NSAIDS Objectives and Nursing Implications – Flashcards
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What is cyclooxygenase?
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the enzyme that converts arachidonic acid into prostaglandins.
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Where is cyclooxygenase found?
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In all tissues and acts locally (goes to site, can't effect sites from a distance)
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What does COX-1 do?
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Housekeeping! 1) protects gastric mucosa (secretes HCO3) 2) Stimulates platelet aggregation 3) Promote contractions
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What does COX-2 do?
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1) Promotes inflammation 2) Sensitizes receptors to painful stimuli 3) Brain - induces fever and pain 4) Vasodilation - blood vessels/supports kidney function 5) Colon - contributes to cancer
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Which cox has beneficial actions?
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Cox-1, "good COX"
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Which cox has primarily harmful actions?
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Cox-2, "bad COX"
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What effects does inhibiting cox-1 cause?
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Bad effects: Gastric erosion/ulcers Bleeding Renal Impairment Good effect: Protection from MI/CVA
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What effects does inhibiting Cox-2 cause?
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Bad effects: Renal Impairment Promotes MI/CVA Good Effects: Suppresses Inflammation Alleviates Pain Reduces Fever Protects against colorectal cancer
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What are the 2 categories of COX-Inhibitors?
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1) Anti-inflammatory Drugs (NSAIDs) 2) Drugs that lack anti-inflammatory properties (The only one: Acetaminophen)
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What is a first generation NSAID?
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inhibit COX-1 and COX-2
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What is a second generation NSAID?
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a selective COX-2 Inhibitor *Was meant to be safer with less S/E because it "doesn't inhibit COX-1," but it increases risk of MI/CVA and has some COX-1 effects...even though its not supposed to.
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What are the uses for 1st gen NSAIDS?
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Tx: Inflammation - RA, Osteoarthritis, Bursitis Alleviate mild/moderate pain Suppress Fever Relieve Dysmenorrhea *GI Ulcers - largely used drugs that put many people in the hospital
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What is the oldest 1st gen NSAID?
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ASA
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What is the difference between ASA and other non-asa 1st Gen NSAIDS?
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Others inhibit COX-1/COX-2 as well, but bind "reversibly" whereas ASA binds to COX "irreversibly" *Also, they don't protect against MI/CVA - they increase the risk (relatively low risk)
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What does irreversible inhibition in ASA cause?
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it irreversibly inhibits platelet aggregation. That means that it prevents the present platelets it comes in contact with from forming clots for the life of the platelet. You would have to wait for new platelets to be produced.
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How long does a platelet live?
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about 8 days (a single dose of ASA effects that platelet for its 8 day lifespan)
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What are the names of the other non-asa NSAIDS we need to know?
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Ibuprofen Naproxen Ketorolac
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How could we minimize the risk of MI/CVA in Non-ASA NSAIDS?
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Use lowest effective dose possible for the shortest time needed * Don't use before CABG surgery or 14 days after
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S/E of 1st gen NSAIDS
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Gastric Ulcers Bleeding Renal Impairment
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T/F: Patients who are hypersensitive to ASA can usually take other NSAIDs without any adverse reaction.
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False ASA hypersensitivity = likely cross-hypersensitivity in other NSAIDS
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What people are more likely to have a hypersensitivity to ASA?
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Adults with hx of asthma, rhinitis, and nasal polyps
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T/F: Women are encouraged to use NSAIDS during pregnancy
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False
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Why were 2 second gen NSAIDS withdrawn from the market?
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Because they caused serious cardiovascular risks and didn't prevent ulcers as well as they'd hoped. Basically: "The risks outweighed any benefits." *Those names were rofecoxib/valdecoxib, though probably not relevant to remember since they're not on the market
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What are the uses for 2nd-Gen NSAIDS?
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COX-2: Suppress pain/inflammation Possible S/E *less risk of GI s/e, but ulcers/bleeding can still develop * Impaired renal function (HTN/Edema)
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What is the only 2nd-Gen NSAID that is still approved by the FDA?
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Celecoxib (Celebrex) * Last choice drug for long-term management of pain *Has equal effects at relieving joint pain/stiffness/edema as Naproxen
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What are the uses for Acetaminophen and what does it lack that NSAIDS have?
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Analgesic Antipyretic Not anti-inflammatory/antirheumatic Does not suppress platelet aggregation Does not cause Gastric Ulcers Does not cause renal impairment
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What can an Acetaminophen overdose cause?
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Liver damage
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Why doesn't acetaminophen cause ulcers or other adverse effects like ASA?
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It only inhibits prostaglandins in the CNS Only acts on the brain part - fever and pain
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What drug is used more for pain than any other analgesic?
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Acetaminophen
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Why isn't acetaminophen used for inflammatory conditions?
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Cause its not anti-inflammatory
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What are the 2 metabolic pathways for acetaminophen?
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Minor and Major
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What happens in the major pathway?
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Acetaminophen conjugates with glucuronic acid to form nontoxic metabolites
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What happens in the minor pathway?
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Acetaminophen is oxidized by P450 system in the liver to a highly toxic metabolite. It can be converted to non-toxic form by "Glutathione," but most of it is converted by the Major pathway.
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What happens in the minor pathway in an overdose?
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An overload of toxic metabolite is produced which the liver cannot clear because "glutathione" is rapidly depleted. The toxic metabolite accumulates, damaging the liver.
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How does alcohol increase risk of injury from Acetaminophen?
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Alcohol increases P450 system, making toxic metabolites accumulate faster. It depletes glutathione Chronic abusers often have pre-existing liver damage *Probably doesn't increase risk in therapeutic doses
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What is the antidote for acetaminophen?
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Mucomyst - acetylcysteine Unpleasant odor, can induce vomiting May be given IV/oroduodenal tube
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How does acetylcysteine work?
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substitutes for glutathione and converts toxic metabolites to nontoxic form 100% effective at preventing severe liver damage if given within 8-10 hrs of overdose. PO or IV
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What happens with the interaction between warfarin and acetaminophen?
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Increases the risk of bleeding Acetaminophen may inhibit warfarin metabolism, causing an accumulation of warfarin. (Warfarin is an anticoagulant)
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What can happen when you take acetaminophen with vaccines?
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It can blunt the immune response
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Why is acetaminophen preferred in children?
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Because it does not associated with Reye's Syndrome like ASA
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Why the mnemonic ASA?
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Acetyl Salicylic Acid - chemical name
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What does ASA inhibit?
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Cox-1 and Cox-2
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Once again, what are the 4 therapeutic uses for ASA?
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anti-inflammatory analgesic anti-pyretic anti-thrombolytic
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What are the 5 adverse effects of ASA?
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GI distress Bleeding Renal Impairment Salicylism Reye's Syndrome
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What are the s/s of ASA poisoning?
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Initial Compensatory Respiratory Alkalosis Progresses to: Respiratory depression Adicosis Hyperthermia Sweating Dehydration Electrolyte Imbalance Stupor/Coma Death - from respiratory failure
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What is going on with ASA poisoning?
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ASA is acidic. pH partitioning occurs. Acidosis of ASA promotes the movement of ASA into the CNS. This increases respiratory depression, which increases CO2 levels in the blood, making it even more acidic, causing even more ASA to move out and into the CNS. This cycle continues until RR stop. EEK!
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Nursing Implications: Preadministration Assessment: Identifying high risk patients with NSAIDS
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Contraindications: hx of hypersensitivity, children (ASA), sulfa allergy (celecoxib), pregnancy, peptic ulcer disease, bleeding disorders, taking anticoagulants, glucocorticoids, ACE inhibitors, ARBs. Caution in elderly, hx MI, HTN, hypovolemia, hepatic cirrhosis, renal dysfunction, asthma/hay fever, urticaria, nasal polyps, alcoholism/smoking
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Nursing Implications: Implementation How are NSAIDS administered and what method of delivery is suggested for use?
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Administration: Route PO: all NSAIDS Topical: Diclofenac Intranasal: Ketorolac IM: Ketorolac IV: Ibuprofen, Ketorolac Rectal: ASA, Indomethacin Method: Take PO NSAIDS /c food, milk, or glass of water Do not crush/chew enteric-coated or sustained-release Discard ASA that smells like vinegar
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Nursing Implications: Ongoing Evaluation/Interventions
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Minimize Adverse Effects: use correct method of administration, give short-term, avoid /c risk factors, test for H pylori prior to long-term therapy, give proton pump inhibitor, use celecoxib in high-risk pt, don't consume alcohol, have pt notify HCP if gastric irritation persists, give an antiulcer medication *Educate pt about all of this
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Considerations in NSAIDs for renal impairment
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can cause acute renal insufficiency Monitor for renal impairment: I/O, weight, rapid elevated Serum creatinine/BUN Avoid Prolonged NSAID use if possible (can cause renal papillary necrosis)
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Considerations for NSAID use in pt's /c CV risk
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Avoid non-ASA NSAIDS or give at lowest dose possible for shortest time and not before a CABG or 14 days after
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When should high-dose ASA be D/C for surgery?
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7-10 days prior
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When should high-dose ASA be continued?
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in minor dental, dermatologic, or cataract surgeries
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When should low-dose ASA be D/C for surgery?
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- if pt has low risk of MI and having noncardiac surgery - intracranial surgery
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When should low-dose ASA be continued?
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- CABG - within 6 weeks of bare metal coronary stent - within 12 months of drug-eluting coronary stent - high risk of CV event - cataract, minor dental, and dermatologic procedures
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When should you D/C Ibuprofen and other nonASA NSAIDS?
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5 half lives prior to elective surgery
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What drugs are preferred for use in surgical patients and pts with bleeding disorders?
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Magnesium salicylate (nonacetylated salicylates) because they have minimal effects on platelet aggregation Celecoxib can minimize risk of bleeding
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What 4 drugs are "probably" safe if you have to give an NSAID-like drug /c hx of hypersensitivity?
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Celecoxib, salsalate, meloxicam, acetaminophen
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What is salicylism?
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tinnitus, sweating, H/A, dizziness
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What is Reye's Syndrome?
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a deadly disease that causes Encephalopathy and a fatty liver, associated with a recent viral illness, especially chicken pox/influenza
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What drug causes premature closure of the ductus arteriosus?
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Ibuprofen
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What are the risks in pregnancy?
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Maternal anemia Prolonged labor Premature closure of the ductus arteriosus
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What does taking other NSAIDs with ASA do?
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decrease protection against MI/Stroke (antagonizes antiplatelet action of ASA)
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When should you take ASA to avoid interactions with other NSAIDS?
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2 hrs before taking another NSAID
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T/F: Taking ACE inhibitors and ARBs with NSAIDs increases the risk of acute renal failure.
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True, avoid high-dose NSAIDS
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How do you manage ASA toxicity?
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external cooling IV fluids for dehydration/electrolyte loss Bicarbonate (reverses acidosis) Mechanical ventilation in severe respiratory depression Gastric lavage/activated charcoal (this really only works if overdose occurred within hrs of ingesting) Dialysis
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Preadministration Ax /c acetaminophen
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Use for pain/fever, preferred in children and peptic ulcer disease Identify high risk patients - chronic alcohol abuse, moderate alcohol use, warfarin, recent vaccine use Can cause HTN in women taking >500mg/d Increases asthma risk, rarely causes anaphylaxis, risk of liver damage, decrease dose in malnutrition/alcoholics
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What is the dose of acetaminophen for undernourished pts?
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3,000 mg/d
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What is the dose of acetaminophen when consuming over 3 drinks/d?
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2,000 mg/d
