Action Potentials and Electrolyte Imbalance Flashcards
action potentials allow nerves to transmit
information through the brain and spinal cord
efferent vs afferent neurons
- efferent: conduct action potentials down a motor nerve resulting in skeletal muscle contraction (myoneural transmission)
- afferent: conduct action potentials from peripheral receptors
what does it mean that an action potential has a stereotypical size and shape ?
a normal action potential for a given cell type looks identical, depolarizes to the same potential and repolarizes back to the same resting potential
what is action potential propagation?
action potential at one site causes depolarization at adjacent sites which can bring those adjacent sites to threshold (nondecremental)
what does it mean that an action potential is an all or nothing response?
- it will either occur or not occur, the stimulus must reach threshold in order for an action potential to occur
what happens if a stimulus is applied during the relative refractory period?
- no action potential will occur
or - it will occur but not have the stereotypical size and shape
what channels must you have in order to maintain resting potential?
Na+/K+ leak channels
what happens during depolarization once an action potential is stimulated?
voltage gated Na+ channels are active once threshold is reached
what happens during the repolarization stage?
voltage gated Na+ channels close and voltage gated K+ channels open
what happens during the hyperpolarization stage?
voltage gated K+ channels are open longer than needed and hyperpolarize the cell below its resting potential
what is used to determine the equilibrium potential of an ion?
Nernst equation
what is Ohm’s law used to calculate?
the relationship between voltage, current and resistance in an electric circuit
what is conductance?
measure of the ability of a material to carry electric current
conductance is inversely related to?
resistance
what is the Ohm’s Law equation?
V=IR
V: voltage difference between membranes
I: current
R: resistance
conduction velocity is determined by
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
what is the formula for the time constant
T= Rm x Cm
Rm: membrane resistance
Cm: membrane capacitance
what happens to the time constant if either the membrane resistance or capacitance is high?
the time constant will increase causing the cell to take a longer amount of time to depolarize or hyperolarize
what is the formula for length constant (lambda)
L = √ Rm/Ri
Rm: membrane resistance
Ri: internal resistance
what would happen to Lambda if there is a high membrane resistance or low internal resistance??
increase in length constant (increase in conduction velocity)
what are the two mechanisms that will help increase conduction velocity?
- increasing nerve diameter
- myelination will increase membrane resistance and decrease membrane capacitance
what causes saltatory conduction?
myelination with nodes of Ranvier
are time and length constants low or high for UNmyelinated axons?
low
what disease can significantly decrease the conduction velocity?
demyelination diseases such as multiple sclerosis
how do lidocaine and procaine (anesthetics) block conductance?
inhibiting voltage gated Na+ channels
what do Tetrodotoxin (TTX) and tetraethyl ammonium block (TEA)?
TTX: blocks voltage gated Na+
TEA: blocks voltage gated K+
potassium balance is done primarily in
the kidneys
hyperkalemia
increase in extracellular blood potassium levels (>5.5 mEq/L)
hypokalemia
decrease in extracellular blood potassium levels (<3.5)
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
what are the major causes for HYPOkalemia due to excess renal loss or GI loss?
- diuretics
- aldosterone excess
- chronic metabolic alkalosis
- vomiting
- diarrhea
what are the major causes for HYPOkalemia due to inter-compartmental shift?
- insulin therapy
- hyperthyroidism
- Beta,2-adrenergic agonist
what is the effect of HYPOkalemia on an action potential?
less likely to hit threshold
what are the clinical symptoms of HYPOkalemia?
- skeletal muscle weakness
- hyporeflexia
- muscle cramping
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
what are the ways HYPERkalemia can occur?
- inter-compartmental shift (ICF to ECF)
- decreased urinary excretion
- increased potassium intake
- renal insufficiency / renal failure
what are the major causes for HYPERkalemia due to inter-compartmental shift?
- excess exercise or trauma
- acidosis
- hypertonicity
- drugs
- beta-blockers
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
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
what are the clinical symptoms of HYPERkalemia?
- skeletal muscle weakness
- hyperreflexia
ca you give someone with hyperkalemia a neuromuscular blocker?
no, must correct high K+ levels first
neural accommodation
failure for potassium to leave the neuron will cause for prolonged cellular depolarization and inactivation of the voltage-gated sodium channels.
calcium balance is primarly done within
the GI tract
hypercalcemic
sodium is less likely to get into the neuron
hypocalcemic
sodium is more likely to get into the neuron
what are the causes of HYPOcalcemia?
- hypoparathyroidism
- Vit D deficiency
- IBS
- hyperphosphatemia
- hypomagnesemia (lowers PTH release)
- alkalosis
what are the clinical symptoms of HYPOcalcemia?
- hyperreflexia
- skeletal muscle tetany
- paresthesia, confusion possible seizures
- carpopedal spasm
- masseter spasm
what happens when you give a person with HYPOcalcemia a neuromuscular blocker?
not predictable but muscle tone is often increased
what are the causes of HYPERcalcemia?
- hyperparathyroidism (increased osteoclast function)
- cancer (malignancy)
- excessive vit D intake
- drugs (diuretics)
what are the clinical symptoms of HYPERcalcemia?
- hyporeflexia
- skeletal muscle weakness (Ca2+ blocks Na+ channels)
what happens when you give a person with HYPERcalcemia a neuromuscular blocker?
not predictable, but muscle tone is often reduced
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
