Non-Opioid Analgesics Flashcards
Selectivity for COX-1 and COX-2 are associated with which AEs?
COX-1 = undesirable GI effects
COX-2 = increased CV risk
Non-opioid used for self-limiting painful conditions like tension headaches, mild/mod MSK pain, OA, low back pain, mild/mod non-inflammatory nociceptive pain, pts w/gastric problems, analgesic/antipyretic of choice in children
Acetaminophen
APAP usually turns into glutathione and is excreted, but if too much is taken, produces what toxic metabolite that kills the liver?
NAPQI
Clinical presentation of APAP OD
First 24hrs: minimal/no symptoms
24-72hrs: ab pain, liver tender, inc. transaminases, dec. urine, maybe jaundice
4days - 2wks: resolution or death from hepatic failure
Antidote to APAP OD
N-acetylcysteine (Mucomyst)- metabolized to cysteine (a glutathione precursor)
-when not used for this, primarily used for chronic bronchopulm disease, CF, atelectasis from mucous obs.
Acetadote: injectable antidote for APAP OD
How do you treat APAP OD immediately before the antidote?
Activated charcoal
Max adult dose of APAP remains what currently? (Daily)
4g/day
What is the children’s dose for APAP?
10-15mg/kg/dose every 4-6 hrs
AHA recommendations for pain in PTs w/CV risk in order or precedence:
APAP -> ASA -> Tramadol -> Opioids -> Non-acetylated salicylates -> NSAIDs with low COX-2 -> NSAIDs with some COX-2 -> COX-2 selective (celecoxib)
See purple chart for NSAID-related ulcer complications
…
NSAID preferred to lower the risk of CV complications
Naproxen
ASA should be used cautiously in respiratory patients because of what illness?
Asthma
Caution when NSAIDs are combined with ACEI/ARBs because of what?
ACEI/ARB can decrease renal function…and so can NSAIDs
In the presence of both NSAIDs and ACEI/ARB we see a decrease in perfusion pressure of the glomerular, leading to what?
Low GFR
Salicylate toxicity can lead to hyperventilation, children may not have this response, which leads to respiratory alkalosis…sodium bicarbonate is then excreted leading to metabolic acidosis…what is this called?
Mixed acid/base disorder
As little as how much ASA can be fatal?
3000mg…severe intoxication is >300mg/kg
There is no antidote for salicylate toxicity, so what do we do?
Activated charcoal and gastric lavage, O2, glucose if there is AMS, REPLENISH BICARBONATE EVEN IF PH IS UP TO 7.55
All NSAIDs are equally effective
Lower doses are for?
Higher doses are for?
Lower = analgesia Higher = inflammation
NSAIDs should be avoided in the 1st and 3rd trimesters, why?
Can lead to cleft pallet and premature closure of the ductus arteriosus
APAP is the preferred analgesic/antipyretic during pregnancy
List of common NSAIDs
Non-A Salicylates: Salsalate
Aspirin Toradol Naproxen Indomethacin Ibuprofen Nabumetone Meloxicam Diclofenac Celecoxib (Celebrex)
All salicylates cross the BBB and placenta and are absorbed through intact skin, with one exception that doesn’t cross the BBB…
Diflunisal
Non-A Salicylates are less effective than ASA, but also have less effects on platelets, fewer GI SEs, less renal toxicity, and may be preferred when?
When COX-1 inhibition is undesirable in pts with asthma, clotting issues, or renal dysfunction
The Non-A Salicylates, including salsalate, trilisate, and diflunisal are all primarily indicated to treat what?
Rheumatic things, RA and OA…pepto (bismuth subsalicylate) is for GI, AE is the black/dark tongue
Anti-platelet effect of ASA lasts how long?
7-10 days, aka the life of the platelet b/c it’s irreversible
