VOCABULARY (So you know what I'm talking about)
Gout - Hyperuricemia (elevated blood uric acid level), arthritis caused by the buildup of uric acid crystals in tissues and joints causing pain
Inflammation - Localized protective response stimulated by injury to tissues that serves to destroy, dilute or wall up both the injurious agent and the injured tissue.
Nonsteroidal antiinflammatory drugs (NSAIDs) - A large and chemically diverse group of drugs that possesses analgesic, antiinflammatory, antirheumatic, and antipyretic activity



I. Nonsteroidal Antiinflammatory Drugs

- OTC uses: analgesic, antiinflammatory, antipyretic

Arachidonic Acid Pathway: Activation causes inflammatory responses such as pain, headache, fever, inflammation
- Arachidonic acid is released from phospholipids in cell membranes from triggering event (Injury)
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- Metabolized on one of 2 pathways: Prostoglandin (COX 1, COX 2), Leukotriene. Both result in inflammation, edema, headache, etc.

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Contradictions:
- Pregnancy category C in first 2 trimester
- Pregnancy category D in last trimester
- Also excreted through the breast milk
- Stop NSAIDs one week before surgery because inhibition of platlet aggregation
- Increased risk of bleed so be aware of epistaxis, rhinitis, vit k deficiency, hemophiliac.
Mechanism of Action:
Pain:
- Cyclooxygenase (COX) 1: promotes synthesis of prostoglandins, keeps GI mucosa intact
- COX 2: promotes synthesis of prostoglandins that are further involved in the inflammatory process
- NSAIDs inhibit prostoglandin pathway, block COX. Most NSAIDs only block COX 2 only limiting GI ulcers
Fever:
- Inhibit prostaglandin E2 within the hypothalmus to regulate temperature
Groups:
Acetic acids, propionic acids, pyrrollzine carboxylic acids, COX 2 inhibitors, fenamic acids, enolic acids, napthylalkanones
Acetic Acids:
Aspirin:
- Max dose 4g per day, 325-650mg 4-6 times per day, pediatric 80-100mg/kg/day
- Prophylactic for adults with strong risk factors for coronary artery disease and stroke
- Prevents platelet . 81mg and 325mg shown to have some equal thrombotic effects.
- Only PO, onset 15-30 min, peak 1-2 hours, duration 4-6 hours
- Commonly used for headache, neuralgia, pain associated with inflammation
Aspirin Toxicity Signs
- Adults: tinnitus, nausea, vomiting
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- Children: hyperventilation (leading to respiratory alkalosis), CNS: dizziness, drowsiness, behavioral changes, metabolic acidosis
Propionic Acids:
- Ibuprofen (Motrin, Advil): PO: Commonly used for arthritis, fever, pain, dysmenorrhea.
- Naproxen (Naprosyn): PO: better side effect profile than ibuprofen
Pyrrollizine Carboxylic Acids
- Ketorolac (Torodol): powerful analgesic, used for post surgical pain and pain in narcotic addicted individuals. PO and IV forms. Adverse effect is bleeding
COX 2 Inhibitors:
- Blocks inflammatory process without disrupting GI mucosa.
- Blocks cyclooxgenase from continuing inflammatory response
- Vioxx - Recalled for adverse cardiovascular events such as clotting during surgery (oops)
Enolic Acids
- Piroxicam (Feldene): mild rheumatoid, osteo, and gouty arthritis, PO form only, severe GI toxicity as an adverse effect.
- Prescribed for 30 days or less
NSAIDs Side Effects:
- GI: heartburn, nausea, vomiting, GI bleed, mucosal lesions
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- Renal: acute tubular necrosis with renal failure
- Cardiovascular: pulmonary edema

II. Antigout Drug

Gout:
- Increased uric acid production, decreased uric acid excretion, or a combo of both
- Hyperuricemia results (high uric acid in the blood)
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- Uric acid crystal deposits gather in tissues and joints: causes inflammation response and pain.
Uric acid production:
- Purine metabolism
- Hypoxanthine converted to xanthine and eventually to uric acid
- Antigout drugs can interrupt either of these conversions

Hypoxanthine ----> Xanthine ----> Uric Acid

Antigout Drugs:
- Allopurinol (Zyloprim): Inhibits xanthine oxidase which converts hypoxanthine to xanthine and xanthine to uric acid, thus reduces production of uric acid. Long term treatment
- Colchicine: reduces inflammatory response to deposits of crystals, used for acute attacks since one adverse effect is leukopenia
- Probenecid (Benemid): Inhibits reabsorption of uric acid in kidneys, thus, more is excreted.
- This kind of drug is called a "Uricosuric" and increases uric acid excretion. (Think "diuretic" as a similar word to "uricosuric")

III. Nursing Implications

NSAIDs:
- assess contradictions (GI lesions, bleeding disorders)
- look at labs
- better tolerated if taken with food/water. Avoids GI upset
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- medication history for drug interactions
- NOT given to children under 12 (risk of Reye's syndrome)
- teach patients side effects and to alert you of GI bleed (blood in stool)




QUIZZZZZZZZZZZZZzzzzzzzzzzz

Q:What lab values would drop if a patient had GI bleeding as an adverse reaction to a NSAID?
A: Hematocrit, HGB, RBC

Q: Why wouldn't you give anticoagulants along with NSAIDs?
A: One of the effects of NSAIDs is inhibition of platelet aggregation, thus, bleeding time would be further increased by giving anticoagulants also.

Q: A patient is prescribed 325mg of aspirin q4h. How many mg will the patient receive in the course of 24 hours and is this a valid order and why?
A: 1950mg, yes it is valid because it doesn't exceed the maximum dosage of 4g/day

Q: Antigout drugs work to inhibit what enzyme when hypoxanthine is converted to xanthine, and xanthine later to uric acid?
A: Xanthine oxidase

Q: What is the action of a "Uricosuric" antigout drug?
A: Decreases uric acid reabsorption in the kidney, thus, more is excreted.

Q: COX 2 inhibitors are a better choice of NSAID because the absence of what side effect that is only present in COX 1 inhibitors?
A: COX 1 also keeps the GI mucosa intact, thus, COX 2 doesn't have side effects such as GI ulcers

Q: Activation of the Arachidonic starts with what trigger?
A: Arachidonic acid is released from phospholipids in cell membranes from triggering event (Injury).

Citation: Anne, L., Rainforth, S., Harrington, S., & S., J. (2010). Pharmacology and the Nursing Process. St. Louis: Mosby.