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NSAID Pharmacology Cheat Sheet by

NSAID pharmacology for podiatry

How Do NSAIDs Work?

NSAIDs have anti-i­nfl­amm­atory, antipy­retic, analgesic and anti-p­latelet proper­ties.
Goal is to inhibit the cox-me­diated generation of pro-in­fla­mmatory eicosa­noids and to limit extent of inflam­mation, pain and fever.
They do this by blocking the site in cycloo­xyg­enase enzyme in which substrate arachi­donic acid binds to
Most NSAIDs are metabo­lized in the liver by oxidation and conjug­ation to inactive metabo­lites which are typically excreted in urine
*patient sensitive to one NSAID may be sensitive to any other NSAID. Studies show that meloxicam can be a good option for NSAID intolerant patients

COX-1 Function

Contri­butes to homeos­tasis
Ongoing consti­tutive physio­logic "­house keepin­g", vascular homeos­tasis, mainte­nance of renal, myocardial and GI blood flow, platelet function, intestinal mucosal prolif­era­tion, antith­rom­bog­enesis

COX-1 Inhibition

Decreases mucosal defense
Increase GI acid, and decreases GI mucus
Decreases HCO2 secretion
Decreases mucosal blood flow

Special Consid­eration for NSAIDs

1. Both ibuprofen and naproxen may reduce the effects of furosemide (diuretic) and may reduct the effect­iveness of several antihy­per­tensive agents
2. Indome­thacin is the NSAID most likely to cause nephro­tox­icity

COX 2 Inhibitors

Due to sometimes severe GI adverse effects associated with long-term NSAID therapy, selective cox 2 inhibitors are used
Inhibition of the chemical mediators respon­sible for inflam­mation while mainta­ining the cytopr­ote­ctive effects of the products of COX-1 activity
Inhibition of COX-2 may generate some problems in wound healing, angiog­enesis and the resolution of inflam­mation
Lower GI and renal problems
Cox 2 may induce hypert­ension, renal failure and cardiac failure
Naproxen has some cardio­pro­tective properties

Contra­ind­ication for NSAIDs

Reye's Syndone
For patients under 18 years old
Compro­mised Renal Function
NSAIDs reduce renal blood flow and therefore may further reduce renal function which may have an impact on the effects of concurrent meds and elimin­ation of the NSAID and other meds and toxins
Compro­mised Liver Function
Most NSAIDs are metabo­lised in liver
Happens more in asthmatics

COX 2 Function

Works at the site of pain and inflam­mation
Source of prosta­cyclin- platelet stabil­ity­/dilate blood vessels

COX 2 Inhibition

Decrease pain and inflam­mation
Increases CV risk as it shifts the balance between platelet production TxA2 and PGI2, predis­posing to platelet aggreg­ation, thrombus formation and vasoco­nst­riction


Includes Aspirin which acts in an irreve­rsible manner by acetyl­ating the active site serine residue in both COX-1 and COX-2
Daily low dose aspirin is used as an anti-t­hro­mbo­genic agent for prophy­laxis and post event management of MI and stroke
Aspirin is antith­rom­bogenic because of its irreve­rsible inhibition of COX, which prevents platelets from biosyn­the­sizing TxA2
Within an hour of aspirin, the effects of COX-1 activity on newly formed platelets is irreve­rsibly destroyed (acety­lated) therefore TXA2 cannot be produced
A single admini­str­ation of aspirin decreases for several days the amount of thromb­oxane that can be generated, shifting the vascular TxA2-PGI2 balance toward PGI2 mediated vasodi­lation, platelet inhibi­tion, and antith­rom­bog­enesis
Long term use of aspirin can lead to GI ulceration and hemorr­hage, nephro­tox­icity and hepatic injury
Two unique toxicities of aspirin: induced airway hypera­ctivity in asthmatics and reye's syndrome

NSAID Drug to Drug Intera­ction

Wendy's LAMP
mnemonic for rememb­ering drug intera­ctions
May increase risk of bleeding- Monitor PT and INR
May increase lithium plasma levels and decrease its clearance renally- need to monitor
ACE Inhibitors
may decrease antihy­per­ten­siuve effects so need to monitor BP and CV function
NSAIDs increase BP and decrease affects of diuretics, ACE inhibitors and ARB which all relax blood vessels as NSAIDs inhibit cox-2 in kidneys which decreases sodium excretion due to a decrease in prosta­gla­ndins
NSAIDs may increase fluid retention and decrease blood flow to the kidneys as they block prosta­gla­ndins which dilate blood vessels and allow O2 to reach kidneys
May lead to an increase in methot­rexate toxicity- don't administer within 10 days of high dose methot­rexate
May lead to reversal or uricosuric effects

Non-Se­lective COX 1 and COX 2 Inhibition

GI irritation due to decreased protection of gastric mucosa.- N&V, GI ulcer, diarrhea
Skin reactions - mild rash, hives, photos­ens­itivity
Inhibition of platelet function- increase risk of bleeding
Decreased renal blood flow- decreases GFR can cause renal ischemia- look out for pts w/ renal disease
CVD risk
Respir­atory- bronch­ospasm- look out for asthmatic pts

Risk Factors for GI compli­cations

Over 60 in age
history of peptic ulcer
use of anti coagulants or cortic­ost­eroids
History of pylori infection
High NSAID dose or use of two NSAIDs
Severe illness

Reducing GI risks

Synthetic prosta­gla­ndin- Protects gastric mucosa from irritation
Protein Pump Inhibitors
Long lasting reduction of gastric acid production
Drugs end in -"pr­azo­le"
H2 Receptor Antago­nists
Blocks the action of histamine on parietal cells in the stomach decreasing the production of acid by these cells
Drugs end in -"di­ne"
Not enough evidence that these alone will work in reducing GI issues
COX-2 Inhibitor
Allow continued protective COX-1 function


Not an NSAID
Has analgesic and antipy­retic effects similar to aspirin
anti-i­nfl­amm­atory effects are insign­ificant because of its weak inhibition of COX
May be a third functional COX isoform (COX-3)
MOA believed to involve the prosta­glandin pathways within the CNS with little influence on peripheral prosta­glandin synthesis
Adverse effect= hepato­tox­icity as it is metabo­lized by hepatic cytochrome p450 enyzmes which produces a reactive molecule which is normally detoxified by conjug­ation with glutat­hione. An overdose of acetam­inophen can overwhelm glutat­hione stores, leading to cellular and oxidative damage and in severe cases to acute hepatic necrosis
4000mg daily limit for adults. For those who are alcoholics or multiple medication patients and patients with liver disorders, even doses within the therap­eutic range may be hepato­toxic


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