Intro to Pain Management Flashcards
1
Q
What is the definition of pain?
A
- unpleasant sensory and emotional experiences associated with action or potential tissue damage or described in terms of such damage
2
Q
What is nociceptive pain?
A
- due to activation of pain pathways be ongoing tissue damage
- subcategories of nociceptive pain include somatic and visceral (can be activated by mechanical, thermal and chemical means)
3
Q
What is somatic pain?
A
- pain arising in the tissues of the body
- sharp, sometimes burning, aching, relatively localized
- osteomyelitis, OA, bone fractures
4
Q
What is visceral pain?
A
- pain arising in the organs of the body cavity
- deep, aching, cramping, diffuse and poorly localized
- may illicit symptoms such as nausea, sweating and cardiovascular changes (systemic symptoms)
- endometriosis, crohn’s disease, angina
- not often managed with OTC agents
5
Q
What is the definition of neuropathic pain?
A
- caused by direct nerve damage or may be due to abnormal processing of a pain signal in the CNS pain pathways due to sensitization of pain neurons
- more commonly chronic, but can be acute
- it can be paroxysmal or spontaneous
- generally described as burning, tingling, shock-like or shooting
(diabetic neuropathy, post-herpetic neuralgia, MS, phantom limb pain)
6
Q
What is considered hyperalgesia?
A
altered perception such that stimuli which would normally induce a trivial discomfort cause significant pain
7
Q
What is allodynia?
A
- pain due to stimulus that does not normally evoke pain
8
Q
After what timeframe is pain considered to be chronic?
A
if it lasts more than 12 weeks
9
Q
What is the difference in cause of both acute and chronic pain?
A
Acute: tissue damage often associated with inflammation
Chronic: neuronal or CNS abnormality
10
Q
What is incident pain?
A
a type of breakthrough pain that is made worse by movement
11
Q
What is breakthrough pain?
A
- a temporary increase in pain to greater than moderate intensity that occurs on a baseline pain of moderate intensity or less
- causes increased level of psychological distress and significant decrease in function
12
Q
What are the three tools of assessing pain?
A
- Numerical rating scale: patients assess their pain on a scale from 0-10, where 0 represents no pain and 10 means that worst pain imaginable
- mild pain (1-3), mild to moderature (4-7) and moderate to severe (8-10) - Visual analogue scale: 100 mm horizontal line, with the left side mean no pain and the right side is the worst pain
- Wong-baker FACES pain rating scale: faces ranging from happy to sad based on how the person is feeling
13
Q
What is the most accurate evidence of pain/intensity based on?
A
- based on the patients description and self-reporting
14
Q
What are the 4 main pieces that are essential to pain information gathering?
A
- severity of pain
- location of pain
- onset and how long the pain lasts
- quality of pain (description of pain - dull ache, sharp pain, tingling or burning)
15
Q
What are the global treatment goals of pain management?
A
- choose pain control options that are appropriate for the patient, family and setting
- delivery interventions in a timely, logical and coordinated manner
- empower patients and their families, enable them to control their course to the greatest extent possible
- many other adjuvant or complimentary therapies, available to patients (massage, chiropractic, OT/PT, acupuncture) – this is considered a multi-modal therapy
16
Q
What is the role of OTC pain medication?
A
- effective when treating mild-moderate somatic pain from skin, muscle and joints
- also effective in the treatment of dysmenorrhea and headache
- less useful in the treatment of visceral pain
- effectiveness in neuropathic pain often demonstrates a variable response
(usually not used past a pain level of 4)
17
Q
What is the mechanism of action of acetaminophen?
A
- produced analgesic effect through central inhibition of PGs (fever and pain perception) and peripherally blocking the generation of pain impulses
- does NOT have an anti-inflammtory effect because there is minimal effect on the peripheral PG’s
18
Q
For what conditions is acetaminophen first line treatment for?
A
mild to moderate pain (low back pain, OA, some headaches) and fever
19
Q
Where is acetaminophen usually metabolized?
A
the liver
20
Q
Where is acetaminophen absorbed from?
A
from the GI tract
21
Q
When does acetaminophen usually provide pain relief?
A
24 to 48 hours
- may be 2-4 weeks in OA
22
Q
What is the duration of effect in acetaminophen? What about the half life?
A
4-6 hours
- half life is 1-4 hours (same in immediate and extended release tabs)
23
Q
What is the adult dose of acetaminophen?
A
325-650 mg q4-6h (max 4g/day)
24
Q
acetaminophen is ___ dependent
A
dose
25
What is the therapeutic range of acetaminophen?
narrow
26
What is the paediatric dose of acetaminophen?
PO: 10-15 mg/kg/dose given Q4-6H
PR: 15-20 mg/kg/dose given Q4-6H (max 65 mg/kg/day) (5 doses/day)
27
Dosing adjustments may be necessary for patients with _______ (CrCl <10 mL/min dose q8h); not used in the elderly
renal dysfunction
28
What is the drug of choice in patients taking warfarin?
acetaminophen
29
Are there any drug interactions with acetaminophen?
no
30
What lifestyle issues can cause liver toxicity?
- hepatitis, liver disease (cirrhosis, alcohol use, binge drinking and fasting
31
What causes acetaminophen overdose?
acetaminophen forms a toxic metabolite which is normally detoxified by glutathione. This system can be overwhelmed in an overdose as glutathione becomes depletes (starts to use hepatocytes instead)
32
What is considered a toxic dose of acetaminophen?
7.5 - 10 g or above 150 mg/kg in children over an 8 hour period
33
What are some of the strategies that can prevent an unintentional overdose of acetaminophen in children?
- can put a warning label on the box, can sell acetaminophen in package sizes that are smaller and can make all doses for kids the same (80 mg/ml vs 160 mg/5ml)
34
What are the main symptoms of acetaminophen overdose?
- flu like symptoms
- may experience symptoms such as: nausea, vomiting, drowsiness, confusion,, sweating (12-24 hours post ingestion)
- liver damage in 24-48 hours
- hepatic damage may not be apparent for 4-6 days
35
What is the difference between rapid, extended and immediate release Tylenol?
rapid release: has an effect in 5 minutes earlier than regular extended release acetaminophen
extended release: doses every 6-8 hours, they do this by adding a coating to the outside of the pill that causes immediate pain relief, and then the interior will dissolve and cause additional relief
36
Why does alcoholism lower the threshold for acetaminophen liver damage?
- possible induction of enzymes
- hepatic dysfunction
- decrease stores of glutathione
- chronic alcohol may result in higher blood levels of NAPQ which is toxic to the liver calls and reduced blood levels of acetaminophen due to increased metabolism of acetaminophen by CYP2E1
- - this may result in a higher risk of kidney disease
- patients with a G6PD deficiency should be cautious when they are taking acetaminophen
37
Does ASA act mostly on the periphery or the central NS?
mostly the periphery - some evidence to show that it provides analgesia through the central mechanism however
38
Why is ASA not considered to be first line therapy?
- because of all of the SE associated with its use - GI irritation, nausea
39
What is the recommended dosing of ASA?
325-650 mg Q4-6H (max 4g/day)
40
How long after starting ASA will that anti-inflammatory dose usually be noticed?
2-4 weeks
41
What is the general onset of action of ASA?
60 minutes, for a duration of 4-6 hours
42
What are the most common AE associated with ASA?
- abdominal pain with cramping, heartburn, dyspepsia, GI irritation
- GI bleeding, skin rash, allergic reaction, sodium and water retention, platelet dysfunction
43
What are the contraindications associated with ASA?
- under 18 y/o, active GI lesions, history of recurrent GI lesions, bleeding disorders, hypersensitivity, concomitant alcohol use, patients relying on vasodilatory renal PGs for renal function
- precaution in renal failure and severe hepatic insufficiency
44
What kind of pain is ibuprofen indicated for?
- minor pain, headache, common cold, toothache, fever and dysmenorrhea
45
What is the MOA of ibuprofen?
inhibits PG synthesis both centrally and peripherally
46
Ibuprofen has a ____ duration of action compared to ASA and acetaminophen
longer
47
Ibuprofen only exhibits anti-inflammatory effects at ____ dose ranges
high (usually takes 2-4 weeks)
48
What is the adult dose of ibuprofen?
200-400 mg/dose Q6-8H (max 1.2g/day)
49
What is the adult dose of ibuprofen for Inflammatory disease?
400-800 mg/dose Q6-8H (max 3.2 g/day)
50
What is the dose of ibuprofen for children?
5-10 mg/kg q6-8h (max 40 mg/kg/day)
51
What is the dosing of naproxen in adults? (cannot use in children)
220 mg q8-12h (1tab)
52
What is the dosing of naproxen in individuals over 65 years old or with renal insufficiencies?
1 tablet every 12 hours
53
What is the onset of action of naproxen?
30-60 minutes
54
Why is taking NSAIDs so hard on the body?
- PGs are mucosally protective
- mucosal damage via NSAID use is primarily a consequence of COX 1 inhibition
- short term use of NSAIDs in a healthy individual is unlikely to cause GI toxicity
55
Who is considered a high risk individual in taking NSAIDs?
- those with PUD, GI bleeds or perforation, concomitant alcohol or NSAID use
56
What are the 2 mechanisms of action by which ASA causes GI adverse effects?
- local irritation effects resulting from the drug contracting the gastric mucosa
- systemic effects from prostaglandin inhibition
57
What are the risk factors for upper GI bleeding?
- age 60 +
- concomitant use of alcohol
- concomitant use of other NSAIDS, anticoagulants, anti-platelets, bisphosphonates, SSRIs or systemic corticosteroids
- history of uncomplicated or bleeding peptic ulcer
- infection with helicobacter pylori
- NSAID related dyspepsia
- rheumatoid arthritis
58
Enteric coated forms of ASA have been shown to reduce mucosal lesions and local irritation but do not reduce the risk of what?
major GI bleeding
59
Risk of GI complications may often be ____ dependent
dose (although even 81 mg ASA can cause major GI bleeding)
60
What medications can be given as prophylaxis to stop GI irritation after giving ASA?
- can give misoprostol (usually given in combination with diclofenac) or can give a proton pump inhibitor (omeprazole or pantoprazole) -- can also switch to a COX-2 agent such as Celebrex
61
Why are NSAIDs often hard on the kidneys?
- because prostaglandins are important for the maintenance of renal blood flow and tubular transport of electrolytes
- increase in PG release occurs to compensate for increased levels of angiotensin 2 and NE
- NSAIDs inhibit this compensatory mechanism, which can lead to increased bp, worsening of CHF, renal and systemic vascular resistance
62
What class of drugs do NSAIDs often interfere with?
- antihypertensive agents
63
What patients are at most risk of renal failure when using NSAIDs?
- volume depletion states
- severe CHF
- hepatic cirrhosis
- clinically significant dehydration
- creatinine clearance under 30 ml/min
- intrinsic renal disease secondary to diabetes, nephrotic syndrome or hypertension
64
What is ASA induced asthma?
- clinical syndrome characterized by the onset of asthma 30 minutes to 3 hours post ingestion of ASA
65
What is the proposed mechanism of ASA-induced asthma?
- decreased PG result in increased leukotrienes (important mediator in asthma and allergies)
66
Will patients that have ASA induced asthma have a similar reaction to acetaminophen?
- only potentially at high doses
- acetaminophen has only weak cyclo-exygenase inhibitory properties, so patients who are sensitive to ASA may have adverse reactions to high doses of acetaminophen
67
Why is ASA instead of ibuprofen used to inhibit platelet aggregation?
Ibuprofen - shorter duration and is reversible upon discontinuation of the drug
ASA - effects are irreversible and lasts for the entire life of the platelet (usually 5-9 days)
68
What is used widely as an anti-platelet to reduce cardiovascular risk (MI, stroke)
Low dose ASA
69
Regular use of _____ may interfere with the cardioprotective effect of low dose ASA when they are taken at the same time
ibuprofen
70
What should the patients be advised of if they are taking both low dose ASA and ibuprofen?
patient should be advised to take the ibuprofen dose at least 2 hours after the ASA (gives the ASA time to bind irreversibly to the platelet)
71
What is the drug interaction of ASA and NSAIDs?
increased risk of GI bleed
72
What is the drug interaction of warfarin and ASA?
increased INR and bleed risk
73
What is the interaction between warfarin and ibuprofen/naproxen?
- there may be an increase in anticoagulant activity and risk of bleeds
74
It is generally not recommended for ASA to be used in what population?
should not be use in influenza like illness, chickenpox, in infants, children, teenagers and young adults (under 18)
75
Can ASA and ibuprofen be used in pregnancy?
- not recommended that it be used in the third trimester of pregnancy (risk of ASA induced platelet dysfunction predisposing bleeding in neonates)
76
Patients that are taking ASA for cardioprotective benefits should stop taking the ASA ____ prior to surgery
7 days
77
What is acetaminophen considered first line therapy for?
- ASA sensitive asthma
- PUD
- increased risk of bleeding
- patients with renal dysfunction
- CV or hypertensive patients
- multiple concurrent drug therapy
- pregnancy or breastfeeding (esp 3rd trimester)
78
What is the rationale of using codeine as a pain medication?
- different from PG inhibition
| - changes to its active analgesic metabolite - morphine
79
What dose of codeine is considered effective in pain relief?
- 30-60 mg codeine (8 mg is questionable)
80
What is the purpose of caffeine in a tylenol 1 tablet?
- to enhance the analgesic effect of ASA and acetaminophen (usually necessary at a dose of 65 mg)
81
NSAIDs should be used with caution in patients with what disease states?
- renal, cardiovascular or GI disease states
82
What is generally the best choice to use in women that are pregnant/lactating?
acetaminophen
83
What is the potential consequence of using NSAIDs in the third trimester of pregnancy?
- can induce premature closure of the ductus arteriosis of the unborn child
84
What should be used when a patient describes their pain level as 1-4? (mild/moderate)
start with acetaminophen/ASA/ibuprofen/naproxen,
| at OTC doses - monitor according to type of pain and agent selected (24-48 hours vs 2-4 weeks)
85
What should be used when a patient describes their pain level as 4-8? (moderate/severe)
consider addition of codeine combination or alternative (2-3 days); may need to switch to T3 of tramadol (weak opioids)
86
What should be used when a patient describes their pain level as 8-10? (severe)
- refer depending on acute/chronic situation, patient history of pain complaints and/or red flags
- likely will require a stronger opioid (oxycodone/morphine)
87
What are some of the general red flags for pain?
- pain is escalating
- pain has not responded to the appropriate therapy
- pain is severe
- patient with pain is pregnant
- patient uses concurrent therapies or has other illnesses
88
Children's pain medication should be dosed based on what?
based on weight or body surface area
89
What is a migraine?
- a neurovascular disorder that consists of headache pain, ANS dysfunction and potentially neurologic symptoms
- can have migraine with aura or a migraine without an aura
- thought that a trigger causes CNS dysfunction resulting in:
- - dilation of intracranial and extra cerebral blood vessels
- - activation of trigeminal sensory nerves
- - leads to pain signals in the brain
90
An aura is thought to be due to what?
neuronal dysfunction
- - develops over 5-20 minutes and usually lasts less than 1 hour
- - migraine occurs within 60 minutes after the aura ends, but in a small percentage the aura begins at the onset or during the migraine
- - usually visual and may encompass half of the visual field
- - may include sensory and motor symptoms (numbness, tingling, burning, dysphagia or aphasia, weakness and partial paralysis on one side of the body)
91
What is the pathophysiology of a tension headache?
- most common type of headache
- thought to occur due to mental stress and tension, but the exact pathophysiology is unknown
- more prevalent in women
92
What is the difference in quality between the three types of headaches?
Tension: dull, pressing and persistent (nonpulsating)
Migraine: pulsating/throbbing
Cluster: penetrating
93
What is the severity/intensity of the three types of headaches?
Tension: mild to moderate
Migraine: usually moderate to severe
Cluster: severe
94
What is the location of all three of the headaches?
Tension: bilateral
Migraine: mainly unilateral (can spread to bilateral)
Cluster: strictly unilateral
95
What is the duration of all three of the headaches?
Tension: 30 minutes to 7 days
Migraine: may develop over minutes to hours- ad lasts 4-72 hours (3 days_
Cluster: reaches max intensity over several minutes losing 15-180 minutes
96
What are the other symptoms associated with three headaches?
Tension: generally not associated with aura, nausea, vomiting or light sensitivity
Migraines: nausea/vomiting, light and sound sensitivity may occur (at least one of these) - may be with or without an aura
Cluster: may be accompanied by lacrimation, nasal congestion, miosis, congestion, rhinorrhea, and facial flushing (no nausea, vomiting and light sensitivity)
97
What is a common reason of a tension headache?
a medication overuse headache (used when there is frequent use >15 days/month for several months -- this usually occurs with acetaminophen or ASA (not as common with NSAIDs)
98
What is the treatment for a medication overuse headache?
- discontinue implicated drugs, relieve withdrawal symptoms, treat recurrent headaches with appropriate rx migraine therapies -- need to refer
99
What are the red flags for a physician referral for a headache?
- severe or abrupt onset (can be a bleed in the brain)
- age of onset over 40 years
- recent head trauma
- medication induced headache (due to medication or analgesic overuse)
- progressive severity and/or increased frequency (headaches are getting worse and occur daily)
- neurological signs or symptoms (stiff neck, fever, reduced consciousness)
- systemic signs
- nocturnal occurence or upon early morning awakening
- onset with exercise
100
What are some common non-pharos for headaches?
(usually these are all to treat migraines)
- cryotherapy
- relaxation techniques (quiet, dark room)
- massage, acupuncture
- stress management
- exercise helps some people
101
What are some recommendations for patients to avoid migraines?
- avoidance of triggers such as: foods, other chemicals and hormones
- lifestyle changes: regular sleeping and eating times, decrease stress and decrease caffeine
102
When are rx treatments for migraines often necessary?
- when an OTC trial does not help or when a treatment is being used for more than 15 days per month
103
What are the typical rx treatments for migraines?
- acute treatments with triptans
- or preventative treatments: propanolol, amitriptyline
- OTC treatment can be used from here to manage breakthrough pain
