TIAs/Strokes Flashcards
1
Q
CNS and strokes
A
- Strokes can affect any region
- Vast majority affect brain
- Spinal stroke= cord stroke, symptoms largely dependent on location
- Brain stroke= cerebrovascular accident
2
Q
Cerebrovascular accidents
A
- Stoke= brain deprived of blood
- As a result regions become poorly perfused and brain cells begin to die
- Ischaemic strokes- occur as result of blood vessel blockage, around 87% of. Aka thromboembolic stroke
- Haemorrhagic stroke- occur as result of blood vessel rupturing and haemorrhage occurring in or around brain, account for 13%
3
Q
Blood supply to the brain
A
- Int carotid arteries and circle of Willis
- Majority of blood arrives through int carotid arteries
- These supply to a circle of Willis
- Brain receives smaller amounts of blood through vertebral arteries which run up the vertebral column and connect to basilar artery (feeds into circle of Willis)
- Circle of Willis can be thought of as functioning like a distribution hub with multiple vessels emerging which supply different lobes of brain
4
Q
TIAs
A
- Temporary disruption to blood flow and tissue prefusion within brain
- Aka mini strokes, usually resolve rapidly
- For stroke to be classed as TIA, symptoms should resolve within 24 hours
- Symptoms are highly variable depending on which region of brain was affected
- Commonly involve numbness (down one cheek or an arm of leg), may be visual disturbance, sometimes speech is affected (slurring)
- Generally blood supply restored and effects disappear
- Can lead to micro-infarctions, where tiny amounts of brain tissue die leaving microscopic infarctions
- In older people TIAs are common, loss of neural tissue can lead to dementia
5
Q
TIA risk factors
A
- Atherosclerotic occlusion of carotid arteries
- Atrial fibrillation- turbulent blood flow and clot formation
6
Q
Cerebral thrombosis
A
- Where blood clot forms in cerebral circulation
- Frequently seen in people suffering atherosclerosis or clotting disorders
- Pregnancy is a risk as liver produces more clotting factors (blood= hypercoagulable)
- Virchow’s triad predisposes thrombosis
7
Q
Virchow’s triad
A
- Hypercoagulable blood
- Endothelial injury (e.g., from smoking)
- Circulatory stasis (blood flow stops commonly as a result of immobility)
8
Q
Atherosclerotic occlusion
A
- Chronic injury to endothelium, initiates inflammatory response
- Largest leukocyte (monocyte) attach to areas of damaged endothelium and squeeze underneath by process of diapedesis
- Monocytes progressively enlarge into macrophages
- Mature macrophages reside under endothelial layer trap and accumulate lipids from circulating blood and puff up fat-laden foam cells
- Foam cells form atherosclerotic plaque that progressively builds up inside blood and restricts flow
- Also causes hardening of arteries
9
Q
Plaque rupture, endothelial damage and thrombosis
A
- Fatty plaque causing atherosclerotic occlusion can become unstable and rupture
- Rupturing of plaque can trigger thrombosis by exposing collagen fibres that support the endothelium
- Once clotting cascade is initiated the clot can expand progressively blocking blood vessels
10
Q
Platelet activation and aggregation
A
- Thrombosis is frequently triggered by damage to endothelial lining of blood vessels, since endothelial layer is only one cell thick it is easily disrupted
- When endothelial cells die supporting collagen layer is exposed and platelets rapidly attach, platelets circulate in dormant state but when they attach to exposed collagen fibres they become activated
- Activated platelets produce a variety of chemicals including ADP, serotonin and thromboxane’s- promote platelet aggregation whereby circulating platelets aggregate (collect) at site of injury and become active to release ADP, serotonin and thromboxane’s
11
Q
Cerebral embolism
A
- Embolus is a piece of solid material that is freely circulating in blood
- Most emboli are blood clots which have formed in another region before detaching and becoming mobile
- More rarely, emboli come from pieces of fatty plaque which have detached from occluded blood vessels, bone fragments which have punctured blood vessels followed fracture or air bubbles introduced via saline drops
- Majority of emboli will become trapped in pulmonary circulation of lungs leading to pulmonary embolism
- Where embolus locates in cerebral circulation= cerebral embolism
- Cerebral emboli are common in Px with atrial fibrillation
12
Q
DVT and emboli
A
- Many emboli arise from DVT
- Common risk factors
1. Immobility
2. Varicose veins - Blood collecting in varicose veins of the immobile can stop moving leading to venous stasis (static non-circulatory blood) which can rapidly clot
- DVT can also activate Virchow’s triad
13
Q
Cerebral haemorrhage
A
- This form of stroke occurs when blood vessels rupture
- Can occur as result of head trauma
- Major risk is hypertension- causes weakening in blood vessels leading to aneurysms, can become unstable and burst
- Aneurysms common where arteries bifurcate
14
Q
Berry aneurysm and cerebral haemorrhage
A
- Aneurysm thought to occur in 1/20-25 people, significantly inc risk of haemorrhagic stroke
- Most aneurysms are asymptomatic and may only be revealed during MRI or CAT scan
- May remain stable, hypertension inc risk of rupture
15
Q
Astrocytes and blood brain barrier
A
- Small vessels of cerebral circulation= neuroglial cells- astrocytes
- Have thin cytoplasmic processes which wrap around wall of the vessel
- Astrocytes form blood brain barrier which keeps metabolic environmental toxins together with blood-borne pathogens away from active neurons
- When cerebral haemorrhage occurs BBB is breached and toxic materials such as urea, uric acid or other soluble toxins in blood can directly damage neural tissue within brain. In effect the leaked blood acts as toxic slurry inflicting widespread damage
- Blood collecting in or around brain can also begin to rapidly clot inc intracranial pressure, can compress blood vessels restricting cerebral blood flow and causing further tissue damage
