Flashcards
Lecture 1 Week 6 Stroke
Cards in this deck (26)
- 1Stroke85% of strokes are ischemic, thrombus, embolus
15% are hemorrhagic are intraparenchy, subarachnoid - 2Types of StrokeLarge vessel
Small vessel
Cardioembolic
Cryptogenic
Stroke of other known etiology - 3ThromboticOccurs when a clot acutely occludes a vessel
Large vessel or small vessel occlusion
Typically forms a white thrombus
RIch in platelets and fibrin
Anti-platelets are effective treatment - 4Plaque and ThrombusPlaque on endothelium often acts as a nidus for platelet aggregation
Plaque often forms at a bifurcation of large vessels
Turbulet flow of blood, and other inflammatory mediators irritates the endothelium
Cholestrol, calcium, inflammatoy cells and collagen wall of inflammatory zone
Rupture of the plaque exposes the core which is highly thrombogenic - 5Large Vessel DiseaseAtheroma develop in large vessels
Carotid bifurcation, vertebral arteries and proximal MCA are commomest site
Thrombus can develop at site of atheroma and occlude vessel or embolism
Large vessel strokes can evolve over days
- Due to shower of emboli, gradual accumulation of clot, acute occlusion of large vessel - 6Small Vessel DiseaseSmall perforating arteries off the major vessels are prone to small vessel disease
This includes
- Lenticulostriate
- Pontine perforators
- Anterior Choroidal artery
- Thalamic perforators
Causes small, subcortical strokes - lacunar infarcts
Lack cortical signs: dysphasia, sensory neglect, hemianopia, agnosia - 7Small vessel disease - lipohyalinosisSmall arteries branch directly off large arteries
Under high pressure from larger arterty
High pressure causes lipohyalinosis
This causes the vessel to hypertrophy with reduction of vessel calibre
May also be due to inflammatory response within the endothelium of small artery - 8Small vessel disease - Other mechanismsAtherosclerosis of the parent vessel and encroaches and occludes the origin of the small vessel
Microembolisation from a parent or downstream artery
Microembolisation from aortic arch or atria - 9EmbolicForms at a distant site and moves to occlude a vessel
Often due to blood stasis
Typically a red thrombus
Cardioembolic and ESUS
Anticoagulation is effective treatment
Often do not have fluctuating symptoms - 10Stasis causing thrombiLamniar flow not maintained bringing platelets in contact with endothelium
Fresh flowing blood often dilutes or moves activated clotting factors
Does not allow inflow of clotting factors inhibitors, allowing build up of thrombi
Promotes endothelial cell activation allowing local thrombus formation - 11EmbolicAtrial Fibrillation is most common cause of embolic stroke
Fibrillation of the left atrium causes blood stasis and coagulation
Presence of left atrial appendage increase risk
People with AF who are not anti coagulated tend to have more severe strokes - 12Patent foraman ovaleCan cause paradoxial embolism whereby a venous clot transverse the atrium and causes systemic occlusion
- 13Breakdown of clotAcute stroke tissue Plasminogen Activator
Plasminogen is inactive and tPA activates this to plasmin
Plasmin then degrades the fibrin clot releasing fibrin degradation products
Plasmin is inactivated by a2-antiplasmin - 14Anti-coagulationWarfarin
- inhibits Factors II, VII, IX and X
Rivaroxaban and Apixaban
- Direct Factor Xa inhibitors - 15Molecular PathophysiologyBrain tissue is very oxygen dependent
15% of cardiac output goes to brain
20% of total body oxygen consumption from brain
Survival is based on
Good collateral flow
Duration of oxygen deprivation
Degree and speed of oxygen deprivation - 16Cerebral AutoregulationVasoconstriction reduces and vasodilation increases
Mechanisms and signling are not weel understoof
Brain is able to maintain auto regulation
Pressures outside this range can cause problems - 17Molecular consequences of IschemiaAnerobic metabolism depletes ATP
Loss of ATPase pump from lack of ATP
Increases release of glutamate in synapse
Stimulates K+ out of cell and Ca and Na into cell
Increased Glutamate results in activation of NMDA and AMPA receptors allow more Ca to enter cell - 18Molecular consequences of IschemiaAs Na enters the cell, so does H2O which causes intracellular edema
Increased Na leads to reduced glutamate resorption leading to increased glutamate levels
This stimulates neutron more leading to excitotoxicity
NMDA receptor activatiion leads to increased NO
NO can be free radical and too much can damage with normal cellular components
NO can react with superoxide to make peroxynitrile
Peroxynitrile can cause DNA damage leading to cell death
With lack of ATP, cellular function ceases and cells becomes necrotic - 19Cell DeathCell death occurs within minutes
Cells in core die by necrosis
Cells in penumbra die by apoptosis
Apoptosis requires ATP to occur
Inflammatory cytokines released
Macrophages enter the area and phagocytise infarcted tissue - 20Post Stroke cerebral EdemaInflammatory mediators attract an inflammatory response
Vasogenic edema
Blood brain barrier is disrupted and edema occurs
Cytotoxic edema
- Cells becomes necrotic and release their contents into interstitial fluid
- This attracts fluid to maintain the osmotic gradient
Hemicraniectomy
- Removal of a portion of skull allows a brain swelling to occur outward rather than inward - 21Hemorrhagic StrokeHypertension is most common cause of ICH
Amyloid angiopathy is the most common cause of non-traumatic ICH in elderly
Vascular malformations are the most cause in the young - 22Hemorrhagic Stroke - Direct Neuronal injuryHemorrhage deprives downstream tissues of blood supply, possibly causing local ischemia
Hemorrhage causes a hematoma
Hematoma causes localised mass effect
Occlude surrounding vessels causing an ischemic injury
Hematoma also exerts mass effect causing herniation - 23Hemorrhagic Stroke - Indirect Neuronal injuryHematoma generates thrombin
Causes an inflammatory response
- leads to direct neuronal injury
- Can lead to breakdown of blood brain barrier
- Can lead to deem, further increasing the mass effect
- Breakdown of hematoma releases heme and Fe
Can direct injurious effects to neurons through free radical formation and oxidative stress - 24Hypertensive HemorrhageHemorrage from hypertension occurs in basal ganglia and pons
Small perforating vessels are prone to disease from hypertension
High pressures in small lumen cause micro-aneurysms
These micro-aneurysms can rupture causing ICH
Prone to lacunar strokes from lipohyalinosis or haemorrhage from miacro-aneurysms - 25Cerebral Amyloid AngiopathyCommon cause of non-traumatic lobar haemorrhage in elderly
Amyloid accumulates in cortical vessels
Weakens the vessels making them prone to rupture
Can see microhemorrhages on MRI scan
Thalamus, pons, basal ganglia from hypertensive microangiopathy - 26Convexity SAHMicrohemorrhage occuring on cortical surface can cause convexity SAH
can present a transient focal neurological event
Patients develop recurrent, sensory changes or motor deficits often affecting the face or hand
Confused for recurrent TIAs
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- PATHOPHYSIOLOGY MMED3937 Flashcards on Lecture 1 Week 6 Stroke, created by Paras Chrysostomou on 10/04/2017.
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