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    ACD, Lead Poisoning, Sideroblastic

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    Aftab Khalil
    This document provides information about anemia of chronic disease (ACD): - ACD is the second most common anemia worldwide and most frequent in hospitalized/chronically ill patients. It is caused by impaired red blood cell production associated with chronic diseases that produce systemic inflammation. - The pathogenesis of ACD involves inflammatory processes that increase hepcidin production, which decreases iron absorption and availability for erythropoiesis. This traps iron in storage cells and contributes to the anemia. - Therapy for ACD should be directed at treating the underlying chronic disease. Most cases do not require specific treatment as the anemia is self-limited. Transfusions should generally be avoided.

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    ACD, Lead Poisoning, Sideroblastic

    Uploaded by

    Aftab Khalil
    19 views28 pages
    This document provides information about anemia of chronic disease (ACD): - ACD is the second most common anemia worldwide and most frequent in hospitalized/chronically ill patients. It is caused by impaired red blood cell production associated with chronic diseases that produce systemic inflammation. - The pathogenesis of ACD involves inflammatory processes that increase hepcidin production, which decreases iron absorption and availability for erythropoiesis. This traps iron in storage cells and contributes to the anemia. - Therapy for ACD should be directed at treating the underlying chronic disease. Most cases do not require specific treatment as the anemia is self-limited. Transfusions should generally be avoided.

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    Lead poisoning

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    This document provides information about anemia of chronic disease (ACD): - ACD is the second most common anemia worldwide and most frequent in hospitalized/chronically ill patients. It is caused by impaired red blood cell production associated with chronic diseases that produce systemic inflammation. - The pathogenesis of ACD involves inflammatory processes that increase hepcidin production, which decreases iron absorption and availability for erythropoiesis. This traps iron in storage cells and contributes to the anemia. - Therapy for ACD should be directed at treating the underlying chronic disease. Most cases do not require specific treatment as the anemia is self-limited. Transfusions should generally be avoided.

    Copyright:

    © All Rights Reserved
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    Download as pptx, pdf, or txt
    19 views28 pages

    ACD, Lead Poisoning, Sideroblastic

    Uploaded by

    Aftab Khalil
    This document provides information about anemia of chronic disease (ACD): - ACD is the second most common anemia worldwide and most frequent in hospitalized/chronically ill patients. It is caused by impaired red blood cell production associated with chronic diseases that produce systemic inflammation. - The pathogenesis of ACD involves inflammatory processes that increase hepcidin production, which decreases iron absorption and availability for erythropoiesis. This traps iron in storage cells and contributes to the anemia. - Therapy for ACD should be directed at treating the underlying chronic disease. Most cases do not require specific treatment as the anemia is self-limited. Transfusions should generally be avoided.

    Copyright:

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    of 28

    Anemia of chronic disease

    (ACD)
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    CONTENTS

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    Introduction

    Impaired red cell production assoicated with chronic


    diseases that produce systemic inflammaiton
    Second most common anemia worldwide
    Most frequent anemia in hospitalized and chronically ill
    patients
    Causes
    Infectious Inflammatory
    Tuberculosis Rheumatoid arthritis
    Endocarditis Systemic lupus
    HIV Vasculitis

    Malignant Miscelneous
    Metastatic cancers Chronic kidney disease
    Lymphomas Congestive heart failure
    Myeloma Advanced atherosclerosis
    Anemia of critical illness
    Pathogenesis of ACD
    Mechanisma of ACD

    Inflammatroy proccesses in iron homeostasis


    Systemic inflammation → ↑ circulation cytokines, interleukin 1 (IL1), interleukin 6 (IL6),
    tumor necrosis factor α (TNF α), interferon beta (IFN beta), interferon gamma(IFN
    gamma)
    • ↑ hepcidin secretion by liveer → ↓ iron absorption from gastrointestinal (GI) tract, ↓
    iron sequestraion in reticuloendothelial system → ↓ iron available for erythropiesis
    • ↓ secretion of erythropoietin
    • Direct inhibition of erythropoiesis
    • ↓ erythrocyte lifespan
    Mechanisma of ACD
    Hepcidin

    Acute phase protein


    • Produced in liver
    • Has anti-bacterial properties
    Affects iron metabolism
    • Inhibits iron transport
    • Binds to ferroportin in enterocytes, macrophages
    Iron trapped in cells as ferritin
    Contributes to anemia of chronic disease
    Key finding ACD: ↑ ferritin
    Diagnosis

    Serum iron is low


    • Thought to be protective
    • Bacteria may use iron for growth/metabolism
    Ferritin is usually increased
    • Iron trapped in storage from
    • Ferritin is acute phase reactant
    • Increase may not represent increased storage iron
    Transferrin (TIBC) is usually decreased
    • Transferrin rises when total body iron low
    %saturation usually normal
    1. Therapy should be directed to underlying disease.

    2. Most patients have self-limited anemia that needs no specific therapy.

    3. Correct co-existent Fe deficiency and other disorders

    4. Transfusions should be avoided


    Lead Poisoning
    Introduction

    Exoposure to lead:
    • Adults: inhalation from industrial work (battery factory)
    • Children: Eating lead paint (old house)
    Inhibits heme sysnthesis via 2 enzymes in RBCs
    • Delta-aminolevulinic acid (δ-ALA) dehydratase
    • Ferrochelatase
    ↓ heme synthesis → microcytic, hypochromic anemia
    Heme Synthesis
    Symptoms

    Abdomial pain (“lead colic”)


    Constipation
    Headache
    “Lead lines”
    • Blue pigments a gum - tooth line
    • Caused by reaction of lead with dental plaque
    Nephropathy
    • Injury to proximal tubules (Fancol-type syndrome)
    • Glucose, amino acids, and phospate wasting
    Neuropathy
    • Common sysmptom: Drop wrist and foot
    Symptoms

    Children may have prominent neurologic effects


    • Behavioral issues
    • Developmental delay
    • Failure to reach milestone (i.e. language)
    Many states screen children with lead level testing
    • Usually at 1-2 years of age
    Signs and Symptoms
    Diagnosis

    Plasma lead level


    ↑ delta - aminolevulinic acid (δ-ALA)
    ↑ erythrocyte protoporphyrin
    Diagnosis

    Blood smear: basophilic stippling


    • Blue granules in cytoplasm of red cells
    • Lead inhibits pyrimidine 5’ nucleotidase
    • Normally digests pyrimidines in ribosomes/RNA
    • Leads to accumulation of pyrimidines/RNA in RBCs
    Also seen in thalassemia, other anemias
    Treatment

    Removal of exposure to lead


    Chelation therapy
    • Dimercaprol (2, 3-dimercapto-1-propanol)
    • Calcium disodium EDTA (ethylenediaminitetraacetate)
    • DMSA (2, 3-dimercaptosuccinic acid; succimer)
    Sideroblastic anemia
    Introduction

    Sideroblasts:
    • Found in normal bone marrow
    • Nucleated red cell precursors
    • Contain granules with non-heme iron
    • 1-4 siderotic granules in cytoplasm Correlate with TIBC saturation
    SIderoblastic anemia
    • Usually microcytic anemia
    • Sideroblast in peripheral blood
    • ≥ 5 granules, coarse, form rings, reflect accumulation of mitochondrial ferritin
    Pathophysiology

    Failure to make protoporphyrin


    Iron cannot bind → heme
    Iron accumulation in mitochondria
    Pathophysiology

    Usually secondary to a toxin


    Alcohol (mitochondrial poison
    Vitamin B6 deficiency (isoniazid)
    Lead poisoning
    Pathophysiology

    X-linked sideroblastic anemia


    • Rare, inherited deficiency of ALA synthase
    • Most common hereditary sideroblastic anemia
    Often responds to treatment with vitamin B6
    A
    THANK YOU

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