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physiology
the study of function and integration
fluid compartments in the body
intracellular and extracellular
intracellular fluid
within cells (ex.cytoplasm)
extracellular fluid
outside cells
types of extracellular fluids
interstitial fluid and plasma
what do interstitial fluid and plasma have in common
similar composition
how much of the cell does intracellular fluid take up
2/3
how much of the cell does extracellular fluid take up
1/3
what percentage of total body water does plasma take up
7%
what percentage of total body water does interstitial fluid take up
26%
what percentage of total body water does intracellular fluid take up
67%
dynamic constancy
fluctuation within a normal range
homeostasis
physiological variables in a state of dynamic constancy; not a static
blood sugar feedback loop
meal, blood sugar rises
pancreas receives signal about high glucose, Bcells release insulin
insulin tells fat, muscle cells to store sugar(out of blood, into cells)
decreases blood sugar
shuts off insulin release
labor and delivery feedback loop
baby head pushes on cervix-stimulates release of oxytocin from posterior pituitary
oxytocin binds to receptors on smooth muscle cells of uterine wall-uterus contracts
baby head pushes more
enhancement of original stimulus
what is the cell most permeable to
K+
what is the charge of inside the cell
negative
what is the resting membrane potential
-70mV
what ion does extracellular fluid have a lot of
na+
what do Na+ and K+ pumps do
pumps na+,k+ against their gradients, uses active transport(ATP),
what is pumped out of the cell with the na+/k+ pump
na+
what is pumped in the cell with the na+/k+ pump
k+
K+ and na+ leak channels
always open, ions travel with/down gradient
what is the ration btwn K+ and na+ leak channels
lots of k+ leak channels, few na+ leak channels
what is the movement of na+ and K+ in the leak channels
na+ in and k+ out
K+ and na+ voltage gated channells
ions travel down/with gradient, similar in #, open via voltage,
movement of na+ and K+ in the voltage gated channels
na+ in, and k+ out
why is the cell most permeable to K+
bc there are lots of k+ leak channels in the cell
where is na+ high: inside or outside the cell?
outside
where is K+ high: inside or outside the cell?
inside
where are the ratios of na+ and k+ like this?
bc of the na+/k+ pump
the na/k pump pumps out how many na+ for what amount of K that comes in
3 na+ out for every 2k’ in
what does the 3na’s being pumped out for every 2k going into the cell generate
net negativity in inside of the cell
what creates negative charge on membrane
K+ flows out through leak channels
driving force
willingness of ion to move
what does depolarizing mean
becoming more positive
hyperkalemia
high k+ in blood/extracellualr
what causes hyperkalemia
kidney’s not excreting potassium well
what are the effects of hyperkalemia
depolarizes the cell membrane, prevents repolarization, and prolongs ap duration
hypokalemia
decreased k+ outside of the cell
effects of hypokalemia
hyperpolarizes the cell membrane and shortens ap duration
excitability
how close rmp is to threshold
what does it mean rmp is closer to threshold
cell is more excitable
does na+ have an effect on rmp
no just k+
what are the phases/steps of an action potential
1: rmp, 2: threshold, 3: depolarization, 4: peak, 5: repolarization, 6: hyperpolariztion, 7: rmp
what is the average threshold point
-55 mV
what causes depolarization during action potential
after hits threshold, current through opening voltage gated Na+ channels rapidly depolarize, causing more Na+ channels to open
what happens when a cell reaches its threshold
Na+ channels open, allowing positively charged sodium ions into the cell
what usually causes cell to reach its threshold
na+ flowing into the cell
what happens when the action potential reaches its peak
na+ channels close, voltage gated K+ channles open:k+ out of cell
what happens during repolarization of the cell
outward current through open voltage gated K+ channels: basically caused by K+ leaving the cell
what during hyperpolarization of an action potential
persistent current through slowly closing voltage gated K+ channels, na+ channels fully closed
what happens at the end of action potential
cell returns back to rmp because voltage gated K+ channels close
what causes a steady resting potential at -70mv
K+ leak channels
hyperpolarzing
becoming more negative
grade potentials
hyperpolarzing or depolarizing
mediated via ligand-gated channels
height, magnitude dependent on stimulus strength
decremental: can sum
action potential
depolarizing
mediated via voltage gated channels
heigh, magnitude independent of stimulus strength
non decremental: cannot sum
what effects the spike height of an action potential
the na+
more sodium on the outside of the cell means what for the spike of the ap
it will be higher
more sodium on the inside of the cell means what for the spike on the ap
it will be lower
what happens to the driving force if depolarization occurs
it goes down
what happens to driving force if hyper polarization occurs
it goes up
what happens to driving force if sodium is greater on the outside/ decreased on the inside
it goes up
what happens to driving force if sodium is greater on the inside/ decreased on the outside
it goes down
hypernatremia
increased na+ outside the cell
effects of hypernatremia
no effect on rmp or ap duration
hyponatremia
decreased na+ outside the cell
effects of hyponatremia
no effect on rmp, and no effect on ap duration
what is a synapse
cell to cell junction between two neurons or a neuron and another cell
electrical synapse
uses gap junctions: direct physical connections btwn cells
chemical synapse
uses neurotransmitters into synaptic cleft
steps in chemical transmission
ap probates down pre synaptic neuron
voltage change from ap opens vg Ca2+ channels, ca2+ rushes into presynaptic terminal
ca2+ helps synaptic vesicles fuse w/ pre-synaptic membrane, get release of neurotransmitters into synaptic cleft
neurotransmitters bind to receptors in post synaptic cell membrane.
response in post synaptic cleft(general)
neurotransmitter removed from synaptic cleft
is na+ inhibitory or excitatory
excitatory
excitatory neurotransmitters
make post synaptic cell more positive(depolarize) by opening na+ channels
inhibitory neurotransmitters
make post synaptic cell more negative(hyper polarize) by opening K+ channels
what direction does na+ travel when excitatory neurotransmitters open na+ channels
into the cell
what does na+ moving into the cell when neurotransmitters open na+ channels cause
depolarization and increased likelihood of firing ap
is K+ inhibitory or excitatory
inhibitory
what direction does K+ flow when inhibitory neurotransmitters open up k+ channels
out of the cell, with the gradient
what are the effects of K+ flowing out of the cell when neurotransmitters open K+ channels
hyperpolarization, decreased likelihood of ap firing
ionotropic receptors
receptor and channel, ligand binds-channel opens- ions flow into pot synaptic cell
metabotropic receptors
-receptor and binding of ligand begins 2nd messenger cascade
SSRI’s
selective serotonin reuptake inhibitors- block reuptake protein so that more serotonin stays in the synaptic cleft which causes more post synaptic excitation
what issue does ssri help solve
less serotonin at some synapses
what is the issue when anxiety is occurring
not enough inhibition at Gaba synapse
what does Cl do in anti anxiety meds
it is the ion causing the inhibitory response for neurotransmitter GABA
benzodiazepines
gaba agonists, promote more gaba transmission and get more post synaptic inhibition, anti-anxiety meds
examples of benzodiazepines
xanax, valium
what do local anesthetics do
they prevent the generation of ap(ap inhibition) by blocking voltage gated channels which prevents them from opening in response to na+ depolarization