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Ana/Phys/Patho I > Unit 7: skeletal muscle > Flashcards

Unit 7: skeletal muscle Flashcards

1
Q

the vast majority of skeletal muscles have cells that are innervated by this many motor neurons

A

ONE

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2
Q

where do the motor neuron cell bodies lie in the spinal cord?

A

the ventral (anterior) horns

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3
Q

what are two pathways for motor neurons to get “excited”?

A
  1. the descending pathways from the brain
  2. the reflex arcs
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4
Q

what is the sarcoplasmic reticulum (SR)?

A

where skeletal muscle stores Ca2+

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5
Q

what are the transverse (T) - tubules

A

these tubules helps propogate the AP across the muscle fibers

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6
Q

what are the two contraction elements in a skeletal muscle fiber?

A

actin + myosin

these structures shorten the muscle fibers during contraction

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7
Q

what is the mitochondria’s role in the skeletal muscle?

A

helps provide ATP to the skeletal muscle

also located in presynaptic neuron for ATP use in ion channels

provides “acetate” for ACh formation

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8
Q

differentiate primary vs secondary clefts

A

primary: one infolding
secondary: two infoldings within one groove

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9
Q

Where are the ACh receptors located on the subneural clefts?

A

typically on the more superior/surface of the subneural cleft

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10
Q

where do VG Na+ channels lie in the subneural cleft?

A

they are congregated deeper inside the cleft at the base and along the inferior walls

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11
Q

what is AChE?

A

an enzyme that breaks down ACh
expressed by the skeletal muscle and parks it in the NMJ
it shuts the stimulus (ACh) down to allow neuronal repolarization

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12
Q

how does AChE break down ACh?

A

hydrolysis to form acetyl/acetate and choline

choline can be recycled into the neuron

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13
Q

how many ACh-Rs are at a typical NMJ?

A

5 million

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14
Q

how many ACh-Rs get activated at a typical NMJ during AP?

A

500,000 or 10% of 5 million

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15
Q

how many ACh molecules typically get released into the NMJ during an AP?

A

1 million at bare minimum (to elicit muscle contraction)

typically 2 million, but not all the ACh makes it to the skeletal muscle (d/t AChE)

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16
Q

on a N-ACh-R, which subunit binds the ACh molecules?

A

the alpha subunits bind the 2 ACh molecules

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17
Q

what is an example of a n-ACh-R antagonist?

A

curare

18
Q

curare can bind to ___ subunit on the n-ACh-R to shut it down

A

ONE

(does not need to bind to both alpha subunits)

19
Q
A
20
Q

this sets up exocytosis for ACh release into NMJ

A

Ca2+

21
Q

what are the voltage sensors in a skeletal muscle cell and what do they do?

A

voltage sensors located in the t-tubules & cellular wall recognize an AP that is propogated by the fast Na+ channels

these voltage sensors are AKA dihydropyridine (DHP) receptors

in response to an AP, DHPRs will “tug” on their attachment to the calcium release channels to liberate Ca2+ “popping the cork”

SOME Ca2+ can influx via the dihydropyridine receptors (but not much)

22
Q

what is a RyR (ryanodine receptor)?

A

RyR is a Ca2+ release channel gatekeeping Ca2+ in the SR

23
Q

what is SERCA?

A

“sarcoplasmic endoplasmic reticulum calcium ATPase”

this structure burns ATP to put Ca2+ BACK into the SR against it’s [ ] gradient

24
Q

list all the steps to excitation-contraction coupling:

A
  1. motor neuron depolarizes from brain/or reflex arcs
  2. Ca2+ influx to motor neuron – primarily thru voltage sensitive p-type Ca2+ channels
  3. ACh storage vesicles fuse to presynaptic neural cell wall/membrane
  4. ACh released into NMJ via exocytosis
  5. 2 ACh bind to 1 n-ACh-R; primarily sodium INFLUX and secondarily Ca2+ influx
  6. threshold potential met generating EPP/local depol and (as long as skeletal tissue is healthy) turns into an AP
  7. AP spreads down muscle fibers in bidirectionally
  8. AP spreads via VG Na+ channels
  9. muscle depolarization sensed by DHPRs (in t-tubules and cell wall)
  10. DHPRs pull on RYR “doors” to release Ca2+ from SR
  11. Ca2+ influx into sarcoplasm; recycled into SR via SERCA
  12. Ca2+ removed from sarcoplasm terminates contraction
25
Q

how does Ch get recycled back into presynaptic neuron?

A
  1. Ch pump (ATP)
  2. Ch/Na+ co-transporter
26
Q

what structure is located in cell wall to store Ch for later use?

A

phosphatidylcholine

27
Q

there are more leaky Na+ channels on a neuron than leaky K+ channels: true or false

A

false
leaky K+ ch > leaky Na+ ch

28
Q

describe how myasthenia gravis affects skeletal muscle

A

MG is an autoimmune disorder where the body produces antibodies to target n-ACh-Rs; usually due to an abnormal thymus gland

if plenty of Ab get destroyed by immune system, there is less surface area for n-ACh-Rs (covered by scar tissue; usually in the clefts) and less fast Na+ channels

this would lead to impaired ability to conduct AP > leads to progressive neuromuscular dysfunction

the disease gets worse throughout the day

29
Q

what are the treatments to MG?

A
  1. thymectomy
  2. plasmapherisis (filter out Abs)
  3. NMJ drugs
    +drugs that target AChE (AChE-inhibitors)//”-stigmine” drugs
30
Q

how would “-stigmine” drugs help MG patients?

A

by inhibiting the degradation of ACh in the synapse, this allows more ACh to interact with n-ACh-Rs; this will increase the overall probability to open the receptors

31
Q

what is LEMS/ELMS?

A

“lambert-eaton myasthenic syndrome”

a paraneoplastic syndrome that develops in CA patients

involves Abs against P-type Ca2+ channels; this results in a Ca2+ deficiency in the motor neuron

32
Q

what are some treatments for LEMS/ELMS patients?

A
  1. plasmapheresis
  2. remove the cancerous tumor
  3. K+ channel blockers
    +depolarization will be enhanced; depolarization will be longer and repolarization will become SLOWER

this increases the opportunity of p-type Ca2+ channels opening for Ca2+ release

33
Q

why don’t AChE-Is work for LEMS patients?

A

AChE-Is will prevent ACh from getting broken down; with the P-type Ca2+ channels being targeted, there is a Ca2+ deficiency and Ca2+ is needed to release ACh from the synapse

therefore if there is no Ca2+ to be released, there is no ACh in the synapse

34
Q

what are some examples of K+ channel blockers?

A
  1. TEA - tetraetyhlammonium
  2. 4,5-diaminopyrimidine

these drugs are very dangeous as they are non-specific to K+ channels

(unlike amiodarone – amio is a poor K+ channel blocker)

35
Q

describe a non-depolarizing paralytic

A

curare is a non-depolarizing NMBA

it binds to the alpha subunit of the n-ACh-R which will cause the skeletal muscle to relax and prevents AP from occuring

36
Q

describe an give an example of a depolarizing paralytic

A

succinylcholine (sux)

a depolarizing paralytic means that the succinylcholine molecule will bind to n-ACh-R, and keep the receptors OPEN

if the receptor is open for a prolonged period of time, this causes a sustained depolarization

initially fasiculations occur, then repolarization is prolonged d/t a sustained AP d/t Na+ influx and VG Na+ channels will close their H gates to remain in their inactive state

if all VG Na+ channels are in inactive state, the channels cannot open the activation gate and will NOT produce new APs

37
Q

why does sux not get broken down by AChE?

A

sux is not broken down by AChE – sux is 2 ACh molecules joined at the acetyl groups and AChE has a hard time breaking the ester bonds

38
Q

describe how sux can cause a potassium leak

A

K+ leak channels don’t ever close; but the K+ channels will start to efflux d/t prolonged depolarization and membrane potential will become more positive for a prolonged period of time

this will allow K+ to efflux thru the leaky K+ channels to flow across the electrochemical gradient

39
Q

by how much does sux raise ECF K+ levels in a healthy person? in a person with skeletal muscular issues?

A

in a normal person: 0.5
in someone who might have skeletal muscle issues: hyperkalemia

40
Q

why would a CVA patient be at risk for hyperkalemia if given sux?

A

CVA patients have acute neuromuscular issues which can cause denervation

if they are not using their muscles as often there will be an increase in n-ACh-Rs that are not confined to just the NMJ

if sux is given, potassium leak channels will also leak throughout areas not confined to the NMJ and will cause hyperkalemia

Ana/Phys/Patho I (16 decks)

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