Vision Physio & Clinical Flashcards

1
Q

What benefits do convergence and divergence have? at what cost?

A

Conv: increased sensitivity, decreased acuity (i.e. rods)
Div: decreased sensitivity, increased acuity (i.e. cones, and projections from occ cx)

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2
Q

What are M cells and P cells?

A

Magno- and parvo-cellular RGCs. M: large receptive field, sensitive, for peripheral/night vision. P: small receptive field, good acuity, central/macular vision

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3
Q

To which cells does center-surround antagonism apply?

A

Bipolar neurons, RGCs, LGN

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4
Q

What are ON and OFF cells?

A

ON: light in center excites neuron, dark inhibits
OFF: light in center inhibits, dark excites

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5
Q

How do center and surround cells affect bipolar cell?

A

Center: direct to bipolar cell
Surround: via inhibitory horizontal cell (lateral inhibition)

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6
Q

What is the function of ocular dominance columns? Ocular orientation columns? Blob channels?

A

ODC: depth perception
OOC: where/mvmt and what/shape
Blob: color

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7
Q

What is amblyopia?

A

“Lazy eye” that affects ocular dominance columns to avoid diplopia; causes loss depth/spatial perception

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8
Q

What is strabismus?

A

Misaligned eyes due to muscle problems, CN problems, etc. May cause diplopia, loss of depth/spatial perception

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9
Q

What are treatment options for amblyopia?

A

Patch good eye and force use of bad eye, blur good eye with cholinergic blockers

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10
Q

Describe the M-channel/movement pathway.

A

M-RGC (periphery retina) -> certain LGN layers -> certain V1 areas (OOC) -> certain visual assc areas -> post par cx

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11
Q

Describe the P-channel/shape pathway.

A

P-RGC (central retina) -> certain LGN layers -> certain V1 areas (OOC) -> certain visual assc areas -> fusiform gyrus

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12
Q

What deficit occurs with lesion of fusiform gyrus?

A

Inability to recognize familiar faces, even your own

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13
Q

Describe the blob channel/color pathway.

A

Non-P/M-RGC (central) -> certain LGN layers -> certain V1 areas -> certain assc cx areas -> fusiform gyrus

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14
Q

What is diabetic retinopathy? How does it affect type 1 and type 2 differently? What are signs of it?

A

Type 1: nearly all have some
2: Most (60%) have some
Microvessel problems lead to micro-aneurysms, -hemorrhages, vessel proliferation

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15
Q

What are the clinical features and progression of retinitis pigmentosa?

A

Slowly progressive photoreceptor degen causing rod loss, tunnel vision, then cone loss and retinal degeneration

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16
Q

How does light cause a neural signal?

A

Photopigments isomerize, increase cGMP PDE to decrease cGMP, close cGMP-gated Na channels -> hyperpolarize by decreasing glutamate release

17
Q

How do vitamins A and E and lutein affect retinitis pigmentosa?

A

E: adverse effects
A: beneficial effects
Lutein: no effects except positive in non-smokers with vit A

18
Q

How many people are affected by AMD? What is a recommended treatment?

A

20-50% >85 yoa; fruits, veggies, many antioxidants for 25% decreased progression; NOT lutein, zeaxanthin, omega-3 FAs

19
Q

What are three non-AMD age-related changes in vision?

A

Decreased contrast sensitivity (worse with AD), adaptation to change in light intensity, and depth perception

20
Q

What is a detached retina?

A

Neural retina detached from pigmented epithelium layer of retina leading to scotoma, floaters, flashes

21
Q

What is the pretectal area important for?

A

Consensual pupillary light reflex; input from RGCs, output to both CN3 nuc

22
Q

What is the superior colliculus involved in?

A

Reflexive head/eye movement to novel stimuli, and fixation to stimuli

23
Q

What is the pulvinar nuc of the thalamus?

A

Possible relay from retina to visual cortex, allowing “blind sight” in cortical blindness

24
Q

What does the suprachiasmatic nucleus produce, and what receptors does it have?

A

Produces vasoactive intestinal peptide (VIP), receptors for melatonin

25
Q

How does the foot activate visual cortex?

A

Lateral foot “vision acupoint” (sural, lateral planter nn) activates visual cortex in fMRI