iron deficiency anaemia.pptx

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IRON DEFICIENCY ANAEMIA:

IRON DEFICIENCY ANAEMIA BY Dr A RADHAKRISHNAN M.D PROF OF MEDICINE INSTITUTE OF INTERNAL MEDICINE MMC & RGGGH

PREVALENCE OF ANAEMIA (Increasing colour indicates increased frequency):

PREVALENCE OF ANAEMIA (Increasing colour indicates increased frequency )

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SOME NUMBERS

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The total body iron in a 70-kg man is about 4 g. This is maintained by a balance between absorption and body losses. Although the body only absorbs 1 mg daily to maintain equilibrium, the internal requirement for iron is greater (20-25 mg). An erythrocyte has a lifespan of 120 days so that 0.8% of red blood cells are destroyed and replaced each day . A man with 5 L of blood volume has 2.5 g of iron incorporated into the hemoglobin, with a daily turnover of 20 mg for hemoglobin synthesis and degradation and another 5 mg for other requirements. Most of this iron passes through the plasma for reutilization. Iron in excess of these requirements is deposited in body stores as ferritin or hemosiderin.

DIETARY IRON:

DIETARY IRON There are 2 types of iron in the diet; haem iron and non-haem iron Haem iron is present in Hb containing animal food like meat, liver & spleen Non-haem iron is obtained from cereals, vegetables & beans Milk is a poor source of iron, hence breast-fed babies need iron supplements

IRON ABSORPTION:

IRON ABSORPTION Haem iron is not affected by ingestion of other food items. It has constant absorption rate of 20-30% which is little affected by the iron balance of the subject. The haem molecule is absorbed intact and the iron is released in the mucosal cells.

IRON ABSORPTION (2):

IRON ABSORPTION (2) The absorption of non-haem iron varies greatly from 2% to 100% because it is strongly influenced by: The iron status of the body The solubility of iron salts Integrity of gut mucosa Presence of absorption inhibitors or facilitators

INHIBITORS OF IRON ABSORPTION:

INHIBITORS OF IRON ABSORPTION Food with polyphenol compounds Cereals like sorghum & oats V egetables such as spinach and spices Beverages like tea, coffee, cocoa and wine. A single cup of tea taken with meal reduces iron absorption by up to 11%.

OTHER INHIBITORS:

OTHER INHIBITORS Food containing phytic acid i.e. Bran, cereals like wheat, rice, maize & barely. Legumes like soya beans, black beans & peas. Cow’s milk due to its high calcium & casein contents.

INHIBITION-HOW?:

INHIBITION-HOW? The dietary phenols & phytic acids compounds bind with iron decreasing free iron in the gut & forming complexes that are not absorbed. Cereal milling to remove bran reduces its phytic acid content by 50% .

Promoters of Iron Absorption:

Promoters of Iron Absorption Foods containing ascorbic acid like citrus fruits, broccoli & other dark green vegetables because a scorbic acid reduces iron from ferric to ferrous forms, which increase s its absorption . Foods containing muscle protein enhance iron absorption due to the effect of cysteine containing peptides released from partially digested meat, which reduces ferric to ferrous salts and form soluble iron complexes.

IRON ABSORPTION (3):

IRON ABSORPTION (3) Some fruits inhibit the absorption of iron although they are rich in ascorbic acid because of their high phenol content e.g strawberry banana and melon. Food fermentation aids iron absorption by reducing the phytate content of diet

Mechanism of Iron absorption:

Mechanism of Iron absorption

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WHO IS AT RISK?

Risk factors in development of iron deficiency :

Risk factors in development of iron deficiency Age –Infants (especially if history of prematurity); adolescents; postmenopausal women; old age Sex –Increased risk in women Reproduction –Menorrhagia Drug histor y –Especially aspirin and non-steroidal anti-inflammatories Social history –Diet, especially vegetarians Physiological –Pregnancy; infancy; adolescence; breast feeding; age of weaning

AT RISK :

AT RISK

Causes of iron deficiency anaemia:

Causes of iron deficiency anaemia

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Elaboration of selected causes

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Dietary factors Meat provides a source of heme iron, which is less affected by the dietary constituents that markedly diminish bioavailability than nonheme iron is. The prevalence of iron deficiency anemia is low in geographic areas where meat is an important constituent of the diet. In areas where meat is sparse, iron deficiency is common

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Hemorrhage Bleeding for any reason produces iron depletion. If sufficient blood loss occurs, iron deficiency anemia ensues .A single sudden loss of blood produces a posthemorrhagic anemia that is normocytic. The bone marrow is stimulated to increase production of hemoglobin, thereby depleting iron in body stores. Once they are depleted, hemoglobin synthesis is impaired and microcytic hypochromic erythrocytes are produced. Maximal changes in the red blood cell (RBC) cellular indices occur in approximately 120 days, at a time when all normal erythrocytes produced prior to the hemorrhage are replaced by microcytes. Before this time, the peripheral smear shows a dimorphic population of erythrocytes, normocytic cells produced before bleeding, and microcytic cells produced after bleeding. This is reflected in the red blood cell distribution width (RDW); thus, the earliest evidence of the development of an iron-deficient erythropoiesis is seen in the peripheral smear, in the form of increased RDW.

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Two thirds of body iron is present in circulating red blood cells as hemoglobin. Each gram of hemoglobin contains 3.47 mg of iron; thus, each mL of blood lost from the body (hemoglobin 15 g/dL) results in a loss of 0.5 mg of iron Bleeding is the most common cause of iron deficiency , either from parasitic infection (hookworm) or other causes of blood loss. Patients report a history of bleeding from most orifices (hematuria, hematemesis, hemoptysis) before they develop chronic iron deficiency anemia; however, gastrointestinal bleeding may go unrecognized, and excessive menstrual losses may be overlooked.

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Malabsorption of iron Prolonged achlorhydria may produce iron deficiency because acidic conditions are required to release ferric iron from food. Then, it can be chelated with mucins and other substances (eg, amino acids, sugars, amino acids, or amides) to keep it soluble and available for absorption in the more alkaline duodenum. Starch and clay eating produce malabsorption of iron and iron deficiency anemia. Specific inquiry is required to elicit a history of either starch or clay eating because patients do not volunteer the information. Extensive surgical removal of the proximal small bowel or chronic diseases (eg, untreated sprue or celiac syndrome) can diminish iron absorption. Rarely, patients with no history of malabsorption have iron deficiency anemia and fail to respond to oral iron therapy. Most merely are noncompliant with therapy.

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CLINICAL FEATURES

ANGULAR CHEILITIS AND SMOOTH TONGUE+ IN IRON DEFICIENCY :

ANGULAR CHEILITIS AND SMOOTH TONGUE+ IN IRON DEFICIENCY

Pallor Depression:

Pallor Depression

Easy fatiguability:

Easy fatiguability

COMPLICATIONS:

COMPLICATIONS Iron deficiency anemia diminishes work performance by forcing muscles to depend on anaerobic metabolism to a greater extent than they do in healthy individuals. This change is believed to be attributable to deficiency in iron-containing respiratory enzymes rather than to anemia. Severe anemia due to any cause may produce hypoxemia and enhance the occurrence of coronary insufficiency and myocardial ischemia. Likewise, it can worsen the pulmonary status of patients with chronic pulmonary disease Plummer-Vinson syndrome Cold intolerance develops in one fifth of patients with chronic iron deficiency anemia and is manifested by vasomotor disturbances, neurologic pain, or numbness and tingling.

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Rarely, severe iron deficiency anemia is associated with papilledema, increased intracranial pressure, and the clinical picture of pseudotumor cerebri . These manifestations are corrected with iron therapy Impaired immune function is reported in subjects who are iron deficient Behavioral disturbances - Children deficient in iron may exhibit behavioral disturbances. Neurologic impairment in infants and scholastic performance is reduced in children of school age. The neurologic damage to an iron-deficient fetus results in permanent neurologic injury Low IQ -The intelligence quotients (IQs) of schoolchildren deficient in iron are reported to be significantly lower than those of their nonanemic peers.

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DIAGNOSIS OF IDA

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Hypochromic microcytic red cells

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Pencil Cell

Serum transferrin receptor and serum transferrin receptor log/ferritin index :

Serum transferrin receptor and serum transferrin receptor log/ferritin index sTfR reflects erythropoiesis and inversely the amount of iron available for erythropoiesis. Values of sTfR are elevated in IDA due to the upregulation of synthesis of transferrin receptors on the erythrocytes so the cells can compete for iron more efficiently. Unlike serum ferritin, sTfR concentrations are not affected by the presence of inflammation . The ratio between sTfR and serum ferritin concentrations, or sTfR-F index, is also considered a good indicator for evaluation of iron deficiency . The sTfR-F index was found to be a useful measure in classifying patients with ACD and coexistent IDA (80%) versus patients with pure ACD (20%). They also determined that sTfR-F index values of less than 2.2 mg/l excludes IDA, whereas values of more than 2.9 mg/l confirmed IDA. Yang et al . compared the plasma ferritin concentrations alone with the sTfR-F ratio in infants, school-aged children and pregnant women measuring plasma ferritin, sTfR and C-reactive protein (CRP). They concluded that iron status can be effectively measured using plasma ferritin concentrations alone, provided a biomarker such as CRP is also measured to avoid falsely elevated plasma ferritin secondary to concurrent inflammation .

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Normal serum iron- 9-27 micromol /L Normal TIBC -54-64 micromol /l Normal transferrin saturation- 25%-50% Normal serum ferritin males-100microgram/l females 30microgram/l

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ABSENT IRON STORES IN BONE MARROW IN IRON DEFICIENCY Iron deficiency Normal control

Zinc protoporphyrin/heme ratio :

Zinc protoporphyrin/heme ratio Evaluation of iron status using the ZPP/H is another diagnostic indicator of IDA diagnostic of early iron depletion . The ZPP/H ratio reflects iron status in the bone marrow during the formation of Hb . When iron supply is diminished, Zn utilization increases resulting in a high ZPP/H ratio . Das and Philip compared the utility of ZPP/H ratio as a diagnostic measure of IDA with bone marrow iron store aspirates. In tandem with Hb and red blood cell indices, ZPP was reliable in reflecting the bone marrow iron status except in the prelatent phase of iron deficiency; however, it lacked the ability to distinguish between ACD and IDA . As zinc is also influenced by inflammation , ZPP interpretation can be challenging .

Reticulocyte hemoglobin content {CHr} :

Reticulocyte hemoglobin content {CHr} CHr assesses the amount of Hb in reticulocytes Measurement of CHr provides a snapshot of iron immediately available for erythropoiesis over the previous 3-4 days , making it functional as an early indicator of iron stores. Blood CHr has also been identified as an early indicator of the response to parenteral iron therapy , increasing within 2-4 days if sequential measurements are observed

Newer diagnostic biomarkers: hepcidin :

Newer diagnostic biomarkers: hepcidin Hepcidin is considered a key regulator of iron metabolism; it regulates iron concentrations and tissue iron distribution via inhibition of intestinal iron absorption, iron reclamation by macrophages and iron mobilization from hepatic stores . Its production is decreased in IDA and increased during inflammation and iron overloading. The overproduction of hepcidin during an acute phase response results in reduced iron absorption, mobilization, or both, contributing to the disease of anemia Hepcidin levels have the potential to improve accuracy when differentiating between IDA and ACD.

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TREATMENT

Treatment:

Treatment The treatment of iron deficiency anemia is replenishment of body iron stores. However, the underlying cause should always be investigated before treatment is begun, Oral Administration The preferred route of iron administration is oral. Oral iron is most readily absorbed in the absence of food ,. The major obstacle to oral iron replacement is unacceptable side effects, chiefly epigastric discomfort or nausea, although diarrhea or constipation also occurs in some patients. Reducing the dose often eliminates nausea and epigastric discomfort. Despite the development of a number of orally effective iron-containing compounds, the original salt, ferrous sulfate (325 mg three times daily), remains the most useful. Although some newer oral iron preparations, such as ferrous gluconate (300 mg two or three times daily ) or ferrous fumarate (325 mg two or three times daily) may induce less GI side effects per milligram of iron, they are also less well absorbed, so there is no net advantage to these costlier formulations except for patients who cannot tolerate ferrous sulfate.

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Given both the low toxicity and the low cost of oral iron replacement, a therapeutic trial is a complementary means for confirming a diagnosis of iron deficiency anemia

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The treatment of IDA should include a strategy for measuring response to iron therapy. Historically, a 2g/dl improvement in Hb levels has been considered an appropriate response to iron supplementation . When refractory IDA is nonresponsive to oral iron therapy, H. pylori infection and chronic gastritis are often to blame. The eradication of H. pylori is warranted to maximize oral iron therapy in the recovery from IDA

Other causes of poor response to oral iron:

Other causes of poor response to oral iron

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Parenteral Administration In situations in which primary blood loss is uncontrollable, iron cannot be absorbed due to severe malabsorption, or oral iron is not tolerated despite concerted efforts to minimize side effects, parenteral iron is an effective alternative treatment. Intramuscular dosing is limited to 100 mg per injection, so intravenous (IV) administration of iron is recommended. Sodium ferric gluconate (given intravenously as a 125-mg dose over 10 minutes ) is the preferred form of parenteral iron for routine use due to the low incidence of adverse reactions.. One limitation of serum ferric gluconate is that the maximum dose that can be delivered in a single injection is approximately 125 mg, and a total dose of 500 to 2000 mg is usually required for adequate repletion. Although iron dextran can be used to deliver very large doses of iron in a single IV injection, it is currently reserved for situations in which rapid iron replacement is required, because of the life-threatening anaphylactic and delayed adverse reactions that occur in 0.6% and 2.5% of cases, respectively. If iron dextran is to be given intravenously, premedication with diphenhydramine and a slow test dose injection of 30 to 40 mg diluted in normal saline is recommended.

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The response to iron repletion therapy is usually quite rapid, with elimination of symptoms within a few days. Increased reticulocytosis usually begins within 4 to 5 days, and the hemoglobin level often rises within 1 week and reaches a normal level after 6 weeks of therapy if adequate iron replacement is achieved. The goal of therapy, which is to reach a serum ferritin level of greater than 50 mg/L , usually takes 4 to 6 months. Therapy must be continued after adequate replacement is achieved if the underlying cause of iron deficiency is not reversible. Because of the avidity of transferrin receptor–rich erythroid precursors for transferrin-bound iron, the serum ferritin level usually will not rise until hemoglobin levels reach normal. An incomplete response, as determined by failure to normalize the hemoglobin level, usually means either that iron replacement has not been adequate or that another condition, such as anemia of chronic disease, is coexistent

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Parenteral iron sucrose Intravenous iron sucrose is approved to treat anemia related to chronic kidney failure (CKF). However, minimal data exist on using i.v. iron sucrose infusions inpatients without CKD.

When to transfuse:

When to transfuse Severe symptoms of anaemia Cardiovascular insufficiency Continued excessive blood loss AIM- to stabilise the patient while cause is being worked up

Prevention :

Prevention Certain populations are at sufficiently high risk for iron deficiency to warrant consideration for prophylactic iron therapy. These include pregnant women, women with menorrhagia, consumers of a strict vegetarian diet, infants, adolescent females, and regular blood donors. Pregnant women have been given supplemental iron since World War II, often in the form of all-purpose capsules containing vitamins, calcium, and iron. If the patient is anemic (hemoglobin < 11 g/dL), administer the iron at a different time of day than calcium because calcium inhibits iron absorption. The practice of routinely administering iron to pregnant females in affluent societies has been challenged; however, it is recommended to provide prophylactic iron therapy during the last half of pregnancy, except in settings where careful follow-up for anemia and methods for measurement of serum iron and ferritin are readily available. Iron supplementation of the diet of infants is advocated. Premature infants require more iron supplementation than term infants. Infants weaned early and fed bovine milk require more iron because the higher concentration of calcium in cow milk inhibits absorption of iron. Usually, infants receive iron from fortified cereal. Additional iron is present in commercial milk formulas. Iron supplementation in populations living on a largely vegetarian diet is advisable because of the lower bioavailability of inorganic iron than heme iron. The addition of iron to basic foodstuffs in affluent nations where meat is an important part of the diet is of questionable value and may be harmful. The gene for familial hemochromatosis ( HFe gene) is prevalent (8% of the US white population). Excess body iron is postulated to be important in the etiology of coronary artery disease, strokes, certain carcinomas, and neurodegenerative disorders because iron is important in free radical formation.

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