Minerals Flashcards
Storage form of iron in liver, spleen, bone marrow, intestinal mucosa, pancreas, myocardium, and other tissues
More abundant storage form when the tissue stores are low
Ferritin
About 3-4g present in the body, 2/3 of which is in hemoglobin
Iron
Partially denatured derivatives of ferritin
Predominates when tissue stores are high
Hemosiderin
Iron transport protein in plasma
Transferrin
Most common micronutrient deficiency worldwide
When iron becomes scarce in the body:
- storage iron is mobilized first
- impairment of hemoglobin synthesis causes anemia
- impairment of iron- containing enzymes, impairing multiple cellular functions
⬇️ total plasma iron, ⬇️ transferrin saturation, ⬇️ serum ferritin, ⬆️ total iron binding capacity
Iron deficiency anemia
Iron overload syndrome with progressive hemosiderosis and resulting organ damage
May lead to liver cirrhosis, liver cancer, diabetes mellitus, cardiomyopathy, hyperpigmentation of the skin, endocrine disorders, and joint pain
Seen mainly in older men
⬆️ total plasma iron, ⬆️ transferrin saturation, ⬆️ serum ferritin, ⬆️ total iron binding capacity
Treated by repeated phlebotomy
Hemochromatosis
Most abundant trace mineral in the body after iron
Total body stores of about 1.5 to 2.5g
Constituent of the zinc metalloenzymes
- include carbonic anhydrase, cytoplasmic superoxide dismutase, alcohol dehydrogenase, carboxypeptidases A and B, DNA and RNA polymerases, and many others
In zinc finger proteins, it serves a structural role by stabilizing small loops in the polypeptide
Dietary sources: meat, nuts, beans, wheat germ
Zinc
Leads to dermatitis and poor wound healing, hair loss, neuropsychic impairment, decreased taste acuity, and, in children, poor growth and testicular atrophy
Zinc deficiency
Rare excessively inherited disease with dermatitis, diarrhea, and alopecia due to impaired intestinal zinc absorption
Treated with high doses of oral zinc
Unable to produce zinc
Acrodermatitis enteropathica
About 80-110mg in the adult human body
Major cofactor of enzymes that use either molecular oxygen or an oxygen derivative as one of their substrates
- cytochrome oxidase, dopamine B-hydroxylase, monoamine oxidase, tyrosinase,
Copper
Present with macrocytic hypochromic anemia, leukopenia, hemorrhagic vascular changes, bone demineralization, Hypercholesterolemia, and neurological problems
Seen in patients receiving total parenteral nutrition and in infants being fed copper-deficient formulas
Copper deficiency
X- linked recessive disorder caused by the deficient of an ATP-dependent membrane transporter for copper
Impaired transfer of copper from intestinal mucosal cells to the blood, and intracellular transport is abnormal as well
Growth retardation, mental deficiency, seizures, arterial aneurysms, bone demineralization, brittle hair
Kinky hair
Unable to absorb copper
Menkes syndrome
Hepatolenticular degenration
Intestinal absorption of copper is intact, but it’s biliary excretion is blocked
Copper accumulation in liver and brain, with resulting liver damage, neurological deterioration, or both
Kayser-Fleisher rings
Treated with D-penicillamine, which forms a soluble, excretable copper complex
Accumulation of copper on the liver and brain
Wilson disease
Stimulates the activity of many enzymes, but can be replaced by magnesium in most cases
MANGANESE
Manganese madness: excess can cause psychosis and Parkinsonism
Occurs in a few oxidase enzymes, including xanthine oxidase
Tx: allopurinol (gout)
Molybdnenum
