Physiology of Vision Flashcards

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1
Q

the lens is suspended by _________ from __________

A

the lens is suspended by ZONULAR FIBERS from CILIARY MUSCLE

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2
Q

relaxed lens

A
  • thick lens

- near vision

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3
Q

vitreous humor: location, consistency

A
  • posterior chamber

- jelly like

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4
Q

aqueous humor: location, consistency

A
  • anterior chamber

- serous (less jelly)

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5
Q

accomodation

A
  • change the shape of the lens to focus near

- relax ciliary muscle to thicken lens

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6
Q

image created on back of retina

A
  • inverted L to R

- inverted up/down

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7
Q

cones

A
  • high acuity
  • low sensitivity
  • daytime
  • color vision
  • cone shaped
  • concentrated in fovea
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8
Q

rods

A
  • decreased acuity
  • increased sensitivity
  • nighttime
  • black/white
  • blunt tip
  • more numerous than cones
  • none in fovea
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9
Q

proteins on rods (and fxn)

A

OPSIN protein

  • absorbs light
  • changes NT released at each layer, which changes firing potential of ganglion cells
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10
Q

order the light hits the (main) cells

A
  • ganglion (first)
  • bipolar
  • photoreceptors (last)
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11
Q

layers of the retina

A
  • inner limiting membrane
  • nerve fiber layer
  • ganglion cells
  • amacrine cells
  • bipolar cells
  • horizontal cells
  • Muller cells
  • outer limiting membrane
  • rods/cones
  • pigment epithelium
  • choroid
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12
Q

choroid

A
  • blood vessels
  • supply outer 1/2 of retina
  • deepest layer
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13
Q

inheritance of colorblindness

A

x-linked

-men more likely to be colorblind

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14
Q

optic disc

A
  • where optic nerve exits
  • blind spot
  • ganglion leave
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15
Q

retinal artery supplies

A

-inner 2/3 of retina

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16
Q

fovea

A
  • increased acuity
  • daytime
  • mostly cones
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17
Q

macula lutea

A
  • surrounds fovea
  • specialized for high acuity daylight vision
  • yellowish
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18
Q

the optic disc is ________ to fovea (medial/lateral)

A

the optic disc is LATERAL to fovea

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19
Q

temporal retina

  • light from _________
  • goes ________
A

temporal retina

  • light from MEDIAL field
  • goes IPSILATERALLY
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20
Q

nasal retina

  • light from _________
  • goes ________
A

nasal retina

  • light from LATERAL field
  • goes CONTRALATERALLY
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21
Q

information from right visual field projects to ________ side of the brain

A

information from right visual field projects to LEFT side of the brain

-info from left visual field projects to right side of brain

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22
Q

lesion of lower bank of calcarine fissure

A
  • affects Meyers loop (inferior retinal fibers, superior visual field)
  • contralateral superior quadrantanopia
  • “pie in the sky” deficit
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23
Q

lesion of upper bank of calcarine fissure

A

-affects superior fibers of optic radiation

superior retina, inferior visual field

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24
Q

lateral geniculate nucleus

A
  • Carries input from retina to primary visual cortex
  • Involved in vision and visual recognition

Lesion:

  • Visual agnosia
  • Alexia without agraphia
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25
Q

visual cortex = Broddman area ____

A

visual cortex = Broddman area 17

26
Q

visual processing pathways

A
  • from visual cortex (Broddman 17) to anterior
  • medial: WHERE (analysis of motion and spatial relations)
  • lateral: WHAT (analysis of form/color)

occipital lobe

27
Q

distribution of cones

A
  • concentrated in center

- peak in fovea

28
Q

distribution of rods

A
  • more in periphery

- none in fovea

29
Q

why does the fovea have a high visual acuity?

A
  • almost 1:1 ratio of photoreceptors to ganglion (no convergence)
  • farther from fovea, the photoreceptor:ganglion ratio is much higher (100:1) –> sacrifices acuity for increased sensitivity CONVERGENCE
30
Q

dark adaptation

A
  • threshold for seeing light in dark gets progressively lower as you adjust to the dark
  • can see things better in low light the longer you are in that lighting
  • takes about 30 min
31
Q

phototransduction

A

there is a current flowing through photoreceptors in the dark that is reduced in the light via a biochemical cascade on the discs of the outer segments that shuts cGMP sensitive channels and thereby reduces Na+ influx.

this causes a hyperpolarization of the photoreceptor in response to light and a reduction in neurotransmitter release

32
Q

when light hits a photoreceptor, the current flowing through is ________. This ________ Na+ influx, which __________ the photoreceptor and ___________ neurotransmitter release

A

when light hits a photoreceptor, the current flowing through is REDUCED. This REDUCES Na+ influx, which HYPERPOLARIZES the photoreceptor and DECREASES neurotransmitter release

33
Q

rhodopsin

A
  • on membranous discs of outer segments of rods/cones
  • phototransduction occurs

Mechanism

  • Closes cation channels, hyperpolarizing membrane and reduction of NT release
  • Closes channel via conformational change (cis to trans) ISOMERIZATION
34
Q

isomerization of rhodopsin

A
  • cis to trans
  • closes Na+ channel, leading to hyperpolarization of photoreceptor
  • decreased release of neurotransmitter
35
Q

prevalence of age-related macular degeneration

A
  • 1 in 3 over age 65
  • most common cause of blindness in elderly
  • rare if under 55
36
Q

symptoms of age-related macular degeneration

A

EARLY:
-none

MIDDLE:
-blurred CENTRAL vision, distortion, faded colors

LATER
-not able to recognize faces until close

usually does not affect peripheral vision

37
Q

“dry” AMD

A
  • beginning stages of AMD
  • DRUSEN DEPOSITS on macula
  • retinal pigment epithelium cells degenerate (GEOGRAPHIC ATROPHY)
  • neighboring photoreceptors start to die too
38
Q

“wet” AMD

A
  • late stages of AMD
  • sprouting of new blood vessels from choroid that invade subretinal space
  • new vessels leak blood and plasma
  • degeneration of underlying photoreceptors
39
Q

cause of AMD

A
  • unknown

- involves complement system

40
Q

treatment for wet and dry AMD

A

DRY
-none

WET

  • lucentis and macugen (VEGF antagonists, block abnormal vessel growth)
  • inject ^^ regularly into eye (5-6 weeks)
41
Q

prognosis for AMD

A
  • most will NOT have disabling central vision loss
  • no way to predict who will progress to severe form
  • NEVER causes complete blindness
42
Q

prevalence of retinitis pigmentosa

A
  • est. 1 in 3000 in US
  • 84% autosomal recessive
  • 10% autosomal dominant
  • 6% x linked
43
Q

symptoms of retinitis pigmentosa

A
  • decreased vision at night or in low light
  • usually starts in childhood
  • loss of peripheral vision (tunnel vision)
  • loss of central vision in advanced cases
44
Q

causes of retinitis pigmentosa

A
  • genetic disease
  • mutations in rhodopsin (AD)
  • mutations of cGMP phosphodiesterase (AR)
45
Q

Tx for retinitis pigmentosa

A

-none

46
Q

prognosis of retinitis pigmentosa

A
  • disorder will continue to progress, slowly

- complete blindness is uncommon

47
Q

visual clues of retinitis pigmentosa

A

-black bone-spicule pigmentation

48
Q

prevalence of diabetic retinopathy

A
  • 40% in adults over 40 (US) with DM

- vision threatening retinopathy: 8.2%

49
Q

symptoms of diabetic retinopathy

A
  • no symptoms untl severe damage done
  • blurred vision
  • gradual vision loss
  • floaters
  • shadows/missing areas
  • difficult seeing at night
50
Q

nonproliferative diabetic retinopathy

A
  • blood vessels become larger (microaneurysms)
  • blood vessels become blocked
  • small retinal hemorrhages, with fluid leaking into retina
  • noticeable problems with eyesight
51
Q

proliferative diabetic retinopathy

A
  • more advanced and severe form of disease
  • new blood vessels start to grow in eye
  • fragile new vessels bleed
  • scars develop on retina
  • vision loss
52
Q

causes of diabetic retinopathy

A

-high blood glucose associated with long-term diabetes mellitus

53
Q

treatment of diabetic retinopathy

A
  • laser eye surgery (photocoagulation) keeps vessels from leaking and to get rid of abnormal fragile vessels
  • focal laser photocoagulation to treat macular edema
  • scatter laser treatment or panretinal photocoagulation to treat large retinal area
  • virectomy when there is bleeding into eye
54
Q

prognosis of diabetic retinopathy

A
  • outcomes improved by keeping good control of blood sugar and blood pressure
  • Tx effective at reducing vision loss, but do NOT reverse damage
55
Q

prevalence of glaucoma

A
  • leading cause of blindness worldwide
  • 3 million people in US
  • most common over age of 40
  • runs in families
  • people of african descent at 5x higher risk
56
Q

causes of glaucoma

A
  • build up of pressure in eye leads to damage of optic nerve head
  • –trabecular meshwork messed up (drainage channels)
57
Q

types of glaucoma

A
  • open angle 90%
  • closed angle (emergency)
  • congenital due to improper development of trabecular meshwork
58
Q

open angle glaucoma symptoms

A
  • no Sx until severe damage

- slow loss of peripheral vision that can lead to blindness

59
Q

closed angle glaucoma symptoms

A
  • sudden, severe pain in one eye
  • decreased/cloudy vision
  • nausea and vomiting
  • rainbow-like halos around lights
  • red eye
  • eye feels swollen
60
Q

progression of glaucoma

A
  • untreated leads to severe vision loss or blindness (irreversible)
  • lowering eye pressure can prevent further vision loss

retinal cup widens

61
Q

treatment of glaucoma

A
  • eye drops
  • –beta adrenergic antagonists: reduce production of aqueous humor
  • –prostaglandins: increase outflow of aqueous humor
  • iridotomy: laser therapy to open trabecular meshwork
  • eye surgery to bypass trabecular meshwork
62
Q

glaucoma prognosis

A

-most people go blind if they do not follow their treatment plan