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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
Angle closure glc
what is the mechanism of primary angle closure glc with pupil block
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
what is iris bombe
iris bulges anteriorly due to posterior pressure buildup seen in pupil block
signs and symptoms of primary angle closure glc with pupil block
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
patient profile for angle closure glc
white>black
females>males
old>young
hyperopes>myopes
Eskimos >>>
Asians
sulfa meds
the typical profile of an angle closure glc patient is
old hyperopic female; if asian greater risk
mid dilated pupil
iris is closest and tightest apposition to lens
signs and symptoms of ACUTE primary ACG
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
after alleviating angle closure, why can IOP still be elevated
because TM damaged
goal of LPI in primary angle closure glc
reestablish communication btw AC and PC thereby relieving PC pressure and allowing bombe to relax and open angle
ddx of angle closure glc
uveitic glaucoma
high IOP in this case is caused by inflammation; will have AC rxn

DON'T USE PILO makes INFLAMMATION WORSE
what is the goal of treatment in angle closure glc
to change angle anatomy not to decrease IOP
tx of acute primary angle closure glc
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
when/what % of pilo be used in primary acute angle closure glc with pupil block
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
what treatment is always required in AACG
LPI
what happens with LPI
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
what is the purpose of giving meds in AACG
give meds in prep for LPI
to break pupil block and let iris work again
what is the role of laser iridoplasty
burns are made and at each point the iris contracts causing the iris to be pulled taut and outt of the angle
how do you clear corneal edema in AACG
topical glycerin
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
are pressures normal or abnormal in subacute intermittent ACG with pupil block
IOP can be normal
what is the tx of subaucte ACG with pupil block
LPI
dont need long term meds
what is the most common type of angle closure glc
chronic primary ACG 80%
acute primary ACG 20%
characterized by asymptomatic closed angle (PAS superior) that is discovered on routine examination
chronic primary angle closure glc with pupil block
what is chronic primary ACG with pupil block misdiagnosed as commonly
POAG
tx of chronic primary ACG with pupil block
LPI
meds
trabeculolectomy if meds dont work
what other factor is attributed to ACG
choroidal expansion
what is choroidal expansion
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
what drug can cause ACG
topomax
medical tx is given in what cases of primary angle closure as first line tx
acute with pupil block only but soley for prep for sx
what tx should be used if PAS is present in ACG
lasers wont work therefore need trabeculolectomy
what is the cause of primary ACG without pupil block
plateau iris
gonio description of any eye with deep AC and narrow angles due to last roll of iris that draps over forward displace ciliary processes
plateau iris configuration
angle that remains closed or occludable after LPI
plateau iris syndrome
how is plateau iris syndrome dx
LPI
causes of secondary angle closure with pupil block
phacolytic
uveitic
phacomorphic
aphakia
pseudoaphakia - reverese pupil block
subluxlated lens
causes of secondary angle closure without pupil block
peripheral iris pulled/pushed onto K

NVG
Neoplastic
ICE
Ciliary Block Glc
corneal endothelial cells oversecrete causing DM to migrate and extend over the TM causing PAS
ICE
progressive angle closure by PAS
displaced pupil towards PAS
ectopian uvaea
stromal atrophy
full thickness iris hole formation
essential iris atrophy
mild changes in iris and corneal edema with normal IOP
chandler's syndrome
malignant glaucoma due to aqueous misdirection syndrome anterior displacement of the iris and ciliary body; causes misdirection of aqueous into the vitreous and PC
ciliary block glaucoma
if one quadrant is closed on gonio, what should you do?
refer for LPI
what is the treatment for ciliary block glaucoma?
atropine and acetazolamide
pilo and LPI do not work!
patient profile for pigment dispersion glc
young myopic white males
is the angle open or closed in pigmentary glc
open
what is the prescursor for pigmentary glc
PDS

about 50% convert to pigmentary glc
what is seen in pigmentary glacuoma
high diurnal IOP fluctuations
what is the mechanism of pigmentary glc
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
layering of pigment seen centrally on corneal endothelium
kruckenberg's spindle
the prescense of kruckenberg spindle should prompt you to do what test
check for TID
where are TID in pigmentary glc located
midperpipheral iris
TID should prompt you to do what test
gonio
how does glc arise in PDS
pigmented is accumulated in TM and the TM breaks down from having to process it

IOP from clogged and overworked TM
when is pigment released in PDS
after dilation --> see it in AC
after exercise can see IOP rise
pigment on lens equator
scheie line
what is pathognmic for PDS/PG
scheie line
in which patients is scheie line seen
black patients with PDS/PG
where is pigment from PDS/PG mostly seen in gonio
inferiorly
pigment reversal sign
more pigment seen superiorly due to burning out of TM
how is the iris configured in PDS/PG
concave
pigment on Schwalbe's line
Sampoaelsi's line
T/F endo pigment and TID are uncommon in blacks with PDS/PG
true

see lots of TM pigment though
tx of PG
treat like POAG but dont use MIOTICS due to risk of RD
why are miotics CI in PG
because they can cause RDs and these pts have a higher incidence of retinal pathology
what tx can be used in PG
ALT or SLT since they are pigment dep it will be versy successful
how often should you follow PDS/PG pts
every 3-6 months bc of high diurnal variation
what is reverse pupil block
pressure builds up in AC and forces the iris backwards onto lens zonules as seen in PG/PDS
why must PDS/PG patients be monitored frequently
because of high diurnal variations
peeling of anterior lens capsule due to heat/radiation
exfoliation
what is the difference btw exfoliation and PXE
exfoliation - material is peeled off

PXE- material is being deposited on lens
deposiition of abnormal BM on anterior lens capsule and in TM
PXE
where does the abnormal BM arise from in PXE
lens
iris
CB
uvea
T/F PXE is systemic disorder
true
is the angle opened or closed in PXE
open
patient characteristics of PXE
60's-80's
bilateral
asymetric
northern Europeans
rare in blacks
what is an important indicator of PXE
peripupillary TID
what condition is worse PXE or POAG
PXE
tx of PXE
more meds
ALT
SLT
trabeculolectomy
where is pigment released from in PXE
pupil border
mechanism of PXE
abnormal BM deposits in TM which blocks TM and leads to its dysfunction
Is a lensectomy a viable tx option for PXE
NO bc material doesn't come from lens!
OHTN develops in what % of pts with PXE
22-81%
what is the likelihood of developing glc in PXE
40% within 10 yrs
what progresses faster POAG or PXE
PXE
is PXE easy to manage
NO
complications that arise in PXE
cataract surgery is more difficult due to loss of zonular support
characterized with inflammation, hyphema, TM changes occuriing within hours to days of trauma
early traumatic glc
characterized by angle recession and PAS that takes weeks to years
late traumatic glc
tear in CB (longitudinal m) occurring within 7 days of injury characterized by blood in AC
hyphema
can rebleeds occur in hyphema
yes within 5-7 days
what % of patients with hyphema develop angle recession
50-90%
the prognosis of developing angle recession after trauma depends on what
the size of the hyphema

1/3 good
2/3 fair
>2/3 poor
how does IOP become elevated in hyphema
pupil block secondary to clot; the RBCs clot the AC angle
tx of hyphema
bed rest
atropine 1% BID
Pred forte q1h
aqueous suppressants
what drugs should be avoided in tx of hyphema
PG, MIOTICS --> make inflammation worse

Asprin
what is the 24/24 rule for sickle positive pts with hyphema
if IOP > 24 for 24 hrs then paracentisis is needed
husks of old RBCs floating around in AC following traumatic persistent hyphema or vitreous heme
ghost cell glc
tx of ghost cell glc
paracentis
cleavage of CB muscles causing widening and deepening of angle
angle recssion
when does angle recession occur
yrs after trauma
unilateral glc should lead you to suspect
angle recession glc
what is the etiology of angle recession glc
TM scarring and sclerosis
what % of angle recession pts develop angle recession glc
10-20%
what must be done when diagnosing angle recessiom
look at the fellow eye
etiology of steroid induced glc
steroids change the TM ability to process AH

GAGs accumulate
IOP increase is more common with topical or systemic steroids
topical
when does steroid induced glc occur
2 weeks after onset
what amount of pop are steroid responders
2/3
what % of steroid responders develop glc
5%
who is at greater risk of developing steroid induced glc
myopes
POAG pts
kids
steroid response depends on
frequency
dose
uveitis and elevated IOP on association with hypermature cataract
phacolytic glc
hypermature cataract acuity
LP only
acute onset of pain and redness in non-seeing eye with hypermature cat
phacolytic glc
mechanism of phacolytic glc
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
is the angle open or closed in phacolytic glc
open but if inflammation is severe enough can have posterior synechiae, pupil block, and angle closure without pupil block
tx of phacolytic glc
lensectomy
vitrectomy

temp meds - steroids, cycloplege, beta blockers, alpha agonists, CAI

AVOID PG and MIOTICS
broken lens capsule due to trauma or surgery
lens particle glc
uveitis s/p cat extraction leading to inflammatory secondary glc that can be open or closed angle
phacoanaphylactic uveitis

autoimmune response to lens antigens
unilateral or asymetric cat associated with asymetric shallowing of AC - see acute to intermitten red painful eye at nigh with blur and corneal edema
phacomorphic glc
ddx of phacomorphic glc
primary angle closure
cause of phacomorphic glc
due to increasing lens thickness- the iris and lens appose each other can have secondary pupil block, bombe, and closure with PAS
tx of phacomorphic glc
treats with meds then do LPI
cat extraction
when should phacomorphic glc be suspected
glaucoma with angle closure shallow chamber and asymmetric advanced cat
what can occur due to lens ectopia lentis
pupil block and angle closure
causes of NVG
ischemia to retina

CRVO
DR
Carotid artery dz
how does NVG arise
hypoxia --> VEGF release -> neo in posterior iris --. NVI, angle neo
what happens when neo of angle occurs
vessels bridge scleral spur and arborize on TM forming fibrovascular membranes

tent like PAS which eventually zipper angle shut
what is the prognosis of NVG
POOR
what is seen in NVG
inflammation and high IOP
what is NVG refered to
90 day glc bc it occurs 90 days after vascular occlusion
what is unique about NVG
secondary angle closure without pupil block
what is the worst glc a pt can gave
NVG
what tests should be ordered in patients over 60 with anterior seg neo
ESR and CRP
tx of NVG
atropine and Pred forte for inflammation
temp aqueous suppressants
trabeculectomt
PRP
avastin and lucentis
what happens if episcleral venous pressure is elevated
IOP will increased
how can elevated episcleral venous pressure be diagnosed
indirectly via gonio

see blood in SC
causes of elevated episcleral venous pressure
carotid cavernous fistula
sturge weber syndrome
cavernous sinus thrombosis
retrobulbar tumor
thyroid
idiopathic
what is the only med that is useful in tx elevated episcleral venous pressure
PG bc they bypassepiscleral venous system
what should be suspected in a pt with unilateral red eye and ipsilateral IOP elevation
acute angle closure
uveitic glc
low flow carotid cavernous fistula
hot eye with pronounced episcleral injection and profuse AC rxn, high IOP, and variable discomfort
acute anterior uveitis
quiet and insidious IOP elevation
chronic uveitis
what type of uveitis is most likely to cause glc
chronic uveitis
how does glc arise in uveitis with pupil block
iris and lens adhere cause posterior synchiae leading to bombe
PAS forms
how does glc arise in \uveitis without pupil block
inflammatory debris is deposited and contracted within angle and pulls peripheral iris over TM causing closure by PAS
how does open angle glc arise from uveitis
TM outflow impeded by accumulation of inflammatory debris AND outflow infacility of proteins in AQ with excess flare

trabeculitis

steroid responses
what leads to IOP rise in open angle glc due to uveitis
flare greatly reduces outflow facility
aqueous becomes viscous
tx of glc due to uveitis
pred forte be agressive
cycloplege
phenylephrine to break syncheiae if cycloplege doesnt work

beta blockers, alpha 2, CAI
what should not be used in tx of uveitic glc
MIOTICS and PG make inflammation worse
what type of glc drug is most effective in uveitic glc
CAI
cause of glc due to chronic iridocyclytis
trabeculitis
IOP varies from 10-30 weekly
how does glc arise in young patients with uveitis
inflammation must be SEVERE
how does glc arise in old pts with uveitis
chronic -. cummulative efefcts of inflammation and steroid use

min amounts of inflammation are needed to cause TM dysfunction
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
what is seen in gluacomatocycltic crisis
IOP rise is dispproprtionate to inflammation

IOP precedes inflammation
patients with glaucomatocycltic crisis ONH and fields are
normal
how long does glaucomatocycltic crisis last
hours to weeks

self limiting
mechanism of glaucomatocyclitic cirsis
decreased outflow due to trabeculitis
PG E seen in high amounts which increases blood aq barrier permeability and leads to increased aq prod
what can cause trabeculitis
herpres
tx of glaucomatocycltic crisis
self limiting
tx inflammation first then IOP
NO MIOTICS or PG

steroids are treatment of choice
beta blockers, alpha 2, CAO
what should you look for in glaucomatocyclitic crisis
AC cells
KPs
characterized by triad of heterochromia, iridocyclytic and cataract after secondary glc seen in young pts
fuch's heterochromatic iridocylctis
mech of fuch's hetero iridocycltic glc
sclerosis of TM