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Neuropysch > Intro to Eye Path > Flashcards

Intro to Eye Path Flashcards

1
Q

Eye Pathology: ITMIINDIO:

A

Inborn errors, Trauma, Meds, Infection, Ischemia, Neoplasm, Degeneration/age, Immune dyregulation, Other organ system

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2
Q

What makes up the Vital signs of the visual system

A

Comprehesive eye exam: Visual actuity, visual fields, pupil exam, extraoccular mvmt, intraocular pressure, exam ocular adnex +antoer segment structures + fundus exam (anatomical assessment)

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3
Q

What makes up teh function eye assement

A

 Visual acuity

 Visual fields

 Pupil exam

 Extraocular movements

 Intraocular pressure

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4
Q

You are looking at eye that is glassy on 2 day old baby, follows light, attracted to ligt in all 4 quads has round pupil R in rt eye with normal red reflex

in Left eye there is no red reflex and lack of pupillary reaciton, next step

A

Exam under anesthesia

check Intraocular pressure/ Corneal diameter/thickness

 Ultrasound of anterior and posterior segments/ Refraction/retinoscopy and Dilated fundus exam

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5
Q

indentify anatomy of cornea

A

key: transparent cover of teh eye or the ‘window”

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6
Q

What are the layers of the cornea

A

Epithelium: protection and replicates

Bowmans

Stroma (acellular so light passes)

Descements

Endothelium

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7
Q

Anatomy of cornea:

 Made of parallel fibers of _______and keratocytes (special fibroblasts).

 Needs_____ structure to maintain optical clarity (not to interfere with light coming into the eye).

A

type 1 collagen

parallel

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8
Q

Cornea:

 Absence of____ (to not disturb the parallel fibers).

 O2 and nutrients obtained through___ anteriorly and _____ posteriorly.

 Layer of _______ to continually pump out fluid from inside to maintain relatively dehydrated structure.

A

vessels

tears

aqueous humor

endothelial cells

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9
Q

What is the funtion of the retina

A

Fnx: let light to retina/ refractive thus bends rays to retina/ global to maintain shape eye

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10
Q

 Rare eye malformation resulting in congenital corneal opacity

 Part of a spectrum of developmental anomalies of the cornea, iris and lens termed “anterior segment dysgenesis.”

A

Peters anomaly

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11
Q

characterized by central corneal opacity with iridocorneal adhesions

A

Peters type I

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12
Q

central corneal opacity and cataracts or corneolenticular adhesions

A

Peters II

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13
Q

Peters anomaly and short stature, developmental delay, dysmorphic facial features including cleft lip/palate along with cardiac and genital abnormalities

A

Peters-plus syndrome

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14
Q

Peters anomaly has a wide spectrum of severity. Sporadic or genetic in the ___ gene

Corneal opacification is bilateral in approximately 80% of cases

A

PAX6 gene

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15
Q

What is teh pathological issue in Peter’s anamoly

A

 The endothelium and Descemet’s membrane do not form correctly (fluid is not removed from that cornea efficiently) – opacity

 Corneal collagen fibers are disturbed in that area - opacity

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16
Q

DDx for corneal opacity in newborn

A

Peters anomaly, Forceps delivery or Non-accidental trauma , TORCH infections

Metabolic disorders: Mucopolysaccharidoses or Sphingolipidoses

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17
Q

How does the cornea respond to injury

A

Epithelial cell injury and death

Disruption of Bowman’s layer and stromal lamellae

Keratocyte injury and death

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18
Q

MOre info on corneal repair;

A

 Epithelial hyperplasia  Stromal contraction  Epithelial repair
 Keratocyte activation  Synthesis of type I collagen, keratan sulfate and type VI collagen
 Blood vessel formation  Keratocyte apoptosis  Blood vessel apoptosis

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19
Q

Why do we get corneal scars with traum adn risk losing clarity

A

bc shit grows in, try to repari and resport type I collegens adn keratocytes, but at the end they apoptos to ensure clarity and insread scar d/t lack of parellel structure

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20
Q

Fuch’s corneal dystrophy

 ______ corneal dystrophy, more common in _____

 Affects vision starting in the ____

A

Autosomal dominant

women

50s

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21
Q

Dysfunction of corneal endothelial cells with growth of Descemet’s membrane “bumps”, called gutttae.

 In end stage of disease there is loss of endothelial cell

A

Fuchs corneal dystrophy

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22
Q

 Thickened stroma with fluid-filled spaces

 Cysts in epithelium
 Hazy cornea

A

Fuchs dystrophy

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23
Q

Transparent biconvex structure
Located behind the pupil, attached in place by the zonule

A

lens

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24
Q

Three main parts of lens

A

lens epithilum, lens capsule, lens fiber cells

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25
Q

lens fibers cells are

A

 Long, thin, transparent cells
 Arrange intracellular content and dispose of unnecessary organelles

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26
Q

Functions of the lens

A

 Transparency- let light reach the retina

 Refractive structure/accommodation- bend rays to reach the retina

 Lens is flexible – by changing the curvature of the lens one can focus for distance, intermediate or nea

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27
Q

 Caused by maternal infection by RNA toga virus  Infection of lens fiber cells by virus

A
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28
Q

What would be result of viral infection of lens fiber cells

A

disorganization of lens intraocular organelles and opacification of lens fibers

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29
Q

What happens when Rubella infects lens fibers

A

 Lens cells retain nucleus and organelles

 Pearly white focal nuclear opacification

 Can progress to complete cataract

 Live virus can be recovered from lens up to 3yrs after birth

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30
Q

“Salt and pepper” appearance
Due to damage of the retina pigmented epithelium layer

Vision, in most instances is preserved

A

Rubellar retinopathy

31
Q

Triad seen in congenital rubella infection

A

 Sensorineural deafness

 Eye abnormalities (70% of pts)

 Congenital heart disease

32
Q

Anatomy of retina and funx

A

Layer of eye that converts light–> neuronal impulse

33
Q

nourishes and supports photoRs, absorbs scat light, supply nutrient, BBR layer, participate in visual cycle, phatocytosis of photoR in outer segment

A

Fnx retinal pigmented epithelium:

34
Q

 Function of the photoreceptors:

A

specialized neuron that converts light into neuronal signal

35
Q

Transmit information to the brain (thalamus, hypothalamus and midbrain

A

inner plexiform layer

36
Q

Houses the bipolar, horizontal and amacrine cells

A

inner nuclear layer

37
Q

Contains the cell bodies of the rods and cones photoreceptors

A

Outer nuclear layer

38
Q

see these bone spicules in retina with pale reitna

A

Retinitis pigmentossa

39
Q

 Most common form of inherited retinal degeneration.

 Caused by abnormalities in photoreceptors (rods and cones) or the retinal pigmented epithelium.

A

Retinitis Pigmentosa

40
Q

15% of retinitis pigmentosa d/t

A

mutation in rhodopsin

41
Q

 Light sensitive receptor protein found in rod photoreceptors

 Composed of the protein opsin and the cofactor chromophore retinal

A

Rhodopsin

42
Q

 Retinol is produced in the retina from ____

 Isomerization of _____ to ______by light changes the shape of the opsin activating a G-protein cascade

 In addition to rhodopsin there are four other____ found in the cone cells

A

Vitamin A

11-cis-retinal to all-trans-retinal

opsins

43
Q

 15% of all RP are due to a mutation in_____.
 The mutations usually cause misfolding of the____ protein.; this leads to faulty outer rod segment recycling.

A

rhodopsin

opsin

44
Q

Mutations in 35 other genes that encode for proteins needed for the visual transduction cascade can cause RP. Some of these mutated genes encode for a

A

pre-mRNA splicing factor expressed in all cells.

45
Q

Why would mutations that would affect all cells in the body cause retinitis pigmentosa?

A

The photoreceptors are very metabolically active and would be affected more than other cells.

46
Q

 Inherited AD, AR and X-linked (dominant or recessive).

 3 types:

A

 Non-syndromic

 Syndromic (ex. combined with deafness – Usher syndrome)

 Secondary to other systemic diseases (ex.Refsum’s disease- abnormal build up of phytanic acid, a type of fatty acid)

47
Q

Other retinal degenerations seen:

A

There are more than 30 other retinal degenerations/dystrophy caused by a dysfunction of one or more of the retinal cells

48
Q

 Degeneration of the retinal pigmented epithelium

 Accumulation of drusen excrescences believed to represent byproducts of vision

A

Age-related macular degeneration : see drusen

49
Q

Differnce btwn Dry and Wet macular degeneration

A

Dry macular degeneration – progressive accumulation of druse

 In wet age-related macular degeneration, blood vessels from the choroidal layer invade the disrupted Bruch’s membrane causing bleeding in the outer layers of the retina.

 Disruption of normal retina architecture then leads to loss of photoreceptors and retinal pigmented epithelium.

50
Q

 In wet age-related macular degeneration, blood vessels from the _____ invade the disrupted Bruch’s membrane causing bleeding in the_____of the retina.

 Disruption of normal retina architecture then leads to loss of ____ and _____

A

choroidal layer

outer layers

photoreceptors and retinal pigmented epithelium.

51
Q

IN macular degeneration, Eventually, loss of retinal pigmentation epithelium causes loss of

A

photoreceptors

52
Q

Abnormal development of the vasculature of the retina in babies born pre-term.

 Increase risk if

A

born <1250 grams or earlier than 31 weeks.

53
Q

 Posterior circulation: blood from the____ feeds the posterior 1/3 of the retina

 Anterior circulation: blood from the ______ feeds the anterior 1/3 of the retina

A

choroid

central retinal artery

54
Q

 Baby born prior to full retinal vascular maturation.

 Factors associated with birth and leaving the womb result in :

 Vessels and retina become:

A

halting of normal vascular migration to the peripheral retina.

abnormal (forming ridges, vessels growing towards the vitreous)

55
Q

What happens to untreated premature retinopathy?

How do you treat it?

A

 If untreated, retina will detach.

 Untreated retinal detachment causes blindness in baby.

Laser or VEGF

56
Q

 Leading cause of blindness for people aged 20 to 64 years

 Retinal dysfunction due to hyperglycemia

 Pericyte loss in retinal capillaries

 Weak vessels bleed in the retina

A

Diabetic retinopathy

57
Q

Hyperglycemia causes ___ loss in retinal capillaries and Weak vessels bleed in the___

A

Pericyte

retina

58
Q

Development of vascular abnormalities and bleeding:

Microaneurysms

Dot-blot hemorrhages

Flame hemorrhages

A

seen in diabetic retinal neuraopathy

59
Q

In diabetic retinal neurapapthy: Underperfused retina secretes ________ thus

 Abnormal blood vessels grow towards the_____ and over other structures. Fragile blood vessels bleed.

 Contraction of the abnormal vasculature pulls the retina causing _____

A

vascular endothelial growth factor

vitreous

retinal detachment

60
Q

 Lack of blood flow through the central retinal artery.

 Causes include atherosclerosis of the carotid artery or embolism

see cherry red spot

A

Central retinal artery occulsion

61
Q

Causes of central retinal artery occlusion

A

Causes include atherosclerosis of the carotid artery or embolism

62
Q

Outcomes for pts with CRAO

A

Patients with visualized retinal artery emboli have a 56% mortality rate over 9 years, compared to 27% for an age- matched population without retinal artery emboli. Life expectancy of patients with CRAO is 5.5.

63
Q

Central retinal artery occlusion resluts in loss of

A

 Loss of the inner retina

64
Q

 Cancer of the immature retinal cells

 Most common malignant tumor of the eye in children

 2 forms: 55% non-heritable (new mutation) and heritable (familial gene)

A

Retinoblastoma

65
Q

 Bilateral retinoblastoma are usually_____, unilateral can be _____

 Inheritance is _______

A

heritable

non-heritable

AD (90% penetrance)

66
Q

Retinoblastoma: Mutation in _______(tumor suppressor protein that prevents excessive cell growth)

A

Ch 13 on the RB1 gene (

67
Q

You see this on histology of someones eyeball

A

Flexner-Wintersteiner rosettes in retinoblastoma

68
Q

Optic nerve or _____; transfer ocular neuronal impulses to the brain

A

Cranial nerve 2

69
Q

 The optic nerve is composed of the axons of the _______

 Contains approximately 1 million nerve fibers that end at the _______

A

retinal ganglion cells (and glial cells).

lateral geniculate nucleus

70
Q

Funtion of optic nerve

A

 The optic nerve transmits sensory information regarding brightness and contrast perception (visual acuity), color perception and visual field information. It also transmits the fibers that control pupillary response

71
Q

Describe traumatic optic neuropathy

A

 Direct or indirect injury (transmitted shock from orbital impact) to the optic nerve results in traumatic optic neuropathy

 Common mechanisms of injury include motor vehicle accident, bike accident, fall and assault.

72
Q

As a result of traumatic optic neuropathy:_____ loss appears to occur either through direct trauma, hemorrhagic infarction, direct compression of the nerve fibers from an extrinsic nerve sheath hematoma, shearing forces, or a combination of these mechanisms.

Loss of_____ support appears to occur followed by replacement of the axons with____.

A

Axonal

astrocyte

microglia

73
Q

Progressive optic neuropathy due to slow loss of optic nerve fibers

A

glaucoma

74
Q

Risk factors for glaucoma, which is modifiable

A

 Intraocular pressure ***** modifiable
 Age
 Central cornealt hickness

 Race

Neuropysch (18 decks)

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