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All trace minerals Flashcards

1
Q

Where does copper absorption occur?

A 
Small intestine
(location of absorption was not specified for other trace minerals)
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2
Q

What increases copper absorption?

A

acidic milieu (milieu=environment)
- I got you
(acidic environment also increases absorption of non-heme iron)

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3
Q

What decreases copper absorption?

A

Calcium, phytates, fiber and zinc (again, also decreases absorption of non-heme iron)

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4
Q

How is copper transported from intestine to tissues?

A

Bound to ALBUMIN (same as zinc except zinc can also bind to transferrin)

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5
Q

How is copper transported from liver to tissues?

A

Bound to CERULOPLASMIN

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6
Q

Functions of Copper?

A

involved with collagen, ROS, neurotransmitters and iron recycling
(1) component of lysly oxidase (important for elastin and collagen)
(2) cofactor for superoxide dismutase (removes reactive oxygen species)
(3) cofactor for monoamine oxidase system (involved in the synthesis of neurotransmitters)
(Note: iron is also important in synthesis of neurotransmitters)
(4) when bound to ceruloplasmin (basal membrane of mucosal cell), promotes iron transportation (note: ceruloplasmin also transports copper from liver to tissues)

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7
Q

What is ceruloplasmin?

A

Major copper-containing protein in plasma, calcium transporter, involved in iron absorption and iron recycling from macrophages

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8
Q

Why is ceruloplasmin important?

A

For recycling of iron in macrophages (from RBCs to circulation)
** Further explained ** RBCs age (called senescent erythrocyte). These aged RBCs can be phagocytosed by macrophages. Ceruloplasmin retrieves the ferrious iron in the macrophage after it “eats” the aged RBC. Retrieves ferrious iron and then converts it to ferric iron so it can bind to transferrin

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9
Q

Symptoms from a copper deficiency?

A

anemia, connective tissue damage (affects hair and skin growth), excessive bleeding (copper is important for clotting)

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10
Q

What is the syndrome resulting from a copper deficiency?

A

Menkes syndrome (genetic syndrome but can be see in malnourished children)

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11
Q

Symptoms of copper toxicitiy?

A

Abdominal pain, nausea, vomiting and diarrhea

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12
Q

Disease resulting from copper toxicity?

A 
Wilson disease
(Remember the copper related diseases start with M/W -> flip letter upside down - wombo mode)
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13
Q

What is wilson disease?

A

copper deposits in the brain, kidney, corna and liver with low blood copper levels

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14
Q

What is the concern with acidic beverages and copper containers?

A

Acidic beverages in containers made with copper. Increases the amount of copper absorption.

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15
Q

Treatment for copper toxicity?

A

(1) zinc toxicity

(2) penicillamine

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16
Q

Sources of Selenium?

A

Brazil nut, seafood, meats, nuts, grains (content of food varies depending on the selenium content of soil)

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17
Q

Biologically active form of selenium?

A

selenocysteine

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18
Q

Storage pool form of selenium?

A

selenomethionine

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19
Q

Describe absorption of selenium

A

efficient, not regulated

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20
Q

Where are the highest concentrations of selenium found?

A

liver, pancreas, muscle, kidneys and thyroid

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21
Q

Functions of selenium?

A
  • antioxidant enzymes, thyroid enzymes (necessary for 5’ deiodinase which converts T4 to T3), immune enzymes

component of 25 proteins, part of the antioxidant enzymes essential for normal thyroid function, essential for normal imune function

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22
Q

What are some of the antioxidant enzymes that selenium is a part of?

A

glutathione peroxidase, thioridexin reductase, selenoprotein P

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23
Q

Describe the connection between selenium and vitamin E.

A

Selenium works in concert with vitamin E to prevents lipid peroxidation and cell membrane damage

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24
Q

What does glutathione peroxidase do?

A

Glutathione peroxidase, along with selenium, converts hydrogen peroxide to water (reduction reaction)

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25
Who may have a selenium deficiency?
(1) patients on total parenteral nutrition (Parenteral nutrition, also known as intravenous feeding, is a method of getting nutrition into the body through the veins.) (This also applies to zinc deficiency - total parenteral nutrition before 1971 - no zinc was added) (2) people with gastrointestinal problems
26
What is keshan disease?
Selenium deficiency with complications resulting in poor cardiac function and an enlarged heart
27
Symptoms from a selenium toxicity?
GI upset, joint pain, hair loss, nail discoloration, fatigue
28
Toxicity in selenium - How?
industrial accidents or supplementation
29
Major source of fluoride?
fluoridated water, tea, seafood, seaweed (also toothpaste)
30
Does fluoride have a metabolic function?
No known metabolic function
31
Then, if it has no metabolic function, why is fluoride important?
increases tooth mineralization and bone density, reduces development of dental caries (dental caries=tooth decay; due to activities by bacteria), promote enamel re-mineralization (hydroxlylapatite vs fluorapaptite)
32
What should be known about fluorapatite?
The presene of fluoride converts hydroylapatite to fluprapatite
33
What is fluorosis?
a chronic condition caused by excessive intake of fluorine compounds, marked by mottling of the teeth, discoloration of teeth and pitting of the enamel
34
Any health risks with fluoride toxicity?
no health risk
35
How does fluoride toxicity usually happen?
accidental poisoning of children who swallow toothpaste
36
Sources of iodine
saltwater, seafood, seaweed and iodized salt, vegetables (depending on the amount of iodine in soil), milk products (iodine used in cattle feeds and santizing solutions)
37
What are goitrogens?
Foods that are going to decrease absorption of iodine in the gut
38
What are examples of goitrogens?
Vegetables - sweet potatoes (decrease iodine absorption in the gut)
39
Where is a large percentage of iodine found?
40% of body's iodine in the thyroid gland
40
Roles of iodine in the body?
Part of the thyroid hormone which means it regulates body temperature, metabolic rate, reproduction, growth, blood cell production, nerve and muscle function
41
Consequence of iodine deficiency in fetal growth and infancy?
cretinism (most common cause of preventable mental retardation and brain damage)
42
How does an iodine deficiency affect the secretion of TSH?
When thyroid hormone production declines, greater secretion of thyroid-stimulating hormone results (leads to a goiter)
43
Treatment for iodine deficiency?
Iodized salt
44
Consequence of iodine toxicity?
Can cause enlargement of the thyroid gland
45
Sources of chromium?
egg yolks, whole grains, pork, nuts and mushrooms
46
Function of chromium?
Enhances insulin action
47
Results of a deficiency in chromium?
Blood glucose levels remains elevated after meals
48
Sources of cobalt?
Animal foods containing vitamin B12
49
Function of cobalt?
constituent of vitamin B12 | constituent - being part of a whole
50
Results of a deficiency in cobalt?
Same symptoms as vitamin B12 deficiency
51
Factors that enhace Non-heme absorption
body need, acid (ascorbic, citric and lactic acid), sugar and animal tissue (heme and meat protein factor - mpf)
52
Factors that inhibit Non-heme absorption
competition (other minerals with 2+ charge - calcium, zinc, manganese or binding agents - oxalates, phytates, polyphenols, and fibers), low gastic acid, infection, gastrointestinal disease
53
Why did we not discuss factors that inflence HEME absorption?
Heme absorption is much easier than the absorption of non-heme. Remember, non-heme iron is usually in the ferric state but can only be absorbed by the mucosal cell if in the ferrous state.
54
Where is excess iron stored after ingestion?
Mucosal cells in the intestine store excess iron in mucosal ferritin
55
What is ferritin?
a storage protein
56
What is the body's response if it needs iron and iron is stored in mucosal cells?
Mucosal ferritin releases iron to mucosal transferrin, which hands off iron to another transferrin that travels through the blood to the rest of the body
57
What is transferrin? How many types of transferrin are there in the body?
A transport protein. There are two types: mucosal and one that travel through the blood to the rest of the body
58
What is the body's response if it does not need iron and iron is stored in mucosal cells?
Iron is not absorbed and is excreted in shed intestinal cells instead. Thus, iron absorption is reduced when the body does not need iron. There is constant turn over of mucosal cells.
59
Ferric state iron
(1) can bind to transferrin | (2) when eating, iron is usually in the oxidized form
60
Ferrous state iron
(1) only form that can exist in the mucosal cell
61
What does ceruloplasmin do?
(1) oxidizes ferric iron which allows it to bind to transferrin (2) transports copper from the liver to tissues
62
important protein in the mucosal cell
(1) ferritin - storage protein (2) ceruloplasmin (Basal membrane) - oxidizes ferric iron (3) ferroportin (basal membrane) - transports ferric iron outside of mucosal cell to then be oxidized
63
Main targets for transferrin?
(1) muscle cells | (2) bone marrow
64
Where else, besides the mucosal cell, can ferritin be found?
liver, spleen and bone marrow
65
Which organs dismantle red blood cells?
Liver and spleen dismantles red blood cells, packages iron into transferrin, and stores excess iron in ferritin (and hemosiderin). This is iron recycling - can chose to store or transfer iron
66
Deficiency in what things are the consequence of iron deficiency?
energy metabolism(requires O2) and neurotransmitter synthesis (affect motivation)
67
Understanding the assessent of iron deficiecy table
if someone is iron deficiency, you should expect a few things: (1) anything related to storing iron will decrease in synthesis (ferritin, tissue iron) (2) because iron is so low, and the body needs iron for the brain (for that O2 transport), everything related transportation or iron and hemoglobin precursors increases in synthesis (transferrin, free erythrocyte protopohyrin) (3) hemoglobin production decreases because ya can't have hemoglobin without iron
68
Stages to iron deficiency?
decrease iron storage -> decrease iron transport -> decrease hemoglobin and hematocrit
69
What is the type of anemia that develops from an iron deficiency?
microcytic, hypochromic (rbcs are paler in color) anemia
70
What are epithelial changes that accompany iron deficiency?
glossitis, angular stoatitis (corner of lips), koilonychia "spoon nails"
71
Review: what are the consequences of iron deficiency?
(1) epithelial changes (2) microcytic, hypochromic anemia (3) disrupted neurotransmitter synthesis (4) disrupted energy metabolism (5) low IQ
72
Consequences of iron overload?
(1) hemochomatosis (bronze diabetes) - excess iron in fibrotic tissue damage (2) risks for cancer and heart disease in elderly
73
What are enterocytes?
A cell of the intestinal lining
74
Describe the circulation of zinc
enteropancreatic circulation (from enterocytes to the pancreas)
75
Where is excess zinc stored after ingestion?
mucosal cells in the intestine store excess zinc in metallothionein
76
What is the body's response if it needs zinc and zinc is stored in mucosal cells?
metallothionein releases zinc to albumin and transferrin for transport to the rest of the body
77
What is the body's response if it does not need zinc and zinc is stored in mucosal cells?
zinc is not absorbed and is excreted in shed intestinal cells instead
78
What organ uses zinc?
pancreas uses zinc to make digestive enzymes and secretes them into the intestine
79
What's a zinc finger? Why does it matter?
The zinc finger is a common structural motif in many protein DNA binding domains. It is found in roughly 3%(!) of all proteins and performs a diverse range of functions not limited to enhancing or inhibiting one specific gene. They are one of several domains that evolved to solve the problem of sequence specific binding of nucleic acids. A zinc ion coordinates with the protein and helps stabilize an alpha helix that can recognize DNA in a sequence specific manner. (Zinc fingers explain the functions of zinc)
80
What are the functions of zinc?
(1) cofactor for enzymes in carbohydrate, fat, and protein metabolism (2) synthesis of heme, DNA, and RNA (3) Gene expression (4) Immune function (5) Sexual maturation (6) Sense of taste and smell
81
diseases resulting from zinc deficiency?
(1) adolescent zinc deficiency (2) acrodermatitis enterophathic - rashes resulting from inflammation of skin around the orifices (acro - means around the limbs, enteropathica - means problem with the intestine)
82
Symptoms of Zn deficiency?
poor appetite, , changes in taste, loss of sense of smell, hair loss, skin problems, poor wound healing, impaired imunity, growth retardation and delayed sexual maturation
83
What are selenomethionine and selenocysteine?
Amino acids

GI (27 decks)

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