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Pain and Analgesics Lecture Review

PAIN AND ANALGESICS

NURS 309 PATHO-PHARM I

Chapter 15
S. Tullos, EdD, MNSC, RN

OBJECTIVES

  • Differentiate between A-delta and C fiber pain.

  • List examples of mechanical, thermal, chemical pain triggers.

  • Compare endorphins and dynorphins.

  • Define diffuse noxious inhibitory control and placebo effect.

  • List types of pain and an example of each.

  • Define chronic pain syndrome and provide examples.

  • Define nociplastic pain.

  • Identify the most common type of pain.

PAIN

Afferent Pathway

  • Definition: Pathway that carries sensory information from the peripheral nervous system (PNS) to the central nervous system (CNS).

  • Components:

    • PNS to dorsal horn, ascending to CNS.

  • Interpretive Center:

    • Involves the brain stem, midbrain, diencephalon, cerebral cortex.

  • Efferent Pathway:

    • Descending from the CNS to the dorsal horn.

STIMULI THAT ACTIVATE NOCICEPTORS

Table 15.1: Stimuli That Activate Nociceptors (Pain Receptors)

  • Location of Receptor:

    • Skin

    • Gastrointestinal tract

    • Skeletal muscle

    • Joints

    • Arteries

    • Head

    • Heart

    • Bone

  • Provoking Stimuli:

    • Skin: Pricking, cutting, crushing, burning, freezing.

    • Gastrointestinal Tract: Engorged/inflamed mucosa, distention or spasm of smooth muscle, traction on mesenteric attachment.

    • Skeletal Muscle: Ischemia, injuries of connective tissue sheaths, necrosis, hemorrhage, prolonged contraction, injection of irritating solutions.

    • Joints: Synovial membrane inflammation.

    • Arteries: Piercing, inflammation.

    • Head: Traction, inflammation, or displacement of arteries, meningeal structures, and sinuses; prolonged muscle contraction.

    • Heart: Ischemia and inflammation.

    • Bone: Periosteal injury due to fractures, tumors, or inflammation.

NOCICEPTORS

  • Definition: Pain receptors characterized by free nerve endings in the afferent pathway.

  • Action: When stimulated, they cause "nociceptive" pain (mechanical, thermal, chemical).

PAIN TRANSDUCTION

  • A-Delta Fibers:

    • Characteristics: Myelinated, large, rapid, sharp pain signals.

    • Function: Spinal reflex withdrawal.

  • C Fibers:

    • Characteristics: Unmyelinated, small, slow, dull pain signals.

    • Function: Generally associated with chronic pain.

PAIN TRANSMISSION

  • Anterior Spinal Thalamic Tract:

    • Characteristics: Fast impulse; conveys acute sharp pain.

  • Lateral Spinal Thalamic Tract:

    • Characteristics: Slow impulse; conveys dull, chronic pain.

  • Projection: Impulses are projected to the somatosensory cortex for interpretation.

PAIN PERCEPTION

  • Conscious Awareness: The awareness of pain, its character, location, and intensity.

  • Affective Motivational: Involves conditioned avoidance and emotional responses.

  • Cognitive Evaluative: Influences how pain is perceived based on context and thought processes.

THRESHOLD VS. TOLERANCE (SUBJECTIVE)

  • Threshold:

    • Definition: Lowest intensity of a stimulus recognized as pain.

    • Influenced by stress, physical exertion (increases circulating neuromodulators), and masking effects.

  • Tolerance:

    • Definition: Greatest intensity of pain one can endure.

    • Can decrease over time due to repeated exposure, fatigue, anger, apprehension, or sleep deprivation.

    • Increases with alcohol, opioid use, distraction, or faith.

PAIN MODULATION

  • Excitatory: Related to tissue injury and inflammation including substances such as prostaglandins, histamine, bradykinin, glutamate, aspartate, and substance P.

  • Inhibitory: Include neurotransmitters such as GABA, glycine, serotonin, and norepinephrine.

ENDOGENOUS OPIOIDS

  • Enkephalins: Most prevalent type of endogenous opioid.

  • Endorphins: Produced in the brain; specifically, beta-endorphin produces the greatest sense of exhilaration and pain relief.

  • Dynorphins: Most potent, impede pain signals.

  • Endomorphins: Provide potent analgesic effects.

MODULATION PATHWAYS

  • Descending inhibitory or facilitatory pathways can inhibit or facilitate pain by activating opioid receptors.

  • Segmental Inhibition of Pain: A-beta fibers stimulate inhibitory interneurons to decrease pain transmission.

  • Diffuse Noxious Inhibitory Control (DNIC): Pain may be relieved when two noxious stimuli occur simultaneously from different sites.

  • Expectancy-Related Cortical Activation (Placebo Effect): Cognitive expectations can lead to physiological changes influencing pain perception.

TYPES OF PAIN

  • Acute (Nociceptive):

    • Somatic Pain:

    • A-delta fibers: sharp and well localized.

    • C fibers: dull, aching, and poorly localized.

    • Visceral Pain: Poorly localized, aching, gnawing, throbbing, or intermittent cramping.

    • Referred Pain: Pain experienced in one location but originating from another site.

  • Chronic Pain:

    • Lasts a minimum of 3 to 6 months.

    • Pain is out of proportion to visible tissue injury, and neuroimaging may reveal brain changes.

    • Associated issues may include cognitive deficits, difficulty coping with pain, depression, anorexia, and altered sleep patterns.

  • Neuropathic Pain:

    • Peripheral Neuropathic Pain: Caused by peripheral nerve lesions.

    • Central Neuropathic Pain: Caused by lesions or dysfunction in the brain or spinal cord, can present as burning, shock-like, or tingling sensations.

COMPARING ACUTE AND CHRONIC PAIN

Table 15-3: Comparison of Acute and Chronic Pain

  • Characteristic: Experience, source, onset, duration, pain identification, significance, pattern, course, and actions taken.

  • Acute Pain:

    • Source: Event

    • Onset: Sudden

    • Duration: Transient (usually short-term)

    • Significance: Protective, informs something is wrong

    • Pattern: Easily identifiable

    • Course: Suffering decreases over time

    • Actions: Leads to actions to address pain.

  • Chronic Pain:

    • Source: Unknown or prolonged state

    • Onset: May be sudden or develop gradually

    • Duration: Lasts beyond expected healing time (months to years)

    • Significance: Individual seeks meaning; serves no useful purpose.

    • Pattern: Less identifiable; may interfere with quality of life.

    • Course: Suffering usually increases over time.

CHRONIC PAIN SYNDROMES

Common Chronic Pain Syndromes

  • Persistent Low Back Pain: Most common; results from poor muscle tone and sudden or vigorous exercise.

  • Myofascial Pain Syndromes: Includes conditions like fibromyalgia with localized and generalized pain.

  • Chronic Postoperative Pain: Occurs after surgical interventions due to nerve disruption; risk factors include preexisting pain.

  • Cancer Pain: Often associated with disease progression or treatment.

  • Deafferentation Pain: Resulting from alterations in sensory input into the CNS.

  • Phantom Limb Pain: Pain perceived in an amputated limb.

  • Complex Regional Pain Syndrome: Associated with peripheral nerve injury; characterized by severe, burning pain.

CENTRAL NEUROPATHIC PAIN

  • Caused by lesions or dysfunction in the brain or spinal cord.

  • Central Sensitization: Increased sensitivity of central pain-signaling neurons due to progressive stimulation of group C neurons (wind-up phenomenon).

  • Examples: Trauma, tumors, multiple sclerosis, etc.

NOCIPLASTIC PAIN

  • Definition: Pain arising from altered nociception without true tissue damage or disease.

  • Commonly associated with conditions such as fibromyalgia and irritable bowel syndrome.

FIBROMYALGIA SYNDROME

  • Characteristics: Chronic diffuse musculoskeletal pain, increased sensitivity to sensory input, and fatigue.

  • Can begin localized (e.g. neck and shoulders) and become generalized.

  • Symptoms include headaches, irritable bowel syndrome, and sleep difficulty.

ANALGESICS

Chapter 25
Objectives

  • Define how acetaminophen affects the liver and identify the antidote for overdose.

  • List side effects and adverse effects of opioids.

  • Identify opioid overdose treatment and contraindications for use.

  • Discuss adjuvant medications for neuropathic pain relief, examples being morphine, naloxone, and naltrexone.

GATE CONTROL THEORY

  • Developed by: Melzack & Wall (1965).

  • Concept: Pain involves emotional and cognitive components.

  • Mechanism: CNS gating mechanisms regulate pain impulses, allowing for manipulation through non-pharmacological interventions.

PATHO ASSOCIATION WITH MEDS

  • Neurohormones such as endorphins can suppress pain.

  • Opioids activate similar receptors to reduce pain perception.

  • NSAIDs block cyclooxygenase, impacting pain conveyed through prostaglandins.

  • Corticosteroids inhibit inflammation pathways and reduce pain signals.

ACETAMINOPHEN

  • Brand: Tylenol

  • Type: Analgesic & antipyretic with no anti-inflammatory properties.

  • Pharmacodynamics: Inhibits prostaglandin synthesis in CNS only.

  • Pharmacokinetics: Well absorbed orally, with dosing every 4 hours.

  • Adverse Effects: Rare but includes risk for severe liver injury with overdose.

  • Drug Interactions: Not recommended with alcohol or warfarin.

ACETAMINOPHEN TOXICITY

  • Serum Range: Therapeutic range is 10-20 mcg/mL.

  • Symptoms of Toxicity: Nausea, vomiting, diarrhea, abdominal pain.

  • Severe outcomes: Hepatic necrosis, hepatic failure.

  • Treatment: Acetylcysteine (Mucomyst, Acetadote) is effective when given within 8-10 hours of overdose.

NURSING IMPLICATIONS

  • High-Risk Factors: Alcohol use and warfarin increase risks.

  • Dose Management: Ensure recommended doses are not exceeded and manage potential toxicity.

NSAID PATIENT EDUCATION

  • Advice to take with food or milk.

  • Avoid crushing or chewing.

  • Discard if preparations smell like vinegar and avoid alcohol consumption.

  • Monitor for symptoms of salicylism (tinnitus, headache).

OPIOIDS

  • Definition: Opioid agonists used for moderate to severe pain.

  • Controlled Substances Act (1970): Classifies drugs with high potential for abuse across five categories.

  • Dependence: Can be both physical and psychological with long-term use.

OPIOID ANALGESIC

  • Source: Derived from natural opium; includes Morphine, Codeine, and Meperidine.

  • Effects: Alter perceptions of pain and cause side effects depending on receptor binding.

SIDE EFFECTS OF OPIOID ANALGESICS

  • Most common: Constipation due to decreased GI motility.

  • Other effects: Drowsiness, dizziness, nausea, vomiting, histamine release leading to pruritus.

ADVERSE EFFECTS OF OPIOIDS

  • Respiratory Depression: A potential critical effect; requires monitoring.

  • Other issues: Urinary retention, orthostatic hypotension, and risk of dependence.

CONTRAINDICATIONS

  • Avoid in head injuries, respiratory disorders, or low blood pressure conditions.

  • Adjust doses as necessary for older adults.

COMBINATION DRUGS

  • Use of smaller doses from combinations (e.g., ibuprofen/hydrocodone, acetaminophen/codeine) to minimize side effects and dependency risk.

PATIENT-CONTROLLED ANALGESIA (PCA)

  • Mechanism: Allows self-administration of pain relief medication via a programmed pump, ensuring safety and effectiveness.

ADJUVANT THERAPY

  • These drugs enhance the effects of opioids or non-opioid medications and include anticonvulsants, antidepressants, and corticosteroids.

OPIOID ANTAGONISTS

  • Function: Reverse opioid effects, especially respiratory depression (primary drug: naloxone).

  • Monitoring: Monitor for potential withdrawal symptoms after administration.

CONCLUSION

  • Understanding pain mechanisms, management, and various types of analgesics are critical in effective patient care and pain management strategies.

GASTROINTESTINAL DYSFUNCTION

NURS 309 Pathophysiology

Chapter 49
S. Tullos, EdD, MNSC, RN

OBJECTIVES

  • List the components of the GI tract and their functions.

  • Review gastric emptying mechanisms.

  • Explain the primary function of the small intestine.

  • Define clinical manifestations of GI dysfunction.

  • Discuss mechanisms of diarrhea and conditions like dysphagia and gastroparesis.

GASTROINTESTINAL TRACT FUNCTIONS

  • Functions include ingestion and breakdown of food, propulsion, secretion (mucus, water, enzymes), digestion (mechanical and chemical), absorption of nutrients, and waste elimination.

COMPONENTS OF THE GASTROINTESTINAL TRACT

  • Mouth: Chewing and salivation.

  • Throat: Swallowing process.

  • Esophagus: Regulation by upper and lower esophageal sphincters.

  • Stomach: Fundus, body, antrum; controlled by the pyloric sphincter.

  • Small Intestine: Divided into duodenum, jejunum, ileum; the ileocecal valve regulates flow into the large intestine.

  • Large Intestine: Includes cecum, appendix, and colon, culminating at the rectum and anus.

STOMACH GASTRIC MOTILITY

  • Mechanism: Peristaltic waves facilitate food movement.

  • Regulation Factors: Gastrin, motilin (increase rate), sympathetic activity, and secretin (decrease rate).

SMALL INTESTINE

  • Major site for digestion and absorption.

  • Enzymatic action and nutrient breakdown facilitated by bile salts and pancreatic enzymes.

LARGE INTESTINE

  • Structure: Cecum connects to the appendix; colon divided into segments (ascending, transverse, descending, sigmoid).

  • Functionality: Fecal mass formation, gastrocolic reflex, and defecation reflex.

CLINICAL MANIFESTATIONS OF GI DYSFUNCTION

  • Include anorexia, nausea, vomiting, constipation, diarrhea, and abdominal pain.

  • Nausea: Subjective sensation of discomfort associated with various conditions.

  • Vomiting (Emesis): Forceful expulsion of stomach contents.

CONSTIPATION

  • Defined by infrequent or difficult bowel movements; factors include diet, medications, and various disorders.

DIARRHEA

  • Characterized by loose watery stools; classified into acute or persistent forms with varying volume causes.

ABDOMINAL PAIN

  • Caused by mechanical, inflammatory, or ischemic factors; can present as parietal or visceral pain, or referred pain.

GASTROINTESTINAL BLEEDING

  • Classified as upper or lower GI bleeding with distinct manifestations and physiological responses.

MOTILITY DISORDERS

Dysphagia

  • Difficulty swallowing due to mechanical obstruction or functional disorders such as achalasia.

GASTROPARESIS

  • A condition of delayed gastric emptying without mechanical obstruction; commonly linked to diabetes mellitus.

PHARMACOLOGY OF NAUSEA AND VOMITING

DOPAMINE ANTAGONISTS

  • Examples: Prochlorperazine, Promethazine; effects include sedation and potential extrapyramidal symptoms.

SEROTONIN ANTAGONISTS

  • Examples: Ondansetron, Granisetron used to control chemotherapy-induced nausea.

PROKINETIC AGENTS

  • Mechanism: Increase GI motility; Metoclopramide is a key agent for gastroparesis.

ANTI-DIARRHEALS

  • Mechanism: Decrease GI motility; includes opioids and combination medications like loperamide.

LAXATIVES

  • Types: Osmotic, stimulant, bulk-forming, with various side effects and usage recommendations detailed.

CONCLUSION

  • A thorough understanding of gastrointestinal function, disorders, and treatment mechanisms is essential for effective patient care in gastrointestinal dysfunction.

REFERENCES

  • Huether & McCance, 8th ed, 2026.

  • McCuistion, 12th ed, 2026.