Decreased production

Hemoglobin synthesis: iron deficiency, thalassemia, anemia of chronic disease

DNA synthesis: megaloblastic anemia
Stem cell: aplastic anemia, myeloproliferative leukemia
Bone marrow infiltration: carcinoma, lymphoma
Pure red cell aplasia

Increased destruction
Blood loss
Hemolysis (intrinsic)
Membrane: hereditary spherocytosis, elliptocytosis
Hemoglobin: sickle cell, unstable hemoglobin
Glycolysis: pyruvate kinase deficiency, etc
Oxidation: glucose-6-phosphate dehydrogenase deficiency
Hemolysis (extrinsic)
Immune: warm antibody, cold antibody
Microangiopathic: thrombotic thrombocytopenic purpura, hemolytic-uremic
syndrome, mechanical cardiac valve, paravalvular leak
Infection: clostridial
Hypersplenism

Classification of anemias by mean cell volume.

Microcytic
Iron deficiency
Thalassemia
Anemia of chronic disease
Macrocytic
Megaloblastic
Vitamin B12 deficiency
Folate deficiency
Nonmegaloblastic
Myelodysplasia, chemotherapy
Liver disease
Increased reticulocytosis
Myxedema
Normocytic
Many causes

Iron Deficiency Anemia

Essentials of Diagnosis

Serum ferritin < 12 ug/L.

Caused by bleeding in adults unless
proved otherwise.
Response to iron therapy.

ANEMIA OF CHRONIC DISEASE

Common causes include chronic infection or
inflammation, cancer, and liver disease.

Red blood cell survival is modestly reduced, and

the bone marrow fails to compensate adequately
by increasing red blood cell production.
Decrease in erythropoietin is rarely an important
cause of underproduction of red cells except in
renal failure.

 The diagnosis should be suspected in patients with known

chronic diseases
Confirmed by the findings of low serum iron, low TIBC, and
normal or increased serum ferritin (or normal or increased bone
marrow iron stores).
Decreased dietary intake of folate or iron is common in these ill
patients, and many will also have ongoing gastrointestinal blood
losses.
Patients undergoing hemodialysis regularly lose both iron and
folate during dialysis.

THE THALASSEMIAS
Essentials of Diagnosis
Microcytosis out of proportion to the degree of
anemia.
Positive family history or lifelong personal history
of microcytic anemia.
Abnormal red blood cell morphology with
microcytes, acanthocytes, and target cells.
In -thalassemia, elevated levels of hemoglobin
A2 or F.

 The a-thalassemia syndromes are seen primarily in

persons from southeast Asia and China, and, less

commonly, in blacks.
Three genes are present: the patient is a
hematologically normal (silent carrier).
Two a-globin genes are present: a-thalassemia trait.
These patients are clinically normal with a mild
microcytic anemia.
Only one a-globin chain is present: hemoglobin H
disease. This is a chronic hemolytic anemia of variable
severity (thalassemia minor or intermedia).
Physical examination: pallor and splenomegaly.
Although affected individuals do not usually require
transfusions, they may do so during periods of hemolytic
exacerbation caused by infection or other stresses.
All four a-globin genes are deleted, the affected fetus is
stillborn as a result of hydrops fetalis.

 -Thalassemia primarily affects persons of Mediterranean origin

(Italian, Greek) and to a lesser extent Chinese, other Asians, and

blacks.
Homozygous for -thalassemia have thalassemia major. Affected
children are normal at birth but after 6 months, develop severe
anemia requiring transfusion. Numerous clinical problems ensue,
including growth failure, bony deformities (abnormal facial structure,
pathologic fractures), hepatosplenomegaly, and jaundice.
Hemosiderosis results in a clinical picture similar to
hemochromatosis, with heart failure, cirrhosis, and
endocrinopathies.
A milder form of -thalassemia (allowing a higher rate of globin gene
synthesis) have thalassemia intermedia: chronic hemolytic
anemia but do not require transfusions except under periods of
stress. They survive into adult life but with hepatosplenomegaly
and bony deformities.
Patients heterozygous for -thalassemia have thalassemia minor
and a clinically insignificant microcytic anemia.

HEMOLYTIC ANEMIAS
Intrinsic

Membrane defects: hereditary spherocytosis, hereditary elliptocytosis,

paroxysmal nocturnal hemoglobinuria

Glycolytic defects: pyruvate kinase deficiency, severe hypophosphatemia
Oxidation vulnerability: glucose-6-phosphate dehydrogenase deficiency,
methemoglobinemia
Hemoglobinopathies: sickle cell syndromes, unstable hemoglobins,
methemoglobinemia

Extrinsic

Immune: autoimmune, lymphoproliferative disease, drug toxicity

Microangiopathic: thrombotic thrombocytopenic purpura, hemolytic-uremic
syndrome, disseminated intravascular coagulation, valve hemolysis,
metastatic adenocarcinoma, vasculitis
Infection: plasmodium, clostridium, borrelia
Hypersplenism
Burns

Kesimpulan
Anamnesis dan fisik diagnostik merupakan kunci

utama untuk menegakan diagnosis Anemia

Lakukan anamnesis dan fisik diagnostik sesuai
dengan patofisiologi dari anemia yang terjadi
Lakukan selalu reanamnesis untuk mencari data
baru berdasar data yang sudah ada
Lakukan allo dan auto anamnesis untuk
mendapat data yang valid.
Pakailah bahasa komunikasi yang dimengerti
oleh pasien.