Painunpleasant 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 painPain of sudden in onset, usually subsides when treated, &
typically occurs over less than 6-week period of time (injury healing time).
Chronic painPersistent or recurring pain that is often difficult to treat.
Typically lasts longer than 3 months (beyond injury healing time).
Pain thresholdLevel of stimulus needed to produce a painful sensation
Analgesia: Absence of pain
Pain: An unpleasant sensory & emotional experience with actual or potential
tissue damage or described in terms of such damage
Mechanism of pain: Stimulus (cause of pain) detected by pain receptors
(nociceptors) sensory nerve pain centre (perception) emotional
reaction (pain threshold)
Relief of pain
Analgesics

Narcotic analgesics (Opioid analgesics)

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

Anaesthetic agents

General anaesthetics
Local anaesthetics

Narcotic analgesics

Used to control moderate to severe pain.

Properties

Control moderate to severe pain by acting on opioid receptors: mu (),

kappa (k), delta (), alters perception of & response to painful stimuli
while producing generalized CNS depression
receptor both spinal & supraspinal analgesia, euphoria,
dependence, respiratory depression and inhibition of gut motility
k receptor analgesia at spinal cord level and dysphoria, do not
contribute to dependence

receptor may contribute to spinal analgesia, respiratory depression

and inhibition of gut motility

Classification of narcotic analgesia

Pure agonists (primarily at , perhaps at k & ): morphine,

methadone
Partial agonist and mixed agonist antagonists: nalorphine(partial
agonist)
Antagonist (all receptors): naloxone

Morphine

Papaver somniferum
prototype of opioids

CNS stimulation (excitation)

Miosis
Vomiting
Mood changes

CNS depression
Sedation
Respiratory depression
Analgesia

Impairs sympathetic vascular reflexes

reduces mental distress
retention of urine

PA

Uses

relieve moderate to serve pain

relive dyspnea
relieve anxiety
Suppressing cough
control of diarrhea

Asthma
drug allergy
Paralytic ileus
Morbid obesity with sleep apnea
Patients with severe head injuries

CI

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
agonist
Drug of choice for detoxification treatment for opioid addiction

Meperidine(Pethidine)

Synthetic ( & k), with lower analgesic action

has anticholinergic action (dry mouth, 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, Tremors, seizures
Non-narcotic analgesics

Non-steroidal analgesic, antipyretic & anti-inflammatory drugs

(NSAIDs)
Classification
Para-aminophenol derivative: paracetamol (acetaminophen)
Salicylic acid derivatives: Aspirin (acetylsalicylic acid)
Propionic acid derivatives: Ibuprofen, naproxen
Indoleacetic acids derivatives: Indomethacin diclofenac*,etodolac*
Fenamic acid (Anthranilic acids) derivatives: Mefenamic acid
Oxicams: Piroxicam, 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

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
Reyes Syndrome(Caused by aspirin & other salicylates)

PARACETAMOL

Therapeutic efficacy: equal to aspirin in analgesic

less effect on platelets, 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, nausea, abdominal pain

not be used in pregnant women & children
Severe frontal headache

DICLOFENAC

Non-selective COX inhibitor, most used among NSAIDs

Potency against COX-2
Rapidly & completely absorbed

Uses

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, rheumatoid arthritis

ADE & CI

Hypertension & oedema.

Selective COX-2 inhibitors depress PGI2 formation by endothelial cells

thrombosis
CI in cardiovascular or cerebrovascular diseases

INFLAMMATION
Remove harmful stimuli, includi damaged cells, irritants, or pathogens - &
begin the healing process.
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,
NOT curative and used when other measures fall
Gradual withdrawal (after use for 2 weeks), A 50% reduction in dose
may be made on each day

ADE

Fat redistribution
Hypertension
Glucose intolerance
Risk of infection
Cataracts

Infection
Peptic ulcer
Heart disease

CI

GOUT

deposition of Na urate crystals in the joint painful arthritis.

Acute attacks indomethecin, naproxen, or other NSAIDs, but not with
aspirin (plasma urate levels at low doses by inhibiting uric acid
secretion in renal tubules).
Colchicine inhibits phagocytic activity & migration of leukocytes to
the area of uric acid deposition and inflammatory response.
Allopurinol lowers plasma urate by inhibiting xanthine oxidase
(xanthine uric acid).

Uricosuric drugs (probenicid ) inhibit renal tubular reabsorption of uric

acid excretion.
Should drink plenty of H2O

Acute Treatment

NSAIDS (indomethacin)
Corticosteroids

Chronic Treatment

Allopurinol
Uricosuric drugs
Low-dose colchicine

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, preserve joint structure & function, improve patients
symptoms & lower health care costs
Steroids are often used along with DMARDs DMARDs may take weeks
to months to have effects. Prednisolone is most often used with
DMARDs

RA