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NSAIDs: Types, Uses, and Effects

The document provides an overview of Non-Steroidal Anti-Inflammatory Drugs (NSAIDs), detailing their classification, mechanism of action, and effects including analgesic, antipyretic, and anti-inflammatory properties. It discusses various types of NSAIDs, such as nonselective COX inhibitors, selective COX-2 inhibitors, and their pharmacokinetics, uses, and adverse effects. Additionally, it compares aspirin and paracetamol, highlighting the advantages and disadvantages of each, as well as the role of topical NSAIDs.
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0% found this document useful (0 votes)
5 views28 pages

NSAIDs: Types, Uses, and Effects

The document provides an overview of Non-Steroidal Anti-Inflammatory Drugs (NSAIDs), detailing their classification, mechanism of action, and effects including analgesic, antipyretic, and anti-inflammatory properties. It discusses various types of NSAIDs, such as nonselective COX inhibitors, selective COX-2 inhibitors, and their pharmacokinetics, uses, and adverse effects. Additionally, it compares aspirin and paracetamol, highlighting the advantages and disadvantages of each, as well as the role of topical NSAIDs.
Copyright
© All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PDF, TXT or read online on Scribd

Dr.

Anadil Fidaa Anver


Dept of Pharmacology
INTRODUCTION
❑ Also called non-narcotic/ non- opioid/aspirin
like analgesics

❑ NSAIDs have :-
• Analgesic action
• Antipyretic action
• Anti-inflammatory action

❑ They act by inhibiting prostaglandin synthesis


CLASSIFICATION
A. Nonselective COX inhibitors

1. Salicylates
Aspirin
2. Para-aminophenol derivatives
Paracetamol
3. Propionic acid derivatives
Ibuprofen, naproxen, ketoprofen, Flurbiprofen
4. Acetic acid derivatives
Indomethacin, Ketorolac
CLASSIFICATION

5. Fenamates (anthranilic acids)


Mefenamic acid
6. Pyrazolone derivatives
Phenylbutazone, azapropazone
7. Oxicams (Enolic acid derivatives)
Piroxicam, tenoxicam
CLASSIFICATION
B. Preferential COX-2 inhibitors

Diclofenac, aceclofenac, meloxicam, nimesulide

C. Selective COX-2 inhibitors


Celecoxib, parecoxib, etoricoxib
MOA
• During inflammation, arachidonic acid liberated from
membrane phospholipids is converted to prostaglandins
(PGs), catalysed by the enzyme cyclo-oxygenase (COX)
• These prostaglandins produce hyperalgesia—they sensitize
the nerve endings to pain
• NSAIDs inhibit the PG synthesis by inhibiting the enzyme
cyclo-oxygenase
Aspirin is the prototype drug

1. Analgesic effect:

 Prevent PG mediated sensitisation of peripheral nerve


endings

 Increase pain threshold

 Mainly used for relieving musculoskeletal pain,


dysmenorrhoea and pain associated with
inflammation or tissue damage
2. Antipyretic effect:

 Reset the hypothalamic thermostat by inhibiting


synthesis of PGs in the hypothalamus and reduce the
elevated body temperature during fever

 Promote heat loss by enhanced sweating & cutaneous


vasodilatation
3. Anti-inflammatory effect:

 Anti-inflammatory effect seen at high doses


(4-6 g/day)
 Signs of inflammation like tenderness, swelling,
erythema and pain reduced
 But, the progression of the disease is not affected
 The anti-inflammatory action of NSAIDs is mainly due
to inhibition of PG synthesis at the site of injury
(PGs present in inflammatory tissues responsible for
oedema, erythema & pain)
 4. Antiplatelet (antithrombotic) effect:
 Aspirin in low doses irreversibly inhibits platelet TXA2
synthesis and produces antiplatelet effect, which lasts
for 8–10 days, i.e. the life time of the platelets.
 Aspirin in high doses inhibits both PGI2 and TXA2
synthesis, hence antiplatelet effect is lost
5. Acid–base and electrolyte balance:

 In therapeutic doses, salicylates produce significant


respiratory stimulation → more CO2 is washed out
resulting in respiratory alkalosis which is compensated
by excretion of bicarbonate

 In toxic doses, the respiratory centre is depressed →


CO2 accumulates → can lead to respiratory acidosis.
Later, there is uncompensated metabolic acidosis
6. GIT:
 Aspirin irritates the gastric mucosa and produces
nausea, vomiting and dyspepsia.
 Aspirin also stimulates CTZ and produces vomiting
 Erosive gastritis, gastric ulceration and GI bleeding
can occur at higher doses
Mechanism:
 PGs are cytoprotective to gastric mucosa because they
reduce acid secretion & increase mucus production.
 Salicylates increase gastric acid secretion & suppress
the protective effect of prostaglandins by inhibiting
their synthesis
7. CVS:

 Prolonged use may cause salt and water retention →


worsen CCF & hypertension

8. Urate excretion:

 Salicylates, in therapeutic doses, inhibit urate secretion


into the renal tubules and increase the plasma urate levels.

 In high doses, salicylates inhibit the reabsorption of uric


acid in the renal tubules and produce uricosuric effect.
Pharmacokinetics
 Absorption : stomach & small intestine
 Rapidly deacetylated salicylic acid
 80-90% plasma protein bound
 Enters brain and crosses placenta
Uses
1. As Analgesic
 Headache
 Myalgia
 Neuralgia
 Joint pain
 Tooth ache
 Dysmenorrhea

2. Fever

3. Inflammatory conditions
 Arthritis
 Fibromyositis etc
4. A/c rheumatic fever:
 4-6 g/day

5. Rheumatoid arthritis:
 Pain, swelling, morning stiffness reduced

 Do not alter the progress of the disease

6. Osteoarthritis:
 Symptomatic relief
7. Post myocardial infarction & stroke:

 Aspirin in low dose - Inhibit platelet aggregation

 Reduces reinfarction in post MI patients

 Reduces TIA & stroke


8. Other uses

 Delay labour
 PIH & pre eclampsia
 P D A closure in new born
 Prevent colon cancer
Adverse effects
1. GI tract
 Nausea, vomiting
 Peptic ulcer
 Occult blood loss in stools
2. Allergic reactions
 Rashes, urticaria, angio-oedema & asthma
3. Haemolysis in G6PD deficient patients
4. Nephrotoxicity on long term use
5. Hepatotoxicity
6. Salicylism

 High doses given for long term causes salicylism

 Charecterised by

➢ Headache, vertigo, dizziness, tinnitus,

➢ Mental confusion, sweating,

➢ Difficulty in hearing,

➢ Vomiting, diarrhoea, thirst & dehydration


7. Reye’s syndrome:
 Hepatic dysfunction seen in children
 Develops a few days after a viral infection like influenza
& varicella
 Increased incidence when aspirin used to treat fever

8. Pregnancy & infancy


 Aspirin given at term delays labor (due to inhibitionof
PG synthesis)
 Increases postpartum bleeding (due tom inhibition of
platelet aggregation)
 Premature closure of ductus arteriosus → portal
hypertension in baby
PARACETAMOL
 Acetaminophen
 Relatively safe and effective analgesic

❑ACTIONS
 Good antipyretic
 Analgesic action
 Weak anti inflammatory action
Advantages of Paracetamol over
Aspirin
 Do not stimulate respiration
 Do not affect acid base balance
 No gastric irritation
 Do not affect platelet function
 Safe and well tolerated in antipyretic doses
 No risk of Reye’ s syndrome in children
ADVERSE EFFECTS
 Antipyretic dose – safe and well tolerated
 Nausea & rashes may occur
 Higher doses - Hepatotoxic

USES
 Analgesic – painful conditions like toothache,
headache, myalgia
 Antipyretic - fever
SELECTIVE COX-2 INHIBITORS
 COXIBS – Celecoxib, parecoxib, etoricoxib
MERITS
 Inhibit COX -2 without affecting COX-1
 Do not inhibit platelet aggregation
 Less gastric mucosal damage
DEMERITS
 Prothrombotic - increased cardiovascular &
cerebrovascular complications → increase risk of
myocardial infection & stroke
USES
 In patients who cannot tolerate other NSAIDs & are at high
risk of developing peptic ulcer
TOPICAL NSAIDs
 Systemic toxicity is minimal.

 Diclofenac, ibuprofen, naproxen, etc. - useful topically


for musculoskeletal pain.

 Used in backache, osteoarthritis, sprain, etc.

 Flurbiprofen and diclofenac eye drops used in


ophthalmic practice.

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