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!!!!! Pharm Spring 16 Exam 2 !!!!! > Pain Basics COPY COPY > Flashcards

Pain Basics COPY COPY Flashcards

1
Q

Pain most paitients feel in the perioperative period

A

Protective physiologic pain from tissue damage

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2
Q

Peripehral nociceptive neuron stimulated by noxious stimuli asrnd signal to CNS - brain and spinal cord for input and sensation of pain

A

Protective physiologic pain from tissue damage

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3
Q

firing of a neuron that is not indicative of of physical damage, but is a pathalogical firing

A

Neuropathic pain

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4
Q

Pain out of proportion to noxious stimuli

A

Hyperalgesia

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5
Q

Pain evoked by a non-noxious stumuli

A

Allodynia

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6
Q

pain with no apparent stimuli - it is NERVE pain

A

spontaneous pain

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7
Q

Peripheral nociceptive neuron activated by intense noxious stimimuli (tissue damage) via

A
  1. Mechanical
  2. thermal
  3. chemical
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8
Q

slow conduction, dull, burning, diffuse

A

non-mylinated C fibers

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9
Q

fast conduction - sharp and well localized

A

A-delta fibers

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10
Q

nociceptiv impulse depends on the balance between

A

excitatory and inhibatory receptors

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11
Q

excitatory catioon channel activated by:

  1. Protons
  2. heat
  3. capsaisin
  4. Endovanilloids
A

TRIP1

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12
Q

Blocking this TRPV1

A

Pain medicine too good, lost protective mechanism ad could not perceive pain

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13
Q
  1. inhibatory
  2. Bind to GPCR to initiate cascade (PKA)
  3. increase K conductance hyperpolarizing the cell
A

Opioids

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14
Q

hyperpolarizing the cell with opioids means

A

cells will need a stronger stimulus to fire

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15
Q

Locations of opioid receptors

A
  1. Peripheral tissues
  2. dorsal horn of spinal cord
  3. Brain (this is wher opioids work)
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16
Q

promotes depolarization and stimulates pain

A

Bradykinin and Prostaglandins

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17
Q

Area of dorsal horn that is very rich in opioid peptides and receptors

A

substantia geletinosa

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18
Q

Synapse in dorsal horn at lamina I, II, III, V

A

A-delta fibers

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19
Q

Synapse in dorsal horn at lamina I and II

A

C-fibers

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20
Q

Located in lamina II and III

A

Substantia gelatinosa

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21
Q

what is in the substantia gelatinosa

A
  1. short inhibatory neurons that receive afferent fibers from A-delta and C fibers
  2. descending pathways that are moculating pain signals (they are inhibatory)
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22
Q

Determine weather a pain signal is sent to the higher centers for processing or modulated

A

Internurons

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23
Q

sends pain signals to the thalamac which then sends pain signals to the somatosensory cortes

A

neospinothalamic tract

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24
Q

responsible for the experience of pain

A

neospinathalamic tract

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25
Q

sends pain signals to the brainstem which then signals to the thalamus, hyptothalamus and elsewhere

A

peleospinothalamic tract

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26
Q

Causes the stress response to pain

A

paleaospinothalamic tract

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27
Q

tract we want to supress with pain that causes the SNS to release a ton of cortisol

A

paleospinothalamic tract

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28
Q

Opioids releive not only the ____________ aspect of pain, it also releves the ___________ aspect thereby preventing ___________ or _____________ from the exaggerated stress response.

A
  1. somatosensory
  2. physiologic
  3. MI
  4. prolonged healing
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29
Q

descending _____________ pathways originate in the ____________/ __________ including areas such as _____________, ____________, ___________, ______________

A
  1. inhibatory
  2. midbrain/brainstem
  3. Periaquaductal gray
  4. amygdala
  5. corpus striatum
  6. Hypothalmus
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30
Q

In descending pathways neurons from the midbrain/brainstem project into the ______________which then sends its descending neurons __________ to synapse in the ____________

A
  1. nucleus raphe magnus
  2. down the spinal cord
  3. substantia gelatinosa
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31
Q

opioids and the brain

A

act pre and post synaptically to activate descending inhibatory pathways

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32
Q

opioids and the spinal cord

A

work directly on the dorsal horn of the spinal cord

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33
Q

opioids and the periphery

A

act on peripheral teminals of nociceptive neurons

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34
Q

why is the perception of noxious stimuli not the same as pain?

A

it is lacking the emotional component

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35
Q

Opioids can change patients __________ without necessarily changing the patients ability to __________ noxious stimuli

A
  1. tolerance of pain
  2. perceive

ie- they can still tell you where the wound is

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36
Q

Opioids are effective for both ________ and _______ pain

A

somatic and visceral

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37
Q

The main use of opioids on anestehsia

A

Attenuate the SNS response to noxious stimuli- Laryngoscopy

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38
Q

During inductons opioids are used to _____________and causes the patient to have _______________

A
  1. maintain stable hemodynamics
  2. less Cardiovascualr comprimise
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39
Q

If opioids are not given to someone with coranary artery disease durring laryngoscopy

A

could have an MI with a really fast heart rate

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40
Q

opoids and inhaled anesthetics

A

act as an adjunct allowing for less use of inhaled agent

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41
Q

cardiac anestheisia and opioids

A

opioids are used as a sole anesthetic

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42
Q

natrurally occuring drugs derrived from opium from the poppy plant

A

Opiate

  1. Morphine
  2. Codeine
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43
Q

Natural and synthetic substances that bind to opioid receptors and produce and agonist effect

A
  1. Opioid
    1. anything that acts like an opiate
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44
Q

Term for DEA regualtions

A

narcotics

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45
Q

therepeutic agents with the general opioid structure

A

Opioids

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46
Q

Opioids produce analgesia without loss of

A
  1. Touch
  2. Propioception
  3. Conciousness
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47
Q

Unique characteristics that set opioids apart

A
  1. no ceiling effect or max dose
  2. tolerance and cross tolerance
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48
Q

Tolerance with opiods is associated with ____________ but not necessarily __________ - this is expected

A
  1. Physical dependance
  2. psychological
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49
Q

naturally occuring opioids

A
  1. Morphine
  2. Codeine
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50
Q

semisynthetic: analogs of morphine

A
  1. heroine and dihydromorhone
  2. heroine and fentanyl are very structurally similar
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51
Q

Synthetic Opioids

A
  1. Exogenous
  2. Has 4 classifications
    1. agonist
    2. partial aginist
    3. mixed agonist/antagonist
    4. antagonist
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52
Q

Synthetic antagonist

A

Narcan

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53
Q
  1. can reach maximum eficacy on dose response curve
  2. their potency is what varries
A

Synthetic agonists (full)

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54
Q
  1. will have a ceiling effect
  2. cannot reach maximum effect on dose response curve
A

Synthetic partial agnosts

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55
Q

Synthetic opioid agonist / antagonist

A
  1. agonist at kappa receptors
  2. antagonist and mu receptors
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56
Q

if their is any potential you will need to switch to a full agonist you want to start with

A

a parial agonist and NOT an agonist / antagonist

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57
Q

OPIOIDS MECHANISM OF ACTION

Activate ___________________ and act

  1. _______________to directly decrease neurotransmission by:
    1. increase K conductance (_______________)
    2. Ca++ channnel inactivation (_________________)
    3. inhabitionof ____________ (______________)
    4. Modulation of___________- signaling cascade for phospholipase C
  2. _______________
    1. Decrease ____,__________,________and ___________
    2. anytime you hyperoplarize a membrane you decrease _______________
A

OPIOIDS MECHANISM OF ACTION

Activate stereo-specific G-protein coupled receptors and act

  1. post-synaptically to directly decrease neurotransmission by:
    1. increase K conductance (hyperpolarization)
    2. Ca++ channnel inactivation (decreased NT release)
    3. inhabitionof adenylate cyclase (decreased cAMP)
    4. Modulation of phospinositide- signaling cascade for phospholipase C
  2. Pre synaptically
    1. Decrease ACh, dopamine, norepi and Substance p release
    2. anytime you hyperoplarize a membrane you decrease NT release
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58
Q

anytime you hyperpolarize a cell you

A

decrease neurotransmitter release

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59
Q

Opioids POST-synaptic mechanism of action

A
  1. increase K conductance (hyperpolarization)
  2. Ca++ channel inactivation (decreases NT release)
  3. Modulationo of phospinositide- signaling cascade for phospholipase C
  4. Inhabition of adenlyate cyclase (decrese cAMP)
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60
Q

Opioids PRE-synaptic mechanism of action

A
  1. inhibits the release of excitatory neurotransmitters
    1. ACh
    2. Dopamine
    3. Norepi
    4. Substance P
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61
Q

Opioid receptors

A
  1. Mu (agnoist binding site)
  2. Kappa (antagonist binding site)
  3. Delta
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62
Q

When opioids bind to receptors they

A

activate endogenous pain modulating systems

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63
Q

All endogenous and exogenous opiois agonists work at these receptors

A

Mu-1 and Mu-2

64
Q

May actually cause immunosupression and accelerate some types of cancer

A

Mu-3

65
Q

Mu receptors location

A
  1. brain- supraspinal
  2. spinalcord
  3. periphery
66
Q

Supraspinal is thought to be the principal site of action but also works at spinal cord and periphery

A

Mu-1

67
Q

Mu-1 receptor activation causes

A
  1. euphoria
  2. miosis pupil constriction
  3. Bradycardia
  4. Urinary retention
  5. hypothermia- impairment of thermal regulation
68
Q

Mu-2 receptor activation effects

A

Most of the bad effects

  1. Hypoventilation
  2. physical dependence
  3. constipation
69
Q

receptor that principal site of action is the spinal cord, but also has some supruaspinal action as well

A

Mu-2

70
Q

opioid agonist/antagonists have principal site of action

A

kappa receptor

71
Q

responsibe for supraspinal , spinal and peripheral analgesia

A

Kappa receptor

72
Q

Kappa receptor activation effects

A
  1. Dysphoria
  2. sedation
  3. Miosis- pupillary constriction
  4. Diuresis
73
Q

dysnorphins act on these receptors

A

Kappa receptors

74
Q

endogenouas ligand of enkephalin

A

Delta receptor

75
Q

Main site of action is peripheral (but also acts supraspinal and spinal)

A

Delta Receptor

76
Q

receptors involved in hypoventilation from opioids

A

Mu-2 and Delta

77
Q

Delta receptor activation

A
  1. Peripheral analgesia
  2. Hypoventilation
  3. Constipation
  4. Urinary Retention
78
Q

Located on Chromosome 6q24-q25

A

Mu opoid receptor

79
Q

aspartated in place of asparagine

10-20% of the population

A
  1. Nucleotide 118 polymorphism
  2. Gene Effects agonist binding to Mu receptor
80
Q

valine in place of alanine

1-10% of population

A
  1. Nucleotide 17 polymorphism
  2. Gene Effects agonist binding to Mu opioid receptor
81
Q

Why are opioids more of an art than a science

A
  1. there are polymorphisms that effect opioid binding
  2. incidences can vary with racial/ethnic groups
82
Q

Two things genetics can influence

A
  1. Receptors
  2. CYP 450 metabolism
83
Q

5 common polymorphisms can alter the metabolism of codine

A

CYP2D6

84
Q

Codine is a ______________.

Its active form is ____________.

Black box warning with _____________.

__________________ dont get adequate pain controll and may get increased nausea.

_____________ get a build up of morphine and can have respiratory depression

A
  1. Prodrug
  2. Morphine
  3. Children
  4. Fast Metabolizers
  5. Slow Metabolizers
85
Q

Increased metabolizers associated with the CYP2D6 gene may have increased nausea and decreased pain controll with…

A
  1. Oxycodone
  2. Hydrocodone
  3. methadone
86
Q

Codine has unpredictable pharmacokinetics and half lives due to

A

CYP2D6 gene polymorphisms

87
Q

Opioid least likely to be impacted by genetic variability. Predictable pharmacokinetics.

A

Fentanyl

88
Q

side effect rate can be influenced by ….

A

The rate of metabolism

89
Q

Ultra-rapid metabolizers are at risk for

A

PONV

90
Q

Prototype for Opioids

A

Morphine

91
Q

Opioids and Perioperative cardiovasucular effects (4)

A
  1. Minimal impairment of CV function but has additive effect with other analgesics
  2. profound vasodilation/ decrease SVR- most evident in patients with hypovolemia
  3. Dose dependant bradycardia- via vagal stimulation (nuclei in medula) andDirect SA/AV nodal depression
  4. Impairmennt of SNS responseand baseline toneorthostatic hypotension that is pronounced with hypovolemia
92
Q

morphine and meperedine and cardiovascular effects

A

Have a dose dependant histamine release

  1. risk more vasodilation - decreased BP and SVR
  2. risk bronchospasm
93
Q

Why is meperidine an exception to the CV effects of opioids

A

It will cause tachycardia - due to its atropine like structure

94
Q

When a large dose of opioids are given and the BP drops what is it likely due to?

A

Hypovolemia with vasodilation it is NOT likely a contractility isusse, Opioids are pretty cardiac stable

95
Q

Opioids and HR

A
  1. Dose dependant bradycardia
    1. Central vagal stimulation
    2. act directly on SA/AV nodal depression
96
Q

Opioids and vascualture

A

Vasodilation/ Decreased SVR

  1. decreased SNS response and baseline tone
  2. decreased CO and venous pooling = orthostatic hypotension
  3. Pronounced effect on vasculature
97
Q

What opiods do we want to avoid in astmatics? Why?

A

Morphine and meperidiene-

  1. dose and infusion rate dependant histamine release
  2. causes more vasodilation and BRONCHOSPASM
98
Q

Do opioids produce amnesia

A

No

99
Q

Opioids and patients with increased ICP

A
  1. Must have ventilations controlled prior to giving opioids
  2. Hypoventilation and Increased CO2 will cause cerebral vasodilation and increased ICP
100
Q

As long as ____________________ Opioids will cause a modest decrease in ICP

A
  1. ventilations are controlled
101
Q

Opioids and urination

A
  1. Increased Uregency and reduced ability to void
  2. Increased tone and peristaltic activity of ureter
  3. incresed tone of detrusor
102
Q

Opioids can cause a spasm of the ________________and ____________ contraction with ____________ billiary pressure. This smooth muscle contraction may feel like an _____ and can be releived with __________ or ___________. __________ will make the patient vomit.

A
  1. Sphincter of Oddi
  2. gallbladder
  3. increased
  4. MI
  5. Glucagon
  6. Nitroglycerine
  7. Glucagon
103
Q

Constipation, decreased gastric motility and prolonged gastric emptying are caused by

A

Spasm of GI smooth muscle from opioids

104
Q

Why do opioids cause nausea and vomiting

A
  1. decreased gastric emptying
  2. stimulation of chemoreceptor zone of the 4th ventricle
    1. balanced depression of medulary vomiting center
105
Q

Puritis and Opioids

A

cause is unknown, could be the histamine release with morphine and meperidine, but fentanyl it is unknown

  1. fentanyl nose itch
106
Q

drugs that cause adverse affect: muscle rigidity in chest, abdomen, jaw and extremeties

A
  1. Fentanyl
  2. Sufentanyl
  3. Hydromorphone (Dilaudid)
107
Q

issues with adverse affect: muscle rigidity from opioids

A
  1. High airway pressures from increased intrathoracic pressure and decreased veonus return
  2. difficult/impossible to Venltilate
  3. only releived my non-depolarizing muscle relaxant
  4. glottic rigidity and closure reported
108
Q

Increased Tidal voume and decreased RR

A

Smaller dose of opioids

109
Q

Increased CO2 and decrease O2

A

Ventilatory effects of smaller doses of opioids

110
Q

Decreased TV and Decreased RR

A

Larger dose of opioids

111
Q

decreased ventilation and decreased response to CO2

A

Hypercarbia

112
Q

Perioperative ventalitory effects of opioids

A
  1. Dose dependant respiratory depression
  2. Decreased chest wall compliance
  3. constriction of pharyngeal and laryngeal muscles
  4. cough supression
  5. Dramatically decreased response to hypercarbia and hypoxia
113
Q

Factors that increase the magnitude and duration of opioid induced respiratory depression

A
  1. more pain = less respiratory depression/sedation
  2. Intermittent boluses have higher degree of respiratory depression than contiuous infusion
  3. Speed of injection
  4. Concurrent admin with other anesthetics
  5. Decreased clearance- active metabolites build up
  6. Age- older an younger
114
Q

consiterable first pass effect - dose seems really large

A

Morphine

115
Q

Abuse of this very bad because of the APAP component

A

Vicodin / Hydrocodone

116
Q

1/2 live 3-4 hours, then converted to an active metablolite

A
  1. Morphine
  2. converted to morphine-6-glucuroninde
117
Q

prodrug- active form is morphine

A

Codeine (3-methylpmorphine)

118
Q
  1. Long plasma half life 8-59 hours or 13-100, sources vary
    1. High variability among individuals
A

Methadone

119
Q

Oxycodone

  1. long acting
  2. with acetomenophen
  3. with ASA
A
  1. Oxycontin
  2. Percocet
  3. Percodan
120
Q

Hydrocodone is ALWAYS combined with

A
  1. APAP
  2. ASA
  3. Ibuprofun
  4. antihistamine
121
Q

Antitussive affects reamin without conversion- lower doses needed

A

Codeine (3-methylmorphine)

122
Q

No active metabolites - safer in patients with renal dysfunction

A
  1. Oxycodone
  2. Methadone
123
Q

Ineffective in 10% caucasions and 30% asians due to the lack in 2D6

A

Codeine (3-methymorphine)

124
Q

dosed QD for opioid addiction treatment

A

Methadone

125
Q

Synthetic opioid

A

Methadone

126
Q

Combined with

  1. APAP
  2. Gusifenesin
  3. promethazine
A

Codeine (3-methyl-morphine)

127
Q

analgesic and antitussive

A

Hydrocodone Vicodin

128
Q

mild paine relief

A

Codiene (3-methylmorphine)

129
Q

used for chronic pain

A

Hydrocodone/vicodin

130
Q

severe acute pain

A

morphine

131
Q

Moderate to severe pain, chronic pain and post op pain

A

oxycodone

132
Q
  1. chronic pain syndrome treatmentbecause of its long half life
  2. dosed BID or TID (q 4-8 hours) to maintain steady plasma concentrations
A

Methadone

133
Q

Used for neuropathic pain

A

Methadone

134
Q

At risk for respiratory depression secondary to its long unpredictable half time

A

Methadone

135
Q

How long does it take to develop tolerance to opioids?

A

48 hours - need to taper

136
Q

Timeline of tolerance

A
  1. reduction of adverse effects
  2. shorter duration of analgesia
  3. decrease in effectiveness
  4. does not work
137
Q

how can tolerance be surmounted?

A

increase the dose

138
Q

in addition to tolerance of analgesic effects, tolerance also occurs to

A

Respiratory and CNS adverse effects

139
Q

____________ exists amung all ___________, but it is not 100% so when switching drugs start at ______ _____________ dose

A

Cross-Tolerance exists amung all full agonists, but it is not 100% so when switching drugs start at half the equianalgesic dose

140
Q

switching opioid tolerant patients to _______ may improve pain releif

A

Methadone

141
Q

What side effect dies NOT go away with tolerance

A

Constipation- a stimulant laxative w/ or without stool softener should be started early in treatment

142
Q

With tolerance __________ and _________ effects go away

A

sedative and emetic

143
Q

causes abstinance symptoms on sudden d/c

A

dependence

144
Q

addiction involves ___________ , ____________, and ___________ factors

A
  1. psychological dependence
  2. Biologic
  3. social
145
Q

Dosages of opioids

A

No minimum or maximum unless they have APAP or ASA

146
Q

what type of dosong should be used in chronic pain

A

sustained release- so they tond have peaks and valleys

147
Q

among individuals a __________ varioation of analgesia is obtained with a single dose

A

10 fold

148
Q

Neuralaxial analgesia (diffusion)

A
  1. Cross the dura onto mu receptors to the substantia geletinosa
  2. difuses into the vascularture to get systmeic effect
149
Q

given neuroaxial: very lipid soluable

A

fentanyl

150
Q

Given neuroaxial: very water soluable - will circulate with CSF

A

Morphine

151
Q

Opioids in the epeidural space may diffuse into

  1. _______
  2. _______
  3. _______
A
  1. fat
  2. systemic absorbtion (vasculature)
  3. CSF
152
Q

Cephalad movemnt of ipoid in CSF depends on ____________.

A

Lipid solubility

153
Q

Fentanyl which has ____________ will be _____________ by uptake into the spinal cord,

Where as, _________ opioid will __________fro transfer to the cephald location such as _______

A
  1. lipid solubility
  2. limited in migration
  3. les soluable
  4. remain in CSF
  5. Morphine
154
Q

More lipid soluabel = ____________

A

Quicker peak in CSF and systemic concentration

155
Q

Why is the dose for an epidural 5x higher than that for a spinal?

A

Because the spinal is directly at the site

156
Q

Using local anesthesia such as spinals and epidurals may decrease

A

overall anesthetic requirements

157
Q
A

!!!!! Pharm Spring 16 Exam 2 !!!!! (11 decks)

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