Robbins Ch.

29 The Eye Review

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1.

>> Figure 29-1 Anatomy of the Eye

7.

Clinically, what does proliferative diabetic retinopathy look like?

2.

Actinic band keratopathy develops due to what? Both pterygium and pinguecula appear in submucosal elevations in conjunctiva. What causes them? Calcific band keratopathy is characterized by what? Cellulitis and mucormycosis

chronically high levels of UV light

3.

sunlight
8.

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 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 (Fig. 29-21) - A mutation at each allele of RB is required to produce retinoblastoma; A child can inherit one germ line mutation and have a sporadic mutation OR - A child can have two sporadic mutations occur - Corneal degenerations may be either unilateral or bilateral and are typically nonfamilial. - By contrast, corneal dystrophies are typically bilateral and are hereditary. Corneal dystrophies may affect selective corneal layers (e.g., Reis-Bckler dystrophy affects Bowman layer, and posterior polymorphous dystrophy affects the endothelium), or the changes may be distributed throughout multiple layers

Describe Knudson's two-hit hypothesis.

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deposition of calcium in Bowman's layer

9.

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The floor of the orbit is the roof of the maxillary sinus, and the medial wall of the orbit-the lamina papyracea-separates the orbit from the ethmoidal sinuses. - Thus, uncontrolled sinus infection may spread to the orbit either as an acute infection (orbital cellulitis) or as a component of a fungal infection (mucormycosis) in immunosuppressed individuals, in patients with diabetic ketoacidosis, or, rarely, in persons without any predisposition. Descement membrane

Difference between corneal degenerations and dystrophies

10.

Figure 29-4 Anatomy of the conjunctiva and eyelids

6.

Chronic herpes simplex keratitis will be associated with a granulomatous reaction involving what membrane?

11.

In the conjunctiva you can see changes from mild dysplasia through carcinoma in situ, which is designated, as what?

conjunctival intra-epithelial neoplasia

12.

In the eye, do melanomas spread via lymphatics? In these conditions, stromal deposits generate discrete opacities in the cornea and may compromise vision? In this condition there is abnormal Descement membrane with progressive loss of endothelial cells? Iris, choroid, ciliary body make up what? Know why sclera might appear blue

no

19.

13.

stromal dystrophies
20.

Mutations of the RB gene predispose to other cancers besides retinoblastoma, what are they? Phthisis Bulbi

osteosarcoma, glioblastoma, and carcinomas of the breast, lung, colon and bladder

Trauma, intra-ocular inflammation, chronic retinal detachment, and many other conditions can give rise to an eye that is both small (atrophic) and internally disorganized: phthisis bulbi - decrease in surface mucin - prevents tears from adhering to corneal epithelium then you get dry eye

14.

Fuch's endothelial dystrophy

21.

Reduction in number of goblet cells due to conjunctival scarring leads to what? What does that do? True or False: Retinoblastoma is the most common primary intraocular malignancy in children. What are cataracts? What are the 2 types of age related macular degeneration? What are the two forms of retinoblastoma and which type is more common? What can happen when this becomes pretty severe? What happens in keratoconus? What is a dellen? Where are these seen?

22.

True

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uvea

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- It may become thin following episodes of scleritis, and the normally brown color of the uvea may appear blue clinically because of the optical Tyndall effect. - Sclera may also be thinned in eyes with exceptionally high intraocular pressure and because this zone of scleral ectasia is lined by uveal tissue, the resulting lesion, known as a staphyloma, also appears blue. - The sclera may appear blue in osteogenesis imperfecta. - Finally, the sclera may appear blue because of a heavily pigmented congenital nevus of the underlying uvea, a condition known as congenital melanosis oculi. When accompanied by periocular cutaneous pigmentation, this condition is known as nevus of Ota uveal melanoma

23.

cataract describes lenticular opacities that may be congenital or acquired non-neovascular and neovascular

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25.

Heritable (30-40%) and Sporadic (60-70%)

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retinal detachment

27.

17.

Most common intra-ocular malignancy in adults is what? Most common malignancy of the eyelid is what?

thinning and ectasia of the cornea resulting in conical shape rather than spherical shape - saucer-like depression in corneal tissue (a consequence of focal dehydration) - pinguecula

28.

18.

basal cell carcinoma

29.

What is a Morgagnian cataract, and what can it lead to?

- the lens cortex may liquefy nearly 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; phacolytic glaucoma is an example of secondary open-angle glaucoma. Chemoreduction

37.

What is the most common primary neoplasm of the optic nerve? What is the most important feature that adversely affects prognosis? What is the second most common malignancy of eyelid? What know a Hollenhorst plaque is (pg 1362) What step of the cell cycle does the RB protein help regulate? Where are the most likely areas that you will see BCC? Where do melanomas spread to first if they MET? Where do you see copper deposition in Wilson's disease? Where does the third tumor usually occur in trilateral retinoblastoma? Why does retrolental fibroplasia happen? Why is infection of the eye with Chlamydia bad? With optic nerve cupping, what would you suspect?

glioma and meningioma

38.

Extension into the optic nerve, particularly if the tumor is present at the surgical margin sebaceous carcinoma

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40.

30.

What is generally the treatment option used in cases when the sight has a high chance of being saved? What is papilledema? What is the difference between open angle glaucoma or angle closure glaucoma? What is the location of the RB gene? What is the main reason for corneal transplantation in the US? What is the most common presenting sign of retinoblastoma? Briefly describe it. What is the most common primary intraocular malignancy of children?

fragments of atherosclerotic plaques can lodge within retinal circulation G1 to S transition

41.

42.

lower lid and medial canthus

31.

edema of head of optic nerve - open-angle glaucoma = high pressure and aqueous can get through, access to trabecular meshwork - angle-closure glaucoma = there is something blocking it, no access to trabecular meshwork Chromosome 13, region 14

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liver

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Descement membrane

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Pineal or suprasellar region

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46.

34.

Fuch's endothelial dystrophy

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administration of oxygen as a premature baby, low birth weight conjunctival scarring increased intra-ocular pressure

48.

35.

Leukocoria- is an abnormal white reflection from the retina (instead of "redeye" you get a "white-eye" reflection b/c the light reflects off of the white tumor)

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retinoblastoma