Musculoskeletal Flashcards
Sarcomere is from ____ to ____
Z disk to Z disk
Can a skeletal muscle undergo hyperplasia or hypertrophy? Can it increase number of nuclei?
It can undergo hypertrophy only
It can increase number of nuclei when it gets bigger
Are A band and I bands dark or light? Which gets shorter with contraction?
A is dArk (myosin and overlapping actin)
I is light (actin only)
I band gets shorter with contraction, A stays the same
Middle of A band is ____
Middle of I band is ____
Middle of A band is M line
Middle of I band is Z disk
What are the steps that a neuromuscular junction gets activated
Action potential comes down axon, when depolarization gets to axon terminus, voltage gated ca channel opens and ca moves into the axon
Axon terminus releases Ach into cleft and binds Ach-ligand gated Na channel on muscle cell, Na moves into the cell and cell depolarizes, as cell potential goes up, voltage-gated Na channel opens and more Na comes in
More depolarization opens voltage-gated ca channel, ca moves into the cell from outside via T-tubules, which opens ca-gated ca channel and ca comes into cell from SR too causing contraction.
List the 4 steps of the sliding filament model. Bind. Flick. Release. Reposition.
- ATP binds to myosin head, causing dissociation from actin
- As ATP is hydrolyzed, a conformation change occurs. ADP and Pi remain associated with the myosin head
- Myosin head attaches to actin filament, causing release of Pi
- Pi release triggers a ‘power stroke’, a conformation change in the myosin head that moves actin and myosin filaments relative to each other. ADP is released
Talk about troponin, tropomyosin, actin, and myosin, how does the binding occur?
Calcium binds to TnC on the troponin, which exposes the myosin binding site on actin. Tropomyosin was blocking the binding site originally.
Myosin releases, repositions, binds, and ficks until _____ (3 reasons)
1 Run out of actin and can’t contract any further
2 Ca is removed from SR (muscle is relaxed)
3 Cell runs out of ATP, myosin can’t release and muscle can’t relax bc myosin attached (rigor mortis)
Note: ATP has to bind in order for myosin to release, when repositioned, ATP is broken down to ADP (ATP not used to bind or flick)
Compare and contrast slow oxidative and fast glycolytic musle fiber types
Slow: low ATPase, slow speed of contraction, resists fatigue, high oxidative capacity, low anaerobic enzyme content, lots of mitochondria and capillaries, high myoglobin content, red, low glycogen, small fiber diameter, ex. tongue (can talk for a long time)
Fast: high ATPase, fast contractions, fatigues quickly, low oxidative, high anaeorbic content, not much mitochondria or capillaries, low myoglobin content, white, high glycogen content, large fiber diameter, ex. Lats (can’t do a lot of pull-ups)
Osteoclasts
Osteoblasts
Osteocytes
Osteoclasts: macrophage syncytium that breaks down bone
Osteoblasts: build bone
Osteocytes: mature osteoblasts
Duchenne muscular dystrophy: would an old person leak CK after vigorous activity?
Severe muscle wasting
No, he doesn’t have muscle left to leak CK
Duchenne muscular dystrophy: what is mutated?
Dystrophin, a protein that anchors the sarcomere. When defected, actin attached to membrane along cell isn’t anchored properly, it rips plasma membrane every time a person exercises, micro-tears in the sarcolemma allows CK to leak out (if there is any). Normally, the tear repairs, but is DMD, it doesn’t repair.
Most common is X-linked, almost always affects males
Myasthenic syndrome: what happens on a cellular level to lead to weakness? Does an Acetylcholinesterase-Inhibitor help?
Progressive autoimmune disease
Antibodies bind to Ca channel, calcium can’t come in, no Ach is released, paralysis, they are weak all day
Note: an Ach inhibitor WOULDN’T help (there’s no Ach)
Myasthenia Gravis: what happens on a cellular level to lead to weakness? Does an Ach-inhibitor help?
Progressive autoimmune disease
Antibodies against Ach receptors, Ca comes in, vesicles fuse, Ach is released but CAN’T bind, cell can’t depolarize, paralysis
They can do things in the morning, but weakness gets worse during the day, with use (starts with droopy eyelids)
Acetylcholinesterase inhibitor DOES help so that Ach has time to read with receptors
MG blocks ___
Curare blocks _____
Clostridium botulinum blocks ____
Clostrididum tetani works by ___
MG blocks Ach receptors
Curare blocks neuromuscular blockade (on post-synaptic membrane)
Botulinum blocks the neurotransmitter from being released (blocks vesicle fusing with membrane)
Tetani releases an excessive amount of neurotransmitters (overstimulation of muscle membrane leads to lock jaw)