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Physio Lecture > Test 2 - Packet 1 > Flashcards

Test 2 - Packet 1 Flashcards

1
Q

Three types of muscles

A

Skeletal, Smooth, Cardiac

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2
Q

Thin filament components

A

Actin microfilaments
Tropomyosin
Troponin

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3
Q

What does troponin do?

A
  • Binds Calcium

- Causes tropomyosin to move when calcium increases

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4
Q

What does tropomyosin do?

A

Cover’s actin’s binding sites for myosin

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5
Q

What does myosin consist of?

A

Two globular heads, each with a tail on a hinge

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6
Q

What enzyme does the globular head on the myosin contain?

A

Myosin-ATP ase

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7
Q
  • Four total

- Attached to the globular heads of the myosin

A

Light chains

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8
Q

Contact between myosin and actin

A

Crossbridges

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9
Q

Sarcomeres are the units of a ____ muscle between two _____

A

Striated

Z lines

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10
Q

Where do the thin filaments attach?

A

Attached to the Z lines

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11
Q

What are Z lines made out of?

A

Cytoskeletal structures made of various intermediate filaments

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12
Q

Where do thick filaments attach?

A

To the M lines –> Their tail ends of the myosin are orientated towards the M-line from both sides

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13
Q

Filaments that attach the Z lines to the M lines

A

Titin

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14
Q

Characteristics about Titin

A
  • Largest protein

- MW is several million daltons

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15
Q

Contraction of the sarcomere

A

The Sliding Filament Theory

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16
Q

H bands

A

Thick filaments with no thin filament overlap

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17
Q

I band

A

Thin filaments with no thick filament overlap

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18
Q

A band

A

The entire length of the thick filament

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19
Q

When the sarcomere contracts, what happens to the bands

A

I and H bands = small, or disappear

A bands = remain the same size

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20
Q

The power for shortening of the sarcomeres comes from where?

A

Myosin-ATPase

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21
Q

Overview of the power for shortening of the sarcomere

A
  1. Hinge region extends = ADP and/or phosphate bound
  2. Myosin has low affinity for actin = ATP is bound
  3. Myosin bound to actin = no ATP
  4. Muscles relax = myosin prevented from binding to actin
22
Q

Control of myosin’s access to actin

A

Excitation-Contraction Coupling

23
Q

Sequence of events during EC-coupling: Contraction

A
  1. AP –> presynaptic terminal of motor neuron
  2. Synapse at neuromuscular junction –> exocytosis of ACH onto motor end plate
  3. ACH –> Nicotinic receptors in motor end plate. Nicotinic cation channels open.
  4. EPSP trigger AP in the sarcolemma
  5. AP across sarcolemma and down into the T-tubules
  6. Dihydropyridine (DHP) receptors in t-tubule membrane respond to AP by opening Ca channels known as Ryanodine receptors in the SR
  7. Ca diffuses into cytoplasm through RyR
  8. Ca binds to troponin, tropomyosin moves away from binding sites
  9. Myosin begins its ATPase cycle and pulls on actin, sarcomere shortens
24
Q

EC-coupling: relaxation phase

A
  1. Ca is pumped into SR by Ca-ATPase
  2. Ca binds to calsequestrin in the SR
  3. Decreased in cytoplasmic Ca, troponin emptied and tropomyosin covers myosin binding sites, stops the myosin ATP ase cycle
25
Q

Response to one AP

A

Twitch

26
Q

What is the latent period?

A

The time between stimulus and beginning of twitch. When EC-coupling is occurring

27
Q

What is the contraction phase?

A

The beginning of the twitch, when muscle active force in increasing

28
Q

What is the relaxation phase?

A

The end of the twitch, when active force is decreasing

29
Q

The twitch of a single muscle fiber is ____

A

All or nothing

30
Q

Changes in heart rate are called ______ effects

A

Chronotropic effects

31
Q

What is stroke volume dependent on

A
  • Cytoplasmic ca concentrations

- Preload of the muscle

32
Q

Changes in the force of contraction are known as ____ effects

A

Inotropic

33
Q

Increased force of contraction results in an increased ____

A

Stroke volume

34
Q

What is Frank-Starling Law of the Heart say?

A

Change in force development as a function of preload

35
Q

Resting length of cardiac muscle is such that increases in preload cause increased force and therefore increased ____ of blood

A

Ejection

36
Q

Change of contraction strength by control of Ca++ is a change in ___

A

Contractility

37
Q

What is ejection fraction?

A

The fraction of the blood in the ventricle that is ejected into the artery

38
Q

How is ejection fraction calculated

A

Stroke volume/End diastolic volume

39
Q

When does calcium leave the cytoplasm?

A

Between the beats of the heart

40
Q

What moves calcium out of the cell?

A

Secondary active mechanism called Na/Ca exchanger

41
Q

What effect is due to the change in contractility

A

The Staircase Effect

42
Q

When the excess calcium that builds up in the cell is taken up by the SR, since the CaATPase not as limited as the Na/Ca exchanger

A

Calcium loading of the sarcoplasmic reticulum

43
Q

Calcium loading leads to what?

A

Increased contractility of the heart (increased rate, stroke volume)

44
Q

What is the equation for flow velocity?

A

Flow rate/cross sectional area

45
Q

What are known as the resistance vessels?

A

Arterioles

46
Q

What kind of vessels are veins?

A

Capacitance vessels

47
Q

What is perfusion pressure?

A

MAP-VP

48
Q

An increase in blood flow due to local conditions and paracrines

A

Hyperemia

49
Q

Tissue responds to it own increased metablosim

A

Active hyperemia

50
Q

Tissue responds to period of reduced blood flow

A

Reactive Hyperemia

51
Q

The venous return equation

A

(VP-R)/R

52
Q

Why is CVP lower than VP?

A

Because of low pressure inside thoracic cavity

Physio Lecture (4 decks)

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