Eye Parts Flashcards
Sclera
White dense connective tissue that covers the globe posterior to the cornea. It provided attachment for extraocular muscles and the ciliary muscle
Cornea
mechanically strong and transparent connective tissue. The most powerful focusing element of the eye, twice as powerful as the lense.
Lens
Transparent epithelial tissue that fine tunes the image projected on the retina
Choroid
Capillary bed nourishing the photoreceptors and outer retina
Ciliary muscle
controls the refractive power of the lens
Ciliary Epithelium
produces the aqueous humor filling the anterior chamber
Iris
controls size of the pupil
Vitreous humor
Thick gelatinous substance filling the space btw the back of the lens and the surface of the retina
Retina
contains neurons that absorb light and process visual information
Macula
oval spot containing a yellowish pigment. Supports high acuity
fovea
small depression at the center of the macula
optic disk
where retinal axons leave the eye, and where blood vessels supplying the inner retina enter the eye
Retinal supply
Delivery of metabolic substrates and oxygen by the inner retinal vascular system and choroidal vascular system.
Myopia
nearsightedness
eyeball is too long (cornea is too curved)
can focus clearly on objects closer to the eye
fixed with concave lens
Hyperopia
farsightedness
eyeball is too short (cornea is not curved enough)
can focus clearly on objects far from the eye
fixed with convex lens
Positive lens
convex
moves the focal point foward
Negative lens
concave
moves the focal point further from the lens
Presbyopia
lens enlarges and becomes denser and more rigid. Losses ability to accommodate.
Scotoma
a portion of the Visual Field that is missing
Arcuate
arc-like shape defect produced by retinal nerve fiber bundle damage
Altitudinal
superior or inferior defect that splits horizontally
Hemianopia
nasal or temporal defect that splits vertically
Quadrantopia
defect that affects one quarter
Cataracts
- clouding of the lens due to disruption of the organization of the lens cell fibers or aggregation of the proteins.
- leading cause of blindness
- need surgical removal of the cloudy lens and replacement with an artificial one
Accommodation
- contraction of the ciliary muscle cause reduced tension of the zonule fibers which allows the lens to thicken.
- increased lens curvature decreases the focal length
Open- Angle Glaucoma
- slow development of pathology
- obstruction of drainage canals causes pressure to build in the anterior chamber
Closed -Angle Glaucoma
- Sudden increase in intraocular pressure (IOP)
- Closed or narrow angle btw the iris and the cornea
Glaucoma General Symptoms and Treatment
Symptoms: Non until its too late, decreased peripheral vision
Treatment: Eye drops to decrease aqueous production and/or increase drainage, or surgery
Layers of the retina
light comes through the: 1) nerve fiber layer 2) Ganglion Cell Layer 3) Inner plexiform layer 4) Inner nuclear layer 5) Outer plexiform layer 6) Outer nuclear layer and then reaches the Photoreceptor outer segment
lateral information flow in the retina
mediated by horizontal and amacrine cells (release GABA or Glycine)
vertical information flow in the retina
photoreceptors to bipolar cells to ganglion cells (release Glutamate)
pigmented epithelium
melanin containing cells behind the photoreceptors that maintain phototransduction machinery.
Photoreceptor structure
Outer segment - phototransduction machinery
Cillium- connects the outer to inner segment
Inner segment- housekeeping machinery
Synaptic terminal- contacts bipolar and horizontal cells and uses glutamate
Photoreceptors in the dark vs light
Photoreceptor in depolarized in the dark and continually releasing glutamate
When light contacts the photoreceptor it causes a graded hyperpolarization and it decreases the release of glutamate.
Photoreceptors in the Dark
1) constant current with Na+ & Ca+ flowing in to depolarize the cell (occurs in the outer segment)
2) K+ current flowing out to hyperpolarize the cell (occurs in the inner segment)
the two actions combine to create a steady sight depolarized membrane potential around -40 mV
Photoreceptors in the Light
1) light absorption decreases cGMP levels in the (outer segment)
2) Na+ and Ca2+ channels are cGMP gated so they shut down
3) the K + channels are fine so the K+ keeps flowing out and hyperpolarizes the cell
4) Since the cell is hyperpolarized the release of glutamate decreases.
Phototransduction steps
1) Absorption of a photon changes the conformation of retinal 11-cis (inside the opsin molecule) to 11-trans
2) this is then able to activate rhodopsin (R to R)
3) R catalyzes the activation of heterotrimeric G-protein known as transducin
4) this decreases cGMP
Dark Adaptation
1) Once 11-cis retinal has absorbed the photon and transformed into 11-trans it dissociates from the opsin
2) 11- trans retinal is transported to the pigment epithelium where it is converted back to 11- cis retinal
3) 11-cis is transportd back to recombine with opsin
fovea
small depression at the center of the macula which is mainly populated by cones.
Has 0.01% of the retinal area and uses 10 to 50% of the optic nerve
Scotopic
rod only vision
Photopic
cone only vision
mesopic
normal vision
Retinitis Pigmentosa (RP)
- Genetic, leads to incurable blindness
- Caused by mutations of genes for rhodopsin & other rod protein, leading to degeneration of rods and eventually cones
Symptoms:
night blindness, tunnel vision, legally blind by 40
Diagnosis:
loss of ERG
Treatment:
None
ERG
Electroretinogram - record electrical activity of the eye after a large field flash of light
AMD, symptoms and risk factors
Age-related Macular Degeneration
leading cause of vision loss
Symptoms:
Loss of central vision and acuity
Risk Factors:
ageing, smoking, inheritance
Wet form AMD
Abnormal blood vessels behind the retina grow under the macula, leaking and rapidly damaging the retina
Treatment:
lazer coagulation of vessels and intravitreal injection of anti-neovascular agents
Dry form AMD
- accounts for 85% of cases
- RPE & photoreceptors of the macula degenerate
- Accumulation of drusen (yellow deposits)
Treatment:
Antioxidants
Non-proliferative Diabetic Retinopathy
Hyperglycemia-inducted pericyte death leads to incompetence of vascular walls, micro-aneurysms & “dot and blot” hemorrhages
Proliferative Diabetic Reintopathy
New fragile vessels grow, which leak blood
Diabetic Retinopathy, risk, symptoms, and treatment
Risk:
Up to 80% in people who have had diabetes for 10+ yrs
Symptoms:
Early stage has no symptoms, late stage has blurry vision with macular edema.
Treatment:
Lazer surgery to reduce edema and injections with anti-neovascular factors
sign invert synapse
for on-center bipolar cells
- have metabotropic receptors that hyperpolarize (cation channels close) in response to glutamate
sign conserving synapse
for off-center bipolar cells
-have ionotropic receptors, cells depolarize (cation channels open) in response to glutamate
cone opsins
member of the G-protein coupled receptor family
-the opsin sequence tunes the absorption of light to a particular region of the spectrum
protanope
No L cones
deuteranope
No M cones
Tritanopia
No S cones
M cells
- large receptive fields
- good light, motion, and contrast sensitivity
- Origin of the magnocellular pathway
P cells
- also called midget cells
- small receptive fields
- high acuity and color sensitivity
- origin of parvocellular pathway
K cells
- bi-stratified ganglion cells
- carry short wavelength info
Intrinsically photosensitive retinal ganglion cells
- contain the primitive opsin
- autonomous response to bright lights
Roles:
1) Inform ambient light intensity
2) Synchronize circadian rhythms
3) Control Pupil resonse
Tangent Screen
an instrument for determining the integrity of the central field of vision
Goldman Perimeter
- hollow white sphere a set distance from the pt
- Examiner moves a test light of variable size and intensity
Humphrey Perimeter
-Goldman perimeter but done by a computer
Complete/ incomplete VFD
extension of type of defect
relative/ absolute
to the type of stimuli
Homonymous
the defect is the same side for both eyes
Heteronymous
the defect is in different sides
Congruous
the defect is similar in both eyes
incongruous
the defect is different in both eyes
retina VFD
general defects, arcuate in glaucoma, central scotoma in foveal lesion
Optic Nerve VFD
can product any type of defect
including alititudinal field defect
Optic Chiasm VFD
- usually caused by tumors, or carotid aneurysms
- usually bitemporal field defect
Optic tract VFD
Homonymous and incongruous ( the more posterior the more congruous it becomes)
Lateral Geniculate VFD
usually congruous sectoranopia, or incongruous hemianopia
Temporal VFD
superior homonymous quadrantanopia
Parietal VFD
inferior homonymous quadrantanopia
Calcarine cortex VFD
macular sparring
cortical magnification
mapping in the visual cortex is proportional to the density of photoreceptors, not the area of the visual field.
cone opponency
any single cone type cannot inform about both intensity and wavelength by itself
Neocortex
2&3- output to high level cortical targets (Ex. V1 toV2)
4- input from lower layers
5- output to subcortical targets (Ex. Superior Colliculus)
6- input from higher levels (Ex. cortex)
lateralized lesion in parietal cortex
hemispatial neglect
prosopagnosia
inability to recognize faces, from lesions in certain parts of the temporal cortex
amblyopia
one eye is weaker in the brain
use patching of the strong eye to fix
Strabismus
improper alignment of the eyes
if you have alternation strabismus, your brain has two strong eyes and has to switch btw them
Hebbian Mechanisms
Cells that fire together, wire together
- explains how in amblyopia one eye can take over the brain
