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A&P 1 > Exam 3 Lecture 7 > Flashcards

Exam 3 Lecture 7 Flashcards

1
Q

Active Tension
*Shape on diagram

A

Amount of force when you shock a muscle with an AP [contraction]
*Upside down U or V

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2
Q

Passive Tension
*Weight example

A

Pulling the muscles at the tendons to stretch them out
*The weight on the picture example

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3
Q

Total Tension
*Formula

A

Stretching the Muscle out by the tendons and applying and Action Potential
*Active + Passive Tension

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4
Q

Increased Load on Muscle = ? Contraction Speed

A

Decreased Muscle Contraction Speed

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5
Q

Decreased Load on Muscle = ? Contraction Speed

A

Increased Muscle Contraction Speed

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6
Q

3 Kg of Weight on a muscle, per diagram

A

Muscle can barely contract

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7
Q

1 Kg of weight on a muscle, per diagram

A

Muscle is able to contract faster

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8
Q

Load/Contraction is Important in Heart, why?

A

Increased afterload = lower CO, and longer filling time (Higher preload)

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9
Q

Increased Voltage on a motor neuron?

A

Increased motor neurons recruited

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10
Q

Temporal Summation (time)
*compared to Quantal Summation (#)
*Unit of Measurement

A

Force generation in comparison to rate of stimulation
*> than Quantal Summation
*In Hz

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11
Q

Quantal Summation

A

Number of MN activated/recruited; voltage the CNS uses to recruit MN

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12
Q

1 Hz = ? sec

A

1 stimuli per Sec

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13
Q

<10 Hz in terms of muscle contractions

A

Individual Contractions

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13
Q

40 Hz = ? sec
*Another name for this
*patho of this

A

40 stimuli per sec
*Known as Tetany
* So much Ca++ that we lose twitches and Ca++ receptors are almost saturated

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14
Q

> 10 Hz in terms of muscle contracts
*Patho of this

A

Stacked contractions; additive (no complete relaxation between muscle contractions)
*Ca++ is coming out of the SR faster than it is being put back in the SR

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15
Q

Atrophy
*Causes
*1st and 2nd to disappear

A

Shrinking of the muscle from denervation or disuse
*1st to disappear - Myofibrils
*2nd to disappear, after a long time of no use - Skeletal muscle cells

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16
Q

Hyperplasia
*cause
*Can we generate new skeletal muscle?

A

Generating new skeletal muscle cells, very slowly, by working out a lot over a long period of time

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16
Q

Hypertrophy
*Cause
*What increases and/or grows

A

Increased muscle size from exercising
*More myofibrils and growing blood vessels

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17
Q

What % of the TBW is Smooth Muscle?

A

10%

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18
Q

Smooth Muscle vs Skeletal Muscle
*Which is stronger
*Which is slower and why?
*Which is more efficient and why?
*Which cells are smaller?

A

*Smooth stronger per gram of muscle
*Smooth is slower, b/c it takes longer for myosin head to release from actin filaments - which maintains force and conserves tension
*Smooth is more efficient b/c has Latch mechanism, which is ultra low energy state that barely allows for Myosin head to detach
*Smooth cells smaller

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19
Q

Where is smooth muscle located?
*4 examples

A

Intestines, lungs, eyes, blood vessels

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20
Q

Skeletal Muscle: Actin to Myosin Ratio

A

2:1 ratio

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20
Q

Smooth Muscle: Actin to Myosin Ratio

A

10-20:1 Ratio

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20
Q

Smooth Muscle SR
*Where does smooth muscle get Ca++
*Causes of Tone in Muscle?

A

Less developed than skeletal muscle SR
*Some Ca++ in SR, mostly get from V-G Ca++, Ligand Ca++, Leaky Ca++
*Leaky Ca++ and Na+

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21
What is the Smooth Muscle version of a Z-Disc? *Function of this
Dense Bodies *Anchor actin and myosin and link to neighbor smooth muscle cells to help produce force
22
In Vascular Smooth Muscle, if you have a Ca++ of 0, why do you not have a BP? *2 Reasons, in order
1. No contraction of vascular smooth muscle, as no Ca++ and no tone 2. Heart does not induce Ca++ that it does with each heart beat
23
Adventitia *other name *purpose
Structural support on outside of smooth muscle *Tunica Adventitia/Externa
24
Smooth Muscle *other name *what can it talk to
Middle layer between adventitia and endothelium *Tunica Media *Can talk to endothelium
24
Visceral (Unitary) Smooth Muscle *How do they communicate *Where are they located *Patho
Gap junctions to talk to other neighbor cells *hollow organs and vascular smooth muscle *Na+ and little bit of Ca++ sneak through to cause contractions with neighbor cells
25
Endothelium *other name *purpose
1 cell thick layer lining inside smooth muscle in entire CV system *Can talk with smooth muscle *Tunica Intima
26
Multi-Unit Smooth Muscle *Function *Location
Graded/delicate control [depend on NTM] *Ciliary and Iris Muscles
27
Esophagus *What type of muscles are used
Skeletal muscle and Visceral Smooth muscle *Only Hybrid Organ
27
Only place that has endothelium, but no smooth muscle?
Capillaries
28
Skeletal Muscle Myosin Anatomy *Mline
Mline gap that separates L and R side of Sarcomere [no myosin heads and gap b/c myosin heads are different angles]
29
Smooth Muscle Myosin Anatomy
No mline; Myosin heads different patterns
30
Which can contract more: Smooth or Skeletal?
Smooth; due to different anatomy can shorten 1/2 of the normal length Skeletal - only a little shorten/contraction
31
Examples of mACh-R that relax
Vascular Smooth Muscle [GPCR]
32
Example of mACh-R that excites?
Intestines [contract]
33
Where is the Site of Regulation in Smooth Muscle? *How does this get activated? *Is Tropomyosin in the way?
Heavy Chains w/ Myosin Heads *Inactive until phosphorylated *Still there, but not in the way
34
Difference between Kinase and Phosphotase?
Kinase - Adds Phosphate Phosphotase - Pulls off Phosphate
35
When is the MLCK activated?
Ca++ has to bind with CaM to change shape and make MLCK activated When the Myosin head is phosphorylated [this causes contraction]
36
How does MLCK become activated?
Ca++ binds with Calmodulin, changes shape, and binds to MLCK
36
How does Ca++ get into the cell to bind to Calmodulin?
Ca++ Leak Channel, V-G L Type Ca++ Channels, Ligand Gated Ca++ Channels, and some from the SR
36
What does Myosin Phosphatase do? *What does this cause
Pulls phosphate off Myosin head, resulting in inactivation *This stops muscle contractions
37
Another Way to slow down the contraction process, besides Myosin Phosphatase? *3 Ways
Removing Ca++, so MLCK never gets activated at all * SERCA Pump to SR, Plasma Membrane Calcium ATPase pump [PMCA], and Na+ Ca++ Exchanger [3Na+ in and 1 Ca++ out]
38
Main Process to get Ca++ out of the cell? *Ion differences
The Na Ca++ Exchanger *3 Na+ in *1 Ca++ out
39
How can NO reduce the amount of MLC?
increasing amount of cGMP, which in turn increases the amount of PKG
39
What is Protein Kinase G [PKG] *How is it activated *What 2 areas does it work on
Enzyme that sticks phosphates on MLCK and reduces its activity [in cGMP side] *Activated by cGMP *Works by adding phosphates to cGMP and by adding phosphates to the Ca++ entry channels, preventing Ca++ from coming into the cell
40
Pathway for NO being created
ACh or Bradykinin bind to receptor - Binding releases Ca++ from ER, which then binds with Calmodulin - This changes shape and increases the activity of ENOS to turn L-Arginine to NO - NO diffuses into Vascular Smooth Muscle
41
Pathway for NO in Vascular Smooth Muscle
After diffusing into smooth muscle, it interacts with soluble Guanylyl Cyclase - this takes GTP to cGMP - cGMP upregulates PKG - PKG phosphorylates MLCK and Ca++ entry, which results in relaxation of vascular smooth muscle
42
What does Phosphodiesterase do?
Shuts down cGMP [speeds up the process of shutting it down]
43
Alpha 1 Receptor Pathway/Serotonin Pathway
Activates PLC - Snips compound into IP3 and DAG - IP3 binds w/ Ca++ released from SR - this activates myosin heads for CBC
43
What is Sildenafil? *MOA
PDE5 Inhibitor *Blocks Phosphodiesterase, which increases the length of cGMP and PKG, which increases the duration of relaxation of the vascular smooth muscle
44
What is the only NTM that can constrict Brain Blood Vessels?
5-HT
44
What is IP3 Mediated vascular smooth muscle contraction?
IP3 Pathway w/ PLC
45
How do SSRI help with headaches?
they help dilate the brain blood vessels
45
Does smooth muscle need an AP to contract?
No; if enough Ca++ leaking in, can cause contraction
46
Slow Waves AP in Smooth Muscle *Shape, what type of waveform *Which organ uses this
Periodic, Oscillation Waveform [PM rhythmic activity] Small Intestine - think cramps in rhythmic motion
47
Long, Prolonged AP in Smooth Muscle
Quarter of a sec - L Type Ca++
47
What is Calsequestrin? *What pump does this help
Takes Ca++ out of circulation to put into SR *Helps the SERCA pump, as it changes the concentration of Ca++ i/s the cell
48
What is Phospholamban? *Where is it only located
Inhibits SERCA pump, allowing for more Ca++ in the Sarcoplasm = longer contraction in the heart [technically slowing HR] *Only located in Cardiac Muscle
48
What does Sequestrin mean?
To take something out of circulation
49
What happens if you give a drug that blocks Phospholamban?
Allows Ca++ to be tucked into SR quicker, resulting in faster HR and faster resetting of the cell
50
What does the Cardiac Myocyte get most of its' Ca++?
The SR
51
What is Calcium Induced Calcium Release [CICR] *Why is this important
Calcium coming into the cell to release Ca++ *Important b/c this is how the Cardiac Myocyte functions
52
How does Ca++ Come into the Cardiac Myocyte? *What triggers Ca++ influx
T-Type 1st, L-Type *Triggered by AP and Na+ influx; Ca++ follows via T-Type, then longer term in L-Type
53
Ca++ removal to outside the Myocyte *with % of Each
Na+Ca++ Exhchanger [3Na+ in, 1 Ca++ out] - 15% Ca++ ATPase [PMCA] - 5%
53
Ca++ from SR in Myocyte?
80%
53
What does beta activity stimulate in the heart?
Adenylyl Cyclase - ATP to cAMP - cAMP signals PKA, giving stronger contraction and faster HR
53
What does mACh-R response to do myocyte?
ACh binding causes mACh-r to slow down Adenylyl Cyclase - decreasing cAMP, which decreases PKA, which slowers HR, slower resetting of the cell, and weaker contraction

A&P 1 (24 decks)

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