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1damen power point ans anemia
1. The document discusses hematologic disorders including hematopoiesis, anemia, polycythemia, and hematologic malignancy. 2. It provides details on the pathophysiology of hematopoiesis, the definition and classification of anemia, the general approach to evaluating anemic patients, and discussions of common anemia types and their treatments. 3. Key anemia types covered include iron deficiency anemia, megaloblastic anemia due to vitamin B12 and folate deficiencies, and the morphological features seen in peripheral blood and bone marrow in these conditions.
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1damen power point ans anemia
- 1. Hematologic disorder Hematopoiesis Anemia Polycytemia Hematologic malignancy by Dr. Damena M.
- 2. Presentation outline • Pathophysiologyof hematopoiesis • Definition of anemia • Classification • General approach to anemic patient • Discussion of commonest types of anemia with respective treatment
- 3. Pathophysiology of hematopoiesis Hematopoiesis-the process by which circulating blood cells are formed in bone marrow. it is estimated that 1010 erythrocytes and 108 to 109 leukocytes are produced per hour in the steady state. they can be greatly amplified on demand. These huge cell numbers are immediate descendants of maturing precursors that arise from a smaller pool of progenitors. The progenitors in turn arise from an even smaller pool of hematopoietic stem cells (HSC)
- 4. hematopoietic stem cells(HSC)- are thought to be mostly in a resting or nondividing state and have the capacity to self-renew (and thus maintain their numbers). Hematopoietic stem cells are multipotent and have the capacity to differentiate into the cells of all 10 blood lineages — erythrocytes, platelets, neutrophils, eosinophils, basophils, monocytes, T and B lymphocytes, natural killer cells, and dendritic cells
- 7. Normal values RBC Profile •RBC= • Hgb= • Hct= • MCH= • MCHC= WBC Profile • WBC= • NEUTROPHIL= • EOSINOPHIL=
- 8. Anemia Pathophysiological definition: Reduction inred cell mass from circulation Laboratory definition: Reduction in haemoglobin concentration below normal WHO criteria: Males Hgb<13 gm/dl, Females Hgb<12gm/dl
- 9. classification • Pathophysiologic • Hypoproliferetive •Hemolytic anemia • Anemia of blood lose • RBC Morphology • Normocytic normochromic- acute blood lose, anemia of chronic illness(70%) • Microcytic hypochromic:- e.g iron deficiency, lead poisoning • Macrocytic anemia:- folat and cobalamin deficiency, drug like zidovudine
- 10. 1. Hypoproliferative anemia Impairedred cell production due to luck of substrate or impaired bon marrow function by infiltration Iron deficiency anaemia .Anaemia of chronic disease Bone marrow failure syndromes: BM infiltration withleukemia, lymphoma, metastatic malignancy and Metabolic and endocrine failure syndromes: hypothyroidism, hypopituitarism; malnutrition Vitamin b12 0r B9 deficiency Drugs ;- zidovudine’ ,mthotrixate
- 11. 2 Anemia ofhemolysis/Blood loss a. Hereditary hemolytic disorders Hemoglobinopathies: Sickle cell disease,Thalassemia, Membronopathies: Hereditary spherocytosis, elliptocytosis, Enzymopathies: G6PD deficiency, Pyruvate Kinase deficiency b. Acquired hemolytic disorders Immune haemolytic anemia: Autoimmune, drug-induced Intravascular hemolysis:Aortic stenosis,Microangiopathic hemolytic anemia (TTP-HUS), Dic Hypersplenism Direct toxic effects: Malaria, burn, sepsis, Snake and Spider envenomation
- 12. 3. Animia ofblood lose • Any obvious bleeding or occult bleeding
- 13. • Normocytic normochromicanemia – Anemia of chronic illness (70% of the cases) – CKD – Early iron deficiency anemia – Acute blood loss • Microcytic hypochromic anemia – Iron deficiency – Lead poisoning – Sideroblastic anemia – Thalassemia – Anemia of chronic illness (30% of the cases)
- 14. •Macrocytic normochromic anemia – Folatedeficiency – Cobalamin deficiency – Any condition causing marked reticulocytosis – Alcohol abuse, hypothyroidism – Drugs- zidovudine, methotrexate, and
- 15. Approch to thept • History • physical examination • Diagnostic invstigation
- 16. Iron deficiency anemia The most common nutritional disorder world wide Globally, 50% of anemia is attributable to iron deficiency Prevalence higher in developing countries Africa and Asia bear 71% of the global mortality burden due to iron deficiency anemia Common also in US-toddlers, adolescent girls
- 17. Iron metabolism Thenormal diet of western diet contains-10-20mg per day The total body iron content is normally about 2gm in women & 6 gm in men It is divided into functional & storage comportment About 80% of functional found in Hb, myoglobin and enzymes The storage pool is represented by ferritin & hemosiderin-15-20% of total body
- 18. • So totaliron binding capacity of serum is 300-350µg/dL • Most Fe is absorbed in duodenum through two distinct pathways • Since body loss of Fe is limited, Fe balance is maintained by regulating absorptive intake • Mechanisms are still incompletely understood
- 19. Etiology Decreased intake Rare in industrialized countries(Can occur in infants, children, elderly) Increased demand Growing infants, children and adolescents during pregnancy Impaired absorption Celiac disease,Tropical sprue Gasterectomy Chronic blood loss Commonest cause in western
- 20. Stages in thedevelopment of IDA 1. Depletion of iron stores Decreased level of serum ferritin (<20µg/L) and BM iron stain 0 to1+ NB: serum ferritin of 50-200µg/L and marrow iron store of 1-3 + is expected in normal state Normal level of SI, TIBC,% saturation, RBC protoporphyrin level Pt not symptomatic /not anemic
- 21. 2. Iron deficienterythropoiesis Serum ferritin <15µg/L and BM iron stain 0 Reduced SI (<50 µg/dl) and % saturation (<20%) Increased TIBC (>360 µg/dl ) and RBC protoporphyrin level (>100 µg/dl)
- 22. 3. Iron deficiencyanemia SI<30 µg/dl, % saturation <10%, Microcytic, hypochromic RBCs, Aniso-poikilocytosis, (SMALL SIZE) Cigar and pencil-shaped RBCs
- 24. Clinical prentation • Nonspecific Sx and Sn of anemia • In addition to the anemia other changes can occur with severe deficiency – koilonychia, alopecia, atrophic changes in tongue & gastric mucosa and intestinal malabsorption • The dominating Sn and Sx relate to the underlying cause
- 25. Morphology In peripheral smearRBCs are Small (microcytic) & Pale (hypochromic) Poikilocytosis in the form of small elongated red cells (pencil cells) are characteristic In bone marrow, Erythroid hyperplasia The disappearance of stainable iron from mononuclear phagocytic cells is a diagnostic finding-Prussian blue st
- 26.
- 28. Prussian Blue Stain ofBone Marrow
- 29. treatment • Red celltransfusion- indications – Cardiovascular instability – HCT <15% – Continued and excessive blood loss – Patients requiring immediate intervention • Oral iron therapy – 300mg of elemental iron per day – Ideally, should be taken on empty stomach – Should continue for a period of 6-12 months after correction of the anemia – Response- the reticulocyte count begin to increase after 4-7days of therapy and peak at 10 days – S/E include abdominal pain, nausea, vomiting, and constipation
- 30. • Parental irontherapy- indicated for patients – Who are unable to tolerate oral iron – Whose needs are relatively acute – Who need iron on an ongoing basis, usually due to persistent GI blood loss – Taking EPO • Preparations include – Iron dextran – Ferric gluconate • Feared complication- anaphylaxis, especially with iron dextran infusion – Anaphylaxis is much rarer with the newer preparations
- 31. Megaloblastic anemia • Twoprincipal types 1. Cobalamin deficiency anemia 2. Folate deficiency anemia • It results in defect in DNA synthesis which lead to Enlargement of erythroid precursors (megaloblast) Large cells in peripheral blood (macrocytes) Hypersegmented neutrophils • The precise basis for the changes is not fully understood
- 32. • Vitamin B12and Folate are coenzymes required for synthesis of thymidine • Deficiency or impairment in their metabolism results in defective nuclear maturation • Delay or block cell division • The synthesis of RNA and protein is relatively unaffected • Cytoplasmic maturation proceeds in advance of nuclear maturation- Nuclear/Cytoplasmic asynchrony
- 33. morphology Certain morphologic featuresare common to all Pancytopenia Marked variation in size and shape of red cells(Anisopoikliocytosis) RBC-macrocytic & oval(Macro-ovalocytes) MCV > 100fl Reticulocyte count is low Nucleated red cells occasionally
- 34. • Neutrophils Larger –Macropolymorphonuclear Hypersegmented-Fiveor six nuclear lobules • Marrow is hypercellular • Megaloblastic change is detected in all stages of red cell development • The nucleus fails to undergo the chromatin clumping
- 35. • Granulocytes precursorsalso display nuclear/cytoplasm asynchrony • Megakaryocytes-Abnormally large and have bizarre, multilobed nuclei • The anemia is further exacerbated by increased hemolytic destruction • Mild to moderate Fe overload
- 36. Anemia due tovitamin B12 deficiency
- 37. Vit B12 metabolism •Human are totally dependent on diet • Daily requirement-1-3µg. • Absorption require intrinsic factor • Vit B12 freed from binding protein by pepsin • Free Vit B12 binds to cobalophilins(R-binder) • This complexes are broken down by pancreatic protease • Vit B12 then associates with intrinsic factor • Endocytosis • Binding with transcobalamin II
- 38. Etiology • Inadequate diet-stricts vegans • Impaired absorption Intrinsic factor deficiency Gasterectomy Ileal resection Tape worm infestation Diffuse intestinal disease Chronic pancreatitis • Increased requirement Pregnancy, cancer, chronic infection, hyperthyroidism
- 39. Clinical feature The sameas other type of anemia CNS manifestations • Found in 3/4th patients • The spinal cord Degeneration of myelin in the dorsal and lateral tract Sometimes followed by loss of axon • Degenerative change in the ganglia of posterior roots and peripheral nerves • Psychiatric features are also seen in some patients with cobalamin or folate deficiencies
- 40. Folate deficency • Adeficiency of folic acid result in megaloblastic anemia • Have the same characteristic as vit B12 but no neurologic change • Depressed synthesis of DNA is the immediate cause
- 41. • Diagnosis canbe made only by demonstration of decreased folate levels in the serum or red cells • Elevated homocystein with normal MMA level • Hematologic symptoms of vit B12 deficiency anemia respond to Folate therapy • But doesn’t prevent the progression of neurologic deficits ( May even exacerbate
- 42. Treatment of megaloblasticanemia • Cobalamin deficiency – Lifelong regular cobalamin injections – Hydroxycobalamin or cyanocobalamin can be used – Hydroxycobalamin 1000µg IM weekly for 6 wks followed by 1000µg IM every 3 months lifelong • Folate deficiency – Folic acid 5-15 mg po/day – Rule out cobalamin deficiency before initiating folic acid – Duration of treatment depends on the underlying cause • Prophylactic folic acid is indicated during – Pregnancy – Premature infants – Chronic dialysis patients – Patients on total parentral nutrition
- 43.