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A&P (Fall 2022) > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

What is usually the cause of ELMS?

A

Paraneoplastic syndrome related to lung cancer.

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2
Q

What are the anesthetic consideration in ELMS?

A

AChE inhibitors don’t have much of an effect. Much more sensitive to paralytics. Use NDMB & sugammadex as reversal, not succinylcholine.

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3
Q

How can ELMS be treated?

A

With 4,5 amino pyridine, which blocks the Ca2+ activated K+ channel –> prolonged depolarization. Or use TEA (Tetraethyl ammonium, a non-selective K+ blocker, only as last resort. Or plasmapheresis to filter out antibodies.

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4
Q

What happens in ELMS on the cellular level?

A

Antibodies attach & block the P-type Ca2+ channel –> decreased neurotransmitter release.

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5
Q

What is the difference between MG & ELMS S/S?

A

In ELMS the S/S get better with activity.

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6
Q

Where do ELMS S/S usually start and what are they?

A

Weakness in peripheral muscles & fatigue

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7
Q

What are the anesthetic considerations for MG?

A

Lower dose of NDMB, inhalation gases or sedation alone, or higher dose of Scc due to fewer receptors available.

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8
Q

What are the treatments for MG?

A

AChE inhibitors, Thymus gland removal, plasmapheresis

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9
Q

What test is used to diagnose MG?

A

Tensilon test, Give AChE inhibitor & if response gets better then positive for MG

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10
Q

What are later S/S of MG?

A

Larger muscle group weakness & eventually the diaphragm

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11
Q

What are some early signs of MG?

A

Small central weakness, droopy eyelids, double vision due to gaze muscles & gets worse throughout the day.

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12
Q

Which nACh receptor is not affected by paralytics?

A

The Neuronal ACh receptor. It has five 𝝰7 subunits

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13
Q

What happens in Myasthenia Gravis?

A

Auto immune antibodies attach to nACh receptor & destroys them

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14
Q

Why is the Adductor pollicis used to check paralyzation?

A

It gives a good indication of diaphragm function. The diaphragm recovers before the thumb.

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15
Q

What happens in a SCc phase 2 block?

A

The nACh receptors on the muscle do not work well.

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16
Q

What is the TOF target & what does that tell us?

A

Ratio of 0.9, means plenty of muscle function has returned to support own breathing.

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17
Q

Why is there a drop-off in TOF response in non-depolarizing blockers?

A

The 𝝰3β2 receptor is blocked

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18
Q

How is the TOF ration calculated & when is it used?

A

Last twitch divided by first twitch. Only used with non-depol blockers.

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19
Q

What is accommodation?

A

nACh receptors do not like interacting with SCc & will shut down with continuous administration.

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20
Q

What are 3 alternative locations for nerve stimulation?

A

Ophthalmic branch of facial nerve, Peroneal nerve, & Posterior tibial nerve

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21
Q

What is an EMG and what would an abnormal measurement mean?

A

Directly stimulate a muscle. If direct stimulation is better then there is a problem in the CNS.

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22
Q

What is an example to check for quantitative force?

A

Pressure transducer under the thumb

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23
Q

Which nerve stimulation would be used to recruit all motor units via all motor neurons?

A

Supramaximal Stimulus.

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24
Q

What is the reason to use tetanic nerve monitoring, how can one tell?

A

To check for residual NMJ blockage. The plateau would fall off if there is residual blockage.

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25
Q

How is Double Burst Stimulation performed?

A

At a high frequency with short breaks in between

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26
Q

Using 2Hz per second over 2 seconds is an example of what?

A

Train of Four nerve stimulation

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27
Q

What is the typical monitoring interval for single twitch?

A

1 twitch / 10 sec

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28
Q

What current flows through a nerve stimulator?

A

20-50mA

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29
Q

How does depolarization work with nerve stimulator?

A

The outside of the cell is made negative same as the inside.

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30
Q

Which muscle is stimulated by the ulnar nerve?

A

Adductor pollicis

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31
Q

How long does it take for immature ACh receptors to be produced?

A

~ 12hrs

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32
Q

Which patients should not receive succinylcholine, what is the body’s natural skeletal muscle response & what wold happen if they received SCc?

A

Stroke, spinal cord injury, or someone with denervation. The body places more ACh receptors at the NMJ but they are the immature receptors & some get placed at the post-junctional area. If they receive SCc, that will lead to abnormal high K+ levels.

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33
Q

How fast in the onset & long do the effects of succinylcholine last?

A

~ 47sec & last ~ 4mins

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34
Q

What happens after the initial depolarization when SCc is given?

A

The V-G Na+ channels in the Junctional & Perijunctional area become inactivated. The receptors that SCc binds to still allow Na+ influx. The K+ channels stay open

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35
Q

What is the acetate methyl linkage?

A

The bond that binds the 2 ACh molecules end to end forming succinylcholine.

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36
Q

What & where cleans up succinylcholine?

A

By Butyrylcholinesterase in the plasma.

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37
Q

What is the relationship of hypocalcemia & resting membrane potential?

A

With normal Ca2+ levels, the Ca2+ blocks some of the leaky Na+ channels, preventing Na+ from entering the cell. In hypocalcemia there is less Ca2+ to block those channels –> increased RMP & cell excitability.

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38
Q

What are the 2 types of secretory vesicles in skeletal presynapses?

A

VP-2: Are ready to go vesicles close to the membrane. VP-1: Farther back & move towards the membrane.

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39
Q

What are the 3 types of calcium channels and where are they found & what is the benefit?

A

L-type: found all over the body & primarily in the heart. P-type: are unique to axons in the motor system. Benefit is redundancy. T-type are found in cardiac tissue.

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40
Q

For which condition is succinylcholine contraindicated for?

A

An eye issue. It increases IOP substantially. Also, ocular muscle is innervated by multiple motor neurons, which can lead to multiple fasciculations/contractions.

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41
Q

What is the difference between high & low conductance channels?

A

High= in adults the nACh receptors open wide for a very short time. Low are only present in fetal nACh receptors. The channels open slower but stay open for a much longer time, allowing for a higher net movement of cations.

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42
Q

Is hyperplasia in skeletal muscle possible?

A

Yes, but it takes a very long time.

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43
Q

What all happens in hypertrophy in relation to skeletal muscles?

A

There is an increase in myofibrils, not cells themselves. Also, the blood vessels will increase in size & amount (angiogenesis).

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44
Q

What does the term denervation refer to?

A

Extreme non-use of skeletal muscle. Ex: spinal cord injury.

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45
Q

What is temporal summation in skeletal muscle?

A

A second stimulus is applied to a muscle before completion of relaxation (Ca2+ build up).

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46
Q

What happens at the cell level when we reach 10-12Hz in muscle contraction?

A

More Ca2+ enters the cell than can be removed –> sustained contraction.

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47
Q

At what level do we not see any temporal summation?

A

Between 1-10Hz

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48
Q

What does tetanization refer to?

A

Max contraction at max force.

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49
Q

What does quantal summation?

A

The quantity of motor units

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50
Q

In which circumstance are heavy loads detrimental?

A

In the cardiac muscle. High afterload –> increased time the ventricle walls need to contract.

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51
Q

Explain the velocity difference in skeletal muscles between light & heavy loads.

A

In light loads the velocity of muscle contraction is very fast. In heavy loads the contraction slows down –> prolonged contraction.

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52
Q

What is the Load/Contraction Velocity diagram used for?

A

It can quantify the rate of speed of contraction to the force.

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53
Q

What is passive tension?

A

Tension used to stretch out the muscle (pre-tension)

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54
Q

What is active tension?

A

The force a muscle produces when contracted.

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55
Q

What are some side effects (3), mentioned in class, of too much ACh in the body?

A

Increased mucus, bradycardia, increased alertness.

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56
Q

What condition would an AChE blocker be used for?

A

Alzheimers, MG

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57
Q

What class of drug inhibits AChE?

A

The “stygmine’s”

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58
Q

What chops up ACh that diffuses away from the NMJ?

A

Plasma AChE

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59
Q

What produces AChE?

A

Skeletal muscle

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60
Q

What is the purpose of Calsequestrin?

A

It binds & stores Ca2+ out of solution

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61
Q

How is calcium released from the SR in a skeletal muscle?

A

The dihydropyridine receptor (DHP) in the T-tubules sense a voltage change and then pulls the Ryr open.

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62
Q

What is an end plate potential?

A

The initial & minimum amount of depolarization of the postsynaptic cell needed for an action potential

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63
Q

What all moves through an nACh receptor into the cell?

A

Primarily Na+ but Ca2+ can also move through

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64
Q

Which subunits of an nACh must bind for the receptor to open?

A

Both alpha subunits

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65
Q

How many & what are the subunits on a mature nACh receptor?

A

5 & 2 alpha, 1 beta, 1 delta & 1 epsilon

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66
Q

About how many nACh receptors are there in each NMJ?

A

About 5 million

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67
Q

About what % of receptors are activated at any given time & why?

A

Only about 10% & it is a safety factor, to ensure muscle are only activated when needed.

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68
Q

Where would V-G Na+ channels be located in the synapse?

A

Towards the end of the cleft closer to the neuron

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69
Q

What is the first thing ACh neurotransmitter encounters when released from the pre-synapse?

A

AChE

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70
Q

What increases NMJ surface area & their 2 names?

A

Invaginations or Subneural clefts

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71
Q

Where are Teloglial cells present & their functions?

A

At the NMJ & help maintain the myelin sheath.

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72
Q

What happens to crossbridge cycling in rigor mortis?

A

There is an ATP depletion –> the myosin head is stuck to the Actin filament.

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73
Q

How does the myosin head release from Actin & gets its tension back?

A

The ADP on the myosin head gets replaced with ATP then the ATP is hydrolyzed and the myosin has now ADP & Pi.

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74
Q

What are the 3 Troponins that play a role in muscle contraction & what do they bind to?

A

Troponin I binds to F-Actin, Troponin T binds to Tropomyosin, Troponin C binds to calcium.

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75
Q

How does crossbridge cycling happen?

A

Troponin C binds to calcium –> Actin strands unwind exposing the active sites & myosin binds & pulls.

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76
Q

What hides the active sites on Actin filaments?

A

The Tropomyosin

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77
Q

What are the 4 parts of Actin filaments?

A

Active sites, Troponin complex, F-Actin, Tropomyosin

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78
Q

What do Myosin heads bind to?

A

The active sites on F-Actin

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79
Q

What is the function is myosin light chains?

A

ATPase activity & act as regulatory chain

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80
Q

What is each myosin molecule composed of?

A

2 heavy chains (Tail), 4 light chains (Heads)

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81
Q

What is the best way to repair an achilles tendon? What is usually done?

A

Suture back together. Usually it is overstretched & drilled.

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82
Q

What happens when muscles lose stretch?

A

We lose force

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83
Q

What muscle pulls up into a ball when the Achilles tendon tears?

A

The Gastrocnemius muscle

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84
Q

What is the reason for a muscle cell to have multiple nuclei?

A

Muscles are very long and get worn out quickly, so multiple nuclei can repair & support the muscle better plus no space for transport system.

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85
Q

Which muscle is purposely under stretched?

A

The heart muscle

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86
Q

What happens to the I band during a contraction?

A

It gets very narrow or disappears.

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87
Q

What happens at the Sarcomere level during a contraction?

A

The myosin head pulls the Actin filaments towards the middle.
The I band shrinks, H band disappear, Z disk move closer together.

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88
Q

Does the A-band width change during contraction?

A

No

89
Q

What makes up the Z disk?

A

Actin filaments anchoring into each other.

90
Q

Where are Z disks located?

A

At the end of each sarcomere

91
Q

What is the H Zone/band composed of?

A

Only myosin

92
Q

What is the A band composed of?

A

Actin & Myosin

93
Q

What is the I band composed of?

A

Only Actin

94
Q

What does Titin do?

A

It locks myosin filament to the Z-disk

95
Q

What make up the different kind of bands on Myofibrils?

A

Actin & Myosin. Myosin are thicker & Actin are thinner

96
Q

What is the purpose of Transverse Tubules?

A

They help with signal propagation deep into skeletal muscle

97
Q

What is the special function of the sarcoplasmic reticulum in muscle?

A

It stores calcium

98
Q

What is the Sarcoplasm?

A

Fluid inside the Sarcolemma

99
Q

What is the sarcolemma?

A

The outer membrane of a skeletal muscle

100
Q

Why could eating too much red meat cause cancer?

A

The myoglobin can cause oxidative stress, which can lead to cancer.

101
Q

What is an example of a Type 1 muscle?

A

The Soleus muscle (calf muscle)

102
Q

What is an example of a Type 2 muscle?

A

The Ocular muscle

103
Q

What is the purpose of myoglobin?

A

It has O2 binding sites & helps with O2 unloading from blood vessels into muscle.

104
Q

What type of muscle is darker in color and why?

A

Type 1 due to the myoglobin (iron heme)

105
Q

What surrounds each muscle fiber?

A

The sarcolemma

106
Q

What is the difference between Type 1 & Type 2 muscles?

A

o Type 1: darker in color “red” due to myoglobin, have lots of mitochondria for long uses, bearing heavy loads
o Type 2: For fast twitch muscles, very little myoglobin, fewer mitochondria & not as efficient as type 1

107
Q

What is the make up of skeletal muscles from smallest to largest?

A

Sarcomere -> Myofibril -> Muscle fiber -> fascicle -> muscle.

108
Q

What is a fasciculus?

A

A group of skeletal muscle fibers/cells that contract when told by CNS

109
Q

What makes up muscle fibers?

A

Myofibrils

110
Q

What components make up a motor unit?

A

Somatic motor axon & Neuromuscular junctions

111
Q

Which are easier to excite, small or larger motor neurons?

A

Smaller ones are easier to excite

112
Q

What is graded force?

A

Small motor units are activated first then larger motor units

113
Q

How does a somatic motor axon/neuron connect to skeletal muscle fibers?

A

Via Neuromuscular junctions

114
Q

What type are most somatic motor neurons?

A

A-alpha fibers

115
Q

What is the functional unit of a skeletal muscle?

A

Sarcomere

116
Q

What are some of the most common reason that cause injuries to tendons & ligaments?

A

Trauma, sports injury, lifting too much weight.

117
Q

Where do tendons connect to & an example?

A

Muscle to bone & Achilles tendon

118
Q

Where do ligaments connect to & an example?

A

Bone to Bone like ACL, MCL

119
Q

What type of muscles are in the voice box?

A

Skeletal

120
Q

What are we most concerned with, with damaged cells leaking?

A

Proteolytic enzymes & potassium.

121
Q

How does glucose get into muscle cells?

A

Via GLUT-4 insulin dependent transporter

122
Q

What is vasoactive tone?

A

Small skeletal muscle contractions to upkeep body temp

123
Q

How does the body control body temperature when sleeping?

A

Deep skeletal muscles continuously have small contractions

124
Q

What happens on a cellular level with malignant hyperthermia?

A

There is a dysfunction with the Ryr receptor –> continued Calcium release from the SR.

125
Q

What is the first sign of malignant hyperthermia in the OR & when will it be seen?

A

A spike in EtCO2 & relative quickly after start of inhaled anesthetics.

126
Q

What are the steps in treating MH in the OR?

A

D/C volatile agent, give dantrolene & cool the Pt

127
Q

What is the function of Dantrolene?

A

It blocks calcium release channels.

128
Q

What is the downside of giving magnesium to a paralyzed patient?

A

Reversal will take longer as Mg slows down the NMJ’s.

129
Q

What are some characteristics of smooth muscle?

A

The cells are shorter/smaller, have no defined sarcomere, cells are attached to each other, do not need multiple nuclei, the SR is less developed & relies on external calcium.

130
Q

How does hypocalcemia relate to smooth muscle?

A

In hypocalcemia we will have problems maintaining BP, the cardiac output will be reduced & have a lower SVR tone.

131
Q

What is the ratio of Actin to Myosin in smooth & in skeletal muscle?

A

Smooth 10:1 & skeletal 2:1

132
Q

What is the purpose of dense bodies, what are they made of, & where are they found?

A

Found in smooth muscle, made of collagen & fibrin, & act as connection points for Actin & connect cells together.

133
Q

What are some examples for smooth muscle locations?

A

Pupillary muscle, uterus, GI & GU systems, small & medium airways.

134
Q

What are the cut-outs in smooth muscle called & their function?

A

Caveolae & easy place for neurotransmitters to get close to the SR.

135
Q

What is the main difference in smooth muscle cross-bridge cycling?

A

The release step of the myosin head. It binds, pulls & hangs on to the thin filament even with ATP around.

136
Q

What is the advantage of smooth muscle cross-bridge cycling?

A

It’s more efficient overall. It uses much less ATP than skeletal muscle & can maintain force longer at a lower energy cost.

137
Q

What is the speed of smooth muscle cycling compared to skeletal?

A

Smooth muscle contracts at 1/10th to 1/300th the speed compared to skeletal muscle.

138
Q

What is the driving force of smooth muscle cycling?

A

ATP hydrolysis of myosin heads

139
Q

Where is the latch mechanism not functionally used?

A

In the lungs and vascular system.

140
Q

What is the latch mechanism and what happens in it?

A

The myosin head is dephosphorylated before letting go of the actin resulting in maintained contraction.

141
Q

What is the myosin head layout in smooth muscle & what is the benefit of it compared to skeletal muscle?

A

The myosin heads are staggered, allowing for much greater relaxation & contraction. It can shorten by 80% compared to 30% of skeletal muscle, which runs into the Z-disk.

142
Q

What are the two smooth muscle arrangements?

A

Visceral/Unitary & Multi-unit.

143
Q

Where are unitary arrangements found & how are they set up?

A

Found in blood vessels, uterus, ureters, GI, larger organs. Cells talk to each other via gap junctions (Na+ is the primary Ion).

144
Q

What is an example multi-unit arrangement?

A

Ciliary smooth muscle of the eye.

145
Q

What is the set-up for multi-unit arrangements, what is their benefit?

A

They are isolated from each other, each cell receives instructions. Fibrous coating of glycoproteins prevents electrical signaling between cells. The benefit is very fine control of smooth muscles.

146
Q

What is an example of a hybrid muscle?

A

The esophagus.

147
Q

What smooth muscle fibers determine SVR?

A

Arterioles

148
Q

What are the 3 layers of arteries?

A

Tunica Intima (endothelium), Tunica Media (smooth muscle) & Tunica Adventitia (Externa)

149
Q

What is different about capillary structure & what is their function?

A

Only contain endothelial cells, no smooth muscles & are good for gas & nutrient exchange.

150
Q

What is the outer most layer of an artery called & what is it made of?

A

Adventitia & made of elastin.

151
Q

Why are veins less resilient than arteries?

A

Their Adventitia layer is smaller.

152
Q

What is the resting membrane potential for skeletal muscle?

A

~ -80mV

153
Q

What is different about the GI smooth muscle membrane potential?

A

It is an oscillating potential with fluctuating Na+ & K+ permeability. Action potentials happen on and off.

154
Q

What is the resting membrane potential of the uterus?

A

~ -50mV

155
Q

What is the pathway for smooth muscle contraction?

A

Calcium enters the cell or from SR then binds to calmodulin (CaM) to form the Ca2+ calmodulin complex –> which activates MLCK –> the MLCK phosphorylates the myosin head regulatory chain –> enables cross-bridge cycling.

156
Q

What are the 2 options for vascular smooth muscle relaxation?

A

Wait for the phosphate to fall off or pull them off with myosin phosphatase.

157
Q

What is the pathway for smooth muscle relaxation?

A

ACh, bradykinin or muscarinic ligand binds to GPCR –> Ca2+ is released & binds with CaM –> that stimulates eNOS –> NO is formed from eNOS & arginine –> NO stimulates guanylyl cyclase –> GC takes GTP & turns it into cGMP –> cGMP stimulates PKG –> PKG phosphorylates cell wall Ca2+ channels &/or speeds up activity of myosin phosphatase.

158
Q

What does a PDE inhibitor do & lead to?

A

It inhibits phosphodiesterase that recycles cGMP into GMP leading to more cGMP.

159
Q

What increases NO release?

A

Increased flow thru (shear force) vessels or via neurotransmitters.

160
Q

How can a particular organ’s cGMP be targeted?

A

With specific PDE inhibitors

161
Q

What sends signals to smooth muscle cells?

A

Autonomic neuron varicosity

162
Q

Where are alpha-1 receptors not present?

A

Capillaries & brain arterial blood vessels

163
Q

How do brain blood vessels constrict?

A

Via vascular smooth muscle. It does not involve neurotransmitters.

164
Q

What is special about smooth muscle contractions vs skeletal?

A

Smooth muscles can contract without an action potential.

165
Q

What kind of muscle is located in the bladder and what can it do?

A

Smooth muscle & it can relax after being stretched.

166
Q

What are the ways that calcium levels gets reset?

A

SERCA pump, Na+/Ca2+ exchanger & PMCA (plasma membrane Ca2+ ATPase

167
Q

How does calcium released from the SR affect membrane potential?

A

It does not.

168
Q

Explain the pathway of an agonist binding to a receptor causing smooth muscle contraction.

A

Alpha subunit replaces GDP with GTP, which activates PL-C –> PL-C cleaves Phosphatidyl inositol into IP3 & DAG –> IP3 frees up Ca2+ from SR –> Ca2+ interacts with CaM –> increases MLCK phosphorylation. DAG increases activity of PK-C –> speeds up MLCK & activates Ca2+ membrane channels.

169
Q

What are the resting membrane potentials in the SA node & ventricular myocytes?

A

-55mV & -80mV

170
Q

What channels are present in nodal tissues?

A

Slow calcium channels

171
Q

How does Lidocaine affect the SA node?

A

It does not as there are no Na+ channels in the SA node.

172
Q

What is the key difference in cardiac action potentials?

A

It is calcium induced, calcium released. The SR only releases Ca2+ from the SR with an influx of external Ca2+.

173
Q

What is the difference in cardiac T-tubules vs skeletal?

A

Cardiac tubules contain L-type Ca2+ channels.

174
Q

What stores Ca2+ in the SR and how much can it store?

A

Calsequestrin & each can store 40 Ca2+ molecules out of solution.

175
Q

How much Ca2+ is removed via the exchanger & ATPase?

A

15% thru exchanger & 5% thru the Ca2+ATPase.

176
Q

What is the VRM for purkinjie fibers?

A

-90mV

177
Q

What is the action potential threshold for nodal tissue?

A

-40mV

178
Q

Activating what kind of nodal tissue receptor would result in a decrease in HR?

A

mACh-receptor

179
Q

What increases the surface area for gap junctions?

A

Intercalated discs

180
Q

What makes up the visceral pericardium?

A

Epicardium, Parietal pericardium & the fibrous pericardium.

181
Q

What is the fiber layout of the cardiac muscle & what are they called?

A

Crisscross pattern of endocardial & epicardial fibers.

182
Q

What causes the plateau in cardiac cycle?

A

Calcium entering the cell via the L-type channels.

183
Q

Besides gap junctions what is the other junction in cardiac muscle?

A

Desmosomes

184
Q

In cardiac muscle how much calcium comes from the outside & how much from the SR?

A

20% from outside & 80% from SR

185
Q

What are the two gates in slow calcium channels in nodal tissue?

A

D-gate= activation & F-gate= inactivation

186
Q

What slows down or inhibits the SERCA pump in cardiac muscle?

A

Phospholamban

187
Q

What important structure takes the grunt of the damage in an MI?

A

The Na+/K+ ATPase

188
Q

What troponins would one expect to find in the serum after an MI?

A

cardiac troponin T (cTNT) & troponin I (cTnI)

189
Q

What is the excitatory pathway via catecholamines thru beta-1 receptors?

A

Gs –> alpha subunit replaces GDP with GTP –> adenylate cyclase –> activates cAMP –> which activates PK-A –> which phosphorylates Troponin I on thin filaments –> rendering them more sensitive to calcium. Or PK-A phosphorylates L-type Ca2+ channels or phospholamban, which leads to loss of inhibition of SERCA pump -> faster reset= faster HR.

190
Q

What is the inhibitory pathway for beta-1 receptors?

A

Gi –> alpha subunit replaces GDP with GTP –> which then inhibits adenylate cyclase.

191
Q

What is an over-the-counter PDE inhibitor & what does it lead to?

A

Caffeine –> stronger & faster heartbeat

192
Q

What would cause a more gradual phase 0 slope?

A

Hyperkalemia, Lidocaine (-caine drugs), or an issue with Na+ channel reset

193
Q

What is & happens in phase 4?

A

Diastole & K+ has the highest permeability during phase 4

194
Q

What happens during phase 0?

A

Fast Na+ channels open. At the end T-type Ca2+ channels open briefly.

195
Q

What happens during phase 1?

A

Na+ inactivation gates close. Transient outward K+ channels open for a very short time.

196
Q

What creates the waveform of phase 1?

A

The Transient outward K+ channels open briefly causing some repolarization.

197
Q

What happens during phase 2?

A

Brief influx of Ca2+ thru V-G T-type Ca2+ channels, prolonged influx through L-type Ca2+ channels, some Na+ sneaks into the cell through the L-type Ca2+ channels.

198
Q

What channels are not affected by beta adrenergists?

A

T-type Ca2+ channels.

199
Q

What happens in phase 3?

A

Na+ channels reset and K+ permeability increases.

200
Q

Why does K+ permeability decrease in phase 0, 1, & 2 & what are the benefits?

A

Closure of the V-G Inward Rectifying K+ channels due to inward current of other ions. This Prevents a big K+ loss & increases the plateau phase.

201
Q

What does an atrial action potential look like?

A

A combination of Fast & slow action potentials, more like fast AP.

202
Q

Where are T-type Ca2+ channels found?

A

In ventricular muscle & purkinjie conduction system

203
Q

Rank the 3 ion permeabilities in phase 4 of nodal tissue from highest to least?

A

Na+, Ca2++, (both increase) K+ (decrease)

204
Q

What is the main determined of the nodal phase 4 slope?

A

Influx/leaking of Na+ into cell

205
Q

Which channel is activated during hyperpolarization?

A

HCN channels, or iChannels or If channels.

206
Q

What happens during phase 1 & 2 of nodal tissue?

A

Nothing, there is no phase 1 & 2.

207
Q

What happens in phase 3 of nodal tissue?

A

Repolarization, K+ permeability increases.

208
Q

What part of the heart has the fastest action potential?

A

Phase 4 of nodal tissue.

209
Q

What happens in phase 0 of nodal tissue?

A

Influx of Ca2+ thru L-type channels.

210
Q

What happens during nodal tissue phase 4?

A

Na+ leaking in, K+ Inward Rectifying channels close due to Na+ & Ca2+ influx.

211
Q

During what phase/s do inward rectifier channels close?

A

During phase 4, 0, 1, & 2.

212
Q

What would all result in a prolonged phase 4?

A

ACh interacting with its receptors increasing K+ permeability, Hypercalcemia

213
Q

What are examples of a less than usual time spent in phase 4?

A

Atropine, it blocks ACh receptors  increased RMP. Hypocalcemia

214
Q

What is the difference between Na+ & K+ channel changes in phase 4?

A

Opening or blocking K+ channels will change the resting membrane potential starting point & the slope of phase 4. Changes in Na+ will not change the starting point but it will change the phase 4 slope accordingly.

215
Q

What governs the nodal tissue Na+ permeability & through what?

A

Beta-agonist availability through HCN channels

216
Q

What can change threshold potential & how does it relate?

A

Calcium. Increased Ca2+ leads to a decreased threshold & low Ca2+ leads to an increased threshold potential.

217
Q

Spell HCN channel & when do they become active?

A

Hyperpolarization cyclic nucleotide & activated at end of phase 3 thru phase 4.

218
Q

What is another name for HCN?

A

iChannels or If (I= current & f= funny)

A&P (Fall 2022) (12 decks)

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