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TOB > Session 8 > Flashcards

Session 8 Flashcards

0
Q

Which types of muscle are striated/non-striated?

A
  • Striated: skeletal; cardiac

- Non-striated: smooth

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1
Q

What are the 3 types of muscle?

A
  • Skeletal
  • Cardiac
  • Smooth
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2
Q

What is the differences in the types of muscle in terms of morphology?

A
  • Skeletal: Long parallel cylinders; multiple peripheral nuclei; strait ions
  • Cardiac: Short, branched cylinders; single (or 2) central nucleus; striations
  • Smooth: Spindle-shaped; tapering ends; single central nucleus; no striations
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3
Q

What are the differences in the types of muscle in terms of connections?

A
  • Skeletal: Fasicle bundles; tendons
  • Cardiac: Junctions join cells end to end
  • Smooth: Connective tissue; gap and desmosome-type junctions
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4
Q

What are the differences in the types of muscle in terms of control?

A
  • Skeletal: Somatic motor neurone (voluntary control)
  • Cardiac: Autonomic modulation (involuntary control); intrinsic rhythm
  • Smooth: Autonomic (involuntary); intrinsic activity; local stimuli
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5
Q

What difference are there in the types of muscle in terms of power?

A
  • Skeletal: Rapid; forceful
  • Cardiac: Lifelong variable rhythm
  • Smooth: Slow, sustained and rhythmic
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6
Q

How does skeletal muscle develop?

A
  • Myoblasts develop from multipotent myogenic stem cells from the mesoderm
  • Myoblasts fuse to form a primary myotube with a chain of multiple central nuclei
  • Centrally positioned nuclei are displaced to the cell periphery by newly synthesised actin and myosin microfilaments
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7
Q

What types of skeletal muscle fibres are there?

A
  • Red
  • Intermediate
  • White
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8
Q

What are some differences between red and white muscle fibres?

A
  • Diameter: Red-smaller; white-larger
  • Vascularisation: Red-rich; white-poor
  • Mitochondria: Red-numerous; white-few
  • Contractions: Red-slow, repetitive, weak; white-faster, stronger
  • Fatigue: Red-slowly; white-rapidly
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9
Q

What are the different layers of connective tissue surrounding muscle?

A
  • Endomysium (surrounds a cell/fibre)
  • Perimysium (surrounds a fasicle)
  • Epimysium (surrounds whole muscle)
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10
Q

What does nuclei of skeletal muscle look like in transverse and longitudinal sections?

A
  • Transverse: Peripheral

- Longitudinal: Rows

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11
Q

What do muscle fibres contain?

A
  • Myofibrils (made up of actin and myosin microfilaments)
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12
Q

What is the thin filament in a skeletal muscle cell?

A
  • Actin
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13
Q

What is the thick filament in skeletal muscle cells?

A
  • Myosin
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14
Q

Describe the structure of a sarcoma re

A

(MHAZI)

  • M line is within the H band, which is within the A band
  • Z line is within the I band
  • H band contains only myosin
  • A band is the length of the myosin including overlapping actin
  • I band is only actin
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15
Q

What is the thin myofilament made up of?

A
  • Actin
  • Tropomysosin
  • Troponin
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16
Q

Describe the binding of the Troponin molecule in actin

A
  • Has 3 binding sites
  • TnI to actin
  • TnC to calcium
  • TnT with tropomysosin
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17
Q

Describe the structure of thick filaments

A
  • Each filament contains many myosin molecules

- Mysoin is a rod-like structure from which 2 heads protrude

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18
Q

Describe the structure of thin filaments

A
  • Actin filament forms a helix
  • Tropomysosin molecules coil around to reinforce
  • Troponin complex is attached to each Tropomysosin molecule
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19
Q

What is the role of ionic calcium in contraction?

A
  • Ionic calcium binds to TnC of Troponin
  • Causes a conformational change
  • Moves Tropomysosin away from actin binding sites
  • Myosin heads can now bind to actin and begin contraction
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20
Q

What are the stages of contraction?

A
  • Stage 1 Attachment: Mysoin head is tightly bound to actin molecule
  • Stage 2 Release: ATP binds to the myosin head, causing it to uncouple from the actin filament
  • Stage 3 Bending: Hydrolysis of the ATP causes uncoupled myosin head to bend and advance a short distance (5nm)
  • Stage 4 Force Generation: Myosin head binds weakly to actin causing release of inorganic phosphate which strengthens binding, causes power stroke which returns myosin head to former position
  • Stage 5 Reattachment: ATP binds to myosin head causing detachment from actin
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21
Q

What happens at a neuromuscular junction?

A
  • Small terminal swelling of the axon that contains vesicles of acetylcholine
  • Nerve impulses cause the release of acetylcholine which binds to receptors on the Sarcolemma
  • This initiates an action potential which propagates along the muscle
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22
Q

What are the stages leading to contraction of skeletal muscle?

A
  • Initiation: nerve impulse along motor neuron axon arrives at neuromuscular junction
  • Impulse prompts release of acetylcholine (Ach) into synaptic cleft causing local depolarisation of the sarcolemma
  • Voltage gated Na+ channels open allowing Na+ into cell
  • General depolarisation spreads over sarcolemma and into T tubules
  • Voltage sensor proteins of the T tubule membrane changes their conformation
  • Gated Ca2+ release channels of adjacent terminal cisternae are activated by this conformation change
  • Ca2+ is rapidly released from the terminal cisternae into the sarcoplasm
  • Ca2+ binds to the TnC subunit of Troponin
  • The contraction cycle is initiated and Ca2+ returns to the terminal cisternae of the sarcoplasmic reticulum
23
Q

What are the distinguishing features of cardiac muscle?

A
  • Striations
  • Centrally positioned nuclei (1/2 per cell)
  • Intercalated discs (for electrical and mechanical coupling with adjacent cells)
  • Branching
  • Adherens-type junctions (anchor cells and actin)
  • Gap junctions (electrical coupling)
24
Q

What is the difference between skeletal and cardiac muscle in terms of Myofibrils?

A
  • Skeletal: Distinct myofibrils

- Cardiac: Myofibrils are absent, instead the myofilaments actin and myosin form continuous masses in the cytoplasm

25
Q

Where do the T tubules lie in skeletal and cardiac muscle?

A
  • Skeletal: junction of A and I bands

- Cardiac: Z line

26
Q

Do skeletal and cardiac muscle have triads or dials of T tubule and sarcoplasmic reticulum?

A
  • Skeletal: Triads

- Cardiac: Diads

27
Q

What is the structure of Purkinje fibres?

A
  • Large cells with:
    ~ Abundant glycogen
    ~ Sparse myofilaments
    ~ Extensive gap junction sites
28
Q

What is the function of Purkinje fibres?

A
  • Transmit action potentials to the ventricles from the atrioventricular node
  • Conduct action potentials rapidly compared to regular cardiac muscle
  • Allows ventricles to contract synchronously
29
Q

What are the features of smooth muscle?

A
  • Spindle-shaped (fusion) with central nucleus
  • Not striated, no star omers or T tubules
  • Contraction still relies on actin-myosin interactions
  • Contraction is slower, more sustained and requires less ATP
  • May stay contracted for days
  • Capable of being stretched
  • Responds to stimuli from nerve signals, hormones, drugs or local concentrations of blood gases
  • Forms sheets, bundles or layers containing thousands of cells
  • Thick and thin filaments are arranged diagonally within the cell, spiralling so that smooth muscle contracts in a twisting way
30
Q

Can skeletal muscle repair itself?

A
  • Cells cannot divide
  • Tissue can regenerate by mitosis activity of satellite cells, so that hyperplasia follows muscle injury
  • Satellite cells can also fuse with existing muscle cells to increase mass (skeletal muscle hypertrophy)
31
Q

Can cardiac muscle repair itself?

A
  • Incapable of regeneration

- Fibroblasts invade, divide and lay down scar tissue following damage

32
Q

Can smooth muscle repair itself?

A
  • Cells retain mitosis ability and can form new smooth muscle cells
  • Particularly evident in pregnant uterus where muscle wall becomes thicker by hypertrophy (swelling) and hyperplasia (mitosis) of individual cells
33
Q

Describe the remodelling of muscles

A
  • Is continual
  • Contractile proteins are replaced in 2 weeks
  • Atophy: muscle wastes away when destruction of proteins is more than replacement
  • Hypertrophy: muscle cells increase in size when replacement of proteins is more than destruction
34
Q

What is the difference between hypertrophy and hyperplasia?

A
  • Hypertrophy: increase in cell size

- Hyperplasia: increase in cell numbers

35
Q

What is the effect of exercise on skeletal muscle?

A
  • Sarcoplasmic reticulum swells
  • Increased volume of mitochondria
  • Increased z band width
  • Increased ATP synthase
  • Increased density of T tubule systems
  • Increase in number of contractile proteins
  • Little evidence for hyperplasia
36
Q

How does high resistance exercise affect skeletal muscles?

A
  • Stimulates contractile protein synthesis, fatter muscle fibres, larger muscle
  • Increased muscle mass and strength and may lead to hypertrophy with the help of myosatellite cells
37
Q

How does endurance exercise affect skeletal muscle?

A
  • Increased endurance without hypertrophy
  • Stimulates synthesis of mitochondrial proteins, vascular changes allowing for greater oxygen utilisation, shift to oxidative metabolism of lipids
38
Q

What is disuse atrophy?

A
  • Occur with bed rest, limb immobilisation, sedentary behaviour
  • Causes loss of protein, which leads to reduced fibre diameter, which leads to loss of power
39
Q

What happens to skeletal muscles as we age?

A
  • Atrophy with age from age 30 onwards

- Loss of 50% muscle mass by 80 (sarcopenia)

40
Q

What is denervation atrophy?

A
  • Also called neurogenic muscular atrophy
  • Muscle no longer receives contractile signals that are required to maintain normal size
  • Signs of lower motor neuron lesions: weakness, flaccidity, muscle atrophy with spontaneous twitching, degeneration 10-14 days after injury
  • Innervation past 3 months has a low chance of recovery, not possible after 2 years
  • Muscle fibres are replaced by fibrous and fatty tissue
  • Fibrous tissue leads to contractures and as muscle shortens leads to debilitating/disfiguring contractures (needs daily stretching)
41
Q

How can muscle length be adjusted?

A
  • Sustained stretching
  • Addition of sacromeres; changes in neurology (pain, stretch receptors and stretch reflex); viscose lactic properties (connective tissue alignment)
  • Reduced muscle length if immobilised
42
Q

What stops acetylcholine?

A
  • Acetylcholinesterase
  • At high motor neuron firing rates, ACh release decreases
  • Only 25% of Ach receptors need to be occupied for an action potential to be triggered
43
Q

What is myasthenia gravis?

A
  • Autoimmune destruction of end-plate ACh receptors
  • Loss of junctional folds at end-plate
  • Widening of synaptic cleft
  • Crisis point when it affects respiratory muscles
44
Q

What are the symptoms of myasthenia gravis?

A
  • Fatigability and sudden falling due to reduced ACh release
  • Drooping upper eyelids
  • Double Vision
  • Affected by General state of health, fatigue and emotion, symptoms fluctuate
45
Q

What is the treatment for myasthenia gravis?

A
  • Acetylcholine inhibitors eg pyridostigmine
  • Immune suppressants
  • Plasmapheresis: removal of harmful antibodies from patients serum
  • Thymetomy
  • Ice on eyelids decreases Acetylcholinesterase activity
46
Q

How is neuromuscular transmission disrupted in botulism poisoning?

A
  • Toxins block ACh release

Botox cosmetic treatment

47
Q

How is neuromuscular transmission disrupted in organophosphate poisoning?

A
  • Irreversibly inhibits acetycholinesterase

- ACh remains in receptors and muscles stay contracted

48
Q

What are muscular dystrophies?

A
  • Genetic faults that cause the absence or reduced synthesis of specific proteins that normally anchor actin filaments to the sarcolemma
  • in absence causes muscle fibres cells can tear themselves apart when contracting
49
Q

What causes Duchenne muscular dystrophy?

A
  • There is a complete lack of dystrophin
  • Muscle fibres tear themselves apart on contraction
  • Enzyme creatine phosphokinase liberated into serum
  • Calcium enters cell causing necrosis
  • Pseudohypertrophy (swelling) before fat and connective tissue replace muscle tissue
50
Q

What are the signs and symptoms of Duchenne muscular dystrophy?

A
  • Early onset - Gower’s sign (hands on knees to generate strength)
  • Contractures (imbalance between agonist and antagonist muscle)
  • Steroid therapy (prenisolone)
  • Ataluren drug trials in humans, ribosomal interaction to produce dystrophin
51
Q

What is malignant hyperthermia?

A
  • A rare, autosomal dominant disorder

- Causes a life threatening reaction to certain drugs used for general anaesthesia

52
Q

How do general anaesthetic drugs work normally?

A
  • Are volatile anaesthetic agents and the neuromuscular blocking agent succinylcholine
  • Succinylcholine inhibits action of ACh, acting non-competitively on muscle-type nicotinic receptors
  • Is degraded by butyrylcholinesterase much more slowly than the degradation of ACh by Acetylcholinesterase
53
Q

How do anaesthetic drugs cause malignant hyperthermia?

A
  • In susceptible individuals, drugs can induce a drastic and uncontrolled increase in skeletal muscle oxidative metabolism
  • Overwhelms body’s capacity to supply O2, remove CO2 and regulate body metabolism
  • Leads to circulatory collapse and death if not treated quickly
54
Q

How is malignant hyperthermia treated?

A
  • Correction of hyperthermia, acidosis and organ dysfunction
  • Discontinuation of triggering agents
  • Administration of dantrolene (muscle relaxant - prevents calcium release)

TOB (12 decks)

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