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Analgesics

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Medications that relieve pain without causing loss of consciousness -'painkillers' -opioid analgesics -adjuvant analgesic drugs

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Pain

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An unpleasant sensory and emotional experience associated with actual or potential tissue damage (personal/individual, subjective pt to pt)

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nociceptors

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sensory nerve fibers that when stimulated result in pain (transmit pain signals from various body regions to the spinal cord and brain)

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noxious stimous

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pain stimulus -Travels through dorsal form of the spinal column: two main fibers: A-fibers and C-fibers receptors for opiates: Kappa, Delta, Mu This stimulus activates the inflammatory cascade and coagulation cascade

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Main Chemicals of the Inflammatory Cascade

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Histamine, prostaglandin**, bradykinin and leukotrianase -prostaglandin: leads to vasodilation(attracts WBC in order to protect area that is injured) -histamine: leading to local vasodilation -->stacking of platelets causes the coagulation cascade to begin

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Pain Threshold

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Level of stimulus needed to produce the perception of pain

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Pain Tolerance

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The amount of pain a person can endure without it interfering with normal function -varies from person to person, subjective response to pain (not physiologic funct), varies by attitude, environment, culture and ethnicity

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Chronic vs. Acute Pain

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Acute: Sudden onset, usually subsides after treatment , 3-6 months, often difficult to treat

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Somatic Pain

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Normally a pain that is localized; most of the time described as "sharp" pain or knife like; non radiating (need opiates or sometimes anti-inflammatory)

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Visceral Pain

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Pain that is poorly localized that feels deep and may be radiating; most of the time described as "dull" aching nagging pain; most of the time related to an infected organ

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Superficial Pain

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Pain linked to the somatic

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Deep Pain

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Pain that is linked to visceral

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Vascular Pain

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Pain type (ex when walking only feel not when moving) related to vascular condition, when blood flows- don't need to know this one well Referred pain: pain that is not localized to actual problem (ex- spleen problem causes shoulder pain)

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Neuropathic Pain

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A pain maybe from diabetes or shingles - described as burning, electric and hypersensativity, secondary to nerves being inflammed

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Phantom Pain

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A pain that the brain modulators still exist even if limb is not longer there- pain or problem is not actually there

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Cancer Pain

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A pain that can be acute or chronic depending on cancer (difficult to treat- sometimes develop opiate tolerance)

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Gate Theory of Pain Transmission

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A theory of pain that uses the analogy of a gate to describe how impulses from damaged tissues are sensed in the brain. Many current pain management strategies are aimed at altering this system If 'gate' is closed no pain stimulus can come though Gate can be closed by other means... something else is 'occupying that nerve' or pathway to stop it Or if experience new pain- smash foot and back pain not felt)

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Pain Transmission: Tissue Injury Causes the Release of

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-bradykinin -histamine -potassium -prostaglandins -serotonin these substances stimulate nerve endings and start the pain process

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PCA- pain control

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Patient controlled analgesia Proxy PCA- someone else is pushing the button for pain relieve NOT the patient- research shows that when family does this the person can die sooner, or possible lead to opiate overdose (fine line better comfortable and toxic levels) PCA's should always be locked

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NSAIDS

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N: non S: steroidal AI: anti-inflammatory D: Drugs *anti inflammatory properties, analgesic properties, antipyretic properties, asprin-platelet inhibition Used for: mild headaches, myalgia, neuralgia, arthralgia, postoperative pain, arthritic disorders, ankylosing spondylitis and osteoarthritis, treatment of gout and hyperuricemia

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Contraindications of NSAIDS

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Ulcer- NSAIDS contraindicated Platelet drugs: NSAIDS contraidicated Nephrotoxicity and Renal Issues from NSAIDS: this is due to **if decreases prostaglandin any med then that med should not be given to someone with renal issues

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How do NSAIDS work?

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-->works by decreasing prostaglandin COX-1 and COX-2 COX-1: has to do with prostaglandin(esp. at level of GI and renal), platelet aggregation, COX-2: has to do with prostaglandin peripherally (at the site of the injury but in theory should not effect GI etc) * You want prostaglandin activated in the kidney/..... Reread this concept in the book (don't understand what teacher said) NSAIDS can be selective or non-selective **typical example: Aleve or Motrin ect: block COX-1 and COX-2 (THEY ARE NOT SELECTIVE) inflammatory reduction and pain reduction BUT they affect GI and renal area- pt at risk for GI bleeding b/c it blocks COX-1 and COX-2 (prostaglandin involved in protective lining of the stomach), take with antacid or food Ulcer- NSAIDS contraindicated Platelet drugs: NSAIDS contraidicated Nephrotoxicity and Renal Issues from NSAIDS: this is due to **if decreases prostaglandin any med then that med should not be given to someone with renal issues A&F Afferent (takes blood to nephron)and efferent (takes blood away nephron) this must be balanced in amt and pressure to keep up a healthy GFR Increasing blood flow dilates afferent- constrict efferentbrings blood into and opposite takes blood away (THIS IS NORMAL) This mechanism above is controlled by prostaglandin Efferent constrictin is controlled by angiotension II

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Adjuvant Drugs

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NSAIDs- anti-inflammatory properties Antidepressants- effect levels of seratonin Anticonvulsants- reduce action potential Corticoalsteroids* the most potient anti-inflammatory meds with have (they reduce prostaglandin, reduce vasodilation and chem mediators of inflammation)

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Opioid drugs

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Synthetic drugs that bind to opiate receptors to relieve pain (very strong pain relievers)-agonists *always assess bowl sounds before any opiate

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Opioid Analgesics: Three Classifications

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-agonist -partial agonist -antagonist

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Opioid Agonists

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Bind to an opioid pain receptor in the brain and cause an analgesic response (reduction of pain sensation) ex: morphine, hydromorphone, meperidine, fentanyl, codeine

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Opioid Agonist and ANtagonists

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Bind to pain receptor -cause a weaker neurologic reponse than a full agonist Also called partial agonists or mixed agonist

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Opioiod Antagonist

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Reverse the effects of these drugs on pain receptors -bind to a pain receptor and exert no response Also known as competitive antagonists Ex: main antagonist NARCAN -->pain will return after administered

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Opioid receptors and their characterisitics

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MU----morphine-------supraspinal analgesia, respiratory depression, euphoria, sedations(moderate) KAPPA----ketocyclazoncine----spinal analgesia, sedation, miosis DELTA-----Enkephalins-------Analgesia

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Opiod Analgesics: Indications

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Main use: to alleviate moderate to severe pain -often given with adjuvant analgesic durgs to assist primary drugs with pain relief *other uses: cough center suppression, treatment of diarrhea, balanced anesthesia

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Opioid Analgesics Adverse Effects

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CNS- depression respiratory depression, nausea, vomiting, urinary retention, diaphoresis/flushing, pupil constriction (miosis), constipation, itching (sendary release of histamine not allergic rxn)

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Opiod Tolerance

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A common physiologic reslut of chronic opiod treatment Result: larger dose is required to maintain the same level of analgesia

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Opioids: Physical Dependence

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Physiologic adaption of the body to the presences of an opioid --opiodi tolerance and physical dependence are expected with long-term opiod treatment and should not be confused with psychologic dependence (addiction) *a nurse must still treat pain even if they have an addiction (addiction withdrawl is a genuine pain)

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Opioid Analgesics: Toxicity and Management of Overdose**

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Regardless of withdrawl symptoms, when a patient experiences severe respiratory depression, an opiod antagonist should be given Ex- naloxone (narcan) and naltrexone(ReVia)j Withdrawl symptoms: anxiety, irritability, chills/hot flashes, joint pain, lacrimation, rhinorrhea, diaphoresis, nausea, vomiting, abdominal cramps, diarrhea, and confusion

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Opiod Analgesics: Interactions

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Alcohol, antihistamines, barbiturates, benzodiazepines, monoamine oxidase inhibitors *these meds will potentuate or increase the effects of opiates

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Nonopioid Analgesics

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-->fever, mild pain, alternative for thosee that cannot take aspirin non-opiate analgesic medication also an antipyretic (means it lowers your fever) -->decrease prostaglandin centrally which is why it helps with pain; little to no anti-inflammatory effect -Good for mild to moderate pain (over the counter med) -Can be given orally, rectally or IV -Highly hepatotoxic- this means liver toxicity (look for pt with hepatitis, cirrhosis or alcholism- do not use in these patients) *daily recc dose adults 3g or 3,000mg/day (above this may lead to hepatoxicity) Good medication for fever or patients that cannont take asprin (pediatric cannot to asprin due to raye's syndrome OR if they are on cumadin (acetaminophen-tylenol)

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Acetaminopen: Contraindications

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Do NOT take with: drug allergy, liver dysfunction, possible liver failure, G6PD deficiency Dangerous interactions may occur if taken with alcohol or other drugs that are hepatotoxic G6PD deficiency: glucose6proteindehydrogenase?- problem where RBC do not have mitocondria -RBC usually use G6PD protein bar(energy source) but pt with this disease lack this (strained by lack of source of energy) If a pt has this disease they should not be on tylenol This cause lysis of RBC

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Acetaminophen: Toxicity and Overdose

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-over the counter but if overdose =lethal -overdose whether intentional or resultling from chronic unintentional misuse, causes hepatic necrosis: hepatotoxicity ANTIDOTE: acetylcysteine(mucomyst)

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Salicylates

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NSAIDS Salicyclic acid (asprin) Inhibits platelet aggregation- >risk of bleeding Antithrombotic effect: used in the treatment of MI and other thromboembolic disorders

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NSAID: Salicylate Toxicity

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Cardiovascular: Increased heart rate Central nervous: Tinnitus, hearing loss, dimness of vision, headache, dizziness, mental confusion, lassitude, drowsiness Gastrointestinal: Nausea, vomiting, diarrhea Metabolic: Metabolic acidosis, Sweating, thirst, hyperventilation, hypoglycemia, or hyperglycemia

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COX-2 Inhibitor

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NSAIDS celecoxib (Celebrex) First and only remaining COX-2 inhibitor Indicated for osteoarthritis, rheumatoid arthritis, acute pain symptoms, ankylosing spondylitis, and primary dysmenorrhea Adverse effects include headache, sinus irritation, diarrhea, fatigue, dizziness, lower extremity edema, and hypertension Little effect on platelet function Celecoxib is not to be used in patients with known sulfa allergy Does not affect GI mucosa when compared to non selective NSAIDs.

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Propionic Acid Derivatives NSAIDS

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fenoprofen (Nalfon) flurbiprofen (Ansaid) ibuprofen (Motrin, Advil) ketoprofen (Orudis KT) naproxen (Naprosyn, Aleve) oxaprozin (Daypro) Used to treat Used for their analgesic effects in treating rheumatoid arthritis, osteoarthritis, primary dysmenorrhea, gout, dental pain, and musculoskeletal disorders Also used for antipyretic effects Naproxen has fewer drug interactions with angiotensin-converting enzyme inhibitors given for hypertension

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NSAIDS Adverse Effects

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Gastrointestinal Dyspepsia, heartburn, epigastric distress, nausea GI bleeding* Mucosal lesions* (erosions or ulcerations) * Misoprostol (Cytotec) can be used to reduce these dangerous effects. Renal Reductions in creatinine clearance Acute tubular necrosis with renal failure Cardiovascular Noncardiogenic pulmonary edema *all nsaids except asprin can lead to clot forming at the level of the heart leading to a heart attack watch patients already at risk (coagulation specifiically) for heart issues

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Analgesics: Nursing Implications

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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 Be sure to medicate patients before the pain becomes severe so as to provide adequate analgesia and pain control Pain management includes pharmacologic and nonpharmacologic approaches; be sure to include other interventions as indicated Patients should not take other medications or OTC preparations without checking with their physician Instruct patients to notify physician for signs of allergic reaction or adverse effects --assess: pain, bowel sounds, vitals, and history

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Opiod Analgesics Nursing Implications

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Oral forms should be taken with food to minimize gastric upset Ensure safety measures, such as keeping side rails up, to prevent injury Withhold dose and contact physician if there is a decline in the patient's condition or if vital signs are abnormal, especially if respiratory rate is less than 10 to 12 breaths/min, may need Narcan Constipation is a common adverse effect and may be prevented with adequate fluid and fiber intake Instruct patients to follow directions for administration carefully and to keep a record of their pain experience and response to treatments Patients should be instructed to change positions slowly to prevent possible orthostatic hypotension Assess bowel sounds before administration

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Examples of NSAIDS (propionic acid derivatives)

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iburofen (motrin or advil) naproxen (naprosyn, aleve) celebrex (only selective one learned)

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NSAID Interactions

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***anticoagulants ***corticosteroid protein bound drugs diuretics and ACE inhibtors

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NSAIDS: Nursing Implications

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-contraindicated with GI lesions and peptic ulcer, bleeding disorders -Do not give to children (Reye's syndrome) -B/C of GI distress they are better tolerated with food, milk and antacids - 3-4 wks for effects to show sometimes -do not crush enteric tab

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Migraine Medications

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(stop and prevent) -Two classes of med: triptans(serotonin agonists) and ergot alkaloids Triptans (migraine specific ex: imitrex and Maxalt) stimulate 5-HT receptors in cerebral arteries and vasoconstrict + reduce inflammatory neuropeptides Ergot alkaloids (migranal) narrow or constrict blood vessels in brain ; note these are category x (not for pregnant women) Sometimes BP meds can be used as preventive drugs for migraine (ca channel blockers and beta blockers)

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Triptans + Ergot Alkaloids Contraindications and adverse effects

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Contraindicated:Hypotensive pt with Cardiac disease(drugs will vasocontrict vessels) Adverse: Triptans: vasoconstrict, irritation @injection site, tingling/flushing Ergot: nausea/vom, cold/clammy hands/feet, muscle pain, dizziness

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Anesthetias

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Drugs that reduce pain by depressing the CNS and PNS (alters the ion channels) types: general and local note: balanced anesthesia is medication that reduces pain and then sedations

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General Anesthetic Types

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-Inhalation: ex nitrous oxide -Parenteral (IV): ex etomidate (amidate) and propofol (diprivan) *note propofol is lipid based and will raise triglycerides over time also it contains warnings able egg sensativities; high doses of meds cause metabolic acidosis and hyperkalemia *note etomidate: decreases brainstem activity and lowers RR

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Anestesia Adverse Effects

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-commonly effects: heart, peripheral circulation, liver, kidney and respiratory tract ***malignant hyperthermia: severe rxn to general anesthesia, elevated body temp above 104, tachypenea, tachycardia, muscle rigidity, LIFE THREATENING EMERGENCY-->treat with life support and dantolene(skeletal muscle relaxant)

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Moderate Sedation (conscious sedation)

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Combination of IV benzodiazepine and opiate analgeics (like fentanyl or morphine) -for minor procedures, safe/rapid recovery, pt still maintain own airway and respond to verbal commands, axiety/pain sensativity reduced, pt cannot recall the procedure

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Local Anesthetics

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Used to render a specific portion of the bdy insenstive to pain by interfering with the nerve impulse transmission to specific areas of the body, do not cause LOC Topical(skin on membrane) or parenteral(injection): -spinal intraspinal (intrathecal(spinal) OR epiduralcatheter placed in between the dura matter of the spinal column) -infiltration -nerve block -topical (ex-lidocaine)

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Ansestsia Indications

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-small procedures, dental pain, chronic pain, child birth, -Inflitration anesthesisa (lidocaine with epi) use nerve block+ are combined with vasoconstrictors to prevent systemic absorp, confine to area, reduce blood loss BUT do not use on nose/finger/toes/genitals B/C vasoconstrict could lead to necrosis of small vessels *usually limited adverse effects if wrong injection site, excessive doses etc "spinal headache"

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Neuromuscular Blocking Drugs (NMBD)

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-prevent nerve transmission in certain muscles, resulting in muscle paralysis -when used during surgery articial mechanical ventialation is required b/c drug paralyzes respiratory and skeletal muscles (pt cannot breathe on own) *do not sedate or relief pain... pt may be paralyzed and conscious!

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NMBD: Depolarizing Drugs

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-Succinylcholine: works similarly to neurotransmitter acetylcholine causing depolarization -They bind to the Acetylcholine receptors causing paralysis (nerve cell membran is not depolarized-no muscle stimulation) -effects small moving muscle first (like fingers and eyes) then intercostal (diaphragm), then *causes flaccid muscle paralysis **need to watch out for malignant hyperthermia ex long acting: *pancuronium(pavulon)

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NMBD Adverse Effects

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-hypotension (blocks autonomic ganglia) -Tachycardia (blocks muscarinic receptors) -Hypotension (release of histamine) ***Always check vitals signs and ABC's

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CNS Depressants

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1. Sedatives: Drugs that inhibit CNS (nervousness, excitability and irritability) 2. Hypnotics: Cause sleep, more potent effect on CNS, sedatives can become a hypnotic if given in large dose

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Stages of Sleep

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Stage 1: Non-REM (1st 7min of sleep-easily aroused) Stage 2: Non REM( 50% of sleep time) rest is occurring/restoration Stage 3: Non REM(HR, BP and temp drop/slow) Stage 4: Deep Non REM Stage: (sleep walking can happen here) Usually after Non REM Deep (but ongoing): REM (Dreaming, memory, cognition, adaptation occur) REM (active sleep-essential in learning and cognition—adaptation to life)

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Types of Insomnia

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-short term (stress #1 cause) -long term (1month+) -rebound insomnia (abrupt discontinuation of sedative use) Diagnosis: EEK, brainwave activity, nonrapid eye movement vs REM,

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CNS Depressant: Benzodiazepines

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Sedative hyponotic drugs: CNS depressants; affect the hypothalmic, thalamic and limbic system of the brain (benzodiazepine receptros--gamma aminobutyric acid (GABA)) Classes: Sedative hypnotic and Axiolytic (meds that relieve anxiety) Know: diazepam(valium)long acting alprazolam(xanax), lorazepam(ativan) and temazepam(restoril)-intermediate acting **do NOT suppress REM as bad as barbituates and do NOT increase metabolism of other drugs

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CNS Depressant: Benzopdaizepine: Adverse Effects

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***drowiness, respiratory depression(overdose and interactions), "hangover" effect/day time sleepiness*** -only cause hypotension and respiratory depression if taken with other CNS depressants(like alcohol and opioids) Treatment for overdose: flumazeil (antidote)

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CNS Depressant: nonbenzodiazepine

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used to treat insomnia

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Barbiturates

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-Low dose: sedative; High does: hypnotic *low therapuetic index and is an enzyme inducers -potentializes action of GABA then nerve impulses traveling down corex are inhibited (brainstem/motor funct) adverse: vasodilation, hypotension, drowsy, lethargy, vertigo, rr, cough, nausea/vom, diarrhea/constip, agranulocytosis and thrombocytopenia, steven johnson syndrome

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Six Major Anxiety Disorders

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OCD: excessive thoughts about something (@least 1 hr) repetitive motions/thoughts/activities—disrupts day and lifestyle PTSD: triggered by a terrifying event (nightmares/flashbacks) GAD: chronic anxiety Panic Dis: panic attacks (rxn disproportion to situation) hyperventialtion, chest pain... Social Phobia: excess fear of social situations Simple Phobia: object of fear

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Drugs for Anxiety

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*reduced overactivity of the CNS -Benzodiapenine -buspirone (BuSpar)

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Antidepressants

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1. Tricyclic antidepressants (ex: amitriptyline-Elavil 2. Monoamine oxidase inhibitors (MAOIs)By inhibiting the reuptake of serotonin-norepinephrine it increase the amount in the body (serotonin and norepinephrine and dopamine) ex: phenelzine (nardil) 3. Second generation antidepressants: selective serotonin reuptake inhibitors (SSRIs) and (SNRIs)

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Epilepsy/Convulsion/Seizure

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-Seizure Brief episode of abnormal electrical activity in nerve cells of the brain -Convulsion Involuntary spasmodic contractions of any or all voluntary muscles throughout the body, including skeletal, facial, and ocular muscles -Epilepsy Chronic, recurrent pattern of seizures

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Classifications of Epilepsy

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1. Generalized Onset Seizures (grand mal): -effect whole body -loss of conscious/effects all muscles 2.Partial onset: Do not have loss of consciousness simple: one focal area complex: secondary generatlized tonic-clonic: partial then a general seizure (LOC)

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Antiepileptic Drugs (AEDs)

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aka anticonvulsants -control and prevent seizures -AED therapy is lifelong +combo of drugs may be used **black box warning: suicidal thoughts and behaviors

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Carbamazepine (Tegretol)

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Antiepileptic Drug (1st line) Stabilized neuronal sodium channels to make neurons less excitable adverse: blood cell abnormalities, low sodium levels, aplastic anemia, agranulocytosis *Normal level: 4-12mcg/mL ***take w/food BUT DO NOT TAKE WITH GRAPEFRUIT (brks dwn juice but not drug=more in system and increases toxicity)

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Valproic Acid (Depakote)

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Antiepileptic Drug +bipolar disorders(1st line) CNS Depression *hepatic dysfunction possible in 1st 6mo(monitor Liver Function tests****) -Therapeutic level 50-100mcg/mL PO adverse: GI irritation: don't chew extended release or mix with carbonated beverage, throat/mouth irritation, sedation, prolonged bleeding time, muscle weakness, wt gain, rash, photosensativity -interactions: dilantin and phenobarb levels increase levels

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Phenytoin (dilantin)

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Antiepileptic Drug(1st line) Stabilizes sodium channels (decreases action potential leading to cardiac effects dysrhythmias IV form only with saline b/c can crystalize and become and embolism IV form can cause purple glove syndrome and damage tissues***Avoid extravasation of dilantin to stop tissue necrosis -monitor steven johnson syndrome *narrow therapeurtic range 10-20mcg/mL NO IM Administration b/c lead to necrosis -adverse: hyperglycemia, hypotension, v-fib, muliple blood dycrasias, drowiness, wakness, gingival hyperplasias ***Enzyme inducers, may need to increase drug dose

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phenobarbital

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Antiepileptic Drug (1st line) ***Enzyme inducers, may need to increase drug dose

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Parkinson's Disease

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Chronic Progressive, degenerative disorder that affects the dopamine producing neurons in the brain -imbalance of neurotransmitters dopamine and acetylcholine (symptoms start when 80% of dopamine stored in substantia nigra is depleted (gets worse when too little dopamine is available) and dyskinesia(abnormal involuntary movement-flopping around) Symptoms: -akinesia(loss of movement), bradykinesia(slow), rigidity, tremor, postural instability, staggering gait, drooling the effectiveness of this drug will wear off after about 4-5 years of using this drug Wait as long as possible to give drug b/c of this

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Levodopa Therapy

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Used to treat parkinson's disease -it is a precursor of dopamine -blood brain barrier does not allow exogenously supplied dopamine to enter but does allow levodopa --it is taken up by the dopaminergic terminal and converted into dopamine then released as disease progresses levadopa no longer controls PD -->after 5-10 yrs the therapy no longer works

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Carbidopa

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Parkinson's Disease Treatment is given with levodopa Carbidopa does not cross the blood-brain barrier and prevents levodopa breakdown in the periphery As a result, more levodopa crosses the blood-brain barrier, where it can be converted to dopamine

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Anticholinergic Therapy

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-blocks effects of ACh -treats muscle tremors and rigidity caused by excessive cholinergic activity *DOES NOT RELIEVE BRADYKINESIA(slowness) -benztropine mesylate(cogentin) is also used to treat extrapyramidal symptoms cause by use of antipsychotic drugs *benadryl also used?

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GABA

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GABA: main inhibitory neurotransmitter in the brain, so the more GABA you have the less action potential you have. If you have less action potenital you have less activity of CNS. Atimodate, doproval and diprovan do not effect BP as much propofol. Hypotension and cardiac issues they should not get propofol b/c it will cause issues with arrhythmias and BP Atomidate: don't use in septic shock or

Analgesics: Relieving Pain without Loss of Consciousness

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