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STROKE

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on 6 July 2015

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Transcript of STROKE

STROKE
Hemorrhagic Strokes
Intracerebral Hemorrhage
Ischemic Stroke
Types of Strokes:
Hemorrhagic
Intracerebral
Subarachnoid
Ischemic

Thrombotic
Embolic
Risk Factors
Neuronal Injury
Ischemic
Hemorrhagic
Hypertension
Atherosclerosis
Hypercholesterolemia
Smoking
Diabetes
Obesity & physical inactivity
Atrial fibrillation
Oral contraceptives
Sickle cell disease
Brain aneurysm
Arteriovenous malformation
Atherosclerosis
Rupture of blood vessel in brain
Hypertension
Vasculitis
Vascular malformation
 
 
 
 
Formation of hematoma
Compressing brain tissue
Increased pressure in the brain
 
 
 
 
Ischemia and damage to brain tissue
Increased intracranial pressure (blood pooling)
Headaches
Nausea, Vomiting
If unresolved: coma, death

Diagnosis

Determine areas of increased pressure
Differentiate between Ischemic and Hemorrhagic
Extent of brain tissue damage

Blood vessel damage
Endothelial cell injury
Migration of inflammatory cells. monocytes attach to endothelial layer.
Monocytes migrate into intimal lining
Transform into Macrophages
Engulf LDL from blood
Attract smooth muscle cells, collagen and elastin fibers
Formation of fibrous cap
Rupture or erosion
Platelets activated, clot forms, obstruction
Stroke
Fatty streak formed
Hypertension
High blood pressure
Weakening of vessel wall over time
Vessel wall bursts
Hemorrhagic stroke
Damage to endothelial layer of vessel
Inflammatory response/atherosclerosis
Blockage in artery
Diminished blood flow to
small arteries
TIA
Fibrous cap rupture
Platelets activated, formation of clot
Blood vessel occluded
Ischemic stroke
Smoking
Increased
BP
Cholesterol
Effects
Blood
Viscosity
Nicotine stimulates SNS
Increased heart rate
Vasoconstriction and increased BP
Occlusion of vessels in brain
Stroke
Smoking increases LDL, decreases HDL
Contribute to enlargement of atherosclerotic plaque
Cholesterol movement decreased, accumulates in vessels
Occlusion of vessels in brain
Stroke
Increased thickness of blood
Risk for clot forming in vessel
Occlusion of vessels in brain
Stroke
Carbon monoxide decreases the amount of oxygen the blood can carry
Less oxygen reaches brain tissue
TIA/Stroke
Increased BP
Cholesterol
Blood Viscosity
Hypercholesterolemia
Increased levels of LDL in the bloodstream
Damage to blood vessels
Atherosclerosis
Stroke
Diabetes
Individuals with diabetes are four times more likely to experience a stroke, largely because of other risk factors (hypertension, atherosclerosis, high cholesterol)
Increased blood glucose levels at the time of a stroke makes brain damage more severe and extensive when compared to controlled blood glucose levels
Obesity &
Physical Inactivity
Hypertension

Atherosclerosis

High Cholesterol

Diabetes
Atrial Fibrillation
Atria of heart quiver
Blood collects and forms clot
Ventricle contracts
Clot sent into circulation
Clot travels to brain
Clot lodges in small cerebral artery
Blood flow to area diminished
Stroke
Sickle Cell Disease
Cells take on sickled shape
Become lodged at bifurcations
Obstruct blood flow
Decreased blood flow to area of brain
Stroke
Non-modifiable Risk Factors
Age
: Vessels narrow and become more stenotic with increased age
Race
: African Americans, American Indians, and Native Americans are at increased risk
Gender
: Men are at increased risk at younger age
Previous stroke/TIA
Family History
Oral Contraceptives
Cerebral Aneurysm
AVM
"over-reaction" of neurotransmitters
glutamate, aspartate
excitotoxity
Cause: depletion of energy stores
removal of glutamate and aspartate from EC space requires energy
no oxygen increased concentrations in EC space
glutamate binds to NMDA and AMPA receptors
influx of calcium, sodium, chloride
eflux of potassium
production of reactive oxygen species
(O2, H2O2)
production of reactive nitrogen species
(NO, ONOO)
calcium activates destructive enzymes
proteases, lipases, endonucleases
loss of cell integrity
Inflammatory Response
Leukocyte recruitment to ischemic areas 30 mins after ischemia and reperfusion
obstruct microcirculation
activate vasoactive substances (oxygen free radicals, nitric acid) leading to...
Effects of Ischemia
Endothelial Damage
Cells swell and form microvilli at luminal surface of cell
Reduction of luminal patency
Mechanical plugging by erythrocytes, leukocytes, platelets
Endotheliail adhesion molecules activated
Leukocytes adhere to endothelial wall
Inflammation
Ischemic Penumbra
Core of infarction surrounded by oligemic zone
below 10-25% of normal blood flow
"Window of Opportunity"
Can be partly or completely reversed by reperfusing within 2-4 hours

CBF 25-50% of normal level preserves metabolic processes
Neuronal Death
Coagulation Necrosis
Apoptosis

Individual cells die among living cells without eliciting inflammatory response
Cause: physical chemical, osmotic changes in plasma membrane
6-12 hour process
Chromatolysis in cell body
Astrocytes swell and fragment, myelin sheaths degenerate
Begins 6 hours after arterial occlusion
Neurons "programmed" to die under ischemic conditions

Subarachnoid Hemorrhage
Complications
"Brain Attack"
Injury to brain tissue as a result of an acute focal deficit
Risk for recurrence
(treat risk factors- hypertension and cholesterol levels)
Motor deficits
Contralateral weakness
(Often a result of a ruptured aneurysm)

Rupture typically occurs with increased intracranial pressure (such as straining for bowel movement)


Increase in pressure of damage or malformed vessels in the subarachnoid space cause rupture


Blood pools in the subarachnoid space causing increased pressure and damage to brain cells


Results in severe headache, nuchal rigidity
and loss of consciousness (if large)
Subarachnoid Complications
-Pituitary Dysfunction
Diabetes insipidus
-Sudden release of catecholamines
Resulting in cardiac dysrhythmias
Impairments based on area of cell death within the brain
Cerebrum
Movement and Sensation
Speech/Language
Swallowing
Vision
Orientation/Surroundings
Bowel/Bladder Control
Right Hemisphere
Left sided weakness (hemiparesis/hemiplegia)
Homonymous hemianopsia (unable to see left half of visual field in each eye)
Memory problems
Behavioral changes (depression/impulsiveness)
Left Hemisphere
Right hemiparesis/Right hemiplegia
Aphasia
Behavioral changes (cautiousness/hesitancy)
Homonymous hemianopsia (of the right visual field)
Inability to do math/disorganization
Cerebellum
Dizziness
Headache
Nausea/Vomiting
Loss of coordination/balance
Ataxia (impaired gait)
Strokes in this area of the brain are considered less common but more severe
Brain Stem
Affects vital signs (breathing rate and cardiovascular function)
Thermoregulation
Balance
Paralysis
Dysphagia
Aphasia (difficulty speaking)
Coma (possible death)
Generalized Stroke
Complications
References
Thrombotic
(Local)
Damage to the blood vessel
Thrombus forms at the area affected
Vessel becomes occluded/narrowed
Decreasing blood flow to the cerebral tissue
Ischemia & damage to
cerebral tissue
**Atherosclerosis is the most common cause
Emoblic
(Distant)
Foreign object in an area other than the brain, most commonly in the heart.
Object loose into the bloodstream
Travels through the brain vessels until it reaches a small vessel it cannot pass thru
Occludes blood flow to cerebral tissue
Ischemia and death of cerebral tissue
Includes: clot, fibrin, and pieces of atheromatous plaque, fat, air, tumor or metastasis, bacterial clumps, and foreign bodies
Images of the Brain, Skull or Spinal Cord:
1. CT Scan
2. MRI
Images of the Blood Vessels Supplying the Brain:
1. Carotid Doppler
2. Transcranial Doppler
3. MRA
4. Cerebral Arteriogram
Images of Heart Function
1. Echocardiogram
2. EKG
CT: Total occlusion of the right middle cerebral artery
Increased Intracrainal Pressure
Hemorrhagic Stroke Ischemic Stroke
Pooling of blood in brain Ischemic brain edema
TIA
Brief episode of focal ischemia that does not result in infarction
Vessel becomes temporarily occluded
Decreased blood and oxygen to area
Cell injury
Reperfusion
Focal enlargement of vessel
Weakening of vessel wall as it stretches
Rupture
Hemorrhagic Stroke
Bleeding into the brain
Cell injury/cell death
Sequelae (long term effects of stroke)
Increased ICP
(Seen especially in hemorrhagic strokes)
Blood pooling/edema due to inflammatory healing process
Increased pressure on brain structures


Coma


Death
Seizure Activity
Cellular biochemical disfunction


Electrically Irritable Tissue
Tissue Ischemia



Increased extracellular glutamate (Excitatory neurotransmitter)






Seizure actitivty
Early
Late (Epilepsy)
Glial (Nervous cell) scarring


Persistant changes in neuron excitibility
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http://www.lipidworld.com/content/9/1/47/figure/F1?highres=y
http://nursingcrib.com/nursing-care-plan/nursing-care-plan-cerebrovascular-accident-cva/
https://www.google.com/url?sa=i&rct=j&q=&esrc=s&source=images&cd=&cad=rja&uact=8&ved=0CAUQjhw&url=http%3A%2F%2Fwww.yakimamemorial.org%2Fmedical-services-act-fast.asp&ei=_KeRVYaDPMOlyASMmo2gAQ&bvm=bv.96783405,d.aWw&psig=AFQjCNE4bf3QknYmZ26HuBbB7B-5_kOSuA&ust=1435695481551418
https://www.google.com/url?sa=i&rct=j&q=&esrc=s&source=images&cd=&cad=rja&uact=8&ved=0CAUQjhw&url=https%3A%2F%2Fneuro4students.wordpress.com%2Fpathophysiology%2F&ei=ZKiRVe_IFsiHyAT3zIDQAw&bvm=bv.96783405,d.aWw&psig=AFQjCNG_tThERR2q-55OoqYmceXy4Zgo6A&ust=1435695581998408
https://www.google.com/url?sa=i&rct=j&q=&esrc=s&source=images&cd=&cad=rja&uact=8&ved=0CAUQjhw&url=http%3A%2F%2Fctrnd.med.ufl.edu%2Fresearch%2Fstroke%2Fstroke-background%2F&ei=paiRVYHgAoGmyASnjJG4Ag&bvm=bv.96783405,d.aWw&psig=AFQjCNG_tThERR2q-55OoqYmceXy4Zgo6A&ust=1435695581998408
https://www.google.com/url?sa=i&rct=j&q=&esrc=s&source=images&cd=&ved=0CAUQjhw&url=https%3A%2F%2Fwww.studyblue.com%2Fnotes%2Fnote%2Fn%2F3l-patho%2Fdeck%2F2000827&ei=yqmRVbuuJNSlyASl17WICQ&bvm=bv.96783405,d.aWw&psig=AFQjCNHPOPbPrjZ87IkhiGGcTLiIbyet8Q&ust=1435695945817344
Other Neurologic
Tests:
1. Lumbar Puncture
2. Electroencephalogram
Carotid Doppler
http://www.mayfieldclinic.com/PE-CarotidStenosis.htm#.VZLmqWC4mqA
Lab Tests
http://a-fib.com/2-overview-of-atrial-fibrillation/
http://creationwiki.org/Sickle_cell_anemia
Stroke risk associated with estrogen component
Information largely based on high-dose estrogens
Increased number of circulating clotting factors
Increased risk of thrombosis
Stroke
, PE, MI
Lack of capillary network
Blood moves directly from high-pressure artery to low-pressure vein
Rupture of veins
Elevated pressure in AVM
Less blood reaches surrounding tissues
Impaired tissue perfusion
Hemorrhage
Stroke
CBC
PT & INR
PTT
Blood Glucose
Electrolytes
Cholesterol levels

MRI of a Stroke Patient
http://www.webmd.com/stroke/stroke-mri
begins 1 hr after ischemic damage
ischemia activates "suicide proteins"
mitochondrial and plasma damage late in process
nuclear damage first
vasodilation
increased permeability
increased platelet aggregation
increased leukocyte adherence to endotheilial wall
supplied with blood by collateral arteries (not adequate long term)
1. proteases damage cellular structure
2. lipids peroxidized
3. microglia produce cytotoxic factors
4. mitochondria function disrupted
5. pyknosis induced (chromatin condensation)
destruction of nucleus
Neuronal Death


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http://classroom.sdmesa.edu/eschmid/Chapter14-Zoo145.htm
Increased Intracranial Pressure
Blood, cerebral spinal fluid (CSF), and brain tissue are the components of the cranial cavity



Blood Increases in the crainial cavity (Hemorrhage)



Other components (CSF and brain tissue) must decrease to prevent pressure increase (Monro-Kellie hypothesis)



Pressure increases due to limited ability of brain tissue to compensate



Tissue ischemia and death
Full transcript