Pharmfr7

Cards (70)

  • Calcitonin Gene-Related Peptide (CGRP) receptor antagonist
  • Serotonin 5-HT Receptor Agonists
  • Salicylates
    .
  • Opioid Antagonist
  • Opioid Agonist-Antagonist
  • Opioid Agonist
  • Opioid Agonist
  • Centrally acting non-opioid
  • nonsalicylate analgesic
    .
  • COX2 Inhibitors
    .
  • Cox1 and COX 2 inhibitors
    .
  • Acute pain has a short duration of less than 3 to 6 months
  • Chronic pain lasts more than 6 months
  • The antipyretic effect of salicylates is caused by the lowering of body temperature by the dilation of peripheral blood vessels
  • Salicylates
    Analgesic and anti-inflammatory—inhibit the production of prostaglandins
  • Aspirin prolongs bleeding time by inhibiting the aggregation of platelets
  • Salicylates—Adverse
    GI bleeding
  • Aspirin Toxicity
    dizziness; tinnitus, nausea; vomiting; rapid, deep breathing; tachycardia; diarrhea; mental confusion; and coma
  • in children or teenagers who have influenza or chickenpox (Reye syndrome)
  • tylenol/ nonsalicylates
    • Analgesic and antipyretic activity: same as salicylates 
    •No anti-inflammatory action 
    •Nonopioid drug—mechanism of action unknown
  • Monitor blood glucose levels in diabetic pts taking acetaminophen
  • Nonsalicylates—Adverse
    • Skin eruptions, urticaria
    • Hypoglycemia
    • Jaundice, hepatotoxicity, and hepatic failure
  • habitual alcohol use – a person who drinks alcohol consistently should take no more than 2000 mg of acetaminophen a day
  • Acute overdosage of acetaminophen treated with gastric lavage within 4 hours of ingestion and acetylcysteine via nebulizer within 24 hours to prevent liver damage
  • Document description of pain and an estimate of when the pain began
  • NSAIDs inhibit the activity of two cyclooxygenase enzymes:
    • COX1
    • COX2
  • cyclooxygenase-1 (COX-1): Enzyme helps to maintain the stomach lining
  • cyclooxygenase-2 (COX-2): Enzyme triggers pain and inflammation
  • Celecoxib: specifically inhibits only COX-2; less potential for GI adverse reactions
  • All NSAIDs may increase risk of serious cardiovascular thrombosis, myocardial infarction, and stroke, which can be fatal
  • NSAIDS
    Notify provider for the following symptoms:
    •Chest pain
    •Visual disturbances
    •Skin rash
  • NSAIDS
    flushing,sweating
  • Ubrogepant
    block nociception so nerves are not stimulated, and pains and vasodilation do not occur
  • Activation of the serotonin 5-HT receptors causes vasoconstriction and reduces the neurotransmission, which in turn produces pain relief
  • NSAID administered with food, milk, or antacids
  • The “pain ladder” directs the use of both opioids and nonopioids in the treatment of mild to severe pain
  • Butorphanol
    Binds to the mu receptor as an antagonist and the kappa receptor as an agonist
  • tramadol
    Binds to the opioid receptor to block the reuptake of serotonin and norepinephrine.
  • morphine
    Bind to the with the Mu receptors to cause analgesia, sedation, euphoria and respiratory depression, weakness, headache
  • Opioid Analgesics AR
    • Depression of rate and depth of breathing
    •Coach the client to breathe if respirations are depressed