Anemia means deficiency of hemoglobin in the blood, which can be caused by either too few RBCs or too little hemoglobin in the cells. Some types of anemia and their physiological causes are described in the following sections.

Blood Loss Anemia. After rapid hemorrhage, the body replaces the fluid portion of the plasma in 1 to 3 days, but this response results in a low concentration of RBCs. If a second hemorrhage does not occur, RBC concentration usually returns to normal within 3 to 6 weeks.

When chronic blood loss occurs, a person frequently cannot absorb enough iron from the intestines to form hemoglobin as rapidly as it is lost. RBCs that are much smaller than normal and have too little hemoglobin inside them are then produced, giving rise to microcytic, hypo chromic anemia, which is shown in Figure1.

Fig1. Genesis of normal red blood cells (RBCs) and characteristics of RBCs in different types of anemias.

Aplastic Anemia Due to Bone Marrow Dysfunction. Bone marrow aplasia means lack of functioning bone marrow. For instance, exposure to high-dose radiation or chemotherapy for cancer treatment can damage stem cells of the bone marrow, followed in a few weeks by anemia. Likewise, high doses of certain toxic chemicals, such as insecticides or benzene in gasoline, may cause the same effect. In autoimmune disorders, such as lupus erythematosus, the immune system begins attacking healthy cells such as bone marrow stem cells, which may lead to aplastic anemia. In about half of aplastic anemia cases the cause is unknown, a condition called idiopathic aplastic anemia.

People with severe aplastic anemia usually die unless they are treated with blood transfusions—which can temporarily increase the numbers of RBCs—or by bone marrow transplantation.

Megaloblastic Anemia. Based on the earlier discussions of vitamin B12, folic acid, and intrinsic factor from the stomach mucosa, one can readily understand that loss of any one of these can lead to slow reproduction of erythroblasts in the bone marrow. As a result, the RBCs grow too large, with odd shapes, and are called megaloblasts. Thus, atrophy of the stomach mucosa, as occurs in pernicious anemia, or loss of the entire stomach after surgical total gastrectomy can lead to megaloblastic anemia. Also, megaloblastic anemia often develops in patients who have intestinal sprue, in which folic acid, vitamin B12, and other vitamin B compounds are poorly absorbed. Because in these states the erythroblasts cannot proliferate rapidly enough to form normal numbers of RBCs, the RBCs that are formed are mostly oversized, have bizarre shapes, and have fragile membranes. These cells rupture easily, leaving the person in dire need of an adequate number of RBCs.

Hemolytic Anemia. Different abnormalities of the RBCs, many of which are hereditarily acquired, make the cells fragile, so they rupture easily as they go through the capillaries, especially through the spleen. Even though the number of RBCs formed may be normal, or even much greater than normal in some hemolytic diseases, the life span of the fragile RBC is so short that the cells are destroyed faster than they can be formed, and serious anemia results.

In hereditary spherocytosis, the RBCs are very small and spherical rather than being biconcave disks. These cells cannot withstand compression forces because they do not have the normal loose, baglike cell membrane structure of the biconcave disks. Upon passing through the splenic pulp and some other tight vascular beds, they are easily ruptured by even slight compression.

In sickle cell anemia, which is present in 0.3 to 1.0 per cent of West African and American blacks, the cells have an abnormal type of hemoglobin called hemoglobin S, containing faulty beta chains in the hemoglobin molecule, as explained earlier in the chapter. When this hemoglobin is exposed to low concentrations of oxygen, it precipitates into long crystals inside the RBC. These crystals elongate the cell and give it the appearance of a sickle rather than a biconcave disk. The precipitated hemoglobin also damages the cell membrane, so the cells become highly fragile, leading to serious anemia. Such patients frequently experience a vicious circle of events called a sickle cell disease “crisis,” in which low oxygen tension in the tissues causes sickling, which leads to ruptured RBCs, which causes a further decrease in oxygen tension and still more sickling and RBC destruction. Once the process starts, it progresses rapidly, eventuating in a serious decrease in RBCs within a few hours and, in some cases, death.

In erythroblastosis fetalis, Rh-positive RBCs in the fetus are attacked by antibodies from an Rh-negative mother. These antibodies make the Rh-positive cells fragile, leading to rapid rupture and causing the child to be born with a serious case of anemia. This condition is discussed in Chapter 36 in relation to the Rh factor of blood. The extremely rapid formation of new RBCs to make up for the destroyed cells in erythroblastosis fetalis causes a large number of early blast forms of RBCs to be released from the bone marrow into the blood.

EFFECTS OF ANEMIA ON FUNCTION OF THE CIRCULATORY SYSTEM

The viscosity of the blood, which was discussed in Chapter 14, depends largely on the blood concentration of RBCs. In persons with severe anemia, the blood viscosity may fall to as low as 1.5 times that of water rather than the normal value of about 3. This change decreases the resistance to blood flow in the peripheral blood vessels, so far greater than normal quantities of blood flow through the tissues and return to the heart, thereby greatly increasing cardiac output. Moreover, hypoxia resulting from diminished transport of oxygen by the blood causes the peripheral tissue blood vessels to dilate, allowing a further increase in the return of blood to the heart and increasing the cardiac output to a still higher level—sometimes three to four times normal. Thus, one of the major effects of anemia is greatly increased cardiac output, as well as increased pumping workload on the heart.

The increased cardiac output in persons with anemia partially offsets the reduced oxygen-carrying effect of the anemia because even though each unit quantity of blood carries only small quantities of oxygen, the rate of blood f low may be increased enough that almost normal quantities of oxygen are actually delivered to the tissues. However, when a person with anemia begins to exercise, the heart is not capable of pumping much greater quantities of blood than it is already pumping. Consequently, during exercise, which greatly increases tissue demand for oxygen, extreme tissue hypoxia results and acute cardiac failure may ensue.

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مواضيع ذات صلة

Polycythemia

Clinical Manifestations of Infective Endocarditis

Definition of Anemia

Acute circulatory failure (cardiogenic shock)

Pulmonary hypertension

Pulmonary thromboembolism

Giant cell (temporal) arteritis

ابيضاض الدم النقوي المزمن Chronic myelocytic leukaemias

Abdominal aortic aneurysm

Infective endocarditis

تليف النقيMyelofibrosis

فقر الدم اللا مصنع ( اللا تنسجي ) Aplastic anemia