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Posterior Seg Lecture > Exam One Flashcards > Flashcards

Exam One Flashcards

1
Q

what supplies the inner 2/3 of the retina up to the ELM

A

central retinal artery system

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2
Q

what system supplies and drains the outer 1/3 of the retina

A

choroidal- choriocapillaris system

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3
Q

which structure divides the inner and outer retina

A

ELM

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4
Q

what drains the inner retina

A

central retinal vein

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5
Q

What is the diff between the inner and outer retinal blood supplies

A

inner retina has a closed system, so the blood should be tight and not fenestrated; the outer retina has a free flow of nutrients and oxygen , so it is NOT a closed system

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6
Q

which system supplies the developing eye for 4 mos during gestation

A

hyaloid vascular system

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7
Q

T or F: during development, there is a reduction of bf from peripheral retina back to the ON, and this redirection is the development of the retinal veins

A

T

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8
Q

T or F: capillaries develop for several years after full gestation, up to 3-5 YO

A

T

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9
Q

WHy do we have Retinopathy of prematurity

A

bc during development, bv reach nasal ora at the same time as they reach the temporal equator

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10
Q

this is the end artery that enters the ON and supplies blood to the inner 2/3 of retina

A

central retinal artery ( as it enters through lamina cribrosa it narrows / tapers)

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11
Q

what are the artery vessel layers

A

intima, internal elastic lamina, media, and adventitia

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12
Q

T or F: as the bv work their way to the ora, they become more narrow

A

T

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13
Q

T or F: The bv stop 1.5 mm from ora, and this is where there is a VASCULAR zone

A

F: this is an AVASCULAR ZONE

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14
Q

which vessel layer makes up the lumen of the artery and is a single layer of tissue

A

intima

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15
Q

which vessel layer functionally separates the intima from the media , and is very thin in arteries and arterioles

A

internal elastic lamina

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16
Q

Are arteries rigid

A

YES

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17
Q

this vessel layer is smooth muscle

A

media ( arterioles are abundant )

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18
Q

this vessel layer is the outermost layer made of ct ; tightly binds the vessels to the retina

A

adventitia

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19
Q

these vessels extend from the central retinal artery; contain smooth muscle in the vascular wall ; internal elastic lamina is d/c or minimal

A

retinal arterioles

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20
Q

what happens to the vessels with high CO2

A

they dilate and vice versa with oxygen

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21
Q

how are the retinal arteries and arterioles regulated

A

via auto regulation- they respond to Oxygen or CO2, hormones, and chemicals in the body; bv narrow if the pt has high oxygen content and dilate in response to high CO2 content

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22
Q

how do the retinal arteries and arterioles attach

A

via the glial perivascular limiting membrane of Kruckman ; they are located in the NFL or GCL

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23
Q

which structure wraps over the entire retina and covers bv

A

ILM

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24
Q

which structure drains blood from the capillaries

A

retinal venules and veins

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25
Q

these vessels expand in diameter as they develop to form the central retinal vein; they have elastic tissue and small amts of smooth muscle; they are not rigid

A

veins

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26
Q

how are the veins attached

A

via the glial perivascular limiting membrane of Kruckman

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27
Q

T or F: Veins are loosely attached to the ILM

A

T: this means there can be changes in the appearance of the veins such as tortuosity

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28
Q

what can occur if the central retinal vein bifurcates anterior to the lamina cribrosa

A

central retinal vein occlusion

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29
Q

what happens if the central retinal vein bifurcates posterior to the lamina cribrosa

A

hemi retinal vein occlusion

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30
Q

what vessels supplies the inner 1/3 of the retina

A

retinal capillaries:

remember: central retinal artery supplies inner 2/3

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31
Q

in this network you will find arteries and veins; this is the post arteriolar network and is assoc with artery based diseases like HTN; more superficial

A

inner capillary network

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32
Q

this network is the inner nuclear layer; its prevenular ; assoc with venous based diseases like diabetes; more deep

A

outer capillary network

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33
Q

where are the capillary free zones

A

there are three

1) ora capillary free zone
2) foveal avascular zone ( fovea gets supply from deeper outer 1/3 retina)
3) capillary free zone around arteries and arterioles ( as opposed to veins, capillaries bump against veins )

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34
Q

these vessels do not have smooth muscle or elastic tissue ; the endothelial cells form the inner blood retinal barrier; pericytes responsible for Autoregulation of the microvascular circulation

A

retinal capillaries

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35
Q

what happens when the pericytes break down

A

can lead to microaneurysms ( diabetes)

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36
Q

what causes peripheral retinal hemorrhages

A

with age, the breakdown of the endothelial cells and pericytes

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37
Q

what are the three capillary zones

A

circumpapillary zone, perifoveal zone, and ora zone

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38
Q

this zone is the area around the ON and two disc diametes away from it

A

circumpapillary zone

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39
Q

this zone is where the two networks merge into one network before the foveal avascular zone

A

perifoveal zone

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40
Q

this zone is where the capillaries merge as the retina begins to thin near the retina

A

ora zone

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41
Q

cotton wool spots are due to what?

A

ischemia

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42
Q

exudate is due to what?

A

edema

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43
Q

make sure you know the retinal layers s

A

slide 14, lecture 1

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44
Q

what are the layers of Bruchs Membrane

A
  1. RPE basement membrane
  2. inner collagenous layer
  3. elastic layer
  4. outer collagenous layer
  5. choriocapillaris basement membrane
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45
Q

will inner or outer capillary networks have the cotton wool spots and flame shaped hemorrhages

A

inner capillary network

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46
Q

this network is located in the inner nuclear layer and is assoc with diabetes ( will have exudative changes, edema, or dot blot /intra retinal hemorrhages)

A

deep/outer capillary network

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47
Q

how is the connection between the RPE and photoreceptors and RPE and overlying sensory retina

A

space between RPE and PR is filled with mucopolysaccharide “glue” / But the glue is very loose . Its loosely adherent to the overlying sensory retina, but RPE cells tightly adherent to each other

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48
Q

T or F: the basement membrane of Bruchs and RPE form a tight bond

A

T

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49
Q

What serves as a barrier between the sensory retina and the choroid

A

RPE

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50
Q

this is a multi layered structure that extends from the optic nerve to the ora serrata; breaks down with age

A

bruchs membrane

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51
Q

what is it called when the RPE is pulled away from Bruchs

A

pigmented epithelial detachment

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52
Q

which vessels feed into the choriocapillaris

A

short posterior ciliary arteries, recurrent branches of the long posterior ciliary arteries, and branches of the anterior ciliary arteries

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53
Q

where does the greatest activity of the choriocapillaris occur

A

at the fovea

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54
Q

how do Elschnig spots happen

A

they are due to infarcts, due to rapid increase in bp, then rapid reduction in bp; this damages the choriocapillaris and everything anterior to that ( Bruchs membrane, PR, ) which stops functioning; aka a window defect/ RPE defect

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55
Q

what can normally occur in someone with HTN, where the choroid and choriocapillaris system has been damaged and inflamed, causing deep scar tissue

A

Siegrist streak

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56
Q

where do peripheral changes happen

A

by the ora - called pavingstone degeneration or cobblestone degeneration

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57
Q

what results due to infarcts involving the choroid or choriocapillaris

A

Elschnig spots, siegrist streaks, and cobblestone degeneration

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58
Q

what supplies nutrition to the RPE and outer 1/3 of the retina

A

choroid

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59
Q

this structure removes heat that is generated by light absorption of the RPE and metabolic activity of the retina

A

Choroid

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60
Q

what is the deepest structure of the choroid; its the basement membrane of the system and is adjacent to sclera

A

suprachoroidal lamina

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61
Q

are the bv of the choroid fenestrated

A

Yes

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62
Q

T or F: The RPE absorbs the short wavelength of energy and the choroid pulls heat away from it

A

T

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63
Q

which layer of the choroid has the smaller caliber vessels

A

Sattlers

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64
Q

Which layer of the choroid has the larger caliber vessels

A

Hallers

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65
Q

what can cause a sudden loss of SVP

A

can be increased ICP, glaucoma, increased blood volume, CRVO, tumor,

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66
Q

T or F: It is possible for you to have an SVP with increased ICP

A

F: its impossible for you to have an SVP with an increased ICP

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67
Q

what determines SVP

A

ventricular heart rate

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68
Q

T or F: the inner 2/3 of the retina does not respond to the sympathetic or parasympathetic innervation

A

T ( the ophthalmic artery, as it runs through the ON it does respond to sympathetic and parasympathetic innervation, but once those retinal vessels and veins are located within retina ( past ON) they are only going to respond to metabolic changes

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69
Q

what influences innervation of the bv

A

oxygen content, carbon dioxide content, and hormone levels

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70
Q

what is a sign that the underlying health of the pt must be evaluated; usually its a manifestation of vascular disease

A

hemorrhages

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71
Q

which layer is most affected by artery disease

A

superficial capillary layer

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72
Q

which layer is most affected by vein disease

A

deep capillary bed

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73
Q

this hemorrhage is located between layers 9 and 10 ( ILM and NFL); this is more superficial retina ; assoc with the superficial capillary network or radial network of the circumpapillary zone

A

pre-retinal hemorrhage

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74
Q

where is the circumpapillary zone

A

two disc diameters away from the ON

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75
Q

where are pre retinal hemorrhages located

A

within the posterior pole ( can get a dramatic change in the VA)

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76
Q

which hemorrhage presents with a demarcated superior horizontal line ( aka keel shape or D shape)

A

pre retinal hemorrhage ( refer to slide 7 lec 2 for pic)

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77
Q

will the blood leak out during a pre retinal hemorrhage

A

not usually; the blood pockets like a blister and the layers gently separate away from each other; it doesn’t leak into deeper tissue; pts will resolve normally

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78
Q

what happens to the color of the blood in a pre retinal hemorrhage once it begins to heal

A

as the blood becomes deoxygenated, the blood becomes yellow, then white, and then the blood reabsorbs completely

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79
Q

what are the main causes of pre retinal hemorrhages

A

Valsalva maneuver, idiopathic, HTN, embolization, anemia, leukemia, PVD, and diabetes are common causes

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80
Q

which hemorrhages mainly occur in children and has to do with shaken baby syndrome

A

subdural hemorrhages

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81
Q

which hemorrhage occurs in adults and has to do with leukemia

A

subarachnoid hemorrhages

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82
Q

these type of hemorrhages are localized within the NFL; assoc with the superficial capillary network or radial network of the circumpapillary zone

A

superficial or flame shaped hemorrhages ( see slide 8 , lec 2 for pic)

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83
Q

how do you get the” flamed shaped appearance on flame shaped hemorrhages?

A

bc the nerve fibers are going to be very tightly packed together; blood can get in between these fibers, and that’s why you get the flamed appearance

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84
Q

these hemorrhages are typically assoc with retinal ischemia ; usually resolve in a few weeks ; do not leak into deeper retinal tissue but can spread t.o NFL

A

flame shaped hemorrhages

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85
Q

this hemorrhage represents an area of localized retinal hypoxia and artery based disease

A

flame shaped or superficial hemorrhage

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86
Q

what is a circular shaped hemorrhage with a white center that is superficial in nature

A

roth spot ( see slide 10, lec 2 for pic)

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87
Q

what are some potential presentations of the roth spot

A

white spot could be a collection of wbc surrounded by a hemorrhage assoc with inflammatory disease, may be assoc with bacterial endocarditis, or a serious cardiac issue

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88
Q

what are some common causes of flame shaped hemorrhages

A

caused by something in the eye or something systemic, low tension glaucoma ( will have a drane hemorrhage located at the ON with a flame shaped appearance), BRVO/CRVO , oral contraceptives, and smoking

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89
Q

these are dot blot or deep retinal hemorrhages; located in the inner nuclear layer, outer plexiform layer, and may extend to the outer nuclear layer ; assoc with the deep capillary network

A

intra retinal hemorrhages ( slide 13, lec 2 for pic)

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90
Q

these hemorrhages are more assoc with venous diseases ( ie Diabetes),

A

intra retinal / dot blot

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91
Q

what is the diff between a dot blot hemorrhage and a microaneurysm

A

microaneurysms are a change in the capillary networks and a dot blot hemorrhage is the result of the development of microaneurysms

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92
Q

what happens with age that can cause dot blot hemorrhages

A

as we age, the capillary networks, endothelial cells, and pericytes break down, which can cause dot blot hemorrhages in the retina ( would cause a bilateral presentation; if its unilateral, that is suggestive of internal carotid stenosis )

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93
Q

these hemorrhages can stretch from the inner plexiform layer to the outer nuclear layer

A

intra retinal / dot blot

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94
Q

will you have any acuity loss, scotoma, or change in VF with dot blot

A

N: unless it leaks into the fovea

95
Q

whats the prognosis of intra retinal hemes

A

normally resolve over time,

96
Q

what are the common causes of intra retinal / dot blot hemes

A

diabetes is the most common , HTN ( if serious enough), carotid blockage , blood disorders, high cholesterol, fiber levels out of wack , age

97
Q

refer to slide 16, lec 2 for a great review slide

A

slide 16, lec 2

98
Q

this heme is located between RPE and photoreceptors or between RPE and Bruchs; results from bleeding of a choroidal neovascular membrane ; located in the outer 1/3 or deep retina ; tends to be lobulated

A

subretinal heme ( slide 17, lec 2)

99
Q

T or F: pre retinal hemes, flame shapes hemes, and dot blot hemes are all located in the inner 2/3 of the retina

A

T

100
Q

what are the main causes of sub retinal hemes

A

CNV or trauma

101
Q

where do sub retinal hemes tend to be located

A

in the posterior pole, mid periphery and equator

102
Q

how does the color of sub retinal hemes change

A

when its fresh expect it to have a bright red color, as heme resolves it turns from red to yellow to white, but the white reps scar tissue that has developed as a result of the heme

103
Q

what is the color of the sub retinal heme if between RPE and Bruchs

A

Green /grey color : bc RPE filters out red light , causing it to look grey/green

104
Q

what happens visually if heme between PR and RPE layer

A

you expect the blood to resolve over time and the retina will come back together, and the visual outcome tends to be positive

105
Q

what happens If heme between RPE and Bruchs

A

you expect more scarring and a worse visual outcome

106
Q

which can eventually develop with sub retinal hemorrhages which can be devastating to visual outcome

A

scar tissue

107
Q

what are the common causes of sub retinal hemes

A

trauma and ARMD, coats disease, sickle cell anemia, diabetes, and ROP

108
Q

this heme is located between the detached vitreous hyaloid membrane and internal limiting membrane ; occurs from a break in the ILM ; assoc with retinal breaks or neovascularization

A

vitreous hemorrhage ( see slide 20, lec 2 )

109
Q

this type of vitroeus heme is when the pt has had a retina vitreous detachment - the hyaloid membrane has pulled away from the ILM - there will be blood in that pocket and it will be located in one area

A

retro vitreal heme

110
Q

this type of vitreous heme is not a PVD- and there is bleeding directly into the vitreous ( tomato soup appearance)

A

complete vitreal hemorrhage

111
Q

these hemes are not flayed, not lobulated, not boat shaped, but has a funky pattern

A

vitreous heme ( pt can have floaters)

112
Q

potential tx of vitreous heme

A

anti vegf medication or vitrectomy

113
Q

most common cause of vitreous heme

A

diabetes

114
Q

these are caused by an infarct in the inner capillary network; located within the NFL and GCL ; artery based disease and ischemia of the NFL

A

cotton wool spots

115
Q

what does it mean if you see a cotton wool spot

A

means there may be some hypoxia going on - there may be compromise in the epithelium of the capillary network which damages the NFL

116
Q

T or F: the cotton wool spot reflects and appreciates the contour of the NFL

A

T

117
Q

these objects blur retinal vessels in acute stages with “fuzzy” borders ; immediate precursor to neovascularization; resolve over time ; can find them mainly in posterior pole

A

cotton wool spots

118
Q

what’s the outcome of cotton wool spots

A

no compromise to the retina if there is a short duration of the infarct ; no vision loss bc it doesn’t affect the FAZ ( unless its large),

119
Q

what is the number one cause of cotton wool spots

A

HTN is the main cause; other common causes are diabetes, medications , etc

120
Q

these are located in the outer plexiform layer ; can extend from the outer nuclear layer to the internal limiting membrane ; located in henles layer when involving the macula; assoc with the outer capillary network and venous based disease

A

retinal exudate

121
Q

where can exudates occur

A

in posterior pole, equator, or retinal periphery

122
Q

T or F: If exudate at equator think something else going on like coats disease ; if in retinal periphery think retinal tumor

A

T

123
Q

T or F: exudative changes are assoc with the development of microaneurysms

A

T ( as a microaneurysm leaks, the whole area becomes edematous and the exudative material is going to work its way to the edge of the edematous retina and normal retina

124
Q

what is ALWAYS assoc with retinal edema

A

exudate ( see slide 30, lec 2 for examples)

125
Q

what are the tx options for retinal exudate

A

anti VEGF medication, monitoring, treating underlying disease

126
Q

clumped exudate assoc with what systemic illness

A

Coats Disease

127
Q

random exudative spots more assic with what

A

diabetes

128
Q

in which retinal layer will we expect to see exudative changes in acute disease

A

outer plexiform layer

129
Q

in which retinal layers will we expect to see exudative changes in long term disease

A

extend all the way from the outer nuclear layer to the ILM

130
Q

with circinate patterns of exudate what vessel anomaly do you expect to see

A

microaneurysms

131
Q

what is the most common cause of retinal exudate

A

diabetes

132
Q

can exudates resolve on their own

A

Y: if systemic diseases are controlled bu ti y may not , it may be there forever

133
Q

this is located between and within the inner nuclear layer and outer nuclear plexiform layer, but can extend from the ILM to the RPE which also involves the PR; usually assoc with the outer capillary network

A

retinal and macular edema

134
Q

which networks is diffuse edema assoc with

A

inner and outer capillary networks

135
Q

T or F: cotton wool spots should not be in the FAZ

A

T

136
Q

whats the diff in appearance between local and diffuse edema

A

local edema is well defined and diffuse edema is poorly defined bc landmarks are difficult to bserve - retinal “thickening”

137
Q

how do we treat pre retinal heme

A

monitor ; if pt cant handle scotoma or visual disturbance we may refer to retina surgeon which can do a hyloidotomy - but that is aggressive

138
Q

what is the tx option for flame shaped and cotton wool spots

A

no really effective tx except to figure out the systemic cause and take care of those issues , so just monitor

139
Q

what is the tx option for dot blot and exudates

A

these both involve the deep retina and the deep capillary network ; if they don’t havge diabetes do more tests

140
Q

what is the tx option for sub retinal hemes

A

secondary care like Anti VEGF tx

141
Q

what is the tx option for vitreous heme

A

vitrectomy or anti vegf injection

142
Q

what is the tx option for retinal edema

A

laser photocoagulation, anti vegf injection

143
Q

this is the starting point when ordering blood work

A

complete blood count with differential

144
Q

what does the CBC differential mean

A

that you are going to be breaking down red blood components and wbc components

145
Q

whats the CBC count for males and females for RBCs

A

male = 106

female =106

146
Q

whats the CBC count for WBC

A

4500-11000

147
Q

whats the platelet count for CBC

A

150,000-400,000

148
Q

this term is the volume of packed rbc as a % per 100 mL of blood ( % of rbc to blood volume )

A

Hematocrit

149
Q

Whats the hematocrit for males

A

39-49$%

150
Q

whats the hematocrit for females

A

33-43%

151
Q

this is the total Hb in whole blood

A

Hb

152
Q

whats the Hb level in males

A

13.6-17.2

153
Q

whats the Hb level in females

A

12.0-15.0

154
Q

this is the average volume of RBCs; tells you the tupe of of edema; 76-100 fl

A

mean cell volume

155
Q

this is the average concentration of Hb per 100 mL of packed RBCs; 33-37 g/ dL

A

mean cell Hb concentration

156
Q

this is the average mass of weight of Hb per individual RBC; 27-33 pg

A

mean cell Hb

157
Q

whats the CBC of neutrophils

A

1500-7800

158
Q

whats the CBC of eosinophils

A

15-500

159
Q

whats the CBC of basophils

A

0-200

160
Q

whats the CBC of lymphocytes

A

850-3900

161
Q

whats the CBC of monocytes

A

200-950

162
Q

whats the normal BP for an adult

A

16-20 respirations a min

163
Q

whats a normal pulse

A

60-100 beats/ min

164
Q

these are 50-100 microns in size and easily observable with IVFA; assoc with hypoxia of the deep capillary network

A

microanuerysms ( these autoflouresce in IVFA called starry night)

165
Q

this anomaly involves microscopic ballooning of the capillary ; may appear as focal or isolated, or as a cluster like “grapes” on a vine ; proliferation of capillary endothelium as a result of hypoxia

A

microaneurysms

166
Q

what maintains the blood retinal barrier in microaneurysms

A

the endothelial cells ; these are non fenestrated so they shouldn’t leak unless damaged

167
Q

what is responsible for the Autoregulation through the capillaries

A

perictyes

168
Q

in microaneurysms, what is a sign of active leakage

A

dot blot hemorrhages and exudate; there will always be edema assoc with it

169
Q

whats the predicted visual outcome for microaneurysms

A

if it leaks into the foveal zone then we could have acuity probs

170
Q

tx option for microaneurysm

A

photocoagulation guided by fluorescein angiography, anti vegf

171
Q

in this aneurysm multiple layers of the retina may be involved: intra retinal, sub retinal, pre retinal, and vitreous; reps isolated ballooning of a major bcv - focal or local bv damage

A

macroaneurysms

172
Q

these aneurysms are assoc with arteries and arterioles ; tend to be more superficial; tend to be assoc. with circinate exudate

A

macroaneurysms

173
Q

these aneurysms are assoc with atherosclerosis , embolization, or HTN

A

macroaneurysms

174
Q

what three things can happen with a macroaneurysm

A

hemorrhaging, edema, and exudate ( refer to slide 10, lec 3 for a great slide ref )

175
Q

whats the tx option for macroaneurysms

A

it could involute and scar, resolving on its own, but you MUST have them to go to the PCP to make sure they are okay ; see these pts back in 3 mos and monitor ; if enough scarring around the retina , it could cause a scotoma. It VA is threatened they may need surgery

176
Q

which vessel networks do micro and macro aneurysms tend to involve

A

microaneurysms involve the deep capillary network ; macroaneurysms involve the arteries or arterioles

177
Q

this is unilateral or bilateral with dilated/ tortuous retinal bv or capillaries near the FAZ; developmental anomaly with assoc aneurysms, edema, and exudate ; loose association with systemic disease

A

parafoveal telangiectasia ( affects M more than F)

178
Q

this type of parafoveal telangiectasia tends to be unilateral and congenital in nature; affects males in 40-50 YO

A

1A unilateral congenital ( ref slide 12, lect 3)

179
Q

this type of parafoveal telangiectasia is called “focal” bc there is one microaneurysm located around the macula ; they don’t leak; confined to small area; these pts tend to do well; in 5th decade of life ; mainly affects males

A

1B unilateral idiopathic focal

180
Q

this type of parafoveal telangiectasia is normally temporal to the macula; with reduced VA; usually some foveal changes and the possibility of CMV development, meaning RPE and Bruchs membrane may be involved

A

2A bilateral idiopathic acquired

181
Q

this type of parafoveal telangiectasia is same as 2A but no CNV or RPE changes, therefore the VA tends to be a little bit better; affects younger people

A

2B- bilateral familial occult

182
Q

this type of parafoveal telangiectasia has to do with some neurological problems ( leukemia, multiple myeloma, polycythemia vera) ; may have significant VA loss

A

occlusive telangiectasia

183
Q

what are the two subtypes of occlusive telangiectasia

A

3A idiopathic occlusive and 3BB idiopathic occlusive

184
Q

these are bv that develop within the framework of the existing vessel network

A

collateral bv

185
Q

these types of collaterals are congenital in nature- when you have the artery-vein

A

AV shunt

186
Q

are collateral vessels beneficial

A

yes: unlike neovasvularization

187
Q

where are the collateral bv located

A

on or within the superficial retina, or on the surface of the ON

188
Q

do collateral vessels leak

A

NO

189
Q

this type of shunt develops around the ON

A

optociliary shunt ( can occur bc something is pushing on the ON and central retinal vein, causing pressure , OR if a pt had a CRVO or BRVO )

190
Q

prognosis of collateral bv

A

can resolve over time if blood flow is reestablished

191
Q

this is a variation of shunt/collateral damage , but only found in diabetic pts; AV connections that by pass capillary networks

A

Inta retinal microvascular anomalies

192
Q

whats the diff between IRMA and collateral bv

A

IRMA develops over ischemic retinal tissue ; collateral vessels develop over healthy retina

193
Q

when the retina hyperflouresces upon FA , what does that mean

A

the bv are leaky

194
Q

this is new bv growth in response to hypoxia secondary to capillary non perfustion

A

neovascularization

195
Q

what are the 3 types of neovascularization

A

NVI: neovascularization of the iris
NVD: neovascularization of the disc and nerve
NVE: neovascularization not involving disc or iris, another pt of retina

196
Q

describe the vessels involved with neovascularization

A

they are weak, leaky, fenestrated, and assoc with fibrosis

197
Q

which type of neovasc. is most likely to cause a vitreal heme

A

NVD

198
Q

where can you find neovasc?

A

junction between poorly perfused tissue and well perfused tissue and it occurs at that border

199
Q

T o F: IRMA can grow over the ischemic tissue, neovasc. cannot! It needs well perfused tissue

A

T

200
Q

what is the gold standard for ID’ing neovasc.

A

IVFA

201
Q

whats the most common cause of neovas.

A

diabetes and HTN

202
Q

whats the current tx option for neovasc

A

anti VEGF or PRP laser photocoagulation

203
Q

what does PRP do ?

A

destroys healthy retina in hopes to reduce the oxygen demand of the retina so there will be no new bv growth

204
Q

this is associ, with venous stasis , retinal hypoxia, or localized vascular occlusion; vessels take on a loopy appearance

A

vessel tortuosity

205
Q

T or F: nonisolated vessel toruosity is concerning

A

F: Isolated vessel tortuosity is concerning

206
Q

this type of tortuosity involves extreme changes in all quadrants, the same degree of changes in both eyes, and involves both vein and artery changes

A

congenital tortuosity

207
Q

is vessel tortuosity in one quadrant congenital or acquired

A

acquired

208
Q

main causes of vessel tortuosity

A

BRVO, CRVO, and hemi retinal occlusion, diabetic retinopathy, ROP

209
Q

this is caused by proliferation of retinal glial cells through the ILM

A

preretinal or epimacular membrane ( can be unilateral or bilateral)

210
Q

type of preretinal membrane: this is a change in the appearance of the internal limiting membrane that can cause tortuosity of the retinal bv

A

cellophane maculopathy ( pt may not have reduced VA but may have metamorphopsia )

211
Q

type of pre-retinal memrbane this is a diff degree of glial tissue that has entered into the ILM

A

macular pucker ( can cause reduced VAs and metamorphopsia)

212
Q

what is the idiopathic cause of pre retinal memrbane

A

elderly ; usually caused by a PVD; tends to be bilateral can results in cellophane maculopathy or macular pucker

213
Q

what is the secondary cause of pre retinal membrane

A

there is an insult or injury usually assoc with surgery ; tend to be unilateral

214
Q

tx options for preretinal membrane

A

if asymptomatic don’t do anything, if reduced VAs and metamorphopsia sx may be indicated like a vitrectomy and membrane peel

215
Q

what is the formula for total cholesterol

A

TC = HDL + LDL + VLDL

216
Q

VLDL= ?

A

triglyceride / 5

217
Q

what is the lipid profile ration

A

TC/ HDL

for males this should be 5.0 or less and for females it should be 4.4 or less

218
Q

what is the diff between congenital and acquired vessel sheathing

A

if congenital both arteries and veins are sheathed and it should be two dd away from ON, if only arteries or veins are sheathed then its acquired

219
Q

this type of sheathing is assoc with periphlebitis “ halo sheathing “; more peripheral in nature

A

acquired vein sheathing

220
Q

this type of sheathing is assoc with arteriosclerosis “copper or silver wire “ appearance

A

acquired arterial sheathing

221
Q

Tx option for sheathing

A

no tx currently available, can only monitor

222
Q

are all the venous sheathing causes inflammatory in nature

A

Yes

223
Q

what three things cause artery and venous sheathing simultaneously

A

papilledema, papillitis, and papillophlebitis

224
Q

this is when elevated triglyceride levels cause retinal bv to assume a salmon or creamy color; triglyceride levels range from 2500-20000

A

lipemia retinalis

225
Q

T or F: the appearance of vessel changes begins with peripheral vessels and slowly involve the vessels located in the posterior pole

A

T

226
Q

visual outcome of lipemia retinalis

A

may be asymptomatic; happens in 2-3rd decade of life ; if we did FA on these pts the fill time would be reduced

227
Q

these originate from carotid disease, heart valve vegetation, cardiac atheromas, or chronic IV drug abuse ; only involve arteries; strong association with CVD; will get atherosclerosis and local intima thickening

A

retinal emboli

228
Q

what are the 4 types of retinal emboli

A

cholesterol plaque ( Hollenhorst), calcium, platelet/ fibrin, talc

229
Q

these emboli originate from carotid artery atheromas, and appear as glistening yellow opacities; tend to be located in artery bifurcation areas ; over time they resolve

A

cholesterol emboli

230
Q

these emboli originate from eroding cardiac atheromas or cardiac valves, and appear as larger , gray to white opacities; located near the ON or 1 dd away , blood cant flow around this plaque and can cause a CRAO or BRAO

A

calcific emboli

231
Q

these emboli originate from the carotid arteries or cardiac valves and appear longer, dull white, and stretched; multiple pts of artery involved like it “skips” ; assoc with amarosis fugax

A

platelet/fibrin emboli

232
Q

these emboli tend to the shiny red or yellow and involve capillaries; assoc with cotton wool spots and usage of IV drugs

A

talc emboli

233
Q

what are some usual suspects for retinal emboli

A

HTN, diabetes, smoking, elevated LDL, homocysteinemia

234
Q

What are the magic numbers for lipid profile

A

TC

Posterior Seg Lecture (1 decks)

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