Exam 3 Flashcards
1
Q
What is usually the cause of ELMS?
A
Paraneoplastic syndrome related to lung cancer.
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.
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.
4
Q
What happens in ELMS on the cellular level?
A
Antibodies attach & block the P-type Ca2+ channel –> decreased neurotransmitter release.
5
Q
What is the difference between MG & ELMS S/S?
A
In ELMS the S/S get better with activity.
6
Q
Where do ELMS S/S usually start and what are they?
A
Weakness in peripheral muscles & fatigue
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.
8
Q
What are the treatments for MG?
A
AChE inhibitors, Thymus gland removal, plasmapheresis
9
Q
What test is used to diagnose MG?
A
Tensilon test, Give AChE inhibitor & if response gets better then positive for MG
10
Q
What are later S/S of MG?
A
Larger muscle group weakness & eventually the diaphragm
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.
12
Q
Which nACh receptor is not affected by paralytics?
A
The Neuronal ACh receptor. It has five 𝝰7 subunits
13
Q
What happens in Myasthenia Gravis?
A
Auto immune antibodies attach to nACh receptor & destroys them
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.
15
Q
What happens in a SCc phase 2 block?
A
The nACh receptors on the muscle do not work well.
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.
17
Q
Why is there a drop-off in TOF response in non-depolarizing blockers?
A
The 𝝰3β2 receptor is blocked
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.
19
Q
What is accommodation?
A
nACh receptors do not like interacting with SCc & will shut down with continuous administration.
20
Q
What are 3 alternative locations for nerve stimulation?
A
Ophthalmic branch of facial nerve, Peroneal nerve, & Posterior tibial nerve
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.
22
Q
What is an example to check for quantitative force?
A
Pressure transducer under the thumb
23
Q
Which nerve stimulation would be used to recruit all motor units via all motor neurons?
A
Supramaximal Stimulus.
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.
25
How is Double Burst Stimulation performed?
At a high frequency with short breaks in between
26
Using 2Hz per second over 2 seconds is an example of what?
Train of Four nerve stimulation
27
What is the typical monitoring interval for single twitch?
1 twitch / 10 sec
28
What current flows through a nerve stimulator?
20-50mA
29
How does depolarization work with nerve stimulator?
The outside of the cell is made negative same as the inside.
30
Which muscle is stimulated by the ulnar nerve?
Adductor pollicis
31
How long does it take for immature ACh receptors to be produced?
~ 12hrs
32
Which patients should not receive succinylcholine, what is the body’s natural skeletal muscle response & what wold happen if they received SCc?
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.
33
How fast in the onset & long do the effects of succinylcholine last?
~ 47sec & last ~ 4mins
34
What happens after the initial depolarization when SCc is given?
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
35
What is the acetate methyl linkage?
The bond that binds the 2 ACh molecules end to end forming succinylcholine.
36
What & where cleans up succinylcholine?
By Butyrylcholinesterase in the plasma.
37
What is the relationship of hypocalcemia & resting membrane potential?
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.
38
What are the 2 types of secretory vesicles in skeletal presynapses?
VP-2: Are ready to go vesicles close to the membrane. VP-1: Farther back & move towards the membrane.
39
What are the 3 types of calcium channels and where are they found & what is the benefit?
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.
40
For which condition is succinylcholine contraindicated for?
An eye issue. It increases IOP substantially. Also, ocular muscle is innervated by multiple motor neurons, which can lead to multiple fasciculations/contractions.
41
What is the difference between high & low conductance channels?
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.
42
Is hyperplasia in skeletal muscle possible?
Yes, but it takes a very long time.
43
What all happens in hypertrophy in relation to skeletal muscles?
There is an increase in myofibrils, not cells themselves. Also, the blood vessels will increase in size & amount (angiogenesis).
44
What does the term denervation refer to?
Extreme non-use of skeletal muscle. Ex: spinal cord injury.
45
What is temporal summation in skeletal muscle?
A second stimulus is applied to a muscle before completion of relaxation (Ca2+ build up).
46
What happens at the cell level when we reach 10-12Hz in muscle contraction?
More Ca2+ enters the cell than can be removed --> sustained contraction.
47
At what level do we not see any temporal summation?
Between 1-10Hz
48
What does tetanization refer to?
Max contraction at max force.
49
What does quantal summation?
The quantity of motor units
50
In which circumstance are heavy loads detrimental?
In the cardiac muscle. High afterload --> increased time the ventricle walls need to contract.
51
Explain the velocity difference in skeletal muscles between light & heavy loads.
In light loads the velocity of muscle contraction is very fast. In heavy loads the contraction slows down --> prolonged contraction.
52
What is the Load/Contraction Velocity diagram used for?
It can quantify the rate of speed of contraction to the force.
53
What is passive tension?
Tension used to stretch out the muscle (pre-tension)
54
What is active tension?
The force a muscle produces when contracted.
55
What are some side effects (3), mentioned in class, of too much ACh in the body?
Increased mucus, bradycardia, increased alertness.
56
What condition would an AChE blocker be used for?
Alzheimers, MG
57
What class of drug inhibits AChE?
The “stygmine’s”
58
What chops up ACh that diffuses away from the NMJ?
Plasma AChE
59
What produces AChE?
Skeletal muscle
60
What is the purpose of Calsequestrin?
It binds & stores Ca2+ out of solution
61
How is calcium released from the SR in a skeletal muscle?
The dihydropyridine receptor (DHP) in the T-tubules sense a voltage change and then pulls the Ryr open.
62
What is an end plate potential?
The initial & minimum amount of depolarization of the postsynaptic cell needed for an action potential
63
What all moves through an nACh receptor into the cell?
Primarily Na+ but Ca2+ can also move through
64
Which subunits of an nACh must bind for the receptor to open?
Both alpha subunits
65
How many & what are the subunits on a mature nACh receptor?
5 & 2 alpha, 1 beta, 1 delta & 1 epsilon
66
About how many nACh receptors are there in each NMJ?
About 5 million
67
About what % of receptors are activated at any given time & why?
Only about 10% & it is a safety factor, to ensure muscle are only activated when needed.
68
Where would V-G Na+ channels be located in the synapse?
Towards the end of the cleft closer to the neuron
69
What is the first thing ACh neurotransmitter encounters when released from the pre-synapse?
AChE
70
What increases NMJ surface area & their 2 names?
Invaginations or Subneural clefts
71
Where are Teloglial cells present & their functions?
At the NMJ & help maintain the myelin sheath.
72
What happens to crossbridge cycling in rigor mortis?
There is an ATP depletion --> the myosin head is stuck to the Actin filament.
73
How does the myosin head release from Actin & gets its tension back?
The ADP on the myosin head gets replaced with ATP then the ATP is hydrolyzed and the myosin has now ADP & Pi.
74
What are the 3 Troponins that play a role in muscle contraction & what do they bind to?
Troponin I binds to F-Actin, Troponin T binds to Tropomyosin, Troponin C binds to calcium.
75
How does crossbridge cycling happen?
Troponin C binds to calcium --> Actin strands unwind exposing the active sites & myosin binds & pulls.
76
What hides the active sites on Actin filaments?
The Tropomyosin
77
What are the 4 parts of Actin filaments?
Active sites, Troponin complex, F-Actin, Tropomyosin
78
What do Myosin heads bind to?
The active sites on F-Actin
79
What is the function is myosin light chains?
ATPase activity & act as regulatory chain
80
What is each myosin molecule composed of?
2 heavy chains (Tail), 4 light chains (Heads)
81
What is the best way to repair an achilles tendon? What is usually done?
Suture back together. Usually it is overstretched & drilled.
82
What happens when muscles lose stretch?
We lose force
83
What muscle pulls up into a ball when the Achilles tendon tears?
The Gastrocnemius muscle
84
What is the reason for a muscle cell to have multiple nuclei?
Muscles are very long and get worn out quickly, so multiple nuclei can repair & support the muscle better plus no space for transport system.
85
Which muscle is purposely under stretched?
The heart muscle
86
What happens to the I band during a contraction?
It gets very narrow or disappears.
87
What happens at the Sarcomere level during a contraction?
The myosin head pulls the Actin filaments towards the middle.
The I band shrinks, H band disappear, Z disk move closer together.
88
Does the A-band width change during contraction?
No
89
What makes up the Z disk?
Actin filaments anchoring into each other.
90
Where are Z disks located?
At the end of each sarcomere
91
What is the H Zone/band composed of?
Only myosin
92
What is the A band composed of?
Actin & Myosin
93
What is the I band composed of?
Only Actin
94
What does Titin do?
It locks myosin filament to the Z-disk
95
What make up the different kind of bands on Myofibrils?
Actin & Myosin. Myosin are thicker & Actin are thinner
96
What is the purpose of Transverse Tubules?
They help with signal propagation deep into skeletal muscle
97
What is the special function of the sarcoplasmic reticulum in muscle?
It stores calcium
98
What is the Sarcoplasm?
Fluid inside the Sarcolemma
99
What is the sarcolemma?
The outer membrane of a skeletal muscle
100
Why could eating too much red meat cause cancer?
The myoglobin can cause oxidative stress, which can lead to cancer.
101
What is an example of a Type 1 muscle?
The Soleus muscle (calf muscle)
102
What is an example of a Type 2 muscle?
The Ocular muscle
103
What is the purpose of myoglobin?
It has O2 binding sites & helps with O2 unloading from blood vessels into muscle.
104
What type of muscle is darker in color and why?
Type 1 due to the myoglobin (iron heme)
105
What surrounds each muscle fiber?
The sarcolemma
106
What is the difference between Type 1 & Type 2 muscles?
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
What is the make up of skeletal muscles from smallest to largest?
Sarcomere -> Myofibril -> Muscle fiber -> fascicle -> muscle.
108
What is a fasciculus?
A group of skeletal muscle fibers/cells that contract when told by CNS
109
What makes up muscle fibers?
Myofibrils
110
What components make up a motor unit?
Somatic motor axon & Neuromuscular junctions
111
Which are easier to excite, small or larger motor neurons?
Smaller ones are easier to excite
112
What is graded force?
Small motor units are activated first then larger motor units
113
How does a somatic motor axon/neuron connect to skeletal muscle fibers?
Via Neuromuscular junctions
114
What type are most somatic motor neurons?
A-alpha fibers
115
What is the functional unit of a skeletal muscle?
Sarcomere
116
What are some of the most common reason that cause injuries to tendons & ligaments?
Trauma, sports injury, lifting too much weight.
117
Where do tendons connect to & an example?
Muscle to bone & Achilles tendon
118
Where do ligaments connect to & an example?
Bone to Bone like ACL, MCL
119
What type of muscles are in the voice box?
Skeletal
120
What are we most concerned with, with damaged cells leaking?
Proteolytic enzymes & potassium.
121
How does glucose get into muscle cells?
Via GLUT-4 insulin dependent transporter
122
What is vasoactive tone?
Small skeletal muscle contractions to upkeep body temp
123
How does the body control body temperature when sleeping?
Deep skeletal muscles continuously have small contractions
124
What happens on a cellular level with malignant hyperthermia?
There is a dysfunction with the Ryr receptor --> continued Calcium release from the SR.
125
What is the first sign of malignant hyperthermia in the OR & when will it be seen?
A spike in EtCO2 & relative quickly after start of inhaled anesthetics.
126
What are the steps in treating MH in the OR?
D/C volatile agent, give dantrolene & cool the Pt
127
What is the function of Dantrolene?
It blocks calcium release channels.
128
What is the downside of giving magnesium to a paralyzed patient?
Reversal will take longer as Mg slows down the NMJ’s.
129
What are some characteristics of smooth muscle?
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
How does hypocalcemia relate to smooth muscle?
In hypocalcemia we will have problems maintaining BP, the cardiac output will be reduced & have a lower SVR tone.
131
What is the ratio of Actin to Myosin in smooth & in skeletal muscle?
Smooth 10:1 & skeletal 2:1
132
What is the purpose of dense bodies, what are they made of, & where are they found?
Found in smooth muscle, made of collagen & fibrin, & act as connection points for Actin & connect cells together.
133
What are some examples for smooth muscle locations?
Pupillary muscle, uterus, GI & GU systems, small & medium airways.
134
What are the cut-outs in smooth muscle called & their function?
Caveolae & easy place for neurotransmitters to get close to the SR.
135
What is the main difference in smooth muscle cross-bridge cycling?
The release step of the myosin head. It binds, pulls & hangs on to the thin filament even with ATP around.
136
What is the advantage of smooth muscle cross-bridge cycling?
It’s more efficient overall. It uses much less ATP than skeletal muscle & can maintain force longer at a lower energy cost.
137
What is the speed of smooth muscle cycling compared to skeletal?
Smooth muscle contracts at 1/10th to 1/300th the speed compared to skeletal muscle.
138
What is the driving force of smooth muscle cycling?
ATP hydrolysis of myosin heads
139
Where is the latch mechanism not functionally used?
In the lungs and vascular system.
140
What is the latch mechanism and what happens in it?
The myosin head is dephosphorylated before letting go of the actin resulting in maintained contraction.
141
What is the myosin head layout in smooth muscle & what is the benefit of it compared to skeletal muscle?
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
What are the two smooth muscle arrangements?
Visceral/Unitary & Multi-unit.
143
Where are unitary arrangements found & how are they set up?
Found in blood vessels, uterus, ureters, GI, larger organs. Cells talk to each other via gap junctions (Na+ is the primary Ion).
144
What is an example multi-unit arrangement?
Ciliary smooth muscle of the eye.
145
What is the set-up for multi-unit arrangements, what is their benefit?
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
What is an example of a hybrid muscle?
The esophagus.
147
What smooth muscle fibers determine SVR?
Arterioles
148
What are the 3 layers of arteries?
Tunica Intima (endothelium), Tunica Media (smooth muscle) & Tunica Adventitia (Externa)
149
What is different about capillary structure & what is their function?
Only contain endothelial cells, no smooth muscles & are good for gas & nutrient exchange.
150
What is the outer most layer of an artery called & what is it made of?
Adventitia & made of elastin.
151
Why are veins less resilient than arteries?
Their Adventitia layer is smaller.
152
What is the resting membrane potential for skeletal muscle?
~ -80mV
153
What is different about the GI smooth muscle membrane potential?
It is an oscillating potential with fluctuating Na+ & K+ permeability. Action potentials happen on and off.
154
What is the resting membrane potential of the uterus?
~ -50mV
155
What is the pathway for smooth muscle contraction?
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
What are the 2 options for vascular smooth muscle relaxation?
Wait for the phosphate to fall off or pull them off with myosin phosphatase.
157
What is the pathway for smooth muscle relaxation?
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
What does a PDE inhibitor do & lead to?
It inhibits phosphodiesterase that recycles cGMP into GMP leading to more cGMP.
159
What increases NO release?
Increased flow thru (shear force) vessels or via neurotransmitters.
160
How can a particular organ’s cGMP be targeted?
With specific PDE inhibitors
161
What sends signals to smooth muscle cells?
Autonomic neuron varicosity
162
Where are alpha-1 receptors not present?
Capillaries & brain arterial blood vessels
163
How do brain blood vessels constrict?
Via vascular smooth muscle. It does not involve neurotransmitters.
164
What is special about smooth muscle contractions vs skeletal?
Smooth muscles can contract without an action potential.
165
What kind of muscle is located in the bladder and what can it do?
Smooth muscle & it can relax after being stretched.
166
What are the ways that calcium levels gets reset?
SERCA pump, Na+/Ca2+ exchanger & PMCA (plasma membrane Ca2+ ATPase
167
How does calcium released from the SR affect membrane potential?
It does not.
168
Explain the pathway of an agonist binding to a receptor causing smooth muscle contraction.
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
What are the resting membrane potentials in the SA node & ventricular myocytes?
-55mV & -80mV
170
What channels are present in nodal tissues?
Slow calcium channels
171
How does Lidocaine affect the SA node?
It does not as there are no Na+ channels in the SA node.
172
What is the key difference in cardiac action potentials?
It is calcium induced, calcium released. The SR only releases Ca2+ from the SR with an influx of external Ca2+.
173
What is the difference in cardiac T-tubules vs skeletal?
Cardiac tubules contain L-type Ca2+ channels.
174
What stores Ca2+ in the SR and how much can it store?
Calsequestrin & each can store 40 Ca2+ molecules out of solution.
175
How much Ca2+ is removed via the exchanger & ATPase?
15% thru exchanger & 5% thru the Ca2+ATPase.
176
What is the VRM for purkinjie fibers?
-90mV
177
What is the action potential threshold for nodal tissue?
-40mV
178
Activating what kind of nodal tissue receptor would result in a decrease in HR?
mACh-receptor
179
What increases the surface area for gap junctions?
Intercalated discs
180
What makes up the visceral pericardium?
Epicardium, Parietal pericardium & the fibrous pericardium.
181
What is the fiber layout of the cardiac muscle & what are they called?
Crisscross pattern of endocardial & epicardial fibers.
182
What causes the plateau in cardiac cycle?
Calcium entering the cell via the L-type channels.
183
Besides gap junctions what is the other junction in cardiac muscle?
Desmosomes
184
In cardiac muscle how much calcium comes from the outside & how much from the SR?
20% from outside & 80% from SR
185
What are the two gates in slow calcium channels in nodal tissue?
D-gate= activation & F-gate= inactivation
186
What slows down or inhibits the SERCA pump in cardiac muscle?
Phospholamban
187
What important structure takes the grunt of the damage in an MI?
The Na+/K+ ATPase
188
What troponins would one expect to find in the serum after an MI?
cardiac troponin T (cTNT) & troponin I (cTnI)
189
What is the excitatory pathway via catecholamines thru beta-1 receptors?
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
What is the inhibitory pathway for beta-1 receptors?
Gi --> alpha subunit replaces GDP with GTP --> which then inhibits adenylate cyclase.
191
What is an over-the-counter PDE inhibitor & what does it lead to?
Caffeine --> stronger & faster heartbeat
192
What would cause a more gradual phase 0 slope?
Hyperkalemia, Lidocaine (-caine drugs), or an issue with Na+ channel reset
193
What is & happens in phase 4?
Diastole & K+ has the highest permeability during phase 4
194
What happens during phase 0?
Fast Na+ channels open. At the end T-type Ca2+ channels open briefly.
195
What happens during phase 1?
Na+ inactivation gates close. Transient outward K+ channels open for a very short time.
196
What creates the waveform of phase 1?
The Transient outward K+ channels open briefly causing some repolarization.
197
What happens during phase 2?
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
What channels are not affected by beta adrenergists?
T-type Ca2+ channels.
199
What happens in phase 3?
Na+ channels reset and K+ permeability increases.
200
Why does K+ permeability decrease in phase 0, 1, & 2 & what are the benefits?
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
What does an atrial action potential look like?
A combination of Fast & slow action potentials, more like fast AP.
202
Where are T-type Ca2+ channels found?
In ventricular muscle & purkinjie conduction system
203
Rank the 3 ion permeabilities in phase 4 of nodal tissue from highest to least?
Na+, Ca2++, (both increase) K+ (decrease)
204
What is the main determined of the nodal phase 4 slope?
Influx/leaking of Na+ into cell
205
Which channel is activated during hyperpolarization?
HCN channels, or iChannels or If channels.
206
What happens during phase 1 & 2 of nodal tissue?
Nothing, there is no phase 1 & 2.
207
What happens in phase 3 of nodal tissue?
Repolarization, K+ permeability increases.
208
What part of the heart has the fastest action potential?
Phase 4 of nodal tissue.
209
What happens in phase 0 of nodal tissue?
Influx of Ca2+ thru L-type channels.
210
What happens during nodal tissue phase 4?
Na+ leaking in, K+ Inward Rectifying channels close due to Na+ & Ca2+ influx.
211
During what phase/s do inward rectifier channels close?
During phase 4, 0, 1, & 2.
212
What would all result in a prolonged phase 4?
ACh interacting with its receptors increasing K+ permeability, Hypercalcemia
213
What are examples of a less than usual time spent in phase 4?
Atropine, it blocks ACh receptors increased RMP. Hypocalcemia
214
What is the difference between Na+ & K+ channel changes in phase 4?
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
What governs the nodal tissue Na+ permeability & through what?
Beta-agonist availability through HCN channels
216
What can change threshold potential & how does it relate?
Calcium. Increased Ca2+ leads to a decreased threshold & low Ca2+ leads to an increased threshold potential.
217
Spell HCN channel & when do they become active?
Hyperpolarization cyclic nucleotide & activated at end of phase 3 thru phase 4.
218
What is another name for HCN?
iChannels or If (I= current & f= funny)
