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ESA1 Callum's cards > TOB S8 - Muscle and Disorders > Flashcards

TOB S8 - Muscle and Disorders Flashcards

1
Q

What are the 3 forms of muscle?

A

Skeletal muscle
Cardiac muscle
Smooth muscle

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2
Q

Which forms of muscle are striated and which are not?

A

Cardiac and skeletal = Striated

Smooth muscle = Non-striated

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3
Q

Describe the ultrastructure appearance of striated sarcomeres

Hint: It’s probably helpful to draw it out then compare your drawing to the description given in the answer.

A

MHAZI

M-line central

H-band containt the M-line

H band lies within the A band

A band flanked by the I bands

Z-line is central in the I bands

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4
Q

What are the two types of filament that appear in a sarcomere?

A

Thin filament - Actin

Thick filament - Myosin

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5
Q

Which types of filaments appear in which bands of a striated muscle sarcomere?

A

I-band = Actin

A-band = Myosin

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6
Q

What are the component molecules of an Actin filament?

A

Actin
Troponin
Tropomyosin

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7
Q

Describe the molecular structure of an Actin/Thin filament

A

2 actin molecules form a helix

Tropomyosin wraps around the actin chain

Each tropomyosin has a troponin complex attached to it (which covers the Actin binding site)

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8
Q

Describe the structure and functions of each subunit in a troponin complex

A

Complex contains TnI, TnC and TnT

TnI binds to Actin

TnC binds to calcium

TnT binds to tropomyosin

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9
Q

Describe how calcium ions initiate contraction in a sarcomere

A

Increased amounts of calcium ions bind to TnC subunit of troponin

A conformational change occurs, moving tropomyosin away from actin’s binding site

This displacement allows myosin heads to bind to actin, and contraction begins

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10
Q

What are the 5 stages of muscle contraction?

A 
Attachment
Release
Bending
Force generation
Reattachment
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11
Q

Describe the attachment phase of muscle contraction (phase 1)

Also, how might this be useful to a doctor writing a death certificate?

A

Rigor conformation seen.

Myosin head is bound tightly to the actin molecules

In death, Lack of ATP perpetuates this binding, causing rigor mortis, an obvious clinical sign of death.

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12
Q

Describe the release phase of muscle contraction (phase 2)

A

ATP binds to the myosin head causing it to uncouple from the actin filament

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13
Q

Describe the bending phase of muscle contraction (phase 3)

A

Hydrolysis of ATP causes uncoupled myosin to bend and advance a short distance (5nm)

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14
Q

Describe the force generation phase of muscle contraction (phase 4)

A

Myosin head binds weakly to the actin filament causing the release of Pi

Release of Pi strengthens binding and causes a ‘power stroke’ in which the myosin head returns to its former position

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15
Q

Describe the reattachment phase of muscle contraction (phase 5)

A

Myosin head binds tightly to actin again and the cycle can then repeat.

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16
Q

What structures can be found surrounding myofibrils?

A

Mitochondria

T tubules

Sarcoplasmic reticulum

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17
Q

Describe in detail how excitatory nerve impulses result in muscle contraction

A
  1. Action potential arrives pre-synaptic neurone terminal. Opens voltage gates calcium channels.
  2. Influx of Ca2+ causes vesicles full of Acetylcholine to be released into the synaptic cleft. These bind with Nicotinic acetylcholine receptors on the motor end plate
  3. Ach binding opens ligand gated ions channels (Na+ flows in, K+ flows out of muscle cytosol) causing membrane depolarisation of the sarcolemma.
  4. Depolarisation spreads to T-tubules which change conformation
  5. Gated Ca2+ release channels of adjacent terminal cisternae of the sarcoplasmic reticulum which rapidly releases Ca2+ into the sarcoplasm
  6. Ca2+ binds to TnC of troponin
  7. Contraction initiated and Ca2+ returned to the sarcoplasmic reticulum
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18
Q

Describe the organisation and composition of muscle sheath layers around structures in skeletal muscle

A

Epimysium surrounds whole muscle

Perimysium surrounds muscle fascicles

Endomysium surrounds individual muscle fibres

Layers are made up of connective tissue

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19
Q

Describe the basic structure of the attachment between a muscle and a tendon

What is the proper name for this structure?

A

Skeletal muscle fibres and collagen bundles of the tendons interdigitate at the myotendinous junctions

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20
Q

Where is collagen found in striated muscle?

A

In bundles between microfilaments of the muscle fibres

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21
Q

Describe the hierarchal composition of a typical skeletal muscle

A

Skeletal muscle composed of…

Fascicles composed of…

Muscle fibres (cells) composed of…

Myofibrils composed of….

Myofilaments (Actin + Myosin)

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22
Q

Describe the location and appearance of the nucleus in muscle fibres

A

Periphery of the cell

Cigar shaped

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23
Q

If skeletal muscle is damaged, what is the role of satellite cells in repair?

A

Muscle fibres cannot divide, therefore satellite cells used in repair via two modes of action:

Tissue can regenerate via mitotic activity of satellite cells so hyperplasia follows injury

Satellite cells can also fuse with existing muscle cells to increase muscle cell mass (hypertrophy)

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24
Q

What is the effect of gross damage to a skeletal muscle?

A

Satellite cells cannot repair the damage therefore:

Repaired by connective tissue forming a scar

If nerve or blood supply is interrupted the muscle cells degenerate and are replaced by fibrous tissue

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25
Q

What happens in the event of damage to cardiac muscle?

A

Cant regenerate

Following damage, fibroblasts invade and lay down fibrous scar tissue

26
Q

What happens in the event of damage to smooth muscle?

A

Cells retain mitotic ability and can form new cells

27
Q

Where are the T tubules found in cardiac cells and skeletal muscle cells?

A

Cardiac - Overlying the Z disk

Skeletal - Overlying the I-A band junction

28
Q

Describe the key histological features of cardiac muscle

A 
Striated
Branching
Centrally positioned nuclei
Intercalated disks between cells
Adherens and gap type junctions
T tubules inline with Z-disk
29
Q

What are adherens junctions, whaere are they found and what is their function?

A

Ribbon like protein couplings between cardiomyocytes

Found at the intercalated disks of cardiomyocytes

They anchor actin to the intercalated disks

30
Q

What is the function and location of gap junctions in a cardiomyocyte?

A

Gap junctions found in the intercalated disks allow ions passage, hence allowing depolarisation to propagate through the cells.

31
Q

Describe the histological features of smooth muscle cells

A

Spindle shape (fusiform)

Central nucleus

Not striated, no sarcomeres or T-tubules

Contraction still relies on actin-myosin interaction
Thick and thin filaments arranged diagonally within the cell, spiralling down the long axis

32
Q

How does contraction of smooth muscle differ from cardiac or skeletal muscle

A

Smooth muscle is slower to contract

Requires less ATP

May remain contracted for hours or days

33
Q

What stimuli might provoke smooth muscle contraction?

A

Nerve signals
Hormones
Drugs
Local concentration of blood gases

34
Q

What is the function of Purkinje fibres and where are they found?

A

Found in the tracts through Cardiac muscle

They transmit action potentials fro the atrioventricular node to the ventricles

35
Q

What are the key features of a Purkinje fibre?

A

Abundant glycogen
Sparse myofilaments
Extensive gap junction sites
Conduct action potentials very quickly, allowing synchronous contraction of ventricles

36
Q

How often are contractile proteins in skeletal muscle replaced?

A

~Every 2 weeks

37
Q

What are the processes behind skeletal muscle atrophy or hypertrophy?

A

Atrophy = Destruction of contractile proteins > Replacement

Hypertrophy = Replacement > Destruction

38
Q

What are the 3 major causes of skeletal muscle atrophy?

A

Disuse
Age
Denervation

39
Q

Explain why and how disuse atrophy of skeletal muscles occurs

Give some examples of when this might occur

A

Maintenance of muscle requires frequent movement against resistance, without this, muscles will shrink and weaken (not die).

Atrophy is the loss of proteins in muscle cells, leading to loss of muscle fibre diameter and subsequent loss of power

Eg. Bed rest, Limb immobilisation, Sedentary behaviour

40
Q

When does age atrophy of skeletal muscle first begin?

How much muscle mass has been lost by age 80?

A

Past age 30

50% of muscle mass lost by 80yrs

41
Q

What is denervation atrophy of skeletal muscle?

A

Muscle is no longer receiving contractile signals that are required to maintain normal size, so muscle atrophies.

42
Q

What is a major cause of denervation muscle atrophy and what are its short term symptoms?

A

Lower motor neurone lesions

Weakness
Flaccidity
Atrophy with fasciculations (spontaneous twitching of small groups of muscle fibres)
degeneration of muscle fibres in 10-14 days
Hypo or areflexia (absent or decreased reflexes)

43
Q

When Denervation atrophy occurs in skeletal muscle what are the effects long term if innervation isn’t re-established?

A

If innervation not re-established within 3 months then there’s a very poor recovery
Muscle completely unviable after 2 years.

Muscle fibres are replaced with fibrous and fatty tissue.
Fibrous tissue leads to contractures
As the muscle shortens it can lead to disfiguring and debilitating contractures (daily stretching required)

44
Q

What is muscle hypertrophy and how does it come about?

What metabolic changes are seen in skeletal muscle hypertrophy?

A

Increase in muscle mass, more contractile proteins and increase in fibre diameter

Due to work performed against load

Metabolic effects are:
Increased enzymes for glycolysis, mitochondria, stored glycogen and blood flow.

45
Q

How is acetylcholine deactivated?

A

By acetylcholinesterase

46
Q

What is the effect of high motor neurone firing rates on acetylcholine release?

Why?

A

Ach release decreases

Only 25% of Ach receptors need to be occupied to open ion channels, therefore release decreases at high firing rates as less is needed to maintain the 25% Ach receptor occupancy.

47
Q

What are the key biochemical features of Myasthenia Gravis?

When does this condition cause a crisis?

A

Auto-immune destruction of Ach receptors on motor end plate

Loss of junctional folds at synaptic cleft

Widening of synaptic cleft

Crisis point occurs when if affects respiratory muscles

48
Q

What are the symptoms of Myasthenia Gravis?

What is the treatment?

A

Fatigability and sudden falling due to reduced Ach release

Drooping eyelids

Double vision

Aceytlcholinesterase inhibitors (eg. Neostigmine)

49
Q

Why does placing ice on the eyelids of someone with Myasthenia Gravis help treat their drooping eyelids?

A

Ice inhibits the action of acetylcholinesterase

50
Q

How does Botulism affect muscular function?

A

Toxins block acetylcholine release at the neuromuscular junction

51
Q

How does organophosphate poisoning affect muscular function?

A

Irreversibly inhibits acetylcholinesterase, therefore acetylcholine remains in the receptors and muscle remains contracted.

52
Q

What is the cause of muscular dystrophy?

A

Genetic faults leading to reduced or absent synthesis of particular proteins that anchor actin filaments to the sarcolemma.

53
Q

What effect does muscular dystrophy have on muscle fibre cells?

A

Causes them to tear apart upon contraction

54
Q

What is the cause of Duchenne muscular dystrophy?

A

Complete absence of Dystrophin in muscle fibres

55
Q

What are the physiological effects of Duchenne muscular dystrophy on the body?

Hint: Not signs and symptoms, think cellular level

A

Muscle fibres tear themselves apart upon contraction

Creatine kinase liberated into serum

Calcium enters cell causing necrosis

Pseudohypertrophy (swelling) before fat and connective tissue replace muscle fibres

56
Q

What are the signs and symptoms of Duchenne muscular dystrophy?

A

Early onset of Gower’s sign (using hands on knees to generate strength

Contractures

57
Q

How might Duchenne muscular dystrophy be treated?

A

Steroid therapy (prednisolone)

58
Q

What is the cause of malignant hyperthermia?

A

autosomal dominant genetic disease

59
Q

In a patient with malignant hyperthermia, what should not be administered to them and why?

Hint: Go into detail on the why, explain the biochemical basis

A

Don’t administer:
Volatile anaesthetic agents
Succinylcholine (neuromuscular blocking agent)

Why:

Cause a drastic and uncontrolled increase in skeletal muscle oxidative metabolism

This quickly overwhelms the body’s ability to remove CO2 and supply O2

This leads to circulatory collapse and death

60
Q

How is malignant hyperthermia treated?

A

Correction of hyperthermia, acidosis and organ dysfunction

Discontinuation of triggering agent

Administration of dantrolene (muscle relaxant)

61
Q

What is Succinylcholine’s method of action and how is it degraded?

A

Inhibits action of Acetylcholine by non-competitively binding to Nicitonic Ach receptors.

Is degraded by butyrylcholinesterase (however, this process is slower than Ach degradation by Achesterase)

ESA1 Callum's cards (34 decks)

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