Functions and Properties of Blood

The study of blood is called [1]. Blood is classified as a [2] tissue whose ground substance is the [3] and whose cellular components are collectively called the [4]. The blood's "thickness" or resistance to flow, called [5], is important in determining the workload on the heart. It is determined primarily by two components of whole blood, the [6] and [7]. The [8] of blood determines its absorption and retention of water and therefore strongly affects blood volume and pressure. That portion of it which is due to plasma protein is called the [9]. The other two major determinants of 8 are [10] and [11].

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Plasma

The most abundant dissolved matter in blood plasma (by weight) is [12]. Most types of 12 are produced by the [13], but one category is produced by plasma cells. The most abundant proteins are the [14], which contribute to blood osmolarity and help transport various solutes. Lipids and other solutes are transported by a and ß [15], while g 15s are antibodies produced by the immune system. Another abundant plasma protein is a clotting protein called [16]. When blood is allowed to clot and then the solids are removed, the remaining fluid is called [17], a useful vehicle for vaccines. Blood plasma also contains various toxic, nitrogen-containing end products of metabolism called [18]. The most abundant of these is [19]. Some other components of blood plasma include gases, nutrients, and inorganic salts called [20].

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Blood Cell Formation

[21] is the process by which all formed elements of the blood are produced. It begins in the [22] of an embryo and later involves the fetal liver, spleen, thymus, and bone marrow. When the process occurs in the bone marrow, it is called [23]; when occurs in such places as the lymph nodes and thymus, it is called [24]. All types of formed elements arise ultimately from pluripotent stem cells called [25].

RBC production, or [26], is stimulated by the hormone [27], which is secreted mainly by the [28]. Proerythroblasts have receptors for this hormone. In response to it, they transform into [29], which begin synthesizing hemoglobin and then lose their nucleus. The major stimulus for 27 secretion is a low level of oxygen in the blood, called [30]. This can result from an increased oxygen demand, as in a higher level of exercise, or from a lower level of oxygen in the atmosphere, as in the mountains. One of the nutritional requirements for RBC production is [31], a mineral that becomes part of the hemoglobin molecule. This binds to a transport protein in the stomach called [32], it is absorbed by the small intestine, and then it binds to a transport protein in the blood called [33]. This mineral may be used right away for RBC production, or if there is an excess, it may be stored in the [34] in the form of [35], available for later use.

WBC production, called [36], is stimulated mainly by interleukins and [37], which come from T lymphocytes and macrophages. WBCs travel briefly in the blood stream but spend most of their lives in the connective tissues. Here, monocytes transform into [38]. Platelets are produced by large bone marrow cells called [39].

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Erythrocytes

Erythrocytes (RBCs) can stretch and bend due to the proteins [40] and actin associated with the plasma membrane. They contain little or no trace of organelles, but do contain an enzyme called [41] that catalyzes a reaction between carbon dioxide and water, and a 33% solution of the pigment [42]. This pigment is made of four polypeptides called [43], two called a chains and two called ß chains. Each chain has a nitrogenous ring called the [44] part of the molecule, and each of these has a [45] ion at the center of it, where oxygen is carried. The oxygen transport capacity of the blood is measured in three ways: RBC count; [46], which is the percent of whole blood composed of RBCs; and [47] concentration, expressed in terms of grams per deciliter of blood.

An RBC lives about 120 days and eventually breaks apart. The rupture of RBCs, called [48], releases cell fragments that are disposed of by macrophages in the spleen and liver, and hemoglobin, whose disposal is more complex. The heme part is modified to form biliverdin and [49], which are collectively called [50] because they are excreted as part of the fluid in the gall bladder. The globin part is broken down into [51], which can be reused by the body for any protein synthesis.

[52] is a state in which the RBC count is elevated by cancer of the hemopoetic tissue, whereas [53] results from air pollution, emphysema, vigorous exercise, or other such causes. A deficiency of RBCs or hemoglobin is called [54]. This is called [55] when it is due to excessive bleeding and [56] when it is due to a high rate of RBC destruction. It can also result from nutritional factors and depressed erythropoiesis, as in the case of [57] anemia resulting from vitamin B₁₂ deficiency. This usually results from a failure of the stomach to produce a substance called [58] that is needed to absorb vitamin B₁₂. If radiation or poisons cause a complete cessation of erythropoiesis, the result is called [59] anemia. A mutation originating in Africa confers resistance to malaria where this disease is prevalent, but when present in a homozygous recessive state it also causes [60] anemia. Whatever the cause, anemia can lead to tissue death, or [61]; accumulation of fluid in the tissues, called [62]; and reduced blood pressure.

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Blood Types

The two blood groups of primary importance in transfusion compatibility are the [63] and [64] groups; the latter was named after the rhesus monkey, in which it was discovered. Transfusion compatibility is based on glycoproteins and glycolipids called [65] on the RBC membrane and g globulins called [66] in the plasma. These g globulins are produced soon after birth in response mainly to [67], but they cross-react with blood cells. A type O person has 66s called [68] and [69] in the blood plasma. If type A, B, or AB blood is transfused into a type O person, one or both of these agents will clump, or [70], the introduced RBCs and initiate a reaction that hemolyzes them. The clumped RBCs can block small blood vessels, causing death of tissues whose blood flow is cut off. In addition, when the RBCs hemolyze, they release hemoglobin, which blocks tubules of the [71] and leads to their failure. Blood type [72] was once called the universal recipient and type [73] the universal donor, but in reality no blood type is universal and great caution must be used whenever the donor and recipient have different blood types. [74] of the newborn results when an Rh^- mother has been sensitized by a previous Rh⁺ pregnancy and is carrying another Rh⁺ child. It is treated by a combination of transfusion and [75] using ultraviolet light.

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Leukocytes

Three types of leukocytes are called [76] because of conspicuously staining granules in their cytoplasm. One of these, the [77], stain with both acidic and basic dyes and function especially to destroy bacteria. The rarest of all WBCs, [78], secrete the anticoagulant [79] and vasodilator [80]. The third, [81], attack parasites and oppose allergies. There are two kinds of agranulocytes. The [82] are the smaller and more abundant of the two, and have several types that function in immune responses. The larger [83] transform into large tissue phagocytes called macrophages.

A WBC count below normal, called [84], can result from radiation sickness, chemical poisoning, AIDS, and certain other infections. An elevated WBC count, or [85], is usually due to infection or allergy, but is also characteristic of [86], cancer of the blood-forming tissues. Various forms of 86 are called [87] when they have a sudden onset and short time course, [88] when onset and duration are longer, [89] when they involve the bone marrow, and [90] when they involve the lymphatic organs. One of the dangers of 86 is susceptibility to [91] infections that take hold because the person's immune defenses are compromised by the immaturity of the WBCs. People with form 89 of the disease also exhibit clotting deficiencies because stem cells of the bone marrow are diverted into making WBCs instead of [92].

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Hemostasis

Platelets are involved not only in clotting but in several other aspects of [93], the stoppage of bleeding. The quickest mechanism to reduce bleeding is [94], the prompt vasoconstriction of an injured vessel. In part, this is stimulated by a platelet secretion called [95]. Platelets also adhere to areas of damaged endothelium and form a mass called a [96], which helps to seal the broken vessel. In a process called [97], certain cytoplasmic granules appear to dissolve as they release factors such as ADP by exocytosis. ADP stimulates more platelets to undergo the same process, creating a self-amplifying [98] loop. Clotting, or [99], occurs when a plasma protein called [100] is converted to sticky threads of [101]. This goal can be reached by two routes. One is called the [102] mechanism because it is activated by factors from the damaged tissues, not from the blood itself. The other is called the [103] mechanism because all the clotting factors arise from the blood. The former mechanism begins with the release of factor III, or tissue [104], whereas the latter mechanism begins with the release of factor [105] from the platelets. Several other steps in clotting require an inorganic cofactor, [106] ions. Both pathways lead to the conversion of a plasma protein called factor II, or [107], into an enzyme that converts 100 into 101. The shrinkage of a clot after it has formed, called [108], helps to draw the edges of a broken vessel together and reduce bleeding. After the vessel has been repaired, an enzyme called [109] dissolves the clot.

In the absence of injury, clotting is inhibited by a platelet repellent called [110] on the endothelial cells. A little thrombin is formed anyway, but a liver enzyme called [111] usually deactivates it before it can trigger clotting. Clotting is also inhibited by a mast cell secretion, [112], which is also used to coat laboratory glassware to prevent clotting in clinical blood work. Clotting deficiencies can result from a low platelet count, called [113], and from [114], a hereditary deficiency of factor VIII or other clotting factors. However, clotting deficiencies kill fewer people than [115], the unwanted formation of blood clots in unbroken vessels. When a clot breaks free and travels in the bloodstream, it is called a/an [116] and presents a danger of obstructing the circulation through vital organs such as the lungs, brain, heart, and kidneys.

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