The properties of blood icon

The properties of blood




Скачати 230.22 Kb.
НазваThe properties of blood
Сторінка3/5
Дата24.08.2012
Розмір230.22 Kb.
ТипДокументи
1   2   3   4   5

247









In addition, a very small amount of carbon dioxide is carried in the blood combined with a-amino groups on plasma proteins in the form of carbamino compounds formed by the general reaction:

R-NH, + CO,

^ R-NHCOO- + H~

The reactions involved in the carriage of carbon dioxide in the form of both bicarbonate ions and carbamino compounds are illustrated diagrammatically in Fig. 13.9.

To summarize, each deciliter of arterial blood has a Pco2 of 5.3 kPa (40 mmHg) and contains about 2.8 ml of CO2 in solution, 43.9 ml as bicarbonate and 2.3 ml as carbamino com-

Fig 13.9 A schematic representation of CO2 and O2 transport in the blood, (a) The exchange of CO2 and O2 that occurs between the blood and the tissues; and (b) the exchange that occurs in the lungs between the blood and the alveolar air.

pounds, making a total of 49 ml dl l. Mixed venous blood has a Pco2 of 6.1 kPa (46 mmHg) and each deciliter contains approxi­mately 3.2 ml of CO2 in solution, 47 ml as bicarbonate and 3.8 ml as carbamino compounds (mainly carbaminohemoglobin), equivalent to a total of 54 ml CO, per deciliter.

The carbon dioxide dissociation curve

The amount of carbon dioxide present in solution depends on the PCO2 and this in turn will determine the amount of bicar­bonate and carbamino compounds that will be formed in the blood. The relationship between the PCO2 (in kPa or mmHg) and the total CO2 (mlCO2dl~1 blood) is called the CO2 dis­sociation curve. It differs from the oxyhemoglobin dissociation curve in that it does not become saturated even at high PCO2 (Fig. 13.10). Across the physiological range of PCO2 for whole blood (5.3 kPa (40 mmHg) in arterial blood to 6.13 kPa (46 mmHg) in mixed venous blood) the CO2 dissociation curve is roughly linear. The quantity of CO2 carried in the blood is, however, dependent on the degree of oxygenation of hemo­globin. This is called the Haldane effect and is also illustrated in Fig. 13.10.

Two main factors are responsible for the changes in carbon dioxide affinity of the blood seen when HbO2 levels vary:

  1. Oxyhemoglobin is less able to form carbamino compounds
    than reduced hemoglobin.

  2. Oxyhemoglobin is a less efficient buffer of hydrogen ions
    than reduced hemoglobin. As a result of this, in the tissues
    (where less of the hemoglobin is in the form of HbO2),
    hydrogen ions are mopped up more rapidly than in the
    pulmonary capillary blood, thereby driving the reaction:

H2O + CO2 ^ HCOj + H+

to the right and encouraging more CO2 to be carried as bicarbonate ion.


Fig. 13.10 The carbon dioxide dissociation curve for whole blood and the Haldane effect. Point a is for arterial blood and v is the value for mixed various blood.

In the lungs, where about 97 per cent of the hemoglobin is in the form of oxyhemoglobin, the carbon dioxide content of

248

13 The properties of blood


the blood is relatively lower than it is in the tissues where oxy­hemoglobin makes up around 75 per cent of the total Hb. In other words, more carbon dioxide may be carried when HbO2 is low. This makes good sense physiologically, as a major purpose of blood gas transport is to load the blood with CO2 in the tissues and unload it for expiration in the lungs.

Summary

  1. The blood must supply oxygen to all the tissues of the body and
    transport the carbon dioxide produced by metabolism to the lungs
    for removal from the body.

  2. Only a small amount of oxygen is carried by the plasma in physical
    solution, most is carried loosely bound to hemoglobin within the red
    blood cells. The amount of oxygen carried in the blood depends on
    the partial pressure of oxygen and is described by the oxyhemoglobin
    dissociation curve, which has a sigmoidal shape

  3. The position of the dissociation curve with respect to the PO2 (i.e.
    the affinity of hemoglobin for oxygen) varies with temperature, pH,
    .PCO2, and the concentration of 2,3-DPG in the red cells. The curve
    is shifted to the right by an increase in PCO2) an increase in rhe level
    of 2,3-DPG, an increase in temperature, and by a fall in pH.

  4. Carbon dioxide is carried in the blood in three forms: in physical
    solution, as bicarbonate ions, and as carbamino compounds. Carbon
    dioxide combines with water to form carbonic acid. This reaction is
    catalyzed by carbonic anhydrase in the red blood cells. The carbonic
    acid dissociates to H* and bicarbonate. The H* is buffered by hemo­
    globin and other blood buffers while the bicarbonate diffuses out of
    the red cells in exchange for Cl~ (the chloride shift).

  5. The carbon dioxide dissociation curve is virtually linear in the physi­
    ological range of blood PCO2. The exact position of the dissociation
    curve, i.e. the affinity of the blood for CO2, is determined by the
    degree of oxygenation of the hemoglobin. More CO7 may be carried
    by the blood as the level of oxyhemoglobin falls. This is the situation
    for blood perfusing the tissues. This is known as the Haldane effect.

^ 13.7 Major disorders of the red and white blood

cells

This section focuses on the consequences arising from changes in the rate of production or destruction of the cellular elements of the blood. Broadly, blood cell disorders fall into two categories, proliferative disorders (where there is an excess of cells, often with abnormal function) and deficiency disorders (where there are too few cells). Red and white cells will be considered here, while abnormalities of platelet function will be considered in Section 13.8.

Red cell abnormalities

Anemia

This term covers a variety of blood disorders characterized by a reduced number of red cells, a reduced hemoglobin concen-

tration, or both. All types of anemia result in a reduction in the oxygen-carrying capacity of the blood. Anemia may arise for a number of reasons:

  1. A reduction in red cell number—this can arise as a result
    of acute hemorrhage after which plasma volume is restored
    in a short time but red cell production takes much longer
    (see also Section 28.5).

  2. A reduction in the hemoglobin content of the red cells, for
    example as a result of iron deficiency due to chronic blood
    loss or to pregnancy.

  3. A reduction in red cell size. Mean corpuscular (red cell)
    volume is generally 80-95 X 1СГ15 liters (80-95 fl). This
    condition is also seen in cases of iron deficiency and is
    known as microcytic anemia.

  4. Pernicious or macrocytic anemia is seen in patients lacking
    vitamin B19 (cyanocobalamin), which is essential for
    the normal maturation of erythrocytes in the bone mar­
    row (Section 13.4). This situation arises when there is
    inadequate absorption of vitamin B12 due to a lack of
    intrinsic factor in the gastric mucosa (Chapter 18). In this
    disorder, the red cells that are produced are much larger,
    and contain more hemoglobin than normal (megaloblasts),
    but are present in greatly reduced numbers.

  5. Occasionally the bone marrow fails to function normally.
    This results in so-called aplastic anemia and can arise spon­
    taneously or as a consequence of damage to the marrow,
    for example by irradiation.

  6. Abnormalities in hemoglobin structure can lead to acceler­
    ation of red cell destruction. One such abnormality is
    sickle-cell anemia, in which there is a defect in one of the
    chains of the hemoglobin molecule. Sickle hemoglobin
    (HbS) is transmitted by recessive inheritance and the
    disease is prevalent in black African populations. In
    homozygous individuals, the HbS becomes sickled when
    deoxygenated, causing deformation of the red cells. The
    deformed cells obstruct the blood flow in the capillaries,
    causing tissue hypoxia with subsequent damage and
    intense pain. Virtually every organ is affected, but the
    liver, spleen, heart, and kidneys are especially vulnerable
    to damage because of the increased risk of blood clot-
    formation caused by the sluggish blood flow. A small but
    significant advantage of this disease is that people who
    carry the HbS gene have a high resistance to malaria. This
    is because the parasite that causes malaria cannot live in
    blood cells containing HbS.

  7. Thalassaemia is the name given to a group of anemias
    caused by the hereditary inability to produce either the
    a- or the /3-chain of hemoglobin. It is found pre­
    dominantly amongst Mediterranean, African, and Afro-
    American populations and is characterized by a reduction
    in Hb synthesis, damage to red cell membranes, and
    abnormal oxygen-binding characteristics.


13.8 Mechanisms of hemostasis 249

Polycythemia

This condition is the tesult of overstimulation of red blood cell production. It brings about an increase in the hematocrit value (to as much as 60—80 per cent) and a rise in blood viscosity. It is often seen in people living at high altitude who experience chronic hypoxia as a result of the low prevailing atmospheric oxygen tension (see Chapter 30 for further details), although it can also arise under other circumstances. The increase in red blood cell numbers increases the oxygen-carrying capacity of the blood but, at the same time, it increases the viscosity of the blood and this places an extra load upon the heart. Over time, the heart hypertrophies (enlarges) to adapt to the increased work load.

White cell abnormalities

As with the red cells, disorders of the leukocytes fall into two broad categories; deficiency disorders and proliferative disorders.

Leukopenia

This term describes an absolute reduction in the numbers of white blood cells. It may affect any of the different types of leukocyte but most often involves the neutrophils, which are the predominant type of granulocyte. In this case the disorder is known as neutropenia. It can result from defective neutrophil pro­duction or from an increase in the rate of removal of neutrophils from the circulation. The former may arise as part of a genetic impairment of the regulation of neutrophil production, aplastic anemia, in which all the myeloid stem cells are affected, or as a result of certain types of chemotherapy. It may also be a con­sequence of the overgrowrh of neoplastic cells characteristic of some forms of leukemia, which suppresses the function of the neutrophil precursor cells.

Occasionally, leukopenia arises as a result of an accelerated rate of neutrophil removal from the circulation rather than a reduction in the rate of production. This is most usually a conse­quence of chemotherapy but may also be seen in certain infections or autoimmune disorders in which neutrophils are destroyed. The neutrophils are essential in the inflammatory response. Infections are, therefore, common in people with neutropenia and these may be severe or even life-threatening.

^ Proliferative disorders of the white blood cells

Malignant proliferative diseases of the blood include the leukemias, lymphomas, and myelomas. Self-limiting pro­liferative disorders such as infectious mononucleosis (glandular fever) can also occur.

Leukemia is characterized by greatly increased numbers of abnormal white blood cells circulating in the blood. There are several different types of leukemia, classified according to their cells of origin (lymphocytic or myelocytic) and whether the disease is acute or chronic. Lymphocytic leukemias are most commonly seen in children and involve the lymphoid precursors that originate in the bone marrow. Cancerous production of lym­phoid cells then spreads to other tissues such as the spleen,

lymph nodes, and CNS. Myelocytic disease, which is more common in adults, involves the pluripotent myeloid stem cells in the bone marrow. The maturation of all the blood cell types, including granulocytes, erythrocytes, and thrombocytes is affected.

Leukemic cells are usually nonfunctional and therefore cannot provide the normal protection associated with white blood cells. Common consequences of the disease include the development of infections, severe anemia, and an increased tendency to bleed, as a result of a lack of platelets (thrombocytopenia). Furthermore, the leukemic cells of the bone marrow may grow so rapidly that they invade the surrounding bone itself. This causes pain and an increased risk of fractures.

Almost all forms of leukemia spread to other tissues, par­ticularly those which are highly vascular, such as the spleen, liver, and lymph nodes. As they invade these regions the growing cancerous cells cause extensive tissue damage and place heavy demands on the metabolic substrates of the body, espe­cially amino acids and vitamins. The energy reserves of the patient are thus depleted and the body protein broken down. Weight loss and excessive fatigue are characteristic symptoms of leukemia.

Summery

  1. Disorders of both the red and white cells fall into two broad
    categories: deficiency and excess production.

  2. Anemia is a general term to describe disorders of the red blood cells
    characterized by a reduced hematocrit. It may arise from reductions
    in red blood cell number or size, reduction of the hemoglobin
    content of red cells, or abnormalities of hemoglobin structure.

3- An important consequence of all types of anemia is a reduction in the oxygen-carrying capacity of the blood.

  1. Polycythemia results from overstimulation of red blood cell pro­
    duction and leads to a rise in both hematocrit and blood viscosity.

  2. Leukopenia is denned as an absolute reduction in white blood cell
    numbers and may be due either to defective production or accelerated
    removal of white cells from the circulation. Infections are common in
    patients suffering from leukopenia.

  3. Proliferation disorders of rhe white blood cells include leukemias,
    lymphomas, and myelomas. In leukemia there are high numbers of
    abnormal white blood cells which are usually nonfunctional. Patients
    suffer from severe anemia, infections, weight loss, and excessive
    fatigue.

13.8 Mechanisms of hemostasis

When a blood vessel is damaged by mechanical injury of some kind, excessive blood loss from the wound is prevented by a process called bemostasis. This involves a series of events— vasoconstriction, platelet aggregation, and blood coagulation (clot fotmation). Later, blood-vessel repair, clot retracrion, and dissolution complete the healing process.

250

13 The properties of blood


Vasoconstriction

When the vascular endothelium (Section 15.9) is damaged, there is a localized contractile response by the vascular smooth muscle, causing the vessel to narrow. This may be mediated by humoral factors or directly by mechanical stimulation, and in arterioles and small arteries closure may be virtually complete. However, this response lasts for only a short time and, to prevent serious loss of blood, further hemostatic mechanisms are initiated.

The role of platelets

Within seconds of a vascular injury, platelets start to build up and adhere to the site of damage. This process is self-perpetuating as the adhering platelets secrete ADP and 5-hydroxytryptamine. They also synthesize arachidonic acid and thromboxane A2. These factors trigger a change in the surface characteristics of the platelets (see also Sections 5.5 and 5.7) which causes them to adhere to the walls of damaged vessels and to each other. This process results in the formation of я platelet plug, which may be sufficient to stem the flow of blood from minor wounds.

In addition to sealing damaged vessels, the platelets play a continuous role in maintaining normal vascular integrity. This is illustrated by the increased capillary permeability seen in people suffering from platelet deficiency (thrombocytopenia). Such indi­viduals often develop spontaneous tiny hemorrhages in the skin and mucous membranes (petechiae), giving the patient a curious blotchy appearance, with further bleeding into subcutaneous

Blood coagulation

This is the process by which fibrin strands create a mesh that binds blood components together to form a blood clot. It is a complex process that involves the sequential activation of a number of factors that are normally present in the blood in an inactive form. A cascade of reactions occurs by which one activated factor activates another according to the following scheme:



Many clotting factors are synthesized in the liver and their manufacture is dependent upon vitamin K. The major reactions in the clotting process are shown in Fig. 13.11, from which it is evident that there are two pathways which may lead to the for­mation of a fibrin clot. These are the intrinsic and extrinsic path­ways, both are needed for normal hemostasis and both involve a number of enzyme factors. Throughout the medical and scientific literature these enzymes are known by a variety of names and/or Roman numerals (Table 13.4). In this account the factors are assigned the nomenclature by which they are most commonly known.

Table 13.4 The nomenclature of the clotting factors of blood



Factor

Names and synonyms

I

Fibrmogen

II

Prothrombin

Ha

Thrombin

III

Tissue factor, tissue thromboplastin

IV

Calcium (Ca2+)

V

Proaccelerin, labile factor, accelerator globulin

VI

Not assigned

VII

VIII

IX

X XI

XII XIII

Proconvertin, SPCA, stable factor, autoprothrombin I

Antihemophilic factor, antihemophilic globulin, antihemophilic factor A, platelet cofactor I

Plasma thromboplastic component, Christmas factor, antihemophillic factor B, platelet cofactor II

Stuart—Prower factor, autoprothrombin III

Plasma thromboplasitin antecedent (РТА), antihemophilic factor С Hageman factor Fibrin stabilizing factor, Laid—Lorand factor

Note that factors I-IV are generally known by their names while factors V-XIII are generally referred to by their Roman numeral. Activated factors are designated by the letter 'a' after the numeral, e.g. activated Factor X is called Xa.

Both systems are activated when blood passes out of the vas­cular system. The intrinsic system (which is the slower of the two) is activated as blood comes into contact with the injured vessel wall, while rhe extrinsic system is activated when blood is exposed to the products of damaged tissue—specifically tissue factor or thromboplastin. The intrinsic pathway is so-called because all of the elements required to activate it are present in normal blood while the extrinsic pathway is activated by a factor from outside the blood, i.e. tissue factor. Both pathways lead to the formation of activated Factor X (Factor Xa) at the end of the first stage of coagulation. Further steps in the clotting reaction are common to both pathways and involve the enzymatic conversion of inactive prothrombin to thrombin. This then initiates the poly­merization offibrinogen to fibrin strands within which plasma and blood cells are trapped to form a clot.

The intrinsic pathway

The initial step in this series of reactions is dependent upon a plasma protein called Factor XII (Hageman factor). When there is vascular damage and blood comes into contact with collagen, Factor XII is converted to 'activated Factor Х1Г. At the same time, platelets release phospholipid which plays a role in subsequent steps of the process.

Activated Factor XII converts Factor XI to 'activated Factor XI' which subsequently converts Factor IX (Christmas factor) to 'activated Factor IX' by a calcium-dependent process. Activated Factor IX then acts together with the phospholipids from the traumatized platelets and with Factor VIII ( antihemophilic



13.8 Mechanisms of hemostosis
1   2   3   4   5

Схожі:

The properties of blood iconOptical properties of urine, blood plasma and pulmonary condensate of the patients with pulmonary form of tuberculosis

The properties of blood iconOptical properties of urine, blood plasma and pulmonary condensate of the patients with pulmonary form of tuberculosis
move to 195-25479
The properties of blood iconДокументи
1. /ФАРМ__курс_модуль 1/At a Chemist's/~$льов_ навчаюч_ завдання_друга мова.doc
2....

The properties of blood iconShalapska T., Stryganyuk G., Demchenko P., Voloshinovskii A., Dorenbos P. Luminescent properties of LiGdP

The properties of blood iconPhysiology of the blood system

The properties of blood iconMechanical properties and defect nanostructure of Si + SiO2
Рис. 1 к статье О. В. Ляшенко, А. П. Онанко ²ияние электрического тока на упругие и неупругие характеристки g 963S 037²
The properties of blood iconDaily monitoring of blood pressure in the study of current hypertension

The properties of blood iconElectronic absorption spectra of blood plasma of patients with various forms of goiter

The properties of blood iconNotional module 2 Morphology of blood supply and limphokinesis disturbance Lectures – 4 hours

The properties of blood iconУдк 631. 445 Pol’chyna S. M., Savitska I. V., Dumih I. V
Н 3, physico-chemical properties – by standard methods. The indexation of genetic horizons was carried out both by the Ukrainian...
Додайте кнопку на своєму сайті:
Документи


База даних захищена авторським правом ©zavantag.com 2000-2013
При копіюванні матеріалу обов'язкове зазначення активного посилання відкритою для індексації.
звернутися до адміністрації
Документи