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Sensory Neuroscience 316 > Physiological basis of retinal degeneration lecture 9 > Flashcards

Physiological basis of retinal degeneration lecture 9 Flashcards

1
Q

What are the retinal diseases looked at in this lecture/

A

Age related macular degeneration
Diabetic Retinopathy
Retinitis pigmentosa

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2
Q

What field of vision is lost with age related macular degeneration?

A

Central vision.

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3
Q

What is diabetic retinopathy in short?

A

Two stages:

Non-proliferative- Where bulges from micro aneurysms in the choroid impact vision.

Proliferative- Blood vessels create smaller blood vessels off themselves which are very leaky and leak blood+fluid onto the retina. Sometimes these blood vessels enter the vitreous.

All parts of visual field can be affected as the blood vessels could grow or leak anywhere.

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4
Q

What is retinitis pigmentosa?

A

Genetic condition where there is a mutation in the opsin protein, rods are effected first therefore resulting in tunnel vision.

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5
Q

What sort of view does an optometrist use to access retina damage?

A

Fundus view

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6
Q

Describe what is seen in a fungus view:

A

To one side there will be the optic disc which leads to the optic nerve, it is bright orange/yellow when the light is shone on it.

There is also a central point called the fovea (dark point) and a ring around it (macula)

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7
Q

What is found on the fundus view of someone with age related macula degeneration and what are they called?

A

Yellow spots in the macula area. They are called droosum

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8
Q

What are droosum?

A

Extracellular deposits of debris i.e fat etc

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9
Q

Why are droosum produced?

A

Due to RPE dysfunction

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10
Q

What is seen in a fungus view of retinitis pigmentosa?

A

Black spots i.e bone deposits

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11
Q

How many people over 50 have age related macula degeneration?

A

1.3%

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12
Q

Does age related macula degeneration affect one or two eyes?

A

Bilateral i.e two eyes.

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13
Q

What are the symptoms of AMD?

A
  • Painless
  • Blurring of central vision despite glasses
  • Blind spot may develop in central vision (sertoma)
  • Lines may appear wavy
  • Need a brighter light to read
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14
Q

What is the definition of AMD?

A

An abnormality of the retinal pigment epithelium that leads to degeneration of the photoreceptors in the macula and consequent loss of central vision

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15
Q

What is found between the choroid and the RPE?

A

Bruchs membrane

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16
Q

What characterises the pathophysiology of AMD?

A

Characterised by the accumulation of debris underneath the RPE basement membrane which forms drusen.

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17
Q

What is drusen?

A

Drusen are small, yellowish extracellular deposits of lipid, cellular debris and protein

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18
Q

What are the types of drusen?

A
  1. Hard drusen-develop in people over the age of 40; yellow, small in size and look round in shape
  2. Soft drusen-prevelant cause of AMD; pale yellow, no rigid border, larger in size than hard drusen and vary in size and shape
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19
Q

Is hard or soft drusen normal?

A

Hard druse is normal and is a physiological consequence of ageing. Soft drusen is the problem.

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20
Q

What are the forms of AMD?

A

Dry and Wet

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21
Q

What is the difference between dry and wet AMD?

A

Classified on the absence (dry AMD) or

presence (wet AMD) of blood vessels that have disruptively invaded the retina

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22
Q

What is more common dry or wet AMD?

A

Dry AMD

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23
Q

What are the stages of DRY AMD?

A

Early
Intermediate
Advanced (a.k.a geographic atrophy)

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24
Q

How is the stage of dry AMD determined?

A

By the size and presence of drusen

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25
Q

What defines the early stage of DRY AMD?

A

Early -defined by the presence of multiple (>5) small drusen or the presence of at least one intermediate drusen (drusen size of ≥63 μm but <125 μm).

26
Q

What defines the intermediate stage of DRY AMD?

A

Intermediate -refers to retina with many intermediate drusen or at least one large drusen (drusen size of ≥125 μm).

27
Q

What defines the advanced stage of DRY AMD?

A

Advanced-also known as geographic atrophy where there are large areas on depigmentation , especially in the macula

28
Q

Where does the drusen tend to cluster?

A

Around the macula

29
Q

What is wet AMD also known as?

A

Choroidal neovascularisation

30
Q

What defines wet AMD?

A

Growth of blood vessels into the retina which leak fluid or blood

31
Q

Describe the regions of the retina in terms of photoreceptors and sensitivity:

A

Fovea:

  • High density of cones, no rods at all
  • High visual acuity detailed vision

Periphery

  • Mostly rods
  • Sensitivity is high, resolution is optimised for courser information.
32
Q

What is the problem with AMD?

A

Photoreceptors in the macula area are damaged and die.

33
Q

What is typical of AMD onset?

A
  1. A patient may be unaware of the presence of retinal changes leading to AMD.
  2. Common ocular symptoms of early AMD are the slow, insidious onset of blurred vision
34
Q

What tests can optometrists use to diagnose AMD?

A

AMSLER grid:

  • Grid with parallel and perpendicular lines
  • Look at marked spot on grid and if lines appear wavy or blurry then possible effects of AMD
35
Q

Why do AMD patients have lines appear blurry?

A

Abnormal blood vessels leak blood and fluid and cause scar tissue, which push against the macula. This changes the macula’s shape and cause it to send distorted images
to your brain.

36
Q

What are the current treatment for wet AMD?

A
  1. Photodynamic laser surgery. This reduces the number of vessels and slows their leaking. (only lasts 1 year)
  2. Intravitreal injection of anti-VEGF
37
Q

What is the current treatment for dry AMD?

A

No treatment

38
Q

The dark spot of vision loss in AMD is known as?

A

Scartoma

39
Q

What is the underlying pathology in wet AMD?

A

Abnormal neovascularization, or angiogenesis, is the underlying pathology in wet AMD

40
Q

What is used in treatment of wet AMD?

A

Blockade of Vascular Endothelial Growth Factor-A (VEGF-A), a potent angiogenic factor, is the basis of available therapies for wet AMD.

41
Q

Describe how blood vessels form:

A
  1. Angiogenic stimuli activate endothelial cells (intracellular signalling cascade)
  2. Endothelial cells proliferate and migrate into the perivascular area, forming “primary sprouts”
  3. Lumenation of these primary sprouts, blood vessel maturation to complete tube like structures
42
Q

What drugs prevent VEGF binding?

A

Ranibizumab=Lucentis
Bevacizumab= Avastin

(requires an injection every 6 weeks)

43
Q

Whats another site of drug action to prevent angiogenesis?

A

Tyrosine kinase inhibitors that prevent the production of angiogenic factors

44
Q

What drugs target tyrosine kinases?

A

sirolimus

45
Q

What’s an alternative solution that is being heavily researched to prevent/ reduce the extent of vision loss?

A

Neuroprotective agents

- the end point of AMD is the apoptosis of retinal neurons, so we attempt to stop this.

46
Q

Whats of note when it comes to the AMD pathways?

A

There are a lot of different pathways and cross talk.

47
Q

Describe the AMD pathway:

A
  • Chronic oxidative stress (happens to everyone)
    + Iipofuscin (from visual cycle)
  • retina structure
  • chronic inlammation
    + abnormal compliment activity
  • Accumulation of extra+intracellular debris
  • Drusen formation and damage to photoreceptors and RPE
48
Q

Describe AMD pathway crosstalk:

A

Debris increase inflammation

Inflammation increases oxidative stress.

49
Q

What are some other targets of AMD therapy?

A
  • Antioxidants
  • Visual cycle inhibitors
  • Anti-inflammatory agents
50
Q

What do doses of antioxidants to for dry and wet AMD?

A
  • No effect for advanced dry AMD

- Reduces progression of CNV (wet AMD)

51
Q

What actually happened when antioxidants were given?

A

Antioxidants inhibit autophagy therefore be counterproductive to the removal of biological garbage.

52
Q

What do visual cycle inhibitors aim to do?

A

Reduce lipofuscin which is a toxic derivative of vitamin A.

53
Q

Is lipofuscin accumulation normal?

A

Yes, they are composed of lipid-containing residues of lysosomal digestion.

54
Q

What happens to lipofuscin in the presence of light?

A

It releases ROS

55
Q

What other pathologies are analogous to lipofuscin?

A

Beta-amyloid or tau proteins – Alzheimer’s Huntington proteins-Huntington’s
Lewy bodies-Parkinson’s

56
Q

Oxidative stress tends to form what in the retina?

A

Oxidative stress to the retina tends to promote lipofuscin formation.

57
Q

Describe how the visual cycle can contribute to lipofuscin formation?

A

all-trans retinal can leave the visual cycle pathway and bind to a protein called A2PE and this forms A2E protein that is toxic and contributes to lipofuscin formation.

58
Q

What have studies of visual cycle inhibitors found?

A

Slight to moderate inhibition of the visual cycle can significantly reduce the formation of toxic vitamin A derivatives without severely impairing normal vision • BUT despite these promising results, the existing visual cycle inhibitors are chemicals that may have undesirable side effects, including the potential to inflict further damage on the retina.

59
Q

What is the current though as to inflammatory origin in the retina?

A

Currently thought that it could be of endothelium origin, however part of the research community believes it is the RPE though.

60
Q

What is compliment activity?

A

They compliment the response of antibodies to infection.

61
Q

What have studies modulating the activity of compliment proteins found?

A
  • Replacement of defective complement compounds
  • Inhibition of the complement system
  • BUT the complement system is an important component of the immune system
  • Local or systemic complement inhibition may increase the risk of infections

Sensory Neuroscience 316 (32 decks)

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