Muscles Flashcards

0
Q

Classify the 3 histology all forms of muscle

A

Skeletal Muscle (striated), Cardiac Muscle (striated), Smooth Muscle (non-striated)

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1
Q

Describe, in ascending order of size, the structure of muscle.

A

Many myofilaments in a myofibril, many of which, make up
a single muscle fibre (cell) wrapped in endosmysium. Arranged into fascicles wrapped in perimysium. Arranged into whole muscles wrapped by epimysium.

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2
Q

Describe the ultrastructure appearance of skeletal muscle. (Bands)

A

MHAZI. M line is in the H band which is in the A band. The Z line is in the I band

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3
Q

In sarcomeres which filament is thick and which is thin

A

Actin is Thin

Myosin is Thick

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4
Q

Name the constituent parts of actin filaments

A

Actin wrapped in tropomyosin, interspersed with troponin complexes

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5
Q

Describe the structure of the thick, myosin, filament.

A

Many myosin molecules, whose heads protrude at opposite ends.

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6
Q

Describe stage 1 of 4 of muscle contraction (Cocking)

A

Hydrolysis of the ATP attached to the myosin head cocks the head into a high energy state.

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7
Q

Describe stage 2 of 4 of muscle contraction (Binding)

A

In the presence of Ca+, which binds to troponin exposing binding sites on the tropomyosin, the myosin head binds lightly to the actin filament.

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8
Q

Describe stage 3 of 4 of muscle contraction (power stroke)

A

The release of the ADP and Pi causes the myosin head to bind tightly moving the actin filament 5nm (the head is now uncocked)

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9
Q

Describe stage 4 of 4 of muscle contraction (detachment)

A

ATP binds to the myosin head, releasing it from the actin filament.
The cycle then repeats

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10
Q

Describe the the mechanism of innervation of muscle. (~6 steps)

A
  1. Nerve impulse arrives at neuromuscular junction
  2. This releases Acetyl Choline causing depolarisation of sarcolema
  3. Voltage gated Na Channels open, Na enters cell
  4. Depolarisation spreads through T tubules
  5. The gated Ca channels open and Ca enters sarcolemoplasm
  6. Ca allows muscle contraction (exposes myosin binding sites)
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11
Q

Explain the attachment of muscle to tendons

A

Skeletal muscle fibres interdigitate with tendon collagen bundle at myotendenous junction.

The sarcolema always lies between collagen bundles and microfilaments.

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12
Q

Describe the nature of repair in skeletal muscle

A

Cells cannot divide but tissue can regenerate by mitotic activity of satellite cells, the can fuse with existing muscle cells to increase mass.
Gross damage is repaired with connective tissue, which leaves scars

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13
Q

Describe the nature of repair in cardiac muscle

A

Incapable of regeneration.

Following damage, fibroblasts invade and lay down scar tissue.

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14
Q

Describe the nature of repair in smooth muscle

A

Cells undergo mitosis

Particularly evident in the pregnant uterus where the muscle wall becomes thicker.

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15
Q

Define muscular hyperplasia

A

The increase in muscle size due to mitotic division (exclusive to smooth muscle)

16
Q

Define muscular hypertrophy

A

The increase in muscle size due to swelling of individual cells. Often caused by an increase in number of myofibrils.

17
Q

Describe the histology of cardiac muscle

A
Striated
Branching
Central nuclei
Intercalated disks (for mechanical and electrical coupling)
Gap junctions
T tubules are in line with the Z disk
18
Q

Describe the histology of smooth muscle

A

Cells are fusiform (like a bronchasuharus with no legs)
Non striated
Contraction is slower and requires less ATP
Can be stretched
Responds to hormones, nerves, drugs, [blood gasses]
Filaments spiral along the cell

19
Q

Outline the structure and function of the Purkinje fibres

A

Abundant glycogen
Sparse myofilaments
Extensive gap junction sites
Rapid conduction of action potentials

20
Q

How long does the remodeling of skeletal muscle take?

A

2 weeks

21
Q

Define muscular atrophy

A

Muscular atrophy is the loss of muscular tissue caused by a greater rate of destruction than replacement.

22
Q

List the causes of muscular atrophy

A

Disuse of muscle (muscle fibres shrink)
Age
Denervation reduced nervous activity leads to disuse

23
Q

Outline the role of acetyl choline in the neuromuscular junction

A

Acetyl choline (ACh) is released across the junction.
25% of ACh receptors need to be occupied to…..
Open sodium channels to…..
Start depolarisation of sarcolema

24
Q

Describe the pathophysiology of Myasthenia Gravis

A

Autoimmune destruction of ACh receptors
Loss of junctional folds at the end-plate
A widening of the synaptic cleft

25
Q

Describe the symptoms of Myasthenia Gravis

A

Fatigability and sudden falling due to reduced ACh release
Drooping eyelids
Double vision
Crisis at point at which respiratory muscles are affected

26
Q

Describe the treatment of Myasthenia Gravis

A

Acetyl Cholinesterase inhibitors which prevent the breakdown of Acetyl Choline

27
Q

Describe the pathophysiology of muscular dystrophy

A

Genetic faults cause reduced synthesis of specific proteins which anchor actin filaments to the cell wall.

Muscle fibres tear themselves apart upon contraction

28
Q

Describe the pathophysiology of Duchenne Muscular Dystrophy

A

Complete absence of dystrophin causing :
Muscle fibres to tear themselves apart on contraction
Enzyme creatine (phospho)kinase liberated in blood serum
Calcium enters and causes necrosis
Pseudohypertrophy before fat on connective tissue replace muscle

29
Q

Describe the signs and symptoms of Duchenne muscular dystrophy

A

Early onset Gower’s sign (use of hands on knees when standing)
Contractures (imbalance between muscle pairs)

30
Q

Describe the treatments of Duchenne muscular dystrophy

A

Steroid therapy

Ataluren (PCT124) drug trails (promotes dystrophin production)

31
Q

Outline the pathophysiology of malignant hyperthermia

A

Rare autosomal dominant
Causes a life-threatening reaction with Succinylcholine
Causes uncontrolled increase in skeletal muscle oxidative metabolism

32
Q

Outline the treatment of malignant hyperthermia

A

Dantrolene (a muscle relaxant which prevents Ca release)

Correction of hyperthermia, acidosis and organ dysfunction