Vitreous Flashcards

1
Q

vitreous is ___ the eye’s volume and ___ the eye’s weight

A

2/3 volume of the eye

3/4 of eye weight

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2
Q

2 components of vitreous

A

water (99%) which is held in a gel-like state by hyaluronic acid and solids (1%) mainly collagenous filaments

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3
Q

what adds viscosity to vitreous and how does it change with age?

A

hyaluronic acid and we have a lot less hyalocytes as we age, so ability to hold water is reduced and vitreous becomes more fluid

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4
Q

vitreous viscosity is ___x viscosity of water

A

4x

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5
Q

what is the area of the strongest adhesion of vitreous to retina

A

vitreous base

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6
Q

describe the location and size of the vitreous base

A
  • straddles ora serrata
  • about 2-4mm wide
  • can extend significantly posterior to ora
  • usually more posterior to ora nasally
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7
Q

what is the vitreous base susceptible to and why?

A
  • vitreous traction in this area can cause retinal tears or retinal dialysis (tear at ora)
  • anterior limit of a PVD almost always posterior edge of vitreous base
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8
Q

what is a common location of tractional retinal tears (15% of them)?

A

posterior border of vitreous base

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9
Q

clinical appearance of vitreous base

A
  • anterior border is grayish ridge on pars plana

- posterior border is hard to see but may have increased pigmentation under vitreous base if you can see it

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10
Q

5 areas of normal vitreo-retinal adherence

A
  • vitreous base
  • optic nerve head
  • macular region
  • retinal vasculature
  • ILM
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11
Q

the 2nd strongest vitreo-retinal attachment, the ONH: has insertions where?
what does detachment cause?

A
  • inserts into glial peripapillary ring

- detachment can disinherit this glial ring and cause Gartner’s/ Vogt’s/ Weiss ring

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12
Q

what type of vitreo-retinal attachment is at the macular region and how does it change with age?

A
  • usually attached in circular ring around macular region

- this adhesion weakens with age

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13
Q

areas of abnormal vitreo-retinal adherence

A
  • lattice degeneration
  • chorioretinal scars
  • retinal vasculature
  • meridional folds
  • granular tufts, tractional tufts
  • unusual posterior extensions of vitreous base
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14
Q

the anomalous vitreo-retinal adhesions area almost always in the

A

equatorial region or further anteriorly

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15
Q

what would be the set up and technique used to evaluate the vitreous

A
  • dark room (dark adapt) and dilated pupil
  • optic section to “slice” vitreous, low mag
  • angle beam at least 15-30
  • use Tyndall effect (have pt shift fixation)
  • observe subtle structures snd shadows directly or indirectly illuminated
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16
Q

symptoms of vitreous disease

A
  • floaters
  • flashes (photopsias)
  • blurred vision
  • metamorphopsia
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17
Q

what is the most common symptom of vitreous diease

A

floaters

sudden onset of floaters highly significant indicator for retinal tear or tear with detachment

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18
Q

what is muscae volitantes

A

a type of floater from remnants of hyaloid artery system trapped in Cloquet’s canal

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19
Q

what can cause white cells in vitreous

A
  • uveal, vitreal, retinal, or optic nerve head inflammation

- iritis

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20
Q

what can cause pigment in vitreous?

A
  • pathogomic of retinal tear (RPE released into vitreous called Tobacco dust or Shafer’s sign)
  • uveitis
  • intraocular surgery
  • trauma
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21
Q

vitreal or pre-retinal blood strongly associated with:

A

retinal tear (91%) in patients without retinal vascular diseases such as diabetic retinopathy

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22
Q

if there is blood in the vitreous and the retina cannot be viewed, what can you do?

A

consider it a retinal tear until proven otherwise and a B scan may be needed to differentiate cause

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23
Q

what are some possible other symptoms of floaters

A
  • asteroid hyalosis
  • syneretic vitreous changes, fibrillary degeneration
  • PVD
  • tear film debris
  • scotoma
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24
Q

flashes (photopsias) may signify

A

vitreo-retinal traction

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25
Q

which eyes are affected with flashes in vitreo-retinal causes vs. neurovascular

A

VR: unilateral
NV: bilateral

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26
Q

what types of flashes are seen in VR vs. NV

A

VR: color or black/white, bright sparks or lines, flash bulb like or lightening streak
NV: angular or zigzag patterned flashes (think chevron on side, consumed whole vision)

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27
Q

timing of flashes in VR vs. NV

A

VR: very brief (second or two)
NV: longer (minutes)

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28
Q

how can ambient lighting affect flashes in VR vs. NV

A

VR: more apparent in dark
NV: apparent in dark or light

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29
Q

if floaters can be elicited with eye/head movement it is more likely to be due to:

A

vitreal traction

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30
Q

what vitreal things can cause blurred vision?

A
  • debris in vitreous such as Gartner’s ring (rapid transient blue to clear), vitreous heme, macular disruption
  • chronic traction on macular region can cause CME
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31
Q

how common is metamorphosia in virtreal disease and what can cause it?

A

very rare symptom

-vitreous traction on macula and/or associated CME may cause it

32
Q

2 types of congenital anomalies of vitreous

A
  • Mittendorf’s dot

- Hyaloid remnants

33
Q

what are 3 hereditary vitreoretinal disorders

A
  • X-linked Juvenile Retinoschisis
  • Wagner’s Hyaloid Retinal Degeneration
  • Goldmann Favre Disease
34
Q

what causes Mittendorf’s dots? what do they appear as?

A
  • remnant of the attachment of HA to posterior lens capsule

- appears as small black dot on retro view or white dot on direct view

35
Q

list of hyaloid artery remnants

A
  • Muscae Volitantes
  • Bergmeister’s Papilla
  • Persistant Hyaloid Artery
  • Persistent Hyperplastic Primary Vitreous (PHPV): both anterior and posterior
36
Q

type of hyaloid artery remnants that are:

  • very common
  • remnants of HA system trapped within Cloquet’s canal
  • more apparent with uncorrected ametropia
A

Muscae Volitantes

37
Q

when can Muscae Volutantes be best visualized by a patient

A

when viewing bright, optically empty area- blue sky, pastel wall,etc.

38
Q

type of hyaloid artery remnants that are:

  • posterior end of HA
  • grayish-whiteish epipapillary membrane due to incomplete regression of hyaloid system
  • may obscure disc margins
A

Bergmeister’s Papilla

39
Q

type of hyaloid artery remnants that are:

-persistent through nonfunctional HA without fibrous component of primary vitreous

A

persistent hyaloid artery

40
Q

type of hyaloid artery remnants and type of PHPV that is:

  • less common
  • dense opaque white membrane (retinal fold) from ONH to retinal periphery
A

posterior PHPV

41
Q

type of hyaloid artery remnants and type of PHPV that is:
-failure of regression of HA system and primary vitreous with hyperplasia of primary vitreous as the fibrovascular mass at posterior lens capsule

A

anterior PHPV

42
Q

characteristics of anterior PHPV

A
  • observable at birth (seen as leukocoria)
  • unilateral (90%)
  • unusual characteristics: whitish mass with vessels on posterior capsule with long ciliary processes inserting, micro ophthalmia, long ciliary processes
  • shallow AC
  • cataract
  • colobomas of uveal tract
43
Q

what type of prognosis for anterior PHPV

A

poor because of amblyopia and glaucoma

44
Q

treatment for anterior PHPV

A

lensectomy

45
Q

type of hereditary vitreoretinal disorder that:

  • X-linked recessive
  • retina splits into two at the RNFL
  • macular schisis with cystoid like maculopathy
A

X-linked juvenile retinoschisis

46
Q

what is different about X-linked juvenile retinoschisis vs. aquired/ senile retinoschisis

A

in senile- retina split is at the OPL and can extend to ora

in juvenille- retina split at RNFL and usually does not extend to ora

47
Q

some other characteristics of X-linked juvenile retinoschisis

A
  • 50% of the peripheral retinoschisis can be found inferior temporal
  • vitreous veils
  • vitreous heme (25%)
  • hyperopia refraction
  • ERG: reduced B wave with normal A wave
48
Q

type of hereditary vitreoretinal disorder that is

  • autosomal dominant
  • vitreoretinal degeneration characterized by optically empty vitreous cavity due to vitreous liquefaction and avascular pre-retinal vitreous membranes
A

Wagner’s Hyaloid retinal degeneration

49
Q

some other characteristics of Wagner’s hyaloid retinal degenerations

A
  • myopic stance
  • whole retina involved
  • radial perivascular lattice degeneration with perivascular pigmentation
  • cataracts
  • may mimic appearance of RP
50
Q

type of hereditary vitreoretinal disorder that is the worst of them all, autosomal recessive, has optically empty vitreous, central and peripheral retinoschisis, RD common, night blindness from RP like changes, and cataracts

A

Goldmann Favre Disease

51
Q

2 normal aging changes of the vitreous

A
  • liquifaction

- syneresis

52
Q

4 further degenerations of the vitreous

A
  • fribrillary degeneration
  • vitreous collapse
  • ring of Gartner
  • PVD
53
Q

describe the process of liquifaction

A
  • depolymerization of hyaluronic acid (release of water and vitreous becomes more liquid)
  • collagenous fibrils move more freely (perception of floaters possible)
  • formation of optically empty spaces (lacunae) within the formed vitreous (no collagenous fibrils, black on SLE, no tyndall effect)
54
Q

what is fibrillary degeneration

A
  • the clinical appearance of frayed fragmented vitreous fibers
  • greater movement of fibers and can result in PVD
55
Q

in fibrillary degeneration, the vitreous begins to collapse and a break in the post-hyaloid membrane occurs. where does the collapse usually happen first?

A

-usually collapses first at the region of the macula where liquefaction has its greatest effect on provoking a break in the membrane

56
Q

explain how the fibrillary degeneration can lead to a PVD

A

-the vitreous fibers tend to contract towards the central vitreous with time -> pulls cortical vitreous from retinal posteriorly first -> detachment of posterior hyaloid membrane from retina and ONH -> PVD

57
Q

what is the ring of Gartner

A

glial ring avulsed from ONH

-not a true PVD until a posterior hyaloid membrane detachment occurs

58
Q

rapid aging of vitreous is ore likely in:

A
  • myopia
  • intraocular inflammation
  • diabetes
  • vitreous heme
  • ocualr trauma
  • surgery (ICCE, retinal procedures)
59
Q

define posterior vitreous detachment

A

detachment of posterior hyaloid membrane from retina

60
Q

complicated PVD includes

A
  • retinal breaks
  • retinal detachment
  • vitreous hemorrhage
  • retinal hemorrhage
61
Q

how many PVD patients have retinal breaks?

A

10-15% of acute, symptomatic PVDs have retinal breaks

62
Q

2 types of retinal tears:

A
  • operculated tear (less likely to cause RD)

- horseshoe tear

63
Q

describe a horseshoe tear

A
  • more likely to result in RD due to continued traction
  • usually superior retina, often at posterior edge of vitreous base
  • can be very small
  • scleral depression and 3M eval helpful
64
Q

how common is vitreous heme and Shafer’s sign in PVD

A
  • 2/3 PVDs with retinal tear have vitreous heme

- almost all will have Shafer’s sign

65
Q

how many visits for follow up on PVD

A

re-evaluate within 1-3 months until flashes submitted

-if a lot of flashes, follow at 1 or 2 week intervals

66
Q

asteroid hyalosis

A

golden or whitish round spherical opacities associated with vitreous fibers in elderly

  • composed of calcium soaps
  • usually unilateral
  • usually no symptoms but maybe slightly decreased VA and floaters
67
Q

Synchisis Scintillans

A
  • cholesterol crystals within the vitreous cavity
  • severely diseased- blind eyes, rare
  • looks like asteroid hyalosis but really bad vision
68
Q

what are the 2 types of vitreous hemorrhages

A
  • intravitreal

- retrovitreal

69
Q

which type of vitreous hemorrhage has a quicker resolution (usually months)

A

retrovitreal

70
Q

which type of vitreous hemorrhage is bright red, boat shaped, and shifts with head position movements

A

retrovitreal

71
Q

which type of vitreous hemorrhage clots quickly and forms masses of blood with projections- fixed in location

A

intravitreal

72
Q

etiologies of vitreous hemorrhages

A
  • tear in normal retinal vessel
  • rupture in “new” vessels - neo
  • increased venous pressure
  • increased arterial pressure
  • retinal angiomas
73
Q

what is a pre-retinal membrane

A

glial cell proliferation over ILM usually at macula

-possibly related to PVD

74
Q

possible etiologies of pre-retinal membranes

A
  • PVD results in small tears in ILM, astrocytes proliferate
  • thin layer of cortical vitreous left
  • proliferation of vitreous cells over surface of ILM
75
Q

signs/symptoms of pre-retinal membranes

A
  • vision good usually
  • metamirphopsia unusual
  • 80% are unilateral
  • glistening, irregular reflection off ILM in macular region with DO or SLE with fundus lens
  • retinal striae (tension lines)
76
Q

vitrectomy

A
  • removal of vision-reducing vitreal opacity
  • peeling and vacuuming up of the vitreous
  • gas bubble substituted in, patient has to lie face down after surgery