Glaucoma Classification Flashcards
Define Glaucoma
A group of ocular diseases with varying presentation with a common denominator: An acquired, progressive optic neuropathy
Usually results in abnormal IOP
Leads to ONH damage and ganglion cell loss
Which leads to VF loss and potential blindness
What are the 4 classifications we discussed and their sub-classifications
Primary Open Angle Glaucomas: High tension and normal tension
Primary Closed angle Glaucoma: With pupillary block and without pupillary block
Secondary glaucomas: open-angle secondary and closed angle secondary
Developmental/congenital Glaucoma
What are the characteristics of Primary Glaucomas
Not associated with any other apparent ocular or systemic disorder
In primary open-angle
-aqueous outflow is reduced on a submicroscopic and or biomechanical level
The angle is usually ()
What are the characteristics of Secondary Glaucoma
Caused ocular and systemic disorders
-Causes decrease in aqueous outflow leading to either open or closed angle glaucoma
Glaucoma is a result of the disorder
can be inherited or acquired
can be unilateral or bilateral
Developmental glaucoma
Due to abnormalities in the anterior chamber angle
abnormalities occuring during gestation
- secondary type glaucoma
- chronic
Describe Open Angle Glaucoma
Blockage of the TB slows drainage of the aqueous humor, which increases intraocular pressure.
The aqueous flow is not obrstructed by iris anatomy
(most) common form of adult glaucoma
Closed angle glaucoma
Aqueous flow is obstructed by the iris root
The angle formed by the cornea and the iris narrow, preventing the aqueous humor from draining out of the eye. This can lead to a rapid increase in IOP
Describe Long Anterior Zonule associated PDS
Long anterior zonules inserted onto the central lens capsule which may cause mechanical disruption of the pigment epithelium at the pupillary ruff and the central iris leading to pigment dispersion
What Percent of patients with PDS will develop PG
Approx: 35% of PDS individuals eventually go on to manifest pigmentary glaucoma
What are the theories behind PDS/PG
1) Pigment release: pigment dispersion results from an abnormality of the iris pigment epithelium
2) Mechanical Disruption: radial folds of the iris pigment epithelium rub agains the lens capsule and/or zonular fibers to release pigment
Describe the pathophysiology behind PDS/PG
Liberated pigment deposits in the TB clogging it. This leads to a disruption in aqueous out-flow and increased IOP
Who is PG/PDS most common in
Occurs most commonly in younger age 20-40 and is more common in caucasions
PDS is equal in men and women
PG is more common in men
What refractive error is associated wit PDS
approx 90% of pts with PDS have MYOPIA
-PDS is more prevalent in pts with deeper anterior chamber angles–> Patients with higher myopia and deeper angles develop PDS at an earlier age and have a more difficult clinical course.
Most commonly is bilateral, though often asymmetrical–> with the MORE affected eye tending to be more MYOPIC
What is the classical clinical triad that presents with PDS
Krukenberg spindle
Iris transillumination defects
Piment deposition in the TM
What would you expect to see upon gonioscopy in PDS?PG
homogenous pigment over the Trabecular Meshwork
Pigment may be observed on or anterior to Schwalbe’s line this is referred to as Sampaolesis line
What is the classical clinical presentation of Pigmentary Glaucoma
Krukenberg spindle
Transillumination defect
Pigment in TM
Zentmeyer ring aka Scheie’s line (pigment on the zonules)
T or F PDS and PDG pts have an increased risk for retinal detachment?
True: occurs in as many as 6-7% of patients
Retinal Breaks and lattice degeneration occurs twice as frequently when compared to age and refraction-matched patients
What conditions would you want to rule out as the mimic PDS process when considering PDS/PG
Exfoliation syndrome
Uveitis
Ocular melanosis
POAG with excessive pigmentation
How would you treat PG?
IOP may fluctuate and is more difficult to control but:
- Topcial B-adrenergic antagonists
- A2 adrenergic agonists
- CAI
- Prostaglandin analogues
- Miotics: can used before exercise but should be careful as there are SE
What “surgical” tx may be considered in PG
laser peripheral iridotomy (LPI or PI) –> may be effective to eliminate any posterior iris bowing
Argon Laser Trabeculoplasty (ALT)
What is Pseudoexfoliative Sydrome characterized by? (PXS)
gray-white flakes of granular material depositing throughout the surfaces of the anterior chamber structures
What type of glaucoma is PXS associated with?
Psuedoexfoliation Glaucoma:when there is optic nerve involvement
-A secondary open-angle glacuma–> is the most identifiable form of secondary open angle glaucoma worldwid
Describe the pathophysiology of PXS
PXM is a fibrogranular material of a protein nature and is amyloid like.
Is possibly secondary to distrubances in the biosynthesis of basement membranes in epithelial cells
The iris pigment epithelium, ciliary epithelium and the peripheral anterior lens epithelium are thought to produce the PXM
-exact origin is uncertain.
T or F PXM is has been found widely distributed throughout the body?
True: Has been found in the walls of the vortex veins and the central retinal artery.
Extraocular tissues involved include: lungs, skin, liver, heart, kidneys, gallbladder, blood vessels. extraocular muscles, connective tissue in the orbit and meninges
What age group is PXS/PG more common in?
More prevalent in ages 60-80 and is rarely seen before the age of 50.
Is PXS more common in men or women? what about PG?
PXS is more common in women
-however, Men with PXS are more likely to develop glaucoma.
What percent of PXS patients will develop glaucoma (PXG)
approximately 15% of patients with PXS developed glaucoma after 10years
-Even more will develop increased IOP
What systemic conditions has PXS been linked to?
Alzheimer disease Senile dementia Stroke TIA Heart disease Hearing loss Higher homocysteine levels (risk factor for cardiovascular disease)
What are the clinical signs of PXS/PG
3 ring sign
greyish-white deposits on the anterior lens surface: classic presentation
-a bulls eye pattern
What are the 3 identifiable zones on the lens with PXS/PG
Central Translucent disc zone
Intermediate clear zone
Peripheral granular zone
What type of Cataract is more prevelant in PXS pts
NS
Where is PXM found in the anterior chamber and how does the pressure compare to POAG
Found in the inferior angle and leads to higher IOP than POAG
What is the pigment deposition like in PXS/PXG?
A more spotty distribution and less dense than PDS
What are the two surgical treatments for PXS and PXG and advantage to each
Argon laser trabeculoplasty(ALT): often used earlier in treatment and has good initial success
Selective laser trabeculoplasty (SLT): Equal efficacy the advantage is that it is a repeatable surgery
can also do surgical trabeculectomy
Describe neovascular glaucoma
IOP elevation due to angle closure resulting form fibrovascular membrane formation obstructing aqueous outflow–> A result of RETINAL hypoxia/ischemia
What are the disorder that predispose a pt to Neovascular Glaucoma
Central Retinal Vein Occlusion, Diabetic Retinopathy and Carotid Artery Dissection
Describe the Early phase of NG
small vessels at the pupillary margin. Earliest sign of vascular proliferation
Rine tortuous randomly orientated tufts of vessels on the surface of the iris
Describe the middle phase of NG
the angle becomes involved
Neo progresses from the pupillary margin toward the angle
-neo of the angle in the absence of pupillary involvement may occur
This is when a Fibrovascular membrane can grow along with NVA obstructing the TM leading to NVG
Describe the late phase of NG
Fibrovascular membrane within the AC contracts producing a peripheral anterior synechia
can progress to 360 angle closure
How would you treat and manage NG
Treat underlying idsease
Topical steroids for inflammation
Anti-VEGF therapy
Panretinal Photocoagulation (PRP) has been the first line therapy
In order to have AACG pts must have 2 of the following sxs what are they?
Ocular pain, Nausea/vomiting, history of intermittent blurring of vision with halos
In order to have AACG pts must have at least 3 of the following signs, what are they?
IOP greater than 21mmhg, conjunctival injection, corneal epithelial edema, mid-dilated nonreactive pupil, shallower chamver in the presence of occlusion
Describe AACG with Pupil Block
Adherence between the back of the iris and the front of the lens
Rapid increase in IOP
Most commonly trigered when the pupil is mid-dilated
-think dark activities
AACG without pupil block
Plateaue iris configuration
Last iris roll will be bunched and forced against the TM upon pupil dilation
What causes Plateaue Iris
Large or anteriorly positioned ciliary processes
Accounts for more than 50% of young pts with recurrent angle closure
AACG due to phacomorphic glaucoma
Due to lens swelling leading to shallower AC
Malignant glaucoma AACG
posterior misdirection of the aqueous into the vitreous
Rod associated signs and Symptoms with HRD
Loss of night vision peripheral field loss ERG: Scotopic loss acuity and color vision affected late photosensitivity
Cone associated signs and symptoms with HRD
Decreased acuity central scotoma ERG: Photopic loss color vision affected photosensitivity
What are the peripheral rod diseases we covered
Retinitis pimentosa family: Lebers congenital amaurosis
CSNB
Oguchis
What are the central cone diseases we covered
Achromatopsia
cone dystrophy
Juvenile Macular dystrophies: Stargardts, Bests
Retinitis Pigmentosa
most common hereditary retinal dystrophy
Involves rhodopsin gene
Initially affects the rods and then with progrssion the cones are affected
Describe autosomal recessive RP
The most common and most severe form
Night vision and peripheral field loss in early childhood, central vision loss by adult hood
X-linked has similar progression
Descrive autosomal dominant RP
Least severe form with central vision intact until 40s or 50s
What are the symptoms of RP
Night blindness (nyctalopia): initial symptom
Reduced mobility especially in low light
Some asymptomatic despite large field loss
Eventual central acuity loss
RP Signs
Arterial attenuation (sometimes earliest sign)
Waxy looking ONH pallor (atrophy)
Classic bone spicule pigmentary pattern
-Begins in mid-periphery
-corresponding visual field loss (ring scotoma)
Cataracts PSC develop in 50% of cases
Macular edema in late stages- always look at the arteries right away the may look narrow
What is the initial ERG show in RP
Scotopic ERG will usually be abnormal before retinal signs are present
What is Retinitis Sine Pigmento
no or minimal pigmentary changes (may be atrophic looking retina)
May be just early stage of disease
Arterial attenuation and wxy nerve may be prominent
What is sector RP
Inferior quadrants only
Ushers syndrome
congenital sensori-neural hearing loss and RP
accounts for 50% of deaf-blind individuals
What can you do to manage/treat RP
Short wavelength blocking tints: red, orange, amber
Oral 9-cis B Carotene
Omega-3 rich diet
Describe Leber’s Congenital Amaurosis
Similar to RP except early onset
Think a visually unresponsive baby with nystagmus
In LCA what do you expect in the ERG
Severely diminished or absent rod and cone response
Need to be sedated for ERG
What is Congenital sensory nystagmus
an afferent pathway defect, secondary to disease disrupting the foveal pathway early in life.
-Bilateral retinal or optic nerve disease that is congenital or develop over 2 years
What is Congenital motor nystagmus
An efferent pathway defect, duet to primary abnormality in the ocular motor system
usually hereditary pattern
-idiopathic infantile motor nystagums
Define congenital Stationary Night blindness
Night blindness is primary symptom Mild acuity reduction to 20/30-20/60 Normal to near normal retina Nystagmus in severe cases ERG Pattern is diagnostic
Define oguchis Disease
Variant of CSNB in Japenese
-Yellow-gray retina color reversed by 2-3hrs of dark adaptation
Gyrate distrophy
Associated with hyperornithinemia due to deficient enzyme activity
high myopia early in life
Night blindness and RPE changes in 2nd decade
RPE and choroidal atrophy leaving bare sclerar
tx: B6 supplements low protein diet
Define Stargardts Macular dystrophy
Most common hereditary juvenile macular dystrophy
usual onset is 8-16yrs
Macular changes subtle at first
-FLR lost as mottling appears
-Yellow pisciform flecks in surrounding posterior pole
-Beaten bronze appearance at endstage
Usually stablizies by early 20s with acuities in 20/200-20/400
Define Fundus Flavimaculatus
variant of stargardts
pisciform lesions are primary presentation
macualr disease and acutiy loss develops later in 40-50s
Define Vitelliform Dystrophy (Bests Disease)
AD inherited
Begins early childhood
central retinal dystrophy
Previtellifrom stage
abnormal EOG
Bitellifrom Stage
Yellow spots coalesce into Egg Yold macula appearance
-VA still near normal
Pseudohypopyon stage
lesion Partially reabsorb
Vitelliruptive stage
lesion breaks up into scrambled egg
VA drops to 20/200
How would you treat Best
anti-VEGF
What are the 2 forms of Achromatopsia
Rod monochromatism = AR
Blue Cone Monochromatism = x-linked
What are the signs of Achromatopsia
Photophobia Nystagmus VA in 20/100-20/200 range Normal fundus in young pts No color vision Photopic ERG severly diminished
What tint would you give to someone with Achromotopsia
Red tint is best for achrmomat
Magenta is best for blue-cone achromat
What are the signs of progressive cone dystrophy
Reduced VA-20/60-20/200
Photophobia (Day blindness)
Most common: Bulls eye macular lesion
Extremely diminished ERG, Normal or slighly diminished scotopic ERG
Being it is progressive you would NOT see NYSTAGMUS
Define central areolar choroidal dystrophy
Later onset: Usually after 40
Atrophy involving choriocapillaris–> RPE–> retina
Normal electrodiagnostics
abnormal color vision
loss of central vision with acutiy dropping below 20/200
What causes albinism
varying degrees of amelanosis due to deficiency of tyrosinase or other player in melanin biosynthesis
What is vision like in those with albinism
Foveal hypoplasia (major factor affecting acuity) Amelanosis of iris and retina Nystagmus strabismus and impaired BV Astigmatism
Define the choroidal Flush
1st fluorescence in 10-12sec
Fluid remains in choroid as long as RPE and Bruchs are intact
cilioretinal artery will fill as choroidal fluorescence begins
Define the arterial phase
10-15sec after injection central retinal artery begins to fill
arteries are bright, veins are dark
Define arterial-venous phase
20-25sec after injection
arteries –> arterioles –> capillaries –> venules –> veins vill
Optic disc capillaries fill via posterior cilliary artery
perifoveal capillaries fill at 20-25sec
Define the venous phase
early venous phase: Laminar flow of veins, arteries still bright
Venous phase:veins and arteries fully bright
Late phase
10min post injection
arteries and veins almost empty
choroidal flush is at its minimum
leakage of dye remains in tissue
What causes hypfluorescence
Filling defect
blocking defect
What causes hyperfluorescence
autofluorescence(drusen) Psuedofluorescence(sclera showing) Transmission or window defect (scar) Leakage (neovascular vessel) Pooling (sub-retinal leakage) Staining (ONH)
what creates shadowing in OCT
blood vessels as the block and absorb light
What creates hyper-reflectivity in OCT
Excess blood, drusen, or exudates
What creates hypo-relfectivity in OCT
other fluids: plasma, vitreous, water
where would you see fluid pockets in CME
Between inner plexiform layer (IPL) and the outer nuclear layer (ONL)
what is the most common cause of serous detachment
Choroidal neovascular membrane (CNVM)
Define a Retrovitreal hemorrhage
Bright red blood behind vitreous, shifts readily with eye movement
What is an intravitreal hemorrhage
varied appearance within vitreous, clots quickly, settles in lacunae.
What are the common causes of intravitreal hemorrhage
Secondary to rupture of neovascular net development of retinal tear associated with PVD Bleeding from neo ischemic retinopathy trauma
How do you manage a intravitreal hemorrhage
Determine cause and refer to retinal specialist
Resting with head 30-45deg elevated
antiplatelet tx
What are the 2 types of retrovitreal hemorrhages and where are they located
1) subhyaloid: between posterior vitreous (Hyaloid) base and the ILM
2) Preretinal: posterior to the ILM and anterior to the NFL
What are the characteristics of a retrovitreal hemorrhage
usually posterior pole
Boat shaped with variable size
FANG: blockage of choroidal fluorescein
Causes: Neo, PVD retinal break, valsalva
Describe a superficial/Flame shaped Heme
Follows NFL Ruans parallel to retinal surface Can have a white center: Roth spot FANG: appears black (hypofluorescent) No compromise to visual function
What are some causes of a flame heme
HTN, vein occlusions, optic neuropathies
Where is a Dot/Blot heme located?
INL, OPL, ONL
What are dot/blot hemes associated with?
Common with diabetes, and HTN
Associated with venous based congestive disease
Where are sub-retinal hemes located
Between RPE and Sensory retina
Appear large with lobulated border
What are the two types of subretinal hemes
Subretinal: above RPE = a red color
Sub RPE = grey/green color
What is the common cause of Sub retinal heme
Ruptured CNVM (wet amd) often visually devastating
What is a roth spot
Retinal heme surrounding a white center
White center is presumed to be WBCs, CWS, leukemic cell foci or firin
What conditions are associated with Roth SPots
Diabetic Retinopathy Pernicious anemia Bacterial endocarditis leukemia HIB
What sizes classifies a macro/micraneurysm
Micro:50-100um diam
Macro: 280um diam
What are the characteristics of a microaneurysm
Originate from inner retinal capillaries /INL
Very small often missed or confused for dot hemees
Hyperfluoresence with FA
What conditions are associated with microaneurysms
DM, HTN, Blood dyscrasias, leukemias
Describe a macroaneurysm
Isolated dilation of major artery branch
Secodnary edema, exudates and hemes can occur
usually in females and older 50-80
What conditions are commonly associated with Macroaneurysm
HTN, arteriosclerosis and retinal emboli
What is the management plan for macroaneurysm
Asymptomatic and (-) exudate/hem 6mo follow up Asymptomatic and (+) exudate/heme 1-3mo follow up Symptomatic and threatens macula --> retinal consult
What are hard exudates
Lipid deposits associated with deep retina edema
where do exudates typically deposit
In the OPL throuought the retina and Henles layer in macula
What are exudates associated with
Choroidal neovascular membrane
Intra-retinal edema (leaky MA, tlangictastic vessel)
Retinal tumors (coats)
What conditions are associated with Hard exudates? How would you manage
DM, HTN, Venous occlusive disease, Retinal Mass, Lebers, VHL, COats
consult specialist if within 1-2DD of macula
What are cotton wool spots
Area of NFL ischemia
white fluffy non-distinct shape
-resolve in 5-7 weeks
What are the causes of Cotton Wool spots
HTN, DM, Anemia, HIV/AIDS, Carotid artery disease
How to Cotton wool spots appear on FANG
black
Neovascularization is due to retinal ischemia. What can neo cause
Retinal edema
Vitreous hemorrhage
Retinal detachment
What is Intra-Retinal- Micrvascular Anomalies (IRMA)
represents an intra-retianl shunting system
Tortuous capillaries in an area of severe capillary non perfusion
IRMA does not leak or bleed
May be a precursor to neo at a later time
what is collateral
New BV that give A-A or V-V communication
What is a shunt
New BV that gives A-V or V-A communication
Descrive Congenital Vascular Tortuosity
All quadrants
symmetric OU
Can be linked with syndromes
Describe Acquired Retinal vascular tortuosity
Previously documented normal
Sectoral involvement
Associated thickening and darkening of the BV column
Indicator of hypoxia
What is venous beading and what does it indicate
Looks like bulging of the vein wall. Result of sludging of venous blood causes venous dilation
Indicates widespread retinal ischemia/hypoxia
Describe NA-AION
Small BV diseas that affects the pre-laminar portion of the disc, creating an imbalance in the pressure perfuion ration
Vast majority of cases are due to hypoperfusion of the ONH specifically a nocturnal hypotension
What are the risk factors for NA-AION
Noctural arterial hypotension--> especially pts on antihypertension medications/topcial BB DM Ischemic HEART disease Renal dialysis Coronary bypass surgery
What systemic meds are associated with NA-AION
ED meds Amiodorone Nasal decongestants Interferon therapy oral antihypertensives
Define AAION
Arteritic AION: an autoimmune inflammatory conditionUsually in Patients over the age of 60 and associated with Females
A TRUE ocular emergency associated with Giant cell arteritis
What vessels are affected in AAION
Disease presents as inflammation of the elastic tissue in the medium or large sized arterial walls leading to occlusion
What is tested when doing an RBCC
number of RBCs x10^6 ml of blood
What is tested when doing a hemoglobin test
Level of oxygen carrying protein found in the blood in g/dl
What is tested when doing a Hematocrit level test
Percentage of red cells in whole blood
Mean cell volume ?
Size of the average RBC in microns
Mean cell hemoglobin
amount of hemoglobin in picograms
mean cell hemoglobin concentration
Grams of hemoglobin in dL
What is being tested in a white blood cell differential
Percent of the five types of WBCs in blood -neutrophils eosinophils basophils lymphocytes monocytes
List the cuases of anemia
Vitamin B12/ Iron deficiencies (pernicious) Increased destruction of RBCs Blood Loss Genetic or acquried defect Disease (Leukemia)
What are the characteristics of Iron deficiency anemia
Most common anemia in the US
Deficiency of iron more common in women
Menstrual blood loss
usually due to inadequate intake
What findings are associated with poor iron absorption
Cold feet, Tiredness, pale skin color, SOB, Typically no retinal changes unless severe
Tx: iron supplements
What is the mechanism for Pernicious anemia
An autoimmune disease directed against intrinsic factor or parietal cells themselves which leads to an intrinsic factor deficiency and malabsorbtion of B12 –> Subseqeunt megaloblastic anemia
What retinal findings are associated with Pernicious anemia
crossing changes in AV with nipping
may see black coagulated blood
How would you treat pernicious anemia
Sublingual or parenteral vitamin supplement
Describe hemolytic anemia
RBCs are destroyed prematurely body can not replace RBC fast enough
What are the causes of hemolytic anemia
Infections
Medications
Immune attack (Autoimmune)
What is aplastic anemia
Bone marrow damage –> inefficiency to make enough RBCs
what are some causes of aplastic anemia
viral infection
toxic chemicals
radiation
medications
What causes temporal atrophy
Toxic and Nutritional ON
Autosomal Dominant ON
Lebers Heriditary ON
Optic Neuritis
What causes Superior/Inferior Atrophy
Ischemic ON
What causes band or Bow tie atrophy
Chiasm or optic tract
What is Papilledema?
Disc edema due to raised ICP
What is idiopathic intracranial Hypertension?
Increased ICP
Normal CSF composition
Not anatomcal abnormality that casues increased ICP
What can cause pseudotumor cerebri?
Pregnancy, anemia, HTN, Sleep apnea, Hypo or Hyper thyroid
Tetracyclines, corticosteroids, retinoids, lithium
what are the sytemic symptoms of IIH or Papilledema
Nausea and vomitting
Pulsatile tinnitus
Dizziness
What are the visual symptoms of IIH or Papilledema
Transient visual obscuractions
Horizontal diplopia
what is the 15 year rule for Demyleniating Optic Neuritis
In terms of lesions
0 = 25%
1-2 = 50%
3> = 75%
What are the indications to begin Glaucoma tx
Established POAG POAG in one eye, ocular HTN in the other Ocular HTN in one or both eyes IOP Level: treat over 30 Rising IOP Family Hx The patient is monocular IOP>21 with history of retinal vascular occlusive disease
What is the conventional (Trabecular) outflow
TM–> Schlemms canal–> Collector channels/venous plexi–>Episcleral veins
What classes are used to reduce aqueous production
Beta-blockers, CAI, Alpha-2 Agonist
What classes are used to increase outflow
Miotics, adrenergic/alpha-2 agonists, Protaglandings/prostamides, docosanoids
What is the only Beta1 selective Topical drop
Betaxolol
By what amount do Beta blockers decease IOP
22-33%
By what amount do CAI decrease IOP
15-20%
What systemic SE should you be concerned about with CAI
Sulfa allergies, dyscrasias
CAI are CI in sulfa allergies, sickle cell anemia or other blood dyscrasias and corneal surgery
Mechanism of Dipivefrin
A pro-drug that is converted to epinephrine
Direct stimulation of both alpha and beta receptors
-Enhances aqueous outflow primarily (uveoscleral pathway)
By what percent does dipiverfrin decrease IOP
15-20%
what is the indication for .5% apraclonidien
short-term therapy of patients on maximally tolerated pharmacotherapy sho require additional IOP drop
Indication for 1% apraclonidine
Reduce incidence an magnitude of IOP spikes after anterior segment laser therapy
can drop up to 40%
Characteristics of Latanoprost/Travaprost/Bimatoprost
Prostaglandin analog
Reduces IOP by 30-35%
What is the mechanism of prostaglandin analogs
Increases uveoscleral outflow
Loosens the intercellular spaces on the ciliary body allowing outflow
What are the SE of Prostaglandins
Darkening of light or mixed iris Increased size of lashes Eyelid darkening CME Uveitis or conjunctivitis Onset of herpes simples
When are Prostaglandins CI
Aphakia/pseudophakia Hx of uveitis YAG posterior capsulotomy hx of herpes simples cosemetic concerns
When are hyperosmotics indicated
indicated in cases of acute angle closure glaucoma or other highly elevated glaucoma situations
What is the only disc change that is completely diagnostic of glaucomatous damage?
progressive thinning of the neural rim
At what C/D is the risk of glaucoma increased
.6/.6
What patterns/combinations of the C/D are highly associated with glaucoma
Vertical elongation of C/D
Temporal thinning/unfolding
What are the characteristics of a healthy NFL
seen as fine silver glistening striations
Normal NFL is brightest and thickest in the superior and thickest in the superior and inferior aracades close to the optic disc
What is the most obvious NFL defect?
Inferior temporal wedge defect and usually corresponds with inferior temporal notching and superior visual field loss
What is the total field covered in each eye by a 30-2 and a 24-2
30-2: covers 60 degrees total field per eye
24-2: covers 48degrees
What is usually the first field defect in glaucoma
small areas of depressed sensitivity (relative paracentral scotomas) between 5 and 20 degrees of fixation
List 3 other common findings on VF with glaucoma pts
Nasal step
Temporal wedge defect
overall gerealized depression of sensitivity