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Y2 > MSK - NMJ > Flashcards

MSK - NMJ Flashcards

1
Q

what innervates skeletal muscle?

A

fast conducting alpha motor neurons with myelinated axons and cell Bodies in the spinal cord or brain stem

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2
Q

where does the axon divide into unmyelinated branches?

A

near the muscle to innervate individual muscle fibres

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3
Q

what is the motor unit?

A

the neurone and the number of fibres it innervates

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4
Q

what is the end of the branches?

A

terminal bouton that synapses with the muscle membrane at NMJ

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5
Q

what does an action potential cause?

A

release of transmitter Ach

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6
Q

where exactly is the synapse?

A

endplate region of skeletal muscle fibre

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7
Q

what contains the Ach?

A

synaptic vesicles which cluster at active zones

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8
Q

where are the nicotinic Ach receptors?

A

junctional folds that face the active zones

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9
Q

where is Ach synthesised?

A

cytoplasm of bouton

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10
Q

where is Ach stored?

A

synaptic vesicles

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11
Q

how is Ach released from the vesicles into the clefts?

A

Ca2+ dependant release by exocytosis

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12
Q

what happens once Ach is released?

A

brief activation of nicotinic receptors by reversible binding

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13
Q

what terminated the binding of Ach?

A

acetylcholinesterase

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14
Q

what terminates the binding of Ach?

A

acetylcholinesterase

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15
Q

pre-synpatically, how is choline transported into the terminal?

A

choline transporter (symport with Na+)

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16
Q

what is combined to produce Ach and by which enzyme?

A

choline and acetyl coenzyme A

choline acetlytransferase

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17
Q

what concentrates Ach in the vesicles?

A

vesicular Ach transporter

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18
Q

what does arrival of the action potential at the terminal cause?

A

depolarisation
opening of voltage gated Ca2+ channels
Ca2+ entry to the terminal

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19
Q

what does Ca+ cause the docked vesicles to do?

A

undergo exocytosis

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20
Q

how many ACh molecules activate each nicotinic receptor?

A

2

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21
Q

what are nAChRs?

A

pentamers of glycoprotein subunits surrounding a central cation selective pore

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22
Q

when does the pore/gate open?

A

when ACh binds

23
Q

what is the channel equally permeable to and not permeable to?

A

Na+ and K+

anions

24
Q

what happens when the gate is open?

A

Na+ enters and K+ exits simultaneously

25
Q

how is a depolarising end plate potential generated?

A

influx of Na+ is greater (driving force at resting potential)
simultaneous opening of many nAChrs

26
Q

what does each vesicle of Ach contain?

A

a quantum of neurotransmitter

27
Q

what is a miniature end plate potential?

A

the electrical response to one quantum of transmitter

28
Q

what is the graded electronic response?

A

when many MEPPs summate to produce an end plate potential

29
Q

what is the condition for the end plate potential to cause contraction?

A

all or none reaction

it must exceed threshold to trigger contraction but this always occurs normally

30
Q

what causes the contraction once the action potential is released?

A

release of Ca2+ from intracellular stores

31
Q

how does the AP enter the muscle fibre?

A

transverse T tubules

32
Q

what are transverse T tubules?

A

invaginations of cell membrane that dip into muscle cell

33
Q

what do APs arriving at T tubules trigger?

A

release of Ca2+ from the SR

34
Q

how does Ca2+ release cause the contraction?

A

by interacting with troponin assoc with myofibrils

35
Q

what causes rapid termination of transmission?

A

hydrolysis of ACh by acetylcholinesterase

36
Q

where do the end products choline and acetate go?

A

choline is taken up by the choline transporter

acetate diffuses from the synaptic cleft

37
Q

how is the termination so rapid?

A

extremely efficient

some Ach molecules are hydrolysed before the transmitter has even bound to nicotinic receptors

38
Q

which drugs reversibly block the action of AChE?

A

anti-cholinesterase

39
Q

what is neuromyotonia?

A

disorders of muscle function including cramps, stiffness, slow relaxation and twitches

40
Q

what causes acquired neuromyotonia?

A

AI

antibodies against K+ channels disrupt function

41
Q

what do the antibodies in neuromyotonia cause?

A

hyper-excitability and repetitive firing

prolonged epp and repetitive AP discharge

42
Q

what are used to treat neuromytonias?

A

anticonvulsants which block Na+ channels

43
Q

main symptom of Lambert eaton myasthenic syndrome?

A

muscle weakness in limbs

44
Q

what is assoc with LEMS?

A

small cell carcinoma of lung

45
Q

origin of LEMS?

A

AI

antibodies against Ca+ channels

46
Q

what are used to treat LEMS?

A

anticholinesterases to increase duration of ACh in cleft

potassium blockers to increase release of ACh

47
Q

main symptoms of MG?

A

progressively increasing muscle weakness during period of activity
eye and eyelid weakness

48
Q

origin of MG?

A

antibodies against ACh receptors

49
Q

treatment of MG?

A

anticholinestrases and immunosuppressants

50
Q

what is botulin toxin?

A

endotoxin that acts at motor neurone terminals to irreversibly inhibit ACh release
high death rate

51
Q

what can a low dose of botulin toxin treat?

A 
overactive muscles (dystopias)
extra ocular muscles for squints or eyelids 
smoothing out wrinkles
52
Q

what are curate like compounds?

A

interfere with the postsynaptic action of ACh by acting as competitive antagonists of the nicotinic receptors

53
Q

what do curate like compounds cause?

A

reduction of amplitude of the epp to below the threshold for AP generation

54
Q

what are curate like compounds used for?

A

induce reversible muscle paralysis in certain surgeries

Y2 (8 decks)

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