ToB - muscles Flashcards
describe the structure of skeletal muscle
multiple peripheral nuclei
connections via fascicle bundles and tendons
controlled via somatic (voluntary) and motor neurones
rapid and forceful
mesoderm derived
vary in colour
which bands remain the same length and which bands narrow during contraction?
A band remains same
I and H band narrow during contraction
describe how skeletal muscle develop (fusion)
myoblasts (muscle cells) from myogenic stem cells (through cell division)
fuse to form primary myotube (cytoplasms join, few nuclei present from few muscle cells fusing)
nuclei displaced (to peripheral) by newly synthesised actin and myosin
(in cardiac and smooth muscle there is no fusion)
Describe red muscle fibres structure and contraction
small, rich in blood supply, myoglobin and mitochondria weaker contraction, slower rich in oxidative enzymes (not ATP) less junctions normally limb muscles, back
describe white muscle fibres structure and contraction
large, low vascularisation, myoglobin and mitochondria
fast, strong contractions (rapid contractions)
rich in ATPase, poor in oxidative enzymes
more junctions
fingers, eyes
what are myotendinous junctions?
skeletal muscle fibres connect (interdigitate) with tendon collagen bundles
the sarcolemma always lies between the collagen bundles and the muscle fibre’s myofilaments (actin + myosin)
(tendons made of collagen)
Describe the repair of skeletal muscle
peripheral satellite cells can undergo mitosis and fuse with muscle cells to increase mass
muscle fibres cannot divide
describe the initiation of contraction
- nerve impulse travels down motor neuron
- impulse releases ACh into synaptic cleft causing depolarisation of sarcolemma (through influx of Ca2+)
- Na+ voltage gated channels open, Na+ enters cells (of post synaptic cleft)
- depolarisation spreads from sarcolemma to T tubules
- then down terminal cisternae
- causing release of Ca2+ from terminal cisternae to sarcoplasm
- the Ca2+ then bind to TnC causing interaction between myosin and actin
describe the sliding filament theory
myosin head binds to actin with ATP (form cross bridge)
myosin head bends pulling actin filament towards M line (in hydrolysis of ATP) - working stroke
a new ATP molecule binds to the myosin head causing it to detach from actin, hydrolysis of the ATP causes the myosin head to cock back to original position for process to begin again
describe cardiac muscle?
short branched cylinders
single central nucleus
connected via junctions - end to end
controlled via an intrinsic rhythm
cells are connected via intercalated disk which allow electrical and mechanical coupling
T tubules line with Z line not A-I junction
describe Purkinje fibres
specialised myocytes abundant glycogen sparse myofilaments extensive gap junction sites rapid conduction
describe the structure of smooth muscles
spindle shaped, tapering ends
single central nucleus
connected via gap and desmosome type junctions
involuntary control - local stimuli
slow sustained power, contraction requires less TP (ox/phos)
may remain contracted for hours or days
capable of being stretched
respond to nerve signals, hormones, drugs or blood gas conc
what are the different types of atrophy?
disuse - bed rest, limb immobilisation, less fibres and cross bridges but same number of cells (fibre diameter decreases)
age - 30+ (muscle mass decrease)
denervation - motor neurones damage
what is hypertrophy of muscle? structural changes?
increased fibre diameter and metabolic changes e.g. increased enzymes, mitochondria, glycogen and blood flow
replacement > destruction
what happens in increasing frequency of stretching to muscle?
increase flexibility as increase sarcomeres (e.g. yoga)
what happens in myasthenia gravis?
autoimmune destruction of ACh end plate receptors
end plate is less convolute
widening of synaptic cleft
this leads to fatigbility and sudden falling e.g. drooping eyelids and double vision
treated with AChesterase inhibitors
What is botulism?
toxins block ACh release
can come from soil
what is organophosphate poisoning
inhibit acetylcholinesterase so leads to constant depolarisation of sarcoplasm
death by asphyxiation commonly (abnormal breathing - body deprived of O2)
what is DMD?
lack of dystrophin molecule to anchor muscle fibres to sarcolemma
muscles rip themselves apart during contraction
Ca2+ release into cell causing cell necrosis
produces pseudohypertrophy of muscle via fibrosis of the muscle (become fat & CT replace muscle fibres)
individuals wheelchair bound and respiratory failure common cause of death
what are symptoms of DMD and treatment?
symptoms: gower’s sign (use hands and knees to support oneself upright), shortening and hardening of muscles
treatment: steroid therapy (slow down muscle damage)
what is malignant hyperthermia?
susceptibility altered by an autosomal dominant gene
general anaesthetics e.g. succinylcholine can cause an overwhelming increase in skeletal muscle oxidative phosphorylation
depletes O2, increases CO2 production and increase temperature
treatment for malignant hyperthermia?
treat with dantrolene (prevent skeletal muscle oxidative phosphorylation) & stop general anaesthetia
how does general anesthetics make malignant hyperthermia worse?
inhibit ACh, causes buildup of Ca2+ in cells (influx of Ca2+ to release ACh)
for body to send Ca2+ to stores in SR requires ATP
