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severe face and arm muscle spasms with dysphasia secondary to Clostridium…
severe face and arm muscle spasms with dysphasia secondary to
Clostridium tetani
Infection
Background Information
Physiology
The process of Excitation-Contraction Coupling
Action potential travels along neuron by the temporary changing of charges
Nerve impulse cause the release of acetylcholine (ACh)
ACh travels across neuromuscular junction, binding to muscle cell membrane
ACh binding initiates an electrical impuse which travels across membrane and into T tubules
Impulse stimulates release of Ca+ from SR
Ca+ binds with t-t complex of the actin filaments, shifting it's position exposing myosin binding sites
Myosin binds to actin; Ca+ presence also cause enzymatic actions of myosin to breakdown ATP in ADP + P + energy
Energy of ATP degradation causes shape change of myosin head, pulling actin molecule toward center of sacromere
After sliding, a new ATP binds to myosin, breaking the myosin-actin bond, releasing the myosin head
If Ca+ is still present, the process repeats itself until sarcomere has shortened completely
If a nerve impulse ceases, the Ca+ is reabsorbed by the SR and the muscle relaxes
The process of summation
Wave Summation and Tetanus
(a) Twitch: a single stimulus is delivered; the muscle contracts and relaxes
(b) Wave Summation: stimuli are delivered more frequently, so that the muscle does not have adequate time to relax
(c) Unfused (incomplete) tetanus: more complete twitch fusion occurs as stimuli are delivered more rapidly
(d) Fused (complete) tetanus: a smooth continuous contraction without any evidence of relaxation
Wave summation occurs when a given set of cells is repeatedly stiulated without complete relaxation. Tetany is the sustained contraction resulting from high frequency stimulation
Clostridium tetani
Causes Tetanus Toxin
Tetanus toxin binds to motor neuron and is taken up by endocytosis
The A subunit exits endosome
The A subunit is transported to CNS and into inhibitory neuron
The A subunit cleaves synaptobrevin
Vesicle fusion and release of gycine or GABA blocked
Vesicle fusion and acetylcholine release cannot be stopped
Cell is stimulated
Muscle contracts continousely
Anatomy
The difference between excitatory & inhibitory postsynaptic potentials
Excitatory Neurons
Neurons that release neurotransmitters to make the post-synaptic neuron generate an action potential
Excitatory neurons in the cerebral cortex are pyramidal neurons
Project either locally or long-range projections between different cortical areas
Glutamic acids is the main excitatory neurotransmitter
Epinephrine, norepinephrine, and nitric oxide are some other neurotransmitters
Make the post-synaptic neurons depolorize
Information flow can be either unidirectional or bidirectional
Responsible for the transmission of nerve signals, stimulating the brain
Transmit a flow of information
Neurotransmitters of the excitatory neurons cause the opening of sodium channels
Inhibitory Neurons
Neurons that release neurotransmitters to make the post-synaptic neuron less-likely to generate an action potential
There are three types in the cerebral cortex; stellate neurons, chandelier neurons, and basket neurons
Project within localized regions that are small
GABA is the main inhibitory neurotransmitter
Glycine, serotonin, and dopamine are some other neurotransmitters
Make the post-synaptic neurons less-likely to depolarize
Responsible for the control of bidirectional excitation
Counterbalance the action of excitatory neurons
Regulate the activation of excitatory neurons
Neurotransmitters of the inhibitory neurons cause the opening of chloride channels
The NORMAL structures & functions of the organ systems malfunctioning in this patient neurons
Action Potential
Action potential reaches axon terminal and depolarizes membrane
Voltage-gated Ca+ channel is open and Ca+ flows in
Ca+ influx triggers synaptic vesicles to release neurotransmitter
Neurotransmitter binds to receptors on target cell, causing ions to flow in
Action Potential neuron flow
Cell Body: the cell's life support center
Dendrites: receive messages from other cells
Axon: passes message away from the cell body to other neurons, muscles, or glands
Neural impulse: electrical signal traveling down the axon
Myelin sheath: covers the axon of some neurons and helps speed neural impulses
Terminal branches of axon: from junctions with other cells
Functional Classes of Neurons
Association neuron: multipolar and connects other neurons together such as connection a sensory with a motor neuron
Motor Neuron: multipolar neuron that innervates an effector such as a muscle, gland. heart, ect.
Sensory neuron: unipolar single axon connects to dendrites at the peripheral end which receives stimuli from a receptor, and then the axon enters the CNS to connect to motor or interneurons
Upstream Cause
Direct Cause
Direct cause – what is happening at the neuromuscular junction
See Background Information: Physiology: Clostridium tetani
Indirect Cause
Pt. obtained new tattoo at a "sketchy" tattoo location and did not have a tetanus vaccine
The spores can get into the body through broken skin, usually through injuries from contaminated objects. Tetanus bacteria are more likely to infect certain breaks in the skin
Causes
Wounds contaminated with dirt, poop (feces), or spit (saliva)
Wounds caused by an object puncturing the skin (puncture wounds), like a nail or needle
Burns
Crush injuries
Injuries with dead tissue
Downstream Cause
Downstream effects: If the toxin remains in the patient’s bloodstream, what other effects might the toxin have?
Nervous System
effects the anterior horns cells, the brain stem, and autonomic neurons and are long lasting because recovery requires the growth of new axonal nerve terminals
Muscular system
Respiratory
Laryngospasm and/or spasms of muscles of respiration
Skeletal System
Fractures of spine and/or long bones from sustained contractions
Cardiovascular System
Hypertension and/or abnormal heart rhythm due to hyperactivity of autonomic nervous system
Immune system
Nosocomial infections
sepsis from indwelling catheters
decubitus ulcers
hospital-acquired pneumonia
Disability
Treatment involves powerful sedatives to control muscle spasms
prolonged immobility due to use of sedatives could lead to permanent disability
If recovery does occur, there are usually no long-term side effects. Recovered individuals do not necessarily develop "natural immunity" against the infection because the very small amount of tetanus toxin produced during the infection does not elicit a strong protective immune response which would produce enough antibodies against future re-injeciton