Iron Flashcards
Gut Involvement in Iron Metabolism
Decrease stomach pH solubilizes Fe-containing compounds
Transport molecules facilitate absorption into blood
Blood Involvement of Iron Metabolism
Fe3+ bound to Transferrin and transported to tissues
- Maintains solubility
- Keeps Fe unreactive
Cells Involvement with Iron Metabolism
Transferrin endocytosis is receptor mediated
Results in Fe3+ release
Fe distributed in cells
Usage of Iron in Cells
Protein components (Heme)
Storage of Iron in Cells
Ferritin (Fe2+)
Excess Iron in cells
Causes toxicity
Normal Iron Ranges
55-160 ug/dL (Male)
40-155 ug/dL (Female)
Total Iron Binding Capacity
Sites on transferrin saturated with iron
Reference range: 255-450 ug/dL
Percent transferrin saturation
20-50%
Increased Total Iron Binding Capacity
Situations that cause increase in transferrin
- Late pregnancy
- Iron deficiency anemia (compensation)
- Acute hemorrhage
- Acute destruction of liver cells
Decreased Serum Iron
Dietary deficiency or malabsorption
Loss of iron (blood loss or late pregnancy)
Impaired release of stored iron
Decreased Total Iron Binding Capacity
Decreased synthesis of Transferrin
Increased loss of protein as in renal disease
Total Serum Iron Principle of Assay
Dissociate ferric iron from transferrin and reduce to ferrous form
Iron + Color Reagent = Color Change
TIBC Principle of Assay
Saturate transferrin with ferric iron
Remove excess free iron from reaction tube
Dissociate ferric iron from transferrin and reduce to ferrous form
Measure iron as in total serum iron procedure
Calculation for % Saturation
(Serum Iron/TIBC) x 100
Other forms of Iron
Ferritin
Transferrin
Hemosiderin
Hemochromocytosis
Ferritin
Tissue Storage form
Sensitive indicator of Iron Deficiency Anemia
Transferrin
Transport molecule for iron
Hemosiderin
Insoluble iron deposits in tissue and bone marrow
Hemochromocytosis
Excess iron deposition in tissues
Defective iron control
Multiple transfusion
Ceruloplasm
Alpha-2-glycoprotein
Enzyme with 6 Cu atoms
Carries >95% of total Cu in plasma
Participates in conversion of ferrous iron to ferric iron
Works in association with transferrin after release from RES
Wilson’s Disease
Autosomal recessive disorder
Causes Cu buid-up in tissues
Genetic defect of Cu-ATPase ATP7B
Cu incorporation into ceruloplasmin is diminished
Wilson’s Disease Symptoms
Cirrhosis
Kayser-Fleischer rings in cornea
May cause brain and kidney damage from Cu deposition
Kayser-Fleischer rings
Ring of golden-brown or brownish-green pigment behind the limbic border of cornea
Porphyrin Derivatives
4 Tetrapyrrole ring linked by methane bridges
Oxidative compounds of Porphyrins
Hemoglobin
Myoglobin
Vitamin B12
Chlorophyll
Cytochromes
Porphyrin ring
Metal chelates
Hgb = Iron
Myoglobin = Iron
Vit B12 = Cobalt
Chlorophyll = Magnesium
Cytochromes = Cu & Fe
Three Clinically Significant Porphyrins
Uroporphyrins (URO)
Coprophyrins (COPRO)
Protoporphyrins (PROTO)
Uroporphyrins
8 Carboxyl groups
Highly soluble because of large number of -COOH side chains
Excreted primarily in urine
Soluble in blood & tissues
Coproporohyrins
4 carboxyl groups
Demonstrates intermediate solubility
Excreted primarily in feces but also appears in urine
Protoporphyrins
2 carboxyl groups
Least soluble
Located primarily within erythrocytes
Excreted only in feces
Most soluble in lipid solvents
Biosynthesis of Porphyrins
Intermediate products in heme biosynthesis
Have no role in body function in free form
Appear in tissue and body fluids only as an abnormality in enzyme function
Lead Toxicity
Binds to any compound with a sulhydryl group
Inhibits multiple enzymes in heme biosynthesis
Get elevations in delta ALA
Lead Toxicity Test
Whole blood screening is the test of choice
Hair analysis for lead concentration is alternative marker for exposure
Other heavy metals & organic solvents poisoning
Have been associated with porphyria
