Pathology (eye2/retina/ optic nerve/uvea)

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  1. ................... constitute the uvea
    iris, choroid and ciliary body
  2. True or false: retina and uvea has no lymphatics
  3. What is uveitis?
    Uveitis is restricted to a diverse group of chronic diseases that may be either components of a systemic process or localized to the eye
  4. Anterior uveitis is a feature of .....
  5. What are the causes of uveitis?
    infectious agents (e.g., Pneumocystis carinii), may be idiopathic (e.g., sarcoidosis), or may be autoimmune in origin (sympathetic ophthalmia)
  6. What are the features of sarcoid uveitis?
    • Granulomatous uveitis
    • In the anterior segment it gives rise to an exudate that evolves into “mutton-fat” keratic precipitates.
    • In the posterior segment, sarcoid may involve the choroid and retina. Thus, granulomas may be seen in the choroid.
    • Retinal pathology is characterized by perivascular inflammation; this is responsible for the well-known ophthalmoscopic sign of “candle wax drippings.” Conjunctival biopsy can be used to detect granulomatous inflammation and confirm the diagnosis of ocular sarcoid
  7. What are some infectious causes of uveitis?
    • Retinal toxoplasmosis is usually accompanied by uveitis and even scleritis.
    • Individuals with AIDS may develop cytomegalovirus retinitis and uveal infection such as pneumocystis or mycobacterial choroiditis
  8. What are the features of Sympathetic ophthalmia?
    • 1) Bilateral granulomatous inflammation typically affecting all components of the uvea: a panuveitis
    • 2) May complicate a penetrating injury of the eye
    • 3) In the injured eye, retinal antigens sequestered from the immune system may gain access to lymphatics in the conjunctiva and thus set up a delayed hypersensitivity reaction that affects not only the injured eye but also the contralateral, noninjured eye
    • 4) The condition may develop from 2 weeks to many years after injury. Enucleation of a blind eye (which can be the sympathizing eye rather than the directly injured eye) may yield diagnostic findings. Sympathetic ophthalmia is treated by the administration of systemic immunosuppressive agents.
    • 6) It is characterized by diffuse granulomatous inflammation of the uvea (choroid, ciliary body, and iris). Plasma cells are typically absent, but eosinophils may be identified in the infiltrate

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    •  The granulomatous inflammation depicted here was identified diffusely throughout the uvea. The uveal granulomas may contain melanin pigment and may be accompanied by eosinophils.
  9. The most common intra-ocular malignancy of adults is ....................................
    is metastasis to the uvea, typically to the choroid
  10. What is the significance of intraocular metastasis?
    Short survival
  11. .................. is the most common primary intra-ocular malignancy of adults
    Uveal melanoma
  12. What are the general features of uveal melanoma?
    • Incidence increases with age
    • Not increased like cutaneous melanoma
    • Uveal nevi, especially choroidal nevi are common but rarely progress to melanoma
  13. What is the route of extension of uveal melanoma?
    • Hematogenous
    • There are no lymphatics within the eye; hence, uveal melanomas, with very rare exception, spread exclusively by a hematogenous route (the only exception being the rare case of melanoma that spreads through the sclera and invades the conjunctiva, thereby gaining access to conjunctival lymphatics).
    • Most uveal melanomas spread first to the liver
  14. Most uveal melanoma first metastasize to the .....
  15. What is the histology of uveal melanoma?
    • Two types of cells, spindle and epithelioid
    • Spindle cells are fusiform in shape and have little atypia, whereas epithelioid cells are spherical and have greater cytologic atypicality
    • Melanomas situated exclusively in the iris tend to follow a relatively indolent course, whereas melanomas of the ciliary body and choroid are more aggressive.
    • Presence of looping patterns rich in laminin that surround packets of tumor cells.These “spaces” (which are not blood vessels) connect to blood vessels and serve as extravascular conduits for the transport of plasma and possibly blood
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  16. What are the prognostic factors of uveal melanoma?
    • (1) size (in contrast to cutaneous melanoma, the lateral extent of the tumor rather than tumor depth is the size dimension related to adverse outcome)
    • (2) cell type (tumors containing epithelioid cells have a worse prognosis than do those containing exclusively spindle cells)
    • (3) and proliferative index.
    • In contrast to cutaneous melanomas, large numbers of tumor-infiltrating lymphocytes are associated with an adverse outcome
    • Extra-ocular extension is related to poor prognosis.
    • Monosomy 3 and trisomy 8, and the presence of looping patterns rich in laminin that surround packets of tumor cells
  17. The neurosensory retina, like the optic nerve, is an embryologic derivative of the ........................
  18. The retina responds to injury by means of .....................
  19. Retina contains no lymphatics: true or false
  20. What are the functional anatomy of exudate and bleeding in retina?
    • Hemorrhages in the nerve fiber layer of the retina are oriented horizontally and appear as streaks or “flames;”
    • the external retinal layers are oriented perpendicular to the retinal surface, and hemorrhages in these outer layers appear as dots (cross-sections of cylinders).
    • Exudates tend to accumulate in the outer plexiform layer of the retina, especially in the macula
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  21. What is the cause of flame-shaped hemorrhage?
    The retinal nerve fiber layer is oriented parallel to the internal limiting membrane, and hemorrhages of this layer appear to be flame-shaped ophthalmoscopically
  22. What is the cause of dot hemorrhage?
    The deeper retinal layers are oriented perpendicular to the internal limiting membrane and hemorrhages in this location appear as cross-sections of a cylinder or “dot” hemorrhages
  23. Exudates that originate from leaky retinal vessels accumulate in the ......................
    outer plexiform layer
  24. What is the significance of retinal pigment epithelium (RPE)?
    • The retinal pigment epithelium (RPE), like the retina, is derived embryologically from the primary optic vesicle, an outpouching of the brain.
    • Separation of the neurosensory retina from the RPE defines a retinal detachment.
    • The RPE has an important role physiologically in the maintenance of the outer segments of the photoreceptors.
    • Disturbances in the RPE-photoreceptor interface may play important roles in hereditary retinal degenerations such as retinitis pigmentosa.
  25. What is retinal detachment?
    Separation of the neurosensory retina from the RPE defines a retinal detachment
  26. What is the cause of persistent hyperplastic primary vitreous?
    The adult vitreous humor is avascular. Incomplete regression of fetal vasculature running through the vitreous humor can produce significant pathology as a retrolental mass (persistent hyperplastic primary vitreous).
  27. The vitreous humor can be opacified by .......................
    hemorrhage from trauma or retinal neovascularization
  28. What are the changes of vitreous with age?
    • With age the vitreous humor may liquefy and collapse, creating the visual sensation of “floaters.”
    • Also, with aging, the posterior face of the vitreous humor—the posterior hyaloid—may separate from the neurosensory retina (posterior vitreous detachment)
  29. How is retinal detachment classified?
    Retinal detachment (separation of the neurosensory retina from the RPE) is broadly classified by etiology based on the presence or absence of a break in the retina
  30. What are the features of Rhegmatogenous retinal detachment?
    • Rhegmatogenous retinal detachment is associated with a full-thickness retinal defect.
    • Retinal tears may develop after the vitreous collapses structurally, and the posterior hyaloid exerts traction on points of abnormally strong adhesion to the retinal internal limiting membrane. Liquefied vitreous humor then seeps through the tear and gains access to the potential space between the neurosensory retina and the RPE.
    • Re-attachment of the retina to the RPE generally requires relief of vitreous traction through indenting of the sclera by surgical procedures.
    • Rhegmatogenous retinal detachment may be complicated by proliferative vitreoretinopathy, the formation of epiretinal or subretinal membranes by retinal glial cells (Müller cells) or RPE cells
  31. What are the complications of rhegmatogenous detachment?
    Rhegmatogenous retinal detachment may be complicated by proliferative vitreoretinopathy, the formation of epiretinal or subretinal membranes by retinal glial cells (Müller cells) or RPE cells
  32. What are the features of Non-rhegmatogenous retinal detachment?
    • Non-rhegmatogenous retinal detachment (retinal detach-ment without retinal break) may complicate retinal vascular disorders associated with significant exudation and any condition that damages the RPE and permits fluid to leak from the choroidal circulation under the retina.
    • Retinal detachments associated with choroidal tumors and malignant hypertension are examples of non-rhegmatogenous retinal detachment.
  33. What is the pathophysiology of retinal detachment?
    • Retinal detachment is defined as the separation of the neurosensory retina from the RPE. Retinal detachments are classified broadly into non-rhegmatogenous (without a retinal break) and rhegmatogenous (with a retinal break) types. 
    • Top, In non-rhegmatogenous retinal detachment the subretinal space is filled with protein-rich exudate. Note that the outer segments of the photoreceptors are missing (see Fig. 29-16 for orientation of layers). This indicates a chronic retinal detachment, a finding that can be seen in both non-rhegmatogenous and rhegmatogenous detachments. 
    • Middle, Posterior vitreous detachment involves the separation of the posterior hyaloid from the internal limiting membrane of the retina and is a normal occurrence in the aging eye
    • Bottom, If, during a posterior vitreous detachment, the posterior hyaloid does not separate cleanly from the internal limiting membrane of the retina, the vitreous humor will exert traction on the retina, which will be torn at this point. Liquefied vitreous humor seeps through the retinal defect, and the retina is separated from the RPE. The photoreceptor outer segments are intact, illustrating an acute detachment
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  34. Missing outer segments of the photoreceptors indicates.............
    chronic retinal detachment
  35. What are the changes of retinal vessels in HTN?
    • Normally, the thin walls of retinal arterioles permit a direct visualization of the circulating blood by ophthalmoscopy.
    • In retinal arteriolosclerosis the thickened arteriolar wall changes the ophthalmic perception of circulating blood: vessels may appear narrowed, and the color of the blood column may change from bright red to copper and to silver depending on the degree of vascular wall thickness.
    • Retinal arterioles and veins share a common adventitial sheath. Therefore, in pronounced retinal arteriolosclerosis the arteriole may compress the vein at points where both vessels cross.
    • Venous stasis distal to arteriolar-venous crossing may precipitate occlusions of the retinal vein branches
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    • The retina in hypertension. A, The wall of the retinal arteriole (arrow) is thick. Note the exudate (e) in the retinal outer plexiform layer. B, The fundus in hypertension. The diameter of the arterioles is reduced, and the color of the blood column appears to be less saturated (copper wire–like). If the wall of the vessel were thicker still, the degree of red color would diminish such that the vessels might appear clinically to have a “silver-wire” appearance. In this fundus photograph, note that the vein is compressed where the sclerotic arteriole crosses over it.
  36. What are the retinal changes in malignant HTN?
    • Vessels in the retina and choroid may be damaged.
    • Damage to choroidal vessels may produce focal choroidal infarcts, seen clinically as Elschnig pearls.
    • Damage to the choriocapillaris, the internal layer of the choroidal vasculature, may, in turn, damage the overlying RPE and permit the exudate to accumulate in the potential space between the neurosensory retina and the RPE, thereby producing a retinal detachment.
    • Exudate from damaged retinal arterioles typically accumulates in the outer plexiform layer of the retina.
    • The ophthalmoscopic finding of a macular star—a spokelike arrangement of exudate in the macula in malignant hypertension—results from exudate accumulating in the outer plexiform layer of the macula that is oriented obliquely instead of perpendicular to the retinal surface
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    • Hypertensive retinopathy with scattered flame (splinter) hemorrhages and cotton-wool spots
  37. What is the pathophysiology of cotton-wool spot?
    • Occlusion of retinal arterioles may produce infarcts of the nerve fiber layer of the retina (axons of the retinal ganglion cell layer populate the nerve fiber layer).
    • Axoplasmic transport in the nerve fiber layer is interrupted at the point of axonal damage, and accumulation of mitochondria at the swollen ends of damaged axons creates the histologic illusion of cells (cytoid bodies).
    • Collections of cytoid bodies populate the nerve fiber layer infarct, seen ophthalmoscopically as “cotton-wool spots”.
    • Seen in HTN and retinal occlusive vasculopathies
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    • cytoid body arrowhead.. hemorrhage arrow.. cottonwool
  38. Cotton wool spots are indeed:.............
    Accumulation of mitochondria in the end of swollen axon as a result of nerve fiber layer infarct
  39. What is the most reliable marker of diabetes in the eye?
    • Thickening of the basement membrane of the epithelium of the pars plicata of the ciliary body is a reliable histologic marker of diabetes mellitus in the eye
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  40. What are the hallmarks of Background (preproliferative) diabetic retinopathy?
    • Confined beneath the internal limiting membrane of the retina
    • Basement membrane of retinal blood vessels is thickened.
    • Number of pericytes relative to endothelial cells diminishes. 
    • Microaneurysms (not seen by ophthalmoscope)
    • Breakdown in the blood-retinal barrier--> leak--> macular edema
    • Exudates that accumulate in the outer plexiform layer
    • Although the retinal microcirculation is often hyperpermeable it is also subject to the effects of micro-occlusion
  41. Background diabetic retinopathy showing microaneurysms (small arrows) and hard exudates. The blood vessels can be seen running over the hard exudates (large arrow), indicating that the exudates are due to leakage in the deeper retinal layers (in contrast to soft exudates, which are microinfarcts in the superficial retinal layers with obliterated blood vessels). Many of the hard exudates are clustered around the macula, which is at the periphery at about four o'clock.
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  42. What is the pathophysiology of diabetic proliferative retinopathy?
    • Nonperfusion of the retina due to the microcirculatory change described above is associated with up-regulation of VEGF and retinal angiogenesis.
    • The development of intraretinal angiogenesis—new vessels confined within the retina beneath the internal limiting membrane—can be included with lesions termed intraretinal microangiopathy
  43. What are the features of diabetic proliferative retinopathy?
    • Clinically, proliferative diabetic retinopathy is defined by the appearance of new vessels that sprout from existing vessels—angiogenic vessels—on the surface of either the optic nerve head, which is termed neovascularization of the disc, or the surface of the retina, which is designated by the nebulous term neovascularization elsewhere.
    • The newly formed vessels breach the internal limiting membrane of the retina.
    • The web of newly formed vessels is called a neovascular membrane both clinically and histopathologically. It is composed of angiogenic vessels with or without a substantial supportive fibrous or glial stroma
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  44. What are the complications of proliferative retinopathy?
    • If the vitreous humor has not detached and the posterior hyaloid is intact, neovascular membranes extend along the potential plane between the retinal internal limiting membrane and the posterior hyaloid. Thus, the separation of the vitreous humor from the internal limiting membrane of the retina (posterior vitreous detachment) after retinal neovascularization may precipitate massive hemorrhage from the disrupted neovascular membrane.
    • Organization of the retinal neovascular membrane may wrinkle the retina, disrupting the orientation of retinal photoreceptors and producing visual distortion, and may exert traction on the retina, separating it from the RPE (retinal detachment). 
    • Traction retinal detachment may begin as a non-rhegmatogenous detachment, but severe traction may tear the retina, producing a traction rhegmatogenous detachment
    • Retinal neovascularization may be accompanied by the development of a neovascular membrane on the iris surface, presumably secondary to increased levels of VEGF in the aqueous humor. 
    • Contraction of the iris neovascular membrane may lead to adhesions between the iris and trabecular meshwork (anterior synechiae), thus occluding a major pathway for aqueous outflow and thereby contributing to elevation of the intra-ocular pressure (neovascular glaucoma).
    • Ablating nonperfused retina by laser photocoagulation or cryopexy triggers regression of both retinal and iris neovascularization.
  45. Absence of the ganglion cell and nerve fiber layers is a hallmark of ..................
  46. What are the features of ROP?
    • At term, the nasal (medial) aspect of the retina is vascularized, but the temporal (lateral) aspect of the retinal periphery is incompletely vascularized.
    • In premature or low-birth-weight infants treated with oxygen, the immature retinal vessels in the temporal retinal periphery can constrict, rendering the retinal tissue distal to this zone ischemic.
    • Retinal ischemia can result in up-regulation of pro-angiogenic factors such as VEGF and lead to retinal angiogenesis.
    • Contraction of a peripheral retinal neovascular membrane may result in “dragging” of the temporal aspect of the retina toward the temporal peripheral zone such that the macula (situated temporal to the optic nerve) is displaced laterally. With significant contraction the retina can detach.
  47. What are the characteristics of sickle retinopathy?
    • Nonproliferative (intraretinal angiopathic changes) and proliferative (retinal neovascularization). The final common pathway in both types is vascular occlusion.
    • Low oxygen tension within the blood vessels in the retinal periphery results in sickling and red cell deformation causing microvascular occlusions.
    • In the nonproliferative form (which occurs in individuals with SS, and SC hemoglobins), vascular occlusions are thought to contribute to preretinal, intraretinal, and subretinal hemorrhages. 
    • Salmon patches, iridescent spots, and black sunburst lesions.
    • Organization of pre-retinal hemorrhage may result in retinal traction and retinal detachment.
    • Up-regulation of both VEGF and basic fibroblast growth factor-->retinal neovascularization in the periphery, described clinically as “sea-fans.
  48. Neovascularization also seen in..............
    peripheral retinal vasculitis, and irradiation
  49. What is the pathophysiology of CRAO?
    • Thrombosis or emboli from heart or carotid
    • Fragments of atherosclerotic plaques can lodge within the retinal circulation (Hollenhorst plaques).
    • Total occlusion of a branch retinal artery can produce a segmental infarct of the retina.
    • With sudden cessation of blood supply, the retina (an embryologic derivative of brain tissue) swells acutely and becomes optically opaque. By ophthalmoscopy the fundus in the affected area appears white instead of red or orange, because the retinal opacity blocks the view of the richly vascular choroid
    • Total occlusion of the central retinal artery can produce a diffuse infarct of the retina. The fovea and foveola are physiologically thin; therefore, the normal orange-red of the choroid is not only visible but highlighted by the surrounding opaque retina—the origin of the cherry-red spot of the central retinal artery occlusion.
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  50. What is the pathophysiology of Cherry red spot in storage diseases?
    • The cherry-red spots seen in rare storage diseases such as Tay-Sachs and Niemann-Pick diseases also have their basis in the anatomic variations of the macula.
    • The storage material accumulates in retinal ganglion cells: the ganglion cell layer of the macula surrounding the fovea is thick, but there are no ganglion cells in the center of the macula, the fovea.
    • Thus, the fovea is relatively transparent to the underlying choroidal vasculature but is rimmed by relatively opaque retina, the result of storage material accumulating in the perifoveal macular ganglion cells
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  51. True or false: retinal arterial occlusions are seldom complicated by either retinal or iris neovascularization
    True (it is acute--> no upregulation of angiogenic factors)
  52. What are the features of CRVO?
    • Retinal vein occlusion may occur with or without ischemia.
    • In ischemic retinal vein occlusion, VEGF and other proangiogenic factors are up-regulated in the retina, leading to neovascularization of the retina and surface of the optic nerve head as well as neovascularization of the iris and subsequent angle-closure glaucoma.
    • Non-ischemic retinal vein occlusion may be complicated by hemorrhages, exudates, and macular edema but is seldom complicated by retinal or iris neovascularization.
    • Blood and thunder
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  53. True or false: most ARMD are heritable
  54. What are the major RF for ARMD?
    Individuals with the CFH CC (Complement factor H) genotype who have smoked at least 10 pack-years
  55. Where is the disturbance in ARMD located?
    • Structural and functional unit composed of the retinal pigment epithelium (RPE), Bruch membrane (which contains the basement membrane of the RPE), and the innermost layer of the choroidal vasculature, the choriocapillaris.
    • Disturbance in any component of this “unit” affects the health of the overlying photoreceptors, producing visual loss
  56. What are the two types of ARMD?
    • nonneovascular (atrophic or dry)--> diffuse or discrete deposits in the Bruch membrane (drusen) and geographic atrophy of the RPE/20% develop choroidal neovascular membranes (loss of vision more severe)
    • neovascular (exudative or wet)-->presence of angiogenic vessels that presumably originate from the choriocapillaris and penetrate through the Bruch membrane beneath the RPE/ This neovascular membrane may also penetrate the RPE and become situated directly beneath the neurosensory retina. The vessels in this membrane may leak, and the exuded blood may be organized by RPE cells into macular scars.
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  57. What are the symptoms of ARMD?
    • Patients with dry AMD may complain of gradual loss of vision in one or both eyes.
    • Wet AMD may present as acute visual distortion or loss of central vision as a result of subretinal hemorrhage or fluid accumulation.
    • Symptoms of wet AMD usually appear in one eye, although the disease is often present in both eyes. Distortion of straight lines (metamorphopsia) is one of the earliest changes with wet AMD
  58. What are the features of Retinitis Pigmentosa?
    • Retinitis pigmentosa is linked to mutations in genes that regulate the functions of either the photoreceptor cells or the RPE.
    • Typically, both rods and cones are lost to apoptosis, though in varying proportions.
    • Loss of rods may lead to early night blindness and constricted visual fields. As cones are lost, central visual acuity may be affected.
    • Clinically, retinal atrophy is accompanied by constriction of retinal vessels and optic nerve head atrophy (“waxy pallor” of the optic disk) and the accumulation of retinal pigment around blood vessels, thus accounting for the “pigmentosa” in the disease's name.
  59. What is the morphological feature of RP?
    retinal atrophy is accompanied by constriction of retinal vessels and optic nerve head atrophy (“waxy pallor” of the optic disk) and the accumulation of retinal pigment around blood vessels
  60. What are the general features of retinoblastoma?
    • Most common primary intra-ocular malignancy of children
    • Origin of retinoblastoma is neuronal
    • germline mutation of one RB allele
    • Also associated with pinealoblastoma and osteosarcoma
  61. Origin of retinoblastoma is ..........
  62. What is the morphology of retinoblastoma
    • Tumors may contain both undifferentiated and differentiated elements.
    • The former appear as collections of small, round cells with hyperchromatic nuclei.
    • In well-differentiated tumors there are Flexner Wintersteiner rosettes and fleurettes reflecting photoreceptor differentiation.
    • Differentiation does not appear to be associated with the prognosis.
    • Viable tumor cells are found encircling tumor blood vessels with zones of necrosis typically found in relatively avascular areas.
    • Focal zones of dystrophic calcification are characteristic of retinoblastoma.
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    • Dystrophic calcification (dark arrow) is present in the zones of tumor necrosis. Flexner-Wintersteiner rosettes—arrangements of a single layer of tumor cells around an apparent “lumen”
  63. What are the prognostic features of retinoblastoma?
    • Retinoblastoma tends to spread to the brain and bone marrow and seldom disseminates to the lungs.
    • Prognosis is adversely affected by extra-ocular extension and invasion along the optic nerve, and by choroidal invasion
  64. What are the features of retinal lymphoma?
    • Primary retinal lymphoma is analogous to primary large-cell lymphoma of the brain; therefore, it involves the two retinal layers derived from brain: the neurosensory retina and the RPE.
    • The underlying choroid is typically filled with a cytologically benign lymphoid infiltrate.
    • The diagnosis depends on a demonstration of lymphoma cells in vitreous aspirates
  65. the most common primary neoplasms of the optic nerve are .....................
    glioma (typically pilocytic astrocytomas) and meningioma
  66. What are the features of ANTERIOR ISCHEMIC OPTIC NEUROPATHY?
    • AION includes a spectrum of injuries to the optic nerve varying from ischemia to infarction
    • Transient partial interruptions in blood flow to the optic nerve can produce episodes of transient loss of vision, whereas total interruption in blood flow can produce an optic nerve infarct, either segmental or total. Zones of relative ischemia may surround segmental infarcts of the optic nerve. Optic nerve function in these poorly perfused but not infarcted zones may recover. The optic nerve does not regenerate, and visual loss from infarction is permanent
    • Interruption in the blood supply to the optic nerve can result from inflammation of the vessels that supply the optic nerve, known as arteritic AION, or from embolic or thrombotic events, known as non-arteritic AION. Bilateral total infarcts of the optic nerve resulting in total blindness have been reported in temporal arteritis (arteritic AION)
  67. What is the cause of papilledema?
    • Edema of the head of the optic nerve may develop as a consequence of compression of the nerve (as in a primary neoplasm of the optic nerve) or from elevations of cerebrospinal fluid pressure surrounding the nerve. The concentric increase in pressure encircling the nerve contributes to venous stasis both at the nerve head and in axoplasmic transport, leading to nerve head swelling.
    • Swelling of the optic nerve head in elevated intra-cranial pressure is typically bilateral (unless the affected individual has experienced previous unilateral optic atrophy) and is commonly termed papilledema.
    • Typically, acute papilledema from increased intra-cranial pressure is not associated with visual loss.
    • Ophthalmoscopically, the optic nerve head is swollen and hyperemic; by contrast, the optic nerve head in the relatively acute phases of anterior ischemic optic neuropathy appears swollen and pale because of decreased nerve perfusion.
    • In papilledema secondary to increased intra-cranial pressure, the optic nerve may remain congested for a prolonged period of time
  68. What is the the histologic explanation for the blurred margins of the optic nerve head in papilledema?
    Normally, the termination of Bruch membrane is aligned with the beginning of the neurosensory retina, as indicated by the presence of stratified nuclei, but in papilledema the optic nerve is swollen, and the retina is displaced laterally.
  69. mutations in the .................gene are seen in individuals with normal-tension glaucoma but are not seen in individuals with primary open-angle glaucoma, in which pressure is elevated chronically
  70. What are the characteristic findings of optic nerve in glaucoma?
    • Characteristically, there is a diffuse loss of ganglion cells and thinning of the retinal nerve fiber layer, which can be measured by optical coherence tomography.
    • In advanced cases, the optic nerve is both cupped and atrophic, a combination unique to glaucoma.
    • Elevated intra-ocular pressure in infants and children can lead to diffuse enlargement of the eye (buphthalmos) or enlargement of the cornea (megalocornea). After the eye reaches its adult size, prolonged elevation of intra-ocular pressure can lead to focal thinning of the sclera, and uveal tissue may line ectatic sclera (staphyloma).
  71. The retina and optic nerve in glaucoma
    • A, Left panel, normal retina; right panel, the retina in long-standing glaucoma (same magnification). The full thickness of the glaucomatous retina is captured (right), a reflection of the thinning of the retina in glaucoma. In the glaucomatous retina, the areas corresponding to the nerve fiber layer (NFL) and ganglion cell layer (GC) are atrophic; the inner plexiform layer (IPL) is labeled for reference. Note also that the outer nuclear layer of the glaucomatous retina is aligned with the inner nuclear layer of the normal retina due to the thinning of the retina in glaucoma. See Figure 29-16 for orientation. B, Glaucomatous optic nerve cupping results in part from loss of retinal ganglion cells, the axons of which populate the optic nerve. C, The arrows point to the dura of the optic nerve. Notice the wide subdural space, a result of atrophy of the optic nerve. There is a striking degree of cupping on the surface of the nerve as a consequence of long-standing glaucoma.
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  72. What is the ophthalmoscopic view of glaucoma?
    Optic atrophy +Cupping
  73. Why do mitochondrial disorders cause optic abnormalities?
    Since neuronal health is dependent on axoplasmic transport of mitochondria, mitochondrial dysfunctions give rise to neurologic disorders including optic neuropathy
  74. optic neuritis is used to describe a loss of vision secondary to .....................
    demyelinization of the optic nerve
  75. What are the features of CMV retinitis?
    • Yellow-white fluffy or granular retinal lesions near vessels
    • Hemorrhage
    • Retinal detachment
    • Painless
  76. What are the features of toxoplasma retinitis?
    • Painful+reduced acuity
    • Raised yellow-white cotton lesions 
    • Nonvascular
    • Retinal necrosis
    • CNS involvement in 50%
Card Set:
Pathology (eye2/retina/ optic nerve/uvea)
2013-10-10 20:03:39
Pathology eye2

Pathology (eye2)
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