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brain and behaviour > eye and retina physiology > Flashcards

eye and retina physiology Flashcards

1
Q

what is visible light?

A

electromagnetic radiation between the wavelengths of about 400 nanometers (blue) and 750 nm (red)

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2
Q

what length of EM radiation can we absorb?

A

shorter wavelengths

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3
Q

what is colour blindness?

A

inability to detect some wavelengths

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4
Q

how many people are affected by colour blindness in the UK?

A

affects 8% of UK men and 0.5% of UK women

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5
Q

what is the lacrimal apparatus?

A

lacrimal glands and associated ducts

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6
Q

what do lacrimal glands do?

A

secrete tears which provide an optically smooth refracting surface

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7
Q

what is the function of tears?

A

provide an optically smooth refracting surface

contain antibodies and lysozymes to prevent bacterial growth

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8
Q

what is lacrimation?

A

secretion of tears

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9
Q

what stimulates lacrimation?

A

stimulated by parasympathetic stimulation via the facial nerve

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10
Q

describe the steps of lacrimation stimulation

A

o Preganglionic parasympathetic efferents travel in the facial nerve (VII)
o Branch off in the greater petrosal nerve which goes to the pterygopalatine ganglion (PPG).
o Post ganglionic fibres from the PPG innervate the lacrimal glands and also stimulate nasal secretions over the olfactory mucosa

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11
Q

what are the layers of the eye and what do they contain?

A

outer - sclera, surrounds eyeball. continuous with the dura mater around optic nerve
middle - blood vessels, connective tissue, includes the iris, ciliary body and the choroid
inner - retina

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12
Q

what does the sclera become on the front of the eye?

A

the cornea

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13
Q

what is the sclera visible as?

A

the white of the eye

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14
Q

describe the structure of the sclera

A

continuous with the dura mater around the optic nerve
exterior is smooth and white
interior is brown and grooved
tendons attach to it

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15
Q

describe the properties of the sclera

A

tendons attach to it

flexibility adds strength

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16
Q

what controls the size of the pupil?

A

sphincter muscles

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17
Q

what is the pupil? what is its average size?

A

the hole through which light passes – diameter between 3-7mm

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18
Q

what does eye colour depend on?

A

the amount and distribution of the pigment melanin

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19
Q

what is the cornea?

A

the clear bulging surface in the front of the eye

the main refractive surface on the eye

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20
Q

what is the index of refraction of the cornea?

A

1.37

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21
Q

describe the structure of the cornea

A

o Normally transparent, uniformly thick
o Nearly avascular
o Richly supplied with sensory unmyelinated nerve fibres from trigeminal nerve
o Sensitive to foreign bodies, cold air and chemical irritation

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22
Q

where does the cornea get its nutrition from?

A

the aqueous humour

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23
Q

how do tears help the cornea?

A

maintain oxygen exchange and water content – prevent scattering and improve optical quality

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24
Q

what is the conjunctiva?

A

Layer of stratified columnar epithelium, goblet cells and capillaries that covers the sclera and the inside of the eyelids

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25
Q

what are the layers of the conjunctiva?

A
  • Palpebral conjunctiva – on the inner eyelid

* Bulbar conjunctiva – on the eyeball

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26
Q

what is the function of goblet cells in the conjunctiva?

A

Layer of stratified columnar epithelium, goblet cells and capillaries that covers the sclera and the inside of the eyelids

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27
Q

where does light go after entering the cornea?

A

anterior chamber –> pupil –> lens –> posterior chamber

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28
Q

what is the anterior chamber filled with?

A

aqueous humour

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29
Q

what is the posterior chamber filled with?

A

vitreous humour

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30
Q

what produces the vitreous humour?

A

glial cells in the retina

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31
Q

what is the function of the vitreous humour?

A

o Holds the shape of the eye to make sure its constant – maintains focusing accuracy

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32
Q

what is the aqueous humour?

A

like CSF – a nearly protein free filtrate of blood

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33
Q

what makes the aqueous humour?

A

the ciliary body

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34
Q

describe the passage of the aqueous humour in the eye

A

• Formed by the ciliary body –> circulates behind the iris –> through the pupil –> into the anterior chamber –> drains into the canal of Schlemm

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35
Q

what is the canal of Schlemm?

A

a venous sinus

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36
Q

what keeps the cornea as a sphere?

A

intraocular pressure

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37
Q

what is the normal intraocular pressure of the cornea?

A

between 10 and 21 mmHg

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38
Q

where is visual acuity highest?

A

fovea

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39
Q

what is the fovea?

A

a small central point composed of closely packed cones (centre of the macula)

40
Q

what is the blind spot?

A

where visual axons leave the eye to form the optic nerve. Slightly lateral to fovea - no photoreceptors here

41
Q

what produces the intraocular pressure?

A

the difference between the formation and drainage of aqueous humour

42
Q

how can you measure the intraocular pressure?

A

by pressing on the cornea and measuring the indentation

43
Q

what happens if aqueous humour drainage is blocked?

A

pressure in the anterior chamber rises

Increases pressure on the vitreous humour –> presses on the retina

Prolonged pressure damages the retina and causes glaucoma

44
Q

what are the 2 main sub-groups of glaucoma?

A

open angle glaucoma (chronic simple)

closed angle glaucoma (acute)

45
Q

what is open angle glaucoma? what is the angle between the cornea and the iris?

A

slowly progressive condition which occurs when Sclemm’s canal gradually becomes blocked.

Angle between the cornea and the iris is open – normal (abt 40 degrees)

46
Q

what is closed angle glaucoma? what is the angle between the cornea and the iris?

A

occurs when the iris is pushed forward. Angle between cornea and iris is reduced (may decrease to near 0). Blocks canal of Schlemm and causes a rapid rise in pressure inside the eye –> extreme pain and vision loss

47
Q

how can glaucoma be treated?

A

surgery

drugs

48
Q

describe how the surgery for glaucoma works?

A

incision is made in the sclera at the cornea-sclera junction

o Allows aqueous fluid to drain out onto the surface of the eye –> lowers pressure

49
Q

what is the aim of drug treatments for glaucoma?

A

to reduce intraocular pressure by reducing aqueous humour formation or increasing drainage

50
Q

how are drugs for glaucoma applied?

A

topically to the eye

51
Q

what do prostaglandin analogs do?

A

increase outflow of aqueous humour through Schlemm’s canal

52
Q

what do • Beta-Adrenergic Receptor Antagonists do?

A

decrease aqueous humour production

53
Q

what do Alpha 2 Adrenergic Agonists do?

A

decreasing aqueous production, increasing outflow

54
Q

what do Parasympathomimetic Agonists do?

A

anticholinesterases, contraction of ciliary muscle (opens canal)

55
Q

what do carbonic anhydrase inhibitors do?

A

inhibit carbonic anhydrase in ciliary body: lower secretion of humour

56
Q

why is surgery the preferred treatment for glaucoma?

A

Decreasing production of aqueous humour can have adverse effects

57
Q

why is UV light harmful to humans?

A

catalyses the formation of free radicals in the cells

58
Q

what cells protect us against UV light and how?

A

Melanocytes produce melanin (darkens skin) which absorbs the UV light and stops it damaging other skin cells

59
Q

how are the lens and inner cornea protected against free radial damage?

A

Aqueous humour contains antioxidants (Vitamin C etc)

Slightly alkaline nature activates vitamin C –> increases antioxidant activity

60
Q

how do cataracts occur?

A

antioxidant level is too low/too much UV light absorbed –> lens becomes gradually opaque bc UV light cross links protein in the lens –> eye is unable to see
as by products of another condition

61
Q

what conditions can cause cataracts?

A

diabetes

hypertension

62
Q

what are risk factors of cataracts?

A

exposure to UV light, infrared light or microwaves

63
Q

how can you decrease the risk of cataracts?

A

if the diet is high in Vitamin C and E

64
Q

what is the treatment for cataracts?

A

surgical replacement of lens

65
Q

what cells are found in the fovea?

A

cones

66
Q

which is more detrimental to vision; foveal damage or peripheral retina damage? why?

A

foveal damage

cones are most closely packed in the fovea

67
Q

where in the eye are photoreceptors not found?

A

blind spot

68
Q

what are the photoreceptors?

A

rods and cones

69
Q

what sight do cones allow for? when are they active?

A

Allow us to see in detail, active in daylight

70
Q

what are the types of cones and how are they different?

A

3 types of cones with slightly different sensitivities to wavelength of light allow us to see different colours

71
Q

which photoreceptor is most dense?

A

rods

72
Q

where are rods found?

A

outside the fovea

73
Q

how many types of rods are they?

A

1

74
Q

what sight do rods allow for? when are they active?

A

o Active in the dark

o No colour differentiation – suppressed in daylight

75
Q

why are we able to differentiate colour?

A

our brains compare the signal occurring in two or more cone populations

76
Q

describe the structure of photoreceptors?

A

outer segment - photoreceptive part

inner segment - cell body and synaptic terminal

77
Q

what do the outer segments of rods contain?

A

disks of membrane with rhodopsin

78
Q

what is rhodopsin?

A

a protein complex that reacts to light

79
Q

what is the cone equivalent of rhodopsin?

A

cone opsins

80
Q

what is the advantage of rods having a stacking arrangement in their outer segment?

A

means that light passes through all plates in sequence, maximising chance of a photon interacting with a molecule of photopigment.

81
Q

why do cones fold their membrane?

A

shorter outer segment –> enough light in daylight to guarantee photon will interact with a photopigment

82
Q

why does the eye require so much oxygen?

A

bc photoreceptors are the most metabolically active cells in the body

83
Q

what is dark current?

A

o In the dark, there’s a constant inward leak of sodium in the outermost  keeps the cell depolarized and tonically releasing glutamate from its synaptic ending

84
Q

how does light affect the dark current?

A

• Light hyperpolarizes the cell –> stops tonic glutamate release

85
Q

how does light absorption affect rhodopsin?

A
  • Absorption of light changes the shape of rhodopsin
  • Changed rhodopsin acts via G-protein to reduce level of cyclic GMP in the rod
  • Reduction of c-GMP closes the sodium channel  cell hyperpolarizes and stops releasing glutamate  synaptic transmission
86
Q

what do bipolar cells do?

A

convert constant release of glutamate into varying depolarization

Transmitted to ganglion cells which project their axons into the optic nerve

87
Q

what are the 3 main neurons in the path from photoreceptor to optic nerve?

A
  1. photoreceptors that connect to
  2. bipolar cells that connect to
  3. ganglion cells that send axons into the optic nerve
88
Q

what are horizontal cells?

A

interneurons that modulate transmission at the synapse between photoreceptor and bipolar cell

89
Q

why does the retina have a dual blood supply?

A

to cope with the demands of photoreceptors for oxygen

90
Q

what forms the inner retina?

A

ganglion and bipolar cells

91
Q

what blood vessel supplies the inner retina?

A

central retinal artery

92
Q

what supplies the photoreceptors?

A

choroid

93
Q

what is the choroid?

A

network of capillaries supplied by the ciliary arteries – branch off the ophthalmic artery and penetrate the sclera at the back of the eye

94
Q

how does oxygen diffuse into photoreceptors?

A

from choroid capillaries through pigment epithelium

95
Q

when photoreceptors grow new membranes, what happens to the old membrane?

A

new membrane at the cell body gradually gets transported outwards –> old, worn out membrane is being shed at the distal tip of the cell
Epithelial cells phagocytose the worn-out ends of the photoreceptors and transfer the debris into the capillaries of the choroid

96
Q

what happens in retinitis pigmentosa?

A

pigment epithelial cells don’t carry away the cellular debris fast enough –> accumulates as black pigment in pigment epithelial layer
o Gradually thickens and decreases the diffusion of O2 to photoreceptors
o Photoreceptors become so hypoxic they die –> patient slowly goes blind

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