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Flashcards in Session 8 Deck (55):

What are the 3 types of muscle?

- Skeletal
- Cardiac
- Smooth


Which types of muscle are striated/non-striated?

- Striated: skeletal; cardiac
- Non-striated: smooth


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

- 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


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

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


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

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


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

- Skeletal: Rapid; forceful
- Cardiac: Lifelong variable rhythm
- Smooth: Slow, sustained and rhythmic


How does skeletal muscle develop?

- 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


What types of skeletal muscle fibres are there?

- Red
- Intermediate
- White


What are some differences between red and white muscle fibres?

- 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


What are the different layers of connective tissue surrounding muscle?

- Endomysium (surrounds a cell/fibre)
- Perimysium (surrounds a fasicle)
- Epimysium (surrounds whole muscle)


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

- Transverse: Peripheral
- Longitudinal: Rows


What do muscle fibres contain?

- Myofibrils (made up of actin and myosin microfilaments)


What is the thin filament in a skeletal muscle cell?

- Actin


What is the thick filament in skeletal muscle cells?

- Myosin


Describe the structure of a sarcoma re

- 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


What is the thin myofilament made up of?

- Actin
- Tropomysosin
- Troponin


Describe the binding of the Troponin molecule in actin

- Has 3 binding sites
- TnI to actin
- TnC to calcium
- TnT with tropomysosin


Describe the structure of thick filaments

- Each filament contains many myosin molecules
- Mysoin is a rod-like structure from which 2 heads protrude


Describe the structure of thin filaments

- Actin filament forms a helix
- Tropomysosin molecules coil around to reinforce
- Troponin complex is attached to each Tropomysosin molecule


What is the role of ionic calcium in contraction?

- 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


What are the stages of contraction?

- 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


What happens at a neuromuscular junction?

- 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


What are the stages leading to contraction of skeletal muscle?

- 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


What are the distinguishing features of cardiac muscle?

- 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)


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


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

- Skeletal: junction of A and I bands
- Cardiac: Z line


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

- Skeletal: Triads
- Cardiac: Diads


What is the structure of Purkinje fibres?

- Large cells with:
~ Abundant glycogen
~ Sparse myofilaments
~ Extensive gap junction sites


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


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


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)


Can cardiac muscle repair itself?

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


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


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


What is the difference between hypertrophy and hyperplasia?

- Hypertrophy: increase in cell size
- Hyperplasia: increase in cell numbers


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


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


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


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


What happens to skeletal muscles as we age?

- Atrophy with age from age 30 onwards
- Loss of 50% muscle mass by 80 (sarcopenia)


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)


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


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


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


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


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


How is neuromuscular transmission disrupted in botulism poisoning?

- Toxins block ACh release
(Botox cosmetic treatment)


How is neuromuscular transmission disrupted in organophosphate poisoning?

- Irreversibly inhibits acetycholinesterase
- ACh remains in receptors and muscles stay contracted


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


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


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


What is malignant hyperthermia?

- A rare, autosomal dominant disorder
- Causes a life threatening reaction to certain drugs used for general anaesthesia


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


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


How is malignant hyperthermia treated?

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