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MS2 Unit 3 > Rubin's 33: The Eye > Flashcards

Rubin's 33: The Eye Flashcards

1
Q

blowout fracture

A

Blunt trauma increases intraorbital pressure momentarily and may cause the bones in the floor of the orbit to fracture into the maxillary sinus

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2
Q

enophthalmos

A

The inferior rectus muscle may become entrapped in a blowout fracture, thereby causing the eye to sink into the orbit

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3
Q

siderosis bulbi

A

retinal degeneration and discoloration of the eye from iron

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4
Q

Blepharitis

A

inflammation of the eyelids. It is common and sometimes produces an acute, red, tender, inflammatory mass.

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5
Q

Hordeolum (sty)

A

an acute, inflammatory, focal lesion of the eyelid

  • Acute inflammation involving the meibomian glands is termed an INTERNAL hordeolum
  • acute folliculitis of the glands of Zeis is an EXTERNAL hordeolum.
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6
Q

Chalazion

A
  • granulomatous inflammation centered around the meibomian glands or the glands of Zeis
  • a reaction to extruded lipid secretions, usually produces a painless swelling in the eyelid
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7
Q

Xanthelasma

A

a yellow plaque of lipid-containing macrophages, usually involving the nasal aspect of the eyelids.
- often seen in older persons and patients with disorders of lipid metabolism

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8
Q

exophthalmos

A

bilateral abnormal forward extrusion of the eyeball

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9
Q

proptosis

A

unilateral abnormal forward extrusion of the eyeball

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10
Q

What happens to the eye in Graves disease?

A

Exophthalmos,may precede or follow other manifestations of thyroid dysfunction

  • occurs in early adult life, especially in women (female-to-male ratio, 4:1)
  • may be severe and progressive, particularly in middle life, when exophthalmos no longer correlates well with the state of thyroid function.
  • edema of the eyelids, chemosis (conjunctival edema) and limitation of ocular motion
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11
Q

Inflammatory pseudotumor

A
  • a chronic idiopathic inflammatory condition associated with a variable degree of fibrosis
  • a common cause of proptosis and partial immobility of the eyeball
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12
Q

Conjunctival hemorrhage

A
  • may result from blunt trauma, anoxia, severe coughing, or spontaneously
  • does NOT spread into the cornea because of the barrier imposed by the close apposition of corneal epithelium to the underlying substantia propria
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13
Q

conjunctivitis

A
  • may be allergic or infectious
  • infectious caused by microorganism lodging on the surface of the eye or by hematogenous spread
  • iatrogenic infxns may follow ophthalmic manipulations, such as corneal grafts, intraocular implantation of lens prostheses or use of infected eyedrops or diagnostic instruments
  • hyperemic conjunctival blood vessels
  • inflammatory exudate that accumulates in the conjunctival sac commonly crusts, causing the eyelids to stick together in the morning. May be purulent, fibrinous, serous or hemorrhagic
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14
Q

trachoma

A
  • a chronic, contagious conjunctivitis caused by Chlamydia trachomatis
  • virtually always bilateral and involves the upper half of the conjunctiva more than the lower
  • cellular infiltrate is predominantly lymphocytic, and conjunctival lymph follicles with necrotic germinal centers are characteristic.
  • lymphocytes and blood vessels invade the superior portion of the cornea between the epithelium and Bowman zone.
  • Scarring of the conjunctiva and eyelids distorts the eyelids.
  • On microscopic examination, the desquamated conjunctival epithelium exhibits glycogen-rich intracytoplasmic inclusion bodies and large macrophages containing nuclear fragments (Leber cells). Secondary bacterial infections occur commonly.
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15
Q

inclusion blennorrhea

A
  • a purulent conjunctiviti that develops in newborns, who become infected during passage through the birth canal.
  • also acquired by swimming in nonchlorinated pools or from contact with dis- charges of infected urethra or cervix.
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16
Q

inclusion conjunctivitis

A
  • follicular conjunctivitis with focal lymphoid hyperpla- sia caused by Chlamydia in older children and adults
  • in contrast to trachoma, the lower tarsal conjunctiva is involved
  • Scarring and necrosis do not develop, and keratitis is rare and mild.
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17
Q

Ophthalmia neonatorum

A
  • severe, acute conjunctivitis with a copious purulent discharge, especially in the newborn, caused by Neisseria gonorrhoeae.
  • complicated by corneal ulceration, perforation, scarring and panophthalmitis.
  • treated with 5% Betadine eye drops.
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18
Q

Pinguecula

A

a yellowish conjunctival lump usually located nasal to the corneoscleral limbus.
- MC conjunctival lump, consists of sun-damaged connective tissue

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19
Q

Pterygium

A
  • a fold of vascularized conjunctiva that grows horizontally onto the cornea in the shape of an insect wing
  • often associated with a pinguecula and frequently recurs after excision.
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20
Q

HSV difference in primary ifxn and reactivation

A

Primary infxn:

  • subclinical or undiagnosed localized ocular lesions are caused by HSV type 1 in childhood.
  • accompanied by regional lymphadenopathy, systemic infection and fever.
  • Most corneal lesions due to HSV are asymptomatic plaques of diseased epithelial cells that contain replicating virus.
  • usually heal without ulceration, but an acute unilateral follicular conjunctivitis may occur. Corneal ulcers appear after serum antibody levels increase.

Reactivation of latent infxn:

  • Unlike primary HSV infection, reactivation disease is characterized by corneal ulceration and a more severe inflammatory reaction.
  • may be precipitated by ultraviolet light, trauma, menstruation, emotional and physical stress, exposure to light or sunlight, vaccination and other factors
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21
Q

HSV lesions in primary infxn

A
  • multiple, minute, discrete, intraepithelial corneal ulcers (superficial punctate keratopathy).
  • some of these lesions heal, others enlarge and eventually coalesce to form linear or branching fissures (dendritic ulcers).
  • The epithelium between the fissures desquamates, leading to sharply demarcated, irregular geographical ulcers
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22
Q

How are HSV ulcers visualized?

A

Fluorescin

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23
Q

HSV lesions in secondary infxn

A
  • central disc-shaped corneal opacity develops beneath the epithelium, owing to edema and minimal inflammation (disciform keratitis)
  • thinning of corneal stroma, Descemet membrane may bulge into it (descemetocele)
  • Corneal perforation can also occur.
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24
Q

Onchocerciasis

A
  • caused by parasite
  • accounts for blindness in at least half a million people in regions of Africa and Latin America in which it is endemic.
  • Microfilariae released from fertilized adult female worms migrate into the superficial cornea, bulbar conjunctiva, aqueous humor and other ocular tissues.
  • intracorneal microfilariae die and elicit an inflammatory response that leads to corneal opacification and visual impairment (river blindness).
  • Tx: ivermectin
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25
Q

annulus lipoides

A
  • frequent in the elderly

- accompanies certain disorders of lipid metabolism

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26
Q

Arcus Lipoides

A

a white arc due to lipid deposition in the peripheral cornea

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27
Q

Band Keratopathy

A
  • an opaque horizontal band across the cornea

- may contain calcium phosphate (calcific band keratopathy) or noncalcified protein (chronic actinic keratopathy)

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28
Q

calcific band keratopathy

A
  • calcium phosphate deposits in a horizontal band across the superficial central cornea in conditions associated with hypercalcemia
  • most often occurs in the absence of hypercalcemia, as in chronic uveitis.
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29
Q

Chronic actinic keratopathy

A
  • most severe in regions in which people spend a consider- able amount of time outdoors
  • unprotected eyes are exposed to excessive ultraviolet light, such as that reflected from desert, water or snow.
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30
Q

Meesmann dystrophy

A
  • epithelial dystrophy caused by dominant mutations in the KRT3 or KRT12 genes, which encode keratin 3 and keratin 12, respectively
  • result in aggregations of abnormal cytokeratin filaments and severely impair cytoskeletal function in the affected cells
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31
Q

familial subepithelial corneal dystrophy

A
  • AR bilateral epithelial dystrophy where the TACSTD2 gene is mutated
  • amyloid is found beneath the corneal epithelium in gelatinous drop-like deposits
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32
Q

macular corneal dystrophy

A

a defect in the CHST6 gene, which encodes a sulfotransferase that catalyzes sulfation of N-acetyl glucosamine and galactose in keratan sulfate

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33
Q

Genes implicated in stromal dystrophies

A
  • TFGBI (many)
  • CHST6 (macular corneal dystrophy)
  • PIP5K3 (fleck corneal dystrophy)
  • DCN (congenital stromal corneal dystrophy)
  • UBIAD1 (Schnyder corneal dystrophy)
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34
Q

Fuchs endothelial corneal dystrophy

A
  • wartlike excrescences form on the Descemet membrane (guttae), and progressive visual loss follows corneal edema and endothelial cell degeneration
  • missense mutations in COL8A2 (encodes the α2-chain of type VIII collagen)
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35
Q

cataracts

A
  • opacifications in the crystalline lens
  • causes: old age, diabetes, nutritional deficiencies, toxins, drugs, physical agents
  • may develop in ocular diseases such as uveitis, intraocular neoplasms, glaucoma, retinitis pigmentosa and retinal detachment
  • congenital rubella virus infection, some skin diseases, various systemic diseases
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36
Q

What happens in the development of cataracts?

A
  • clefts appear between the lens fibers, degenerated lens material accumulates in these spaces
  • Degenerated lens material exerts osmotic pressure, causing the damaged lens to imbibe water and swell, obstructing the pupil and causing glaucoma (phacomorphic glaucoma)
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37
Q

What happens in a mature cataract?

A
  • entire lens degenerates, and the lenticular debris escapes into the aqueous humor through the lens capsule, diminishing the volume of the lens
  • the extruded lenticular material is engulfed by macrophages and may obstruct aqueous outflow and produce glaucoma (phacolytic glaucoma)
  • compressed lens fibers in the center of the lens normally harden with aging (simple nuclear sclerotic cataract) and may become brown or black
  • If the peripheral part of the lens becomes liquefied (morgagnian cataract), the sclerotic nucleus may sink within the lens by gravity
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38
Q

Presbyopia

A
  • a failure of accommodation due to aging
  • the near point of distinct vision becomes located farther from the eye
  • displacement of lenticular fibers causes loss of elasticity so lens can’t become spherical –> accomodation is shitty
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39
Q

Phacoanaphylactic dndophthalmitis

A
  • an autoimmune granulomatous reaction to lens proteins
  • an inflammatory lesion occurs around or within the lens (or its remains) in an eye with a traumatized or cataractous lens and sometimes after surgical removal of a cataractous lens
  • similar reaction may occur spontaneously in the contralateral eye months or years later.
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40
Q

uveitis

A

inflammation of the uvea

41
Q

iritis

A

inflammation of the iris

42
Q

cyclitis

A

inflammation of the ciliary body

43
Q

iridocyclitis

A
  • inflammation of the iris and the ciliary body
  • causes red eye, photophobia, moderate ocular pain, blurred vision, a pericorneal halo, ciliary flush and slight miosis.
  • flare in anterior chamber on slit-lamp biomicroscopy,
  • keratic precipitates or a hypopyon (leukocytic exudate in the anterior chamber)
44
Q

Peripheral anterior synechiae

A

adhesions between the peripheral iris and the anterior chamber angle

45
Q

Posterior synechiae

A

adhesions that develop between the iris and the lens

46
Q

sympathetic ophthalmitis

A
  • an autoimmune disease where the entire uvea develops granulomatous inflammation after a latent period in response to an injury in the other eye.
  • Nodules containing reactive retinal pigment epithelium, macrophages and epithelioid cells commonly appear between the Bruch membrane (lamina vitrea) and retinal pigment epithelium (Dalen-Fuchs nodule)
  • antigen = arrestin, in photoreceptors
47
Q

Sarcoidosis in eye

A
  • granulomatous disease, calcific band keratopathy, retinal vascularization, vitreous hemorrhage and bilateral enlargement of the lacrimal and salivary glands (Mikulicz syndrome)
48
Q

retinal hemorrhage

A

CAUSES: hypertension, diabetes mellitus, central retinal vein occlusion, bleeding diatheses and trauma (shaken baby syndrome)

  • hemorrhage in nerve fiber layer have flame-shaped appearance on funduscopy
  • deep retinal hemorrhages tend to be round.
  • when located between the retinal pigment epithelium and Bruch membrane, blood appears as a dark mass, may resemble melanoma (spooky)
49
Q

retinal vascular occlusion

A
  • small emboli often do not interfere with retinal function, septic emboli may cause foci of ocular infection
  • white fluffy patches that resemble cotton on ophthalmoscopic examination (cotton-wool spots), consisting of aggregates of swollen axons in the nerve fiber layer of the retina.
  • affected axons contain numerous degenerated mitochondria and dense bodies related to the lysosomal system, which accumulate because of impaired axoplasmic flow
50
Q

central retinal artery occlusion

A
  • Permanent blindness follows central retinal artery obstruction, unless the ischemia is of short duration
51
Q

amaurosis fugax

A

Unilateral blurred vision, lasting a few minutes, that occurs with small retinal emboli in the central retinal artery.

52
Q

central retinal vein occlusion

A
  • results in flame-shaped hemorrhages in the nerve fiber layer of the retina, especially around the optic nerve head.
  • Edema of the optic nerve head and retina occurs because absorption of interstitial fluid is impaired.
  • Vision is disturbed but may recover surprisingly well, considering the severity of the funduscopic changes.
53
Q

What spooky thing happens after a central retinal vein occlusion?

A

An intractable, closed-angle glaucoma, with severe pain and repeated hemorrhages, commonly ensues 2–3 months after central retinal vein occlusion

This spooky complication is caused by neovascularization of the iris and adhesions between the iris and the anterior chamber angle.

54
Q

Features of hypertensive retinopathy

A

-Arteriolar narrowing
- Flame shaped hemorrhages in the retinal nerve fiber
- Exudates, including some that radiate from the center of
the macula (macular star)
- cotton wool spots
- microaneurysms

55
Q

arteriovenous nicking

A

In hypertensive retinopathy, veins look kinked where the arterioles cross over them.

  • reflects sclerosis within the venous walls, because retinal arteries and veins share a common adventitia at sites of arteriovenous crossings
56
Q

arterial sheathing

A

abnormal retinal arterioles appear as parallel white lines at sites of vascular crossings on fundoscopy

57
Q

copper wiring

A

In hypertensive retinopathy, INITIALLY the narrowed lumen of the retinal vessels decreases the visibility of the blood column and makes it appear orange on ophthalmoscopic examination

58
Q

silver wiring

A

In hypertensive retinopathy, LATER, as the blood column eventually becomes completely obscured, light reflected from the sclerotic vessels appears as threads of silver wire

59
Q

malignant hypertension

A

characterized by necrotizing arteriolitis, with fibrinoid necrosis and thrombosis of precapillary retinal arterioles

60
Q

proliferative retinopathy

A
  • does not appear until at least 10 years of diabetes, after which its incidence increases rapidly
  • T1DM: frequency of proliferative retinopathy correlates with the degree of glycemic control
  • T2DM: relationship between retinal microvascular disease and blood glucose levels in type 2 diabetes is less clear
61
Q

What accounts for most of the features of diabetic retinopathy?

A

retinal ischemia

62
Q

what are the two stages of diabetic retinopathy?

A

Background and proliferative

63
Q

Background diabetic retinopathy

A
  • venous engorgement, small hemorrhages (dot and blot hemorrhages), capillary microaneurysms and exudates
  • does not impair vision unless associated with macular edema
64
Q

exudative diabetic retinopathy

A

In elderly diabetic people, there is accumulation of “waxy” exudate in the vicinity of microaneurysms, which are not seen with type 1 diabetes

65
Q

waxy exudates

A
  • Exudates seen in exudative diabetic retinopathy

- due to hyperlipoproteinemia of diabetics, the exudates are rich in lipid and thus appear yellowish

66
Q

proliferative diabetic retinopathy

A
  • occurs after many years of retinopathy
  • neovascularization
  • newly formed vessels bleed easily, and resultant vitreal hemorrhages obscure vision
  • neovascularization a/w proliferation and immigration of astrocytes, which grow around the new vessels to form delicate white veils (gliosis)
  • often causes retinal detachment and blindness
67
Q

rubeosis iridis

A

iris neovascularization that occurs in diabetics with severe retinopathy
- can cause blindness secondary to glaucoma

68
Q

Diabetic Cataracts

A
  • Patients with T1DM develop bilateral “snowflake” cataracts, a blanket of white needle-shaped opacities in the lens immediately beneath the anterior and posterior lens capsule.
  • The opacities coalesce within a few weeks in adolescents, and within days in children, until the whole lens becomes opaque.
  • caused by accumulation of sorbitol
69
Q

Retinal Detachment

A

Separation of the sensory retina from the pigment epithelium

70
Q

rhegmatogenous retinal detachment

A

associated with a retinal tear and also often with degenerative changes in the vitreous body or peripheral retina

71
Q

tractional retinal detachment

A

the retina is pulled toward the center of the eye by adherent vitreoretinal adhesions (as occurs in proliferative diabetic retinopathy, in retinopathy of prematurity and after intraocular infection)

72
Q

exudative retinal detachment

A

Accumulation of fluid in the potential space between the sensory retina and the retinal pigment epithelium in disorders such as choroiditis, choroidal hemangioma andchoroidal melanoma

73
Q

Retinitis pigmentosa

A

refers to a variety of bilateral, progressive, degenerative retinopathies characterized clinically by night blindness and constriction of peripheral visual fields and pathologically by loss of retinal photoreceptors (rods and cones) and pigment accumulation within the retina

74
Q

macular degeneration

A

occurs with aging, in certain drug toxicities (e.g., chloroquine) and in several inherited disorders

  • loss of central vision
  • mutations in ABCA4 allow drusen to accumulate
75
Q

What causes a cherry-red macula?

A
  • lysosomal storage diseases

- central retinal artery occlusion

76
Q

Angioid streaks

A
  • characteristic irregular lines that radiate beneath the retina from the optic nerve head when the Bruch membrane fractures
  • happens spontaneously in pseudoxanthoma elasticum, sickle cell and Paget disease of bone.
77
Q

Retinopathy of prematurity

A
  • a bilateral, iatrogenic, retinal disorder that occurs predominantly in premature infants treated with high levels of inspired oxygen after birth
  • the developing retinal blood vessels become obliterated, and the peripheral retina does not vascularize
78
Q

Optic nerve head edema

A
  • swelling of the optic nerve head where the retinal axons leave the globe
  • caused by increased intracranial pressure
  • swollen optic nerve head that displays blurred margins and dilated vessels
79
Q

optic atrophy

A

thinning of the optic nerve caused by loss of axons within its substance d/t long-standing edema of the optic nerve head, optic neuritis, optic nerve compression, glaucoma or retinal degeneration

80
Q

glaucomatous cupping

A

excavation of the the optic nerve in optic atrophy following glaucoma

81
Q

glaucoma

A
  • a collection of disorders that feature an optic neuropathy accompanied by a characteristic progressive loss of visual field sensitivity and eventual excavation of the optic nerve head
  • often a/w increased intraocular pressure
  • almost always follows a congenital or acquired lesion of the anterior segment of the eye that mechanically obstructs the aqueous drainage
82
Q

Congenital Glaucoma

A
  • caused by obstruction to aqueous drainage by developmental anomalies
  • MC in boys
  • X linked recessive
  • a/w deep anterior chamber, corneal cloudiness, photophobia, excessive tearing and buphthalmos
83
Q

Primary open-angle glaucoma

A
  • the angle of the anterior chamber is open and appears normal, but there is increased resistance to the outflow of the aqueous humor in the vicinity of the canal of Schlemm.
  • intraocular pressure increases asymptomatically, almost always bilateral
  • damage to the retina and optic nerve causes irreversible loss of vision.
  • a/w DM, myopia
84
Q

Primary closed-angle glaucoma

A
  • Mydriasis of the iris obstructs the drainage of aqueous humor from the eye, resulting in sudden episodes of intraocular hypertension.
  • accompanied by ocular pain, and halos or rings around lights
  • intraocular pressure may also increase if the pupil becomes blocked and aqueous humor accumulates in the posterior chamber
  • AN OCULAR EMERGENCY EEEEEEKKKK
85
Q

low-tension glaucoma

A

has all the characteristic visual field defect and all of the ophthalmoscopic features of chronic open-angle glaucoma occur, but without increased intraocular pressure

86
Q

Effects of increased intraocular pressure

A
  • glaucomatous cupping
  • bulging of the cornea or sclera
  • optic atrophy
  • degeneration of ganglion cell and nerve fiber layers of the retina
  • buphthalmos in children
87
Q

Myopia

A
  • “nearsightedness”
  • a refractive ocular abnormality in which light from the visualized object focuses at a point in front of the retina because of a longer than usual anteroposterior diameter of the eye
88
Q

emmetropization

A

adjustment of the eye’s axial length to the refraction by the anterior segment of the eye in myopia

89
Q

Phthisis bulbi

A
  • nonspecific, end-stage eye that is disorganized and atrophic
  • MC after trauma or inflammation
  • intraocular bone formation, lens displacement, disorganization of ocular contents
90
Q

Malignant melanoma

A
  • arises from melanocytes in the uvea
  • mostly circumscribed, commonly invades the Bruch membrane
  • spindle-shaped cells without nucleoli (spindle A cells), spindle-shaped cells with prominent nucleoli (spindle B cells), polygonal cells with distinct cell borders and prominent nucleoli (epithelioid cells) or a fourth cell type that is similar to epithelioid cells but smaller with indistinct cell borders.
  • no lymphatic spread
  • hematogenous spread, also traverses the sclera to enter the orbital tissues
  • liver MC site of metasteses
91
Q

Prognostic factors of malignant melanoma

A
  • tumor size, tumor location and cell type
  • BAD: tumor hyperploidy, high mitotic activity, high microvascular density, high tumor-infiltrating lymphocyte counts, chromosome 3 monosomy and high serum melanoma inhibitory activity protein
  • tumors composed purely of epithelioid cells have the worst prognosis.
92
Q

retinoblastoma

A
  • originate from immature neurons
  • a/w inherited or acquired deletions of, or mutations in the Rb tumor suppressor gene, located on the long arm of chromosome 13 (13q14)
  • cream-colored tumor that contains scattered, chalky white, calcified flecks within yellow necrotic zones
93
Q

endophytic retinoblastoma

A

grow toward the vitreous body and can be seen with an ophthalmoscope

94
Q

exophytic retinoblastoma

A

extend between the sensory retina and the retinal pigment epithelium, thereby detaching the retina

95
Q

diffuse retinoblastoma

A

spreads diffusely within the retina without forming an obvious mass

96
Q

Flexner-Wintersteiner rosettes

A

when cells in retinoblastoma are arranged radially around a central cavity

97
Q

how do retinoblastomas disseminate?

A
  • extend into optic nerve

- hematogenously

98
Q

Clinical features of retinoblastoma

A
  • white pupil (leukocoria), squint (strabismus), poor vision, spontaneous hyphema or a red, painful eye
  • light entering the eye commonly reflects a yellowish color similar to that from the tapetum of a cat (cat’s eye reflex).
  • fatal if untreated, 90% survival with tx

MS2 Unit 3 (21 decks)

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