Anatomy of the cornea Flashcards
Anatomy of cornea
5 layers Epithelium, bowmans , stroma, desemcents membrane and endothelium
Parallel fibers of type 1 collagen and keratocytes, paralell structure allows for opticla clarity
no vesels o2 and nutrient obtainaed thru tears anteriorly and aqueus humor psoterior, endothelial cells pump out fluid from inside to maintain dehydration
Function of cornea
refractic and mechanical strengths
Peters anomaly
rare eye malformation resulting in congential corneal opacity, part of spectrum of developmental anomalies of the cornea, iris and lens termed anterior segment dysgenesis
type 1- characterized by central corneal opacity with iridocorneal adhesions
type 2- central opactity and cataracts or coneolensticular adhesion
Peters plus- peters with short, dev delay, dysmorphic face (cleft lip) cardiac, CNS and genital abnormalities
Sporadic or genetic (PAX6), can be bilateral
Peters anomoly pathophys
The endothelium and descements membrane dont form correctly (fluid is not removed from the area) leading to opacity
Corneal collagen fibers are disturbed in that area leading to opacity
Corneal response to trauma
Injury–> epithelial cell injury and death, disruption of bowmans layer and stromal lamellae, keratocyte injury and death
Corneal response to trauma
Corneal repair epithelial hyperplasia, stromal contraction
Epithelial repair, keratocyte activation, synthesis of type 1 collagen, keratan sulfate and type 6 collagen, blood vessel formation
Fuchs corneal dystrophy
Autosomal dominant corneal dystrophy, more common in women, affects vision starting in the 50s
dysfunction of cornial endothelial cells with growth of descemets membrane (bumps–guttate)
End stage loss of of endothelial cells
Thickened stroma with fluid filled spaces, cysts in epithelium, hazy cornea
Anatomy of the lens
transparent biconvex structure, located behind the pupil, attached in place by zonules
3 parts, lens capsule, epithelium and lens fibers, the newest in the periphery
fibers- long thin transparent cells, arrange intracellular content and dispose of unnecessary organelles
rubella cataract
caused by maternal infection by RNA toga virus, infection of lens fibers cells by the virus
Infection of lens fiber cells by virus, lens cells retain nucleus and organelles, pearly white focal nuclear opacification, can progress to complete cataract, live virus can be recovered from lens up to 3 yrs after birth
Rubella retinopathy
salt and pepper apearance, due to damage of the the pigmented epithelium layer, vision in most instances is preserved
Congenital rubella infection
triad- sensorineural deafness, eye abnormality (70%), congenital heart disease
Other manifestation- microcephaly, hepatomegaly or other liver problems, thrombocytopenia purpura, other bone marrow problems, learning disability
adult cataracts
age associated, diabetic, traumatic or post ocular surgery, steroid-induced
Anatomy of retina
layer of eye that converts light into a neuronal impulse, in to out- retina, choroid, sclera
Function of the retina
function of the photoreceptors- specialized neuron that converts light into neuronal signal
Function of the RPE (retinal pigment epithelium) - nourishes and supports the photoreceptors
Absorption of scattered light, formation of the Blood retina barrier, supply of nutrients to photo receptors and elimination of waste
Phagocytosis of photo receptor outer segments
REtinitis pigmintosa
most common form of inherited retinal degeneration
Caused by abnormalities in photoreceptors (rods, followed by cones) and the RPE
Visual impairment usually manifest as night blindness and progressive visual field loss (rods)
1/3000 to 1/5000
Histopathologic studies suggest that RP results from a primary defect in the rod and cones- final common pathway is photo receptor cell death by apoptosis
No risk other than genetics, rhodopsin gene mutation
Retinitis pigmentosa
inherited AD, AR and X linked dominant or recessive
3 types- Non-syndromic, syndromic (combined with deafness- Usher syndrome), Secondary to other systemic diseases (refsums disease-abnormal buildup of phytanic acid, a type of Fatty acid)
Age related macular degeneration (ARMD)
Degneration of retinal pigment epithelium (RPE), accumulation of drusen excrecences believed to represent byproducts of vision
Dry macular degeneration- progressive accumulatio of drusen
eventually Loss of RPE-> loss of photoreceptors
Wet ARMD- blood vessels from the choroid layer invade the inner most layer (Bruchs membrane) causing disruption and bleeding in the outer layers of the retina
Disruption of normal retina architection–> photoreceptor loss and RPE loss
Treatment of armd
vision preservation with injection of antiVEGF
Retinopathy of prematurity (ROP)
Abnormal development of the vasculature of the retina in premature infants, increased risk if born <1500 grams or earlier than 30 weeks
occurs in premies born prior to full retinal vascular maturation, factors associated with birth result in halting of normal vascular migration to the peripheral retina
Retinal vessels may grow abnormally (lines, ridges and abnormal neovascularization
If undiagnosed/untreated, retinal and vitreous hemorrhages may occur and the retina detach, untreated and treated retinal detachment portend a poor visual outcome
Diabetic retinopathy
Leading cause of blindness for people 20-64 yrs, retinal dysfunction due to hyperglycemia, pericyte loss in retinal capillaries, weak vessels bleeds in the retina
can leed to microaneurysms, dot-blot hemorrages, flame hemorrhages
Under perfused retina in Diab ret
underperfused retina secretes vascular endothelial growth factor (VEGf)
Proliferative diabetic retinopathy- abnormal blood vessels grow towards the vitreous and over other structures, fragile blood vessels bleed
Contraction of the abnormal vasculature pulls the retina causing retinal detachment
Central retinal artery occlusion
Lack of blood flow through the central retinal artery
Etiology- occlusion of the blood flow in the retinal blood vessel (usually embolic, but can be thrombotic, inflammatory or traumatic)
painless sudden viual loss, cherry red spot on fundus
retinoblastoma
cancer of the immature retinal cells, most common malignant tumor of the eye in kids, non heritable heritable
Bilateral = heritable unilateral can be non heritable
AD Ch13 on the Rb1 gene (tumor suppressor protein)
Flexner-Wintersteiner rosettes in retinoblastoma
Optic nerve
tCN2 transfers optic to brain
Composed of axons of the retinal ganglion cells and glial cells, optic nerve contains approximately 1 million nerve fibers that end at the lateral geniculate nucleus
sensory and pupillary response control
traumatic optic neuropathy
Direct or indirect injury (transmitted shock from orbital impact) to the optic nerve results in traumatic optic neuropathy
Common mechanisms of injury includ car/bike fall and beat
axonal loss via direc trauma or hemorrhagic infarct, compression from a sheat hematoma, loss of astorcyte support after replacement with microglia
Pale- ethambutol alcohol
Glaucoma is another cause
Glaucosa
Progressve optic neuropathy due to slow loss of optic nerve fibers, risk factors- intraocular pressure, age, central corneal thickness, ethnicity
