section 2, chapter 14: blood plasma


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section 2, chapter 14: blood plasma

  1. 1. Plasma Overview 1. Plasma is the liquid portion of blood 2. Makes up 55% of blood volume 3. Straw colored 4. Components include Plasma proteins, Dissolved gasses, Wastes, Electrolytes, Nutrients, Hormones Chapter 14, Section 2 of 2.
  2. 2. Plasma proteins 1. Albumin • 60% of plasma proteins • Synthesized in liver • Creates an osmotic that helps maintain blood pressure 2. Globulins • 36% of plasma proteins • Alpha & Beta globulins o Are produced by liver o Transports lipids • Gamma globulins o Are produced by lymphatic tissues o function as antibodies 3. Fibrinogen • 4% of plasma proteins • Primary role in blood coagulation
  3. 3. Plasma proteins
  4. 4. Plasma Gasses & Nutrients • Blood Gasses: • Oxygen •Most is bound to hemoglobin. Less than 2% of oxygen is dissolved in plasma • Carbon dioxide •Most CO2 is transported as bicarbonate (HCO3-) • About 7% is dissolved in plasma • Nutrients: • Amino acids • Simple sugars • Nucleotides • Lipids • Hydrophobic lipids are bound to plasma proteins within the plasma
  5. 5. Nonprotein Nitrogenous Substances • These are molecules containing nitrogen but are not proteins • In plasma they include: • Urea – product of protein catabolism; about 50% of nonprotein nitrogenous substances • Uric acid – product of nucleic acid catabolism • Amino acids – product of protein catabolism • Creatine – biproduct of creatine phosphate metabolism • Creatinine – product of creatine metabolism Common tests that evaluate kidney functions: •Creatinine test – measures creatinine •BUN – blood urea nitrogen; indicates health of kidney
  6. 6. Plasma Electrolytes • Plasma contains a variety of these ions called electrolytes • They are absorbed from the intestine or released as by-products of cellular metabolism • They include: • Sodium (most abundant with chloride) • Potassium • Calcium • Magnesium • Chloride (most abundant with sodium) • Bicarbonate • Phosphate • Sulfate
  7. 7. Hemostasis • Hemostasis refers to the stoppage of bleeding • Actions that limit or prevent blood loss include: 1. Blood vessel spasm (vasospasm) 2. Platelet plug formation 3. Blood coagulation
  8. 8. hemostasis, step 1: vasospasm • Blood vessel spasm (vasospasm) • Cutting or breaking a vessel wall stimulates the smooth muscles in its walls to contract. •Vasospasm reduces blood loss almost immediately, and may close small blood vessels completely.
  9. 9. hemostasis, step 2: platelet plug formation 1. Platelet adhesion – platelets adhere to collagen fibers that become exposed due to the damage in a vascular walls 2. Platelets undergo a shape change, producing several processes to which additional platelets bind. 3. In addition, platelets secrete thromboxanes, which attract additional platelets to the site of injury. 4. A platelet plug may control blood loss from a small break.
  10. 10. hemostasis, step 3: coagulation • Blood coagulation • Is triggered by cellular damage and blood contact with foreign surfaces • Coagulation is a cascade reaction involving several biochemicals (clotting factors) • The major event is formation of a blood clot when fibrin (a thread-like protein) forms a mesh surrounding the damaged vessel. • The 1. 2. 3. cascade is divided into three events Extrinsic mechanism Intrinsic mechanism Common pathway
  11. 11. Coagulation • Extrinsic clotting mechanism • A chemical released from tissue outside the blood vessels trigger the extrinsic pathway •Damaged tissues releases thromboplastin (also called factor III) •Factor III initiates a cascade reaction that, in the presence of Calcium, activates factor X. •Activation of factor X initiates the common pathway
  12. 12. Coagulation • Intrinsic clotting mechanism • An inactive clotting factor within the blood (Hageman, or factor XII) is activated when foreign tissue, such as collagen enters the bloodstream. •Factor XII proceeds through a cascade of reactions in the presence of Calcium to activate factor X. •Activation of factor X initiates the common pathway.
  13. 13. Coagulation •Common Pathway •Is the point at which intrinsic & extrinsic pathways converge •Activated factor X (with help of Calcium & factor V) leads to the release of prothrombin activator from platelets. •Prothrombin activator converts prothrombin into thrombin. •Thrombin, in turn converts fibrinogen into long threads of fibrin. •Fibrin forms an insoluble clot at the site of injury.
  14. 14. Coagulation Figure 14.19c. Schematic of the common pathway in the blood clotting mechanism Figure 14.18 A scanning electron micrograph of fibrin threads. The insoluble fibers trap blood cells and platelets, which contribute to the blood clot formation.
  15. 15. hemostasis: review
  16. 16. Blood Clot Dissolution • After a blood clot forms it retracts and pulls the edges of a broken blood vessel together while squeezing the fluid serum from the clot • Platelet-derived growth factor stimulates smooth muscle cells and fibroblasts to repair damaged blood vessel walls • Plasmin digests the blood clots
  17. 17. Blood Clot Disorders •A thrombus is an abnormal blood clot •Deep vein thrombosis – prolonged immobility causes blood to pool, especially in the deep veins of the legs or pelvis. • An embolus is a blood clot moving through the blood vessels •Pulmonary embolism – may occur when part of a thrombus breaks away from the clot and lodges in a pulmonary artery. Rapidly fatal. •Atherosclerosis – accumulation of fatty deposits along arterial lining •May cause inappropriate clotting •Most common cause of thrombosis in medium-sized arteries •Arteriosclerosis – hardening of an artery. •Stenosis – abnormal narrowing of a passage in a body •Atherosclerosis of an artery narrows the passage through which blood flows in an artery, and increases the likelihood of an embolism at that site.
  18. 18. Blood Clot Disorders Figure 14.20 Artery cross sections. (a) light micrograph of a normal artery. (b) The inner wall of an artery changed as a result of atheroclerosis. Ultrasound image of stenosis within the internal carotid artery.
  19. 19. Blood Typing Blood typing is the process of identifying an individual’s blood group. (eg. Type A, B, AB or O) • Terms to become familiar with: •Antigen – a chemical (or membrane protein) that stimulates cells to produce antibodies • Foreign antigens in the body stimulate the immune response. • Antibodies – a plasma protein that reacts against a specific antigen • Agglutination – clumping of red blood cells in response to a reaction between an antibody and an antigen
  20. 20. ABO Blood Group • This blood group is based on the presence (or absence) of two antigens on red blood cell membranes: Antigen A & Antigen B antigens Type A blood contains A-antigens on the surface of its RBCs. Type B blood contains B-antigens on the surface of its RBCs. and anti-A antibodies in its plasma. Type AB blood contains A-antigens and Bantigens on the surface of its RBCs. and has neither antibody Type O blood contains neither A or B antigen on the surface of its RBCs
  21. 21. Blood Typing antibodies Type A blood plasma contains anti-B antibodies. Type B blood plasma contains anti-A antibodies. Type AB blood plasma contains neither antibody Type O blood plasma contains both anti-A and anti-B antibodies.
  22. 22. ABO Blood Group
  23. 23. Rh Blood Group • The Rh blood group was named for the rhesus monkey •Rh positive (Rh+) indicates the presence of D-antigen (or other Rh antigen) on the red blood cell membranes • Rh negative (Rh-) lacks the D-antigen • When Rh- blood is exposed to the D antigen, it becomes sensitized and develops anti-D antibodies • Anti-D antibodies are formed only after a person is exposed to Dantigen (Rh sensitization).
  24. 24. erythroblastosis fetalis •The seriousness of the Rh blood group is evident in a fetus that develops the condition erythroblastosis fetalis or hemolytic disease of the newborn. • If the mother is Rh- and has been sensitized to the D-antigen, her own antibodies may attack the red blood cells of a fetus that is Rh+.
  25. 25. erythroblastosis fetalis •Erythroblastosis fetalis can be prevented for women at high risk by administering a serum that contains anti-D antibodies into the mother during the pregnancy and after birth (before she becomes sensitized to D-antigen). •The injected antibodies quickly agglutinate any fetal red blood cells, thereby preventing her from becoming sensitized to the D-antigen. End of Section 2 of 2.