Anemia
Mazin Abdelgadir
General features
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Decrase RBCs
Pallor
Hypoxia
Peripheral blood changes
BM hyperplasia
Extra medullary hematopoiesis
Process of RBCs production
iron
Vit b12
Folic acid
BM
(Aplastic anemia)
RBCs (hemolysis)
Iron deficiency anemia
• Very common
• 25% to 50% of people in developing countries .
• Causes:
1. Chronic blood loss is the most important cause :peptic ulcers,
colonic cancer, hemorrhoids,menorrhagia, metrorrhagia, cancers).
2. low intake
3. Increased demands (pregnancy and infancy.)
4. Malabsorption (celiac disease or after gastrectomy)
• iron deficiency develops insidiously.
• Iron stores are depleted , marked by :
1. a decline in serum ferritin
2. and the absence of stainable iron in the bone marrow.
3. decrease in serum iron and
4. a rise in the serum transferrin.
5. Microcytic hypochromic anemia,
6. impaired work and cognitive performance,
7. reduced immunocompetence.
Clinical feature:
1. weakness, and pallor,
2. figernails, thinning, flttening, and “spooning,”
3. pica, the compunction to consume non food stuffs such as dirt or clay.
4. In peripheral smears red cells are microcytic and hypochromic
Diagnostic criteria:
1. anemia, hypochromic and microcytic
2. low serum ferritin and iron levels,
3. low transferrin saturation,
4. increased total iron-binding capacity,
5. For unclear reasons, the platelet count often is elevated.
6. Erythropoietin levels are increased, but marrow cellularity usually is
only slightly increased.
Microcytosis hypochromia
There is also increased anisocytosis (variation in size) and
poikilocytosis (variation in shape).
Aplastic anemia
• Aplastic anemia is a disorder in which multipotent myeloid stem cells
are suppressed, leading to bone marrow failure and pancytopenia.
• pure red cell aplasia, :only erythroid progenitors are affected
and anemia is the only manifestation.
Causes
1. 50% is idiopathic.
2. a drug or a chemical,( alkylating agents, antimetabolites), benzene,
and chloramphenicol.
3. viral hepatitis.
4. Cancer affecting the bone marrow
5. Chemotherapy
Pathogenesis
• autoreactive T cells play an important role.
• 5% to 10% of patients with “acquired” aplastic anemia have inherited
defects in telomerase,.
Morphology
• The bone marrow in aplastic anemia is markedly hypocellular, with
greater than 90% of the intertrabecular space being occupied by fat.
• Thrombocytopenia and granulocytopenia may result in hemorrhages
and bacterial infections, respectively.
• The requirement for transfusions may eventually lead to
hemosiderosis.
Clinical course
• The slowly progressive anemia causes the insidious development of weakness, pallor,
and dyspnea.
• Thrombocytopenia often manifests with petechiae and ecchymoses.
• Granulocytopenia may be manifested by frequent and persistent minor infections or by
the sudden onset of chills, fever, and prostration.
• Aplastic anemia does not cause splenomegaly
• the red cells are normochromic and normocytic
• Reticulocytes are reduced in number(reticulocytopenia)
Tx & Px
• The prognosis is unpredictable.
• Withdrawal of drugs sometimes leads to remission,
• Bone marrow transplantation often is curative, particularly in
nontransfused patients younger than 40 years of age.
• Transfusions sensitize patients to alloantigens, producing a high rate
of engraftment failure
Myelophthisic Anemia
• anemia is caused by extensive infitration of the marrow by tumors or other
lesions.
• It most commonly is associated with metastatic breast, lung, or prostate cancer.
• Other tumors, advanced tuberculosis, lipid storage disorders, and osteosclerosis
• . The principal manifestations include anemia and thrombocytopenia.
• the white cell series is less affected.
• Characteristically misshapen red cells, some resembling teardrops, are seen in
the peripheral blood.
• Immature granulocytic and erythrocytic precursors also may be present
(leukoerythroblastosis)
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