Pain, Analgesia, and Anesthesia

pharm exam 3

What is pain?

• a protective signal → indicates tissue injury or threat

• generated by nociceptors → CNS processing → perception

What is the gold standard for pain assessment?

• patient report of their pain

3 factors influencing pain and perception of it

• biological → injury, inflammation

• psychological → anxiety, past experience

• social → culture, support

Pain pathway

• Transduction

  • tissue injury → inflammatory mediators → nociceptor activation

• Transmission

  • signal travels → peripheral nerve → spinal cord → brain

• Perception

  • brain interprets signal → “pain experience”

• Modulation

  • CNS up or down regulates pain signal (endorphins, descending pathways)

What do all analgesics target?

• all analgesics target the pain pathway

• drugs act at different steps in this pathway

What activates pain? (transduction)

• Mechanical → pressure, stretch, injury

• Thermal → extreme heat/cold

• Chemical → inflammation

  • prostaglandins, bradykinin, ATP

What actually happens?

• stimulus → ion channels open

  • action potential occurs → signal sent to CNS

What does inflammation do to pain threshold?

• inflammation lowers pain threshold

• sensitivity is increased

Pain facilitators (increase pain)

• Prostaglandins → sensitize nociceptors (not direct pain cause) (KEY target of NSAIDs)

• Bradykinin → direct nociceptor activation

• Substance P → amplifies signal in spinal cord, released by neuron

• Histamine → inflammation + swelling

Pain inhibitors (decrease pain)

• Endorphins → natural opioids

• Endocannabinoids → modulate pain

Acute vs Chronic pain

Acute Pain (symptom)

• protective → signals injury

• sympathetic activation → increased HR, BP, RR, diaphoresis

• resolves with healing

Chronic Pain (not a symptom)

• no longer protective

• CNS remodeling + persistent signaling

• minimal physiologic response

• psychological + functional impact

• disease, not just a symptom

Types of acute pain

Nociceptive (tissue injury)

• Somatic → sharp, localized

• Visceral → deep, diffuse

Neuropathic (nerve damage)

• burning, tingling, electric

Inflammatory

• swelling, aching, throbbing

Central (no processing disorder)

• no clear injury (fibromyalgia), always chronic

IDENTIFYING PAIN TYPE GUIDES DRUG CHOICE!

Where do different pain drugs work?

• Transduction → NSAIDs, corticosteroids

• Transmission → local anesthetics

• Perception → opioids

• Modulation → antidepressants, anticonvulsants

NSAIDs

MOA → inhibit COX → decrease prostaglandins

Effects → decrease pain, decrease inflammation, decrease fever

Why they work → prostaglandins = key pain sensitizers

ADRs

• GI bleeding → decreased protective prostaglandins

• Renal injury → decreased renal perfusion, especially in hypovolemia or older adults

• Increased BP

Nursing Considerations

• monitor GI, renal function, dosing limits

Acetaminophen

MOA → acts in CNS → decreases prostaglandins in brain (minimal peripheral effect)

Effects → decreased pain, decreased fever → NO anti-inflammatory effect

Major ADR → hepatotoxicity → dose dependent

Max Dose

• 4 g/day (healthy)

• ≤ 3 g/day (high risk)

What is the max dose for Acetaminophen?

• 4 g/day (healthy)

• ≤ 3 g/day (high risk)

Opioid Agonists (central pain modulators)

MOA → bind µ receptors → decreased pain perception + emotional response

Effects → analgesia, sedation, euphoria (if taken for non-pain reason)

Major ADR

• Highest risk → respiratory depression

• severe constipation, dependence

Pain signal still present, but perception and emotional response reduced!

What is the antidote for opioids?

• Naloxone → reverses opioid effects

• person will feel pain again, so its important to titrate dosage

What is the most important opioid receptor?

• µ (mu) → analgesia, respiratory depression, euphoria

What are combination opioids?

• Opioid + non-opioid (ex. acetaminophen)

  • benefit: better pain control

  • risk: dose ceiling → toxicity from the non-opioid

Common examples of combination opioids

• Hydrocodone/APAP → Vicodin, Norco

• Oxycodone/APAP → Percocet

• Codeine/APAP → Tylenol #3

What to question with combination opioids?

• is the patient taking multiple APAP-containing products?

  • percocet + OTC tylenol, cold/flu meds?

• is the total daily acetaminophen dose exceeding 3-4 g/day?

• Liver disease, alcohol use, malnutrition?

Key danger of combination opioids?

• Acetaminophen overdose → liver failure

Assessment of pain

Onset → sudden or gradual

Location → where + does it radiate

Quality → sharp, dull, burning, etc.

Intensity → 0-10 scale

Aggravating/relieving factors → what makes it worse/better

Effect on function → ADLs, mobility

Influencing Factors

• biological

• psychological

• social

Effects of ineffective pain management?

Cardiovascular → increased HR, BP, cardiac workload

Pulmonary → hypoventilation, atelectasis, infection

GI → post-op ileus, constipation, urinary retention

Muscular → weakness, fatigue

Psychological → anxiety, fear, frustration

Long-Term → chronic stress impacts heart, lungs, immune system

Pain Management Principles (what we do)

• Goal is to decrease pain and improve function

  • not to completely eliminate pain, may not be possible

• Multimodal → non-pharm + pharmacologic intervention

• Individualize dosing + manage ADRs

• Reassess pain + function

Non-pharm interventions

Physical → heat/ice, PT, TENS

Cognitive → distraction, biofeedback

Mind-body → acupuncture, meditation, yoga

Adjuvant meds

• Not primary analgesics, used to enhance pain control

Antidepressants (TCAs, SSRIs) → neuropathic pain

Anticonvulsants (gabapentin, pregabalin) → neuropathic pain

Corticosteroids → inflammatory pain

Morphine → class, MOA, effects

Class → opioid agonist (narcotic analgesic)

MOA → minds to opioid receptors in the CNS to alter pain perception

Therapeutic Effects → severe acute pain, chronic pain, preanesthetic sedation

Morphine ADRs

• respiratory depression

• sedation

• nausea/vomiting

• constipation

• urinary retention

Morphine warnings

• Black box warning → Schedule II

  • high risk physical/psychologic dependence

• Extended release for opioid-tolerant patients only

  • not intended for prn use

Morphine nursing considerations

• Monitor for sedation, respiratory depression

• monitor bowel function

• use naloxone (Narcan) for overdose

• Routes → oral, IV, subcutaneous

Fentanyl → class, MOA, effects

Class → opioid agonist (IV anesthetic)

MOA → binds to mu/kappa opioid receptors for potent, rapid analgesia

Therapeutic Effects

• short-duration analgesia

• chronic pain management

• severe pin in controlled settings (surgery)

50-100 times more potent than morphine! Most powerful opioid!

Fentanyl ADR/warning

ADR → respiratory depression, bradycardia, hypotension, muscle rigidity

Black box warning → schedule II controlled substance

• high abuse potential

• risk of misuse, overdose, and CNS depressant interaction

Fentanyl nursing considerations

• ensure airway support

• monitor for respiratory depression

• titrate carefully, especially in opioid-naive patients

• routes: IV, transdermal patches, lozenges

Tramadol → class, MOA, effects

Class → synthetic opioid analgesic

MOA → minds to mu receptor, weak opioid agonist

• inhibits norepinephrine/serotonin reuptake

• inhibits pain transmission impulse

Therapeutic Effects → moderate pain, off-label for neuropathic pain, restless leg syndrome

Tramadol → ADRs, contraindications

ADRs → dizziness, N/V, lethargy, CNS stimulation, seizures (lowers seizure threshold)

Contraindications

• history of seizures

• use of SSRIs/MAOIs

• sudden death if combined with ethanol

Tramadol → nursing considerations

• monitor for seizures

• patients should avoid alcohol/CNS depressants

• assess for risk of serotonin syndrome

• schedule IV controlled substance

What is anesthesia?

• medically induced, reversible state of loss of sensation

  • with or without loss of consciousness

  • used to prevent pain during procedures

Levels of CNS depression

• Sedation → calm, awake

• Moderate sedation → drowsy, arousable

• Deep sedation → difficult to arouse

• General anesthesia → unconscious

Drugs move patients along this continuum

Types of anesthesia

General

• loss of sensation + loss of consciousness

• used for major surgery

Regional

• loss of sensation in a body region

• consciousness intact

• used for procedures below level, like a spinal/epidural

Local

• loss of sensation in a small area

• consciousness intact

• used for minor procedures

Sedation

• reduced awareness

• consciousness variably depressed

• used for procedures requiring relaxation/anxiolysis

General Anesthesia → MOA, result, risks

MOA

• increased GABA (inhibitory) and decreased NMDA (excitatory)

Result

• global CNS depression → unconsciousness

Risks

• respiratory depression

• hypotension