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51 Cards in this Set
- Front
- Back
Epimysium is made of what kind of CT?
What vasculature lies in epimysium? |
Dense CT
Bld vessels, nerves |
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What vasculature lies in perimysium?
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Bld vessels, nerves
Muscle spindles |
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What vasculature lies in endomysium?
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Capillaries
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Purpose of satellite cells
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Stem cells
Remain in basal lamina Can divide & fuse with myofibers to create large myofibers |
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Characteristics of Myofibers
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1. Multinucleated, along perimenter
2. Striated 3. Basal lamina made by myoblast 4. Angular-looking cells 5. Cannot divide (take on more nucleus by fusing with satellite cells) |
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Difference between Pennate & Strap
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Pennate can undergo greater changes in tension
Strap capable of greater changes in length |
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Is there more stress at the ends(musculotendinous jxn) of myofibers or midsection?
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-The ends have larger SA
-When F develops-->transmitted to tendon and because of large SA less stress at jxn. More stress at the midsection. |
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Golgi Tendon organ
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-Force
-lie at the jxn btw myofibers & tendons/aponeurosis -axon embedded in collagen -Upon contraction-->distorts axon endings-->AP |
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Muscle spindles
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-Lie within the perimysium
-Stretch reflex -Upon stretching-->spindles activated-->depolarization |
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Trophism
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Neurons secrete tropic factors which bind to receptors on myofibers causing altered cellular activity.
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Embryonic development of skeletal m?
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Mesoderm
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Embroyonic devopment of myofibers
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Mesenchymal cells-->myoblast-->myotube-->myofiber
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Why would a myofiber need additional nuclei?
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Large myofibers need to maintain protein synthesis for fiber growth
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Sarcoplasmic reticulum
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Another name for the ER
Storage area for calcium, released with an action potential in T-tubule |
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Sarcolemma
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-PM of muscles
-has voltage-gated Na/K channels |
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Invaginations of the sarcolemma is called?
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T-tubules that allows AP conduction interior
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Thin filaments are linked where?
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Z-line
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thick filaments are anchored to?
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M-line
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What does contraction do?
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Thin filaments slide towards M-line
Pulls Z-disc towards center |
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Tropomyosin
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Regulatory proteins that blocks binding of thick filaments
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What happens with Ca++ present with tropomyosin
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Ca binds to Troponin-->binds to to tropomyosin-->exposes myosin binding sites
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What are the 3 subunits of Troponin?
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1. Tn-T: where tropomyosin binds
2. Tn-C: where Ca binds 3. Tn-I: inhibition |
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Myosin head has what important feature?
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It has ATPase
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A band
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Where thick & thin filaments overlap
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I-band
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Thin filaments only
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Titin
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extends from z-line to m-line
limits stretch |
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Desmin
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-Not in smooth
-links Z-line of one myofibril to adjacent myofibril -genetic errors result in weak muscle bc no coordination |
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Dystrophin
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achors actinof cell on inside to glycoproteins of the CM
genetic error, change in length no transmitted to glycoproteins externally |
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Duchenne muscular dystrophy
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No dystrophin
No structural stability linking contractile proteins to CM death of muscle fibers, look large bc filled with fat |
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Hypertrophy
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Inc. in cell size, NOT #
Stretch signal-->Inc. protein synthesis-->inc. cell size-->recruitment of satellite cells |
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Stimulant of satellite cells
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IGF-1-->hypertrophy
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Inhibitor of satellite cell proliferation
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Myostatin
No inhibition of satellite cell proliferation |
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Hyperplasia
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Increase cell #, NOT size
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Atrophy
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Dec. in myofiber # or size
Caused by loss of innervation |
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What happens to motor neurons that lose innervation and then motor neurons grow back
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New motor units larger than normal, will not be in normal mosaic pattern
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What happens in aging
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Atrophy-->loss of myofibers-->replaced by fat cells
Satellite pool dec-->limits repair ability-->loss of myofiber Dec. in # of motor units |
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Attachment (rigor)
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-Crossbridge formation
-High affinity for ATP |
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Release
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ATP binds to myosin-->conformational change in head-->dec. myosin affinity for actin-->release crossbridge
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Hydrolysis/Bending
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-ATP hydrolyzed
changes shape of myosin head-->moves towards Z-line Resting state (low Ca++)-->tropomyosin & troponin block myosin on actin |
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Power stroke
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-release of ADP + pi-->inc. affnity for myosine & actin-->pull of myosin towards sarcomere-->shortening
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Postsynaptic terminal for skeletal muscule
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-Junctional folds
-Ach binds to nicotinic cholinergic receptors |
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Role of Ca++
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Depolarization-->Voltage sensing DHSR change conformation-->signals RyR-->opens Ca++ channels in SR
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How does relaxation occur involving Ca++?
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Ca ++ ATPase on SR moves Ca++ back into SR
Ca++ ATPase has a higher affinity for Ca++ than troponin does. |
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If we administer Lidocaine (blocks AP) what would happen?
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everything downstream will be blocked
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If we block or dec. Ach receptors what would happen?
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End plate potential dec.
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If we block or dec. SR Ca++ ATPase what would happen?
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dec. in sarcomere Ca++ reuptake
inc. duration of cross bridge cycling inc. myofiber shortening or force |
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Defect in dystrophia (muscle weakening & atrophy)
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dec. myofiber shortening or force
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Blocking AchE
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Inc. end plate potential, myofiber AP, sarcomere Ca++ release, sarcomere Ca++ reuptake, cross bridge cycling, dec. myofiber shortening for force
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What records electrical activity of the motor unit
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EMG (electromyologram)
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Spontaneous contraction of myofiber (independent of motor neuron)
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Fibrillation
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Spontaneous firing of a motor unit
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Fasciculation
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