Module 4 : Cerebrovascular Pathophysiology Flashcards
14 risk factors for cerebrovascular pathology
- hypertension
- diabetes
- smoking
- obesity/diet
- dyslipidemia
- hypercholesterimia
- sex
- age
- patent foramen ovale
- physical inactivity
- genetic predisposition/ family history
- homocystinaemia
- cardiac disease
- previous TIA or stroke
risk factors - hypertension
- physical force injuries
risk factors - diabetes
- chronic systemic disease with vascular atherosclerosis occurring at an early age being a primary complication
risk factors - smoking
- associated with irritation of the endothelial lining
risk factors - obesity/diet
- high fat high cholesterol
risk factors - dyslipidemia
- abnormal levels of plasma lipids closely associated with development of atherscerlosis
risk factors - hyperscholesterolemia
- genetic defect in LDL receptors
risk factors - sex
- male predominance
risk factors - age
- time allows for build up of plaque
risk factors - patent foramen ovale
- clot or particles in the blood traveling in the right side of the heart can cross the PFO, enter the left atrium and travel out of the heart and to the brain or into coronary artery
risk factors - genetic predisposition/ family history
- stroke, cardiac disease, or diabetes
risk factors - homocystinaemia
- increased homocysteine level in blood which is associated with an increased risk of strokes
2 parts of the physical examination for cerebrovascular pathology
- carotid auscultation for a bruit
- bilateral blood pressures
what is a carotid auscultation for a bruit
- indicates abnormal flow is present
- turbulent blood flow vibrates the vessel wall and creates a bruit
when will a bruit might not be detected
- in the case of a severe stenosis due to significantly diminished flow
what is a thrill
- the palpable bruit
physical exam - bilateral blood pressure
- difference of > 20 mmmHG between the sides indicates a possible subclavian steal
is hemispheric/ anterior flow lateralizing or non lateralization
- lateralizing
is vertebrobasilar/ posterior flow lateralizing or non lateralizing
- non lateralizing
what does lateralizing mean
- usually stays on one side of the body
with anterior circulation are symptoms contralateral or ipsilateral to diseased artery and why
- anterior circulation from the ICA supplies flow to the cerebral hemispheres and because body is often not always controlled by contralateral hemispheres
- symptoms are contralateral to the diseased artery
what is an important exception to anterior circulation symptoms being on the contralateral side of diseased artery
- unilateral vision symptoms from ipsilateral side
- because of ophthalmic artery
5 hemispheric / anterior circulation disease signs and symptoms
- hemiparesis/ hemiplegia
- paresthesia
- aphasia/dysphasia
- amaurosis fugax
- homonomous hemianopsia
hemiparesis/ hemiplegia
- weakness or complete loss of function to one limb or one side of body
paresthesia
- tingling , numb, or burning sensation
aphasia/dysphasia
- inability to speak or comprehend language (ALWAYS LEFT)
- speech is controlled by the left
amaurosis fugax
- aka transient monocular blindness
- often beginning as a black curtain coming over one (if vascular) eye vertically and sometime stopping
- ipsilateral symptom if vascular
homonomous hemianopsia
- blindness or visual defect in half of the field of vision in both eyes
- occurs because the right brain has visual control for the left side of both eyes and the left has visual control of the right side of both eyes
unilateral visual disturbances are what type of symptoms
- ipsilateral
bilateral visual disturbances are caused from disease of what circulation
- can be anterior or posterior
8 signs and symptoms of vertebrobasilar/ posterior circulation disease
- diplopia
- ataxia
- bilateral visual blurring
- drop attacks
- dysphagia
- motor/sensory disturbances
- vertigo
- subclavian steal syndrome
diplopia
- double vision (occipital lobe)
ataxia
- lack of muscle coordination which can affect walking, swallowing, eye movements, speech
drop attacks
- sudden fall while walking or standing that is recovered from quickly
dysphagia
- difficulty swallowing
motor/sensory disturbances
- unilateral, bilateral, or alternating
vertigo
- spinning or sensation that your surrounding are moving around you
signs and symptoms of subclavian steal
- supraclavicular bruit
- arm weakness
- decreased arm pulses
- arm pressures that are discrepant by more than 20mmHg
- usually asymptomatic
5 non localizing signs and symptoms
- dizziness
- syncope
+ transient loss os consciousness - dysarthria
+ abnormal speech or difficulty with speech - headache
- confusion
5 classifcations of neurological deficits
- asymptomatic
- transient ischemic attacks
- resolving/reversing/ ischemic neurological deficits
- cerebrovascular accident
- vertebrobasilar insufficiency
asymptomatic classification of neurological deficits
- patients present with no cerebral and retinal symptoms of vascular disease
- AUSCULTATION OF A BRUIT is most common indication for a duplex ultrasound in these patients
transient ischemic attack TIA class of neurological deficits
- brief episode of neurological symptoms in which cell death does not occur
- lasts 1-30minutes
- neurologic deficit last less than 24 hours an consistent with ischemia is TIA
resolving/reversing ischemic neurological deficit RIND
- neurologic event with symptoms lasting longer than 24 hours to within 3 weeks and with no permanent neurological damage
cerebrovascular accident (CVA/stroke) class of neurological deficit
- results from a loss of blood supply that has left some permanent brain damage and subsequent loss of motor, sensory or cerebral function
- may be further classified
what further 3 classification can be apart of cerebrovascular accident
- acute sudden onset
- unstable in evolution, symptoms come and go
- completed, no progression or resolution stable
vertebrobasilar insufficiency (VBI) class of neurological defect
- causes BILATERAL symptoms of visual blurring, vertigo, ataxia, and drop attacks
2 mechanisms of disease
- thrombosis
- emboli
what is thrombosis
- formation of a blood clot over the plaque site which further decreased the lumen and contributes to ischemia or infarction
what is emboli
- thrombus may. break off and become and embolus
- travels to areas downstream that are too narrow for it to pass causing ischemia and infarction
what is arteriosclerosis
- hardening of arteries
- directly related to age resulting in degenerative changes of the arteries that include loss of elasticity and a thickening of the intima over time
what is atherosclerosis
- form of arteriosclerosis
- refers to both hard and soft plaque beyond the intimal thickening of arteriosclerosis
- MOST COMMON arterial disease
- plaque builds in the arterial wall and limits or stops the blood flow by either narrowing the lumen or blocking the artery
What is considered to be a hemodynamically significant lesion
- a stenosis or occlusion resulting in decreased pressure or flow distal to the obstruction
- > 50% reduction in diameter
What tends to be the cause of atherosclerosis
- injury to the endothelial lining of the vessel wall
What are the 4 stages of development of atherosclerosis
- stage one = early atherosclerosis, injury
- stage two = inflammatory response
- stage three = atheromatous thickening - plaque formation
- stage four = advanced atherosclerosis - late changes
Stage one one of atherosclerosis
- injury could be due to a wide range of causes including
+ risk factors
+ vasculitis
+ hemodynamics stress
Stage 2 of atherosclerosis
- injury exposes areas of the intimacy layer allowing lipids from blood to enter leading to the fatty streak
Stage three of atherosclerosis
- platelets are deposited at the site and teh muscle cells become consumed with fat
- body’s attempt to repair results in teh formation of scar tissue or fibrosi leaving a tough fibrous cap overlying the soft fatty portion of the plaque
Stage 4 of atherosclerosis
- fibrous cap can be disturbed by hemorrhage calcification leading to further disruption of teh endothelial layer resulting in ulcerative plaque
- this type of plaque is unstable adn can release emboli into blood stream
- hemorrhage from the vast vasorum into the plaque causes ischemia leading to break down of fibrous cap and endothelium
Two different descriptions of plaque surface
- smooth
- irregular
Smooth plaque surface
- continuous with no irregularities
Irregluar plaque surface
- plaque surface is discontinuous
- ulceration is possible on these surfaces but the presence of ulcers cannot be confirmed by us
What is the echogenicity of plaque determine by and what 4 ways can it be described
- determined by composition of lipids, collagen, hemorrhage and calcification with the plaque
- anechoic, hypoechoic, hyperechoic, calcific
Anechoic plaque
- no echogenicity
- contains lipid or intraplaque hemorrhage
Hypoechoic plaque
- low echogenicity
- fibrofatty plaque