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Dr. Soban sadiq. Oral Therapy: Ferrous Sulphate Ferrous Fumarate Ferrous Gluconate Parenteral Therapy: Iron Dextran Iron-sucrose complex Iron sodium.

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Presentation on theme: "Dr. Soban sadiq. Oral Therapy: Ferrous Sulphate Ferrous Fumarate Ferrous Gluconate Parenteral Therapy: Iron Dextran Iron-sucrose complex Iron sodium."— Presentation transcript:

1 Dr. Soban sadiq

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3 Oral Therapy: Ferrous Sulphate Ferrous Fumarate Ferrous Gluconate Parenteral Therapy: Iron Dextran Iron-sucrose complex Iron sodium gluconate complex

4  Iron deficiency anemia in  Infants  Pregnant and lactating women  Children during rapid growth periods

5 Common adverse effects:  Nausea  Epigastric discomfort  Abdominal cramps  Constipation/diarrhea These effects are usually dose-related and can often be overcome by lowering the daily dose of iron or by taking the tablets immediately after or with meals Patients taking oral iron develop black stools; this has no clinical significance in itself but may obscure the diagnosis of continued gastrointestinal blood loss

6 Parenteral therapy should be reserved for patients who are unable to tolerate or absorb oral iron and for patients with extensive chronic blood loss.  Postgastrectomy conditions  Small bowel resection  Inflammatory bowel disease(proximal small bowel)  Malabsorption syndromes

7 Essential in two reactions: 1. Conversion of methylmalonyl-coenzyme A to Succinyl-CoA 2. Conversion of Homocysteine to Methionine The second reaction is linked to folic acid metabolism and synthesis of deoxythymidylate (dTMP) dTMP is a precursor for DNA synthesis

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10 In Vitamin B12 deficiency, folate accumulates as N-Methyltetrahydrofolate The supply of tetrahydrofolate is depleted This slows production of RBCs Folic acid replacement can correct B12 deficiency anemia, but not the neurological manifestation of B12 deficiency.

11 Absorption: Vitamin B12 binds to Intrinsic factor (secreted by gastric parietal cells) It prevents digestion of B12 In bound state,it binds to receptors on brush border of mucosa These receptors are located in ileum Bound intrinsic factor and B12 are absorbed with pinocytosis

12 DISTRIBUTION: Vitamin B12 is distributed to various cells bound to a plasma glycoprotein,Transcobalamin II STORAGE: Excess vitamin B12 (upto microgram) is stored in liver

13 ELIMINATION : Trace amounts of vitamin B12 are normally lost in urine and stool. Significant amount of vitamin B12 are excreted in urine (when large amounts are given parenterally)

14 ABOSRPTION: Form: Dietary folates in polyglutamate forms; first undergo hydrolysis by conjugase (present in brush border of intestinal mucosa) and form monoglutamate Site: Proximal jejunum Only modest amounts of folic acid are stored in body,therefore a decrease in diet will lead to anemia in few months

15 Distribution: Widely distributed through out the body via blood stream Storage: Normally, 5-20 mg is stored in liver and other tissues Elimination: Excreted in urine and stool, and also destroyed by catabolism

16 These are used in anemia (megaloblastic) Pernicious anemia ( Vitamin B12, basically IF) Prophylaxis for neural tube defects (folic acid before conception) Neuropathy (Vitamin B12) Cancer chemotherapy Certain drug therapies lead to deficiency of folic acid so replacement is requir ed

17 Tablet and syrup forms: Cyanocobalamin, Hydroxycobalamin Parenteral: I/M, I/V. Use:  To corrects major depletion of B12 quickly  If patient is unable to take orally  Required in patients with pernicious anemia(IF deficiency) Parenteral therapy can lead to pain at injection site

18 Both are very well tolerated There are no remarkable adverse effects of therapy

19  The side effect which primarily limits acceptability of oral iron therapy is  Black stools  Epigastric pain and bowel upset  Staining of teeth  Metallic taste

20  Choose the correct statement about iron therapy  Iron is given in megaloblastic anemia  Iron must be given orally except in pernicious anemia  Prophylactic iron therapy must be given during pregnancy  Infants on breast feeding do not require medicinal iron

21  A 23 year old pregnant woman is referred by her obstetrician for evaluation of anemia.If this woman has macrocytic anemia,an increased serum concentration of vitamin B12,the most likely cause of her anemia is deficiency of,  Cobalamin  Erythropoietin  Folic acid  Intrinsic factor  Iron

22  If the patient had folic acid deficiency,her infant would have a higher than normal risk of  Cardiac abnormality  Kidney damage  Limb deformity  Neural tube defect

23  A pregnant patient is found to have microcytic anemia.Optimal treatment of microcytic anemia is  A high fibre diet  Erythropoietin injections  Ferrous sulphate tablet  Folic acid supplements  Hydroxocobalamin injections

24  The iron stored in intestinal mucosal cells is complexed to  Intrinsic factor  Transcobalamin II  Transferrin  Ferritin

25  An important biochemical consequence of vitamin B12 deficiency is accumulation of  Dihydrofolate  dTMP  Folic acid  Tetrahydrofolate  Methyltetrahydrofolate

26  Mr. Abid, 25 years of age was suffering from chronic lethargy and weakness On examination he was very pale and he had signs of neuropathy as well. His Laboratory tests showed megaloblastic type of anemia. His physician performed Schilling’s test, which was positive. Choice of management would be:   Cyanocobalamin orally  Folic acid orally  Vitamin B12, I/V  Folic acid+Vitamin B12 orally  Intrinsic factor orally


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