Muscle Flashcards
state what is in each band of skeletal muscle - MHAZI
m line is in the h-band within the h- band is myosin within the a band is actin and myosin in the i band there is the z line the i band is made up of actin only
give the structure of actin
the actin molecule is helixal
it contain tropomysoin coiled around it to reinforce the helix
troponin complexes are bound to the tropomyosin.
describe the structure of myosin
rod like structure from which two heads protrude
many myosin molecules together make a filament and heads protrude at opposite ends of filament
describe the role of calcium in contraction
calcium ions bind to the TnC of troponin causing a confomational changes that moves the tropomyosin away from actin’s binding sites
allows myosin heads to bind to actin and contraction begins
describe the sliding filament model
calcium binds to troponin causing tropomyosin to pull away from binding sites on actin
myosin head attaches to actin - cross bridge
head of myosin changes angle moving actin filament along and ADP released
*ATP molecule binds to myosin head and cross bridge breaks
myosin head bends back as ATP hydrolysis occurs
head of myosin reattaches to actin
and pivots and bends pulling actin towards the m line
describe the events leading to a contraction
- nerve impulse along motor neurone arrives at neuromuscular junction.
- the impulse causes the release fo acetyl choline into the synaptic cleft and there si a localised depolarisation of the sarcolemma
- voltage gated sodium channels open and sodium enters the cell
- this causes a general depolarisation which spreads over the sarcolemma and down the t tubules
- the action potential triggers calcium release from terminal cisternae of sarcoplasmic reticulum.
- calcium binds to troponin TnC
Describe the continuity of muscle with tendon
the muscle fibres interdigitate with the collagen bundles of the tendon
the sarcolemma is always present between myofibrils of the muscle fibres and the collagen bundles
Give some features of cardiac muscle
and ultra structure
striated centrally positioned nuclei intercalated discs branches The endomysium is rich in capillaries - white spaces between pink fibrils
myofibrils are continuous masses in the cytoplasm
mit and er are between the myofibrils
gap junctions are dark black squiggly lines
give the t tubule position in the skeletal and cardiac muscle
Skeletal - t tubules are in line with the A-I band junction
forms triad
Cardiac - t tubules are inline with the z lines
form diads
give the structure and function of the purkinje fibres
specialised myocardial cells of which distal conducting cells carry impulses to ventricular muscle from the AVN (down bundle of His, branches into purkinje fibres) allows the wave of contraction to occur from the apex causing ventricular systole
allows ventricles to contract in synchronous manor. ( areas close to AVN = thin PF and regions far from AVN = thick fibres
large cells with abundant glycogen, sparse myofilaments and extensive gap junctions
describe histology of smooth muscle
fusiform
central nuclei
no striations, sarcomeres or t tubules
describe smooth muscle contractions
slow and sustained
requires less ATP
can be stretched
can be contracted for days/ hours
responds to nerve impulses, hormones, local blood gas concentrations and drugs
give examples of modified smooth msucle cells
myoepithelial cells - in secretory units of exocrine glands
myofibroblasts - at sites of wound healing producing a cartilaginous matrix and contract
which nervous system innovates smooth muscles and from where?
the autonomic nervous system
neurotransmitters from varicosities
which muscle cells can divide?
skeletal muscle cells cannot divide
cardiac muscle cannot regenerate
smooth muscle cells retain their mitotic activity
what can change in muscle to adapt it?
SR swells increase in actin and myosin proteins increase in z band width increase in ATPase increase volume of mit increase density of t tubule system little hyperplasia
give the changes to muscles in endurance and high resistance exercise
high resistance
increase in actin and myosin, fatter muscle fibres and muscle mass and strength
may lead to hypertrophy
endurance
stimulates syntehsis of mit proteins, vascular changes to allow fro greater oxygen utilization - shift to oxidative metabolism
what can cause atrophy
sedentary life style - bed rest
loss of protein = reduced fibre diabeter = loss of power
Age
denervation -
describe events of impulse transmition from motor neurone to muscle
opening of voltage gated calcium channels on presynaptic membrane causes vesicles containing acetyl choline to be released into the synaptic cleft
ach binds to recpeotrs on the motor end plate
ach opens sodium channels
sodium entry depolarises the muscle sarcolemma causing calcium release from the sacroplasmic reticulum hence muscle contraction
describe myasthenia gravis and give symptoms
autoimmune destruction of the end plate ACh receptors
loss of junctional folds at end-plate
widening of synaptic cleft
fatigability and sudden falling
drooping upper eyelids and double vision
fatigue, emotions, symptoms change
give treatments for myasthenia gravis
acetylcholinesterase inhibitors
immune suppressants
thymectomy
plasmapheresis - removal of harmful antibodies from serum
describe Duchennes muscular dystrophy
lack of dystrophin
sarcolemma and actin and myosin filaments are not connected anymore
describe the damage to muscle fibres in Duchenne
muscle fibres tear on contraction
creatine phosphokinase is released into blood
calcium ions enter cells causing necrosis
pseudohypertrophy - swelling before fat and CT replace muscle fibres
describe presentation and treatments of Duchenne muscular dystrophy
early onset gowers signs
contractures
steriod therapy
genetic research into gene threapy and stem cells
