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BOARDS2: Retina/vitreous > Wavy Vision > Flashcards

Wavy Vision Flashcards

1
Q

Top differentials for floaters

A

PVD
Vit heme
Vitritis

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2
Q

Chance of there being a retinal break in a symptomatic PVD

A

10-15%

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3
Q

Chance of there being a retinal break in a symptomatic PVD with a vit heme

A

80%

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4
Q

Common differentials for metamorphopsia

A 
ERM
CSR
AMD
Histo 
Laquer cracks
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5
Q

Stats on ERM

A

More common in females and prevalence increases with age; occurs in 2% of patients over 50, and 20% of patietns over 75.

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6
Q

Signs of mild ERMS

A

Fine glistening membrane on the macular surface (cellophane maculopathy)

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7
Q

Signs of advanced ERMS

A

Thick, gray-white membranes associated with retinal folds due to contraction of the glial membrane (macular pucker)

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8
Q

What happens when the glial membrane in an ERM contracts on itself

A

Macular pucker
Lamellar hole (straight down and inwards)
CME
Pseudohole

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9
Q

Difference between ERM and VMT

A

VMT=pulling up

ERM=just wrinkling

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10
Q

Symptoms of ERMS

A

Often asymptomatic but mild metamorphopsia and/or decreased vision are the most commonly reported symptoms

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11
Q

CSCR

A

Idiopathic condition that results in RPE and/or choroidal dysfunction with resulting accumulation of submacular serous fluid. Puts often complain of unilateral sudden onset of blurred vision (20/20 to 20/200), metamorphopsia, and/or relative scotoma (if macula is involved)

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12
Q

Stats on CSCR

A

Young to middle aged men (20-50) with type A personality, the condition is also assocaited with stress, pregnancy, oral steroids, hypochondriasis, Cushing’s syndrome, SLE, organ transplant, and HTN

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13
Q

Fundus appearance of CSCR

A

Localized macula serous detachemnt; 3% of cases will have an RPE detachment as well

  • FA shows gradual pooling of Fl into the pigment epithelial detachment or a “smokestack” appearance.
  • OCT shows PED
  • may have hyperopic shift in the refractive error and loss of the foveal light reflex
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14
Q

SRF + PED =

A

CNVM

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15
Q

Stats on AMD

A

Most common in patients over the age of 50. It is the second leading cause if blindness in patients 45-64 yo.; wet AMD is the chief cause of vision loss in pts over the age of 50

Framingham eye study: 6.4% of patients 65-74yo and 19.7% of pts older than 75 have signs of AMD.

More common in caucasians and females, additional risks

  • older (esp >75)
  • +Famhx
  • light iris color
  • SMOKING (2.5x more likely)
  • hyperopia
  • HTN
  • HLD
  • cardiovascular disease
  • nutritional factors and light toxicity
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16
Q

Which is more common, wet or dry AMD

A

Dry

-85-90% of cases

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17
Q

Signs of dry AMD

A

Presence of macualr drusen (hallmark), associated RPE abnormalities (mottling, granularity, GA, focal hyperpigmentation) may also be present

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18
Q

Symptoms of dry AMD

A

Most patients do not have sever evision loss, metamorphopsia, gradual vision loss (over months to years), and blurred vision are common complaints

12% of patients with dryAMD will develop severe vision loss (>6 lines of VA); most result from GA or drusenoid PEDs

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19
Q

The macular photocoagulation study discovered 4 risk factors that increase the likelihood of progression to wet AMD

A

A. Multiple soft drusen (especially if confluent)
B. Focal hyperpigmentation
C. HTN
D. Smoking

Hard drusen in isolation are NOT a risk factor for more advanced forms of ARMD

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20
Q

Wet AMD

A

Accounts for 10-15% of cases of AMD. 88% of legal blindness attributed to ARMD is caused by the wet form

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21
Q

Symptoms of wetAMD

A

Metamorphopsia, central scotoma, and rapid vision loss

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22
Q

Signs of wet AMD

A

Drusen associated with signs of a CNVM. CNVMs can leak blood or plasma into two potential spaces, subRPE or subretinal. This creates 4 potential presentations of wet AMD

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23
Q

What are the 4 potential presentations of wetAMD

A

Subretinal hemorrhage (blood under retina, red)
Sub-RPE hemorrhage (blood under RPE, green)
Subretinal detachment (plasma under retina, AKA serous RD)
Sub-RPE detachment (plasma under RPE, AKA PED)

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24
Q

Incidence of involving the fellow eye in wet AMD

A

Is estimated to be about 28-36% during the first two years, the annual rate of bilaterality is about 6-12% per year for the next 5 years, the overall 5 year risk ranges from 40-85%

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25
Q

Histoplasmosis

A

Infection caused by histoplasma capsulatum, a fungus that grows in soil and material contaminated with bird or bat droppings. Most commonly in the Mississippi-OH river valleys.

26
Q

Signs of histo

A

Choroiditis and a classic clinical triad of PPA, multifocal chorioretinal lesions in the periphery, and maculopagthy

NO VITRITIS

27
Q

Symptoms of histo

A

Asymptomatic unless the macula is involved; the earliest symptom is metamorphopsia

  • CNVM is a late manifestation of histoplasmosis and is most likely to occur between the ages of 20 and 45
  • if the macula is involved, the chance of a symptomatic recurrence is appx 20% over 3 years
28
Q

Lacquer cracks

A

Fine, yellow, linear, irregualr lines that represent large breaks in bruchs membrane; they occur in 5% of high myopes. CNVMS can develop in associate with these, resulting in metamorphopsia and severe vision loss. This may be one of the earliest findings in pathological myopia

29
Q

Most patients with ERMS have an associated

A

PVD

30
Q

Risk factors for ERMS

A 
PVD
Retinal breaks
Cataract or other intraocular surgeries 
Trauma
Intraocular inflammation
31
Q

Cause of ERM

A

Glial cell proliferation on the ILM of the retina, vitreous traction can result in residual glial cells from the posterior hyaloid membrane of the vitreous on the ILM, or can cause small pores to develop in the ILM; this allows intraretinal glial cells to gain access to the anterior side of the ILM for proliferation

32
Q

Cause of histo

A

Fungus histo capsulatum

33
Q

What causes CSCR

A

Idiopathic dysfunction of the RPE

34
Q

Cause of laquer cracks

A

Due to thinning and atrophy of the choroids due to increased axial length in patietns with pathological myopia

35
Q

Cause of ARMD

A

Progressive degeneration of the RPE, BRuchs membrane and the choriocapillaris due to the accumulation of drusen within bruchs membrane

36
Q

Treatment of ERMS

A

PPV with membrane peel
-with a VA of 20/50 or worse, or pts with intolerable metamorphopsia complaints secondary to an ERM may benefit; overall prognosis is good after sx, as 75% of pts experience an improvement in symptoms and VA. If the patients vision is better than 20/50, the fain in visual acuity after surgery is relatively insignificant.

37
Q

Treatment for CSCR

A

Most improve without treatment in 1-3 months. 94% of pts will regain >20/30 vision, and 66% of patietns will achieve 20/20 vision. After resolution of the condition, pts often have permanent residual RPE changes within the macula, recurrences occur in up to 40-50% of cases. Although most cases of CSR are observed, laser photocoagulation should be considered in the following cases

  • persistent RD after 4 months
  • previous CSR episode that results in permanent vision reduction
  • patient demand for more immediate visual recovery

Can also use CAIs and PDT

38
Q

Laser photocoagulation and CSCR

A

Can expedite the recovery process, but does not result in better final VA

39
Q

Treatment of dry and wet AMD

A
  • cessation of smoking (#1 risk factor)
  • daily monitoring with amsler grid
  • consideration of high dose antioxidants for pts iwth cat 4 AMD
40
Q

cat 1 AREDS

A

No ARMD (<5 small drusen), BCVA 20/32 or better in both eyes

41
Q

Cat 2 AREDS

A

Borderline to mild ARMD (multiple small drusen/single intermediate drusen/pigment abnormalities) and BCVA 20/32 or better in both eyes

42
Q

Cat 3 AREDS

A

Moderate ARMS with a least 1 large drusen, extensive intermediate drusen, or non central GA, BCVA 20/32 or better in 1 eye

43
Q

Cat 4 AREDs

A

No signs of advanced ARMD in the study eye with BCVA 20/32 or better, with advanced ARMD (central GA or CNVM) or BCVA worse than 20/32 that could be attributed to ARMD in the fellow eye

44
Q

What category of ARMD did AREDs 1 determine would benefit from high dose antioxidants

A 
Cat 4 (10 year results)
(5 year results say cat 3 and 4)
45
Q

What is relative risk reduction

A

100-((incidence of the outcome in the treatment group)/(incidence of the outcome in the control group))

46
Q

What is absolute risk reduction

A

(Incidence of the outcome in the control group)-(incidence of the outcome in the treatment group)

More meaningful stat as it takes into account the absolute incidence of the disease

47
Q

Original AREDs formula

A 
15mg beta carotene
500mg VitC
400IU Vit E
80mg Zinc
2mg copper
48
Q

AREDs 2

A

Lutein and xeazanthine weren’t that beneficial
Omega 3 FAs proven ineffective
Eliminated beta carotene and reduced zinc (had no effect on positive outcomes)
Give low dose antioxidants for cat 1 and 2, and with strong famHx
Low vision rehab for pts with functional vision loss
Smokers should use formulation with lutein in place of beta carotene

49
Q

Subfoveal CNVM

A

Located directly underneath the FAZ

50
Q

Juxtafovea lCNVM

A

1-199 microns from the center of the FAZ or in extrafoveal CNVM that has leaked fluid within 1-100um of the FAZ

51
Q

Extrafoveal CNVM

A

200-250um from the center of the FAZ

52
Q

How wide is FAZ

A

500um in diameter

53
Q

Classic CNVMs

A

Well defined membrane that fills with dye during the early phase of FA

54
Q

Occult CNVM

A

Poorly defined membrane with less intense and late appearing FA leakage

55
Q

Occult vs classic CNVM

A

Most patietns with ARMD have a CNVM that has a combination of both. The term “predominantly classic” means that over 50% of the entire leasing is composed of a classic CNVM

56
Q

Treatment for wet ARMD

A

Thermal laser photocoagulation
Verteporfin
AntiVEGF

57
Q

Thermal laser photocoagulation for ARMD

A

Used to treat extrafoveal and juxtafoveal CNVMs. It is no longer used to treat subfoveal CNVMs because the laser damages the retina, resulting in a permanent scar and blind spot. Patients should be carefully monitored after treatment as recurrences are common

58
Q

Verteprofin for ARMD

A

PDT, used for subfoveal CNVMs. Effective at treating subfoveal, predominantly classic CNVMs, no longer DOC because of AntiVEGF

  • injected IV and has a predilection for lipoproteins concentrated in the areas of proliferating capillaries. PDT is used to activate the molecules and destroy the CNVM
  • slows the rate of progression, but does not improve the visual outcome in patients with wet AMD
  • 3m intervals are required due the high recurrence of CNVMs. Patients should also be advised to avoid direct sun light or bright indoor light for at least 48 hours after treatment
59
Q

ANCHOR study

A

Compared PDT to lucentis for treatment of predominantly classic CNVMs in patients with wet AMD; more than 1/3 of pts on lucentis had improvement in vision of more than 15 EDTRS letters, compared to only 6% of patients who received PDT

60
Q

MARINA study

A

Effectiveness of lucentis injections for the treatment of minimally classic or occult CNVMs in patietns with wet AMD. Lucentis improved VA to 20/40 in more than 1/3 of patients at 2 years compared to sham injections; less than 5% of patients receiving lucentis suffered severe vision loss at 2 years compared to 23% of sham injections

61
Q

Why is eyelea different

A

High binding affinity,
Can be used every 2 months

More expensive

BOARDS2: Retina/vitreous (8 decks)

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