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Ellie's MEH > Sesh 5- Haemopoiesis, Iron and Anaemia > Flashcards

Sesh 5- Haemopoiesis, Iron and Anaemia Flashcards

1
Q

What is the normal range for blood platelet count?

A

150-400 X 10^9/L

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2
Q

What is the lifespan of a red blood cell?

A

120 days

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3
Q

What happens to the globin chains following Hb breakdown?

A

Broken down into their constituent amino acids which are then recycled

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4
Q

What is bilirubin excreted as in the faeces?

A

Stercobilin

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5
Q

What are the 2 main metabolic pathways in red blood cells?

A
  1. glycolysis

2. pentose phosphate pathway

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6
Q

Where is EPO produced, and in response to what?

A

Peritubular cells of the kidney in response to hypoxia

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7
Q

What is the action of EPO?

A

Stimulates maturation and release of red blood cells from the bone marrow

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8
Q

Why are the levels of iron in the body tightly controlled?

A

There is no specific mechanism for its excretion

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9
Q

Name 2 ways iron is stored in the body.

A
  1. 95% Ferritin in hepatocytes

2. 5% as Haemosiderin in Kupffer cells

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10
Q

Where does most active Fe come from?

A

Rbc (Hb) breakdown

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11
Q

Why are haem iron sources better than non-haem sources?

A

They don’t have to be converted from the ferric (Fe 3+) to the ferrous form (Fe 2+) to be transported across the intestinal epithelium

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12
Q

Roughly how much iron do we need in our diet per day?

A

10-15 mg

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13
Q

What does Fe2+ bind before being absorbed into the small intestine?

A

Transferrin

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14
Q

In what parts of the small intestine is iron absorbed?

A

Duodenum and upper jejunum

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15
Q

How is iron exported out of the enterocyte into the bloodstream?

A

Bound to ferroportin

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16
Q

How is iron transported in the bloodstream?

A

Bound to transferrin

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17
Q

How is iron taken into red blood cells?

A

Iron-transferrin complex binds to transferrin receptor

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18
Q

Which cells have the highest number of transferrin receptors?

A

Erythroid cells

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19
Q

What is the effect of vitamin C on iron absorption?

A

Enhances absorption of non-haem iron

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20
Q

Name 3 things that inhibit Fe absorption

A
  1. Tea
  2. Chapatis
  3. Antacids
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21
Q

What is hepcidin?

A

A negative regulator of iron absorption produced by the liver

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22
Q

What is the action of hepcidin?

A
  • Binds ferroportin for internalisation and degradation
  • Fe can’t pass from enterocytes into the blood
  • Recycled Fe from macrophages cannot enter blood
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23
Q

What 3 things is hepcidin regulated by?

A
  • HFE gene
  • Inflammatory cytokines
  • Transferrin Receptor
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24
Q

In what circumstance would hepcidin synthesis and release be up-regulated?

A

Iron overload

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25
Q

List some signs of iron deficiency

A
  • Pallor and pale conjunctiva
  • Tachycardia
  • Increased respiratory rate
  • Glossitis
  • Angular stomatitis
  • Koilonychia- spooning of nails
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26
Q

What epithelial changes are associated with iron deficiency?

A
  • Glossitis
  • Angular stomatitis
  • Koilonychia
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27
Q

Red blood cells on a blood film from a patient with iron deficiency would be ____chromic and ______cytic.

A
  1. Hypo

2. Micro

28
Q

What is the problem with using serum ferritin to assess iron deficiency?

A
  • It is an acute phase protein that would be raised in inflammation, malignancy, liver disease, alcoholism etc
  • Normal or increased ferritin levels don’t exclude iron deficiency
29
Q

What is a better test to identify functional Fe deficiency?

A

CHr test- tests reticulocyte Hb content

30
Q

What needs to be done once a patient is identified to have Fe deficiency?

A

Need to find underlying cause

31
Q

List some causes of Fe deficiency

A
  1. Inadequate dietary Fe intake
  2. Increased loss of Fe e.g. via bleeding stomach ulcer
  3. Excessive Fe use e.g. pregnancy
  4. Heavy periods etc etc
32
Q

How would you advise a patient to take their iron supplement tablets?

A
  • Take on an empty stomach
  • Take with orange juice
  • Don’t take with tea
33
Q

How can Fe2+ cause damage to lipid membranes, DNA and proteins?

A

Can cause production of hydroxyl and lipid radicals

34
Q

What is haemochromatosis?

A

A disorder of iron excess resulting in end organ damage due to iron deposition

35
Q

What is hereditary haemochromatosis due to?

A

An autosomal recessive inherited mutation in the HFE gene

36
Q

Why do patients with hereditary haemochromatosis have excess iron in cells?

A

HFE protein is mutated, so it can no longer compete with transferrin for the transferrin receptor on cells

37
Q

What is the treatment for hereditary haemochromatosis?

A

Venesection

38
Q

How much iron is contained in a 400ml bag of blood?

A

200mg

39
Q

Fe3+ is the ______ form of iron, and Fe2+ is the ______ form.

A
  1. Ferric

2. Ferrous

40
Q

Which form of iron can be absorbed into the intestinal enterocytes?

A

The ferrous form

41
Q

The ___________ count provides a good estimate of the amount of erythropoiesis going on in the patient’s marrow.

A

Reticulocyte

42
Q

Name 4 proteins involved in vertical interaction between the red blood cell plasma membrane and its cytoskeleton. What disorder is caused by mutations in these proteins?

A
  1. Ankyrin
  2. Spectrin
  3. Band 3 protein
  4. Protein 4.2
    - Hereditary spherocytosis
43
Q

In which organs/tissues are the highest concentrations of stored iron found?

A
  • Liver
  • Spleen
  • Bone marrow
44
Q

What is pancytopenia?

A

-Below normal levels of red blood cells, white blood cells and platelets

45
Q

What 2 main factors underlie the aetiology of anaemia of chronic disease?

A
  1. Increased macrophage activity reduces rbc lifespan

2. Increased cytokine production e.g. IL-6 increase hepcidin production- reduces intestinal Fe absorption

46
Q

Vit B12 and folate deficiency can give rise to what form of anaemia?

A

Megaloblastic anaemia- a macrocytic anaemia

47
Q

Why would anaemia due to vit B12 deficiency present later than folate deficiency?

A

-Can store via B12 for long time, so won’t become deficient for years

48
Q

Which mutation underlies sickle cell anaemia?

A

Substitution from glutamate to valine in beta- globin chain of Hb.

49
Q

In brief, what does thalassaemia result from?

A

Genetic reduction or absence of production of Hb’s alpha or beta chains, resulting in excess of the other type, which then precipitates.

50
Q

What are target cells, and in what patients might they be seen?

A
  • Nucleated, immature red blood cells that have escaped the marrow and are present in the periphery.
  • Seen in blood film of patients with thalassaemia
51
Q

What 2 errors in rbc metabolism can lead to haemolytic anaemia?

A
  1. Glucose-6-phosphate dehydrogenase deficiency

2. Pyruvate kinase deficiency

52
Q

What is myelofibrosis?

A

Haemopoetic tissue in marrow replaced by fibrotic tissue, leading to pancytopenia.

53
Q

What is polycythaemia vera?

A

Myeloproliferative neoplasm in bone marrow causes excessive production of rbc’s, resulting in an increased haematocrit >55%

54
Q

Why can anaemia arise from chronic kidney disease?

A

Kidneys don’t produce enough EPO to stimulate adequate erythropoiesis

55
Q

What is a major complication of polycythaemia vera?

A

Arterial thrombosis

56
Q

Despite increased haemolysis, which is the mean cell volume often normal in patients with hereditary spherocytosis?

A

-Increased reticulocyte count- larger than spherocytes and red blood cells, so compensate

57
Q

What type of anaemia does lack of intrinsic factor result in and why?

A
  • Pernicious anaemia

- Cannot absorb vitamin B12- needed for DNA synthesis

58
Q

Why does pyruvate kinase deficiency lead to haemolytic anaemia?

A
  • Red blood cells cannot make ATP
  • Na/K ATPase can’t function so K moves out of rbcs
  • Rbcs shrink, so are broken down
59
Q

Which gene is commonly mutated in many myeloproliferative neoplasms?

A

JAK2

60
Q

What are the main sites of haematopoiesis in an adult?

A
  • Skull
  • Ribs
  • Vertebrae
  • Pelvis
  • Sternum
61
Q

How might you treat a patient with polycythaemia vera?

A
  • Venesection to reduce haematocrit
  • Aspirin to reduce risk of thrombosis
  • Only use cytoreduction agents if venesection poorly tolerated, or patient is progressing
62
Q

Roughly when does the switch from foetal to adult Hb occur?

A

3-6 months old

63
Q

What facilitates Fe2+ uptake from the GIT lumen into enterocytes?

A

Divalent metal transporter 1 (DMT1)

64
Q

Define anaemia.

A

A Hb concentration lower than the normal range.

65
Q

Why might 2,3-BPG concentration increase in anaemia?

A

To shift the oxygen dissociation curve to right, so O2 is more readily released to the tissues

Ellie's MEH (12 decks)

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