Non-Steroidal Anti- Inflammatory Drugs. ATPE 410 Chapter 6

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1 Non-Steroidal Anti- Inflammatory Drugs ATPE 410 Chapter 6

2 Inflammatory Process A normal, beneficial process that begins immediately after injury to facilitate repair and return the tissue to normal function Initiated by stimulus including physical trauma, radiation, chemicals, heat, infection, and hypersensitivity Causes the release of chemical mediators

3 Chemical mediators Definition: are compounds released by one cell type that attach to the receptor of a second cell type to affect the response by that second cell Contained in mast cells and basophils Histamine- increases vascular permeability, increases blood flow to injured area Leukotrienes and prostaglandins- pain response, vascular permeability, and chemotaxis Phagocytes- neutrophils and macrophages remove debris Serotonin- increases capillary blood flow and vascular permeability

4 Chemical mediators Have a relatively short half-life, life, so their site of action is at or near the tissue that produces them. Known as local hormones. Plasma protein systems are biochemical sequences that produce proteins that have specific functions in the inflammatory response Kinin system Bradykinin - Increases vascular permeability and pain Complement system also impacts inflammation

5 Arachidonic Acid Metabolites Arachidonic acid is an unsaturated fatty acid that is the substrate for the production of compounds (metabolites) that contribute to the inflammatory response Metabolites of arachidonic acid are also known as eicosanoids Arachidonic acid contributes to symptoms of inflammation, including redness, swelling, and pain Phospholipase A 2 catalyzes the intracellular release of arachidonic acid from the phospholipids

6 Arachidonic Acid Metabolites Follows one of two pathways: cyclooxygenase (COX) lipoxygenase (leukotriene) Pathways lead to four eicosanoid mediators prostaglandins (PGs) prostacyclin (PGI 2 ) thromboxanes (TXs) leukotrienes (LTs) The COX pathway leads to the production of TX, PG, and PGI 2 Two forms of COX enzyme, known as isoforms COX-1- produced in most tissues at a stable rate COX-2- produced in the brain, female reproductive tract, blood vessel walls, and kidneys Production is also induced by tissue injury

7 Non-Steroidal Anti- Inflammatory Drugs (NSAIDs) Most frequently prescribed and frequently used OTC drugs Major mechanism of action is to decrease PG production by inhibiting one or both of the cyclooxygenase isoforms (COX-1, COX-2) COX-2 2 is enhanced in response to pain and inflammation so NSAIDs primarily inhibit this isoform rather than both COX-1 1 and COX-2

8 Therapeutic Uses of NSAIDs Treat both acute and chronic inflammation A week or 2 of therapy is typically long enough to determine whether the anti-inflammatory inflammatory effect is sufficient Treats inflammation associated with musculoskeletal disorders such as osteoarthritis, rheumatoid arthritis, gout, tendonitis, sprains, and strains Reduces pain, swelling, stiffness, and increases mobility Questionable if it decreases healing time to increase return to activity Selection of the NSAID, dosing, and duration impacts the potential for improved healing rate Use of other modalities simultaneously with NSAIDs helps decrease inflammation All NSAIDs have analgesic and antipyretic (fever reducing) activity ity Aspirin and ibuprofen most commonly used to reduce fever Acetaminophen (Tylenol)- not a NSAID but also reduces fever

9 Therapeutic Uses of NSAIDs Inhibit uterine synthesis of eicosanoids that contribute to cramps and excessive bleeding in menstruation COX-1 1 inhibitors have antiplatelet activity and thus have and anticoagulant effect Platelet aggregation stimulates activation of blood coagulation that can lead to thromboembolism, myocardial infarction, transient ischemic attack, or stroke COX-1 1 produces TXA 2, which stimulates platelet aggregation COX-2 2 produces PGI 2, which inhibits platelet aggregation Aspirin differs from other NSAIDs because it is an irreversible inhibitor of the COX enzymes All other NSAIDs are reversal inhibitors and therefore less effective for antiplatelet therapy Low-dose aspirin ( mg/day) is effective for antiplatelet therapy

10 Pharmacokinetics and Dosage of NSAIDs Absorption All NSAIDs are absorbed rapidly from the gastrointestinal tract, and thus almost all NSAIDs are available only as oral preparations Gastrointestinal upset can occur, so it should be taken with food d or milk, or at least a glass of water Enteric-coated coated aspirin can reduce stomach upset but it delays absorption Distribution NSAIDs distribute into the central nervous system, in breast milk, and across the placenta Extensively bound to plasma protein (especially some COX-2 inhibitors) Ibuprofen, fenoprofen, naproxen, and tolmetin are 99% bound to plasma p protein Metabolism and Excretion Metabolized by the liver and excreted through urine Both glomerular filtration and/or renal tubular excretion are used in the kidneys to get NSAIDs and their metabolites into the renal tubulet

11 Pharmacokinetics and Dosage of NSAIDs Aspirin Dosage The antipyretic dose for aspirin and ibuprofen is similar to the dose for relief of mild to moderate pain Risk of Reye s s syndrome associated with the use of aspirin in children with fever NSAID Dosage The anti-inflammatory inflammatory and analgesic dosage for NSAIDs varies between patients and the extent of their inflammation Anti-inflammatory inflammatory dosage is typically greater than analgesic dosage Toxicity Symptoms include tinnitus, nausea, vomiting, hyperthermia, sweating, disorientation Outdated bottles of aspirin have an odor of vinegar (acetic acid)

12 Adverse Effects of NSAIDs Most common adverse effects are gastrointestinal irritation, heartburn, nausea, gastrointestinal bleeding, and gastric and duodenal ulcers Side effects occur more commonly with aspirin than NSAIDs Signs include indigestion, dark stools, nausea, vomiting, and abdominal pain Two mechanisms develop gastrointestinal adverse effects Direct local irritation when drug is in contact with gastric mucosa Systemic action of inhibiting COX Avoiding irritation Administer with milk, food, or antacids (except for coated products) Proton pump inhibitor- reduces the amount of acid pumped into the stomach to decrease negative effects

13 Adverse Effects of NSAIDs Hypersensitivity is another adverse effect Symptoms begin within 3 hours of ingestion Include rhinitis, bronchospasm, asthma attack Liver and Renal toxicity (hepatoxicity) Renal toxicity is more common than liver toxicity Symptoms include nausea, fatigue, jaundice, right upper quadrant abdominal pain, flu-like like symptoms Use caution when administering to those with history of heart failure, hypertension, or kidney disease

14 Drug Interactions with NSAIDs Aspirin must be used with caution with Warfarin (Coumadin) COX-2 2 inhibitors may also affect warfarin response because of plasma protein binding or inhibition of CYP450 enzyme metabolism Acetaminophen does not have these anticoagulant effects NSAIDs diminish effect of antihypertensive drugs Includes diuretics, angiotensin-converting enzyme inhibitors, B-blockersB

15 NSAID Therapy Guidelines The lowest dose for the shortest duration of therapy that accomplishes the therapeutic goal should be used Most NSAIDs are not used in children, however ibuprofen is an exception

16 Corticosteroids The adrenal gland produces two types of corticosteroids Glucocorticoids cortisol (hydrocortisone) is primary Mineralocorticoids aldosterone is primary

17 Therapeutic Uses of Corticosteroids Major use is to suppress the immune and inflammatory responses Corticosteroids inhibit the activity of phospholipase A 2 to decrease both prostaglandin and leukotriene production Reduces the swelling and pain associated with inflammation Inhibit infiltration of phagocytes and lymphocytes at the site of o inflammation Inhibit release of other chemical mediators that affect the inflammatory and immune responses, like histamine and some cytokines Also used to treat rheumatoid and gouty arthritis, systemic lupus erythematosus, bronchial asthma, inflammatory bowel disease, tendonitis, bursitis, allergic reactions, and dermatologic diseases

18 Pharmacokinetics and Dosage Administration Inhalation for asthma Topical application for local, non-systemic effects (dermatological) Local and intramuscular injections Oral beneficial because they are usually almost completely absorbed by the GI tract Metabolism and Excretion Liver metabolism Urine excretion

19 Adverse Effects of Corticosteroids The amount of corticosteroid produced by the adrenal gland is regulated through a feedback regulation process by the amount of corticosteroid in the blood Hypothalamic-Pituitary Pituitary-Adrenal (HPA) axis When corticosteroid level in the blood decreases, the hypothalamus releases corticotrophin-releasing releasing hormone (CRH) which signals the anterior pituitary to release adrenocorticotropic hormone (ACTH), which signals the adrenal gland to produce more corticosteroid (cortisol)( When corticosteroid level is sufficient, the adrenal gland signals the hypothalamus and pituitary to stop releasing hormone If adrenal suppression occurs and the dose of corticosteroid is removed too quickly, the patient can experience various symptoms including nausea, vomiting, anorexia, headache, lethargy, fever, and muscle and joint pain

20 Drug Interactions with Corticosteroids Patients on NSAIDs have an increased risk of peptic ulcers when corticosteroids are added to therapy

21 Corticosteroid Therapy Guidelines Dosage Short-term term therapy is less than one week As doses of prednisone increase above 5 mg/day, the dose is considered supraphysiologic and capable of causing adrenal suppression Discontinued therapy should be tapered off in patients with adrenal suppression to allow the HPA axis to recover

22 Glucosamine Classified as a dietary supplement Use and Effects Not analgesic or anti-inflammatory inflammatory (does not affect COX pathway) Aminomonosaccharide that is used to make glycosaminoglycans, components of proteoglycans used to make cartilage Used to stop or reverse the progression of osteoarthritis Causes reduced restriction of active and passive movement, articular pain, and joint tenderness and swelling Pharmacokinetics and Dosage Absorbed orally First pass effect reduces bioavailability to about ¼ the oral dose Most common dosage is 500 mg three times a day in the form of glucosamine sulfate Excreted by the kidneys Also marketed as chondroitin sulfate, another glycosaminoglycan Chondroitin is more expensive and possibly less effective than glucosamineg Adverse Effects Gastrointestinal discomfort, headache, skin rash, itching

23 Topical Anti-Inflammatory Products Salicylate Applied to site of strains, sprains, and muscle soreness Has not been shown to be more effective than oral NSAIDs Absorption Penetrate directly into the skin Rate is dependent on site of application and number of applications Amount absorbed is too low for systemic therapeutic purposes Should be used with the same caution as other NSAIDs in patients with risk factors like hypersensitivity, renal disease, liver disease, and alcohol use

24 Topical Anti-Inflammatory Products Counterirritants Sometimes a component of anti-inflammatory/analgesic inflammatory/analgesic products Produce less severe pain by distracting patient with another type of pain Should not be applied to wounded, damaged, or open skin Other Topical NSAIDs Capsicum - inhibits Substance P, a neurotransmitter that is involved with peripheral pain Camphor and Menthol relieve itching Hydrocortisone topical corticosteroid All topical drugs, as with other drugs, can have a placebo effect

25 Role of the Athletic Trainer Alter the dose and duration of the treatment according to the therapeutic goal Considerations The benefits and risks must be weighed for each athlete NSAIDs should be taken with food or milk, and especially water, to reduce gastric upset Only one NSAID should be used at a time Recognize the long-term effects of NSAIDs Recognize at-risk athletes who should not take NSAIDs Inform athletes of all risks, dosage procedures, and symptoms of adverse effects caused by NSAIDs

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