Anti-inflammatories - NSAIDs Flashcards
Which level do NSAIDs works?
perception, projection, modulation, transmission, transduction?
transduction (skin, muscle, bone, joint, viscera) - reduces inflammation that causes the pain
Inflammation can be caused by insults to the body. What is the common insult?
disruption of cell membrane integrity. Membrane phospholipids are exposed to enzymatic attack
Name the types of stimuli for inflammation…
physical trauma thermal ichhaemia Ag-Ab interaction infection
Draw ‘review of Inflammation 1-3 flow chart… It forms the basis of the whole lecture!
slide 9…
NSAIDs are most effective during which phases?
acute & subacute phases
Isoform COX-1 is also known as …? what are its functions?
‘constitutive’ - functions as ‘house-keeping’ and protective roles in blood vessels, GASTROintestinal mucosa & kidney
PGE2 & PGI2
Isoform COX-2 is also known as …? what are its functions?
‘induced’ - after insult (ischaemia, infection…) -> mediators of inflammation, pain & pyrexia
Most NSAIDs inhibit COX-?
COX-2
How does inhibition of COX-2 reduce side effects?
by sparing “good” COX-1
How does a drug “know” the difference between a COX-2 & COX-1?…
COX-2 channel is a little wider than COX-1, allowing NSAID to enter & bind to COX-selective site
Why is nanna’s knee not cured after admin. of celecoxib when she says she feels better?
The drug (NSAID) stops further ACUTE inflammation via COX-2 -> knee feels better….but….damage from chronic pain is almost permanent -> this treatment aka -> “bandaid solution” in terms of chronic arthritis
Firocoxib vs Carprofen…Which NSAID is more potent? Which is more effective as an NSAID? Which is safer?
firocoxib more potent, effective & safer as it is more selective for COX-2
Paracetamol pros & cons…
pros - inhibits COX via arachadonic acid, no GIT ulceration
cons - peroxides inactivate paracetamol; only works in brain or mild inflammation; can cause hepatic necrosis in cats
How many human deaths in US due to NSAIDs?
16.5k
Side effects of NSAIDs are commonly seen where?
- GI tract
- Altered PLATELET FUNCTION
- kidney
NSAID side effects are nearly entirely related to the inadvertent inhibition of COX-?
COX-1
How do NSAIDs cause side effects in the GI tract…?
inhibiting “good” PGs which inhibit acid secretion, increase mucosal blood flow & mucous production -> erosion, ulceration & haemorrhage
Re. side effects in the GI tract…how can they be alleviated? 3 methods…
- H-2 blockers (ranitidine) & PPI (omeprazole) - GOLD STANDARD FOR TREATING ULCERS -> decreases acid secretion
- PGE1 analogue (misoprostol) (ulcer prevention)
- sucralfate (protects ulcers already formed)
How do NSAIDs cause ALTERED PLATELET FUNCTION…?
NSAIDs decrease thromboxane & PGI2 -> a net decrease in platelet aggregation potentially resulting in abnormal bleeding
How do NSAIDs cause side effects in the kidney…?
PGE2 & PGI2 (increase salt & water excretion & blood flow to kidney) & when NSAIDs inhibits them -> Water retention → hypertension & decreased renal blood flow papillary → necrosis and nephritis
Safest NSAID & why?
celecoxib as it targets COX-2 moreso than COX-1
List the NSAID indications…
- analgesia: sx (desexing, orthopedics), trauma, arthritis
- anti-inflammatory
NSAIDs commonly used in small animals…List & briefly discuss their clinical use and potential side-effects (SE)
- meloxicam: good analgesic (peri-operative); good for exotics; cat-friendly preps [low]
- firocoxib: lowest SEs (COX-2 selective); good analgesia (esp chronic therapy)
- carprofen: very commonly used, good analgesia (peri-op)
NSAIDs commonly used in production animals…List & briefly discuss their clinical use and potential side-effects (SE)
- flunixin: old, cheap, established WHPs, trusted
- tolfenamic acid: more $, possibly fewer SEs than flunixin, established WHPs
