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Retina and Vitreous > ARMD, CNV, and Retinal Vascular Disease Associated with Diabetes and Cardiovascular Disease and Other Causes > Flashcards

ARMD, CNV, and Retinal Vascular Disease Associated with Diabetes and Cardiovascular Disease and Other Causes Flashcards

1
Q

leading cause of blindness in the developed world of people over 50

A

AMD

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2
Q

risk factors for AMD

A

age, female sex, HTN, HLD, CVD, fam hx, smoking, hyperopia, light iris color, caucasian

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3
Q

2 major susceptibility genes for AMD

A

CFH and ARMS2

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4
Q

where are basal laminar and basal linear deposits located

A

basal laminar: between RPE plasma membrane and basement membrane

basal linear: within the inner collagenous zone of Bruch membrane

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5
Q

size categories of drusen

A

small: < 64 microns
intermediate: 64-124 microns
large: >124 microns

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6
Q

at which stage of dry AMD is there a significant increase in risk for progression to geographic atrophy (stage 4 )?

A

stage 3, definied by many intermediate drusen or one large drusen, has 18% chance on developing into stage 4 (only 1.3% for stage 2)

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7
Q

which type of drusen incur a greater risk to progress to CNV

A

confluent, and soft (which correspond to basal linear deposits), as opposed to hard

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8
Q

FA appearance of different types of drusen

A

hard: hyperfluoresce early (window defect)

soft and/or confluent: slowly and homegenously increase fluorescence (pooling defect in PED)

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9
Q

T or F:

  1. geographic atrophy from AMD tends to spare the fovea until late in disease
  2. reticular pseudodrusen carry a greater risk for geographic atrophy and CNV than soft or hard drusen
A

both true

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10
Q

Initial AREDS formula? AREDS 2 formula? Why changes? Indications?

A

AREDS: zinc, copper, beta-carotene, vitamins C and E
AREDS2: zinc, copper, lutein, zeaxanthin, vitamins C and E

-beta-carotene a/w increased lung cancer in smokers

Indicated for intermediate or stage 3 dry AMD (defined by a least 1 large druse or nonsubfoveal GA)

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11
Q

Three types of CNV with OCT appearance

A

I: Originates in choriocapillaris, grows through defect in Bruch’s membrane. PED on OCT
II: CNV occupies subneurosensory compartment between photoreceptors and RPE (less common in AMD). hyperreflective subretinal band with SRF and/or IRF
III: Intraretinal NV that grows downward toward RPE. Hyperreflecive intraretinal focus

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12
Q

FA patterns of CNV

A
  • classic: well-defined early hyper + progressive leakage
  • occult:
  • -type I: fibrovascular (progressive stippling) or serous PED (rapid pooling w/ hot spot)
  • -late leakage from undetermined source
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13
Q

multiple, recurrent serosanguinous RPE detachments with vitreous hemorrhage. network of polyps and feeder vessels like a “string of pearls.” Predilection for peripapillary region

A

polypoidal choroidal vasculopathy.

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14
Q

What did the following studies conclude:
MARINA
ANCHOR
PIER and EXCITE

A

MARINA: ranibizumab > placebo for minimally classic CNV
ANCHOR: ranibizumab > PDT for for classic CNV
PIER and EXCITE: monthly treatment with ranibizumab > quarterly treatment

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15
Q

mechanism of aflibercept v ranibizumab

A

aflibercept: soluble VEGF receptor (VEGF trap)
ranibizumab: humanized antibody fragment that binds VEGF

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16
Q

anti-VEGF v anti-VEGF + PDT

A

adding PDT decreases total injections but lead to worse visual oucomes

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17
Q

DDx for angioid streaks

A 
"PEPSI-B"
Psedoxanthoma elasticum (PXE, aka Gronbald-Stranberg syndrome), Ehlers-Danlos, Paget's disease of the bone, sickle cell, idiopathic, beta-thalassemia
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18
Q

what do angioid streaks represent, and what is vision loss from them usually related to

A

breaks in Bruch’s membrane. CNV, or submacular hemorrhage from trauma (high risk for choroidal rupture)

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19
Q

plucked chicken skin, angioid streaks, peau d/orange RPE. diagnosis and treatment? Inheritance and gene defect?

A

PXE (Gronbald-Stranberg syndrome). safety glasses (high risk of choroidal rupture after minor blunt trauma). anti-VEGF for CNV as needed. AR, ABCC6

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20
Q

definitions of high myopia and pathologic myopia

A

high: spherical equivalent of -6.00 or less; axial length of 26.5 or more
pathologic: spherical equivalent of -8.00 or less; axial length of of 32.5 or more

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21
Q

spontaneous breaks in Bruch’s membrane in -7.00 myope? small dark spots of RPE hyperplasia in same patient?

A

lacquer cracks

Forster-Fuchs spots (represent regressed CNV)

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22
Q

first line treatment for CNV in myopia

A

anti-VEGF

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23
Q

percentage of type I and II diabetics who get NPDR and PDR at 20 years

A

Type I: 99% NPDR, 50% PDR

Type II: 60% NPDR, 25% PDR

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24
Q

management of high risk PDR in pregnancy?

A

PDT

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25
criteria for CSME
1. retinal thickening located within 500 um of fovea 2. hard exudates located within 500 um of the fovea with adjacent retinal thickening 3. zone of thickening larger than 1 disc diameter if located within 1 disc diameter of the fovea
26
describe the findings of ETDRS
- focal photocoagulation indicated for DME - early scatter photocoagulation indicated for severe NPDR but not helpful in mild or moderate NPDR - Aspirin had no effect on NPDR
27
patient with severe NPDR with CSME as well as visually significant cataracts. steps in management?
treat DME before performing scatter photocoagulation. remove cataracts after laser, as long as view is clear enough to perform laser first. use preoperative anti-VEGF or perioperative steroids injections to help prevent post-op DME.
28
criteria for severe and very severe NPDR
Any 1 of the following for severe, any 2 for very severe: 1. severe intraretinal hemorrhages and MAs in all 4 quadrants 2. venous beading in 2 or more quadrants 3. IRMA in 1 or more quadrants
29
chance of progression from severe NPDR to PDR in 1 year? for very severe NPDR?
15% | 45%
30
initial treatment of severe NPDR
PRP
31
criteria for high-risk PDR?
Any one of the following: - mild NVD with vit heme - moderate to severe NVD (1/4-1/3 disc area) +/- vit heme - moderate NVE (1/2 disc area) with vit heme OR at least 3 of the following: - vitreous or preretinal heme - new vessels - new vessels located on or near the disc - moderate to severe extent of new vessels
32
significant adverse effect of anti-VEGF for PDR?
contracture of fibrovascular membrane causing tractional RD
33
mainstay of treatment for PDR?
PRP
34
indications for PPV in diabetic retinopathy
- nonclearing vitreous hemorrhage - tractional RD involving or threatening the macula - diffuse DME associated with posterior hyaloid traction - combined tractional and rhegmatogenous RD - significant recurrent vit heme despite PRP - secondary glaucoma - anterior segment NV with media opacities - dense premacular subhyaloid heme
35
management for tractional RD?
observe if macula not involved. prompt vitrectomy when macula is affected
36
screening recommendations for diabetics
Type I: 5 years after diagnosis, then annually Type II: at diagnosis and continue annually Type I or II w/ prengancy: soon after conception or in first trimester
37
follow up intervals for diabetic retinopathy
``` none or mild NPDR: 12 months any stage with ME: 2-6 months any stage w/ CSME: 1 month moderate NPDR w/o ME: 6 months severe NPDR w/o ME: 4 months PDR w/o ME: 4 months inactive/involuted PDR w/o ME: 6-12 months ```
38
In DRVS (Diabetic Retinopathy Treatment Study), what subclass of patients benefited form early vitrectomy?
Type I diabetics with severe vit heme (although, with improved vitreoretinal surgical techniques including use of endolaser, most surgeons will also perform vitrectomy on type II diabetics with severe vit heme)
39
grades of hypertensive retinopathy
0: no changes 1: mild arterial narrowing 2: obvious arterial narrowing 3. grade 2 + retinal heme or exudates 4. grade 3 + disc edema
40
signs of hypertensive choroidopathy
Elschnig spots: lobular areas of chronic choroidal nonperfusion; appear as hyperpigmented spot surrounded by margins of hypopigmentation Siegrist streaks: linear aggregations of Elschnig spots:
41
chronic complications of retinal vein occlusions
neovascularization, anterior segment ischemia +/- NVI +/- NVG, optociliary shunt vessels, retinal microaneurysms and telangiectasias
42
location of BRVO? most common quadrant? | location of CRVO?
- BRVO at AV crossing (vein compressed by artery); most common superotemporal (and nasal is rare) - CRVO at level of lamina cribrosa
43
risk factors for BRVO v CRVO
BRVO: age, HTN, glaucoma, smoking (NOT diabetes), BMI CRVO: age, HTN, glaucoma, HLD, diabetes, OCPs, diuretics, hypercoagulable states (NOT BMI)
44
What is extensive retinal ischemia as determined by the Branch Retinal Vein Occlusion Study, and what risk factors does this entail?
ischemia > 5 disc areas | neovascularization and vit heme
45
describe the different causes of vision loss in diabetic retinopathy
- capillary leakage: CME - capillary occlusion: macular ischemia - sequelae of neovascularization (glaucoma, tractional RD, vit heme)
46
criteria for severe CRVO
> 10 disc areas or retinal capillary nonperfusion on FA
47
most important risk factor for NVI from CRVO?
poor vision acuity at onset
48
treatment for CRVO and BRVO
treat macular edema, and possibly for for ischemia > 5 disc areas. anti-VEGF probably first line. can also use intraocular steroids, macular laser (only for BRVO). PRP indicated for at least 2 clock hours of NVI systemic anticoagulation is NOT indicated for treatment or prevention of CRVO
49
symptoms to differentiate CRVO from ocular ischemic syndrome (OIS)
OIS usually slowly progressive from hypoperfusion. CRVO usually acute
50
mechanism of deceased IOP in ocular ischemic syndrome?
impaired aqueous production from ciliary body ischemia
51
ophthalmodynamometer difference between CRVO and ocular ischemic syndrome?
high retinal artery pressure in CRVO, low pressure in OIS
52
ERG appearance in ocular ischemic syndrome?
global amplitude depression not limited to inner segments (in contrast to negative ERG of CRAO or CRVO)
53
most common etiology of ocular ischemic syndrome
carotid atherosclerosis
54
approximate degree of carotid stenosis necessary to cause ocular ischemic syndrome
90%
55
5 year mortality rate of ocular ischemic syndrome?
40%
56
most definitive treatment of ocular ischemic syndrome? additional treatments?
CEA with stenting is most definitive. PRP can lead to regression of NVI in 2/3 of cases. Anti-VEGF and steroids have not been investigated. may need to manage IOP after laser, as ciliary body reperfusion can lead to ocular hypertension
57
most common cause of cotton wool spot
diabetic retinopathy
58
percentage of people with a cilioretinal artery
20-23%
59
irreversible damage to the retina occurs after ____ minutes/hours of infarction
90 minutes
60
percentage of CRAO 2/2 GCA
1-2%
61
treatment of CRAO
nothing with good evidence, but IOP lowering meds and ocular massage are not unreasonable.
62
44 yo F develops complete monocular vision loss after a facial injection for cosmetic purposes
ophthalmic artery occlusion from retrograde flow of facial filler
63
risk factors for retinal macroaneurysms
HTN, previous retinal vascular occlusion
64
first and second highest rates of proliferative retinopathy in the hemoglobinaopthies
hemoglobin SC (33%), then SThal (14%)
65
findings in nonproliferative sickle cell retinopathy
salmon patch hemorrhages, sunburst lesions (RPE hyperplasia, refractile spots (old, resorbed hemorrhages), angioid streaks, hyphema, conjunctival vessel thrombosis and dilatation (comma sign)
66
differences between PDR and PSR
PSR neovacularizations are located more peripherally and often autoinfarct, leading to a white sea fan appearane
67
contraindicated medications in patients with sickle cell
carbonic anyhdrase inhibitors (lead to acidosis which worsens sickling), and alpha agonists (vasoconstriction leads to thrombosis)
68
where do retinal tears generally occur in proliferative sickle cell retinopathy?
at the base of seas fans, and they are often precipitated by photocoagulation
69
primary occlusive retinopathy, affecting mostly veins, and usually in males
Eales disease (may also be associated with tuberculin hypersensitivity)
70
multiple BRAOs, hearing loss, and cognitive delay
Susac syndrome
71
retinal vasculitis, multiple macroaneurysms, neuroretinitis, and peripheral capillary nonperfusion
IRVAN
72
other name for post-surgical CME
Irvine-Gass Syndrome
73
medication that causes CME without leakage on FA?
niacin (nicotinic acid)
74
treatment for CME
topical NSAIDs and topical steroids. periocular steroids for refractory cases. systemic acetazolamide in chronic cases and in RP.
75
findings in Coats disease
peripheral retinal telangiectasias, lipoidal exudates, exudative retinal detachments
76
demographics of Coats disease
usually unilateral. 85% male
77
treatment of Coats disease
retinal photocoagulation and cryotherapy. surgery as needed for RD
78
describe the three types of parafoveal telangiectasias
Type 1 aka Leber miliary aneurysm: unilateral, congenital or acquired, occurs in males, like a macular variant of Coats Type II: bilateral, no sex predilection, a/w abnormal glucose tolerance Type III: bilateral; progressive vision loss from capillary obliteration
79
treatment for parafoveal telangiectasias?
type I responds well to photocoagulation, types II and III do not (leaky vessels not the primary problem with types II and III)
80
chromosome and inheritance of von Hippel-Lindau
chromosome 3, AD
81
systemic findings in patient with red-orange retinal lesion fed by dilated, tortuous artery and drained by engorged vein and with associated exudative maculopathy
VHL; renal cell carcinoma, cerebellar hemangioblastoma, meningioma, pheochromocytoma, multiple organ cysts
82
treatment of retinal hemangioblastomas in VHL
photocoagulation, PDT, or cryo directly to lesion
83
ipsilateral AVMs in retina, brain, face, mandible: diagnosis, pathology, and common presentation
Wyburn-Mason syndrome; blood vessels without an intervening capillary bed (racemose angioma); often present with unexpected hemorrhage during dental extractions (although retinal lesions usually are asymptomatic)
84
grapelike cluster of thin walled angiomatous lesion in inner retinal or optic nerve: diagnosis and FA appearance?
retinal cavernous hemangioma; lesions fill slowly on FA and dye pools superiorly within the lesion
85
appearance of radiation retinopathy? treatment?
looks and acts like diabetic retinopathy. treat with focal laser for edema or PRP for areas of ischemia and neovascularization
86
typical time course of presentation of radiation retinopathy? what amounts of radiation are associated with this disease process?
months to years after therapy; about 18 months post-radiation for external beam and shorter for brachytherapy. exposure to doses of 30-35 Grays or more is generally enough to cause retinopathy.
87
classic finding in valsalva retinopathy
sub-ILM or subhyaloid hemorrhage +/- vit heme +/- subretinal heme
88
decreased vision in patient shortly after sustaining a crushing injury to thorax? retinal findings? mechanism?
Purtscher's retinopathy; many cotton wool spots, also edema and any type of hemorrhage, usually peripapillary. injury-induced compliment activation causes leukoembolization and vascular occlusion.
89
causes of Purtscher-like retinopathy
acute pancreatitis, amniotic fluid or fat embolism, systemic collagen vascular disease, childbirth
90
difference in retinal findings in fat embolism v Purtscher's?
hemorrhages in fat embolism are usually perimacular, and cotton wool spots are smaller and more peripheral
91
findings in Terson syndrome
vitreous heme and subhyaloid or sub-ILM heme occurring after abrupt intracranial hemorrhage

Retina and Vitreous (6 decks)

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