Analgesics Flashcards
(185 cards)
1
Q
what are analgesics?
A
pain killers
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
3
Q
PGs are produced from what precursor?
A
arachidonic acid (AA)
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
5
Q
what is Cox 1?
A
the “good” cox
normal constituent of certain cells
6
Q
what is the role of Cox 1?
A
synthesize PGs to protect cells and maintain fxn
7
Q
which Cox is responsible for platelet aggregation, decreasing acid production, mucus bicarb layer of the gut, and renal vasodilation?
A
Cox 1
8
Q
what is Cox 2?
A
the “bad” Cox
9
Q
what is the role of Cox 2?
A
synthesizing Pgs in injured cells that mediate inflammation, pain, and fever
10
Q
what are the therapeutic classifications for non-steroidal anti-inflammatory drugs (NSAIDs)?
A
analgesic (pain killer), anti-pyretic (anti-fever), anti-inflammatory
11
Q
what is an anti-pyretic?
A
a fever reducing drug
12
Q
what does a non-selective (traditional) NSAID block?
A
both Cox 1 and 2
13
Q
are aspirin, ibuprofen, and naproxen non-selective or selective NSAIDs?
A
non-selective NSAIDs
14
Q
what does a selective NSAID block?
A
just Cox 2
15
Q
are celecoxib (celebrex) and Meloxicam (mobic) selective or non-selective NSAIDs?
A
selective NSAIDs
16
Q
are Cox 2 inhibitors selective or non-selective NSAIDs?
A
selective NSAIDs
17
Q
what are the only 2 selective NSAIDs on the market by prescription in the US?
A
celecoxib (celebrex) and Meloxicam (mobic)
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
19
Q
what are some examples of non-selective NSAIDs?
A
aspirin, ibuprofen (Motrin and Advil), naproxen (Aleve), ketoprofen, piricam (feldene), and indomethacin (indocin)
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
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
22
Q
what are common indications for Aspirin?
A
headache, fever, arthritis, tooth aches, body aches, and after an MI
23
Q
why is baby aspirin used after an MI?
A
bc low doses of aspirin provide them with good clot prevention
24
Q
in what age range is baby aspirin good for prevention of CVD?
A
50-59 yo
25
should other NSAIDs be taken while taking baby aspirin? why or why not?
no, bc higher doses of NSAIDs will block the cardioprotective effect
26
why is resistance training unsafe while taking daily aspirin?
bc the aspirin increases the risk of internal bleeding
27
describe the absorption of aspirin
absorbs rapidly from the GI tract
transformed into salicylate in the stomach and liver
may cross the placenta and into breast milk
28
what is the bioavailability of aspirin?
50-70%
29
what is the 1/2 life of aspirin?
2 hours
30
how is aspirin eliminated?
depends largely on hepatic biotransformation
renal excretion of unchanged drugs is usually small (<5% of the dose)
31
describe the absorption of ibuprofen
oral dose is rapidly absorbed
32
does ibuprofen undergo a lot of the 1st pass effect?
no
33
what is the bioavailability of ibuprofen?
90-99%
34
how is ibuprofen eliminated?
rapidly by the kidneys w/ 95% eliminated w/in 4 hours
35
what is the 1/2 life of ibuprofen?
1.8-2 hours
36
what is the peak plasma concentration of ibuprofen?
1-2 hours after a single dose
37
what are the side effects of non-selective NSAIDs?
headache, dizziness
GI irritation
bleeding
peripheral edema
renal dysfxn, tinnitus, confusion, metabolic acidosis
Reye's syndrome (pediatrics)
pseudoarthosis following a spinal fusion
38
when non-selective NSAIDs are used long term, what should be taken with it?
proton pump inhibitor (PPI) to reduce stomach acids
misoprostol (synthetic PG)
39
what can result from bleeding from non-selective NSAID use?
anemia and abnormal bleeding
40
what is Reye's syndrome?
relatively rare pediatric condition from use of aspirin in children 4-12
swelling in the brain and liver
41
what are the s/s of Reye/s syndrome?
lethargy, confusion, vomiting, seizures
42
why isn't Reye's syndrome very common anymore?
bc asprin is not routinely given to children anymore
43
what are the advantages of topic NSAIDs?
min side effects
relief of local superficial pain without changes to good PGs
44
what is pseudoarthrosis?
slow fusion or nonunion
45
why does pseudoarthrosis occur with non-selective NSAID use?
bc it stops Cox 2 mediated osteogenesis
46
non-selective NSAIDs should be avoided for how many months post-op?
6
47
after opioids are no longer needed post-op, what meds are recommended for pain?
Tylenol
48
are Cox 2 inhibitors selective or non-selective NSAIDs?
selective
49
how do Cox 2 inhibitors work?
by selectively inhibiting the synthesis of inflammatory PGs
50
what are the therapeutic effects of Cox-2 inhibitors?
analgesic (pain reducer), antipyretic (reduce fever), and antiinflammatory
same as non-selective NSAIDs
51
t/f: cox 2 inhibitor have a lower incidence of gastric irritation
true
52
t/f: cox 2 inhibitors allow for normal platelet activity
true
53
what NSAID is preferred in pts at risk for bleeding (pts on blood thinners)?
Cox 2 inhibitors
54
why are cox 2 inhibitors recommended for pts at risk for bleeding?
bc they allow for normal platelet activity
55
are cox 2 inhibitors slow or fast absorbing?
fast
56
when is the peak concentration of Cox 2 inhibitors?
about 3 hours
57
are cox 2 inhibitors metabolized by the liver?
yes
58
t/f: cox 2 inhibitors have extensive distribution
true
59
what is the 1/2 life of cox 2 inhibitors?
8-12 hours
60
what are the side effects of Cox 2 inhibitors?
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
61
what is acetaminophen?
a non-NSAID analgesic and antipyretic
62
is acetaminophen an antiinflammatory/anticoagulant?
no!
63
what is the mechanism of action of acetaminophen?
unique mechanism not clearly defined
64
t/f: acetaminophen has fewer side effects than NSAIDs
true
65
how long does the onset of action of acetaminophen take?
orally less than 1 hour
66
t/f: acetaminophen is rapidly and well absorbed in the GI tract
true
67
t/f: acetaminophen crosses the placenta and breast milk
true
68
what is the 1/2 life of acetaminophen in adults?
1-3 hours
69
what is the 1/2 life of acetaminophen in neonates?
4-10 hours
70
can young children take acetaminophen? why or why not?
yes bc it is free of the risk of Reye's syndrome
71
when is the peak concentration of acetaminophen?
about 2 hours
72
t/f: acetaminophen is metabolized by the liver
true
73
t/f: high doses of acetaminophen can lead to liver toxicity
true
74
how is acetaminophen usually excreted?
by the kidneys
75
what are the side effects of acetaminophen?
nausea, vomiting, constipation
headache
rash
hepatic toxicity/failure
renal failure w/high dosage/chronic use
leukopenia, neutropenia, and pacytopenia
76
what is leukopenia?
reduced WBCs
77
what is neutropenia?
reduced neutrophils (a type of WBC)
78
what is pancytopenia?
reduced WBCs and RBCs
79
can acetaminophen be used safely in pts with liver disease?
yes, as long as the pt doesn't consume alcohol
80
why is acetaminophen often preferred in pts with liver disease over NSAIDs?
bc of the absence of platelet impairment, GI toxicity, and nephrotoxicity associated with NSAIDs
81
t/f: pts with chronic liver disease have a prolonged 1/2 life of acetaminophen
true
82
what are the therapeutic effects of NSAIDs?
analgesic, antipyretic, anti-inflammatory, antithrombotic/anticoagulant, and anticancer (not well supported)
83
what are the therapeutic effects of acetaminophen?
analgesic
antipyretic
84
combining NSAIDs and acetaminophen is advantageous for ____ to ____ pain
mild, moderate
85
what are some other non-opioid analgesics?
anticonvulsants
SNRIs (serotonin NE reuptake inhibitors)
tricyclic antidepressants (TCAs)
86
how do anticonvulsants, SNRIs, and TCAs work to relieve pain?
they are membrane stabilizing drugs so they make it less likely that an AP with be fired to cause pain
87
what is the downside of TCAs?
they can have an anticholinergic effect in higher doses
88
what drugs are involved in CNS pharmacology?
opioids, antiparkinsonism drugs, pyschopharmacology, antiepileptic drugs, and antispastic drugs
89
what are opioid analgesics?
very powerful analgesics
90
how do opioids work?
they use endogenous peptides already in the system (enkephalin, B-endorphins, dynorphins)
91
what are the endogenous peptides?
enkephalin, B-endorphins, dynorphins
92
t/f: opioid use the body's built in anti-nociceptive system
true
93
where are the opioid receptors?
on the presynaptic terminals of C and a delta fibers (pain fibers)
94
what were opioids originally used as?
sleep aids
95
how do opioids work?
by blocking the pain-mediating NTs
96
what are the 3 opioid receptors?
mu, kappa, and delta
97
what are mu receptors?
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
what receptor is the primary target of opioids?
mu receptors
99
what is the primary effect of the mu receptors?
analgesic
100
what are the side effects of the mu receptors?
euphoria, respiratory depression, bradycardia, decreased GI motility, and dependence
101
what are k (kappa) receptors?
located in the limbic and other diencephalon areas, BS, and SC
primary effect: spinal analgesia
side effects: sedation, respiratory depression, dependence
102
where is the primary location of mu receptors?
in the BS and med thalamus
103
where is the primary location of k receptors?
in the limbic system and other diencephalon areas, BS, and SC
104
what is the primary effect of k receptors?
spinal analgesic
105
what are the side effects of k receptors?
sedation, respiratory depression, dependence
106
what are delta receptors?
primarily located in the brain
effects: psychotomimetric, analgesia
107
what are the effects of delta receptors?
psychotomimetric, analgesia
108
what are psychotomimetric effects?
effects that mimic the symptoms of psychosis or schizophrenia
109
can opioids be selective and nonselective to certain receptors?
yes
110
what is the mechanism of action of opioids?
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
what are common opioid agonists?
morphine
fentanyl
hydromorphone (Dilaudid)
oxycodone/hydrocodone
codeine
methadone
buprenorphine
112
opioid agonists treat ___ to ____ pain
moderate, severe
113
what is morphine?
an analgesic
114
what is fentanyl?
a very potent anesthetic
115
fentanyl is ___ times more potent than morphine
80
116
what is hydromorphone?
an analgesic, antitussive, and anti diarrhea
117
what does antitussive mean?
reduced coughing
118
what is oxycodone/hydrocodone?
analgesic with greater risk for addiction and dependency
dif ions associated with each
119
what is codeine?
an analgesic and antitussive
weak agonist w/low affinity for mu receptors
lower potency
120
codeine is __ as potent as morphine
1/2
121
what is methadone?
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
what is buprenorphine?
used for ppl w/opioid addiction to reduce the drug craving
123
what opioid agonists can be used for withdrawal and addiction?
methodone, buprenorphine, and codeine
124
what are schedule drugs?
drugs that have a risk for dependency
125
are all opioids schedule drugs?
yes
126
is a schedule 1 or schedule 5 drug more dangerous?
schedule 1 drug
127
t/f: the lower the schedule number in schedule drugs, the more dangerous they are
true
128
what are common opioid antagonists?
Naloxone (Narcan)
Naltrexone
129
what does Naloxone (Narcan) do?
blocks all types of opioid receptors
130
what is Naltrexone used for?
opioid and alcohol abuse to treat w/drawal symptoms
131
what does PO mean?
oral
132
what does SQ mean?
subcutaneous
133
what does IM mean?
intramuscular
134
what does IV mean?
intravenous?
135
t/f: patches are transdermal
true
136
t/f: patches have a much longer onset of action
true
137
are patches meant for acute or chronic pain?
chronic
138
after the removal of a fentanyl patch, how long can the effects last?
up to 24 hours
139
what precaution should PTs know about their pts with fentanyl patches?
don't directly touch the patch with your bare skin
140
what are the consequences of opioid use?
tolerance
dependence
addiction
141
what is tolerance?
the need for more of the drug to achieve a particular effect
142
pts will respond to the same amount of a drug for ___ weeks after stopping a drug
1-2
143
what is dependence?
the need for the receptors to be occupied (stimulated), resulting is w/drawal upon removal of the drug
144
is dependence physiological or psychological?
it can be either or both
145
what addiction?
disease of the brain reward and motivation pathways
pathological pursuit of addiction substance knowing they have a problem
146
when are drugs most addictive
when they are taken in a way other than as prescribed (ie snorting an oral med)
147
t/f: taking opioids for more than a few days increase the risk for abuse
true
148
pts are more likely to become addicted after only __ days of opioid use
5
149
what is the most common side effect of opioids?
sedation
150
what are the side effects of opioids?
sedation
nausea
respiratory depression
delirium/confusion (psychosis symptoms)
bowel dysfunction (mostly constipation)
miosis (constricted pupils)
pruritis (intense itching)
151
what are the s/s of opioid withdrawal?
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
what is neonatal abstinence syndrome?
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
what are the contraindications for opioid use?
hx of substance abuse
hypersensitivity
IBS/Chron's
uncontrolled asthma
154
why would someone with a hypersensitivity be contraindicated for opioids?
bc opioid can increase pain sometimes (don't really know why but may have to do with genetics)
155
why would someone with IBS/Chron's be contraindicated for opioids?
bc of the GI issues related to opioid use
156
why would someone with uncontrolled asthma be contraindicated for opioids?
bc respiratory depression is a common side effect of opioids
157
what are medications used for opioid use disorder?
methadone
naltrexone
buprenorphine
(weaker opioid agonists to reduce w/drawl symptoms)
158
what do meds for opioid use disorder do?
they substantially reduce w/drawal symptoms
decrease relapse rates and time to relapse
reduce risk for death
159
what is opioid use disorder characterized by?
maladaptive use of opioid causing harm to the patient
160
what is a common comorbidity of opioid use disorder?
chronic musculoskeletal conditions
161
what is a patient controlled analgesia (PCA)?
a button that can be used and controlled by the patient to release pain killers
162
what drug is primarily used in PCAs?
opioid analgesics
163
what is demand dose in PCAs?
the dose delivered when the button is pressed by the pt
164
what is the lockout interval in PCAs?
the few minutes when the PCA will not release more drugs even if the patient is pressing the button
165
what conditions are PCA's used in?
acute surgical pain, cancer pain, and chronic pain
166
t/f: PCAs provide a safer and more effective way to reduce pain
true
167
t/f: opioid work better for improving pain related functioning than non-opioids
false
168
what is the most effective pain relief pharmacologically?
ibuprofen with acetaminophen
169
why do we believe that opioids are so much stronger?
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
t/f: children have differences in pharmacodynamics and pharmacokinetics with opioid analgesics
true
171
do infants have more or less opioid receptors?
more
172
what is the consequence of infants having more opioid receptors?
they are more sensitive to opioids
173
why does opioid dosing in children vary with body surface area?
bc in children, body surface area I used rather than weight to estimate metabolism
174
what non-pharmacological interventions can PT counsel pts in?
relaxton techniques, mediation, pain management team, etc
175
what are precautions PTs should be aware of with pts on opioids?
psychosis, respiratory depression, constipation, bradycardia, nausea and vomitting, sedation (fall risk), hyperalgesia, and allodynia
176
is neuropathic pain responsive to NSAIDs?
no
177
what is the first line of treatment in neuropathic pain?
antidepressants
178
why are antidepressants used to treat neuropathic pain?
bc they are membrane stabilizers that work by modifying the sensitization of the pain fibers
179
what are some drugs used for the pharmacological management of neuropathic pain?
opioids, local anesthetics, anticonvulsants, NMDA antagonists
180
what are the descriptors of neuropathic pain?
burning, electric shock-like, tingling, choosing, numbness and tingling, paresthesias
181
what are common populations affected by neuropathic pain?
pts with diabetes, post-herpetic neuralgia, CRPS, HIV, MS, fibromyalgia, and amputations
182
why may analgesics fail to work?
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
what do PTs need to do in pain management?
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
t/f: pts with depression are more at risk for developing an addiction
true
185
t/f: women are more at risk for more debilitating symptoms
true
