brief seminar on various ANEMIA SEMINAR.pptx

anemia

1. Case scenario 1 A 35 year old female presented with easy fatigue for 5 months. She is 24weeks pregnant with her 3 rd child 3years back. She does not visit any obstetrician and not taken any medication. She developed taste for eating ice and no other complaints. She doesn’t smoke or drink. Physical examination : pallor(+), spooning of nails (+) and systolic murmur at left lower sternal border. Lab values : CBC  7.1/5400/450*10 3 MCV  72fl ; RDW  17.1; MCH  25 Hematocrit  23% ; reticulocyte index  1.5 Vitamin B12, folate: normal LFT, RFT: normal, stool for occult blood: normal Hemolytic w/u : normal. Iron profile: S.ferritin 10, S.iron : 30, TIBC: 378. %SATURATION : 20%

2. Content Basic iron metabolism Factors effecting iron metabolism Causes of IDA Stages of IDA Clinical features Diagnosis of IDA (PBF and iron profile) Differential diagnosis Treatment of IDA Response assessment and follow up Prevention of IDA

3. Basic iron metabolism Total body iron stores 50mg/kg in male 40mg/kg in female Average intake of iron  10-20mg/day ( 10% is adsorbed) Iron form Percentage Hemoglobin 65% Myoglobin 3-4% Ferritin and hemosiderin 25% Transferrin iron 0.08% Individual Minimum daily requirement Adult male 1mg Adult female 2mg Pregannt 3mg Children 0.5mg

4. In the duodenal enterocyte, dietary iron is reduced to the ferrous state by duodenal ferric reductase ( Dcytb ) Transported into the cell by divalent metal transporter 1 (DMT1), and released by way of ferroportin into the circulation. Hephaestin facilitates enterocyte iron release. Hepatocytes take up iron from the circulation either as free iron or transferrin-bound iron (through transferrin receptor 1 and transferrin receptor 2). Transferrin receptor 2 may serve as a sensor of circulating transferrin-bound iron, thereby influencing expression of the iron regulatory hormone, hepcidin. The hepcidin response is also modulated by HFE and hemojuvelin . Hepcidin is secreted into the circulation, where it down-regulates the ferroportin -mediated release of iron from enterocytes, macrophages and hepatocytes.

5. Factors effecting iron metabolism Favorable factors Inhibitory factors Acidic pH Alkaline pH Heme iron Phytates ,tannins, oxalates Ferrous state Antacids Reducing agents Dietary calcium Ascorbic acid Soy protein

6. Causes of iron deficiency Increased demand for iron Rapid growth in infancy or adolescence Pregnancy Erythropoitein therapy Increased iron loss Chronic blood loss Menses Acute blood loss Blood donation Phlebotomy as treatment for polycythemia vera Decreased iron intake or absorption Inadequate diet Malabsorption from disease Malabsorption from surgery Acute or chronic inflammation

7. Symptoms of IDA Pagophagia Pica Beeturia Restless leg syndrome

8. DIAGNOSIS OF IDA

9. Differential diagnosis

10. Differential diagnosis

11. Management Prevention Dietary interventions Deworming Iron Supplementation in high risk groups Treatment Oral Iron Parenteral Iron Transfusion

12. Oral Iron: First line 200 mg elemental Fe daily Divided dosages ES/2-3 hours after food Not with tea/coffee/calcium 15 -20%%: GI effects Black stools: reassure patients 3-6 months of therapy If Compliance is an Issue advice with meals DOSE CALCULATION: 2.3 X BW X (Target HB-Patient’s Hb) + 500-1000 mg

13. Indications of parenteral Iron Poor adherence or GI side effects of oral iron Preferred to replace iron stores in one or two visits rather than course of several months On going blood loss that exceeds the capacity of oral iron to meet needs Anatomic or physiologic conditions that interfere with oral iron absorption Co existing inflammatory state that interferes with iron homeostasis

14. Precautions before giving Parenteral Iron Obtain consent Administer in the presence of a doctor No need for anti-histamine prophylaxis Steroid prophylaxis if H/O allergy/atopy or past h/o reaction (Hydrocortisone: 100 mg iv) Test dose in the form of initial slow infusion of around 5 ml Avoid in first trimester of pregnancy Keep adrenaline (1:10000 dilution) and IV hydrocortisone(100 mg) ready for anaphylaxis

15. Monitoring of response to therapy Earliest improvement seen in pagophagia when present with initiation of oral or IV iron therapy Improved feeling of well-being within few days Restless leg syndrome complete or near complete response within 72hrs Reticulocytotis will be seen after 1 st week Hb concentration will rise slowly and reach to normal levels at about 6-8weeks Iron is generally given until levels of transferrin saturation and ferritin normalizes

16. Case scenario 2 A 57 year old male patient presented to his physician with marked fatigue, nausea with occasional diarrhoea and sore and swollen tongue. Lately he also has been experiencing a tingling feeling in toes and feeling of clumsiness. He had h/o of partial gastrectomy at the age of 40years for morbid obesity on irregular vitamin b12 therapy. O/E he had pallor, red shiny beefy Tongue. There is no other significant physical findings: Lab findings CBC  8.4/ 7500/ 250*10 3 MCV  115fl ; reticulocyte index 2.0 PBF: megaloblatic RBC with hypersegmented neutrophils. Iron studies: normal, hemolytic w/u: normal Serum folate: 22 ng/l, VITAMIN B12: < 55 pg /l

17. Megaloblastic anemia Causes Vitamin B12 absorption and causes for deficiency Folate absorption and causes for deficiency Pathophysiology Clinical features Diagnosis Treatment

18. Causes of megaloblastic anemia Cobalamin deficiency Folate deficiency Therapy with antifolate drugs Other causes : some cases of AML, myelodysplasia Drugs interfering with DNA synthesis Orotic aciduria Thiamine responsive Copper deficiency

19. Vitamin B12 absorption Only source to humans from animal origin Daily requirement around 1-3 mcg /day Total body stores 2-3mg

20. Deficiency of vitamin B12

21. Folate absorption Richest source of folate : Spinnach Liver Yeast Nuts RDA of folic acid  100mcg Total body folate in adults  10mg

22. Causes for folate deficiency

23. Clinical features of vit B12 and folate deficiency Glossitis and angular cheilosis Anorexia, weight loss, diarrhea or constipation Anemia and related symptoms Jaundice,mild fever Personality changes Hyper homocysteinemia leads to CVA, CAD Skin hyperpigmentation

24. Neurological manifestations of Vit B12 Subacute combined degeneration of the dorsal (posterior) and lateral spinal columns Numbness Symmetric neuropathy legs>arms Severe weakness, spasticity, clonus, paraplegia Memory loss

25. Diagnostic work-up

26. Lab findings PBF Macro ovalocytic anemia with MCV > 100fl Reticulocytes, WBC & platelets normal to low, Hyper segmented neutrophils Serum vitamin B12 level (< 200pg/ml) Serum folate level (< 2ng/ml)

27. Treatment of B12 and folate deficiency First step is to diagnose whether it is isolated folate or B12 deficiency or combined deficiency. Vitamin B12 available in two forms cyanocobalamin, hydroxy cobalamine Folic acid available in either folate or folinic forms Oral (preferred) Parenteral(preferred) Asymptomatic anemia patients Dietary deficiency patients Severe anemia or neurological manifestations Malabsorption Increased demand (pregnancy and infancy) Long-term maintenance

28. Treatment of B12 and folate deficiency Replacement of body stores of vitamin b12 should be complete with 6 doses of inj hydroxycobalamin 1000mcg every week For maintenance therapy will give either hydroxycobalamin 1000mcg /3monthly or cyanocobalamin 1000mcg/ monthly. Life long therapy needed for individual with conditions that is not recovered Very rare cases of hypersensitivity or acneiform eruptions with vitamin B12 have been reported

29. Treatment of B12 and folate deficiency Folic acid: oral doses of 5 -15 mg folic acid daily for 4 months Before large doses of folic acid therapy we should rule out concomittent vitamin B12 deficiency. Long term folic acid therapy is required in conditions like chronic dialysis, hemolytic anemias, gluten induced enteropathy. Prophylactic folic acid will be given in pregnancy, infancy and childhood period Folinic acid will be given orally or parenterally in toxicity of methotrexate or other DHF reductase inhibitors.

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