Autacoidstu

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Autacoidstu

  1. 1. Autacoids and Inflammation
  2. 2. An 8-year-old boy is stung by a bee. Within 5 minutes he develops a 2 cm, raised, red, swollen lesion an the site of injury. Which of the following findings will be predominant in tissue from a lesion? <ul><li>A. Foreign body reaction </li></ul><ul><li>B. Hemorrhage </li></ul><ul><li>C. Lymphocytic Infiltration. </li></ul><ul><li>D. Neutrophilic migration. </li></ul><ul><li>E. Vasodilation </li></ul>
  3. 3. Inflammation <ul><li>Pathologic state. </li></ul><ul><li>Pain, Redness, Heat, Swelling. </li></ul><ul><li>Vascular permeability. </li></ul><ul><li>Variety of compounds or chemicals can elicit an inflammatory response. </li></ul><ul><li>Eicosanoids and Autacoids. </li></ul>
  4. 4. Eicosanoids <ul><li>“ Eicosa ” greek for 20 . </li></ul><ul><li>Synthesized from oxygenation of 20-carbon fatty acids. </li></ul><ul><li>Most potent regulator of cellular function. </li></ul><ul><li>Produced in almost every cell. </li></ul><ul><li>Participates in inflammation response. </li></ul>
  5. 5. Eicosanoids <ul><li>Forms blood cloths. Pain, swelling and fever. </li></ul><ul><li>Regulate smooth muscle contraction. </li></ul><ul><li>Increase water and Na excretion. (BP) </li></ul><ul><li>Bronchoconstriction and Bronchodilation . </li></ul><ul><li>Gastric protection . </li></ul>
  6. 6. Eicosanoids <ul><li>Prostaglandins and Tromboxanes effects : </li></ul><ul><li>Airway, Gastrointestinal, reproductive and vascular. </li></ul><ul><li>Platelets, monocytes, CNS, presynaptic nerve terminals, sensory nerve endings. </li></ul><ul><li>Endocrine organs, adipose tissue, eye. </li></ul>
  7. 7. Eicosanoids <ul><li>Arachidonic Acid chief precursor. </li></ul><ul><li>Derived dietary linoleic acid (essential) or as a component of meat. </li></ul><ul><li>Store in phospholips of the cell membrane (esterification). </li></ul><ul><li>Phospolipase A 2 release arachidonate. </li></ul>
  8. 8. Eicosanoids <ul><li>Four separate pathways. </li></ul><ul><li>Ciclooxygenase : Prostaglandins. </li></ul><ul><li>Lipoxygenase : Leukotrienes. </li></ul><ul><li>P450 epoxygenase (epoxides). </li></ul><ul><li>Isoprostane pathway (isoprostanes). </li></ul>
  9. 9. Prostaglandins <ul><li>First found on human semen. </li></ul><ul><li>Two Isoenzimes COX-1, COX-2 . </li></ul><ul><li>Converts AA into prostaglandin endoperoxide. </li></ul><ul><li>COX-1 : present in most cells. “housekeeping” stomach lining protection, reduction fever, promotes platelet aggregation. </li></ul>
  10. 10. Prostaglandins <ul><li>COX-2 : Inducible by cytokines, growth factors, tumor promoters. Stimulus dependent. Associated with pain and inflammation. </li></ul><ul><li>LPS (endotoxin) potent stimulus. </li></ul><ul><li>Tissue specific </li></ul><ul><li>Lungs, spleen: synthesize all types. </li></ul><ul><li>Endothelia: PGI 2 . </li></ul><ul><li>Platelets: TXA 2 . </li></ul>
  11. 11. Leukotrienes <ul><li>Lipoxygenase: lungs, platelets, leukocytes. </li></ul><ul><li>Converts AA to 5-HPETE. </li></ul><ul><li>5-HPETE to 5-HETE or Leukotriene A4 (LTA 4 ). </li></ul>
  12. 12. Organ System Effects
  13. 13. Cardiovascular <ul><li>Prostaglandins </li></ul><ul><li>Potent vasodilators ( PGI 2 , PGE 2 ), and vasoconstriction in specific sites and species (TXA 2 , PGF 2a ). </li></ul><ul><li>Vasodilatation = Increase HR and CO. </li></ul><ul><li>TXA 2 : contracts vascular smooth muscle </li></ul>
  14. 14. Cardiovascular <ul><li>L eukotrienes </li></ul><ul><li>Initial increase BP, then prolong hypotension. </li></ul><ul><li>Leukotriene-induce reduction coronary blood flow and reduction cardiac contractibility, leads to CO reduction. </li></ul><ul><li>LTC 4 , LTD 4 . </li></ul>
  15. 15. Blood <ul><li>Platelet: Inhibit aggregation, PGI 2 most potent. </li></ul><ul><li>TXA 2 : promotes aggregation. </li></ul><ul><li>Prostaglandins promote erythropoietin release kidney. </li></ul><ul><li>LTB 4 : leukocyte chemoattractant. </li></ul><ul><li>LTD 4 , LTC 4 : chemoattractants eosinophils (oxygen radical formation). </li></ul>
  16. 16. Kidney <ul><li>PGI 2 , PGE 2 , PGE 1 : increase renal blood flow. Na, K excretion. </li></ul><ul><li>TXA 4 : decreases renal blood flow (vasoconstriction). </li></ul><ul><li>PGE 2 , PGI 2 : stimulate renin release. </li></ul><ul><li>Leukotrienes: role is speculative. </li></ul>
  17. 17. Smooth Muscle <ul><li>Bronchial </li></ul><ul><li>PGF 2 , TXA 2 : Bronchoconstriction. </li></ul><ul><li>PGE 2 : dilates bronchial muscle . </li></ul><ul><li>LTC 4 , LTD 4 : potent bronchoconstrictors, mucus secretion, increase microvascular permeability. </li></ul>
  18. 18. Smooth Muscle <ul><li>Uterus </li></ul><ul><li>PGE, PGA, PGD: uterine relaxation. </li></ul><ul><li>PGF: uterine contractions. </li></ul><ul><li>Gastrointestinal muscle </li></ul><ul><li>Prostaglandins: Variable. decrease gastric time, diarrhea, cramps. </li></ul>
  19. 19. Gastrointestinal <ul><li>Prostaglandins </li></ul><ul><li>PGE 2 , PGI 2 : inhibit gastric secretion. </li></ul><ul><li>PGE 2 , PGF 2 : increase small bowel secretion. </li></ul><ul><li>Leukotrienes </li></ul><ul><li>LTB 4 : produced in colonic cells, chemoattractant for neutrophiles. </li></ul>
  20. 20. CNS <ul><li>PGE 1 , PGE 2 : increase body temperature. </li></ul><ul><li>Intraventricular injections PGEs: sedation, stupor or catatonia. </li></ul><ul><li>PGEs inhibit release of norepinephrine. </li></ul><ul><li>PGFs: stimulates release norepinephrine. </li></ul><ul><li>PGEs causes pain when injected intradermally. </li></ul>
  21. 21. Endocrine System <ul><li>PGE 1 : stimulates release ACTH, GH, Prolactin, Gonadotropins. </li></ul><ul><li>PGE 2 : facilitates release LH,TSH, insulin and steroids. </li></ul><ul><li>PGEs: inhibit lipolysis. </li></ul>
  22. 22. Mechanism Action <ul><li>Receptors for prostaglandins: 5 groups according to the PG which are more selective (DP, EP, FP, IP, TP) </li></ul><ul><li>DP-PGD, EP-PGE, TP-TXA 2 , etc. </li></ul><ul><li>Leukotrienes receptors activate phospholipase C. </li></ul>
  23. 23. Processes <ul><li>TXA 2 and PGI 2 : opposite actions in modulating platelet interactions. </li></ul><ul><li>High Prostaglandins synthesis play a role in the genesis in dysmenorrhea. </li></ul><ul><li>Prostaglandins are elevated in labor. Inhibition COX delays labor. </li></ul><ul><li>PGI 2 , PGE 2 maintains patency of the ductus arteriosus. </li></ul>
  24. 24. Processes <ul><li>PGE 2 : dilates bronchial smooth muscle. </li></ul><ul><li>PGF 2 , TXA 2 : bronchoconstriction. </li></ul><ul><li>Leukotrienes ( LTC 4 ) major responsible for allergic bronchoconstriction in asthma. </li></ul><ul><li>Medullary carcinoma of the thyroid and breast carcinoma, associated with high serum prostaglandins. </li></ul><ul><li>PGEs: high osteolytic activity (hypercalcemia of malignancy) </li></ul>
  25. 25. Processes <ul><li>PGE 2 , PGI 2 : increase blood flow to areas of inflammation. </li></ul><ul><li>Leukotrienes: increase vascular permeability and attracts leukocytes. </li></ul>
  26. 26. Clinical Uses <ul><li>PGE 1 (Alprostadil) </li></ul><ul><li>Maintains a patent ductus arteriosus . </li></ul><ul><li>Treatment of erection dysfunction (intracavernosal injection or urethral suppository. </li></ul><ul><li>Apnea, bradycardia, hypotension, hyperpyrexia. Prolong erection, priapism, pain (less frequent). </li></ul>
  27. 27. Clinical Uses <ul><li>PGE 1 (Misoprostol) </li></ul><ul><li>Prevention of NSAID-induce peptic ulcers . </li></ul><ul><li>Cytoprotective (low doses), inhibits gastric secretion (high doses). </li></ul><ul><li>Adverse Effects: diarrhea, abdominal discomfort (dose-related). </li></ul>
  28. 28. Clinical Uses <ul><li>PGE 2 (Dinoprostone) </li></ul><ul><li>Inducing abortions in the second trimester, missed abortion, benign hydatidiform mole, ripening of the cervix. </li></ul><ul><li>Induction of full term labor. </li></ul><ul><li>Adverse Effects: vomiting, diarrhea, fever, bronchoconstriction, hypotension, syncope, dizziness and flushing. </li></ul>
  29. 29. Clinical Uses <ul><li>PGF 2a (Carboprost) </li></ul><ul><li>Second trimester abortions. </li></ul><ul><li>Withdrawn of market. </li></ul><ul><li>Adverse: Cardiovascular collapse (severe). Anaphylactic shock, pulmonary hypertension . </li></ul>
  30. 30. Clinical Uses <ul><li>Prostacyclin PGI 2 (epoprostenol) </li></ul><ul><li>Substitute Heparin in Hemodialysis. </li></ul><ul><li>Primary and secondary pulmonary hypertension. </li></ul><ul><li>Improves symptoms and prolongs survival. Extremely short half-life. </li></ul><ul><li>Treprostinil: longer half life. </li></ul>
  31. 31. Clinical Uses <ul><li>PGF 2a (Latanoprost) </li></ul><ul><li>Glaucoma </li></ul><ul><li>Bimatoprost, Travaprost, Unoprostone. </li></ul><ul><li>Adverse: irreversible brown pigmentation of the iris and eyelashes, drying of the eye and conjunctivitis. </li></ul>
  32. 32. Inhibition <ul><li>Aspirin and NSAIDs (COX-1, COX2). </li></ul><ul><li>Celecoxib, Rofecoxib (COX-2 specific) </li></ul><ul><li>Corticosteriods (Inh.Phospholipase A 2 ) </li></ul><ul><li>Zileuton (inh. Lypoxygenase) </li></ul><ul><li>Zafirlukast, Montelukast (leukotriene receptor inhibitors) </li></ul>
  33. 33. Dietary manipulation <ul><li>Different fatty acids produce different eicosanoids. </li></ul><ul><li>Two approaches. </li></ul><ul><li>1.- Use corn or sunflower oil (Linolenic C18:2)to produce PG 1 class (PGI 1 , PGE 1 ) </li></ul><ul><li>2.- Use fish oil “OMEGA-3” (C20:5) produces PG 3 class (PGI 3 , PGE 3 ). </li></ul><ul><li>Reduction in TXA 2 , PGI 2 . </li></ul><ul><li>Beneficial changes in platelet aggregation, vasomotor spasm, cholesterol metabolism. </li></ul>
  34. 34. Autacoids <ul><li>Endogenously produced subtances of intense pharmacologic activity. </li></ul><ul><li>Don’t fit into other specific classes. </li></ul><ul><li>“ Local hormones”. “autopharmacologic agents”. </li></ul><ul><li>Histamine, Serotonin, Kinins, Angiotensins, Eicosanoids. </li></ul>
  35. 35. Histamine <ul><li>Decarboxylation of amino acid Histidine </li></ul><ul><li>Found in nearly all tissues. Highest concentrations skin, lung, GI mucosa. </li></ul><ul><li>Stored circulating basophils and tissue mast cells . </li></ul><ul><li>Release: secretory process triggered by binding of specific antigen to a IgE surface “Degranulation”. </li></ul><ul><li>Immediate hypersensibility, allergy and anaphylaxis. </li></ul><ul><li>Reduce cAMP or cGMP favors release. B-adrenergic stimulation and glucocorticoids decrease release . </li></ul>
  36. 36. Organ System Effects
  37. 37. Cardiovascular <ul><li>Dilatory effect on the vasculature. Causes flushing, hypotension, low peripheral resistance, increase capillary permeability. </li></ul><ul><li>Inotropic and Chronotropic effect (H 2 ) </li></ul><ul><li>“ Triple Response ” (intradermal injection) </li></ul><ul><li>1.- Localized erythema (vasodilatation) </li></ul><ul><li>2 .- Bright red flare surrounding the local spot (axon reflexes, more vasodilatation) </li></ul><ul><li>3.- Wheal of edema (increase permeability of postcapillary venules) </li></ul>
  38. 38. Smooth Muscle <ul><li>H 1 agonist: contraction; Bronchial muscle very sensitive . Fatal bronchoconstriction. </li></ul><ul><li>H 2 agonist: relaxation. </li></ul>
  39. 39. Exocrine Glands <ul><li>Common mediator of gastric secretions. </li></ul><ul><li>High production of acidic gastric juice is produce in response to histamine (H 2 ) </li></ul><ul><li>Stimulates secretion from Pancreas, Salivary Glands and Bronchial glands. </li></ul>
  40. 40. Nerve Endings <ul><li>Sensations of pain (dermis) and itch (epidermis). Part of the triple response. </li></ul><ul><li>Stimulates the adrenal medulla to release catechols. </li></ul>
  41. 41. Metabolism <ul><li>Acts rapidly when given parentally, oral histamine inactivated by bowel flora. </li></ul><ul><li>Metabolized by methylation (N-methyltrasferase), yielding N-methylhistamine. </li></ul><ul><li>Most of the N-methylhistamine is converted by Monoamine oxidase (MAO) to N-methyl imidazol acetic acid, then excreted by the kidney. </li></ul><ul><li>Alternatively, some is oxidatively deaminated by diamine oxidase (DAO), excreted as ribose conjugates. </li></ul>
  42. 42. Histamine-Receptors agonist <ul><li>Compounds release histamine without IgE interaction (drugs, amides, alkaloids, antibiotics) </li></ul><ul><li>Some venoms and toxins may be mediated by histamine release. </li></ul><ul><li>Pathologic aggregation of mast cells (urticaria pigmentosa, mastocytosis, carcinoid syndrome , myelogenous leukemia) are associated with urticaria, pruritus, headache, weakness, flushing and gastric distress. </li></ul>
  43. 43. Histamine-Receptors agonist <ul><li>No therapeutic uses, but is used in clinical function tests . </li></ul><ul><li>Gastric function test: low acid production = pernicious anemia, atrophic gastritis. High acid production= Zollinger-Ellison syndrome. </li></ul><ul><li>Sensory Nerve Test. </li></ul><ul><li>Bronchial reactivity. </li></ul>
  44. 44. Histamine antagonist <ul><li>Physiologic = epinephrine . Opposite effects, different receptors. </li></ul><ul><li>Cromolyn and nedocromil reduce the degranulation of the mast cells. </li></ul>
  45. 45. H 1 -Receptors antagonist
  46. 46. Pharmacokinetics <ul><li>Well-absorbed orally </li></ul><ul><li>Metabolized by the liver. </li></ul><ul><li>Excreted by kidney. </li></ul>
  47. 47. Pharmacologic effects <ul><li>Occupies the H 1 receptor without initiating a response (Competitive inhibition). </li></ul><ul><li>No effect on gastric secretions. </li></ul><ul><li>Antagonize bronchoconstrictor activity , as well as the “triple response”. </li></ul><ul><li>Cough suppression via presumed CNS effect. Also acts on the “vomiting center”. </li></ul><ul><li>Relief motion sickness via CNS effect. </li></ul><ul><li>Nighttime sleep aids because their sedative effects. </li></ul>
  48. 48. Indications <ul><li>Palliation of symptoms of allergy, hay fever, allergic rhinitis. Also for cutaneous allergies associated with urticaria, atopic and contact dermatitis. </li></ul><ul><li>Rhinitis associated with the common cold. </li></ul><ul><li>Motion sickness and vestibular disturbances (Meniere’s disease). </li></ul><ul><li>Mildly useful as secondary agents for anaphylaxis and angioedema. </li></ul><ul><li>Antipsychotic side effects . </li></ul><ul><li>Not useful in the treatment of asthma. </li></ul>
  49. 49. Side Effects <ul><li>Sedation : very common, except the piperidines. </li></ul><ul><li>CNS: dizziness, lack of coordination, tremors, diplopia. </li></ul><ul><li>GI: anorexia, nausea, vomiting, constipation, diarrhea. </li></ul><ul><li>Dryness of mucous membranes and urinary retention (antimuscarinic) </li></ul><ul><li>Cardiovascular: palpitations, hypotension. Prolongation QT interval (serious), associated with astemizol and terfenadine, especially when used with an azole derivative ( ketoconazol ) or macrolide antibiotic. </li></ul>
  50. 50. Side Effects <ul><li>Peripheral Nerves: paresthesias and weakness. </li></ul><ul><li>Teratogenicity may occur (Piperazines). </li></ul><ul><li>Acute poisoning: hallucinations, excitement, lack of coordination, seizures, dilated pupils and fever. </li></ul>
  51. 51. H2-Receptor antagonist <ul><li>Acts selectively on H 2 receptors with virtually no effect on H 1 receptors. </li></ul><ul><li>Block gastric acid secretion </li></ul><ul><li>Cimetidine </li></ul><ul><li>Ranitidine. </li></ul><ul><li>Famotidine. </li></ul>
  52. 52. Serotonin 5-HT <ul><li>Produced by hydroxylation and subsequent decarboxylation of AA tryptophan. </li></ul><ul><li>Neurotransmitter for the CNS . </li></ul><ul><li>GI tract: enterochromaffin cells 90%, regulates smooth muscle function. </li></ul><ul><li>Platelets: regulates platelet function. </li></ul><ul><li>Produces hallucinogenic activity (LSD, psilocybin) </li></ul>
  53. 53. Organ System Effects <ul><li>Respiratory system: transient increase in respiratory rate. Bronchoconstriction. </li></ul><ul><li>Cardiovascular: vasoconstriction (splanchnic and renal beds), vasodilatation on skeletal muscle beds. Inotropic and chronotropic effect. </li></ul><ul><li>Coronary chemoreflex: hypotension and bradycardia (vagal and sympatholytic effect). </li></ul><ul><li>Produces venous constriction and enhances platelet aggregation. </li></ul>
  54. 54. Organ System Effects <ul><li>Smooth muscle: inhibits and enhances gastric and large intestine motility (various receptors). Stimulates small bowel motility. </li></ul><ul><li>Exocrine glands: reduces volume and acidity of gastric secretions. </li></ul><ul><li>Nerves: generally stimulatory, produces pain at site of injection, stimulates autonomic effect . </li></ul><ul><li>Depolarizes adrenal medullary chromaffin cells to induce catechol secretion. </li></ul>
  55. 55. Organ System Effects <ul><li>CNS </li></ul><ul><li>Acts as an inhibitory neurotransmitter. Localized in the raphe nucleus of the brain stem. </li></ul><ul><li>Precursor of melanotonin in the pineal gland. </li></ul><ul><li>Carcinoid tumors : malignant tumor of the enterochromaffin cells, excess serotonin production. Diarrhea, abdominal cramps, malabsorption, flushing. </li></ul>
  56. 56. Metabolism <ul><li>Oxidative deamination by MAO to 5-hydroxyindoleacetaldehyde acid, then oxidized 5-hydroxyindoleactic (5-HIAA) by aldehyde dehydrogenase. </li></ul><ul><li>Renally excreted. </li></ul>
  57. 57. Serotonin <ul><li>No therapeutic uses. </li></ul><ul><li>Multiple receptors identified. 5-HT. </li></ul><ul><li>5-HT 2 , 5-HT 4-7 are g-protein-coupled. </li></ul><ul><li>5-HT 3 is Na/K ligand-gated ion channel. </li></ul>
  58. 58. Bradykinin <ul><li>Produced by a group of enzymes called kininogenases. </li></ul><ul><li>Half-life of 10-20 seconds. Most inactivated in the pulmonary beds by kinase II. </li></ul><ul><li>Potent vasodilator s and flushing effect . Increase microcirculatory permeability and edema formation. </li></ul><ul><li>Regulate urine volume and compositions. </li></ul><ul><li>Smooth muscle constriction of the tracheobronchial muscle </li></ul>
  59. 59. Bradykinin <ul><li>Powerful pain stimulators. </li></ul><ul><li>If injected, mimic inflammation. </li></ul><ul><li>Powerful stimuli for cathecol discharge. </li></ul><ul><li>Mechanism of action: not completely understood. </li></ul><ul><li>Two receptors: B1, increase during inflammation. B2, mediates actions in the absence of inflammation. </li></ul>
  60. 60. Bradykinin <ul><li>No clinical uses. </li></ul><ul><li>ACE Inhibitors . </li></ul><ul><li>Cough common complain. </li></ul><ul><li>Adds vasodilator effect to the ACE Inhibitors. </li></ul>
  61. 61. An 8-year-old boy is stung by a bee. Within 5 minutes he develops a 2 cm, raised, red, swollen lesion an the site of injury. Which of the following findings will be predominant in tissue from a lesion? <ul><li>A. Foreign body reaction </li></ul><ul><li>B. Hemorrhage </li></ul><ul><li>C. Lymphocytic Infiltration. </li></ul><ul><li>D. Neutrophilic migration. </li></ul><ul><li>E. Vasodilation </li></ul>
  62. 62. USMLE STEP1
  63. 63. Histamine 2 receptors <ul><li>Important in gastric secretion. </li></ul><ul><li>Indirectly stimulate proton pump. </li></ul>
  64. 64. H2 Antagonist <ul><li>Used in management of peptic ulcer and gastroesophageal disease. </li></ul><ul><li>Cimetidine, Ranitidine, Famotidine. </li></ul>
  65. 65. H2 Antagonist <ul><li>Adverse Effects </li></ul><ul><li>Safe drugs </li></ul><ul><li>Cimetidine inhibits multiple CYP450 enzymes. </li></ul><ul><li>Many drug-drug interactions. </li></ul><ul><li>Classical Cimetidine vs. Aminophylline </li></ul>
  66. 66. Serotonin 5-HT <ul><li>Synthesized and store in GI cells. Neurons and platelets. </li></ul><ul><li>5-HT release by carcinoid tumors </li></ul><ul><li>Diagnosis added by assays for metabolites as 5-HIAA. </li></ul><ul><li>Somatostatin analog “ ocreotide ” to treat carcinoid. </li></ul>
  67. 67. Serotonin Receptors <ul><li>Numerous receptors </li></ul><ul><li>Seven receptors subtype families. </li></ul><ul><li>All couple to G-protein second messenger. </li></ul><ul><li>Except 5-HT 3 , couple directly to ion channel. </li></ul>
  68. 68. Lipid-derived Autacoids <ul><li>Mediators, derived from membrane phospholipids. </li></ul><ul><li>Including: Prostaglandins, Prostacyclin, Leukotrienes, TXA 2 . </li></ul><ul><li>Usually present in low concentration. </li></ul><ul><li>Increased amounts: Inflammation, Trauma, Toxins. </li></ul>
  69. 69. Prostaglandins <ul><li>Form by COXs or prostaglandins synthases. </li></ul><ul><li>COX-1: express in most tissues, protects gastric mucosa. </li></ul><ul><li>COX-2: Express in brain, kidney and sites of inflammation. </li></ul>
  70. 70. Prostaglandins Drugs <ul><li>Misoprostol </li></ul><ul><li>PGE 1 . </li></ul><ul><li>Use to protect the gastric mucosa, in treatment of NSAID-induce ulcers. </li></ul><ul><li>Also used as abortifacient. </li></ul>
  71. 71. Prostaglandins Drugs <ul><li>Alprostadil </li></ul><ul><li>PGE 1 . </li></ul><ul><li>Maintains patency of ductus arteriosus in infants waiting for corrective surgery. </li></ul><ul><li>Also used transurethrally for erectile dysfunction. </li></ul>
  72. 72. Prostaglandins Drugs <ul><li>PGE 2 </li></ul><ul><li>Used to progress labor by inducing uterine smooth muscle contraction. </li></ul>
  73. 73. Leukotrienes <ul><li>Formed by action of lipoxygenases on Arachidonic Acid. </li></ul><ul><li>Leukotriene B 4 (LTB 4 ) is an inflammatory mediator. </li></ul><ul><li>LTA 3 , LTC 4 , LTD 4 : cause anaphylaxis and bronchoconstriction. </li></ul>

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