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Body log > Muscle > Flashcards

Muscle Flashcards

1
Q

Describe the muscle cell hierarchy spider diagram

A

Pg 9

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2
Q

What does haemoglobin do to myoglobin and why?

A
  • Haemoglobin gives up oxygen to myoglobin, especially at low pH
  • Myoglobin has a higher affinity for oxygen than haemoglobin
  • When the muscle work hard it produces carbon dioxide to the blood which make the blood acidic.
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3
Q

What happens when striated muscle dies (muscle necrosis)?

A

Myoglobin is released into the blood (myoglobinaemia) and travels to the kidney where it is excreted into the urine (myoglobinuria).

Can cause renal damage:

  • Kidney has to remove the myoglobin from the blood and it can block the tubes and tubules causing Ischaemia and their is no oxygen to the kidney.
  • Tea-coloured urine
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4
Q

Where are the nucleus of the skeletal muscle cells

A

On the peripheral

Pg 16- 27 for histology pictures

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5
Q

What is a striated muscle cell called and what is within it ?

A

It is called a muscle fibre

  • Each fibre contains numerous myofibrils
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6
Q

What are the different types of muscle speeds?

A
  • Slow (red) , fast (white ) and intermediate (pink)

- Intermediate can sometimes be classified as fast

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7
Q

What are the characteristics of slow twitch fibres?

A

Type 1

  • rich capillary supply
  • aerobic
  • high myoglobin level
  • many mitochondria and cytochrome
  • fatty acids, make glucose to make ATP
  • Lots of ATP/Co2
  • fatigue resistant
  • red
  • endurance type activities e.g. walking and standing
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8
Q

What are the characteristics for intermediate?

A

Type 2A

  • rich blood supply
    Aerobic
  • high myoglobin level
  • high to intermediate level of mitochondria
  • many cytochrome
  • red to pink
  • Fatty acids and glycogen
  • initially lots of CO2, then lost of lactate (causes fatigue)
  • fatigue resistant
  • assist type 1 and 2B
  • standing and walking ( recruited 2nd)
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9
Q

What are the characteristics of fast twitch fibres?

A

Type 2B

  • poor capillary supply
  • anaerobic
  • low myoglobin level
  • few mitochondria and cytochrome
  • white (pale)
  • Glycogen - breaks down to form glucose which can then produce (below)
  • lots of lactate and little ATP
  • rapidly fatigue
  • strength and anaerobic tube activities
    E.g. standing, walking recruited last

Jumping/running sprinting

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10
Q

What does continued muscle contraction depend on? And what type of twitch does oxidative phosphorylation and anaerobic glycolysis lead to?

A
  • Ca2+ ions
  • Amounts of ATP
  • OP: Slow twitch (red fibres)
  • AG: Fats twitch (white fibres)
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11
Q

What are features of cardiac muscle fibres in LS?

A
  • Striations
  • Centrally positioned nucleus (1or 2 per cell)
  • Intercalated discs (for electrical -connexins and mechanical coupling with adjacent cells)
  • Branching

Pg 34

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12
Q

When is hypertrophy and hyperplasia seen in cardiac myocytes?

A
  • Cardiac myocytes can’t do hyperplasia as adults but children up to the age of 8 can
  • As the heart grows at age 8
  • When you hit puberty hyperplasia stops and hypertrophy takes over
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13
Q

What are the similarities and differences between cardiac and skeletal muscle?

A

Similarities

  • Both striated
  • Cintraction mechanisms are similar

Difference

  • Nuclei on cardiac is central and skeletal is peripheral
  • Sacromere not so developed in cardiac
  • Few/no Tubule in sacroplasmic reticulum (cardiac)
  • Only one contractile cell type - cardiomyocytes ( found in the bundle of his, bachmann’s bundles and purkinje fibres)
  • cardiomyocytes communicate through gap junctions (in intercalated discs).
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14
Q

What is the structure of smooth muscle cells?

A
  • Spindle-shaped (fusiform) with a single central large nucleus.
  • Not striated, no sacromere, no T-tubule
  • Capable of being stretched and sustained ( the cells overlap each other, so it has a massive capacity to stretch).
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15
Q

What are the features of the contraction of the smooth muscle cell? And what do smooth muscle respond to?

A
  • Contraction still relies on actin-myosin interactions
  • Contraction is slower, more sustained and relies on less ATP
  • May remain contracted for hours or days
  • Responds to stimuli form of nerve signals, hormone, drugs or local concentrations of blood gas.
  • Numerous caveolae (small cave-like invaginations - used pinocytosis).
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16
Q

How does muscle contraction occur in smooth muscle

A
  1. There are lots of little tiny myofilaments and intermediate filaments that are sitting in the cytoplasm waiting for a signal to come through, which can come through the caveolae.
  2. When they assemble they assemble in the dark areas called the dense bodies/plaques. The dense bodies/plaques are often on the sarcolemma and can be in the centre in the cytoplasm.
  3. When contraction comes together, the filaments join the dense plaque/bodies together with the contraction machinery and contract to move smooth muscle in whatever direction they have been brought together.
  4. When they come together in a kriss Kross pattern across adjacent cells, so when they do contract the smooth muscle cells contract in all direction
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17
Q

How are smooth muscle cells joined?

A
  • Smooth muscle cells join to another via gap junctions which have a lot of connexins.
  • These connexins allow free movement of small molecules from one cell to another. So you get the whole series of the smooth muscle cells to contract together acting almost like a syncitium.
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18
Q

What are smooth muscle innervated by?

A
  • Innervated by the autonomic nervous system fibres, that release their neurotransmitters from varicosities into wide synaptic cleft.

This is found in smooth muscles in the gut.

Pg 50-52

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19
Q

Can mature muscle repair occur in smooth muscle?

A
  • Skeletal muscle cells cannot divide but can regenerate by mitotic activity of satellite cells, so that hyperplasia follows muscle injury.
  • Satellite cells can also fuse with existing muscle cells to increase mass (skeletal muscle hypertrophy)
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20
Q

Can mature muscle repair occur in cardiac muscle?

A
  • Adult cardiac muscle is incapable of regeneration
  • Following damage, fibroblast invade, divide and lay down scar tissue
  • Muscle cannot grow over scar tissue and scar tissue doesn’t conduct electricity
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21
Q

Can mature muscle repair occur in smooth muscle.

A

Smooth muscle retain their mitotic activity and can form new smooth muscle cells

E.g.

  • Particularly evident in the pregnant uterus where the muscle wall
    (myometrium) becomes thicker by hypertrophy (cell enlargement)
  • Hyperplasia (cell division/mitosis) of individual cells increases muscle mass
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22
Q

What are the similarities and differences between cardiac and smooth muscle cells?

A

Similarities

  • Both have central nucleus not peripheral
  • One contractile cel type (cardiomyocytes and smooth muscle cell)
  • Communicate through gap junctions
  • Acts as a syncytium (wave-like function)

Difference

  • Smooth muscle doesn’t contain sarcomere
  • Electrical conduction - specialised cells/routes in cardiac muscle
  • No troponins in smooth muscle
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23
Q

What occurs for in smooth muscle cells for contraction to take place?

A
  1. When calcium enter the smooth muscle cell it binds to a protein called calmodulin, four molecules of calcium bind to calmodulin.
  2. When they bind to calmodulin a new enzyme binds to the calmodulin/calcium complex to create an activated enzyme , the enzyme is called myosin light chain kinase and its job is to phosphorylate the myosin light chain.
  3. Myosin usually sits in a circle and it’s two heads are not activated, but when it’s activated by ATP or phosphorylated it opens up.
  4. The two heads can now bind to actin and causes contraction, the contraction continues as long as there is calcium.
  5. When calcium decreases, an enzyme called phosphatase takes the phosphate off and the myosin turns back to the cell and can no longer contract.

Pg 11

24
Q

How is skeletal muscle innervated?

A

Through the neuromuscular junction.

  • Small terminal swellings of the axon
  • Contain vesicles of acetylcholine
  • Nerve impulse releases acetylcholine
  • Binds receptors on the sarcolemma
  • Initiates an action potential propagated along the muscle
25
Q

What is the action of the Kranocyte in the neuromuscular junction?

A

Anchors the end of the nerve to the muscle

  • not a lot of information on it yet to allow for a conclusion of its function.

Pg 13

26
Q

What are the events leading to the contraction of the Skeletal muscle?

A
  1. Initiation: nerve impulse along motor neuron axon arrives at neuromuscular junction
  2. Impulse prompts release of acetylcholine (Ach) into synaptic cleft causing local depolarisation of sarcolemma
  3. Voltage-gated Na+ channels open; Na+ ions enter cell
  4. General depolarisation spreads over sarcolemma and into T tubules
  5. Voltage sensor proteins of T tubule membrane change their
    conformation
  6. Gated Ca2+ ion-release channels of adjacent terminal cisternae are
    activated by step 5.
  7. Ca2+ ions are rapidly released into the sarcoplasm
  8. Ca2+ binds to the TnC subunit of troponin and the contraction cycle is initiated
  9. Ca2+ ions are returned to the terminal cisternae of sarcoplasmic reticulum

Calcium is put back into the sacroplasmic reticulum by SERCA (Ca2+ ATPase).

27
Q

What is the pathophysiology of myasthenia gravis?

A
  • Autoimmune disease
  • Antibodies directed against Ach receptor (block)
  • 30% reduction in receptor number sufficient for symptoms
  • Endplate ‘invaginations’ in synaptic clefts reduced leading to
  • Reduced synaptic transmission leading to
  • Intermittent muscle weakness
28
Q

What does each individual myosin molecule look like?

A

A rod-like structure with 2 protruding heads.

  • each thick filaments consisted of many myosin molecules, whose heads are protrude at opposite ends of the filament.
29
Q

What are the two protein components of actin and what complex sits over the binding site where actin will bind?

A
  1. F-actin fibres
  2. G-actin globules
  • Tropomyosin-Troponin complex sits over binding sites
  • Troponin complex prevents the acting and myosin from coming together.

Pg 21

30
Q

What complex is found in skeletal and cardiac muscle?

A

Actin, tropomyosim and troponin molecules complex to form thin filaments of the skeletal and a cardiac muscles.

Troponin complex is made up of TnC, TnI and TNT

TnC response to calcium

Pg 22

31
Q

Describe the contractile unit.

A
  • Tropomyosin molecules coil around the actin helix, reinforcing it(holding it in place.
  • A troponin complex is attached to each tropomyosin molecule.
  • In the centre of the sarcomere, the thick filaments have no myosin heads. (H zone).
  • The myosin heads extend towards the actin filaments in regions of potential overlap.

Pg23

32
Q

What is the role of ionic calcium in the contraction mechanism?

A
  • As Ca2+ binds to TnC of troponin, a conformational change moves tropomyosin away from actin’s binding sites
  • This allows myosin heads to bind actin, and contraction begins
  • The tropomyosin sits in the cleft of the G-actin ‘spheres’

Pg 24

33
Q

Hat is the sequence of events that occurs in contraction?

A

Pg25

34
Q

What happens to the length of the actin and myosin filaments?

A
  • The length stays the same as they just slide past each other.
  • It is the sacromere that shortens as the z line come closer to each other

Pg 26

35
Q

What is the meaning of origin?

A
  • It’s the start point
  • Bone, typically proximal, which has greater mass and is more stable during contraction than the muscle’s insertion.

Pg 27

36
Q

What is insertion?

A

• Structure the muscle attaches to

• Tends to be moved by
contraction

• Tends to be distal

• May be bone, tendon or
connective tissue (usually tendon
to bone).

• Greater motion than origin
during contraction.

Pg 27

37
Q

What is the meaning of agonist and what is an antagonist?

A
  • Agonists: Prime movers (main muscles responsible for a particular movement).
  • Antagonists: Oppose prime mover.

Pg 28

38
Q

What is a Synergists, neutralisers and fixators?

A
  • Synergistis - Assist prime movers (acting alone they cannot perform the movement but their angle of pull Synergists assists)
  • Neutralisers: Prevent the unwanted actions that an agonist can perform.

Fixators: Act to hold a body part immobile whilst another body part is moving.

Pg 28

39
Q

What are the different types of levers?

A

First class lever - effort at one end and load at the other e.g. extension/flex ion of head

Second class lever - effort at one end and fulcrum at the other end 
E.g. Plantar flexion of foot

Third class lever - Effort between load and fulcrum

  • mechanical disadvantage
  • most common in the body

Pg 30

40
Q

What is compartment syndrome?

A
  • Limbs divided into compartments separated (boundary) by fascia
  • Trauma in one compartment could cause internal bleeding which exerts pressure on blood vessels and nerves
  • Can give rise to compartment syndrome
41
Q

What are the symptoms of compartment syndrome?

A
  • Deep constant poorly localised pain
  • Aggravated by passive stretch of muscle group
  • Paresthesia (altered sensation e.g., “pins & needles”)
  • Compartment may feel tense and firm.
  • Swollen shiny skin, sometimes with obvious bruising.
  • Prolonged capillary refill time.
42
Q

What is muscle tone regulated by?

A
  • Motor neuron activity
  • Muscle elasticity
  • Use
  • Gravity
43
Q

What is muscle tone?

A
  • Healthy muscles never fully ‘relaxed’ (pre relaxed state)
  • Retain amount of tension and stiffness (muscle tone)
  • Makes muscle ready to react
  • Improves with exercise

Pg 33

44
Q

How does muscle remodelling occur?

A
  • Continual exercise
  • Replacement of contractile protein in 2 weeks
  • Destruction more than replacement = atrophy
  • Replacement is more than destruction = hypertrophy

Pg 34

45
Q

What is the mechanism of muscle hypertrophy?

A
  1. Overstretching such that the A and I bands can no longer re-engage.
  2. Leads to new muscle fibrils produced.
  3. New sarcomeres are added in the middle of existing sarcomeres.
  4. New muscle fibres arise from mesenchymal cells.
    - Over-stretching is thought to feature in some cardiac pathologies (i.e. enlarged ventricles).

Pg 35

46
Q

What is the mechanism of muscle atrophy?

A

Disuse: bed rest, limb immobilisation (broken bone), sedentary behaviour, age, etc.

Surgery: denervation of muscle

Disease: Muscular dystrophies

  • Loss of protein
  • reduced fibre diameter
  • loss of muscle power
47
Q

What is muscle dystrophy?

A

• Inherited through X-linked recessive pattern ( mainly boys get it than girls)

  • Mutation of the dystrophin gene
  • Muscle cells that have burst are replaced by adipose tissue (satellite cells are destroyed when it bursts).
48
Q

In Duchene muscular dystrophy, What does the absence of dystrophin allow?

A

• Absence of dystrophin allows:

  • Excess calcium to enter the muscle cell
  • Calcium taken up by mitochondria
  • Water taken with it
  • Mitochondria burst
  • Muscle cells burst (rhabdomyolysis - striated muscle destruction)
  • Creatine kinase and myoglobin levels are extremely high in the blood
49
Q

What are the situations in which creatine kinase is released into the blood?

A
  • by damaged skeletal muscle and brain.

A rise in plasma CK can result from:
• intramuscular injection (e.g. vaccinations)

  • vigorous physical exercise (overdoing it in the gym!)
  • a fall (especially in the elderly)
  • rhabdomyolysis (severe muscle breakdown)– compartment syndrome, crush injuries, earthquakes and war, etc.
  • muscular dystrophy
  • acute kidney injury (myoglobin not being cleared)
50
Q

How is Troponin Assay a useful diagnostic tool in myocardial cell damage?

A
  • Troponin (I & T forms) used as a marker for cardiac ischaemia
  • Released from ischaemic cardiac muscle within an hour.
  • Must measure within 20 hours for absolute accuracy
  • The smallest changes in troponin levels in the blood are indicative of cardiac muscle damage
  • Quantity of troponin is not necessarily proportional to the degree of muscle damage

• Used by many Emergency Departments as the assay of choice,
superseding muscle enzyme assays

51
Q

What is Botulism toxin

A
  • Toxin produced by Clostridium botulinum
  • Blocks neurotransmitter release at the motor end plate

• Causes non-contractile state of skeletal muscle
- Flaccid paralysis

• Clinically used to treat muscle spasms (e.g. cervical dystonia) • Used cosmetically to treat ‘wrinkles’

Pg 43

52
Q

What occurs in organophosphate poisoning?

A

Organophosphates are used as pesticides

  • Inhibits the normal function of Ach esterase
  • Ach activity at the neuromuscular junction is potentiated/increased
  • Leads to multiple symptoms and signs:
  • Effects on both somatic and autonomic signalling

Pg 44

53
Q

What is malignant hyperthermia?

A

• Severe reaction to anaesthetics – particularly Succinylcholine

  • Autosomal dominant inheritance pattern - RyR1 gene.
  • Males>Females

• Massive contractile fasciculation

  • Muscle rigidity caused by ↑Ca2+ release
  • Outcome – excessive heat and metabolic acidosis

• ↑Muscle breakdown and hyperkalaemia (high blood [K+]) • Mortality risk 5% with treatment; 75% without treatment

54
Q

How are megakaryocytes (platelets) produced?

A
  1. Osteoblasts are receiving signals. When the MSC receives a signal ( hormone,growths factor, cytokines or interleukin) telling them to divide.
  2. They divide into haematopoietic stem cells (HSC) or haematopoietic progenitor cells (HPC) and some of the cells go back and become mesenchymal stem cell and attach to the blastocyst.
  3. Two cells come together and start to develop, they fuse and fuse again and you get four cells with four nuclei.
  4. There mechanical stiffness and changing of the viscosity from the extracellular matrix and fat cells acting on the developing cell, changing the phenotype of the developing cell called a megakaryocyte ( mega -large, Karyo - DNA, Cyte -cell), they have lots of DNA in the.

Pg 17

55
Q

How does the megakaryocyte enter into the blood and what do they form?

A
  1. This is how it differs from other cells in the formation of blood cells. It makes large pseudo podia, using parts of its cytoplasm , that forces out between the epithelial cells, but not through the sinusoidal gaps, it’s going through fenestrations.
  2. The pseudo podia go through the sinusoidal space and lose a little part of them by apocrine secretion, so in the blood vessel there are lots of different fragments of the megakaryocyte which then become the platelets
  3. Platelets have convex shape.

• Loss of blood, so a drop in blood pressure or flow rate in the blood, change in viscosity of blood or decrease temperature will stimulate the release of the platelets.

Pg 17

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