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23 year old male has severe face and arm muscle spasms and can hardly…

- - - - Calcium entry at the Synaptic Knob:
        
        Electrical signal passes down an axon, along a motor neuron of the somatic nervous system
        
        Nerve signal triggers opening of voltage-gated Ca2+ channels in synaptic knob
        
        Ca2+ moves down concentration gradient through open channels until it binds w/ membrane proteins on external surface of synaptic vesicles
        
        Release of Acetylcholine from Synaptic Knob:
        
        Binding of acetylcholine (ACh) across synaptic cleft bind w/ ACh receptors at the motor end plate, which causes excitation of skeletal muscle. fiber
        
        Nerve signals to continue to propagate down the motor axon, continuing stimulation of the skeletal muscle fiber
        
        After stimulation stops, acetylcholinesterase breaks down ACh in synaptic cleft
        
        Excitation-Contraction Coupling
        
        Development of End-Plate Potential (EPP) at Motor End-Plate
        
        Binding of ACh to ACh receptors triggers opening of channels; Na+ diffuses into muscle fiber as K+ slowly diffuses out
        
        EPP reached when membrane potential changes from -90 to -65 mV from Na+ diffusion
        
        Initiation & Propagation of Action Potential along Sarcolemma & T-Tubules
        
        Voltage-gated Na+ channels open, Na+ diffuses through causing depolarization
        
        Secondly, voltage-gated K+ channels open & K+ moves out to cause repolarization
        
        Release of Ca2+ from Sarcoplasmic Reticulum (SR)
        
        2 more items...
        
        Muscle Contraction Continued
    - - Transmissive segment of a neuron = synaptic knob
        
        Release of neurotransmitters from synaptic vesicles
        
        Substances/Conditions that Decrease Response at NMJ
        
        Muscular Paralysis & Neurotoxins
        
        Botulinum toxin, Cobratoxin & curare act as competitive inhibitors of ACh receptors (prevent binding of ACh)
        
        Myasthenia Gravis
        
        Loss of ACh receptors which causes decreased response at NMJ, expressed through weakness in muscles
        
        Substances/Conditions that Increase Response at NMJ
        
        Acetylcholinesterase Inhibitors
        
        Interfere w/ the breaking down of ACh at NMJ
        
        Organophosphates (insecticides)
        
        Leads to increase response at NMJ which is expressed in overstimulation of muscles, including muscles for breathing
        
        NMJ Transmitters & Receptors
        
        Acetylcholine
        
        Neurons that synthesize & release ACh are cholinergic neurons
        
        Cholinergic Receptors bind ACh to nicotinic receptors at the motor end plate
  - - - Severe muscle spasms from the bacteria, causing continued contractions which can lead to muscle fatigue
    - - Skin directly impacted from the tattoo needle & propelling bacteria further into his skin near blood vessels, allowing bacteria to spread
    - - Action potential events at NMJ are continuing to fire, causing the overwhelming amount of muscle spasms
    - - Bacteria reaches the bloodstream which causes systemic effects of the bacterium: sepsis, tetany/ spasms of the body, septic shock, etc.
      - Spasms can spread to other parts of the body & cause muscle fatigue of the heart, then flatline
    - - Severe spasms can spread to both the internal airway & diaphragm, causing insufficient oxygen supply & death
  - - - Vesicle membrane fuses w/ plasma membrane
        
        Plasma membrane opens to outside of cell
        
        Release of vesicle contents into the interstitial fluid & integration of vesicle membrane components into the plasma membrane
        
        Phospholipid molecules of vesicle & plasma membrane bilayers rearrange; requires cell to expend energy by splitting ATP
  - - - Voltage is increased in increments until a muscle responds, mainly producing a twitch; minimum voltage needed to generate twitch is the threshold
      - Latent Period: occurs after stimulus is applied & before contraction of skeletal fiber begins
      - Contraction Period: repetitive power stroke pulls on thin filaments, shortens sarcomeres; muscle tension increasing
      - Relaxation Period: begins w/ release of crossbridges as Ca2+ returned to storage of Ca2+
      - Twitch depends on predominant type of skeletal muscle fibers; fast-twitch vs slow-twitch
      - Summation: additive effect of several electrical impulses at NMJ
        
        Multiple Motor Unit Summation: increase in muscle tension that occurs with an increase in stimulus intensity (recruitment)
        
        All-or-None Law: if a skeletal muscle fiber contracts in response to stimulation, it will contract completely; stimulus not sufficient, it will not contract
        
        Wave Summation: stimulation that occurs so rapidly that complete relaxation of a skeletal muscle does not occur before next stimulation event
        
        Due to this, a summation of contractile forces from the new wave is added to the previous wave
        
        Temporal Summation: addition of waves depending upon the increasing frequency of the stimulation
        
        Tetany: continuous, sustained contraction
        
        With continuous contraction, muscle will fatigue (decrease in muscle tension from repetitive stimulation)
        
        Incomplete Tetany: tension tracing continues to increase and the distance between waves decreases
  - - - Tetanospamin then moves through the nervous system trans-synaptically into nerve terminals which release inhibitory neurotransmitters
        
        When blocked, ability to inhibit lower motor neurons is disrupted which causes muscle rigidity & spasm
        
        It inhibits nerve functions by targeting VAMP (vesicle-associated membrane protein) which regulates the release of neurotransmitters from nerve endings
- - - - Any muscle fatigue affecting the heart, throat, or diaphragm = death
    - - Interference of breathing
        
        Lack of oxygen
        
        Death
    - - Most commonly the spine
    - - Respiratory failure
        
        Death
    - - Acute renal failure
        
        Death
        
        Loss of kidney function
  - - - Cardiac arrest
        
        Death
      - Pleural Effusion
        
        Lung scarring: Chronic
        
        Increased difficulty for lungs to transfer oxygen to bloodstream
        
        Pneumothorax
        
        Respiratory failure
        
        Cardiac arrest
        
        Death
        
        Pulmonary edema
        
        Acute respiratory distress syndrome
        
        Breathing impaired
        
        Death
        
        Possible spontaneous pneumothorax years later
        
        Empyema (collection of pus within pleural space)
        
        Fibrosis
        
        Chronic, difficulty breathing
        
        Empyema Necessitatis (extension of infection into chest wall & soft tissue)
        
        Sepsis or septic shock
        
        Continued spreading of infection
  - - - Death
    - - Empyema
        
        Fibrosis
        
        Empyema Necessitatis
      - Pleurisy
        
        Increased pain
    - - Death
    - - Destroy blood vessel
        
        Internal bleeding
  - - - Death