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Basic Haem > Iron/ B12 & Folate > Flashcards

Iron/ B12 & Folate Flashcards

1
Q

Biological functions of folate/vit B9?

A

DNA synthesis, RNA synthesis, DNA methylation, methionine and thymidylate synthesis, theres more cant bother

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2
Q

What is the Folate Trap?

A
  • B12 deficiency cause folate to be trapped in methyl form (methyl THF) and it can escape without being used.
  • needs to be in the THF so it can be used
  • DNA synthesis is affected, large RBCs with nuclear retention and flimsy membrane are formed-megaloblastic anaemia
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3
Q

Plant foods contain cobalamin. True or False.

A

FALSE!!! B12 found in animal sources like beef, liver, fish, diary products.
PS. folate is mainly from plant sources

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4
Q

Describe the transport & absorption of Cobalamin (B12).

A
  1. Mouth: Haptocorrin/R protein in saliva binds to dietary B12 & carries it to the stomach.
  2. Stomach: Gastric acid and pepsin cleaves the B12 from haptocorrin (TCI carries it to the duodenum).
  3. Duodenum & jejenum: pancreatic juices and enzymes degrade the TC I and releases the cobalamin, which is now taken up by intrinsic factor.
    - IF protects the cobalamin and carries it to the cubulin in the ileum.
  4. Ileum: the IF-cobalamin complex binds to cubulin and is taken up into the enterocyte (by Ca2+ dependent passive transport)
  5. Enterocyte: the IF-cobalamin complex is engulfed by lysosomes, where enzymes degrade the IF and release the cobalamin into the cytoplasm where it is taken up by TCII.
    - TC II/Cobalamin complex exit the enterocyte into systemic circulation- to the bone marrow & tissues.
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5
Q

B12 is never left unattended. True or False

A

True- it is always bound to something.

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6
Q

Describe TCI?

A
  • Binds 70% of cobalamin, protects cobalamin from the acid environment of the GI tract, n neutralizes the function of cobalamin- cobalamin appears functionally dead.
  • Largely synthesized by granulocytes and macrophages.
  • Aka haptocorrin and R protein
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7
Q

Describe TCII?

A
  • Binds 30% of circulating cobalamin, and transports cobalamin to target cells where they are used, like in bone marrow.
  • Congenital TC deficiency causes megaloblastic anaemia because of failure of B12 to enter marrow
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8
Q

What is megaloblastic anaemia?

A
  • Caused by a deficiency (or defective metabolism) of B12 and folate which in turn causes impaired DNA synthesis-ineffective erythropoiesis.
  • Results in abnormal RBCS; features- anaemia, macrocytosis, hypersegmented neutrophils, red cell fragments, raised LDH and thrombocytopenia.
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9
Q

The dietary forms of B12 and folate are the same as that in the circulation. True or false.

A

False-the form in circulation is different

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10
Q

Normal dietary intake of B12 and folate?

A

7-30 micrograms and 200-250 micrograms resp.

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11
Q

Cooking has a little effect on folate. T or F.

A

F- folate is easily destroyed by over-cooking

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12
Q

Body stores of B12 and folate?

A

2-3 mg and 10-12 mg resp.

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13
Q

Absorption site for B12 and folate

A

Ileum and duodenum/jejunum resp.

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14
Q

In order to be absorbed folate is converted to what?

A

methyltetrahydrofolate- reduced monoglutamate form which circulates the plasma.

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15
Q

Severe deficiency of B12 is usually caused by what?

A

pernicious anaemia
note: less commonly in veganism

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16
Q

What is pernicious anaemia?

A
  • an autoimmune attack on the gastric mucosa leading to atrophy of the stomach and the secretion of intrinsic factor (IF) is absent.
  • Therefore, there is malabsorption of B12 due to lack of IF.
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17
Q

Why do pregnant women require an increased need for folate?

A

Due to excess cell turnover, because folate is degraded due to an increase in DNA synthesis (thymidylate synthesis).

18
Q

How does a folate deficiency cause megaloblastic anaemia?

A

Folate deficiency inhibits thymidylate synthesis which is the rate limiting step of DNA synthesis.

19
Q

How does B12 deficiency cause megaloblastic anaemia?

A

B12 deficiency indirectly reduces the amount of folate coenzyme which is necessary for thymidylate synthesis. In turn, affects DNA synthesis.

20
Q

Iron deficiency is the main cause of what kinda anaemia?

A
  • Microcytic, hypochromic anaemia (red cells are small and pale)
  • low MCV and MCH
    note: iron deficiency is the main cause of anaemia.
21
Q

which enzyme other than hephaestin catalyses oxidation of iron to the ferric form?

A

caeruloplasmin (copper-containing enzyme)

22
Q

iron is mobilised after what?

A

reduction to the ferrous form (Fe2+)

23
Q

transport and storage of iron is largely mediated by which proteins?

A
  • transferrin
  • transferrin receptor 1
  • ferritin
24
Q

What does hepcidin do?

A
  • It’s a hormone produced by the liver that inhibits the release of iron from macrophages and from enterocytes (by closing the ferroportin) into the plasma.
  • If increased, it reduces iron absorption
25
Q

Too much iron leads to an increase in hepcidin, and iron deficiency leads to a decrease in hepcidin. T or F.

A

T- amt of iron is directly proportional to the amt of hepcidin

26
Q

Why does ineffective erythropoiesis, increase iron absorption?

A

Because erythroblasts secrete 2 proteins that suppress the hepcidin synthesis, and a decrease in hepcidin allow for an increase in iron absorption.
note: hypoxia also suppresses hepcidin synthesis

27
Q

Inflammation, IL-6 and other cytokines increase hepcidin synthesis. T or F.

A

T- reduces iron absorption

28
Q

Most dietary iron is absorbed. T or F.

A

F- most dietary iron remains unabsorbed
- 5-10 % is absorbed normally
- 20-30 % is absorbed in iron deficiency and pregnant women (bcuz 35% of 300 mg of iron is transferred to the fetus)

29
Q

major causes of iron deficiency?

A
  • chronic blood loss (uterine, gastrointestinal)
  • increased demands (pregnancy, growth)
  • malabsorption
  • poor diet (rarely the sole cause of iron deficiency)
30
Q

In iron deficiency, the iron stores are completely depleted. T or F.

A

T- takes a while before it reaches anaemia cuz the iron stores will be used up

31
Q

what is hemochromatosis?

A
  • disorder in iron metabolism where there is excess iron absorption, saturation of iron-binding proteins and deposition of hemosiderin in the tissues.
  • excess iron deposition leads to liver cirrhosis bronze diabetes (bronze skin + diabetes).
32
Q

iron is absorbed mainly where?

A

the duodenum
note: in the ferrous state

33
Q

iron varies directly with what?

A

rate of erythropoiesis

34
Q

what factors favour iron absorption? hint: 8

A
  • ferrous form
  • inorganic iron
  • acids- HCl, vit C
  • solubizing agents- sugar, amino acids
  • iron deficiency
  • ineffective erythropoiesis
  • pregnancy
  • primary haemochromatosis

*decreasing hepcidin

35
Q

what factors reduce iron absorption? hint:9

A
  • ferric form
  • organic iron
  • alkalis- antacids
  • precipitating agents-phosphates
  • iron excess
  • decreased erythropoiesis
  • infection/ inflammation
  • tea
  • desferrioxamine

*increasing hepcidin

36
Q

describe the process of iron transport/absorption?

A
  • first, dietary iron is reduced from the ferric state (Fe3+) to the ferrous state (Fe2+) by DCYTB.
  • Fe2+ can now enter the enterocyte but its transferred in by DMT1
  • in the enterocyte, Fe2+ can either be stored as mucosal ferritin then shed as stool or it can be transported through ferroportin into circulation
  • Fe2+ outside of the enterocyte is oxidized back to the Fe3+ by hephaestin
  • Fe3+ now in the blood vessel is bound to transferrin which carries it either to the bone marrow for erythropoiesis or to the liver to stimulate hepcidin
37
Q

what does low plasma iron concentrations (hypoferremia) cause?

A

anaemia (cuz of decreased Hb synthesis)

38
Q

Iron is transported in the ferric form (Fe3+) by transferrin and absorbed in the ferrous form (Fe2+) by DMT-1. T or F.

A

T

39
Q

the majority of storage iron is present as ferritin, and haemosiderin is predominantly found in macrophages rather than hepatocytes. T or F.

A

T

40
Q

TC deficiency causes metaloblastic anaemia because of failure of B12 to enter marrow (and other cells) from plasma but the serum B12 level in TC deficiency is normal. T or F.

A

T

41
Q

Folate deficiency is thought to cause megaloblastic anaemia by inhibiting the thymidylate synthesis, a rate-limiting step in DNA synthesis. T or F.

A

T
note: Lack of B12 prevents the demethylation of methyl THF, thus depriving cells of THF and so of folate polyglutamate coenzyme- which is needed for thymidylate synthesis

42
Q

clinical features of megaloblastic anaemia?

A
  • mild jaundice- excess breakdown of haemoglobin resulting from increased ineffective erythropoiesis in the bone marrow
  • Glossitis, angular stomatitis and mild symptoms of malabsorption with loss of weight

Basic Haem (9 decks)

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