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Disease Iron-Deficiency Anemia of Chronic Aplastic Anemia Megaloblastic Anemia

Anemia Disease
Etiology 1. Chronic blood 1. Chronic 1. Idiopathic (50% 1. Folate deficiency
loss inflammation 70%) - Celiac disease
- PUD - Autoimmune - Alcoholism
- Hookworm diseases 2. Drugs - Drug inhibition
(Ancyclostoma - (Rheumatoid - Pregnancy / lactation
Duodenale, arthritis) 3. Chemical agents
Necator - Infections 2. Vitamin B12 deficiency
Americanus) (Tuberculosis (TB)) 4. Infection (EBV, - Pernicious anemia
- Polyps / colorectal - Crohn disease CMV, HCV) - Gastritis
cancer - Gastric bypass
- Menorrhagia 2. Alcoholism 5. Whole body - Fish tapeworm
- Pregnancy ionizing radiation - Malnutrition
3. Malignancy - Pregnancy, lactation
2. Decreased intake 6. Pregnancy

3. Decreased 7. Thymoma
absorption
- Celiac sprue 8. Paroxysmal
- Gastric surgery nocturnal
- Atrophic gastritis hemoglobinuria
- Achlorhydria

4. Intravascular
Hemolysis
- Microangiopathic
hemolytic anemia
Paroxysmal
nocturnal
hemoglobinuria

Decreased Chronic disease Immunologic Megaloblastic states result


synthesis of heme such as chronic alterations occur in from defective DNA
(iron + inflammation the myeloid stem synthesis. RNA synthesis
protoporphyrin) releases (progenitor) cells, continues, resulting in a
leads to a inflammatory causing T-cell large cell with a large
decreased cytokines. activation and release nucleus. All cell lines have
synthesis of Hb of cytokines that dyspoiesis, in which
Inflammatory suppress or destroy cytoplasmic maturity is
cytokines shorten the myeloid stem greater than nuclear
RBC survival and cells, that results in a maturity; this dyspoiesis
Macrophage- loss of blood cell produces megaloblasts in the
derived cytokines precursors, marrow before they appear
(eg, IL-1-beta, hypoplasia or aplasia in the peripheral blood.
tumor necrosis of bone marrow, and Dyspoiesis results in
factor-alpha, cytopenias in two or intramedullary cell death,
interferon-beta) more cell lines (RBCs, making erythropoiesis
contribute to WBCs, and/or ineffective. Because
hepatic synthesis platelets. dyspoiesis affects all cell
of acute phase lines, reticulocytopenia and,
reactants during later stages
e.g. Hepcidin. leukopenia and
thrombocytopenia develop.
Hepcidin causes Large, oval RBCs (macro-
reticuloendothelial ovalocytes) enter the
cells to retain iron circulation.
from senescent Hypersegmentation of
RBCs, polymorphonuclear
sequestering iron neutrophils is common.
in storage sites
making iron
unavailable for Hb
synthesis. It limits
iron transfer from
macrophages to
erythroid
precursors,
inhibits iron
absorption and
recycling. When
the erythroid
precursors dont
have iron, there is
decreased heme
synthesis.

Hepcidin can also


suppress
erythropoietin
(EPO) production
and decrease bone
marrows
responsiveness to
EPO, decreasing its
drive to produce
more cells.
Decreased
available iron
leads to low heme
synthesis.

Hemoglobin
synthesis become
low resulting in
anemia.

Clinical Findings 1. Fatigue, loss of 1. Fever, due to 1. GIT Manifestations


stamina, shortness infection associated (diarrhea, glossitis, and
of breath, with neutropenia anorexia)
weakness, 2. Petechiae, 2. Neurologic manifestations
dizziness, and ecchymosis, and (peripheral neuropathy, gait
pallor bleeding from the instability, subacute
gums, into the combined degeneration, and
2. Chronic iron conjunctivae, or dementia)
deficiency other tissues, due to
- Esophageal web thrombocytopenia
(Plummer-Vinson 3. Weakness and
syndrome) fatigue, due to
- Achlorhydria anemia
- Glossitis and 4. Agranulocytosis
angular cheilosis commonly causes
- Spoon / concave life-threatening
nails (koilonychias) infections.
5. Splenomegaly is
2. Pallor of the absent unless
conjunctivae and induced by
palmar skin creases transfusion
hemosiderosis.
3. Craving (pica) for
ice
Clinical tests Serum test Serum test Peripheral smear Peripheral smear
Peripheral smear Peripheral Smear Bone Marrow Biopsy Bone Marrow Biopsy
Bone marrow Schilling Test
examination

RBC Morphology - From normocytic Normocytic to Normocytic - Megaloblasts with high RBC
normochromic Microcytic (in hypoplastic distribution width (RDW) is
anemia to setting of high
microcytic Rheumatoid - Macro-ovalocytosis,
hypochromic RBCs Arthritis and Anisocytosis, and
Crohns disease) Poikilocytosis
- Increased red cell
distribution width
(RDW) -
anisopoikilocytosis
Laboratory findings - Decreased serum - Decreased serum - Pancytopenia - Decreased serum vitamin
iron iron (anemia, B12 and folic acid
- Decreased iron % - Decreased iron % thrombocytopenia, - Increased serum
saturation saturation and leukopenia) homocysteine and
- Decreased serum -Reticulocytopenia methylmalonic acid (95%
ferritin cases)
- Increased TIBC - Increased or - Hypocellular bone - Howell-Jolly bodies
- Increased serum normal serum marrow replaced by (residual fragments of the
free erythrocyte ferritin large adipose cells nucleus)
protoporphyrin - Decreased serum with scattered - Reticulocytopenia
(FEP) transferrin, lymphocytes in - Hypersegmented
typically low to between from bone neutrophils
normal marrow examination - Pancytopenia
- Decreased TIBC (Neutropenia,
- Increased serum thrombocytopenia)
free erythrocyte - Oval macrocytes
protoporphyrin - Megaloblastic nucleated
(FEP) cell with primitive open
- Low reticulocyte chromatin pattern

Treatment Supplemental iron 1. Treat underlying 1. Cessation of Treatment of vitamin B12


given orally cause causative drugs, if it is deficiency
(Ferrous sulfate) 2. Recombinant responsible - Intramuscular injections of
erythropoietin 2. Hematopoietic vitamin B12
(EPO) stem cell
3. Iron transplantation Treatment of folic acid
supplements (to 2.Immunosuppressive deficiency
ensure adequate therapy - Oral administration of
response to EPO) monoglutamic folic acid
4. Hepcidin
antagonists