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ESA2 > MEH - Haemopoiesis & Iron > Flashcards

MEH - Haemopoiesis & Iron Flashcards

1
Q

What is anaemia?

A

Low Hb or low total RBC count in the blood

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2
Q

How does the distribution of haemopoiesis change from child to adult? Why is this relevant in cancer?

A

More widespread child
Adult - skull, sternum, pelvis, vertebrae, skull, ribs
These are the common places for bone mets due to the blood supply and marrow microenvironment that is favourable for cancers

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3
Q

What is the name of a bone marrow biopsy?

A

Trephine

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4
Q

What is G-CSF?

A

Granulocyte colony stimulating factor - is a cytokine and hormone

Stimulates granulocytes to be made

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5
Q

What controls haematopoiesis?

A

Cytokines (interleukins)/Hormones (growth factors)

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6
Q

What are the hormones/cytokines that control:

1) Erythrocytes
2) Megakaryotcytes/platelets
3) Granulocytes
4) Lymphocytes

A

1) Epo an CM-CSF
2) CM-CSF, TPO
3) G-CSF, GM-CSF
4) ILs TNFs

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7
Q

What is GM-CSF? What three kinds of blood cell does it stimulate?

A

Erythrocytes
Granulocytes
Megakaryocytes

(myeloid cells)

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8
Q

What is Tpo and what does it stimulate production of?

A

Thrombopoeitin and stimulates platelets

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9
Q

What is the reticuloendothelial system? Where is it? What are the main RE organs?

A

Tissues and cells around body that are part of the immune system containing phagocytic cells - destroy old and damaged cells particularly RBCs
Spleen and liver

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10
Q

5 roles of RBC?

A 
Carry O2
Carry Hb
Keep Hb in reduced (ferrous) state
Generate ATP
Maintain osmotic equilibrium
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11
Q

What is the diamter of a RBC? Can a capillary be less than this?

A

8micrometres

Yes down to 3.5 - RBC need to fold and squeeze through

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12
Q

When is Epo released?

A

In response to hypoxia

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13
Q

What is the structure of Hb? R state T state? What is the role of the global chains (3)?

A

2 alpha 2 beta globin chains each with a haem bound
R- relaxed - O2 bound
T - tense - deoxy

Role of globin chains:

1) Prevents haem from oxidation
2) Confers solubilty
3) Permits shape change of molecule for O2 affinity change (R and T)

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14
Q

What is the catabolism of Haem to excretion?

A

Haem –> bilirubin —> travels to liver with albumin –> conjugated to glucoronic acid —> more soluble —> forms bile –> bile duct –> intestine –> here either formed into stercobilin or urobilinogen (for faeces or urine excretion)

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15
Q

What is Hb recycled to in the liver?

A

Spleen –> Haem –> bilirubin to live

Globin –> amino acids

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16
Q

What are the two main metabolic pathways of RBCs?

A

Glycolysis - Glucose metabolised to lactate ATP generated

Pentose phosphate pathway - G6P metabolised, generates NADPH

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17
Q

Why does the RBC use pentose?

A

As its intermediates can go into glycolysis

As it regernates glutathione which helps protect from Ros as RBC vulnerable to Ros damage - membrane damage particularly

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18
Q

Can we excrete iron?

A

No

Only lose a bit a day e.g. bleeding

19
Q

What are two major functions of iron in the body?

A

Transports and stores oxygen

Integral part of many enzymes - eg. cytochromes

20
Q

Name some available stores of iron?

A

Hb
Myoglobin
Tissue iron - cytochromes
Transported iron - serum iron

21
Q

Name some stored iron, which is soluble which isn’t?

A

Ferritin - soluble

Haemosiderin - not

22
Q

Does most iron come from gut absorption or recycling?

A

Recycling

23
Q

How are RBC recycled? Where is most iron stored in the liver?

A

Mostly by splenic macrophages and liver kupffer cells

Most of iron stored in the liver is in hepatocytes

24
Q

How much iron enters and leaves the body each day?

A

1-2mg

25
Q

Why is haem a better source of iron?

A

Doesn’t need to be reduced to ferrous form as already is ferrous form

26
Q

How is iron absorbed in the gut (3 major things to remember)?

A

Absorbed via binding to transferrin –> into enterocyte. Then either stored as ferritin or transported into the blood via ferroportin, then travels with transferrin to cells e.g. to RBC to then be taken up and used in Hb. Taken into RBC by transferrin receptor. Or taken to be stored in liver/muscle

27
Q

What is the foetal special ferroportin?

A

lactoferrin - allows transfer of lactose iron from enterocyte cell to blood

28
Q

What inhibits/increases iron absorption in the gut?

A

Ascorbic acids (vit C/citric acid) increases

Chelation inhibits - tea, chapatis, antacids

29
Q

How are dietary iron levels sensed?

A

By villi of eneterocytes

30
Q

What 4 ways can iron absorption be controlled?

A

Regulation of transporters e.g. ferroportin
Expression of receptors e.g. HFE protein (human haemochromatosis protein) has an effect on regulating the interaction between transferrin receptor and transferrin
Hepcidin and cytokines
Cross talk between macrophages and epithelial cells

31
Q

How does hepcidin work in iron absorption regulation?

A

negative regulator of iron storage
binds to ferroportin and degrades it
1) So iron can get into gut cell but can’t go further
2) Iron can’t be released from macrophages so can’t be used

32
Q

Where is hepcidin synthesised and excreted?

A

Synthesised in liver

Excreted in gut

33
Q

When is hepcidin synthesis increased and why?

A

High iron as it acts to reduce usable iron

34
Q

What is hepcidin regulated by?

A

HFE
Transferrin receptor
Inflammatory cytokines (increase release)

35
Q

Iron deficiency is a symptom not a diagnosis - what else must you look for?

A

Reason - e.g. malnutrition, pregnancy, bleeding e.g. GI

36
Q

What can happen to the sides of the lips and the nails in anaemia?

A

Angular stomatitis

Spooning of nails

37
Q

How do you treat iron deficiency? What is the problem with giving iron IV?

A 
Dietary advice
Oral iron supplements
IM Iron
IV iron - high risk of anaphylaxis
Transaction - not unless severe anaemia with imminent cardiac compromise
38
Q

What response are you looking for with iron deficient anaemia treatment?

A

Improvement in symptoms

raise of 20g/L Hb in 3 weeks

39
Q

What is the problem with excess iron - what happens?

A

When it exceeds the binding capacity of transferrin can be reduced and form hydroxyl and lipid radicals - damage membranes, nucleic acids and proteins

40
Q

Where is excess iron deposited?

A

In tissues

41
Q

What happens in haemochromatosis? How do you treat?

A

Autosomal recessive mutation in gene HFE
Deposition of iron in organs leading to damage
Pigmented skin
Hereditary or transfusion associated haemosiderosis
Treat with venesection

42
Q

What is the normal role of HFE?

A

Normally competes for binding with transferrin on transferrin receptor
Mutated HFE can’t bind so transferrin has no competition

43
Q

What is a risk of treatment of thalassemia/transfusion dependent anaemias?

A

Risk of transfusion associated haemosiderosis due to excess iron - iron chelating agents delay but don’t stop effects of iron overload

ESA2 (37 decks)

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