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NMSP Exam 1 > Eye > Flashcards

Eye Flashcards

1
Q

What can be a complication of proptosis?

A
  • Chronic corneal ulcer and/or infection from exposure to air
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2
Q

What is the most common cause of unilateral or bilateral exophthalmos?

A
  • Graves
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3
Q

What causes exophthalmos in Graves?

A
  • Enlargement of the extraocular muscles with non-granulomatous inflammation (tendons and adipose not inflamed)
  • Increased glycosaminoglycans
  • Endomysial fibrosis
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4
Q

What are some complications of Graves?

A
  • Visual loss due to compression of optic nerve

- Corneal complications due to exposure

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5
Q

What happens in idiopathic orbital inflammation (pseudotumor)?

A
  • Lymphs, plasma cells, and eosinophils infiltrate

- Orbital fat and tendons replaced by fibrosis

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6
Q

Where around eyes does idiopathic orbital inflammation affect?

A
  • Lacrimal only
  • Extraocular muscles
  • Tendon capsule
  • Fascial layer
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7
Q

How is Graves distinguished from pseudotumor?

A
  • In pseudotumor, the tendons and adipose have fibrosis
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8
Q

What are some causes of orbital inflammatory disease?

A
  • Sinus infection can spread
  • Granulomatosis with polyangiitis
  • Sarcoid
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9
Q

What is seen in sarcoid that causes orbital inflammatory disease?

A
  • Systemic disease
  • Granulomatous uveitis
  • Sympathetic ophthalmia
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10
Q

What do you see on ophthalmic exam in sarcoid?

A
  • “Mutton fat” in anterior segment and keratic ppt

- “Candle wax drippings” on ophthalmic exam, perivascular inflammation of retina

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11
Q

What is blepharitis?

A
  • Chronic inflammation of eyelid margin
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12
Q

What is a chalazion?

A
  • Lipid extravasated into tissue provokes granulomatous response –> lipogranuloma
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13
Q

What are some neoplasms that affect the eyelid?

A
  • Basal cell carcinoma
  • Sebaceous carcinoma
  • Melanoma
  • Kaposi sarcoma
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14
Q

Who mainly has basal cell carcinoma of the eyelid?

A
  • Younger patients with a lot of sun exposure

- Lower eyelid most common location

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15
Q

What does basal cell carcinoma of the eyelid look like?

A
  • Pearly nodules
  • Telangiectatic vessels
  • Central ulcer (rodent ulcer)
  • Rolled edges
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16
Q

What is a sebaceous carcinoma?

A
  • Common as squamous cell carcinoma of eyelid

- Chalazion that returns after treatment

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17
Q

What is seen in sebaceous carcinoma?

A
  • Pagetoid spread –> intraepithelial spread

- Nuclei larger, increased pleomorphic, hyperchromatic and more atypical than BCC

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18
Q

What stain is used to help identify sebaceous carcinoma?

A
  • Oil Red O –> fat stain but only used on frozen tissue
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19
Q

Where do sebaceous carcinomas most likely to metz too?

A
  • Regional LN (parotid and submandibular)
  • Lung
  • Liver
  • Brain
  • Skull
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20
Q

What are sebaceous carcinomas associated with?

A
  • Muir-Torre syndrome –> skin tumors in association with internal cancers
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21
Q

What is the palpebral conjunctiva?

A
  • Tightly tethered to tarsus

- Papillary folds with allergic and bacterial conjunctivitis

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22
Q

What is the fornix?

A
  • Contains accessory lacrimal tissue and lymphoid tissue
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23
Q

What does the fornix contain?

A
  • Pseudostratified columnar epith rich in goblet cells
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24
Q

What is seen in viral conjunctivitis?

A
  • Enlarged lymphoid follicles
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25
Q

What is the bulbar conjunctiva?

A
  • Covers the surface of the eye
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26
Q

What epithelial covers the bulbar conjunctiva?

A
  • Non Keratinizing stratified squamous
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27
Q

What are some causes of conjunctival scarring?

A
  • Chlamydia trachomatis
  • Exposure of the ocular surface to caustic alkalis or as a sequela to ocular cicatricial pemphigoid
  • Dry eye –> reduction in number of goblet cells
  • Iatrogenic damage –> drug and/or surgery
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28
Q

What is a pinguecula?

A
  • Limbus, small yellowish submucosal elevation near iris
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29
Q

What causes a pinguecula?

A
  • Thin epithelium
  • Fragmented stromal collagen
  • Basophilic degeneration
  • May contain sun induced SCC or melanoma
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30
Q

Does a pinguecula affect vision?

A
  • NO
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31
Q

What is a pterygium?

A
  • Similar to pinguecula but encroaches on the cornea in winglike fashion
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32
Q

What is seen in conjunctival melanoma?

A
  • Unilateral and in fair complexion individuals in middle age
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33
Q

What mutation is a big cause of conjunctival melanoma?

A
  • BRAF V600
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34
Q

What is a precursor lesion of conjunctival melanoma?

A
  • Primary acquired melanosis, with atypia

- 50-90% when untreated develop melanoma

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35
Q

What are some causes of blue sclera?

A
  • Scleritis thins sclera
  • Increased intraocular pressure thins sclera
  • Osteogenesis imperfecta
  • Congenital melanosis oculi, accompanied by periocular cutaneous pigmentation –> nevus of ota
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36
Q

Why is a corneal transplant able to be done so often?

A
  • Lacks blood vessels and lymphatics
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37
Q

What are some reasons for a corneal transplant rejection?

A
  • Loss of endothelial cells and subsequent corneal edema
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38
Q

What is a hypopyon?

A
  • Exudate and cells leaking from iris and ciliary body vessels into anterior chamber
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39
Q

What are some bacteria that can infect the cornea?

A
  • S. aureus
  • S. pneumoniae
  • P. aeruginosa
  • Enterobacteriaceae
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40
Q

What is acanthamoebic keratitis?

A
  • May lead to corneal ulcers or even blindness

- Most often in people who wear contact lens and do not properly disinfect their lenses

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41
Q

How can people prevent acanthomoebic keratitis?

A
  • Use hydrogen peroxide based solutions
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42
Q

What is the treatment for acanthamoebic keretitis?

A
  • No single medication eliminates both trophozoite and cystic forms
  • Corneal transplant
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43
Q

What is granulomatous amoebic encephalitis? What does it cause?

A
  • Often in immunosuppressed patients
  • Amoebae enter body through open wound
  • Can cause massive brain swelling resulting in death
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44
Q

What is seen in herpes simplex virus keratitis?

A
  • Dendrite –> linear arborizing pattern of opacification and swelling of epithelial cells
  • Infected cells may coalesce to form multinucleated giant cells
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45
Q

What does a giemsa stain reveal in HSV keratitis?

A
  • Intranuclear viral inclusions
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46
Q

How does HSV keratitis affect descemets membrane?

A
  • Granulomatous reaction –> histologic hallmark
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47
Q

What are some causes of corneal degenerations?

A
  • Inflammation, maturity, or systemic disease

- May see deposition, thinning, or vascularization

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48
Q

How do you differentiate between corneal degenerations and dystrophies?

A
  • Degenerations are not familial while dystrophies are
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49
Q

What is calcific band keratopathy?

A
  • Calcium deposition in bowman layer
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50
Q

What is the source of calcific band keratopathy?

A
  • Chronic uveitis, especially with juvenile rheumatoid arthritis
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51
Q

What causes actinic band keratopathy?

A
  • Chronic exposure to high amount of UV light

- Extensive solar elastosis develops in superficial layers of corneal collagen in sun-exposed interpalpreal fissure

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52
Q

What is keratoconus associated with?

A
  • Downs
  • Marfans
  • Atopic disorders
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53
Q

What is keratoconus?

A
  • Progressive bilateral centra ectasia of cornea with anterior protrusion of cornea
  • Causes irregular astigmatism that is NOT correctable with glasses
54
Q

What can help correct keratoconus?

A
  • Rigid contact lenses
55
Q

What is the histologic hallmark of keratoconus?

A
  • Thinning of the cornea with breaks in the bowman layer
56
Q

What is fuchs dystrophy?

A
  • Descemet’s diffusely thickened with focal anvil-shaped excrescences of basement membranes material protruding into anterior chamber
57
Q

What is seen in fuchs dystrophy?

A
  • Endothelial cells sparse or absent –> leading cause of bullous keratopathy
58
Q

What is pseudophakic bullous keratopathy?

A
  • Decrease in endothelial cells following cataract surgery
59
Q

What is the most common cause of corneal transplants in the US?

A
  • Fuchs dystrophy
60
Q

What is a cataract?

A
  • Lenticular opacities that may be congenital or acquired
61
Q

What are some risk factors for cataracts?

A
  • DM
  • Wilson disease
  • Atopic dermatitis
  • Drugs
  • Radiation
  • Trauma
62
Q

What is nuclear sclerosis?

A
  • Age related cataracts typically results from opacification of the lens nucleus
63
Q

What is a posterior subcapsular cataract?

A
  • Migration of the lens epithelium posterior to the lens equator
64
Q

What is phacolysis?

A
  • HMW proteins form liquefied lens cortex leaks through the lens capsule, may clog the trabecular meshwork and increases intraocular pressure
  • Form of secondary open angle glaucoma
65
Q

What is glaucoma?

A
  • Collection of diseases with distinctive changes in the visual field and in the cup of the optic nerve
66
Q

What is glaucoma most associated with?

A
  • Increased intraocular pressure
67
Q

What are some risk factors of glaucoma?

A
  • Age
  • Race
  • Family history
  • DM
  • HTN
  • Trauma
  • Prolonged corticosteroid use
68
Q

What is open angle glaucoma?

A
  • Complete open access to trabecular meshwork

- Increased resistance to aqueous outflow causing increased intraocular pressure

69
Q

What is angle closure glaucoma?

A
  • Peripheral zone of iris adheres to trabecular meshwork which physically impedes outflow of fluid
70
Q

What are the two types of open angle glaucoma?

A
  • Primary –> angle is open and few structural changes

- Secondary –> Pseudoexfoliation most common form; deposition of fibrillary material throughout anterior segment

71
Q

What are the two types of angle closure glaucoma?

A
  • Primary –> pupillary block; iris bombe

- Secondary –> pathologic membranes over iris causing occlusions

72
Q

What is seen in primary angle closure glaucoma?

A
  • Increased intraocular pressure damages lens epithelial which causes opacities, plus corneal edema and bullous keratopathy
73
Q

What is seen in secondary angle closure glaucoma?

A
  • Chronic retina ischemica (increase in VEGF) –> neovascular glaucoma
74
Q

What is an anterior synechiae?

A
  • Adhesions between iris and trabecular meshwork
75
Q

What do anterior synechiae cause?

A
  • Increased intraocular pressure causing optic nerve damage

- Anterior subcapsular cataract –> decreased aqueous causing fibrous metaplasia of lens epithelial

76
Q

What is a posterior synechiae?

A
  • Adhesions between iris and anterior surface of lens
77
Q

What is endophthalmitis?

A
  • Inflammation in vitreous humor
78
Q

What are some causes of endophthalmitis?

A
  • Exogenous –> originating in environment that gains access to interior of eye
  • Endogenous –> enters hematogenously
79
Q

What could suppurative inflammation of the vitreous humor cause?

A
  • A few hours of it could cause irreversible retinal injury
80
Q

What is panophthalmitis?

A
  • Interior inflammation also involving retina, choroid, sclera, and extends into orbit
81
Q

What is uveitis?

A
  • Any type of inflammation involving uvea (iris, choroid, and ciliary body)
82
Q

What are some causes of posterior segment uveitis?

A
  • Infection (P. carinii)
  • Idiopathic
  • Autoimmune
83
Q

What is seen in granulomatous uveitis?

A
  • Sarcoidosis

- “Candle wax drippings”

84
Q

What is sympathetic ophthalmia?

A
  • Noninfectious uveitis limited to eye
  • Bilateral granulomatous inflammation of all components of uvea –> no plasma cells and eosinophils
  • Complicates penetrating eye injury
85
Q

What is the treatment for sympathetic ophthalmia?

A
  • Systemic immunosuppressive agents
86
Q

What is the most common primary intraocular malignancy in adults?

A
  • Uveal melanoma
87
Q

What are some deposits of uveal melanoma?

A
  • No link to UV light

- Genetic events are required for development of melanoma

88
Q

What are some mutations seen in uveal melanoma?

A
  • GNAQ and GNA11 GPCRs

- May have something to do with BAP1 on chr 3

89
Q

What is the worst kind of uveal melanoma?

A
  • Epithelioid –> spherical, greater cytological atypically
90
Q

What is seen in epithelioid melanoma?

A
  • Large nuclei
  • Prominent nucleoli
  • Infiltrating plasma cells and lymphs
91
Q

Where is the first place uveal melanoma metz to?

A
  • Livers hematogenously
92
Q

What is retinal detachment?

A
  • Separation of neurosensory retina from retinal pigment epithelium
93
Q

What is retinitis pigmentosa?

A
  • Hereditary retinal degeneration –> X-linked rec

- Age of onset correlates with inheritance pattern

94
Q

What does retinitis pigmentosa affect?

A
  • Rods and cones of RPE
95
Q

What happens when the vitreous liquifies?

A
  • Collapses and causes floaters
96
Q

What is posterior vitreous detachment?

A
  • Posterior hyaloid separates from neurosensory retina due to aging
97
Q

What is rhegmatogenous retinal detachment?

A
  • Full thickness retinal defect?
98
Q

How is rhegmatogenous retinal detachment treated?

A
  • Scleral buckling –> application of strips of silicon to the surface of the eye
  • Vitrectomy –> removal of vitreous material (last resort)
99
Q

What is a non rhegmatogenous retinal detachment?

A
  • Retinal detachment without retinal break

- Retinal detachments associated with choroidal tumors and malignant hypertension

100
Q

What is retinal arteriolosclerosis?

A
  • Thickened arteriolar walls appear narrowed

- Color of the blood column varies from bright red to copper to silver

101
Q

What can happen in retinal arteriolosclerosis?

A
  • Arteriole may compress the vein at points where vessels cross due to sharing a common adventitial sheath
  • This venous stasis may precipitate occlusions of the retinal vein branches
102
Q

What happens in malignant hypertension?

A
  • Retinal and choroid vessels damaged

- Macular star is seen

103
Q

What is the macular star seen in malignant hypertension?

A
  • Poke-like arrangement of exudate in the macula
104
Q

What are elschnig spots?

A
  • Damaged choroidal vessels causing focal choroidal infarcts
105
Q

What are cytoid bodies that may be seen in malignant hypertension?

A
  • Accumulation of mitochondria at the swollen ends of damaged axons
  • Found in the nerve fiber layer infarct of a “cotton wool spot”
106
Q

What is the main histologic hallmark of diabetic retinopathy?

A
  • Thickening of the basement membrane of the par plicata of the ciliary body
107
Q

What occurs in non-proliferative diabetic retinopathy?

A
  • Basement membrane of retinal blood vessels thickened
  • May have microaneurysms
  • Macular edema –> may cause vision loss
  • Exudates
  • Micro-occlusions
108
Q

Where do the exudate accumulate in diabetic retinopathy?

A
  • Outer plexiform layer, due to vascular changes
109
Q

What occurs in proliferative diabetic retinopathy?

A
  • New vessels sprouting from optic nerve head or surface of retina
  • “Retinal neovascularization” –> new branches breach internal limiting membrane of retina
110
Q

What are some complications of diabetic retinopathy?

A
  • Hemorrhage from neovascularization
  • Posterior vitreous detachment
  • Retinal detachment
  • Neovascular glaucoma
111
Q

What is the treatment for diabetic retinopathy?

A
  • Ablating nonperfused retina by laser photocoagulation or cryopexy regression of both retinal and iris neovascularization
  • Injection of VEGF inhibitors into vitreous have been used
112
Q

How does retinopathy of prematurity occur?

A
  • In premature infants who are treated with oxygen, immature retinal vessels in the temporal retinal periphery constrict, rendering the retinal tissue distal to this zone ischemic
113
Q

What are some complications of retinopathy of prematurity?

A
  • Neovascularization of retina and vitreous –> proliferation of new vessels between vascularized and avascular peripheral retina
  • Fibrovascular proliferation into vitreous causing tractional retinal detachment
114
Q

What is dry age related macular degeneration?

A
  • No neoangiogenesis
  • Vision loss may be severe
  • No treatment
115
Q

What is wet age related macular degeneration?

A
  • Choroidal neovascularization

- Tx –> inject VEGF antagonists into vitreous

116
Q

What gene and chromosome is responsible for retinoblastomas?

A
  • RB on Ch 13

- Only one gene is sufficient in suppresses mutant genes but since it is so bad, the mutant gene is expressed

117
Q

Where do retinoblastomas typically spread?

A
  • Brain
  • Bone marrow
  • RARELY to the lungs
118
Q

What association is seen with trilateral retinoblastoma?

A
  • Pinealoblastoma
119
Q

What does a retinoblastoma look like histologically?

A
  • Round, oval, or spindle shaped hyperchromatic nuclei with scant cytoplasm
  • Necrosis with calcification and perivascular cuffs of viable tumor cells
120
Q

What rosettes are seen in retinoblastomas?

A
  • Flexner-Wintersteiner –> central lumen lined by columnar tumor cells that contain peripherally oriented nuclei
121
Q

What determines prognosis with retinoblastomas?

A
  • Affected by extraocular extension and invasion of optic nerve and choroidal invasion
122
Q

What is the treatment for retinoblastomas?

A
  • After chemoreduction, tumors may be obliterated with laser treatment or cryopexy
123
Q

What are some secondary effects of retinoblastomas?

A
  • Pseudohypopyon
  • White reflex
  • Proptosis
124
Q

What is anterior ischemic optic neuropathy?

A
  • Spectrum of injuries to the optic nerve varying from ischemia to infarction
  • Transient partial interruptions of blood flow cause transient loss of vision
  • Total interruption is due to optic nerve infarct
125
Q

What happens to the optic nerve in an infarct?

A
  • Does not regenerate so vision loss is permanent
126
Q

What should you think about if there is bilateral swelling of optic nerve?

A
  • Increased intracranial pressure
127
Q

What should you think about if there is unilateral papilledema?

A
  • Compression of the nerve
128
Q

What is normal tension glaucoma?

A
  • Small group that develops visual field and optic nerve changes typical of glaucoma with normal
129
Q

What is buphthalmos?

A
  • Increased intraocular pressure in infants causing diffuse enlargement of eye
130
Q

What is optic neuritis?

A
  • Loss of vision secondary to demyelination of optic nerve

- Seen in MS

131
Q

What is phthisis bulbi?

A
  • End stage eye –> eye is small and internally disorganized

- Could be due to trauma, intraocular inflammation, chronic retinal detachment

NMSP Exam 1 (12 decks)

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