14 - Retina/Choroid2 Flashcards
Hyperviscosity retinopathy
-pathophys
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
Hyperviscosity retinopathy
- most common cause
- signs
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%
HIV retinopathy
Most common ocular manifestation of HIV/AIDS
CWS, hemorrhages
Asymptomatic
Non-infectious
Interferon retinopathy
Used for hepatitis (with ribaviron) and cancer
CWS, hemorrhages within post pole
Typically within 3-5mo of starting
Resolves with discontinuation
Talc retinopathy
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
Vascular sheathing/periphlebitis
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
Idiopathic juxtafoveolar retinal telangiectasia
- pathophys
- signs/symp
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
Coat’s disease
- epidemiology
- pathophys
Males, <20yo (2/3 cases <10yo)
Progression more rapid in children <4yo, simulating retinoblastoma
IDIOPATHIC peripheral vascular dz
Untreated -> total EXUDATIVE RD
Coat’s disease
-signs/symp
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)
Retinopathy of prematurity
- epidemiology
- pathophys
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)
Retinopathy of prematurity
- signs
- concerns
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
Retinoblastoma
- epidemiology
- pathophys
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
Retinoblastoma
- heritable vs non
- signs/symp
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
Leukocoria DDx (4)
Coats
Toxocariasis
Retinoblastoma
ROP
Congenital hypertrophy of retinal pigmented epithelium (CHRPE)
- epidemiology
- signs
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
Choroidal nevus
- epidemiology
- pathophysiology/signs
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)
Choroidal nevus
-risk factors for transformation
“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
Age-related macular degeneration (ARMD) -overview —what it is —epidemiology —risk factors
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)
Non-exudative/dry AMD
- epidemiology
- characteristics
- signs/symp
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)
Age-related macular degeneration (ARMD)
-pathophys of drusen (hallmark of AMD)
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
The Macular Photocoagulation Study Group identified these 4 main risk factors that incr the risk of progression from dry to wet ARMD
1) multiple soft drusen (esp confluent)
2) focal hyperpigmentation
3) HTN
4) smoking
Exudative/wet AMD
- epidemiology
- symptoms
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
Exudative/wet AMD
-characterized by __ assoc with signs of __, which can lead to 4 potential presentations of wet AMD
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
Age-related macular degeneration (ARMD)
-PEDs
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
Exudative/wet AMD
-classic vs occult CNVMs on FA
C: well-defined
O: poorly-defined, less intense leakage
Most pts with wet AMD have a combo of features, “predominantly classic”
Central serous chorioretinopathy (CSCR)
-epidemiology
Young to mid-age men (20-50) Type A Stress Pregnancy Corticosteroid use (#1) HTN Recurrences occur as high as 50%
Central serous chorioretinopathy (CSCR)
- pathophys
- signs/symp
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
