Pain Flashcards
(117 cards)
1
Q
Autonomic responses of acute pain
A
Guarding Grimacing Diaphoresis Increased HR Increased RR Increased BP
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
3
Q
Pain assessment
A
P-provoking/palliative factors Q-quality R-region/radiate S- severity/intensity T- temporal/time (onset, duration, frequency)
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
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)
6
Q
Tramadol drug interactions
A
SSRIs/SNRIs- serotonin syndrome, GI bleeds
Tryptan migraine abortants (serotonin syndrome as well)
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
8
Q
Severe serotonin syndrome sx
A
High fever
Seizures
Irregular heartbeat
Unconsciousness
9
Q
Tramadol monitoring
A
Achievement of goals
S/Sx tolerance
Misuse/abuse
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)
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
12
Q
What are the opioid receptors?
A
Mu
Kappa
Delta
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
14
Q
Chemical classes of opioids
A
Phenanthrenes
Phenylpiperidine derivatives
Diphenylheptane derivative
15
Q
Phenanthrenes
A
Morphine Codeine Hydromorphone Oxycodone Oxymorphone
16
Q
Phenylpiperidine derivatives
A
Meperidine
Fentanyl
17
Q
Diphenylheptane derivative
A
Methadone
18
Q
Pure opioid products
A
Effective for moderate to severe pain Immediate and ER products available -Morphine -Oxycodone -Hydromorphone -Oxymorphone -Fentanyl -Methadone
19
Q
Absorption of opioids
A
Most agents are well-absorbed, however some may undergo first-pass metabolism reducing overall bioavailability
20
Q
Common opioid adverse effects
A
Constipation (80%) Dry mouth Nausea (20%)/vomiting (15%) Sedation Pruritis (2-10%)
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
22
Q
Nociceptive pain
A
Usually propagated by mediators or noxious stimulus often localized
- Somatic: bone, joint, muscle, connective tissue
- Visceral: Organ
23
Q
Neuropathic pain
A
Interruption or damage to the actual impulse transmission pathway often regional or radiating
24
Q
Mediators of nociceptive pain
A
Prostaglandins
Prostacyclins
Histamine serotonin
Substance P
25
Functional pain
Pain in response to abnormal functioning of the nervous system
26
What is the time span for determining chronic pain?
Persistent pain lasting > 3 mos
27
Time span for acute pain
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
28
Common types of chronic pain
```
Back pain
Arthritis
Headaches
Knee pain
Cancer
```
29
Responses to chronic untreated pain
Anxiety
Hostility
Insomnia
Depression
30
Malignant pain
Usually implies cancer pain
| Usually is associated with a terminal condition
31
Nonmalignant pain
Not usually associated with an acute cause of death frequently but not always neuropathic
32
Step 1 of the modified WHO pain ladder
Mild pain
Non-opioids +/- adjuvant
Non-opioids: APAP, ASA, NSAIDS, Tramadol
33
Step two of modified WHO pain ladder
```
Mild to moderate pain
Mild-mod. opioids
+/- non-opioids
+/- adjuvant
Mild-mod opioids: Vicodin (Hydrocodon/APAP)
Percocet (Oxycodone/APAP)
```
34
Step 3 of the modified WHO pain ladder
```
Mod-severe pain
Mod-severe opioids
+/- non-opioids
+/- adjuvant
Mod-severe opioids:
Morphine
Oxycodone
Dilaudid
Opana
Duragesic
Methadone
```
35
Non-opioid analgesics
Acetaminophen
NSAIDs
Tramadol
36
General info about acetaminophen
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
37
Effects of acetaminophen
Analgesic and antipyretic
38
MOA of acetaminophen
Likely centrally, generally unknown, however does NOT have anti-inflammatory properties in vivo
39
Uses for acetaminophen
Utilized for mild-moderate pain, headache, and fever
Onset- 30 mins
DOA- 4 hrs, longer with ER formulation
40
Absorption of acetaminophen
Can be given orally and rectally with excellent bioavailability
Peak: 30-60 min after oral administration
41
Distribution of acetaminophen
Similar concentrations throughout body fluids
42
Metabolism of acetaminophen
Undergoes glucuronidation, hydroxylation, and several other mechanisms of hepatic metabolism
Half-life: around 2 hours
43
Elimination of acetaminophen
Metabolites excreted predominately in urine
44
Drug interactions of acetaminophen
Alcohol
Cirrhosis/liver disease
Concommitant use with other products containing acetaminophen
45
Dosing interval of acetaminophen
Q4-6h
46
Max dose of acetaminophen
3.0 g/day
| Optimal synergistic/additive effects seen with 500 mg dose in some injuries
47
Side effects of acetaminophen
```
Nausea
Rash, less common
Hepatotoxicity
Bone marrow suppression
Combination with other hepatotoxic agents increases risks; generally tolerated.
```
48
Side effects of NSAIDs
```
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
Tramadol side effects
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
Opioids side effects
Constipation
Dry mouth
CNS effects (sedation, dizziness, N/V, etc), respiratory depression
Long-term use can allow tolerance to most of these effects
51
Acetaminophen monitoring
Long term/chronic: AST/ALT, Alk phosphatase, GGT
Any s/sx of hepatitis
Caution with other products containing acetaminophen
Drug interactions?
52
Effects of NSAIDs
Analgesic, anti-inflammatory, and antipyretic
53
MOA of NSAIDs
Inhibition of cyclooxygenase enzymes interrupting prostaglandin synthesis and inflammation
54
COX-1
Platelet function, protective prostaglandins
55
COX-2
Inflammation, pain, and fever
56
Bone pain and NSAIDs
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
Absorption of NSAIDs
Most agents are rapidly and completely absorbed
| Food may slow absorption with no effect on bioavailability
58
Distribution of NSAIDs
Well distributed into body fluids
59
Metabolism of NSAIDs
Hepatic metabolism via glucuronidation and CYP450
60
Elimination of NSAIDs
Renal elimination with some biliary excretion
61
NSAIDs drug interactions
Anticoagulants
EtOH
SSRIs, SNRIs
ACE inhibitors
62
ASA peak, half-life
Peak: 1 hr
1/2 life: 2-3 hours
Not typically used; low tolerance due to side effects
63
Ibuprofen peak, 1/2 life
Peak: 15-30 mins
1/2 life: 2-4 hrs
Commonly used due to rapid onset and moderate duration
64
Naproxen peak, 1/2 life
Peak: 1 hr
1/2 life: 14 hrs
Commonly used for longer duration of action
65
Etodolac peak, 1/2 life
Peak: 1 hr
1/2 life: 7 hrs
Slightly more selective for COX-2 than other NSAIDs
66
Diclofenac peak, 1/2 life
Peak: 2-3 hrs
1/2 life: 1-2 hours
Higher rate of SEs than other NSAIDs (esp. GI)
67
Mefoxicam peak, 1/2 life
Peak: 5-10 hrs
1/2 life: 15-20 hrs
More selective for COX-2 than other NSAIDs, but less selective than coxibs
68
Celecoxib peak, 1/2 life
Peak: 2-4 hrs
1/2 life: 6-12 hrs
Highly selective for COX-2
69
Ketorolac (toradol) peak, 1/2 life
Peak: 2-4 hrs
1/2 life: 4-6 hrs
IV/IM
70
Acetaminophen adult doses
Starting dose: 325-600 mg q4-6 hrs OR
1000 mg 3-4 times daily
Max dose: 1000 mg/dose
3000 g/day
71
Ibuprofen adult doses
Starting: 400-800 mg 3-4 times daily
Max: 2400 mg/day
72
Naproxen adult doses
250-500 mg twice daily
| Max: 1000 mg/day
73
NSAID adverse events
```
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
Cardiac adverse effects, NSAIDs
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
NSAID monitoring
Achievement of goals
Side effects- renal, GI
CIs
76
Contraindications of NASAIDs
```
Renal insufficiency (BUN, SrCr)
GI bleeds/gastritis, duodenal ulcers (blood, tarry stools, upset stomach)
CV disease (CHF, MI, CVA)
```
77
Selection of NSAIDs
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
Mneumonic to use for any drug consideration
```
Allergy
Age
Race
Sex
Sx
Disease considerations
Drug-drug interactions
Labs
```
79
Tramadol or tramadol/apap primary action
Central activity (serotonin, norepinephrine)
80
Tramadol or tramadol/apap secondary action
Very weak Mu-1 receptor activity
81
Use for tramadol or tramadol/apap
Second or third line option for neuropathic pain
| Caution in pts at risk for seizures
82
Tramadol dosing
Max dosing: 400 mg/day
Very short half-life
Frequent dosing
83
Combination products with tramadol
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
Kappa receptor
Analgesia, sedation, miosis, decreased GI motility
| Dysphoria/euphoria, psychotomimetic effects
85
Tolerance
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
Physical dependence
Discontinuation of medication causes physiologic sx of withdrawal (NOT psychiatric need for the drug...no drug craving, compulsions, etc)
87
Addiction
A psychiatric disease characterized by cravings, compulsions, continued use despite consequences, loss of control
88
Combination opioid products
Effective for moderate to severe nociceptive pain (visceral and somatic)
Currently only available in immediate release products
-Hydrocodone/APAP
-Oxycodone/APAP
-Codeine/APAP
89
Absorption of opioids
Most agents are well-absorbed, however some may undergo first-pass metabolism reducing overall bioavailability
90
Distribution, metabolism, elimination of opioids
Distribute into well-perfused tissues such as the brain
Metabolism: Hepatic metabolism, largely through glucuronidation
Elimination: Primarily renal elimination with some biliary excretion
91
Cmax after opioid dose
Depends on ROA
92
Half-life of opioids at steady state
Half-life: 3-4 hrs
| Steady state: 4-5 half lives
93
Acute pain opioid dosing immediate-release preparation
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
Dosing for extended-release preparations of opioids
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
Dosing for extended-release preparations of opioids
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
Breakthrough dosing
Utilized in pain management as back up to a scheduled regimen
Use immediate-release opioids
-5-15% of 24-h dose (generally 10%)
97
Morphine
All opioids are compared to morphine on a mg/mg basis or Morphine Equivalent Doses (MED)
-MEDD (Morphine equivalent daily dose)
98
Multiple dosage forms of morphine
```
Immediate release liquid and tablets
Sustained release q12-24 hrs
Sustained release pellets for sprinkle or G-tube
Injectable
Cost effective
```
99
Impact of morphine metabolites
```
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
Hydromorphone
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
Oxymorphone
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
Codeine
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
Hydrocodone
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
Meperidine
Currently NOT routinely recommended but may be used 1-2 doses IV/IM acute pain
105
IV admin Fentanyl
Immediate onset of action
Easy to titrate
Fast elimination
Generally less hypotensive effects than morphine
106
Transdermal (patch) Fentanyl
```
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
Methadone indications
Addiction
Chronic pain
Acute pain
Half-life between 25-120 hrs
108
Buprenorphine
Considered a partial mu-agonist
| Used in Subxone, Subutex for opioid addiction
109
Buprenorphine patches
5, 10, and 20 microgram/hr patches, schedule CII
| Applied once weekly to manage chronic moderate to severe pain
110
Uncommon opioid adverse effects
```
Bad dreams/hallucinations
Dysphoria/delirium
Myoclonus/seizures
Urinary retention
Respiratory depression
```
111
How to treat constipation from opioids
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
Prokinetic agents
```
Selective opioid antagonist
-Naloxegol
-Methylnaltrexone
Bulk forming agents
-Avoid in debilitated pts
```
113
N/V in opioids
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
Tx of n/v in opioids
```
Prevent or treat with dopamine-blocking antiemetics
-Prochlorperazine
-Haloperidol
-Metoclopramide
-Promethazine
Second line
-Serotonin antagonists
-Anticholinergics
```
115
Tx for pruritis in opioids
Opioid rotation
Antihistamines
5HT3 antagonists
Other txs (Topical emollient (Sarna lotion))
116
Sedation tx in opioids
Distinguish from exhaustion due to pain
Avoid other sedating medications
Reduce dose, alternative opioid or route of administration
117
Management of respiratory depression in opioids
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
