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NSAID

NSAID 
(Nonsteroidal anti - inflammatory drugs)


• NSAIDs are used alone or in combination.
• They provide symptomatic relief but should not be taken on a long term basis
• Ex= aspirin, naproxen , diclofenac ,paracetamol ,mefenamic acid



• CLASSIFICATION:-

,A. Non selective COXinhibitors (traditional NSAIDs)

1. Snlicylates: Aspirin.
2. Propionic acid derivatives: Ibuprofen,
Naproxen, Ketoprofen, Flurbiprofen.
3. Anthranilic acid derivative: Mephenamic
acid.
4. Aryl-acetic acid derivation: Diclofenac.
Aceclofenac.
5. Oxicam derivatives: Piroxicam, Tenoxica
6. Pyrrolo-pyrrolc derivative: Ketorolac.
7. Indole derivative: Indomethacin.
8. Pymzolone derivatives: Phenylbutazon,
Oxyphenbutazone.

B.Preferential COX-2 inhibitors
Nimesulide, Meloxicam, Nabumetone

C. Selective COX-2 tnhibitors
Celecoxib, Etoricoxib, Parecoxib.

D. Analgesic- antipyretics with poor
antiinflammatory action:

1. Paraalllinophmol derivative: Parae, :
(Acetaminophen).
2. Pymzolone daivatives: Metamizol
rone), Propiphenazone.
3. Bcnzoxazocine derivatiuc: Nefopam

• Strongest NSAIDs= NSAID efficacy generally varied with the dose but acetaminophen was ineffective at all doses tested,
• In constant ,diclofenac 150mg/day was the most effective treatment for both pain and physical disability
• Superior to the maximal doses of ibuprofen,naproxen and celecoxib.


• Indication for NSAIDs include the following :=
1. Inflammatory condition
2. Chronic joint disease
3. Headache
4. Dental pain
5. Menstrual pain
6. Postoperative mild to moderate pain



• How are they taken?????
• They are available as tablets, liquids ,suppositories or creams and gels,
• They dosage will depend on the type of drug.

• NSAID half -life also influences treatment choice :=
• NSAIDs can be divided into short acting and long acting
• Short acting NSAIDs with half -lives less than six hours
• Ex=ibuprofen, have a relatively quick onset of action and are better suited for the treatment of acute pain.
• NSAIDs with longer half -lives :=
• Ex:=naproxen or in long acting formulation are more suited for the treatment of chronic condition.
• As they require only once or twice daily dosing


• Overall mechanism of action and other responses=
• A) anti -inflammatory action=
• 1)inhibition of P.G. bio synthesis = Arachidonic a —>cox(-) PG
• 2)inhibition of chemotaxis =decrease proinflammatory mediator
• 3)down regulation of interleukin -1 production
• 4)decrease production of free radicals =decrease oxidative stress
• 5)decrease sensisitivity of blood vessels to bradykinin and histamine


B)anti - pyretic effect=
• Action =reset the hypothalamic "Thermostate -mechanism" (decrease PGE2)

C)Analgesic effects = decrease mild and inflammatory pain (–cox-2)
• ACTION=
• 1)decrease PG synthesis = decrease sensitivity of nociceptive response
• 2)decrease inflammatory mediator (bradykinin) = decrease pain of arthritis, toothache,musculoskeletal,dysmenorrer,pain dur to other,

• D)Anti-platelet action =All NSAID decrease platelet aggregation =increase bleeding
• Except=1)Cox-2 selective
• 2)non- Acetylated salicylate =Sod. Salicylate

• E)nwqnted effect =(—cox-1)G1-Erosin ,G1Bleeding ,ulcer, decrease renal activity .



• Adverse effects of NSAIDs:-
• Gastrointestinal :-Gastric irritation, erosions, peptic ulceration, gastric bleeding/ perforation, esophagitis

• Renal:-Na+ and water retention, chronic renal failure, interstitial nephritis, papillary necrosis (rare)

• Hepatic:-Raised transaminases, hepatic failure (rare)

• CNS :-Headache, mental confusion, behavioural disturbances, seizure precipitation

• Haematological :- Bleeding, thrombocytopenia, haemolytic anaemia, agranulocytosis

• Others :-Asthma exacerbation, nasal polyposis, skin rashes, pruritus, angioedema


• Drug interaction with NSAIDs:-

• Pharmacodynamic:-
• Diuretics = decrease diuresis
• Beta- blocker =decrease antihypertensive effect
• ACE inhibitors =decrease antihypertensive effect
• Anticoagulants = increase risk g.i.bleed
• Sulfonylureas =increase of hypoglycaemia
• Alcohol = increase risk g.i. bleed
• Cyclosporine = increase nephrotoxicity
• Corticosteroids = increase risk g.i. bleed

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