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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
Q

criteria for CSME

A
  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
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26
Q

describe the findings of ETDRS

A
  • 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
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27
Q

patient with severe NPDR with CSME as well as visually significant cataracts. steps in management?

A

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.

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28
Q

criteria for severe and very severe NPDR

A

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
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29
Q

chance of progression from severe NPDR to PDR in 1 year? for very severe NPDR?

A

15%

45%

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30
Q

initial treatment of severe NPDR

A

PRP

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31
Q

criteria for high-risk PDR?

A

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
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32
Q

significant adverse effect of anti-VEGF for PDR?

A

contracture of fibrovascular membrane causing tractional RD

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33
Q

mainstay of treatment for PDR?

A

PRP

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34
Q

indications for PPV in diabetic retinopathy

A
  • 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
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35
Q

management for tractional RD?

A

observe if macula not involved. prompt vitrectomy when macula is affected

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36
Q

screening recommendations for diabetics

A

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

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37
Q

follow up intervals for diabetic retinopathy

A 
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
Q

In DRVS (Diabetic Retinopathy Treatment Study), what subclass of patients benefited form early vitrectomy?

A

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
Q

grades of hypertensive retinopathy

A

0: no changes
1: mild arterial narrowing
2: obvious arterial narrowing
3. grade 2 + retinal heme or exudates
4. grade 3 + disc edema

40
Q

signs of hypertensive choroidopathy

A

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
Q

chronic complications of retinal vein occlusions

A

neovascularization, anterior segment ischemia +/- NVI +/- NVG, optociliary shunt vessels, retinal microaneurysms and telangiectasias

42
Q

location of BRVO? most common quadrant?

location of CRVO?

A
  • BRVO at AV crossing (vein compressed by artery); most common superotemporal (and nasal is rare)
  • CRVO at level of lamina cribrosa
43
Q

risk factors for BRVO v CRVO

A

BRVO: age, HTN, glaucoma, smoking (NOT diabetes), BMI
CRVO: age, HTN, glaucoma, HLD, diabetes, OCPs, diuretics, hypercoagulable states (NOT BMI)

44
Q

What is extensive retinal ischemia as determined by the Branch Retinal Vein Occlusion Study, and what risk factors does this entail?

A

ischemia > 5 disc areas

neovascularization and vit heme

45
Q

describe the different causes of vision loss in diabetic retinopathy

A
  • capillary leakage: CME
  • capillary occlusion: macular ischemia
  • sequelae of neovascularization (glaucoma, tractional RD, vit heme)
46
Q

criteria for severe CRVO

A

> 10 disc areas or retinal capillary nonperfusion on FA

47
Q

most important risk factor for NVI from CRVO?

A

poor vision acuity at onset

48
Q

treatment for CRVO and BRVO

A

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
Q

symptoms to differentiate CRVO from ocular ischemic syndrome (OIS)

A

OIS usually slowly progressive from hypoperfusion. CRVO usually acute

50
Q

mechanism of deceased IOP in ocular ischemic syndrome?

A

impaired aqueous production from ciliary body ischemia

51
Q

ophthalmodynamometer difference between CRVO and ocular ischemic syndrome?

A

high retinal artery pressure in CRVO, low pressure in OIS

52
Q

ERG appearance in ocular ischemic syndrome?

A

global amplitude depression not limited to inner segments (in contrast to negative ERG of CRAO or CRVO)

53
Q

most common etiology of ocular ischemic syndrome

A

carotid atherosclerosis

54
Q

approximate degree of carotid stenosis necessary to cause ocular ischemic syndrome

A

90%

55
Q

5 year mortality rate of ocular ischemic syndrome?

A

40%

56
Q

most definitive treatment of ocular ischemic syndrome? additional treatments?

A

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
Q

most common cause of cotton wool spot

A

diabetic retinopathy

58
Q

percentage of people with a cilioretinal artery

A

20-23%

59
Q

irreversible damage to the retina occurs after ____ minutes/hours of infarction

A

90 minutes

60
Q

percentage of CRAO 2/2 GCA

A

1-2%

61
Q

treatment of CRAO

A

nothing with good evidence, but IOP lowering meds and ocular massage are not unreasonable.

62
Q

44 yo F develops complete monocular vision loss after a facial injection for cosmetic purposes

A

ophthalmic artery occlusion from retrograde flow of facial filler

63
Q

risk factors for retinal macroaneurysms

A

HTN, previous retinal vascular occlusion

64
Q

first and second highest rates of proliferative retinopathy in the hemoglobinaopthies

A

hemoglobin SC (33%), then SThal (14%)

65
Q

findings in nonproliferative sickle cell retinopathy

A

salmon patch hemorrhages, sunburst lesions (RPE hyperplasia, refractile spots (old, resorbed hemorrhages), angioid streaks, hyphema, conjunctival vessel thrombosis and dilatation (comma sign)

66
Q

differences between PDR and PSR

A

PSR neovacularizations are located more peripherally and often autoinfarct, leading to a white sea fan appearane

67
Q

contraindicated medications in patients with sickle cell

A

carbonic anyhdrase inhibitors (lead to acidosis which worsens sickling), and alpha agonists (vasoconstriction leads to thrombosis)

68
Q

where do retinal tears generally occur in proliferative sickle cell retinopathy?

A

at the base of seas fans, and they are often precipitated by photocoagulation

69
Q

primary occlusive retinopathy, affecting mostly veins, and usually in males

A

Eales disease (may also be associated with tuberculin hypersensitivity)

70
Q

multiple BRAOs, hearing loss, and cognitive delay

A

Susac syndrome

71
Q

retinal vasculitis, multiple macroaneurysms, neuroretinitis, and peripheral capillary nonperfusion

A

IRVAN

72
Q

other name for post-surgical CME

A

Irvine-Gass Syndrome

73
Q

medication that causes CME without leakage on FA?

A

niacin (nicotinic acid)

74
Q

treatment for CME

A

topical NSAIDs and topical steroids. periocular steroids for refractory cases. systemic acetazolamide in chronic cases and in RP.

75
Q

findings in Coats disease

A

peripheral retinal telangiectasias, lipoidal exudates, exudative retinal detachments

76
Q

demographics of Coats disease

A

usually unilateral. 85% male

77
Q

treatment of Coats disease

A

retinal photocoagulation and cryotherapy. surgery as needed for RD

78
Q

describe the three types of parafoveal telangiectasias

A

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
Q

treatment for parafoveal telangiectasias?

A

type I responds well to photocoagulation, types II and III do not (leaky vessels not the primary problem with types II and III)

80
Q

chromosome and inheritance of von Hippel-Lindau

A

chromosome 3, AD

81
Q

systemic findings in patient with red-orange retinal lesion fed by dilated, tortuous artery and drained by engorged vein and with associated exudative maculopathy

A

VHL; renal cell carcinoma, cerebellar hemangioblastoma, meningioma, pheochromocytoma, multiple organ cysts

82
Q

treatment of retinal hemangioblastomas in VHL

A

photocoagulation, PDT, or cryo directly to lesion

83
Q

ipsilateral AVMs in retina, brain, face, mandible: diagnosis, pathology, and common presentation

A

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
Q

grapelike cluster of thin walled angiomatous lesion in inner retinal or optic nerve: diagnosis and FA appearance?

A

retinal cavernous hemangioma; lesions fill slowly on FA and dye pools superiorly within the lesion

85
Q

appearance of radiation retinopathy? treatment?

A

looks and acts like diabetic retinopathy. treat with focal laser for edema or PRP for areas of ischemia and neovascularization

86
Q

typical time course of presentation of radiation retinopathy? what amounts of radiation are associated with this disease process?

A

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
Q

classic finding in valsalva retinopathy

A

sub-ILM or subhyaloid hemorrhage +/- vit heme +/- subretinal heme

88
Q

decreased vision in patient shortly after sustaining a crushing injury to thorax? retinal findings? mechanism?

A

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
Q

causes of Purtscher-like retinopathy

A

acute pancreatitis, amniotic fluid or fat embolism, systemic collagen vascular disease, childbirth

90
Q

difference in retinal findings in fat embolism v Purtscher’s?

A

hemorrhages in fat embolism are usually perimacular, and cotton wool spots are smaller and more peripheral

91
Q

findings in Terson syndrome

A

vitreous heme and subhyaloid or sub-ILM heme occurring after abrupt intracranial hemorrhage

Retina and Vitreous (6 decks)

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