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Oc Disease III > Glaucoma Classification > Flashcards

Glaucoma Classification Flashcards

1
Q

Define Glaucoma

A

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

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2
Q

What are the 4 classifications we discussed and their sub-classifications

A

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

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3
Q

What are the characteristics of Primary Glaucomas

A

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 ()

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4
Q

What are the characteristics of Secondary Glaucoma

A

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

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5
Q

Developmental glaucoma

A

Due to abnormalities in the anterior chamber angle

abnormalities occuring during gestation

  • secondary type glaucoma
  • chronic
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6
Q

Describe Open Angle Glaucoma

A

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

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7
Q

Closed angle glaucoma

A

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

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8
Q

Describe Long Anterior Zonule associated PDS

A

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

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9
Q

What Percent of patients with PDS will develop PG

A

Approx: 35% of PDS individuals eventually go on to manifest pigmentary glaucoma

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10
Q

What are the theories behind PDS/PG

A

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

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11
Q

Describe the pathophysiology behind PDS/PG

A

Liberated pigment deposits in the TB clogging it. This leads to a disruption in aqueous out-flow and increased IOP

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12
Q

Who is PG/PDS most common in

A

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

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13
Q

What refractive error is associated wit PDS

A

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

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14
Q

What is the classical clinical triad that presents with PDS

A

Krukenberg spindle
Iris transillumination defects
Piment deposition in the TM

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15
Q

What would you expect to see upon gonioscopy in PDS?PG

A

homogenous pigment over the Trabecular Meshwork

Pigment may be observed on or anterior to Schwalbe’s line this is referred to as Sampaolesis line

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16
Q

What is the classical clinical presentation of Pigmentary Glaucoma

A

Krukenberg spindle
Transillumination defect
Pigment in TM
Zentmeyer ring aka Scheie’s line (pigment on the zonules)

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17
Q

T or F PDS and PDG pts have an increased risk for retinal detachment?

A

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

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18
Q

What conditions would you want to rule out as the mimic PDS process when considering PDS/PG

A

Exfoliation syndrome
Uveitis
Ocular melanosis
POAG with excessive pigmentation

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19
Q

How would you treat PG?

A

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
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20
Q

What “surgical” tx may be considered in PG

A

laser peripheral iridotomy (LPI or PI) –> may be effective to eliminate any posterior iris bowing

Argon Laser Trabeculoplasty (ALT)

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21
Q

What is Pseudoexfoliative Sydrome characterized by? (PXS)

A

gray-white flakes of granular material depositing throughout the surfaces of the anterior chamber structures

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22
Q

What type of glaucoma is PXS associated with?

A

Psuedoexfoliation Glaucoma:when there is optic nerve involvement

-A secondary open-angle glacuma–> is the most identifiable form of secondary open angle glaucoma worldwid

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23
Q

Describe the pathophysiology of PXS

A

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.

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24
Q

T or F PXM is has been found widely distributed throughout the body?

A

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

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25
Q

What age group is PXS/PG more common in?

A

More prevalent in ages 60-80 and is rarely seen before the age of 50.

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26
Q

Is PXS more common in men or women? what about PG?

A

PXS is more common in women

-however, Men with PXS are more likely to develop glaucoma.

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27
Q

What percent of PXS patients will develop glaucoma (PXG)

A

approximately 15% of patients with PXS developed glaucoma after 10years
-Even more will develop increased IOP

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28
Q

What systemic conditions has PXS been linked to?

A 
Alzheimer disease
Senile dementia
Stroke
TIA
Heart disease
Hearing loss
Higher homocysteine levels (risk factor for cardiovascular disease)
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29
Q

What are the clinical signs of PXS/PG

A

3 ring sign
greyish-white deposits on the anterior lens surface: classic presentation
-a bulls eye pattern

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30
Q

What are the 3 identifiable zones on the lens with PXS/PG

A

Central Translucent disc zone
Intermediate clear zone
Peripheral granular zone

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31
Q

What type of Cataract is more prevelant in PXS pts

A

NS

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32
Q

Where is PXM found in the anterior chamber and how does the pressure compare to POAG

A

Found in the inferior angle and leads to higher IOP than POAG

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33
Q

What is the pigment deposition like in PXS/PXG?

A

A more spotty distribution and less dense than PDS

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34
Q

What are the two surgical treatments for PXS and PXG and advantage to each

A

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

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35
Q

Describe neovascular glaucoma

A

IOP elevation due to angle closure resulting form fibrovascular membrane formation obstructing aqueous outflow–> A result of RETINAL hypoxia/ischemia

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36
Q

What are the disorder that predispose a pt to Neovascular Glaucoma

A

Central Retinal Vein Occlusion, Diabetic Retinopathy and Carotid Artery Dissection

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37
Q

Describe the Early phase of NG

A

small vessels at the pupillary margin. Earliest sign of vascular proliferation
Rine tortuous randomly orientated tufts of vessels on the surface of the iris

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38
Q

Describe the middle phase of NG

A

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

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39
Q

Describe the late phase of NG

A

Fibrovascular membrane within the AC contracts producing a peripheral anterior synechia
can progress to 360 angle closure

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40
Q

How would you treat and manage NG

A

Treat underlying idsease
Topical steroids for inflammation
Anti-VEGF therapy

Panretinal Photocoagulation (PRP) has been the first line therapy

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41
Q

In order to have AACG pts must have 2 of the following sxs what are they?

A

Ocular pain, Nausea/vomiting, history of intermittent blurring of vision with halos

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42
Q

In order to have AACG pts must have at least 3 of the following signs, what are they?

A

IOP greater than 21mmhg, conjunctival injection, corneal epithelial edema, mid-dilated nonreactive pupil, shallower chamver in the presence of occlusion

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43
Q

Describe AACG with Pupil Block

A

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

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44
Q

AACG without pupil block

A

Plateaue iris configuration

Last iris roll will be bunched and forced against the TM upon pupil dilation

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45
Q

What causes Plateaue Iris

A

Large or anteriorly positioned ciliary processes

Accounts for more than 50% of young pts with recurrent angle closure

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46
Q

AACG due to phacomorphic glaucoma

A

Due to lens swelling leading to shallower AC

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47
Q

Malignant glaucoma AACG

A

posterior misdirection of the aqueous into the vitreous

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48
Q

Rod associated signs and Symptoms with HRD

A 
Loss of night vision
peripheral field loss
ERG: Scotopic loss
acuity and color vision affected late
photosensitivity
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49
Q

Cone associated signs and symptoms with HRD

A 
Decreased acuity
central scotoma
ERG: Photopic loss
color vision affected
photosensitivity
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50
Q

What are the peripheral rod diseases we covered

A

Retinitis pimentosa family: Lebers congenital amaurosis
CSNB
Oguchis

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51
Q

What are the central cone diseases we covered

A

Achromatopsia
cone dystrophy
Juvenile Macular dystrophies: Stargardts, Bests

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52
Q

Retinitis Pigmentosa

A

most common hereditary retinal dystrophy
Involves rhodopsin gene
Initially affects the rods and then with progrssion the cones are affected

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53
Q

Describe autosomal recessive RP

A

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

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54
Q

Descrive autosomal dominant RP

A

Least severe form with central vision intact until 40s or 50s

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55
Q

What are the symptoms of RP

A

Night blindness (nyctalopia): initial symptom
Reduced mobility especially in low light
Some asymptomatic despite large field loss
Eventual central acuity loss

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56
Q

RP Signs

A

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

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57
Q

What is the initial ERG show in RP

A

Scotopic ERG will usually be abnormal before retinal signs are present

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58
Q

What is Retinitis Sine Pigmento

A

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

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59
Q

What is sector RP

A

Inferior quadrants only

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60
Q

Ushers syndrome

A

congenital sensori-neural hearing loss and RP

accounts for 50% of deaf-blind individuals

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61
Q

What can you do to manage/treat RP

A

Short wavelength blocking tints: red, orange, amber
Oral 9-cis B Carotene
Omega-3 rich diet

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62
Q

Describe Leber’s Congenital Amaurosis

A

Similar to RP except early onset

Think a visually unresponsive baby with nystagmus

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63
Q

In LCA what do you expect in the ERG

A

Severely diminished or absent rod and cone response

Need to be sedated for ERG

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64
Q

What is Congenital sensory nystagmus

A

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

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65
Q

What is Congenital motor nystagmus

A

An efferent pathway defect, duet to primary abnormality in the ocular motor system
usually hereditary pattern
-idiopathic infantile motor nystagums

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66
Q

Define congenital Stationary Night blindness

A 
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
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67
Q

Define oguchis Disease

A

Variant of CSNB in Japenese

-Yellow-gray retina color reversed by 2-3hrs of dark adaptation

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68
Q

Gyrate distrophy

A

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

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69
Q

Define Stargardts Macular dystrophy

A

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

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70
Q

Define Fundus Flavimaculatus

A

variant of stargardts
pisciform lesions are primary presentation
macualr disease and acutiy loss develops later in 40-50s

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71
Q

Define Vitelliform Dystrophy (Bests Disease)

A

AD inherited
Begins early childhood
central retinal dystrophy

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72
Q

Previtellifrom stage

A

abnormal EOG

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73
Q

Bitellifrom Stage

A

Yellow spots coalesce into Egg Yold macula appearance

-VA still near normal

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74
Q

Pseudohypopyon stage

A

lesion Partially reabsorb

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75
Q

Vitelliruptive stage

A

lesion breaks up into scrambled egg

VA drops to 20/200

76
Q

How would you treat Best

A

anti-VEGF

77
Q

What are the 2 forms of Achromatopsia

A

Rod monochromatism = AR

Blue Cone Monochromatism = x-linked

78
Q

What are the signs of Achromatopsia

A 
Photophobia
Nystagmus
VA in 20/100-20/200 range
Normal fundus in young pts
No color vision 
Photopic ERG severly diminished
79
Q

What tint would you give to someone with Achromotopsia

A

Red tint is best for achrmomat

Magenta is best for blue-cone achromat

80
Q

What are the signs of progressive cone dystrophy

A

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

81
Q

Define central areolar choroidal dystrophy

A

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

82
Q

What causes albinism

A

varying degrees of amelanosis due to deficiency of tyrosinase or other player in melanin biosynthesis

83
Q

What is vision like in those with albinism

A 
Foveal hypoplasia (major factor affecting acuity)
Amelanosis of iris and retina 
Nystagmus
strabismus and impaired BV
Astigmatism
84
Q

Define the choroidal Flush

A

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

85
Q

Define the arterial phase

A

10-15sec after injection central retinal artery begins to fill
arteries are bright, veins are dark

86
Q

Define arterial-venous phase

A

20-25sec after injection
arteries –> arterioles –> capillaries –> venules –> veins vill
Optic disc capillaries fill via posterior cilliary artery
perifoveal capillaries fill at 20-25sec

87
Q

Define the venous phase

A

early venous phase: Laminar flow of veins, arteries still bright
Venous phase:veins and arteries fully bright

88
Q

Late phase

A

10min post injection
arteries and veins almost empty
choroidal flush is at its minimum
leakage of dye remains in tissue

89
Q

What causes hypfluorescence

A

Filling defect

blocking defect

90
Q

What causes hyperfluorescence

A 
autofluorescence(drusen)
Psuedofluorescence(sclera showing)
Transmission or window defect (scar)
Leakage (neovascular vessel)
Pooling (sub-retinal leakage)
Staining (ONH)
91
Q

what creates shadowing in OCT

A

blood vessels as the block and absorb light

92
Q

What creates hyper-reflectivity in OCT

A

Excess blood, drusen, or exudates

93
Q

What creates hypo-relfectivity in OCT

A

other fluids: plasma, vitreous, water

94
Q

where would you see fluid pockets in CME

A

Between inner plexiform layer (IPL) and the outer nuclear layer (ONL)

95
Q

what is the most common cause of serous detachment

A

Choroidal neovascular membrane (CNVM)

96
Q

Define a Retrovitreal hemorrhage

A

Bright red blood behind vitreous, shifts readily with eye movement

97
Q

What is an intravitreal hemorrhage

A

varied appearance within vitreous, clots quickly, settles in lacunae.

98
Q

What are the common causes of intravitreal hemorrhage

A 
Secondary to rupture of neovascular net
development of retinal tear associated with PVD
Bleeding from neo
ischemic retinopathy 
trauma
99
Q

How do you manage a intravitreal hemorrhage

A

Determine cause and refer to retinal specialist
Resting with head 30-45deg elevated
antiplatelet tx

100
Q

What are the 2 types of retrovitreal hemorrhages and where are they located

A

1) subhyaloid: between posterior vitreous (Hyaloid) base and the ILM
2) Preretinal: posterior to the ILM and anterior to the NFL

101
Q

What are the characteristics of a retrovitreal hemorrhage

A

usually posterior pole
Boat shaped with variable size
FANG: blockage of choroidal fluorescein
Causes: Neo, PVD retinal break, valsalva

102
Q

Describe a superficial/Flame shaped Heme

A 
Follows NFL
Ruans parallel to retinal surface
Can have a white center: Roth spot
FANG: appears black (hypofluorescent)
No compromise to visual function
103
Q

What are some causes of a flame heme

A

HTN, vein occlusions, optic neuropathies

104
Q

Where is a Dot/Blot heme located?

A

INL, OPL, ONL

105
Q

What are dot/blot hemes associated with?

A

Common with diabetes, and HTN

Associated with venous based congestive disease

106
Q

Where are sub-retinal hemes located

A

Between RPE and Sensory retina

Appear large with lobulated border

107
Q

What are the two types of subretinal hemes

A

Subretinal: above RPE = a red color

Sub RPE = grey/green color

108
Q

What is the common cause of Sub retinal heme

A 
Ruptured CNVM (wet amd)
often visually devastating
109
Q

What is a roth spot

A

Retinal heme surrounding a white center

White center is presumed to be WBCs, CWS, leukemic cell foci or firin

110
Q

What conditions are associated with Roth SPots

A 
Diabetic Retinopathy
Pernicious anemia
Bacterial endocarditis
leukemia
HIB
111
Q

What sizes classifies a macro/micraneurysm

A

Micro:50-100um diam
Macro: 280um diam

112
Q

What are the characteristics of a microaneurysm

A

Originate from inner retinal capillaries /INL
Very small often missed or confused for dot hemees
Hyperfluoresence with FA

113
Q

What conditions are associated with microaneurysms

A

DM, HTN, Blood dyscrasias, leukemias

114
Q

Describe a macroaneurysm

A

Isolated dilation of major artery branch
Secodnary edema, exudates and hemes can occur
usually in females and older 50-80

115
Q

What conditions are commonly associated with Macroaneurysm

A

HTN, arteriosclerosis and retinal emboli

116
Q

What is the management plan for macroaneurysm

A 
Asymptomatic and (-) exudate/hem 6mo follow up
Asymptomatic and (+) exudate/heme 1-3mo follow up
Symptomatic and threatens macula --> retinal consult
117
Q

What are hard exudates

A

Lipid deposits associated with deep retina edema

118
Q

where do exudates typically deposit

A

In the OPL throuought the retina and Henles layer in macula

119
Q

What are exudates associated with

A

Choroidal neovascular membrane
Intra-retinal edema (leaky MA, tlangictastic vessel)
Retinal tumors (coats)

120
Q

What conditions are associated with Hard exudates? How would you manage

A

DM, HTN, Venous occlusive disease, Retinal Mass, Lebers, VHL, COats

consult specialist if within 1-2DD of macula

121
Q

What are cotton wool spots

A

Area of NFL ischemia
white fluffy non-distinct shape
-resolve in 5-7 weeks

122
Q

What are the causes of Cotton Wool spots

A

HTN, DM, Anemia, HIV/AIDS, Carotid artery disease

123
Q

How to Cotton wool spots appear on FANG

A

black

124
Q

Neovascularization is due to retinal ischemia. What can neo cause

A

Retinal edema
Vitreous hemorrhage
Retinal detachment

125
Q

What is Intra-Retinal- Micrvascular Anomalies (IRMA)

A

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

126
Q

what is collateral

A

New BV that give A-A or V-V communication

127
Q

What is a shunt

A

New BV that gives A-V or V-A communication

128
Q

Descrive Congenital Vascular Tortuosity

A

All quadrants
symmetric OU
Can be linked with syndromes

129
Q

Describe Acquired Retinal vascular tortuosity

A

Previously documented normal
Sectoral involvement
Associated thickening and darkening of the BV column
Indicator of hypoxia

130
Q

What is venous beading and what does it indicate

A

Looks like bulging of the vein wall. Result of sludging of venous blood causes venous dilation

Indicates widespread retinal ischemia/hypoxia

131
Q

Describe NA-AION

A

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

132
Q

What are the risk factors for NA-AION

A 
Noctural arterial hypotension--> especially pts on antihypertension medications/topcial BB
DM
Ischemic HEART disease
Renal dialysis
Coronary bypass surgery
133
Q

What systemic meds are associated with NA-AION

A 
ED meds
Amiodorone
Nasal decongestants
Interferon therapy 
oral antihypertensives
134
Q

Define AAION

A

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

135
Q

What vessels are affected in AAION

A

Disease presents as inflammation of the elastic tissue in the medium or large sized arterial walls leading to occlusion

136
Q

What is tested when doing an RBCC

A

number of RBCs x10^6 ml of blood

137
Q

What is tested when doing a hemoglobin test

A

Level of oxygen carrying protein found in the blood in g/dl

138
Q

What is tested when doing a Hematocrit level test

A

Percentage of red cells in whole blood

139
Q

Mean cell volume ?

A

Size of the average RBC in microns

140
Q

Mean cell hemoglobin

A

amount of hemoglobin in picograms

141
Q

mean cell hemoglobin concentration

A

Grams of hemoglobin in dL

142
Q

What is being tested in a white blood cell differential

A 
Percent of the five types of WBCs in blood 
-neutrophils
eosinophils
basophils
lymphocytes
monocytes
143
Q

List the cuases of anemia

A 
Vitamin B12/ Iron deficiencies (pernicious)
Increased destruction of RBCs
Blood Loss
Genetic or acquried defect
Disease (Leukemia)
144
Q

What are the characteristics of Iron deficiency anemia

A

Most common anemia in the US
Deficiency of iron more common in women
Menstrual blood loss
usually due to inadequate intake

145
Q

What findings are associated with poor iron absorption

A

Cold feet, Tiredness, pale skin color, SOB, Typically no retinal changes unless severe
Tx: iron supplements

146
Q

What is the mechanism for Pernicious anemia

A

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

147
Q

What retinal findings are associated with Pernicious anemia

A

crossing changes in AV with nipping

may see black coagulated blood

148
Q

How would you treat pernicious anemia

A

Sublingual or parenteral vitamin supplement

149
Q

Describe hemolytic anemia

A

RBCs are destroyed prematurely body can not replace RBC fast enough

150
Q

What are the causes of hemolytic anemia

A

Infections
Medications
Immune attack (Autoimmune)

151
Q

What is aplastic anemia

A

Bone marrow damage –> inefficiency to make enough RBCs

152
Q

what are some causes of aplastic anemia

A

viral infection
toxic chemicals
radiation
medications

153
Q

What causes temporal atrophy

A

Toxic and Nutritional ON
Autosomal Dominant ON
Lebers Heriditary ON
Optic Neuritis

154
Q

What causes Superior/Inferior Atrophy

A

Ischemic ON

155
Q

What causes band or Bow tie atrophy

A

Chiasm or optic tract

156
Q

What is Papilledema?

A

Disc edema due to raised ICP

157
Q

What is idiopathic intracranial Hypertension?

A

Increased ICP
Normal CSF composition
Not anatomcal abnormality that casues increased ICP

158
Q

What can cause pseudotumor cerebri?

A

Pregnancy, anemia, HTN, Sleep apnea, Hypo or Hyper thyroid

Tetracyclines, corticosteroids, retinoids, lithium

159
Q

what are the sytemic symptoms of IIH or Papilledema

A

Nausea and vomitting
Pulsatile tinnitus
Dizziness

160
Q

What are the visual symptoms of IIH or Papilledema

A

Transient visual obscuractions

Horizontal diplopia

161
Q

what is the 15 year rule for Demyleniating Optic Neuritis

A

In terms of lesions
0 = 25%
1-2 = 50%
3> = 75%

162
Q

What are the indications to begin Glaucoma tx

A 
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
163
Q

What is the conventional (Trabecular) outflow

A

TM–> Schlemms canal–> Collector channels/venous plexi–>Episcleral veins

164
Q

What classes are used to reduce aqueous production

A

Beta-blockers, CAI, Alpha-2 Agonist

165
Q

What classes are used to increase outflow

A

Miotics, adrenergic/alpha-2 agonists, Protaglandings/prostamides, docosanoids

166
Q

What is the only Beta1 selective Topical drop

A

Betaxolol

167
Q

By what amount do Beta blockers decease IOP

A

22-33%

168
Q

By what amount do CAI decrease IOP

A

15-20%

169
Q

What systemic SE should you be concerned about with CAI

A

Sulfa allergies, dyscrasias

CAI are CI in sulfa allergies, sickle cell anemia or other blood dyscrasias and corneal surgery

170
Q

Mechanism of Dipivefrin

A

A pro-drug that is converted to epinephrine
Direct stimulation of both alpha and beta receptors
-Enhances aqueous outflow primarily (uveoscleral pathway)

171
Q

By what percent does dipiverfrin decrease IOP

A

15-20%

172
Q

what is the indication for .5% apraclonidien

A

short-term therapy of patients on maximally tolerated pharmacotherapy sho require additional IOP drop

173
Q

Indication for 1% apraclonidine

A

Reduce incidence an magnitude of IOP spikes after anterior segment laser therapy
can drop up to 40%

174
Q

Characteristics of Latanoprost/Travaprost/Bimatoprost

A

Prostaglandin analog

Reduces IOP by 30-35%

175
Q

What is the mechanism of prostaglandin analogs

A

Increases uveoscleral outflow

Loosens the intercellular spaces on the ciliary body allowing outflow

176
Q

What are the SE of Prostaglandins

A 
Darkening of light or mixed iris
Increased size of lashes
Eyelid darkening
CME
Uveitis or conjunctivitis
Onset of herpes simples
177
Q

When are Prostaglandins CI

A 
Aphakia/pseudophakia
Hx of uveitis 
YAG posterior capsulotomy
hx of herpes simples
cosemetic concerns
178
Q

When are hyperosmotics indicated

A

indicated in cases of acute angle closure glaucoma or other highly elevated glaucoma situations

179
Q

What is the only disc change that is completely diagnostic of glaucomatous damage?

A

progressive thinning of the neural rim

180
Q

At what C/D is the risk of glaucoma increased

A

.6/.6

181
Q

What patterns/combinations of the C/D are highly associated with glaucoma

A

Vertical elongation of C/D

Temporal thinning/unfolding

182
Q

What are the characteristics of a healthy NFL

A

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

183
Q

What is the most obvious NFL defect?

A

Inferior temporal wedge defect and usually corresponds with inferior temporal notching and superior visual field loss

184
Q

What is the total field covered in each eye by a 30-2 and a 24-2

A

30-2: covers 60 degrees total field per eye

24-2: covers 48degrees

185
Q

What is usually the first field defect in glaucoma

A

small areas of depressed sensitivity (relative paracentral scotomas) between 5 and 20 degrees of fixation

186
Q

List 3 other common findings on VF with glaucoma pts

A

Nasal step
Temporal wedge defect
overall gerealized depression of sensitivity

Oc Disease III (1 decks)

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