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NS2 Test 2 > Chapter 29 part 2 > Flashcards

Chapter 29 part 2 Flashcards

1
Q

Anterior chamber bound by?

A
  • anteriorly–cornea
  • laterally-trabecular meshwork
  • posteriorly–iris
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2
Q

aqueous humor formed by?

A

pars plicate of ciliary body

  • enters posterior chamber, bathes lens
  • circulates through pupil to anterior chamber
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3
Q

cataracts–describes?

A

lenticular opacities–congenital or acquired

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4
Q

age-related cataract

A
  • pacification of lens nucleus (nuclear sclerosis)

- accumulation of urochrome pigment–lens nuclear brown–distorts the perception of blue color

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5
Q

posterior subcapsular cataract

A
  • migration of lens epithelial posterior to lens equator

- secondary to enlargement of abnormally positioned lens epithelium

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6
Q

morgagnian cataract

A

lens cortex liquefies

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7
Q

phacolysis

A
  • proteins may leak through lens capsule

- can clog trabecular meshwork-elevation in intraocular P and optic nerve damage

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8
Q

glaucoma–what is it?

A
  • distinctive changes in visual field and cup of optic nerve
  • most associated with elevated intraocular pressure
  • normal or low-tension glaucoma–with normal intraocular pressure
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9
Q

2 major categories of glaucoma

A
  • open angle

- angle closure

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10
Q

open angle glaucoma

A
  • aqueous humor has complete physical access to trabecular meshwork
  • the elevation in intraocular pressure results from an increased resistance to aqueous outflow in the open angle
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11
Q

primary open-angle glaucoma–genes

A
  • most common–few changes are apparent structurally
  • MYOC gene mutation–juvenile and adult
  • OPTN mutation–adults
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12
Q

secondary open-angle glaucoma–most common type?

A
  • pseudoexfoliation glaucoma
  • deposition of fibrillar material throughout anterior segment
  • SNPs in LOX1 gene (lyse oxidase like)
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13
Q

secondary open-angle glaucoma–particulate material?

A
  • particulate material can clog up trabecular meshwork
  • proteins (phacolysis)
  • senescent red cells after trauma (ghost cell glaucoma)
  • iris epithelial pigment granules (pigmentary glaucoma)
  • necrotic tumors (melanoma lytic glaucoma)
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14
Q

angle closure glaucoma

A
  • peripheral zone of iris adheres to trabecular meshwork

- physically impedes aqueous humor

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15
Q

primary angle-closure glaucoma

A
  • in eyes with shallow anterior chambers, often in patients with hyperopia
  • pupillary margin of iris on anterior surface of lens–pupillary block
  • continued production of aqueous humor by ciliary body–causes iris to bow forward (iris bombe)
  • lens epithelium–gets its nutrition from aqueous humor–can be damaged–leads to minute anterior subcapsular opacities (glaukomflecken)
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16
Q

secondary angle closure galucoma

A
  • pathologic membranes can form over surface of iris, causing iris to draw over trabecular meshwork
  • chronic retinal ischemia–upregulates VEGF–VEGF in aqueous humor induces thin, fibrovascular membranes over iris–contraction of these in membranes leads to occlusion of trabecular meshwork–neovascular glaucoma
  • can also be caused by tumors in ciliary body–compresses iris onto trabecular meshwork
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17
Q

in intraocular inflammation, what happens?

A

vessels in ciliary body and iris become leaky–exudate accumulate in anterior chamber

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18
Q

keratic precipitates

A

inflammatory cells adhere to corneal endothelium

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19
Q

presence of exudate in anterior chamber can facilitate the formation of adhesion bw?

A
  • iris and trabecular meshwork or cornea (anterior synechiae)–leads to increased intraocular P
  • iris and anterior surface of lens (posterior synechiae)–deprive lens epithelium of aqueous humor–fibrous metaplasia of lens epithelium–anterior sub capsular cataract
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20
Q

endopthalmitis

A
  • inflammation in vitreous humor
  • retina lines the vitreous cavity
  • inflammation in vitreous humor–poorly tolerated by retina–causes irreversible injury
  • exogenous–from environment–gains access through a wound
  • endogenous–to eye hematogenously
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21
Q

panopthalmitis

A

-inflammation within eye–retina, choroid, sclera, extends into orbit

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22
Q

uvea–consits of?

A
  • iris, choroid, ciliary body

- choroid–richly vascularized

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23
Q

uveitis

A
  • inflammation in 1 or more tissues that compose the urea

- chronic disease

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24
Q

granulomatous uveitis

A
  • complication of sarcoidosis
  • anterior segment–exudate–“mutton fat” keratin precipitates
  • post segment–choroid and retina
  • retina–perivascular inflammation–“candle wax drippings”
25
Q

retinal toxoplasmosis

A

-accompanied by uveitis

26
Q

sympathetic ophthalmia–what is it? caused by? diagnostic findings?

A
  • non-infectious uveitis
  • bilateral granulomatous inflammation–panuveitis (all urea)
  • can complicate a penetrating injury to eye–retinal ags gain access to lymphatics in conjunctiva–delayed hypersensitivity reaction–affects injured and uninjured eye
  • diagmostic findings–enucleation of a blind eye–diffuse granulomatous inflammation of uvea
27
Q

most common inraocular malignancy in adults

A

metastasis to uvea, typically the choroid

28
Q

uveal melanomas–genes

A
  • GNAQ and GNA11 (GPCRs–promote proliferation)

- loss of chromosome 3–deletion of BAP1 (tumor suppressor gene)

29
Q

uveal nevi-genes

A
  • GNAQ and GNA11 mutations

- but rarely transform into melanomas

30
Q

uveal melanomas–2 types of cells

A
  • spindle cells–fusiform in shape

- epithelioid cells-spherical

31
Q

uveal melanomas–spread by?

A
  • vasculogenic mimicry

- hematogenous route–first to liver

32
Q

retina responds to injury by?

A

gliosis

33
Q

retinal detachment

A
  • separation of neurosensory retina from RPE (retinal pigment epithelium)
  • RPE–role in maintenance of outer segments of RPE
34
Q

persistent hyperplastic primary vitreous

A

-incomplete regression of fetal vasculature running through vitreous humor (adult humor is avascular)

35
Q

posterior vitreous detachment

A

-with aging–posterior face of vitreous humor may separate from the neurosensory retina

36
Q

retinal detachment classified by

A

-presence or absence of break in retina

37
Q

rhegmatogenous retinal detachment

A

-full thickness retinal defect

38
Q

retinal tears develop by?

A
  • vitreous collapses structurally–posterior hyaloid (post face of vitreous humor) exerts traction on points of strong adhesion to retinal internal limiting membrane
  • vitreous humor seeps through tear–goes to potential space bw neurosensory retina and RPE
39
Q

hypertension–opthalmoscopy

A
  • retinal arteriosclerosis–thickened arteriolar wall changes
  • vessels appear narrowed
  • color of blood column changes from bright red to copper to silver (depending on vascular wall thickness)
40
Q

malignant hypertension–what happens?

A
  • retina and choroid vessels damaged
  • produce focal choroid infarcts–Elsning spots
  • exudate from damaged retinal arterioles–accumulate in outer plexiform layer of retina–macular star! (exudate in macula)
  • occlusion of retinal arterioles–infarcts of n fiber layer of retina–cytoid bodies–cotton wool spots
41
Q

diabetes mellitus–reliable histologic marker

A

-thickening of basement membrane of epithelium of pars plicate of ciliary body

42
Q

retinal vasculopathy of diabetes mellitus–classifed into?

A
  • non-profliferative diabetic retinopathy

- proliferative diabetic retinopathy

43
Q

non proliferative diabetic retinopathy

A
  • basement membrane of retinal BVs thickens
  • microaneurysms–important manifestation
  • retinal microcirculation becomes leaky–macular edema
  • exudates–accumulate in outer plexiform layer
44
Q

proliferative diabetic retinopathy

A

-appearance of new vessels sprouting on surface of the optic n head (neovascularization of disc), or on surface of retina (neovascularization elsewhere)

45
Q

proliferative diabetic retinopathy–new vessels go where?

A

-breach the internal limiting membrane of retina

46
Q

posterior vitreous detachment

A

if vitreous humor separates from internal limiting membrane of retina–massive hemorrhage from the disrupted neovascular membrane

47
Q

retinal neovascular–accompanied by?

A
  • neovascular membrane on iris surface (due to VEgF)
  • contraction of iris nonvascular membrane–adhesions bw iris and trabecular meshwork (anterior synechiae)–occludes aqueous outflow neovascular glaucoma
48
Q

retinopathy of prematurity (retrolental fibroplasia)

A
  • at term–temporal aspect of retinal periphery is incompletely vascularized
  • in premature babies treated with oxygen–immature retinal vessels constrict–retinal tissue distal to the zone is ischemic
  • retinal ischemia–up regulation of VEGF–retinal angiogenesis–contraction of neovascular membrane–drag the temporal aspect of retina toward peripheral zone–displace macula laterally–retinal detachment
49
Q

retinopathy that affects patients with sickle hemoglobinopathies–2 types

A
  • non-proliferative
  • proliferative
  • both cause vascular occlusion
50
Q

retinopathy that affects patients with sickle hemoglobinopathies–what happens? visible changes?

A
  • infarct of retina

- retina swells, becomes optically opaque–fundus appears white instead of red or orange

51
Q

hollenhorst plaques

A

-fragments of atherosclerotic plaques can lodge in retinal circulation

52
Q

total occlusion of central retinal a–produces

A
  • diffuse infarct of retina
  • retina appears opaque
  • normal orange-red of choroid, highlighted by surrounding opaque retina (cherry red spot)
53
Q

cherry red spot occurs in?

A
  • occlusion of central retinal a

- Tay-sachs and Riemann-Pick diseases

54
Q

AMD (age-related macular degeneration)

A
  • dry AMD–deposits in Bruch membrane, atrophy of RPE
  • wet AMD–choroidal neovascularization–penetrate through RPE–becomes directly beneath the neurosensory retina–vessels can leak–exudated blood cause macular scars
55
Q

AMD gene

A

CFH (complementary regulatory gene)

56
Q

Retinitis pigmentosa

A
  • inherited mutations that affect rods and cones or RPE
  • visual impairment
  • rods and cones lost to apoptosis
  • retinal atrophy–constriction of retinal vessels and optic nerve head atrophy (waxy pallor of optic disc)
57
Q

retinitis pigmentosa

A
  • inherited mutations that affect rods and cones, or RPE
  • visual impairement
  • rods and cones lost to apoptosis
  • retinal atrophy–constriction of retinal vessels and optic n head atrophy (waxy pallor of optic disc)
58
Q

retinitis pigments pathogenesis

A
  • candida- can disseminate to retina hematogenously–causes retinal abscesses
  • CMV–in immunocompromised

NS2 Test 2 (16 decks)

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