This document summarizes the biosynthesis, receptors, and pharmacological actions of eicosanoids including prostaglandins, thromboxanes, prostacyclins, and leukotrienes. It describes that these molecules are derived from arachidonic acid and produced via the cyclooxygenase and lipoxygenase pathways. The document outlines the different receptors for each eicosanoid class and their downstream signaling effects. It also provides details on the physiological and pathological roles of eicosanoids in various organ systems such as the cardiovascular, pulmonary, gastrointestinal, renal and immune systems.
A Powerpoint presentation on the basics of Eicosanoids which includes Prostaglandins, Leukotrienes (LTs) ad Platelete Activating Factors (PAF) suitable for Undergraduate level Medical students.
A Powerpoint presentation on the basics of Eicosanoids which includes Prostaglandins, Leukotrienes (LTs) ad Platelete Activating Factors (PAF) suitable for Undergraduate level Medical students.
This ppt provides the detailed about the bradykinin and their physiological and pharmacological actions and their generation and their mechanisms in detailed manner.
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.
(Eicosanoids) Prostaglandins, leucotrienes, and platelet activating factorsPranatiChavan
Prostaglandins (PGs) and Leukotrienes (LTs) are biologically active derivatives of 20 carbon atom polyunsaturated essential fatty acids that are released from cell membrane phospholipids. They are the major lipid derived autacoids.
Part VII-IX: Autocoids- Prostaglandins, Leukotrienes (Eicosanoids) and Platel...Shaikh Abusufyan
This slide deck give detail presentation on Pharmacology of Prostaglandins, Leukotrienes (Eicosanoids) and Platelet Activating Factor.
For all IX video lecture series of this topic click:
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organic compound, any of a large class of chemical compounds in which one or more atoms of carbon are covalently linked to atoms of other elements, most commonly hydrogen, oxygen, or nitrogen. The few carbon-containing compounds not classified as organic include carbides, carbonates, and cyanides. See chemical compound.
This ppt provides the detailed about the bradykinin and their physiological and pharmacological actions and their generation and their mechanisms in detailed manner.
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.
(Eicosanoids) Prostaglandins, leucotrienes, and platelet activating factorsPranatiChavan
Prostaglandins (PGs) and Leukotrienes (LTs) are biologically active derivatives of 20 carbon atom polyunsaturated essential fatty acids that are released from cell membrane phospholipids. They are the major lipid derived autacoids.
Part VII-IX: Autocoids- Prostaglandins, Leukotrienes (Eicosanoids) and Platel...Shaikh Abusufyan
This slide deck give detail presentation on Pharmacology of Prostaglandins, Leukotrienes (Eicosanoids) and Platelet Activating Factor.
For all IX video lecture series of this topic click:
https://www.youtube.com/playlist?list=PLBVbJ9HCa1BYfo1EfxdCJtJDf8EjT0ffl
- For More Such Learning You Can Subscribe to My YouTube Channel.
https://www.youtube.com/channel/UC5o-WkzmDJaF7udyAP2jtgw/featured?sub_confirmation=1
Facebook Page: https://www.facebook.com/asacademylearningforever
Website Blog: https://itasacademy.blogspot.com/
organic compound, any of a large class of chemical compounds in which one or more atoms of carbon are covalently linked to atoms of other elements, most commonly hydrogen, oxygen, or nitrogen. The few carbon-containing compounds not classified as organic include carbides, carbonates, and cyanides. See chemical compound.
I have taken the reference from Essentials of Medical Pharmacology by K.D. Tripathi and tried to present the material in the form of short notes. I hope these slides will help you understand and learn things in a better way. Thank You.
Dr. Jibachha Sah,M.V.Sc( Veterinary pharmacology, TU,Nepal),posted lecturer notes on AUTONOMIC AND SYSTEMIC PHARMACOLOGY for B.V.Sc & A.H. 6 th semester veterinary students of College of veterinary science,Nepal Polytechnique Institute, Bharatpur, Bhojard, Chitwan, Nepal.I hope this lecture notes may be beneficial for other Nepalese veterinary students. Please send your comment and suggestion .Email:jibachhashah@gmail.com,moble,00977-9845024121
The principal eicosanoids of biological significance to humans are a group of molecules derived from the 20:4 (20 carbons: 4 sites of unsaturation) fatty acid, arachidonic acid.
By Dr. Vishal Pawar, MD pharmacology
considering the complex nature of this topic, i am hereby providing a comprehensive review of prostaglandins and its various effects in the body, which after a through go through should be enough for simplifying the understanding of prostaglandins
Eicosanoids is the class of lipids derived from arachidonic acid. Eicosanoids play an important role in the growth and development, cellular signalling, drug response, platelet action and maintenance of body homeostasis.
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
micro teaching on communication m.sc nursing.pdfAnurag Sharma
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New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
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Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
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Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
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Evaluation of antidepressant activity of clitoris ternatea in animals
Eicosanoids
1.
2. INTRODUCTION
•Prostaglandins (PGs) and Leukotrienes (LTs) are
biologically active derivatives of 20 carbon atom
polyunsaturated essential fatty acids that are released from
cell membrane phospholipids.
•In the body PGs, TXs and LTs are all derived from Eicosa
(referring to 20 C atoms) enoic acids.
•Therefore, they can be collectively called Eicosanoids.
02
4. •Cyclo-oxygenase is known to exist in two isoforms
COX-1 and COX-2.
•While both isoforms catalyse the same reactions,
COX-1 is synthesized in most cells.
•The other hand, COX-2 present in insignificant
amounts, is inducible by cytokines, growth factors
and other stimuli during the inflammatory response.
04
5. •Eicosanoids produced by COX-1 participate in
physiological (house keeping) functions such as secretion of
mucus for protection of gastric mucosa, haemostasis and
maintenance of renal function.
•While those produced by COX-2 lead to inflammatory and
other pathological changes.
•Certain sites in kidney, brain and the foetus constitutively
express COX-2 which may play physiological role.
05
6. •Lipoxygenase pathway appears to operate mainly in
the lung, WBC and platelets.
•Its most important products are the LTs, (generated
by 5-LOX) particularly LTB4 (potent chemotactic)
and LTC4, LD4 which together constitute the ‘slow
reacting substance of anaphylaxis’.
06
7. INHIBITION OF SYNTHESIS OF EICOSANOIDS
•Synthesis of COX products can be inhibited by nonsteroidal anti-
inflammatory drugs (NSAIDs).
•Aspirin acetylates COX at a serine residue and causes irreversible
inhibition while other NSAIDs are competitive and reversible
inhibitors.
•Most NSAIDs are nonselective COX-1 and COX-2 inhibitors, but
some later ones like Celecoxib, Etoricoxib are selective for COX-2.
07
8. •NSAIDs do not inhibit the production of
LTs.
•Zileuton inhibits LOX and decreases the
production of LTs. It was used briefly in
asthma, but has been withdrawn.
08
9. •Glucocorticosteroids inhibit the release of
arachidonic acid from membrane lipids (by
stimulating production of proteins called
Annexins which inhibit phospholipase A2)
indirectly reduce production of all eicosanoids
PGs, TXs and LTs.
09
10. DEGRADATION OF EICOSANOIDS
•Biotransformation of Eicosanoids occurs rapidly in most
tissues, but fastest in the lungs.
•Most PGs, TXA2 and prostacyclin have plasma t½ of a few
seconds to a few minutes.
•Metabolites are excreted in urine.
•PGI2 is catabolized mainly in the kidney.
10
11. PROSTANOID RECEPTORS
•All Prostanoid receptors are G-protein coupled receptors which can be
functionally categorized into ‘excitatory’ or ‘contractile’ and ‘inhibitory’
or ‘relaxant’ groups.
•The contractile group (EP1, FP, TP) couple primarily with Gq protein and
generate IP3 and DAG. These second messengers release Ca2+
intracellularly resulting in excitatory responses like smooth muscle
contraction, platelet aggregation, etc.
•The relaxant group (DP1, EP2, EP4 and IP) couple with Gs protein and
activate adenylyl cyclase to generate intracellular second messenger cAMP.
11
12. DP
•This receptor has strongest affinity for PGD2, but PGE2
can also activate it.
•Two subtypes DP1 and DP2 have been identified, but both
have limited distribution in the body.
•DP1 is a relaxant receptor which dilates certain blood
vessels and inhibits platelet aggregation.
•DP2 receptor couples with Gi protein and inhibits cAMP
generation.
12
13. FP
•This contractile receptor is highly
expressed in the female genital tract,
and is present in many other organs.
•It exhibits strong affinity for PGF2α.
13
14. TP
•Characterized by high affinity for TXA2,
this contractile receptor is abundant in
platelets (aggregatory), cardiovascular
system, immune cells and many other
organs.
•PGH2 can also activate TP.
14
15. EP
•This receptor is characterized by highest affinity for
PGE2.
•Four subtypes have been recognized:
EP1 is a contractile receptor—contracts visceral
smooth muscle, but is less abundant in the body.
EP2 and EP4 are relaxant in nature, act by increasing
cAMP in smooth muscle, but the same second messenger
enhances Cl¯ and water secretion by the intestinal mucosa.
15
16. •While EP2 is present in few
organs, EP4 has wide distribution.
EP3 is inhibitory, decreases
cAMP generation by coupling with
Gi protein.
16
17. IP
•This relaxant receptor is defined by
highest affinity for PGI2, but PGE2
also acts on it.
•It is expressed in heart, lungs, kidney,
platelet (anti-aggregatory), etc.
17
18. LEUKOTRIENE RECEPTORS
•Separate receptors for LTB4 (BLT1 and BLT2) and
for the cysteinyl LTs (LTC4, LTD4) have been found
out.
•Two subtypes, cysLT1 and cysLT2 of the cysteinyl
LT receptor have been cloned.
18
19. •All LT receptors couple with Gq protein and
function through the IP3/DAG transducer
mechanism.
•The BLT receptors are chemotactic and
primarily expressed in leucocytes and spleen.
19
20. •BLT1 receptor has high, while BLT2 receptor has lower
affinity for LTB4. The cysLT1 receptor is mainly expressed
in bronchial and intestinal muscle and has higher affinity
for LTD4 than for LTC4.
•The primary location of cyslt2 receptor is leucocytes and
spleen, and it shows no preference for LTD4 over LTC4.
•The cyslt1 receptor antagonists, viz. Montelukast,
zafirlukast, etc.
20
23. •1.CVS
•PGE2 and PGF2α cause vasodilatation in most, but not all, vascular
beds.
•PGF2α constricts many larger veins including pulmonary vein and
artery. Fall in BP occurs when PGE2 is injected i.v. But,PGF2α has
little effect on BP.
•PGI2 is uniformly vasodilatory and is more potent hypotensive than
PGE2.
23
24. •TXA2 consistently produces vasoconstriction.
•PG endoperoxides (G2 and H2) are inherently
vasoconstrictor, but often produce vasodilatation by rapid
conversion to other PGs, especially PGI2 in the blood
vessels themselves.
•PGE2 and PGF2α stimulate heart by weak direct but more
prominent reflex action due to fall in BP. The cardiac output
increases.
24
25. •2.PLATELETS
•TXA2, which can be produced locally by platelets, is a potent
inducer of aggregation and release reaction.
•The endoperoxides PGG2 and PGH2 are also pro-aggregatory.
•PGI2 (generated by vascular endothelium) is a potent inhibitor of
platelet aggregation.
•PGD2 has anti-aggregatory action, but much less potent than PGI2.
•PGE2 has dose dependent and inconsistent effects.
25
26. •3.UTERUS
•PGE2 and PGF2α uniformly contract human uterus,
in vivo, both pregnant as well as non-pregnant.
•The sensitivity is higher during pregnancy.
•During early stages, uterus is quite sensitive to PGs
though not to oxytocin.
26
27. •PGs increase basal tone as well as amplitude of
uterine contractions.
•When tested in vitro, PGF2α consistently produces
contraction while PGE2 relaxes non-pregnant but
contracts pregnant human uterine strips.
•PGs soften the cervix at low doses and make it more
compliant.
27
28. •4.BRONCHIAL MUSCLE
•PGF2α, PGD2 and TXA2 are potent
bronchoconstrictors.
•PGE2 is a powerful bronchodilator.
•PGI2 produces mild dilatation. Asthmatics are more
sensitive to constrictor as well as dilator effects of
PGs.
28
29. •PGE2 and PGI2 also inhibit histamine
release..
•Antiasthmatic effects of PGE2 and PGI2
cannot be exploited clinically because they
produce irritation of the respiratory tract and
have a brief action.
29
30. •5.GIT
•In isolated preparations, the longitudinal muscle of gut is
contracted by PGE2 and PGF2α while the circular muscle
is either contracted (usually by PGF2α) or relaxed (usually
by PGE2).
•Propulsive activity is enhanced in man, especially by PGE2
→ colic and watery diarrhoea are important side effects.
30
31. •PGE2 acts directly on the intestinal mucosa
and increases water, electrolyte and mucus
secretion.
•PGI2 does not produce diarrhoea and in fact
opposes PGE2 and toxin induced fluid
movement.
31
32. •6.KIDNEY
•PGE2 and PGI2 increase water, Na+ and K+
excretion and have a diuretic effect.
•PGE2 has been shown to have a furosemide-like
inhibitory effect on Cl¯ reabsorption as well.
•They cause renal vasodilatation and inhibit tubular
reabsorption.
32
33. •PGE2 antagonizes ADH action, and this adds to
the diuretic effect.
•In contrast, TXA2 causes renal vasoconstriction.
•PGI2, PGE2 and PGD2 evoke release of renin.
33
34. •7.CNS
•PGs injected i.v. penetrate brain poorly, so that central
actions are not prominent.
•However, injected intracerebroventricularly PGE2 produces
a variety of effects—sedation, rigidity, behavioural changes
and marked rise in body temperature.
•PGI2 also induces fever, but TXA2 is not pyrogenic.
34
35. •8.EYE
•PGF2α induces ocular inflammation and lowers I.O.T by
enhancing uveoscleral and trabecular outflow.
•Non irritating congeners like Latanoprost are now first line
drugs in wide angle glaucoma.
35
36. •9.ENDOCRINE SYSTEM
• PGE2 facilitates the release of anterior pituitary
hormones—growth hormone, prolactin, ACTH, FSH and
LH as well as that of insulin and adrenal steroids.
•PGF2α causes luteolysis and terminates early pregnancy in
many mammals, but this effect is not significant in humans.
•Though PGs can terminate early pregnancy in women, this
is not associated with fall in progesterone levels.
36
37. •10.METABOLISM
•PGs are antilipolytic, exert an insulin like effect on
carbohydrate metabolism and mobilize Ca2+ from
bone.
•They may mediate hypercalcaemia due to bony
metastasis.
37
39. •1.CVS AND BLOOD
•LTC4 and LTD4 injected i.v. evoke a brief rise
in BP followed by a more prolonged fall.
•LTs increase capillary permeability and are
more potent than histamine in causing local
edema formation.
39
40. •LTB4 is highly chemotactic for neutrophils and
monocytes.
•Migration of neutrophils through capillaries and their
clumping at sites of inflammation in tissues is also
promoted by LTB4.
•The cysteinyl LTs (C4, D4) are chemotactic for
eosinophils.
40
41. •2.SMOOTH MUSCLES
•LTC4 and D4 contract most smooth muscles.
•They are potent bronchoconstrictors and induce
spastic contraction of G.I.T. at low concentrations.
•They also increase mucus secretion in the airways.
41
42. •3.AFFERENT NERVES
• Like PGE2 and PGI2, the LTB4 also
sensitizes afferents carrying pain impulses—
contributes to pain and tenderness of
inflammation.
42
43. THERAPEUTIC USES OF PROSTAGLANDINS,
THROMBOXANES, PROSTACYCLIN & LEUKOTRIENES
•Maintenance of patent ductus arteriosus
•Treatment of dysmenorrhoea
•Therapeutic abortion
•Treatment of asthma
43
49. •1. PLATELETS
• Aggregation and release reaction and also
releases TXA2.
•i.v. injection of PAF results in intravascular
thrombosis.
49
50. •2. WBC
• PAF is a potent chemotactic for neutrophils,
eosinophils and monocytes.
•It stimulates neutrophils to aggregate, to stick to
vascular endothelium and migrate across it to the
site of infection.
50
51. •It also prompts release of lysosomal enzymes
and LTs as well as generation of superoxide
radical by the polymorphs.
•The chemotactic action may be mediated
through release of LTB4.
• It induces degranulation of eosinophils.
51
52. •3. BLOOD VESSELS
• Vasodilatation mediated by release of EDRF
occurs → fall in BP on i.v. injection.
•Decreased coronary blood flow has been
observed on intracoronary injection.
52
53. •PAF is the most potent agent known to increase
vascular permeability.
•Wheal and flare occur at the site of intradermal
injection.
•Injected into the renal artery PAF reduces renal
blood flow and Na+ excretion by direct
vasoconstrictor action.
53
54. •4. STOMACH
• PAF is highly ulcerogenic.
•Erosions and mucosal bleeding occur shortly
after i.v. of PAF.
•The gastric smooth muscle contracts.
54
55. •5. VISCERAL SMOOTH MUSCLES
•Contraction occurs by direct action of PAF.
•Aerosolized PAF is a potent Bronchoconstrictor.
•It produces mucosal edema, secretion and a delayed
and long-lasting bronchial hyper-responsiveness.
•It also stimulates intestinal and uterine smooth
muscle.
55
56. REFERENCES
•K.D.Tripathi. Essentials Of Medical Pharmacology Jaypee
Publishers Seventh Edition 2008.
•Goodman & Gilman. Manual Of Pharmacology &
Therapeutics.
•Charles R Craig. Modern Pharmacology with Clinical
Applications Fifth Edition.
56