NSAIDs Flashcards
explain inflammation
achidonic acid is released from phospholipids in cell membranes in response to a triggering event (e.g., an injury). It is metabolized in either the prostaglandin
Leukotrienes are responsible for
vasoconstriction, bronchoconstriction and
increased vascular permeability
Prostaglandins induce inflammation through
vasodilation and increase vascular permeability.
They also potentiate histamine as well as
produce pain and edema.
what are the classes of saids?
what happens when you use nonspecific NSAIDS?
it blocks COX-1 and COX-2. by blocking COX-1, it increases stomach acid which can cause ulcers and GI bleed as COX-1 produces prosonglandins which help protect the mucosa
too little COX-1 results in?
too much gastric juice
what about platelets?
COX-1 convert prostongladin to thromboxane which helps platelet aggregation at the site of injury now if you are having a heart attack you dont want platelet aggregation thats why they take ASPRIN acts as an irreversible inhibitor of COX-1.
which medication helps reduce platelet aggregation? (platelet forming fibrin/clot)
aspirin ONLY
Which medication is apart of the nonspecific NSAID?
aspirin, ibuprofen, naproxen
what medication is COXIBs (specific COX-2 inhibitor)
celecoxib
What is cox-1 and cox-2
1 - physiological (always present in body)
2- inflammation only
what are the 3 reasons why NSAIDs are used?
1) analgesic
2) anti-inflammatory
3) antipyretic effects, and for platelet inhibition.
what is the common drug interaction you should be careful with when it comes to NSAIDs?
dont mix ACE inhibitors or ARBS with NSAIDs as it can cause vasoconstriction to kidneys leading to kidney failure
what lab value should we look at for ARBS/ACE with NSAIDs?
GFR
and even liver enzymes ALT, AST
for bleeding, Hgb, Hct, RBC
