1
Q
orbit anatomy
A
= 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
2
Q
functions of orbit
A
- Protection and cushioning of globe
- Conduit for vessels and nerves
through multiple foramina - Attachment for extraocular muscles
3
Q
orbital changes in volume
A
- Exophthalmos – eye
pushed forward, space- occupying lesions (something behind eye in orbital) - Neoplasia, inflammation
- Enophthalmos – eye sinks backward
- Dehydration, atrophy of
orbital fat
4
Q
eyelid function
A
- 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
5
Q
Eyelid pathology
A
- 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
6
Q
Blepharitis
A
-(inflammation of eyelid) Infectious, immune-mediated
7
Q
Eyelid neoplasia
A
- Meibomian gland adenoma,
squamous cell carcinoma,
melanocytoma
8
Q
- Bulbar conjunctiva
A
- Conjunctival epithelium extending
from limbus to conjunctival fornix
9
Q
- Palpebral conjunctiva
A
- Conjunctival epithelium extending from eyelid margin to conjunctival fornix
10
Q
Conjunctival physiology
A
- Provides smooth, lubricated surface for blinking
- Conjunctival goblet cells – secrete mucin component of tears
- Lymphoid follicles – respond to antigens as part of immune surveillance
11
Q
Conjunctivitis
A
-inflammation of conjunctiva
- Primary conjunctivitis in cats –
etiologies such as FHV-1,
Chlamydophila felis
* Non-specific and secondary in
most other species
12
Q
Lacrimal “anatomy 3 layers of tear composition
A
- 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
13
Q
lacrimal physiology (function)
A
- Provide optically uniform corneal
surface - Flush foreign material and debris
- Permit passage of oxygen and
nutrients to cornea - Antimicrobial enzymes
14
Q
Pathology of lacrimal system
A
-Alterations of quantity (aqueous tears) or quality (mucin, oil) affect
corneal health and clarity
* Vascularization (red)
* Keratinization
* Pigmentation (brown)
* Lackluster cornea
* Scarring
* Corneal ulceration
15
Q
lacrimal deficiency in quantity (aqueous)
A
= keratoconjunctivitis sicca
16
Q
lacrimal deficiency in quantity (mucin, oil)
A
= tear film quality disorder
17
Q
Nasolacrimal pathology
A
- Lacrimal punctal atresia
- Supernumerary puncta
- Nasolacrimal cysts
- Dacryocystitis
18
Q
corneal anatomy layers
A
- Epithelium (5-7 cell layers) outer layer
- Stroma
* Collagen lamellae - Descemet’s membrane
* Basement membrane of endothelium - Endothelium
* One inner layer of cells
19
Q
corneal physiology / function
A
- 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
20
Q
loss of corneal clarity =disease causes
A
- Pigmentation
- Keratinization
- Vascularization
- Edema
- Cellular, lipid, mineral infiltrates
- Corneal ulceration
- Superficial – corneal
epithelium only - Deep – corneal stromal involvement
- Scarring
21
Q
Corneal epithelial pathology
A
- Epithelial hyperplasia, keratinization,
pigmentation - Response to chronic inflammation
- Superficial corneal ulceration
22
Q
Corneal stromal pathology
A
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
23
Q
keratitis (ulcerative and non-ulcerative)
A
-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
24
Q
Scleral/episcleral anatomy
A
- Episclera: Loose connective tissue between conjunctiva and
sclera - Sclera: Dense connective tissue between episclera and uvea
25
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
26
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.
27
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
28
Uveal anatomy
-Uvea = Vascular tunic of the eye
-posterior uvea: choroid
-anterior uvea: iris and ciliary body
29
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
30
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
31
Blood-Ocular Barriers
Blood-Aqueous Barrier: breakdown of BAB results in anterior uveitis
blood-retinal barrier: * Breakdown of BRB results in
posterior uveitis
32
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
33
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
34
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
35
Uveitis
Uveitis = Breakdown in Blood-Ocular Barriers
-can be anterior, posterior, and panuveitis.
36
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
37
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
38
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
39
Panuveitis
* BOTH anterior and posterior uveitis
*also called Endophthalmitis
-filled with suppurative material
40
Phthisis bulbi
-Chronic, uncontrolled
uveitis can lead to
a small, shrunken
globe
41
Uveitis caused by? two types
1. 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)
2. Systemic disease
* Infectious disease: Bacterial
-neoplasia
-immune-mediated disease
-septicemia and endotoxemia.
42
pigmented Melanocytic tumor of the anterior uvea
-uveal neoplasia
-Large, heavily pigmented
mass arising from iris and
ciliary body
43
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
44
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
45
acute glaucoma causes
* Cornea:
* Endothelial cell dysfunction → edema
* Iris:
* Muscle dysfunction → dilation
* Retina and optic nerve:
* Cellular dysfunction → temporary vision loss
46
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
47
lens anatomy
Outer capsule:
* Anterior and posterior lens capsule
Anterior lens epithelium and lens fibers:
* Cortex = outer, newer fibers
* Nucleus = inner, older (harder) fibers
48
Lens physiology
* Transparent:
* Dehydrated state
* Avascular - obtains nutrition from
aqueous humor
* Biconvex:
* Functions to bend light to
produce a focused image on the retina
49
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
50
lens pathology
* Congenital – aphakia (no lens), microphakia (small lens): Embryologic errors in development
* Lens instability – luxation,
subluxation: Due to breakdown of zonules
51
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
52
* 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
53
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)
54
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
55
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
56
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.
57
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
58
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
59
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
60
optic nerve anatomy
* Optic nerve = cranial nerve II
* Optic nerve > Optic chiasm > optic tracts > Optic radiations > Visual cortex
61
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
62
Optic neuritis
* Signs:
* Optic disc may be elevated, enlarged,
fuzzy
* Exudates, hemorrhages of optic disc
* Causes:
* Immune-mediated
* Systemic infection
* Trauma
63
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
veterinary systemic pathology
flashcards
Decks in class (13)
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