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Physiology > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

what is the main function of the nervous system

A

coordinates body functions

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2
Q

when is nervous system control used

A

when speed or complex integration is required

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3
Q

what kind of specificity does the nervous system have

A

anatomical specificity

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4
Q

what determines target cells of nervous system

A

the “wiring”

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5
Q

what kind of signals is information carried by in the nervous system

A

electrical and chemical

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6
Q

what does the input region of a neuron do

A

receives incoming signals

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7
Q

where is the input region

A

dendrites (and soma)

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8
Q

what is another name for the integrative region

A

the trigger zone

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9
Q

where is the trigger zone located

A

at the axon hillock (initial segment of axon)

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10
Q

what does the trigger zone do

A

combines inputs from different dendrites and the soma

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11
Q

what is the function of the conductive region

A

long-distance propagation

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12
Q

where is the conductive region located

A

axon

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13
Q

what does the output region do

A

transmits signal to the target cell

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14
Q

where is the output region located

A

axon terminal

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15
Q

can the membrane potentials be different at different regions of the cell

A

yes

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16
Q

what are the two types of electrical signal in neurons

A

graded and action potentials

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17
Q

what are graded potentials

A

local signals

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18
Q

what is the purpose of a graded potential

A

to carry information from the input region (transduction site or synapse) to the trigger zone

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19
Q

what is an action potential

A

long distance signal (spikes)

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20
Q

what is the purpose of an action potential

A

to carry information from the trigger zone to the axon terminal

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21
Q

what types of electrical signals can occur at the trigger zone

A

both graded and action potentials

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22
Q

what are electrical signals

A

temporary changes in membrane potential

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23
Q

how does the cell accomplish temporary changes in membrane potential to produce an electrical signal

A

there is a temporary change in membrane permeability (conductance) via gated ion channels

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24
Q

do electrical signals appreciably change ion concentrations

A

no

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25
Q

what do electrical signals change

A

the charge separation across the membrane (membrane potential)

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26
Q

where do graded potentials originate

A

in input region

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27
Q

how do graded potentials start

A

due to opening of gated channels

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28
Q

do graded potentials increase or decrease in amplitude as they travel

A

decrease

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29
Q

where do graded potentials carry information to

A

the integrative region

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30
Q

are graded potentials excitatory or inhibitory

A

can be either depending on ion flow

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31
Q

what happens to a cell with an excitatory graded potential

A

the cell depolarizes

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32
Q

what is the effect on APs when the cell depolarizes

A

it is easier to produce an AP

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33
Q

what happens to the cell with an inhibitory graded potential

A

the cell hyperpolarizes

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34
Q

what is the effect on APs when the cell hyperpolarizes

A

it is harder to produce an AP

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35
Q

what is the graded potential called when it occurs on a sensory neuron

A

a receptor potential

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36
Q

are receptor potentials excitatory or inhibitory

A

always excitatory

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37
Q

what is the graded potential called when it occurs on an interneuron or a motor neuron

A

postsynaptic potential

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38
Q

what are the different types of postsynaptic potentials

A

excitatory (EPSP)
inhibitory (IPSP)

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39
Q

what is the graded potential called when it occurs on a skeletal muscle

A

end-plate potential (EPP)

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40
Q

are end-plate potentials excitatory or inhibitory

A

always excitatory

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41
Q

what two qualities are graded

A

amplitude and duration

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42
Q

what two qualities are directly proportional to triggering stimulus

A

amplitude and duration

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43
Q

what does it mean to ‘summate at the trigger zone’

A

all of the neurons inputs are integrated at the trigger zone to determine whether action potentials are produced

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44
Q

what are the two types of summation

A

temporal and spatial

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45
Q

what is temporal summation

A

summation of graded potentials from the same source at different times

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46
Q

what is spatial summation

A

summation of graded potentials from two or more sources (locations)

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47
Q

what happens is summed activity is subthreshold

A

no AP produced

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48
Q

what happens if summed activity is suprathreshold

A

AP is produced

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49
Q

what type of potentials can occur at the trigger zone

A

both graded and action potentials

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50
Q

where can graded potentials occur on the neuron

A

soma, dendrites, trigger zone

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51
Q

where is the transition from local to long-distance signal

A

at the trigger zone

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52
Q

what kind of signals are APs

A

long-distance signals

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53
Q

where do AP carry information

A

from trigger zone to axon terminal (at synapse)

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54
Q

what happens to the polarization of a cell during an AP

A

rapid depolarization followed by repolarization

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55
Q

do APs increase or decrease in amplitude as they travel

A

neither, they are regenerated

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56
Q

what is the all-or-none part of an AP

A

APs don’t summate and are not graded

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57
Q

what can vary an AP

A

drugs/diseases that alter ion flow

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58
Q

what does the frequency of AP code for

A

stimulus amplitude (intensity)

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59
Q

what does the duration of the spike train of an AP code for

A

stimulus duration

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60
Q

what are action potentials produced by

A

sequential opening and closing of voltage-gated ion channels

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61
Q

what are the two types of ion channels related to APs

A

voltage-gated K+ channels
voltage-gated Na+ channels

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62
Q

what are the two states of the voltage-gated K+ channel

A

closed (resting) and open

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63
Q

what are the states of the voltage-gated Na+ channel

A

closed (resting)
open
inactivated (refractory)

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64
Q

what are the orientations of the activation and inactivation gates in the voltage-gated Na+ channel during the closed (resting ) state

A

activation gate: closed
inactivation gate: open

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65
Q

what are the orientations of the activation and inactivation gates in the voltage-gated Na+ channel during the open state

A

activation gate: open
inactivation gate: open

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66
Q

what are the orientations of the activation and inactivation gates in the voltage-gated Na+ channel during the inactivated (refractory) state

A

activation gate: open
inactivation gate: closed

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67
Q

what is the resting membrane potential

A

-70 mV

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68
Q

what are the steps in the rising phase of the generation of an AP

A
  1. depolarization past the threshold and all 3 gates start to transition
  2. Na+ gates open more rapidly allowing Na+ influx
  3. Na+ influx depolarizes the inside of the cell more
  4. more gates open (positive feedback)
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69
Q

what are the steps in the falling phase of an AP

A
  1. Na+ gates close
  2. K+ channels open
  3. K+ efflux which repolarizes the cell
  4. all 3 gates begin transitioning to resting state
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70
Q

what are the steps in the hyperpolarization phase of an AP

A
  1. K+ channels remain open
  2. cell begins to hyperpolarize
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71
Q

how does the cell return to Vrest after an AP is generated

A

the K+ channels will close

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72
Q

what are the two different refractory periods

A

absolute and relative

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73
Q

is it possible to generate another AP during the absolute refractory period

A

no

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74
Q

is it possible to generate another AP during the relative refractory period

A

AP initiation is possible but the threshold is higher

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75
Q

when does the absolute refractory period begin

A

when Vm exceeds threshold and the AP begins

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76
Q

when does the absolute refractory period end

A

when some Na+ channels have reset

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77
Q

does the relative refractory period come before or after the absolute refractory period

A

after

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78
Q

what are the Na+ and K+ channels doing during the relative refractory period

A

some Na+ channels have reset
K+ channels still open

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79
Q

what are the steps to an AP propagating from the trigger zone

A
  1. Na+ influx spreads to the neighboring region
  2. neighboring region reaches the threshold and a new AP begins
  3. the recently active region is refractory, preventing backward propagation
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80
Q

where do AP propagate to

A

over long distances to the output region

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81
Q

when is the speed of propagation the fastest

A

for axons with a large diameter and myelin

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82
Q

what is the purpose of myelin

A

insulated axon and causes the signal to conduct more effectively

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83
Q

what kind of conduction do myelinated axons have

A

saltatory conduction

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84
Q

what is located at the nodes of Ranvier

A

gaps in myelin with voltage-gated channels

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85
Q

what happens at the nodes of Ranvier

A

the AP is regenerated

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86
Q

what do action potentials convey

A

information to synapses where it is then passed along to the target cell

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87
Q

what are the two types of synapses

A

electrical and chemical

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88
Q

what kind of junctions are electrical synapses

A

gap junctions

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89
Q

what do electrical synapses do to activity

A

synchronize activity

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90
Q

what kind of signal conduction does an electrical synapse have

A

rapid, potentially bidirectional signal conduction

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91
Q

what kind of synapses are the majority of synapses

A

chemical synapses

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92
Q

where are most NT stored

A

in vesicles

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93
Q

how are most NT released

A

they are exocytosed due to an action potential

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94
Q

where does the NT diffuse after it is released

A

diffuses across synaptic cleft

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95
Q

what kind of signal conduction does a chemical synapse have

A

slower but more flexible
allows for amplification

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96
Q

what is the purpose of an AP

A

open voltage gated Ca2+ channels for exocytosis

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97
Q

what is an example of a neurocrine

A

neurotransmitters

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98
Q

what does it mean to say that neurocrine secretion is graded

A

there can be any number of neurotransmitters released

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99
Q

what does the amount of neurocrine released depend on (2 things)

A

frequency of APs
duration of spike train

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100
Q

what are the three major neurocrines of the PNS

A

ACh
norepinephrine
epinephrine

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101
Q

what happens when a NT is released

A

it diffuses across the synaptic cleft and binds to a receptor

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102
Q

what are the two types of postsynaptic receptors

A

ionotropic and metabotropic

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103
Q

how are ionotropic receptors gated

A

directly gated (receptor channel)

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104
Q

what is the speed of an ionotropic receptor

A

fast

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105
Q

how are metabotropic receptors gated

A

indirectly gated (GPCR or receptor enzyme)

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106
Q

what is the speed of a metabotropic receptor

A

slow

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107
Q

what are the two types of postsynaptic responses

A

excitatory (EPSP)
inhibitory (IPSP)

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108
Q

what are the three ways to terminate neurotransmitter activity

A

inactivate
reuptake
diffuse away

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109
Q

what is signal transduction

A

information is conserved at each transduction step (as information changes form)

eg: as information changes from chemical to electrical signals etc, the information is conserved

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110
Q

what is the function of sensory receptors

A

to perform sensory transduction

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111
Q

what is sensory transduction

A

conversion of stimulus into receptor potential (or graded potential)

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112
Q

where is the postsynaptic response excitatory (sensory/afferent) division

A

in most senses

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113
Q

where is the postsynaptic response inhibitory (sensory/afferent) division

A

vision

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114
Q

what does the receptor look like for most general senses (touch, pressure, temp)

A

receptive nerve ending of sensory neuron

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115
Q

what does the receptor look like for most special senses (hearing, vision, taste)

A

a receptor cell
- which then releases NT onto sensory neuron

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116
Q

what are the three sensory transduction types

A
  1. directly gated
  2. indirectly gated
  3. direct depolarization
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117
Q

what type of receptors are directly gated (ionotropic)

A

thermoreceptors
mechanoreceptors

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118
Q

what type of receptors are indirectly gated (metabotropic)

A

vision
olfaction
gustation (bitter, sweet, umami)

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119
Q

how are indirectly gated receptors usually gated

A

by GPCR

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120
Q

how does direct depolarization occur

A

through leakage channels

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121
Q

what type of receptors are stimulated by direct depolarization through leakage channels

A

gustation (salty, sour)

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122
Q

what are the two different motor divisions of the PNS

A

somatic motor
visceral motor

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123
Q

what type of muscle does the somatic motor system control

A

skeletal muscle

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124
Q

is the somatic motor system voluntary or involuntary

A

voluntary

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125
Q

what type of neuron is involved in the somatic motor system

A

single motor neuron

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126
Q

where is a neuron of the somatic motor system found

A

extending from the CNS to a muscle cell

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127
Q

what is a neuromuscular junction

A

the synapse between axon terminal or somatic motor neuron and motor end place of skeletal muscle fiber

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128
Q

what are the two basic steps that occur after a neuronal action potential

A
  1. voltage gated Ca2+ channels open
  2. exocytosis of ACh from axon terminal
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129
Q

what kind of receptors are located in the sarcolemma (skeletal muscle fiber membrane)

A

nicotinic acetylcholine receptors (nAChR)

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130
Q

are nicotinic ACh receptors excitatory or inhibitory

A

excitatory - tonic control

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131
Q

what kind of receptor is a nAChR

A

receptor channel

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132
Q

what are the two steps that occur after the binding of ACh to a nAChR

A
  1. binding of ACh allows ion flow
  2. depolarization of sarcolemma
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133
Q

is the nAChR an ionotropic or metabotropic receptor

A

ionotropic

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134
Q

what kind of potential is an end plate potential (EPP)

A

graded potential

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135
Q

what are the three steps that occur after an EPP is produced

A
  1. voltage gated Na+ channels open
  2. sarcolemmal action potential (always produced)
  3. muscle contraction
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136
Q

what are the four steps in the ACh lifecycle at a neuromuscular junction

A
  1. ACh made from choline and acetyl CoA
  2. ACh broken down by acetylcholinesterase (AChE) in the synaptic cleft
  3. choline is transported back into the axon terminal
  4. choline is reused to make ACh
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137
Q

what kind of effectors are controlled by the visceral motor (autonomic) system

A

involuntary
- cardiac and smooth muscle
- glands

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138
Q

what kind of neuron(s) is involved in the visceral motor system

A

two motor neurons in a series

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139
Q

where are the neurons in the visceral motor system found

A

extending from the CNS to the effector cell

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140
Q

what are the two branches of the visceral motor system

A

sympathetic and parasympathetic

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141
Q

what kind of control do the sympathetic and parasympathetic nervous systems have

A

antagonistic control

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142
Q

what kind of effects do the sympathetic and parasympathetic nervous systems have

A

excitatory and inhibitory

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143
Q

do the EPSP and IPSP work separate or simultaneously in the visceral motor system

A

simultaneously

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144
Q

why do the sympathetic and parasympathetic systems work together

A

to balance shifts with physiological and mental state

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145
Q

what is autonomic tone

A

normal balance between the branches (sympathetic and parasympathetic)

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146
Q

what is the difference between a graded potential and an action potential

A

both are changes in membrane potential but graded potentials can vary in size as opposed to being all-or-none

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147
Q

what are the autonomic control centers of the CNS

A

pons
medulla
hypothalamus

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148
Q

what are the three different types of responses that are integrated under CNS control

A

autonomic
endocrine
behavioral

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149
Q

what are the CNS control responses influenced by (2)

A

cerebral cortex
limbic system

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150
Q

are most internal organs under tonic or antagonistic control

A

antagonistic control

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151
Q

what happens to the pupil under sympathetic and parasympathetic control

A

S: dilates
P: constricts

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152
Q

what happens to the heart under sympathetic and parasympathetic control

A

S: tachycardia (increase)
P: bradycardia (decrease)

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153
Q

what happens to the lung bronchioles under sympathetic and parasympathetic control

A

S: dilate
P: constrict

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154
Q

what happens to the GI tract motility/secretion under sympathetic and parasympathetic control

A

S: decrease
P: increase

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155
Q

what happens to the exocrine pancreas under sympathetic and parasympathetic control

A

S: decrease
P: increase

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156
Q

what happens to insulin secretion under sympathetic and parasympathetic control

A

S: decreases
P: increases

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157
Q

if a system is only innervated by the sympathetic branch, what kind of control is it under

A

tonic

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158
Q

what are the two systems only innervated by the sympathetic branch

A

sweat glands
smooth muscle of most blood vessel

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159
Q

what NT is released by the preganglionic neuron

A

ACh

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160
Q

what kind of receptor is on the post ganglionic neuron

A

nicotinic AChR

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161
Q

what kind of receptor is the nicotinic AChR

A

ionotropic (fast response)

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162
Q

what kind of NT is released at the post ganglionic neuron

A

S: NE
P: ACh

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163
Q

what kind of receptor is on the target/effector

A

S: adrenergic receptors
P: muscarinic AChR

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164
Q

what kind of receptors are the adrenergic and muscarinic receptors

A

GPCR (slow response)

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165
Q

what are the 4 adrenergic receptor subtypes

A

alpha 1
alpha 2
beta 1
beta 2

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166
Q

what is the function of alpha 1 receptors

A

vasoconstriction

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167
Q

what is the function of alpha 2 receptors

A

inhibit digestive system function

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168
Q

what is the function of beta 1 receptors

A

cardiac muscle (excitatory)

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169
Q

what is the function of beta 2 receptors

A

vasodilation
bronchodilation

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170
Q

what do autonomic postganglionic neurons end in

A

varicosities

171
Q

what do varicosities do

A

store and release NT

172
Q

what is NE synthesized from

A

tyrosine

173
Q

where is NE stored

A

in vesicles

174
Q

what are the 3 steps to the release of NE

A
  1. AP
  2. voltage gated Ca2+ channels open
  3. exocytosis of NE
175
Q

after NE is released, where is it transported back into

A

back into varicosity

176
Q

what happens after NE is transported back into the varicosity (2)

A

repackaged in vesicle
broken down by monoamine oxidase (MAO)

177
Q

what is the adrenal medulla an example of

A

a modified sympathetic ganglion

178
Q

what pathway is produced by the adrenal medulla

A

sympathoadrenal pathway

179
Q

what are the postganglionic neurons called in the sympathoadrenal pathway

A

chromaffin cells

180
Q

what do chromaffin cells do

A

release epinephrine into the blood

181
Q

what is epinephrine

A

stress neurohormone that activated “fight or flight” response

182
Q

what receptor is present at the first synapse at all 4 motor pathways

A

nAChR
nicotinic AChR

183
Q

what are the two different types of reflexes

A

autonomic reflexes
skeletal muscle reflexes

184
Q

what do autonomic reflexes involve

A

autonomic neurons and effectors

185
Q

what neurons are involved in skeletal muscle reflexes

A

somatic motor neurons

186
Q

what is the muscle spindle organ

A

proprioceptors scattered among contractile muscle fibers

187
Q

what does the muscle spindle organ monitor

A

muscle length (stretch)

188
Q

what kind of channels are in the muscle spindle organ that produce graded (receptor) potentials

A

mechanically-gated channels

189
Q

what does the muscle spindle (stretch) reflex mediate

A

postural corrections

190
Q

what is the reflex response of the muscle spindle organ due to

A

unexpected changes in length

191
Q

what is an example of a reflex due to the muscle spindle organ

A

patellar reflex

192
Q

what are the two efferent pathways of the muscle spindle organ

A

contract agonist
relax antagonist

193
Q

what kind of pathway is the contract agonist

A

monosynaptic pathway

194
Q

what kind of pathway is the relax antagonist

A

polysynaptic pathway

195
Q

is the relax antagonist excitatory or inhibitory

A

inhibitory interneuron

196
Q

what does it mean to say that motor neurons tonically control skeletal muscle

A

there is no inhibitory, just excitatory

197
Q

what does more excitation of the muscle spindle organ lead to

A

contraction

198
Q

what does less excitation of the muscle spindle organ lead to

A

relaxation

199
Q

where does the EPP (end plate potential) occur

A

at the motor end plate of the sarcolemma

200
Q

what is the sarcolemma

A

membrane of muscle cell

201
Q

what does an EPP cause

A

sarcolemmal action potential

202
Q

what will each AP of the sarcolemma evoke

A

a single twitch

203
Q

what is excitation-contraction coupling

A

the sequence of muscle action potentials and Ca2+ release that initiates contraction

204
Q

where do sarcolemmal AP propagate

A

along t-tubules

205
Q

what are t-tubules

A

inward extensions of sarcolemma

206
Q

what part of the SR are t-tubules associated with

A

terminal cisternae of sarcoplasmic reticulum

207
Q

what does the AP in a skeletal muscle activate

A

the DHP receptor in the t-tubule (voltage-gated)

208
Q

what does the DHP receptor do

A

mechanically opens (directly attached to) the ryanodine receptor (RyR) in sarcoplasmic reticulum

209
Q

what happens when the RyR receptor is opened

A

stored Ca2+ from the SR is released

210
Q

what is a contraction cycle

A

the contraction/relaxation cycle

211
Q

what does Ca2+ bind to to move tropomyosin

A

troponin

212
Q

what happens Ca2+ binds to troponin

A

tropomyosin moves out of the way of the actin binding sites

213
Q

what happens as the actin and myosin filaments slide

A

muscle shortens

214
Q

what is bound to myosin in the resting state

A

ADP and Pi
*weakly bound to actin

215
Q

what is the power stroke activated by

A

Ca2+

216
Q

what causes the myosin head to swivel toward the M line

A

Pi released

217
Q

what causes myosin to enter the rigor state

A

ADP is released

218
Q

what causes myosin to release actin

A

ATP binds to myosin

219
Q

what causes myosin to move back to the “cocked” starting position

A

ATP hydrolysis

220
Q

what are the steps of muscle contraction in skeletal muscle

A
  1. myosin starts in resting state with ADP and Pi bound (weakly bound to actin)
  2. Pi is released and the myosin head swivels toward the M line (strongly bound to actin)
  3. ADP is released and myosin enters rigor state (bound strongly to actin)
  4. ATP binds to myosin (releases actin)
  5. hydrolysis of ATP moves myosin back to resting position (weakly bound to actin)
221
Q

how is the contraction cycle terminated in skeletal muscle

A

Ca2+ is pumped back into the sarcoplasmic reticulum by Ca2+-ATPase

222
Q

what kind of transporter is Ca2+-ATPase

A

uniporter

223
Q

what are the three types of skeletal muscle

A

type 1 - slow oxidative
type 2a - fast oxidative-glycolytic
type 2b - fast glycolytic

224
Q

which type of skeletal muscle is the fastet/slowest

A

fastest: type 2b
slowest: type 1

225
Q

which type of skeletal muscle has the fastest/slowest myosin ATPase activity

A

fastest: type 2a and 2b
slowest: type 1

226
Q

which type of skeletal muscle has the smallest/largest diameter

A

smallest: type 1
largest: type 2b

227
Q

which type of skeletal muscle is the most/least fatigue resistant

A

most: type 1 and 2a
least: type 2b

228
Q

which type of skeletal muscle is aerobic

A

type 1

229
Q

which type of skeletal muscle is anaerobic

A

type 2b

230
Q

which type of skeletal muscle has high/low capillary density, mitochondria, and myoglobin content

A

high: type 1
low: type 2b

231
Q

do muscles have both type 1 and type 2 fibers

A

yes

232
Q

what type of muscle fibers mostly make up postural muscles

A

mostly type 1

233
Q

what type of muscle fibers mostly make up muscles used in short bursts

A

mostly type 2

234
Q

when is the optimal force generated in skeletal muscles

A

with moderate initial fiber length (moderate filament overlap)

235
Q

what can increase force

A

summation

236
Q

what increases to produce summation

A

stimulus frequency

237
Q

what happens when stimulus frequency increases

A

there is insufficient time to pump Ca2+ back into the sarcoplasmic reticulum between twitches

238
Q

what does the continuing contraction do to the series elastic elements

A

allows them to be pulled taut

239
Q

what happens when the series elastic elements are pulled taut

A

more tension (force) is produced

240
Q

what is tetanus

A

state of maximal contraction

241
Q

what is unfused tetanus

A

muscles relax slightly between stimuli

242
Q

what is fused tetanus

A

sustained maximal tension of the muscles

243
Q

what is a motor unit

A

somatic motor neuron and all the muscle fibers it innervates

244
Q

are all the muscle fibers in a motor unit the same type

A

yes

245
Q

how many motor neurons innervate each muscle fiber

A

one

246
Q

what is motor unit force dependent on

A

the number of fibers

247
Q

what kind of movements are produced from MUs with few fibers

A

fine movements, slow twitch

248
Q

what kind of movements are produced from MUs with 1000s of fibers

A

gross movements, fast twitch

249
Q

what are two ways that muscles can vary force

A

MU recruitment
frequency coding

250
Q

what kind of motor unites are recruited first

A

small, slow-twitch units

251
Q

what kind of motor units are held in reserve

A

large, fast twitch units

252
Q

what happens with increased AP frequency

A

summation –> increased force

253
Q

is the adaptive response of muscle reversible or irreversibe

A

reversible

254
Q

what happens with hypertrophy

A

muscle fibers thicken
(increased myosin and actin so more cross bridges can form)

255
Q

what happens with muscle disuse

A

atrophy - muscle fibers get thinner
(body uses energy elsewhere)

256
Q

what is isotonic contraction

A

any contraction in which the muscle changes length

257
Q

what is isotonic contraction used for

A

body movements and moving objects

258
Q

what are the two types of isotonic contraction

A

concentric contraction
eccentric contraction

259
Q

how does the muscle force compare to the load in concentric contraction

A

muscle force is greater than the load

260
Q

what happens to the muscle in concentric contraction

A

muscle shortens

261
Q

how does the muscle force compare to the load in eccentric contraction

A

load is greater than the muscle force

262
Q

what happens to the muscle in eccentric contraction

A

muscle lengthens

263
Q

what does the muscle force do in eccentric contraction

A

slows muscle lengthening

264
Q

what is isometric contraction

A

muscle contracts but does not change length

265
Q

how does the muscle force compare to the load in isometric contraction

A

they are equal

266
Q

what is isometric contraction used for

A

posture and supporting objects

267
Q

why is length constant in isometric contraction

A

the sarcomeres shorten but the series elastic elements (CT) stretch

268
Q

what happens to the velocity of muscle shortening when the load increases

A

the velocity decreases

269
Q

what happens to the velocity when the load=0

A

maximal velocity of concentric contraction

270
Q

what are the two causes of excitation in cardia muscle cells

A

spontaneous (rhythmic)
via gap junctions from other cardiac muscle cells

271
Q

what are the cardiac muscle contraction rate and force influenced by

A

autonomic input

272
Q

where is the AP propagated from in the contraction of a cardiac contractile cell

A

propagated from adjacent cell

273
Q

in cardiac muscle cell, what does the AP result in

A

voltage-gated Ca2+ channels in t-tubule open

274
Q

in cardiac muscle cell, what causes extracellular Ca2+ to enter cytosol

A

voltage gated Ca channels opening

275
Q

in cardiac muscle cell, what is the result of the extracellular Ca entering the cell (cytosol)

A

the RyR on the SR opens

276
Q

in cardiac muscle cell, what happens when the RyR is opened

A

Ca2+ from the SR enters cytosol
(Ca2+ induced Ca2+ release)

277
Q

in cardiac muscle cell, what does the Ca2+ that was released from the SR do

A

binds to troponin

278
Q

how do cardiac muscles relax

A

Ca2+ is pumped back into the SR and out of the cell

279
Q

what are the 5 causes of contraction in smooth muscle

A

autonomic neurons
hormones/paracrines
stretch
via gap junctions from other smooth muscle cells
spontaneous (rhythmic)

280
Q

what does a smooth muscle contraction result in

A

increased cytosolic Ca2+ from
1. SR (IP3 activated receptor)
2. extracellular fluid (cell membrane channels)

281
Q

in smooth muscle, what causes the contraction mechanism to start

A

increased Ca2+ in cytosol

282
Q

in smooth muscle, what does Ca2+ bind to

A

calmodulin (CaM)

283
Q

in smooth muscle, what does Ca2+-CaM activate

A

myosin light chain kinase (MLCK)

284
Q

in smooth muscle, what does MLCK do

A

phosphorylates myosin

285
Q

in smooth muscle, what happens when myosin is phosphorylated

A

myosin ATPase activity increases

286
Q

does smooth muscle contraction use cross bridges like skeletal muscle

A

yes

287
Q

where does Ca2+ come from in smooth muscle

A

extracellular fluid and SR

288
Q

is an AP required for Ca2+ release in smooth muscle

A

no

289
Q

how does Ca2+ initiate smooth muscle contraction

A

through cascade and phosphorylation

290
Q

how does smooth muscle relax

A
  1. myosin light chain phosphatase (MLCP) dephosphorylates myosin
  2. Ca2+ is pumped back out of cell and into SR
291
Q

in smooth muscle, what happens when myosin is dephosphorylated

A

myosin ATPase activity decreases

292
Q

what happens to the cytosolic Ca in smooth muscle when Ca is pumped back into the SR

A

it decreases

293
Q

in smooth muscle, what happens to Ca2+-CaM when Ca2+ is pumped back into the SR

A

Ca unbinds from CaM

294
Q

in smooth muscle, what happens to MLCK activity when Ca is pumped back into the SR

A

it decreases

295
Q

in smooth muscle, what happens to myosin ATPase activity when Ca is pumped back into the SR

A

it decreases

296
Q

in smooth muscle, what determines the contraction rate

A

MLCK/MLCP ratio
(kinase/phosphatase ratio)

297
Q

what are cardiomyocytes

A

cardiac muscle cells

298
Q

what are the two kinds of cardiomyocytes

A

autorhythmic cells (fibers)
contractile cells (fibers)

299
Q

how do autorhythmic cells generate APs

A

spontaneously generate AP

300
Q

how do autorhythmic cells conduct APs

A

via gap junctions

301
Q

are autorhythmic cells contractile

A

no (have no myosin/actin to generate force)

302
Q

how do contractile cells conduct APs

A

via gap junctions

303
Q

what is a pacemaker potential in autorhythmic cells

A

unstable membrane potential (no resting potential)

304
Q

in a pacemaker potential, what kind of channels open at -60mV

A

special ion channels (If)

305
Q

what are If channels permeable to

A

both Na+ and K+

306
Q

does Na+ or K+ movement predominate in an If channel? why?

A

Na+ influx predominates due to stronger driving force

307
Q

does a pacemaker potential have a slow or fast depolarization

A

slow

308
Q

what happens to If channels as they approach threshold

A

the If channels close

309
Q

what triggers an AP in autorhythmic cells

A

the pacemaker potential reaches threshold so the voltage-gated Ca2+ channels open

310
Q

in autorhythmic cell AP, what happens when the Ca2+ channels open

A

depolarization phase of AP

311
Q

in autorhythmic cell AP, what causes the repolarization phase of the AP

A

delayed closing of Ca2+ channels and opening of voltage-gated K+ channels

312
Q

how are contractile cells depolarized to the threshold for an AP

A

by adjacent cells via gap junctions

313
Q

in a contractile cell AP, what causes the depolarizing phase

A

Na+ channels open

314
Q

in a contractile cell AP, what causes the initial repolarizing phase

A

Na+ channels close
fast K+ channels open

315
Q

in a contractile cell AP, what causes the plateau phase

A

balance between Ca2+ channels and slow K+ channels

316
Q

in a contractile cell AP, what causes the final repolarizing phase

A

Ca2+ channels close
slow K+ channels fully open

317
Q

what kind of channels are all of the channels involved in the contractile cell AP

A

voltage-gated

318
Q

what are the 4 phases of contractile cell AP

A
  1. depolarizing phase
  2. initial repolarizing phase
  3. plateau phase
  4. final repolarizing phase
319
Q

what is the length of a cardiac AP compared to neuronal and skeletal muscle AP

A

cardiac AP is very long

320
Q

what part of the cardiac contractile cell AP is long

A

the refractory period

321
Q

what does the long refractory period in a cardiac contractile cell allow for the heart to do

A

relax between contractions

322
Q

can cardiac contractile AP summate

A

no (because of long refractory period)

323
Q

what is the pacemaker of the heart

A

sinoatrial node (SA node)

324
Q

why is the SA node the pacemaker

A

because it has the fastest intrinsic rhythm

325
Q

what is the conduction pathway comprised of

A

autorhythmic cells

326
Q

where do the autorhythmic cells of the conduction pathway spread conduction to

A

contractile cells

327
Q

do electrical or mechanical events come first

A

electrical events trigger and precede mechanical events

328
Q

which node has slower conduction

A

AV node (AV node delay)

329
Q

why is the AV node delay present in the heart

A

to allow the ventricles to fill before they contract

330
Q

what part of the heart contracts first? second? third?

A

apex –> base of heart –> arteries

331
Q

what is the contraction of the heart coordinated by

A

purkinje fibers

332
Q

what does an electrocardiogram reflect

A

the electrical activity of the heart

333
Q

where is the ECG/EKG recorded from

A

the body surface

334
Q

what does the ECG?EKG represent

A

summed electrical activity of all heart cells
(NOT a single AP)

335
Q

what are the three different things that electrical activity is divided into

A

waves
segments
intervals

336
Q

what are the waves of the heart

A

PQRST
deflections above/below baseline

337
Q

what are the segments of the heart

A

P-R, S-T
sections between 2 waves that are zero/electroneutral

338
Q

what are the intervals of the heart

A

PR, QT
combination of waves and segments

339
Q

what does the P wave correspond to

A

atrial depolarization

340
Q

what does the P-R or P-Q segment coorespond to

A

conduction time through AV node and AV bundle
atrial contraction occurs

341
Q

what does the QRS complex coorespond to

A

ventricular depolarization

342
Q

what does the S-T segment correspond to

A

most of the ventricular contraction occurs

343
Q

what does the T wave correspond to

A

ventricular repolarization

344
Q

what does the T-P segment correspond to

A

heart electrically silent between cycles

345
Q

what are four things that are provided by the ECG

A

heart rate
heart arrhythmias
extra beat (PVCs)
heart block

346
Q

what is the heart rate

A

time between 2 P or R waves

347
Q

what is the normal resting heart rate

A

60-100bpm

348
Q

what is tachycardia

A

above normal heart rate

349
Q

what is bradycardia

A

below normal heart rate

350
Q

what is a type of heart arrhythmia

A

fibrillation

351
Q

what is fibrllation

A

disorganized contraction

352
Q

what happens with an extra beat/PVC

A

one part of the conducting circuit fires too early and is out of sync with the rest

353
Q

what happens with a heart block

A

conduction through the AV node is disrupted

354
Q

where does blood flow in correspondence to pressure

A

blood flows from area of higher pressure to area of lower pressure

355
Q

what is systole

A

contraction

356
Q

what is diastole

A

relaxation

357
Q

what does systole do to pressure

A

increases pressure

358
Q

what does diastole do to pressure

A

decreases pressure

359
Q

what are the five stages of the cardiac cycle

A
  1. late atrial and ventricular diastole
  2. atrial systole
  3. isovolumic ventricular contraction (part of ventricular systole)
  4. ventricular ejection (part of ventricular systole)
  5. isovolumic ventricular relaxation (part of ventricular systole)
360
Q

when does the late atrial and ventricular diastole stage begin

A

when ventricular pressure drops below atrial pressure

361
Q

what happens to AV valves during the first step in the cardiac cycle

A

they open

362
Q

where does blood flow in the first step in the cardiac cycle

A

into the ventricles

363
Q

what happens to the atria during the first step in the cardiac cycle

A

the atria fill with blood from the veins

364
Q

what happens to atrial pressure during atrial systole

A

atrial pressure rises

365
Q

what ends during atrial systole

A

ventricular diastole

366
Q

what is the end-diastolic volume (EDV) at the end of ventricular diastole

A

~135mL

367
Q

what does end-diastolic volume mean

A

the volume of blood in either ventricle at the end of ventricular diastole

368
Q

when is there the greatest ventricular volume in the cardiac cycle

A

at the end of atrial systole

369
Q

when does isovolumic ventricular contraction begin

A

when ventricular pressure exceeds atrial pressure

370
Q

what happens to AV valves during step 3 of the cardiac cycle

A

AV valves close

371
Q

when does the first heart sound (lub) occur

A

S1 occurs during isovolumic ventricular contraction (step 3)

372
Q

are all 4 valves open or closed during step 3 of the cardiac cycle

A

closed

373
Q

what happens to the EDV during step 3

A

it continues

374
Q

what happens to the ventricular pressure during step 3 of the cardiac cycle

A

it increases

375
Q

as the atria begin to relax in step 3 of the cardiac cycle, what happens to blood

A

it begins to flow from veins into atria

376
Q

when does ventricular ejection begin

A

when ventricular pressure exceeds pressure in aorta

377
Q

what happens to SL valves and blood when ventricular ejection starts

A

SL valves open and blood flows into arteries

378
Q

does al blood leave ventricles during step 4 of cardiac cycle

A

no

379
Q

what is the end systolic volume (ESV) during ventricular ejection

A

~65mL

380
Q

what is the end systolic volume (ESV)

A

volume of blood in either ventricle at the end of ventricular systole

381
Q

when is the minimum ventricular volume in cardiac cycle

A

at the end of ventricular systole

382
Q

when does the isovolumic ventricular relaxation step of the cardiac cycle begin

A

when ventricular pressure drops below the pressure in the aorta

383
Q

what happens to the SL valves during the 5th step in the cardiac cycle

A

SL valves close

384
Q

when does the second heart sound (dub) occur in the cardiac cycle

A

during step 5 (S2 heart sound)

385
Q

what occurs in the fifth step of the cardiac cycle due to rebound

A

dicrotic notch

386
Q

are the four valves open or closed during the fifth step of the cardiac cycle

A

closed

387
Q

what happens to ESV during isovolumic ventricular relaxation

A

it continues

388
Q

what does wiggers diagram integrate

A

mechanical and electrical events

389
Q

what does the crossing of pressure lines on wiggers diagram indicate

A

reversal in pressure gradient

390
Q

what is cardiac output

A

volume of blood pumped by one ventricle per minute
heart rate x stroke volume

391
Q

what is stroke volume (SV)

A

mL of blood pumped by a ventricle per contraction

392
Q

what is heart rate (HR)

A

number of beats per minute (bpm)

393
Q

what is the average cardiac output (CO) at rest

A

5 L/min

394
Q

what is the average stroke volume (SV) at rest

A

70 mL/beat

395
Q

what is the average heart rate (HR) at rest

A

72bpm

396
Q

what happens to CO if SV or HR change

A

CO will also be affected

397
Q

what can lead to a change in HR (therefore affecting CO)

A

autonomic nervous system can alter heart rate at SA node

398
Q

what are the steps leading to decreased heart rate

A

(parasympathetic NS (dominates at rest))
1. ACh binds to mAChR receptor
2. higher K+ efflux and lower Ca2+ influx
3. hyperpolarizes membrane potential (Vm) of the autorhythmic cells and slows pacemaker depolarization
4. HR decreases

399
Q

what are the steps leading to increased heart rate

A

(sympathetic NS)
1. NE and Epi bind to beta-1 receptor
2. higher Na+ and Ca2+ influx
3. depolarizes membrane potential (Vm) of autorhythmic cells and speed up pacemaker depolarization
4. HR increases

400
Q

what are the three factors that influence stroke volume (SV)

A
  1. contractility
  2. end-diastolic volume (EDV)
  3. afterload
401
Q

what is the stroke volume equation

A

SV= EDV - ESV

402
Q

what is the stroke volume (mL/beat) related to

A

the force of contraction

403
Q

what is contractility

A

intrinsic forcefulness (independent of fiber length) due to Ca2+ interaction with troponin

404
Q

what does end-diastolic volume (EDV) affect (muscular)

A

affects contraction force via muscle fiber length at start of contraction

405
Q

what is afterload

A

force a ventricle must overcome in order to eject blood

406
Q

what will increase contractility (therefore increasing force of contraction)

A

catecholamines (epi and NE)

407
Q

is the increased force of contraction of the heart considered a positive or negative ionotropic effect

A

positive

408
Q

are the contractile cells innervated by the parasympathetic or sympathetic NS

A

sympathetic innervation of contractile cells only

409
Q

when NE and epi bind to a beta-1 receptor, what happens (in reference to contractility)

A

phosphorylation of
1. Ca2+ channels: more Ca2+ entry from extracellular fluid (more Ca2+ entry into the cell)
2. phospholamban: Ca2+ is pumped into the SR faster

410
Q

what happens when phospholamban is phosphorylated

A
  1. Ca2+ is pumped into SR faster
  2. higher stored Ca2+ –> stronger contractions
  3. less Ca2+ - troponin binding time –> briefer contractions
411
Q

what is the frank-starling law

A

stroke volume increases as EDV increases

412
Q

what happens when there is more blood in the heart

A

fibers stretch more and a more forceful contraction occurs

413
Q

what is preload

A

degree of stretch

414
Q

what is EDV normally determined by

A

venous return

415
Q

what is venous return

A

amount of blood entering heart from the veins

416
Q

what three factors increase venous return

A

skeletal muscle pump
respiratory pump
venoconstriction (vasoconstriction of veins)

417
Q

how does the skeletal muscle pump increase venous return

A

active skeletal muscles squeeze veins

418
Q

how does the respiratory pump increase venous return

A
  1. diaphragm lowers during inspiration
  2. increased abdominal pressure and decreased thoracic pressure
419
Q

how does venoconstriction increase venous return

A

from sympathetic innervation of smooth muscle in veins

420
Q

what is afterload

A

force a ventricle must overcome in order to eject blood

421
Q

what is afterload due to

A

arterial blood pressure

422
Q

what does increased afterload lead to

A

decreased stroke volume and increased ESV

423
Q

what can prolonged high blood pressure lead to? why?

A

heart failure because heart is unable to keep pace with body’s demands

Physiology (5 decks)

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