6. Pain Management Flashcards
(132 cards)
1
Q
Amnestic
A
agent suppressing formation of memories
2
Q
Hypnotic
A
promotes onset of sleep
3
Q
Narcotic
A
opioid agent with various CNS depressant
4
Q
Opiate vs opioid
A
<div>
<div>
<div>
<div>
<div>Opiate—naturally occurring derivative of opium alkaloid that binds opiate
</div>
<div>receptors and produces effects similar to those of the endogenous endor-
</div>
<div>phins<br></br>
Opioid—naturally occurring or semisynthetic derivative of opium alkaloid
</div>
<div>(includes all opiates) that binds opiate receptors and produces effects sim-
</div>
<div>ilar to those of endogenous endorphins<br></br>
</div>
</div>
</div>
</div></div>
5
Q
Nociceptive vs neuropathic pain
A
<div>
<div>
<div>
<div>
<div>Nociceptive pain results from the activation of sensory neu-
rons that signal pain (nociceptors) in response to noxious stimuli. </div><div><br></br></div><div>Neuropathic pain results from signal-processing changes in the cen-
tral nervous system (CNS) </div>
</div>
</div>
</div></div>
6
Q
<img></img>
A
7
Q
Pain conduction pathways - 4?
A
pain detection<br></br>transmission<br></br>modulation<br></br>expression
8
Q
Pain detection: what are receptors for pain?
A
nociceptors
9
Q
Subtypess of nociceptors and where
A
<div>
<div>
<div>
<div>
<div> cutaneous tissues, including mechanoreceptors, polymodal
nociceptors (PMNs), and a variety of thermoreceptors. </div>
</div>
</div>
</div></div>
10
Q
What are ways that nociceptor activation can be modified?
A
PG<br></br>CAMP<br></br>leukotrienes<br></br>bradykinins<br></br>serotonin<br></br>substance P<br></br>thromboxanes<br></br>plt activating factor<br></br>endorphines
11
Q
How does trigger pointing work?
A
pain detection - freq o constant low level senosry stim developed peripheral sensitized nociceptors that perceive pain from otherwise innocuous stimuli (allodynia)
12
Q
How do peripheral nerve fibers work?
A
sensory neurons of cell body in neurons axon fibers with sn receptors in number of body sites - dermatomes from skin, sclerotomes from bone and myotomesfrom m
13
Q
Peripheral nerve fibers - which 2 responsible for pain?
A
alpha delta C
14
Q
Sharp initial pain peripheral n fibers?
A
sharp and initial pain
15
Q
Transmission of dull, aching burning pain fibers?
A
C fibers
16
Q
Which lasts longer alpha delta or c fibers for pain?
A
c - even after stim gone
17
Q
<img></img>
A
18
Q
<img></img>
A
19
Q
Pain transmission: dorsal horn - what is this?
A
gray mater in posterior aspect of SC, acts as integration system prior to passing on to other spinal cord segments
20
Q
in transmission: dorsal horn - how does this work with nociceptive input?
A
modulatesc in when it comes in
21
Q
pain transmission: dorsal horn -how does it differentiate between innocuous stimuli and noci input?
A
wide dynamic range neurons: get modulating input rom opioids, substance P, inflammatory factors from both efferent and afferent
22
Q
How does visceral and somatic pain differ?
A
smatic: sharp, later burn/throb<br></br>visc: poorly localized, burn or throb with pronounced autonomic activation, then may become sharp and referred as modulated
23
Q
What are the predominant pathways for pain conduction through the SC?
A
spinothalamic<br></br>spinomesencephalic<br></br>spinoreticular tracts <br></br><br></br>all in anterolat aspect of SC
24
Q
What are two primary descending pathways in SC involved in nociceptor modulation?
A
serotonin<br></br>noradrenergic
25
Where to serotonergic and noradrenergic pathways for pain modulation originate?
midbrain
medulla
go to SC through dorsolateral funiculus
medulla
go to SC through dorsolateral funiculus
26
27
What is central sensitization?
amplification of nociceptive signals
28
Central sensitization: what is this involved in? (dis)
chr pain - damage at any point in pain transmission system
also seen in thalamic stroke, MS, parkinson's, arnold chiari formation, cervical stenosis
also seen in thalamic stroke, MS, parkinson's, arnold chiari formation, cervical stenosis
29
30
Two reflex responses to nociceptor input:
spinal segmental/suprasegental
cortical
cortical
31
Responses to noci input: spinal reflex: generation?
gen-
erated by the transmission of nociceptive impulses from the dorsal
horn to motor and autonomic neurons in the spinal cord, provoking
a range of responses, including tachycardia, vasoconstriction, para-
lytic ileus, and muscle spasm
Suprasegmental reflexes are
transmitted through ascending tracts to the brainstem, hypothala-
mus, and cortex, where withdrawal reflexes and autonomic responses
occur in connection with conscious responses. The autonomic reflex
responses to pain are variable and cannot be used to quantify pain in
an individual.
32
Endorphin system - how does this work?
scattered neurons producing beta-endorphine, met and leuk enkephalins, dnyorphins
to act on mu delta kappa opioid receptors and produce analgesia
to act on mu delta kappa opioid receptors and produce analgesia
33
LT endorphin system - does it work well?
prolonged pain no
During prolonged periods of pain with high
stimulation levels, the system can become less responsive and less
effective at modulating the pain response.
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35
36
Acute vs chronic pain distinctions
acute: identifiable pathologic cause
adaptive
expected to stop/injury fized
adaptive
expected to stop/injury fized
37
*The treatment of recurrent pain in the ED incorporates
elements of the treatment of acute pain and chronic pain, and
prevention of recurrent pain events must be considered part of the
treatment strategy.
38
What med to use liberally in cancer pain?
opioids
39
CRPS 1 - what causes this? what is this?
CRPS type 1 (often referred to as reflex sympathetic dystrophy)
develops after a painful injury and typically follows the distribution of a
peripheral nerve. It is associated with hyperalgesia, allodynia, changes
in skin blood flow, and sympathetic dysfunction. This syndrome
develops during the healing and recovery phases of acute painful
injuries and is generally described as a burning, tingling sensation in
the area of the previous injury. This pain is likely related to ongoing
stimulation leading to the development of self-sustaining modulation
of the pain transmission system
40
CRPS type 2 - what is this?
causalgia, is associated with
burning pain and allodynia in the distribution of an injured nerve, with
no association with sympathetic symptoms.
41
What meds are more helpful in treating CRPS?
clonidine
NMDA rec antagonists
GABA agonists
*gabapentin first line
NMDA rec antagonists
GABA agonists
*gabapentin first line
42
What anticonvulsant meds can be used for neuropathic pain?
gabap
phenytoin
carbamaz
VPA
phenytoin
carbamaz
VPA
43
How do opioids work?
-bind specific endorphin system receptors throughout NS
-suppress pain dtection peripherally, modify at thal and SC, alter pain perception at cortex
-suppress pain dtection peripherally, modify at thal and SC, alter pain perception at cortex
44
MC SE of opioids?
constipation
45
Opioids side effects
constip
n/v
n/v
46
47
Why may patients get itchy face/trunk after IV opioids?
histamine release from opioid rec on mast cells
not allergy
can cause urticaria, pruirtis, orthostatic hypotension
rarely bronchospasm
resp depression
not allergy
can cause urticaria, pruirtis, orthostatic hypotension
rarely bronchospasm
resp depression
48
49
Why prefer IV titration over other forms of meds
titration aspect
50
Morphine: peak action time?
15-20mins
51
Morphine:half life
1.5-2 hours
52
Morphine: duration of action
3-4 hours
53
Morphine: first pass metabolism rate
only 20% reaches tissues
54
Morphine: metabolized by what organ?
liver
55
*Morphine is primarily metabolized by conjugation into three- and
six-conjugate forms in the liver. The six-conjugate form morphine
metabolite is a strong mu and delta receptor agonist. This form plays
an important role in the efficacy and duration of clinical effects. The
three-conjugate form (normorphine) has no opioid analgesic activity
but has been associated with CNS side effects (e.g., tremors, myoclo-
nus, delirium, seizures) when it accumulates. This risk is greatest in
older patients and those with renal insufficiency.
56
57
58
What is a significant disadvantage of meperidine?
cytochrome p450 into normeperidine
--> can cause cns toxicity at therapeutic dosing, lasts 12-16 hours, signficiant anticholinergic effcts
DO NOT USE
--> can cause cns toxicity at therapeutic dosing, lasts 12-16 hours, signficiant anticholinergic effcts
DO NOT USE
59
Hydromorphone: how many more times potent than morphine?
About 7
60
Hydromorphone: SE vs morphine
less
61
Hydromorphone: excretion of H3g (metabolite) through ?
renal
62
Fentanyl: time to onset via IV?
1-2 mins
63
Fentanyl: duration of action
30-60 mins
64
Fentanyl release of histamine compared to morphine?
less
65
Fentanyl duration of action vs half life
short
long
therefore concerns for build up of tox
long
therefore concerns for build up of tox
66
Bronchospasm or pruritis hx - opioid of choice?
fent
67
High or repeated doses of fentanyl may produce ?
m rigidity
rigid chest syndrome
can interfere with resp
tx with naloxone or NM blockade if not successful nalox
rigid chest syndrome
can interfere with resp
tx with naloxone or NM blockade if not successful nalox
68
fentanyl recommended dose for neb/IN
1-3 mcg/kg
69
Sufentanil: what is this?
highly lipophilic synth opid
fewer cardiac se than other opioids, no breakdown products
fewer cardiac se than other opioids, no breakdown products
70
ideal med for cardiac surgery, renal or hepatic disease? (opioid)
sufentanil
71
sufentanil: high risk of __
apnea
72
Buprenorphine: what is this?
synthetic opioid with high affinity for receptor
moreso used as reduction of opioid cravings when combined with naloxone for suboxone
moreso used as reduction of opioid cravings when combined with naloxone for suboxone
73
suboxone - why add naloxone to Buprenorphine?
deterrant - it is absrobed in GI tract bu SL or oral form is insert whereas IV = sign uptake to block receptors and = withdrawal sx
74
Oxycodone: bioavailability oral compared to other opioids?
much higher
75
Oxycodone: high abuse potential factors?
quickly and efficiently absorbed
76
Oxycodone: ___ metabolism to oxymorphine that accounts for analgesia. how many pt do not generate this functional metabolite?
hepatic
10%
10%
77
Oxycodone: what meeds can compete with it for CYP2D6 metabolism?
neuroleptics
tca
ssri
tca
ssri
78
Hydrocodone: metabolized by __ to hydromorphone
liver
79
Hydrocodone: best synergistic effect with ?
tyl
nsaid
nsaid
80
Hydrocodone: lasts?
4 hours
81
Codeine: 10% of pop metabolizes this __
poorly
82
Methadone: why is this a good, new option?
no known neurtoxic or active metabolites, high bioavailability
NMDA antagonist and serotonic reuptake inhib qualities
slow clearance (up to 27 hours) helps to maintenance therapy as delays withdrawal for 24h
NMDA antagonist and serotonic reuptake inhib qualities
slow clearance (up to 27 hours) helps to maintenance therapy as delays withdrawal for 24h
83
Methadone: action of onset?
6-8 hours
84
Naloxone: typical dose
0.2mg IV and titrated
85
Naloxone: autoinjection dose?
0.4mg
86
What receptors does tramadol work on?
weak my agonist
nmda
serotonin and norepi reuptake qualities
nmda
serotonin and norepi reuptake qualities
87
How is tramadol metabolized?
liver
cytochrom -450
cytochrom -450
88
MC se tramadol?
nausea/v
dizzy
orthos hypotension
sedation
dizzy
orthos hypotension
sedation
89
Acetaminophen - MOA
analgesic and antipyretic
inhibit PG endoperoxidase H2 synthase and cyclooxygenase isoenzyme centrally, beta endorphine centrally
inhibit PG endoperoxidase H2 synthase and cyclooxygenase isoenzyme centrally, beta endorphine centrally
90
Acetaminophen - metabolized where?
liver
91
Acetaminophen - how does metabolizism in liver work?
1. conjugation to sulfate or glucuronide
2. also has minor withway oxidative metabolism to produce NAPQI
2. also has minor withway oxidative metabolism to produce NAPQI
92
NAPQI requires ? for detoxi and elimination
glutathione
93
When does hepatic toxicity occur with Acetaminophen?
glutathiaone pathways overwhelmed by increase in NAPQI or decr glutathione level
94
Acetaminophen - rare SE?
mild rash
bm suppresion - neutropenia, thrombcytopenia, granulocytosis
bm suppresion - neutropenia, thrombcytopenia, granulocytosis
95
Acetaminophen - chronic use avoid in which diseases?
hepatic or renal disease
96
NSAID: MOA?
inhibi cyclooxygenase and therefore synthesis of PG which mediate inflamm
decrease PG peripherlly and raise threshold activation of nociceptors
decrease PG peripherlly and raise threshold activation of nociceptors
97
Cox-1 vs cox2 = where present?
cox1 all cells, homeostatic function
cox2 injury or inflamm to produce inflamm process
cox2 injury or inflamm to produce inflamm process
98
Nonselective NSAIDs effect which cox?
both
99
NSAID: SE
GIB
renal failure
anaphylaxis
plt dysfunction
renal failure
anaphylaxis
plt dysfunction
100
NSAID: concern in __ healing
bone and cartilage healing
101
102
103
COX promotes prostacyclin which increases risk of?
vasodilator -- GI mucosa perforation as coxx1 incr mucus production and bicarb to protect in lining
104
cox1 and 2: effects on cardiovascular system
endothelial prostacyclin - vasodilation and thromboxane (plt aggregation) - cox1 inhibits plt >vasodil, whereas cox 2 inhibits prostacyclin >plt and may have prothrombotic effects to incr risk cv events
105
COX_ may incr risk of cv events
2
106
cox1 produces PG which causes what effect on kidney?
renal vasodilation -- renal blood flow and GFR
107
What drugs may interact with nsaids?
aspirin
oral anticoagulants
acei
diuretics
Glucocorticoids
Li
oral anticoagulants
acei
diuretics
Glucocorticoids
Li
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109
Pt at risk for adverse events during NSAID therapy:
1. dehydration/hypovol or impaire renal function -- risk failure
2. liver disease/chf
3. older
4. asthma - risk bronchospasm
5. in third trim pregnancy = prolong gest or premature closure of DA
6. tobacco/etoh hx of gastric/pud at increased risk for ulcer/GIB
2. liver disease/chf
3. older
4. asthma - risk bronchospasm
5. in third trim pregnancy = prolong gest or premature closure of DA
6. tobacco/etoh hx of gastric/pud at increased risk for ulcer/GIB
110
NO:O2 safe ratio?
50:50
111
NO - MOA thoughts?
similar to low dose opioids and or benzoes through effect on GABA
112
NO is contraindicated in pregnancy as it can cause...
folate antagonist, risk of Spina bifuda
113
Who to avoid NO in ?
decreased LOC
cannot follow instructions
sev copd - risk of hypercapnia with high o2
PTX
bowel obstruction (diffusion into cavities)
cannot follow instructions
sev copd - risk of hypercapnia with high o2
PTX
bowel obstruction (diffusion into cavities)
114
NO side effects
lightheaded
parasthesia
nausea
parasthesia
nausea
115
Low dose ketamine for analgesia - dose?
0.1-0,3mg/kg IV
116
117
SE of ketamine
dysphoria
vomit
hypersalivation
vomit
hypersalivation
118
Ketamine: receptor
NMDA
119
Less potent local anestheticc must be given in __ concentrated forms and __ doses to achieve equivalent effect
more
larger
larger
120
*Low tissue pH (5 or 6) in surrounding infected tissue delays the
onset of local anesthesia in cases such as abscess incision and drainage
by keeping more of the agent in an ionized state.
121
What increases/makes it faster local anesthesia onset of action?
alkalinization
vasodilators shorten duration of anesthesia
injection into vascular tissues
vasodilators shorten duration of anesthesia
injection into vascular tissues
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123
Techniques to reduce pain of infection
buffer local
counterirritation
slower rate injection
use of topic anesthetics
warming of solutions
distraction technique
counterirritation
slower rate injection
use of topic anesthetics
warming of solutions
distraction technique
124
More lipophilic __ cardiotoxic
more
125
Local anesthetic toxicity sx
lightheaded
h/a
tinnitus
paresthesia
m spasm
confusion
seizure
h/a
tinnitus
paresthesia
m spasm
confusion
seizure
126
Typical local anesthetic toxicity progression
begins with circumoral paresthesias,
dysarthria, and tinnitus or similar auditory phenomenon. These events
may be followed by a decreased level of consciousness progressing to
confusion, seizures, and coma. Longer-acting, more potent agents (e.g.,
bupivacaine, etidocaine) are more likely than lidocaine to cause CNS
symptoms at lower blood levels. Local anesthetic-induced seizures
should be treated with IV benzodiazepines and may be refractory to
normal dosing of neuroleptic medications.
127
**to decrease pain: A standard solution of sodium bicar-
bonate (8.4% in 50 mL) can be added to a syringe containing lidocaine
in a ratio of 1 : 10 (e.g., 1 mL bicarbonate to 10 mL lidocaine, or 0.5 mL
to 5 mL). Buffered lidocaine can be stocked in the ED and is effective
for up to 1 week.
128
Topical agent to mucosa examples
cocainelidocaine
tetracaine
benzocaine
tetracaine
benzocaine
129
Topical agents able to apply to open skin/wound for pain?
lido
epi
teracaine
epi
teracaine
130
1.Which of the following statements is true regarding pain trans-
mission?
a. Cardiac pain is transmitted via the sympathetic system.
b. Central post-stroke neuropathic pain is associated with
parietal infarcts.
c. Descending modulation of pain is mediated primarily
c. Descending modulation of pain is mediated primarily
through γ-aminobutyric acid (GABA).
d. Peripheral neurotransmitters include prostaglandins,
d. Peripheral neurotransmitters include prostaglandins,
histamines, and substance P.
Answer: A. As a general rule, all visceral pain is carried via sym-
pathetic afferents to ganglia and then to the spinal cord. Prostaglan-
dins, substance P, and histamine sensitize peripheral afferents but are
not neurotransmitters. The dorsal column tracts can down-modulate
ascending pain signals. Central post-stroke pain is clinically seen most
often after thalamic strokes. Descending tracts that modulate pain pro-
cessing at the dorsal horn use norepinephrine and serotonin, with the
effect of the former being most important regarding analgesia.
131
A 32-year-old male patient undergoing treatment for an ankle
sprain returns to the emergency department (ED) because of
inadequate pain relief from the medicines he was prescribed. He
is currently taking oxycodone, 10 mg PO every 4 hours, and ibu-
profen, 400 mg every 4 hours. What is the next most appropriate
medicine to add to his pain treatment regimen?
a. Add acetaminophen, 650 mg q4h.
b. Add tramadol, 50 mg PO q4h.
c. Increase ibuprofen to 800 mg.
d. Increase oxycodone to 15 mg.
c. Increase ibuprofen to 800 mg.
d. Increase oxycodone to 15 mg.
a
132
2.
Which of the following analgesics is matched with the correct
feature?
a. Fentanyl—prolongedQTintervalonelectrocardiography
b. Hydromorphone—active metabolites
a. Fentanyl—prolongedQTintervalonelectrocardiography
b. Hydromorphone—active metabolites
c. Meperidine—musclerigidity
d. Oxycodone—serotonin syndrome
D. Oxycodone has been associated with serotonin syn-
drome when coadministered with selective serotonin reuptake inhib-
itor (SSRI) medications. This is due to an active metabolite it shares
with morphine, hydromorphone, hydrocodone, and codeine. The fol-
lowing are the other correct associations:
