贫血及贫血性心脏病-夜.ppt

Anemia AND Anemia Heart Disease,本文档由医学百事通高端医生网专家制作 在线咨询医生网址:,2,Chest Hospital,Definition,Anemia is defined as a decrease in the circulating RBC, hemoglobin or the hematocrit ,and a corresponding decrease in the oxygen-carrying capacity of the blood. Normal values of the hemogram (In sea level): TEST WOMEN MEN HCT (%) 37-48 40-50 Hb (g/L) 110-150 120-160 RBC Count(1012/L) 3.5-5.0 4.0-5.5,PS: The HB of Newborn is170-200g/L.,3,Chest Hospital,Diagnosis,WOMEN MEN PREGNANT,Hb (g/L) 110 120 100,WOMEN, Anemia isnt a diagnosis, it is a sign of the presence of disease. Correct diagnosis: include underlying cause of the anemia They can be altered by the plasmatic volumes . The mean normal value depends on :altitude of residence, age and gender. Difference between women and men values are due to androgen hormones.,4,Chest Hospital,Diagnosis,First step : detection of the presence of anemia,and the severity. Second step: laboratory investigation of the morphological classification. Third step: investigation of the pathogenesis of anemia.,5,Chest Hospital,Diagnosis,Classification according to severity,First step:,6,Chest Hospital,Diagnosis,cell morphological type MCV（fl） MCH(pg) MCHC (%) Macrocytic anemia 100 34 3236 Normocytic anemia 80100 27 34 3236 Microcytic hypochromic anemia Simple microcytic anemia,(80-100),(32-36),(27-34),80 27 32,80 27 3236,Second step: cell morphological classification,PS: According to Bone marrow proliferative degree and peripheral RBC morphology .,7,Chest Hospital,Diagnosis,Third step: according to etiology/pathogenesis 1.Blood loss-acute hemorrhage chronic hemorrhage 2. Increased RBC destruction -hemolytic anemia(HA),The chronic hemorrhage often combine with IDA, caused by ITP,bronchiectasis,tuberculosis,tumor,etc.,8,Chest Hospital,Diagnosis,RBC internal defect (1)RBC membrane defect acquired: PNH hereditary : hereditary spherocytosis (2) enzyme deficiency: G6PD deficiency (3) Hb abnormality: hemoglobinopathy, Thalassemia (4) porphyrin metabolism : porphyrinopathy Exopathic immunologic (AIHA), chemical, biological, or phisical factors,Usually 6.5 m diameter Microspherocytes: 4 m diameter Lacks area of central pallor. Additional causes: Immunologic reaction Physical trauma,(dacryocyte),(spherocyte),(elliptocyte),(stomatocyte),9,Chest Hospital,Diagnosis,3. Decresed RBC production,BM stem cells abnormality AA BM injured by abnormal tissues/cells Leukemia Cell dysmaturity(deficiency of essential substances ) (1). DNA dyssynthesis Megaloblastic anemias (2). Hb dyssynthesis IDA 4. Abnormality in haematopoiesis modulation AA,10,Chest Hospital,Diagnosis,Complete diagnosis 1. Anemia 2. Degree of anemia 3. Classification of anemia 4. Cause of anemia,11,Chest Hospital,Clinical manifestations,1.The clinical manifestations is related to tissue hypoxia which decreases work tolerance. 2.The Related factor: Cause of anemia Degree of decrease of oxygen carrying capacity Degree of decrease of blood volume Speed of anemia genesis Compensation and tolerance of blood and others 3.The associated manifestations of the underlying disorders.,12,Chest Hospital,Clinical manifestation,Skin Pallor can be the most evident sign mucous membranes of mouth and lips, nail bed, palpebral conjunctiva Neuromuscular system headache, vertigo, tinnitus, faintness, lack of mental concentration, muscular weakness Gastrointestinal system common in anemic patients anorexia, nausea, vomiting, glossitis, atrophy of papillae of tongue(mirror surface tongue), etc. The dysphagia(Plummer Vinson Syndrome) and pica can be seen in chronic IDA patients. Genitourinary system slight proteinure is common. Other signs mild fever, basal metabolic rate be increased.,13,Chest Hospital,Clinical manifestation,Cardiorespiratory system: 2,3-diphosphoglyceric acid (2,3-DPG)affect hemoglobin bind and release of oxygen. In chronic anemia, 2,3-DPG concentration increased making the oxygen dissociation curve right,oxygen affinity of hemoglobin falls compensate for oxygen deficit. General symptoms(accelerated breath, short breath) are noticeable after exertion. In severe or HBC is less than 7g/dl -cardiac output is increased and heart murmurs are common sign in anemia.,14,Chest Hospital,History Taking and Examination,History: 1.symptoms and their duration 2.past history(Gastrectomy, haemorrhoids, peptic ulcer, jaundice, bleeding disorder ) 3.hereditary background, menses and childbearing history 4.diet habit, exposure to risk factors(such as chemicals or toxins) Examination: Jaundicemay point to hemolytic anemia, liver disease Hepatomegalysuggeste liver disease, lymphoma, leukemia Splenomegalyleukemia, hemolytic anemia, liver disorder sternal tendernessshows leukemia flating of finger nailmean iron defiency anemia,15,Chest Hospital,Laboratory investigation,Hematologic-blood RT, platelet count, hematocrit(HCT), MCV, MCH, MCHC, RBC morphological change, bone marrow, reticulocyte count ,etc. reticulocyte count lower than normalaplastic anemia reticulocyte count higher than normalhemolytic anemia Blood smeareasy, quickly, useful for much information Bone marrowshow all hemocytic changes Hypochromia, Microcytosisiron difiencey Microspherocytehereditary sherocytosis PS: HA Urinalysis Hemoglobinuria or methemoglobinuria Hemosiderinuria Urobilinogen,16,Chest Hospital,Laboratory investigation,MA: Nuclear maturation lags behind cytoplasmic maturation,IDA: Cytoplasmic maturation lags behind nuclear maturation,Seed Stem cell deficiency,Worm Immunological changes,Soil Microenvironment deficiency-,17,Chest Hospital,Treatment,The principle of treatment-Pathogenetic therapy,to Eradicate the cause of anemia.,Nutritional anemia IDA: Oral Iron. A Ret rise in 35 days and Hb increase in 12 wk after the initiation of iron therapy. Patients should be continue iron therapy for two months after Hb levels is normal to reestalbish adequate iron stores. MA: First correct the basic problem ,then the Vit B12 and folic should been completed simultaneously.,18,Chest Hospital,Treatment,AA: 1.Supportive care RBC transfusion(Hb60g/L),platelet transfusion (BP20109L, spontaneous bleeding), management of infection. 2. Stimulate hemotopoiesis androgen,EPO,G-CSF 3. Immunosuppressive agents CsA,ALG,MMF,CTX 4. Bone marrow transplantationSAA,HAAIHA glucocorticoids, Splenectomy, Immunosuppressive agents, Washed Red Blood Cells transfusion,19,Chest Hospital,Anemia heart disease,Sinus tachycardia, pulse pressure increased, arterial pulsation strengthened, cardiac output increased, cardiac systolic murmurs.,Circulation system has not changed much. No specific symptoms.,20,Chest Hospital,Anemia heart disease,30% of the patients of anemia can have ECG changes, performance for low voltage, ST segment depression, T wave inversion or flattened . The serious can have Long QT Syndrome , atrial fibrillation etc. The patients of very severe anemia ( 30 g/L) or acute anemia progress, can have the whole heart to expand obviously. Finally because of the myocardial nutrition barriers for increasing high output, the anemia leading to a state of congestive heart failure. Corrected the hypovolemia, the symptoms can get a certain recovery.,21,Chest Hospital,Anemia heart disease,Anemia in heart failure (HF) is increasingly recognized and treated, but little is known about the prevalence and its relation to outcomes in patients hospitalized for decompensated HF in a situation of both reduced and preserved systolic function. Data from 48,612 patients at 259 hospitals showed that half of the total cohort had low hemoglobin (12.1 g/dl) and that 25% were moderately to severely anemic (lowest hemoglobin quartile, 5 to 10.7 g/dl). Anemic patients had higher in-hospital mortality (4.8% vs 3.0%, lowest vs highest quartile), longer hospital length of stay (6.5 vs 5.3 days), and more readmissions by 90 days (33.1% vs 24.2%) (all p 0.0001). In conclusion, these data reveal a higher prevalence of low hemoglobin in hospitalized patients than noted in randomized HF trials and outpatient registries. Lower hemoglobin is associated with higher morbidity and mortality in hospitalized patients with HF . Young JB, Abraham WT, Albert NM, et al. Relation of low hemoglobin and anemia morbidity and mortality in patients with heart failure (Insight from the OPTIMIZE-HF Registry) J. Am J Cardiol.2008, 101 (2): 223-230.,22,Chest Hospital,Anemia heart disease,In the present study we therefore report the long-term effect of anaemia over 13 to 15 years of follow up. We furthermore explore differences in mortality rates between subgroups of anaemic patients in order to identify patients with a particularly high risk. We also perform landmark analysis to investigate whether the presence of anaemia remains significant during follow up. The present study concludes that anaemia is present in one third of patients at the time of diagnosis of heart failure and that anaemia at the time of diagnosis of heart failure is an independent factor for mortality in the following 2-5 years. The presence of mild or severe anaemia loses its influence on mortality after 2 years while moderate anaemia loses its influence on mortality after 5 years. Charlot M，Torp-Pedersen C, Valeur N, et al. Anaemia and long term mortality in heart failure patients: a retrospective study J.Open Cardiovasc Med J, 2010, 4(9):173-177