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Anemia ppt

To brief introduction of anemia its cause, classification and management .

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Anemia ppt

  1. 1. ANEMIA AND DIETARY MANAGEMENT Presented by Dev Ram SUNUWAR M.Sc.Nutrition and dietetics1
  2. 2. OUTLINE  Definition  Overview of anemia  Causes of anemia  Classification  Dietary management 2
  3. 3. DEFINITION  Anemia from the Greek word ( ναιμία)(an-haîma) meaning "without blood", is a deficiency of red blood cells (RBCs) and/or hemoglobin.  WHO definition: “ a condition in which the haemoglobin content of blood is lower than normal as a result of a deficiency of one or more essential nutrients, regardless of the cause of such deficiency.  Anaemia refers to a state in which the level of haemoglobin in the blood is below the reference range appropriate for age and sex. ( Davidsons principle and practice of medicine) 3
  4. 4. OVERVIEW According to WHO  Worldwide prevalence = over 30% of the world’s population are anaemic, many due to iron deficiency.  In developing countries every second pregnant woman and about 40% of preschool children are estimated to be anaemic.  40% in young children  50% of pregnant women and 35% of non-pregnant women affected  18% adult males Prevalence of anemia in Nepal  Anemia affects 35% of all women (close to 48% of pregnant women)  However, Nepal demonstrated a huge reduction in anemia prevalence among women between 2001 and 2006 ,Hookworm infestation may be a particular driver of iron deficiency and anemia in Nepal, particularly in the Terai, where one study found that 75% of pregnant women had hookworms, 73% were anemic, and 88% of anemia cases were due to iron deficiency (Dreyfuss et al. 2000).  Anemia among women and children still higher:- (35% in women 15-49 years and 46% 6-59 months children anemic (NDHS 2011) 4
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  6. 6. CAUSE OF ANEMIA Decreased or ineffective marrow production • Lack of iron, vitamin B12 or folate • Hypoplasia/myelodysplasia • Invasion by malignant cells • Renal failure • Anaemia of chronic disease Normal marrow production but increased removal of cells • Blood loss • Haemolysis • Hypersplenism 6
  7. 7. Diagnosis of anemia  Patient history Dietary habits Medication Possible exposure to chemicals and/or toxins Description and duration of symptoms  Tiredness  Muscle fatigue and weakness  Headache and vertigo (dizziness)  Dyspnea (difficult or labored breathing) from exertion  G I problems  Overt signs of blood loss such as hematuria (blood in urine) or black stools 7
  8. 8. Diagnosis of anemia  Physical exam General findings might include Hepato or splenomegaly Heart abnormalities Skin pallor Specific findings may help to establish the underlying cause: In vitamin B12 deficiency there may be signs of malnutrition and neurological changes In iron deficiency there may be severe pallor, a smooth tongue, and esophageal webs In hemolytic anemias there may be jaundice due to the increased levels of bilirubin from increased RBC destruction 8
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  12. 12. IRON-DEFICIENCY ANEMIA  Clinical Manifestations  Most common: pallor  Second most common: inflammation of the tongue (glossistis)  Cheilitis=inflammation/fissures of lips  Sensitivity to cold  Weakness and fatigue  Diagnostic Studies  CBC  Iron studies Diagnostics:  Iron levels: Total iron-binding capacity (TIBC), Serum Ferritin.  Endoscopy/Colonscopy 12
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  17. 17. MANAGEMENT  Collaborative Care  Treatment of underlying disease/problem  Replacing iron  Diet  Drug Therapy  Iron replacement  Oral iron  Feosol, DexFerrum, etc  Absorbed best in acidic environemtn  GI effects  Parenteral iron  IM or IV  Less desirable than PO 17
  18. 18. IRON-DEFICIENCY ANEMIA MANAGEMENT  Diet counseling—foods rich in iron  Provide periods of rest  Supplemental iron  Discuss diagnostic studies  Iron therapy for 2-3 months after the hemoglobin levels return to normal 18
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  21. 21. Guidelines for oral iron and folate therapy to treat severe anaemia Age Group Dose Duration < 2 years 25 mg iron + 100-400μg folic acid daily 3 months 2-12 years 60 mg iron + 400μg folic acid daily 3 months Adolescents and adults, including pregnant women 120 mg iron + 400μg folic acid daily 3 months  After completing 3 months of therapeutic supplementation, pregnant women and infants should continue preventive supplementation regimen.  Children with Kwashiorkor or marasmus should be assumed to be severely anaemic. However, oral iron supplementation should be delayed until the child regains appetite and starts gaining weight, usually after 14 days Source: Rebecca J. Stoltzfus and Michele L. Dreyfuss, Guidelines for the use of Iron Supplements to Prevent and Treat Iron Deficiency Anaemia, INACG, WHO and UNICEF, 1998 21
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  23. 23. FOOD FORTIFICATION  Ministry of Health and Population (MoHP) has also started home fortification programs in Nepal with multiple micronutrient powders (MNPs) under the World Health Organization’s guidelines  This does not ask for a change in food habits as the powders are sprinkled on the food that the children usually eat.  This has also helped a timely initiation of complementary food. This program has targeted children completing 6 months.  Simultaneously, the second anemia control plan 2012– 2016 is being formulated by MoHP addressing anemia among all strata, particularly the most vulnerable ones like children of 6-23 months young, children of 6-59 months, adolescents, pregnant women's 23
  24. 24. MEGALOBLASTIC ANEMIAS  Characterized by large RBCs which are fragile and easily destroyed  Common forms of megaloblastic anemia 1. Cobalamin deficiency 2. Folic acid deficiency 24 This picture shows large, dense, oversized, red blood cells (RBCs) that are seen in megaloblastic anemia.
  25. 25. COBALAMIN (VITAMIN B12) DEFICIENCY  Cobalamin Deficiency--formerly known as pernicious anemia  Vitamin B12 (cobalamin) is an important water- soluble vitamin.  Intrinsic factor (IF) is required for cobalamin absorption  Causes of cobalamin deficiency  Gastric mucosa not secreting IF  GI surgery loss of IF-secreting gastric mucosal cells  Long-term use of H2-histamine receptor blockers cause atrophy or loss of gastric mucosa.  Nutritional deficiency  Hereditary defects of cobalamine utilization 25
  26. 26. COBALAMIN (VITAMIN B12) DEFICIENCY  Clinical manifestations  General symptoms of anemia  Sore tongue  Anorexia  Weakness  Parathesias of the feet and hands  Altered thought processes  Confusion  dementia 26
  27. 27. COBALAMIN DEFICIENCY DIAGNOSTIC STUDIES  RBCs appear large  Abnormal shapes  Structure contributes to erythrocyte destruction  Schilling Test: a medical investigation used for patients with vitamin B12 deficiency. The purpose of the test is to determine if the patient has pernicious anemia. 27
  28. 28. COBALAMIN DEFICIENCY  Collaborative Care  Parenteral administration of cobalamin  ↑ Dietary cobalamin does not correct the anemia  Still important to emphasize adequate dietary intake  Intranasal form of cyanocobalamin (Nascobal) is available  High dose oral cobalamin and SL cobalamin can use be used 28
  29. 29. FOLIC ACID DEFICIENCY  Folic Acid Deficiency also causes megablastic anemia (RBCs that are large and fewer in number)  Folic Acid required for RBC formation and maturation  Causes  Poor dietary intake  Malabsorption syndromes  Drugs that inhibit absorption  Alcohol abuse  Hemodialysis 29
  30. 30. FOLIC ACID DEFICIENCY  Clinical manifestations are similar to those of cobalamin deficiency  Insidious onset: progress slowly  Absence of neurologic problems  Treated by folate replacement therapy  Encourage patient to eat foods with large amounts of folic acid  Leafy green vegetables  Liver  Mushrooms  Oatmeal  Peanut butter  Red beans 30
  31. 31. THALASSEMIA  Etiology  Autosomal recessive genetic disorder of inadequate production of normal hemoglobin  Found in Mediterranean ethnic groups  Clinical Manifestations  Asymptomatic  major retardation  life threatening  Splenomegaly, hepatomegaly  No specific drug or diet are effective in treating thalassemia  Thalassemia minor  Body adapts to ↓ Hb  Thalassemia major  Blood transfusions with IV deferoxamine (used to remove excess iron from the body) 31
  32. 32. ANEMIA OF CHRONIC DISEASE  Underproduction of RBCs, shortening of RBC survival  2nd most common cause of anemia (after iron deficiency anemia  Generally develops after 1-2 months of sustained disease  Causes  Impaired renal function  Chronic, inflammatory, infectious or malignant disease  Chronic liver disease  Folic acid deficiencies  Splenomegaly  Hepatitis 32
  33. 33. APLASTIC ANEMIA  Characterized by Pancytopenia  ↓ of all blood cell types  RBCs  White blood cells (WBCs)  Platelets  Hypocellular bone marrow  Etiology  Congenital  Chromosomal alterations  Acquired  Results from exposure to ionizing radiation, chemical agents, viral and bacterial infections 33
  34. 34. APLASTIC ANEMIAEtiology  Low incidence - Affecting 4 of every 1 million persons  Manageable with erythropoietin or blood transfusion  Can be a critical condition  Hemorrhage  Sepsis Clinical Manifestations Gradual development Symptoms caused by suppression of any or all bone marrow elements General manifestations of anemia Fatigue/ Dyspnea, Pale skin Frequent or prolonged infections Unexplained or easy bruising Nosebleed and bleeding gums Prolonged bleeding from cuts Dizziness headache 34
  35. 35. APLASTIC ANEMIA  Treatment  Identifying cause  Blood transfusions  Antibiotics  Immunosuppressants (neoral, sandimmune)  Corticosteroids (Medrol, solu-medrol)  Bone marrow stimulants  Filgrastim (Neupogen)  Epoetin alfa (Epogen, Procrit)  Bone marrow transplantation 35
  36. 36. ANEMIA CAUSED BY BLOOD LOSS  Acute Blood Loss  Chronic Blood Loss 36
  37. 37. ACUTE BLOOD LOSS  Result of sudden hemorrhage  Trauma, surgery, vascular disruption  Collaborative Care 1. Replacing blood volume 2. Identifying source of hemorrhage 3. Stopping blood loss Chronic Blood Loss  Sources/Symptoms  Similar to iron deficiency anemia  GI bleeding, hemorrhoids, menstrual blood loss  Diagnostic Studies  Identifying source  Stopping bleeding  Collaborative Care  Supplemental iron administration 37
  38. 38. ANEMIA CAUSED BY INCREASED ERYTHROCYTE DESTRUCTION  Hemolytic Anemia  Sickle Cell disease  Acquired Hemolytic Anemia  Hemochromatosis  Polycythemia 38
  39. 39. HEMOLYTIC ANEMIA  Destruction or hemolysis of RBCs at a rate that exceeds production  Third major cause of anemia  Intrinsic hemolytic anemia  Abnormal hemoglobin  Enzyme deficiencies- G6PD deficiencies  RBC membrane abnormalities  Extrinsic hemolytic anemia  Normal RBCs  Damaged by external factors  Liver  Spleen  Toxins  Mechanical injury (heart valves) 39
  41. 41. ACQUIRED HEMOLYTIC ANEMIA  Causes  Medications  Infections  Manifestations  S/S of anemia  Complications  Accumulation of hemoglobin molecules can obstruct renal tubules  Tubular necrosis  Treatment  Eliminating the causative agent 41
  42. 42. SICKLE CELL ANEMIA  First described in Chicago in 1910 by James Herrick as an inherited condition that results in a decrease in the ability of red blood cells to carry oxygen throughout the body  A serious condition in which red blood cells can become sickle-shaped  Normal red blood cells are smooth and round. They move easily through blood vessels to carry oxygen to all parts of the body.  Sickle-shaped cells don’t move easily through blood. They’re stiff and sticky and tend to form clumps and get stuck in blood vessels.  The clumps of sickle cell block blood flow in the blood vessels that lead to the limbs and organs. Blocked blood vessel can cause pain, serious infection, and organ damage. 42
  43. 43. NORMAL AND SICKLE RED BLOOD CELLS IN BLOOD VESSELS 43 Figure A shows normal red blood cells flowing freely in a blood vessel. The inset image shows a cross-section of a normal red blood cell with normal hemoglobin. Figure B shows abnormal, sickled red blood cells clumping and blocking the blood flow in a blood vessel. The inset image shows a cross-section of a sickled red blood cell with abnormal strands of hemoglobin. Source from http://www.nhlbi.nih.gov/health/dci/Diseases/Sca/SCA_WhatIs.html
  44. 44. Genetics  2 copies of the gene for Hb (each parent)  HbS – Recessive  S=Sickle  A=Normal 44
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  46. 46. SIGNS AND SYMPTOMS  Individual signs and symptoms varies. Some have mild symptoms, others have very severe symptoms and may be hospitalized for treatment  Present at birth, many infants doesn’t show signs until after 4 months of age  Anemia: Fatigue (tiredness), pale skin and nail beds, jaundice, and shortness of breath  Pain (Sickle Cell Crisis): Sudden episode of pain throughout the body. Common sites: bones, lungs, abdomen, and joints. Lack of blood flow can cause pain and organ damage. 46
  47. 47. Medical Complications 1. pain episodes 2. strokes 3. increased infections 4. leg ulcers 5. bone damage 6. yellow eyes or jaundice 7. early gallstones 8. lung blockage 9. kidney damage and loss of body water in urine 10. painful erections in men (priapism) 11. blood blockage in the spleen or liver (sequestration) 12. eye damage 13. low red blood cell counts (anemia) 14. delayed growth 47
  48. 48. TREATMENT & PREVENTION  Taking the folic acid (folate) daily to help make new red cells  Drinking plenty of water daily (8-10 glasses for adults)  Identify what can trigger the “Crisis” such as stress, avoid extremes of heat and cold weather  Maintain healthy lifestyle habits  Eating healthy  Avoid dehydration  Exercise regularly  Get enough sleep and rest  Avoid alcohol and don’t smoke  Regular medical checkups and treatment are important 48
  49. 49. SIDEROBLASTIC ANEMIA  Sideroblastic anemias, a group of heterogeneous disorders, produce a common defect-failure to use iron in Hb synthesis, despite the availability of adequate irons stores.  Disease that interfere with production of heme. May be microcytic and hypochromic 49
  50. 50. ETIOLOGY  Hereditary  X- linked (isolated/ genetic syndrome) autosomal  Acquired  Drugs (chloramphenicol, isoniazid)  Heavy metals (e.g. lead)  Chemotherapeutics agents 50
  51. 51. SIGNS AND SYMPTOMS  Non specific clinical effects,  Anorexia, weakness, fatigue, dizziness, pale skin and mucous membrane and occasionally enlarged lymph node  Heart and liver failure may developed from excessive iron accumulation in these organs causing angina, slight jaundice and hepatosplenomegaly  Hereditary sideroblastic anemia is associated with increased GI absorption of iron causing sign of hemosiderosis. 51
  52. 52. TREATMENT  Hereditary sideroblastic anemia usually respond to several weeks treatment with high doses of pyridoxine 52
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  55. 55. REFERENCES  Advance text book on food & nutrition vol -2, Dr. M. Swaminathan  Davidsons principle and practice of medicine 22nd edition; Brian R. Walker, Nicki R. Colledge, Stuart H. Ralston, Ian D. Penman  Hematologic System, Oncologic Disorders & Anemias, Dr Ibrahreem Bashayreh, RN, PhD  Sickle cell anemia, Gregg Selke, Ph.D. 11/28/06  NDHS 2011 55
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  57. 57. CLASSIFICATION Anemias may be classified morphologically based on the average size of the cells and the hemoglobin concentration into: 1. Normochromic, normocytic anemia (normal MCHC, normal MCV).These include:  anemias of chronic disease  hemolytic anemias (those characterized by accelerated destruction of RBC's)  anemia of acute hemorrhage  aplastic anemias (those characterized by disappearance of RBCs precursors from the marrow) 2. Hypochromic, microcytic anemia (low MCHC, low MCV).These include:  iron deficiency anemia  thalassemias  anemia of chronic disease (rare cases) 3. Normochromic, macrocytic anemia (normal MCHC, high MCV).These include:  vitamin B12 deficiency  folate deficiency 57
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