analgesics and anesthetics

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analgesics and anesthetics
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2011-10-28 16:06:35
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analgesics anesthetics
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analgesics and anesthetics
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  1. local anesthetics work by
    sodium blockade in the CNS neutrons
  2. Basic pharmacology are
    local anesthetics have either an ester-bond or amide bond
  3. What are the differences between a ester-bond and a amide bond local anesthetics?
    • ester type are procaine/novocain, marcaine, cocaine and are metabolized by plasma enzymes.
    • amide type are lidocaine and are metabolized by the liver.
  4. what are the adverse effects of local anesthetics?
    • CNS excitation and seizures
    • anaphylaxis
    • respiratory depression
    • bradycardia
    • tachycardia - especially cocaine
    • relaxation of the cardiac muscle - cardiac arrest
  5. forms of local anesthetics include:
    • injectable solutions - .5%, 1%, 2%, 10%
    • lidocaine- topical cream, ointment, patches (lidoderm), jelly, aerosol are available as well as solutions for injections also used as a sodium block.
    • cocaine HCl- powder and topical solutions
    • tetracaine- topical forms and eyedrops
  6. what are the advantages of local anesthetics?
    rapid onset, usually takes 2-3 minutes, short half life
  7. ways to administer local anesthetics include:
    • topically
    • infiltration injection of a local site usually with lidocaine & epinephrine - NEVER use on fingers, toes, or nose.
  8. nerve block IV regional anethesia has to be used with
    • a tourniquet to prevent rapid circulatory absorption, the lidocaine is injected into distal vein in the area, ex. hand or arm
    • epidural injection
    • spinal injection
  9. risks and dangers of local anesthetics:
    • the most invasive techniques of injection are the highest risk for adverse reactions:
    • hypotension due to blockade of the sympathetic nervous system.
    • vagal response: causes bradycardia, possible cardiac arrest
    • epidurals for birth can cause CNS depression in the newborn.
  10. nursing implications for local anesthetics:
    • check patient allergies, anesthesia reactions prior to procedure and communicate to the physician.
    • constantly monitoring vital signs: respiratory rate and effort, blood pressure, heart rate
    • have epinephrine conveniently available for anaphylaxis
    • monitor injection site for signs of swelling or infection
    • check sensorium distal to injection site - ex. wiggle toes
  11. GAS is
    general inhaled anesthetics
  12. MAC is
    minimum alveolar concentration is the minimum concentration of the drug that will produce immobility in 50% of patients exposed to a painful stimulus. The more concentrated the the air the fater the uptake. Which is why gas is given by a mask.
  13. history of gas
    • was first invented in the 1800's. Nurses administered gases doctors did not take over till after WW2.
    • nitrous oxide was used by sigmond freud in sniff parties
  14. preanethesia agents consist of:
    • benzodiazapines (anti-anxiety sedatives), ex: midazolam, valium, ativan
    • muscle relaxants
    • opioids - morphine and fentanyl
    • anticholinergics - to counteract the parasympathetic reflex, vagal response of the heart = severe bradycardia and hypotension
    • using these drugs to induce relaxation helps the anesthetist to use less gas.
    • barbituates = thiopental (pentothal) "truth serum"
    • propofol (diprivan)- most commonly used
    • etomidate (amidate)
    • ketamine (ketalar) not used as much cause hallucinations
    • neuroleptics- fentanyl mixed with drosperidol, name brand is innovar.
  15. Anesthetic gases = ANE's include
    • halothane
    • isoflurane
    • enflurane
    • desflurane
    • sevo flurane
    • all of these drugs have a risk for malignant hypthermia and in combination with succynocholine is a higher risk
  16. risks of GAS include:
    • respiratory depression
    • cardiac vagal response and cardiac arrest
    • anaphaylaxis
    • hepatotoxicity and renal toxicity
    • DRT- dead right there
    • prolonged sedation
    • malignant hypothermia
    • decreased bowel motility and constipation
    • nausea and vomiting.
  17. GAS and nursing implications
    • 1. airway
    • 2. circulation- continuous monitoring of cardiac status and blood pressure
    • 3. temperature- watch out for a high rise as a result of GAS, malignant hypothermia
    • 4. pain management
    • 5. LOC
  18. Pre- op nursing implications
    • patient teaching- reduce patient anxiety
    • allergy history
    • communication with healthcare team about previous adverse reactions and anesthesia
  19. opiods pharmacology is
    • opiods work on the Mu receptors primarily (MOO makes you happy) and some Kappa receptors = sedation and less pain.
    • These receptors block the pain receptors so the patient does not "feel pain". Th problem with these receptors is the patient may become dependent and go through some withdrawal symptoms.
  20. the most common opioid is
    morphine
  21. opiods include:
    • alfentanil
    • fentanyl IV
    • hydromorphone
    • levorphanol
    • morphine
    • heroin
    • oxymorphone
    • meperidine
    • sulfentanil
    • methadone
  22. opoids ususal side effects include:
    • itching
    • pupil constriction
    • hypotension - morphine is a vasodilator
    • constipation and urinary retention
    • nausea and vomiting
    • euphoria (MU)
    • involuntary orgasm in some patients
  23. opioid adverse reactions:
    • anaphylaxis
    • respiratory failure: the client respirations are 12/minute or less
    • neurotoxicity
    • hepatotoxicity
    • oversedation
    • drug tolerance- builds up to a larger dose required to kill pain
    • physical dependence
  24. what is the antidote to opioids?
    • naloxone (narcan) used to reverse overdose or respiratory suppresion , blocks the MU and Kappa receptors.
    • problem: if your patient has any kind of pain they will feel it immediatly x 10
  25. opioid agonists include:
    • codeine
    • oxycodone
    • hydrocodone
    • prophoxyphene
  26. opioids agonists are given in the following forms:
    • orally or IV, used to control mild to moderate pain
    • problem: number one abused drug class in the USA
  27. opioid agonists have similiar actions as
    morphine
  28. usual side effects of opioid agonists are:
    • analgesia
    • sedation
    • euphoria
    • cough suppression- used in cough syrups
    • miosis- pinpoint pupils
  29. adverse reactions of opiod agonists include:
    nausea/vomiting, respiratory depression, constipation, urinary retention.
  30. NSAIDS - means
    Non Steroidal Anti Inflammatory Drugs
  31. Most NSAIDS are
    OTC
  32. NSAIDS are used for
    mild to moderate pain levels and inflamed disease processes.
  33. NSAIDS work by
    blocking arachnadonic acid cycle ehich produces prostaglandins. As a result can trigger asthma in asthmatics.
  34. The metabolism in NSAIDS is
    absorbed 90% by the GI tract, metabolized by the liver. Some are cleared by the kidneys so doses need to be adjusted for people with renal disease or just avoid them
  35. Ibuprofen is the generic version of and has a T1/2 of
    • motrin, advil, midol, and 2-4 hours
    • NSAIDS
  36. Naproxyn is the generic of and has a T1/2 of
    • Aleve, 10-20 hours
    • NSAIDS
  37. Indomethacin is the generic of and has a T1/2 of
    • Indocin 2.6 - 11 h
    • NSAIDS
  38. Meloxicam is the generic of and has a T1/2 of
    • Mobic, 20 h
    • NSAIDS
  39. Colchicine is the generic of and has a T1/2 of
    • specifically used for gout, 30 hours
    • NSAIDS
  40. ketorolac is the generic of and has a T1/2 of
    • toradol, 4.5 hours
    • NSAIDS
  41. What are the side effects of NSAIDS?
    GI bleeds from chronic use, asthma attack, increased BUN, creatinine
  42. Nursing implication for NSAIDS are
    take only with food, not to be taken with aspirin or other anticoagulants, avoid alcohol with use. Since T1/2 lives vary, the client may prefer longer acting NSAIDS.
  43. What are forms do NSAIDS come in?
    mostly oral, some can be given IV or IM (colchicine and toradol
  44. Cox-2 inhibitors are used for
    moderate and inflammatory pain. Also used as a blocker for familial polyptosis (colon polyps) which has an 80% genetic link.
  45. Cox - 2 inhibitors mechanism is
    inhibits the enzyme cox 2 which creates prostaglandins metabolized by the liver.
  46. Cox -2 inhibitors have a wider tissue abosoprtion compared to
    NSAIDS
  47. Cox 2 inhibitors still have the risk for _______ but not as much as NSAIDS
    GI complications
  48. The only Cox 2 inhibitor on the market right now is
    • Celecoxib (Celebrex) 100mg-200mg
    • T1/2 is 12 hours

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