Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Nutrition AKA The most boring class on earth > Minerals > Flashcards

Minerals Flashcards

1
Q

Name five factors that influence mineral absorption.

A
  1. Redox state
  2. Intraluminal pH
  3. Formation of chelates
  4. Formation of insoluble complexes
  5. Protein-mineral complexes must be digested
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the bioavailability of iron from food? What is done with the absorbed iron?

A

15%, it is used in RBCs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How much iron is lost per day from normal metabolic processes?

A

1-2 mg/day

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Which is most bioavailable: Heme or non-heme iron?

A

Heme (15-35%)

Non-heme is 5-15%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the food sources of heme and non-heme iron, respectively?

A

Heme: Meat

Non-heme: plants (grains, fortified grains), nuts, fruits, veggies.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Can iron be actively excreted?

A

Nope

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Compare heme iron absorption vs. non-heme iron absorption.

A

Heme iron can diffuse through the heme transporter (heme carrier protein 1) in intestinal mucosal cells, then is incorporated into mucosal ferritin in the cell. After that, it can go to the blood through Ferroportin 1. On the blood side it is oxidized by Hephaestin to Fe3+ so it can bind to plasma transferrin to go to the liver and bone marrow.

Non-heme iron must first be reduced with either duodenal Cytochrome B in the mucosal brush border, or is naturally reduced in acid. Fe2+ then gets into the cell through DMT1 (divalent metal transporter 1). The rest of the steps are the same after that.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Hephaestin is ________ dependent.

A

Copper

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Name two ways in which iron absorption is regulated.

A
  1. Upregulation of duodenal cytochrome B and DMT1 (non-heme).
  2. Hepcidin regulation of iron release from cells.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

In which organ is hepcidin made? Does hepcidin increase or decrease iron release from cells?

A

Made in liver. Hepcidin BLOCKS release from cells (so it is made when iron levels are adequate)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the mechanism of hepcidin?

A

When it binds to cells Ferroportin transporters are internalized and degraded.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Name the host factors that affect iron absorption. Which one is most important.

A
  1. Iron status (hepcidin levels) - most important
  2. GI pH
  3. Inflammation (from sepsis, RA, etc.) upregulates hepcidin
  4. Absorptive capability (eg. Celiac, Chron’s etc.)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How do phytates affect mineral absorption?

A

They chelate to minerals and prevent absorption.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Does alcohol help absorb iron?

A

Yeah, by inhibiting hepcidin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Which amino acid can form a complex with iron that allows for its absorption?

A

Cysteine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Name three factors that increase non-heme iron absorption.

A
  1. Acids in the small intestine, which helps to solubilize iron.
  2. Chelation by organic molecules, which are absorbed.
  3. Iron deficiency, which results in upregulation of brush border DMT1, which increases absorptive capacity.
17
Q

Name four factors that decrease non-heme iron absorption.

A
  1. Polyphenols such as tannic acid in tea and red wine.
  2. Oxalic acid in vegetables, fruits and some grains.
  3. Phytates in vegetables, fruits, and some grains.
  4. DMT 1 competition with other minerals like Zinc
18
Q

Name the populations at risk for iron deficiency (7).

A

Infants/young children, pregnant women, peeps with malabsorption syndromes, vegetarians, athletes, peeps with chronic GI diseases, peeps with intestinal parasites.

19
Q

What results from iron deficiency (12)?

A

Anemia, fatigue, lethargy, cold intolerance, impaired psychomotor development, impaired intellectual performance, impaired immunity, adverse pregnancy outcomes, increased risk of lead poisoning due to upregulation of DMT1 transporter, angular stomatitis, glossitis and koilonychia (depression of nails).

20
Q

Glossitis, angular stomatitis (inflammation at the corners of the mouth), and koilonychia may be indicative of ______ deficiency.

A

iron

21
Q

What is hereditary hemochromatosis and what is the treatment?

A

It is when hepcidin is mutated or absent, resulting in iron toxicity. Treatment is periodic phlebotomy.

22
Q

What is the TUL of iron?

A

45 mg/day

23
Q

What is Bantu syndrome and how is it treated?

A

Genetic disorder that results in iron toxicity, treated by diet modification.

24
Q

What are the food sources of copper (7)?

A

Liver, shellfish, meats, whole grains, nuts, seeds, legumes.

25
Q

What are the biological roles for copper (3)?

A

Cofactor for enzymes, key roles in nerve function and transport of iron out of the enterocyte.

26
Q

Where in the GI tract is copper absorbed?

A

Some in stomach, most in duodenum, jejunum

27
Q

What is the defect with Menke’s disease?

A

Mutated ATP7A that normally allows copper to enter the golgi of an enterocyte for packaging and release to the portal circulation.

28
Q

What is the defect with Wilson’s disease?

A

Defective ATP7B that normally allows copper to enter the golgi of a hepatocyte for packaging into either bile or ceruloplasmin –> organs. Liver fills with copper, cells die and release copper into blood which damages other organs.

29
Q

Who is at risk for copper deficiency (2)?

A

People after upper GI surgery, malabsorptive diseases.

30
Q

What are the symptoms of copper deficiency (6)?

A

Neuro: tremors, dysphagia, balance loss. Hematologic problems, osteoporosis, cardiomyopathy.

31
Q

What are the biological roles of zinc (12 listed)?

A

Gene expression, cell division, metalloenzyme cofactor, protein/hormone synthesis, immunity, antioxidant function, vitamin A metabolism, taste, wound healing, growth, sexual maturation, fertility and reproduction.

32
Q

What are the food sources of zinc (4)?

A

Animal foods, cereal grains, veggies, supplements.

33
Q

Where in the GI tract is zinc absorbed? Which transporters are involved?

A

Small intestine by ZIP4 and DMT1

34
Q

Zinc toxicity may cause ______ deficiency.

A

copper

35
Q

What is acrodermatitis enteropathica?

A

Autosomal recessive defect of zinc transporter that results in zinc deficiency.

36
Q

Who is at risk for zinc deficiency (5)?

A

Peeps with malabsorptive diseases, vegetarians, alcoholics, peeps with DM and chronic kidney disease

37
Q

What is the relationship among copper, zinc, and metallothionein?

A

Zinc upregulates metellothionein in enterocytes. Mettalothionein binds copper with high affinity and MT-Cu is excreted in feces. Zn supplementation –> high MT levels –> high Cu excretion and Cu deficiency.

38
Q

Copper deficiency can mimic deficiency of ______.

A

Vitamin B12

Nutrition AKA The most boring class on earth (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions