Physio Test 1 - Muscle

Front 1

Sodium levels

Back 1

higher in ECF; lower in ICF (145 vs 15mM)

Front 2

Potassium levels

Back 2

higher in ICF; lower in ICF (4.5 vs 120mM)

Front 3

Calcium levels

Back 3

higher in ECF; lower in ICF (1.2 vs .0001)

Front 4

Chloride levels

Back 4

higher in ECF, lower and variable in ICF

Front 5

Osmolarity

Back 5

290

Front 6

NA-K-ATPase

Back 6

uses energy from hydrolyzing ATP to pump 3 NA out, 2 K into cell. Creates gradients for active transport, RMP, AP

Front 7

Calcium ATPase

Back 7

pumps calcium out of cytoplasm to maintain low intracellular level.

Front 8

PMCA

Back 8

plasma membrane calcium ATPase; high affinity but low capacity

Front 9

SERCA

Back 9

pumps calcium into SR or ER; high affinity and capacity

Front 10

NaCaX

Back 10

Sodium Calcium exchanger (antiporter) pumps Calcium out of cell in exchange for letting sodium in. low affinity but high capacity

Front 11

Resting Membrane Potential

Back 11

Most cells highly permeable to K and less permeable to Na at rest.

Front 12

Polarization or Hyperpolarization

Back 12

negative shift in membrane potential

Front 13

depolarization

Back 13

positive shift in membrane potential (influx of sodium)

Front 14

Action potential

Back 14

transient change in predominant permeability to ions (increase in perm to sodium)

Front 15

Positive feedback loop for activation of voltage-gated Na channels.

Back 15

Local stimulus (depolarization) opens voltage-gated Na channels, causing an influx of Na. This influx causes more depolarization, which makes more Na channels open.

Front 16

Threshold

Back 16

voltage required to get enough Na channels open to initiate positive feedback loop 50% of time.

Front 17

Repolarization

Back 17

Closure of Na channels and opening of voltage-gated K channels to allow more K out of cell (accelerates repolarization)

Front 18

Afterhyperpolarization

Back 18

occurs due to having both leak and voltage-gated K channels open. Greater than usual permeability to K, so membrane potential gets closer to Ek.

Front 19

Absolute Refractory period

Back 19

physically impossible to fire another action potential because Na channels are engaged or inactivated

Front 20

Relative Refractory period

Back 20

When K conductance is elevated and some Na channels still inactivated; higher threshold needed to achieve depolarization.

Front 21

How to increase propagation along axon

Back 21

1. increase axon diameter: this increases electronic conduction and velocity. 2 Myelination: decreases capacitance and increases resistance of membrane, aka keeps more charge moving down axon. Charge dissipates less. Reduces leak of Na into cyto, K out of cyto

Front 22

Nodes of Ranvier

Back 22

unmyelinated sections that have lots of Na channels to give a little extra charge of current, recharge what is lost due to lack of myelin.

Front 23

Na-K-Cl pump

Back 23

uphill influx of K, Cl and downhill influx of Na (symport)

Front 24

local anesthetics

Back 24

block Na channels; so higher stimulus (greater amt of pain) needed

Front 25

key for snare complex activation

Back 25

Ca++ binds synaptotagamin, initiates conformational change

Front 26

Tetanus and Botox

Back 26

inhibit snare complex, prevent release of Ach. paralytics.

Front 27

magnitude of end-plate potential on post-synaptic membrane

Back 27

depends on amt of Ach receptors and amt of Ach released.

Front 28

Myasthenia Gravis

Back 28

autoimmune disease in which body attacks Ach receptors. Fewer receptors = smaller EPP. Subthreshold EPP causes muscle weakness and paralysis.

Front 29

Calcium and muscle contraction

Back 29

skeletal muscle needs intracellular Ca to contract. Smooth/cardiac need extracell.

Front 30

T-tubule activation

Back 30

Have voltage sensor proteins that detect depolarization of action potential. Undergo conformational change, which causes SR (in physical contact) to release Ca. Ca released into cyto, binds troponin.

Front 31

3 troponin proteins

Back 31

TN-I and TN-T block binding sites; TN-C binds Ca.

Front 32

Termination of contraction

Back 32

Ca release is deactivated; Ca is returned to SR by SERCA

Front 33

temporal summation

Back 33

AP leads to a twitch. A rapid series of AP's can cause temporal summation.

Front 34

Strength of contraction

Back 34

based on frequency of stimulation by motor neuron and # of motor units activated.

Front 35

spatial summation

Back 35

CNS controls # of motor units that are stimulated.

Front 36

Type I myosin

Back 36

Slow myosin
Lots of mitochondria, myoglobin
Oxidative production of ATP

Front 37

Type 2a myosin

Back 37

Fatigue-resistant fast-twitch (type IIa)
Faster myosin
Mitochondria, myoglobin, and glycolytic enzymes
Production of ATP by oxidation and glycolysis

Front 38

2b myosin

Back 38

Fastest myosin
Glycolytic enzymes but few mitochondria, no myoglobin
ATP produced by glycolysis