Analgesia and Analgesics

Download as ppt, pdf, or txt
Download as ppt, pdf, or txt
You are on page 1of 113
At a glance
Powered by AI
The document discusses a variety of topics over many pages in detail without providing an overt summary.

The concepts seem to be organized by topic, moving from general discussions to more specific details across several pages in a mostly chronological fashion.

Some of the main topics discussed include organizational structures, processes, relationships, and conclusions based on evidence and analysis presented earlier in the document.

ANALGESIA AND ANALGESICS

What is PAIN?

Pain is defined as an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage.

PATHWAYS OF PAIN

STEPS IN CONDUCTION


TRANSDUCTION TRANSMISSION MODULATION PERCEPTION

PAIN MODULATION


Neural impulses re altered, changed or modulated as they travel up neural axis Experience of pain is more complex than simple perception reaction mechanism

PAIN MODULATION


In the trigeminal spinal tract based on the Gate control theory of pain

Pain modulation in reticular formation for example locus cerulus - norepinephrine nucleus raphe - serotonin substantia nigra - Dopamine

DESCENDING INHIBITORY SYSTEM

Modulation effects of endorphins. Pain modulation by psychological factors Excitatory modulating factors Inhibitory modulating factors

TERMINOLOGIES ANALGESIA  ANALGESICS  HYPOALGESIA  HYPERALGESIA  ALLODYNIA




TREATMENT OF PAIN
GOALS OF THERAPY Decrease the frequency and / or severity of the pain General sense of feeling better Increased level of activity Return to work Decreased health care utilization Elimination or reduction in medication usage

MANAGEMENT OF OROFACIAL PAIN




PHARMACOLOGICAL THERAPY PHYSICAL THERAPY PSYCOLOGICAL COUNSELLING

PHARMACOLOGICAL THERAPY
VASOACTIVE AGENTS NOREPINEPHRINE BLOCKERS ANTIMICROBIALS ANTIVIRALS ANTIHISTAMINE AGENTS NEUROLYTICS URICOSURIC AGENTS ETC

ANALGESIC AGENTS ANAESTHETIC AGENTS ANTIINFLAMMATORY MUSCLE RELAXANTS ANTI DEPRESSANTS ANTICONVULSIVE ANTIANXIETY

B. PHYSICAL THERAPY 1 MODALITIES A. SENSORY STIMULATION CUTANEOUS TRANSCUTANEOUS PERCUTANEOUS B. ULTRASOUND C. ELECTROGALVANIC STIMULATION D. DEEP HEAT 2. MANUAL TECHNIQUES A. MASSAGE B. SPRAY & STRETCH TECH. C. EXERCISE D. PHYSICAL ACTIVITY

C. PSYCHOLOGIC THERAPY 1. COUNSELLING 2. BEHAVIORAL MODIFICATION TRAINING A. STRESS REDUCTION TRAINING  B.RELAXTION PROGRAMME

OPIOID ANALGESICS


Opioid refers to all compound related to opium Opium derived from opos the Greek word for juice

poppy flower Papaver somniferam

1st mentioned in Ebers papyrus 1500 BC. Opium contains more than 20 alkaloids. 1806 Serturner isolated and named morphine after Morpheus the Greek god of dreams . 1975 Hughes and associates identified endogenous opioid enkephalin

 

Natural opioids occur in 2 places:


1) In the juice of the opium poppy (morphine and codeine)  2) As endogenous endorphins  All other opioids are prepared from either morphine (semi synthetic opioids such as heroin) or they are synthesized from precursor compounds (synthetic opioids such as fentanyl)


Endogenous Opioids


 

ProPro-opiomelanocortin peptides:  F-endorphin ProPro-enkephalin peptides:  met-enkephalin and leu-enkephalin metleuProdynorphin peptides:


Dyn- DynDyn-A, Dyn-B and E-neo-endorphin neo-

Endomorphins:  Endomorphin-1 and Endomorphin-2 EndomorphinEndomorphin-

MECHANISM


3 TYPES OF RECEPTORS
MU  KAPPA  DELTA  N/OFQ


ACTION produced on binding of these receptors by opioids.

Binding of opioid agonist Inhibition of adenyl cyclase activity activation of receptor operated k+ current suppression of voltage gated Ca+ current hyperpolarisation of membrane potential

Blockade of neurotransmitter release and pain transmission

Classification of OPIOIDS


Natural
  

morphine 10% codeine 0.5% thebaine 0.2%

semi synthetic
  

heroin oxymorphone Hydromorphone meperidine methadone morphinians benzamorphans

synthetic
   

Opioid Agonists
A. Opium alkaloids and derivatives B. Synthetic compounds

Antagonists Mixed agonist-antagonists agonistPartial agonists

Morphine
prototypic opioid analgesic Trade names Rumorf ,Duramor ,Rilimorf etc Dose 10 -100mg alone or in combination

Pharmacological actions
Analgesia Dose dependent Symptomatic relief involves sensory discriminative component and motivational affective component, action with in limbic system Changes our reaction and perception of pain  most effective against continuous dull aching pain  Pain relief increases with age. Peripheral analgesia

Sedation  Euphoria sense of well being, tranquility loss of apprehension reason why morphine is abused Mediated by dopamine release in nucleus accumbance Inhibition of noradrenalin release - allay fear and apprehension. Convulsions At high doses


Temperature Alters equilibrium pt of hypothalamus- body temp hypothalamusfalls slightly




Cough centre is depressed Vasomotor centre Depressed at high doses resulting in fall in BP.

Depression of respiration related to dose  decrease rate  decrease volume  decrease tidal exchange  CNS becomes less responsive to pCO2 thereby causing a build up of CO2  Indifference to breathing seen Pure oxygen produces apnea loss pf hypoxic drive

Pupillary reaction
   

miosis (pinpoint pupils) kappa receptor effect pinpoint pupils still responsive to bright light Edinger Westphal nucleus ooculomotor nerve (CN3) is stimulated Nausea and vomiting Stimulation of CTZ, in area postrema of medulla Has a vestibular component as more common in ambulatory patients

Neuro endocrine Effects




inhibit the release of GnRH and CRF,thus decreasing circulating concentrations of LH, FSH, ACTH, and bendorphin; the concentrations of testosterone and cortisol in plasma decline. Prolactin and growth hormone levels are increased. Secretion of thyrotropin is relatively unaffected.

 

Effects on GIT


increase in tone and decrease in mobility leads to constipation increased tone in stomach, small intestine, and large intestine delay of passage of food (gastric contents) so more reabsorption of water tolerance does not develop to this constipation effect

 

Cardiovascular effects


  

Cardiovascular effects of morphine lead to vasodilation, thus a decrease in blood pressure esp orthostatic hypotension release of histamine suppression of central adrenergic tone and suppression of reflex vasoconstriction

Effects on other smooth muscles




biliary tract  marked increase in the pressure in the biliary tract increase due to contraction of Sphincter of Oddi urinary bladder tone of detrusor muscle and sphincter is increased urinary urgency, urinary retention bronchial muscle bronchoconstriction contraindicated in asthmatics, particularly before surgery uterus contraction of uterus can prolong labor

ANS Mild hyperglycaemia




SKIN Skin appears flushed Urticaria Immune system Suppression of immune system

PHARMACOKINETICS
Routes of administration Oral (preferred) latency to onset 15 60 mins it is also sniffed, swallowed and injected. duration of action 3 6 hours FirstFirst-pass metabolism results in poor availability from oral dosing.  30% is plasma protein bound Metabolism conjugation with glucoronic acid Morphine-3-glucuronideMorphine-6-glucuronide Excretion by kidney 90% in 1st day

    

Side effects Idiosyncrasy and allergy Apnea and respiratory depression Constipation and urinary retention Acute morphine poisoning

due to respiratory depression 50mg severe toxicity 250mg lethal. Rx naloxone 0.4-0.8mg 0.4 

Tolerance Dependence

Tolerance


is a diminished responsiveness to the drugs action Tolerance can be demonstrated by a decreased effect from a constant dose of drug or by an increase in the minimum drug dose required to produce a given level of effect Physiological tolerance involves changes in the binding of a drug to receptors or changes in receptor transductional processes related to the drug of action This type of tolerance occurs in opioids

1997, Gies and colleagues stated that activation of glutamate NMDA receptors correlates with development of tolerance No tolerance to its effect on GIT and miotic effect on pupil

Cross-tolerance person who is tolerant to morphine will also be tolerant to the analgesic effect of fentanyl, heroin, and other opioids

DEPENDENCE

Dependence
   

Physiological dependence Psychological dependence Withdrawal reactions are usually the opposite of the physiological effects produced by the drug Treatment use of methadone 20-30 mg 20antagonist naltrexone

OPIOID WITHDRAWAL

          

Pain and irritability Hyperventilation Dysphoria and depression Restlessness and insomnia Fearfulness and hostility Increased blood pressure Diarrhea Pupillary dilation Hyperthermia Lacrimation, runny nose Severe craving for drug

PRECAUTIONS AND CONTRAINDICATION


In infants and elderly more respiratory depression  Contraindicated in bronchial asthma Head injury  Unstable personalities are liable to continue and become addicts


DRUG INTERACTIONS WITH OPIOIDS


Phenothiazines, tricyclic antidepressants, MAO inhibitors amphetamine, neostigmine, potentiate morphine and other opioids. Delays absorption of many orally administered drugs.

OTHER RELATED OPIOID AGONISTS


Codeine  Methyl morphine  one tenth the potency of morphine  absorbed readily from GI tract  the absorption is more regular and more predictable  less first pass metabolism  metabolized through glucuronic acid  about 10% converted to morphine  antitussive drug for cough

Heroin (diacetylmorphine)  at 3 and 6 hydroxy positions, there are acetyl groups instead of hydroxyl groups  it is 3 to 4 times the analgesic potency of morphine  heroin is the most lipophilic of all the OPIOID  morphine is the least lipophilic of all the OPIOID  OPIOID withdrawal is NOT fatal  Used as brown sugar as a drug of abuse

Meperidine
     

Semisynthetic phenylpiperidine same CNS actions as morphine sedation, analgesia, respiratory depression Dose 50 -100mg im/sc Dose to dose1/8 to1/10 in analgesic potency however analgesic efficacy is near to morphine Plasma half life3 hrs

Pethidine

hydrolysis

meperidinic acid norpethidine

       

unlike morphine: less constipation no antitussive activity it causes mydriasis drug absorbed orally drug most abused by health care professionals due to its availability withdrawal similar to morphine toxic effects similar to atropine Side effects overdose produces excitatory

used as analgesic

Tramadol
     

Trade name Dolotram Synthetic codeine analog Opioid receptor agonist (mu and delta) NE and 5-HT reuptake blocker (antidepressant) 5These actions are synergistic for analgesia Dose 50-100mg orally/im 50-

Fentanyl
Trade names Durogesic patch, Sublimaze
       

synthetic drug related to phenylepiperidine 80 to 100 times more potent than morphine rapidly acting drug due to high lipid solubility used as iv supplement during GA short acting (30-45 min) (30onset of action is 5 minutes Patch delivers 25ug,50ug/75ug /hr highly abused ,known as china white .

Methadone Trade name Physeptone  pharmacologically similar to morphine, long duration of activity  absorbed well orally(1:2)  24 to 36 hrs duration of action on chronic use  powerful pain reliever  used in maintenance program for narcotic treatment

Complex action opioids


Mixed agonist-antagonists agonistNalorphine and cyclazocine not used as analgesic Pentazocine Butorphanol Nalbuphine

has analgesic action

Pentazocine Trade name Fortwin ,Pentawin mostly spinal analgesia obtained but efficiency lower. sedation ,respiratory depression 1/3-1/2 of morphine. 1/3less vomiting, biliary spasms and constipation Dose 25-100mg 4 times daily. 25-

Butorphenol Trade name Butrum More potent analgesic than pentozocine

Partial agonist: Buprenorphine

Trade names Norphin, Tidigesic inj or sl tablets  25 times more potent than morphine  Partial agonist at mu receptors  6-8 hrs action  Lower efficacy analgesic than morphine


Naloxone
Trade name Narcotan,Nalox

competitive antagonist at mu, kappa, and delta receptor  Short half-life ,not effective orally half Antagonizes all action of morphine,nalorphine pentazocine even endogenous opioids.  it will precipitate withdrawal  Drug of choice for morphine poisoning


Naltrexone
Trade name Naltrema  same effect of naloxone except it is used orally so can't use it if for person with acute toxicity  long duration of activity 1-2 days 1 Used for opioid blockade therapy Dose 50mg per day  also used for treatment of alcoholism


Nalmefene
Intermediate duration (4-6 hr) (4orally active no hepatotoxicity with long term use

Opioid therapy is the mainstay approach for


Acute pain Cancer pain Pain in advanced illnesses

But under treatment is a major problem

opiphobia

ALTERNATIVE ROUTES OF ADMINISTRATION


       

Patient controlled analgesia Transdermal Iontophoresis Oral Tran mucosal Rectal route Inhalation computer assisted continuous infusion Intraspinal intrathecal

NSAIDS
NON STEROIDAL ANTI INFLAMMATORY DRUGS

4 Major actions
analgesic  antipyretic  anti-coagulant anti anti-inflammatory anti

MOA OF NSAIDS


inhibit prostaglandin production reduction of activation of T lymphocytes stabilizing the mast cell inhibits bradykinin from stimulating pain receptors May unmask T cell suppressing activity thus decrease production of rheumatoid factor

The anti-inflammatory properties of the antiNSAIDs insure that the release of the prostaglandins, histamines, thromboxanes and leukotrienes is inhibited . Do not produce tolerance Has ceiling effect

CLASSIFICATION


NON SELECTIVE COX INHIBITORS Salicylates :aspirin pyrazolone derivatives : phenylbutazones, Indole : indomethacin Propionic acid : ibuprofen ,Ketoprofen Anthranilic acid : mephanamic acid Aryl acetic acid : diclofenac Oxicam : piroxicam PyroloPyrolo-pyrole :ketorolac

PREFERENTIAL COX2 INHIBITORS Nimesulide meloxicam nabumetone  SELECTIVE COX2 INHIBITORS celecoxib rofecoxib valdecoxib WITH POOR ANTIINFLAMMATORY PROPERTY Paracetamol Metamizol Nefopam


NSAIDS AND COX


Inhibits COX COX1 COX2


Beneficial action due to inhibition of PG Analgesia Antipyretic Anti-inflammatory Antithrombotic

Adverse effect due to inhibition GI mucosal damage Bleeding Decreased renal blood flow ANALGESIC HYPERSENSITIVITY


NSAIDs... A Host Of Drugs




ASPIRIN

Trade name ASPIRIN, ECOSPIRIN,DISPIRIN Acetylsalicylic acid MOA inactivates COX by irreversibly acetylating the enzyme. May inhibit cell migration and formation of rheumatoid factor. decreased capillary permeability, decreased antibody response

PHARMACOLOGICAL PROPERTIES
ANALGESIA Mainly peripheral but central action of raising subcortical action also cotributes.


Shows ceiling effect Do not affect emotional reaction to pain Difficult to separate analgesic and antiantiinflammatory action.

ANTIPYRETIC EFFECT

resets hypothalamic thermal set Promotes heat loss by sweating and vasodilatation But does not reduce heat production.

ANTI INFLAMMATORY EFFECT AND ANTIRHEUMATOID EFFECT

Exerted at a higher dose 3-6gm/day 3Inhibit PG synthesis Reduce capillary permeability So decreased fluid exudation and edema Inhibition neutrophil aggregation Suppression of antigen-antibody reaction antigenInhibit mucopolysaccharide biosynthesis


1.

EFFECT ON RESPIRATION

Increase O2 consumption CO2 stimulates respiration. 2. Direct stimulation of respiratory center Hyperventilation resp. alkalosis renal compensation Plasma conc of 350ug/ml hyperventilation 500ug/ml hyperpnea.

ACID BASE AND ELECTROLYTE BALANCE


RESPIRATORY ALKALOSIS

RESPIRATORY ACIDOSIS

UNCOMPENSATED METABOLIC ACIDOSIS

GIT Epigastric distress, due to Loss of protective mucosal barrier Ion trapping in gastric mucosal cell trapping Back diffusion of acid
 

URATE EFFECTS

<2gm/day<2gm/day- urate retention 2-5gm/day variable effect >5gm/day increase urate excretion

BLOOD

inhibits platelet aggregation platelet COX acetylation occurs presystemically.so selective TXA2 suppressed,no effect on antiaggregatory PGI2. Also lowers leucocytosis and high ESR in acute rheumatic fever.


CVS

At toxic dose depress vasomotor centre BP falls.

METABOLIC EFFECTS

Cellular metabolism increased Large dose cause hyperglycaemia Cause negative nitrogen balance Decrease free plasma FFA


ENDOCRINE

Induce release of adrenaline Interferes with binding of thyroxine to their binding proteins

SALICYLATE AND PREGNANCY

premature closure of ductus arteriosus Low birth weight babies Prolongs labour Greater postpartum blood loss


LOCAL ACTION

salicylic acid and methyl salicylate are irritants Salicylic acid is keratinolytic used in the treatment of warts.

PHARMACOKINETICS
   

taken orally rapidly absorbed from stomach and small intestine. Rate limiting step is disintegration and dissolution 80% is plasma protein bound Plasma t1/2 is 15 20 min,together with salicylic acid is 3 4 hrs.t1/2 anti-inflammatory dose 8 12hrs. antiConjugated in liver with glycine and with glucoronic acid Excreted by glomerular filtration and tubular secretion Elimination dose dependent

ADVERSE EFFECTS


Side effects - nausea ,vomiting, epigastric distress, peptic ulcerations Hypersensitivity and idiosyncrasy Salicylism prolonged use of salicylates develops when plasma conc.>25mg% On kidneys dose dependent water and sodium retention renal artery vasoconstriction Analgesic associated nephropathy

  

Reyes Syndrome is associated use of aspirin in children recovering from viral infections Signs/Symptoms  cerebral edema  encephalopathy  disorientation & confusion  liver damage  liver failure  fatty infiltration of the brain  fatty infiltration of the liver

ACUTE SALICYLATE POISONING


Seen more in children Fatal adult dose 15 30 gm

       

Headache - tinnitus - dizziness hearing impairment dim vision Confusion and drowsiness Sweating and hyperventilation Nausea, vomiting Marked acid-base disturbances Hyperpyrexia Dehydration Cardiovascular and respiratory collapse, coma convulsions and death

Aspirin Toxicity - Treatment




Enhance excretion - alkalinize urine, forced diuresis, hemodialysis Decrease absorption - activated charcoal, emetics, gastric lavage Supportive measures - fluids, decrease temperature, bicarbonate, electrolytes, glucose, etc

CONTRAINDICATIONS AND PRECAUTIONS


        

Peptic ulcer Asthma Diabetes Gout Chronic liver disease G6PD deficient individual In children Hypo coagulation state Aspirin should be stopped 1 wk before elective surgery

DRUG INTERACTIONS


Warfarin, heparin , ethanol increase internal bleeding Phenytoin, methetrexate - plasma conc. increases Probencid, silfinpyrazone decreased uricosuric effect Sulfonylureas, insulin unpredictable effect Diuretics action of furosimide and thiazide is blunted

 

 

USES
      

Analgesic Antipyretic In acute rheumatic fever Rheumatoid arthritis and osteoarthritis Post myocardial infarction patients Closure of ductus arteriosus pregnancy induced hypertension etc

DIFLUNISAL

Trade name DOLOBID


More potent and longer duration than aspirin No antipyretic action PYRAZOLONES include phenylbutazone, oxybutazone antipypyrine, phenylbutazone, antipypyrine, aminopyrine etc. High chances of bone marrow depression, agranulocytosis Recently 2 other pyrazolones available in India Trade name Metamizol NOVALGIN,ANALGIN Propophenazone SARIDON,(in combination with SARIDON,(in paracatamol) paracatamol)


INDOMETHACIN Trade name INDICIN, ARTICID ETC




Use closure of patent ductus arteriosus Malignancy associated fever Rheumatoid arthritis. Use in dentistry not known.  SULINDAC Prodrug of indomethacin  ETODOLAC 3 times more selective COX2 inhibitor t1/2 7hrs

PROPIONIC ACID DERIVATIVES

Ibuprofen BRUFEN, EMFLAM Dose 400 800 mg thrice daily Naproxen Ketoprofen Flurbiprofen Better tolerated than aspirin side effects similar but milder ppt of asthma occurs . Special features: Naproxen inhibit leucocyte migration Ketoprofen stabilizes lysosomes Fluriprofen used as occular anti inflammatory.

MEPHANEMIC ACID MEFTAL Exerts peripheral as well central analgesic action




Adverse effect severe diarrhoea,this limits its use in dental pain management Use analgesic in muscle ,joint ,soft tissue pain where stong anti inflammatory action not required.

DICLOFENAC SODIUM

DICLONAC ,VOVERAN

Dose 100 150 mg in 2-3 divided dose 2Inhibits COX, short lasting antiplatelate action, may reduce intracellular concentration of free arachidonic acid, T1/2 1 -2 hrs Good tissue permeability Adverse effect increase chance of hepatotoxicity DICLOFENAC POTASSIUM
VOLINI,VOLTAFLAM

suited for patients on sodium free diet, hypertensives

OXICAM DERIVATIVES

PIROXICAM MELOXICAM MICROPEC PIRICAM OXYCAM long acting potent analgesic T is 50 hrs Single daily dosing used for long term therapy KETOROLAC KETOROL, ZOROVON Given im or orally Potent analgesic and modest anti inflammatory equal efficincy as morphine in management of post operative pain Adverse effects high incidence of GI ulcerations and postoperative bleedings Not to be used more than 5 days


COXCOX-2 Selectivity

PREFERENTIAL COX2 INHIBITOR ,

NIMESULIDE, MELOXICAM, NABUMETONE


NIMESULIDE Nimulid Dose 100mg BD inhibits cyclooxygenase inhibits neutrophil activation,exhibits antioxidant properties Adverse effect hepatc toxicity so banned in some countries Usefulness lies in patients whoare asthmatics and those who are intolerant to aspirin and other NSAIDs,

MELOXICAM Melflam Newer congener of piroxicam NABUMETONE Nabuflame

Selective COX-II Inhibitors COX   

Celecoxib rofecoxib Valdecoxib

CELECT ROFIBAX VALUS

Anti-inflammatory with less adverse effects, especially GI events. Potential toxicities: kidney and platelets increased risk of thrombotic events due to reduction ofPGI2 JUXTAGLOMERULAR cox2 inhibition salt and water retention, pedal edema, rise in BP ,ppt CHF

PARACETAMOL(ACETOMINOPHEN) Crocin, metacin,calpol

equal efficacy as aspirin for noninflammatory conditions Poor anti-inflammatory effect due to poor ability to inhibit COX in presence of peroxides ,has central analgesic action raises pain threshold. Does not stimulate respiration, affect acid base balance, or cause GI ulcerations. do not effect platelet function .

Adverse effect: occasional nausea and rashes analgesic nephropathy Acute paracetamol poisoning

ACUTE PARACETAMOL POISONING occurs mostly in children with low glucuronide conjugation. Serious toxicity in adults at dose>10gm Features Nausea, vomiting Abdominal pain 12 18 hrs later Centrolobular hepatic necrosis Hypoglycemia Coma Jaundice Hepatic failure and death


Mechanism of toxicity
due to formation of NABQI binds to hepatic cells and renal tubules and cause necrosis.

Treatment
induce vomiting give gastric lavage Activated charcoal is given Specific antidote N acetylcysteine

Contraindicated
in alcoholics In premature children

ADJUVANT ANALGESICS
 

ANESTHETIC AGENT topical anesthetic mainly used as


solutions sprays ointments or lozenges.

injectable local anesthetic


mainly used to control surgical pain, as analgesic agent has 4 facets : to arrest primary pain to interrupt pain cycle to resolve myofascial trigger point activity to induce a sympathetic block

ANTI INFLAMMATORY AGENT

use of corticosteroids esp useful for infalmmatory pain, suppress the symptoms Induce lipocortin thus blocks phospholipaseA2 Suppress synthesis of cyclooxygenase in e Inhibit synthesis of endothelial adhesion molecules

MUSCLE RELAXANTS Used for myogenous pain Depress spinal and sopraspinal reflexes needed to maintain muscle tone.

 drugs such as Diclomine ,methacarbamol used


 

ANTIDEPRESSANTS Tricyclic antidepressants like amitriptyline is used. they increase availability of 5HT and norepinephrine. SSRI used.


ANTIANXIETY AGENTS Phenothiazines, Diazepam Clonazepam for neuropathic pain Useful in pain control by reducing the modulating effect of anxiety and apprehension Their muscle relaxation action is also useful Precaution Long term use may cause dependence and tolerance

ANTICONVULSIVE Carbamazepine Tegretal Gabapentin topiramide Oxycarbamazepine Useful in neuralgic pain Side effects bone marrow suppression Blood dyscrasia


NEUROLYTIC AGENTS

95% ETHYL ALCOHOL GLYCEROL

Others VASOACTIVE AGENTS ANTIHISTAMINICS ANTIMICROBIALS ANTIVIRALS URICOSURIC AGENTS DIETARY CONSIDERATIONS tryptophan

PHYSICAL THERAPY


Sensory stimulation Cutaneous- rubbing the skin


counterirritants, vapocoolants, hydrotherapy

Transcutaneous- TENS, Acupuncture Percutaneous

CutaneousCutaneous-

rubbing the skin counterirritants, hydrotherapy, vapocoolants

VAPOCOOLANT SPRAY

TENS
   

Kane & Tub reviewed history of electric fish to minimize pain Current of low intensity at frequency of 50 to 100 Hz Stimulation of thick A- beta fibers ARelease of serotonin & dynorphins

ACUPUNCTURE
   

Utilizes a low frequency 2hz but high intensity electric current. Applied at acupoints infraorbital acupoint ,Hoku acupoint. Activation of endogenous antinociception Release of B endorphin.

Ultrasound increases temperature at deeper tissue interface thus increases blood flow.

Heat therapy - Short wave diathermy

Indicated in patient with pain in masticatory muscles




mechanical vibration and partly by deeply penetrating thermal energy this increases blood flow

Manual techniques
MASSAGE CAN MAKE A DIFFERENCE

EXERCISE AND PHYSICAL ACTIVITY

PSYCOLOGICAL THERAPY

Counseling Behavioral modification

CHOICE OF ANALGESICS
  

Cause of pain Past h/o pain Anticipation of degree of pain

HIERCHY OF ANALGESIC PRESCRIPTION The most important concept in pain management..

References


 

Goodman and Gilmans The pharmacological basis of therapeutics,10th edition. K D Tripathi ,Essentials of medical pharmacology, 5th edition. Satoskar, Bhandarkar, Ainapure, Pharmacology and pharmacotherapeutics, 18th edition. Okesson JP,Bells orofacial pains, 6th edition Yagiela, Dowd, Neidle,Pharmacology and therapeutics for dentistry,5th edition .

 

THANK YOU

You might also like