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HEAMATOLOGICAL FINDINGS OF ANAEMIA STUDY.pptx

The document discusses the pathology and diagnosis of anemia, detailing its definition, clinical presentations, classifications, and diagnostic approaches. Anemia is characterized by a reduction in red blood cells or hemoglobin, leading to insufficient oxygen-carrying capacity, with various forms including microcytic, macrocytic, and normocytic anemia. The document outlines the diagnostic process, including history-taking, clinical examination, and laboratory investigations necessary for identifying the underlying causes of anemia.

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VICTORIA UNIVERSITY KAMPALA BPHARM-STUDENTS PRESENTED BY KAWALYA STEVEN
Pathology and Diagnosis of a case of Anemia • Anaemia is decrease in total number of erythrocytes in circulating blood. • Or Its a decrease in quality & quantity of Haemoglobin.
Learning Objectives • Definition of anemia. • Clinical presentation of anemia. • Classification of anaemia • Distinct features of each type of anemia. • Approach to diagnosis of anemia
Definition of anaemia • Anaemia is a condition in which the number of red blood cells goes low • or a reduction in the concentration of circulating haemoglobin below the level that is expected for healthy persons of same age and sex in the same environment. • Their oxygen-carrying capacity is insufficient to meet physiologic needs. • The WHO criteria for anemia as hemoglobin (Hb) levels <12.0 g/dL in non- pregnant women and <13.0 g/dL in men(in adults). • Anemia in pregnancy is defined as a hemoglobin concentration of less than 11 g/dL .
Clinical presentation of anemias • Fatigue and weakness • Headache • Dizziness • Tinnitus • Numbness and coldness • Pallor in cornea and palms • Dyspnea and palpitations • Angina pectoris • Intermittent claudication • Hemorrhages in the fundus of eyes • Jaundice • Menorrhagia • Anorexia • Flatulence • Nausea • Constipation
Clinical presentation of anaemias
Grading of anaemia Grade of anemia Hb concentration Mild Hb from lower limit of normal to 10g/dl Moderate 10.0 to 7.0 g/dl Severe < 7.0 g/dl Reference Hemoglobin values (ranges): Non pregnant women: 13.0 – 16.0 g/dl Men: 14.0 – 18.0 g/dl
Classification of anemia • Morphological classification • Etiological classification • Classification based on reticulocyte response
Morphological classification of anemia Microcytic anemia (MCV<80fl) Macrocytic anemia (MCV>100fl) Normocytic anemia (MCV 80-100 fl) Iron deficiency anemia Megaloblastic anemia Reticulocyte production normal Thalassemia Non-megaloblastic anemia • Recent blood loss • Hemolytic anemias Sideroblastic anemia • liver disease Reticulocyte production deficient Anemia of chronic disease • hemolytic anemias • Anemia of chronic disease • alcoholism • aplastic anemia • myelodysplastic syndrome • chronic kidney disease • hypothyroidism • hypothyroidism
11 1 Microcytic/hypochromic 3 1 2 2 Macrocytic/Normochromic 3 Normocytic/Normochromic Morphologic Categories of Anemia N.B. The nucleus of a small lymphocyte (shown by the arrow) is used as a reference to a normal red cell size
Macrocytic Hypochromic anemia • Low/normal reticulocyte count, macrocytosis (oval and round) • Elevated MCV,MCHC • Basophilic stippling • Howell-jolly bodies • Cabot rings • Pancytopenia • Hypersegmented neutrophils • Bone marrow- megaloblastic maturation, sieve like chromatin, nuclear-cytoplasmic asynchrony, maturation arrest
Normocytic Normochromic anaemia with effective erythropoiesis
Normocytic Normochromic Anemia MCV 82 – 92 MCHC > 30 • 1. Blood loss with Hemorrhage • 2. Increased plasma volume : Pregnancy, Over-hydration • 3. Hemolytic anemia : depend on each cause • 4. Hypoplastic marrow : Aplastic anemia, RBC aplasia • 5. Infiltrate BM : Leukemia, Multiple myeloma, Myelofibrosis, etc. • 6. Abnormal endocrine : Hypothyroidism, Adrenal insufficiency, etc. • 7. Kidney disease / Liver disease / Cirrhosis
Etiological Classification of Anaemias
Basic Approach to a diagnosis of anemia
Evaluation of microcytic-hypochromic anaemia
Evaluation of macrocytic anaemia
Evaluation of Haemolytic anaemia
A simplified approach to diagnosis of haemolytic anaemias
Clinical Diagnosis of anemia History • Diet history - vegeterian or non-vegeterian • H/o- chronic blood loss (menorrhagia, hemorrhoids) • H/o- drugs like anticancerous agents, chloramphenicol, gold, penicillamine (aplastic anemia) Dapsone, quinine(hemolytic anemia) • Family history of anemia (thalassemia, sickle cell anemia) • H/o- alcohol addiction • H/o- renal disease, rheumatologic disease • History of systemic symptoms like fever , weight loss, night sweats. • Obstetric and menstrual history
Clinical examination General examination- • Pallor • Icterus • Edema • Lymphadenopathy • Petechiae Systemic examination • CVS- flow murmur, loud S1 • Chest – crepts • P/A-splenomegaly
Laboratory Investigations • CBC • Reticulocyte count • ESR • Peripheral blood smear • LFT(recent viral hepatitis) • RFT • Iron profile • LDH, uric acid • Bone marrow examination • Hg electrophoresis • Flowcytometry • Direct and indirect coombs test • Screening test for Hepatitis (A, B and C) • Vitamin B12 and folic acid level
COMPLETE BLOOD COUNT RED CELL INDICES • Hb • Red cell count • Hematocrit: Proportion of the volume of red cells relative to the volume of blood • Mean Corpuscular Volume: Dividing the total volume of red cells by the number of red cells • Index for average size of red cells • Mean Corpuscular Hemoglobin: Average amount of haemoglobin in each red cell. • Mean Corpuscular Hemoglobin Concentration: This represents the average concentration of haemoglobin in a given volume of packed red cells. • MCHC raised in hereditary spherocytosis. • Decreased in hypochromic anaemia. • Red cell distribution width: Variation in red cell size • High in iron deficiency anaemia • Normal in anaemia of chronic disease
Laboratory Findings • Chemistry Hyperbilirubinemia: predominantly unconjugated bilirubin due to breakdown of heme ring by reticuloendothelial cells in the liver. Elevated LDH: released from destroyed cells. Hemoglobinemia: free hemoglobin level increases in hemolysis esp. intravascular hemolysis: levels of 10-20 mg/dl gives plasma amber color and 50-100 gm/dl reddish color.
Hemoglobinuria: red-brown color of urine due to free hemoglobin and methamoglobin. Decreased Heptaglobin level: it is a alpha-2-globin produced in the liver. It binds free hemoglobin thus level is reduced in hemolysis. Hemosidrinuria: it reflects extensive hemolysis for a prolonged period of time. - When hemoglobin is filtered by nephron, proximal tubular cells metabolize hemoglobin and iron accumulate in the cells. - Cells then exfoliate in the urine and iron can be detected by Prussian blue reaction.
Basic approach to diagnosis of anemia
Evaluation of microcytic hypochromic anemia (50-150ng/ml)
Microcytic Hypochromic Anemia • MCV < 80 • MCHC < 31 • 1. Fe deficiency anemia • 2. Abnormal globin synthesis : Thalassemia with or without Hemoglobinopathies • 3. Abnormal porphyrin and heme synthesis : Pyridoxine responsive anemia, etc. • 4. Other abnormal Fe metabolism
Iron deficiency anemia Cause – Chronic Blood loss (Hypermennorhoea, GI blood loss i.e ulcers and hookworm infestation) - Malabsorption in Celiac disease - H.pylori infection - Inadequate Fe diet, - Increased demand • History of pica (consumption of substances • such as ice, starch, or clay) • Koilonychia (“spoon nail”) • Glossitis (Plummer-Vinson's syndrome) seen in severe iron deficiency anemia
Investigations for Fe++ D • CBC and red cell indices-↓Hb, ↓MCV, ↓MCH, ↓MCHC, ↓PCV, ↑RDW • Reticulocyte count-normal or decreased • PBS – Microcytic and hypochromic RBCs anisocytosis and poikilocytosis • Iron profile- Serum ferritin decreased (<10ng/ml in women and <20ng/ml in men) Serum iron ↓, TIBC↑ and transferrin saturation is less than 10 percent • Increased soluble transferrin receptor in serum • Free erythrocyte protoporphyrin is increased. • BM biopsy-absent or ↓ staining for iron. Severe iron deficiency anemia (Normal serum iron - 50-150 µ/Dl Normal TIBC - 300-360 µ/dL)
Thalassemia • The thalassemia syndromes are inherited disorders of α- or β-globin biosynthesis. • Alpha and beta thalassemia. Alpha beta thalassemia Silent carrier Minor trait intermedia Hemoglobin H Major (cooley’s anemia) Hydrops fetalis
Features of Thalassemia • Decreased or absent globin chains • Alpha and beta thalassemias • Microcytic hypochromic, target cells, basophilic stippling • Reticulocytosis • Hb F elevated in electrophoresis
Diagnosis of Thalassemia • The diagnosis of β Thalassemia major made during childhood. • Minor and intermedia remains asymptomatic • On examination – jaundice, hepatosplenomegaly, Investigation – • CBC- ↓MCV, ↓MCH • Reticulocytosis • Peripheral smear- microcytic hypochromic RBCs with poikilocytosis ,target cells
Peripheral blood smear of thalassemia Microcytic and hypochromic resembling severe iron-deficiency anemia. Many elliptical and teardrop-shaped red blood cells are noted. Target cells have a bull’s-eye appearance
Diagnosis of Thalassemia contd…. • Hb electrophoresis is diagnostic for β –thalassemia • HbF(α2γ2), HbA2 (α2δ2) or both increased. • In α thalassemia trait HbA2 and HbF levels are normal. (Normal HbF<1%, HbA2 - 2.5-3.5%) • Hb H disease have increased β tetramers.
Differential diagnosis of Microcytic anemia Tests Iron Deficiency Inflammation Thalassemia Sideroblastic Anemia PB-smear Micro/hypo Normal Micro/hypo Micro/hypo with targeting variable Serum iron(μg/dL) <30 <50 Normal to high Normal to high TIBC(μg/dL) >360 <300 normal normal Percent saturation <10 10-20 30-80 30-80 Ferritin(μg/L) <15 30-200 50-300 50-300 Hemoglobin pattern on electrophoresis Normal Normal Abnormal with β thalassemia; Normal
Evaluation of Macrocytic anemia
Macrocytic Anemia MCV > 94 and MCHC > 31 Megaloblastic dyspoiesis 1. Vit. B12 deficiency : Pernicious anemia 2. Folic acid deficiency : Nutritional megaloblastic anemia, Sprue, and Other malabsorption syndromes 3. Inborn errors of metabolism : Orotic aciduria etc. 4. Abnormal DNA synthesis : Chemotherapy, Anticonvulsant, Oral contraceptives
Synthesis of Purines and dTMP
Megaloblastic anemia • Megaloblastic anemia is a term used to describe disorders of impaired DNA synthesis in hematopoietic cells but affects all proliferating cells. • Resulting Erythrocytes are larger than normal • Due to folic acid or vitamin B12 deficiency Diagnosis- • In addition to sx of anemia; peripheral neuropathy, paresthesias, seizures and dementia may found due to vit b12 deficiency • On examination - Jaundice or splenomegaly • Decreased vibratory and positional sense, ataxia,
Pernicious Anaemia • Vit B12 deficiency. • Malabsorption of Vit B12. • Absence of Intrinsic Factor (Gastric Intrinsic Factor). • GIF is secreted by parietal cells in ileum. • GIF absorbs vit B12
45 Macrocytic Ovalocytes Blood NRBC Blood Howell-Jolly body Teardrop Schistocyte Stippled RBC & Cabot Ring Giant Platelet Pap bodies PBS for Megaloblastic anemia
Investigations of megaloblastic anemia • Increased MCV & MCH, normal MCHC • Low RBC , WBC, and platelets • Peripheral smear-oval macrocytes, anisocytosis, poikilocytosis, Hypersegmented neutrophils • LDH and indirect bilirubin are elevated • Raised urine urobilinogen • Serum vitamin B12 , or folate or both decreased (Normal serum vit B12levels 160–200 ng/L and normal serum folate 2 -15 μg/L) • Serum methylmalonic acid (MMA) and homocysteine (HC) are elevated in vitamin B12 deficiency; and only HC is elevated in folate deficiency. • Detecting antibodies to intrinsic factor is specific for the diagnosis of PA.
Tests • Folate and B12 levels • Schilling test may be useful to establish etiology of B12 deficiency • Assesses radioactive B12 absorption with and without exogenous IF • Other tests if pernicious anemia is suspected • Anti-parietal cell antibodies, anti-IF antibodies • Secondary causes of poor absorption should be sought (gastritis, ileal problems, etc.)
Evaluation of normocytic anemia
Aplastic anemia • Aplastic anemia is pancytopenia with bone marrow failure (hypocellularity). • Decreased production of all cell lines and replacement of marrow with fat. • Causes: • Inherited: -fanconi anemia and dyskeratosis congenita • Acquired • Radiations: X-ray and radioactive drugs 196 Au and 34 I • Drugs: cytotoxic drugs, benzene, chloramphenicol, NSAIDS, sulfonamides, mercury, hydantoin • Infection: Parvovirus B19, Hepatitis A,B & C, EB-virus, HIV-1
Diagnosis of aplastic anemia • History-of bleeding, easy bruising, nose bleeds, heavy menstrual flow • Family history of hematologic ds • Examination-petechiae and ecchymoses • Lymphadenopathy and splenomegaly are highly atypical of aplastic anemia. Cafe au lait spots and short stature suggest Fanconi anemia • MCV-increased, reticulocytes are absent or few • Peripheral smear - shows large erythrocytes and a paucity of platelets and granulocytes. • Bone Marrow-only red cells, residual lymphocytes, mainly fat • Chromosome studies of bone marrow cells for Myeloid Dysplastic Syndrome • Flow cytometry to rule out PNH.
Anemia of chronic kidney disease • Primarily due to decreased endogenous EPO production • Other causes are-Diminished red blood cell survival, Bleeding diathesis • Iron deficiency • Hyperparathyroidism/bone marrow fibrosis • Chronic inflammation • Folate or vitamin B12 deficiency • Comorbid conditions: hypo-/hyperthyroidism, pregnancy,
Anemia of chronic disease • Normocytic anemia with ineffective erythropoiesis (reduced reticulocyte count) • Normochromic • Results from; • Chronic inflammation (e.g. rheumatologic disease): Cytokines released by inflammatory cells cause macrophages to accumulate iron and not transfer it to plasma or developing red cells (iron block anemia) • Inflammation • Malignancy • Bone marrow suppression (EPO is elevated)
Diagnosis Anemia of chronic kidney disease • CBC-normal MCV • Reticulocyte count-normal • PBS-normocytic, normochromic, echinocytes (burr cell) • Decreased serum iron, decreased total iron binding capacity and normal or raised ferritin • Increased marrow storage iron • ESR is high
Normochromic, normocytic anemia with effective erythropoiesis INCREASED reticulocyte count • Acute blood loss • Very acutely, with hypovolemia, may have normal blood counts, will become anemic with volume replenishment • Hemolytic anemia • Increased reticulocyte production cannot keep pace with loss of RBCs peripherally. • Response to specific therapy in nutritional anemias
Hemolytic anemia • Abnormality intrinsic to red cells- 1. Hereditary spherocytosis 2. Sickle cell disease 3. Thalassemia 4. G-6PD deficiency • Abnormality extrinsic to red cells 1. Autoimmune antibodies 2. Mechanical (malaria parasites)
Evaluation of hemolytic anemia
Evaluation of haemolytic anaemia
Diagnosis of hemolytic anemia • General examination- Jaundice, pallor • Other physical findings Splenomegaly; bossing of skull • Hemoglobin level From normal to severely reduced • MCV, MCH Usually increased • Reticulocytes Increased • Bilirubin Increased (mostly unconjugated) • LDH Increased • Haptoglobin Reduced to absent • direct Coombs test [DAT] is an indicator of the presence of antibodies attached to RBC. • The indirect Coombs test indicates the presence of free antibody in the plasma. • A peripheral blood smear-in Intravascular hemolysis may show red cell fragmentation (i.e., schistocytes,helmet cells)
• Inherited defect in the red cell membrane cytoskeleton (spectrin, ankyrin or band 3) leading to the formation of spherocytic red cells. • PBS - normocytic, microspherocytes • Screening test - osmotic fragility test • Definitive dx by molecular studies of gene - Autosomal dominant • Clinical presentations; • Mild to moderate anaemia, MCHC increased • Intermittent jaundice • Splenomegaly • Pigment gall stones Hereditary Spherocytosis
Sickle cell anemia • Due to point mutation in 6th place of beta chain substitution of, • glutamic acid with → valine • On deoxygenation of Hb, Hb chains polymerise and then sickle cells are formed Clinical presentation • Vaso-occlusive crisis - acute chest syndrome, pain crisis • Aplastic crisis-by parvovirus B19 • Hemolytic crisis - gall stones • Infections
Sickle cell anaemia Tests • Sickling test is positive. • Solubility test is positive. • Electrophoresis shows HbS. • In sickle cell trait, electrophoresis shows 60 percent of Hb A and 40 percent Hb S
Diagnostic testing of sickle cell anemia • CBC: • Reticulocytosis, indirect bilirubin↑, LDH↑, leukocytosis, thrombocytosis • Peripheral smear; • shows sickle shaped RBCs, target cells and Howell-jolly bodies
Diagnostic testing of sickle cell anemia Sickling slide test; positive Sickling and solubility test – is a screening test of sickle cell anemia Solubility test; positive
Diagnostic testing of sickle cell anemia • HPLC- Hb analysis by High Performance Liquid Chromatography and Hb electrophoresis Homozygote Heterozygote
• X linked disorder • Reduced activity of G6PD • Inability to remove ROS esp. H2O2 • Accumulated H2O2 leads to oxidation of hemoglobin with precipitation of globin chains • Forming Heinz-bodies • Red cells with heinz bodies destroyed in spleen(extravascular hemolysis) Glucose-6-phosphate dehydrogenase deficiency
Glucose-6-phosphate dehydrogenase deficiency • Asymptomatic • May present as Neonatal jaundice • Acute hemolytic anaemia • Chronic hemolytic anaemia • PBS- Bite cells and Heinz bodies (precipitated Hb within RBCs). • Polychromasia, fragmented red cells, spherocytes, half ghost cells • Biochemistry; -increased bilirubin, hemoglobinemia and hemoglobinuria
Drug-Induced Acute Hemolysis • Drugs that have been linked to G6PD: • Primaquine (an antimalarial) • Sulphonamide antibiotics • Sulphones (e.g. dapsone, used against leprosy) • Other sulphur-containing drugs: glibenclamide (an anti-diabetic drug) • Nitrofurantoin (an antibiotic often used for urinary tract infections) • Vitamin K analogues • Several others • Henna can cause a hemolytic crisis in G6PD deficient infants
Glucose-6-phosphate dehydrogenase deficiency • Screening tests-fluorescent spot test • Methemoglobin reduction test • Dye decolorisation test
Autoimmune Hemolytic Anemias Warm antibody AIHA-by an IgG autoantibody • mild jaundice and splenomegaly, red cells coated with IgG, • Form spherocytes. • Causes: Seen in autoimmune disorders Blood grouping Antibody ds, SLE, collagen vascular ds eg Scleroderma and Lymphomas e.g CLL. Cold antibody AIHA-by an IgM autoantibody, acrocyanosis • Seen in cold agglutinin ds, Paroxysmal cold hemoglobinuria (PCH), mycoplasma, EB virus
Blood Transfusion • Blood from one individual is given to another individual. • Red blood Cell donation is Required during: Acute Blood Loss; via Surgery, mechanical injuries and RT-accidents Less blood formation Excess destruction of blood by intracellular parasites, bacteria and autoimmune Antibodies Chronic blood loss; Hypermennorhoea, GIT ulcer bleeding and Hookworm parasitic infestation.
Hazards Of Blood Transfusion Mis-matched Blood Transfusion • Immediate: - Haemolysis Shock - Renal Failure - Deep vein thrombosis • Delayed: - Jaundice Matched Blood Transfusion • Immediate: - Circulatory Overload - Hyperkalaemia - Hypocalcaemia • Delayed: - Transmission of Disease pathogens
Erythroblastosis Foetalis • Newborn Infant disease • Characterized by gradual agglutination & phagocytosis of erythrocytes. • Haemolytic Disease of the Newborn and feotus (HDNF).
Diagnosis- • CBC; marked reticulocytosis, • Biochemistry tests; elevated LDH, and indirect hyperbilirubinemia. • Peripheral blood smear: may show spherocytes, occasional fragmented RBCs, • Positive DAT (direct coombs test) • Warm AIHA: IgG +and/or C3+ • Cold AIHA: IgG-and C3+
Coomb’s test • Detects presence of either antibody on RBC or of antibody in serum • Helpful in determining if a hemolytic anemia is immune-mediated
Non-Immune Hemolytic Anemias Hemolytic anaemias due to mechanisms or agents other than antibodies +/or complement Excessive destruction E.g.: • Mechanical (traumatic) • Toxins • Infections e.g clostridium tetanae, staphylococcus aureaus • Splenomegaly (hypersplenism) • Burn (physical) • Renal failure and liver failure • Chemicals
Mechanical (Traumatic) (Fragmentation) • This is due to direct trauma (stress) to the RBCs causing fragmentation of the RBCs & intra-vascular hemolysis. • The fragmented cells can be seen on peripheral blood smears & are called (schistocytes). Due to: 1. Prosthetic valves 2. Patches 3. Valvular diseasse e.g., stenosis
Mechanical (Traumatic) (Fragmentation) 2. Microangiopathic Hemolytic Aneamia: mechanical hemolysis due to contact between the RBCs & the abnormal intema of thrombosed, narrowed, necrotic small vessels or fibrin strand formation. MAHA Caused by many diseases e.g., • DIC (disseminated intravascular coagulation) • Malignant hypertension • Disseminated malignancies especially mucin secreting adenocarcinomas, • TTP (thrombocytopenic purpura) • Hemolytic uremic syndrome (HUS).
Take home message • Anemia is one of the important cause of morbidity and mortality in women. • Iron deficiency anemia is the most common type of anemia • Iron deficiency in adult male means GI blood loss until proven otherwise. • Hb electrophoresis is diagnostic for thalassemia • Megaloblastic anemia may present as pancytopenia • Reticulocytosis present in hemolytic anemia • Microcytic hypochromic –iron deficiency anemia • Macrocytic-megaloblastic anemia • Normocytic normochromic-hemolytic anemia
THANK YOU!

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HEAMATOLOGICAL FINDINGS OF ANAEMIA STUDY.pptx

  • 1.
  • 2.
    Pathology and Diagnosisof a case of Anemia • Anaemia is decrease in total number of erythrocytes in circulating blood. • Or Its a decrease in quality & quantity of Haemoglobin.
  • 3.
    Learning Objectives • Definitionof anemia. • Clinical presentation of anemia. • Classification of anaemia • Distinct features of each type of anemia. • Approach to diagnosis of anemia
  • 4.
    Definition of anaemia •Anaemia is a condition in which the number of red blood cells goes low • or a reduction in the concentration of circulating haemoglobin below the level that is expected for healthy persons of same age and sex in the same environment. • Their oxygen-carrying capacity is insufficient to meet physiologic needs. • The WHO criteria for anemia as hemoglobin (Hb) levels <12.0 g/dL in non- pregnant women and <13.0 g/dL in men(in adults). • Anemia in pregnancy is defined as a hemoglobin concentration of less than 11 g/dL .
  • 5.
    Clinical presentation ofanemias • Fatigue and weakness • Headache • Dizziness • Tinnitus • Numbness and coldness • Pallor in cornea and palms • Dyspnea and palpitations • Angina pectoris • Intermittent claudication • Hemorrhages in the fundus of eyes • Jaundice • Menorrhagia • Anorexia • Flatulence • Nausea • Constipation
  • 7.
  • 8.
    Grading of anaemia Gradeof anemia Hb concentration Mild Hb from lower limit of normal to 10g/dl Moderate 10.0 to 7.0 g/dl Severe < 7.0 g/dl Reference Hemoglobin values (ranges): Non pregnant women: 13.0 – 16.0 g/dl Men: 14.0 – 18.0 g/dl
  • 9.
    Classification of anemia •Morphological classification • Etiological classification • Classification based on reticulocyte response
  • 10.
    Morphological classification ofanemia Microcytic anemia (MCV<80fl) Macrocytic anemia (MCV>100fl) Normocytic anemia (MCV 80-100 fl) Iron deficiency anemia Megaloblastic anemia Reticulocyte production normal Thalassemia Non-megaloblastic anemia • Recent blood loss • Hemolytic anemias Sideroblastic anemia • liver disease Reticulocyte production deficient Anemia of chronic disease • hemolytic anemias • Anemia of chronic disease • alcoholism • aplastic anemia • myelodysplastic syndrome • chronic kidney disease • hypothyroidism • hypothyroidism
  • 11.
    11 1 Microcytic/hypochromic 3 1 2 2Macrocytic/Normochromic 3 Normocytic/Normochromic Morphologic Categories of Anemia N.B. The nucleus of a small lymphocyte (shown by the arrow) is used as a reference to a normal red cell size
  • 14.
    Macrocytic Hypochromic anemia •Low/normal reticulocyte count, macrocytosis (oval and round) • Elevated MCV,MCHC • Basophilic stippling • Howell-jolly bodies • Cabot rings • Pancytopenia • Hypersegmented neutrophils • Bone marrow- megaloblastic maturation, sieve like chromatin, nuclear-cytoplasmic asynchrony, maturation arrest
  • 15.
    Normocytic Normochromic anaemiawith effective erythropoiesis
  • 16.
    Normocytic Normochromic Anemia MCV82 – 92 MCHC > 30 • 1. Blood loss with Hemorrhage • 2. Increased plasma volume : Pregnancy, Over-hydration • 3. Hemolytic anemia : depend on each cause • 4. Hypoplastic marrow : Aplastic anemia, RBC aplasia • 5. Infiltrate BM : Leukemia, Multiple myeloma, Myelofibrosis, etc. • 6. Abnormal endocrine : Hypothyroidism, Adrenal insufficiency, etc. • 7. Kidney disease / Liver disease / Cirrhosis
  • 17.
  • 18.
    Basic Approach toa diagnosis of anemia
  • 19.
  • 20.
  • 21.
  • 22.
    A simplified approachto diagnosis of haemolytic anaemias
  • 23.
    Clinical Diagnosis ofanemia History • Diet history - vegeterian or non-vegeterian • H/o- chronic blood loss (menorrhagia, hemorrhoids) • H/o- drugs like anticancerous agents, chloramphenicol, gold, penicillamine (aplastic anemia) Dapsone, quinine(hemolytic anemia) • Family history of anemia (thalassemia, sickle cell anemia) • H/o- alcohol addiction • H/o- renal disease, rheumatologic disease • History of systemic symptoms like fever , weight loss, night sweats. • Obstetric and menstrual history
  • 24.
    Clinical examination General examination- •Pallor • Icterus • Edema • Lymphadenopathy • Petechiae Systemic examination • CVS- flow murmur, loud S1 • Chest – crepts • P/A-splenomegaly
  • 25.
    Laboratory Investigations • CBC •Reticulocyte count • ESR • Peripheral blood smear • LFT(recent viral hepatitis) • RFT • Iron profile • LDH, uric acid • Bone marrow examination • Hg electrophoresis • Flowcytometry • Direct and indirect coombs test • Screening test for Hepatitis (A, B and C) • Vitamin B12 and folic acid level
  • 26.
    COMPLETE BLOOD COUNTRED CELL INDICES • Hb • Red cell count • Hematocrit: Proportion of the volume of red cells relative to the volume of blood • Mean Corpuscular Volume: Dividing the total volume of red cells by the number of red cells • Index for average size of red cells • Mean Corpuscular Hemoglobin: Average amount of haemoglobin in each red cell. • Mean Corpuscular Hemoglobin Concentration: This represents the average concentration of haemoglobin in a given volume of packed red cells. • MCHC raised in hereditary spherocytosis. • Decreased in hypochromic anaemia. • Red cell distribution width: Variation in red cell size • High in iron deficiency anaemia • Normal in anaemia of chronic disease
  • 27.
    Laboratory Findings • Chemistry Hyperbilirubinemia:predominantly unconjugated bilirubin due to breakdown of heme ring by reticuloendothelial cells in the liver. Elevated LDH: released from destroyed cells. Hemoglobinemia: free hemoglobin level increases in hemolysis esp. intravascular hemolysis: levels of 10-20 mg/dl gives plasma amber color and 50-100 gm/dl reddish color.
  • 28.
    Hemoglobinuria: red-brown colorof urine due to free hemoglobin and methamoglobin. Decreased Heptaglobin level: it is a alpha-2-globin produced in the liver. It binds free hemoglobin thus level is reduced in hemolysis. Hemosidrinuria: it reflects extensive hemolysis for a prolonged period of time. - When hemoglobin is filtered by nephron, proximal tubular cells metabolize hemoglobin and iron accumulate in the cells. - Cells then exfoliate in the urine and iron can be detected by Prussian blue reaction.
  • 29.
    Basic approach todiagnosis of anemia
  • 30.
    Evaluation of microcytichypochromic anemia (50-150ng/ml)
  • 31.
    Microcytic Hypochromic Anemia •MCV < 80 • MCHC < 31 • 1. Fe deficiency anemia • 2. Abnormal globin synthesis : Thalassemia with or without Hemoglobinopathies • 3. Abnormal porphyrin and heme synthesis : Pyridoxine responsive anemia, etc. • 4. Other abnormal Fe metabolism
  • 32.
    Iron deficiency anemia Cause– Chronic Blood loss (Hypermennorhoea, GI blood loss i.e ulcers and hookworm infestation) - Malabsorption in Celiac disease - H.pylori infection - Inadequate Fe diet, - Increased demand • History of pica (consumption of substances • such as ice, starch, or clay) • Koilonychia (“spoon nail”) • Glossitis (Plummer-Vinson's syndrome) seen in severe iron deficiency anemia
  • 33.
    Investigations for Fe++ D •CBC and red cell indices-↓Hb, ↓MCV, ↓MCH, ↓MCHC, ↓PCV, ↑RDW • Reticulocyte count-normal or decreased • PBS – Microcytic and hypochromic RBCs anisocytosis and poikilocytosis • Iron profile- Serum ferritin decreased (<10ng/ml in women and <20ng/ml in men) Serum iron ↓, TIBC↑ and transferrin saturation is less than 10 percent • Increased soluble transferrin receptor in serum • Free erythrocyte protoporphyrin is increased. • BM biopsy-absent or ↓ staining for iron. Severe iron deficiency anemia (Normal serum iron - 50-150 µ/Dl Normal TIBC - 300-360 µ/dL)
  • 34.
    Thalassemia • The thalassemiasyndromes are inherited disorders of α- or β-globin biosynthesis. • Alpha and beta thalassemia. Alpha beta thalassemia Silent carrier Minor trait intermedia Hemoglobin H Major (cooley’s anemia) Hydrops fetalis
  • 35.
    Features of Thalassemia •Decreased or absent globin chains • Alpha and beta thalassemias • Microcytic hypochromic, target cells, basophilic stippling • Reticulocytosis • Hb F elevated in electrophoresis
  • 36.
    Diagnosis of Thalassemia •The diagnosis of β Thalassemia major made during childhood. • Minor and intermedia remains asymptomatic • On examination – jaundice, hepatosplenomegaly, Investigation – • CBC- ↓MCV, ↓MCH • Reticulocytosis • Peripheral smear- microcytic hypochromic RBCs with poikilocytosis ,target cells
  • 37.
    Peripheral blood smearof thalassemia Microcytic and hypochromic resembling severe iron-deficiency anemia. Many elliptical and teardrop-shaped red blood cells are noted. Target cells have a bull’s-eye appearance
  • 38.
    Diagnosis of Thalassemiacontd…. • Hb electrophoresis is diagnostic for β –thalassemia • HbF(α2γ2), HbA2 (α2δ2) or both increased. • In α thalassemia trait HbA2 and HbF levels are normal. (Normal HbF<1%, HbA2 - 2.5-3.5%) • Hb H disease have increased β tetramers.
  • 39.
    Differential diagnosis ofMicrocytic anemia Tests Iron Deficiency Inflammation Thalassemia Sideroblastic Anemia PB-smear Micro/hypo Normal Micro/hypo Micro/hypo with targeting variable Serum iron(μg/dL) <30 <50 Normal to high Normal to high TIBC(μg/dL) >360 <300 normal normal Percent saturation <10 10-20 30-80 30-80 Ferritin(μg/L) <15 30-200 50-300 50-300 Hemoglobin pattern on electrophoresis Normal Normal Abnormal with β thalassemia; Normal
  • 40.
  • 41.
    Macrocytic Anemia MCV >94 and MCHC > 31 Megaloblastic dyspoiesis 1. Vit. B12 deficiency : Pernicious anemia 2. Folic acid deficiency : Nutritional megaloblastic anemia, Sprue, and Other malabsorption syndromes 3. Inborn errors of metabolism : Orotic aciduria etc. 4. Abnormal DNA synthesis : Chemotherapy, Anticonvulsant, Oral contraceptives
  • 42.
  • 43.
    Megaloblastic anemia • Megaloblasticanemia is a term used to describe disorders of impaired DNA synthesis in hematopoietic cells but affects all proliferating cells. • Resulting Erythrocytes are larger than normal • Due to folic acid or vitamin B12 deficiency Diagnosis- • In addition to sx of anemia; peripheral neuropathy, paresthesias, seizures and dementia may found due to vit b12 deficiency • On examination - Jaundice or splenomegaly • Decreased vibratory and positional sense, ataxia,
  • 44.
    Pernicious Anaemia • VitB12 deficiency. • Malabsorption of Vit B12. • Absence of Intrinsic Factor (Gastric Intrinsic Factor). • GIF is secreted by parietal cells in ileum. • GIF absorbs vit B12
  • 45.
    45 Macrocytic Ovalocytes Blood NRBCBlood Howell-Jolly body Teardrop Schistocyte Stippled RBC & Cabot Ring Giant Platelet Pap bodies PBS for Megaloblastic anemia
  • 46.
    Investigations of megaloblasticanemia • Increased MCV & MCH, normal MCHC • Low RBC , WBC, and platelets • Peripheral smear-oval macrocytes, anisocytosis, poikilocytosis, Hypersegmented neutrophils • LDH and indirect bilirubin are elevated • Raised urine urobilinogen • Serum vitamin B12 , or folate or both decreased (Normal serum vit B12levels 160–200 ng/L and normal serum folate 2 -15 μg/L) • Serum methylmalonic acid (MMA) and homocysteine (HC) are elevated in vitamin B12 deficiency; and only HC is elevated in folate deficiency. • Detecting antibodies to intrinsic factor is specific for the diagnosis of PA.
  • 47.
    Tests • Folate andB12 levels • Schilling test may be useful to establish etiology of B12 deficiency • Assesses radioactive B12 absorption with and without exogenous IF • Other tests if pernicious anemia is suspected • Anti-parietal cell antibodies, anti-IF antibodies • Secondary causes of poor absorption should be sought (gastritis, ileal problems, etc.)
  • 48.
  • 49.
    Aplastic anemia • Aplasticanemia is pancytopenia with bone marrow failure (hypocellularity). • Decreased production of all cell lines and replacement of marrow with fat. • Causes: • Inherited: -fanconi anemia and dyskeratosis congenita • Acquired • Radiations: X-ray and radioactive drugs 196 Au and 34 I • Drugs: cytotoxic drugs, benzene, chloramphenicol, NSAIDS, sulfonamides, mercury, hydantoin • Infection: Parvovirus B19, Hepatitis A,B & C, EB-virus, HIV-1
  • 50.
    Diagnosis of aplasticanemia • History-of bleeding, easy bruising, nose bleeds, heavy menstrual flow • Family history of hematologic ds • Examination-petechiae and ecchymoses • Lymphadenopathy and splenomegaly are highly atypical of aplastic anemia. Cafe au lait spots and short stature suggest Fanconi anemia • MCV-increased, reticulocytes are absent or few • Peripheral smear - shows large erythrocytes and a paucity of platelets and granulocytes. • Bone Marrow-only red cells, residual lymphocytes, mainly fat • Chromosome studies of bone marrow cells for Myeloid Dysplastic Syndrome • Flow cytometry to rule out PNH.
  • 51.
    Anemia of chronickidney disease • Primarily due to decreased endogenous EPO production • Other causes are-Diminished red blood cell survival, Bleeding diathesis • Iron deficiency • Hyperparathyroidism/bone marrow fibrosis • Chronic inflammation • Folate or vitamin B12 deficiency • Comorbid conditions: hypo-/hyperthyroidism, pregnancy,
  • 52.
    Anemia of chronicdisease • Normocytic anemia with ineffective erythropoiesis (reduced reticulocyte count) • Normochromic • Results from; • Chronic inflammation (e.g. rheumatologic disease): Cytokines released by inflammatory cells cause macrophages to accumulate iron and not transfer it to plasma or developing red cells (iron block anemia) • Inflammation • Malignancy • Bone marrow suppression (EPO is elevated)
  • 53.
    Diagnosis Anemia ofchronic kidney disease • CBC-normal MCV • Reticulocyte count-normal • PBS-normocytic, normochromic, echinocytes (burr cell) • Decreased serum iron, decreased total iron binding capacity and normal or raised ferritin • Increased marrow storage iron • ESR is high
  • 54.
    Normochromic, normocytic anemiawith effective erythropoiesis INCREASED reticulocyte count • Acute blood loss • Very acutely, with hypovolemia, may have normal blood counts, will become anemic with volume replenishment • Hemolytic anemia • Increased reticulocyte production cannot keep pace with loss of RBCs peripherally. • Response to specific therapy in nutritional anemias
  • 55.
    Hemolytic anemia • Abnormalityintrinsic to red cells- 1. Hereditary spherocytosis 2. Sickle cell disease 3. Thalassemia 4. G-6PD deficiency • Abnormality extrinsic to red cells 1. Autoimmune antibodies 2. Mechanical (malaria parasites)
  • 56.
  • 57.
  • 58.
    Diagnosis of hemolyticanemia • General examination- Jaundice, pallor • Other physical findings Splenomegaly; bossing of skull • Hemoglobin level From normal to severely reduced • MCV, MCH Usually increased • Reticulocytes Increased • Bilirubin Increased (mostly unconjugated) • LDH Increased • Haptoglobin Reduced to absent • direct Coombs test [DAT] is an indicator of the presence of antibodies attached to RBC. • The indirect Coombs test indicates the presence of free antibody in the plasma. • A peripheral blood smear-in Intravascular hemolysis may show red cell fragmentation (i.e., schistocytes,helmet cells)
  • 59.
    • Inherited defectin the red cell membrane cytoskeleton (spectrin, ankyrin or band 3) leading to the formation of spherocytic red cells. • PBS - normocytic, microspherocytes • Screening test - osmotic fragility test • Definitive dx by molecular studies of gene - Autosomal dominant • Clinical presentations; • Mild to moderate anaemia, MCHC increased • Intermittent jaundice • Splenomegaly • Pigment gall stones Hereditary Spherocytosis
  • 60.
    Sickle cell anemia •Due to point mutation in 6th place of beta chain substitution of, • glutamic acid with → valine • On deoxygenation of Hb, Hb chains polymerise and then sickle cells are formed Clinical presentation • Vaso-occlusive crisis - acute chest syndrome, pain crisis • Aplastic crisis-by parvovirus B19 • Hemolytic crisis - gall stones • Infections
  • 61.
    Sickle cell anaemiaTests • Sickling test is positive. • Solubility test is positive. • Electrophoresis shows HbS. • In sickle cell trait, electrophoresis shows 60 percent of Hb A and 40 percent Hb S
  • 62.
    Diagnostic testing ofsickle cell anemia • CBC: • Reticulocytosis, indirect bilirubin↑, LDH↑, leukocytosis, thrombocytosis • Peripheral smear; • shows sickle shaped RBCs, target cells and Howell-jolly bodies
  • 63.
    Diagnostic testing ofsickle cell anemia Sickling slide test; positive Sickling and solubility test – is a screening test of sickle cell anemia Solubility test; positive
  • 64.
    Diagnostic testing ofsickle cell anemia • HPLC- Hb analysis by High Performance Liquid Chromatography and Hb electrophoresis Homozygote Heterozygote
  • 65.
    • X linkeddisorder • Reduced activity of G6PD • Inability to remove ROS esp. H2O2 • Accumulated H2O2 leads to oxidation of hemoglobin with precipitation of globin chains • Forming Heinz-bodies • Red cells with heinz bodies destroyed in spleen(extravascular hemolysis) Glucose-6-phosphate dehydrogenase deficiency
  • 66.
    Glucose-6-phosphate dehydrogenase deficiency •Asymptomatic • May present as Neonatal jaundice • Acute hemolytic anaemia • Chronic hemolytic anaemia • PBS- Bite cells and Heinz bodies (precipitated Hb within RBCs). • Polychromasia, fragmented red cells, spherocytes, half ghost cells • Biochemistry; -increased bilirubin, hemoglobinemia and hemoglobinuria
  • 67.
    Drug-Induced Acute Hemolysis •Drugs that have been linked to G6PD: • Primaquine (an antimalarial) • Sulphonamide antibiotics • Sulphones (e.g. dapsone, used against leprosy) • Other sulphur-containing drugs: glibenclamide (an anti-diabetic drug) • Nitrofurantoin (an antibiotic often used for urinary tract infections) • Vitamin K analogues • Several others • Henna can cause a hemolytic crisis in G6PD deficient infants
  • 68.
    Glucose-6-phosphate dehydrogenase deficiency •Screening tests-fluorescent spot test • Methemoglobin reduction test • Dye decolorisation test
  • 69.
    Autoimmune Hemolytic Anemias Warmantibody AIHA-by an IgG autoantibody • mild jaundice and splenomegaly, red cells coated with IgG, • Form spherocytes. • Causes: Seen in autoimmune disorders Blood grouping Antibody ds, SLE, collagen vascular ds eg Scleroderma and Lymphomas e.g CLL. Cold antibody AIHA-by an IgM autoantibody, acrocyanosis • Seen in cold agglutinin ds, Paroxysmal cold hemoglobinuria (PCH), mycoplasma, EB virus
  • 70.
    Blood Transfusion • Bloodfrom one individual is given to another individual. • Red blood Cell donation is Required during: Acute Blood Loss; via Surgery, mechanical injuries and RT-accidents Less blood formation Excess destruction of blood by intracellular parasites, bacteria and autoimmune Antibodies Chronic blood loss; Hypermennorhoea, GIT ulcer bleeding and Hookworm parasitic infestation.
  • 71.
    Hazards Of BloodTransfusion Mis-matched Blood Transfusion • Immediate: - Haemolysis Shock - Renal Failure - Deep vein thrombosis • Delayed: - Jaundice Matched Blood Transfusion • Immediate: - Circulatory Overload - Hyperkalaemia - Hypocalcaemia • Delayed: - Transmission of Disease pathogens
  • 72.
    Erythroblastosis Foetalis • NewbornInfant disease • Characterized by gradual agglutination & phagocytosis of erythrocytes. • Haemolytic Disease of the Newborn and feotus (HDNF).
  • 74.
    Diagnosis- • CBC; markedreticulocytosis, • Biochemistry tests; elevated LDH, and indirect hyperbilirubinemia. • Peripheral blood smear: may show spherocytes, occasional fragmented RBCs, • Positive DAT (direct coombs test) • Warm AIHA: IgG +and/or C3+ • Cold AIHA: IgG-and C3+
  • 75.
    Coomb’s test • Detectspresence of either antibody on RBC or of antibody in serum • Helpful in determining if a hemolytic anemia is immune-mediated
  • 77.
    Non-Immune Hemolytic Anemias Hemolyticanaemias due to mechanisms or agents other than antibodies +/or complement Excessive destruction E.g.: • Mechanical (traumatic) • Toxins • Infections e.g clostridium tetanae, staphylococcus aureaus • Splenomegaly (hypersplenism) • Burn (physical) • Renal failure and liver failure • Chemicals
  • 78.
    Mechanical (Traumatic) (Fragmentation) •This is due to direct trauma (stress) to the RBCs causing fragmentation of the RBCs & intra-vascular hemolysis. • The fragmented cells can be seen on peripheral blood smears & are called (schistocytes). Due to: 1. Prosthetic valves 2. Patches 3. Valvular diseasse e.g., stenosis
  • 79.
    Mechanical (Traumatic) (Fragmentation) 2.Microangiopathic Hemolytic Aneamia: mechanical hemolysis due to contact between the RBCs & the abnormal intema of thrombosed, narrowed, necrotic small vessels or fibrin strand formation. MAHA Caused by many diseases e.g., • DIC (disseminated intravascular coagulation) • Malignant hypertension • Disseminated malignancies especially mucin secreting adenocarcinomas, • TTP (thrombocytopenic purpura) • Hemolytic uremic syndrome (HUS).
  • 80.
    Take home message •Anemia is one of the important cause of morbidity and mortality in women. • Iron deficiency anemia is the most common type of anemia • Iron deficiency in adult male means GI blood loss until proven otherwise. • Hb electrophoresis is diagnostic for thalassemia • Megaloblastic anemia may present as pancytopenia • Reticulocytosis present in hemolytic anemia • Microcytic hypochromic –iron deficiency anemia • Macrocytic-megaloblastic anemia • Normocytic normochromic-hemolytic anemia
  • 81.

Editor's Notes

  • #61 Sickling test : When red cells containing HbS are subjected to deoxygenation, the become sickle-shaped while cells that do not contain HbS remain normal. Certain reducing chemical agents such as 2% sodium metabisulphite or sodium dithionite can deprive red cells of oxygen. Solubility test: Small amount of blood is added to a solution that contains high-phosphate buffer, a reducing agent (sodium dithionite) and saponin. Red cells are haemolysed and HbS, if present, is reduced by dithionite. Reduced HbS forms insoluble polymers, which refract light, and solution becomes turbid. A reader scale is held at the back of the tube; in negative test lines will be clearly seen since HbA is soluble in phosphate buffer, while lines will not be seen in positive test due to formation of polymers of HbS (Fig. 4.10).