Exam 1 Quiz Flashcards
(127 cards)
Name a presynaptic and postsynaptic acting disorder and explain how each works specifically and what each causes generally.
Pre- botulism–blocks Ach from binding the presyanptic membrane for release into synaptic cleft so nerve impulse fails to be transmitted across neuromuscular junction which causes muscle paralysis.
Post- MG– antibodies to ACh change the shape of the post synaptic membrane to be wider and have less receptors so ACh has less chance of finding a receptor to bind before it is hydrolyzed by AChesterase which causes increased muscle weakness.
Name 2 types of MG
ocular–symptoms in extraocular muscles only= diplopia and ptosis (10-15% of cases) and generalized (85%)
Where does MG weakness symptoms start?
BUE and BLE weakness starts proximal and moves distal
What is the action of recovery from botulism?
create NEW terminal nerve filaments and formation of NEW synapses at the NMJ
When using BOTOX as a tx what happens in PT?
as soon as BOTOX starts to take effect in 4-7 days PT is MANDATORY. should utilize active stretching with care to not overstretch and tear weak muscles, + reciprocal inhibition and serial casting/dynasplint if necessary AND strengthen the ANTAGONIST muscle
What kinds of pts can use BOTOX?
SCI, TBI, CVA, MS, Dystonia, hypertonicity–focal spasticity
How long does BOTOX tx last? how long until NMJ takes up? How long until see effects in pt?
3-4 months, 12 hours, 4-7 days
How does one contract botulism?
food bourne, improperly preserved foods/canned foods, wounds
Prevention for botulism?
no honey for <1 y/o, wounds clean, boil food for 10 minutes
Onset and Recovery time frame for botulism
12-36 hours for sxs, gradual full recovery in wks/months
Intervention for MG?
thymectomy(10-15% have tumor, 70% have enlargement)
anticholinesterase drugs
immunosuppressives-prednisone, cyclosporine, mycophenolate, azathioprine
IVIG
plasmaphoresis–lasts 4-6wks
Dx of MG?
Ab in blood for ACh receptors
Decremental EMG–decreased strength in repeated stimulation
Tensilon test–Achesterase inhibitor, so it acts to prevent ACh breakdown which will allow more time for it to bind to receptors= increased strength/endurance
Muscle biopsy- count ACh receptors
Symptoms of botulism
flaccid symmetrical paralysis diplopia, blurred vision, ptosis dry mouth N&V lethargy difficult swallow and speech Respiratory distress Autonomic involvement--symp/parasymp
Symptoms of MG
ocular--diplopia, ptosis=CN3 facial weakness=CN7 oropharyngeal weakness chewing/swallowing/speaking difficulty BUE/BLE weakness starts prox to dist respiratory muscle weakness Fluctuates over days/hours--better in AM, declines with day/exercise
What type of population does MG affect?
specific term needed
Bimodal–30 year old women, 60 year old men
1 in 10-20,000 in US
15-30, 60-75 y/o
females>males 3:2
What is normal in both botulism and MG?
sensory. MG also reflexes and coordination
MG crisis
respiratory or choking
Intervention for Botulism
ABE serum antitoxin, antibiotics, debridement, gastric lavage, IV, mechanical vent
example of dendritic arborization
purkinje cell in cerebellum, tree like, many inputs to 1 output for slots of integration of information
neurons–types and where seen
multipolar- motor neurons–many dendrite 1 axon
bipolar–interneuron, 1 dendrite, 1 axon
unipolar–sensory–many dendrites 1 axon, cell body is removed usually in DRG
Glial cells 4 functions
structure and support
nutrients and oxygen
myelination
destroy pathogens, remove dead cells
Glial cell types and where found
PNS-Schwann cells
CNS-oligodendrocytes, astrocytes, microglia
Schwann cell functions
myelination of 1 neuron–wraps around axon, forms nodes of Ranvier
Oligodendrocyte functions
myelination of MANY neurons
insulate and protect
increase NCV
involved in Alzheimer’s and MS