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haematology > iron in health disease]] > Flashcards

iron in health disease]] Flashcards

1
Q

iron important in electron transport e.g.?

A

mitochondria production of ATP

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2
Q

ferric ?

A

fe3

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3
Q

ferrous

A

fe2

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4
Q

iron present in ? (3)

A

haemoglobin, myoglobin, enzymes eg cytochroms

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5
Q

why is iron dangerous?

A

it induces oxidative stress

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6
Q

assessment of iron status

A

functional - haemoglobin
transport (% saturation with transferrin)
storage (ferritin)

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7
Q

what transports iron from donor tissues to tissues expressing receptors ?

A

transferrin

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8
Q

ferritin - large intracellular protein - stores up to ?

A

4000 iro arims

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9
Q

tiny amount of serum ferritin reflects intracellular ferritin synthesis in response to iron - indirect measure of storage iron

A

y

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10
Q

how is iron absorption regulated?

A

intraluminal factors - solubility or iron, reduction of ferric to ferrous.
mucosal factors - DMT 1 and ferroportin at mucosal surface
hepcidin - major negative regulator of iron uptake.

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11
Q

where is hepcidin produced?

A

liver

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12
Q

what is it produced in response to?

A

iron load and inflammation

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13
Q

what facilitates iron export from the enterocyte?

A

ferroportin

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14
Q

what is iron passed on to to be transported elsewhere?

A

transferrin

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15
Q

what does hepcidin do?

A

down regulates ferroportin

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16
Q

normal amount of iron in the body?

A

4g

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17
Q

lack of iron?

A

angular stomatitis, koilonychia, skin changes

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18
Q

iron deficiency can be confirmed by?

A

combination of anaemia and low storage iron (ferritin)

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19
Q

causes of iron deficiency?

A

diet, bleeding, malabsorption

20
Q

bleeding

A

menorrhagia, GI tumours, haematuria

21
Q

GI bleeds can occurr without any symptoms

A

y

22
Q

what is the maximum iron absorption of iron per day?

A

4-5mg

23
Q

this can balance with GI blood loss i.e. no symptoms

A

y

24
Q

anaemia of chronic disorders, what happens?

A

old red cell broken down. increased transcription of ferritin mRNA stimulated by inflammatory cytokines. get increased ferritin synthesis and increase in hepcidin, which blocks ferroportin mediated release of iron

25
Q

results in?

A

impaired iron supply to marrow erythroblasts and eventually hypchromic red cells

26
Q

primary iron overload?

A

long term excess iron absorption with parenchymal rather than macrophage iron loading and eventual organ damage

27
Q

what is the parenchyma?

A

functional part of the organ

28
Q

clinical features of hereditary haemocromatosis?

A

weakness, fatigue, joint pains, arthritis, cirrhosis, diabetes, cardiomyopathy, impotence

29
Q

haemocromatosis can cause deposits anywhere

A

hypogonadism, cancer, cirrhosis, cardiomyopathy, diabetes, arthropathy

30
Q

presentation usually in middle age or later

A

> 5g

31
Q

mutations of HFE gene, in particular which mutations?

A

C282Y, H63D

32
Q

main effect thought to be through?

A

reduced hepcidin synthesis

33
Q

diagnosis: phenotype

A

transferrin saturdation >50%, serum ferritin >300 in men or >200 in pre menopausal women

34
Q

why would you consider doing a liver biopsy?

A

can get cirrhosis in haemacromatosis

35
Q

treatment of hereditary haemacromotosis?

A 
weekly phlebotomy (400-500ml)
200-250mg iron
36
Q

how much iron in 100ml blood?

A

50mg

37
Q

initial aim to exhaust iron stores

A

ferritin below 20

38
Q

thereafter keep ferritin below?

A

50

39
Q

causes of death in hereditary haemocromotosis?

A

diabetes, infections, cardiac failure, hepatic failure, bleeding varies, hepatoma

40
Q

first degree relatives: especially siblings risk 1/4

A

HFE genotype and iron status

41
Q

why important to do family studies?

A

haemocromatosis may be asymptomatic until irreversible organ damage has occurred. this underlines the importance of family studies

42
Q

secondary iron overload

A

repeated red cell transfusions, excessive iron absorption related to over active erythropoesis

43
Q

regular blood transfusions

A

each unit of blood contains 200-250 mg iron

44
Q

patients with thalassaemia may require transfusion every 2-3 weeks lifelong

A

red cell transfusion (iron overload (total >5g)) or liver >15mg/g dry weight

45
Q

treatment of secondary iron overload?

A

iron chelating agents (desferrioxamine)

46
Q

why?

A

venesection not usually an option in already anaemic patients

haematology (20 decks)

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