Pharm - Pain Management

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What is pain?: - unpleasant sensory and emotional experience associated with actual or potential tissue damage

*pain is whatever the client says it is
What is pain threshold?: LOWEST threshold at which a stimulus is perceived as pain
What is perceptual dominance?: intense pain in one area may increase the pain threshold in another

(ex. headache vs. appendicitis)
Pain tolerance: length of time or intensity a person will endure before asking for pain relief
What factors influence pain experience?: - culture (may not express feelings)
- past experience
- meaning
- attention, anxiety
- suggestion & placebo (meds that have no active ingredients & cause a psychological belief that it's working)
- feelings of control
What are the different types of pain?: 1. Nociceptive Pain
- somative pain
- visceral pain
2. Neuropathic Pain
What is somative pain?: - arises from bone, joint, muscle, skin or CT
- usually aching or throbbing
- well localized
What is visceral pain?: - arises from organs
- aching & not well-localized
(ex. GI tract or tumor involvement of organ)
What is neuropathic pain?: - abnormal processing of sensory input by peripheral or CNS
- Neuralgias: pain in one or more nerves that occurs without stimulation of pain receptor
- opioids are not effective (ONLY adjuvant analgesics)
What is acute pain?: - usually sudden onset
- short-lived
- easily treated with meds
- symptoms are easily observed
What is chronic pain?: - constant pain
- long duration (3-6 months)
- no specific symptoms
What are the consequences of pain?: - impaired ambulation, gait disturbances, & falls
- decreased socialization
- sleep disturbances
- deconditioning - weakness, muscle atrophy
- depression
- polypharmacy (taking more than one med)
- cognitive dysfunction
- malnutrition
- increased health care use & costs
Pain management strategy:: A - ASK about pain regularly & ASSESS pain systematically
B - BELIEVE the patient & family reports of pain & what relieves it
C - CHOOSE pain control options appropriately
D - DELIVER intervention in a timely manner
E - EMPOWER patients & families
ENABLE patients to control their treatment to the greatest extent possible
What are some non-drug interventions for pain?: - massage
- TENS (transcutaneous electrical nerve stimulation)
- touch
- heat
- cold
- acupuncture
- relaxation
What is the pain pathway?: 1. Stimulation of nociceptors
2. Impulse is conducted to the dorsal horn via:
- A-delta fibers
- A-beta fibers
- C fibers
3. Dorsal horn is relay station & sensory processing area (substantia gelatinosa)
4. Impulses are conducted to brain via spinothalmic tracts:
- brainstem - input signal is integrated in periaqueductal gray in midbrain
- thalamus - perception of pain
- limbic system - emotional response
- reticular - memory of pain
- cerebrocortex
5. Pain is perceived and a response is initiated
What are A-delta fibers?: - large
- fast
- myelinated
- sharp, localized pain

(ex. stub toe, bite cheek, or hit elbow)
What are A-beta fibers?: - large
- mechanical
- can close pain gate

(ex. touch, pressure, or vibration)
What are C fibers?: - small
- slow
- unmyelinated
- dull/burning
- diffuse pain (unlocalized)

(ex. chronic pain, aching)
What are nociceptors?: - small nerve endings of A-delta, A-beta, & C fibers
- do not adapt to repeated stimuli
What chemicals are released when a tissue is injured?: - H1 (histamine)
- PGs/Lts (prostaglandins & leukotrienes)
- 5HT (serotonin)
- Bradykinin
- substance P
What is the MOA of inflammation?: cell membrane damage --> release of lipo-oxygenase --> Lts & cyclo-oxygenase (COX 1&2) --> release of thromboxanes & PGs
What are the functions of COX 1?: house keeping duties:
- protection of GASTRIC mucosa
- support RENAL function
- promotes PLATELET aggregation (thromboxane)
- stimulates UTERINE contractions
What is the function of COX 2?: synthesis of PGs associated with pain & inflammation
What drugs can be taken for mild to moderate pain WITH anti-inflammatory properties?: 1. NSAIDS
2. ASA - Acetylsalicyclic acid (aspirin)
3. Ibuprofen (Advil & Motrin)
What is the MOA of NSAIDS?: inhibit COX-2 --> blocks the synthesis of PGs --> prevents pain from inflammatory process (prevents vasodilation & vascular permeability & chemical mediators)
- also blocks PGs effect on hypothalamus --> antipyretic

**NSAIDS have reversible inhibition (except ASA which is irreversible)
What are 1st generation NSAIDS??: blocks COX 1 & COX 2
ex. ASA (Aspirin) & Ibuprofen (Advil & Motrin)
What are 2nd generation NSAIDS?: blocks only COX 2
ex. Celecoxib (Celebrex)
What is the MOA and pharmakinetics of ASA (aspirin)?: - MOA: IRREVERSIBLE inhibition of COX 1 & COX 2
- Pharmakinetics:
- absorbed rapidly from GI tract
- metabolized in liver
- half life: 2 hours (low levels) vs. 20 hours (high levels)
- distribution: highly bound to albumin (competes with other NSAIDS for binding sites; will displace other drugs such as Ibuprofen and they will be used up more quickly)
- excretion: kidneys
What are the adverse effects of ASA (aspirin)?: - GI upset (nausea & heartburn)
- bleeding (blocks platelet aggregation)
- renal dysfunction (blocks COX 1 which is necessary for normal functioning) --> Na & H20 retention
- salicylism (tinnitus, sweating, headache)
- Reye's syndrome (no NSAID use in children & teenagers with influenza or chickenpox because of high correlation)
Which inhibitors cause Na & H20 retention?: COX 1 inhibitors
What drugs interact with ASA (aspirin)?: - Anti-coagulants (Wararin) - because ASA blocks platelet aggregation
- Glucocorticoids (exacerbate effects)
- alcohol (increase metabolism of drugs in the liver)
Education about ASA:: patient should report signs of:
- hepatotoxicity:
- dark urine
- clay-colored stools
- yellow sclera/skin
-itching
-abdominal pain
- renal toxicity
- visual changes
- ototoxicity
- allergic reactions
- bleeding (long-term therapy)
Ibuprofen?: - anti-inflammatory
- analgesic
- antipyretic (anti-fever)
- milder side affects than ASA
- preferred choice for inflammation

- ex. Advil & Motrin
- 1st generation NSAIDS
Drugs for mild-moderate pain (WITHOUT anti-inflammatory effects)?: ACETAMINOPHEN:
- adverse effects are rare
- can cross placenta (but not harmful to fetus)
- inhibits PG synthesis in CNS --> reduces pain & fever
- Drug interactions: alcohol & warafin (coumadin) - anticoagulant
Opioid Agonists:: MORPHINE
- binds to opioid receptors
- inhibits neurotransmitter release
- decreases firing rate
- blocks impulse transmission
- decreases perception of pain
- triggers release of H1
- high first pass effect (only 25% PO dose bioavailable)
Opioid receptor Mu point of action & effects?: Mu - limbic system, thalamus, brainstem, & dorsal horn

- analgesia
- respiratory depression
- euphoria
Opioid receptor Kappa point of action & effects?: - cerebral cortex & spinal cord

Effects:
- analgesia
- sedation
- pupil constriction
Opioid receptor SIGMA point of action & effects?: - mid to lower brain

Effects:
- dysphoria (dissatisfaction)
- psychotomimetic effects
Opioid receptor DELTA point of action & effects?: - bowel

Effects:
constipation (decreased GI motility)
Direct stimulation of vomiting center from?: - brain (anticipation, fear, memory)
- senses (sight, smell, pain)
- inner ear (H1 & M)
Indirect stimulation of vomiting centre from?: - stomach (5HT, DA)
- drugs (chemotherapy, opioids)

*activation of chemo-receptor trigger zone (CTZ) - 5HT, DA, M
Opioid Effects:: - analgesia
- euphoria
- sedation
- respiratory depression
- nausea
- decreased GI motility (causing constipation)
- restlessness/confusion
- pupillary constriction
- peripheral vasodilation
- itching
- cough suppression
Respiratory Depression effects of opioids?: - may occur at therapeutic doses
- rate & depth can be decreased
- not a deterrent to patients with normal respiratory function
- CAUTION with people who have COPD
- more problematic in post-op/trauma pts than cancer patients
Considerations when giving opioids:: - give anti-emetics to start to prevent nausea
- start bowel regimen to deal with constipation
- observe for over-sedation (wake people for next dose & observe pupils - indictor of reaching toxicity)
opioids to avoid "chronic pain": - METHADONE & LEVORPHANOL (long half-life)
- CODEINE (side effects)
- MEPERIDINE (toxic metabolite accumulates if long term use)
- agonist/antagonists (their effects will be diminished - net effect action decreased)
NALOXONE (NARCAN): - structurally like morphine
- competitive opioid antagonist
- blocks access of opioid agonists to opioid receptors
- reverses opioid actions & side effects
- bumps opioid molecules out of receptor
- 0.4 mg IV, repeat at 2-3 min intervals
Neuropathic pain: - injury to nerves: shooting, jabbing, burning
- responds poorly to opioids
- treat with adjuvants
Adjuvants:: - Imipramine - antidepressants
- Carbamazepine - anti-convulsants
- Lidocaine - local anesthetics
Anti-depressant adjuvant:: Imipramine
Anti-convulsive adjuvant:: carbamazeprine
Local anesthetic adjuvant:: Lidocaine
What are adjuvants?: - not pain meds per se
- assist with pain control when used with pain meds
- used for neuropathic pain
- can allow for reduced analgesic dosing
- side effects can be a problem (sometimes unpredictable)
Brain Target for pain relief:: - support & augment endorphins
- give opioids
- relaxation response
- imagery
- distraction
- enhance control
- meditation (short term)
Targeting spinal cord to interrupt message: - opioids by epidermal
- peripheral stimulation by massage & TENS (stimulate large A-delta fibers) - close pain gate
- therapeutic touch
Non-pharm pain methods:: - ultrasound (promotes circulation in deep tissue)
- heat - dilates blood vessels --> speed up removal of chemical stimulating nocicpetors (OLD injury)
- cold - vasoconstriction --> decreases inflammatory response & decreases stimulation of nociceptors (ACUTE injury)
- acupuncture/acupressure - opens energy paths/fields in body
What is tolerance?: - loss of a particular effect at a given dose
- receptors adapt to the presence of drug
- occurs in the absence of addiction
Physical dependence?: - physiological changes occur so that one needs continued use of drug to prevent withdrawal - usually takes several weeks to occur -
Abuse?: - use of drug outside of normally accepted standard
Addiction?: - preoccupation with the acquisition of, compulsive use of, and relapses to use
- less than 1% become addicted
Summary:: - treat the pain & not the behaviour
- start low and go slow
- drugs/non-drug interventions are more effective
4 receptors involved in emetic response?: 1. DA - dopamine
2. H1 - histamine
3. M - muscarinic cholinergic
5. 5-HT - serotonin

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Created By daisy497