10 - OTC Pain Management Flashcards
What are the two kinds of pain?
Nociceptive
- Somatic
- Visceral
Neuropathic
_____ pain: due to the activation of pain pathways by ongoing tissue damage
Nociceptive
Define somatic pain
- Pain arising in the tissues of the body
- Sharp, sometimes burning, aching, relatively localized
- Osteomyelitis, osteoarthritis, bone fractures
ex. ankle sprain, tooth being pulled out
Define visceral pain
- Pain arising in the organs of a body cavity
- Deep, aching, cramping, diffuse and poorly localized
- Could have nausea, sweating, and CV changes involved (i.e. systemic symptoms)
- Endometriosis (pelvic), Chron’s disease (abdomen), angina (thorax)
- Not often managed with OTC agents (Referral)
Define neuropathic pain
- 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
- Can be paroxysmal or spontaneous
- Generally described as burning, tingling, shock-like or shooting
Hyperalgesia
Altered perception such that stimuli which would normally induce a trivial discomfort cause significant pain
Allodynia
Pain due to a stimulus that does not normally evoke pain
Phantom pain
Pain in a limb that is no longer there
Acute Pain:
Cause
Tissue damage often associated with inflammation
Acute Pain:
Duration
Days to weeks (2-4 weeks)
Sub-acute = 4-12 weeks
May depend on the cause
Acute Pain:
Course or prognosis
Predictable
Acute Pain:
Emotional response
Anxiety or overt pain behaviours (grimacing, limping, etc)
Acute Pain:
Treatment
Primarily analgesic
Chronic Pain:
Cause
Neuronal or CNS abnormality (sensitization)
Chronic Pain:
Duration
> 12 weeks (3 months)
Associated with a pattern of recurrence over months or years
May be associated with chronic disease (Rheumatoid arthritis, back pain)
Chronic Pain:
Course or prognosis
Unpredictable
Chronic Pain:
Emotional response
Quiet, depressed
Flat affect
May also have anxiety issues
Chronic Pain:
Treatment?
Multimodal
-Have to try different options, different HCP’s, different therapies, etc.
What is break-through pain?
- 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
What is incident pain?
A type of breakthrough pain that is made worse by movement
List some tools for assessing pain
1) Numerical Rating Scale (NRS)
- Patients rate their pain on a scale of 0-10
2) Visual Analogue Scales (VAS)
- 100mm horizontal line, with the left side marked no pain and the right side marked the worst pain
3) Wong-Baker FACES Pain Rating Scales
- Faces ranging from happy to sad based on how they are feeling
* Good for children or people who don’t speak english
What are the 4 main pieces that are essential to pain information gathering?
- 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)
What is the role of OTC Pain medication
- Effective when treating mild-moderate somatic pain from skin, muscle and joints
- Also effective in treatment of dysmenorrhea and headache
- Less useful in treatment of visceral pain (refer)
- Effectiveness in neuropathic pain often demonstrates variable response
- Treatment of neuropathic pain may involve a wide range of therapy
List the types of non-prescription pain medications
1) NSAIDs
- ibuprofen
- ASA
- naproxen
2) Acetaminophen
3) Opioids
- Codeine (8mg)
MOA of Acetaminophen?
Produces analgesic effect through central inhibition of PG (fever and pain perception) & peripherally blocking the generation of pain impulses.
- Effective analgesic and antipyretic
- Does not possess anti-inflammatory activity
Oral onset of action for acetaminophen ?
30 minutes
PR onset of action for acetaminophen ?
slowly and incompletely absorbed
Duration of effect for acetaminophen ?
4-6 hours
Acetaminophen:
Adult dosing
325-650 (1000) mg every 4-6 hours
max 4g/day
Acetaminophen is _____-dependent
dose
*meaning that 1000mg produces greater analgesia than 650 or 500 mg dose.
Acetaminophen:
Ceiling effect at ?
1000 mg - no further pain management, just further liver damage
Acetaminophen:
Pediatric dosing
PO: 10-15 mg/kg/dose every 4-6 hours
PR: 15-20 mg/kd/dose every 4-6 hours
Max 65 mg/kg/day (max 5 doses/day)
T or F: Acetaminophen is safe for short term use in children, pregnancy and lactation
true
Describe Acetaminophen Overdose
-It forms a toxic metabolite which is normally detoxified by glutathione. This system can be overwhelmed in an overdose as glutathione becomes depleted (starts to use hepatocyte instead)
What is the minimum toxic single dose in a healthy adult and healthy child?
Adult: 7.5-10g over 8 hours
Child: 150mg/kg over 8 hours
What strategies can be used to prevent accidental or unintentional overdose?
- limit pack size
- change the scheduling
- make font of acetaminophen very large
- just have one strength available for children
- increase patient awareness on the dangers of acetaminophen overdose
Describe the symptoms of Acetaminophen OD
Flu like symptoms
-nausea, vomiting, drowsiness, confusion, sweating (12-24 hours after ingestion)
What is the antidote for Acetaminophen OD and when will you see results from it?
acetylcysteine
-optimal result with antipodal therapy seen within 16-24 hours
Why would an alcoholic have a lower threshold for acetaminophen liver damage?
- possible induction of enzymes
- hepatic dysfunction
- decreased stores of glutathione
*severe liver injury reported in alcoholics who claimed to have taken less than 4g/day
Chronic alcoholism may result in higher blood levels of _____
NAPQ
What is NAPQ?
Acetaminophen metabolite which is toxic to liver cells and reduced blood levels of acetaminophen due to increased metabolism of acetaminophen by CYP2E1
List some non-Rx NSAIDs
ASA
Ibuprofen
Naproxen
What are the pharmacological properties of non-Rx NSAIDs
- Analgesic
- Antiplatelet
- Antipyretic
- Anti-inflammatory
ASA acts primarily in the _____
periphery
What benefit do NSAIDs have over acetaminophen?
anti-inflammatory properties
Why is ASA not a first line analgesic?
Higher ADR’s - Gastric irritation, nausea
Do we give ASA to kids?
No - Risk of Reye’s syndrome
ASA:
Adult dosing
325-650 mg every 4-6 hours
Max = 4g/day
What are the other types of dosing for ASA?
80 or 81mg every 2 days to 325 mg TID
*antiplatelet often seen OD
ASA:
Onset of action
within 60 minutes
ASA:
Duration of action
4-6 hours
ASA:
Adverse effects
abdominal pain, cramps, dyspepsia, GI irritation
Ibuprofen:
MOA
inhibit PG synthesis both centrally and peripherally
Ibuprofen:
Duration of action
6-8 hours
Ibuprofen:
Onset of action
30-60 minutes
Ibuprofen:
When should you not take it?
if allergic to ASA or other NSAIDs
Ibuprofen:
Adult dosing for pain, fever, dysmenorrhea
200-400 mg every 6-8 hours
Max 1.2 g/day
Ibuprofen:
Adult dosing for inflammatory disease
400-800 mg every 6-8 hours
Max 3.2 g/day
Ibuprofen:
Child dosing for pain/fever
PO: 5-10 mg/kg every 6-8 hours
Max = 40 mg/kg/day
Ibuprofen:
Child dosing for anti-inflammatory effects
PO: 30-45 mg/kg/24 hours divided every 6-8 hours
Naproxen:
MOA
inhibits PG synthesis both centrally and peripherally
Naproxen: Adult dosing (we do not give this drug to kids)
For 12-65 year olds:
220 mg every 8-12 hours
Max 440 mg/day
For >65:
220 mg every 12 hours
Max 440 mg/day
Naproxen:
Onset of action
30-60 minutes
Naproxen:
When should you not take it?
If allergic to ASA or other NSAIDs
Naproxen:
How should you take it?
Take with good and a full glass of water (to decrease GI irritation)
Why should NSAIDs be taken with food?
Because you are inhibiting PGs which are mucosally protective.
How are NSAIDs able to cause GI damage?
1) Local irritant effect resulting from the drug contacting the gastric mucosa
2) Systemic effect from PG inhibition
Risk factors for upper GI bleeding?
- over 60
- alcohol abuse
- concomitant use of other NSAIDs, anticoagulants, anti platelet agents, bisphosphonates, SSRIs or systemic corticosteroids
- history of uncomplicated or bleeding peptic ulcer
- infection with H. pylori
- NSAID related dyspepsia
- rheumatoid arthritis
Do EC forms help reduce GI bleeding?
No - EC forms only reduce mucosal lesions and local irritation
How do you prevent GI bleeding when considering pain control?
Consider prophylaxis with:
- Misoprostol
- PPI’s (Omeperazole)
- Cox-2 Agent (Celebrex)
How do NSAIDs affect the kidneys?
- PGs are important for maintenance of renal blood flow and tubular transport of electrolytes
- Increase in PG release occurs to compensate for the increased level of angiotensin 2 and NE
- NSAIDs inhibit PGs therefore it can lead to:
- renal and systemic vascular resistance
- increase BP
- worsening of pre-existing CHF
What is an important drug interaction with NSAIDs?
Antihypertensive agents
-ACEi, diuretics, beta blockers
ASA-induced Asthma:
MOA
decreased PGs result in decreased leukotrienes (important mediator in asthma and allergies)
ASA-induced Asthma:
Characterized by ??
onset of asthma 30 mins - 3 hours post ingestion of ASA
What drugs inhibit platelet aggregation?
ASA and ibuprofen
Ibuprofen anti platelet properties are _______
reversible
ASA anti platelet properties are _______
irreversible
Average lifespan of a platelet ?
5-9 days
How long before surgery should ASA be discontinued?
about 7-10 days
See on Page 8 important drug-drug interactions
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Limitations of ASA?
don’t use in people under 18, for influenza-like illnesses or for chicken pox
Limitations of ASA and ibuprofen regarding pregnancy?
Both not recommended in 3rd trimester
Patients with asthma should avoid ___
ASA
When is acetaminophen considered 1st line therapy?
- ASA-sensitive asthma
- gastritis or PUD
- increased risk of bleeding
- patients with renal dysfunction
- CV or hypertensive patients
- multiple concurrent drug therapy
- Pregnant or breast feeding (especially 3rd trimester)
Is codeine 8mg recommended for pain management?
No - too low of a dose to produce any significant analgesic effect
Codeine 8mg:
MOA
-changes to it’s active analgesic metabolite (morphine)
Is caffeine effective for pain management?
Yes - dose of caffeine was around 64-65mg
*it enhances the analgesic effect of ASA and acetaminophen
Are tylenol #1 good for pain?
not really at all
- dose of caffeine is too low for it to be effective (soda or coffee has higher levels of caffeine)
- dose of codeine is too low to be effective
What age do you refer pain?
under 2
For ages 2-18, what do you recommend?
acetaminophen or ibuprofen
When should NSAIDs be cautioned?
in patients with renal, CV or GI disease states
What is the best choice for pregnant/lactating women?
acetaminophen
**NSAIDS need to be avoided in the 3rd trimester
Red flags for pain
- Pain is escalating
- Pain has not responded to appropriate therapy
- Pain is severe
- Patient with pain is pregnant (need to determine underlying cause)
- Patient uses concurrent therapies or has other illnesses
Pathophysiology of migraines
-Neurovascular disorder that consists of headache pain, autonomic nervous system dysfunction and potentially neurologic symptoms
It is thought that a trigger causes CNS dysfunction resulting in:
- dilation of intracranial and extracerebral blood vessels
- activation of trigeminal sensory nerves
- leads to pain signals in the brain
2 types of migraines
with aura
without aura
Describe an aura
- develops over 5-20 mins
- usually lasts less than 1 hour
- migraine occurs within 60 mins after the aura ends
When do you refer migraines?
If there has been no initial diagnosis.
*Mild, diagnosed symptoms can be treated OTC
Pathophysiology of Tension headaches
- Most common type of headache
- Occurs due to mental stress and tension, but exact pathophysiology unknown
- More prevalent in women but declines with age for both males and females
See the modified CTMA 2 Table 1 on page 11
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Describe a MOH (medication overuse headache)
- Defined as frequent use (>15 days/month) for several months
- Often mimics tension-type headaches
- Most common with combo products containing caffeine and/or opioids
Treatment for MOH (medication overuse headache)
- Discontinue implicated drugs
- Relieve withdrawl symptoms
- Treat recurrent headaches with appropriate Rx migraine therapies
Prevention for MOH (medication overuse headache)
Educate patients to try and avoid regular or daily use of pain relievers for headache/pain.
Frequency should be less than 15 days/month
Red flags for Headaches
- Severe or abrupt onset
- Age of onset > 40 yrs
- Recent head trauma
- Medication-induced headache
- Progressive severity and/or increased frequency
- Neurological signs or symptoms (stiff neck, fever, reduced consciousness)
- Systemic signs (fever, nausea, vomiting)
- Nocturnal occurence or upon early morning awakening
- Onset with exercise or exertion
Non-pharm treatment for headaches
- Cryotherapy
- Relaxation techniques (quiet, dark room, sleep)
- Massage, acupuncture
- Stress management, CBT
- Exercise helps some patients
How do you prevent headaches?
- Avoid triggers (food, chemicals, hormones)
- Lifestyle changes: regular sleeping and eating times, decrease stress, decrease caffeine
- *See table 3 - migraine triggers
Pharmacological treatment for a migraine?
- OTC therapy often helps with mild-moderate migraines
- Will require Rx therapy if OTC trial does not help or if treatment is being used >15 days per month
- RX options include: Triptans (treatment) or preventative therapies (propranolol, amitriptyline)
- OTC pain relievers can still be used to manage breakthrough migraine pain
Pharmacological treatment for a tension headache?
Acetaminophen, ASA, Ibuprofen, Naproxen
Pharmacological treatment for an MOH?
Refer
Monitoring ?
- Relief of headache within 2 hours after taking meds
- If additional symptoms present, relief of those symptoms should also occur in that time
