Muscle Phys Flashcards
What are the 3 connective layers of mm (from in to out)
- Endomysium- surrounds indv mm fibres
- Perimysium- surrounds groups of mm cells (fasicles)
- Epimysium- Surrounds entiraty of mm
What are myofibrils and what are they made up of
Functional unit of the mm fibre
-Myofibrils are comprised of pro filaments called myofilaments which can be differentiated into thicc and thin filaments
Myosin- characteristics, binding sites
Thick filament (creates pulling motion)
- has binding site for actin
- has binding site for ATP (for energy breakdown)
What are the 3 protein subunits of actin
- Actin- double helix along length of myofilament
- Tropomyosin- Blocks actin binding sites when contraction isn’t supposed to happen
- Troponin- located along tropomyosin (ensures tropomyosin stays in its blocking pos)
What line borders each sarcomere
Z disc
Where is titan located along the sarcomere, what does it act to do + disease that affects it
z disc to m line (acts to hold myosin in place for contraction to occur)
Tibial muscle dystrophy
What does dystrophin connect and what is its function
connects actin filaments to the transmembrane pro B- dystroglycan which is located in sarcolemma
What is in the A band
Formed by overlapping bands of actin/myosin
What is the h zone
middle portion of myosin where there is no overlap
What is the m line
small portion in h zone that is composed of m pro molecules that connect adjacent myosin
What is the I band
Segment of the sarcomere that includes the z discs and the ends of the actin filaments
What is the sarcolemma punctured by and the function of it
T tubules
-important for when the action pot needs to propagate along the mm
Sarcoplasmic reticulum- how it is layed out, what does it do
chambers called terminal cisternae on either side of the t tubules and runs longitudinally along myofibril
-It stores ca when mm is not contracting
What is the triad
A single t tubule with 2 surrounding terminal cisternea
What are subneural clefts
numerous smaller folds in the mm membrane (greatly increases the surface area for which synaptic transmission can occur)
Steps at neuromuscular junction
- Ap reaches and voltage gated Ca open
- aCH is released and binds to ligand channels
- NA comes in and triggers depolarization
Where are volatage gated channels located in relation to ligand gated channels
Located very close in relation to ligaand gated- if membrane pot created by the ligand gated channels is great enough to reach threshold required by voltage gated AP will begin
What type of feedback mechanism is voltage gated channels
Positive feedback mechanism (opening of voltage gated sodium channels allows more to keep opening)
Where is dihydropyrindine receptor located and function
Located in walls of t tubules
- ca channels that are activated by depolarization which causes conformational change in ryanodine receptor which causes it to open and release ca into SR
Once Ca is released into the SR what will it bind to
Will bind to troponic C, which pulls tropomyosin out of the way and exposing actin active sites
How are cross bridges formed
form when myosin interact with exposed actin sites
- atp binds to myosin head and atpase breaks it down which puts myosin head in high energy state to bind to actin
How is skeletal mm contraction ended
Ach removed by achesterase
- SR recaptures Ca off tropinin C (pumped back in by atp dependent Ca pump)
- Tropmyosin is brought back to cover actin sites
Why does rigor mortis occur
Atp is depleted
-Without ATP Ca pumps cant work to detach myosin heads from cross bridges (mm will remain stiff)
Myasthenia Gravis- pathophys
Autoimmune disease where body forms antibodies against ach receptors in motor end plate
Myasthenia Gravis- age, clinical picture, tx
age- 20w, 60s m
clinical- Symetrical/asymetric weakness affecting smol mm first
Tx- anticholinesterase drugs (inhibits achesterase)
Lambert eaton myasthenic syndrome- pathophys
autoimmune disorder that target presynaptic voltage gated calcium channels resulting in less ach released at NMJ
Botulism- pathophys and when does occur
Inhibits/blocks release of ach from the nerve terminals
-occurs 6-48hrs after ingestion
Tetanus- pathophys
Tetnus toxin travels retrograde axonal transport where it binds to presynaptic inhibitory neurons (blocks inhib nt release)
-net effect is disinhibition of spinal motor reflexes
Tetanus- clinical pic
Sustained contraction of skeletal mm with periodic painfully mm spasms
-starts w small mm and moves to larger ones
