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Vascular 2 > M4: Cerebrovascular Pathophysiology > Flashcards

M4: Cerebrovascular Pathophysiology Flashcards

1
Q

risk factors for carotid disease that can be related to life style

A 
HTN
diabetes
smoking
obesity
dyslipidemia
physical inactivity
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2
Q

risk factors for carotid disease related to the heart and blood

A

homocystinaemia
cardiac disease
previous TIA or stroke

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3
Q

genetic and/or uncontrollable risk factors for carotid disease

A 
sex
age
hypercholesterolemia
genetic predisposition/fam Hx
patent foramen ovale
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4
Q

carotid disease is most common in which gender

A

male

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5
Q

what is hypercholesterolemia

A

genetic defect in the LDL receptors

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6
Q

3 parts to a physical exam to assess for carotid disease

A
  1. carotid auscultation for bruits - indicates if abnormal flow is present, caused by turbulent blood flow due to a stenosis, that creates a vibration in the surrounding tissue
  2. palpate for a thrill - thrill is a bruit that is felt
  3. bilateral BP - difference of > 20 mmHg b/w sides indicates possible disease/subclavian steal
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7
Q

what are the 2 types of circulation to the brain

A
  1. Hemispheric/anterior

2. vertebrobasilar/posterior

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8
Q

in general, what types of symptoms will a stenosis in the Hemispheric/anterior and vertebrobasilar/posterior circulations cause

A
  1. Hemispheric/anterior: lateralizing, symptoms on one side of the body
  2. vertebrobasilar/posterior: non-lateralizing, symptoms on both sides of the body
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9
Q

if an artery supplying anterior circulation to the brain was diseased, where would symptoms be experienced

what can be an exception to this rule and why

A

on the contralateral side of the diseased artery…
….since the body is often controlled by the cerebral hemisphere on the contralateral side

unilateral vision problems, due to the ophthalmic artery

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10
Q

which arteries supply the anterior circulation of the brain

A

ICAs

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11
Q

cerebral hemispheres are supplied by which circulatory system of the brain

A

anterior

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12
Q

general symptoms of disease effecting the hemispheric/anterior circulation (ICA)

A

hemiparesis/hemiplegia - weakness or loss of function to 1 limb or one side of the body

paresthesia - tingling, numb or burning sensation

aphasia/dysphasia - inability to speak or understand language

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13
Q

if a patient has aphasia/dysphasia, which side of anterior circulation is always effected

A

always the left

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14
Q

vision symptoms of disease effecting the hemispheric/anterior circulation (ICA)

A

amaurosis fugax (transient monocular blindness TMB) - black curtain coming over 1 eye vertically, if its a vascular cause

homonomous hemianopsia - blindness or visual defect in half the field of vision in both eyes

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15
Q

if amaurosis fugax is occurring due to a vascular cause, which eye will be affected

A

ipsilateral

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16
Q

why does homonomous hemianopsia occur

A

b/c the R brain has visual control for the L side of both eyes, and vice versa

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17
Q

rule for unilateral visual disturbances for anterior circulation

A

they are always an ipsilateral symptom (artery on same side affected)

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18
Q

can bilateral visual disturbances be due to either anterior or posterior disease

A

yes

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19
Q

general symptoms of disease effecting the vertebrobasilar/posterior circulation

A 
ataxia - lack of muscle coordination
drop attacks - sudden fall that is recovered from quickly
dysphagia - difficulty swallowing
motor/sensory disturbances
vertigo
subclavian steal syndrome
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20
Q

vision symptoms of disease effecting the vertebrobasilar/posterior circulation

A

diplopia - double vision

bilateral visual blurring

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21
Q

define a subclavian steal

A

reversal of a vertebral artery to collateralize the ipsilateral SCA

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22
Q

localized signs and symptoms of a subclavian steal

A

supraclavicular bruit
arm weakness
decreased arm pulse
arm BP discreptent by > 20 mmHg

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23
Q

is the patient usually asymptomatic w/ a subclavian steal

A

yes, so no treatment

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24
Q

non-localized signs and symptoms of a subclavian steal

A 
dizziness
syncope
dysarthria
headache
confusion
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25
Q

norm LDL/HDL cholesterol level

A

3:1

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26
Q

describe arteriosclerosis

directly related to which factor

A

hardening of arteries leading to degenerative changes

directly related to age

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27
Q

describe the degenerative changes of arteriosclerosis

A

loss of elasticity and thickeneing of intima over time, may lead to atherosclerosis

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28
Q

describe atherosclerosis

A

hardening of arteries along w/ the formation of plaque

plaque builds up in the artery wall and limits or stops blood flow by narrowing (stenosis) or occlusion

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29
Q

whats the most common arterial disease

A

atherosclerosis

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30
Q

what is considered a hemodynamically significant lesion

A

a stenosis or occlusion that reduces the diameter of an artery by 50% or >, leading to decreased BP or flow distal to the obstruction

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31
Q

4 stages of development of atherosclerosis

A

stage 1: early atherosclerosis and injury
stage 2: inflammatory response
stage 3: atheromatous thickening - plaque formation
stage 4: advanced atherosclerosis - late changes

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32
Q

describe stage 1 of atherosclerosis

A

injury to the endothelial that can be due to a variety of causes

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33
Q

what is vasculitis

A

swelling or a vein or artery wall

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34
Q

describe stage 2 of atherosclerosis

A

the injury to the endothelial lining leads to an inflammatory response which leads to fatty streaking.

there is endothelial thickening

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35
Q

what is fatty streaking

do we see it on US

A

collection of fat and monocytes inside the vessel wall

no

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36
Q

describe stage 3 of atherosclerosis

A

muscle cells become infiltrated w/ fat…

repair leads to the formation of scar tissue/fibrosis that leaves a fibrous cap over the soft fatty plaque

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37
Q

how does stage 3 of atherosclerosis appear on US

A

hypoechoic thickened wall and echogenic cap

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38
Q

does plaque for on or in the vessel wall

A

inside

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39
Q

describe stage 4 of atherosclerosis

A
  • hemorrhage and/or calcification leading to possible ulcerative plaque, emboli, and further narrowing
  • there can be hemorrhage from the vasa vasorum into the plaque which will lead to the breakdown of the fibrous cap and endothelium
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40
Q

why is ulcerative plaque concerning

A

its unstable and can embolize

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41
Q

is atherosclerosis reversible

A

no

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42
Q

after a vasa vasorum hemorrhage, can the artery repair itself

A

no

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43
Q

what determines plaque echogenicity

A

its composition - lipids, collagen, hemorrhage and/or calcifications

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44
Q

what causes plaque to be anechoic

A

lipids or hemorrhage

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45
Q

what causes plaque to be hypo

A

fibrofatty plaque

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46
Q

what causes plaque to be hyper

A

fibrous plaque

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47
Q

US appearance of intraplaque hemorrhage

A

hypo regions w/ thin fibrous cap… eggshell pattern

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48
Q

what should you include when describing plaque

A

location, echogenicity, echotexture, surface contour, composition (sometimes)

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49
Q

can we confirm plaque ulcerations on US

A

no

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50
Q

describe a thrombus

A

formation of blood clot over the plaque site which further restricts the lumen and contributes to ischemia or infarction

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51
Q

describe an emboli

A

thrombus that breaks off into the blood streak, can cause ischemia or infarction if it travels to an area too narrow for it to pass

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52
Q

if patients are asymptomatic but have disease, what is the most common indication for a duplex US

A

auscultation of a bruit

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53
Q

describe a TIA

A

brief neurological event that lasts 1-30 minute… cell death do not occur… due to a reduction of blood flow

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54
Q

how long to neuro deficits last w/ a TIA

A

< 24 hrs

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55
Q

what is RIND

A

resolving/reversing ischemic neurological deficits… a neurological event w/ symptoms lasting b/w 24 hrs - 3 wks w/ no permanent damage

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56
Q

what is a cerebrovascular accident (CVA/stroke)

A

loss of blood supply that results in some permanent brain damage including a loss of motor, sensory or cerebral function

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57
Q

how can CVAs be classified

A
  • acute
  • unstable evolution, symp come and go….
  • completed, no progression or resolution and stable
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58
Q

if AR is present, how will this effect flow in the CCAs

A

bilaterally, there will be a longer period of reversed flow

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59
Q

what are the NASCET trials

A

north american symptomatic carotid endarterectomy trial

-study that showed benefit of endarterectomy versus medical treatment in symp patients severe stenosis

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60
Q

what is ACAS

what did it show

A

asymptomatic carotid atherosclerosis study

showed that endarterectomy reduced stroke risk by 6% over 5 years in asymp patients w/ >60% diameter stenosis

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61
Q

how did NASCET and ACAS measure the diameter of a stenosis

A

measured the norm lumen distal to the stenosis, and the diameter at the stenosis

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62
Q

see diagram on pg 50

A

/

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63
Q

factor effecting stenosis velocity

A 
length and diameter
roughness/irregularity
flow rate
physiological factors (BP, CO, etc)
collateral circulation
norm vessel anatomy
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64
Q

what 2 factors that limit colour doppler assessment of carotid stenosis

A

vessel tortuosity and shadowing from calcific plaque

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65
Q

what other diagnostic imaging can US be correlated w/ for carotid stenosis

A

MRA (MR angio), CTA (CT angio)

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66
Q

which parameter is the most important for carotid stenosis

A

peak systolic velocity….. its important to search the lumen for the highest velocity

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67
Q

a significant stenosis will produce what type of sound on PW

A

high pitched hissing

68
Q

w/ carotid stenosis, when will EDV remain in the normal range…. when will it increase

A

norm if theres a diameter reduction of <50%

> 50% reduction will cause an increases in diastolic velocity…. >70% there will be a rapid rise in EDV

…. valuable for detecting high grade stenosis

69
Q

what is the systolic velocity ratio

what physiological factors can effect this ratio

A

ratio of the PSV in the ICA / PSV in the CCA

HTN, reduced CO

70
Q

when will the systolic velocity ratio be invalid

A

if theres stenosis in the CCA or the bulb

71
Q

describe trickle flow

A

occurs when a stenosis is so severe that the blood trickles through the residual lumen

72
Q

another term for trickle flow

A

pre-occlusive stenosis

73
Q

to confirm occlusion, or when it’s being considered, how must we alter the machines controls

A

set the controls for low flow…. low wall filter, low PRF, increase colour gains, power doppler, increase sample size

scan distal to the bulb w/ PW and colour if occlusion in the CCA

74
Q

describe a total occlusion

A

when no flow is detected by colour or spectral doppler w/ appropriate settings

75
Q

what can happen to arterial pulsations w/ total occlusion

A

they can be absent

76
Q

how may the vessel appear w/ total occlusion

A
  • isoechoic or slightly echogenic to the surrounding tissue, making it hard to see the walls
  • reduction of vessel size w/ longstanding occlusion
77
Q

when is the string sign seen

A

w/ nearly occluded vessels

78
Q

ratio of ICA to CCA occlusion

A

10 : 1

79
Q

what is internalization of the ECA

A

when the ECA has increased flow w/ a higher diastolic velocity than norm

80
Q

w/ total occlusion in the CCA, how would flow in the contralateral and ipsilateral CCA change

what sound will you hear on the ipsilateral CCA

A

contralateral: may have increased compensatory flow w/ increased velocities
ipsilateral: will show decreased PSV and an absent or reversed diastolic flow, will have a thump sound

81
Q

w/ ICA occlusion, what happens to diastolic flow in the CCA

a downstream occlusion of the ICA is indicated by what type of waveform

A

may be absent

staccato

82
Q

describe the waveform proximal to a significant stenosis

this type of waveform is often accompanied by what sound

A

staccato… increased pulsatility, decreased systolic velocity, little diastolic flow and reversal in early diastole

thump

83
Q

describe the waveform distal to a significant stenosis

A

post stenotic turbulence directly after the stenosis, flow retunrs to laminar 3 cm distal to stenosis

84
Q

where is max disturbance experienced distal to a stenosis

A

1 cm

85
Q

if a stenosis is obscured by calcific plaque, what may be the only clue to a severe stenosis

A

post stenotic turbulence

86
Q

what waveform is seen more distal to a significant stenosis

A

tardus parvus… slow to peak and lower PSV increased diastolic flow

87
Q

other terms for tardus parvus

A

pulsus tardus

pulsus parvus

88
Q

is there an abnorm velocity value for the CCA

A

no

89
Q

what might low or no EDV in the CCA indicate

A

distal CCA, bulb or prox ICA severe stenosis

90
Q

if theres a velocity difference of >/= 30 cm/s b/w the bilateral CCAs, what 3 things should be considered

A

prox CCA obstruction
the vessel is tortuous
compensatory flow due to contralateral occlusion/stenosis

91
Q

norm PSV and EDV for ICA

abnorm?

A

PSV: <125 cm/s
EDV: <40 cm/s

anything above these values indicated stenosis

92
Q

W/ severe ICA stenosis or occlusion, what can happen to the blood flow in the ECA

Why

A

It may have a low resistance waveform as the ECA would be acting as a collateral to supply the brain

93
Q

How can you tell the ECA from the ICA if both have a low resistance waveform due to ECA collateralization to supply the brain

A

Look for branches from the ECA

OR

Do a temporal tap (tapping the superficial temporal artery), and the spectral tracing will oscillate if you’re in the ECA

94
Q

If the CCA is occluded what often happens to the direction of flow in the ECA

A

It will reverse in order to supply blood to the ICA and profuse the brain

95
Q

Is a healthy patient, should waveforms be fairly symmetrical on both sides

If not?

A

Yes

if no apparent cause, use other modalities to determine cause

96
Q

3 basic routes for intracranial collateral circulation

A
  1. Large inter-arterial connections through the circle of willis
  2. Intracranial-extracranial anastomoses or Pre-willisian anastomoses
  3. Leptomeningeal
97
Q

Large inter-arterial connections through the circle of willis connect which vessels in the event of occlusion

A

Provide path b/w both carotids or b/w the basilar A and the R or L carotid

98
Q

Intracranial-extracranial anastomoses or Pre-willisian anastomoses connect which vessels in the event of occlusion

A

ECA to ICA (ophthalmic)
Or
ECA (occipital) to vertebral (Atlantic)

99
Q

Which Intracranial-extracranial anastomosis is the most common

A

ECA to ICA

100
Q

Leptomeningeal collaterals connect which vessels in the event of on occlusion

A

main cerebral arteries

101
Q

If the vertebrals are occluded what are the most common extracranial collaterals

A

The opposite vertebral which will become enlarged

Or flow is shunted to the thyrocervical and costocervical branches

(on exam)

102
Q

If the larger AO branches are occluded what are the most common extracranial collaterals

A

Intercostal and internal mammary arteries connecting to the subclavian

(On exam)

103
Q

When assessing the parameters for stenosis, why is it important to look at both the velocites and ratios

A

Velocites can be falsely elevated due to compensatory flow

104
Q

Would an endarterectomy ever be done on an fully occluded ICA

A

No

105
Q

When the ICA is occluded, how can the path of the vessel change

Where in the vessel are these changes usually seen

Is this more common in W or M

A

Can become tortuous or coiled and appear S or C shaped…. usually seen W/in first 2-3 cm of occlusion

W, 4x more common

106
Q

Causes of posterior circulation ischemia (vertebral basilar insufficiency)

Which is most common

A

Atherosclerosis

Emboli
Extrinsic compression
Subclavian steal
Heart dysfunction

107
Q

Most common site for stenosis in the vertebral A

2nd most common

A

Origin of vertebral A/proximal portion, up to C6 where the vertebrals enter the vertebrae

Intracranially, just past C1 before the vert form the basilar A

108
Q

Other DI to identify occlusion/stenosis in the vertebrals (since US for vert are limited)

A

Angiography

MRAngio

109
Q

Norm flow in vert A

A

Low resistance, laminar flow

110
Q

Why is US for vert stenosis limited

A

We don’t directly image the prox portion of the vert and we can’t see around the shadowing of the vertebrae

111
Q

Is there a ratio we use for the vert to indicate disease

A

No

112
Q

Can flow in the vert velocities vary from L to R?

Why or why not

A

Yes

One side is usually dominant, often the L side

113
Q

Most obvious finding in the vert for subclavian steal syndrome

A

Reversal of flow in the vert A to feed the arm

114
Q

How is a subclavian steal confirmed (3 ways)

A

Abnorm subclavian waveform
Reversed flow in vert
Or bilateral BP >/= 20 mmHg different (lower BP will be on the affected side)

115
Q

What kind of waveform in the vert indicates a subacute or pre-subclavian steal

A

Pendulum waveform/bunny ears where ONLY the systolic portion of the waveform with me reversed.

116
Q

Review triphasic/multiphasic, etc

A

Page 100 of notes

117
Q

Norm waveform of the Subc A

Is there a norm value for PSV

A

Triphasic or multiphasic, can be biphasic in older adult

No, but the velocity is usually higher than the carotids

118
Q

A hemodynalically significant stenosis of >50% is defined by which parameters

A

Focal velocity increas (at least double)
Post stenotic turbulence
Possible colour bruit

119
Q

What ratio can you use for assessing the subc A for disease

A

V2 PSV/V1 PSV

V2: PSV of stenosis
V1: PSV of prox norm segment

120
Q

Which 3 indirect signs of subc steal are important to identify when a proximal velocity of the vert are hard to obtain

A
  1. Compare the arterial waveforms at the same site on both arteries (for test)
  2. spectral waveform changes (for any vessel)
  3. increased velocities with lumen reduction and post stenotic turbulence
121
Q

If the prox vert A is occluded, what will the flow direction be in it’s collaterals

A

Reversed to feed the vert

122
Q

What is it called if a patient has neurological deficits or symptoms due to subclavian steal

A

subclavian steal syndrome/phenomenon

123
Q

Which artery other than the vert, may have reversed flow w/ a subclavian steal

A

Reversal of the basilar artery

124
Q

Medical treatment for carotid artery disease

A

Reduce risk factors
Tissue plasminogen activator (to treat ischemic stroke)
Anticoagulants

125
Q

Surgical treatment for carotid artery disease

A

Endarterectomy (most common)
Thrombectomy
Focal repairs
Bypass

126
Q

Endovascular treatment for carotid artery disease

A

Carotid angioplasty
Carotid stent

These are often done w/ an endarterectomy

127
Q

When is the first US done after a endarterectomy

A

W/in 30 days

128
Q

Complications from an endarterectomy

A 
-Re-stenosis/occlusion:
myointimal/neointimal hyperplasia (w/in 2-3 years)
primary atherosclerosis (after 3 years)
  • residual plaque
  • tissue flaps
  • narrowing
  • hematoma
  • endovascular leak
  • pseudoaneurysm
  • stent displacement/poor placement/kinking
129
Q

Describe a myointimal/neointimal hyperplasia

A

Tissue overgrowth, often a rxn to a stent

130
Q

Is the normal intimal seen on US after a endarterectomy

How will the sutures appear

A

No

Bright reflectors

131
Q

Will you see some normal wall thickening post endarterectomy

Is this important

A

Yes

No. Unless associated w/ lumen reduction and increased PSV

132
Q

Are PSV unpredictable w/ a carotid stent

How can we monitor them

A

Yes

Compare PSV from exam-exam in the same location

133
Q

Describe a carotid artery dissection

A

A tear in the intimal lining, blood enters the media of the vessel and creates a false lumen

134
Q

Causes of carotid artery dissection

A

Trauma
Medical complications
Spontaneous

135
Q

Can a false lumen be blind ended or reconnect distal to the origin

A

Yes

136
Q

How can a carotid artery dissection obstruction

A

Expansion of the false lumen which can narrow the true lumen

137
Q

Where in the ICA does a dissection usually occur

risk factors for spontaneous carotid dissection

A

In the first 2-4 cm of the ICD

HTN, fibromuscular dysplasia, marfans, ehlers-danlos syndrome, cystic medial necrosis

138
Q

A CCA dissection can be the extension of what other type of dissection

A

AO, usually will effect the left CCA

139
Q

US appearance of carotid dissection

A

Intimal flutter
Duplicated lumen
Narrowed true lumen, false may be thrombosed

140
Q

How is carotid dissection treated

A

Anticoagulation therapy

141
Q

Describe fibromuscular dysplasia

What’s it characteristic appearance

A

Non-atherosclerotic disease characterized by tandem stenosis caused by vessel wall abnormalities
-affects medium and large arteries

String of beads/pearls

142
Q

Which arteries do fibromuscular dysplasia most commonly effect

A

Renal arteries
ICA

Can coexist in these locations

143
Q

Fibromuscular dysplasia is most predominant in which gender

Where in the ICA does it most commonly occur

A

Women

2-6 cm of the Mid, extracranial segment of the ICA
For test

144
Q

Symptoms of fibromuscular dysplasia

A

Incidental or TIA

145
Q

Describe a carotid body tumor (CBT)

Where are they located

A

Sm cluster of highly vascular chemoreceptor cells that are part of the autonomic nervous sys

at the bulb

146
Q

What kind of tumor is a CBT

What tissue does it arise from

A

Paraganglioma

Arises from the ganglion of the glossopharyngeal nerve

147
Q

Are CBTs usually benign

More common in M or W

A

Yes

women, 3-5 X

148
Q

Where does a CBT get its blood supply

A

ECA usually, if it gets larger, ICA may supply it as well, or the VA or thyrocervical trunk

149
Q

US appearance of CBT

A

Ovoid

Widening or bulging of the bifurcation, highly vascular

150
Q

Symptoms of CBT

Complications of CBT

A

palpable mass, headache, neck pain, hoarseness

Compression of the laryngeal nerve or invasion of surrounding tissue

151
Q

2 Treatments for CBT

A

Surgical removal

Embolization with angiography

152
Q

Are aneurysms and pseudo aneurysms common or rare in the carotid sys

A

Rare

153
Q

Describe a pseudoaneurysm

A

Weakening/tear in the artery wall, creating a collection of blood b/w the media and Adventitia

154
Q

What’s the most common cause of aneurysms in the carotid sys

Which location is the most common

A

Atherosclerosis

CCA

155
Q

Treatment of extra cranial aneurysms

A

Surgical resection

Endovascular therapy

156
Q

Describe vasculitis

A

Inflammation of the wall of an artery/vein leading to wall damage

157
Q

Causes and treatment for vasculitis

A

Causes: genetics, infectious, toxins

Treatment: steroids

158
Q

4 diseases that cause vasculitis

A

Takayasu’s arteritis
Temporal arteritis
Polyarteritis
Buergers disease

159
Q

What types of injuries can radiation cause

A

Injury to the vasa vasorum, endothelial cells and necrosis of the vessel wall

160
Q

What are normal duplex and doppler findings after a carotid endarterectomy.

A
  • smooth velocity increase into the stent
  • Slight narrowing of the lumen at the ends of the stent with no significant velocity increase
  • Laminar or only slightly disturbed flow
161
Q

Whats the definitive diagnostic test to identify obstructive lesson in the carotid system

A

angiography

162
Q

what’s needed to diagnose a subclavian steal

A

reversal in a vert. A combined with a significant difference in arm pressures

163
Q

which ares need to be sampled post endarterectomy

A 
prox native artery
prox stent attachment site
prox, mid, distal within the stent
dist stent attachment site
native artery distal to the stent
164
Q

most common complication post endarterectomy within the first 2-3 years

what about 3 + years

A

restenosis by neointimal hyperplasia

complications from atherosclerosis

165
Q

US appearance of FMD

A

tandem stenosis and dilations, with moderate-severe increase is PDV with extensive turbulence

166
Q

how can arterial flow be altered in collaterals with occlusion

A

increased flow to compensate
increased velocity to compensate
flow reversal
decreased or changes in pulsatility

167
Q

What PSV in the ECA indicates 50% or greater stenosis?

A

Greater than 150-200 cm/s

Vascular 2 (6 decks)

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