Vision Flashcards

1
Q

What are the second order neurons in the retina?

A

Bipolar cell

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2
Q

What is the third order neuron in the retina?

A

Retinal ganglion cells

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3
Q

What do the retinal ganglion cells connect?

A

Retina to LGN

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4
Q

What are the interneurons of the retina?

A
  • horizontal cells

- Amacrine cells

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5
Q

What supplies blood to the photoreceptors?

A

Choroidal vasculature

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6
Q

Are there any blood vessels in the fovea?

A

no

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7
Q

In their normal state, are photoreceptors depolarized or hyperpolerized? Why?

A

Depolarized

-more open Na channels, increased Na conductivity

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8
Q

What does light do to photoreceptor?

A
  • decrease cGMP
  • closes cGMP dependent Na channels
  • Cell hyperpolarizes, graded
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9
Q

What is the main function of the retinal pigmented epithelium?

A
  • phagocytose the most apical outer segment discs of photoreceptors and recycle
  • Rods and cones produce about 100 new discs each every day
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10
Q

What are the 5 functions of the Retinal pigmented epithelium?

A
  1. Form the blood/PR barrier
  2. Daily phagocytosis of outer segment discs
  3. Vitamin A metabolism – reisomerize from trans back to cis
  4. Melanin production to allow for high acuity
    - High density of melanosomes and microvilli around cones – directional
    - Low density of melanosomes and microvilli around rods – scatter
  5. Neovascular barrier to prevent choroidal vasculature from entering the subretinal space
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11
Q

Close to _____ ratio of cone to retinal ganglion cell at the fovea.

A

1:1

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12
Q

Genes for long and middle wavelength opsins are tightly linked on the _____ chromosome.

A

X

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13
Q

What does the dorsal stream process?

A

“Where”

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14
Q

What does the ventral stream process?

A

“What”

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15
Q

What is an agnosia?

A

-failure of recognition

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16
Q

What is an apraxia?

A
  • failure to execute learned purposeful movements

e. g. inability to fixate in visual space

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17
Q

What is a scotoma?

A
  • Areas of blindness resulting from damage to V1

- Blind in corresponding contralateral visual field of both eyes

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18
Q

Which layer do neurons of the LGN input to in V1?

A

Layer 4 = simple cells

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19
Q

Which layer of V1 are simple cells located?

A

Layer 4

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20
Q

Which layer of V1 are complex cells located?

A

Layer 2/3

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21
Q

Tonic Pupils = _____

A

sector iridoplegia (vermiform)

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22
Q

What are versions?

A

-binocular movements in the same direction

=saccades & smooth pursuit

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23
Q

What is supraversion?

A

Up gaze

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24
Q

What is infraversion?

A

down gaze

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25
Q

What is levotorsion?

A

When eyes rotate (wheel) tot he left

26
Q

What are vergence eye movements?

A
  • binocular, disconjugate eye movements

- convergence & divergence

27
Q

What are vestibulo-ocular eye movements?

A
  • reflexive

- compensate for change in head position (semicircular canals)

28
Q

What is esotropia?

A
  • inward eye deviation

- usually unilateral

29
Q

What is exotropia?

A

outward eye deviation

30
Q

What is hypertropia?

A

vertical eye deviation

31
Q

What is the clinical term for double vision?

A

Diplopia

32
Q

What is cranial nerve palsy vs paresis?

A
  • Palsy: Complete paralysis of muscle innervated by a cranial nerve (can’t get past midline)
  • Paresis: Incomplete paralysis of muscle innervated by a cranial nerve
33
Q

Where is the origin of the inferior oblique?

A

anterior-medial orbit

34
Q

What is Herring’s law?

A
  • law of parallel innervation
  • voluntary and involuntary eye movements
  • muscles are “yoked” and movements conjugate
35
Q

What is Sherington’s law?

A
  • law of reciprocal innervation to extraocular muscles

- when agonist is activated, antagonist is suppressed

36
Q

What is the leading cause of blindness in patients 20-64?

A

Diabetic Retinopathy

37
Q

What is the pathogenesis of Non-proliferative diabetic retinopathy?

A
  • vessels are abnormal
  • endothelial cells die
  • VEGF
  • random fragile vessels develop
  • these vessels burst
38
Q

What is the pathogenesis of proliferative diabetic retinopathy?

A
  • large tufts of vessels growing out of retina

- vitreous hemorrhage

39
Q

Does diabetic retinopathy cause an afferent pupilary defect?

A

rarely

40
Q

Does diabetic retinopathy cause scotomas?

A
  • usually not

- may have relative scotoma in areas of severe edema or ischemia

41
Q

How do we treat diabetic retinopathy?

A
  1. blood sugar control
  2. Blood pressure control
  3. discussion with internist
    others: pan-retinal photocoagulation (PRP); VEGF inhibitor
42
Q

What is the most common cause of central acuity loss in patients over 50?

A

Age related Macular degeneration (AMD)

43
Q

What is the pathogenesis of age related macular degeneration (AMD)?

A
  • Drusen accumulates between RPE & choroid
  • small round yellow lesions, contain lipids
  • product of lipid peroxidation
  • RPE can atrophy over time
44
Q

Is there afferent pupilary defect in age related macular degeneration?

A

no

45
Q

What may be an early finding in age related macular degeneration?

A

metamophopsia

46
Q

What is the treatment for age related macular degeneration?

A
  • vitamins (antioxidants and zinc)

- Injection of VEGF inhibitor

47
Q

What is retinitis pigmentosa?

A
  • genetic disease of rods
  • night blindness
  • progressive peripheral vision loss
  • genetic
48
Q

What is the pathogenesis of retinitis pigmentosa?

A

-degeneration of rods, with secondary loss of RPE, and 3’ loss of cones

49
Q

Is there afferent pupilary defect with retinitis pigmentosa

A

no

50
Q

What is the treatment for retinitis pigmentosa

A

none available

51
Q

What is the pathogenesis of glaucoma?

A
  • RGC axons die at optic nerve head
  • squeezed by lamina cribrosa
  • CUPPING
52
Q

Is there afferent pupilary defect in glaucoma?

A

Not at first, will develop later

53
Q

What is the treatment for glaucoma?

A

-lower intraocular pressure

54
Q

What is central retinal artery occlusion (CRAO)?

A

-clot of central retinal artery

55
Q

How does a patient present with a central artery occlusion?

A
  • sudden, massive loss of vision
  • cherry red spot
  • big afferent pupilary defect
56
Q

What are the possible treatments of central retinal artery occlusion?

A
  • ocular massage
  • IOP reduction
  • tPA
57
Q

What is a risk factor for central retinal artery occlusion?

A

-giant cell arteritis (GCA)

58
Q

What is optic neuritis?

A
  • sudden loss of vision in one eye, often central
  • pain with eye movments
  • massive afferent pupilary defect
59
Q

What is the most common cause of optic neuritis?

A

MS

60
Q

What is the pathogenesis of optic neuritis?

A

MS: demyelination of ganglion cell axons in optic nerve

Other: infiltration, inflammation, ischemia, infection

61
Q

What is the treatment of optic neuritis?

A
  • IV Steroids

- vision will return, often to baseline

62
Q

Is there afferent pupilary defect in retinal detachment?

A

-no, unless massive and of long duration