Physiology of Vision HY Flashcards
1
Q
image created on back of retina
A
- inverted L to R
- inverted up/down
2
Q
cones
A
- high acuity
- low sensitivity
- daytime
- color vision
- cone shaped
- concentrated in fovea
3
Q
rods
A
- decreased acuity
- increased sensitivity
- nighttime
- black/white
- blunt tip
- more numerous than cones
- none in fovea
4
Q
proteins on rods (and fxn)
A
OPSIN protein
- absorbs light
- changes NT released at each layer, which changes firing potential of ganglion cells
5
Q
order the light hits the (main) cells
A
- ganglion (first)
- bipolar
- photoreceptors (last)
6
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
7
Q
choroid
A
- blood vessels
- supply outer 1/2 of retina
- deepest layer
8
Q
inheritance of colorblindness
A
x-linked
-men more likely to be colorblind
9
Q
optic disc
A
- where optic nerve exits
- blind spot
- ganglion leave
10
Q
retinal artery supplies
A
-inner 2/3 of retina
11
Q
fovea
A
- increased acuity
- daytime
- mostly cones
12
Q
macula lutea
A
- surrounds fovea
- specialized for high acuity daylight vision
- yellowish
13
Q
the optic disc is ________ to fovea (medial/lateral)
A
the optic disc is LATERAL to fovea
14
Q
temporal retina
- light from _________
- goes ________
A
temporal retina
- light from MEDIAL field
- goes IPSILATERALLY
15
Q
nasal retina
- light from _________
- goes ________
A
nasal retina
- light from LATERAL field
- goes CONTRALATERALLY
16
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
17
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
18
Q
lesion of upper bank of calcarine fissure
A
-affects superior fibers of optic radiation
superior retina, inferior visual field
19
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
20
Q
visual cortex = Broddman area ____
A
visual cortex = Broddman area 17
21
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
22
Q
distribution of cones
A
- concentrated in center
- peak in fovea
23
Q
distribution of rods
A
- more in periphery
- none in fovea
24
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
25
dark adaptation
- 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
26
phototransduction
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
27
when light hits a photoreceptor, the current flowing through is ________. This ________ Na+ influx, which __________ the photoreceptor and ___________ neurotransmitter release
when light hits a photoreceptor, the current flowing through is REDUCED. This REDUCES Na+ influx, which HYPERPOLARIZES the photoreceptor and DECREASES neurotransmitter release
28
rhodopsin
- 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
29
isomerization of rhodopsin
- cis to trans
- closes Na+ channel, leading to hyperpolarization of photoreceptor
- decreased release of neurotransmitter
30
symptoms of age-related macular degeneration
EARLY:
-none
MIDDLE:
-blurred CENTRAL vision, distortion, faded colors
LATER
-not able to recognize faces until close
usually does not affect peripheral vision
31
"dry" AMD
- beginning stages of AMD
- DRUSEN DEPOSITS on macula
- retinal pigment epithelium cells degenerate (GEOGRAPHIC ATROPHY)
- neighboring photoreceptors start to die too
32
"wet" AMD
- 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
33
cause of AMD
- unknown
| - involves complement system
34
treatment for wet and dry AMD
DRY
-none
WET
- lucentis and macugen (VEGF antagonists, block abnormal vessel growth)
- inject ^^ regularly into eye (5-6 weeks)
35
prognosis for AMD
- most will NOT have disabling central vision loss
- no way to predict who will progress to severe form
- NEVER causes complete blindness
36
prevalence of retinitis pigmentosa
- est. 1 in 3000 in US
- 84% autosomal recessive
- 10% autosomal dominant
- 6% x linked
37
symptoms of retinitis pigmentosa
- 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
38
causes of retinitis pigmentosa
- genetic disease
- mutations in rhodopsin (AD)
- mutations of cGMP phosphodiesterase (AR)
39
Tx for retinitis pigmentosa
-none
40
prognosis of retinitis pigmentosa
- disorder will continue to progress, slowly
| - complete blindness is uncommon
41
symptoms of diabetic retinopathy
- no symptoms untl severe damage done
- blurred vision
- gradual vision loss
- floaters
- shadows/missing areas
- difficult seeing at night
42
nonproliferative diabetic retinopathy
- blood vessels become larger (microaneurysms)
- blood vessels become blocked
- small retinal hemorrhages, with fluid leaking into retina
- noticeable problems with eyesight
43
proliferative diabetic retinopathy
- 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
44
causes of diabetic retinopathy
-high blood glucose associated with long-term diabetes mellitus
45
treatment of diabetic retinopathy
- 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
46
prognosis of diabetic retinopathy
- outcomes improved by keeping good control of blood sugar and blood pressure
- Tx effective at reducing vision loss, but do NOT reverse damage
47
causes of glaucoma
- build up of pressure in eye leads to damage of optic nerve head
- --trabecular meshwork messed up (drainage channels)
48
types of glaucoma
- open angle 90%
- closed angle (emergency)
- congenital due to improper development of trabecular meshwork
49
open angle glaucoma symptoms
- no Sx until severe damage
| - slow loss of peripheral vision that can lead to blindness
50
closed angle glaucoma symptoms
- sudden, severe pain in one eye
- decreased/cloudy vision
- nausea and vomiting
- rainbow-like halos around lights
- red eye
- eye feels swollen
51
progression of glaucoma
- untreated leads to severe vision loss or blindness (irreversible)
- lowering eye pressure can prevent further vision loss
retinal cup widens
52
treatment of glaucoma
- 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
53
glaucoma prognosis
-most people go blind if they do not follow their treatment plan
