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76 Cards in this Set

  • Front
  • Back
characteristic of POAG
1. progressive
2. chronic optic neuropathy
3. open anterior chamber angle
4. atrophy of optic nerve
5. loss of retinal ganglion cells
6. visual field damage
7. IOP involvment
what are the FOUR theories of how glaucoma causes damage
1. mechanical compression
2. ischemic vascular
3. excitotoxicity of neural cells
4. genetically pre-programmed cellular suicide
what are the main characteristics of MECHANICAL COMPRESSION IN POAG
1. fiber distortion due to pressure resulting in vertical cupping
2. increased IOP causes stretching of lamina connective tissue (only bad in POAG)
3. connective tissue collapses on itself
what are the main characteristics of ISCHEMIA in POAG
1. vascular stasis to the short posterior ciliary arteries which supplies the anterior ONH
2.disrupts axonal transport
3. increased IOP compresses vessels with lower interluminal pressure
4. causes decreased metabolic activity (increases exotoxins, glutamate)
5. deprivation of neutrophins and RGC death due to low axonal transport
what are the main characteristics of EXCITOTOXICITY in POAG
1. low glutamate= neurotransmitter
2. high glutamate= neurotoxin
3. due to neutrophin deprivation due to ischemia
4. when cells die they release glutamate which kills healthy adjacent cells
what is the mechanism of glutamate in the eye
1. acts on sodium channels
2. increases calcium levels
3. activates nitric oxide synthase
4. increases nitric oxide
5. form free radicals
6. result in retinal cell death
what is the current pathophysiology of glaucoma
1. deforms lamina cribosa
2. impairs blood flow to the optic nerve
3. decreases ocular perfusion pressure
4. block axonal transport
5. deprives the ganglion cells of nerve growth
6. APOPTOSIS occurs
7. dead cells release glutamate to adjacent cells
8. pressure and ischemia also plays a contributing factor
what is preperimetric glaucoma
1. glaucomatous damage to the optic nerve with noticeable visual field loss
2. glaucoma can be diagnosed based upon disc appearance in the absence of visual field loss
uveitis in relation to glaucoma
1. uveitis can cause IOP elevation (uveitic glaucoma)
2. not TRUE glaucoma, but if the condition is not treated, glaucoma pathology will develop.
what is ocular hypertension
IOP of 21+ mmHg in the absence of structural and functional change
what are SEVEN characteristics to SUSPECT glaucoma
1. elevated IOP/OHTN
2. suspicious disc appearance
3. family history of glaucoma
4. increase age
5. race
6. suspicious VF loss
7. suspicious NFL
what are the characteristics of POAG (7)
1. most prevalent type of glaucoma
2. DECREASED OUTFLOW (not increased inflow)
3. elevated IOP
4. Rim Notching
5. NFL defects
6. OPEN ANGLE
7. MUST RULE OUT SECONDARY CAUSES
what is the main problem in the ANTERIOR SEGMENT in relation to POAG
DECREASED OUTFLOW
increased resistance to outflow at the level of the juxtacanalicular tissues in the trabecular meshwork
what is the main problem in the POSTERIOR SEGMENT in relation to POAG
1. compression of laminar sheets
2. distortion of laminar pores
3. blockage of axonal transport
4. death of ganglion cells
5. deepening and enlargement of optic cup
6. posterior and lateral displacement of laminar sheet
where does the visual field loss occur in glaucoma?

what is the earliest detectable visual field loss
1. 90-93% of all field loss in glaucoma occurs within the central 30 degrees
2. not a disease where the patient loses peripheral vision
3. earliest detectable field defect is SMALL FLUCTUATING SCOTOMA
how should you consider IOP in glaucoma
1. MOST significant risk factor OVERALL
2. however IOP is different between individuals and should not be made a prerequisite for glaucoma
3. half of all glaucoma patients have IOP <21mmHg
4. increase with age
5. decrease with exercise (transiently)
6. increased blood osmolarity decreases IOP
Diurnal Variuation of IOP
normal?
when is IOP is highest?
1. normal: <5mmHg
2. highest IOP occurs when the patient is sleeping in the supine position
READ OVER THE STUDIES ON PAGE 9 OF THE POAG PACKET
READ OVER THE STUDIES ON PAGE 9 OF THE POAG PACKET
what are the most significant risk factors for glaucoma today (5)
1. elevated IOP
2. thin central cornea
3. old age
4. race (blacks and older hispanics)
5. lower OPP
gonioscopy and glaucoma??
CANNOT accurately diagnose or categorize any glaucoma unless you do GONIOSCOPY
what where the results of the advanced glaucoma intervention study (AGIS)
1. black pts. with advanced glaucoma should receive LASER FIRST
2. white pts. with advanced glaucoma should receive SURGERY FIRST
3. Low IOP is associated with reduced progression of visual field defects
what were the key features in the Ocular Hypertensions Treatment Study
1. determines if lowering IOP in OHTN pt will reduce glaucoma
2. OHTS is the first and only NEI funded study that used an optometrist and an optometry college as a principal investigator
3. lowering IOP in patients with OHTN reduced the risk of developing glaucoma in five years
4. central corneal thickness appears to be a powerful predictor of the progression from OHTN to POAG
5. Blacks in the study had twice the risk of developing POAG
gonioscopy in relation to anterior angles (5)
1. artificially opens closed angles by creating suction
2. false impression of angle (more open than it truely is)
3. excess light or near fixation may make an angle appear more open than it typically is
4. best performed in light and dark
5. TONO BEFORE GONIO
what are the anterior structures seen in gonioscopy from posterior to anterior
1. iris
2. angle recess
3. ciliary body
4. scleral spur
5. trabecular meshwork
6. schwalbes line
what is the best anatomical landmark to find in gonioscopy?
why?
SCLERAL SPUR
1. anterior to it is TM
2. posterior to it is ciliary body

massive angle recession can cause TWO scleral spurs
what type of pigmentation is most important to notice?
degree of pigmentation of the TRABECULAR MESHWORK is more important than ciliary body
what structure is highly indicative of pigment dispersion syndrome
SAMPAOLESI'S LINE
what is the difference between angle recess and angle recession
1. angle recess: area between iris and cornea
2. angle recession: traumatic dialysis of the iris from the ciliary body
what is peripheral anterior synchiae?
what causes it
permanent adhesion between the iris and TM caused by:
1. inflammation
2. angle closure
3. neovascularization
4. trauma/hyphema/surgery
5. congenital
characteristics of angle recession
1. blunt trauma
2. CB tear
3. TM scarring
4. angle appears very open
5. need contralateral comparison
6. antecedent trauma usually included hyphema
what is diagnostic for chronic angle closure glaucoma
SUPERIOR ANGLE PERIPHERAL ANTERIOR SYNCHIAE (PAS)
what helps to differentiate between PAS and appositional closure
indentation gonioscopy
what type of notching do you usually see with glaucoma
1. vertical elongation via inferior and superior notching
2. occurs only from inside cup to inner rim (not outside)
3. hemorrhages and visual defects usually accompanies notching
what are disc hemorrhages usually located?
1. superior and inferior
2. nasal and temporal hemorrhages tend to not be associated with glaucoma
3. typically where notching occurs
4. resides in the retinal nerve fiber layer, NOT IN CUP

*resolves in 6 weeks
what are two criterias of NFL defect
1. they are at least the same caliber as an arteriole
2. they must extend to the disc

*anything that doesnt meet these criteria are pseudodefects
what is parapapillary atrophy?
what are the zones
1. atrophic peripapillary retina shoud suspect glaucoma
2. ZONE BETA: adj to nerve, scleral tissue and more associated with glaucoma
3. ZONE ALPHA: pigment adj to zone beta
what is the SAME in tumors and glaucomas
1. isolated
2. painless
3. progressive
4. visual dysfunction
5. cupped disc
what is DIFFERENT about tumor and glaucoma
1. visual acuity
2. color vision
3. RAPD
4. visual field defect
5. disc appearance (pallor is not glaucoma, obliteration of rim IS glaucoma)
other than glaucoma, what notches a cup?
1. AION
2. Compression
3. Inflammation
4. Trauma
5. Hereditary

*rim pallor is NOT glaucoma
*remember the ISNT rule of THICKNESS
what are the visual field changes in glaucoma (scotoma) (7)
types of scotomas:
1. relative
2. fluctuating
3. absolute
4. paracentral (5-15 degrees)
5. nasal step
6. arcuate (Bjerrum)
7. altitudinal defect
what is the earliest visual defect?
what is the earliest DETECTABLE defect?
1. earliest: increased short term fluctuations
2. earliest detectable: shallow fluctuating scotoma
what are the visual field testing that can be done to diagnose glaucoma
FT, SITA, SITA FAST
1. 30-2 (30 deg)
2. 24-2 (24 deg)
3. 10-2 (10 deg)

*24-2 most used and accurate for glaucoma
*cannot compare results from different test strategies and testing algorithms
how does fixation loss occur in visual field testing
1. pt gaze often drifts from fixation
2. presumed location of blind spot is incorrect
3. pt readjusted head position after the blind spot had been plotted
what function in the visual field machine helps manage fixation loss
eye tracking system (gaze monitor)
1. deviation up: pt gaze was not on the fixation target
2. deviation down: indicates a blink
what is indicative of a high false NEGATIVE value
1. fatigue
2. changed personal criteria for response
3. true indicator of actual field loss where sensitivities are variable
what is indicative of a high false POSITIVE value
1. suprathreshold levels
2. MD has a high positive value
3. fixation loss high
4. patchy loss on grayscale
5. PD is worse than TD

*unreliable field
*most devasting to interpretation (10+% should be discarded)
what is the best representation of the TRUE retro-lenticular visual field defect
PATTERN DEVIATION
what is mean deviation in the visual field testing
weighted average of the numbers on the total deviation plot each value weighted according to the magnitude of the normal range at that point
what can the mean deviation signify
1. overall severity of the field loss
2. interpret the severity of the field loss at individual locations and the area of the field involved
what can a POSITIVE mean deviation signify?
NEGATIVE?
1. positive: average sensitivity is above the normal for age
2. negative: average sensitivity is below the average age matched normal
abnormalities in mean deviation can indicate:
1. widespread damage
2. general depression
3. many small depressions
what is the relationship between MD and PSD
1. MD worsen and PSD relatively the same is WORSENING CATARACT
2. MD remains stable, PSD worsens, PROGRESSING GLAUCOMA
3. Both worsening, both glaucoma and cataract is getting worse
what should be measured when giving a beta blocker
pulse rate
blood pressure
what is the biggest failure of treatment
NONCOMPLIANCE
monocular trials?
what are the misconceptions?
DO NOT GIVE VALUABLE INFO

MISCONCEPTIONS:
1. diurnal IOP is identical between eyes
2. diurnal IOP is similiar between days, weeks, months
3. response of medication is identical between eyes
how would you initiate a combo
1. CAI and BB effective, discontinue both and ADD COSOPT
2. A2 Agonist and BB effective, discontinue both and ADD COMBIGAN
3. Pilocarpine and CAI (po) are NOT great choices and NOT typically used

each medication added has diminishing returns
how is adherence often measured
1. self reporting (greatly overestimated)
2. electronic monitoring (theoretically ideal, not practical)
3. pharmacy records (still pretty useless)
what drugs have the highest degree of adherence and persistence?
why?
1. prostaglandins analogs
2. lowest prevalence of adverse effects
how do you improve patient adherence and persistance
1. easy dosing
2. ask open ended questions
3. acknowledge that dosages are going to be missed
4. provide printed information and internet sources
5. glaucoma social groups
6. preset next appointment or send reminders to schedule
what are the characteristics of the Scanning Laser Polarimetry
1. double pass laser along the NFL, records retardation times to measure thickness.
2. near infra red wavelength
3. <3min for both eyes
4. completely objective
5. clear corneal surface required
6. undilated pupil works best
when it comes to imaging, what is the greatest indicator of glaucoma vs. normalcy
SYMMETRY between the two eyes
what is the mechanism for PROSTAGLANDIN ANALOGS?

dosing?
enhance uveoscelral outflow

QD (NEVER INCREASE)
what is the mechanism for MIOTICS?

dosing?
Increases outflow of aqueous through trabecular meshwork

QID
what is the mechanism for ALPHA AGONIST?

dosing?
aqueous suppressors

TID
what is the mechanism for BETA BLOCKER?

dosing?
aqueous suppressors

BID
what is the mechanism for CARBONIC ANHYDRASE INHIBITORS?

dosing?
aqueous suppressors

TID
contraindication of prostaglandins analogs
1. secondary inflammatory glaucoma
2. uveitis
3. anterior segment inflammation
contraindication for miotics?
1. NEVER use miotics with inflammation
2. NEVER let the person fet up after taking medication (vasovagal response)
3. uveitic glaucoma
4. neovascular glaucoma
5. aphakia
6. retinal detachment
7. cataracts
8. pre-presbyopes
what are the most significant effect of alpha 2 agonist
1. drowsiness
2. fatigue
3. dry mouth
4. headache

DO NOT USE ON KIDS
what drugs is most likely to cause systemic side effects
beta blockers
what type of medication do you use for atheletes
OCUPRESS (beta blocker)
1. has intrinsic sympathetic activity
2. least likely to cause bradycardia even though its NON SELECTIVE
characteristics of OSMOTICS
1. osmotic dehydrations (sucks fluid out of patients, TWSS)
2. serve this with cracked ice (like a COCKtail, haha)
3. EMESIS
4. NOT for use in chronic care (USE ONLY ONCE!!!)
what are the contraindications for carbonic anhydrase inhibitors
1. sulfa allergies (SJ syndrome)
2. sickle cell
3. hypokalemia
4. renal/liver diseases
5. COMPROMISED CORNEA!!
what is the best companion for a prostaglandin analog
CARBONIC ANHYDRASE INHIBITOR!!!
what are the combo medications?

dosing
1. COSOPT (BB+CAI)
dosing: BID

2. COMBIGAN (BB+AA)
dosing: BID
what are the criteria for neuroprotection?

what glaucoma drug class has this?
1. must reach target
2. must have receptors on the target organ
3. has to confer some resistance to stress
4. has to be proven effective in humans

*alpha agonist has been said to have neuro-protective effects