Session 6 - Muscles Flashcards

1
Q

Histologically distinguish between skeletal, cardiac and smooth muscle types

A
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2
Q

Describe the ultrastructural appearance of striated muscle and state which bands contain actin, myosin or both

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3
Q

Explain the hierarchical composition of a typical skeletal muscle outlining the principal components at the molecular, organelle, cellular, histological and regional anatomical levels

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4
Q

Compare and contrast the structural significance of fast and slow striated muscle fibres

A
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5
Q

Fast vs slow twitch Muscle fibres when they are working

A
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6
Q

Describe the limited nature of repair possible in a mature muscle

A
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7
Q

Recognise the following in photomicrographs, discuss their anatomical locations and salient histological features in relation to their function:
* skeletal muscle in longitudinal and transverse section (and be able to distinguish it from tendon)
* cardiac muscle (and be able to distinguish it from skeletal muscle)
* smooth muscle (and be able to distinguish it from connective tissue)

A
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8
Q

Understand the concepts of the origin and insertion of a muscle, and relate these to its actions

COME BACK TO

A
  • To contract, a skeletal muscle needs at least two points of attachment, an origin and an insertion.
  • In most cases, one end of the muscle is fixed in position (usually the origin), while the other end moves during contraction (usually insertion)
  • The insertion is usually distal, or further away, while the origin is proximal, or closer to the body, relative to the insertion.
    (For example, one could say the wrist is distal to the elbow. Conversely, you can say the elbow is proximal to the wrist.)
  • Points of origin
  • Points of insertion
  • If these cross a joint, then movement occurs
  • Movement is dependent on the direction of muscle fibre (cell) contraction
  • Lots of different shapes of mucscle
  • Movement is always along the direction of a fascicle
  • Tension created at the origin tendon point
  • Movement created at the insertion tendon point
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9
Q

Describe the structure and organisation of skeletal muscle fibres

A
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10
Q

Understand the different roles muscles can play in coordinated movement e.g. agonist, antagonist, synergist, neutraliser and fixator

A
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11
Q

Understand the difference between superficial and deep fascia

A
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12
Q

Outline the function of the Purkinje fibres of the heart

A
  • The Purkinje fibres conduct action potentials rapidly (3-4 m/s, compared to 0.5 m/s for cardiac muscle fibres)
  • This rapid conduction enables the ventricles to contract in a synchronous manner
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13
Q

Outline the structure Purkinje fibres of the heart

A

Purkinje fibres are large cells with: - abundant glycogen
- sparse myofibrils
- extensive gap junction sites

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14
Q

What is this arrow pointing to?

A

Purkinje Fibres

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15
Q

Label this diagram (the 3 arrows) and describe what is happening in the image

A

Tracts of Purkinje fibres (modified myocytes) transmit action potentials to the ventricles from the atrioventricular node

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16
Q

What are Purkinje fibres?

A
  • Large modified myocytes with: abundant glycogen, sparse myofilaments and extensive gap junction sites.
  • Conduct APs rapidly, enabling ventricles to contract in a synchronous manner.
17
Q

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

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18
Q

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

A
19
Q

Outline the physiology of the neuromuscular junction

A
20
Q

Describe the clinical features of myasthenia gravis

A

Ptosis (Ptosis is when the upper eyelid droops, sometimes restricting or blocking vision)

21
Q

Describe the pathogenesis 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
  • Reduced synaptic transmission
  • Intermittent muscle weakness
22
Q

outline the mechanisms of the sliding filament model of muscle contraction

A
23
Q

State how neuromuscular transmission is disrupted in botulism

A
  • Toxin produced by Clostridium botulinum
  • Blocks neurotransmitter release at the motor end plate
  • Causes non-contractile state of skeletal muscle - Flaccid paralysis
24
Q

Describe the use of Botulism toxin and botox

A
  • Clinically used to treat muscle spasms (e.g. cervical dystonia)
  • Used cosmetically to treat ‘wrinkles’
25
Q

State how neuromuscular transmission is disrupted in organophosphate poisoning

A

Organophosphates are used as pesticides
* Inhibits the normal function of Ach esterase
* Ach activity at the neuromuscular junction is
potentiated
* Leads to multiple symptoms and signs:
* Effects on both somatic and autonomic signalling

26
Q

describe the pathophysiology of Duchenne muscular dystrophy

A
  • Most common muscular dystrophy
  • Inherited through X-linked recessive pattern
  • Mutation of the dystrophin gene
  • 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)
  • Creatine kinase and myoglobin levels are extremely high in the blood(sodium, phosphate, uric acid, potassium are also released)
  • Multiple skeletal muscle related symptoms and signs
  • Muscle cells replaced by adipose tissue
27
Q

What are the signs and symptoms of Duchenne muscular dystrophy? (10)

A
28
Q

What is happening in this image?

A

Muscle cells are being replaced with adipose tissue (occurs in Duchenne muscular dystrophy)

29
Q

Break down the word ‘rhabdomyolysis’

A

Rhabdo = striated; myo = muscle; lysis = destruction

30
Q

Describe the pathophysiology of malignant hyperthermia

A
  • Severe reaction to anaesthetics – 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
31
Q

State the muscarinic and nicotinic symptoms of cholinergic toxidrome

A