Neurohistology and Neuromuscular Junction DD Flashcards
What is a multipolar neuron
Multiple dendrites and one axon
What is a bipolar neuron
Has one dendrite and one axon attached to the cell body
What is a unipolar neuron
Has one process from the cell body an axon
List the 4 main functions of glial cells
- Provides structure for the neurons
- Forms the myelin sheath
- Supplies nutrients and oxygen to neurons
- Destroys pathogens and removes dead neurons
What are the glial cells of the PNS
Schwann cells
What are the glial cells of the CNS
Oligodendrocytes
Astrocytes
Microglia
T or F: Schwann cells myelinate many neurons
False - they only myelinate one
T or F: Oligodendrocytes can myelinate many neurons
True - they myelinate many neurons
Which type of glial cell is involved in pathologies such as Alzheimer’s disease and MS
Oligodendrocytes and Microglia
What is the most common glial cell?
Astrocytes
What are the functions of Astrocytes
- Structural support and insulation
- Blood-brain barrier maintenance
- Divide and wall off damaged areas
- Scavengers to remove NT from the synaptic cleft
What type of glial cells have a major phagocytic role?
Microglia
What are the x roles of microglia?
a) Protective
b) Destructive
a) Mobilize after injury, important for brain development, phagocytosis
b) Alzheimer’s disease and aging, HIV/AIDs
Which disease has the oligodendrocytes attacked by their own antibodies?
Multiple Sclerosis
What is the etiology of botulism
Neurotoxin produced by C. Botulinium From: - food-borne -wound - unclassified
How does Botulism poisoning occur
1) Enters presynaptic terminals
2) Blocks fusion of ACh vesicles w/presyn mem
3) Inhibit ACh release into Neuromuscular junction
4) Nerve Impulse fails to transmit
5) Mm paralysis
How long until s/s develop w/botulism ? What is the incidence rate?
12-36 hours following ingestion
10 adult and 100 infant each year
What are the s/s of botulism?
- Flaccid symmetrical paralysis
- Blurred & double vision, photophobia, ptosis
- Lethargy
- Dry mouth, nausea, and vomiting
- Respiratory mm
BoTox use
- Temporarily treat a focal spasticity by preventing the release of ACh from the presynaptic nerve terminal
- Occurs gradullat over 4-7 days and is taken up w/in 12 hours
What should we do post-injection of PT?
- Increase mm strength of opposing mm groups
- Do NOT over-stretch the weakend mm
What is myasthenia Gravis
Post-synaptic membrane disease at neuromuscular junction that is slow and progressive
What is the mechanism of myasthenia gravis?
- widened synaptic cleft, loss of folds
- dec # and density of ACh receptors
- Results in weakness or paresis
What are the classifications of MG and percentages
- Ocular myasthenia - confined to extra-ocular mm (10-15)
- Generalized weakness (85)
- Myasthenic crisis (resp failure)
s/s of Myasthenia gravis
- ptosis
- diplopia
- facial weakness
- oropharyngeal weakness
- chewing, swallowing and speaking difficulties
- weakness (BUE or LE, respiratory mm, fluctuates)
What are some interventions of myasthenia gravis?
- Anticholinesterase drugs
- immunosuppressive drugs
- IVIG
- Plasmaphoresis
- Thymectomy