3 Flashcards

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1
Q

Iron Significance:

A

• Part of hemoglobin & myoglobin to carry O2 in blood & in muscles.
• Part of heme molecules of iron-binding proteins.
• Part of cytochromes and many oxidation/reduction reactions, so, it is important for energy utilization, being a part of cytochromes.
• Iron is found in 2 forms; reduced ferrous iron (F2+) & oxidized ferric
iron (F3+). So, it acts as both an electron donor & electron acceptor.
• A component of iron-sulfur proteins.

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2
Q

Iron is found in 2 forms in food:

A
  1. Heme iron: Only foods derived from
    animal flesh provide heme. So, it’s found in meats, poultry, fish, (they also contain non-heme iron). - It’s readily absorbed.
  2. Non-heme iron: In plants.
    - It’s less absorbed.
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3
Q

Intestinal iron absorption increases with:

A

• Vitamin C.
• ↓ iron stores.
• ↑ erythropoietic activity.
• Anaemia.
• Hypoxia.

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4
Q

Intestinal iron absorption decreases in:

A

Inflammation

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5
Q

Excess iron absorption relative to body iron stores:

A

Hereditary hemochromatosis.

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6
Q

• The majority of iron is absorbed in the ………..

A

duodenum

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7
Q

Inorganic iron is taken up by the intestinal mucosal cells and is bounded to the intracellular protein “…………….”.
Once ….. is saturated with iron, no more can enter.

A

ferritin

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8
Q

Iron absorbed from intestine is stored as ……….. in the intestinal epithelial cells or transported in plasma as ……………….

A

ferritin
transferrin.

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9
Q

Absorption of both inorganic & heme iron is impaired by ………….. .

A

Calcium

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10
Q

Iron is toxic to human body if left free in plasma or in fluid portion of the cells as it can generate the highly toxic
………….

A

hydroxyl free radical (HO -).

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11
Q

In duodenal cells , dietary iron (Fe3+) is reduced to the ferrous state Fe2+ (more soluble) by …

A

duodenal cytochrome B (ferric reductase).

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12
Q

Then Fe2+ →transported into the cell by

A

divalent metal transporter-1

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13
Q

In enterocytes, Fe2+ is released from heme by ………….. ……… ……..
• Fe2+ is released into circulation by another protein called ………….

A

In enterocytes, Fe2+ is released from heme by heme oxidase enzyme.
• Fe2+ is released into circulation by another protein called ferroprotein-
1.

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14
Q

Fe2+ iron is then oxidized to Fe3+ iron by & before binding to transferrin.

A

Fe2+ iron is then oxidized to Fe3+ iron by ceruloplasmin & ferroxidase II,
before binding to transferrin.

Hephaestin, a protein similar to ceruloplasmin, is thought to have a
ferroxidase activity which is also important to release iron from the
cells as Fe3+, to be transported in plasma by transferrin

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15
Q

……………….secreted into the circulation, where it down-regulates
ferroprotein-mediated release of iron from enterocytes, macrophages &
hepatocytes.

A

Hepcidin

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16
Q

There are 2 broad categories that describe iron in the body:

A

A. Essential (or functional) iron. B. Storage iron.

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17
Q

Essential or functional Iron: • The iron which is involved in the normal metabolism of the cells. They
are mainly divided into 3 groups:

A
  1. Heme Proteins: as Hb, myoglobin & others as catalases, peroxidases.
  2. Cytochromes.
  3. Iron Requiring Enzymes: as xanthine oxidase, cytochrome-C reductase, acyl-CoA dehydrogenase, NADH-reductase &others
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18
Q

Storage Iron: present in 2 major compounds;

A

Ferritin & Hemosiderin

19
Q

Ferritin

Storage Sites……, keeps iron in a l…..,

A

protein complex. It is the intracellular iron-storage protein.
• Ferritin keeps iron in a soluble & non-toxic form.
• Up to 4,500 Fe3+ atoms are found stored in a ferritin complex.
• Ferritin that is not combined with iron is called “apo-ferritin”.
• Storage Sites: Liver, Bone marrow & Spleen.

20
Q

…………glycoprotein that binds Fe very tightly but reversibly  It is the true carrier of iron.

A

Transferrin

21
Q

Excretion by 3 main sites :Iron

A
  1. GIT.
  2. Kidneys.
  3. Shedding cells of the skin.
22
Q

Iron Deficiency
• There are three stages of iron deficiency which are:

A
  1. Iron Storage Depletion : not usually recognized by the patient in which
    serum ferritin ↓.
  2. Iron Deficiency: Fe stores are almost exhausted. Biochemically, serum
    ferritin & transferrin saturation are low.
  3. Iron Deficiency Anemia : hypochromic microcytic anemia .
23
Q

Causes For Iron Deficiency Anemia:

A

 Blood loss.
 Increased demand for Fe,
Inflammation
 Inability to absorb Fe
 Phytates

24
Q

Iron Overload
• Iron stores may increase due to :

Cells start to fill with excess of hemosiderin → 2 broad types of Fe overload:

A
  • Excessive absorption, or
  • Parental iron therapy or
  • Repeated transfusions.
  1. Hemosiderosis: Iron overload without cell damage. 2. Haemochromatosis: iron overload associated with injury to cells.
25
Q

SELENIUM:
Biochemical Functions;

A

SELENIUM:
Biochemical Functions;
Serves as a catalytic component in enzymes & proteins as:
• Glutathione peroxidase (destroys H 2O2).
• Acts with other antioxidants and free radical scavengers.
• Overlaps with vitamin E for antioxidant effects.
• Iodo-thyronine 5’- deiodinase to form rT3; playing an important role
in regulating thyroid hormones during embryological development .
• Thio-redoxin reductase.

26
Q

Selenium:
Sources:

A

Meat, sea food, whole grains & vegetables.

27
Q

Selenium is stored in the body as …

Selenium Deficiency: may lead to ……

A

is stored in the body as seleno-cysteine in seleno-proteins.

CVDs

28
Q

Most of cobalt is stored with

A

vitamin B12

29
Q

Cobalt Sources and Intakes:

A

Humans obtain vitamin B12 and cobalt from animal foods such as
organ and muscle meat.

30
Q

increased the Absorption and Excretion Cobalt:

A

• Shared with iron.
• Absorption is increased in patients with:
- deficient iron intake,
- portal cirrhosis
- hemochromatosis.

• Excretion: mainly through urine & small amounts in feces, hair & sweat.

31
Q

IODINE: • The body normally has ……. mg of iodine. More than 75% in ………….. The remaining part in: ………

A

• The body normally has 20-30 mg of iodine.
• More than 75% in thyroid gland. The remaining part in: Mammary gland, Gastric mucosa & Blood.

32
Q

IODINE Function, Sources

A

Function: synthesis of thyroid hormones, T4 & T3.
• Food Sources: Foods of marine origin, processed foods, iodized salt.

33
Q

Absorption and Excretion:

IODINE

A

• Iodine is absorbed in the form of iodide.
• Its excretion is mainly by urine & small amounts from bile are
excreted in feces.

34
Q

Iodine Deficiency:

A
  1. GOITER 2. Endemic Cretinism: o Short stature o Protuberant abdomen o Swollen features
35
Q

ZINC:
Main functions in the body:

A

• Part of many enzymes, especially enzymes for transfer of CO 2.
• Associated with the insulin hormone.
• Involved in making genetic material & proteins.
• Important to wound healing, taste perception, reproduction (for
sperms), vision (transports, activates Vitamin A) & immune function.

36
Q

ZINC sources, Deficiency symptoms:

A

Significant sources: Protein-containing foods, red meats, shellfish and
whole grains.

oIn children: growth retardation & delayed sexual maturation. o Impaired immune function & poor wound healing. o Hair loss and eye and skin lesions. o Loss of appetite and abnormal taste.

37
Q

Toxicity symptoms:

ZINC

A

• Loss of appetite,
• Low HDL.
• Copper & iron deficiencies.

38
Q

Copper Source

A

Organ meats, seafood, nuts, seeds, cereals & whole grains.
• Milk and milk-products are poor sources.

39
Q

Copper Absorption: mainly from ………… by specific transporters, (Cu+2 ions
are highly insoluble).
• Serum Copper: It circulates in blood bounded to ………..
• Excretion: by ……

A

• Absorption: mainly from duodenum by specific transporters, (Cu+2 ions
are highly insoluble).
• Serum Copper: It circulates in blood bounded to ceruloplasmin.
• Excretion: by liver into bile → GIT to be excreted in feces.

40
Q

Ceruloplasmin: (6 Cu atoms/molecule).
 Functions: …………….
 Congenital absence of ceruloplasmin → ……………

A

oxidize Fe+2 to Fe+3 iron for binding to transferrin.
 Congenital absence of ceruloplasmin → tissue iron accumulation
→ “hemochromatosis”.

41
Q

Biochemical Functions of Copper:

A

 Healing wounds,
 Maintaining the myelin sheath nerve fibers.
*
Essential catalytic cofactor for many cupro-enzymes including:
- Cu, Zn-superoxide dismutase (antioxidant).
- Cytochrome C oxidase (ATP synthesis, neurologic function).
- Lysyl oxidase (stabilizes connective tissue proteins).
- Tyrosinase (melanin synthesis).
- Part of several enzymes required for collagen synthesis.

42
Q

Copper Deficiency:

A

Acquired deficiency is rare . Manifestations are:
Hypochromic microcytic anemia.
Hypopigmentation of hair and skin
Structural abnormalities in connective tissue (hair, teeth, bone
demineralization) Reduced levels of circulating copper and ceruloplasmin

43
Q

Inborn Errors of Copper Metabolism

A

Wilson’s
Disease
(Hepato-lenticular Degeneration)

44
Q

Wilson’s
Disease
(Hepato-lenticular Degeneration)

A

• Autosomal recessive disease due to a mutation in Wilson’s disease
protein gene (ATP7B) → protein that transports excess copper into
the bile,

It is a copper storage disease (mainly liver, CNS & cornea of eye)

Diagnosis based on:
Low Ceruloplasmin levels. *
Corneal copper deposition, Kayser-Fleisher Ring.
*
High liver copper levels.