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Flashcards in Muscular System Deck (15)
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Actions to stimulate a muscle fiber

1) Somatic motor neuron = release of AcH - binds to nicotinic AcH-R on motor end plate
2) Na+ channels open ...depolarization of sacrolemma


Excitation contraction coupling

1) Ca2+ channels open ( T-tubule) -> Ca2+ moves into myoplasm
2) Ca2+ channels open (sacroplasmic recticulum) -> Ca2+ moves into myoplasm
3) Ca2+ binds to toponin , tropomyosin moves, cross bridge formation, power stroke, New ATP causes release (contraction cycle)


Ache (Acetylcholinesterae)

Breaks down ACH



*Stimulation at motor end plate is short lived due to AcHe
*ca2+ in sarcoplasm is brief/Ca2+ is actively transported back into ECF and SR
*Once contraction has ended, relaxation occurs
* muscle fiber returns to resting length


Motor End Plate

Point of connection between somatic motor neurons and sacrolemma



Succinylcholine (depolarizing agent)
Rocuronium ( non-depolarizing agent)
Vecuronium ( non-depolarizing agent )



Short duration of action > most drug broken down by plasmacholinesterase before reaching neuromuscular Junction

Once bound , not broken down by ACHE. Diffuses away from R site after several Min


Functions of the Skeletal System

-Produce skeletal movement
-Maintain posture/ body position
- support soft tissues/weight of visceral organs
- Guard entrances and exits (sphincters)
- Maintain Body temp
- Store nutrients


Rigor mortis

Within a Few hours of death, no new 02 is circulating, no new ATP can be formed, Ca2+ cannot be pumped out of myoplasm and ATP is unavailable to separate actin + myosin muscles stiffen to become Rigor

Generally lasts for 15-24 which point lysosomes break down tissues and body begins to decompose.



Widespread simultaneous depolarization > all cells simultaneously release K+...may place plasma K+ in lethal range
*Observe low amplitude or sinusoidal wave on ECG
*As indicators of severe HyperK beyond peaked Ts/Flat Ps


Common causes of HyperK+

Dialysis (did not go today)
Burns >1 day
*May impair peripheral nerve connections. Nerves attempt to regrow up regulation # of ACH R on skeletal muscle.
Increased ion exchange includes K+


Depolarizing neuromuscular blocker

Binds to nicotinic ACH-R causes initial wave of WIDESPREAD NEUROMUSCULAR DEPOLARIZATION, then stays bound preventing any further muscle stimulation (flaccid)



Malignant Hyperthermia

Mutation of ryanodine receptor > significant increase in Ca2+ release.
WIDESPREAD SIMULATANEOUS DEPOLARIZATION => disproportionate increase in Ca2+ release > hyper metabolic state
*Increased RR , Increased 02 consumption , Increased ATP, Increased heat production = HYPERTHERMIA
Rigor acidosis Rhabdomyolysis



The muscle cells are damaged, breaking down and releasing K+ resulting in HyperK+.

Brown urine ominous sign
*can lead to renal failure


What is the role of Ca2+ in muscle contraction and how does it arrive?

Calcium binds to troponin, causes tropomyosin to move off of actin binding site for myosin - allows for cross-bridge formation. Calcium is released from the sarcoplasmic reticulum and enters from ECF through T-tubules.