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NEUROANATOMY > ANALGESIA > Flashcards

ANALGESIA Flashcards

1
Q

circulating beta-endorphin is derived predominantly from the __________ where it is released

A

pituitary

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2
Q

circulating proenkephalins are derived from the ___________ and exocrine glands of the stomach and intestine

A

adrenal medulla

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3
Q

what is the precursor molecule for beta-endorphin?

A

proopiomelanocortin (POMC)

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4
Q

which type of analgesics modulate initial signal transduction for pain?

A

NSAIDs

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5
Q

which type of drugs blocks signal conduction in nociceptive fibers?

A

Na+ channel blockers (local anesthetics)

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6
Q

how do opioids antidepressants, NSAIDs and alpha-adrenergic agonists all modulate transmission of pain?

A

modulate transmission of pain sensation in the spinal cord by decreasing the signal relayed from peripheral to central pain pathways

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7
Q

activating a peripheral nerve leads to influx of what two cations which results in depolarization of the polarized nerve membrane and generation of an action potential?

A

influx of sodium & Calcium

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8
Q

sensitizing agents act via what two intracellular signaling systems can modulate both the extent of originating ion influx and the sensitivity of the voltage-gated sodium channels to increase the likelihood of propagation and conduction of the pain impulses?

A

G-proteins coupled receptor either activates Phospholipase C to increase Ca2+ release from intracellular stores and activates protein kinase C, OR increases cAMP, activates protein kinase A and phosphorylates sodium channels

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9
Q

What effect do Norepinephrine (acting via alpha-2 receptors), GABA (acting via GABAb receptors) and endogenous opiates, endorphin and encephalin have on the pre synaptic terminal in the spinal cord?

A

Norepinephrine, GABA, endogenous opiates, endorphin and encephalin all inhibit calcium entry to teh pre-synaptic terminal

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10
Q

what effect do norepinephrine, GABA, endogenous opiates, endorphin and encephalin have on the post-synaptic membrane in the spinal cord?

A

activate potassium channels, leading to an increase in K+ conductance and hyperpolarization of the cell
(reduces the likelihood of the depolarization and the onward transmission of the pain signal is interrupted)

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11
Q

what effect does activating mu opiate receptors have on the presynaptic terminal?

A

decreases calcium influx

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12
Q

what effect does activating mu opiate receptors have on the post-synaptic membrane?

A

increases potassium efflux

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13
Q

how do NMDA receptors cause sustained or intense activation of central transmission?

A

activating NMDA receptors leads to postsynaptic calcium influx (Ca2+ influx activates signal transduction ascades that can enhance both short-term and long term excitability of the synapse)

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14
Q

what are the two drugs that block NMDA receptors?

A

ketamine

dextromethorphan

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15
Q

how can ketamine and dextromethorphan be used to prevent surgery-induced sensitization?

A

preemptive block of NMDA receptors

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16
Q

what are some of the adverse effects of ketamine?

A

hallucinations, amnesia, CV pressor, increased ICP

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17
Q

what are some of the adverse effects of dextromethorphan?

A

dizziness, confusion, fatigue

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18
Q

what is allodynia?

A

normally innocuous stimuli are now painful

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19
Q

what is hyperalgesia?

A

high intensity stimuli perceived as more painful

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20
Q

what are some of the extra-neuronal inflammatory components?

A

bradykinin, protons, histamine, PGE2, Nerve growth factor (NGF)

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21
Q

how do the extra-neuronal inflammatory components (bradykinin, protons, histamine, PGE2, NGF) cause increased pain perception?

A

G-protein coupled effects
reduced activation threshold
increased current conducted

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22
Q

what are the intra-neuronal mechanisms that increased the pain perception?

A

Substance P & CGRP (released from termini of primary afferents)

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23
Q

how do the intra-neuronal molecules like substance P & CGRP increase pain perception?

A

stimulates inflammatory cells to release histamine and TNF-alpha, recruits granulocytes to the site of inflammation

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24
Q

what is neuropathic pain?

A

pain arising from transection of mechanical damage to the nerve axon

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25
Q

explain how neuropathic pain lead to the continued perception of injury

A

loss of neurotrophic support alters gene expression in the injured nerve fiber
-inflammatory cytokines alter gene expression in both injured and adjacent uninjured nerve fibers (changes in gene expression lead to altered sensitivity and activity of nociceptive fibers)

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26
Q

what Na+ channel blocking drug is used to treat trigeminal neuralgia?

A

CARBAMAZEPINE

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27
Q

The rewiring of the peripheral and central pain pathways following nerve damage involves changes in expression of what ion channel?

A

Na+

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28
Q

what are the adverse effects of opioids?

A 
Sedation
Resp. depression
N/V
increased ICP
Constipation
Urinary Retention
Itching around nose, urticaria
postural hypotension
behavioral restlessness
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29
Q

opioids act mainly as an agonist on what receptor?

A

mu-receptor agonist

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30
Q

what are the adverse effects of acetaminophen?

A

hepatic toxicity and liver failure at high doses, hypersensitivity

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31
Q

what are the main adverse effects of NSAIDs?

A

GI irritation, platelet inhibition, renal insufficiency or failure, cardiovascular hypersensitivity

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32
Q

what is the MOA of the gabapentinoids?

A

inhibition of voltage gated Ca2+ channels

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33
Q

how are the gabapentinoids (gabapentin, pregabalin) administered?

A

PO

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34
Q

what are the main adverse effects of the gabapentinoids?

A

sedation, peripheral edema, GI, decrease dose for renal insufficiency

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35
Q

what is the MOA for clonidine and dexmedetomidine?

A

alpha-2 receptor agonist

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36
Q

what are the adverse effects of clonidine?

A

sedation, hypotension, bradycardia

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37
Q

what are the functions of the Mu opioid receptor (OP-3)?

A

supraspinal & spinal analgesia; sedation; decrease respiration; decrease GI transit; modulation of hormone & NT release

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38
Q

what are the functions of the delta opioid (OP-1) receptors?

A

supraspinal & spinal analgesia; modulation of hormone and NT release

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39
Q

what are the functions of the kappa opioid (OP-2) receptors?

A

supraspinal & spinal analgesia; psychotomimetic effects; decrease GI transit

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40
Q

Name the opioid receptor type: endorphins> enkephalins> dynorphins

A

mu opioid receptor (OP-3)

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41
Q

name the opioid receptors type: enkephalins > endorphins & dynorphins

A

delta opioid receptors (OP-1)

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42
Q

name the opioid receptor type: dynorphins&raquo_space; endorphins & enkephalins

A

kappa opioid receptor (OP-2)

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43
Q

what are the american pain society and the american academy of pain medicine’s five MAIN recommendations?

A
  1. Try other treatments first
  2. assess the risk for abuse
  3. Keep expectations realistic
  4. Start w/ a short term trial
  5. Weight individuals potential harm / benefit ratio
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44
Q

for the opioids that are considered full agonist, which receptor do they mostly act on?

A

OP-3

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45
Q

which 4 full agonist (at the mu receptor) opioids have a low oral:IV potency ratio?

A

morphine
hydromorphone
oxymorphone
fentanyl

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46
Q

which full agonist at the mu receptor opioid drug has a high oral:IV potency ratio?

A

methadone

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47
Q

Name the 7 opioids that are considered full agonists at the mu receptor?

A 
Morphine
hydromorphone
oxymorphone
methadone
meperidine
fentanyl
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48
Q

which drug is the only full agonist opioid that also has some activity on kappa receptors?

A

morphine

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49
Q

name the 7 opioids that are only partial agonists at the mu receptor

A 
codeine
hydrocodone
oxycodone
pentazocine
nalbuphine
buprenorphine
butorphanol
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50
Q

which two opioids that are partial agonists at the mu receptor are only available in IV form?

A

Nalbuphine

Butorphanol

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51
Q

which opioid is often given as a patch to provide 48-72 hours of relatively stable drug delivery?

A

fentanyl

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52
Q

what is the benefit to the peripheral analgesia devise (PCA)?

A

the dose rate and max delivery/hr dose is set by te nurse or physician and the controls locked to prevent tampering

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53
Q

why does oral morphine have a low bioavailability?

A

it has a high first pass metabolism

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54
Q

which organ serves as the main reservoir for opiate distribution because it has greater relative bulk?

A

skeletal muscle

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55
Q

what can happen with frequent high dose administration or continuous infusion of highly lipophilic & slowly metabolized opioids (e.g. fentanyl)?

A

can lead to accumulation (depot storage site, can release drug slowly, once dosing is terminated)

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56
Q

opiates would really like to accumulate in what kind of tissue, but is limited by the poor blood supply to this tissue?

A

adipose tissue

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57
Q

explain how enkephalin signaling can persist, yet morphine has a loss of drug activity?

A

Enkephalin has a relative balance b/w desensitization and resensitization.
Morphine has a slow persistent desensitization and little recycling, favoring loss of drug activity

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58
Q

which adverse effects of opioids have a minimal chance of tolerizing?

A

miosis
constipation
convulsions

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59
Q

which adverse effects of opioids have a high chance of tolerizing?

A 
Analgesia
euphoria, dysphoria
mental clouding
sedation
resp. depression
antidiuresis
N/V
Cough Suppression
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60
Q

what is the most common and persistent side effect from opioids?

A

CONSTIPATION

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61
Q

what is the prophylactic treatment for opioid-induced constipation?

A

stool softener & laxatives (also increased consumption of fluids and dietary fiber)

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62
Q

what class of drugs may be useful to treat refractory constipation due to opioid agonists?

A

opioid antagonists (avoid in the presence of bowel obstruction)

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63
Q

what is the mechanism behind opiates causing constipation?

A

opiates have direct & anticholinergic actions to reduce motility

64
Q

what can be done to manage the somnolence caused by opioid therapy?

A
  • reduce or eliminate non-essential centrally-acting drugs
  • adjust analgesia dose-opioid rotation
  • consider drug treatment directed at symptom (e.g. methylphenidate)
65
Q

how can you help prevent persistent nausea in the context of opioid therapy?

A

gradual rather than rapid upward titration of the opioid dose (could also try changing the route of drug delivery)

66
Q

what are the mechanisms that explain why opioids can cause emesis?

A

direct effect on the chemoreceptor trigger zone
enhanced vestibular sensitivity
delayed gastric emptying

67
Q

when is there a major risk of respiratory depression with opioid therapy?

A
  • if opioids are titrated too rapidly
  • w/ sleep apnea syndrome (obesity, short neck, snoring)
  • if combined w/ sedative hypnotic
68
Q

what should you do if you start to see respiratory depression in a pt who is being treated with opioids?

A

withhold the dose until the respiration improves, or you can use naloxone

69
Q

what drug can you give in the event of opioid abuse/overdose induced respiratory depression that will help reverse the respiratory depression?

A

naloxone (opiate antagonist)

70
Q

what are the risks associated with use of naloxone with the treatment of opioid abuse induced respiratory depression?

A

risks of abstinence, aspiration, and severe pain

71
Q

how do you treat the pruritis caused by opioid therapy?

A

antihistamine drugs

72
Q

what is the classic triad of opiate overdose?

A

pinpoint pupils
coma
respiratory depression

73
Q

other than the classic triad of opioid overdose, what are some other adverse effects of opioid overdose?

A

altered mental status, severe perspiration, sock, pulmonary edema, unresponsiveness

74
Q

what are the 3 opiate antagonists?

A

Naloxone
Naltrexone
Nalmefene

75
Q

which opiate antagonist has the shortest half life?

A

naloxone (used to treat opiate intoxication and has a short duration of action)

76
Q

which opiate antagonist has the longest half life and is used to treat addiction?

A

Naltrexone

77
Q

opiate antagonists work at which opiate receptors?

A

all 3: mu, delta, kappa

78
Q

what is a major downside to using opiate antagonists?

A

can precipitate withdrawal in dependent pts

79
Q

how does Naltrexone decrease alcohol craving in alcoholics?

A

decreasing baseline beta-endorphin release

80
Q

what are the 3 major drug groups that can cause further CNS depression when used with opioids?

A

sedative-hypnotics
antipsychotic tranquilizers
MAO inhibitors

81
Q

what happens if you use sedative-hypnotics with opioids?

A

increased CNS depression, particularly resp. depression

82
Q

what happens if you use antipsychotic tranquilizers with opioids?

A

increased sedation

accentuation of CV effects (antimuscarinic and alpha-blocking actions)

83
Q

what happens if you use MAO inhibitors with opioids?

A

relative contraindication to all opioid analgesics b/c high incidence of hyperpyrexic coma; HTN

84
Q

codeine is converted to morphine by what enzyme?

A

CYP2D6 (normally accounts for up to 15% conversion of codeine to the more potent morphine)

85
Q

what happens to a pt taking codeine if they have renal insufficiency?

A

metabolites accumulate

86
Q

why is it a bad idea for nursing moms to be taking codeine?

A

mom can metabolize the drug to morphine and this morphine can accumulate in the neonatal system and prove fatal

87
Q

what is the adverse effect associated with high first pass metabolism of meperidine to normeperidine?

A

CNS toxicity

88
Q

which opioid is was originally synthesized as an anticholinergic?

A

meperidine

89
Q

which opioid can cause serotonin syndrome by inhibiting both 5-HT and NE reuptake?

A

meperidine

90
Q

why is meperidine such a crappy opioid?

A

less effective analgesic than other drugs, and has peripheral anticholinergic effects and central anticholinergic effects

91
Q

what factor facilitates increased fentanyl absorption?

A

increased skin temperature

92
Q

what makes methadone a unique and useful opioid agonist?

A

has long elimination half life (used in the treatment of opiate withdrawal)

93
Q

which opiate agonist is an aromatase inhibitor and has a long elimination half life?

A

methadone

94
Q

meperidine and its active metabolite ___________ accuulates with renal dysfunction or prolonged use at high doses

A

normeperidine

95
Q

morphine _________ are renally-excreted and can accumulate and lead to unanticipated changes in potency or side effects in pts with renal failure

A

glucuronides

96
Q

which two opioid drugs lack active metabolites and could be considered safe in the setting of renal failure?

A

hydromorphone & fentanyl

97
Q

why are adjuvant nonopioid agents used in the treatment for cancer pain?

A

to permit the lowest level of opiate dosing that can be effective and to maximize the pain relief

98
Q

the onset of opiate withdrawal depends on what?

A

the half-life of the abused drug

99
Q

opiate withdrawal peaks at what time and lasts for about how many days?

A

peaks at 36-48 hrs and lasts about 7-10 days

100
Q

what are the first signs of opiate withdrawal?

A

craving and drug-seeking behavior

101
Q

what are some of the symptoms and signs of opiate withdrawal that occur after the craving and drug-seeking behavior?

A

crawling sensation in skin, diaphoresis, rhinorrhea

Also, anxiety, fear, & sleep disturbance

102
Q

fever, seizures, hallucination and delirium do not occur with what drug withdrawal?

A

opioid

103
Q

the physical exam findings of agitation, diaphoresis, increased lacrimation, piloerection, and dilated pupils are all indicative of what?

A

opiate withdrawal

104
Q

ethanol and sedative-hyponotic withdrawal produces what signs/symptoms?

A

seizures, hyperthermia, HTN, tachycardia

105
Q

sympathomimetic intoxication may produce what symptoms and signs?

A

mydriasis, agitation, tachycardia, HTN

106
Q

what are the signs/symptoms of cholinergic agent intoxication?

A

diarrhea, vomiting

107
Q

how can you distinguish cholinergic intoxication from opioid withdrawal?

A

cholinergic intoxication has salivation, bradycardia & altered level of consciousness

108
Q

what is the short term inpatient treatment for opiate withdrawal?

A

methadone

109
Q

what is the outpatient treatment for opiate withdrawal?

A

clonidine (very effective for treating drug craving, sweating, piloerection, anxiety, and agitation)

110
Q

clonidine is an ineffective treatment of what opiate withdrawal symptoms?

A

insomnia, muscle cramps, GI symptoms

111
Q

term for physical dependence

A

dependence

112
Q

term for psychological dependence

A

addiction

113
Q

what defines dependence clinically?

A

once availability of the drug lapses and there is an appearance of withdrawal syndrome

114
Q

________ consists of compulsive, relapsing drug use despite negative consequences (often triggered by cravings in response to contextual clues)

A

addiction

115
Q

___________invariably occurs with chronic exposure, addiction does not

A

dependence

116
Q

which drug is a long acting opiate and is formulated with the antagonist naloxone to prevent pts from shooting the drug up?

A

buprenorphine (if drug is taken as indicated the naloxone isn’t absorbed and so the pt gets what they need, however if the pt shoots the drug up then the naloxone blocks any euphoric feelings)

117
Q

if you are in methadone maintenance therapy less than 180 days it is considered what?

A

detoxification

118
Q

if you are in methadone maintenance therapy more than 180 days it is considered what?

A

maintenance

119
Q

why can’t pts undergoing methadone maintenance therapy take additional opiates and experience euphoria?

A

the methadone has a very long half life and is preventing additional opioids from binding

120
Q

what is the treatment of choice for opioid dependent pregnant women?

A

methadone

121
Q

what are the adverse effects of methadone maintenance therapy?

A 
constipation, mild drowsiness, excess sweating, peripheral edema
reduced testosterone (reduced libido and sexual performance, erectile dysfunction)
Prolonged QTc and arrhythmia
122
Q

regarding buprenorphine: what is the result of very tight binding to opioid receptors?

A

displaces other opioids from receptors
triggers withdrawal in pts physically dependent on opioids
blocks the analgesic action of other opioids

123
Q

regarding buprenorphine: what is the result of slow dissociation from opioid receptors?

A

long duration of action, relieves withdrawal and cravings for greater than 24 hrs

124
Q

regarding buprenorphine: what is the result of no bioaccumulation?

A

allows quick titration to effective dose

125
Q

regarding buprenorphine: what is the result of the fact that it is a partial agonist with celiing effect?

A

has a very low risk of overdose, might be less effective than higher doses of methadone

126
Q

regarding buprenorphine: what is the result of Sublingual and IV absorption; poor oral absorption?

A

can be abused intravenously

127
Q

what is the test used to identify morphine, heroin, hydrocodone, and codeine in urine?

A

antibody-based enzymatic immunoassays

128
Q

if you want the exact drug and concentration of morphine, heroin, hydrocodone, and codeine what test do you have to perform?

A

GC-MS

129
Q

which metabolite of heroin is definitive evidence of heroin use?

A

6-MAM

130
Q

what does it mean if you have a morphine: codeine ration > 2:1?

A

indicates heroin or poppy seed use (if ratio is less than 2:1 then think codeine use)

131
Q

Synthetic opiates (fentanyl, meperidine, methadone) are ______________ negative

A

Enzymatic immunoassays (EIAs)

132
Q

which antibiotics can produce false-positive EIAs?

A

fluroquinolones (ciprofloxacin)

133
Q

how does gabapentin (pregabalin) work?

A

drugs bind to alpha2-delta subunit, preventing trafficking to cell surface (upreg. of voltage-gated Ca2+ channels occurs in hypersensitization)

134
Q

what is the pharmacological effect of gabapentin in dense synaptic connectionsn of neocortex, amygdala, & hippocampus?

A

inhibition of neuronal excitability

135
Q

how is gabapentin (pregabalin) excreted?

A

renal

136
Q

what are the 2 most common adverse effects of gabapentin-pregabalin?

A

dizziness & drowsiness

137
Q

how does lamotrigine-carbamazepine work?

A

blocks sodium channel function

138
Q

Lamotrigine-Carbamazepine has a BB warning fr what?

A

rash-Stevens Johnson syndrome

139
Q

what are the most common adverse effects of lamotrigine-carbamazepine?

A

diplopia, blurred vision

140
Q

anticonvulsants carry an increased risk for what adverse effect?

A

suicidal ideation

141
Q

regarding lamotrigine-carbamazepine: you need ot adjust the dose in __________ failure

A

hepatic

142
Q

both ketamine and dextromethorphan are limited by what adverse effect?

A

psychomimetic effects

143
Q

hepatic metabolism of tricyclic antidepressants with what CYP enzyme could cause drug interactions?

A

CYP2D6

144
Q

what are the adverse effects of TCAs?

A 
dizziness
headache
fatigue
drowsiness
lethargy
uneasiness
hypersomnia
difficulty concentrating
memory impairment
145
Q

TCAs work by blocking reuptake of what two molecules?

A

norepinephrine and 5-HT

146
Q

TCAs work on serotonin and norepinephrine in ________________ pathways

A

cortciospinal monoamines

147
Q

what are the adverse effects of dextromethorphan if they are abused?

A

hallucinogenic and habit forming

148
Q

name the drug: nonprescription opioid agonist that has no analgesia or potential for addiction (no BBB) access

A

Loperamide

149
Q

name the drug: prescription opioid agonist that is used as an antidiarrheal and contains atropine to discourage abuse

A

diphenoxylate

150
Q

which drug is used to treat alcohol dependence and craving by blocking? the elevation of dopamine levels arising from signals in the ventral tegmental area in the arcuate nucleus

A

naltrexone

151
Q

what is the toxicity associated with capsaicin?

A

increased pain, burning of eyes or mucus membrnaes

152
Q

what is the benefit of cod-liver oil?

A

alleviates musculoskeletal & osteoarthritic pain

153
Q

what is the toxicity associated with cod-liver oil?

A

increased bleeding risk oral anticoagulants, additive w/ antihypertensives, increased blood sugar

154
Q

what is the toxicity associated with devil’s claw?

A

adversely affects acid-inhibiting, BP & CV drugs

155
Q

what is the toxicity associated with epsom salts?

A

GI irritation, interacts with drugs affecting excretion and skeletal muscle relaxants

156
Q

what is the toxicity associated with white willow?

A

contains salicylates; potential interaction with anticoagulants, antiplatelet & oral drugs

NEUROANATOMY (11 decks)

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