• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/65

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

65 Cards in this Set

  • Front
  • Back
EXCITATORY neurotransmitters do what function
EITHER depolarize or HYPOpolarize the postsynaptic neuron
INHIBITORY neurotransmitters do what function
HYPERpolarize the postsynaptic neuron making it more difficult to propagate an AP
g-proteins do what
either stimulate or inhibit adenylate cyclase to convert ATP into cyclic AMP
what is the major INHIBITORY neurotransmitter in the brain
GABA
GABA does what to neurons
HYPERpolarizes them making them less excitable
GABAa receptors do what
open Cl- channels
activation of GABAa receptors is increased by what
*bzd

*barbs
GABAb receptors do what
act via a second messenger to either open K+ channels or close Ca+ channels
what is the major EXCITATORY neurotransmitter of the brain
GLUTAMATE
glutamate does what function
depolarizes neurons increasing the number of AP generated
what are the 3 major glutamate receptors
*AMPA

*kainate

*NMDA
AMPA and kainate receptors do what
allow Na+ and K+ to pass through channels
NMDA receptors are activated when
neurons are already depolarized and are permeable to Na, K & Ca
activation of NMDA receptors is associated with what
*long-term changes in neuron activity

*learning

*memory
what receptors have been associated with neuron injury after anoxia
GLUTAMATE
the brain consumes what amt of total o2 uptake at rest
20%
approx how much of the energy of cerebral metabolism is used to support the ionic gradients necessary for the electrical activity of the brain
60%
after each AP Na+ and Ca+ are transported how
to the OUTSIDE of the membrane
after each AP K+ and Cl- are transported how
to the INSIDE of the membrane
Name the original thirteen colonies.
Connecticut, Delaware
Georgia,Maryland,
Massachusetts,New Hampshire,
New Jersey, New York,
North Carolina, South Carolina,
Pennsylvania, Rhode Island
Virginia
approx what amt of energy of cerebral metabolism is used to support the normal "housekeeping" fxns of the neurons & glial cells
40%
the brain relies on what substrates
*o2

*glucose
the brain closely couples neuronal activity with what
BLOOD FLOW
cerebral metabolism requires mostly what type of pathway
AEROBIC
with sufficient o2 how many ATP molecules are produced for each glucose molecule metabolized
38
withOUT sufficient o2 how many ATP molecules are produced for each molecule of glucose metabolized
2
the carotid arteries supply what amt of blood flow to the brain
80%
the vertebral arteries supply what amt of blood flow to the brain
20%
the amt of cerebral blood flow (CBF) varies according to what
CEREBRAL METABOLIC RATE (CMR)
CMR is greatest where in the brain
GRAY MATTER
what is normal CBF
~ 50 ml/100 g/min
what is CBF in the GRAY matter
~ 80 ml/100 g/min
what is CBF in the WHITE matter
~ 20 ml/100 g/min
functional impairment occurs at around what CBF
23 ml/100 g/min
evoked potentials and synaptic transmission disappear around what CBF
15 ml/100 g/min
cellular integrity is lost at around what CBF
10 ml/100 g/min
regarding duration of ischemia what time frame and CBF is probably irreversible damage
*longer than 2 hours

*below 12 ml/100 g/min
what is flow metabolism coupling
any change in CMR is rapidly matched by an appropriate change in CBF
what borders on all cerebral vessels
GLIAL CELLS
what are glial cells involved in
control of extracellular K+ concentration in their vicinity
when neurons depolarize what happens to extracellular K+
it INCREASES
what is the MOST potent physiologic determination of CBF
PaCo2
H+ ions cause what to occur with cerebral blood vessels
VASODILATION
CBF reaches a new steady state within how long after a step-change in PaCo2
~ 1 min
CBF increases or decreases what amt for each 1 torr increase/decrease in PaCo2
~ 1 ml/ 100 g/min
changes in CBF r/t PaCo2 are transient and return to normal in approx how long
6-8 hours
when PaO2 is at what level CBF begins to increase
below 60 torr
when PaCo2 reaches what level hypoxemia begins to cause dramatic increases in CBF
below 50 torr
what is autoregulation
maintenence of a constant CBF in the face of changes in perfusion pressure
CBF normally remains constant at what mean arterial pressures (MAP)
50-150
when MAP is out of normal levels CBF becomes what
PRESSURE DEPENDENT-relying on the CPP
what is CPP
MAP-ICP
mean arterial pressures above 150 can do what
disrupt the integrity of the blood brain barrier causing cerebral edema or hemorrhage
mean arterial pressures below 50 can do what
cause cerebral ischemia and reduced energy levels for cellular function
the cerebral autoregulation curve is shifted how with CHRONIC HTN
to the RIGHT
complete loss of autoregulation is common with what pts
*tumors

*AVM's

*ruptured aneurysms

*strokes
cerebral autoregulation is controlled via what factors
*myogenic

*metabolic
what type of cell appears necessary for the maintanence and development of the blood brain barrier
GLIAL cells
what of the endothelial membranes prevent passage of POLAR molecules
LIPID bilayer
what type of substance passes easily through the BBB
LIPID soluble
water moves how across the BBB
FREELY d/t bulk flow
acute HYPERtonicity results in what kind of water movement in the brain
net movement OUT of the brain
acute HYPOtonicity causes what type of movement of water in the brain
net movement INTO the brain
mannitol does what in regards to the brain
causes an increase in tonicity of the plasma causing a sustained decrease in brain water and volume
the blood brain barrier can be disrupted by what factors
*acute HTN *shock
*stroke *tumor
*trauma *radiation
*sz *ischemia