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OD1 Semester 2 - Integrated Ophthalmic Sciences and Preclinical Optometry > BIOSYSTEMS: SEMINARS (2) - tear quality, bionic eye, colour therapy > Flashcards

BIOSYSTEMS: SEMINARS (2) - tear quality, bionic eye, colour therapy Flashcards

1
Q

What are the roles of the tear film? [tear quality #1]

A
  1. Protects and lubricates the eyes
  2. Prevents and reduces the risk of eye infection
  3. Washes away foreign particles
  4. Smooth refractive surface for clear vision
  5. Provides oxygen and nutrients to the surface of the cornea
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2
Q

Describe the chemical composition (in terms of polarity) of the lipid layer of the tear film [tear quality #1]

A

Hydrophobic outer layer: non-polar lipids (60-70%)

Hydrophilic inner layer: polar lipids (30-40%)

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3
Q

Which layer of the tear film is the main bulk of the tear film? [tear quality #1]

A

Aqueous layer

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4
Q

What are meibomian glands? [tear quality #1]

A

Oil glands located in the upper and lower eyelids

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5
Q

Roles of meibomian glands? [tear quality #1]

A
  • prevents tears from evaporating too quickly
  • role in increasing surface tension
  • protecting against bacterial infection
  • help maintain quality of tear film
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6
Q

What is Meibomian Gland Dysfunction (MGD)? [tear quality #2]

A

Either too much or too little secretion of meibum

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7
Q

How does inadequate meibum affect the eye? [tear quality #2]

A

Tears evaporate too quickly: get dry eyes

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8
Q

Name the pathophysiological mechanisms of MGD. [tear quality #2]

A
  • eyelid inflammation
  • cytokine release onto the cornea
  • microbial factors
  • lipid deficiencies
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9
Q

List the symptoms of MGD. [tear quality #2]

A
  • dryness
  • burning
  • itching
  • stickiness/crustiness
  • watering
  • light sensitivity
  • red eyes
  • foreign body sensation
  • chalazion/styes
  • intermittent blurry vision
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10
Q

What can cause a corneal infection? [tear quality #3]

A
  • bacteria
  • virus
  • injury
  • allergy
  • chemicals
  • dry eye
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11
Q

How can MGD lead to a corneal infection? [tear quality #3]

A
  • accumulation of inflammatory molecules at ocular surface
  • quantitative reduction or qualitative aberration of tear film
  • destruction of epithelial tight junctions resulting in sloughing of ocular surface epithelia
  • disrupting corneal epithelium allows opening for microbial invasion

Therefore, if you have MGD induced dry eye and bacterial colonisation: then you have increased risk of corneal infection

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12
Q

List the management strategies for MGD. [tear quality #4]

A
  • warm compress
  • gland probing
  • emulsion eye drops
  • lipiflow
  • N-acetylcysteine
  • topical azithromycin
  • oral supplements (omega 3)
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13
Q

Describe the steps of Gland probing. How effective is it? [tear quality #4]

A
  1. numb eye with aesthetic drop
  2. probe with 2mm probe at slit lamp
  3. (switch to 4mm probe if persistant tendernes)

24/25 patients had immediate relief (25/25 had long term relief)

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14
Q

When might warm compress be a problem for a px? [tear quality #4]

A

Might be a problem if px experiences burning eye sensation

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15
Q

Which MGD management techniques are most useful to target burning? [tear quality #4]

A

Emulsion eye drops and topical azithromycin

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16
Q

List the 10 layers of the retina in order [bionic eye #1]

A
  1. RPE
  2. Photoreceptor layer
  3. OLM
  4. ONL
  5. OPL
  6. INL
  7. IPL
  8. Ganglion cell layer
  9. Nerve fibre layer
  10. ILM
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17
Q

Describe the RPE: What constitutes it? Where is it? What is it’s role? [bionic eye #1]

A
  • single layer of melanin containing cells
  • between neural retina and choroid
  • part of blood-retinal barrier: transports nutrients to outer retina
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18
Q

Describe the barrier function of OLM: barrier between what? [bionic eye #1]

A

Barrier b/w subretinal space and neural retina proper

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19
Q

How does Retinitis Pigmentosa change the retina? [bionic eye #1]

A
  • impaired function and death of photoreceptors
  • bone-spicule pigment: RPE cells around inner retinal blood vessels
  • outer nuclear layer thinning
  • inner nuclear layer thickness remains the same in some cases (sometimes thickens, possibly due to aqueous flare)
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20
Q

What is the goal of retinal prosthesis? [bionic eye #2]

A

To restore vision by providing a sensory input to replace impaired/lost photoreceptors in Retinitis Pigmentosa

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21
Q

For retinal prosthesis to work, what must remain intact in RP patients? [bionic eye #2]

A

There needs to be an intact ganglion cell layer to transmit the signal to the brain

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22
Q

What happened in 1929 that helped lead to the development of retinal prosthesis? [bionic eye #2]

A

Discovery that electrical stimulation of visual pathways could result in phosphates being seen

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23
Q

What was the first retinal prosthesis? and when was it made? [bionic eye #2]

A

Argus I, in 2002.

24
Q

What was the first retinal prosthesis to be approved for retinitis pigmentosa? and when? [bionic eye #2]

A

Argus II, 2013

25
Q

Describe the features of Argus I and Argus II prostheses [bionic eye #2]

A

Argus I: a cochlear implant which ran a cable into the eye to stimulate 16 electrodes

Argus II: uses an external pair of glasses combined with an internal electrode array with a total of 60 electrodes

26
Q

How does the number of electrodes in a retinal prosthetic implant affect resolution? [bionic eye #2]

A

More electrodes = greater resolution

27
Q

Name 4 types of epiretinal implants/prosthetics [bionic eye #2]

A
  • Argus I
  • Argus II
  • Epi-Ret
  • IRIS V2
28
Q

How does the Epi-Ret differ from Argus II? [bionic eye #2]

A

Epi-Ret only has 25 electrodes (lower resolution). Although the main difference is that:
- to be able to implant Epi-Ret, you must remove the intraocular lens and vitreous

29
Q

How many electrodes does IRIS V2 have? [bionic eye #2]

A

Has 2 versions: 49 electrode and 150 electrode version

30
Q

Briefly describe the relative success of Argus II vs Epi-Ret vs IRIS V2 [bionic eye #2]

A

Argus II: moderate success in various aspects of vision
Epi-Ret: no published test results (however have been successfully implanted in humans)
IRIS V2: Subjects were able to perceive basic patterns like horizontal bars

31
Q

Where are subretinal prostheses implanted, and how can they be divided? [bionic eye #2]

A

Are implanted in that common location where photoreceptors are typically found. Can be divided into active and passive systems

32
Q

List one advantage and one disadvantage for suprachoroid retinal prosthesis? [bionic eye #2]

A

Advantage: minimal surgery needed for electrode array implementation
Disadvantage: Electrodes are further away from target rGCs compared to epiretinal (signal has to travel further)

33
Q

Where are S, M, and L cones located? [Colour Therapy #1]

A

S cones: Perifoveal

M and L cones: dense in fovea

34
Q

Describe the differences between:

Protan, Duetan, Tritan [Colour Therapy #1]

A

Protan: red-green deficiency (insensitive to red, overcompensate with green)
Duetan: red-green deficiency (insensitive to green)
Tritan: blue-yellow deficiency

35
Q

What 3 theories work together to explain how colour vision works? [Colour Therapy #1]

A
  • trichromatic theory
  • opponent processes theory
  • retinex theory
36
Q

On what chromosomes are the s-cone, m-cone and l-cones located? [Colour Therapy #1]

A

S-cones: Chromosome 7

M and L cones: Chromosome X

37
Q

Describe the visual pathway to the Anterior Infero-Temporal Cortex [Colour Therapy #1]

A

Cones – bipolar cells – ganglion cells – LGN – V1 – V2 – PIT (posterior IT) complex – anterior IT complex

38
Q

How does the anterior infero-temporal cortex contribute to colour vision? [Colour Therapy #1]

A

Contains colour selective neurons, presumably connecting from glob cells

39
Q

Why are M and L cone pigments prone to homologous recombination? [Colour Therapy #1]

A

Because they are 98% identical

40
Q

True or False: Tritan deficiencies affect males and females equally [Colour Therapy #1]

A

True

41
Q

Where are CVD frequencies highest? [Colour Therapy #1]

A

In Europe

42
Q

Describe the ratio of L:M cones in normal trichromats. Do they vary? [Colour Therapy #2]

A

Generally 2:1, and they are highly variable

43
Q

Why is it difficult to determine L:M cone ratio? [Colour Therapy #2]

A

Due to:

  • amino acid homology
  • large individual differences in the maximum wavelength of the L-cone photopigment
44
Q

Do L and M cones share a locus control region? [Colour Therapy #2]

A

Yes they do

45
Q

What factors influence the ratio of L:M cones? [Colour Therapy #2]

A

LCR (locus control region), mRNA and epigenetic changes influence this ratio

46
Q

What might be the reason why there are more L cones than M cones? [Colour Therapy #2]

A

Closer proximity of L genes to LCR (LCR has a slight bias for L-cones due to this proximity)

47
Q

Provide evidence for Neural Plasticity mechanisms in colour vision? [Colour Therapy #3]

A

1) Long term chromatic filter exposure in one eye in adults induced long term changes in colour perception for both eyes
2) and the fact that normal trichromats have variations in L:M cone ratio but still have similar colour perception to each other
- so the visual system uses experience information to compensate for genetic variation

48
Q

How do you maximise colour vision perception through neural plasticity? [Colour Therapy #3]

A

By adjusting post-receptoral gains at the nervous system level (R/G channels), based on experiences at the photoreceptor level

49
Q

How can neural plasticity help anomalous trichromats? [Colour Therapy #4]

A

can help them maximise their colour perception

50
Q

What type of anomalous trichromats have an abnormal cone, and what does this result in? [Colour Therapy #4]

A

X-linked anomalous trichromats have an abnormal cone which has a spectral sensitivity distribution shifted towards that of the other x-linked cone, resulting in decreased sensitivity of stimuli of different wavelengths

51
Q

How does the ‘gain’ of L cones in anomalous trichromats compare to normal trichromats? [Colour Therapy #4]

A

L cone gain is greater in anomalous trichromats

Anomalous: L cone gain = 0.92
Normal: L cone gain = 0.64

The result is that the higher gain allows unique yellow to still be perceptible, thus allowing some discrimination of red-green

52
Q

How can anomalous trichromats distinguish colours that normal trichromats cannot? [Colour Therapy #4]

A

Neural adaptation allows the perception and differentiation of colours that are otherwise expected to be metamers (based on cone spectral sensitivities)

53
Q

What is Gene Therapy? [Colour Therapy #5]

A

Treatment of a disease through the introduction of a functional gene copy into cells

54
Q

How does gene therapy for colour vision work? [Colour Therapy #5]

A

A recombinant adeno-associated virus (rAAV) delivers functional L-opsin to cones via subretinal injection

55
Q

How did the injection of functional opsin gene affect colour vision in monkeys? [Colour Therapy #5]

A

Injection with enough functional opsin gene was able to achieve a change in colour vision for red-green CVD monkeys

  • however changes in colour perception take a bit of time to occur

OD1 Semester 2 - Integrated Ophthalmic Sciences and Preclinical Optometry (49 decks)

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