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CLIN MED - SPRING EXAM 2 > Pharm - Pain & NSAIDs/Opioids > Flashcards

Pharm - Pain & NSAIDs/Opioids Flashcards

1
Q

What kind of drugs are step 1 on the analgesic ladder?

A

aspirin, acetaminophen, NSAIDs

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2
Q

What type of pain do step 1 drugs on the analgesic ladder address?

A

MILD pain

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3
Q

What kind of drugs are step 2 on the analgesic ladder?

A

weaker opioids

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4
Q

What type of pain do step 2 drugs on the analgesic ladder address?

A

mild to MODERATE pain

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5
Q

What are step 3 drugs on the analgesic ladder?

A

stronger opioids

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6
Q

What kind of pain do step 3 drugs on the analgesic ladder address?

A

Moderate to SEVERE pain

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7
Q

What should be used at each step of the analgesic ladder?

A

Combinations of medicines

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8
Q

What can the PT implement outside of the analgesic ladder to help with pain?

A

Non-medication options

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9
Q

What are the pharmacological effects of NSAIDs?

A
  • reduce inflammation
  • provide mild to moderate pain relief
  • reduce body temp associated with fever
  • reduce blood clotting by inhibiting platelet aggregation
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10
Q

What is the mechanism of action for NSAIDs?

A

inhibit synthesis of prostaglandins

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11
Q

What does the effect of prostaglandins depend on?

A
  • organ or tissue involved
  • receptor
  • bodily function or physiological situation
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12
Q

What are prostaglandins?

A

fatty acid derivatives of arachidonic acid that have diverse hormone-like effects dependent on body region

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13
Q

Are prostaglandins present in most cells?

A

YES

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14
Q

What should we know about the prostaglandin half-life?

A

SHORT

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15
Q

Do prostaglandins have a short or long duration?

A

Short duration of action

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16
Q

What cells does prostaglandin ONLY affect?

A

Those that are close by

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17
Q

What are some of the varied effects of prostaglandins?

A
  • add or subtract platelet buildup for blood clot formation
  • vasodilation or constriction
  • bronchoconstriction
  • fever
  • modulate pain perception
  • cause uterine contractions
  • inhibit gastric acid secretions
  • modulate ?? in GI tract
  • regulate several hormones
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18
Q

How do NSAIDs inhibit prostaglandin synthesis?

A

by inhibiting cyclooxygenase (COX 1 and COX2)

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19
Q

What does COX 1 enzyme do?

A
  • expressed in most tissue
  • regulates normal cell processes
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20
Q

When is COX2 enzyme expressed?

A

in response to injury/inflammation

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21
Q

What does low dose asprin do?

A

irreversably inhibits platelet cox 1

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22
Q

What side effects do COX 1 enzymes have on the GI mucosa?

A
  • gastic protection
  • increase mucus secretion
  • increase bicarbonate
  • increase mucosal blood flow
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23
Q

What can COX 1 inhibition cause?

A
  • peptic ulcers
  • GI bleeding
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24
Q

What can COX 1 and 2 enzymes do to the kidneys?

A
  • afferent arteriolar vasodilatoin
  • increase Na and water excretion
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25
Q

What side effects can COX inhibition have on the kidneys?

A
  • na and water retention
  • hypertension
  • hemodynamic acute kidney injury
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26
Q

What are the cardiovascular effects that COX 2 enzymes have?

A
  • vasodilation
  • inhibit platelet aggregation
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27
Q

What are the cardiovascular affects that COX 1 enzymes have?

A
  • platelet aggregation
  • vasoconstriction
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28
Q

What side effects can COX 1 & 2 inhibition have on the cardiovascular system?

A
  • stroke
  • myocardial infarction
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29
Q

What are some COX 1 selective medications?

A

asprin
naproxen (ALEVE)

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30
Q

What are some nonselective NSAIDs?

A
  • ibuprofen (advil, motrin)
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31
Q

What is an example of a 5-50-fold COX 2 selective medication?

A

Celecoxib

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32
Q

What is an example of a >50-fold COX 2 elective medication?

A

Etoricoxib (arcoxia)

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33
Q

Do Cox 1 selective or cox2 selective have more GI effects?

A

COX 1 selective

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34
Q

Do COX 1 selective or COX 2 selective medications have increased cardiovascular effects?

A

COX 2 selective

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35
Q

What do COX 2 selective NSAIDs do?

A
  • increase risk for CV events
  • decrease risk for GI side effects
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36
Q

What do semiselective NSAIDs do?

A
  • increase affinity for COX2 but still retain activity for COX1
  • use with caution in patients at increased CV risk
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37
Q

What do NON selective NSAIDs do?

A
  • decreased risk for CV events
  • increased risk for GI side effects
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38
Q

What do irreversible nonselective NSAIDs do?

A
  • cardio-protective at low doses
  • increased risk for GI side effects
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39
Q

What should we know about acetaminophen and its efficacy compared to aspirin and NSAIDs?

A
  • equal efficacy to aspirin and NSAIDs for analgesia and antipyeretic effects
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40
Q

Does acetaminophen have GI effects?

A

no

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41
Q

What can happen with acetaminophen at high doses?

A

liver toxicity

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42
Q

What can nonopioids treat?

A
  • mild/mod pain
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43
Q

What are examples of nonopioids?

A
  • NSAIDs
  • Acetaminophen
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44
Q

What can opioids treat?

A

moderate/severe pain

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45
Q

Are opioids controlled substances?

A

yes

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46
Q

What do opioids bind to?

A

specific CNS receptors

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47
Q

What are the sources of opioid analgesics?

A
  • natural (opium poppy)
  • synthetic
  • semisynthetic
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48
Q

How do opioids work?

A

interact with opioids receptors and reduce intensity of pain signals and feelings of pain

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49
Q

What are some examples of natural opioid analgesics?

A

opiates
- morphine
- codene

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50
Q

What are some examples of opioids analgesics?

A

opioids
- methadone
- tramadol
- fentanyl

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51
Q

What are some examples of semisynthetic opioids?

A

opioids
- oxycodone
- hydrocodone

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52
Q

What does endogenous mean?

A

within the spinal cord

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53
Q

What are some endogenous receptors?

A
  • mu
  • kappa
  • delta
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54
Q

What are the functions of mu receptors?

A
  • supraspinal and spinal analgesia, sedation
  • inhibition of respiration, slowed GI transit
  • modulation of hormone and neurotransmitter release
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55
Q

What are the functions of delta opioid receptors?

A
  • supraspinal and spinal analgesia, sedation
  • modulation of hormone and neurotransmitter release
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56
Q

What are the functions of kappa receptors?

A
  • supraspinal and spinal analgesia, sedation
  • psychotomometic effects
  • slowed GI transit
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57
Q

What are the endogenous opioid peptide affinity of mu receptors?

A

endorphins>enkephalines>dynorphins

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58
Q

What are the endogenous opioid peptide affinity of delta receptors?

A

enkephalins> endorphins and dynorphins

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59
Q

What are the endogenous opioid peptide affinity of kappa receptors?

A

dynorphins» endorphins and enkephalins

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60
Q

What are the ionic mechanics opioid analgesics?

A

opioid analgesics inhibit synaptic activity partly through direct activation of opioid receptors and partly through release of endogenous opioids

61
Q

Where are all three types of receptors found?

A
  • in high concentration in the dorsal horn
  • in the brainstem
    > medulla, locus ceruleus and midbrain periaqueductal grey
62
Q

Where have mu receptors been found also?

A

on the peripheral terminal of sensory neurons

63
Q

What are strong agonists for?

A

severe pain

64
Q

What receptor do strong agonists have an affinity for?

A

Mu receptors

65
Q

What are examples of strong agonists?

A

morphine, methadone, meperidine (demerol), fentanyl

66
Q

What are moderate agonists for?

A

moderate pain

67
Q

What affinity do moderate agonists have?

A

less affinity or efficacy

68
Q

What are examples of moderate agonists?

A
  • codeine, oxycodone
69
Q

What are weak agonists for?

A

moderate pain

70
Q

What affinity do weak agonists have?

A

less affinity or efficacy

71
Q

What is an example of a weak agonist?

A

propoxyphene (darvon)

72
Q

What is an agonist?

A

A drug which produces a pharmacological effect when combined with a receptor

73
Q

What is an antagonist?

A

a drug which reduces the effect of an agonist

74
Q

What are mixed agonist-antagonists?

A
  • exhibit some agonist and some antagonist activity
75
Q

What can mixed agonist-antagonists do?

A

provide pain relief without some side effects

76
Q

What are some examples of mixed agonist-antagonists?

A

buprenophine, nalbuphine (nubain)

77
Q

What do antagonists do?

A

block all opioid receptors

78
Q

What are antagonists used for?

A

overdose and addiction

79
Q

What are some examples of antagonists?

A

naloxone, naltrexone

80
Q

What is the half life of codeine?

A

2.5-3 hours

81
Q

What are the side effects of codeine?

A

constipation, nausea

82
Q

What are prescribing considerations for codeine?

A

> 65mg may not be appropriate particularly in elderly

83
Q

What is the potency of codeine relating to morphine?

A

15% of morphine

84
Q

What is the half life of fentanyl?

A

10-20 mins

85
Q

What are some side effects of fentanyl?

A

somnolence, diarrhea, nausea, constipation

86
Q

What are some prescribing considerations for fentanyl?

A

fast acting transmucosal formulations are suitable for breakthrough pain

87
Q

What is the potency of fentanyl compared to morphine?

A

80x more potent than morpine

88
Q

What is the half life of hydromorphone?

A

2-3 hours

89
Q

What are the side effects of hydromorphone?

A

somnolence, constipation, nausea, dizziness

90
Q

What are the prescribing considerations for Hydromorphone?

A

metabolites can build up in those with compromised renal function

91
Q

What is the potency of hydromorphone compare to morphine?

A

8-10x more potent than morphine

92
Q

What is the half life of mepheridine?

A

3 h

93
Q

What are the side effects of merpheridine?

A

tachycardia, mydriasis, dysphoria

94
Q

What are some prescribing considerations for merpheridine?

A

normerperidine is neurotoxic, so meperidine should not be used to treat chronic pain syndromes

95
Q

What is the potency of merpheridine compared to morphine?

A

Morphine is 10x more potent than merperidine

96
Q

What is the half life of morphine?

A

2-3 h

97
Q

What are some side effects of morphine?

A

sedation, conception, nausea, morphine toxicity

98
Q

What are some prescription considerations for morphine?

A

should not be used in patients with renal dysfuction

99
Q

What is morphine considered?

A

the standard by which other drugs are measured

100
Q

What is the half life of oxycodone?

A

3-4.5 hours

101
Q

What are some side effects of oxycodone?

A

constipation, fatigue, dizziness

102
Q

What are some prescription considerations for oxycodone?

A

some patients may be “fast metabolizers”

103
Q

What is the potency of oxycodone compared to morphine?

A

1.5-2x more potent than morphine

104
Q

What is the half life of tramadol?

A

5.5-7 hours

105
Q

What are some side effects of tramadol?

A

nausea, vomiting, constipation

106
Q

What are some prescribing considerations for tramadol?

A

dual mechanism of action because these agents also inhibit serotonin and norepinepherine reuptake

107
Q

What is the potency of tramadol compared to morpheine?

A

higher for neuropathic pain than for nociceptive

108
Q

When are most pharmacokinetics well absorbed ? (method of intake)

A

when given by subcutaneous, intramuscular, and oral routes

109
Q

What is there an extensive list of with some pharmacokinetics?

A

first pass effect
- may need a higher dose orally than parenteral

110
Q

Where are pharmacokinetics widely distributed?

A

body tissue

111
Q

Where are pharmacokinetics localized?

A

in higher concentration in higher perfused tissue (brain, lung, liver, kidneys, and spleen)

112
Q

What are CNS effects of pharmacokinetics?

A
  • analgesia
  • euphoria
  • sedation
  • respiratory depression
  • antitussive
  • miosis (constricted pupils)
  • N&V
  • truncal rigidity
113
Q

What are peripherial effects of pharmacokinetics?

A
  • cardiovascular system
  • GI tract
  • smooth muscle
  • renal
  • pruritis (itching)
114
Q

When can problems arise with opioids?

A

when used in combination with other CNS depressents

115
Q

What is a relaxive contraindication of opioids?

A

use wit MAO (can cause serotonin toxicity)

116
Q

What should we know about analgesic activity with agonist-antagonist drugs?

A

varied, less activity than strong gonists

117
Q

What receptors are there for agonist-antagonist drugs?

A
  • nalbuphine and pentazocine are kappa agonists with weak mu receptor antagonist activity
  • Buprenorphine is a mu-receptor with weak kappa and receptor antagonist activity
118
Q

What are the effects of agonist-antagonist drugs?

A

pain relief without SE

119
Q

What are some qualities of anatagonists?

A
  • pure opioid receptor antagonists
  • have few other effects
  • greatest affinity for mu receptors
120
Q

What is the primary clinical use of antagonists?

A

in the management of acute opioid overdose

121
Q

What is naltrexone also used for?

A

treatment of ethanol dependency

122
Q

What are opioid clinical uses?

A
  • analgesia
  • cough suppression
  • treatment of diarrhea
  • management of acute pulmonary edema
  • anesthesia
123
Q

When are analgesic applications of opioids most effective?

A
  • with mod/severe constant pain
  • also appropriate for acute or chronic pain
  • frequently alter the perception of pain
124
Q

What is a benefit of oral administration?

A

easiest, most convinient

125
Q

What is IM?

A

intramuscular

126
Q

What are benefits of IV administration?

A
  • more complete and rapid
127
Q

What is PCA??

A

Patient Controlled Analgesia

128
Q

What are adverse side effects of opioids?

A
  • behavioral restlesssness, hyperactivity
  • respiratory depression
  • N&V
  • increased intracranial pressure
  • postural hypotension
  • constipation
  • urinary retention
  • itching
129
Q

What is addiction?

A

repeated seeking and ingestion of substance for mood-altering and pleasurable experiences

130
Q

What is tolerance?

A

the gradual loss of effectiveness with repeated administration of therapeutic levels of morphine or its surrogates

131
Q

What is physical dependency?

A

marked by a relatively specific withdrawal or abstinence syndrome

132
Q

What is psychological dependency?

A

reinforced by the development of the physical dependency
- euphoria, indifference, and sedation tend to promote their compulsive use

133
Q

What are symptoms of narcotic withdrawl?

A
  • Body aches
  • Diarrhea
  • Fever
  • Chills
  • Insomnia
  • Irritability
  • Loss of appetite
  • Nausea/vomiting
  • Runny nose
  • Shivering
  • Sneezing
  • Stomach cramps
  • Sweating
  • Tachycardia
  • Uncontrolled yawning
  • Weakness/fatigue
134
Q

What are the characteristics of opioid overdose?

A

– Pupillary constriction,
comatose state, and respiratory
depression

135
Q

When is opioid overdose confirmed?

A
  • Overdose is confirmed if prompt recovery is gained through the use
    of naloxone
136
Q

What are some specific PT considerations for pain medications?

A
  • Pain can negatively impact efficacy of PT
    intervention
  • Total pain relief can negatively impact
    efficacy of PT intervention
  • Intermittent pain control can result in
    higher drug use with less pain control
    *Need =Appropriate Type & Dose
    *Timing for optimum PT rx
    *Monitoring of effects, efficacy
137
Q

What are some types of chronic pain?

A

Neuropathic pain
Migraines
Fibromyalgia
Trigeminal neuralgia
Central pain syndromes
Complex regional pain syndrome

138
Q

What are some adjuvant analgesic medications?

A
  • Anticonvulsants
  • Tricyclic antidepressants
  • Norepinephrine and serotonin reuptake
    inhibitors
  • Muscle relaxants
  • Antihistamines
  • Local anesthetics
  • Psychostimulants
  • Nerve blocks
139
Q

What is neuropathic pain?

A

burning or shooting

140
Q

What is neuropathic pain associated with?

A
  • associated with migraine, post-herpetic
    neuralgia, diabetic neuropathy, peripheral
    neuropathy, malignant nerve infiltration
  • May lead to continuous or stimulus-evoked
    pain; pain is not necessarily related to the
    amount of nerve damage
  • Allodynia may occur
141
Q

What are some condition based pain medications?

A
  • Migraines
  • Fibromyalgia
  • Trigeminal neuralgia
  • Cancer-related pain
  • OA and RA medications
  • Gout medications
142
Q

What are some abortive therapy migraine headache agents?

A

Abortive therapy
– NSAIDs – decrease inflammation
– Triptans – target serotonin (Imitrex)
– Ergot alkaloids - cause vasoconstriction of carotid artery beds (Ergotamine tartrate)

143
Q

What are some preventive therapy migraine agents?

A

Preventative therapy
– Beta blockers
– Tricyclic antidepressants
– Monoamine oxidase inhibitor antidepressants
– Selective serotonin reuptake antidepressants
– Anticonvulsants
– Calcium channel blockers
– NSAIDs

144
Q

What is fibromyalgia characterized by?

A

chronic muscle and joint pain,
extreme fatigue, and tender points

145
Q

What are some medications for fibromyalgia?

A

Medications
– Anticonvulsants
* Gabapentin and pregabalin
– Selective serotonin and norepinephrine
reuptake inhibitor antidepressants
* Duloxetine (Cymbalta) and milnacipran
(Savella)

146
Q

What is trigeminal neuralgia?

A

Tic douloureux – produces sudden, severe, recurrent unilateral face pain

147
Q

What are some medications therapies for trigeminal neuralgia?

A

Medication therapy
– Anticonvulsants
* First line: carbamazepine (Tegretol)
* Second line: gabapentin and phenytoin
(Dilantin)

148
Q

What is cancer pain described as? How do we manage it?

A

Cancer Pain
* Pain can be a mixture of acute pain related to the disease and pain related to the therapeutic interventions
* Non-pharmacologic therapies for managing pain include physical and cognitive modalities, nerve blocks

149
Q

What are some pain medications for cancer?

A
  • Opiates
  • Corticosteroids
  • Anticonvulsants
  • Tricyclic antidepressants
  • Norepinephrine and serotonin reuptake inhibitor
    antidepressants
  • Muscle relaxants
  • Antihistamines
  • Anesthetics
  • Psychostimulants

CLIN MED - SPRING EXAM 2 (4 decks)

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