Copper (Cu) Flashcards

1
Q

In what state is Cu present in food and what is the process it must go through for absorption to occur?

A

Most of the Cu in food is in the Cu2+ state and bound to organic compounds like a.a. Similar to Zn and non-heme iron, Cu needs the acidic environment in the stomach (gastric secretions, HCL, pepsin) to release the bound Cu before it is absorbed in the small intestine especially duodenum.

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2
Q

Is Cu homeostasis is maintained by absorption or excretion? Explain the process.

A

Cu homeostasis is maintained primarily by excretion. For instance, when Cu stoes increases, biliary Cu excretion increases.

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3
Q

What dietary factors inhibits Cu absorption?

A

Phytates, dietary fiber, Zn, Fe, large doses of Ca gluconate, molybdenum, and large doses of Vit C.

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4
Q

After transport from intestinal cell to the liver, how is Cu transported?

A

Cu is transported via ceruloplasmin (60-95%), an acute phase protein or incorported into liver enzymes.

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5
Q

What are the functions of Cu?

A
  1. Cu functions in oxidation-reduction and electron transfer rxt (e.g. cytochrome)
  2. Plays a role in antioxidant defense via Cu enzymes (3), e.g. ceruloplasmin, which is also responsible for oxidation of Mn and Fe2+ (ferrous)
  3. Via enzymes, Cu also plays a role in collagen and elastin development, (de)activation of peptide hormones, conversion of dopamine to norepinepherineetc
  4. Cu is necessary for cholesterol and glucose metabolism.
  5. Formation of melatonin pigment.
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6
Q

What are good sources of Cu? What are the DRIs?

A
  1. Liver, cocoa, beans, nuts, whole grains, dried fruits.

2. 890/700mcg/day M/F 14-18, and 900/900mcg/day M/F for all other groups.

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7
Q

What are the symptoms of Cu deficiency?

A

Hypochromic and microcytic anemia, leukopenia, neutropenia, hypercholesterolemia, decreased ceruloplasmin and erythrocyte Cu/Zn superoxide dismutases (SOD),increased erythrocyte turnover, and abnormal electrocardiographic patterns.

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8
Q

Who are at risk for developing Cu deficiency?

A

Those at greater risk for developing Cu def include those w/ malabsorptive disorders like celiac disease, those recovering from undernutrition associated w/ chronic diarrhea, those consuming milk-based diet, pts recovering from intestinal surgery,
Pts on hemodialysis, where Cu losses can be excessive.
2. Individuals receiving excessive Zn supplementation.

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9
Q

What conditions can cause Cu toxicity?

A
  1. Since the body regulate Cu storage via biliary excretion, impaired excretion or cholestasis (arrest of bile flow) may cause Cu retention in the hepatocyte, which could lead to oxidative damage.
  2. Chronic ingestion of excessive Cu could lead to liver cirrhosis (e.g. Wilson’s disease) w/ an accumulation of Cu in liver and other organs.
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10
Q

What is a contraindication or what indicates a cautious approach to Cu supplementation?

A

Pts with hepatic dysfunction because it is excreted via the liver.

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11
Q

What measures are used to assess Cu status?

A

Serum Cu concentrations or serum ceruloplasmin levels. However, since both of these measures are elevated during systematic inflammatory response syndrome (SIRS), measurement of serum c-reactive protein concentration may be helpful in determining SIRS.

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12
Q

What is the daily parenteral supplemental dose for adults?

A

.3 - .5 mg/day and 500mcg/d additional for GI losses.

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13
Q

In what condition/disease state Cu supplementation should be given prophylactically?

A

Cu supplementation is prophylactically advocated in individuals with celiac disease when anemia or neutropenia is present because in this condition could result in irreversible neurological deficits.

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