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2 Review Course > Pharmacology 2 > Flashcards

Pharmacology 2 Flashcards

1
Q

The ability of LA’s to block the conduction of nerve fibers depends on what three factors?

A

the nerves being blocked, chemical structure, and physiochemical properties of the LA

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2
Q

What is the functional unit of peripheral nerves?

A

axon

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3
Q

What is the function of Schwann cells?

A

support and insulate axons

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4
Q

What are nodes of Ranvier?

A

segments of axon that do not contain myelin, where conduction is propagated.

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5
Q

What is the primary site of action of LA’s and where are they located?

A

Na channels, in the nodes of ranvier.

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6
Q

What is saltatory conduction?

A

action potentials jumping between nodes of Ranvier

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7
Q

Describe the difference myelin makes in nerve conduction.

A

Myelinated nerves are larger, conduct impulses faster, and are more difficult to block.

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8
Q

What are the three layers of connective tissue of nerves?

A

Epineurium - outer
perineurium
endometrium - inner

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9
Q

Which connective tissue layer holds fascicles together to form a peripheral nerve?

A

epineurium

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10
Q

What is the resting membrane potential of peripheral nerves?

A

-70 to -90mV

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11
Q

What is the primary mechanism that creates the ionic gradient for electrical potential?

A

Na-K/ATPase

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12
Q

What equation expresses the charge created by the K concentration gradient?

A

Nernst

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13
Q

Besides K, what ions have a minor role in establishing intracellular resting membrane potential?

A

Na and Cl

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14
Q

What happens to membrane potential when an electrical impulse is generated?

A

Na channels open, and membrane potential reaches +20 mV then the concentration reverses. Na channels close, K channels open. Na is removed by the NaK/ATPase (3 Na out, 2 K in)

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15
Q

What state of Na channels do LA’s bind?

A

Open and inactive.

Not the closed state.

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16
Q

What is the guarded receptor or modulated receptor hypothesis of LA’s?

A

LA’s preferentially bind to Na channels when they are in the resting or open states.

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17
Q

What is a use-dependent or phasic block?

A

LA’s work faster as the Na channels is repetitively depolarized.
The more frequently the channel is stimulated the more time it is in the open or resting state.

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18
Q

Where are the Na channel binding sites for LA’s located?

A

internal opening

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19
Q

Is the ionized or nonionized portion of a LA more likely to bind to Na channels?

A

ionized

The nonionized portion crosses the cell membrane, but the ionized portion actually binds the Na channels

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20
Q

Which LA can penetrate the lipid bilayer and can directly inhibit the Na channel without entering the axoplasm first?

A

Benzocaine (secondary amine)

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21
Q

What is the order of differential block?

A 
autonomic function - first
superficial pain perception
temperature
motor function
proprioception
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22
Q

What are characteristics and function of A-alpha fibers?

A

largest diameter (12-20)
heavily myelinated
fast conduction
motor function and proprioception

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23
Q

What are characteristics and function of A-beta fibers?

A

diameter 5-12
myelinated
motor function, touch and pressure

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24
Q

What are characteristics and function of A-gamma fibers?

A

diameter 3-6
myelinated
muscle spindles and reflexes

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25
Q

What are characteristics and function of A-delta fibers?

A

diameter 1-5
myelinated
slowest conduction of the A fibers
pain and temperature sensation

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26
Q

What are characteristics and function of B fibers?

A

smaller diameter and less myelin than A fibers.

preganglionic autonomic nerves

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27
Q

What are characteristics and function of C fibers?

A

smallest diameter 0.3-1.3
slowest conduction
pain and temperature

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28
Q

What is the ratio between the magnitude of the action potential and the magnitude of the critical membrane potential?

A

safety factor or conduction safety

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29
Q

What are the two type of LA’s used in clinical practice?

A

aminoesters

aminoamides

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30
Q

What are the three characteristic segments of LAs?

A

intermediate ester or amide carbon group
unsaturated aromatic ring
amine end

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31
Q

What parts of LA structure are hydrophilic and lipophilic?

A

lipophilic benzene ring

hydrophilic amine

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32
Q

Name the LA.

A
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33
Q

How are ester LAs metabolized?

A

plasma and tissue cholinesterase via hydrolysis

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34
Q

How are amide LAs metabolized?

A

liver by CYP1A2 and CYP3A4

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35
Q

Which class of LA is more likely to cause an allergic reaction?

A

ester

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36
Q

Which class of LAs tend to be shorter acting?

A

esters due to metabolism. Tetracaine is the exception

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37
Q

What is the mechanism for amide LAs being longer acting?

A

more lipophilic and protein bound and require transport to the liver for metabolism

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38
Q

What determines offset and termination of LAs effect?

A

systemic absorption

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39
Q

What factors have a significant impact on LA duration of action?

A

vascularity and blood flow of injection area, lipid and protein binding, and vasoconstrictors

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40
Q

What determines local anesthetic potency?

A

lipid solubility

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41
Q

What does increased lipid solubility correlate to?

A

increased protein binding, increased potency, longer DOA, higher tendency for cardiac toxicity

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42
Q

The addition of a butyl group to the amide end of mepivicaine yields what LA?

A

bupivicaine

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43
Q

The addition of a butyl group to the aromatic end of procaine yields what LA?

A

tetracaine

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44
Q

What determines a LAs duration of action?

A

protein binding and lipid solubility

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45
Q

What proteins do LAs mainly bind?

A

alpha1-acid glycoprotein. They are weak bases

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46
Q

What is the most important determinant of LAs onset of action?

A

ionization.

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47
Q

Do LAs with a pKa closer to physiologic pH have a slower or faster onset?

A

Faster, the nonionized fraction will be a higher.

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48
Q

Despite its high pKA which LA has a rapid onset of action? Why is this?

A

Chloroprocaine, due to high concentrations injected

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49
Q

Which two LAs have low potency and short DOA?

A

procaine and chloroprocaine

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50
Q

Which two LAs have intermediate potency and DOA?

A

mepivicaine and lidocaine

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51
Q

Which 3 LAs have high potency and long DOA?

A

tetracaine, bupivicaine, and ropivicaine

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52
Q

Which LAs do not produce relaxation of vascular smooth muscle? 3

A

cocaine, ropivicaine, and lidocaine

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53
Q

What are the consequences of LAs causing vasodilation?

A

increased absorption, limits DOA, increase potential for toxicity

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54
Q

What is the mechanism of cocaine causing vasoconstriction?

A

it blocks reuptake of NE

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55
Q

What is the order of tissue absorption from greatest to least?

A

interpleural > intercostal > caudal > epidural > brachial plexus > sciatic femoral > subcutaneous

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56
Q

What determines the peak plasma concentration of a LA?

A

total dose

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57
Q

The addition of epinephrine to what two LAs for epidural does not decrease peak plasma levels?

A

prilocaine and bupivicaine

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58
Q

What is the concentration of epi added to LAs?

A

1:200,000 or 5mcg/mL

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59
Q

How does the addition of sodium bicarbonate affect LA?

A

speeds onset of sensory and motor block

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60
Q

How does the addition of hyaluronidase affect LAs?

A

facilitates diffusion of LA in the tissues

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61
Q

What are the undesirable effects of adding hyaluronidase to LAs?

A

allergic reactions, shortened DOA, increased risk of toxicity

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62
Q

What tissue group receives the greatest amount of LA from redistribution?

A

muscle

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63
Q

How are ester LAs metabolized?

A

plasma cholinesterase

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64
Q

How are amide LAs metabolized?

A

in the liver by P450 enzymes mainly 1A2 and 3A4

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65
Q

What is the primary factor that determines the elimination of amide LAs?

A

hepatic blood flow

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66
Q

What are the most common causes of LAST?

A

IV injection or absorption from large volumes injected into vascular tissues

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67
Q

Are inhibitory or excitatory neurons blocked first in LAST?

A

inhibitory - mechanism of seizure (lack of inhibition of excitatory neurons)

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68
Q

What is the first observed arrhythmia of LAST and the most serious?

A

Bradycardia

V-fib

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69
Q

Most reported deaths from LAST are involve which LA?

A

Bupivicaine

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70
Q

What is the progression of symptoms in last?

A

agitation, tinnitus, circumoral numbness, blurred vision, metallic taste, muscle twitching, coma and seizures, cardiac and respiratory arrest

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71
Q

What are the preferred medications for seizure suppression in LAST?

A

benzos

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72
Q

What is the treatment of LAST?

A

20% lipid emulsion 1.5mL/kg over 1 minute

infusion 0.25mL/kg

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73
Q

What medications are avoided in treating LAST?

A

vasopressin, CCBs, B-blockers

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74
Q

What are essential first steps in managing LAST?

A

avoid hypoxia and acidosis

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75
Q

Which class of LAs has the higher incidence of allergic reactions? Why?

A 
Esters
Metabolite PABA (para-aminobenzoic acids)
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76
Q

What preservatives of LAs can cause allergic reactions?

A

methylparaben, paraben, metabisulfite

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77
Q

What is methemoglobin?

A

oxidized form of hemoglobin with reduced O2 carrying capacity. Causes Left shift of oxygen-Hgb response curve

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78
Q

What is the formula for methemoglobin?

A

HbFe3OH

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79
Q

What are clinical symptoms of methemoglobinemia?

A

hypoxia unresponsive to increased O2
abnormal colored blood
Normal PaO2, with low SpO2
Cyanosis

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80
Q

Which local anesthetics are most likely to cause MetHgb?

A

benzocaine and prilocaine

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81
Q

What is the mechanism of Prilocaine causing MetHgb?

A

metabolite o-toulidine oxidizes Hgb to MetHgb

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82
Q

What is the treatment for MetHgb?

A

Methylene Blue 1-2mg/kg over 3-10 minutes

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83
Q

What complication of LA’s presents as bowel and bladder dysfunction, bilateral LE weakness and sensory impairment?

A

Cauda equina syndrome

84
Q

What is the only naturally occurring LA?

A

cocaine

85
Q

What is the maximum dose of cocaine?

A

5mL of 4% or 200mg

86
Q

What is the onset and duration of EMLA cream?

A

1 hour onset

2-3 hour duration

87
Q

What are the concentrations of Tetracaine, Epinephrine and Cocaine used for traumatic lacerations?

A

Tetracaine: 1%
Epi: 1:200,000
Cocaine: 4%

88
Q

What is the maximum dose of exparel?

A

266mg

89
Q

What makes up tumescent local anesthesia?

A

lidocaine, sodium bicarb and epinephrine

90
Q

What is the maximum dose of lido for tumescent anesthesia?

A

35-55mg/kg

91
Q

Where are supraspinal opioid receptors primarily located?

A

midbrain and medulla

92
Q

Spinal anesthesia occurs by activation of what receptors?

A

presynaptic opioid receptors

93
Q

What are the cellular mechanisms of opioids?

A

activation of G-proteins, decrease adenylate cyclase, decrease cAMP, decease pre- and postsynaptic Ca conduction, increase K conduction

94
Q

What are the effects of Mu receptors?

A

supraspinal analgesia, euphoria, decreased ventilation

95
Q

What are the effects of kappa receptor stimulation?

A

spinal anesthesia, sedation and miosis

96
Q

What are the effects of delta receptor stimulation?

A

spinal analgesia, response to enkephalins, and modulate mu receptors

97
Q

How does dose of opioids effect their termination?

A

small doses- effect is terminated by redistribution

large doses- effect is terminated by metabolism

98
Q

Which opioid metabolite is neurotoxic and may accumulate in the elderly or those with decreased liver or kidney function?

A

meperidine - normeperidine

99
Q

How are opioids excreted?

A

primarily by the kidney

secondarily by the billiard system and GI tract

100
Q

What type of pain are opioids most effective for?

A

visceral continuous dull pain

101
Q

Where do the analgesic properties of opioids come from? 2

A
  1. directly inhibit ascending transmission of pain signals from the dorsal horn
  2. activate pain control pathways descending from the midbrain to the dorsal horn
102
Q

How do opioids increase ICP?

A

from respiratory depression induced hypercarbia

103
Q

Rank the potency of opioids used in anesthesia?

A

Sufent > fent = remi > alfent

104
Q

Which opioid receptor is most likely to cause dysphoria?

A

kappa receptors

105
Q

opioid agonists at what receptors are more likely to cause respiratory depression>

A

Mu and kappa

106
Q

How do opioids effect the CO2 response curve?

A

right shift. Require a higher CO2 to stimulate repirations

107
Q

How do opioids stimulate N/V?

A

stimulate the chemoreceptor trigger zone, and vestibular system.

108
Q

What are the cardiac effects of opioids?

A

bradycardia from vagal stimulation

vasodilation

109
Q

Which opioids cause histamine release leading to HoTN?

A

morphine, meperidine, and codeine

110
Q

What are the GU effects of opioids?

A

detrusor muscle relaxation, urinary spincter contraction -> urinary retention.
Kappa receptor agonist cause diuresis.

111
Q

Skeletal muscle rigidity is most often caused by what opioids?

A

Fentanyl and its derivatives

especially Remi infusions

112
Q

opioid induced muscle rigidity is mediated by what receptors?

A

central mu

113
Q

Stimulation of what opioid receptors cause pruritis?

A

Mu

114
Q

What medication is considered first line treatment of opioid induced pruritis?

A

nalbuphine

115
Q

What are the endocrine effects of opioids?

A

release of vasopressin

inhibition of corticotropin, gonadotropin, and thyrotropin

116
Q

What are the most common side effects of spinal administration of opioids?

A

pruritis and urinary retention

117
Q

What is the most common serious complication of intrathecally administered opioids?

A

respiratory depression

118
Q

Which intrathecally administered opioid has the longest duration of action?

A

morphine`

119
Q

What are the uses of methadone?

A

chronic pain, opioid abstinence syndromes, heroin addiction

120
Q

What receptors is meperidine an agonist at?

A

mu

121
Q

What is the metabolite of meperidine and its effects?

A

normeperidine - decreases the seizure threshold

122
Q

Which opioid can induce serotonin syndrome if combined with MAOIs?

A

meperidine

123
Q

Which opioid reduces shivering? What receptor does it act on?

A

Meperidine. Kappa

124
Q

How is alfentanil metabolized?

A

N-dealkylation and O-demethylation by P450

125
Q

Which medication can prolong the metabolism of alfentanil leading to respiratory depression and sedation?

A

erythromycin

126
Q

How is fentanyl cleared and metabolized?

A

cleared by hepatic blood flow

metabolized by N-dealkylation and hydroxylation

127
Q

Which phenylpiperidine opioid is the most potent?

A

sufentanil

128
Q

Which receptors is sufentanil an agonist at?

A

Mu

129
Q

How is sufentanil metabolized?

A

O-demethylation and N-dealkylation

130
Q

Sufentanil causes the most respiratory depression in which age group? Why?

A

elderly. smaller Vd

131
Q

How does tramadol exert its effects?

A

mu agonist
inhibits NE and serotonin
stimulates 5-hydroxytryptamine release

132
Q

What are the three opioid agonist/antagonists (partial agonists)?

A

Buprenorphine, Nalbuphine, Butorphanol

133
Q

What do you need to know about buprenorphine?

A

mu agonist
long DOA = 8 hours
naloxone not effective
significant respiratory depression

134
Q

What do you need to know about Butorphanol?

A

Kappa agonist, mu antagonist
more potent than morphine
can be given intranasal
treats shivering

135
Q

What do you need to know about Nalbuphine?

A

Kappa agonist, Mu antagonist
reverse respiratory depression but maintain analgesia
Naloxone ineffective
antagonist pruritis

136
Q

What are the three opioid antagonists?

A

naltrexone, naloxone, nalmefene

137
Q

What is the MOA of naloxone?

A

blocks the opioid receptors and reverses respiratory depression and opioid analgesia

138
Q

What are the potential side effects of naloxone?

A

pulmonary edema and increased catecholamine release leading to V-Fib

139
Q

What do you need to know about nalmefene?

A

half life 10 hours
DOA 8 hours
dose is 0.1-0.5 mcg/kg
not for opioid dependent patients

140
Q

What do you need to know about naltrexone?

A

longest DOA - 24 hours
used in alcohol withdrawal programs
prevents euphoric effects of opioids
active metabolite half life exceeds that of the parent compound

141
Q

What enzymes do NSAIDs and acetaminophen inhibit?

A

cyclooxygenase

142
Q

What are the beneficial effects of NSAIDs and acetaminophen?

A

NSAIDs: analgesic, antipyretic, anti-inflammatory
Acetaminophen: analgesic, antipyretic

143
Q

In which patients is toradol avoided?

A

asthma, elderly, renal or GI dysfunction, bleeding disorders

144
Q

What is the dose of acetaminophen in children?

A

15mg/kg

145
Q

What is the preferred method to determine neuromuscular blockade?

A

quantitative method with a numerical value

MMG, AMG, KMG, EMG

146
Q

What is the preferred site for determining the level of neuromuscular blockade?

A

adductor muscle of the thumb via the ulnar nerve

147
Q

What brach of the facial nerve is stimulated to assess NMB’s? What are the muscles stimulated?

A 
temporal.
Corrugator supercilii (eyebrow)
Orbicularis oculi (around the eye)
148
Q

What is the order of NMB onset and recovery?

A

Eye muscles, then extremities, neck and chest trunk muscles, abdominal muscles, diaphragm.
Recovery is opposite

149
Q

Which muscle of the eye is more resistant to NMB?

A

corrugated supercilii

150
Q

Describe single twitch monitor.

A

0.1-1Hz for 0.1-0.2 milliseconds.
muscle movement = not 100% paralyzed
no movement = 100% paralyzed

151
Q

Describe TOF monitor.

A

4 stimuli every 0.5 seconds at 2 Hz for 2 seconds

152
Q

How much paralysis occurs with each amount of twitches?

A

0/4: 100%
1/4: 90-95%
2/4: 80-85%
3/4: 75-80%

153
Q

What is the ideal degree of paralysis for surgery?

A

1 or 2 twitches (85-90% block)

154
Q

Describe Double burst stimulation

A

two short bursts of 50 Hz tetanus separated by 0.75 seconds.

155
Q

Describe tetanus?

A

continuous stimulation for 5 seconds at 50 or 100Hz

156
Q

Describe post-titanic count.

A

50 Hz for 5 seconds, wait 3 seconds, then a series of single 1 Hz twitch stimulations

157
Q

What is the ED95 of succinylcholine?

A

0.3 mg/kg

158
Q

How does NMB potency affect speed of onset?

A

Lower the potency the faster the speed of onset

159
Q

How do patients with atypical pseudocholinesterase respond to succinylcholine?

A

prolonged response

160
Q

For Succinylcholine what is the:
half life:
DOA:
full recovery:

A

half life: 2-4 min
DOA: 5-10 min
full recovery: 12-15 min

161
Q

How is succ metabolized?

A

By pseudocholinesterase into succinylmonocholine and choline

162
Q

How does succ affect ICP?

A

increases by 10-15 for 5-8 minutes.

Prevented with a nondepolarizer

163
Q

What medications should be given before a second dose of succ?

A

Atropine or Glyco

164
Q

A second dose of succ is most likely to cause bradycardia in which patient population?

A

peds

165
Q

Which of the following are “nonspecific esterases”?

A

paraoxonase and albumin esterase

166
Q

What are all the names for AchE?

A 
"The 1 and True Specific Genie"
Type 1
True
Specific
Genuine
167
Q

What are all the names for pseudocholinesterase?

A

“The 2nd But False Plasma Princess”
Type 2, Butylcholinesterase, False, Plasma, Pseudocholinesterase

Serum, benzoyl, nonspecific

168
Q

What populations is PChe decreased in?

A

Pregnant, newborns, infections, PE, muscular dystrophy, MI

169
Q

What type of PChE does dibucaine inhibit?

A

typical or usual PChE

Not atypical

170
Q

What drugs may inhibit Cholinesterase?

A

Donepezil, Rivastigmine, Galantamine

171
Q

What is the dose of Succ for obese patients?

A

1mg/kg based on TBW

172
Q

How does succ affect IOP?

A

increases by 5-15 mmHg for 10 minutes.

Airway is the priority, seeing is overrated

173
Q

What situations cause an up regulation of AChR’s?

A

upper/lower motor neuron denervation, infection, muscle trauma, muscle tumor, muscle inflammation, burns, immobilization, chemical denervation

174
Q

Succ is safe within what time period after a burn?

A

48 hours

175
Q

Where are succ induced myalgias most likely to occur?

A

subcostal region, trunk, neck, upper abs, shoulders

176
Q

What does of nondepolarizers reduce the incidence of myalgias and fasciculations?

A

10-30% of ED95

177
Q

How can we prevent fasciculations?

A

Lidocaine, NSAIDS, higher dose of Succ

178
Q

Who is most prone to fasciculations?

A

young, physically inactive women

179
Q

What populations have the lowest incidence of myalgias?

A

extremes of age, pregnant

180
Q

What are the doses of vec, roc, and Atracurium to prevent fasciculations?

A

0.04mg/kg Roc, 1.5mg Atracurium, 0.3mg Vec

181
Q

What dose of Succ causes a phase 2 block?

A

6-8mg/kg

182
Q

What is the preferred nondepolarizer for RSI?

A

Roc

183
Q

What is the relationship between NDNMB potency and onset?

A

inverse.

The lower the potency the faster the onset

184
Q

Giving 10% of the intubating dose of a NDNMB prior to induction is referred to as what?

A

priming. It speeds the onset but produces respiratory depression in some patients

185
Q

What is the dose, onset, DOA, and elimination of Roc?

A

Dose: 0.6-1.2mg/kg
Onset: 45-90 seconds
DOA: 30-60 minutes
Elimination: biliary excretion unchanged

186
Q

What is the dose, onset, DOA, and elimination of Vec?

A

Dose: 0.1mg/kg
Onset: 3 minutes
DOA: 30-45 minutes
Elimination: Liver and kidney

187
Q

What is the dose, onset, DOA, and elimination of Pancuronium?

A

Dose: ED95 0.14mg
Onset: 4 minutes
DOA: 60-90 minutes
elimination: kidneys,

188
Q

What is the dose, onset, DOA, elimination, and metabolite of Atracurium?

A 
Dose: 0.1-0.25mg/kg
Onset: 1-3 minutes
DOA: 30-60 minutes
elimination: Hoffman
Metabolite: laudanosine
Histamine release
189
Q

What is the dose, onset, DOA, elimination, and metabolite of Cisacurium?

A 
Dose: 0.1mg/kg
Onset: 2-4 minutes
DOA: 30-60 minutes
elimination: Hoffman
Metabolite: laudanosine
190
Q

What is the dose, onset, DOA, elimination, and metabolite of Mivacurium?

A

Dose: 0.08mg/kg
Onset: 2-4 minutes
DOA: 15-20 minutes
elimination: plasma cholinesterase

191
Q

What are the CV effects of Atracurium and mivacurium? What causes this?

A

increased HR and decreased BP

Histamine release

192
Q

Which NMB has vagolytic properties?

A

Pancuronium

193
Q

What NMB’s are preferred for patients with liver and kidney disease?

A

Atracurium and Cisatracurium

194
Q

How should you dose NMB’s for obese?

A

Ideal body weight

195
Q

How does core temperature affect DOA of NMB’s?

A

hypothermia prolongs DOA

196
Q

What two categories of drugs are most likely to cause allergic reactions/

A

Antibiotics and NMB’s

197
Q

What are the main components of the allergic sites on NMB’s?

A

quaternary and tertiary ammonium ions

198
Q

Which of the cholinesterase inhibitors is used to treat myasthenia gravis, and rarely used in anesthesia?

A

Pyridostigmine

199
Q

What is the gold standard type of monitoring to determine residual paralysis?

A

Quantitative

200
Q

What is the most rapid acting cholinesterase inhibitor?

A

edrophonium. 30-60 seconds, DOA 5-10 minutes. Renal elimination

201
Q

Neostigmine

A

Onset 4-8 minutes
DOA 30-120 minutes
Liver and Kidney metabolism

202
Q

What are the vagal effects seen if you only give a cholinesterase inhibitor?

A

Diarrhea, Urination, Miosis, Bradycardia, Bronchoconstriction, Emesis, Lacrimation, Laxation, Salivation

203
Q

Which anticholinergics are tertiary amines?

A

Atropine and scopolamine

204
Q

What are adverse reactions to sugammadex?

A

N/V, allergy, HTN, bradycardia

205
Q

What increases potency of LAs?

A

increasing lipid solubility, increased carbon atoms, adding a halide to the aromatic ring, an ester linkage, or the presence of large alkyl groups on the tertiary amide nitrogen.

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