Nsaids new/cosmetic dentistry courses

NSAIDs
INDIAN DENTAL ACADEMY
Leader in continuing Dental Education
www.indiandentalacademy.com

Contents
• Introduction
• History
• Classification
• Autocoids
• General properties of NSAIDs
• Mechanism of action of NSAIDs
• Descriptions of various drugs
• Choice of NSAIDs
• Adverse drug interactions
• Role of NSAIDs in periodontics
• conclusionwww.indiandentalacademy.com

Introduction
• NSAIDs are also called non narcotic , non opioids or
aspirin like analgesics
• In contrast to the opioid analgesics, the non opioid
analgesics as a group:
1. Relieve pain without interacting with opioid receptors
2. Reduce elevated body temperature
3. Possess antiinflammatory action in different measures.
4. Have antiplatelet activity to varying degrees
5. Do not cause sedation and sleep
6. Are non addicting

History
Medicinial effect of bark of willow-active ingredient
SALICIN
this was converted to sodium salicylate which was first
used in the treatment of rheumatic fever and as
antipyretic in 1875
• Acetyl salicylic acid (Aspirin) was introduced in 1899
• The next major advance was the development of phenyl
butazone
• Recently some selective COX2 inhibitors have been
added

Autocoids
• Are diverse substances produced by wide variety of
cells in the body, having intense biological activity.
Some of the classical autocoids are
1. Amine autocoids –Histamine, 5HT
2. lipid derived autocoids-prostaglandins,
leucotriens,platelet activating factor(PAF)called as
eicosanoids
3. Peptide autocoids- plasma
kinins(Bradykinin,Kallidin,angiotensin
In addition, cytokines,(IL,TNF ) and several peptides like
gastrin may also be considered as autocoids.

Prostaglandins(PGs)
• In 1930 Kurzok and Lieb demonstrated the activity of
human semen on human uterine muscle
• Bergstrom and associates showed that the various PGs
are closely related derivatives of lipid soluble prostanoic
acid
• PGs also present in various other tissue extracts such as
iris, lung,human menstrual fluid, brain, thymus, pancreas
and kidneys.

Biosynthesis of PGs
• Biosynthesized from polyunsaturated fatty acids belonging
either to the linoleic or the alfa lenolenic series.
• The 2 principal PGs are PGE2 & PGF2
• most tissues are capable of synthesizing PGs from the
dietary essential fatty acids.
• In human tissues ,the fatty acid released from membrane
lipids in largest quantity is arachidonic acid
• The chemical, bacterial and thermal insults activate the
phospholipase A and release arachidonic acid from the cell
membrane.
• Thus PGs &LTs are synthesized locally by the release of
arachidonic acid from membrane lipids in response to
appropriate stimuli.

Pharmcological actions of PGs
• On smooth muscles-
cause contraction of uterine muscle in both pregnant and
non pregnant women in vivo.
Pathophysiological role-
• It has been postulated that PGs mediate initiation and
progression of labour
• Dysmenorrhoea in many women is associated with
increased PG synthesis by the endometrium.this induces
incoordinated uterine ischaemia->pain.

On gastrointestinal system-
• PGE2 & PGI2 synthesized by cox, inhibit the gastric acid
secretion, enhance the mucosal flow & thus have
cytoprotecyive effect on gastric and duodenal mucosa in
humans.
• On CVS-
PGE2 & PGF2 cause vasodilationin most of the vascular
beds.(whereas TXA2 consistently produces
vasoconstriction.)
The vasodilator effect is mainly localised to the arterioles,
precapillary spinchter and post capillary venules.The BP
falls and the blood flow to most of the organs increases.

On platelets
• The PGI2 (synthesized by the endothelium) is a
vasodilator and inhibits platelet aggregation;where as
TXA2 is a platelet derived prostaglandin,it activates
platelet aggregation and is a potent vasoconstrictor.
• Thus PGI2 and TXA2 are opposite in function.
• Its role
Because of its opposing action there is a balance
mechanism of human platelet function
Role in inflammation
PGE2 and PGF2 and PGD2 are the major metabolites in the
cyclooxygenase pathway in the mast cells.
It causes vasodilation & potentiates edema formation.
The PGs are also involved in the pathogenesis of pain and
fever in inflammation
•Some of the beneficial action due to PG synthesis inhibition:•Some of the beneficial action due to PG synthesis inhibition:

Some of the beneficial actions due to
PG synthesis inhibition:
• Analgesia
• Antipyresis
• Anti inflammatory
• Anti thrombotic
• Closure of ductus arteriosis

Shared toxicities due to PG synthesis
inhibition
• Gastric mucosal damage
• Bleeding:inhibition of platelet function
• Limitation of renal blood flow:Na and water retention
• Delay/ prolongation of labour
• Asthma and anaphylactoid reactions in susceptible
individuals

Difference between
opioids Non-opioids
•Act within the CNS
•used in severe type of
pain as in MI,
burns,fracture
•Do not have anti pyretic
action
•No antiinflammatory
action
•No uricose uric effect
•Have drug dependence
and drug addiction
•Act peripherally at the
peripheral nerve endings
•Used in mild to moderate
inflammatory pain
•Reduce fever;have
antipyretic action
•Reduce cardinal signs of
inflammation
•Have uricose uric effect
•No drug dependence

Classification
A). Nonselective COX inhibitors (conventional NSAIDS).
1. Salicylates: Aspirin, Diflunisal.
2. Pyrazolone derivatives: Phenylbutazone, oxyphenbutazone.
3. Indole Acetic Acid derivatives:Indomethacin, Sulindac.
4. Propionic Acid derivatives: Ibuprofen, Naproxen, Ketoprofen,Flurbiprofen.
5. Fenamates: Mephenamic acid, Enphenamic acid, Fluphenamic acid.
6. Phenyl acetic acid derivatives: eg. Diclofenac,ketorolac
7. Oxicam derivatives: Piroxicam, Tenoxicam.
B). Preferential COX-2 inhibitors: Nimesulide, Meloxicam, Nabumetone
C). Selective Cox-2 inhibitor: Celecoxib, Rofecoxib, Valdecoxib.
D). Analgesic- antipyretics with poor anti-inflammatory action.
1. Paraaminophenol derivative: Paracetamol (Acetaminophen).
2. Pyrozolone derivatives: Metamizol (Dipyrone), propiphenazone.
3. Benzoxazocine derivative: Nefopam.

Mechanism of action of NSAIDs
• In 1971,Vane & coworkers made the landmark observation
that aspirin and some NSAIDs blocked PG generation.this
is now considered to be the major mechanism of action of
NSAIDs.
• There is a well known fact that PG participated in the
pathogenesis of inflammation & fever.Inhibition of
biosynthesis of these autocoids will explain the action of
the drug
• The cyclooxygenase enzymes exist in 2 isoforms
COX1 AND COX2

• The COX1 is constitutive.cox1 is present in nearly all
cell types at a constant level and is involved in tissue
homeostasis.
• COX2 normally present in small quantities is absent
from cells except those of kidney and brain)
COX2 is induced by cytokines IL2 and TNF, in activated
leucocytes and other inflammatory cells.
Thus cox1 is physiological while cox2 is usually but not
always) pathological.
Most NSAIDs inhibit cox1 & cox 2 non selectively,but now
selective cox-2 inhibitors have been produced.

Mechanism of action of analgesia
PG induced hyperalgesia by affecting the transducing
property of free nerve endings.
PGs sensitize the chemical receptors of the afferent
pain endings to other mediators such as
bradykinin,and histamine.
NSAIDS when administered,they block the pain
sensitizing mechanism induced by bradykinin and
other algesic substances.

MECHANISM OF ACTION AS ANTI
PYRETIC
:
• NSAIDS reduce body temperature in fever but don’t
cause hypothermia in normothermic individuals
• Fever during infections is produced through the
generation of pyrogens,ILs,TNF,interferons which
induce PG production in hypothalamus.
• They raise the temperature set point in hypothalamus.
• NSAIDs block the action of pyrogens and fever is
reduced

ANTI INFLAMMATORY ACTION
The anti inflammatory potency of different compounds
roughly corresponds with their potency to inhibit
cox
Certain NSAIDs may act by additional mechanism
inducing inhibition of activity of some of the other
mediators.
Other mechanisms also play an important role
Ex:indomethacin inhibits phosphodiesterase and
increases the intra cellular conc.of cyclic AMP.
Cyclic AMP has been shown to stabilize membranes
including lysosomal membranes in PMNs.
This prevents the release of enzymes important in the
inflammatory response
Further the anti inflammatory drug appear to act
inhibiting the activation of T lymphocytes and thus
inhibits release of cytokines.

SALICYLATES:
• Salicylates are esters of salicylic acid
• Ex:methyl salicylate and sodium salicylate
• Can also occur as esters of salicylic acid
• Aspirin is one of the oldest analgesic, anti
inflammatory drug and is still widely used
• Pharmacological actions:
• 1) analgesic,anti pyretic anti inflammatory action:
• Aspirin is weaker analgesic than morphine type
drugs
• Aspirin 600mg <= 60mg codine.
• Salicylates unlike the opioid analgesics produces
relief of pain with out hypnosis or inducing sleep
• The analgesic action is mainly due to blocking of
peripheral pain receptors and prevention of PG
mediated sensitization of nerve endings.

• As anti pyretic:
• As salicylates act centrally and reset the thermostatic
mechanism at normal level and there by bring down the
temperature.
• Anti inflammatory activity:
• Salicylates suppress the clinical signs of inflammation
• Vaso dilation and leukocyte infiltration are suppressed
they reduce the inflammatory component of the
disease by
• Inhibiting PG synthesis in the peripheral tissues
• Reducing the capillary permeability there by minimizing
the exudation of fluid and development of inflammatory
edema.
• Inhibition of neutrophil aggregation and activation

• METABOLIC EFFECTS:
• Cellular metabolism is increased specially in,skeletal
muscles.due to oxidative phosphorelation by
salicylates there is increased heat production
• Large doses of salicylates may lead to
hyperpyrexia,increased protein catabolism.large doses
of salicylates produce hyperglycemia and glycosuria in
normal individuals.
• This is due to central sympathetic stimulation which
causes release of adrenaline and corticosteroids

On respiration
• Salicylates stimulate respiration as a result of direct
and indirect actions.
• Therapeutic doses of salicylates increase the
consumption of oxygen by the skeletal muscles.this
results in increased co2 production .increased co2
causes direct production of the respirator centre
producing an increased in the depth and rate of
respiration.
• Salicylates also stimulates the medullary respiratory
centre directly.
• They also stimulate the chemoreceptors. This
produces an increase in the rate as wellm as the
depth of respiration leading to hyperventilation.

Acid base balance & electrolytes
• When there is respiratory ankylosis produced by
therapeutic doses of salicylates,to compensate this
there is excretion of alkaline urine containing bi
carbonate.
• Along with it Na,K are also excreted.
• In addition water is also lost.Dehydration rapidly
occurs.since more water is lost through the lungs and
by sweating,dehydration is associated with
hypernatremia.

Effect on GIT
• The ingestion of salicylates may produce
• Dyspepsia,nausea and vomiting as a result of gastric
irritation
• Peptic ulceration with GI bleeding leading to
hematemesis or melena
• The salicylates remain un ionised because of the acidic
Ph of the stomach the non ionised form of salicylates is
water soluble;hence it tends to adhere to the gastric
mucosa ther by producing irritation.
• Salicylates also reduce the motility of the stomach and
increase the period of contact of salicylates with the
gastric mucosa.

Immunological effect
• Salicylates suppress a variety of Ag-Ab reactions in
vivo including systemic anaphylaxis in rabbits and
serum sickness in man.
• They also prevent the release of histamine as a result
of Ag-Ab reaction.
• They suppress cell mediated immunity
• Interfere with vitamin K in liver
• Reduce pro thrombin level
• Reduce ESR
• Reduce leukocyte count

Blood and platelets
• When there is leukocytosis the salicylates lower the
leukocyte count
• Aspirin inhibits platelet aggregation.aspirin action is
unique in that it irreversibly inhibits cox by
acetylation thus by inhibiting cyclo oxygenase,it
supresses the synthesis of thromboxane A2 in the
platelets
• This property is made use in post myocardial
infarction and post stroke patients

Uricosuric effects
• Dose related effects is seen
• In small doses less than 2 gm per day
urate retention and antagonism of all other
uricosuric drugs
• In moderate dose 2-5gm/day.
variable effects,often no change
• In large doses >5gm/day
cause increased urate excretion

CVS effects
• Therapeutic doses of salicylates donot produce any
deleterious effects on the CVS
• But larger doses increase cardiac output to meet
increased peripheral oxygen demand and cause vaso
dilation and BP falls.

Endocrine effects
• Salicylate interfere with the binding of thyroid
hormones with their binding proteins,especially
thyroxine binding albumin.
• Thus T3 and thyroxine values are altered.

Pharmacokinetics
• Both salicylic acid methyl salicylate are absorbed from
intact skin when applied locally
• Given orally salicylates are absorbed from the stomach
and largely from the small intestine.
• microfining the drug particles and inclusion of an alkalie
enhances absorption.
• A single therapeutic dose is absorbed with in 30 min
peak plasma levels is achieved with in 2 hours
• After absorption 80% of salicylate is bound to plasma
protein
• Excretion –the metabolites are excreted by glomerular
filtration as well as tubular secretion

• The plasma half life of salicylates ranges from 2-8 hours
• The plasma t1/2 of aspirin is 15 to 20 minutes
• That means salicylates exihibit dose dependent
excretion

Adverse reaction of aspirin
a) Side affects- occur at analgesic dose (o.3-1.5g/day)
nausea, vomitting, epigastric distress increased occult
blood loss in stools.
most important-gastric mucosal damage and peptic
ulceration
b)Hypersensitivity and idiosyncracy
Reactions include rashes, fixed drug eruptions,
urticaria,rhinorrrhoea, angioedema, asthama and
anaphylactoid reactions.
Aspirin is sometimes involved in the precipitation of
bronchospasm
Aspirin can induce idiosyncratic, mild hemolysis in
individuals with G6PD deficiency.

c)Salicylism-
this syndrome develops when plasma level exceeds
25mg%.
Characterised by headache, dizziness,vertigo, tinnitus,
reversible impairment of hearing& vision
Drowsiness lethargy and mental confusion may also
occur.
In such cases the dosage has to be reduced

d) Reye’s syndrome
• Seen in children <12 years
• Is a rare form of hepatic encephalopathy seen in
children having viral infection
• An association with aspirin therapy and reye’s
syndrome has been noted

Acute salicylate poisoning
• Seen in overzealous therapy in infants or on
accidental ingestion by children.
• Serum salicylate level of 50mg% indicates mild
toxicity.
• Levels above 75mg% is fatal(15-30gm in saliva)
• Manifestations are
vomitting, dehydration,electrolyte
imbalance,acidotic breathing,hyperglycemia
hyperpyrexia,GI irritation and occasional
hemorrhage.
• Treatment –external cooling & i.v fluid with
Na,K, HCO3
-
and glucose if hypoglycemia is
seen.

Precautions and contraindications
• Aspirin is contraindicated in patient who are sensitive to it
and in peptic ulcer, bleeding tendencies,in children
suffering from chicken pox or influenza
• In chronic liver diseases cases of hepatic necrosis
• Avoided in diabetics and congestive heart failure
• Aspirin to be stopped 1 week before elective surgery and
dental extraction
• In pregnant women, latating mothers
• Avoid high doses in G6PD deficient individuals since
hemolysis can occur.

Preparations and dosage
1. Aspirin as acetyl salicylic acid as 300-600mg tablets
2. Dose :4-6 hourly maxi.4gm/day for relief of moderate
pain
3. In the Rx of acute rheumatism 4-8gm daily in divided
doses.
4. Soluble aspirin tablet as 300-600mg
5. Buffered aspirin – contain aspirin along with antacid
like magnesium hydroxide, aluminium hydroxide
6. Sodium salicylate 500mg tab
7. Lysine acetyl salicylate – i.v infusion of this
preparation may be used to treat post operative pain

Interactions of aspirin
1. Aspirin displaces warfarin, naproxen, sulfonyl
ureas,phenytoin and methotrexate from binding sites
on plasma proteins; toxicity of these drugs may occur.
2. It inhibits tubular secretion of uric acid (at analgesic
doses) and antagonizes uricoseuric action of
probenicid.
3. It blocks the diuretic action of furosemide or thiazides
and reduces K+ conserving action of spironolactone.
4. Aspirin interferes with vit K synthesis in liver and
thereby reduce prothrombin level and prolong the
bleeding time.
Aspirin like drugs are synergistic with anticoagulants

Uses of aspirin
1. Local application-salicylic acid is used for its
keratolytic,fungistaticand mild antiseptic
activity.
2. As analgesic-for headache, tooth ache,
backache, myalgia, joint pain, muscle pull,
neuralgias and dysmenorrhoea.
• Used alone or in combination
• Analgesic effect is maximal at 1gm.
3. As antipyretic
effective in fever of any origin.
dose is same as for analgesia
However paracetamol being safer is generally
preferred www.indiandentalacademy.com

4. In acute rheumatic fever- first drug to be used in all
cases
5. In rheumatoid arthritis
6. Osteo arthritis- it affords symptomatic relief only .
7.Postmyocardial infarction and post stroke patients

Drug Combination Effect Management
Options/Considerat
ions
Oral anticoagulants
with all NSAIDs
Increased oral
warfarin activity
Increased risk of
bleeding
(especially GI)
Monitor
prothrombin time
and for occult
blood in stool and
urine
Avoid concurrent
use of aspirin
Lithium with all
NSAIDs
Increased steady
state lithium
concentration
Lithium toxicity
Monitor lithium
concentrations
carefully
Interactions less
likely with aspirin
than naproxen
sodium or
ibuprofen

Antihypertensive agents
(beta-blockers, ACE
inhibitors, vasodilators,
diuretics) with several
NSAIDs
Antihypertensive effect
antagonized
Hyperkalemia may occur
with potassium-sparing
diuretics and ACE
inhibitors
Monitor blood pressure
and cardiac function
Monitor potassium
concentration
Low-dose aspirin (e.g., 75
mg/day) may not interact
with ACE inhibitor
Digoxin with NSAIDs Renal clearance inhibited Monitor digoxin
concentrations
Adjust dose as necessary
Valproate with aspirin Oxidation of valproate
inhibited
Up to 30% reduction in
clearance
Possible valproate toxicity
Avoid aspirin with
valproate
Naproxen sodium is an
alternative
Phenytoin with ibuprofen and
high-dose salicylates
Increased phenytoin
levels: phenytoin is
displaced from serum
protein binding sites, if
phenytoin metabolism is
saturated or folate
concentrations are low
Monitor unbound
phenytoin concentrations
and adjust dose, if
necessary
Ensure patient has
sufficient folate intake

Methotrexate with all
NSAIDs
Reduced renal clearance
Increased plasma
methotrexate
concentration
Avoid NSAIDs with high-
dose methotrexate
Monitor concentrations
with concurrent therapy
Antacids (in high doses)
with salicylates, aluminum
hydroxide,and naproxen
sodium
Salicylate concentrations
possibly reduced by 25%
Aluminum hydroxide
decreases naproxen
sodium absorption
Monitor clinical status
Determine if salicylate
dose needs to be
increased
Probenecid with naproxen
sodium
Cephalosporins with
aspirin
Reduced clearance of
naproxen sodium
Possible increased
bleeding risk
Monitor for adverse effects
Avoid concurrent use
H2-blocking agents with
salicylates, naproxen
sodium
Potential salicylate toxicity
Potentially reduced
naproxen sodium effect
Monitor salicylate
concentration
Monitor clinical status

Corticosteroids with
aspirin; salicylates (high
doses)
Possible decreased
salicylate effect due to
increased clearance
Monitor salicylate
concentration when
changing corticosteroid
dose
Insulin with salicylates Possible decreased
hypoglycemic effect with
large salicylate doses
Monitor blood glucose
Sulfonylureas with
salicylates (moderate to
high-dose
Hypoglycemic activity
increased
Avoid concurrent use
Monitor blood glucose
concentrations
when changing salicylate
dose
Aminoglycoside antibiotic
sand NSAIDs
Inhibits aminoglycoside
renal clearance
Monitor antibiotic
concentrations and adjust
dose as needed

Uses of aspirin
1. Local application-salicylic acid is used for its
keratolytic,fungistaticand mild antiseptic activity.
2. As analgesic-for headache, tooth ache, backache,
myalgia, joint pain, muscle pull, neuralgias and
dysmenorrhoea.
• Used alone or in combination
• Analgesic effect is maximal at 1gm.
3. As antipyretic
effective in fever of any origin.
dose is same as for analgesia
However paracetamol being safer is generally preferred
4. In acute rheumatic fever- first drug to be used in all
cases
5. In rheumatoid arthritis

Paraaminophenol derivatives
• Eg.paracetamol, phenacetin, acetanilid
• Paracetamol is the deethylated active metabolite of
phenacetin.
• Actions
Exerts analgesic and antipyretic effects like salicylates i.e
it raises pain threshold.
Has a weak peripheral anti inflammatory action.
more active on cox in the brain.
• Compared to salicylates, it does not produce
gastrointestinal irritation, Acid –base balance, electrolyte
imbalance, nor does it effect clotting.

Pharmacokinetics
• Paracetamol is well absorbed orally.(only 1/3 is protein
bound in plasma).
• Peak plasma levels are reached within ½ to 1 hour.
• Plasma t1/2 is 2-3 hours
• It is metabolised in the liver and the metabolites excretd
in urine as conjugation products of glucuronic and
sulfuric acids

Adverse effects
• Hepatic and renal toxicity –occurs after years of heavy
ingestion of analgesics.it causes hepatocellular
damage and renal tubular necrosis and may cause
death.
• Pathological lesions like tubular atrophy followed by
renal fibrosis is seen.
• Paracetamol may ause fever, neutropenia,
thrombocytopenia, nephropathy and skin reactions.
• It may rarely produce anemia as a result of
hemolysis.individuals with G6PD deficiency may
exhibit increased sensitivity to this drug.

Therapeutic uses of paracetamol
• It is a suitable substitute for aspirin for analgesic or
antipyretic uses, particularly
• valuable for patients in whom aspirin is
contraindicated.eg.those with peptic ulcer.
it does not prolong bleeding time.
• One of the most commonly used over the counter
analgesic for headache, musculoskeletal pain,
dysmenorrhoea etc
• Recommended as first choice analgesic for
osteoarthritis
• One of the best drugs to be used as antipyretic
• Can be used in all age groups
• Does not have significant drug interaction.

• Dose:500 mg is used as analgesic and antipyetic.
• Total daily dose should not exceed 2.5gm in adults
• It can be used in a liquid form in children
• Can be used as injection Febrinil(150mg/dl)
• Aspirin+ Paracetamol gives an additive synergestic effect. i

Pyrazolone derivatives
a. These are aminopyrine & antipyrine
b. Phenylbutazone &oxyphenbutazone
c. Metamizol (dipyrone) & prophenazone
The first group is not used because there was high
incidence of agranulocytosis.
The second group are also rarely used coz of increased
risk of bone marrow deoression.
The third group are now available in India and are
primarily used as analgesic and antipyretic ,
But is a poor antiinflammatory.
Dose : 0.5-1.5 g oral/ i.m/ i.v

Metamizol available as Analgin 0.5g tab
novalgin,Baralgam0.5g tab, 0.5/ml in
2ml
•Propiphenazone: dose 300-600mg TDS
preparation available as SARIDON
(propiphenazone150mg+paracetamol 250mg tab )

Indole Derivatives
• Eg. Indomethacin
• Is a potent antipyretic and analgesic
• Is a potent inhibitor of PG synthesis and suppress
neutrophil motility
• pharmacokinetics-
Is well absorbed orally.It is 90% bound to plasma
protein, partly metabolised in liver to inactive
products and excreted by kidney,
• Dose :25-50mg QID.
• Available as Indocid, Indoflam.
• Uses : indicated in rheumatoid arthritis, not
controlled by aspirin.
• Acts rapidly in acute GOUT.

Propionic Acid Derivative
• Eg. Ibuprofen, naproxen, ketoprofen, flurbiprofen
• Ibuprofen was the first member of this group to be
introduced.
• The analgesic antipyretic and antiinflammatory effect is
similar to aspirin
• All inhibit PG synthesis and also prolong bleeding time
• Pharmacokinetics-
all are well absorbed orally, highly bound to plasma
protein(90-99%) and like aspirin displace drugs such as
Hydantoins, Sulfonyl ureas and Warfarin

Adverse effects
• Ibuprofen and all its congeners are better tolerated than
aspirin.
• Side effects are milder and their incidence is lower.
• Gastric irritation, nausea, vomitting are common.
gastric erosion and occult blood loss are rare.
• CNS side effects include headache, dizziness, blurring of
vision, tinnitus and depression.
• Not prescribed to pregnant women and should be avoided
in peptic ulcer patient.
• These drug may precipitate aspirin induced Asthma

uses
• Widely used in rheumatoid arthritis, osteoarthritis and
other musculoskeletal disorders
• Are indicated in soft tissue injuries ,fractures,
Vasectomy, tooth extraction,postpartum and post
operatively suppress swelling and inflammation.
• Ibuprofen –has been related as the safest conventional
NSAID by the SPONTANEOUS ADVERSE DRUG
REACTION REPORTING SYSTEM IN U.K

ARYL Acetic Acid derivatives
• Eg. Diclofenac
• This drug has substantially greater activity than
Indomethacin, Naproxen and other NSAID.
• It inhibits PG synthesis and has short lasting antiplatelet
action.
• It is well absorbed orally, 99% protein bound.
• Metabolized and excreted both in urine and bile.
• Plasma t1/2 is 1-2 hours.
• Diclofenac accumulates in synovial fluid after oral
administration

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