iron metabolism

Question 1

what are microcytic anaemias caused by

Answer 1

mainly caused by iron deficiency and TAILS (thalassaemia(reduced global chain synthesis), anaemia of chronic disease, iron diefeicney, lead poisoning = acquired defect which inhibits enzymes involved in harm synthesis and sidrobalstic)

Question 2

how to recognise microcytic anaemias

Answer 2

reduced hb synthesis, smaller RBC and paler nucleus (hypo chromic)

Question 3

why is iron important

Answer 3

carter of o2 in myoglobin and haemoglobin. its also an important cofactor in enzymes including cytochromes, Krebs cycle enzymes, cytochrome p450 and catalase

Question 4

problem with iron

Answer 4

its very toxic in its free form and the body has no mechanism of removing it

Question 5

difference between ferrous and ferric and what needs to be converted

Answer 5

ferrous = fe2+ and ferric = fe3+. iron can only be absorbed in the body in the for, of fe2+ and therefore ferric iron must be reduced before it can be absorbed

Question 6

alkaline and acid cause oxidation or reduction?

Answer 6

alkaline causes oxidation and acid causes reduction

Question 7

difference between haem and non-haem iron

Answer 7

they are both absorbed in the duodenum and jejunum. haem iron is the best source because it is readily absorbed. haem= from animal products e.g burger and non-haem is found in oats and barley ect.

Question 8

explain the process of how iron is absorbed

Answer 8

1. Haem (fe2+) is readily absorbed into the enterocyte. non-haem fe2+ is absorbed via a DMT1 cotransporter which pumps H+ out and Fe2+ in. Fe3+ non haem must be first converted using enzyme reductase and then can also be absorbed via DMT1.
2. once Fe2+ has been absorbed it can be stored as ferritin (in fe3+ form) or enter the blood

Question 9

function of vitamin C

Answer 9

it is a cofactor for the enzyme reductase

Question 10

describe how Fe2+ enters the blood from an enterocyte

Answer 10

1. enters blood via ferroportin transporter.
2. once enters blood fe2+ is converted to FE3+ by hephaestin so it is able to bind to transferin transporter to take it around the body

Question 11

what is hepcidin

Answer 11

it is a molecule which inhibits the actions of ferroportin to prevent iron entering the blood
its synthesis is increased when there is high iron and decreased when high erythropoietic activity

Question 12

positive and negative factors which affect absorption of non-haem iron from the the blood

Answer 12

negative;(prevent the absorption of iron)
tannins (found in tea)
phytates (in chapattis)
fibre
antacids
positive (help the absorption of iron);
citrate and vitamin C- these help reductase and prevent iron turning insoluble

Question 13

difference between functional and stored iron

Answer 13

functional is found in haem and myoglobin swell as enzymes and as its being transported. stored iron is found in the form of ferritin(soluble) held in globular protein. the other source of stored protein is haemosiderin (insoluble) which accumulates in macrophages.

Question 14

how cells take up iron

Answer 14

1. fe bound to feraportin enters cytosol by receptor mediated endocytosis
2. Fe3+ is converted to Fe2+ by the acidic microenvironment
3. fe2+ enters the cytosol via DMT1
4. can be exported, stored in ferritin or used in mitochondria for cytochrome enzymes

Question 15

how is iron recycled

Answer 15

most iron is recycled so don’t need that much from the diet. it is recycled by the breaking down old RBC in that they are engulfed by macrophages (especially splencic and kupfer cells) and within the macrophages the haem is catabolised and Fe is then transferred via trasnferin and stored as ferritin

Question 16

how is iron absorption

Answer 16

this is something thats not really understood yet
mechanisms include;
regulation of ferraportin and other transporters
hepcidin and cytokine used to regulate how much iron enters the blood
cross talk by epithelial cells and macrophages to see how much iron there is

Question 17

how chronic disease leads to anaemia

Answer 17

increased release of cytokines because of the disease increases porucditon of hepcidin by the liver. more hepcidin leads to ferroportin inhibition decreased iron absorption in the gut and decreased iron release from RES because ferritin stores full. overall reduces plasma iron.
cytokines also inhibit eryhtropoetin production by kidneys
swell as that cytokines themselves also inhibit erythropoiesis in bone marrow

Question 18

talk about how iron is recycled

Answer 18

iron enters iron pool via macrophages and dietary absorption and leaves via bone marrow and loss due to sweat or pregnancy

Question 19

causes of iron deficiency

Answer 19

1. insufficient intake
2. malabsorption
3. bleeding e.g menstrual cycle
4. increased requirement e.g during pregnancy
5. anaemia of chronic disease e.g rheumatoid arthritis

Question 20

which groups are at risk of developing anaemia

Answer 20

infants and children, women of child bearing age (because need more) and elderly people

Question 21

symptoms of anaemia

Answer 21

physiological;
tieredness
pallow
reduced exercise tolerance due to reduced oxygen carrying capacity
cardiac - angina, palpitations and heart failure because the heart is compensating for lack of oxygen
increased respiratory rate because of less o2
headache, dizziness and light-headedness
pica (cravings for weird things e.g dirt)
cold hands and feet
epitelial chances

Question 22

what epithelial changes are seen anaemic patients

Answer 22

glossy tongue, koilonychia (spoon nails and angular cheilitis which are cold sores on the edge of mouth

Question 23

blood film features of iron deficient anaemia

Answer 23

microcytic, low hb, high platelets and WBC, low keratin, iron and transferin, low reticulocyte.
definitely iron deficient if low ferritin BUT normal value doesn’t disclude it (because levels increase in cancer and other diseases). instead CHr (reticulocyte count) used because stays low in other diseases EXCEPT thalassaemia

Question 24

treatment of iron deficiency

Answer 24

dietary changes 
oral supplements 
intramuscular injection 
intravenous 
blood transfusion (rare and only used if have cardiac compromise)
=should see improvement with oral and dietary changes within 3 weeks because RBC have life span of 120 days

Question 25

what does excess iron cause

Answer 25

if there is excess iron it is store in organs as haemosiderin. iron promotes free radical formation which can cause damage to cells

Question 26

what is hereditary haemochromostosis

Answer 26

autosomal resecive disease where there is a mutation in the HFE gene. HFE usually interacts with transferin and reduces its affinity for iron BUT mutated HFE can’t bind transferin so more iron enters cells, accumulate and damages. treated with venesetion

Question 27

side effects of hereditary haemochromostosis and transfusion associated hamesiderosis

Answer 27

liver cirrhosis 
diabetes 
hypogandism 
athropathy 
cardiomyopathy 
increased skin pigmentation

Question 28

what is transfusion associated hamesiderosis

Answer 28

repeated blood transfusions lead to the accumulation of iron. desferrioxamine can delay but to stop iron overload effects. its inevitable