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  1. GI
    • epigastric distress, nausea/vomiting
    • gastric ulseration, GI hemorrhage, erosive gastritis
    • low dose of aspirin for CV benefits associated with 2- to 4- increases in upper GI
    • none acetylated salicylates > less effect on cytoprotective PGs in GI
  2. blood
    • antiplatelet effect = inc. risk of bleeding
    • dec. plasma iron
    • dec. life or RBC
  3. avoid aspirin
    patients at risk of GI bleeding, ethanol use, platelet bleeding disorder, post surgery
  4. cardiovascular
    patients with already present congestive heart failure or renal disease = dec. renal function + salt and water retention caused by salicylates > inc. in blood volume can be up to 20%

    non-cardiogenic: older patients who ingest salicylates regularly > cardiogenic pulmonary edema 

    cardiogenic: compromised cardiac function (e.g. congestive heart failure) > and pulmonary edema
  5. respiration
    oxid. phosphorylation uncoupling > inc. production of CO2 > inc. respiration (mainly by an increase in depth with only a slight increase in rate) > Pco2 dec., >  blood alkalosis > renal acidosis.

    oxid. phosphorylation uncoupling (large aspirin doses) > depletion of glycogen = heat = and dec. aerobic metabolism

    direct effect on respiratory center in the medulla (at higher conc.)
  6. acid-base and electrolyte balance
    at therapeutic doses

    plasma alkalosis = renal acidosis > renal excretion of bicarbonate > Na+ and K+ excretion > dec. plasma bicarbonate  > blood pH returns to normal > homeostasis
  7. uricosuric effect
    at low doses > inhibit urate excretion > inhibit uricosuric agents (e.g. probenecid)

    at intermediate doses > no effect

    at high doses > inc. urate excretion > renal calculi

    note: avoid treatment for gout
  8. nephrotoxicity

    • prolonged and excessive ingestion of analgesic mixtures containing salicylates in
    • combination with acetaminophen or other analgesic-antipyretic compounds can produce
    • papillary necrosis and interstitial nephritis
  9. hepatotoxicity
    • in patients with prolonged use
    • onset is slow and damage is reversible with cessation of aspirin
  10. reye’s syndrome
    fatal disease: acute onset of encephalopathy, liver dysfunction, and fatty infiltration of the liver and other viscera

    likely mechanism: epidemiological evidence suggests an association between aspirin use and Reye’s syndrome 

    aspirin is contraindicated in children < 16yo who have or are recovering from chickenpox or flu-like symptoms
  11. hypersensitivity
    aspirin-induced anaphylactoid reactions are not immunological

    incidence of hypersensitivity estimated at 10-25% in patients with asthma, nasal polyps, chronic urticaria

    1% in healthy individuals. Aspirin intolerance is a contraindication to the use of any other NSAIDs 

    aspirin induced airway hyperreactivity in asthmatics, leading to bronchoconstriction, ocular and nasal congestion

    • aspirin triad:
    • Image Upload
    • possible mechanism: inhibition of COX pathways shunts AA to LOX, resulting in increased formation of leukotrienes > cross-reactivity with NSAIDs
Card Set:
2013-11-01 22:08:27

aspirin/salicylates adverse side effects and precautions
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