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50 Cards in this Set
- Front
- Back
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Pain |
Whatever the experiencing person says it is, existing whenever he says it does |
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Pain Threshold |
Lowest threshold at which a stimulus is perceived as pain |
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Pain TOlerance |
Length of time or intensity a person will endure before asking for pain relief |
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Somative Pain |
Arises from bone, joints, muscles, skin or CT, usually aching or throbbing in quality and well localized |
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Visceral Pain |
Arises from organs |
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Neuropathic Pain |
Abnormal processing of sensory input by peripheral or central nervous system; treatment usually involves adjuvant analgesics |
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Acute Pain |
Usually of sudden onset, short-lived, or transient; easily treated with medications for short durations; easily observed symptoms |
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Chronic Pain |
Constant pain of long duration (5-6 months); no specific symptoms |
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Consequences of Pain |
Impaired ambulation, gait disturbances, falls Decreased socialization Sleep disturbances Depression Polypharmacy Cognitive dysfunction Malnutrition Increase health care use and costs |
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Principles of Pain Management |
Believe the person's self-report, establish cause of pain and initiate appropriate treatment Evaluate and discuss the potential negative consequences of unrelieved pain with the person on overall quality of life |
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Pain Management Strategy |
A- Ask, assess B- Believe C- Choose pain control D- Deliver intervention E- Empower, enable |
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Pain Pathway |
1. Stimulation of nociceptors 2. Conducted to dorsal horn via fibres 3. Dorsal horn is relay station 4. Impulses are conducted to brain via spinothalamic tract 5. Pain is perceived and a response initiated |
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Inflammation Response |
Cell membrane destruction--> Release of lipo-oxygenase--> Lts and Cox 1 and Cox 2 which then results in--> release of thromboxanes and pGs |
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COX-1 |
House-keeping duties; protection of gastric mucosa, support renal function, and promotes platelet aggregation (thromboxane), stimulates uterine contractions |
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COX-2 |
Synthesis of pGs associated with pain and inflammation |
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NSAIDs MOA |
Act by inhibiting COX 2 which blocks synthesis of pGs preventing pain from inflammatory process (prevents vasodilation/ vasc perm/ chemical mediators); blocks pGs effect on hypothalamus |
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1st Gen NSAIDs |
Block both COX-1 and COX-2 (ASA) |
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2nd Gen NSAIDs |
Targets COX-2 (Celecoxib) |
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Acetylsalicyclic Acid (ASA) MOA |
Irreversible inhibition COX-1 and COX-2 |
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Acetylsalicyclic Acid (ASA) Pharmacokinetics |
Absorbed rapidly from GI tract Metabolism: liver Half-life: 2 hours (low levels) vs. 20 hours (high levels) Distribution: highly bound to plasma albumin Excretion: kidneys |
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Acetylsalicyclic Acid (ASA) Adverse Effects |
GI upset (nausea/ heartburn) Bleeding (decrease platelet aggregation) Renal dysfunction (blacks COX-1 needed for normal renal function, Na/ H2O retention) Salicyclism (Tinnitus, sweating, headache) Reyes Syndrome (No kids with Chicken Pox/ Influenza) |
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Acetylsalicyclic Acid (ASA) Drug Interactions |
Anti-coagulants (Warfarin) Glucocorticoids (exacerbate effects) Alcohol (increase risk of gastric bleeding) |
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Acetylsalicyclic Acid (ASA) Nursing Implications |
Report signs of: - Hepotoxicity (dark urine, clay-colored stools, yellow skin/ edema, itching, abdo pain) - Renal toxicity - Ototoxicity - Allergic reactions - Bleeding (long term therapy) |
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Ibuprofen (Advil, Motrin) |
Anti-inflammatory, analgesic, antipyreutic Inhibits COX-1 and COX-2 but reversible Milder side effects Preferred now for inflammation |
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Acetaminophen (Tylenol) MOA |
Inhibits pG synthesis in CNS Reduce pain and fever |
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Acetaminophen (Tylenol) Pharmacokinetics |
Easily absorbed/ distributed Metabolism: non-toxic metabolite easily converted to toxic metabolite in liver Maximum daily dosage: 4000mg/ 4g Half life: 2 hours Excretion: metabolites in urine |
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Acetaminophen (Tylenol) Drug Interactions |
Alcohol, Warfarin (Coumadin) anticoagulant Caution with liver impairment |
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Acetaminophen (Tylenol) Nursing Implication |
Crosses placenta |
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Morphine MOA |
Binds to opioid receptor: inhibits neurotransmitter release--> decrease excitability and firing rates--> blocks transmission of impulses--> decrease perception of pain and decrease emotional response; triggers H1 from mast cells |
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Morphine Pharmacokinetics |
Absorption: good via all route; Onset: slower via PO than parenteral- effects last 4-5 hrs; Intrathecal (spinal) and epidural- effects can last 24 hrs Distribution: wide Metabolism: half-life (2-3 hrs all routes- significant hepatic first pass effect, only 25$ PO dose is bioavailable) Excretion: 90% appears in urine in 24 hrs |
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Mu Opioid Receptor |
Limbic system, thalamus, brainstem, dorsal horn- analgesia, respiratory depression, euphoria |
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Kappa Opioid Receptor |
Cerebral cortex, spinal cord- analgesia, sedation, pupil constriction |
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Delta Opioid Receptor |
Bowel- constipation |
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Opioid Effects |
Analgesia Euphoria Sedation Restlessness, confusion Peripheral vasodilation (warm, flushed, decreased BP) Respiratory depression Nausea Decreased GI motility Pupil constriction Cough suppression |
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Respiratory Depression |
May occur at therapeutic doses Decrease rate and depth Not a deterrent to pts. with normal respiratory function, but caution in pts. with compromised respiratory depression (ex. COPD), more problematic in post-op/ trauma pts than cancer pts |
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Opioids: Nursing Care |
Constipation: always start a bowel regime when giving opioids Nausea: offer antiemetics to start, nausea will disappear in time, unless sensitive Sedation: observe for over sedation; remove any other drugs with sedating effect; wake people for next dose when sleeping Give pain meds around the clock Oral route- less expensive Rectal route- underused, useful if person nauseated |
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Breakthrough Pain Management |
Manage pain before it can break through |
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Methadone |
Very long half life Treatment of drug addictions |
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Hydromorphone (Dilaudid) |
5x as powerful as morphine |
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Codeine |
Side effect of constipation |
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Meperidine (Demerol) |
Toxic (active 18 hr metabolite so can build up) if long term use |
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Naloxone (Narcan) |
Opioid Antagonist Structurally like Morphine Competitive Antagonist: blocks access of opioid agonists to opioid receptors; reverses opioid actions and side effects, bumps opioid molecules out of receptor Dose/ Route: 0.4mg IV, repeat at 2-3 min intrevals |
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Neuropathic Pain Treatment |
Responds poorly to opioids, but much better with adjuvant analgesics (ex. andidepressants, anti-consultants, and local anaesthetics) |
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Adjuvants |
Not pain medication per se, but assist with pain control when used in conjunction with pain medications, especially with neuropathic pain Can allow for reduced analgesic dosing, but can be unpredictable and side effects a problem |
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Ultrasound |
Promotes circulation in deep tissue |
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Heat |
Dilates blood vessels- speed up removal of chemical stimulating nociceptors (old injury) |
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Cold |
Decrease inflammatory response (vasoconstriction); decrease stimulation of nociceptors (acute injury) |
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Tolerance |
Loss of an effect at a given dose; receptors adapt to the pressure of the drug; occurs in absence of addiction |
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Physical Dependence |
Physiologic changes occur so that one needs continued use of drug to prevent withdrawal/ abstinence syndrome <2% of opiate naive pts receiving prescribed opioids become dependent |
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Abuse |
Use of a drug that is outside the normally accepted standard of use |
