Eye

EYE PATHOLOGY

OCULAR PATHOLOGY

ORBIT

NORMAL

  • § Palpebral conjunctiva: nonkeratinizing squamous lining[1]
  • § Conjunctiva at fornix: columnar rich in goblet cells with submucosal accessory lacrimal glands and prominent lymphoid aggregates[2]à fornix biopsy can be used for sarcoidosis with 50% sensitivity!!!
  • § Bulbar conjunctiva: nonkeratinizing squamous lining
  • § Limbus: junction between bulbar conjunctiva and cornea, contains epithelial stem cells
  • § Corneal epithelium: same as bulbar conjunctiva but never goblet cells
  • § ECM accumulation and fibrosis of rectus muscleà axial proptosis[3]

THYROID OPHTHALMOPATHY

IDIOPATHIC ORBITAL INFLAMMATION*** IOI

Clinical

  • § Unilateral vs bilateral
  • § All orbital tissue vs limited (lacrimal gland, extraocular muscles, Tenon’s capsule, fascial layer)
  • § Sometimes with sclerosing inflammation elsewhere (RP, mediastinum, thyroid)

Micro

  • § Chronic inflammation[4] with variable fibrosis
  • § Vasculitis should raise possibility of Wegener
  • § No1 tumors of orbit are vascular: capillary hemangioma, lymphangioma, cavernous hemangioma[5]
  • § Periorbital ecchymosis: Wilms, neuroblastoma
  • § Orbital chronic inflammation: metastatic prostatic carcinoma
  • § Lacrimal gland tumors staged as SG tumors

TUMORS

EYELID

  • § Accessory lacrimal glands in fornixè tear
  • § Sebaceous glands (Zeis and Meibomian glands)à lipid to delay tear evaporationà chalazion[6] if lipid extravasates into tissue when tear drainage is blocked[7]
  • § BCC[8] is no1, sebaceous carcinoma no2

TUMOR

SEBACEOUS CARCINOMA

How and where does sebaceous carcinoma spread

  • § Pagetoid mimicking blepharitis or ocular pemphigoid
  • § To parotid and submandibular LN

Micro

  • § Cytoplasmic vacuolation
  • § Chlamydia
  • § Chemical
  • § Pemphigoid
  • § Surgery
  • § Mostly at limbus
  • § Squamous papilloma and CIS may be associated with HPV 16/18!
  • § SCC indolent vs MEC aggressive
  • § Conjunctival nevi benign[9]
  • § Conjunctival melanoma: fair-complexioned persons, mid-aged, from primary acquired melanosis with atypia[10], spreads to parotid and submandibular LN[11]
  • § Bacteria
  • § Viruses (HSV[12])
  • § Fungi
  • § Protozoa (Acanthamoeba)
  • § Band keratopathies: calcific[13] vs actinic[14]
  • § Keratoconus: thin cornea with rupture of Bowman’s layer[15]
  • § Fuchs endothelial dystrophy[16]
  • § Stromal dystrophies
  • § Systemic disease (DM, Wilson, atopic dermatitis)
  • § Drugs (CTSD)
  • § Radiation
  • § Trauma
  • § Age-related (nuclear sclerosis)
  • § Posterior subcapsular cataract[17]

CONJUNCTIVA

CONJUNCTIVAL SCARRING

PINGUECULA

PTERYGIUM

TUMOR

SCLERA

CORNEA

KERATITIS AND ULCER

CORNEAL DEGENERATIONS

CORNEAL DYSTROPHIES

ANTERIOR SEGMENT

CATARACT

GLAUCOMA

ENDOPHTALMITIS/PANOPHTHALMITIS

UVEA

UVEITIS

UVEAL MELANOMA

Treatment

  • § Radiation or enucleation
  • § Rhegmatogenous
  • § Non-rhegmatogenous

RETINA, VITROUS

RETINAL DETACHMENT

RETINAL VACULAR DISEASE

HTN

Changes

  • § Atherosclerosis of retinal BV[18]à silver copper color[19] and artery compressing vein at crossing
  • § Choroidal artery damage[20]à choroidal infarcts (Elschnig spots)
  • § Exudate leakage from damaged BVà retinal detachment[21]
  • § Retinal artery occlusionà retinal nerve infarct

DM

Changes

  • § Microvascular injury and thick BMà edema, hemorrhage
  • § Pericyte lossà microaneurysms

2 phases

  • § Preproliferative: changes below internal limiting membrane

 

  • § Proliferative: neovascularization breaching internal limiting membrane
  • § O2à vasoconstriction of still immature BVà local ischemia
  • § Sicklingà microvascular occlusion

RETINOPATHY OF PREMATURITY

SICKLE RETINOPATHY

RETINAL ARTERY/VEIN OCCLUSION

Differences

  • § Atherosclerosisà artery occlusionà retinal infarct[22]
  • § HTNà thickened arterioles compressing venulesà ischemia[23]

MACULAR DEGENERATION

Variants

  • § Atrophic (dry)[24]
  • § Exudative (wet)[25]
  • § Inherited disorder
  • § Loss of both rods and cones to apoptosis with perivascular pigment accumulation
  • § No1 intraocular malignant in kids[26]

RETINITIS PIGMENTOSA

RETINOBLASTOMA

Prognosis

  • § Extraocular extension by optic nerve or choroidal invasion
  • § Trilateral (with pinealoblastoma)

Micro

  • § Undifferentiated: SRBC
  • § Differentiated[27]: Flexner-Wintersteiner rosettes, fleurettes
  • § Extensive necrosis with residual viable tumor cells around BV
  • § Dystrophic calcification characteristic

Spread: 2B

  • § Brain
  • § Bone
  • § Not lung

Treatment

  • § Shrink before excision
  • § Systemic lymphoma: uvea[28]
  • § Primary lymphoma: involves two retinal layers[29][30][31] derived from brain

RETINAL LYMPHOMA

OPTIC NERVE[32]

2 common tumors

  • § Gliomas (pilocytic astrocytoma)
  • § Meningiomas
  • § Stroke of optic nerve
  • § By temporal arteritis, embolism or thrombosis
  • § Optic nerve head is swollen and hyperemic[34]
  • § Unilateral if local compression
  • § Bilateral if increased intracranial pressure

ANTERIOR ISCHEMIA OPTIC NEUROPATHY

PAPILLEDEMA[33]

GLAUCOMATOUS OPTIC NERVE DAMAGE

Micro

  • § Atrophy
  • § Optic nerve head cupping
  • § Small atrophic, internally disorganized eye

PHTHISIS BULBI[35]

Etio

  • § Trauma
  • § Intraocular inflammation
  • § Chronic retinal detachment

Micro

  • § Ciliochoroidal effusion[36][37]
  • § Cyclitic membrane[38]
  • § Chronic retinal detachment
  • § Optic nerve atrophy
  • § Intraocular bone from osseous metaplasia of retinal pigment epithelium
  • § Thickened sclera
  • § Idiopathic orbital inflammation IOI
  • § Wegener
  • § Lymphoma
  • § Metastatic prostatic carcinoma to orbit!
  • § Spindle vs epithelioid

LYMPHOCYTES IN ORBIT***

OCULAR MELANOMA CLASSIFICATION AND PROGNOSIS***

Prognosis

  • § Location (indolent if limited to iris vs more aggressive in ciliary body and choroid)
  • § Epithelioid more aggressive than spindle cell
  • § Lateral growth bad[39]
  • § Mitoses
  • § Heavy intratumoral lymphocytic infiltrate bad
  • § Extraocular extension
  • § Looping patterns rich in laminin (vasculogenic mimicry) bad

PINGUECULA AND PTERYGIUM

Pinguecula Pterygium
Actinic injury Actinic injury
Raised white-yellow spots on limbus Grows from limbus to cornea
-Does not invade Bowman’s

-Solar elastosis+/-granulomas

-Submucosal FV tissue proliferation that migrates into cornea

-Dissects Bowman’s layer[40]

Focal dehydration causing depression (dellen) No vision problem
  Benign but rarely SCC and melanoma

NORMAL LAYERS OF CORNEA

  • § Nonkeratinizing squamous epithelium
  • § BM
  • § Bowman’s layer (acellular)[41]
  • § Stroma[42]
  • § Descemet membrane[43]=BM (PAS+)
  • § Endothelium[44]
  • § Inflammation
  • § High intraocular pressure (staphyloma)
  • § OI
  • § Congenital nevus

BLUE SCLERA

 


[1] Can form papillae when inflamed

[2] Very large in viral conjunctivitis and favorite site for lymphoma

[3] Independent of thyroid function in Graves

[4] Lymphocytes, plasma cells, eosinophils

[5] First 2 are non-encapsulated and in kids whereas cavernous hemangioma is encapsulated and in adult

[6] Provoking granulomas

[7] By blepharitis or tumor

[8] Distinct ppredilection for lower eyelid and medial canthus

[9] May become really inflamed at late childhood or adolescence with tons of lymphocytes, plasma cells and eosinophilsà inflamed juvenile nevus

[10] Equivalent to melanoma in situ

[11] Similarly to sebaceous carcinoma of eyelids

[12] Chronic HSV can cause granulomatous reaction to Descemet’s membrane!!!

[13] Calcium in Bowman’s layer. Complicate chronic uveitis

[14] Solar elastosis in superficial layer of corneal stroma

[15] Non-inflammatory, non-vascular. Treated with corneal transplantation

[16] Causes stromal edema and bullous keratopathy

[17] Migration of lens epithelium posterior to lens equator

[18] Most vascular

[19] Instead of red

[20] In malignant HTN

[21] Exudate accumulation dissects between neurosensory and pigmented layers of retina

[22] Sudden, no prolonged infarction, no neovascularization

[23] Neovascularization

[24] Geographic atrophy of retinal pigment epithelium

[25] Due to leaky choroidal neovascular membranes

[26] Intraocular melanoma is no1 malignancy in adults

[27] No prognostic value

[28] ICC=iris, ciliary body, choroid

[29] Neurosensory retina and retinal pigment epithelium

[30] Outer-lying choroid is not infiltrated by malignant lymphocytes

[31] Diagnosis by FNA of vitreous fluid

[32] Considered part of CNS (not PNS)

[33] Optic nerve edema

[34] Because it’s due to venous compression by CSF. In contrast, optic nerve stroke is swollen and pale due to arterial blockage

[35] End-stage eye

[36] Blood or fluid between ciliary body-choroid and sclera

[37] Leading to hypotony (low intraocular pressure)

[38] Bridging membrane from ciliary body to the other across eye

[39] Different from cutaneous melanoma where radial growth has not clinical value

[40] Just underneath BM

[41] Efficient barrier against penetration by malignancy

[42] No BV, no lymphatics

[43] Thickens with age and also site of copper deposition (Kayser-Fleischer ring)

[44] Malfunction of endotheliumà stromal edemaà bullous keratopathy

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