Stroke
Pathology: lack O2, cell death, ILB produced, bind receptors,
intracellular signalling, nuclear factor kappa B, ILB into cell, trascr
factor for IL6 and TNF-a
Craniotomy: surgery for bleed
Crush tablets: cytotoxic inhailed
Sub haemor: nimodipine 60mg 4 days after
High bp: IV nicardipine, labetalol, GTN
Risk bleed: anticoag stop, warfarin INR>1.4 vit k, prothrombin complex
conc, DOAC-> andexanet alfa
What is an ischemic stroke?
more common
80% strokes
blood clot supply disrupted
a clot or plaque is the cause
causing atherosclerosis
Causes of ischaemic stroke
cerebral thrombosis from atherosclerosis (atherosclerosis, fatty deposits causing a
plaque, sticks and becomes a clot in a vessel)
distal embolism from cardioembolic disease (e.g. AF where a clot forms in the heart
and travels to the brain and causes an occlusion)
How do we treat ischaemic stroke?
alteplase
o tissue plasminogen activator
o has a thrombolytic effect
o must be given within 4.5 hr
o otherwise, won’t be as effective
What is a haemorrhagic stroke?
less common
bleeding into the brain
Cause of haemorrhagic stoke
depends on where the bleed is
intracerebral haemorrhage (rupture small vessel in brain)
Subarachnoid haemorrhage (rupture of intracranial aneurysm in the subarachnoid
space, lining of the brain)
How do we treat haemorrhagic stroke?
surgery: craniotomy
repair the blood vessel
clot removal
manage blood pressure:
o reduces blood flow to the brain
o ACE inhibitors
o beta blockers
o lifestyle changes-diet and exercise
What is a TIA?
, transient ischaemic attack
symptoms of stroke that resolve within 24 hours
Pathophysiology behind a stroke
cells are deprived of nutrients and oxygen
leading to cell death and brain damage
umbra: area of irrecoverable damage
penumbra: area of potential recovery
in stroke cytokine interleukin-1Beta is produced
o leads to brain inflammation
o exacerbates the brain damage
o a pro-inflammatory cytokine
Following a stroke:
interleukin 1 beta binds to interleukin 1 receptor on nearby cells
o e.g. endothelial, neural cells
triggers intracellular signalling pathways
including the activation of transcription factor nuclear factor kappa B (NFkB)
This activation prompts the translocation of IL-1β into the cell and ultimately into the
nucleus.
IL-1β acts as a transcription factor, influencing the expression of various genes
involved in inflammation and immune response regulation.
One of the genes activated by IL-1β is that encoding interleukin 6 (IL-6).
IL-6 is a pro-inflammatory cytokine that plays a significant role in the acute phase
response to injury or infection. It promotes inflammation and recruits immune cells
to the site of injury.
further amplifies the inflammatory response within the brain tissue.
IL-1β can also induce the production of tumour necrosis factor-alpha (TNF-α),
another pro-inflammatory cytokine exacerbating a stroke
How do we treat a stroke? Pathophysiology behind treatment
interleukin-1 receptor antagonist
this reduces the infarct volume
o volume or size of the area of tissue in an organ that has undergone infarction
o resulting in tissue death and unoxygenated blood supply to the area
How do we diagnose a stroke?
droopy face, speech, lose power down one side
might not be a stroke that causes these symptoms
but investigate to exclude stroke first
this is a medical emergency
look for other causes
Examples of conditions that can cause a stroke
e.g. seizures
drug toxicity (e.g. overdose)
brain tumour
migraine
spinal cord lesion
Risk factors of stroke
age
o risk doubles with every decade over age 55
Pathology: lack O2, cell death, ILB produced, bind receptors,
intracellular signalling, nuclear factor kappa B, ILB into cell, trascr
factor for IL6 and TNF-a
Craniotomy: surgery for bleed
Crush tablets: cytotoxic inhailed
Sub haemor: nimodipine 60mg 4 days after
High bp: IV nicardipine, labetalol, GTN
Risk bleed: anticoag stop, warfarin INR>1.4 vit k, prothrombin complex
conc, DOAC-> andexanet alfa
What is an ischemic stroke?
more common
80% strokes
blood clot supply disrupted
a clot or plaque is the cause
causing atherosclerosis
Causes of ischaemic stroke
cerebral thrombosis from atherosclerosis (atherosclerosis, fatty deposits causing a
plaque, sticks and becomes a clot in a vessel)
distal embolism from cardioembolic disease (e.g. AF where a clot forms in the heart
and travels to the brain and causes an occlusion)
How do we treat ischaemic stroke?
alteplase
o tissue plasminogen activator
o has a thrombolytic effect
o must be given within 4.5 hr
o otherwise, won’t be as effective
What is a haemorrhagic stroke?
less common
bleeding into the brain
Cause of haemorrhagic stoke
depends on where the bleed is
intracerebral haemorrhage (rupture small vessel in brain)
Subarachnoid haemorrhage (rupture of intracranial aneurysm in the subarachnoid
space, lining of the brain)
How do we treat haemorrhagic stroke?
surgery: craniotomy
repair the blood vessel
clot removal
manage blood pressure:
o reduces blood flow to the brain
o ACE inhibitors
o beta blockers
o lifestyle changes-diet and exercise
What is a TIA?
, transient ischaemic attack
symptoms of stroke that resolve within 24 hours
Pathophysiology behind a stroke
cells are deprived of nutrients and oxygen
leading to cell death and brain damage
umbra: area of irrecoverable damage
penumbra: area of potential recovery
in stroke cytokine interleukin-1Beta is produced
o leads to brain inflammation
o exacerbates the brain damage
o a pro-inflammatory cytokine
Following a stroke:
interleukin 1 beta binds to interleukin 1 receptor on nearby cells
o e.g. endothelial, neural cells
triggers intracellular signalling pathways
including the activation of transcription factor nuclear factor kappa B (NFkB)
This activation prompts the translocation of IL-1β into the cell and ultimately into the
nucleus.
IL-1β acts as a transcription factor, influencing the expression of various genes
involved in inflammation and immune response regulation.
One of the genes activated by IL-1β is that encoding interleukin 6 (IL-6).
IL-6 is a pro-inflammatory cytokine that plays a significant role in the acute phase
response to injury or infection. It promotes inflammation and recruits immune cells
to the site of injury.
further amplifies the inflammatory response within the brain tissue.
IL-1β can also induce the production of tumour necrosis factor-alpha (TNF-α),
another pro-inflammatory cytokine exacerbating a stroke
How do we treat a stroke? Pathophysiology behind treatment
interleukin-1 receptor antagonist
this reduces the infarct volume
o volume or size of the area of tissue in an organ that has undergone infarction
o resulting in tissue death and unoxygenated blood supply to the area
How do we diagnose a stroke?
droopy face, speech, lose power down one side
might not be a stroke that causes these symptoms
but investigate to exclude stroke first
this is a medical emergency
look for other causes
Examples of conditions that can cause a stroke
e.g. seizures
drug toxicity (e.g. overdose)
brain tumour
migraine
spinal cord lesion
Risk factors of stroke
age
o risk doubles with every decade over age 55
