DRUGS USED TO TREAT PAIN
AND INFLAMMATION
Dr. Haji Bahadar, PhD, Assistant Professor
KMU-IPMS
WHAT IS INFLAMMATION?
Inflammation is the body's protective response to
injury.
Physical: Burns, Frostbite, Physical injury
Biological: Infection by pathogens
Chemical: toxin or toxicant
Immune system activation
Types: Acute and chronic
SIGNS OF INFLAMMATION
Pain - the inflamed area is likely to be painful
.Chemicals that stimulate nerve endings are
released, making the area much more
sensitive.
Redness - this is because the capillaries are
filled up with more blood than usual.
Immobility - there may be some loss of
function.
Swelling - caused by an accumulation of
fluid.
Heat - more blood in the affected area
makes it feel hot to the touch.
SYNTHESIS OF PROSTAGLANDINS
Synthesis of prostaglandins: Arachidonic acid
is the primary precursor of the prostaglandins
Arachidonic acid is present as a component of
the phospholipids of cell membranes.
Free arachidonic acid is released from tissue
phospholipids by the action of phospholipase
A2 via a process controlled by hormones
There are two major pathways in the synthesis
of the eicosanoids from arachidonic acid, the
cyclooxygenase and the lipoxygenase
pathways
Rheumatoid arthritis
CHEMICALS INVOLVED
Cytokines (fever sensitizing)
Histamine (swelling sensitizing)
Prostaglandins (pain sensitizing)
PAIN
Pain is an unpleasant sensory and emotional
experience associated with actual or
potential tissue damage.
Pain has many causes – cancer, injury,
infection, surgery – and people experience
pain in many different ways.
Analgesics
Non-opioid
Opioid analgesics
analgesics or NSAIDs
CYCLOOXYGENASE PATHWAY
COX-1 is an enzyme that regulates normal
cellular processes,
1. Gastric protection,
2. Vascular homeostasis,
3. Platelet aggregation
4. Reproductive and kidney functions
COX-2 is expressed in tissues such as the
brain, kidney, and bone. Its expression at
other sites is increased during states of
chronic inflammation
NONSTEROIDAL ANTI-INFLAMMATORY DRUGS
(NSAIDS) TRADE NAMES (DRUG MANNUAL)
1. Non selective COX
inhibitors
Aspirin
Diclofenac
Indomethacin
2. COX-2 inhibitors
Selective COX-2 inhibitors are a type of non-
Ketorolac
steroidal anti-inflammatory drug (NSAID) that
Meloxicam directly targets cyclooxygenase-2, COX-2,
Piroxicam an enzyme responsible
Fenoprofen for inflammation and pain. Targeting
Flurbiprofen selectivity for COX-2 reduces the risk
of peptic ulceration. Drugs are
Ibuprofen
celecoxib, rofecoxib
Ketoprofen
Naproxen
Paracetamol
(no anti inflammatory)
STEROIDAL ANTI INFLAMMATORY
DRUGS
Steroid is an organic compound with
four rings.
The steroid core structure is composed
of seventeen carbon atoms, bonded in
four "fused" rings.
DIFFERENCE BETWEEN NON STEROID
AND STEROID STRUCTURES
Aspirin Dexamethasone
MECHANISM OF ACTION
During inflammation prostaglandins are
produced which stimulate peripheral nerve
endings producing pain impulses that are carried
to the CNS. NSAIDs cause the inhibition of COX-
1/2, decreasing prostaglandin synthesis. Aspirin
irreversibly inhibit cyclooxygenase. The other
NSAIDs are all reversible inhibitors of
cyclooxygenase.
INDICATIONS
Headache (nonmigraine)
Muscle aches and pain
Toothache
Dysmenorrhea
Joint Pain (osteoarthritis)
Inflammation
Removal of acne(salicylic acid)
Salicylic acid 6 % topical gel
SIDE EFFECTS
• Nausea due to erosion of stomach lining
• Decrease cytoprotective mucus secretion.
SIDE EFFECTS
Vomiting
Peptic ulcer disease
Gastrointestinal bleeding
Prolong bleeding time (Aspirin)
Hepatotoxicity (elevated serum enzymes like
alkaline phosphatase, serum glutamic-
pyruvic transaminase SGPT or ALT)
(Paracetamol)
Hypersensitivity (in sensitive patients)- rash,
laryngeal edema, asthma (Aspirin)
Kidney damage
CONTRAINDICATIONS
Severe hepatic diseases (Aspirin, diclofenac,
paracetamol)
Vitamin K deficiency (Aspirin)
Hemophilia (bleeding disorder) (Aspirin)
Children (Aspirin) causing Reye syndrome(self)
Patients receiving anticoagulants such as warfarin
and heparin (aspirin)
Asthma (aspirin)
ANTIPYRETIC ACTION
Antipyretic action: Fever occurs when the
set-point of the anterior hypothalamic
thermoregulatory center is elevated. This can
be caused by PGE2 synthesis, which is
stimulated when endogenous fever-
producing agents (pyrogens), such as
cytokines, are released from WBCs that are
activated by infection, hypersensitivity,
malignancy, or inflammation. The NSAIDs
lower body temperature in patients with
fever by impeding PGE2 synthesis and
release
ANALGESICS AND PAIN RELIEF IN PREGNANCY
AND BREASTFEEDING
Paracetamol
Mefanamic acid
