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95 Cards in this Set

  • Front
  • Back
what is angle closure glaucoma
A type of glaucoma caused by the APPOSITION OF THE IRIS TO THE TM, obstructing the outflow of aqueous.
1. what is considered PRIMARY ANGLE CLOSURE SUSPECT?
2. PAS?
3. Status of Disc and IOP?
4. Medical Therapy?
1. pigmented TM blocked by iris
2. NO PAS
3. disc and IOP NORMAL
4. no clear medical therapy (probe of symptoms)
1. what is considered PRIMARY ANGLE CLOSURE?
2. PAS?
3. Status of Disc and IOP?
4. Medical Therapy?
1. pigmented TM blocked by iris 180 degrees
2. either PAS or high IOP present
3. NO DISC DAMAGE nor FIELD LOSS
4. pathological
5. LPI recommended
what is considered PRIMARY ANGLE CLOSURE GLAUCOMA?
PAS?
Status of Disc and IOP?
Medical Therapy?
1. Pigmented TM is blocked by iris for 180 degrees
2. Have either PAS or elevated IOP
3. Glaucomatous neuropathy and field loss
4. LPI recommended
what is primary angle closure attack?
what are the classic signs?
medical therapy?
1. near complete apposition of iris to pigmented TM
2. injection, vision loss, nausea, emesis, halos, corneal edema, high IOP, inflammation, mid dilated fixed pupil
3. iridotomy, iridoplasty, trabeculectomy
what is the classic profile of an angle closure glaucoma patient
OLD, HYPEROPIC ASIAN FEMALE

1. white>black
2. asian: ACG>POAG
3. females>males
4. older>younger
5. hyperopes>myopes
6. ESKIMOS
7. sulfa medications
what is iris bombe?
bowing forward of iris due to posterior pressure buildup
what is the mechanism for primary angle closure with pupil block
1. mid dilated state causes most problems
2. IRIS BOMBE
3. irido corneal apposition causing angle closure via PAS
4. irido lenticular apposition causing posterior synechiae
5. dramatic IOP elevation (40+ mmHg)
medical therapy for posterior synechiae
dilation or miosis
1. miosis has long been standard of care
2. dilation will also work (atropine)
3. basically anything that will get that sucker loose
what are the anatomical features of primary angle closure with pupil block
1. small corneal diameter
2. small axial length
3. moderate hyperope
4. thick lens
5. shallower AC depth (75% ACG with AC depth < 1.5mm)
DO NOT mistake acute angle closure glaucoma with...
UVEITIC GLAUCOMA
1. uveitic glaucoma will have a very active anterior chamber reaction
2. acute angle closure will have a quiet anterior chamber
what are the symptoms of acute primary angle closure GLAUCOMA
1. entire angle closed
2. vision loss in days
3. NFL damage by 48 hours
4. profound signs and symptoms
5. may result in chronic IOP elevation after breaking attack and alleviating angle closure due to TM damage
What is the treatment for Primary Angle Closure Attack?
1) Medical therapy
2) LPI
3) Iridoplasty
4) Trabeculectomy
What is the treatment for Acute Primary Angle Closure?

What is the goal of this treatment?
To relieve Corneal Edema:
1) Glycerin
2) Corneal Indentation

AQS
- Beta Blocker (1 DROP)
- Iopidine or Alphagan (x2)
- CAI - Diamox 500 mg

Pilocarpine 2% (if <40mmHg)
Prostaglandin (may not work fast enough in an acute situation)

Pred Forte Q15min-Q30min

Osmoglyn

Surgical therapy:
LPI
Iridectomy with Trabeculectomy
Argon Laser Iridoplasty

Goal is not to reduce the IOP, but to change the Angle Anatomy. Pressure reduction is merely part of the process.
what must be a part of every treatment plan for primary angle closure with pupil block
laser peripheral iridotomy is the definitive treatment
What is the mechanism for Subacute or Intermittent Angle Closure?
1. A partial angle closure that can seen in dim lighting which leads to pupil dilation and block
2. ONH cupping and field loss are often first indications

*not narrow angle glaucoma, angle chronically narrow and occludable
What is the correct treatment for Subacute Angle Closure?
1. LPI followed by iridoplasty if necessary
2. filtering surgery

*long term medical management not appropriate (allows PAS to form)
what is the most common type of primary angle closure
CHRONIC (80%)
what is the mechanism of CHRONIC primary angle angle closure glaucoma?
less pupil block and more creeping angle closure

PAS in superior angle
what is the medical therapy for CHRONIC primary angle angle closure glaucoma
1. DO GONIO!!
2. iridotomy then filtering surgery if necessary
3. topical medication following iridotomy to control IOP due to chronic trabecular damage
4. prostaglandin analogs work well!!!
what is the role of the choroid in angle closure glaucoma
1. likely to contribute heavily to ACG
2. choroidal expansion takes up volume
3. leads to forward movement of lens and iris, and AC flattening with ACG
4. change in choroidal vessel permeability leads to choroidal expansion (SCLERITIS)
what is the main highlighted drug that causes angle closure glaucoma
sulfa based drugs:
TOPIRAMATE (TOPAMAX)

and viagra haha...
what is the difference between pupil block and choroidal expansion in acute angle closure
PUPIL BLOCK:
1. IRIS BOMBE PRESENT
2. treat with BB, PILOCARPINE, AA, CAI, PGA, tp steroids
3. LPI

CHOROIDAL EXPANSION:
1. flat AC, NO IRIS BOMBE
2. treat with tp steroids, ATROPINE, BB, AA, d/c adverse medication
3. NO LPI
what is the difference between iris plateau configuration and syndrome
Gonioscopy: (CONFIGURATION)
1. any eye with deep AC and narrow angle due to large last roll of the iris draping forward.
2. displaced ciliary processes, forward rotation

SYNDROME:
the angle remains either closed or potentially closed following LPI

*treat with pilocarpine
what are the 7 SECONDARY ANGLE CLOSURE WITH PUPIL BLOCK
1. uveitic
2. phacomorphic
3. aphakia
4. vitreous prolapse
5. pseudophakia
6. reverse pupil block with AC lens
7. subluxated lens
What is the treatment for Plateau Iris Syndrome?
1. Argon Laser Iridoplasty
2. Pilocarpine.
What is the mechanism for Ciliary Block Glaucoma?
Anterior displacement of the iris and ciliary body which causes misdirection of aqueous into the vitreous and the posterior chamber with anterior displacement of the structure of the eye.

This is most typically occurs following ocular surgery for angle closure glaucoma (Trabecuectomy)

1. disparity in AC depth between eyes
2. MIOTIC will aggravate or cause condition
3. NO LPI
What are the two names given for CBG?
1. Malignant Glaucoma
2. Aqueous Misdirection Syndrome
What is the treatment for Ciliary Block Glaucoma?
Best managed with Cycloplege and Steroids:
- Atropine 1% BID
- Topical Steroids
- AQS --> Possible Diamox 1 gram PO QD (dehydrates and shrinks the vitreous
(Eventually everything is tapered but Atropine.)

Surgical options include:
1. Vitrectomy
2. Lensectomy
3. Chandler's Procedure
after successful treatment for angle closure glaucoma, the IOP is still high...whats wrong?
cause by compromise to the angle structures (TM) from the angle closure

"residual stage of angle closure glaucoma"
how would you PROPHYLAX for primary angle closure glaucoma
1. LPI for AC < 2.0mm
2. Gonio to identify areas of reversible closure
3. provocative tests
what is the mechanism for ICE syndrome
1. corneal endothelial cells over-secrete leading to Descemet's membrane migrating and extending over the TM.
2. membrane contraction forms PAS
3. UNILATERAL seen more in WOMEN
ICE syndrome: essential iris atrophy
1. gonioscopy shows progressive angle closure by PAS
2. pupil displaced towards PAS
3. ectropion uveae, stromal atrophy, and full thickness iris hole formation opposite PAS
ICE syndrome: chandlers
1. iris normal to mild change
2. corneal edema
3. normal IOP
ICE syndrome: Cogan-Reese
gonioscopy shows progressive angle closure by PAS except that an iris nevus covers the anterior iris
what are THREE secondary glaucomas that are ALWAYS or ALMOST ALWAYS OPEN ANGLED
1. Pigmentary
2. Pseudo-exfoliative
3. Steroid induced
what is the ONLY secondary glaucoma that is ALWAYS CLOSED ANGLED
NEOVASCULAR
what are the FOUR secondary glaucomas that has equal prevalence of being open or closed angled
1. traumatic
2. lens induced
3. inflammatory
4. miscellaneous causes
pigmentary glaucoma is typically seen in what type of patient?

what is a precursor to this disease?
OPEN ANGLE:
1. young myopic white male (20-45)
2. can be seen in BLACK FEMALES too (distinctly different appearance)
3. BILATERAL, asymmetric
4. high diurnal fluctuations

pigment dispersion syndrome is a precursor
what is the difference between the presentation of pigmentary glaucoma in whites and blacks
WHITES:
1. endothelial pigments
2. transillumination defects
3. TM pigments
4. backwards bowing of iris

BLACKS:
1. rare endothelial pigment
2. no transillumination defects
3. HEAVY TM pigment
what is SCHEIE LIINE
1. pigment on the lens equator
2. was considered diagnostic for PDS/PG
3. certain patterns are more indicative of exfoliation syndrome
4. more common in BLACKS
what type of secondary glaucoma will present with IOP spike after exercise and dilation
PIGMENTARY GLAUCOMA
what are legitimate treatments for pigmentary glaucoma
1. BB, AA, CAI, PGA
2. Pilocarpine (not a real option because of the risk for ret detach)
3. argon laser trabeculoplasty (or selective laser)
4. trabeculectomy
5. for PDS f/u Q3-6 months for IOP check due to diurnal fluctuations (DFE and VF also)
what is the primary indicator for pseudoexfoliative glaucoma
presence of development of peripupillary transilluminations defects (TIDs)
what is the mechanism for pseudoexfoliative glaucoma
1. and age related abnormal basement membrane deposition from the lens epithelium and other tissues on the anterior lens capsule, and clogging TM.
2. posterior synechiae
3. #1 notable cause of OPEN ANGLE GLAUCOMA
PXE glaucoma in comparison to POAG
1. PXEG MORE SEVERE!!
2. more medication and surgery required for PXEG
3. PXEG one of the worse glaucomas to encounter regularly in clinic
4. PXEG easily missed w/o a dilation
management of PXEG
1. BB, AA, CAI, PGA
2. ALT/SLT
3. trabeculectomy
what is very diagnostic for PXEG
1. IOP rise after dilation due to pigment liberation

*highest IOP typically outside office hours
transillumination defects for pigmentary glaucoma vs. PXEG
pigmentary glaucoma:
1. mid periphery

PXEG:
1. peri-pupillary
2. pt. with radial oriented pigment on the anterior lens, pigment liberation with dilation (with or w/o IOP spike) and peripupillary TIDs can be considered exfoliation suspects
what is the #1 cause of unilateral glaucoma
ANGLE RECESSION

gonioscopy must be done on both eyes to compare
hyphema management
1. bed rest at 30 deg incline (with bathroom privileges only)
2. atropine
3. pred forte q1h
4. aq. suppressers

AVOID:
1. PGA
2. MIOTICS
3. ASPIRIN (blood thinners)
angle recession management
1. monitor IOP and disc, glaucoma can develop years after trauma
2. BB, CAI, AA, PGA
3. trabeculectomy
4. POAG more common in fellow uninjured eye

DOESNT WORK WELL:
1. miotics due to TM change
2. ALT/SLT, poor response if recession > 180
steroid induced glaucoma management
1. d/c steroids (after prolonged use, IOP may not lower with medication cessation)
2. BB, AA, CAI, PGA
3. trabeculoplasty (poor)
4. trabeculectomy (better)
what percentage of the population will respond to steroids with IOP spike

what demographic is most significant
1. 66%
2. 2-5 week for IOP spike to become apparent
3. <10% of population ever become a significant problem
4. MOST SIGNIFICANT IN KIDS, ELDERLY and POAG PTS.
what is photocoagulation
1. laser is focused on pigmented tissue (melanin dependent) and absorbed, converted to heat
2. photocoagulatin occurs when tissue is warmed by 10-20 degrees.
3. blood coagulation and inflammation serves to create desired scarring and adhesions
4. warms collagen stimulating it to contract
5. tissue atrophy arises surrounding each photocoagulation scar
what is photovaporization
1. dependent upon light absorption by pigment
2. heated by 60-100 degrees
3. more powerful and short burst of light
4. ONLY desirable in thermal iridotomies
5. UNDESIRABLE in thermal laser photocoagulations
what is photodisruption
1. non pigment dependent
2. CONSIDERED NON THERMAL
3. infrared spectrum
4. highly localized instantaneous temperature rise (15000C)
5. ionization of tissue occurs
6. coagulation DOES NOT OCCUR
7. Nd:YAG capsulotomies and iridotomies
complications associated with anterior segment laser procedures
1. elevation of IOP from intraocular inflammation (pre and post op. glaucoma medication)
2. corneal burns (edematous or shallow corneals)
3. ret. detach and intraocular hemorrhage (mostly cold lasers)
what is argon laser trabeculoplasty?

what are the indications?
thermal laser alteration of the TM to increase aq outflow

1. PXEG
2. pigmentary glaucoma
3. POAG
4. non-compliance with meds
5. inadequate medical controls
what are the theories for the pressure lowering mechanism of ALT
1. laser burns causes stretching of TM causing pores
2. burns attract phagocytes that clean up debris in TM improving flow
3. destroys endothelial cells stimulating the production of new, more viable cells

ALT will fail over time and retreatment generally not beneficial
whats the difference between SLT and ALT
ALT:
1. mechanical alterations, due to collateral thermal effects

SLT:
1. no apparent tissue alterations, due to lack of such thermal effects
2. can be performed more than once (most of the time only once)
3. obliterated macrophages leaves the non-pigmented lining TM cells intact
what are the laser therapies for closed angle glaucoma
1. argon laser iridoplasty
2. laser peripheral iridotomy
3. argon laser LPI
4. Nd:YAG laser LPI
5. trabeculectomy
6. antimetabolites
what are the indications for LPI
1. angle closure with pupil block
2. prophylaxis in narrow, occluded angles

*allowing flow between the anterior and posterior chamber, relieving pupil block
indication for ALT
1. irido-retraction procedure
2. breaking attack of acute angle closure (phacomorphic glaucoma and plateau iris syndrome)
what is the difference between argon LPI and Nd:YAG
Argon Laser LPI:
1. photocoagulation leading to photovaporization
2. unlikely to bleed
3. less likely to disrupt lens and vitreous
4. difficult to penetrate iris
5. pigment dependent (CONTRAINDICATED IN BLUE IRIS)
6. morely like to close in time

Nd:YAG
1. photodisruption
2. more likely to bleed
3. more likely to disrupt lens and vitreous
4. much easier to penetrate iris
5. less likely to close in time
6. pigment INDEPENDENT (CAN BE USED IN BLUE IRIS)
comparison between post surgical trabeculectomy vs. malignant glaucoma
post trabeculectomy:
1. shallow chamber
2. low IOP
3. indicates overfiltration or bleb leakage

malignant glaucoma:
1. shallowing chamber
2. rising IOP
what are considerations for surgery
1. maximal medical and progression
2. poor patient compliance with medications
3. failure or contraindication of LT
4. need for very low IOP
what are signs of surgical failures
1. hypotony from wound leaks and over secretions
2. shallow anterior chamber with low IOP
3. residual elevated IOP
4. bleb encapsulation
5. overfiltrations
6. ciliochoroidal detachment
7. cyclodialysis
what are antimetabolites used for in trabeculectomy
1. inhibits fibroblasts preventing scarring after surgery
2. mitomycin and 5-fluorouracil
procedure of trabeculectomy
1. creates fistula through the TM and creates a communication between the anterior chamber and subconjunctival space
2. creates anther channel for aqueous to exit the chamber
3. iridectomy is also performed so that the iris doesnt block and adhere to the surgical filter
what are the characteristics of CONGENITAL/INFANTILE glaucoma
1. ABNORMAL angle
2. LARGE globe
3. corneal EDEMA
4. onset near birth
5. MEGALOCORNEA
6. symptomatic (blepharospasm, photophobia, lacrimation)
what are the characteristics of Juvenile Open Angle/Secondary glaucoma
1. NORMAL angle
2. NORMAL axial length
3. CLEAR cornea
4. onset LATER
5. NORMAL corneal size
6. ASYMPTOMATIC
what is important in detection of glaucoma in children
1. IOP does not have to be high in a child for glaucoma to develop.
2. 20+ mmHg IOP in a child in concerning
3. ALWAYS DO TONOMETRY
medical therapy for kids with glaucoma?

what is good to use?
what shouldnt be used?
GOOD TO USE:
1. CAI (drug of choice)
2. beta blockers

NOT SO GREAT:
1. PGA (not effective, BEST in JOAG >15yrs old)
2. DONT USE BRIMONIDINE!!!
what is the classic triad of congenital glaucoma
1. epiphora
2. photophobia
3. blepharospasm
what are surgical options for congenital glaucoma
1. goniotomy
2. trabeculotomy
3. viscocanalostomy
4. filtering surgery
5. cyclocryotherapy
6. YAG cyclophotocoagulation
7. diode laser photoablation
NOTE:
any childhood glaucoma caused by TRABECULODYSGENESIS is considered PRIMARY CONGENITAL GLAUCOMA

a child with glaucoma but WITHOUT angle abnormalities has JOAG
NOTE:
any childhood glaucoma caused by TRABECULODYSGENESIS is considered PRIMARY CONGENITAL GLAUCOMA

a child with glaucoma but WITHOUT angle abnormalities has JOAG
trend analysis
1. looks at significance of rate of change over time
2. identifies progression by looking at patient behavior over time
3. uses all data points and a linear regression formula

weakness: progressioni is not necessarily linear
event analysis
1. compares baseline to most recent data
2. change as dictated by criteria has occurred or not
mechanism for steroid responders
accumulation of GAGs in the TM
what are the TWO anti VEGF drugs?
Avastin
Lucentis
phacolytic mechanism?
1. hypermature cataract leaks proteins into AC
2. bloated macrophages with lens material in TM
3. outflow blockage
phacolytic management
1. pred forte
2. atropine
3. BB, AA, CAI

AVOID PGA and PILOCARPINE!!!
phacomorphic mechanism?
1. unilateral
2. increasing lens thickness causes irido-lenticular apposition
3. pupil block and posterior chamber pressure increase
4. iris bombe
5. ANGLE CLOSURE/PAS
neovascular mechanism?
mostly likely caused by...
most likely caused by...
1. central retinal vein occlusion
2. diabetic retinopathy
3. carotid artery disease

1. hypoxia
2. rubeosis
3. angle neovascularization
4. SECONDARY ANGLE CLOSURE W/O PUPIL BLOCK
neovascular manangement
1. atropine
2. pred forte
3. Avastin/Lucentis

overal poor prognosis
a person 60+ yrs old comes in with rubeosis and neovascularization...what must you get on the patient
1. ESR
2. C-reactive protein
DIAGNOSIS and TREATMENT of glaucoma associated with elevated episcleral venous pressure
Dx: BLOOD in Schlemm's Canal in gonio

Tx: PGA!!!
pt comes in with unilateral and ipsolateral IOP elevation, you should think THREE causes
1. acute angle closure
2. uveitic glaucoma
3. low-flow carotid cavernous fistula
how do you break a stubborn posterior synchiae

best treatment for uveitic glaucoma
10% phenylephrine

1. steroids
2. cycloplegia
3. CAI's
what medications should you avoid in uveitic glaucoma
1. MIOTICS
2. PGA
what are the FOUR unilateral glaucomas
1. glaucomatocyclitic crisis (GCC)
2. phacomorphic
3. angle recession
4. increased episcleral venous pressure
cloudy cornea...cant look through it to do gonio.

what do you do?
1. Osmoglyn
2. Isosorbide FOR DIABETICS!!
3. Glycerin

LOOK AT OTHER EYE!!
what FOUR conditions do you use MIOTICS
1. phacomorphic
2. acute primary angle closure
3. acute angle closure with pupil block
4. Plateau Iris Syndrome (primary angle closure w/o pupil block)
what are the SIX conditions do you DILATE
1. hyphema
2. phacolytic
3. neovascular
4. uveitic
5. acute angle closure secondary to choroidal expansion
6. ciliary block glaucoma