Session 8 Flashcards
(55 cards)
0
Q
Which types of muscle are striated/non-striated?
A
- Striated: skeletal; cardiac
- Non-striated: smooth
1
Q
What are the 3 types of muscle?
A
- Skeletal
- Cardiac
- Smooth
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
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
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
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
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
7
Q
What types of skeletal muscle fibres are there?
A
- Red
- Intermediate
- White
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
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)
10
Q
What does nuclei of skeletal muscle look like in transverse and longitudinal sections?
A
- Transverse: Peripheral
- Longitudinal: Rows
11
Q
What do muscle fibres contain?
A
- Myofibrils (made up of actin and myosin microfilaments)
12
Q
What is the thin filament in a skeletal muscle cell?
A
- Actin
13
Q
What is the thick filament in skeletal muscle cells?
A
- Myosin
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
15
Q
What is the thin myofilament made up of?
A
- Actin
- Tropomysosin
- Troponin
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
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
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
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
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
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
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
What is the difference between skeletal and cardiac muscle in terms of Myofibrils?
- Skeletal: Distinct myofibrils
| - Cardiac: Myofibrils are absent, instead the myofilaments actin and myosin form continuous masses in the cytoplasm
25
Where do the T tubules lie in skeletal and cardiac muscle?
- Skeletal: junction of A and I bands
| - Cardiac: Z line
26
Do skeletal and cardiac muscle have triads or dials of T tubule and sarcoplasmic reticulum?
- Skeletal: Triads
| - Cardiac: Diads
27
What is the structure of Purkinje fibres?
- Large cells with:
~ Abundant glycogen
~ Sparse myofilaments
~ Extensive gap junction sites
28
What is the function of Purkinje fibres?
- 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
What are the features of smooth muscle?
- 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
Can skeletal muscle repair itself?
- 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
Can cardiac muscle repair itself?
- Incapable of regeneration
| - Fibroblasts invade, divide and lay down scar tissue following damage
32
Can smooth muscle repair itself?
- 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
Describe the remodelling of muscles
- 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
What is the difference between hypertrophy and hyperplasia?
- Hypertrophy: increase in cell size
| - Hyperplasia: increase in cell numbers
35
What is the effect of exercise on skeletal muscle?
- 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
How does high resistance exercise affect skeletal muscles?
- 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
How does endurance exercise affect skeletal muscle?
- Increased endurance without hypertrophy
- Stimulates synthesis of mitochondrial proteins, vascular changes allowing for greater oxygen utilisation, shift to oxidative metabolism of lipids
38
What is disuse atrophy?
- 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
What happens to skeletal muscles as we age?
- Atrophy with age from age 30 onwards
| - Loss of 50% muscle mass by 80 (sarcopenia)
40
What is denervation atrophy?
- 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
How can muscle length be adjusted?
- 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
What stops acetylcholine?
- 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
What is myasthenia gravis?
- 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
What are the symptoms of myasthenia gravis?
- 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
What is the treatment for myasthenia gravis?
- Acetylcholine inhibitors eg pyridostigmine
- Immune suppressants
- Plasmapheresis: removal of harmful antibodies from patients serum
- Thymetomy
- Ice on eyelids decreases Acetylcholinesterase activity
46
How is neuromuscular transmission disrupted in botulism poisoning?
- Toxins block ACh release
| Botox cosmetic treatment
47
How is neuromuscular transmission disrupted in organophosphate poisoning?
- Irreversibly inhibits acetycholinesterase
| - ACh remains in receptors and muscles stay contracted
48
What are muscular dystrophies?
- 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
What causes Duchenne muscular dystrophy?
- 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
What are the signs and symptoms of Duchenne muscular dystrophy?
- 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
What is malignant hyperthermia?
- A rare, autosomal dominant disorder
| - Causes a life threatening reaction to certain drugs used for general anaesthesia
52
How do general anaesthetic drugs work normally?
- 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
How do anaesthetic drugs cause malignant hyperthermia?
- 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
How is malignant hyperthermia treated?
- Correction of hyperthermia, acidosis and organ dysfunction
- Discontinuation of triggering agents
- Administration of dantrolene (muscle relaxant - prevents calcium release)
