9/13 Eye Conditions - Woodbury Flashcards
eye formation: retina and lens
- optic vesicle induces overlying ectoderm to differentiate → lens epithelium
- optic vesicle folds on itself and pulls forming lens from the surface ectoderm
- lens placode becomes detached from ectoderm
- outer retinal layer differentiates → Retinal Pigmented Epithelium & Neural Retina (inner layer)
- surrounded mesenchyme becomes tough outer sclera and inner Uvea (vascular choroid and Ciliary body/muscle)
adult eye ends up with 3 distinct layers:
- tough, fibrous outer layer: sclera/cornea
- vascular uvea
- cornea
optic sheath and relation to meninges
optic sheath is continuous with meninges as a result of devpt (eyes develop as extensions from same tissue as brain)
implication: optic nerve is surrounded by subarachnoid space in which csf flows
- high ICP leads to compression of optic nerve → impaired venous return
- causes head of optic nerve to swell
- can be visualized as papilledema
fun fact: swelling from other causes = intraocular optic neuritis or papillitis
terms:
- canthus (lat vs med)
- caruncle
- iris
- cornea
- sclera
- limbus - importance?
canthus: corners of eyes (lateral vs medial)
caruncle: area near medial canthus
iris: colored portion plus pupil
sclera: white of eye
cornea: clear layer over iris; continuous with sclera
limbus: jx between cornea and sclera
- imp bc it contains stem cells that can repair cornea if damaged
muscles/nerves involved with opening and closing eye
corneal reflex review
CLOSING
obicularis oculi m. [CN VII → motor limb of corneal reflex]
- orbital portion
- palpebral portion [eyelid]
OPENING
levator palpebrae [skeletal CN III]
superior tarsal m. [sm muscle - SNS innervation. application: drooping eyelid when tired!]
→ both connect to tarsal plate (conn tissue connection to tip of lid)
corneal reflex:
- touch conveyed by afferent of CN V → chief sensory nucleus → facial motor nucleus bilaterally → signal to close conveyed on efferent of CN VII → blink!
lacrimation
innervations that make it possible
dry eye lacrimation pathway
lacrimal gland is superior and lateral to eye
both SNS and PSNS innervation
- PSNS: CN VII → greater petrosal → pterygopalatine ganglia
- application: dry eye signaled via CN V, lacrimation stimulated via component of CN VII (similar pathway to corneal reflex)
lacrimation is swept by blinking toward medial side → drained via lacrimal ducts near caruncle → inf nasal meatus
eye structure
three concentric spheres
- complete tough outer layer : sclera & cornea
- vascular middle layer : uvea
- ends anteriorly at ciliary body and iris
- appears to have a hole in it at the pupil BUT actually sealed off by lens posterior to pupil
- inner layer : retina
* incomplete anteriorly
fluid-filled segments of eye
- posterior segment: retina to back of lens
- filled with gelatinous vitreous humor
- stable; slow turnover
- anterior segment: lens forward to cornea
- filled with aqueous humor
- constantly replenished
- further subdivided into…
- posterior chamber (behind iris)
- anterior chamber (in front of iris)
- communicate with each other through the pupil
functions of anterior eye
1. regulate light intensity
- iris has 2 opposing muscle groups that regulate pupil diameter
- sphincter pupillae [parasymp CN III]
- loss of PSNS fx → blown pupil (mydriasis
- dilator pupillae [symp]
- loss of SNS fx → miosis
- dilator can pull on sphincter → spasm in segment of dilator causing misshapen “tadpole” pupil
2. focus light on retina
- light refracted by cornea and lens → focuses rays on retina
- cornea = FIXED : does most of bending (dependent on tear film and air/liq interface)
- lens = VARIABLE : fine tuning
- RECALL: retina receives images 180deg flipped → issue with upper visual field is issue with lower part of retina!
normal vision vs nearsighted vs farsighted
normal: image focused on retina
myopia (near): image focused ant to retina
hypermetropia (far): image focused post to retina
- all issues with either focusing apparatus or with structure of eye
lens anatomy
variable lens
zonules (suspensory ligaments) : pull on lens, flatten it when focusing on distant obj
ciliary muscle (component of ciliary body)
- when relaxed, internal diameter is large → puts tension on zonules, lens is flattened
- when contracted, releases tension on zonules → lens is rounded
radial muscle fibers (unknown fx, unknown innervation)
accomodation reflex
why your eyes get tired after prolonged reading
- convergent eye movement
- pupillary constriction
- lens accomodation
* 2&3 primarily PSNS, involve sphincter muscles (iris, ciliary mm; innervation from CN III → ciliary ganglia → ciliary nerves)
accomodation for visualizing things that are close requires muscle tension! → eyes get tired after accomodating for a while (ex. after reading for a long time)
lens and aging
accomodation is PASSIVE for the lens, limited only by elasticity
early in life, lens is pliable → shape determined primarily by elastic capsule
as a person ages, lens compliance changes → ability to change shape is compromised
functions of ciliary body
1. control lens shape (accomodation)
2. produce aqueous humor (fills ant and post chambers)
- aqueous humor flows towards uvea-sclera jx, collects in Canal of Schlemm → drains to venous system
- imbalance? increased IOP! glaucoma!
functions of posterior eye
- converting light image into neural signal
retina maturation
- development of original retinal layers
- relationship to retinal detachment
early retina has 2 discrete layers
- outer layer → Retinal Pigmented Epithelium
* NOT a neural layer - inner layer differentiates → 3 distinct neural sublayers, and space between layers disappears
* all four layers of the retina become intimately associated*
during retinal detachment, space that exists during devpt reappears (i.e. neural layers separate from RPE)
layers of retina
- retinal pigmented epithelium (RPE)
- outer nuclear layer : photoreceptors
- inner nuclear layer : interneurons
-
retinal ganglion cells (RGCs)
- output cells of retina : only axons that leave retina, eye → form optic nerve
also have a few notable structures between retinal layers
- outer plexiform layer: synapses between photoreceptors and interneurons (inner/outer nuc layers)
- inner plexiform layer: synapses between interneurons (inner nuc layer) and RGCs
photoreceptors
rods : low light conditions
cones : bright light, color vision
- long/med/short wavelength cones (correspond to R/G/B)
structure
-
outer segment: filled with photoreceptors (absorbing light, starting signaling cascade)
- apex is buried in RPE - critical for normal fx.
-
inner segment: powerplant (mito, ribo → generating proteins for outer segment)
- comprise outer nuclear layers
-
synaptic body
- comprise outer plexiform layer
rods : use stacks of discs studded with photoreceptors (generated at top, migrate/degraded at bottom in RPE)
cones : pl membrane is loaded with photopigments, travels in a sinusoidal path
what is the relationship between photoreceptors and RPE?
photoreceptors need RPE fx for survival!
why? ex. rods
- discs containing photoreceptors are continually generated at Inner:outer segment jx
- new discs are pushed towards apex over approx 2 weeks
- “spent” discs are phagocytized by RPES
implication: pathologies that compromise RPES compromise photoreceptors → threaten vision!
corneal layers
corneal fx
pathology
tx
- tear film
- corneal epithelium (stratified squamous)
- Bowman’s membrane
- substantia propria (thick)
- Descemet’s membrane
- corneal endothelium
- constantly pumps fluid out of cornea to maintain transparency
underneath: aqueous humor
pathology: failure of corneal endothelium → vision issues, clouding of cornea (hydrops)
tx: cadaveric transplant
- successful bc cornea is avascular, so v little immune surveillance (don’t have to donor match)
Alport Syndrome
mutation in any of Type IV collagen genes → affects basement membrane formation
- 2 out of 3 genes on X chromosome, so males preferentially affected
complications: kidney failure is most serious; vision/hearing can be compromised
- keratoconus
- anterior lenticonus (v strong corr)
- hearing bc basement membrane of Organ of Corti also affected
- kidney issues bc blomerular basement membrane altered → fibrosis/kidney failure
Wilson’s Disease
aka hepatolenticular degeneration
single gene mutation affects Cu handling
- Cu accumulates in liver
- plasma ceruloplasmin drops
- plasma free Cu increases
- Cu deposits in body tissues
Cu in liver → fibrosis/cirrhosis
Cu in cornea → Kayser-Fleisher ring
damage to putamen → neuro sx
glaucoma
what it affects
types: diffs
pathology of anterior/posterior chamber
- affects optic nerve, but has origins in anterior segment
- issues with overproduction or poor reabs of fluid will lead to exit at point of least resistance : optic nerve (where RGC axons coalesce and turn 90deg)
two forms: open angle and closed angle (named for location of aq humor reabs - anterior chamber angle, jx of sclera/uvea)
-
open angle: fluid has unimpeded access to angle, but reabs is reduced
- slow onset of optic nerve damage
-
closed angle: angle is blocked
- often due to ant displacement of lens → ant displacement of iris at angle
- rapid onset, acute loss of vision
glaucoma pathophys
pathology within anterior segment affects optic nerve and retina
- incr IOP compromises axons in optic nerve, leads to cupping
- untreated, neurons generating axons die & downstream targets of axons in LGN (lat geniculate nucleus) die
glaucoma tx
- pharmacological
- mechanical
- stent in anterior chamber to reinforce connection to Canal of Schlemm
- IF having cataract removed as well
presbyopia
lens becomes less pliable with age
- capsule can squeeze, but lens is not pliable enough to change shape
full accomodation usually compromised by 5th decade
cataracts
loss of optical function of the lens
- lens grows naturally throughout life, thickening
- can eventually grow to a point where it obstructs the vision it’s supposed to facilitate
most common cause : senile cataract
macular degeneration
what is the macula?
2 forms & characteristics
macula: region of retina encompassing fovea
- where best vision occurs
macular degeneration begins in retina or underlying choroid
two forms of age-related:
- DRY : drusen (debris) accumulation between choroid and RPE → interrupts vascular supply of RPE → interrupts fx of photoreceptor cells
- most common
- slow progression
- no current tx
- WET : abnormal angiogenesis → leaking exudate into area between choroid and RPE → formation of scar tissue, interrupting nutrient supply
- less common
- rapid progression
- tx: block new vessel formation
Stargardt disease
mutation leading to buildup of toxic vitA derivative in outer segment
- toxin is passed to RPEs when outer segment membranes are phagocytized
- pathology in photoreceptors → death of RPEs → death of photoreceptors
fovea affected first : pts lose vision in early teens
- vision loss similar to MD, but sooner
Retinitis Pigmentosa
mutations in any of multiple geners involved in signal transduction
signal transduction: light → activates receptor → activates transducin → activates PDE → inactivates cGMP → closes channels
initially affects rods → night blindness, loss of peripheral vision
- “tunnel vision”
diabetes and vision
vision loss consequent to vascular changes due to diabetes
- leading cause of blindness in adults 20-74
diabetic retinopathy (neovascularization between retina & vitreous humor)
- damaged vessels leak → retinal edema, ischemia
- retina releases angiogenic factors → new vessels formed
- more leaking → scar formation and adhesions to overlying vitreous
- scar contraction pulls on neural retina → separation from underlying RPEs
→→→ photoreceptors are detached from blood supply and will die unless reattached
diff between wet macular degen and diabetic retinopathy
wet MD : angiogen between choroid and RPEs
diabetic retinopathy : angiogen between retina and vitreous humor
blood supply to eye
what happens when you occlude vein or artery???
internal carotid → opthalmic artery
- many orbital and ocular branches
- CENTRAL RETINAL A/V (down middle of optic nerve)
- perfuse and drain inner 2/3 of retina
Central Retinal Artery Occlusion (CRAO)
- pale retina
- attenuated branches
- no hemmorhage
Central Retinal Vein Occlusion (CRVO)
- hemorrhage, edema
- “squashed tomato sign”
retinoblastoma
most common malignant cancer of eye in young children
cause: mutations in Rb gene (chr13)
- Rb is normally tasked with inactivating E2F protein
- exception: during division, when G1 CDKs P and inactivate it temporarily
mutation leads to permanent inactivation → E2F not sequestered → aberrant proliferation, destroys retina architecture
sx: leukocoria when testing light reflex
- unilat = spontaneous
- bilat = familial
