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E2 NSP > Action Potentials + Electrolyte imbalance > Flashcards

Action Potentials + Electrolyte imbalance Flashcards

1
Q

when are the most voltage gated Na channels open?

A

at the height of depolarization

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2
Q

where in the AP is the K closest to equilibrium?

A

just passed the deepest point in hyperpolarization

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3
Q

neurons are _____ modulated, not ____ modulated

A

frequency
amplitude (height always the same, just the amount it fires changes)

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3
Q

go over the membrane potential chart

A

!!!

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4
Q

why do neurons use a lot of ATP?

A

because of the NA/K ATPase channels that require energy

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5
Q

A somatogram with lines very close and equally spaced is showing:

A

firing potential slowly adapting
no adaptation
(tonic pain receptors, big pain stimulus)

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6
Q

A neuron with stimulus but no AP means?

A

the neuron adapted

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7
Q

what does the somatogram of a adapted neuron look like?

A

fire fire fire, break, fire fire fire

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8
Q

what is a neuron that just keeps firing at a continuous rate called?

A

tonic

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9
Q

what are equilibrium potentials?

A

depending of the charge of the ion tells you its directionality

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10
Q

what is ohms law?

A

calculates relationship between current, resistance and voltage in a circuit

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11
Q

what is the equation for ohms law?

A

V=I*R

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12
Q

what is conductance?

A

ability of a material to carry current (inversely proportional to resistance)

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13
Q

what ensures the AP goes in a unidirectional manner?

A

propagation of AP by local NA current

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14
Q

what determines conduction velocity?

A

length constant (lambda) divided by the time constant (tau)

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15
Q

what is the time constant?

A

the amount of time it takes following injection of current or the potential to change to 63% of its final value

(how quickly the cell membrane can depolarize in response tot an inward current or how quickly it can hyperpolarize in response to outward current)

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15
Q

what is the equation for the time constant?

A

T=RC
(time=resistancecapacitance)

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16
Q

what happens if membrane resistance or capitance is high?

A

time increases

this means it will take longer for cell to de/hyperpolarize (if take longer to depolarize then conduction velocity will decrease)

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17
Q

what is the length constant?

A

distance from the site of current injection where the potential has fallen by 63%

(indicates how far along a depolarizing current will spread down the axon)

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18
Q

what kind of axons have lower internal resistance?

A

bigger ones

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19
Q

what does low time constant high length constant cause?

A

nerve with high conduction velocity

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20
Q

what are the two mechanisms that increase conduction velocity?

A

increasing diameter of nerve
myelinating the nerve

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21
Q

why does myelination increase conduction velocity?

A

increase resistance, decreases the membrane capacitance, decreasing the time constant

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22
Q

what effect do nodes of ranvier have on conduction?

A

cause saltatory conduction (jumping of AP across the non-mylinated portions)

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23
what do non-myelinated axons rely on for conductance?
local current paths that degrade easily to leaky membranes (non M have low time and length constants)
24
why does myelination impact conduction velocity?
dramatically increases the conduction velocity by decreasing the time constant and thus increasing the length constant
25
why does diseases like MS cause muscular problems?
because the axons are less or non myelinated causing the conduction velocity to decrease and action potentials to potentially not propagate down the axon
26
how do anesthetics like lidocaine impact nerves?
block Na conductance by inhibiting the voltage gated Na channels
27
what direction does K, Na and Ca want to travel? (intra/extracellular)
K wants to go out Na, Ca want to go in
28
where is potassium balance mostly done?
kidneys
28
what is hyperkalemia?
INCREASE in extracellular (blood) potassium levels (above 5.5)
29
what is hypokalemia?
DECREASE in extracellular (blood) potassium
30
what happens to concentration gradient with hypokalemia?
increase in concentration gradient (more K will be leaving the cells)
31
what happens to the concentration gradient with hyperkalemia?
decreased concentration gradient (K wants to leave cell less)
32
what are some causes of hypokalemia?
1) intercompartmental shift of K from ECF to ICF 2) increase in K loss (from kidneys) 3) inadequate intake
33
how does hypokalemia impact action potential?
decreasing the resting potential making axons fire LESS, harder to fire, need greater stimulus
34
what are some clinical symptoms of hypokalemia?
skeletal muscle weakness hyporeflexia (low neuronal activity) muscle cramps
35
what effect does hypokalemia have on neuromuscular blocker/skeletal muscle reactants?
increased sensitivity because the muscles are already at a weakened state (these patients will need to be prescribed less)
36
what can cause hyperkalemia?
renal issues (usually the kidneys can handle extra K and just excrete it
37
use of NSAIDs, ace inhibitors, decrease in aldosterone release can cause ______
decreased K excretion
38
what effect does hyperkalemia have on action potential?
moves resting potential closer to threshold allowing action potentials to fire more easily
39
what are some symptoms of hyperkalemia?
hyperreflexia, skeletal muscle weakness if K level exceeds 8
40
how can hyperkalemia be treated?
rid body of K by loop diuretic or dialysis
41
what effect does hyperkalemia have on neuromuscular blocker/skeletal muscle reactants?
DO NOT give a pt NMB or succinylcholine when having hyperkalemia!! must treat` Hyper K first
42
what helps maintain a negative resting membrane potential?
Na/K pump
43
where is Ca balance mostly done?
GI tract
44
in what forms can Ca be found in the blood?
free, ionized, bound to albumin, complexed to together anions
45
how does changes in blood pH impact Ca?
affect degree of Ca binding to albumin increasing or decreasing the ionized Ca content
46
what concentration should Ca be?
8.5-10
47
if hypercalcemic what happens?
Ca less likely to get into neurons
48
if hypocalcemic what happens?
Ca more likely to get into neuron
49
how should hypocalcemia be diagnosed?
at the basis of free, ionized Ca level
50
what are some causes of hypocalcemia?
blood transfusions, alkalosis, vit D deficiency, hypothyroidism
51
what are clinical symptoms of hypocalcemia?
hyperreflexia skeletal muscle tetany infusion, seizures carpopedal spasm (trousseau) masseter spasm (chvostek)
52
what effect does hypocalcemia have on neuromuscular blocker/skeletal muscle reactants?
response not predictable, muscle tone often increased
53
what causes hypercalcemia?
hyperthyroidism, cancer, excessive vit D
54
what organ is responsible for maintenance of ionized calcium?
parathyroid
55
what are the clinical symtoms of hypercalcemia?
hyporeflexia, skeletal muscle weakness (treatment loop diuretic and rehydration)
56
what effect does hypercalcemia have on neuromuscular blocker/skeletal muscle reactants?
often unpredictable, but muscle tone often reduced
57
what is neural accommodation?
because K is responsible for repolarizing the cell, if K doesnt leave the cell the Na channels will be inactivated
58
what effect does Ca have on Na intake in cells?
they oppose each other so if Ca is high in the cells Na cant enter (remember his example with the classroom door)
59
what does AVP do?
water reabsorption in collecting duct (when AVP inc there is more water in the blood lowering the solute concentration)

E2 NSP (8 decks)

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