Iron in Health and Disease Flashcards

(34 cards)

1
Q

what is iron used for

A

oxygen transport
electron transport - mitochondrial production of ATP

present in:
Hb
myoglobin
enzymes

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2
Q

what makes iron dangerous

A

chemical reactivity
-can take part in oxidative reactions and free radical production

requirements are:

  • safe transport
  • safe storage
  • regulation of iron absorption
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3
Q

where is the majority of iron in the body found

A

haemolytic

Fe2 sits in a porphyrin ring to form Haem

1 Haem group per globulin

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4
Q

what happens to iron in Hb after RBCs are broken down

A

binds to transferrin and re-enters the plasma

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5
Q

how much iron to be absorb/loose per day

A

absorb 1mg/day

lose 1mg/day (bleeding, worn out skin cells etc, cannot be controlled)

iron in Hb is constantly recycled

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6
Q

where is iron absorbed

A

duodenum - uptake into cells of duodenal mucosa

influenced by dietary factors

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7
Q

what enhances iron absorption

A

Haem-vs non-harm iron
-haem iron from animal products absorbed better

ascorbic acid (vit C) helps reduced iron to Fe2+ to make it absorbed more easily

alcohol

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8
Q

what inhibits iron absorption

A

tannins eg. tea
phytates eg. cereals, bran, nuts and seeds
calcium eg. dairy products

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9
Q

what is the mechanism of iron absorption

A

Duodenal cytochrome B

  • found in luminal surface
  • reduced Fe3+ (ferric) to Fe2+ (ferrous)

DMT (divalent metal transporter)
-transports ferrous iron into the duodenal enterocyte
OR
Haem transporter
-transfers Haem into the duodenal enterocyte

Ferroportin

  • facilitates iron export from enterocyte
  • passed on to transferrin
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10
Q

what regulated iron absorption

A

Hepcidin

-hepcidin production in the liver increases due to increased iron load or inflammation

binds to ferroportin and causes its degradation

iron therefore ‘trapped’ in the duodenal cells

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11
Q

what happens to heptocidin levels in iron deficiency

A

decreases to facilitate absorption of more iron

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12
Q

how do you asses iron status

A

functional iron

  • Hb concentration
  • where iron in use is

transport iron/supply to tissues
-% saturation of transferrin with iron

storage iron

  • serum ferritin
  • tissue biopsy (rarely needed)
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13
Q

what is transferrin

A

protein which binds two iron atoms

transports irons from donor tissues (macrophages, intestinal cells, hepatocytes)
to tissue expressing transferrin receptors (erythroid marrow)

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14
Q

what does transferrin saturation measure

A

iron supply
-serum iron/total iron binding capacity

reflects proportion of diferric transferrin

transferrin saturation - 20-50%

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15
Q

what is ferritin

A

spherical intracellular protein - stores up to 4000 ferric irons

tiny amounts of serum ferritin reflects intracellular ferritin synthesis

therefore serum ferritin is a surrogate marker to tissue ferritin

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16
Q

what causes increased ferritin

A

iron overload

inflammation
sepsis
malignancy
liver injury

17
Q

what are the disorders of iron metabolism

A

iron deficiency
iron malutilisation ‘anaemia of chronic disease’
iron overload

18
Q

what are the consequences of iron deficiency

A

exhaustion of iron stores

iron deficiency erythropoiesis
-falling red cell MCV

microcytic hypochromic anaemia

epithelial changes

  • skin
  • koilonychia
  • angular stomatitis
19
Q

what causes microcytic anaemias

A

deficient haemoglobin synthesis

Haem deficiency

  • lack of iron
  • anaemia of chronic disease
  • congenital sideroblastic anaemia

globing deficiency
-thalassaemias

20
Q

how can iron deficiency be confirmed

A

anaemia (decreased Hb iron)

reduced iron storage (low serum ferritin)

21
Q

causes of iron deficiency

A

insufficient intake

  • women and children
  • diet

loosing too much
-bleeding

not absorbing
-coeliac disease

22
Q

causes of chronic blood loss

A
menorrhagia 
GI 
-tumours
-ulcers
-NSAIDS 
-parasitic infection 
haematuria
23
Q

what is Iron Malutilisation (anaemia of chronic disease)

A

up regulating of ferritin production stimulated by inflammation -
iron stores increase

hepcidin increases

iron becomes stuck in duodenal enterocyte as transferrin

leads to microcytic hypochromic red cells

24
Q

why does anaemia of chronic disease occur

A

protective mechanism to reduce iron supply to pathogens

25
causes of iron overload
primary -herreditary haemochromatosis secondary - transfusional - iron loading anaemias
26
what is hereditary haemochromatosis
long-term excess iron absorption with parenchymal iron loading HFE gene mutation decreased hepcidin synthesis increased iron absorption gradual iron accumulation with risk of end organ damage
27
clinical features of hereditary haemochromatosis
``` weakness/fatigue joint pains impotence arthritis cirrhosis diabetes cardiomyopathy ``` usually presents in middle age or later iron overload >5g
28
treatment of hereditary haemochromatosis
weekly venesection 450-500ml 200-250mg of iron initial aim to exhaust iron stores then once its norm just do it when ferritin comes back up thereafter keep ferritin below 50
29
causes of death in hereditary haemochromatosis
``` diabetes infection cardiac failure hepatic failure hepatoma ```
30
who else do you test in hereditary haemochromatosis
family screening first degree relative 1/4 risk HFE genotype and iron status may be undetectable until irreversible organ damage occurs
31
what causes secondary iron overload
Repeated red cell transfusion Excessive iron absorption related to over-active erythropoiesis
32
disorders causing iron overload
massive ineffective erythropoiesis - thalasaemia - sideroblastic anaemias - bone marrow not working - red cell aplasia - myelodysplasia
33
what is the treatment of secondary iron overload
ironchelating drugs as venesection is not an option in already anaemic patients
34
what iron chelating agents are used
desferrioxamine subcutaneous or IV