ANALGESICS

(PAIN KILLERS)
MECHANISM OF ACTION OF
ANALGESICS

 Pain can be treated in three principle ways

1. Peripherally acting agents: acts on peripheral receptive terminals and thus
prevent discharge and sensitization of the nociceptors e.g. NSAIDs block
formation of inflammatory and pain mediators e.g. prostaglandins etc.
2. Anesthetic agents: Nociceptive signal can be interrupted between its peripheral
source and its central target in brain and spinal cord.

3. Centrally acting agents: Interact with specific receptors in central nervous

system interrupting both the pain message in CNS and its emotional response e.g.
opioid analgesics.
TYPES OF ANALGESICS USED
 NSAIDs (NON-STEROIDAL ANTI-INFLAMMATORY DRUGS)
1. Salicylate (Aspirin)
2. Non-Salicylate (Diclofenac, Naproxen, Indomethacin, Ibuprofen)
3. Acetaminophen
 Opioid Analgesics
1. Morphine
2. Codeine
3. Hydrocodone/Oxycodone
4. Fentanyl
5. Tramadol
NSAIDS

 NSAIDs work by inhibiting the activity of cyclooxygenase enzymes. In cells,

these enzymes are involved in the conversion of arachidonic acid into key
biological mediators, namely prostaglandins which are involved in
inflammation and pain.
 NSAIDs are drug of choice for the treatment of mild to moderate pain.
 NSAIDs are very affective for treating different types of acute ocular pain.
ASPIRIN

 Clinical uses of aspirin includes

1. Pain associated with inflammation
2. Used in combination with narcotics for severe pain due to ocular trauma or
inflammation.
 Side effects of aspirin includes
1. Gastric ulceration and GIT bleeding
2. Renal failure
3. Increase bleeding time by thinning the blood
DIFFERENCE BETWEEN SALICYLATE
AND NON- SALICYLATE NSAIDS

Salicylate NSAIDs Non-Salicylate NSAIDs

Irreversibly inhibit the cyclooxygenase Reversibly inhibit the cyclooxygenase

enzyme enzyme

It has shorter half life Longer half life than aspirin

Produces more toxicity Produces less toxicity

ACETAMINOPHEN

 Acetaminophen inhibits prostaglandin synthesis in central nervous system but

has less effect on cyclooxygenase in peripheral tissues due to peripheral
inactivation thus having very less anti-inflammatory activity than aspirin.

 It replaces aspirin in pain and fever treatment because it do not affect

prothrombin time and having less toxic effect.
 Clinical uses of acetaminophen includes
1. Patient allergic to aspirin
2. In patients in which aspirin is contraindicated
3. In patient with upper GIT disease and bleeding disorder
4. NSAID of choice for mild to moderate pain during pregnancy and lactation.

 Toxic effects of acetaminophen includes

1. Hepatotoxicity (At high doses)
 OPIOID ANALGESIC

 Opioids are natural, semi-synthetic or synthetic compounds that produces

morphine like effects e.g. analgesia, treatment of diarrhea, antitussive,
anesthesia etc.

 Opioid analgesics produces their effect by binding to opioid receptors.

Activation of the opioid receptor decreases calcium influx in response to
incoming action potential. This decreases releases of excitatory
neurotransmitters such as glutamate.
 Morphine is standard opioid against which all other narcotic analgesics are
compared.

 Codeine is rarely used individually. Mostly it is used in combination with

other NSAIDs.

 Oxycodone and hydrocodone are codeine congener and much more potent
than their parent compound.

 Tramadol is synthetic analogue of codeine and used in surgical pain.

 Clinical Uses:
 It is mostly used for short term treatment of acute ocular pain due to risk of
addiction
 These agent are mostly indicated for moderate to severe pain
 Sometime it can also be used with NSAIDs to increase the effectiveness.

 Side Effects:
 Pupillary constriction
 Respiratory depression
 Nausea
 Constipation