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Physiology > Lecture 5-7 > Flashcards

Lecture 5-7 Flashcards

1
Q

Myofilament

A

Actin and myosin filaments that make up a sarcomere

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2
Q

Myofibrils

A

A chain of sarcomeres w/in a myofiber

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3
Q

Myofiber

A

Individual multinucelated muscle cell

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4
Q

Sarcolemma

A

Cell membrane of muscle fiber

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5
Q

Endomysium

A

Delicate CT around each myofiber

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6
Q

Fascicle

A

A bundle of myofibers

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7
Q

Perimysium

A

CT surrounding individual Fascicle

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8
Q

Muscle

A

Made up of fascicles “bundle of sticks”

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9
Q

Epimysium

A

CT surrounding entire muscle

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10
Q

Z discs [lines]

A

Anchor actin filaments

Located at each end of a sarcomere

Z-between

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11
Q

I bands

A

Composed entirely of actin

Width changes during contraction

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12
Q

A bands

A

Actin and myosin

With doesn’t change during contraction

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13
Q

H bands

A

Composed entirely of myosin

Width changes during contraction

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14
Q

How many t-tubules to sarcomere?

A

2 t tubules to a sarcomere

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15
Q

Changes that occur during sarcomere contraction

A

HI changes

A band doesn’t change

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16
Q

Sliding filament mechanism events:

A
  1. AP at terminal end of nerve fiber
  2. Opening of voltage-gated Ca++ channels o nerve fiber ending
  3. Release of Ach from synaptic vesicles into synaptic cleft
  4. Opening of ligand-gated Na+ channels of sarcolemma
  5. Generation of AP on sarcolemma
  6. Voltage-gated channels on T tubules interact w/ ryanodine receptors on SR
  7. Opening of ryanodine-sensitive Ca+ ion release channels
  8. increase Ca++ [ ] in cytosol
  9. Activation of sliding filament mechanism
  10. released Ca+ binds to troponin.
  11. Tropomyosin uncovers myosin binding sites on actin.
  12. ATPase heads of myosin molecules split ATP and bind to actin.
  13. Stored energy in myosin head causes deformation so that thick /thin filaments slide past one another
  14. A 2nd ATP binds to myosin and causes it to release actin.
  15. Repeated over and over
  16. Contractions ends when ATP-dependent Ca+ pump gets Ca+ back to SR.
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17
Q

Does binding of myosin head or release of myosin head req’ ATP?

A

Release after the powerstroke

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18
Q

Describe role of SR and T tubules in muscle contraction:

A

T-tubules: When depolarizer by AP, conformational change in DHP receptor and ryanodine receptor= opening of ryanodine Ca+ channels

SR: Ca+ released after its ryanodine receptor is opened by DHP on T tubule

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19
Q

Role of Ca++ in muscle contraction

A

Ca+ binds to troponin which allows tropomyosin to uncover myosin binding sites on actin—–

Exposes active site

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20
Q

Function of SERCA

A

Sarcoplasmic reticulum Ca++ ATPase: recycles Ca++ against [ ] gradient…ATP-dependent.

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21
Q

Function of calsequestrin

A

Takes Ca+ out of sol’n makes job easier for SERCA…

Lessens the [] of Ca++gradient to lower resistance

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22
Q

Function of DHP

A

Voltage gated L-type calcium channels arranged in quadruplets

On sarcolemma of t tubules; conformational change results in opening of SR ryanodine channels allowing Ca++ into the cytosol

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23
Q

Function of ryanodine channels

A

Allow Ca+ to flow into cytosol to initiate muscle contraction…must be activated by DHP

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24
Q

Preload

A

load on a muscle in the relaxed state

Results: passive tension-stretching

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25
Q

Afterload

A

Load the muscle works against

Results: if more force is generated than afterload =isotonic contraction

If muscle generates less force than afterload=. Isometric contraction

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26
Q

Active vs passive tension

A

Active: produced by cross-bridge cycling-contraction

Passive: produced by preload

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27
Q

What is meant by cross-bridge cycling?

A

Contraction is the continuous cycling of cross-bridging. ATP is not req’d to form the cross-bridge linking to actin but is req’d to break the link w/ actin.

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28
Q

Muscle length-tension relative to changes in sarcomere length…why?

A

Length

  1. 5microm —0 tension
  2. 2—Max. Tension
  3. 65—max. Tension
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29
Q

Where is ATP req’d for muscle contraction

A

Most used during sliding filament mechanism

Pumping Ca++ from sarcoplasm to SR.

Pumping Na+ and K+ through the sarcolemma to reestablish resting potential

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30
Q

Sources of rephosphorylation during muscle contraction and significance:

A

Phosphocreatine: releases energy rapidly…reconstitutes ATP.. ATP+phosphocreatine =5-8 sec of contraction

Glycolysis: Lactic acid build-up
Can sustain contraction for 1 minute

Oxidative metabolism: Provides > 95% energy needed for long-term contraction.

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31
Q

Compare isotonic and isometric contractions

A

Isometric:
Increase in tension but not length…ex: wall sit

Isotonic:
Muscle length changes…ex: push-up

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32
Q

Concentric isotonic muscle contraction

A

Contraction when muscle shortens

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33
Q

Eccentric isotonic muscle contraction

A

Contraction when the muscle lengthens

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34
Q

Fast fibers-light fibers

A

Contract rapidly but have less endurance

Fewer mito. –primarily anaerobic resp.
Little myoglobin, LARGER [ ] of ATPase

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35
Q

Slow fibers-dark fibers

A

Contract slowly but more endurance

More mito. -use aerobic resp.

More myoglobin..smaller [ ] of ATPase

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36
Q

Define motor unit

A

A neuron and the myofibers it innervates makes up a motor unit.

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37
Q

Summation

A

Additional spike can occur before the previous Ca++ ions have been returned to the SR.

Increase in Total amt. Ca++ in cytosol and increases the rate of cycling btw myosin and actin cross-bridging.

Leading up to tetany…motor units are becoming locked up

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38
Q

Tetany

A

Muscle remains at maximal contraction. No time for relaxation btw spikes

39
Q

3 types of lever systems:

A

1st, 2nd, and 3rd class

40
Q

1st class muscle lever system

A

Fulcrum in the middle

Ex: seesaw

In and out force move in OPPO directions

41
Q

2nd class muscle lever system

A

resistance is in the middle

Ex: wheelbarrow

Both in and out force on same side of fulcrum

42
Q

3rd class muscle lever system

A

Effort [in-force] is in the middle

Ex: lifting a weight in palm

Both forces are same side of fulcrum

43
Q

Describe cellular characteristics of single axon

A

Many mito. Synaptic vesicles w/ Ach
Dense bars
Synaptic gutter
Synaptic cleft

44
Q

How many Ach released via exocytosis:

A

300,000

45
Q

Dense bars

A

Anchored to the presynaptic membrane and asso. W/ synaptic vesicles to which they are tethered by short filaments

Hypothesis: help guide exocytosis…not truly known.

46
Q

Synaptic gutter(trough)

A

Groove or furrows in the surface of a sarcolemma in which the axon terminal makes contact w/ the sarcolemma

Subneural clefts are smaller clefts in the bottome of the synaptic trough.

47
Q

Synaptic cleft

A

20-30 nm wide

Narrow but real gap btw the axolemma of the axon terminal and the sarcolemma of the innervated muscle fiber.

48
Q

structure of Ach gated channel

A

Sarcolemma of skeletal muscle:

  • has Ach-gated channels
  • 275,000mw
  • 2 alpha,1 beta,1 gamma, and 1 delta protein
  • tubular channel remains closed until 2 Ach molecules attach to its alpha subunits
49
Q

Which subunit does Ach attach?

A

Must attach to the 2 alpha proteins to open channels

50
Q

Where are vesicles for neurotransmitters formed in the neuron? How are they transported?

A

Formed in the Golgi and are carried by axonal transport to axon terminus -this is where they are filled w/ Ach

51
Q

Compare Ca++ [ ]outside and inside the axoplasm:

A

[Ca++] =
ECF: 1-2 mM
Intracellular:

52
Q

How does calcium enter the axon during the transmission of an action potential

A

When AP arrives at the terminus of the axon, voltage gated channels open and Ca+ enter axon terminus…

AP activates dihydropyridine channels and the conformational Change allows Ca+ to flow out of ryanodine channels

53
Q

Number of Ach molecules that attach to each ligand gated channel?

A

125 vesicles fuse to the neuronal membrane and empty their contents into the synaptic cleft

54
Q

Define end plate potential

A

Created by large numbers of Na+ to pass through muscle fiber membrane…[50-75mV] initiates a AP on the sarcolemma

55
Q

Steps in skeletal muscle contraction beginning w/ release of Ach from neuron:

A

1: Release of Ach into synaptic cleft
2: diffusion across cleft
3: Binding of Ach to Ach receptors on sarcolemma
4: opening ligand-gated channels
5: Na+ influx
6: End plate depolarization
7: Opening of voltage gated Na+ channels—>sarcolemma AP
8: depolarization of T-tubule
9: conformational change in DHP receptor –>change in ryanodine
10: Ca+ release from SR d/t open ryanodine channels
11: Ca+ [ ] increase in cytosol
12: binding of Ca+ to troponin C
13: Conformational change in troponin
14: Tropomyosin is pulled away from active sites on actin-exposure
15: binding of myosin heads to actin active sites

56
Q

How is Ach removed from synaptic cleft? Acetylcholinesterase?

A

Degradation into choline and acetate by aceytlcholinesterase

Resp take of choline by axon end terminal

Diffusion of Ach away from site.

57
Q

Drugs that mimic Ach but are not broken down by aceytlcholinesterase and describe their effect on muscle contraction:

A

Methacholine, carbachol, and nicotine:
same effect on muscle fiber as Ach, but aren’t broken down byacteylcholinesterase-cause spasm

Neostigmine, physostigmine, and diisopropyl flourophosphates:
Inactivate acetylcholinesterase- cause spasm

Curare:
Prevents passage of impulses from nerve ending into muscle-cause paralysis

58
Q

Cause of myasthenia gravis and effects:

A

Autoimmune disease where antibodies attack Ach recptors…End plate potentials are too weak to initiate opening of the voltage-gated Na+ channels.

Effects: muscle weakness/spasm

59
Q

How neostigmine alleviate effects of MG?

A

Inactivated aceytlcholinesterase to allow movement

60
Q

Tricuspid valve

A

3 leaf valve on R side

61
Q

Bicuspid/mitral valve

A

2 leaf valve on L side

62
Q

Cardiac muscle tissue vs. skeletal

A

Cardiac:
Syncytium- 1 cell coupled to a neighbor via gap junctions

Striated[ skeletal also], mononucleated, intercalated discs, and cell branching did

63
Q

T tubules in skeletal and cardiac fibers

A

Skeletal: at the ends of thick filaments. 2 cisternae, triads w/ SR. SR more extensive.

Cardiac: along the Z line. One cisterna per T, form diads w/ SR. SR is less extensive

64
Q

Fast cardiac muscle APs:

A

Fast: found in atria,ventricles, and conduction system

Rapidly conducting but non-contractile in purkinje fibers

Rapidly conducting and contractile in atrial and ventricular fibers

High amplitude [100mV]

65
Q

Slow cardiac muscle AP’s

A

Found in SA and AV nodal tissues

Conducts slowly

Automatically depolarizes during resting phase-faster in SA[why it’s pacemaker]

Low Amplitude [60mV]

66
Q

Five phases of cardiac muscle AP

A 
Phase 4: resting 
Phase 0: rapid depolarization
Phase 1: initial, incomplete repolarization
Phase2: plateau or slow decline of membrane potential
Phase 3: Repolarization
 1 I\_2_
   I.     \
0 I       \ 3
 _I         \\_\_\_\_\_4
67
Q

Fast action potentials

A

D/t changes in conductance of K+,Na+, and Ca+

Conductance pattern is mostly d.t voltage dependent gates

Greater AP amp. , rapid rate of rise of phase 0, and larger cell diameter result in faster conduction velocity

68
Q

Slow AP

A

No fast Na+ ion gates

Upstroke (- to +) of AP is due to Ca+—slow!

Resting phase potential 4 is close to -60mV rather than -90mV[fast AP]

Change in potential is less than fast

SA and AV nodal tissue will spontaneously depolarize slowly to reach threshold during phase 4

69
Q

Characteristics of fast type contractile myocytes:

A

Large diameter

High amplitude

Rapid onset of AP

70
Q

Characteristics of fast type non-contractile myocytes:

A

VERY large diameter

VERY rapid upstroke

71
Q

Characteristics of slow type non-contractile myocytes:

A

small diameter

Low amplitude

Slow rate of depolarization

72
Q

Role of ions in creation of cardiac muscle AP

A

Action potential plateau:

NA+ channels close rapidly [like skeletal] BUT the Ca++ channels open slowly and stay open for a longer period.

There is a delay in the opening of the K+ channels

the large [ ] of both Ca+ and K+ are responsible for the plateau.

73
Q

SA node is pacemaker b/c

A

It’s depolarization occurs more rapidly than any other and reaches threshold first. THis becomes the norm rhythm.

74
Q

APs that originate anywhere besides SA node are called:

A

Ectopic

75
Q

Resting membrane potential for SA node fiber:

A

-55mV to -60mV [threshold-40mV]

Phase 4: slow depolarization: d/t inactivated fast Na+ gates, only slow Na+-Ca+ channels open [slow leak of Na+ ions back into cells]-membrane potential becomes more positive. At -40mV Sodium-calcium channels become activated

Large # of K+ channels open when Na+-Ca+ channels become inactivated…nodal cells become repolarized.

76
Q

Ventricular resting membrane potential

A

-85 to -90 mV

77
Q

Atrial AP sequence

A

Phase 4: resting potential is gradual to
Phase 0: Ca+ influx
Phase 1and 2not noted
Phase 3: K+ efflux [cell becomes more - again

78
Q

Ventricular AP sequence

A 
phase 4: resting -90mV
Phase 0: depolarization rapid Na+ influx
Phase 1: fast K+ efflux
Phase 2: Ca+ influx and K+ efflux
Phase 3:Delayed K+ efflux
79
Q

Faster the ion channels return to phase 4,

A

the shorter the refractory period

80
Q

Sinus rhythm

A

Originates in SA

81
Q

Mechanism of Ca+ release during contraction of cardiomyocyte w/ DHP and Ryanodine compared to skeletal muscle.

A

AP travels along sarcolemma to T-tubules

Ca+ enters from the ECF through voltage-dependent Ca+ channels (DHP) of T-tubule

ELevated cytosolic Ca+ triggers more CA+ to enter from cisternae of the sarcoplasmic tubules though ryanodine receptors

Elevated Ca++ binds to troponin and results in myofilament contraction

Skeletal muscle Req’s conformational change in DHP and ryanodine receptor for influx of ICF ca++

82
Q

SERCA cardiac muscle relaxation

A

SR Ca+ ATPase

Stimulated by phosphorylation via an integral SR protein called phospholambian, which reduces its ability to inhibit SERCA pump

Returns Ca+ to SR during diastole

This allows for even greater Ca+ release on the next beat.

Also allows for a fast clearance of Ca+ from sarcoplasm.

83
Q

Sodium-calcium exchanger in cardiac muscle relaxation

A

Transports Ca+out of the cell

84
Q

Atria primer pumps

A

About 80% of blood flows from the atria to the ventricles before the atria contract

Atria can therefore add an additional 20% by contraction

85
Q

Ventricular systole

A

AV valves closed during systole

86
Q

End of ventricular systole

A

AV valves open at end of systole b/c of increased pressures in atria

87
Q

Cardiac cycle

A

1st 1/3 diastole: rapid filling

Middle 1/3: small amt. blood flows into ventricles blood continues to flow into atria

Last 1/3:atria contract to push last 20% of blood into ventricles.

Isometric contraction: ventricles contract but semilunar valves do not open for .02-.03 s

88
Q

Period of rapid ejection:

A

Occurs when L ventricular pressure is a little above 80 mmHg and R ventricular pressure is above 8 mmHg

Semilunar valves open.

About 70% blood ejected

Occurs during first 1/3 of ejection

89
Q

Period of slow ejection

A

Remaining 30 % blood is ejected from ventricles

Occurs during the last 2/3 of ejection

90
Q

Frank-starling law

A

More stretch =strongest contraction= most blood pumped into aorta

Stretching brings actin and myosin to optimum degree of overlap

91
Q

Blood in proximal aorta

A

Mean velocity = 40cm/s

Flow is phasic

Velocity ranges form 120 cm/s (systole) to - value before aortic valves close in diastole. [- d/t backflow]

92
Q

Blood in distal aorta and arteries

A

Velocity is greater in systole than diastole

Forward flow is continuous b/c of elastance of vessel walls during diastole

93
Q

Forces altering flow

A

Active tissue may req’ 20-30X as much blood flow than at rest

CO can’t exceed 4-7x > at rest

Microvessels at each tissue monitor tissue needs–act directly on local blood vessels

Nervous control and hormones help tissue blood flow

Physiology (10 decks)

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