Muscle And Pathologies Of Muscle Flashcards

0
Q

What are the lengths and diameters of the cells of the different muscle types?

A

Skeletal 1mm-20cm long, 10-100um diameter
Cardiac 50-100um long, 10-20um diameter
Smooth 20-200um long, up to 0.5mm in uterus. 5-10um diameter

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1
Q

What are the three types of muscle?

A

Skeletal, cardiac and smooth.

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2
Q

How does skeletal muscle develop?

A

Myogenic stem cells give rise to myoblasts, which fuse to give a primary motive with multiple central nuclei, which are then displaced to the periphery by actin and myosin filaments.

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3
Q

What are the three different types of skeletal muscle fibres, and how do they differ? (7 points)

A

Red, white and intermediate.
Red are narrower
Red have more mitochondria
Red are more abundant in muscles that don’t contract as powerfully, but they can sustain a contraction for a long time, such as postural muscles of the back, limb muscles.
Red fibres are richly vascularised
Red fibres have more myoglobin
Red fibres have fewer neuromuscular junctions
Red fibres are rich in oxidative enzymes, but poor in ATPase

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4
Q

Describe the locations of the connective tissues found in a muscle, and their names.

A

Epimysium surrounds muscle belly.
Perimysium surrounds individual fascicles.
Endomysium surrounds each muscle fibre.

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5
Q

List seven different arrangements of muscle fibres in muscle.

A
Circular (orbicularis orbis)
Convergent (pectoralis major)
Parallel (sartorius)
Unipennate (extensor digitorum longus)
Multipennate (deltoid)
Fusiform (biceps brachii)
Bipennate (rectus femoris)
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6
Q

What is the difference between intrinsic and extrinsic muscles of the tongue?

A

Extrinsic muscles have insertions in bone or cartilage, allow the tongue to change position.
Intrinsic muscles are not attached to bone or cartilage, allow the tongue to change shape.

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7
Q

Where are the nuclei found in skeletal muscle fibres?

A

Peripherally, in rows.

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8
Q

How do skeletal muscles of the tongue terminate?

A

Interdigitation with matrix and collage of surrounding connective tissue.

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9
Q

What is found in a dark staining streak in a micrograph of skeletal muscle?

A

Mitochondria.

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10
Q

What is found in the endomysium?

A

Capillaries and nerves. (And other constituents of connective tissue!)

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11
Q

How are actin and myosin arranged in a skeletal muscle fibre?

A

Arranged in sarcomeres.
Z discs lie within the I bands
M lines lie within H zones, lie within A bands
I bands consist of actin filaments, not including where they overlap with myosin.
A bands consist of myosin filaments, including overlap with actin filaments.
H zones consist of myosin filaments not overlapped with actin.

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12
Q

What are the changes in the appearance of the sarcolemma during muscle contraction?

A

Z discs get closer together and sarcomeres shorten.
I Bands get shorter.
A bands stay the same
H zones get shorter.

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13
Q

What is the structure of troponin, what does each subunit bind?

A

Three subunits.
TnT binds tropomyosin
TnC binds calcium
TnI binds actin, preventing myosin heads from binding.

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14
Q

What happens when calcium binds troponin?

A

Tropomyosin is bound to actin via troponin to form the thin filament.
When calcium binds troponin this causes a conformational change in troop myosin which exposes the site for myosin heads to bind on actin, so muscle contraction can occur.

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15
Q

What makes troponin useful in diagnosis?

A

Released from cardiac muscle within an hour of MI

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16
Q

What is the structure of myosin?

A

Rod like protein from which two heads protrude

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17
Q

Describe the process of muscle contraction.

A

Myosin head (bound to ADP and Pi) binds exposed binding site on actin filaments.
The myosin head pivots and pulls the actin filament towards the M line (working stroke). ADP and Pi released.
ATP binds, myosin heads detach.
ATP is hydrolysed, cocking of myosin heads occurs.

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18
Q

What is rigor mortis?

A

In the absence of ATP myosin heads remain tightly bound to actin.

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19
Q

How are the T tubules and sarcoplasmic reticulum arranged in skeletal muscle?

A

Triad (cross section would show 2 terminal cisternae of sarcoplasmic reticulum and a t tubule). T tubules in line with A-I junction.

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20
Q

What is a t tubule?

A

Invagination of plasma membrane, allows propagation of depolarisation into the muscle.

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21
Q

Describe how a contraction is initiated.

A

Nerve impulse arrives at neuromuscular junction.
Acetylcholine is released into synaptic cleft.
Binds with receptors on post synaptic membrane, causes voltage gated sodium ion channels to open, sodium ions flood into the cell.
This causes a depolarisation of the membrane that propagates along the sarcolemma and into the t tubules.
This causes a conformational change in voltage sensor proteins in the t tubules membrane, which causes calcium ion channels in the sarcoplasmic reticulum to open. Calcium ions flood out of the sarcoplasmic reticulum and bind to troponin, initiating muscle contraction.

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22
Q

What are the salient features of cardiac muscle?

A

Striated
Centrally positioned nuclei (one or two per cell)
Branched.
Cells joined by intercalated discs - for electrical and mechanical conduction.

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23
Q

How are myofilaments arranged in cardiac and skeletal muscle?

A

In cardiac muscle, they form continuous masses in the cytoplasm.
In skeletal muscle they are arranged in distinct myofibrils within each muscle fibre.

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24
Q

Name two features of intercalated discs, and their purpose.

A

Gap junctions for electrical coupling

Adherens junctions to join cells and anchor actin filaments.

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25
Q

How are T tubules arranged in cardiac muscle?

A

In line with Z bands.

Diad arrangement with terminal cisternae of sarcoplasmic reticulum.

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26
Q

What is the structure and function of purkinje fibres?

A

Purkinje fibres are modified myocytes with abundant glycogen, sparse myofilaments and extensive gap junctions. They often stain pale.
They conduct action potentials rapidly to enable the ventricles to contract in a synchronous manner.

27
Q

How are the nuclei positioned in a smooth muscle cell?

A

Centrally

28
Q

What is the shape of a smooth muscle cell?

A

Fusiform.

29
Q

How does smooth muscle contract?

A

Sliding filament mechanism.

They are not striated, don’t have t tubules, don’t have sarcomeres.

30
Q

Does contraction of smooth muscle require more or less ATP? How long may a contraction last for?

A

Less.

Hours or days.

31
Q

How do smooth muscle cells aggregate?

A

Into sheets, bundles or layers containing thousands of cells!!!

32
Q

What stimulates contraction of smooth muscle cells?

A

Hormones, nerve signals, local concentrations of blood gases, drugs.

33
Q

Where is smooth muscle found?

A

Walls of blood vessels, GI system, respiratory tract, genitourinary tract.

34
Q

In what conditions might smooth muscle be of clinical significance?

A
Abnormal gut motility
Dysmenorrhea
Asthma
Atherosclerosis
Hypertension
35
Q

Explain the role of myoepithelial cells.

A

Myoepithelial cells are modified myocytes that are present as single cells.
They are stellate, and form a basket work around the secretory portions of some glands, such as mammary glands, sweat glands and salivary glands. Their contraction assists secretion.
They are also present in the iris, and contract to dilate the pupil.

36
Q

Explain the role of myofibroblast cells.

A

They are present at sites of wound healing and tooth eruption. They produce collagen, and also contract (contain actin and myosin)

37
Q

How is smooth muscle innervated?

A

By the autonomic nervous system. Varicosities release neurotransmitters into a wide synaptic cleft.

38
Q

How are thick, thin and intermediate filaments arranged in a smooth muscle cell?

A

Thick and thin filaments are arranged diagonally in the cell - they spiral down the long axis.
Intermediate filaments are attached to dense bodies in the sarcoplasm and anchored in the sarcolemma.

39
Q

What repair is possible in:

a) skeletal muscle
b) cardiac muscle
c) smooth

A

a) limited repair possible - satellite cells can divide, but muscle fibres cannot. Dividing satellite cells increase numbers of muscle fibres (hyperplasia) and can also fuse with existing muscle fibres making them larger (hypertrophy)
b) incapable of regeneration. Following damage fibroblasts invade and lay down scar tissue.
c) smooth muscle cells can undergo mitosis - particularly evident in pregnant uterus.

40
Q

Name four functions of skeletal muscle:

A

Movement
Posture
Stability of joints
Heat generation

41
Q

What is hypertrophy?

A

Increase in the number of myofilaments, muscle fibres increase in size.

42
Q

What is atrophy?

A

Decrease in the number of myofilaments resulting in smaller muscle fibres.

43
Q

List 7 changes to skeletal muscle due to exercise.

A
Metabolic adaptation.
Sarcoplasmic reticulum swells.
Increased volume of mitochondria
Increased Z band width
Increased ATPase 
Increase in number of contractile proteins
Increased density of t tubule systems.
44
Q

What might high intensity exercise lead to?

A

Hypertrophy - more myofilaments synthesised, fatter muscle fibres, larger muscle with increased strength.

45
Q

What is the potential effect of low intensity exercise on muscle fibres?

A

Not hypertrophy
Switch to oxidative metabolism - lipids
Vascular changes and synthesis of mitochondrial proteins to support greater oxygen utilisation.

46
Q

What can cause atrophy?

A

Age - 50% by age 80 (sarcopenia) - implications for temperature regulation.
Disuse
Denervation - must innervate within 3 months to regain use

47
Q

What is the affect of sustained stretching on a muscle fibre?

A

Elongates - possible addition of sarcomeres?

48
Q

How is acetylcholine removed from synaptic cleft?

A

Acetylcholinesterase

49
Q

What proportion of receptors need to be occupied to stimulate muscle contraction?

A

25%

50
Q

What is myasthenia gravis?

A

Autoimmune destruction of acetylcholine receptors, causes loss of junctional folds and a widening of the synaptic cleft.

51
Q

What are the symptoms of myasthenia gravis?

A

Fatigability and sudden falling
Ptosis and double vision
Affected by general state of health, fatigue and emotion

52
Q

How can you treat myasthenia gravis?

A

Acetylcholinesterase inhibitors - eg pyridostigmine.
Immune suppressants
Thymectomy
Plasmapheresis- removal of antibodies from serum

53
Q

Want cause duchenne muscular dystrophy?

A

Complete absence of dystrophin.

54
Q

What causes beckers muscular dystrophy?

A

Truncated, altered dystrophin

55
Q

What causes limb girdle muscular dystrophy?

A

Deficiency of sarcoglycans

56
Q

What causes congenital mersosin deficient muscular dystrophy?

A

50% deficiency of mersosin.

57
Q

What is the consequence of an absence of dystrophin in DMD?

A
Muscle fibres tear themselves apart - Creatine kinase released into circulation.
Calcium floods into fibres, causing necrosis.
Muscles swell (pseudohypertrophy) then fat and connective tissue replace muscle fibres.
58
Q

What is Gowers sign?

A

Children using their arms to stand, as leg muscles aren’t strong enough.

59
Q

What are contractures?

A

Imbalance between strengths of agonist and antagonist muscles (may be present in DMD)

60
Q

How may you treat DMD?

A

Prednisolone (steroid)

61
Q

What is thyrotoxicosis?

A

Hyperthyroidism leads to catabolism of muscle

62
Q

What is malignant hyperthermia?

A

A life threatening allergy to volatile anaesthetic - intracellular calcium increases causing sustained contraction of muscles.

63
Q

What is the effect of hypoparathroidism on muscle?

A

Decreased calcium levels cause tetany - contraction of muscles

64
Q

Name three causes of inflammatory myopathy:

A

Polymyosotis (autoimmune muscle wasting -cancer and old age)
Myalgia
Influenza

65
Q

How might diuretics cause cramps?

A

They reduce the levels of electrolytes including potassium