14 - Retina/Choroid2 Flashcards

1
Q

Hyperviscosity retinopathy

-pathophys

A

Incr in resistance to blood flow secondary to elev levels of plasma proteins, RBCs, and/or WBCs -> impaird circulation of blood/O2

As flow decr -> vessel walls become damaged -> leakage of fluid, retinal ischemia

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2
Q

Hyperviscosity retinopathy

  • most common cause
  • signs
A

Hyperglobulinemia: found in Waldenstrom’s macroglobulinemia, multiple myeloma, serum positive RA, SLE, and HIV infxns

Retinal venous dilation, hemorrhage, CWS, exudates
CRVO may occur, bilateral in 10%

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3
Q

HIV retinopathy

A

Most common ocular manifestation of HIV/AIDS
CWS, hemorrhages
Asymptomatic
Non-infectious

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4
Q

Interferon retinopathy

A

Used for hepatitis (with ribaviron) and cancer
CWS, hemorrhages within post pole
Typically within 3-5mo of starting
Resolves with discontinuation

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5
Q

Talc retinopathy

A

Bilateral in IV drug users who use talc as a filler
Talc gets caught in retinal capillaries, app as multiple, yellow, refractile deposits, tend to be CLUSTERED NEAR MACULA
May cause cap occlusion, ischemia

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6
Q

Vascular sheathing/periphlebitis

A

INFLAMMATORY condn
-assoc with SARCOID, syphilis, pars planitis, sickle cell
Exudates around vessels (white cuffing), walls will stain on FA
Retinal edema, ischemia, hemorrhage may occur

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7
Q

Idiopathic juxtafoveolar retinal telangiectasia

  • pathophys
  • signs/symp
A

aka MacTel

Abnormal perifoveal caps present within juxtafoveal region
Most common form = unilateral idiopathic (mid-age men, 20/25 or better)

Signs: right-angle venules, dilated tortuous vessels, hemes, exudate, macular edema and/or CNVM

Symp: decr vision

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8
Q

Coat’s disease

  • epidemiology
  • pathophys
A

Males, <20yo (2/3 cases <10yo)
Progression more rapid in children <4yo, simulating retinoblastoma

IDIOPATHIC peripheral vascular dz
Untreated -> total EXUDATIVE RD

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9
Q

Coat’s disease

-signs/symp

A

Signs: unilateral (80-95%), TELANGIECTATIC dilated vessels in “LIGHTBULB” app

  • progression -> MARKED HARD EXUDATES, intraretinal hemorrhages, EXUDATIVE RD, and NVG*
  • results in red, painful, potentially blind eye
  • from chronic extensive serous RD -> ischemia -> ant seg neo

Symp: decr vision, strabismus, leukocoria (scarring)

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10
Q

Retinopathy of prematurity

  • epidemiology
  • pathophys
A

aka retrolental fibroplasia
Premature infants <32weeks, low birth weight <1500g), rec’vd oxygen therapy

Immature BVs vasoconstrict, stop developing in response to high O2 concentration -> proliferative retinopathy (DRVOS)

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11
Q

Retinopathy of prematurity

  • signs
  • concerns
A

Leukocoria (fibrovascular scarring secondary to tractional RD), strabismus
Most susceptible area of retina is anterior TEMPORAL (last to achieve mature vascular development)
Often have high RE, esp HIGH MYOPIA

DRVOS: preret/vit heme, tractional RD, NVG

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12
Q

Retinoblastoma

  • epidemiology
  • pathophys
A

Most common intraocular malignancy in children (2nd most for all age groups behind choroidal melanoma)
No gender/race predilection
High cure rate unless optic nerve is involved

Tumor derived from retinoblasts due to mutations in Rb tumor-suppressor gene

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13
Q

Retinoblastoma

  • heritable vs non
  • signs/symp
A

Heritable (40%): ALL BILATERAL, 15% unilateral

  • bilat: 50% chance of passing to offspring
  • unil: only 6% have positive fam hx, due to high spontaneous mutation rate

Non-heritable (60%): 85% unilateral

Signs/symp: leukocoria (50%), strabismus, intraocular inflammation, decr vision

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14
Q

Leukocoria DDx (4)

A

Coats
Toxocariasis
Retinoblastoma
ROP

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15
Q

Congenital hypertrophy of retinal pigmented epithelium (CHRPE)

  • epidemiology
  • signs
A

Congenital, no predilections

Benign, pigmented (brown-black), non-progressive lesions with sharp borders, central hypopigmented lacunae

  • typically unilateral, solitary, 1-6mm
  • bilateral, multifocal (4+) assoc with Gardner’s syndrome
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16
Q

Choroidal nevus

  • epidemiology
  • pathophysiology/signs
A

1-6% pop, esp WHITES

Common benign focal acumm of melanocyets within choroid
-flat/slightly elevated, <5mm, overlying drusen
Present at birth, non-progressive*
-*growth during puberty is not unusual, but during adulthood should raise concern for conversion to malignant melanoma (10% of suspicious progress)

17
Q

Choroidal nevus

-risk factors for transformation

A
“To Find Small Ocular Melanomas, Use Helpful Hints”
Thickness: >2mm elev
Fluid (subret)
Symptoms (blur, floaters)
Orange pigment (lipofuscin)
Margins (irreg borders)
Ultrasonographic Hollowness
Halo absence

Also diameter >6mm (4DD) or close proximity to optic nerve

18
Q
Age-related macular degeneration (ARMD)
-overview
—what it is
—epidemiology
—risk factors
A

Progressive dz of RPE, Bruchs, choriocapillaris

Most common in pts >50
#2 cause of blindness in pts 45-64 (behind diabetes)

Risks: age (esp 75+), Caucasians, family hx, light iris color, SMOKING*, HYPEROPIA**, HTN, hypercholesterolemia, females, CV dz

  • possibly nutritional and light toxicity factors
  • smoking think AMD, TED
  • *hyperopia >0.75D is assoc with 2.5x incr risk of wet AMD, same for current smokers (who also have incr risk for recurrence of CNV)
19
Q

Non-exudative/dry AMD

  • epidemiology
  • characteristics
  • signs/symp
A

85-90% of AMD cases

Presence of drusen - incl DRUSENOID PED (#1 CONCERN)
Assoc RPE abnormalities - mottling, granularity, focal hyperpigmentation

Common: metamorphopsia, gradual vision loss, blurred visoin
Uncommon: severe vision loss (12%, defined as loss of >6 lines) - majority due to GEOGRAPHIC ATROPHY (worst, no tx for)

20
Q

Age-related macular degeneration (ARMD)

-pathophys of drusen (hallmark of AMD)

A

Normal: RPE lysosomes phagocytose PR outer segs -> sends to choriocapillaris, which pumps nutrients to RPE

AMD: dysfunction in RPE/bruchs/chcap -> acumm of undigested material from outer segs (lipofuscin) and phospholipids (drusen) in INNERCOLLAGENOUS region of BRUCHS (b/w basement membrane of RPE + innercollag layer) -> bruch’s becomes HYDROPHOBIC -> dysfunction in passage of nutrients/waste/metabolites/water ->RPE cell death

21
Q

The Macular Photocoagulation Study Group identified these 4 main risk factors that incr the risk of progression from dry to wet ARMD

A

1) multiple soft drusen (esp confluent)
2) focal hyperpigmentation
3) HTN
4) smoking

22
Q

Exudative/wet AMD

  • epidemiology
  • symptoms
A

10-15% of AMD cases
88% of legal blindness attributed to AMD
Involvement of fellow eye: ~30% first 2 years, overall 40-85%

Metamorphopsia, central scotoma, rapid vision loss

23
Q

Exudative/wet AMD

-characterized by __ assoc with signs of __, which can lead to 4 potential presentations of wet AMD

A

DRUSEN assoc with CNVMs

1) sub-ret hem = blood under retina, red
2) sub-RPE hem = blood under RPE, GRAY-GREEN
3) sub-ret detach = plasma under retina (aka serous RD), no color change
4) sub-RPE detach* = plasma under RPE (aka PED), no color change
* 1-3 seen in wet, 4 seen in both

24
Q

Age-related macular degeneration (ARMD)

-PEDs

A

Can occur with dry or wet

Dry: drusenoid PED
-due to build-up of confluent soft drusen on bruch’s membrane -> creates space b/w RPE and choroid

Wet: due to small break in bruch’s, plasma

25
Q

Exudative/wet AMD

-classic vs occult CNVMs on FA

A

C: well-defined

O: poorly-defined, less intense leakage

Most pts with wet AMD have a combo of features, “predominantly classic”

26
Q

Central serous chorioretinopathy (CSCR)

-epidemiology

A
Young to mid-age men (20-50)
Type A
Stress
Pregnancy 
Corticosteroid use (#1)
HTN
Recurrences occur as high as 50%
27
Q

Central serous chorioretinopathy (CSCR)

  • pathophys
  • signs/symp
A

UNKNOWN ETIOLOGY
Results in RPE and/or choroidal dysfunction -> accumm of submacular serous fluid (= PLASMA)

Signs: localized MACULAR SEROUS DETACHMENT, angio shows SMOKESTACK app (10%), may also have HYPEROPIC SHIFT, loss of FLR

  • often have PERMANENT RESIDUAL RPE CHANGES in macula
  • 67% IMPROVE W/O TX IN 1-3MO (if needed, do photodynamic therapy)

Symp: UNILATERAL, sudden onset blur (20/20-20/200), metamorphopsia, relative scotoma