ocular Flashcards
orbit anatomy
= Cavity that encloses the eye
1. Bony orbit formed by fusion of 5-7 bones depending on species
* Incomplete bony orbit: Dog, cat, pig have a lateral orbital ligament
* Complete bony orbit: Horse, cow, sheep
2. Retrobulbar tissues
* Extraocular muscles, nerves, vessels, fat, lacrimal gland
functions of orbit
- Protection and cushioning of globe
- Conduit for vessels and nerves
through multiple foramina - Attachment for extraocular muscles
orbital changes in volume
- Exophthalmos – eye
pushed forward, space- occupying lesions (something behind eye in orbital) - Neoplasia, inflammation
- Enophthalmos – eye sinks backward
- Dehydration, atrophy of
orbital fat
eyelid function
- Sensation given by cilia and vibrissae surrounding the eye
- Meibomian gland secretions –
lipid layer of tearfilm - Physical protection of eye
- Reduction of tear evaporation
- Distribution of tears
- Pumping of tears down the
nasolacrimal duct
Eyelid pathology
- Eyelid agenesis (coloboma) usually cats
- Blepharitis (inflammation of eyelid) Infectious, immune-mediated
- Eyelid laceration leading to fibrosis
- Trauma
- Eyelid neoplasia: Meibomian gland adenoma,
squamous cell carcinoma,
melanocytoma
Blepharitis
-(inflammation of eyelid) Infectious, immune-mediated
Eyelid neoplasia
- Meibomian gland adenoma,
squamous cell carcinoma,
melanocytoma
- Bulbar conjunctiva
- Conjunctival epithelium extending
from limbus to conjunctival fornix
- Palpebral conjunctiva
- Conjunctival epithelium extending from eyelid margin to conjunctival fornix
Conjunctival physiology
- Provides smooth, lubricated surface for blinking
- Conjunctival goblet cells – secrete mucin component of tears
- Lymphoid follicles – respond to antigens as part of immune surveillance
Conjunctivitis
-inflammation of conjunctiva
- Primary conjunctivitis in cats –
etiologies such as FHV-1,
Chlamydophila felis
* Non-specific and secondary in
most other species
Lacrimal “anatomy 3 layers of tear composition
- Lipid layer – produced by meibomian glands of eyelid
- Aqueous layer – produced by lacrimal gland (60%) and third
eyelid gland (40%) - Mucin layer – produced by conjunctival goblet cells
lacrimal physiology (function)
- Provide optically uniform corneal
surface - Flush foreign material and debris
- Permit passage of oxygen and
nutrients to cornea - Antimicrobial enzymes
Pathology of lacrimal system
-Alterations of quantity (aqueous tears) or quality (mucin, oil) affect
corneal health and clarity
* Vascularization (red)
* Keratinization
* Pigmentation (brown)
* Lackluster cornea
* Scarring
* Corneal ulceration
lacrimal deficiency in quantity (aqueous)
= keratoconjunctivitis sicca
lacrimal deficiency in quantity (mucin, oil)
= tear film quality disorder
Nasolacrimal pathology
- Lacrimal punctal atresia
- Supernumerary puncta
- Nasolacrimal cysts
- Dacryocystitis
corneal anatomy layers
- Epithelium (5-7 cell layers) outer layer
- Stroma
* Collagen lamellae - Descemet’s membrane
* Basement membrane of endothelium - Endothelium
* One inner layer of cells
corneal physiology / function
- Refracts light: Corneal curvature bends light rays to create focused image
- Clear for vision!!!
- Non-pigmented
- Non-keratinized
- Non-vascularized: Aqueous humor and tears provide nutrition and oxygen
- Organized collagen lamellae
- Dehydrated state:
- Active pumping in endothelium via Na/K ATPase
- Physical barrie
loss of corneal clarity =disease causes
- Pigmentation
- Keratinization
- Vascularization
- Edema
- Cellular, lipid, mineral infiltrates
- Corneal ulceration
- Superficial – corneal
epithelium only - Deep – corneal stromal involvement
- Scarring
Corneal epithelial pathology
- Epithelial hyperplasia, keratinization,
pigmentation - Response to chronic inflammation
- Superficial corneal ulceration
Corneal stromal pathology
Corneal edema – 3 mechanisms
1. Disruption of epithelium: ulcer
2. Loss of endothelial pump function
* Reduced number of endothelial cell or function
3. Leakage from newly formed vessels
* Corneal vascularization
-keratitis
keratitis (ulcerative and non-ulcerative)
-of the stromal layer of the cornea
* Inflammation – neutrophils, lymphocytes
and plasma cells
* Vascularization – vessels migrate to areas
of injury
* Corneal ulceration – takes ~4 days for vessels
to start growing, then they grow at a rate of 1 mm/day
Scleral/episcleral anatomy
- Episclera: Loose connective tissue between conjunctiva and
sclera - Sclera: Dense connective tissue between episclera and uvea
Scleral/episcleral function
- Continuous with cornea, together comprise fibrous layer of the eye to
provide structural support - Protection of intraocular structures
- Insertion of extraocular muscles
Episcleritis
-inflammation of the episclera
* Nodular, focal, and diffuse
forms
* Superficial disease, does NOT affect deeper ocular structures
* Immune-mediated
inflammation of episclera
* Mixed inflammation – plasma cells, lymphocytes, macrophages.
Sclera pathology
- Scleral coloboma: Focal absence of sclera
- Scleritis
- Causes include immune-mediated, traumatic,
infectious agents - Deep disease, affects deeper structures - uvea,
retina - Necrotizing scleritis
- Collagen degradation
Uveal anatomy
-Uvea = Vascular tunic of the eye
-posterior uvea: choroid
-anterior uvea: iris and ciliary body
Uveal physiology
Iris:
* Forms the pupil
* Sphincter muscle
constricts
* Dilator muscle dilates
Choroid:
* Blood supply to outer retina
* Contains tapetum lucidum
dorsally in the fundus
* Bright structure that increases light capture
Ciliary body:
* Produces aqueous humor
* Attachment site for zonules
that suspend the lens
Uveal physiology - Aqueous humor production
Aqueous humor is produced by ciliary
body and circulates:
* posterior chamber, pupil, anterior
chamber, filtration angle, collecting
veins into systemic circulation
Function:
* Maintains intraocular pressure (IOP)
* Provides nutrition and waste removal
for lens, inner cornea
Blood-Ocular Barriers
Blood-Aqueous Barrier: breakdown of BAB results in anterior uveitis
blood-retinal barrier: * Breakdown of BRB results in
posterior uveitis
Blood-Aqueous Barrier:
Epithelial portion
* Tight junctions of non-pigmented
ciliary epithelium
Endothelial portion
* Tight junctions of iridal vessels
* Breakdown of BAB results in anterior uveitis
Blood-Retinal Barrier:
Epithelial portion
* Tight junctions of retinal pigment
epithelium
Endothelial portion
* Tight junctions of retinal vessels
* Breakdown of BRB results in posterior uveitis
uveal pathology
- Congenital:
- Persistent pupillary membranes =
vascular strands of iris that failed to regress - Iris hypoplasia
- Heterochromia iridis
- Inflammation: Uveitis
- Neoplasia:
- Ciliary body adenoma
- Melanocytomas and melanomas
Uveitis
Uveitis = Breakdown in Blood-Ocular Barriers
-can be anterior, posterior, and panuveitis.
Anterior Uveitis
- Iridocyclitis = inflammation of iris and ciliary body
-Protein and cellular leakage into aqueous
humor - Protein – aqueous flare
- White blood cells – hypopyon
- Red blood cells – hyphema
- Fibrin
- Keratic precipitates
Anterior uveitis sequelae
- Disruption of normal nutrition and waste
removal - Cornea – edema, degeneration
- Lens – cataract, zonular breakdown
- Adhesions and scar tissue formation inside
the eye: Secondary glaucoma
Posterior Uveitis
- Choroiditis = inflammation of the choroid
- Chorioretinitis = inflammation of choroid and retina
- Tapetal hyporeflectivity:
- Fuzzy, gray exudates within or behind retina or within vitreous
that obstruct view of tapetum lucidum - Hemorrhage, retinal detachment, granulomas
Panuveitis
- BOTH anterior and posterior uveitis
*also called Endophthalmitis
-filled with suppurative material
Phthisis bulbi
-Chronic, uncontrolled
uveitis can lead to
a small, shrunken
globe
Uveitis caused by? two types
- Ocular disease
* Ocular trauma (blunt, penetrating)
* Complex corneal ulceration or laceration
* Lens-induced (phacolytic, phacoclastic,
lens instability)
* Pigmentary uveitis (Golden Retriever)
* Equine recurrent uveitis (ERU) - Systemic disease
* Infectious disease: Bacterial
-neoplasia
-immune-mediated disease
-septicemia and endotoxemia.
pigmented Melanocytic tumor of the anterior uvea
-uveal neoplasia
-Large, heavily pigmented
mass arising from iris and
ciliary body
Filtration angle anatomy and function
Anatomy
* Iridocorneal angle = located where iris and cornea meet
* Pectinate ligaments span opening of filtration angle
Function
* Drainage of aqueous humor and return to systemic circulation
filtration angle pathology = glaucoma
- Glaucoma = Elevated intraocular pressure
due to DECREASED drainage of aqueous humor
-mechanisms: blockage at filtration angle, blockage at pupil (posterior synechia where iris is adhered to lens)
-causes: - Congenital glaucoma = embryologic errors
- Primary glaucoma = inherited
- Secondary glaucoma = ocular disease
acute glaucoma causes
- Cornea:
- Endothelial cell dysfunction → edema
- Iris:
- Muscle dysfunction → dilation
- Retina and optic nerve:
- Cellular dysfunction → temporary vision loss
chronic glaucoma causes
- Globe stretching/enlargement
(buphthalmos) - Retina and optic nerve ischemia and
oxidative stress
: Permanent retinal ganglion cell death - End-stage eye
1. Irreversible blindness
2. Pain
lens anatomy
Outer capsule:
* Anterior and posterior lens capsule
Anterior lens epithelium and lens fibers:
* Cortex = outer, newer fibers
* Nucleus = inner, older (harder) fibers
Lens physiology
- Transparent:
- Dehydrated state
- Avascular - obtains nutrition from
aqueous humor - Biconvex:
- Functions to bend light to
produce a focused image on the retina
Lens aging leads to
- Nuclear sclerosis:
- Lens fibers proliferate throughout life
- Newer outer fibers push older inner
fibers concentrically toward lens nucleus - Normal old age change
lens pathology
- Congenital – aphakia (no lens), microphakia (small lens): Embryologic errors in development
- Lens instability – luxation,
subluxation: Due to breakdown of zonules
Lens instability
- Zonular breakdown:
- Primary = inherited zonular
degeneration (Terriers) - Secondary:
- Uveitis causing zonular degeneration
- Trauma causing zonular disruption
- Glaucoma causing zonular disruption
- Consequence for the eye:
- Uveitis due to microtrauma of
unstable subluxated lens - Glaucoma due to disrupted aqueous
humor outflow
- Cataract (white eye)
- Due to protein and/or hydration changes in lens metabolism.
- Metabolic disturbance affects lens protein and/or fluid content
- Results in altered organization of lens fibers
- Manifests as an opacity in the lens (cataract)
- Causes:
- Inherited, metabolic (diabetes), nutritional, congenital, traumatic, toxic, retinal degeneration, uveitis
- Consequences for the eye
1. Disrupts vision
2. Causes inflammation due to leakage of lens proteins across intact lens capsule - Phacolytic uveitis – lymphocytic plasmacytic inflammation
Phacoclastic uveitis
- Penetrating lens trauma with capsule rupture:
- Cataract with massive release of lens protein through the rent in lens capsule
- Severe (phacoclastic) uveitis leading to glaucoma (severe)
Vitreal Anatomy & Physiology
- Composition of vitreous:
- Water (99%)
- Collagen fibers which serve as a skeleton for
the gel - Cells (hyalocytes)
- Hyaluronic acid
- Maintains ocular shape
- Maintains lens and retina in their normal
anatomic position - Transmits light
Pathology of the vitreous
- Persistent hyperplastic primary vitreous
- Vitritis
- Vitreal hemorrhage
- Liquefaction/Degeneration/Syneresis: due to old age or preveous vitritis
- Asteroid Hyalosis: Suspended calcium and phospholipid concretions
in vitreous
Retinal anatomy
- Optic cup formation
embryologically - Layers appose but are not firmly attached
- RPE and neurosensory retina detach easily
- Retinal pigment epithelium (RPE) = one cell layer
- Neurosensory retina = multiple layer
-space between these two layers and if unattached leads to degeneration.
Retinal physiology
- Neurosensory retina
- Phototransduction by photoreceptors: Conversion of light energy into electrical signals
- Blood supply and nutrients
- Retinal pigment epithelium (RPE)
- One cell layer thick
- Supports retina through transport of ions, removal of waste products, and regeneration of photoreceptors
Retinal degeneration
- Retinal thinning:
- Dorsal fundus – tapetal hyperreflectivity
- Ventral fundus – pigment clumping and
depigmentation - Retinal vascular attenuation
-less vascular, hyperreflective, pigment clumping. - Causes
- Inherited photoreceptor degenerations,
toxicity, nutritional, glaucoma
Retinal detachment
- Separation between photoreceptor layer of retina and RPE
- Embryologic potential space between them.
- Acute – vision loss due to loss of contact between retina and RPE
- Chronic – death of photoreceptors due to loss of support from RPE
- Mechanisms of detachment
1. Rhegmatogenous retinal detachment - Tears or holes in retina, expand due to liquified vitreous entering subretinal
space
2. Non-rhegmatogenous retinal detachment (looks like seagull Y) - Fluid
- Cells
optic nerve anatomy
- Optic nerve = cranial nerve II
- Optic nerve > Optic chiasm > optic tracts > Optic radiations > Visual cortex
optic nerve pathology
- Congenital:
- Optic nerve hypoplasia – reduction in retinal ganglion cells
- Optic nerve aplasia – retinal ganglion
cells absent - Acquired
- Inflammation: Optic neuritis
- Degeneration: Optic nerve atrophy
- Neoplasia
Optic neuritis
- Signs:
- Optic disc may be elevated, enlarged,
fuzzy - Exudates, hemorrhages of optic disc
- Causes:
- Immune-mediated
- Systemic infection
- Trauma
Optic nerve degeneration signs and causes
- Signs
- Disc appears darker, smaller, cupped
- Causes
- Chronic glaucoma – loss of retinal
ganglion cells - Post-optic neuritis
- Post-traumatic
