1. Describe the composition and physical characteristics of whole blood. Explain why it is classified as a connective tissue.
2. List the functions of blood.
3. Discuss compositions and functions of plasma. Define serum.
4. Describe functional characteristics, function, and production of erythrocytes. (Production ‑ hypoxia, erythropoietin, stem cell commitment, necessity of iron, folic acid, B‑12, and intrinsic factor, extrusion of nucleus).
5. Describe the structural and functional features of hemoglobin.
6. List the classes, structural characteristics, and functions of leukocytes. Describe leukocyte genesis (CSF, stem cell commitment, myeloid and lymphoid branches).
7. Describe structure and function of platelets.
8. Explain the mechanism of each disorder of the blood given in the handout.
9. Describe the process of hemostasis using the following terms: platelet plug, vasoconstriction, clot formation, healing process, platelet products and their functions (serotonin, ADP, PDGF, calcium), what stimulates intrinsic and extrinsic pathways, common point of the two pathways, thrombin, fibrinogen, fibrin, plasminogen, plasminogen activator, plasmin).
I. Describe the composition and physical characteristics of whole blood. Explain
why it is classified as connective tissue.
Whole blood is 55% plasma, < 1% leukocytes, 45% erythrocytes (percentage of erythrocytes is known as the hematocrit). ph 7.35 ‑ 7.45 A healthy male has 5‑6 liters and a healthy female has 4‑5 liters.
Blood is a connective tissue because it contains the three elements of connective tissue: cells, ground substance (the fluid component) and fibers (Coagulation fibers are present in a soluble form until damage occurs to a vessel and then they become insoluble.)
II. List functions of blood.
(1) delivering oxygen and nutrients to body cells
(2) transporting waste to lungs and kidney
(3) transporting hormones
(1) maintaining body temperature
(2) maintaining normal pH
(3) maintaining adequate fluid volume
(1) coagulation pathway prevents blood loss
(2) leukocytes, antibodies, and other substances defend against infection
III. Discuss plasma and serum.
Plasma is straw‑colored, sticky fluid. It is mostly water but has many solutes such as: nutrients, gases, hormones, wastes, ions, and proteins. Most plasma proteins are produced by the liver. Albumin is an important plasma protein because it (1) acts as a carrier for other molecules (2) buffers the blood and (3) is a major contributor to blood osmotic pressure (which keeps water in the blood vessels and keeps it from leaking out into the tissues). Sodium ions also contribute to osmotic pressure.
Serum is plasma from which the clotting proteins have been removed.
IV. Functional characteristics, function, and production of erythrocytes.
Erythrocytes (rbcs) are biconcave disks, without nuclei, which contain large amounts of hemoglobin (the oxygen carrier). They are the most numerous blood cell (5 million cells per milliliter). They have a lifespan of 120 days. Production of rbc (erythropoiesis) occurs in the bone marrow from a precursor cell, the hemocytoblast. Production is stimulated by the hormone erythropoietin, produced by the kidney in response to hypoxia. (Hypoxia may result from low numbers of rbcs, malfunctioning rbcs, reduced availability of oxygen, or increased tissue demands for oxygen.) Substances necessary for production of rbcs are iron (stored inside cells in a protein‑iron complex called ferritin and transported in blood bound to the transport protein transferrin), and the B‑complex vitamins B‑12 and folic acid (for DNA synthesis). Intrinsic factor is necessary for vitamin B‑12 to be absorbed from the intestinal tract.
Hemoglobin is made up of 4 polypeptide chains (globin), each containing a heme group. In the middle of the heme group is an iron atom. Oxygen binds to the iron atom. (oxyhemoglobin, deoxyhemoglobin). Carbon dioxide mostly travels in the blood as part of the bicarbonate buffer system. The small amount that binds to hemoglobin binds to the globin protein (carbaminohemoglobin).
See Table 17.2 for description, structure, number (don't memorize exact numbers, but know the leukocytes in order of prevalence), and function.
In general, leukocytes are defensive cells. They have the ability to travel to areas of inflammation and infection where they can leave the circulatory system by squeezing through the capillary walls (diapedesis). Leukocytes proliferate during an infection. A white blood cell count of over 11,000 cells per ml is indicative of an infection.
Leukopoiesis (making of new leukocytes) occurs in the bone marrow and is stimulated by a group of hormones called colony stimulating factors produced by macrophages and T lymphocytes. CSF's stimulate wbc precursors to divide and mature and make the already mature leukocytes more active. Early commitment occurs in which the hemocytoblast commits to either the myeloid cell line (eventually becoming granulocytes and monocytes) or the lymphoid cell line (eventually becoming lymphocytes).
Platelets (sometimes called thrombocytes) are actually cytoplasmic fragments from large cells called megakaryocytes. The cytoplasm of the megakaryocyte becomes compartmentalized by membranes, and the plasma membrane then fragments, liberating the platelets. Platelets stick to a damaged blood vessel, making a plug and also secrete, important substances for the clotting and repair process.
VIII. Disorders of blood.
Anemias ‑ blood has abnormally low oxygen carrying capacity
1. Insufficient numbers of red cells.
hemorrhagic anemia ‑ due to blood loss
hemolytic anemia ‑ due to blood cell destruction
aplastic anemia ‑ due to bone marrow destruction /inhibition
2. Low hemoglobin content.
iron deficiency anemia ‑ small pale rbcs (microcytes)
pernicious anemia ‑ deficiency of vitamin B12 and/or intrinsic factor
3. Abnormal hemoglobin
thalassemias ‑ depressed synthesis of globin chains
sickle‑cell anemia ‑ abnormal hemoglobin causes red blood cells to sickle
Polycythemia ‑ abnormal excess of rbc's leading to increased blood viscosity
Leukopenia ‑ abnormally low wbc count
Leukemia ‑ cancerous condition of wbc, from a single clone, cells are dysfunctional
acute leukemia ‑ derives from immature, blast type cells
chronic leukemia ‑ derives from a cell in a later stage of maturation
hemostasis ‑ stopping of bleeding
1. Vascular spasms ‑ contraction of smooth muscle around blood vessel walls to reduce blood loss; triggered by injury, pain, chemicals
2. Platelet plug formation ‑ seal damaged blood vessels. Platelets do not usually stick to each other or blood vessels, but when the blood vessel is damaged, underlying collagen is exposed. Platelets bind to the collagen and release substances stored in their granules. These substances enhance vascular spasms, attract more platelets, and cause them to release their granules. Within a minute a platelet plug is formed.
3. Coagulation ‑ series of reactions the end result of which is the production of fibrin, a tough insoluble protein, that forms part of the blood clot (along with platelets). The precursors of the coagulation cascade exist in the blood in soluble, inactive forms. Note that there are 2 coagulation pathways which join at a common point. The intrinsic pathway is triggered by blood vessel endothelium damage which exposes underlying collagen. The extrinsic pathway is triggered by damage to surrounding tissue cells. In the extrinsic pathway the damaged cells release tissue thromboplastin which shortcuts part of the process.
Each of the cascade reactions involves a product activating the formation of the next product of the pathway. Eventually thrombin is formed which catalyzes the polymerization of fibrinogen (soluble, inactive) to fibrin (insoluble, clot protein). Fibrin forms the framework of the clot to stop the bleeding and also to facilitate repair. Note that calcium is important for several steps of the coagulation pathway. The clot is stabilized further by the process of clot retraction mediated by a platelet contractile protein. The clot is compacted and brings damaged edges closer together. Platelets also release (PDGF) platelet derived growth factor which stimulates the rebuilding of the vessel wall.
When healing is finished, the clot needs to be removed. When the clot was initially formed a blood protein plasminogen (inactive) was incorporated into the clot. When healing is finished a chemical released by the endothelial cells activates plasminogen into plasmin. Plasmin degrades fibrin and destroys the clot.