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Ocular Disease 4 > Lecture 7 - AMD > Flashcards

Lecture 7 - AMD Flashcards

1
Q

what are the hallmark findings of dry AMD?

A

drusen, RPE hyperpigmentation and RPE atrophy

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2
Q

what are the hallmark findings of wet AMD?

A

choroidal neovascularization, sub-retinal/sub-RPE fluid, and sub-retinal/sub-RPE blood

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3
Q

what is the risk of conversion from dry to wet AMD?

A

1-5% chance after 1 year and 13-18% chance after 3 years

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4
Q

who typically gets AMD?

A

12-30% over age 80, 89% white and 65% female

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5
Q

what is the biggest risk factor for AMD?

A

age = risk advances with increased age (2nd is race = caucasian because RPE pigmentation is protective)

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6
Q

what are other risk factors for AMD besides age and race?

A

family history (Tyr402His and Ala69Ser - part of complement factor H gene), smoking, UV exposure, systemic diseases (cardiovascular disease, obesity, HTN, high cholesterol)

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7
Q

how do you calculate the risk based on smoking?

A

pack years = if they smoked 1 pack a day for 1 year they have a 1 pack year smoking history (if they smoke 1/2 pack a day for 50 years they have a 25 year pack history)

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8
Q

what are the 5 layers of bruch’s membrane?

A

basement membrane of RPE, inner collagenous zone, elastic fiber layer, outer collagenous zone, basement membrane of the choriocapillaris

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9
Q

what happens to bruch’s with aging, what increases and what decreases?

A 
increases = type 1 collagenm debris, filamentous material, glycosaminoglycans
decreases = laminin, fibronectin and type 4 collagen
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10
Q

what is the pathophysiology of dry AMD?

A

problem with RPE, bruch’s or choriocapillaris = ultimately affects the photoreceptor function as a result of oxidative stress and inflammation

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11
Q

what happens during oxidative stress?

A

radiation (UV) and oxygen side effects (pro-oxidants) produce free radicals - damaged photoreceptors are taken in by RPE cells - RPE cells cannot handle amount and results in RPE damage

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12
Q

what happens during inflammation?

A

inflammation induces complement system - forms the membrane attack complex (MAC) - MAC injures RPE cells and endothelial cells of choriocapillaris

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13
Q

how does RPE damage occur?

A

damage to matrix metalloproteins (cannot get rid of byproducts like normal) - backed up byproducts get deposited between basal lamina of RPE and bruch’s = Drusen and RPE cells disorganize = atrophy and hypertrophy

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14
Q

what is the composition of drusen?

A

basal laminar deposits = lipid and collagen

basal linear deposits = phospholipid vesicles and granules

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15
Q

what are the sizes of drusen?

A

small less than 63um, intermediate between 64-124um, and large larger than 125um

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16
Q

what is the histology of drusen?

A

hyaline material accumulations and lipid rich

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17
Q

what is the result of hydrophobic and hydrophilic drusen?

A 
hydrophobic = predispose RPE detachments
hydrophilic = predispose formation of CNVM
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18
Q

what causes RPE atrophy?

A

photoreceptor death, large drusen push pigment away, perfusion abnormalities and decreased vascular density, flattening of RPE detachments and regression of confluent drusen

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19
Q

what is geographic atrophy?

A

may be the end stage of Dry AMD - will never develop wet (neo) the RPE is dead

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20
Q

what is the pathophysiology of wet AMD?

A

damage to RPE stimulates neo from choroid - new vessels contain fibroblasts (aka network or membrane) = VEGF and CNVM occur

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21
Q

what are the symptoms of dry AMD?

A

may be asymptomatic, gradual vision loss, central scotomas, and amsler grid defects

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22
Q

what are the signs of dry AMD?

A

hard/soft/confluent/calcified drusen - RPE hyperpigmentation - RPE hypopigmentation - RPE atrophy - geographic atrophy

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23
Q

what do hard drusen look like?

A

small (less than 64 microns), discrete and well demarcated

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24
Q

what do soft drusen look like?

A

larger than 64 microns, poorly defined borders, yellow-white

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25
Q

what do confluent drusen look like?

A

soft drusen that have coalesced - can cause focal RPE detachment

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26
Q

what do calcified drusen look like?

A

calcification of soft drusen - more white and refractile than soft

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27
Q

what is RPE hyperpigmentation?

A

migration of RPE cells and the photoreceptor layer

28
Q

what is RPE hypopigmentation?

A

areas where RPE cells are absent of not-pigmented, usually counter to RPE hyperpigmentation or indicates a larger area of RPE atrophy, geographic atrophy

29
Q

what is RPE atrophy?

A

results from = large are of hypopigmentation, previous drusen, RPE detachment, choroidal neo - the choroid is visible and photoreceptors are absent (VA loss)

30
Q

what is geographic atrophy?

A

end of cycle = large areas of contiguous RPE atrophy - causes the most visual dysfunction of dry AMD (12-20% legal blindness)

31
Q

what are RPE atrophy symptoms?

A

decreased vision/central scotoma, missing areas on amsler grid, and may have metamorphopsia

32
Q

what are the symptoms of wet AMD?

A

vision loss is more sudden (over 1 weeks time), metamorphopsia, and central scotoma

33
Q

what are the clinical findings of wet AMD?

A

CNVM/gray-green CNV lesion, sub-RPE or sub-retinal (fluid, blood, lipid), sub-retinal pigment ring, irregular elevation of RPE, and pigment epithelial detachment (PED)

34
Q

what are the types of PED?

A

serous (coalesced drusen - fluid accumulates from choroid) and vascular (CNVM pushes RPE from bruchs)

35
Q

what are the 2 types of CNVM?

A

classic = uniform lesion with typical IVFA pattern, easier to treat
occult = irregular lesion with typical IVFA pattern
most are a combination of both

36
Q

what is a disciform scar in wet AMD?

A

also called fibrovascular scar or net = end stage of CNVM (fibrous tissue proliferation - hemorrhage or hyperplasia of RPE)

37
Q

what are normal aging changes?

A

only druplets (small drusen

38
Q

what is early AMD?

A

medium drusen (greater than 63um and less than 125um) and no AMD pigmentary abnormalities

39
Q

what is intermediate AMD?

A

large drusen ( greater than 125um) and/or any AMD pigmentary abnormalities

40
Q

what is late AMD?

A

neovascular AMD and/or any geogrphic atrophy

41
Q

what are the different tests used in AMD?

A

amsler grid, macula OCT, IVFA, ICG

42
Q

what does drusen look like in an OCT?

A

within the RPE layer - local elevations/irregularities

43
Q

what does RPE atrophy look like in an OCT?

A

missing areas of RPE layer, window defect - choroid is directly visible (more hyper-reflectivity)

44
Q

what does a PED look like on an OCT?

A

serous PED = elevated dome shape, sharply demarcated edges, black or optically empty - fluid
fibrovascular PED = irregular borders, not black but shadowed, no dome shape pattern

45
Q

what does a CNVM look like on an OCT?

A

looks like a fibrovascular PED, no typical dome shape, irregular borders and interior is filled with material

46
Q

what does a disciform scar look like on an OCT?

A

intraretinal cyst - large area of scar tissue, elevated in OCT scan

47
Q

what does dry AMD look like on FA?

A

all components will hyperflouresce except pigment with hypofluoresce (drusen hard/soft will stain directly) and the RPE hypertrophy will block NaFl

48
Q

what does geographic atrophy look like on FA?

A

early hyperfluorescent and late scleral staining

49
Q

what does a classic CNVM look like on FA?

A

well-demarcated lacy pattern
early phase = bright uniform hyperfluorescence
transit phase = progressively intensifies
late phase = dye leakage outside the borders

50
Q

what does an occult CNVM look like on FA?

A

early phase = elevation of RPE, granular irregular

late phase = progressive leakage, still granular and not as diffuse/uniform as classic

51
Q

when is ICG used in AMD?

A

most advantageous in occult CNVM in determining exact location

52
Q

what is the follow up for dry AMD?

A 
6-12 months (depends on appearance)
early hard drusen = 12 months
some soft drusen = 9 months
extensive soft drusen = 6 months
geographic atrophy = 6-12 months
53
Q

what is the follow up for wet AMD?

A

any new area of CNVM, bleeding, fluid = refer to OMD for treatment and will follow up every 1-3 months until CNVM resolves

54
Q

what is the follow up for a disciform scar?

A

if scarring is extensive = new treatment will not be affective, monitor every 12 months

55
Q

what can patients do to self-monitor?

A

amsler grid 1x per week = look for metamorphopsia and missing lines, decreased vision, and central scotoma

56
Q

what are some lifestyle changes for AMD?

A

stop smoking, sun protection, manage chronic conditions, diet

57
Q

what tests do you perform if you suspect a CNVM?

A

OCT, FA, and preferential hyperacuity perimeter (highly sensitive to changes in photoreceptors)

58
Q

what groups are AREDS 1 most effective for?

A

intermediate AMD and advanced AMD in 1 eye (no benefit for early AMD, geographic atrophy, CNVM or disciform scar)

59
Q

what is in the AREDS 1 formula?

A

500mg Vitamin C, 400 IU Vitamin E, 15mg Beta Carotene, 80mg Zinc oxide, 2mg cupric oxide (copper)

60
Q

what were the issues with AREDS 1?

A

beta-carotene is a concern with smokers (lung cancer), high levels of zinc may cause a copper deficiency, and new studies showed lutein/zeathanthin/omega 3 fatty acids may help

61
Q

what did the AREDS 2 study conclude?

A

overall no benefit for = lutein/zeathanthin, lowering zinc dose, removing beta-carotene and adding omega 3 (only benefited smokers and those with little lutein/zeathanthin in diet)

62
Q

what is the AREDS 2 formula?

A

500mg Vitamin C, 400 IU Vitamin E, 80mg Zinc oxide, 2mg cupric oxide (copper), 10mg Lutein, 2mg Zeathanthin

63
Q

what are the vitamin recommendations?

A

multivitamin, AREDs 2 formula for moderate dry AMD and advanced dry/wet AMD in 1 eye

64
Q

what are the treatments for CNVM?

A

anti-VEGF = lucentis, avastin, macugen, eylea (upon sign of CNVM inject every 3-6 months as needed)

65
Q

what are other treatments for wet AMD besides anti-VEGF?

A

laser (at leaking vessels - rarely used), PDT (rarely used) and low vision aids

Ocular Disease 4 (6 decks)

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