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95 Cards in this Set
- Front
- Back
what is angle closure glaucoma
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A type of glaucoma caused by the APPOSITION OF THE IRIS TO THE TM, obstructing the outflow of aqueous.
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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) |
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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 |
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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 |
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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 |
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what is the classic profile of an angle closure glaucoma patient
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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 |
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what is iris bombe?
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bowing forward of iris due to posterior pressure buildup
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what is the mechanism for primary angle closure with pupil block
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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) |
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medical therapy for posterior synechiae
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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 |
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what are the anatomical features of primary angle closure with pupil block
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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) |
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DO NOT mistake acute angle closure glaucoma with...
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UVEITIC GLAUCOMA
1. uveitic glaucoma will have a very active anterior chamber reaction 2. acute angle closure will have a quiet anterior chamber |
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what are the symptoms of acute primary angle closure GLAUCOMA
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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 |
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What is the treatment for Primary Angle Closure Attack?
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1) Medical therapy
2) LPI 3) Iridoplasty 4) Trabeculectomy |
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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. |
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what must be a part of every treatment plan for primary angle closure with pupil block
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laser peripheral iridotomy is the definitive treatment
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What is the mechanism for Subacute or Intermittent Angle Closure?
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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 |
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What is the correct treatment for Subacute Angle Closure?
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1. LPI followed by iridoplasty if necessary
2. filtering surgery *long term medical management not appropriate (allows PAS to form) |
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what is the most common type of primary angle closure
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CHRONIC (80%)
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what is the mechanism of CHRONIC primary angle angle closure glaucoma?
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less pupil block and more creeping angle closure
PAS in superior angle |
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what is the medical therapy for CHRONIC primary angle angle closure glaucoma
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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!!! |
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what is the role of the choroid in angle closure glaucoma
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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) |
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what is the main highlighted drug that causes angle closure glaucoma
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sulfa based drugs:
TOPIRAMATE (TOPAMAX) and viagra haha... |
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what is the difference between pupil block and choroidal expansion in acute angle closure
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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 |
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what is the difference between iris plateau configuration and syndrome
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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 |
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what are the 7 SECONDARY ANGLE CLOSURE WITH PUPIL BLOCK
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1. uveitic
2. phacomorphic 3. aphakia 4. vitreous prolapse 5. pseudophakia 6. reverse pupil block with AC lens 7. subluxated lens |
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What is the treatment for Plateau Iris Syndrome?
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1. Argon Laser Iridoplasty
2. Pilocarpine. |
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What is the mechanism for Ciliary Block Glaucoma?
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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 |
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What are the two names given for CBG?
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1. Malignant Glaucoma
2. Aqueous Misdirection Syndrome |
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What is the treatment for Ciliary Block Glaucoma?
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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 |
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after successful treatment for angle closure glaucoma, the IOP is still high...whats wrong?
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cause by compromise to the angle structures (TM) from the angle closure
"residual stage of angle closure glaucoma" |
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how would you PROPHYLAX for primary angle closure glaucoma
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1. LPI for AC < 2.0mm
2. Gonio to identify areas of reversible closure 3. provocative tests |
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what is the mechanism for ICE syndrome
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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 |
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ICE syndrome: essential iris atrophy
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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 |
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ICE syndrome: chandlers
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1. iris normal to mild change
2. corneal edema 3. normal IOP |
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ICE syndrome: Cogan-Reese
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gonioscopy shows progressive angle closure by PAS except that an iris nevus covers the anterior iris
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what are THREE secondary glaucomas that are ALWAYS or ALMOST ALWAYS OPEN ANGLED
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1. Pigmentary
2. Pseudo-exfoliative 3. Steroid induced |
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what is the ONLY secondary glaucoma that is ALWAYS CLOSED ANGLED
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NEOVASCULAR
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what are the FOUR secondary glaucomas that has equal prevalence of being open or closed angled
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1. traumatic
2. lens induced 3. inflammatory 4. miscellaneous causes |
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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 |
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what is the difference between the presentation of pigmentary glaucoma in whites and blacks
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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 |
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what is SCHEIE LIINE
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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 |
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what type of secondary glaucoma will present with IOP spike after exercise and dilation
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PIGMENTARY GLAUCOMA
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what are legitimate treatments for pigmentary glaucoma
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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) |
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what is the primary indicator for pseudoexfoliative glaucoma
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presence of development of peripupillary transilluminations defects (TIDs)
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what is the mechanism for pseudoexfoliative glaucoma
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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 |
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PXE glaucoma in comparison to POAG
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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 |
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management of PXEG
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1. BB, AA, CAI, PGA
2. ALT/SLT 3. trabeculectomy |
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what is very diagnostic for PXEG
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1. IOP rise after dilation due to pigment liberation
*highest IOP typically outside office hours |
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transillumination defects for pigmentary glaucoma vs. PXEG
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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 |
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what is the #1 cause of unilateral glaucoma
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ANGLE RECESSION
gonioscopy must be done on both eyes to compare |
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hyphema management
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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) |
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angle recession management
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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 |
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steroid induced glaucoma management
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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) |
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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. |
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what is photocoagulation
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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 |
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what is photovaporization
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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 |
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what is photodisruption
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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 |
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complications associated with anterior segment laser procedures
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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) |
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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 |
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what are the theories for the pressure lowering mechanism of ALT
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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 |
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whats the difference between SLT and ALT
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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 |
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what are the laser therapies for closed angle glaucoma
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1. argon laser iridoplasty
2. laser peripheral iridotomy 3. argon laser LPI 4. Nd:YAG laser LPI 5. trabeculectomy 6. antimetabolites |
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what are the indications for LPI
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1. angle closure with pupil block
2. prophylaxis in narrow, occluded angles *allowing flow between the anterior and posterior chamber, relieving pupil block |
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indication for ALT
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1. irido-retraction procedure
2. breaking attack of acute angle closure (phacomorphic glaucoma and plateau iris syndrome) |
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what is the difference between argon LPI and Nd:YAG
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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) |
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comparison between post surgical trabeculectomy vs. malignant glaucoma
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post trabeculectomy:
1. shallow chamber 2. low IOP 3. indicates overfiltration or bleb leakage malignant glaucoma: 1. shallowing chamber 2. rising IOP |
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what are considerations for surgery
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1. maximal medical and progression
2. poor patient compliance with medications 3. failure or contraindication of LT 4. need for very low IOP |
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what are signs of surgical failures
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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 |
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what are antimetabolites used for in trabeculectomy
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1. inhibits fibroblasts preventing scarring after surgery
2. mitomycin and 5-fluorouracil |
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procedure of trabeculectomy
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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 |
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what are the characteristics of CONGENITAL/INFANTILE glaucoma
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1. ABNORMAL angle
2. LARGE globe 3. corneal EDEMA 4. onset near birth 5. MEGALOCORNEA 6. symptomatic (blepharospasm, photophobia, lacrimation) |
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what are the characteristics of Juvenile Open Angle/Secondary glaucoma
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1. NORMAL angle
2. NORMAL axial length 3. CLEAR cornea 4. onset LATER 5. NORMAL corneal size 6. ASYMPTOMATIC |
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what is important in detection of glaucoma in children
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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 |
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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!!! |
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what is the classic triad of congenital glaucoma
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1. epiphora
2. photophobia 3. blepharospasm |
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what are surgical options for congenital glaucoma
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1. goniotomy
2. trabeculotomy 3. viscocanalostomy 4. filtering surgery 5. cyclocryotherapy 6. YAG cyclophotocoagulation 7. diode laser photoablation |
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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 |
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trend analysis
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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 |
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event analysis
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1. compares baseline to most recent data
2. change as dictated by criteria has occurred or not |
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mechanism for steroid responders
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accumulation of GAGs in the TM
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what are the TWO anti VEGF drugs?
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Avastin
Lucentis |
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phacolytic mechanism?
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1. hypermature cataract leaks proteins into AC
2. bloated macrophages with lens material in TM 3. outflow blockage |
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phacolytic management
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1. pred forte
2. atropine 3. BB, AA, CAI AVOID PGA and PILOCARPINE!!! |
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phacomorphic mechanism?
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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 |
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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 |
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neovascular manangement
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1. atropine
2. pred forte 3. Avastin/Lucentis overal poor prognosis |
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a person 60+ yrs old comes in with rubeosis and neovascularization...what must you get on the patient
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1. ESR
2. C-reactive protein |
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DIAGNOSIS and TREATMENT of glaucoma associated with elevated episcleral venous pressure
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Dx: BLOOD in Schlemm's Canal in gonio
Tx: PGA!!! |
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pt comes in with unilateral and ipsolateral IOP elevation, you should think THREE causes
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1. acute angle closure
2. uveitic glaucoma 3. low-flow carotid cavernous fistula |
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how do you break a stubborn posterior synchiae
best treatment for uveitic glaucoma |
10% phenylephrine
1. steroids 2. cycloplegia 3. CAI's |
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what medications should you avoid in uveitic glaucoma
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1. MIOTICS
2. PGA |
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what are the FOUR unilateral glaucomas
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1. glaucomatocyclitic crisis (GCC)
2. phacomorphic 3. angle recession 4. increased episcleral venous pressure |
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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!! |
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what FOUR conditions do you use MIOTICS
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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) |
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what are the SIX conditions do you DILATE
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1. hyphema
2. phacolytic 3. neovascular 4. uveitic 5. acute angle closure secondary to choroidal expansion 6. ciliary block glaucoma |