Anemia
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Anemia

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    Anemia Anemia Presentation Transcript

    • Anemias Dr. Pablo Parenti
    • • La evaluación del hematocrito depende del volumen – Deshidratación – embarazo
    • Complicaciones• Hipoxia – Shock – Hipotensión – Insuficiencia coronaria y pulmonar
    • EtiologíasPérdida de sangreHemólisisProducción
    • Genéticas• Hemoglobinopatías• Talasemias• Anormalidades enzimáticas• Defectos del citoesquelétdo del GR• Anemia diseritropoyética congénita• Enfermedad Rh• Xerocitosis hereditaria• Abetalipoproteinemia• Anemia de Fanconi
    • Nutricionales• Hierro• Vitamina B-12• Folato• Malnutrición
    • Físicas• Trauma• Quemaduras• Congelamiento• Válvulas protésicas
    • Neoplasias y enfermedades crónicas• Renal• Hepática• Infecciones crónicas• Neoplasias• Colagenopatías
    • Infecciosas• Viral – Hepatitis, mononucleosis, citomegalovirus• Bacteriana – Clostridia, sepsis gram-negativo• Protozoos – Malaria, leshmaniasis, toxoplasmosis
    • Factores demográficos• Geográficas• Raciales• Género• Edad
    • Anamnesis• Duración anemia• Historia familiar• Ocupación, hábitos, exposición, drogas.• Historia gineco-obstétrica• Síntomas gastrointestinales• Nutrición, deficiencias vitamínicas• Fiebre, lesiones piel, enfermedades metabólicas, colagenopatías• Orina• Anamnensis por aparatos
    • Examen físico• Aspecto general• Piel• Ojo• Adenopatías y edemas• Hepatoesplenomegalia• Recto y pelvis• Sistema nervioso• Aparato cardiovascular
    • Hb g/dl OMS USAAdultos 12.5 13.5Femeninos 12.56m-6a 116ª-14a 12
    • Frotis
    • Hipocrómica microcítica Total Iron- Bone Marrow Condition Serum Iron Binding Capacity Comment Iron (TIBC)Iron deficiency ↓ ↑ 0 Responsive to iron therapyChronic ↓ ↓ ++ Unresponsive toinflammation iron therapyThalassemia ↑ N ++++ Reticulocytosismajor and indirect bilirubinemiaThalassemia N N ++ Elevation of A ofminor fetal hemoglobin, target cells, and poikilocytosisLead poisoning N N ++ Basophilic stippling of RBCsSideroblastic ↑ N ++++ Ring sideroblasts in marrowHemoglobin N N ++ Hemoglobin electrophoresis
    • Macrocitosis (MCV >95)Megaloblastic bone marrow Deficiency of vitamin B-12 Deficiency of folic acid Drugs affecting deoxyribonucleic acid (DNA) synthesis Inherited disorders of DNA synthesisNonmegaloblastic bone marrow Liver disease Hypothyroidism and hypopituitarism Accelerated erythropoiesis (reticulocytes) Hypoplastic and aplastic anemia Infiltrated bone marrow
    • Alteración en la forma GRMacrocyte Larger than normal (>8.5 µm diameter). See Table 2.Microcyte Smaller than normal (< 7 µm diameter). See Table 1.Hypochromic Less hemoglobin in cell. Enlarged area of central pallor. See Table 1.Spherocyte Loss of central pallor, stains more densely, often microcytic. Hereditary spherocytosis and certain acquired hemolytic anemiasTarget cell Hypochromic with central "target" of hemoglobin. Liver disease, thalassemia, hemoglobin D, and postsplenectomyLeptocyte Hypochromic cell with a normal diameter and decreased MCV. ThalassemiaElliptocyte Oval to cigar shaped. Hereditary elliptocytosis, certain anemias (particularly vitamin B-12 and folate deficiency)Schistocyte Fragmented helmet- or triangular-shaped RBCs. Microangiopathic anemia, artificial heart valves, uremia, and malignant hypertensionStomatocyte Slitlike area of central pallor in erythrocyte. Liver disease, acute alcoholism, malignancies, hereditary stomatocytosis, and artifactTear-shaped Drop-shaped erythrocyte, often microcytic. Myelofibrosis and infiltration of marrow withRBCs tumor. ThalassemiaAcanthocyte Five to 10 spicules of various lengths and at irregular intervals on surface of RBCsEchinocyte Evenly distributed spicules on surface of RBCs, usually 10-30. Uremia, peptic ulcer, gastric carcinoma, pyruvic kinase deficiency, and preparative artifactSickle cell Elongated cell with pointed ends. Hemoglobin S and certain types of hemoglobin C and l
    • evaluación• Pérdida
    • hemólisis Hereditary AcquiredIntracorpuscular defect Hereditary spherocytosis Vitamin B-12 and folic acid deficiency Hereditary elliptocytosis Paroxysmal nocturnal hemoglobinuria Hemoglobinopathies Severe iron deficiency Thalassemias Congenital dyserythropoietic anemias Hereditary RBC enzymatic deficiencies Rarer hereditary abnormalities
    • Hereditario adquiridoExtracorpuscular Physical agents: Burns, cold exposuredefect Traumatic: Prosthetic heart valves, march hemoglobinemia, disseminated intravascular coagulation (DIC), graft rejection Chemicals: Drugs and venoms Infectious agents: Malaria, toxoplasmosis, mononucleosis, hepatitis, primary atypical pneumonia, clostridial infections, bartonellosis, leishmaniasis Hepatic and renal disease Collagen vascular disease Malignancies: Particularly hematologic neoplasia Transfusion of incompatible blood Hemolytic disease of the newborn Cold hemagglutinin disease Autoimmune hemolytic anemia Thrombotic thrombocytopenic purpura (TTP) and hemolytic-uremic syndrome (HUS)
    • Exámenes complementarios• Imágenes• Endoscopías digestivas y RX• Medula osea
    • Tratamiento
    • Tratamiento• Transfusión• Sulfato ferroso• Nutrición (hierro, vit B12, Ac fólico)• Aplasias• Esplenectomía• Transplante MO y células madre
    • Productos sanguineosFresh frozen plasma coagulation factors, as well as protein C and protein S. treatment of coagulopathies and TTP and the reversal of Coumadin. FFP does not transmit infections. treatment of Von Willebrand disease.Cryoprecipitate It contains fibrinogen, factor VIII, and von Willebrand factor and can be used in lieu of factor VIII concentrate if the latter is unavailable.Platelets Patients who are thrombocytopenic and have clinical evidence of bleeding should receive a platelet transfusion. Patients with platelet counts of less than 10,000/mcL are at risk for spontaneous cerebral hemorrhage and require a prophylactic transfusion. The preferred treatment for TTP and hemolytic-uremic syndrome is large- volume plasmapheresis with FFP replacement. ITP is rarely treated with transfusion, as the transfused platelets are destroyed rapidly. In stable patients, initial treatment is with prednisone. High-dose immunoglobulin and splenectomy are very effective treatments.Factor IX (BeneFix, Mononine) Hemophilia B is treated with factor IX concentrate. Recombinant factor IX currently is undergoing clinical trials (the current treatment is FFP or prothrombin-rich plasma concentrate).Recombinant factor VIII treat hemophilia A.(Advate, Helixate FS, Xyntha)
    • Suplementos minerales Mineral supplements are used to provide adequate iron for hemoglobinFerrous sulfate (MyKidz synthesis and to replenish body stores of iron. Iron is administeredIron 10, Fer-Iron, Slow-FE) prophylactically during pregnancy because of the anticipated requirements of the fetus and the losses that occur during delivery.Carbonyl iron (Feosol, Iron Csrbonyl iron is used as a substitute for ferrous sulfate. It has a slower release ofChews, Icar) iron and is more expensive than ferrous sulfate. The slower release affords the agent greater safety if ingested by children. On a milligram-for-milligram basis, it is 70% as efficacious as ferrous sulfate. Claims are made that there is less gastrointestinal (GI) toxicity, prompting use when ferrous salts are producing intestinal symptoms and in patients with peptic ulcers and gastritis. Tablets are available containing 45 mg and 60 mg of iron.Dextran-iron (INFeD, Dextran-iron replenishes depleted iron stores in the bone marrow, where it isDexferrum) incorporated into hemoglobin. Parenteral use of iron-carbohydrate complexes has caused anaphylactic reactions, and its use should be restricted to patients with an established diagnosis of iron deficiency anemia whose anemia is not corrected with oral therapy. The required dose can be calculated (3.5 mg iron/g of hemoglobin) or obtained from tables in the Physicians Desk Reference. For intravenous (IV) use, this agent may be diluted in 0.9% sterile saline. Do not add to solutions containing medications or parenteral nutrition solutions.
    • VitaminasCyanocobalam Deoxyadenosylcobalamin and hydroxocobalamin are active forms of vitaminin ( Calo-Mist, B12 in humans.Ener-B, Microbes synthesize vitamin B12, but humans and plants do not.Nascobal) Vitamin B12 deficiency may result from intrinsic factor (IF) deficiency (pernicious anemia), partial or total gastrectomy, or diseases of the distal ileum. Folic acid is an essential cofactor for enzymes used in the production of redFolic acid blood cells (RBCs).(Folvite)Vitamin K A decrease in levels of vitamin K–dependent factors (II, VII, IX, X, protein C, protein S) can lead to bleeding. Vitamin K is also used to treat hemorrhagic disease of the newborn, Coumadin- induced bleeding, and hypothrombinemia from other causes (eg, antibiotic, aspirin).
    • electrolítosPotassium Essential for transmission of nerve impulses, contraction of cardiac muscle,Chloride (K- maintenance of intracellular tonicity, skeletal and smooth muscles, andTab, Klor-Con, maintenance of normal renal function.microK, Gradual potassium depletion occurs via renal excretion, through GI loss orEpiklor) because of low intake. Depletion usually results from diuretic therapy, primary or secondary hyperaldosteronism, diabetic ketoacidosis, severe diarrhea, if associated with vomiting, or inadequate replacement during prolonged parenteral nutrition. Potassium depletion sufficient to cause 1 mEq/L drop in serum potassium requires a loss of about 100 to 200 mEq of potassium from the total body store.
    • vasopresoresVasopressin Vasopressin causes vasoconstriction of vascular smooth muscles and(Pitressin) increases water permeability and reabsorption in the collecting tubules. It decreases portal pressure in patients with portal hypertension.Somatostatin Somatostatin diminishes blood flow to the portal system due to(Zecnil) vasoconstriction, thus decreasing variceal bleeding. It has similar effects to vasopressin but does not cause coronary vasoconstriction.
    • Antihistamínicos H2Cimetidine The primary indication is to reduce symptoms and accelerate healing of(Tagamet) gastric ulcers. In the acutely bleeding patient, it has limited benefit.Ranitidine Ranitidine inhibits histamine stimulation of the H2 receptor in gastric parietal(Zantac) cells, which, in turn, reduces gastric acid secretion, gastric volume, and hydrogen ion concentrations.Famotidine Famotidine competitively inhibits histamine at H2 receptor of gastric parietal(Pepcid) cells, resulting in reduced gastric acid secretion, gastric volume, and hydrogen ion concentrations.Nizatidine (Axid) Nizatidine competitively inhibits histamine at the H2 receptor of the gastric parietal cells, resulting in reduced gastric acid secretion, gastric volume, and reduced hydrogen concentrations.
    • GlucocorticoidesPrednisone Glucocorticoids inhibit phagocytosis of antibody-covered platelets. Treatment of ITP during pregnancy is conservative unless the condition is severe. For severe cases, use the lowest dose of glucocorticoids. In neonates, if the platelet count drops below 50,000-75,000 platelets/µL, consider prednisone and exchange transfusions and immunoglobulin.