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SKIN/MS FINAL > TRACHTE > Flashcards

TRACHTE Flashcards

1
Q

How many efferent fibers come from spinal cord in somatic nervous system?

A

1

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2
Q

neurotransmitter in somatic nervous system

A

acetylcholine

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3
Q

receptor in somatic nervous system

A

nicotinic

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4
Q

What can activate nicotinic receptor

A

acetylcholine or nicotine

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5
Q

6 steps that activation results in - step 1

A

Na influx

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6
Q

6 steps that activation results in - step 2

A

depolarization

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7
Q

6 steps that activation results in - step 3

A

muscle action potential

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8
Q

6 steps that activation results in - step 4

A

opening of voltage sensitive calcium channel

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9
Q

6 steps that activation results in - step 5

A

release of calcium from sarcoplasmic reticulum

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10
Q

6 steps that activation results in - step 6

A

contraction

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11
Q

efferent nerves from the spinal column virtually always release..

A

acetylcholine

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12
Q

toxin from krait that blocks neuromuscular nicotinic ion channel

A

alpha - bungarotoxin or cobra venom

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13
Q

Do somatic nerves have a synapse outside the spinal cord?

A

No (that’s autonomic nerves)

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14
Q

Nerve activation leads to 9 things….1

A

acetylcholine release

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15
Q

Nerve activation leads to 9 things….2

A

nicotinic receptor activation

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16
Q

Nerve activation leads to 9 things….3

A

sodium influx

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17
Q

Nerve activation leads to 9 things….4

A

muscle endplate depolarization

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18
Q

Nerve activation leads to 9 things….5

A

muscle action potential

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19
Q

Nerve activation leads to 9 things….6

A

calcium influx

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20
Q

Nerve activation leads to 9 things….7

A

calcium induced calcium release from sarcoplasmic reticulum

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21
Q

Nerve activation leads to 9 things….8

A

calcium interaction with troponin

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22
Q

Nerve activation leads to 9 things….9

A

myosin-actin interaction (muscle contraction)

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23
Q

What drugs could prolong acetylcholine actions?

A

anticholinesterases: neostigmine, pyridostigmine, edrophonium

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24
Q

If something blocks acetylcholine release, what is prevented (2 things)

A
  1. muscle depolarization
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25
Q

Something that blocks nicotinic receptors will prevent.. (2 things)

A

muscle depolarization

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26
Q

drug that prevents AcH release

A

botulinum toxin

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27
Q

drugs that block nicotinic receptors (useful in surgery)

A

mivacurium

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28
Q

Something that blocks calcium induced calcium release will block…

A

contraction! (but not depolarization)

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29
Q

drug that blocks calcium induced calcium release

A

dantrolene

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30
Q

What is useful for treating myasthenia gravis

A

anticholinesterases

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31
Q

What do anticholinesterases do?

A

increase acetylcholine concentrations in the vicinity of the nicotinic receptor (outside the somatic nerve)

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32
Q

charge of acetylcholine

A

negative (comes from aspartic acid)

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33
Q

what does acetylcholine get broken down to?

A

acetic acid and choline

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34
Q

2 carbamate drugs

A

neostigmine

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35
Q

stimulates nicotinic receptors, useful for myasthenia gravis, abdominal distension or atony of detrusor muscle. More often used in the hospital only though.

A

Neostigmine (quaternary ammonium)

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36
Q

delivery of neostigmine

A

oral or parenteral

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37
Q

Used in myasthenia gravis or to reverse competive neuromusclar antagonism; can also be used prophylactically to prevent action of nerve gas.

A

Pyridostigmine

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38
Q

Why is pyridostigmine used more in patients?

A

It is better absorbed orally.

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39
Q

Why can pyridostigmine be used with nerve gas/

A

It could occupy some sites of Ach and prevent acetylcholinesterases from binding there

40
Q

Therapeutic idea in myasthenia gravis

A

increase Ach concentrations to increase interactions with nicotinic receptors. Nicotinic receptors are depleted in MG so must increase Ach to get interaction w/Nic receptor.

41
Q

On a response vs acetylcholine concentration plot, what way would it shift if neostigmine was administered?

A

left shift

42
Q

Reversilbe anticholinesterase that is administered parenterally and is very SHORT ACTING

A

Edrophonium

43
Q

What is edrophonium good for?

A

diagnosing myasthenia gravis and treating paraoxysmal supraventricular tachycardia

44
Q

If an increase in strength is seen after administering edrophonium…

A

myastenic crisis

45
Q

if a decrease in strength is seen after administering edrophonium…

A

cholinergic crisis

46
Q

cholinergic crisis

A

If there person is getting too much acetycholinesterase, the edrophonium will make them weaker.

47
Q

unique property of acetylcholine related to activation:

A

excessive stimulation desensitizes the organ to further stimulation (principle behind cholinergic crisis)

48
Q

Acetycholinesterase toxicity

A

Sludge

49
Q

S

A

sweating

50
Q

L

A

lacrimation

51
Q

u

A

urination

52
Q

D

A

diarrhea

53
Q

G

A

GI distress

54
Q

E

A

emesis (vomiting)

55
Q

What causes SLUDGE

A

stimulation of organs in body that respond to parasympathetic innervation, lung constriction, pinpoint pupils

56
Q

Where are neuromuscular blockers used?

A

surgery

57
Q

2 types of neuromuscular blockers

A

competitive and depolarizing

58
Q

Mechanism of neuromuscular competitive blockers

A

competitively compete for nicotinic receptor sites

59
Q

What parts of contraction, etc. are blocked w/neuromuscular competitive blockers?

A

Na influx (compete for nicotinic sites)

60
Q

How do depolarizing agents work?

A

depolarize END PLATE OF MUSCLE - leads to chronic Na influx

61
Q

How do competitive agents work on muscles..

A

affect smaller muscles first then larger ones

62
Q

What can reverse competitive blockers?

A

acetylcholinesterase (neostigmine, etc)

63
Q

What is most sensitive to depolarizing agents?

A

chest and abdomen

64
Q

What does acetylcholinesterase do to depolarizing agents/

A

may augment block (increase intensity)

65
Q

What do you see with depolarizing agents?

A

twitching before paralysis

66
Q

What effects occur from neuromuscular blockers (4)

A

paralyze skeletal muscle

67
Q

When don’t you want to use neuromuscular blockers

A

burn patients

68
Q

Examples of competitive blockers

A

d-tubocurarine

69
Q

examples of depolarizing agents

A

succinylcholine

70
Q

what can enhance competitive block?

A

ether

71
Q

What has slight ability to reverse competitive blockade due to beta 2 receptors on muscle

A

epinephrine

72
Q

toxic effects of neuromuscular blockers

A

apnea

73
Q

what can cause malignant hyperthermia

A

halothane

74
Q

treatment for malignant hyperthermia

A

dantrolene

75
Q

what does dantrolene do?

A

inhibits calcium release from sarcoplasmic reticulum by blocking the Ryanodine receptor

76
Q

What does dantrolene prevent?

A

CONTRACTION

77
Q

Absorption of neuromuscular blockers

A

intravenously (quaternary ammonium)

78
Q

How are neuromuscular blockers usually excreted

A

kidneys

79
Q

what drug is not excreted by the kidneys

A

atracurium

80
Q

uses of neuromuscular blockers

A

anesthetics

81
Q

What are resistant to succinylcholine

A

myasthenics

82
Q

what potentiates succinylcholine effects

A

anticholinesterases

83
Q

What should you check for in patient before giving succinylcholine

A

butyrylcholinesterase

84
Q

What does butyrylcholinesterase do?

A

degrades succinylcholine (gives short duration due to rapid metabolism)

85
Q

Other side effects of succinylcholine

A

can produce malignant hyperthermia

86
Q

when is succinylcholine used

A

shorter procedures

87
Q

what does succinylcholine do to the contraction/acetylcholine concentration curve

A

flat lines (no contraction occurs)

88
Q

what does tubocarine do to the contraction/acetylcholine concentration curve

A

shifts curve to the right - decreases contraction of muscle (need higher Ach for contraction to occur)

89
Q

prevents acetylcholine release by cleaving proteins (SNAP25) necessary for acetylcholine exocytosis

A

botulinum toxin A (botox)

90
Q

where is botox injected

A

region of spastic muscle

91
Q

how long does botox last

A

3 months

92
Q

what can botox treat

A

spasms of eye

93
Q

most potent lethal toxin known (8 serotypes, only 3 have antisera)

A

botulinum toxin

94
Q

Prevents CONTRACTION and malignant hyperthermia

A

dantrolene

95
Q

Potentiate contraction w/antichoinesterases

A

neostigmine

96
Q

What drug would BLOCK action potential from occuring

A

tubocurarine (competitive)

SKIN/MS FINAL (6 decks)

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