2. Musculoskeletal system Flashcards
(23 cards)
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