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Anemia
- 1. • By Dr / Mona Mohsen
- 2. What is anemia ? (definition) • Anemia is strictly defined as a decrease in red blood cell (RBC) mass . • The function of RBC is to deliver oxygen from the lungs to the tissues and carbon dioxide from the tissues to the lungs. • Anemia ,like a fever is a sign that requires investigation to know the underlying etiology.
- 5. Blood loss • trauma • Burns • Frostbite Increase destruction • Thalassemias • Sickle cell anemia • Hemoglobinopathies • Protozoal (malaria). Decrease production • Iron deficiency • Vit b12 and folate deficiency • Anemia of chronic disease • A plastic anemia
- 6. Another etiological classification: • Thalassemias. • Sickle cell anemia. • Glucose 6 phosphate dehydrogenase deficiency(G6PD). Genetic • Iron deficiency • Vitamin B12 deficiency • Folate deficiency. Nutritional • Viral hepatitis • Bacterial gram negative sepsis • protozoal-malaria,leishmaniasis,toxoplasmosisInfectious • Renal disease • Hepatic disease • neoplasia Chronic Disease
- 7. Morphological classification: Microcytic (<80fl) • Iron deficiency anemia • Thalassemia • Anemia of chronic disease . macrocytic(>96fl) • Vitamin B12 deficiency • folate deficiency • hypothyroidism Normocytic(80-96fl) • Acute blood loss • Anemia of chronic disease • Marrow infiltration
- 8. epidemiology: • In underprivileged countries ,nutritional factors are the major factors for the etiology of anemia . • Even though geographic diseases such as sickle cell anemia ,malaria, hookworm and chronic infections are responsible for a portion of the increase . • Thalassemia and Sickle cell anemia are common in regions of Saudi Arabia and the Mediterranean basin.
- 9. hemoglobin:13-17g/dl (men) 12-15g/dl(women). Hematocrit : 40%-52%(men) 36%-47% women Mean corpuscular volume(MCV): 80-100fl Red blood cell distribution width(RDW): 11.5-14.5 % Mean corpuscular hemoglobin (MCH): 0.4- 0.5fmol/cell Mean corpuscular hemoglobin concentration (MCHC) : 30-35g/dl Reticulocytes: 0.5%-1.5% Normal parameters : Type of HB levels indication Hemoglobin A1 (2 α 2β) 12-16 gm/dl ,90% of total hemoglobin in adult Low levels indicate anemia or blood loss HemoglobinA2 (2α 2δ) 1.5%-3.5% of total hemoglobin High levels may indicate thalassemia Hemoglobin F (2 α 2γ) 50-90% in neonates 0-1% of total hemoglobin in adult Normally high in neonates Long term elevations may indicate thalassemia Hemoglobin S Presence is abnormal Indicative of sickle cell anemia
- 10. Iron deficiency anemia • Def : this type of anemia develops when body stores of iron too low to support normal red blood cell production. • Causes : inadequate dietary intake, impaired absorbtion,bleeding,or loss of iron in urine. • 2/3 of body iron is in the circulation as hemoglobin (2.5-3gm). • 1/3 stored as ferritin and hemosiderin(.5- 1.5gm). • Average daily iron requirements 10- 12mg/day. • Daily requirements increase in case of childhood ,pregnancy , breast feeding .
- 11. Iron deficiency anemia cont • Clinical presentation: I. Fatigue. II. Poor school performance. III. Pallor. IV. Impaired growth. V. Angular stomatitis. VI. Koilonychia . • Workup: I. MCV II. MCHC III. Low serum iron . -men(55-160µg/dl). -women(40-155µg/dl). I. Low ferritin level -men (23-336ng/ml) -women(11-306ng/ml) I. total iron binding capacity (255-450µg/dl).
- 12. Iron deficiency anemia cont • Management : I. Oral iron therapy Adult:120 mg/day for three months Children:3mg/kg per day Adequate response 1 gm per dl increase in HG level after one month therapy.
- 13. IMCI Severe palmer and or mucous membrane pallor Severe anemia Treat the child to prevent low blood sugar Some palmer and or mucous membrane pallor Anemia •Give iron daily for 14 days. •If family history of chronic hemolytic anemia don’t give iron and refer for assessment. •Advise mother when to return immediately . •Follow up in 14 days . No palmer or mucous membrane pallor No anemia •If child aged 6-30 months give one dose of iron weekly . •If family history of chronic hemolytic anemia don’t give iron and refer for assessment.
- 14. Age or weight Iron syrup (30mg/5ml) 2months up to 4 months (4-<6kg) 2.5ml 4 months up to 12 months (6-<10kg) 5ml 12 months up to 3 years (10-<14kg) 7.5ml 3 years up to 5 years (14-19kg) 10ml IMCI ….dose of iron
- 15. Megaloblastic Anemia Vitamin B12 deficiency (rare) Daily requirement:2-3µg stores: 2-3mg mainly in liver sufficient for 2 years. Found in meat,fish,milk Not destroyed by cooking Folic acid deficiency Daily requirement:100µg stores: minimal amounts Depleted in few weeks Found in green leafy vegetables, liver Destroyed by cooking
- 16. Megaloblastic Anemia cont • Vitamin B12 deficiency (rare) Etiology : -Low dietary intake -Decreased absorption (pernicious anemia) -ileal disease or resection • Folic acid deficiency Etiology: -poor intake -anti folate drugs Anticonvulsants methotrexate
- 17. Megaloblastic Anemia cont • Vitamin B12 deficiency (rare) Clinical picture: -Pallor -Glossitis -Neurological (Parathesia in toes and fingers, Weakness , ataxia Optic atrophy). • Folic acid deficiency Clinical picture: -pallor -Glossitis - Asymptomatic
- 18. Megaloblastic Anemia cont • Vitamin B12 deficiency (rare) Workup: MCV Nucleated RBCs and megaloblasts in blood smear Serum B12 <150mg/l normal(200-900Рg/ml) • Folic acid deficiency Workup: MCV Nucleated RBCs and megaloblasts in blood smear Serum folate <2.5ng/ml normal(2.5-20ng/ml)
- 19. Megaloblastic Anemia cont • Vitamin B12 deficiency (rare) Management : • Hydroxocobalamin 1000 μg can be given intramuscularly to a total of 5–6 mg over the course of 3 weeks. • 1000 μg is then necessary every 3 months for the rest of the patient’s life. • Folic acid deficiency Management: • Folate deficiency can be corrected by giving 1- 5 mg of folic acid daily. • Treatment should be given for about 4 months to replace body stores.
- 20. Folic acid and pregnancy Prophylactic folic acid (400 μg daily_0.4 mg ) is recommended for all women planning a pregnancy to reduce neural tube defects. Women with a previous history of neural tube defects (NTDs) are advised to undergo at least( 4 mg )folic acid supplementation daily . Folic acid supplementation should start at least one month and preferably two or three months prior to conception . The use of folinic acid (calcium levofolinate )in preventing NTDs is inappropriate as it is different from folic acid .
- 21. thalassemia • Pathogenesis : Imbalance in globin chain synthesis. Unstable hemoglobin which precipitate within the cell Forming insoluble inclusion bodies (Heinz bodies) That damage the red cell membrane Leading to excessive hemolysis. In addition diminished hemoglobinization of individual red blood cells results in damage to erythrocyte precursors and in effective erythropoisies In the bone marrow . Hypochromia .
- 22. thalassemiascont • Β thalassemia Absent beta chains or very small amounts leading to ineffective erythropoisies and hemolysis . I. Thalassemia major II. Thalassemia intermedia III. Thalassemia minor • α thalassemia • healthy individuals have 4 alpha- globin genes ,2 on each chromosome 16. • Alpha thalassemia syndromes are caused by deficient expression of 1 or more of the 4 alpha globin genes.
- 23. Β thalassemia 1. thalassemia major : homozygous β-thalassaemia Usually presented in the first year of life . Clinical picture severe anemia. Extra medullary haemopoiesis that soon leads to hepato splenomegaly and bone expansion, giving rise to the classical thalassaemic facies. (sun ray skull appearance)
- 24. Β thalassemia 1. thalassemia major Work up : -MCV -target cells in peripheral smear -elevation of Hb A2 in electrophoresis
- 25. Β thalassemia 1. thalassemia major Management : Regular transfusions should be given to keep the Hb above 10 g/dL. iron-chelating agent desferrioxamine. Long-term folic acid supplements. splenectomy may be needed.
- 26. Β thalassemia 2. Thalassemia intermedia Thalassaemia intermedia includes patients who are symptomatic with moderate anemia (Hb 7–10 g/dL) and who do not require regular transfusions. Patients may have splenomegaly and bone deformities. Recurrent leg ulcers. these patients are also iron overloaded. 3. Thalassemia minor (trait) This common carrier state (heterozygous β thalassaemia) is asymptomatic. Anemia is mild or absent.
- 27. α thalassemia 1. Alpha (0) thalassemia : Deletion of both pairs of alpha-globin genes (--/--) . Can’t produce any functional hemoglobin and so it is in compatible with life . Clinically referred to as : Hydrops fetalis . Alpha thalassemia major . Hemoglobin Bart’s.
- 28. α thalassemia 2. Silent carrier Silent carriers (-α/αα) are essentially asymptomatic . CBC,MCV,MCH , HB electrophoresis are all normal . 3. Alpha thalassemia trait Individuals with alpha thalassemia trait (-α/-α) are asymptomatic . Normal CBC Blood smear shows microcytosis ,target cells HB electrophoresis may be normal or increased HB F
- 29. α thalassemia 3. Hemoglobin H disease (--/-α) Clinical picture: asymptomatic. chronic hemolytic anemia needing periodic transfusions. Severe anemia with hepato - splenomegaly. Hydrops fetalis . Complications : Hepato-splenomegaly. A plastic crises . Gall stones . Skeletal changes . Management : Blood transfusions . Iron chelating agents. Splenectomy.
- 30. Glucose-6-phosphate dehydrogenase (G6PD) deficiency • The enzyme G6PD holds a vital position in the hexose monophosphate shunt oxidizing glucose-6-phosphate to 6-phosphoglycerate with the reduction of NADP to NADPH. • The reaction is necessary in red cells where it is the only source of NADPH, which is used via glutathione to protect the red cell from oxidative damage
- 31. Glucose-6-phosphate dehydrogenase (G6PD) deficiency • The gene for G6PD is localized to chromosome X . The deficiency is more common in males than in females. Clinical picture: 1. Acute drug-induced hemolysis usually dose related 2. Favism (ingestion of fava beans). 3. Chronic haemolytic anaemia. 4. Neonatal jaundice 5. Infections and acute illnesses will also precipitate haemolysis in patients with G6PD deficiency Drugs causing hemolysis in G6PD deficiency Analgesics: Aspirin Phenactin Antimalarias: Primaquine pyrimethamine Antibacterials: Sulphonamides Quinolones Chloramphenicol Miscellaneous Vit k probenicid
- 32. Glucose-6-phosphate dehydrogenase (G6PD) deficiency Work up: Blood account is normal between attacks. During the attack Jaundice is evident MCV G6PD deficiency Management: • Any offending drugs should be stopped. • Underlying infection should be treated. • Blood transfusion may be life-saving.
- 33. References : • www.medscape.com • www.who.int • www.ncbi.nlm.nih.gov • Askhematologist.com • www.news-medical.net • Kumar and Clark 7th edition • www.mayoclinic.com • Medlineplus.gov • www.webmed.com
- 34. Thank you