Pathology of the eye Flashcards
What is an immune privilege site
-Site that is able to tolerate the introduction of antigens without eliciting an inflammatory immune response
-Causes immune tolerance of T cells
What is the sclera and cornea
-Fibrous protective outer layer
-Transparent at the cornea
-Limbus= where the sclera meets the cornea
What is the uvea
-Choroid, ciliary body, and iris
-Main vascular layer
-No lymphatic vessels
-provides nutrition to the lens and outer retina
-Tapetum=dorsal choroid
-Blood eye barrier, tight junctions making systemic treatment of the eye difficult
What do the retina and optic nerve do
-Retina: photoreceptors, convert photons of visible light into electrical impulses which are transmitted to the visual cortex
-Optic nerve: contains axons from the ganglion cells of the retina, transmits impulses to the visual cortex in the brain
What do the aqueous humor and lens do
-Aqueous humor: provides nutrition to the lens and cornea, removes metabolites
Lens: focuses light on retina, avascular, held in place by zonules
How does aqueous humor flow through the eye
Starts at ciliary process, moves via pupil to anterior chamber, moves again to filtration angle, and is resorted via scleral venous plexus. This flow is very slow, can take years
What is Collie eye anomaly (CEA) and what ophthalmoscopic findings are present
-CEA is a patchy to diffuse choroidal hypoplasia in smooth and rough follicles and collie-related breeds
-Ophthalmoscopic findings: retinal vessel tortuosity, focal to diffuse choroidal and tapetal hypoplasia, optic nerve coloboma-retinal separation with intraocular hemorrhage
This disease is always bilateral but not necessarily equal
What is the general pathology of edema within the uvea, cornea, retina, and lens
-Uveal edema: no lymphatic drainage, uveitis because of increased volume and pressure
-Corneal edema: vascular leakage or limbal inflammation, loss of corneal endothelial cell function or overload or the corneal pump (glaucoma), will have problem with vision as cornea needs to be dehydrated
-Retinal edema: disruption of retinal blood barrier (tight junctions), hypersensitivity vasculopathy, retinitis, diabetic retinopathy
-Lens: osmotic cataract, diabetic cataract from increased sorbitol
What are the regenerative capacities of the retina, corneal endothelium, corneal stroma, and lens
-Retina and corneal endothelium: no regenerative capacity
-Corneal stroma and lens: poor regenerative capacity
-Fibrous meta plasma is very common as a response of corneal endothelium, lens epithelium, and retinal pigmented epithelium
Is the cornea vascular and keratinized
No, the cornea is avascular and it’s epithelium is non-keratinized
What does the transparency of the cornea depend on
-Parallel arrangement of fibers
-Hydration state: tight junctions and Na/K pumps
What is the cornea’s response to injury
-Necrosis, inflammation, and cutaneous metaplasia
-Depends on depth of injury and if sepsis present
-Damage to epithelium can lead to edema and migration of leukocytes
-No sepsis heals rapidly, but substantial injury or infection causes delayed healing, new stroma granulation tissue
What changes are seen with adaptive cutaneous metaplasia of the cornea
-Keratinization
-Epithelial hyperplasia
-Epithelial/stromal pigmentation
-Subepithelial fibrosis
-Vascularization
-Some changes can be reversed
What are some causes of keratitis (inflammation of the cornea)
-Trauma
-Infectious agents
-Chemical agents
-Can be ulcerative or non-ulcerative, commonly associated with conjunctivitis
What is keratoconjunctivitis sicca and what happens in the acute and chronic forms
-It is also known as dry eye, and it is corneal desiccation leading to decreased lacrimal gland secretion, reduced tear flow, mucus accumulation, or bacterial infections
-Acute: ulcerative keratitis
-Chronic: vascularization, fibrosis, cutaneous metaplasia
What happens in acute and chronic infectious bovine keratoconjunctivitis
-Acute: bulbar conjunctival edema and hyperemia, 24-48 hours forms a shallow central corneal ulcer, corneal abscess can form, stromal liquefaction from Moraxella derived leukotoxins causing WBCs to rupture and die releasing contents
-Chronic: 1 week+, extensive stromal edema and vascularization, keratomalacia which frequently leads to forward coning of the weakened cornea, heals by sloughing of necrotic tissue and filling of the defect by granulation tissue
What are some causes of infectious bovine keratoconjunctivitis
-Mycoplasma and chlamydial species
-Mycoplasma conjunctivae
-Chlamydophila pecorino
-Lambs: conjunctivitis
-Adults: keratitis and corneal ulceration
What causes bacterial keratitis
-Direct contact with listeria monocytogenes usually through silage (happensto cows and sheep on self fed silage)
-Commonly unilateral
What causes viral keratitis
-FHV-1 leading to acute to chronic keratitis in cats
-Virus infects epithelial cells causing epithelial necrosis (ulcers), activation of latent infections possible
-BHV-1 (IBR) causes severe conjunctivitis and corneal edema (ulceration is uncommon)
What cause fungal keratitis and what are predisposing factors
-Aspergillus and mucor, opportunistic infections of corneal wound leading to keratomalacia
-Steroid treatment and prolonged antibiotic treatment are predisposing factors
What happens during eosinophilic keratitis
-Granular white proliferative lesion extends inwards from limbus, can be unilateral or bilateral, non-ulcerative
-Superficial stroma infiltrated by eosinophils, plasma cells, macrophages and mast cells, cause and pathogenesis unknown
What happens within chronic superficial keratitis
-Superficial fleshy vascularized stroma, begins at lateral limbus,, bilateral
-Histologically similar to discoid lupus
-Interface:plasma cells, basal cell degeneration, and fibrovascular tissue
-Exacerbated by exposure to UV light
-Immunological pathogenesis is suspected
What happens in keratomalacia
-Necrosis of stroma caused by collagenases/proteases produced by pathogenic organisms and neutrophils (Pseudomonas, Strep, or fungus) leading to mass immune response and neutrophilic degranulation
What happens in lipid keratopathy
-Histology: deposition of lipid, cholesterol, lipid-filled histiocytoma within the stroma
-Gross: bilateral, central, slightly white roughening of the corneal surface
-Can be genetic or associated with high cholesterol diets or storage diseases
What is band keratopathy
-Band like area of calcification following trauma or due to hyperparathyroidism, Vit D toxicity
What is melanosis
-Sequel to chronic keratitis where melanocytes are deposited in epithelium and stroma
What is congenital dermoid
-Focal skin differentiation (skin on cornea)
-Hair can grow an cause irritation
-Can cause blepharospasm, ulceration
What is persistent pupillary membrane
-Mesoderm containing blood vessels that should atrophy in fetus
-Connects iris to cornea or anterior lens
-Focal corneal opacity or anterior pole cataract
What are the types of uveitis and what parts of the eye do they involve
-Anterior uveitis: iris and ciliary body
-Posterior uveitis: ciliary body and choroid
-Panuveitis: diffuse uveitis
-Chorioretinitis: choroid, retina (less severely)
-Endophthalmitis: uvea, retina, ocular cavities
-Panophthalmitis: all ocular structures, including sclera
What are some sequels to uveitis
-Circumferential peripheral corneal stroma hyperemia (hallmark of anterior uveitis)
-Fibrin, leukocytes and erythrocytes plug filtration angle: glaucoma
-Atrophy of the iris: severe and necrotizing inflammation
-Vitreous: liquefied in severe uveitis and contraction of fibrin in posterior chamber, fractional retinal separation
-Cataracts are common
-Phthisis bulbi: hypotonic, shrunken, structurally disorganized eye, end stage of severe opthalmitis
