Unit 12: Trace Minerals and Nutrients for Blood Health Flashcards

1
Q

For Vitamin K:

Identify the functions of vitamin K in the body.

A

The primary role of vitamin K is in blood clotting. It is involved in the synthesis of blood‑clotting proteins, one of which is prothrombin. It is also involved in synthesis of bone proteins.

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2
Q

For Vitamin K:

Describe the prevalence of deficiency and its associated symptom.

A

Primary vitamin K deficiency in humans is rare because of intestinal vitamin K synthesis. Mixed diets contribute more than adequate amounts of vitamin K, and the vitamin is stored in the liver. However, vitamin K deficiency may be seen in

  • people on long‑term antibiotic therapy;
  • newborn infants
  • people suffering fat malabsorption caused by bile obstruction or pancreatic insufficiency.

The symptom of vitamin K deficiency is very specific—the inability of blood to clot. Upon injury, hemorrhages can occur internally as well as externally, and if vitamin K is severely deficient, uncontrolled bleeding can lead to death.

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3
Q

For Vitamin K:

Describe the toxicity symptoms.

A

Vitamin K toxicity is also rare. No adverse effects have been reported with high intakes of vitamin K and consequently a UL has not been set.

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4
Q

For Vitamin K:

List some of its major food sources.

A

Major food sources of vitamin K are green leafy vegetables, such as spinach, kale, turnip greens, cabbage, and broccoli.
Dairy products, eggs, and whole grains are also good sources.
Most fruits and non‑leafy vegetables are poor sources, as are highly refined foods.
Bacterial synthesis in the digestive tract

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5
Q

Classify the general functions of trace minerals in the body.

A
  1. Catalytic roles: Many trace minerals serve as cofactors for enzymatic reactions. As coenzymes, they work with enzymes to facilitate chemical reactions. An example is zinc, which functions in DNA and RNA polymerase during cell division and growth.
  2. Structural roles: Some trace minerals are integrated into the structure of specific molecules or types of tissue. Since many of these molecules or tissues have regulatory functions, the trace mineral exerts its effect in this manner.
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6
Q

Briefly describe the absorption, transport, and excretion of trace minerals

A

Absorption: absorption of trace minerals is generally regulated at the mucosa of the small intestine. It depends greatly on the physiological need. Oxalic and phytic acids can interfere with the absorption of trace minerals by binding with them to form insoluble complexes. Nutrient interactions can also affect the absorption of trace minerals.
Transportation: trace minerals are transported by binding to protein carriers, which may be specific (e.g., transferrin for iron) or general (e.g., albumin). Specific protein carriers are usually only about 30% saturated; the remaining capacity is reserved to buffer excesses of the minerals. After this buffering capacity is exhausted, toxicity results.
Excretion: The excretion of trace minerals—if any—is generally through feces, urine, shed cells, bile, and menses. Some losses may occur in sweat and breath, especially in hot climates.

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7
Q

Describe the distribution and functions of iron in the body

A

Three to five grams of iron are distributed throughout the body of healthy adults. Of this, about 70–80% is found in hemoglobin with the remainder in myoglobin, body stores, and iron‑containing enzymes. The major storage sites of iron are the liver, the spleen, and the bone marrow.

The iron in the body can be divided into two forms:

  1. Functional iron serves a metabolic role (in hemoglobin and myoglobin) or an enzymatic role (in enzymes containing iron as cofactor).
  2. Stored iron is found in ferritin and hemosiderin.

Functions of iron:
Oxygen transport from lungs to body tissues.
Cellular respiration during the process of energy production.
Other functions.

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8
Q

Describe how iron is absorbed

A

Special proteins help the body absorb iron from food. The iron-storage protein ferritin captures iron from food and stores it in the cells of the small intestine. When the body needs iron, ferritin releases some iron to an iron transport protein called transferrin. If the body does not need iron, it is carried out when the intestinal cells are shed and excreted in the feces; intestinal cells are replaced about every three to five days. By holding iron temporarily, these cells control iron absorption by either delivering iron when the day’s intake falls short or disposing of it when intakes exceed needs.

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9
Q

Describe how iron is transported

A

The blood transport protein transferrin delivers iron to the bone marrow and other tissues. The bone marrow uses large quantities of iron to make new red blood cells, whereas other tissues use less. When dietary iron has been plentiful, ferritin is constantly and rapidly made and broken down, providing an ever-ready supply of iron.

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10
Q

Describe how iron is stored

A

Surplus iron is stored in the protein ferritin, primarily in the liver, but also in the bone marrow and spleen. When iron concentrations become abnormally high, the liver converts some ferritin into another storage protein called hemosiderin. Hemosiderin releases iron more slowly than ferritin does. Storing excess iron in hemosiderin protects the body against the damage that free iron can cause. Free iron acts as a free radical, attacking cell lipids, DNA, and protein.

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11
Q

Describe how iron is recycled

A

The average red blood cell lives about four months; then the spleen and liver cells remove it from the blood, take it apart, and prepare the degradation products for excretion or recycling. The iron is salvaged: the liver attaches it to transferrin, which transports it back to the bone marrow to be reused in making new red blood cells. Thus, although red blood cells live for only about four months, the iron recycles through each new generation of cell

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12
Q

Describe how the body maintains iron balance

A

Maintaining iron balance depends on the careful regulation of iron absorption, transport, storage, recycling, and losses. The hormone hepcidin is central to the regulation of iron balance.9 Produced by the liver, hepcidin helps to maintain blood iron within the normal range by limiting absorption from the small intestine and controlling release from the liver, spleen, and bone marrow. Hepcidin production increases in iron overload and decreases in iron deficiency

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13
Q

Describe the symptoms of iron deficiency

A

Anemia: weakness, fatigue, headaches; impaired work performance and cognitive function; impaired immunity; pale skin, nail beds, mucous membranes, and palm creases; concave nails; inability to regulate body temperature; pica

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14
Q

Define Iron Deficiency

A

The state of having depleted iron stores.

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15
Q

Define Iron Deficiency Anemia

A

Severe depletion of iron stores that results in low hemoglobin and small, pale red blood cells. Anemias that impair hemoglobin synthesis are microcytic (small cell).

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16
Q

Identify the biochemical tests used to determine iron deficiencies and anemia.

A

In the first stage of iron deficiency, iron stores diminish. Measures of serum ferritin (in the blood) reflect iron stores and are most valuable in assessing iron status at this earliest stage. Unfortunately, serum ferritin increases with infections, which interferes with an accurate diagnosis and estimate of prevalence.
The second stage of iron deficiency is characterized by a decrease in transport iron: serum iron falls, and the iron-carrying protein transferrin increases (an adaptation that enhances iron absorption). Together, measurements of serum iron and transferrin can determine the severity of the deficiency—the more transferrin and the less iron in the blood, the more advanced the deficiency is. Transferrin saturation decreases as iron stores decline.
The third stage of iron deficiency occurs when the lack of iron limits hemoglobin production. Now the hemoglobin precursor, erythrocyte protoporphyrin, begins to accumulate as hemoglobin and hematocrit values decline.
Hemoglobin and hematocrit tests are easy, quick, and inexpensive, so they are the tests most commonly used in evaluating iron status. Their usefulness in detecting iron deficiency is limited, however, because they are late indicators. Furthermore, other nutrient deficiencies and medical conditions can influence their values.

17
Q

Describe the causes and effects of iron overload.

A

The iron overload disorder known as hemochromatosis is usually caused by a genetic failure to prevent unneeded iron in the diet from being absorbed. Some of the signs and symptoms of iron overload are similar to those of iron deficiency: apathy, lethargy, and fatigue.
Iron overload is characterized by tissue damage, especially in iron-storing organs such as the liver. Infections are likely because viruses and bacteria thrive on iron-rich blood.
Symptoms are most severe in alcohol abusers because alcohol damages the small intestine, further impairing its defenses against absorbing excess iron. Untreated hemochromatosis increases the risks of diabetes, liver cancer, heart disease, and arthritis Treatment involves iron-chelation therapy. Chelation therapy uses a compound to sequester a toxic substance, rendering it inactive or less harmful.
Iron overload is much more common in men than in women
Toxicity Symptoms:
GI distress
Iron overload: infections, fatigue, joint pain, skin pigmentation, organ damage

18
Q

Describe the forms of dietary iron and their sources

A

There are two forms of iron in foods: heme iron and non‑heme iron. Bound in hemoglobin and myoglobin, heme iron makes up about 40% of the total amount of iron in animal tissues. The remaining 60% is non‑heme iron and consists of ionized iron (Fe+++ or Fe++) or ferritin iron found in tissues.

The heme portion of the hemoglobin molecule is absorbed intact by the mucosal cells. Once inside a cell, iron is released, then transported across the cell to be picked up by the plasma transferrin and delivered to other body cells.
Heme iron is absorbed as a heme complex; therefore, it is not affected by enhancing or inhibiting factors in the diet. The absorption is relatively high, at a constant rate of about 25%. The major sources are meat, fish, and poultry.

The major part of dietary iron is non‑heme iron (ferrous and ferric). It is found in the non‑heme portion of meats, fruits, vegetables, cereals, eggs, dairy products, iron added to foods as part of enrichment programs, and iron found in mineral supplements. Non‑heme iron can become bound to binding agents such as phytates; thus, non‑heme iron has lower bioavailability than does heme iron.

19
Q

Identify the dietary factors that enhance and inhibit iron absorption.

A

Factors that inhibit nonheme iron absorption:
• Phytates (legumes, grains, and rice)
• Vegetable proteins (soybeans, legumes, nuts)
• Calcium (milk)
• Tannic acid (and other polyphenols in tea and coffee)
Factors that enhance nonheme iron absorption:
• MFP factor
• Vitamin C (ascorbic acid)
• Acids (citric and lactic)
• Sugars (fructose)

20
Q

Identify the major functions of zinc in the body

A

The main role of zinc is as the cofactor for over 100 enzymes. Some of the major functions are

  • -DNA and RNA synthesis. Zinc is required for growth, for wound healing, and, especially in males, for sexual maturation.
  • -Vitamin A metabolism. Zinc is required in the mobilization of stored vitamin A from the liver when dietary vitamin A is low. Night blindness can result from zinc deficiency.
  • -Insulin synthesis. Zinc is a structural component of insulin. It also seems to be involved in the storage and release of insulin.
  • -Taste and appetite. Zinc deficiency can cause a decrease of taste acuity and loss of appetite.
  • -Prevention of heavy metal poisoning. Zinc deficiency enhances both lead and cadmium accumulation and sensitivity to their effects.
  • -Immunity. The immune system is particularly sensitive to a zinc deficiency.
21
Q

Describe the causes and effects of zinc deficiency

A

Zinc deficiency is not widespread in developed countries, where meat is readily available. However, marginal deficiency resulting from unusual dietary practices may occur. Those susceptible to zinc deficiency are children who consume little meat and people who are pregnant, elderly, or poor.
Symptoms:
Growth retardation, delayed sexual maturation, impaired immune function, hair loss, eye and skin lesions, loss of appetite

22
Q

Describe the causes and effects of zinc toxicity

A

In children, toxicity can occur at two to three times the RDA. It can be caused by an overdose of a zinc supplement, or from storing acidic foods in galvanized cans. The principal toxic effect of zinc is its interference with normal copper metabolism (i.e., it tends to deplete the body’s copper level). As a result, it causes heart muscle degeneration, increases low-density lipoprotein, and decreases high-density lipoprotein in the blood. Each of these effects can accelerate atherosclerosis.
Symptoms:
Loss of appetite, impaired immunity, low HDL, copper and iron deficiencies

23
Q

List some major dietary and non‑dietary sources of zinc.

A

The rich dietary sources of zinc are protein‑rich foods, such as meats, poultry, liver, and shellfish (e.g., oysters and crabs).
Zinc Supplements

24
Q

Discuss the need for vitamin and mineral supplements.

A

For Supplements: Vitamin-mineral supplements may be appropriate in some circumstances; they can prevent or correct deficiencies or they can reduce the risk of diseases.
Against Supplements: Foods rarely cause nutrient imbalances or toxicities, but supplements can.
Folic acid (i.e., the form of folate used in supplements) is used for women of childbearing age to prevent neural tube defects in infants
Vitamin D supplements may be valuable for people in northern latitudes during the winter.
Iron supplements may be required by women with high menstrual blood loss.

25
Q

Define Pica

A

A curious behaviour seen in some iron-deficient people, especially in women and children of low-income groups, is pica—the craving and consumption of ice, chalk, starch, and other nonfood substances. images These substances contain no iron and cannot remedy a deficiency; in fact, clay actually inhibits iron absorption, which may explain the iron deficiency that accompanies such behaviour. Pica is poorly understood. Its cause is unknown, but researchers hypothesize that it may be motivated by hunger, nutrient deficiencies, or an attempt to protect against toxins or microbes. The consequence of pica is anemia.

26
Q

Define Transferrin Saturation

A

Transferrin saturation—the percentage of transferrin that is saturated with iron—decreases as iron stores decline.

27
Q

Define Metalloenzyme

A

enzymes that contain one or more minerals as part of their structures.

28
Q

Define Ferrous Iron (Fe++)

A
The remaining 60% is non‑heme iron and consists of ionized iron (Fe+++ or Fe++) or ferritin iron found in tissues.
Ferrous iron (reduced): Fe++
29
Q

Define Ferric Iron (Fe+++)

A
The remaining 60% is non‑heme iron and consists of ionized iron (Fe+++ or Fe++) or ferritin iron found in tissues.
Ferric iron (oxidized): Fe+++
30
Q

Define Cytochromes

A

The iron-containing electron carriers of the electron transport chain are known as cytochromes

31
Q

Define Hemoglobin

A

Hemoglobin is the oxygen-carrying protein of the red blood cells that transports oxygen from the lungs to tissues throughout the body; hemoglobin accounts for 80% of the body’s iron.

32
Q

Define Myoglobin

A

the oxygen-holding protein of the muscle cells.

33
Q

Define Microcytic Hypochromic Anemia

A
Iron-deficiency anemia is a microcytic (my-cro-SIT-ic) hypochromic (high-po-KROME-ic) anemia.
• micro = small
• cytic = cell
• hypo = too little
• chrom = colour
34
Q

Define Hemochromatosis

A

a genetically determined failure to prevent absorption of unneeded dietary iron that is characterized by iron overload and tissue damage.

35
Q

Define MFP Factor

A

a peptide released during the digestion of meat, fish, and poultry that enhances nonheme iron absorption.

36
Q

Non-Heme Iron

A

the iron in foods that is not bound to proteins; found in both plant-derived and animal-derived foods.

37
Q

Heme Iron

A

the iron in foods that is bound to the hemoglobin and myoglobin proteins; found only in meat, fish, poultry, and eggs.

38
Q

Define Subclinical Definiceny

A

Deficiency of a nutrient sufficient to affect health but not severe enough to cause classic deficiency symptoms.
Subclinical deficiencies are subtle and easy to overlook—and they are also more likely to occur. People who do not eat enough food to deliver the needed amounts of nutrients, such as habitual dieters and the elderly, risk developing subclinical deficiencies. Similarly, vegetarians who restrict their use of entire food groups without appropriate substitutions may fail to fully meet their nutrient needs. If there is no way for these people to eat enough nutritious foods to meet their needs, then vitamin-mineral supplements may be appropriate to help prevent nutrient deficiencies.