z EBOD Flashcards
most common FA pattern in CSR
Expanding dot or “ink blot”. Smoke-stack only in 10%
ICGA in CSR
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.
FFA in CSR
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
The outer retina is supplied by the
ciliary arteries through the choriocapillaris
Inner retina receives its blood supply from the
central retinal artery
CRAO - OCT
normal macular profile with diffuse hyperreflectivity and loss of definition of the retinal inner layers
gyrate - gene, metabolism
OAT, deficient activity of ornithine aminotransferase, increased levels of ornithine
Purtscher’s retinopathy - signs
cotton-wool exudates and flame-shaped retinal haemorrhages around the optic nerve head, which are associated with a severe loss of vision
Purtscher-like retinopathy
acute pancreatitis, childbirth, kidney failure and as a presenting sign of systemic lupus erythematosus
Immune recovery uveitis
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.
Lacquer cracks
breaks in Bruch’s membrane
myopic macular degeneration - men, women or equal
women
Sympathetic ophthalmia - time
65% of cases present between two weeks and two months after the trauma and 90% within the first year
Sympathetic ophthalmia - signs
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
Degenerative retinoschisis - quadrant
inferotemporal
Paving-stone degeneration - where
quadrants inferior and anterior to the equator
Lattice degeneration - what is it
abnormality in the vitreoretinal interface
X-linked retinitis pigmentosa
least common form of RP but the most severe
XLRP carriers
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
Do anti-VEGF injections increase risk of cataract
No. Steroids do
anti-VEGF - complications
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
anti-VEGF in vitrectomized eyes
the drug’s half-life is reduced
choroidal rupture - where
post-equatorial retina
MacTel 2 - signs
blunting of the foveal reflex, crystalline deposits on the retinal surface, capillary ectasia, progression to pigment hyperplasia and foveal atrophy
MacTel 2 - OCTA
changes in the deep capillary plexus
indications for pneumatic retinopexy
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
indications for PPV
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
demage in commotio
outer retina
Sea fan neovascularization
sickle cell retinopathy, thrombocytosis, sarcoidosis, retinitis pigmentosa, Eales
hemoglobin disease - most common proliferative in which
SC and S-thal
Signs of sickle cell
comma sign, sea fan (neovasc), salmon patches (intraretinal hemorrhages), black sunburst (chorioretinal scars), angioid streaks
hemorrhages in all retinal layers
retinal macroaneurysm
radiation retinopathy - how many gray
30-35 grays
OIS syndrome - 5 year mortality
40-50%
saccular aneurysms (light-bulb dilations), intraretinal cholesterol depositions
Coats
temporal to fovea
MacTel 2
MacTel types nad prognosis
1 good, 2, 3 guarded
MacTel 3
bi, later, capillary obliteration
The Diabetic Retinopathy Clinical Research Network (DRCR.net) protocol I study
intravitreal anti-VEGF therapy (Ranibizumab) achieves better visual acuity than focal laser for central macular oedema
T protocol
superiority of Aflibercept over Bevacizumab and Ranibizumab in improving ETDRS visual acuity in the treatment of diabetic macular oedema
most common CNV type
Type 1
sign of CNV 1
serous or fibrovascular RPE detachment, subretinal fluid
sign of CNV 2
grey-green lesion
sign of CNV 3
small, reddish areas, with associated intraretinal or subretinal fluid
a-wave generated by
the photoreceptors
b-wave originates
in the bipolar cell layer
The c-wave originates
from the RPE
multiple evanescent white dot syndrome - fundoscopy
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
multiple evanescent white dot syndrome - ERG
reduction in the a-wave
multiple evanescent white dot syndrome - OCT
disruption of the ellipsoid zone
Haemangiomas - USG
acoustically solid lesion (high internal reflectivity) with a well-defined anterior surface
Haemangiomas - FA
very early filling of the large vessels with mottled hyperfluorescence in the early phase and diffuse intense late hyperfluorescence
Most breaks (60%) are located in
superior temporal quadrant. Around 50% of RRDs have more than one break, often separated by less than 90º.
indicative of chronic RRD
Retinal thinning, a demarcation line, subretinal precipitates and macrophages
After blunt trauma - where are the breaks
often multiple breaks, predominantly in the inferotemporal and superonasal quadrants
Choroidal haemangioma - most helpful imaging test and whats shows
Indocyanine green angiography. hypercyanescence observed in early stages and hypocyanescence “washout” in late stages
Circumscribed Choroidal haemangioma - treatment
photodynamic therapy
Diffuse Choroidal haemangioma - treatment
complicated and can consist of radiotherapy, several sessions of photodynamic therapy or oral propranolol
Sclerochoroidal calcifications - manifest as
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
Sclerochoroidal calcifications - study for
Calcium metabolism disorders such as hyperparathyroidism, parathyroid adenomas, and the Gitelman and Bartter syndromes
Primary vitreoretinal lymphoma - uni or bi
bi
Primary uveal lymphoma - uni or bi
uni
inflammation in the outer retina that leads to punch-out lesions
multifocal choroiditis (MFC) and punctate inner choroidopathy (PIC)
AZOOR - perimetry
increase in the blind spot
AZOOR - fundus
appears normal or manifests mild vitritis, but as the disease progresses patients develop RPE atrophy, pigment deposits and arteriolar attenuation
APMPPE - where and what are the lesions
Lesions are generally located in the posterior pole and measure less than the papillary diameter
Sorsby pseudoinflammatory fundus dystrophy - genetics
autosomal dominant maculopathy caused by a mutation in the gene that codes for tissue inhibitor of metalloproteinase-3 (TIMP3)
Sorsby pseudoinflammatory fundus dystrophy - age
third to fifth decades
Sorsby pseudoinflammatory fundus dystrophy - prognosis
subsequently progresses to choroidal neovascularisation, haemorrhagic maculopathy and even disciform fibrosis and atrophy which can extend beyond the macula
cuticular drusen - what and where are on OCT
clustered, uniform and yellowish deposits located below the RPE
FA - “starry night” appearance
cuticular drusen
cuticular drusen - FA
“starry night” appearance
cuticular drusen - prognosis
can develop acquired vitelliform lesions, or large drusen, which eventually constitute a risk factor for further progression to choroidal neovascularisation
cuticular drusen - FAF
hypoautofluorescent appearance with a hyperautofluorescent halo
cuticular drusen - other name
Basal Laminar Drusen
drusen - where on OCT
below the RPE
Reticular Drusen - where
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
X-linked retinoschisis - FA
no leakage
Fabry disease - genetics
X-linked lysosomal disorder caused by a mutation in the GLA gene which results in insufficient α-galactosidase A levels
Fabry disease - ocular manifestations
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
Fabry disease - systemic manifestations
left ventricular dysfunction, early stroke and severe kidney failure
CNV in pathological myopia
Myopic neovascularisation is type 2, so it develops above the RPE
RAP - which layer
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)
RAP - where in fundus
Initially it respects the peripapillary location and the foveal avascular zone
Polypoidal choroidal vasculopathy - presentation
The usual symptoms are serohaemorrhagic detachments and lipid exudation
Aflibercept - blocks what
VEGF-A, VEGF-B and PlGF
Aflibercept - Mechanism of Action
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
Osteoma - Visual loss is the result of
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
Retinal capillary haemangioma - evolution
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
Retinal capillary haemangioma - complications
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
Retinal capillary haemangioma - uni or multifocal
uni or multifocal
Retinal capillary haemangioma - in whom diagnosed
It is usually diagnosed in children and young adults
Vasoproliferative retinal tumour - where in fundus
located pre-equatorially and inferotemporally
Vasoproliferative retinal tumour - leads to what
retinal exudates, macular oedema and epiretinal membranes
Vasoproliferative retinal tumour - causes
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
Vasoproliferative retinal tumour - age
detected between the ages of 40 and 60 years
risk factors for growth of choroidal nevi into melanoma - Thickness
tumour thickness > 2 mm
Stargardt disease - fundus
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
Stargardt disease - FA
dark choroid with hyperfluorescent pisciform flecks
Stargardt disease - FAF
hyperautofluorescence in areas of lipofuscin accumulation and hypoautofluorescence in areas of RPE atrophy
Pseudoxanthoma Elasticum (PXE) - gene
ABCC6 gene
multifocal uveitis - type of CNV
Type 2
