Anti-Inflammation

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Bobopudge
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57098
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Anti-Inflammation
Updated:
2010-12-23 08:53:32
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  1. What are eicosanoids?
    • 20 carbon molecule (essential fatty acid) derived from plasma membrane
    • Main EFA is Arachadonic Acid
    • Lead to production of leukotrienes and prostanoids
  2. Name the 3 prostanoids and how their formed
    Prostaglandins (E and D), Prostacyclin (PGI2), Thromboxane (TXA2)

    • Formation
    • - Common step: Breaking off phospholipid to make Arachadonic acid (by phospholipase C)
    • - Formation of PGH2 by COX 1 or 2

    • PGD2: is formed from PGD synthase
    • PGE2: from PGE synthase
    • PGF2: from PGE2
    • PGI2: from prostacyclin synthase
    • TXA2: from thromboxane synthase
  3. What are leokotriense?
    • Act on G-protein linked receptors
    • Involved in:
    • - allergic reactions and athma
    • - sustain inflamatory reactions
    • Function:
    • - chemotaxis
    • - vaso- and broncho constriction
    • - vascular permeabillity
  4. Name 2 leokotriene receptor antagonists
    • Montelukast
    • Zafirlukast
    • Used to treat asthma
  5. State the functions of the following prostanoids:
    • PGD2: in mast cells. vasodilation, inhibit platelet aggregation
    • PGF2: in smooth muscle and corpus luteum. Uterin contraction, vasoconstriction
    • PGI2: in endothelium. Vasodilation, Inhibits platelet aggregation, maintains renal bloodflow and glomerular filtration
    • PGE2: mediates fever, contraction of GIT smooth muscle, relaxation of bronchial, vascular and GIT smooth muscle, maintanance of renal bloodflow and glomerular filtration. Gastric mucosal protection
    • TXA2: vasocontrictor. Platelet aggregation.
  6. describe two active sites in COX
    • COX site: converts AA to PGG2
    • POX site: converts PGG2 to PGH2
  7. True or False? The conversion of AA to PGH2 is the rate limiting step in prostaglandin production.
    True
  8. State 3 types of Cyclo-oxygenase
    • COX 1: constitutive
    • COX 2: induced
    • COX 3: splice variant of COX 1 gene
  9. Name three properties of NSAIDS
    • Analgesic
    • Antipyretic
    • Anti-inflammatory
  10. Discuss classification of NSAIDS by Mode of Action and give examples of each
    • Class I: simple, competetive
    • - i.e. ibuprofen, naproxen
    • Class II: competetive, time-dependent, reversible
    • - i.e Diclofenac, indomethacin
    • Class II: competetive, time-dependent, irreversible
    • - i.e. Aspirin
  11. Describe drug interaction of Aspirin:
    • Mainly Warfarin:
    • - displaces warfarin from plasma proteins
    • - risk of hemmorage
    • Decreases effects of:
    • - ACE inhibitors, B-blockers, Diuretics
    • Increase effects of:
    • - Lithium, methotrexate, phenytoin
  12. Side effects of NSAIDS
    • GI disturbance:
    • - nausea, vomitting, ulceration, hemmorage, perforation
    • Skin:
    • - rashes, photosensitivity
    • Kidneys:
    • - Papillary necrosis
    • - interstitial nephritis
    • - hypertension
    • Liver:
    • - Reye’s syndrom in children
    • Bone:
    • - bone marrow toxicity
    • Lungs:
    • - bronchospasm
    • CNS:
    • - headache, confusion, seizures, drowsiness
    • Salicilism:
    • - fatal
  13. Name 3 main uses of aspirin
    • Thrombosis
    • Inflammation
    • Allergy
  14. What is the mechanism of action of Aspirin?
    • Irreversible acetylation of: Ser529 on COX active site
    • Prevents: eicosanoid production in platelets
    • Duration: life cycle of platelet
  15. *Note: in higher doses it causes toxicity and prevents PGI in endothelium
  16. How does Aspirin affect the GI mucosa?
    • Inhibits prostaglandins
    • PG are responsible for protection
    • - mucous production
    • - bicarbonate production
    • - inhibition of acid
    • causes bleeding and ulceration
  17. Breifly discuss ibuprofen in terms of:
    • Indications: RA, Osteoarthritis, pain, Dysmenorrhea, fever
    • Mode of Action: inhibition of COX 1 more than 2 less GI reactions
  18. Briefly discuss Diclofenac in terms of:
    • Indications: RA and osteoarthrits, spondylitis
    • Mode of Actions: COX inhibition, inhibition of DNA synthesis
  19. Discuss the actions of paracetemol
    • Analgesic, anti-pyretic
    • Inhibits COX 2 more than COX 1
    • Does not inhibit TXA2 production
  20. Discuss the properties of Parecetemol
    • half life of 1-4 hours
    • metabolized in liver
    • excreted in urine
    • few side effects: (allegic skin rxn and GI disturbance)
    • long term use: analgesic nephropathy
  21. Discuss paracetemol Overdose
    • Hepatic necrosis
    • - depletes glutathione
    • - accumalation of toxic metabolites
    • Hypoglycemic coma
    • Thrombocytopenia
  22. What are the symptoms and treatment of Paracetemol overdose?
    • Symptoms: nausea, vomitting, diaphoresis (excess sweating)
    • Treatment: activated charcoal, N-acetylcystein (makes glutathione in liver)
  23. What is Nimesulide?
    preferentially inhibits COX-2
  24. Discuss COX-2 inhibitors
    • Examples: rofecoxib; celecoxib
    • Anti-inflammatory agents
    • Less risk of GI damage
    • Greater risk of Myocardial Infarction and Stroke
  25. State 3 types of corticosteroids
    • glucocorticoids
    • minealocorticoids
    • androgens
  26. Discuss mechanism of action of corticosteroids
    • 1. Activation of anti-inflammatory genes
    • annexin-1, SLPI
    • 2. Inhibition of pro-inflammatory gene
    • - Activator Protein-1 and Nuclear factor kappa B
    • -- responsible for IL-1, IL-2, IL-6, IL-8, TNF-a and TNF-b
    • - NO
    • - Phospholipase A2, COX-2
  27. Discuss side effects of cortocosteroids
    • Osteoperosis
    • Growth retardation
    • Metabolic effects

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