MUSCULOSKELETAL - muscle cells / contraction
*Muscle cells
https://doctorlib.info/physiology/medical/48.html
*Fast twitch / slow twitch muscle cells
- type 1 = ONE SLOW RED OX
--> slow twitch arobic / mito with NO glycogen - type 1 = TWO RED OXes are FASTER
--> type 2a and 2b
*Sarcoplasmic reticulum Release of Calcium Pathway
- Ryanodine Receptors
- DHR = Di Hydro Pyridine Receptors
--> these are either mechanical or Ca+ induced - Skeletal muscle = coupled DHR/Ryanodine Receptors
--> the conformational change of
--> DHR MECHANICALLY attached to the RYR releases the Ca++ from the SPR - Cardiac muscle = SEPARATE DHR/Ryanodine Receptors
--> the release of Ca++ from teh SPR comes from
--> calcium induced calcium release from the SPR
*Skeletal vs Cardiac DHR / RYR
- Skeletal muscle = coupled DHR/Ryanodine Receptors
--> the conformational change of
--> DHR MECHANICALLY attached to the RYR releases the Ca++ from the SPR - Cardiac muscle = SEPARATE DHR/Ryanodine Receptors
--> the release of Ca++ from teh SPR comes from
--> calcium induced calcium release from the SPR
*Sarcomere Structures
Allelic Heterogeneity
Case example:
Notes:
- note that whenever talking about ___ heterogeneity, this means there is difference = hetero- within that object that results in the same phenotype
--> the exception is phenotypic heterogeneity ofcourse where it means different phenotypes from the different mutations on the same gene - in allelic heterogeneity we are talking about possibly different mutations within the same allele, but they all manifest as the same phenotype
- in genetic heterogeneity we are talking about possibly different gene mutations within different genes, but they all manifest as the same phenotype
- in phenotypic heterogeneity we are talking about different phenotypes arising from the same gene undergoing different mutations
- note in the above that polygenic disease means that a disease is cause by defects in multiple other genes
--> best example is T2 DM which is clearly hereditary, but so many different genes are involved that we don't know of
Skeletal muscles move MYAA TITZ
- My = M line in the middle = Myosin
--> A band surrounds it - TITZ = titin holds M line = myosin to the Z line
--> TITZ has an I in it
--> I band goes with the Z line
Pathophys:
- recall MY TITZ for sarcomeres
--> M line has MYocytes - connects with Titin to Z line
--> where actin are attached - most common mutation that leads to DCM
--> TTN gene mutation for titin protein
--> myosin are loosley held on Z lines by defective titin
--> leads to dilation of the cardiomyocytes
- tropomyosin = TROMPS on you
--> troponin = bodyguard of the myosin - Ca++ binds to the bodyguard = tropomyosin
--> actin can then bind the myosin heads
*Frank Starling Mechanism
- the more muscles are stretch = end-diastolic sarcomere length
--> the more powerful they contract
Frank Starling and Sarcomere length in giving saline for shock case
Clinical Case
Notes:
- note that
*Negative feedback systems of muscles
- muscle TESNILE strength feedback = Golgi Tendon
- muscle length and stretch = msucle spindles
*Golgi Tendon organs
- muscle TESNILE strength feedback = Golgi Tendon
- used for TENDONS under pressure = weight lifting
*muscle spindles - negative feedback system
- muscle length and stretch = muscle spindles
*Calcium regulation in Muscle cells from
- entering in the sarcolemma through the L type Dihydropyridine Rs
- to entering the Rannodine receptors on the sarcoplasma reticulum
- SERCA2 pumps bring the Ca++ back into the Sarco Retics
*Transverse T tubules
- these are actually very important to get the Ca++ to the sarcoplasmic retic sites in a coordinated way
--> this way all the muscle cells can contract together - if you don't have proper t tubules you can get limb girdle dystrophies since muscles can't contract together
