CNS Flashcards
(96 cards)
two mechanisms of brain death
anaerobic metabolism
deterioration of ion gradients
critical factor in determining neuronal cell fate
ATP depletion
if we decrease blood flow to the brain
we decrease washout of waste products
causes K+ to leave the cell and Na+, Cl+, and Ca++ to come in
Anoxic depolarization
NT important in learning/memory
glutamate
Excititatoy NT, binds with NMDA receptor to allow Ca++ to flow into cell
Glumamate
Excessive glumamate release with ____________
impaired membrane integrity
Glutamate reuptake is dependent on ____________. When repute fails glutamates now _____________.
ATP
Excitotoxic
Excess glutamate release and Open NMDA receptors leads to
Calcium overload
ca++ overload and swell in
cytotoxic edema and swelling
NMDA receptor activation and calcium overload stimulates nitrous oxide production and body cannot clear
reactive nitrogen species
lipid peroxidation causes
injury to the cell membrane and inflammatory response
formation of arachidonic acid leads to MORE free radials and inflammatory mediators
lipid peroxidation
Work- stimulates to bring in new bold flow and carry out wast products
metabolic vasodilation
influenced by pH, CO2 and O2
metabolic vazodilation
cases hyper perfusion and edema
impaired vasoconstriction
Normal ICP
0-15
can occur with vasogenic or cytotoxic (glutamate or Ca++) edema, space occupying lesions, or obstruction/excess production CSF
increased ICP
cytotoxic edema
increased brain TISSUE volume
Vasogenic Edema
Increased brain TISSUE volume
Ischemia and Necrosis
Increased brain TISSUE volume
obstructive and non-obstructie hydrocephalus
Increase CSF volume
Acidosis
Increased BLOOD volume
High arterial PaCO2
Increased BLOOD volume