pharmacology midterm 2

go through pain slideshow and notes

NSAID stands for

non steriodal anti inflammatory drugs

inflammation

localised protective response stimulated by tissue injury, serves to desroy dilute or wall off the injurious agent and injured tissue, s+s: pain, fever, loss of function, redness and swelling, mediated by: endogenous compounds, including proteins of complement system, histamine, serotonin, bradykinin, leukotrienes and prostaglandins

NSAIDS define

most commonly prescribed drug (10 million per year in Canada), many available over the counter, some may work better for some people, 15 different NSAIDS available, large and chemically diverse group of drugs

NSAIDS uses

relief of headaches, relief of myalgia (muscle pain), neuralgia, arthralgia, postoperative pain, relief of arthritic disorders (rheumatoid, juvenile, ankylosing spondylitis- inflammed arthritis affecting spine, osteoarthritis), treatments of gout and hyperuricemia (high uric acid levels- leads to gout or kidney stones)

properties of NSAIDS

anti pyuretic (reduce fever), analgesic (reduce pain), anti inflammatory

Aspirin (special)- platelet inhibition, protective against CV events

history of aspirin

acetylcalicyclic acid (ASA), marketed in 1899 and became the most widely used drug, had adverse affects (GI bleeding, kidney impairment), unable to use long term- but prompted need to develop similar medications

NSAIDS mechanism of action

inhibition of leukotriene pathway and/or prostaglandin pathway (called Arachidonic Acid pathway), blocks chemical activity of enzyme COX (cyclo-oxygenase)- COX-1: role in maintaining GI mucosa (side effects) and COX-2: promotes synthesis of prostaglandins involved in inflammatory process (lowers inflammation)

quick summary of arachidonic acid pathway insert image

FINISH

NSAIDS contraindications

allergies, conditions that place pt at risk for bleeding- rhinitis, vitamin k deficiency, peptic ulcer disease

NSAIDS adverse effects

heartburn, sever GI bleeding, acute kidney injuries (bc prostaglandins are important for kidneys), non cardiogenic pulmonary edema, altered hemostasis, hepatotoxicity, skin erruption sensitivity, tinnitus —MOST of these risks are more extreme with taking aspirin

NSAIDS adverse renal affects

reduction in creatine clearance, acute tubular necrosis with acute kidney injury

NSAIDS adverse cardiovascular affects

non cardiogenic pulmonary edema

NSAIDS and kidney function

when prostaglandins are disrupted, could enhance acute or chronic kidney failure, can compromis existing kidney function, kidney toxicity can occur in pt with dehydration, heart failure, liver dysfunction, use of diuretics or angiotensin-converting enzyme inhibitors

NSAIDS interactions

alcohol- increased GI bleeding, anticoagulants- increased bleeding, acetylsalicylic acid- GI toxicity, corticosteroids- increased ulcers, natural health products- fever (garlic, ginger and ginkgo have resulted in increased bleeding risk)

NSAIDS health canada warning

all NSAIDS except aspirin- increased risk of acute cardiovascular thrombotic events including MI and stroke, older people at risk FINISH

NSAIDS: acetic acid deriveratives

diclofenac sodium (voltaren), ketorolac (toradol)

ketoralac tromethamine (toradol)

powerful analgesic- comparable to morphine, short term for acute pain FINISH

propionic acid derivatives

ibuprofen (advil or motrin), naproxen (naprosyn, aleve)

ibuprofen

most commonly used, analgesic effects in management with arthritis, fevers, dental pain, period pain, cardiovascular event risk with over 2,400mg/day

naproxen (aleve)

second most commonly used NSAID, better adverse affect profile than ibuprofen, fewer drug interactions with angiotensin-converting enzyme inhibitors given for hypertension

salicylates

acetylsalicylic acid (aspirin)- most common- sold as oral tablets, topical cream (aspercreme), oral liquids or rectal suppositories, aspirin-antacid combinations (Alka-seltzer)- enteric coated aspirin (ASA-EC)

aspirin

inhibits platelet aggregation (clumping), irreversible inhibitor of COX-1 receptors within platelets, reduced formation of thromboxane (more antiplatelet), antithrombotic effect (treats MIs and other thromboembolic disorders), can lead to reye’s syndrome, pt with systemic lupus may benefit, OTHER NSAIDS lack these antiplatelet effects

aspirin during MI

reduces cardiac death after MI, should be administered at first signs of MI if no contraindications present, one of the first drugs given by ed, daily aspirin tablet for preventative therapy for adults with strong risk factors for cardiovascular event- effective after MI, FINISH

uses for aspirin

headache, neuralgia, myalgia, arthralgia, pain resulting from inflammation, systemic lupus erthematosus- antirheumetic effects, antipyertic action

Reye’s syndrome

affects children or teens, acute life threating syndrome, can lead to liver damage, neurological defects and liver damage, caused by viral illness like flu or chicken pox as well as by salicylate therapy in presence of viral illness (aspirin)