Analgesic Drugs Chapter 10 PDF

CHAPTER 10 Analgesic Drugs Important aspect of nursing care Pain one of the most common reasons for seeking health care PAIN MANAGEMENT Pain can lead to: Suffering Economic burden 2 Opioid analgesics Adjuvant analgesic drugs Medications that relieve pain without causing loss of consciousness “Painki...

CHAPTER 10 Analgesic Drugs Important aspect of nursing care Pain one of the most common reasons for seeking health care PAIN MANAGEMENT Pain can lead to: Suffering Economic burden 2 Opioid analgesics Adjuvant analgesic drugs Medications that relieve pain without causing loss of consciousness “Painkillers” ANALGESICS 3 PAIN An unpleasant sensory and emotional experience associated with actual or potential tissue damage A personal and individual experience Whatever the patient says it is Exists when the patient says it exists Pain involves: Physical factors Psychologic factors Cultural factors 4 NOCICEPTION The sensation of pain o Pain results from stimulation of sensory nerve fibers called nociceptors. o Transmission of pain signals  Mu receptors-dorsal horn of the spinal cord  Kappa and delta receptors. Pain receptors  central nervous system (CNS) and various body tissues. 5 6 Level of stimulus needed to produce the perception of pain PAIN THRESHOLD A measure of the physiologic response of the nervous systemsimilar for most 7 The amount of pain a person can endure without it interfering with normal function Varies from person to person: age, gender, culture, previous pain experience, and anxiety level. PAIN TOLERANCE Varies by attitude, environment, culture, ethnicity 8 CLASSIFICATION OF PAIN BY ONSET AND DURATION Acute pain Sudden onset Usually subsides once treated Chronic pain Persistent or recurring Lasts 3 to 6 months Often difficult to treat Tolerance Physical dependence 9 CLASSIFICATION OF PAIN Somatic Visceral Superficial Deep Vascular Referred Neuropathic Phantom Cancer Central 1 0 TREATMENT OF PAIN IN SPECIAL SITUATIONS PCA and “PCA by proxy” Patient comfort vs. fear of drug addiction Opioid tolerance Recognizing patients who are opioid tolerant Breakthrough pain Synergistic effect 11 Assist primary drugs in relieving pain NSAIDs Antidepressants Anticonvulsants Corticosteroids Example: adjuvant drugs for neuropathic pain Amitriptyline (antidepressant) Gabapentin or pregabalin (anticonvulsants) 12 WORLD HEALTH ORGANIZATION THREE-STEP ANALGESIC LADDER Step 1 nonopioids (with or without adjuvant medications) after the pain has been identified and assessed. If pain persists or increases, treatment moves to Step 2 opioids with or without nonopioids and with or without adjuvants. If pain persists or increases, management then rises to Step 3 opioids indicated for moderate to severe pain, administered with or without nonopioids or adjuvant medications. 13 OPIOID DRUGS Synthetic drugs that bind to the opiate receptors to relieve pain Mild agonists: codeine, hydrocodone Strong agonists: morphine, hydromorphone, oxycodone, meperidine, fentanyl, and methadone OPIOID CEILING EFFECT Drug reaches a maximum analgesic effect. Analgesia does not improve, even with higher doses. Pentazocine Nalbuphine COMPARISON MECHANISM OF ACTION Antagonists  Reverse the effects of these drugs on pain receptors  Bind to a pain receptor and exert no response Agonist  Bind to an opioid pain receptor in the brain  Cause an analgesic response (reduction of pain sensation) Agonist-Antagonist  Bind to a pain receptor  Cause a weaker neurologic response than a full agonist  Also called partial agonist 16 EQUIANALGESIA Ability to provide equivalent pain relief by calculating dosages of different drugs or routes of administration that provide comparable analgesia Hydromorphone (Dilaudid): seven times more potent than morphine Example: if morphine 10 mg was given to a patient followed 1 hour later by hydromorphone 1 mg, then the patient would have received an equivalent of 17 mg of morphine. 17 18 OPIOID ANALGESICS: INDICATIONS Main use: to alleviate moderate to severe pain Often given with adjuvant analgesic drugs to assist primary drugs with pain relief Opioids are also used for: Cough center suppression Treatment of diarrhea Balanced anesthesia 20 OPIOID ANALGESICS: CONTRAINDICATIONS Known drug allergy Severe asthma Use with extreme caution in patients with: Respiratory insufficiency Elevated intracranial pressure Morbid obesity or sleep apnea Paralytic ileus Pregnancy 20 OPIOID ANALGESICS: ADVERSE EFFECTS CNS depression Leads to respiratory depression Nausea and vomiting Urinary retention Diaphoresis and flushing Pupil constriction (miosis) Constipation Itching 21 OPIOIDS Psychologic Dependence  A pattern of compulsive drug use characterized by a continued craving for an opioid and the need to use the opioid for effects other than pain relief Physical Dependence  Physiologic adaptation of the body to the presence of an opioid  Opioid tolerance and physical dependence are expected with long-term opioid treatment and should not be confused with psychologic dependence (addiction). Opioid Tolerance  A common physiologic result of chronic opioid treatment  Result: larger dose is required to maintain the same level of analgesia 22 OPIOID ANALGESICS TOXICITY AND MANAGEMENT OF OVERDOSE  Naloxone (Narcan)  Naltrexone (ReVia) Regardless of withdrawal symptoms, when a patient experiences severe respiratory depression, an opioid antagonist should be given. Pure opioid antagonist Indicated in cases of suspected acute opioid overdose Failure of reversal available without a prescription and is being used by 1st responders 23 OPIOID ANALGESICS: TOXICITY AND MANAGEMENT OF OVERDOSE (CONT.) Opioid withdrawal or opioid abstinence syndrome Manifested as: Anxiety, irritability, chills and hot flashes, joint pain, lacrimation, rhinorrhea, diaphoresis, nausea, vomiting, abdominal cramps, diarrhea, confusion 24 OPIOID ANALGESICS: INTERACTIONS Alcohol Antihistamines Barbiturates Benzodiazepines 25 CODEINE SULFATE Opioid agonist Natural opiate alkaloid (Schedule II) obtained from opium Less effective Ceiling effect Often combined with acetaminophen Schedule III More commonly used as an antitussive drug Most common adverse effect: GI disturbance 26 Synthetic opioid (Schedule II) used to treat moderate to severe pain Parenteral injections, transdermal patches (Duragesic), buccal lozenges (Fentora), and buccal lozenges on a stick (Actiq) FENTANYL Fentanyl patch for chronic, long-term pain management 27 Hydromorphone: very potent opioid analgesic; Schedule II drug 1 milligram of IV or IM hydromorphone is equivalent to 7 mg of morphine HYDROMORPHONE (DILAUDID) 28 Naturally occurring alkaloid derived from the opium poppy Drug prototype for all opioid drugs; Schedule II controlled substance Indication: severe pain High abuse potential MORPHINE SULFATE Oral, injectable, and rectal dosage forms; also extended-release forms 29 NONOPIOID ANALGESICS: ACETAMINOPHEN (TYLENOL) Analgesic and antipyretic effects Little to no antiinflammatory effects Available over-the-counter (OTC) and in combination products with opioids 30 ACETAMINOPHEN: MECHANISM OF ACTION/INDICATIONS MOA  Similar to salicylates  Blocks pain impulses peripherally by inhibiting prostaglandin synthesis Indications  Mild to moderate pain  Fever  Alternative for those who cannot take aspirin products 31 ACETAMINOPHEN: DOSAGE Maximum daily dose for healthy adults is being lowered to 3000 mg/day.  2000 mg for older adults and those with liver disease Inadvertent excessive doses may occur when different combination drug products are taken together. Be aware of the acetaminophen content of all medications taken by the patient (OTC and prescription). 32 ACETAMINOPHEN: CONTRAINDICATIONS AND INTERACTIONS Should not be taken in the presence of:  Drug allergy  Liver dysfunction  Possible liver failure Dangerous interactions may occur if taken with alcohol or other drugs that are hepatotoxic. 33 ACETAMINOPHEN: TOXICITY AND MANAGING OVERDOSE Overdose, whether intentional or resulting from chronic unintentional misuse, causes hepatic necrosis: hepatotoxicity Long-term ingestion of large doses also causes nephropathy. Recommended antidote: acetylcysteine regimen 34 LIDOCAINE, TRANSDERMAL Topical anesthetic Indications: postherpetic neuralgia Left in place no longer than 12 hours Minimal adverse effects Skin irritation may occur 35 ANALGESICS: NURSING PROCESS: ASSESSMENT Perform Thorough history regarding allergies and use of other medications, including alcohol, health history, and medical history. Obtain Baseline vital signs and I&O. Assess Potential contraindications and drug interactions. 36 ANALGESICS: NURSING PROCESS: ASSESSMENT (CONT.) Perform a thorough pain assessment, including pain intensity and character, onset, location, description, precipitating and relieving factors, type, remedies, and other pain treatments.  Pain is now considered a “fifth vital sign.”  Rate pain on a 0 to 10 or similar scale  Use appropriate scale for age, cognition 37 38 ANALGESICS: NURSING IMPLICATIONS Medicate patients before the pain becomes severe Take with food to minimize gastric upset. Pain management includes pharmacologic and nonpharmacologic approaches Check dosages carefully. Instruct patients to follow directions for administration carefully and to keep a journal Instruct patients about signs of allergic reaction or adverse effects. Constipation is common Patients should be instructed to change positions slowly to prevent possible orthostatic hypotension. OPIOID ANALGESICS: NURSING IMPLICATIONS (CONT.) Monitor for therapeutic effects  Decreased complaints of pain  Decreased severity of pain  Increased periods of comfort  Improved activities of daily living, appetite, and sense of well-being  Decreased fever (acetaminophen) 42 CHAPTER 44 Antiinflammatory and Antigout Drugs INFLAMMATION Localized protective response stimulated by injury to tissues, which serves to destroy, dilute, or wall off (sequester) both the injurious agent and the injured tissue  Pain, fever, loss of function, redness, and swelling  Endogenous compounds, including proteins of the complement system, histamine, serotonin, bradykinin, leukotrienes, and prostaglandins NSAIDS NSAIDs are also used for the relief of:  Mild to moderate headaches  Myalgia  Neuralgia  Arthralgia  The pain associated with arthritic disorders, such as rheumatoid arthritis (RA), juvenile arthritis, ankylosing spondylitis, and osteoarthritis (OA)  Treatment of gout and hyperuricemia 45 NSAIDS (CONT.) Large and chemically diverse group of drugs with the following properties:  Antipyretic  Analgesic  Antiinflammatory Salicylates  Aspirin-antiplatelet NSAIDS Acetic acid derivatives Diclofenac sodium (Voltaren) Ketorolac (Toradol) Cyclooxygenase-2 Celecoxib (Celebrex) (COX-2) inhibitors Enolic acid derivatives Propionic acid derivatives Nabumetone (Relafen) Meloxicam (Mobic) Ibuprofen (Motrin, Advil, others) Naproxen (Naprosyn, Aleve) 47 NSAIDS: MECHANISM OF ACTION Inhibition of the leukotriene pathway, the prostaglandin pathway, or both Blocking the chemical activity of the enzyme COX COX-1 maintains the gastrointestinal (GI) mucosa COX-2 promotes the synthesis of prostaglandins that are involved in inflammatory processes. NSAIDS: CONTRAINDICATIONS Known drug allergy Patients with documented aspirin allergy must not receive NSAIDs. Conditions that place the patient at risk for bleeding: Vitamin K deficiency Peptic ulcer disease pregnancy category C NSAIDS: ADVERSE EFFECTS GI: heartburn to severe GI bleeding Acute renal failure Hepatotoxicity Increased risk of MI and stroke Skin eruption, sensitivity reaction Altered hemostasis Tinnitus, hearing loss NSAIDS AND RENAL FUNCTION Renal function depends partly on prostaglandins. Disruption of prostaglandin function by NSAIDs is sometimes strong enough to precipitate acute or chronic renal failure. Use of NSAIDs can compromise existing renal function. Renal toxicity can occur in patients with dehydration, heart failure, liver dysfunction, or use of diuretics or angiotensinconverting enzyme (ACE) inhibitors. NSAIDS: INTERACTIONS Serious interactions can occur when given with  Anticoagulants  Aspirin  Corticosteroids and other ulcerogenic drugs  Protein bound drugs NSAIDS: BLACK BOX WARNING All NSAIDs (except aspirin) share a black box warning regarding an increased risk of adverse cardiovascular thrombotic events, including fatal MI and stroke. NSAIDs may counteract the cardioprotective effects of aspirin. SALICYLATES Salicylic acid (aspirin) Aspirin  Antipyretic Analgesic Anti-inflammatory + Antithrombotic effect: used in the treatment of MI and other thromboembolic disorders Irreversible inhibitor of COX-1 receptors within the platelets themselves Reduced formation of thromboxane A2, a substance that normally promotes platelet aggregation Inhibits platelet aggregation Examples: aspirin, salsalate (Salsitab); Topical cream (Aspercreme), rectal suppositories; Combination products: aspirin– acetaminophen–caffeine combinations such as Excedrin; Enteric-coated aspirin (Ecotrin) 53 Shown to reduce cardiac death after MI Should be administered at the first sign of MI ASPIRIN Daily tablet (81 mg or 325 mg): prophylactic therapy for adults who have strong risk factors for developing coronary artery disease or cardiovascular accident  Indications  Headache, neuralgia, myalgia, and arthralgia Pain syndromes: arthritis Antipyretic action 54 ASPIRIN: REYE’S SYNDROME Acute and potentially lifethreatening condition involving progressive neurologic deficits that can lead to coma and may also involve liver damage Triggered by viral illnesses such as influenza as well as by salicylate therapy itself in the presence of a viral illness Survivors of this condition may or may not have permanent neurologic damage. ACETIC ACID DERIVATIVES Ketorolac (Toradol)  Some antiinflammatory activity  Used primarily for its powerful analgesic effects which are comparable to those of narcotic drugs such as morphine  Indication: short-term use (up to 5 days) to manage moderate to severe acute pain  Adverse effects: renal impairment, edema, GI pain, dyspepsia, and nausea PROPIONIC ACID DERIVATIVES Ibuprofen (Motrin, Advil) Most commonly used NSAID Uses: analgesic effects in the management of RA, OA, primary dysmenorrhea, gout, dental pain, musculoskeletal disorders, antipyretic actions Naproxen Second most commonly used NSAID Somewhat better adverse effect profile than ibuprofen Fewer drug interactions with ACE inhibitors given for hypertension GOUT Gout: condition that results from inappropriate uric acid metabolism  Underexcretion of uric acid  Overproduction of uric acid Uric acid crystals are deposited in tissues and joints, resulting in pain Hyperuricemia Allopurinol (Zyloprim) ANTIGOUT DRUGS Colchicine (Colcrys) Probenecid (Benemid) 63 ANTIGOUT DRUGS: INDICATIONS Allopurinol (Zyloprim) Used to prevent uric acid production and to prevent acute tumor lysis syndrome Exfoliative dermatitis, Stevens-Johnson syndrome, and toxic epidermal necrolysis Probenecid (Benemid) Inhibits the reabsorption of uric acid in the kidneys and thus increases the excretion of uric acid Must have good renal function Colchicine Reduces inflammatory response to the deposits of urate crystals in joint tissue Used for short-term management or prevention of gout May cause short-term leukopenia and bleeding into the GI or urinary tracts NSAIDS: NURSING IMPLICATIONS Assess for conditions that may be contraindications GI lesions or peptic ulcer disease Bleeding disorders Do not give salicylates to children and teenagers because of the risk of Reye’s syndrome Perform laboratory studies as indicated (cardiac, renal, and liver function studies; complete blood count; platelet count). Educate patients to notify prescribers if bleeding or GI pain occurs. assess for potential drug interactions. Enteric-coated tablets should not be crushed or chewed. Monitor for therapeutic effects Decrease in swelling, pain, stiffness, and tenderness of a joint or muscle area 65 CHAPTER 47 Biologic Response– Modifying and Antirheumatic Drugs BIOLOGIC RESPONSE–MODIFYING DRUGS Alter the body’s response to diseases such as cancer and autoimmune, inflammatory, and infectious diseases.  Hematopoietic drugs  Immunomodulating drugs  Interferons (IFNs)  Monoclonal antibodies (MABs)  Interleukin (IL) receptor agonists and antagonists  Disease-modifying antirheumatic drugs (DMARDs) 63 IMMUNOMODULATING DRUGS Therapeutically alter a patient’s immune response.  Alter a patient’s immune response to malignant tumor cells  Modify the body’s own immune response so that it can destroy various viruses and cancerous cells  Stimulate a patient’s hematopoietic (blood-forming) function and prevent disease. Fourth part of cancer therapy, in addition to:  Surgery  Chemotherapy  Radiation Also used for other diseases  Autoimmune  Inflammatory  Infectious 64 Enhancement or restoration of the host’s immune system defenses against the tumor. Direct toxic effect on the tumor cells, which causes them to lyse, or rupture Adverse modification of the tumor’s biology, which makes it harder for the tumor cells to survive and reproduce BIOLOGIC RESPONSE– MODIFYING DRUGS: MECHANISMS OF ACTION 69 70 THE IMMUNE SYSTEM Two components of the immune system work together to recognize and destroy foreign particles and cells in the blood or other body tissues. Humoral immunity Mediated by B-cell functions (antibodies) Cell-mediated immunity Mediated by T-cell functions THE IMMUNE SYSTEM (CONT.) Tumors Genetic Mutation Tumor antigens (chemical or tumor “markers”) label tumor cells as abnormal cells. Antibodies attack tumor cells.  B-lymphocytes (B cells) from the humoral immune system  T-lymphocytes (T cells) from the cell-mediated immune system 71 HUMORAL IMMUNE SYSTEM 72Antibodies also known as immunoglobulins (Ig) bind to specific antigens, forming an antigen-antibody complex that inactivates disease-causing antigens. Five major types of naturally occurring immunoglobulins  A, D, E, G, and M  B lymphocytes differentiate into memory cells.  exact characteristics of a particular foreign invader or antigen, stronger and faster immune response in the event of reexposure 73 CELL-MEDIATED IMMUNE SYSTEM T-lymphocytes (T cells)  Originate from bone marrow but mature in the thymus gland Three types with different functions  Cytotoxic T cells  T-helper cells  T-suppressor cells Cytotoxic T cells directly kill their targets by causing cell lysis or rupture. 74 CELLMEDIATED IMMUNE SYSTEM (CONT.) T-helper cells direct the actions of many other components of the immune system. T-suppressor cells serve to limit or control the immune response. A healthy immune system has about twice as many T-helper cells as T-suppressor cells at any one time. Overactive T-suppressor cells may be responsible for clinically significant cancer cases by permitting tumor growth beyond immune system control. THERAPEUTIC EFFECTS OF BIOLOGIC RESPONSE– 75 MODIFYING DRUGS Enhancement of hematopoietic function Regulation or enhancement of the immune response, including cytotoxic or cytostatic activity against cancer cells Inhibition of metastases, prevention of cell division, or inhibition of cell maturation HEMATOPOIETIC DRUGS 76 Promote the synthesis of various types of major blood components by promoting the growth, or differentiation, and function of proginitor cells in the bone marrow. Produced  recombinant DNA technology HDs are used to:  Decrease the duration of chemotherapyinduced anemia, neutropenia, and thrombocytopenia  Enable higher doses of chemotherapy to be given HEMATOPOIETIC DRUGS (CONT.) Erythropoietic drugs Epoetin alfa Darbepoetin alfa Colonystimulating factors (CSFs) Filgrastim Pegfilgrastim Sargramostim Plateletpromoting drugs Oprelvekin Romiplostim 73 HEMATOPOIETIC DRUGS (CONT.) Filgrastim (Neupogen) Granulocyte colony-stimulating factor (G-CSF) Stimulates precursor cells for the type of white blood cells known as granulocytes (including basophils, eosinophils, and neutrophils) Administered before patient develops infection Pegfilgrastim (Neulasta) Longer acting form of filgrastim Usually discontinued when the ANC rises above 10,000 mm3 74 HEMATOPOIETIC DRUGS: M 79ECHANISM OF ACTION Decrease Allow duration of chemotherapy-induced anemia, neutropenia, and thrombocytopenia higher dosages of chemotherapy Decrease bone marrow recovery time after bone marrow transplantation or irradiation Stimulate other cells in the immune system to destroy or inhibit the growth of cancer cells, as well as virus- or fungus-infected cells destruction of bone marrow cells as a result of cytotoxic chemotherapy Decrease the duration of low neutrophil counts, thus reducing the incidence and duration of infections HEMATOPOIETIC DRUGS: INDICATIONS Enhance the functioning of mature cells of the immune system, resulting in greater ability to kill cancer cells as well as viraland fungal-infected cells Also enhance red blood cell and platelet counts in patients with bone marrow suppression resulting from chemotherapy Allow for higher doses of chemotherapy, resulting in the destruction of a greater number of cancer cells 76 Fever Usually mild HEMATOPOIETIC DRUGS: ADVERSE EFFECTS Most common include: Muscle aches Bone pain Flushing 77 82 MONOCLONAL ANTIBODIES Treatment of cancer, rheumatoid arthritis (RA), MS, and organ transplantation Specifically target cancer cells and have minimal effect on healthy cells Fewer adverse effects than traditional antineoplastic medications Adalimumab MONOCLONAL ANTIBODIES (CONT.) Alemtuzumab Bevacizumab Cetuximab Rituximab 79 ADALIMUMAB MOA  Specificity for human TNF.  Naturally occurring cytokine involved in normal inflammatory and immune responses. Preventing TNF molecules from binding to TNF cell surface receptors, adalimumab also modulates the inflammatory biologic responses induced or regulated by TNF.  Indications  RA, Crohn’s disease, ulcerative colitis, plaque psoriasis, and psoriatic arthritis.  Contraindicated  active infectious process, whether localized or systemic, acute or chronic. 80 MONOCLONAL ANTIBODIES Contraindications Very few Adverse effects: Flulike symptoms Vary--see specific drugs 81 Autoimmune disorder causing inflammation and tissue damage in joints Diagnosis primarily symptomatic RHEUMATOID ARTHRITIS Treatment consists of nonsteroidal antiinflammatory drugs (NSAIDs) and DMARDs. 82 87 DISEASE-MODIFYING ANTIRHEUMATIC DRUGS Modify the disease of RA Exhibit antiinflammatory, antiarthritic, and immunomodulating effects Inhibit the movement of various cells into an inflamed, damaged area, such as a joint Slow onset of action of several weeks versus minutes to hours for NSAIDs Also referred to as slow-acting antirheumatic drugs 88 NONBIOLOGIC DISEASE-MODIFYING ANTIRHEUMATIC DRUGS Methotrexate Leflunomide Hydroxychloroquine Sulfasalazine BIOLOGIC DISEASE-MODIFYING ANTIRHEUMATIC DRUGS Adalimumab Golimumab Tofacitinib Infliximab Anakinra Abatacept Certolizumab Rituximab Etanercept Tocilizumab 89 90 DISEASE-MODIFYING ANTIRHEUMATIC DRUGS Abatacept (Orencia) Used to treat RA Caution if the patient has a history of recurrent infections or chronic obstructive pulmonary disease Patients must be up to date on immunizations before starting therapy. May increase risk of infections associated with live vaccines May decrease response to vaccines 91 DISEASE-MODIFYING ANTIRHEUMATIC DRUGS (CONT.) Methotrexate Anticancer drug commonly used to treat RA in much lower doses Weekly dosing (oral or by injection) Adverse effects: bone marrow suppression Once a week medication Advise to take folic acid supplement to lessen likelihood of adverse effects Takes 3 to 6 weeks for onset of antirheumatic action NURSING IMPLICATIONS 92 Assess allergies, specifically allergies to egg proteins, IgG, or neomycin. Assess conditions that may be contraindications. Assess baseline blood counts; perform cardiac, renal, and liver studies. Assess & Teach Follow for presence of infection. Sore throat, Diarrhea, and /or Vomiting Fever of 100.5°F (38.1°C) or higher specific guidelines for preparation and administration of drugs. Monitor for therapeutic responses: Decrease in growth of lesion or mass Improved blood counts Absence of infection, anemia, and hemorrhage Monitor for adverse effects. 93 NURSING IMPLICATIONS (CONT.)