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Pharmacology > Induction agents cont and pain management - Quiz 3 > Flashcards

Induction agents cont and pain management - Quiz 3 Flashcards

1
Q

What CNS effect does etomidate provide

A

hypnosis

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2
Q

Does etomidate have any analgesic properties

A

No

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3
Q

What is important about the chemical structure in etomidate?

A

imidazole derivative ring
Ring only closes with a physiologic ph (8.1)
2 isomers – R+ isomer is hypnotic

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4
Q

How is etomidate metabolized?

A

78% metabolized by hepatic microsomal enzymes

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5
Q

Is the etomidate metabolite active or inactive?

A

Inactive

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6
Q

Can etomidate accumulate?

A

Can accumulate but less of an accumulation because of its rapid clearance

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7
Q

What is one of the main limiting factors to use of etomidate?

A

Transient depression of adrenocortical function.

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8
Q

In transient depression of adrenocortical function, what inhibited?

A

11-betahydroxylase

Reduction of CS and mineralocorticoid production

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9
Q

How long can transient depression of adrenocortical function last?

A

4-8 hrs

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10
Q

After how many doses of etomidate can transient depression of adrenocortical function happen?

A

after 1 dose

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11
Q

What is the MOA of etomidate?

A

Potentiation of GABAA mediated chloride shift

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12
Q

What are the CNS effects of etomidate?

A

Decreased CMRO2, CBF, ICP, IOP

CPP is maintained because CO is not changed!

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13
Q

What are the CV changes with etomidate in a healthy individual?

A

Minimal change in HR, BP, CVP (one of the most stable CV induction agents)

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14
Q

Patient’s with aortic or mitral valvular disease may experience what with etomidate?

A

significant decrease in systemic BP, PAP, PCWP.

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15
Q

Respiratory effects of etomidate

A

decrease in minute volume and response to C)2 accumulation.

Brief periods of apnea followed by hyperventilation.

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16
Q

Does etomidate increase or decrease incidence of PONV?

A

Increase

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17
Q

Etomidate has a lower incidence of true allergic reaction, what could this be from?

A

No histamine release

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18
Q

MOA of precedex

A

Highly selective α2-adrenergic agonist

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19
Q

What is the active component of precedex

A

D-isomer of medetomidine

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20
Q

Alpha 2 receptors in the CNS have what in regards to releasing norepinephrine?

A

negative feedback loop

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21
Q

How is precedex bounds?

A

highly protein bound

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22
Q

How is precedex metabolized?

A

Rapidly metabolized by hepatic microsomal enzymes

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23
Q

how is precedex excreted?

A

Metabolites excreted in urine and bile

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24
Q

How do you awaken from precedex?

A

naturally and easily

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25
Q

hypnosis from precedex occurs how?

A

from stimulation of α2 receptor at locus ceruleus.

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26
Q

Where does analgesia effects from precedex originate?

A

at the level of the spinal cord

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27
Q

How do sedative effects work with precedex?

A

activates endogenous sleep pathways

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28
Q

Does precedex have a potential for tolerance?

A

yes - negative feedback loop

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29
Q

What should be your maximum length of time for precedex gtt?

A

24 hours. It is causing long term suppression of sympathetic nervous system

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30
Q

CNS effects of precedex

A

Decrease in CBF

No change in CMRO2 / ICP

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31
Q

does precedex increase or decrease in MAC requirement for inhaled anesthetics

A

Decrease

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32
Q

True to False, precedex causes a decrease in anesthetic requirement for opioid

A

True

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33
Q

CV affects from precedex

A

Moderate decrease in heart rate and SVR

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34
Q

What are the respiratory effects from precedex?

A

minimal changes

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35
Q

Why don’t you see many respiratory effects from precdex?

A

Norepi does not have significant beta 2 effects (bronchodilator, bronchoconstriction) This is why you don’t see many respiratory effects from precedex.

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36
Q

What is neuropathic pain and how is it described by patients?

A

No physical injury but nerve is firing inappropriately

Burning, electric shock, lightening bolt

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37
Q

What is nociceptive pain and how is it described by patients?

A

Any pain that has happened to body structure

Stabbing, pressure, sharp, dull, achy

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38
Q

Will opiates help with neuropathic pain?

A

No, never

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39
Q

Nociceptive pain must have what in order to send pain signals to spinal cord?

A

Stimulation

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40
Q

In neuropathic pain, do you need to have a stimulus?

A

NO, sometime you do (pinched nerve) but you DO NOT need to have one

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41
Q

In nociceptive pain, what is transmission?

A

Action potential moves from site of stimulus to the dorsal horn of the spinal cord, then to the CNS.
There are several pathways

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42
Q

In nociceptive transmission, what type of pain does A delta fibers transmit?

A

sharp localized pain

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43
Q

In nociceptive transmission, what type of pain does C fibers transmit?

A

dull/ achy pain, poorly localized

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44
Q

Calcitonin related peptides are now being targeted for what?

A

New migraine medications

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45
Q

In nociceptive pain, what is perception?

A

Conscious experience of pain

Pain impulse relayed through thalamus
Higher cortical structures transmit pain

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46
Q

In nociceptive pain, what is modulation?

A

Inhibition of impulses via the brain stem.

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47
Q

Neuropathic pain is sustained by what?

A

abnormal processing of sensory input

Nerve damage, persistent stimulation, autonomic dysfunction

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48
Q

What is hyperalgesia

A

abnormally heightened sensitivity to pain

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49
Q

What is allodynia?

A

pain resulting from a stimulus, such as light touch, which would not normally provoke pain

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50
Q

How do you differentiate acute vs chronic pain?

A

Chronic Pain >3 months OR past the time of normal tissue healing

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51
Q

How many patients presenting to physician offices with noncancer pain symptoms or pain-related diagnoses received and opopioidiod prescription?

A

1/5 or 20%

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52
Q

What is the PQRST monitoring of pain?

A 
P: palliative and provocative factors
Q: Quality
R: Radiation
S: Severity
T: Temporal relations
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53
Q

Besides the pt telling you they are in pain, what else could you look for?

A

Grimacing, guarding, sweating, nausea

Hypertension, tachycardia, tachypnea

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54
Q

People who use opiates for > 5 days, have an exponential increase at still using that medication at ______ days

A

30

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55
Q

6% of patients s/p elective surgery (minor or major, all types) continue to use opiates for at least ____ days

A

90

56
Q

The GREATEST percentage (44%) of people dying of opioid overdose is

A

middle age 45-64 years old

57
Q

Which groups of people are at risk for inadequate pain control

A 
Racial and ethnic minority groups 
Women
Elderly
Persons with cognitive impairment
Cancer and at the end of life
58
Q

The optimal length of opioid prescriptions for

General surgery
Womens health
Musculoskeletal

A

General surgery 4-9 days
Womens health 4-13 days
Musculoskelatal 6-15 days

59
Q

Where are opioid receptors located?

A

Located throughout the brain, spinal cord, GI tract

60
Q

What are the 4 subtypes of opiod receptors?

A

Delta
Kappa
Mu
Nociceptive

61
Q

Where are the delta opioid receptors and what are they responsible for?

A

Brain and peripheral nerves

Analgesia, antidepressant, DEPENDENCE

62
Q

Where are the kappa opioid receptors and what are they responsible for?

A

Brain, spinal cord, periphery

Analgesia, sedation, miosis, dysphoria, ADH inhibition (urinary hesitancy)

63
Q

Where are the Mu opioid receptors and what are they responsible for?

A

Brain, spinal cord, periphery, intestine

Mu1: analgesia, dependence
Mu2: respiratory depression, euphoria, reduced GI motility, dependence, constipation
Mu3: unknown

64
Q

Where are the nociceptive opioid receptors and what are they responsible for?

A

Brain, spinal cord

Anxiety, depression, appetite, tolerance to mu agonists

65
Q

What is andenylate cyclase

A

an enzyme that takes ATP and changes it to cyclic AMP

66
Q

How do opiates respond to Mu receptors?

A

in an inhibitory way.

Morhine stops cAMP, By morphine binding, it reduces the amount of Ca that is coming in, so it reduces the amount of neurotransmitter that are being released, stopping the signal.

67
Q

Opioid stimulation of the NMDA receptor may cause what in regards to opioid effectiveness?

A

reduced opioid effectiveness

68
Q

Overstimulation by glutamate may be the cause to?

A

Neuropathic pain

69
Q

What is our natural opiate?

A

Morphine

70
Q

What are some examples of our semisynthetic opiates?

A

dilaudid, fentanyl

71
Q

What plant does morphone come from and where is it grown?

A

Comes from the poppy plant – majority plants grown in Afghanistan

72
Q

Our S anteomere and only levo-rotatory forms of opioid have

A

agonistic activity

73
Q

Opioids must exist in the ______ state in order to form a strong bond at the opioid receptor.

A

Ionized

74
Q

Of the opioids, which is the most ionized?

A

Morphine

75
Q

What routes can you give morhine?

A

PO, IM, IV, SQ, IT, Epidural

76
Q

What effects does morphine provide?

A

analgesia, sedation, and euphoria

77
Q

How does morphine change the threshold of pain?

A

Increases the pain threshold and modifies the perception of noxious stimuli so that it is no longer experienced as pain.

78
Q

What type of pain is relieved the best by morphine?

A

Continuous dull pain is relieved more effectively than intermittent sharp pain.

79
Q

When does morphine peak?

A

15-30 minutes

80
Q

How much IV morphine enters the CNS?

A

<0.1%

binding is mostly along spinal cord on dorsal horn peripherally

81
Q

Morphine creates 2 metabolites, what is the M3G metabolite?

A

inactive

(bulk of metabolite) 75-85%

82
Q

Morphine creates 2 metabolites, what is the M6G metabolite?

A

active
5-10%
Inside the CNS M6G is 100x more potent than morphine.

(The hydrophilicity of M6G normally prevents its entrance to the CNS. HOWEVER, Chronic administration or renal failure can cause M6G to enter the CNS by mass action.)

83
Q

What is the biggest reason people die of opiate overdose

A

respiratory depression

84
Q

When we give morphine, suppression of sympathetic nervous system and vasodilation

A

hypotension, bradycardia

85
Q

Morphine causes a histamine release which leads to what?

A

Itching

vasodilation- hypotension

86
Q

Which opioid agonist produce dose dependent & gender specific depression of ventilation.

A

ALL of them

Women seem to have higher risk (unsure why)

87
Q

What does rapid injection of morphine cause?

A

chest wall rigidity - can make intubation difficult

88
Q

Why do we need to use caution when administering morphine to its with head injuries?

A

causes an increase in ICP

89
Q

Morphine causes pupil

A

constriction

90
Q

effects of morphine on an EEG

A

Resembles sleep associated change

91
Q

Explain sedation and pain control of morphine

A

People will feel tired and lethargic before they feel pain control

92
Q

What is the side effect of morphine in the biliary system?

A

May cause spasm of biliary smooth muscle.

During cholecystectomy – opioid induced spasm of the sphincter of oddi

93
Q

What is the treatment for biliary spasms caused by morphine?

A

glucagon

it increases amount of cAMP

94
Q

When does opiate induced constipation go away?

A

never, PREVENTION is key

95
Q

Genitourinary side effects of morphine

A

hesitancy

96
Q

Does morphine have any effect on neuromuscular blocking agents?

A

No

97
Q

Patients on MAO inhibitors may experience _______ CNS depression and hyperpyrexia after an opioid agonist (esp demerol)

A

exaggerated

98
Q

In comparison to morphine, what is different about dilaudid?

A

Semisynthetic
More potent
Does NOT have an active metabolite

99
Q

Fentanyl is a ______ agonist

A

synthetic

100
Q

Fentanyl analgesia is _______ times more potent than morphine

A

75-100

101
Q

Single dose fentanyl demonstrates more rapid _____ and _____ duration of action than morphine

A

Onset

Shorter

102
Q

Fentanyl effect-site equilibration time between blood and brain is about ___ minutes

A

6

103
Q

Is fentanyl more hydrophilic or lipophilic than morphine

A

lipophilic

More rapid onset
Greater potency
Greater passage across BBB

104
Q

Why does first dose of fentanyl wear off

A

d/t redistribution, not from clearance

105
Q

The ____ serve as a large inactive storage site with an estimated 75% of a single fentanyl dose undergoing 1st pass pulmonary reuptake

A

Lungs

106
Q

Fentanyls metabolite is ______, and can be detected in urine for up ______

A

Inactive

72 hrs

107
Q

does fentanyl increase ICP

A

yes, modest increase 6-9 mmHg

108
Q

CV effects from fentanyl

A

Bradycardia, hypotension, decreased CO (from reduced SNS stimulation NOT histamine release)

109
Q

Does fentanyl release histamine?

A

NO

110
Q

When you take opiates and benzos, what is the effect?

A

exponential/synergistic effects when it comes to hypnotic effects, depression and ventilation

you should does at least 2 hours apart

111
Q

What might you have to do an opiate dose if pt is on cardiopulmonary bypass? esp fentanyl

A

increase the dose, a significant portion of the drug adheres to the circuit of the cardiopulmonary bypass circuit.

112
Q

What are the different fentanyl routes?

A

Intrathecal, Oral transmucosal fentanyl - “oralet”, patch

113
Q

When you take off a fentanyl patch, how much medication is still left on the patch?

A

approx 90%

114
Q

What allows for fentanyl to be used by other routes?

A

Its lipophallicity

115
Q

Sufentani is _______ times more potent than fentanyl and _______ times more potent that morphine

A

5-10

1000

116
Q

What is the SL form of sufentanil?

A

Dsuvia

117
Q

Elimination time for Sufentanil is

A

intermediate

Fentanyl>sufentanil>alfentanil

118
Q

Is elimination of Sufentanil effected by liver disease?

A

No

119
Q

Sufentanil Vd and elimination half-time is increased in obese patients due to

A

high lipid solubility

120
Q

How much first pass pulmonary reuptake does Sufentinal go though?

A

60%

121
Q

Is sufentanils metabolite active or inactive?

A

inactive

122
Q

How is sufentanil eliminated?

A

Less than 1% is excreted unchanged in the urine

Normal renal function is important for elimination of sufentanil
Patients with chronic renal failure may have prolonged depression of ventilation and abnormally high plasma concentrations of sufentanil

123
Q

Does Sufentanil have an increase or decrease in CMRO2 and CBF

A

decrease

124
Q

CV effects of Sufentanil

A

Bradycardia

Decreased CO, secondary to bradycardia

125
Q

Why would you use Sufentanil or fentanyl?

A

When there is a shortage of fentanyl

126
Q

Alfentanil is ______ the potency of fentanyl

A

1/5 - 1/10

127
Q

Alfentanil is ______ the duration of action of fentanyl

A

1/3

128
Q

What is the unique advantage about its rapid effect-site equilibration time.

A

Even MORE rapid onset of action

Alfentanil 1.4 minutes
Fentanyl 6.8 minutes
Sufentanil 6.2 minutes

129
Q

The short elimination half-time if alfentanil makes it useful for what?

A

useful drug for quick, single, brief stimulus procedure.

130
Q

How is alfentanil metabolized?

A

Highly dependent on the liver

131
Q

Why is alfentanil different from other fentanyl products?

A

quicker onset and quicker clearance

132
Q

Remifentanil is similar to _______ for quick site equilibrium

A

Alfentanil

133
Q

How is remifentanil metabolized?

A

by esterases to inactive metabolites

134
Q

how fast is remifental metabolized?

A

6 minutes or less

135
Q

Why does remifentanil have more mild effects?

A

it is metabolized so fast it does not have time to get into conduction pathways

136
Q

If you use this medication during a procedure, what might happen post-op?

A

This medication is metabolized so quick that the pt will probably need additional pain medication.

Pharmacology (8 decks)

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