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Blood loss Hemolysis (intrinsic) Membrane: hereditary spherocytosis, elliptocytosis Hemoglobin: sickle cell, unstable hemoglobin Glycolysis: pyruvate kinase deficiency, etc Oxidation: glucose-6-phosphate dehydrogenase deficiency Hemolysis (extrinsic) Immune: warm antibody, cold antibody Microangiopathic: thrombotic thrombocytopenic purpura, hemolyticuremic syndrome, mechanical cardiac valve, paravalvular leak Infection: clostridial Hypersplenism
myeloproliferative leukemia Bone marrow infiltration: carcinoma. Decreased production Hemoglobin synthesis: iron deficiency. anemia of chronic disease DNA synthesis: megaloblastic anemia Stem cell: aplastic anemia. lymphoma Pure red cell aplasia . thalassemia.
chemotherapy Liver disease Increased reticulocytosis Myxedema Normocytic Many causes .Classification of anemias by mean cell volume. Microcytic Iron deficiency Thalassemia Anemia of chronic disease Macrocytic Megaloblastic Vitamin B12 deficiency Folate deficiency Nonmegaloblastic Myelodysplasia.
.Iron Deficiency Anemia Essentials of Diagnosis Serum ferritin < 12 ug/L. Response to iron therapy. Caused by bleeding in adults unless proved otherwise.
and liver disease. cancer. and the bone marrow fails to compensate adequately by increasing red blood cell production. Red blood cell survival is modestly reduced.ANEMIA OF CHRONIC DISEASE Common causes include chronic infection or inflammation. . Decrease in erythropoietin is rarely an important cause of underproduction of red cells except in renal failure.
•Decreased dietary intake of folate or iron is common in these ill patients. and normal or increased serum ferritin (or normal or increased bone marrow iron stores). and many will also have ongoing gastrointestinal blood losses. •Patients undergoing hemodialysis regularly lose both iron and folate during dialysis. low TIBC.•The diagnosis should be suspected in patients with known chronic diseases •Confirmed by the findings of low serum iron. .
acanthocytes. elevated levels of hemoglobin A2 or F. • In ß-thalassemia.THE THALASSEMIAS Essentials of Diagnosis • Microcytosis out of proportion to the degree of anemia. • Positive family history or lifelong personal history of microcytic anemia. . • Abnormal red blood cell morphology with microcytes. and target cells.
Two a-globin genes are present: a-thalassemia trait. The a-thalassemia syndromes are seen primarily in persons from southeast Asia and China. in blacks. Only one a-globin chain is present: hemoglobin H disease. they may do so during periods of hemolytic exacerbation caused by infection or other stresses. and. the affected fetus is stillborn as a result of hydrops fetalis. . Physical examination: pallor and splenomegaly. Three genes are present: the patient is a hematologically normal (silent carrier). These patients are clinically normal with a mild microcytic anemia. All four a-globin genes are deleted. less commonly. Although affected individuals do not usually require transfusions. This is a chronic hemolytic anemia of variable severity (thalassemia minor or intermedia).
hepatosplenomegaly. develop severe anemia requiring transfusion. A milder form of ß-thalassemia (allowing a higher rate of globin gene synthesis) have thalassemia intermedia: chronic hemolytic anemia but do not require transfusions except under periods of stress. pathologic fractures). and endocrinopathies. including growth failure. Homozygous for ß-thalassemia have thalassemia major. Hemosiderosis results in a clinical picture similar to hemochromatosis. Numerous clinical problems ensue. They survive into adult life but with hepatosplenomegaly and bony deformities. bony deformities (abnormal facial structure. Patients heterozygous for ß-thalassemia have thalassemia minor and a clinically insignificant microcytic anemia. and jaundice. Affected children are normal at birth but after 6 months. . with heart failure. Greek) and to a lesser extent Chinese. cirrhosis. ß-Thalassemia primarily affects persons of Mediterranean origin (Italian. and blacks. other Asians.
methemoglobinemia Hemoglobinopathies: sickle cell syndromes. severe hypophosphatemia Oxidation vulnerability: glucose-6-phosphate dehydrogenase deficiency. hereditary elliptocytosis. methemoglobinemia Extrinsic Immune: autoimmune. vasculitis Infection: plasmodium. valve hemolysis. paroxysmal nocturnal hemoglobinuria Glycolytic defects: pyruvate kinase deficiency. lymphoproliferative disease. drug toxicity Microangiopathic: thrombotic thrombocytopenic purpura. clostridium. hemolytic-uremic syndrome. unstable hemoglobins. borrelia Hypersplenism Burns .HEMOLYTIC ANEMIAS Intrinsic Membrane defects: hereditary spherocytosis. disseminated intravascular coagulation. metastatic adenocarcinoma.
Pakailah bahasa komunikasi yang dimengerti oleh pasien.Kesimpulan Anamnesis dan fisik diagnostik merupakan kunci utama untuk menegakan diagnosis Anemia Lakukan anamnesis dan fisik diagnostik sesuai dengan patofisiologi dari anemia yang terjadi Lakukan selalu reanamnesis untuk mencari data baru berdasar data yang sudah ada Lakukan allo dan auto anamnesis untuk mendapat data yang valid. .