Glaucoma

Front 1

EPI: Definitions
-What are the 3 factors that determine IOP?
-What is the general etiology of open angle glaucoma?
-What are causes of combined mechanism glaucoma?

Back 1

Definitions
-3 factors that determine IOP: 1) aqueous production; 2) aqueous outflow; 3) episcleral venous pressure
-OAG: abnormality in TM extracellular matrix & in TM cells in the juxtacanalicular region
-Combined mechanism glaucoma: pt w/ OAG who develops secondary angle closure from other causes OR patient successfully treated for narrow angles who still has decreased outflow facility and elevated IOP

Front 2

EPI: Open angle glaucoma
-Prevalence of POAG in US pts > 40 yo?
-POAG is the most frequent cause of irreversible blindness in which pt population?
-The different types of glaucoma account for what % of worldwide blindness?

Back 2

Open angle glaucoma
-Prevalence of 1.86% in US individuals > 40 yo
-POAG is the most frequent cause of irreversible blindness in BLACKS
-Glaucoma accounts for 15% of blindness worldwide (follows cataracts & river blindness)

Front 3

EPI: Open angle glaucoma
-How much more prevalent is glaucoma in older pts compared to younger? How does this vary with black pts?
-Risk factors for POAG? (list proven and controversial)

Back 3

Open angle glaucoma
-Older pts (70s) are 3-8x more likely than pts in 40s to have glaucoma
-Prevalence in blacks is 3-4x higher than for whites; 4x higher risk of blindness
-Risk factors (proven): increased IOP, positive family history, advanced age, decreased corneal thickness, race (blacks are 3-4x more likely to have glaucoma than whites)
-Risk factors (some data): Diabetes, myopia

Front 4

EPI: Open angle glaucoma
-What did the Baltimore Eye Survey show re: glaucoma prevalence in older vs young and blacks vs whites?
-What are some reasons behind why blacks are more at risk for glaucoma?

Back 4

Open angle glaucoma
-Baltimore Eye Survey: prevalence of glaucoma among whites was 3.5x higher for 70 yo than for 40 yo (ratio was 7.4 in blacks)
-Black pts have larger discs, more nerve fibers, thinner central corneas

Front 5

EPI: Primary angle closure glaucoma
-What population of pts worldwide has the highest prevalence of PACG?
-What is the prevalence in Asian populations?
-Is there a gender association for PACG?

Back 5

Primary angle closure glaucoma
-Inuits from Arctic regions have the highest known prevalence of PACG (30-40x higher than for whites)
-Asians have prevalence rate b/w Inuits and whites
-Females more at risk for acute angle closure --> have shallower ACs than men

Front 6

EPI: Primary angle closure glaucoma
-How does the AC change with age? What is the most common age of presentation of PACG?
-What refraction is assoc w/ PACG?
-Is there any association w/ positive family history and PACG?

Back 6

Primary angle closure glaucoma
-AC volume & depth decreases w/ age --> may predispose to pupillary block
-PACG most common b/w ages of 55-65 yo
-Hyperopia is assoc w/ increased risk of PACG
-Relatives of PACG pts have higher risk of angle closure than general population (b/c some anatomic features predisposing to pupillary block - lens position/thicknes - may be inherited)

Front 7

EPI: Genetics
-What is the contribution of genetics vs environmental factors to development of glaucoma?
-What is the prevalence of glaucoma among siblings?
-What is the inheritance pattern of many glaucomas?

Back 7

Genetics
-UNKNOWN relative contributions of environmental vs genetic factors to development for glaucoma
-Known genes account for only a small % of glaucoma
-Prevalence of glaucoma among siblings = 10%
-Many glaucomas are autosomal dominant, polygenic, late onset, incomplete penetrance

Front 8

EPI: Genetics of OAG
-What is the location and product of the GLC1A gene?
-What % of pts w/ adult onset POAG have this mutation?
-What are 2 loci identified for normal tension glaucoma
-What are these mutations thought to be assoc with (pathophysiologically)?
-What type of glaucoma is assoc w/ GLC1C and GLC1D mutations?

Back 8

Genetics of OAG
-GLC1A gene: produces myocilin protein (induced by TM cells treated w/ dexamethasone) --> chromosome 1
-GLC1A reported in 3% of pts w/ POAG
-2 loci for normal tension glaucoma: GLC1B (ch 2), GLC1E (ch 10) --> may render optic nerve more sensitive to IOP or faciliate optic neuropathy independent of IOP
-GLC1C (ch 3),GLC1D (ch 23) cause high pressure glaucoma w/ late onset, moderate response to meds

Front 9

EPI: Genetics
-What inherited ocular condition is assoc w/ higher frequency of angle closure glaucoma? which chromosome are these defects mapped to?
-What gene is assoc w/ the majority of inherited congenital glaucomas? What is the gene product?
-Name 2 other genes assoc w/ anterior segment dysgensis that can cause glaucoma

Back 9

Genetics
-Nanophthalmos is assoc w/ angle closure glaucoma --> 3 genes found on ch 11
-Primary congenital glaucoma maps ot GLC3A --> cytochrome P450 mutation
-PITX2 and PAX6 are assoc w/ anterior segment dysgenesis & assoc glaucoma

Front 10

AQUEOUS/IOP: Aqueous humor formation
-How does aqueous exit the eye? (2 ways)
-What is the structure, blood supply andnumber of ciliary processes?
-What component of the ciliary processes comprises a major part of the blood-aqueous barrier?

Back 10

Aqueous humor formation
-Aqueous exits the eye via TM --> Schlemm's canal --> venous channels
-Aqueous also exits via root of iris and ciliary muscle --> suprachoroidal space --> sclera
-Ciliary processes: 80+ in number, double layer of epithelium arranged apex-to-apex over core of stroma and fenestrated capillaries - supplied by major arterial circle of iris
-Blood-aqueous barrier created by tight junctions b/w apical surfaces of pigmented and nonpigmented epithelial cells of ciliary processes

Front 11

AQUEOUS/IOP: Aqueous humor formation
-What structures are found within the outer pigmented and inner nonpigmented cells of ciliary processes?

Back 11

Aqueous humor formation
-Inner nonpigmented cells: protrude into posterior chamber, many mitochondria & microvilli --> major site of aqueous production
-Outer pigmented cells: contain many melanin granules, face ciliary stroma and vessels

Front 12

AQUEOUS/IOP: Aqueous humor formation
-What are the 3 mechanisms by which aqueous humor is produced and secreted into posterior chamber?
-What is the rate of aqueous production?

Back 12

Aqueous humor formation
-Active secretion (majority of aqueous production): involves carbonic anhydrase II enzyme
-Ultrafiltration: pressure-dependent movement of fluid into/out of eye (hydrostatic pressure b/w capillaries and IOP favors fluid movement into eye & oncotic pressure resists movement into eye)
-Diffusion: passive movement of ions across a membrane related to charge/concentration
-Rate of aqueous production: 2-2.5 uL/min

Front 13

AQUEOUS/IOP: Aqueous humor formation
-What substances are found in excess and in deficit in aqueous compared to plasma?
-What is the protein concentration of aqueous relative to plasma?
-What is the major protein in the aqueous?

Back 13

Aqueous humor formation
-Aqueous contains EXCESS H and Cl ions & ascorbate relative to plasma
-Aqueous contains DEFICIT of bicarbonate relative to plasma
-Aqueous protein concentration is 1/200-1/500 that of plasma --> allows optical clarity, reflects integrity of blood-ocular barrier
-Albumin accounts for 50% of aqueous protein

Front 14

AQUEOUS/IOP: Aqueous humor formation
-How does aqueous production vary during sleep and during the day?
-How does aqueous production and outflow facility change with age?
-What are some factors affecting the rate of aqueous production?

Back 14

Aqueous humor formation
-Aqueous production varies diurnally and decreases during sleep
-Age causes decrease in aqueous formation and in outflow facility
-Factors affecting aqueous production: 1) integrity of blood-aqueous barrier; 2) blood flow to CB; 3) neurohumoral regulation of vascular tissue/ciliary epithelium --> therefore, aqueous production decreases s/p trauma, intraocular inflammation, general anesthetics and systemic hypotensives, carotid occlusive disease

Front 15

AQUEOUS/IOP: Aqueous outflow
-What is the rate of aqueous outflow?
-What are the 3 parts of the trabecular meshwork? Which of these is the major site of outflow resistance?

Back 15

Aqueous outflow
-Rate of outflow: 0.22-0.3 uL/min/mmHg
-3 parts of TM: 1) uveal (adjacent to AC, bands that extend from iris root/CB to peripheral K); 2) corneoscleral (from SS to lateral wall of scleral sulcus); 3) juxtacanalicular (adjacent to, forms inner wall of, Schlemm's canal) --> major site of outflow resistance

Front 16

AQUEOUS/IOP: Aqueous outflow
-What type of outflow occurs in the TM?
-What is a function of the TM cells?
-What are some histologic changes that occur in TM w/ age?
-How many trabecular cells are present per eye?

Back 16

Aqueous outflow
-Pressure-dependent outflow occurs via TM
-TM cells are phagocytic
-Aging changes to TM: increased pigment granules, decreased trabecular cells, thickened basement membrane beneath them
-200,000-300,000 trabecular cells per eye on average

Front 17

AQUEOUS/IOP: Aqueous outflow
-What is the structureof Schlemm's canal?
-Where does aqueous go after entering Schlemm's canal?

Back 17

Aqueous outflow
-Schlemm's canal: inner wall contains giant vacuoles that communicate w/ intertrabecular spaces & outer wall lined w/ endothelial layer w/o continuous BM
-Aqueous travels from Schlemm's canal --> episcleral veins --> anterior ciliary & superior ophthalmic veins --> cavernous sinus

Front 18

AQUEOUS/IOP: Aqueous outflow
-What type of outflow occurs by the uveoscleral mechanism?
-What is the path of aqueous movement via uveoscleral outflow?
-What % of total aqueous outflow is accounted for by uveoscleral outflow?
-What agents increase and decrease uveoscleral outflow?

Back 18

Aqueous outflow - Uveoscleral
-Pressure-independent outflow
-Aqueous travels from AC --> ciliary muscle --> supraciliary and suprachoroidal space --> sclera
-Accounts for 5-15% of total aqueous outflow
-Increased by: prostaglandin analogs, cycloplegia, adrenergic agonists
-Decreased by: miotics

Front 19

AQUEOUS/IOP: Tonography
-What instrument is used in tonography?
-How is tonography performed?
-What is tonography used for today?

Back 19

Tonography
-Shiotz tonometer
-Measures facility of aqueous outflow --> place tonometer on cornea to acutely increase IOP --> rate at which pressure declines w/ time is related to ease of aqueous outflow
-Used as a research tool primarily

Front 20

AQUEOUS/IOP: Episcleral venous pressure
-Normal range of episcleral venous pressure?
-How much does IOP rise by every 1 mm Hg increase in episcleral venous pressure?
-What is the mechanism by which episcleral venous pressure impairs aqueous outflow?
-What situations/diseases are assoc w/ increased episcleral venous pressure?

Back 20

Episcleral venous pressure
-Normal range: 8-10 mm Hg
-IOP rises 1 mm Hg for every 1 mm Hg increase in eipscleral venous pressure
-Mechanism by which episcleral venous pressure impairs aqueous outflow: collapse of Schlemm's canal and increase in outflow resistance
-Conditions causing increase in episcleral venous pressure: Sturge Weber, thyroid eye disease, orbital disease obstructing venous return

Front 21

AQUEOUS/IOP: IOP epidemiology
-What type of distribution does IOP have within the general population?
-How many pts w/ glaucoma would be missed if only IOP > 21 was used for screening?
-List factors that cause variation in IOP readings

Back 21

IOP epidemiology
-IOP has a non-Gaussian distribution --> skew towards higher IOP in pts > 40 yo
-Screening for glaucoma based only on IOP > 21 would cause 50% of pts w/ glaucoma to be missed!
-IOP influenced by: time of day, heartbeat, respiration, exercise, fluid intake, systemic meds (i.e., EtOH decreases IOP, cannabis decreases IOP, caffeine has no effect), topical meds, body position (higher when recumbent b/c of increased episcleral venous pressure)

Front 22

AQUEOUS/IOP: IOP measurement
-What is the normal range of variation of IOP over a 24 hr period?
-Are higher IOPs assoc w/ greater or less variation?
-When do post pts reach daytime peak pressures?
-What is the impact of IOP fluctuations on optic nerve?

Back 22

IOP measurement
-Normal variation of IOP is 2-6 mm Hg over 24 hour period
-Higher IOP is assoc w/ greater fluctuation --> diurnal fluctuation of > 10 mm Hg suggests glaucoma
-Daytime peak pressures usually reached in morning hours --> poss 2/2 recent long period of supine positioning during sleep
-Impact of IOP fluctuation on optic nerve = UNKNOWN
-Systemic hypotension during sleep may account of optic nerve damage (malperfusion)

Front 23

AQUEOUS/IOP: IOP measurement
-What does the Goldmann applanation tonometer measure?
-Is the Goldmann tonometer affected by ocular rigidity?
-How does too much/too little fluorescein affect IOP readings?

Back 23

IOP measurement
-Goldmann tonometer measures force necessary to flatten 3.06 mm diameter area of cornea
-Goldmann tonometer is unaffected by ocular rigidity
-Excess fluorescein = inaccurately high reading (wide mires)
-Inadequate fluorescein = inaccurately low reading (thin mires)

Front 24

AQUEOUS/IOP: IOP measurement
-How does K edema and scarring affect IOP reading?
-How does measurement over soft CL affect IOP reading?
-What are other possible sources of error in tonometry?

Back 24

IOP measurement
-K edema --> low readings
-K scarring --> high readings
-Soft CL --> low readings
-Other sources of error: squeezing eyelids, valsalva, breath holding, tight collar/tie, obesity, straining, high K astigmatism, abnormal K thickness

Front 25

AQUEOUS/IOP: IOP measurement
-For what K thickness is the Goldmann tonometer most accurate?
-What is the estimated relationship b/w K thickness and IOP readings w/ Goldmann tonometer?
-What was a major finding of the OHTN treatment study re: K thickness and glaucoma?

Back 25

IOP measurement
-Goldmann tonometer is most accurate w/ CCT of 520 um
-For every 10 um difference in CCT from population mean (542 um) --> IOP changes by 0.5 mm Hg w/ Goldmann tonometer
**NOTE: there is no current accepted correction factor available to modify IOP interpretation depending on CCT!
-OHTN treatment study: thinner central cornea is strong predictor for development of glaucoma in pts w/ OHTN (3x increased risk of POAG)

Front 26

AQUEOUS/IOP: IOP measurement
-What are disadvantages of the non-contact (air-puff) tonometers?
-What are advantages of Tono-Pen and pneumatic tonometers?
-When is it useful to use digital pressure on globe to assess IOP?

Back 26

IOP measurement
-Air puff tonometers obtain widely variable readings & overestimate IOP
-TonoPen & pneumatic tonometers are useful in presence of K scarring or edema
-Digital palpation of globe only useful for detecting large IOP differences b/w 2 eyes (inaccurate in determining actual IOP)

Front 27

AQUEOUS/IOP: IOP measurement
-What are different strategies to clean tonometer tips after use?

Back 27

IOP measurement
-Soaked in household bleach (1:10 sodium hypochlorite), 3% hydrogen peroxide or 70% isopropyl alcohol x 5 minutes
-Tips can also be thoroughly wiped w/ alcohol sponge

Front 28

EVALUATION: History/exam
-What systemic conditions/diseases are important to ask about in a glaucoma eval?
-What associations do myopia and hyperopia (respectively) have with glaucoma?
-What information can be gained from assessing pupils in glaucoma pts?

Back 28

History/exam
-Systemic associations: diabetes, cardiac/pulmonary disease, HTN, history of shock or systemic hypotension, sleep apnea, Raynaud, migraine, renal stones, corticosteroid use, trauma
-Hyperopia: assoc w/ angle-closure glaucoma
-Myopia: increased risk of pigment dispersion, disc morphology can be confused w/ glaucoma
-Pupils: can use to monitor compliance w/ miotic tx OR to check for APD
**Note: if pt does not have reactive pupils, can check relative optic nerve function by asking pt to make subjective comparison b/w brightness of test light b/w eyes

Front 29

EVALUATION: History/exam
-What conjunctival signs are visible in pts on long term prostaglandins, epinephrine?
-What qualities of a bleb should be assessed on evaluation?

Back 29

History/exam
-Conjunctiva: adrenochrome deposits (epinephrine use), injection (sympathomimetics & prostaglandins)
-Bleb qualities to note: size, height, degree of vascularization, integrity, Seidel test

Front 30

EVALUATION: History/exam
-Name corneal signs to look for in glaucoma pts?
What is the Van Herick method?

Back 30

History/exam
-Corneal signs: K spindle, KPs, exfoliation material deposition, guttae, "beaten bronze" appearance (ICE syndrome)
-Van Herick method: measures depth of AC --> direct narrow slit beam at 60 deg angle onto cornea just anterior to limbus --> if distance from iris to posterior K is less than 1/4 thickness of cornea, angle may be narrow

Front 31

EVALUATION: History/exam
-What is iris bombe?
-What are iris signs to look for in glaucoma eval?
-What are lens signs to look for in glaucoma eval?
-What is the significance of a posterior subcapsular cataract in glaucoma?

Back 31

History/exam
-Iris bombe: AC is deep centrally, shallow/flat peripherally
-Iris signs: heterochromia, TI defects, atrophy, ectropion uveae, corectopia, nevi/nodules, exfoliation material
-Lens signs: pseudoexfoliation material, phacodonesis, subluxation, dislocation
-PSC may indicate long term steroid use

Front 32

EVALUATION: Gonioscopy
-What is the critical angle at the air-tear interface? What does this have to do with gonioscopy?
-What lenses can be used for direct gonioscopy?
-Difference b/w direct and indirect gonioscopy?

Back 32

Gonioscopy
-Critical angle at air-tear interface is at 46 degrees --> at this point, all light is totally reflected into corneal stroma --> prevents visualization of angle structures
-Need to eliminate air-tear interface to visualize angle
-Direct gonio lenses: Koeppe, Barkan, Richardson, Swan-Jacob or Wurst lens
-Direct gonioscopy: erect view of angle structures --> good for surgery (i.e., goniotomy)
-Indirect gonioscopy: angle viewed by seeing reflection from mirror within the lens (not direct visualization) --> note that image is inverted but right-left orientation does not change

Front 33

EVALUATION: Gonioscopy
-Which indirect goniolenses allow exam of all 4 quadrants of angle without having to rotate lens?
-What is the corneal wedge technique? What does it show?

Back 33

Gonioscopy
-Posner, Sussman and Zeiss 4-mirror goniolenses permit evaluation of entire angle without rotating lens
-Corneal wedge: allows determination of exact junction b/w cornea and TM
-Use narrow slit beam, will see 2 linear reflections (one from external surface of cornea and junction w/ sclera, other from internal surface of cornea --> both reflections meet at Schwalbe line

Front 34

EVALUATION: Gonioscopy
-Describe the 5 grades in the Shaffer system
-What angle features does the Spaeth grading system use?

Back 34

Gonioscopy
-Shaffer system: looks at angle b/w TM and iris
-Grade 4: 45 degree
-Grade 3: greater than 20, less than 45
-Grade 2: 20 degrees
-Grade 1: 10 degrees
-Grade 0: iris is against TM (angle closure is present)
-Spaeth system: peripheral iris contour, iris root insertion, angle configuration

Front 35

EVALUATION: Gonioscopy
-When is blood visible in Schlemm's canal?
-What are normal blood vessels in the angle?
-What are signs of abnormal blood vessels?
-Characteristic vessels in Fuchs heterochromic iridocyclitis?

Back 35

Gonioscopy
-Blood in Schlemm's canal: seen as faint red line in posterior portion of TM
-Pathophysiology: episcleral pressure > IOP (often because episcleral veins compressed by lip of goniolens) --> may also be 2/2 hypotony & high episcleral venous pressure diseases
-Normal angle vessels: radial iris vessels, vertical branches of anterior ciliary arteries
-Abnormal angle vessels: cross scleral spur to reach TM (i.e., in NVA, trunklike vessels cross CB & SS --> arborize over TM)
-Fuchs vessels: fine, branching, meandering vessels within angle (not neovascularization)

Front 36

EVALUATION: Gonioscopy
-What diseases are associated w/ heavy pigmentation of the angle?
-How does pigmentation vary depending on age and iris color?
-What is a Sampaolesi line?

Back 36

Gonioscopy
-Pigmentation of TM increases w/ age and w/ darkly pigmented irises
-Pathologic pigmentation: PXF syndrome (patchy), PDS (uniform)
-Sampaolesi line: line of pigmentation anterior to Schwalbe line, seen in PXF

Front 37

EVALUATION: Gonioscopy
-What findings are seen in post-traumatic angle recession?
-What is cyclodialysis? How does it appear gonioscopically?

Back 37

Gonioscopy
-Post-traumatic angle recession: abnormally wide CB band, increased prominence of SS, torn iris processes, variation of ciliary face width/depth in different quadrants of the same eye
-Cyclodialysis: separation of CB from SS --> on gonioscopy, looks like deep angle recess w/ gap b/w SS and CB

Front 38

EVALUATION: Optic nerve
-How many axons in the optic nerve?
-How does the diameter of the optic nerve change as it crosses the lamina cribosa?

Back 38

Optic nerve
-1.2-1.5 million axons
-Intraocular optic nerve: 1.5 mm diameter
-Retrolaminar optic nerve: 3-4 mm diameter (2/2 formation of axonal myelination, glial tissue, leptomeninges)

Front 39

EVALUATION: Optic nerve
-M cells: function, size?
-P cells: function, size?

Back 39

Optic nerve
-M cells: large axons, senstivie to luminance changes in dim conditions (scotopic), process info related to motion perception & DO NOT respond to color
-P cell: 80% of all ganglion cells, concentrated centrally, smaller axons, slower conduction, subserve color vision, active under high luminance and discriminate fine detail --> motion INsensitive!

Front 40

EVALUATION: Optic nerve
-What is the anatomy of retinal nerve fiber distribution within the optic nerve?
-What is the structure of the lamina cribosa?

Back 40

Optic nerve
-In optic nerve, peripheral retinal fibers run closer to the choroid and exit in the periphery of the nerve (central fibers situated closer to vitreous and occupy more central portion of nerve)
-Lamina cribosa: sheets of fenestrated connective tissue & elastic fibers --> provide main support for optic nerve as it exits the eye

Front 41

EVALUATION: Optic nerve
-Blood supply to different parts of optic nerve: NFL? Prelaminar? Laminar? Retrolaminar?

Back 41

Optic nerve
-NFL supplied by recurrent retinal arterioles branching from CRA
-Prelaminar and Laminar supplied by direct branches of short posterior ciliary arteries & branches of circle of Zinn-Haller
-Retrolaminar supplied by same branches as laminar region and also pial arteries coursing adjacent to optic nerve (originate from both CRA & short posterior ciliary arteries)

Front 42

EVALUATION: Optic nerve
-What area is supplied by the short posterior ciliary arteries in addition to optic nerve?
-What is the circle of Zinn-Haller?

Back 42

Optic nerve
-Short posterior ciliary arteries supply peripapillary choroid & anterior optic nerve
-Circle of Zinn-Haller: noncontinuous arterial circle within the perineural sclera

Front 43

EVALUATION: Optic neuropathy
-What is the appearance of advanced glaucomatous optic neuropathy?
-Where does tissue loss begin in glaucoma?
-What is the appearance of cupping in children/infants?

Back 43

Optic neuropathy
-Begins at level of lamina cribosa (compaction, fusion of laminar plates) & worst at superior and inferior poles of disc
-Advanced glaucoma: tissue loss extends behind cribiform plate, lamina bows backwards (looks like "bean pot" on DFE)
-Children/infants: glaucomatous cupping assoc w/ expansion of scleral ring --> explains why cupping occurs earlier in peds pts and why it is reversible w/ treatment

Front 44

EVALUATION: Optic neuropathy
-What is the mechanical theory of glaucomatous optic neuropathy?
-What is the ischemic theory of optic neuropathy?
-Which of these is more plausible in glaucoma?

Back 44

Optic neuropathy
-Mechanical theory: direct compression of axonal fibers and support structures of nerve --> distortion of lamina cribosa & interrruption of axoplasmic flow --> death of RGC
-Ischemic theory: intraneural ischemia caused by decreased optic nerve perfusion
-BOTH vascular and mechanical factors likely responsible for glaucomatous damage (glaucomas are likely a heterogeneous family of disorders w/ many causative factors)

Front 45

EVALUATION: Optic neuropathy
-What is the normal size of the optic disc?
-How can the 78D/90D lens be used at the slit lamp to calculate disc size?

Back 45

Optic neuropathy
-Normal diameter of optic disc: 1.5 - 2.2 mm
-Using 78D/90D lens, adjust height of slit beam until it is the same as the vertical diameter of disc --> take this value and multiply by 1.1 (78D) or 1.3 (90D) to obtain disc diameter in millimeters

Front 46

EVALUATION: Optic neuropathy
-How is disc size different b/w races and refractive errors?
-What is the normal vertical C:D?
-What level of asymmetry is considered abnormal?
-What are some non-glaucomatous causes for asymmetric cupping?
-Where does focal optic nerve atrophy tend to occur in glaucoma?

Back 46

Optic neuropathy
-Myopes, African Americans have larger discs than hyperopes/emmetropes, Caucasians
-Normal vertical C:D is 0.1-0.4
-Asymmetry should be < 0.2 C:D
-Abnormal C:D asymmetry may be familial or assoc w/ high myopia
-Focal optic neuropathy in glaucoma: follows ISNT rule (inferior, superior, nasal, temporal) --> order of thickest to thinnest areas of neuroretinal rim

Front 47

EVALUATION: Optic neuropathy
-Name early signs of glaucomatous optic nerve damage

Back 47

Optic neuropathy - early signs of glaucomatous damage
-generalized or focal cup enlargement
-splinter hemorrhage at disc (occur in 1/3 of glaucoma pts at some point in disease course)
-loss of NFL (use red-free to examine)
-translucency of neuroretinal rim
-vessel overpass (blood vessels overlying rim look like they are suspended over but not in contact with underlying tissue)
-asymmetric cupping
-peripapillary beta zone atrophy

Front 48

EVALUATION: Optic neuropathy
-What type of glaucoma is more likely to be assoc w/ disc hemorrhages?
-What clinical exam finding can be seen following resolution of disc hemorrhage?
-What are other etiologies of splinter disc hemorrhages?

Back 48

Optic neuropathy
-Normal tension glaucoma = more likely to be associated w/ disc hemorrhage
-Disc heme is often followed by localized notching of rim & VF
-Other causes of splinter hemorrhages: PVD, DM, BRVO, anticoagulation use

Front 49

EVALUATION: Optic neuropathy
-What is the difference b/w alpha zone and beta zone peripapillary atrophy?
-Is OCT able to provide an absolute measurement of NFL thickness?

Back 49

Optic neuropathy
-Alpha zone: temporal crescent seen in myopia (areas of hyper and hypopigmentation) --> no known impact on glaucoma
-Beta zone: loss of choriocapillaris & RPE, leaving large choroidal vessels and sclera (white appearance adjacent to disc margin) --> assoc w/ glaucoma and corresponding VF defects
-NFL OCT is able to yield an absolute measurement of NFL thickness

Front 50

EVALUATION: Perimetry
-What is SWAP?
-What is FDT? Which cells are activated using FDT?

Back 50

Perimetry
-SWAP (short-wavelength automated perimetry): projects blue stimulus onto yellow background --> sensitive for early ID of glaucoma
-FDT (frequency-doubling technology): low spatial frequency sinusoidal grating undergoing rapid flicker --> preferentially activates M cells --> may be good for early detection of glaucoma

Front 51

EVALUATION: Perimetry
-Define the following terms:
-Threshold
-Kinetic testing
-Static testing
-Isopter
-Scotoma

Back 51

Perimetry - definitions
-Threshold: light sensitivity at which a stimulus of given size/duration of presentation is seen 50% of the time (dimmest spot detected during testing)
-Kinetic testing: target is moved from area in which it is not seen to area in which it is seen
-Isopter: a line on VF representation connecting points w/ the same threshold
-Static testing: stationary stimulus presented at various locations
-Scotoma: area of decreased retinal sensitivity surrounded by area of increased sensitivity

Front 52

EVALUATION: Perimetry
-What are 6 patterns of glaucomatous VF defects?
-Describe each
-Which parts of VF tend to be preserved longest in glaucoma?

Back 52

Perimetry - Glaucomatous VF defects
-Generalized depression
-Paracentral scotoma (within 10 deg of fixation)
-Arcuate/Bjerrum scotoma (10-20 deg from fixation): a Bjerrum scotoma arches from blind spot and ends at nasal raphe, becoming closer to fixation on nasal side
-Nasal step
-Superior altitudinal defect: near complete or complete loss of superior VF field (fixation splitting)
-Temporal wedge
-Longest preserved areas of VF in glaucoma: central island of vision & inferior temporal VF

Front 53

EVALUATION: Perimetry
-What are standard sizes of stimuli in VF testing?
-What is the standard presentation time of a stimulus?
-What pupil size can induce artifacts during testing?

Back 53

Perimetry
-Stimuli sizes: 0-V (range from 1/16 mm2 to 64 mm2)
-Standard presentation time of stimulus is 0.2 seconds
-Pupil size should be recorded for each test --> if < 3 mm, may induce artifacts (should be constant from test to test)

Front 54

EVALUATION: Automated perimetry
-Purpose of suprathreshold testing?
-Threshold-related strategy?
-Threshold testing?
-Efficient threshold strategies (i.e., SITA)?
-Purpose of SITA fast VF?

Back 54

Automated perimetry
-Suprathreshold testing: screens for moderate to severe defects --> not useful for screening or follow up (uses suprathreshold stimuli at various locations)
-Threshold-related strategy: threshold determined at a few points & presumed hill of vision extrapolated from these points --> detects only moderate to severe defects (misses mild defects)
-Threshold testing: current standard for automated perimetry --> can use efficient or full threshold strategies to test VF
-Efficient theshold strategies (i.e., SITA): 50% shorter than full threshold testing, less fatigue for pt, less variability than full threshold --> SITA standard found to be comparable to full threshold testing
-SITA fast: 30% faster than SITA standard --> use for pts who are unable to perform SITA standard due to mental/physical limitations **SHOULD NOT be used in routine glaucoma eval**

Front 55

EVALUATION: Perimetry
-What are the most common program for threshold testing?
-When should serial 10-2 VF be used in glaucoma?

Back 55

Perimetry
-Most common programs for threshold testing: HVF 24-2 or 30-2
-Central 10-2 VF should be used for advanced VF loss that threatens fixation --> enables following many more test points within central island and earlier detection of progression

Front 56

EVALUATION: Perimetry
-How does VF quality and variability change with glaucoma?
-What is more suspicious: a cluster of 2 or more points depressed 5 dB or a single point depressed > 10 dB?
-Which part of VF is normally more depressed: the superior or inferior field?

Back 56

Perimetry
-VF variability and rate of false negatives increases in areas of glaucomatous damage
-A cluster of 2+ points with decreased sensitivity is more suspicious than a single severely depressed point b/c cluster points confirm one another
-Superior VF is normally 1-2 dB more depressed compared to inferior VF

Front 57

EVALUATION: Perimetry
-How is the association b/w glaucoma and short-wavelength (blue) color vision used in perimetry?
-What is the type of perimetry usd to measure blue vision?

Back 57

Perimetry
-Sensitivity to blue stimuli is mediated by a small population of bistratified ganglion cells (large receptive fields, little receptive field overlap, large axon diameter) --> if early ganglion cell loss in glaucoma preferentially affects sparse cell groups or thos w/ larger axons, these ganglion cells should be affected early
-SWAP (short wavelength automated perimetry) isolates these axons within the visual field for testing --> can detect early glaucomatous defects

Front 58

EVALUATION: Perimetry
-Describe possible sources of artifact in perimetry (lens rim, incorrect corrective lens, cloverleaf, high false positives, high false negatives)

Back 58

Perimetry - sources of artifact
-Lens rim: if lens is decentered or set too far from the eye
-Incorrect corrective lens: generally depressed VF, less of a problem w/ FDT
-Cloverleaf: if pt stops paying attention and ceases to respond half way through VF test OR malingering
-High false positives: "white scotomata" (impossibly high retinal sensitivity) --> can occur if pt responds when no stimulus presented OR when instrument records fixation losses by presenting stimuli in blind spot
-High false negatives: pt fails to respond to stimulus in location where dimmer stimulus previously seen --> may be seen in pts w/ significant VF loss including scotomata w/ steep edges (in this case, does not indicate unreliability)

Front 59

EVALUATION: Perimetry
-How should VF be used in mgmt of glaucoma?
-What are criteria to determine if VF defects are progressing?

Back 59

Perimetry
-Need good baseline VF (get at least 2 VF early in course of mgmt as pts may learn how to perform test after doing it once)
-All VF w/ new findings should be repeated to confirm changes from baseline
-Criteria for progression: 1) deepening of existing scotoma (depression of existing scotoma point by >7dB); 2) enlargement of existing scotoma (depression of point adjacent to scotoma by >9 dB); 3) development of new scotoma (depression of previously normal point by >11 dB or 2 adjacent previously normal points by >5 dB)

Front 60

EVALUATION: Perimetry
-Under what situations would VF defects be suspected to occur from cause other than glaucoma (using both VF and optic disc appearance together)

Back 60

Perimetry - Suspect nonglaucomatous defect if...
-Disc is less cupped than expected for degree of VF loss
-Pallor of disc is more impressive than cupping
-VF progression seems excessive
-Uncharacteristic pattern of VF loss (i.e., respects vertical midline)
-Location of cupping/thinning of rim does not correspond to location of VF defect

Front 61

OAG: POAG
-What % of screened individuals w/ "normal" IOP have glaucoma?
-What is the diurnal variation in IOP in normal pts and in those w/ glaucoma?
-What accounts for diurnal IOP elevation?

Back 61

POAG
-30-50% of individuals w/ IOP < 22 have glaucomatous damage to optic nerves/VF
-Diurnal variation of IOP in normal pts: 2-6 mm Hg
-Diurnal variation of IOP in glaucoma: may be >/= 10 mm Hg over 24 hours
-Diurnal variation thought to be 2/2 shift from daytime upright posture to supine night time posture (increased nocturnal IOP)

Front 62

OAG: POAG
-What is average CCT?
-What group of pts have increased CCT?
-What group of pts tend to have decreased CCT?

Back 62

POAG
-Average CCT = 530-545 in eyes without glaucoma
-OHTN pts tend to have HIGHER CCT
-Normal tension glaucoma pts tend to have LOWER CCT

Front 63

OAG: POAG
-What did the Baltimore Eye Survey, OHTS and the CIGTS find re: age as risk factor for glaucoma?
-What is the relationship b/w glaucoma/blindness and AA race?

Back 63

POAG
-Baltimore Eye Survey: increased risk of glaucoma w/ age, especially in blacks (>11% in >80 yo)
-OHTS: increased risk of OAG w/ age per decade
-CIGTS: VF defects 7x more likely in pts >60 yo
**Age is an independent risk factor for OAG!**
-Glaucoma is 3-4x more prevalent in AA pts, 4x greater risk of blindness in AA pts
-Glaucoma more likely to be diagnosed at an advanced stage in black pts

Front 64

OAG: POAG
-What did the Baltimore Eye Survey find re: family history as risk factor for glaucoma?
-Name other risk factors for POAG

Back 64

POAG
-Baltimore Eye Survey: 3.7x higher risk of glaucoma in pts who have sibling w/ POAG
-Othe risk factors: myopia (? selection bias as myopes more likely to seek eye care and be diagnosed), DM (higher IOP readings in DM pts, susceptibility of optic nerve to ischemic damage), CV disease (i.e., lower systolic pressure may cause progression), RVO (CRVO assoc w/ later neovascular or angle closure glaucoma AND glaucoma is a risk factor for CRVO also) --> elevated IOP in fellow eye of CRVO pt must be kept as low as possible!

Front 65

OAG: POAG
-What was the purpose and findings of the Ocular HTN Treatment Study?

Back 65

POAG - OHTS
-Purpose: safety/efficacy of meds in preventing VF loss/optic nerve damage in pts w/ OHTN
-22.5% decrease in IOP of treatment group assoc w/ decreased development of POAG from 9.5% to 4.4%
-CCT was strong predictor of POAG (risk of POAG increased 81% for every 40 um thinner)

Front 66

OAG: POAG
-What was the purpose and findings of the Early Manifest Glaucoma Trial?

Back 66

POAG - Early Manifest Glaucoma Trial
-Purpose: compare immediate lowering of IOP w/ observation for newly dx POAG
-Results: Treatment reduced IOP by 25% --> reduced progression from 62% to 45%

Front 67

OAG: POAG
-What were the purpose and findings of the Collaborative Initial Glaucoma Treatment Study?

Back 67

POAG - CIGTS
-Purpose: comparing initial treatment of POAG w/ meds vs filtering surgery
-Findings: similar VF outcomes and QOL impact in both groups at 5 yrs, but early VA loss greater in surgical group
-IOP reduction greater in surgical group than medical group, but higher rate of cataract surgery in surgical group

Front 68

OAG: POAG
-What were the purpose and findings of the Advanced Glaucoma Intervention Study?

Back 68

POAG - AGIS
-Purpose: comparing 2 treatment sequences for uncontrolled OAG (laser-trabeculotomy-trabeculectomy VS trabeculotomy-laser-trabeculectomy)
-Findings: Black pts benefited more when treated w/ laser first (white patients had opposite results)
-Lower IOP assoc w/ less VF loss
-78% increased risk of cataract formation w/ trabeculectomy, but trabeculectomy retards progression of glaucoma more in white pts than black (laser slightly more effective in blacks)

Front 69

OAG: Normal tension glaucoma
-Presumed pathophysiology?
-What did the Collaborative Normal-Tension Glaucoma Study show?
-What differences exist b/w neuroretinal rim thinning in normal tension glaucoma vs POAG?

Back 69

Normal tension glaucoma
-Pathophysiology: thought to be 2/2 local vascular factors inducing ischemia (may be subject to different risk factors than POAG)
-Collaborative normal tension glaucoma study: lowering IOP by at least 30% reduced VF progression from 35% to 12% --> IOP has a clear role in disease
-In eyes matched for VF loss, the neuroretinal rim is thinner in pts w/ normal tension glaucoma

Front 70

OAG: Normal tension glaucoma
-Describe differences in optic nerve appearance in senile sclerotic vs focal ischemic groups of normal tension glaucoma
-What do VF defects in NTG typically look like?

Back 70

Normal tension glaucoma
-Senile sclerotic group: shallow, pale sloping of neuroretinal rim
-Focal ischemic group: deep, focal notching of neuroretinal rim
-VF defects in NTG tend to be more FOCAL, DEEPER, CLOSER TO FIXATION (i.e., dense paracentral scotoma encroaching on fixation)

Front 71

OAG: Normal tension glaucoma
-What population of pts tend ot have a high proportion of NTG?
-What historical and exam features should be considered in the diagnosis of NTG?

Back 71

Normal tension glaucoma
-Japanese pts have a high proportion of NTG
-Prior to dx: measure IOP at different times during day, gonioscopy, check history of precipitating event (record of CV disease, hypotensive event, use of topical steroids)

Front 72

OAG: Normal tension glaucoma
-How variable is the clinical course in NTG?
-What is the proposed benefit of systemic CCBs for NTG?

Back 72

Normal tension glaucoma
-Variable clinical progression: pts may not progress despite lack of treatment but in some pts progression occurs depsite aggressive IOP reduction --> general rule: get IOP as low as possible
-CCBs: though to increase capillary perfusion of optic nerve head

Front 73

OAG: Glaucoma suspect
-What findings are required for diagnosis of glaucoma suspect?
-What testing methods may increase ability to recognize early glaucomatous field loss in glaucoma suspects?
-What risk factors were identified by the OHTS for development of glaucoma in pts w/ OHTN?

Back 73

Glaucoma suspect
-SUSPECT needs ONE of the following criteria: 1) optic nerve changes (asymmetric or enlarged C:D, focal notching, disc heme); 2) glaucomatous VF change; 3) IOP > 21
-POAG needs TWO of those criteria
-Early detection of glaucomatous defects in glaucoma suspects: Short-wavelength & frequency-doubled perimetry
-OHTS risk factors for glaucoma in pts w/ OHTN: increased C:D, elevated IOP, reduced CCT

Front 74

OAG: PXF syndrome
-What is the nature of the deposited material?
-Pathophysiology (presumed)?
-Clinical exam?
-What is a Zentmayer line?

Back 74

PXF syndrome
-Fibrillar, amyloid-like, PAS+ material deposited in ant segment
-Pathophys: generalized basement-membrane disorder
-Clinical: target-like pattern on ant lens capsule (central area and peripheral zone of deposition separated byclear zone), deposits also on pupil margin, K endothelium, inferior AC angle; pupillary margin atrophy
-Gonio findings: increased pigmentation, Sampaolesi line, poss narrow angle due to anterior movement of lens/iris diaphgram from zonular weakness
-Zentmayer line: pigment deposits on anterior hyaloid

Front 75

OAG: PXF syndrome
-Name complications that can occur in cataract surgery for PXF patients
-What population of patients has a high prevalence of PXF syndrome related glaucoma?
-Mechanism of glaucoma?
-Mgmt?

Back 75

PXF syndrome
-Cataract surgery complications: zonular dehiscence, dropped lens, poor pupillary dilation, phacodonesis, iridodonesis, vitreous loss, late IOL dislocation
-Scandanavian countries: PXF accounts for > 50% of cases of OAG! --> strongly age related (seen more commonly in > 70 yo)
-Glaucoma mechanism: fibrillar material obstructs flow through and causes damage to TM --> IOP often higher w/ greater fluctuation
-Mgmt: prognosis worse than in POAG; SLT very effective; removal of lens does NOT alleviate condition
**note: all forms of ocular surgery can induce increased intraocular inflammation in PXF pts**

Front 76

OAG: Pigmentary glaucoma
-What are signs of PDS on exam?
-Pathophysiology of K spindle?
-Pathophysiology of PDS?

Back 76

Pigmentary glaucoma
-Clinical: K spindle, mid-peripheral iris TI defects (mechanical contact b/w zonules and iris causes pigment release), homogenous & densely pigmented TM, Sampaolesi line, Zentmayer line (pigment on anterior hyaloid)
-Pathophys of K spindle: aqueous convection currents & phagocytosis of pigment by K endothelium causes vertical K spindle
-Pathophys of PDS: increased IOP in anterior chamber relative to post chamber --> backward bowing of iris ('reverse pupillary block") --> iris rubs against zonules --> pigment release

Front 77

OAG: Pigmentary glaucoma
-Pathophysiology of PDS-related glaucoma?
-What % of PDS pts develop glaucoma?
-Other epidemiologic associations w/ PDS-assoc glaucoma?
-What activities can produce IOP spike in PDS-related glaucoma?
-Does cataract surgery help resolve PDS?

Back 77

Pigmentary glaucoma
-Pathophys of PDS-glaucoma: pigment release --> clogs TM --> TM cells phagocytose pigment --> TM degeneration --> uncontrolled pigmentary glaucoma (ie., dysfunction of TM causes increased IOP)
-25-50% of PDS pts develop glaucoma
-Higher risk in MALES w/ MYOPIA who are 20-50 yo
-High IOP induced by exercise or pupillary dilation --> causes increased pigment release into aqueous
-Cataract surgery can help induce remission of PDS

Front 78

OAG: Pigmentary glaucoma
-Mgmt of PDS glaucoma?
-Natural course of PDS?

Back 78

Pigmentary glaucoma
-Natural course: Tends to improve over time (decreased IOP, decreased TM pigment, loss of TI defects)
-Mgmt: medical mgmt first, good response to SLT (can use lower settings due to pigmentation - increased absorption of laser energy)
**Note: caution in filtering surgery - increased risk of hypotony maculopathy**

Front 79

OAG: Phacolytic glaucoma
-Mechanism?
-Clinical presentation?
-Are KPs present? Why is this significant?
-Definitive mgmt?

Back 79

Phacolytic glaucoma
-Mechanism: mature/hypermature cataract --> leakage of lens protein through intact anterior capsule --> lens proteins, phagocytozing macrophages and inflammatory debris obstruct TM
-Clinical: elderly pt w/ poor vision --> sudden onset pain, injection, worsening vision
-Exam: markedly elevated IOP, K edema, prominent cell/flare, wrinkled anterior capsule and mature cataract
**NO KPs present** (distinguish from phacoantigenic glaucoma)
-Definitive mgmt: cataract extraction

Front 80

OAG: Lens particle glaucoma
-Mechanism?
-When does it occur in relation to surg/trauma?
-Clnical findings?
-Mgmt?

Back 80

Lens particle glaucoma
-Mechanism: following eye surgery/trauma, lens cortex particles obstruct TM --> glaucoma
-Can occur weeks - years s/p surgery or trauma
-Clinical: AC reaction, post synechiae, K edema, PAS
**No KPs**
-Mgmt: medical tx while lens material resorbs --> aqueous suppressants, mydriatics (for post synechiae), topical steroids (inflammation)

Front 81

OAG: Phacoantigenic glaucoma
-Mechanism? How does it differ from lens particle glaucoma?
-Clinical presentation?
-Are KPs present?
-Mgmt?

Back 81

Phacoantigenic glaucoma
-Mechanism: pts become sensitized to their own lens protein s/p surgery/trauma --> granulomatous inflammation
**Note: lens particle --> no granulomatous inflammation
-Clinical: AC reaction WITH KPs on lens capsule and endothelium, synechiae, vitritis
-Mgmt: medical mgmt w/ steroids, aqueous suppressants
-May need to remove residual lens material if medical mgmt unsuccessful

Front 82

OAG: Intraocular tumors
-Name the different mechanisms by which intraocular tumors cause glaucoma
-Which of these is the most common mechanism?

Back 82

Intraocular tumors - mechanisms of glaucoma
-Direct tumor invasion of angle (most common mechanism)
-Rotation of CB or anterior lens-iris diaphragm displacement (ciliary body tumors, choroidal tumors)
-Intraocular hemorrhage
-NVA (choroidal melanomas, medulloepitheliomas, retinoblastomas)
-Deposition of cells/inflammatory debris in TM

Front 83

OAG: Inflammatory glaucoma
-What is the general principle behind glaucoma in setting of intraocular inflammation?
-Name diferent mechanisms of OAG in inflammation

Back 83

Inflammatory glaucoma
-General etiology: IOP elevation occurs when TM dysfunction exceeds ciliary body hyposecretion with acute inflammation
-Mechanisms of glaucoma: TM edema, endothelial dysfunction, blockage by fibrin/inflammatory cells; Schlemm's canal blockage by inflammatory cells; prostaglandins mediating breakdown of blood-aqueous barrier; steroid induced reduction in aqueous outflow through TM

Front 84

OAG: Inflammatory glaucoma
-What etiologies of uveitis (both infection and non-infectious) are most associated w/ OAG?
-Why should miotic agents be avoided in pts w/ iritis?

Back 84

Inflammatory glaucoma
-Uveitic conditions most commonly assoc with glaucoma: herpesvirus infection, toxoplasmosis, rheumatoid arthritis, pars planitis
-Miotics are avoided in iritis because they increase inflammation and cause posterior synechiae

Front 85

OAG: Glaucomatocyclitic crisis
-Clinical picture?
-Typical IOP range?
-Mgmt?
-Etiology?

Back 85

Glaucomatocyclitic crisis (Posner-Schlossman)
-Clinical: recurrent bouts of markedly increased IOP (40-50 range) & low grade AC inflammation (few KP, mild iritis)
-Etiology unknown
-Mgmt: topical NSAIDs or mild steroids prevent attacks

Front 86

OAG: Fuchs heterochromic iridocyclitis
-Clinical picture?
-What % of pts develop glaucoma?
-Characteristic gonioscopy finding?
-Mgmt?

Back 86

Fuchs heterochromic iridocyclitis
-Clinical: unilateral, iris heterochromia (lighter eye = affected eye except in blue eyed pts), low grade AC reaction, small stellate KP, PSC
-15% of pts develop glaucoma
-Gonio: fine vessels crossing the TM (but do not lead to PAS or secondary angle closure) --> may bleed w/ surgery or trauma
-Mgmt: steroids NOT effective, glaucoma does not respond to degree of inflammation --> give aqueous suppressants

Front 87

OAG: Episcleral venous pressure
-Normal range?
-Goniosopic finding?
-Mgmt?

Back 87

Episcleral venous pressure
-Normal range 8-10 mm Hg
-Gonio: blood in Schlemm's canal
-Mgmt: aqueous supresssants --> more efficacious than drugs that improve TM outflow; laser NOT effective usually
-Generally: surgery better than medical tx (otherwise will be unable to lower IOP below episcleral venous pressure w/ drops/laser only)
-Note: surgery can result in choroidal effusions/hemorrhage

Front 88

OAG: Episcleral venous pressure
-List causes of episcleral venous pressure elevation

Back 88

Episcleral venous pressure
-AVMs (Sturge-Weber, orbital varix, CCF)
-Venous obstruction (orbital tumors, thyroid eye disease)
-SVC syndrome
-Idiopathic (familial)

Front 89

OAG: Trauma
-List the possible anterior segment injuries caused by blunt ocular trauma

Back 89

Trauma - AC effects of blunt eye injury
-Hyphema
-Angle recession (cleavage) --> indicates damage to TM
-Iridodialysis (does not cause glaucoma but indicates severity of injury)
-Cyclodialysis (separation of CB and scleral spur)
-Iris sphincter tear
-Lens subluxation

Front 90

OAG: Trauma
-Describe gonioscopy findings and mgmt of cyclodialysis clefts

Back 90

Trauma - cyclodialysis cleft
-Gonio: wide scleral spur, missing CB band (due to separation of CB and SS)
-Mgmt: 1) atropine (dilation can mechanically close the cleft); 2) high power argon laser (induces inflammation/edema to close cleft)
-GOAL of treatment: prevent hypotony and macular injury

Front 91

OAG: Traumatic hyphema
-Over what time frame does rebleeding occur?
-Is high IOP more common w/ initial hyphema or w/ rebleed?
-What is the mechanism of increased IOP in hyphema?

Back 91

Traumatic hyphema
-Increased IOP more common w/ rebleeding
-Time frame for rebleeding: 3-7 days s/p original hyphema
-Mechanism of increased IOP: obstruction of TM by RBC, inflammatory cells, debris, fibrin OR direct injury to TM from trauma

Front 92

OAG: Traumatic hyphema
-Why do sickle cell pts have increased risk of elevated IOP after hyphema?
-For what other reason do we worry about sickle cell pts losing vision after hyphema/blunt injury?

Back 92

Trauma - hyphema
-Sickle cell pts have increased risk of elevated IOP s/p hyphema: RBCs sickle in AC due to acidity of aqueous --> dificulty passing out through TM --> block TM
**Therefore, even small hyphema can cause significant IOP elevation in sickle patients
-Optic nerves of sickle pts more sensitive to elevated IOP --> more risk of ischemic optic neuropathy, CRAO

Front 93

OAG: Trauma - hyphema
-What are the general principles of mgmt of an uncomplicated hyphema?
-What is the benefit of aminocaproic acid in preventing rebleeding?

Back 93

Trauma - hyphema
-Mgmt: elevate HOB, eye shield, limited activity, topical/systemic steroids, cycloplegics (but do not prevent rebleeding)
-Aminocaproic acid: shown in some studies to prevent rebleeding but has significant sstemic sfx (GI, CV)
-General strategy: 1) medical mgmt first; 2) AC washout; 3) orphan trabeculectomy (w/o MMC to ensure that it is temporary)

Front 94

OAG: Traumatic hyphema
-What medical agents are used first in mgmt of a hyphema?
-What drugs should be avoided in all pts w/ hyphema?
-What drugs should be avoided in sickle cell pts?
-Surgical intervention in sickle cell pts?

Back 94

Traumatic hyphema
-Medical mgmt: aqueous suppressants & hyperosmotic agents
-Parasympathomimetics should be avoided in all hyphema pts
-Drugs that should be avoided in sickle cell pts: 1) carbonic anhydrase inhibitors (increase aqueous acidity --> increased sickling tendency); 2) alpha agonist (cause anterior segment vasoconstriction)
-Surgery: have low threshold in sickle cell pts --> risk of ischemic optic neuropathy, corneal bloodstaining, amblyopia

Front 95

OAG: Trauma
-What is the most common cause of hemolytic or ghost cell glaucoma?
-What is the mechanism of glaucoma in each condition? Clinical presentation?

Back 95

Trauma
-VITREOUS hemorrhage (not hyphema!) can lead to hemolytic or ghost cell glaucoma after 1-3 months
-Mechanism (hemolytic): hemoglobin-laden macrophages block TM --> will see red cells in AC, reddish discoloration of TM
-Mechanism (ghost cell): degenerated RBCs (ghost cells) block TM --> AC filled w/ small khaki colored cells w/o significant conj injection or flare

Front 96

OAG: Trauma
-What is the mgmt of hemolytic/ghost cell glaucoma? Prognosis?

Back 96

Trauma
-Mgmt of hemolytic/ghost cell glaucoma: resolve when hemorrhage has cleared --> use medical tx w/ aqueous suppressants as initial approach
-If ghost cells or RBCs present in vitreous --> need PPV for effective treatment of increased IOP

Front 97

OAG: Trauma - angle recession
-What is the definition of angle recession?
-When does it occur after ocular trauma?
-Classic gonio findings?

Back 97

Trauma - angle recession
-Definition: tear b/w longitudinal and circular muscle fibers of CB (the greater the degree of angle recession, the greater risk of glaucoma)
-May occur soon or months-years after ocular trauma
-Gonio: 1) broad angle recess; 2) absent/torn iris processes; 3) white, glistening scleral spur; 4) depression in TM; 5) PAS at border of recession

Front 98

OAG: Trauma - angle recession
-What proportion of fellow eyes develop increased IOP in angle recession?
-When should the diagnosis of angle recession glaucoma be considered? (presentation)
-Mgmt?

Back 98

Trauma - angle recession
-50% of fellow eyes develop increased IOP (pts w/ angle recession glaucoma may be predisposed to OAG)
-Typical pt presentation: pt presenting w/ unilateral elevation in IOP (may not recall history of trauma!)
-Mgmt: aqueous suppressants, prostaglandin analogs, alpha-2 agonists --> laser has a limited role

Front 99

OAG: Surgical trauma
-What are possible mechanisms for transient IOP elevation following ocular surgery?

Back 99

Surgical trauma - mechanisms of transient IOP rise
-Pigment release
-Inflammatory cells/debris
-TM deformation
-Angle closure
-Viscoelastic: dispersives (most common cause!) or cohesives

Front 100

OAG: IOL-induced glaucoma
-What is the definition of UGH syndrome?
-Pathophysiology?
-What are 2 other forms of secondary glaucoma caused by an IOL implant?

Back 100

IOL-induced glaucoma
-UGH (uveitis-glaucoma-hyphema): chronic irritation 2/2 malpositioned or rotating ACIOL (usually) -> chornic inflammation, secondary iris NV, recurrent hyphemas
**Note: may also be caused by PCIOL or SS-IOL
-2 other forms of secondary glaucoma caused by IOL implant: secondary pigmentary glaucoma, pseudophakic pupillary block

Front 101

OAG: PK-induced glaucoma
-What are mechanisms by which PK causes increased IOP?
-Which types of corneal procedures are assoc with decreased risk of elevated IOP?

Back 101

PK-induced glaucoma
-Mechanisms: wound distortion of TM and progressive angle closure = most common cause
-Highest frequency in aphakic/pseudophakic patients & with repeat grafts
-Lower risk of IOP elevation with lamellar or endothelial grafts

Front 102

OAG: Schwartz-Matsuo syndrome
-Definition?
-When is IOP actually LOW in this condition?

Back 102

Schwartz-Matsuo syndrome
-Definition: chronic RRD --> liberation of photoreceptor outer segments --> reach AC and block TM --> IOP elevation
**Note: photoreceptor segments can be mistaken for AC cell or pigment
-IOP improves after successful reattachment
-IOP can be LOW in acute RRD 2/2 increased outflow of fluid through exposed RPE

Front 103

OAG: Steroid-induced glaucoma
-What % of all pts demonstrate some response to steroids? Are many of these pts POAG pts?
-Mechanism of elevated IOP?
-When during steroid administration does steroid-induced glaucoma develop?

Back 103

Steroid-induced glaucoma
-1/3 of pts develop some steroid response (only small % have clinically significant elevation in IOP)
-High % of POAG pts have this response to topical steroids
-Mechanism: increased resistance to outflow in TM
-Glaucoma can develop at any time during long-term steroid administration

Front 104

OAG: Steroid-induced glaucoma
-What % of pts who get intravitreal steroids have transient elevation of IOP?
-What % of these pts need medication to control IOP and what % need filtering surgery?
-What populations of pts on cycloplegic therapy have increased IOP from cycloplegics?

Back 104

Steroid-induced glaucoma
-50% of pts who get intravitreal steroids have transient IOP elevations
-25% of these may require medical mgmt
-1-2% require filtration sugery
-Intravitreal steroid implants often assoc w/ increased IOP --> may require filtration surgery
-Cycloplegics: cause increased IOP in PDS, POAG, PXF, and pts on miotics

Front 105

ACG: PACG
-What % of bilateral blindness in China is accounted for by PACG?
-In which part of the world is PACG the most common glaucoma?
-What is the primary pathology?
-What are 2 general mechanisms of angle closure?

Back 105

PACG
-Accounts for 91% of blindness in China
-The most common glaucoma in East Asia
-Primary pathology: ANATOMIC (peripheral iris impedes aqueous access to TM)
-2 mechanisms: 1) iris pushed forward from behind - ie, pupillary block 2) iris pulled forward into TM - ie, PAS

Front 106

ACG: Pupillary block
-What is the pathophysiology of angle closure?
-What is absolute and relative pupillary block?
-How can pupillary block be broken?

Back 106

Pupillary block
-Most frequent cause of angle closure!
-Pathophysiology: blocked aqueous flow through PC to pupil --> increased pressure in PC relative to AC --> iris pushed forward
-Pupillary block is maximal in mid-dilated position
-Absolute block: 360 degrees posterior synechiae (no aqueous movement through pupil)
-Relative pupillary block: causes 90% of PACG
-How to break: PI

Front 107

ACG: Lens-induced angle closure
-What are the 2 causes of lens induced angle closure?

Back 107

Lens-induced angle closure
-Intumescent lens
-Dislocated lens (Marfan, homocystinuria, PXF): increased ant-post lens excursion, especially in prone position, causes pupillary block)

Front 108

ACG: Iris-induced angle closure
-What are the 3 causes of iris-induced angle cosure?

Back 108

Iris-induced angle closure
-Anterior iris insertion into SS (thick peripheral iris "rolls" into TM with dilation)
-Plateau iris (anterior displaced ciliary processes, rotate peripheral iris forward)
-Aniridia (rudimentary iris leaflets rotate into angle)

Front 109

ACG: PACG
-What is the prevalence of angle closure in the Inuit population?
-What type of angle closure is most frequent in Africans and Asians?
-What are ocular structural factors that contribute to risk of angle closure?

Back 109

PACG
-Inuits: 2.1-5% of population have PACG
-Africans & Asians more commonly have asymptomatic chronic angle closure
-Predisposing anatomical factors: 1) shallow AC (if depth < 2.5 mm, increased risk of PAS formation and angle closure); 2) thick lens; 3) increased anterior curvature of lens; 4) small K diameter; 5) short axial length

Front 110

ACG: PACG
-Is PACG affected by age?
-What gender predilection does PACG have?
-Most common refractive error?

Back 110

PACG
-Incidence increases w/ each decade after age 40 (poss 2/2 increased lens thickness and resultant iridolenticular contact)
-2-4x more common in females (unclear reason)
-Associated w/ hyperopia (if occurs in myopia, should look for secondary causes of angle closure)

Front 111

ACG: PACG
-What are ocular signs of acute PACG?
-Why can pigment be released during acute PACG?
-What are glaukomflecken?

Back 111

PACG
-Ocular signs: iris bombe, sluggish/mid-dilated and irregular pupil, K epithelial edema, mild cell/flare in AC, shallow AC, congested episcleral/conj vessels
-Pigment may be released by ischemic sectoral iris atrophy --> dusts K ednothelium and iris surface
-Glaukomflecken: small anterior subcapsular lens opacities --> evidence of prior episodes of angle closure

Front 112

ACG: PACG
-Defintiive treatment?
-What medical agents are most helpful?
Why might the pupillary sphincter be unresponsive to miotics alone in acute PACG?
-What medications should be avoided?

Back 112

ACG: PACG
-Definitive mgmt: laser or surgical PI
-Medical mgmt: Pilo 2-4% (pulls peripheral iris away from TM)
-Pupil may be unreponsive to miotic because if IOP markedly elevated (40-50) --> pupil sphincter may be ischemic and doesn't respond to mioitcs alone
Meds to AVOID: nonselective or alpha-1 alpha agonists (further dilation and iris ischemia)

Front 113

ACG: PACG
-What is 1 mechanism by which PACG in one eye can induce pupillary block and PACG in the other eye?
-What is the % risk of developing acute angle closure in the fellow eye in pts who have received treatment
-What is the treatment of choice?

Back 113

PACG
-In acute PACG, pain and emotional upset from sx in first eye may increase sympathetic flow to other eye and cause pupillary dilation --> bilateral acute PACG
-40-80% risk of acute angle closure attack in untreated fellow eye at 5-10 yrs
-Treatment of choice: PI

Front 114

ACG: PACG
-Why does improved IOP not necessarily indicate opening of the angle s/p laser PI?
-What is the preferred mechanism to confirm angle opening s/p laser PI?

Back 114

PACG
-Improved IOP not always 2/2 resolution of angle closure --> IOP can be low due to ciliary body ischemia and reduced aqueous production!
-Repeat gonioscopy = preferred method of confirming that angle has opened s/p laser PI

Front 115

ACG: PACG
-Describe clinical picture of subacute or intermittent angle closure (IOP range, changes in sleep, differential dx)
-Gonioscopic appearance?
-Treatment of choice? Other treatments?

Back 115

PACG
-Subacute/intermittent chronic angle closure: spontaneous sx resolution (esp during sleep-induced miosis), nl IOP b/w episodes
-Laser PI = treatment of choice
-Other treatment options: primary lensectomy, goniosynechiolysis

Front 116

ACG: PACG
-What is the definition of chronic angle closure?
-In which part of the world is this a major cause of blindness?

Back 116

PACG
-Chronic angle closure: slow, creeping synechial closure over time w/ PAS formation --> slow IOP rise as angle function becomes more and more compromised
-Major cause of blindness in Asia

Front 117

ACG: PACG
-What is the clinical course of chronic angle closure?
-Ddx?
-Mgmt?

Back 117

PACG: Chronic angle closure
-Clinical course: no symptoms, modest IOP elevation, progressive glaucomatous optic neuropathy & VF loss --> VERY SIMILAR TO POAG
-Mgmt: PI necessary to relieve pupillary block component (otherwise PAS will continue to progress) + long term ocular hypotensive meds

Front 118

ACG: PACG
-Definition of an occludable, or narrow, angle?
-How to diagnose?
-When is a PI indicated for narrow angle?

Back 118

PACG - Narrow angles
-Definition: anatomic description (not synonymous w/ glaucoma)
-Diagnosis: provocative testing (pharmacologic dilation and prone-darkroom testing) --> no longer used!
-Indications for PI: presence of PAS, pigmentation of TM, history of angle closure, AC depth < 2 mm, strong family history --> not all pts w/ narrow angle need PI!

Front 119

ACG: PACG
-What factors/meds can precipitate angle closure in pts w/ narrow angle?
-What medications can REVERSE pharmacologic dilation?

Back 119

PACG - Narrow angle
-Precipitating factors: pain, emotional upset, fright
-Precipitating meds: mydriatics, miotics (relax zonules, forward movement of lens-iris diaphragm, pupillary block)
-Systemic sympathomimetics or anti-parasympathetics (allergy/cold meds, antidepressants) --> can precipitate angle closure in susceptible pts
-Drugs that REVERSE pharmacologic dilation: dapiprazole & thymoxamine --> alpha blockers (can be used for acute angle closure)

Front 120

ACG: Plateau iris
-Definition?
-Mechanisms of angle closure glaucoma in plateau iris?
-When should plateau iris be suspected?

Back 120

Plateau iris
-Definition: anteriorly positioned ciliary processes --> push peripheral iris forward --> narrow angle (gonioscopic diagnosis!)
-Mechanisms of angle closure: peripheral iris bunches up against TM s/p dilation, pupillary block component usually present also
-Suspect plateau iris when: central AC deep but peripheral AC flat in eye w/ angle closure OR in young myopic pt w/ angle closure

Front 121

ACG: Plateau iris
-Mgmt?
-What is the difference b/w PAS that form as a result of plateau iris vs PAS resulting after pupillary block?

Back 121

Plateau iris
-Mgmt: laser PI (to remove pupillary block component), long term miotics
-NOTE: even w/ patent PI, eyes w/ plateau iris remain predisposed to angle closure due to peripheral iris anatomy
-PAS in plateau iris: start at Schwalbe line and extent posteriorly over TM, SS and angle recess
-PAS in pupillary block angle closure: form in posterior to anterior direction (reverse)

Front 122

ACG: Lens-induced angle closure
-What are distinguishing features of phacomorphic glaucoma compared to PACG?
-Clinical features to suspect phacomorphic process?
-Mgmt?

Back 122

Lens-induced angle closure - Phacomorphic glaucoma
-PACG vs phacomorphic: rapid onset of anatomic predisposition in phacomorphic glaucoma (vs slow/gradual in PACG) --> marked lens swelling (intumescence) 2/2 cataract formation and development of pupillary block and AC shallowing in eye that is not normally predisposed to angle closure
-Clinical features of phacomorphic: disparities b/w the 2 eyes in AC depth, gonioscopy and degree of cataract
-Mgmt: laser PI f/b CE in quiet eye

Front 123

ACG: Lens-induced angle closure
-Definition of ectopia lentis?
-Causes of ectopia lentis?
-Mgmt?

Back 123

Lens-induced angle closure - Ectopia lentis
-Definition: displacement of lens from normal anatomic position --> forward movement --> pupillary block --> iris bombe, AC shallowing, secondary angle closure
-Causes: Marfan, homocystinuria, Weill-Marchesani, PXF, trauma, microspherophakia
-Mgmt: laser PI 180 deg apart = treatment of choice (followed by definitive lensectomy)

Front 124

ACG: Lens-induced angle closure
-What is microspherophakia and how does it cause glaucoma?
-What meds make glaucoma worse or better in these pts?
-Systemic associations w/ microspherophakia?
-Most common etiology of acquired lens subluxation?

Back 124

Lens-induced angle closure - Microspherophakia
-Definition: congenital spherical/globular shape of lens --> pupillary block, angle closure
-Cycloplegics: tighten zonules, flatten lens, pull it posteriorly --> BREAK pupillary block
-Miotics: loosen zonules, anterior rotation of CB, increase globularity of lens --> WORSEN pupillary block
-Systemic associations: Weill-Marchesani, Marfan
-PXF is most common acquired form of lens subluxation

Front 125

ACG: Lens-induced angle closure
-Mechanism of angle closure in aphakic/pseudophakic eyes?
-Mgmt?
-Mechanism of angle closure w/ ACIOL?

Back 125

Lens-induced angle closure - Aphakic/Pseudophakic
-Mechanism: pupillary block via intact vitreous face (aphakia or pseudophakia w/ dislocated IOL) or lens (pseudophakia)
-Mgmt: mydriatics, cycloplegics (but may make it difficult to perform PI), may need > 1 PI
-ACIOL induced angle closure: pupillary block 2/2 vitreous face, iris or lens optic --> periph iris bows forward around ACIOL to occlude angle --> central chamber remains deep
-Same mgmt as for other types of pseudophakic ACG

Front 126

ACG: Secondary angle closure w/o pupillary block
-What are the 2 mechanisms of glaucoma in these cases?

Back 126

Secondary angle closure w/o pupillary block
-Mechanisms: 1) PAS formation 2/2 inflammation, NV or heme; 2) forward displacement of lens-iris diaphgram & anterior rotation of CB

Front 127

ACG: Neovascular glaucoma
-Most common underlying etiologies of NVG?
-Clinical appearance of angle?
-Appearance of iris?

Back 127

Neovascular glaucoma
-Most common etiologies: DM, CRVO, ocular ischemic syndrome
-Angle appearance: fine arborizing blood vessels on surface of iris, pupil margin, TM accompanied by fibrous membrane --> contracts to form PAS
**Note: PAS end at Schwalbe line --> do not grow over healthy K endothelium!
-Iris NV: starts w/ fine vascular tufts at pupil --> vessels then grow radially over iris --> cross CB, SS and then branch until they reach TM

Front 128

ACG: Neovascular glaucoma
-Name some diseases in which AC neovascularization occurs w/o evidence of retinal ischemia
-Can angle NV occur w/o NVI?
-What % of pts w/ CRVO develop NVG?
-How should pts w/ CRVO induced NVG be treated?

Back 128

Neovascular glaucoma
-Diseases causing AC neovascularization w/o retinal ischemia: Fuchs heterochromic iridocyclitis, PXF, uveitis, iris melanoma, carotid occlusive disease
-Angle NV CAN occur w/o iris NV
-10% of pts w/ CRVO develop NVG
-Mgmt of NVG 2/2 CRVO: PRP to decrease retinal ischemia --> may decrease NV and normalize IOP (if significant PAS has not yet formed)

Front 129

ACG: Neovascular glaucoma
-Mgmt: medical vs surgical?
-When should filtering surgery be done?

Back 129

Neovascular glaucoma
-Medical mgmt: temporizing measure --> need definitive surgical or laser tx
-When to do filtering surgery: when NV has regressed and PRP has been performed
-Aqueous shunt may be the procedure of choice

Front 130

ACG: ICE syndrome
-Definition and subtypes?
-What % of pts w/ ICE develop glaucoma?
-Which ICE syndrome is most common?
-Epidemiology?

Back 130

ICE syndrome
-Definition: group of disorders w/ abnormal K endothelium ("beaten bronze" appearance) w/ resulting microcystic K edema & varying degrees of iris atrophy and secondary angle closure glaucoma w/o pupillary block
-Subtypes: 1) Chandler (K and angle findings only); 2) essential iris atrophy (severe heterochromia, corectopia, ectropion uveae, hole formation); 3) iris nevus/Cogan-Reese (less severe iris atrophy, tan nodules on iris vs diffuse pigmentation)
-50% of pts develop glaucoma --> more severe in iris atrophy & Cogan-Reese subtypes
-Chandler syndrome is the most common form of ICE syndrome
-Epi: F>M, unilateral, 20-50 yo

Front 131

ACG: ICE syndrome
-What type of PAS are characteristic of ICE syndrome?
-Mgmt of glaucoma and K edema?
-Which glaucoma therapies are INEFFECTIVE for ICE?

Back 131

ICE syndrome
-High PAS are characteristic: extend anterior to Schwalbe line (since K pathology is root cause) --> multiple layers of endothelial cells & fibrous tissue cause PAS formation and extend from anterior to posterior to cover TM --> glaucoma
-Mgmt: hypertonic saline and IOP reduction (for K edema) + aqueous suppressants or filtering surgery (for glaucoma)
-Ineffective therapies: miotics, laser trabeculoplasty

Front 132

ACG: Tumors
-What are the 3 most common tumors to cause secondary angle closure?
-General mechanisms of angle closure w/ tumors?

Back 132

Tumors
-Most common: choroidal melanoma, ocular mets, retinoblastoma --> most commonly assoc w/ ACG
-Mechanisms: 1) shift lens-iris diaphragm forward; 2) breakdown blood-aqueous barrier --> inflammation --> PAS, post synechiae; 3) NVI

Front 133

ACG: Inflammation
-Mechanism of angle closure via inflammation?
-Most common part of angle to be affected?
-What is one mechanism by which inflammatory disease can cause lens-iris diaphragm forward displacement?
-Primary medical agents used?

Back 133

Inflammation
-Mechanism of ACG: breakdown of blood-aqueous barrier --> increased protein/fibrin in AC --> posterior synechiae & PAS
-PAS most frequently occur in INFERIOR angle (unlike in PACG --> occur superiorly) & are irregular in appearance
-Mechanisms of forward displacement of lens-iris diaphragm in inflammation: posterior uveitis w/ massive exudative RD OR choroidal effusions
-Medical mgmt: steroids + aqueous suppressants

Front 134

ACG: Aqueous misdirection
-Typical clinical setting in which this occurs?
-Clinical presentation? (distinguish from PACG)
-Pathophysiology?
-Vitreous appearance?

Back 134

Aqueous misdirection
-Occurs in pts s/p ocular surgery w/ history of angle closure or PAS
-Clinical: uniform flattening of central & peripheral AC (asymmetric to fellow eye) --> note that in PACG, iris bombe occurs w/ flatter peripheral AC
-Pathophysiology: anterior rotation of CB and posterior misdirection of aqueous flow + relative block at vitreous face
-Vitreous may show optically clear zones of aqueous within

Front 135

ACG: Aqueous misdirection
-Medical mgmt?
-Which agents should NOT be used?
-Is laser helpful?
-What % of pts can be controlled medically?

Back 135

Aqueous misdirection
-Medical mgmt: intensive cycloplegia, aggressive aqueous suppression (beta blockers, alpha-2 agonists, CAIs) & vitreous shrinking w/ hyperosmotics
-AVOID miotics! --> make condition worse
-Nd:YAG laser can be used to disrupt vitreous face
-50% of pts able to be medically controlled

Front 136

ACG: non-RRD & uveal effusions
-What is a suprachoroidal effusion/hemorrhage?
-How is an RRD different from a non-RRD in terms of risk of ACG?
-Mechanism of ACG?

Back 136

non-RRD & uveal effusions
-Suprachoroidal effusion/heme: blood or fluid in potential space b/w choroid and sclera
-In a non-RRD, subretinal fluid accumulates & acts as space-occupying lesion within vitreous (in RRD, fluid escapes through retinal tear that is present)
-Mechanism of ACG: forward movement of lens-iris diaphragm

Front 137

ACG: Epithelial downgrowth
-Which is more prevalent: epithelial or fibrous downgrowth?
-Risk factors?
-3 forms of epithelial proliferation in AC? Which of these cause secondary glaucoma?
-Appearance of fibrous ingrowth?
-Histologic appearance of epithelial ingrowth?

Back 137

Epithelial/Fibrous downgrowth
-Fibrous is more prevalent than epithelial, progresses more slowly and is often self limited
-Risk factors: prolonged inflammation, wound dehiscence, delayed wound closure, Descemet's tear
-3 forms of epithelial proliferation: 1) pearl tumors of iris; 2) epithelial cysts; 3) epithelial ingrowth (latter 2 cause glaucoma)
-Fibrous downgrowth: thick gray-white retrocorneal membrane, vascular, irregular border --> causes PAS and TM destruction
-Histo of epithelial ingrowth: nonkeratinized, stratified squamous epithelium w/ avascular connective tissue layer

Front 138

ACG: Nanophthalmos
-Definition?
-Why are these eyes susceptible to ACG?
-Is surgical mgmt generally successful?

Back 138

Nanophthalmos
-Definition: unusually small eye (shortened AP diameter), normal shape, large lens for eye volume, thickened sclera (impaired drainage from vortex veins)
-Hyperopic --> susceptible to ACG
-High rate of surgical complications --> avoid!

Front 139

ACG: PFV
-How can PFV cause narrowing of angle?
-Associated ocular conditions?

Back 139

Persistent fetal vasculature
-Causes narrow angles via contraction of retrolental tissues --> narrowing of ant chamber angle
-Unilateral
-Assoc w/ microphthalmos & elongated ciliary processes

Front 140

ACG: Flat AC
-Which is better tolerated by cornea: iridocorneal contact or corneolenticular contact?

Back 140

Flat AC
-Corneolenticular touch (or contact b/w cornea and hyaloid face or IOL) is poorly tolerated by cornea --> need to reform chamber ASAP
-Iridocorneal touch better tolerated

Front 141

ACG: Drug-induced angle closure
-What drug is sometimes assoc w/ acute ACG?
-Mechanism?
-Medical mgmt?
-Does PI help?
-Prognosis?

Back 141

Drug-induced ACG - Topiramate
-Topamax/topiramate: acute myopic shift (>6 D) + acute bilateral ACG
-Mechanism: ciliocoroidal effusions --> relaxation of zonules --> significant anterior displacement of lens-iris complex --> angle closure
-Medical mgmt: aqueous suppressants, cycloplegia
-PI does NOT help (pupillary block is not a cause)
-Prognosis: ACG resolves over 24-48 hrs, myopia resolves in 1-2 weeks

Front 142

CHILDHOOD GLAUCOMA: PCG
Definition of infantile/congenital vs juvenile glaucoma?
-What % of congenital glaucomas is accounted for by primary congenital glaucoma?
-Epidemiology of PCG?
-Major loci of AR PCG?

Back 142

PCG
-Primary juvenile glaucoma occurs after age 3 or in early adulthood (infantile/congenital occurs at birth or first few years of life)
-PCG accounts for 50-70% of congenital glaucomas
-65% male, 70% bilateral
-3 genetic loci in AR disease: GLC3A, GLC3B, GLC3C (ch 2, 1 and 14)

Front 143

CHILDHOOD GLAUCOMA: Pathophysiology
-Primary pathophysiologic mechanism?

Back 143

Pathophysiology
-Anatomic abnormality of TM --> cellular or membranous abnormality (i..e, impermeable TM or Barkan membrane covering TM)

Front 144

CHILDHOOD GLAUCOMA: Clinical
-Classic triad?
-Corneal findings?
-How do general anesthetics affect IOP measurement?

Back 144

Clinical findings
-Classic triad: photophobia, blepharospasm, epiphora
-Corneal findings: enlarged K diameter (>12 mm in 1st yr of life), Haab striae (tears in Descemet's oriented horizontally or concentric to limbus)
-Anesthetic agents and sedatives tend to LOWER IOP (exception: ketamine can raise IOP) --> must measure IOP as soon as possible after induction of anesthesia

Front 145

CHILDHOOD GLAUCOMA: Clinical
-Anterior chamber appearance (iris, angle, depth of AC)
-How is cupping different in children compared to adults?

Back 145

Clinical
-AC is deep, normal iris (may have high or flat insertion, absence of angle recess, peripheral iris hypoplasia, thickened TM), open and avascualr angle
-Cupping looks like adult cupping EXCEPT scleral canal enlarges w/ increased IOP --> entire cup enlarges --> may be reversible

Front 146

CHILDHOOD GLAUCOMA: Mgmt
-Initial procedures of choice?
-What medical agents are most frequently used as temporizing measures?
-Why should alpha-2 agonists be avoided in children?
-What are sfx of medical therapy for each type?

Back 146

Mgmt
-Procedures of choice: goniotomy (if K view is good) or trabeculotomy (can do with cloudy K)
-Medical mgmt: beta blockers, topical CAI --> best agents for children
-AVOID alpha-2 agonists: risk of CNS depression, apnea --> never give to pt < 3 yo
-B blockers can also cause apnea, hypotension, cough
-Oral CAI can cause acidosis, hypokalemia, feeding problems

Front 147

CHILDHOOD GLAUCOMA: Axenfeld-Rieger
-Definition?
-Inheritance?
-What % of cases are assoc w/ glaucoma?

Back 147

Axenfeld-Rieger
-Bilateral abnormal development of AC angle, iris, corneal endothelium and TM (neural-crest derived tissues)
-Posterior embryotoxon (anteriorly displaced Schwalbe line) + adherent iris strands, iris hypoplasia & corectopia
-Systemic findings: hypospadias, pituitary abnormalities, dental problems
-Autosomal dominant
-50% of cases assoc w/ glaucoma

Front 148

CHILDHOOD GLAUCOMA: Peters anomaly
-Definition?
-Laterality?
-Inheritance?
-% of cases assoc w/ glaucoma?
-Which patients have a higher likelihood of ocular and systemic anomalies in Peter's?

Back 148

Peter's anomaly
-Definition: central corneal opacity w/ adhesions b/w central iris & posterior cornea + clear/cataractous lens
-Annular corneal opacity ("leukoma") in central visual axis w/ iris strands from collarette to corneal opacity --> corresponds to central defect in K endothelium and underlying Descemet's
-Bilateral in 80%
-50% of cases assoc w/ glaucoma
-Pts w/ corneolenticular adhesions have higher risk of ocular and systemic abnormalities!

Front 149

CHILDHOOD GLAUCOMA: Aniridia
-Definition?
-Associated ocular abnormality that is most important to be aware of?
-Inheritance?
-Which pts have aniridia assoc w/ Wilm's tumor (WAGR)?
-% of pts that develop glaucoma?
-What is Gillespie syndrome?

Back 149

Aniridia
-Variable iris hypoplasia w/ assoc limbal stem cell abnormalities (results in pannus)
-Important ocular abnormality: foveal hypoplasia --> pendular nystagmus & poor VA
-Autosomal dominant (1/3 of cases sporadic) --> both 2/2 PAX6 mutations
-20% of sporadic cases assoc w/ Wilm's tumor
-50-75% of pts develop glaucoma when rudimentary iris stump rotates into TM
-WAGR (Wilm's tumor, aniridia, GU abnormalities, MR)
-Gillespie syndrome: aniridia, cerebellar ataxia, MR) --> occurs in 2% of pts w/ aniridia

Front 150

CHILDHOOD GLAUCOMA: Systemic disease
-What important eye finding is assoc w/ increased risk of glaucoma in Sturge Weber and NF?

Back 150

Systemic disease
-When upper eyelid involved in Sturge Weber or NF --> increased risk of developing glaucoma

Front 151

CHILDHOOD GLAUCOMA: Sturge Weber
-Features of Sturge Weber?
-What % of pts develop glaucoma?
-Mechanism of glaucoma?
-Risks related to surgical therapy in these patients?

Back 151

Sturge Weber
-Unilateral facial cutaneous hemangioma & ipsilateral choroidal cavernous hemangioma & leptomeningeal angiomas
-Glaucoma occurs in 30-70%
-Mechanism of glaucoma: congenital AC abnormalities (infants), elevated episcleral venous pressure (after 1st decade)
-Caution w/ surgery --> high risk of choroidal hemorrhage

Front 152

CHILDHOOD GLAUCOMA: Neurofibromatosis
-Which is associated w/ glaucoma: NF1 or NF2?
-Inheritance?
-Characteristic findings of NF1 and NF2?

Back 152

Neurofibromatosis
-NF1 is assoc w/ glaucoma, NF2 is NOT
-Autosomal dominant
-NF1: chromosome 17, Lisch nodules, optic gliomas, eyelid neurofibromas, glaucoma (systemic: axillary freckling, cafe au lait spots, cutaneous neurofibromas)
-NF2: chromosome 22, PSC cataracts, bilateral acoustic neuromas

Front 153

MEDICAL: Studies
-What were the findings of OHTS re: IOP reduction in OHTN?
-What amount of initial IOP reudction is suggested at baseline?

Back 153

Studies
-OHTS: 22.5% decrease in IOP w/ meds --> decreased risk of POAG from 9.5% to 4.4% at 5 years (treatment vs observation)
-Treatment should be considered in those w/ moderate or high risk of POAG
-Initial IOP reduction: 20% of baseline (continuously reassess depending on VF progression/optic nerve changes)

Front 154

MEDICAL: Prostaglandins
-Mechanism of action?
-Most common drugs and how much they tend to lower IOP?

Back 154

Prostaglandins
-Mechanism: exact mechanism unknown --> thought to increase aqueous OUTFLOW (increased spaces b/w muscle fascicles of CB, increased uveoscleral outflow)
-Latanoprost/travoprost: lower IOP by 25-32%
-Bimatoprost: lowers IOP by 27-33%

Front 155

MEDICAL: Prostaglandins
-Most unique side effect for this class of med?
-What % of pts w/ blue iris have increased pigmentation compared to those w/ light brown/blue-green eyes?
-Other ocular side effects?

Back 155

Prostaglandins
-Most unique side effects: iris and periocular skin darkening --> increased # of melanosomes within melanocytes
-Blue iris pts have increased pigmentation in 10-20% but pts w/ light brown/green iris have 60% risk of pigmentation!
-Other ocular side effects: conj hyperemia, hypertrichosis, trichiasis, distichiasis, eyelid skin pigmentation, hair growth around eyes --> all reversible

Front 156

MEDICAL: Beta blockers
-Mechanism of action?
-When are these drugs MOST effective? How does this impact dosing?
-How effective are topical beta blockers in pts already on systemic beta blocker?

Back 156

Beta blockers
-Mechanism: decrease cAMP production in ciliary epithelium --> 20-50% reduction in aqueous secretion --> 20-30% reduction in IOP
-Much more effective in the day than during sleep --> AM dosing is best to blunt early AM pressure spikes and for efficacy
-May have lower IOP in contralateral eye due to systemic absorption
-If pt already on systemic beta blocker, adding topical beta blocker is much less effective

Front 157

MEDICAL: Beta blockers
-Which beta blocker is a selective b1 blocker?
-What organ systems are affected by b1 and b2, respectively?
-What is a unique feature of carteolol?

Back 157

Beta blockers
-All are NONselective except betaxolol (b1 selective) --> may have less IOP lowering than nonselective BBs
-B1 = cardiac
-B2 = pulmonary
-Carteolol: intrinsic sympathomimetic activity --> may cause slight to moderate activation of receptors --> decreased effect on CV and respiratory systems

Front 158

MEDICAL: Beta blockers
-Most common side effects?
-Important questions to ask pts before prescribing beta blocker?
-Does the use of gel vehicle decrease or increase systemic beta blocker concentration?

Back 158

Beta blockers
-Most common side effects: bradycardia, bronchospasm (ask about history of asthma!), heart block, hypotension, CNS depression
-Use of a gel vehicle decreases plasma concentration of beta blocker compared to solution modalities

Front 159

MEDICAL: Parasympathomimetics
-Which are the direct and indirect acting parasympathomimetics?
-Mechanism of action?
-Amount of IOP lowering?

Back 159

Parasympathomimetics
-Direct: pilocarpine (affect motor endplates in same way as Ach)
-Indirect: carbachol (both direct and indirect), echothiophate (inhibit anticholinesterase)
-Mechanism: both types cause contraction of longitudinal ciliary muscle --> pulls scleral spur --> tightens TM --> increase OUTFLOW of aqueous
-Reduce IOP by 15-25%

Front 160

MEDICAL: Parasympathomimetics
-Most important systemic side effects?
-Why should miotics be avoided in uveitic glaucoma?
-Why should miotics be avoided in phakic patients?
-What are some other ocular side effects?

Back 160

Parasympathomimetics
-Systemic side efects: GI, abd pain, increased salivation, bronchospasm, enuresis, inability to give depolarizing agents (succinylcholine)
-Ocular side effects: induced myopia (from CB contraction), brow ache, poor vision in dim light, retinal detachment
-Avoid in uveitic glaucoma b/c miotics can break down blood-aqueous barrier
-Avoid in phakic pts b/c miotics are cataractogenic & can cause paradoxical angle closure (CB contraction --> forward movement of lens-iris complex, increased AP diameter of lens, miotic pupil --> pupillary block)

Front 161

MEDICAL: CAIs
-Mechanism of action?
-How much of the CB carbonic anhydrase activity must be abolished to produce effect?
-Onset of action of topical vs systemic CAIs?
-Any advantage to using BOTH topical and systemic CAI?

Back 161

CAIs
-Mechanism: decrease aqueous formation by antagonizing ciliary carbonic anhydrase --> need to abolish > 90% of enzyme activity to produce IOP reduction
-Oral CAIs act within 1 hour of administartion
-IV Diamox starts within 2 minutes of administration
-No advantage to using both topical and systemic CAI in combination

Front 162

MEDICAL: CAIs
-Systemic side effects?

Back 162

CAIs
-Systemic side effects: paresthesias, GI sx, weight loss, lassitude/loss of energy, loss of libido, impotence, unpleasant taste, mental depression, renal stones
-Avoid in pts w/ sulfa allergy!

Front 163

MEDICAL: Alpha agonists
-Mechanism of action?
-Which are selective and which are nonselective?
-Are alpha agonists effective when combined w/ beta blockers?

Back 163

Alpha agonists
-Mechanism: increase trabecular and uveoscleral outflow (epinephrine-related agents can initially increase and then long term decrease aqueous production)
-Nonselective: epinephrine & dipivefrin
-Alpha2 selective: apraclonidine, brimonidine
-Modest additional pressure lowering when combined with beta blockers

Front 164

MEDICAL: Alpha agonists
-What are the main side effects of nonselective alpha blockers (epinephrine, dipivefrin) that prevent their use today?

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Alpha agonists - NONselective side effects
-Adrenochrome deposits from oxidized metabolites in conj, cornea, lacrimal system
-Pupillary dilation --> can precipitate angle closure in susceptible pts
-CME in aphakic/pseudophakic eyes w/o intact posterior capsule

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MEDICAL: Alpha agonists
-What are the main ocular alpha-1 and alpha-2 effects?
-Which is more selective for alpha-2 receptor: brimonidine or apraclonidine?
-Mechanism of apraclonidine?
-Why is apraclonidine not used for long term IOP control?

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Alpha agonists
-Alpha 1: vasoconstriction, pupil dilation, eyelid retraction
-Alpha 2: IOP reduction, possible neuroprotection
-Brimonidine is more selective for Alpha-2 than apraclonidine
-Mechanism (apraclonidine): inhibits norepinephrine release at nerve terminal --> decrease aqueous PRODUCTION, episcleral venous pressure & improves trabecular outflow
-Apraclonidine is not good for long term IOP control due to tachyphylaxis

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MEDICAL: Alpha agonists
-Mechanism of brimonidine?
-What is brimonidine-purite?
-Why should brimonidine be avoided in infants/young children?
-Peak IOP reduction?
-What other drugs should be avoided in pts on brimonidine?

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Alpha agonists
-Mechanism (brimonidine): decreased aqueous production & increased uveoscleral outflow
-Brimonidine-Purite: lower concentration, no benzalkonium chloride, neutral pH --> as efficacious and with reduction of ALL side effects compared to brimonidine
-Avoid in infants: somnolence, CNS depression, apnea, seizures, hypotension
-Peak IOP reduction: 25%
-Avoid in pts on MAOI or TCA antidepressants!

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MEDICAL: Hyperosmotics
-What agents are used?
-Mechanism of action?
-Side effects?

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Hyperosmotics
-Oral glycerin & IV mannitol
-Mechanism: increase blood osmolality --> osmotic gradient b/w blood and vitreous --> draws water from vitreous --> reduces IOP
-Side effects: transient (rapid re-equilibration of osmotic gradient), HA, confusion, CHF, MI, SDH/SAH, hyperglycemia (glycerin)

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MEDICAL: OAG
-What are reasonable first line choices for medical mgmt?
-Which of these is the most commonly used?
-Which are the best tolerated?
-What accounts for intolerance to many topical agents? What are alternatives in this case?

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OAG
-First line: prostaglandins, beta blockers, alpha-2 agonists, topical CAI
-Prostaglandins: most effective for IOP lowering, best safety profile
-Beta blockers: best tolerated in/around the eye
-Benzalkonium chloride (preservative): most common cause of medication intolerance
-Alternatives: preservative free timolol, brimonidine-purite, gel forming timolol, BAK-free travoprost

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MEDICAL: ACG
-What is the general purpose of medical therapy in mgmt of ACG?

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ACG
-Purpose of medical therapy is to prepare for laser iridectomy --> rapid IOP reduction, clearing of cornea, reduce intraocular inflammation, pupil constriction, prevent formation of PAS and post synechiae

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MEDICAL: Pregnancy
-Which is the only class B agent? (all others are class C)
-What are specific pregnancy-related side effects of CAIs and prostaglandins?
-When are beta blockers specifically not recommended?

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Pregnancy
-Brimonidine = class B
-CAIs: teratogenic in rodents
-Prostaglandins: increase uterine contractility
-Beta blockers: avoid in nursing mothers (concentrated 5x in breast milk) --> also avoid alphagan in nursing mothers