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Friedman's Ophthalmology > Posterior Segment > Flashcards

Posterior Segment Flashcards

1
Q

<p>What are the components of Vitreous?</p>

A

<p>99% Water, Type II and IX collagen, hyaluronic acid</p>

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2
Q

<p>What is the volume of vitreous cavity?</p>

A

<p>4 cubic cm</p>

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3
Q

<p>Name the attachment points of vitreous</p>

A

<p>Ora serrata, optic nerve, blood vessels, and macula</p>

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4
Q

<p>Name the layers of retina</p>

A

<p>ILM (foot processes of muller's cells, true BM)NFL (unmyelinated glaglion cell axons)GCL (single layer of cells near the optic disc and multilayered at the macula)IPL (synapses between ganglion cells and bipolar cells)INL (Bipolar cells, Amacrine and horizontal cells)OPL (synapses between photoreceptors and bipolar cells)ONL(Photoreceptor cell bodies and nuclei)ELM (not a true BM)Photoreceptor layer (rods and cones)</p>

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5
Q

<p>On average, how many rods are in the retina?</p>

A

<p>120 million rods</p>

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6
Q

<p>On average how many cones are in the retina?</p>

A

<p>6 million cones</p>

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7
Q

<p>Few facts about rods:</p>

A

<p>95% of photoreceptors are filled with rodsNo rods in the center of the foveaMaximal rhodopsin is found as a ring around fovea in a 20-40 degree roundRod disks are not attached to the cell membraneThey are 1000 times more sensitive than cones in dark</p>

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8
Q

<p>Few facts about cones:</p>

A

<p>Provide high acuity of color visionSensitive in bright light50% are present in the maculaMaximal density in the foveaCone disks are attached to the cell membrane</p>

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9
Q

<p>Name the 3 types of visual pigment present in the cones</p>

A

<p>S: Short wavelength: sensitive to blueM: Medium wavelength: Sensitive to greenL: Long wavelength: Sensitive to Red</p>

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10
Q

<p>What supplies the inner retina?</p>

A

<p>Central retinal artery</p>

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11
Q

<p>What supplies the outer retina?</p>

A

<p>Choriocapillaries</p>

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12
Q

<p>What layer of retina separates the outer retina from inner retina?</p>

A

<p>OPL: middle limiting membrane in OPL acts as a water shed region between inner retinal vascular supply and outer retinal vascular supply</p>

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13
Q

<p>When does macula finishes its differentiation?</p>

A

<p>4-6 months of age</p>

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14
Q

<p>What are the predominant cones in the macula?</p>

A

<p>Red and Green</p>

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15
Q

<p>Name the carotenoids in the macula?</p>

A

<p>Lutein (antioxidant) and Zeaxanthin (light screening)</p>

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16
Q

<p>What is the diameter of the fovea?</p>

A

<p>1500 um</p>

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17
Q

<p>What is the diameter of FAZ?</p>

A

<p>250-600 um</p>

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18
Q

<p>What is the diameter of the foveola?</p>

A

<p>350 um</p>

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19
Q

<p>What acts as inner blood retinal barrier?</p>

A

<p>Retinal vascular endothelial cells (Zonula occludens-tight junctions)</p>

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20
Q

<p>What acts as outer blood retinal barrier?</p>

A

<p>RPE</p>

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21
Q

<p>Describe the architecture of the following hemorrhages?Flame or splinter hemorrhages:Dot blot:Boat shaped (scaphoid):Dark hemorrhage:</p>

A

<p>Flame or splinter hemorrhages: Superficial, tracks along NFLDot blot: Deep layers of retina, confined by axons oriented perpendicular to bruch's membraneBoat shaped (scaphoid): Sub-ILM (hemorrhagic detachment of ILM) Sub-Hyaloid (between ILM and hyaloid)Dark hemorrhage: Sub-RPE</p>

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22
Q

<p>What type of cells make up RPE?</p>

A

<p>Monolayer of hexagonal cells with apical microvilli</p>

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23
Q

<p>What type of arrangement is noted between RPE and outer segments of photoreceptors?</p>

A

<p>Apical to apical arrangement resulting on potential subretinal space</p>

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24
Q

<p>What are the functions of RPE?</p>

A

<p>Forms outer blood retinal barrierPhagocytoses of waste products and renewal of outersegments every 10 daysAbsorption of lightMelanin production Heat exchangeVitamin A cycle Provide nourishment of outer retinal cells</p>

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25
Q

<p>Name the layers of Bruch's membrane</p>

A

<p>Basement membrane (inner basal lamina of RPE)Inner CollagenElastic tissueOuter collagenBasement membrane (outer basal lamina of choriocapillaries)</p>

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26
Q

<p>What cells produce myelin in peripheral nervous system?</p>

A

<p>Schwann cells</p>

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27
Q

<p>What cells produce myelin in the CNS?</p>

A

<p>Oligodendrocytes</p>

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28
Q

<p>What are the attachments of choroid to sclera?</p>

A

<p>Scleral spur, at optic nerve, vortex veins and long and short posterior ciliary vessels</p>

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29
Q

<p>What are the layers of choroid?</p>

A

<p>Bruch's membrane (true BM)Choriocapillaries (endothelial cells with wide fenestrations)Stroma (mainly blood vessels)Suprachoridal space</p>

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30
Q

<p>What is the major source of nutrition for RPE and outer retinal layers?</p>

A

<p>Choriocapillaries</p>

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31
Q

<p>Name the arterial blood supply of choroid?</p>

A

<p>1-2 long and 15-20 short posterior ciliary arteries</p>

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32
Q

<p>Where does choriocapillaries drain?</p>

A

<p>Drain via vortex veins to superior and inferior ophthalmic veins</p>

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33
Q

<p>When do rods and cones shed outer segments?</p>

A

<p>Rods shed outer segments during the day (dawn)Cones shed in the night (dusk)</p>

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34
Q

<p>What are the visual pigments of retina?</p>

A

<p>3 cone pigments and 1 rod pigment. Each consists of 11-cis-retinal+protein opsin</p>

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35
Q

<p>What is the peak sensitivity of rods?</p>

A

<p>505 nm (blue)</p>

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36
Q

<p>What is the peak sensitivity of cones?</p>

A

<p>555 nm</p>

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37
Q

<p>Name the cells that contribute to flash ERG?</p>

A

<p>Photoreceptors, Muller's and bipolar cells. Ganglion cells do not respond or participate in ERG.</p>

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38
Q

<p>What are the components of ERG?</p>

A

<p>a-wave (photoreceptors)b-wave (bipolar and muller's cells)Oscillatory potentials (Generated in inner retinal layers by inner plexiform cells and amacrine cells)</p>

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39
Q

<p>Name the conditions with decreased b-wave amplitude or electronegative ERG?</p>

A

<p>CRAO, ischemic CVO, DM</p>

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40
Q

<p>What is Arden ratio?</p>

A

<p>Ratio of light to dark peak (2:1 is normal, <1.65 is abnormal)Decreased ratio is due to photoreceptor disorder or RPE disorder</p>

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41
Q

<p>Describe the ultrasound characteristics of retinal lesions? (in the following sequence below)LESION-SHAPE-INTERNAL REFLECTIVITYMelanomaChoroidal hemangiomaMetastasisNevusChoroidal hemorrhageDisciform lesion</p>

A

<p>Melanoma-Dome or collar button-Low to mediumChoroidal hemangioma-Dome-HighMetastasis-Diffuse irregular-Medium to HighNevus-Flat-HighChoroidal hemorrhage-Dome-VariableDisciform lesion-Dome irregular-High</p>

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42
Q

<p>Define reflectivity on A-scan and B-scan?</p>

A

<p>A-scan: Height of spikeB-scan: Signal brightness</p>

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43
Q

<p>What frequency of light is absorbed by Fluorescein?</p>

A

<p>Absorbs blue light at 465-490 nm and emits yellow-green light at 520-530 nm</p>

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44
Q

<p>\_\_\_\_\_% of Fluorescein is bound to albumin and serum proteins. \_\_\_\_\_\_% excreted from \_\_\_\_\_ and \_\_\_\_\_with in 24-36 hours.</p>

A

<p>80% bound to albumin. 90% excreted from kidneys and liver.</p>

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45
Q

<p>Is pregnancy a contradiction for FA?</p>

A

<p>Only the first trimester</p>

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46
Q

<p>Describe the types of Hyper fluorescence?</p>

A

<p>Leakage(NV), staining (scar, collagen), Pooling (CSR, PED), Window defects (GA, RPE defects)</p>

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47
Q

<p>Describe the types of hypofluorescence?</p>

A

<p>Blockage (RPE, blood, xanthophyll)Filling defect (ischemia)</p>

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48
Q

<p>Why is macula dark on FA?</p>

A

<p>Dark spot is due to blockage by xanthophyll in OPL and excess of melanin and lipofusin</p>

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49
Q

<p>What frequency of light is absorbed by ICG?</p>

A

<p>ICG absorbs light in near infrared range (790-805 nm) and emits at 770-88- nm</p>

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50
Q

<p>How is ICG excreted from the body?</p>

A

<p>Excreted via liver into bile</p>

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51
Q

<p>What are the contraindications for ICG?</p>

A

<p>Allergic to Iodine, uremic syndrome and liver disease</p>

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52
Q

<p>What is the best way to look at retinal pathology in patients with asteroid hyalosis?</p>

A

<p>FA</p>

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53
Q

<p>What is asteroid hyalosis?</p>

A

<p>Refractile particles (calcium soaps) suspended in vitreous</p>

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54
Q

<p>Describe the pathology of asteroid hyalosis?</p>

A

<p>Gray spheres with "Maltese cross" birefringence on polarization</p>

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55
Q

<p>What is synchisis scintillans?</p>

A

<p>Cholesterol deposits derived from old vitreous hemorrhage. Rare, unilateral, s/p trauma. crystals sink to the bottom due to liquefaction of vitreous</p>

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56
Q

<p>What is Berlin's edema?</p>

A

<p>Not a true edema. It is called Commotio retinae - transient retinal whitening due to disruption of photoreceptor outer segments</p>

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57
Q

<p>Describe the mechanism of Choroidal rupture?</p>

A

<p>Tear in RPE, bruch's membrane and choroid. Sclera is resistant due to high tensile strength and retina is resistant due to elasticity. </p>

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58
Q

<p>What is the most common location of choroidal rupture?</p>

A

<p>Direct injury: Occurs anterior to the site of impact, oriented parallel to ora serrataIndirect injury: Occurs posterior to the site of impact, crescent shaped, concentric with optic disc and temporal to it. Associated with VH.</p>

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59
Q

<p>Name the trauma to the retina and choroid caused by transmitted shock waves and necrosis from high velocity injuries.</p>

A

<p>Retina sclopetaria?</p>

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60
Q

<p>What are the findings of sclopetaria?</p>

A

<p>Rupture of retina and choroid with commotio and VH. Lesion heals with white fibrous scar and RPE changes</p>

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61
Q

<p>What is the most common retinal tear associated with trauma?</p>

A

<p>Retinal dialysis. </p>

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62
Q

<p>What are the most common locations of retinal dialysis?</p>

A

<p>Inferotemporal 31% and Superonasal 22%</p>

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63
Q

<p>What is the pathognomonic sign for retinal trauma?</p>

A

<p>Avulsion of vitreous base</p>

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64
Q

<p>Name the 4 most common retinal breaks?</p>

A

<p>Horseshoe tear, operculated hole, retinal dialysis and macular hole</p>

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65
Q

<p>Describe the treatment options for common retinal breaks?1. Horseshoe tear2. Operculated hole3. Retinal dialysis with RD4. Macular hole</p>

A

<p>1. Horseshoe tear - Laser or cryo (peripheral lesions)2. Operculated hole - laser or cryo3. Retinal dialysis with RD- Scleral buckle, w/o RD-laser4. Macular hole-PPV with tamponade or Ocriplasmin</p>

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66
Q

<p>Name few causes of Purtscher's retinopathy?</p>

A

<p>Head trauma, compression injury to the lungs or trunk, fat /amniotic/ air embolism, pancreatitis, dermatomyositis.</p>

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67
Q

<p>What are the unique findings of Purtscher's retinopathy?</p>

A

<p>CWS, retinal whitening, hemorrhages, papillitis, ?RAPD</p>

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68
Q

<p>Name the syndrome that causes VH secondary to subarachnoid hemorrhage?</p>

A

<p>Terson's syndrome</p>

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69
Q

<p>The fracture of what kind of bones result in fat emboli syndrome?</p>

A

<p>Long medullated bone fractures</p>

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70
Q

<p>What are the unique features of fat emboli syndrome?</p>

A

<p>CWS, small blot hemorrhages, rarely CRAO</p>

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71
Q

<p>What type of injury is associated with Whiplash retinopathy?</p>

A

<p>Severe flexion/extension of head and neck without direct eye injury</p>

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72
Q

<p>Name the unique features of whiplash retinopathy?</p>

A

<p>Mild reduction of vision (20/30), gray swelling of fovea, foveal pit</p>

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73
Q

<p>What causes ERM?</p>

A

<p>contraction of proliferations at vitreoretinal junction cause retinal striae, folds and macular edema</p>

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74
Q

<p>What are the statistics of ERM?</p>

A

<p>12% prevalence in 43-86 yo, 20% bilateral, 2% association with retinal folds</p>

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75
Q

<p>Name the conditions associated with ERM?</p>

A

<p>DM, retinal vascular occlusions, anomalous, PVD, high myopia, retinal hole/tears, previous ocular or laser surgery, and increasing age.</p>

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76
Q

<p>What causes a full thickness macular hole (FTMH)?</p>

A

<p>Tangential traction on foveal region by posterior cortical vitreous</p>

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77
Q

<p>Name the factors associated with FTMH?</p>

A

<p>Age (senile), may develop after trauma, surgery, CME or inflammation</p>

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78
Q

<p>What is Watzke-Allen sign?</p>

A

<p>Positive: If patient perceives a "break" in the line when a narrow slit beam is shone in the eye over the macular hole.</p>

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79
Q

<p>What are the treatment options for macular hole?</p>

A

<p>Stage 1: Observation or Ocriplasmin (Jetrea)Stages 2-4: PPV/MP/gas tamponade</p>

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80
Q

<p>What is the prognosis of macular hole?</p>

A

<p>Good: recent onset and <400umPoor: For >1 year duration and larger holes</p>

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81
Q

<p>What frequency of light can cause solar retinopathy?</p>

A

<p>Blue (441nm) and near UV light (325-250 nm). >90 seconds of sun gazing can cause photochemical retinal damage</p>

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82
Q

<p>What factors are associated with solar retinopathy?</p>

A

<p>solar eclipse, psychiatric disorders, religious rituals, or ingestion of hallucinogens</p>

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83
Q

<p>What factors are associated with CSR?</p>

A

<p>HTN, steroid use, psychiatric medication, type A personality</p>

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84
Q

<p>What is the buzzword for leakage on FA for CSR?</p>

A

<p>"Smokestack" appearance (10%)"Expansile dot" of hyperfluorescence (80%)</p>

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85
Q

<p>Name the findings of CSR on OCT?</p>

A

<p>serous retinal elevation, PED or SRF, thick choroid</p>

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86
Q

<p>What are the treatment options for CSR?</p>

A

<p>Laser for parafoveal spotsPDT for subfoveal spotsSpironolactone to eplerenone for chronic CSR</p>

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87
Q

<p>What are the indications for treatment of CSR?</p>

A

<p>Persistent serous detachment (>3 months)Episode of vision loss in fellow eyePrior episode of CSR with vision loss in the contralateral eyeOccupational reasons</p>

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88
Q

<p>What are the risk factors for AMD?</p>

A

<p>Age, Fam hx, female, Caucasian race, smoking, nutrition, light iris color, hyperopia, HTN, photic exposure</p>

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89
Q

<p>What are the characteristics of dry or non-exudative AMD?</p>

A

<p>Drusen (80-90%), pigmentary changes and RPE atrophy</p>

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90
Q

<p>What are the characteristics or wet or exudative AMD?</p>

A

<p>CNV</p>

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91
Q

<p>What is the drusen size classification?</p>

A

<p>Small: <64 umIntermediate: 64-124 umLarge: >/= 125 umin diameter</p>

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92
Q

<p>What is the Ddx for yellow foveal spot?</p>

A

<p>Solar retinopathy, Adult vitelliform dystrophy, Best's dz, CSR, lamellar hole, CME, pattern dystrophy, old subretinal hemorrhage</p>

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93
Q

<p>What are the types of CNV?</p>

A

<p>Type 1: CNV under RPE. Eg: PCV Type 2: CNV above RPE or subretinalType 3: Retinal angiomatous proliferation (RAP)</p>

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94
Q

<p>What type of AREDS is recommended for smokers and why?</p>

A

<p>AREDS2 was recommended for smokers due to lack of beta carotene. </p>

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95
Q

<p>What are the adverse affects reported with AREDS?</p>

A

<p>Beta carotene is associated with lung cancerZinc with BPH in men and stress incontinence in womenVitamins E and C with MI in postmenopausal women</p>

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96
Q

<p>What additional components were tested in AREDS 2?</p>

A

<p>Lutein, Zeaxanthin, and omega-3 fatty acids</p>

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97
Q

<p>What VEGF isoform does Macugen binds to?</p>

A

<p>Isoform 165 of VEGF-A</p>

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98
Q

<p> Which anti-VEGF acts a fusion receptor decoy?</p>

A

<p>Aflibercept or Eylea</p>

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99
Q

<p>Which anti-VEGF binds to all isoforms of VEGF?</p>

A

<p>Bevacizumab (Avastin)</p>

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100
Q

<p>What is the mnemonic for angioid streaks?</p>

A

<p>PEPSI: Pseudoxanthoma elasticumEhler's Danlos, Paget's dz, SCD, idiopathic and B-thal</p>

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101
Q

<p>How to define pathologic myopia?</p>

A

<p>High myopia: AL>26mm, >-6D of myopiaPathologic myopia: AL>32.5 mm, >-8D of myopia</p>

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102
Q

<p>What are the few adverse but rare side effects of anti VEGF injections?</p>

A

<p>Anti-thrombotic events (ATE) such as HTN, stroke and MI</p>

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103
Q

<p>What type of organism cause POHS and which part of US is it endemic to?</p>

A

<p>Histoplasma capsulatum (dimorphic fungus). Endemic to Mississippi and Ohio river valley. </p>

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104
Q

<p>What percent of patients with ocular signs are positive for skin test?</p>

A

<p>90%</p>

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105
Q

<p>What type of autoimmune diseases are associated with POHS?</p>

A

<p>HLA-B7, HLA-DRW2</p>

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106
Q

<p>What are the signs of primary infection of POHS?</p>

A

<p>Mostly systemic with self limited flu like illness with dissemination to liver, spleen and choroid.</p>

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107
Q

<p>What are the signs of primary choroidal inflammation?</p>

A

<p>Granulomatous lesions with unapparent inflammation that resolves with small atrophic scars (Histo spots) which may disrupt Bruch's membrane.</p>

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108
Q

<p>What is the triad of POHS?</p>

A

<p>Peripapillary atrophy, multiple punched out lesions, and maculopathy (CNV).</p>

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109
Q

<p>What is the risk of CNV in POHS?</p>

A

<p>1% if no signs of POHS in the fellow eye4% if peripapillary atrophy25% if histo spots are in the macula</p>

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110
Q

<p>What are angioid streaks?</p>

A

<p>Peripapillary linear cracks in thickened, degenerated, and calcified Bruch's membrane</p>

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111
Q

<p>What is the risk with angioid streaks?</p>

A

<p>Subretinal hemorrhage can occur with minor trauma</p>

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112
Q

<p>What are the findings of pathologic myopia?</p>

A

<p>Long oval disk, tilted, shallow cup, temporal crescent, posterior staphyloma, tigroid fundus with choroidal show, lacquer cracks (breaks in BM), Foerster Fuchs' spot (macular hemorrhage), </p>

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113
Q

<p>What was the objective of macular photocoagulation study (MPS) and what were the results?</p>

A

<p>Objective: To evaluate the efficacy of laser in preventing visual loss from CNV in patients with AMD, POHS and idiopathicResults: Tx extrafoveal CNV with laserTx juxtafoveal CNV with Krypton laserTx subfoveal CNV with argon or Krypton laserClassic CNV responds better than occult CNV</p>

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114
Q

<p>What was the objective of TAP (Tx of AMD with photodynamic therapy (PDT) trial) and what were the results?</p>

A

<p>Objective: To evaluate Verteporfin (PDT) in the management of subfoveal CNV in AMD patientsResults: PDT is beneficial for "predominantly classic" CNV in AMD</p>

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115
Q

<p>What was the objective of AREDS study and what were the results?</p>

A

<p>Objective: To evaluate the effect of "high dose supplements" on the progression of AMD and on the development and progression on cataractsResults: Supplements are beneficial in reducing the risk of progression in intermediate and severe stages of AMD. NO benefit in early AMD. No effect on cataract development and progression. Caution should be exercised in smokers with high dose of B-carotene</p>

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116
Q

<p>What was the objective of "AREDS 2" study and what were the results?</p>

A

<p>O: To evaluate the effect of "high dose supplements, carotenoids and Omega-3 fatty acids" in the progression of AMDR: NEI recommended to adjust AREDS with removal of B-carotene and addition of Lutein and Zeaxanthin</p>

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117
Q

<p>What was the objective of "VISION" (VEGF inhibition in neovascular AMD) trial and what were the results?</p>

A

<p>O: To evaluate intravitreal pegaptanib (Macugen) for subfoveal CNV in AMDR: Macugen was better than sham and PDT for subfoveal CNV In AMD</p>

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118
Q

<p>What was the objective of "MARINA" (minimally classic/occult trial of Ranibizumab in the txt of wet AMD) trial and what were the results?</p>

A

<p>O: Compare monthly Ranibizumab injections with shamR: Ranibizumab is better than sham for occult CNV with no classic or minimally classic CNV in wet AMD</p>

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119
Q

<p>What was the objective of "ANCHOR" trial and what was the conclusion? (Anti-VEGF for predominantly classic CNV in AMD)</p>

A

<p>O: Compare Ranibizumab with PDT for subfoveal CNV in AMDR: Ranibizumab is superior to PDT</p>

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120
Q

<p>What was the objective of "VIEW 1/2" trial and what was the conclusion? (Aflibercept for CNV in AMD)</p>

A

<p>O: Compared Aflibercept of 3 different doses (0.5 mg/ 4 weeks, 2 mg/4 weeks, 2 mg/8 weeks) with Ranibizumab at 0.5 mg /4 weeksR: Aflibercept injected every 2 months was equivalent to monthly Ranibizumab injections after 3 monthly loading doses</p>

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121
Q

<p>What are the generic names of antivegf injections?Aflibercept:Ranibizumab:Bevacizumab:Pegabtanib:</p>

A

<p>Aflibercept: EyleaRanibizumab: LucentisBevacizumab: AvastinPegabtanib: Macugen</p>

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122
Q

<p>What was the objective and conclusion of "CATT" trials? (Comparison of AMD treatment trials)</p>

A

<p>O: To compare Avastin and Lucentis with monthly and prn schedulesR: With both drugs, patients with monthly injections gained more lines of VA compared to prn injections. Patients with monthly injections suffered macular atrophy than prn.Considering anatomic outcomes, Avastin was found to be inferior to Lucentis</p>

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123
Q

<p>What was the objective and what were the results of "IVAN" study? (Alternative tx options to inhibit VEGF in CNV from AND)</p>

A

<p>O: Lucentis vs Avastin for treatment of CNV in AMDR: Review of all studies including CATT, IVAN, MANTA, LUCAS, and GEFAL found that monthly treatment with Avastin or Lucentis was equally effective in treating CNV with AMD in upto 2 years. </p>

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124
Q

<p>How does edema appears histologically?</p>

A

<p>clear cystoid spaces</p>

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125
Q

<p>Histologically, how does lipid deposits look like?</p>

A

<p>Yellow lesions, hard exudates with eosinophilic and PAS positive</p>

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126
Q

<p>What are microaneurysms?</p>

A

<p>Outpouching of capillary walls</p>

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127
Q

<p>What are cotton wool spots?</p>

A

<p>Infarction of NFL(usually secondary to occlusion of retinal arteriole)</p>

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128
Q

<p>What is the mnemonic for ddx for CME?</p>

A

<p>DEPRIVENDM, Epinephrine use, Parsplanitis, RP, Vein occlusions, Irvine Gass, E2 prostaglandins, and Nicotinic acid maculopathy</p>

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129
Q

<p>Name the causes of CME that DOES NOT LEAK on FA?</p>

A

<p>Juvenile retinoschisisNicotinic acid maculopathyGoldmann-Favre syndromeRP variants</p>

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130
Q

<p>What is macular telangiectasia? (MacTel)</p>

A

<p>Microaneurysmal and saccular dilation of parafoveal vessels. Formerly called parafoveal/juxtafoveal telangiectasia</p>

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131
Q

<p>What is the classification of MacTel?</p>

A

<p>Type 1: Unilateral, Males>females, onset during middle age, in spectrum of coats diseaseType 1A: Congenital, macular edema localized to temporal fovea and exudationType 1B: idiopathic, capillary telengiectasia confined to FAZType 2A: most common, b/l, males=females, 5-6th decade of life, symmetricType 3: b/l, idiopathic, M=F, capillary occlusion predominates</p>

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132
Q

<p>What are the findings of hypertensive retinopathy?</p>

A

<p>AV nicking "copper or silver wiring", hemorrhages, exudates, CWS</p>

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133
Q

<p>What are the findings of hypertensive choroidopathy?</p>

A

<p>Elsching's spots (non perfusion of choriocapillaries), Siegrist streak (reactive RPE hyperplasia along sclerosed choroidal vessel) and exudative RD</p>

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134
Q

<p>What are the findings of hypertensive optic neuropathy?</p>

A

<p>Florid disc edema with macular exudate, linear flame hemorrhages</p>

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135
Q

<p>Describe severe NPDR "4-2-1 rule"?</p>

A

<p>4 quadrants of intraretinal hemorrhages/MAs2 quadrants of venous bleeding1 quadrant of IRMAVery severe NPDR: 2 or more of the above criteria</p>

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136
Q

<p>Define PDR and HR-PDR?</p>

A

<p>PDR: NV of disc or elsewhereHR-PDR: 1. NVD >/= 1/4 to 1/3 disc area2. NVD w/ VH3. NVE w/ VH</p>

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137
Q

<p>Define CSME?</p>

A

<p>1. Retinal thickening w/in 500 um from the fovea2. Retinal thickening with hard exudates w/in 500 um from the fovea3. 1 D area of retinal thickening w/in one 1DD of the macular center or fovea</p>

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138
Q

<p>What are the main causes of vision loss in NPDR?</p>

A

<p>Macular edema or ischemia</p>

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139
Q

<p>What are the main causes of vision loss in PDR?</p>

A

<p>TRD, NVG, and VH</p>

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140
Q

<p>What is a diabetic cataract?</p>

A

<p>Aldose reductase pathway. converts glucose to sorbitol and fructose. </p>

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141
Q

<p>What is diabetic iridopathy?</p>

A

<p>Iris NV, lacy vacuolization of iris pigment epithelium, PAS+</p>

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142
Q

<p>What is the histologic signs of diabetic retinopathy?</p>

A

<p>Selective loss of pericytes, thickening of BM, lacy vacuolization of iris pigment epithelium, intraepithelial vacuoles containing glycogen</p>

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143
Q

<p>What are the adverse effects of PRP?</p>

A

<p>Decrease night vision (due to loss of extramacular rods)Angle closure glaucoma (choroidal effusion)RD (regression of NV fronds can contract)Central scotoma (Worsening of CME)Progression of cataract</p>

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144
Q

<p>What are the indications for vitrectomy?</p>

A

<p>NCVHcombined RRD and TRD of the foveaMacular threatening TRDRefractory macular edema from tractional hyaloid faceProgressive fibrovascular proliferation despite PRP 360Ghost cell glaucoma</p>

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145
Q

<p>What conditions exacerbate diabetic retinopathy?</p>

A

<p>HTN, puberty, pregnancy, renal disease, anemia</p>

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146
Q

<p>What was the objective of "DRS" study and what were the results?</p>

A

<p>O: To evaluate whether PRP prevents vision loss in DRR: Defined severe NPDR and HR-PDRPRP is indicated only for NV and high risk characteristics</p>

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147
Q

<p>What was the objective for ETDRS and what were the results?</p>

A

<p>O: To evaluate if PRP is effective for DME2. Effect of Aspirin on the course of DR3. When to initiate PRP for DRR: Defined CSME. No benefit from Aspirin. Treat all patients with CSME regardless of VA</p>

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148
Q

<p>What was the objective for "DRVS" (Diabetic retinopathy vitrectomy study) and what were the results?</p>

A

<p>O: To observe patients with severe DR in type 1 and type2R: Type1 DM benefit from early vitrectomyVision loss form NCVH in T1DM and monocular patients despite the type of diabetes</p>

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149
Q

<p>What was the objective for "DCCT" (Diabetes control and complications trial) and what were the results?</p>

A

<p>O: To evaluate the effect of tight vs conventional control of blood sugar on diabetic complications on T1DMR: Patients with HbA1C<8% had significantly reduced risk of retinopathy. Tight control is beneficial. Rapid fluctuations lead to initial worsening of retinopathy.</p>

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150
Q

<p>What was the objective for "UKPDS" (United Kingdom prospective diabetes study) and what were the results?</p>

A

<p>R: Type 2 diabetic patients benefit from intensive glycemic control, as do type 1 diabetic patients</p>

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151
Q

<p>What was the objective for "UKPDS-HDS" (United Kingdom prospective diabetes study-HTN in diabetes study) and what were the results?</p>

A

<p>R: Tight BP control reduced the risk of complications from DR</p>

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152
Q

<p>What are the results of "RISE, RIDE, RESTORE/RESOLVE" studies?</p>

A

<p>All these studies looked at efficacy of Ranibizumab for DME and found that Lucentis is superior to focal laser for DME treatment</p>

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153
Q

<p>What are the conclusions of DRCR.net?</p>

A

<p>1. Triessence is NOT superior to focal/grid laser2. Lucentis w or w/o focal/grid laser is superior to laser alone3. Lucentis is superior to PRP in PDR treatment4. When initial VA loss was mild, there was no difference among eylea, Lucentis and Avastin. At worse levels of initial VA, Lucentis and Eylea were more effective than Avastin.</p>

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154
Q

<p>What are the few facts of SCR?</p>

A

<p>It is a form of proliferative retinopathy, usually equatorial or pre-equatorial. Most severe in HbSC disease. </p>

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155
Q

<p>What is the prevalence of SCR in SC patients?</p>

A

<p>SC>SThal>SS>SA</p>

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156
Q

<p>What are the findings in SCR?</p>

A

<p>Salmon patch (intraretinal hemorrhage), black sun burst ((chorioretinal scar), Sea fan (peripheral NV), refractile spots (old resorbed hemorrhages), angioid streaks, vascular occlusions, peripheral nonperfusion.</p>

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157
Q

<p>What are the stages of SCR?</p>

A

<p>Stage 1: Peripheral arterial occlusionsStage 2: Peripheral anastomosesStage 3: NV (sea fan) at posterior border of areas of non-perfusionStage 4: VHStage 5: VH with RD</p>

158
Q

<p>What are the treatment options for SCR?</p>

A

<p>PRP or cryo for NVPPV for RD and VHSB and Gas fill are contraindicated due to risk of anterior segment ischemiaAvoid epinephrine in the bottle during sx</p>

159
Q

<p>What is Eales' disease?</p>

A

<p>Idiopathic retinal perivasculitis and peripheral NV Occurs in young men, 90% bilateralMostly seen in middle East and IndiaIncreased risk of BVO</p>

160
Q

<p>Describe the stages of Eales' disease?</p>

A

<p>Stage 1: Sheathing of retinal venules, retinal edema, hemorrhagesStage 2: Vitreous hazeStage 3: Peripheral NVStage 4: Proliferative retinopathy with VH and TRD</p>

161
Q

<p>What are the systemic findings of Eales' disease?</p>

A

<p>Sensironeural hearing loss, vestibular dysfunction, PPD+, cerebral vasculitis and epistaxis</p>

162
Q

<p>What is the most common site of occlusion in BRVO?</p>

A

<p>Site of occlusion is at AV nicking usually in ST quadrant</p>

163
Q

<p>What are the risk factors of BRVO?</p>

A

<p>Age, HTN, BMI, CAD, high serum alpha-globulins, glaucoma, papilledema, optic disc drusen. Diabetes is NOT a risk factor for BRVO.</p>

164
Q

<p>What factors decrease the risk of BRVO?</p>

A

<p>High HDL levels and moderate consumption of alcohol</p>

165
Q

<p>What are the types of BRVO?</p>

A

<p>Ischemic: >/= 5DD of capillary nonperfusionNon-ischemic: < 5 DDof capillary nonperfusion</p>

166
Q

<p>What is pathognomonic sign of BRVO?</p>

A

<p>Numerous deep and superficial hemorrhages in Wedge shaped distribution with the tip pointing toward the etiologic crossing. </p>

167
Q

<p>What are the treatment options for BRVO?</p>

A

<p>Sectoral PRP for NV or VH. Intravitreal injections for macular edema (new txt)Grid laser for macular edema if VA < 20/40 for >3 months (old txt)</p>

168
Q

<p>What was the conclusion of "BVOS" study? (Branch vein occlusion study)</p>

A

<p>Grid argon laser for macular edema and VA < 20/440 for at least 3 months PRP for >/=5DD of nonperfusion if NV develops</p>

169
Q

<p>What was the conclusion of "BRAVO" study? (Branch Retinal vein occlusion)</p>

A

<p>Lucentis for macular edema</p>

170
Q

<p>What was the conclusion of "VIBRANT" study? (Eylea for mac Edema in Branch vein occlusion)</p>

A

<p>Eylea for macular edema</p>

171
Q

<p>What is the conclusion of "GENEVA" study? (Global evaluation of implantable Dexa in RVO with ME)</p>

A

<p>Intravitreal injection of sustained release dexa intravitreal implant for macular edema (Ozurdex) from vein occlusion</p>

172
Q

<p>What are the complications of nonischemic BRVO?</p>

A

<p>Macular edema</p>

173
Q

<p>What are the complications of ischemic BRVO?</p>

A

<p>NV, ME, VH, TRD</p>

174
Q

<p>What is the pathology behind CRVO?</p>

A

<p>Thrombosis of central retinal vein at or posterior to the lamina cribrosa</p>

175
Q

<p>What are the types of CRVO?</p>

A

<p>Ischemic: >/= 10 DD of capillary nonperfusionNon-ischemic: < 10 DDof capillary nonperfusion</p>

176
Q

<p>What are the risk factors of CRVO?</p>

A

<p>Age (>50), HTN, DM< CAD, glaucoma, syphilis, sarcoidosis, vasculitis, hyperviscocity syndromes, high homocysteine levels, sickle cell, HIV</p>

177
Q

<p>What are the findings of CRVO?</p>

A

<p>Venous dilatation, tortuosity, hemorrhages in all quadrants, disc edema and macular edema</p>

178
Q

<p>What are the high risk characteristics of CRVO?</p>

A

<p>Positive RAPD, central scotoma, CWS, wide spread nonperfusion, and electronegative ERG</p>

179
Q

<p>What are the treatment options for CRVO?</p>

A

<p>Intravitreal injections for macular edemaPRP for NVMonthly gonioscopy for 6 months to r/o NVG</p>

180
Q

<p>What was the conclusion of "CVOS" study? (Central vein occlusion study)</p>

A

<p>No benefit from early PRP. Wait until the first sign of NVNo benefit from focal laser for macular edema</p>

181
Q

<p>What was the conclusion of "CRUISE" study? (Central vein occlusion study with Ranibizumab)</p>

A

<p>Lucentis is effective for macular edema</p>

182
Q

<p>What was the conclusion of "COPERNICUS/GALILEO" study? (Central vein occlusion study with Eylea)</p>

A

<p>Eylea for macular edema from CRVO</p>

183
Q

<p>What are the complications of CRVO?</p>

A

<p>NVI (more common than NVE or NVD), NVG, TRD, VH, and macular edema</p>

184
Q

<p>What are the risk factors of hemiretinal vein occlusion (HRVO)?</p>

A

<p>HTN, DM, glaucoma</p>

185
Q

<p>What is the significance of HRVO compared to CVO or BVO?</p>

A

<p>Higher risk of NVD (30%) and NVE (40%) compared to BVO/CVO. NVI is 10%</p>

186
Q

<p>What is the pathology behind BRAO?</p>

A

<p>90% is caused by emboli (cholesterol, calcium, fibrin and platelets). Most common occlusion at arterial bifurcations. 10% risk in the fellow eye.</p>

187
Q

<p>What is the most common cause of cherry red spot?</p>

A

<p>CRAO</p>

188
Q

<p>What is the etiology of CRAO?</p>

A

<p>Atherosclerosis: CRA at lamina cribrosaEMBOLI: cholesterol (hollenhorst plaque)-73%, Platelet fibrin (carotid plaque)-15%, Calcium (from heart valves), tumor (atrial myxoma), lipid emboli (pancreatitis), talc</p>

189
Q

<p>What are the retinal findings of CRAO?</p>

A

<p>Severe vision loss, LP or poor vision, retinal whitening in posterior pole with cherry red spot, box-carring of vessels, emboli, positive RAPD, pale disc and attenuated vessels </p>

190
Q

<p>What is the ddx of cherry red spot?</p>

A

<p>Sphingolipidosis (Tay-sachs dz, Niemann-Pick, Gaucher's, Fabry's dz), Quinine toxicity, commotio retinae, macular hole with surrounding RD, macular hemorrhage, ocular ischemia, and methanol toxicity</p>

191
Q

<p>What are the ERG findings of CRAO?</p>

A

<p>electronegative ERG with depressed b-wave, normal/supernormal a-wave, loss of oscillatory potentials</p>

192
Q

<p>What are the treatment options available for CRAO?</p>

A

<p>Lower arterial pressure: paracentesis, ocular massage, carbogen, or breath into paper bag, oral and topical hypotensive agents, PRP for NV</p>

193
Q

<p>What are the complications of CRAO?</p>

A

<p>Rubeosis(NVI)</p>

194
Q

<p>What is the difference in VA between CRAO and ophthalmic artery occlusion?</p>

A

<p>CRAO: LP or HM visionOphthalmic artery occlusion: NLP and no cherry red spot</p>

195
Q

<p>What is the difference in ERG findings between CRAO and ophthalmic artery occlusion?</p>

A

<p>CRAO: Depressed b-wave and normal a-waveOphthalmic artery occlusion: Absent a-wave</p>

196
Q

<p>What causes ocular ischemic syndrome (OIS)?</p>

A

<p>Reduced blood flow to globe produces anterior and/or posterior segment ischemia</p>

197
Q

<p>What is the etiology of OIS?</p>

A

<p>Carotid occlusion (most common usually >90% stenosis)Carotid dissection, arteritis (rare)</p>

198
Q

<p>What is associated with OIS?</p>

A

<p>DM(56%), HTN(50%), CAD(38%), CVA/TIA(31%)</p>

199
Q

<p>What are the symptoms of OIS?</p>

A

<p>Amaurosis fugax, gradual or sudden vision loss, dull pain, transient vision loss precipitated by bright light due to photoreceptor degeneration</p>

200
Q

<p>What causes radiation retinopathy?</p>

A

<p>Slowly progressive microangiopathy following exposure to radiation (6 months to 3 years after radiation txt)</p>

201
Q

<p>What is the threshold of radiation to eyes?</p>

A

<p>300 rads (3Gy)</p>

202
Q

<p>What is the mean dose of radiation that causes radiation retinopathy?</p>

A

<p>15,000 rads (150 Gy) for plaque brachytherapy5000 rads (50 Gy) for external beam radiation</p>

203
Q

<p>What are the findings of radiation retinopathy?</p>

A

<p>Hemorrhage, exudates, MAs, CNP, CWS, NV , optic disc swelling, optic neuropathy, proliferative retinopathy</p>

204
Q

<p>What are the symptoms of neuroretinitis?</p>

A

<p>Usually unilateral with viral prodrome in 50% of cases. Decreased VA, colors appear washed out, retrobulbar pain, pain with EOM, or HA</p>

205
Q

<p>What are the ocular findings in neuroretinitis?</p>

A

<p>Optic nerve swelling or atrophy, peripapillary NFL hemorrhages, serous RD, iritis, vitritis, +/- scleritis</p>

206
Q

<p>What are the demographics of Leber's idiopathic stellate neuroretinitis (LISN)?</p>

A

<p>Affects individuals 8-55 years of ageMost commonly 3rd decadeM=F, >70% unilateral, 5% viral prodrome</p>

207
Q

<p>What are the findings of LISN?</p>

A

<p>Decreased VA, +RAPD, central scotoma, vitreous cell, Optic nerve edema with macular star, ?exudative peripapillary RD</p>

208
Q

<p>What are the FA findings of LISN?</p>

A

<p>Hot disc with no perifoveal capillary leakage or macular abnormalities</p>

209
Q

<p>What are the infectious causes of Neuroretinitis?</p>

A

<p>Syphilis, LymeViral (Influenza A, Mumps, Coxsackie B, EBV)Cat scratch disease (Bartonella Henselae)TB, salmonella, Typhi, parasites (Toxocara, Toxoplasma, DUSN)</p>

210
Q

<p>What causes diffuse unilateral subacute neuroretinitis DUSN?</p>

A

<p>A subretinal nematode: Ancyclostoma Caninum(dog hookworm), Balisascaris procyonis (racoon worm)</p>

211
Q

<p>Does DUSN carry the same characteristics of neuroretinitis?</p>

A

<p>NO. Typically the decrease in VA is out of proportion to findings on clinical exam</p>

212
Q

<p>What are the findings in DUSN on clinical exam?</p>

A

<p>Multifocal pigmentary changes due to movement of the worm, minimal intraocular inflammation, decreased VA, possible RAPD.Late findings: VF defects, optic nerve pallor, chorioretinal atrophy and attenuated vessels</p>

213
Q

<p>How do you diagnose DUSN?</p>

A

<p>Stool sample for ova and parasites, CBC with diff (for eosinophils), LDH and SGOH on liver functional panel are elevated.</p>

214
Q

<p>What are the FA findings in DUSN?</p>

A

<p>Perivascular leakage with disc staining, early hypoflourescence with late staining of the lesions, multifocal window defects in late disease</p>

215
Q

<p>What are the ERG findings in DUSN?</p>

A

<p>Subnormal with electronegative ERG (loss of b-wave)</p>

216
Q

<p>What is the treatment for DUSN?</p>

A

<p>Focal laser for the worm or subretinal surgery(controversial)Systemic anithelmintic medications are controversial and not effective.Steroids are usually added because the death of the worm can create inflammation</p>

217
Q

<p>What is the prognosis of DUSN? </p>

A

<p>Poor w/o treatment. variable if worm is killed with txt</p>

218
Q

<p>What is the Ddx for optic nerve swelling and macular star?</p>

A

<p>LISN, syphilis, HTN, trauma, acute febrile illness (measles, flu, TB, coccidiomycosis, CSD, papillitis, papilledema) DUSN and AION (macular star is rare)</p>

219
Q

<p>Describe HIV retinopathy?</p>

A

<p>Microangiopathy in 50% of HIV infected individuals, patients are usually asymptomatic and non-progressive</p>

220
Q

<p>What are the findings of HIV retinopathy?</p>

A

<p>CWS, roth spots, hemorrhages, MAs in posterior pole</p>

221
Q

<p>What is the cause of early presbyopia in HIV patients?</p>

A

<p>Inflammation of the ciliary body with loss of accommodative amplitude.</p>

222
Q

<p>How do you diagnose HIV retinopathy?</p>

A

<p>HIV antibody test, CD4 count, HIV viral load</p>

223
Q

<p>What is the treatment of HIV retinopathy?</p>

A

<p>None. Spontaneous resolution in 1-2 months with HAART therapy.</p>

224
Q

<p>Which aminoglycoside is found to be toxic with intracameral injection?</p>

A

<p>Gentamicin/Tobramycin/Amikacin. </p>

225
Q

<p>What is the toxic side effect of Gentamicin?</p>

A

<p>Acute, severe, permanent vision loss after intracameral injection.</p>

226
Q

<p>What are retinal findings of toxic retinopathy with gentamicin intracameral injection?</p>

A

<p>Retinal whitening in the macula, retinal hemorrhages, and pigmentary changes later</p>

227
Q

<p>What is the etiology of chloroquine toxicity?</p>

A

<p>Chloroquine binds to melanin in RPE and also directly affects ganglion cells</p>

228
Q

<p>What is the toxic dose of hydroxychloroquine and chloroquine?</p>

A

<p>Chloroquine is >2.3mg/Kg real weightHydroxychloroquine is 5 mg/Kg real weight</p>

229
Q

<p>What are the risk factors of chloroquine toxicity?</p>

A

<p>Daily dose, usage for >5 years, liver disease, kidney disease, concomitant tamoxifen use, older age, preexisting retinal/macular disease</p>

230
Q

<p>What are the ocular findings of chloroquine toxicity?</p>

A

<p>Early, mild mottling of perifoveal RPE with decreased foveal reflex, bull's eye maculopathy, pigmentary retinopahty, eyelash whitening and corneal vortex keratopathy</p>

231
Q

<p>What are the imaging findings of chloroquine toxicity?</p>

A

<p>VF: paracentral scotomasERG: Enlarged a-wave and decreased b-waveEOG: depressedOCT: ring of outer retinal thinning (UFO sign)FAF: bulls eye pattern is often seen</p>

232
Q

<p>What is the ddx of bull's eye maculopathy?</p>

A

<p>Cone dystrophy, AMD, stargardt's , fundus flavimaculatus, albinism, central areolar choroidal dystrophy, clofazimine toxicity, fucosidosis</p>

233
Q

<p>Which ocular tissue is affected by Thioridazine (Mellaril)?</p>

A

<p>Mellaril concentrates in uveal tissue with RPE damage</p>

234
Q

<p>What are the symptoms of Thioridazine toxicity?</p>

A

<p>Decreased VA, nyctalopia, and altered color vision </p>

235
Q

<p>What is the toxic dose of Mellaril?</p>

A

<p>>1200mg/day</p>

236
Q

<p>What are the ocular findings of Thioridazine toxicity?</p>

A

<p>Peripheral pigmentary retinopathy, pigment deposition of retinopathy, cornea and lens</p>

237
Q

<p>What are the ERG findings of Mellaril toxicity?</p>

A

<p>Depressed a and b waves</p>

238
Q

<p>What are the ocular findings of chlorpromazine (Thorazine) toxicity?</p>

A

<p>Pigment deposition (crystals) in eyelids, cornea, lens and retina</p>

239
Q

<p>What are the ocular findings of Chloramphenicol toxicity?</p>

A

<p>Atrophy of maculopapillar bundle VF: cecocentral scotoma</p>

240
Q

<p>What are the ocular findings of Quinine toxicity?</p>

A

<p>Fine RPE mottling, retinal vascular attenuation, disc pallor</p>

241
Q

<p>What are the symptoms of quinine toxicity?</p>

A

<p>Blurred vision, visual field loss, photophobia, transient blindness and sometimes patient may comatose</p>

242
Q

<p>What are symptoms of acute toxicity of Quinine?</p>

A

<p>blurred vision, nyctalopia, loss of hearing, retinal opacification with cherry red spot, dilated retinal vessels. </p>

243
Q

<p>What are the ocular signs of tamoxifen toxicity?</p>

A

<p>Fleck like crystalline retinopathy with refractile retinal deposits in a ring around macula and mild CME</p>

244
Q

<p>What are the signs of tamoxifen toxicity on FA?</p>

A

<p>Macular edema</p>

245
Q

<p>What is canthaxanthine?</p>

A

<p>Oral tanning agent which can cause toxicity at higher cumulative doses of >35g</p>

246
Q

<p>What are the signs of canthaxanthine toxicity?</p>

A

<p>Refractile yellow deposits in a ring around the fovea, "gold-dust" retinopathy</p>

247
Q

<p>Name the agent that causes crystalline retinopathy due to oxalate crystals?</p>

A

<p>Methoxyflurane. These crystals are permanent</p>

248
Q

<p>Describe the etiology of talc retinopathy?</p>

A

<p>Talc deposits in the lungs and cause pulmonary AV shunts, and eventually passes in to the systemic circulation. It can cause arteriolar occlusions, resulting in ischemic maculopathy, retinal NV and VH</p>

249
Q

<p>Describe NIctotinic acid maculopathy?</p>

A

<p>Atypical non leaking CME due to intracellular edema of Muller's cells</p>

250
Q

<p>What are the symptoms of nicotinic acid maculopathy?</p>

A

<p>Blurred vision with metamorphopsia. CME DOES NOT leak on FA</p>

251
Q

<p>What ocular structure is damaged by Digoxin?</p>

A

<p>Direct effect on cones.</p>

252
Q

<p>What are the symptoms of Digoxin toxicity?</p>

A

<p>Xanthopsia (yellow vision), blurred vision, paracentral scotomas</p>

253
Q

<p>What are the adverse effects of Ergotamine? migraine medication</p>

A

<p>It is a vasocontrictor of retinal vessels resulting in CME, CVO, papillitis, optic disc pallor, orthostatic hypotension, postpartum hemorrhages</p>

254
Q

<p>Which medicine causes transient blue hue to the vision 1-2 hours after ingestion?</p>

A

<p>Sildenafil (viagra), Tadalafil (Cialis), Vardenafil (Levitra)</p>

255
Q

<p>What is oral bay?</p>

A

<p>Oval island of pars plana epithelium immediately posterior to ora serrata</p>

256
Q

<p>What is meridional fold?</p>

A

<p>Elevated fold of retina in upper nasal quadrant</p>

257
Q

<p>What is meridional complex?</p>

A

<p>Meridional fold extending to posterior aspect of a ciliary process. It is a normal variation of anatomy at ora serrata</p>

258
Q

<p>What is vitreoretinal tuft?</p>

A

<p>Small retinal projection of retinal tissue</p>

259
Q

<p>Give a list of lesions NOT predisposed to RD?</p>

A

<p>White without pressure, pigment clumping, diffue chorioretinal atrophy, peripheral microcystoid changes, paving stone degeneration, oral pigmentary degeneration, Degenerative "senile" retinoschisis</p>

260
Q

<p>Name the retinal lesions that predispose to RD?</p>

A

<p>Lattice degeneration, Snail track degeneration, Zonuloretinal traction tufts, snow flake degeneration</p>

261
Q

<p>Explain white without pressure?</p>

A

<p>Geographic areas of peripheral retinal whiteningMore common in young individuals, AA and myopes</p>

262
Q

<p>Describe degenerative "senile" retinoschisis?</p>

A

<p>Splitting of OPL, bilateral, elderly patients, no risk of RD</p>

263
Q

<p>Describe reticular retinoschisis?</p>

A

<p>Splitting of NFL, 41% bilateral, 18% of adults population, , always posterior to peripheral cystoid</p>

264
Q

<p>What are the signs that differentiate RD from retinoschisis?</p>

A

<p>In Reitnoschisis: NO RPE degeneration, Neg shafer's sign, absolute scotoma (in RD, it is relative scotoma), PRP blanches underlying RPE (RD will not blanch), no shifting fluid and appears dome shaped</p>

265
Q

<p>What is the most common location of paving stone/cobblestone degeneration?</p>

A

<p>Usually inferior and 33% bilateral. Increased incidence with age and myopia</p>

266
Q

<p>What is the pathology of paving stone degeneration?</p>

A

<p>Degeneration of choroid and retina, loss of outer retinal layers, RPE absent and firm adhesion between retina and bruch's membrane/choroid. No predispostion to RD</p>

267
Q

<p>What is the prevalence of lattice degeneration?</p>

A

<p>Occurs in 7% of population, more common in myopic eyes, no sex predilection. Often bilateral and usually superotemporal. Usually found in 20-35% of eyes with RD. 0.5% risk that pt with lattice will develop an RD</p>

268
Q

<p>What is the pathology behind lattice degeneration?</p>

A

<p>Discontinuity of ILM, overlying pocket of liquid vitreous, condensation and adherence of vitreous at margin of lesion, focal area of retinal thinning with loss of inner retinal layers, melanin-laden macrophages, fibrous thickening of retinal vessel walls</p>

269
Q

<p>What are the treatment options for lattice?</p>

A

<p>Consider txt of fellow eye if hx of RD from lattice. No proof that prophylactic treatment prevents RD. </p>

270
Q

<p>What is the etiology of RRD?</p>

A

<p>A retinal break allows liquid vitreous access to subretinal space</p>

271
Q

<p>What is the most common location for RRD?</p>

A

<p>Most tears are located superiorly between 10 and 2'O clock positions</p>

272
Q

<p>What is a giant retinal tear?</p>

A

<p>A tear that is >3 clock hours or 90 degrees, associated with trauma, myopia, 50% risk of RD in fellow eye</p>

273
Q

<p>What are the risk factors for retinal tear?</p>

A

<p>age, hx of RD in the fellow eye, high myopia, fam hx, lattice, trauma, cataract sx, DM, YAG laser capsulotomy</p>

274
Q

<p>What are the ocular findings of RD?</p>

A

<p>Detached retina is opaque, corrugated and undulates, +shafer's sign, decreased IOP, VH, non shifting SRF</p>

275
Q

<p>What are the signs of lang standing RD?</p>

A

<p>Thin retina, small breaks or dialysis, demarcation lines, underlying RPE atrophy, PVR, macrocysts, subretinal precipitates, may have increased IOP</p>

276
Q

<p>What are the ddx of RD?</p>

A

<p>RRD, TRD and Exudative RD</p>

277
Q

<p>What is the criteria for pneumatic retinopexy?</p>

A

<p>Single break in superior 8 clock hoursMultiple breaks within 1-2 clock hoursConfidence that all breaks are foundPhakic patients </p>

278
Q

<p>What are the intraocular gases commonly used and what is the duration of those in the eye?</p>

A

<p>In the order of decreasing time in the eye:C3F8>C2F6>SF6>air</p>

279
Q

<p>What are the complications of cryo therapy?</p>

A

<p>PVR, CME, Uveitis, intraocular hemorrhage, chorioretinal necrosis</p>

280
Q

<p>What are the complications of scleral buckle surgery?</p>

A

<p>Ischemia (anterior or posterior segments), infection, perforation, strabismus, erosion or extrusion of implant, change in refractive error, ERM, cataract, glaucoma, new retinal tears, PVR and buckle failure</p>

281
Q

<p>What are the complications of SRF drainage?</p>

A

<p>hemorrhage, retinal tears, retinal incarceration, hypotony, vitreous loss and infection.</p>

282
Q

<p>What are the characteristics of silicone oil?</p>

A

<p>Higher surface gravity than waterHigher surface tension than other gasesALWAYS make iridotomy inferiorly (as oil floats to the top)</p>

283
Q

<p>What are the complications of silicone oil?</p>

A

<p>Cataract (100%), band keratopathy (24%), glaucoma (19%), corneal decompensation (8%)</p>

284
Q

<p>What is the prognosis of RD?</p>

A

<p>Scleral buckle has 91% success rateFinal vision depends on macular involvementWorse if macula is detached and also for longer duration.</p>

285
Q

<p>What is PVR?</p>

A

<p>Retinal break allows cells (RPE, glial cells and myofibroblasts) to prolferate on inner and outer surfaces of retina along scaffold of detached vitreous</p>

286
Q

<p>What is the most common reason for failure of retinal reattachment surgery?</p>

A

<p>PVR formation which usually happens in 4-6 weeks after initial repair</p>

287
Q

<p>How does PVR appear on B-scan?</p>

A

<p>Detached retina with triangle sign (transvitreal membrane connecting the 2 sides)</p>

288
Q

<p>What is the treatment for PVR?</p>

A

<p>Vitreoretinal surgery, successful in 70% of the cases, leading to anatomical success</p>

289
Q

<p>What is the etiology of exudative RD?</p>

A

<p>Uveitis (VKH, SO, para planitis, viral retinitis), tumors, glomerulonephritis, HTN, eclampsi/preeclampsia, hypothyroidism, coats disease, nanophthalmos, scleritis</p>

290
Q

<p>What are the signs of exudative RD?</p>

A

<p>shifting fluid, smooth retinal surface, no retinal break, retina right behind the lens (pathognomonic sign)</p>

291
Q

<p>What is the etiology of traction RD?</p>

A

<p>Penetrating trauma (PVR), proliferative retinopathies, PHPV, toxoplasmosis, vitreous degeneration</p>

292
Q

<p>What are the retinal findings of traction RD?</p>

A

<p>taut retinal surface, immobile, concave shape, no retinal break, no extension to the ora serrata.</p>

293
Q

<p>What is the pathology of traction RD?</p>

A

<p>SRF. photoreceptor degeneration, cystoid degeneration, glial membrane formation</p>

294
Q

<p>What causes folds on NFL?</p>

A

<p>ERM and RRD, only seen on OCT</p>

295
Q

<p>What causes folds on choroid? (choroidal folds)</p>

A

<p>Shrinkage of inner choroid or Bruch's membrane causing undulations of overlying RPE and outer retina</p>

296
Q

<p>What is the etiology of choroidal folds?</p>

A

<p>Mnemonic: THIN RPETumors, Hypotony, Inflammation(Thyroid eye disease)/idiopathic, NVM, retrobulbar mass, papilledema, extraocular hardware</p>

297
Q

<p>What are the FA findings of choroidal folds?</p>

A

<p>Light bands/crests contain thinner RPE, producing prominent choroidal fluorescence, dark bands/troughs contain compressed RPE, producing relative hypofluorescence </p>

298
Q

<p>What is the etiology of choroidal detachment?</p>

A

<p>Hypotony, uveitis, idiopathic, uremia, nanophthalmos (thickened sclera impedes vortex venous drainage), intraocular surgery (rapid change in IOP shears choridal perforating arteries), intense PRP</p>

299
Q

<p>What are the causes of suprachoroidal hemorrhage?</p>

A

<p>Rupture of small vessels with sudden decrease of IOP (open globe or surgery), may be expulsive with loss of intraocular contents through wound</p>

300
Q

<p>What is the clinical appearance of choroidal detachment?</p>

A

<p>Dark dome shaped retina</p>

301
Q

<p>What is the appearance of choroidal detachment on B-scan?</p>

A

<p>Echogenic convexity attached at scleral spur and vortex veins (not at optic nerve)</p>

302
Q

<p>What are the treatment options of choroidal detachment?</p>

A

<p>Treat the underlying disorderIf happens during surgery, close the globe and give mannitol IV; may require sclerotomies for drainageAlso can consider partial thickness scleral windows near vortex vein exit sites in 3 or 4 quadrants</p>

303
Q

<p>What causes choroidal ischemia?</p>

A

<p>Hypertensive retinopathy</p>

304
Q

<p>What is polypoidal choroidal vasculopathy?</p>

A

<p>Branching of inner choroidal vessels external to the choroicapillaries with polyp like terminal dilations. Classified as CNV 1, PCV is idiopathic and peripapillary</p>

305
Q

<p>In what patient population is PCV more commonly seen?</p>

A

<p>AA and Asians</p>

306
Q

<p>What are the risk factors for PCV?</p>

A

<p>HTN, smoking, genetic mutations in ARMS2, HTRA1, Y402H, C2, and CFH genes</p>

307
Q

<p>How to diagnose PCV?</p>

A

<p>ICG</p>

308
Q

<p>What are the treatment options for PCV?</p>

A

<p>Anti-VEGF injections or PDT</p>

309
Q

<p>What is the other name for PCV?</p>

A

<p>Posterior Uveal Bleeding Syndrome (PUBS)</p>

310
Q

<p>What is the most common intraocular benign tumor?</p>

A

<p>Choroidal nevus</p>

311
Q

<p>What is the most common intraocular malignant tumor?</p>

A

<p>Choroidal melanoma</p>

312
Q

<p>What are the demographics of choroidal nevus?</p>

A

<p> Usually unilateral, unifocal, increased frequency with age, prevalence in US population>49 years of age</p>

313
Q

<p>Which disease is associated with multifocal nevi?</p>

A

<p>Neurofibromatosis </p>

314
Q

<p>What are the clinical findings of choroidal nevi?</p>

A

<p>Flat slate-gray to dark brown choroidal lesion will ill-defined margins, surface drusen common, SRF and orange clumps of pigment are rare</p>

315
Q

<p>What are the risk factors for malignant transformation?</p>

A

<p>Mnemonic TFSOM: (To Find Small Ocular Melanoma)THICKNESS: >2 mmFLUID: SRFSYMPTOMS: dec VA, flashes or floatersORANGE pigment: LipofuscinMARGIN: Juxtapupillary location, =3mm from optic nerve</p>

316
Q

<p>What is the pathology of choroidal nevus?</p>

A

<p>Benign spindle cells with pigment</p>

317
Q

<p>What are the characteristics of choroidal cavernous hemangioma?</p>

A

<p>Congenital, unilateral vascular tumor</p>

318
Q

<p>What are the types of choroidal hemangioma?</p>

A

<p>Diffuse: Associated with Sturge-Weber syndromeCircumscribed: NOT associated with systemic disease</p>

319
Q

<p>What are the symptoms of choroidal hemangioma?</p>

A

<p>Blurred vision, micropsia, metamorphopsia, VA loss due to cystic macular retinal degeneration or adjacent exudative RD</p>

320
Q

<p>What are the ocular findings in "diffuse" type of hemangioma?</p>

A

<p>Generalized red-orange choroidal thickening, ("tomato catsup" fundus), may have elevated IOP </p>

321
Q

<p>What are the ocular findings in "circumscribed" type of hemangioma?</p>

A

<p>Red-orange dome shaped choroidal mass within 2DD of optic disc or fovea</p>

322
Q

<p>What is choroidal osteoma?</p>

A

<p>Tumor composed of bone</p>

323
Q

<p>What are the characteristics of Osteoma?</p>

A

<p>Sporadic, unifocal, bilateral in 20%, more common in women (90%)</p>

324
Q

<p>What are the clinical findings of osteoma?</p>

A

<p>Yellow-white to pale orange circumpapillary lesion with well defined pseudo-pod like margins. CNV and RPE disruption can cause progressive visual impairment</p>

325
Q

<p>What is the pathology of osteoma?</p>

A

<p>Plaque of mature bone involving full thickness choroid usually spares RPE </p>

326
Q

<p>What is the B-scan appearance of Choroidal osteoma?</p>

A

<p>Highly reflective plate-like lesion with orbital shadowing beyond the lesion</p>

327
Q

<p>What is the CT scan appearance of osteoma?</p>

A

<p>Plate like thickening of eye wall</p>

328
Q

<p>What is the other name for retinal capillary hemangioma?</p>

A

<p>Hemangioblastoma (vascular tumor)</p>

329
Q

<p>What disease is hemagioblastoma associated with ?</p>

A

<p>Von-Hippa-Lindau disease</p>

330
Q

<p>What is the inheritance pattern of hemagioblastoma?</p>

A

<p>SD, sporadic, Chromosome 3</p>

331
Q

<p>What are the systemic associations of VHL disease?</p>

A

<p>Bilateral retinal capillary hemangiomas (40-60%)Cystic cerebellar hemagioblastomas (60%)Renal cell carcinomaPheochromocytomaLiver, pancreas and epididymis cysts</p>

332
Q

<p>What is the most common cause of death in VHL?</p>

A

<p>Cerebellar hemangioblastoma</p>

333
Q

<p>What are the clinical findings of hemangioblastoma?</p>

A

<p>Red globular mass with prominent dilated tortuous afferent and efferent retinal blood vessels, exudative RD may develop</p>

334
Q

<p>What are the FA findings of hemangioblastoma?</p>

A

<p>Feeding arteriole fills rapidly and dye leaks unto vitreous and subretinal space</p>

335
Q

<p>What are the treatment options of hemagioblastoma?</p>

A

<p>PRP, cryotherapy or PDT</p>

336
Q

<p>What is retinal CAVERNOUS hemangioma?</p>

A

<p>Vascular tumor, congenital, associated with similar CNS or skin vascular lesions, unilateral, rarely progressive</p>

337
Q

<p>What are the ocular findings of retinal cavernous hemangioma?</p>

A

<p>Cluster of dark red intraretinal vascular sacs ("bunch of grapes" appearance) typically associated with an anomalous retinal vein, associated overlying gliosis, no exudates or detachments, may be VH</p>

338
Q

<p>What are the FA findings of retinal cavernous hemangioma?</p>

A

<p>Fluid levels within the vascular sacs</p>

339
Q

<p>What is the treatment for retinal cavernous hemangioma?</p>

A

<p>vitrectomy for nonclearing VH</p>

340
Q

<p>What is retinal astrocytoma?</p>

A

<p>Glioma arising from retinal glial cells (Astrocytic Hamartoma)</p>

341
Q

<p>Retinal hamartomas are associated with what diseases?</p>

A

<p>Tuberous sclerosis (multifocal, bilateral) and neurofibromatosis</p>

342
Q

<p>What are the clinical findings of retinal hamartomas?</p>

A

<p>yellow-white masses obscuring retinal vessels, calcification in some larger lesions, may have glistening, mulberry appearance or softer, fluffy appearance</p>

343
Q

<p>How is a combined hamartoma different from retinal hamartoma?</p>

A

<p>Combined hamartoma is a tumor composed of neurosensory retina and RPE, where as retinal hamartoma is a glioma from glial tissue. </p>

344
Q

<p>What is combined hamartoma associated with?</p>

A

<p>NF 2</p>

345
Q

<p>What are the characteristics of combined hamartoma?</p>

A

<p>Congenital, unilateral, unifocal, minimal progression</p>

346
Q

<p>What is the pathology of combined hamartoma?</p>

A

<p>Cords of proliferated pigment epithelium with excess blood vessels and glial tissue</p>

347
Q

<p>What is the treatment for combined hamartoma?</p>

A

<p>No treatment is available currently. Treat the symptoms.</p>

348
Q

<p>What is racemose hemagioma?</p>

A

<p>Congenital AV malformation</p>

349
Q

<p>What is racemose hemagioma associated with ?</p>

A

<p>Wyburn-Mason syndrome with AVM of the brain</p>

350
Q

<p>Where does choroidal malignant melanomas arise from?</p>

A

<p>85% from choroid, 10% from ciliary body and 5% from iris.</p>

351
Q

<p>What is the most common intraocular malignant tumor?</p>

A

<p>Choroidal malignant melanoma</p>

352
Q

<p>What are the risk factors of choroidal melanoma?</p>

A

<p>Ocular melanocytosis, sunlight exposure, uveal nevi, caucasian race, rare in AA and Asians, smoking, NF, dysplastic nevus syndrome, BDUMP syndrome</p>

353
Q

<p>What are the symptoms of choroidal melanoma?</p>

A

<p>Flashes or floaters, decreased VA and VF defect</p>

354
Q

<p>What are the clinical findings of choroidal melanoma?</p>

A

<p>Brown, dome shaped or mushroom shaped lesion orange pigment clumps (lipofuscin accumulation in RPE), sentinel vessel (dilated tortuous episcleral vessel), secondary glaucoma, may be amelanotic and appear as a pale mass</p>

355
Q

<p>What kind of cells are found in melanomas?</p>

A

<p>Spindle A and spindle B cells</p>

356
Q

<p>Describe Spindle A cells?</p>

A

<p>Slender, cigar shaped nucleus, with finely dispersed chromatin, no mitotic figures, low nucleus-chromatin ratio, tumors are considered benign nevi</p>

357
Q

<p>Describe Spindle B cells?</p>

A

<p>Oval larger nucleus and nucleolus with coarser chromatin, mitotic figures, tumors with both spindle A and spindle B cells are called spindle cell melanomas. </p>

358
Q

<p>What are epithelioid cells?</p>

A

<p>Polyhedral with abundant cytoplasm, poorly cohesive, distinct borders, most MALIGNANT, prominent eosinophilic or purple nucleolus ("look back at you") WORST prognosis</p>

359
Q

<p>What is mixed cell melanoma?</p>

A

<p>Composed of spindle and epithelioid cells</p>

360
Q

<p>What structure is required for identification to r/o tumor extension on gross examination?</p>

A

<p>Vortex veins</p>

361
Q

<p>How does choroidal melanoma appears on MRI?</p>

A

<p>Bright on T1, dark on T2</p>

362
Q

<p>What are the treatment options of melanoma?</p>

A

<p>Enucleation: Large tumor, optic nerve invasion, painful eye with poor visual potentialPlaque brachytherapy: Medium sized tumor with visual potential, or failure of laserResection: Most irido and iridociliary tumors, some ciliary body tumors and choroidal tumorsTranspupillary thermotherapy: small tumors</p>

363
Q

<p>What are the complications of melanoma treatment?</p>

A

<p>Cataracts, radiation retinopathy</p>

364
Q

<p>What are the methods of COMS? (Collaborative ocular melanoma study)</p>

A

<p>Defined small/medium/large tumors.Small: apical height: 1.5-2.4mm, basal diameter: 5-16mmMedium: apical height: 2.5-10mm, basal diameter =16mmLarge: apical height: >10mm, basal diameter: >16mm</p>

365
Q

<p>What is the treatment criteria of COMS?</p>

A

<p>Small tumors: Observation Vs treatmentMedium: Randomized to enucleation vs plaque brachytherapyLarge: Randomized to enucleation vs external beam radiation for 5 days and then enucleation</p>

366
Q

<p>What are the conclusions of COMS?</p>

A

<p>Small tumors: Low risk of death with in 5 yearsMedium: High risk of substantial vision loss from brachytherapy and does not change survivalLarge: Pre-enucleation radiation (PERT) does not change survival with tumors with metastases or w/o metastases</p>

367
Q

<p>What is the most common primary intraocular lymphoma?</p>

A

<p>Non-Hodgkin's B-cell lymphoma, large cell type</p>

368
Q

<p>What patient demographics are affected by intraocular lymphoma?</p>

A

<p>Older population (>70 years), immunocompromised patients, usually bilateral and multifocal</p>

369
Q

<p>What is the risk of concurrent systemic lymphoma?</p>

A

<p>Very high increased risk of primary CNS lymphoma</p>

370
Q

<p>What are the symptoms of intraocular lymphoma?</p>

A

<p>Blurred vision, floaters, dementia may occur</p>

371
Q

<p>What are the findings of primary intraocular lymphoma?</p>

A

<p>Creamy white, diffuses sub-RPE, vitritis, AC reaction, hypopyon, secondary glaucoma, multifocal atrophic or punched out lesions and exudative RD</p>

372
Q

<p>How to diagnose primary intraocular lymphoma?</p>

A

<p>MRI, LP, vitreous bx (low yield, atypical lymphocytes with prominent nucleoli, mitoses, cellular necrosis)</p>

373
Q

<p>What is the pathognomonic sign of lymphoma?</p>

A

<p>"leopard spots" on FA</p>

374
Q

<p>What are the treatment options for lymphoma?</p>

A

<p>Chemotherapy or XRT</p>

375
Q

<p>What is the prognosis of intraocular lymphoma?</p>

A

<p>Poor, mortality often within 2 years (mean survival is 22 months)</p>

376
Q

<p>What is the most common intraocular malignancy?</p>

A

<p>Metastases</p>

377
Q

<p>What is the most common site of primary tumor that metastases to choroid in women?</p>

A

<p>Breast carcinoma</p>

378
Q

<p>What is the most common site of primary tumor that metastases to choroid in men?</p>

A

<p>Lung carcinoma</p>

379
Q

<p>what is the ddx of AMelanotic choroidal mass?</p>

A

<p>Amelanotic melanoma, old SRH, choroidal osteoma, granuloma and posterior scleritis</p>

380
Q

<p>What causes carcinoma associated retinopathy?</p>

A

<p>Paraneoplastic syndrome from mainly small cell lung cancer, breast cancer and gynecologic cancer, rare, loss of photoreceptors without inflammation</p>

381
Q

<p>What antibodies are found in CAR?</p>

A

<p>Recoverin antibodies</p>

382
Q

<p>What causes bilateral diffuse uveal melanocytic proliferation? (BDUMPS)</p>

A

<p>Paraneoplastic syndrome (ovarian, uterine, lung cancer most common)</p>

383
Q

<p>What are the clinical findings of BDUMPS?</p>

A

<p>Orange or pigmented fundus spots, iris thickening and pigmentation</p>

384
Q

<p>What are the ERG findings of CAR?</p>

A

<p>Extinguished ERG due to photoreceptor loss without inflammation</p>

385
Q

<p>What are the ERG findings of BDUMPS?</p>

A

<p>Markedly reduced</p>

386
Q

<p>What are the retinal structures that absorb laser?</p>

A

<p>Melanin, Hemoglobin, Xanthophyll</p>

387
Q

<p>What are the wavelengths of the following lights?</p>

A

<p>Blue-green 488 and 514 nmGreen 514 nmYellow 577 nmRed 647 nmInfrared 810 nmNd:YAG 532 nm</p>

388
Q

<p>What are the parameters of PRP?</p>

A

<p>500 um spot size, 0.1-0.5 s duration1200-2000 spots, moderate white burn, 1 burn-width apart, 2 DD from fovea, 1 DD from optic nerve, 2 or more sessions</p>

389
Q

<p>What are the complications of PRP?</p>

A

<p>Choroidal effusion, exudative RD, permanent mydriasis, impairment of accommodation, VH, CME, CNV, angle-closure, retinal vascular occlusion</p>

390
Q

<p>What are the parameters of focal laser?</p>

A

<p>50-100 um spot size, 0.1 s duration, grid pattern, 1 burn-width apart, </p>

Friedman's Ophthalmology (12 decks)

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