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139 Cards in this Set

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Definition: Glaucoma
Group of disorders characterized by progressive structural/functional damage to the eye, particularly the ONH. IOP may be statistically normal at all times!
Becker-Schafer Definition of Glaucoma
That IOP which produces damage to the optic nerve is glacumomatous. Glaucoma is not an IOP, it is a disorder characterized by damaging intraocular pressure in some patients
Definition: Low Tension Glaucoma aka: Normal tension Glaucoma (form of POAG)
ONH damage consistent with glaucoma in presence of consistently 'normal' IOP
Definition: Ocular Hypertension
Elevated IOP no accompanied by clinically apparent ocular damage characteristic of glaucoma
What __% of ocular hypertensives develop glaucoma over a 10 year period?
What ___% of ocular hypertensives per year develop glaucoma over time?
.5 - 1 %
OHTS: Conclusion?
Untreated: 9.5% developed ONH or VF damage over 5 years Treated: 4.4% of ocular hypertensives developed glaucoma over 5 years
True or False? Risk of glaucoma increases with IOP
True: at IOP > 21 the risk of glaucomatous VF loss is 5-6x greater than IOP < 21
Definition: Angle Closure Glaucoma
Glaucoma caused by clinically evident obstruction of aqueous flow TO the TM
True or false? Pupillary Block (obstruction of flow thru the lens-iris diaphragm) is the least common cause of angle closure
False - Pupillary Block is the most common cause of angle closure glaucoma
Open Angle Glaucoma
aqueous flow does get thru the lens-iris diaphragm and TO the TM but not THRU the TM
True or False: POAG is the 2nd leading cause of blindness in the U.S.?
False: 3rd (after cataract and ARMD)
T or F? <75% of glaucoma-caused blindness in the U.S. is due to POAG
False: > 75%
T or F? Angle Closure Glaucoma is much less common but can quickly damage the ONH and cause blindness in 2-3 days if untxed
True. High IOPs can be reached in and can be as quick as 1 day
T or F? POAG accounts for ~70% of all adult glaucoma cases in the US
T or F? Only 20-30% of U.S. population have an angle narrow enough to possibly close (grade 1 or 2)
False: 2-6%. ACG is uncommon in the U.S. Only about 5% of these actually go on to close = PACG
T or F? < 10% of all glaucomas in the US are PACG
List two common sx of congenital/infantile glaucoma
Photophobia (cornea becomes edematous which causes glare) and lacrimation
List 6 common signs of congenital/infantile glaucoma
Eye rubbing, Megalacornea, Buphthalmos, Hobbs striae (breaks in descmets), Elevated IOP and Large cups (reversible)
Adult onset glaucoma is classified by three ways... list them
1. By etiology, 2. By anatomy of filtration angle, 3. Mixed
Is Primary or Secondary glaucoma the result from a clinically evident systemic or ocular disorder causing obstruction of flow to the TM or increased resistance to outflow?
Secondary. Primary is NOT the result of a clinically evident systemic or ocular disorder
Can Primary glaucoma be bilateral, inherited, open angle and angle closure
Yes, all of these are characteristics of Primary Glaucoma
OAG and ACG are differentiated by what technique?
Define OAG
aqueous flow to the TM is NOT blocked by an anomaly. Accounts for the vast majority of glaucoma. Aqueous outflow obstruction is not clinically evident - the obstruction is within the TM
T or F? Secondary OAG accounts for most OAG
False. Primary OAG does
Define ACG
Aqueous flow to TM IS blocked, usually obstruction is either at the pupil (PUPILLARY BLOCK), at the angle (ANGLE CLOSURE) or both. Only occurs in anatomically at risk eyes - narrow angles = Primary ACG or obstruction due to a condition = Secondary ACG
Define Mixed glaucoma
Both angle closure and open angle glaucoma in the same eye. Ex. a POAG pt experiencing an angle closure is not uncommon. Periodic gonio on all glaucoma suspects
Name the two mechanisms of Aqueous production
1. Ultrafiltration = 20% of production, 2. Active Secretion = 75-80% (from non-pigmented ciliary epithelium)
T or F? Ultrafiltration is a pressure-dependent mechanism
True. If IOP increases --> ultrafiltration is reduced (homeostatic). If perfusion thru capillaries in the ciliary processes decreases, then ultrafiltration decreases
List 3 classes of glaucoma meds that INCREASE TM outflow
1. Miotics (Pilocarpine, Carbachol), 2. Non-specific adrenergic agonists (Epi and Propine), 3. Prostaglandins and prostamides (Lumigan)
List 3 classes of glaucoma meds that INCREASE Uveoscleral outflow
1. Prostaglandin analogs (Xalatan, Travatan) and prostamides (Lumigan), 2. Non-specific adrenergic agonists (Epi and Propine), 3. Alpha-2 agonists (Alphagan, Iopidine)
List 3 classes that Reduce Ultrafiltration --> decreases aqueous production
1. Beta Blockers, 2. Alpha-2 adrenergic agonists (Iopidine, Alphagan), 3. Osmotics
List the class that reduces active secretion (hint: think about the enzyme required for active secretion)
Carbonic anhydrase inhibitors (Azopt, Trusopt, Diamox, Neptazane)
Review the Glaucoma meds and their mechanism of action pg. A11-12
Describe the method for max overall effect of a glaucoma med
For best additivity, combine two meds that have different mechanisms of action. Ex. One that works on aqueous production and the other on increasing outflow
What happens in the early stages of inflammation (ant. uveitis) on IOP?
Early uveitis or iritis decreases IOP due to decreased aqueous production of the ciliary processes; increases WBC, Fibrin in aqueous
What about in later stages of inflammation? (Later iritis)
WBC, fibrin and protein can clog TM outflow path causing increased IOP
Name two mechanisms of Primary Angle Closure Glaucoma (breakdown the name into steps)
1. Pupillary Block - most common. Lens-iris diaphragm is tightest when pupil is mid-dilated - increases pressure of PC and bows iris forward (Iris Bombe), 2. Plateau Iris - narrow angle approach - as pupil dilates it bunches into the narrow angle. Laser PI will be ineffective
T or F? Almost all elevated IOP/glaucoma is due to an over production of aqueous
False. Almost all due to OUTFLOW problem, - TM is major site of obstruction in POAG (specifically the Juxtacanalicular TM)
T or F? Uveoscleral outflow does not depend on the pressure of the episcleral venous plexus
True. Not pressure dependent (unlike TM outflow)
List the 6 components of the Filtration angle and related physiology
1. Uveal Trabeculum: Adjacent to AC - Large openings = little resistance to outflow, 2. Corneo-scleral Trabeculum: from schwalbes ring to SS and CB - Smaller holes decreasing in size away from AC, 3. Intratrabecular space: MPS (GAGs) = substance filling space between trabecular sheets. MPS secreted by trabecular endo. , 4. Juxtacanalicular: Immediately adjacent to Schlemms. Endo cells different than other areas. Site of greatest resistance, 5. Schlemm's: Lined by endo cells w/ TJ. Aqueous transported by vacuoles (pressure dependent), 6. Episcleral Plexus: 30-35 channels dumping into intrascleral veins then into episcleral plexus. 1:1 pressure change in plexus.
List a few factors that cause an increase in Episcleral venous plexus pressure (inturn raises IOP)
Sturge-Weber, Valsalva, enthusiastic gonio, carotid cavernous fistula, etc..
T or F? Most ACG is primary AND most primary ACG is the result of pupillary block
True. Most ACG has no apparent cause thus it's primary
T or F? The narrow angle can be detected with SLE only
False. Gonioscopy is needed
Which condition has a anatomically narrow angle, often little or no pupillary block and dilation crowds the iris root into the angle causing ACG
Plateau Iris
List 6 risk factors for PACG due to pupillary block
1. Age: increased with age due to increased thickness of lens, 2. Race: Increased rate in Eskimos, chinese, vietnamese, 3. Sex: Females tend to have shallower ACs, 4. FHx: 3.5-6x greater risk in first degree relatives of patients with PACG, 5. RE: Hyperopes have a smaller globe = smaller AC, 6. Cortical Cataracts: lens thickened
T or F? Pupillary block is often times caused by the doctor during dilation
False. It is very infrequently Iatrogenic. Most causes are spontaneous
T or F? Must inform patient if they are anatomically at risk for ACG
True. Should also further evaluate with gonio or prophylactic laser PI to minimize risk
Describe the mechanism to differentiate Primary angle closure glaucoma
Gonioscopy. If angle closes in the presence of PI --> this suggests that pupillary block is NOT playing a major role - plateau iris is.
Describe the treatment of ACG secondary to pupillary block
Control IOP - to minimize damage, -Use Meds (know the list), Clear cornea if edemous- NaCl solution, Pull iris root out of angle (miosis) - allows for shot at PI - use 2% pilo q15 min for total of 4 doses, May use corneal indentation to force fluid into TM to open angle - indent for 30s followed by 30s of rest. several times for 15 min, Laser PI- produces alternative path, Provocative Dilation test - plateau iris component
Describe the treatment for PACG secondary to plateau iris
Control IOP, Pull iris out of angle, LPI, Provocative test (dilate), Gonioplasty/iridoplasty if positive provocative test
Acute IOP increases cause what symptoms of corneal edema
Halos and glare
At what level of IOP is pilo non-effective due to an ischemic sphincter muscle
> 45-50 mmHg
What is Lens-glaukomflecken?
Lens-induced epithelial necrosis due to acute increase in IOP. Appears as Ant. Subcapsular gray-white opacities
T of F? Optic nerve fibers are affected in about 3 days and Disc edema occurs in about 4-5 days of acute IOP increase. Also Axon dropout in 6-7 days and Cupping 1-2 weeks
False. ON - 1 day, Disc Edema 3-4 days, Axon dropout 5-7 days, Cupping 1-2 months
When could vision loss and blindness occur in an episode of acute IOP spike?
Vision loss within 24 hours and blindness within 2-3 days
List 6 signs of an old acute ACG
1. Pupil not round due to segmental sphincter paralysis, 2. Iris atrophy, 3. Glaucomflecken, 4. Peripheral anterior synchiae, 5. Posterior synechiae or pigment on ant. lens capsule, 6. Iridotomy near 12 o clock
Chronically elevated IOP (symptoms unlikely), 1. Cornea, 2. Iris, 3. Lens, 4. Choroid, 5. Sclera, 6. ON
1. Generally no effect. Possible edema, 2. Iris atrophy (unlikely), 3. cataract (unlikely), 4. Choriocapillaris atrophy?, 5. in young, staphyloma, generally posterior, 6. most devastating and damaging from increased IOP
RNFL normal anatomy: Where are the ganglion cell bodies located?
Ganglion cell layer of retina
List the 3 major nerve bundles of the RNFL
1. Papillomacular bundle: 80-90% of the fibers, 2. Arcuate bundles, 3. Nasal radial fibers
Describe the papillomacular bundle fibers
From macula to temporal ONH. Small, compact bundles with alot of overlap. Damage hard to detect on VF. Hard to see clinically cause of size. Make up most fibers of ON but occupy little space in the ONH
Describe the Arcuate Fibers
Do not cross horiontal raphe temporal to the macula. Large diameter fiber bundles. Less overlap so damage seen quickly in VF. All temporal retina innervated by arcuate - nasal step
Describe Nasal Radial Fibers
From nasal fundus to nasal side of ONH. Temporal wedge of the VF. Affected later in glaucoma thus a temporal island is often left.
Where are the axons from the periphery located in the RNFL?
They are the deepest axons. They also enter more peripherally of the ONH
What part of the VF is affected first in glaucoma and why?
Central field is because axons from the central retina enter the ONH closest to the cup. As cup enlarges, these fibers are affected first.
Descibe the visualization of RNFL
Reflect light - red free reflected more. Thicker bundles reflect more light. Glial cells separate fibers = striations. Astrocytes allow redfree light to pass thru to RPE where it is absorbed. Most evident Superior and Inferiorly
How many axons are in the ON?
1 - 1.3 million bundles- bundles surrounded by astrocytes
List the regions of the ONH
1. Surface nerve fiber layer, 2. Prelaminar region, 3. Laminar region, 4. Retro-laminar region
T or F? Cup size increase is due mostly to axon loss --> loss of rim tissue
True. Cup itself is filled with Glial cells - outside of the cup is axons.
What is the correlation of cupping and RNFL changes to VF changes in early and late glaucoma?
Early: structural damage might be evident with NO VF loss, Late: changes in VF are often not accompanied by observable ONH/RNFL change
In the laminar region, Why is the size of the scleral canal important clinically?
A small scleral canal = small diameter of ONH = small cup. Direct relationship
Which region does the myelin sheath (oligodendrocytes) start (less astroglia)?
Retro-Laminar region
List 4 major theories and some characteristics of ON damage
1. Vascular: Imbalance b/w IOP and perfusion pressure in capillaries of laminar region causes hypoperfusion --> ischemia --> ON damage, 2. Mechanical: Elevated IOP causes mechanical damage to axons --> not due to direct pressure on axons but changes in lamina cribosa (shearing pressure), 3. Combo of both vascular and mechanical --> Individual variation, 4. Axoplasmic: likely that both ischemia (lowered perfusion) and mechanical factors can reduce axoplasmic flow
List 3 major problems with the mechanical theory
1. Low tension glaucoma, 2. Ocular hypertension, 3. Vascular disease relationship to glaucoma
List the 4 stages in the pathogenesis of glaucoma
Stage 1: Primary event - primary factors such as mechanica, vascular, genetic, Stage 2: Damaging stimulus - Molecular changes in and around the ganglion cells, Stage 3: Apoptosis of ganglion cells - preprogrammed death (not by necrosis), Stage 4: Ganglion cells are dead
What is the main excitatory NT in the CNS under normal physiological conditions?
Glutamate. High [] levels are toxic to ganglion cells. Ischemia can cause glutamate release from ganglion cells
What is BDNF?
Neurotrophin = brain derived neurotrophic factor. Produced by LGN and move by retrograde axoplasmic flow to ganglion cells. Necessary for cell viability
T of F? Axon loss occurs very early in natural history of glaucoma, before evident structural changes but not before VF loss
False. Axon loss comes before structural changes and long before VF Loss. Therefore you will need substantial axon loss before recognizable VF loss on SAP
___% axon loss before recognizable VF defect on Goldmann perimeter
___% axon loss before detectable VF loss on white-on-white threshold perimetry
30-40%. 20% ganglion cell loss corresponds to ~5 dB of VF loss on SAP
Explain why there is such extensive axon loss before VF loss is detected
Because of the redundancy of axon bundles. Overlapping of the visual fields allows for significant bundle loss before any changes can be detected.
T of F? Pallor precedes cupping (loss of axons) in glaucoma
False. Cupping precedes pallor. Highly specific to glaucomatous optic neuropathy compared to other optic neuropathies
Which pattern of structural damage is characterized by general cup enlargement, general RNFL dropout, late onset VF loss and a B-Y color defect?
Diffuse axon loss. May cause up to 50% axon loss before detection possible.
Describe some characteristics of Focal axon loss
1. Poles of ONH - arcuate by far most common (large diameter axons). Temporal = least , common. , 2. Notch in sup/inf rim, 3. Slit defects in arcuate RNFL, 4. Localized VF defects: Nasal steps, paracentral scotomas, 5. More quickly detected than diffuse, 6. Tend to occur more in elderly patients with normal or slightly elevated IOP.
T or F? Most often a combination of diffuse and focal axon loss develops
What are the average CCT of white ocular hypertensives according to the OHTS study? African Americans?
Whites=579 microns, Blacks = 555, All = 573
OHTS: which two factors correlated to development of glaucoma?
1. CCT: strongest correlation - for every 40 micron decrease in CCT --> 70% increase of glaucoma damage, 2. IOP: for every 1 mmHg increase --> 10% greater risk of glaucoma
When should you perform pachymetry? (at what step in the workup)
Should be done before any measurement is needed that involves touching the cornea. Tono, Gonio, Dilation, -Take 3 hours after arising, -Take > 3 months after cataract surgery and, > 6 months after refractive surgery
How do you perform a Ultrasonic pachymetry reading?
1. Anesthetize cornea, 2. Be sure cornea is moist: Blinking periodically, Use AT, 3. Probe should be parallel to visual axis, 4. CENTRAL cornea, 5. Multiple readings (>5), delete outlyers
List some factors that effect the IOP reading
1. Valsalva maneuver: Holding breath increases IOP; Body inversion substantially increases IOP, 2. Aerobic exercise: Can result in 20% decrease in IOP, -Is not sustained once patient stops, -Additive to meds, -may enhance perfusion to ONH, , Factors that influence IOP during actually measurement, 1. Accommodation: Decreases IOP, 2. Apprehension: Increases IOP; significant in NCT, 3. Tight tie/collar: Increases IOP, 4. Holding lids/pressure on globe can substantially increase, 5. Corneal Edema: falsely low, 6. Corneal Scarring: False High
Besides the procedure used, pressures and time of day, what other piece of info is needed?
If patient on glaucoma med, need to know the TIME the medication was taken
When is post-dilated Tonometry indicated?
1. Glaucoma patients on miotics, 2. Glaucoma patients, 3. Narrow, potentially occludable angles, 4. Pseudoexfoliation (post-dilated IOP spike), 5. Pigment dispersion
When can you bill for serial tonometry?
If more than one IOP reading is taken in a day
List some factors that are characteristic of a higher risk of glaucoma
1. Consistent high IOP >30 or IOP spikes over 30, 2. Upward trend of IOPs over time, 3. IOP asymmetry > 5, 4. Large (diurnal) IOP variation or at least spikes (>5 suspicious, >10 abnormal), 5. large post-dilated IOP spike > 8 mmHg
According to evidence, does significant structural damage occur prior to earliest recognizable, classical VF defects in many cases?
Yes; Quigley showed that 50% of axons are gone at the 1st sign of VF defect on Goldmann, -Reports of Drance hemes, RNFL defects before VF defects
What is the value of perimetry in glaucoma?
1. Detection: In ~15% of patients you will notice VF defects before ONH changes, 2. Important in glaucoma management: once a defect is detected, VFs are accepted to be more sensitive to glaucoma changes, Why? Because once significant axon damage, it is very hard to detect any further change except thru VF changes (no more redundancy)
Is Goldmann or current automated perimeters better for detecting early changes and for monitoring progression?
Current automated perimeters are better at detecting, quantifying and monitoring progression
Name three 'must haves' for perimetry to be effective for picking up progression in glaucoma patients
1. Must be able to identify:, -Fluctuations of sensitivity: depth changes = most common change in VF defect over time, -Size changes, -New defects, 2. must have consistently repeatable testing conditions and process --> results will fluctuate under normal conditions and even more as VF loss onsets, 3. Must be able to minimize the variability of the VF due to the test instrumentation, process and examiner in order to identify that fluctuation caused only by disease
T or F? Degree of VF loss at diagnosis is a major risk factor for blindness
List 3 phases of field loss in glaucoma
1. Elevated IOP, VF normal or non-specific defect, -Early/subtle ONH changes, 2. Unstable, shallow field defects, transient nature, -Static threshold testing necessary, 3. Unequivocal early VF defect, -irreversible damage and field loss
List 3 field defects that MAY be glaucomatous in nature - no definitively glaucomatous
1. Baring of BS, 2. *Generalized Depression: many other causes; small pupil, fatigue, wrong lens, media opacity, age, glaucoma, 3. Vertical BS enlargement: may be due to peripapillary atrophy
List 3 CLASSIC (localized) VF defects in 'early' glaucoma
1. Paracentral scotoma: Commonly recognized as the earliest single VF defect and earliest to occur in combo with other defects (Nasal step ~ 50%). Use static threshold perimetry, 2. Nasal Step: sensitivity drop across the nasal horizontal midline due to arcuate damage sup or inf --> only in or more so in one vs the other. , -Centrally far more common, -~75% occurs as earliest defect combined with paracentral scotoma, 3. Temporal sector/Wedge: nasal radial fibers, points toward temporal side of BS, may cross midline
What is the criteria for nasal step on Goldmann?
Width: > 5 - 10 degrees (if consistently repeatable then any size), Depth: > 5 - 10 db, Compare threshold to those of mirror image, -Points across the nasal horizontal midline
What is the main goal of glaucoma therapy?
To maintain maximal visual function- index currently is VF
Is improvement from glaucoma therapy common? What about stabilization?
No. <2><10%
According to Midelberg/Drance by what percentage does damage increase
79% of all VF defects become denser, - 52% increase in size, - 50% develop new VF defects , - 87% progressed, 2% improved, 10% stabilized
What are the optimal testing conditions of VF
1. Pupil at least 3 mm on every test - dilate, 2. Appropriate correction to distance, 3. Align pts eye and maintain thruout test - adjust if necessary, 4. Do not leave the room during test
List 2 types of VF testing
1. Screening: good for routine exams (FDT N30), 2. Threshold testing: standard of care in management and detection. Use on glaucoma suspects (ex. Large C/D), those at high risk (high IOPs), -Types of Threshold, a. White on White: standard, b. SWAP: good if you detect that white on white isn't picking up the defect, c. FDT
T or F? VF are more important in glaucoma management than is IOP
True. VF testing, ONH and RNFL eval are more important that IOP
Which two structures do you need to assess for structural damage?
ONH eval: Best technique?
For stereoscopic view --> high mag, fine slit beam = Fundus lens
ONH eval: T or F? You want to evaluate color when judging cup
False. Cup is defined by contour., *Cupping of neural rim w/o pallor w/in the cup is highly specific to early glaucomatous ONH damage - difficult to see, -Keys to judging contour changes, a. use smaller vessels -deflect at edge, b. narrow slit beam - deflection, c. stereopsis optimal at high mag - but may not be too helpful
ONH eval: What is the significance of a ONH evaluation
Important to R/O non-glaucomatous causes of RNFL dropout, VF loss --> both not very specific for glaucoma. R/O ONH atrophies (pallor), -Pallor outside of cup = Optic neuropathy, *Harder to slow progression if damage is significant
ONH eval: List 2 patterns of ONH damage
1. Diffuse/generalized: enlarged round cup. Most common; 50% pts present diffuse - hard to detect. Associated with general RNFL loss, color decrease (BY), general VF loss, 2. Focal/Localized: Most commonly inferior rim; superior is second. Associated with focal VF defects (nasal step), RNFL defects (slits), Drance hemes
ONH eval: List 4 components of a systematic ONH strategy
1. ONH size: Cup size related to ONH size (Increased ONH = Increased C/D), 2. Rim tissue: most important aspect of ONH in glaucoma, 3. Cup/Disc: Indirect indicator of rim width, 4. Parapapillary atrophy: Zone beta - Closer to ONH; Zone Alpha - more peripheral to beta
T or F? Cup size is not strongly related to ONH size
False. Larger ONH --> Larger C/D ration, -AA tend to have the largest ratio > Asians/Hispanics > Caucasians, - Larger ONH for higher myopes and small for higher hyperopes, *Always check ONH size before evaluating C/D, - 60D lens best for estimating size because least amount of mag (closer to pt RE)
T or F? Rim tissue is the most important feature of the ONH to evaluate in glaucoma
Localized thinning usually appears inferior (notched) rather than superior. But rim tissue is NORMALLY slightly thicker where?
ISNT rule: Inferior > sup > nasal > temp; Inf/Sup 1.5-2x thicker than Temporal, - Cup is normally oval horizontally while the ONH is a vertical oval, -Also compare Superior OD vs. Superior OS (also other areas too)
Which part of the rim tissue should display this PINKEST color?
Nasal is the pinkest. Then Sup/Inf, -Temporal is variable in color (stretching in high myopes), **Pallor of rim tissue (outside of cup) strongly suggests nonglaucomatous optic neuropathy; pallor fills into the cup in glaucoma and PRECEDES the cup in nonglaucomatous atrophy
What is considered the most critical characteristic when evaluating the rim tissue?
Contour., -Saucerization/shelving = cupping w/o pallor in the shelf resulting in two level saucer-shaped cup - must judge contour to detect
C/D is judged by contour - not color. T or F?
True, -C/D ratio is an indirect indicator of rim width, -2% of normals have C/D > .7
What two components of parapapillary atrophy (PPA) are considered in glaucoma?
Zone Beta: closer to ONH - has large choroidal vessels showing. More significant, Zone Alpha: more peripheral to Beta, irregular pigment
List common signs/changes of the ONH that are highly suggestive of glaucoma
1. Overall decrease in rim tissue --> Increase in C/D ratio, 2. Focal decrease rim width/focal notching/polar notching, 3. Saucerization - subtle, 4. C/D asymmetry in OD vs OS, 5. Vertical Cupping: normal cup is horizontally oval, 6. PPA: can be due to age; *increase in Beta predictive of onset, 7. Pallor: fills cup; *cupping precedes pallor toward disc margin, 8. Laminar dot sign: *In location where they were not previously - more slit shapped, 9. Drance hemes: at edge of disc usually at 12 and 6 oclock, 10. Focal constrictions of arterioles as they leave the ONH, 11. Baring of the circumlinear vessel - cup has progressed beyond vessel, 12. Acquired pit of ONH (APON): focal excavation of rim tissue often precedes focal VF loss
T or F? Drance hemes are highly specific to glaucoma (LTG > POAG) and they precede focal ONH/RNFL damage and local VF loss by years
True., -Suggests inadequate IOP control, -#1 ddx of Drance Heme = LTG or POAG
RNFL evaluation: ___% of axon damage occurs before a RNFL defect appears
30-50%., -RNFL defect can precede ONH damage and usually precedes VF loss.
RNFL loss can be used to predict presence of and the TYPE of subsequent VF defect. What are the two types?
1. Diffuse RNFL loss: general depression of VF possible but r/o artifacts, 2. Focal RNFL loss (slit or wedge) may have localized VF loss (scotoma, NS) in corresponding area of VF
RNFL loss appears:, 1. ___% axon loss on Goldmann, 2. ___% axon loss on white-on-white threshold perimetry, 3. ____% axon loss on SWAP
1. 40-50%, 2. 20-40%, 3. 20-30%
Which type of RNFL pattern loss is easier to detect and why?
Localized/Focal defects are easier because of the difference in appearance from the surrounding fibers (appear darker), -Most often inferior or superior arcuate, -Diffuse much more common in early glaucoma, -In diffuse look for: increased visibility and contrast of larger vessels close to disc
What would you do in this situation... Glaucoma suspect presents with a RNFL defect with no associated VF loss
Initiate Glaucoma therapy, *10-15% of normals have slit defects - if you have not seen this pt before then you cannot be certain this is a change. If other signs then follow as a suspect.
Pseudo-slit defects (slit defects in normals) are narrow ( < 1 vessel width) defects. But how do you differentiate them from a TRUE defect of the RNFL?
Pseudo defects don't continue into the ONH. , -Any cause of ONH damage causes RNFL loss - RNFL loss is NOT very specific to glaucoma. Evaluate ONH or other findings to DDx
What is the most reliable way to decide if glaucomatous suspects have early glaucoma damage?
Review Fundus photos. Documenting is the easiest and most reliable way to follow change, *Gold standard = 20 degree stereo photos of ONH at high magnification
What are some advantages of these new technology devices such as OCT, HRT, and GDx?
1. Identify glaucoma now; however wide variation in normal, 2. Identify change over time that could not be detected by other instruments
Which instrument measures the retardation of polarized light from the RNFL and which one generates a 3-D image from a series of focal cuts thru the long axis of the ONH?
1. GDx: Polarized change is directly proportional to RNFL thickness, 2. HRT: Calculates quantitative characteristics of the ONH relative to a reference plane
Which instrument is similiar to a B scan ultrasound but uses low coherence light which analyzes the backscatter from the retinal layers?, Which one uses a digital fundus cmera with scanning slit lamp to capture images of the x-section of the retina?
1. OCT, 2. Retinal thickness analyzer
When should you use ONH/RNFL imaging?
*1. High risk: high IOP, numerous strong risk factors, 2. Possible evidence of ONH/RNFL damage, 3. Glaucomatous appearing VFs with high IOP but no apparent structural damage, 4. Anomalous ONHs which make glaucoma changes difficult (i.e. tilted disc), 5. Early to moderate stage glaucoma
According to the OHTS study - what was the strongest risk factor related to progression to POAG in OC hypertensive pts?
Thin corneas, *Pachymetry has become the standard of care in diagnosis/management of ocular hypertensives.
Are provocative tests for OAG used?
Not really, 1. Water provocative: too many false positives/negatives, 2. Dilation/cycloplegic
What are the provocative tests for Narrow AG?
1. Prone Dark Room (PDRP): most physiologic test, -positive > 8mmHG rise, 2. Dark Room: sitting up instead, 3. Dilation: Positive if > 8mmHg
List other tests of visual function
1. Color: Good evidence of color defect in early glaucoma, 2. Contrast sensitivity, 3. Dark adaptometry, 4. ERG/VER, 5. Color Fields, 6. SWAP/FDT/High pass resolution perimetry