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NSP Exam 2 > Action Potentials and Electrolyte Imbalance > Flashcards

Action Potentials and Electrolyte Imbalance Flashcards

(52 cards)

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1
Q

action potentials allow nerves to transmit

A

information through the brain and spinal cord

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2
Q

efferent vs afferent neurons

A
  • efferent: conduct action potentials down a motor nerve resulting in skeletal muscle contraction (myoneural transmission)
  • afferent: conduct action potentials from peripheral receptors
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3
Q

what does it mean that an action potential has a stereotypical size and shape ?

A

a normal action potential for a given cell type looks identical, depolarizes to the same potential and repolarizes back to the same resting potential

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4
Q

what is action potential propagation?

A

action potential at one site causes depolarization at adjacent sites which can bring those adjacent sites to threshold (nondecremental)

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5
Q

what does it mean that an action potential is an all or nothing response?

A
  • it will either occur or not occur, the stimulus must reach threshold in order for an action potential to occur
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6
Q

what happens if a stimulus is applied during the relative refractory period?

A
  • no action potential will occur
    or
  • it will occur but not have the stereotypical size and shape
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7
Q

what channels must you have in order to maintain resting potential?

A

Na+/K+ leak channels

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8
Q

what happens during depolarization once an action potential is stimulated?

A

voltage gated Na+ channels are active once threshold is reached

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9
Q

what happens during the repolarization stage?

A

voltage gated Na+ channels close and voltage gated K+ channels open

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10
Q

what happens during the hyperpolarization stage?

A

voltage gated K+ channels are open longer than needed and hyperpolarize the cell below its resting potential

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11
Q

what is used to determine the equilibrium potential of an ion?

A

Nernst equation

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12
Q

what is Ohm’s law used to calculate?

A

the relationship between voltage, current and resistance in an electric circuit

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13
Q

what is conductance?

A

measure of the ability of a material to carry electric current

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14
Q

conductance is inversely related to?

A

resistance

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15
Q

what is the Ohm’s Law equation?

A

V=IR

V: voltage difference between membranes
I: current
R: resistance

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16
Q

conduction velocity is determined by

A

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

Tau: how quickly a cell membrane can depolarize
Lambda: how far a depolarizing current will spread down the axon

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17
Q

what is the formula for the time constant

A

T= Rm x Cm

Rm: membrane resistance
Cm: membrane capacitance

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18
Q

what happens to the time constant if either the membrane resistance or capacitance is high?

A

the time constant will increase causing the cell to take a longer amount of time to depolarize or hyperolarize

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19
Q

what is the formula for length constant (lambda)

A

L = √ Rm/Ri

Rm: membrane resistance
Ri: internal resistance

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20
Q

what would happen to Lambda if there is a high membrane resistance or low internal resistance??

A

increase in length constant (increase in conduction velocity)

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21
Q

what are the two mechanisms that will help increase conduction velocity?

Study These Flashcards
A
  1. increasing nerve diameter
  2. myelination will increase membrane resistance and decrease membrane capacitance
22
Q

what causes saltatory conduction?

Study These Flashcards
A

myelination with nodes of Ranvier

23
Q

are time and length constants low or high for UNmyelinated axons?

24
Q

what disease can significantly decrease the conduction velocity?

Study These Flashcards
A

demyelination diseases such as multiple sclerosis

25
how do lidocaine and procaine (anesthetics) block conductance?
inhibiting voltage gated Na+ channels
26
what do Tetrodotoxin (TTX) and tetraethyl ammonium block (TEA)?
TTX: blocks voltage gated Na+ TEA: blocks voltage gated K+
27
potassium balance is done primarily in
the kidneys
28
hyperkalemia
increase in extracellular blood potassium levels (>5.5 mEq/L)
29
hypokalemia
decrease in extracellular blood potassium levels (<3.5)
30
what are the ways HYPOkalemia can occur
- inter-compartmental shift of K+ (from ECF to ICF) - increase in potassium loss through the kidneys or GI tract - inadequate potassium intake
31
what are the major causes for HYPOkalemia due to excess renal loss or GI loss?
- diuretics - aldosterone excess - chronic metabolic alkalosis - vomiting - diarrhea
32
what are the major causes for HYPOkalemia due to inter-compartmental shift?
- insulin therapy - hyperthyroidism - Beta,2-adrenergic agonist
33
what is the effect of HYPOkalemia on an action potential?
less likely to hit threshold
34
what are the clinical symptoms of HYPOkalemia?
- skeletal muscle weakness - hyporeflexia - muscle cramping
35
what is the effect of neuromuscular blockers on a person with hypokalemia ?
they are more sensitive to them because the skeletal muscle is already in a weakened state
36
what are the ways HYPERkalemia can occur?
- inter-compartmental shift (ICF to ECF) - decreased urinary excretion - increased potassium intake * renal insufficiency / renal failure
37
what are the major causes for HYPERkalemia due to inter-compartmental shift?
- excess exercise or trauma - acidosis - hypertonicity - drugs - beta-blockers
38
what are the major causes for HYPERkalemia due to decreased potassium excretion?
- kidney failure or uremia - K+ sparing diuretic - NSAIDs - ACE inhibitors - decrease in aldosterone release
39
what is the effect of HYPERkalemia on an action potential?
no as much stimulus is needed or no action potential can develop due to sodium channels unable to reset
40
what are the clinical symptoms of HYPERkalemia?
- skeletal muscle weakness - hyperreflexia
41
ca you give someone with hyperkalemia a neuromuscular blocker?
no, must correct high K+ levels first
42
neural accommodation
failure for potassium to leave the neuron will cause for prolonged cellular depolarization and inactivation of the voltage-gated sodium channels.
43
calcium balance is primarly done within
the GI tract
44
hypercalcemic
sodium is less likely to get into the neuron
45
hypocalcemic
sodium is more likely to get into the neuron
46
what are the causes of HYPOcalcemia?
- hypoparathyroidism - Vit D deficiency - IBS - hyperphosphatemia - hypomagnesemia (lowers PTH release) - alkalosis
47
what are the clinical symptoms of HYPOcalcemia?
- hyperreflexia - skeletal muscle tetany - paresthesia, confusion possible seizures - carpopedal spasm - masseter spasm
48
what happens when you give a person with HYPOcalcemia a neuromuscular blocker?
not predictable but muscle tone is often increased
49
what are the causes of HYPERcalcemia?
- hyperparathyroidism (increased osteoclast function) - cancer (malignancy) - excessive vit D intake - drugs (diuretics)
50
what are the clinical symptoms of HYPERcalcemia?
- hyporeflexia - skeletal muscle weakness (Ca2+ blocks Na+ channels)
51
what happens when you give a person with HYPERcalcemia a neuromuscular blocker?
not predictable, but muscle tone is often reduced
52
what are the effects of arginine vasopressin (AVP)?
AVP causes water reabsorption in the collecting ducts so - HIGH AVP will significantly LOWER the solute concentrations within the blood - LOW AVP will significantly INCREASE the solute concentrations within the blood

NSP Exam 2 (8 decks)

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