Chemical mediators.docx

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Department
Biochem. and Medical Genetics
Course
BGEN 3020
Professor
Jason Leboe- Mcgowan
Semester
Fall

Description
Chemical mediators: 1. Histamine: the king of chemical mediators of acute inflammation a) What does it do to arterioles? Vasodilates b) Venules? Increased vessel permeability 2. Serotonin: a) What amino acid makes serotonin? Tryptophan b) Is serotonin a neurotransmitter? Yes c) In a deficiency, you get depression (also decreased NE) d) a vasodilator and increases vascular permeability 3. Complement system: Anaphylatoxins – C3a, C5a. Function: stimulate mast cells to release histamine, leading to vasodilation and increased vessel permeablility. They also play a role in shock, b/c when there is inflammation the compliment system is activated, therefore there will be mast cells and histamine, therefore C3a, and C5a will both be there. 4. Nitric oxide – made mainly in endothelial cells, and is a potent vasodilator. It is used for treating pulmonary hypertension. It has a big time role in septic shock. 5. IL-1 associated with a fever, it is a pyrogen, therefore stimulates the hypothalamus to make PG’s, which stimulate thermoregulatory system to produce fever. Aspirin works by inhibiting the synthesis of prostaglandins thereby reducing the fever. 6. Arachidonic acid metabolites: a) Corticosteroids inhibits Phospholipase A ,2therefore do not release arachidonic acid from phospholipids, therefore not making PG’s or leukotrienes. This is the supreme antiflammatory agent b/c BOTH PG’s and leukotrienes are blocked by blocking phospholipase A . 2rachidonic acids make linoleic acid (omega 3), which is found in fish oils and walnuts. It is very good for you b/c it acts like aspirin, and blocks platelet aggregation, and that’s how omega 3 protects your heart. b) Lipoxygenase pathway: Zileutin blocks 5-lipoxgenase, other drugs act by blocking the receptors, example: zirkufulast, etc. Leukotriene (LT) C4, D4, E4 (the slow reactor substances of anaphylaxis) seen in bronchial asthma. They are potent bronchoconstrictors; therefore it can be seen why zileutin works well in asthma b/c it blocks the leukotrienes, including these (LT-C4, D4, and E4). LT B4 is an adhesion molecule in chemotaxis. c) Cyclooxygenase pathway: Aspirin blocks cycoloxygenase, irreversibly in platelets. PGH2: where everything seems to be derived from. PGI2: derives from endothelial cells, it’s also called prostacyclin synthase; is a vasodilator and inhibits platelet aggregation (exact the opposite of TxA2). Thrombaxane A2 (the enemy of PGI2) is made in the platelet; it’s a vasoconstrictor, a bronchoconstrictor, and promotes platelet aggregation. What drug blocks thrombaxane synthase and is used to stress testing for CAD? Dipyrramidal blocks the enzyme, TxA2 synthase, therefore does not have to perform a treadmill stress test, all you have to do is use the drug dipyrramidal. PGE2: vasodilator in kidney; keeps patent ductus patent in baby heart; makes the mucous barrier in GI (stomach) thereby preventing ulcers; can cause dysmenorrhea woman and increased uterine contractility, and it an abortifactant, to get rid of fetal material. d) COX 2-make sure you know how this works! e) Corticosteroids blocks phospholipase A2, and it also decreases adhesion molecule synthesis, along with other steroids like epinephrine and NE. Decreased adhesion molecule synthesis, will lead to increased neutrophils on CBC; in immuno, 50% neutrophils are stuck to the endothelial vessels, and the other 50% are circulating, therefore, decreasing adhesion molecule synthesis will lead to doubled WBC (b/c the 50% of neutrophils that were stuck are now circulating). Corticosteroids destroy B-cells b/c they are lymphocytotoxic. Mechanism: decrease WBC’s (B and T cells) via apoptosis; therefore, corticosteroids are the signal to activate the caspasases. Eosinophils, mainly seen in type one HPY rxn, corticosteroids
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