis, DUSN, toxoplasmosis

masquerate process: ocular lymphoma, mtz dz, choroidal lymphoproliferative dz

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34
Q

Birdshot work-up

A

FA findings?
subtle compared with ophthalmoscopic appearance (mild hyperF early with active lesions my hypoF early) and late stianing

Late views: vascular incompetence with leakage
CME, 2ndary retinal staining

“quenching” (dye disappears quickly from vessels)

HLA-A29 (90-98%) although 7% of general population positive for HLA-A29

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35
Q

Other signs of birdshot

A
Mild vitritis; vascular attenuation & leakage
Optic disc edema or atrophy; CME
Painless eye
Decreased scotopic  ERG
CNV is rare
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36
Q

Birdshot demographics

A

Usually occurs in middle-age (age 40-60) females = 70% almost exclusively in Caucasians of N. european descent

37
Q

Birdshot Treatment & Prognosis?

A

Treatment & Prognosis?
Early aggressive IMT (cyclosporine, azathioprine, MTX, Cellcept)
Intravitreal triamcinolone
Poor prognosis chronic & recurring

38
Q

Neuroretinitis/macular exudate DDx

A
B. henseale
syphilis
lyme
TB
tularemia
toxoplasmosis
viral retinitis (HSV, HZV, EBV)
DUSN
toxocariasis

Non-infectious; HTN, DM, AION, RVO, acute macular neuroretinopathy, sarcoidosis, papilledema

39
Q

Neuroretinitis/macular exudate work-up

A
BP
VDRL/RPR
FTA-ABS/MHA-TP
PPD
indirect fluorescent antibody test for B. Henselae
40
Q

Neuroretinitis etiology and Rx

A

2/2 pleomorphic gram negative bacillus called B. henseale (also assoc/w/ cat-scratch dz)

No definite Rx: controversial to use systemic antibiotics (Doxy, cipro, Bactrim)

immunocompetent: doxycycline for 2-4 weeks, IV doxycycline can also be given along with rifampin

41
Q

Neuroretinitis px

A

good with 67% regaining >= 20/20 vision and 97% regaining > 20/40 vision
Disc edema resolves over 8-12 weeks vs. macular star takes 6-12 mo

optic atrophy and RPE changes may develop late

42
Q

Presumed Ocular Histoplasmosis Syndrome (POHS) findings and ddx

A
Findings?
Over 60% bilateral
Punched-out “histo spots” in the midperiphery and posterior pole
Peripapillary atrophy
CNV (peripapillary)
No vitritis

DDX: pathologic myopia, inflammatory disorder (multifocal choroiditis or PIC)

43
Q

POHS work-up and demographics

A

OCT/FA to look for CNV

Lab testing is unnecessary - althoug histoplasmin antigen skin testing can be performed (60% of the adult population of the Ohio and Mississippi River Valleys have a positive reaction to histoplasmin skin testing)

Ohio-Mississippi River Valley
San Joaquin Valley

dimorphic fungus: histoplasma capsulatum
Present on feathers of chickens, pigeons, bat droppings –> humans inhale the droppings. Rare in AfrAms. Assoc/w/HLA-B7

44
Q

POHS Treatment and Px?

A

Extra/juxtafoveal CNV Rx: laser (MPS), anti-VEGF (but not subfoveal CNV)

Subfoveal CNV: PDT, steroids, anti-VEGF
Prognosis?

44% severe VA loss (>6 lines) in 5 yrs
Risk of CNV in fellow eye (

45
Q

Bull’s eye DDx

A

Stargardt’s disease

Cone (and rod) dystrophy

Chloroquine/Hydroxychloroquine toxicity

AMD

Chronic macular hole

Also: central areolar choroidal dystrophy, olivopontocerebellar atrophy, ceroid lipofuscinosis

46
Q

Bull’s eye work-up

A

FA: classic “bull’s eye” = hypoF with ring of hyperF visible before the fundus lesion

Use it to R/O dark choroid seen in Stargard

OCT: thinning of retina at Bull’s eye without IS/OS junction in ring

47
Q

Bull’s eye history

A

SLE, RA
short-term treatment for GVH disease
amebiasis
toxic medications - quinolones (hydoxychloroquine/chloroquine)

FH - stargard, cone/rod dystrophy

48
Q

Risk factors for hydoxychloroquine/chloroquine

A

Plaquenil >6.5mg/kg/day
Chloroquine >3mg/kg/day

Total daily dose more critical than cumulative dose

Increased toxicity w/ age, obesity, liver or renal dx. Maculopathy can progress even s/p medication discontinued b/c the drug concentrates in the eye.

Findings?
Decreased color (red) vision 
Paracentral scotomas
Bull’s eye maculopathy
RP-like changes late
49
Q

hydoxychloroquine/chloroquine work-up and Px?

A

Red 10-2 HVF @ baseline and q6 mo (chloroquine) or 12 mo (hydroxychloroquine)
color fundus photos if abnml
SD-OCT (loss of IS/OS jn) and color vision (blue-yellow axis)
Multifocal ERG

visual loss rarely improves and can even progress s/p drug is discontinued

50
Q

Potentially lethal forms of albinism?

A

Chediak-Higashi syndrome
>Recurrent pyogenic infections/anemia/thrombocytopenia
>White forelock & silvery hair

Hermansky-Pudlak syndrome
>Platelet dysfunction
>Puerto-Rican heritage

51
Q

Oculocutaneous Albinism vs. ocular albinism

A

Oculocutaneous Albinism (sytemic)
Less MELANIN in all melanosomes - tyrosinase positive (some pimgnet which increases with age) vs. tyrosinase negative (no pigment)
Inheritance: AR

Ocular Albinism (only in eye)
Less MELANOSOMES but each melanosome has pigment
Inheritance: XR, AR

52
Q

ocular albinism description and DDx

A

generalized fundus hypopigmentation with deep choroidal vasculature visible. Foveal hypooplasia with no luteal pigment or foveal light reflex present

DDx: blond fundus (variant of normal) or ocular albnism

53
Q

True albinism vs. albinoidism

A

degree of ocular involvement:
1) true albinism: pts have low VA (20/100 to 20/400) and nystagmus 2/2 foveal hypoplasia

2) albinodism: pts have normal or only slightly diminished VA w/o nystagmus

54
Q

albinism demographics and Px

A

AfrAms have higher incidence of albinism than caucasians but often have incomplete forms of ablinism

Px variable depending on form of albinism but dz is not degenerative and VA can improve over 1st two decades of life.

55
Q

Severe NPDR

A
4:2:1 rule, any one of:
4 quads: IRH + MAs
2 quads: venous beading
1 quad: IRMA
15% chance of progression to high-risk PDR within 1 year
CWS are NOT predictive
56
Q

Very severe NPDR

A

Any 2 of the 4:2:1 rule

45% chance of progression to high-risk PDR within 1 year

57
Q

CSME:

A

Any edema within 500μm of fovea
Hard exudates within 500μm of fovea + adjacent edema
Edema >1 disc area in size within 1 disc diameter of fovea

58
Q

Macular Ischemia:

A

FA: microaneurysms at margins of zone of capillary nonperfusion
FAZ enlargement >1000um usu. associated with visual loss

59
Q

High risk PDR

A

Any NVD with VH
1/4-1/3 disc area NVD (≥standard photo 10A)
1/2 disc area NVE with VH (standard photo 7)

60
Q

Why do we care about high-risk PDR? What study is it from?

A

Diabetic Retinopathy Study: if high-risk, immediate PRP

61
Q

DCCT (Diabetes Control and Complications Trial) and UKPDS (United Kingdom Prospective Diabetes Study) studies

A

DCCT
Intensive > conventional glycemic control in DM1 pts, reduces onset & progression of DR & macular edema

UKPDS
Intensive > conventional glycemic control in DM2 pts, reduces onset & progression of DR
Intensive BP control slowed progression of DR
No difference bet. ACEi & BB

62
Q

ETDRS (Early Treatment Diabetic Retinopathy Study)

A
Early PRP (for severe NPDR)
Small improvement in risk of severe VA loss (
63
Q

Retinitis Pigmentosa (RP) 2 types?

A

type 1 rod-cone; type 2 cone-rod

64
Q

RP Clinical Findings?

A
Bone spicules
Waxy optic disc pallor 
Attenuated vessels
Pigmented vitreous cell
Macular edema w/o leakage on FA
PSC
Progressive loss of night vision
Tritan color deficiency (blue)
mild hearing loss (30%, excluding Usher's pts)
50% of female carriers with X-linked form have golden reflex in posterior pole

HVF: mid-peripheral scotomas, eventually becomes ring scotoma

65
Q

RP DDx

A

V: congenital rubella syndrome, syphilis, DUSN
I: thioridazine/chloroquine drug toxicity
T
A
M: CSNB, vitamin A deficiency
I
N: CAR

66
Q

Sector RP/inverse RP

A

Sector RP
RP in part of retina (usu. Inferotemporal) that doesn’t enlarge, good ERG response

Inverse RP
RP in macula and posterior pole (central/color vision reduced earlier than other types, pericentral/central scotoma)

67
Q

Retinitis punctata albescens & RP sine pigmento

A

Retinitis punctata albescens
RP + white spots (50-100 um) at level of RPE scattered in mid-periphery with attenuated vessels & bone spicules. Slowly progressive (as opposed to fundus albipunctatus)

RP sine pigmento
RP without RPE changes (20% cases, assoc/w/more profound cone dysfunction)

68
Q

Bassen Kornzweig (abetalipoproteinemia)

A

RP + hereditary abetalipoproteinemia
>minimal pigmentary changes

Poor vitamin A absorption & steatorrhea (malabs of fat-soluble vitamins - A, D, E, K and TG/chloesterol)
Also: ataxia, acanthocytosis
Inheritance: AR

Treatment?
Low fat diet, vitamin A + E

69
Q

Refsum Disease

A

RP + phytanic acid oxidase deficiency
>minimal pigmentary changes

High phytanic acid, copper & ceruloplasmin

No bone spicules; enlarged K nerves
Also: Ataxia, deafness, anosmia, ichthyosis, cardiomyopathy, symmetric short 4th toes

Inheritance: AR (7q21-22; PEX1)

Treatment?
low phytanic acid diet (avoid fats, milk)

70
Q

Spielmeyer-Vogt-Batten-Mayou (neuronal ceroid lipofuscinosis)

A

RP + neuronal ceroid lipofuscinosis
>infantile, juvenile, or adult onsets

Lipofuscin accumulates in lysosomes

Also: seizure, dementia, ataxia, vacuolization of peripheral lymphocytes

conj bx: granular lipopigments that also accumulate in neurons causing retinal and CNS degeneration.

Inheritance: AR, usu. Jewish girls

71
Q

Usher Syndrome

A

RP + deafness (congenital, neurosensory)
Cilia defect (photoreceptors & hair cells)
MC syndrome assoc/w/RP (5%)

Also: ataxia, MR, low phosphate (rickets)
Inheritance: AR (Ch 1q41; USH2A)

72
Q

Alstrom Syndrome

A

RP + deafness + obesity + endocrine dx
(DM, hypertriglceridemia, etc.)
>early profound visual loss, baldness, renal failure, cataracts

73
Q

CPEO / Kearns-Sayre

A
RP + CPEO (EOM limitations + ptosis)
Also: heart block (Kearns-Sayre)
Path findings: ragged red fibers on muscle bx
Inheritance: mitochondrial
Treatment?
Coenzyme Q10
74
Q

Choroidal melanoma work-up

A

U/S to differentiate between tumor and other diseases. B-scan: shows shape of tumor

A-scan: low to medium internal reflectivity with reduction in amplitudes from front to bck and high-amplitude spikes consistent with break in Bruchs’ membrane.

FA: “double” circulation within tumor from filling of both the retinal and choroidal vasculature. Lesion itself would be hypoF early with pinpoint leakage late.

Although not required, neuroimaging can be performed. Melanoma is bright on T1 and dark on T2 MRI imaging

75
Q

Choroidal melanoma Risk factors?

A

Risk factors?
Melanosis oculi, nevus of Ota
Mushroom-shaped when tumor breaks through Bruch’s membrane

76
Q

Choroidal melanoma other findings

A

Glaucoma develops from liberation of melanin clogging TM

Sentinel vessel?
Sign of ciliary body melanoma

77
Q

Choroidal melanoma Metastasis to?

A

Metastasis to?
Hematogenous to liver

(also lung/bone/skin, CNS). LFTs and CT of chest/abdomen

78
Q

Collaborative Ocular Melanoma Study (COMS) - large

A

Large (>10mm height, >16mm dia)
Enucleation = pre-XRT + enucleation

Large tumors: ~ 50% pts have mtz within 5 yrs

79
Q

Collaborative Ocular Melanoma Study (COMS) - medium

A

Medium (2.5-10mm height,

80
Q

Collaborative Ocular Melanoma Study (COMS) - small

A

Small (1.5-2.4mm height, 5-16mm dia)

81
Q

Choroidal melanoma Risk factors

A

To Find Small Ocular Melanomas Using Helpful Hints Daily

Thickness >2mm
Fluid (SRF)
Symptom
Orange (pigment)
Margin (near optic nerve)
Hollowness (on B-scan)
Halo (absence)
Drusen (absence)

0 factors = risk of 4%, each risk increases relative risk ~ 3x

82
Q

Choroidal melanoma Factors predicting survival?

A
Size of scleral contact and cell type
Mean of 10 largest melanoma cell nuclei (MLN)
Monosomy 3 (correlates with mets)
83
Q

Callender classification?

A

Spindle cell nevus = Spindle A cells = slender, cigar-shaped nucleus with finely dispersed chromatin. low nuclear to cytoplasmic ratio, no miotic figures
Spindle B cells = oval with larger nucleus and prominent nucloelus

Spindle cell melanoma = Best prognosis
Mix of spindle A & B cells
25% 15-year mortality

Mixed
50% 15-year mortality

Epithelioid melanoma
Worst prognosis
Epithelioid cells = abundant ctyoplasm and large nueclues with peripheral margination of chromatin, pooly cohesive with distnct borders
75% 15-year mortality

84
Q

Complications of melanoma radiation Rx

A

radiation retinopathy
Cataracts (PSC in 42% w/in 3 years of proton beam therapy)
dry eye
I-125 brachytherapy (high risk of substantial visual loss) - up to 49%

85
Q

ERM risk factors

A

Can be idiopathic or secondary to vascular occlusions, inflammation, surgery, trauma, or retinal breaks (allows RPE migration onto retina)
Stable (>75% maintain >20/50)

86
Q

ERM Treatment?

A

PPV/MP if VA

87
Q

DDx of optociliary shunt vessels?

A

RVO, ON meningioma, low-grade ON glioma, chronic papilledema, chronic glaucoma

88
Q

DDx of submacular fibrosis in a child?

A
Coat’s disease
ROP
FEVR
Fascioscapulohumeral muscular dys.
VHL