Muscle Flashcards
Describe the general functions of skeletal muscle.
- movement
- posture
- stability of joints
- heat generation
Describe the general structure of skeletal muscle.
Mesoderm-derived
H & E = red fibres - intermediate fibres - white fibres
Epimysium —> Perimysium (surrounding fascicles - groups of fibres) —> Endomysium (surrounding individual fibres) —> Myofibrils —> Myofilaments
Myotendinous junctions: interdigitation of skeletal muscle fibres and tendon collagen bundles (sarcolemma in between)
T tubules within A-I band junction
Multiple peripheral nuclei
Calcium-binding protein = troponin
Stimulated by somatic & voluntary nerve supply
Cannot divide, but tissue can regenerate by mitotic activity of satellite cells
Damage = hyperplasia & hypertrophy
Outline the formation of skeletal muscle.
Myogenic stem cells —> Myoblasts —> Primary myotube (chain of central nuclei) —> Actin & myosin displace nuclei to periphery
What is:
- the Z line?
- the M line?
- the I band?
- the H band?
- the A band?
Z line = disc between I bands (bisection of actin & myosin)
M line = myosin filaments perpendicular to muscle fibres
I band = zone of actin filaments in between myosin filaments (not superimposed with myosin filaments)
H band = zone of myosin filaments in between actin filaments (not superimposed with actin filaments)
A band = entire length of myosin filament
What is the definition of a sarcomere?
Basic unit of muscle (contractile unit of a myofibril)
Consisting of myosin and actin filaments
Describe the structure of an actin (thin) filament.
Helix of actin filaments associated with tropomyosin, which has the regulatory protein troponin (C, I & T) on its surface
Calcium binds to troponin, which changes the conformation of the actin & tropomyosin, allowing formation of myosin cross-bridges.
Describe the structure and function of myosin filaments.
2 interlocking chains
Tail region & head region (2 heads)
Myosin head binds to actin filaments during power stroke
Outline the sliding filament model.
Calcium binds to troponin
Change in conformation allows myosin head forms cross bridge with actin
Power stroke: ADP & Pi released, myosin head bends as it pulls the actin filament, sliding it towards the M line
ATP attaches to the myosin head & cross-bridge detaches
ATP hydrolysed, cocking the myosin head
What happens when ATP is unavailable for muscle contraction?
Rigor mortis = permanent contraction until decomposition breaks down the muscle fibre
Describe what happens during contraction at the neuromuscular junction.
Action potential travels down nerve
Acetylcholine released from synaptic vesicles
Acetylcholine binds to receptors on sarcolemma (acetylcholinesterase terminates binding)
Na+ entry into sarcolemma depolarises end plate
Depolarisation travels down T-tubules
Calcium released from terminal cisternae on sarcoplasmic reticulum
Calcium binds to troponin, causing contraction
Active transport removes calcium to the sarcoplasmic reticulum
Tropomyosin blocks binding site so contraction ends
Describe how contractions travel in the heart.
Myogenic cells spontaneously contract
Sino-atrial node sends electrical impulses to atrioventricular node
Atrioventricular node sends electrical impulses down Bundle of His and up the Purkinjie fibres
Describe the general features of cardiac muscle.
Mesoderm-derived
Single centrally positioned nuclei
Intercalated discs
Gap junctions & adherens-type junctions
Branching muscle fibres
T tubules in line with Z bands
Calcium-binding protein = troponin
Stimulated by myogenic cells
Incapable of regeneration
Damage -> fibroblasts lay down scar tissue
Describe the general features of smooth muscle.
Mesoderm & neural crest origin
Non-striated
Gap junctions
Spindle-shaped (fusiform) cells
Single central nuclei
No T-tubules
No sarcomeres
Capable of being stretched
Calcium binding protein = calmodulin
Stimulated by nerve signals (involuntary), hormones, drugs, [blood gases]
Cells retain mitotic activity and can form new smooth muscle cells
….+++
What is the definition between myoepithelia & myofibroblasts?
Myoepithelia = single, stellate cells forming the basketwork around secretory units of some exocrine glands to assist with secretion
Myofibroblasts = single cells at sites of wound healing which secrete collagen, but can also contract (bring wound edges together)
Outline how smooth muscle contracts.
ANS innervates
ANS releases neurotransmitters from varicosities into a wide synaptic cleft
Actin intermediate filaments attach to dense bodies
What is the difference between atrophy and hypertrophy? What is hyperplasia?
Atrophy = destruction > replacement
(muscle wasting)
e.g. bed rest, limb immobilisation, sedentary behaviour
Hypertrophy = destruction < replacement
(increased glycolysis, mitochondria, glycogen, & blood flow —> increased fibre diameter; increased sarcomeres —> increased flexibility)
Hyperplasia = increase in cell number
What is denervation atrophy?
Loss of nerve supply to muscles so muscles do not receive contractile signals.
Muscle replaced with fibrous tissue
S&S = weakness, flaccidity, muscle atrophy
What is the pathology of myasthenia gravis?
Autoimmune destruction of end-plate AchR, loss of junctional folds at end-plate, widening of synaptic cleft
S&S:
- fatigue
- sudden falling: as Ach falls over time —> muscle relaxes & loses tension
- drooping eyelids (ptosis)
- double vision
- immune state affected (reduced general health & emotional state)
- respiratory muscles affected —> DEATH
Treatment: acetylcholinesterase inhibitors
What are the effects of botulism toxin and organophosphate poisoning on the neuromuscular junction?
Botulism toxin = block Ach release, therefore no transmission of action potential, therefore no muscle contraction
Respiratory muscles —> stop breathing —> DEATH
Treatment: anti-toxin
Organophosphate poisoning = inhibits Ach-ase irreversibly, therefore there is constant action potential transmission and constant muscle contraction —> fatigue, excessive secretions, cramps, confusion, paralysis, etc.
Treatment: atropine, gastric lavage, activated charcoal
What is tetany? Why does tetanus NOT cause tetany?
Involuntary contraction of muscles e.g. due to action potential changes, lack of calcium, excess of phosphate etc.
Tetanus cramps are caused by a blocking of the inhibition of nerves suppling muscles
What are muscular dystrophies? Give some examples.
Genetic disorders characterised by progressive muscle wasting and weakness
e.g. Duchenne’s, Becker’s
Describe the pathology of Duchenne’s muscular dystrophy.
Complete absence of dystrophin (which anchors actin & myosin to the sarcolemma)
Proximal muscles affected
Sarcolemma does not move with fibres —> shearing forces tear muscle fibres during contraction —> creatine kinase released —> calcium enters muscle cells and causes necrosis —> muscle fibres replaced by fat and connective tissue (pseudohypertrophy)
S&S:
- contractures (permanent shortening of muscles)
- difficulty rising to feet (see Gower’s sign)
- proximal limb weakness
- disabled by 10yrs, dead in teens/20s
Treatment: steroids (prednisolone) to build up muscle
Give some examples of myopathies.
Polymyositis (chronic inflammation of muscle by virus/auto-immune) —-> myalgia (pain)
Hypokalaemia —> hyperpolarisation —> arrhythmias (cardiac muscle)
Thryotoxicosis (hyperthyroidism) —> increased BMR —> muscle wasting
Hypoparathyroidism —> lack of PTH —> low [Ca2+] —> tetany
Malignant hyperthermia (increased [Ca2+] —> muscle contraction —> lots of heat released)
What are some of the specialisations of the Purkinjie fibres ?
- abundant glycogen
- sparse myofilaments
- extensive gap junctions
Outline the mechanism of malignant hyperthermia.
Rare autosomal dominant disorder
Uncontrolled skeletal muscle oxidation in response to anaesthetic agents or muscle relaxant succinylcholine —> acidosis, heat production, organ failure —> circulatory collapse
Treat with dantrolene to prevent calcium release
