NSAIDS treatment of Gout Flashcards
What are the classic signs of inflammation?
Redness(rubor), swelling(tumor), Heat(calor), Pain(dolor)
What are the first reactions upon initiation of inflammation?
Vasodilation, leaky BVs
kinins(bradykinin), neuropeptides(SubstanceP), vasoactive amines(histamine, 5HT)
Arachadonic acid metabolites (Prostaglandin
Thromboxanes, Prostacyclin), and cytokines(TNF-alpha) Oxy FR, and proteases.
What are the actions of NSAIDS?
Anagesia, AntiPyretic, Antiinflammatory, Primary target is COX-1 and COX-2
Is acetaminophen and NSAID?
no
What are the main two prostzglandins involved in infalmmation?
PGE2 and PGI2
What is the function of the COX enzymes?
Convert Arachadonic Acid into Prostaglandins.
What is the unique function of COX-1?
Continually Expressed, widely distributed. Housekeeping functions. Protects Stomach lining from gastric acid.
What is the unique function of COX-2?
Inducible, production of inflammatory molecules. Renal perfusion
Vascular Endothelium: Prostacyclin(PGI2)
What are the different types of NSAIDS?
Non-Selective:Acetacylic Acid(aspirin), Ibuprofen, Indomethacin
Selctive for COX-2: Celecoxib
What are rhe clinical uses of NSAIDS?
Pain, Fever, Inflammation, Antithrombotic, Misc uses.
What can Aspirin be hydrolysed to?
Salicylic acid
What are the low dose effects of aspirin?
Analgesia, antipyretic
HL 3-5 hrs
What are the high dose effects of aspirin?
Anti inflammatory
HL > 12hrs
What form is aspirin in the Plasma?
Bound to Albumin
How is Salicylic acid excreted in urine?
Conjugated with glucuronic acid.
What are the pharmacologic Considerations of Aspirin?
Acetylation and inhibition of COX are irreversible.
How does Aspirin decrease inflammation?
Inhb. of COX2 and PG
Inhb. Inflammatory cell migration.
How does Aspirin decrease fever?
Blocks Prostaglandins to CNS to reset temp control. Dilates superficial BVs
How does Aspirin prevent coagulation?
Inhibits Thromboxane synthesis
What are the adverse effects of Aspirin?
GI tract upset (COX-1) GI irritation (decrease PG E2 and PGI2) Platelet inhibition Hepatic and Renal Tox. (decreases kidney function) Hypersensitivity Tinnitus Reyes Syndrome: Encephalopathy
What is the primary treatment for gout?
Indomethacin
What is the benefit of using COX-2 selective inhibitors?
Similar benefits with less GI symptoms (higher risk for Cardiac events)
What are the contraindications for COX-2 selective inhibitors
Underlying Cardiac disease
What are the theraputic actions of Acetaminophen?
Pain and fever reducer
No antiinflammatory efects
What is the main drawback to acetaminophen?
Acute toxicity is very dangerous! Acute Liver failure ==> Transplant!
What is the MOA of Capscacin?
activates vanilloid receptors ==> Release of Substance P
What are the drug reactions of NSAIDS?
Displacement of protein binding, diuretic, anticoagulants, GI effects
What chemical builds up in Gout?
Monosodium urate.
What is the treatment course for gout?
Terminate acute gouty attack
Control of pain and inflammation,
Prevent future attack
Low purine foods and limit alcohol
What is the use of Colchicine?
Reduces pain and inflammation in Gout. Inhibits leukocyte migrationand phagocytosis
What are adverse effects of Colchicine?
Diarrhea
What is used for Gout Prophylaxis?
Xanthine Oxidase inhibitors(Allopurinol, Febuxostat) Uricosuric Drugs (Probenecid or sulfinpyrazone)
