Paperchase Review 3.2 PDF

Unit 3.2 Paperchase 1. During vigorous exercise, you generate lactic acid, which can produce a local “acidosis” in the exercising tissues. What effect would this local “acidosis” have on the level of oxyhemoglobin? Provide support for your answer. It would create a shift of Hb to carbaminohemoglob...

Unit 3.2 Paperchase 1. During vigorous exercise, you generate lactic acid, which can produce a local “acidosis” in the exercising tissues. What effect would this local “acidosis” have on the level of oxyhemoglobin? Provide support for your answer. It would create a shift of Hb to carbaminohemoglobin because of the decreased pH. This is consequent ot the Bohr/Haldane phenomenon. This is appropriate because during exercise you would want Hb to give up O2 and pick up CO2 at a faster rate. Make sure you know the Bohr/Haldane parameters! Pg 7-9 Blood 2. After diffusing from the tissues into the blood, what is the fate of CO2? Pg 11 Blood 3. What is the role for thrombin in clotting? Pg 20 & 22 Blood 4. What is the major pathway for secondary hemostasis? Tissue Factor Pathway Pg 22 Blood 5. Why would a vitamin K deficiency create a clotting disorder? It is an essential factor for making 2, 7, 9, and 10 in the liver Pg 23 Blood 6. What is heparin, and how does it influence clotting? Protein that triggers anti-thrombin, stops progression of a clot. Pg 22 & 25 7. List some triggers for clotting. Collagen, vWF, Tissue Factor, and Thrombin Pg 15-23 8. What are the components of Virchow’s triad? What does it represent? The three causes of intravascular clotting: Stasis Hypercoagubility Endothelial injury 9. Diagram the cascade of proteins in secondary hemostasis. Pg 19 Blood 10. Make a list of the important events, in order, that occur in humoral activation. Macrophage which has encountered antigen processes it, display it with MHC II protein on surface. Via T cell receptor and CD4, T helper cell binds to this. APC secretes Il-1 which activates the T helper cell. T-helper cells bind to B cells and release Il-4 which activates B cell. The B cell then becomes a plasma cell and releases antibodies. Pg 25 Immunity 11. What is meant by “cell-mediated immunity”? CD8 T cells (cytotoxic or killer cells) are activated by the release of Il-2 from T helper cells. CD8 cells recognize antigens on the surface of infected cells, attach to these cells and secrete perforins Perforins punch holes into the infected cells, killing them. Pg 9 Immunity 12. Explain how the use of a vaccine can prevent illness. Vaccine creates antibody response (humoral) by injecting a foreign antigen. This in turn creates memory B & T cells. If the antigen is ever again encountered, the memory cells will rapidly create a response to eliminate it. Pg 26 Immunity 13. Describe how interleukins, interferons, and TNF work. Flow charts Pg 11-14 14. What does complement do? Pg 15 15. What are the cardinal signs of inflammation? Heat, redness, swelling, pain, and loss of function Pg 17 16. Why is chronic inflammation bad? Basically, inflammation creates additional tissue damage, which leads to continued inflammation. Pg 18 17. Describe the different kinds of acquired immunity. Active Artificial: Immunization Active Natural: Disease followed by Recovery Passive Artificial: Intravenous antibodies (IgG) Passive natural: Breastfeeding Pg 19 18. What is an antigen? An antigen is a substance that confers identity. Pg 20 19. What is an antibody? Protein molecules produced by activated B cells (Plasma Cells). Pg 20 20. What do antibodies do? Antibodies attach to antigens. Agglutination: Antibodies links cells, viruses together to make clumps that attract macrophages. Opsonization: an opsonin is something that promotes phagocytosis. Complement fixation (activation) Precipitation: toxin molecules come out of solution, which is good...but what if the precipitates stick to the host tissues? Neutralization: toxins, viruses inactivated. Pg 22