Posterior Segment Flashcards
<p>What are the components of Vitreous?</p>
<p>99% Water, Type II and IX collagen, hyaluronic acid</p>
<p>What is the volume of vitreous cavity?</p>
<p>4 cubic cm</p>
<p>Name the attachment points of vitreous</p>
<p>Ora serrata, optic nerve, blood vessels, and macula</p>
<p>Name the layers of retina</p>
<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>
<p>On average, how many rods are in the retina?</p>
<p>120 million rods</p>
<p>On average how many cones are in the retina?</p>
<p>6 million cones</p>
<p>Few facts about rods:</p>
<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>
<p>Few facts about cones:</p>
<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>
<p>Name the 3 types of visual pigment present in the cones</p>
<p>S: Short wavelength: sensitive to blueM: Medium wavelength: Sensitive to greenL: Long wavelength: Sensitive to Red</p>
<p>What supplies the inner retina?</p>
<p>Central retinal artery</p>
<p>What supplies the outer retina?</p>
<p>Choriocapillaries</p>
<p>What layer of retina separates the outer retina from inner retina?</p>
<p>OPL: middle limiting membrane in OPL acts as a water shed region between inner retinal vascular supply and outer retinal vascular supply</p>
<p>When does macula finishes its differentiation?</p>
<p>4-6 months of age</p>
<p>What are the predominant cones in the macula?</p>
<p>Red and Green</p>
<p>Name the carotenoids in the macula?</p>
<p>Lutein (antioxidant) and Zeaxanthin (light screening)</p>
<p>What is the diameter of the fovea?</p>
<p>1500 um</p>
<p>What is the diameter of FAZ?</p>
<p>250-600 um</p>
<p>What is the diameter of the foveola?</p>
<p>350 um</p>
<p>What acts as inner blood retinal barrier?</p>
<p>Retinal vascular endothelial cells (Zonula occludens-tight junctions)</p>
<p>What acts as outer blood retinal barrier?</p>
<p>RPE</p>
<p>Describe the architecture of the following hemorrhages?Flame or splinter hemorrhages:Dot blot:Boat shaped (scaphoid):Dark hemorrhage:</p>
<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>
<p>What type of cells make up RPE?</p>
<p>Monolayer of hexagonal cells with apical microvilli</p>
<p>What type of arrangement is noted between RPE and outer segments of photoreceptors?</p>
<p>Apical to apical arrangement resulting on potential subretinal space</p>
<p>What are the functions of RPE?</p>
<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>
<p>Name the layers of Bruch's membrane</p>
<p>Basement membrane (inner basal lamina of RPE)Inner CollagenElastic tissueOuter collagenBasement membrane (outer basal lamina of choriocapillaries)</p>
<p>What cells produce myelin in peripheral nervous system?</p>
<p>Schwann cells</p>
<p>What cells produce myelin in the CNS?</p>
<p>Oligodendrocytes</p>
<p>What are the attachments of choroid to sclera?</p>
<p>Scleral spur, at optic nerve, vortex veins and long and short posterior ciliary vessels</p>
<p>What are the layers of choroid?</p>
<p>Bruch's membrane (true BM)Choriocapillaries (endothelial cells with wide fenestrations)Stroma (mainly blood vessels)Suprachoridal space</p>
<p>What is the major source of nutrition for RPE and outer retinal layers?</p>
<p>Choriocapillaries</p>
<p>Name the arterial blood supply of choroid?</p>
<p>1-2 long and 15-20 short posterior ciliary arteries</p>
<p>Where does choriocapillaries drain?</p>
<p>Drain via vortex veins to superior and inferior ophthalmic veins</p>
<p>When do rods and cones shed outer segments?</p>
<p>Rods shed outer segments during the day (dawn)Cones shed in the night (dusk)</p>
<p>What are the visual pigments of retina?</p>
<p>3 cone pigments and 1 rod pigment. Each consists of 11-cis-retinal+protein opsin</p>
<p>What is the peak sensitivity of rods?</p>
<p>505 nm (blue)</p>
<p>What is the peak sensitivity of cones?</p>
<p>555 nm</p>
<p>Name the cells that contribute to flash ERG?</p>
<p>Photoreceptors, Muller's and bipolar cells. Ganglion cells do not respond or participate in ERG.</p>
<p>What are the components of ERG?</p>
<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>
<p>Name the conditions with decreased b-wave amplitude or electronegative ERG?</p>
<p>CRAO, ischemic CVO, DM</p>
<p>What is Arden ratio?</p>
<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>
<p>Describe the ultrasound characteristics of retinal lesions? (in the following sequence below)LESION-SHAPE-INTERNAL REFLECTIVITYMelanomaChoroidal hemangiomaMetastasisNevusChoroidal hemorrhageDisciform lesion</p>
<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>
<p>Define reflectivity on A-scan and B-scan?</p>
<p>A-scan: Height of spikeB-scan: Signal brightness</p>
<p>What frequency of light is absorbed by Fluorescein?</p>
<p>Absorbs blue light at 465-490 nm and emits yellow-green light at 520-530 nm</p>
<p>\_\_\_\_\_% of Fluorescein is bound to albumin and serum proteins. \_\_\_\_\_\_% excreted from \_\_\_\_\_ and \_\_\_\_\_with in 24-36 hours.</p>
<p>80% bound to albumin. 90% excreted from kidneys and liver.</p>
<p>Is pregnancy a contradiction for FA?</p>
<p>Only the first trimester</p>
<p>Describe the types of Hyper fluorescence?</p>
<p>Leakage(NV), staining (scar, collagen), Pooling (CSR, PED), Window defects (GA, RPE defects)</p>
<p>Describe the types of hypofluorescence?</p>
<p>Blockage (RPE, blood, xanthophyll)Filling defect (ischemia)</p>
<p>Why is macula dark on FA?</p>
<p>Dark spot is due to blockage by xanthophyll in OPL and excess of melanin and lipofusin</p>
<p>What frequency of light is absorbed by ICG?</p>
<p>ICG absorbs light in near infrared range (790-805 nm) and emits at 770-88- nm</p>
<p>How is ICG excreted from the body?</p>
<p>Excreted via liver into bile</p>
<p>What are the contraindications for ICG?</p>
<p>Allergic to Iodine, uremic syndrome and liver disease</p>
<p>What is the best way to look at retinal pathology in patients with asteroid hyalosis?</p>
<p>FA</p>
<p>What is asteroid hyalosis?</p>
<p>Refractile particles (calcium soaps) suspended in vitreous</p>
<p>Describe the pathology of asteroid hyalosis?</p>
<p>Gray spheres with "Maltese cross" birefringence on polarization</p>
<p>What is synchisis scintillans?</p>
<p>Cholesterol deposits derived from old vitreous hemorrhage. Rare, unilateral, s/p trauma. crystals sink to the bottom due to liquefaction of vitreous</p>
<p>What is Berlin's edema?</p>
<p>Not a true edema. It is called Commotio retinae - transient retinal whitening due to disruption of photoreceptor outer segments</p>
<p>Describe the mechanism of Choroidal rupture?</p>
<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>
<p>What is the most common location of choroidal rupture?</p>
<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>
<p>Name the trauma to the retina and choroid caused by transmitted shock waves and necrosis from high velocity injuries.</p>
<p>Retina sclopetaria?</p>
<p>What are the findings of sclopetaria?</p>
<p>Rupture of retina and choroid with commotio and VH. Lesion heals with white fibrous scar and RPE changes</p>
<p>What is the most common retinal tear associated with trauma?</p>
<p>Retinal dialysis. </p>
<p>What are the most common locations of retinal dialysis?</p>
<p>Inferotemporal 31% and Superonasal 22%</p>
<p>What is the pathognomonic sign for retinal trauma?</p>
<p>Avulsion of vitreous base</p>
<p>Name the 4 most common retinal breaks?</p>
<p>Horseshoe tear, operculated hole, retinal dialysis and macular hole</p>
<p>Describe the treatment options for common retinal breaks?1. Horseshoe tear2. Operculated hole3. Retinal dialysis with RD4. Macular hole</p>
<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>
<p>Name few causes of Purtscher's retinopathy?</p>
<p>Head trauma, compression injury to the lungs or trunk, fat /amniotic/ air embolism, pancreatitis, dermatomyositis.</p>
<p>What are the unique findings of Purtscher's retinopathy?</p>
<p>CWS, retinal whitening, hemorrhages, papillitis, ?RAPD</p>
<p>Name the syndrome that causes VH secondary to subarachnoid hemorrhage?</p>
<p>Terson's syndrome</p>
<p>The fracture of what kind of bones result in fat emboli syndrome?</p>
<p>Long medullated bone fractures</p>
<p>What are the unique features of fat emboli syndrome?</p>
<p>CWS, small blot hemorrhages, rarely CRAO</p>
<p>What type of injury is associated with Whiplash retinopathy?</p>
<p>Severe flexion/extension of head and neck without direct eye injury</p>
<p>Name the unique features of whiplash retinopathy?</p>
<p>Mild reduction of vision (20/30), gray swelling of fovea, foveal pit</p>
<p>What causes ERM?</p>
<p>contraction of proliferations at vitreoretinal junction cause retinal striae, folds and macular edema</p>
<p>What are the statistics of ERM?</p>
<p>12% prevalence in 43-86 yo, 20% bilateral, 2% association with retinal folds</p>
<p>Name the conditions associated with ERM?</p>
<p>DM, retinal vascular occlusions, anomalous, PVD, high myopia, retinal hole/tears, previous ocular or laser surgery, and increasing age.</p>
<p>What causes a full thickness macular hole (FTMH)?</p>
<p>Tangential traction on foveal region by posterior cortical vitreous</p>
<p>Name the factors associated with FTMH?</p>
<p>Age (senile), may develop after trauma, surgery, CME or inflammation</p>
<p>What is Watzke-Allen sign?</p>
<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>
<p>What are the treatment options for macular hole?</p>
<p>Stage 1: Observation or Ocriplasmin (Jetrea)Stages 2-4: PPV/MP/gas tamponade</p>
<p>What is the prognosis of macular hole?</p>
<p>Good: recent onset and <400umPoor: For >1 year duration and larger holes</p>
<p>What frequency of light can cause solar retinopathy?</p>
<p>Blue (441nm) and near UV light (325-250 nm). >90 seconds of sun gazing can cause photochemical retinal damage</p>
<p>What factors are associated with solar retinopathy?</p>
<p>solar eclipse, psychiatric disorders, religious rituals, or ingestion of hallucinogens</p>
<p>What factors are associated with CSR?</p>
<p>HTN, steroid use, psychiatric medication, type A personality</p>
<p>What is the buzzword for leakage on FA for CSR?</p>
<p>"Smokestack" appearance (10%)"Expansile dot" of hyperfluorescence (80%)</p>
<p>Name the findings of CSR on OCT?</p>
<p>serous retinal elevation, PED or SRF, thick choroid</p>
<p>What are the treatment options for CSR?</p>
<p>Laser for parafoveal spotsPDT for subfoveal spotsSpironolactone to eplerenone for chronic CSR</p>
<p>What are the indications for treatment of CSR?</p>
<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>
<p>What are the risk factors for AMD?</p>
<p>Age, Fam hx, female, Caucasian race, smoking, nutrition, light iris color, hyperopia, HTN, photic exposure</p>
<p>What are the characteristics of dry or non-exudative AMD?</p>
<p>Drusen (80-90%), pigmentary changes and RPE atrophy</p>
<p>What are the characteristics or wet or exudative AMD?</p>
<p>CNV</p>
<p>What is the drusen size classification?</p>
<p>Small: <64 umIntermediate: 64-124 umLarge: >/= 125 umin diameter</p>
<p>What is the Ddx for yellow foveal spot?</p>
<p>Solar retinopathy, Adult vitelliform dystrophy, Best's dz, CSR, lamellar hole, CME, pattern dystrophy, old subretinal hemorrhage</p>
<p>What are the types of CNV?</p>
<p>Type 1: CNV under RPE. Eg: PCV Type 2: CNV above RPE or subretinalType 3: Retinal angiomatous proliferation (RAP)</p>
<p>What type of AREDS is recommended for smokers and why?</p>
<p>AREDS2 was recommended for smokers due to lack of beta carotene. </p>
<p>What are the adverse affects reported with AREDS?</p>
<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>
<p>What additional components were tested in AREDS 2?</p>
<p>Lutein, Zeaxanthin, and omega-3 fatty acids</p>
<p>What VEGF isoform does Macugen binds to?</p>
<p>Isoform 165 of VEGF-A</p>
<p> Which anti-VEGF acts a fusion receptor decoy?</p>
<p>Aflibercept or Eylea</p>
<p>Which anti-VEGF binds to all isoforms of VEGF?</p>
<p>Bevacizumab (Avastin)</p>
<p>What is the mnemonic for angioid streaks?</p>
<p>PEPSI: Pseudoxanthoma elasticumEhler's Danlos, Paget's dz, SCD, idiopathic and B-thal</p>
<p>How to define pathologic myopia?</p>
<p>High myopia: AL>26mm, >-6D of myopiaPathologic myopia: AL>32.5 mm, >-8D of myopia</p>
<p>What are the few adverse but rare side effects of anti VEGF injections?</p>
<p>Anti-thrombotic events (ATE) such as HTN, stroke and MI</p>
<p>What type of organism cause POHS and which part of US is it endemic to?</p>
<p>Histoplasma capsulatum (dimorphic fungus). Endemic to Mississippi and Ohio river valley. </p>
<p>What percent of patients with ocular signs are positive for skin test?</p>
<p>90%</p>
<p>What type of autoimmune diseases are associated with POHS?</p>
<p>HLA-B7, HLA-DRW2</p>
<p>What are the signs of primary infection of POHS?</p>
<p>Mostly systemic with self limited flu like illness with dissemination to liver, spleen and choroid.</p>
<p>What are the signs of primary choroidal inflammation?</p>
<p>Granulomatous lesions with unapparent inflammation that resolves with small atrophic scars (Histo spots) which may disrupt Bruch's membrane.</p>
<p>What is the triad of POHS?</p>
<p>Peripapillary atrophy, multiple punched out lesions, and maculopathy (CNV).</p>
<p>What is the risk of CNV in POHS?</p>
<p>1% if no signs of POHS in the fellow eye4% if peripapillary atrophy25% if histo spots are in the macula</p>
<p>What are angioid streaks?</p>
<p>Peripapillary linear cracks in thickened, degenerated, and calcified Bruch's membrane</p>
<p>What is the risk with angioid streaks?</p>
<p>Subretinal hemorrhage can occur with minor trauma</p>
<p>What are the findings of pathologic myopia?</p>
<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>
<p>What was the objective of macular photocoagulation study (MPS) and what were the results?</p>
<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>
<p>What was the objective of TAP (Tx of AMD with photodynamic therapy (PDT) trial) and what were the results?</p>
<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>
<p>What was the objective of AREDS study and what were the results?</p>
<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>
<p>What was the objective of "AREDS 2" study and what were the results?</p>
<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>
<p>What was the objective of "VISION" (VEGF inhibition in neovascular AMD) trial and what were the results?</p>
<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>
<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>
<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>
<p>What was the objective of "ANCHOR" trial and what was the conclusion? (Anti-VEGF for predominantly classic CNV in AMD)</p>
<p>O: Compare Ranibizumab with PDT for subfoveal CNV in AMDR: Ranibizumab is superior to PDT</p>
<p>What was the objective of "VIEW 1/2" trial and what was the conclusion? (Aflibercept for CNV in AMD)</p>
<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>
<p>What are the generic names of antivegf injections?Aflibercept:Ranibizumab:Bevacizumab:Pegabtanib:</p>
<p>Aflibercept: EyleaRanibizumab: LucentisBevacizumab: AvastinPegabtanib: Macugen</p>
<p>What was the objective and conclusion of "CATT" trials? (Comparison of AMD treatment trials)</p>
<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>
<p>What was the objective and what were the results of "IVAN" study? (Alternative tx options to inhibit VEGF in CNV from AND)</p>
<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>
<p>How does edema appears histologically?</p>
<p>clear cystoid spaces</p>
<p>Histologically, how does lipid deposits look like?</p>
<p>Yellow lesions, hard exudates with eosinophilic and PAS positive</p>
<p>What are microaneurysms?</p>
<p>Outpouching of capillary walls</p>
<p>What are cotton wool spots?</p>
<p>Infarction of NFL(usually secondary to occlusion of retinal arteriole)</p>
<p>What is the mnemonic for ddx for CME?</p>
<p>DEPRIVENDM, Epinephrine use, Parsplanitis, RP, Vein occlusions, Irvine Gass, E2 prostaglandins, and Nicotinic acid maculopathy</p>
<p>Name the causes of CME that DOES NOT LEAK on FA?</p>
<p>Juvenile retinoschisisNicotinic acid maculopathyGoldmann-Favre syndromeRP variants</p>
<p>What is macular telangiectasia? (MacTel)</p>
<p>Microaneurysmal and saccular dilation of parafoveal vessels. Formerly called parafoveal/juxtafoveal telangiectasia</p>
<p>What is the classification of MacTel?</p>
<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>
<p>What are the findings of hypertensive retinopathy?</p>
<p>AV nicking "copper or silver wiring", hemorrhages, exudates, CWS</p>
<p>What are the findings of hypertensive choroidopathy?</p>
<p>Elsching's spots (non perfusion of choriocapillaries), Siegrist streak (reactive RPE hyperplasia along sclerosed choroidal vessel) and exudative RD</p>
<p>What are the findings of hypertensive optic neuropathy?</p>
<p>Florid disc edema with macular exudate, linear flame hemorrhages</p>
<p>Describe severe NPDR "4-2-1 rule"?</p>
<p>4 quadrants of intraretinal hemorrhages/MAs2 quadrants of venous bleeding1 quadrant of IRMAVery severe NPDR: 2 or more of the above criteria</p>
<p>Define PDR and HR-PDR?</p>
<p>PDR: NV of disc or elsewhereHR-PDR: 1. NVD >/= 1/4 to 1/3 disc area2. NVD w/ VH3. NVE w/ VH</p>
<p>Define CSME?</p>
<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>
<p>What are the main causes of vision loss in NPDR?</p>
<p>Macular edema or ischemia</p>
<p>What are the main causes of vision loss in PDR?</p>
<p>TRD, NVG, and VH</p>
<p>What is a diabetic cataract?</p>
<p>Aldose reductase pathway. converts glucose to sorbitol and fructose. </p>
<p>What is diabetic iridopathy?</p>
<p>Iris NV, lacy vacuolization of iris pigment epithelium, PAS+</p>
<p>What is the histologic signs of diabetic retinopathy?</p>
<p>Selective loss of pericytes, thickening of BM, lacy vacuolization of iris pigment epithelium, intraepithelial vacuoles containing glycogen</p>
<p>What are the adverse effects of PRP?</p>
<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>
<p>What are the indications for vitrectomy?</p>
<p>NCVHcombined RRD and TRD of the foveaMacular threatening TRDRefractory macular edema from tractional hyaloid faceProgressive fibrovascular proliferation despite PRP 360Ghost cell glaucoma</p>
<p>What conditions exacerbate diabetic retinopathy?</p>
<p>HTN, puberty, pregnancy, renal disease, anemia</p>
<p>What was the objective of "DRS" study and what were the results?</p>
<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>
<p>What was the objective for ETDRS and what were the results?</p>
<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>
<p>What was the objective for "DRVS" (Diabetic retinopathy vitrectomy study) and what were the results?</p>
<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>
<p>What was the objective for "DCCT" (Diabetes control and complications trial) and what were the results?</p>
<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>
<p>What was the objective for "UKPDS" (United Kingdom prospective diabetes study) and what were the results?</p>
<p>R: Type 2 diabetic patients benefit from intensive glycemic control, as do type 1 diabetic patients</p>
<p>What was the objective for "UKPDS-HDS" (United Kingdom prospective diabetes study-HTN in diabetes study) and what were the results?</p>
<p>R: Tight BP control reduced the risk of complications from DR</p>
<p>What are the results of "RISE, RIDE, RESTORE/RESOLVE" studies?</p>
<p>All these studies looked at efficacy of Ranibizumab for DME and found that Lucentis is superior to focal laser for DME treatment</p>
<p>What are the conclusions of DRCR.net?</p>
<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>
<p>What are the few facts of SCR?</p>
<p>It is a form of proliferative retinopathy, usually equatorial or pre-equatorial. Most severe in HbSC disease. </p>
<p>What is the prevalence of SCR in SC patients?</p>
<p>SC>SThal>SS>SA</p>
<p>What are the findings in SCR?</p>
<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>