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Pharmacology > Pain Management and Local Anesthetics - Quiz 4 > Flashcards

Pain Management and Local Anesthetics - Quiz 4 Flashcards

1
Q

How is meperidine classified?

A

Synthetic opioid agonist at mu and kappa receptors

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2
Q

Meperidine is structurally related to

A

the fentanyls and atropine

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3
Q

Why has Meperidine fallen out of favor?

A

From all the side effects, particularly neuro

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4
Q

How is meperidine metabolized

A

Extensive hepatic metabolism (90%)

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5
Q

Meperidine is broken down into 2 different metabolites, what is the first metabolite?

A

Initial demethylation to normeperidine

  • Active metabolite
  • Becomes a problem in ppl with renal dysfunction
  • Seizure, confusion, agitation
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6
Q

Meperidine is broken down into 2 different metabolites, what is the second metabolite?

A

Second breakdown to meperidinic acid

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7
Q

How are the 2 metabolites from meperidine excreted?

A

Primarily excreted by the kidneys

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8
Q

What is the elimination half time of meperidine

A

3-5 hours

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9
Q

What percentage of meperidine is bound to protein

A

60%

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10
Q

How potent is meperidines first metabolite, normeperidine

A

One half the analgesic properties of meperidine

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11
Q

How long is the elimination half time of normeperidine

A

Elimination half-time is 15 hours

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12
Q

How long is the elimination half time of normeperidine in patients with renal failure?

A

> 35 hours

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13
Q

Normeperidine produces CNS stimulation, what is some of the toxic side effects?

A

Seizures, myoclonus, agitation, hallucinations

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14
Q

What are the cardiac side effects of meperidine?

A
  1. Interferes with compensatory SNS reflexes
  2. therapeutic doses is associated with orthostatic hypotension
  3. May increase heart rate (reflection of its atropine like qualities)
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15
Q

What are the respiratory side effects of meperidine?

A

respiratory depression

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16
Q

Meperidine taken with an SSRI can cause what?

A

Serotonin Syndrome

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17
Q

Serotonin syndrome has a low risk of occurrence, but when it does, what is the main symptoms you will see?

A

First you will see accelerated HTN

then tachycardia, diaphoresis, hyperreflexia

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18
Q

What does meperidine cause post up? and at what dosage?

A

Post-op shivering

12.5-25 mg

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19
Q

Will one time dose of meperidine build up an active metabolite?

A

no

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20
Q

When doing medication equivalents, what is everything based off of?

A

Morphine

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21
Q

What is the MOA of methadone?

A

Mu agonist with NMDA antagonism

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22
Q

How is methadone eliminated?

A

renal and fecal

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23
Q

What is significant about the variable half life of methadone?

A

has the ability to last 8-60 hours, difficult to pull equivalence to other medications, can build up and accumulate – increase resp depression and death

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24
Q

What is significant about the EKG and methadone?

A

QT prolongation, which can lead to tornadoes

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25
Q

Why were opioid agonist, antagonist created?

A

Created in response to overage of resp depression and deaths from pure opiate agonist

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26
Q

Where do opioid agonist-antagonist work?

A

at the Mu receptor

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27
Q

Does the agonist/antagonist opioids have more or less affinity?

A

Affinity is LESS than a pure agonist

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28
Q

What happens if you increase the dose of an opioid agonist/antagonist?

A

You reach a ceiling effect, increasing the dose does not produce an additional response

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29
Q

Opioid agonist/antagonist produce analgesia with little effect on what?

A

with limited depression of ventilation

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30
Q

Agonist /antagonist drugs should be reserved for patients who

A

cannot tolerate pure agonist.

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31
Q

Cross tolerance can happen between

A

all opioids

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32
Q

What is cross tolerance

A

You can switch opioid medication but you will still have a tolerance to its medication equivalence. Just a new agonist is hitting the receptor.

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33
Q

Can tolerance occur without dependacne?

A

yes

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34
Q

Can dependance occur without tolerance?

A

no, this is addiction

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35
Q

When are you considered opioid tolerant?

A

if you are using more than 60 mg morphine or equivalent per week

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36
Q

What is one way to combat cross tolerance to opioids?

A

to add adjunct medication – Tylenol, lyrica, Neurontin, clonidine

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37
Q

Minor changes in the structure of an opioid agonist convert the drug into an opioid antagonist, Naloxone is the N-alkyl derivative of

A

oxymorphone

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38
Q

Opioid antagonist are which type of antagonism?

A

Competitive antagonism – fighting for mu receptors (hopefully antagonist kicks off agonist)

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39
Q

After displacement from the Mu receptor, does binding of the pure antagonist activate the mu receptor?

A

No

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40
Q

Do opioid antagonist have a high or low affinity for the receptor

A

high affinity

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41
Q

Naloxone is a ________ antagonist, having effects at all 3 receptors (gamma, kappa, mu)

A

nonselective

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42
Q

What is naloxone used for?

A

Treatment of Opioid-induced depression of ventilation post-op and overdoses

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43
Q

How fast does naloxone produce reversal effects in IV vs nasal spray?

A

IV - under 1 minute

Nasal spray - under 2 minutes

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44
Q

What is the duration of action of naloxone and what does this mean?

A

30-45 minutes? may need to re-dose, opioid effects of opioid will last longer than naloxone

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45
Q

How is naloxone metabolized?

A

hepatic ally

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46
Q

What are the side effects of naloxone?

A

Very CV stimulating - tachycardia, HTN

N/V

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47
Q

Why do you need to be careful when reversing a potential overdose on someone who is a chronic opioid user?

A

risk of putting them into withdrawal. What is worse? - withdrawal symptoms or overdose (can we put them on a vent for now?) both can be fatal

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48
Q

Where are the neuraxil opioid receptors located that allow placement of opioids in epidural or subarachnoid space?

A

opioid receptors (mu) are present in the substantia gelatinosa of the spinal cord

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49
Q

What happens if you inject a highly lipophilic medication into a epidural space?

A

Its going to move right out of epidural tissue into general circulation, just as if you gave it IM/IV

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50
Q

CSF concentration of fentanyl will peak ___ minutes after epidural administration of fentanyl.

A

20

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51
Q

Epidural administration of opioid produces blood/plasma concentrations that are ______ to IM administration of drug at equivalent dose.

A

similar

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52
Q

Why would you add Epi to a neuraxail opioid epidural?

A

causes vasoconstriction, making blood vessels smaller, makes it more difficult for lipophilic meds to move out of area

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53
Q

When giving an epidural, what moves the medication of the intended spot?

A

blood flow

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54
Q

What happens if you inject into a highly vascular area?

A

you are going to have a much short duration in that location because its going to get swept up by blood flow faster than if you put it SQ (low vascular, highly fatty)

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55
Q

Movement of intrathecal opioid is dependent on bulk flow of

A

CSF

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56
Q

in intrathecal neuraxial opioids, what can affect movement in CSF?

A

coughing or straining

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57
Q

What is the main side effect of neuraxial opioids?

A

Puritus! - ITCHING doesn’t necessarily mean they are having allergic reaction (is there depression of ventilation?)

Other s.e. are N/V, urinary retention, response depression

58
Q

What is an unusual side effect of neuraxial opioids?

A

Viral reactivation - reactivation of latent and viral infection (shingle, chicken pox, TB)

59
Q

What class is ketoralac?

A

NSAID

60
Q

What is the black box warning on ketoralac?

A

5 days - max use of toradol before have to be seen by provider. Increased risk of GI bleed

61
Q

When using ketoralac, which COX system helps prevent GI upset?

A

COX1 is inhibiting the prostaglandin production work to maintain mucus layer around stomach and GI tract that is protective. When that goes away,, increased risk for GI bleed.

62
Q

What are the side effects of ketoralac?

A

ARF - common cause
GI bleed - reduced COX 1
CHF - cause you to hold onto fluids
platelet malfunction - antiplatlet effect

63
Q

What is a specific COX2 inhibitor that should lower risk of GI upset, GI bleed?

A

Celebrex

Give this pre-op, esp. when NPO and becoming dehydrated – possibly safer

64
Q

What is the onset and duration of Acetaminophen

A

Onset 15 min

Duration 4-6 hours

65
Q

What is the main concern about taking too much Acetaminophen?

A

Hepatotoxicity

66
Q

What is the treatment for Tylenol overdose?

A

N-acelycistine

67
Q

what is the MOA of Tylenol?

A

Questionable mechanism

68
Q

What is the max mg each dose of tylonal can have?

A

325 mg

69
Q

What is the recommend maximum daily dose of Tylenol?

A

3gram (used to be 4g)

70
Q

What is the MOA of tramadol (ultram)

A

mu agonist, weak SNRI

71
Q

Does tramadol have an active metabolite?

A

No

72
Q

What is a major side effect of tramadol?

A

lowers the seizure threshold. Even someone who has never had seizures before can get them.

73
Q

Local anesthetics do what to nerve fibers?

A

reversibly block the conduction of electrical impulses along nerve fibers.

74
Q

Do LA cause any nerve damage?

A

no evidence of structural damage to nerve fibers.

75
Q

What will change the onset of action of LA’s

A

pKa and chemical structure

76
Q

What will change the duration of action of a LA?

A

lipophalicity

77
Q

What is a saltatory conduction?

A

jumping electrical conduction down a nerve, accelerating with each jump

78
Q

What are Schwann cells?

A

any of the cells in the peripheral nervous system that produce the myelin sheath around neuronal axons

79
Q

What does unmyelinated mean?

A

Action potential travels as continuous waves (not jumping) in a “push” pattern

80
Q

What does myelinated mean?

A

Action potentials “jump” or propagate by saltatory conduction. (+Na)

81
Q

What is Nodes of Ranvier?

A

the gap in the myelin sheath of a nerve, between adjacent Schwann cells

82
Q

What is the site of action for local anesthetics

A

Na channels

83
Q

What is the Resting membrane potential of a peripheral nerve

A

-70mV

84
Q

When a chemical, mechanical, or electrical impulse is applied to a resting nerve, the membrane potential is reversed due to

A

intracellular movement of Na+.

85
Q

The Na,K, ATpase pump works in what ratio

A

3:2 ratio, 3 Na in - 2K out

86
Q

Describe A Alpha fibers

A

Largest in diameter (15-20µm)
The most heavily myelinated
Fastest conduction velocity of all the fibers
Motor function and proprioception

87
Q

Describe A Beta fibers

A

Diameter (4-15µm)
Second fastest conduction velocity
Motor function, touch and pressure sensation

88
Q

Describe A Gamma fibers

A

Diameter (4-15µm)

Muscle spindles and reflex

89
Q

Describe A Delta fibers

A

Diameter (3-4µm) – smaller the diameter – pumps up conduction
Slower conduction velocity than other A fibers
Pain and temperature sensation

90
Q

Describe B fibers

A

Diameter (4µm)
Slower conduction velocity and less myelination than A fibers.
Preganglionic autonomic nerves

91
Q

Describe C fibers

A

Diameter (1-2µm)
Slowest speed of conduction
Conduct pain and temperature impulses
The only fibers that are unmyelinated

92
Q

Is motor function sensitive to the effects of LAs?

A

No - person can still move, just don’t want them to feel

93
Q

Where is the first place the LA will act?

A

1st effect will be at B fibers (autonomic effects) – change in signal transmission from blockade of Na channels

94
Q

Why are higher doses of LA needed in order to blunt motor function?

A

not as susceptible to effect of local anesthetic

95
Q

For LAs where is the receptor site?

A

INSIDE the nerve fiber

96
Q

To bind to its receptor site, the LA has to be

A

IONIZED

97
Q

Once inside the cell the ionized portion more avidly binds the

A

sodium channel inside the cell

98
Q

Our bodies have a neutral pH, why did we create weak basis

A

so they maintain stability and liopphilicity when injected into neutral body environment

99
Q

You have to have a weak base injected into a neutral pH to stay ______ to move inside nerve terminal where it is more ______ - becomes ionized through the Henderson Hasselback equation, too bind to receptor.

A

lipophilic

acidic

100
Q

EVERY local anesthetic is made up of 3 compounds, what are they?

A

An unsaturated aromatic ring system
An intermediate carbon group
A tertiary amine

101
Q

What do we get from the intermediate group?

A

where you get amid vs ester

102
Q

How do you tell apart the esters vs the amides?

A

the amides all have i’s in the first part

Lidocaine
Mepivacaine
Prilocaine
Bupivacaine
Levobupivacaine
Ropivacaine
Etidocaine

the esters do not

Procaine
Chloroprocaine
Tetracaine
Cocaine

103
Q

Onset of action: Lipid solubility-major determinant is amount of LA that is in

A

the non ionized state

104
Q

Onset of action: pKa is the pH of the LA at which the amount of

A

ionized and non-ionized drug is equal

105
Q

LA with a pKa closet to physiologic pH will have a higher concentration of non-ionized form that can

A

readily pass thru the nerve cell membrane.

106
Q

Ion trapping results from changes in pH in relationship to the agent’s

A

pKa

107
Q

What is the pharmacokinetics of LAs all they way through the body

A

When we inject, it goes into the nerve terminal, picked up by blood flow to move it to the site of action, metabolized by liver and renally excreted

108
Q

Highly or poorly lipid soluble LA have a longer duration of action, because they are less likely to be cleared by blood flow

A

highly lipid soluble (gets sequestered in lipid depot) (less likely to be taken away by blood stream)

109
Q

If the pKa is slightly above 7.5, what does that mean?

A

they are weak bases

110
Q

Intracostal will have a shorter duration of action that SQ, why?

A

the intercostal area is more vascular than SQ, more blood flow

111
Q

the addition of epi to a LA is a vasoconstrictor and increases the duration of action by roughly how long?

A

increase duration of action by 25% roughly

112
Q

What are some advantages of adding epi to LAs

A 
Decreases vascular absorption
Increases nerve cell uptake
Enhances the quality of analgesia
Prolongs the duration of action
Limits toxic side effects
113
Q

All LAs except for ________ have natural dilatory effects (works against us). It shortens its own duration of action, that’s why we give epi.

A

Cocaine

114
Q

Highly perfused organs are responsible for initial uptake, what are they?

A

Brain, lung, liver, kidney, and heart

115
Q

Esters are predominately metabolized by

A

pseudocholinesterase

116
Q

Procaine and benzocaine are metabolized to

A

p-aminobenzoic acid (PABA) ~ associated with allergic reactions

117
Q

What pts are at risk for a toxic reaction when taking esters?

A

Pts with genetically abnormal pseudocholinesterase

118
Q

How are Amides metabolized?

A

Metabolized by microsomal P-450 enzymes in liver

119
Q

Which metabolism is faster, esters or Amides?

A

esters

120
Q

The metabolites of what 2 LA’s can cause Methemoglobinemia

A

Prilocaine and benzocaine

121
Q

Hight concentrations of Methemoglobinemia will show what S/S?

A

Brownish gray cyanosis
Tachypnea
Metabolic acidosis

Severe S/S
Tissue hypoxia
Headache
Irritability
Loss of consciousness
122
Q

What is the treatment for Methemoglobinemia

A

Spontaneous recovery in 2-3 hours

Immediate reversal with methylene blue IV if having true CV ischemia

123
Q

Why would you add sodium bicarb to a LA?

A

will bring it back to a more neutral or basic area to improve its non ionized form

124
Q

What happens if you have Inadvertent intravascular injection of an LA

A

Local anesthetic systemic toxicity (LAST)

Instead of local reaction, can get cardio and CNS effects

125
Q

Explain the symptoms have CV toxicity from low to high

A

HTN, tachycardia

Bradycardia/hypotension

up to Asystole

126
Q

Explain the symptoms have cerebral toxicity from low to high

A

acting abnormal

confusion, dizziness, tinnitus, metallic taste

up to seizures

127
Q

Which LA has very commonly makes people “speak gibberish” and act strange

A

Lidocaine

128
Q

CV toxicity in LA administrations have what in regards to outcomes?

A

Very grave clinical outcomes

129
Q

Why do all LA depress myocardial automaticity

A

the are Na channel blockers

130
Q

Which LA has a very common occurrence of CV toxicity?

A

Bupivacaine

131
Q

What is the treatment if LAs get into systemic circulation?

A

Use and intralipid solution (10-30%)

propofol does NOT work!!!

132
Q

What are the Transient Neurologic Symptoms from spinals?

A

Tingling, burning aching in lower extremities and backside

133
Q

Which LA has a high incidence of TNS with spinal anesthesia?

A

Lidocaine has 13% incidence (this is high)

bupivicaine #2

134
Q

are TNS sysmtoms permanent?

A

no but can last up to 10 days

135
Q

higher risk of allergic reactions come from esters or amides?

A

esters

136
Q

What 2 LA mixtures is EMLA cream made up of?

A

Mixture of lidocaine and prilocaine

137
Q

Where is the site of action of EMLA cream

A

acts at little nerve endings at site of application

138
Q

How long does EMLA cream take to work?

A

1 hr

139
Q

Where should you NOT put topical anesthesia unless being supervised for a specific case?

A

nose, mouth - absorbed more rapidly into vena cava

140
Q

Topical cocaine cause

A

vasoconstriction

Pharmacology (8 decks)

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