Neuromuscular Physiology Flashcards Preview

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Flashcards in Neuromuscular Physiology Deck (110)
1

Motor Neurons to skeletal muscle originate where?

Anterior (ventral) horn

2

Sensory neurons from skeletal muscle carry action potentials to the spinal cord via the what?

Dosal Horn

3

Motor neurons are what type of fibers?

A=Alpha

4

A-Alpha fibers are the ___, most heavily ___ fibers, thus have the ____ conduction velocity

Largest

Mylinated 

fastest

5

Just to see a picture

Nothing to know just look at pic

6

Look at the cleft

know and understand the parts

 

7

Release of ACh from the nerve terminal:

an ation potential travels along the motor nerve axon and ultimately invades the ______ nerve terminal

Presynaptic

8

Release of ACh from the nerve terminal:

Depolarization of the presynaptic nerve teminal causes voltage-gated ____ channels to open.

Ca++

9

Release of ACh from the nerve terminal:

Ca++ difuses down the concentration gradient _____ the nerve terminal

into

10

Release of ACh from the nerve terminal:

inside the nerve terminal Ca++ causes ____ ____ vesicles to fuse with the nerve cell membrane and open to the exterior. 

release pool

11

Release of ACh from the nerve terminal:

ACh spills out into the synaptic cleft called ______.

Exocytosis

12

Release of ACh from the nerve terminal:

just a picture for reference. Notice Ca++ in and teh release of ACh

 

13

Release of ACh from the nerve terminal:

The presynaptic nicotinic receptor responds to ACh in the cleft by how? what is this also known as?

by increasing the synthesis of ACh and mobilization of ACh-containing vessicles (storage pools) know as positive feedback

14

Release of ACh from the nerve terminal:

what is the purpose of the positive feedback system?

prevents the depletion of ACh at the NMJ and also accounts for the phenomenon of fade seen with nondepolorizing MR (and Phase II block w/ SCh)

15

Release of ACh from the nerve terminal:

again notice the presynaptic Nicotinic receptors. the are the positive feedback system

 

16

Events at the POSTsynaptic membrane:

ACh combines with nicotinic ACh receptors (nAChR) on the postsynaptic membrane. When _____ Alpha subunits or the nicotinic receptor are occupied the ACh. The ion channel snaps open

Both

17

Events at the POSTsynaptic membrane:

ACh combines with nicotinic ACh receptors (nAChR) on the postsynaptic membrane. When _____ Alpha subunits or the nicotinic receptor are occupied the ACh. The ion channel snaps open and the ions ___ and ____ diffuse into the cell and the ion ___ diffuses out of the cell into the extracellular space?

Ca++ and Na+

K+

18

Events at the POSTsynaptic membrane:

notice the binding if ACh and the influx of Ca++ and Na+ and the Efflux of K+

 

19

Events at the POSTsynaptic membrane:

the diffusion of the 3 ions (Ca++, Na+, and K+) through the channel causes the motor end-plate to ______.

Depolarize.

 

20

Termination of Neurotransmitter Action:

________ breaks down ACh.

Acetycholinesterase

21

Termination of Neurotransmitter Action:

Acetylcholinesterase in also called?

true

specific

genuine

type I

22

Termination of Neurotransmitter Action:

Acetylcholinesterase breaks down ACh to ____ and ___

Choline and Acetate

23

Termination of Neurotransmitter Action:

the breakdown of ACh into choline and actate by acetylcholinesterase occurs by what?

hydrolysis

24

Termination of Neurotransmitter Action:

the ____ is transported back into the nerve terminal where it is used to re-synthesize ACh

Choline

25

Termination of Neurotransmitter Action:

Picture to help. 

Notice the termination and breakdown of the ACh

 

26

Postsynaptic Receptors and Channels:

Note 2 of the 5 subunits are identical.

AKA the Alpha subunits

 

27

Postsynaptic Receptors and Channels:

An ACh molecule must attach to each of these 2 identical subunits where the nicotinic receptors are located in order to ____ the channel

open

28

Postsynaptic Receptors and Channels:

stated another way: ___ ACh molecules are needed to open each nicotinic ACh receptor?

2

29

Postsynaptic Receptors and Channels:

Acetylcholinesterase is anchored to the ______ surface of the membrane

External (extracellular)

30

Nondepolarizing block:

Nondepolarizing agents are ______ _______

compettive inhibitors

31

Nondepolarizing block:

when a nondepolarizing agent (dark diamond) binds to either ACh binding site on the nicotinic receptor, ACh cannot attach to that receptor and the channel cannot _____.

open (it remains shut)

32

Nondepolarizing block:

notice in the picture the channel remains closed (no ions are passing)

 

33

Nondepolarizing block:

how many Nondepolarizing molecules are needed to bind to close the channel? 

1

34

Nondepolarizing block:

just a side note to remember.

ACh opens the gate (channel) like SCh. a NDMR closes the gate or prevents it from opening, thus no K+ is leaking. thats why you get Hyperkalemic from SCh not NDMR

35

Depolarizing Block:

SCh binds to the Nicotinic receptors and ____ the channels in the same way that ACh does.

 

opens

 

36

Depolarizing Block:

unlike ACh bc SCh is not metabolized by true acetylcholinesterase, the voltage gated sodium channels in the perijunctional are become and remain ______. 

Inactive 

that is they do not reset to the closed position

37

Depolarizing Block:

due to the fact the channel remains open what is common in 60-90% of patients?

fasiculations

and myalgia

38

Depolarizing Block:

notice in th picture how the channels remian open.

 

39

NonDepolarizing: Mechanics

After IV administration a NDMR circulates to all tissues including skeletal muscle. It them Diffuses from the vascular department into the ___ ___ of the NMJ

Synaptic cleft

40

NonDepolarizing: Mechanics

Once in the synaptic cleft is combines with the nAChR of the motor end plate. Does it have a direct effect on the nAChR? how do you know?

No direct effect

b/c the ion channel does not open

41

NonDepolarizing: Mechanics

although it doesnt have a direct effect, it does however completly block ____ from attaching to its receptor so the channel cannot open

ACh

42

NonDepolarizing: Mechanics

since the channel cannot open it stays closed and the postsynaptic membrane remained ______.

Polarized 

(it is a nondepolarizer)

43

NonDepolarizing: Mechanics

what are the characteristics of the Nondepoalarizing block (Aka Phase II) (5)

  1. Competitive inhibition
  2. has fade
  3. Post-tetanic facilitation
  4. Antagonized by anticholinesterases (neostigmine)
  5. No fasciculations

44

Depolarizing Block: Mechanics

SCh is composed of 2 what? 

2 ACh molecules linked together

(thus mimics ACh)

45

Depolarizing Block: Mechanics

SCh after administration IV diffuses into ____ from bood

tissues

46

Depolarizing Block: Mechanics

the SCh molecules that reach the motor nerve terminal causes the motor end-plate to depolarize and a single _____ occure

contraction

47

Depolarizing Block: Mechanics

Bc true acetylcholinesterase doesn't metabolize SCh the SCh remains attached to the receptors and cause the channel to remain ____ until SCh diffuses back into circulation

open

48

Depolarizing Block: Mechanics

SCh is metabolized by what? what are the other names its called

Plasma cholinesterase

Pseudo-

butyro-

benzoyl-

false-

nonspecific- 

type II cholinesterase

49

Depolarizing Block: Mechanics

As circulating SCh is metabolized a ______ develops for SCh to diffuse from skeletal muscle motor end-plate back into the plasma and the effect of SCh is terminated

 

50

Depolarizing Block: Mechanics

6 Characteristics of depolarizing blocks (phase I)

  1. Decreased single twitch height
  2. Response to high freq stimulation is maintained (no Fade)
  3. Minimal or no fade after TOF
  4. Antagonized by Nondepolarizers
  5. Potentiated by anticholinesterases (neostigmine)
  6. Muscle fasiculations preceed block

51

Depolarizing Block: Mechanics

when the motor end plate depolarizes in response to SCh, the voltage gated Na+ channels in the membrane adjacent to it snap into the inactive state. as long as SCh maintains the depolarized state, the volage gated Na+ channels remaoin inactive, and action potentials cannot be elicited.

 

See picture 

 

52

Depolarizing Block: Mechanics

when the gated Na+ channel is in inactivated state, another action potential cannot be fired no matter how intense the stimulus. this is termed what?

the absolute refractoty period 

53

Pharmacology of NMB:

what is the relationship between twitch depression and dose. 

potency

54

Pharmacology of NMB:

the ED95 represents what?

when 95% block of a single twitch, compared tto a control single twitch

55

Pharmacology of NMB:

what is the time to maximum blockade after administration of an agent. usually compared at 2 x ED95

onset time

56

Pharmacology of NMB:

what is the time from injection to return of 25% twitch height? 

Duration of action

57

Pharmacology of NMB:

what is their structural compounds

Quaterany Ammoniums

58

Pharmacology of NMB:

Nondepolarizing agents are classified into what 2 classes? how do you differentiate tham?

  • Aminosteroids (-curonium)
  • Benzylisoquinolines (-curium)

59

Pharmacology of NMB:

what 2 NDMR are monoquaternary aminosteroids?

 

Roc

Vec

 

60

Pharmacology of NMB:

what 1 NDMR are bisquaternary aminosteroids

Panc

61

Pharmacology of NMB:

What 2 NDMR are Bisquaternary benzylisquinolines?

 

 

Atracurium

Cisatracurium

62

Pharmacology of NMB:

____% ionized at physiologic pH

 

100%^

63

Pharmacology of NMB:

they are Very (high or low) protein bound

high

64

Pharmacology of NMB:

do they cross the BBB?

Nope

65

Pharmacology of NMB:

do they cross the Placenta

nope

66

Pharmacology of NMB:

All MR can be excreted by ______ is other routes are unavailable?

Kidneys

67

Pharmacology of NMB:

The termination of Atracurium, cisatracurium, Vecuronium, and Rocuronium is by what?

redistribution

68

Adverse reactions of SCh:

Plasma Levels of K+ can increase how much 

0.5 mEq/L

69

Adverse reactions of SCh:

Plasma levels of K+ in pts with burns, trauma, or closed head injuries can increase how much

5-10 mEq/L

70

Adverse reactions of SCh:

muscle pains (myalgia's) occur most commonly where?

Subcostal

Trunk of neck

upper abdomen

shoulders

71

Adverse reactions of SCh:

Myalgia's usually occur when after administrations

24-48 hours

72

Adverse reactions of SCh:

you can get Increased IOP of how much after administration

5-15 mmHg

73

Adverse reactions of SCh:

what does it do to ICP?

Increases it

74

Adverse reactions of SCh:

Can it cause myoglobinuria?

yep

75

Adverse reactions of SCh:

what happens to intragastric pressures?

increases

76

Adverse reactions of SCh:

will you get fasiculations?

yeppers

77

Adverse reactions of SCh:

what are 5 conditions that can accenuate SCh induced hyperkalemia

  1. Burns
  2. Spinal cord transection, paraplegia, hemiplegia
  3. Skeletal muscle trauma
  4. Upper body neuron injury ( head injury, CVA, Parkinson's Dz)
  5. Prolonged immobility

78

Malignant Hyperthermia:

the diagnosis of MH is made upon the unexplained signs of what?

  • increased ETcO2
  • Pyrexia
  • tachycardia
  • cyanosis
  • rigidity
  • masseter muscle spasm (trismus)
  •  

79

Malignant Hyperthermia:

what are the Serum compesition seen with MH

  • Increased H+
  • Increased K+
  • Increased Ca++
  • Increased CO2
  • Decreased 02

80

Malignant Hyperthermia:

the defect in MH is a mutation in what receptor

ryanodine receptor RyR1

81

Malignant Hyperthermia:

where is the RyR1 receptor located at

in the SR of the skeletal muscle cells

82

Malignant Hyperthermia:

how does MH cause muscle contractions

the SR releases Ca++ continuously, leading to sustained contractions with increased metabolism

83

Malignant Hyperthermia:

what is used to treat MH

Dantrolene

84

Malignant Hyperthermia:

How does dantrolene work

acts on the SR to decrease the release of Ca++ to contractile proteins

85

Malignant Hyoerthermia:

What is one of the Earliest , most sensitive and specific signs of MH?

 

EtCO2 elevation

 

86

Malignant Hyoerthermia:

the inital signs of tachycardia and tachypenea result from what?

SNS stimulation secondary to underlying hypermetabolism and hypercarbia

87

Malignant Hyoerthermia:

SNS hyper activity manifested by tachycardia is also an early sign of increased metabolism but an Increased ______ PRECEEDS increased HR

EtCO2

88

Malignant Hyoerthermia:

other S/S

  • Increased PaCO2 (poss >100 mmHg)
  • Decreased pH (poss
  • Cyanosis
  • Unstable B/P
  • Dysrhythmias
  • Hyperkalemia

89

Nondepolarizing Neuromuscular Block:

6 charachteristics

  • NO Fasiculations prior to paralysis
  • Antagonized by true acetylcholinesterase (neo)
  • Amplitude of single twitch contractions decreases w/ increasing intensity of block
  • FADE w/ TOF and tetanic stimulation
  • Post-tetanic facilitation (potentiaion) is present
  • TOF ratio (amplitude of fourth beat to amplitude of first beat) is LESS thean 70% (T4/T1

90

Blockade:

what % is complete paralysis- flaccid pt (no twitches in TOF)

99-100%

91

Blockade:

what % blocked is the diaphragm moves (no twitches in TOF)

95%

92

Blockade:

what % blocked is Abd relaxation adequate for mos intra-abdominal procedures (1 twitch present in TOF)

90%

93

Blockade:

what % bloocked is when TV returns to normal (> 5 mL/Kg) single twitch as strong as baseline. (NOT an indicator of recovery)

75-80%

94

Blockade:

what % blocked when there is NO palpable fade in TOF, and usefull as gauge of recovery

70-75%

95

Blockade:

what % blocked w/ sustained tetanus @ 50 Hz for 5 sec, reliable indicator of recovery; VC at least 20 mL/kg

70%

96

Blockade:

what % blocked when there is NO palpable fade in Double bust stimulation, More sensitive than TOF as indicator

60-70%

97

Blockade:

what % blocked if passes inspiratory pressure test, at least -40 cmH2O; head lift (from supine) for 5 sec, sustained strong hand grip; sustained bite, reliable indicator of recovery

50%

98

Blockade:

what % of blockade is good for intubation? and what is the clinical response look like?

greater than 95%

- Diaphragm moves (no twitches on TOF)

99

Blockade:

what % block is good for abd procedures? what does the clinical response look like?

greater than 90% block.

- Abd relaxation 1 twith on TOF

 

100

Depolarizing Neuromuscular Block:

do you have fasiculations?

yep

101

Depolarizing Neuromuscular Block:

What happens to the block with cholinesterase inhibitors (neostigmine)

Augmented (agonized)

102

Depolarizing Neuromuscular Block:

what happens to the amplitude of the single twitch contraction in proportion to the severity of the block?

decreases

103

Depolarizing Neuromuscular Block:

does fade occur 

nope

104

Depolarizing Neuromuscular Block:

what happens to amplitude with tetanic contration or TOF 

decreases (no fade)

105

Depolarizing Neuromuscular Block:

what is the TOF ratio

greater the 70%

T4/T1 > 70% (>0.7)

106

Depolarizing Neuromuscular Block:

is there post tetanic facilitation?

nope

107

Depolarizing Neuromuscular Block:

what happens to the block when NDMR are administered

antagonized

108

What can cause a Phase II block?

treatment w/ higher doses of SCh or prolonged exposure os teh motor end plate to SCh 

109

what are teh characteristics of a Phase II block?

nondepolarizing block 

110

Thats it Memory master pages

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