7. Pain Management Flashcards
The Concept of Pain
Pain is an unpleasant sensory
and emotional experience in which
the body is made urgently aware
of actual or potential tissue damage.
Pain Threshold
– The lowest intensity of painful stimulation at
which the patient becomes aware of the pain.
The Anatomy of Pain
Chemical agents that occur naturally
in the environment of pain receptors after
acute tissue damage are algogenic substances.
These include adenosine, adenosine triphosphate,
serotonin, histamine, bradykinin, cytokines, and
prostaglandins.
The release of these substances leads to
nociceptor activation, producing the pain impulse.
The Anatomy of Pain
Inflammation promotes the formation of
prostaglandins which enhance the effects of
the other algogenic substances on nociceptors.
Traumatic injury may also provoke an initial
efferent sympathetic reflex, producing
vasoconstriction.
Decreased microcirculation in the injured tissue,
produces ischemia, further amplifying nociceptor
stimulation.
Non-Opioid Analgesics
(COX Inhibitors)
Slide 11
Aspirin Pharmacologic effects
– Antiplatelet
• Used to reduce platelet aggregation
– Antipyretic
• Lowers body temp if above normal
– Analgesic
• Used to treat mild to moderate pain
– Antiinflammatory
• Decreases pain, redness and swelling
Aspirin
Adverse reactions
–Gastrointestinal ulceration
• Decreased protective prostaglandins
– Decreased protective mucous
– Increased gastric acid secretion
- Nausea and vomiting
- GI bleeding
Aspirin
Adverse reactions
–Gastrointestinal ulceration
• Decreased protective prostaglandins
– Decreased protective mucous
– Increased gastric acid secretion
- Nausea and vomiting
- GI bleeding
– Altered bleeding time
• Irreversibly reduces platelet aggregation
– Effect extends for the life of the platelet
– Replacement of platelets needed for normal clotting to resume
–May result in excessive or prolonged
bleeding after procedures
Aspirin
Drug interactions
– Increased effectiveness of other drugs
–Mechanism
• Plasma-protein binding
– Common Drugs Affected
• Coumadin (warfarin)
– Result
• Increased risk of hemorrhage
2019 Thomas A. Viola, R.Ph. All Rights Reserved 17
Aspirin
Drug interactions
– Increased effectiveness of other drugs
–Mechanism
• Plasma-protein binding
– Common Drugs Affected
• Coumadin (warfarin)
– Result
• Increased risk of hemorrhage
© 2019 Thomas A. Viola, R.Ph. All Rights Reserved 18
Aspirin
Drug interactions
– Decreased effectiveness of other drugs
–Mechanism
• Increase sodium/fluid retention
– Common Drugs Affected
• Antihypertensives
– Result
• Exacerbated cardiovascular disease
Aspirin
Contraindications
– Peptic ulcer
– Pregnancy
–Gout
– Hemophilia
– History of hypersensitivity
• Cross-sensitivity with NSAIDs
Aspirin
Contraindications
– Peptic ulcer
– Pregnancy
–Gout
– Hemophilia
– History of hypersensitivity
• Cross-sensitivity with NSAIDs
NSAIDs
Types
– ibuprofen (Motrin, Advil)
– naproxen sodium (Anaprox, Aleve)
– naproxen (Naprosyn)
– etodolac (Lodine)
– nabumetone (Relafen)
–meloxicam (Mobic)
Types
–Other NSAIDs offer no apparent advantage over
ibuprofen in the treatment of dental pain
- diclofenac (Voltaren / Cataflam)
- diflunisal (Dolobid)
- ketoprofen (Orudis)
- meclofenamate (Meclomen)
NSAIDs
Pharmacologic effects
– Antipyretic
• Lower body temp if above normal
– Analgesic
- Treatment of mild to moderate pain
- More effective if administered before pain
– Anti-inflammatory
- Treatment of inflammatory joint disease
- Treatment of dysmenorrhea
NSAIDS: Patient care considerations
– Hypersensitivity reactions
• Cross-sensitivity with ASA and other NSAIDs
– Dermatological reactions
- Stevens Johnson Syndrome (SJS)
- Toxic epidermal necrolysis (TEN)
Patient care considerations (continued)
– Teratogenic effects
- Premature closures in fetal circulation
- Prolonged gestation
– Iatrogenic disease
- Not listed as medications on medical history
- Interfere with cardioprotective effects of once daily
aspirin
–Maximum daily dose of ibuprofen: 3200mg
NSAIDs
Adverse reactions
–Gastrointestinal ulceration
- Decrease protective mucous
- Increase gastric acid secretion
- Nausea and vomiting
- Gastrointestinal bleeding
Adverse reactions (continued)
– Altered bleeding time
• Reversibly reduce platelet aggregation
– Effect lasts only until NSAID is excreted
– Normal clotting resumes
– Lesser effect than aspirin
NSAIDs
Drug interactions
– Increased effectiveness of other drugs
- Mechanism
- Plasma-protein binding
- Common Drugs Affected
- Coumadin (warfarin)
- Result
- Increased risk of hemorrhage
Drug interactions (continued)
– Increased effectiveness of other drugs
- Mechanism
- Decreased renal excretion
- Common Drugs Affected
- Lithium
- Result
- Increased muscle rigidity
NSAIDs
Drug interactions (continued)
– Decreased effectiveness of other drugs
–Mechanism
• Increase sodium/fluid retention
– Common Drugs Affected
• Antihypertensives
– Result
• Exacerbated cardiovascular disease
NSAIDs
Drug interactions (continued)
– Decreased effectiveness of other drugs
–Mechanism
• Increase sodium/fluid retention
– Common Drugs Affected
• Antihypertensives
– Result
• Exacerbated cardiovascular disease
Contraindications
– Asthma
– Cardiovascular disease with fluid retention
– Peptic ulcer/ulcerative colitis
– Renal function impairment
– Pregnancy
– History of hypersensitivity to aspirin
Acetaminophen (APAP)
Types
– Tylenol, Panadol
Mechanism of action
– Unknown (hypothesized)
- Elevates overall pain threshold
- Reduces fever
Acetaminophen (APAP)
Pharmacologic effects
– Antipyretic
• Lowers body temp if above normal
– Analgesic
- Effective in treatment of mild to moderate pain
- Considered the most “safe” analgesic
Acetaminophen (APAP)
Adverse reactions
– Hepatotoxicity
• Converted to a liver-toxic metabolite
– Inactivated by gluthathione in liver
• Possible liver failure with either:
– Acute ingestion of supratherapeutic doses
– Chronic ingestion of high therapeutic doses
–Maximum daily dose of APAP: 3000mg
Adverse reactions
– Hepatotoxicity (continued)
– Exacerbated by liver-enzyme inducers:
– Alcohol
– Cigarette smoke
– Drugs
– phenytoin (Dilantin)
– Delayed reaction
– Peak hepatotoxicity occurs 3 to 4 days
after acute intoxication
Acetaminophen (APAP)
Contraindications
– Hepatitis or other known decreased liver function
– Chronic alcohol ingestion
–Other liver microsomal enzyme inducing drugs
– Impaired renal function
Opioid Analgesics
(Substance P Inhibitors)
For a person to feel pain, the pain
impulse must be transmitted to the
spinal cord and then to the cerebral cortex.
The pain impulse is transmitted to the spinal cord
by peripheral nerve fibers.
At the dorsal horn of the spinal cord, peripheral
nerve fibers interface with CNS neurons to
transmit the pain signal.
Opioid Analgesics
Substance P facilitates the transfer
of pain impulse from peripheral
neurons to CNS signaling neurons.
In the dorsal horn of the spinal cord, peripheral
pain neurons meet CNS signaling neurons.
At the synapse, the peripheral pain neurons
release substance P, a pain neurotransmitter.
The CNS signaling neurons carry the pain impulse
to the brain.
Opioid Analgesics
Spinal interneurons respond to stimulation from
CNS neurons by releasing endogenous opiates,
which block transmission of pain impulses.
Endogenous opiates (endorphins) bind to opiate
receptors on the peripheral pain neuron to inhibit
the release of substance P.
Opioid Analgesics
Spinal interneurons respond to stimulation from
CNS neurons by releasing endogenous opiates,
which block transmission of pain impulses.
Endogenous opiates (endorphins) bind to opiate
receptors on the peripheral pain neuron to inhibit
the release of substance P.
Opioid Analgesics
By binding with any free opiate receptors,
opioid analgesics further inhibit the release of
substance P and thus further block transmission
of pain impulses to the brain.
Opioid analgesics supplement and mimic the
pain-blocking effect of the endogenous opiates.
Opioid Analgesics
Opioid Analgesics used in Dentistry
– Codeine
• Combination with APAP (Tylenol w/codeine)
– Hydrocodone
• Combination with APAP (Vicodin, Lortab)
– Oxycodone
• Combination with APAP (Percocet, Endocet)
Opioid Analgesics
Pharmacologic effects
– Analgesia
• Treatment of moderate to severe pain
– Cough suppression
• Treatment of severe non-productive coughs
–GI hypo-motility
• Treatment of diarrhea and traveler’s sickness
Opioid Analgesics
Patient care considerations
– Addiction and dependence
- Tolerance develops to most effects
- Withdrawal symptoms upon abrupt cessation
– Respiratory effects
• Respiratory depression leads to death
Opioid Analgesics
Adverse reactions
– GI effects
• Constipation (OIC)
– Reduced GI motility
• Nausea and emesis
– Direct stimulation of
the chemoreceptor
trigger zone
– Hypersensitivity reactions
• Dermatological reactions
Opioid Analgesics
Drug interactions
– Increase risk of additive CNS depression
– Increase risk of additive respiratory depression
– Increase risk of additive constipation
Opioid Analgesics
Contraindications
– Chronic respiratory disease (COPD)
– Head injuries
– Hepatic, renal function impairment
– Prostatic hypertrophy, constipation
Treatment of Opioid Analgesic Addiction
Vivitrol (naltrexone)
– Administered once-monthly via IM injection
– Blocks effects if opioids are taken
Sublocade (buprenorphine)
– Administered once-monthly via SC injection
– Blocks effects if opioids are taken
Suboxone (buprenorphine plus naloxone)
– Taken sublingually by patient
– Blocks effects if opioids are taken
