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1、内科学 贫血总论谢彦晖第1页，本讲稿共55页DIAGNOSIS AND CLASSIFICATION Anemia is an absolute decrease in hematocrit,hemoglobin concentration,or the RBC count.Anemia is not a diagnosis,but a sign of underlying disease.第2页，本讲稿共55页Hemoglobin(Hb):male(adult)120g/L female(adult)110g/L female(gestation)100g/LRed cell count m
2、ale4.5x1012 /L female4.0 x1012 /LHemocrit(HCT)male0.42 female0.37 female(gestation)0.30第3页，本讲稿共55页I.Determination of the cause:A.History1.Drug administration.2.Exposure to toxic chemicals 3.Family occurrence.4.Recent transfusions 5.menstruation(woman)6.ingestion(child)7.chronic disease8.Age at onset
3、.第4页，本讲稿共55页 B.Physical findings and complaintsa.Pale mucous membranes and skinsb.Weakness,loss of stamina,and exercise intolerance,Hypersensitivity to cold,fever.c.Tachycardia and polypnea,Heart murmur.anemia associated cardiac disease:Hb1/2blood volume lost in short period.第6页，本讲稿共55页C.Laboratory
4、findings1.The Hct is the easiest,most accurate method for detecting anemia.Its result should be interpreted with knowledge of the hydration status and any alteration caused by splenic contraction.第7页，本讲稿共55页2.Hb and RBC may be used to further classify the anemia.第8页，本讲稿共55页II.ClassificationA.Size(MC
5、V)and Hb Concentration(MCHC)1.Normocytic,macrocytic,microcytic.2.Normochromic,hypochromic.(Hyperchromia does not occur)第9页，本讲稿共55页Type MCV(fl)MCHC(%)MCH(pg)disorderMacro 100 32 32-35 megaloblastic anemia MDSNormo 80-100 26-32 32-35 aplastic anemia,blood lost,hemolytic anemiaMicro 80 26 32 iron defic
6、iency anemia sideroblastic anemia thalassemia 第10页，本讲稿共55页 B.Bone marrow response1.Regenerativea.Bone marrow actively responds by increasing its production of RBCs.b.Findings:(1)Polychromasia.(2)Reticulocytosis第11页，本讲稿共55页.(3)Macrocytosis(increased MCV)and hypochromia associated with reticulocytosis
7、.(4)Hypercellular bone marrow with a low M/E ratio.(5)Increase in MCV and RDW第12页，本讲稿共55页c.The presence of regeneration suggests an extramarrow cause.(1)Blood loss(2)Erythrocyte destruction(hemolysis)d.Bone marrow examination would reveal erythropoietic hyperplasia.第13页，本讲稿共55页2.Non-Regenerativea.In
8、adequate bone marrow response because of a bone marrow disorder.b.Polychromasia and reticulocytosis are absent.第14页，本讲稿共55页C.Pathophysiologic mechanism1.Blood losshemorrhagic anemia.2.Accelerated erythrocyte destructionhemolytic anemia.3.Reduced or defective erythropoiesis 第15页，本讲稿共55页ANEMIA FROM AC
9、CELERATED ERYTHROCYTE DESTRUCTION(HEMOLYTIC ANEMIA)第16页，本讲稿共55页A.Clinical findings1.Clinical signs of hemorrhage are absent.2.Jaundice may be seen in acute and severe cases.3.Hemoglobinuria and red plasma is seen if significant intravascular hemolysis occurs第17页，本讲稿共55页B.Laboratory findings1.Reticul
10、ocyte counts are higher in hemolytic anemias than externalhemorrhagic anemias 2.Plasma protein concentration is normal or increased.第18页，本讲稿共55页3.Neutrophilic leukocytosis and monocytosis may occur.4.Evidence of Hb degradation(hyperbilirubinemia,hemoglobinuria).5.Abnormal erythrocyte morphology(Hein
11、z bodies,erythrocytic parasites,spherocytes,or poikilocytes).第19页，本讲稿共55页I.Differentiation of the Causes of Hemolytic AnemiasA.Extravascular hemolysis第20页，本讲稿共55页1.Mechanismsa.Autoimmune Mediated-Antibody and/or C3 mediated(AIHA,infection,drug,immune system disorder)b.Decreased erythrocyte deformabi
12、lity(a)Shistocytes of microangiopathic anemia(b)Spherocytes of immune-mediated anemia(c)Parasitized erythrocytes(d)Heinz body-containing cells第21页，本讲稿共55页c.Reduced glycolysis and ATP content of the erythrocyte(PK deficiency)d.Increased macrophage activity (hypersplenism)第22页，本讲稿共55页e.Intravascular c
13、auses of hemolysis do not lyse all erythrocytes;some altered cells may remain that are removed by phagocytosis.第23页，本讲稿共55页2.Clinical and laboratory characteristics of phagocytic(extravascular)hemolysis.a.Usually chronic with insidious onset.b.A regenerative response.c.Hemoglobinemia and hemoglobinu
14、ria are absent.第24页，本讲稿共55页d.Hyperbilirubinemiae.Neutrophilia,monocytosis,and thrombocytosisf.Splenomegaly.第25页，本讲稿共55页h.Low-grade extravascular hemolysis occurs in many anemias that are primarily nonhemolytic(e.g.,anemia of chronic renal disease,iron-deficiency anemia).Referred to as the“hemolytic
15、component”of other types of anemia第26页，本讲稿共55页B.Intravascular hemolysisErythrocytes are destroyed within the circulation,releasing hemoglobin into the plasma where it is either removed by the liver or excreted by the kidneys.第27页，本讲稿共55页1.Mechanisms:The erythrocyte membrane must be significantly dis
16、rupted to allow escape of the Hb molecule into the plasma.Most of the mechanisms of intravascular hemolysis are extrinsic or extracorpuscular defects the erythrocyte is initially normal.第28页，本讲稿共55页a.Complement-mediated lysis.(neonatal isoerythrolysis and transfusion reactions,PNH)b.Physical injury(
17、Traumatic,microangio-pathic anemia,DIC,Coagulation,Vasculitis)c.Oxidative injury(Heinz body,methemo-globin)d.Osmotic lysis(hypotonic intravenous fluids)第29页，本讲稿共55页e.Other membrane alterations.(1)Castor beansricin.Causes direct lysis(2)Snake venoms(3)Bacterial toxins(4)Parasites(Babesia)第30页，本讲稿共55页
18、2.Clinical and laboratory characteristics of intravcascular hemolytic anemia.a.Most cases present as peracute or acute episodes.b.History may reveal exposure to causative drugs or plants,recent transfusion of blood,or recent ingestion of colostrum.c.A regenerative response occurs,but it may not be e
19、vident in early stages.第31页，本讲稿共55页d.Hemoglobinemia is the principal feature of intravascular hemolysis.(1)Red discoloration of plasma(2)Increased MCHCe.Hemoglobinuria f.Hemosiderinuriag.Hyperbilirubinemia第32页，本讲稿共55页h.Additional laboratory findings may include schistocytes,keratocytes,Heinz bodies,
20、erythrocytic parasites,positive Coombs test.第33页，本讲稿共55页 ANEMIA FROM REDUCED OR DEFECTIVE ERYTHROPOIESIS reduced or defective erythropoisis long or onset insidious clinic course第34页，本讲稿共55页I.General considerations.A.Mechanisms:1.Precursor cells Nutrients(iron and B vitamins)Stimulation(erythropoieti
21、n)第35页，本讲稿共55页2.Bone marrow failure(intramarrow disease and extramarrow causes)3.Bone marrow failure may be selective for the erythroid series or may also affect the other cell lines.第36页，本讲稿共55页B.Bone marrow response1.When the number of precursor cells or erythropoietic stimulation is inadequate,th
22、e erythroid marrow is hypocellular.2.Maturation abnormalities which characterize the nutritional deficiencies,are associated with a Hypercellular marrow and ineffective erythropoiesis.第37页，本讲稿共55页3.All degrees of bone marrow failure can occur,from complete aplasia to a suboptimal response of the ery
23、throid marrow following hemorrhage or hemolysis.第38页，本讲稿共55页II.Differentiation of anemias caused by reduced or defective erythropoiesis.erythrocyte morphology,u blood neutrophil u platelet numbersu bone marrow cellularity.第39页，本讲稿共55页 A.Normocytic,normochromic anemia;normal or increased neutrophil a
24、nd platelet numbers;increased M/E ratio caused by hypocellular erythroid marrow.1.Anemia of erythropoietin lack.a.Chronic renal disease.Anemia proportional to severity of the uremia.第40页，本讲稿共55页 b.Endocrinopathies (1)Cushings (2)Hypoandrogenism (3)Hypopituitarism第41页，本讲稿共55页 2.Anemia of chronic diso
25、rders(ACD)a.Occurs in chronic infectious,inflammatory,or neoplastic disorders.b.Cytokines involved with the inflammatory process initiate the anemia.c.Erythrocyte life span reduced第42页，本讲稿共55页d.Laboratory findings include:(1)Low serum iron (2)Low total iron binding capacity (3)Increased bone marrow
26、macrophage iron (4)Mild-moderate anemia that is usually nonprogressive 第43页，本讲稿共55页 3.Pure red cell aplasia a.Characterized by a selective loss of erythroid precursors in the bone marrow.b.Thought to be immune mediated.4.Unknown mechanisms a.Liver disease b.Vitamin E deficiency第44页，本讲稿共55页 B.Normocy
27、tic,normochromic anemia;neutropenia and/or thrombocytopenia;M/E ratio is difficult to determine because of hypocellularity.第45页，本讲稿共55页1.Aplastic anemia a.pancytopenia.b.shorter life spans of the cells.c.Causes (1)Drugs,chemicals,plants (2)Irradiation (3)Cytotoxic T cells or antibody (4)Infectious a
28、gents 第46页，本讲稿共55页 2.Myelophthisic anemia a.The bone marrow is physically replaced by an abnormal proliferation of cells.(1)Myeloproliferative disordersleukemias (2)Myelofibrosis (3)Osteosclerosis (4)Diffuse granulomatous osteomyelitis (5)Metastatic cancer第47页，本讲稿共55页 3.Anemia caused by infectious a
29、gents a.Ehrlichiosis(埃里西提病）埃里西提病）b.FeLV（猫白血病病毒）（猫白血病病毒）第48页，本讲稿共55页 C.Microcytic,hypochromic anemia;variable neutrophil and platelet number;usually a hypercellular marrow with a variable M/E ratio.第49页，本讲稿共55页1.Iron deficiency a.Chronic hemorrhage b.Dietary deficiency,especially in young milk-fed c.
30、Ineffective erythropoiesis early;第50页，本讲稿共55页 d.Laboratory findings:(1)Low serum iron (2)Variable iron-binding capacity (3)Microcytosis (4)Hypochromasia (5)Poikilocytes (6)Hypercellular bone marrow 第51页，本讲稿共55页 2.Pyridoxine deficiency.This vitamin is a cofactor in heme synthesis and a deficiency lea
31、ds to a failure to utilize iron.3.Copper deficiency.Copper-containing ceruloplasmin is important in iron absorption and transfer between gut,macrophages,and transferrin.第52页，本讲稿共55页 D.Macrocytic,normochromic anemia;variable neutrophil and platelet number;M/E ratio usually low because of hypercellula
32、r erythroid marrow.1.Vitamin B12 and folic acid deficiency.2.Erythemic myelosis or erythroleukemia.3.FeLV infection.第53页，本讲稿共55页 Treatment principle of anemia(1)causes treatment(2)supporting-trnsfusion(3)giving nutrition elements for hematopoiesis such iron agent,vitamine B12,folate acid(4)immunosuppression agent such glucocorticoid,antithymocyte globulin,cyclosporine A (5)auto-or allogeneic hematopoietic stem cell transplantation(6)hematopoietic growth hormone(EPO)or stimulating factor(androgen)(7)splenectomy第54页，本讲稿共55页THANKSTHANKS第55页，本讲稿共55页