Colour Vision Flashcards

1
Q

What are colour vision tests used for

A

Managing paediatric cases, giving vocational advice, detecting ocular disease, monitoring ocular disease, careers, police armed forces, safety, electrician, education, pathology, traffic lights, wires etc
Telling parents capabilities of vision

Change in colour vision- could be a potential sign of pathology

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2
Q

Facts about colour and light
How many colours can an individual see
What 2 things is colour produced by
What wavelengths can the human eye detect

A

Normal individuals can see around 150 colours
Colour is produced by sources which emit a limited spectral range and by filters which transmit a portion of white light

Light is electromagnetic radiation
Human eye can detect wavelengths between 380-780nm
1nm= 1 times 10^-9 of a metre.

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3
Q

Wavelengths and light timeline

A

Red orange yellow green blue indigo violet
Long wavelength
Low frequency
700nm. 500nm. 400nm

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4
Q

Essentially what can all visible hues be matched by
And explain what newton did

A

All visible hues can be matched by an additive mixture of 3 primary colours taken from red green and blue parts of the visible spectrum.

Newton- demonstrated that a prism could decompose white light into a spectrum of colours and a 2nd prism and a lens could recompose the multicoloured spectrum back into white light

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5
Q

Basic colour theory dates and names of the 3 theories

A

1773- young-helmhotz theory
1870- herrings opponent colour theory
1881- donders zone theory

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6
Q

Young helmhotz theory

A

Trichromatic theory
Human eye has 3 types of colour receptors: red, green and blue which work together to create the perception of all of the colours in the visible spectrum.

Helmhotz later discovered that the 3 retinal receptors had overlapping spectral sensitivities.

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7
Q

Opponent colour theory

A

Proposed 4 primary colours red yellow blue and green arranged these opponent colours
R vs G and Y vs B
When you look at one colour for too long the opponent colour appears

This is due to bleaching of colour opponent colours taking away any stimulus
Also discovered luminance mechanisms- white vs black

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8
Q

Zone theory

A

Combines 2 previous theories and this is the basis of modern cv theories
Cv is processed in a series of zones along the visual pathway
Depending on what zone you are in depicts what theory stands

3 zones
Receptor level- the cones themselves, vision is trichromatic
Ganglion cell level- colour info coded into opponent channels
Luminance channels- derives input from the long and medium wavelength cones and a small 10 percent input from short wavelength cone

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9
Q

The diagram of light incident on the retina

A

Light comes through the pupil through everything plexiform layer etc ganglion cells and it bounces off the rpe to go to the photoreceptors. Rpe is important for nutrients, metabollic waste disposal and overall barrier for light to bounce off it

In the human eye the retina is back to front so but it follows a similar theory. Light incident on retina hits cones (reality it bounces off rpe and then hits cones)

Plexiform layer- neurons to process signals
Horizontal and miller cells- combine signals from photoreceptors and these also connect ganglion cells laterally within the plexiform layer.
Bipolar and horizontal cells-> ganglion cell
Ganglion cels- sends signals to brain via ON= respond to colour, contrast, motion + regulate size of pupils

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10
Q

Rods
Function
Where and where not are they present

A

Function at low light levels. Rods everywhere so no directional sensitivity.

Not present at the fovea and diminish in density towards the far periphery. Most dense at the periphery. More rods than cones. 5 degrees from fovea.

Spatial summation= multiple rods to one axon= faster aps generated but cant differentiate. High sensitivity low visual acuity. No colour vision with rods. Better in scotopic conditions.

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11
Q

cones
Function and
Where are they the most dense
What are these not ideal for which conditions

A

Function at higher levels of illumination
Most dense at the fovea, diminish in density towards the periphery

One cone to one axon so high va low sensitivity less aps generated. Can distinguish between photons and can process colour.
Populates the central 2 degrees.

Not ideal for scotopic conditions, sensitivity diminishes if light enters eye obliquely= stiles Crawford effect. Only in centre really.

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12
Q

The stiles Crawford effect

A

Rods are stimulated from any direction to generate an action potential.
Cones are stimulated only from central rays to generate the same action potential.

Brightness curve relating to distance from pupil centre. Central pupil= brightest and away from pupil edges are less bright. -3mm and 3mm from pupil is lowest and 0 is the highest so its a curve from -3 to 3mm. Pupil bright and edges lower

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13
Q

When is colour vision present and when is it not present- numbers

A

Colour vision is present when cones are stimulated so either in mesopic or photopic conditions. More than 3cd/m^3

Cv is absent during scotopic conditions so anything less than 0.001cd/m^3

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14
Q

Normal colour vision is what 3 classes of..

A

3 classes of photopigment which have overlapping spectral sensitivity allowing us to see a range of shades

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15
Q

Proportion of cones in the central retina and the near fovea

A

Central retina- R:G:B
40:20:1 so blue is scarce

Near fovea- R:G
1.2:1
3.9:1 so no blue at near fovea.

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16
Q

Clinically if we detect early damage to blue cones.. and what is this called
What degree field size is optimal and when is it scarce

A

Early sign of glaucoma

Small field tritanopia= losing sensitivity of blue wavelength photoreceptors. This can be observed due to a scarcity of short wavelength cones at the fovea.

2 degree field size is optimal and scarcity if field sizes subtend less than 0.5 degrees

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17
Q

If we do suspect tritanopia, how can we test this or detect it

A

Using short wavelength automated perimetry
This involves blue and yellow light sources in a normal visual fields analyser to detect early damage to blue cones

This effects a persons ability to see blue and yellow due to scarcity of short wavelength cones found at the fovea.

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18
Q

Brunescence of the crystalline lens

A

Browning or yellowing of it as we age
This acts as a blue light filter and it absorbs blue light

Crystalline lens also loses flexibility which can lead to presbyopia

Px who had cataracts may now be able to see lots of blue so they may need yellow tinted glasses to absorb some of that blue

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19
Q

retinal pigments at the back of the eye

A

Retinal pigments amounts may vary at the back of the eye for individuals
Different concentrations can impact AMD and the perception of colour will be different based on absorption characteristics present in the eye.

Different pxs have diff amounts of macular pigment and you can supply them w drugs to increase this to protect their eyes against amd. Supplements could also change absorption characteristics in the eyes impacting their perception of colour.

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20
Q

Trichromacy vs monochromacy

A

Trichromacy- all 3 cone pigments present and functioning

Monochromacy- truly colour blind as there is only 1 functioning pigment either one cone or just rods due to a genetic mutation. No overlapping on graph so no other shades seen.

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21
Q

Monochromat graph

A

Colour blind- only one functioning pigment. Caused by a genetic mutation that affects all 3 cone cells no overlapping.

Peaks at 100 percent which is wavelength a, wavelength b is absorbed 50 percent of the time but when light is absorbed it cant differentiate between a and b so it either produces an ap or it doesnt. A is 2 times as likely of being absorbed than b however can’t differentiate.

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22
Q

why does a monochromat have no colour discrimination

A

Absorption spectrum for a hypothetical photopigment
A photon of light wavelength A has the highest probability of being absorbed whereas wavelength b has half the probability of being absorbed. Eventhough a is 2 times as likely to be absorbed than b the pigment has no way of knowing which is which. There may be a difference in brightness but this is due to intensity no way of discriminating them

A monochromat is unable to distinguish between objects on the basis of wavelength alone. So there are 2 photons of light but when light is absorbed by this pigment it doesnt know if it is a or b it just either produces an action potential or it doesnt

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23
Q

Dichromat graph and why are these distinguishable

A

Spectra overlap a bit
But px cant see shades outside of that overlap

The quanta absorbed by the 2 photopigments is different so photons are distinguishable by their wavelength

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24
Q

Dichromats
Anomalous trichromats

A

Dichromates- anopes
If one pigment is missing. Long wavelength pigment missing so red (protanope) same for medium and short for green and blue. Pro deu Tritanope

Anomalous trichromats- anomalys
Pigment is there but it isnt fully functional
Abnormal long wavelength pigment Protanomaly same for medium and short wavelength pigments so deuteranomaly or Tritanomaly for green and blue respectively.

25
Q

The different forms of dichromacy

A

Typem Men. Women
Protanopes 1.0. 0.01
Deuteranope. 1.0. 0.01
Tritanope. 0.001. 0.001

26
Q

Anomalous trichromacy

A

Type. Men. Women
Protanomaly 1.0. 0.03
Deuteranomaly 4.9. 0.35
Tritanomaly unknowns for both

27
Q

Why does it affect men more

A

Bc they are recessive x linked defect
Men xy so only need one copy of defective allele

Mother -> son

Affects 8 percent of males and 0.5 percent of females
5 percent of males have Deuteranomaly check young males monocularly 1/12 have a cv defect.

28
Q

What are acquired colour vision defects

A

These are secondary features to pathology,
need to check eyes monocularly as these manifest often in one eye only.
Good eye can mask the other eye and defects can often also fluctuate in severity

29
Q

What type of drug can produce cv defects and how and how to monitor changes

A

Hydroxychloroquine in excessive amounts or in allergic reaction may produce a colour vision defect
Can use Oct to monitor changes

30
Q

Type 1 acquired cv defect

A

Type 1=
Similar to a protan defect. So red green
1MD found in macular dystrophy

31
Q

Type 2

A

Type 2 acquired defect is similar to deutan defect and is also red green
N2R
Retrobulbar neuritis and it affects the optic nerve

32
Q

type 3 acquired defect

A

Similar to a tritan defect
Blue yellow
CPR= (PX Is blue)
Found in many central and peripheral retinal lesions and in lesions of the visual pathway

33
Q

Acquired have what associated with more than 1 type
What pathway is vulnerable to acquired defects
What defect commonly occurs insidiously for what type

What is common with optic nerve defects

A

Acquired have a combination of characteristics normally associated with more than 1 type

The blue pathway is vulnerable to acquired defects so retinal lesions

Type 3 defects commonly occur insidiously

Red green defects are common with optic nerve defects

34
Q

What may an acquired cv defect be an early indication for

A

Indication of pathology if symptomatic
Can be used to monitor pathology progression

35
Q

Ishihara viewing distance and what are some facts about ishihara
How long do you view each plate for
Illumination
What light should be used

A

Ishihara= 75cm. Bc 8 letters 80-5=75cm
View each plate for a max 4 seconds bc ishi= 4 letters
Illumination= at least 250lux
No tungsten light bc sounds ugly and can lead to a slight red bias allowing px with a slight red defect to pass
Use fluorescent lighting if available= sounds beautiful.

36
Q

What is the ishihara test and what does it do

And what cant it do

A

Ishihara is a pseudoisochromatic test that makes use of confusion lines and if px confuse certain colours this can be plotted on a cie chromaticity diagram in order to detect the type of defect they have.

Pass or fail test. But it doesn’t test for severity or test for tritanopia. Screening test is very sensitive and even mild cv defects can lead to failure on several plates.

37
Q

Describe the standard test vs ones they have in practice

Describe the screening and classification plates

What is the criteria like for pass fail

A

Standard test= 38 plate ver. In practices= 24 plate abridged version.

Screening plates are used to detect the defect and if defect is found then we use classification plate in order to detect the type of defect. There are 2 classification plates which are plate 26,42

Screening plates:
Transformation plate- normal and abnormal see diff numbers, vanishing- abnormal doesnt see it, hidden digit= only seen by abnormal. Efficiency of test increased if hidden digit are excluded from the test bc it makes it fair.

2 mistakes = pass for 24 plate ver
3 mistakes= pass for 32 plate ver
8 mistakes or more= fail for 38 plate ver
Studies say 6 mistakes or more= cv defect

38
Q

City university test distance and what is it

A

Viewing distance= 35cm bc city=4 so 40-5 is 35

Derived from d 15, overcomes difficulties with sequencing and soiling of colour caps, can identify type and severity of defect.

39
Q

1st and 2nd version
What is it and what lighting

A

5 colours
Need to detect the one that is more similar
3 of the surrounding colours are average isochromatic confusions of protanopes, deutanopes and Tritanopes and the remaining one is the one that is the most similar to central spot.

Macbeth lamp should be used with this as this light source signs with the CIE chromaticity diagram, most practices dont have one which means= limited spectral lightband so this can bias some wavelengths

5 coloured targets per plate, subtends 1.5 degrees

40
Q

3rd edition

A

3 colour plates
Now detect colour that is different
Has 2 sections that can be used separately or in sequence

41
Q

D-15 test distance and what is it

A

50cm viewing distance bc 15=50
Arrangement test. Pilot cap placed and rest in sequence by the px

15 coloured caps, classifies defect and severity.
Plotted on diagram, more transverse along the circle more crossings= more severe
Orientation= type of defect.

42
Q

100 hue test what is it

A

Another sequencing one
85 coloured caps takes time to conduct and analyse. Computerised software for the data= polar diagram

This one is more sensitive at picking up cv defects
Angle of the spikes on polar diagram= what type of defect it is and how far they come out= severity

43
Q

Hardy rant Ritler
HRR

A

Like ishihara but it is with shapes, uses plates with shapes and patterns
Higher sensitivity than ishihara and can test for tritanopia. Can tell you severity.

24 plates
HRR tests for a wider range of deficiencies- blue or yellow loss as well which can help w diagnosing early glaucoma

44
Q

What do pseudoisochromatic tests involve

A

Involve looking for asymmetry in results

45
Q

CIE chromaticity diagrams what are they
What colours do cv defects confuse

A

2d dimensional representation of colour space
Different colours are arranged in x and y coordinates
Spectral colours are arranged along the arc of the perimeter of the diagram- different cv defects confuse colours that are placed along certain orientations

Protans confuse red purple with grey
Deutans confuse blue purple with grey

46
Q

Describe CIE chromaticity diagram again and confusion lines

A

Different px confuse colours along certain orientations which is then plotted on a CIE chromaticity diagram in order to detect their colour defect. Ultimately if a px has a cv defect depending upon which photoreceptor is affected they will confuse certain colours.

Protans confuse colours along one orientation and deutan another. Tritan confuse colours in an orientation of almost 90 degrees.

Confusion lines are made use of in designing pseudoisochromatic cv tests for example ishihara so if they pass the plate they arent confusing lines but if they fail then they are confusing lines that plot along certain confusion lines.
Introduce terms like dichromats and trichromats monochromats anomalous trichromats and how that differs for severity

47
Q

D-15 for normal vs protanopes deutanopes and tritanopes

A

Normal- all the caps should be connecting one after the other dot to dot
Protanope- starts from reference cap and goes straight down and then up. Lines are sort of left
Deutanopes- reference then to 1 and then goes down, more right compared to protanopes.
Tritanopes- connects till 7 then goes down to 18 then zig zags in sort of a almost 180 degree direction so facing to the right but almost straight right.

48
Q

D 15 rod monochromacy

A

Random so you can start from pilot to 1 then go down and then just random

49
Q

Severity with d15

A

More severe= greater numbers of crossings

50
Q

What are polar diagrams used with and what are they

A

Used with 100 hue test bc lots of data
Results are turned into a score and then plotted on polar diagram
Confusion lines relate to type of defect

Results of 100 hue tests can be plotted on a polar diagram cp 1234 all the way around to 85 in a circle. If cap 5 is plotted where cap 2 was we are out by 2. The angle and how far the spikes come out. Angle= what type of defect. Spikes coming out= severity of the cv defect

More sensitive than d15 at picking up cv defects

51
Q

Errors for protans Deutans and tritans

A

Protan= 15-26 and 58-68
Deutan= 12-17 and 53-60
Tritan= 4-6 and 45-46

52
Q

What are the 4 factors colour vision is important for

And list 4 reasons why we measure cv

A

Career
Education
Safety
Pathology

Managing paedtriatic cases
Giving vocational advice
Detecting ocular diseases
Monitoring ocular disease

53
Q

Rods vs cones illuminations numbers

A

Rod function at low levels of illumination (~120M)
Cones function at high levels of illumination (~7M)

54
Q

Ishihara standard is 38 plate ver
But for the 24 plate abridged version commonly found in practices (how many screening plates and classification plates are there)
What lighting is best

A

14 screening plates and 2 classification plates (26,42)

Daylight is best but not usually available so we use fluorescent which is acceptable
Tungsten shouldnt be used as it produces a slight red bias so may allow people with a slight red defect to pass

55
Q

Percent of colour vision deficiencies
What is the most common and whats the percentage

What are the statistics of men and women having a colour vision defect

A

Deuteranomaly 4.9 percent

Men= 8 percent (1/12)
Women= 0.5 percent (1/250)

56
Q

What can produce a cv defect if used excessively or in allergic reactions

A

Chloroquine

57
Q

What are acquired defects associated with? Loss of what

A

Loss of visual acuity and visual field defects (eg SWAP algorithm)

58
Q

Why is type III defects more common

A

As the blue pathway is more vulnerable to acquired defects (retinal lesions)