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PPO > week 3 > Flashcards

week 3 Flashcards

1
Q

Vitreous is attached to posterior lens surface by:

A

Vitreous is attached to posterior lens surface by Wieger’s ligament (not a true ligament)

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2
Q

Vitreous base divides the vitreous into:

A

Vitreous base divides the vitreal cortex into the anterior and posterior portions

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3
Q

vitreous composed of:

A

99% water…. increases as we get older
1% of solids: eg: proteins, hyaluronic acid, collagen filaments, hyalocytes,
albumin, glucose, absorbic acid, galactose

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4
Q

where is the vitreous base?

A

landmark is at the ora serrata and it extends anteriorly towards the pars plana and posteriorly to the peripheral retina (2 mm)

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5
Q

where are the anterior and posterior hyaloid membranes?

A
  • anterior and posterior hyaloid membrane covers the vitreal cortex
  • anterior is in front of vitreous base, posterior is behind it
  • Ant hyaloid membrane runs from post lens surface to ora (extends from zonules to Weiger’s ligament)
  • Posterior Hyaloid membrane runs from post edge of vitreal abse to ONH
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6
Q

what is Weiss’s ring?

A

detached/floating ring of Gartner at optic nerve/peripapillary vitreous attachment

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7
Q

3rd weakest vitreal attachment?

A

macular attachment

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8
Q

what is Cloquet’s Canal? where is it?

A
  • S shaped optically empty space.
  • runs from the lens to the optic disc.
  • represents atrophic primary vitreous
  • less visible with increasing age.
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9
Q

how can you examine the vitreous with a B scan?

A

B-Scan consists of focused, short wavelength, acoustic waves. Wavefront’s intraocular and orbital velocity
differs as it passes through various ocular structures.

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10
Q

rheology:

A

shift of vitreal cortex from gel to liquid

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11
Q

aging vitreal changes occur sooner for what type of people?

A

high myopes

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12
Q

what % of people with symptomatic PVD will develop retinal breaks?

A

15-35%

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13
Q

3 features of youthful vitreous?

A

avascular acellular fine collagen fibrils

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14
Q

what is synchisis senilis?

A

hyaluronic acid macromolecules break down and release water (liquefaction); allows collagen fibers to coalesce into larger fibers more visible in slit lamp

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15
Q

what is syneresis?

A

vitreous collapses and shrinks

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16
Q

How can “lacunae” in vit lead to PVD?

A

Can!lead!to PVD:!lacunae!may!coalesce!in!sup[post!cortex!and!break!through!
hyaloid!membrane.!Vitreous!collapses!and!shrinks!(Vitreal+Syneresis),!lifts!away!
from!ONH!and!macular!attachments!=!PVD

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17
Q

What gives vitreous its visco-elastic properties?

A

hyaluronic acid

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18
Q

what mainly contributes to strength of vitreal attachment at vit base?

A

alignment of fibers contributes to strength of attachment

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19
Q

what is vitrosin?

A

concentration of collagen-like material in the vitreous;

determines viscosity of vitreous, which is 4x that of water

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20
Q

what are lacunae made out of?

A

Lacunae contain hyaluronic acid and no collagen

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21
Q

Liquefaction and syneresis = ?

A

fibrillary degeneration

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22
Q

flashes are caused by:

A

phosphenes produced by traction on retina, opposite to site of traction

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23
Q

floaters are caused by:

A

Particles of vitreous, blood, retina, casting shadows on the retina

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24
Q

how long do floaters typically last?

A

~4-6w
(brain suppresses the floater so it is no longer bothersome)
**Should not change size or shape over time!

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25
Q

what are a few ways to check for PVD in slit lamp exam?

A

1) Weiss’s ring
2) optically empty space between a loose veil-like posterior membrane with direct focal illumination
“Inverted “J” space in between vitreous base and macula”
3) Look for small opacity temporal to macula

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26
Q

If it is Weiss’s ring, the floaters will be seen where in field?

A

Weiss’s ring- the floater will usually be in central vision

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27
Q

With symptomatic patients w/ PVD, there is a greater chance that there will be a retinal tear within ____

A

1 week

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28
Q

what can cause the vitreal heme?

A
  • retinal tear will cause retinal vessels to bleed when the vitreous tugs on them – can also occur with a retinal detachment
  • *Remember, often caused by NVE, NVD in diabetes
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29
Q

asteroid hyalosis commonly found in what kind of patients?

A

DM HTN atherosclerosis

30
Q

what is asteroid hyalosis made up of?

A

opacities consists of complex phospholipid and calcium phosphate complexes

31
Q

asteroid hyalosis is often: uni or bilateral?

A

unilateral

32
Q

Shaffer’s sign:

A

pigment in the vitreous

33
Q

If you see Shafer’s sign, what should you rule out?

A

assume retinal tear until proven otherwise! (could be from cataract surgery though)

34
Q

why do you get pigment in vitreous with retinal tears?

A

lots of holes/tears of periph retina near vitreous base detachment of sensory retina from RPE
-physical separation damages RPE cells> pigment released from RPE cells can go into anterior vitreous

35
Q

when might you consider vitrectomy from vit heme?

A

if it still hasn’t cleared in 5-6 months

36
Q

Lutein is found primarily where in macula?

A

dominates parafoveal region (just outside FAZ)

37
Q

Zeaxanthin is found primarily where in macula?

A

dominates center part of fovea

38
Q

Lutein is reduced in what kinds of people?

A

smokers, females, light-eyed people

39
Q

Function of Lutein and Zeaxanthin?

A

Protects the macula by blocking blue light reduced oxidative stress, which causes tissue damage

40
Q

how do you perform the photostress test?

A

project one line above BCVA at dist, shine light into one eye for 10 sec, then measure how long it takes them to read the line again (usually 50 sec or less is normal)

41
Q

what is the Farnsworth D-15 test?

A

Farnsworth D-15 is designed to test acquired color defects

Testing: line colors up in order, monocularly. Detects subtle color defects

42
Q

Amselr is performed at what distance and tests how much of your visual field?

A

33cm

-tests 20deg field (10deg on either side of dot)

43
Q

List 8 risk factors related to AMD:

A

1) Age
2) UV light exposure
3) Light irises/fair skinned ie Caucasians
4) Smoking**- biggest risk factor
5) Vascular problems, decreased perfusion (Arteriosclerotic disease, vascular problems, HTN)
6) Obesity
7) Hyperopic: 2.5x higher risk
8) Genetics=parent has AMD, 40% chance child might get it

44
Q

What is the end stage of dry AMD:

A

Atrophic= end stage of dry form

45
Q

how quickly does dry AMD progress?

A

Very slow ~10 years for progression

46
Q

what is one of the first signs of aging RPE layer?

A

RPE mottling

47
Q

what are basal laminar deposits

A

Basal laminar deposits= hard drusen

48
Q

what are basal linear deposits?

A

soft drusen

49
Q

where do hard drusen accumulate?

A

accumulation bw RPE cell membrane and BM of RPE (Bruch’s)

50
Q

What was the avg age of AREDS 1 trial? what kind of participants?

A

~4000 people, ~25% had no AMD but genetic predisposition, rest had varying levels
Age group: 55-80 years, Mean age: 69 years
**interesting to note: 57% of subjects were already taking multivitamins; 67% chose to add Centrum - implications for dosing

51
Q

what were the vitamins in the AREDS 1 formula?

A

o Vitamin C: 500 mg
o Vitamin E: 400 IU (IU- international units)
o Beta-carotene: 15mg or 25,000 IU
o Zinc oxide: 80mg * controversy over how much
o Copper oxide: 2 mg- this was added b/c when we take zinc, it depletes our copper levels

52
Q

Describe how category 1 was classified for the AREDS 1 findings:

A

No AMD:

  • less than 5 small drusen (<63 microns)
  • 20/32 vision or better in both eyes
53
Q

Describe how category 2 was classified for the AREDS 1 findings:

A

Mild AMD:
-Multiple small drusen
-single or non-extensive intermediate drusen (63-124 um)
-Pigment abnormalities
(Or any combination of these in one or both eyes)
-With 20/32 vision or better in both eyes
**2% rate of progression to advanced AMD at 5 years

54
Q

Describe how category 3 was classified for the AREDS 1 findings:

A

Moderate AMD:
-at least one eye with 20/32 vision of better
-at least one large drusen (125 microns),
-Extensive intermediate drusen,
-Geographic atrophy not involving the center of the macula
(Or any combination of these)

55
Q

Describe how category 4 was classified for the AREDS 1 findings:

A

Advanced AMD:

  • Geographic atrophy, involving the center of the macula
  • Or features of choroidal neovascularization (wet AMD)
56
Q

What were the variables in treatment for the AREDS 1 study?

A

Zinc only, Antioxidant only, Zinc & Antioxidant or Placebo

57
Q

what were the outcomes for the zinc only study group for the AREDS 1 study?
Reduced development of Advanced AMD by __% ?
Reduced risk of vision loss by ___%

A

Reduced development of Advanced AMD by 21%

Reduced risk of vision loss by 11%

58
Q

what were the outcomes for the antioxidant only study group for the AREDS 1 study?
Reduced development of Advanced AMD by __% ?
Reduced risk of vision loss by ___%

A

Reduced development of Advanced AMD by 17%

Reduced risk of vision loss by 10%

59
Q

what were the outcomes for the antioxidant AND zinc study group for the AREDS 1 study?
Reduced development of Advanced AMD by __% ?
Reduced risk of vision loss by ___%

A

Reduced development of Advanced AMD by 25%

Reduced risk of vision loss by 19%

60
Q

Was the AREDS 1 formula helpful for early AMD or those with genetic predisposition?

A

NO

61
Q

what were some of the risks associated with a few of the vitamins in the AREDS 1 formula?

A

1) Increased lung cancer in active smokers taking vitamin A / Beta-carotene
2) Higher doses of Zinc caused GI problems
3) Men taking selenium or vitamin E might double their risk of prostate cancer, depending on levels of selenium already in their bodies

62
Q

Name 4 modifications to the vitamin formula the AREDS 2 study made:

A

1) Adding Omega 3 fatty acids (1000 mg)
-Reduces inflammatory cytokines, may help in rebuilding PR and retinal cell membrane
2) Adding Lutein (10mg) and Zeaxanthin (2mg)
Increase macular pigment density (remember our bodies don’t replenish)
3) Eliminate Beta carotene
4) Reduce zinc dosing (Reduce GI problems)

63
Q

4 categories pts were divided into for AREDS 2 study?

what about the 4 subgroups of this?

A
  1. AREDS 1 formula
  2. AREDS 1 formula w/o Beta carotene
  3. AREDS 1 formula w/ low amounts of zinc (25 mg)
  4. AREDS 1 formula w/ reduced zinc and w/o beta carotene

a. Lutein & Zeaxanthin
b. Omega 3 fatty acids
c. Lutein & zeaxanthin & omega 3 fatty acids
d. Placebo

64
Q

what kind of people benefited from AREDS 1 WITH Lutein & Zeaxanthin in the AREDS 2 study?

A

Patients with low diet intake of Lutein & zeaxanthin benefitted from additional supplement

65
Q

T/F: • No overall benefit from adding omega 3 fatty acids OR lutein & zeaxanthin to the original AREDS formulary

A

true

66
Q

AREDS 1 WITHOUT beta carotene and WITH Lutein & zeaxanthin risk of developing advanced AMD over 5 years was reduced by __% compared to AREDS 1 formulary?

A

reduced by 18% compared to AREDS 1 formulary (in those with intermediate/moderate AMD)
**Possible that: Beta-carotene and Lutein & Zeaxanthin are competing for absorption in the body and B carotene may be masking the overall effects

67
Q

How do the AMD genetic risk markers Complement factor H (CFH) and Age-Related Maculopathy Sensitivity 2 (ARMS2) benefit from the different possible vitamins?

A

1) 1 or 2 risk alleles of CFH: maximum benefit from AREDS formula minus zinc
2) ARMS2 risk alleles: maximum benefit from zinc alone
- No benefit from other supplements in AREDS formula
3) CHF & ARMS2 risk alleles: no benefit from AREDS

68
Q

what are pigment epithelial defects?

A
  • soft drusen physically separate RPE & Bruch’s causing PEDs

* *PEDs increase the risk of choroidal neovascular membrane formation

69
Q

what is the protein released by the PRs that keeps VEGF in check?

A

Pigment Epithelial Derivative factor (PEDF)

70
Q

what are the 2 types of CNV?

A

1) Classic
=Well demarcated borders
=Seen clearly in early phase of FA
=Area of hyper-FL but stays confined to that area
=Easier to get rid of
2) Occult
=Ill-defined borders
=Persistence of leakage of FL post FA (10+ mins)
=Spread and surround more of retinal area
=Highly associated with wet AMD
=More difficult to get rid of; worse prognosis

71
Q

where is juxtafoveal CNV? extrafoveal? subfoveal?

A

subfoveal is underneath
juxta=1-199 um
extra=200-2000um

72
Q

2nd most common reason for CNVM?

A

1st=wet AMD

2nd=POHS=presumed ocular histoplasmosis

PPO (10 decks)

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