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
norm LDL/HDL cholesterol level
3:1
26
describe arteriosclerosis directly related to which factor
hardening of arteries leading to degenerative changes directly related to age
27
describe the degenerative changes of arteriosclerosis
loss of elasticity and thickeneing of intima over time, may lead to atherosclerosis
28
describe atherosclerosis
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
29
whats the most common arterial disease
atherosclerosis
30
what is considered a hemodynamically significant lesion
a stenosis or occlusion that reduces the diameter of an artery by 50% or >, leading to decreased BP or flow distal to the obstruction
31
4 stages of development of atherosclerosis
stage 1: early atherosclerosis and injury stage 2: inflammatory response stage 3: atheromatous thickening - plaque formation stage 4: advanced atherosclerosis - late changes
32
describe stage 1 of atherosclerosis
injury to the endothelial that can be due to a variety of causes
33
what is vasculitis
swelling or a vein or artery wall
34
describe stage 2 of atherosclerosis
the injury to the endothelial lining leads to an inflammatory response which leads to fatty streaking. there is endothelial thickening
35
what is fatty streaking do we see it on US
collection of fat and monocytes inside the vessel wall no
36
describe stage 3 of atherosclerosis
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
37
how does stage 3 of atherosclerosis appear on US
hypoechoic thickened wall and echogenic cap
38
does plaque for on or in the vessel wall
inside
39
describe stage 4 of atherosclerosis
- 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
40
why is ulcerative plaque concerning
its unstable and can embolize
41
is atherosclerosis reversible
no
42
after a vasa vasorum hemorrhage, can the artery repair itself
no
43
what determines plaque echogenicity
its composition - lipids, collagen, hemorrhage and/or calcifications
44
what causes plaque to be anechoic
lipids or hemorrhage
45
what causes plaque to be hypo
fibrofatty plaque
46
what causes plaque to be hyper
fibrous plaque
47
US appearance of intraplaque hemorrhage
hypo regions w/ thin fibrous cap... eggshell pattern
48
what should you include when describing plaque
location, echogenicity, echotexture, surface contour, composition (sometimes)
49
can we confirm plaque ulcerations on US
no
50
describe a thrombus
formation of blood clot over the plaque site which further restricts the lumen and contributes to ischemia or infarction
51
describe an emboli
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
52
if patients are asymptomatic but have disease, what is the most common indication for a duplex US
auscultation of a bruit
53
describe a TIA
brief neurological event that lasts 1-30 minute... cell death do not occur... due to a reduction of blood flow
54
how long to neuro deficits last w/ a TIA
< 24 hrs
55
what is RIND
resolving/reversing ischemic neurological deficits... a neurological event w/ symptoms lasting b/w 24 hrs - 3 wks w/ no permanent damage
56
what is a cerebrovascular accident (CVA/stroke)
loss of blood supply that results in some permanent brain damage including a loss of motor, sensory or cerebral function
57
how can CVAs be classified
- acute - unstable evolution, symp come and go.... - completed, no progression or resolution and stable
58
if AR is present, how will this effect flow in the CCAs
bilaterally, there will be a longer period of reversed flow
59
what are the NASCET trials
north american symptomatic carotid endarterectomy trial -study that showed benefit of endarterectomy versus medical treatment in symp patients severe stenosis
60
what is ACAS what did it show
asymptomatic carotid atherosclerosis study showed that endarterectomy reduced stroke risk by 6% over 5 years in asymp patients w/ >60% diameter stenosis
61
how did NASCET and ACAS measure the diameter of a stenosis
measured the norm lumen distal to the stenosis, and the diameter at the stenosis
62
see diagram on pg 50
/
63
factor effecting stenosis velocity
``` length and diameter roughness/irregularity flow rate physiological factors (BP, CO, etc) collateral circulation norm vessel anatomy ```
64
what 2 factors that limit colour doppler assessment of carotid stenosis
vessel tortuosity and shadowing from calcific plaque
65
what other diagnostic imaging can US be correlated w/ for carotid stenosis
MRA (MR angio), CTA (CT angio)
66
which parameter is the most important for carotid stenosis
peak systolic velocity..... its important to search the lumen for the highest velocity
67
a significant stenosis will produce what type of sound on PW
high pitched hissing
68
w/ carotid stenosis, when will EDV remain in the normal range.... when will it increase
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
what is the systolic velocity ratio what physiological factors can effect this ratio
ratio of the PSV in the ICA / PSV in the CCA HTN, reduced CO
70
when will the systolic velocity ratio be invalid
if theres stenosis in the CCA or the bulb
71
describe trickle flow
occurs when a stenosis is so severe that the blood trickles through the residual lumen
72
another term for trickle flow
pre-occlusive stenosis
73
to confirm occlusion, or when it's being considered, how must we alter the machines controls
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
describe a total occlusion
when no flow is detected by colour or spectral doppler w/ appropriate settings
75
what can happen to arterial pulsations w/ total occlusion
they can be absent
76
how may the vessel appear w/ total occlusion
- isoechoic or slightly echogenic to the surrounding tissue, making it hard to see the walls - reduction of vessel size w/ longstanding occlusion
77
when is the string sign seen
w/ nearly occluded vessels
78
ratio of ICA to CCA occlusion
10 : 1
79
what is internalization of the ECA
when the ECA has increased flow w/ a higher diastolic velocity than norm
80
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
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
w/ ICA occlusion, what happens to diastolic flow in the CCA a downstream occlusion of the ICA is indicated by what type of waveform
may be absent staccato
82
describe the waveform proximal to a significant stenosis this type of waveform is often accompanied by what sound
staccato... increased pulsatility, decreased systolic velocity, little diastolic flow and reversal in early diastole thump
83
describe the waveform distal to a significant stenosis
post stenotic turbulence directly after the stenosis, flow retunrs to laminar 3 cm distal to stenosis
84
where is max disturbance experienced distal to a stenosis
1 cm
85
if a stenosis is obscured by calcific plaque, what may be the only clue to a severe stenosis
post stenotic turbulence
86
what waveform is seen more distal to a significant stenosis
tardus parvus... slow to peak and lower PSV increased diastolic flow
87
other terms for tardus parvus
pulsus tardus | pulsus parvus
88
is there an abnorm velocity value for the CCA
no
89
what might low or no EDV in the CCA indicate
distal CCA, bulb or prox ICA severe stenosis
90
if theres a velocity difference of >/= 30 cm/s b/w the bilateral CCAs, what 3 things should be considered
prox CCA obstruction the vessel is tortuous compensatory flow due to contralateral occlusion/stenosis
91
norm PSV and EDV for ICA abnorm?
PSV: <125 cm/s EDV: <40 cm/s anything above these values indicated stenosis
92
W/ severe ICA stenosis or occlusion, what can happen to the blood flow in the ECA Why
It may have a low resistance waveform as the ECA would be acting as a collateral to supply the brain
93
How can you tell the ECA from the ICA if both have a low resistance waveform due to ECA collateralization to supply the brain
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
If the CCA is occluded what often happens to the direction of flow in the ECA
It will reverse in order to supply blood to the ICA and profuse the brain
95
Is a healthy patient, should waveforms be fairly symmetrical on both sides If not?
Yes if no apparent cause, use other modalities to determine cause
96
3 basic routes for intracranial collateral circulation
1. Large inter-arterial connections through the circle of willis 2. Intracranial-extracranial anastomoses or Pre-willisian anastomoses 3. Leptomeningeal
97
Large inter-arterial connections through the circle of willis connect which vessels in the event of occlusion
Provide path b/w both carotids or b/w the basilar A and the R or L carotid
98
Intracranial-extracranial anastomoses or Pre-willisian anastomoses connect which vessels in the event of occlusion
ECA to ICA (ophthalmic) Or ECA (occipital) to vertebral (Atlantic)
99
Which Intracranial-extracranial anastomosis is the most common
ECA to ICA
100
Leptomeningeal collaterals connect which vessels in the event of on occlusion
main cerebral arteries
101
If the vertebrals are occluded what are the most common extracranial collaterals
The opposite vertebral which will become enlarged Or flow is shunted to the thyrocervical and costocervical branches (on exam)
102
If the larger AO branches are occluded what are the most common extracranial collaterals
Intercostal and internal mammary arteries connecting to the subclavian (On exam)
103
When assessing the parameters for stenosis, why is it important to look at both the velocites and ratios
Velocites can be falsely elevated due to compensatory flow
104
Would an endarterectomy ever be done on an fully occluded ICA
No
105
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
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
Causes of posterior circulation ischemia (vertebral basilar insufficiency) Which is most common
Atherosclerosis Emboli Extrinsic compression Subclavian steal Heart dysfunction
107
Most common site for stenosis in the vertebral A 2nd most common
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
Other DI to identify occlusion/stenosis in the vertebrals (since US for vert are limited)
Angiography | MRAngio
109
Norm flow in vert A
Low resistance, laminar flow
110
Why is US for vert stenosis limited
We don’t directly image the prox portion of the vert and we can’t see around the shadowing of the vertebrae
111
Is there a ratio we use for the vert to indicate disease
No
112
Can flow in the vert velocities vary from L to R? Why or why not
Yes One side is usually dominant, often the L side
113
Most obvious finding in the vert for subclavian steal syndrome
Reversal of flow in the vert A to feed the arm
114
How is a subclavian steal confirmed (3 ways)
Abnorm subclavian waveform Reversed flow in vert Or bilateral BP >/= 20 mmHg different (lower BP will be on the affected side)
115
What kind of waveform in the vert indicates a subacute or pre-subclavian steal
Pendulum waveform/bunny ears where ONLY the systolic portion of the waveform with me reversed.
116
Review triphasic/multiphasic, etc
Page 100 of notes
117
Norm waveform of the Subc A Is there a norm value for PSV
Triphasic or multiphasic, can be biphasic in older adult No, but the velocity is usually higher than the carotids
118
A hemodynalically significant stenosis of >50% is defined by which parameters
Focal velocity increas (at least double) Post stenotic turbulence Possible colour bruit
119
What ratio can you use for assessing the subc A for disease
V2 PSV/V1 PSV V2: PSV of stenosis V1: PSV of prox norm segment
120
Which 3 indirect signs of subc steal are important to identify when a proximal velocity of the vert are hard to obtain
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
If the prox vert A is occluded, what will the flow direction be in it’s collaterals
Reversed to feed the vert
122
What is it called if a patient has neurological deficits or symptoms due to subclavian steal
subclavian steal syndrome/phenomenon
123
Which artery other than the vert, may have reversed flow w/ a subclavian steal
Reversal of the basilar artery
124
Medical treatment for carotid artery disease
Reduce risk factors Tissue plasminogen activator (to treat ischemic stroke) Anticoagulants
125
Surgical treatment for carotid artery disease
Endarterectomy (most common) Thrombectomy Focal repairs Bypass
126
Endovascular treatment for carotid artery disease
Carotid angioplasty Carotid stent These are often done w/ an endarterectomy
127
When is the first US done after a endarterectomy
W/in 30 days
128
Complications from an endarterectomy
``` -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
Describe a myointimal/neointimal hyperplasia
Tissue overgrowth, often a rxn to a stent
130
Is the normal intimal seen on US after a endarterectomy How will the sutures appear
No Bright reflectors
131
Will you see some normal wall thickening post endarterectomy Is this important
Yes No. Unless associated w/ lumen reduction and increased PSV
132
Are PSV unpredictable w/ a carotid stent How can we monitor them
Yes Compare PSV from exam-exam in the same location
133
Describe a carotid artery dissection
A tear in the intimal lining, blood enters the media of the vessel and creates a false lumen
134
Causes of carotid artery dissection
Trauma Medical complications Spontaneous
135
Can a false lumen be blind ended or reconnect distal to the origin
Yes
136
How can a carotid artery dissection obstruction
Expansion of the false lumen which can narrow the true lumen
137
Where in the ICA does a dissection usually occur risk factors for spontaneous carotid dissection
In the first 2-4 cm of the ICD HTN, fibromuscular dysplasia, marfans, ehlers-danlos syndrome, cystic medial necrosis
138
A CCA dissection can be the extension of what other type of dissection
AO, usually will effect the left CCA
139
US appearance of carotid dissection
Intimal flutter Duplicated lumen Narrowed true lumen, false may be thrombosed
140
How is carotid dissection treated
Anticoagulation therapy
141
Describe fibromuscular dysplasia What’s it characteristic appearance
Non-atherosclerotic disease characterized by tandem stenosis caused by vessel wall abnormalities -affects medium and large arteries String of beads/pearls
142
Which arteries do fibromuscular dysplasia most commonly effect
Renal arteries ICA Can coexist in these locations
143
Fibromuscular dysplasia is most predominant in which gender Where in the ICA does it most commonly occur
Women | 2-6 cm of the Mid, extracranial segment of the ICA For test
144
Symptoms of fibromuscular dysplasia
Incidental or TIA
145
Describe a carotid body tumor (CBT) Where are they located
Sm cluster of highly vascular chemoreceptor cells that are part of the autonomic nervous sys at the bulb
146
What kind of tumor is a CBT What tissue does it arise from
Paraganglioma Arises from the ganglion of the glossopharyngeal nerve
147
Are CBTs usually benign More common in M or W
Yes women, 3-5 X
148
Where does a CBT get its blood supply
ECA usually, if it gets larger, ICA may supply it as well, or the VA or thyrocervical trunk
149
US appearance of CBT
Ovoid | Widening or bulging of the bifurcation, highly vascular
150
Symptoms of CBT Complications of CBT
palpable mass, headache, neck pain, hoarseness Compression of the laryngeal nerve or invasion of surrounding tissue
151
2 Treatments for CBT
Surgical removal | Embolization with angiography
152
Are aneurysms and pseudo aneurysms common or rare in the carotid sys
Rare
153
Describe a pseudoaneurysm
Weakening/tear in the artery wall, creating a collection of blood b/w the media and Adventitia
154
What’s the most common cause of aneurysms in the carotid sys Which location is the most common
Atherosclerosis CCA
155
Treatment of extra cranial aneurysms
Surgical resection | Endovascular therapy
156
Describe vasculitis
Inflammation of the wall of an artery/vein leading to wall damage
157
Causes and treatment for vasculitis
Causes: genetics, infectious, toxins Treatment: steroids
158
4 diseases that cause vasculitis
Takayasu’s arteritis Temporal arteritis Polyarteritis Buergers disease
159
What types of injuries can radiation cause
Injury to the vasa vasorum, endothelial cells and necrosis of the vessel wall
160
What are normal duplex and doppler findings after a carotid endarterectomy.
- 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
Whats the definitive diagnostic test to identify obstructive lesson in the carotid system
angiography
162
what's needed to diagnose a subclavian steal
reversal in a vert. A combined with a significant difference in arm pressures
163
which ares need to be sampled post endarterectomy
``` prox native artery prox stent attachment site prox, mid, distal within the stent dist stent attachment site native artery distal to the stent ```
164
most common complication post endarterectomy within the first 2-3 years what about 3 + years
restenosis by neointimal hyperplasia complications from atherosclerosis
165
US appearance of FMD
tandem stenosis and dilations, with moderate-severe increase is PDV with extensive turbulence
166
how can arterial flow be altered in collaterals with occlusion
increased flow to compensate increased velocity to compensate flow reversal decreased or changes in pulsatility
167
What PSV in the ECA indicates 50% or greater stenosis?
Greater than 150-200 cm/s