Classification and IDA
Classification and IDA
Classification and IDA
anemia.
Dr. Manasa GC
Assistant professor
Dept of Pathology
“The only person who never makes a mistake is a person who never does anything”
- Theodore Roosevelt
Classification
A. PATHOPHYSIOLOGIC
• I. Anaemia due to increased blood loss
– a) Acute post-haemorrhagic anaemia
– b) Chronic blood loss
• II. Anaemias due to increased red cell destruction
(Haemolytic anaemias)
– A. Extrinsic (extracorpuscular)
– B. Intrinsic (intracorpuscular) red cell abnormalities
• III. Anaemias due to impaired red cell production
– Inherited genetic defects
• Defects leading to stem cell depletion: Fanconi anemia, telomerase
defects
• Defects affecting erythroblast maturation :Thalassemia syndromes
– Nutritional deficiencies
• Deficiencies affecting DNA synthesis :B12 and folate deficiencies
• Deficiencies affecting hemoglobin synthesis: Iron deficiency anemia
– Erythropoietin deficiency: Renal failure, anemia of chronic disease
– Immune-mediated injury of progenitors Aplastic anemia, pure red cell
aplasia
– Inflammation-mediated iron sequestration Anemia of chronic disease
– Primary hematopoietic neoplasms Acute leukemia, myelodysplasia,
myeloproliferative disorders
– Space-occupying marrow lesions Metastatic neoplasms, granulomatous
disease
– Infections of red cell progenitors Parvovirus B19 infection Unknown
mechanisms Endocrine disorders, hepatocellular liver disase
B. MORPHOLOGIC
• I. Microcytic, hypochromic
– iron deficiency anaemia, sideroblastic anaemia,
Thalassaemia, anaemia of chronic disorders
• II. Normocytic, normochromic
– acute blood loss, haemolytic anaemias, bone
marrow failure, anaemia of chronic disorders
• III. Macrocytic, normochromic
– deficiency of vitamin B12 or folic acid
IRON DEFICIENCY ANAEMIA
Iron metabolism
ABSORPTION
Ferric reductase
Ferric--------------------------------->Ferrous
1. Haem
DMT1
2. Non-haem
FERRIC
medicinal
ascorbicantacids,
acid
milk,citric
pancreatic
acid,
secretions,
amino acids,
phytates,
sugars, gastric
phosphates,
secretions FERRITIN FERROPORTIN
ethylene
and diamine AND
tetra-acetic
hydrochloric
acid HEPHAESTIN
(EDTA)
acid.
and
tannates contained
in tea.`
TRANSFERRIN
Transferrin
300 - 350ug/dl Fe
Normal Transferrin - 1/3 Filled With Iron
FERRITIN AND
HAEMOSIDERIN
30%
TRANSFERRIN
BOUND IRON HEMOGLOBIN
0.5% 65%
HAEM AND NON
HAEM ENZYMES
0.5%
MYOGLOBIN
4%
Etiopathogenesis
1. Increased blood loss
2. Increased requirements
3. Inadequate dietary intake
4. Decreased intestinal absorption.
Etiology
I. INCREASED BLOOD LOSS
1. Uterine e.g. excessive menstruation in reproductive years, repeated
miscarriages, at onset of menarche, post-menopausal uterine bleeding.
• Atrophic glossitis
• Angular stomatitis
…Why?
Koilonychia in Iron def.
…Why?
Laboratory Findings
1.BLOOD PICTURE AND RED CELL INDICES.
2.BONE MARROW FINDINGS.
3.BIOCHEMICAL FINDINGS.
1.BLOOD PICTURE AND RED CELL INDICES.
i) Haemoglobin.
iv) Red cell indices:MCV (below 50 fl), MCH (below 15 pg), and
MCHC (below 20 g/dl).
ii)Erythropoiesis:
– normoblastic erythropoiesis with predominance of small
polychromatic normoblasts (micronormoblasts).
– The cytoplasmic maturation lags behind so that the late
normoblasts have pyknotic nucleus but persisting
polychromatic cytoplasm
2.BONE MARROW FINDINGS.
iii) Other cells. Myeloid, lymphoid and megakaryocytic cells are
normal in number and morphology.
ii) Total iron binding capacity (TIBC) (normal 250- 450 ug/dl)
rises to give less than 10% saturation (normal 33%).
3.BIOCHEMICAL FINDINGS.
iii) Serum ferritin (normal 30-250 ng/ml)
low indicating poor tissue iron stores.
iv) Red cell protoporphyrin (normal 20-40 ug/dl)
is very low as a result of insufficient iron supply to form haem.
v) Serum transferrin receptor protein (normal level 4-9 ug/L ).
which is normally present on developing erythroid cells and
reflects total red cell mass, is raised in iron deficiency due to
its release in circulation
Treatment
• 2 essential principles:
– correction of disorder causing the anaemia, and
– correction of iron deficiency.
• Oral iron therapy
– to correct the anaemia and to replenish the body
iron stores.
– The response to oral iron therapy is observed by
reticulocytosis which begins to appear in 3-4 days
with a peak in about 10 days.
• ii) Parenteral therapy.
– intolerant to oral iron therapy,
– The haematological response to parenteral iron
therapy is no faster than the administration of
adequate dose of oral iron but the stores are
replenished much faster.
– The adverse effects with iron dextran include
hypersensitivity or anaphylactoid reactions,
haemolysis, hypotension, circulatory collapse,
vomiting and muscle pain.