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146 Cards in this Set
- Front
- Back
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what is the most significant modifiable risk factor for AMD
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SMOKING
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in AMD...drusen are signs of (2)
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1. RPE Abnormality
2. RPE Atrophy -associated with RPE thinning and atrophy |
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what is drusen
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1. RPE cells deposit collagenous basement membrane into Bruch's
2. mucopolysaccharides and lipids |
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what are the two types of DRUSEN
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HARD
1. typically seen in DRY AMD SOFT 1. amorphous stuff between inner and outer layers of Bruch's Membrane 2. more inclined to lead to exudative AMD (wet) 3. allows formation of CNVM |
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what age has the highest prevalence of AMD
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75+ years
Framingham: 20/30 or worse |
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what type of AMD is more prevalent
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DRY: 80%
WET: 20% MACULAR DRUSEN is a risk factor in BOTH |
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DRY AMD is diagnosed by...
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combination of...
1. drusen 2. RPE atrophy 3. functional vision loss 4. RPE pigment changes ranging from normal aging changes to severe vision loss |
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what are the characteristics of Geographic Atrophy in Dry AMD
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1. progressive loss of RPE and choriocapillaris
2. macrophages replace drusen with fibrous tissue/dystrophic calcification 2a. once this occurs, CNVM WILL NO LONGER FORM 3. loss of photoreceptor function and retinal layers 4. 20/25 - 20-400 |
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management for DRY AMD
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1. photodocument
2. home amsler 3. UV protection 4. anti-oxidant vitamins with zinc supplement |
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complications of antioxidant supplement plus zinc for AMD
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1. beta carotene increases risk of lung cancer in current smokers
2. increase risk even if the patient has stopped smoking for a few years |
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what is the chronic inflammation theory in respects of WET AMD
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1. higher number of lymphocytes, macrophages, fibroblasts found in Bruch's membranes of patients with AMD
2. inflammation causes break in Bruch's membrane |
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what layer does CNVM involve
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1. CNVM infiltrates from the choriocapillaris
2. under the RPE and sensory retina 3. may cause RD (look for fluid and blood) |
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which type of CNVM is most prevalent
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OCCULT CNVM
1. 90% 2. ill defined membrane on angiogram CLASSIC CNVM 1. 10% 2. well defined membrane on angiogram |
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Bruch's disruption in relation to CNVM
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1. diffuse thickening of Bruch's with soft drusen which predisposes to breaks in Bruch's membrane
2. presence of VEGF enhances development |
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CNVM in respects to imaging
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1. FA/ICG: hot spot with late spread of hyperfluorence
2. must get 72hr because CNVM will grow 10 microns/day 3. OCULAR URGENCY |
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what is disciform scarring in wet AMD
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1. fibrovascular material following CNVM development
2. disciform will replaces most of sensory retina, RPE 3. results in death of tissue (RPE HYPERPLASIA) and severe vision loss -most cases of CNVM will lead to disciform scarring |
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what are all possible management options for WET AMD
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1. LASER PHOTOCOAGULATION
2. PHOTODYNAMIC THERAPY 3. INTRAVITREAL STEROID INJECTION 4. ANTI-VEGF TREATMENT 5. ANTI-OXIDANT VITAMIN THERAPY 6. UV protection 7. macular drusen-home amsler 8. low vision consult |
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laser treatment in respects of CNVM position around the fovea in WET AMD
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Krypton:
- Juxtafoveal - specificity of choroidal layers Argon - Extrafoveal - laser absorbed by the RPE and choroidal pigment |
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treatment of subretinal/subfoveal hemorrhage in WET AMD
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NO GOOD TREATMENT
-maybe gas bubble injection into the retina to tamponade the hemorrhage and spread the blood out |
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what is photodynamic therapy
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1. IV infusion of Verteporfin (Visudyne)
2. low power laser activates the drug 3. causes platelet aggregation and thus CNVM thrombosis 4. chemical obliteration of CNVM without damaging overlying retina and RPE |
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what are problems associated with photodynamic therapy
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1. causes upregulation of VEGF which increase leakage and propensity to from neovascularization
Verteporfin 1. high rate of side effects 2. highly photosensitizing 3. high degree of skin necrosis LEAKAGE REDUCTION BUT NOT STOPPED!! |
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PDT
stand alone or in conjunction with something else |
1. PDT is a well accepted therapy for wet AMD, though the STAND ALONE RESULTS ARE NOT GREAT.
2. best used in conjunction with other therapies |
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what are intravitreal steroid injections used to treat
what does it do?? |
EDEMA SECONDARY TO...
1. vascular occlusions 2. diabetes 3. cystoid macular lesions 4. wet AMD -stabilizes vascular membranes and reduces vascular permeability |
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what is the most significant complications of intravitreal steroid injections?
others? |
1. ENDOPHTHALMITIS
2. IOP rise 3. cataract formations |
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what are the THREE anti-VEGF drugs?
which ones are FDA approved? |
1. Macugen (FDA)
2. Lucentis (FDA) 3. Avastin (NOT APPROVED) -binds to VEGF and prevents uptake by endothelial receptors |
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what are the main causes of CNVM formations
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1. Wet AMD
2. Idiopathic CNVM 3. Degenerative Myopia 4. Ocular Histoplasmosis syndrome |
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what is the usual profile for central serous chorioretinopathy
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1. Caucasian Male
2. mid 30's 3. type A personality |
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characteristics of central serous chorioretinopathy
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1. serous retinal or pigment epithelial detach in macular area
2. loss of foveal reflex 3. focal conduit through RPE into sensory retina 4. NO DRUSEN!! |
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age in relation to central serous chorioretinopathy (ICSC)
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1. ERROR to diagnose ICSC in a patient over the age of 55
2. consider CNVM!!! |
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management of ICSC
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1. home amsler and observation
2. DISCONTINUE ALL STEROIDS!!! |
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what should you always consider in the case of mild paramacular hemorrhaging
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IDIOPATHIC JUXTAFOVEAL RETINAL TELANGIECTASIA
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compare serous and hemorrhagic RPE detachment
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serous:
1. round, small, well demarcated dome with CLEAR fluid hemorrhagic: 1. blood in sub-RPE, indicates CNVM 2. occasionally, blood goes through RPE and gives hemorrhagic RD and may even break through retina to give vitreous hemorrhage |
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how does RPE detachment usually look?
how does it show up on FA |
RPE detach tends to be:
1. SMALL 2. well localized 3. fills early on FA 4. DOES NOT SPREAD |
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RPE detachment usually occurs simultaneously with what??
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ICSC
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what is cystoid macular edema
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1. not a disease, but a FINDING
2. honeycomb appearance 3. occurs almost always from LEAKY CAPILLARIES |
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what layer of the retina can cystoid macular edema (CME) be seen
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1. initial fluid accumulates in MULLERS CELLS
2. gets into EXTRACELLULAR SPACES 3. causes CYSTOID SPACE in OPL |
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how is cystoid macular edema diagnosed?
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1. Petalloid appearance on FA
2. cystic appearance on OCT 3. acuity may be 20/20 (asymptomatic) |
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what is Irvine-Glass syndrome
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CME following complicated intracapsular cataract extraction
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CME Management
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1. steroids (oral and topical)
2. NSAIDS (oral and topical) 3. Diamox 4. vitrectomy and/or grid photocoagulation 5. intravitreal steroid and anti-VEGF long term CME may result in foveal cyst formation and macular hole |
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what are the stages of MACULAR HOLE
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1. foveal cyst from CME or disruption to vitreoretinal site. LAMELLAR HOLE PARTIAL THICKNESS (late hyperfluorescence on FA)
2. lamellar hole more likely to occur and retinal tear possible 3. full thickness macular hole with REMAINING VITREOUS ATTACHMENT 4. full thickness macular hole with POSTERIOR VITREOUS SEPARATION (early hyperfluorescence on FA) |
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what is the main difference about stage 1 and stage 4 macular hole in respects to FA
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stage 1:
late hyperfluorescence on FA stage 4: early hyperfluorescence on FA |
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macular hole management
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VITRECTOMY
stage1: vision may improve stage 2: vision stabilization full thickness: expanding bubble flattens out the edges of the hole and the recontact with the RPE stimulate fibroblastic activity, filling in the hole. |
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what are the TWO types of solar retinopathy
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type 1:
1. rhodopsin action spectrum 2. mediated by visual pigments 3. primary lesion on the photoreceptors type 2: 1. RPE absorbs the radiation and converts to heat 2. burns in the RPE are often permanent |
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small, symmetrical foveal cysts should be investigated for...
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solar retinopathy
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describe what solar retinopathy will look like after several days...
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1. reddish spot with pigment halo
2. progresses to red lamellar foveal depression 3. cystic change may develop 4. simulate hole or progress to hole |
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pathophysiology of preretinal/epiretinal membrane
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aka: CELLOPHANE MACULOPATHY
1. caused by break in ILM with retinal glial cells proliferating on surface 2. occurs from VMT |
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what causes macular pucker
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cellophane maculopathy:
3-5% of cases due to vitreous shrinkage following surgery (proliferative vitreoretinopathy) |
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treatment from cellophane maculopathy
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1. vitrectomy with membrane peeling
2. typically has a rapidly advancing course initially, then stabilizes and doesn't change |
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what is the difference between CHOROIDAL FOLD and EPIRETINAL MEMBRANE
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1. choroidal folds are HORIZONTAL
2. epiretinal membrane often radiate from the MACULA |
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choroidal folds are strongly indicative of...
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1. RETRO-ORBITAL TUMOR
2. need orbital imaging |
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what are FUCH'S SPOTS?
what are special about them? |
1. RPE hyperplasia overlying CNVM
2. FIRST SIGN of CNVM formation 3. pathognomonic for CNVM in degenerative myopia!!!!! |
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what are lacquer crack?
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1. breaks in Bruch's Membrane
2. conduit for CNVM 3. similar to angoid streaks, but DO NOT always connect with the disc or radiate |
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what is degenerative myopia
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1. myopic stretching of photoreceptors, posterior pole and disc area
2. true alteration of globe structure (elongation) |
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what percentage of android streaks are associated with systemic disease?
most common? |
50%
1. Pseudoxanthoma elasticum, PXE (80-90%) 2. Ehler's Danlos syndrome (8-15%) 3. Sickle Cell Disease (1-2%) |
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combination of angioid streaks and PXE is known as...
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Groinblad-Stanberg Syndrome
-vascular changes are most problematic |
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what is the difference between benign nevus and malignant melanoma
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benign nevus:
1. drusen 2. shallow RD 3. minimal growth 4. less than 2mm thick 5. gradual elevation 6. focal orange pigment 7. no blood vessels malignant melanoma 1. lipofuscin 2. bullous detachment 3. profound growth 4. more than 2mm thick 5. abrupt elevation (mushroom shape) 6. diffuse orange pigment 7. blood vessels |
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size and thickness of choroidal nevus?
best management |
1. 5mm in size
2. no more than 2mm thick best managed by serial photography to document growth |
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what is the difference between tyrosinase (-) and (+) OculoCutaneous Albinism
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tyrosinase (-) OCA:
congenital inactivity of enzyme Tyrosinase prevents melanin formation Tyrosinase (+) OCA: enzyme activity is normal, but melanin can not be sequestered into melanosomes |
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what is Hermansky Pudlak syndrome
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subset of Tyrosinase POSITIVE OCA which as associated abnormal bleeding patterns
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describe Ocular Albinism
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1. melanin NORMAL
2. melanosomes are DEFICIENT in number 3. systemic pigmentation is nearly normal BUT ocular pigmentation is variable |
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what are the visual dysfunctions that corresponds with albinisms
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due to lack of pigmentation and hence lack of normal substrate for macular and retinal development
1. subnormal acuity 2. strabismus 3. nystagmus (due to macular hypoplasia) 4. photophobia 5. astigmatism and refractive error |
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what is the main cause of visual difficulty in albinism?
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MACULAR HYPOPLASIA
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do not confuse albinism with what?
how do you tell the difference? |
do not diagnose BENIGN BLONDE FUNDI with ocular albinism
TRUE ALBINISM has a hypoplastic macula and nystagmus |
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what causes retinopathy in prematurity
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1. due to changing oxygen environments immediately post natal
2. vasculature is stopped before the retina is matured |
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what are the three stages of retinopathy of prematurity
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1. VASO-OBLITERATIVE: high oxygen content in incubation shunts normal maturation of vessels
2. VASO-PROLIFERATIVE: 2nd to return to normal oxygen levels in room air. deficiency that cant be met by the infants vessels (vitreous hemorrhage and tractional RD) 3. CICATRICIAL: vitreoretinal membranes, dragged vessels, retinal folds, retrolental mass in pupil region, and dragged macula |
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what are the stages of FEVR
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1. zone of avascular retina is seen in 100% of patients
2. proliferative and exudative changes with neovascularization 3. tractional forces from cicatricial lesion in periphery, rhegmatogenous RD more common |
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when you see peripheral exudation, think...
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1. FEVR
2. Coat's Disease |
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what characteristics should you think FEVR and NOT ROP
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NO HISTORY OF PREMATURE BIRTH OR LOW BIRTH WEIGHT
BOTH: 1. ectopic macula 2. dragged retinal vessels 3. peripheral vitreoretinopathy with incomplete peripheral retinal vascularization |
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definition:
any full thickness disruption in the sensory retina providing a conduit for fluid to enter the potential space between the sensory retina and RPE |
RETINAL BREAK
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what are the three types of retinal breaks
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1. rhegmatogenous (only type caused by an RD)
2. tractional 3. serous/exudative |
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what causes a PVD?
leading to what?? |
1. hyaluronic acid concentration decreases with age
2. collagen fibrils lose support, aggregate, forms pockets of liquefied vitreous 3. vitreous then collapses 4. traction exerted on areas of vitreoretinal adhesion leading to RD |
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most floaters in patients under the age of 50 are due to...
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benign vitreous syneresis
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sudden onset of floaters could be a sign of...
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1. PVD
2. vitreous hemorrhage secondary to retinal tear 3. liberated pigment cells from RD 4. vitreous cells from a posterior inflammation |
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PVD typically presents as...
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one big ass floater
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what is lattice degeneration
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1. thinning of all 10 retinal layers due to dropout of peripheral retinal capillaries
2. resulting in ischemia with subsequent retinal collapse and glial fibrosis |
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how does lattice degeneration look
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1. white fibrotic tracks across retina
2. snail tracks 3. almost always runs circumferentially around the eye 4. pigmentation in 80-90% of cases |
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management of lattice degeneration
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**LATTICE ALONE AND ATROPHIC HOLES ARE NOT TREATED**
1. treated prophylactically if the patient previously had RD from lattice in the fellow eye 2. or lattice in the eye of a monocular patient 3. tears along the border of lattice lesions are treated |
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describe flap tears
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1. retina is incompletely pulled away from RPE
2. base towards vitreous base and apex towards pole 3. initially symptomatic but may stop by the time pt gets to office |
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what type of flap tears need prophylactic therapy
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1. symptomatic flap tears
2. asymptomatic flap tears with subclinical RD (fluid) |
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what are subclinical retinal detachments
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1. retinal elevation extending more than 1DD beyond the edge of a break
2. not more than 2 DD posterior to the equator 3. any amount of subretinal fluid is bad |
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what are operculated breaks
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1. retinal tissue is completely pulled free of RPE
2. traction may or may not remain on the edges of the hole |
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management of operculated breaks
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DO NOT TREAT asymptomatic operculated breaks without fluid!!!
-symptomatic operculated breaks and those with subretinal fluid need prophylax |
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what is retinoschisis
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1. splitting of the retina into an inner and outer layer
2. results from the coalescence of microcystoid degeneration of the peripheral retina 3. inner layer is thin and transparent and contains blood vessels 4. shadow case on the outer retina by the vessels |
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which quadrant is retinoschisis usually seen in
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72% in inferiotemporal
25% in superiotemporal 82% BILATERAL NOWHERE ELSE!!! |
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management of retinoschisis
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DO NOT treat retinoschisis unless progressive RD is present simultaneously or macula is threatened
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DDx of RD vs. Retinoschisis
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Retinoschisis
1. sharp borders 2. transparent 3. no demarcation line 4. smooth Retinal detachment: 1. graduated border 2. translucent 3. demarcation line 4. undulated and uneven 5. rhegmatogenous RD often has fixed folds (only RRD) |
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presence of what makes retinal breaks a little safer
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1. pigment surrounding the break
- RPE becomes hyperplastic and invades the retina surrounding the break, sealing the rbeak |
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what is the most significant risk factor for progression to rhegmatogenous retinal detachment
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PHOTOPSIA
-FLASHES OF LIGHT |
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management of rhegmatogenous retinal detachment
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1. scleral buckle (most common)
2. pneumatic retinopexy 3. intraocular silicone oil tamponade |
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retinal breaks and detachment:
what do you NOT treat |
1. lattice degeneration (w/o history of lattice RD)
2. atrophic holes in lattice degeneration 3. asym flap tears without fluid 4. asym flap tears without PVD 5. asym operculated breaks without fluid 6. retinoschisis (unless macula is threatened) |
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retinal breaks and detachment:
what DO you treat |
BREAKS that are...
1. symptomatic 2. with fluid 3. in fellow eye 4. cataract extractions 5. vitreous hemorrhage 6. recent and tractional 7. trauma |
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management of retinal break in respects to location
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1. anterior: cryoretinopexy
2. posterior: laser photocoagulation |
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possible complications of pars planitis
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1. posterior subcapsular cataract
2. PVD 3. neovascularization (mostly posterior segment) 4. glaucoma |
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treatment of pars planitis
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1. OBSERVATION
2. steroids 3. transscleral cryoretinopexy 4. thermal laser photocoagulation 5. vitrectomy |
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what is the #1 cause of pediatric vitreous hemorrhage
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PARS PLANITIS
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pars planitis is associated with what systemic diseases
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1. crohn's disease
2. multiple sclerosis |
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what do you look for with pars planitis in young patients??
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1. when encountering a true PVD in a young patient
2. look for vitreal cells and other signs of pars planitis |
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active toxoplasmosis produces retinitis that appears as...
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1. "headlights in a fog" due to focal vitritis
2. arteritis 3. periphlebitis 4. lesions heal within 3wk-6mths |
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toxoplasmosis is the #1 cause of what??
what should you consider in acquired toxo in a young patient |
1. posterior uveitis
2. focal chorioretinitis consider AIDS in acquired young patients |
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what are some treatments for toxoplasmosis
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1. Sulfadiazine 1g p.o. QID
2. Bactrim DS QD 3. Pyrimethamine 25mg p.o. QD (w/ folate supplement) 4. Clindamycin 250mg QID 5. Prednisone 40mg QD (only in conjunction with above) |
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how does toxocariasis infect the eye
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1. nematode parasitic in dirt and fecal matter
2. larvae travel in blood and lymph fluid |
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what are the two types of toxocariasis
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1. OCULAR and SYSTEMIC
2. NEVER seen together 3. occurs in CHILDREN and UNILATERAL |
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treatment and diagnosis of toxocariasis
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1. ELISA
2. photocoagulation and cryo 3. steroids (po) for inflammation |
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where is histoplasmosis found?
how does it infect the body? |
1. Ohio-Mississippi River Valley
2. fungal infection (soil, bird and bat feces) 3. mycelial spores inhaled and transform to yeast phase in lungs 4. spread via bloodstream |
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DDx between ocular histoplasmosis and multifocal choroidopathy
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1. OHS never causes cells to appear in the vitreous
2. purely CHOROIDITIS |
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diagnosis of ocular histoplasmosis
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1. **peripapillary scarring**
2. **at least one peripheral Histo spot** 3. granulomatous inflammatory mass 4. circumpapillary choroidal scarring |
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what are the signs of maculopathy in histoplasmosis
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1. macular granuloma
2. bruch's disruption 3. 4th most common cause of CNVM 4. Sub-RPE hemorrhage with subsequent disciform scarring 5. lipid exudates |
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most common population for sarcoidosis
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BLACK FEMALES!!!
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pts. comes in with...
1. retinal periphlebitis 2. vasculitis 3. candle wax drippings immediately think... |
1. sarcoidosis
2. syphilis |
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how do you diagnose for sarcoidosis...(if you dont know this...just kill yourself)
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1. ACE
2. chest xray (hilar adenopathy) 3. Gallium scan 4. biopsy |
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Eale's disease targets what population
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YOUNG HEALTHY MALES
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what are the two key features in diagnosing Eale's Disease
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1. venous peri-phlebitis
2. venous obstruction |
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you should suspect Eales Disease when you see a patient with...(5)
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1. posterior segment neovascularization
2. vitreous hemorrhage 3. tractional detachment 4. symptoms in young healthy male with no diabetes 5. perivascular scarring |
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what must you rule out with Eale's Disease
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TUBERCULOSIS
-high association to tuberculoprotein sensitivity |
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Vogt-Koyanagi-Harada syndrome is characterized by...
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rare systemic disease involving various melanocyte-containing organs
**PRECEDED BY PRODROMAL STAGE (headache, touch sensitivity, vertigo, nausea, nuchal rigidity, vomiting, fever)** 1. bilateral granulomatous panuveitis 2. serous retinal detachment 3. optic disc edema 4. neurological abnormalities 5. skin pigmentary changes |
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what causes APMPPE
what is seen in the retina |
1. obstructive choroidal vasculitis
2. post viral autoimmune disorder 3. spirochete disease WHITE PLACOID LESIONS |
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what test highly correlates to birdshot retinochoroidopathy
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(+) HLA A29
FA: filling delay and vessel leakage |
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what are the A/R in congenital fundus dystrophies
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1. Retinitis Pigmentosa
2. Stargardt 3. Reticular Dystrophy 4. Gyrate Atrophy |
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what are the A/D in congenital fundus dystrophies
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1. Adult Vitelliform
2. Best Disease 3. Butterfly Dystrophy 4. Cone Dystrophy 5. Central Areolar Dystrophy 6. Reticular Dystrophy 7. Retinitis Pigmentosa (Sectoral) |
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what are the X Linked in congenital fundus dystrophies
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1. Cone Dystrophy
2. Choroideremia |
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what is the most common
hereditary dystrophy |
retinitis pigmentosa
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in terms of vision what will the patient complain of in Cone Dystrophy vs. Retinitis Pigmentosa
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Retinitis Pigmentosa:
NIGHT BLINDNESS Cone Dystrophy: DAY BLINDNESS |
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clinical triad for retinitis pigmentosa
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1. arteriolar attenuation
2. waxy pallor of ONH 3. retinal bone spicule pigmentation along perivascular area (SALT AND PEPPER FUNDUS) |
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pathophysiology of retinitis pigmentosa
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defect of RPE metabolism:
disturbance in the disc renewal process of the outer segment of photoreceptors and lipofuscin accumulation within the RPE with eventual death of photoreceptors |
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what are the two notable systemic associations with retinitis pigmentosa
|
1. Usher's Syndrome
RP with hearing loss 2. Bardet-Biedl Syndrome RP with obesity, mental retardation, polydactyly, hypogenitalism and renal disease |
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diagnostic test for retinitis pigmentosa
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1. VF:
-ring scotoma 2. ERG -abnormal dark adapation -decrease A or B amplitudes -increased latency for scotopic responses |
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retinitis pigmentosa management
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1. vitamin A palmitate
2. DHA in patients beginning Vitamin A therapy 3. Lutein in NON SMOKERS 4. hearing test 5. test associated conditions |
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clinical appearance of Cone Dystrophy
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1. bull's eye maculopathy
2. golden reflex due to atrophic RPE surrounding darker macula 3. pigment clumping 4. geographic atrophy 5. loss of color vision |
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diagnostic test for Cone Dystrophy
|
1. ERG
-reduced or absent photopic and cone response 2. OCT -retinal atrophy in macula area 3. Visual field -central scotoma |
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what are the the type of Cone Dystrophy
characteristics? use what test to DDx? |
STATIONARY:
-rod monochromatism -no progression -associated with nystagmus PROGRESSIVE: -ONLY CONES -gradually worsens CONE-ROD DISEASE: -eventually affects rods |
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what is the most common macular dystrophy?
second most?? |
MOST COMMON:
-Stargardt's Macular Dystrophy SECOND MOST COMMON: -Best's Vitelliform Macular Dystrophy |
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what are the FIVE stages of Best's Vitelliform Macular Dystrophy
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1. Pre-Vitelliform: abnormal EOG in asymptomatic patients
2. Vitelliform: elevated "egg-yolk" macular lesion 3. Pseudo-Hypopyon: part of lesion reabsorbed 4. Vitelliruptive: "scramble egg" appearance 5. End Stage Atrophy: moderate to sever acuity loss with macular scar |
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diagnostic test for Best's Vitelliform Macular Dystrophy
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1. EOG: SEVERELY ABNORMAL
2. OCT may reveal lipofuscin just about RPE 3. FA hypofluorecent due to block by lipofuscin in macula (R/O CNVM) |
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what causes Stargardt's Macular Dystrophy
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1. enzymatic defect within RPE
2. enlarged RPE with lipofuscin |
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what is the clinical presentation for Stargardt's Macular Dystrophy
|
1. oval macular lesion with a BEATEN BRONZE appearance
2. mottling of fovea |
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diagnostic test for Stargardt's Macular Dystrophy
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1. FA: DARK CHOROID
2. ERG: flash ERG normal and mfERG ABNORMAL 3. OCT reveals thinning 4. visual field will have central defect but normal periphery |
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what is adult vitelliform
|
1. bilateral and symmetric
2. abnormal accummulation of lipofuscin in RPE 3. GOOD PROGNOSIS 4. EOG USUALLY NORMAL |
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diagnostic testing for Gyrate Atrophy
management? |
1. Ornithine levels are highly elevated
2. ERG and EOG both abnormal management: 1. B6 (pyridoxine) in attempt to normalize plasma and urine ornithine levels 2. reduce protein intake and restrict arginine (AA) |
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what does central areolar dystrophy present as...
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bilateral and symmetric destruction of CHORIOCAPILLARIS within the posterior pole
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what are the two types of mechanism for traumatic retinopathy
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1. Coup:
-local trauma at the sit of impact 2. Contrecoup: COMMOTIO RETINAE -injuries at the opposite side of the skull caused by shock waves that traverse the brain |
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what is seen in COMMOTIO RETINAE
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1. trauma induced swelling and disorganization of outer retinal layers
2. white and opaque (confused with white without pressure) |
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what do you do if you see peripapillary hemorrhage associated with head trauma?
what is the syndrome called? |
TERSON'S SYNDROME:
1. EMERGENCY 2. IMMEDIATE RADIOLOGICAL SCAN |
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what is Valsalva Hemorrhage
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preretinal hemorrhages arising from sudden increases in internal pressure through exertion or strangling
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what type of maculopathy is significant with Plaquenil
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BULL'S EYE MACULOPATHY
-fine pigmentary mottling within the macular area |
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what are the FOUR main risk factors for PLAQUENIL
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a FAT OLD (60+) person taking 1000g HCQ or 460g CQ for more than FIVE YEARS
1. DOSAGE: >1000g HCQ or >460g CQ 2. OBESITY: CQ/HCQ is not retained in fat tissue, standard 400mg/day may represent overdosage. should be dosed based on height of pt 3. DURATION: greater than 5 years 4. age >60yrs 5. liver/renal impairment or preexisting retinal condition |
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Tamoxifen Maculopathy
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1. reversible early, IRREVERSIBLE LATE
2. white crystalline macular deposits 3. visual acuity decreases are usually secondary to foveal cyst development |
