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2.2 Haematology > Iron Metabolism and Iron Disorders > Flashcards

Iron Metabolism and Iron Disorders Flashcards

(85 cards)

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1
Q

Write about iron
(3)

A

A component of haemoglobin

A rate limiting step in erythropoiesis

Haem iron/ferrous iron and non haem iron/ferric iron

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2
Q

What is haem iron derived from?

A

Derived from haemoglobin, particularly myoglobin from food of animal origin

It is ferrous and in the form Fe++

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3
Q

What is Non-haem iron?
(3)

A

Ferric iron in the Fe+++ form

It is converted to the ferrous form before absorption

It is reduced in the stomach because of its acid environment

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4
Q

How many mg of iron do we need a day

A

1-2mg

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5
Q

Give some sources of iron
(3)

A

Red meat, liver, green vegetables, poultry and dried form

Organic iron already in the haem form Fe2+ derived from red meat and liver is more rapidly absorbed

Inorganic iron found in vegetables which is in the Fe3+ form is less easily absorbed

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6
Q

What can increase iron absorption and how?
(2)

A

Foods containing ascorbic acid and muscle protein increase iron absorption

They do so by reducing ferric iron to ferrous iron

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7
Q

What can inhibit iron absorption?

A

Caffeine

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8
Q

How much iron does the human body contain

A

3-5grams

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9
Q

Why do we need iron?
(3)

A

Synthesis of haem, myoglobin, cytochromes
Co-factor in DNA synthesis
Connective tissue production

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10
Q

Why do we not want excess iron

A

Excess iron is toxic to the body

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11
Q

Where is iron primarily found?

A

In RBCs, macrophages, hepatocytes, enterocytes

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12
Q

How much iron do we lose everyday

A

1-2mg lost per day through blood loss, urine, faeces, or sloughed mucosal epithelial cells

This must be replaced through the day

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13
Q

What are the three types of iron found in the body and what % of total iron are they

A

Functional iron (80%)
Transport iron (0.1%)
Storage iron (20%)

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14
Q

What is included in functional iron?

A

Haemoglobin
Myoglobin
Enzymes

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15
Q

What is meant by transport iron

A

Transferrin

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16
Q

What is meant by storage iron

A

Ferritin
Haemosiderin

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17
Q

Briefly describe the life cycle of iron in the body
(4)

A

Transit of iron from the bone marrow to RBCs

To the spleen for removal by macrophages

With iron recycled to the bone marrow via transferrin

The intestine absorbs iron to balance the iron that is lost daily

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18
Q

How is iron excreted?

A

There is no physiological mechanism for excretion of iron

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19
Q

Where is iron balance controled

A

Controlled at the level of iron absorption in the duodenum and jejunum

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20
Q

How do we modify the absorption of iron by the intestine?
(5)

A

Modified by:
- availability of iron in the body
- blood oxygen content/hypoxia
- Blood haemoglobin concentration
- EPO activity in bone marrow/rate of erythropoiesis
- Inflammation can minimise iron availability

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21
Q

What might cause iron excess?
(4)

A

Dietary excess (over supplementation)
Inherited protein defect (haemochromatosis)
Anaemia (ineffective erythropoiesis)
Iatrogenic (red cell transfusions)

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22
Q

Write about the steps in iron absorption
(7)

A

Iron released from protein complexes by acid/proteolytic enzymes in stomach

Free iron is absorbed by interstitial epithelial cells (enterocytes) via a specific cell membrane molecule called divalent metal transporter-1 (DMT-1)

Ferric iron Fe3+ is converted to Fe2+ by ferroreductase enzymes on surface of enterocytes

Haem iron is released from haem by enzyme Haemoxygenase-1

Iron moves from enterocyte into the circulation through a membrane protein called Ferroportin

The movement of iron into plasma by Ferroportin is regulated by a liver derived enzyme called Hepcidin

Hephaestin oxidises iron to Fe3+ the form required for binding to apotransferin

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23
Q

What is the first step in iron absorption - food has just reached the stomach

A

Iron released from protein complexes by acid/proteolytic enzymes in stomach

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24
Q

What is the second step in the absorption of iron, iron has just been released from protein complexes?

A

Free iron is absorbed by interstitial epithelial cells (enterocytes) via a specific cell membrane molecule called divalent metal transporter-1 (DMT-1)

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25
How does iron get absorbed into the enterocytes?
Via a specific cell membrane molecule called divalent Metal Transporter-1 (DMT)
26
What is the third step in iron absorption, iron has just been absorbed by enterocytes?
Ferric iron Fe3+ is converted to Fe2+ by ferroreductase enzymes on surface of enterocytes
27
What does ferroreductase do?
Converts ferric iron (Fe3+) to ferrous iron (Fe2+)
28
What is the fourth step of iron absorption, Ferrous iron (Fe2+) has been formed?
Haem iron/ferrous iron is released from haem by enzyme Haemoxygenase-1
29
What does haemoxygenase-1 do?
it releases haem iron/ferrous iron from haem
30
What is the fifth step in iron absorption, haem iron has just been released from haem?
Iron moves from enterocyte into the circulation through a membrane protein called ferroportin (port for iron)
31
What is ferroportin?
A membrane protein that iron can move through
32
What is the sixth step of iron absorption, iron has just moved into circulation
At this step hepcidin, a liver derived enzyme, regulates the movement of iron into plasma
33
What is hepcidin and what does it do?
a liver derived enzyme Regulates the movement of iron into plasma
34
What is the seventh step of iron absorption
Hephaestin oxidises iron to Fe3+ (ferric) form required for binding to apotransferrin
35
What does hephaestin do
Oxidises iron to Fe3+ form required for binding to apotransferrin
36
List 9 factors favouring iron absorption
Haem iron Ferrous iron Acids (HCl, vitamin C) Solubilizing agents e.g. sugars, amino acids Reduced serum hepcidin e.g. iron deficiency Ineffective erythropoiesis Pregnancy Hereditary haemochromatosis Increased expression of DMT-1 in duodenal enterocytes
37
List 8 factors decreasing absorption
Inorganic iron Ferric form Alkalis -> antacids, pancreatic secretions Precipitating agents - phytates, phosphates, tea Increased serum hepcidin, e.g. iron excess Decreased erythropoiesis Inflammation Decreased expression of DMT-1 in duodenal enterocytes
38
What is hepcidin (4)
The master regulator 25 amino acid length peptide Coded by the HAMP gene on Ch19 Produced in the liver
39
What are some of the functions of Hepcidin (5)
Has antibacterial and antifungal activity Circulating hepcidin regulates iron export by binding to ferroportin and inducing its degradation in lysosomes Blocks intestinal Fe absorption Inhibits release of Fe from macrophages Decreases export of Fe from liver cells
40
What are the three main iron transporters in the body?
Transferrin, lactoferrin and albumin
41
List the seven steps in iron transport
Plasma iron taken up by iron transporters synthesised in the liver (transferrin, lactoferrin, albumin) Iron is best transported as ferric iron (Fe3+) which is converted from ferrous iron by ceruloplasmin and ferroconvertase Apotransferrin bound to iron is termed transferrin Transferrin delivers iron to the bone marrow Transferrin is also termed the total iron binding capacity (TIBC) The amount of iron being transported as transferrin can be used as an indication of body iron status Aprroximately 85% of iron from degraded Hb is promptly recycled from the macrophage to the plasma and delivered by transferrin to the bone marrow
42
What is the best form of iron for transport
Ferric iron (Fe3+)
43
What converts ferrous iron to ferric iron
Ceruloplasmin and ferroconvertase
44
What does ceruloplasmin and ferroconvertase do?
Converts ferrous iron to ferric iron
45
What is transferrin and what does it do (4)
Apotransferrin bound to iron It delivers iron to the bone marrow It is also termed the total iron binding capacity (TIBC) This amount of iron being transported as transferrin can be used as an indication of body iron status
46
What percentage of iron from degraded Hb is recycled and how?
85% Recycled from the macrophage to the plasma and delivered by transferrin back to the bone marrow
47
Explain how iron is incorporated into the developing red blood cell in the bone marrow (5)
In BM the iron-transferrin complex enters the developing RC by receptor mediated endocytosis by attaching to TfR on the RC membrane Iron is incorporated into haem molecule in the mitochondria 80-90% of iron taken up is converted to haem within 1 hour Any excess iron taken up is stored as ferritin Apotransferrin returns back to plasma to collect more iron from intestines TfR expression responds to changes in iron i.e. down-regulated by high iron conditions
48
What receptor is needed for the uptake of iron by developing erythroblasts?
TfR Transferrin receptor
49
How long does it take for 80-90% of iron to be converted to haem
1 hour
50
What happens to excess iron taken up by rbcs
Stored as ferritin
51
What does apotransferrin do after giving it's iron to rbcs
Goes back into plasma to travel to intestine for more iron
52
What does TfR expression depend on? (4)
Responds to change in iron status Down-regulated by high iron condition Up-regulated by low iron conditions Soluble TFR (sTfR) are receptors shed from red cells and can be used as an indication of increased erythropoiesis
53
Where is iron stored in the body
Bone marrow Liver Pancreas Spleen
54
What are the storage forms of iron
Ferritin Haemosiderin
55
What is haemosiderin
Formed from aggregates of ferritin
56
Ferritin vs Haemosiderin (4)
Release of iron from Haemosiderin is slow and considered long term storage of iron Ferritin is the primary iron storage protein Plasma ferritin used as an indicator of iron status Ferritin is an acute phase protein
57
What stain do we use for iron stores?
Perls Prussian Blue
58
Why is it important to remember that ferritin is an acute phase protein? (3)
Ferritin levels may increase in inflammation Ferritin is used to determine iron levels Storage form of iron may be inadequate but may appear normal
59
Write about iron deficiency anaemia (5)
Most common cause of anaemia Affects 500 million people worldwide Microcytic, hypochromic anaemia MCV and MCH are reduced Small and pale red cells due to defect in Hb synthesis
60
What are some signs of Iron deficiency anaemia
Tachypnea Koilonychia Angular cheilitis Atrophic glossitis Angular Stomatitis
61
What would we test for to determine iron status on a FBC
Haemoglobin - would be low MCV = low MCH = low Blood film - hypochromic, microcytic rbcs
62
How do we carry out iron studies in the lab
Serum iron Transferrin measured as total iron binding capacity (TIBC) % transferrin saturation Serum ferritin
63
What can serum iron by influenced by? (4)
Iron absorption from meals Infection Inflammation Diurnal variation
64
What is TIBC
The amount of transferrin that is available to bind to and transport is reflected in measurements of the total iron binding capacity (TIBC)
65
How do you determine % transferrin saturation
Serum iron/ TIBC x100
66
What is considered normal % transferrin saturation
30%
67
What is considered iron deficient % transferrin saturation
Less than 15%
68
What is considered iron overload % transferrin saturation
Greater than 55%
69
What are the laboratory findings of IDA
Decreased: - Hb - MCV and MCH - Reticulocytes - Ferritin - Serum iron - % Transferrin saturation Increased - TIBC
70
What are the two ways of managing iron deficiency anaemia?
Identification and treatment of the underlying cause Correction of the deficiency by therapy with inorganic iron - oral iron therapy
71
What is failure to respond to iron therapy often caused by (3)
Not taking the oral therapy Or taking it incorrectly i.e. with coffee not orange juice etc (most common) Continued haemorrhage Malabsorption
72
What should you do if a patient has microcytic anaemia but isn't responding to iron deficiency?
Reassess the diagnosis to exclude other cause of the anaemia
73
What might cause a microcytic anaemia (4)
A poor response to infection Renal or hepatic failure Underlying malignant disease Anaemia of inflammation due to high hepcidin levels
74
What would be the clinical findings of anaemia of chronic disorders
Decreased - Hb - Serum iron - (or normal) Transferrin saturation - (or normal) TIBC Increased - ferritin (or normal) - CRP
75
What would indicate iron overload?
High transferrin saturation High non-transferrin bound iron in plasma
76
What are the two main affects of non-transferrin bound iron in plasma as seen in iron overload? (2)
Excess iron promotes the generation of free hydroxyl radicals, which cause damage to oxygen related tissues Insoluble iron complexes are deposited in the tissues and initiates toxicity to organ
77
What are the symptoms of iron overload (5)
Hydroxyl radicals cause - cardiac failure - liver cirrhosis/fibrosis/cancer - diabetes mellitus Iron deposition causes - diabetes mellitus - infertility - growth failure
78
What is Hereditary Haemochromatosis (6)
Increased absorption of iron from the GIT High Fe protein is involved in Hepcidin production HFE is encoded on chromosome 6 Arises due to a single point mutation (G>A at nucleotide position 845) which results in a substitution of Cyt with Tyr at position 282 in HFE protein Causes decreased hepcidin production Mutation is called C282Y, less common is H63D
79
What causes Hereditary Haemochromatosis?
Mutation in HFE gene on chromosome 6 Arises due to a single point mutation (G>A at nucleotide position 845) which results in a substitution of Cyt with Tyr at position 282 in HFE protein
80
What are the two most common HH mutations?
282Y (most common) (on HFE) H63D (on HFE) Mutations have also been found on TfR2, HJV and ferroportin that are known to cause HH
81
Comment on HH in Irish population
Approximately 10% of Europeans are heterozygous 1 in 83 carry the mutation
82
What happens in HH (3)
Hepcidin is released from the liver but in low amounts This causes the uncontrolled release of iron from macrophages and duodenal enterocytes Low levels of hepcidin causes too much iron to be absorbed from the GIT
83
How does HH progress? (5)
Asymptomatic Non-specific symptoms Signs of organ damage Bronze diabetes Early death
84
What are the clinical findings of HH (7)
Haemoglobin increased Normochromic, normocytic cells Serum ferritin very high Serum iron increased % Transferrin saturation >45% Haemosiderin staining of bone marrow and liver positive Demonstration of mutations by PCR
85
How is HH treated? (4)
Phlebotomy -> this is donated to IBTS Done weekly for 6 months When iron stores are exhausted the frequency of phlebotomy should be reduced to two to four units each year to continue indefinitely Early diagnosis to prevent cirrhosis, hepatocellular carcinoma etc

2.2 Haematology (38 decks)

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