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Human Physiology > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

What are the functional regions of a neuron?

A

Input region: dendrites & soma
Integrative/trigger zone: Initial segment of axon
Conductive region: Axon body
Output region: axon terminal

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2
Q

What are the 2 types of electrical signals?

A
  1. Graded potentials
  2. Action potentials
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3
Q

What is the purpose of a graded signal?

A

Local signals to carry information from input region to trigger zone.

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4
Q

What is the purpose of an action potential?

A

Used for long-distance signals to carry information from trigger zone to axon terminal.

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5
Q

What are electrical signals?

A

Temporary changes in membrane potential due to temporary changes in membrane permeability via gated ion channels.

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6
Q

Electrical signals only change _______?

A

Separation of charge across membrane.

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7
Q

What are the characteristics of graded potentials?

A

-Originate in input region due to opening of gated channels
-Decrease in amplitude as they travel
-Carry information to integrative zone
-Can be excitatory or inhibitory

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8
Q

What does an excitatory signal do?

A

Depolarize the cell to make it easier to produce an action potential.

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9
Q

What does an inhibitory signal do?

A

Hyperpolarize the cell to make it harder to produce an action potential.

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10
Q

What is a receptor potential? Is it excitatory or inhibitory?

A

A receptor potential is a graded potential in the input region of a sensory neuron.
-Always excitatory

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11
Q

What is an EPSP?

A

An excitatory postsynaptic potential is a graded potential in the input region of an interneuron and motor neuron.

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12
Q

What is an IPSP?

A

An inhibitory postsynaptic potential is a graded potential in the input region of an interneuron or motor neuron.

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13
Q

What is an EPP? Is it excitatory or inhibitory?

A

An end-plate potential is an excitatory graded potential in the input region of a skeletal muscle.

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14
Q

How are amplitude & duration graded in a graded potential?

A

-Directly proportional to triggering stimulus
-Conveys information about stimulus amplitude (intensity) & duration

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15
Q

Why do neurons summate graded potentials?

A

A typical neuron receives many inputs which it integrates at the trigger zone to determine whether an action potential is produced.

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16
Q

What is temporal summation?

A

Summation of graded potentials from the same source at different times.

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17
Q

What is spatial summation?

A

Summation of graded potentials from two or more sources

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18
Q

What kind of potenial(s) occur at the trigger zone?

A

Both graded & action

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19
Q

What is the transition from local to long-distance signal?

A

Trigger zone

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20
Q

What are the characteristics of action potentials?

A

-Long-distance signals
-Rapid depolarization followed by repolarization
-Don’t decrease in amplitude as they travel
-All or none
-Don’t summate
-Regenerated

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21
Q

What does it mean to have a graded potential?

A

To have various amplitudes possible

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22
Q

What is a measure of intensity in action potentials?

A

Frequency

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23
Q

How many K+ voltage gates are there? How many states?

A

1 gate, 2 states (closed/resting vs. open)

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24
Q

How many voltage-gated Na+ channels are there? How many states?

A

2 gates: Activation & Inactivation gate
3 states: Closed/resting, open, inactivated

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25
Q

What are the phases/steps of an action potential?

A
  1. Depolarization past threshold (~-55 mV)
  2. Rising phase = Na+ activation gates open rapidly and causes Na+ influx
  3. Falling phase = Other 2 gates transition
    -Na+ inactivation gates closing and
    -K+ channels opening allowing K+ to leave the cell.
  4. Repolarization = all gates begin transitioning to resting state
  5. After-hyperpolarization: K+ channels remain open
  6. K+ channels close –> return to Vrest
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26
Q

How do Na+ voltage-gated channels exhibit positive feedback?

A

As Na+ enters, the cell depolarizes which opens up more Na+ channels.

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27
Q

What is the absolute refractory period?

A

-Impossible to initiate another action potential
-Begins when Vm exceeds threshold
-Ends when some Na+ channels have reset

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28
Q

What is the relative refractory period?

A

-Some Na+ channels have reset
-K+ channels still open
-Action potential possible, but threshold is higher

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29
Q

How does an action potential propagate from trigger zone?

A

-Na+ influx spreads to neighboring region
-Neighboring region reaches threshold to generate a new action potential

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30
Q

Why can’t an action potential travel backwards?

A

Recently active region is refractory which prevents backward propagation

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31
Q

What increases the speed of propagation of an action potential?

A

-Large diameter
-Myelin

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32
Q

How do myelin increase speed of propagation?

A

Insulates axon to conduct signal more effectively

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33
Q

What is saltatory conduction?

A

Myelinated axons have saltatory conduction because voltage gated Na+ and K+ channels are only found at the nodes of Ranvier (gaps in myelin) and re-generate action potentials here.

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34
Q

What are the characteristics of electrical synapses?

A

-Gap junctions
-Synchronize activity
-Rapid, potentially bidirectional signal conduction

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35
Q

What are the characteristics of chemical synapses?

A

-Majority of synapses
-Most NT stored in vesicles & exocytosed due to action potential
-Diffuses across synapse
-Slower, but more flexible & allows amplification

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36
Q

What is the purpose of an action potential in chemical signaling?

A

Open voltage-gated Ca2+ channels that allow vesicles to have exocytosis

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37
Q

What does the amount of neurocrine released depend on?

A

Depends on frequency of action potentials & duration of spike train = graded potentials

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38
Q

What are the major neurocrines of the SNS?

A

-Acetylcholine (ACh)
-Norepinephrine (NE)
-Epinephrine (E)

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39
Q

What are the 2 types of postsynaptic receptors? Define each.

A
  1. Ionotropic = directly-gated receptor-channel
  2. Metabotropic = indirectly-gated GPCR or receptor enzyme
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40
Q

Which postsypantic receptor is fast?

A

Ionotropic

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41
Q

Which postsynaptic receptor is slow?

A

Metabotropic

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42
Q

How can a NT be terminated?

A

-Inactivate
-Reuptake
-Diffuse away

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43
Q

What is sensory transduction?

A

Conversion of stimulus into a graded potential

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44
Q

Are sensory receptors in the PSNS excitatory or inhibitory?

A

-Excitatory in typical senses
-Inhibitory in vision

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45
Q

What anatomy does a sensory receptor consist of?

A

Consist of either:
-Receptive ending of sensory neuron (general senses)
-Receptor cell which releases NT onto sensory neuron (special senses)

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46
Q

What are the types of sensory transduction?

A

-Directly-gated (ionotropic)
- Thermoreceptors
- Mechanoreceptors
-Indirectly-gated (metabotropic)
- Vision
- Olfaction
- Gustation

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47
Q

A somatic motor controls what type of effector muscle?

A

Skeletal

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48
Q

What are the characteristics of somatic motor neurons?

A

-controls skeletal muscle
-mostly voluntary
-A single motor neuron extends from CNS to muscle cell

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49
Q

What is a neuromuscular junction?

A

Synapse between axon terminal of somatic motor neuron & motor end plate of skeletal muscle fiber

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50
Q

What occurs at the neuromuscular junction?

A

Neuronal action potential opens voltage-gated Ca2+ channels and allows exocytosis of Acetylcholine from axon terminal

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51
Q

Where can nicotinic acetylcholine receptors be found at the neuromuscular junction?

A

Skeletal muscle fiber membrane (sarcolemma)

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52
Q

What is the response from Ach release at the neuromuscular junction?

A

Always excitatory - tonic control = signal always “on” with no possibility of inhibition

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53
Q

What kind of receptor is nAChR?

A

Ionotropic: binding of ACh allows ion flow to depolarize the sarcolemma

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54
Q

What kind of potential is an end-plate potential (EPP)?

A

A graded potential - always excitatory

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55
Q

How does EPP potential produce muscle contraction?

A

EPP opens voltage-gated Na+ channels which always produces a sarcolemmal action potential that causes muscle contraction

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56
Q

What is the life cycle of acetylcholine at the neuromuscular junction?

A
  1. ACh made from choline and acetyl coA
  2. In synaptic cleft, ACh broken down by acetylcholinesterase (AChE)
  3. Choline transported back into axon terminal - reused to make ACh
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57
Q

What are the characteristics of visceral motor (autonomic) neurons?

A

-Controls involuntary effectors
-2 motor neurons in series (preganglionic –> postganglionic)
-2 branches: sympathetic & parasympathetic

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58
Q

What kind of control are the SNS and the PSNS under?

A

Antagonistic control: act simultaneously - balance shifts with physiological & mental state

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59
Q

What is autonomic tone?

A

Normal balance between the SNS & PSNS branches

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60
Q

What are the autonomic control centers of the CNS?

A

pons, medulla, hypothalamus

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61
Q

What are the integrated responses of the CNS?

A

autonomic, endocrine, behavioral responses

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62
Q

What is CNS control influenced by?

A

Cerebral cortex & limbic system

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63
Q

Most internal organs are under __________ control.

A

Antagonistic

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64
Q

What is the SNS & PSNS inputs to the pupil of the eye?

A

SNS: dilate
PSNS: constrict

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65
Q

What is the SNS & PSNS inputs to heart rate?

A

SNS: increase (tachycardia)
PSNS: decrease (bradycardia)

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66
Q

What is the SNS & PSNS inputs to the lung bronchioles?

A

SNS: dilate
PSNS: constrict

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67
Q

What is the SNS & PSNS inputs to GI tract motility & secretion?

A

SNS: Decrease
PSNS: increase

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68
Q

What is the SNS & PSNS inputs to the exocrine pancreas?

A

SNS: Decrease secretion
PSNS: Increase secretion

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69
Q

What is the SNS & PSNS inputs to insulin secretion?

A

SNS: Decrease secretion
PSNS: Increase secretion

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70
Q

What are the systems that are only innervated by the sympathetic branch?

A

-Sweat glands
-Smooth muscle of most blood vessels

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71
Q

What NT is secreted by the pre-ganglionic neuron in both the SNS & PSNS?

A

Acetylcholine

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72
Q

What is the type of receptor found on post-ganglionic neurons in both the SNS & PSNS?

A

Nicotinic AChR

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73
Q

What NT does the post-ganglionic neuron of the PSNS secrete?

A

Acetylcholine

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74
Q

What NT does the post-ganglionic neuron of the SNS secrete?

A

Norepinephrine

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75
Q

What is the type of receptor found on target cells of the SNS?

A

Adrenergic receptors

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76
Q

What is the type of receptor found on target cells of the PSNS?

A

Muscarinic

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77
Q

What does the Alpha-1 subtype of adrenergic receptors do?

A

Vasoconstriction

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78
Q

What does the Alpha-2 subtype of adrenergic receptors do?

A

Inhibit digestive system functions

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79
Q

What does the Beta-1 subtype of adrenergic receptors do?

A

Cardiac muscle (excitatory)

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80
Q

What does the Beta-2 subtype of adrenergic receptors do?

A

-Vasodilation
-Bronchodilation

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81
Q

What are varicosities?

A

The end of autonomic postganglionic neurons that store & release NT

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82
Q

What is the life cycle of Norepinephrine at a sympathetic neuroeffector junction?

A

-NE synthesized from Tyrosine & stored in vesicles
-Action potential opens voltage-gated Ca2+ channels and allows exocytosis of NE
-NE can be transported back into varicosity by being repackaged in vesicle or broken down by MAO

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83
Q

What are chromaffin cells?

A

Postganglionic neurons in the sympathoadrenal pathway that release epinephrine into the blood to activate “fight-or-flight” response.

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84
Q

What are autonomic neural reflexes? What are examples?

A

Involve autonomic neurons & effectors (involuntary). Ex: urination, blood pressure, heart rate

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85
Q

What are skeletal muscle reflexes?

A

Involve somatic motor neurons

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86
Q

How does a muscle spindle organ participate in skeletal muscle reflexes?

A

-proprioceptors scattered among contractile muscle fibers that monitor muscle stretch
-when stretched, mechanically-gated channels open and created a graded potential

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87
Q

What is the purpose of the the muscle spindle reflex?

A

Mediated postural corrections in response to unexpected change in muscle stretch

88
Q

What are the 2 efferent pathways involved in skeletal muscle reflexes?

A
  1. Contract agonist: monosynaptic pathway where somatic motor neuron contracts muscle
  2. Relax Antagonist: polysynaptic pathway where inhibitory interneuron inhibits somatic motor neuron of opposing muscle
89
Q

Can motor neurons inhibit skeletal muscles?

A

No, motor neurons tonically control skeletal muscle.
-more excitation = contract
-less excitation = relax

90
Q

What is excitation -contraction coupling?

A

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

91
Q

What are t-tubules? What do they do?

A

Inward extensions of sarcolemma that propagated sarcolemmal action potentials.

92
Q

What is the sarcoplasmic reticulum?

A

Similar to endoplasmic reticulum, sequesters Ca2+ in a muscle cell.

93
Q

What happens after an action potential has propagated a long a t-tubule?

A

The action potential activates the DHP receptor that mechanically opens the ryanodine receptor in the sarcoplasmic reticulum to release Ca2+.

94
Q

What is the contraction cycle?

A

Ca2+ binds to troponin –> moves tropomyosin –> exposes entire binding site on actin –> sliding filaments allow muscle to shorten

95
Q

What are the steps of the contraction cycle?

A
  1. Myosin in resting “cocked” state
  2. Power stroke activated by Ca2+
  3. Enters rigor state
  4. Myosin releases actin
96
Q

What happens when myosin is in the “cocked” phase?

A

-Bound to ADP and Phosphate
-Weakly bound to actin

97
Q

What happens in the power stroke phase?

A

-Myosin bound strongly to actin
-Phosphate released
-Myosin head swivels toward M line

98
Q

What happens in the Rigor state?

A

-Myosin releases ADP
-Myosin strongly bound to actin (stuck until another ATP can come & release myosin)

99
Q

What causes Myosin to release actin?

A

ATP binds to myosin

100
Q

What moves Myosin back to the “cocked” position?

A

ATP hydrolysis

101
Q

What terminates the contraction cycle?

A

Calcium pumped back into SR by Ca2+ ATPase

102
Q

What are the types of skeletal muscle fibers?

A
  1. Type 1 (slow oxidative)
  2. Type 2a (fast oxidative-glycolytic)
  3. Type 2b/x (Fast glycolytic)
103
Q

What are the characteristics of Type 1 skeletal muscle fibers?
Speed:
Myosin ATPase activity:
Diameter:
Endurance:

A

Speed: Slowest
Myosin ATPase activity: slow
Diameter: small
Endurance: fatigue resistance

104
Q

What are the characteristics of Type 1 skeletal muscle fibers?
Metabolism:
Capillary Density:
Mitochondria:
Myoglobin content:

A

Metabolism: Aerobic (uses O2)
Capillary Density: High
Mitochondria: Many
Myoglobin content: High

105
Q

What are the characteristics of Type 2a skeletal muscle fibers?
Speed:
Myosin ATPase activity:
Diameter:
Endurance:

A

Speed: Intermediate
Myosin ATPase activity: Fast
Diameter: Medium
Endurance: Fatigue Resistence

106
Q

What are the characteristics of Type 2b/x skeletal muscle fibers?
Speed:
Myosin ATPase activity:
Diameter:
Endurance:

A

Speed: Fastest
Myosin ATPase activity: Fast
Diameter: Large
Endurance: Easily fatigued

107
Q

What are the characteristics of Type 2a skeletal muscle fibers?
Metabolism:
Capillary Density:
Mitochondria:
Myoglobin content:

A

Metabolism: Intermediate
Capillary Density: Medium
Mitochondria: Moderate
Myoglobin content: Moderate

108
Q

What are the characteristics of Type 2b/x skeletal muscle fibers?
Metabolism:
Capillary Density:
Mitochondria:
Myoglobin content:

A

Metabolism: Anaerobic (uses glycolysis & fermentation)
Capillary Density: Low
Mitochondria: Few
Myoglobin content: Low

109
Q

What type of muscle fibers mostly make up postural muscles?

A

Type 1

110
Q

What type of muscle fibers mostly make up short bursts?

A

Type 2

111
Q

What are the factors influencing force production?

A

-Fiber length
-Summation
-Motor Units

112
Q

How does summation increase force in a muscle?

A

Increased stimulus frequency causes insufficient time to pump Ca2+ back into SR between twitches. The continuing contraction allows more force to be produced.

113
Q

What is tetanus?

A

State of maximal contraction

114
Q

What is unfused tetanus?

A

Relaxes slightly between stimuli

115
Q

What is fused tetanus?

A

Sustained maximal tension

116
Q

What is a motor unit?

A

Somatic motor neuron and all the muscle fibers it innervates.

117
Q

What are the characteristics of motor units?

A

-all muscle fibers in motor units are same type & twitch together
-each muscle fiber only innervated by 1 motor unit

118
Q

A muscle unit with few fibers produces what kind of movement?

A

Fine movements, slow twitch

119
Q

A muscle unit with 1000s of fibers produces what kind of movement?

A

Big movements, fast twitch

120
Q

How do muscles vary force?

A

-Motor unit recruitment
-Frequency coding

121
Q

Which muscles are recruited first and why?

A

Small, slow-twitch muscle units are recruited first while large, fast twitch units are held in reserve because you can wait until you need a lot of force since they are easily fatigued.

122
Q

How does frequency coding vary muscle force?

A

Increase in AP frequency leads to summation which increase the muscle force.

123
Q

What is hypertrophy?

A

Resistance exercise can lead to muscle fibers thickening & getting bigger

124
Q

What is atrophy?

A

Disuse of muscles can lead to the muscle fibers getting thinner & shrinking

125
Q

What are the types of muscle contraction?

A
  1. Isotonic contraction
    1a. Concentric contraction
    1b. Eccentric contraction
  2. Isometric contraction
126
Q

What is isotonic contraction?

A

Any contraction in which the muscle changes length.

127
Q

What is concentric contraction?

A

-Muscle force > external load
-Muscle shortens

128
Q

What is eccentric contraction?

A

-Muscle force < external load
-Muscle lengthens
-Muscle force slows its lengthening (“putting the brakes on gravity”)

129
Q

What is isometric contraction?

A

Muscle contracts but does not change length. Used for posture & supporting objects.

130
Q

Why is the length constant in isometric contractions?

A

The sarcomeres shorten but tendons and elastic tissues around the muscle lengthen.

131
Q

How are cross bridges broken & distorted?

A

Myosin and actin form crossbridges. They want to pull one direction, but the external force is pulling the opposite direction. With each contraction cycle, there is some slippage & distortion to the cross bridges.

132
Q

If you increase the external load, what happens to the velocity of shortening?

A

Decreases

133
Q

If the load is 0, what happens to the velocity of concentric contraction?

A

Maximal

134
Q

If the load is equal to the muscle force, what kind of contraction is prefromed?

A

Isometric

135
Q

What are the causes of excitation in cardiac muscle?

A

-Spontaneous (intrinsic rhythmic)
-Via gap junctions from other cardiac muscle cells

136
Q

How does the autonomic nervous system affect contraction rate & force?

A

Can influence rate to increase or decrease, but can not directly change contraction.

137
Q

What is the mechanism of contraction in cardiac muscle cell?

A
  1. Action potential propagated from adjacent cell
  2. Opens voltage-gated Ca2+ channels in t-tubule
  3. Extracellular Ca2+ enters cytosol
  4. Opens ryanodine receptor on SR
  5. Ca2+ from SR enters cytosol
  6. Ca2+ binds to troponin and moves tropomyosin from binding site
  7. Relaxation: Ca2+ pumped back into SR and out of cell
138
Q

What are the causes of contraction in smooth muscle?

A

-Autonomic neurons
-Hormones & paracrines
-Stretch
-Via gap junctions from other smooth muscle cells
-Spontaneous (rhythmic)

139
Q

What is the mechanism of contraction in smooth muscle?

A
  1. Increased Ca2+ cytosol
  2. Ca2+ binds to calmodulin (CaM)
  3. Ca2+&CaM activate myosin light chain kinase (MLCK)
  4. MLCK phosphorylates myosin
    5.Increases myosin ATPase activity
  5. Contraction cycling
140
Q

The causes of contraction in smooth muscle result in increased cytosolic Ca2+ from where?

A

-SR via IP3 pathway
-ECF via cell membrane channels

141
Q

What are the differences in smooth muscle vs. skeletal muscle?

A
  1. Ca2+ comes from ECF & SR
  2. Action potential not required for Ca2+ release
  3. Ca2+ initiates contraction through cascade & phosphorylation instead of troponin
142
Q

What are the mechanisms of relaxation in smooth muscle?

A

-Myosin light chain phophatase dephosphorylates myosin leading to decreased myosin ATPase activity
-Pump Ca2+ back out of cell & into SR

143
Q

What determines contraction state in smooth muscle?

A

MLCK/ MLCP ratio

144
Q

What are the 2 types of cardiac muscle cells?

A
  1. Autorhythmic cells
  2. Contractile cells
145
Q

What is the pacemaker potential?

A

Unstable membrane potential in autorhythmic cells

146
Q

What are special ion channels?

A

Contribute to the pacemaker potential in autorhythmic cells that open at -60mV and are permeable to both Na+ and K+ to lead to slow depolarization.

147
Q

How does an action potential occur in autorythmic cells?

A
  1. When pacemaker potential reaches threshold, voltage-gated Ca2+ channels open
  2. Depolarizes phase
  3. Delayed closing of Ca2+ channels and opening of voltage-gated K+ channels
  4. Repolarization phase
148
Q

What are the characteristics of autorhythmic cells?

A

-Spontaneously generate AP
-Conduct AP via gap junctions
-Not contractile

149
Q

What are the characteristics of contractile cells?

A

-Conduct AP via gap junctions
-Contractile

150
Q

How are action potentials generated in contractile cells?

A
  1. Depolarized to threshold by adjacent cell via gap junctions
  2. Depolarizing phase: Na+ channels open
  3. Initial repolarizing phase: Na+ channels close & fast K+ channels open
  4. Plateau phase: balance between Ca2+ channels and slow K+ channels
  5. Final repolarizing phase: Ca2+ channels close & slow K+ channels fully open
151
Q

What kind of channels are found in contractile cells?

A

Voltage-gated

151
Q

What kind of channels are found in contractile cells?

A

Voltage-gated

152
Q

Why do cardiac contractile cells have very long refractory periods?

A

No summation of action potentials allows to the heart to relax between contractions.

153
Q

Why is the SA node the pacemaker of the heart compared to other nodes?

A

It has the fastest intrinsic rhtym

154
Q

What is the conduction pathway comprised of and what does it spread to?

A

Comprised of autorhythmic cells that spread to contractile cells

155
Q

What do electrical events trigger?

A

Mechanical events

156
Q

Why is there an AV node delay?

A

Allows ventricles to fill before they contract

157
Q

What do the purkinje fibers coordinate?

A

Contraction of ventricles from apex to base to arteries.

158
Q

What does an ECG/EKG represent? How is it recorded?

A

Reflects electrical activity of the heart recorded from the body surface. It represents summed electrical activity of all heart cells, not a single action potential.

159
Q

What are waves of an EKG?

A

P, Q, R, S, T
-deflections above/below baseline

160
Q

What are segments of an EKG?

A

P-R & S-T
-sections between 2 waves

161
Q

What are intervals of an EKG?

A

PR, QT
-combinations of waves & segments

162
Q

What does the P-wave represent?

A

Atrial depolarization

163
Q

What does the P-R or P-Q segment represent?

A

Atrial contraction

164
Q

What does the QRS complex represent?

A

Ventricular depolarization

165
Q

What does the S-T segment represent?

A

Most of ventricular contraction

166
Q

What does the T-wave represent?

A

Ventricular repolarization

167
Q

What does the T-P segment represent?

A

Heart electrically silent between cycles

168
Q

What is the information provided by an EKG?

A

Heart rate, heart arrhythmias, extra beat, and heart block

169
Q

What is a heart arrhythmia?

A

Fibrillation = disorganized contraction

170
Q

What causes heart block?

A

Conduction through AV node is disrupted

171
Q

In the heart, blood flows from area of ______ pressure to area of ______ pressure.

A

In the heart, blood flows from area of higher pressure to area of lower pressure.

172
Q

What is systole?

A

Contraction / increase in pressure

173
Q

What is diastole?

A

Relaxation / decrease in pressure

174
Q

What are the steps in the mechanical events of the cardiac cycle?

A
  1. Late atrial & ventricular diastole (both atria & ventricles are relaxed)
  2. Atrial systole
  3. Isovolumic ventricular contraction
  4. Ventricular ejection
  5. Isovolumic ventricular relaxation
175
Q

What happens in late atrial & ventricular diastole?

A

-begins when ventricular pressure drops below atrial pressure
-AV valves open
-blood begins to flow into ventricles
-atria fill with blood from veins

176
Q

What happens in atrial systole?

A

-atrial pressure rises
-ventricular diastole ending

177
Q

What is the EDV?

A

End-diastolic volume ~135 mL = volume of blood in either ventricle at end of ventricular diastole

178
Q

What occurs during isovolumic ventricular contraction?

A

-begins when ventricular pressure exceeds atrial pressure
-All 4 valves close
-ventricular pressure increases
-as atria relax, blood begins to flow from veins into atria

179
Q

What occurs during ventricular ejection?

A

-begins when ventricular pressure exceeds pressure in aorta
-semi-lunar valves open & blood flows into arteries

180
Q

What is ESV?

A

End-systolic volume ~65mL = volume of blood in either ventricle at end of ventricular systole

181
Q

What occurs during isovolumic ventricular relaxation?

A

-begins when ventricular pressure drops below pressure in aorta
-All 4 valves are closed
-dicrotic notch due to rebound of blood off closed valves

182
Q

What does Wiggers diagram do?

A

Integrates mechanical & electrical events

183
Q

What occurs at point A?

A

AV valve opens

184
Q

What occurs at point B?

A

SL valve closes

185
Q

What occurs at point C?

A

AV valve closes

186
Q

What occurs at point D?

A

SL valve opens

187
Q

What occurs at point E?

A

Isovolumetric contraction

188
Q

What occurs at point F?

A

Isovolumetric relaxation

189
Q

What is cardiac output?

A

-volume of blood pumped by one ventricle per min
=heart rate x stroke volume

190
Q

What is stroke volume?

A

mL blood pumped by a ventricle per contraction

191
Q

How does the parasympathetic nervous system change HR?

A

PSNS stimulates ACh that binds to mAChR to increase K+ effulx and decrease Ca2+ influx which causes hyperpolarization of the Vm and slows pacemaker depolarization

192
Q

How does the SNS change HR?

A

SNS release NE and Epi that bind to B1 receptor which increase Na+ and Ca2+ influx to depolarize the Vm and speed up pacemaker depolarization

193
Q

What is the equation for stroke volume?

A

SV = EDV - ESV

194
Q

What are the factors affecting stroke volume?

A
  1. Contractility
  2. EDV
  3. Afterload
195
Q

How does contractility affect SV?

A

Catechloamines (NE & Epi) increase contractility which increases the force of contraction.

196
Q

The influence of contractility on SV is an example of what?

A

Positive inotropic effect

197
Q

How do NE & Epi affect contractility?

A

-NE & Epi bind to B1 receptor which stimulates phosphorylation to :
-open Ca2+ channels to increase Ca2+ entry from ECF
-phospholamban to pump Ca2+ into SR
-increased stored Ca2+ leads to stronger contractions

198
Q

How does EDV affect SV?

A

-Frank-Starling Law: stroke volume increases as EDV increases because:
- more blood = more fibers stretch = more forceful contraction

199
Q

What is preload?

A

Degree of stretch in heart fibers

200
Q

What kind of nervous system input affects contractile cells of the heart?

A

Sympathetic

201
Q

What is EDV normally determined by?

A

Venous return = amount of blood entering heart from the veins

202
Q

What factors increase venous return?

A

-Skeletal muscle pump = active skeletal muscles squeeze veins
-Respiratory pump = diaphragm lowers during inspiration which increases abdominal pressure and decreases thoracic pressure
-Venoconstriction

203
Q

How does afterload affect SV?

A

Force a ventricle must overcome in order to eject blood, mainly due to arterial blood pressure

204
Q

What does prolonged high blood pressure cause?

A

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

205
Q

What is the sequence of events for skeletal muscle contraction?

A
  1. ACh binds to receptors on the motor end plate
  2. End plate potentials trigger action potential
  3. T-tubules convey potentials into the interior of the cell
  4. Voltage-gated DHP receptors are activated that open mechanically gated ryanodine receptors
  5. Ca2+ is released from the SR
  6. Ca2+ binds to troponin, pulling on tropomyosin
  7. Binding sites on actin are uncovered, allowing myosin to bind
  8. Tension increases
  9. Ca2+ is pumped back into SR
  10. Tension decreases
206
Q

Starting with a skeletal muscle in the resting state, what is the sequence of events of the contraction cycle?

A
  1. Release of phosphate
  2. Myosin head swivels toward M line
  3. ADP release
  4. Myosin enters rigor state
  5. ATP binds to myosin
  6. Myosin detaches from actin
  7. ATP hydrolysis
  8. Myosin head rotates to “cocked” position
207
Q

What are the states of each gate during the rising phase of a neuronal action potential?

A

-Na+ activation gate = open
-Na+ inactivation gate = open
-K+ gate = closed

208
Q

What are the states of each gate during the falling phase of a neuronal action potential?

A

-Na+ activation gate = open
-Na+ inactivation gate = closed
-K+ gate = open

209
Q

What are the states of each gate during the hyper-polarization/refractory period of a neuronal action potential?

A

-Na+ activation gate = open
-Na+ inactivation gate = closed
-K+ gate = open

210
Q

What are the states of each gate during repolarization of a neuronal action potential?

A

-Na+ activation gate = closed
-Na+ inactivation = open
-K+ gate = closed

211
Q

Describe the generation of an AP in an autorythmic cell.

A
  1. Special channels (If) are leaky for Na+ and K+
  2. Leaky input contributes to pacemaker potential drifting towards threshold
  3. Once it hits threshold, Ca2+ channels open and If channels clause. Ca2+ influx causes cell to depolarize.
  4. Once the AP peaks, K+ channels open and K+ leaves to repolarize the cell.
212
Q

When is the lub heart sound created in the heart?

A

When the AV valves close & blood bounces off of it trying to go back in

213
Q

When is the dub hearted sound created?

A

When the SL valves close

214
Q

What does the crossing of pressure lines in the Wiggers diagram mean?

A

Reversal in pressure gradient

Human Physiology (10 decks)

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