EICOSINOIDS LIPID DERIVED AUTOCOIDS HAP T
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The document details lipid-derived autocoids, specifically prostaglandins and leukotrienes, which are biologically active derivatives of essential fatty acids. It discusses their chemical structure, biosynthesis, degradation, and various physiological roles across different body systems, including cardiovascular, central nervous, and gastrointestinal systems. The document also highlights the actions and receptors of these compounds, their roles in conditions like asthma and dysmenorrhea, as well as their therapeutic uses and potential adverse reactions.
EICOSINOIDS LIPID DERIVED AUTOCOIDS HAP T
- 3. PROSTAGLANDINS & LEUKOTRIENES Also known as EICOSANOIDS, They are biologically active derivatives of 20 CARBON ATOM POLY UNSATURATED ESSENTIAL FATTY ACID. They released from CELL MEMBRANE PHOSPHOLIPIDS.
- 4. CHEMISTRY,BIOSYNTHESIS & DEGRADATION: Prostaglandins are DERIVATIVES OF PROSTANOIC ACID. It does not naturally occurs in the body. Five membered ring , two side chains in opposite directions at right angle to the plane of ring. LEUCOTRIENES are named because - Obtained from leucocytes – LEUKO. Have 3 conjugated double bonds – TRIENE. Both of them have Designated A,B,C,……I. A,B,C,….F. Subscript 1,2,3. 1,2,3,4.
- 6. DEGRADATION: Arachidonic acid – degradation occurs rapidly in most of the tissues. Occurs fastly in lungs. Most of PG’s, TXA2 have t1/2 of few seconds – few min.
- 7. ACTIONS: PROSTAGLANDINS,THROMBAXANES, CVS: PGE2 & PGF2(AIPHA) vasodilation, fall in BP, stimulate heart, decrease in BP, increase in cardiac output. ROLE: PGI2 - REGULATION OF LOCAL VASCULAR TONE- AS DIALATOR. PGE2 and PGI2 – produced in the DUCTUS ARTERIOSUS during foetal life. PG – internal regulator of blood flow and tubular reabsorption in kidney, renin release.
- 8. CNS: IV-injection- PENETRATE BRAIN POORLY Central effects are not prominent. INTRACEREBROVENTRICULAR injection of PGE2- SEDATION, RIGIDITY, BEHAVIOURAL CHANGE, DECREASE IN BODY TEMPERATURE. PGI2- induces fever. TXA2- is not pyrogenic. ROLE: PGE2- mediate the PYROGEN INDUCED FEVER and MALAISE (uneasyness) PG’s- may function as NEUROMODULATORS in the BRAIN by regulating NEURAL EXCITABILITY and role in pain perception, sleep.
- 9. ANS: Depending on PG’s type and tissue – INHIBITION and STIMULATION OF N.A RELEASE from the adrenergic nerve endings. ENDOCRINE SYSTEM: PGE2- facilitates the RELEASE OF ANTERIOR PITUITARY HORMONE, GROWTH HORMONE, PROLACTINE, ACTH, FSH and LH. PGF2(alpha)- LUTEOLYSIS ( structural and functional degradation of the corpus luteum) and TERMINATES EARLY PREBNANCY.
- 10. PLATELETS: PGI2- produced by vascular endothelium. Potent INHIBITOR OF PLATELET AGGREGATION. PGD2- anti aggrigatory action. ROLE: Prevent aggregation of platelet - in circulation. Inducing aggregation of platelet – on injury.
- 11. UTERUS: PGE2 & PGF2(alpha) contraction of uterus. sensitivity high during pregnancy. Increase in conc. on process of pregnancy. ROLE: PG’s – INITIATION and PROGRESSION OF LABOUR. Present in high conc in SEMEN, Rapidly absorbed when lodged in the vagina Which coordinate movements of the femalegenetial tract Transport of sperm and fertilization.
- 12. DYSMENORRHOEA: Due to increase in PG synthesis by endometrium. Induce uncoordinated uterine contraction Compress blood vessels, uterine ischemia pain.
- 13. BRONCHIAL MUSCLE: PGF2(alpha), PGD2, TXA2 - potent bronchoconstrictors. PGE2 - powerful bronchodilator. PGI2 - mild dilatation. ROLE: Due to IMBALANCE – ASTHMA.
- 14. GIT: PGE2 & PGF2 - CONTRACTION OF GUT MUSCLE. PGE2 – colic and watery diarrhea by acting on intestinal mucosa. ROLE: PG’s involved in – MEDIATING TOXIN INDUCED INCREASED FLUID MOVEMENTS IN DIARRHOEAS. PGE2 – decrease acid secretion in stomach. PGI2 – regulate gastric mucosal blood flow, act as ulcer protectives by ENHANCING GASTRIC MUCUS PRODUCTION.
- 15. KIDNEY: PGE2increase water, Na+, k+ excretion in urine- diuretic effect PGI2 - renal vasodilatation. TXA2 – renal vasoconstriction.
- 16. ACTIONS OF LEUKOTRIENES: CVS AND BLOOD: LTC4 and LTD4 – on IV injection brief rise in BP and prolonged fall. It is not due to VASODILATATION. ROLE: LT’s – important mediators for inflammation they produce locally at the site of injection.
- 17. SMOOTH MUSCLE: LTC4 & LTD4: CONTRACT SMOOTH MUSCLE. POTENT BRONCHODILATOR. At low conc: SPASTIC CONTRACTION OF GIT. ROLE: LTC4 & LTD4 - IMPORTANT MEDIATORS OF ASTHMA
- 18. RECEPTORS: PROSTAGLANDIN RECEPTORS: DP- greater affinity for- PGD2, PGE2- inhibit platelet aggregation. EP- greater affinity for- PGE2- smooth muscle contraction,relaxation, chloride and water secretion in intestinal mucosa. FP- greater affinity for- PGF2(alpha)- smooth muscle contraction. IP- greater affinity for- PGI2,PGE- inhibit platelet aggregation, smooth muscle relaxation. TP- greater affinity for- TXA2, PGH2- platelet aggregation, smooth muscle contraction.
- 19. LEUCOTRIENE RECEPTOR: LT1 & LT2 - valuable drugs for bronchial asthma USES: Abortion Induction/augmentation of labour Cervical priming Post partum haemorrhage Peptic ulcer Glaucoma Prevent platelet aggregation.
- 20. ADR: 1.Nausea 2.Vomiting 3.Watery diarrhea 4.Uterine contractions 5.Uterine cramps 6.Vaginal bleeding 7.Fall in BP 8.Chest pain 9.Tachycardia.
- 21. THANK U ALL