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ZANDER CNOR > pharmacology part 2 > Flashcards

pharmacology part 2 Flashcards

1
Q

What is a depolarizing agent?

A

succinylcholine

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2
Q

Succinylcholine is also called what?

A

anectine

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3
Q

What is succinylcholine (anectine) primarily used for?

A

induction to facilitate tracheal intubation

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4
Q

What is acetylcholine? what 2 things is it for?

A

a neurotransmiter for your parasympathetic nervous system and muscle contraction

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5
Q

what is the MOA?

A

motor neuron throws acetylcholine down. Acetylcholine gets in receptors on motor end plate, which stimulates depolarization (sodium potassium exchange). Sodium potassium exchange creates a voltage or charge across that cell membrane or an action potential, which causes muscle contraction.

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6
Q

What is succinylcholine really doing physiologically?

A

it is acting like acetylcholine (which is what our body produces), so it can interact with acetylcholine receptors. which causes muscle contractions.

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7
Q

During an action potential, sodium and potassium do what?

A

sodium moves into the cell and potassium moves out of the cell

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8
Q

How can you tell the succinylcholine has hit the motor end plate?

A

fasiculations

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9
Q

What is the onset of succinylcholine?

A

1 minute

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10
Q

What is the duration of succinylcholine?

A

5-10 minutes

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11
Q

Succinylcholine is metabolized by what? which is a what?

A

pseudocholinesterase, which is an enzyme from liver

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12
Q

Succinylcholine causes what? how?

A

paralysis, because it holds the depolarization before pseudocholinesterase comes through

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13
Q

What is an adverse reactions of succinylcholine?

A
  1. bradycardia - rest and digest
  2. increases intraocular pressure - caused by fasiculations
  3. hyperkalemia - sodium moves in and potassium moves out. PVCs are normal
  4. oxygen depletion -
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14
Q

What are 2 contraindications of succinylcholine?

A
  1. malignant hyperthermia family history
  2. degenerative neuromuscular disorders
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15
Q

What are 2 meds that are contraindicated in glaucoma patients?

A
  1. succinylcholine - increase intraocular pressure
  2. anticholinergics (atropine, robinol) - causes pupil to dilate which further constricts the ocular drainage system
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16
Q

What is the treatment med for glaucoma?

A

Pilocarpine

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17
Q

Pilocarpine is the reversal agent for what group of meds?

A

anticholinergics

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18
Q

So if glaucoma patients are given atropine and are taking pilocarpine, what happens?

A

atropine doesn’t work because pilocarpine is the reversal agent

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19
Q

Is there a reversal agent for succinylcholine?

A

no

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20
Q

effects of succinylcholine are reversed how?

A

effects reversed quickly by metabolism from pseudocholinesterase only

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21
Q

There is a rare deficiency of what that can be an issue with succinylcholine?

A

pseudocholinesterase

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22
Q

What does pseudocholinesterase deficiency look like?

A

you go to wake them up and monitor is going nuts but they can’t move anything including their own diaphragm, but they are awake.

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23
Q

What is a non-depolarizing muscle relaxant? how does it work?

A

blocking agent. they block the motor end plate, form a film over top of motor end plate so the acetylcholine just bounces off resulting in no depolarization

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24
Q

what are non-depolarizing muscle relaxants also called?

A

acetylcholine competitive antagonists

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25
Q

Acetylcholine does not interact with what with non-depolarizing muscle relaxants?

A

with receptor

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26
Q

Non-depolarizing muscle relaxants work slower than what?

A

succinylcholine

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27
Q

large doses of what med come close to succinylcholine?

A

rocuronium comes close

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28
Q

Rocuronium and vecuronium only lasts about how long?

A

15 minutes

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29
Q

Vecoronium likes the what muscle?

A

heart muscle

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30
Q

vecuronium decreases the what demand on the heart?

A

oxygen demand on the heart

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31
Q

what are NDMR reversal agents?

A

anticholinesterases

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32
Q

How do anticholinesterases work?

A

block acetylcholinesterase

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33
Q

How do anticholinesterases work?

A
  1. increases acetylcholine concentration in the neuromusclar junction
  2. displaces the muscle relaxant from the acetylcholine receptor
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34
Q

When would they give anticholinesterases?

A

when patient starts to move a little big, that’s how you know the film at the motor end plate is peeling back so it’s safe to give it.

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35
Q

What are the 4 unwanted side effects with anticholinesterases?

A
  1. bradycardia
  2. bronchospasm
  3. enhanced GI peristalsis
  4. enhanced oral secretions
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36
Q

Anticholinesterases, because of their side efffects, are usually combined with what?

A

typically combined with a muscarinic antagonist (anticholinergic)

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37
Q

What are 2 anticholinergics?

A
  1. glycopyrrolate
  2. atropine
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38
Q

What are 2 anticholinesterases?

A
  1. edrophonium
  2. neostigmine
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39
Q

neostigmine is always mixed with what anticholinergic?

A

glycopyrrolate

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40
Q

Who’s effects come first atropine or neostigmine?

A

atropine effects occur before neostigmine

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41
Q

What anticholinergic is mixed with edrophonium or enlon plus?

A

atropine

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42
Q

What is sugammadex?

A

it is an NDMR reversal agent

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43
Q

What is the difference between edrophonium and neostigmine with sugammadex?

A

sugammadex is an active reversal agent

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44
Q

Suggammadex selectively does what?

A

Sugammadex selectively binds rocuronium or vecuronium

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45
Q

How does sugammadex work?

A

It does 1:1 binding of rocuronium or vecuronium, so it engulfs these things so your body just thinks it’s sugammadex. It sucks up these meds too

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46
Q

Due to sugammadex 1:1 binding it is able to do what?

A

reverse any depth of neuromuscular block

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47
Q

sugammadex is NOT a what?

A

not an anticholinesterase

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48
Q

What is the strongest inhalation gas?

A

halothane

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49
Q

What can halothane cause in conjuction with epi?

A

cause arrhythmias

50
Q

Do we use halothane anymore?

51
Q

What is the gas that is most often related to MH?

52
Q

What is Isoflurane also known as?

53
Q

What is isoflurane most used for?

A

neuro procedures

54
Q

What are 2 huge negatives of isoflurane?

A
  1. you can’t give it to patients with a pneumatic tourniquet. When you exsanguinate, the blood engorges surrounding organs. The blood brain barrier protects cerebral vascular system from this, but because isoflurane brings down the blood brain barrier it increases intracranial pressure
  2. smells terrible
55
Q

What do we have with isoflurane?

A

rapid recovery

56
Q

Isoflurane makes people lucid in how much time?

A

(lucid in 15-30 minutes)

57
Q

What is the benefit of sevoflurane?

A

rapid onset and offset

58
Q

Sevoflurane is the chosen drug for what?

A

inhaled induction in children

59
Q

Does sevo have issues with pneumatic tourniquet?

60
Q

What is ethrane contraindicated in?

A

in people with seizures, because it lowers the seizure threshold

61
Q

What gas has the fastest onset and offset?

A

desflurane

62
Q

Who do we not give desflurane to?

A

neuro patients because coughing is common

63
Q

Desflurane is terrible for what?

A

bad for the environment

64
Q

where do we mostly use desflurane?

A

in ambulatory surgery

65
Q

What is common with desflurane?

66
Q

What are 2 characteristics of nitrous oxide?

A

it is a gas and it is odorless. It is different from the rest of the inhaled anesthetics

67
Q

What is something unique about nitrous oxide?

A

it is the only thing that is not an opioid that is also going to interact with opioid receptors - has some analgesic properties

68
Q

Is nitrous oxide a good anesthetic

A

NO it is a weak anesthetic, not very good at being a sedative and suppressing consciousness around painful stimuli

69
Q

Nitrous oxide can support what?

A

combustion like oxygen

70
Q

Why is nitrous oxide different from halothane, isoflurane, sevoflurane, ethrane, and desflurane?

A

the -anes are all volatile agents, meaning they are liquids under pressure

71
Q

Because nitrous oxide is an oxidizer it can cause what?

A

diffusion hypoxia

72
Q

What will anesthesia providers commonly do with nitrous oxide?

A

combine it with another inhaled anesthetic because it has analgesic properties

73
Q

All of the inhaled anesthetics are all exhaled in a what?

A

unchanged form

74
Q

When nitrous oxide is exhaled it can cause what?

A

leaving blood into the alveoli it can displace oxygen out of the alveoli

75
Q

What is a nursing intervention for nitrous oxide?

A

patient needs to have nasal cannula postoperatively until they are done off gassing the nitrous oxide

76
Q

Inhalation gases are exhaled in what kind of form?

A

in an unchanged form

77
Q

What are neuro effects of inhalation gases?

A

headaches, irritability, cognitive changes

78
Q

What are hormonal changes that can happen with inhalation gases?

A

miscarriage, birth defects, female and male sterility

79
Q

what are systemic things that inhalation gases can cause?

A

renal and hepatic disease, cancer

80
Q

Safety data sheet includes info on what?

A

chemical hazards, special handling and exposure

81
Q

Where is a lot of our exposure from anesthesia gases coming from?

A
  1. leaking anesthesia circuits
  2. when someone is extubated
82
Q

What can nitrous oxide effect?

A

DNA synthesis

83
Q

MH is what kind of syndrome?

84
Q

MH is autosomal what?

85
Q

MH has no racial boundaries, but, at least in america, who are most commonly affected?

86
Q

MH happens more frequently in who?

A

older children and young adults

87
Q

How can we test for MH?

A
  1. blood test - but if you get negative test doesn’t mean you don’t really have it
  2. string muscle biopsy - oxygenated solution, throw halothane, give MH outside of the body
88
Q

MH is consistently more frequent in men or women?

89
Q

We do what more specifically with MH?

A

pre-op family history

90
Q

How does a normal muscle contraction work?

A

DHP receptor acts as the foot that kicks open the door to calcium channel. The calcium channel is also known as the ryanidid receptor. When door opens the calcium comes out of the sarcoplasmic reticulum and causes muscle contraction

91
Q

What is really the ryanidid receptor?

A

the MAMA, it tell the calcium to come back in

92
Q

What is the issue with MH as far as mechanism of action for a muscle contraction?

A

the triggering agents (succinylcholine and halothane) act as a door stop in the ryanidid receptor. Door can’t close or open, so it causes calcium so stay out causing CONTRACTION CONTRACTION CONTRACTION ENERGY ENERGY ENERGY which is an MH crisis

93
Q

To trigger an episode of MH what kind of patient do you have to have?

A

genetically susceptible patient

94
Q

What is the most common triggers of MH?

A

succinylcholine, especially when used in conjunction with an inhaled anesthetic such as desflurane, isoflurane, and halothane

95
Q

An MH susceptible patient should never receive what?

A

never receive succinylcholine or one of these anesthestics

96
Q

Early signs of MH cause what?

A

trismus or jaw tightening

97
Q

Is trismus or jaw tightening consistent indicator of MH?

98
Q

What is a consistent early indicator of MH?

A

a rapid rise in end tidal CO2 and metabolic acidosis

99
Q

Why is rise in exhaled in CO2 and metabolic acidoses a consistent early sign?

A

because the muscle cell is sucking in oxygen and throwing out co2 and heat, so it is going to throw out tons of CO2

100
Q

MH causes intense what?

A

muscle rigidity - xtreme rictus

101
Q

MH increases what 2 hemodynamic things?

102
Q

People in MH burn what faster than you can what?

A

burn oxygen faster than you can push it into their lungs

103
Q

What are late signs of MH?

A
  1. rapidly rising body temp
  2. change in color of soda lime
  3. hyperkalemia - bc of the depolarization, potassium is thrown out of their cells
  4. hypoxia - metabolic acidosis
  5. myoglobinuria - muscle cells fly apart
  6. cardiac arrest
104
Q

It is not uncommon for patients who have MH to go on what afterwards?

A

dialysis, because muscle tissue is toxic to the kidneys

105
Q

What 3 things can cause cardiac arrest?

A
  1. hyperkalemia
  2. hypoxia
  3. acidosis
106
Q

What are the steps for intervening with MH?

A
  1. immediately discontinue all triggering agents -
  2. switch over to nitrous oxide
  3. hyperventilate the patient with 100% oxygen
  4. call MHAUS 1-899-MH-HYPER
  5. Dontrolene 2-3 mg/kg
  6. sodium bicarb IV for metabolic acidosis
  7. treat hyperkalemia with calcium, insulin, glucose
  8. treat myoglobinuria with diuretics, bicarb, fluids
107
Q

What is 1 dose of dantrolene?

108
Q

In an adult you would get a 2.5 mg/kg out of how many vials?

A

9 vials is one dose

109
Q

Dantrolene has to be mixed with what?not what?

A

PF sterile water, not saline

110
Q

You have to have how many doses of dantrolene on your cart?

111
Q

How many vials do you need on your MH cart?

112
Q

What is ryanedex?

A

powdered dantrolene

113
Q

Do you have to mix ryanadex?

A

yes with pf sterile water

114
Q

How many mL’s in a dantrolene vial?

A

60 mL’s, so you need a liter bag of sterile water to reconstitute (with 60 mL syringe to pull out sterile water, and put it in the dantrolene vials 9 times, and then do redraw it and put it back into the sterile water bag).

115
Q

What is the issue with ryanodex?

A

it is 3 times more costly than all 9 vials of dantrolene

116
Q

No what type of meds for MH?

A

no calcium channel blockers - prolongs MH crisis

117
Q

Verapimil (calcium channel blocker) has a very bad lethal drug interaction with what med?

A

dantrolene; causes severe hyperkalemia

118
Q

How can we cool MH patients down?

A

ice packs and hypothermia blanket

119
Q

Give what kind of fluids? not what?

A

iced NSS - avoid ringers (has potassium and lactate)S

120
Q

Send what and correct what during MH?

A

send labs and correct electrolyte imbalances

121
Q

Monitor what and correct what during MH?

A

monitor ECG and correct arrhythmias

122
Q

Where will the patient be transferred post MH crisis

A

transfer patient to ICU when stable and monitor for 36 hours for recurrence and complications

ZANDER CNOR (15 decks)

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