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Semester 1 TxWes > A/P Unit 3 > Flashcards

A/P Unit 3 Flashcards

1
Q

What are the arteries that supply the brain?

A

The internal carotids (2) and the vertebral arteries (2)

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2
Q

What, other than the brain, does the internal carotid perfuse?

A

Top of the head, top of the forehead

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3
Q

What does the term “a very protected system” indicate for the internal carotid artery?

A

It gets what it wants, meaning if it wants more blood flow, it will get it. It can “override” other bodily demands for blood

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4
Q

What is the range for brain blood flow? Typical resting number?

A

750 - 900 ml/min, resting is 750 mmHg

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5
Q

What percentage of CO does the brain consume?

A

15%

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6
Q

How is the energy divvied up between white/grey matter?

A

Grey matter = 80%
White matter = 20%

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7
Q

What is the vast majority of energy spent doing?

A

Ion movement, running the pumps, or use the term “electrophysiology”

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8
Q

What is the process of brain blood flow changing in response to MAP?

A

Autoregulation

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9
Q

What is the usual set point, LLA and ULA of BBF, also define those terms.

A

set point = 100 mmHg
LLA = lower limit of autoregulation
ULA = upper limit of autoregulation
BBF = brain blood flow
the range is 65 - 150 mmHG

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10
Q

What happens as map decreases, what is the relationship if you go past LLA?

A

Cranial vessels dilate to allow more blood to flow in. If you go past LLA, there is a linear relationship to BBF and Map (both go down on a linear rate)

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11
Q

What happens as map increases, what is the relationship if you go past ULA?

A

Cranial vessels constrict to limit blood flow. If you go past ULA, there is a linear relationship to BBF and Map (both go up on a linear rate)

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12
Q

Why is having a chronic setpoint of 120 mmHg bad?

A

Because LLA increases (now 85 instead of 65) meaning if something catastrophic happens (such as an MI) the blood vessels can’t relax as much as they should, which will limit BBF

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13
Q

What other tissues than the brain exhibit autoregulation?

A

Spinal cord, kidneys

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14
Q

What circulation has no adrenergic receptors?

A

Cerebral circulation

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15
Q

What is the term for blood vessels constricting in response to changes in MAP independent of neurotransmitters?

A

Myogenic constriction

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16
Q

Give a basic description of the circle of willis

A

It is a circle that allows several arteries in the brain to “communicate” with each other. Its a kind of fail safe system, if something goes wrong, then the collateral circulation can pick up the slack until the problem gets fixed.

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17
Q

What artery provides the greatest portion of blood to the brain?

A

MCA

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18
Q

What are the 3 main cerebral arteries?

A

Anterior cerebral artery, middle cerebral artery and posterior cerebral artery (ACA, MCA, and PCA)

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19
Q

What artery eventually turns into the MCA? Where are they in terms of the circle of willis?

A

Internal carotids, roughly the “middle” of the circle

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20
Q

Describe nomenclature for circle of willis arteries

A

1 means pre-communicating, 2 means post communicating (communicating meaning before the little bridges that complete the circle). So the anterior cerebral artery, A1 = pre communicating, A2 = post communicating. For the posterior, P1 = pre communicating, P2 = post communicating. The MCA does not have any special nomenclature.

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21
Q

When is an artery no longer a part of the circle of willis?

A

When it becomes post-communicating

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22
Q

What are the 3 main blood vessels feeding into (but not a part of) the circle of willis?

A

The basilar artery and the internal carotids (2).

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23
Q

What are the 3 main arteries of the cerebellum?

A

The superior cerebellar artery, the anteroinferior cerebellar artery, and the posteroinferior cerebellar artery

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24
Q

What artery is the progenitor of the superior and anteroinferior cerebellar arteries?

A

The basilar artery

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25
Q

What artery is the progenitor of the posteroinferior artery?

A

The vertebral arteries

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26
Q

What is CPP? How does it impact blood flow to the head?

A

Cerebral perfusion pressure, and a high CCP will decrease how much blood gets up to the head.

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27
Q

What is the formula to calculate CPP?

A

Map - ICP, so for example, 100 - 10 = 90, which would be the cerebral perfusion pressure

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28
Q

What is CRMO? What is its relationship to BBF?

A

Cerebral metabolic rate, generally a direct relationship. If CRMO goes up, generally, BBF does as well to provide nutrients

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29
Q

How does a CO2 increase affect BBF?

A

It increases it, CO2 disassociates into bicarb and protons this increase in waste products will increase CRMO and BBF

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30
Q

What is a way to decrease CRMO?

A

Hypothermia

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31
Q

How much does therapeutic hypothermia decrease O2 demand?

A

6 - 7% per 1 degree drop in Celsius

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32
Q

What is the relationship of BBF and dissolved CO2 (PaCO2)? What actually drives the change in BBF?

A

Generally direct. While the trend does follow the change in PaCO2 (both go up or both go down) it is actually the protons that drive the change

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33
Q

How much does BBF change to each 1 mmHg change in PaCO2?

A

2 - 4% in either direction

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34
Q

What is a temporary measure to reduce ICP? How long does it last?

A

Hyperventilate, 6 hours

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35
Q

What drugs mentioned in lecture can increase BBF?

A

NO, ketamine

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36
Q

Describe the relationship of volatile anesthetics to BBF/CRMO, why is the net change negligible?

A

So they are potent vasodilators (which would increase BBF), but at the same time, the decrease CRMO. This combination of effects kind of neutralize each other. However, at high doses, the vasodilatory effect wins

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37
Q

Give examples of cerebral vasoconstrictors

A

Serotonin, Propofol, barbiturates, hyperthermia

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38
Q

How much blood flow does the anterior spinal artery take? The posterior spinal arteries?

A

75%, and 12.5% each for a total of 25%

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39
Q

What is the name for arteries that run in-between the ribs? What is their purpose?

A

Intercostal arteries, and to feed into the posterior/anterior spinal arteries.

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40
Q

Describe what happens to the intercostal artery coming off the thoracic aorta

A

It extends towards the back, then splits. One goes towards anterior/posterior spinal artery, the other becomes the dorsal branch (perfuses the back), which can then split into the spinal branch

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41
Q

Where does the spinal branch artery terminate? What happens after termination?

A

Generally in the dorsal root ganglion, however from this point it can split and extend into the spinal cord, making them radicular arteries

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42
Q

Describe the general occurrence per level in the spinal cord, of feed arteries

A

You may have one on the left or right side, but they rarely occur on both sides of a level at the same time.

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43
Q

Give the common term used in lecture to describe feed arteries

A

Radicular arteries

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44
Q

What is the most important feed artery?

A

The artery of Adamkiewicz, or the GRA (great radicular artery)

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45
Q

What is the primary function of the GRA?

A

Provides blood supply for the bottom 2/3 of the cord, primarily the anterior cord

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46
Q

How long can the cord survive occlusion of the GRA? What is the most likely outcome if this timeframe is exceeded?

A

30 minutes, and motor paralysis

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47
Q

What procedure puts you at risk for motor paralysis due to intentional GRA occlusion?

A

Aortic aneurysm repair

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48
Q

In general, where are the locations for feed arteries?

A

C3/4, C5/6, C7/T1, T3/4, T11/12

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49
Q

Why is there minimal chance of paralysis of the upper extremities if you clamp the aorta?

A

Because you have feed arteries coming off the vertebral arteries that should be able to keep perfusing the top 1/3 of the cord

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50
Q

What is the range of vertebrae that the GRA can enter? What is the most common range in the population, and what percentage of them fall within the common range?

A

Total range: T5 - L5
Common range: T9 - T12
Common range occurrence: 75%

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51
Q

What is the origin for the posterior spinal arteries?

A

The vertebral arteries and the posteroinferior cerebellar artery and the radicular arteries

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52
Q

What is the origin for the anterior spinal artery?

A

The vertebral arteries and radicular arteries

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53
Q

What would be a good target map to try and over perfuse when the aorta is clamped?

A

150 mmHg

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54
Q

What arm will you place an art-line for any case that involves aortic clamping?

A

Right arm

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55
Q

What are the ULA and LLA for the spinal cord?

A

50 - 125 mmHg

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56
Q

What determines flow rate in the spinal cord?

A

Distal aortic pressure - CSF pressure

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57
Q

What could you do to improve spinal cord perfusion without changing BP?

A

Decrease CSF

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58
Q

What does CSF spike up to during an aortic aneurysm repair?

A

20

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59
Q

Why do you overperfuse the cord during cross clamp?

A

The goal is that the high map will hopefully get down to the radicular arteries and provide collateral circulation while the aorta is clamped

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60
Q

Why are sensory cell bodies easier to perfuse than motor?

A

Sensory cell bodies are outside of the cord in ganglia, motor cell bodies are physically inside the cord

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61
Q

Describe what happens during reperfusion injury

A

Cells that have been hypoxic suddenly get oxygen again. The problem is the cell isn’t ready to handle the sudden influx, and oxygen is a potent oxidation agent. This can actually harm the inside of the cell and cause damage.

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62
Q

Describe the rate of oxygen delivery to an average cell.

A

The delivery is generally the same as the rate of consumption

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63
Q

What is lateral inhibition?

A

The ability of a neuron to affect their neighbor, even if its a different kind of neuron

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64
Q

Give an example of lateral inhibition

A

You injure a body part, this causes pain. When you apply pressure, the pressure neurons can “turn off” nearby pain neurons. This is why we reflexively try to grab at an injured body part, because we instinctively know that pressure could help reduce the pain.

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65
Q

What homeotherapy is based off the principles of lateral inhibition?

A

Acupuncture

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66
Q

What tract does pain run parallel to?

A

The DCML pathway

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67
Q

During lateral inhibition, what type of fiber inhibits the pain fiber?

A

A-beta fibers

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68
Q

Why is a laminectomy a temporary fix? How does it create a vicious cycle?

A

Because eventually the loss of bone creates instability in the spine, and will require fusion. The problem with fusion, is that the vertebrae just above/below the fusion will wear down, and they themselves will eventually need fusion. Generally, each surgery is good for 5 - 10 years.

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69
Q

According to Dr. Schmidt, who should you see to have a back surgery done?

A

A neurosurgeon rather than an ortho one.

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70
Q

What stretches are good to help promote lower spine stability?

A

Hamstring stretches

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71
Q

Which reflexes are localized to one side of the spinal cord?

A

Stretch, tendon and withdrawal reflexes

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72
Q

Which reflex involves both sides of the cord?

A

Crossed extensor reflexes

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73
Q

Which reflex relies on direct connections only?

A

Stretch reflexes

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74
Q

Which reflexes rely on interneurons?

A

Tendon, withdrawal and crossed extensor reflexes

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75
Q

Which reflex is the most complex?

A

Crossed extensor

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76
Q

What reflex makes use of information gathered by the golgi bodies and muscle spindles?

A

The stretch reflex

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77
Q

Describe the goal/process of the stretch reflex

A

Its goal is to keep the muscles at a constant length. It can manipulate extending/relaxing muscle groups to accomplish this. If someone pushes you off balance, the quads to stretch, in response this reflex would try to get the quads to contract or relax to keep them at the same length

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78
Q

Describe what happens to the quads and the antagonistic muscle if the quads are contracting

A

The quads contract in response to a stimulus. To augment this, we can have the antagonistic muscle do the opposite, which would be the hamstrings relaxing

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79
Q

What is the goal of the tendon reflex?

A

To prevent injury, keep tendons attached to their insertion points

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80
Q

What happens during the tendon reflex if tensions gets to dangerous levels?

A

In the emergency situation, these reflexes will do everything they can to get the muscle to relax to prevent injury. It would accomplish this using an inhibitory interneuron. So step 1: get the quad to relax. Step 2:, get the antagonistic muscle to contract (hamstring).

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81
Q

What is a unique feature that withdrawal and crossed extensor reflexes share?

A

The ability of pain signals to go up/down levels in the spinal cord via the tract of Lissauer

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82
Q

Describe what happens during the withdrawal reflex

A

You have an unpleasant stimuli and want to pull your foot away. The quad relaxed and the hamstrings flex to pull the foot away.

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83
Q

Why is it advantageous for pain information to go up/down levels via the tract of Lissauer?

A

This allows a single stimuli (such as pain) to recruit numerous muscles to participate in a reflex in a short period of time

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84
Q

Describe what happens during a crossed extensor reflex?

A

So you have a painful stimuli mid stride and the body wants to stabilize itself. It pulls the right leg away (relaxing extensors and exciting flexors) and extending the left leg for stabilization (exciting extensors, relaxing flexors).

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85
Q

Where do neurons cross over during a crossed extensor reflex?

A

Lamina X

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86
Q

What is a pain receptor called?

A

A nocioceptor

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87
Q

What senses (other than pain) are sensed by free nerve endings?

A

Crude pressure and temperature

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88
Q

Describe how cellular death could elicit a pain response

A

The cell dies and releases all of its intracellular contents. There is a lot of K in the cell. This massive release of K could raise the Vrm of nearby pain sensors, making it easier to send of pain APs

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89
Q

Per lecture, why would a dialysis pt be more likely to report pain?

A

They have a buildup of inflammatory markers and waste products. So if K and acids are hanging around, they can elicit pain signals.

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90
Q

What hormone can cause nociceptors to become excitatory?

A

Serotonin

91
Q

What is histamine released from?

A

Mast cells

92
Q

What is bradykinin involved with?

A

Inflammation/swelling

93
Q

What causes chest pain during an MI?

A

The buildup of waste products such as lactic acid

94
Q

How do prostaglandins cause pain?

A

Indirectly, they increase the bodies sensitivity to other chemicals that excite pain

95
Q

What is visceral pain?

A

Internal hollow organ pain, generally slow, achy, poor localization, c-fibers

96
Q

What is parietal pain?

A

Pain in the connective tissue surrounding the organ. Tends to be fast, sharp pain, highly localized

97
Q

What is referred pain? Give an example

A

This is when pain is felt in a part of the body that is not the source of the pain. Such as a kidney stone causing back pain. The back isn’t in pain, but that is where you feel the pain

98
Q

What is the pain threshold?

A

The ease or difficulty of eliciting a painful feelings. Some people will have a high pain threshold, some will be low, there is a wide variance

99
Q

Why do you want to control post-op pain early?

A

Because you become more sensitive to pain if it continues. So if you let someone after surgery stay in pain, it will only get worse.

100
Q

Where specifically do you feel visceral and parietal pain from appendicitis?

A

The visceral pain is around the umbilicus (T10) and the parietal (sharp pain) is about L1.

101
Q

Describe pain receptor location trends in a hollow organ

A

Sparse receptors are inside the organ, however you will find a very high concentration of them in the connective tissue surrounding the organ

102
Q

How could you reduce how much visceral/parietal pain is being sent to the nervous system? For what chronic condition would this be useful for?

A

Sever the autonomic ganglia of the affected area. Generally done for hospice care, and cancer was the mentioned condition.

103
Q

What are the categories of glutamate receptors?

A

Metabotropic and ionotropic

104
Q

Describe the difference between metabotropic and ionotropic

A

Metabotropic is not involved with pain signaling and is GPCR related. Ionotropic is highly involved with pain signaling and is ion current related

105
Q

What the 3 ionotropic receptor subtypes?

A

AMPA, NMDA and Kainite

106
Q

Describe an AMPA channel

A

They have a binding site for glutamate, allows for Na to rush in (K can leave, but the rush of Na prevents this) and causes rapid depolarization. They are the primary glutamate pain receptors found throughout the body

107
Q

Describe an NMDA channel

A

Slower than AMPA, structurally very similar. This allows Ca and Na to enter, this also allows Ca to act as a secondary messenger. A key feature, is that NMDA can’t open on their own. They require prior cell depolarization to work.

108
Q

What can the body do to “ramp up” pain signaling?

A

Place NMDA receptors in areas with high AMPA receptor activity (this would lower pain threshold, making pain more “intense.”)

109
Q

What is NMDA involved with other than pain?

A

Learning and memories. Along with glutamate, they can create “pathways”, this is why repetition with something like basketball can lead to improvement

110
Q

What are examples of NMDA antagonists?

A

Ketamine (does not fully block pain, just reduces awareness), alcohol, NO, tramadol, and Lead

111
Q

What similarities does heart muscle share with skeletal?

A

Both are striated and use Ca for contraction

112
Q

How much of our mass is made up by skeletal muscle?

A

40%

113
Q

What is calsequestrin? How does it work?

A

It is a calcium storage protein in the SR. It has binding sites for Ca, as the Ca binds it reduces the concentration of dissolved Ca in the SR, lowering the concentration gradient and making it easier for Ca to be pumped into the SR

114
Q

What is the name of the receptor that pulls the “cork” to allow Ca out of the SR?

A

The ryanodine receptor

115
Q

What is an early sign of malignant hyperthermia?

A

Sudden rise in CO2 without an obvious cause

116
Q

What causes malignant hyperthermia?

A

A gene mutation of the ryanodine receptor that causes the channel to stay open, allowing Ca to flood into the muscle and cause constant contractions causing the body to rapidly heat up.

117
Q

What are the basic steps muscle AP generation?

A

Motor neuron depolarizes, Ca influx into the motor neuron, ACh vesicles fuse to the membrane, ACh is secreted, ACh binds with the nicotinic ACh receptors, Na floods into the muscle cell, Ca is released from the SR, and an AP is generated in the EPP

118
Q

What is the name of a local potential?

A

End plate potential

119
Q

What happens after EPP AP propagation?

A

Local depolarization creates an AP, it spreads L/R down the muscle cell via voltage gated Na channels, this is sensed by the DHP (dihydropyridine) sensors that then pulls on the ryanodine receptors which pulls the cork and allows Ca influx into the sarcoplasm

120
Q

Where can you find acetylcholinesterase?

A

In the synapse, in the plasma and the liver

121
Q

What are AChE inhibitors?

A

‘Stygmines

122
Q

What condition can AChE inhibitors treat (non skeletal related)?

A

Alzheimers

123
Q

What is the difference between L type and P type calcium channels?

A

L type (t-tubules) close as a result of a certain time period passing, P type (usually in motor neurons) close in response to depolarization

124
Q

What occurs with ELMS/LEMS disease?

A

Auto-immune disorder: anti-bodies attack the P-type calcium channels, making it harder for APs in the muscle to propagate

125
Q

What drug can help treat ELMS/LEMS, how does it work?

A

TEA, and by blocking K channels, this keeps the neuron depolarized for a longer period of time, which gives the body more time to allow Ca to come in via P-type channels that have not been destroyed

126
Q

What are other treatment options for ELMS/LEMS?

A

A K channel blocker, steroids to slow down the immune system, plasmapheresis to remove antibodies or removing the thymus gland (which is producing the anti-bodies),

127
Q

What is a downside to giving sux?

A

It can cause hyperkalemia

128
Q

How much can sux raise K in a healthy person?

A

By .5, so 4 -> 4.5

129
Q

What is a common condition that causes the body to start placing ACh receptors all over the muscle?

A

After a stroke

130
Q

What is the primary source of body heat?

A

The muscles

131
Q

Describe the organization of muscle tissue, from smallest to largest

A

Sarcomere -> Myofibril -> Muscle cell or fiber -> Fasciculus -> Muscle

132
Q

What composes a motor unit?

A

A single motor neuron, and a muscle cell or cells

133
Q

What is excited first, large or small motor units? What is this process referred as?

A

Small, then recruit larger ones if needed. This is called a graded reaction

134
Q

What neuron type innervates muscle?

A

A-alpha

135
Q

What is type 1 muscle? What is its characteristics?

A

Red due to presence of myoglobin, good for doing a lot of work over a long period of time.

136
Q

What is type 2 muscle? What is its characteristics?

A

White muscle or fast twitch muscles, good for quick contractions but not as strong.

137
Q

Why is red meat a potential carcinogen?

A

Due to the iron content, there is speculation too much iron can be cancerous

138
Q

What is the skeletal muscle cell wall?

A

The sarcolemma

139
Q

What replaces the endoplasmic reticulum in the muscle?

A

Sarcoplasmic reticulum

140
Q

What is the primary purpose of the SR?

A

To store calcium

141
Q

List from least to most how well developed the SR is in muscle tissue

A

Smooth < Cardiac < Skeletal

142
Q

What does an AP travel through in muscle tissue?

A

T-tubules (transverse tubules)

143
Q

What is the basic functional unit of the muscle?

A

The sarcomere

144
Q

What are the thick and thin filaments?

A

Myosin and Actin

145
Q

What is the I band?

A

Actin only

145
Q

What is the Z disc?

A

The ends of the sarcomere

146
Q

What is the A-band?

A

Actin + Myosin

147
Q

What is the H zone/band?

A

Only myosin

148
Q

What is the M line?

A

A dark line in the middle of the H zone

149
Q

What anchors the filaments to the z disc?

A

Titin

150
Q

What is myosin pulling on during contraction? Where is it headed?

A

Actin, and going “towards” the Z disc

151
Q

What bands disappear during contraction?

A

The I and H bands

152
Q

What is the process of myosin “walking” to and pulling on actin called?

A

The sliding filament mechanism

153
Q

Muscle cells do not have the “cellular train tracks” that neurons have to overcome length. How do the muscles solve this problem?

A

By having nuclei spread throughout the cell

154
Q

What makes up myosin?

A

6 chains, 2 heavy chains wrapping around each other to make the tail, 4 light chains, 2 making up the regulatory light chains, and 2 making the essential light chains

155
Q

What is the difference between essential and regulatory light chains?

A

The regulatory chains are always “on”, and the essential help stabilize the myosin head

156
Q

What hides the active sites on actin?

A

Tropomyosin

157
Q

What is the regulatory complex on actin, its constituent parts and function of each?

A

The troponin complex. Troponin I binds to actin, Troponin T binds to tropomyosin and Troponin C binds to calcium

158
Q

How does calcium reveal the active site?

A

By binding to troponin C, which changes troponin I’s affinity to actin, and allows the actin strand to unravel and reveal the active site

159
Q

What is the cycle of the myosin head binding, pulling and resetting called?

A

Cross bridge cycling

160
Q

Describe the basic process of the myosin head binding to the active site cycle.

A

The head it attached to actin and has gone through power-stroke. ATP comes along, binds, and using energy frees the myosin head and reloads it into a cocked state bound to ADP. Once in this state, if the active site is revealed, the myosin head will bind to it, go through power-stroke and shorten the sarcomere.

161
Q

What happens if there is no ATP to reset the myosin head?

A

It becomes stuck, this is what happens with rigor mortis

162
Q

What are schawnn cells called in the NMJ?

A

Teloglial cells

163
Q

What is the neurotransmitter of motor neurons?

A

ACh

164
Q

What would you find at the entrance of the synaptic cleft? The inner part?

A

The ACh receptors, and voltage gated Na channels

165
Q

How many ACh receptors are in the synapse? Why is this the case?

A

20x more than needed. It is thought to be a safety mechanism

166
Q

What makes up a nicotinic ACh receptor?

A

ADBAE - alpha subunit, delta subunit, beta subunit, alpha1 subunit and the epsilon subunit

167
Q

What is the difference in ACh receptor makeup in adults vs a neonate?

A

Adult ACh follows ADBAE, when young the configuration of the subunits is different

168
Q

Describe the process of Ca being released from the SR

A

An AP travels down the T-tubules, the electrical signal is sensed by the DHP (dihydropyridine) receptor, which then pulls on the ryanodine receptor pulling the “cork” out which allows Ca to rapidly enter the sarcoplasm

169
Q

Why is parietal pain better localized than visceral?

A

Because parietal feeds into the cord at the same level as the sensory information, whereas visceral comes into the cord, ascends in the tract of lissauer before crossing over.

170
Q

What are treatment options for myasthenia gravis?

A

Removing the thymus gland, AChE inhibitor

171
Q

What are some of the side effects of giving neostigmine?

A

Bradycardia (counter with atropine) and increasing respiratory secretions via M3 stimulation

172
Q

What principle does sarin nerve gas operate?

A

Overstimulation of muscarinic receptors: causing bradycardia, but killing you by increasing pulmonary secretions to the point where you drown. Treat using atropine

173
Q

Describe the length-tension relationship

A

A muscle will be able to have ideal contraction at a certain length, under or over leads to less than ideal contraction or tension.

174
Q

What muscle rests in an under-relaxed (meaning a lot of overlap or minimal stretch, close to the Z-disks)? Why?

A

Heart muscle. It doesn’t get passive tension from attachment points, it gets it from blood. So as the blood comes in, this provides the passive stretch for the heart.

175
Q

How would you fix an achilles tear?

A

Try to overlap the remaining tendons, sew them together, and screw them into the heel bone. Because the muscle is now more “overstretched” at rest, it will never be able to contract like it did before the injury.

176
Q

Describe Isometric muscle force generation

A

You hold the muscle at a fixed length, apply a stimulus, and see how much force is generated. The sarcomeres shorten, but we don’t see it due to stretchy tissue masking the contraction.

177
Q

Describe Isotonic muscle force generation

A

You place a weight/load on the muscle, apply a stimulus, and allow the muscle to contract and measure the contraction.

178
Q

Describe the frank-starling law

A

The force of contraction is proportional to the stretch of the heart muscle. Meaning; the ability of the heart to contract depends on how much blood is “stretching” the heart prior to contraction

179
Q

What is passive tension? Active?

A

Passive = the tension from the stretch of the muscle at rest, aka the tendons
Active = the tension created during contraction

180
Q

What happens if you increase/decrease passive tension?

A

If you increase passive tension, this will increase total tension up to a point (because the more you stretch, you hit a point where the muscle can no longer contract effectively). If you decrease passive tension, total tension will decrease (think a muscle severed from its insertion point, it can’t contract with no passive tension).

181
Q

What is passive tension for the heart?

A

Preload

182
Q

How can you diagnose a motor problem?

A

Using EMG (electro-myography)

183
Q

Describe the relationship between load and contraction for skeletal and cardiac muscle

A

S: The lighter the load, the quicker the muscle can shorten, the heavier the load the longer it takes for the muscle to shorten.
C: A low BP (lighter load) the heart can contract faster, a high BP (higher load) it takes the ventricular walls longer to contract

184
Q

Describe the difference between quantal and temporal summation

A

Q = how many motor units are recruited (we generally recruit all of them)
S = the rate of stimulation per second, generally directly correlates to strength of contraction (if rate goes up, strength of contraction goes up). Or, think of it as: more Aps per unit of time

185
Q

How does increasing temporal summation increase force of contraction?

A

Ca is being released from the SR faster than it can be pumped back in, this extra Ca allows for near constant cycles of muscle contractions.

186
Q

Define atrophy, hypertrophy and hyperplasia

A

A: the a decrease in size or loss of myofibrils or worse entire muscle cells
HT: increase in size of myofibrils/cells, due to working out usually
HP: increase in the actual number of myofibrils, rare, usually present in extreme body builders

187
Q

What is an option to try and prevent atrophy from long term disuse (think Christopher reeves)?

A

Electrical stimulation - buy time to keep the myofibrils from wasting away and hope a cure/treatment is developed for the underlying cause

188
Q

How does an electrical current (tazer, electrodes) depolarize a cell?

A

The flow of electrons (negative charge) makes the outside of the cell more negative, voltage gated Na channels sense this as depolarization and open up to allow Na to flood in and create an AP

189
Q

Why can an electrical stimulus cause muscle contraction in the presence of a paralytic?

A

Because paralytics only augment the NMJ, the rest of the muscle has reset. If the electrical current happens near a T-tubule (release Ca) or to an ACh receptor errantly placed on the muscle, depolarization and then AP can occur leading to contraction.

190
Q

What triggers the exocytosis of ACh from the pre-synaptic motor neuron?

A

Ca coming in via the P-type Ca channels. Exocytosis can now occur

191
Q

What potassium channel blocker can treat ELMS/LEMS?

A

TEA - tetra ehtyl-ammonium

192
Q

What is a low conductance nACh channel? High conductance? 7 alpha?

A

Low = immature channel
High = mature channel
7 alpha = in the CNS or neuronal in nature

193
Q

What is the difference between immature and mature nACh channels?

A

Immature replaces the epsilon subunit with a gamma.
Mature = conducts more current, opens/closes faster
Immature = less current flows through it, but it stays open much longer

194
Q

What is the rate of hertz to stimulations?

A

Generally 1:1, 1 hertz = 1 pulse a second, 10 hertz = 10 pulses a second

195
Q

Why does Ca being released from the SR affect membrane potential?

A

Membrane potential current depends on resistance which in this case in the cell wall. In order to contribute to resistance, it must cross the cell wall, which this Ca does not.

196
Q

Why does a hertz of 50 allow 50 contractions a second?

A

Because the muscle functions similarly to a nerve axon, it stimulates and resets very quickly, what is slower is pumping Ca back into the SR

197
Q

What muscle is the adductor pollicis? What would you see with electrical stimulus?

A

Muscle of the forearm, pinky twitch is the primary outcome, thumb twitch can occur as well

198
Q

Why would electrical stimulation to the ulnar nerve hurt?

A

Because it is a mixed nerve, you have motor fibers and pain fibers.

199
Q

How many twitches would you get with 0.1 Hertz?

A

1 every 10 seconds. 0.1 hertz = twitches per second (isolate twitches) -> 1 / 0.1 = 10

200
Q

Which lasts longer, sux of NDMR?

A

NDMR

201
Q

What is train of 4 ratio? What is the difference between the ratio for sux vs NDMR?

A

It is the difference in twitch “strength” of each of the 4 twitches. Sux should always be about equal, or 1:1 (the twitch strength will get stronger as time goes on, but the strength is equal whenever you check it). Early in the recovery from NDMR, the ratio could be 4:1, then gradually lessen to 3:1, 2:1, until it has worn off completely and the ratio is back to 1:1, so the first twitch will be stronger than the second which will be stronger than the third until it fully wears off

202
Q

Why is the TOF ratio so different between Sux and NDMR?

A

With sux, it does not affect pre-synaptic ACh, the only thing affected is the NMJ. So over the 2 seconds you check TOF, the twitches should be similar or 1:1. With NDMR, the pre-synaptic ability to secrete ACh is impaired, so you get the most ACh released with the first twitch, a little less with the second, and less with the third and so on. This is why the TOF ratio is higher early on with NDMR.

203
Q

What is the difference between VP1 and VP2 vesicles? What gets them to release?

A

VP2 = ready to release ACh vesicles, VP1 = the reserve or storage pool. And exocytosis is mediated by calcium

204
Q

What is the name of the ACh auto-receptor on motor neurons?

A

the Alpha 3 Beta 2 receptor

205
Q

Why would the Adductor Pollicis paralyze before the diaphragm?

A

It is likely a safety mechanism, the diaphragm is more important that the AP muscle, so the body has more safety mechanisms (such as more ACh receptors) in place for more important muscles

206
Q

Which muscle would recover faster from a paralytic, Adductor Pollicis or diaphragm? why?

A

Diaphragm, it is a more important muscle

207
Q

How many of the nACh receptors are blocked with a 3/4 TOF? Continue through 0/4.

A

3/4 = 75 - 80% blockade
2/4 = 85% blockade
1/4 = 85 - 90% blockade
0/4 = 90 - 95% blockade

208
Q

What is the nACh receptor blockade with a reasonable head lift?

A

70%

209
Q

With V = IR, what is the body most sensitive to? What is resistance governed by?

A

Current, or I. And resistance = the cell wall

210
Q

Basic difference between smooth and skeletal muscle

A

Smooth is shorter, more efficient, only 1 nucleus, poorly developed SR and slower at cross-bridge cycling

211
Q

What is ratio of actin to myosin in smooth muscle? Skeletal?

A

10 - 20:1 , 2:1

212
Q

What provides actin and intercellular anchor points for smooth muscle?

A

Dense bodies

213
Q

What is the difference in cross bridge cycling with smooth muscle?

A

It is slower, and the myosin head can bind, pull and hold on rather than release. This ability to hold on is called the latch mechanism. This makes smooth muscle far more energy efficient.

214
Q

Gram per gram, which is stronger, smooth or skeletal?

A

Smooth

215
Q

What provides control of the smooth muscle?

A

autonomic nerve endings

216
Q

What is an example of a hybrid muscle (smooth and skeletal)?

A

Esophagus

217
Q

What are the layers of a blood vessel, inner to outer?

A

Inner = Endothelium or tunica intima (endothelial layer)
Middle = Tunica Media (smooth muscle)
Outer = Tunica Adventitia/Externa (outer connective tissue)

218
Q

Do capillaries qualify to be smooth muscle?

A

No

219
Q

What is the difference between visceral and multi-unit smooth muscle?

A

Visceral = connected via dense bodies, and gap junctions to allow for coordinated contraction
MU = varied response, may or may not be attached to each other, and behavior can vary based on the neurotransmitter or stimulus.

220
Q

What is the difference between skeletal and smooth myosin?

A

The smooth myosin’s regulatory chains dictate if it is turned on or off via phosphorylation status

221
Q

What is the difference in myosin head of the skeletal/smooth muscle?

A

Skeletal heads are oriented in similar directions from the tail
Smooth heads alternate in direction from each other

222
Q

Why is it advantageous that vascular muscle is smooth?

A

Because it is so energy efficient, it won’t wear out like skeletal muscle does. This is important, because it is constantly contracting/relaxing.

Semester 1 TxWes (7 decks)

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