This document discusses NSAIDs (non-steroidal anti-inflammatory drugs). It begins by defining NSAIDs and describing their mechanisms of action, including inhibiting cyclooxygenase enzymes to reduce prostaglandin production. It then classifies different types of NSAIDs and describes their individual properties, mechanisms of action, effects, and potential adverse reactions. The document provides detailed information on the pharmacology of NSAIDs.
NSAIDs are the chemically diverse class of drugs that have anti-inflammatory, analgesic & antipyretic properties.
They are also called as Non Narcotic, Non Opioid, Aspirin like analgesics.
They are among the widely used therapeutic agents world wide and often taken without prescription for minor aches and pain.
They are used to suppress the symptoms of inflammation associated with rheumatic disease.
Non-steroidal anti-inflammatory drugs (NSAIDs) are a group of often chemically unrelated compounds with some common therapeutic actions and side effects. They have potent anti-inflammatory, analgesic and antipyretic activity, and are among the most widely used drugs worldwide.
A presentation describing pain, analgesia, formation of prostaglandins along with a detailed description of NSAIDS, the mechanism of action, classification and an in depth discussion of each class along with key points to be kept in mind for dentists
NSAIDs are the chemically diverse class of drugs that have anti-inflammatory, analgesic & antipyretic properties.
They are also called as Non Narcotic, Non Opioid, Aspirin like analgesics.
They are among the widely used therapeutic agents world wide and often taken without prescription for minor aches and pain.
They are used to suppress the symptoms of inflammation associated with rheumatic disease.
Non-steroidal anti-inflammatory drugs (NSAIDs) are a group of often chemically unrelated compounds with some common therapeutic actions and side effects. They have potent anti-inflammatory, analgesic and antipyretic activity, and are among the most widely used drugs worldwide.
A presentation describing pain, analgesia, formation of prostaglandins along with a detailed description of NSAIDS, the mechanism of action, classification and an in depth discussion of each class along with key points to be kept in mind for dentists
GEMC- Pharmacology of Pain Medications- for NursesOpen.Michigan
This is a lecture by Michelle Munro from the Ghana Emergency Medicine Collaborative. To download the editable version (in PPT), to access additional learning modules, or to learn more about the project, see http://openmi.ch/em-gemc. Unless otherwise noted, this material is made available under the terms of the Creative Commons Attribution Share Alike-3.0 License: http://creativecommons.org/licenses/by-sa/3.0/.
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Analgesics in maxillofacial surgery by Dr. Amit T. Suryawanshi, Oral Surgeon...All Good Things
Hi. This is Dr. Amit T. Suryawanshi. Oral & Maxillofacial surgeon from Pune, India. I am here on slideshare.com to share some of my own presentations presented at various levels in the field of OMFS. Hope this would somehow be helpful to you making your presentations. All the best.
Brufen Tablets for Treatment of Arthritis, Dysmenorrhoea, and PyrexiaThe Swiss Pharmacy
Brufen Tablets (Ibuprofen) is used for relief of the signs and symptoms of Rheumatoid arthritis, Osteoarthritis, Juvenile rheumatoid arthritis, Primary dysmenorrhoea, and Pyrexia. Brufen is also used for the relief of acute and/or chronic pain states in which there is an inflammatory component
NSAIDs have an extremely safe profile when used for acute dental pain.
Within a group they tend to have similar characteristics & tolerability. There is little difference in clinical efficacy among the NSAIDs when used at equivalent doses.
Rather, differences among compounds usually relate to dosing regimens (related to compound’s elimination half –life), route of administration, & tolerability profile.
So, clinician should have a thorough knowledge of mechanism of action, pharmacokinetics, pharmacodynamics, dosage & adverse effects of each drug before prescribing the same.
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.
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.
This whole slide is all about the NSAIDs in detail
it contents - 1. Inflammation 2. NSAIDs 3. Salicylate (Aspirin)
4. Propionic Acid Derivatives (Ibuprofen) 5. Anthranilic Acid Derivatives[Fenamate] (Mephenamic Acid)
Related questions about above topics
A PowerPoint presentation on "NSAIDS" suitable for reading by UG and PG Medical/Paramedical students of Pharmacology and Pharmacy sciences. This Ppt. is prepared for academic purpose only and already presented to my students in one of the theory classes of mine.
The eicosanoids are oxygenation products of polyunsaturated
long-chain fatty acids. They are ubiquitous in the animal kingdom
and are also found—together with their precursors—in a variety
of plants. They constitute a very large family of compounds that
are highly potent and display an extraordinarily wide spectrum of
biologic activity. Because of their biologic activity, the eicosanoids,
their specific receptor antagonists and enzyme inhibitors, and
their plant and fish oil precursors have great therapeutic potential.
Opportunity for Dentists (BDS/MDS )to relocate to United kingdom -Register as a DENTAL HYGIENIST/ DENTAL THERAPIST without Board exams and after approval you can register in GDC as a DH/DT and start working as a DH/DT Immediately and get paid.
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Indian Dental Academy: will be one of the most relevant and exciting training center with best faculty and flexible training programs for dental professionals
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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.for more details please visit
www.indiandentalacademy.com
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.for more details please visit
www.indiandentalacademy.com
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The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
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The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
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The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
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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.for more details please visit
www.indiandentalacademy.com
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.for more details please visit
www.indiandentalacademy.com
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.for more details please visit
www.indiandentalacademy.com
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.for more details please visit
www.indiandentalacademy.com
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.for more details please visit
www.indiandentalacademy.com
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.for more details please visit
www.indiandentalacademy.com
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.for more details please visit
www.indiandentalacademy.com
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.for more details please visit
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Embracing GenAI - A Strategic ImperativePeter Windle
Artificial Intelligence (AI) technologies such as Generative AI, Image Generators and Large Language Models have had a dramatic impact on teaching, learning and assessment over the past 18 months. The most immediate threat AI posed was to Academic Integrity with Higher Education Institutes (HEIs) focusing their efforts on combating the use of GenAI in assessment. Guidelines were developed for staff and students, policies put in place too. Innovative educators have forged paths in the use of Generative AI for teaching, learning and assessments leading to pockets of transformation springing up across HEIs, often with little or no top-down guidance, support or direction.
This Gasta posits a strategic approach to integrating AI into HEIs to prepare staff, students and the curriculum for an evolving world and workplace. We will highlight the advantages of working with these technologies beyond the realm of teaching, learning and assessment by considering prompt engineering skills, industry impact, curriculum changes, and the need for staff upskilling. In contrast, not engaging strategically with Generative AI poses risks, including falling behind peers, missed opportunities and failing to ensure our graduates remain employable. The rapid evolution of AI technologies necessitates a proactive and strategic approach if we are to remain relevant.
Synthetic Fiber Construction in lab .pptxPavel ( NSTU)
Synthetic fiber production is a fascinating and complex field that blends chemistry, engineering, and environmental science. By understanding these aspects, students can gain a comprehensive view of synthetic fiber production, its impact on society and the environment, and the potential for future innovations. Synthetic fibers play a crucial role in modern society, impacting various aspects of daily life, industry, and the environment. ynthetic fibers are integral to modern life, offering a range of benefits from cost-effectiveness and versatility to innovative applications and performance characteristics. While they pose environmental challenges, ongoing research and development aim to create more sustainable and eco-friendly alternatives. Understanding the importance of synthetic fibers helps in appreciating their role in the economy, industry, and daily life, while also emphasizing the need for sustainable practices and innovation.
Instructions for Submissions thorugh G- Classroom.pptxJheel Barad
This presentation provides a briefing on how to upload submissions and documents in Google Classroom. It was prepared as part of an orientation for new Sainik School in-service teacher trainees. As a training officer, my goal is to ensure that you are comfortable and proficient with this essential tool for managing assignments and fostering student engagement.
The Roman Empire A Historical Colossus.pdfkaushalkr1407
The Roman Empire, a vast and enduring power, stands as one of history's most remarkable civilizations, leaving an indelible imprint on the world. It emerged from the Roman Republic, transitioning into an imperial powerhouse under the leadership of Augustus Caesar in 27 BCE. This transformation marked the beginning of an era defined by unprecedented territorial expansion, architectural marvels, and profound cultural influence.
The empire's roots lie in the city of Rome, founded, according to legend, by Romulus in 753 BCE. Over centuries, Rome evolved from a small settlement to a formidable republic, characterized by a complex political system with elected officials and checks on power. However, internal strife, class conflicts, and military ambitions paved the way for the end of the Republic. Julius Caesar’s dictatorship and subsequent assassination in 44 BCE created a power vacuum, leading to a civil war. Octavian, later Augustus, emerged victorious, heralding the Roman Empire’s birth.
Under Augustus, the empire experienced the Pax Romana, a 200-year period of relative peace and stability. Augustus reformed the military, established efficient administrative systems, and initiated grand construction projects. The empire's borders expanded, encompassing territories from Britain to Egypt and from Spain to the Euphrates. Roman legions, renowned for their discipline and engineering prowess, secured and maintained these vast territories, building roads, fortifications, and cities that facilitated control and integration.
The Roman Empire’s society was hierarchical, with a rigid class system. At the top were the patricians, wealthy elites who held significant political power. Below them were the plebeians, free citizens with limited political influence, and the vast numbers of slaves who formed the backbone of the economy. The family unit was central, governed by the paterfamilias, the male head who held absolute authority.
Culturally, the Romans were eclectic, absorbing and adapting elements from the civilizations they encountered, particularly the Greeks. Roman art, literature, and philosophy reflected this synthesis, creating a rich cultural tapestry. Latin, the Roman language, became the lingua franca of the Western world, influencing numerous modern languages.
Roman architecture and engineering achievements were monumental. They perfected the arch, vault, and dome, constructing enduring structures like the Colosseum, Pantheon, and aqueducts. These engineering marvels not only showcased Roman ingenuity but also served practical purposes, from public entertainment to water supply.
Welcome to TechSoup New Member Orientation and Q&A (May 2024).pdfTechSoup
In this webinar you will learn how your organization can access TechSoup's wide variety of product discount and donation programs. From hardware to software, we'll give you a tour of the tools available to help your nonprofit with productivity, collaboration, financial management, donor tracking, security, and more.
Macroeconomics- Movie Location
This will be used as part of your Personal Professional Portfolio once graded.
Objective:
Prepare a presentation or a paper using research, basic comparative analysis, data organization and application of economic information. You will make an informed assessment of an economic climate outside of the United States to accomplish an entertainment industry objective.
Francesca Gottschalk - How can education support child empowerment.pptxEduSkills OECD
Francesca Gottschalk from the OECD’s Centre for Educational Research and Innovation presents at the Ask an Expert Webinar: How can education support child empowerment?
June 3, 2024 Anti-Semitism Letter Sent to MIT President Kornbluth and MIT Cor...Levi Shapiro
Letter from the Congress of the United States regarding Anti-Semitism sent June 3rd to MIT President Sally Kornbluth, MIT Corp Chair, Mark Gorenberg
Dear Dr. Kornbluth and Mr. Gorenberg,
The US House of Representatives is deeply concerned by ongoing and pervasive acts of antisemitic
harassment and intimidation at the Massachusetts Institute of Technology (MIT). Failing to act decisively to ensure a safe learning environment for all students would be a grave dereliction of your responsibilities as President of MIT and Chair of the MIT Corporation.
This Congress will not stand idly by and allow an environment hostile to Jewish students to persist. The House believes that your institution is in violation of Title VI of the Civil Rights Act, and the inability or
unwillingness to rectify this violation through action requires accountability.
Postsecondary education is a unique opportunity for students to learn and have their ideas and beliefs challenged. However, universities receiving hundreds of millions of federal funds annually have denied
students that opportunity and have been hijacked to become venues for the promotion of terrorism, antisemitic harassment and intimidation, unlawful encampments, and in some cases, assaults and riots.
The House of Representatives will not countenance the use of federal funds to indoctrinate students into hateful, antisemitic, anti-American supporters of terrorism. Investigations into campus antisemitism by the Committee on Education and the Workforce and the Committee on Ways and Means have been expanded into a Congress-wide probe across all relevant jurisdictions to address this national crisis. The undersigned Committees will conduct oversight into the use of federal funds at MIT and its learning environment under authorities granted to each Committee.
• The Committee on Education and the Workforce has been investigating your institution since December 7, 2023. The Committee has broad jurisdiction over postsecondary education, including its compliance with Title VI of the Civil Rights Act, campus safety concerns over disruptions to the learning environment, and the awarding of federal student aid under the Higher Education Act.
• The Committee on Oversight and Accountability is investigating the sources of funding and other support flowing to groups espousing pro-Hamas propaganda and engaged in antisemitic harassment and intimidation of students. The Committee on Oversight and Accountability is the principal oversight committee of the US House of Representatives and has broad authority to investigate “any matter” at “any time” under House Rule X.
• The Committee on Ways and Means has been investigating several universities since November 15, 2023, when the Committee held a hearing entitled From Ivory Towers to Dark Corners: Investigating the Nexus Between Antisemitism, Tax-Exempt Universities, and Terror Financing. The Committee followed the hearing with letters to those institutions on January 10, 202
Unit 8 - Information and Communication Technology (Paper I).pdfThiyagu K
This slides describes the basic concepts of ICT, basics of Email, Emerging Technology and Digital Initiatives in Education. This presentations aligns with the UGC Paper I syllabus.
Acetabularia Information For Class 9 .docxvaibhavrinwa19
Acetabularia acetabulum is a single-celled green alga that in its vegetative state is morphologically differentiated into a basal rhizoid and an axially elongated stalk, which bears whorls of branching hairs. The single diploid nucleus resides in the rhizoid.
Read| The latest issue of The Challenger is here! We are thrilled to announce that our school paper has qualified for the NATIONAL SCHOOLS PRESS CONFERENCE (NSPC) 2024. Thank you for your unwavering support and trust. Dive into the stories that made us stand out!
2. Contents
• Introduction
• History
• Classification
• Autocoids
• General properties of NSAIDs
• Mechanism of action of NSAIDs
• Descriptions of various drugs
• Choice of NSAIDs
• Adverse drug interactions
• Role of NSAIDs in periodontics
• conclusionwww.indiandentalacademy.com
3. Introduction
• NSAIDs are also called non narcotic , non opioids or
aspirin like analgesics
• In contrast to the opioid analgesics, the non opioid
analgesics as a group:
1. Relieve pain without interacting with opioid receptors
2. Reduce elevated body temperature
3. Possess antiinflammatory action in different measures.
4. Have antiplatelet activity to varying degrees
5. Do not cause sedation and sleep
6. Are non addicting
www.indiandentalacademy.com
4. History
Medicinial effect of bark of willow-active ingredient
SALICIN
this was converted to sodium salicylate which was first
used in the treatment of rheumatic fever and as
antipyretic in 1875
• Acetyl salicylic acid (Aspirin) was introduced in 1899
• The next major advance was the development of phenyl
butazone
• Recently some selective COX2 inhibitors have been
added
www.indiandentalacademy.com
5. Autocoids
• Are diverse substances produced by wide variety of
cells in the body, having intense biological activity.
Some of the classical autocoids are
1. Amine autocoids –Histamine, 5HT
2. lipid derived autocoids-prostaglandins,
leucotriens,platelet activating factor(PAF)called as
eicosanoids
3. Peptide autocoids- plasma
kinins(Bradykinin,Kallidin,angiotensin
In addition, cytokines,(IL,TNF ) and several peptides like
gastrin may also be considered as autocoids.
www.indiandentalacademy.com
6. Prostaglandins(PGs)
• In 1930 Kurzok and Lieb demonstrated the activity of
human semen on human uterine muscle
• Bergstrom and associates showed that the various PGs
are closely related derivatives of lipid soluble prostanoic
acid
• PGs also present in various other tissue extracts such as
iris, lung,human menstrual fluid, brain, thymus, pancreas
and kidneys.
www.indiandentalacademy.com
7. Biosynthesis of PGs
• Biosynthesized from polyunsaturated fatty acids belonging
either to the linoleic or the alfa lenolenic series.
• The 2 principal PGs are PGE2 & PGF2
• most tissues are capable of synthesizing PGs from the
dietary essential fatty acids.
• In human tissues ,the fatty acid released from membrane
lipids in largest quantity is arachidonic acid
• The chemical, bacterial and thermal insults activate the
phospholipase A and release arachidonic acid from the cell
membrane.
• Thus PGs <s are synthesized locally by the release of
arachidonic acid from membrane lipids in response to
appropriate stimuli.
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8. Pharmcological actions of PGs
• On smooth muscles-
cause contraction of uterine muscle in both pregnant and
non pregnant women in vivo.
Pathophysiological role-
• It has been postulated that PGs mediate initiation and
progression of labour
• Dysmenorrhoea in many women is associated with
increased PG synthesis by the endometrium.this induces
incoordinated uterine ischaemia->pain.
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9. On gastrointestinal system-
• PGE2 & PGI2 synthesized by cox, inhibit the gastric acid
secretion, enhance the mucosal flow & thus have
cytoprotecyive effect on gastric and duodenal mucosa in
humans.
• On CVS-
PGE2 & PGF2 cause vasodilationin most of the vascular
beds.(whereas TXA2 consistently produces
vasoconstriction.)
The vasodilator effect is mainly localised to the arterioles,
precapillary spinchter and post capillary venules.The BP
falls and the blood flow to most of the organs increases.
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10. On platelets
• The PGI2 (synthesized by the endothelium) is a
vasodilator and inhibits platelet aggregation;where as
TXA2 is a platelet derived prostaglandin,it activates
platelet aggregation and is a potent vasoconstrictor.
• Thus PGI2 and TXA2 are opposite in function.
• Its role
Because of its opposing action there is a balance
mechanism of human platelet function
Role in inflammation
PGE2 and PGF2 and PGD2 are the major metabolites in the
cyclooxygenase pathway in the mast cells.
It causes vasodilation & potentiates edema formation.
The PGs are also involved in the pathogenesis of pain and
fever in inflammation
•Some of the beneficial action due to PG synthesis inhibition:•Some of the beneficial action due to PG synthesis inhibition:
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11. Some of the beneficial actions due to
PG synthesis inhibition:
• Analgesia
• Antipyresis
• Anti inflammatory
• Anti thrombotic
• Closure of ductus arteriosis
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12. Shared toxicities due to PG synthesis
inhibition
• Gastric mucosal damage
• Bleeding:inhibition of platelet function
• Limitation of renal blood flow:Na and water retention
• Delay/ prolongation of labour
• Asthma and anaphylactoid reactions in susceptible
individuals
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13. Difference between
opioids Non-opioids
•Act within the CNS
•used in severe type of
pain as in MI,
burns,fracture
•Do not have anti pyretic
action
•No antiinflammatory
action
•No uricose uric effect
•Have drug dependence
and drug addiction
•Act peripherally at the
peripheral nerve endings
•Used in mild to moderate
inflammatory pain
•Reduce fever;have
antipyretic action
•Reduce cardinal signs of
inflammation
•Have uricose uric effect
•No drug dependence
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15. Mechanism of action of NSAIDs
• In 1971,Vane & coworkers made the landmark observation
that aspirin and some NSAIDs blocked PG generation.this
is now considered to be the major mechanism of action of
NSAIDs.
• There is a well known fact that PG participated in the
pathogenesis of inflammation & fever.Inhibition of
biosynthesis of these autocoids will explain the action of
the drug
• The cyclooxygenase enzymes exist in 2 isoforms
COX1 AND COX2
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16. • The COX1 is constitutive.cox1 is present in nearly all
cell types at a constant level and is involved in tissue
homeostasis.
• COX2 normally present in small quantities is absent
from cells except those of kidney and brain)
COX2 is induced by cytokines IL2 and TNF, in activated
leucocytes and other inflammatory cells.
Thus cox1 is physiological while cox2 is usually but not
always) pathological.
Most NSAIDs inhibit cox1 & cox 2 non selectively,but now
selective cox-2 inhibitors have been produced.
www.indiandentalacademy.com
17. Mechanism of action of analgesia
PG induced hyperalgesia by affecting the transducing
property of free nerve endings.
PGs sensitize the chemical receptors of the afferent
pain endings to other mediators such as
bradykinin,and histamine.
NSAIDS when administered,they block the pain
sensitizing mechanism induced by bradykinin and
other algesic substances.
www.indiandentalacademy.com
18. MECHANISM OF ACTION AS ANTI
PYRETIC
:
• NSAIDS reduce body temperature in fever but don’t
cause hypothermia in normothermic individuals
• Fever during infections is produced through the
generation of pyrogens,ILs,TNF,interferons which
induce PG production in hypothalamus.
• They raise the temperature set point in hypothalamus.
• NSAIDs block the action of pyrogens and fever is
reduced
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19. ANTI INFLAMMATORY ACTION
The anti inflammatory potency of different compounds
roughly corresponds with their potency to inhibit
cox
Certain NSAIDs may act by additional mechanism
inducing inhibition of activity of some of the other
mediators.
Other mechanisms also play an important role
Ex:indomethacin inhibits phosphodiesterase and
increases the intra cellular conc.of cyclic AMP.
Cyclic AMP has been shown to stabilize membranes
including lysosomal membranes in PMNs.
This prevents the release of enzymes important in the
inflammatory response
Further the anti inflammatory drug appear to act
inhibiting the activation of T lymphocytes and thus
inhibits release of cytokines.
www.indiandentalacademy.com
20. SALICYLATES:
• Salicylates are esters of salicylic acid
• Ex:methyl salicylate and sodium salicylate
• Can also occur as esters of salicylic acid
• Aspirin is one of the oldest analgesic, anti
inflammatory drug and is still widely used
• Pharmacological actions:
• 1) analgesic,anti pyretic anti inflammatory action:
• Aspirin is weaker analgesic than morphine type
drugs
• Aspirin 600mg <= 60mg codine.
• Salicylates unlike the opioid analgesics produces
relief of pain with out hypnosis or inducing sleep
• The analgesic action is mainly due to blocking of
peripheral pain receptors and prevention of PG
mediated sensitization of nerve endings.
www.indiandentalacademy.com
21. • As anti pyretic:
• As salicylates act centrally and reset the thermostatic
mechanism at normal level and there by bring down the
temperature.
• Anti inflammatory activity:
• Salicylates suppress the clinical signs of inflammation
• Vaso dilation and leukocyte infiltration are suppressed
they reduce the inflammatory component of the
disease by
• Inhibiting PG synthesis in the peripheral tissues
• Reducing the capillary permeability there by minimizing
the exudation of fluid and development of inflammatory
edema.
• Inhibition of neutrophil aggregation and activation
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22. • METABOLIC EFFECTS:
• Cellular metabolism is increased specially in,skeletal
muscles.due to oxidative phosphorelation by
salicylates there is increased heat production
• Large doses of salicylates may lead to
hyperpyrexia,increased protein catabolism.large doses
of salicylates produce hyperglycemia and glycosuria in
normal individuals.
• This is due to central sympathetic stimulation which
causes release of adrenaline and corticosteroids
www.indiandentalacademy.com
23. On respiration
• Salicylates stimulate respiration as a result of direct
and indirect actions.
• Therapeutic doses of salicylates increase the
consumption of oxygen by the skeletal muscles.this
results in increased co2 production .increased co2
causes direct production of the respirator centre
producing an increased in the depth and rate of
respiration.
• Salicylates also stimulates the medullary respiratory
centre directly.
• They also stimulate the chemoreceptors. This
produces an increase in the rate as wellm as the
depth of respiration leading to hyperventilation.
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24. Acid base balance & electrolytes
• When there is respiratory ankylosis produced by
therapeutic doses of salicylates,to compensate this
there is excretion of alkaline urine containing bi
carbonate.
• Along with it Na,K are also excreted.
• In addition water is also lost.Dehydration rapidly
occurs.since more water is lost through the lungs and
by sweating,dehydration is associated with
hypernatremia.
www.indiandentalacademy.com
25. Effect on GIT
• The ingestion of salicylates may produce
• Dyspepsia,nausea and vomiting as a result of gastric
irritation
• Peptic ulceration with GI bleeding leading to
hematemesis or melena
• The salicylates remain un ionised because of the acidic
Ph of the stomach the non ionised form of salicylates is
water soluble;hence it tends to adhere to the gastric
mucosa ther by producing irritation.
• Salicylates also reduce the motility of the stomach and
increase the period of contact of salicylates with the
gastric mucosa.
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26. Immunological effect
• Salicylates suppress a variety of Ag-Ab reactions in
vivo including systemic anaphylaxis in rabbits and
serum sickness in man.
• They also prevent the release of histamine as a result
of Ag-Ab reaction.
• They suppress cell mediated immunity
• Interfere with vitamin K in liver
• Reduce pro thrombin level
• Reduce ESR
• Reduce leukocyte count
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27. Blood and platelets
• When there is leukocytosis the salicylates lower the
leukocyte count
• Aspirin inhibits platelet aggregation.aspirin action is
unique in that it irreversibly inhibits cox by
acetylation thus by inhibiting cyclo oxygenase,it
supresses the synthesis of thromboxane A2 in the
platelets
• This property is made use in post myocardial
infarction and post stroke patients
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28. Uricosuric effects
• Dose related effects is seen
• In small doses less than 2 gm per day
urate retention and antagonism of all other
uricosuric drugs
• In moderate dose 2-5gm/day.
variable effects,often no change
• In large doses >5gm/day
cause increased urate excretion
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29. CVS effects
• Therapeutic doses of salicylates donot produce any
deleterious effects on the CVS
• But larger doses increase cardiac output to meet
increased peripheral oxygen demand and cause vaso
dilation and BP falls.
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30. Endocrine effects
• Salicylate interfere with the binding of thyroid
hormones with their binding proteins,especially
thyroxine binding albumin.
• Thus T3 and thyroxine values are altered.
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31. Pharmacokinetics
• Both salicylic acid methyl salicylate are absorbed from
intact skin when applied locally
• Given orally salicylates are absorbed from the stomach
and largely from the small intestine.
• microfining the drug particles and inclusion of an alkalie
enhances absorption.
• A single therapeutic dose is absorbed with in 30 min
peak plasma levels is achieved with in 2 hours
• After absorption 80% of salicylate is bound to plasma
protein
• Excretion –the metabolites are excreted by glomerular
filtration as well as tubular secretion
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32. • The plasma half life of salicylates ranges from 2-8 hours
• The plasma t1/2 of aspirin is 15 to 20 minutes
• That means salicylates exihibit dose dependent
excretion
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33. Adverse reaction of aspirin
a) Side affects- occur at analgesic dose (o.3-1.5g/day)
nausea, vomitting, epigastric distress increased occult
blood loss in stools.
most important-gastric mucosal damage and peptic
ulceration
b)Hypersensitivity and idiosyncracy
Reactions include rashes, fixed drug eruptions,
urticaria,rhinorrrhoea, angioedema, asthama and
anaphylactoid reactions.
Aspirin is sometimes involved in the precipitation of
bronchospasm
Aspirin can induce idiosyncratic, mild hemolysis in
individuals with G6PD deficiency.
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34. c)Salicylism-
this syndrome develops when plasma level exceeds
25mg%.
Characterised by headache, dizziness,vertigo, tinnitus,
reversible impairment of hearing& vision
Drowsiness lethargy and mental confusion may also
occur.
In such cases the dosage has to be reduced
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35. d) Reye’s syndrome
• Seen in children <12 years
• Is a rare form of hepatic encephalopathy seen in
children having viral infection
• An association with aspirin therapy and reye’s
syndrome has been noted
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36. Acute salicylate poisoning
• Seen in overzealous therapy in infants or on
accidental ingestion by children.
• Serum salicylate level of 50mg% indicates mild
toxicity.
• Levels above 75mg% is fatal(15-30gm in saliva)
• Manifestations are
vomitting, dehydration,electrolyte
imbalance,acidotic breathing,hyperglycemia
hyperpyrexia,GI irritation and occasional
hemorrhage.
• Treatment –external cooling & i.v fluid with
Na,K, HCO3
-
and glucose if hypoglycemia is
seen.
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37. Precautions and contraindications
• Aspirin is contraindicated in patient who are sensitive to it
and in peptic ulcer, bleeding tendencies,in children
suffering from chicken pox or influenza
• In chronic liver diseases cases of hepatic necrosis
• Avoided in diabetics and congestive heart failure
• Aspirin to be stopped 1 week before elective surgery and
dental extraction
• In pregnant women, latating mothers
• Avoid high doses in G6PD deficient individuals since
hemolysis can occur.
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38. Preparations and dosage
1. Aspirin as acetyl salicylic acid as 300-600mg tablets
2. Dose :4-6 hourly maxi.4gm/day for relief of moderate
pain
3. In the Rx of acute rheumatism 4-8gm daily in divided
doses.
4. Soluble aspirin tablet as 300-600mg
5. Buffered aspirin – contain aspirin along with antacid
like magnesium hydroxide, aluminium hydroxide
6. Sodium salicylate 500mg tab
7. Lysine acetyl salicylate – i.v infusion of this
preparation may be used to treat post operative pain
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39. Interactions of aspirin
1. Aspirin displaces warfarin, naproxen, sulfonyl
ureas,phenytoin and methotrexate from binding sites
on plasma proteins; toxicity of these drugs may occur.
2. It inhibits tubular secretion of uric acid (at analgesic
doses) and antagonizes uricoseuric action of
probenicid.
3. It blocks the diuretic action of furosemide or thiazides
and reduces K+ conserving action of spironolactone.
4. Aspirin interferes with vit K synthesis in liver and
thereby reduce prothrombin level and prolong the
bleeding time.
Aspirin like drugs are synergistic with anticoagulants
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40. Uses of aspirin
1. Local application-salicylic acid is used for its
keratolytic,fungistaticand mild antiseptic
activity.
2. As analgesic-for headache, tooth ache,
backache, myalgia, joint pain, muscle pull,
neuralgias and dysmenorrhoea.
• Used alone or in combination
• Analgesic effect is maximal at 1gm.
3. As antipyretic
effective in fever of any origin.
dose is same as for analgesia
However paracetamol being safer is generally
preferred www.indiandentalacademy.com
41. 4. In acute rheumatic fever- first drug to be used in all
cases
5. In rheumatoid arthritis
6. Osteo arthritis- it affords symptomatic relief only .
7.Postmyocardial infarction and post stroke patients
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42. Drug Combination Effect Management
Options/Considerat
ions
Oral anticoagulants
with all NSAIDs
Increased oral
warfarin activity
Increased risk of
bleeding
(especially GI)
Monitor
prothrombin time
and for occult
blood in stool and
urine
Avoid concurrent
use of aspirin
Lithium with all
NSAIDs
Increased steady
state lithium
concentration
Lithium toxicity
Monitor lithium
concentrations
carefully
Interactions less
likely with aspirin
than naproxen
sodium or
ibuprofen
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43. Antihypertensive agents
(beta-blockers, ACE
inhibitors, vasodilators,
diuretics) with several
NSAIDs
Antihypertensive effect
antagonized
Hyperkalemia may occur
with potassium-sparing
diuretics and ACE
inhibitors
Monitor blood pressure
and cardiac function
Monitor potassium
concentration
Low-dose aspirin (e.g., 75
mg/day) may not interact
with ACE inhibitor
Digoxin with NSAIDs Renal clearance inhibited Monitor digoxin
concentrations
Adjust dose as necessary
Valproate with aspirin Oxidation of valproate
inhibited
Up to 30% reduction in
clearance
Possible valproate toxicity
Avoid aspirin with
valproate
Naproxen sodium is an
alternative
Phenytoin with ibuprofen and
high-dose salicylates
Increased phenytoin
levels: phenytoin is
displaced from serum
protein binding sites, if
phenytoin metabolism is
saturated or folate
concentrations are low
Monitor unbound
phenytoin concentrations
and adjust dose, if
necessary
Ensure patient has
sufficient folate intake
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44. Methotrexate with all
NSAIDs
Reduced renal clearance
Increased plasma
methotrexate
concentration
Avoid NSAIDs with high-
dose methotrexate
Monitor concentrations
with concurrent therapy
Antacids (in high doses)
with salicylates, aluminum
hydroxide,and naproxen
sodium
Salicylate concentrations
possibly reduced by 25%
Aluminum hydroxide
decreases naproxen
sodium absorption
Monitor clinical status
Determine if salicylate
dose needs to be
increased
Probenecid with naproxen
sodium
Cephalosporins with
aspirin
Reduced clearance of
naproxen sodium
Possible increased
bleeding risk
Monitor for adverse effects
Avoid concurrent use
H2-blocking agents with
salicylates, naproxen
sodium
Potential salicylate toxicity
Potentially reduced
naproxen sodium effect
Monitor salicylate
concentration
Monitor clinical status
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45. Corticosteroids with
aspirin; salicylates (high
doses)
Possible decreased
salicylate effect due to
increased clearance
Monitor salicylate
concentration when
changing corticosteroid
dose
Insulin with salicylates Possible decreased
hypoglycemic effect with
large salicylate doses
Monitor blood glucose
Sulfonylureas with
salicylates (moderate to
high-dose
Hypoglycemic activity
increased
Avoid concurrent use
Monitor blood glucose
concentrations
when changing salicylate
dose
Aminoglycoside antibiotic
sand NSAIDs
Inhibits aminoglycoside
renal clearance
Monitor antibiotic
concentrations and adjust
dose as needed
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51. Uses of aspirin
1. Local application-salicylic acid is used for its
keratolytic,fungistaticand mild antiseptic activity.
2. As analgesic-for headache, tooth ache, backache,
myalgia, joint pain, muscle pull, neuralgias and
dysmenorrhoea.
• Used alone or in combination
• Analgesic effect is maximal at 1gm.
3. As antipyretic
effective in fever of any origin.
dose is same as for analgesia
However paracetamol being safer is generally preferred
4. In acute rheumatic fever- first drug to be used in all
cases
5. In rheumatoid arthritis
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52. 4. In acute rheumatic fever- first drug to be used in all
cases
5. In rheumatoid arthritis
6. Osteo arthritis- it affords symptomatic relief only .
7.Postmyocardial infarction and post stroke patients
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53. Paraaminophenol derivatives
• Eg.paracetamol, phenacetin, acetanilid
• Paracetamol is the deethylated active metabolite of
phenacetin.
• Actions
Exerts analgesic and antipyretic effects like salicylates i.e
it raises pain threshold.
Has a weak peripheral anti inflammatory action.
more active on cox in the brain.
• Compared to salicylates, it does not produce
gastrointestinal irritation, Acid –base balance, electrolyte
imbalance, nor does it effect clotting.
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54. Pharmacokinetics
• Paracetamol is well absorbed orally.(only 1/3 is protein
bound in plasma).
• Peak plasma levels are reached within ½ to 1 hour.
• Plasma t1/2 is 2-3 hours
• It is metabolised in the liver and the metabolites excretd
in urine as conjugation products of glucuronic and
sulfuric acids
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55. Adverse effects
• Hepatic and renal toxicity –occurs after years of heavy
ingestion of analgesics.it causes hepatocellular
damage and renal tubular necrosis and may cause
death.
• Pathological lesions like tubular atrophy followed by
renal fibrosis is seen.
• Paracetamol may ause fever, neutropenia,
thrombocytopenia, nephropathy and skin reactions.
• It may rarely produce anemia as a result of
hemolysis.individuals with G6PD deficiency may
exhibit increased sensitivity to this drug.
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56. Therapeutic uses of paracetamol
• It is a suitable substitute for aspirin for analgesic or
antipyretic uses, particularly
• valuable for patients in whom aspirin is
contraindicated.eg.those with peptic ulcer.
it does not prolong bleeding time.
• One of the most commonly used over the counter
analgesic for headache, musculoskeletal pain,
dysmenorrhoea etc
• Recommended as first choice analgesic for
osteoarthritis
• One of the best drugs to be used as antipyretic
• Can be used in all age groups
• Does not have significant drug interaction.
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57. • Dose:500 mg is used as analgesic and antipyetic.
• Total daily dose should not exceed 2.5gm in adults
• It can be used in a liquid form in children
• Can be used as injection Febrinil(150mg/dl)
• Aspirin+ Paracetamol gives an additive synergestic effect. i
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58. Pyrazolone derivatives
a. These are aminopyrine & antipyrine
b. Phenylbutazone &oxyphenbutazone
c. Metamizol (dipyrone) & prophenazone
The first group is not used because there was high
incidence of agranulocytosis.
The second group are also rarely used coz of increased
risk of bone marrow deoression.
The third group are now available in India and are
primarily used as analgesic and antipyretic ,
But is a poor antiinflammatory.
Dose : 0.5-1.5 g oral/ i.m/ i.v
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59. Metamizol available as Analgin 0.5g tab
novalgin,Baralgam0.5g tab, 0.5/ml in
2ml
•Propiphenazone: dose 300-600mg TDS
preparation available as SARIDON
(propiphenazone150mg+paracetamol 250mg tab )
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60. Indole Derivatives
• Eg. Indomethacin
• Is a potent antipyretic and analgesic
• Is a potent inhibitor of PG synthesis and suppress
neutrophil motility
• pharmacokinetics-
Is well absorbed orally.It is 90% bound to plasma
protein, partly metabolised in liver to inactive
products and excreted by kidney,
• Dose :25-50mg QID.
• Available as Indocid, Indoflam.
• Uses : indicated in rheumatoid arthritis, not
controlled by aspirin.
• Acts rapidly in acute GOUT.
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61. Propionic Acid Derivative
• Eg. Ibuprofen, naproxen, ketoprofen, flurbiprofen
• Ibuprofen was the first member of this group to be
introduced.
• The analgesic antipyretic and antiinflammatory effect is
similar to aspirin
• All inhibit PG synthesis and also prolong bleeding time
• Pharmacokinetics-
all are well absorbed orally, highly bound to plasma
protein(90-99%) and like aspirin displace drugs such as
Hydantoins, Sulfonyl ureas and Warfarin
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62. Adverse effects
• Ibuprofen and all its congeners are better tolerated than
aspirin.
• Side effects are milder and their incidence is lower.
• Gastric irritation, nausea, vomitting are common.
gastric erosion and occult blood loss are rare.
• CNS side effects include headache, dizziness, blurring of
vision, tinnitus and depression.
• Not prescribed to pregnant women and should be avoided
in peptic ulcer patient.
• These drug may precipitate aspirin induced Asthma
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63. uses
• Widely used in rheumatoid arthritis, osteoarthritis and
other musculoskeletal disorders
• Are indicated in soft tissue injuries ,fractures,
Vasectomy, tooth extraction,postpartum and post
operatively suppress swelling and inflammation.
• Ibuprofen –has been related as the safest conventional
NSAID by the SPONTANEOUS ADVERSE DRUG
REACTION REPORTING SYSTEM IN U.K
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64. ARYL Acetic Acid derivatives
• Eg. Diclofenac
• This drug has substantially greater activity than
Indomethacin, Naproxen and other NSAID.
• It inhibits PG synthesis and has short lasting antiplatelet
action.
• It is well absorbed orally, 99% protein bound.
• Metabolized and excreted both in urine and bile.
• Plasma t1/2 is 1-2 hours.
• Diclofenac accumulates in synovial fluid after oral
administration
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