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Pathology > The Eye Robbins > Flashcards

The Eye Robbins Flashcards

1
Q

Diseases that increase orbital contents; chronic corneal exposure to air is

A

displace the eye forward: PROPTOSIS;

injurious, leading to pain and predisposing to corneal ulceration and infection

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2
Q

What can cause proptosis?

A

Enlargement of lacrimal gland from inflammation or neoplasm (displaces eye inferiorly and medially)

QandA: most common cause of this is THYROID DISEASE (then orbital dermoid cysts and hemangiomas); you see extraocular muscles swell because of mucinous edema, accumulation of fibroblasts, and infiltration by lymphocytes

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3
Q

Two most common primary tumors of the optic nerve

A

Glioma and meningioma (produce axial proptosis b/c optic nerve is positioned within muscle cone)

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4
Q

Idiopathic orbital inflammation: cause, where, histo

A

Cause: inflamm condition affecting orbit
Where: maybe be bilateral or unilateral, confined to lacrimal gland (sclerosing dacryoadenitis), extraocular muscles (orbital myositis), or Tenon’s capsule (fascial layer around eye, or posterior scleritis) LET!!!
Histo: thinks lymphocytes, plasma cells, and occasionally eosinophils; maybe vasculitis (think Wegener’s)

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5
Q

Most common primary tumors of the orbit are

A

vascular in origin (capillary hemangioma of infancy and early childhood, and lymphangioma; and the encapsulated cavernous hemangioma found typically in adults

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6
Q

In eyelid, most common malignancy is what? Clinical?

A

Basal cell carcinoma;

can distort tissue and prevent eyelids from closing completely; MUST TREAT PROMPTLY!! Think LOWER EYELID!!

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7
Q

Sebaceous carcinoma: presentation, spread, histo, sequelae

A

Presentation: can mimic chalazion or diffusely thicken the eyelid; can resemble blepharitis or ocular cicatricial pemphigoid
Spread: spread first to the parotid and submandbular nodes
Histo: vacuolization of the cytoplasm; Pagetoid spread; can go through conjunctival epithel and epidermis to lacrimal drainage system and nasopharynx; also lacrimal gland;
Sequelae: think Kaposi sarcoma in either eyelid or conjunctiva (could have purple hue in eyelid, but bright red in conjunctiva!!)

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8
Q

Primary lymphoma of the conjunctiva is

A

typically indolent marginal zone B-cell lymphoma, most likely to develop in the fornix

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9
Q

When can conjunctival scarring occurring? Sequelae?

A
  1. Chlamydia trachomatis (significant conjunctival scarring)
  2. Exposure of ocular surface to caustic alkalis
  3. Sequela to ocular cicatricial pemphigoid;
    number of goblet cells reduced and leads to decrease in surface mucin (without this can get DRY EYE)

Robbins QandA: trachoma with initial inflamm followed by progressive scarring of conjunctiva and cornea

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10
Q

Dry eye most commonly occurs from

A

deficiency in the aqueous component of the tear film generated by accessory lacrimal glands embedded within the eyelid and fornix

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11
Q

Removal of a conjunctival neoplasm or precursor lesion may

A

leave the affected individual with a painful dry eye that can compromise vision; try to remove ONLY the invasive components of conjunctival neoplasms when possible!!!

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12
Q

Pterygium and pinguecula: causes, where, potential sequelae

A

Causes: actinic damage (sun-exposed regions of conjunctiva)
Where: pterygium originates in conjunctiva astride the limbus, dissecting into plane occupied normally by the Bowman layer, and won’t pose a threat to vision; pinguecula is astride the limbus and is yellowish, won’t invade cornea and can result in uneven distribution of tear film over adjacent cornea
Sequelae: usually benign for ptery (could be SCC and melanoma) and pinguecula can create saucer-like depression in corneal tissue, or DELLE!!)

QandA: if there’s mention of an insect wing and a fold of vascularized conjunctiva, think PTERYGIUM (pterydactyl!!)

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13
Q

Conjunctival SCC: progression, causes;

A

Progression: mild dysplasia through CIS (Conjunctival intraepi neoplasia)
Causes: HPV types 16 and 18 for squamous papillomas and CIN

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14
Q

Conjunctival nevi: progression, results

A

Progression: late childhood or adolescence you have inflamm component with lymphocytes, plasma cells, eosinophils
Results: inflamed juvenile nevus

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15
Q

Conjunctival melanomas: causes, who, treatment

A

Causes: unilateral neoplasms
Who: fair-complexioned individuals in middle age
Treatment: Prevention through extirpation of its precursor lesion (could spread to parotid or submandibular lymph nodes)

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16
Q

Blue sclerae can be seen in

A
  1. optical Tyndall effect after episodes of scleritis
  2. High intraocular pressure could thin sclera and with staphyloma, you get blue color
  3. OI
  4. Congenital melanosis oculi (uvea with congenital nevus that’s highly pigmented); could evolve into nevus of Ota
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17
Q

Corneal ulceration: causes, clinical, histo

A

Causes: pathogens like bacteria, fungi, viruses (think herpes simplex and zoster) and protozoa
Clinical: slit-lamp examination and can see exudate and cells leaking from iris and ciliary body vessels in anterior chamber; penlight examination (hypopyon)
Histo: exudate and cells leaking from iris and ciliary body vessels into anterior chamber (think lymphocytes, plasma cells, viral inclusions within cornela epi cells if chronic)

Robbins QandA: most common cause is HERPES SIMPLEX

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18
Q

Two examples of corneal degeneration and causes

A
  1. Calcific band keratopathy: deposition of Ca in Bowman layer; one can complicate chronic uveitis
  2. Actinic band keratopathy: chronically exposed to high levels of UV light; extensive solar elastosis in superficial layers of corneal collagen
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19
Q

Keratoconus: causes, histo, sequelae

A

Causes; thinning and ectasia of the cornea, bilateral, conical shape rather than spherical shape
Histo: thin cornea with breaks in Bowman layer; Descemet membrane could rupture precipitously: could lead to corneal hydrops
Sequelae: might need corneal transplantation or just rigid contact lens; associated with Down syndrome, Marfan syndrome, and atopic disorders!!!

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20
Q

Fuchs Endothelial Dystrophy: Causes, histo, presentation, sequelae

A

Causes: Loss of endothelial cells and resulting edema and thickening of the stroma;
Histo: droplike deposits of abnormal BM material (guttata) produced that resemble fetal component of Descemet membrane, and can see guttata by slit-lamp
Presentation: vision is blurred
Sequelae: might need corneal transplantation (pseudophakic bullous keratopathy); fibrous CT may be deposited between epi and Bowman layer (degenerative pannus) perhaps by ingrowht from limbus or fibrous metaplasa of corneal epi

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21
Q

Stromal dystrophies: causes, where, one particular mutation

A

Causes: TGFB1 gene which encodes ECM protein keratoepithelin; stromal deposits generate discrete opacities in the cornea that could eventually compromise vision
Where: think epi, BM, and Bowman layer leading ultimately to compromised vision

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22
Q

Cataract: causes, some examples

A

Causes: Think systemic disease (diabetes mellitus, Wilson disease, atopic dermatitis), drugs (corticos) radiation, trauma, UV light, leading to LENTICULAR OPACITIES that could be congenital or acquired
Examples: 1. age-related cataract (nuclear sclerosis),
2. urochrome pigment distorting person’s perception of blue color,
3. posterior subcapsular cataract (due to lens epithelium enlarging)
4. Morgagnian cataract (lens cortex liquefies nearly entirely)

RobbinsQandA: nuclear sclerosis will have opacification of the lens due to compression of the lens fibers in the central portion of lens, but peripheral vision will be okay

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23
Q

Glaucoma causes, types,

A

Cause: elevated intraocular pressure (sometimes normal intraocular pressure) leading to optic nerve and visual field changes;
Types: 1. Open-angle glaucoma where you have increased resistance to aqueous outflow and elevated intraocular pressure
2. Angle-closure glaucoma (peripheral iris adheres to trabecular network and impedes egress of aqueous humor if e.g. pupil dilates)

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24
Q

In primary open-angle glauma, the most ____ form of glaucoma, what can be associated with this?

A 
common;
myocilin gene (MYOC) for juvenile and adult primary open-angle glaucoma vs. optineurin (OPTN) for adults
25
Q

For secondary open-angle, list some causes

A
  1. Pseudoexfoliation glaucoma (deposition of fibrillar material of varying composition throughout anterior segment; think polymorphism in lysyl oxidase like 1, LOX1, gene)
  2. Ghost cell glaucoma (senescent red cells after trauma clogging trabecular network
  3. Pigmentary glaucoma (iris epi pigment granules)
  4. Necrotic tumors (melanoma-lytic glaucoma)
26
Q

For primary angle-closure glaucoma, what can cause this? Sequelae?

A

Causes: shallow anterior chambers and seen in those with HYPEROPIA (Robbins QandA); maybe pupillary block, iris bombe, eventually DAMAGED LENS EPI
Sequelae: elevated intraocular pressure can produce corneal edema and bullous keratopathy

27
Q

Secondary angle-closure glaucoma: causes

A

Causes:

  1. Chronic retinal ischemia (up-regulation of VEGF and presence of membrane over iris surface; can lead to neovascular glaucoma)
  2. Retinoblastomas
  3. Tumors in ciliary body
28
Q

For endophtalmitis and panophthalmitis, list causes

A

Causes: vessles in ciliary body and iris become leaky, allowing cells and exudate to accumulate in the anterior chamber (formation of adhesions b/w iris and trabecular meshwork or cornea, anterior synechiae, OR b/w iris and anterior surface of lens, aka posterior synechiae)

29
Q

Endophthalmitis is reserved for inflamm within _____, and panophthalmitis applies to _____

A 
vitreous humor (leads to retina poorly tolerating suppurative inflammation), and can be endogenous or exogenous;
inflamm within eye the involves retina, choroid, and sclera and extends into orbit
30
Q

Uvea consists of

A

iris, choroid, and ciliary body

31
Q

Uveitis causes, examples, treat

A

Causes: in posterior segment, think infectious agents (e.g. Pneumocystis carinii), idiopathic (sarcoid), or maybe autoimmune (sympathetic ophthalmia)
Examples: granulomatous uveitis due to sarcoidosis (in posterior segment sarcoid can involve choroid and retina) and CANDLE WAX DRIPPINGS; retinal toxoplasmosis can be accompanied by uveitis; sympathetic ophthalmia is noninfectious (bilateral granulomatous inflamm and panuveitis): think DELAYED HYPERSENSITIVITY REACTION and enucleation of blind eye yielding diagnostic findings;
Treat: systemic immunosuppressants and look for EOSINOPHILS!!

Robbins QandA: symp ophthalmia is complication of penetrating ocular trauma resulting from release of antigen from one eye and causing inflamm reaction in opposite eye (remove traumatized eye first)

32
Q

Most common intraocular malignancy of adults is ____, typically to where? What is the most common primary intraocular malignancy of adults? Causes, histo, clinical

A

metastasis to uvea, typically the choroid;
UVEAL MELANOMA;
Causes: oncogenes are GNAq and GNA11 (G protein receptors), also loss of chromosome 3 (deletion of BAP1, a tumor suppressor that normally places repressive marks on chromatin and gets gene silencing)
Histo: look for spindle cells (fusiform) and epithelioid cells (spherical and cytologic atypicality)
Sequelae: mets particularly to liver; prognosis depends on size (lateral worse than deeper), cell type (epithelioid worse than spindle), and proliferative index); think eye-sparing radiotherapy

Robbins QandA: as though a shade had been pulled across!!! can cause retinal detachment, choroidal hemorrhage, or macular edema

33
Q

What defines a retinal detachment?

A

Separation of the neurosensory retina from the retinal pigment epi (latter derived from primary optic vesicle)

34
Q

RPE-photoreceptor interface disturbance implicated in

A

hereditary retinal degenerations like RETINITIS PIGMENTOSA!!

35
Q

Retinal detachment classified based on

A

presence or absence of a break in the retina

36
Q

Rhegmatogenous retinal detachment is; treatment; complications

A

associated with a full-thickness retinal detachment and liquefied vitreous can gain access to space between NEUROSENSORY RETINA AND RPE!!
Treat: scleral buckling (application of strips of silicon to eye surface) and vitrectomy to remove vitreous removal;
complications: proliferative vitreoretinopathy (formation of epiretinal or subretinal membranes by retinal glial cells or RPE cells)

37
Q

Non-rhegmatogenous retinal detacment permits

A

fluid to leak from the choroidal circulation under the retina (think choroidal tumors and malignant HTN)!!!

38
Q

In retinal arteriolosclerosis in context of malignant HTN, the thickened arteriolar wall

A

changes the ophthalmic perception of circulating blood: vessels appear narrowed, and coloar of blood could go from bright red to copper and maybe silver!!

39
Q

In malignant HTN, vessels in ___ and ___ maybe damaged; what is a major sequelae with damage to choriocapillaris?

A

choroid, retina; think potential retinal detachment and also Elschnig spots if CHOROIDAL VESSELS are damaged

40
Q

Exudate from damaged ____ arterioles typically accumulates where? What would you see with ophthalmoscope?

A

retinal; outer plexiform layer of retina;

macular star

41
Q

If retinal arterioles are occluded, what could happen?

A
  1. Infarcts of nerve fiber layer of the retina
  2. Cytoid bodies with swollen ends of damaged axons
  3. Collection of cytoid bodies populate nerve fiber layer infarct (look for COTTON-WOOL SPOTS)
42
Q

Diabetes mellitus: histo, types and key points for each

A

Histo: thickening of basement membrane of epi of pars plicata of ciliary body;

  1. Nonprolif diabetic retinopathy (BM of retinal bv’s thickened, microaneurysms, macular edema due to leaky vessels, exudates formed in outer plexiform layer, upregulation of VEGF)
  2. Prolif diabetic retinopathy (new vessels of optic nerve head or surface of retina, could be posterior vitreous detachment if vitreous humor separates from internal limiting membrane of the retina); traction retinal detachment could start as non-rheg detachment but could lead to traction rheg detachment

Robbins QandA: hemorrhages, arteriolar hyalinization, cotton-wool spots, neovascularization, fibroplasia; renal failure; cardiovascular disease

43
Q

Retinopathy of prematurity (retrolental fibroplasia): what is it?

A

In premature or LBW infants treated with O2, immature retinal vessles in temporal retinal periphery CONSTRICT, rendering retinal tissue distal to this zone ISCHEMIC!! (VEGF can be up-regulated)

RobbinsQandA: can actually have scarring and retinal detachment

44
Q

Give examples of retinal artery and vein occlusions:

A
  1. Atherosclerosis of central retinal artery
  2. Emboli from heart thrombi or ulcerated atheromatous plaques in carotid arteries (Hollenhorst plaques)
  3. Retinal opacity (blocks view of vascular choroid);
    Retinal vein occlusion with VEGF upregulated

QandA: look for flame-shaped hemorrahges and intraocular pressure elevated in central retinal vein occlusion

45
Q

Cherry-red spots can be seen in

A

diffuse infarct of the retina; also in Tay-Sachs and Niemann-Pick diseases (stuff builds up in retinal ganglion cells but fovea is relatively transparent)

Robbins QandA: can have thromboembolization from diseased heart to cause diffuse retinal infarct in central retinal artery

46
Q

AMD: causes, forms, treat

A

Causes: damage to macula which is required for central vision; excess complement activity, cig smoking, or intense light exposure!!
Forms: 1. Atrophic/dry AMD (deposits in Bruch membrane, or drusen, and geographic atrophy of the RPE
2. Neovascular/wet AMD (choroidal neovascularization with angeiogenic vessels originating from choriocapillaris and penetrates throgh Bruch membrane beneath the RPE)
Treat: VEGF antagonists for neovascular AMD

47
Q

Retinitis pigmentosa: cause, sequelae

A

Causes: inherited condition resulting from mutations affecting rods and cones, or RPE; part of something like Bardet-Biedl syndrome, Usher syndrome, or Refsum disease or isolation
Sequelae: lose rods and cones to apoptosis, leading to night blindness and central visual acuity

QandA: think accumulation of pigment within the retina (retinal pigment epi cells migrate into sensory retina)

48
Q

In histo of retinoblastoma, what can be seen in well-differentiated tumors?

A

Flexner-Wintersteiner rosettes (cluster of cuboidal or short columnar cells around central lumen; can spread to orbit or along optic nerve) and fleurettes

49
Q

Retinal lymphoma involves _____: who, what nerve is involved usually?

A

neurosensory retina and RPE;
think older individuals (usually DLBCL);
optic

50
Q

In papilledema, how can this develop? How does it differ from AION?

A

Edema of the head of the optic nerve could develop with:
1. compression of the nerve (primary neoplasm of optic nerve with swelling of nerve head and unilateral disc edema)
2. elevations of CSF pressure surrounding the nerve (bilateral disc edema);
optic nerve head is SWOLLEN AND HYPEREMIC in papilledema, but swollen and PALE in AION

51
Q

In normal-tension glaucoma, what can be seen with optic nerve? With elevated intraocular pressure, what can be seen?

A

Cupped and atrophic, combination UNIQUE TO GLAUCOMA!!;

  1. diffuse enlargement of the eye (buphthalmos)
  2. enlargement of the cornea (megalocornea)
  3. in adulthood more so, think ectatic sclera (staphyloma)
52
Q

For optic neuritis, what does this describe and what’s a main cause?

A

Multiple sclerosis; see loss of vision secondary to demyelinzation of the optic nerve

53
Q

Hypertensive retinonaphy results from

A

long-standing hypertension, with progressive changes beginning with generalized narrowing of arterioles; look for flame-shaped hemorrhages (retinal nerve fiber layer), cotton-wool spots, HARD, WAXY exudates (if they radiate from macula, they will be the macular star)!

54
Q

Corneal stromal dystrophy

A

is usually autosomal dominant; most severe is macular dystrophy, but this is actually AUTOSOMAL RECESSIVE and is a form of mucopolysaccharidosis confined to cornea where KERATAN SULFATE is deposited

55
Q

Pannus is

A

due initially to C. trachomatis and the cornea being invaded by blood vessels and fibroblasts forming this trachomatous pannus; conjunctiva was focally hypertrophic and scarred

56
Q

Causes of secondary glaucoma

A

include inflamm, hemorrhage, neovascularization of iris, adhesions

57
Q

Xanthelasmas are

A

yellow plaques of lipid-containing macrophages usually located on EYELIDS (think familial hypercholesterolemia maybe)

58
Q

Snowflake cataracts can be associated with

A

patients with type 1 diabetes with accumulation of sorbitol in the lens

59
Q

Myopia (near-sightedness) is basically

A

increase in anteroposterior diameter of eye and leads to ligh from object focusing on point in front of retina

Pathology (40 decks)

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