ARDD Flashcards
Classes of drugs used in rheumatic diseases:
1) NSAIDS/COX-2 selective inhibitors
2) Glucocorticoids
3) Methotrexate
4) Colchicine
What is the major mechanism targeted by anti-inflammatory drugs?
Endothelium activation, leukocyte adhesion, transmigration, and chemotaxis. If the cells can’t get there, they can’t cause inflammation. Blocking ET activation also decreases edema.
Can COX2-inhibitors and NSAIDS decrease chronic inflammation- why or why not?
No, because the process is very complex (vascular growth effects, chronic response of ET cells hard to control), BUT these drugs CAN help with pain.
This drug inhibits PG production
NSAIDS
Used for acute and chronic inflammation and pain
NSAIDS, but not disease modifying.
Prostaglandins are made from what?
Arachidonic acid by COX enzymes.
COX1 is present where?
COX1: platelets, GI mucosa
COX3: injury/inflammation sites, EC, kidney
How do non-acetylated salicylates function?
They inhibit COX expression but not enzyme activity, and stimulate AMPK activity (which is anti-inflammatory).
How do carboxylic acids work?
COX-inhibitors (like ibuprofen)
How do COX-2 selective inhibitors work?
“-coxib” drugs work by being more selective for COX2 and reduce GI-related toxicity.
How to prostaglandins play into the pain pathway?
They produce mediators, such as bradykinins, histamine (which do produce pain, thus they enhance pain). They also cause “hyperalgesia by sensitizing nerves in the CNS and in primary afferent nerve terminals.
Where do NSAIDS function?
Periphery AND CNS PG synthesis
NSAIDS are more effective:
analgesic, less effective at anti-inflammation
