11.3 cellular reactions to cerebral ischaemia Flashcards Preview

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Flashcards in 11.3 cellular reactions to cerebral ischaemia Deck (10)

What are the 3 broad groups of cerebral ischaemia and what causes each?

Global: cardiac arrest, neonatal borth asphyxia, drowning
Focal: acute stroke and intracerebral hemorrhage
Traumatic brain injury


What are the 3 patterns of cellular injury?

Immediate cell death
Delayed cell death
Late cells death


What causes immediate cell death and what are the consequences?

Due to direct cellular trauma and anoxia. This represents the minimum deficit once the patient has presented - irreversible damage


What causes delayed cell death, where does it occur and what are the consequences?

Due to peri-infarct depolarisations, excitotoxicity and inflammation

Occurs in the penumbra (area surrounding the ischaemic area) causing reduced ATP and glucose utilisation


When is infarcted tissue vulnerable to secondary neuronal damage?

48-72 hours


What causes excitotoxicity?

Increased intracellular Ca causing glutamate to be released binding to NMDA and AMPA channels causing increased post synaptic Ca


What causes pre synaptic depolarisation leading to excitotoxicity?

Failure of pumps and exchange mechanisms allowing Ca in and large amounts of glutamate causing pre and post synaptic depolarisation


What causes inflammation?

Activation of nNOS - membrane damage, protein and DNA damage
Glial cell activition: TNF and IL-1 release, ICAM selectin expression and leukocyte mediated injury
Eicosanoid production: COX2 induction


What are the 3 strategies for cerebral protection?

Increase cerebral oxygen delivery
Reduce cerebral oxygen demand
Improve cellular integrity on the presence of a corrupt supply/demand balance


What is a non pharmacological treatment for cerebral protection?

Hypothermia - best evidence in global ischaemia as it reduces the oxygen consumption