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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
Q

What is the Smooth Muscle version of a Z-Disc?
*Function of this

A

Dense Bodies
*Anchor actin and myosin and link to neighbor smooth muscle cells to help produce force

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22
Q

In Vascular Smooth Muscle, if you have a Ca++ of 0, why do you not have a BP?
*2 Reasons, in order

A
  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
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23
Q

Adventitia
*other name
*purpose

A

Structural support on outside of smooth muscle
*Tunica Adventitia/Externa

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24
Q

Smooth Muscle
*other name
*what can it talk to

A

Middle layer between adventitia and endothelium
*Tunica Media
*Can talk to endothelium

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24
Q

Visceral (Unitary) Smooth Muscle
*How do they communicate
*Where are they located
*Patho

A

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
Q

Endothelium
*other name
*purpose

A

1 cell thick layer lining inside smooth muscle in entire CV system
*Can talk with smooth muscle
*Tunica Intima

26
Q

Multi-Unit Smooth Muscle
*Function
*Location

A

Graded/delicate control [depend on NTM]
*Ciliary and Iris Muscles

27
Q

Esophagus
*What type of muscles are used

A

Skeletal muscle and Visceral Smooth muscle
*Only Hybrid Organ

27
Q

Only place that has endothelium, but no smooth muscle?

A

Capillaries

28
Q

Skeletal Muscle Myosin Anatomy
*Mline

A

Mline gap that separates L and R side of Sarcomere [no myosin heads and gap b/c myosin heads are different angles]

29
Q

Smooth Muscle Myosin Anatomy

A

No mline; Myosin heads different patterns

30
Q

Which can contract more: Smooth or Skeletal?

A

Smooth; due to different anatomy can shorten 1/2 of the normal length
Skeletal - only a little shorten/contraction

31
Q

Examples of mACh-R that relax

A

Vascular Smooth Muscle [GPCR]

32
Q

Example of mACh-R that excites?

A

Intestines [contract]

33
Q

Where is the Site of Regulation in Smooth Muscle?
*How does this get activated?
*Is Tropomyosin in the way?

A

Heavy Chains w/ Myosin Heads
*Inactive until phosphorylated
*Still there, but not in the way

34
Q

Difference between Kinase and Phosphotase?

A

Kinase - Adds Phosphate
Phosphotase - Pulls off Phosphate

35
Q

When is the MLCK activated?

A

Ca++ has to bind with CaM to change shape and make MLCK activated

When the Myosin head is phosphorylated [this causes contraction]

36
Q

How does MLCK become activated?

A

Ca++ binds with Calmodulin, changes shape, and binds to MLCK

36
Q

How does Ca++ get into the cell to bind to Calmodulin?

A

Ca++ Leak Channel, V-G L Type Ca++ Channels, Ligand Gated Ca++ Channels, and some from the SR

36
Q

What does Myosin Phosphatase do?
*What does this cause

A

Pulls phosphate off Myosin head, resulting in inactivation
*This stops muscle contractions

37
Q

Another Way to slow down the contraction process, besides Myosin Phosphatase?
*3 Ways

A

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
Q

Main Process to get Ca++ out of the cell?
*Ion differences

A

The Na Ca++ Exchanger
*3 Na+ in
*1 Ca++ out

39
Q

How can NO reduce the amount of MLC?

A

increasing amount of cGMP, which in turn increases the amount of PKG

39
Q

What is Protein Kinase G [PKG]
*How is it activated
*What 2 areas does it work on

A

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
Q

Pathway for NO being created

A

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
Q

Pathway for NO in Vascular Smooth Muscle

A

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
Q

What does Phosphodiesterase do?

A

Shuts down cGMP [speeds up the process of shutting it down]

43
Q

Alpha 1 Receptor Pathway/Serotonin Pathway

A

Activates PLC - Snips compound into IP3 and DAG - IP3 binds w/ Ca++ released from SR - this activates myosin heads for CBC

43
Q

What is Sildenafil?
*MOA

A

PDE5 Inhibitor
*Blocks Phosphodiesterase, which increases the length of cGMP and PKG, which increases the duration of relaxation of the vascular smooth muscle

44
Q

What is the only NTM that can constrict Brain Blood Vessels?

A

5-HT

44
Q

What is IP3 Mediated vascular smooth muscle contraction?

A

IP3 Pathway w/ PLC

45
Q

How do SSRI help with headaches?

A

they help dilate the brain blood vessels

45
Q

Does smooth muscle need an AP to contract?

A

No; if enough Ca++ leaking in, can cause contraction

46
Q

Slow Waves AP in Smooth Muscle
*Shape, what type of waveform
*Which organ uses this

A

Periodic, Oscillation Waveform [PM rhythmic activity]
Small Intestine - think cramps in rhythmic motion

47
Q

Long, Prolonged AP in Smooth Muscle

A

Quarter of a sec - L Type Ca++

47
Q

What is Calsequestrin?
*What pump does this help

A

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
Q

What is Phospholamban?
*Where is it only located

A

Inhibits SERCA pump, allowing for more Ca++ in the Sarcoplasm = longer contraction in the heart [technically slowing HR]
*Only located in Cardiac Muscle

48
Q

What does Sequestrin mean?

A

To take something out of circulation

49
Q

What happens if you give a drug that blocks Phospholamban?

A

Allows Ca++ to be tucked into SR quicker, resulting in faster HR and faster resetting of the cell

50
Q

What does the Cardiac Myocyte get most of its’ Ca++?

A

The SR

51
Q

What is Calcium Induced Calcium Release [CICR]
*Why is this important

A

Calcium coming into the cell to release Ca++
*Important b/c this is how the Cardiac Myocyte functions

52
Q

How does Ca++ Come into the Cardiac Myocyte?
*What triggers Ca++ influx

A

T-Type 1st, L-Type
*Triggered by AP and Na+ influx; Ca++ follows via T-Type, then longer term in L-Type

53
Q

Ca++ removal to outside the Myocyte
*with % of Each

A

Na+Ca++ Exhchanger [3Na+ in, 1 Ca++ out] - 15%
Ca++ ATPase [PMCA] - 5%

53
Q

Ca++ from SR in Myocyte?

A

80%

53
Q

What does beta activity stimulate in the heart?

A

Adenylyl Cyclase - ATP to cAMP - cAMP signals PKA, giving stronger contraction and faster HR

53
Q

What does mACh-R response to do myocyte?

A

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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