Exam 1 Flashcards
(172 cards)
1
Q
What does OCT look at?
A
- Retinal nerve fiber layer (RNFL)
- Optic nerve head
-Looks for a loss of tissue
2
Q
Thinning on OCT
A
- Inferior thinning corresponds with a superior defect
- thinning will be red
3
Q
What test looks at macular region?
A
Ganglion cell Analysis (GCA)
4
Q
Visual field combined report
A
- Combines VF and OCT so you can correlate and compare
- if the info conflicts with each other, less sure of the diagnosis
- allows for comparison of structural dmg to fxnal loss
5
Q
What determines the stage of glaucoma a patient has?
A
- VF loss
- how close it is to fixation
6
Q
What is the coding system for the stages of glaucoma?
A
-VF ONLY
7
Q
Better term for glaucoma suspect
A
open angle with borderline findings
8
Q
Glaucoma and patient education
A
- educate but don’t overwhelm at first visit.
- interaction is patient dependent
- the disease is life long and can never go away. Will need treatment for the rest of their life
9
Q
History of Glaucoma diagnosis
A
- pre 1980s –> elevated IOP meant glaucoma
- 1980s to mid 1990s –> elevated IOP with VF defect meant glaucoma
- Mid 1990s to present –> glaucomatous optic disc AND RNFL loss with/without VF defect means glaucoma (IOP is NOT included in the definition anymore)
10
Q
Why do you not have to have a VF defect to have glaucoma
A
-VF defects are not always present at the beginning stages of the defect
11
Q
structure vs. function
A
Function: -visual fields/perimetry -functionally assesses patient's vision Structure: -OCT devices scan structure and anatomy (RNFL, ONH, etc)
12
Q
cupping
A
- implies loss of tissue to neuroretinal rim (made up of retinal ganglion cell axons)
- cup enlarges due to the loss of tissue (the loss of tissue is what impairs vision)
13
Q
VF in glaucoma
A
- key baseline work-up/evaluation of someone suspected to have glaucoma
- used regularly and repeatedly to monitor change over time
- needed to assess what is a true glaucomatous defect
14
Q
What comes first: structural damage or functional loss?
A
- USUALLY structural: RNFL injury observed up to 6 years before VF defects
- eyes with mild VF loss have already lost many axons (the most mild VF loss associated with 10-50% axon loss
15
Q
What is used to identify functional loss?
A
- Standard automated perimetry (SAP)
- Short wave automated perimetry (SWAP)
- Frequency doubling perimetry (FDP)
16
Q
Standard automated perimetry
A
SAP
-white on white perimetry (ie Humphrey Visual field)
17
Q
Short wave automated perimetry (SWAP)
A
- no longer used
- blue light on yellow backgroun
18
Q
frequency doubling perimetry
A
FDP
-screen VF
19
Q
Normal vs early vs advanced glaucoma optic nerve
A
early
- enlargement of cup due to loss of tissue
- changes to lamina cribrosa
advanced
- severe excavation and loss of tissue
- loss of GC axons leading to VF loss, blindness and functional impairment of patient’s vision
20
Q
Structural damage and the progression to functional vision loss
A
Undectable 1. Normal 2. acceleration of apoptosis 3. ganglion cell death/axon loss 4. RNFL change (undectable ) Asymptomatic 5. RNFL change (detectable) 6. short wavelength automated perimetry VF changes
Functional Impairment
- Standard automated perimetry VF change
- VF change (moderate)
- VF change (severe)
- Blindness
21
Q
Glaucoma risk factors
A
- IOP
- C/D ratio
- CCT
- Age
22
Q
POAG prevalence in the US 40 years and older
A
about 2%
Overall affects 2.22 million people (half are undiagnosed)
23
Q
glaucoma and diagnosis
A
- we can treat glc in every state
- it is our legal responsibility
- if we miss a diagnosis, we can get sued
24
Q
Glc definition
A
Glaucoma is a FAMILY of diseases in which an optic neuropathy develops that is manifested by the death of ganglion cell axons, which results in excavation of the optic nerve head
This damage causes characteristics nerve fiber bundle defects which lead to visual field loss and other abnormalities of visual function.
more common among those persons with elevated intraocular pressure, however a significant number of individuals will develop the same type of neuropathy with consistently normal intraocular pressures
25
What to emphasize when explaining glc
- primarily a disease of the optic nerve (blindness results from nerve damage and not necessarily from elevated IOP
- appearance and function of the optic nerve are the main factors in managing any patient with glc
- **Any IOP can be misleading**
26
Glc classification
- Primary
- Secondary
- Developmental
27
Primary glc
- open angle
- Primary open angle glc (POAG)
- normal tension glc (NTG)
- closed angle
- Primary Angle closure glc (PACG)
- acute angle closure (AAC)
28
Secondary glc
-increased intraocular pressure and glaucomatous changes which are a direct result of some other ocular or systemic abnormality
Types:
-open angle
-closed angle
29
Developmental glc
primary
secondary
less common than the others
30
Primary Open Angle Glaucoma
POAG
| -patient has been examined and secondary glc mechanisms have been ruled out (ie narrow angles or angle recession)
31
Secondary open angle glaucoma
```
pigmentary
exfoliation
uveitic
angle recession
etc
```
32
Secondary closed angle glaucoma
```
neovascular
uveitic
subluxed lens
iridocorneal endothelial syndrome (ICE)
ocular tumors
etc
```
33
Types of developmental glaucoma
```
congenital glc
juvenile open angle glc
aniridia
axenfeld-reiger syndrome
Marfan's Syndrome
Microcornea
micropthalmus
Sturge-Weber syndrome
Peter's anomaly
neurofibromatosis
```
34
Requirements for diagnosing POAG
1. GLAUCOMATOUS damage to the optic nerve head
AND/OR
2. GLAUCOMATOUS visual field defects
WITH
3. elevated IOP (>21 mm Hg) with open angles and normal anterior segment (no secondary mechanisms)
35
What is considered an elevated IOP for POAG
>21 mm Hg
36
Ocular hypertension
OHTN
IOP repeatedly over 21 mm Hg
AND
NO glaucomatous changes to the optic nerve head/nerve fiber layer/visual field
37
OHTN patients that develop glc
- 0.3 to 10% with OHTN will develop glc
- 1 to 2% with OHTN convert per year
- 90% with OHTN never develop glc
38
OHTN key risk factor
pachymetry (ie thickness of the cornea)
39
Normal Tension Glaucoma
NTG
AKA low tensioon glc
-neuropathy and VF loss develops in the absence of IOP greater than 21 mm Hg
-usually caused by poor blood flow that doesn't serve the needs of ganglion cell axons
40
Diagnosis of NTG
- used to be diagnosis of exclusion
| - now the disease is more common
41
NTG treatment
- Still a significant challenge
| - still lower IOPs (has been proven to be helpful by slowing progression, but it is more difficult)
42
Glaucoma Suspect
-findings suspicious for glc without definitive damage
43
Glaucoma suspect HVF or RNFL OCT
- not enough to be definitively glc, but enough to be suspicious
- falls into a gray area
44
Glaucoma suspect ONH
- one of the main triggers for labeling and diagnosing as suspect
- large C/D
45
Glaucoma suspect family history
-patient may be normal but due to strong family history may be labeled as glaucoma suspect
46
Glaucoma suspect IOP
-elevated WITH additional suspicious findings
47
Glaucoma suspect based on ONH cupping
- healthy ONH with physiologically large C/D ratio often corresponding with a larger ONH size
- large C/D ratio may be a normal variation for a pt
- Normal IOP
- Order VF or RNFL OCT
- monitor patient over time if there is still a risk for disease
48
Physiologic Cupping
- healthy ONH
- Physiologic C/D ratio
- not considered at risk
- noted in posterior exam findings, not specifically assess in assessment and plan
- can be genetic
- large discs have large cups
49
POAG/NTG characteristics
- bilateral but often asymmetric (not same level of disease in each eye)
- chronic; doesn't go away, not curable
- slowly progressing (usually)
- ONH cupping (excavation and loss of ON tissue
- GLAUCOMATOUS RNFL and VF loss
50
What percent of people in the US are undiagnosed and unaware of condition
50%
51
Glaucoma as cause of blindness
```
2nd leading cause world wide
#1 cause of vision loss in African Americans
```
52
Worldwide glaucoma stats
- 65 million people affected
- 44 million with open-angle
- 21 million with angle-closure
- 10 million bilaterally blind (10% of the open angle patients; 25% of the angle closure patients)
53
Rotterdam Study
determined that family history alone cannot account for the observed proportion of the disease suggesting that non-genetic factors play a significant role in overall occurrence of glc
-the lifetime absolute risk of glc at age 80 is almost 10x higher in patients having relatives with glc
54
Diabetes as a risk factor for glc
about 1.35x greater risk
- not the strongest risk factor we look at
- only considered a MODEST risk factor compared to family history and CCT
55
Studies that look at diabetes and glc
Beaver Dam Eye Study
Blue Mountain Eye Study
Nurses' health study
Los Angeles Latino Eye Study
-does not provide a definitive link between DM and POAG
-vascular dysregulation has a component in glc but is likely NOT a sole, initiating cause of glc
56
Systemic blood pressure
- controversial
- no associations in several studies
- HTN may be protective (more blood to optic nerve helps protect retinal ganglion cells)
- HypoTN is a factor in ocular perfusion pressure (less blood flow, more damaging)
57
Strongest risk factor correlation to glc
IOP
- higher pressure means greater risk
- BUT most patients with IOP>21 mmHg will not develop glc
58
True/False: Increased C/D ratio is a definitive risk for glc
FALSE
| not definitive
59
Optic disc parameters
- C/D ratio
- NFL integrity
- Neural retinal rim
* asymmetry is an important feature
60
Expected C/D ratios from vertical height of discs
```
Height (mm)-->Expected C/D
2.4-->0.8
2.2-->0.6
2.0-->0.4
1.8-->0.2
1.6-->0.0
for ever .2 the height drops, the C/D drops by .2
```
61
Refractive error and glc
- myopia 2x more common amoung POAG patients (may be selection bias since myopes seek eye exams more than hyperopes or emmetropes)
- very high myopes (> -14 D) are definitely at high risk
62
Pachymetry
- measures CCT
- Thinner corneas increase risk of developing glc from OHTN
- Thinner cornea indicates higher true GAT on average
- POSSIBLE anatomic weakness in the ONH or laminar region (not proven)
63
Which combo of ONH size and C/D ratio is the most concerning?
a. 1.8 mm / 0.3 C/D
b. 1.9 mm / 0.7 C/D
c. 2.2 mm / 0.6 C/D
d. 2.4 mm / 0.8 C/D
B.
| smaller disc size with a large cup
64
Global Risk Assessment
- Estimates patient's overall risk for onset and progression based on MULTIPLE rather than single risk factors
- Ideally based on evidence from well controlled clinical trials and long term studies
- Used for many diseases other than glc
- helps guide treatment
65
Global Risk Calculator for OHTN
- identifies the global risk of developing glc in the next 5 years (so it must be repeated)
- identify who will benefit from treatment
- calculator is accurate and has been validated
- answer is given at the bottom in a %
```
Factors:
untreated IOP (3 from dif visit)
CCT
Vertical C/D
Pattern SD (HVF)
```
66
What percentage of VF defects go away after 3 tests?
85%
| early stage VF defects are not permanent
67
aqueous humor production
in the pigmented epithelium of the CB iris processes via Na/K/Cl symport. Relies on carbonic anhydrase
-CB stroma has a net + charge
68
Aqueous humor flow
- CB processes
- posterior chamber
- iris and lens
- through pupil
- anterior chamber
- Exit via Trabecular or uveoscleral outflow
69
Trabecular outflow
Pressure dependent
80% of outflow
Route
- TM
- Schlemm's canal
- intrascleral collector channels
- episcleral veins
70
Uveoscleral outflow
outflow independent of IOP
20% of outflow
Route
- iris root
- between CB muscle bundles
- suprachoroidal space
- venous circulation
CB contraction/relaxation will affect uveoscleral outflow
71
outflow vocab
resistance is opposition
| facility is ease
72
Resistance to outflow
- outflow becomes more difficult with age (lose endothelial cells in TM, can't form giant vacuoles in schlemm's)
- high IOP glc is usually due to poor outflow not too much production
73
Major players in resistance outflow
TM
Schlemm's canal
episcleral veins
aqueous humor
74
Trabecular meshwork
single layer of phagocytic endothelial cells that clean up obstructive debris
75
Primary site of outflow resistance
-juxtacanalicular meshwork: ECM with proteoglycans, GAGs, MMPs
76
Schlemm's Canal
- has giant vacuoles
- receives bulk of aqueous flow
- flow here is pressure dependent
- drains into episcleral veins
77
episcleral veins
- receive aqueous from Schlemm's
| - pressure here can increase via laying on back or increasing thoracic pressure
78
Normal IOP
-defined as pressure which does not lead to optic nerve damage
79
Average IOP
- 15.4 mm Hg +/- 2.5 SD
| - upper limit is 21 mm Hg
80
Paradox of IOP
- 90% of patients with elevated IOP do not develop glc
| - 30 to 50% of patients with glc DO NOT have IOP over 21 mm Hg
81
Characteristics of IOP
- increases slightly with age
- higher in women
- symmetrical between eyes (within 2 to 4 mm Hg)
- asymmetry can mean a disease or angle pathology, so do gonio
- has diurnal fluctuations
82
Factors that increase IOP
- external pressure on eye
- Steroids (topical and oral)
- increased episcleral venous pressure (i.e. more fluid behind the eye means less drainage)
83
Factors that decrease IOP
- exercise
- acute (early stage) uveitis
- retinal detachment
- alcohol and marijuana (not that well - patient would have to be high the entire day)
84
YOGA and IOP
2x increase in IOP when in a headstand
- study did not show high prevalence of OHTN
- still, advise glc pts to not do headstand
85
CCT and IOP
-thicker cornea does not alter IOP, just impacts measurements
86
24 hour rhythm of aqueous flow and formation
Time/Rate/Volume/% day total
6 AM to 12 PM/3.0/1087/33%
12 to 10/2.7/1602/50%
10 to 6AM/1.2/585/17%
shows reduction of aqueous humor production at night, but thats when IOP is theoretically the highest
87
Sleep studies and IOP
- **showed highest IOP spike while sleeping and supine (likely due to decreased drainage)
- measured during sleep with pneumatonometer that does not require anesthetic - patients remained asleep
- largest peak around 4 to 6 AM
- higher IOP in AM than PM
- glc patients have higher nightime spike
- older and younger healthy pt have similar spikes
88
Serial tonometry
Patient comes into office in the morning and you measure IOP every 30 minutes for a few hours
89
Sensimed Triggerfish
- FDA approved as of this month
- doesn't measure pressure - measures change in shape of cornea and graphs it
- extrapolating that when the cornea changes shape, IOP is changing as well
- allows for continuous IOP monitoring
90
beta antagonists MOA
inhibit aqueous production
day time
minimal nocturnal effect
91
prostaglandins MOA
increase outflow
92
CAI MOA
inhibit aqueous production
93
alpha agonist
inhibit aqueous production
| increase outflow
94
drugs affect on diurnal IOP
- beta blocker (timolol) not as effective at night as PG (latanaprost)
- alpha agonist (brimonidine) not effective at night
95
add-on efficacy
- latanaprost with:
- timolo: helps during the day not at night
- azopt: helps during the day and at night
96
Summary:
• IOP fluctuates throughout the day
• IOP is usually highest in the overnight hours
• A single measurement of IOP during office hours is truly insufficient for glaucoma management
• The diagnosis and treatment of glaucoma should include measurement of IOP at various times throughout the day/night, if possible
o Ex. patients shouldn’t only come for appointments during lunch hour
• Consider the effectiveness of anti-glaucoma medications lowering 24-hour IOP
• The optimal way to estimate 24-hour IOP peak to enhance diagnosis and treatment of glaucoma is not known
asdg
97
How to measure CCT
- pachymetry
| - take 3 readings on central cornea and record the average
98
thinner corneas and IOP
lead to lower Goldmann readings (NEVER adjust the reading you get)
99
Ocular Hypertension Treatment Study
OHTS
- the ONLY rock solid evidence that lowering IOP reduces the risk of developing POAG
- prior to this it was assumed all OHTN pts should be treated even without glaucomatous changes
100
OHTS Objective
To determine whether topical hypotensive medication can delay or prevent the onset of POAG in patients with ocular hypertension and assess the safety of topical hypotensive medication.
101
OHTS methods
```
5 year
longitudinal
multicenter
radomized
controlled
```
1636 patients
102
OHTS patients
1636 pts
- IOP from 24 to 32 mm Hg in one eye and 21 to 32 mm Hg in the other
- NO glaucomatous damage
- randomized into control or treatment group
Target IOP: less than or equal to 24 mm Hg or 20% reduction in IOP from baseline
103
OHTS Results
reduce risk of OHTN pts from developing glc at 5 years by 50%
104
OHTS and CCT
For ALL IOPs, a thinner cornea increased the risk of developing glc at 5 years
Thin cornea
-588 is low risk
105
The Big Four Risk factors
Age
IOP
VERTICAL C/D
CCT
106
OHTS and the big four risk factors
Age: 20-40% increase per decade (older=more risk)
IOP: >26 mm Hg (higher=more risk)
Vertical C/D: >0.5 (larger=more risk)
CCT:
107
OHTS Results and Conclusions
- pts with elevated IOP, hypotensive treatment was effective in delaying the probability of onset of POAG
- for patients with a MODERATE TO HIGH risk of developing POAG, IOP lowering treatment should be considered
- borderline pts should still be considered
108
Risk calculator recommendations
15%: treatment recommended
109
How much does an increase in IOP increase your risk?
1 mm Hg increase above 22 increases risk by 10%
110
Early Manifest Glaucoma Triel (EMGT)
every 1 mm Hg of Iop reduction lowers risk of progression by 10%
111
Advanced Glaucoma Intervention Trial (AGIS)
IOP always under 18 mm Hg has a lower risk of progression
112
Collaborative Normal-Tension Glaucoma Study
30% reduction of IOP reduces risk of progression
113
Clicker: What is a normal IOP
A pressure which does not lead to optic nerve damage
114
Ocular Perfusion Pressure
OPP
- new risk factor for glc
- Defined as: the differential between arterial BP and IOP
- regulated to maintain constant blood flow to the optic nerve despite fluctuating blood pressure and IOP
- can have low OPP without glc
115
Cause of abnormal OPP
secondary to vascular dysregulation in susceptible patients resulting from abnormal/insufficient auto-regulation
116
OPP Formula
OPP = BP - IOP
BP is mean arterial pressure, diastolic pressure or systolic pressure
can be low but still have a normal autoregulation
117
Ocular hemodynamics
-normal blood flow despite fluctuations in blood pressure
118
Diastolic Perfusion Pressure
DOPP = DBP - IOP
use their lowest diastolic BP and highest IOP
119
Systolic Perfusion Pressure
SOPP = SBP - IOP
120
Mean Perfusion Pressure
MOPP = 2/3(mean arterial pressure) - IOP
121
Baltimore Eye Survey
AA and whites
| -6x excess of POAG with lowest category of OPP
122
Egna-Numarkt Study
Caucasians
| -lower DOPP associated with increase in freq of POAG
123
Barbados 4 year eye study
black Caribbeans
| -4 year risk in developing glc increased dramatically at lower OPP
124
Proyecto Ver
Hispanic
- lower DOPP associated with increase in OPP
- looks at patients who already have POAG to see what their DOPP is (rather than predicting if they will get it)
- at 50 mm Hg you see an increase in slope of the graph
125
POAG Risk Factors for Barbados Eye Study
1=increased risk
the further the black bar is to the right on the graph the higher the risk
126
Los Angeles Latino Eye Study (LALES)
cross-sectional study of 6357 latinos older than 40 in LA
-patients with low DOPP and SOPP had higher risk of POAG
***DOPP
127
Why is IOP of limited clinical use
- research uses lowest OPP (nocturnal BP and IOP used)
| - clinically we see patient during the day sitting so research doesn't translate too great
128
Clinical control of OPP
- lower IOP improves OPP
| - measure BP on all pts even if not dilating to identify potential risk factors (higher BP imporves OPP)
129
Nocturnal BP and OPP
- BP decreases 15% in normal pts, 50% in HTN pts
- lower BP at night with higher IOP at night can significantly compromise OPP
Treatment options
- Adjust BP meds (use in AM to minimize nocturnal hypoTN)
- Use IOP lowering meds that lower IOP while sleeping (but avoid IOP meds that can lower systemic BP at night like beta blockers or alpha agonists)
- potentially sleep with head elevated
130
Your pt with POAG is still progressing despite low IOP measured in office. Which med can you add to latanoprost OU. assuming no contraindications?
a. timolol QAM OU
b. alphagan P BID OU
c. Combigan BID OU
d. dorzolamide BID OU
D. dorzolamide
131
CSF and glc
correlation between CSF and glc risk
| -specifically looks at translaminar pressure
132
Translaminar pressure
TLP=IOP-CSFp
- pressure differential between intracranial CSF and pressure which surrounds the optic nerve and IOP (Intracranial pushes forward when IOP pushes backward and TP is the difference between the two)
- CSF around optic nerve is in the optic nerve subarachnoid space (ONSAS)
133
CSF pressure vs. translaminar pressure
```
CSF is a value like IOP
Translaminar pressure (TLP) is a differential
```
134
TLP risk factor
increase in pressure differential increases risk
i.e. decrease CSFp or increase IOP
This might explain why people with normal IOPs can have nerve damage
135
TLP clinical limitations
- cannot measure CSF easily (lumbar puncture)
- lumbar CSF pressure may not equate to ONSAS CSF pressure
- currently CSFp is not modifiable (we cannot increase a low CSFp)
136
Why can a patient progress if their IOPs are normal
unidentified IOP fluctuation (diurnal) + increase nocturnal IOP + low nocturnal BP = low DOPP
137
Causes of glaucomatous damage to the ONH
- Elevated IOP
- causing mexhanical force which compresses the ganglion cell axons (GCA)
- Anatomic weakening of lamina cribrosa
- results in less physical support of GCA
- Ischemia, hypoxia
- due to poor OPP
- Neurotoxic processes (excitotoxins leading to apoptosis) AKA trophic support failure
138
What are the signs of glaucomatous damage to ONH
1. axonal necrosis leading to cupping
2. loss of supporting glial tissue
3. deep excavation within the ONH (called cupping) - some can remain shallow
4. disc pallor and atrophy (looks pale due to loss of tissue) - paired with cupping
- light reflecting off of lamina cribrosa has a whiter appearance
139
Process of ganglion cell death
- pressure kills axons
- dying axons release toxic glutamate
- glutamate acts on surrounding axons causing a cascade of events to occur
- causes loss of thousands of axons leading to visible change in ONH
140
Nasal Step
-defect stepping on the horizontal midline in the nasal field
141
Superior arcuate defect
- almost all sup VF is gone
142
Superior nasal step defect
- a portion of the nasal field is missing towards the periphery, close to the horizontal midline
143
How to identify which eye is on a VF
-the blind spot is on the right means a right eye
144
Nerve Fiber layer drop out: focal
can see dark arcs of where the RNFL has died
| a focal change is easier to see
145
Diffuse loss of RNFL
- move past focal stage and become progressive
- visual field loss across the entire VF
- very thin rim
146
Lamina Cribosa
- superior and inferior regions have larger pores
- these larger ones provide less physical support and allow greater damage to RGC axons due to mechanical deflection of the axons
147
blood supply relating to OPP
- SPCA
- Circle of Zinn-Haller
- CRA supplies disc and RNFL
148
Axonal transport
- energy dependent requiring oxygen and glucose from normal blood flow
- blood must flow to the entire length of the axon
- disruption of axonal transport can be due to low OPP or high IOP (IOP will compresses the microtubules in the axon stopping transport
149
Pathogenesis of ONH excavation and cupping
- damage occurs at lamina cribrosa
- primarily involves superior and inferior
- loss of axonal tissue results in excavation of optic nerve
- dmg often begins within the cup
150
Mechanical Force theory
-misalignment of lamina cribrosa or movement and displacement of GCA bundles causes blocking of axonal transport
151
Lamina deformation
-if we learn to measure it we can see which pts have greater deformation that could lead to cupping
152
Vascular theory
- ischemia lowers axonal transport rate
| - can be reduced or initiated by mechanical constriction
153
Generality of cup depth and glc
-deeper cupping (can see more laminar dots) is more suggestive of glc but not always (myopes tend to have deeper cups)
154
Optic disc size variations
- blacks have larger than whites
| - hyperopic disc smaller, myopic larger (outside of range from +5 to -5 D)
155
Normal optic disc size
- 2.1 mm diameter vertical
| - 2.8 mm diameter horizontal
156
Grouping Glacomatous Disc Appearances
- Focal: polar notching
- Myopic: tilted insertion with temporal crescents
- Senile sclerotic disc: shallow, sloping cup with PPA (not used much anymore)
- generalized enlargement: uniform enlargement of cup or thinning of NRR
157
Myopic Glaucomatous Optic Disc
- sloped and tilted contour
- very difficult to evaluate
- Very high myopia has a high risk (>15 D)
- scanning laser tests won't help diagnose but may help diagnose changes
- may rely more heavily on VF testing
158
Senile Sclerotic Disc
- pale, shallow sloping cup with PPA
- age related change to sclera and tissue in ONH
- due to decreased OPP
159
Cup shapes
- normal: funnel shaped
- deep, cylindrical, steep-walled cup
- temporal sloping (VERY COMMON): makes it hard to assess C/D
160
Focal enlargement of discs
- NRR notching
- easier to detect
- early stages
161
Concentric enlargement
diffuse
- even thinning of NRR
- advanced stages
162
Notching
thining of the NRR
| AKA saucerization
163
Staphyloma
degeneration and thinning of scleral tissue around the ONH related to progressive myopic change
- patient can get glc even with normal IOP due to poor blood flow
- OCT are useless
164
Peripapillary Atrophy (PPA)
irregular pigmentation around the ONH
- non-specific (seen in normal eyes) age related change (should not see in young adults)
- should raise suspicion for POAG and NTG (SERVES AS A RED FLAG FOR GLC)
Two zones
165
Alpha zone
outermost zone appearing as irregular peripapillary pigmentation
166
Beta zone
exposed choroidal vessels and sclera
| -found right next to the disc margins and adjacent to alpha zones
167
Normal vs. glc PPA
Normal: alpha zone larger;
Glc: beta zone larger/more frequent; nasal zones more frequent
PPA more frequent in NTG
168
Vascular signs of Glc
-Optic disc (Drance) hemorrhages: on disc margin
AKA splinter hemorrhage
-Baring of circumlinear vessel: vessel is bared or exposed because NRR has receded; rides along inner cup margin (white of cup on both sides of a vessel)
-Bayonetting: very advanced stage change; very sharp bending and turning of vasculature at disc margin
169
Optic disc hemorrhage
Drance
TRANSIENT
-occurs in EARLY stages (before NFL loss, notching or VF loss)
-present means 20x greater risk in progressive VF loss or OHTN esp in females
-More frequent in NTG
-if present, pt is undiagnosed or poorly controlled
170
Nerve Fiber layer evaluation
- use red free filter
- dark slit like defects may be noticed in glc patients
- indicates axonal loss
- THE EARLIEST of all objective signs, but only detectable with experience and optimal conditions
- NOT a common clinical technique
171
Diffuse Retinal NFL defects
- most common of NFL defects
- most difficult to identify
- compare S/I and R/L striations
- look for raked appearance/loss of brightness
172
Wedge Retinal NFL defects
- territorial loss of NFL
| - easiest to identify, but least common
