2. Musculoskeletal system Flashcards
What are the Skeletal muscle diseases gone over in this lecture?
Rhabdomyolysis
and Duchenne Muscular dystrophy
What are the bone diseases gone over in this lecture?
- Paget’s disease
- Gout
What is the patient case gone over in this lecture?
- osteoporosis
What is a sarcomere?
- most basic functional cell unit of a muscle cell
thick filaments aka?
myosin
thin filaments aka?
actin filaments
which zones in the saromere get shorter during contraction?
and which one stays the same length?
- H zone (from actin filament to actin filament)
- I band ( end of actin- Z line to other end of actin)
- A band ( just the myosin)
3 components of actin filaments?
- actin molecules
- troponin - Ca+ binds to troponin inducing conformational change
- tropomyosin –> covers myosin binding site
2 components of the myosin filaments ?
- myosin molecules
2. myosin heads
2 binding sites on myosin head?
- Actin AtPase
- Myosin ATPase –> induce relaxation after contraction and stops binding of myosin head to actin binding site
what is the point of the globular heads?
- build cross bridges to actin
Role of Ca+ in muscular contractions?
- Ca+ comes from sarcoplasmic reticulum
- T tubules transmit Action Potential signal to lateral sacs
- Ca+ released and induces vesicle exocytosis for Ach at the NMJ synaptic cleft
Ca+ role at the sarcomere?
- Ca+ attaches and binds to troponin, pulls off tropomyosin from actin , myosin head binds to and forms cross bridges to actin -> power stroke etc….
what did we learn about eccentric muscle contractions?
- actin and myosin are far apart
- TITIN pulls them together to allow eccentric contractions –> LOTS OF CROSS BRIDGING –> MORE CONTRACTION –> PASSIVE TENSION
Aging on the musculoskeletal system?
- sarcopenia –> involuntary loss of muscle mass
- Muscle loss: decrease in contractile proteins, and circulating hormones, MU changes
- fiber type distribution: 2 is faster, 1 is slower
- MU firing rates decrease
Rhabdomyolysis ?
And what is the population most affected?
- rapid breakdown of muscles –> relase of intracellular contents ( myoglobin) in to the bloodstream
- Detrained athletes that are asked to do something strenuous or difficult (ie hell week)
Rhabdo pathophysiology?
- Excessive muscular contraction over a long period of time, direct trauma, toxins, drug, hereditary enzyme disorders
clinical manisfestations?
- DARK URINE
- muscle pain, weakness
- also can happen via direct trauma (ie car crash)
DMD? what is this?
- Duchenne muscular dystrophy
- progressive muscle fiber loss due to weakness of mostly voluntary muscles (diaphragm)
DMD pathophys?
- mutations in dystrophin gene
DMD clinical manisfestations ?
- sway back thick lower leg muscles (due to fat deposition), foot drop, poor balance, frequent falls
Most important protein we talked about for DMD?
- Dystrophin gene getting fucked –> helps anchor sarcolemma with cytoskeletal proteins better and helps with force transmission.
Bone overview: what is an osteoid?
- unmineralized, organic portion of bone matrix: bone’s tensile strength, precipitation of Ca phosphate
- Forms prior to maturation of bone tissue
