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A 23yr old male patient is demonstrating severe face and muscle spasms,…

- - - - opens muscle gates allowing Na to enter the muscle
        
        once gates are opened, "zap" continues down the cell membrane
  - - - progresses to lockjaw and spasms of trunk and limb muscles
- - - - 2.Voltage-gated Ca2+ channels open. Ca2+ enters the axon terminal moving down its electrochemical gradient
        
        3.Ca2+ entry causes ACh (a neurotransmitter) to be released by exocytosis
        
        4.ACh diffuses across the synaptic cleft and binds to ACh receptors on the sarcolemma
        
        5.AC binding opens chemically gated ion channels that allow simultaneous passage of Na+ into the muscle fiber and K+ out of the muscle fiber.
        
        More Na+ ions enter than K+ ions exit which produces a local change in the membrane potential called end plate potential
        
        7. ACh effects are terminated by its break down in the synaptic cleft byacetylcholinesterase and diffusion away from the junction
  - - - 2. Calcium attaches to the axon terminal (synaptic bulb)
        
        3. Contact with calcium releases Acetylcholine
  - - - 2. Period of Contraction: cross bridges are active from the onset to the peak of tension development (peak on graph)
        
        3. Period of Relaxation: Ca2+ is pumped back into the sarcoplasmic reticulum
  - - - tetanolysin: which causes local tissue destruction
      - tetanospasmin: which causes clinical tetanus
- - - - nerve cannot stimulate the muscle to contract
        
        toxin spreads through out body
        
        paralysis
        
        respiration failure
        
        death
  - - - a doctor may need to remove infected tissue surgically
    - - antitoxin attaches itself to toxin that's still circulating in your bloodstream and keeps it from harming your nerves
    - - hese medications are not advised for other types of botulism because they can speed up the release of toxins.