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Pharm I > Pain > Flashcards

Pain Flashcards

1
Q

Autonomic responses of acute pain

A 
Guarding
Grimacing
Diaphoresis
Increased HR
Increased RR
Increased BP
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2
Q

Goals of therapy

A

Not to be 100% pain free, but to reduce the sensation of pain such that appropriate care or ADLS can be provided or achieve without causing disability or impairment
The expectations of the pt and the practitioner should support goal
Pt-prescriber mismatch- goals should be the same

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3
Q

Pain assessment

A 
P-provoking/palliative factors
Q-quality
R-region/radiate
S- severity/intensity
T- temporal/time (onset, duration, frequency)
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4
Q

Acetaminophen IV injection formulation

A 
Ofirmev
Expensive
Many restrictions for hospital use
Must inject slowly over 15 mins
Monotherapy in mild to moderate pain
Adjunct therapy in opioids in moderate to severe pain
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5
Q

Tramadol side effects

A

Seizures- contraindicated in patients with a seizure history (may lower threshold)
GI- upset stomach, diarrhea
Physical dependence- physiological withdrawal
Abuse- “psychological dependency” (C1V in TN)

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6
Q

Tramadol drug interactions

A

SSRIs/SNRIs- serotonin syndrome, GI bleeds

Tryptan migraine abortants (serotonin syndrome as well)

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7
Q

S/Sx of serotonin syndrome

A 
Agitation or restlessness
Confusion
Rapid HR and htn
Dilated pupils
Loss of muscle coordination or twitching muscles
Diarrhea
HA
Shivering 
Goose bumps
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8
Q

Severe serotonin syndrome sx

A

High fever
Seizures
Irregular heartbeat
Unconsciousness

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9
Q

Tramadol monitoring

A

Achievement of goals
S/Sx tolerance
Misuse/abuse

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10
Q

General principles of opioid management

A

Always assess risk of abuse and addiction
All acute principals to pain management apply
Always try to eliminate causes
Try to limit doses and duration
Want to meet goals while minimizing side effects
Utilize adjuvant medications, esp in situations where a combo of issues could be occurring simultaneously (depression, anxiety, etc)

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11
Q

Opiates and opioids- MOA

A

Modify both sensory and affective aspects of pain
Inhibit the transmission of input from the periphery to the spinal cord
Also activates descending inhibitory pathways that modulate transmission to the spinal cord

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12
Q

What are the opioid receptors?

A

Mu
Kappa
Delta

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13
Q

Mu receptors

A

Appears to be the most important in mediating morphine (and other strong opioids) effects
Analgesia, resp depression, sedation, euphoria, miosis, physical dependence, decreased GI motility

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14
Q

Chemical classes of opioids

A

Phenanthrenes
Phenylpiperidine derivatives
Diphenylheptane derivative

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15
Q

Phenanthrenes

A 
Morphine
Codeine
Hydromorphone
Oxycodone
Oxymorphone
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16
Q

Phenylpiperidine derivatives

A

Meperidine

Fentanyl

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17
Q

Diphenylheptane derivative

A

Methadone

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18
Q

Pure opioid products

A 
Effective for moderate to severe pain
Immediate and ER products available
-Morphine
-Oxycodone
-Hydromorphone
-Oxymorphone
-Fentanyl
-Methadone
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19
Q

Absorption of opioids

A

Most agents are well-absorbed, however some may undergo first-pass metabolism reducing overall bioavailability

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20
Q

Common opioid adverse effects

A 
Constipation (80%)
Dry mouth
Nausea (20%)/vomiting (15%)
Sedation
Pruritis (2-10%)
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21
Q

Constipation from opioids

A

Common to all opioids
Opioid effect on CNS, spinal cord, myenteric plexus of gut
Easier to prevent than treat
Tolerance does not develop to constipation
Dietary interventions alone usually not sufficient

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22
Q

Nociceptive pain

A

Usually propagated by mediators or noxious stimulus often localized

  • Somatic: bone, joint, muscle, connective tissue
  • Visceral: Organ
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23
Q

Neuropathic pain

A

Interruption or damage to the actual impulse transmission pathway often regional or radiating

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24
Q

Mediators of nociceptive pain

A

Prostaglandins
Prostacyclins
Histamine serotonin
Substance P

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25
Q

Functional pain

A

Pain in response to abnormal functioning of the nervous system

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26
Q

What is the time span for determining chronic pain?

A

Persistent pain lasting > 3 mos

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27
Q

Time span for acute pain

A

Comes on quickly, can be moderate to severe in intensity and only lasts a short period (less than 1-2 weeks) of time

  • Usually nociceptive in type
  • Usually considered a beneficial process warning us of potential harmful situations
  • Severe or undertreated acute pain can lead to negative consequences
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28
Q

Common types of chronic pain

A 
Back pain
Arthritis
Headaches
Knee pain
Cancer
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29
Q

Responses to chronic untreated pain

A

Anxiety
Hostility
Insomnia
Depression

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30
Q

Malignant pain

A

Usually implies cancer pain

Usually is associated with a terminal condition

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31
Q

Nonmalignant pain

A

Not usually associated with an acute cause of death frequently but not always neuropathic

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32
Q

Step 1 of the modified WHO pain ladder

A

Mild pain
Non-opioids +/- adjuvant
Non-opioids: APAP, ASA, NSAIDS, Tramadol

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33
Q

Step two of modified WHO pain ladder

A 
Mild to moderate pain
Mild-mod. opioids
\+/- non-opioids
\+/- adjuvant
Mild-mod opioids: Vicodin (Hydrocodon/APAP)
Percocet (Oxycodone/APAP)
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34
Q

Step 3 of the modified WHO pain ladder

A 
Mod-severe pain
Mod-severe opioids
\+/- non-opioids
\+/- adjuvant
Mod-severe opioids:
Morphine
Oxycodone
Dilaudid
Opana
Duragesic
Methadone
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35
Q

Non-opioid analgesics

A

Acetaminophen
NSAIDs
Tramadol

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36
Q

General info about acetaminophen

A

Commonly used agent and a part of a multitude of combination products
Of all agents utilized for pain, acetaminophen is the most tolerated with the least number of side effects

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37
Q

Effects of acetaminophen

A

Analgesic and antipyretic

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38
Q

MOA of acetaminophen

A

Likely centrally, generally unknown, however does NOT have anti-inflammatory properties in vivo

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39
Q

Uses for acetaminophen

A

Utilized for mild-moderate pain, headache, and fever
Onset- 30 mins
DOA- 4 hrs, longer with ER formulation

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40
Q

Absorption of acetaminophen

A

Can be given orally and rectally with excellent bioavailability
Peak: 30-60 min after oral administration

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41
Q

Distribution of acetaminophen

A

Similar concentrations throughout body fluids

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42
Q

Metabolism of acetaminophen

A

Undergoes glucuronidation, hydroxylation, and several other mechanisms of hepatic metabolism
Half-life: around 2 hours

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43
Q

Elimination of acetaminophen

A

Metabolites excreted predominately in urine

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44
Q

Drug interactions of acetaminophen

A

Alcohol
Cirrhosis/liver disease
Concommitant use with other products containing acetaminophen

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45
Q

Dosing interval of acetaminophen

A

Q4-6h

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46
Q

Max dose of acetaminophen

A

3.0 g/day

Optimal synergistic/additive effects seen with 500 mg dose in some injuries

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47
Q

Side effects of acetaminophen

A 
Nausea
Rash, less common
Hepatotoxicity
Bone marrow suppression
Combination with other hepatotoxic agents increases risks; generally tolerated.
48
Q

Side effects of NSAIDs

A 
GI toxicity (ulceration, abd pain)
Decreased renal perfusion
CV effects
Platelet dysfunction
Tinnitus
If using for cardioprotection, aspirin must be taken prior to other NSAIDs, take with food to reduce SEs
49
Q

Tramadol side effects

A

Side effects similar to opioids: seizures, serotonin syndrome, sweating, dry mouth
Do not use with MAOI; dosing limit 400 mg/day due to seizures.

50
Q

Opioids side effects

A

Constipation
Dry mouth
CNS effects (sedation, dizziness, N/V, etc), respiratory depression
Long-term use can allow tolerance to most of these effects

51
Q

Acetaminophen monitoring

A

Long term/chronic: AST/ALT, Alk phosphatase, GGT
Any s/sx of hepatitis
Caution with other products containing acetaminophen
Drug interactions?

52
Q

Effects of NSAIDs

A

Analgesic, anti-inflammatory, and antipyretic

53
Q

MOA of NSAIDs

A

Inhibition of cyclooxygenase enzymes interrupting prostaglandin synthesis and inflammation

54
Q

COX-1

A

Platelet function, protective prostaglandins

55
Q

COX-2

A

Inflammation, pain, and fever

56
Q

Bone pain and NSAIDs

A

Often an effective tx option for cancer, dental, fracture related bone pain. One of the most common causes of tumor-related pain
May affect bone healing long-term but does not affect short term

57
Q

Absorption of NSAIDs

A

Most agents are rapidly and completely absorbed

Food may slow absorption with no effect on bioavailability

58
Q

Distribution of NSAIDs

A

Well distributed into body fluids

59
Q

Metabolism of NSAIDs

A

Hepatic metabolism via glucuronidation and CYP450

60
Q

Elimination of NSAIDs

A

Renal elimination with some biliary excretion

61
Q

NSAIDs drug interactions

A

Anticoagulants
EtOH
SSRIs, SNRIs
ACE inhibitors

62
Q

ASA peak, half-life

A

Peak: 1 hr
1/2 life: 2-3 hours
Not typically used; low tolerance due to side effects

63
Q

Ibuprofen peak, 1/2 life

A

Peak: 15-30 mins
1/2 life: 2-4 hrs
Commonly used due to rapid onset and moderate duration

64
Q

Naproxen peak, 1/2 life

A

Peak: 1 hr
1/2 life: 14 hrs
Commonly used for longer duration of action

65
Q

Etodolac peak, 1/2 life

A

Peak: 1 hr
1/2 life: 7 hrs
Slightly more selective for COX-2 than other NSAIDs

66
Q

Diclofenac peak, 1/2 life

A

Peak: 2-3 hrs
1/2 life: 1-2 hours
Higher rate of SEs than other NSAIDs (esp. GI)

67
Q

Mefoxicam peak, 1/2 life

A

Peak: 5-10 hrs
1/2 life: 15-20 hrs
More selective for COX-2 than other NSAIDs, but less selective than coxibs

68
Q

Celecoxib peak, 1/2 life

A

Peak: 2-4 hrs
1/2 life: 6-12 hrs
Highly selective for COX-2

69
Q

Ketorolac (toradol) peak, 1/2 life

A

Peak: 2-4 hrs
1/2 life: 4-6 hrs
IV/IM

70
Q

Acetaminophen adult doses

A

Starting dose: 325-600 mg q4-6 hrs OR
1000 mg 3-4 times daily
Max dose: 1000 mg/dose
3000 g/day

71
Q

Ibuprofen adult doses

A

Starting: 400-800 mg 3-4 times daily
Max: 2400 mg/day

72
Q

Naproxen adult doses

A

250-500 mg twice daily

Max: 1000 mg/day

73
Q

NSAID adverse events

A 
Gastropathy
-Gastric cytoprotection if appropriate
-COX-2 selective inhibitors less irritating
-ASA diminishes benefit
Renal insufficiency
-Maintain adequate hydration
Effect on platelet aggregation
-Assess for coagulopathy
74
Q

Cardiac adverse effects, NSAIDs

A

Lots of data is available, some is conflicting
Even short-term use of NSAIDs in pts with preexisting heart disease increases risk for recurrent MI and death, the exception is ASA
Most common cause of drug-induced CHF exacerbations in geriatric pts

75
Q

NSAID monitoring

A

Achievement of goals
Side effects- renal, GI
CIs

76
Q

Contraindications of NASAIDs

A 
Renal insufficiency (BUN, SrCr)
GI bleeds/gastritis, duodenal ulcers (blood, tarry stools, upset stomach)
CV disease (CHF, MI, CVA)
77
Q

Selection of NSAIDs

A

If one product does not work, consider switching NSAID classes
ASA has the most clinically significant effect on platelets
Avoid ASA in children if they have the flu, flu-like sx, viral infections or chickenpox!

78
Q

Mneumonic to use for any drug consideration

A 
Allergy
Age
Race
Sex
Sx
Disease considerations
Drug-drug interactions
Labs
79
Q

Tramadol or tramadol/apap primary action

A

Central activity (serotonin, norepinephrine)

80
Q

Tramadol or tramadol/apap secondary action

A

Very weak Mu-1 receptor activity

81
Q

Use for tramadol or tramadol/apap

A

Second or third line option for neuropathic pain

Caution in pts at risk for seizures

82
Q

Tramadol dosing

A

Max dosing: 400 mg/day
Very short half-life
Frequent dosing

83
Q

Combination products with tramadol

A

When combined with APAP, the analgesic effect of tramadol is increased by about 1 hr (additive effect)
APAP dose is typically 500 mg for best effects
2 tabs orally every 4-6 hrs as needed for 5 days or less (each tablet contains tramadol 37.5 mg and acetaminophen 325 mg); MAX 8 tabs/day

84
Q

Kappa receptor

A

Analgesia, sedation, miosis, decreased GI motility

Dysphoria/euphoria, psychotomimetic effects

85
Q

Tolerance

A

An increased amount of medication needed to achieve the same pharmacological effects
We generally develop tolerance to sedative and euphoric effects occasionally long term some tolerance to analgesia and may occur but NOT to constipation, miosis or anxiolysis

86
Q

Physical dependence

A

Discontinuation of medication causes physiologic sx of withdrawal (NOT psychiatric need for the drug…no drug craving, compulsions, etc)

87
Q

Addiction

A

A psychiatric disease characterized by cravings, compulsions, continued use despite consequences, loss of control

88
Q

Combination opioid products

A

Effective for moderate to severe nociceptive pain (visceral and somatic)
Currently only available in immediate release products
-Hydrocodone/APAP
-Oxycodone/APAP
-Codeine/APAP

89
Q

Absorption of opioids

A

Most agents are well-absorbed, however some may undergo first-pass metabolism reducing overall bioavailability

90
Q

Distribution, metabolism, elimination of opioids

A

Distribute into well-perfused tissues such as the brain
Metabolism: Hepatic metabolism, largely through glucuronidation
Elimination: Primarily renal elimination with some biliary excretion

91
Q

Cmax after opioid dose

A

Depends on ROA

92
Q

Half-life of opioids at steady state

A

Half-life: 3-4 hrs

Steady state: 4-5 half lives

93
Q

Acute pain opioid dosing immediate-release preparation

A

Dose q4h for pain requiring around the clock coverage
Dose q4h PRN for intermittent pain
Adjust dose daily
-Mild/moderate pain increase 25-50%
-Severe/uncontrolled pain increase 50-100%
Adjust more quickly for severe uncontrolled pain

94
Q

Dosing for extended-release preparations of opioids

A

For the management of pain severe enough to require daily, around-the-clock opioid tx and for which alternative txs are inadequate
Dose q8, 12, or 24h (product specific)

95
Q

Dosing for extended-release preparations of opioids

A

For the management of pain severe enough to require daily, around-the-clock opioid tx and for which alternative txs are inadequate
Dose q8, 12, or 24h (product specific)
-Don’t crush or chew tablets
-May flush time-release granules down feeding tubes
Adjust dose q2-3 days (once steady state reached)

96
Q

Breakthrough dosing

A

Utilized in pain management as back up to a scheduled regimen
Use immediate-release opioids
-5-15% of 24-h dose (generally 10%)

97
Q

Morphine

A

All opioids are compared to morphine on a mg/mg basis or Morphine Equivalent Doses (MED)
-MEDD (Morphine equivalent daily dose)

98
Q

Multiple dosage forms of morphine

A 
Immediate release liquid and tablets
Sustained release q12-24 hrs
Sustained release pellets for sprinkle or G-tube
Injectable
Cost effective
99
Q

Impact of morphine metabolites

A 
Oral morphine is metabolized in the liver and oral mucosa to:
M6G
-Mu agonist activity (analgesic activity)
-Concentrations in men > women
M3G
-Myoclonus
-Neurotoxicity/allodynia
-Accumulates in pts with renal failure
100
Q

Hydromorphone

A

May be more appropriate than morphine in pts with
-High dose opioid needs
-Side effects from morphine
Available in oral and parenteral dosage forms
-ER formulation available
Caution in renal failure long term
-Metabolism is similar to morphine

101
Q

Oxymorphone

A

May be more appropriate than morphine in pts with:
-High dose opioid needs
-SEs from morphine
-Does not induce or inhibit the CYP2C9 or 3A4 pathways
Currently available in immediate and extended release tablets

102
Q

Codeine

A

Metabolized to morphine in the liver
Only effective for mild to moderate pain
Rapidly converted to active form…codeine
1/10 pts genetically do not convert codeine to morphine
VERY HIGH incidence of constipation and nausea/vomiting
Antitussive and antidiarrheal properties

103
Q

Hydrocodone

A

Recently classified as a CII
Mild to moderate pain when combined with APAP
Available as a single agent for more moderate to severe pain
Cannot write refills
Don’t use first or second line for neuropathic pain

104
Q

Meperidine

A

Currently NOT routinely recommended but may be used 1-2 doses IV/IM acute pain

105
Q

IV admin Fentanyl

A

Immediate onset of action
Easy to titrate
Fast elimination
Generally less hypotensive effects than morphine

106
Q

Transdermal (patch) Fentanyl

A 
Slow onset of action
Difficult to dose correctly
Difficult to respond to changing pain
Dependent on physiological state of pt
Useful as an alternative for parenteral administration
107
Q

Methadone indications

A

Addiction
Chronic pain
Acute pain
Half-life between 25-120 hrs

108
Q

Buprenorphine

A

Considered a partial mu-agonist

Used in Subxone, Subutex for opioid addiction

109
Q

Buprenorphine patches

A

5, 10, and 20 microgram/hr patches, schedule CII

Applied once weekly to manage chronic moderate to severe pain

110
Q

Uncommon opioid adverse effects

A 
Bad dreams/hallucinations
Dysphoria/delirium
Myoclonus/seizures
Urinary retention
Respiratory depression
111
Q

How to treat constipation from opioids

A

Combination stimulant with or without softeners are useful first-line medications
-Senna
-Senna + docusate sodium
Osmotic Cathartic- requires adequate hydration
-Milk of magnesia
-Lactulose (Chronulac)
-Polyethylene Glycol 3350 (Miralax)

112
Q

Prokinetic agents

A 
Selective opioid antagonist
-Naloxegol
-Methylnaltrexone
Bulk forming agents
-Avoid in debilitated pts
113
Q

N/V in opioids

A

Occurs with initiation or increased dose of opioids

  • Caused by stimulation of receptors in the brain and decreased GI motility
  • Try decreasing dose or changing the route of administration
  • Alternative opioid if refractory
114
Q

Tx of n/v in opioids

A 
Prevent or treat with dopamine-blocking antiemetics
-Prochlorperazine
-Haloperidol
-Metoclopramide
-Promethazine
Second line
-Serotonin antagonists
-Anticholinergics
115
Q

Tx for pruritis in opioids

A

Opioid rotation
Antihistamines
5HT3 antagonists
Other txs (Topical emollient (Sarna lotion))

116
Q

Sedation tx in opioids

A

Distinguish from exhaustion due to pain
Avoid other sedating medications
Reduce dose, alternative opioid or route of administration

117
Q

Management of respiratory depression in opioids

A

Identify those at highest risk
-Opioid naive pts- esp very young and old
-COPD, obesity, and recent abdominal surgery
If stable, treat contributing causes
-Reduce opioid dose and monitor
If unstable vital signs, pinpoint pupils
-Naloxone, 0.1 mg IV q 1-2 min

Pharm I (10 decks)

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