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AAO Retina > z EBOD > Flashcards

z EBOD Flashcards

1
Q

most common FA pattern in CSR

A

Expanding dot or “ink blot”. Smoke-stack only in 10%

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2
Q

ICGA in CSR

A

vascular abnormalities of the choroid, including filling delays of the choroidal arteries and the choriocapillaris, venous dilation, vascular hyperpermeability and characteristic multifocal patchy areas of choroidal hypercyanescence that appear in early phases and slowly extend as the study progresses. A washout pattern is often seen as well.

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3
Q

FFA in CSR

A

hypoautofluorescence corresponding to sensory retinal detachment, and mottled pigmentation in the affected area of the RPE. There is also hyperautofluorescence on the outer edge of the elevated retina

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4
Q

The outer retina is supplied by the

A

ciliary arteries through the choriocapillaris

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5
Q

Inner retina receives its blood supply from the

A

central retinal artery

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6
Q

CRAO - OCT

A

normal macular profile with diffuse hyperreflectivity and loss of definition of the retinal inner layers

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7
Q

gyrate - gene, metabolism

A

OAT, deficient activity of ornithine aminotransferase, increased levels of ornithine

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8
Q

Purtscher’s retinopathy - signs

A

cotton-wool exudates and flame-shaped retinal haemorrhages around the optic nerve head, which are associated with a severe loss of vision

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9
Q

Purtscher-like retinopathy

A

acute pancreatitis, childbirth, kidney failure and as a presenting sign of systemic lupus erythematosus

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10
Q

Immune recovery uveitis

A

inactive CMV retinitis in the previously affected eye that occurs after CD4 recovery with HAART. Clinically, onset is insidious with vitritis and anterior uveitis. If left untreated, it follows a progressive course.

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11
Q

Lacquer cracks

A

breaks in Bruch’s membrane

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12
Q

myopic macular degeneration - men, women or equal

A

women

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13
Q

Sympathetic ophthalmia - time

A

65% of cases present between two weeks and two months after the trauma and 90% within the first year

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14
Q

Sympathetic ophthalmia - signs

A

may or may not be granulomatous, and vitritis; it may be associated with macular oedema, papillitis, choroiditis with exudative retinal detachment and Dalen–Fuchs nodules. The course is progressive and implacable with exacerbations of the disease that may lead to a poor visual prognosis

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15
Q

Degenerative retinoschisis - quadrant

A

inferotemporal

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16
Q

Paving-stone degeneration - where

A

quadrants inferior and anterior to the equator

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17
Q

Lattice degeneration - what is it

A

abnormality in the vitreoretinal interface

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18
Q

X-linked retinitis pigmentosa

A

least common form of RP but the most severe

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19
Q

XLRP carriers

A

tapetal-like reflex, changes in the retinal pigment epithelium and variable visual function. Optic disc pallor is another common clinical sign. slight reduction or delay in b-wave responses

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20
Q

Do anti-VEGF injections increase risk of cataract

A

No. Steroids do

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21
Q

anti-VEGF - complications

A

increase in IOP, retinal detachment (0.04-0.9%), intraocular haemorrhage (0.02-1.3%), uveitis/iritis (0.14-6.3%) and, less frequently, ocular hypotension, optic atrophy, traumatic cataract and retinal vascular obstruction

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22
Q

anti-VEGF in vitrectomized eyes

A

the drug’s half-life is reduced

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23
Q

choroidal rupture - where

A

post-equatorial retina

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24
Q

MacTel 2 - signs

A

blunting of the foveal reflex, crystalline deposits on the retinal surface, capillary ectasia, progression to pigment hyperplasia and foveal atrophy

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25
Q

MacTel 2 - OCTA

A

changes in the deep capillary plexus

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26
Q

indications for pneumatic retinopexy

A

certainty that all the breaks have been identified, breaks confined to the superior 8 clock hours, single or multiple breaks separated by no more than 1-2 clock hours, absence of grade C or D PVR, patient who is able to hold a specific posture and no media opacity. It can be performed in both phakic and pseudophakic patients and in vitrectomized or non-vitrectomized eyes. After retinal apposition (the fluid is usually reabsorbed in 6-8 hours), laser retinopexy or cryopexy can be performed

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27
Q

indications for PPV

A

pseudophakic patients, especially if it is not possible to locate the breaks, if the breaks are posterior, in giant tears, re-detachments, in cases of advanced proliferative vitreoretinopathy or when there is media opacity

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28
Q

demage in commotio

A

outer retina

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29
Q

Sea fan neovascularization

A

sickle cell retinopathy, thrombocytosis, sarcoidosis, retinitis pigmentosa, Eales

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30
Q

hemoglobin disease - most common proliferative in which

A

SC and S-thal

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31
Q

Signs of sickle cell

A

comma sign, sea fan (neovasc), salmon patches (intraretinal hemorrhages), black sunburst (chorioretinal scars), angioid streaks

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32
Q

hemorrhages in all retinal layers

A

retinal macroaneurysm

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33
Q

radiation retinopathy - how many gray

A

30-35 grays

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34
Q

OIS syndrome - 5 year mortality

A

40-50%

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35
Q

saccular aneurysms (light-bulb dilations), intraretinal cholesterol depositions

A

Coats

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36
Q

temporal to fovea

A

MacTel 2

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37
Q

MacTel types nad prognosis

A

1 good, 2, 3 guarded

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38
Q

MacTel 3

A

bi, later, capillary obliteration

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39
Q

The Diabetic Retinopathy Clinical Research Network (DRCR.net) protocol I study

A

intravitreal anti-VEGF therapy (Ranibizumab) achieves better visual acuity than focal laser for central macular oedema

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40
Q

T protocol

A

superiority of Aflibercept over Bevacizumab and Ranibizumab in improving ETDRS visual acuity in the treatment of diabetic macular oedema

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41
Q

most common CNV type

A

Type 1

42
Q

sign of CNV 1

A

serous or fibrovascular RPE detachment, subretinal fluid

43
Q

sign of CNV 2

A

grey-green lesion

44
Q

sign of CNV 3

A

small, reddish areas, with associated intraretinal or subretinal fluid

45
Q

a-wave generated by

A

the photoreceptors

46
Q

b-wave originates

A

in the bipolar cell layer

47
Q

The c-wave originates

A

from the RPE

48
Q

multiple evanescent white dot syndrome - fundoscopy

A

Multiple white dots (100-200 microns) are seen on the fundus of the eye at the level of the RPE or deep retina, typically perifoveal. These dots are transient and sometimes may not even be visible, but they leave a granular appearance on the macula

49
Q

multiple evanescent white dot syndrome - ERG

A

reduction in the a-wave

50
Q

multiple evanescent white dot syndrome - OCT

A

disruption of the ellipsoid zone

51
Q

Haemangiomas - USG

A

acoustically solid lesion (high internal reflectivity) with a well-defined anterior surface

52
Q

Haemangiomas - FA

A

very early filling of the large vessels with mottled hyperfluorescence in the early phase and diffuse intense late hyperfluorescence

53
Q

Most breaks (60%) are located in

A

superior temporal quadrant. Around 50% of RRDs have more than one break, often separated by less than 90º.

54
Q

indicative of chronic RRD

A

Retinal thinning, a demarcation line, subretinal precipitates and macrophages

55
Q

After blunt trauma - where are the breaks

A

often multiple breaks, predominantly in the inferotemporal and superonasal quadrants

56
Q

Choroidal haemangioma - most helpful imaging test and whats shows

A

Indocyanine green angiography. hypercyanescence observed in early stages and hypocyanescence “washout” in late stages

57
Q

Circumscribed Choroidal haemangioma - treatment

A

photodynamic therapy

58
Q

Diffuse Choroidal haemangioma - treatment

A

complicated and can consist of radiotherapy, several sessions of photodynamic therapy or oral propranolol

59
Q

Sclerochoroidal calcifications - manifest as

A

accumulations of calcium with choroidal compression and alterations to the retinal pigment epithelium. The calcifications can sometimes be observed within the lesion. The overlaying retina and vitreous tend to be normal

60
Q

Sclerochoroidal calcifications - study for

A

Calcium metabolism disorders such as hyperparathyroidism, parathyroid adenomas, and the Gitelman and Bartter syndromes

61
Q

Primary vitreoretinal lymphoma - uni or bi

A

bi

62
Q

Primary uveal lymphoma - uni or bi

A

uni

63
Q

inflammation in the outer retina that leads to punch-out lesions

A

multifocal choroiditis (MFC) and punctate inner choroidopathy (PIC)

64
Q

AZOOR - perimetry

A

increase in the blind spot

65
Q

AZOOR - fundus

A

appears normal or manifests mild vitritis, but as the disease progresses patients develop RPE atrophy, pigment deposits and arteriolar attenuation

66
Q

APMPPE - where and what are the lesions

A

Lesions are generally located in the posterior pole and measure less than the papillary diameter

67
Q

Sorsby pseudoinflammatory fundus dystrophy - genetics

A

autosomal dominant maculopathy caused by a mutation in the gene that codes for tissue inhibitor of metalloproteinase-3 (TIMP3)

68
Q

Sorsby pseudoinflammatory fundus dystrophy - age

A

third to fifth decades

69
Q

Sorsby pseudoinflammatory fundus dystrophy - prognosis

A

subsequently progresses to choroidal neovascularisation, haemorrhagic maculopathy and even disciform fibrosis and atrophy which can extend beyond the macula

70
Q

cuticular drusen - what and where are on OCT

A

clustered, uniform and yellowish deposits located below the RPE

71
Q

FA - “starry night” appearance

A

cuticular drusen

72
Q

cuticular drusen - FA

A

“starry night” appearance

73
Q

cuticular drusen - prognosis

A

can develop acquired vitelliform lesions, or large drusen, which eventually constitute a risk factor for further progression to choroidal neovascularisation

74
Q

cuticular drusen - FAF

A

hypoautofluorescent appearance with a hyperautofluorescent halo

75
Q

cuticular drusen - other name

A

Basal Laminar Drusen

76
Q

drusen - where on OCT

A

below the RPE

77
Q

Reticular Drusen - where

A

superficial to the RPE. more commonly found at the superotemporal quadrant of the macula. more prominent in blue light. very difficult to appreciate in fluorescein angiogram

78
Q

X-linked retinoschisis - FA

A

no leakage

79
Q

Fabry disease - genetics

A

X-linked lysosomal disorder caused by a mutation in the GLA gene which results in insufficient α-galactosidase A levels

80
Q

Fabry disease - ocular manifestations

A

Retinal vascular tortuosity can be discerned in 77% of males and 19% of females. Other ocular manifestations include tortuosity of the bulbar conjunctiva, cornea verticillata and posterior lens opacity

81
Q

Fabry disease - systemic manifestations

A

left ventricular dysfunction, early stroke and severe kidney failure

82
Q

CNV in pathological myopia

A

Myopic neovascularisation is type 2, so it develops above the RPE

83
Q

RAP - which layer

A

originates in the retina, close to the outer plexiform layer. It tends to progress towards the subretinal space (IIA) and continues across the RPE, growing into the sub-RPE space (IIB)

84
Q

RAP - where in fundus

A

Initially it respects the peripapillary location and the foveal avascular zone

85
Q

Polypoidal choroidal vasculopathy - presentation

A

The usual symptoms are serohaemorrhagic detachments and lipid exudation

86
Q

Aflibercept - blocks what

A

VEGF-A, VEGF-B and PlGF

87
Q

Aflibercept - Mechanism of Action

A

Aflibercept is a 115 kDa fusion protein. It consists of an IgG backbone fused to extracellular VEGF receptor sequences of the human VEGFR1 and VEGFR2.[2] [3] As a soluble decoy receptor, it binds VEGF-A with a greater affinity than its natural receptors

88
Q

Osteoma - Visual loss is the result of

A

atrophy of the retinal pigment epithelium covering a decalcified osteoma; serous retinal detachment over the osteoma from decompensated retinal pigment epithelium; and most commonly from choroidal neovascularisation

89
Q

Retinal capillary haemangioma - evolution

A

At first, the tumour may not be clinically visible and may only be seen on FA. As it increases in size, the vessels become more dilated and tortuous

90
Q

Retinal capillary haemangioma - complications

A

This tumour can produce subretinal fluid, subretinal and intraretinal exudation and vitreoretinal fibrosis. The exudation has a tendency to accumulate selectively in the macular area as a macular star

91
Q

Retinal capillary haemangioma - uni or multifocal

A

uni or multifocal

92
Q

Retinal capillary haemangioma - in whom diagnosed

A

It is usually diagnosed in children and young adults

93
Q

Vasoproliferative retinal tumour - where in fundus

A

located pre-equatorially and inferotemporally

94
Q

Vasoproliferative retinal tumour - leads to what

A

retinal exudates, macular oedema and epiretinal membranes

95
Q

Vasoproliferative retinal tumour - causes

A

Approximately 75% of cases are idiopathic and 25% are secondary to other ocular diseases, such as retinitis pigmentosa, uveitis, retinal detachment, congenital toxoplasmosis and Coats disease

96
Q

Vasoproliferative retinal tumour - age

A

detected between the ages of 40 and 60 years

97
Q

risk factors for growth of choroidal nevi into melanoma - Thickness

A

tumour thickness > 2 mm

98
Q

Stargardt disease - fundus

A

often normal early. Later, typical fundus manifestations appear, including pigmented lesions, frank macular atrophy, bull’s eye maculopathy and fundus flecks. atrophic macular changes surrounded by diffuse pisciform flecks

99
Q

Stargardt disease - FA

A

dark choroid with hyperfluorescent pisciform flecks

100
Q

Stargardt disease - FAF

A

hyperautofluorescence in areas of lipofuscin accumulation and hypoautofluorescence in areas of RPE atrophy

101
Q

Pseudoxanthoma Elasticum (PXE) - gene

A

ABCC6 gene

102
Q

multifocal uveitis - type of CNV

A

Type 2

AAO Retina (4 decks)

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