Painunpleasant sensory & emotional experience associated with either

actual or potential tissue damage. The processes in the body involved in
perception of pain are called "nociception"

Acute painPain of sudden in onset, usually subsides when treated, &
typically occurs over less than 6-week period of time (injury healing time).

Chronic painPersistent or recurring pain that is often difficult to treat.
Typically lasts longer than 3 months (beyond injury healing time).

Pain thresholdLevel of
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painful sensation


Mechanism of pain: Stimulus (cause of pain) detected by pain receptors
(nociceptors) → sensory nerve → pain centre (perception) → emotional
reaction (pain threshold)

Relief of pain


 Narcotic analgesics (Opioid analgesics)
 Non narcotic analgesics (Non steroidal anti- inflammatory drugs)
 Adjuvant analgesics or Co-analgesics

Anaesthetic agents

 General anaesthetics
 Local anaesthetics

do not contribute to dependence  δ receptor – may contribute to spinal analgesia. delta (δ). euphoria. kappa (k). methadone  Partial agonist and mixed agonist antagonists: nalorphine(partial μ agonist)  Antagonist (all receptors): naloxone Morphine  Papaver somniferum  prototype of opioids PA CNS stimulation (excitation)  Miosis  Vomiting  Mood changes CNS depression  Sedation  Respiratory depression  Analgesia  Impairs sympathetic vascular reflexes  reduces mental distress  retention of urine Uses . Properties  Control moderate to severe pain by acting on opioid receptors: mu (μ). respiratory depression and inhibition of gut motility Classification of narcotic analgesia  Pure agonists (primarily at μ.Narcotic analgesics  Used to control moderate to severe pain. perhaps at k & δ): morphine. dependence. respiratory depression and inhibition of gut motility  k receptor – analgesia at spinal cord level and dysphoria. alters perception of & response to painful stimuli while producing generalized CNS depression  μ receptor – both spinal & supraspinal analgesia.

 relieve moderate to serve pain  relive dyspnea  relieve anxiety  Suppressing cough  control of diarrhea CI  Asthma  drug allergy  Paralytic ileus  Morbid obesity with sleep apnea  Patients with severe head injuries ADE  Physical & psychological dependence  Tolerance  Respiratory depression  Cerebral vasodilatation Overdose: coma. pinpoint pupil (miosis). depressed respiration (with injection morphine > 30 mg) Treatment: opioid antagonist  antidote for opioid poisoning Naloxone competitively blocks effects of opioids Naloxone  Pure competitive antagonist  treatment of acute opiate overdose  High first-pass effect (IV) Codeine  Natural alkaloid  Generalized CNS depression  mild to moderate pain  combination with other analgesics Tylenol with codeine Methadone  Synthetic opioid  Physical dependence  μ agonist  Drug of choice for detoxification treatment for opioid addiction Meperidine(Pethidine) .

blurred vision)  Does not interfere birth or uterine involution  Pethidine differs from morphine in that: Does not suppress cough usefully. not constipate  less likely to cause urinary retention  Does not interfere birth or uterine involution  Same uses & adverse effects as morphine ADE neurotoxic metabolism with chronic use CNS agitation Hallucinations. naproxen Indoleacetic acids derivatives: Indomethacin diclofenac*. Tremors.  Synthetic (μ & k). seizures Non-narcotic analgesics Non-steroidal analgesic.etodolac* Fenamic acid (Anthranilic acids) derivatives: Mefenamic acid Oxicams: Piroxicam. antipyretic & anti-inflammatory drugs (NSAIDs) Classification Para-aminophenol derivative: paracetamol (acetaminophen) Salicylic acid derivatives: Aspirin (acetylsalicylic acid) Propionic acid derivatives: Ibuprofen. meloxicam* Cyclo-oxygenase (COX-2) inhibitors: Celecoxib Salicylate PA  Analgesia  Anti-inflammatory action  Antipyretic action  Antiplatelet effect Inhibit platelet aggregation/adhesion Uses Systemic administration:  Non-specific relief of certain types of pain headache . with lower analgesic action  has anticholinergic action (dry mouth.

most used among NSAIDs  Potency against COX-2  Rapidly & completely absorbed Uses . nausea. on bleeding time and on GI irritation  control pain or fever as substitute for aspirin ADE  chronic renal failure  hepatic necrosis & failure INDOMETHACIN  Methylated indole derivatives  relieve pain & inflammation ADE  anorexia.  To reduce inflammation acute rheumatic fever  Prophylaxis of thromboembolic diseases coronary heart disease Local application:  Topical application for muscle and joint pain  Oral for ulcerative colitis ADE  Nausea/vomiting  Salt-water retention  Increased bleeding tendency  hypersensitivity reaction  Reye’s Syndrome(Caused by aspirin & other salicylates) PARACETAMOL  Therapeutic efficacy: equal to aspirin in analgesic  less effect on platelets. abdominal pain  not be used in pregnant women & children  Severe frontal headache DICLOFENAC  Non-selective COX inhibitor.

 Long-term symptomatic t/m in moderate pain & inflammation rheumatoid arthritis  Orally  Short-term treatment in MSK disorders CELECOXIB  Highly-selective potent COX2 inhibitor  Sulphonamide derivative  Used mainly for osteoarthritis.  Selective COX-2 inhibitors depress PGI2 formation by endothelial cells  thrombosis  CI in cardiovascular or cerebrovascular diseases INFLAMMATION Remove harmful stimuli. CHRONIC autoimmune conditions  damage is too severe to be resolved CORTICOSTEROID  Suppresses all types of hypersensitivity & allergic phenomenon  Acute short-term therapy Very high single dose  Prolong therapy(> 20 mg prednisolone x > 2 weeks) Only palliative. or pathogens .& begin the healing process. rheumatoid arthritis ADE & CI  Hypertension & oedema. includi damaged cells. A 50% reduction in dose may be made on each day ADE  Fat redistribution  Hypertension  Glucose intolerance  Risk of infection  Cataracts CI  Infection  Peptic ulcer . irritants. NOT curative and used when other measures fall  Gradual withdrawal (after use for 2 weeks).

 Acute attacks indomethecin. naproxen.  Colchicine inhibits phagocytic activity & migration of leukocytes to the area of uric acid deposition and inflammatory response. but not with aspirin (plasma urate levels at low doses by inhibiting uric acid secretion in renal tubules).  Heart disease GOUT  deposition of Na urate crystals in the joint € painful arthritis.  Allopurinol lowers plasma urate by inhibiting xanthine oxidase (xanthine € uric acid).  Uricosuric drugs (probenicid ) inhibit renal tubular reabsorption of uric acid € excretion. Prednisolone is most often used with DMARDs . preserve joint structure & function.  Should drink plenty of H2O Acute Treatment  NSAIDS (indomethacin)  Corticosteroids Chronic Treatment  Allopurinol  Uricosuric drugs  Low-dose colchicine RA  auto-immune  Causes inflammation & swelling  Disease-modifying anti-rheumatic drugs (DMRDs) are recommended for almost all RA patients within 3 months of diagnosis to reduce joint damage. or other NSAIDs. improve patient’s symptoms & lower health care costs  Steroids are often used along with DMARDs DMARDs may take weeks to months to have effects.