The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and offering a wide range of dental certified courses in different formats.
Indian dental academy provides dental crown & Bridge,rotary endodontics,fixed orthodontics,
Dental implants courses.for details pls visit www.indiandentalacademy.com ,or call
0091-9248678078
Dental tissues and their replacements/ oral surgery courses
Nonsteroidal anti inflammatory drugs (nsai ds) /certified fixed orthodontic courses by Indian dental academy
1. Nonsteroidal Anti(inflammatory Drugs (NSAIDs
INDIAN DENTAL ACADEMY
Leader in continuing dental education
www.indiandentalacademy.com
www.indiandentalacademy.com
5. Salicylates
Acetyl salicylic acid (aspirin).
Sodium salicylates.
Diflunisal (dolobid, difluorophenyl salicylate).
Acetyl salicylic acid (aspirin).
Kinetics:
Well absorbed from the stomach, but better from the upper small
intestine (large surface area). Distributed allover the body, 50-80%
bound to plasma protein (albumin).
Metabolized to acetic acid and salicylates (active metabolite).
Salicylates is conjugated with glucuronic acid and glycine.
Excreted by the kidney.
Alkalinization of the urine increases the rate of salicylates excretion.
www.indiandentalacademy.com
6. Low dose of aspirin 0.6 g is eliminated by
1st order kinetics and its t 1/2 is 3-5 h.
while high dose (more than 4 g/day) is
eliminated by zero-order kinetics and its t
1/2 may increase up to 15 h.
Mechanism of action:
Aspirin irreversibly inhibits cyclooxygenase enzyme, so blocks synthesis of
prostaglandins and thromboxane A2.
www.indiandentalacademy.com
7. Pharmacological effects of aspirin:
Anti-infammatory effects:
Inhibits prostaglandin synthesis.
Blocks action of kinins which are mediated
through prostaglandin synthesis.
Inhibits granulocyte adherence to damaged
vasculature.
Stabilizes lysosomes.
Inhibits migration of PMN leukocytes &
macrophages into the site of inflammation.
www.indiandentalacademy.com
8. Analgesic effects:
Centrally: it inhibits prostaglandin synthesis, so
increasing pain threshold in the thalamus.
Peripherally: inhibits prostaglandin synthesis, so
inhibiting inflammation and diminishes activation
of peripheral pain sensors.
Aspirin alleviates mild to moderate pain of
muscular and dental origin, postpartum states,
arthritis & bursitis.
www.indiandentalacademy.com
9. Antipyretic effect:
It inhibits prostaglandin synthesis in the CNS
Resetting of temperature control in the
hypothalamus.
VD of the superficial BV, so increasing heat
dissipation & sweating.
NB: aspirin lowers elevated temperature while
normal body temperature is only slightly
affected.
www.indiandentalacademy.com
10. Platelet effect:
Aspirin in small dose (75-100 mg /day)
irreversibly inhibits thromboxane A2 synthesis in
the platelets without affecting prostacyclin
synthesis in the vascular endothelium.
Aspirin must be stopped one week prior to
surgery if potential bleeding complications are a
concern.
Aspirin has longer duration as antiplatelet than
ticlopidine, dipyridamole and phenylbutazone.
www.indiandentalacademy.com
11. Uses:
Antipyretic (0.5-2 g / day).
Analgesic for mild to moderate superficial pain
(headache, arthritis, toothache, myalgia) 0.5-2 g/day.
Acute rheumatic fever (6-12 g/ day).
Rheumatoid arthritis (6-8 g / day).
Prophylaxis in thromboembolic diseases e.g. transient
ischemic attack, unstable angina, & MI (75-100 mg /
day).
Other uses under investigation e.g. aspirin may reduce
cataract formation and the incidence of cancer colon.
www.indiandentalacademy.com
12. A/E:
GIT upset: nausea, vomiting, gastritis, ulceration &
bleeding (prevented by misoprostol).
Hypersensitivity: bronchial asthma, angioedema &
rashes.
Idiosyncracy: aspirin causes hemolytic anemia in
patient with G-6-PD deficiency.
Hypoprothrombinemia and bleeding tendency as
aspirin competes with vitamin K, so decreasing
prothrombin synthesis.
Salicylism: aspirin in large doses for long time therapy
causes headache, tinnitus, hearing difficulty, blurring of
vision, GIT upset, irritability & hyperventilation (these
symptoms disappear on stopping aspirin).
www.indiandentalacademy.com
13. At low toxic dose: aspirin produces
respiratory alkalosis followed by acidosis
Teratogenicity
Nephropathy.
Reye's syndrome : aspirin in children with
viral infection may cause liver injury and
encephalopathy.
www.indiandentalacademy.com
14. Acute aspirin poisoning:
Restlessness, tremors, convulsion, vomiting,
dehydration, hypotension, hyperventilation, hyperreflexia,
hyperpyrexia & coma.
Treatment:
Activated charcoal 50g p.o to adsorb salicylates and
prevents its absorption.
Alkalinization of urine (to enhance excretion) by i.v Na
HCO3 which also corrects acidosis.
Anticonvulsant e.g. i.v diazepam.
Cold fomentation and ice bags.
Correct dehydration by i.v fluids (5% dextrose).
Correct acid / base balance (alkalosis or mixed
alkalosis/acidosis need no specific treatment).
Correct hypoprothrombinemia by i.v vitamin K.
Hemodialysis may be needed.
www.indiandentalacademy.com
15. Contraindications:
Peptic ulcer, esophageal varices,
bronchial asthma, idiosyncrasy, allergy,
viral infection in children, bleeding
tendency and small dose in gout
(competes with uric acid excretion).
www.indiandentalacademy.com
16. Interactions:
Alcohol increases aspirin-induced GIT bleeding.
Aspirin displaces oral anticoagulants and oral
hypoglycemics from their plasma protein binding sites,
so increasing their activities and may lead to toxicity.
Aspirin inhibits the uricosuric effects of sulphinpyrazone
and probenecid.
Barbiturates increase the analgesic effect of aspirin.
NB: Diflunisal (difluorophenyl salicylate): it has analgesic
and anti-inflammatory effects like aspirin, but has no
antipyretic action.
www.indiandentalacademy.com
17. Locally acting salicylates
Salicylic acid: keratolytic, antiseptic & fungistatic.
Methyl salicylate (wintergreen oil): used as
counterirritant for muscle and joint pain.
Sulfasalazine : it is a combination of
sulfapyridine and 5-aminosalicylic acid (5-ASA).
Sulfasalazine liberates 5-ASA in the colon where
it blocks the synthesis of leukotriene B4 locally
and used in ulcerative colitis.
www.indiandentalacademy.com
19. Non-acidic NSAIDs
Selective COX-2 inhibitors.
are not concentrated in the gastric mucosa.
and are less likely to produce peptic ulcers
Examples:
Nabumetone: it is a pro-drug, changed in the body to its
active metabolite. It is relatively selective COX-2
inhibitor.
Meloxicam, rofecoxib & celecoxib are selective COX-2
inhibitors.
Rofecoxib and celecoxib may cause cardiac toxicity
(myocarditis).
www.indiandentalacademy.com
20. ).Acetaminophen (paracetamol
It is only analgesic and antipyretic,
it has no anti-inflammatory effect as it
acts centrally only.
It doesn’t cause gastritis.
It doesn’t cause bronchial asthma.
www.indiandentalacademy.com
21. Kinetics:
Well absorbed orally and rectally,
Conjugated with glucuronic acid and
sulforic acid
Excreted in urine.
www.indiandentalacademy.com
22. Dynamics: inhibits PG synthesis in the CNS
only.
Uses: analgesic, antipyretic especially in
children and those who cannot tolerate
aspirin e.g. patients with bronchial asthma,
peptic ulcer or gout.
A/E: Rashes, blood dyscrasias
www.indiandentalacademy.com
23. Toxicity of paracetamol
Large toxic dose causes liver cell
necrosis.
Treated by:
N-acetylcysteine and methioneine which
supply the S-H group necessary to
detoxify the toxic metabolites.
www.indiandentalacademy.com
24. Thank you
For more details please visit
www.indiandentalacademy.com
www.indiandentalacademy.com