Exam 1 Flashcards

1
Q

Explain the rationale fro studying physiology

A

Knowing the function of underlying mechanisms and how they are integrated into the human body can allow us to become better well rounded clinicians and it provides overlap of other topics such as pharmacology, biochem, immunology etc.

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2
Q

Describe homeostasis and provide examples

A

Homeostasis is a dynamic and responsive ability of the body to respond to stimuli and internal/external changes that allow regulation. BP, kidney intake and release of water, etc.

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3
Q

What is a negative feedback loop, give an example

A

A response loop that can be shut off by counteracting the stimulus causing it. Example—control of blood glucose levels.

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4
Q

What is a positive feedback loop, give examples.

A

A positive feedback loops is a response loop that reinforces the stimulus, sending the variable farther from set point. Ex—blood clotting, child birth, menstrual cycle, digestion, nerve signaling.

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5
Q

What is a feed forward loop? Give example

A

A feed forward loop is a response that helps prepare the body for a stimulus. The salivation response that happens when you see/smell/think of food.

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6
Q

What are the components of a response loop

A

Stimulus-change in internal environment
Sensor- detects environmental change
Input- afferent signal sent to integrating center
Integrating center- receives input signal
Output- efferent signal a message that is sent out
Target- cells, tissues, or organs that receive efferent signal for change
Response- change occurs

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7
Q

Where it cortisol made

A

The adrenal glands

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8
Q

What is cortisol and what does it do

A

Hormone that increases blood glucose, regulates BP, anti inflammatory response.

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9
Q

How does cortisol provide homeostasis

A

It uses negative feedback loops to counter stimuli causing change

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10
Q

How is cortisol related to corticosteroid-based medications and why are corticosteroids prescribed

A

Corticosteroids closely mimic cortisol and they are prescribed to people with inflammatory diseases

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11
Q

Is it better to have dental surgery while your body levels of cortisol are high or low

A

When cortisol is low and there is less stress. Cortisol decreases in the evening when preparing for bed.

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12
Q

What is the difference between osmolarity and tonicity

A

Osmolarity is a measurement of of osmotic pressure (osmol/L) and tonicity is a behavioral/functional term that is used to describe what a solution would do to a cells volume

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13
Q

If a cells volume shrinks, the ECF is?

A

Hypertonic and fluid leaves

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14
Q

If a cells volume swells, the ECF is?

A

Hypotonic and water enters the cell

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15
Q

If there is no change to a cells volume the ECF is?

A

Isotonic

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16
Q

Isosmotic

A

Same number of particles/electrolytes in solutions

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17
Q

Hyperosmotic

A

One solution has more electrolytes that the other

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18
Q

Hyposmotic

A

One solution has less electrolytes than the other

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19
Q

Why Is the osmolarity of a solution not an accurate predictor of its tonicity

A

Because the cell isn’t permeable to all particles and electrolytes

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20
Q

What electrolytes easily penetrate the cell membrane

A

Glucose/dextrose

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21
Q

What will happen to the tonicity of your blood plasma if you drink excessive amounts of “pure” water (no electrolytes)

A

Blood plasma becomes hypotonic

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22
Q

If a solution is .9% saline what is the osmolarity and tonicity

A

Isosmotic and isotonic

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23
Q

If a solution is 5% dextrose in .9% saline (D5) what will the osmolarity and tonicity be?

A

Hyperosmotic and isotonic

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24
Q

If a solution is 5% dextrose in water (D5W) what will the osmolarity and tonicity be?

A

Isosmotic and hypotonic

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25
Q

Ina .45% saline solution (half-normal saline) what will happen to the osmolarity and tonicity?

A

Hyposmotic and hypotonic

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26
Q

In a 5% dextrose in .45% saline (D5 half normal saline) solution what will the osmolarity and tonicity be?

A

Hyperosmotic and hypotonic

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27
Q

If a cell has a higher intracellular fluid concentration of nonpermeable particles/electrolytes than the surrounding extracellular fluid, which way will fluid move? What is the ECF tonicity?

A

Fluid will move in. The ECF is hypotonic relative to ICF

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28
Q

If a cell has a LOWER ICF concentration of non permeable particles/electrolytes than the surrounding ECF, which way will fluid move? What is the ECF tonicity?

A

Fluid will move out. The ECF is hypertonic relative to the ICF

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29
Q

What are the primary divisions of the nervous system

A

CNS and PNS

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30
Q

What are the two basic categories of nervous system cells and their functions

A

Neurons- transmit signals
Glial Cells- support cells. They do transmit signals but they do not depolarize

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31
Q

What is the difference between a neuron and a nerve

A

A neuron is a single cell and a nerve is a compilation of neurons.

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32
Q

What are components of the synaptic cleft

A

Presynaptic axon terminal and postsynaptic dendrite

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33
Q

Where is a signal received from a neuron

A

Dendrite

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34
Q

Synapse

A

The region where an axon terminal communicates with its postsynaptic target cell

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35
Q

Resting potential

A

The difference in electrical charge between the extra and intracellular sides of the neuron membrane. When an axon is not firing. The membrane polarization remains around -70mV

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36
Q

How is resting potential created

A

Extra/intracellular K+ concentration gradient, cell membrane permeability to K+, Na+, and Cl-. Osmotic pressure.

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37
Q

How does resting potential occur

A

Na/K pump carrier proteins move large number of Na out of cell creating the + extracellular charge. Simultaneously the protein moves K+ into the cell cytoplasm. Because more Na is moved out than K in the becomes positive on the outside and negative on the inside

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38
Q

How are nerve impulses transmitted?

A

Action potentials

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39
Q

Action potential

A

Movement of ions across the neurons membrane resulting in rapid depolarization, followed by a repolarization, then a brief hyperpolarization (greater than -70mV), and then a return to RMP.

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40
Q

What is the threshold level for depolarization to occur

A

-55mV

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41
Q

Steps of action potential

A

1)depolarizing stimulus brings RMP to -55mV
2)voltage gated Na+ and K+ channels begin to open
3)rapid Na+ entry depolarizes cell
4)Na+ channels close and slow gated K+ channels open
5)K+ moves from the ICF to ECF
6)K+ channels remain open and additional K+ leaves the cell causing it to hyperpolarize
7)voltages gated K+ channels close, less K+ leaks out of cell
8)cell returns to resting ion permeability and RMP

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42
Q

Absolute refractory period

A

Membrane can’t depolarize again or receive a stimulus (during hyperpolarization)

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43
Q

Relative refractory period

A

Cell can depolarize but b/c of hyperpolarization stimulus needs to be stronger in order for cell to reach threshold.

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44
Q

The resting potential of peripheral and central nervous system neurons can and will vary (I.e. their excitability levels will fluctuate) T/F

A

True. One example is variability from day to day in pain sensitivity

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45
Q

In action potential conduction why does size matter

A

The larger the neuron the quicker the transmission speed

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46
Q

Saltatory conduction

A

The ability of the signal to leap in a neuron because of the myelin insulated segments. Sodium channel opening only occurs periodically at the uninsulated spots (nodes of ranvier)

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47
Q

What area of communication between neurons will be most affected by drugs.

A

The activity in the synaptic cleft

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48
Q

Two types of synapses

A

Chemical or electrical

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49
Q

Electrical synapse

A

Consists of a direct physical connection (gap junction) between two neurons which allows ions to flow from one to the next.

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50
Q

What synapse is the fastest form of communication

A

Electrical

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51
Q

Groups of neurons connected by electrical synapses fire altogether in a synchronized fashion T/F

A

True

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52
Q

Chemical synapses

A

A neuron with a presynaptic ending that contains neurotransmitter filled vesicles meets with a post synaptic neuron ending that contains receptors.

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53
Q

Excitatory post synaptic potential

A

When a neurotransmitter of a presynaptic cell makes the postsynaptic neuron more likely to reach an AP

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54
Q

Inhibitory postsynaptic potential

A

When the neurotransmitter of the presynaptic cell makes the post synaptic cell les likely to reach an AP

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55
Q

Neuroplasticity

A

The variation of neuron signaling intensity due to the amount of neuro transmitter released and the number of receptors available.

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56
Q

Temporal summation

A

Sensory summation that involves the addition of single stimuli over a short period of time. A single presynaptic neuron is responsible for generating the AP by generating subthresholds over a period of time. Less efficient process due to time it takes to generate AP

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57
Q

Spatial Summation

A

Sensory stimulation that involves stimulation of several spatially separated neurons at the same time. Multiple presynaptic neurons are responsible for generating the AP and generating subthresholds. More efficient

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58
Q

Where does the integration of EPSP’s and IPSP’s at an individual synapse occur

A

Axon hillock

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59
Q

What determines the frequency of action potentials carried by the axon

A

Level and Duration of depolarization at the axon hillock

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60
Q

What is a divergent synapse pathway and give an example

A

When one presynaptic neuron branches to affect a larger number of postsynaptic neurons. Pain quality and intensity is interpreted within the CNS when a sensory signal reaches the brain and interconnect with MANY different areas in addition to the sensory homonculus. Or reflex when you touch something hot.

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61
Q

What is convergent synapse pathway and give n example

A

Many presynaptic neurons converge to influence a smaller number of postsynaptic neurons. Part of the reason referred pain occurs is due to multiple primary sensory neurons converging on a single ascending tract.

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62
Q

Two classifications of neurotransmitter receptor

A

Ionotropic and G-coupled receptors

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63
Q

Ionotropic receptor

A

Ligand activated ion channels. These integral carrier proteins span these postsynaptic cell membrane and respond to binding a specific neurotransmitter known as a ligand or molecule/ion.

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64
Q

What happens to Ionotropic receptors when a neurotransmitter binds to them

A

They change shape that creates a small channel opening that only allows a specific ion to flow through

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65
Q

G protein coupled receptor

A

Also known as metabotropic receptors that are secondary signaling receptors.

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66
Q

How does a G-coupled receptor work

A

Neurotransmitters bind to receptor triggering a g-protein pathway. G protein activates one or more other molecules known as secondary messengers. This can open or close channels. Secondary messengers can travel throughout the cell and create a wider range of responses than Ionotropic. Is slower and longer acting (sometimes) than Ionotropic

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67
Q

endocannabinoids

A

Neurotransmitters that do not require a cell membrane receptor.

68
Q

Gasotransmitters

A

Soluble gasses that aren’t stored in a synaptic vesicle and diffuse directly through the cell membrane and act directly on molecules inside cell

69
Q

Norepinephrine

A

GPCR, ANS and CNS. Alertness and arousal. Excitatory and inhibitory functions

70
Q

Dopamine

A

GPCR, CNS. Primarily inhibitory and influences movement, learning, attention and emotion. Reward activity/motivation.

71
Q

Serotonin

A

Ionotropic and GPCR. CNS. Primarily inhibitory but regulates anxiety, appetite, mood, sleep cycle and body temp. Involved in circadian rythmicity and neuroendocrine function.

72
Q

Histamine

A

GPCR, CNS. Primarily excitatory. Increases wakefulness, stomach acid production, and itchiness, decreases hunger.

73
Q

GABA

A

Ionotropic and GPCR. CNS. Major inhibitory functions like decrease of muscle tone and anxiety, increases relaxation and sedation. Improves focus

74
Q

Glutamate

A

Ionotropic and GPCR. CNS. Major excitatory functions and involved with learning and memory

75
Q

“Work” performed by the body specifically by contraction

A

Pumping blood, moving food through digestive tract, moving the body, absorbing shock and distributing loads.

76
Q

What percentage of the total body weight that is muscle

A

40-50%

77
Q

How much skeletal muscle mass is lost between ages of 30-50. And then by age 80

A

An estimated 10%. 40% by 80

78
Q

Three types of muscular tissue

A

Skeletal, cardiac, smooth

79
Q

Skeletal muscle

A

Attaches to bone, skin or fascia. Striated with light and dark bands visible microscopically. Voluntary control of contraction and relaxation. Strong and quick.

80
Q

Cardiac muscle

A

Striated in appearance. Involuntary control. Autorythmic because of built in pacemaker. Strong and quick.

81
Q

Smooth muscle

A

Nonstriated in appearance, involuntary control, strong in general but slow in most cases.

82
Q

Which type of muscle store and move substance

A

Cardiac, smooth, and skeletal (sphincters, venous and lymph flow)

83
Q

Example of involuntary skeletal muscle contraction

A

Shivering

84
Q

What type of muscle produce heat

A

Skeletal muscles

85
Q

Contractility

A

Ability to develop tension in response to a chemical and or electrical stimulus. This enables movement of structures to which the muscles are attached.

86
Q

Electrical excitability

A

Like a neuron, muscle can conduct or transmit electrical impulses.

87
Q

Extensibility

A

Ability to stretch

88
Q

Elasticity

A

Ability to return to normal resting length. Retractility or recoil.

89
Q

Tenosynovitis/tendonitis

A

Inflammation due to overuse or strain.

90
Q

Strains

A

Contractile tissue injuries

91
Q

Wear do tears most often occur

A

Myotendinous junction

92
Q

What is tendinitis or teninopathy

A

Tendon is abnormal and can’t handle stress. Chronic degenerative changes in the tissue w out inflammation

93
Q

Sarcolemma

A

Muscle fiber/cell membrane

94
Q

Endomysium

A

Surrounds the individual muscle fibers and insulates the individual cells form one another. Rich in capillaries.

95
Q

Perimysium

A

Ensheathes muscle fiber cells to form fascicles (bundles of muscle fibers). Penetrated by neurovascular bundles

96
Q

Epimysium

A

Wraps around the entire gross structure of a muscle (bundles of fascicles). Send septa inward (contains neurovascular bundles)

97
Q

“Bundles of bundles”

A

That each subsequent layer of muscle connective tissue is tougher and thicker than the previous one.

98
Q

Are endomysium and sarcolemma the same?

A

NO. Sarcolemma is the cell membrane. Endomysium covers outside of muscle cell.

99
Q

What are the pros and cons of a neurovascular bundle

A

Efficiency is pro. But if the area gets damage both structures are at risk.

100
Q

Somatic motor neurons

A

Nerve cells within the peripheral nerve found in the neurovascular bundle that connect the nervous system to the muscle cell

101
Q

Myogenesis

A

Multiple mesodermal stem cells fusing together to form a muscle fiber in utero.

102
Q

What cells remain to help with trauma in skeletal muscle

A

Myoblasts (satellite cells)

103
Q

Myofibril

A

Structural and functional subunit of a muscle fiber. Composed of organized bundles of myofilaments that extend the entire length of the cell.

104
Q

Sarcoplasmic reticulum

A

Fluid filled system of membranous sacs (sER) encircling each myofibril within the muscle fiber. Stores Ca2+ until needed.

105
Q

Transverse tubules

A

Invaginations of sarcolemma into the cell that rapidly convey action potentials to all myofibrils inside the muscle fiber.

106
Q

What fluid is in the T tubules

A

Extracellular

107
Q

Basic contractile component of a myofibril

A

Sarcomere

108
Q

What happens when a muscle contraction occurs (to bands and zones)

A

Z discs-move closer together
I bands- shrink
H zone- narrows
A band- does not change

109
Q

What proteins make up a myofibril

A

Contractile-actin and myosin
Regulatory- tropomyosin and troponin
Structural- titi, nebulin, alpha actin, myomesin, dystrophin

110
Q

Titin

A

Anchors thick filaments to Z line, its elasticity prevents excessive stretch of sarcomere/helps sarcomere return to resting length.

111
Q

Nebulin

A

Aligns thin filaments

112
Q

Alpha actin

A

Bundles thin filaments into parallel arrays and anchors them at Z line

113
Q

Myosin

A

Holds thick filaments in place at M-line

114
Q

Dystrophin

A

Absence is associated with ms cell death due to membrane ruptures—resulting in progressive weakness (muscular dystrophy)

115
Q

List components of a muscle from smallest to largest

A

Sarcomere, myofibril, fiber, fascicle.

116
Q

When a joint is immobilized for healing what do you think happens to the microstructure of those muscles?

A

Function decreases due to atrophy and stability decreases.

117
Q

The NMJ consists of

A

Synapse, synaptic cleft, neurotransmitter, axon terminal (synaptic end bulb, synaptic vesicles, ACh), motor end plate

118
Q

One neuron innervates multiple muscle fibers. T/F

A

T. The number 0n muscle fibers interacted varies based on need for fine motor control.

119
Q

Steps of nerve impulse at NMJ

A

1-release of ACh
2-opening of ACh gated sodium channels
3-production of muscle cell AP (influx Na+ an other ions from ECF to ICF)
4-closing of ACh gated channels (Na+ low and K+ high) ACh is broken down by acetylcholinesterase.
ACh has to be removed for contraction to end

120
Q

Difference between myasthenia gravis and Bell’s palsy

A

MG is an autoimmune disease that causes progressive damage to the NMJ causing early on muscle fatigue and progressive weakness and muscle atrophy (ACh can’t bind or be released) Bell’s palsy is compression of facial nerve which impairs the ability of nerve to propagate an AP. ACh can’t get past compression to cause AP but once compression resolves it can.

121
Q

Botulinum

A

“Miracle poison” that blocks ACh release form efferent motor neuron synaptic end bulb this preventing muscle contraction.

122
Q

How many contractions can occur from ATP storage in a muscle cell

A

5-8

123
Q

What is a back up energy source to ATP

A

Phosphocreatine. Contains high energy phosphate bonds and transfers phosphate to ADP via creatine kinase enzyme

124
Q

How many ATP does glycolysis produce

A

About 30

125
Q

How many ATP does anaerobic glycolysis produce

A

About 2

126
Q

What is ATP required for

A

1-cross bridge formation and release (myofilament sliding)
2-active pump of calcium ions from sarcoplasm back into SR
3-sodium-potassium pump to restore muscle fiber membrane potential.

127
Q

Type I muscle fibers

A

Slow oxidative or “slow twitch” red muscle fibers. High resistance to fatigue, high # mitochondria, aerobic respiration. Slow use of ATP, red in color and low force production.

128
Q

Type II A muscle fibers

A

Fast oxidative-glycolytic (FOG) or “intermediate twitch”. Pinkish in color moderate # mitochondria and resistance to fatigue. Anaerobic and aerobic respiration. Fast Rae of ATP use, fast contraction velocity and high force production.

129
Q

Type II X

A

Fast glycolysis (FG) or fast twitch fibers. Low number mito, low resistance to fatigue. Anaerobic respiration. Fastest rate of ATP use and contraction velocity. High force production and white in color

130
Q

Your patient has a genetic disorder that causes their skeletal muscle mitochondria to be under produced and or abnormal. Which of the following problems would you expect this patient to have

A

Muscle fatigue/loss of endurance and muscle weakness.

131
Q

What muscle fibers are affected with age

A

Type I and II A decrease in muscle mass with age. There is a preferential loss of type II fibers (power/strength versus endurance)

132
Q

How and or why do we get stronger with resistance exercises

A

Neural adaptations at around 2 weeks cause improved synchrony of muscle cells, more ACh production/ release, GTO sensory feedback is down modulated. This reflex normally inhibits muscle contraction to prevent injury/tearing of tissues.

133
Q

Muscle spindle reflex

A

also deep tendon reflex. Afferent NS initiated. Receptors w/in muscle cells sense quick stretch of muscle cel fibers due to tendon tap and send afferent signal to SC. SC will immediately send efferent signal to muscle fiber to contract and counteract stretch. Descending inhibition moderates response to make it less hyperactive.

134
Q

CNS/UMN injury/disease cause what.

A

Loss of descending inhibition. Allowing excessive MSR response to occur.

135
Q

No response on one side to the MSR /tendon Tap indicates what

A

Issue with the PNS

136
Q

No response on either side to the MSR/tendon tap

A

Bilateral lesion or reflex is being covered by tension

137
Q

Hyperactive response on both sides to MSR/tendon tap

A

Damage to CNS b/c loss of descending inhibition

138
Q

Golgi Tendon Organ reflex

A

Afferent NS initiated. GTO stimulation=relaxation. Afferent signal from muscle tendon to SC, interconnections w/in SC from brain CNS system moderate motor output (descending inhibition)

139
Q

UMN injury/diseas most commonly results in

A

Increased tone/spasticity due to lack of CNS inhibition of muscle reflexes.

140
Q

Muscle spasticity is most likely to be caused by which of the following mechanisms

A

Loss of CNS inhibition of muscle reflexes

141
Q

Smooth muscle contraction pattern

A

Phasic- undergo periodic contraction and relaxation cycles(GI)
Tonic- maintain some level of tone (bladder sphincter)

142
Q

Smooth muscle cell communication

A

Unitary-work together in a coordinated fashion. Connect via gap junctions which allow rapid spread of AP’s among neighboring fibers. Found in walls of vasculature and hallow organs.
Multi unit- Act independently and only when they receive neuronal input. Found in walls of larger arteries, bronchioles, erector pilli and iris of eye.

143
Q

Can smooth muscle regenerate

A

Yes, more than skeletal and cardiac. Capable of mitosis and regeneration.

144
Q

Why does smooth muscle relax and contract more slowly than cardiac or skeletal

A

To save energy, maintain absorption.

145
Q

Give an example of smooth muscle that can withstand significant stretching and still function

A

Bladder

146
Q

Where does calcium come from in a smooth muscle contraction and what protein does It lack that skeletal muscle has

A

Some form SR and ECF and smooth muscle does not have troponin

147
Q

In smooth muscle how are contractions initiated

A

Mechanically by stretching, electrically by the ANS stimulation, chemically

148
Q

Why does it take longer for calcium to reach filaments in smooth muscle

A

There are no t tubules in smooth muscle. Results in lower contraction response than skeletal ms

149
Q

Caveolae

A

Flask shaped invaginations of the plasma membrane in smooth muscle. Similar function to t tubules as in it deliver Ca2+ to cytoplasm which stimulates SR Ca release and or contraction

150
Q

Protein in smooth muscle that is not found in cardiac or skeletal

A

Calmodulin. Myosin binding sites blocked by caldesmon. When calcium calmodulin complex binds or caldesmon the myosin binding sites are exposed and myosin actin cross bridges can form.

151
Q

Differences in smooth muscle contractions to skeletal.

A

Calcium ions from ECF, Ca binds to calmodulin which then binds myosin light chain kinase, the enzyme complex breaks ATP to ADP, when ca pumped out of cell or back into SR inorganic phosphate gets removed from myosin by another enzyme

152
Q

How is cardiac muscle similar to smooth

A

Single nucleus, contains gap junctions, under ANS and hormonal control

153
Q

What is unique to cardiac muscle

A

Shorter muscle fibers than skeletal, branched muscle fibers.

154
Q

How is cardiac muscle similar to skeletal

A

Striated, sarcomere, sarcolemma has t tubules that spread depolarization. Terminal Cisternae, mechanism of muscle contraction (sliding filament)

155
Q

Differences between cardiac and skeletal muscle

A

Cardiac muscle fibers have smaller diameter than most skeletal. Cardiac muscle contraction is involuntary, cardiac muscle fibers are formed by individual muscle cells with one or two centrally placed nuclei.

156
Q

Intercalated disc

A

There region where the ends of the cells in cardiac muscles are connected to another cell. Contains gap junctions, adhering junctions, and desmosomes.

157
Q

Why are the cisternae of skeletal muscle larger than that of cardiac

A

Cardiac muscle is highly vascularized and has more abundant mitochondria because it need to have a lot of endurance.

158
Q

Ischemia

A

Coronary artery blockage results in cell death called a myocardial infarction or hear attack

159
Q

Muscle at rest

A

ATP+creatine——->ADP + phosphocreatine

Via creatine kinase

160
Q

Working muscle

A

Phosphocreatine+ADP——>creatine+ATP (needed for contraction)—->Myosin ATPase(contraction), ca2+ATPase(relaxation), Na-K ATPase restores ions that cross cell membrane during AP)

161
Q

Simple diffusion

A

Non specific, non saturable. Lipid soluble/steroid hormone, small non-polar, non polar gases,water, lipid soluble drugs

162
Q

Facilitated diffusion

A

Specific, saturable, no energy required. Down concentration gradient. Charge molecules, large polar molecules, amino acids, metabolic by products, proteins, non diffusable drugs. Carrier proteins involved.

163
Q

Active transport

A

Specific, saturable, ATP used, carrier proteins involved. Charge molecules, large polar molecules, amino acids, proteins, lipid insoluble drugs, drugs are are endogenously similar to molecules.

164
Q

Vesicular transport

A

ATP requires, specific, saturable, receptor proteins involved, large particles in large quantities, drug complexes, common mechanism for targeted drug delivery

165
Q

Peripheral proteins

A

Loosely adhere to other membranes surface inner or outer membrane through hydrogen bonds. Allows disconnection without affecting the structure of the membrane. Receptor, provides structural support, facilitates movement.

166
Q

Integral proteins

A

Channel- allows small ions to passively move through cell membrane
Carrier- ions specific bonding sites that transport ions passively or actively