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45 Cards in this Set

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Two solutions with the same osmolarity
Having the same osmolarity as ECF (300mOsm/L)
*molar concentration x number of dissociable particles
*inversely related to water concentration
*determined largely by Na+ and Cl-
*normal = 300 mOsm/L
*water flows from low osmolarity to high osmolarity
[K+] = 120mM
[Na+] = 15mM
[Cl-] = 20mM
[K+]= 3.5-5.0mM
[Na+]= 135-145mM
[Cl-]= 100-111mM
Action of cardiac glycosides
Competitively inhibit K+ binding on the extracellular side of the Na+/K+ ATPase
(e.g. ouabain, digitalis)
Main functions of the Na+/K+ ATPase
1. Regulate cell volume
2. Establish RMP through K+ and Na+ concentration gradients.
3. Set up Na+ concentration gradient to power secondary active transporters.
Blocking the Na+/K+ ATPase causes...
Cell swelling and lysis: Na+ continues to leak back into the cell and is accompanied by Cl-. The increased osmotic pressure results in an influx of water.
Examples of Na+ powered secondary active transport (3)
1. Na+/glucose symporter in kidney tubules and gut.
2. Na+/amino acid transporter in most cells
3. Na+/Ca++ (3:1) antiporter in cardiac muscle.
Action of digitalis on cardiac tissues
Partially inhibits Na+/K+ ATPase on cardiac myocytes. This reduces the Na+ concentration gradient and thus reduces Na+/Ca++ antiporter action. As a result Ca++ is accumulated in the cell. Increased Ca++ in cytoplasm and SR of cardiac muscle increases contractility.
Equilibrium (for an ion)
When the concentration gradient and electrical gradient are equal but opposite. There is no net flux of the ion.
Nernst equation
E = 58log([X1]/[X2])
The electrical equivalent of permeability which connotes the ease of passage of an ion through a membrane; equal to 1/resistance.
Absolute refractory period (neural)
*No additional AP can be generated regardless of stimulus strength or frequency.
*Occurs because all Na+ channels are either all open already or all inactivated
*lasts from initiation to midway through repolarization
Relative refractory period
*a new AP may be generated with a stimulus of greater strength or frequency
*lasts from midway through repolarization until after hyperpolarization
*enough Na+ channels have lost their inactivation, but it takes more to reach threshold
During an AP, why does Em never reach E-Na?
*Na+ channels are inactivated at a voltage less than E-Na
*K+ channels open at a voltage less than E-Na
*the driving force on Na+ decreases as the electrical gradient lessens
tetrodotoxin (TTX)
*Blocks Na+ channels from the outside
*prevents AP transmission
*can be used to decrease the amplitude of the AP
tetraethylammonium (TEA)
*blocks K+ channels from the inside
*prevents AP transmission
*can be used to increase the duration of an AP
Na+ channel structure
*4 domains (I-IV), each consisting of 6 transmembrane segments (S1-S6)
*voltage-sensor at S4 of each domain
*inactivation plug made from III-IV linker
*channel formed by S5-S6 linker of each domain
Passive electrical properties
*electrotonic - movement of e-
*decrements over distance
*conducts signals along inexcitable membranes
*conducts signals through areas where Na+ channels are blocked
Factors which change nerve conduction velocity
*Increasing the axon diameter decreases the resistance and thus increases velocity
*increasing myelination increases velocity because it insulates against the loss of local current and decreases capacitance
Why are AP's in nerves "all or none"?
Once a depolarizing stimulus has caused a membrane to reach threshold, all available V-gated Na+ channels will open.
Electrical synapses
*very fast
*typically made by gap junctions
*found in cardiac and smooth muscle, and some neurons
Lambert-Eaton Syndrome (LES)
*autoimmune disorder in which autoantibodies attack the presynaptic Ca++ channels
*this results in decreased ACh release
*correlated with small cell cancer of the lung
End plate potential
*the potential that is generated when Na+ enters the motor end plate through ACh-gated channels
*graded response that is directly related to the [ACh]
*electrotonic signal that then depolarizes adjacent membrane enough to cause an AP
Myasthenia gravis
*autoimmune disease where autoantibodies attack ACh receptors on the motor end plate
*treated with ACh-esterases
Used to increase the amount of Ca++ stored in the SR forty-fold
Recruitment of motor units
*occurs by the size principle: the smallest units are recruited first and the largest last
*is a means of increasing the power of a contraction
chemical synapses
*slower than electrical synapses
*may be excitatory or inhibitory
*modulated by NT
repetitive stimulation of a single fiber
*a means of increasing strength of contraction
*involves the stretching of series elastic components (SEC)
*NOT due to increase of [Ca++]
*can lead to summation and tetanus
A fiber is not allowed to return to normal tension before being stimulated again
A fiber reaches maximum tension
excitation-secretion coupling
The sequence of events beginning with the arrival of an AP and ending with the exocytosis of ACh.
*Inhibits ACh-esterase and thus increases [ACh] in the cleft
*can be used to terminate the action of non-depolarizing paralytic agents
*can also be paralyzing thru a depolarizing synaptic blockade
What is the mode of action of curare?
It competes with ACH and prevents it from ginding the ACh receptor, thus keeping it closed. It is a reversible non-depolarizing blocker.
*ACh-R agonist which hold the receptor in the open state
*cause paralysis through chronic depolarization
*Na+ channels are unable to remove their inactivation plugs
Irreversibly binds ACh-R in the closed state.
What are the two main types of neuromuscular blocking agents?
Those that inhibit the opening of the ACh-ion channel and those that hold the ACh-ion channel open.
What would be 3 characteristics of an ideal muscle relaxant?
1.Specificty for the NMJ
2.Rapid onset of action
3.Predictable duration
Curare affects only the ACh channels at the NMJ.
False: It can affect other ACh-mediated channels, this is a cause for ssome of its side effects.
Why must curare be used with caution in patients with renal disease?
It is excreted unmetabolized from the kidney, thus a decrease in renal function can allow accumulation of the active form.
What is a side effect shared by succinylcholine and curare?
They both stimulate release of histamine from mast cells.
How is succinylcholine metabolized?
It is hydrolyzed by a plasma pseudocholinestrase.
How is succinlycholine able to produce cardiac arrhythmias? There are 2 ways.
*prolonged use can lead to hyperkalemia, which can lead to spontaneous depolarization of cardiac muscle cells
*can directly stimulate muscarinic ACh receptors in the sinus node
Can anticholinesterases like neostigmine be used to terminate the action of succinylcholine?
No - actually they would prolong the action of a depolarizing blocker.