Eye Stuff (Gianani / Heck) Flashcards
Two compartments divided by the lens, suspensory ligaments and ciliary body
Anterior compartment
- Filled with aqueous humor
- Contains anterior and posterior chambers separated by the iris
Posterior compartment
- Filled with vitreous humor
Three tissues
Corneo-scleral layer (fibrous tunic)
- Makes up the sclera in the posterior (5/6) wall of the eye
Uveal layer (vascular tunic) - Makes up the choroid in the posterior (5/6) wall of the eye
Retinal layer (neural tunic)
Accessory Structures
Conjunctiva
Lacrimal Gland
Eyelid
Corneo-scleral layer
The Sclera
Opaque white posterior 5/6 of the eye
Nearly avascular
Composed of collagen and elastin
The Cornea
Transparent in the anterior 1/6 of the eye
Avascular but highly innervated
5 layers
Refractive Error (not on the test)
Myopia Nearsightedness Light rays are focused in front of the retina Cornea is too curved or lens is too powerful for length of globe
Hyperopia
Farsightedness
Light rays are focused behind the retina
Lens and cornea too weak for length of globe
LASIK
Laser assisted in-situ keratomileusis
For both myopia and hyperopia
Procedure:
- A corneal flap is raised using a microkeratome
- — About 160 microns thick
- An ultraviolet or “cool laser” is used to ablate a precise amount of the exposed corneal stroma
- The flap is irrigated and replaced
- NO sutures are applied
- — The flap remains in place due to the dehydration pump action of the corneal endothelium
- Corneal epithelial cells are replaced by mitotic cells found in the periphery, which migrate into the wound
Uveal layer
The Choroid
Posterior pigmented portion of the vascular layer
Components:
- Loose connective tissue
- Fibroblasts
- Melanocytes
- Bruch’s Membrane
Separates it from the retina
Choriocapillaris
- Area next to the retina, rich in capillaries
The Ciliary Body
Forward continuation of the Uveal (vascular) layer
- Making up the Choroid in the posterior 5/6
Wedge shaped - Between the iris and vitreous body - Contains: Loose connective tissue Pigmented epithelium Nonpigmented epithelium *** Filtrate plasma to create aqueous humor Smooth Muscle Zonule Fibers - Radiate from ciliary processes to lens - Form suspensory ligaments of lens
Accommodation
Ciliary Muscle:
- Three bundles
- Opens the canal of Schlemm
- Two stretch the ciliary body
- —- Occulomotor innervation
Altering the shape of the lens
- Via suspensory ligaments
- – As ciliary muscles contract, ciliary body stretches in length, thereby releasing tension on the suspensory ligaments
- – Lens gets thicker and more convex
- – Permits focus on nearby objects
Circulation of Aqueous Humor
Ciliary Processes
- On medial surface radiating from core
- Epithelial folds with a core rich in fenestrated capillaries
- Continuous production of aqueous humor
- Flow:
- – Enters the posterior chamber, passes through the papillary aperture between the iris and lens and enters the anterior chamber.
- – Drains through the trabecular meshwork into the Canal of Schlemm and directly into venous circulation.
Corneal-irideal angle
The area between Descemet’s membrane of the cornea and the anterior surface of the iris
Canal of Schlemm forms a complete circle here
Clinical correlation
Glaucoma***
Refers to a group of diseases characterized by optic neuropathy resulting in loss of vision due to retinal ganglion cell death
The number one risk factor for glaucoma is increased intraocular pressure, however, not only does high IOP not occur in all patients but management may not slow progression
Open-Angle Glaucoma
The most common form
Corneal-irideal angle is open
Usually presents with increased IOP
- May be due to increased production or decreased outflow
Slow neurodegenerative process with characteristic optic nerve cupping
Treatment:
- Prostaglandins
- Beta-blockers
- Alpha adrenergic agonists
- Trabeculectomy or trabeculoplasty
Angle-Closure Glaucoma*
Corneal-irideal angle is obstructed
Aqueous outflow is impeded
Primary: Unknown anatomical cause
Secondary: Inflammation
Hemorrhage, neovascularization or tumor growth
Patient may show characteristic conjunctival redness
Cataract
Leading cause of blindness in the world
Mechanism yet unknown, but we do know:
- Lens does not shed nonviable cells
- Lens fibers do not have intracellular mechanism to deal with accumulation of substances
cataract risk factors**
- Advanced age
- Smoking
- Sun exposure
- Alcohol consumption
(Metabolic syndrome
Diabetes mellitus
Malnutrition
Inactivity)
This leads us to believe the cause is photo/oxidative injury
cataract treatment
Currently no pharmaceuticals available
Changes in lifestyle may slow progression but damage is irreversible
Surgical replacement with synthetic intraocular lens
- Lens nucleus removed leaving lens capsule to support prosthetic
The Retina
Histology
Cell types: Neurons - Photoreceptor cells ----- Rods and cones - Retinal ganglion cells - Interneurons (integrating neurons) ---- Bipolar cells, horizontal cells and amacrine cells
Retinal pigment epithelial cells (RPE)
— Outermost layer separating the retina from the choroid
Neuron support cells
structures of the retina
Fovea: Visual axis of the cornea - Depression in the retina ---- Flattening of the inner layers to let more light in - Greatest visual discretion ---- The most neuronal interconnections for the most representation in the visual cortex - Almost exclusively cones ---- Poor in low light
Optic nerve: Convergence of the axons of retinal ganglion cells - Unmyelinated afferent fibers - Myelination begins at optic disc Absence of photoreceptor - Blind spot
Blood supply
of the retina
Choroid:
Maintenance of the outer retina
Central retinal artery:
Rises from the optic nerve head
Maintenance of inner retina
- Has branches that supply three layers of capillary networks
Branches run posterior to the inner limiting membrane, within the nerve fiber layer
- Capillaries can be found running through the retina but generally no deeper than the outer plexiform or nuclear layer
Retinal Detachment
Detachment of the photoreceptor cell layer from the pigment epithelial layer can result in blindness
RPE needed to maintain support of visual function
Choroid needed to nourish and maintain cells
Diabetic Retinopathy
an ocular complication of diabetes.
Prevalence
60-80% of all diabetics develop some sort of retinopathy
15-20 years after diagnosis
Nearly all type 1 diabetics after 20 years
50% of which will have proliferative
Preproliferative (Nonproliferative)
diabetic retinopathy
Increased size and number of intraretinal hemorrhages
Most vision loss occurs from macular edema
- Would not treat unless clinically significant
Proliferative
diabetic retinopathy
Includes the formation of new blood vessels Neovascularization - Can protrude into vitreous --- Hemorrhage here and cloud vision --- Detach retina
Can eventually extend into and grow from other structures in the eye
- Causing secondary forms of blindness
