ANEMIA3231334556467687898790909-7654.ppt

Anemia

1. ANEMIA

2. WHAT IS ANEMIA
•Anemia is a sign, not a disease.
•Decrease in whole red cell mass
•Causes:
•1. decreased in RBC production
•2. increased RBC loss

4. IRON METABOLISM
•Only 5-10 % or about 1.0 mg of dietary iron is absorbed as
ferrous iron (Fe++), mainly in the duodenum and upper
jejunum.
•The mucosal cells oxidize the ferrous iron to ferric iron
•complexed with apoferritin to form ferritin;
•Apoferritin a protein present in the intestinal mucosa that binds
and stores iron by combining with a ferric hydroxide-
phosphate compound to form ferritin.
•some of the ferritin is transported out of the mucosal cell
into the plasma bound to transferrin

5. TRANSFERRIN
•Are iron binding blood plasma glycoprotein that control the
level of free iron in biological fluids.
•The major function of transferrin is to transport iron to cells.
•iron has to be bound to transferrin because unbound iron is
toxic .
•Serum iron has a normal concentration of 60-150 ug/dL and
largely reflects iron bound to transferrin.

6. TIBC
•Is a medical lab. test that measures the blood’s capacity to bind iron
with transferrin.
•Total iron binding capacity (TIBC) is the sum of the unbound
apotransferrin plus the iron bound transferrin
•represents the maximum capacity for iron binding
•Serum iron in males: 65- 177ug/dL
•Females: 50- 170ug/dL

7. IRON STORES
•stored as either ferritin or hemosiderin
• The main storage site is liver.
•The receptor-transferrin-iron complex is then incorporated into
the cytosol by endocytosis.
•at an acid pH the iron (Fe++) is released from transferrin
•transported to mitochondria where it is incorporated into heme.
•the bulk of body iron is found in erythrocytes
•Large amounts of iron are required during growth periods in
infant, childhood and teenage years

9. IRON-DEFICIENCY ANEMIA
•Major cause in adults: chronic blood loss, insufficient
absorption of iron, parasitic inf.
menorrhagia ( heavy menses)
bleeding from GIT
•Dietary deficiency is common after 6 months of age in infants
•Pallor, fatigue, dyspnea on exertion, anxiety, hair loss, mouth
ulcers.

10. IRON-DEFICIENCY ANEMIA
•Low hemoglobin
•Low hematocrit
•Low RBC count
•Hypochromic, microcytic RBC on smear
•Low serum iron
•High total iron binding capacity(TIBC)
•Low iron store; low ferritin

11. MEGALOBLASTIC ANEMIA
•Presence of large, abnormal-looking erythroid precursor cells or
MEGALOBLASTS in the bone marrow
•Impaired RBC production
•Mostly due to B12 or folate deficiency

12. HYPERSEGMENTED NEUTROPHILS

13. MEGALOBLAST

14. MEGALOBLASTIC ANEMIA
•Folate deficiency
•Seen in alcoholics
•Pregnancy
•Contraceptive pills
•Dilantin, anticonvulsant drugs
•Chemotherapy agents
•Same presentation as B12
deficiency
•Women with folate deficiency
who become pregnant are
more likely to give birth to low
birthweight, premature infants
with neural tube defects.

15. PERNICIOUS ANEMIA
•Pernicious anemia is one of many types of the larger
family of megaloblastic anemia. It is caused by loss of
gastric parietal cells which are responsible, in part, for the
secretion of intrinsic factor, a protein essential for
subsequent absorption of vitamin B
12
in the ileum.

16. ANEMIA OF CHRONIC DISEASE
•Impaired red cell production associated` with chronic
diseases Second most common form
•May be due to rheumatoid arthritis,regional enteritis,
chronic infection, neoplasms.
•Normochromic, normocytic
•Low TIBC

17. APLASTIC ANEMIA
•Aplastic anemia is a condition where bone marrow does not
produce sufficient new cells to replenish blood cells. The
condition, as the name indicates, involves both aplasia and
anemia. Typically, anemia refers to low red blood cell counts, but
aplastic anemia patients have lower counts of all three blood cell
types: red blood cells, white blood cells, and platelets, termed
pancytopenia.

18. APLASTIC ANEMIA
•Anemia with malaise, pallor and associated symptoms such
as palpitations
•Thrombocytopenia(low platelet counts), leading to
increased risk of hemorrhage, bruising and petechiae
•Leukopenia (low white blood cell count), leading to
increased risk of infection
•Reticulocytopenia (low reticulocyte counts)

19. APLASTIC ANEMIA
•Most common cause: toxic exposure
radiation
chemicals – benzene
antibiotics – chloramphenicol
cancer drugs
viruses – hepatitis C and Parvovirus

20. SIDEROBLASTIC ANEMIA
•a sideroblastic anemia caused by a deficiency of pyridoxine
(vitamin B
6
). The most common cause of pyridoxine deficiency
is isoniazid therapy for tuberculosis. Sideroblastic anemias are
due to defects in heme synthesis in the mitochondria of
developing RBC precursors in the bone marrow.

21. HEMOLYTIC ANEMIA
•Hemolytic anemia is a form of anemia due to hemolysis,
the abnormal breakdown of red blood cells , either in the
blood vessels (intravascular hemolysis) or elsewhere in the
human body (extravascular).

22. HEMOLYTIC ANEMIAS
•Shortened life span of RBC
•Increased destruction
•Hemoglobinemia, hemoglobinuria
•Hemosiderosis

23. IMMUNE HEMOLYTIC ANEMIA
•immune hemolytic anemia is a condition in which there is a
reduced blood cell count due to the premature destruction of
red blood cells by the immune system.
•Immune hemolytic anemia occurs when antibodies form against
the body's own red blood cells. The antibodies destroy the blood
cells because the immune system mistakenly recognizes these
blood cells as foreign material within the body.

24. IMMUNE HEMOLYTIC ANEMIA
•The antibodies may be caused by:
•Complication of another disease
•Past blood transfusions
•Pregnancy (if the baby's blood type is different from the
mother's)
•Reaction to certain medications
•Reaction to certain infections

25. THALASSEMIAS
•The thalassemia are a group of disorders in which the normal
hemoglobin protein is produced in lower amounts than usual.
•Deficient production of either alpha or beta-globin chains
•Beta-thalassemia: most common form; defect in the genes
coding for Beta-globin gene
•

26. BETA-THALASSEMIA MAJOR
•A usually fatal form of thalassemia
appearing in infancy or childhood
in which normal hemoglobin is
absent, characterized by severe
anemia, enlargement of the heart,
liver, and spleen, and skeletal
deformation.
•Decrease Hb synthesis
•Short RBC lifespan (due to
insoluble, excess alpha-chains)
•Ineffective RBC production
•Skull, facial bones and long
bones distortion
•Microcytosis, hypochromic
anemia
•Hemosiderosis
•Increase Hb F throughout life