Medical School, Notes, Pharmacy

Narcotic and Non-Narcotic Analgesics

Analgesic is a drug, which relief pain without impairing the degree of consciousness is called analgesics.

We can describe pain as a displeasing sensory, emotional experience associated with actual or potential tissue damage or described in terms of such damage.

There are various types of pain. Such as-

Somatic pain: Somatic pain comes from the skin, muscles and soft tissues.

For Example: Headache, pain in muscles, joints etc.

Visceral pain: Visceral pain arrive from the internal organs. 

For Example: Kidney’s pain, stomach pain, urinary bladder pain, liver pain etc.

There are two types of Analgesic:

1) Narcotic Analgesics

2) Non-Narcotic Analgesics

Narcotic Analgesic

Drugs which reduce pain arising from the viscera and produce narcosis and addiction is called narcotic analgesic.


  • Highly potent analgesics
  • Addicting analgesics
  • Mainly act on CNS
  • No anti-inflammatory action
  • No anti-pyretic action
  • No anti-platelet action

Classification of Narcotic Analgesics

1. Natural Analgesics

  • Example: Opium alkaloids (Morphine, Codeine)

2. Semi-synthetic opiates

  • Example: Oxymorphine, Hydromorphine

3. Synthetic Analgesics

  • Mepredine and related phenyl-piperidine.
    • Example: Piminodine
  • Methadone and related drugs.
    • Example: Methadone
  • Benzomorphanes.
    • Example: Pentazocine
  • Morphinan derivatives.
    • Example: Levorphanol
  • Narcotic antagonists.
    • Example: Naloxone, Nalophine, Levorpheine

Mechanism of Morphine (Natural Analgesics)


Stimulation of opioid receptors (mu) in the CNS

Hyperpolarisation and inhibition of presynaptic neurons

Inhibition of cell firing by increasing the threshold for pain

Exclusion of pain and also allows subjects to tolerate pain.

So basically morphine bind with opioid receptors (mu) then reduce potassium ion from cell and inhibit the presynaptic neurons then cell firing is inhibit and threshold of pain is raising so eliminated the pain and raising the capacity or tolerance of pain.

Non-Narcotic Analgesic

The agents that produce analgesia without producing generalized depression of CNS and addiction are known as non-narcotic analgesics.

The effects of Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) given below:

  1. Analgesic action
  2. Anti-inflammatory action
  3. Anti-pyretic action
  4. Anti-platelet action

Classification of NSAIDs

1. Drug with analgesic but with negligible anti-inflammatory action.

  • Example: Acetaminophen (paracetamol)

2. Drug with analgesic and mild to moderate anti-inflammatory action.

  • Propionic acid derivative:
    • Example: Neproxen
  • Fenamates:
    • Example: Flufenamic acid
  • Nabumetone

3. Drug with analgesic and strong anti-inflammatory action

  • Salicylic acid derivatives:
    • Example: Acetyl salicylic acid

Mechanism of action of NASIDs

Membrane Phospholipid

Arachidonic acid (by the help of Cyclooxygenase enzyme)


Mediators of inflammation

Phospholipid can be synthesized while it is converted to the Arachidonic acid. This Arachidonic acid converted to the Prostaglandins by the action of Cyclooxygenase enzyme. This Cyclooxygenase enzyme can be reversibly and not rapidly by paracetamol/ Aspirin/ Ibuprofen.

Mechanism of action of Aspirin


Acetylates the alpha amino group of terminal serine of the cyclooxygenase enzyme; forming a covalent bond.

Irreversible inactivation of cyclooxygenase enzyme

Prostaglandin (PG) synthesis is arrested

Analgesic response

Anti-inflammatory response

Anti-pyretic response

Anti-platelet response

Anti-inflammatory response action of aspirin

Prostaglandin is an important mediator of inflammation. Anti-inflammatory action of aspirin is due to inhibition of the synthesis of prostaglandin by inhibiting the enzyme cyclooxygenase. Aspirin interferes with the chemical mediators of inflammation. So aspirin inhibits granulocyte adherence to injured vasculature, freezes lysosomes and inhibits the migration of polymorphonuclear leukocytes and macrophages into the site of inflammation.

Anti-pyretic action of aspirin

Aspirin inhibits the synthesis of PGE2 in the hypothalamus. This PGE2 is responsible for elevating hypothalamic set point of temperature. Due to decrease PGE2 the set point back to normal level. Aspirin also blocks the CNS response to interleukin-I, which is produced by the macrophages and is released during inflammatory responses. Aspirin has no payoff on normal body temperature.

Mechanism of action of Pyrexia

Bacterial or viral endotoxin

Release of pyrogen from leukocytes

Generation of PGE1 and E2

Stimulation of heat regulating center in thalamus

Reduce sweating and increase vasoconstriction

Rise of temperature


Anti-platelet action of aspirin

Aspirin causes inevasible inhibition of cyclooxygenase enzyme, which is responsible for prostaglandin (thromboxane) synthesis. Thereby it prevents platelet aggregation. The result is prolongation of bleeding time.

Mechanism of action of Anti-platelet

Aspirin (low dose)

Inhibits platelets cyclooxygenase

Decrease TX-A2 (thromboxane-A2) synthesis

Inhibition of platelet aggregation

So prevents thromboembolism

Indication of Aspirin

Systemic uses:

1. To relieve mild to moderate pain (non-visceral):

  • Headache, toothache, migraine.
  • Myalgia, arthralgia.
  • Dysmenorrhea.
  • Osteoarthritis.

2. As anti-pyretic:

  • To reduce fever.

3. As anti-rheumatic and anti-inflammatory agent:

  • Acute rheumatic fever.
  • Ankylosing fever.
  • Osteoarthritis.
  • Acute Rh-arthritis.
  • Acute and chronic glomerulonephritis.

4. As anti-thrombic agent:

  • Cerebrovascular accident.
  • Venous thrombosis, coronary thrombosis.
  • Pulmonary embolism.
  • Atherosclerotic disease.
  • Myocardial infraction.
  • Postoperative deep vein thrombosis.

Local uses:

  1. Antiseptic
  2. Fungicidal and
  3. Keratolytic agent

Other uses:

  1. Primary dysmenorrhea.
  2. Patent ductus arteriosus.
  3. Bartter’s syndrome.

Recent uses:

  1. Cholera: Vibrio cholera release PG which increase the GIT motility (loose motion). But aspirin blocks the PG synthesis, thus prevents cholera.
  2. Inferility: Aspirin may help in sperm synthesis.

Cardiovascular indications of aspirin:

1. Acute myocardial infraction.

  • Loading dose: 300mg.
  • Maintenance dose: 100-150mg.

2. Acute rheumatic fever.

  • Dose: 75-100mg/kg body weight/day.

3. Acute pericarditis.

4. Prophylaxis of arterial thromboembolism.

Contraindication of Aspirin:

  1. Peptic ulcer.
  2. Patients with bleeding disorders.
  3. Hepatic and renal disease.
  4. Pregnancy (last trimester).
  5. Asthma.
  6. Gout.
  7. Patient intolerance to aspirin.

Adverse effect of aspirin:

  1. Gastric and duodenal ulceration.
  2. Bleeding tendency (impaired clotting).
  3. Renal irritation.
  4. Tinnitus, deafness (overdose).
  5. Reye’s syndrome.
  6. Iron deficiency anemia.
  7. Allergic manifestations. Such as;
  • Severe rhinitis
  • Urticarial
  • Angioneurotic oedema

Dose of aspirin

Normal dose: 300mg 8 hourly (900 mg/day)

In Rh. Fever: 50mg/kg/day (3000mg/day of 60kg man)

In Rh. Arthritis: 4-6mg/day

Pharmacokinetics of Aspirin

Routes of administration: oral (buffer, soluble, effervescent, enteric coated tablets), parenteral.

Absorption: well absorbed from stomach and upper gastrointestinal tract (GIT).

Distribution: highly protein bound.

Metabolism: hydrolysis, conjugation with glycine.

Excretion: renal (tubular secretion).

Difference between narcotic analgesics and non-narcotic analgesics:

Narcotic analgesicNon-narcotic analgesics
Centrally acting.Peripherally acting.
Relieve visceral pain.Relieve somatic pain.
Produce addiction.Doesn’t produce addiction.
Depress CNS.Inhibits cyclooxygenase or PG synthetize enzyme.
Used parenterally.Used orally.
No anti-inflammatory action.Anti-inflammatory action.
Therapeutic index is less.Therapeutic index is more.