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DPT 530 > Analgesics > Flashcards

Analgesics Flashcards

1
Q

what are analgesics?

A

pain killers

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2
Q

what are prostaglandins (PGs)?

A

non-opioid analgesics that initiates pain, inflammation, and fever in injured tissue or protect the GI tract and mediate clotting in healthy tissue

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3
Q

PGs are produced from what precursor?

A

arachidonic acid (AA)

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4
Q

what is the process of PG biosynthesis?

A

cell damage causes a release of AA

AA is converted to PGs by cyclooxygenase (Cox) 1 and 2

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5
Q

what is Cox 1?

A

the “good” cox

normal constituent of certain cells

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6
Q

what is the role of Cox 1?

A

synthesize PGs to protect cells and maintain fxn

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7
Q

which Cox is responsible for platelet aggregation, decreasing acid production, mucus bicarb layer of the gut, and renal vasodilation?

A

Cox 1

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8
Q

what is Cox 2?

A

the “bad” Cox

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9
Q

what is the role of Cox 2?

A

synthesizing Pgs in injured cells that mediate inflammation, pain, and fever

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10
Q

what are the therapeutic classifications for non-steroidal anti-inflammatory drugs (NSAIDs)?

A

analgesic (pain killer), anti-pyretic (anti-fever), anti-inflammatory

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11
Q

what is an anti-pyretic?

A

a fever reducing drug

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12
Q

what does a non-selective (traditional) NSAID block?

A

both Cox 1 and 2

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13
Q

are aspirin, ibuprofen, and naproxen non-selective or selective NSAIDs?

A

non-selective NSAIDs

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14
Q

what does a selective NSAID block?

A

just Cox 2

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15
Q

are celecoxib (celebrex) and Meloxicam (mobic) selective or non-selective NSAIDs?

A

selective NSAIDs

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16
Q

are Cox 2 inhibitors selective or non-selective NSAIDs?

A

selective NSAIDs

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17
Q

what are the only 2 selective NSAIDs on the market by prescription in the US?

A

celecoxib (celebrex) and Meloxicam (mobic)

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18
Q

what is the mechanism of action of NSAIDs?

A

they block Cox 1 and/or 2 to stop the conversion of AA into PGs

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19
Q

what are some examples of non-selective NSAIDs?

A

aspirin, ibuprofen (Motrin and Advil), naproxen (Aleve), ketoprofen, piricam (feldene), and indomethacin (indocin)

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20
Q

do selective or non-selective NSAIDs inhibit pain, fever, and inflammation and cause GI damage and increase clotting risk?

A

non-selective NSAIDs

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21
Q

what results from long-term Cox-1 inhibition from non-selective NSAIDs?

A

decrease in GI mucosa and GI damage

decrease in clotting mechanism and increased bleeding risk

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22
Q

what are common indications for Aspirin?

A

headache, fever, arthritis, tooth aches, body aches, and after an MI

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23
Q

why is baby aspirin used after an MI?

A

bc low doses of aspirin provide them with good clot prevention

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24
Q

in what age range is baby aspirin good for prevention of CVD?

A

50-59 yo

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25
Q

should other NSAIDs be taken while taking baby aspirin? why or why not?

A

no, bc higher doses of NSAIDs will block the cardioprotective effect

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26
Q

why is resistance training unsafe while taking daily aspirin?

A

bc the aspirin increases the risk of internal bleeding

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27
Q

describe the absorption of aspirin

A

absorbs rapidly from the GI tract

transformed into salicylate in the stomach and liver

may cross the placenta and into breast milk

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28
Q

what is the bioavailability of aspirin?

A

50-70%

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29
Q

what is the 1/2 life of aspirin?

A

2 hours

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30
Q

how is aspirin eliminated?

A

depends largely on hepatic biotransformation

renal excretion of unchanged drugs is usually small (<5% of the dose)

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31
Q

describe the absorption of ibuprofen

A

oral dose is rapidly absorbed

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32
Q

does ibuprofen undergo a lot of the 1st pass effect?

A

no

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33
Q

what is the bioavailability of ibuprofen?

A

90-99%

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34
Q

how is ibuprofen eliminated?

A

rapidly by the kidneys w/ 95% eliminated w/in 4 hours

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35
Q

what is the 1/2 life of ibuprofen?

A

1.8-2 hours

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36
Q

what is the peak plasma concentration of ibuprofen?

A

1-2 hours after a single dose

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37
Q

what are the side effects of non-selective NSAIDs?

A

headache, dizziness

GI irritation

bleeding

peripheral edema

renal dysfxn, tinnitus, confusion, metabolic acidosis

Reye’s syndrome (pediatrics)

pseudoarthosis following a spinal fusion

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38
Q

when non-selective NSAIDs are used long term, what should be taken with it?

A

proton pump inhibitor (PPI) to reduce stomach acids

misoprostol (synthetic PG)

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39
Q

what can result from bleeding from non-selective NSAID use?

A

anemia and abnormal bleeding

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40
Q

what is Reye’s syndrome?

A

relatively rare pediatric condition from use of aspirin in children 4-12

swelling in the brain and liver

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41
Q

what are the s/s of Reye/s syndrome?

A

lethargy, confusion, vomiting, seizures

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42
Q

why isn’t Reye’s syndrome very common anymore?

A

bc asprin is not routinely given to children anymore

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43
Q

what are the advantages of topic NSAIDs?

A

min side effects

relief of local superficial pain without changes to good PGs

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44
Q

what is pseudoarthrosis?

A

slow fusion or nonunion

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45
Q

why does pseudoarthrosis occur with non-selective NSAID use?

A

bc it stops Cox 2 mediated osteogenesis

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46
Q

non-selective NSAIDs should be avoided for how many months post-op?

A

6

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47
Q

after opioids are no longer needed post-op, what meds are recommended for pain?

A

Tylenol

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48
Q

are Cox 2 inhibitors selective or non-selective NSAIDs?

A

selective

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49
Q

how do Cox 2 inhibitors work?

A

by selectively inhibiting the synthesis of inflammatory PGs

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50
Q

what are the therapeutic effects of Cox-2 inhibitors?

A

analgesic (pain reducer), antipyretic (reduce fever), and antiinflammatory

same as non-selective NSAIDs

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51
Q

t/f: cox 2 inhibitor have a lower incidence of gastric irritation

A

true

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52
Q

t/f: cox 2 inhibitors allow for normal platelet activity

A

true

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53
Q

what NSAID is preferred in pts at risk for bleeding (pts on blood thinners)?

A

Cox 2 inhibitors

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54
Q

why are cox 2 inhibitors recommended for pts at risk for bleeding?

A

bc they allow for normal platelet activity

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55
Q

are cox 2 inhibitors slow or fast absorbing?

A

fast

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56
Q

when is the peak concentration of Cox 2 inhibitors?

A

about 3 hours

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57
Q

are cox 2 inhibitors metabolized by the liver?

A

yes

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58
Q

t/f: cox 2 inhibitors have extensive distribution

A

true

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59
Q

what is the 1/2 life of cox 2 inhibitors?

A

8-12 hours

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60
Q

what are the side effects of Cox 2 inhibitors?

A

some GI distress

increased CV incidents (acute heart attack, stroke, sudden coronary death) with long term use (over 9 mo)

contraindicated in pts with CABG

decreased effectiveness of ACE inhibitors

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61
Q

what is acetaminophen?

A

a non-NSAID analgesic and antipyretic

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62
Q

is acetaminophen an antiinflammatory/anticoagulant?

A

no!

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63
Q

what is the mechanism of action of acetaminophen?

A

unique mechanism not clearly defined

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64
Q

t/f: acetaminophen has fewer side effects than NSAIDs

A

true

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65
Q

how long does the onset of action of acetaminophen take?

A

orally less than 1 hour

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66
Q

t/f: acetaminophen is rapidly and well absorbed in the GI tract

A

true

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67
Q

t/f: acetaminophen crosses the placenta and breast milk

A

true

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68
Q

what is the 1/2 life of acetaminophen in adults?

A

1-3 hours

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69
Q

what is the 1/2 life of acetaminophen in neonates?

A

4-10 hours

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70
Q

can young children take acetaminophen? why or why not?

A

yes bc it is free of the risk of Reye’s syndrome

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71
Q

when is the peak concentration of acetaminophen?

A

about 2 hours

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72
Q

t/f: acetaminophen is metabolized by the liver

A

true

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73
Q

t/f: high doses of acetaminophen can lead to liver toxicity

A

true

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74
Q

how is acetaminophen usually excreted?

A

by the kidneys

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75
Q

what are the side effects of acetaminophen?

A

nausea, vomiting, constipation

headache

rash

hepatic toxicity/failure

renal failure w/high dosage/chronic use

leukopenia, neutropenia, and pacytopenia

76
Q

what is leukopenia?

A

reduced WBCs

77
Q

what is neutropenia?

A

reduced neutrophils (a type of WBC)

78
Q

what is pancytopenia?

A

reduced WBCs and RBCs

79
Q

can acetaminophen be used safely in pts with liver disease?

A

yes, as long as the pt doesn’t consume alcohol

80
Q

why is acetaminophen often preferred in pts with liver disease over NSAIDs?

A

bc of the absence of platelet impairment, GI toxicity, and nephrotoxicity associated with NSAIDs

81
Q

t/f: pts with chronic liver disease have a prolonged 1/2 life of acetaminophen

A

true

82
Q

what are the therapeutic effects of NSAIDs?

A

analgesic, antipyretic, anti-inflammatory, antithrombotic/anticoagulant, and anticancer (not well supported)

83
Q

what are the therapeutic effects of acetaminophen?

A

analgesic

antipyretic

84
Q

combining NSAIDs and acetaminophen is advantageous for ____ to ____ pain

A

mild, moderate

85
Q

what are some other non-opioid analgesics?

A

anticonvulsants

SNRIs (serotonin NE reuptake inhibitors)

tricyclic antidepressants (TCAs)

86
Q

how do anticonvulsants, SNRIs, and TCAs work to relieve pain?

A

they are membrane stabilizing drugs so they make it less likely that an AP with be fired to cause pain

87
Q

what is the downside of TCAs?

A

they can have an anticholinergic effect in higher doses

88
Q

what drugs are involved in CNS pharmacology?

A

opioids, antiparkinsonism drugs, pyschopharmacology, antiepileptic drugs, and antispastic drugs

89
Q

what are opioid analgesics?

A

very powerful analgesics

90
Q

how do opioids work?

A

they use endogenous peptides already in the system (enkephalin, B-endorphins, dynorphins)

91
Q

what are the endogenous peptides?

A

enkephalin, B-endorphins, dynorphins

92
Q

t/f: opioid use the body’s built in anti-nociceptive system

A

true

93
Q

where are the opioid receptors?

A

on the presynaptic terminals of C and a delta fibers (pain fibers)

94
Q

what were opioids originally used as?

A

sleep aids

95
Q

how do opioids work?

A

by blocking the pain-mediating NTs

96
Q

what are the 3 opioid receptors?

A

mu, kappa, and delta

97
Q

what are mu receptors?

A

the primary target of opioids

located primarily in the BS and med thalamus

primary effect: analgesic

side effects: euphoria, respiratory depression, bradycardia, decreased GI motility, and dependence

98
Q

what receptor is the primary target of opioids?

A

mu receptors

99
Q

what is the primary effect of the mu receptors?

A

analgesic

100
Q

what are the side effects of the mu receptors?

A

euphoria, respiratory depression, bradycardia, decreased GI motility, and dependence

101
Q

what are k (kappa) receptors?

A

located in the limbic and other diencephalon areas, BS, and SC

primary effect: spinal analgesia

side effects: sedation, respiratory depression, dependence

102
Q

where is the primary location of mu receptors?

A

in the BS and med thalamus

103
Q

where is the primary location of k receptors?

A

in the limbic system and other diencephalon areas, BS, and SC

104
Q

what is the primary effect of k receptors?

A

spinal analgesic

105
Q

what are the side effects of k receptors?

A

sedation, respiratory depression, dependence

106
Q

what are delta receptors?

A

primarily located in the brain

effects: psychotomimetric, analgesia

107
Q

what are the effects of delta receptors?

A

psychotomimetric, analgesia

108
Q

what are psychotomimetric effects?

A

effects that mimic the symptoms of psychosis or schizophrenia

109
Q

can opioids be selective and nonselective to certain receptors?

A

yes

110
Q

what is the mechanism of action of opioids?

A

has actions at several levels of the NS

inhibition of NT released

increase K+ outward current

activation of descending inhibitory controls in the midbrain

111
Q

what are common opioid agonists?

A

morphine

fentanyl

hydromorphone (Dilaudid)

oxycodone/hydrocodone

codeine

methadone

buprenorphine

112
Q

opioid agonists treat ___ to ____ pain

A

moderate, severe

113
Q

what is morphine?

A

an analgesic

114
Q

what is fentanyl?

A

a very potent anesthetic

115
Q

fentanyl is ___ times more potent than morphine

A

80

116
Q

what is hydromorphone?

A

an analgesic, antitussive, and anti diarrhea

117
Q

what does antitussive mean?

A

reduced coughing

118
Q

what is oxycodone/hydrocodone?

A

analgesic with greater risk for addiction and dependency

dif ions associated with each

119
Q

what is codeine?

A

an analgesic and antitussive

weak agonist w/low affinity for mu receptors

lower potency

120
Q

codeine is __ as potent as morphine

A

1/2

121
Q

what is methadone?

A

analgesic

used for withdrawal and addiction

weak agonist w/low affinity for mu receptors

unique synthetic opioid (can be used in ppl with opioid allergies)

122
Q

what is buprenorphine?

A

used for ppl w/opioid addiction to reduce the drug craving

123
Q

what opioid agonists can be used for withdrawal and addiction?

A

methodone, buprenorphine, and codeine

124
Q

what are schedule drugs?

A

drugs that have a risk for dependency

125
Q

are all opioids schedule drugs?

A

yes

126
Q

is a schedule 1 or schedule 5 drug more dangerous?

A

schedule 1 drug

127
Q

t/f: the lower the schedule number in schedule drugs, the more dangerous they are

A

true

128
Q

what are common opioid antagonists?

A

Naloxone (Narcan)

Naltrexone

129
Q

what does Naloxone (Narcan) do?

A

blocks all types of opioid receptors

130
Q

what is Naltrexone used for?

A

opioid and alcohol abuse to treat w/drawal symptoms

131
Q

what does PO mean?

A

oral

132
Q

what does SQ mean?

A

subcutaneous

133
Q

what does IM mean?

A

intramuscular

134
Q

what does IV mean?

A

intravenous?

135
Q

t/f: patches are transdermal

A

true

136
Q

t/f: patches have a much longer onset of action

A

true

137
Q

are patches meant for acute or chronic pain?

A

chronic

138
Q

after the removal of a fentanyl patch, how long can the effects last?

A

up to 24 hours

139
Q

what precaution should PTs know about their pts with fentanyl patches?

A

don’t directly touch the patch with your bare skin

140
Q

what are the consequences of opioid use?

A

tolerance

dependence

addiction

141
Q

what is tolerance?

A

the need for more of the drug to achieve a particular effect

142
Q

pts will respond to the same amount of a drug for ___ weeks after stopping a drug

A

1-2

143
Q

what is dependence?

A

the need for the receptors to be occupied (stimulated), resulting is w/drawal upon removal of the drug

144
Q

is dependence physiological or psychological?

A

it can be either or both

145
Q

what addiction?

A

disease of the brain reward and motivation pathways

pathological pursuit of addiction substance knowing they have a problem

146
Q

when are drugs most addictive

A

when they are taken in a way other than as prescribed (ie snorting an oral med)

147
Q

t/f: taking opioids for more than a few days increase the risk for abuse

A

true

148
Q

pts are more likely to become addicted after only __ days of opioid use

A

5

149
Q

what is the most common side effect of opioids?

A

sedation

150
Q

what are the side effects of opioids?

A

sedation

nausea

respiratory depression

delirium/confusion (psychosis symptoms)

bowel dysfunction (mostly constipation)

miosis (constricted pupils)

pruritis (intense itching)

151
Q

what are the s/s of opioid withdrawal?

A

sweating

shaking

headahce

nausea, vomiting, diarrhea

abdominal cramping

inability to sleep

confusion, agitation, depression, anxiety, and other behavioral changes

allodynia and hyperalgesia

neonatal abstinence syndrome

152
Q

what is neonatal abstinence syndrome?

A

babies born from a mother w/opioid abuse problems

w/drawal from a drug as a newborn bc they become detached from mom who had been on opioids

153
Q

what are the contraindications for opioid use?

A

hx of substance abuse

hypersensitivity

IBS/Chron’s

uncontrolled asthma

154
Q

why would someone with a hypersensitivity be contraindicated for opioids?

A

bc opioid can increase pain sometimes (don’t really know why but may have to do with genetics)

155
Q

why would someone with IBS/Chron’s be contraindicated for opioids?

A

bc of the GI issues related to opioid use

156
Q

why would someone with uncontrolled asthma be contraindicated for opioids?

A

bc respiratory depression is a common side effect of opioids

157
Q

what are medications used for opioid use disorder?

A

methadone

naltrexone

buprenorphine

(weaker opioid agonists to reduce w/drawl symptoms)

158
Q

what do meds for opioid use disorder do?

A

they substantially reduce w/drawal symptoms

decrease relapse rates and time to relapse

reduce risk for death

159
Q

what is opioid use disorder characterized by?

A

maladaptive use of opioid causing harm to the patient

160
Q

what is a common comorbidity of opioid use disorder?

A

chronic musculoskeletal conditions

161
Q

what is a patient controlled analgesia (PCA)?

A

a button that can be used and controlled by the patient to release pain killers

162
Q

what drug is primarily used in PCAs?

A

opioid analgesics

163
Q

what is demand dose in PCAs?

A

the dose delivered when the button is pressed by the pt

164
Q

what is the lockout interval in PCAs?

A

the few minutes when the PCA will not release more drugs even if the patient is pressing the button

165
Q

what conditions are PCA’s used in?

A

acute surgical pain, cancer pain, and chronic pain

166
Q

t/f: PCAs provide a safer and more effective way to reduce pain

A

true

167
Q

t/f: opioid work better for improving pain related functioning than non-opioids

A

false

168
Q

what is the most effective pain relief pharmacologically?

A

ibuprofen with acetaminophen

169
Q

why do we believe that opioids are so much stronger?

A

when given IV, opioids have no ceiling effect

psychotherapeutic effects of opioids relieve emotional distress of pain and is likely much stronger than the pain relieving effects

the WHO pain ladder

marketing

170
Q

t/f: children have differences in pharmacodynamics and pharmacokinetics with opioid analgesics

A

true

171
Q

do infants have more or less opioid receptors?

A

more

172
Q

what is the consequence of infants having more opioid receptors?

A

they are more sensitive to opioids

173
Q

why does opioid dosing in children vary with body surface area?

A

bc in children, body surface area I used rather than weight to estimate metabolism

174
Q

what non-pharmacological interventions can PT counsel pts in?

A

relaxton techniques, mediation, pain management team, etc

175
Q

what are precautions PTs should be aware of with pts on opioids?

A

psychosis, respiratory depression, constipation, bradycardia, nausea and vomitting, sedation (fall risk), hyperalgesia, and allodynia

176
Q

is neuropathic pain responsive to NSAIDs?

A

no

177
Q

what is the first line of treatment in neuropathic pain?

A

antidepressants

178
Q

why are antidepressants used to treat neuropathic pain?

A

bc they are membrane stabilizers that work by modifying the sensitization of the pain fibers

179
Q

what are some drugs used for the pharmacological management of neuropathic pain?

A

opioids, local anesthetics, anticonvulsants, NMDA antagonists

180
Q

what are the descriptors of neuropathic pain?

A

burning, electric shock-like, tingling, choosing, numbness and tingling, paresthesias

181
Q

what are common populations affected by neuropathic pain?

A

pts with diabetes, post-herpetic neuralgia, CRPS, HIV, MS, fibromyalgia, and amputations

182
Q

why may analgesics fail to work?

A

overestimating efficacy of the drug

underestimating the analgesic requirement of the pt

lack of knowledge in analgesics

pt noncompliance due to drug fears

pt wants to pls the PT by not complaining when the meds aren’t working as intended

183
Q

what do PTs need to do in pain management?

A

ID pts at high risk for developing persistent pain

lower pt dependence on pain meds by providing and actively engaging them in a more sustainable plan (AKA PT!)

184
Q

t/f: pts with depression are more at risk for developing an addiction

A

true

185
Q

t/f: women are more at risk for more debilitating symptoms

A

true

DPT 530 (14 decks)

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