Pathology (eye)

Card Set Information

Pathology (eye)
2013-10-10 12:50:16
Pathology eye

Pathology (eye)
Show Answers:

  1. the most common cause of irreversible visual loss in the United States
    age-related macular degeneration (ARMD)
  2. What are the two types of proptosis?
    • Proptosis may be axial (directly forward) or positional
    • Any enlargement of the lacrimal gland from inflammation  or neoplasm produces a proptosis that displaces the eye inferiorly and medially
    • Masses contained within the cone formed by the horizontal rectus muscles generate axial proptosis: the eye bulges straight forward. The two most common primary tumors of the optic nerve  glioma and meningioma, produce axial proptosis because the optic nerve is positioned within the muscle cone
  3. What are the features of thyroid ophthalmopathy?
    • Proptosis is caused by the accumulation of extracellular matrix proteins and variable degrees of fibrosis in the rectus muscles
    • Tendons are spared
  4. Which conditions of sinus can cause orbital involvement?
    • Bacterial, fungal
    • Wegener
  5. The presence of necrotic collagen along with vasculitis in orbital inflammation should raise the suspicion of .............
    Wegener granulomatosis
  6. What is the mc primary neoplasm of orbit?
  7. Structure of eyelid
  8. What is a chalazion?
    • Chronic inflammatory lesion that develops when a Zeis or meibomian tear gland of the eyelid becomes obstructed
    • A chalazion may first present with eyelid swelling and erythema and then evolve into a painless, rubbery, nodular lesion
  9. What is hordeolum?
    • A hordeolum is an acute purulent inflammation of the eyelid.
    • It may be sterile or may show both inflammatory cells and bacteria, most commonly Staphylococcus aureus.
    • An internal hordeolum represents inflammation of a meibomian gland just under the conjunctival side of the eyelid.
    • An external hordeolum (stye) arises from an eyelash follicle or a lid-margin tear gland
  10. The most common malignancy of the eyelid is ........................
    basal cell carcinoma
  11. The second most common malignancy  of eyelid is .............
    sebaceous carcinoma
  12. Where is the location for BCC of eyelid?
    Lower eyelid and the medial canthus
  13. What are the features of sebaceous carcinoma?
    • May mimics chalazion or may diffusely thicken the eyelid or inflammatory processes.
    • Tends to spread first to the parotid and submandibular nodes
    • High mortality
  14. What is the morphology of sebaceous carcinoma?
    • vacuolization of the cytoplasm
    • Pagetoid spread
    • Sebaceous carcinoma may spread through the conjunctival epithelium and the epidermis to the lacrimal drainage system and the nasopharynx.
    • It may also extend into the lacrimal gland ductules and thereby into the main lacrimal gland.
  15. What is the functional anatomy of palpebral conjunctiva?
    The conjunctiva lining the interior of the eyelid, the palpebral conjunctiva, is tightly tethered to the tarsus and may respond to inflammation by being thrown into minute papillary folds as may occur in allergic conjunctivitis and bacterial conjunctivitis.
  16. What is the functional anatomy of conjunctival fornix?
    • The conjunctiva in the fornix is a pseudostratified columnar epithelium rich in goblet cells. 
    • The fornix also contains accessory lacrimal tissue, and the ductules of the main lacrimal gland pierce through the conjunctiva in the fornix superiorly and laterally. 
    • The lymphoid population of the conjunctiva is most noticeable in the fornix, and in viral conjunctivitis, lymphoid follicles may enlarge sufficiently to be visualized clinically by slit-lamp examination. 
    • Granulomas (sarcodiosis) and marginal zone lymphoma are seen in the fornix
  17. What is the characteristic of bulbar conjunctiva?
    The bulbar conjunctiva—the conjunctiva that covers the surface of the eye—is a nonkeratinizing stratified squamous epithelium.
  18. How is the lymphatics of conjunctiva and eyelid?
    The conjunctiva, like the eyelid, is richly invested with lymphatic channels. Malignant neoplasms arising in the eyelid and conjunctiva tend to spread to regional lymph nodes (parotid and submandibular node groups).
  19. What are the causes of conjunctival scarring?
    • Cicatricial pemphigoid
    • Alkali
    • Trachoma
  20. What is the consequence of conjunctival scarring?
    • A reduction in the number of goblet cells due to conjunctival scarring leads to a decrease in surface mucin, which is essential for the adherence of the aqueous component of tears to the corneal epithelium.
    • Thus, even if the aqueous component of the tear film is adequate, the affected individual will suffer from a dry eye, a condition that, when severe, can be painful and can predispose to corneal opacification and ulceration.
    • More commonly, however, dry eye results from a deficiency in the aqueous component of the tear film generated by the accessory lacrimal glands embedded within the eyelid and fornix.
  21. What are the features of pinguecula and pterygium?
    • Both pinguecula and pterygium appear as submucosal elevations on the conjunctiva.
    • They result from actinic damage and are therefore located in the sun-exposed regions of the conjunctiva (i.e., in the fissure between both the upper and lower eyelids—the interpalpebral fissure).
  22. What are the characteristics of Pterygium?
    • Pterygium typically originates in the conjunctiva astride the limbus.
    • It is formed by a submucosal growth of fibrovascular connective tissue that migrates onto the cornea, dissecting into the plane occupied normally by the Bowman layer.
    • Pterygium does not cross the pupillary axis and, aside from the possible induction of mild astigmatism, does not pose a threat to vision.
    • Benign but may contain precursor of SCC
  23. What is the feature of Pingecula?
    • Pinguecula, which, like pterygium, appears astride the limbus, is a small, yellowish submucosal elevation.
    • Although the pinguecula does not invade the cornea as pterygium does, the presence of a focal conjunctival elevation near the limbus can result in an uneven distribution of the tear film over the adjacent cornea.
    • As a consequence of focal dehydration, a saucer-like depression in the corneal tissue—a dellen—may develop
  24. Both squamous neoplasms and melanocytic neoplasms and their precursors tend to develop at the ............of conjunctiva
  25. ...............carcinoma of the conjunctiva tend to have an aggressive course
  26. Pigmented lesions that invade the cornea or appear in the fornix or over the palpebral conjunctiva are..................
  27. ................... of the conjunctiva characteristically contain subepithelial cysts lined by surface epithelium
    • Compound nevi
    • A, B, Cystic compound nevus of the conjunctiva. C, D, Conjunctival malignant melanoma. In C, note the deflection of the beam of the slit lamp over the surface of the lesion, indicative of invasion
  28. What are the features of inflamed juvenile nevus?
    In late childhood or adolescence, conjunctival nevi may acquire an inflammatory component rich in lymphocytes, plasma cells, and eosinophils. The resultant inflamed juvenile nevus is completely benign and not associated with vitiligo or halo nevus.
  29. ....................................................make up the major refractive surface of the eye
    The cornea and its overlying tear film—not the lens—
  30. What are the layers of cornea?
    • Epithelium
    • Basement membrane (PAS+)
    • Bowman membrane (acellular and forms an efficient barrier against the penetration of malignant cells from the epithelium into the underlying stroma)
    • Corneal stroma (lacks blood vessels and lymphatics, precise alignment of collagen)
    • Descemet membrane (BM/ PAS+)
    • Endothelium
  31. What is the importance of lack of blood vessels and lymphatics in corneal stroma?
    transparency of the cornea, high rate of success of corneal transplantation
  32. What is the cause of graft failure in corneal transplant?
    non-immunological graft failure (associated with loss of endothelial cells and subsequent corneal edema)
  33. The risk of corneal graft rejection increases with ..................................
    stromal vascularization and inflammation
  34. A precise alignment of collagen in the corneal stroma also contributes to ...............
  35. How can scarring and edema contribute to corneal opacification?
    both disrupt the spatial alignment of stromal collagen
  36. How is deturgescence of  corneal stroma is maintained?
    by active pumping of fluid from the stroma back into the anterior chamber by the corneal endothelium
  37. The corneal endothelium is derived from .............
    neural crest
  38. How does bulbous keratopathy occur?
    A decrease in endothelial cells or a malfunction of endothelium results in stromal edema, which may be complicated by bullous separation of the epithelium(bullous keratopathy).
  39. Descemet membrane increases in thickness with ...
  40. What is the site of copper deposition in Wilson?
    Descemet membrane
  41. What occurs to corneal stroma in all types of keratitis?
    In all forms of keratitis, dissolution of the corneal stroma may be accelerated by activation of collagenases within corneal epithelium and stromal fibroblasts (also known as keratocytes)
  42. What are the features of hypopyon?
    • Exudate and cells leaking from iris and ciliary body vessels into the anterior chamber may be visible by slit-lamp examination and may accumulate in sufficient quantity to become visible even by a penlight examination (hypopyon).
    • Although the corneal ulcer may be infectious, the hypopyon seldom contains organisms and is an example par excellence of the vascular response to acute inflammation
  43. What is the feature of chronic herpes keratitis?
    chronic herpes simplex keratitis may be associated with a granulomatous reaction involving the Descemet membrane
    • Degeneration--> uni or bilateral/ nonhereditary
    • Dystrophy--> bilateral/ hereditary
  45. What are Band Keratopathies?
    • Degenerations
    • Calcific band keratopathy is characterized by deposition of calcium in the Bowman layer. This condition may complicate chronic uveitis, especially in individuals with chronic juvenile rheumatoid arthritis
    • Actinic band keratopathy develops in individuals who are exposed chronically to high levels of UV. In this condition, extensive solar elastosis develops in the superficial layers of corneal collagen in the sun-exposed interpalpebral fissure, hence the horizontally distributed band of pathology. Similar to pinguecula, the sun-damaged collagen of the cornea appears clinically to be yellow.
  46. What are the general features of keratoconus?
    • Progressive thinning and ectasia of the cornea without evidence of inflammation or vascularization
    • Cornea that has a conical rather than spherical shape. This abnormal shape generates irregular astigmatism that is difficult to correct with spectacles. Rigid contact lenses generate a smooth, spherical surface to the cornea and may provide refractive relief for individuals with keratoconus
    • If not treated by lens--> transplant
    • Bilateral
    • Associated with Down syndrome, and Marfan syndrome, and atopic eczema
    • Activation of collagenases, gelatinases, and matrix metalloproteinases
  47. ...................................are the histologic hallmarks of keratoconus
    Thinning of the cornea with breaks in the Bowman layer
  48. What are the morphological features of keratoconus?
    • Thinning of the cornea with breaks in the Bowman layer are the histologic hallmarks of keratoconus.
    • In some patients the Descemet membrane may rupture precipitously, allowing the aqueous humor in the anterior chamber to gain access to the corneal stroma. The sudden effusion of aqueous humor through a gap in the Descemet membrane—corneal hydrops—may also cause vision to worsen suddenly.
    • An episode of hydrops may be followed by corneal scarring that can also contribute to visual loss.
    • Keratoconus. The tissue section is stained by PAS to highlight the epithelial basement membrane (ebm), which is intact, the Bowman layer (bl), situated between the epithelial basement membrane, and the stroma (s). Following the Bowman layer from the right side of the photomicrograph toward the center, there is a discontinuity, diagnostic of keratoconus. The epithelial separation just to the left of the Bowman layer discontinuity resulted from an episode of corneal hydrops, caused by a break in the Descemet membrane (not shown).
  49. What are the causes of corneal hydrops?
    • Keratoconus
    • Descemet membrane ruptures that develop secondary to extraordinary elevations of intraocular pressure in infantile glaucoma (Haab's striae) or following the now uncommon obstetric forceps injury to the eye
  50. What are the two major clinical manifestations of Fuchs endothelial dystrophy?
    stromal edema and bullous keratopathy
  51. What is the major cause of Fuchs dystrophy?
    Endothelial loss
  52. What is the pathophysiology of Fuchs dystrophy?
    • Early in the course of the disease endothelial cells produce droplike deposits of abnormal basement membrane material (guttata) that resemble the fetal component of the Descemet membrane ultrastructurally.
    • Guttata can be visualized clinically by slit-lamp examination. With disease progression, there is a decrease in the total number of endothelial cells, and the residual cells are incapable of maintaining stromal deturgescence.
    • Consequently the stroma becomes edematous and thickens; it acquires a ground-glass appearance clinically, and vision is blurred.
    • Because of chronic edema, the stroma may eventually become vascularized.
    • On occasion the number of endothelial cells may decrease following cataract surgery even in individuals who do not have early forms of Fuchs dystrophy, and the condition is then known as pseudophakic bullous keratopathy
    • With increasing stromal edema, the epithelium undergoes hydropic change, and the detachment of the epithelium from the Bowman layer produces epithelial bullae that may eventually rupture.
    • Fibrous connective tissue may be deposited between the epithelium and Bowman layer (degenerative pannus) either by ingrowth from the limbus or perhaps through fibrous metaplasia of the corneal epithelium.
  53. Sequences of event in Fuchs dystrophy
    EC produce abnormal BM--> decreased number of EC--> inability to maintain deturgescence-->stromal edema (blurred vision)-> neovascularization--> hydropic changes of epithelium--> detachment of epithelium from Bowman (bullae)--> fibrous CT deposited between epithelium and Bowman (pannus)
  54. Fuchs
    • Fuchs dystrophy. This tissue section is stained by PAS to highlight the Descemet membrane, which is thick. Numerous droplike excrescences—guttata—protrude downward from the Descemet membrane. Endothelial cell nuclei are not seen. Epithelial bullae, not shown in this micrograph, were present, reflecting corneal edema.
  55. What are stromal dystrophies?
    • Stromal deposits generate discrete opacities in the cornea may eventually compromise vision.
    • Deposits in the vicinity of the epithelium, its basement membrane, and Bowman layer may result in painful epithelial erosions.
    • Scarring in the vicinity of Bowman layer may generate an irregular corneal surface, further compromising vision. 
    • Macular corneal dystrophy is so named because early in the disease, small nummular (macular) deposits of keratan sulfate develop in the corneal stroma. Later in the course of this AR dystrophy, keratan sulfate is distributed diffusely throughout the stroma and may affect the endothelium.
  56. Mutation in ..........................cause corneal stromal dystrophy
    • the TGFB1 gene, which encodes an extracellular matrix protein called keratoepithelin
    •  needle-shaped deposits of amyloid (lattice dystrophy); chunky deposits of hyalin (granular dystrophy)
  57. What is the anatomy of anterior chamber?
    • The anterior chamber is bounded anteriorly by the cornea, laterally by the trabecular meshwork, and posteriorly by the iris.
    • Aqueous humor, formed by the pars plicata of the ciliary body, enters the posterior chamber, bathes the lens, and circulates through the pupil to gain access to the anterior chamber.

  58. What is the mcc of conjunctivitis?
  59. What are the features of each type of conjunctivitis?
    • All etiologies of conjunctivitis can cause symptoms of the eyes being stuck closed in the morning
    • Bacterial--> unilateral,  thick purulent discharge that continues throughout the day
    • Viral--> injection, mucoid or serous discharge, and a burning, sandy, or gritty feeling in one eye, second eye become involved in 24-48 hoursprofuse tearing, tarsal conjunctiva may have a follicular or "bumpy" appearance, enlarged tender preauricular LN, has prodrome
    • Allergic--> Allergic conjunctivitis typically presents as bilateral redness, watery discharge, and itching, history of atopy
  60. Which structure in the eye has no neoplasm?
  61. What is the anatomy of lens?
    • The lens is a closed epithelial system; the basement membrane of the lens epithelium (known as the lens capsule) totally envelops the lens.
    • Thus, the lens epithelium does not exfoliate like the epidermis or a mucosal epithelium. Instead, the lens epithelium and its derivative fibers accumulate within the confines of the lens capsule, thus “infoliating.
    • With aging, therefore, the size of the lens increases
  62. What are the systemic conditions associated with cataract?
    • Systemic diseases (such as galactosemia, diabetes mellitus, Wilson disease, and atopic dermatitis)
    • drugs (especially corticosteroids)
    • radiation
  63. What is the major type of cataract in elderly?
    • Age-related cataract typically results from opacification of the lens nucleus (nuclear sclerosis).
    • The accumulation of urochrome pigment may render the lens nucleus brown, thus distorting the individual's perception of blue color
  64. How does posterior subcapsular cataract occur?
    • Migration of the lens epithelium posterior to the lens equator may result in posterior subcapsular cataract secondary to enlargement of abnormally positioned lens epithelium.
    • The technique that is most commonly used to remove opacified lenses extracts the lens contents, leaving the lens capsule intact (extracapsular cataract extraction). A prosthetic intra-ocular lens may be inserted into the eye. Residual lens epithelial cells may migrate over the lens capsule, contributing to opacification of the capsule and reduction in vision after surgery
  65. What is lens induced uveitits?
    • Inflammatory reactions to lens material may develop following exposure of the intact lens cortex caused by rupture of the capsule due to trauma or as a result of cataract extraction.
    • It has been suggested that antigen-antibody complexes containing lens cortical material develop especially in the presence of Propionibacterium acnes (which acts as an adjuvant), generating a lens-induced uveitis.
  66. How can lens abnormality cause open angle glaucoma?
    • The lens cortex may liquefy entirely, a condition known as hypermature or morgagnian cataract. High-molecular-weight proteins from liquefied lens cortex may leak through the lens capsule (phacolysis).
    • This phacolytic protein—either free or contained within macrophages—may clog the trabecular meshwork and contribute to elevation in intra-ocular pressure and optic nerve damage
  67. What is the anatomy of aqueous humor?
    • Aqueous humor is produced in the ciliary body and passes from the posterior chamber through the pupil into the anterior chamber.
    • Although there are multiple pathways for the egress of fluid from the anterior chamber, most of the aqueous humor drains through the trabecular meshwork, situated in the angle formed by the intersection between the corneal periphery and the anterior surface of the iris
  68. What are the two types of glaucoma?
    In open-angle glaucoma the aqueous humor has complete physical access to the trabecular meshwork, and the elevation in intra-ocular pressure results from an increased resistance to aqueous outflow in the open angle.

    • In angle-closure glaucoma the peripheral zone of the iris adheres to the trabecular meshwork and physically impedes the egress of aqueous humor from the eye.
  69. What is the mc type of glaucoma?
    primary open-angle glaucoma
  70. What are the features of primary open-angle glaucoma?
    • In primary open-angle glaucoma, the most common form of glaucoma, the angle is open, and few changes are apparent structurally.
    • Mutations in the MYOC in a subset
    • MYOC is present in the tracetabular meshwork, in other anterior segment tissues, and in the optic nerve
  71. What are the causes of secondary open angle glaucoma?
    • Particulate material such as high-molecular-weight lens proteins produced by phacolysis, senescent red cells after trauma (ghost cell glaucoma), iris epithelial pigment granules (pigmentary glaucoma), fragments of oxytalan fibers (exfoliation glaucoma), and necrotic tumors (melanomalytic glaucoma) can clog the trabecular meshwork in the presence of an open angle.
    • Elevations in the pressure on the surface of the eye (episcleral venous pressure) in the presence of an open angle also contributes to secondary open-angle glaucoma. This type of glaucoma is associated with surface ocular vascular malformations seen in Sturge-Weber syndrome or as a consequence of arterialization of the episcleral veins following a spontaneous or traumatic carotid-cavernous fistula
  72. What is the symptom of open angle glaucoma?
    No symptom
  73. What is DOC for open angle glaucoma?
    topical prostaglandins> topical beta blockers
  74. What are the drugs that are used in glaucoma?
    • Agents that suppress aqueous inflow--> beta blocker/ alpha2 agonist/ CAI
    • Agents that increase aqueous outflow--> PG/alpha agonist/cholinergic agonist
  75. What are the important SE and cautions with antiglaucoma agents that suppress aqueous flow?
    • Beta blocker--> Contraindicated in patients with bradycardia, heart block, heart failure, asthma, or obstructive airway disease
    • Alpha blocker (apraclonidine, brimonidine)--> CNS effects and respiratory arrest in young children (brimonidine). Caution in patients with cerebral or coronary insufficiency, Raynauds, postural hypotension, hepatic or renal impairment
    • CAI( Dorzolamide and brinzolamide (topical), acetazolamide and methazolamide (oral))    --> Oral form can cause transient myopia, nausea, diarrhea, loss of appetite and taste, parasthesiae, lassitude, renal stones, and hematological problems
  76. What are the important SE and cautions with antiglaucoma agents that Agents that increase aqueous outflow?
    • PG--> Brown discoloration of iris, lengthening and darkening of eyelashes, macular edema or iritis in suceptible
    • Alpha agonist
    • Cholinergic agonists (Pilocarpine, carbachol)--> Ciliary spasm leading to headaches especially in younger patients, myopia, dim vision (small pupil). Cataracts and iris-lens adhesions in long term.
  77. What is the pathophysiology of primary angle closure glaucoma?
    • Develops in eyes with shallow anterior chambers, often found in individuals with hyperopia
    • Transient apposition of the pupillary margin of the iris to the anterior surface of the lens may result in obstruction to the flow of aqueous humor through the pupillary aperture (pupillary block). Continued production of aqueous humor by the ciliary body thus elevates pressure in the posterior chamber and may bow the iris periphery forward (iris bombé), apposing it to the trabecular meshwork. These anatomic changes provoke a marked elevation in intra-ocular pressure
    • Since the crystalline lens is avascular and the lens epithelium receives its nutrition from the aqueous humor, unremitting elevation in intra-ocular pressure in primary angle-closure glaucoma can damage the lens epithelium. This leads to minute anterior subcapsular opacities that are visible by slit-lamp examination (glaukomflecken).
    • Although the affected individual might have a normal complement of healthy corneal endothelial cells, sustained elevated intra-ocular pressure can produce corneal edema and bullous keratopathy.
  78. What are the symptoms and signs of primary angle closure glaucoma?
    • Symptoms: Decreased vision, Halos around lights, Headache, Severe eye pain, Nausea and vomiting
    • Signs: Conjunctival redness, Corneal edema or cloudiness, A shallow anterior chamber, A mid-dilated pupil (4 to 6 mm) that reacts poorly to light
    • occurs in evening when mydriasis is present in response to reduced light
  79. What are the causes of secondary angle closure glaucoma?
    • Contraction of various types of pathologic membranes that form over the surface of the iris can draw the iris over the trabecular meshwork, occluding aqueous outflow.
    • For example, chronic retinal ischemia is associated with the up-regulation of VEGF and other pro-angiogenic factors. The appearance of VEGF in the aqueous humor is thought to induce the development of thin, clinically transparent fibrovascular membranes over the surface of the iris. Contraction of myofibroblastic elements in these membranes leads to occlusion of the trabecular meshwork by the iris:neovascular glaucoma
    • Necrotic tumors, especially retinoblastomas, can also induce iris neovascularization and glaucoma.
    • Other mechanisms as well; for example, tumors in the ciliary body can mechanically compress the iris onto the trabecular meshwork, closing off the major pathway of aqueous outflow
  80. What is the medical Tx for angle closure glaucoma?
    • Beta blocker/alpha agonist/ cholinergic agonist (topical)
    • Systemic medications (oral or IV acetazolamide, IV mannitol, or oral glycerol or isosorbide)
  81. What are the morphological features of intraocular inflammation?
    • Vessels in the ciliary body and iris become leaky, allowing cells and exudate to accumulate in the anterior chamber.
    • At times the inflammatory cells may adhere to the corneal endothelium, forming clinically visible keratic precipitates.
    • Aggregates of macrophages on the endothelium in sarcoid produce characteristic “mutton-fat” keratic precipitates.
  82. What is the sequel of presence of exudate in the anterior chamber?
    • 1) It can facilitate the formation of adhesions between the iris and the trabecular meshwork or cornea (anterior synechiae) or between the iris and anterior surface of the lens (posterior synechiae).
    • 2) Anterior synechiae can lead to elevation in intra-ocular pressure, which may lead to optic nerve damage.
    • Prolonged contact between the iris and the anterior surface of the lens can deprive lens epithelium of contact with aqueous humor and can induce fibrous metaplasia of the lens epithelium: anterior subcapsular cataract.
    • The exudate (e) present in the anterior chamber would have been visualized with a slit lamp as an optical “flare.” The iris is adherent focally to the cornea, obstructing the trabecular meshwork (anterior synechia, arrow), and to the lens (posterior synechiae, arrowheads). An anterior subcapsular cataract (asc) has formed. The radial folds in the lens are artifacts
  83. What is the pathophysiologic role for pharmacologic induction of pupillary dilation and cycloplegia in individuals with intra-ocular inflammation ?
    in part to prevent the formation of synechiae and their sequelae
  84. What are anterior and posterior synechiae?
    adhesions between the iris and the trabecular meshwork or cornea (anterior synechiae) or between the iris and anterior surface of the lens (posterior synechiae)
  85. What are the sequels of anterior and posterior synechiae?
    • Anterior--> Glaucoma
    • Posterior--> fibrous metaplasia of lens epithelium and anterior subcapsular cataract
  86. What is endophthalmitis ?
    inflammation within the vitreous humor
  87. What is the major sequel of endophthalmitis?
    The retina lines the vitreous cavity, and suppurative inflammation in the vitreous humor (endophthalmitis) is poorly tolerated by the retina; after only a few hours of exposure to acute inflammation, the retina may be irreversibly damaged
  88. How is endophthalmitis classified?
    exogenous (originating in the environment and gaining access to the interior of the eye through a wound) or endogenous (delivered to the eye hematogenously).
  89. What is panophthalmitis?
    inflammation within the eye that involves the retina, choroid, and sclera and extends into the orbit
  90. What are the features of The End-Stage Eye: Phthisis Bulbi?
    • 1) Small (atrophic) and internally disorganized eye
    • 2) The presence of exudate or blood between the ciliary body and sclera and the choroid and sclera (ciliochoroidal effusion);
    • 3) The presence of a membrane extending across the eye from one aspect of the ciliary body to the other (cyclitic membrane)
    • 4) Chronic retinal detachment 
    • 5) Optic nerve atrophy
    • 6) The presence of intra-ocular bone, which is thought by many to originate from osseous metaplasia of the RPE
    • 7) Thickened sclera, especially posteriorly.
    • 8) Ciliochoroidal effusion is typically associated with the physiologic state of low intra-ocular pressure (hypotony). The normal pull of the extra-ocular muscles on a hypotonous eye may render the appearance of the eye as square rather than round
  91. What is the difference between microphthalmic and endstage eye?
    Microphthalmic eye--> not disorganized internally