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NMSP Exam 1 > The Eye > Flashcards

The Eye Flashcards

1
Q

What is proptosis? What can it lead to?

A

Inc in orbital contents that displaces eye; can lead to corneal ulcers or infection from exposure to air

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2
Q

What are 2 orbital inflammatory diseases?

A
  • Thyroid disease like Graves

- Idiopathic orbital inflammation

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3
Q

What happens to the eye in Graves disease?

Does this affect adipose tissue?

A

Enlargement of extraocular muscles w non-granulomatous inflammation

Note: Adipose tissue is NOT inflammed

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4
Q

What happens to the eye in idiopathic orbital inflammation/psuedotumor?

Does this affect adipose tissue?

A

Lymphocytes, plasma cells, eosinophils infiltrate

Orbital fat and tendons are replaced by fibrosis

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5
Q

What are the 3 things present in idiopathic orbital inflammation that differentiates it from Graves disease?

A

IOI will include eosinophils, adipose tissue (fibrosis), and chronic inflammatory cells

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6
Q

What causes orbital inflammatory disease? (3)

A
  • Sinus infection that spreads to orbit esp in immunosuppressed or DKA pts
  • Granulomatosis e polyangiitis (Wegners)
  • Sarcoid: May produce bilateral granulomatous inflammation secondary to penetrating injury
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7
Q

What are 2 unique signs of sarcoid in orbital inflammatory disease?

A
  • “Mutton fat” in anterior segment (keratic precipitates on cornea)
  • “Candle wax drippings” on ophthalmic exam, perivascular inflammation of retina
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8
Q

Where does eye get dispalced when lacrimal gland is involved?

A

Inferiorly and medially

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9
Q

Two common neoplasms of the orbit?

A

Mostly vascular in origin

  • Capillary hemangioma (infancy & early childhood)
  • Cavernous hemangioma (adults)
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10
Q

What is blepharitis?

What is chalazion?

A
  • Blepharitis: Chronic inflammation of eyelid margin

- Chalazion: Lipid extravasated into tissue provokes granulomatous response -> Lipogranuloma

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11
Q

Two common neoplasms of the eyelid?

A
  • Basal cell carcinoma

- Sebaceous carcinoma

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12
Q

What is the most common malignant tumor of periocular skin?

A

Basal cell carcinoma

- More common in younger pts w sun-exposed skin

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13
Q

What are some characteristics of a BCC tumor?

A
  • Pearly nodules
  • Telangiectatic vessels
  • Central ulcer
  • Rolled edges
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14
Q

Common histo in BCC?

A

Nests of cells that show peripheral palisading

- Look for blue coloring below the epidermis

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15
Q

What is one way to differentiate between a chalazion and a sebaceous carcinoma?

A

Chalazion should not return after removal; if it does, think sebaceous carcinoma

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16
Q

How do sebaceous carcinomas spread?

What is a histo characteristic?

A

Rolls through BM and spreads in epidermis (intraepithelial or bowenoid spread)

Foamy cytoplasm

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17
Q

What stain would you use for a sebaceous carcinoma?

A

Oil Red O (fat stain)

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18
Q

Where are common sites of metastasis for a sebaceous carcinoma?

A

Regional lymph nodes, lung, liver, brain & skull

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19
Q

What will be histo characteristics of squamous cell carcinoma?

A

Full thickness atypia w loss of polarity and keratin pearls in substantia propria

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20
Q

What is a common type of lymphoma in the eye/conjunctiva?

A

B-cell lymphoma

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21
Q

Where is a common site of lymphatic spread w tumors in the eyelid or conjunctiva?

A

Parotid and submandibular nodes

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22
Q

Generally, what are pingueculas & pterygiums?

A

Submucosal elevations of the conjunctiva d/t actinic damage (sun)

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23
Q

Between pingueculas & pterygiums, which can lead to cancer

A

Pingueculas can lead to SCC or melanoma

Pterygium are unlikely to lead to cancers

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24
Q

Between pingueculas & pterygiums, which can impair vision?

A

Pterygiums can lead to visual impairment; encroaches on cornea in a wing-like fashion– excise when it threatens visual axis

Pingueculas do not lead to visual impairment

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25
Q

Where do we the following grow:

  • Junctional nevus
  • Compound nevus
  • Intradermal nevus
A
  • Junctional: Epidermal nests that grow along dermo-epidermal junction
  • Compound: Grow into underlying dermis as nests or cords
  • Intradermal: No more epidermal nests
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26
Q

Immature vs mature nevi?

A
  • Immature superficial nevi are larger, produce melanin, grow in nests
  • Mature nevi are deeper in basal layer, smaller, produce little or no pigment, grow in cords
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27
Q

What do you stain corneal tissue with?

A

PAS to the basement membrane

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28
Q

What is important to note about regeneration of Descemets membrane?

What happens to it with age?

What can we note about it with Wilson’s disease?

A

Does not regenerate; if you damage, you will need a corneal transplant

Thickens with age

Copper deposits here to form Kayser-Fleischer ring

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29
Q

Why is the corneal stroma difficult to repair?

A

Lacks blood vessels and lymphatics (why it’s transparent!)

  • Leads to lack of rejection
  • Vascularization of cornea will opacify it; VEGF antagonists can be used to prevent this
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30
Q

What is a hypopyon?

A

Exudate and cells leaking from iris and ciliary body into anterior chamber (think infection OR retinoblastoma)

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31
Q

Most common bacteria that cause infection in the eye?

A

S. aureus, S. pneumoniae, P. aeruginosa, Enterobaceriaceae

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32
Q

What is a common cause of acanthamoebia keratitis?

A

Contact lenses that are not properly disinfected

- Can cause permanent visual impairment and blindness in healthy persons

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33
Q

Corneal degenerations vs dystrophies:

Unilateral or bilateral?

A

Degenerations are often unilateral but can be bilateral

Dystrophies can be either

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34
Q

Corneal degenerations vs dystrophies:

Inflammatory?

A

Degenerations can be caused by inflammation (or maturity or disease)

Dystrophies are not caused byinflammation

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35
Q

Corneal degenerations vs dystrophies:

Characteristics of where they affect, etc

A

Degenerations are often peripheral and asymmetric; can be deposition, thinning, vascularization, etc; very broad term

Dystrophies affect selective corneal layers or multiple layers; progressive over time
- Deposition of abnormal material

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36
Q

Corneal degenerations vs dystrophies:

Familial?

A

Degenerations are typically not familial

Dystrophies are familial (rare)

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37
Q

What are the two types of band keratopathies?

A
  • Calcific band keratopathy: Calcium deposition in Bowman layer
  • Actinic band keratopathy (aka Climatic droplet keratopathy): D/t chronic exposure to high amount of ultraviolet light
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38
Q

What is keratoconus and what disorders is it associated with?

What is the treatment?

A

Cornea bows out into more of a cone shape
- A/w Downs, Marfans, and other atopic disorders

Can be corrected with rigid contact lenses

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39
Q

Histo of keratoconus? What stain do you use?

A

Thinning of the cornea with breaks in Bowman later

- Use PAS to highlight BM

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40
Q

What is Fuchs dystrophy?

A

Descemet’s membrane is diffusely thickened w focal anvil-shaped excrescences of BM material protruding into anterior chamber; endothelial cells are sparse or absent

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41
Q

What is pseudophakic bullous keratopathy?

A

Dec in endothelial cells following cataract surgery

42
Q

What is primary angle closure glaucoma?

A

Iris attaches to lens to block passage of aqueous humor from posterior to anterior chamber; pressure building in posterior chamber causes iris to bow forward which occludes trabecular meshwork

43
Q

What is neovascular glaucoma?

A

Membrane grows over surface of iris which smooths surface; membrane contracts and blocks trabecular meshwork
- Closed angle glaucoma

44
Q

What is exfoliation syndrome of the lens? Why is this significant with aging

A

Since the lens is closed system, when epithelium sloughs off it stays inside the system
- Lens size increases w age

45
Q

What are some risk factors for cataracts?

A
  • DM
  • Wilson’s
  • Atopic dermatitis
  • Drugs (esp corticosteroids)
  • Radiation
  • Trauma
46
Q

What is a posterior subcapsular cataract?

A

Migration of the lens epithelium posterior to the lens equator

47
Q

What is phacolysis? What disorder can this lead to?

A

HMW proteins leak thru lens capsule and clog trabecular meshwork
- Leads to inc intraocular pressure which leads to phacolytic glaucoma (secondary open angle glaucoma)

48
Q

What is open angle glaucoma?

What is the most common secondary cause of this?

A

There is no blockage to trabecular meshwork, instead there is an inc resistance to aqueous outflow which in intraocular pressure

Pseudoexfoliation is most common form; deposition of fibrillary material throughout anterior segment

49
Q

What happens to the nerve fiber layer and the ganglion cell layer in glaucoma?

A

Both become atrophic

50
Q

What are anterior synechiae?

A

Adhesions between iris and trabecular meshwork

51
Q

What causes an anterior subcapsular cataract?

A

Dec aqueous humor leads to fibrous metaplasia of lens epithelium

52
Q

How can you prevent formation of synechiae in pts w intraocular inflammation?

A

Induction of pupillary dilation and cycloplegia (paralysis of ciliary muscles)

53
Q

What is endophthalmitis?

A

Inflammation in vitreous humor (can be exogenous like wound or endogenous)

54
Q

What is panphthalmitis?

A

Interior inflammation involving the retina, choroid, sclera, can extend into orbit

55
Q

What parts make up uvea?

A

Iris, choroid, ciliary body

56
Q

What are some things that can cause posterior segment uveitis?

A

Frequently involved retinal pathology

  • Infection (like pneumocystis carinii)
  • Idiopathic (like sarcoid)
  • Autoimmune (sympathetic ophthalmia)
57
Q

What is sympathetic ophthalmia?

What cell types are involved?

How long does it take to happen?

Tx?

A

Damage to one eye affects both eyes

+ eosinophils, no plasma cells

Can occur weeks to years after injury

Systemic immunosuppressive agents and possible enucleation of eye

58
Q

What is the most common intraocular malignancy in adults and where does it typically metastasize?

A

Melanoma that metastasizes to the uvea, esp choroid

59
Q

What can cause uveal melanoma and how is this similar to melanoma found elsewhere?

A

GNAQ1 and GNAA11
- Nevi may have these mutations that rarely transform to melanoma

BAP1 predisposes to uveal melanoma among others, need genetic events for dev of melanoma

No link to UV light, no BRAF mutation

60
Q

What is the prognosis with epithelioid melanoma?

A

BAD

61
Q

Where does uveal melanoma metastasize to first?

A

Liver thru hematogenous spread (skips lymph nodes)

- However can spread thru sclera to conjunctiva and into lymphatics

62
Q

How do outcomes compare with melanoma in the iris, ciliary body, choroid?

A

Melanomas in the iris tend to follow a more indolent course whereas melanomas of the ciliary body and choroid are more aggressive

63
Q

Tx for uveal melanoma?

A

No effective treatment for metastatic melanoma

No difference in survivability with radiation vs enucleation

MAPK inhibitors have shown some effectiveness in clinical trials

64
Q

What are Clark’s level and Breslow thickness in melanoma?

A

Clark: Anatomic level of invasion

Breslow: Thickness of tumor– important indicator for prognosis

65
Q

What is retinal detachment?

A

Separation of neurosensory retina from RPE

66
Q

What is retinitis pigmentosa?

A

Hereditary retinal degeneration that affects rods and cones or RPE

67
Q

Blood supply of vitreous humor? What happens if there is persistent fetal vasculature?

A

Avascular

Persistent fetal vasculature will lead to retrolental mass; hemorrhage and neovascularization will lead to opacification of vitreous

68
Q

What are “floaters” that come with age?

A

When the vitreous liquefies and collapses

69
Q

What is posterior vitreous detachment?

A

Vitreous separates from neurosensory retina d/t aging (liquification)

This isn’t too bad or worrisome– unlike retinal detachment

70
Q

What is rhegmatogenous retinal detachment?

Nonrhegmatogenous retinal detachment?

A

Full-thickness retinal defect (“retinal break”)

Non- is when there is no retinal break; a/w choroidal tumors & malignant HTN

71
Q

What are reattachment options for retinal detachmnet?

A
  • Scleral buckling

- Vitrectomy (last choice)

72
Q

What is proliferative vitreoretinopathy?

A

Complication; epi-retinal or sub-retinal membrane formation

73
Q

What does the common adventitial sheath affect with retinal arteriolosclerosis?

A

Retinal arterioles and veins share this sheath so in arteriolosclerosis, arteriole may compress vein at points where the vessels cross

74
Q

Which intraocular vessels are damaged in malignant HTN?

A

Retinal and choroid vessels are damaged

75
Q

What is a macular star?

A

Spoke-like arrangement of exudate in the macula in malignant HTN?

76
Q

What can damaged choiriocapillaries lead to?

A

Lead to damaged RPE, which leads to exudate accumulating, which leads to retinal detachment

77
Q

What are Elschnig spots?

A

Focal choroidal infarcts from damaged choroidal vessels

78
Q

What are cytoid bodies?

A

Accumulation of mitochondria at the swollen ends of damaged axons; found in the nerve fiber layer infarct of a “cotton wool spot”

79
Q

What is proliferative diabetic retinopathy?

A

New vessels sprouting from optic nerve head or surface of retina; referred to as “neovascular membrane”

80
Q

What is non-proliferative diabetic retinopathy? What are some features you will see? (4)

A

BM of retinal blood vessels thicken

  • Microaneurysm
  • Macular edema
  • Exudates
  • Micro-occlusions (inc VEGF and intraretinal angiogenesis)
81
Q

What are some complications of diabetic retinopathy? (4)

A
  • Hemorrhage from neovascularization
  • Posterior vitreous detachment
  • Retinal detachment
  • Neovascular glaucoma
82
Q

What are some treatment options for diabetic retinopathy?

A
  • Ablating nonperfused retina by laser photocoagulation or cryopexy (causes regression of both retinal & iris neovascularization)
  • Injection of VEGF inhibitors into the vitreous has been used to treat diabetic macular edema & retinal neovascularization
83
Q

What is retinopathy or prematurity (aka retrolental fibroplasia)?

A

The lateral aspect of the retinal periphery is incompletely vascularized but the medial aspect is vascularized

84
Q

What causes retinopathy of prematurity (aka retrolental fibroplasia)?

A

Premature or LBW infants are treated with oxygen. This causes immature retinal vessels in the lateral periphery to constrict rendering the retinal tissue distal to this zone ischemic
- Neovascularization forms between vascularized and avascular peripheral retina –> fibrovascular proliferation into vitreous leads to tractional retinal detachment

85
Q

What are the 2 forms of age-related macular degeneration?

A

Dry and wet

Both are a result of damage to the macula (required for central vision)

86
Q

What is dry age-related macular degeneration?

A

No neoangiogenesis; vision loss may be severe –> deposits in Bruch membrane –> atrophy of RPE

87
Q

What is wet age-related macular degeneration?

A

Choroidal neovascularization; vessels penetrate thru the Bruch membrane beneath RPE

88
Q

What is the treatment for dry and wet age-related macular degeneration?

A

Dry: No treatment

Wet: Inject VEGF antagonists into vitreous

89
Q

What are the two main retinal neoplasms?

A
  • Retinoblastoma

- Retinal lymphoma

90
Q

On what chromosome is the mutation for retinoblastoma? What can be said about normal gene suppression of RB alleles?

A

13q14

One normal gene will suppress RB allele; one abn gene is unstable & may lead to mutation of normal gene w loss of suppression

91
Q

Is retinoblastoma typically unilateral or bilateral?

A

RB arising in context of germline mutation are often bilateral

92
Q

Common sites of RB metastasis?

A

Brain & bone marrow

93
Q

In which disorder do we see Flexner-Wintersteiner rossettes?

A

Retinoblastoma

94
Q

What is the prognosis of RB adversely affected by?

A

Extraocular extension & invasion of optic nerve & choroidal invasion

95
Q

Tx of RB?

A

Chemoreduction then laser of cryoplexy obliteration

96
Q

What is anterior ischemic optic neuropathy? What are some examples that can lead to this?

A

Spectrum of injuries to optic nerve varying from ischemia to infarction

  • Inflamed vessels, emboli, thrombosis, temporal arteritis
  • Transient partial interruptions to blood flow in optic nerve (transient loss of vision)
  • Total interruptions in blood flow (optic nerve infarct)
97
Q

How is papilledema r/t vision?

A

Inc intracranial pressure –> Bilateral swelling of optic nerve head –> –? retina laterally displaced; can lead to bilateral vision loss
- Acute papilledema is not a/w vision loss

98
Q

What is normal-tension glaucoma?

A

Small group that develops visual field and optic nerve changes typical of glaucoma but with normal intraocular pressure

99
Q

Define the following:

  • Buphthalmos
  • Megalocornea
  • Staphyloma
A
  • Buphthalmos: Inc in intraocular pressure in infants which leads to diffuse enlargement of the eye
  • Megalocornea: Enlargement of the cornea
  • Staphyloma: Inc intraocular pressure in adults leading to thinning of sclera
100
Q

What is optic neuritis? What disorder does this a/w?

A

Loss of vision secondary to demyelination of optic nerve

- Occurs w multiple sclerosis

101
Q

What is phthisis bulbi?

A

“End-stage eye”

  • Trauma, intraocular inflammation, chronic retinal detachment, and many other conditions can give rise to an eye that s both small (atrophic) and internally disorganized

NMSP Exam 1 (9 decks)

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