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Week 7 Power Point Notes

PAIN AND ANALGESICS

NURS 309 PATHO-PHARM I

CHAPTER 15

Instructor: S. Tullos, EdD, MNSC, RN

OBJECTIVES

  • Differentiate between A-delta and C fiber pain.

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

  • Compare endorphins and dynorphins.

  • Define diffuse noxious inhibitory control and placebo effect.

  • List types of pain and provide an example of each.

  • Define chronic pain syndrome and provide examples.

  • Define nociplastic pain, noting its prevalence.

PAIN

  • Afferent pathway:

    • Pathway from the peripheral nervous system (PNS) to the dorsal horn, ascending to the central nervous system (CNS).

  • Interpretive center:

    • Comprises brain structures including:

    • Brain stem

    • Midbrain

    • Diencephalon

    • Cerebral cortex

  • Efferent pathway:

    • Descending pathways from the CNS to the dorsal horn, which modulates the perception of pain.

STIMULI THAT ACTIVATE NOCICEPTORS

TABLE 15.1

Stimuli That Activate Nociceptors (Pain Receptors)

  • Location of Receptors:

    • Skin

    • Gastrointestinal tract

    • Skeletal muscle

    • Joints

    • Arteries

    • Head

    • Heart

    • Bone

  • Provoking Stimuli:

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

    • Gastrointestinal tract: Engorged or inflamed mucosa, distension/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, fractures, tumors, inflammation.

NOCICEPTORS

  • Definition:

    • Pain receptors characterized as free nerve endings present in the afferent pathway.

  • Function:

    • When stimulated, they cause “nociceptive” pain, which can be mechanical, thermal, or chemical.

PAIN TRANSDUCTION

  • Types of Nerve Fibers:

    • A-delta fibers:

    • Characteristics: Myelinated, large, rapid, causing sharp pain and spinal reflex withdrawal.

    • C fibers:

    • Characteristics: Unmyelinated, small, slow, causing dull pain that is poorly localized.

PAIN TRANSMISSION

  • Anatomical Pathways:

    • Anterior spinal thalamic tract:

    • Transmits fast impulses related to acute sharp pain.

    • Lateral spinal thalamic tract:

    • Transmits slow impulses related to dull, chronic pain.

  • Interpretation:

    • Impulses are projected to the somatosensory cortex for interpretation of pain characteristics.

PAIN PERCEPTION

  • Conscious Awareness:

    • Involves sensory discrimination regarding presence, character, location, and intensity of pain.

  • Affective Motivational Component:

    • Encompasses conditioned avoidance and emotional responses.

  • Cognitive Evaluative Component:

    • Modulates perception of pain, influenced by personal experiences and beliefs.

THRESHOLD VS. TOLERANCE (SUBJECTIVE)

  • Threshold:

    • Definition: The lowest intensity of pain that can be recognized.

    • Influencing Factors: Stress and physical exertion can elevate levels of circulating neuromodulators that raise the pain threshold.

    • Perceptual Dominance:

    • Refers to the phenomenon of masking one pain by another.

  • Tolerance:

    • Definition: The greatest intensity of pain one can endure.

    • Influencing Factors: Can decrease over time due to repeated exposure, fatigue, anger, apprehension, and sleep deprivation. Conversely, tolerance can increase with the use of alcohol, opioids, distraction, and faith.

PAIN MODULATION

  • Excitatory Factors:

    • Tissue injury related to substances like prostaglandin, histamine, bradykinin; chronic inflammation involves lymphokines.

    • Other excitatory compounds include glutamate, aspartate, substance P, and calcitonin.

  • Inhibitory Factors:

    • Include GABA, glycine, serotonin, and norepinephrine, which help reduce pain perception.

ENDOGENOUS OPIOIDS

  • Definition:

    • Naturally occurring peptides that modulate pain perception.

  • Types of Endogenous Opioids:

    • Enkephalins:

    • Most prevalent class of endogenous opioids.

    • Endorphins:

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

    • Dynorphins:

    • Most potent class; they impede pain signaling pathways.

    • Endomorphins:

    • Potent analgesics with strong effects on pain modulation.

MODULATION PATHWAYS

  • Descending Pathways:

    • The inhibitory or facilitatory pathways that inhibit or facilitate pain by activating opioid receptors.

  • Segmental Inhibition:

    • Achieved by A-beta fibers stimulating inhibitory interneurons, thus decreasing pain transmission.

  • Diffuse Noxious Inhibitory Control (DNIC):

    • Defined as the phenomenon where pain is relieved when two noxious stimuli occur simultaneously but from different sites; effectively demonstrates how pain can inhibit pain.

  • Expectancy-Related Cortical Activation:

    • Known as the placebo effect, it describes the physiological effects caused by cognitive expectations.

TYPES OF PAIN

  • Acute Pain (Nociceptive):

    • Types:

    • Somatic Pain:

      • Experienced via A-delta fibers and characterized by sharp and well-localized pain.

    • Visceral Pain:

      • Described as poorly localized, often presenting as an aching, gnawing, throbbing, or intermittently cramping sensation.

      • Notable phenomena include referred pain, where pain in a visceral organ is perceived elsewhere in the body.

  • Chronic Pain:

    • Defined as lasting at least 3 to 6 months and often disproportionate to visible tissue injury.

    • Neuroimaging may reveal brain changes such as cognitive deficits and decreased coping abilities.

  • Neuropathic Pain:

    • Peripheral Neuropathic Pain:

      • Results from lesions in peripheral nerves.

    • Central Neuropathic Pain:

      • Caused by lesions or dysfunction in the brain or spinal cord, manifesting as burning, shock-like, or tingling sensations.

      • Characterized by enhanced sensitivity to both painful and nonpainful stimuli that can lead to hyperalgesia, allodynia, or spontaneous pain.

COMPARING ACUTE AND CHRONIC PAIN

TABLE 15-3

Comparison of Acute and Chronic Pain

  • Characteristics:

    • Experience:

    • Acute pain: An event with a known cause.

    • Chronic pain: A situational state with an often unknown cause.

    • Onset:

    • Acute: Usually sudden.

    • Chronic: May be sudden or develop insidiously.

    • Duration:

    • Acute: Short duration (up to 3 months); resolves with treatment and healing.

    • Chronic: Prolonged for months to years; persists beyond normal healing time.

    • Pain Identification:

    • Acute: Painful and nonpainful areas easily differentiated; visible signs more present, with emotional distress common.

    • Chronic: Areas less differentiated; changes in sensations difficult to evaluate; varied response patterns with fewer overt signs and potential for interference in sleep and quality of life.

    • Course:

    • Acute: Suffering usually decreases over time.

    • Chronic: Suffering often increases over time, leading to behaviors aimed at modifying the pain experience.

    • Prognosis:

    • Acute: Likelihood of complete relief.

    • Chronic: Complete relief often not possible.

COMMON CHRONIC PAIN SYNDROMES

  • Key Conditions Include:

    • Persistent Low Back Pain:

    • Most common chronic pain condition arising from poor muscle tone, inactivity, muscle strain, or sudden vigorous exercise.

    • Myofascial Pain Syndromes:

    • Pain due to muscle spasm, tenderness, and stiffness, including conditions such as myositis, fibrositis, and fibromyalgia.

    • Characterized by hypersensitive trigger points that produce pain in a specific area when stimulated.

    • Chronic Postoperative Pain:

    • Persistent pain occurring after surgery with risk factors including preexisting pain and genetic predisposition, often associated with peripheral and central sensitization.

    • Cancer Pain:

    • Resulting from disease progression or treatment, presenting significant challenges in management.

    • Complex Regional Pain Syndrome:

    • Severe burning pain often associated with significant changes in vasomotor function and muscle wasting after peripheral nerve injury.

    • Phantom Limb Pain:

    • Pain felt in amputated limbs, possibly related to hyperexcitability of peripheral nerves or alterations in brain processing.

CENTRAL NEUROPATHIC PAIN

  • Defined as pain stemming from lesions or dysfunction in the brain or spinal cord, leading to enhanced sensitivity in central pain-signaling neurons due to mechanisms called "wind-up."

  • Associated conditions include: brain or spinal cord trauma, tumors, vascular lesions, multiple sclerosis, Parkinson’s disease, postherpetic neuralgia, and phantom limb pain.

NOCIPLASTIC PAIN

  • Definition:

    • Described as pain emerging from altered nociception without clear evidence of actual or threatened tissue damage, not caused by peripheral nociceptor activation or lesions in the somatosensory system.

  • Commonly associated with:

    • Conditions such as irritable bowel syndrome, complex regional pain syndrome type I (without confirmed nerve injury), and fibromyalgia syndrome, which is the most prevalent.

FIBROMYALGIA SYNDROME

  • Characteristics:

    • chronic diffuse musculoskeletal pain, stiffness, and increased sensitivity to sensory input; etiology and pathophysiology remain poorly understood.

    • marked by no validated biomarkers or clear evidence of somatosensory disease.

  • Manifestations Include:

    • Diffuse, chronic pain often beginning in the neck/shoulder regions, spreading over time.

    • Tender points reflecting a hypersensitivity to touch.

    • Symptoms of fatigue and stiffness worsen upon awakening and during mid-afternoon.

    • Co-morbid symptoms include headaches, irritable bowel syndrome, and temperature sensitivity (e.g., Raynaud’s symptoms).

    • Additional somatic symptoms may also manifest, such as impaired cognition, mood alterations, and sleep disturbances.

ANALGESICS

CHAPTER 25

Objectives:

  • Recognize the organ affected by acetaminophen overdose and the corresponding antidote.

  • Identify the side effects and contraindications associated with opioid use.

  • Discuss adjuvant medications used for neuropathic pain relief.

GATE CONTROL THEORY

  • Proposed by Melzack & Wall (1965):

    • Emphasizes that pain has emotional and cognitive components beyond physical sensation.

    • Introduces the concept of gating mechanisms along the CNS that can regulate or obstruct pain impulses.

  • Mechanism:

    • Pain impulses can pass through a 'gate' which opens or closes based on various stimuli, informing non-pharmaceutical pain management methods alongside analgesic use.

PATHOASSOCIATION WITH MEDICATIONS

  • Neurohormones:

    • Endorphins act to suppress pain conduction.

  • Opioids:

    • Activate similar receptors as endorphins.

  • NSAIDs:

    • Control peripheral conduction by blocking cyclooxygenase (COX) enzymes, interfering with prostaglandin production.

  • Corticosteroids:

    • Block phospholipase, inhibiting prostaglandins and leukotrienes.

  • Anticonvulsants:

    • Used for neuropathic pain by inhibiting nerve transmission.

ACETAMINOPHEN

  • Trade Name: Tylenol.

  • Properties:

    • Functions as an analgesic and antipyretic but lacks anti-inflammatory properties.

  • Pharmacodynamics:

    • Inhibits prostaglandin synthesis solely in the CNS.

  • Pharmacokinetics:

    • Administered orally, well absorbed, and recommended every 4 hours.

    • Metabolized hepatically with renal excretion.

  • Adverse Effects:

    • Rare; however, overdose may lead to severe liver injury.

    • Notable drug interactions with alcohol and warfarin.

  • Pharmacotherapeutic Uses:

    • Indicated for pain and fever; preferred in children with suspected influenza or active chickenpox; also safer for individuals with peptic ulcer disease (PUD).

ACETAMINOPHEN TOXICITY

  • Therapeutic Serum Range:

    • 10-20 mcg/mL.

  • Symptoms of Toxicity:

    • Nausea/vomiting, diarrhea, sweating, and abdominal pain.

    • Severe adverse consequences may include hepatic necrosis, hepatic failure, coma, or death.

  • Treatment:

    • Acetylcysteine (Mucomyst, Acetadote) serves as an antidote for overdose and is most effective when administered within 8-10 hours post-ingestion.

NURSING IMPLICATIONS

  • Risk Factors for Toxicity:

    • Alcohol use, concurrent warfarin therapy.

  • Recommendations:

    • Do not exceed recommended dosages; manage toxicity promptly.

NSAID PATIENT EDUCATION

  • Administration Instructions:

    • Take with food, milk, or water.

    • Avoid crushing or chewing.

    • Discard any aspirin formulations that emit a vinegar-like odor.

    • Refrain from alcohol consumption while on NSAIDs.

    • Report severe or persistent gastric irritation to prescriber.

    • Be aware of salicylism symptoms (e.g., tinnitus, sweating, headache, dizziness) and inform prescriber.

    • Avoid aspirin in children; opt for acetaminophen instead (with a maximum dosage limit of 4 grams/day).

OPIOIDS

  • General Overview:

    • Utilized as opioid agonists for moderate to severe pain.

    • Governed by the Controlled Substances Act of 1970 and categorized into five schedules based on potential for abuse.

  • Addiction:

    • Physical and psychological dependence can develop with prolonged use, often more so than with short-term use.

OPIOID ANALGESIC ACTION

  • Characteristics:

    • Derived from natural opium, mimicking its effects.

    • Noteworthy opioids include morphine (derived from the sap of seed pods), codeine, meperidine (synthetic derivative).

    • Tolerance and dependence develop over longer durations of use, but not generally over short durations of use.

  • Mechanism of Action:

    • Opioids act primarily on CNS receptors (µ - mu, kappa - k, and occasionally delta - d), yielding various side effects determined by receptor type and location.

    • Consideration should be given to interactions with herbal supplements like kava, valerian, and St. John’s wort.

OPIOID ANALGESICS SIDE EFFECTS

  • Common Side Effects Include:

    • Pain relief

    • Respiratory depression

    • Euphoria

    • Sedation

    • Cough suppression

    • Antidiarrheal effects (codeine).

  • Specific Actions:

    • Morphine markedly reduces respiratory rate while codeine functions as an antitussive agent.

    • Dosage Considerations:

    • Morphine: commonly provided at 2-10 mg per 70 kg IV every 3-4 hours as needed for pain.

OPIOIDS ADVERSE EFFECTS

  • Adverse Effects Include:

    • Respiratory Depression:

    • Resulting from diminished sensitivity of the respiratory center to carbon dioxide.

    • Notably, opioid naïve individuals are at higher risk for overdose consequences, including death.

    • Maximum respiratory depression occurs variably with administration route (e.g., IV – within 15 minutes; IM – within 30 minutes).

    • Urinary Retention:

    • Caused by hypertonicity of bladder muscles; patients may require catheterization, with monitoring essential.

    • Orthostatic Hypotension and Pupillary Changes:

    • Indications of toxicity; require careful monitoring.

  • Dependence and Withdrawal Symptoms:

    • Withdrawal symptoms may manifest within 24-48 hours of last dose cessation, characterized by irritability, diaphoresis, restlessness, muscle twitching, tachycardia, and elevated blood pressure.

OPIOID CONTRAINDICATIONS

  • Key Considerations Include:

    • Patients with head injuries due to potential respiratory suppression.

    • Respiratory disorders (asthma) that may be exacerbated by opioid administration.

    • Shock or hypotensive states necessitating dosage adjustment.

    • Special considerations needed for older adults due to altered pharmacodynamics.

COMBINATION DRUGS

  • Examples:

    • Ibuprofen/hydrocodone, acetaminophen/codeine.

  • Combination therapies utilize smaller doses of each medication, thereby decreasing side effects and minimizing dependency.

PATIENT-CONTROLLED ANALGESIA (PCA)

  • Overview:

    • PCA allows for self-administration of analgesics, commonly through infusion pumps programmed with a loading dose followed by patient-activated dosing.

  • Safety Mechanisms:

    • Lockout safety feature prevents overdose by ensuring the patient cannot trigger doses before a predetermined interval.

    • PCA promotes therapeutic efficacy while minimizing wait times for analgesia and empowers patient control over pain management.

ADJUVANT THERAPY

  • Definition:

    • Refers to medications utilized in combination with non-opioid and opioid analgesics to enhance pain relief.

  • Common Classes Include:

    • Anticonvulsants (e.g., Gabapentin for neuropathic pain, migraine prevention), antidepressants (tricyclic antidepressants for peripheral neuropathy), corticosteroids (reduce nociceptive stimuli), and antidysrhythmics (block sodium channels to alleviate pain).

  • Adjuvant medications may allow for diminished dosages of opioids and NSAIDs, reducing potential adverse effects.

OPIOID ANTAGONISTS

  • Function:

    • Antagonists like naloxone are utilized to counteract the adverse effects of opioids, particularly respiratory depression due to overdose.

  • Characteristics:

    • Naloxone acts as a short-acting opioid antagonist administered via IV, IM, or subcutaneously; it is effective in doses of 0.4-2 mg every 2-3 minutes until patient response is noted.

  • Considerations:

    • Naltrexone is another long-acting opioid antagonist with potential life-threatening effects if opioids are resumed after treatment for dependence.

GASTROINTESTINAL DYSFUNCTION

NURS 309 PATHOPHYSIOLOGY

Instructor: S. Tullos, EdD, MNSC, RN

OBJECTIVES

  • List components of the GI tract and discuss influencing factors on each.

  • Review functions encompassing ingestion and breakdown of food, propulsion, secretion, digestion, absorption, and waste elimination.

  • Understand primary functions pertaining to gastric emptying and small intestine activity.

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

  • Explore medications used for vomiting control and categories for diarrhea treatment.

GASTROINTESTINAL TRACT FUNCTIONS

  • Core Functions Include:

    • Ingestion and breakdown of food, propulsion, secretion (mucus, water, enzymes), mechanical and chemical digestion, nutrient absorption, elimination of waste, and immune protection against microbes.

GASTROINTESTINAL TRACT STRUCTURE

  • Comprises:

    • Mouth: Responsible for chewing and secretion of saliva.

    • Throat: Facilitates swallowing.

    • Esophagus: Contains upper and lower esophageal sphincters.

    • Stomach: Divided into fundus, body, antrum, with pyloric sphincter.

    • Small Intestine: Divided into duodenum, jejunum, ileum (concludes with ileocecal valve).

    • Large Intestine: Comprising cecum, appendix, colon (ascending, transverse, descending, sigmoid), and rectum/anus.

GASTRIC MOTILITY

  • Upon swallowing, the fundus relaxes to allow passage of food.

  • Peristaltic Waves: Occur at approximately three per minute, regulated by hormones such as gastrin, motilin, and nervous systems.

  • Influences on gastric emptying rate include volume, osmotic pressure, and chemical composition of the gastric contents.

  • Gastric Secretions:

    • Include intrinsic factor (required for vitamin B12 absorption), gastric acid, pepsin, gastric lipase, and mucus for protection.

SMALL INTESTINE DIGESTION AND ABSORPTION

  • Key Enzymes and Mechanisms:

    • Pancreatic enzymes, intestinal brush-border enzymes, bile salts facilitate these processes.

  • Motility Mechanisms:

    • Includes segmentation and peristalsis.

LARGE INTESTINE FUNCTION

  • Comprising Structures:

    • Cecum, appendix, colon, rectum.

    • Gastrocolic reflex assists with fecal mass movement.

    • Defecation Reflex: Involves contraction and relaxation of circular muscles for waste elimination.

ACUTE & CHRONIC GI DISORDERS

  • Common Conditions:

    • Anorexia: Lack of desire to eat despite physiological hunger.

    • Nausea: Subjective experience often going hand in hand with various conditions.

    • Vomiting (Emesis): Forceful emptying of stomach contents, potentially influenced by multiple stimuli.

CONSTIPATION

  • Definition: Characterized by infrequent or difficult defecation.

  • Primary Factors Include:

    • Normal transit (functional), slow transit, and pelvic floor disorders.

  • Secondary Factors:

    • Various lifestyle and medical conditions including diet and medications contributing to symptoms.

    • Symptoms can progress to sensations of incomplete evacuation and involve fewer than three bowel movements weekly.

  • Management: Treat underlying causes and encourage dietary adjustments.

DIARRHEA

  • Defined by the presence of loose, watery stools that may be acute or persistent.

  • Types:

    • Large-Volume Diarrhea: Results from excessive water/secretion in intestines.

    • Small-Volume Diarrhea: Typically a result of excessive intestinal motility.

  • Mechanisms of Diarrhea:

    • Osmotic, secretory, and motility-related pathophysiological processes.

  • Systemic Effects: Resulting dehydration, electrolyte imbalances, and associated with malabsorption syndromes; management entails fluid restoration and targeted therapeutic interventions.

ABDOMINAL PAIN

  • Types of Pain:

    • Mechanical, inflammatory, or ischemic; usually signals tissue injury and inflammation.

  • Pain can be categorized as parietal (localized) or visceral (diffuse), and can also manifest as referred pain.

GASTROINTESTINAL BLEEDING

  • Classification:

    • Upper gastrointestinal bleeding involves the esophagus, stomach, duodenum.

    • Lower gastrointestinal bleeding involves the jejunum, ileum, colon, rectum.

    • Ocult bleeding presents different clinical responses based on blood loss amount and duration.

ACUTE, MASSIVE GI BLEEDING

  • Causes & Signs:

    • Upper GI bleeding can stem from esophageal varices, bleeding ulcers.

    • Lower GI bleeding can arise from intestinal polyps, inflammatory diseases, and cancers.

    • Physiologic Response:

    • Patient exhibits symptoms based on the extent of blood loss, affecting blood volume, peristalsis, digestion, and influencing neurological and cardiovascular outcomes.

MOTILITY DISORDERS

  • Dysphagia: Characterized by difficulty swallowing, associated with mechanical obstructions and functional disorders.

    • Achalasia: Specific condition related to the loss of inhibitory neurons in the myenteric plexus leading to symptom manifestations including pain, regurgitation, aspiration, and weight loss.

GASTROPARESIS

  • Defined as delayed gastric emptying without physical obstruction, linked with diabetic complications, surgical vagotomy, impacting patient quality of life.

  • Symptoms include nausea, vomiting, and abdominal discomfort.

MEDICATIONS FOR N/V CONTROL

  • Dopamine Antagonists:

    • Phenothiazines (e.g., prochlorperazine, promethazine) and Butyrophenones (e.g., haloperidol).

    • Mechanism of Action: Block H1 receptors and inhibit the chemoreceptor trigger zone (CTZ) to ameliorate nausea and vomiting.

    • Side Effects: Include CNS depression especially if used with other depressants.

SEROTONIN ANTAGONISTS

  • Drugs such as Ondansetron and Granisetron are effective for nausea/vomiting related to chemotherapy.

  • Mechanism of Action: Block 5-HT3 serotonin receptors in CTZ, minimizing adverse effects on extrapyramidal system as it does not block dopamine receptors.

GLUCOCORTICOIDS & CANNABINOIDS

  • Corticosteroids: Used to control N/V in cancer treatment (e.g., dexamethasone).

  • Cannabinoids (e.g., dronabinol): Effective when unresponsive to conventional therapies but contraindicated in patients with psychiatric conditions.

PROKINETIC AGENTS

  • Function: Increase GI tone and motility.

  • Indications Include:

    • Gastroesophageal reflux disease (GERD), chemotherapy-induced N/V, diabetic gastroparesis.

  • Example: Metoclopramide (Reglan) enhances acetylcholine actions to promote upper GI motility but must be monitored closely for extrapyramidal side effects.

OPIATES AND RELATED AGENTS (ANTIDIARRHEALS)

  • Mechanism of Action:

    • Decrease GI motility to ameliorate symptoms of diarrhea.

    • Notable agents include diphenoxylate/atropine and loperamide.

  • Side Effects: Constipation, potential for CNS depression, and caution advised in vulnerable populations (e.g., children, older adults) due to respiratory depression risks.

ADSORBENTS FOR DIARRHEA

  • Examples Include:

    • Kaolin, pectin, and bismuth subsalicylate (OTC); also, Rx colestipol/cholestyramine for excessive bile acids in the colon.

  • Side Effects: Can include dizziness, drowsiness, weakness, and headache.

OSMOTIC LAXATIVES

  • Administered for bowel preparation; side effects include potential fluid and electrolyte imbalances and gastrointestinal distress.

    • Key agents include glycerin, lactulose, magnesium hydroxide, magnesium oxide.

STIMULANT LAXATIVES

  • Utilized for bowel prep/testing; notable for potential side effects like abdominal cramping and changes in urine color.

  • Commonly abused, especially bisacodyl and senna.

BULK-FORMING LAXATIVES

  • Intended to soften stool, with administration instructions emphasizing immediate consumption.

    • Agents include psyllium, methylcellulose, polycarbophil.

CHLORIDE CHANNEL ACTIVATORS

  • Indications primarily for idiopathic constipation in adults, though contraindicated in patients with mechanical obstructions.

EMOLLIENTS (STOOL SOFTENERS)

  • Indications focused on constipation prevention and minimizing defecation strain post-MI; contend with potential for nausea and mild abdominal cramping.

REFERENCES

  • Huether & McCance 8th ed 2026

  • McCuistion 12th ed 2026