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Anemia and Hemolisis

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					Anemia
Anemia

Hb<13 g/dl (male), <11.5 g/dl
(Female)
Associated with reduced in RBC count
Due to failure of RBC production, loss or
destruction of RBC
Rapid blood loss >10% caused tissue
hypoxia and shock.
Anemia in gradually form is more
tolerable
RBC function is to carry oxygen
Sign & Symptom mainly due to tissue
hypoxia
    Lethargy, breathlessness,
    Bounding pulse, tachycardia,
    Pale
    Heart failure,
    Spesific S&S for spesific type of anemia.
    jaundice
  Classification


Production failure
Increased red cell loss, lysis or pooling
Production failure
   Hematinic def;
      iron, vitamin B12, folic acid
   Chronic disorders;
      infection, inflammation and neoplasia
   Dyserythropoiesis;
     sideroblastic anemia
   Bone marrow failure;
     leukemia, non-hematological malignancy
Increased RBC loss, lysis, pooling
 Acute blood loss
 Hemolysis due to RBC abnormality
     Membrane defect: hereditary spherocytosis,
     elliptocytosis
     Enzyme defect: G6PD def, Pyruvat Kinase def
     Hemoglobinophathy: talasemia, sickle cell dis
 Hemolysis due to abnormality outside of
 RBC
     Immune hemolysis, drug, toxin, parasites
 Hypersplenism
Iron def Anemia

 Causes
   chronic blood loss
      Peptic ulcer, hemorrhoid, manorrraghia,
   Poor iron intake
      Malnutrition,
   Increased requirement
      Pregnancy, chilhood
   Malabsorption
      Gastrectomy,
Chronic blood loss and iron def anemia

    Iron status is mainly controlled by absorption
    Limited absorption and blood loss likely to
    result iron def
    Body iron
      60% of iron body is in Hb of RBC
      30% stored in RES in BM as ferritin & hemosiderin
      The rest in tissue, esp. muscle
    Iron from intravascular lysis will remain in
    iron cycle
    Iron for erythropoiesis is from iron cycle
Iron def anemia

 In body iron stored mainly in macrophage of
 bone marrow, spleen and hepatocyte.
 Iron stored in form of ferritin.
 Absorption and loss of iron must be in
 balance
 Req: adult male 1m, female 2 mg, pregnant
 female 1.5-3 mg, child 1.5mg
Daily iron loss 1mg
Normal diet contain 10-20mg but only
10-15 % is absorbed.
1 ml of blood contain 0.5 mg iron.
Chronic small volume of blood loss
cause iron def
At initial stage body will increase iron
absorption
The usage of stored iron for
erythropoiesis
Cause low iron stored
Caused ineffective erythropoiesis
Failure of hemoglobin synthesis–
hypochromic
Increased blast cell devision---
microcytic
Feature of iron def anemia

 Angular stomatitis
 Atrophic glossitis
 Koilonychia (spoon shape nail)
 Dysphagia
   Atrophic glossitis   koilonychia




Angular stomatitis
B12 and Folate deficiency

 Nucleic acid synthesis for cell division is
 defective
 Result in macrocytic anemia
 (megaloblastic anemia)
 Pancytopenia is common
 B12 def mainly due to malabs.
   Pernicious anemia
   Gastrectomy
   Ileal resection
B12 deficiency
  mainly due to malabsorption (pernicious anemia,
  gastrectomy, ileal resection)
  Malnutrition (vegetarian)
Folate deficiency
  Mainly due to malnutrition
Special clinical feature
  Sensory impairment in the feet, altered gait, visual
  disturbance and dimentia due to lesion of nervous
  system (demyelination and neuronal
  degeneration)
Increased RBC loss, lysis, pooling
 Acute blood loss
 Hemolysis due to RBC abnormality
     Membrane defect: hereditary spherocytosis,
     elliptocytosis
     Enzyme defect: G6PD def, Pyruvat Kinase def
     Hemoglobinophathy: talasemia, sickle cell dis
 Hemolysis due to abnormality outside of
 RBC
     Immune hemolysis, drug, toxin, parasites
 Hypersplenism
Thalassemia
 Four gene needed for each alpha and
 beta globin chain
 In thalas production of chain is reduced
 due to gene defect
 Accumulation of an excess of
 uneffected globin chain cause damage
 RBC
 Hemolysis is severe with increase in no
 of gene deleted
Alpha thalassemia
 4 gene   deleted—hydrop fetalis
 3 gene   deleted--- free beta chain form
 Hb                        H (bart)
 2 gene   deleted---talas trait (N Hb)
 1 gene   deleted ---talasemia trait (N Hb)
Beta Thalassemia
 Beta talass major
   Deletion of 2 beta gene
   Reduced in HbA
   High in Hb F
Sickle cell Disease
 Substitution of valine for glutamic acid
 in position 6 in beta chain.
 Formation of Hb S
 Hb S aggregation and polymerization in
 hypoxia condition
 Vascular occlusion---tissue infarction
 Chronic hemolysis----jaundice
 Hyphochromic microcytic anemia

				
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