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Nutritional Deficiency Anemias
DR BINOD KUMAR SINGH Associate Professor, PMCH, Patna CIAP Executive board member- 2015 NNF State president,Bihar IAP State secretary,Bihar NNF State secretary,Bihar - Consultant Neonatologist & Pediatrician Shiv Shishu Hospital :K-208, P.C Colony.Hanuman Nagar, Patna – Web site :
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Anemia Definition Hemoglobin level is more than two standard deviation below the mean for childs age & sex -Cut off for Hb and hematocrit(WHO)
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Mechanisms of Anemia Marrow production defects (hypoproliferation)
Low reticulocyte count Little or no change in red cell morphology (a normocytic, normochromic anemia Red cell maturation defects (ineffective erythropoiesis) Slight to moderately elevated reticulocyte count Macrocytic or microcytic anemia Decreased red cell survival (blood loss/ hemolysis).
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Classification of anemias by MCV
Microcytic (<80 fL) Iron deficiency Thalassemia Anemia of chronic disease Macrocytic (>100 fL) Vitamin B12 deficiency Folate deficiency Myelodysplasia Chemotherapy Liver disease Increased reticulocytosis Myxedema Normocytic Anemia of chronic disease Aplasia Protein-energy malnutrition Chronic renal failure Post-hemorrhagic
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Initial Evaluation Signs: History/Symptoms Pallor, dark knuckles
Koilonychia Laboratory evaluation CBC with differential Peripheral Smear Reticulocyte count Iron Studies B12 level Serum/Folate level R/E of stool & urine History/Symptoms Pica Easy fatigue Poor concentration Dyspnea on exertion pallor Tingling and numbness in extremities Tinnitus Chest Pain Medications
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Nutrient Roles in Erythropoesis
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Iron Stores Humans contain ~2.5 g of iron, with g circulating as part of heme in hemoglobin Another ~0.3 g found in myoglobin, cytochromes, and Fe-S complexes Iron is stored in body primarily as protein complexes (ferritin and hemosiderin) Healthy newborn have body iron store of 250mg(80ppm) decreases to 60ppm in first 6month of life because milk is poor source of iron
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Nutritional Iron Balance
Intake Dietary iron intake Medicinal iron Red cell transfusions Injection of iron complexes Excretion Gastrointestinal bleeding Menses Losses can be as much as mg/menstrual cycle Other forms of bleeding Loss of epidermal cells from the skin and gut
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Iron Absorption Dietary iron content is closely related to total caloric intake (approximately 6 mg of elemental iron per 1000 calories) Iron bioavailability is affected by the nature of the foodstuff, with heme iron (e.g., red meat) being most readily absorbed Heme iron> Organic iron (Ferrous gluconate) > Inorganic iron (ferrous sulfate) Average iron intake in an adult male is 15 mg/d with 6% absorption; average female, the daily intake is 11 mg/d with 12% absorption Acid pH and presence of reducing agents: ascorbic acid (vitamin C) reduces Fe+++ to Fe++ which promotes passage across intestinal mucosa Vegetarians are at an additional disadvantage because certain foodstuffs that include phytates and phosphates reduce iron absorption by about 50% Takes place in the mucosa of the proximal small intestine Absorption increase to 20% in iron-deficient persons
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Dietary Sources of Iron
Red meat > poultry & fish Iron cooking pots Plants are generally not good sources because of oxalate, phytate, tannins, etc. Spinach has a lot of iron, but has ~780 mg oxalate/100 g Note - Heme iron absorption from diet not affected by ascorbate or phytate
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Iron Exchange 80% of iron passing through the plasma transferrin pool is recycled from broken-down red cells Absorption of about 1 mg/d is required from the diet in men, 1.4 mg/d in women to maintain homeostasis
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Iron Deficiency Anemia
Facts and Figures Most common cause of anemia 500 million cases worldwide Prevalence is higher in less developed countries Unique Physical Exam findings Cheilosis fissures at the corners of the mouth Koilonychia spooning of the fingernails
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Plummer vinson syndrome
Marrow iron store
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Causes of Iron Deficiency
Increased demand for iron and/or hematopoiesis Rapid growth in infancy or adolescence Pregnancy Erythropoietin therapy Increased iron loss Chronic blood loss Menses Acute blood loss Blood donation Phlebotomy as treatment for polycythemia rubra vera Decreased iron intake or absorption Inadequate diet Malabsorption from disease (sprue, Crohn's disease) Malabsorption from surgery (post-gastrectomy) Acute or chronic inflammation
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Iron Deficiency Anemia
Hypochromic red cell Microcytic cell Target cell
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Stages of Iron Deficiency
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Stages of Iron Deficiency
Stage 1: moderate depletion of iron stores; no dysfunction Stage 2: Severe depletion of iron stores; no dysfunction Stage 3: Iron deficiency Stage 4: Iron deficiency (dysfunction and anemia)
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Treatment of Iron Deficiency
Red Blood Cell Transfusion Oral Iron Therapy Ferrous sulfate Ferrous fumarate Ferrous gluconate Parenteral Iron
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Children Adults Elemental iron 3-6mg/kg/day, contd.. 4-6 months
Check Hb at 4 weeks Adults Ferrous sulphate/gluconate/fumarate Iron polymaltose complex Elemental iron 200mg/day Parentral Iron:-total dose-iron required(mg)=wt(kg)X2.3X(15-pt hb in gm/dl)+(500 to 1000mg)
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Indication for parentral iron therapy
Intolerance to oral iron. Malabsorption. Ongoing blood loss at a rate where oral replacement cannot match iron loss. Iv route is preferred over im route.
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Reasons for nonresponse to hematinic therapy for iron deficiency anemia
Poor compliance with therapy Poorly absorbed iron preparation Use of H2 blocker or PPI causing achlorhydria. Interaction with food and medication. Associated vit B12 or folic acid deficiency. Underlying hemolytic anemia inflammation or infection.
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Malabsorption eg- coeliac disease giardiasis,H pylori infection
High rate of ongoing blood loss. Alternative etiology eg- sideroblastic anemia.
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Diet for Iron Deficiency:
In adults, limit milk intake mL/day Avoid excess caffeine Eat iron-rich foods Protein foods Vegetables Meats Greens Fish & Shelfish Dried peas & beans Eggs Fruits Grains Dried fruit Iron-fortified breads Juices Dry cereals Most fresh fruits Oatmeal
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Iron Supplementation in special populations
Pregnant Women During the last two trimesters, daily iron requirements increase to 5 to 6 mg Infancy Normal-term infants are born with sufficient iron stores to prevent iron deficiency for the first 4–5 months of life Thereafter, enough iron needs to be absorbed to keep pace with the needs of rapid growth Nutritional iron deficiency is most common between 6 and 24 months of life
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Megaloblastic Anemia Due to impaired DNA synthesis
Affects cells primarily having relatively rapid turnover, especially hematopoietic precursors and gastrointestinal epithelial cells Cell division is sluggish, but cytoplasmic development progresses normally, so megaloblastic cells tend to be large, with an increased ratio of RNA to DNA. Megaloblastic erythroid progenitors tend to be destroyed in the marrow Marrow cellularity is often increased but production of red blood cells (RBC) is decreased
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Causes of Megaloblastic Anemia
Vitamin B12 Deficiency Inadequate intake: vegans (rare) Malabsorption Defective release of cobalamin from food Gastric achlorhydria Partial gastrectomy Drugs that block acid secretion Inadequate production of intrinsic factor (IF) Pernicious anemia Total gastrectomy Disorders of terminal ileum Sprue Regional enteritis Intestinal resection Competition for cobalamin Fish tapeworm (Diphyllobothrium latum) Bacteria: "blind loop" syndrome Drugs: p-aminosalicylic acid, colchicine, neomycin
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Clinical Manifestations of Vitamin B12 Deficiency
Hematologic Macrocytic Anemia Gastrointestinal Glossitis Anorexia Diarrhea Neurologic (found in 3/4th of individuals with pernicious anemia) Numbness and paresthesia in the extremities, Weakness, Ataxia Sphincter disturbances Disturbances of mentation Mild irritability and forgetfulness to severe dementia or frank psychosis. Demyelination, Axonal degeneration, and then Neuronal death Last stage is irreversible
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Megaloblastic Anemia Macrocytic RBC Hypersegmented Neutrophil
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Vitamin B12 Absorption – Oral Phase
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Vitamin B12 Absorption – Gastric Phase
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Vitamin B12 Absorption – Intestinal Phase
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Vitamin B12 Deficiency Any interruption along this path can result in cobalamin deficiency Gastrectomy results in low production of IF Terminal ileal resection (>100 cm), decreases the site of absorption of B12-IF complex
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Pernicious Anemia Most common cause of cobalamin deficiency
Caused by the absence of IF Atrophy of the mucosa Autoimmune destruction of parietal cells Seen in individuals of northern European descent and African Americans Men and women are equally affected Disease of the elderly, the average patient presenting near age 60
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Diagnosis of Vitamin B12 Deficiency
Macrocytosis Peripheral blood smear Cobalamin levels Elevated serum methylmalonic acid and homocysteine levels Schilling Test
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Schilling Test Measures B12 deficiency Detects IF deficiency
Detects abnormal results in patients with genetic defects in B12 absorption, bacterial overgrowth of the small bowel, resection/bypass of terminal ileum, and pancreatic insufficiency
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Stage 1 Oral dose of radiolabeled cobalamin given simultaneously with an IM injection unlabeled cobalamin 24 Hour Urine collection Amount radiolabeled activity is measured Normal absorption of B12 and normal renal function will excrete > 7% of radiolabeled B12
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Stage 2 If stage 1 is abnormal, then test is repeated following 60 mg of oral IF If the level of urinary radiolabeled B12 normalizes, then this indicates pernicious anemia
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Stage 3 Small intestine bacterial overgrowth may cause B12 malabsorption and an abnormal result in stage 1 that is not corrected with IF administration in stage 2 Broad spectrum antibiotics are given for one week to eliminate intestinal bacteria and then stage 1 should normalize
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Stage 4 If pancreatic insufficiency exists, B12 malabsorption may occur Normalization after pancreatic enzyme therapy suggests pancreatic origin
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Causes of Megaloblastic Anemia
Folate Deficiency Inadequate intake: unbalanced diet (common in alcoholics, teenagers, some infants) Increased requirements Pregnancy Infancy Malignancy Increased hematopoiesis (chronic hemolytic anemias) Chronic exfoliative skin disorders Hemodialysis Malabsorption Sprue Drugs: Phenytoin, barbiturates, (?) ethanol Impaired metabolism Inhibitors of dihydrofolate reductase: methotrexate, pyrimethamine, triamterene, pentamidine, trimethoprim Alcohol Rare enzyme deficiencies: dihydrofolate reductase, others
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Treatment of Vitamin B12 Deficiency
Replacement therapy ugm im Young children ugm since tremor & extrapyramidal toxicity Daily for 1-2week the weekly until Hct normal
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Folate Deficiency More often seen in malnourished than those with cobalamin deficiency Gastrointestinal manifestations More widespread and more severe than those of pernicious anemia Diarrhea is often present Cheilosis Glossitis Neurologic abnormalities do not occur
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Stages of folate deficiency
Negative folate balance (decreased serum folate) Decreased RBC folate levels and hypersegmented neutrophils Macroovalocytes, increased MCV, and decreased hemoglobin
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Diagnosis of folate deficiency
Peripheral blood and bone marrow biopsy look exactly like B12 deficiency Plasma folate <3 ng/ml—fluctuates with recent dietary intake RBC folate—more reliable of tissue stores, <140 ng/ml Only increased serum homocysteine levels but NOT serum methylmalonic acid levels
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Treatment of folate deficiency
Oral replacement therapy :1-5mg daily for 3-4wks Folate prophylaxis Women planning pregnancy are advised to take 400 micro gm folic acid daily before conception and until 12 weeks of pregnancy to prevent neural-tube defects (5 mg/day for women with a previous affected pregnancy) Prophylactic folate is also recommended in other states of increased demand such as long-term hemodialysis and chronic haemolytic disorders
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Inappropriate Treatment of Pernicious Anemia With Folate
Vitamin B12 deficiency anemia can be temporarily corrected by folate supplementation However, this does not correct the neurologic deficits Folate “draws” vitamin B12 away from neurologic system for RBC production and can exacerbate combined degeneration of cord
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