Course Name: Introduction To
Pharmacology
Course Code: MLT BA 801
Teacher Introduction:
Hassan Imran
M.Phil. Pharmacology
Lecturer, UIMLT
Faculty of Allied Health Sciences (FAHS)
The University of Lahore
Analgesics & Antipyretics
Learning Objectives:
Definition of Analgesics .
Types of Analgesics (NSAIDs & Opioids).
Classification of NSAIDs.
Mechanism of Action of NSAIDs.
Adverse Effects of NSAIDs.
Analgesics
Analgesics are medicines that are used to
relieve pain. They are also known as
painkillers or pain relievers.
Analgesics
Two most common groups of pain killers
are:
1.Nonsteroidal anti-inflammatory
drugs (NSAIDs).
2.Opioids (narcotics).
Nonsteroidal Anti-
Inflammatory drugs
All the drugs included in this class have
analgesic, antipyretic and anti-
inflammatory actions. In contrast to
morphine they do not depress central
nervous system (CNS). They are also
called nonnarcotic, non-opioid or
analgesics.
Classification of NSAIDs
Nonselective COX inhibitors:
1. Aspirin
2. Ibuprofen
3. Naproxen
4. Ketoprofen
5. Mephenamic acid
Classification of NSAIDs
Nonselective COX inhibitors:
7. Flurbiprofen
8. Diclofenac
9. Aceclofenac
10. Indomethacin
11. Piroxicam
Classification of NSAIDs
Selective COX-2 inhibitors:
1. Celecoxib
2. Etoricoxib
3. Parecoxib
Analgesics-Antipyretics with poor
anti-inflammatory action:
1. Paracetamol (Acetaminophen)
2. Metamizol
Inflammation
Inflammation is a normal, protective
response to tissue injury caused by
physical trauma, noxious chemicals or
microorganisms.
Inflammation
Inflammation is the body's effort to
inactivate or destroy invading organism,
remove irritants and set the stage for
tissue repair. When healing is complete,
the inflammatory process usually
subsides.
Inappropriate activation of the immune
system can result in inflammation and
immune-mediated diseases such as
rheumatoid arthritis (RA).
Features of inflammation
1. Swelling
2. Redness
3. Hotness
4. Pain
Mechanism of NSAIDS
Arachidonic acid is the component of
phospholipids in the cell membrane. In
response to stimuli (injury or microbial
infection) free arachidonic acid is released
from tissue phospholipids by the action of
phospholipase A2.
Arachidonic acid is the primary precursor
of the prostaglandins and related
compounds (Thromboxanes and
leukotrienes).
Mechanism of NSAIDS
(Continue)
There are two major pathways in the
synthesis of eicosanoids from arachidonic
acid:
o Cyclooxygenase Pathway
o Lipoxygenase pathways
Cyclooxygenase Enzyme
The products of COX are then converted
into either:
1. Prostaglandins by prostaglandin
synthase.
2. Thromboxane by thromboxane
synthase.
Cyclooxygenase Pathway
The cyclooxygenase enzyme convert the
arachidonic acid in to Prostaglandin H2,
which is an unstable compound and is
further converted in to prostaglandin E2,
prostaglandin D2, prostaglandin I2 and
thromboxane A2.
Action of Prostaglandins:
The prostaglandins play a major role in
modulating:
i. Pain
ii. Inflammation
iii. Fever
iv. Production of mucus in the
gastrointestinal tract. (PGE)
Action of Thromboxane A2:
i. Aggregation of Platelets
ii. Vasoconstriction
Actions of Prostacyclin PGI2 :
iii. Increase Platelet disaggregation
iv. Increase Vasodilation
Cyclooxygenase Pathway
There are two types of cyclooxygenase
enzymes:
1. Cyclooxygenase 1 (COX-1)
2. Cyclooxygenase 2 (COX-2).
COX-1 is responsible for physiological
production of prostaglandins. COX-1 is an
enzyme that regulates normal cellular
processes, such as gastric cytoprotection,
vascular homeostasis, and platelet
aggregation.
COX-2 occur at the site of inflammation.
Its expression at the site is increased
during inflammation and is induced by
inflammatory mediators like TNF-α and
IL1.
Lipoxygenase Pathway
The lipoxygenase enzyme act on the
arachidonic acid and convert it in to
leukotrienes. The leukotrienes act on the
leukotriene receptor and cause
bronchoconstriction.
Nonsteroidal Anti-
Inflammatory Drugs (NSAIDs)
The NSAIDs act by inhibiting the
cyclooxygenase enzyme, this leads to
decreased prostaglandin synthesis with
both beneficial and unwanted effects.
Adverse effects:
1. Gastrointestinal effects:
Normally prostaglandin E stimulate the
production of protective mucus in both
stomach and intestine.
Adverse effects (Continue)
Agents that inhibit Cyclooxygenase enzyme
reduce the beneficial effects of
prostaglandins and increased acid
secretion resulting in ulceration and GI
bleeding .
Adverse effects
2. Increased risk of bleeding
The inhibition of cyclooxygenase enzyme
also inhibit the thromboxane A2 production
resulting in antiplatelet effect i.e. increased
risk of bleeding.
Adverse effects
Renal effects
NSAIDs prevent the synthesis of
PGE2 and PGI2 , prostaglandins that are
responsible for maintaining renal blood
flow. Decreased synthesis of
prostaglandins can result in retention of
sodium and water and may cause
edema.
Adverse effects
Central nervous system (CNS) adverse
events, such as headache, tinnitus, and
dizziness, may occur.
Learning Outcomes:
The students will learn about:
Definition of analgesics.
Pathophysiology of pain & inflammation.
Classification of analgesic drugs.
Mechanism of action of analgesic drugs.
Therapeutic uses and adverse effects of
these drugs.
References
1. Lippincott, Illustrated Reviews
Pharmacology.
2. Basic and Clinical Pharmacology 12
Edition Katzung.
3. Essentials of Medical Pharmacology 6th
edition, KD Tripathi.
