NSAIDS Flashcards
Non selective NSAIDS
Aspirin Diclofenac Ibuprofen Indomethacin Ketorolac Piroxicam Tolmetin Acetaminophen (not NSAID)
COX-2 Selective
Celecoxib
Etoricoxib
Meloxicam (not as selective)
What happens when you inhibit COX
Decreased PGs and TXA
Which COX is constitutive
1
Where is COX-2 constitutive
Kidney
Brain
What naturally induces COX-2
Growth factors
Tumor promoters
Cytokines
What effects do NSAIDs have
Antipyretic
Analgesic
Anti-inflammatory
Blocking which COX can cause GI damage
1
What does endothelial COX-2 activation lead to
Vascular Prostacyclin
What sensitizes nerve endings to pain
PGE2
NSAIDs or opioid better for inflammatory pain
NSAIDs
What is responsible for fever
COX-2 –> PGE2
What are NSAIDs useful for treating
RA
OA
Gout
DOC closing ductus arteriosis
Indomethacin
DOC gout Sx
Indomethacin
Why can Celecoxib cause HS reactions
Sulfonamide
What happens if you give child with viral fever, Aspirin
Reye’s
What do you give child with viral fever
Acetaminophen/Ibuprofen
Contraindication
Pregnancy
Aspirin is Category D
DOC OA and pregnancy
Acetaminophen
Tx for Colon cancer
Aspirin
Give for niacin flushing
Aspirin
Tx GI ulceration from COX-1 inhibition
Misoprostol
PPIs
H2 blockers
Lowest risk of GI ulceration
Celecoxib
Highest risk of GI ulceration
Piroxicam
Why are there CVS AEs with NSAIDs
Imbalance of TXA2 and PGI2
Higher CV risk but lower GI effects
COX-2 inhibitors
What are the CVS AE of NSAIDs
Vasoconstriction
Platelet aggregation
Thrombosis
Renal AE of NSAIDs
Decreased RBF
AIN
Analgesic nephropathy
What happens with decreased PGE2
Sodium and water retention (Decreased GFR)
What happens with decreased PGI2
Hyperkalemia and ARF
What is the most common cause of AIN
NSAIDs and ABX
What is the effect of chronic NSAID use
Analgesic nephropathy and papillary necrosis
Aspirin effect on uric acid
Low dose reduces secretion
High dose inhibits reabsorption
What is seen in Aspirin HS
Rhinitis
Edema
Asthma
Why does Aspirin HS occur
Excess LT synthesis
Which NSAIDs are irreversible
Aspirin/Salicylates
What happens with Aspirin induced uncoupling of oxidative phosphorylation
Increased CO2 and respiration Hyperventilation (resp centre at high doses) Resp paralysis (toxic levels)
How does Aspirin/Salicylates increase BT
Decreased TXA2 in platelets but unaffected PGI2 levels
What kind of elimination does Aspirin undergo
Zero order
What can chronic Aspirin use cause
Hepatic injury
What is Salicylism
HA
Confusion
Tinnitus
Dizziness
Acid/Base effects of Aspirin
Resp alk
Metab acid
