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NMSP 1 > The Eye > Flashcards

The Eye Flashcards

1
Q

What is Graves Orbitopathy?

A

–thyroid disease (Graves) is the most common cause of U/L or B/L exophthalmos

–enlarged extraocular muscles w/ non-granulomatous inflammation (tendons are spared)

–increased glycosaminoglycans and endomysial fibers

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2
Q

What are two complications of Graves Orbitopathy?

A
  • visual loss d/t compression of the optic nerve

- corneal complications d/t exposure

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3
Q

How does Sarcoidosis affect the eye?

A
  • granulomatous uveitis
  • sympathetic ophthalmia (spared eye injury)
  • “mutton fat” keratic precipitate on anterior segment
  • “candle wax drippings” (retinal perivascular inflammation)
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4
Q

How does Basal Cell Carcinoma affect the eye?

A
  • -most common malignant periocular tumor of the skin
  • -younger patients, sun-exposed skin (lower eyelid)
  • -pearly nodules, telangiectatic vessels, central ulcer
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5
Q

What is seen on histology of Basal Cell Carcinoma?

A
  • basaloid cell nests, w/ peripheral palisading of nuclei
  • “blue” and “below” large masses below epidermis

-morpheaform: cords/tendrils of tumor cells embedded in fibrotic stroma; widely and deeply infiltrative

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6
Q

What is seen on histology of Squamous Cell Carcinoma?

A

-keratin pearls

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7
Q

What is Sebaceous Carcinoma?

A
  • common as SCC of eyelid in Asian women >40yrs
  • “Masquerade Syndrome”
  • -U/L keratoconjunctivitis unresponsive to therapy
  • can metastasize to regional LN’s, lung, liver, brain
  • 15% mortality
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8
Q

What is seen on histology of Sebaceous Carcinoma?

A
  • intraepithelial spread of tumor cells (Pagetoid)
  • larger nuclei, hyperchromatic, greater pleiomorphism
  • neoplastic cells w/ foamy cytoplasm
  • central necrosis
  • -Oil Red O fat stain on frozen tissue
  • -positive Epithelial Membrane Ag (EMA)
  • -positive BRST-1, P-16
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9
Q

What is a pinguecula?

A

-thin epithelium (hyperplastic or dysplastic) w/ fragmented stromal collagen and BASOPHILIC degeneration d/t actinic damage from sun exposure

  • small, yellowish submucosal conjunctival elevation
  • does NOT invade the cornea
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10
Q

What is a pterygium?

A
  • submucosal conjunctival elevation d/t actinic damage
  • fibrovascular tissue that encroaches onto the cornea
  • does not cross pupillary axis
  • does not affect vision (mild astigmatism)
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11
Q

What is a freckle?

A
  • basal keratinocytes w/ increased melanin

- melanocytes are in normal numbers, but enlarged

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12
Q

What is a lentigo?

A

-linear (non-nested) melanocyte hyperplasia restricted to the basal cell layer

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13
Q

What is a nevus?

A
  • melanocytes are rounded and grow into “nests”
  • cells are uniform w/ a round nucleus, inconspicuous nuclei and little to no mitotic activity

Junctional Nevus: epidermal nests along dermo-epidermal junction

Compound Nevus: junctional nevus that grows into the underlying dermis as nests or cords

Intradermal Nevus: epidermal nests are lost completely

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14
Q

What is the difference between superficial nevus cells and deep nevus cells?

A
  • superficial nevus cells are immature, larger, produce melanin and grow in nests
  • deeper nevus cells are more mature, in the basal layer, smaller, produce little to no pigment, and grow in cords
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15
Q

What is the most common primary intraocular tumor in adults?

A

uveal melanoma (comprises 5% of melanomas)

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16
Q

What is the most common intraocular tumor in adults?

A

-cutaneous melanoma that has metastasized to the eye

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17
Q

True or False: uveal melanoma, like cutaneous melanoma, is linked to ultraviolet light exposure.

A

False; there is no clear link b/w UV light and uveal melanoma.

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18
Q

What is the most common primary intraocular tumor in adults?

A

uveal melanoma (account for 5% of all melanomas)

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19
Q

What two oncogenes are associated with uveal melanoma?

A

GNAQ and GNA11

  • code GPCR’s
  • -gain-of-function mutation found in 85%

Note: uveal nevi also have mutations in GNAQ and GNA11, but rarely transform into melanoma

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20
Q

To what organ does uveal melanoma first spread?

A

liver

-spread almost exclusively by a hematogenous route

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21
Q

What two types of cells comprise uveal melanomas and which has a more adverse outcome?

A

-spindle cell and epithelioid cells

–epithelioid cells have more atypia and worse outcome

22
Q

Discuss the two treatments for uveal melanoma and which is preferred.

A

–there is no difference in survivability between melanomas treated w/ enucleation vs. eye-sparing radiotherapy (preferred)

23
Q

How does the structure of the cornea affect corneal transplants?

A
  • corneal stroma lacks blood vessels and lymphatics

- -lack of rejection

24
Q

What happens in non-immunological graft rejection of a cornea?

A

-loss of endothelial cells and corneal edema

25
Q

What are common bacterial infections of the eye?

A
  • S. aureus, Strep pneumo, Pseudomonas, Enterobacter
  • -PMN infiltrates and necrotic debris

(can do a Gram stain, but culture is more accurate)

26
Q

Describe Herpes Simplex Virus Keratitis, in regards to the eye?

A

Dendrite: linear arborizing pattern of opacification and swelling of epithelial cells

Cowdry Bodies (intranuclear inclusions) seen on Giemsa stain

infected cells can coalesce into multinucleated giant cells

27
Q

What is the hallmark pathology of chronic herpes simplex keratitis?

A
  • granulomatous rxn at Descemet Membrane (full thickness involvement)
  • chronic stromal keratitis leads to ulceration and scarring
28
Q

What is a cataract?

A
  • lenticular opacity

- congenital or acquired

29
Q

What are risk factors for cataracts?

A
  • DM
  • Wilson Dz
  • atopic dermatitis
  • corticosteroids
  • radiation
  • trauma
30
Q

What causes age-related cataracts?

A

-opacification of the lens nucleus (nuclear sclerosis)

31
Q

What causes a posterior subcapsular cataract?

A

-migration of the lens epithelium posterior to the lens equator d/t enlargement of abnormally-positioned lens epithelium

32
Q

What is a Morgagnian (hypermature) cataract?

A

-liquefication of lens cortex

–high-molecular-weight proteins may leak through the lens capsule (phacolysis) and clog the trabecular meshwork causing secondary open-angle glaucoma

33
Q

What causes most cases of glaucoma?

A

-increased intraocular pressure

normal or low-tension glaucoma DO exist, however

34
Q

What is open-angle glaucoma?

A

-complete open access to trabecular meshwork, but increased resistance to aqueous outflow, creating increased intraocular pressure

Primary Open-Angle: most common form
-MYOC gene mutations (sometimes OPTN gene)

Secondary Open-Angle:

  • pseudoexfoliation (LOX1 gene)
  • -deposition of fibrillary material through anterior segment
35
Q

What is angle-closure glaucoma?

A

peripheral zone of iris adheres to the trabecular meshwork and physically impedes the aqueous humor from draining

36
Q

What are risk factors for glaucoma?

A
  • race (AA and Hisp)
  • family Hx
  • DM, HTN
  • trauma
  • corticosteroids
  • eye abnormalities
37
Q

What is the leading cause of blindness in people aged 20-64?

A

diabetic retinopathy

38
Q

How does diabetes lead to blindness in diabetic retinopathy?

A

-primary changes in the retinal microcirculation

39
Q

What is the treatment for diabetic retinopathy?

A

Laser Photocoagulation Tx

  • variable destruction of outer retina
  • destruction of retinal pigmented epithelium
  • occlusion of choriocapillaris
  • healing by proliferation of adjacent RPE, glial scarring
40
Q

What is the leading cause of blindness in the US?

A

age-related macular degeneration

–choroidal neovascularization (presence of angiogenic vessels originating from the choriocapillaris)

41
Q

What is the most common intraocular malignancy in children?

A

-retinoblastoma

cell of origin in a neuronal progenitor

42
Q

What is the genetic cause of retinoblastoma?

A
  • germline mutation in RB allele and a subsequent somatic mutation in the other RB allele in a retinal progenitor (germline mutation often B/L phenotype)
  • 13q14 (long arm of chromosome 13)
43
Q

What are the most common symptoms of retinoblastoma?

A
  • leukocoria (white pupillary reflex)
  • strabismus (abnormal eye alignment)
  • ocular inflammation
44
Q

How might a retinoblastoma affect the iris?

A

-cells shed into the anterior chamber, aggregate and form nodules on the iris, or they may settle inferiorly to form a pseudohypopyon

45
Q

Where does retinoblastoma tend to metastasize?

A
  • skull, brain, and spinal cord
  • bone marrow
  • LN’s
  • abdominal viscera

-most commonly escaping via the optic N. (poor prognosis)

46
Q

What is the histology of retinoblastoma?

A
  • -round, oval, or spindle-shaped hyperchromatic nuclei
  • -high mitotic rate
  • -scant cytoplasm
  • -necrosis w/ calcification
  • -perivascular cuffs of tumor cells
47
Q

What is Flexner-Wintersteiner, a characteristic feature of retinoblastoma?

A

-single row of eosinophilic columnar cells w/ peripherally-oriented nuclei surrounding central lumen lined by refractile structure (external limiting membrane)

48
Q

What is Homer Wright in regards to histology of retinoblastoma?

A
  • less common that Flexner-Wintersteiner

- lumen filled w/ tangle of eosinophilic cytoplasmic processes

49
Q

What is fleurette in regards to histology of retinoblastoma?

A

-curvilinear clusters of cells composed of rod and cone inner segments, often attached to abortive outer segments

50
Q

What is papilledema?

A

-edema of the head of the optic N. that develops as a result of compression of the nerve

Increased intracranial pressure
--B/L disc edema
--not associated with vision loss
--optic N. is swollen and hyperemic
(while it's pale in anterior ischemic optic neuropathy)

Neoplasms
–U/L disc edema

NMSP 1 (9 decks)

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