Muscular System Flashcards
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
Relaxation
- 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
Paralytics
Succinylcholine (depolarizing agent)
Rocuronium ( non-depolarizing agent)
Vecuronium ( non-depolarizing agent )
Succinylcholine
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 hrs….at which point lysosomes break down tissues and body begins to decompose.
HyperK+
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+
Rhabdomyolysis 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)
*Fasiculations
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
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.
