IRON and IRON DEFICIENCY ANAEMIA Flashcards

(36 cards)

1
Q

To carry out its functions (oxygen and electron transport) iron must be kept in what state?

A

Fe 2+ ferrous form

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2
Q

Why is its conversion to Fe2+ dangerous?

A

It can cause inflammation and oxidative stress by the formation of free radicals.

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3
Q

Iron is actively excreted T/F?

A

F. No mechanism for active excretion of iron.

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4
Q

Where is the majority of the bodies iron found?

A

Bound to haem

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5
Q

What is the
A) reccomended daily intake of iron
B) amount that should be absorbed
C) normal amount stored?

A

A)10-20mg
B)1mg
C) 4mg

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6
Q

Where is iron absorbed from?

A

DUODENUM

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7
Q

Iron is taken in by the diet in ferric (Fe3+) form what converts it to Fe2+ form for absorption?

A

Vitamin C enzyme on enterocyte apical surface

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8
Q

Once absorbed into enetrocyte Fe2+ can either
A) oxidse to ferric form and be stored bound to ___
B) EXIT the cell via ____ to be transported round the body?

A

A) ferritin

B) Ferroportin

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9
Q

Upon exiting the enterocyte (via ferroportin) Fe2+ is oxides to ferric form and bound to which protein?

A

Transferrin. carrier protein for iron.

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10
Q

MEasuring transferrin saturation is useful to get an idea of?

A

How much iron is being transported/ iron supply

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11
Q

On iron studies what does total iron binding capacity (TIBC) reflect?

A

Availability of iron binding sites on transferrin the blood.

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12
Q

What is the main liver protein which controls iron absorption?

A

HEPCIDIN

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13
Q

How does hepcidin decrease plasma iron concentration in response to increased iron load and inflammation?

A

It down regulates ferroportin (channel responsible for exit of iron from cells) => inhibiting release of iron into the circulation.

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14
Q

Iron bound to transferrin mainly gets taken to?

A

Tissues with transferrin receptors:
BONE MARROW
LIVER
Macrophages

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15
Q

Iron deficiency anaemia will have HIGH/LOW TIBC?

A

HIGH. Stores of iron = low, body compensates by increasing transferrin => increases bodys ability to bind iron.

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16
Q

Causes of iron deficiency anaemia?

A

Dietary
Blood loss
Malabsorption

17
Q

Why must all men with unexplained iron deficiency get GI investigations (endoscopy +/- colonoscopy)?

A

Iron deficiency is uncommon in men. (they have reduced iron requirements) therefore cause is almost always PATHOLOGICAL (GI bleed, malabsoprtion, malignancy)

18
Q

Ferritin is an indirect measure of storage iron. Why is it HIGH in anaemia of chronic disease?

A

Ferritin is also an acute pahse protein => will rise with infection, malignancy etc.

19
Q

Which GI condition should all those presenting with iron deficiency anaemia be screened for?

A

Coeliac. Blood test ttg.

20
Q

1st line treatment for iron deficiency?

A

200mg Ferrous Sulphate or fumerate TDS

21
Q

Side effects of iron supplements?

A

Nasea, constipation, diarrhoea, black stool

22
Q

If there is no response to iron supplementation in ____ then further investigations (GI) are done.

A

3 months. (120 day life span of RBC => 120 days to see repletion)

23
Q

Other than no response to treatment and being male with unexplained iron deficiency, what other circumstances grant immediate GI investigation for iron deficiency?

A

Women with unexplained iron deficiency and NOT menstrating. (menorrhagia = common cause)
Iron deficiency with either dyspepsia (may be stomach ulcer) or rectal bleeding (suggests CRC)

24
Q

How does anaemia of chronic disease affect hepcidin levels?

A

Release of cytokines STIMULATES hepcidin => blockage of Fe++ entering circulation and plasma conc. of iron REDUCES. Anaemia of chronic disease presents as microcytic hypochromic anaemia.

25
What measures functional iron?
Hb
26
Functional iron deficiency (low Hb but normal./high serum ferritin) indicates adequate ____ but problem with ?
Adequate storage but problem with iron mobilisation and transport. e.g. increased hepcidin --> iron cant exit cells (happens in chronic disease) or kidney dysfunction (reduced erythropoesis)
27
Autossomal recessive disorder that causes a mutation in HFE gene which regulates hepcidin synthesis?
Hereditatory haemochromatosis.
28
Consequence of defective HFE gene in hereditary haemochromatosis?
Decreased synthesis of hepcidin protein by the liver => loss of negative feedback => increased iron absoprtion.
29
Early Clinical features of iron overload?
Weakness/fatigue, joint pains (arthritis)
30
Late signs of iron overload?
bronze/ashen grey skin, testicular atrophy, arrythmias
31
Hamachromatosis is more likely in Men/WOMEN?
MEN
32
Iron overloas sign specfic to men?
Testicular failure/impotence. Iron deposits easily in testicles.
33
Why are iron overload patients at an increased risk of infection?
Iron promotes bacterial growth
34
Determining factor in prognosis of iron overload?
Liver involvement.
35
1st line treatment for iron overload?
Regular venosection. (removal of iron loaded blood)
36
Why is genetic screening for families of patients with haemochromatosis so important?
It may be asymptomatic until irreversible damage has occured, Chance of first degree relatives is 1 in 4.