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Physiology I Block 2 > 1 Neuromuscular Junctions > Flashcards

1 Neuromuscular Junctions Flashcards

1
Q

What does MEPP stand for

A

Miniature End-Plate Potential

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2
Q

the synapse b/w axon of motorneuron and skeletal muscle fiber is called what

A

neuromuscular junctions or motor end plate

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3
Q

what is another name for neuromuscular junction

A

motor end plate

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4
Q

What is a MEPP

A

a muscle cell will spontaneously depolarize even if they were not stimulated.

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5
Q

how much does a MEPP depolarize the postsynaptic membrane

A

about .4 mV

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6
Q

will a relesase of 1 quanta of ACh generate an action potential?

A

no

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7
Q

how many ACh are in one quanta?

A

about 10,000 molecules

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8
Q

When will an EPP be generated by MEPP?

A

when they are released in synchronisitc fashion - need 125 quanta

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9
Q

when 125 quanta are released due to summation of MEPP what happens

A

EPP → deplarization at the muscle cell that triggers opening of voltage gated channels for the muscle AP

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10
Q

What does EPP stand for

A

end-plate potential

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11
Q

EPP is always large enough to do what

A

initiate action potential on the muscle membrane

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12
Q

What is the EPP

A

When the motor axon is stimulated, ACh is released from the axon terminal and interacts with the postsynaptic nicotinic receptors to produce an excitatory postsynaptic potential (EPSP) called the end-plate potential (EPP).

EPPs) are the depolarizations of skeletal muscle fibers caused by neurotransmitters binding to the postsynaptic membrane in the neuromuscular junction. They are called “end plates” because the postsynaptic terminals of muscle fibers have a large, saucer-like appearance. (wikipedia)

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13
Q

what is an example of an agent that would block ligand gated channels

A

curare - it’s a nicotinic antagonist

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14
Q

What is the result of transmitter-gated channels

A

end plate potential

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15
Q

What is the result of voltage-gated channels

A

action potential

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16
Q

what produces the end-plate potential

A

ACh engaging ligand gated nicotinic receptors

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17
Q

how can end plate potential cause APP

A

the opening of the cation channels from ACh will stimulate opening of voltage sensitive Na+ and K+ channels

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18
Q

What is myasthenia gravis

A

autoimmune disease

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19
Q

what causes myasthenia gravis

A

Antibodies directed against AChR receptors  destruction of the receptors. Antigen-specific lymphocytes in the thymus recognize and destroy AChR nicotinic receptors.

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20
Q

1) Fatigue, muscle weakness and diminished coordination 2) Blurred or double vision (diplopia) and drooping of one or both eyelids (ptosis) 3) Difficulty swallowing (dysphagia) and speaking (dysarthria) 4) Bladder dysfunction 5) Sensory disturbances
these are symptoms of what

A

myasthenia gravis

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21
Q

what is the general affect of myasthenia gravis

A

muscle weakness or paralysis - b/c neuromuscular junction cannot trasmit signals from nerve fibers to the muscle fiber

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22
Q

what is the EPP of a pt with myasthenia gravis vs. the resto f the population

A

amplitude of EPP for a pt with myasthenia gravis is much smaller

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23
Q

if myasthenia gravis isn’t properly managed what will pt die from

A

paralysis - particulary of respiratory muscles

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24
Q

how can you run diagnostics to see if a pt has myasthenia gravis

A

1) Edrophonium test: a brief improvement of the symptoms. Edrophonium (Tensilon) is a acetylcholinesterase inhibitor that will reduce the muscle weakness by increasing ACh levels at the NM junction.
2) Antibodies against AChR nicotinic receptors in the blood (in 80-90% of the patients)

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25
What is Edrophonium and how is it related to MG
acetylcholinesterase inhibitor that will reduce the muscle weakness by increasing ACh levels at the NM junction. if pt has improvement can point to them having MG
26
what does MG stand for
MYASTHENIA GRAVIS
27
What is used for treatment for MG
Anticholinesterase (Neostigmine)
28
What does MS stand for
multiple sclerosis
29
What is MS
demyelinating disease - esp. demyelination in the brain and spinal cord
30
List out the risk factors for MS
MS can occur at any age but most commonly affects people between 20 and 40 years of age. Women are about twice as likely as men are to develop MS. If one of your parents or siblings has had MS, you have a 1 to 3% chance of developing the disease — as compared with the risk in the general population, which is just 0.1%. There appears to be an association of MS with Epstein-Barr virus, the virus that causes infectious mononucleosis. People of Caucasian descent, especially those whose families originated in northern Europe, are at highest risk of developing MS. People of Asian, African or Native American descent have the lowest risk. A person is slightly more likely to develop MS if she/he has thyroid disease, type 1 diabetes or inflammatory bowel disease. MS is far more common in Europe, southern Canada, northern United States, New Zealand and southeastern Australia, countries with temperate climates. The risk seems to increase with latitude
31
What is believed to cause MS
autoimmune disorder where pts immune system attacks its myelin
32
Numbness or weakness in one or more limbs, which typically occurs on one side of your body at a time or the bottom half of your body.  Partial or complete loss of vision, usually in one eye at a time, often with pain during eye movement (optic neuritis – decrease visual acuity)  Double vision or blurring of vision (diplopia)  Tingling or pain in parts of your body  Tremor, lack of coordination or unsteady gait (ataxia)  Neurogenic pain can be experienced by MS patients from time to time. It results from an abnormal flow of nerve impulses in the CNS.  Cognitive impairment 9  Depression  Fatigue  Dizziness  Problems with bladder, bowel and sexual function  Symptom remissions and relapses as a result of disappearance and occurrence of inflammation of white matter in the CNS. these are all symptoms of what
MS
33
List the symptoms of MS that are most important to remember for physio
Numbness or weakness in one or more limbs, which typically occurs on one side of your body at a time or the bottom half of your body. Tingling or pain in parts of your body Tremor, lack of coordination or unsteady gait (ataxia) Neurogenic pain can be experienced by MS patients from time to time. It results from an abnormal flow of nerve impulses in the CNS.
34
What is ataxia
unsteady gait, loss of full control of body movements
35
what diagnostic tests can be run to see if pt has MS
Spinal tap (lumbar puncture) - Elevated white blood cells and IgG levels in cerebrospinal fluid (CSF). Also helps rule out some infectious or inflammatory diseases that have symptoms similar to MS. Magnetic Resonance Imaging (MRI) - MRI can reveal lesions, indicative of the myelin loss on your brain and spinal cord. Evoked potential test - This test measures the electrical signals sent by your brain in response to stimuli. The measured nerve fiber conduction in various sensory pathways is abnormal in almost all established cases and in about 2/3 of suspected cases of MS.
36
why is spinal tab done to see if pt has MS
the pt would have elevated WBC and can test for IgG levels in CSF can rule out other diseases based on results that might have similar symptoms to MS
37
why is MRI done to see if pt has MS
can reveal lesions which could mean there has been myelin loss (like on brain and spinal cord)
38
What is the most common treatment for MS
Corticosteroids (Prednisone)
39
how do Corticosteroids (Prednisone) function
used to treat MS | reduce inflammation that spikes during a relapse
40
when are Plasma exchange (plasmapheresis) used to treat pts with MS
can be used to help treat pts with severe MS who aren't responding to intravenous steroids
41
How is K+ Channel Blockers (aminopyridines) used to treat MS
Drugs that prolong action potentials and facilitate conduction through demyelinated axons
42
How is Immunosuppressants (interferon beta) used to treat MS
Appear to slow the rate at which multiple sclerosis symptoms worsen over time but have to monitor liver enzymes. Reduces number and severity of exacerbations
43
besides drugs what else can be done to help treat pts with MS
Physical therapy, muscle relaxants, and other medications to treat symptoms.
44
at the end of neuromuscular junction what kind of receptors
nicotinic (ligand gated) receptors
45
normally channels at neuromuscular junction are
closed
46
small depols by MEPP are less than
1 mV
47
what is average depol for MEPP
.4 mV
48
how is EPP generated
have to sum a lot of MPPs
49
how many ACh released in one vesicle
10,000 Ach molecules
50
how many vesicles released in EPP
125 vesicles
51
why are so many Ach needed to generate AP
it is going to get degraded, it is inactivated, might diffuse away, etc. so need a lot released to actually be able to bind and stimualte AP
52
why is muscle cell more negative than nerve
more K leak channels
53
RMP in muscle
is more negative than that of nerve
54
normal muscle cell will never have peak of EPP b/c
voltage gated sodium and potassium channels take over and produce AP
55
describe how Ach nicotine receptor allows for depol.
Ach binds, opens it - Selective ion channel | Lets sodium come in potassium wants to go out. So there will be more sodium in than potassium out, so get depol.
56
1 EPP is created by a
quanta
57
what is ptosis
droopy eyes
58
ptosis is a common symptom of what
myasthenia gravis
59
what does edrophonium do (mechanism of action)
blocks enzyme acetylcholinesterase
60
what does neostigmine do
longer lasting than edrophonium - blocks acetylcholinesterase
61
what does anticholinesterase do
break down enzyme that turns acetylcholine into choline
62
in Mg what makes the muscle more tired
using it more
63
in Mg what makes the muscle better
not using it - relaxing it
64
what are important risk factors of MS
Women are about twice as likely as men are to develop MS. People of Caucasian descent are at highest risk of developing MS.
65
how can K+ channel blockers help with MS
Prolong action potentials & facilitate conduction through demyelinated axons

Physiology I Block 2 (7 decks)

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