7. Pain Management

Question 1

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.

Question 2

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.

Question 3

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.

Question 4

Non-Opioid Analgesics

(COX Inhibitors)

Slide 11

Question 5

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

Question 6

Aspirin

 Adverse reactions

–Gastrointestinal ulceration

• Decreased protective prostaglandins

– Decreased protective mucous

– Increased gastric acid secretion

• Nausea and vomiting
• GI bleeding

Question 7

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

Question 8

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

Question 9

Aspirin

 Contraindications

– Peptic ulcer

– Pregnancy

–Gout

– Hemophilia

– History of hypersensitivity

• Cross-sensitivity with NSAIDs

Question 10

Aspirin

 Contraindications

– Peptic ulcer

– Pregnancy

–Gout

– Hemophilia

– History of hypersensitivity

• Cross-sensitivity with NSAIDs

Question 11

NSAIDs

 Types

– ibuprofen (Motrin, Advil)

– naproxen sodium (Anaprox, Aleve)

– naproxen (Naprosyn)

– etodolac (Lodine)

– nabumetone (Relafen)

–meloxicam (Mobic)

Question 12

Types

–Other NSAIDs offer no apparent advantage over

ibuprofen in the treatment of dental pain

• diclofenac (Voltaren / Cataflam)
• diflunisal (Dolobid)
• ketoprofen (Orudis)
• meclofenamate (Meclomen)

Question 13

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

Question 14

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

Question 15

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

Question 16

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

Question 17

NSAIDs

 Drug interactions (continued)

– Decreased effectiveness of other drugs

–Mechanism

• Increase sodium/fluid retention

– Common Drugs Affected

• Antihypertensives

– Result

• Exacerbated cardiovascular disease

Question 18

Contraindications

– Asthma

– Cardiovascular disease with fluid retention

– Peptic ulcer/ulcerative colitis

– Renal function impairment

– Pregnancy

– History of hypersensitivity to aspirin

Question 19

Acetaminophen (APAP)

 Types

– Tylenol, Panadol

 Mechanism of action

– Unknown (hypothesized)

• Elevates overall pain threshold
• Reduces fever

Question 20

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

Question 21

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

Question 22

Acetaminophen (APAP)

 Contraindications

– Hepatitis or other known decreased liver function

– Chronic alcohol ingestion

–Other liver microsomal enzyme inducing drugs

– Impaired renal function

Question 23

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.

Question 24

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.

Question 25

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.

Question 26

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.

Question 27

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)

Question 28

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

Question 29

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

Question 30

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

Question 31

Opioid Analgesics

 Drug interactions

– Increase risk of additive CNS depression

– Increase risk of additive respiratory depression

– Increase risk of additive constipation

Question 32

Opioid Analgesics

 Contraindications

– Chronic respiratory disease (COPD)

– Head injuries

– Hepatic, renal function impairment

– Prostatic hypertrophy, constipation

Question 33

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