BLOOD Major Functions:
[see Figure] Serum = Plasma minus the clotting elements. The Packed Cell Volume of centrifuged blood averages around 45% (= HEMATOCRIT) Plasma contains: WATER (about 93%) PROTEINS: Serum albumin (contributes to viscosity and oncotic pressure. Serum globulins (transport proteins and immunologic reactions. Fibrinogen (blood coagulation) NUTRIENTS: Glucose (0.1%), lipids, amino acids, salts, etc. CELL PRODUCTS: Enzymes, antibodies, hormones, etc. WASTES: Lactic acid, urea, etc. GASES: Oxygen, carbon dioxide, nitrogen [see Figure] ERYTHROCYTES: Contain HEMOGLOBIN (Hb) and essential for oxygen and carbon dioxide transport. About 5 million per cubic mm. Mature erythrocytes have an average lifespan of 3 - 4 months. About 200 billion "die" every day. New erythrocytes are continuously produced (e.g. in the bone marrow). This is influenced by a hormone (ERYTHROPOIETIN, EPO) from the kidney. Old worn-out erythrocytes are ingested by macrophages but much of the iron (from the Hb) is recycled. BILIRUBIN is a breakdown product of Hb. [see Figure] [Fig. 12-69] ANEMIA = a deficiency of normal hemoglobin. This may be a consequence of a loss (e.g. Hemorrhagic Anemia) or inadequate production (e.g. Pernicious Anemia) of normal erythrocytes, of a nutritional deficiency (e.g. Iron Deficiency Anemia), of abnormal Hb (e.g. Sickle-cell Anemia), etc. [see Figure] The FORMED ELEMENTS of blood also include GRANULOCYTEES (top row), NONGRANULAR LEUKOCYTES (lymphocytes and monocytes), and PLATELETS. [Fig. 12-71] The Neutrophils and Monocytes are active PHAGOCYTES. HEMOSTASIS Mechanisms to prevent blood loss. When a blood vessel is injured, the collagen of the epithelial tissue is exposed to blood. Platelets adhere to the collagen, and secrete ADP, which promotes platelet aggregation and the formation of a PLATELET PLUG. Platelet factors also contribute to COAGULATION (the formation of a blood clot). [see Figure] Undamaged endothelial cells produce both prostacyclin and nitric acid (NO) to inhibit platelet adhesion and aggregation. [Fig. 12-72] There is both an INTRINSIC (i.e. everything necessary is within the blood) and an EXTRINSIC pathway for blood clotting. There is also a system for dissolving a clot (or THROMBUS). [see Figure] [FIG. 12-74] The system of reactions leading to coagulation is called a CASCADE. A clot will form when PROTHROMBIN is converted to THROMBIN, which will convert FIBRINOGEN to FIBRIN. A clot consists of stabilized fibrin plus trapped blood cells. [Fig. 12-76] IMMUNE RESPONSES These can be either nonspecific or specific. NONSPECIFIC: Inflammation (release of histamine, mobilization of phagocytes (CHEMOTAXIS), production of COMPLEMENT proteins (which enhance phagocytosis, etc.), and INTERFERON (which stimulates the synthesis of anti-viral protein). General inflammation = FEVER SPECIFIC: These make the nonspecific responses more efficient. They are responses to particular foreign molecules (or organisms) known as ANTIGENS. Lymphocytes differentiate into two types of cells: T cells (involved in CELL-MEDIATED IMMUNITY) and B cells (involved in HUMORAL IMMUNITY). Immunity can be INNATE or ACQUIRED. There are two types of acquired immunity: ACTIVE IMMUNITY: This occurs when an individual is exposes to an antigen and recovers. This can be induced by injection (usually attenuated) antigen (e.g. VACCINE). PASSIVE IMMUINY: This can be induced by injecting antibodies from another organism. Infants receive some passive immunity across the placenta and via breast milk. CELL-MEDIATED IMMUNITY: This involves both T lymphocytes and MACROPHAGES (which develop from monocytes). In addition to CYTOTOXIC T CELLS (which directly engage and destroy infected cells), there are HELPER T CELLS and SUPRESSOR T CELLS (which prevent runaway immune reactions). Before the T cells can function properly, they must be presented with the antigen (by ANTIGEN-PRESENTING CELLS). HUMORAL IMMUNITY: B cells (with an assist from helper T cells) differentiate into PLASMA CELLS, some of which persist as a MEMORY, but most of which produce ANTIBODIES (about 2,000 antibody molecules per second during their brief (5 - 7 day) life. [see Figure] Some antigens (e.g. bacteria) are protected by a polysaccharide capsule, which is not attacked by phagocytes unless first complexed with OPSONIN (e.g. ANTIBODY). [Fig. 18-9] [see Figure] MAJOR HISTOCOMPATABILITY COMPLEX (MHC) proteins (which are different for every individual other than identical twins) on cell membranes can complex with antigens and are involved in antigen presentation. MHC I = all nucleated cells MHC II = only on macrophages, B cells, and some macrophage-like cells. [Fig. 18-11] The processing of antigen and presentation by (A) a macrophage and (B) a B cell to helper T cells [Fig. 18-12] Activation of helper T cells requires three events: (1) Presentation of the antigen bound to an MHC II protein. (2) A bond of matching nonantigenic proteins between the two cells. (3) Secretion of various cytokinins by the antigen presenting cell. [Fig. 18-13] You will recall that MHC I proteins are synthesized by all nucleated cells. Viral antigens of any infected cell may be processed and presented (via MHC I) proteins to a cytotoxic T cell. Cytotoxic T cells and Natural Killer (NK) cells are similar in some respects. Both bind with and directly attack virus-infected and cancer cells. However, cytotoxic T cells are specific whereas NK cells are non-specific and do not require the participtation of MHC proteins. Nevertheless, although they are essentially nonspecific, NK cell responses are greatly enhanced by certain chemicals (e.g. antibodies and cytokines) secreted by helper T cells, and they thus participate in specific immune responses. [see Figure] [Fig. 18-14] [see Figure] Blood AGGLUTINATION is actually a type of antigen - antibody reaction. Erythrocyte membrane proteins can act as AGGLUTINOGENS (i.e. antigens) and can stimulate the production of AGGLUTININS (i.e. antibodies), which appear in the plasma. Individuals are either positive (Rh+) or negative (Rh-) with respect to a factor found in Rhesus monkey blood. Rh- individuals will produce agglutinins against Rh+ blood. This can be a problem when a Rh- mother is carrying a Rh+ fetus. The anti-Rh agglutinins can cross the placenta and cause agglutination and hemolysis of the fetal blood (ERYTHROBLASTOSIS FETALIS). This is rarely a problem with the first such pregnancy, but may be with the second.
1.Transport
a. Respiratory gases
b. Nutrients
c. Metabolic wastes
d. Heat
e. Hormones
2. Acid - Base Balance
3. Immunologic Reactions