Drugs for Pain Management

1. culture

2. past experiences

3. meaning

4. attention, anxiety

5. suggestion and placebo

6. feelings of control

factors n fluencing pain experience [6]

1. believe person’s self report

2. establish cause of pain

3. initiate appropriate treatment

principles of pain management [3]

Ask about pain regularly/assess pain systematically

believe the patient and family reports of pain and what relieves it

choose pain control options appropriate for the patient, family, and setting

deliver interventions in a timely manner

empower patients to control their treatment to the greater extent possible

Pain management strategy (ABCDE)

adjuvants

drugs that can be used for pain management but are not in anagelsic class

Pain pathway

always consider how pain management strategies work in relation to what?

nociceptors

small nerve endings of a-delta and c fibres

1. histamine

2. bradykinin

3. prostaglandins

4. substance P

5. serotonin

6. leukotrienes

tissue injuries release which chemical(s): [6]

dorsal hornw

relay station and sensory processing area in substantia gelatinosa

cerebral cortex

where muscle response is initiated in pain pathway

thromboxanes and prostaglandins

release of COX1 and COX2 results in the release of what? [2]

Cox-1

cyclo-oxygenase for house-keeping duties: protection of gastric mucosa, support renal function, and promotes platelet aggregation, stimulates uterine conractions

COX-2

cyclo-oxygenase for synthesis of prostaglandins associated with pain and inflammation

Acts by inhibiting COX-2 which blocks the synthesis of prostaglandins.

NSAID MOA:

Aspirin

First generation NSAID

first generation drug

NSAID that blocks both COX-1 and COX-2

Second generation

NSAID that targets cox-2

Celecoxib (Celebrex)

second generation NSAID prototype

Irreversible inhibition (3-5 days) of COX1 and 2

Acetylsalicylic acid (ASA) MOA:

7 days

stop taking aspirin how many days before surgery?

1. absorbed rapidly in GI tract

2. Highly bound to plasma protein

3. excreted in kidneys

Aspirin pharmacokinetics: [3]

1. GI upset

2. bleeding

3. renal dysfunction

ASA (aspirin blocks COX-1, so it will have which adverse effects?

Salicylism

Too much aspirin, causes tinnitus, sweating, and headache

warfarin is an antigoaculant

aspirin decreases platelet aggregation

risk of severe bleeding

Aspirin and warfarin drug interaction

Glucocorticoids act like cortisol. increases gastic secretions.

exaccerabates effects of aspirin

aspirin and glucocorticoids drug interaction

Alcohol increases bleeding risk

aspirin causes bleeding

Alcohol and aspirin drug interaction:

1. hepatotoxicity

2. renal toxicity

3. visual changes

4. alergic reactions

5. bleeding

It is important patients taking aspirin be educated to report signs of what? [6]

1. dark urine

2. claycoloured stool

3. yellow skin/sclera

4. itching

5. abdominal pain

Signs of hepatotoxicity[5]

Ibuprofen (advil, motrin)

First generation NSAID that is an anti-inflammatory, analgesic, antipyretic. Preferred drug now for inflammation over ASA, also has milder side effects

inhibits COX-1 and COX-2 but is reversible

Ibuprofen (Advil) MOA

Acetaminophen (Tylenol)

Drug for mild to moderate pain without anti-inflammatory properties

Inhibits prostaglandin synthesis in CNS to reduce pain and fever

Tyelenol MOA:

Competes for metabolism sites in the liver.

Tyelenol and alcohol drug interaction

causes warfarin to stay around longer

Tylenol and warfarin drug interaction

1. easily distributed

2. half-life of 2 hours

3. excretion: metabolites in urine

Tylenol pharmacokinetics [3]

Opioid agonist

Drug that attaches to opioid receptor and causes something to happen

Opioid agonist/antagonist

Drug that attaches to opioid receptor and works as an agonist in some ways and an antagonist in others:

In the CNS, not an anti-inflammatoryM

where does tylenol work?

morphine

opioid agonist prototype

1. binds to opioid receptors

2. inhibits neurotransmitter release

3. decreases firing rate and excitability

4. decreases transmission of impulses

5. decreased perception of pain and emotional response

6. triggers histamine release from mast cells

Morphine MOA:

It causes histamine release from mast cells, causing itching

Why does morphine cause iching?

1. well absorbed

2. widel distributed

3. half-life: 2-3 hours with significant (25%) hepatic first pass effect

4. 90% appears in urine in 24 hours

Opioid pharmacokinetics: [4]

Mu receptors

opioid receptors in limbic system, thalamus, brainstem, dorsal horn, gut

Kappa

opioid receptors in cerebral cortex, spinal cord

Delta

Opioid receptors in the bowel, no much interaction

1. analgesia

2. euphoria

3. sedation

4. respirator depression

5. nausea

6. decreased GI motility

7. restlessness, confusion

8. pupil ocnstriction

9. peripheral vasodilation

10. itching

11. cough suppression

effects of opioids [11]

less than 8 breaths per minute

respiratory depression rate

1. patients with compromised respiratory system (ex: COPD)

2. patients with head injuries, respiratory centre in medulla could be compromised

patients with what conditions should be cautioned about using opioids due to them causing respiratory depression [2]

always start a bowel regimen (laxatives) when giving opioids

Nursing care for opioids and constipation

offer anti-emetics to start; nausea will disappear in time unless sensitive

nursing care for opioids and nausea

observe for over-sedation; remove/be cautious with any other drugs with sedating effect

nursing care for opioids and sedation

Around the clock (ATC). Manage pain before it can “break through”

when should opioids be given? (schedule-wise)

Hydromorphone (Dilaudid)

Opioid 5X more potent than morphine

codeine

opioid that has the most constipation as a side effect

Meperidine (Demerol)

opioid that should only be given 600mg per day because it has a toxic metabolite that can build up with long term use. half life is 18 hours.

Percocet

combination opioid wit 5mg oxycodone and 325mg tylenol

Tylenol #3 or #4/Atasol 30 or 60

combination opioid with codeine, tylenol, and caffeine

patient-controlled analgesia (PCA)

pump that delivers opioid when patient pushes button

1. a certain amount per hour maximum

2. a lock-out period

Safety features of PCA:

Intrathecal morphine

“spinal” morphine, with or without anesthetic. Usually administered during a procedure in the OR. The effects can last up to 24 hours

1. clocks access of opioid agonists to the opioid receptors

2. reverses opioid actions and side effects

3. bumps opioid molecules out of receptor

Naloxone (Narcan) MOA:

Naloxone (Narcan)

strucurally like morphine. is a competitive antagonist

0.4mg IV; repeat at 2-3 minute intervals

Narcan dosing:

1. severe N+V with cheotherapy

2. loss of appetite and weight with cancer and/or HIV/AIDS

3. muscle spasms

4. palliative/end of life care

when is medical cannabis prescribed? [4]

causes drowsiness

Cannabis and drugs that slow CNS interactions

1. other anti-depressants

2. certain heart meds

3. certain antibiotics

4. antiretroviral drugs (HIV)

5. caution with psychoactive drugs

Medical cannabis should not interact with what? [5]

it is individualized and titrated to effect. Usually no more than 3 grams per day (dried)

Medical cannabis dosing:

1. drowsiness

2. lightheadedness

3. disorientation

4. confusion

side effects of medical cannabis [4]

responds poorly to opioids but much better with adjuvant analgesics

treatment for neuropathic pain:

1. antidepressants (imipramine)

2. Anti-convulsants (Carbomazepine)

3. Local anaesthetics (lidocaine)

examples of adjuvant analgesics for opioids: [3]

the brain to support and augment endorphins

1. opioids

2. relaxation

3. imagery

4. distraction

5. enhance control

6. meditation

targeting the brain for pain relief for neuropathic pain and examples [6]

1. opioids via epidural

2. nerve blocks

3. peripheral stimulation through massage / TENS

methods for pain relief that interrupt spinal cord messages: [3]

Use effective doses on a regular schedule

combine with alternative therapies

should not deter use if needed

Clinical implications for pain relief: [3]