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Stroke Flashcards

1
Q

Stroke facts

A

2nd leading cause of death worldwide
20-33% die within 1-3 months
Largest cause of adult disability in uk
25% of cases on people under 65

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2
Q

What is a stroke

A

Brain attack caused by the disturbance of blood supply to the brain
Rapidly developing clinical symptoms, focal or global, leading to loss of cerebral function that can only be attributed to vascular origin

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3
Q

Acute effect of stroke vs chronic brain disease

A

Rapid presence of symptoms vs build up over time

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4
Q

Obstacle to emergency treatment of stroke

A

Don’t know they are having a stroke
Long time between stroke and getting to the hospital
F - face
A - arms
S - speech
T - time

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5
Q

Ischemic stroke

A

Blood clot so blood flow stops so cells don’t get oxygen

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6
Q

Haemorrhagic stroke

A

Rupture of blood vessels

Intracerebral haemorrhage - blood spilled over brain, 10% of strokes

Subarachnoid haemorrhage - 5% of stroke

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7
Q

Transient ischemia attack (TIA)

A

Ischdmic events
Resolves with 24 hrs
No tissue death

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8
Q

Intracerebral haemorrhage

A

Blood goes into the premnchyal, invades brain tissue, invades neurones and glial cells, haemoglobin comes out (some neurones sub lethal exposure but have effect)
Extracellular haemoglobin induces cell death mainly via oxidation and inflammation

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9
Q

Subarachnoid haemorrhage

A

Venous sinus leak
Invades subarahnoid space and spreads around brain at high pressure
Blood released into subarachnoid space clots almost immediately and disappears via clot lysis which starts shortly after SAH
Highest incidence of death and disability and in younger people

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10
Q

Cerebral venous sinus thrombosis (CVST) EXTRA READING

A
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11
Q

Ischemic stroke

A

Aka thrombotic
85% of strokes
Usually in medial cerebral artery - arm and facial weakness, speech affected but depends on location Lenticulostriate arteries in lacunar stroke (most common, the small areas following MCA) - weakness on one side of the body

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12
Q

The brain needs to be adequately perfumed

A

Uses up most energy
Expensive to run in term of energy (ATP)
20% of energy
15% of cardiac output
(Sodium/potassium pump)

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13
Q

Brainstem stroke syndromes

A

Can affect fibre tracts (eg spinothalamic tract, nuclei (of cranial nerves) and physiological functions (eg consciousness and arousal)

Occlusion of vessel in posterior circulation

Stroke syndromes: medulla - wallenbergs syndrome, midbrain - webers syndrome, pons - locked in syndrome

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14
Q

Clinical features of brainstem strokes: tracts

A

Motor/sensory disturbance
Ataxia
Horners syndrome

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15
Q

Clinical features of brainstem strokes: nuclei

A

Cranial nerve dysfunction

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16
Q

Clinical features of brainstem strokes: physiological centres

A

Loss of consciousness

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17
Q

Stroke progression

A

Rapid - o2 depletion, energy failure, terminal depol, ion homeostasis failure (minutes)
Secondary - excitotoxicity, SD like depols, disturbance of ion homeostasis (hours to days)
Delayed - inflammation, apoptosis (days to weeks)

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18
Q

Current treatments for stroke

A

Antiplatelets
Clot busting agent aka alteplase
Anticoagulants
Carotid endarterectomy
Statins
Anti hypertensives
Neurosurgery- remove blood and repair burst blood vessels

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19
Q

Clot busting agent aka alteplase

A

Mainly used
Has to be given within 4 hrs so only 8% of patients eligible

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20
Q

Correct diagnosis extremely important

A

Eg Haemorrhagic cannot be given clot busting or will bleed to death
Must act fast for treatments

21
Q

How is the clinical outcome of stroke measured

A

National institutes of health stroke scale (NIHSS)
Bigger the score the worse off they are
Improved outcome with earlier treatment

22
Q

Risk factors of stroke

A

High blood pressure
Elevated cholesterol level
Smoking
Physical inactivity
Obesity
Alcohol consumption
60-80 % cumulative stroke risk

Non modifiable risk factors - older age, race (Hispanic, black), maternal history of stroke, sex (makes), diabetes

23
Q

How do risk factors increase the propensity to stroke

A

Structure and function of blood vessels - artherosclerosis, stiffening of arteries, narrowing thickening and tortuosity of aerterioles and capillaries eg atheroma, aneurysm

Interface with circulating blood - reduction/ alteration of cerebral flow (CBF)

Inflammatory cells - macrophages, T lymphocytes, mast cells, cascade - lesion development

24
Q

Stroke triggers can be identified in some patients

A

Neck trauma
Pregnancy/ postpartum
Systemic infection use of drugs
Mental stress

Exacerbation of vascular inflammation, activation of coagulation cascade leading to vascular occlusion and haemodynamic insufficiency

25
Ten point plan for action
Awareness Prevention Patient involment Act on warnings Stroke as medical emergency Stroke uni quality Rehabilitation and community support Participantion Workforce Service improvement <50% of hospitals with acute stroke units have brain scanning available within 3 hrs
26
Stroke (cells involved)
Interactions between glia, neurons, vascular cells, matrix components all relevant
27
Normal aerobic metabolism
Oxygen + glucose lead to mitochondrial respiration to create cellular ATP produces and so ongoing consumption
28
Stroke influence on aerobic respiration
Removal of mitochondrial respiration So depletion of ATP Accumulation of reactive oxygen species so even more ATP usage so intracellular acidification Malfunction and cellular death
29
Malfunction of ATP dependent processes
Enhanced consumption of cellular ATP Profound loss of ioninc gradients so sustained rise in [glu]o (further loss of ionic gradients) and large elevations of intracellular calcium leading to excitotoxicity due to more ROS, proteases and mitochondrial Ca overload
30
Inflammation
Ischemia evokes robust inflammatory response Highly stereotyped and markers used to determine approximate age of cerebrovascular lesions Stimulated glia and blood vessels communicate through complex signalling Innate and adaptive immune systems used
31
Early vascular, peri vascular and parenchyma events triggered by ischemia and reperfusion
Clot - stress/ pressure Clot goes away - perfusion stress/pressure Signals interact with BBB and may open it so may infiltrate the brain Increase in ROE and decrease in nitric oxide produced by blood vessels Interact with neurones and astrocytes
32
Cell death and activation pattern, recognition receptors set the stage adaptive immunity
Neurones may release ATP or UTP in cells that have been opened by force and may leak out signal danger molecules Eg HMGB1, HSP60, AB Activate TLR 2 and 4 Lead to adaptive immunity, leukocyte infiltration, tissue damage and matrix degredation leading to DAMPs activation Inflammation appliqués Ischemic lesion early on
33
Resolution of inflammation and tissue repair
Microglia start to clear away dead cells Start release neuro protective factors eg IL10 and TGF-B Brain repair - neurones release helpful factors eg BDNF, VEGF to repair neurones and blood vessels
34
Peripheral immunological changes after stroke
Blood, bone marrow, spleen and other lymphoid organs White blood cell count and expression of cytokines and inflammatory markers up within hrs after ischemia then down within 1/2 days Marked immuno depression - determinant of stroke morbidity and morality Respiratory and UTIs
35
Ischemia penumbra
Area of reduced perfusion sufficient to cause potentially reversible clinical deficits but insufficient to cause disrupted ionic homeostasis
36
Contribution factors for irreversible damage of brain tissue in penumbra
Ischemic core Irreversibly damaged tissue <20% baseline blood flow levels Depleted ATP stores Failure energy metabolism Ischemic penumbra Perinfract zone Depressed tissue perfusion Basal ATP lvls & o2 metabolism Normal ion gradients Electrical silence Suppressed protein synthesis Goes from salvageable tissue to dead within hrs and days
37
MRI (DWI & PWI) - Acute ischemic stroke
Diffusion weighted imaging Detects areas of restricted diffusion of water - bright in acute Ischemic stroke Perfusion weighted imaging Detects abnormal blood flow Diffusion perfusion mismatch
38
Salvageable brain to infractionsteps
Energy failure Anoxic depol, excitotoxicity, oxidative stress, necrosis Peri infract depol, calcium overload, mitochondrial damage Inflammation, programmed cell death Interacted tissue
39
Studying stroke
Patients (post mortem, clinical trials) Animal models (eg medial cerebral artery occlusion) In vitro studies ( eg oxygen glucose deprivation)
40
Possible stroke treatment - time sundowns and convo therapy approaches (EXTRA READING)
41
Reversal of focal ischemia
Animal model (rat) Mechanical occlusion of middle cerebral artery for 1 hr Imaging of ATP and protein synthesis Restoration of energy metabolism but not protein synthesis Restoration of energy metabolism fails where protein synthesis did not recover
42
Simulated ischemia in neurones causes sharp increase in glutamate receptor activation and anoxic depol (AD)
Glutamate mediate feedback mechanism that doesn’t let recover Under Ischemic conditions, disruptions na+, k+ and pH gradients will cause transported to function in reverse leading to increased [extracellular glutamate]
43
Potential therapy: glutamate/ca receptor blockers
Protect neurons from 1.5 hrs oxygen/glucose depreciation Don’t protect >2 hrs
44
Possible involvement of NMDARs, TRPM2 & 7 channels in anoxic neuronal death
Excessive activation of glutamate receptors Activation of NMDA receptor subtype (voltage dependent) Losing membrane potential, receptors bound to glutamate and open as cell is depolarised Calcium influx Activation of ion channels TRMP2 & 7 Interact with mitochondria so ROS Essential interaction of nitric oxide synthase with PSD95 bound to NMDA receptors Peroxinitrate (ROS) lead to cell death
45
Nitric oxide
Multifunction biological messenger Reduction in nitric oxide in vascular system - bad High levels bad in neurones Endothelial nitric oxide Vasoregikatory effects Antiaggregant Antiprolifarative Anti cell adhesion Nitric oxide loss leads to vasoconstriction- platelet aggregation, leukocyte adhesion to endothelial cells, smooth muscle proliferation, key steps to vascular inflammation
46
Inhibiting NOS reduces number of dead cells by NMDA application in cultured cells
[L-NAME] increase can rescue some cells as it is a NOD inhibitor Knock down PSD-95 reduced number of dead neurons following NMDA application Treatment with agent that perturbs PSD95 interactions - inefficient signalling through PSD 95 bound effector molecules by keeping NOS away
47
Treatment of stroke with PSD95 inhibitor in primate brain
Decreased infraction compared to placebo condition Primate - closer to humans
48
N1-A treatment
40% decrease in morbidity Functional independence - 10% increase Good to give to all stroke types - give in ambulance, more likely to survive

Neurodegenerative (8 decks)

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