11.3 cellular reactions to cerebral ischaemia Flashcards Preview

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Flashcards in 11.3 cellular reactions to cerebral ischaemia Deck (10)
1

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

2

What are the 3 patterns of cellular injury?

Immediate cell death
Delayed cell death
Late cells death

3

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

4

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

5

When is infarcted tissue vulnerable to secondary neuronal damage?

48-72 hours

6

What causes excitotoxicity?

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

7

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

8

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

9

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

10

What is a non pharmacological treatment for cerebral protection?

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