glucocorticoids & nsaids Flashcards
lipids are turned into arachidonic acid by
phospholipase A2
arachidonic acid is turned into leukotrienes by
lipoxygenase
arachidonic is turned into thromboxanes & prostaglandins by
cyclooxygenase
cyclooxygenase has two
isoforms (COX1 & COX2)
COX1 role
imp for GI mucosal function
COX2 role
inducible in inflammatory cells
NSAIDS moa
reversibly inhibits COX1 & COX2
benefits of nsaids
decrease pain, redness, swelling
ADE of nsaids
decreased platelet aggregation
decreased renal blood flow
increased GI ulcers
acute interstitial nephritis is caused by
nsaids
acute interstitial nephritis
inflammation of interstium due to hypersensitivity allergic reaction
classic finding in acute interstitial nephritis
urine eosinophils
PGE2 role
vasodilation, fever, edema, pain, & renal vasodilation
PGE2/PGI2 role
protect GI mucosa
TXA2 role
platelet adhesion
LTC4/LTD4 role
vasodilators and bronchoconstriction (imp role in asthma)
LTB4 role
neutrophils & eosinophils chemotaxis
cox 2 inhibitor name
celecoxib
cox 2 benefits
decreased pain, redness, bleeding
less risk of GI ulcers
ADE of COX2
increased CV events
COX1 main product
TXA2
glucocorticoids MOA
inactivation of NF-KB
inactivation of NF-KB causes
mediates response to TNF alpha
controls synthesis of inflammatory mediators (COX2, PLA2, lipoxygenase)
effects of glucocorticoids
increase neutrophils
decrease cytokines & eosinophils
side effects of glucocorticoids
skin thinning, easy bruising, hyperglycemia, osteoporosis, cushings
major side effect of glucocorticoids
avascular necrosis
avascular necrosis path
bone collapse due to interruption of blood flow & bone thinning
long term steroid use suppresses
HPA axis
abrupt discontinuation of steroids causes
adrenal gland insufficiency
sxs of adrenal gland insufficiency
hypotension, shock, weakness, fatigue