This whole slide is all about the NSAIDs in detail
it contents - 1. Inflammation 2. NSAIDs 3. Salicylate (Aspirin)
4. Propionic Acid Derivatives (Ibuprofen) 5. Anthranilic Acid Derivatives[Fenamate] (Mephenamic Acid)
Related questions about above topics
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2. Overview
1. What’s inflammation – Importance and sign of
inflammation.
2. NSAIDs – Introduction, Mechanism, Physiology of
pain, Classification.
3. Salicylate – (Aspirin) Introduction, Synthesis,
Pharmacology[Pharmacodynamic,Pharmacokinetics],
Adverse Effect, Uses, Interaction, Precaution &
Contraindication.
4. Propionic Acid Derivatives – (Ibuprofen)
Introduction, Pharmacology, Uses, Side Effect.
5. Anthranilic Acid Derivatives [Fenamates]
(Mephenamic Acid) Pharmacology, Uses, Side Effects.
6. Related Questions
3. NSAIDs
• It produces anti-inflammatory action means it
acts against the inflammation.
What’s Inflammation
• Inflammation is derived from Latin word
inflammatio which means to set on fire.
• It’s a complex biological responses of body
tissues to harmful stimuli, such as pathogens,
damaged cells, or irritants.
• this complex process involvesseveral immune
cells, blood vessels and molecular mediators.
4. Importance of Inflammation
• Inflammation occurs in body to eliminate the initial
causes of cell injury, clear out necrotic cells and
tissue damage.
Latin Word Meaning Due to
Calor Heat Local vessel dilation
Dolor Pain Local release of enzymes & increased
tissue pressure
Rubor Redness Local vessel dilation
Tumor Swelling Influx of plasma proteins &
phagocytes cells into the tissue spaces
Functio laesa Loss of functions Lack of oxygen or nutrients, and
insufficient blood flow to the area
5 Signs of Inflammation
6. Introduction of NSAIDs
o The drugs which comes under NSAIDs category have
analgesic, antipyretic and anti-inflammatory action.
o These are the drugs without steroidal ring.
o NSAIDs don’t depress CNS, don’t produce physical
dependence, have no abuse liability and are weaker
analgesic instead morphine shows all characteristics.
o It’s also known as Non-narcotic, non-opoids or
aspirin like analgesic.
o Mainly NSAIDs act on peripheral pain mechanisms,
but also in the CNS to raise pain threshold.
7. Mechanism of Action of NSAIDs
Biochemical
Mechanism
1. Inhibition of hydrolytic enzyme.
2. Inhibition of Arachidonic
metabolism.
3. Inhibition of COX & LOX pathway
4. Inhibition of free radical
generations
Cellular or immunologic
Mechanism
1. Inhibition of Polymorphonuclear
leucocytes.
2. Monocyte modification.
3. Action through lymphocytes.
8. Biochemical Mechanism
• Inhibition of hydrolytic enzyme: This concept is related
with lysosymes, which contains hydrolytic enzyme and
participate in process of inflammation. NSAIDs
inhibited the lysosymes to release of hydrolytic
enzymes.
• Inhibition of Arachidonic metabolism : PGs play an imp
role in erythema, oedema, pain and fever.
• Most of NSAIDs inhibit the formation of PGs and
Leuctotrienes which are metabolic product of
arachodonic acid and are responsible for inflammation.
NSAIDs inhibit COX and LOX enzyme
• COX also known as PGs Synthetase
9. • Inhibition of free radical generations: No. of free
radicals species generated during biosynthesis of PGs
which was inhibited by NSAIDs.
•Inhibition of Polymorphonuclear leucocytes: PMN is
first cell to arrive at site of inflammation and NSAIDs
restrict their arrival at site of inflammation.
•Monocyte modification: Monocyte are central cell in
inflammatory process. NSAIDs modify the function of
movement and function of monocyte.
• Action through lymphocytes: The second line drug such
as penicllamine, gold salts and dapsone used in treatment
of inflammation. Lymphocyte may influence chronic
inflammation.
Cellular or Immunologic Mechanism
10.
11. Physiology of Pain
Sources (Chemical/Thermal)
Pain Receptors (Nociceptors)
Discharge Impulses
Electrical Activity to spinal cord and onto the brain
In brain electrical activity become the experience of
PAIN
12. Classification of Acidic/ Classical
Non-Selective
Cox Inhibitor
Selective COX-II
inhibitors
Preferential
COX-II Inhibitors
Analgesic &
Antipyretics
Classification of NSAIDs
Acidic Drug
Classical & Non-classical
(Gold Compounds)
Basic Drugs
Timegadine (Which
inhibits neutrophil
degranulation)
Non-Acidic Drug
Indoxle, Nicotindole,
Nambumetone
15. Salicylate (Asprin)
• It’s a Prototype OTC drug.
• Aspirin is acetylsalicylic acid.
• After administration in body it converts rapidly into the
salicyclic acid which is responsible for most of the
action.
• Mainly it decreases the body temperature and pain
threshold.
• Regular use or high consumption of aspirin leads to
death or other side effect.
• Natural Sources – Fruits, Vegetables, herbs, spices, nuts
and tea.
16. Synthesis of Asprin
Pharmacology of Aspirin
Pharmacodynamics :-
1. Analgesic, Antipyretic and Anti-inflammatory
• Aspirin Produce analgesic effect by inhibiting the
synthesis of PGs (Prostaglandins) and prevents
sensitization of peripheral nerve ending.
17. • Aspirin Also acts on temperature
regulating centre and increase heat loss but
doesn’t affect the production of heat.
• Aspirin Sometime it also increases the
threshold level in body and decreases the
sensation of pain.
2. Metabolic effect –
• Aspirin Decreases utilization of glucose
from peripheral tissue which produce
hypoglycemia (condition produced mainly in
diabetic patient).
18. • Aspirin at higher dose cause
release of adrenaline which increases
chances of hyperglycemia.
3. CVS (Cardio-Vascular System)-
Aspirin Produces
Depressant effect in
vasomotor centre
Decreases the Blood
Pressure (B.P.)
Vasodilating Effect
Decreases the B.P.
19. 4. Respiratory System Effect –
Aspirin
Stimulate Peripheral & CNS
Increases Respiration
Rate
In case of Salicylate Poisoning
Aspirin
Suppress Respiratory system &
Respiratory Failure occurs
20. 5.Gastro-intestinal Tract (GIT) effect–
Aspirin/Salicyclic acid
Cause hyperacidity in stomach
And produces irritation in gastric mucosa , peptic ulcer, nausea
and vomiting
21. 6. Blood Pressure (B.P.)–
Aspirin
Inhibits
The synthesis of TXs
(Thromboxane)
Interfere in
1. Platelets aggregation
2. Blood coagulation
22. Pharmacokinetics :-
• Aspirin absorbed from the stomach and small
intestine.
• It’s having poor water solubility, which influence
absorption property.
• By introducing the alkali group in aspirin enhance
the absorption power.
•It’s 80% bound to plasma protein.
• Aspirin converts to salicylic acid by deacetylation
process in gut wall, liver, plasma and other tissue.
• It’s metabolites are excreted by glomerular
filtration and tubular secretion.
23. Adverse Effect:-
• Side Effect -
Nausea, Vomiting, Epigastric distress, blood loss in stool,
Gastric Mucosal damage and peptic ulceration.
• Hypersensitivity and idiosyncrasy –
Rashes, urticaria, angioedema, asthma, rhinorrhoea and
anaphylactoid reaction.
• Antiinflammatory doses –
It produces syndrome called salicylism.
Dizziness, tinnitus, vertigo, reversible impairment of
hearing and vision, excitement and mental confusion,
hyperventilation and electrolyte imbalance.
•Acute salicylate poisoning
24. Uses:-
• Analgesic, Antipyretic and Anti-inflammatory
• In Rheumatoid arthritis
• In Postmyocardial infarction
• In Pregnancy induced hypertension
• In Osteoarthritis
Interaction with other drugs:-
• When aspirin is taken with probenecid it inhibits the
tubular secretion of uric acid and antagonizes uricosuric
action of probencid.
•Aspirin blunts diuretic action of furosemide and
thiazides. And also reduce k+ conserving action of
spironolactone.
25. Precautions and Contraindications
• Aspirin displaces naproxen, warfarin, sulfonylureas,
phenytoin from binding sites on plasma protein.
•Its antiplatelets action increases the risk of blood
loss in patients on taking oral anticoagulants.
•Aspirin is contraindicated and avoided by patients
of following conditions :-)
1. In peptic ulcer, bleeding tendencies, in chronic
liver diseases, avoided in diabetics, in juvenile
rheumatoid arthritis, during pregnancy and
breastfeeding time.
26. Propionic Acid Derivatives (Ibuprofen)
• Ibuprofen is NSAIDs and have analgesic, antipyretic
and anti-inflammatory action. Major mechanism is
believed to be inhibition of COX activity and PGs
(prostaglandins) synthesis.
• it’s marketed as Brufen, provided by popular brands
such as Mortin, Advil and etc.
• It have anti-platelets action and act as
vasoconstrictor.
• It’s a “core” drug in the WHO model list of essential
medicines necessary in the minimum medical needs
of basic healthcare system.
27. Pharmacodynamics / Mode of Action
• Ibuprofen acts by inhibiting the Cyclooxygenase
(COX) enzyme, which converts the Arachidonic acid
to prostaglandins (PGs).
• PGs are then converted into two PGs subunits by
enzymatic process into PG G2 & PG H2 (which are
act as mediators in pain, fever, inflammation,
stimulates platelets aggregation and leads to the
formation of blood clots.
28. Pharmacodynamics / Mode of Action
Arachidonic
Acid
Prostaglandins
PG G2
Protect gastric
mucosa
Platelets and
Kidney functions
PG H2
Fever and
Pain
Inflammation
Cyclooxygenase
Ibuprofen
Inhibits
29. Pharmacokinetics
• All Propionic acid derivatives are well absorbed
orally, highly bound to plasma proteins (90-
99%).
• All derivatives enters in brain, synovial fluid and
cross placenta.
• They are largely metabolized in liver by
hydroxylation and glucoronide conjugation.
• Excreted in urine as well as bile.
• Mainly absorbed from the GI system.
• It’s peak level is about 1 to 2 hours.
30. Uses
Fever
Inflammation
Headache
Toothache
Back Pain
Arthritis (rheumatoid arthritis, osteoarthritis)
Minor injuries
Other musculoskeletal disorders
31. Side effects
Nausea
Dyspepsia
GI ulceration
Bleeding
Diarrhoea
Constipation
Hypertension
CNS side effect (Headache, Dizziness, Blurring
of vision and depression)
32. Anthranilic Acid Derivatives (Fenamate)
It’s used to treat pain and typically prescribed for
oral administration.
It exhibits anti-inflammatory, analgesic and
antipyretic effects.
The pharmacodynamic of Mefenamic Acid is quite
similar to othre NSAIDs, isn’t completely
understood but may be related to prostaglandins
(PGs) inhibition.
Pharmacodynamics
33. After oral administration usually reaches peak
plasma level 2 to 4 hours with a half life of 2 hours.
Mefenamic acid and its metabolites are bound to
plasma proteins.
Of a single dose 67% of the total dose is excreted
in the urine as unchanged drug or as one of the two
metabolites.
20% to 25% of the dose is excreted
in the faeces during the first three days.
Pharmacokinetics
34. Treatment of primary dysmenorrhoea
inflammation and fever
Soft tissue and dental pain
It also treat the symptoms of pain and
inflammation. They don’t treat the disease that
causes those symptoms.
Uses of Mefenamic Acid
Side Effect
Constipation, diarrhoea, dizziness, gas, headache,
heartburn, nausea, stomach upset..
Severe allergic reaction are:-
Rashes, Hives, itching, trouble breathing, tightness in
the chest, swelling of mouth, face, lips, or tongue.
35. Related Questions
• Write mechanism involved in inflammation?
• Write structural classification of NSAIDs?
• Write MOA of NSAIDs?
• Give SAR of each categories of NSAIDs?
• Write synthesis of asprin ?
• Explain pharmacology of aspirin?
• Explain pharmacology of Mefenamic Acid ?
• Explain pharmacology of Ibuprofen ?
• Write short note on inflammation ?