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166 Cards in this Set
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malignant glaucoma caused by apposition of the iris to the cornea and/or the TM obstructing AH outflow
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Angle closure glc
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what is the mechanism of primary angle closure glc with pupil block
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iris and lens adhere; AH builds up in the PC and a pressure gradient btw the PC and AC form which pushes the iris forward towards the cornea (BOMBE) which thus blocks the TM
if PAS form permanent closure can result |
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what is iris bombe
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iris bulges anteriorly due to posterior pressure buildup seen in pupil block
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signs and symptoms of primary angle closure glc with pupil block
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elevated IOP (40-70+)
mid dilated pupl CRAO or CRVO bc of high IOP possible corneal edema NFL damage within 24 hrs haloes HA pain nausea |
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patient profile for angle closure glc
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white>black
females>males old>young hyperopes>myopes Eskimos >>> Asians sulfa meds |
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the typical profile of an angle closure glc patient is
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old hyperopic female; if asian greater risk
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mid dilated pupil
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iris is closest and tightest apposition to lens
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signs and symptoms of ACUTE primary ACG
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entire angle is involved
VA loss in days redness photophobia K edema haloes blurred vision nausea/emesis IOP > 45 mid dilated pupil mild AC rxn NFL loss within 48 hrs |
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after alleviating angle closure, why can IOP still be elevated
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because TM damaged
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goal of LPI in primary angle closure glc
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reestablish communication btw AC and PC thereby relieving PC pressure and allowing bombe to relax and open angle
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ddx of angle closure glc
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uveitic glaucoma
high IOP in this case is caused by inflammation; will have AC rxn DON'T USE PILO makes INFLAMMATION WORSE |
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what is the goal of treatment in angle closure glc
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to change angle anatomy not to decrease IOP
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tx of acute primary angle closure glc
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glycerin topical for K edema
beta blocker 2 drops pilo 2% if IOP <40 iopodine or alphagan 2 drops pred forte q 15 min diamox 500 mg osmoglyn isosorbide if DM LPI |
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when/what % of pilo be used in primary acute angle closure glc with pupil block
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2% bc > % causes increased CB congestion and greater pupil block
it should only be used if IOP < 40 bc with IOP>40, ischemia will prevent miotic effect only use when certain its AACG bc if its uveitic glc --> BAD |
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what treatment is always required in AACG
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LPI
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what happens with LPI
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new hole in iris is a new place for AH to go through this causes iris to flatten and relieves the bombe the angle should open
no longer have to rely on pupil bc the new hole does what the pupil does |
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what is the purpose of giving meds in AACG
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give meds in prep for LPI
to break pupil block and let iris work again |
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what is the role of laser iridoplasty
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burns are made and at each point the iris contracts causing the iris to be pulled taut and outt of the angle
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how do you clear corneal edema in AACG
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topical glycerin
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recurrent attack of angle closure that occurs with dim lighting that leads to pupil block but opens during sleep; see partial angle closure and PAS
characterized by episodic blur, haloes |
subacute intermittent ACG with pupil block
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are pressures normal or abnormal in subacute intermittent ACG with pupil block
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IOP can be normal
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what is the tx of subaucte ACG with pupil block
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LPI
dont need long term meds |
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what is the most common type of angle closure glc
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chronic primary ACG 80%
acute primary ACG 20% |
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characterized by asymptomatic closed angle (PAS superior) that is discovered on routine examination
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chronic primary angle closure glc with pupil block
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what is chronic primary ACG with pupil block misdiagnosed as commonly
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POAG
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tx of chronic primary ACG with pupil block
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LPI
meds trabeculolectomy if meds dont work |
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what other factor is attributed to ACG
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choroidal expansion
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what is choroidal expansion
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choroid expands into AC thereby collapsing the AC causing the iris and AC to rotate forward and flatten causing the chamber to shut and iris to lay over the cornea
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what drug can cause ACG
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topomax
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medical tx is given in what cases of primary angle closure as first line tx
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acute with pupil block only but soley for prep for sx
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what tx should be used if PAS is present in ACG
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lasers wont work therefore need trabeculolectomy
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what is the cause of primary ACG without pupil block
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plateau iris
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gonio description of any eye with deep AC and narrow angles due to last roll of iris that draps over forward displace ciliary processes
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plateau iris configuration
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angle that remains closed or occludable after LPI
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plateau iris syndrome
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how is plateau iris syndrome dx
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LPI
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causes of secondary angle closure with pupil block
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phacolytic
uveitic phacomorphic aphakia pseudoaphakia - reverese pupil block subluxlated lens |
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causes of secondary angle closure without pupil block
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peripheral iris pulled/pushed onto K
NVG Neoplastic ICE Ciliary Block Glc |
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corneal endothelial cells oversecrete causing DM to migrate and extend over the TM causing PAS
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ICE
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progressive angle closure by PAS
displaced pupil towards PAS ectopian uvaea stromal atrophy full thickness iris hole formation |
essential iris atrophy
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mild changes in iris and corneal edema with normal IOP
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chandler's syndrome
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malignant glaucoma due to aqueous misdirection syndrome anterior displacement of the iris and ciliary body; causes misdirection of aqueous into the vitreous and PC
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ciliary block glaucoma
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if one quadrant is closed on gonio, what should you do?
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refer for LPI
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what is the treatment for ciliary block glaucoma?
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atropine and acetazolamide
pilo and LPI do not work! |
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patient profile for pigment dispersion glc
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young myopic white males
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is the angle open or closed in pigmentary glc
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open
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what is the prescursor for pigmentary glc
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PDS
about 50% convert to pigmentary glc |
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what is seen in pigmentary glacuoma
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high diurnal IOP fluctuations
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what is the mechanism of pigmentary glc
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iris and lens zonules come in contact
due to posterior bowing of mid peripheral iris AH is trapped in AC causing reverse pupil block iris rubs on lens and piment is relased |
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layering of pigment seen centrally on corneal endothelium
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kruckenberg's spindle
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the prescense of kruckenberg spindle should prompt you to do what test
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check for TID
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where are TID in pigmentary glc located
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midperpipheral iris
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TID should prompt you to do what test
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gonio
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how does glc arise in PDS
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pigmented is accumulated in TM and the TM breaks down from having to process it
IOP from clogged and overworked TM |
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when is pigment released in PDS
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after dilation --> see it in AC
after exercise can see IOP rise |
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pigment on lens equator
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scheie line
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what is pathognmic for PDS/PG
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scheie line
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in which patients is scheie line seen
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black patients with PDS/PG
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where is pigment from PDS/PG mostly seen in gonio
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inferiorly
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pigment reversal sign
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more pigment seen superiorly due to burning out of TM
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how is the iris configured in PDS/PG
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concave
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pigment on Schwalbe's line
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Sampoaelsi's line
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T/F endo pigment and TID are uncommon in blacks with PDS/PG
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true
see lots of TM pigment though |
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tx of PG
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treat like POAG but dont use MIOTICS due to risk of RD
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why are miotics CI in PG
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because they can cause RDs and these pts have a higher incidence of retinal pathology
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what tx can be used in PG
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ALT or SLT since they are pigment dep it will be versy successful
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how often should you follow PDS/PG pts
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every 3-6 months bc of high diurnal variation
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what is reverse pupil block
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pressure builds up in AC and forces the iris backwards onto lens zonules as seen in PG/PDS
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why must PDS/PG patients be monitored frequently
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because of high diurnal variations
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peeling of anterior lens capsule due to heat/radiation
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exfoliation
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what is the difference btw exfoliation and PXE
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exfoliation - material is peeled off
PXE- material is being deposited on lens |
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deposiition of abnormal BM on anterior lens capsule and in TM
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PXE
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where does the abnormal BM arise from in PXE
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lens
iris CB uvea |
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T/F PXE is systemic disorder
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true
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is the angle opened or closed in PXE
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open
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patient characteristics of PXE
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60's-80's
bilateral asymetric northern Europeans rare in blacks |
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what is an important indicator of PXE
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peripupillary TID
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what condition is worse PXE or POAG
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PXE
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tx of PXE
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more meds
ALT SLT trabeculolectomy |
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where is pigment released from in PXE
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pupil border
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mechanism of PXE
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abnormal BM deposits in TM which blocks TM and leads to its dysfunction
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Is a lensectomy a viable tx option for PXE
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NO bc material doesn't come from lens!
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OHTN develops in what % of pts with PXE
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22-81%
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what is the likelihood of developing glc in PXE
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40% within 10 yrs
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what progresses faster POAG or PXE
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PXE
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is PXE easy to manage
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NO
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complications that arise in PXE
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cataract surgery is more difficult due to loss of zonular support
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characterized with inflammation, hyphema, TM changes occuriing within hours to days of trauma
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early traumatic glc
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characterized by angle recession and PAS that takes weeks to years
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late traumatic glc
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tear in CB (longitudinal m) occurring within 7 days of injury characterized by blood in AC
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hyphema
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can rebleeds occur in hyphema
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yes within 5-7 days
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what % of patients with hyphema develop angle recession
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50-90%
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the prognosis of developing angle recession after trauma depends on what
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the size of the hyphema
1/3 good 2/3 fair >2/3 poor |
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how does IOP become elevated in hyphema
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pupil block secondary to clot; the RBCs clot the AC angle
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tx of hyphema
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bed rest
atropine 1% BID Pred forte q1h aqueous suppressants |
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what drugs should be avoided in tx of hyphema
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PG, MIOTICS --> make inflammation worse
Asprin |
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what is the 24/24 rule for sickle positive pts with hyphema
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if IOP > 24 for 24 hrs then paracentisis is needed
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husks of old RBCs floating around in AC following traumatic persistent hyphema or vitreous heme
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ghost cell glc
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tx of ghost cell glc
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paracentis
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cleavage of CB muscles causing widening and deepening of angle
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angle recssion
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when does angle recession occur
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yrs after trauma
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unilateral glc should lead you to suspect
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angle recession glc
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what is the etiology of angle recession glc
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TM scarring and sclerosis
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what % of angle recession pts develop angle recession glc
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10-20%
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what must be done when diagnosing angle recessiom
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look at the fellow eye
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etiology of steroid induced glc
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steroids change the TM ability to process AH
GAGs accumulate |
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IOP increase is more common with topical or systemic steroids
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topical
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when does steroid induced glc occur
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2 weeks after onset
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what amount of pop are steroid responders
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2/3
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what % of steroid responders develop glc
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5%
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who is at greater risk of developing steroid induced glc
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myopes
POAG pts kids |
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steroid response depends on
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frequency
dose |
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uveitis and elevated IOP on association with hypermature cataract
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phacolytic glc
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hypermature cataract acuity
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LP only
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acute onset of pain and redness in non-seeing eye with hypermature cat
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phacolytic glc
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mechanism of phacolytic glc
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hypermature cat leaks out proteins which act as antigens; they go into AC and cause immune rxn resulting inflammation which cause macrophages to engulf them and go into TM where they block TM and cause IOP rise due to uveitis
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is the angle open or closed in phacolytic glc
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open but if inflammation is severe enough can have posterior synechiae, pupil block, and angle closure without pupil block
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tx of phacolytic glc
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lensectomy
vitrectomy temp meds - steroids, cycloplege, beta blockers, alpha agonists, CAI AVOID PG and MIOTICS |
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broken lens capsule due to trauma or surgery
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lens particle glc
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uveitis s/p cat extraction leading to inflammatory secondary glc that can be open or closed angle
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phacoanaphylactic uveitis
autoimmune response to lens antigens |
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unilateral or asymetric cat associated with asymetric shallowing of AC - see acute to intermitten red painful eye at nigh with blur and corneal edema
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phacomorphic glc
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ddx of phacomorphic glc
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primary angle closure
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cause of phacomorphic glc
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due to increasing lens thickness- the iris and lens appose each other can have secondary pupil block, bombe, and closure with PAS
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tx of phacomorphic glc
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treats with meds then do LPI
cat extraction |
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when should phacomorphic glc be suspected
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glaucoma with angle closure shallow chamber and asymmetric advanced cat
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what can occur due to lens ectopia lentis
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pupil block and angle closure
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causes of NVG
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ischemia to retina
CRVO DR Carotid artery dz |
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how does NVG arise
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hypoxia --> VEGF release -> neo in posterior iris --. NVI, angle neo
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what happens when neo of angle occurs
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vessels bridge scleral spur and arborize on TM forming fibrovascular membranes
tent like PAS which eventually zipper angle shut |
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what is the prognosis of NVG
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POOR
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what is seen in NVG
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inflammation and high IOP
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what is NVG refered to
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90 day glc bc it occurs 90 days after vascular occlusion
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what is unique about NVG
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secondary angle closure without pupil block
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what is the worst glc a pt can gave
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NVG
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what tests should be ordered in patients over 60 with anterior seg neo
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ESR and CRP
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tx of NVG
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atropine and Pred forte for inflammation
temp aqueous suppressants trabeculectomt PRP avastin and lucentis |
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what happens if episcleral venous pressure is elevated
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IOP will increased
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how can elevated episcleral venous pressure be diagnosed
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indirectly via gonio
see blood in SC |
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causes of elevated episcleral venous pressure
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carotid cavernous fistula
sturge weber syndrome cavernous sinus thrombosis retrobulbar tumor thyroid idiopathic |
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what is the only med that is useful in tx elevated episcleral venous pressure
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PG bc they bypassepiscleral venous system
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what should be suspected in a pt with unilateral red eye and ipsilateral IOP elevation
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acute angle closure
uveitic glc low flow carotid cavernous fistula |
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hot eye with pronounced episcleral injection and profuse AC rxn, high IOP, and variable discomfort
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acute anterior uveitis
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quiet and insidious IOP elevation
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chronic uveitis
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what type of uveitis is most likely to cause glc
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chronic uveitis
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how does glc arise in uveitis with pupil block
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iris and lens adhere cause posterior synchiae leading to bombe
PAS forms |
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how does glc arise in \uveitis without pupil block
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inflammatory debris is deposited and contracted within angle and pulls peripheral iris over TM causing closure by PAS
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how does open angle glc arise from uveitis
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TM outflow impeded by accumulation of inflammatory debris AND outflow infacility of proteins in AQ with excess flare
trabeculitis steroid responses |
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what leads to IOP rise in open angle glc due to uveitis
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flare greatly reduces outflow facility
aqueous becomes viscous |
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tx of glc due to uveitis
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pred forte be agressive
cycloplege phenylephrine to break syncheiae if cycloplege doesnt work beta blockers, alpha 2, CAI |
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what should not be used in tx of uveitic glc
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MIOTICS and PG make inflammation worse
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what type of glc drug is most effective in uveitic glc
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CAI
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cause of glc due to chronic iridocyclytis
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trabeculitis
IOP varies from 10-30 weekly |
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how does glc arise in young patients with uveitis
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inflammation must be SEVERE
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how does glc arise in old pts with uveitis
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chronic -. cummulative efefcts of inflammation and steroid use
min amounts of inflammation are needed to cause TM dysfunction |
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abrupts increased elevation of IOP with minimal pain, blur and haloes due to corneal edema; recurrent - eye is white and quiet may see some KPS
min. sympyomatic |
glaucomatocyclitic crisis aka Possner Schlossman Syndrome
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what is seen in gluacomatocycltic crisis
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IOP rise is dispproprtionate to inflammation
IOP precedes inflammation |
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patients with glaucomatocycltic crisis ONH and fields are
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normal
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how long does glaucomatocycltic crisis last
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hours to weeks
self limiting |
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mechanism of glaucomatocyclitic cirsis
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decreased outflow due to trabeculitis
PG E seen in high amounts which increases blood aq barrier permeability and leads to increased aq prod |
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what can cause trabeculitis
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herpres
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tx of glaucomatocycltic crisis
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self limiting
tx inflammation first then IOP NO MIOTICS or PG steroids are treatment of choice beta blockers, alpha 2, CAO |
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what should you look for in glaucomatocyclitic crisis
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AC cells
KPs |
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characterized by triad of heterochromia, iridocyclytic and cataract after secondary glc seen in young pts
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fuch's heterochromatic iridocylctis
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mech of fuch's hetero iridocycltic glc
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sclerosis of TM
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