muscles Flashcards
what muscle is striated
skeletal and cardiac
smooth is non-striated
what I the difference between striated and non striated muscle
myoglobin is present in striated
what is myoglobin and what does it do
- red protein that is similar to a single unit of haemoglobin.
- oxygen storing molecule providing oxygen to working striated muscles.
what causes tea coloured urine
when striated muscle die or is damaged (rhabdomyolysis) myoglobin is released into the blood stream, (myoglobinaemia).
this can cause renal damage as kidneys remove myoglobin from blood into the urine (myoglobinuria)
what is the sarcolemma
outer membrane of muscle cell
what is a sarcoplasm
cytoplasm of a muscle cell
what is the sarcosome
mitochondrion of muscle cell
what is a sarcomere
contraction unit in striated muscle
what is a sarcoplasmic reticulum
smooth endoplasmic reticulum of a muscle cell
how are skeletal muscle fibres arranged
each fibre is surrounded by a loose connective tissue called the endomysium. the fibres are then arranged in bundles called fascicles that are enclosed in a slightly thicker loose connective tissue called perimysium. bundles of fascicles are then enclosed by an even thicker , denser connective tissue called epimysium. this collectively becomes muscle.
what is a striated muscle cell called
muscle fibre
learn slide 15-22 muscles 1
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how do the different types of skeletal muscle fibres stain
fast-pale
slow- dark
intermediate- brown
compare slow twitch and fast twitch fibres
slow twitch fibres- rich capillary supply, aerobic, high myoglobin levels , many mitochondria and cytochromes, red, fatigue resistant
fast twitch- poor capillary supply, anaerobic, low myoglobin , few mitochondria and cytochromes, white, rapidly fatigue.
how can you histologically tell the difference between cardiac and skeletal muscle
in cardiac muscle :
muscle fibres are not as wide as those of skeletal muscle
nuclei positioned centrally and cigar-shaped
usually one 1 or 2 nuclei per cell.
muscle fibres branch and joint together
intercalated discs form the junctions between the individual cells
what is hypertrophy
enlargement of individual cells
what is hyperplasia
multiplication of cells
structure os smooth muscle cells
spindle-shaped (fusiform) with a single central large nucleus
not striated , no sarcomeres, no T tubules
can the 3 types of muscle repair
skeletal muscle cells -cannot divide. regenerate by mitotic activity of satellite cells so that hyperplasia follows muscle injury. dstellitye cells can also fuse with existing muscles to increase mass (hypertrophy).
cardiac muscle cells- incapable of regeneration.
smooth muscle- retain their mitotic activity and can form new smooth muscle cells. good at repairing themselves.
how is skeletal muscle innervated
neuromuscular junction - interaction between motor nerve ending and sarcolemma
contains synaptic knob( boutons)- dilated tip of a nerve fibre that contains synaptic vesicles of ACh.
nerve impulse can release ACh which binds to receptors on sarcolemma and initiates an action potential propagated along the muscle.
events leading to contraction of skeletal muscle
- nerve impulse arrives at neuromuscular junction.
- ACh released into synaptic cleft causing local depolarisation of sarcolemma.
- voltage gated Na+ channels open and `Na+ ions enter the cell.
- general depolarisation spreads over sarcolemma and into T tubules.
- voltage sensor proteins of T tubule change their confirmation.
- this activates opening of gated Ca2+ channels so Ca2+ is rapidly released into sarcoplasm and binds to TnC of troponin initiating the contraction cycle.
- Ca2+ are returned to the terminal cistern of sarcoplasmic reticulum.
what is myasthenia gravis and what are the symptoms
- Chronic autoimmune disease causing weakness in muscles
- normla communication between nerve and muscle is interrupted at neuromuscular junction.
- antibodies block , alter or destroy the ACh receptors at the neuromuscular junction preventing muscle from contracting.
symptoms: eye drooping , blurred vision due to weakness of muscles that control eye movements, difficulty swallowing, shortness of breath ,weak arms legs etc
sliding filament theory
- Myosin head forms a cross bridge with actin filaments.
- attached heads pull on the actin filament through a form of relaxation towards the M line (passive movement).
- ATP attaches to myosin head breaking bond with actin filament.
- ATP hydrolyses and makes the myosin head go back to original position (active moevement).
* movement of myosin filaments along actin cause I band to shrink.
what is the troponin complex made up of?
TnC
TnT
TnI
role of calcium in contraction of muscle
- As Ca2+ binds to TnC of troponin a conformational change moves tropomyosin away from actin binding sites.
- allows myosin heads to bind actin and contraction begins.
- the tropomyosin sits in the cleft of the G actin ‘spheres’.
what happens to the length of actin and myosin during contraction
remain the same they just slide past each other.
its the sarcomere itself that shorten as the z lines come closer to each other.
muscle hypertrophy- what’s the mechanism
overstretching such that A and I bands can no longer re-engage
- new muscle fibrils are produced
- new sarcomeres are added in the middle of the existing sarcomeres
muscle atrophy -whats the mechanism
muscle disuse
surgery - e.g denervation of muscle
disease
what is duchene muscular dystrophy
mutation of dystrophin gene which joins the sarcolemma to actin myofibril.
absence of dystrophin allows: excess Ca2+ to enter the ,muscle cell and it is taken up by mitochondria. water is taken with it so mitochondria bursts , the muscle cells burst(rhabdomyolysis).
muscle cells are replaced by adipose tissue
how does duchene muscular dystrophy present
shoulders and arms are held back when walking
belly stocks out
sway back
weak butt muscles
weak muscles in front of leg causes foot drop
tight heel cord so child may walk on toes
what is botulism toxin and botox
- toxin produced by clostridium botulinum (bacteria)
- blocks neurotransmitter release at the motor and end plate causing a non-contractile state of skeletal muscle (flaccid paralysis).
used for : treat muscle spasms, cosmetically on wrinkles, severe underarm sweat.
side effects: pain, swelling , bruising
organophosphate poisoning
organophosphate is used as a pesticide
- inhibits normal function of ACh esterase so stops it from breaking down ACh so you get more action potentials.
muscarinic symptoms- salivation , lacrimation , urination , defecation , GI cramping , emesis
nicotinic symptoms- muscle cramps, tachycardia, weakness, twitching , fasciculations
what is malignant hyperthermia
severe reaction to anaesthetics
e.g succinylcholine
defective RyR1 gene
muscle rigidity causes increased calcium release which causes muscle contraction which generates heat and metabolic acidosis.
-increased muscle breakdown and hyperkalaemia
