The Eyelids, Blepharitis Basic Pathology of the Eye

anterior

Nicola G. Ghazi

posterior

Introduction
• A subspecialty on its own • Focus on generalities and most common conditions in each major disease category • Suggested readings:
– Spencer WH (ed): Ophthalmic pathology: An atlas and textbook, 4th ed. Philadelphia: WB Saunders, 1996. – Yanoff M, Fine BS: Ocular pathology, 5th ed. St. Louis: MosbyYear Book, 2002 – Klintworth GK: The eye pathologist, an eye pathology tutor and disease database. http://www.eyepathologist.com

The Eyelids, Hordeolum
• Hordeolum:
– Acute, purulent, focal inflammatory lesion of the eyelid – Usually due to a bacterial infection – May involve hair follicles or glandular structures

The Eyelids, Blepharitis
• Blepharitis:
– Inflammation of the eyelids – Several types:
• • • • seborrheaic staphylococcal anterior mixed meibomia gland dysfunction (posterior) • others
Anterior lamella Posterior lamella

The Eyelids, Hordeolum
• Hordeolum:
– May be:
• external: starts as folliculitis perifolliculitis nearby glands • internal: involves meibomian glands

– Both may cause abscess formation

The Eyelids, Chalazion
• Chalazion:
– Chronic localized lipogranlomatous inflammation – Centered around the sebaceous glands of the eyelid – Reaction to extruded lipid – May also be external (marginal) or internal

The Orbit, Graves
• Exophthalmos or proptosis: forward protrusion of the eye • Thyroid orbitopathy in Graves disease is the most common cause of unilateral or bilateral eye protrusion in adults

The Eyelids, Chalazion
External

The Orbit, Graves
• Exophthalmos in Graves disease may precede or follow other manifestations of thyroid dysfunction • May manifest in any dysthyroid state of the disease

External (marginal)

Internal

The Eyelids, Chalazion
• Chalazion:
– May be caused by infectious, inflammatory or neoplastic processes – The common etiology is obstruction of the sebaceous gland orifice – lipogranlomatous inflammation:
• predominantly chronic inflammatory cells around lipid vacuoles

The Orbit, Graves
• Autoimmune disease • Female: male= 4:1 • Bilateral or unilateral eye protrusion • Upper lid retraction: stare (may indicate hyperthyroid state)

Graves • Eyelid swelling • Chemosis (conj swelling) • EOM restriction with ocular motility disturbance and diplopia • Exposure keratopathy • Compressive optic neuropathy The Conjunctiva. Graves • Eyelid swelling • Chemosis (conj swelling) • EOM restriction with ocular motility disturbance and diplopia • Exposure keratopathy • Compressive optic neuropathy The Orbit. Conjunctivitis • May be: – Allergic (papillae) – Infectious: • viral (follicles) • bacterial Vision loss .The Orbit. Graves • Eyelid swelling • Chemosis (conj swelling) • EOM restriction with ocular motility disturbance and diplopia • Exposure keratopathy • Compressive optic neuropathy The Conjunctiva. Graves • Pathologically: – Chronic inflammatory cells. mainly lymphocytes and plasma cells – Mucopolysaccharide – Involves EOM belly but not the tendon Vision loss The Orbit. Conjunctivitis • Most common of eye diseases • Hyperemic conj blood vessels (pink eye) • Crusting • Discharge • Matting in the morning Vision loss The Orbit.

fomites and flies The Conjunctiva. Trachoma • Bilateral Chronic cicatricial conjunctivitis • Caused by Chlamydia trachomatis serotypes A. Trachoma • Pathology: – Superior limbal subepithelial inflammatory fibrovascular pannus Inflamed pannus Non-inflamed pannus The Conjunctiva.The Conjunctiva. and C • Highly contagious – spread by fingers. Trachoma • Pathology: – Lymphocytic infiltrate – Epithelial cells: intracytoplasmic inclusion bodies The Conjunctiva. the Middle East and Africa The Conjunctiva. Trachoma • Pathology: – Superior limbal subepithelial inflammatory fibrovascular pannus Inflamed pannus Non-inflamed pannus . Trachoma • Affects upper conjunctiva especially the palpebral part • Still the most common cause of blindness in underdeveloped areas in Asia. Trachoma • Pathology: – Superior limbal subepithelial inflammatory fibrovascular pannus The Conjunctiva. B.

Epithelial Dystrophies • Faulty maturation and turnover of epithelial cells: – Microcysts (cytoplasmic epithelial accumulations) – Basement membrane duplication/migration – Faulty desmosomal and hemidesmosomal junctions (recurrent erosions) • Meesmann • Map-dot-fingerprint . Dystrophies • Varied genetic disorders • Non-inflammatory • Most are autosomal dominant • Most widely classified by the layer of the cornea primarily involved • Many involve more than one layer The Conjunctiva. elastotic degeneration of collagen – Giant cells may be seen The Cornea. Pingueculum • Yellowish conjunctival lump • Usually affects nasal conjunctiva • Sun-damaged collagen • Pathology: – accumulations of amorphous. Pterygium • Pingueculum that grows onto the cornea • Insect wing shape (hence the name) • Forms a fold of vascularized conjunctiva The Cornea. granular collagen fragments – Stain with elastin stains but are elastase resistant.The Conjunctiva. Trachoma • Pathology: – Herbert pits The Cornea. Dystrophies Epithelial dystrophies Basement membrane Bowman layer dystrophies dystrophies Stromal dystrophies Endothelial dystrophies The Conjunctiva.

Stromal Dystrophies • Lattice: amyloid Red-green Congo red Plane polarized . Stromal Dystrophies • Macular: mucopolysaccharide Colloidal iron (may use Alcian Blue) The Cornea. Stromal Dystrophies • Deposition of abnormal material in the stroma – amyloid (lattice) – mucopolysaccharides (macular) – unidentified proteins. Epithelial Dystrophies • Faulty maturation and turnover of epithelial cells: – Microcysts (cytoplasmic epithelial accumulations) – Basement membrane duplication/migration – Faulty desmosomal and hemidesmosomal junctions (recurrent erosions) • Meesmann • Map-dot-fingerprint The Cornea. Epithelial Dystrophies • Faulty maturation and turnover of epithelial cells: – Microcysts (cytoplasmic epithelial accumulations) – Basement membrane duplication/migration – Faulty desmosomal and hemidesmosomal junctions (recurrent erosions) • Meesmann • Map-dot-fingerprint The Cornea.The Cornea. hyaline (granular) – Lipids (numerous) – Some may be associated with systemic manifestations The Cornea. Stromal Dystrophies • Granular: hyaline The Cornea.

The Cornea. cortical cataract) – Posterior polymorphous dystrophy (PPD) – Congenital hereditary endothelial dystrophy (CHED) The Lens. toxic. Cataract • Most commonly associated with age • Path: varies with type – Lens fibers harden and are compressed centrally (nuclear sclerosis) The Cornea. metabolic. Cataract • Path: varies with type – Peripheral cortical fibers degenerate. Cataract • Path: varies with type – Anterior lens epithelial cells migrate posteriorly and swell up (bladder cells of Wedl. Stromal Dystrophies • • • • • • • • • Marilyn: Macular Monroe: Mucopolysaccharide Always: Alcian Blue Gets: Granular Her: Hyaline Men: Massson-Trichrome In LA: Lattice/Amyloid County: Congo red The Lens. posterior subcapsular cataract) . Endothelial Dystrophies • Accompanied by Descemet membrane (DM) changes – Fuchs: • Endothelial cell loss • DM thickening • DM wartlike excrescences (guttata) • corneal edema with vision loss The Lens. physical and other conditions The Lens. Cataract • Most common cause of reversible vision loss in the elderly • Opacification of the crystalline lens • Possible role for ultraviolet light • Multiple ocular and nonocular causes for secondary cases • Genetic. fragment and form globules (Morgagnian corpuscles.

Cataract • May cause glaucoma: – Phacomorphic: due to continuous osmotic lens swelling which eventually obstructs outflow of aqueous – Phacolytic: due to lens debris seeping out through lens capsule and accumulating in macrophages that eventually obstruct outflow (phacolytic cells) The Lens. Cataract • May cause glaucoma: – Phacomorphic: due to continuous osmotic lens swelling which eventually obstructs outflow of aqueous – Phacolytic: due to lens debris seeping out through lens capsule and accumulating in macrophages that eventually obstruct outflow (phacolytic cells) The Lens. Cataract The Lens. hemorrhage • A feature of many retinal disorders • Appearance varies with location: – Dot/blot (round): outer retina (outer plexiform layer) – Splinter (flame)shaped: inner retina (nerve fiber layer) – Melanoma-like: subRPE or suprachoroidal .The Lens. Cataract • Path: varies with type – Cortex liquefies completely and nucleus sinks down (morgagnian cataract) The Lens. Cataract • May cause glaucoma: – Phacomorphic: due to continuous osmotic lens swelling which eventually obstructs outflow of aqueous – Phacolytic: due to lens debris seeping out through lens capsule and accumulating in macrophages that eventually obstruct outflow (phacolytic cells) The Retina.

The Retina. retinal occlusive disease • Venous: – Central (CRVO) – Branch (BRVO) • Arterial – Central (CRAO) – Branch (BRAO) • Effect depends: – on size and location of involved vessel – degree of ischemia The Retina. arterial occlusion • Pathology: – Early: • • • • Cotton wool spots Retinal swelling Thin artery Cherry red spot (in CRAO) • Arterial – Central (CRAO) – Branch (BRAO) • Effect depends: – on size and location of involved vessel – degree of ischemia – Late: • Inner retinal atrophy • Optic nerve atrophy Cytoid bodies (micro-infarcts with impaired axoplasmic flow) . hemorrhage • A feature of many retinal disorders • Appearance varies with location: – Blot (round): outer retina (outer plexiform layer) – Dot (round): inner plexiform – Splinter (flame)shaped: inner retina (nerve fiber layer) – Melanoma-like: subRPE or suprachoroidal The Retina. retinal occlusive disease • 2nd most common retinal vascular disease after DR • May be: – Arterial – Venous The Retina. retinal occlusive disease • Venous: – Central (CRVO) – Branch (BRVO) The Retina. compressive. vasculitic. thrombotic. and idiopathic – Embolic is main cause: • Carotid • Heart • Major vessels The Retina. arterial occlusion • The etiology of both branch or central artery occlusion: – Embolic. vasospastic. stenotic.

arterial occlusion No inner retina The Retina.The Retina. venous occlusion • The etiology of occlusion not well understood • Thought to be: – thrombotic in CVO – compressive in BVO – Late: • Inner retinal atrophy • Optic nerve atrophy Atrophy involves inner retina but spares the outer aspect of INL . arterial occlusion • Leads to permanent visual loss if circulation not restored within a short time • Amaurosis fugax: transient vision loss due to micro-emboli to CRA • Pathology: – Early: • Cotton wool spots • Inner retinal swelling/infarction • Cherry red spot (in CRAO) – Late: • Inner retinal atrophy • Optic nerve atrophy Stenotic CRAO due to an atheromatous plaque The Retina. arterial occlusion • Pathology: – Early: • Cotton wool spots • Retinal swelling • Cherry red spot (in CRAO) The Retina. arterial occlusion No inner retina The Retina. venous occlusion • The etiology of occlusion not well understood • Thought to be: – thrombotic in CVO – compressive in BVO • Pathology: – Early: • Cotton wool spots • Inner retinal swelling/infarction • Cherry red spot (in CRAO) – Late: • Inner retinal atrophy • Optic nerve atrophy Stenotic CRAO due to an atheromatous plaque The Retina.

venous occlusion • Neovascular glaucoma (NVG): – “90-day glaucoma” – Angle neovascularization • Open angle early • Closed later on (peripheral anterior synechiae) The Retina. mainly venous – Microaneurysms – Flame shaped hemorrhages – Cotton-wool spots – Exudates – Macular star (exudates radiating from macula) – ONH swelling in malignant hypertension The Retina. hypertensive retinopathy • Ophthalmoscopic findings: – Exudates – Macular star (exudates radiating from macula) – Malignant hypertension • ONH swelling • Fibrinoid necrosis of precapillary arterioles – Painful – Worst prognosis . hypertensive retinopathy • Ophthalmoscopic findings: – Arteriolar narrowing and sheathing (“cupper” and “silver wiring”) due to arteriosclerosis – AV nicking – Retinal vascular occlusion. venous occlusion • Both have similar fundus findings along the distribution of occlusion: – Venous/capillary tortuousity – Cotton-wool spots – Retinal hemorrhages (splinter mainly) – Retinal and ONH swelling – Cystoid macular edema (CME) – Retinal/ONH/anterior segment neovascularization – Neovascular glaucoma (within 3 months) The Retina. venous occlusion • CME: – Leakage of fluid from compromised retinal capillaries – Patelloid appearance on angiography – Pathology: fluid accumulation mainly in outer plexiform layer (OPL) The Retina.The Retina. hypertensive retinopathy • Chronic hypertension affects retinal and choroidal arterioles through the process of arteriosclerosis • This leads to thickening of arteriolar wall and narrowed lumen • Arterioles compress veins at AV crossings – Some believe that no compression occurs but venous sclerosis The Retina.

Diabetic retinopathy (DR) • Vascular disease • 20-40% of diabetics develop ocular symptoms and retinopathy • The rate of proliferative DR correlates with: – Type of diabetes – Degree of glycemic control The Retina. Diabetic retinopathy • 2 types of DR: – Non-proliferative (NPDR) – Proliferative (PDR) • The difference is neovascularization The Retina. nonproliferative • Previously called background – Retinal dot/blot hemorrhages – Hard exudates – Cotton-wools spots – Retinal swelling – Venous beading – Microaneurysms – IRMA – Narrowing of central retinal or ophthalmic arteries from atherosclerosis • Diabetes causes incompetence of retinal circulation with leakage: – Endothelial cell damage – Loss of pericytes (1:1 ratio disrupted) . Diabetic retinopathy. Diabetic retinopathy. nonproliferative • Previously called background – Retinal dot/blot hemorrhages – Hard exudates – Cotton-wools spots – Retinal swelling – Venous beading – Microaneurysms – IRMA • Almost all type 1 and most type 2 diabetics develop some form of retinopathy by 15 years • The better the glycemic control the lower the rate of retinopathy • Proliferative retinopathy (worse type) usually appears after 10 years of diabetes The Retina. Diabetic retinopathy • Diabetes causes retinal ischemia: – Narrowing/occlusion of retinal arterioles and capillaries: • Arteriosclerosis • Platelet thrombi • Lipid deposition in vessel wall The Retina. hypertensive retinopathy • Ophthalmoscopic findings: – Exudates – Macular star (exudates radiating from macula) – Malignant hypertension • ONH swelling • Fibrinoid necrosis of precapillary arterioles The Retina.The Retina.

Diabetic retinopathy. Diabetic retinopathy. Diabetic retinopathy. nonproliferative • These lesions do not affect vision unless: – they involve the macula or PM bundle – associated with macular edema • These lesions are more prominent in type 2 DM • Hard exudates are rich in lipids due to lipoproteinemia of diabetics The Retina. nonproliferative • Previously called background – Retinal dot/blot hemorrhages – Hard exudates – Cotton-wools spots – Retinal swelling The Retina. Diabetic retinopathy. nonproliferative • Previously called background – Retinal dot/blot hemorrhages – Hard exudates – Cotton-wools spots – Retinal swelling – Venous beading – Microaneurysms – IRMA The Retina. nonproliferative • Previously called background – Retinal dot/blot hemorrhages – Hard exudates – Cotton-wools spots – Retinal swelling – Venous beading – Microaneurysms – IRMA The Retina. nonproliferative • Pathology: – IRMA: • close to areas of venous beeding • rich in endothelium but rare to no pericytes . Diabetic retinopathy.The Retina. nonproliferative • Pathology: – Microaneurysms: focal capillary dilatations at areas of wall weakness The Retina. Diabetic retinopathy.

Diabetic retinopathy. proliferative • Neovascularization: – At the disc (NVD) – Elsewhere (NVE) – May be associated with vitreous hemorrhage – Tractions retinal detachment – Iris neovessels The Retina. proliferative • Neovascularization: – At the disc (NVD) – Elsewhere (NVE) – May be associated with vitreous hemorrhage – Tractions retinal detachment – Iris neovessels The Retina. Diabetic retinopathy. proliferative • Neovascularization : – Due to VEGF release from ischemic retina – Stimulates endothelial cell and astrocyte proliferation – Fibrovascular proliferation . Diabetic retinopathy. proliferative • Neovascularization: – At the disc (NVD) – Elsewhere (NVE) – May be associated with vitreous hemorrhage – Tractions retinal detachment – Iris neovessels The Retina. proliferative • Neovascularization: – At the disc (NVD) – Elsewhere (NVE) – May be associated with vitreous hemorrhage – Tractions retinal detachment – Iris neovessels The Retina.The Retina. Diabetic retinopathy. proliferative • Neovascularization: – At the disc (NVD) – Elsewhere (NVE) – May be associated with vitreous hemorrhage – Tractions retinal detachment – Iris neovessels The Retina. Diabetic retinopathy. Diabetic retinopathy.

Diabetic retinopathy. Diabetic retinopathy. proliferative • Pathology: – New blood vessels with glial tissue (gliosis) from surface of retina or ONH into vitreous • NVE • NVD The Retina. proliferative • Pathology: Retina – NVE – NVD – Traction RD • AP forces (asterisk) • Tangential forces (arrowhead) • Foci of VR attachments at NVE (arrows) The Retina. lost by processing – New blood vessels in the iris (rubeosis iridis) or angle The Retina. proliferative • Pathology: – New blood vessels with glial tissue (gliosis) from surface of retina or ONH into vitreous • NVE • NVD The Retina. Diabetic retinopathy.The Retina. Diabetic retinopathy • Pathology: – DME: • May occur in NPDR or PDR • Main cause of vision loss in diabetics • Swelling/hard exudates in or close to the macula – Patholohy: • Lipoprotein and fluid accumulation mainly in OPL . Diabetic retinopathy. Diabetic retinopathy. proliferative • Pathology: Iris – Lacy vacuolization of the iris pigment epithelium (IPE): • Due to hyperglycemia • Glycogen storage in IPE. proliferative • Pathology: Iris – Rubeosis iridis: fibrovascular membrane on the iris surface • PAS with angle closure (neovascular glaucoma) • Posterior synecahiae • Ectropion uveae • Hyphema – New blood vessels in the iris (rubeosis iridis) or angle The Retina.

Diabetic retinopathy • Retinal ischemia and incompetence of retinal circulation with leakage may explain all the signs of DR The Retina. Retinal detachment (RD) Fluid leads to RD • Vision loss from DR has a bad prognosis – Life expectancy < 6yrs – Only 20% survive 10 yrs – Death from RF/CAD often follows • Vision loss due to: – – – – DME Vitreous hemorrhage Retinal detachment NVG • BS control can not be overemphasized Other ophthalmic manifestations of diabetes • “Snowflake” cataract: – White spoke-shaped opacities – Adjacent to lens capsule – Rapidly progressing over days to week – Due to an osmotic effect of sorbitol in the lens The Retina. tumors .The Retina. Diabetic retinopathy • One of the 3 leading causes of irreversible vision loss in the USA: – DR – AMD – Glaucoma The Retina. RD • 3 types of RD – Rhegmatogenous: • Rhegma= break • Common after trauma and cataract surgery • Most common type – Tractional: • No break usually • Due to pulling on retina • PDR. Retinal detachment (RD) The Retina. ROP • Earlier onset and faster growing than age-related NSC – Exudative: • No break/traction • Fluid accumulates under retina • Inflammation.

Age-related macular Agedegeneration (AMD) • May be: – Wet: subretinal fibrovascular tissue – Dry: drusen/RPE atrophy – RPE demarcation line – Cystic degeneration of the retina – Subretinal dense proteinaceous material . Age-related macular Agedegeneration (AMD) • May be: – Wet: subretinal fibrovascular tissue – Dry: drusen/RPE atrophy – RPE demarcation line – Cystic degeneration of the retina – Subretinal dense proteinaceous material The Retina. is: – Point of maximal visual acuity – Highest cone concentration The Retina. RD • Pathology: – Photoreceptor atrophy: • due to separation from RPE and choroid The Retina. RD • Pathology: – Photoreceptor atrophy: • due to separation from RPE and choroid The Retina.The Retina. Age-related macular Agedegeneration (AMD) • Most common cause of vision loss in the elderly (>60) • The macular center. the foveola. Rhegmatogenous RD • Factors required for a rhegmatogenous RD to occur: – Retinal break – Traction – Fluid The Retina.

Optic nerve head (ONH) edema The Optic Nerve. Optic atrophy • Loss of optic nerve axons • Many causes: – – – – – – Chronic edema Optic neuritis Optic compression Retinal conditions Infarction Toxicity (ethambutol.The Retina. infarction. Age-related macular Agedegeneration (AMD) • May be: – Wet: subretinal fibrovascular tissue – Dry: drusen/RPE atrophy The Optic Nerve. late (atrophic stage) – – – – – – – – The Optic Nerve. Optic nerve head (ONH) edema • Swelling of the nerve where it enters the globe (optic disc) • Increased ICP is the most important cause – Usually bilateral – Papilledema The Optic Nerve. Optic atrophy Atrophic papilledema Glaucomatous excavation . venous drainage obstruction are other causes The Optic Nerve. isoniazid) – Hereditary (Leber) – GLAUCOMA • Clinically: – – – – Thin disc rim Pale ONH Flat ONH Excavated (cupped) in GLAUCOMA • Inflammation. Optic nerve head (ONH) edema • Clinical findings: Optic disc swelling Disc elevation Blurred margins Dilated vessels Hemorrhages Exudates CWS Concentric folds of choroid and retina – Central vision is preserved initially (no syx’s) – Vision loss.

IOP rises – Usually aqueous drainage rather than production involved Normal Post inflammation (optic neuritis) Glaucomatous excavation Glaucoma • Collection of disorders: – Optic neuropathy – Characteristic ONH excavation – Progressive visual field loss Glaucoma • High IOP may lead to vision loss: – ONH damage – Corneal edema Glaucoma • Most commonly associated with increased intraocular pressure (IOP) • Normal tension glaucoma (NTG) is one exception • Increased IOP does not always lead to glaucoma • Types: – Congenital – Acquired • Open angle – Primary – Secondary Glaucoma •Closed angle –Primary –Secondary . Optic atrophy • Aqueous flow: Glaucoma – A delicate balance between production and filtration maintains physiologic IOP – When aqueous accumulates.The Optic Nerve.

1ry closed angle – With pupil block: • In patients with small eyes or anterior segments • Pupil blocked by lens • Peripheral iris pushed forward (iris bombe) • Angle obstructed and IOP rises . 1ry open angle Glaucoma. asymmetric • Asymptomatic.Glaucoma • Types: – Congenital – Acquired • Open angle – Primary – Secondary Glaucoma. insidious: – ONH damage – Irreversible field loss Glaucoma. 1ry closed angle • Affects patients who have an abnormally narrow angle – Without pupil block: • Peripheral iris displaced anteriorly • When pupil is constricted (miotic) angle widens • When dilated (mydriatic) angle narrows and IOP increases Glaucoma. 1ry open angle • Normal AC and angle • Most common type • Major cause of blindness • 6th decade • Bilateral. 1ry open angle • Pathology: – Increased resistance to aqueous outflow – Usually in the vicinity of Schlem’s canal •Closed angle –Primary –Secondary • Multiple genes may determine predisposition to glaucoma Glaucoma.

not in infants – Nasalization of blood vessels – Buphthalmos: in pts < than 3 years of age – Optic atrophy – Ganglion cell layer atrophy Glaucoma. 1ry closed angle • Symptoms: – – – – – – – Decreased vision Ocular pain Headache Nausea/vomiting Red eye Halos Light sensitivity Glaucoma.Glaucoma. Low-tension LowGlaucoma • Also called normal tension glaucoma – ONH glaucomatous damage – Visual field loss – Normal IOP • May represent patients with hypersensitivity to IOP Glaucoma. 1ry closed angle • Ocular emergency • Start treatment as soon as possible (within 24-48 hrs) • Treat the other eye prophylactically Glaucoma • Effects of increased IOP: – ONH excavation. 2ry Glaucoma • May be open or closed angle too • Many causes: – – – – – Inflammation Hemorrhage Neovascularization Tumors Many others Pigment dispersion syndrome Glaucoma .

Melanoma Neoplasms. Melanoma Neoplasms. • Pathology: – Circumscribed – Some are flat (diffuse) – Mushroom-shaped after breaking through Bruch membrane – Orange lipofuscin pigment on surface Neoplasms. Melanoma Neoplasms. • Malignant • Arises from uveal melanocytes • Most commonly from the choroid • Most common 1ry intraocular malignancy Neoplasms. Melanoma Neoplasms. Melanoma Neoplasms. • Pathology: 3 cell types: – – – – – Spindle A Spindle B Epithelioid (worst px) Variable pigmentation Some cells may contain abundant lipid (ballon cell degeneration) – Variable amount of necrosis Neoplasms. • Pathology: 3 cell types: – – – – – Spindle A Spindle B Epithelioid (worst px) Variable pigmentation Some cells may contain abundant lipid (ballon cell degeneration) – Variable amount of necrosis Neoplasms.Neoplasms. • Pathology: 3 cell types: – – – – – Spindle A Spindle B Epithelioid (worst px) Variable pigmentation Some cells may contain abundant lipid (ballon cell degeneration) – Variable amount of necrosis Neoplasms. Retinoblastoma Neoplasms. • Malignant • Arises from retinal neuroblasts • Most common 1ry intraocular malignancy in children • Occurs within the 1st 2 years of age .

• More common than 1ry tumors • May be 1st manifestation • Most common: – Leukemias – Breast – Lung • Orbit: Partially differentiated Photoreceptors. • Presentation: – – – – – – Leukocoria (white pupil) Strabismus (squint) Poor vision Spontaneous hyphema Glaucoma Painful red eye RB. less specific . Metastasis Neoplasms. Pathology • Neuroblastic cells • May arise in any nucleated layer • Perivascular cuffing • Calcification • Necrosis • Rosettes: – Flexner-Wintersteiner – Homer-Wright Neoplasms. Pathology • Neuroblastic cells • May arise in any nucleated layer • Perivascular cuffing • Calcification • Necrosis • Rosettes: – Flexner-Wintersteiner – Homer-Wright • Fleurettes • Seeds Poorly differentiated cells. may be seen in medulloepithelioma and pineoblastoma • Fleurettes • Seeds – Neuroblastoma in children (bilateral) – From periorbital structures RB.Neoplasms. Pathology • Neuroblastic cells • May arise in any nucleated layer • Perivascular cuffing • Calcification • Necrosis • Rosettes: – Flexner-Wintersteiner – Homer-Wright • Fleurettes • Seeds More differentiated Photoreceptors with outer and inner segments RB. Retinoblastoma Neoplasms.

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