Arachidonic Acid Flashcards
PGE2 effects
Pain, fever, vasodilation, uterine contraction (inflammation)
Increased capillary permeability
Leukotrienes role
–participants in allergic responses such as asthma
–Appreciate role of leukotrienes in some side-effects of nonsteroidal anti-inflammatory agents
Some Cyclooxygenase Inhibitors
- Acetylsalicylic acid (Aspirin)
- Celecoxib (Celebrex) (only Cox2 inhibitors)
- Diclofenac (Votaren)
- Fenoprofen (Nalfon)
- Ibuprofen (Motrin etc)***
- Indomethacin (Indocin)
- Ketoprofen (Orudis)
- Ketorolac (Toradol)
- Meclofenemate (Meclomen)
- Naproxen (Votaren)***
- Oxaprozin (Daypro)
- Piroxicam (Feldene) - more long acting
- Sulindac (Clinoril)
- Tolmetin (Tolectin)
Why aspirin specifically for preventing heart attacks?
Permanent (not reversible)
Celecooxib (mechanism, advantage, disadvantage)
Doesn’t block COX1 (particularly in stomach) → Less gastric ulceration
COX2 inhibition in endothelium of coronary and cerebral circulation → suppressed prostacyclin synthesis - too much clotting → MIs
**Many COX2 have been withdrawn from market (increased risk of cardiovascular thrombosis**
Acetaminophen (Tylenol)
Blocks cyclooxygenase in CNS but not in periphery
* NOT anti-inflammatory
*Both anti-pyretic and analgesic
Aspirin (Acetylsalicylic Acid)
Irreversible COX inhibitor
Eliminate thromboxane A2 for platelet’s entire life (14d) (platelet doesnt have nucleus, can’t generate more cyclooxygenase)
Used to eliminate thrombosis (MI)
Gastric ulceration and blood thinning (in accidents, hemorrhagic strokes)
Prostaglandins and inflammatory effects of rheumatoid arthritis
Ibuprofen and other NSAIDs used to tx sxs, but don’t halt or reverse disease progression
Arachidonic acid –> ____ –> _________
PGE2
Inflammation
Treat arthritis sxs by blocking Cyclooxygenase w/ agents such as:
Ibuprofen, Naproxen, Celebrex
Glucocorticoids are _________ regulators
transcriptional
***Takes a little bit of time
Corticosteroids reduce numbers of _________ but increase numbers of ___________
Reduce lymphocytes, eosinophils, monocytes, and basophils
Increase polymorphonuclear leukocytes
Corticosteroids reduce release of _______ and ___________ (immuno)
Arachidonic acid and cytokines (interleukin 1 & 6 and TNF)
Examples of Corticosteroids
- Dexamethasone (Decadron)
- Hydrocortisone
- Methylprednisolone (Medrol)
- Prednisone (Deltasone)
Steroids are incredibly effective _____________
anti-inflammatories
Toxicites of steroids
–Osteoporosis
–Immune suppression
–Peptic ulcers
–Myopathy (less prevalent)
–Cataracts
–Fluid accumulation and hyperglycemia
Steroids are/are not considered disease modifying agents (DMARD) in RA
NOT (those are more biological modifiers and nonbio)
Corticosteroids suppress immune responses (specifics)
–Suppress leukocyte numbers
–Suppress arachidonic acid release
——Synthesize proteins inhibiting phospholipase A2
–Suppress release of inflammatory cytokines such as interleukins and TNF
Eicosapentaenoic Acid
Fish Oil
Fish oil results in
PGE3, Thromboxane A3 or PGI3
–Produce thromboxane but Thromobxane A3 is not effective – Major outcome is a bleeding tendency and a virtual resistance to Cardiovascular disease
•Example is maritime diet characteristic of Inuits
Fish oil is promoted as a treatment for ____________
Rheumatoid Arthritis
–Not mainstream at the moment
–Mechanism suggests that PGE3 is not inflammatory
Prostaglandin E2 causes symptoms of ________________:
Inflammation:
–Edema
–Pain
–Redness
–Warmth
Inhibitors of prostaglandin synthesis are useful in treating ___________ rheumatoid arthritis
inflammatory symptoms of
Both Cyclooxygenase inhibitors and corticosteroids inhibit _____________ synthesis
prostaglandin
Major effects of Corticosteroids
–Reduction in white blood cells
–Reduced arachidonic acid liberation, resulting in suppression of both prostaglandin and leukotriene synthesis
