Sherman's Stuff
Terms
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- normal salicylates obtained in the diet everyday
- 10-200 mg
- autoimmune inflammation; not from wear and tear
- rheumatism
- salicylates inhibit the biosynthesis of
- PGE2, a mediator of inflammation and pain
- peptide assoc with pain and inflammation
- bradykinin
- dose of salicylate required to see analgesic activity (for inflammation and musculoskeletal-type pain)
- 600-1200 mg
- cause of heat and redness assoc with inflammation
- leakage of protein
- found in all sites where PGs have an action
- COX I
- found only in sites of inflammation, so targeted to decrease ADRs
- COX II
- dose of NSAID required for antopyretic activity
- 600 mg
- how NSAIDs reduce fevers
- induction of PGE2 in the temp regulating hypothalamic center
- causes vasoconstriction and increases aggregation of platelets
- COX I
- causes vasodilation and decreases aggregation of platelets
- COX II
- associated with Thromboxane which causes vasoconstriction
- COX I
- makes vessel walls sticky allowing platelets to clog the lumen
- TX
- PGI2 works against __ to prevent clogging of vessels
- TX
- NSAIDs have a "dose-related elimination half life" which means
- increased dose of NSAID increases dose of salicylic acid which is more difficult to excrete
- and important factor in the CL of salicylates
- urinary pH
- liquid aspirin
- arthropan
- arthropan is aka
- choline salicylate
- NSAIDs have cross-sensititvity with
- tetrazine dye
- oral synthetic analog of PG which is used to decrease NSAID-related ulcers
-
Misoprostol, Cytotec
50-200 mcg qid - toxic dose of NSAID which produces respiratory depression in the medulla
- 10 g
- associated with ASA and viral infections, so you don't give ASA to children under 16
- Reyes' Syndrome
- causes brain swelling, erratic behavior, coma, and maybe death; has no antidote
- Reyes' Syndrome
- decreases synthesis of PG but is weaker than ASA
- Acetaminophen
- APAP is __% less potent than ASA
- 20
- why doesn't APAP have an anti-inflammatory effect?
- peroxides, etc, won't allow it to enter inflammed tissue
- why do peds normally use APAP?
- is available as a liquid because more soluble than ASA (and the Reyes' thing)
- toxic dose of APAP; cross-links DNA
- 8-10g
- generates a toxic intermediate from APAP which can't be conjugated as normal by
- glutathione
- early sx of hepatotoxicity with APAP
- n/v, cramps, jaundice
- antidote for APAP tox
-
Mucomyst (N-acetylcysteine)
oral, 140 mg/kg - how does Mucomyst work against APAP tox?
- will help conjugate the toxic intermediate
- decreases viscosity of secretions with cystic fibrosis
- mucomyst
- may or may not be grouped as an NSAID
- ASA
- Ibuprofen was introduced in __ for this reason
- 1974, circumvent gi probs of ASA
- although __ are more effective at treating arthritis and the like, why aren't they used?
- steroids, like Prednisone; MANY more ADRs
- why were COX II inhibitors designed?
- to decrease gi problems assoc with COX I inhibitors
- inducible in inflammation but also found in gi and renal sites
- COX II
- when you inhibit COX I and PG in mucosal cells, you __ HCL, and __ HCO3 and __ mucus
- increase, decrease, and decrease
- __% patients experience gi distress, ulcers, gasritis, etc. with NSAIDs
- 30-45
- __ of every 1000 patients using NSAIDs for arthritis have serious gi event
- 15
- constitutive housekeeping gene
- COX I
- Relafen, Lodine, Clinoril, and COX II selectives all have a __ GI risk
- decreased
- retains renal blood flow which ppl with acute renal failure rely on
- COX I
- thought to circumvent renal blood flow issue, but not the case
- COX II
- ppl who should not take NSAIDs
- ppl with acute renal failure