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Anemias: Table Showing Types of Anemias and Causes Reticulocyte Count Microcytic Normocytic Macrocytic LOW
Anemias: Table Showing Types of Anemias and Causes Reticulocyte Count Microcytic Normocytic Macrocytic LOW
MICROCYTIC
NORMOCYTIC
MACROCYTIC
Iron deficiency
Lead poisoning
Chronic disease
Aluminium toxicity
Copper deficiency
protein malnutrition
Chronic disease
RBC aplasia (TEC
infection, drug
induced)
Malignancy
Juvenile Rheumatoid
arthritis
Endocrinopathies
Renal failure
Folate deficiency
Vit B12
Aplastic anemia
Congenital bone
Marrow Dysfunction
(Diamond-Blackfan or
Fanconi syndromes)
Drug Induced
Trisomy 21
Hypothyroidism
NORMAL
Thalassemia trait
Sideroblastic Anemia
HIGH
Thalassemia
syndromes
Hemoglobin C
disorders
Acute bleeding
Hypersplenism
Dyserythropoietic
anemia II
Anti-body mediated
hemolysis
Hypersplenism
Microangiopathy (DIC,
TTP, hemolytic uremic
syndrome)
Membranopathies
(spherocytosis,
elliptocytosis)
Enzyme disorders
(G6PD, Pyruvate
kinase)
Hemoglobinopathies
Dyserythropoietic
anemia I, III
Active hemolysis
ANEMIA
CAUSES
LAB
RESULTS
TREATMENT SYMPTOMS
IRON
DEFICIENCY
Inadequate intake of
iron (less than
2mg/day)prolonged
unsupplemeted
breast/bottle feeding
during rapid growth
phases, iron
malabsorption,
blood loss from
drug-induced GI
bleeding, heavy
menses, traumatic
hemorrhage, peptic
ulcer, cancer,
excessive blood
loss, pregnancy,
mechanical trauma.
Congenital
membranopathies,
hemoglobinopathies
, enzymopathies,
metabolic defects,
immune-mediated
destruction.
Low reticulocyte
Low MHC and
MCV (<13.5
suggests iron
deficiency- with
high RDW; <11.5
suggests
thalassemia
minor)
Low serum iron,
serum ferritin
(first to fall) or
transferrin and
elevated TIBC)
Identify cause
then give iron
replacement in
combination
with ascorbic
acid.
Iron therapy
(increased
reticulocyte
count in 2-3
days and
increased
hematocrit in 14 weeks)
Iron stores
repleted within 3
months of
therapy.
Blood
transfusion
Supplements
Diet
maintenance
HEMOLYTIC
RBC APLASIA
Acquired- infection
(parvovirus in
children:infects
precursors of RBC
hence rapid
turnover, EBV, CMV,
HIV; transient
Reticulocyte
count elevated
(shows
compensation),
CRC >1.5increased RBC
production as a
result of
hemolysis or
blood loss
Plasma
aspartate
aminotransferas
e and lactate
dehydrogenase
elevated,
Coombs test,
Osmotic fragility
test (hereditary
sperocytosis or
ABO
incompatibility),
G6PD assay,
Heinz body
(precipitated Hb
with RBCs)
Variable cell size,
low reticulocyte
count, variable
platelet and
WBC count,
bone marrow
aspiration (bone
Dyspnea on
exertion,
fatigue,
listlessness,
increased
cardiac output,
tachycardia,
nails that are
coarsely rigid,
koilonchyia,
sore, red
burning
tongue, sore,
dry skin at
corners of
mouth
SICKLE CELL
erythroblastopenia
of childhood: 6m to
4 yrs with normal or
slightly low MCV
and low reticulocyte
count; Radiation,
drug and chemical
exposure)
Congenital
(Fanconipancytopenia before
age 10, causes
chromosomal
fragility; Diamondblackfan oski
syndrome)
Genetic
marrow
dysfunction,
neoplasm or
infection)
Newborn screen
with Hb
electrophoresis
Pneumococcal,
meningitis, and
influenza
vaccine,
prophylaxis of
penicillin,
supplement with
folic acid and
hydroxyurea.
Fever, vasoocclusive
crisis, acute
chest
syndrome,
splenic
sequestration,
aplastic crisis
REFERENCE:
Bessman, J. D., Gilmer Jr, P. R., & Gardner, F. H. (1983). Improved classification
of anemias by MCV and RDW. American journal of clinical pathology, 80(3), 322326.
Dallman, P. R., Yip, R., & Oski, F. A. (1993). Iron deficiency and related nutritional
anemias. Hematology of infancy and childhood, 4, 413-450.
Petz, L. D., & Garratty, G. (1980). Acquired immune hemolytic anemias. Churchill
Livingstone.
Herbert, V. (1959). The megaloblastic anemias (Vol. 18). Grune & Stratton.