Muscle Tissues Flashcards

1
Q

What is the difference between skeletal, cardiac and smooth muscle

A

Skeletal Muscle - Voluntary muscle responsible for the movement of the skeleton and structures such as the eye, tongue, etc.
Cardiac muscle - Involuntary muscle found only in the heart
Smooth muscle - Involuntary visceral (organ) muscle, found in the uterus/bladder and associated with tube-like structure e.g., GI tract, blood vessels and conducting airways of the respiratory tract

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2
Q

Describe different muscle definitions and derivations

A

Myalgia - Muscle pain
Myasthenia - Weakness of the muscles
Myocardium - Muscular component of heart
Myopathy - Any diseases of the muscles
Myoclonus - Sudden spasm of muscles

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3
Q

Describe muscle cell components

A

Sarcolemma - Outer membrane of a muscle cell
Sarcoplasm - Cytoplasm of a muscle cell
Sarcosome - The mitochondrion
Sarcomere - Contraction unit in striated muscle
Sarcoplasmic Reticulum - Smooth endoplasmic reticulum of muscle cell

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4
Q

Describe the striated muscle and which bands contain actin, myosin or both

A

I band - Contains only actin filaments
A band - Contains myosin (and actin filaments)
H zone - Contains only myosin filaments
M line - Centre of a sarcomere

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5
Q

Describe the structure of skeletal muscles

A

Skeletal muscles are joined to bone using tendons. They contain Fascicles which are covered by the Epimysium, Perimysium and endomysium, and also contain muscle fibres.

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6
Q

What is the Epimysium, Perimysium and Endomysium

A

Epimysium - The external connective-tissue sheath of a muscle. It surrounds the entire muscle tissue and contains many bundles (fascicles).
Perimysium - Connective tissue that surrounds each bundle of muscle fibres.
Endomysium - The connective tissue that covers each single muscle fibre or myofiber or muscle cell.

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7
Q

What controls direction of movement

A

There are lots of different muscles shapes e.g., circular, bipennate etc. Movement is always along the direction of a fascicle. Tension is created at the origin tendon point. Movement is created at the insertion tendon point.

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8
Q

Explain the structure of slow twitch muscle fibres.

A

Slow twitch fibres have:
- Rich capillary supply
- Aerobic
- High myoglobin levels
- Many cytochromes
- Red
- Fatigue resistant
- Endurance type activities
- Standing/walking

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9
Q

Explain the structure of fast twitch muscle fibres

A

Fast twitch muscle fibres have:
- Poor capillary supply
- Anaerobic
- Low myoglobin levels
- Fewer mitochondria
- Few cytochromes
- White (pale)
- Rapidly fatigue
- Strength/anaerobic type activities
- Jumping/sprinting

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10
Q

Explain the limited nature of repair possible in mature muscle

A

Skeletal muscle - They cannot divide. They regenerate by mitotic activity of satellite cells, so hyperplasia follows muscle injury. Satellite cells can fuse with existing muscle cells to increase mass.
Cardiac muscle - Generally considered to be incapable of regeneration. Following damage, fibroblasts invade, divide and lay down scar tissue.
Smooth muscle - Retain their mitotic activity and can form new smooth muscle cells. Very good at repairing themselves. Show particularly in the pregnant uterus

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11
Q

Explain skeletal muscles in longitudinal and transverse section and how it relates to its function.

A

Skeletal muscles in the transverse section contain peripheral nuclei whilst skeletal muscles in the longitudinal section contain nuclei in rows. Skeletal muscle fibres are surrounded by a thin layer of connective tissue (perimysium) which bears capillaries and nerves.
A main way to distinguish between skeletal muscles and tendons is that tendons do not contain stripes in the longitudinal section.

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12
Q

Explain cardiac muscle and its function and how to determine it from skeletal muscle.

A

Cardiac muscles in the longitudinal section contain:
- Striations
- Centrally positioned nuclei
- Intercalated discs for electrical and mechanical coupling with adjacent cells
- Branching

To distinguish between skeletal muscles, cardiac muscles:
- Have nuclei in the centre and not peripheral
- Reduced number of T-tubules associated with sarcoplasmic reticulum
- Only one contractile cell type (cardiomyocyte)
- Cardiomyocytes communicate through gap junctions in the intercalated disc

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13
Q

Explain how tissues increase and decrease in size.

A

To increase in size tissues can do so by:
- Hypertrophy which is the enlargement of individual cells
- Hyperplasia which is the multiplication of their cells
To decrease in size, tissue can do so by atrophy where individual cells decrease in size.

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14
Q

Explain ANP and BNP

A

Atrial natriuretic peptide (ANP) is released by the atria and causes congestive heart failure
Brain-type natriuretic peptide (BNP) is released by ventricles and causes left ventricular hypertrophy causing mitral valve disease

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15
Q

Explain smooth muscle and its function and be able to distinguish it from connective tissue.

A

Smooth muscle cells have a spindle shaped (fusiform) with a single central large nucleus. It is not striated with no sarcomeres or T tubules and is capable of being stretched substantially.
There are multiple adjacent capillaries. There is also one flattened nucleus per cell in the centre and smooth muscle are packed very tightly together.
Tissue in skeletal membrane sits below the basement membrane unlike in connective tissue where it sits on the basement membrane.

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16
Q

How does smooth muscle cell contraction and distribution work

A

Contraction still relies on actin-myosin interactions. Contraction is slower, more sustained and requires less ATP and may remain contracted for hours or days.
Smooth muscle can often form contractile walls of passages or cavities e.g., in the gut, respiratory tract and genitourinary system. However, involuntary muscle can sometimes develop a mind of it own and cause disorders such as:
- high blood pressure
- painful mensturation
- lung disease

17
Q

Describe the structure and organisation of skeletal muscle fibres

A

Skeletal muscles are attached to skeletons allowing it to move. They are also called striated muscle because its cells (fibres) are composed of striations.
The fibres of skeletal muscle are grouped into bundles (fascicles) which are organised into various architectural patterns. It is the specific pattern that determines the range of movement.
Skeletal muscles are covered and held together by fibrous connective tissue which are structurally arranged (as epimysium, perimysium, and endomysium).

18
Q

What is the origin and insertion of a muscle.

A

Skeletal muscles act as levers. They have two endpoints:
- Attachment to bone (normally at proximal end) is called the muscle origin
- Attachment to bone through a tendon (normally at the distal end), is called the muscle insertion.
This causes movement

19
Q

What is an agonist and antagonist muscle

A

Agonist - An agonist muscle is a muscle that contracts to provide the main force to move or rotate a bone through its joint.
Antagonist - An antagonist muscle has an opposing effect and contract across the opposite edge of a joint

20
Q

What is a synergist, neutraliser and fixator muscle

A

Synergist - The synergist in a movement is the muscle that stabilises a joint around which movement is occurring, which in turn helps the agonist function effectively. Synergist muscles also help to create the movement.
Neutraliser - Neutralizing muscles provide important support during exercise to prevent injury and restrict movement.
Fixator - The fixator in a movement is the muscle that stabilises the origin of the agonist and the joint that the origin spans (moves over) in order to help the agonist function most effectively.

21
Q

What is the difference between superficial and deep fascia

A

The primary difference is that superficial fascia is composed of loose connective tissue and is found in the layer between the dermis layer of your skin and muscles, while deep fascia contains dense connective tissue and is found within and between your muscles, all working together in the extracellular matrix.

22
Q

What is the structure and function of Purkinje fibres in the heart

A

Purkinje fibres are large cells found in the ventricular walls with:
- Abundant glycogen
- Sparse myofibrils
- Extensive gap junction sites
The Purkinje fibres conduct action potentials rapidly. This rapid conduction enables the ventricles to conduct in a synchronous manner. Tracts of Purkinje fibres transmit action potential to the ventricles from the AV node

23
Q

Describe the process of skeletal muscle remodelling and its relevance to atrophy, hypertrophy and during injury

A

Atrophy occurs is muscle destruction is greater that muscle replacement. This can occur from:
- disuse, e.g., bed rest,
- surgery e.g., denervation of the muscle
- Disease e.g., Muscular dystrophies
Hypertrophy occurs from overstretching such that A and I bands can no longer re-engage. New muscle fibrils are produced. New sarcomeres are added in the middle of existing sarcomeres, and new muscle fibres arise from mesenchymal cells

24
Q

Describe the innervation of muscle and excitation contraction coupling (the motor end plate)

A

1) Acetylcholine released by axon of motor neuron and binds to receptors on motor end plate
2) AP generated and subsequent end plate potential is propagated across surface membrane and down T tubules of muscle cells.
3) AP triggers Ca2+ release from sarcoplasmic reticulum
4) Ca ions released from lateral bind to troponin and tropomyosin physically moves exposing the binding site
5) Myosin cross bridges attach to actin and pull actin filaments toward centre of sarcomere. Energy provided by ATP
6) Ca2+ actively taken up by sarcoplasmic reticulum when there is no longer AP
7) With Ca2+ gone, tropomyosin covers binding site over again. Contraction ends and actin slides back to original resting position

25
Q

Outline the physiology of the neuromuscular junction

A
26
Q

Describe the pathogenesis and clinical features of myasthenia gravis

A

Myasthenia gravis is an autoimmune disease where the antibodies are directed against Ach receptor (block). A 30% reduction in receptor number is sufficient for symptoms. Endplate ‘invaginations’ in synaptic clefts is reduced. There is reduced synaptic transmission and intermittent muscle weakness. Symptoms include:
- Difficulty chewing/swallowing
- Slurred speech/ husky quiet voice
- Chocking bits of food and shortness of breath
- Difficulty holding the head up
- Difficulty with physical tasks

27
Q

What happens to the actin and myosin lengths during muscle contraction

A

The lengths of the actin and myosin filaments remain the same. It’s the sarcomeres that shorten. Z lines come closer together.

28
Q

State how neuromuscular transmission is disrupted in botulism

A

Toxin is produced by Clostridium botulinum. This blocks the neurotransmitter release at the motor end plate which cause non-contractile state of the skeletal muscles (flaccid paralysis).
Botox is clinically used to treat muscle spasms but also used cosmetically to treat wrinkles

29
Q

State how neuromuscular transmission is disrupted in organophosphate poisoning

A

Organophosphates are used as pesticides. They inhibit the normal function of Ach esterase. Ach activity at the neuromuscular junction is potentiated This leads to multiple symptoms and signs such as:
Muscarinic Symptoms - Salivation, Lacrimation, Urination, Defecation, GI cramping, Emesis (vomiting)
Nicotinic symptoms - Muscle cramps, Tachycardia, Weakness, Twitching, Fasciculations

30
Q

Describe the pathophysiology of Duchenne muscular dystrophy

A

Duchene muscular dystrophy
- Most common muscular dystrophy
- Inherited through X-linked recessive pattern
- Mutation of dystrophin gene
- Absence of dystrophin allows:
Excess calcium enter muscle cell which is taken up by mitochondria. Water is taken with it. Mitochondria burst. Muscle cell burst. Creatine kinase and myoglobin levels extremely high.
Multiple skeletal muscle related symptoms and signs. Muscle cells replaced by adipose tissue.

31
Q

What does dystrophin do

A

It attaches to actin filament to the sarcolemma, through a protein A complex that is inserted into the sarcolemma. This membrane bound complex connects to the basal lamina of the muscle endomysium through collagen 4 and 6 using proteoglycans and laminin. When muscle fibre contacts it bursts (rhabdomyolysis).