Microcytic Hypochromic Anemias

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Increased RDW indicates

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anisocytosis

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Microcyte

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Small erythorocyte

<80fL

Diameter <7um

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Microcytic hyochromic anemia

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< 80 FL

<32 g/dL

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Two causes of Hypochromic Anemias

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• Defect in Heme production
• Defect in Globulin production

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Defect in Heme production

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• Iron deficiency
• Iron metabolism defect
• Protoporphyrin metabolism

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Defect in globulin production

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Thalassemias: overload of either alpha or beta chains

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Microcytic Hypochromic Anemias: Classification

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• Iron Deficiency Anemia
• Sideroblastic Anemia (Lead Poisoning)
• Anemia of Chronic disease
• Thalassemias

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Sideropenic anemia

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Iron deficiency Anemia

deficient iron for hemoglobin synthesis:

• Iron metabolism
• Iron absorption and transport
• Iron recycling

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Nutritional Iron

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• Meats and veggies
• 1 mg required a day
• Diet form in ferrous or Ferric
• Stomach acid converts dietary iron to ferrous form

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Iron Absorption and transport

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• Ferrous iron is absorbed in the upper intestines
• Enters the blood stream
• Picked up by transferrin
• Iron to BM for erythropoiesis
• Excess is stored: ferritin and hemosiderin(ferric)

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Iron Absorption depends on:

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• Health of the gastric mucosa
• current iron stores
• Erythropoietic need
• Amount and type of iron available

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How much iron is absorbed

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5-10%

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Absorption increases:

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During high demand

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Where is the majority of Iron come from

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95% recycled from RBC breakdown

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Iron Recycling

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• At the end of 120 days RBC is destroyed by mononuclear phagocytes of the spleen
• Once destroyed heme is separated from globin
• Iron picked up by transferrin
• Delivered to BM, ferritin or hemosiderin

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Total body iron content in adult

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3500mg

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2/3 of iron is found in:

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2500 mg in HgB

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1/3 of iron is found:

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Present as tissue iron (90% as ferritin or hemosiderin)

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The most common cost of microcytic hypochromic anemias

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Iron Deficiency Anemia

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Pathophysiology IDA

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• Red cell cytoplasmic maturation defect
• Ineffective erythropoesis
• Increased cell division

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IDA defect in Heme synthesis

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Iron deficiency

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Causes of IDA

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• Nutritional deficiency is the most common
• Low iron intake (children/pregnant)
• Decreased Absorption
• Increased blood loss: Men- GI bleeding, Women-menorrhagia

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Causes of decreased absorption in IDA

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• Defective gastric function
• Gastrectomy
• GI malignancies
• Low transferrin

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Stage I of IDA

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Iron Depletion:

• Decrease serum ferritin
• Normal Hgb
• Normal MCV

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Stage II IDA

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Iron deficient eythropoiesis

• Decrease in serum ferritin
• Normal or decrease HgB
• Normal MCV

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Stage III IDA

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Iron deficiency Anemia

• Decrease Serum ferritin
• Decrease HgB
• DecreaesMCV

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Clinical Manifestation IDA

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• Anemia: Fatigue, shortness of breath, dizziness, pallor
• Koilonychia
• Cheilitis
• Pica

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Meilonychia

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spooning of the nails

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Cheilitis

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Inflammation of the lips

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Laboratory findiin IDA

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CBC

• Decreased- HgB, Hct, RBC, MCV(<80), MCHC (<32)
• Increased RDW

Peripheral Blood Smear

• Micro/hypo RBCs
• Ovalocytes
• Thrombocytosis

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Bone Marrow Findings in IDA

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• Decreased iron
• Micro normoblast with scanty and "shaggy blue" cytoplasm owing to asynchronism in maturation

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Bone Marrow Stains IDA

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• Prussian Blue; iron looks blue

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Iron Studies in IDA

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• Decreased: Iron, Ferritin, % Saturation
• Increased TIBC
• Increased free erythrocyte protoporphyrin

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Normal Range of Serum Iron

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• Men: 65-176 ug/dL
• Women: 50-170 ug/dL
• Newborns: 100-250 ug/dl
• Children: 50-120 ug/dL

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Normal Range of Ferritin

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• Men 12-300 ng/mL
• Women 12-150 ng/mL

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Normal Range TIBC

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240-450 ug/dL

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Normal Range Saturation

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20-50%

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Treatment of IDA

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Iron supplement

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Sideroblastic Anemia

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• Iron overload
• Abnormal iron metabolism
• iron accum. in mitochondria
• mild-moderate anemia
• inherited or acquired

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SA Inherited

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Primary

• Enzyme deficiency
• Protoporphyrin metabolism

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SA Acquired

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secondary to some other disorder

• Systemic, metabolic, toxic disorder
• Increased alcohol intake
• lead poisoning

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Lead poisoning

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interferes with iron metabolism

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Laboratory findings in SA

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CBC

• Low Hgb, Hct, RBCs
• High RDW
• Marked decreased MCV in inherited
• Normal MCV in aquired
• Low retic count

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Laboratory findings in SA Peripheral blood findings

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• Dimorphic blood picture: M/H and normocytic RBCs
• Peppenheimer bodies
• Basophilic stippling

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Bone Marrow findings SA

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• Erythroid hyperplasia
• Ringed sideroblasts
• increased iron stain

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Iron Studies SA

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• Increased: Serum iron, serum ferritin, % saturation
• N- decreased: TIBC

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Acquired SA

Lead Poisoning

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• Interfers with heme synthesis causing mild micro/hypo anemia
• Basophilic stippling on the peripheral smear

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Treatment of SA

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• Directed at underlying cause: removal of drug or toxin
• Chelation: chelate iron so it can be excreted (salts of EDTA are used)
• Repeated phhlebotomies?

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Anemia of Chronic Disease

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• Associated with infections, malignancies, autoimmune
• Iron trapped in macrophages
• Initially N/N anemia
• May develop M/H (25%)
• Absence of the ringed sideroblast in BM

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Laboratory Findings ACD CBC

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• Mild anemia
• Low HgB (8-12 g/dL)
• MCV low (61 fL)

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Lab findings ACD peripheral blood smear

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N/N-M/H RBC

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Bone Marrow ACD

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Increased Iron store

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Iron Studies ACD

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• Decreased: Serum iron, TIBC, % Saturation
• Normal- Increased: FEP, Serum ferritin

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Treatment of ACD

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• Effective control or removal of underlying condition
• Therapeutic erythoropoietin to correct anemia; iron must be admin. concurrently because body stores will remain sequestered

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Hemosiderosis

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• Excess iron absorption
• Most often asymptomatic

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Hemochromatosis

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• Ferritin deposited in major organs forming fibrotic process
• Genetic defects are present at birth, symptoms in adulthood

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Hereditary Hemochromatosis

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• Autosomal recessive
• 1/200 caucasians have the disease
• 1/8 - 1/12 are carriers
• Metabolic abnormalities
• Intestines absorb excess iron
• Asymptomatic or mimic other diseases
• Therapeutic phlebotomy or iron chelatin

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Porphyrias

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A group of inherited disorder

A block in porphyrin synthesis

Porphyrin heme precursors accumulate in tissues and large amounts are excreted in the urine and/or feces