Glaucoma Classification Flashcards
(186 cards)
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
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
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 ()
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
5
Q
Developmental glaucoma
A
Due to abnormalities in the anterior chamber angle
abnormalities occuring during gestation
- secondary type glaucoma
- chronic
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
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
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
9
Q
What Percent of patients with PDS will develop PG
A
Approx: 35% of PDS individuals eventually go on to manifest pigmentary glaucoma
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
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
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
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
14
Q
What is the classical clinical triad that presents with PDS
A
Krukenberg spindle
Iris transillumination defects
Piment deposition in the TM
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
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)
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
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
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
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)
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
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
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.
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
25
What age group is PXS/PG more common in?
More prevalent in ages 60-80 and is rarely seen before the age of 50.
26
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.
27
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
28
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)
```
29
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
30
What are the 3 identifiable zones on the lens with PXS/PG
Central Translucent disc zone
Intermediate clear zone
Peripheral granular zone
31
What type of Cataract is more prevelant in PXS pts
NS
32
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
33
What is the pigment deposition like in PXS/PXG?
A more spotty distribution and less dense than PDS
34
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
35
Describe neovascular glaucoma
IOP elevation due to angle closure resulting form fibrovascular membrane formation obstructing aqueous outflow--> A result of RETINAL hypoxia/ischemia
36
What are the disorder that predispose a pt to Neovascular Glaucoma
Central Retinal Vein Occlusion, Diabetic Retinopathy and Carotid Artery Dissection
37
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
38
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
39
Describe the late phase of NG
Fibrovascular membrane within the AC contracts producing a peripheral anterior synechia
can progress to 360 angle closure
40
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
41
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
42
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
43
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
44
AACG without pupil block
Plateaue iris configuration
| Last iris roll will be bunched and forced against the TM upon pupil dilation
45
What causes Plateaue Iris
Large or anteriorly positioned ciliary processes
| Accounts for more than 50% of young pts with recurrent angle closure
46
AACG due to phacomorphic glaucoma
Due to lens swelling leading to shallower AC
47
Malignant glaucoma AACG
posterior misdirection of the aqueous into the vitreous
48
Rod associated signs and Symptoms with HRD
```
Loss of night vision
peripheral field loss
ERG: Scotopic loss
acuity and color vision affected late
photosensitivity
```
49
Cone associated signs and symptoms with HRD
```
Decreased acuity
central scotoma
ERG: Photopic loss
color vision affected
photosensitivity
```
50
What are the peripheral rod diseases we covered
Retinitis pimentosa family: Lebers congenital amaurosis
CSNB
Oguchis
51
What are the central cone diseases we covered
Achromatopsia
cone dystrophy
Juvenile Macular dystrophies: Stargardts, Bests
52
Retinitis Pigmentosa
most common hereditary retinal dystrophy
Involves rhodopsin gene
Initially affects the rods and then with progrssion the cones are affected
53
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
54
Descrive autosomal dominant RP
Least severe form with central vision intact until 40s or 50s
55
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
56
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
57
What is the initial ERG show in RP
Scotopic ERG will usually be abnormal before retinal signs are present
58
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
59
What is sector RP
Inferior quadrants only
60
Ushers syndrome
congenital sensori-neural hearing loss and RP
| accounts for 50% of deaf-blind individuals
61
What can you do to manage/treat RP
Short wavelength blocking tints: red, orange, amber
Oral 9-cis B Carotene
Omega-3 rich diet
62
Describe Leber's Congenital Amaurosis
Similar to RP except early onset
| Think a visually unresponsive baby with nystagmus
63
In LCA what do you expect in the ERG
Severely diminished or absent rod and cone response
| Need to be sedated for ERG
64
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
65
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
66
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
```
67
Define oguchis Disease
Variant of CSNB in Japenese
| -Yellow-gray retina color reversed by 2-3hrs of dark adaptation
68
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
69
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
70
Define Fundus Flavimaculatus
variant of stargardts
pisciform lesions are primary presentation
macualr disease and acutiy loss develops later in 40-50s
71
Define Vitelliform Dystrophy (Bests Disease)
AD inherited
Begins early childhood
central retinal dystrophy
72
Previtellifrom stage
abnormal EOG
73
Bitellifrom Stage
Yellow spots coalesce into Egg Yold macula appearance
| -VA still near normal
74
Pseudohypopyon stage
lesion Partially reabsorb
75
Vitelliruptive stage
lesion breaks up into scrambled egg
| VA drops to 20/200
76
How would you treat Best
anti-VEGF
77
What are the 2 forms of Achromatopsia
Rod monochromatism = AR
| Blue Cone Monochromatism = x-linked
78
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
```
79
What tint would you give to someone with Achromotopsia
Red tint is best for achrmomat
| Magenta is best for blue-cone achromat
80
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
81
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
82
What causes albinism
varying degrees of amelanosis due to deficiency of tyrosinase or other player in melanin biosynthesis
83
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
```
84
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
85
Define the arterial phase
10-15sec after injection central retinal artery begins to fill
arteries are bright, veins are dark
86
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
87
Define the venous phase
early venous phase: Laminar flow of veins, arteries still bright
Venous phase:veins and arteries fully bright
88
Late phase
10min post injection
arteries and veins almost empty
choroidal flush is at its minimum
leakage of dye remains in tissue
89
What causes hypfluorescence
Filling defect
| blocking defect
90
What causes hyperfluorescence
```
autofluorescence(drusen)
Psuedofluorescence(sclera showing)
Transmission or window defect (scar)
Leakage (neovascular vessel)
Pooling (sub-retinal leakage)
Staining (ONH)
```
91
what creates shadowing in OCT
blood vessels as the block and absorb light
92
What creates hyper-reflectivity in OCT
Excess blood, drusen, or exudates
93
What creates hypo-relfectivity in OCT
other fluids: plasma, vitreous, water
94
where would you see fluid pockets in CME
Between inner plexiform layer (IPL) and the outer nuclear layer (ONL)
95
what is the most common cause of serous detachment
Choroidal neovascular membrane (CNVM)
96
Define a Retrovitreal hemorrhage
Bright red blood behind vitreous, shifts readily with eye movement
97
What is an intravitreal hemorrhage
varied appearance within vitreous, clots quickly, settles in lacunae.
98
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
```
99
How do you manage a intravitreal hemorrhage
Determine cause and refer to retinal specialist
Resting with head 30-45deg elevated
antiplatelet tx
100
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
101
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
102
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
```
103
What are some causes of a flame heme
HTN, vein occlusions, optic neuropathies
104
Where is a Dot/Blot heme located?
INL, OPL, ONL
105
What are dot/blot hemes associated with?
Common with diabetes, and HTN
| Associated with venous based congestive disease
106
Where are sub-retinal hemes located
Between RPE and Sensory retina
| Appear large with lobulated border
107
What are the two types of subretinal hemes
Subretinal: above RPE = a red color
| Sub RPE = grey/green color
108
What is the common cause of Sub retinal heme
```
Ruptured CNVM (wet amd)
often visually devastating
```
109
What is a roth spot
Retinal heme surrounding a white center
| White center is presumed to be WBCs, CWS, leukemic cell foci or firin
110
What conditions are associated with Roth SPots
```
Diabetic Retinopathy
Pernicious anemia
Bacterial endocarditis
leukemia
HIB
```
111
What sizes classifies a macro/micraneurysm
Micro:50-100um diam
Macro: 280um diam
112
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
113
What conditions are associated with microaneurysms
DM, HTN, Blood dyscrasias, leukemias
114
Describe a macroaneurysm
Isolated dilation of major artery branch
Secodnary edema, exudates and hemes can occur
usually in females and older 50-80
115
What conditions are commonly associated with Macroaneurysm
HTN, arteriosclerosis and retinal emboli
116
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
```
117
What are hard exudates
Lipid deposits associated with deep retina edema
118
where do exudates typically deposit
In the OPL throuought the retina and Henles layer in macula
119
What are exudates associated with
Choroidal neovascular membrane
Intra-retinal edema (leaky MA, tlangictastic vessel)
Retinal tumors (coats)
120
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
121
What are cotton wool spots
Area of NFL ischemia
white fluffy non-distinct shape
-resolve in 5-7 weeks
122
What are the causes of Cotton Wool spots
HTN, DM, Anemia, HIV/AIDS, Carotid artery disease
123
How to Cotton wool spots appear on FANG
black
124
Neovascularization is due to retinal ischemia. What can neo cause
Retinal edema
Vitreous hemorrhage
Retinal detachment
125
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
126
what is collateral
New BV that give A-A or V-V communication
127
What is a shunt
New BV that gives A-V or V-A communication
128
Descrive Congenital Vascular Tortuosity
All quadrants
symmetric OU
Can be linked with syndromes
129
Describe Acquired Retinal vascular tortuosity
Previously documented normal
Sectoral involvement
Associated thickening and darkening of the BV column
Indicator of hypoxia
130
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
131
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
132
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
```
133
What systemic meds are associated with NA-AION
```
ED meds
Amiodorone
Nasal decongestants
Interferon therapy
oral antihypertensives
```
134
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
135
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
136
What is tested when doing an RBCC
number of RBCs x10^6 ml of blood
137
What is tested when doing a hemoglobin test
Level of oxygen carrying protein found in the blood in g/dl
138
What is tested when doing a Hematocrit level test
Percentage of red cells in whole blood
139
Mean cell volume ?
Size of the average RBC in microns
140
Mean cell hemoglobin
amount of hemoglobin in picograms
141
mean cell hemoglobin concentration
Grams of hemoglobin in dL
142
What is being tested in a white blood cell differential
```
Percent of the five types of WBCs in blood
-neutrophils
eosinophils
basophils
lymphocytes
monocytes
```
143
List the cuases of anemia
```
Vitamin B12/ Iron deficiencies (pernicious)
Increased destruction of RBCs
Blood Loss
Genetic or acquried defect
Disease (Leukemia)
```
144
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
145
What findings are associated with poor iron absorption
Cold feet, Tiredness, pale skin color, SOB, Typically no retinal changes unless severe
Tx: iron supplements
146
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
147
What retinal findings are associated with Pernicious anemia
crossing changes in AV with nipping
| may see black coagulated blood
148
How would you treat pernicious anemia
Sublingual or parenteral vitamin supplement
149
Describe hemolytic anemia
RBCs are destroyed prematurely body can not replace RBC fast enough
150
What are the causes of hemolytic anemia
Infections
Medications
Immune attack (Autoimmune)
151
What is aplastic anemia
Bone marrow damage --> inefficiency to make enough RBCs
152
what are some causes of aplastic anemia
viral infection
toxic chemicals
radiation
medications
153
What causes temporal atrophy
Toxic and Nutritional ON
Autosomal Dominant ON
Lebers Heriditary ON
Optic Neuritis
154
What causes Superior/Inferior Atrophy
Ischemic ON
155
What causes band or Bow tie atrophy
Chiasm or optic tract
156
What is Papilledema?
Disc edema due to raised ICP
157
What is idiopathic intracranial Hypertension?
Increased ICP
Normal CSF composition
Not anatomcal abnormality that casues increased ICP
158
What can cause pseudotumor cerebri?
Pregnancy, anemia, HTN, Sleep apnea, Hypo or Hyper thyroid
| Tetracyclines, corticosteroids, retinoids, lithium
159
what are the sytemic symptoms of IIH or Papilledema
Nausea and vomitting
Pulsatile tinnitus
Dizziness
160
What are the visual symptoms of IIH or Papilledema
Transient visual obscuractions
| Horizontal diplopia
161
what is the 15 year rule for Demyleniating Optic Neuritis
In terms of lesions
0 = 25%
1-2 = 50%
3> = 75%
162
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
```
163
What is the conventional (Trabecular) outflow
TM--> Schlemms canal--> Collector channels/venous plexi-->Episcleral veins
164
What classes are used to reduce aqueous production
Beta-blockers, CAI, Alpha-2 Agonist
165
What classes are used to increase outflow
Miotics, adrenergic/alpha-2 agonists, Protaglandings/prostamides, docosanoids
166
What is the only Beta1 selective Topical drop
Betaxolol
167
By what amount do Beta blockers decease IOP
22-33%
168
By what amount do CAI decrease IOP
15-20%
169
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
170
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)
171
By what percent does dipiverfrin decrease IOP
15-20%
172
what is the indication for .5% apraclonidien
short-term therapy of patients on maximally tolerated pharmacotherapy sho require additional IOP drop
173
Indication for 1% apraclonidine
Reduce incidence an magnitude of IOP spikes after anterior segment laser therapy
can drop up to 40%
174
Characteristics of Latanoprost/Travaprost/Bimatoprost
Prostaglandin analog
| Reduces IOP by 30-35%
175
What is the mechanism of prostaglandin analogs
Increases uveoscleral outflow
| Loosens the intercellular spaces on the ciliary body allowing outflow
176
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
```
177
When are Prostaglandins CI
```
Aphakia/pseudophakia
Hx of uveitis
YAG posterior capsulotomy
hx of herpes simples
cosemetic concerns
```
178
When are hyperosmotics indicated
indicated in cases of acute angle closure glaucoma or other highly elevated glaucoma situations
179
What is the only disc change that is completely diagnostic of glaucomatous damage?
progressive thinning of the neural rim
180
At what C/D is the risk of glaucoma increased
.6/.6
181
What patterns/combinations of the C/D are highly associated with glaucoma
Vertical elongation of C/D
| Temporal thinning/unfolding
182
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
183
What is the most obvious NFL defect?
Inferior temporal wedge defect and usually corresponds with inferior temporal notching and superior visual field loss
184
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
185
What is usually the first field defect in glaucoma
small areas of depressed sensitivity (relative paracentral scotomas) between 5 and 20 degrees of fixation
186
List 3 other common findings on VF with glaucoma pts
Nasal step
Temporal wedge defect
overall gerealized depression of sensitivity
