Please enable JavaScript.
Coggle requires JavaScript to display documents.
23 year old male infected with Clostridium Tetani (direct upstream cause…
23 year old male infected with
Clostridium Tetani
downstream effects
severe muscle spasms
cause tetanus (lockjaw)
difficulty chewing
neck
abdominal
break bones
no cure
could be fatal
difficulty breathing
respiratory failure
death
indirect upstream cause
getting tattoo with dirty needle
not having tetanus vaccine
Anatomy
systems involved
integumentary system
epidermis
dermis
Muscular system
skeletal
voluntary
smooth
involuntary
cardiac
involuntary
nervous system
spinal cord
motor neurons
nerve signals
neurotransmitters
skeletal system
protection for vital organs
support for skeletal muscles
motor neurons
axons
axon terminal
motor end plate
neuromuscular junction
synaptic cleft
synaptic vesicles
acetylcholine
clostridium tetani
soil bacterim
bacterial infection
toxin
tetanospasmin
severe muscle spasms
affects motor neuron
cause tetanus
Phisiology
whole muscle contraction
muscle tension
isotonic
muscle shortens
isometric
no shortening
control of movement
increase frequency
causes temporal timulation
unfused tetanus
temporal summation
individual twitch
fused tetanus
greater srength of cntraction
increase strength
more motor neurons are active
muscle fiber contraction
action potentials
acetylcholine
ion channels
chemically gated
voltage gated
muscle twitch
latent period
no muscle contraction
period of contraction
active crossbridge decline
period of relaxation
cross bridge
neurotransmitter
muscle contraction
membrane potential less negative
action potential moves along sarcolemma
excitation contraction coupling
action potential conducted by T tubules
T tubules contract SR
voltage sensitive tubules proteins change shape
1 more item...
along fraid
increased sodium
caused by ACh
exocytosis process
vescicle migrates to plasma membrane
proteins at surface bind with t-SNAREs
vesicle fuse with plasma membrane
vesicle contents are released
exits to cells exterior
a pore opens up
neuromuscular junction
action potential arrives at axon terminal
voltage gated calcium channels open
calcium enters axon terminal
calcium causes ACh to release
exocytosis
ACh crosses synaptic clef
ACh attaches to receptors
ACh stimulates ion channels
allows salt to flow in
potassium to flow out
ACh is broken down by acetylcholinesterase
direct upstream cause
spasms
stiffness
difficulty swallowing
fever
sweating
elevated blood pressure
rapid heart rate