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Pharmacology > Pharm A Test 3 > Flashcards

Pharm A Test 3 Flashcards

1
Q

What value do we use to compare potencies of neuromuscular blockers?

A

ED95

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2
Q

What is ED95?

A

Dose needed to produce 95% suppression of single twitch response

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3
Q

How is the ED95 of neuromuscular blockers changed in the presence of volatile anesthetics?

A

Decreased

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4
Q

What do we use to dose neuromuscular blockers?

A

Nerve stimulator

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5
Q

Which muscles are affected first by neuromuscular blockers?

A

Small, rapidly moving muscles are paralyzed first

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6
Q

What factors determine the onset of the neuromuscular block?

A
  • Fiber type

- Density of Ach receptors

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7
Q

Why do neuromuscular blockers have a limited volume of distribution?

A
  • Highly ionized
  • Limited lipid solubility
  • Don’t cross blood brain barrier or placenta
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8
Q

How are neuromuscular blockers excreted?

A

Unchanged by the kidneys

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9
Q

How is the pharmacokinetics of NMB changed in elderly patients?

A

They may stick around longer because there is decreased blood flow to the liver and kidneys

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10
Q

How is the pharmacokinetics of NMB changed in ESRD/liver disease patients?

A

Longer effect because of a slower clearance

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11
Q

Action of succinylcholine at NMJ

A

Binds to postsynaptic receptor and activates it

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12
Q

Action of non-depolarizing blockers at NMJ

A

Binds to postsynaptic receptor and blocks it

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13
Q

How is acetylcholine cleared from the NMJ?

A

Hydrolyzed by acetylcholinesterase in the NMJ

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14
Q

Where does succinylcholine bind to in order to exert its effect?

A

Alpha subunit of nicotinic receptor

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15
Q

Dose of succinylcholine

A

1-2mg/kg

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16
Q

Onset time of succinylcholine

A

30-60 seconds due to low lipid solubility

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17
Q

Duration of succinylcholine

A

3-5 min

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18
Q

How is succinylcholine cleared from circulation?

A

Plasma cholinesterase

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19
Q

What is the effect of high doses of succinylcholine?

A

Phase II block

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20
Q

How does succinylcholine affect amplitude during tetany?

A

Decreases amplitude

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21
Q

How is the Phase I blockade caused by succinylcholine affected by an anticholinesterase like neostigmine?

A

Phase I blockade is enhanced

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22
Q

With succinylcholine, is the amplitude of each twitch in a TOF the same or different?

A

Each TOF twitch has the same amplitude

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23
Q

What is a phase II blockade with succinylcholine?

A

The nerve response resembles a non-depolarizing blocker, causing fade with TOF and tetany and posttentanic potentiation

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24
Q

What causes a phase II blockade?

A
  • Repeated doses

- Prolonged infusion

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25
Q

What variables can decrease activity of plasma cholinesterase?

A
  • Hepatic failure
  • Low levels of circulation cholinesterases
  • Anticholinesterases
  • Metoclopramide (Reglan)
  • Atypical types
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26
Q

In large male patients with lots of muscle mass, what can be a side effect of the fasciculations caused by sux?

A

Myoglobinuria

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27
Q

How does succinylcholine affect intragastric/intraocular pressure?

A

It increases both - so don’t use if a patient has an open globe injury or if these pressures are already high

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28
Q

What muscular effect is an early sign of MH?

A

Masseter muscle rigidity

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29
Q

Why would you NOT use succinylcholine in patients presenting with the following: muscular dystrophy, T4-T6 lesions, renal failure

A

Because succinylcholine increases K+ release and can cause hyperkalemia

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30
Q

Why would you NOT use succinylcholine in patients presenting with the following: small bowel obstruction, pyloric stenosis, bleeding varices

A

Because succinylcholine increases intragastric pressure

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31
Q

Why would you NOT use succinylcholine in patients presenting with the following: open globe, intracranial hemorrhage

A

Because succinylcholine increases intracranial pressure

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32
Q

What conditions cause susceptibility to succinylcholine-induced hyperkalemia?

A
  • Prolonged total body immobilization i.e. ICU patients
  • Burns
  • Massive trauma
  • Spinal cord injury
  • Stroke
  • Severe Parkinson’s
  • Myopathies
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33
Q

What type of non-depolarizer is cisatracurium?

A

Benzylisoquinolinium

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34
Q

What type of non-depolarizer is rocuronium and vecuronium?

A

Aminosteroid

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35
Q

Non-depolarizing muscle blockers cause a TOF ratio less than __

A

0.7

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36
Q

Which neuromuscular blockers cause fade - depolarizing or nondepolarizing?

A

Nondepolarizing

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37
Q

What is the effect of using aminosteroids and benzylisoquinoliniums together?

A

Flipping between them can prolong the block

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38
Q

Which nondepolarizing muscular blocker has autonomic effects?

A

Pancuronium

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39
Q

Which class of nondepolarizing muscular blockers has hepatic and renal clearance?

A

Aminosteroids

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40
Q

How do volatiles, aminoglycosides (mycin antibiotics), and high doses of local anesthetics affect ND-NMBs?

A

Prolong the block

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41
Q

How does Phenytoin and other seizure meds affect ND-NMBs?

A

They decrease the duration of the block because of the increase in CYP450

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42
Q

How do ganglionic blockers such as trimethaphan affect ND-NMBs?

A

They delay onset and prolong the block

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43
Q

How do diuretics affect ND-NMBs?

A

Prolong the block

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44
Q

How do anti-dysrhythmics affect ND-NMBs?

A

Prolong block

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45
Q

How does hypothermia affect ND-NMBs?

A

Increases the duration because it slows hepatic enzymes

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46
Q

How does hypokalemia affect both succinylcholine and ND-NMBs?

A

It hyperpolarizes the cell so patients are resistant to succinylcholine and sensitive to ND-NMBs

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47
Q

How does hyperkalemia (burn patients) affect both succinylcholine and ND-NMBs?

A
  • Sensitive to succinylcholine

- Resistant to ND-NMB

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48
Q

If a patient has paresis on the right, where should you put the peripheral nerve stimulator?

A

Left

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49
Q

How does magnesium affect ND-NMBs?

A

Enhances the block because Mg2+ decreases Ach release

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50
Q

How will a large dose of ND-NMB given in combination succinylcholine affect the block?

A

The block will be prolonged

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51
Q

Maintenance dose of pancuronium

A

0.01mg/kg (same as vec)

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52
Q

Onset of pancuronium

A

3-5 minutes

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53
Q

Duration of pancuronium

A

60-90 minutes

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54
Q

Cardiovascular effects of pancuronium

A
  • Tachycardia
  • Increased MAP
  • Increased cardiac output
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55
Q

How is clearance of pancuronium affected in patients with renal failure?

A

Decreased up to 50%

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56
Q

Dose of atracurium

A

0.5mg/kg

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57
Q

Onset for intermediate acting NDNBMs (atra, cis, vec, roc)

A

2-5 minutes

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58
Q

Duration for intermediate acting NDNBMs (atra, cis, vec, roc)

A

20-45 minutes

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59
Q

Clearance of atracurium

A
  • Hoffmann elimination
  • Ester hydrolysis
  • Degraded at high pH
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60
Q

Side effects of atracurium

A

Histamine release and the subsequent drop in BP

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61
Q

Considerations for the pH of atracurium

A

The pH is 3.2 so do not mix with thiopental or it will crystallize

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62
Q

How does temperature affect atracurium

A

Hypothermia increases the duration of action because it decreases Hoffmann elimination

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63
Q

How does the dose of atracurium change in pediatrics?

A

Reduced by 50%

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64
Q

What is the metabolite of atracurium that can evoke seizures?

A

Laudanosine

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65
Q

Dose of cisatracurium

A

0.1-0.15mg/kg

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66
Q

Which NDNMB is great to use for ESRD and liver failure patients?

A

Cisatracurium because it is not metabolized by kidneys or liver

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67
Q

How is cisatracurium metabolized

A

Hoffman elimination

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68
Q

Maintenance dose of vecuronium

A

0.01mg/kg

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69
Q

Clearance of vecuronium

A

Excreted unchanged by the liver

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70
Q

How does the action of vecuronium change in pediatrics?

A

The onset is quicker and the duration is longer

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71
Q

How does the action of vecuronium change in elderly?

A

The duration is longer due to decreased liver/kidney blood flow

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72
Q

Intubating dose of rocuronium

A

0.6-1.2mg/kg

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73
Q

Maintenance dose of rocuronium

A

0.1mg/kg

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74
Q

What dose of roc must you use in order to mimic the onset time of succinylcholine?

A

1.2mg/kg

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75
Q

What is the only short acting NDNMB?

A

Mivacurium

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76
Q

Which NDNMBs should be considered in patients with renal and severe hepatic failure?

A
  • Mivacurium
  • Cisatracurium
  • Atracurium
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77
Q

Which NDNMB should be considered in extremely long cases?

A

Pancuronium

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78
Q

Which NDNMBs should be considered in patients with pseudocholinesterase deficiency?

A
  • Rocuronium

- Vecuronium

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79
Q

What allergy correlates with pseudocholinesterase deficiency?

A

Anectine

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80
Q

Anticholinesterase drug used to diagnose myasthenia gravis

A

Edrophonium

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81
Q

Anticholinesterase drug that crosses the blood/brain barrier and treats overdose of anticholinergics

A

Physostigmine

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82
Q

Anticholinesterase drug that is paired with atropine

A

Edrophonium

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83
Q

Anticholinesterase that is paired with glycopyrrolate

A

Neostigmine

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84
Q

Recovery from neuromuscular blocker results from what?

A

Elimination of the drugs from the body

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85
Q

Why can neostigmine prolong the block if you overdose it?

A

Because there is a ceiling effect of anti-cholinesterases on acetylcholinesterase

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86
Q

Which anticholinesterase reversibly inhibits AChase electrostatically?

A

Edrophonium

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87
Q

Which anticholinesterases inhibit AChase via the formation of carbamyl esters?

A
  • Neostigmine
  • Physostigmine
  • Pyridostigmine
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88
Q

Which anticholinesterase inhibits AChase via irreversible activation?

A

Echothiophate

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89
Q

Onset time of neostigmine for 50% antagonism of AChase

A

3 minutes

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90
Q

Onset time of neostigmine for 100% antagonism of AChase

A

7-11 minutes

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91
Q

Onset time of pyridostigmine for 100% antagonism of AChase

A

12 minutes

92
Q

What accounts for 50-75% of anticholinesterase elimination

A

Renal clearance

93
Q

How does a decrease in renal and hepatic blood flow affect neostigmine?

A

The effects of neostigmine are increased

94
Q

Pharmacologic effects of anticholinesterases

A
  • BLUDS
  • Increased intraocular pressure
  • Can be therapeutic for myasthenia gravis
95
Q

Treatment of anticholinesterase overdose

A
  • Atropine

- Pralidoxime

96
Q

Dose of neostigmine

A

0.04-0.07mg/kg

97
Q

How does neostigmine affect a phase 1 block from succinylcholine?

A

It potentiates the block because it inhibits acetylcholinesterase

98
Q

Post-op risk of neostigmine

A

PONV

99
Q

Onset of neostigmine

A

5-10 minutes

100
Q

Peak effect of neostigmine

A

10 minutes

101
Q

Duration of neostigmine

A

1 hour

102
Q

Which anticholinergics are very lipid soluble?

A
  • Atropine

- Scopolamine

103
Q

Which anticholinergics cause sedation?

A
  • Atropine

- Scopolamine

104
Q

Which anticholinergic is the strongest antisialagogue?

A

Scopolamine

105
Q

Which anticholinergic does not cross the blood/brain barrier?

A

Glycopyrrolate

106
Q

Duration of atropine and glycopyrrolate

A

30-60 minutes

107
Q

Clearance of anticholinergics

A

Excreted unchanged by the liver and kidneys

108
Q

With which patients should you use caution when considering using anticholinergics?

A
  • Glaucoma

- Pregnant

109
Q

Anticholinergic used as a pre-operative amnestic

A

Scopolamine

110
Q

IV dose of scopolamine

A

0.4mg

111
Q

Which anticholinergic is best for the treatment of bradycardia due to its quick onset?

A

Atropine

112
Q

How do anticholinergics affect the airways?

A

Cause bronchodilation in the medium/large airways, thus decreasing resistance and increasing deadspace

113
Q

What is Ipratropium?

A

An inhaled anticholinergic that works directly on the airways

114
Q

What is Combivent?

A

A combination of albuterol and ipratropium

115
Q

What are the symptoms of central anticholinergic syndrome?

A
  • Restlessness
  • Hallucinations
  • Somnolence
  • Unconsciousness
116
Q

What is the treatment for central anticholinergic syndrome?

A

Physostigmine

117
Q

What patients are at risk for central anticholinergic syndrome?

A
  • Elderly patients on glaucoma medication or with scope patches
  • Children
118
Q

What are the symptoms of an anticholinergic overdose?

A
  • Dry mouth
  • Blurred vision
  • Tachycardia
  • Increased temp
  • Flushing
  • Irritability
119
Q

For a safe extubation, the TOF ratio must be greater than…

A

0.7

120
Q

For a safe extubation, patients must produce a negative inspiratory pressure greater than…

A

20cmH2O

121
Q

On what nerves do we monitor neuromuscular blockade?

A
  • Ulnar
  • Posterior tibial
  • Peroneal
  • Facial
122
Q

How is residual paralysis from NMB defined?

A

A TOF less than 90% at adductor pollicis

123
Q

How is sugammadex cleared?

A

Renally

124
Q

How is sugammadex supplied?

A

100mg/ml

125
Q

Dose of sugammadex for 0/4 twitches and a PTC of 1-2

A

4mg/kg

126
Q

Dose of sugammadex for 2/4 twitches

A

2mg/kg

127
Q

Dose of sugammadex after an RSI dose of rocuronium

A

16mg/kg

128
Q

What are the side effects caused by sugammadex?

A
  • Bradycardia
  • Hypersensitivity
  • Prolonged PTT/PT
  • Decreased hormonal contraception effectiveness
129
Q

Onset of action of sugammadex

A

~3 minutes

130
Q

Contraindication to sugammadex

A

A prior hypersensitivity reaction to it

131
Q

Cellular membrane resting potential

A

-70mV

132
Q

Cellular membrane threshold potential

A

-55mV

133
Q

Method of action of local anesthetics

A

Bind to Na+ channels in the activated state to prevent achievement of threshold potential and decrease rate of depolarization

134
Q

Which nerve fibers are easier to block - small or large?

A

Small fibers

135
Q

Which nerves are easier to block - motor or sensory?

A

Sensory because they are smaller

136
Q

Which nerves are easier to block - myelinated or non-myelinated?

A

Myelinated

137
Q

How many nodes of Ranvier need to be blocked in order to stop the action potential?

A

2-3

138
Q

What makes nerve bundles difficult to block?

A

They are surrounded by sheath

139
Q

Which local anesthetic is most likely to cause cardiac arrest?

A

Bupivicaine

140
Q

What is the lipophilic group on local anesthetics?

A

Benzene ring

141
Q

What is the hydrophilic group on local anesthetics?

A

Tertiary amine

142
Q

What anesthetic class has an “i” before caine?

A

Amides

143
Q

How are amides metabolized?

A

Hepatically

144
Q

How are esters metabolized?

A

Plasma cholinesterases

145
Q

What is the only ester that has some hepatic metabolism?

A

Cocaine

146
Q

What determines the potency of local anesthetics?

A

Lipid solubility - the more lipid soluble, the more potent

147
Q

Which class of local anesthetics are more potent?

A

Esters

148
Q

What factors determine the onset of local anesthetics?

A
  • Lipid solubility

- pKa

149
Q

What can be added to local anesthetics to speed up their onset?

A

Sodium bicarb because it brings the solution closer to physiologic pH

150
Q

What parameter is the measurement of a local anesthetic’s local potency?

A

Cm (minimum concentration)

151
Q

What affects Cm of local anesthetics?

A

1) Fiber size
2) Type
3) Myelination
4) pH
5) Frequency of stimulation

152
Q

Are nerves that fire a lot easier or harder to block with local anesthetics?

A

Easier

153
Q

Are local anesthetics weak acids or bases?

A

Weak bases

154
Q

What affects the absorption of local anesthetics?

A
  • Dosage
  • Site of injection
  • Local blood flow
  • Vasoconstrictors
  • Drug-tissue binding
155
Q

Why is placental transfer of local anesthetics an issue?

A

When the baby gets stressed, they become acidotic so the local anesthetic shifts towards this acidic environment and becomes trapped in its ionized form

156
Q

What is the metabolite of ester anesthetics that patients may be allergic to?

A

PABA

157
Q

What other allergy may indicate that the patient has an allergy to PABA?

A

Sunscreen because there is PABA in it

158
Q

What 2 local anesthetics produce ortholuidine, the metabolite that causes methemoglobin?

A
  • Prilocaine

- Benzocaine

159
Q

What is the normal metHgB level?

A

Less than 1%

160
Q

What is methemoglobinemia?

A

There is a decrease in oxygen carrying capacity of hemoglobin due to the presence of increased methemoglobin

161
Q

What are the signs and symptoms of methemoglobinemia?

A
  • Sat 85%

- Dark brown blood

162
Q

What is the treatment for methemoglobinemia?

A

Methylene blue 1-2mg/kg

163
Q

How does the addition of vasoconstrictors affect the action of local anesthetics?

A
  • Increases duration of action
  • Limits systemic absorption
  • Maintains drug concentration at the nerve
  • Decreases possibility of systemic toxicity
164
Q

What is the common concentration of epi added to local anesthetics?

A

5mcg/ml (1:200,000)

165
Q

List the vascularity of local injection sites from most to least vascular (I Think I Can Pass Emory But School Sucks)

A

Intravenous > tracheal > intercostal > caudal > paracervical > epidural > brachial plexus > sciatic > subQ

166
Q

CNS symptoms of local anesthetic systemic toxicity

A
  • Circumoral numbness
  • Tinnitus
  • Restlessness
  • Slurred speech
  • Seizure
167
Q

CV symptoms of local anesthetic systemic toxicity

A
  • Hypotension
  • Decreased cardiac conduction
  • Ventricular arrhythmias
168
Q

What is the treatment for seizures assc. with local anesthetic systemic toxicity?

A

Benzodiazepines

169
Q

First sign of local anesthetic toxicity

A

Circumoral numbness

170
Q

Toxic dose of lidocaine without epi

A

5mg/kg

171
Q

Toxic dose of lidocaine with epi

A

7mg/kg

172
Q

Toxic dose of bupivicaine

A

2.5mg/kg

173
Q

Sequence of events for treatment of LAST (local anesthetic systemic toxicity)

A

1) Get help
2) 100% O2
3) Suppress seizures with benzos
4) Manage arrhythmias
5) Lipid emulsion therapy

174
Q

What cardiovascular drugs should be avoided when a patient is having arrhythmias due to LAST?

A

Any drug that interferes with the cardiac conduction system…vasopressin, calcium channel blockers, beta blockers

175
Q

What is the dose of IntraLipid to treat LAST?

A

1.5mg/kg bolus

176
Q

Infusion rate for intralipid

A

0.25ml/kg/min (~18mL/min)

177
Q

What is the recommended upper limit for IntraLipid administration for LAST?

A

10mL/kg over the first 30 minutes

178
Q

What receptors does cocaine block?

A
  • Na+ receptors
  • Alpha 2
  • Dopamine
179
Q

How does cocaine affect NE and DA levels?

A

Increases NE and DA levels by blocking their reuptake

180
Q

What are the most common clinical uses for cocaine?

A

ENT surgeries

181
Q

Peak effect of cocaine

A

30 minutes

182
Q

Cocaine metabolism

A

Liver

183
Q

Adverse effects of cocaine

A
  • HTN
  • Arrhythmias
  • Catecholamine surge
  • Increased O2 demand on the heart
184
Q

How do you treat cocaine toxicity?

A

Supportive therapy of vitals with beta blockers and NTG

185
Q

Duration of a spinal with 5% lidocaine

A

~1.5 hours

186
Q

Duration of a spinal with 0.5% bupivicaine

A

2-2.5 hours

187
Q

Duration of a spinal with 1% tetracaine without epi

A

2-3 hours

188
Q

Duration of a spinal with 1% tetracaine with epi

A

up to 5 hours

189
Q

Which local anesthetic is mainly used in obstetrics because it maintains motor function?

A

Ropivicaine

190
Q

What dose and local anesthetic is commonly used for bier blocks?

A

50cc 5% lidocaine or prilocaine

191
Q

Which local anesthetics are used for topical anesthesia?

A
  • Tetracaine
  • Cocaine
  • Lidocaine w/ oxymetazoline
192
Q

What local anesthetic is in hurricaine spray?

A

20% benzocaine

193
Q

What is EMLA?

A

Eutectic mixture of local anesthetic - a local anesthetic cream that “melts” into the skin

194
Q

What local anesthetics are usually found in EMLA?

A

Lidocaine/prilocaine combo

195
Q

Onset of EMLA cream

A

1 hour

196
Q

Contraindications to EMLA

A
  • Non-intact skin

- Skin less than a month old

197
Q

Dose of EMLA

A

1-2g

198
Q

What can occur during retrobulbar blocks due to the inadvertent administration of local anesthetic into the CSF? What are the symptoms?

A

Brain stem anesthesia - the patient becomes unresponsive and apneic, with hypotension and bradycardia

199
Q

What type of drug is Azathioprine? What is it commonly used to treat?

A

Immunosuppressive agent commonly used to treat rheumatoid arthritis

200
Q

What is Piperacillin-Tazobectam (Zosyn)?

A

PCN class antibiotic effective against gram-negative bacteria

201
Q

Typical allergic reaction to paper tape

A

Contact dermatitis

202
Q

What is Irbesartan? What is it used for?

A

Angiotensin II Receptor Antagonist used to treat hypertension

203
Q

What drug class is Pyridostigmine?

A

Anticholinesterase

204
Q

What is Pyridostigmine used to treat?

A
  • Myasthenia gravis

- Muscle weakness

205
Q

What is myasthenia gravis?

A

Chronic autoimmune disorder caused by a decrease in functional Ach receptors that causes weakness and rapid exhaustion of voluntary muscles

206
Q

Anesthetic considerations of a patient with myasthenia gravis

A
  • Continue myasthenia gravis meds
  • Chance of postop ventilation
  • Resistant to succinylcholine
  • Sensitive to non-depolarizers
  • Potential for phase II block
207
Q

How will a patient with myasthenia gravis react to muscle relaxants if they are on Pyridostigmine?

A
  • Increased sensitivity to nondepolarizers

- Prolonged response to succinylcholine

208
Q

What is the preferred relaxant for a patient with myasthenia gravis?

A

Cisatracurium

209
Q

The initial muscle relaxant dose should be titrated to what?

A

The initial response of the peripheral nerve stimulator

210
Q

Oral dose of morphine

A

30mg q3-4hr

211
Q

Parenteral dose of morphine

A

10mg q3-4hr

212
Q

What drug class is Aspirin in?

A

NSAID

213
Q

Method of action of Aspirin

A

COX1 inhibitor

214
Q

Drug class of Prednisone

A

Adrenocortical steroid for short term use (~1 week)

215
Q

What is the recommendation for when to give a a stress dose of steroids?

A

If the patient has been on a glucocorticoid in the last year

216
Q

Recommended stress dose of hydrocortisone for a major surgery like a colectomy for a 70kg patient

A

100-150mg

217
Q

Recommended stress dose of hydrocortisone for a minor surgery like a herniorrhapy for a 70kg patient

A

25-100mg

218
Q

What nerve should you use to monitor neuromuscular blockade in patients with myasthenia gravis?

A

Temporal branch of the facial nerve to stimulate the orbicularis oculi because it is more sensitive than the ulnar in MG patients

219
Q

List anticholinergics in order of fastest to slowest onset

A

Edrophonium (fastest) –> neostigmine –> pyridostigmine (slowest)

220
Q

Neuromuscular blocker that causes histamine release

A

Atracurium

221
Q

Local anesthetic used mainly in ENT surgeries

A

Cocaine

222
Q

Norepi release is regulated by what receptor

A

Alpha 2

223
Q

How should the dose of succinylcholine be altered if your patient has myasthenia gravis

A

Increase the dose

224
Q

Drug class used to treat myasthenia gravis

A

Anticholinesterase (specifically pyridostigmine)

225
Q

What drugs are combined to make percodan?

A

Oxycodone + aspirin

226
Q

EMLA definition

A

Eutectic mixture of local anesthetics

227
Q

EMLA components

A

Lidocaine + Prilocaine

Pharmacology (6 decks)

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