IRON DEFICIENCY ANEMIA

T.HARYANTO SURIJADI . dr ,SpPK

Definition: Iron deficiency anemia/IDA : Anemia resulting from a demand on stored iron greater than can be met Iron deficiency anemia/IDA : most frequently types of anemia in Indonesia. Clinical manifestation of IDA - similar to those of anemia in other hematologic syndrome and - depend on the degree of anemia present
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Condition may result IDA : 1.Nutritional deficiency ; not enough iron consume in daily diet. 2.Faulty or incomplete iron absorption eq : achlorhydria , following gastric resection, chronic diarrhea , resection small bowel, absence of factor needed for iron absorption. 3.Increase iron demand : during pregnancy, growth period, increase blood regeneration . 4.Excessive loss iron ; eg acute or chronic hemorrhage. 5.Another causes IDA ( less common ) : disorders of iron utilization, sideroblastic anemia, selected hemoglobinopathies, anemia causes chronic disorders, chronic inflammation , parasitic infection as hook worm, deficiency transferin (plasma protein for transport iron).

- HUMAN HAVE 35 50 gm IRON / kg BODY WEIGHT AVERAGE TOTAL IRON IN ADULT : MAN : 3,5 gr , WOMAN : 2,5 - 3 gr Normal iron loss very small --- eg < 1 mg /Day ( Through intestinal, skin cells, bile, urinary excretion .--TO COMPENSATE IT BODY NEED 1 mg/Day). ADDITIONAL IRON NEEDED DURING :
- GROWTH - PREGNANCY AND LACTATION - HEAVY MENSTRUAL BLOOD LOSS.
70 % IRON IS INCORPORATED INTO Hb MOLECULES AN IS RECYCLED 30 % NON ESSENTIAL.

STAGE OF IRON DEFICIENCY Laboratory test results help stage iron deficiency anemia. Stage 1 - Decreased bone marrow iron stores; Hb and serum iron remain normal - Serum ferritin level falls to < 20 ng/mL. - As compensatory increase in iron absorption causes an increase in ironbinding capacity (transferrin level). Stage 2 - Erythropoiesis is impaired. (Erythropoiesis is impaired when serum iron falls to < 50 g /dL and transferrin saturation < 16%). - Transferrin level is increased, the serum iron level decreases; - The serum ferritin receptor level rises (> 8.5 mg/L). Stage 3 Anemia with normal-appearing RBCs and start develops to microcytosis and hypochromia Stage 4 Microcytosis and then hypochromia develop. Stage 5 Iron deficiency affects tissues, resulting in symptoms and signs.

Symptoms Iron deficiency anemia is characterized by 1. PALLOR (reduced amount of oxyhemoglobin in skin or mucous membrane) 2.FATIGUE and WEAKNESS. Tends to develop slowly, adaptation occurs and the disease often goes unrecognized for some time. 3. DYSPNEA/ especially in severe cases. 4. PICA , Unusual obsessive food cravings. Pagophagia or Pica for ice is a very specific symptom and may disappear with correction of iron deficiency anemia. 5.HAIR LOSS AND LIGHT HEADEDNESS 6.OTHER SYMPTOMS : Constipation, Sleepiness , Tinnitus , Palpitations ,Seeing bright colors , Depression ,Breathlessness, twitching muscles ,tingling, numbness, or burning sensations ,Sleep apnea (rare) ,Missed menstrual cycle ,Heavy menstrual period,Sore or swollen tongue ,Koilonychia (spoon-shaped nails)

Diagnosis: 1.Symptoms and signs, but when anemia is mild it may not be diagnosed from mild non-specific symptoms. 2.A sufficiently low hemoglobin must be determine its cause and the exact diagnosis. Anemia is often first shown by routine blood tests, which generally include a Complete Blood Count(CBC) : RBC number : Hb, Ht, RBC count, RBC indices : MCV , MCHC, MCH Platelet count WBC count , WBC diff 3.Examination of a peripheral blood smear will narrow the diagnosis to a microcytic anaemia. The blood smear of a patient with iron deficiency shows many hypochromatic and rather small RBCs, and may also show poikilocytosis(variation in shape) and anisocytosis(variation in size). Microcytic anemia can also be the result of malabsorption phenomena associated with gluten-sensitive enteropathy/coeliac disease.

4.Supporting diagnosis of iron deficiency anemia : 1) appropriate history (e.g., anemia in a menstruating woman) 2) low serum ferritin 3) low serum iron level 4) elevated serum transferrin 5) high Total Iron Binding Capacity (TIBC). Serum Iron, Serum ferritin and TIBC essential lab test for determined iron deficiency anemia. Thalassemia Minor present with many of the same lab results. Important : not to treat a patient with Thalassemia with an iron supplement as this can lead to hemachromatosis (accumulation of iron in the liver). A hemoglobin electrophoresis would provide useful evidence in distinguishing these two conditions ( IDA or Thalassemia ).

GOLD STANDARD A definitive diagnosis requires a demonstration of depleted body iron stores by performing a bone marrow aspiration, with the marrow stained for iron. Bone marrow aspiration is invasive and painful, while a clinical trial of iron supplementation is inexpensive and non-traumatic, patients are often treated without a definitive diagnosis. DETERMINATION OF ETIOLOGY The diagnosis of iron deficiency anemia requires further investigation as to its cause--- sign of other disease, such as colon cancer, which will cause the loss of blood in the stool. In adults, 60% of patients may have underlying gastrointestinal disorders leading to chronic blood loss. Addition causes dietary insufficiency, malabsorption ,diversion of iron to fetal erythropoiesis during pregnancy, intravascular haemolysis and haemoglobinuria or other forms of chronic blood loss .

TREATMENT :
ORAL IRON SUPPLEMENTS. Usually with Ferro sulfate, ferrous gluconate, or iron amino acid
Women who develop iron deficiency anemia in mid-pregnancy : 20-40 mg per day. Search the lower dose effective and produces fewer gastrointestinal complaints. PARENTERAL e.g., as iron dextran Indication : -Patients who do not tolerate or who will not take oral iron -Patients who steadily lose large amounts of blood because of capillary or vascular disorders (eg, hereditary hemorrhagic telangiectasia). Adverse effects of partenteral iron : fever, chills, backache, myalgia, dizziness, syncope, rash, anaphylactic shock and secondary iron overload, thrombophlebitis, and pain.

How long ? Oral or parenteral iron therapy should continue for 6 months ( until 6 8 weeks after normal Hb/ after correction of Hb levels to replenish tissue stores). The response to treatment is assessed by serial Hb measurements until normal RBC values are achieved. Hb rises little for 2 wk but then rises 0.7 to 1 g/wk until near normal. Anemia should be corrected within 2 months. A subnormal response suggests continued hemorrhage, underlying infection or cancer, insufficient iron intake, or, very rarely, malabsorption of oral iron.

BIOAVAILABILITY. There can be a great difference between iron intake and iron absorption, also known as bioavailability. Iron absorption problems when iron is taken in conjunction with milk, tea, coffee and other substances. Solutions for this problem, including: Ascorbic acid, increases bioavailability in both presence and absence of inhibiting substances.

Ferritin : the storage form the iron in the tissue , which is found principally in the reticulo endothelial cells of the liver, spleen and bone marrow. Transferrin : A glycoprotein synthesized in the liver with the primary function of iron transport. Total iron binding cpasity : : (TIBC) : Transferrin is usually measured indirectly by the amount of iron that can find : this is referred to as the TIBC. Hemosiderin : An iron containing pigment derived from hemoglobin upon disintegration of red cells..It is one method where by iron is store until it is needed for making hemoglobin

The End

Iron Deficiency Anemia Iron transport and usage: Iron from intestinal mucosal cells is transferred to transferrin,( an iron-transport protein synthesized in the liver) transferrin can transport iron from cells (intestinal, macrophages) to specific receptors on erythroblasts, placental cells, and liver cells. Transferrin transports iron to the erythroblast mitochondria, which insert the iron into protoporphyrin for it to become heme. Synthesis of transferrin increases with iron deficiency but decreases with any type of chronic disease. Iron storage and recycling: Iron not used for erythropoiesis is transferred by transferrin, (an iron transporting protein) to the storage pool which has 2 forms, : 1.ferritin and 2.hemosiderin. The most important is ferritin (a heterogeneous group of proteins surrounding an iron core), which is a soluble and active storage fraction located in the liver (in hepatocytes), bone marrow, and spleen (in macrophages); in RBCs; and in serum. Iron stored in ferritin is readily available for any body requirement. Circulating (serum) ferritin level parallels the size of the body stores (1 ng/mL=8 mg of iron in the storage pool). Another storage pool of iron is in hemosiderin, which is relatively insoluble and is stored primarily in the liver (in Kupffer cells) and in the marrow (in macrophages). Because iron absorption is so limited, the body recycles and conserves iron. Transferrin grasps and recycles available iron from aging RBCs undergoing phagocytosis by mononuclear phagocytes. This mechanism provides about 97% of the daily iron needed (about 25 mg of iron). Iron deficiency: Deficiency develops in stages. In the first stage, iron requirement exceeds intake, causing progressive depletion of bone marrow iron stores. As stores decrease, absorption of dietary iron increases in compensation. During later stages, deficiency impairs RBC synthesis, ultimately causing anemia. Severe and prolonged iron deficiency also may cause dysfunction of iron-containing cellular enzymes.

5Iron

deficiency anemia is the most common type of anemia overall and it has many causes. RBCs often appear hypochromic (paler than usual) and microcytic (smaller than usual) when viewed with a microscope. Iron deficiency anemia is caused by insufficient dietary intake or absorption of iron to replace losses from menstruation or losses due to diseases.[2] Iron is an essential part of hemoglobin, and low iron levels result in decreased incorporation of hemoglobin into red blood cells. In the United States, 20% of all women of childbearing age have iron deficiency anemia, compared with only 2% of adult men. The principal cause of iron deficiency anemia in premenopausal women is blood lost during menses. Studies[who?] have shown that iron deficiency without anemia causes poor school performance and lower IQ in teenage girls. I ron deficiency is the most prevalent deficiency state on a worldwide basis. Iron deficiency is sometimes the cause of abnormal fissuring of the angular (corner) sections of the lips (angular stomatitis). Iron deficiency anemia can also be due to bleeding lesions of the gastrointestinal tract. Fecal occult blood testing, upper endoscopy and lower endoscopy should be performed to identify bleeding lesions. In men and post-menopausal women the chances are higher that bleeding from the gastrointestinal tract could be due to colon polyp or colorectal cancer. Worldwide, the most common cause of iron deficiency anemia is parasitic infestation (hookworm, amebiasis, schistosomiasis and whipworm).[3]