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Haematology > RBCs And Anaemia > Flashcards

RBCs And Anaemia Flashcards

1
Q

Where does eyrthropoesis take place before and after birth?

A

before: liver
after: bone marrow (pelvis, sternum, skull, ribs, vertebrea)

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2
Q

What hormone stimulates erythropoesis, when and where is it produced?

A
  • erythropoetin (EPO)
  • from kidneys
  • When O2 levels in blood is low
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3
Q

Describe the process of erythrocyte production

A
  • GATA1 and FOG1 expressed in myeloid progenitor cells commit them to erythroid progenitor cell line
  • when hypoxia, EPO produced from kidneys
  • EPO inhibits apoptosis of colony forming units of erythroid cell line (CFU- E)
  • the erythroblasts extrude nucleus and most organelles as they develop to form reticulocytes which are released in to the circulation
  • reticulocytes extrude mitochondria and ribosomes over next 1-2 days and so become erythrocytes
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4
Q

What can be used as a good marker of amount of erythropoesis?

A
  • EPO

- reticulocytes

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5
Q

How does an RBC get its concave and flexible membrane?

A
  • spectrin, ankyrin, band 4 and protein 4.2 vertically interact with the cytoskeleton
  • band 3 goes across membrane
  • protein 4.2 binds band 3 and ankyrin
  • ankyrin binds to spectrin which acts to scaffold the actin cytoskeleton to the membrane
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6
Q

What is normal blood Hb levels and what % of a RBC should be taken up by Hb?

A

130-180 g/L (male), 115-165 (female) and lower of younger ppl
95%

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7
Q

How long will a RBC live in circulation for?

A

120 days

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8
Q

How do RBCs produce energy if they have no mitochondria?

A

pentose- phosphate pathway

glycolysis

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9
Q

What system controls eythryocyte death?

A

Reticuloendothelial system

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10
Q

Where is the reticuloendothilial system? What is it mainly made up of?

A

A network of cells located throughout body- main center is in spleen/ liver though.
Made up of types of macrophages- kupffer cells in liver, langerhans in skin

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11
Q

Describe the process of erythrocyte removal in spleen and haem catabolism

A
  • spleen filters blood
  • removes damaged erythrocytes
  • sensecent RBCs have their globin removed and metabolised to amino acids
  • The Hb is converted to bilirubin, which is conjugated with sugar in the liver, and removed as bile
  • bacteria in the colon metabolise and deconjugate the bilirubin to urobillinogen and then to urobillin and stercobillin which is secreted and gives poo a brown colour
  • urobillinogen may be reabsorbed but its secreted in urine
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12
Q

What is the normal mean cell volume?

A

80-100 fL

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13
Q

What is iron needed for?

A
  • enzymes
  • proteins
  • hb
  • ETC
  • protection against oxidative stress
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14
Q

How much iron is lost each day and due to what?

A

1-2 mg due to bleeding, hair removal, skin loss ect

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15
Q

How is iron excreted?

A

there is no mechanism for iron excretion

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16
Q

Where is excess iron stored and in what form? (non functional iron)

A

ferritin in liver, bone marrow, spleen, epethilial cells

haemosiderin (insoluable, in macrophages)

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17
Q

What is the difference between iron from meats and iron from pulses, nuts and grain?

A
  • from meats it is heam iron- mainly in ferrous state (Fe2+) so can be absorbed directly
  • From nuts ect it is non heam and so mainly in the ferric state ( Fe3+) so first must be reduced to Fe2+ before absorbtion
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18
Q

Describe the location and process of iron absorbtion

A
  • in duodenum and upper jejnuem
  • iron enters epethilial cells through the DMT1, it is either stored as ferritin or transported into blood (as ferritin)
  • ferroportin is responsible for moving ferritin into blood where it binds to a carrier to become transferrin
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19
Q

What is the possible fate of transferrin in the blood?

A
  • taken up into bone marrow for erythropoesis
  • taken up by macrophages in tissues and stored
  • transferin receptor needed for transferrin absorbtion into a cell
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20
Q

How is ferritin release from epithelia and macrophages regulated?

A
  • hepcidin from liver inhibits ferroportin on macrophages and epithilia to increase storage (as it cant leave the cell)
  • hepcidin release depends on dietary factors (sensed by villi of epethillia), body stores and erythropoesis rate
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21
Q

What enhances and decreases absorption of iron?

A
  • acids enhance absorption
  • tea and coffee decreases absorption
  • DMT expression controlled by hepcidin
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22
Q

Where does most active iron come from?

A

80% from recycling within body, only 20% from absorbtion

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23
Q

What can cause iron deficiency?

A
  1. decrease absorbtion/ intake
    - veggies, diarrhoea, gaviscon reduces uptake
  2. increased use
    - physiological: pregnancy, mensuration, aspirin, growth
    - pathological: bleeding (can be due to use of non- steroidal anti inflammatory drugs)
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24
Q

What are symptoms of anaemia caused by iron deficiency?

A
  • tiredness
  • exerisize intolerance
  • angina
  • paleness
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25
Q

what are the signs of anaemia caused by iron deficiency?

A
  • tachycardic
  • high resp rate
  • paleness
  • enlarged and shiney tongue
  • spoon nails
  • ulcers at corners of mouth
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26
Q

What will show up on the blood test and blood film results of someone with iron deficiency

A
  • Low Hb content (hypochromic)
  • low MCV (microcytic)
  • change in size and shape of RBCs (ansiopoikilocytosis)
  • presence of pencil and target cells
  • low serum ferritin, low serum iron and %transferritin saturation
  • low reticulocyte Hb content
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27
Q

What tests can be used to diagnose iron deficiency and what are their limitations

A
  1. can test serum ferritin
    - but this is an acute phase protein so while low ferritin means definatly iron deficient, normal or high ferritin does not exclude iron deficiency
  2. CHR (reticulocytes haemoglobin content)
    - when low they are definatly iron deficient and wont increase unless iron goes up
    - however its also low in pts with thalasaemia
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28
Q

How is iron deficiency treated?

A
  • dietary adivce- meats, seafoods, dark leafy greens (spinach), beans ect
  • IV/ IM injectons (only when severe as dangerous for heart)
  • oral supplements (cause constipation and diarrhoea tho)
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29
Q

What is the result of excess iron?

A
  • haemochromatosis
  • iron is deposited in liver, pancreas, gonads, heart, skin
  • leads to cirrhosis, adrenal insufficiency, heart failure, arthritis, diabetes, bronze skin
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30
Q

How can excess iron absorbtion occur?

A
  • heredeitary (haemochromatosis), HFE gene mutation, decreased HFE, HFE normally competes with transferritin for transferrin receptor, so less HFE means more transferrin absorbed
  • too many transfusions (eg in thallassaemia) mean iron builds up as its rarely lost
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31
Q

How ca hereditary haemochromatosis be treated?

A
  • draining blood (phlebotomy)
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32
Q

How can transfusion associated haemochromatosis be prevented?

A
  • iron chelating agents delay the effects of iron overload
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33
Q

Why might anaemia develop?

A
  • reduced/ ineffective erythropoesis
  • problems with Hb synthesis
  • loss of RBCs from circulation
  • problems with RBC membrane and metabolism
  • folate/ b12 deficiency
  • increased RBC removal
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34
Q

What is anaemia?

A
  • A low Hb concentration
35
Q

What are the symptoms for slow and acute onset anaemia?

A

slow onset: may be asymptomatic as body adjusts- decreased BPG, increased HR, EPO release ect
acute onset: headaches, pallor, fatigue, short of breath, angina

36
Q

What can cause deficancies in RBC production?

A

Radiation, chemicals (benzene), chemotherapy, parovirus
All these mean bone marrow not respond to EPO.
Or deficiencies in feed back look that creates EPO: kidney disease

37
Q

What else on a blood result suggests anaemia is due to reduced red cell production?

A
  • aplastic anaemia (low WBCs, platelets ect)

- low reticulocytes

38
Q

What type of anaemia is caused by iron deficiancy?

A

microcytic

39
Q

What type of anaemia is anaemia of chronic disease?

A

microcytic

40
Q

Describe the pathophysiology of anaemia of chronic disease?

A
  • chronic inflammatory diseases (RA, TB, malignancies ect) mean more activity of macrophages
  • this means shorter RBC life span
  • and cytokines like Il6 increase hepcidin release so more iron stored
  • also decreases sensitivity of bone marrow to EPO
41
Q

What will reticulocyte count, CRP and levels be in anaemia of chronic disease?

A

reticulocyte normal
CRP high
Ferritin high

42
Q

Is thalasamia micro, normo or macrocytic?

A

microcytic

43
Q

What is thallasaemia B major?

A

Both beta- globin chains are defective/ missing- ver severe

44
Q

What is thalassaemia B minor?

A

When only on beta- globin chain is defective/ missing

45
Q

What is thalassemia B intermida?

A

one beta globin gene missing on each chromosome

46
Q

Is someone is only misssing one alpha globin gene will they present with symptoms?

A

no

47
Q

What is HbH disease?

A

3 alpha globin genes are missing, tetramers of Beta globin form (HbH) this is moderately severe anaemia and makes microcytic RBCs

48
Q

What is hydrops fetalis?

A

all 4 alpha globin genes missing

y tetramers in foetus not sufficient so foetus dies

49
Q

If anaemia is due to loss of red cells (bleeding) what will be the MCV?

A

microcytic

50
Q

What can cause chronic excessive bleeding?

A
  • gastric ulcers
  • gastric cancer
  • colon cancer
  • menorrhagia
  • using NSAID such as ibuprofen cause GI bleeding
51
Q

Name some inherited problems of RBC membranes

A
  • spherocytosis (RBCs become spherical)
  • Elliptocytosis (RBCs take cigar shape)
  • Pyropoikliocytosis
  • stomatocytosis (swell and burst as cant hold Na and K well)
52
Q

What is the inheritance pattern of herediatry spherocytosis?

A

auto dominant

53
Q

What are the signs of herediary spherocytosis?

A
  • haemolytic anaemia
  • jaundice
  • spelnomegaly
  • gall stones
  • many ppl asymptomatic
54
Q

What will be the blood test and film results of hereditary spherocytosis? How is it diagnosed?

A
  • Hb low
  • platelets low- they pool in the spleen
  • MCV normal - more reticulocytes and these are larger so will counteract the fact that defctive blood cells are small
  • Reticulocytes high- compensation
  • blood film shows spherical RBCs
  • the EMA binding test will be abnormal
55
Q

What can cause aquired problems with RBC membranes?

A
  • mechanical damage- heart valves, vasculitis, MAHA, DIC
  • Heat damage (burns)
  • osmotic damage (downing)
56
Q

What two metabolic disorders cause anaemia?

A
  • G6PHD deficiency

- Pyruvate kinase deficiency

57
Q

Why does G6PHD deficiency cause anaemia?

A
  • Needed for pentose phosphate pathway
  • This is needed for NADPH production
  • Which is needed for glutathoine reduction
  • This needed to protect against oxidative damage
  • So leads to haemolytic anaemia
58
Q

Why does pyruvate kinase deficiency lead to anaemia?

A
  • needed for final step of glycolysis to create ATP
  • This is the only way RBCs can produce energy (no mitochondria)
  • cant fuel Na/ K pump
  • Cell shrinks and dies
59
Q

What other hereditary condition causes abnormal Hb synthesis?

A

sickle cell disease

60
Q

Why do you get hepatosplenomegaly and bone expansion in thalassaemia?

A
  • They try to compensate for anaemia so enlarge as they increase blood cell production
61
Q

Why do ppl with thalassaemia often get iron overload?

A
  • lots of transfusions is part of their treatment

- excessive absorption of iron due to ineffective haematopoesis

62
Q

What can cause excess removal of RBCs?

A
  • autoimmune conditions
  • antibodies bind to RBCs, so theyre destroyed in spleen
  • increased reticulocytes to compensate, raised billirubin (more heam breakdown), raides LDH (RBCs rich in this enzyme)
63
Q

What enzyme can be tested for in the blood and suggests haemolytic anaemia?

A

LDH

64
Q

How does the MCV change in anaemia due to B12 or folate deficiency and why ?

A

It becomes macrocytic (>100fL)

They’re both needed for DNA synthesis, so the cytoplasm development is faster than cell division and nuclear maturation

65
Q

What is the role of folate ?

A
  • acceptor of a single carbon from amino acids, which can go on to provide the carbon for other compounds (creates the one carbon pool)
  • The one carbon pool is needed for purine base synthesis and transfer of methyl on to B12
  • Role prominent in RBC precursor cells
66
Q

What happens to folate once it is absorbed?

A
  • absorbed by proximal intestine
  • converted to methyl tetrahydrofolate
  • taken to liver
  • stored
67
Q

What foods is folate present in?

A

liver, leafy greens

68
Q

Other than dietary insufficiency, what can cause folate deficiency?

A

pregnancy, severe skin diseases (psoriasis), ALCOHOLISM (damages intestine), proximal small bowel diseases (crohns, coeliac), anticovulsant drugs, liver disease, heart failure

69
Q

Where is B12 obtained from?

A

eating animal based foods, its originally synthesised by microorganisms

70
Q

Describe what happens B12 after ingestion

A
  • B12 binds to hepatocorrins- this complex is digested by pancreatic proteases to release the B12
  • this is combined with intrinsic factor (IF) produced by partietal cells in stomach
  • Binds to illeum, B12 absorbed, IF destroyed
  • B12 bound to transcobalamin which delivers it to bone marrow and other tissues
71
Q

What can cause B12 deficiency?

A
  • vegetarian diet- most from animal foods
  • Auto immune destruction of parietal cells
  • gastroectomy
  • diseases of ileum (crohns ect)
  • congenital defiencies in transcoalbumin
72
Q

How does B12 deficiency lead to functional folate deficiency?

A
  • B12 is needed to remove a methyl group from methyl tetrahydrofolate and put it on a methionine
  • folate therefor not available for purine synthesis
73
Q

How long can you last without eating B12 before you become symptomatic?

A

years because it is in large surpless in the body

74
Q

What other effect is there to B12 deficiency but not folate?

A
  • focal demyelination of some nerves

- leads to depression and dementia

75
Q

What 3 major processes can cause polycytheamia (High RBC conc)?

A
  • myeloproliferative disorders (eg polycythemia vera)
  • EPO receptor mutation so always active
  • a physiological reaction
  • reaction to secondary condition (smoking ect)
  • dehydration leads to low plasma vol so relative polycythaemia
76
Q

What is the cause of most myeloproliferative disorders?

A

usually mutations to JAK2 genes, meaning over activity of progenitor cells

77
Q

What are the key clinical features of polycythaemia vera?

A
  • Pruritis (itching) often after hot shower- unknown cause
  • splenomegaly leads to fullness and abdo discomfort (more RBC destruction)
  • tiredness, muscle aches- more viscous blood
  • headaches, confusion, dizziness- more viscous blood = less to brain
  • increased bleeding (gums) and high risk of thrombus - mutation often also affects platelet formation
  • high haematocrit and Hb
  • JAK2 mutation
78
Q

What is the difference between relative and absolute ertyhrocytosis?

A

relative is normal red cell mass but low plasma volume.

Absolute is normal plasma volume and high red cell mass

79
Q

What could lead to increased EPO (causing erytrocytosis)?

A
  • central hypoxia (chronic lung disease, CO poising, altitude training)
  • renal hypoxia (renal artery stenosis, kidney failure)
  • Many cancers (renal cell cancer, hepatocellular carcinoma)
  • EPO injection in cyclists
80
Q

How is polycythaemia vera managed?

A
  • venesection (remove blood)
  • aspirin (thins blood, reduces clot risk)
  • manage CVS risk factors
  • other drugs can be used if splenomegaly becomes symptomatic/ disease progresses ect
81
Q

What is the difference between primary and secondary polycythaemia?

A

primary is something that directly causes raised haematocrit- polycthaemia vera
secondary is heamatocrit being raised due to an increase in EPO production for example at altitude

82
Q

What genes are expresses in myeloid cells that commits them to the erythroid lineage?

A

GATA1, FOG1 and PU.1

83
Q

How does EPO work to increase erythropoesis?

A

inhibits apoptosis of CFU-E cells (colony forming units of the erythroid cell line)

84
Q

What is pernicious anaemia?

A

lack of intrinsic factor so you cannot absorb b12

Haematology (3 decks)

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