This document discusses the evaluation, causes, and treatment of various types of anemias. It covers topics such as the complications of anemia, genetic and acquired etiologies, nutritional deficiencies, physical causes, infections, neoplasms, and demographic factors. Evaluation involves medical history, physical exam, blood tests including complete blood count and smear, and imaging. Treatment depends on the underlying cause but may include blood transfusions, iron supplementation, bone marrow transplantation, splenectomy, and management of underlying conditions.

1. Anemias
Dr. Pablo Parenti

2. • La evaluación del hematocrito depende del
volumen
– Deshidratación
– embarazo

3. Complicaciones
• Hipoxia
– Shock
– Hipotensión
– Insuficiencia coronaria y pulmonar

4. Etiologías
Pérdida de sangre
Hemólisis
Producción

5. Genéticas
• Hemoglobinopatías
• Talasemias
• Anormalidades enzimáticas
• Defectos del citoesquelétdo del GR
• Anemia diseritropoyética congénita
• Enfermedad Rh
• Xerocitosis hereditaria
• Abetalipoproteinemia
• Anemia de Fanconi

6. Nutricionales
• Hierro
• Vitamina B-12
• Folato
• Malnutrición

7. Físicas
• Trauma
• Quemaduras
• Congelamiento
• Válvulas protésicas

8. Neoplasias y enfermedades crónicas
• Renal
• Hepática
• Infecciones crónicas
• Neoplasias
• Colagenopatías

9. Infecciosas
• Viral
– Hepatitis, mononucleosis, citomegalovirus
• Bacteriana
– Clostridia, sepsis gram-negativo
• Protozoos
– Malaria, leshmaniasis, toxoplasmosis

10. Factores demográficos
• Geográficas
• Raciales
• Género
• Edad

11. 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

12. Examen físico
• Aspecto general
• Piel
• Ojo
• Adenopatías y edemas
• Hepatoesplenomegalia
• Recto y pelvis
• Sistema nervioso
• Aparato cardiovascular

13. Hb g/dl OMS USA
Adultos 12.5 13.5
Femeninos 12.5
6m-6a 11
6ª-14a 12

14. Frotis

15. Hipocrómica microcítica
Total Iron-
Bone Marrow
Condition Serum Iron Binding Capacity Comment
Iron
(TIBC)
Iron deficiency ↓ ↑ 0 Responsive to
iron therapy
Chronic ↓ ↓ ++ Unresponsive to
inflammation iron therapy
Thalassemia ↑ N ++++ Reticulocytosis
major and indirect
bilirubinemia
Thalassemia N N ++ Elevation of A of
minor fetal hemoglobin,
target cells, and
poikilocytosis
Lead poisoning N N ++ Basophilic
stippling of RBCs
Sideroblastic ↑ N ++++ Ring sideroblasts
in marrow
Hemoglobin N N ++ Hemoglobin
electrophoresis

16. 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 synthesis
Nonmegaloblastic bone marrow Liver disease
Hypothyroidism and hypopituitarism
Accelerated erythropoiesis (reticulocytes)
Hypoplastic and aplastic anemia
Infiltrated bone marrow

17. Alteración en la forma GR
Macrocyte 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 anemias
Target cell Hypochromic with central "target" of hemoglobin. Liver disease, thalassemia, hemoglobin D,
and postsplenectomy
Leptocyte Hypochromic cell with a normal diameter and decreased MCV. Thalassemia
Elliptocyte 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 hypertension
Stomatocyte Slitlike area of central pallor in erythrocyte. Liver disease, acute alcoholism, malignancies,
hereditary stomatocytosis, and artifact
Tear-shaped Drop-shaped erythrocyte, often microcytic. Myelofibrosis and infiltration of marrow with
RBCs tumor. Thalassemia
Acanthocyte Five to 10 spicules of various lengths and at irregular intervals on surface of RBCs
Echinocyte Evenly distributed spicules on surface of RBCs, usually 10-30. Uremia, peptic ulcer, gastric
carcinoma, pyruvic kinase deficiency, and preparative artifact
Sickle cell Elongated cell with pointed ends. Hemoglobin S and certain types of hemoglobin C and l

18. evaluación
• Pérdida

19. hemólisis
Hereditary Acquired
Intracorpuscular 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

20. Hereditario adquirido
Extracorpuscular Physical agents: Burns, cold exposure
defect
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)

22. Exámenes complementarios
• Imágenes
• Endoscopías digestivas y RX
• Medula osea

23. Tratamiento

24. Tratamiento
• Transfusión
• Sulfato ferroso
• Nutrición (hierro, vit B12, Ac fólico)
• Aplasias
• Esplenectomía
• Transplante MO y células madre

25. Productos sanguineos
Fresh 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)

26. Suplementos minerales
Mineral supplements are used to provide adequate iron for hemoglobin
Ferrous sulfate (MyKidz synthesis and to replenish body stores of iron. Iron is administered
Iron 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 of
Chews, 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 is
Dexferrum) 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 Physician's 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.

27. Vitaminas
Cyanocobalam Deoxyadenosylcobalamin and hydroxocobalamin are active forms of vitamin
in ( 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 red
Folic 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).

28. electrolítos
Potassium Essential for transmission of nerve impulses, contraction of cardiac muscle,
Chloride (K- maintenance of intracellular tonicity, skeletal and smooth muscles, and
Tab, Klor-Con, maintenance of normal renal function.
microK, Gradual potassium depletion occurs via renal excretion, through GI loss or
Epiklor) 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.

29. vasopresores
Vasopressin 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.

30. Antihistamínicos H2
Cimetidine 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.

31. Glucocorticoides
Prednisone 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.