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    افتراضي الانيميا الانواع والاسباب وطرق المعالجة

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    Anemia, General Principles
    • Definition → Hb < 13.5 g/dL (Hct < 40) in men or Hb < 12 g/dL (Hct < 37) in women
    • Most useful classification of anemia (based on MCV or mean corpuscular volume):
    1. Microcytic (MCV < 80) → Iron-deficiency anemia, sideroblastic anemia, anemia of chronic disease, lead poisoning, thalassemia
    2. Normocytic (MCV 80-100) → aplastic anemia, anemia of chronic disease, myelofibrosis/bone marrow infiltration, chronic renal failure, hemolytic anemia,
    early stages of iron-deficiency anemia, hemorrhage
    3. Macrocytic (MCV > 100) → megaloblastic anemia (vitamin B12 and/or folate deficiency; drug-induced), liver disease, myelodysplasia, reticulocytosis
    • Best initial diagnostic tests : CBC with RBC indices (e.g. MCV), reticulocyte count, blood smear

    1-Microcytic Anemia

    Iron-deficiency Anemia
    • Most common cause of anemia
    • Females > Males
    • Etiology:
    1. Chronic blood loss à most common cause; e.g. GI cancer, menorrhagia
    2. ↓ dietary intake/malabsorption e.g. celiac disease, post-gastrectomy, cow’s milk diet in infants.
    3. ↑ requirements → e.g. pregnancy, growth spurt
    4. Chronic intravascular hemolysis → hemoglobinuria, hemosiderinuria
    • Clinical features specific for iron-deficiency anemia
    1. brittle nails/koilonychia (spoon-shaped nails)
    2. glossitis/angular cheilitis
    3. pica (craving for non-nutritive substances)
    4. dysphagia (Plummer-Vinson syndrome)
    • Initial lab results (CBC, reticulocyte count, etc.) → low Hb and/or Hct, low MCV, ↑ RDW (red blood cell distribution width), ↓ reticulocyte count, possible thrombocytosis
    • Blood smear → hypochromic, microcytic RBCs poikilocytosis (abnormal shapes)
    • Best next step → perform iron studies:
    1. ↓ serum ferritin → most specific laboratory test; lacks sensitivity (falsely elevated in inflammatory conditions, liver disease and/or malignancies)
    2. ↓ serum iron
    3. ↑ TIBC (total iron binding capacity)
    4. ↓ transferrin saturation (serum iron/TIBC ratio, expressed as %)
    • Most accurate diagnostic test à bone marrow biopsy + Prussian blue stain

    Anemia of Chronic Disease
    • Anemia that accompanies any chronic inflammatory
    and/or malignant condition
    • Pathophysiology →
    1. ↓ sensitivity to erythropoietin
    2. Impaired utilization of stored iron due to ↑ levels of TNF-خ± and IL-6
    • Clinical features : symptoms/signs of anemia + that of the underlying disease
    • Initial lab results : low Hb and/or Hct, low or normal MCV, ↓ reticulocyte count, normal RDW
    • Blood smear → hypochromic, microcytic or normochromic, normocytic RBCs

    • Best next step → perform iron studies:
    1. ↓ serum iron
    2. ↓ TIBC
    3. Normal transferring saturation
    4. Normal or ↑ serum ferritin
    • Bone marrow biopsy + Prussian blue stain → ↑stainable iron

    Thalassemia
    • A group of hereditary (autosomal recessive) disorders characterized by decreased to absent globin chain (خ± and/or خ²) synthesis → hypochromic, microcytic anemia
    • خ±-thalassemia (common in Asians and African-Americans)

    • خ²-thalassemia (common in people of Mediterranean origin; also seen in Asians and/or African-Americans) unbalanced production of خ±-chains leads to ineffective
    erythropoiesis, chronic hemolysis and extramedullary hematopoiesis


    • Best initial step → perform iron studies to rule out iron-deficiency (should be normal in both forms of thalassemia)
    • Best next and the most sensitive test is hemoglobin electrophoresis:
    1. خ±-thalassemia : normal levels of HbA2 and HbF
    2. خ²-thalassemia minor : ↑ HbA2 ± ↑ HbF
    3. خ²-thalassemia major : ↑ HbA2 and HbF
    • Most accurate diagnostic test → Genetic analysis

    2-Normocytic Anemia

    Hemolytic Anemia, General Principles
    • Anemia resulting from ↑ premature destruction of RBCs
    • May be classified according to:
    1. time-course → acute vs. chronic
    2. site of hemolysis → intravascular vs. extravascular
    3. causative factor : intrinsic vs. extrinsic (intracorpuscular vs. extracorpuscular)
    • Clinical features suggestive of hemolysis → acute onset, jaundice with dark urine, gallstone disease, chronic leg ulcers, hepatosplenomegaly + symptoms/signs of anemia
    • Lab findings → ↓ Hb, ↓ Hct, normal MCV (possible ↑ MCV due to reticulocytosis), ↑ reticulocyte count, ↑ serum LDH, ↑ serum indirect bilirubin, ↓ serum haptoglobin (binds free hemoglobin; more prominent with intravascular hemolysis)
    • Lab findings consistent with intravascular hemolysis :
    ↓ haptoglobin, presence of serum free hemoglobin, hemoglobinuria, possible hemosiderinuria

    Hereditary Spherocytosis
    • Most common hereditary hemolytic anemia
    • Autosomal dominant (more common, less severe) or autosomal recessive inheritance
    • Etiology → spectrin deficiency resulting from various genetic defects, with mutations involving the ankyrin gene being most common
    • Pathophysiology: RBC membrane defects/instability →assumption of a spherical shape → ↓ elasticity → inability to traverse splenic cords → extravascular (principally splenic) hemolysis
    • Clinical features → family history + triad of mild/moderate anemia + splenomegaly + jaundice/gallstone disease (e.g. biliary colic, acute cholecystitis)
    • Aplastic crisis → worsening of anemia characterized by ↓ reticulocyte count, secondary to parvovirus B19 infection and/or concurrent folate deficiency
    • Lab findings → consistent with extravascular hemolysis (see above) + ↑ MCHC (mean corpuscular hemoglobin concentration)
    • Blood smear → normochromic, normocytic RBCs + presence of spherocytes (small, hyperchromic RBCs with loss of normal central pallor)
    • Most accurate diagnostic test → osmotic fragility test (RBC susceptibility to hemolysis when placed in hypotonic solutions)

    Sickle Cell Anemia
    • Autosomal recessive chronic hemolytic anemia resulting from substitution of valine for glutamic acid at position 6 of the خ²-globin gene → HbS
    • Most common in people of African descent .
    • Both sickle cell trait and anemia protect against falciparum malaria
    • Pathophysiology: deoxygentated HbS tends to polymerize forming rigid crystals → “sickling” of RBCs (irreversible with time) + membrane damage →abnormally sticky and non-deformable RBCs → principally extravascular hemolysis + vaso-occlusion of
    small arterioles and/or larger arteries
    • Clinical manifestations:
    1. chronic hemolytic anemia
    2. jaundice
    3. bilirubin gallstones/acute cholecystitis
    4.growth and/or developmental delay
    5. renal papillary necrosis → hematuria and/or acute renal failure
    6. acute painful crisis (vaso-occlusive crisis):
    7. acute chest syndrome:
    8. aplastic crisis: • secondary to Parvovirus B19 infection
    9. splenic sequestration crisis.
    • Lab findings → ↓ Hb, ↓ Hct, ↑ reticulocyte count (unless in aplastic crisis), ↑ indirect bilirubin, ↑ LDH, ↑ WBC count (in the absence of infection) with eosinophilia
    • Blood smear → normochromic, normocytic RBCs, “sickled” RBCs, target cells.
    • Urinalysis → microscopic hematuria
    • Best initial (screening) test → sickle solubility test (cannot differentiate between trait and disease)
    • Most accurate diagnostic test → Hb electrophoresis with HbS > 80%

    Glucose-6-Phosphate Dehydrogenase (G6PD) Deficiency
    • X-linked recessive
    • Most common in African-Americans
    • G6PD deficiency protects against malaria
    • Pathophysiology: G6PD deficiency → ↓ NADPH →↓ reduced glutathione →susceptibility to oxidant stress → acute intravascular hemolysis
    • Oxidant stress → infections (e.g. pneumonia, hepatitis, typhoid fever), drugs (e.g. primaquine, sulfonamides, nitrofurantoin, dapsone, quinidine, aspirin) and/or fava beans (“favism” →limited to patients with the Mediterranean variant of G6PD deficiency)
    • Clinical features →
    sudden onset of fever/chills, backache, weakness, dizziness, jaundice and/or dark urine within several days of oxidant exposure
    • Lab findings → suggestive of intravascular hemolysis (see above)
    • Blood Smear → normochromic, normocytic RBCs with Heinz bodies (denatured, oxidized Hb) + bite cells (remnants of RBCs after removal of Heinz bodies by splenic macrophages) ± spherocytes
    • Most accurate diagnostic test → G6PD assay (not performed until acute episode subsides → ↑ reticulocyte count → false-positive results)

    Immunohemolytic Anemia, Warm-Antibody Type
    • Autoimmune-mediated hemolytic anemia secondary to production of “warm” antibodies of the IgG type (react at body temperature)
    • Most commonly seen in adult females
    • Usually idiopathic
    • Secondary causes include :
    1. Drugs:
    • خ±-methyldopa .
    • penicillins/cephalosporins .
    • quinidine, sulfonamides/other sulfa derivatives .
    2. NHL (non-Hodgkin lymphoma), Hodgkin’s lymphoma
    3. CLL (chronic lymphocytic leukemia)
    4. SLE/other collagen-vascular disorders
    5. Viral infection (usually transient; predominantly in children)
    • Pathophysiology: IgG and/or complement coating of RBCs → Fc fragment and/or
    complement-mediated adherence to splenic macrophages → extravascular (principally splenic) hemolysis } intravascular hemolysis (from complement activation)
    • Clinical features :
    1. Mild/moderate anemia + splenomegaly and/or
    2. Sudden onset of fever/chills, dark urine, weakness, tachycardia, dizziness/syncope, acute CHF à shock (with massive intravascular hemolysis)
    • Lab findings → consistent with hemolysis .
    • Blood Smear → normochromic, normocytic RBCs + spherocytes
    • Most accurate diagnostic test → direct Coombs’ test showing reaction with anti- IgG ± anti-C3 antibodies:

    Immunohemolytic Anemia, Cold-Antibody Type (Cold Agglutinin Disease)
    • Autoimmune-mediated hemolytic anemia secondary to production of “cold” antibodies
    of the IgM type (react at temperatures < 37oC)
    • Classification:
    1. Chronic → idiopathic, CLL, lymphoma.
    2. Acute/transient → Mycoplasma pneumoniae, infectious mononucleosis, adenovirus
    • Pathophysiology: IgM coating of RBCs + activation of complement cascade → agglutination of RBCs ± hemolysis (usually intravascular and/or intra-hepatic)
    • Clinical features : acrocyanosis (ears, nose, fingers) on cold exposure that disappears with re-warming ±symptoms/signs of anemia
    • Lab findings → consistent with hemolysis .
    • Blood Smear → normochromic normocytic RBCs , agglutination
    • Most accurate diagnostic test → direct Coombs’ test showing reaction with anti-C3 antibodies

    Aplastic Anemia
    • Pancytopenia associated with bone marrow hypocellularity secondary to failure of hematopoietic stem cells
    • Etiology
    1. Idiopathic (most common)
    2. Radiation
    3. Drug- and/or chemical-related.
    4. Infectious hepatitis virus (so called non-A, non-B, non-C), HIV, infectious mononucleosis, parvovirus B19
    5. Congenital (Fanconi’s anemia)
    • Clinical features → symptoms/signs of thrombocytopenia (e.g. easy bruising, nosebleeds,
    petechiae, etc.) + anemia (e.g. pallor, weakness, dyspnea, etc.) ± neutropenia (e.g. ↑ fever, pharyngitis, sepsis, etc.) in the absence of systemic manifestation,
    splenomegaly/lymphadenopathy and/or weight loss
    • Lab findings :↓ Hb (and Hct), ↓ reticulocyte count, ↓ WBC count, ↓ platelet count
    • Most accurate diagnostic test is bone marrow biopsy showing ↓ and/or absent
    hematopoietic precursors with marked fatty replacement .

    3-Macrocytic Anemia
    Megaloblastic Anemia
    • Pathophysiology: Vitamin B12 and/or folate deficiency → ↓ DNA synthesis → arrested nuclear maturation + normal cytoplasmic maturation → large, nucleated RBC
    precursors (megaloblasts)
    • Etiology:
    1. Vitamin B12 deficiency → pernicious anemia (most common), total gastrectomy, atrophic gastritis, malabsorption syndromes (e.g. Crohn’s disease,
    celiac disease, chronic pancreatitis, bacterial overgrowth), resection of the ileum, fish tapeworm (D. latum), strict vegetarianism.
    2. Folate deficiency → ↓ dietary intake (most common; seen in alcoholism, poverty and/or infancy), ↑ requirements (e.g. pregnancy, rapid growth, chronic
    hemolysis, hemodialysis, psoriasis, dermatitis), malabsorption syndromes, drug/chemical induced (e.g. phenytoin, barbiturates, methotrexate, trimethoprim, pyrimethamine, alcohol)
    • Clinical features (common to both forms of disease) : symptoms/signs of anemia, mild jaundice, atrophic glossitis, diarrhea, abdominal pain, ± symptoms/signs of thrombocytopenia
    • Clinical features suggestive of vitamin B12 deficiency → neurologic manifestations:
    1. peripheral neuropathy .
    2. Subacute degeneration of spinal tracts.
    • Lab findings :↓ Hb, ↓ Hct, ↓ reticulocyte count, ↑ MCV, ↓ WBC and/or platelet count, ↑ LDH, ↑ indirect bilirubin
    • Blood smear : macrocytic RBCs (oval macrocytes), hypersegmented neutrophils (>50% with 4 lobes, or >5% with 5 lobes, or at least one with 6 lobes)
    • Bone marrow biopsy → hypercellularity + prominent arrest in nuclear maturation
    • Most accurate diagnostic test is serum vitamin B12 and RBC folate levels, respectively
    • Best next step in confirmed B12 deficiency → anti-intrinsic factor and/or anti-parietal cell autoantibodies (to confirm the diagnosis of pernicious anemia)
    • Best next step if antibodies negative →Schilling test

    Myeloid Malignancies
    Acute Myelogenous Leukemia (AML)
    • Hematopoietic stem cell disorder characterized by clonal proliferation of immature myeloid precursors (myeloblasts) secondary to loss of ability to differentiate à bone marrow failure + peripheral myeloblasts
    • Risk factors → benzene, petroleum products, radiation, post-chemotherapy, Down syndrome, ataxiatelangiectasia.
    • Incidence increases with age

    • FAB classification of AML:
    M0: minimally differentiated
    M1: myeloblastic without maturation
    M2: myeloblastic with maturation
    M3: promyelocytic .
    M4: myelomonocytic .
    M5: monocytic .
    M6: erythroleukemia .
    M7: megakaryoblastic .
    • Clinical features : symptoms/signs of anemia, thrombocytopenia and/or neutropenia, anorexia, weight loss, fever, hepatosplenomegaly, lymphadenopathy±symptoms/signs of tissue infiltration and/or mass lesions
    • Symptoms/signs of leucostasis if ↑↑WBC count →headache, dyspnea, visual disturbances, retinal and/or CNS hemorrhage
    • Lab findings : normochromic, normocytic anemia with ↓ reticulocyte count, ↓ platelet count, ↓, normal or ↑ WBC count, circulating blasts, ↑ LDH, ↑ uric acid
    • Most accurate diagnostic test (for leukemia in general) → bone marrow biopsy showing > 20% blast forms
    • Most accurate diagnostic test to differentiate among AML and ALL and between subtypes of AML → Cytogenetic/molecular and immunophenotypic analysis

    Chronic Myelogenous Leukemia
    • Myeloproliferative disorder characterized by clonal proliferation of a myeloid stem cell harboring the pathognomic t(9;22) trans******** (Philadelphia chromosome)
    • Risk factors : high-dose radiation (e.g. atomic bomb survivor)
    • Incidence increases with age
    • Pathophysiology: t(9;22) → BCR/ABL fusion protein → transformation of myeloid stem cells .
    • Clinical features → asymptomatic (e.g. detected on routine CBC) to night sweats, fatigue, weakness, fever, weight loss, splenomegaly , hepatomegaly, ±symptoms/signs of thrombocytopenia and/or neutropenia (uncommon), ± “leucostasis”
    • Lab findings → ↑↑ WBC count with prominent left shift, blasts < 5%, ↑ basophils and/or eosinophils, ↑ platelet count, normochromic normocytic anemia, ↑ vitamin B12
    level, ↓ LAP activity (differentiates from other myeloproliferative disorders and/or
    reactive leukocytosis (“leukemoid reaction”)
    • Best initial diagnostic test in suspected CML à LAP score
    • Bone marrow biopsy : ↑ cellularity (predominantly myeloid and megakaryocytic), ↑ marrow basophils and/or eosinophils, ↑ fibrosis
    • Most accurate diagnostic test (mandatory for diagnosis) is demonstration of Philadelphia chromosome (e.g. PCR, FISH, etc.)
    Lymphoid Malignancies
    Acute Lymphoblastic Leukemia (ALL)
    • Most common leukemia in children
    • Boys > girls
    • Whites > African-Americans
    • 85% of cases are of B-cell origin
    • Risk factors à radiation, benzene, genetic syndromes (e.g. Down syndrome, Bloom syndrome, etc.)
    • Clinical features → symptoms/signs of anemia, thrombocytopenia and/or neutropenia,
    ↑ temperature, severe bone pain, arthralgias, lymphadenopathy, splenomegaly ±
    hepatomegaly, mediastinal mass (especially with T-cell ALL) ± respiratory distress, possible CNS disease, testicular enlargement and/or tissue infiltration
    • Lab findings à pancytopenia with ↓ reticulocyte count, circulating lymphoblasts, ↑ LDH, ↑ uric acid
    • Most accurate diagnostic test in general → bore marrow biopsy showing > 20% marrow blasts
    • Most accurate diagnostic test to differentiate between AML and ALL and/or different
    forms of ALL → immunophenotypic and/or cytogenetic analysis

    Chronic Lymphocytic Leukemia.
    • Clonal proliferation of mature B lymphocytes
    • Most common form of leukemia
    • Age > 50
    • Males > Females
    • Clinical features → asymptomatic (most common; e.g. detected on routine CBC, etc.)
    to fatigue, splenomegaly, lymphadenopathy, ↑ risk of infections, ± symptoms/signs of anemia and/or thrombocytopenia
    • Complications à autoimmune hemolytic anemia, immune-mediated thrombocytopenia, hypogammaglobulinemia, Richter syndrome (transformation to high-grade large-cell lymphoma)
    • Lab findings → ↑ WBC count with absolute lymphocytosis (lymphocyte count > 5000/خ¼L) ± ↓ RBC and/or platelet counts.
    • Blood smear → small, mature lymphocytes + “smudge” cells
    • Bone marrow biopsy > 30% lymphocytes
    • Most accurate diagnostic test →flow-cytometry

    Platelet/Coagulation Disorders

    Idiopathic Thrombocytopenic Purpura (ITP)
    • Most common cause of thrombocytopenia
    • Pathophysiology: anti-platelet IgG production à coating of platelets → destruction by splenic macrophages
    • ITP is a diagnosis of exclusion
    • ITP is frequently associated with SLE, HIV infection and hematologic malignancies, e.g. CLL .
    • Females > Males; 20-40 years of age
    • Clinical features → epistaxis, menorrhagia, easy bruising, petechiae, purpura, ecchymoses, possible hematuria and/or GI bleeding (so called “platelet-type” bleeding); intracranial hemorrhages in severe cases; NO splenomegaly
    • Best initial diagnostic test → CBC showing ↓ platelets with normal RBC and WBC counts
    • Other Lab findings → normal PT, PTT, blood smear and serum creatinine; ↑ bleeding time.
    • Next step → exclusion of secondary/known causes of thrombocytopenia:
    1. Drug-induced (e.g. quinidine, rifampin, heparin, alcohol)
    2. SLE/connective tissue disorders
    3. HIV infection
    • Bone marrow examination (for definite diagnosis) indicated:
    1. If age > 60
    2. Before splenectomy
    • Bone marrow findings : ↑ megakaryocytes

    Von Willebrand’s Disease (vWD)
    • Most common inherited form of coagulopathy
    • Autosomal dominant (most common) or autosomal recessive
    • Secondary to quantitative or qualitative defects in vWF
    • Pathophysiology: ↓ vWF → ↓ platelet adherence } secondary factor VIII deficiency
    • Clinical features → positive family history + “platelet type” bleeding (epistaxis, menorrhagia, petechiae, easy bruising, etc.), especially after aspirin administration;
    possible hematuria and/or GI bleed.
    • Best initial diagnostic test → CBC showing normal platelet counts .
    • Best next diagnostic test (or best initial, if platelet count already known) → bleeding time, which should be prolonged
    • Other lab findings ↑ aPTT .
    • Most accurate diagnostic test is vWF assay (also known as factor VIIIag assay) showing ↓ vWF levels

    Hemophilia A
    • X-linked recessive (hence males > females)
    • Deficiency of factor VIII (also known as factor VIIIpro)
    • Categorized as mild/subclinical (> 5%), moderate (1-5%) and severe (<1%) based on factor VIII activity
    • Clinical features à positive family history + asymptomatic with unexpected bleeding
    following major trauma and/or surgical procedures to hemarthrosis, deep tissue
    hematomas, GI and/or urinary bleeding, intracranial hemorrhage with minor head
    trauma
    • Repeated hemarthrosis à disabling arthropathy
    • Lab findings : ↑ aPTT with normal PT, bleeding time, platelet count, etc.
    * Hemophilia B (Christmas Disease) → X-linked recessive deficiency of factor IX; otherwise similar to hemophilia A; treat with factor IX concentrates

    Vitamin K deficiency
    • Etiology → malabsorption syndromes, prolonged antibiotic use, dietary deficiency, warfarin therapy, liver disease
    • Asymptomatic to bleeding similar to hemophilia
    • Lab findings : ↑↑ PT, ↑ aPTT, normal bleeding time

    Disseminated Intravascular Coagulation (DIC)
    • Etiology :
    1. Gram-negative sepsis (most common)
    2. Meningococcemia
    3. Massive trauma
    4. Burns
    5. Obstetric complications (abruptio placenta, amniotic fluid embolism)
    6. Snakebites
    • DIC may be classified as acute (most causes of DIC) or chronic (e.g. solid malignancies, retained products of conception)
    • Pathophysiology: activation of coagulation →generation of thrombin → diffuse microthrombi formation à consumption of platelets and coagulation factors
    + microangiopathic hemolytic anemia + activation of fibrinolysic system → diffuse thrombosis
    • Clinical features à symptoms/signs of underlying disease + bleeding and evidence of thrombosis .
    • Lab findings → ↓ platelet count, ↑ PT and aPTT, ↓ Hb and Hct, ↓ fibrinogen and ↑ Ddimer levels (fibrin-split products)
    • Blood smear → evidence of traumatic hemolysis (schistocytes → helmet cells, triangle cells, etc.)





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