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OD3 S1 > D - Ocular Ageing - Week 1 > Flashcards

D - Ocular Ageing - Week 1 Flashcards

1
Q

List 4 extrinsic factors that contribute to ageing pathology

A

Nutrition
Radiation (UV)
Stress
Smoking

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2
Q

Describe the pathogenesis of nuclear cataracts. Explain how the main symptoms of nuclear cataracts arise (2)

A

Nuclear fibres compact with age, increasing the density of the nucleus.
- The denser tissue leads to a higher refractive index = myopic shift.
- compaction leads to development of reflective crystallin deposits = glare

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3
Q

Describe how the increased density of the nucleus affects oxygen transport in nuclear cataracts (3)

A

Increased tissue density from nuclear compaction creates a “tissue density border” (= barrier for transport), resulting in:
- less oxygen flowing to the nucleus
- increased oxidative stress (from O2 pooling/accumulating at edge of nucleus inside)
- reduced antioxidant access to the nucleus

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4
Q

Describe how UV exposure affects a lens with nuclear cataract

A

Light (UV) exposure of oxygen generates free-radicals, which the lens proteins react with, causing protein cross-linking in the lens.

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5
Q

What does protein cross-linking of the lens lead to?

A

Nuclear cataract development.

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6
Q

Why does UV lead to cataract formation in a denser nucleus?

A

Because with a denser nucleus, the tissue density border prevents antioxidants getting in, meaning antioxidants can’t remove the free-radicals that get formed when the oxygen at the nucleus edge reacts with UV

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7
Q

How do antioxidants (such as glutathione/GSH, the one used for the lens) remove free-radicals?

A

They donate an electron to them to make them more stable/less reactive

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8
Q

Briefly outline the 3 key pathological changes that can happen in cortical cataracts

A

Fibre cell degeneration, liquefaction, and fragmentation

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9
Q

Describe the pathogenesis of cortical cataracts.

A

UV light exposure leads to fragmentation of the lens fibres, which release protein and break off into globules.

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10
Q

Describe the pathogenesis behind the progression of cortical cataracts into hypermature cortical cataracts (2)

A

As the cataract progresses, globules and denatured proteins accumulate in a “cleft”, leading to formation of a water diffusion gradient.
- This gradient attracts water to the lens fibre/cell in the cortex: resulting in the lens absorbing fluid and swelling up.

This process is known as “cortical liquefaction”

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11
Q

What is a cleft? (in relation to cortical cataract)

A

it literally just means the space between where the lens fibre has broken apart

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12
Q

What happens to the nucleus of the lens in a hyper-mature cortical cataract?

A

Eventually, the globules/abnormal protein replaces the entire cortex, resulting in complete liquefication of the cortex.
- The nucleus then sinks, by gravity, inferiorly

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13
Q

What does the lens look like in a hypermature cortical cataract?

A

A milk-filed sac.

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14
Q

How can cortical liquefication affect the appearance of the capsule in cortical cataracts?

A

If the fluid is small enough, it can escape through the intact capsule, resulting in a smaller-than-normal lens with a wrinkled capsule.

i.e. the capsule has wrinkles in it. (not always, obv)

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15
Q

How do globules form in a cortical cataract?

A

Fibres comprise a bi-lipid membrane layer which gets broken by UV. Sulphydryl bond crosslinking of lens proteins gives infolding, rounding and aggregation.

Thus causing the formation of globules.

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16
Q

What does the anterior and posterior lens sutures look like?

A

anterior: Y
posterior: upside-down Y

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17
Q

Briefly outline the key pathology behind posterior subcapsular cataracts

A

cytokine induced abnormal epithelial proliferation

18
Q

Describe the pathogenesis of posterior subcapsular cataracts

A

Excess levels of TGF-B at the lens equator result in overgrowth of lens fibre cells and cellular migration to the posterior sub-capsular area, where they form “bladder cells”

19
Q

Why do the fibre cells migrate to the posterior-subcapsular area in posterior-subcapsular cataracts?

A

Because this is where the concentration of TGF-B is lowest

20
Q

What is the role of TGF-B in the lens?

A

promotes growth of fibre cells

21
Q

Where in the lens does TGF-B go?

A

Flows around the lens and accumulates in the (equatorial) bow region as it flows to the AC (anterior chamber probs)

22
Q

Why do posterior sub-capsular cataracts affect vision a lot? What should be considered in response?

A

Because the bladder cells are in the nodal region/location. Consider surgery

23
Q

What may aberrant TGF-B expression in the lens be secondary to? (2)

A

Eye disorder
Corticosteroid use

24
Q

Describe the process of vitreous liquefaction (3)

A
  • UV or AGE (advanced glycation end products) damage the hydrophilic hyaluronan coating on the collagen fibres
  • so the fibres then collapse on each other as water is lost between them
  • results in a loss of gel structure with water pooling
25
Q

How may the collapsed fibres from vitreous liquefaction present?

A

Patients may see them as shadows

26
Q

What happens to the partial pressure of oxygen with vitreous liquefaction? How does this relate to cataract formation?

A

Increases. This increases oxidative stress on the lens which can lead to free radical production which promotes lens cross linking and cataract formation

27
Q

What are the hallmarks of dry and wet AMD respectively?

A

Dry AMD: change in pigmentation (hyper or hypo. Called Geographic Atrophy)
Wet AMD: blood vessel ingrowth

28
Q

How does an end-stage wet AMD patient present?

A

Disciform scar formation

29
Q

Describe the pathogenesis of AMD (6)

A
  1. With age, RPE cells lose ability to fully digest Photoreceptor outer segments
  2. Partially digested material form lipofuscin vesicles (protein+fat)
  3. Lipofuscin come together to form Basal lamina deposits (BLamD), which occupy RPE space, impairing RPE function
  4. BLamD is shed by the RPE, leading to Basal Linear Deposits (BLinD) [fat] and sub-retinal drusen [protein]
  5. Cholesterol coats this material & deposits in bruch’s membrane, which restricts clearance and exchange from RPE
  6. Choroidal vessels fail to get VEGF support = shrink + atrophy
  7. Gives relative hypoxia/exchange
30
Q

What is likely to happen in AMD when a patient is -ve for factor H?

A

immune response promoted. Wet AMD

31
Q

What is likely to happen in AMD when a patient is +ve for factor H?

A

Immune response suppressed, resulting in lower immune response. RPE undergoes apoptosis. Dry AMD

32
Q

What is the earliest detectable change in AMD?

A

basal lamina (BLamD) and basal linear (BLind) deposits

33
Q

Where are basal lamina deposits located?

A

Between RPE membrane and RPE basal lamina

34
Q

Where are basal linear deposits located?

A

Between RPE basal lamina and bruch’s membrane

35
Q

Do we have a way to remove basal deposits? Why can’t AMD patients just use this?

A

Yes, Glia. However with age the number of deposits exceeds the clearing capacity of the glia.

36
Q

Why can cholesterol be found in the space between RPE and bruch’s membrane in AMD patients? What does the cholesterol do there?

A

current theory: cholesterol deposited in bruch’s from the choriocapilaris
- there, they coat the basal deposits

37
Q

What are BLinD and drusen rich in?

A

cholesterol and apolipoproteins

38
Q

Which drusen are normal retinal deposits with ageing? Hard or soft?

A

hard

39
Q

What causes drusen to soften?

A

softened by high composition of lipid (cholesterol + BLinD

40
Q

What does drusen coated with cholesterol affect? (2)

A

impedes metabolic exchange and induces a low grade inflammatory response (C3/C5) to membrane/lipid deposits

41
Q

Why can’t RPE cells fully digest photoreceptor outer segments in AMD?

A

Due to UV exposure, either the RPE cells or outer segments themselves get damaged via oxidative stress from free-radical generation

OD3 S1 (25 decks)

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