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2. PAIN (Algesia)
“Pain is an unpleasant sensory and
emotional experience associated with
actual or potential tissue damage or
described in terms of such damage”
International Association for the Study
of Pain
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3. WHY FEEL PAIN?
• Gives conscious awareness of tissue
damage
• Protection:
– Removes body from danger
– Promotes healing by preventing
further damage
• Elicits behavioural and emotional
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responses
4. LOCALIZATION OF PAIN
• Superficial Somatic Pain arises from
skin areas
• Deep Somatic Pain arises from
muscle, joints, tendons & fascia
• Visceral Pain arises from receptors
in visceral organs
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5. FAST AND SLOW PAIN
• Most pain sensation is a combination of the
two types of message.
– If we prick our finger we first feel a sharp
pain which is conducted by the A fibres,
– and this is followed by a dull pain
conveyed along C fibres.
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6. • FAST PAIN (acute)
– Occurs rapidly after stimuli (0.1
second)
– Sharp pain like needle puncture or cut
– Not felt in deeper tissues
– Larger myelinated A nerve fibers
– Velocity of 80 m/s
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7. • SLOW PAIN (chronic)
– Begins more slowly & increases in
intensity
– In both superficial and deeper tissues
– Smaller unmyelinated C nerve fibers
– Velocity of 0.4 m/s
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9. ANALGESIC
• It is a drug that selectively relieves pain
by acting in the CNS or on peripheral
pain mechanisms,without significantly
altering consciousness
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22. MECHANISM OF ACTIONa) Morphine + receptors
Hyperpolarization of nerve cells
Inhibition of nerve firing
Presynaptic inhibition(transmitter)
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23. b) Morphine + k receptors
Reduces release of substance P
c) Morphine inhibits release of
excitatory transmitters from nerve
terminals carrying nociceptive stimuli
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25. NOCICEPTORS
• Nociceptors are special receptors that
respond only to noxious stimuli and
generate nerve impulses which the brain
interprets as "pain".
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32. MEPERIDINE
• It is a synthetic opioid used for acute pain.
1.MECHANISM OF ACTION:Meperidine+k receptors
2. ACTIONS: Depression of respiration
Dilates cerebral vessels
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34. 5. ADVERSE EFFECTS:Large doses lead to tremors,muscle twitches
6.DRUG INTERACTIONS:It increases depression along with major neuroleptics
7.TOLERANCE:It causes dependence and cross tolerance.
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35. METHADONE
High oral parenteral activity ratio (1:2) and firm
binding to tissue proteins.
1. MECHANISM OF ACTION:Methadone+mu receptors
2. ACTIONS:-Analgesia
-Respiratory depression
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36. 3.THERAPEUTIC USES:a) SUBSTITUTION THERAPY OF OPIOID
DEPENDENCE;
1 mg of oral methadone for 4 mg of opioid ,2
mg of heroin,20 mg of pethidine.
b) MAINTENANCEwww.indiandentalacademy.com
THERAPY :-
38. FENTANYL
It is 80-100 times more potent than morphine.
1.ACTIONS:Analgesia
Respiratory depression
2.THERAPEUTIC USES:Anaesthesia injection form exclusively
Transdermal fentanyl has become available for use
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in cancer or chronic pain
40. PROPOXYPHENE
It is a derivative of methadone
2.USES:d isomer leads to analgesia
l isomer leads to antitussive action
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41. 3.SIDE EFFECTS: Nausea,vomiting
Toxic doses ; respiratory depression
Used with alcohol,sedatives ;severe CNS
depression and death
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42. CODEINE
It is a less potent analgesic than morphine having
higher oral efficacy
ACTIONS:Analgesia
Sedation
Euphoria
Depresses the cough reflex.
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43. PENTAZOCINE
1.MECHANISM OF ACTION:It is an agonist on k receptors and weak antagonist
on mu and delta receptors.
2.USES:Analgesia
Angina
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44. 3.ACTIONS: Analgesia by activating receptors in the spinal
cord
4.ADVERSE EFFECTS:Higher dose;respiratory depression
Tolerance and dependence
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45. BUPRENORPHINE
It is a partial agonist acting at the mu
receptors metabolized in liver and excreted in
bile and urine.
It causes nausea,dizziness,respiratory
depression.
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46. NALOXONE
It reverses coma and respiratory depression of
opioid overdose.
It rapidly displaces all receptor bound opioid
molecules
MECHANISM OF ACTION: It is a competitive antagonist at mu,k,delta receptors
with a ten fold affinity for mu .
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47. NALTREXONE
It has a longer duration of action than
naloxone and a single oral dose blocks the
effect of injected heroin for upto 48 hours.
USES: Opiate dependence maintenance
programs
Chronic alcoholism
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50. ANTI INFLAMMTORY DRUGS
INFLAMMATION:It is the body’s effort to inactivate or destroy
invading microorganisms ,remove irritants
and set the stage for tissue repair.
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57. MECHANISM OF ACTION
• Blocks Prostaglandin synthesis(Peripheral targets)
• Prevents sensitization of pain receptors
• Depresses pain stimuli at subcortical sites
(Thalamus,Hypothalamus)
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58. PHARMACOLOGICAL EFFECTS
1. Antipyretic and analgesic effect:The two effects of aspirin are strong and rapid.
2. Anti inflammatory and anti rheumatic effect:(1) Relatively stronger
(2) Often used to the dose of tolerance
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59. 3.
Inhibits platelet aggregation and prevent
thrombosis
– Inhibits TXA2 synthetase
– Aspirin administrated in low dose can reduce
TXA2 remarkably
– Anticoagulant effect
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60. CLINICAL USES
1. Antipyretic and analgesic: Headache,toothache,myalgia,neuralgia , fever ,
dysmenorrhoea(decreases PGE2 synthesis)
2. Anti-inflammation and antirheumatism: Diagnosis and therapy of acute rheumatic fever
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62. ADVERSE REACTIONS
1.Gastrointestinal reactions:
Irritates gastric mucosa directly:
cause epigastric distress nausea and
vomiting
Irritates chemoreceptor trigger
zone(CTZ): cause nausea ,vomiting
Gastric ulcer: can cause and
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deteriorate ulcer
63. 2. Blood Coagulation Disorders:-
• In usual dose:
Inhibits platelet coagulation and prolongs the
bleeding time.
• In high dose or in long term:
Inhibits the formation of prothombin and
prolongs the prothombin time
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70. ANTHRANILIC ACID
DERIVATIVE
MEPHENAMIC ACID
1) MECHANISM OF ACTION:Inhibits COX as well as antagonises certain actions
of prostaglandins
3)USES:Analgesic in muscle,joint and soft tissue pain
Dysmenorrhoea
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71. ARYL ACETIC ACID
DERIVATIVE
DICLOFENAC SODIUM
1) MECHANISM OF ACTION:Inhibits prostaglandin synthesis and has short
lasting antiplatelet action.
Neutrophil chemotaxis,superoxide production
at the inflammatory site is reduced.
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83. MELOXICAM
1. MECHANISM OF ACTION:It has a COX 2:COX 1 ratio of 10
It inhibits platelet TXA production
2.ADVERSE EFFECTS:Gastric changes
Long term bleeding and perforation
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85. SELECTIVE COX 2 INHIBITORS
They reduce prostaglandin 2 production by
vascular endothelium
CELECOXIB
Time dependent
Irreversible inhibition of COX-2
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88. PARA AMINO PHENOL
DERIVATIVE
PARACETAMOL
1. MECHANISM OF ACTION:It raises pain threshold but has weak peripheral
anti inflammatory component
Inhibits Prstaglandin synthesis
in CNS
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91.
Very large dose is taken
Glucuronidation capacity is saturated
More of minor metabolite is formed
Hepatic glutathione is depleted
Metabolite binds covalently to proteins
Necrosis
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92. TREATMENT: Patient brought early- GASTRIC LAVAGE
Prevent further absorption- ACTIVATED
CHARCOAL
Specific antidote-N-acetylcysteine i.v./oral
4 .USES: Best antipyretic
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Headache,toothache,musculoskeletal pain
93. DRUG INTERACTIONS
• NSAIDs + Hypotensive drugs ( β-blockers, ACEinhhibitors, diuretics ) = ↓ hypotensive effect
• NSAIDs + Ethanol = ↑ risk of bleeding from
gastrointestinal tract
• NSAIDs + Ticlopidine or Clopidogrel = ↑ risk of
bleeding
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94. • NSAIDs + Oral antidiabetic drugs = ↑ risk of
hypoglycemia
• NSAIDs + Coumarines =↑ risk of bleeding
• NSAIDs + Corticosteroids = ↑ risk of gastropathy
and bleeding from gastrointestinal tract
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95. • NSAIDs + Lithium = ↑ lithium toxicity
• NSAIDs + Cylosporine or ACE-inhibitors or
Tacrolimus= ↑ nephrotoxicity of drugs
• NSAIDs + Fluoroquinolons = ↑ toxic action of
fluoroquinolones on CNS
• NSAIDs + Oral antidiabetic drugs = ↑ risk of
hypoglycemia
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98. TRAMADOL+PARACETAMOL:
o Faster onset of action compared to
Tramadol alone (17 minutes)
o Longer duration of action compared
to Paracetamol alone (5 hours)
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99. DICLOFENAC + PARACETAMOL;
Actions of Paracetamol set in
earlier and provides pain relief
before the effects of Diclofenac sets
in.
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100. ACECLOFENAC + PARACETAMOL
Inhibits synthesis
of IL-1b,PGE2 production
Positive cartilage anabolism
Modulating effect on matrix
catabolism( GAG )
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104. DISEASE MODIFYING ANTIRHEUMATIC AGENTS
A.
1.
GOLD SALTS:Are taken up by macrophages
Supresses phagocytosis
Lysosomal enzyme activity
Retards bone, articular destruction
THERAPEUTIC USES:Rheumatoid arthritis that does not respond
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to SALICYLATES or other NSAIDS.
106. •
•
•
•
•
CHLOROQUININE AND HYDROXY
CHLOROQUININE:It inhibits nucleic acid synthesis
Stabilizes lysosomal membranes
Traps free radicals
Reserved for RHEUMATOID ARTHRITIS that has
been unresponsive to NSAIDS
Adverse effects include headache, rashes
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107. PENICILLAMINE: It slows the progress of bone destruction and
rheumatoid arthritis.
Prolonged treatment leads to aplastic
anemia,nephritis
METHOTREXATE: It is used for patients with severe rheumatoid
arthritis
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108. DRUGS FOR GOUT
COLCHICINE:It is a plant alkaloid reserved for the treatment of
acute gouty attacks
2) USE:Alleviates the pain of acute gout
within 12 hours.
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109. ALLOPURINOL: Treats primary hyperuricemia of gout
Hyperuricemia secondary to certain
malignancies.
1. ADVERSE EFFECTS:Hypersensitivity reactions
Nausea,diarrhoea
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110. URICOSURIC AGENTS• PROBENECID is a general inhibitor of the tubular
secretion of organic acids and SULFINPYRAZONE
is a derivative of phenylbutazone.
• At therapeutic doses, they block proximal tubular
absoption of uric acid.
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111. CORTICOSTEROIDS
MECHANISM OF ACTION:-(cellular level)
Corticosteroids
Bind to high affinity
Receptor protein(cytoplasmic)
Migrate into the nucleus
Transcription of m-Rna
Regulation of protein synthesis
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112. • The most important overall mechanism appears
to be limitation of inflammatory cells at the local
site.
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113. IMPLICATIONS IN DENTISTRY
•
•
•
•
Recurrent oral ulceration
Severe oral lesions
TMJ pain and stiffness
In case of patients who have been in recent past on
long term corticosteroid therapy,consideration has to
be given to the need for supplementary prophylactic
corticoid to cover a dental procedure.
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114. • For traumatic procedures and those to be performed
under general anaesthesia ,supplemental steroids
may be needed,particularly if the dose and duration
of steroid therapy are such as to have caused
significant adrenal supression .
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115. PREEMPTIVE DIASICS
Recommended to orthodontic
patients before separator placement
IBUPROFEN(reduces pain
at 6 hours and at bedtime on the
night of separator placement)
NAPROXEN SODIUM
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116. ORTHODONTICS
• Direct injection of prostaglandin into periodontal
ligament increases the rate of tooth movement.
• 2 types of drugs are known to depress the
response to orthodontic force and may
influence current treatment:
BISPHOSPHONATES
PROSTAGLANDIN INHIBITORS
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117. BISPHOSPHONATES:-
• Synthetic analogues of pyrophosphate
+
Hydroxyapatite in bone,acts as specific inhibitors of
osteoclast mediated bone resorption.
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118. PROSTAGLANDIN INHIBITORS:A) Corticosteroids and NSAIDS
B) Other agents
CORTICOSTEROIDS:Reduces PG synthesis
Both children and adults on chronic steroid
therapy- difficulty www.indiandentalacademy.com
in tooth movement.
119. NSAIDS
• Potent prostaglandin inhibitors like Indomethacin
can inhibit tooth movement.
OTHER AGENTS
• Tricyclic antidepressants
• Antimalarial drugs –can affect the response to
orthodontic force
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120. • Phenytoin has been reported to decrease tooth
movement
• Some tetracycline(doxycycline) inhibits osteoclast
recruitment.
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121. 1. Acetaminophen has no effect on the rate
of tooth movement in rabbits
undergoing orthodontic tooth
movement.
2. Acetaminophen, a proven analgesic that
lacks the anti-inflammatory properties
of NSAIDS, appears to be the drug of
choice for the relief of orthodontic pain.
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122. 3. Some test subjects may have exhibited
deleterious effects on somatic growth
due either to acetaminophen toxicity or
to orthodontically induced pain.
4. Misoprostol had an insignificant
inhibitory effect on local PGE2
production; however, the degree and
rate of tooth movement was enhanced
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