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s3 - MSK, Derm, Cardio, Neuro, Pharm > Visual and Auditory Systems > Flashcards

Visual and Auditory Systems Flashcards

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Dermatology Board Prep flashcards
1
Q

What makes the aqueous humor in the eye?

A

Ciliary body

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2
Q

Where is aqueous humour drained?

A

-trabecular meshwork into Schlemm’s canal at the limbus (the joining point of the cornea and sclera)

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3
Q

What does the iris control?

A

how much light enters via pupil size

enough for brightness, not too much for clarity

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4
Q

The layers of the eye are: fibrous, vascular and neural. What are the 4 layers of the neural retina?

A
  • RPE (part of the non-neural retina)
  • Photoreceptor layer
  • inner nuclear layer (interneurones)
  • Ganglion cells
  • (Vitrious)
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5
Q

Why do you have course vision at peripheral retina?

A
  • before light reaches cones it passes through many translucent layers, light gets scattered
  • cones are large, widely spaced and converge to 1 GC
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6
Q

How is vision much clearer in the central retina?

A
  • foveal pit has no overlying layers (no scattering)
  • red and green cones detect detailed vision
  • cones are slender, packed close, + no convergence
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7
Q

Damage infront of the chiasm leads to…

A

different deficits in both eyes

vs behind chiasm would be matching

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8
Q

What is involved in constriction of the pupil?

A
  • SHORT ciliary nerves innervate sphicter pupilae

- CNIII, Ach.

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9
Q

What is involved in dilation of the pupil?

A
  • LONG ciliary nerves to dilator pupilae

- NA, occurs due to a strong emotional drive

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10
Q

What happens in accomodation?

Normally the ciliary muscle is relaxed (suspensory ligaments taut on lens) so lens is flat, poor refractive power…….

A

Accomodation..Ach on short ciliary nerves causes ciliary muscles to contract (suspensory ligaments lax)
-lens bulges, more refractive power to see close

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11
Q

What is myopia? (-)

A
  • optics too strong, focus infront of retina

- ‘short sightedness’

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12
Q

What is presbyopia?

A

Middle age, lens becomes stiff, proteins degenerate

Focus becomes fixed

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13
Q

What is the anatomical axis of the eyes?

A
  • divides orbital pyramid in half

- but 45/2 is 22.5 degrees from midline

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14
Q

In the visual axis, (eyes forward-22 degrees adducted) what actions does contraction of the superior oblique have?

A
  • moves eye down and out

- intorsion

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15
Q

In the abducted eye (by medial rectus) what action does the superior oblique have? (what role does SR have now?)

A 
Pure depressor
(SR will intort eye ball)
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16
Q

The outer part of the photoreceptor contains phospholipid membrane bound stacks for…?
What is the RMP? how?

A
  • they hold chemicals/protiens needed for the transduction of stimuli
  • RMP -40mV as Na+ can leak in meaning theres a small default glutamate released
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17
Q

What happens to the outer segment/RMP when the photoreceptor is illuminated?

A
  • The leak Na+ channels close, cell hyperpolarises

- The glutamate release stops

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18
Q

What happens to the outer segment/RMP when illumination of a photoreceptor decreases?

A
  • More leak Na+ channels open, cell depolarises

- More glutamate release

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19
Q

What apparatus is involved in the membrane discs of photoreceptors to transduce a light signal?

A

-the photopigment (opsin bound to 11-cis retinal)

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20
Q

Upon a photon hitting the photopigment, -the 11-cis bond breaks, now all bonds are trans…what does this trigger?

A
  • triggers activated photopigment which amplifies a biochemical cascade resulting in decreased c.GMP conc
  • c.GMP ususally holds open the Na+ leak channels so now some Na+ close -> hyperpolarisation
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21
Q

How is the activated photopigment response terminated?

A
  • trans retinal is converted back to 11-cis retinal in the RPE and opsin is inactivated, more c.GMP and
  • c.GMP is replenished by an enzyme, Na+ open again
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22
Q

How do photoreceptors adapt to constant levels of illumination?

A
  • as illumination causes hyperpolarisation

- also with constant levels of illumination this becomes the new normal, it adapts

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23
Q

Photoreceptors outer segment have a high RMR and need a rapid O2/nutrient supply..where is this from?

A

-the photoreceptors lie just under the RPE - which is surrounded by the choroid plexus

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24
Q

What happens in retinal detachment?

A
  • Retina is held to the RPE as RPE cells suck fluid out the gaps
  • with a retinal tear the retina pulls away from the RPE
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25
Q

Name 3 functions of the RPE

A
  • blood-retina barrier with TJs controlling flow
  • phagocytic cells -> outersegments replaced often
  • absorbs stray light via pigment granules
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26
Q

What causes damage to the outersegment of photoreceptors?

A

-retinoids and photoxidation

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27
Q

With age what clogs the basement membrane of the RPE? How can they decrease vision/macular degeneration?

A

Lipofusin. Attracts cholesterol and immune cells -> drusen plaques that block supply/kill photoreceptors

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28
Q

What do parvocellular ganglion cells do?

A
  • high resolution & colour of a stable image, which is in the centre of the receptive field
  • cone activates inhibitory interneurones to inhibit surrounding cones via lateral inhibition
  • they see CONTRAST/edges
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29
Q

What do magnocellular ganglion cells do?

A
  • detect fast movements and broad outlines
  • large receptive field, convergence of many rods/cones
  • low resolution
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30
Q

What wavelength of light do the following cones respond to?

Red, Green, Blue

A

Red -> long wavelengths
Green -> medium
Blue -> short wavelengths

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31
Q

What are “off” and “on” Ganglion cells? We have 50/50 of each

A
  • “off cells” excited by decreased illumination of their photoreceptors
  • “on cells” are excited by increased illumination
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32
Q

What 2 things do the retina and LGN encode?

A
  • contrast

- wavelength

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33
Q

What 3 things do the 1 visual cortical cells encode?

A
  • edge orientation ( I or – ), -presence of corners
  • direction of motion
  • binocular disparity -> depth
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34
Q

Which colours do cones compare?

A
  • Red to green

- Blue to yellow

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35
Q

How does binocular disparity work?

A
  • the difference in the location of an object as seen through the 2 eyes
  • in the cortex the input from the 2 eyes relating to same locations make synaptic contacts onto the SAME cortical cells, slight variations from each eye –> depth
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36
Q

What are the 2 pathways of visual cortex, what does each do?

A
  • Inferoremporal ‘what’ pathway - meaning, shape, colour
  • Parietal ‘where’ pathway - where, relations to surroundings, self movement control. The superior temporal areas encode movement and feed in here
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37
Q

Lesion in the Inferoremporal ‘what’ pathway leads to what?

A

Associated agnosia (cant say what an object/face is)

38
Q

Lesion in the Parietal ‘where’ pathway leads to what?

A

Cant see whole image, bump into things, cant reach accurately

39
Q

What is the pathway involved in a Reflexive Saccade?

A

Retina - Superior Colliculus - Gaze centres - EO muscles

so eyes move towards visual stimulus (this is a reflex-no cortex involved)

40
Q

What CN nuclei do the following activate

  • horizontal gaze centres
  • vertical gaze centres
A

Horizontal -> CNIII and CN VI

Vertical -> CNIII and CNIV

41
Q

What is the pathway involved in a Exploratory Saccade?

e.g. explore fine detail in image

A

Retina - V1 - Parietal Cortex- Superior Colliculus - Gaze centres - EO muscles
Scanning to find important features&recognise them

42
Q

What is the pathway involved in a Voluntary Saccade?

e.g. looking at a clock

A

Frontal Cortex - Superior Colliculus - Gaze centres - EO muscles

43
Q

What is smooth pursuit coordinated by?

What 2 things drive it?

A

Pontine nuclei via cerebellum to vestibular nuclei -> EO

  • frontal eye fields (voluntary decision to follow x)
  • superior temporal areas (movement sensitive)
44
Q

Convergence is a disconjugate eye movement.

The cortex projects to the pretectal nucleus, activates CNIII on both sides to MR, at same time what happens?

A

pretectal nucleus -> edingher westpal -> short cililary nerve -> parasympathetic -> pupil constriction and lens bulges, more refractive power

45
Q

What part of the ear is the bony labryrinth? What 3 things does it include? What is it filled with?

A
  • wall of inner ear
  • vestibule, semicircular canals and cochlear
  • Na+ rich periperilymph
46
Q

Inside the bony labyrinth is the smaller membranous labyrinth, which is filled with what?
And its components are..

A

K+ rich endolymph

..utricle, saccule, the lateral, superior and posterior semicircular ducts.

47
Q

The cochlear has 3 chambers, what are they? And what fills them? What membranes separate them?

A
  • scala vestibuli - perilymph, vestibular membrane
  • cochlear duct -endo, basilar membrane
  • scala tympani - peri
48
Q

What sits on the basilar membrane in the cochlear duct? What attached to this?

A

The spiral organ/of Corti, here auditory cells project up

Tectorial membrane overs and attaches to spiral organ

49
Q

What is the difference between inner and outer stereocilia, structurally and functionally?

A
  • inner are closer to origin of tectorial membrane
  • inner do discriminitive hearing at varying pitches
  • outer amplify sensitivity of system upon depolarisation
50
Q

What are tiplinks? What do they do?

A

Glycoproteins. They transduce sound wave to electrical signals

51
Q

What is the function of the ossicles in the middle ear?

A

Capture the vibrations/waves of pressure, allow them to be converted to waves in the fluid (stirrup) & amplify the sound

52
Q

What causes the hair cells to depolarise?

A
  • vibration of basilar membrane as taller stereocilia are pulled away from their shorter neighbours
  • tugging on the tip links
53
Q

What is the ears RMP?

A
  • 40mV partially depolarised

- tonic glutamate release

54
Q

How does sound cause an AP? Sound, vibrating basilar membrane, tugs on tip links…..

A

..tug pulls open some mechanically gated K+ channels on the ADJACENT stereocilia
-K+ influx through the K+ rich endolymph -> big increase in glutamate release and burst of AP

55
Q

When does the stereocilia tug on the tip link?

A

Every time they tilt in the direction of the taller pair, they tug on the tip link

56
Q

The hair cells are sitting in intracellular fluid (high in K+, low in Na+). The top (sterocilia) project up into the endolymph (high K+, low Na+) so how does opening of K+ channel cause depolarisation?

A

The endolymph is +80mV (ion pumps that generate the endolymph pump more + charge into cochlear duct than they remove)
The intracellular part is -40mV so K+ goes down the electrical gradient

57
Q

What is responsible for making the endolymph in the coclear duct?

A

The stria vascularis (exchanges ions from blood to endolymph-making the high K+, positive fluid)

58
Q

Pathology relating to endolymph production/reabsorption imbalance? Commonly in what disease?

A
  • endolymphatic hydrops (high pressure)

- Ménière disease -> vertigo, tinnitis, gradual hearing loss

59
Q

Name 2 things that cause ototoxicity to sterocilia.

A
  • aminoglycoside antibiotics (gentamyacin)

- platinum based anti-cancer drugs (cisplatin)

60
Q

How do we percieve louder sounds? If too loud what happens?

A

Loud=larger vibrations so cause bigger receptor potentials, more APs and more NT released
-damage stereocilia, kill hair cells, excitotoxic damage

61
Q

Low frequency sounds-each wave causes sterocilia to tilt, AP.. at the Hz of sound, what happens with high frequency sounds?

A

-continuous depolarisation as they cant depolarise, hyperpolrise etc that fast

62
Q

Where are high and low frequency sounds detected?

A
  • high (20kHz) at base of cochlear basilar membrane and at the back of the A1 cortex
  • low (20Hz) at apex resonates and at the front of A1
63
Q

Where is the 1ry Auditory Pathway-for discriminative hearing?

A

Inner hair cells -> dorsal cochlear nuclei –> INF colliculus –> MGN –> 1 Auditory Cortex

64
Q

What happens if you wipe out a primary auditory cortex?

If you wipe out both?

A
  • still good hearing through other auditory cortex

- damaged discriminative hearing but not deafness (due to some bypass routes)

65
Q

What is Presbycusis?

A

Loss of ss/tt sound hearing in speech (high frequency), decreases understanding, especially in elderly

66
Q

Where is complex speech comprehension done?

A

Wernicke’s area

67
Q

How is high frequency located?

A
  • (L)ateral superior olivary nuclei comparing the (L)oudness of high frequency sounds in the 2 ears
  • as high frequency sounds are absorbed in the head
68
Q

How is low frequency sound located?

A
  • the medial superior olivary nuclei compares the timing of low frequency sounds in the 2 ears
  • they pass straight through head, are not absorbed
69
Q

What is the pathway involved in sound localisation?

A

VENTRAL cochlear nucleus -> S.O.N (medial/lateral) –> Inf colliculus –> MGN –> A1

70
Q

Which cochlear nucleus does discrimination

A

DORSAL

71
Q

Cochlear has to exit through the inner ear encased in bone. What can happen here and what part?

A

The vestibular part of CNVIII tends to produce an acoustic neuroma’s via out of control replication of schwann cells. Ringing in ears, crushes auditory afferents…

72
Q

What makes up the otolith system. Which acceleration does each part do? (As well as gravity sensing)

A

The Utricle - horizontal movement

Saccule - Vertical movements

73
Q

What makes up the vestibular apparatus? With the 5 sets of patches of hair cells.

A
  • the vestibule (utricle and saccule)

- the semicircular canals (semicircular ducts with the 3 ampullae where they attach to the utricle)

74
Q

What is the purpose of the otoconia?

A

crystals that provide mass and inertia (resistance to change). This lies on top of the otolith (gelatinous membrane on top of sterocilia)

75
Q

If head moves in a linear horizontal direction what happens on each side of head? (Utricle responsible)

A
  • the otolith lags behind, head movement, sterocilia tilt
  • in the ear that the stereocilia tilts towards the tallest sterocillium, channels open, more active afferent
  • in other ear, that they tilt towards shortest one, channels close, hyperpolarise, less glutamate.
76
Q

What is the main output of the vestibular system for? Via what? Which muscles?

A

Postural control via vestibulospinal tract

Targets anti-gravity muscles of legs and trunk

77
Q

The 3 ampullae of the semicircular ducts are responsible for rotation of the head. Explain the arrangement.

A

Stereocilia sit in ampullae crest, projecting into endolymph with a gelatinous material, the cupula.
The upper surface of cells is at interface between the endolymph and normal ECF

78
Q

What happens in the left semicircular canal when head rotates left? (Push-pull system)

A
  • On left, fluid lags behind rotation movement, presses on cupula, tilts sterocilia, all sterocillia point in same direction so are all depolarised and send afferent signal
  • On right they are all silenced by hyperpolarisation
79
Q

What EO muscles do the left and right horizontal canals project to?

A

Medial and lateral rectus muscles that do horizontal eye movements

80
Q

What is the semicircular canals main output, via? e.g. compensate for externally induced movements..

A

-head stability, visually guided movements
-via medial vestibulospinal tract
-bilaterally neck and shoulder muscles
+Vestibulo-ocular reflexes

81
Q

The vestibular nuclei brings together what? To do what?

A

Integrate Vestibular info and Visual info

  • to move the eyes to follow the visual stimulus
  • while compensating for the movements of the head
82
Q

Why is the vestibulo-ocular reflex vulnerable to damage eg. from MS?

A
  • they are heavily myelinated to be so fast

- MLF-medial longitudinal fasiculus links the EO motor nuclei, a plaque here disrupts this coordination

83
Q

Where does the vestibular nucleus receive input from where for pursuit?

A

-parietal cortex to eye fields project to the pontine nucleus which goes to the vestibular nucleus via the floculo-nodular lobe cerebellum

84
Q

What are 2 key roles of the cerebellum?

A
  • controlling and correcting fine delicate movements e.g. smooth pursuit
  • improves performance in motor learning
85
Q

Where do the cerebellum Purkinje cells project to? What do they do here? And if due to a pathology the eye moving pathways are weaker…?

A

To the vestibular nuclei and inhibits it
Inhibition is weaker/stops if a correction to the fine movement is needed
-in a pathology, the purkinje cells will adapt/re-calibrate the level of inhibition they send

86
Q

Name 2 vestibular system dysfunctions.

A
  • Nystagmus
  • Vertigo
  • nausea and vomiting
87
Q

What would happen if you have a dysfunctional left horizontal canal?

A
  • You will have the sensation of your head turning right
  • Your eyes will turn to the left and back again
  • Diziness and nystagmus and nausea
88
Q

What 3 areas involved in the vestibular system can cause Nausea and Vomiting with lesions?

A
  • vestibular apparatus lesions
  • vestibular pathway lesions
  • cerebellar lesions
89
Q

What 4 things can cause motion sickness?

A
  • actual motion (boat)
  • zero gravity
  • extreme vestibular stimulation (roller-coasters)
  • illusion of motion (VR, cinema)
90
Q

Name 3 things that can cause the vestibular nuclei to increase signalling to the NTS to induce Nausea/Vomiting.

A
  • vestibular/cerebellar dysfunction -> abnormal input
  • overstimulation -> abnormal input to vestibular organs
  • sensory conflict between visual system and vestibular organs -> abnormal output. Brain thinks am I poisoned..

s3 - MSK, Derm, Cardio, Neuro, Pharm (9 decks)

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