Mcilwain Material

Front 1

Isosmolar

Back 1

Two solutions with the same osmolarity

Front 2

isotonic

Back 2

Having the same osmolarity as ECF (300mOsm/L)

Front 3

Osmolarity

Back 3

*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

Front 4

Intracellular:
[K+]
[Na+]
[Cl-]

Back 4

[K+] = 120mM
[Na+] = 15mM
[Cl-] = 20mM

Front 5

Extracellular
[K+]
[Na+]
[Cl-]

Back 5

[K+]= 3.5-5.0mM
[Na+]= 135-145mM
[Cl-]= 100-111mM

Front 6

Action of cardiac glycosides

Back 6

Competitively inhibit K+ binding on the extracellular side of the Na+/K+ ATPase
(e.g. ouabain, digitalis)

Front 7

Main functions of the Na+/K+ ATPase

Back 7

1. Regulate cell volume
2. Establish RMP through K+ and Na+ concentration gradients.
3. Set up Na+ concentration gradient to power secondary active transporters.

Front 8

Blocking the Na+/K+ ATPase causes...

Back 8

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.

Front 9

Examples of Na+ powered secondary active transport (3)

Back 9

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.

Front 10

Action of digitalis on cardiac tissues

Back 10

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.

Front 11

Equilibrium (for an ion)

Back 11

When the concentration gradient and electrical gradient are equal but opposite. There is no net flux of the ion.

Front 12

Nernst equation

Back 12

E = 58log([X1]/[X2])

Front 13

conductance

Back 13

The electrical equivalent of permeability which connotes the ease of passage of an ion through a membrane; equal to 1/resistance.

Front 14

Absolute refractory period (neural)

Back 14

*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

Front 15

Relative refractory period

Back 15

*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

Front 16

During an AP, why does Em never reach E-Na?

Back 16

*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

Front 17

tetrodotoxin (TTX)

Back 17

*Blocks Na+ channels from the outside
*prevents AP transmission
*can be used to decrease the amplitude of the AP

Front 18

tetraethylammonium (TEA)

Back 18

*blocks K+ channels from the inside
*prevents AP transmission
*can be used to increase the duration of an AP

Front 19

Na+ channel structure

Back 19

*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

Front 20

Passive electrical properties

Back 20

*electrotonic - movement of e-
*decrements over distance
*conducts signals along inexcitable membranes
*conducts signals through areas where Na+ channels are blocked

Front 21

Factors which change nerve conduction velocity

Back 21

*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

Front 22

Why are AP's in nerves "all or none"?

Back 22

Once a depolarizing stimulus has caused a membrane to reach threshold, all available V-gated Na+ channels will open.

Front 23

Electrical synapses

Back 23

*very fast
*bi-directional
*typically made by gap junctions
*found in cardiac and smooth muscle, and some neurons

Front 24

Lambert-Eaton Syndrome (LES)

Back 24

*autoimmune disorder in which autoantibodies attack the presynaptic Ca++ channels
*this results in decreased ACh release
*correlated with small cell cancer of the lung

Front 25

End plate potential

Back 25

*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

Front 26

Myasthenia gravis

Back 26

*autoimmune disease where autoantibodies attack ACh receptors on the motor end plate
*treated with ACh-esterases

Front 27

calsequestrin

Back 27

Used to increase the amount of Ca++ stored in the SR forty-fold

Front 28

Recruitment of motor units

Back 28

*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

Front 29

chemical synapses

Back 29

*slower than electrical synapses
*unidirectional
*may be excitatory or inhibitory
*modulated by NT

Front 30

repetitive stimulation of a single fiber

Back 30

*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

Front 31

summation

Back 31

A fiber is not allowed to return to normal tension before being stimulated again

Front 32

tetanus

Back 32

A fiber reaches maximum tension

Front 33

excitation-secretion coupling

Back 33

The sequence of events beginning with the arrival of an AP and ending with the exocytosis of ACh.

Front 34

Neostigmine

Back 34

*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

Front 35

What is the mode of action of curare?

Back 35

It competes with ACH and prevents it from ginding the ACh receptor, thus keeping it closed. It is a reversible non-depolarizing blocker.

Front 36

succinylcholine

Back 36

*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

Front 37

alphabungaratoxin

Back 37

Irreversibly binds ACh-R in the closed state.

Front 38

What are the two main types of neuromuscular blocking agents?

Back 38

Those that inhibit the opening of the ACh-ion channel and those that hold the ACh-ion channel open.

Front 39

What would be 3 characteristics of an ideal muscle relaxant?

Back 39

1.Specificty for the NMJ
2.Rapid onset of action
3.Predictable duration

Front 40

T/F:
Curare affects only the ACh channels at the NMJ.

Back 40

False: It can affect other ACh-mediated channels, this is a cause for ssome of its side effects.

Front 41

Why must curare be used with caution in patients with renal disease?

Back 41

It is excreted unmetabolized from the kidney, thus a decrease in renal function can allow accumulation of the active form.

Front 42

What is a side effect shared by succinylcholine and curare?

Back 42

They both stimulate release of histamine from mast cells.

Front 43

How is succinylcholine metabolized?

Back 43

It is hydrolyzed by a plasma pseudocholinestrase.

Front 44

How is succinlycholine able to produce cardiac arrhythmias? There are 2 ways.

Back 44

*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

Front 45

Can anticholinesterases like neostigmine be used to terminate the action of succinylcholine?

Back 45

No - actually they would prolong the action of a depolarizing blocker.