By Stefan Silbernagl, Florian Lang
Books on pathophysiology are inclined to specialise in a definite box corresponding to endocrine or cardiovascular pathophysiology. this can be the single pocket atlas that treats points of pathophysiology for all vital problems. The book's association provides the reader easy access to the informative texts and the 181 finished and transparent colour pictures. Informative photographs exhibit the causal relationships among disturbances of physiological procedures and the ensuing malfunction and disorder. This flexi is designed either as a reference either for the coed getting ready for tests and the expert general practitioner wishing to replace his wisdom on pathophysiology.
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Extra info for Color Atlas of Pathophysiology
They can be severely deformed within the blood capillaries, which greatly facilitates both their passage and the exchange of substances and gases with the surrounding tissues. RBCs that have recently entered the blood will retain net-like residues of organelles (reticulocytes) for another one or two days. With a normal life-span of RBCs of about 110 – 120 days, the proportion of reticulocytes is normally 1 – 2 %. Erythrocytes contain a large amount of hemoglobin (Hb), their mean corpuscular hemoglobin concentration (MCH) normally being 300 – 360 g per litre RBCs (→ A).
Disorders of erythropoiesis (→ B) may occur as a result of 1) lack or absence of differentiation of pluripotent, hemopoietic stem cells (aplastic anemia in panmyelopathy or acute myeloid leukemia); 2) transient (viral infection) or chronic reduction of only the erythrocytic precursor cells (isolated aplastic anemia) due to autoantibodies against erythropoietin or against membrane proteins of the precursor cells; 3) erythropoietin deficiency in renal failure (renal anemia); 4) chronic inflammation or tumors that can activate, among others, erythropoiesis-inhibiting interleukins (secondary anemia); 5) abnormal cell differentiation (ineffective erythropoiesis), which in addition to gene defects may mainly be due to a deficiency in folic acid or vitamin B12 (megaloblastic anemia; → p.
6 Iron Deficiency Anemias Lumen Mucosal cells Heme (duodenum) 2+ Fe Heme Apotransferrin Blood A. Iron (Fe) Deficiency Inhibits Hemoglobin Synthesis Fe recycling Systemic blood Ferritin Fe Hemosiderin Fe storage HemoHeme pexin Fe Haptoglobin Hb Ferritin Hemosiderin Already in bone marrow Erythrocytes 2 Storage, loss and recycling Macrophages in spleen, liver and bone marrow (extravasal) Silbernagl/Lang, Color Atlas of Pathophysiology © 2000 Thieme All rights reserved. Usage subject to terms and conditions of license.