The ageing eye Flashcards

(70 cards)

1
Q

which ocular diseases develop more likely as we age

A

cataract
glaucoma
AMD

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2
Q

what things does a decline in visual function with age have a significant impact on in terms of quality of life

A

affect mobility
are a major contributory factor to falls
are implicated in many road traffic accidents

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3
Q

list the age related changes which occur to the external part of the eye

A
  • enophthalmos - eyes sunken in, loss of fat behind the eye
  • loss of skin elasticity
  • loss of muscle tone
  • ptosis - loss tone of elevator palpebrae, enzymes which destroy collagen up regulate as we age
  • ectropion - decreased muscle tone of orbicularis oculi
  • epiphora - tears pool in eye and spill out
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4
Q

what occurs with the tear film with age

A

change in tear constitution & reduction in tear volume as tear production goes down

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5
Q

what is the consequence in the reduction of tear production as a function of age

A

dry eye

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6
Q

which particular components of the tear film reduces with age, and causes dry eye

A

serous & sebaceous component reduces

mucous component stays the same

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7
Q

list the components of the cornea which does not change with age

A
  • epithelium (as it continually renews by the gimbal stem cells)
  • bowman’s layer
  • stroma
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8
Q

list the components of the cornea which do change with age

A
  • descemet’s layer thickens (10-18um)
  • endothelium - amitotic cells increase in size and lose their regular (hexagonal) outline as neighbouring cells die
    with age, there is a decrease in cell density and an increase in variability of cell size (polymegathism) and shape (pleomorphism)
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9
Q

what is the name for corneal endothelial cells increasing in variability of cell size

A

polymegathism

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10
Q

what is the name for when corneal endothelial cells change in cell shape

A

pleomorphism

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11
Q

what is arcus senilis

A

cholesterol deposits (lipid) in peripheral corneal stroma

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12
Q

what happens to corneal sensitivity with age and why

A

declines, due to loss of nociceptors (pain receptors)

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13
Q

how is corneal sensitivity measured

A

by poking a long piece of nylon into the eye, and shorter and shorter as it gets more stiff until pain is felt, and length of nylon chord indicates corneal sensitivity

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14
Q

what happens to the pupil diameter with age and what is it called

A

decreases, called senile miosis

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15
Q

what is a consequence of senile miosis

A

less light reaches the retina

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16
Q

what is the circular iris sphincter muscle innervated by

A

parasympathetic nervous system

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17
Q

what does the circular iris sphincter muscle cause the pupil to do

A

constrict (miosis)

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18
Q

what is the radial dilatator muscle innervated by

A

sympathetic nervous system

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19
Q

what does the radial dilatator muscle cause the pupil to do

A

dilate (mydriasis)

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20
Q

list the possible reasons why senile miosis can occur

A
  • loss of sympathetic tone = decreases innervation of dilatator muscle (most likely cause)
  • degeneration of the dilatator muscle (although muscle starts to degenerate before senile miosis occurs, so maybe not a possible reason)
  • increased rigidity of iris blood vessels - so pupil can’t dilate as much as it used to
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21
Q

what type of structure is the lens and what layers does it consist of

A

trilaminar structure, consists of:

  • capsule (elastic outer)
  • epithelium (on anterior surface)
  • stroma (elongated lens fibres)
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22
Q

at what rate are new lens fibres laid

A

5 shells every year

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23
Q

what happens to the lens as more fibres are laid every year

A

lens gets bigger (which has consequences)

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24
Q

how are new lens fibres formed

A

formed from epithelial cells at the lens equator,

the epithelial cells immigrate into the stroma & elongate in a back to front direction & form the lens fibres

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25
what does the lens never lose
any of its cells
26
at what age does the eye stop growing, and what implication does this have as the lens keeps growing
eye stops growing at 15, this means anterior chamber depth will decrease with age (angle gets less) = increased risk of glaucoma as it impedes the drainage of aqueous
27
what are the lens sutures, (where the lens fibres join) described as in a young lens
y shaped
28
what are the lens sutures, (where the lens fibres join) described as in an aged lens
star like as numbers increases
29
what do star shaped sutures cause in an old lens
scattered light
30
how much light does a young clear lens allow through
more wavelengths of light, so doesn't remove any visible wavelength
31
how much light does an old 'yellowing' lens allow through
allows less blue wavelength light through
32
what can be a reason for the yellowing of the lens
the amount of soluble crystalline (protein) probably form insoluble aggregates with age (crystallines clump) due to UV exposure and so the soluble crystalline goes down with age, results in reduced transparency and increased scatter
33
as well as an increase in insoluble aggregates of crystalline, what else within the crystalline lens increases with age and what does this cause
crystalline lens fluorescence increases flourophores within the lens excited by UV light emit visible (blue/green) light, this stray light will result in intraocular veiling glare (scattered light) and reduce the contrast of the retinal image
34
at rest, what state is the eye in
emmetropic, focused for distance
35
at rest, what condition is the ciliary muscle in and what does this cause to the lens
ciliary muscle is relaxed and exerts tension on the lens via suspensory ligaments
36
what occurs with the ciliary muscle during accommodation for near vision and what does this cause to the lens
ciliary muscle contracts, moving the ciliary body forwards and inwards. the ciliary body thus acts like a sphincter and approaches the lens. the resulting release in tension allows the elastic nature of the capsule to increase the thickness of the lens increasing its refractive power
37
what does accommodation cause to the tension of the lens
decrease
38
what is presbyopia
loss of accommodative ability with age
39
what are the possible causes of presbyopia
- increased sclerosis (hardening) of lens fibres | - loss of elasticity of lens capsule
40
what is the description of the muscle fibres of the ciliary body of a 1 year old
smooth muscle fibres of the ciliary body, spindle shaped cells
41
what is the description of the muscle fibres of the ciliary body of an elderly person
inclusion of connective tissue 'whorls' make the old ciliary muscle appear degenerate
42
although an elderly persons ciliary body muscle fibres appearing degenerate, what does this indicate about its function
physiological studies indicate it is still functional
43
describe the experiment that was demonstrated to show that the cause of presbyopia reside within the lens
- the ciliary body with the lens attached was stretched - the focal point of the lens was determined with laser beams (to see if it came to the focal point) - while young lens could be deformed (change point where to focus) - older lens could not (change focal point of laser beam)
44
what happens to the rate of aqueous production with age
production rate declines
45
what is the rate of aqueous flow at age 15
3 ul/min
46
what is the rate of aqueous flow by age 80
2.25 ul/min (declines) = 25% of production decreases from 15-80 yrs old
47
what can be the reason for the decrease in rate of aqueous production
epithelium of ciliary body losing cells as we age, (as that produces aqueous)
48
what is the conventional and unconventional ways in which the aqueous drains and decreases as we age
- canal of schlemm (conventional) & - through uveoscleral 9ciliary muscle) pathway (unconventional)
49
why is there an accumulation of debris in the canal of schlemm, ciliary muscle & trabecular meshwork as we age
as trabecular meshwork cells degenerate
50
what changes occur in the vitreous humour as we age
liquid component increases | gel component declines
51
what can the liquefaction of the vitreous humour cause
- increased risk of posterior vitreous detachment (from retina) - floaters
52
what are the minor and major changes which occur in the retina as we age
- minor changes = RGCs decrease | - major changes = in outer retina e.g. RPE & photoreceptors
53
what is the RPE of the retina responsible for
the phagocytosis of spent outer segment dies
54
what happens to the RPE as we age
lipofuscin, the 'waste product' of the process of the phagocytosis of spent outer segment accumulates
55
what does the RPE of young eyes mainly contain
melanin
56
what does the RPE of older eyes mainly contain
lipofuscin granules
57
which photoreceptor in the retina changes significantly with age
the number of rods, (within a region 8mm in diameter centred on the fovea) reduces cones in centred fovea does not change significantly with age
58
what are the reasons for scotopic visual sensitivity (don't see well in low light levels) declining with age
- decreased pupil size - increased opacity of lens (yellowing lets through less photons) - reduced number of rods - more lens sutures
59
what are the neural factors (other than rod loss) are involved in age related loss in scotopic sensitivity
the rate of dark adaptation decreases with age i.e. the rate of rhodopsin (visual pigment) regeneration is impaired in the elderly
60
what is the overall process of pigment regeneration
photons turning all trans retinal into 11 cis
61
list the step by step process of pigment regeneration
- light acting on 11 cis retinal and opsin combined - straightens out the retinal to be all trans retinal, which wants to go back to 11 cis retinal - which can't happen in the photoreceptor - so all trans retinal diffuses out of the photoreceptor & goes into the photoreceptor matrix - and binds onto proteins such as retinal binding protein - and gets transported to the retinal pigment epithelia in the retinal pigment epithelium - the all trans retinal is turned back into 11 cis retinal - this goes all the way back to the photoreceptor which joins onto opsin & forms the visual pigment - so visual pigment regeneration involves the RPE which is less efficient in the elderly
62
how must new retinal which is only consumed via our diet, get transported to the RPE
from the choroidal vasculature and therefore must cross bruch's membrane
63
how may visual pigment regeneration (in which bleached retinal must go from photoreceptors into the RPE) be impaired with age
- bruch's membrane thickens - debris/lipofuscin accumulates between the RPE and bruch's - reduced hydraulic conductivity of bruch's - changes in the RPE cell structure - or there may be problems with transfer from RPE to photoreceptors
64
what effect does high light levels have on the visual function of older people
no major effect (may look bit darker)
65
what effect does low light levels have on the visual function of older people
impairment is more severe
66
which part of contrast sensitivity especially declines with age
intermediate and high frequencies
67
what are the causes of the decline in visual acuity with age
optical component is more important than neural factors eg: - increased intraocular scatter (more sutures in lens) - increased aberration e.g. chromatic and longitudinal spherical aberration - reduced retinal illuminance due to: senile miosis increased lens density
68
how is temporal resolution decreased in old age
fusion flicker frequency decreases so the older find it harder to see moving objects
69
list the things that impaired temporal resolution can lead to
- problems driving - increased search time - mobility problems some of these defects are caused by impaired processing beyond the retina
70
how does the yellowing of the lens with age effect colour vision
decrease in short wavelength sensitivity i.e. can no longer or reduced amount of seeing blue as its like looking through a yellow filter