Microcytic Hypochromic Anemias

Anemias associated with iron and heme

Anemias associated with iron and heme

impaired production=
- lack of raw materials
- iron limiting factor= inflammation
- low protoporphyrin

Causes of Iron Deficiency

- diet
- pregnancy/growing
- chronic blood loss
- impaired absorption

Stages of iron deficiency

- Storage Iron depletion
- Transport Iron Depletion
- Functional Iron Depletion

Stage I: Iron Depletion

- iron stores mobilized
- Ferritin decrease

Stage II: Iron Deficient Erythropoiesis

- no iron storage pools
- hgb falls
- serum Fe= low
- Ferritin= low
- % trasnferrin saturation= low

- transferrin= high
- sTfR high
- ZPP build up

Stage III: Iron Deficiency Anemia

Microcytic, hypochromic RBCs
- hgb <10 mg/dL
- high RDW
- reticuloytes

Koilonychia

spoon nails
- with IDA

Glossitis

smooth tongue
- IDA

Anemia of Chronic Inflammation

Impaired iron mobilization because of chronic inflammation= iron restricted

ACI associated with

- autoimmune= RA, SLE
- infection
- neoplasms

ACI Due to:

1. Impaired ferrokinetics
2. Diminished erythropoiesis
3. shortened rbc life span

ACI lab values

- Decreased TIBC (trasnferrin)
- increased serum ferritin
- increased iron in BM macrophages

Hepcidin

acute phase reactant during inflammation
- regardless of iron levels

Inflammation

- decrease in iron absorption in GI
- increased iron retention in macrophages and hepatocytes

Lactoferrin

Iron binding protein in the granules of neutrophil
- higher avidity for iron than transferrin

Bone Marrow

iron in macrophages but not in erythroblasts

Diminished erythropoiesis

- cytokines= active T cells and macrophages
- erythroid progenitor cells ignore EPO
- EPO decreased by liver

Shortened RBC life span

Impaired ferrokinetics
- not clear

ACI diagnosis

- hgb 9-11 g/dL
- reticulocytes decreased
- inflammation= leukocytosis

ACI iron studies

- Serum iron and TIBC - decreased
- % transferrin saturation - normal or low

- Ferritin - normal to increased*
- ZPP (FEP) - increased
- sTfR - normal
- BM iron= increased

Sideroblastic Anemia type

Interference of Protoporphyrin Production

Sideroblastic anemia characteristics

- Unable to make heme
· Microcytic/ Hypochromic anemia
- iron overload
- Increased ring sideroblasts in BM

Acquired Sideroblastic

- primary= refractory
- secondary= drugs, lead, chemo

Sideroblastic CBC

- dimorphic RBCs= high RDW
- increased platelets
- pappenheimer bodies and basophillic stipplings**

Sideroblastic Iron study

- Ferritin - increased
- Serum iron - increased
- % transferrin saturation - increased
- TIBC - decreased to normal
- sTfR - normal or decreased

Sideroblastic Bone Marrow

- Erythroid hyperplasia
- increased iron in mitochondria= ringed sideroblasts

Lead poisoning

- Plubism
- interferes with 6 enzymes in porphyrin synthesis

ALA dyhydratase (PBG synthase)

- bad conversion of ALA to porphobilinogen (PBG)
- ALA in urine

ferrochelatase (heme synthase)

- incorporation of iron into protoporphyrin IX
- iron and protoporphyrin in mitochondria
- FEP or ZPP in RBCs

Lead RBC changes

- shortened survival
- basophilic stipplings= Lead inhibits pyrimidine 5'-nucleotidase= bad breakdown of RNA
- FEP accumulation

ALcoholism anemias

- Iron deficient= blood loss
- Sideroblastic= Toxic to enzymes for heme synthesis
- Megaloblastic= bad folate metabolism

Porphyria

Impair production of protoporphyrin
- Enzymes in heme synthesis is missing= byproducts accumulate
- fluorescent

Hemochromatosis

iron overload
- bronze diabetes
- iron accumulates in pancreas, liver, and spleen
- treatment= therapeutic phlebotomoies

Hereditary Hemochromatosis

- increased ferritin, serum iron, % transferrin saturation (> 50%)
- normal to decreased TIBC

Hemosiderosis

Accumulation of excessive iron in macrophages
- treatment= iron-chelating drugs