Pain &

Analgesics

Dr.Kumarasingam

 Pain is an unpleasant sensation occurring

in varying degrees of severity as a
consequence of injury, disease, or
emotional disorder
Hyperalgesia increased the pain
sensitivity to noxious stimuli.
Allodynia - phenomenon characterised by
painful sensations provoked by non-noxious
stimuli, (e.g. touch), transmitted by fast
conducting nerve fibers

Pathophysiology of Pain
Pain perceptions are,
1. Peripheral component
2. The central component

Afferent pathways
Impulse
Spinal cord
Brain stem
Thalamus
Central structures of
brain
Pain is processed.

*Transmission through the larger, myelinated Adelta fibers

occurs much more quickly. A - fibers carry
well-localized,
sharp pain sensations
*The small unmyelinated C- neurons are
responsible for the
transmission of diffuse burning or aching
sensations

Descending pathway
Its role: - inhibition of afferent pain signals

There they inhibit or block transmission of

nociceptive signals at the level of dorsal horn

1. Nociceptive pain (stimuli from

somatic and visceral structures)
2. Neuropathic pain (stimuli
abnormally processed by the
nervous system) by injury, surgery
& damaged nerves.

Analgesics
Pain relieving properties by acting in
the CNS or on peripheral pain receptor
without significantly affecting
consciousness.
1. Narcotic / opioid
2. Non-narcotic / NSAIDs

Moderate Pain
4-6/10
Mild Pain 1- Weak opioids +/non-opioids
3/10
ASA, NSAIDS

Severe Pain 710/10

Potent opioids +/non-opioids

Opioids
Originally derived
from poppies
Body possesses
endogenous opioids
Opiate Receptors
mu ()
delta ()
kappa ()
NOP

Papaver
somniferum

Pharmacology of Opioids
1: inhibit transmission of pain
2: respiratory depression, euphoria,
constipation, physical dependence
: inhibit transmission of pain
: inhibit transmission of pain
: autonomic effects, dysphoria,
hallucinations

PHARMACOLOGICAL ACTION
CNS
Endocrine
CVS
GIT
Other
Biliary
Urinary
Bronchi
Uterus

Transducer mechanisms
1. AC
2. k+
3. Ca2+

Adverse effects

Classification of NSAIDs
1.Nonselective Irreversible inhibitors of
COX Aspirin, Sodium
salicylate,Sulfasalazine, Olsalazine, Methyl
salicylate.
2.Nonselective reversible inhibitors of
COX Oxyphenbutazone, Indomethacin,
Sulindac, Ibuprofen, Flurbiprofen,
Naproxen, Mefenamic acid, Tenoxicam,
Piroxicam, ketorolac, Tolmetin, Oxaprozin,
Diflunisal, Diclofenac, Aceclofenac.
3.Weak inhibitor of COX-1< COX-2 plus

4.Preferential COX-2 inhibitors

Meloxicam, Etodolac, Nabumetone
5.Selective COX-2 inhibitors Rofecoxib,
Celecoxib, Valdecoxib, Etoricoxib, Parecoxib
6.COX-3 inhibitor or Reversible inhibitors
of Hypothalamic COX-1 Paracetamol,
Metamizol
7.NSAIDs Which do not inhibit PG
synthesis Nefopam , Diacerein.

BIOSYNTHESIS OF
PROSTAGLANDIN
Membrane
phospholipids
Phospholipase A2

Arachidonic
Li
po
Acid
o-

l
c
y ge
C xy
o

Prostaglandins,
thromboxanes

e
s
na

xy
ge
na

se

Leukotrienes

PHARMACOLOGICAL ACTION
Analgesics
Antipyretic
Anti-inflammatory
Platelet aggregation
Dysmenorrhoea
Closure of DA
Others
Colonic CA
- FCP
Pre eclampsia- Niacin
Alzheimer
- Cataract

Adverse effects
Gastric mucosal damage
Acid-base balance
Bleeding tendency
Hypersensitivity
Renal

COX-2 Inhibitors
Selectively inhibit cyclooxygenase-2
less GI irritation; less platelet effects
other side effects similar to NSAIDs

Role: patients with low cardiovascular

risk who require NSAID therapy & are
at increased risk for GI toxicity

Thank
you