Phys Flashcards
(38 cards)
Describe the action and effect of botulinus toxin
Action: Blocks presynaptic ACh release
Effect: Total blockage can cause paralysis of respiratory muscles, eventual death (flaccid paralysis)
Describe the action and effect of curare
Action: Competitive AChR antagonist
Effect: Decreases the size of the end-plate potential; can relax and paralyze muscles (flaccid paralysis)
Describe the action and effect of neostigmine
Action: AChE inhibitor
Effect: Prolongs and enhances action of ACh at motor end-plate. Used to tx myasthenia gravis or reverse NMJ blockade
Describe the action and effect of hemicholinium
Action: Blocks reuptake of choline into presynaptic terminal
Effect: Depletes ACh stores from presynaptic terminal, leading to weakness
Describe the action and effect of tetrodotoxin
Action: Blocks neuronal Na+ channels
Effect: No Na+ channels = no AP = no ACh release = flaccid paralysis
Describe the pathophys and effect of myasthenia gravis
Pathophys: Autoimmune attack on nicotinic ACh receptors
Effect: Weakening of skeletal muscles; usually first observed in the small facial/eye muscles. Treat with AChE inhibitors such as neostigmine
Describe calcium-induced calcium release
An AP traveling down the sarcolemma causes DHPRs in the T-tubules to open, allowing Ca++ to enter. This Ca++ opens RyRs, allowing Ca++ release from the SR.
When pCa is plotted against muscle force, what does the curve look like and why?
Sigmoidal curve due to cooperative binding
What causes malignant hyperthermia and how is it treated?
Genetic mutations of RyRs result in pathologic opening in response to certain “-ane” anesthetics and depolarizing agents such as succinylchoine.
The pathologic opening allows Ca++ leak, drives muscle contraction, and causes the SERCA pump to work overtime to remove Ca++.
The metabolic ramp up that is required to fuel the SERCA pump with ATP causes malignant hyperthermia.
MH is treated with dantrolene.
What holds the sarcomere together?
Costameres connect the sarcomere of the muscle to the sarcolemma
Describe the pathophys of muscular dystrophy
Lacking or mutated dystrophin results in poor connections in muscle tissue, making it susceptible to damage from eccentric forces. Can see interstitial muscle fibrosis, dislocated nuclei, and patches of necrotic fibers due to this damage.
If/when membrane ruptures, Ca++ floods in from ECF, causing contractures.
What causes the dissociation of the actin-myosin complex?
ATP binding
What allows myosin heads to return to their resting conformation?
ATP hydrolysis
How is the actin-myosin weak cross-bridge state strengthened?
Release of Pi
Which bands change during contraction?
I band
H band
(A does not change)
Stretching a muscle has what effect on passive and active tension?
Increases passive tension
Decreases active tension
Contracting a muscle has what effect on muscle movement and tension?
Limits movement
Reduces tension development
How can muscle force be modulated?
- ) Recruit more motor units
- ) Increase the frequency of stimulation of those unit
- ) Improve synchronization of stimulation
What impact does training have on muscle recruitment and force?
Lowers motor unit thresholds
Provides more myelin (helps increase the frequency of stimulation)
Improves synchronization (highly trained athletes tend to recruit high threshold units FIRST, giving more power or dexterity)
^^ All of these things help increase force
At what points of load and velocity of shortening do muscles have the most power?
High velocity * medium load
Describe Type 1 muscle fibers in terms of twitch speed, size of motor neuron, power, endurance, mitochondria, capillary density, and fuel:
Type I: Slow twitch Small motor neuron Low power High endurance Lots of mitochondria High capillary density Fuel = triglycerides
(aerobic)
Describe Type IIa muscle fibers in terms of twitch speed, size of motor neuron, power, endurance, mitochondria, capillary density, and fuel:
Type IIa: Fast twitch Large motor neuron High power Moderate endurance Lots of mitochondria Intermediate capillary density Fuel = CP/Glycogen
(aerobic)
Describe Type IIb muscle fibers in terms of twitch speed, size of motor neuron, power, endurance, mitochondria, capillary density, and fuel:
Very fast twitch Very large motor neuron Very high power Low endurance Few mitochondria Low capillary density Fuel = GP/Glycogen
(anaerobic)
What are the 4 functions of bone?
Scaffolding/protection
Storage (Ca++ and Pi)
Hematopoiesis/leukopoiesis
Endocrine fxn
