Anemia pathophysiology

Rappaport JM, Nathan DG Acquired aplastic anemias Pathophysiology and treatment. Adv Intern Med 27 547-590, 1982... 

Heimpel H. Epidemiology and etiology of aplastic anemia. In Schrezenmeier H, et al, eds. Aplastic Anemia Pathophysiology and Treatment. Cambridge, UK, Cambridge University Press, 2000 97—116. 

FIGURE 65-1. Sickle gene inheritance scheme for both parents with sickle cell trait (SCT). A, normal hemoglobin S, sickle hemoglobin. Possibilities with each pregnancy 25% normal (AA) 50% SCT (AS) 25% sickle cell anemia (SS). (From Chan CYJ, Moore R. Sickle cell disease. In DiPiro JT, Talbert RL, Yee GC, et al, (eds.) Pharmacotherapy A Pathophysiologic Approach. 6th ed. New York McGraw-Hill 2005 1856.)... 

Graziano JH Columbia University Health Sciences, New York, NY Aim to elucidate the pathophysiologic mechanism(s) whereby Pb exposure induces anemia National Institute of Environmental Health Sciences... 

Fig. 11.1 Pathophysiologic scheme of sickle cell anemia (see color plates, p. XXXIV).

In accord with in vitro studies we should expect that the in vivo effects of MFs must have been the damaging ones. There are only few experimental in vivo and ex vivo studies, which, nonetheless, support this suggestion. Recently, we have showed for the first time (personal communication by LG Korkina, IB Deeva, IB Afanas ev) that MF effects may be much greater under pathophysiological than physiological conditions. We have studied the effects of a weak alternative magnetic field on leukocytes from Fanconi anemia (FA) patients, compared to... 

At present, numerous free radical studies related to many pathologies have been carried out. The amount of these studies is really enormous and many of them are too far from the scope of this book. The main topics of this chapter will be confined to the mechanism of free radical formation and oxidative processes under pathophysiological conditions. We will consider the possible role of free radicals in cardiovascular disorders, cancer, anemias, inflammation, diabetes mellitus, rheumatoid arthritis, and some other diseases. Furthermore, the possibilities of antioxidant and chelating therapies will be discussed. 

Anemias can be classified on the basis of RBC morphology, etiology, or pathophysiology (Table 33-1). The most common anemias are included in this chapter. 

A pressure sore is also called a decubitus ulcer and bed sore. A classification system for pressure sores is presented in Table 47-5. Many factors are thought to predispose patients to the formation of pressure ulcers paralysis, paresis, immobilization, malnutrition, anemia, infection, and advanced age. Four factors thought to be most critical to their formation are pressure, shearing forces, friction, and moisture however, there is still debate as to the exact pathophysiology of pressure sore formation. The areas of highest pressure are generated over the bony prominences. 

In an attempt further to elucidate the anhaptoglobinemia in patients with anemia, Nyman (N7) studied the plasma Hp in 335 cases of anemia (Hb less than 11 g/lOOml) mainly from a department of internal medicine. The partition she found (Table 2) is instructive from a pathophysiological point of view. The frequency of subnormal Hp values found within the different diagnostic groups may fairly well reflect the hemolytic trait in tire different types of anemia. Subnormal Hp possibly secondary to the increased red cell destruction is a common finding also in polycythemia. 

Young NS, Calado RT, Scheinberg P. Current concepts in the pathophysiology and treatment of aplastic anemia. Blood 2006 108 2509-19. 

Different classifications of anemia are based in part on the pathophysiological factor inducing the decreased hemoglobin concentration. Anemias due to cell hy-poproliferation include aplastic anemia and iron deficiency anemia. Hemolytic anemia results from excessive destruction of red blood cells. Megaloblastic anemia, sideroblastic anemia, and iron deficiency anemia result from an abnormality in the maturation of red blood cells. 

The syndrome of acute hypotension, adult respiratory distress syndrome, non-cardiogenic pulmonary edema, anemia, coagulopathy, and anaphylactic reactions after the administration of dextran 70 is referred to as the dextran syndrome (36-39). Factors other than acute volume overload due to intravascular absorption of dextran are thought to account for the syndrome. A combination of diverse pathophysiological factors may be responsible, namely direct pulmonary toxicity, activation of the coagulation cascade, release of vasoactive mediators, hypotension, pulmonary edema, intravascular intravasation of fluids, dilution of blood, and impaired renal and hepatic clearance. Cases of pulmonary edema are described under the section Respiratory. 

De long PE, Statius van Eps LW. Sickle cell nephropathy new insights into its pathophysiology. Kidney Int 1985 27 711-719. Allen M, Lawson L, Eckman IR, Delaney V, Bourke E. Effects of nonsteroidal anti-inflammatory drugs on renal function in sickle cell anemia. Kidney Int 1988 34 500-506. 

IFNy has also been found to be associated with immunodeficiency after allogeneic bone marrow transplantation/ the pathophysiology of aplastic anemia/ and atherogenesis. ... 

The pathophysiology of isoimmune hemolysis is the same for all antigens. The differences in severity of disease are due to differences in the expression of the antigen on the surface of the cells, the intrinsic immunogenicity of the antigen, and peculiarities of the immune response of the mother. Destruction of the fetal erythrocytes, which is the central problem, produces several other problems. Fetal anemia imposes an extra burden on the fetal heart to provide adequate oxygen supply to fetal tissues. Anemia stimulates the fetal marrow and extramedullary erythropoiesis in the liver and spleen to replace the destroyed erythrocytes. Extramedullary erythropoiesis destroys hepatocytes and leads to decreased production of serum albumin and decreased oncotic pressure in tire intravascular space. 

The pathophysiology of anemia of critical illness would lead to the hypothesis that treatment with pharmacologic doses of EPO might be beneficial. Few randomized, controlled trials have evaluated the role of EPO in critically ill patients, and these have resulted in mixed findings regarding EPO s ability to decrease transfusion requirements. A recently published literature review found that EPO cannot be recommended to reduce the need for RBC transfusions in critically ill patients with anemia. Even though EPO administration... 

Young NS, Maciejewski J. The pathophysiology of acquired aplastic anemia. N Engl J Med 1997 336 1365-1372. 

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