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ANAT241 > Lecture 12 > Flashcards

Lecture 12 Flashcards

1
Q

Three main types of muscle

A

Skeletal
Cardiac
Smooth

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2
Q

Structure of skeletal muscle

A

Long, cylindrical, multinucleate cells with obvious striations

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3
Q

Function of skeletal muscles

A
  • voluntary movement
  • locomotion
  • manipulation of the environment
  • facial expression
  • voluntary control
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4
Q

Image of skeltatal muscle

A
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5
Q

Location of skeletal muscles

A

Attached to bones or occasionally skin

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6
Q

Gross anatomy of skeletal muscle. In order - siums

A
  • epimysium
  • endomysium
  • perimysium
  • fascicles
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7
Q

What is epimysium

A

Connective tissue sheathing the muscle

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8
Q

What is endomysium

A

Protecting individual muscle fibres

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9
Q

What is perimysium

A

Sheaths bundles of muscle fibres

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10
Q

What are fascicles

A

Bundles of muscle fibres

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11
Q
A
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12
Q

How many motor neurons per muscle fiber?

A

1

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13
Q

What is in between the motor neuron and the muscle fibre

A

Neuromuscular junction

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14
Q

What is the sacrolemma?

A

Cell membrane of muscle fibre

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15
Q

What a transverse T-tubule?

A

Invagination of sacrolemma into cell

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16
Q

What is the sarcoplasmic reticulum

A

Store and release Ca2+

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17
Q
A
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18
Q
A
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19
Q
A
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20
Q

Myofibrils are made up of individual units called…

A

Sarcomeres

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21
Q

Different lines of the sarcomere

A
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22
Q

What causes muscle contraction

A

Thin and tick filaments attaching to eachother

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23
Q

On the enedtron microphraph picture what do the different colours represent

A

Different degrees of overlapping in different areas

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24
Q

Make sure you know:

A
  • what the thick and thin filaments are made up from
  • what the different striation colour signifies and how it will change during muscle contraction
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25
Q

Main components of the thin filament

A

Actin
- contains binding sites for thick filament

Tropomyosin
- protein strand that covers binding sites in relaxed state

Troponin
- sits on tropomyosin and responds to signals for contraction

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26
Q

Main components of the thick filament

A

Myosin
- main protein of thick filament, elongated with distinctive head
- head binds and “walks” along thin filament

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27
Q

Sarcamere zones will be an essay question

A
28
Q

Different sacromere zones

A
29
Q

What is in the I band?

A

Just thin filament

30
Q

What is in the H-zone

A

Just thick filament

31
Q

What is the A-band

A

Anywhere where there is thick filament

32
Q

What happens when an AP comes down the motor neuron

A

-Acetylcholine is released into the synaptic cleft
-Acetylcholine choline binds to ion channels in the post synaptic cleft which causes depolarisation of the muscle cell plasma membrane
- this sends an action potential along the sacrolemma
- T-tubes allow the AP to penetrate into the muscle
- it then causes calcium to be released by the sacroplasmic reticulum
- calcium can then interact with the sacromeres which make up the myofibrils

33
Q

In the relaxed state what is the state of the actin binding sites

A
  • binding sites of actin to myosin covered by tropomyosin
34
Q

State Actin binding site in the excited state and why

A
  • binding of Ca2+ to troponin causes movement of tropomyosin exposing binding sites
  • myosin (thick filament) binds to actin (thin filament)
35
Q

Process of sarcomeere contraction - after head has bound

A
  • myosin head changes shape and pulls thin filament to centre of sarcomere
  • ATP binds to myosin and energy is utilized to detach myosin, reverting shape
36
Q

Use of ATP in contraction of the myofilaments

A
37
Q
A

Smaller
Same
Smaller
Smaller

38
Q

A I H zones during sarcomere contraction

A
  • size of filaments dont change, just the degree of overlap
39
Q

Molecular basis of muscle contraction

A
  • the ca2+ released from the sarcoplsmic reticulum when the muscle fibre is excised binds to the protein troponin
  • the binding enables the troponin protein complex to “pull tropomyosin aside” so that it no longer covers the active sites on actin
  • the heads of myosin molecules bind to the now exposed active sites on actin
  • swing movement of myosin head pulls thin filament inwards
  • head is detached andshape reverted if bound to ATP
40
Q

Why do animals show rigour morris?

A
  • Ca2+ leaks from sarcoplasmic reticulum into muscle fibres following death, exposing actin binding sites
  • myosin automatically binds and pulls thin filament (no ATP required)
  • new molecules of ATP needed for the unbinding of myosin and actin are not produced
  • thus myosin remains attached to actin and the contracted muscles do not relax
41
Q

What are the sytmptoms of nemaline myopathy?

A
  • muscle weakness, swelling dysfunction, impaired speech
42
Q

What causes nemaline myopathy?

A

Mutations in at least 10 different genes
- NED (~50% of cases) - nebulin - governs length of thin filament
- ACTA1 (15-25% of cases) - actin isoform making up thin filament

43
Q

Cardiac muscle features

A
  • continuous rhythmic activity
  • inherent mechanisms of activation that can be modulated by external autonomic and hormonal stimuli
  • structurally intermediate to skeltetal and smooth muscle
44
Q

Structure of cardiac muscle

A

Branching, striated, generally uninuclueared cells that interdigitate at specailised junctions (intercalated discs)

45
Q

Function of cardiac muscle structure

A
  • as it contracts, it propels blood into the circulation
  • in voluntary control
46
Q

Location of cardiac muscle

A

Walls of the heart

47
Q

Image of cardiac muscle

A
48
Q

What joins the muscle cells together

A

Intecollated discs

49
Q
A
50
Q

3 types of intercollated discs and what they do

A

Desmosomes: anchor cells to eachother via the cytoskeleton
Fascia adherens: anchor actin filaments and transmit contractile forces
Gap junctions: transmit contraction stimulus

51
Q

What do desmosomes do?

A

Anchor cells to eachother via cytoskeleton

52
Q

What do facia adherens do?

A

Anchor actin filaments and transmit contractile forces

  • along the Z line
53
Q

What do gap junctions do

A

Tansmit contraction stimulus

54
Q

Arrhythmogenic right ventricular cardiomyopathy is a disease of…

A

Desmosomes

55
Q

Arrhythmogenic right ventricular cardiomyopathy features

A
  • cardiac muscles die and are replaced by fatty infiltration
  • irregular heart beat - arrhythmia
  • leads to heart attacks in otherwise healthy individuals
  • genes for desmosomes proteins explains the prevelance (1:5000)
56
Q

Desmosomes of someone with arrhythmogenic right ventricular cardiomyopathy

A
  • fewer desmosomes, those that are present, fragmented, different lengths of
  • intracellular gap widening and distruption
  • cell death
  • widening of gap junction may contribute to arrythmogenicity
57
Q

Features of smooth muscle

A
  • muscular component of visceral tissue e.g blood vessels, GI
  • under inherent automatic and hormonal control - involuntary
  • continuous contractions of slow force
  • often whole muscle contracting in a wave like fashion
58
Q

Structure of smooth muscle

A
  • spindle-shaped cells with central nuclei
  • no striations
  • Cells arranged closely to form sheets
59
Q

Function of smooth muscle

A
  • propels substances or objects along internal passages
  • involuntary control
60
Q

Location of smooth muscle

A
  • mostly in the walls of hallow organs
61
Q

Image of smooth muscle

A
  • collagen in between to allow for contraction and expansion
62
Q

Smooth muscle contraction - contractile filaments - where are the anchored

A
  • contractile filaments cross-cross the cell
  • anchored to cell at focal densities (D) in cytoplasm and focal adhesion densities (J) on cell membrane
63
Q

How smooth muscle contraction occurs

A

Ran out of time to make proper cue card

50 minutes in lecture 11

64
Q

Contractile filaments in their contracted and unconrtacted states

A
65
Q
A
66
Q
A

ANAT241 (29 decks)

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