Distribution of Iron
The human body requires iron, one of the metals. Functional and storage compartments comprise the total body iron content. The body recycles a large amount of iron between its storage and functioning pools.
1. Functional: Hemoglobin contains about 80% of the functional iron. Myoglobin and iron-containing enzymes (catalase, cytochromes a, and peroxidases) contain the remaining functional iron.
2. Storage: 15–25% of the iron in the body is in the storage pool. Because free iron can create free radicals, which can cause tissue damage, it is extremely hazardous.
The protein binds to iron, which is then stored. The distribution of iron (measured in milligrams) in young, healthy people's bodies about hemosiderin and ferritin. Iron storage for men and women can be easily mobilized when there is an increase in functional iron requirements, which might happen following blood loss (Hboglobin 2000–2500 1750). • Enzymes and myoglobin, third Three-quarters of the iron is kept as hemosiderin, and the remaining 350–400% is stored as ferritin. • Hemostasin and ferritin 500–1000 400.
• All tissues have ferritin, a protein-iron combination (apoferritin + iron), but the liver, spleen, bone marrow, and skeletal muscles contain most of it. Serum ferritin levels are extremely low, often ranging from 15 to 300 µg/L. Iron reserves are reflected in serum ferritin levels. When there is iron overload, the serum ferritin level can be as high as 5000 µg/L. In iron insufficiency, the level is often less than 12 µg/L. Ferritin is soluble in water and invisible under a light microscope.
Hemosiderin is a protein and iron aggregation that is present in the reticuloendothelial cells of the liver, spleen, and bone marrow. Staining Hemosiderin with standard Hematoxylin and Eosin yields golden yellow granules in the cell cytoplasm. Hemostain absorbs a blue-black hue when exposed to Prussian blue (Perl's) stain, which is caused by an iron-potassium ferrocyanide reaction. The majority of the iron in an iron overload is hemosiderin, which is kept in the cells.
Daily needs: For adult males, the daily need is 5–10 mg, while for females, it is 20 mg.
Food sources: Iron can be found in food either as nonheme iron found in plants or as heme iron found in animal products.
Absorption of Iron
• Site of absorption: The proximal jejunum and duodenum are where iron is absorbed. The primary mechanism for maintaining iron balance in the diet is controlling iron absorption.
• Absorption-influencing factors.
Iron Absorption's Molecular Aspect.
• Heme iron: Heme iron absorbs more readily than nonheme iron. Mostly found in the Fe3+ (ferric) state, nonheme iron is converted to Fe2+ (ferrous) iron by ferrireductases like duodenal cytochrome b.
– Divalent metal transporter 1 (DMT1) then carries Fe2+ iron over the brush border of the cytoplasmic membrane of the enterocyte (duodenal or jejunal epithelial cells).
• Heme transporters allow heme iron to cross the brush boundary of the enterocyte's cytoplasmic membrane and enter the cytoplasm.
Heme or nonheme iron that reaches the enterocyte's cytoplasm can either be transferred to the bloodstream or remain in the mucosa as iron reserves. Ferroportin-1 is responsible for moving Fe2+ iron from the cytoplasm into the bloodstream. Iron oxidase-like hephaestin, which is mostly expressed in enterocytes, is what links this process together by converting Fe2+ iron into Fe3+ form.
Note: Ferroportin and DMT1 are extensively distributed in the body and are also implicated in iron transport in other tissues.
Transportation of Iron
The iron transport protein transferrin, which is produced in the liver, is responsible for moving iron around in plasma. Delivering iron to erythroid precursors for the formation of hemoglobin is plasma transferrin's primary role. Normal humans have transferrin that is around 33% saturated with iron, with men's serum iron levels averaging 120 µg/dL and women's at 100 µg/dL. As a result, the serum's total iron-binding capacity falls between 310 and 340 µg/dL.
Iron Loss
Because the body uses and recycles iron so well, iron metabolism is special. Their iron excretion is not physiologically controlled, and 1 to 2 mg is lost daily by GI tract epithelial cell shedding.
Control of Iron Balance
While iron is necessary for cellular metabolism, too much of it can be extremely harmful. Consequently, appropriate regulation of the body's overall iron reserves is required. The primary method of achieving iron balance in the diet is to control iron absorption. Iron absorption increases as body storage declines and vice versa. The primary modulator of iron homeostasis, hepcidin is produced in the liver and regulates both absorption and storage. By attaching to ferroportin, hepcidin prevents iron from being transferred from the enterocyte to the plasma. Hepcidin causes iron to be stored in enterocytes, where it forms mucosal ferritin, which is then expelled along with the cells.
Why Iron Deficiency Anemia Occurs
Three stages of progressive development are associated with iron deficiency anemia.
Phase 1 (depletion of iron): Serum ferritin levels are the only ones that are reduced during the first phase, and iron levels may be sufficient to sustain normal hemoglobin levels.
Stage 2 (Iron deficient erythropoiesis): Without causing anemia (Hb, MCV, and MCH within normal range), the progressive depletion of iron reserves initially lowers serum iron and transferrin saturation levels. At this point, iron-deficient erythropoiesis is seen in bone marrow.
Stage 3 (iron deficiency anemia): Low serum iron, serum ferritin, and transferrin saturation are the only conditions that accompany reduced iron storage. Hemoglobin formation is hampered when the serum iron level drops and transferrin saturation falls below the crucial value of less than 15%. Red blood cells undergo morphological changes that cause them to first become smaller (microcytic) and then become paler in the center (hypochromic). Increasing the concentration of cytoplasmic hemoglobin normally inhibits normoblast division. Small erythrocytes, or microcytes, are produced during erythropoiesis when there is an iron deficit due to the failure of hemoglobin synthesis.
Clinical Characteristics
The anemia's clinical signs and symptoms are not particular. Presenting signs and symptoms are often associated with the underlying cause of the anemia (malnutrition, pregnancy, gastrointestinal or gynecologic disorders, and malabsorption) as well as the anemia itself.
• Beginning: It is subtle, with symptoms developing as anemia worsens. Patients get symptoms when their hemoglobin level drops below 7 g/dL.
• Nonspecific symptoms: The majority of patients report experiencing nonspecific symptoms such as weakness, palpitations, exhaustion, dyspnea, and agitation. When the anemia becomes more severe, these symptoms get worse.
• Pharyngeal/esophageal webs: At the point where the esophagus and hypopharynx (post-cricoid area) converge, folds (webs) of mucosa occur. Dysphagia, or trouble swallowing, is primarily caused by these webs with solid foods. Major discoveries in either Plummer-Vinson or Patterson-Brown-Kelly syndromes include the following three: - Microcytic hypochromic anemia
- Esophageal webs in middle-aged women; - Atrophic glossitis.
Premalignant mucosal abnormalities can result in the development of carcinoma at the location.
• Congestive heart failure: Patients who suffer from severe anemia may exhibit hyperdynamic circulation and congestive heart failure.
• Central nervous system: Manifestation of pica, an atypical need for certain non-nutritional items such as chalk or clay. The ice craving, or pagophagia, is thought to be the most distinctive sign of an iron shortage.
Physical Discoveries
• Angular stomatitis and glossitis: The tongue surface appears red, smooth, and waxy due to papillae atrophy. Angulatory stomatitis, or fissures and ulcerations at the mouth's angles, may occur.
• Chronic atrophic gastritis: This condition causes hypochlorhydria and is caused by atrophic alterations in the stomach mucosa.
• Koilonychia: This condition causes fingernails to become spoon-shaped, ridged, brittle, thin, and flattened (platynychia). This results from cells' loss of vital iron-containing enzymes.
