Trace Minerals Flashcards
1
Q
What are the macronutrients? Why are they essential?
A
Carbohydrates, proteins, lipids.
Essential because they supply energy for cells whereas micronutrients don’t.
2
Q
What are minerals?
A
Essential, inorganic elements required in maintaining the normal functions of our body. They are important for bone health, growth and development, bone formation and clotting and nerve impulses. They are also important as electrolytes and as antioxidants.
3
Q
What are MAJOR minerals? Define and name.
A
Minerals required > 100 mg per day. Calcium Phosphorous Potassium Sulfur Sodium Chloride Magnesium
4
Q
Factors that increase bioavailability of minerals
A
Deficiency in a mineral increases absorption
Cooking increases the bioavailability of minerals in legumes
Vitamin C increases the absorption of some minerals such as iron
5
Q
Factors that reduce bioavailability of minerals
A
Binders, such as OXALATES found in some veggies.
PHYTATES found in grains
POLYPHENOLS in tea and coffee
Supplementation of single minerals affects absorption of competing minerals
6
Q
Example of an oxalate
A
One that binds with the calcium in spinach.
7
Q
The 10 trace elements are…
A
Iron Zinc Copper Selenium Fluoride Iodine Chromium Cobalt Manganese Molybdenum
8
Q
Sources of Iron
A
Meat, fish, poultry, eggs, dried peas and beans, whole grains and fortified breads and cereals.
9
Q
Forms of Iron
A
3-4 grams of Fe in adult body
Two forms:
Ferrous iron (+2)
Ferric iron (+3)
10
Q
How is iron transported in circulation?
A
Bound to TRANSFERRIN.
11
Q
Most of the iron (70%) is in _ _ _s as part of _ _ _ _ in hemoglobin.
A
RBCs, heme
5% is bound to myoglobin in heart and skeletal muscles.
5% act as cofactor either part of heme or non-heme enzymes.
12
Q
Where is iron stored?
A
RBCs, heme, myoglobin, cofactor…
FERRITIN in liver, spleen, and bone marrow.
13
Q
When iron concentrations are high, liver converts _______ into another storage protein called _______
A
When iron concentrations are high, liver converts FERRITIN into another storage protein called HEMOSIDERIN.
14
Q
Where is Hemosiderin found?
A
In macrophages, especially abundant in situations following hemorrhage (its formation may be related to phagocytosis of RBCs and hemoglobin)
15
Q
What two forms of dietary iron are found in food?
A
- Heme - absorbed slowly, not affected by dietary composition.
- Non-heme - the larger portion of iron consumption is from non-heme iron which includes both plant and animal sources.
16
Q
Non-heme iron is absorbed at a much ______ rate than the heme molecule.
A
SLOWER
17
Q
T or F: Only foods derived from animal flesh provide heme, but they also contain noontime iron.
A
True
18
Q
T or F: All of the iron in foods derived from plants is non-heme iron.
A
True.
19
Q
Which is absorbed better: heme iron or non-heme iron?
A
Heme (25% absorbed), even though it accounts for less (10%) of the average daily iron intake.
Non-heme - accounts for 90% but less well absorbed (about 17%).
20
Q
Factors that ENHANCE non-heme absorption
A
Body need (ex. periods of growth, pregnancy, weight training)
Vitamin C (Ascorbic acid - acidic environment increases iron absorption)
Animal tissues (presence of Meat Protein Factor - MPF: a peptide in meant, fish and poultry that promote the absorption of non-heme iron. Heme iron improves non-heme iron)
Sugars (fructose)
Acids (citric and lactic)
21
Q
Factors that INHIBIT non-heme absorption
A
Binding agents (oxalates, phytates, polyphenolsm, fiber)
Low gastric acid
Infection (body suppresses supply of iron in an attempt to reduce supply to infectious organisms).
GI disease
Calcium, zinc, and manganese
Antacids and proton pump inhibitors
22
Q
Minerals found in CHILI DINNER
A
Provides iron, MFP from meat, iron from legumes, Vitamin C from tomatoes :)
23
Q
Where is excess iron stored? Describe the absorption of iron: When the body needs it vs. when it doesn’t.
A
Mucosal cells in the intestine store excess iron in mucosal FERRITIN (storage protein).
It’s found in food. If body needs iron: Little ferritin is made (more can bind transferrin). Mucosal ferritin releases iron to mucosal TRANSFERRIN (transport protein) which hands off iron to another transferrin that travels through the blood to the rest of the body.
If body does not need iron - iron is not absorbed and is excreted in shed intestinal cells. Thus, absorption is reduced when not needed.
24
Q
Where is iron absorbed?
A
Duodenum
25
Describe the absorption of iron.
Heme iron is transported across brush border and enters same pool as non-heme iron. Dietary non-heme iron (ferric, + 3) must be reduced to ferrous (+2) for transport across the brush border.
Some iron issued or stored within the enterocytes and lost when the intestinal mucosa is sloughed.
Ferroportin helps to transport iron out of enterocytes for incorporation into serum transferrin **Ceruloplasmin - Fe2+ to Fe3+**
The amount of ferritin produced in this cell is proportional to the iron in body stores.
26
What is CERULOPLASMIN?
```
Aka ferroxidase (hephaestin)
1. It takes ferrous form and makes it into ferric form - important because what's need to bind to transferase! If you don't need iron, will be kept as ferritin.
```
2. THE MAJOR COPPER CONTAINING PROTEIN IN PLASMA.
27
How is iron recycled in the body?
Once in circulation, transferrin bound iron is distributed to liver, muscle, bone marrow, other body tissue (bone marrow incorporates iron to hemoglobin of RBCs, excess stored in ferritin and hemosiderin. Some delivered to myoglobin of muscle cells. Some lost if bleeding occurs).
Liver and spleen degrades old RBCs and they harvest iron from them for recycling - pack into transferrin and ferritin and hemosiderin.
*Some is lost with sweat, skin, urine, body tissues and must be replaced by eating iron-containing food*
28
Who is vulnerable to iron deficiency?
Women in reproductive years, pregnancy, infants and young children, adolescents.
Inadequate intake
A diet with low bioavailable iron (ex. infants not given iron-fortified formula or cereal after 6 months of age).
Vegans
29
Symptoms of iron deficiency
Fatigue, feelings of faintness, cold or abnormal sensations of the extremities, shortness of breath (first 4 due to iron-deficiency anemia), greater susceptibility to infections, low IQ infants.
PICA!
HYPOCHROMIC MICROCYTIC ANEMIA
30
Why does iron deficiency lead to immunosuppression?
Role of heme iron as a prosthetic group in several enzymes needed to destroy microorganisms.
31
Why does iron deficiency lead to low IQ?
Due to the altered neurotransmitter synthesis.
| Reduces work capacity and mental productivity. Motivational problems.
32
What is Pica?
The craving and consumption of unusual nonfood substances such as dirt, clay, or ice (comes with iron OR ZINC deficiency)
33
Describe iron's role in neurotransmitter synthesis *enrichment*
Essential for tryptophan hydroxylase (serotonin) and tyrosine hydroxylase (norepi and DA).
Iron is a cofactor for ribonucleotide reductase and is essential for function of a number of electron transfer reactions related to lipid and brain-energy metabolism.
Iron related to monoamine oxidase activity - enzyme critical for proper rates of degradation of these neurotransmitters.
34
Stages of Iron deficiency development:
1. Iron stores diminish (serum ferritin)
2. Transport decreases (TIBC Total Iron-binding Capacity or transferrin saturation)
3. Hemoglobin production and hematocrit falls.
35
Most commonly used tests to uncover iron deficiency:
Hemoglobin and hematocrit
36
As serum iron falls, transferrin levels (increase or decrease)?! as an adaptation mechanism.
Increase.
37
What is Total Iron-Binding Capacity (TIBC)?
A measure of total amount of iron that transferrin can carry.
38
What is Transferrin saturation?
% Transferrin = (serum iron/total iron binding capacity) * 100
39
Serum Ferritin
Provides a good estimate of iron stores.
Not a reliable indicator as the concentrations are increased by infection, inflammation, alcohol consumption, and liver disease.
40
In iron deficiency anemia, hemoglobin synthesis decreases, resulting in red blood cells that are pale (________) and small (_______).
Iron deficiency anemia = ________ ________ anemia!
HYPOCHROMIC MICROCYTIC ANEMIA
41
RWJMS > NJMS
TRUE (sibling schools *twin emoji*).
42
Microcytic, hypochromic anemia symptoms:
Tissue oxygen delivery, producing weakness, fatigue, palpitations, and light-headedness.
43
Epithelial Changes linked with Iron Deficiency
Glossitis, angular stomatits, painful swelling of the tongue.
44
What is koilonychia?
An abnormality of the nails that is also called spoon-shaped (concave) nails. Associated with long standing severe iron deficiency.
Nail substance is soft, so ordinary pressure on fingertips (ex. writing) produces a concave deformity.
Spoon shaped changes are rare.
45
What is hemochromatosis? Common causes?
GENETIC DISEASE in which iron is absorbed at a high rate despite elevated liver stores.
Excess iron in fibrotic tissue damage.
3-4/100 of European descent.
Cirrhosis, diabetes, heart failure, arthritis, sexual dysfunction.
Common causes: Excess ingestion or transfusion.
**Risks for cancer and heart disease in elderly**
Prolonged: may cause "bronze diabetes".
46
What is "bronze diabetes"?
Caused by prolonged hemochromatosis.
| Bronzed pigmentation to the skin and damaged liver and pancreas tissue, possibly causing diabetes.
47
A 22 year old woman with iron deficiency anemia is placed on iron supplements. Which of the following is the most likely result of her therapy?
A. It binds to metallothionein in the blood.
B. It has a rate of reabsorption that is unaffected by iron stores.
C. It is stored as ferritin in body tissues.
D. It is transported in both the ferrous (+2) and ferric (+3) oxidation states.
C.
Metallothionein binds zinc.
48
What are sources of Zinc?
Seafood, especially oysters. Steak, crab.
Meat and eggs.
Legumes - **but the bioavailability of plant sources is limited due to PHYTATES, OXALATE, CALCIUM, IRON, AND COPPER**
49
What protein does zinc bind to once inside mucosal cells?
Metallothionein
50
Absorption of zinc.
If body needs it
If body doesn't need it
1. Mucosal cells in the intestine store excess zinc in metallothionein.
If needed: Metallothionein releases zinc to ALBUMIN and transferrin for transport to the rest of the body. The pancreas uses zinc to make digestive enzymes and secrete them into the intestine.
If not needed: Zinc is not absorbed and is excreted in shed intestinal cells instead.
51
Main protein that participates in zinc transport:
Albumin (some binds to transferrin)
52
Functions of Zinc
Cofactor for enzymes in carbohydrates, fat, and protein metabolism.
Synthesis of heme, DNA and RNA (part of Zn finger proteins!)
Gene expression
Immune function
Sexual maturation
Sense of taste and smell
Stabilizes cell membrane proteins, receptor proteins for vitamin A, D, and thyroid hormone.
53
Who's vulnerable to Zn deficiency?
Vegetarians (low efficiency of Zn absorption from plant sources)
Alcoholics (alcohol inhibits absorption and promotes excretion)
Lactating women (greater need)
Heavy smokers
Patients with chronic ulcers or bed sores
Malabsorption disorders
Total Parenteral Nutrition before 1971 - no zinc was added
Genetic condition: ACRODERMATITIS ENTEROPATHICA
- results in impaired intestinal Zn absorption
54
Symptoms of Zn deficiency
```
Poor appetite
Changes in taste
Loss of sense of smell (anosmia)
Hair loss
Skin problems
Poor wound healing
Impaired immunity
Delayed growth retardation and sexual maturation
**EGYPTIAN FARM BOY**
```
55
Adolescent Zinc Deficiency
Males primarily affected.
Growth retardation, hypogonadism, delayed onset of puberty failure of secondary sexual characteristics to develop.
Syndrome associated with HIGH INTAKE OF UNLEAVENED BREAD + low Zn intakes (yeast fermentation used in bread preparation REDUCES effect of PHYTATES thereby increasing zinc bioavailability) *EGYPTIAN FARM BOY*
56
What is Acrodermatitis enteropathica?
Autosomal recessive metabolic disorder characterized by periorificial (around natural orifices) and acral (in limbs) dermatitis, alopecia (loss of hair) and diarrhea.
Results in impaired intestinal Zn absorption.
57
Zinc Toxicity
RARE
Diarrhea, nausea, vomiting
Chronic toxicity:
- impair COPPER status
- depress immune function
- urintary tract problems including infections
Treatment for WILSON disease (Wilson disease - results in increased copper storage)
58
Sources of Copper
Liver, shellfish, nuts, seeds, lentils, soy products, DARK CHOCOLATE!!
Dried fruits, whole grain products and tap water.
Meat = poor source, but may promote absorption like in non-heme iron absorption.
59
Where does copper absorption occur?
Small intestine.
60
What enhances copper absorption?
Enhanced by acidic medium
61
How is copper transported from intestine to tissues?
Bound to albumin.
62
How is copper transported from liver to tissues?
Bound to ceruloplasmin.
63
Functions of Copper:
Component of lysly oxidase important for elastin and collagen (therefore important for production of skin, hair, CT)
Cofactor for superoxide dismutase (essential for protection of cells from ROS)
Cofactor for monoamine oxidase system involved in the synthesis of neurotransmitters (maintenance of myelin sheath and nervous system)
As part of ceruloplasmin it promotes iron transportation
64
Describe recycling of iron in macrophages.
Senescent erythrocytes are phagocytosed by macrophages.
Hemoglobin is degraded and iron is released from heme.
Ferrous iron is then transported out of the macrophage via ferroportin (Fp). In the plasma, it is oxidized to the ferric form by ceruloplasmin before binding to transferrin (Tf).
65
Copper Deficiency
RARE
Malnourished infants fed only cow's milk (low in copper!)
MENKES SYNDROME - poor copper absorption
Nutritional disorders (ex. KWASHIORKOR, ANEMIA, CELIAC DISEASE).
66
Symptoms of Copper deficiency?
Anemia
CT damage
Excessive bleeding
67
Manifestations of Menkes Disease?
Silvery wiry hair, soft and lax skin, problems of CT and neurologic problems which progress with time.
Children suffering from this are often born before term.
Symptoms identifiable ~3 months after birth.
Hair is sparse, tangled, and can be easily broken.
Cheeks are rosy and chubby.
Nose bridge flattened.
Face devoid of any expression.
68
Causes of Copper Toxicity?
May occur with consumption of acidic beverages in containers made with copper.
69
Symptoms of Copper Toxicity?
Abdominal pain, nausea, vomiting, diarrhea *death in extreme cases*
70
What is Wilson Disease?
Autosomal recessive disorder caused by a defect in incorporation of copper in hepatic lysosomes. Because of faulty storage, copper can't be excreted in bile, so accumulates. Copper deposits in the brain, kidney, cornea, and liver, but with DECREASED BLOOD copper levels.
GOLDEN BROWN / GREENISH BROWN AT EDGES OF CORNEA (because of copper deposition).
71
What is Kayser-Fleischer ring?
GOLDEN BROWN / GREENISH BROWN AT EDGES OF CORNEA (because of copper deposition).
In 97% of patients with neurologic manifestations of Wilson's Disease.
72
Treatments for Wilson's Disease
Zn supplementation
Copper chelation therapy
Penicillamine (chelating agent, binds copper, excreted in urine)
73
Sources of Selenium
```
Content of food varies depending on selenium content of soil (Western U.S. is high, KESHAN, CHINA has low content!!! KESHAN DISEASE).
Seafood, meat, nuts, grains
Brazil nut (shouldn't be consumed regularly).
```
74
What is Keshan Disease?
Selenium deficiency. Keshan, China - where scientists recognized that selenium prevented a cardiac condition in children.
75
Active form of selenium
Selenocysteine
76
Storage form of selenium
Selenomethionine
77
Is selenium absorption regulated?
No. But it's efficient.
| Selenium levels are regulated through URINARY EXCRETION.
78
Highest concentrations of selenium found:
Liver, pancreas, muscle, kidneys, thyroid.
79
Function of Selenium
```
Component of 25 proteins
Part of the antioxidant enzymes
- Glutathione peroxidase
- Thioridexin reductase
- Selenoprotein P
- Prevent lipid preoccupation and cell membrane damage
- Works in concert with Vitamin E
Essential for normal thyroid function (conversion of T4 to T3 requires selenium for proper functioning of deiodinase).
Essential for normal immune function
```
80
What decreases copper absorption?
```
Decreased by:
PHYTATES
CALCIUM
FIBER
ZINC
```
81
***What is Glutathione Peroxidase (GPx)?***
A powerful antioxidant that cells use to prevent oxidative stress particularly important to cell membranes and LDL cholesterol.
It breaks down peroxides such as hydrogen peroxide to water before they form free radicals and damage cells.
This breakdown spares people from need of vitamin E (major free radical scavenger).
82
Selenium Deficiency: who's prone?
Not common in US.
Noted in people on Total Parenteral Nutrition (TPN) for maintenance as their only source of nutrition.
People with GI problems
KESHAN disease (people have enlarged heart with poor cardiac function).
Kids with KWASHIORKOR disease
Areas with low selenium in soil
83
Selenosis (Selenium Toxicity) (what are potential causes?)
Rare
| Related to industrial accidents or from a manufacturing error that led to high dose of selenium in supplements
84
Selenosis (Selenium Toxicity) symptoms:
```
Fatigue
Upset GI
Joint pain
Hair loss
Nail discoloration
```
85
Is fluoride an essential nutrient?
No. All basic functions can occur without it.
86
What are sources of fluoride?
Fluoridated water
Tea, seafood, seaweed
Toothpaste
87
Benefits of Fluoride
Helps prevent development of caries and strengthen bones.
*No known metabolic function*
Increase tooth mineralization and bone density
Promote enamel re-mineralization (Forms Hydroxyapatite crystals - greater resistance to bacteria and acids in mouth)
Inhibits glycolysis in bacteria by inhibiting enolase
88
Fluoride deficiency consequences
Dental caries
89
Fluoride toxicity consequences:
Accidental poisoning of children who swallows toothpaste
Fluorosis
- Mottled teeth
- No health risk
- Discoloration of teeth and pitting of the enamel
90
What are sources of iodine?
(Natural iodine in most foods is low)
Saltwater, seafood, seaweed, iodized salt
Vegetables depending on the amount of iodine in soil
Milk products due to the iodine in the cattle feeds and sanitizing solutions used
91
What are GOITROGENS?
Found in vegetables (turnips, cabbage,Brussel sprout, cauliflower, broccoli, rutabagas, potatoes, peanuts, strawberries) decreasing iodine absorption in the gut.
Also reduce function of thyroid gland.
*not usually a concern, usually destroy activity when we cook food. Trouble for Raw Diet people!!*
92
Iodine Deficiency Disorders
Thyroid hormone production declines (Greater secretion of TSH. Goiter)
If iodine deficiency in fetal growth and infancy - CRETINISM - most common cause of preventable mental retardation and brain damage
93
Treatment for Iodine Deficiency
Iodized salt
94
Iodine Toxicity consequences
Can cause enlargement of the thyroid gland
95
Risk factors for iodine deficiency:
```
Deficient intake
Pregnancy
Excessive tobacco or alcohol consumption
Oral contraceptive use
Excessive Calcium intake
Selenium deficiency
```
96
Symptoms of iodine deficiency
Lethargy, dry skin, THICK LIPS, enlarged tongue, reduced muscle and skeletal growth and mental retardation
97
Function of Chromium?
Enhances insulin action
98
Function of Cobalt?
Constituent of vitamin B12
(therefore cobalt deficiency should give rise to same symptoms as vitamin B12 deficiency).
