The document discusses non-steroidal anti-inflammatory drugs (NSAIDs). It covers their classification, mechanisms of action, uses, and adverse effects. NSAIDs work by inhibiting the cyclooxygenase (COX) enzymes and subsequent prostaglandin production. They are effective for pain, fever, and inflammation but can cause gastrointestinal, renal, hepatic, and bleeding side effects. The document focuses on specific NSAIDs including aspirin, ibuprofen, indomethacin, and mephenamic acid, outlining their pharmacology, dosing, and indications.

1. 1

3. CONTENTS:
 Introduction
 Classification
 Various Forms of Delivery of NSAIDs
 Uses of NSAIDs
 Adverse Effects
 Mechanism of Action
 Contraindications
 Individual drug groups in detail
 Selection of NSAIDs
 Conclusion
 References

4. INFLAMMATION
 Inflammation (Latin-inflamatio, to set on fire) is the complex
biological response of vascular tissues to harmful stimuli,
such as pathogens, damaged cells, or irritants.
 It is a protective attempt by the organism to remove the
injurious stimuli as well as initiate the healing process for
the tissue.

5. CAUSES
 Burns
 Chemical irritants
 Frostbite
 Toxins
 Infection by pathogens
 Physical injury
 Immune reactions due to hypersensitivity
 Radiation
 Foreign bodies

6. The classic signs and symptoms of acute
inflammation
English Latin
Redness Rubor
Swelling Tumor
Heat Calor
Pain Dolor
Loss of Function Functio laesa
√ √√√

7. PAIN
 An unpleasant sensory and emotional experience
associated with actual or potential tissue damage.
 There are three type of Pain:
1) Somatic Pain
2) Visceral Pain
3) Referred Pain

8.  Analgesic is a drug that selectively relieves pain
by acting in the CNS or peripheral pain mechanisms,
without significantly altering consciousness.
 Analgesics relieve pain as a symptom without affecting
its cause
Analge
sic

9.  Analgesics are divided into two groups :
1. Opioid / Narcotic / Morphine like analgesic
2. Non Opioid / Non-Narcotic / Non Steroidal Anti
inflammatory Drugs

10. w
NSAIDS

11. INTRODUCTION
 NSAIDS are most widely used therapeutic agents world wide.
 They are frequently prescribed for ‘rheumatic’ musculo-skeletal complaints and
are often taken without prescription for minor aches and pains.
 They have Analgesic, Antipyretic & Anti-inflammatory actions.
 They act primarily on peripheral pain mechanisms but also in CNS to raise the
pain threshold.

12.  They are also called:
 Non narcotic
 Non opoid analgesics
 Aspirin type or antipyretic analgesic
 Compared to morphine they are:
• Weaker analgesics
• Do not depress CNS
• Do not produce physical dependence and
• Have no abuse liability.

13. CLASSIFICATION
Non Selective COX inhibitors
Salicylates Aspirin, Sodium salicylate Diflunisal
Pyrazolone derivatives Phenylbutazone, Oxyphenbutazone
Indole derivatives Indomethacin, Sulindac
Propionic acid derivatives Ibuprofen, Naproxen, Ketoprofen
Anthranilic acid derivatives Mephenamic acid, Flufenamic acid
Aryl-acetic acid derivatives Diclofenac, Aceclofenac
Pyrrolo-pyrrole derivative Ketorolac
Oxicam derivatives Piroxicam, Tenoxicam

14. Preferential COX-2 inhibitors
Nimesulide, Meloxicam, Nabumatone
Selective COX-2 inhibitors
Celecoxib, Rofecoxib, Valdecoxib
Analgesic –Antipyretics with poor Anti
inflammatory action
Para amino phenol derivatives Paracetamol (Acetaminophen)
Pyrazolone derivatives Metamizol (Dypirone),
Propiphenazone
Benzoxazocine derivative Nefopam

15. Routes of analgesic
administration:
 Oral
 Intramuscular Injection
 Intravenous Injection
 PCA: patient controlled analgesia
 Epidural Administration
 Transdermal, Creams, gels
and foams.
 Suppositories
PCA

16. Mechanism of action of NSAIDs:
 When a tissue is injured, from any cause, prostaglandin synthesis in that
tissue increases.
 PGs have TWO major actions:
• They are mediators of inflammation
• They also sensitize pain receptors at the nerve endings,
lowering their threshold of response to stimuli and allowing
the other mediators of inflammation

17. x
Leukotrienes

18.  Naturally, a drug that prevents the synthesis of PGs is likely to be effective
in relieving pain due to inflammation of any kind.
 In 1971 Vane and coworkers made the landmark observation that aspirin
and some NSAIDs blocked PG generation.
 This is they do by inhibiting Cyclo–oxygenase (COX) enzyme in the
pathway for PGs synthesis

19. COX
 COX exists in two isoforms:
 COX-1 (constitutive)
 COX-2 (inducible)
COX-1:
• Present as part of everyday physiological function.
• Involved in the homeostasis of the entire organism.
• Protects the stomach by limiting acid secretion.
• Improves the distribution of blood flow in the kidney.
• Helps platelets limit bleeding by increasing their adhesiveness.
COX-2: Its expression is induced by various stimuli such as the inflammation
or at the site of the injury

20. x √

21. Actions due to PG synthesis inhibition
Benificial Actions Non beneficial
Actions
Analgesia: prevention of pain nerve
ending sensitization
Gastric mucosal damage
Antipyresis Bleeding: inhibition of platelet
function
Anti inflammatory Asthma and anaphylactoid reactions
in susceptible individuals
Anti thrombotic Delay/prolongation of labour

22. NSAIDS-Adverse effects
► Gastrointestinal:
Gastric irritation, erosions, peptic ulceration, gastric bleeding/ perforation, oesophagitis
► Renal:
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

23. NSAIDS -
ContraindicationsNSAIDs should usually be avoided by people with the following conditions:
► Peptic ulcer or stomach bleeding
► Uncontrolled hypertension
► Kidney disease
► People who suffer with Inflammatory Bowel Disease (Crohn's Disease or Ulcerative
Colitis)
► Past stroke (excluding aspirin)
► Past myocardial infarction (excluding aspirin)
► Coronary artery disease (excluding aspirin)
► Taking aspirin for heart
► In third trimester of pregnancy
► Past transient ischemic attack (excluding aspirin)
► Persons who have a history of allergy to Nsaids (allergic-typeNSAID) or hypersensitivity
reactions, e.g. aspirin-induced asthma
https://en.wikipedia.org/wiki/Nonsteroidal_anti-inflammatory_drug#Contraindications

24. Non Selective COX inhibitor
s

25. Salicylate derivatives
Aspirin
 Acetylsalicylic acid
 It was obtained from ‘willow bark’ (Salicaceae) but is now synthesized.
 Irreversible COX inhibitor
Dose: 300-600mg tid.

26. Aspirin – Pharmacological actions:
 Anti inflammatory action:
 Exerted at high doses (3-6g/day or 100mg/kg/day)
 Signs of inflammation are suppressed
 Acts mainly by inhibiting PG synthesis
 Analgesic action:
 Mild analgesic effect ≤ codeine
 Effective in non -visceral pain
 Inhibition of peripheral PG synthesis

27.  Antipyretic action:
 Reduces body temperature in fever.
 Rapidly reduces fever by heat loss.
 But does not decrease heat production.
 Respiration:
 Stimulated at therapeutic doses by peripheral and central
actions.
 Hyperventilation is prominent in salicylate poisoning.
 Further raise of dose causes respiratory depression and death
due to respiratory failure.

28.  CVS:
 No direct effect in therapeutic doses
 Larger doses increase Cardiac Output
 Toxic doses depress vasomotor center.
 GIT:
 Irritate gastric mucosa and cause epigastric distress, nausea and
vomiting
 Also stimulates CTZ
 Heart burn, dyspepsia, gastritis, erosion, gastric ulcers.

29.  Effect on platelets/coagulation:
 It inhibits TXA2 synthesis thus interferes with platelet aggregation and prolongs bleeding
time
 Local irritant effect:
 Cause irritating to the skin & mucosa and destroys epithelial cells.
 Keratolytic effects.
Aspirin burn

30. Aspirin – Adverse effects:
 Side effects – Nausea, vomiting, epigastric distress and occult blood in stools.
 Hypersensitivity and idiosyncracy – Rashes, urticaria, rhinorrhea, asthma,
angioedema and anaphylactoid reactions.
 Anti-inflammatory doses – produces a syndrome called Salicylism – dizziness,
tinnitus, vertigo, reversible impairment of hearing and vision, excitement and mental
confusion.
 Reye’s syndrome - Reye's syndrome tends to occur in previously healthy children
about a week after common viral infections such as influenza or chickenpox.
 The precise reason is unknown, but using aspirin to treat a viral illness or infection may
trigger the condition in children.

31.  Acute salicylate poisoning: Fatal dose in adults is estimated to be 15-30
gm.
 Serious salicylate toxicity (Salicylism) is seen at serum salicylate levels
of  50 mg/dl. Manifestations are:
 Vomiting, dehydration ,electrolyte imbalance.
 Acidotic breathing.
 Hyper / hypoglycemia.
 Petechial hemorrhage's.
 Restlessness, delirium, hallucinations,
convulsions.
 Hyperpyrexia.
 Coma and death due to respiratory faliure
and cardiovascular collapse.

32. Aspirin – Contraindications:
 Peptic ulcer
 Ulcerative colitis
 Gout
 Renal failure
 Patients hypersensitive to salicylates
 Hemophilias
Aspirin – Uses:
 As analgesic – headache, backache, myalgia, joint pain, toothache,
neuralgias and dysmenorrhea.
 As antipyretic
 Acute rheumatic fever
 Rheumatoid arthritis
 Osteoarthritis
 Post myocardial infarction and post-stroke patients

33. Pyrazolone derivatives
Phenylbutazone:
 Potent anti-inflammatory drug.
 Poor analgesic & antipyretic activity
Pharmacokinetics:
 Absorption- 98% bound to plasma proteins.
 Metabolism- Liver.
 Excretion- Urine.
DOSE: 100-200 mg Bid.

34. Adverse effects : More toxic than aspirin.
 Nausea, vomiting, epigastric distress and peptic ulceration .
 Diarrhea
 Edema
 Hypersensitivity: rashes, serum sickness, hepatitis and stomatitis.
 Bone marrow depression, agranulocytosis and stevens-johnson syndrome.
 Goiter and hypothyroidism on long term use.

35. Uses:
 Because of the serious side effects, these drugs should be used only in severe
cases not responding to any other NSAIDs.
 Rheumatoid arthritis and ankylosing spondylitis: for short periods of 1-2
weeks during an acute exacerbation.
 In Acute gout.

36. Indole derivatives
Indomethacin:
Potent anti inflammatory & antipyretic & good analgesic.
Pharmacokinetics:
 Absorption- 90% bound to plasma proteins.
 Metabolism- Liver.
 Excretion- Urine.
DOSE: 25-50 mg bid.

37. Adverse effects:
 Gastric irritation, nausea, anorexia, gastric bleeding and diarrhea are prominent.
 Frontal headache (very common), dizziness, ataxia, mental confusion,
hallucination, depression and psychosis.
 Rashes and other hypersensitivity reactions can also occur.
 Increased risk of bleeding due to decreased platelet aggregation.
Contraindications:
In machinery operators, drivers, psychiatric patients, epileptics, in kidney diseases,
pregnant women and in children.

38. Uses:
 Indicated in rheumatoid arthritis not controlled by aspirin.
 It is particularly efficacious in ankylosing spondylitis, acute exacerbations of
destructive arthropathies and psoriatic arthritis.
 It acts rapidly in acute gout.
 Malignancy associated fever refractory to other antipyretics may respond to
indomethacin.
 It has been the most common drug used for medical closure of patent ductus
arteriosus.
 Bartter's syndrome responds dramatically, as it does to other PG synthesis
inhibitors.

39. PROPIONIC ACID
DERIVATIVES
Ibuprofen, naproxen, flurbiprofen
and ketoprofen:
 All have similar pharmacodynamic properties but differ considerably in potency and to some extent
duration of action.
 The analgesic, antipyretic and anti-inflammatory activity is rated lower than high dose of the aspirin.
 All inhibit PG synthesis naproxen being most potent.
 They inhibit platelet aggregation and prolong bleeding
time.
Dose: Ibuprofen- 400-800mg tid(BRUFEN)

40. Adverse effects:
 Ibuprofen is better tolerated than aspirin. Side effects are milder and their
incidence is lower.
 Gastric discomfort, nausea and vomiting, less than aspirin or indomethacin,
are still most common side effects.
 CNS side effects include headache, blurring of vision, tinnitus and depression.
 Precipitates aspirin induced asthma.
 Fluid retention is less marked.
 They are not to be prescribed to pregnant women and should be avoided in
peptic ulcer patients.

41. Pharmacokinetics and interactions:
 All are absorbed orally, highly bound to plasma proteins (90-99%), but
displacement interactions are not clinically significant.
 Because they inhibit platelet function, use with anticoagulants should, be
avoided.
 They are likely to decrease diuretic and antihypertensive action of thiazides,
furosemide and -blockers.
 All propionic acid derivatives enter brain, , synovial fluid and cross placenta.
 They are largely metabolized in liver by hydroxylation and , glucornide
conjugation and excreted in urine well as bile.

42. Uses:
 Ibuprofen is used as a simple analgesic and antipyretic.
 Ibuprofen and its congeners are widely used in rheumatoid arthritis,
osteoarthritis and other musculoskeletal disorders, specially where pain is
more prominent than inflammation.
 They are indicated in the soft tissue injuries, fractures, vasectomy, tooth
extraction, postpartum and post-operatively.
 Ibuprofen is rated as the safest NSAID by the spontaneous adverse drug
reaction reporting system in the U.K.

43. ANTHRANILICACIDDERIVATIVE(FEN
AMATE)
Mephenamic acid:
 An analgesic, antipyretic and anti-inflammatory drug, which inhibits COX as well as
antagonises certain actions of PGs.
 Mephenamic acid exerts peripheral as well as central analgesic action.
Dose: 250-500mg tid.
Adverse effects :
 Diarrhea is the most important dose related side effect.
 Epigastric distress is complained, but gut bleeding
is not significant.
 Skin rashes, dizziness and other CNS manifestations have occurred.
 Haemolytic anaemia is rare but serious complication.

44. Uses:
 Mephenamic acid is indicated primarily as analgesic in muscle, joint and soft
tissue pain where strong anti-inflammatory action is not needed.
 It is quite effective in dysmenorrhoea.
 It may be useful in some cases of rheumatoid and osteoarthritis but has no
distinct advantage.

45. ARYL-ACETICACID
DERIVATIVE
Diclofenac sodium :
 An analgesic-antipyretic, anti-inflammatory drug, similar in efficacy to
naproxen.
 It inhibits PG synthesis and has short lasting Antiplatelet action.
 Neutrophil chemotaxis and superoxide production at the inflammatory site
are reduced.
 It is well absorbed orally, 99%protein bound, metabolized and excreted both
in urine and bile.
Dose: 50mg bid-tid.

46.  The plasma t ½ is approximately 2 hours.
 It has good tissue penetrability and concentration in synovial fluid is maintained
for 3 times longer period than in plasma, exerting extended therapeutic action
in joints.
Adverse effects : Diclofenac have generally mild adverse effects
 Epigastric pain
 Nausea
 Headache
 Dizziness
 Rashes.
 Gastric ulceration and bleeding are less common
 Reversible elevation of serum aminotransferases can occur; kidney damage is
rare.

47. Uses: Diclofenac is among the most extensively used NSAID
 Employed in rheumatoid and osteoarthritis
 Bursitis
 Ankylosing spondylitis
 Dysmenorrhea
 Post-traumatic and postoperative inflammatory
 Conditions - affords quick relief of pain and wound edema.

48. OXICAM DERIVATIVES
Piroxicam :
 It is a long acting potent NSAID with anti-inflammatory potency similar to
indomethacin and good analgesic-antiplatelet action.
 It is a reversible inhibitor of COX; lowers PG concentration in synovial fluid
and inhibits the platelet aggregation-prolonging bleeding time.
 Thus, it can inhibit inflammation in diverse ways.
Dose: 20mg od - orally

49. Pharmacokinetics:
 It is rapidly and completed absorbed: 99% plasma protein bound; it is
metabolized in liver by hydroxylation and glucoronide conjugation
 It is excreted in urine and enterohepatic cycling occurs.
Uses:
 It is suitable for use as short term analgesic as well as long term anti-
inflammatory drug
 Rheumatoid and osteo-arthritis
 Ankylosing spondylitis,
 Acute gout,
 Musculoskeletal injuries,
 In Dentistry

50. Adverse effects :
 Common side effects are - burn, nausea and anorexia, but it is
tolerated and less ulcerogenic than indomethacin ;causes less
faecal blood than aspirin.
 Rashes and pruritus are seen in < 1% patients.
 Edema and reversible azotemia, have been observed.

51. Pyrollo pyrolle
Derivatives
Ketorolac :
 A NSAID with potent analgesic and modest anti-inflammatory
activity.
 In postoperative pain it has equaled the efficacy of morphine.
 It inhibits PG synthesis and is believed to relieve pain by a
peripheral mechanism.
Dose: 10mg tid(orally)
30mg/dl qid(IV)

52. Pharmacokinetics:
 ketorolac is rapidly absorbed after oral and i.m. administration.
 It is highly plasma protein bound and 60% excreted unchanged in urine.
Adverse effects:
 Nausea, abdominal pain, dyspepsia, ulceration, loose stools, drowsiness,
headache, dizziness, nervousness, pruritus, pain at injection site.
 Rise in serum transaminases and fluid retention have been noted.

53. Contra-indications: It should not be given to patients on the anti-coagulants.
Uses:
 Ketorolac is frequently used in post-operative and acute musculoskeletal pain:
15-30 mg every 4-6 hours (max. 90 mg/ day).
 It can also be used for renal colic, migraine and pain due to due to bony
metastasis.
 It is used in a dose of 10-20 mg 6 hourly short term management of moderate
pain.
 Use for more than 5 days is not recommended.
 It should not be used for obstetric purposes.

54. PREFERENTIAL COX-2 INHIBI
TORS
54

55. Nimesulide:
 Sulfonamide derivative
 Selective inhibitor of PG synthesis and there is some relative COX-2 selectivity.
Pharmacokinetics:
 Absorption- 99%Plasma bound
 Metabolism-Liver
 Excretion- Urine
DOSE- 50-100mg bid , Children-5mg/kg/day

56. Adverse effects
 Epigastralgia, heart burn, nausea, loose motions
 Dermatological rash, pruritus
 Somnolence , dizziness
USES:
 Short lasting painful inflammatory conditions like sports injuries,
sinusitis and other ear-nose-throat disorders, dental surgery,
bursitis, low backache, dysmenorrhea.
 Postop pain, osteoarthritis & for fever

57. Nabumetone:
 Anti-inflammatory agent.
 It possesses less analgesic, antipyretic activities; effective in the treatment
of rheumatoid and osteoarthritis as well as soft tissue injury.
 Nabumetone has caused a lower incidence of gastric erosions, ulcers and
bleeding, probably because the active COX inhibitor is produced in
tissues after absorption.
Pharmacokinetics:
 Absorption-Gut
 Metabolism-Liver
 Excretion- Urine

58. Dose- 1-2g od. Not recommended in children
Adverse effects :
 GI bleeding, Gastritis, Stomatitis, Anemia, Dizziness, Headache, Nausea,
Abdominal pain, diarrhea, Flatulence, Dyspepsia

59. SELECTIVE COX-2 INHIBITOR
S
59

60.  COX-2 selective inhibitor are Celecoxib, Rofecoxib,
Valdecoxib
 It is a form of (NSAID) that directly targets COX-2 which is produced at
the site of inflammation.
 Selectivity for COX-2 can halve the risk of peptic ulceration.
 Cox-2-selectivity does not seem to affect other side-effects of NSAIDs
(most notably an increased risk of renal failure), and there might be
an increase in the risk for heart attack, thrombosis and stroke by a
relative increase in thromboxane.

61. Pharmacokinetics:
 Absorption- Plasma bounded.
 Metabolism-Liver
 Excretion- Urine
Uses of COX2 inhibtiors:
 Osteoarthritis.
 Rheumatoid Arthritis.
 Ankylosing Spondylitis.
 For the management of acute pain in adults.
 Dysmenorrhea.
Dose :
 Celecoxib- 100-200mg bid
 Rofecoxib- 12.5-50mg od
 Valdecoxib- 20 mg bid

62. Adverse effects:
 Celecoxib:
 Abdominal pain, dyspepsia, dizziness, head ache, peripheral edema, insomnia,
mild diarrhea.
 Rofecoxib:
 It can decrease prostaglandin production in endothelial cells and lead to an
inefficiency in declumping and vasorelaxation.
 Diarrhea, nausea, hypertension, dyspepsia, heart burn, URI, UTI, epigastric
discomfort.
 Valdecoxib:
 Cardiovascular Hypertension, Peripheral edema.
 Dizziness, Headache
 Nausea, Abdominal fullness, Abdominal pain, diarrhea, Flatulence, Dyspepsia

63. TOPICAL NSAIDS

64. Topical NSAIDS
 Diclofenac 1% gel
 Ibuprofen 10% gel
 Naproxen 10% gel
 Ketoprofen 2.5% gel
 Flurbiprofen 5% gel
 Nimesulide 1% gel
 Piroxicam 0.5% gel

65. SELECTION OF NSAID

67. • Paracetamol
• Low dose ibuprofen
Mild/moderate pain
• Ketorolac ,diclofenac,
Post op. pain/ short
lasting pain
• Paracetamol
• Ibuprofen, naproxen,ketoprofen
Musculoskeletal pain
• Naproxen, piroxicam,
• Indomethacin, high dose aspirin
Rheumatoid arthritris, AS ,
Acute gout, Acute rh.fever
• Paracetamol
• Cox-2 inhibitorsGI Irritation
• Paracetamol or COX-2 inhibitors
H/O Hyper Sensitive
reaction to NSAIDS
• Paracetamol, ibuprofen and naproxenPaediatric pts
• ParacetamolPregnancy
Lactation • Ibuprofen,Indomethacin,Naproxen

68. Moderate to severe Pain
Moderate Pain
Mild to Moderate Pain
Opiods or Tramadol
NSAIDS or Tramadol
Acetaminophen or
Ibuprofen
A SUGGESTED TREATMENT ALOGRITHM.AMERICAN JOURNAL OF MEDICINE
105, 535_605,1998.
Management of pain in patients with multiple health problems: a guide for the practicing
physician. Ruoff G, The American Journal Of Medicine [Am J Med], ISSN: 0002-9343, 1998
Jul 27; Vol. 105 (1B), pp. 53S-60S

69. Name Available as Dose / Frequency
Salicylates Aspirin 300-350 mg t.i.d
Ibuprofen Brufen 400-600mg t.i.d
Naproxen Naprosyn 250-500mg b.i.d
Diclofenac voveran 50mg b.i.d
Piroxicam pirox 10-20mg o.d
Paracetamol Crocin 300-500mg t.i.d
Indomethacin Indocid 25-50mg t.id

70. 70
CONCLUSION

71.  NSAID is a safe therapeutic alternative for young healthy patients, but should
be used with caution in the elderly.
 Ulcer complications associated with the use of NSAIDs, in high-risk patients,
are often caused by a failure to identify patients risk factors, concomitant use
of aspirin or multiple NSAIDs, and under utilization of gastroprotective agents.
 COX2 inhibitors & some nonselective NSAIDs increase the risk of myocardial
infarction. Physicians must, therefore, take into account both the
gastrointestinal and the cardiovascular risks of individual patients when
prescribing NSAIDs.
 In patients with a low cardiovascular risk, NSAIDs can be prescribed according
to the level of gastrointestinal risk.
 Patients with a moderate gastrointestinal risk (one or two risk factors) should
receive a COX2 inhibitor or an NSAID plus a Proton pump inhibitors (PPI) or
Misoprostol.

72.  Patients with more than two gastrointestinal risk factors or prior
ulcer complications require the combination of a COX2 inhibitor &
PPI.
 Patients with a high cardiovascular risk (e.g. coronary heart disease or
an estimated 10-year cardiovascular risk greater than 10%) should
receive prophylactic aspirin & combination therapy with a PPI or
Misoprostol irrespective of the presence of gastrointestinal risk
factors. Naproxen is the preferred NSAID because it is not associated
with excess cardiovascular risk.

74. References
► K D Tripathi, Essentials of medical pharmacology, Jaypee brothers medical
publishers(P)Ltd, 6th edition (2008).
► Padmaja udaykumar, Text book of Pharmacology for dental and allied health
sciences, Jaypee brothers medical publishers(P)Ltd, 2nd edition (2007).
► Management of pain in patients with multiple health problems: a guide for
the practicing physician. Ruoff G, The American Journal Of Medicine [Am J
Med], ISSN: 0002-9343, 1998 Jul 27; Vol. 105 (1B), pp. 53S-60S
► https://en.wikipedia.org/wiki/Nonsteroidal_antiinflammatory_drug#
Contraindications.
► AMANDA RISSER et al, NSAID Prescribing Precautions, American Family
Physician, December 15, 2009.Volume 80, Number 12

75. 75