NSAIDS! Flashcards
3 main effects of NSAIDs
- Analgesic
- Antiinflammatory
- Antipyretic
What are the effects of protaglandins
one of the main mediators of inflammation causing sensitization of nociceptors, dilation of peripheral vessels and local edema
How do NSAIDs affect the production of protiglandins
inhibits cyclooxagenases stoping production of prostaglandin from arachonic acid
What is COX-1 used for and where is it found
found throughout body
Important for the productuon of prostaglandins (PGE, PGI2) that are cytoprotective for gastric mucosa (inhibit acid sec)
What is COX 2 and where is it found
Inducable enzyme (low normally but increased w needed) or expressed in kidney, CNS
Responsible for the production of protaglandins that mediate the inflammatory response
Salicutic acid drugs (ASA) effects (3)
- Analgesia peripheral and central
- effect on hypothalamus to decrease heat loss
- increases uric acid secretion (to avoid accumulation in jts)
ASA duration of action and how is it metabolised in the body
-duration of action 4 hours
Hydrolyzed by estarases in blood/tissues to salicylate and acetic acid
excreted in urine (enhanced by alkaline urin)
what is the MOA for antipyretic effects
inhibition of the synthesis of PGE2 (wont be able to increase set point of hypothalamus)
what is the MOA for the antiinflammatory effects
inhibits protaglandins leading to decreased vasodialation, edema, decreased leukocyte migration and stabilization of membranes
Indications of use of ASA (4)
- mild/mod pain
- relief of fever in febile pts
- antiinflamatory
- prevent clot formation in cerebral + coronary vessels
Geneeral Advese affects of ASA
epigastric distress, nausea, vomitting, microscopic bleeding
-gastric ulceration and bleeding due to inhibition of protaglandin protection
What has ASA been associated with in children
in children w chickenpox, influenza administratin of ASA has been associated with development of Reyes syndrome
How can NSAIDs affect BP
NSAIDs tend to promote sodium retention which may cause an increase in BP
What can repeated NSAID taking lead to
tinnitis, mental confusion, kidney tox, prolonged prothrombin time
What does NSAIDS do to uric acid at high/ low doses
at high doses: loss of uric acid in urine
at low doses: retention of uric acid
What is the benifit of Ibuproden
Generally better tolerated than ASA, though may cause some git probs and bleeding
Naproxon use in combonaton
Used in combo with methocarbamol (mm relaxant for tx of mm spasm and backache
Oxicams characteristics (4)
Amphoteric- 2 sites for ionazation depending on PH conditions
Long half life*- 2-3x most nsaids
Low dose
Selectively stops COX2 (less git effects)
Example of oxicam
Meloxicam
What is idomethacin used for/ good at and side effect
Inhibits protaglandin synthesis, very potent anti inflammatory
-may cause more serious git problems and CNS complaints
what is an example of a selective cox 2 inhibitor and what does it not have a major impact on
Celecoxib
claimed no sig affect on platelet aggregation or bleeding time
What does acetaminophen selectively inhibit and its main effects
V weak inhibitor of COX 1/2
-pot inhibitor of COX 3??
-Little antiinflammatory action but more central analgesia and some antipyeretic
Which Nsaids have more Cox 1 selectivity (3) and Cox 2
Cox 1- Ibuprofen, naproxen, asprin
Cox 2- Celecoxib
Which is the tx of choice for arthritic diseases
ASA
What was used for serious inflammation but now not used due to toxicity
Gold salts
