Classification of Findings Flashcards

Question 1

Q

Size and shape

Answer

A

2.1mm2 and 2.8mm2 with a range The average vertical disc diameter is 1.8mm with a horizontal disc diameter of 1.7mm.

Caucasians - Smaller

Mexicans < Asians < Africans

CDR is normally less than 0.60, relative to the size of the disc so that smaller cupping - small-sized disc and larger cupping - large discs

tends to enlarge in the vertical meridian in glaucoma

Question 2

Q

Size, How to classify

(could use bloodvessels as broad guide)

Answer

A

optic disc size as small (vertical diameter <1.5mm),

average or large (vertical diameter >2.2mm)

Use slit beam height to match vert - Using 90D

correction factor will be 1.0x for a 60 D lens, 1.1x for a 78 D and 1.3x for a 90 D lens.

Larger with Biomicroscope

Question 3

Q

ISN’T rule

Answer

A

Neural rim tissue THICKEST

Inferior of the disc, then the Superior and Nasal, being thinnest in the Temporal region

normal neural rim tissue

Question 4

Q

LAMINA CRIBROSA

Answer

A

It is a sieve-like structure of largely connective and glial tissue that is continuous,

although embryologically distinct, with the scleral coat

Question 5

Q

OPTIC NERVE DRUSEN

Answer

A

Bilateral

pseudopapilloedema. They are golden, autofluorescent, glowing, calcific globular deposits that sit in front of the lamina cribrosa

can shear blood vessels and/or nerve fibres, leading to haemorrhages (2-10%) and visual field loss (~75%),

Question 6

Q

Myelinated nerve fibres

Answer

A

Myelin sheathing of the optic nerve fibres that extends beyond the lamina cribrosa and presents a superficial, white, feathery opacification which hides any underlying retinal blood vessels.

Question 7

Q

Classification of Glaucoma

Normal

Answer

A

Good rims
Good IOP
No Family Hx
No Trauma related incidents that can increase risk
No medications that can increase IOP

( Topical and Systemic Steroids / TOPAMAX (Weightloss / seizures / migraines)

Question 8

Q

Nerve fibre layer striations

Answer

A

brightest at the superior and inferior poles, where the nerve fibre layer is thickest and are best seen in young patients, particularly those with heavily pigmented fundi (Figure 9). The striations are caused by the tubes of astrocytes that surround the retinal ganglion cell axon

Question 9

Q

Peripapillary atrophy (PPA)

Answer

A

The RPE and choriocapillaris are lost and all that is visible are the large choroidal vessels and sclera

15% of normal eyes bordering the disc BETA zone

More prevelent in glaucoma

Question 10

Q

Tilted discs & optic disc malinsertion

Answer

A

the disc or discs are commonly tilted inferior nasally with a nasal staphyloma (bulging of the sclera) and situs inversus, where the temporal blood vessels first course towards the nasal retina before sharply changing course

staphyloma can produce a temporal visual field defect

Question 11

Q

Optic disc basic Examination

C x 3

VEINS &ARTERIES

Answer

A

CUP

CONTOUR

COLOUR

Veins - Darker

Arteries Lighter lumen

Question 12

Q

COLOUR of optic disc

Orange - Pink

What Causes Palor?

NIGHT TIC

Answer

A

Neuritis
Ischaemic
Granulomatous
Hereditory
Traumatic
Toxic
Irradiation
Compression

Question 13

Q

Goldman Perimetry

Advantages

Answer

A

Goldmann Perimetry

• Advantages
◦Can use both kinetic and static targets
◦Can test both central and peripheral fields
◦Can change both target luminance and size
◦A specific area of the field may be quickly isolated and tested

• Used mostly in low vision and neuro-ophthalm to map fields•

Question 14

Q

Goldman Perimetry

Disadvantages

Answer

A

Disadvantages

◦Testing the full field is time consuming and tedious
◦The exposure time, speed of movement, and point location are NOT set by the machine, so

there can be variability between users

Question 15

Q

Automated Fields

• HVF 3 - Has a liquid lens, just enter the Rx

Question 16

Q

Automated Perimeters
• HVF Analyzer 2
• Octopus
• Oculus Zeiss

Answer

A

Different Types of Stimulus Presentations

Projection (ie: Humphrey)
Movable LED (ie: Octopus 1-2-3)

Question 17

Q

Automated Perimetry

Advantages

Answer

A

• Advantages

◦Testing conditions are reproducible

◦Accurate

◦Numerical results (Not X or sqaures)

◦Most testing can be done by techs

◦Insurance carriers reimburse

Question 18

Q

Automated Peimetry

Disadvantages

Answer

A

• Disadvantages

◦Interpretation of results can be difficult

◦Variability between different manufacturers —> hard to compare

◦Length of time for threshold testing

◦Initial cost of instrument

Question 19

Q

Automated VF Luminace terminolegy

Apsotilb (Asb)

Decibels (Db)

and the comparison

Answer

A

• Apostilb(asb.)
◦Unit of light intensity
◦Apostilb = candela/pi m = lumens m

*• Decibels (dB)**
*target size** NOT considered or background illumination

◦0.1 log units = 1 dB
‣ 0 dB corresponds to brightest stimulus on a machine
‣ > 0 on a printout means pt cannot see the brightest stimulus
‣ 50 dB corresponds dim stimulus on a given machine
‣ highest you see is about 40 dB

Question 20

Q

Automated Perimetry

Background

Answer

A

For all automated perimeters, the background is in the mesopic range (between 1-100 asb)

◦This range stimulates both rods and cones
◦Humphrey: 31.5 asb
◦Regular Octopus: 4 asb

Octopus 1-2-3: 31.5 asb

Question 21

Q

Threshold vs. Sensitivity

Answer

A

• Automated machines are threshold tests
◦Higher dB = dimmer stimulus = the better vision = more sensitive
• ie: a threshold value of 10 dB has a lower sensitivity than a threshold value of 20 dB
◦10 dB is brighter than 20 dB, which means person is less sensitive if this is their threshold

Question 22

Q

How size of target influence Db and how calculated

Answer

A

Sizes:
◦Humphrey III target is 0.43 deg diameter, 4.00 mm

◦Humphrey V target is 1.72 deg diameter, 64.00 mm
◦Log(4) = 0.6 (6 dB), so going from a III to V would increase the dB by about 12 dB

◦Ie: Test patient in one location with III size and get 20 dB, if you repeat with V size you would

get about 32 dB

Question 23

Q

Gray Scale

Answer

A

◦Visual representation using varying shades of gray to represent sensitivity

◦Darker gray = greater reduction in sensitivity
◦NOT a substitute for numerical chart —> can be misleading at times

◦Skewed to recognize defects
◦Good tool for patient education
◦Gray scale is a simple representation (not an interpretation)

Question 24

Q

Fixation Monitoring

Answer

A

Fixation Monitoring
• Heijl-Krakau Fixation Quotient
◦A blind spot is mapped
◦A stimulus is placed at the center of the already mapped blind spot to ensure the pt is not
tracking the stimulus and to check for alignment changes ◦Expressed as a ratio
‣ Numerator = # times the pt lost fixation
‣ Denominator = # of trials
◦Greater than 0.20-0.25 is usually considered invalid or unreliable

Question 25

Q

Optical monitoring

Answer

A

• Optical monitoring
◦Humphrey system projects infrared light onto the cornea
◦Enables perimeter to calculate the eye rotation from the distance the corneal reflex moves
compared to a baseline measurement taken before VF begins ◦“Gaze tracking”

Question 26

Q

3 Ways to varify Fixation losses

Tech Tips

how to pause test by holding button

Run demo

Pause every 5mins for break - avoid fatigue artifact

• Monitor pt fixation manually through entire test especially if 10 degree

Answer

A

Fixation Losses
◦Blind spot check is easily fooled
‣ Slight tilting of head or anatomical variation
‣ Catch trials are skewed - more in the first few minutes and less as attention decreases
◦Gaze track can lose its lock
‣ Not all patients pass gaze track initialization
‣ Thrown off by head movement and dry eye
‣ Fair accuracy, 1-2 degrees
‣ Interpretation is subjective (no standards!)
◦Gaze track and fixation loss (FL) catch trials often disagree
◦Direct observation by tech is probably best - final arbitration of reliable fixation

Question 27

Q

Rx needed for visual Fields?

Answer

A

• Humphrey bowl is 30cm deep
◦Peripheral field —> No Rx needed , the ring of the lens will interfere with the test

◦Central field (30 deg) —> Rx is needed
• metal rimmed trail lenses
• Patient is dilated with anti-cholinergic (tropicamide) to wipe out accommodation, a +3.25 Add should be used

◦Phenylephrine is a sympathetic agonist,

tropicamide is a parasympathetic antagonist
• For Rx’s with 0.75 cyl or below, the spherical equivalent can be used
• For 1.50 cyl, you must use it in perimetry

Question 28

Q

How to read A Humphries test

+

Considerations.

Answer

A

How to read Humphrey Visual Field Printout
(1). Type of test
◦Threshold or screening?
(2). Name of Patient
◦Always enter the name the same way
(3). Strategy
◦Full Threshold, Fast Pac, SITA Standard, or SITA Fast or SITA Faster
(4). Rx used
(5). Pupil Diameter
◦If pupil is less than 2-3mm, pupil should be dilated

(6). Fixation Losses
◦Predicts validity or reliability, if greater than 20% need to repeat unless there are reasons

(7). False Positives
(8). False Negatives
◦If pt is thresholded at one stimulus, then a stimulus that is 9 dB brighter will be presented at the same point
‣ Ie: 20dB threshold, 9 dB brighter would be 11 dB
◦If the pt does not see this point, it is a false negative
◦May indicate that the pt is tired or no longer attentive to the test

Question 29

Q

Patient and Perimetrist factors to consider

Answer

A

Human Factors to Consider
• Fatigue
• Learning
• Fixation
• Distractions
• Anxiety
• Medical problems (ie: arthritis)
• Droopy lids
• Pupil size
• Long-term fluctuation
• Short-term fluctiation (indicator of pt reliability)

Perimetrist Factors to Consider
• Correct pt instructions
• Correct type of path
• Correct Rx
• Correct alignment of the patient
• Encouragement of pt
• Rx must be metal rimmed lens
• Lens holder must be close to the eye
• Lid must be held open or taped
• Perimetrist should be sensitive to the individual needs of the pt

Question 30

Q

Do not create Pseudo defects

Answer

A

• You lose 1 dB per diopter that you’re out of focus

Dirty trial lens
- lenses instead of - lenses
Not taking away the lens holder when testing periphery
Using wrong cyl axis
Noisy testing room
Using plastic rims instead of metal

Question 31

Q

Evaluating a Field

WANDER

Answer

A

◦What was done?

◦Was the field accurate?

◦Was the field normal?

◦What defects are present?

◦Evaluation of visual defect?

◦Re-revaluation of visual field

Question 32

Q

Visual fields (How many points And location)

24-2

30-2

10-2

24-2C

Answer

A

Usually grid for glaucoma is (24) 54 pts or (30) 76 pts

Macula 10-2 tests 68 points in the central 10 deg

24-2C (new) takes all points of a 24-2 and adds 10 points from 10-2 for a total of 64 points

Full field test goes out to 60 deg —> very useful, but takes too long to threshold

Question 33

Q

How FULL threshold is determined

Answer

A

The threshold at any given point is determined by a staircase method
◦A 4-2-2 staircase with the last seen value taken as the pt’s threshold
◦Once it has crossed the line from seeing to non-seeing or vice versa, it goes in 2 dB steps

◦At each threshold location, a dB number is assigned
◦Can detect very shallow defects
◦Can take up to 18 mins per eye on some pts

Question 34

Q

FASTPAC 3-3

Answer

A

Threshold Strategy: FASTPAC 3-3
• Start with 4 seed points at 25 dB, then uses the FASTPAC strategy to get threshold
• FASTPAC then starts thresholding half the points 1 dB brighter and the other half 2 dB dimmer
• It only makes one transition from seeing to non-seeing or vice versa

Question 35

Q

SITA

SITA FAST

SITA FASTER

Answer

A

SITA (Swedish Interactive Threshold Algorithm)
theoretically better startingpoint
• Data constantly updates as more info is gathered during the test
• Uses frequency of seeing curves
• At the end of exam, threshold values are recomputed using all stimulus luminance with a 50%
probability fo being seen
• It does NOT directly test false positives - uses response time to estimate the false positive response
• It speeds up the rate of stimulus presentation in accordance to how quickly the pt can respond
• Response time is set by the patient
• The machine theoretically calculates when to stop testing points that are fluctuating a lot
• Other algorithms re-threshold if 7 dB off, but this algorithm only retests if 12 dB off 24dB seen
Threshold is 24 dB
SITA Fast
• SITA Faster —> no false negatives and no blindspot checks
◦Rationale: more fields are important and we need to do them quicker

SITA FASTER
◦Rather than using starting point of 25 dB for the 4 primary points, it uses a faster age- corrected normal value
SITA Faster uses only one staircase test reversal
◦The SITA tests use real time determination to stop testing based on full threshold program norms. SITA Faster uses norms from SITA Fast to stop testing a given point
◦Does not re-test absolute blind spots (ie: not seen at 0 dB), while older strategies do

◦Does not test for false negatives
◦Uses gaze tracker for monitoring fixation (does not place a point in the blind spot)

◦Eliminates delay after non-seen stimuli
‣ Older SITA programs had an extra 300ms delay after non-seen stimuli at the end of the response time window before a new stimulus was presented

Question 36

Q

SWAP

Answer

A

SWAP (Short Wavelength Automated Perimetry)

Blue target, yellow background
Do less of this now
Hard to do with cataracts, hard to interpret the threshold testing

Question 37

Q

Interpreting Visual field testing

Answer

A

• Very deep defects are easily spotted

lose a decibel a decade after age 20.

Hill of vision changes roughly 3 dB every
10 degrees throughout the field
Mirror Imaging and Defect Depth (Hirsch)
• If point is 9 dB less than its neighbours, it’s a defect
• If point is 6 dB less than its neighbours, it’s possibly a defect
• If 2 or more points are 6 dB less than neighbouring points, they are probably defects
• Often a collection of points will have a reduced sensitivity (ie: an arcuate or quadrant defect)

◦Comparing the values in different locations on the graph will help identify problems ◦Compare dB values in the same coordinates between eyes

Question 38

Q

MEAN Deviation

Answer

A

◦Mean elevation or depression of the pt’s overall field compared to normal reference field

◦Takes all points, averages them, compares to your age

◦Peripheral points do not weigh as much, central is more important (weighted average)

◦P<2 means less than 2% of the normal population shows an MD larger than the value found in this test

Question 39

Q

Total Deviation and

Patern Deviation

Answer

A

• Total Deviation
◦Point-by-point representation of the difference in dB between pt’s test and age-corrected normals
◦Translates into gray scale symbols
◦ie: 33 is what you should score, but you scored 29 —> -3

• Pattern Deviation
◦Similar to total deviation, except results are adjusted for the overall changes in height of PX’s
measured hill of vision
◦If the pt has overall depression, this is filtered out

Question 40

Q

PSD

Answer

A

◦Pattern standard deviation is a measure of the degree to which the shape of the pt’s measured field departs from the normal age-corrected reference field

◦Low PSD = smooth hill - follows the shape

◦High PSD = irregular hill - all over the place

◦PSD < 3 is abnormal

Question 41

Q

Visual Field Index

VFI

Answer

A

“what % of the field is normal?”

An enhanced MD designed to be less affected by cataract, and more sensitive to changes near the center of the VF to correlate better with ganglion cell loss

Center >> periphery

Reduces cataract contribution to the measurement of VF loss

VFI plotted against age
◦Facilitates estimates of disability risk

Question 42

Q

Glaucoma Hemifield Test

GHT

Answer

A

• In glaucoma, inferior rim of the optic nerve is attacked first
• Glaucoma is known to affect one 1/2 of the field to a greater extent before involving the other half
• Compares one half of pt’s VF to mirror image of the other half
◦Looks for asymmetry
◦Can be fooled by symmetrical loss

• Pattern deviation scores in each of 5 zones in the upper hemifield are compared to findings in mirror-image zones in the inferior visual field
• Scoring differences between mirror image zones are compared to normative significance limits specific to each zone pair
• GHT findings are divided in the following categories:
◦Outside normal limits - whenever at least one zone pair differs by an amount found in fewer than 1% of normal subjects
◦Borderline - whenever at least one zone pair differs by an amount found in fewer than 3% but more than 1% of normal subjects
◦General depression or Abnormally high sensitivity - whenever even the best test point locations are either so low or so high as to be at levels seen in fewer than 0.5% of normal subjects
◦Within normal limits - whenever none of the above conditions are met

Question 43

Q

Which test to do for Gaucoma suspect

Answer

A

• Most doctors do a 24-2 (54 points, 6 deg apart)
• Some do a 30-2 (76 points, 6 deg apart)
• Newest theories on glaucoma: do a 24-2 and a 10-2 (76 points, 2 deg apart)
◦Idea of the 24-2C —> now have 64 points, and the 10 points in the central 10 deg are the ones thought to be the most commonly flagged if glaucoma develops
Which Test Strategy?
• SITA STANDARD vs. SITA Fast vs. SITA FASTER
◦Standard may be more accurate, but not clinically significant
◦Fatigue artifact wins over theoretical
◦SITA FASTER doesn’t do false negatives and doesn’t check fixation (just checks activity at
the bottom)
◦Hanley: SITA Standard >> Fast
‣ Fast misses defects but the data seems to point to not much difference
Which Test to Run: 30 vs. 24 vs. 10?
• For glaucoma, either 24 or 30 is effective, but 24 is faster and lessens fatigue artifacts
◦Eliminates edge points of limited value
◦not involved in early diagnosis, too variable
◦Lessening of fatigue artifact outweighs any theoretical advantage of 30
• For neuro: use 30 with SITA standard or SITA Fast
• For decrease vision and/or endstage glaucoma
◦Always use 10-2 for evaluation of decreased vision ◦2 degree spacing vs. 6 degree
◦24/30 suboptimal for testing decreased vision ◦Potential for detecting early glaucoma with 10-2

Question 44

Q

Evaluating Threshold Fields Over Time

Answer

A

VFI plotted against age (projected loss)

◦Healthy —> lose about 1 dB a decade
◦Glaucoma —> lose about 1 dB a year

Guided Progression Analysis (GPA)
• 2 baseline visual fields and compares the new field
• Possible progression - 3 or more points show deterioration in at least 2 consecutive fields (4 min fields)
• Likely progression - 3 or more points show deterioration on 3 consecutive fields (Min 5 fields)
• A simple linear projection is shown as a dashed line
• A regression line is drawn through the best fit to the VFI data
◦Projected out 5 years to help the pt and doctor understand the anticipated impact of glaucoma progression if things continue along the current course
• Cons of VFI:
◦Estimates are more optimistic than those of experts
◦Rates of change over time with both indices were closely related, but the reliance of the VFI
on pattern deviation probability maps have caused a ceiling effect that may have reduced its sensitivity to change in eyes with early damage
‣ In this group of pts, there’s no evidence to suggest that the VFI is either superior or inferior to the MD as a summary measure of visual field damage
• Pts get cataracts over time, so may have to create new base VFs

Question 45

Q

How many fields are needed to determine progression?

GPA

Answer

A

◦Minimum 5 years with annual testing using linear regression ◦Clinically, minimum of 2, or 3 if major therapeutic intervention planned

◦Suggest 2 in first 6 months, third 4-6 months later

Question 46

Q

Screening Modes/Tests on Humphries

Answer

A

Two-zone strategy
Three-zone strategy
Quantify defects

• 2 different approaches
(1) Four primary points, one in each quadrant are thresholded
Second most sensitive value used to calculate the expected height of the hill of vision

(2) From the age-related norms, the machine will set the hill
Age related is the one most commonly used

Question 47

Q

Two-zone Strategy

Answer

A

Two-zone Strategy

From expected height, theoretical hill of vision is calculated
Targets then presented 6 dB brighter than theoretical hill
If seen at 6 dB brighter, then it is tested a 2nd time
Points missed twice at the 6 dB brighter level are recorded as defects, and a SOLID BLOCK is recorded

Question 48

Q

3 ZONE Strategy

Answer

A

Three-zone Strategy
• Begins same as threshold-related strategy
◦4 primary points, one in each quad, thresholded
◦Second most sensitive value used to calculate the expected height of the hill

◦From expected height, theoretical hill is calculated
◦Targets 6 dB brighter than the theoretical hill
• Points missed twice at the 6 dB level are retested with the brightest stimulus for the machine
• If see at brightest, an X is recorded
• If not seen at brightest level, a solid block is recorded
• Very useful strategy for patients who have had strokes

Question 49

Q

Qauntify Defects

Answer

A

• Begins same as two-zone strategy
◦Targets are presented 6 dB brighter than the theoretical hill
◦ If missed twice, the area is then thresholded
◦The number expressed is the depth of the defect from theoretical threshold, NOT THE

ACTUAL THRESHOLD
◦Ie: expect 33 dB point, but pt misses it twice. Thresholded to 10 dB, so 33 - 10 = 23 dB

‣ 23 dB is shown on the quantify defect graph

Quantify Defects

The higher the number, the deeper (worse) the defect

Do not confuse this with the numbers on the full thresholding tests where higher dB is better

If only one isolated point is missed and the defect depth is less than or equal to 8 dB, it probably

does not represent a defect if it is beyond 20 deg

If one point is missed and the defect depth is greater than 8 dB, it probably represents a defect

If two adjacent points are missed with a defect depth of 6 dB or higher, they probably represent a defect

Question 50

Q

FDP

Answer

A

• Frequency Doubling Perimetry (FDP)
◦Stimulus is a grating of low spatial frequency that is flickered at a high temporal frequency

◦Minimum contrast for each stimulus to be detected is used to determine threshold
◦At a certain frequency, the total number of bars appears to be double

◦When a low spatial frequency undergoes a high temporal frequency, the stimulus display appears to have twice as many light and dark bars than are actually present
• Frequency doubling is controlled by the magnocellular pathway
• The M cells are responsible for low-contrast, high temporal frequency (or motion) stimulus
detection
• They make up only 15% of the total number of axons in the eye
• There is a small subset of M cells called My cells that actually respond to frequency doubling
• My cells are thought to be affected in early glaucoma
• The My cells contribute about 5% of total axons in the eye

Question 51

Q

Anterior Causes of

Visual Field Defects

Answer

A

• Lids - ptosis
◦Superior defect secondary to location of nodal point

• Cornea
◦Dense scars can create VF defects
◦Corneal dystrophy —> MD decreased, total deviation decreased, pattern deviation looks normal, PSD normal
◦Fields are not usually done for corneal problems, however your glaucoma pt may also have a corneal dystrophy

• Cataracts
◦Usually associated with generalized overall depression, especially nuclear opacities
◦Can be associated with scotomas or localized depression depending on locaiton and density

Question 52

Q

4 Main terretories for defects after the Nodal point

Answer

A

• Territory I - retinal rods and cones
‣ Macular degeneration, retinal detachments, retinitis pigmentosa
• Territory II - retinal ganglion cells and axons, nerve fibre layer, optic nerve
‣ Nerve fibre pattern on the retina: papillomacular bundle, inferior arcuate fibres, superior arcuate fibres, horizontal raphe, nasal radial bundles
• Territory III - optic chiasm, usually caused by pituitary adenomas
• Territory IV - optic tract, LGN, optic radiations, visual cortex

Question 53

Q

Visual Field Loss with Glaucoma

Answer

A

• Paracentral scotomas (usually in Bjerrum’s Area 5-20 deg from fixation)
• Central and peripheral nasal steps
◦Inferior macula vulnerability zone

Progression of focal depths
◦Increase in depth (ie: one point goes from 20 dB to 15 dB)
◦Increase in size (ie: 2-3 points affected before, now 4-5 points affected)

◦New scotomas

*◦Isolated paracentral scotomas merge to form arcuates**
*• In end stage glaucoma, usually all that’s left is nasal rim**
*• The last thing to go is 20/20 vision**

Question 54

Q

Terretory 2 Visual field Defects

Answer

A

• Most common is glaucoma
◦Paracentral —> 70%
◦Nasal step —> 5%
◦Both paracentral and nasal step (upon 1st exam) —>10% ◦Temporal wedge —> 5%
due to changes in rim tissue

• Myelinated nerve fibres
• Drusen on ONH
• Papilledema
• Optic neuritis
• Ischemic optic neuropathy

Question 55

Q

Direct Opthalmoscopy

General

Answer

A

• The dioptral power of the wheel should be the sum of your Rx (if you are uncorrected) and the pt’s Rx to get the retina in focus
◦Ie: you are a -2 D myope without correction on, your patient is a -4 D myope. The wheel on your oscope should be -6
◦Ie: you are + 4 D without correction on, your patient is pl. Wheel on your oscope is +4
• Angle your head at a 15 degree angle to view the optic nerve, move temporally to see nasal retina

Question 56

Q

Components to disc Diagraming

Answer

A

• Media - does the disc look clear or hazy
◦Anything along the visual pathway can fog up your view
• Look at disc margins - are they distinct or indistinct
• Crescents - around the disc margins
• Evaluating size of disc
• Evaluating each rim
• Evaluate the size of the cup compared to the disc
• Evaluate the cup rims sloping, undermined, indistinct, etc.
• Proper symbols to be used when drawing an optic nerve

Question 57

Q

Disc Edema

Answer

A

Ask yourself is it unilateral or bilateral?
• Is the vision decreased?
◦Did it come on quickly or gradually?
• Are there any other symptoms / headache, vomiting, electrical impulses, etc?

Question 58

Q

What causes indistinct Margins?

Answer

A

• Increased intracranial pressure - papilledema
• Papillitis - infiltration or inflammation of the optic nerve
• Ischemic optic neuropathy
• Pseudo disc edema
congenital tilted nerves in high myopic astigmatic

*SIGNS**
*• Hemorrhages**
*• Dilated, twisted veins**
*• Tilted discs**
*• Glial veils** (do not make margins indistinct, because they hover above the retina at the disc)
*• Crescents**

Question 59

Q

CRESENTS:

Answer

A

*• Scleral crescents** - white semilunar patch of sclera adjacent to the optic disc due to the fact that the choroid and RPE do not extend to the optic disc
*• Choroidal crescents** - occur because the RPE is not abutted to the optic nerve
*• Pigment crescents** - in almost all eyes, the RPE shows some histological irregularities close to the tip of Bruch’s membrane at the border of the optic disc
*• Peripapillary atrophy (PPA)** - thinning of the retina and RPE in the region immediately surrounding the optic nerve head

Question 60

Q

CD RATIO

Answer

A

Average cup to disc is about 0.35-0.4
Ilarge discs should have large physiological cups, and pts with smaller discs should have small C/D ratios
above 0.6 C/D ratio should get VF done

How to evaluate disc size…
• mid-size oscope light target, that’s about equivalent to average disc size

• If you use a 90, 78, 60 DD lens,
◦Correcting factor:
60 is 1.0x
78 is 1.1x
90 is 1.3x

Question 61

Q

WHICH EYE

Answer

A

If the vessels are not central, if anything, they move nasally
Margins - usually the optic nerve slopes temporally
Fovea will be temporally
Straight vessels tend to go nasally
Vessels arch going toward the fovea

Question 62

Q

Glaucoma Deffinition

New and Old

Answer

A

Chronic neurodegenerative disease characterized by loss or retinal ganglion cells resulting in distinctive changes in the optic nerve head and retinal and nerve fiber layer

• Optic neuropathy that is consistent with remodeling of connective tissue elements of the optic nerve head and with loss of neural tissue associated with eventual development of distinctive patterns of visual dysfunction

Question 63

Q

Chronic Open Angle Glaucoma

POAG

Answer

A

Bilateral with one eye preceding the other
IOP was greater than or equal to 21 mm Hg and the filtration angle (trabecular meshwork) was open by gonioscopy
Glaucoma is the leading cause of irreversible blindness in the US. and 2.7 million who are over 40 have POAG
OAG most common form and affects 95% of individuals with glaucoma. It is more common in African Americans and Hispanics than other ethnic groups. OAG is up to 3-4x more common in African Americans than Caucasians and tends to occur at an earlier age

Question 64

Q

2 Types of Glaucoma:

Answer

A

Open Angle Glaucoma – the aqueous appears to have open access to the trabecular meshwork. The iris does not appear to be blocking the trabeculum. Initially this condition has no symptoms. At some point, side (peripheral) vision is lost and without treatment, an individual can become totally blind.

2. Closed Angle Glaucoma – the trabeculum is blocked by the iris and aqueous cannot drain from the eye causing the IOP to rise

Answer 64

A

Primary Open Angle Glaucoma

Age
African or Latino ethnicity
Family history
Increased IOP
Myopia
Decreased corneal thickness
Diurnal intraocular pressure variation
Long-term intraocular pressure variation
Sleep apnea
Migraine sufferers

Answer 65

A

Angle Closure Glaucoma

Age
Female gender
Asian ethnicity
Shallow anterior chamber
Short axial length
Small corneal diameter
Steep corneal curvature
Shallow limbal chamber depth
Thick or anteriorly positioned lens

Answer 66

A

Genetic loci linked to POAG

underlying genes Myocilin (MYOC),MYOC appears to affect protein unfolding in the trabecular meshwork Optineurin (OPTN) and WD repeat Domain 36, (WDR36) is well established

Answer 67

A

Open angle glaucoma VS Narrow angle glaucoma dt race:

Whites 11:1
African American 150:1 (More OAG)
Chinese 1:3 (More angle closure)

Prevalence of POAG Glaucoma based on race

European descent is about 2.5% for patients over 40

5.6% of African Americans have open angle glaucoma

Filipinos >>> Caucasions to normal tension glaucoma and POAG

Inuit’s over 40, 2-3% have angle closure glaucoma (opposite)

• Asians in general have more normal tension glaucoma and more angle closure (Highest) risk as a large amount of the population have narrow angles

Answer 68

A

Increased risk of glaucoma as you get older. Age serves as a marker for metabolic and degenerative changes of the tissue.

Prevalence is about 0.25% at age 20 and doubles every 10 years.

Answer 69

A

Gender – no significant difference for primary open angle glaucoma.

Females are more prone to angle closure glaucoma, the reason is

unknown. More women have open angle glaucoma mostly because women tend to outlive men

Sample set is larger.

Answer 70

A

Primary Pediatric Glaucomas are classified as follows:

Congenital glaucoma (congenital open angle glaucoma)
Juvenile open angle glaucoma
Glaucoma associated with systemic disease
Glaucoma associated with other ocular anomalies

Answer 71

A

Primary congenital glaucoma – about 20-40% of the cases are caused by increased IOP during life in the womb and the baby has ocular enlargement of the eye (buphthalmos).

Features include: enlarged corneas, Steamy corneas, elevated IOP, Haab striae may present at birth or prior to 1 month (newborn)

Infantile PCG presents within the first 2 years
Late diagnosed PCG may present after the age of 2

Answer 72

A

Congenital Glaucoma is present at birth and bilateral in 2/ 3 of cases.

Males >> than females except in Japanese individuals. It is thought to be due to a developmental defect where the iris inserts more anteriorly than in normal eyes which prevents fluid from draining causing an increase in IOP. The prevalence is higher in cultures with consanguinity, particularly those with a high carrier rate of CYP1B1 gene (GLC3A locus on chromosome 2p21) and LTBP2 within GLC3C locus

Congenital/ infantile glaucoma presents with marked elevated IOP causing the sclera to enlarge and become thinner. The eye looks bluer than normal because the choroid is more easily visualized through the thinned sclera.

The common clinical triad is epiphora, blepharospasm and photophobia.

The cornea appears cloudy due to edema from the increased IOP, horizontal breaks in Descemet’s membrane occur called Haab striae and the scleral canal increases in size. The normal cornea of an infant is 10mm (adult is 11.8mm), > 13mm corneal diameter is suspect before the age of 1 and >14mm is typical of advanced buphthalmos.

Answer 73

A

The normal anterior chamber of an infant compared to an adult

Less pigmented TM
Less prominent Schwalbe line
Less distinct junction between scleral spur and CBB

• In PCG (primary congenital glaucoma)

There is high iris insertion
The angle recess is absent
The iris root appears as a scalloped line of glistening tissue. This glistening membrane is what is referred to as Barkan’s membrane and likely represents thickened and compacted trabecular meshwork.

Answer 74

A

The disease becomes manifest after 2 years, but before 16 years of age.
Most cases of juvenile appear be autosomal dominant with only minor sporadic cases occurring.
These cases are linked to TIGR (trabecular meshwork inducible glucocorticoid response) / MYOC (myocillin ) gene locus GLC1A

Answer 75

A

Axenfeld Riegers Syndrome

Sturge Weber syndrome.

Answer 76

A

Congenital, It is characterized by a facial birthmark and neurological abnormalities.

Ocular manifestation is high IOP in eye with port wine stain. Glaucoma 70% , when birth mark close to eye / the hemangioma is

on the upper lid.

Patients can also have CNS angiomas which can produce seizures.

GLAUCOMA caused due to an isolated trabeculodysgenesis.

As the child ages, elevated IOP is due to elevated episcleral venous pressure that occurs as a result of arterioveonous shunts through the episcleral hemangiomas.

Patient have a marked increase in pigment in one eye and more pigment in TM about 10% have elevated IOP in the hyper pigmented eye.

Answer 77

A

Nevus of Ota presents as a blue or gray patch on the face, which is congenital, with onset at birth or around puberty and is within the distribution of the ophthalmic and maxillary branches of the trigeminal nerve. The nevus can be unilateral or bilateral, and, in addition to skin, it may involve ocular and oral mucosal surfaces

Answer 78

A

Increase in short term fluctuation on threshold fields

Paracentral scotomas (usually in Bjerrum’s Area 5-20 degrees
from fixation)

Central and peripheral nasal steps

Progression of focal depths
o Increase in depth (one point goes from 20 db to 15 db)
o Increase in size (2-3 points affected now 4-5 points affected
o New scotomas

o Isolated paracentral scotomas merge to form arcuates

Answer 79

A

Superior nasal

Paracentral scotoma

Answer 80

A

Superior Arcuate Scotoma

Bjerrum’s Area 5-20 degrees

& Nasal Step

Answer 81

A

Superior arcuate scotoma

Inferior Paracentral scotoma, general depression

Answer 82

A

Temporal island OD

Answer 83

A

Progression of visual field defects

Answer 84

A

Initial Phase - IOP is causing damage to the optic nerve head but the field is normal
Threshold Phase - patient shows an increase influctuationand visualfields are inconsistent andvariable
Manifest Phase - positively reproducible visual field loss

Answer 85

A

Decreased MD / Also with Glaucoma

o Wrong Rx
o Cataracts
o Miosis
o Aging and other ocular conditions

Answer 86

A

Three or more adjacent points in an expected location of the central 24 field* that have P < 5% on the pattern deviation plot, one of which must have P < 1 % on at least 2 consecutive fields
OR
Glaucoma hemifield test“outside normal limits“ on at least 2 fields ‘(Upper and lower differ from each other by P<1% or 2 corresponding zones are both depressed relative to normal at a P< 0.5% level

OR
Corrected pattern standard deviation with PSD flagged at 5% on two consecutive fields
* Must be nonedge points in central 300 field

Answer 87

A

Mean deviation > -6 dB

or

On pattern deviation plot, depressed below the 5% level and fewer than 15% of
points depressed below 1% level

or
No point within central 5 below 15dB

Answer 88

A

Mean deviation worse than -6 dB but not less than 12dB

or

On pattern deviation plot, < 50% of points
depressed below the 5% level and fewer than 25% of
points depressed below 1% level

or
No point within central 5 below 10dB

or

Only 1 hemifield containing a point less than 15 dB within 5 of fixation

Answer 89

A

Mean deviation worse than -12dB

or

On pattern deviation plot, > 50% of points
depressed below the 5% level and more than 25% of
points depressed below 1% level

or
No point within central 5 less than or Eqaul to 0dB

or

Only 1 hemifield containing a point less than 15 dB within 5 of fixation

Answer 90

A

Three contiguous points same side of horizontal
One points p<1% or worse on Pattern Deviation Plot and two other points p<5 or worse

Answer 91

A

The blood supply from the short
posterior ciliary artery and surface of nerve supplied
by retinal arterioles of the CRA
Increased IOP → decreased perfusion → lamina crushes axons → cupping

Perfusion pressure is insufficient to support adequate blood
flow through the nerve

Glaucoma patients do not have good autoregulatory control when their IOP goes up

Answer 92

A

IOP causes compression of the lamina sheets →
mechanical compression of the axons and also
compresses the arteries cupping →

NFL drop out and death of the axons.

Mean of 550 pores in lamina smaller temporally + nasally and bigger Superior and Inferior

Bigger Pores = Easier to crush

Answer 93

A

Axonal transport at the level of lamina and organelles
within the NFL is stopped due to elevated IOP
long enough time, NFL death will occur

o 5 dB loss probably corresponds to a 20 % loss of axons

Y Axoplasmic flow also stops with ocular hypotony ( 4mmHg)
pressure difference across the ONH regardless of high or low IOP, causes
mechanical compression of the axonal bundles

Answer 94

A

Neurotrophin deprivation and Glutamate toxicity

Neurtotrophin are peptides - development and maintenance retinal ganglion cells.

glaucoma there is an obstruction of neurotrophin
transport to the ONH which results in RCG apoptosis
neurotrophic deprivation
dt loss of neurons in the lateral geniculate nucleus

Y Glutamate is a normal neurotransmitter may accumulate to toxic levels secondary to release from apoptosis

Answer 95

A

CONCLUSIONS:
Y These results suggest that patients with glaucoma undergo widespread and complex changes in cortical brain structure and that the extent of these changes correlates with disease severity.

Y Considered together, these data suggest that patients with glaucoma may have volumetric gains in some structures early in disease, but that brain volumes decrease toward and in some cases below control volumes as the disease progresses

Y Also OCT seem to show Ganglion loss with Glaucoma but also
with Alzheimer Disease

Answer 96

A

lack of SVP may be also more important when
we consider POAG
Y Possibly be due to the fact that Px’s
glaucoma have significantly lower CSF pressure than
patients without glaucoma

Answer 97

A

Generalized Enlargment of the cup
Barring of Circumlinear Vessels
Bean Potting
Vertical Elongation ( 0.2 more than Hor cupping)
Notching
Drance Hemhorages (dt notch, inferior disc. Splinter hem dt stretching that it ruptures)
Asymmetry of CD Ratio between eyes (Diff of 0.2 and more)
Distorted Lamina Dots
Aquired Optic pit
PPA (Peripapillary Atrophy) BETA ZONE
NFL Dropout
Nasal cup - extendes past BV / Nasal shift of BV

Answer 98

A

IOP >22 mm Hg
Optic nerve head is normal
Visual field is normal
4-10% of patients over 40 are ocular
hypertensive

IOP 24 to 32 in one eye and at
least 21 in the other eye
30-2 q(6) months and stereo
photos every year

Answer 99

A

Basically thin corneas are considered to be a risk for glaucoma
but one should not convert all IOPs with the chart is what we
do now

Answer 100

A

A 20% reduction in IOP resulted in a 50% reduction in the
development of primary open angle glaucoma in a 5 year
span.
o 4.4% progressed to glaucoma in treated group
o 9.5% progressed to glaucoma in untreated group

>90% of OHTS patients when left untreated did not progress
in 5 years
CCT should be measured

Answer 101

A

Age
IOP 20-32 x3
Central Corneal thickness (475-650) x3 could change DT LASIK SX
Pattern standard deviation x2
Vertical cup disc by contour

*Low < 5%** Observe and monitor
*Moderate 5-15%** Consider treatment
*High >15%** treatment

Answer 102

A

This showed that early IOP-lowering intervention reduces the
cumulative burden of disease,
The absolute effect was greatest in patients with the highest
risk as determined by a prediction model that was developed
and validated using OHTS data. It incorporates age, IOP,
central corneal thickness, cup–to-disc ratio and field pattern
standard deviation as significant risk factors.

Answer 103

A

AAO Def: following findings in at least 1 eye:

Optic nerve or nerve fiber layer defect suggestive of glaucoma ( enlarged cup–disc ratio, asymmetric cup–disc ratio, notching or narrowing of the neuroretinal rim, a disc hemorrhage, or suspicious alteration in the nerve fiber layer)
a visual field abnormality consistent with glaucoma
an elevated IOP greater than 21 mm Hg
Naturally the gonioscopy angle is normal and open
An individual with a suspicious nerve or NFL appearance in the absence of a visual field loss
A visual field defect suggestive of glaucoma in the absence of a corresponding glaucomatous optic nerve abnormality

Answer 104

A

Open-angle glaucoma suspects
(based on the number of risk factors: family history, race,
elevated IOP, optic disc appearance and thin central corneal
thickness):

Open-angle suspect, low risk (one or two risk factors)

Open-angle suspect, high risk (three or more risk factors)

Answer 105

A

Primary open angle glaucoma

Gonioscopy shows an open angle
IOP is > 21 on at least one occasion
Not associated with known ocular or systemic disorders that cause increased resistance to aqueous outflow or damage to the optic nerve(i.e. patient does not have PXE or steroid induced glaucoma)
The optic nerve shows a characteristic optic neuropathy that is consistent with
excavation and undermining of neural and connective elements of the optic disc and eventual
development of distinctive patterns of visual dysfunction.

Answer 106

A

ISNT Rule
Rim notching
NFL dropout
High IOP
Distorted Lamina
Drance Hemorrhages
C/D asymmetry
Greater than .6 cupping
Thin corneas
Abnormal gonioscopy
Abnormal OCT of optic nerve
Hx of hyphema
Hx of ocular trauma
Family Hx of glaucoma esp sibs
Hx of PXE or PDS
Migraine/Raynaud’s
Race - African American

Answer 107

A

To preserve visual function by lowering IOP to a level that is likely to prevent further optic nerve damage
Therapy with the fewest adverse affects
Least amount of disruption to patient’s life
Cost consideration

Can only treat currently by lowering IOP

SX and Laser:
selective laser trabeculoplasty (SLT) in some patients may be a
first line

Injections / MGIS / ALT

Answer 108

A

History
IOP since and multiple readings
Optic nerve evaluation
Visual fields
Pachymetry
Imaging OCT
Gonio (always do gonio before you treat glaucoma)

Answer 109

A

Mild:

Definite optic disc, RNFL, or macular imaging
abnormalities consistent with glaucoma and a normal visual
field

Moderate:

*Definite** optic disc, RNFL, or macular imaging
*abnormalities** consistent with glaucoma

visual field abnormalities in one hemifield that are not within 5 degrees of fixation

Severe:

visual field abnormalities in both hemifields and/or loss
within 5 degrees of fixation in at least one hemifield

Answer 110

A

Establish baseline IOP 3x
Obtain an OCT
Classify amount of glaucoma damage as mild, moderate, severe
Use the highest IOP (Tmax) and set target pressure based on the severity of the glaucoma
Consider lowering target pressure an additional 10% if patient is
* *younger than 50 years, African American, monocular , or has a sibling with advanced glaucoma**

Answer 111

A

Tmax

Highest the IOP ever been recorded in the eye
Importance of this number as the calculation of the
target pressure is based off of Tmax, not the IOP at the time of
diagnosis or starting treatment

Answer 112

A

IOP from baseline (Tmax) by different amounts

o Mild Severity – 20-30% IOP lowering
o Moderate Severity – 30-40% IOP lowering
o Severe Severity – 40-50% IOP lowering

o Though new guidelines from AAO recommend starting with a
minimal of 25% reduction

Ocular hypertension
o Lower the IOP by 20%-30%, or to 20 mm Hg or less.

Answer 113

A

OCTs to monitoring structural
consistent with glaucoma however
Y Once the damage is significant,

*visual fields** are probably best
*to monitor progression**
Stereoscopic viewing of the optic nerve still the way to diagnose glaucoma
OCT have a lot of false positives and false negatives.

Answer 114

A

High myopes : fall outside of the

normal range, showing up as red.

On the other hand, small focal areas of damage show up as green because the instrument averages the thickness
The average is often within the normal range, despite the focal loss.
impression that there is no damage present.

Answer 115

A

3 IOPs
2VF
Gonioscopy ****
Pachymetry (some recommend separate day readings)
OCT
Evaluate risk factors

Answer 116

A

Topical miotic – cholingeric agents

o Alpha adrenergic agonist

o Prostaglandin analogues mostly increase uveoscleral outflow but also affect some increase in trabecular meshwork outflow

Answer 117

A

o Beta Blockers
act on the [beta]-adrenergic receptors in the ciliary processes
o Carbonic Anhydrase Inhibitors
inhibit carbonic anhydrase in the ciliary
epitheliumand decrease aqueous humorsynthesis

o Alpha2-adrenergic Agonists
• Apraclonidine: Relative selective alpha 2 adrenergic agonist but does activate some
alpha - 1 receptors,
• Brimonidine: more alpha 2 selective

Answer 118

A

Increase Uveoscleral Outflow
o Prostaglandins analog: binds and activates receptors in the ciliary smooth muscle and improves uveoscleral outflow
o Selective alpha-adrenergic agonists: Brimonidine

Systemic
o CAI :Diamox (Sigma), Neptazane (Wyeth-Ayerst) and Daranide (Merck,Sharp, & Dohme)
Decrease Aqueous Production and

ORAL CAI reduce vitreous volume
o

Inhibit carbonic anhydrase in the ciliary epithelium and decrease aqueous humor synthesis
o Osmotic agents

Answer 119

A

*latanoprostene bunod 0.024% Vyzulta**
*metabolizing** into two moieties:

latanoprost acid - primarily uveoscleral pathway to increase aqueous humor outflow
butanediol mononitrate, which releases nitric oxide (NO) to increase outflow through the trabecular meshwork and Schlemm’s canal.

nitric oxide-donating prostaglandin F2-alpha receptor agonist

One drop in the affected eye(s) once daily in the evening

Unopened bottles should be refrigerated
Open bottle can be stored at 2° to 25°C for 8 weeks

Vyzulta really only acts the trabeculum and not the retina

Answer 120

A

netarsudil ophthalmic solution 0.02%

Rho kinase inhibitor which is believed to reduce IOP byrelaxing the cells of the meshwork and inner walls of Schlemm’s canal, increasing outflow.
also decreases inflow by inhibiting norepinephrinetransporter therefore reducing the production of aqueous humor. It has also been shown to lower episcleral venous pressure.

Y One drop daily in the evening.
20% will get Vertex Keratopathy (Corneal verticillata) after 4 weeks

Unopened Store in refrigerator
After opening, product may be stored in refrigerator or at room temperature for up to 6 weeks.

Answer 121

A

Conclusion: The monocular trial of therapy is effective in
accurately predicting the response of an untreated eye to
monotherapywith aprostaglandin analogue at all daytime
time points measured

Answer 122

A

Side Effects of Glaucoma Medications

Prostaglandin Analogs: eye color change, darkening of eyelid skin, eyelash growth, droopy eyelids, sunken eyes, stinging, eye redness, and itching
Beta Blockers: low blood pressure, reduced pulse rate, fatigue, shortness of breath; rarely: reduced libido, depression.
Alpha Agonists: burning or stinging, fatigue, headache, drowsiness, dry mouth and nose, relatively higher likelihood of allergic reaction.
Carbonic Anhydrase Inhibitors: in eye drop form: stinging, burning, eye discomfort;
in pill form: tingling hands and feet, fatigue, stomach upset, memory problems, frequent urination.
Rho Kinase Inhibitors: eye redness, corneal deposits, stinging, and small bleeds on the white of the eye.

Answer 123

A

Pilocarpine 1% 2% 4%

Answer 124

A

Mechanism

– Alter the function and the structure of the
uveoscleral pathway to increase aqueous outflow
Y less increase in trabecular outflow facility.

DOSE: 1gtt qhs

twice day dosing is less effective

Two weeks to 6 weeks for maximum overall effect

ALWAYS ASK PX WHEN LAST GTT WAS INSTILLED

Answer 125

A

Increases Uveal Scleral outflow

starts 3-4 hours after installation, maximum effect is
8-12 hours after administration

unopened bottle(s) - regfigerator (transport 8day up to 40C)
opened - room temperature up to 25°C
(77°F) for 6 weeks

ocular redness (worst 30min / better 1hr)

stinging - refrigerator to not sting

21% IOP drop in NTG
No crossover to fellow eye, as low strength and metabolized in
eye

Answer 126

A

Increase Uveal scleral Outflow

starts 2 hours after installation, maximum effect 12
hours

Un-opened - not need refrigeration shelf life of 18 months.

Opened - between 2° - 25°C disgard 6wks

ocular redness (worst 30min / better 1hr)

stinging - refrigerator to not sting

21% IOP drop in NTG
No crossover to fellow eye, as low strength and metabolized in
eye

Answer 127

A

Increases Uveal scleral outflow

starts 4 hrs and maximum effect is 8-12 hrs

Opened Bottel - doesn’t require refrigeration.

Disgard Open container 6wks

ocular redness (worst 30min / better 1hr)

stinging - refrigerator to not sting

21% IOP drop in NTG
No crossover to fellow eye, as low strength and metabolized in
eye

Answer 128

A

Conjunctival hyperemia up to 25%
Foreign body sensation/irritation
Superficial Punctate Keratopathy
Hyperpigmentation of periocular skin
Permanent darkening of the irises
Darkening and increasing length of eyelashes
Anterior Uveitis – rare
Orbital fat atrophy
Problem with Cystoid Macula Edema
Possible herpes simplex activation
Migraine like headaches
Flu like symptoms

Answer 129

A

4.1% are non responders – defined as <15%
reduction
Then you add beta blocker AM

Adding another med from the same family will not show an additive effect on IOP decrease

Switch in prostaglandins discontinuing one d/c and trying another

Side Effects

Macular edema
History of herpes simplex in eye
Active uveitis
Class C for pregnancy

Answer 130

A

The beta-blockers act on the beta-adrenergic receptors in the
ciliary processesandreduce aqueous humor production.

selective (Block beta 1 receptors) or
nonselective (block both beta-1 and B2 receptors equally)

however even the selective can cause pulmonary effects

Non-selective approximately 25% IOP decrease
Levobunolol(Betagan), Timolol(Timoptic)
Cartechol (Ocupress)
Selective approximately 20% decrease
Betaxolol (Betoptic S)
BB most effective when given in the morning

Answer 131

A

Most common beta-blocker is
Non-selective B-blocker Lowers IOP by ~25%

IOP begins to fall in 30-60 minutes and peak in
reduction in 2-3 hours and back to baseline in 24 -48 hours

About 10-20% of patients do not respond with lower IOP

Best results AM

CONTRA Indications!!!!!!!

Answer 132

A

Problems
Short term escape
o Loss of efficacy within 1 month
This is secondary to receptor saturation

Long term drift (tachyphylaxis)
o Extended use of B blockers may reduce their effectiveness because the response of B adrenergic receptors is affected by constant exposure to an agonist.

Need at least 4 weeks for washout from the receptors

Answer 133

A

Patients with or had asthma
Patients with COPD (Chronic obstructive Pulmanory disease)
Patients with Bradycardia
o Check pulse if below 55 – 60 BPM
Patients with myasthenia gravis

*CHF** (Congestive Heart Failure)
*Hypotension**

Controversial if already on a systemic beta blocker if you should also use it to treat glaucoma

Answer 134

A

Dry eye
Corneal anesthesia
Allergic blepharoconjunctivitis

Uveitis

Answer 135

A

Systemic hypotension – left ventricular failure and atrioventricular conduction disturbances
Bronchospasm
Adverse CNS effects – fatigue, depression, amnesi
Ocupress – less effect on bad cholesterol profile
Mask clinical signs of hyperthyroidism (i.e. tachycardia) because of the thyroid storm
Bradycardia – if they have a pace maker it is ok
Mask hypoglycemic signs and symptoms, sometimes resulting in dangerously low blood sugar
Impotence

Answer 136

A

Could be used before Timoptic
A-2 receptors located on presynaptic adrenergic nerve terminal and postsynaptic terminal

*o A2 presynaptic** activation inhibits NE release
*o Postsynaptic A2** activation reduces cAMP levels

Overall these drugs reduce aqueous production as well as increase uveoscleral outflow

Lower IOP by ~20-25%
􏰀 Brimonidine and Apraclonidine which are alpha 2 selective
Alphago”
o Brimonidine is more alpha 2 selective

Answer 137

A

Brimonidine (Alphagan)
1gtt TID (used alone)
o Starts to work in 1 hour ,peak effect after 2 hours lasts for 12 hours

Apraclonidine (Iopidine)
post Sx / Angle closure / Risk procedures
o Starts first hour work peak 3 hours lowers and lasts _for 12 hours but large tachyphylaxis(_Toxic)

so not usually used for long term treatment used for short term ,i.e after and before ALT,LPI Acute Angle Closure

Answer 138

A

Blepharits

Dry Eye

Conjuctival hyperemia

Dry mouth Dry Nose

Allery Conjuctivitis

Follicular Conjuctivitis

Miosis

Answer 139

A

AVOID IN CHILDREN - can cause CYANOSIS and SEIZURES

CONTRAINDICATED for PX taking Monoamine Oxidase Inhibitors

& Px with Severe CARDIOVASCULAR Disease

Hypotension

Vasovagal attack

Anxiety

Answer 140

A

rasagiline (Azilect),
􏰀 selegiline (Eldepryl, Zelapar),

􏰀 isocarboxazid (Marplan),
􏰀 phenelzine (Nardil),
􏰀 tranylcypromine (Parnate)

Answer 141

A

Bicarbonate formation is an essential component of aqueous. Inhibiting carbonic anhydrase activity in the ciliary processes decreases the amount of bicarbonate

􏰀 Results in decreased aqueous production
􏰀 Lower IOP ~ 20%

Azopt Trusopt

􏰀 Appears to work at night thought not as good as prostaglandin

Answer 142

A

Ask when last taken

Azopt – peak 2 hrs trough is 12 hours .

Trusopt peak 2 hours trough is about 12 hours

􏰀 Both TID
􏰀 Some people get a metallic taste

Answer 143

A

SULFA ALLERGY

Endothelium compromise

FUCHS ENDOTHELIAL DYSTROPHY

Answer 144

A

Not used as much today as in the past secondary to ocular problems with miosis and ciliary spasm

Direct acting – activate cholinergic receptors directly at the neuro-junctions of iris sphincter and CB
Indirect acting – exert effect by inhibiting cholinesterase increasing Ach in synaptic cleft
Increase in outflow likely due to stimulation of CB longitudinal muscle which widens scleral spur

􏰀 Lowers IOP by 15-25%
PILOCARPINE
􏰀 Most common pilocarpine 0.5%, 1%, 2% , 4%, 6%

Answer 145

A

Elderly: Decrease in VA dt NS and cataract formation

Young Adults: Decreases the Acc available, unable to read

Answer 146

A

Drops:

Rhopressa

Meds:

Amioderone- Drug for Anarythmia

Plaquenil - Arthritis treatment

(Bulls eye retinopathy)

Answer 147

A

􏰀 Better compliance, better IOP lowering than with
monotherapy of the same components
.
􏰀 ROCKLATAN® (netarsudil/latanoprost ophthalmic solution) 0.02%/0.005% about $300 for 2.5 ml

􏰀 Cons: Dosing regime BID (insead of TID)
􏰀 Timolol-dorzalimide (Cosopt)
􏰀 Timolol-brimonidine (Combigan)
􏰀 Brinzolamide-Brimonidine (Simbrinza)

Answer 148

A

􏰀 Usually at 4-6 weeks but the medication dependent
if someone has severe glaucoma you may need to have them back in a week.

Make sure they can show you how to use the medication.

􏰀 Pilocarpine- immediate effect
􏰀 Beta blocker may take several weeks to stabilize return 4-6 weeks
􏰀 Alphagan can return as early as 2 weeks but usually 4-6 weeks
􏰀 CAI’s can return as early as 2 weeks but usually 4-6 weeks
􏰀 Prostaglandins 2 weeks to possibly 3 months before best results is lowest effect observed

Answer 149

A

􏰀 Depends on severity of disease.

Severe cases frequent follow up, mild cases q 6 months The greater damage, the greater the risk for further damage.

FU - Always IOP / Prelims / Field and OCT Yearly.

1st Year 2-3 fields

** Gonio should be done on all patients before starting a patient on glaucoma meds you need to determine what type of glaucoma they have

Answer 150

A

Optic nerve coloboma

Answer 151

A

See Table

Answer 152

A

direct method, angle observed directly
hand held focal illuminator

patient in supine position
highly convex Koeppe lens is placed on
*anesthetized** cornea
provides a broad view of chamber gives excellent impression of physiological iris contour

and width of angle inlet distorts the angle very slightly relatively low magnification special equipment
time consuming

Answer 153

A

The two most common methods are:

Zeiss 4 mirror lens
Goldmann mirror lens
Sussman lens, Posner lens

Performed at the slit lamp PX seated in upright position
Opposite Qaudrant evaluated

Answer 154

A

Central lens : Posterior pole (Primary gaze)

Evaluate inferior 1st (Largest angle)

1gtt Proparacane

PROS:

Stereo view of Fundus
Faster exam / No Rotation
No need for Gel / Bubbles
Smaller corneal contact

CONS:

Unwanted compression (alter angle appearance)
Need to be steady

Answer 155

A

Requires viscous solution eg: methylcellulose

Past gonio gel(very preserved SPK)
USE- Teargel / Celuvisc
Bubble free / anesthesia (Proparacaine)

Optically excellent views

Answer 156

A

Better for deeper set eyes / Smaller appertures

Able to view posterior pole

Answer 157

A

Smaller - Easier to handle

Less rotation

Central view of fundus

Answer 158

A

Central Lens

clear fundus contact lens
􏰁 allows view of posterior pole
􏰁 provides stereopsis and magnification
􏰁 Image is upright

Answer 159

A

largest trapezoid shape mirror
Equatorial

Eye needs to be very dilated

Able to see vortex veins in periphery

Answer 160

A

rectangular in shape
Dilated pupil needed

Answer 161

A

Used for viewing the angle UNDILATED

Able to view the extreme periphery in a very dilated eye

Answer 162

A

Steps

Align slit lamp for patient and examiner
Scan anterior portion of eye
if corneas are intact, anesthetize cornea
Clean mating surface Dakin’s solution(9:1) 10/10
Rinse with saline
Fill 3/4 CELLUVISC(less viscous) Genteal(More viscous) Gonio scopic(SPK)
Set up slit lamp (low mag.,~ 0° illum. arm, narrow beam, low light intensity), position so the gonioscopy mirror is placed on the eye superiorly
without excessive pressure, fingers not used to brace Px forehead
Look outside the mirror and move the illumination beam into the gonio mirror
identify the pupil edge. Focus on the edge of iris
Focus on the iris and note the color of the iris
Increase the magnification to 16x (medium)

Answer 163

A

Corneal abrasion
􏰁 Penetration injury
􏰁 Hyphema
􏰁 Laceration
􏰁 Recent lasik surgery, corneal transplant

􏰁 Corneal ulcer, infection

Answer 164

A

Always Tonometry first

Arteficially could lower pressure if done first
􏰁
Check the pupillary/iris frill and iris surface before observe the other angle structures

(Signs of EXP exfoliation syndrome)

Answer 165

A

observe and note the flatness or convexity of the iris plane
Iris inserted more posterior in Myopes and Hyperopes

Answer 166

A

CBB

SS

TM

SL / Sampolisi’s line

Answer 167

A

Ciliary Body Band (CBB)

*Darker** in eyes with more iris pigmentation
*Height varies** dependent on iris insertion

Peripheral anterior synechias are formed when peripheral iris adheres to the peripheral cornea

Answer 168

A

Ciliary Body Band

Answer 169

A

Normal variant and remnant of embryological development

􏰁 Histologically iris tissue at its base and uveal tissue at the apex

􏰁 Most dense nasally
􏰁 Does NOT interfere with outflow- it is not an iris adhesions
􏰁 Typically stop at the trabecular meshwork

Answer 170

A

formed when peripheral iris
adheres to the peripheral cornea

Answer 171

A

Avoid compressions when unwanted

Make slight lens excursions

Answer 172

A

Most easily seen in wide angled eyes at the anterior end of the angle recess where the ciliary body inserts

􏰁 narrow white line

Blood fills Schlemm’s canal, or pigment deposits are found in the Trabecular meshwork anteriorly;

it can be easily located

Answer 173

A

can be sometimes discussed as a gray zone just above scleral spur

if blood flows through the canal can stand out

Answer 174

A

*Causes:**
Excessive external pressure on goniscopy
Low intraocular pressure
Increased episcleral pressure

Sturge Weber syndrome

Corotid Carniverous sinus

Answer 175

A

Trabecular pigment band due to
*deposition of pigment of** granules
Denser in pigmentation in brown iris patients than blue eyed patients
With age, band becomes less translucent
Pigment Of TM should be less than CBB

Answer 176

A

condensation of collagenous fibers which runs round the inner peripheral cornea

Marks the anterior insertion limit of the angle structures

Schwalbe’s line is also called
Sampolesi’s line (Pigmented)

Most anterior limit of angle Termination of Descemet’s membrane

White glistening line: sometimes thickened

Answer 177

A

Optical section slitlamp

Angle the illumination arm either temporally or nasally 5-10 degrees off center
Medium magnification
􏰁 Note 2 linear reflection: one from the external surface of the cornea. The other from the internal surface of the cornea
􏰁 Edge formed due to juncture in angle curvature of cornea and sclera in angle

The 2 reflections meet at Schwalbe’s line; identifying the anterior limit of the trabecular meshwork
􏰁 Observe the location of the iris insertion onto angle wall when focal lines are aligned

Answer 178

A

Technique issue: alter tilt of lens, patient looking in different direction

Could be a narrow angle

Bowed Iris

Iris roll preventing observation of iris reces

Answer 179

A

CBB

SS

TM

SL

Answer 180

A

Primary views: when patient is looking straight ahead

Secondary views: when patient looks towards the direction of the mirror the examiner tilts lens towards the angle of observation
If the angle as the gonio- lens does not reach the depth then secondary views are helpfull

Answer 181

A

Change of external stimulus can alter the anterior chamber assessment depth
􏰁 Recommendation: performing gonioscopy
􏰁 Dark Room
􏰁 1mm beam Slitlamp beam
􏰁 Patient position: straight ahead Primary Gaze

􏰁 Adequate illumination

Importance is a false OPEN angle dt Illumination

Answer 182

A

Location of iris insertion

Note presence of iris processes
Grade Trabecular meshwork pigmentation

NORM: CBB <= TM

Answer 183

A

penlight technique: temporally
if iris is FLAT, total illumination
if iris is BOWED, shadow forms

Answer 184

A

Check the pupillary/iris frill and iris surface before observe the other angle structures

Answer 185

A

Age related
Most predominant Scandenavia / Further away from eqautor(Angle of light reflection WATER ICE)
Solar radiation / Outdoors / Geographical Location
High Coffee Consumption
Decr Folate / Incr Homosysteine levels
Genetics LOXLI gene
Amyloid buildup on lens and Surounding structures
Krukenberg spindle

Answer 186

A

Amyloid Material on lens surface - Dilation caused a Bull’s eye appearance

Weakening of Zonules and cilliary processes LENS SUBLAXATION

Cat sx EXO should be taken into consideration

Iris Transillumination at Pupil margin

Krukenberg Spindle

Answer 187

A

Gonioscopy findings
Roughened lens surface abrades iris pigment during pupil movement
Pigment releases from iris and collects on TM and SL Obstruction of outflow through TM
Dysfunction of TM increase in IOP

Krukenberg spindle / endo deposition of pigment

Uneven pigment deposition in Trabecular meshwork

􏰂 “Patchy” lack of homogenous appearance
􏰂 Pigmented Schwalbe’s line
􏰂 Rare to see exfoliated material

Answer 188

A

30-40 Males 10yr before Females MYOPES

Peripheral contour of iris more Concave

Risk of PIGMENTARY GLAUCOMA

Zonular rubbing causes shedding of iris pigmentation into the aqueous humor and thus Trabecular Meshwork (TM)

Answer 189

A

Iris Transillumination (Mid Peripheral)

Krukenburg spindle

Due to convection currents of aqueous, pigment rubbed off from iris
flows into anterior chamber, deposits endothelium

Pigment deposit in a linear fashion at the junction of the
zonules and the posterior lens capsule = called Scheie’s stripe

Answer 190

A

DDX

Krukenburg spindle

Answer 191

A

According to Spaeth grade the amount of pigmentation the posterior portion TM at the 12 o’clock position

Answer 192

A

Trauma create tears in locations between the sclera and uvea at the corneoscleral junction

Hx of injuries blunt TRAUMA

􏰁 history or presence of hyphema(Blood in eye) may be an indication of ocular trauma

Leads disruption of uveal meshwork and
tears in the Trabecular meshwork (TM), ciliary muscle, iris root

SCARRING causes Glaucoma Years later

Answer 193

A

Dt: Trauma 80%

Rubeosis 20% (Caused by Hypoxia at the retina)

Diabetes ALWAYS RECORD -NVI / Rubeiosis

Chec IOP / NO Gonio

***Bed Rest / Head Elevated ***

Answer 194

A

Compare CBB width in all Qauds

Small areas of iridodialysis, iris tears
􏰁 Angle recession: CBB >>> SS + TM
􏰁 Altered anatomical structure that can affect aqueous
outflow and cause angle recession glaucoma many years later

Answer 195

A

Thickening of lens
Shallow AC
IOP outflow Obstruction
Could develop Hypermature Cataract

Answer 196

A

Hypermature cataract can cause Phacolytic glaucoma
Ruptured capsule of mature lens evoking macrophage proliferation into anterior chamber
Cloggs up TM dt hypersensitivety to Protein in AC

Answer 197

A

Rubeosis irides = Iris neovascularization

Hypoxic/ischemic changes in the retina

Diabetics, Vein occlusion, Ocular Ischemic Syndrome

Hyphema

Answer 198

A

PACG is the leading cause of blindness worldwide

80% of PACG Asia 1/6th of Asian pop Narrow ANGLE

*Prevalence** of PACG
1. 5% of Asians over 40yo
0. 1-0.5% of patients over 40yo of European decent
0. 75% in adult Asians
0. 97% in Middle East group
1. 10% in China
1. 19% in Japan group

Answer 199

A

apposition of peripheral iris against the pigmented TM resulting in obstruction of aqueous outflow

relationship between iris and lens regulates the flow of aqueous from the posterior to anterior
5micron space between iris and lens
One way valve to maintain higher pressure in the posterior chamber prevents back flow
relative pupillary block

increase in resistance flow of aqueous

pressure in posterior chamber rises and bows the iris forward

*Iris bombe**
*blocks the TM**, IOP inc

Answer 200

A

older age

6th/7th decade . Iris thickens anteriorly

Gender

2-3x more women / dt anatolmical shallower AC

Family Hx

autosomal dominant and autosomal recessive patterns for anatomy

Hyperopia

Prolonged dark states / Winter - Dilation

Eye anatomy

small corneal diameters
short axial length of globe
anterior displaced lens
increased curvature of the anterior lens
increased thickness of the lens
anterior insertion of iris into ciliary body
*Emotional stress** - Dilates Pupil
*Anterior displacement of the lens** - Accomodation

Answer 201

A

shallow anterior chamber both centrally and peripherally
average depth = 3.15mm
expect 6:1 anterior chamber depth (Van Herrick)

RISK
central depth of <2.2mm risk for angle closure
4:1 anterior chamber depth

Plateau irises

Exeption to the rule

2.4mm -2.0mm Sometimes

much higher risk if = 1.8mm
75% of PACG patients are <1.5mm

Answer 202

A

*medications that causes Dilation or Constriction**
ex. bronchodilators, nasal decongestants, antinausea, antispasmodics, antihistamines, adrenergic agonists, cholinergics, anticholinergics, sulfa-based drugs, SSRIs, TCAs and tetracyclic antidepressants, anticoagulants

Miotics
Pull the peripheral iris away from the anterior chamber angle
strong miotics may also cause the zonular fibers of the lens to relax, allowing the lens-iris interface to move forward results in greater iris-lens contact, potentially increasing pupillary block

General anesthesia
parenteral atropine sulfate during induction of anesthesia or muscle relaxants induce mydriasis

Answer 203

A

Moderate pupillary dilation increases risk for angle closure

posterior vector of force is at a maximum when the pupil is between 3-4.5mm dilated
Moderately dilated, the peripheral iris is under less tension and is easily pushed forward into contact with the TM

thicken the iris and bunch it into the TM

Answer 204

A

Quick - no time to develop
Dilator muscle moves the iris peripherally (slower) and posteriorly (faster)
pulls the sphincter back posteriorly as well maximally dilated
little to no contact between the lens and the iris

Dilation wearing off
occurs slowly, pupillary block can develop as dilation comes down and pupil is mid-dilated

Answer 205

A

NO phenylephrine or iris dilator stimulating agents
forces the iris posteriorly, increasing the pupillary block

0.5% tropicamide is preferred if need to dilate
fast acting

*not safe** to dilate, send for LPI
*1/2 of TM** –> refer
*posterior TM in at least 180** –> refer

Answer 206

A

0.5% tropicamide

Answer 207

A

Need scotopic conditions
different grading systems used
dynamic or static
no clear definition of at risk eyes/occludable angles
ex. 1/4:1 or less
ex. pigmented TM was not visible in 3/4 quadrants in primary gaze without manipulation or indentation
failure to assess the anterior chamber depth

Answer 208

A

Autonomic imbalance with increased sympathetic tone
iris dilator muscles are more developed and stronger
incr sympathetic - emotional distress, low light conditions, sympathomimetic drugs use
contraction - leads thickening of the middle-peripheral iris = AC

Water volume in iris - Some irises stiffer than others Don’t move anterior.

Peripheral iris attached to Trabicular wall.

Answer 209

A

Angle Closure
can start narrow but become broad and/or high as time progresses
Chronic angle closure - PAS are more basal and broad based

Larger PAS, the less likely LPI will be effective

PAS is more common in occludable angles
PAS is more extensive the longer the duration of the angle closure attack

Answer 210

A

Gonioscopy should be performed:

dim to dark room
small 1mm slit beam
patient looks straight ahead
only modestly tilt the lens

Answer 211

A

Primary angle closure suspect
iris touch the anterior chamber angle at the TM on non-comp gonioscopy
ITC 180deg or more
NO PAS, normal IOP, normal nerve and VF

Primary angle closure
ITC 180deg or more
PAS and/or elevated IOP
with no secondary cause for the PAS Trauma
Normal nerve and VF
refer for LPI

Primary angle closure glaucoma
80% is chronic
ITC 180deg or more
PAS and/or elevated IOP
with no secondary cause for the PAS
glaucomatous optic neuropathy and VF loss

Acute angle crisis glaucoma
Angle is occluded suddenly
20% of angle closure glaucoma

Answer 212

A

BOWED IRIS

Narrow angle

Answer 213

A

Progression and further intervention

PAC’S eyes do not receive further intervention after LPI
PAC and APAC and most PACG eyes receive further treatment damaged optic nerve fragile
- GTT(Medication) , cataract surgery, or trabeculectomy
- progression to PACG is uncommon in PACS and PAC

LPI efficacy
LPI increases angle width in all stages of PAC

good safety profile

Answer 214

A

Characteristics

angle is occluded suddenly
can be self-limited and resolve spontaneously
can have mini-attacks when in the dark for prolonged periods
can occur repeatedly
can cause permanent vision loss or blindness

Findings

quickly elevated IOP
ciliary flush/vascular congestion
corneal epithelial edema/steamy
causes intermittent blurring of vision and haloes
ocular pain and/or headache
nausea/vomiting
mid-dilated pupil
ischemia to iris muscles due to high IOP
sphincter is stronger than dilator

Answer 215

A

Acute Angle closure Glaucoma

Answer 216

A

Management

lower IOP (first) and provide comfort (second)
Open the angle and break the attack
Depends on pressure and length of attack most resolve in 4-6hrs if treated

medical treatment

Start with drops GTT, if the IOP does not lower in 1hr start ORALS

aqueous suppressors may be ineffective due to decreased ability to reduce aqueous formation if the ciliary body is ischemic

Answer 217

A

*Beta Blocker**
*1gtt timolol** or levobunolol followed by 2nd drop 10min later
*takes effect within 20min**

Alpha Agonists
0.5-1% iopidine 1gtt followed by second drop 10min later
or 1gtt brimonidine works quickly

Steroid
1gtt 1% prednisolone acetate hourly
decreases inflammation
(raises pressure after 2-3weeks of use )

CAI’S
1gtt dorzolamide
500mg acetazolamide/Diamox orally or IV if nauseous
(not the time release capsule)

hyperosmotic agents
glycerine 50%, isosorbide 45% or mannitol 20%
cause rapid decrease in IOP

anti-cholinergics
controversial, may get more pupillary block
Only use if < 50mmHg
sphincter is ischemic when pressure is too high
1gtt 2% pilocarpine every 15min for 1hr

Answer 218

A

Compression for 30sec on and 30sec off
- 4 mirror gonio lens
- Q-tip perpendicular to the vertical axis
- push on eye with palm of hand
Have patient lay on their back / Moves lens Back
Anterior chamber paracentesis
- apply anesthetic drops (ex. oxybupricaine) and clean eye with povidone iodine 5%
- insert a syringe 9 o’clock at the limbus aiming for the center of the anterior chamber

IOP is lowered too quickly,

retinal hemorrhaging can occur decompression retinopathy

laser iridotomy
- preferred surgical treatment
- favorable risk-benefit ratio
- can’t Dt corneal edema, cornea may be cleared with topical hyperosmotic agents or anterior chamber paracentesis

Answer 219

A

PAS

*Glaucomflecken**
*infarction** of anterior lens epithelium from high IOP
*white deposits** more irregular and no fluff on frill like in exfoliative

iris atrophy

Answer 220

A

YAG (cutting of hole)

Effective alone in thin blue iris
far less effective in thick brown iris more of a cutting laser

Argon Laser (Burning laser)

Used to thin darker irises, then YAG laser is used to create the hole
Argon is more of a burning laser takes longer

Answer 221

A

Preparation

Topical proparacaine (Anestetic)
1% pilocarpine - stretches the iris to reveal the crypts/thinnest areas
0.5% or 1% apraclonidine due to post-laser IOP spike

Procedure
laser at a crypt until bubbles of fluid are seen coming through the iris. 3 or 9 o’clock prevents diplopia, photopsia, and diplopia

Post-LPI
1% prednisolone acetate 4x/day for 5-7days
glaucoma medications

Efficacy
need further treatment (drops, surgery)
0-8% PACS
42-67% with PAC
21-47% with APAC
83-100% with PACG
if the nerve is damaged, have to treat like POAG to keep pressure low and prevent further damage

Risks
6-10% 8-17mmHg IOP spike
2-11% dysphotopsia

30-41% anterior chamber bleeding (hyphema)
23-39% cataract progression

Answer 222

A

Examination:

Sure it is patent before dilating / Thin membrane visible?
check with retro-illumination
can also use OCT to determine
if not sure, check with gonioscopy - Angle should be larger than Pre

check the IOP post dilating a patient with a LPI

Causes for IOP with dilation after LPI
LPI is not patent
incomplete LPI not able to view lens capsule
response to dilating agents
other causes ruled out
pigment liberation will observe anterior chamber shower
PI is patient but patient has plateau iris angle closure
malignant glaucoma
lens causing angle narrowing
phacomorphic, subluxated or abnormally anterior lens

Answer 223

A

recurrent and self-limiting episodes of closure with elevated IOP
DARK lighting leads to pupil dilation and block
Issues going from dim to bright - light like those with AMD and carotid artery disease
bright light and sleep open angle as pupil becomes miotic

Hx

episodic symptoms
blurred vision, haloes, eye pain, headache, eye redness
relatives with acute angle closure glaucoma

Findings

PAS, esp. superiorly superior angle is narrowest
IOP often normal in office can be misdiagnosed as NTG
ONH cupping and VF loss are often the first indications
*Management**
*LPI first**

use medications after LPI

if LPI is not sufficient filtering surgery if needed

Answer 224

A

Findings

asymptomatic
more PAS zippering shut of angle, esp. superior angle
iris atrophy
Mistaken for POAG
perform gonioscopy

Management
iridotomy first / CAT Sx if lens is part of the Cause
require medications after LPI to control IOP due to chronic trabecular damage
prostaglandin analogs are preferred

filtering surgery if not controlled

Answer 225

A

Plateau iris configuration
iris is flat centrally then peripherally then becomes very steep
ciliary body is abnormally anteriorly displaced,

pushing the iris forward gonioscopically,

steep peripheral iris that it is closely apposed to the angle

not be detected on Van Herick - narrow until far periphery

Plateau iris syndrome
angle closure either spontaneously or after pharmacological dilation in an eye with a patent LPI
iris pulls back directly into the angle causing an IOP spike

Answer 226

A

*Subtypes**
*Complete plateau iris syndrome**
*IOP rises** when the angle closes with pupillary dilation

Incomplete plateau iris syndrome
height of the plateau is less and leaves the filtering meshwork either partially or all open covers the SS but not the TM

Primary angle closure
demographics
female younger than with pupil block (45-50yo)
less hyperopia than pupil block
bilateral
wide dilation is a risk
often retrospective diagnosis
perform LPI because you think there is pupillary block ACG and after LPI when pupil dilates the IOP still goes up

must perform compression gonioscopy

won’t pick this up with Van Herick
S shaped hump or double trough sign
results from the iris following the curvature of the lens then drops when the iris reaches the deepest point at the lens equator and then rises again over the ciliary processes before dropping peripherally
normal iris has one hump

Answer 227

A

treat eyes with recurrent high IOP after dilation or if IOP is high after LPI
treat syndrome, not just configuration
if only SS is covered, no need to treat

*Miotics**
*pilogel at night or 1-2% pilocarpine 2-4x/day**

gonioplasty/iridoplasty
evenly spaced burns around peripheral iris
argon laser burn to the stroma
constricts the peripheral iris by pulling it away from the angle

Complications
marked anterior chamber inflammation
corneal endothelial cell damage

Answer 228

A

primary cysts of iris and ciliary body
stationary / no harm

clinically identical to plateau iris, but different cause
anterior chamber is uneven in depth and the angle is variable in width
Van Herick

Management and Treatment
confirmed by UBM (ultrasound)
monitored or puncture cysts with argon or YAG laser

Answer 229

A

*shallow angle chamber** both peripherally and centrally
*high IOP**
*no pupillary block**
*aqueous is misdirected into vitreous** causing rotation of ciliary body causing anterior lens displacement and angle closure
Caused by choroidal expansion with fluid
- after ocular or cataract surgery
- after CRVO
  - edema in uveal tract can cause angle closure
  - can also cause 100day neovascular glaucoma
Scleritis
allergy to sulfa drugs (acetazolamide, sulfamethoxazole, hydrochlorothiazide)
HIV, AIDs, HZ

topirimate/Topamax (rare)
indicated for migraines, seizures, weight loss

swells ciliary body with anterior displacement of the lens-iris diaphragm
increase in minus dt lens moving anteriorly
most attacks happen within 7days of starting the medication
tell patient if there is eye pain or a change in vision to come in that day
85% of cases are bilateral

Answer 230

A

Management
if medication induced d/c medication

MX medications
cycloplegic
atropine may be drug of choice to relax ciliary body
deepens the anterior chamber
Steroids
topical aqueous suppressors

Answer 231

A

*Retinal ischemia** triggers angiogenesis factors to be released
*secondary to variety of ocular and systemic diseases**
*fibrovascula**r membrane grows over the TM leading to increased IOP and glaucoma

Causes
Ocular
post-CRVO 100 day glaucoma, ocular ischemic syndrome, proliferative diabetic retinopathy, BRVO, CRAO, tumor, retinopathy of prematurity, chronic RD

Systemic
sickle cell retinopathy, GCA, lupus, Marfan’s, Sturge Weber Syndrome, syphilis, endophthalmitis, carotid artery occlusive disease

Answer 232

A

treatment
refer NVI in 24-48hrs
despite being blind in that eye because angle closure is very painful
PRP
anti-VEGF

stages
stage 1: pre-glaucoma with abnormal blood vessels at the pupillary margin
want to eliminate neo before pressure goes up
inject anti-VEGF or PRP if there is retinal ischemia
treat inflammation

stage 2: angle is open but IOP is elevated because of the abnormal blood vessels in the angle
PRP and inject anti-VEGF to decrease pain and complications
standard glaucoma treatments to address high IOP
glaucoma surgery if drugs are insufficient

stage 3: angle is closed and IOP is elevated
PRP and inject anti-VEGF
reduce inflammation
treat glaucoma with drugs and surgery
glaucoma drainage implant is needed

Answer 233

A

leakage of proteins from an intact but permeable lens capsule
associated with hyper-mature lens with liquified cortex

non-allergic cellular response
high molecular weight proteins block the TM
glaucoma is very acute and slit lamp shows a very heavy flare and cellular reaction

inflamed, painful, red eye
high IOP
blurry vision
can see the material blocking the angle

Answer 234

A

process
associated with cataract extraction
cortical material is left behind

occurs days to years after cataract extraction
marked uveitis

treatment
medically
remove cortical fragments surgically and washout anterior chamber

Answer 235

A

Lisch nodules

Neurofribromatosis

Answer 236

A

Angle resession

Answer 237

A

Concave bowing peripheral iris / posterior iris rubs on zonules
Bilateral
Young myopic males 20-40yo

Ocular Findings

liberation of pigment from posterior iris
iris transillumination defects Mid peripheral Iris
moth-eaten appearance
Krukenberg’s spindle
pigment deposition on zonules and posterior lens capsule
zonules attach to the capsule, forming Scheie’s stripe
TM hyperpigmentation

Complications

large diurnal variations in IOP as well as spikes in IOP
strenuous exercise activates pigment dispersion

Answer 238

A

Treatment (Aggessive Px younger)

LP Iridotomy

pilocarpine - constricts iris to get the iris off the zonules
causes 3D of myopic fluctuations throughout the day

ALT (argon laser trabeculoplasty)
laser TM to clean it out
SLT (selective laser trabeculoplasty)
laser TM to clean it out
long-term effect is low
success rate decreases over time

AAO study
10% risk at 5yrs and 15% risk at 15yrs
mean age at diagnosis of pigmentary glaucoma was 42 +/- 12yrs
78% of patients were male
58% of patients with PDS were male
other studies don’t show gender bias
underdiagnosed in black patients
hard to transilluminate the iris
most significant risk factor = IOP > 21mmHg at initial exam
most studies say 10-20% convert to glaucoma
some studies report at high as 35% conversion over 17yrs

Answer 239

A

exfoliative material is released AMYLOID - elastic fibers (fibrillin and alpha-elastin) and non-collagenous basement membrane material (laminin) that forms fibrils
Iris rubs on amyloid material
unilateral and becomes bilateral in 5yrs
Older patients 50-70
Geographic away form Eqautor / UV at angle during youth

Findings

white, flaky, dandruff-like deposits at pupillary border, anterior lens, posterior iris and ciliary processes
Bull’s eye appearance scalloped border appearance around area of mid-peripheral clearance on anterior lens
pigment deposition
- patchy hyperpigmentation of the TM
- SL pigmentation Sampolisis LINE Wavy
- Krukenberg’s spindle
must be seen every 6months at minimum

IOP > 21mmHg, lower IOP with glaucoma medications
even if optic nerve, OCT and VF are normal

Answer 240

A

elevated IOP impairment of aqueous humor outflow due to deposition of pigment and exfoliation material in TM
Fluctuations in IOP of 15mmHg or greater in 35% of patients
increased vulnerability of the lamina cribosa toward elevated IOP, facilitating progression of glaucomatous optic neuropathy

CAT sx - Indication - possible sublazation due to weekened Zonules
post-cataract surgery
TM is aspirated intraoperatively
exfoliative material is lavaged out and vacuumed up

ALT and SLT lower IOP
SLT has greater lowering effect in XFG

Answer 241

A

Posterior recessed insertion of the iris onto the CBB
diagnose with gonioscopy
main feature = widening of the CBB in part or all of the angle
Dense large pigment deposits TM and CBB
CBB > TM+SS
wide diurnal IOP curves

Aqueous suppressor drugs work best
TM outflow is impaired, best to decrease inflow
beta blockers, alpha agonists, carbonic anhydrase inhibitors
use whatever works
sometimes prostaglandins can work

Answer 242

A

Multiple IOP readings to Ddx POAG
mutations in GCL1G gene for optineurin
related to ischemic theory
HX: carotid artery disease, cardiovascular disease, major blood loss, systemic hypotension, severe anemia, migraines, Raynaud’s, sleep apnea, hyperviscosity

Findings
splinter/Drance hemes at the disc more than norn
shallower cupping
more peripapillary atrophy
arcuate field loss closer to fixation
should consider a 10-2 or 24-2C

Answer 243

A

Management and treatment
Beta blockers
SLT
filtering surgery

NTG vs. neurological problem
think neurological problem if:
unilateral or marked asymmetry
color vision loss without VF loss
VF loss that is atypical or not proportional to the optic nerve damage

Answer 244

A

20-60yo
unilateral
Mild inflammation AC (few cells)- large increase in IOP (40-70)

Findings
asymptomatic - dull ache in the eye
mild haze from edema if IOP is very high
KP in AC
angles are open
no synechia
40% heterochromia
inflammation may be the TM (trabeculitis) decr Outflow

HSV, VZV, CMV could be triggers

*Treatment**
*first line therapy:**
*steroid and aqueous suppressors**

1% prednisone acetate QID

second line therapy:
oral CAis for IOP
topical or oral NSAIDs for inflammation

NOT
cycloplegics
prostaglandin analogues and miotics

Answer 245

A

Characteristics
very rare chronic form of iridocyclitis
85% unilateral
presents at middle age

Findings

relatively asymptomatic
80% iris heterochromia Lighter affected
small diffuse stellate keratic precipitates
featureless iris no crypts or furrows
can develop PSCs

10-30% have small blood vessels go up the gonio angle
does not come with fibrotic tissue so no peripheral anterior synechiae
60% get anterior vitritis

may be associated with Rubella, toxoplasmosis, herpes
those immunized against Rubella do not develop this condition
Treatment
Aqueous suppressors

Answer 246

A

rare group of disorders characterized by abnormal corneal endothelium progressive iris and angle changes
epithelial-like corneal endothelium grows as a membrane over the angle
leads to peripheral anterior synechiae that usually extend to SL

Forms
Chandler syndrome
predominantly corneal changes
corneal edema = primary feature
essential iris atrophy
iris changes predominate
causes corectopia and polycoria

treatment
difficult to treat
endothelium grows into blebs and shunts
no cholinergics or trabeculoplasty
prostaglandins are not likely very effective
anterior face of ciliary body is covered by synechia
may need penetrative keratoplasty to treat corneal decompensation

Answer 247

A

Argon laser and a gonioscope mirror and delivering approximately 100 burns usually in two treatments of 50 burns usually do ½ the TM first

The laser burns are placed at boarder between the nonpigment and pigmented TM

Pretreat
Pilocarpine to stretch the iris
Iopidine to lower IOP

Post treat
prednisolone acetate 4 times a day for 4-7 days
Glaucoma medication

Answer 248

A

SLT (Non Scarring)

does not cause thermal damage like ALT
delivers just enough energy to target specific melanin-rich cells in pigmented TM

ALT
Pilocarpine to stretch the iris
Iopidine to lower IOP
Argon laser delivers 100 burns over 180deg of the TM
performed in two treatments of 50 burns
laser burns are placed at boarder between non-pigmented and pigmented TM

*Post-treatment**
*prendisolone acetate 4x/day for 4-7days**

Answer 249

A

I-Stent
insert 2-3 during cataract surgery
directs aqueous directly to SC from anterior chamber

Removal of TM
improves aqueous outflow
can perform with or without cataract surgery
TRrabectome
burns off the TM
Kahook
cuts the TM out with a blade

Answer 250

A

XEN Stent
creates a filtering bleb
cylindrical implant made of porcine gelatin that has been cross-linked with glutaraldehyde
small corneal incision - inserted with an injector

CyPass
voluntarily recalled
causes endothelial cell density loss over 5yrs
very good at lowering IOP

Hydrus microstent
inserted into SC to hold it open over 3 clock hours
partial bypass of the TM

Answer 251

A

mitomcyin to prevent scarring
Create a scleral flap
remove a block of peripheral corneoscleral tissue to create an opening under the conjunctiva to the anterior chamber
aqueous is filtered under the conjunctiva into a filtering bleb
peripheral iridectomy is performed so iris doesn’t clog the opening

Complications
choroid effusion
CME
dellen formation
hyphema
hypotony
causes shallow or flat anterior chamber
prone to infection
blebitis can lead to endophthalmitis
malignant glaucoma
wound leak
cataract formation
ptosis

Answer 252

A

Express shunts
stainless steel shunt placed under scleral flap
compared to filtering bleb less risk of hypotony

Ahmed glaucoma valve
large decrease in pressure
can laser in more holes later if more outflow is needed

Answer 253

A

Collaterals
collaterals can form in advanced glaucoma
like those seen with CRVO, BRVO, tumor behind the eye

Answer 254

A

Cataracts (ACC, NS, PSC, PCC)
ex. NS - diffuse overall field loss
decreased MD and total deviation
pattern deviation and PSD are normal

ex. PSC
VF defect closer to fixation, likely a relative scotoma
decreased MD,increased PSD

if defect is right near the nodal point, Affect visual field more

Answer 255

A

BRAO
retro-atrophy of the nerve
ex. inferior arcuate defect
vessels respect the horizontal raphe
could confuse with a glaucomatous defect once retina regains normal coloration
BRVO systemic HTN
example:
macula edema with exudates
will have distorted Amsler grid
more so inferior because edema is worse superior
refer for anti-VEGF injections
flame hemes superiorly

Answer 256

A

BRAO

Hx very important. Won’t be able to see in 3 yrs

Papliomacular bundle spared

Answer 257

A

Retinitis Pigmentosa

20-50 from fixation

Develop PSC earlier

Bone Specules

Answer 258

A

Territory 2: Ganglion Cells and Axons within RNFL and Optic Nerve
disc edema
grade 4 HTN
tilted disc
optic neuritis
example: papillitis
25yo, decreased vision x 3days OD
VA = 20/50 OD
RAPD OD
can get any VF defects
central scotoma, arcuates, altitudinal
have to determine cause (demyelination, sarcoid, etc.)

Answer 259

A

Optic nerve drusen
field loss can be anywhere
can mimic glaucoma
hard to predict VF defects due to potential impact of buried drusen

Answer 260

A

Optic atrophy
pale optic nerve
can occur post-CRAO or post-ION
suspect tumor behind the eye
example:
73yo
VA = 20/80 OD, 20/30 OS
IOP = 24 OU
RAPD OD
has rim tissue but it has atrophied
PPA around the disc

Answer 261

A

Temporal fibers - nasal VF
remain ipsilateral

Macula fibers
travel in center of optic tract
temporal macular fibers remain ipsilateral
macular fibers cross at posterior chiasm to the contralateral optic tract

Nasal fibers - Temporal VF
inferior nasal cross in anterior chiasm and loop into the contralateral optic nerve before joining the optic tract
loop = knee of Willibrand

superior nasal loop into ipsilateral optic tract then cross in posterior chiasm before joining contralateral optic tract

*Inferior fibers** pass inferiorly
*superior VF**
*Superior fibers** pass superiorly
*inferior VF**

Answer 262

A

25% of all chiasmal lesions will affect the junction
important to do fields in both eyes when you have a patient with unexplained VA loss in one eye
example:
20/20 OD, 20/25- OS
nerve and macula look fine, OCT is fine
BIO light looked dimmer OS, red desaturation OS
perform VFs –> bitemporal defects
diagnosed with pituitary tumor

Answer 263

A

Pressure anterior and inferior on OD optic nerve before chiasm
lose OS knee of Willebrand (inferior nasal fibers)
superior temporal defect
lose OD inferior nasal fibers
superior temporal defect
superior bitemporal heteronymous quadrinopsia

Pressure from below the chiasm (pituitary)
fovea is usually preserved
lose inferior nasal fibers from both eyes
superior bitemporal VF defect

Answer 264

A

Aneurysms of Internal Carotid Arteries
aneurysm of one carotid shifts chiasm against the other carotid
compresses chiasm from the sides
produces binasal defects

Answer 265

A

homonymous
symmetric halves or parts of VF
occupy the same side of the VF in both eyes
respect vertical meridian
defects are either “right” or “left”
labeled in terms of defective side
do not have to be congruous
example: right homonymous congruous hemianopsia

congruous
equal in size, shape and intensity in both eyes
have to be homonymous to be congruous

Answer 266

A

Right optic tract carries information from left VF and vice versa
most defects present as homonymous and usually incongruous
fibers from the two eyes are not perfectly aligned in the tract
create incongruous homonymous hemianopsias on left or right
defects usually occur medial or lateral to the tract

*medial lesion** usually affects the contralateral eye more
example: left medial optic tract lesion
right incongruous homonymous hemianopsia*
*lateral lesion** usually affects the ipsilateral eye more
example: left lateral optic tract lesion
right incongruous homonymous hemianopsia*

Answer 267

A

LGN
very complicated
not many patients have LGN lesions, fairly protected
creates half of an hourglass shaped defect
example: right LGN lesion
left homonymous incongruous hemianopsia

Answer 268

A

Temporal lobe lesions
produce an incongruous superior homonymous quadrantopsia with sloping margins
pie in the sky

example: left temporal lobe lesion
right incongruous superior homonymous quadrantopsiaEffects
behavioral disorders, aphasia (defect or loss of power or expression or speech and writing) and/or amnesia (lack or loss of memory)
formed and unformed hallucinations are possible
formed = see a rat
unformed = see flashes of lights

Answer 269

A

Parietal lesions
produce an incongruous inferior homonymous quadrantopsia with sloping margins
pie on the floor
example: left parietal lobe lesion
right incongruous inferior homonymous quadrantopsia

somatic perceptual disorders
extinction phenomenon
neglect on one side of VF
can see stimuli when presented on the defective side of VF alone, but cannot see the stimuli on the defective side if stimuli are presented on both sides of the VF

Answer 270

A

Occipital Striate Cortex
lesions usually produce defects which are:

complete or incomplete congruous homonymous hemianopsia
macular sparing - More POSTERIOR
Macular Splitting - Anterior lesion
produce discrete VF defects

vascular lesions
Thrombosis of posterior cerebral or calcarine artery
produce complete homonymous hemianopsia

vascular lesions of the small vessels quadrantopsia, hemianopic scotomas

symptoms of lesions
alexia (understands what they seen but cannot read out loud)
headaches
failing VA
sometimes cannot read Snellen letters, have them write what they see instead
macular sparing

Answer 271

A

The most anterior portion of the visual cortex receives fibers only from the peripheral nasal retina in the contralateral eye

some lesions spare this anterior portion of the cortex and leave an intact crescent in temporal VF
can get a lesion only in this area and get a monocular crescent defect in temporal VF

example: left posterior occipital lobe lesions
right homonymous congruous hemianopsia with macula sparing
congruous despite temporal crescent

Answer 272

A

Treatment PLAN

Answer 273

A

Glaucoma MEDS

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Classification of Findings Flashcards

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