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Unit 14 Week 1 > Applied anatomy of the eye- diseases of eye > Flashcards

Applied anatomy of the eye- diseases of eye Flashcards

1
Q

What 3 main things do we need to see?

A
  1. clear cornea
  2. clear lens
  3. functioning retina and optic nerve
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2
Q

list other structures needed to see

A

Lateral Geniculate Nucleus

Edinger Westphal nucleus

CN III nucleus

CN IV nucleus

CN VI nucleus

Vestibular nuclei (gaze stability)

Occipital lobe- accommodation reflex, pursuit eye movements

Frontal lobe- voluntary eye movements

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3
Q

The cornea

function

made up of how many layers. name the layers

A

main function: refraction of light so that it correctly lands on the retina

made up of 5 layers

  1. epithelium
  2. Bowman’s layer
  3. Stroma (keratinocytes)
  4. Descemet’s membrane
  5. Endothelium
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4
Q

Epithelium of the cornea

A
  • several layers of cells
  • barrier to water and bacteria entering the cornea
  • maintains a smooth optical surface for refraction

constantly replaced

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5
Q

Endothelium of cornea

A

single layer of hexagonal cells

allows transport of nutrients (inc. glucose)

pumps water out to maintain clairty of stroma

never replaced

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6
Q

what are the 3 types of refractive error

A
  1. myopia (short sight)
  2. hypermetropia (long sight)
  3. astigmatism- defect in the eye lens caused by a deviation from a spherical curvature
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7
Q

what is emmetropia

A

normal vision

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8
Q

what shape of lens is used to fix:

  1. myopia
  2. hypermetropia
  3. astigmatism
A

concave lenses

convex lenses

cylindrical lens with a steeper vertical axis than horizontal

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9
Q

examples of corneal disease

A
  • corneal ulcer
  • corneal dystrophy
  • corneal oedema
  • corneal graft
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10
Q

the lens

does it refract light?

what is its main function

A

some refraction

main function is accomodation/ fine focus: circumferential ciliary muscle contracts, allowing the lens capsule to relax, meaning the lens becomes more spherical

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11
Q

what is cataract

causes of cataracts

how do you treat cataracts

A

clouding of the lens due to degradation of proteins in the lens

  • age
  • diabetes
  • corticosteroids
  • congenital
  • trauma

surgery to remove the lens and replace

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12
Q

the retina

consists of how many layers? name the layers

A

the innermost sensory membrane found on the inner surface of the posterior aspect of the eye. Contains many photoreceptors

13 layers

  1. nerve fibre
  2. ganglion cell
  3. inner plexiform
  4. inner nuclear
  5. outer plexiform
  6. outer nuclear
  7. external limiting membrane
  8. inner segment of photoreceptors
  9. IS/OS junction
  10. outer segment of photoreceptors
  11. retinal pigment epithelium
  12. Bruch’s membrane
  13. choroid
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13
Q
A
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14
Q

districution of cones and rods in the retina

A

cones- increasing concentration towards fovea

rods- none at fovea nit evenly spread throughout retina

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15
Q

what are the 2 kinds of photoreceptor in the eye

what kind of vision does each give

which light pigments are found in each

A

rods and cones

rods-scotopic vision stimulated by light over a wide range of intensities and are responsible for perceiving the size, shape, and brightness of visual images. They do not perceive colour and fine detail,

cones- high light photopic vision- colour vision, works best at high light levels

rods- rhodopsin

cones- iodopsin

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16
Q

how many kinds of opsins are present in cones?

what are the 3 colours

A

there are 3 different opsins found in cones however one type always predominates

blue

green

red

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17
Q

process of phototransduction

A

Light waves enter the pupil after being refracted from the tear layer and cornea.

  1. The lens further refracts the light onto the retina which is where the photoreceptors are populated (specifically the fovea)
  2. Photons from the light are absorbed by the photopigment (rhodopsin/iodopsin), specifically by opsin. This tunes the light and detects the particular wavelength on the spectrum.
  3. The absorption of light triggers the activation of transducin which activates a phosphodiesterase that hydrolyses cGMP.
  4. In darkness, high levels of cGMP in the outer segment keep sodium channels open, however in the light cGMP levels drop and some of the channels close leading to hyperpolarization of the outer segment. This ultimately reduces the opening of Calcium channels at the synaptic membrane and reduces glutamate being released into the synapse
  5. In the dark, the photoreceptors are in a depolarized state (membrane potential of roughly -40mV). As there is a progressive increase in the intensity of light, it causes the potential across the receptor membrane to become more negative (reaching -65mV)
  6. The drop in the glutamate neurotransmitter signals that light is present
  7. Photoreceptors in the outer plexiform layer stimulate horizontal cells which helps to identify the information that is passing through.
  8. Alongside this, the bipolar cells create direct or indirect connections to the ganglion cells in the inner plexiform layer
  9. The ganglion cells process the electrical information (alongside the amacrine cells). Their axons collectively form the initial part of optic nerve.
  10. The optic nerve (cranial nerve II)  exits via the optic disc on the retina
    a. Anything from the nasal visual field is projected onto the temporal retina
    b. Anything from the temporal visual field is projected onto the nasal retina
    c. (for example, light from the right visual field will hit the left eye’s temporal retina while hitting the right eye’s nasal retina)
  11. After the formation of the optic nerve, it leaves the bony orbit via the optic canal, a passageway through the sphenoid bone. It then enters the cranial cavity running along the surface of the middle cranial fossa.
  12. The optic nerve meets at the chiasm in which;
  13. Axons from the nasal retina cross over to the opposite sides, while the temporal retina information remain on the same side (this means that all information from the left visual field stay together and all information from the right visual field stay together)
  14. The optic tract then synapses with the cells in the lateral geniculate nucleus (part of the thalamus)
  15. Information from the contralateral side goes to layers 1, 4 and 6 of the LGN while information from the ipsilateral side goes to layers 2,3 and 5
  16. It then travels to the primary visual cortex in the occipital lobe via two main pathways;
    a. Upper optic radiation – (baum loop) this pathway carries fibres from the superior retinal quadrants (corresponding to the inferior visual field quadrants)
    b. Lower optic radiation – (Meyers loop) carries fibres from the inferior retinal quadrants (corresponding to the superior visual field quadrants)
  17. In the higher visual centre, it takes either the;
    a. Dorsal pathway (to parietal cortex) which subserves spatial vision providing an image of where the object is
    b. Ventral pathway (to inferotemporal cortex) providing an image of what the object is
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18
Q

examples of retinal diseases (5)

A

Colour blindness

Retinal vascular occlusion

Diabetes

Macular degeneration

Retinal detachment

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19
Q

colour blindness

A

anomaly if malfunctioning

anopia if vision is absent

red-green colour blindness is most common

tested for using ishihara plates

can be due to a genetic cause- X linked recessice- affects men more

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20
Q

central retinal artery occlusion

A

If the retina loses blood supply then the retina thins as cells die

Vision is very poor

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21
Q

diabetic retinopathy

A

Small blood vessels leak or get blocked. Leaks lead to oedema, exudation and haemorrhage in inner retinal layers.

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22
Q

Wet age related macular degeneration

A

New blood vessels grow from the choroid through the Retinal pigment epithelium. These leak and bleed causing oedema and haemorrhage in the outer retinal layers. This causes distorted vision as photoreceptors are displaced.

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23
Q

Why do we get distrotion with wet ARMD?

A

Each cone is responsible for seeing one part of the face and that is mapped exactly onto the occipital cortex.

If oedema separates the cones their pixels will be different.

The brain assembles the image as though cones are in the correct place, therefore, the image appears distorted.

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24
Q

retinal detachment

who is at a greater risk (2)

symptoms

A

Myopic or trauma are more prone to it.

As we age the vitreous which acts as a scaffold, keeping the retina in place, degenerates and become more liquid. The retina can move around. If the retina is still attached to some of the vitreous humor, the traction can cause a tear to form, through which fluid can leak behind the retina and cause detachment.

  • Flashing lights
  • Floaters
  • Shadow appearing in vision

Important to get retina attached ASAP, while it is not, the photoreceptors are not receiving adequate blood supply.

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25
Q

the optic nerve

describe the arterial supply to the retina and optic nerve

A

AKA CN II

composed of retinal ganglion cell axons and glial cells

  • extends from the optic disc to the optic chiasma and continues as the optic tract to the lateral geniculate nucleus, pretectal nuclei, and superior colliculus.
  • Fibres from superior part of the retina enter the superior part of the optic nerve with the inferior going inferior. Damage to the superior portion will cause inferior field defect.
  • Central retinal artery does not supply blood to the optic nerve but just to the retina. The optic nerve is perfused by the posterior ciliary arteries.
    *
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26
Q

Optic nerve problems can cause:

can be:

A
  • Reduced visual acuity
  • Altered colour vision
  • Visual field defects
  • Possible RAPD
  • Inflammatory (optic neuritis)
  • Glaucoma
  • Ischaemia
  • Compression
27
Q

optic neuritis

A
  • Presents as a progressive loss of vision over a few days which improves over 6-8 weeks.
  • Associated with red desaturation
  • Optic nerve may look normal
  • 50% of cases are related to MS or be post-viral
28
Q

galucoma cause

pathway of aqeous humor

A

Progressive optic neuropathy causing the loss of nerve fibre layer causing CUPPED OPTIC DISC appearance and corresponding VISUAL FIELD DEFECTS. Commonly associated with raised intraocular pressure.

Aqeous humor is produced by the ciliary body to provide nutrients to the lens and cornea. It flows into the anterior segment, in front of the lens and through the pupil.

It drains via the trabecular meshwork into Schiemm’s canal.

29
Q

anterior ischaemic neuropathy

A

Most commonly caused due to microvascular occlusion related to diabetes, hypertension, atherosclerosis disease but can be due to inflammatory cause including Giant Cell Arteritis. Posterior ciliary arteries affected.

30
Q

optic nerve compression

what can cause it

A

The eye, optic nerve and associated muscles are surrounded by fat and enclosed in a bony box known as the orbit. This provides protection but leaves little room for manoeuvre.

The optic nerve can be compressed by:

  • Inflammatory conditions (thyroid eye disease)
  • Infection (orbital cellulitis)
  • Haemorrhage

The eye, optic nerve and associated muscles are surrounded by fat and enclosed in a bony box known as the orbit. This provides protection but leaves little room for manoeuvre.

Can cause proptosis and compression of the optic nerve

31
Q

eye diseases by part of eye

A
32
Q

visual pathway

A

EXTRACRANIAL

  1. After its formation, the nerve leaves the bony orbit via the optic canal, a passageway through the sphenoid bone.
  2. It enters the cranial cavity, running along the surface of the middle cranial fossa (in close proximity to the pituitary gland).

INTRACRANIAL

  1. Within the middle cranial fossa, the optic nerves from each eye unite to form the optic chiasm. At the chiasm, fibres from the nasal (medial) half of each retina cross over to the contralateral optic tract, while fibres from the temporal (lateral) halves remain ipsilateral
  2. Each optic tract travels to its corresponding cerebral hemisphere to reach the lateral geniculate nucleus (LGN), a relay system located in the thalamus; the fibres synapse here.
  3. Axons from the LGN then carry visual information via a pathway known as the optic radiation. The pathway itself can be divided into:

upper optic radiation- fibres from superior retinal quadrants, through parietal to visual cortex

lower optic radiation- fibres from the inferior retinal quadrants, through temporal to visual

33
Q

visual field defects

A

Knowledge of the visual pathway and corresponding visual field defect allows us to locate the lesion.

The visual field is the portion of the subject’s surroundings that can be seen at any one time. If central field is lost then you’d suspect damage to the fovea.

34
Q

what visual field defect would an occipital infarct cause

A

total hemianopia but the macula area of the visual cortex is supplied by both the middle cerebellar artery and the posterior cerebellar artery.

35
Q

what kind of visual field defect would a pituitary lesion cause?

A

damage to the optic chiasm and the medial side of retina—bitemporal hemianopia

36
Q

if an object we’re looking at is moving, how does our brain still manage to keep it in focus?

A

pursuit eye movements and accomodation

eye movements are controlled by the 3rd CN (occulomotor), 4th (trochlear) and 6th (abducens) so movement info from the occipital lobe is via these nuceli.

pursuit movements- eyes ove in the same direction

accomodation- eyes move inwards

37
Q

accomodation reflex

how does pupil constriction occur

A

3 part reflex that brings near objects into focus through

  1. pupil constriction
  2. lens thickening
  3. inward rotation of eyes

test by asking them to look at a distant point and then a point up close

Edinger-Westphal nucleus supplies paraympathteic fibres to constrict the pupil, converge the eyes and accomodate the lens.

constriction via short ciliary nerve of the short ciliary nerve ganglion. Iris has circumferential muscle fibres.

zonules suspending the lens relax and the elastic capsule is also allowed to relax, allowing the lens to become more spherical.

38
Q

muscles of the eye and their innervation

A

CN III- SR, IR, MR, IO

CN IV- SO

CN VI- LR

39
Q

muscles and movements of the eye

A

Superior rectus: primary action is elevation, secondary actions include adduction and medial rotation of the eyeball.

- Inferior rectus: primary action is depression, secondary actions include adduction and lateral rotation of the eyeball.

- Medial rectus: adduction of the eyeball.

  • Lateral rectus: abduction of the eyeball.

- Superior oblique: depresses, abducts and medially rotates the eyeball.

- Inferior oblique: elevates, abducts and laterally rotates the eyeball.

40
Q

pupil response pathway and the concensual light reflex

A

In this reflex there is no involvement of the visual cortex.

  1. fibres from the optic tract peel off into the pretectal ganglion, which decussates into the Edinger-Westphal ganglion.
  2. Fibres then pass to the ciliary ganglion and via the short ciliary nerve causes constriction of the pupil.

This constriction is bilateral due to the nerve decussation.

In the absence of light, the pupil will then dilate again.

  • As different neurotransmitters are used for each system, we can use this to our pharmaceutical advantage to make topical drops that will either mimic the para constriction or symp dilation of the pupil.
  • Symp dilation useful in examining the fundus.

to test the consenual reflex, put your hand in a chop position over the nose, shine light into one eye and watch for the pupil of the other to constrict

41
Q

which part of the brain contributes to gaze stability

A

Input from the vestibular nuclei causes our eyes to compensate for movement of the head (gaze stability).

42
Q

which pathway in the brain is responsible for determining what we are looking at

A

the ventral stream

(from occipital to temporal lobe)

43
Q

which stream is responsible for where something is

A

the dorsal stream (occipital to frontal lobe)

spatial awareness and ability to find things

44
Q

which lobe of the brain responds to what we’ve seen

A

frontal lobe. connects to motor cortex that generates action plan

45
Q

summary of which parts of the brain are responsible for what

  1. pursuit and accommodation
  2. pupil reflexes
  3. keeping the image still
  4. what is it?
  5. where is it?
  6. what next?
A
  1. occipital cortex
  2. Pretectal and E-W nuclei, Parasympathetic and Sympathetic systems
  3. vestibular input
  4. ventral stream
  5. dorsal stream
  6. frontal lobe
46
Q

what is blindsight

A

Possible to shut off occipital lobes so info goes straight to frontal cortex and our bodies take appropriate actions. E.g., driving normal way to work.

47
Q

what causes pain in the eye

A
  • Foreign body
  • Trauma
  • Reduced tear film
  • Corneal epithelial disturbance
  • Inflammation
  • Raised IOP
48
Q

which 6 CNs are involved in vision?

A
49
Q

mechanisms of eye pain

A

Nociceptive- damage to non-neural tissue

Neuropathic- damage to nerve

Inflammatory- activation of nociceptors by inflammatory mediators

Sudden raised intra-ocular pressure- activation of nociceptors by ATP

50
Q

3 kinds of pain receptor in the eye

A
51
Q

anatomy of eyelid

A
52
Q

what is blepharitis and meibonianitis

A

Blepharitis has multiple types. Inflammation of eyelids/ meibomian glands causing discomfort

Meibomianitis- meibomian glands in the tarsal plate become inflamed or blocked

53
Q

what 2 components are tears made from

A
  1. aqueous aspect from lacrimal gland
  2. oily aspect from the meibomian gland (prevents aqeous component dehydrating)
54
Q

lumps and bumps on the eyelids

  1. cyst of moll
  2. stye
  3. chalazion
A
  1. from gland of moll (modified sweat gland), clear fluid filled blister, very common
  2. infected hair follicles, very painful, blocked sebaceous gland
  3. blocked meibomian gland
55
Q

eyelashes causinf pain

  1. entropion
  2. ectropion
  3. trichiasis
A
  1. eyelid turned in, lashes rubbing on cornea, fat shrinks and eye sinks in
  2. eyelid turned out, lashes do not cause problem, watering eye, fat shrinks and eye sinks in
  3. lashes turned in and rubbing on cornea
56
Q

eyelid summary

A
57
Q

the conjunctiva

bacterial and viral conjunctivitis

A

conjunctiva covers sclera of the eye, folds forward and also joins conjunctiva of inner eye

Bacterial conjunctivitis- sticky discharge,only lasts a few days,,,, viral is more watery and lasts weeks

Allergic conjunctivitis- chemosis, lid changes

58
Q

foreign bodies in eye

A

Subtarsal foreign body- can be easily wiped out

Corneal foreign body

59
Q

common corneal problems

A

Dry eyes- common, aqueous part of tear production not adequate causing epithelial cells to die, common in those with autoimmune diseases and age

Dendritic ulcers-

Corneal abrasions- epithelium continually produced at the limbus so abrasions can heal

Bacterial ulcer-

60
Q

which dye shows lesions or defects in the eye

A

Fluorescein dye shows epithelial defects

61
Q

flow of what fluid through the anterior chamber

A

Ciliary body produces aqueous that travels forward between the iris and the lens into the anterior chamber. Circulates and then leaves via the trabecular network intothe canal of Schlemm. If the outflow is blocked then intraocular pressure will go up.

62
Q

acute angle closure glaucoma

A

Severe pain (ATP mediated)

Vomiting

Reduced vision

Rainbow haloes (around lights as oedema altered refraction)

Aqueous has nowhere to go, goes through cornea and waterlogs it

mechanism for AACG

  • Happens in those that are hypermetropic (long sight, smaller eyes, therefore anterior chamber also smaller).
  • Shallower AC
  • Enlarged lens
  • Pupils dilate in low light
  • Iris sticks to enlarged lens
  • Aqeous cannot flow into AC and pushes iris forward
  • Iris closes off already narrowed angle
  • IOP rises
63
Q

what is yag laser iriditotomy

A

Prevents further attack of AACG- makes a little hole in the iris

64
Q

the iris (uveal tract)

A

Uveitis- inflammation of any or all of these structures (uveal tract- iris, ciliary body and choroid). Can be related to other systemic inflammatory diseases.

Acute anterior uveitis

Commonest form

Inflammation of the iris- causes eye to be red, can see inflammatory cells floating in the anterior chamber, yreat with steroids, can cause iris to stick to lens so dilation causes funny shaped pupil

Unit 14 Week 1 (3 decks)

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