Anemia. for nursing. student.ppt.pptx

Nursing College

1. A nemia Ph. Ali mohsin

2. defined as a reduction from normal of the quantity of haemoglobin in the blood. The WHOdefines anaemia in adults as haemoglobin levels less than 13 g/ dL for males and less than 12 g/ dL for females. The low haemoglobin level results in a corresponding decrease in the oxygen-carrying capacity of the blood.

3. causes • Increased haemoglobin loss due to either: – haemorrhage (red cell loss) or – haemolysis (red cell destruction). • Reduced haemoglobin synthesis due to either: – lack of nutrient or – bone marrow failure.

4. Microcytic anaemias iron deficiency anaemia anaemia of chronic disease sideroblastic anaemia Megaloblastic anaemias folate deficiency vitamin B12 deficiency Haemolytic anaemias autoimmune haemolytic anaemia sickle cell disease thalassaemia glucose-6-phosphate dehydrogenase deficiency

5. Clinical manifestation In its mildest form anaemia results in tiredness and lethargy; at its most severe it results in death unless treated. The reduced oxygen-carrying capacity of the blood leads to reduced tissue oxygenation and widespread organ dysfunction

6. investigation The most important parameter to assess anaemia is the haemoglobin concentration of the blood. It is also usual to count the number of red cells. In addition the size, shape and colour . The mean corpuscular volume (MCV) is a useful parameter that help determine the type of the anaemia .

7. Iron deficiency anaemia Iron deficiency anaemia is the commonest form of anaemia worldwide and may be present in up to 20% of the world's population .

8. etiology In Western societies, the commonest cause of iron deficiency is due to blood loss. In women of childbearing age, this is most commonly due to menstrual loss. Amongst adult males, the most likely cause is GI bleeding . Other causes of blood loss are haemorrhoids , nosebleeds or postpartum haemorrhage .

9. Clinical manifestation Patients at risk of heart failure may present with breathlessness when anaemic . A full blood count is an essential screening test. The cells of the peripheral blood are microcytic and hypochromic .

10. treatment The standard treatment is ferrous sulphate 200 mg two to three times a day. It typically takes between 1 and 2 weeks for the haemoglobin level to rise 1 g/ dL . Nausea or abdominal pains trouble some patients and this tends to be related to the dose of elemental iron .

11. Giving the iron with food makes it better tolerated but tends to reduce the amount absorbed. Alternative salts of iron are sometimes tried; these tend to have fewer side effects simply because they contain less elemental iron. A change in bowel habit is sometimes reported

12. There is a limited place for parenteral iron in iron deficiency anaemia ; it should be reserved for patients who fail on oral therapy . Patients who have lost blood acutely may require blood transfusions . There is a risk of anaphylactoid reactions with IV iron but the incidence appears to be lower with the newer products.

13. iron dextran, iron sucrose, iron III isomaltoside and ferric carboxymaltose should have a test dose . The dose for all products is calculated from the body weight and iron deficit . Iron dextran may also be given by deep intramuscular injection.

14. Anaemia of chronic disease Etiology Impaired response to erythropoietin and the inflammatory cytokines lead to a reduction in the availability of circulating iron. In malignancies,the cytotoxic treatments themselves decrease erythrocyte production through their anti-proliferative effects on the bone marrow.

15. treatment Treating the underlying chronic condition is important . A number of patients with chronic renal failure appear to have a functional iron deficiency that responds to intravenous iron . Intravenous iron in combination with erythropoietin analogues is widely used in chronic kidney disease.

16. Megaloblastic anaemias The two major causes are folate deficiency and vitamin B12 deficiency . Pernicious anaemia is a specific autoimmune disease that causes malabsorption of vitamin B12 due to a lack of intrinsic factor

17. etiology Folate deficiency anaemia dietary deficiency is common, either as the sole cause or in conjunction with increased folate utilisation . Vitamin B12 deficiency anaemia Deficiency occurs from inadequate intake or malabsorption . The only dietary source of vitamin B12 ( cyanocobalamin ) is from food of animal origin. It is present in meat, fish, eggs, cheese and milk .

18. treatment Folate deficiency anaemia Folate deficiency is usually managed by replacement therapy . The normal daily requirement of folic acid is approximately 100 μcg a day; despite this, the usual treatment doses given are 5–15 mg a day The folate requirement increases in pregnancy Folate deficiency regularly occurs in patients with a poor diet who do not take supplements .

19. Prophylaxis with folate (350–500 μcg daily) is now frequently given in pregnancy, often in combination with iron, starting before conception and during the first 12 weeks of pregnancy. It is important that these products with low doses of folate are not used to treat megaloblastic anaemia .

20. Vitamin B12 deficiency anaemia The majority of patients with vitamin B12 deficiency require lifelong replacement therapy The standard treatment is hydroxocobalamin 1 mg intramuscularly three times a week for 2 weeks then 1 mg every 3 months . Where there is neurological involvement , 1 mg on alternate days , until no further improvement then 1 mg every 2 months

21. High (1 mg) daily oral and sublingual doses of cyanocobalamin are absorbed in sufficient quantities to manage Pernicious anaemia

22. Haemolytic anaemias In the haemolytic anaemias , there is a reduced life span of the erythrocytes . Anaemia occurs when the rate of destruction of the erythrocytes exceeds their rate of production

23. Sickle cell anaemia Etiology Patients with sickle cell disease have a different form of haemoglobin . haemoglobin S ( Hb S). Normal haemoglobin is usually designated Hb A.

24. treatment prophylactic antibiotics. Administration of pneumococcal vaccine and Haemophilus influenzae vaccine is now common. Folic acid is commonly used because of the high turn over of red cells.

25. Attempts have been made to increase the proportion of haemoglobin F and reduce the proportion of haemoglobin S in the circulation . Hydroxycarbamide is effective and may reduce the frequency of crises but is limited by its cytotoxicity .

26. Sickle cell crises require prompt and effective treatment. Removal of the trigger factor, hydration and effective pain relief are the mainstays of treatment

27. Thalassaemias Etiology In α thalassaemia , there is either no α chain production (α0 thalassaemia ) or reduced production of a chain (α+ thalassaemia ). Similarly for β thalassaemia

28. Clinical manifestation The anaemia causes erythropoietin production to increase and results in expansion of the bone marrow. In severe disease, this causes bone deformity and growth retardation. The spleen is actively involved in removing the abnormal mature cells from the circulation and becomes enlarged.

29. treatment There is currently no effective treatment. Many patients with severe forms are dependent on blood transfusions from an early age. This inevitably leads to iron overload. Desferrioxamine , deferiprone and deferasirox are routinely needed for such patients Splenectomy helps some patients , and allogeneic stem cell transplant is used in severe cases

30. Glucose-6-phosphate dehydrogenase deficiency Etiology G6PD is essential for the production of (NADPH) in erythrocytes. If there is a deficiency in G6PD, this decreases the production of NADPH which is needed to keep glutathione in a reduced form. Reduced glutathione helps erythrocytes deal with oxidative stress

31. treatment Prevention of haemolysis by avoiding trigger factors ( drugs or food) is important

32. Drugs to be avoided in all variants Ciprofloxacin (and probably other quinolones ) Dapsone Methylene blue Primaquine (reduced dose may be used in milder variants) Nalidixic acid Sulphonamides (including co- trimoxazole ) Drugs to be avoided in more severe variants Aspirin (low dose used under supervision) Chloramphenicol Chloroquine (may be acceptable in acute malaria) Menadione Probenecid Quinidine Quinine (acceptable in acute malaria)

33. There is no specific drug treatment. During acute episodes, the patient should be kept well hydrated to ensure good urine output to prevent haemoglobin damaging the kidney. Blood transfusions may be necessary. Vitamin E (an antioxidant) appears to have little clinical benefit in preventing haemolysis .