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Neuro II - Exam 1 > 3-23 Pathology of the Eye > Flashcards

3-23 Pathology of the Eye Flashcards

1
Q

Familiarize yourself with the normal anatomy of the eye.

A

Yup

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2
Q

More normal eye anatomy.

A
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3
Q

What is the limbus in regards to the eye?

A

structure at edge of anterior chamber that represents the fusion of 3 layers:

conjunctiva, episclera, and sclera all fusing onto cornea

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4
Q

What artery can be occluded to cause blindness? What are the causes of occlusion?

A

1)Retinal artery occlusion (or one of its branches, from ophthalmic artery and/or cavernous int carotid aa)…usually due to

A) atheromatous emboli from ipsilateral internal carotid stenosis;

B) stenosis from HT, diabetes;

C) vasculitis

  • infarction of entire artery (or part of)
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5
Q

What is amaurosis fugax?

A

TIA of retinal artery (or branches of) = “Amaurosis fugax”… “browning out” or “loss of vision” in one eye for about 10 minutes …usually caused by ipsilateral internal carotid stenosis.

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6
Q

What is anterior ischemic optic neuropathy?

A

2) neuropathy…short posterior ciliary arteries (branches of the ophthalmic artery)…supply anterior optic nerve.…occlusion results in sudden vision loss in one eye (common in patients over 50)…classic onset is upon wakening
- sometimes seen in temporal arteritis

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7
Q

What are the tumors of the peri-ocular regions?

A
  • Basal cell carcinoma
  • Squamous cell carcinoma
  • Sebaceous cell carcinoma
  • Nevi (Benign tumors)
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8
Q

What is the most common eyelid malignancy? What structures does it preferentially affect?

A
  • Most common eyelid malignancy (~ 25 times more common than SCC)
  • Lower lid>medial canthus>upper lid>outer canthus
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9
Q

What forms of basal cell carcinoma are present as an eyelid malignancy? What histo and gross forms might it take?

A
  • Nodular, cystic, diffuse
  • Islands of basaloid cells with peripheral palisading, stromal desmoplasia, retraction artifact
  • Ulceration may or may not occur;
  • Pigmentation may occur, simulating a melanoma
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10
Q

Is BCC of the eyelid often metastatic?

A

•Locally invasive, rarely metastasizes

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11
Q

What’s this?

A

BCC

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12
Q

What’s this?

A

BCC

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13
Q

What population is most likely to get SCC on the eyelid? Is it metastatic?

A
  • Elderly fair-skinned individuals
  • Potential for local or distant metastasis
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14
Q

What forms, gross & histo, can SCC take?

A
  • Lower lid most common
  • Typically shallow ulcer surrounded by a wide, elevated, and indurated border
  • Polygonal cells with pink eosinophilic cytoplasm, nuclear atypia, infiltrating cords into dermis, dyskeratotic cells, keratin pearls.
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15
Q

What’s this?

A

SCC

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16
Q

What’s this?

A

SCC

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17
Q

What’s this?

A

SCC

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18
Q

What population is more affected by sebaceous carcinoma of the eye?

A

•Elderly, more female, > Asians

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19
Q

What can sebaceous carcinoma of the eyelid mimic? What part of the eye does it most often arise from?

A
  • Can mimic chalazion or chronic blepharoconjunctivitis
  • 2/3rds in upper lid
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20
Q

What glands can sebaceous carcinoma arise from? What is its appearance histologically?

A
  • Can arise from meibomian, Zeis (lash follicules) or caruncle glands
  • Malignant cells with foamy, lipid-laden cytoplasm, necrosis, pagetoid invasion of the skin
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21
Q

What is the mortality of sebaceous carcinoma? What structures are affected by metastasis?

A

•15% mortality, direct extension and distant metastasis (lung, liver, brain, skull)

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22
Q

What are the tumors of the eye?

A
  • Retinoblastoma
  • Conjunctival Melanoma and Squamous Cell Carcinoma
  • Uveal Melanoma
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23
Q

What is the frequency of retinoblastoma?

A
  • Most common intraocular tumor of childhood (90% dx before age 3)
  • Frequency: 1/14,000 to 1/20,000 live births
  • In the US, approximately 250-500 new cases occur/ yr
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24
Q

What is the difference between b/l and sporadic cases of retinoblastoma?

A
  • 30-40% are bilateral…associated with germ line mutations.
  • Sporadic cases are associated with somatic mutations.

Eighty five percent of retinoblastomas are sporadic. Fifteen percent are autosomal dominant and are often bilateral and multiple.

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25
Q

What are the SSXs of retinoblastoma? What gene is involved?

A

•Signs/symptoms

–Leukocoria, strabismus, red,

–painful eye, poor vision

•Retinoblastoma gene Chr 13 (tumor suppressor)

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26
Q

What type of tumor is retinoblastoma? What is it similar to?

A

Retinoblastoma is a malignant embryonal tumor of the eye similar to medulloblastoma.

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27
Q

What is the cellular composition of retinoblastoma?

A

. It is composed of “small blue cells”, which are frequently arranged in characteristic circular formations, the Flexner-Wintersteiner rosettes.

28
Q

Tumor development in retinoblastoma is due to what genetic problem?

A

Tumor development is due to deletion of the Rb tumor suppressor gene on chromosome 13q14. Familial tumors have a germline mutation resulting in one defective copy of the gene. Tumors develop when the remaining normal copy is altered due to a somatic mutation. The same principle is involved in the pathogenesis of other tumors.

29
Q

What’s this?

A

Retinoblastoma

30
Q

What’s this?

A

Retinoblastoma

31
Q

What’s this?

A

retinoblastoma

32
Q

What’s this?

A

Retinoblastoma

33
Q

What’s this?

A

RB - blue with rosettes

34
Q

What’s this?

A

Flexner-Wintersteiner rosettes

35
Q

What is the Tx for retinoblastoma?

A

–Enucleation, Photocoagulative Ablation and Hyperthermia, Cryotherapy, Chemoreduction Therapy, External-beam Radiation, Plaque Radiotherapy (Brachytherapy)

36
Q

What is the prognosis for retinoblastoma?

A

–Overall survival rates of 95%

–Most important risk factor is extraocular extension of tumor through ON or sclera

37
Q

What’s this?

A

Conjunctival melanoma

  • frequently seen at the limbus
38
Q

What’s this?

A

Conjunctival squamous cell carcinoma

39
Q

What’s this?

A

Uveal (choroidal) melanoma

40
Q

What’s this?

A

Uveal (choroidal) melanoma

41
Q

What are the clinical risk factors for mortality for uveal melanoma?

A

–Larger tumor size, anterior eye location, extraocular extension

42
Q

How long does metastasis usually take to appear in uveal melanoma? What is survival after mets?

A
  • Metastasis usually 2-4 years from time of diagnosis
  • Patients who develop metastasis (usually to the liver) generally survive less than 6 months
43
Q

What is a split nevus?

A

•Split nevus – a form of congenital nevus of the eyelids…rare

44
Q

What are the different types of nests of nevus cells?

A

•Nests of nevus cells

–Interface of the epidermis and dermis (junctional nevus)

–Dermis and epidermis (compound)

–Only in the dermis (dermal)

45
Q

What is an external stye?

A

An external stye or styes /ˈstaɪ/, also hordeolum /hɔrˈdiːələm/, is an infection of the sebaceous glands of Zeis at the base of the eyelashes, or an infection of the apocrine sweat glands of Moll.[

46
Q

What is the appearance of an external stye?

A

External styes form on the outside of the lids and can be seen as small red bumps. Internal styes are infections of the meibomian sebaceous glands lining the inside of the eyelids. They also cause a red bump underneath the lid with only generalized redness and swelling visible on the outside. Styes are similar to chalazia, but tend to be of smaller size and are more painful; they usually don’t cause any lasting damage though.

47
Q

What are the contents of styes? What is the duration and cause?

A

They contain water and pus, and the bacteria will spread if the stye is forcefully ruptured. Styes are characterized by an acute onset and usually short in duration (7–10 days without treatment) compared to chalazia that are chronic and usually do not resolve without intervention. Styes are usually caused by the Staphylococcus aureus bacterium

48
Q

What are the non-neoplastic lesions of the peri-orbital skin and conjunctiva?

A
  • Stye (Hordeolum)
  • Chalazion (Meibomiam gland granuloma)
  • Xantelasma palpebratum
  • Pinguela
  • Pterigium
49
Q

What is a chalazion? What is the duration and treatment?

A

Chalazion
Meibomian gland lipogranuloma

  • Lipogranulomatous inflammatory reaction to sebum in tissues (endogenous “foreign body” reaction)
  • Secondary to obstruction of gland
  • Subacute to chronic and painless nodule
  • Epithelioid cells and giant cells surround lipid vacuoles
  • Usually lasts weeks to months
  • May become secondarily infected
  • Surgical therapy, antibiotics if infected
50
Q

What is xanthelasma palpebratum? What does it look like?

A
  • Aggregates of foamy, lipid-laden histiocytes in dermis
  • Soft, flat or slightly raised yellow papules and plaques
  • Usually more in inner canthus
51
Q

What kinds of patients get xanthelasma? How is it fixed?

A
  • Seen in hyperlipemic and normolipemic patients
  • Cosmetic surgery
52
Q

What’s this?

A

Xanthelasma Palpebratum

53
Q

What is pinguecula? Who gets them?

A
  • Asymptomatic, small yellowish submucosal nodule at the limbus
  • Adults and older patients but younger if >> sun exposure
  • Typical in tropical places
  • Conjunctival equivalent of Solar Elastosis of skin
  • Does not extend to or invade the cornea as a pterygium
54
Q

How is pinguecula treated?

A

no therapy needed

55
Q

What is the clinical correlation for Descemet membrane?

A

Descemet membrane…

Site of copper deposition in Wilson’s disease…Kayser-Fleischer ring

56
Q

How does the corneal surface regenerate?

A

Stem cells in the limbus divide to produce a daughter stem cell and a transient amplifying cell. These transient amplifying cells migrate within the cornea to lie in basal layer of corneal epithelium. Further cellular divisions of transient amplifying cells produce postmitotic cells, which lie in the suprabasal layers. Progressive differentiation of postmitotic cells produce terminally differentiated cells, which lie in the superficial corneal epithelial layers. These terminally differentiated cells are non-keratinized, stratified squamous corneal epithelial cells. These cells are continually sloughed away from the corneal surface and replaced by maturing, underlying cell layers.

57
Q

What is a pterygium? What causes it?

A
  • Submucosal growth of connective tissue that migrates into cornea
  • Results from actinic (UV) damage, dust, wind
58
Q

How is pterygium treated? What should the treatment process include?

A
  • Removed for cosmetic and irritation of conjunctiva reasons
  • Examine histologically to rule-out squamous neoplasia
59
Q

What are some lesions of the cornea?

A
  • Keratitis
  • Keratoconus
60
Q

What are 4 causes of ulcerative keratitis?

A

viral, bacterial, mycotic and parasitic

61
Q

Name some specific causes of ulcerative keratosis.

A
  • Viral: Herpes simplex - most common cause of central corneal ulcer (dendritic ulcer); herpes zoster
  • Bacterial: Pseudomonas aeruginosa and Staphylococcus aureus - especially associated with cosmetics or contact lenses
  • Mycotic: Aspergillosis, Candida, and Fusarium represent over 80% of all fungal keratitis
  • Parasitic: microsporidia
62
Q

What are the SSXs of HSV keratitis?

A
  • Pain
  • Photophobia
  • Blurred vision
  • Tearing and redness
63
Q

What is the earliest sign of HSV keratitis?

A

The earliest sign of active viral replication in the corneal epithelium is the development of small, raised, clear vesicles.

64
Q

How is HSV keratitis dx’ed?

A

HSV keratitis remains primarily a clinical diagnosis based on characteristic features of the corneal lesion.[1] If the diagnosis is in doubt, however, laboratory diagnosis can be made using the following[2] :

• Giemsa stain - Scrapings of the corneal or skin lesions show multinucleated giant cells

65
Q

What is the Tx for HSV keratitis?

A

Since most cases of HSV epithelial keratitis resolve spontaneously within 3 weeks, the rationale for treatment is to minimize stromal damage and scarring. Gentle epithelial débridement may be performed to remove infectious virus and viral antigens that may induce stromal keratitis. Antiviral therapy, topical or oral, is an effective treatment for epithelial herpes infection.

66
Q

What’s this?

A

Herpes Simplex Keratitis

67
Q
A

Neuro II - Exam 1 (6 decks)

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