Anti-inflammatory+&+Antigout+Drugs


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

- 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. 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 Acetic acids, propionic acids, pyrrollzine carboxylic acids, COX 2 inhibitors, fenamic acids, enolic acids, napthylalkanones 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 - Children: hyperventilation (leading to respiratory alkalosis), CNS: dizziness, drowsiness, behavioral changes, metabolic acidosis - Ibuprofen (Motrin, Advil): PO: Commonly used for arthritis, fever, pain, dysmenorrhea. - Naproxen (Naprosyn): PO: better side effect profile than ibuprofen - Ketorolac (Torodol): powerful analgesic, used for post surgical pain and pain in narcotic addicted individuals. PO and IV forms. Adverse effect is bleeding - 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) - Piroxicam (Feldene): mild rheumatoid, osteo, and gouty arthritis, PO form only, severe GI toxicity as an adverse effect. - Prescribed for 30 days or less - GI: heartburn, nausea, vomiting, GI bleed, mucosal lesions - Renal: acute tubular necrosis with renal failure - Cardiovascular: pulmonary edema
 * Contradictions:**
 * Mechanism of Action:**
 * Groups:**
 * Acetic Acids:**
 * Propionic Acids:**
 * Pyrrollizine Carboxylic Acids**
 * COX 2 Inhibitors:**
 * Enolic Acids**
 * NSAIDs Side Effects:**

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

Hypoxanthine > Xanthine > Uric Acid

- 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")
 * 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

=__**III. Nursing Implications**__= - assess contradictions (GI lesions, bleeding disorders) - look at labs - better tolerated if taken with food/water. Avoids GI upset - 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)
 * NSAIDs:**

=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.