Neuromuscular Junction (NMJ)
patient cant speak.
fresh tattoo on shoulder
face and arm muscles spasms
dirty needle was used
muscular
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nervous
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circulatory
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integumentary
anatomy of NMJ
where nerve meets muscle. usually mid region of muscle fiber
synaptic cleft
motor end plate
synaptic knob, axon terminal, synaptic bulb
skeletal muscle is stimulated by somatic motor neuron
each muscle fiber has one NMJ and one motor neuron
motor neuron
axon,long extensions travel from central nervous system to skeletal muscle
each axon divides into many branches as it enters muscle
axon branches at the end of muscle fiber, forming the NMJ or motor end plate
filled with neurotransmitter acetylcholine(ACh) which triggers muscle contraction.
voltage gated Ca2+ channels embedded in plasma membrane
houses synaptic vesicles; small membrane sacs
Ca2+ comes into the s. knob (flows down concentration gradient) if the channel is opened, signaling a neuron action potential.
Narrow space between the synaptic knob and motor end plate
Acetylcholinesterase lives here, an enzyme that breaks down ACh molecules after their release into synaptic cleft
it is a specialized region of sarcolemma; has numerous folds which increase surface area
has many ACH receptors
muscle end of NMJ
receptors have ligand-gated channels that open with attachment of ACH
Na+ enters into muscle cell and K+ exits. More Na in than K out. changes the voltage of the cell membrane.
causes depolarization, membrane potential of muscle fiber becomes less negatives.
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respiratory
NMJ steps
ACh diffuses across the synaptic cleft and binds to ACh receptors on the sarcolemma
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Ca2+ entry causes ACh to be released by exocytosis
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exocytosis
Action potential arrives at axon terminal of motor neuron
Ca2+ enters the axon terminal, moving down its electrochemical gradient
more Na enter that K leaving and changes the membrane potential of -70Mv closer to 0. called end plate potential.
ACh effects are terminated by its breakdown in the synaptic cleft.
Acetycholinesterase breaks down ACh and it diffuses away from the junction.
ACh binding opens the ligand channels. allow Na into and K out of muscle fiber.
voltage gated Ca2+ channels open.
the vesicle and plasma membrane fuse and open a pore
the vesicle contents are released into the cell exterior
proteins at the vesicle surface bind with plasma membrane proteins.
the membrane bound vesicle migrate to the plasma membrane
Breathing difficulties may result from neck and chest muscle stiffness
respiratory muscle failure
sweating
sensitivity to touch
infected needle
rapid heart beat
including peripheral motor end plates, spinal cord, and brain, and in the sympathetic nervous system
tetanus toxin binds to the presynaptic motor nerve terminal and disrupts the release of ACh
Toxins act at several sites within the central nervous system.
muscle tension
spasms
can cause fractures
difference
summation
tetany
twitch
one isolated contraction, produced by one single action potential
twitches increase in force with each stimuli
If stimuli frequency further increase, muscle tension reaches maximum (fused)
tension is measured by a myogram
doesn't produce significant muscle activity
Differences in strength and duration of twitches are due to variations in metabolic properties and enzymes between muscles
latent period; action potential running down sarcolemma and Ca is released
contraction period; Ca binds to troponin
relaxation period; Ca pumping out of sarcoplasm and back into sarcoplasmic reticulum
additional Ca2+ that is released w 2nd stimulus stimulates more shortening.
more frequent than a twitch
Produces smooth, continuous contractions that add up
muscle fibers do not have time to completely relax between stimuli.
results of two stimuli are received by a muscle in rapid succession
contractions “fuse” into one smooth sustained contraction plateau (fused)
quivering contraction (unfused)
Prolonged muscle contractions lead to muscle fatigue
Further increase in stimulus frequency causes muscle to progress to sustained (unfused)
no relaxation at all between stimuli (fused)
caused clostridium tetani
never vaccinated for this bacteria
clostridium tetani
tetanolysin
tetanospasmin
function not known
on the basis of weight, one of the most potent toxins known
neurotoxin and causes the clinical manifestations of tetanus.
the toxin tetnospasm causes spasms instead of paralysis
Interferes with neurotransmitter release to block inhibitor impulses
Leads to unopposed muscle contraction and spasm
spasms continue for 3-4 weeks
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effects on the body
Pulmonary embolism
Nosocomial infections
Hypertension and/or abnormal heart rhythm
fractures
Laryngospasm
Aspiration pneumonia
Death
effect on NMJ
severe muscular spasms develop when the tetanus toxin blocks the release of inhibitory neurotransmitters at the neuromuscular junction.
These spasms often are protracted and can cause death by means of severe resistant laryngospasm and respiratory muscle failure.
Fractures of the spine or long bones may result from sustained contractions and convulsions.
spasm of vocal cords
Hyperactivity of the autonomic nervous system
common because of prolonged hospitalization
. Secondary infections may include sepsis from indwelling catheters, hospital-acquired pneumonias, and decubitus ulcers
particularly a problem in drug users and elderly patients.
common late complication of tetanus, found in 50%-70% of autopsied cases
no obvious pathology is identified and death is attributed to the direct effects of tetanus toxin.
Cases most likely to be fatal are those occurring in persons 60 years of age and older (18%) and unvaccinated persons (22%). In about 20% of tetanus deaths,
In recent years, tetanus has been fatal in approximately 11% of reported cases.
These spasms often are protracted and can cause death by means of severe resistant laryngospasm and respiratory muscle failure.