Iron Flashcards
What is the difference between heme and non-heme iron?
a) Heme iron is derived from hemoglobin and myoglobin and found in animal flesh while the non-heme form is found in plants and minimal amounts in dairy.
b) Heme iron is more efficiently absorbed than non-heme, 40% vs 10 -50% respectively.
c) Non-heme absorption varies depending on other dietary constituents.
D) factors that enhance non-heme absorption are vit c, HCL, lactic acid, and the acidic amino acids aspartic and glutamic acid.
What factors enhance non-heme absorption? How do they increase absorption?
Organic compounds that increase the acidity like Vit C, lactic acid, HCL,and acidic a.a aspartic and glutamic acids.
b) By maintaining the acidic environment, they compounds maintain iron in the ferrous form (Fe2+), which is more absorbable than the ferric form (Fe3+).
How does heme and non heme differ in terms of absorption?
After heme is removed from hemoglobin, it absorbed into the enterocytes and then hydrolyzed to ferrous (Fe2+). However, non-heme is released from food as ferric (fe3+) which is converted to Fe2+ via gastric acid in the stomach. Iron is absorbed in the duodenum and jejunum.
Note: Fe2+ is more absorbable than Fe3+.
What non dietary factors/conditions could lead to decrease iron absorption/iron deficiency?
Malabsorptive states like celiac disease, crohn’s disease, or pernicious anemia and during frank achlorhydria (absence of HCL).
Individuals with decreased HCL prod like aging are at high risk for absorbing less iron.
What dietary factors could reduced the absorption of nonheme iron absorption?
Dietary factors that reduce non heme iron by forming insoluble complexes are phytic acid in grain fiber, oxalic acid in spinach, chard, tea, and chocolate, polyphenols in coffee, tea and cocoa, and other nutrients like Ca, Zn, Mn.
B) Fe absorption may be competitively impaired when Zn or Mn supplements are provided via GI tract; these can contribute to compromise Fe status.
What ultimately determines the fate of iron after absorption? Describe how Iron is transported and stored in the body.
The extent of Iron stores in the body determines the how much Fe absorbed and its fate after absorption. Increased need of iron -> more transferrin receptors to bind iron -> increased transport of Fe in blood. When Fe stores are adequate, transferrin receptors site are saturated and transport of Fe in blood is inhibited. When Fe storage in the body exceeds ferritin storage, some of the ferritin is degraded to insoluble Fe -protein compound hemosiderin, which also acts as a storage site. These mechanism allow the body to control Fe absorption.
What happen when the body exceeds the storage capacity of ferritin?
Ferritin is degraded to the insoluble iron-protein compound hemosiderin,which also acts as an iron storage site.
Why is Iron transport in the blood inhibited following injury and infection? what happen to the iron if not transported in blood?
The sequestering of iron into storage form, Ferritin, following injury/infection is thought to be physiologically protective to the host. It reduces availability of iron for iron-dependent mircoorganisms proliferation, and reduces free radical production and oxidative damage to the membrane and DNA.
What are the functions of iron?
Iron is an essential component of hemoglobin, myoglobin, which is necessary for muscle iron storage, and a imp component of cytochromes, which are necessary for the oxidative production of cellular energy as ATP.
What are the good sources of Iron? what are the DRIs?
Meats, seafood, broccoli, peas,bran, enriched breads.
11/15 mg/d for 14-18 yr old M/F and 8/18 mg/d for all other groups M/F.
What conditions could happen as a result of iron deficiency and what are the symptoms?
Conditions are microcytic (abnormally small RBC) and hypochromic (decreased hemoglobin in RBC) anemia. Symptoms include tachycardia, fatigue, poor capillary refilling, impaired ability to maintain body temps in cold environments, decreased resistance to infection, impaired behavioral and intellectual performance, and increased lead absorption, and adverse outcomes during pregnancy.
Who are at risk for developing iron deficiency?
Women of childbearing age, individuals with malabsorption states like celiac, crohn’s disease, and gastric or intestinal surgery and those hospitalized with excess blood sampling or blood loss.
What hematological indices are measured in the assessment for iron depletion or deficiency?
Hemoglobin, plasma iron, iron binding capacity, ferritin, transferrin, erythropocyte protoporphyrin, transferrin receptor, and mean cell volume
What measures indicate early stages of iron deficiency and ultimately iron deficiency?
a) Decreased transferrin saturation-plasma iron/iron binding capacity, which is characterized by reduced plasma iron and elevated plasma transferrin.
b) If depletion continues, decreased ferritin.
c) Elevated levels of erythropocyte protoporphyrin but this measures has limitation bcuz it is altered when hemoglobin is blunted or in the presence of inflammation.
d) Iron deficiency is determine by a decreased mean corpuscular volume (MCV) and hemoglobin concentration.
What are the recommended treatment for iron deficiency? What are the common oral Fe preparation forms?
Recommended dose equivalent of 150 to 200mg of elemental iron/day. Common oral preparation are ferrous sulphate, gluconate, and fumarate but the preferred forms are ferrous sulphate and gluconate. Parenteral forms should only be considered if inadequate response to oral prep. They include iron dextran, Na ferric gluconate, and iron sucrose. Iron dextran is the preferable form.
