Post on 06-Apr-2018
8/2/2019 REGENCIA CVA PATHO
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CEREBRAL VASCULAR ACCIDENT
Predisposing factors:
1. Advancing age
2. Gender (males)3.Race (African Americans)
4. Family history of stroke
Precipitating factors:
1.Hypertension
2. Heart disease
(atrial fibrillation)
3. Diabetes mellitus4. Sleep apnea
5. Blood cholesterol
levels6. Smoking
7. Sickle cell disease
8. Substance abuse9. Living in the stroke
belt10. Prior stroke, carotid stenosis,
and a history of TIA11.Heavy alcohol consumption
12. Obesity
13. Specific to women: oralcontraceptive use, pregnancy,
childbirth,menopause, migraineheadaches with aura, autoimmune
d/os (diabetes and lupus), clotting
factor disorders
Atherosclerosis
Atherosclerotic plaques
8/2/2019 REGENCIA CVA PATHO
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RELEASE THE
CAN DEVELOP ANYWHERE
enzyme Adenosine
Diphosphate
initiates the clotting
sequence
THROMBUS
FORMS
small, deep penetrating
arteries( lenticulostriate arteries)from the middle cerebral artery
common site: internalcarotid artery, vertebral arteries
and the junction of the vertebral and basilar
arteries
OCCLUSION
LACUNAR
STROKE
thrombus may remain in place
and continue to enlarge
8/2/2019 REGENCIA CVA PATHO
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INITIATES
WITHIN FEW
MONTHS OF THE
INFARCTION
BEGINS
WHEN
INFARCTION
part of it may break off
EMBOLUS
carried through
the arterialsystem
Brain
lodged in a vessel too narrow to permit
further movement (most common
site: left middle cerebral artery)
completely occluding
the lumen of the
vessel
disruption of thecerebral blood
flow
ISCHEMICCASCADE
cerebral blood flow
falls to<25ml/100g/min
DIE
only minor deficits
are seen since theseareas are very small
cells DISTAL tothe occlusion
cells
CRITICALLY
more severemanifestations
may developincluding paralysis
and sensory loss
Necrotic brain cells areREABSORBED by macrophage activity
a very small cavity or
lake is formed
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RENDERS
INCREASING
THE POTENTIAL
neurons can no longer maintain aerobic
respiration
Mitochondria
switch
Anaerobic respiration
large amounts of
lactic acid
change in the pH level
neuron incapable of producing
sufficient quantities of adenosine triphosphate
(ATP)
NA- K pump fails
breaks up into
smaller fragments
not absorbed
>drowsiness, stupor,
coma
>contralateral hemiplegiaof the arm and face
>contralateral sensorydeficits of the arm and face
>global aphasia (if dominanthemisphere is involved)
>homonymous hemianopia
absorbed by the
body
manifestations
will persist
manifestations will
disappear in a few hours
to a few days
weakenedvessel wall
CEREBRAL
HEMORRHA
GE
HPN
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OCCURS WHEN
SUDDEN ENTRY
BLOOD ENTRY OF BLOOD IF CONTINUED
INTO
RESULT
increase in
intracellular calcium
release of glutamate
activate a number of
damaging
pathways
generation of free radicals,
vasoconstriction,
release of more calcium and glutamate,destruction of the cell membrane
Cerebral
vessel ruptures
BRAIN TISSUE
brain tissue affected
by pressure due tomass formation of
blood clot
displaces
brain tissue
decreases cerebral blood flow
rupture of acerebral
aneursym
sudden onsetof a severe
headache
SUBARACHNOID SPACE/VENTRICLES
Irritates the
meningesand brain tissue
Inflammatoryreaction impairing absorption
and circulation of CSF
MINI STROKE/
TRANSIENT ISCHEMICATTACK
sudden onset and
often disappears w/ minutes or hour s
If managed: tPA,
calcium channel blockers
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IF NOT MANAGED
ischemia and
infarction
Blood vessel
spasm
infarction
edema
>weakness of one side(including the face, arm
and leg)>slurred speech
>deviation of theeyes
SEVERE
HEMORRHAGE
>hemiplegia
>fixed and dilated pupils>abnormal body posturing
>coma
Putaminal &Internal
capsule
Hemiplegia with more
sensory than motor lossthalamus
Problems w/ visionand eye movement
subthalamus
>contralateral numbnessor weakness of the leg,
hand, forearm
and corner of themouth( middle cerebral artery involvement)
>aphasia (ischemia
of the left hemisphere);>visual disturbances
such as blurring( posterior cerebral artery
involvement)
IRREVERSIBLECEREBRAL
DAMAGE
release of metalloprotease(zinc & calcium- dependent
enzymes)
breakdown of collagen, hyaluronic acid and other elements of connective tissue
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severe headache, vomiting,
loss of ability to walk,
dysphagia, dysarthria,eye movement
disturbances
cerebellum
pons
>respiration affected>hemiplegia
>paralysis>coma
>abnormal body posturing>fixed pupils
>hyperthermia
>DEATH
structural integrity loss of brainand tissue and blood vessels
breakdown of the protective
blood brain barrier
CEREBRAL EDEMA
VASCULAR
CONGESTION
Compression
of tissue
increase intracranial
pressure
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Impaired perfusion
and function
Contralateralhemiparesis
or hemiplegia,unilateral Neglect,
alteredconsciousness,
homonymous
anopsia,inability to turn
eyes toward
affected side,Vision changes,
dyslexia,Dysgraphia,
Aphasia, agnosia,Memory deficits,
vomiting
ContralateralHemiparesis,Foot and leg deficitsgreater than the arm,
foot drop,gait disturbances,
ContralateralHemisensoryAlterations,
Deviation of Eyes toward
Affected side,Expressive
Aphasia,Confusion,
Amnesia,Flat affect,
Apathy, shortenedAttention span,
Incontinence, acuityApraxia, acuity
Mild contralateralHemiparesis,
Intention tremor,Diffuse sensory
Loss,Pupillary dysfunction,
Loss of conjugateGaze, nystagmus,
Loss of depth
Perception,Cortical blindness,Homonymous
Hemianopsia,Perseveration,
dyslexia,Memory deficits,
Visual hallucinations
Contralateral
Hemiparesis w/
Facial asymmetry,Contralateral
SensoryAlterations,
HomonymousHemianopsia,
Ipisilateral periodsof blindness,aphasia
If dominantHemisphere
is involved,
Horner'ssyndrome
Carotid bruits
Alternating motor Weaknesses,Ataxic gait,dysmetria,
ContralateralHemisensoryImpairments,
Double vision,HomonymousHemianopia, Nystagmus,
Conjugate gaze,Paralysis,Dysarthria,
Memory loss,Disorientation,
Tinnitus,Hearing loss,dysphagia,
vertigo,coma
Ipsilateral
Ataxia, facialParalysis,
Ipsilateral lossof sensation
in face,Sensation changes
onTrunk
and limbs, Nystagmus,
Horner's syndrome,
Tinnitus, hearingloss
Ataxia, paralysis
Of the larynx
And soft palate,Ipsilateral
Loss of sensationIn face,
Contralateral on
Body, Nystagmus,
dysarthria,Horner's
Syndrome,Hiccups
And coughing,
Vertigo, Nausea
And vomting
Anterior cerebral
artery
Posterior cerebralartery
Middle
Cerebral
Artery
InternalCarotid
Vertebrobasilar System
Anteroinferior
cerebellar
Posteroinferior cerebellar
Lateral
hemisphere,
Frontal, parietal
And temporal
Lobes,
basal ganglia
Frontal lobe Occipital lobe;Anterior & medialPortion of temporal
lobe
Branches into
opthalmic,
PCA, anterior
Choroidal,ACA, MCA
Cerebellum,
brain stemCerebellum
Cerebellum
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If managed:Palliative care- monitoring v/s
and neurovital signs, intubation,ICP monitoring, intubation,
Mechnical ventilation, vasodilators,Osmotic, diuretics, ventriculostomy
Poor cerebral perfusion
Poor improvement
If not managed
Continued insufficiency of
Blood flow
Further compressionOf tissues
coma
Cerebral death
Loss of neural
feedback mechanisms
Cessation of
physiologic functions
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Cardiovascular
Loss of cardiac
musclefunction
Relaxationof venous
valves
Decreased
Cardiac output
Bradycardia Hypotension
Cardiopulmonary arrest
Pulmonary
system
Failure of
Accessory
MusclesFor breathing
Loss of lung
movement
GIT GUT Other systems
Relaxation of
intestinesand sphincters
Loss of bowel
control
Neurogenic bladder
Loss
of sphincter control Restlessness,
abnormal
Thermoregulation,
Mental
Confusion,
Increase
Secretions,
Decreased
urinary
output
Systemic failure
apnea
DEATH