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3 HAEM > ANAEMIA > Flashcards

ANAEMIA Flashcards

1
Q

what is the definition of anaemia

A

reduced total red cell mass

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2
Q

which markers are used to assess for anaemia

A

haemoglobin concentration and haematocrit

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3
Q

what are the normal levels of Hb concentration and haematocrit for males and females

A 
males
Hb 130-180
Hct 0.38-0.55
females 
Hb 120-180
Hct 0.37-0.47
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4
Q

how is Hb concentration measured

A 
burst red cells to create Hb solution 
stabilise the Hb molecules with cyanide
measure the optical density 
density is proportional to density 
concentration is calculated against a known standard solution
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5
Q

what does Beer’s law state

A

optical density is proportional to concentration

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6
Q

what is the haematocrit

A

ration of the whole blood that is red cells if the sample was left to settle

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7
Q

in what situation might Hb/Hct not be an accurate marker

A

directly after an acute rapid bleed (falsely reassuring)

after harm-dilution with fluids (falsely worrying)

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8
Q

how do reticulocytes differ from mature RBCs

A

larger than average RBCs
still have remnants of protein making machinery (RNA)
stains purple/deeper red due to presence of RNA

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9
Q

what is a polychromatic blood film

A

shows different colours

presence of reticulocytes

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10
Q

what is the normal reactive response to anaemia

A

reticulocytosis

increased production of reticulocytes by the bone marrow

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11
Q

measured red cell indices

A

Hb concentration
number of red cells
MCV

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12
Q

calculated red cell indices

A

haematocrit
mean cell Hb
(mean cell Hb concentration)

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13
Q

pathophysiological classifications of anaemia

A

decreased production (low reticulocyte count)

  • hypo proliferative
  • maturation abnormality

increased loss/destruction of red cells (high reticulocyte count)

  • bleeding
  • haemolysis
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14
Q

what types of maturation abnormality can occur

A 
cytoplasmic defects (impaired haemoglobinisation)
nuclear defects (impaired cell division)
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15
Q

how can the MCV be used to distinguish maturation abnormalities

A

low MCV consider problems with haemoglobinisation (cytoplasmic)

high MCV consider problems with cell division (nuclear)

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16
Q

define microcytic and macrocytic

A

microcytic = low MCV

macrocytic = high MCV

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17
Q

microscopic features of microcytic anaemias

A

low Hb content
small cells
hypo chromic (lacking in colour)

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18
Q

what is the deficiency in hypo chromic, microcytic anaemia

A

deficient haemoglobin synthesis (cytoplasmic defect)

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19
Q

what is the commonest cause of microcytic anaemia

A

iron deficiency

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20
Q

what is thalassaemia and what type of anaemia is it

A

globin deficiency

hypochromic microcytic

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21
Q

causes of hypo chromic microcytic anaemia

A

haem deficiency

  • lack of iron
  • anaemia of chronic disease (lack of available iron)
  • problems with porphyrin synthesis

globin deficiency
- thalassaemia

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22
Q

what is iron needed for

A

oxygen transport

electron transport

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23
Q

what is the structure of Hb

A

four globin subunit
each globin contains one haem molecule
each haem molecule contains on Fe2+ ion

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24
Q

which molecule transfers iron from liver stored to the erythroid

A

transferrin

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25
Q

what is the name of the molecule that iron is stored as

A

ferritin

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26
Q

where is the main iron store in the body

A

liver

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27
Q

how can ferritin be used to assess iron stores

A

it goes up when iron replete and down when iron deficient

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28
Q

how to assess iron status

A 
Hb (functional iron)
transported iron 
- serum iron
- transferrin
- transferrin saturation
storage iron
- serum ferritin
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29
Q

ow many binding sites are there in a molecule of transferrin

A

2

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30
Q

what does the % saturation of transferrin with iron measure

A

iron supply

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31
Q

in what situations might % saturation of transferrin with iron be abnormal

A

reduced in iron deficiency
reduced in anaemia of chronic disease
increased in genetic haemachromatosis

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32
Q

what does low serum ferritin mean

A

iron deficiency

33
Q

causes of iron deficiency

A

not eating enough
losing too much (bleeding)
not absorbing enough

34
Q

what is the difference between relative deficiency and absolute deficiency of iron

A

relative deficiency = still eating a normal amount but physiological increased demand eg child bearing age woman and children

absolute deficiency = not eating a normal amount eg vegetarian diet

35
Q

what is achlorhydria

A

deficiency of HCl resulting in impaired absorption of non-haem iron

36
Q

common causes of chronic blood loss

A

menorrhagia
GI tumours/ulcers
haematuria

37
Q

what is the equivalent iron loss due to menstrual bleeding per month

A

15-20 mg/month

38
Q

what happens if there is an iron deficiency

A

exhaustion of iron stores

iron deficient erythropoiesis (falling red cell MCV)

microcytic anaemia

epithelial changes (skin, koilonychia)

39
Q

why is occult blood loss a risk factor for microcytic anaemia

A

a small volume of GI blood loss can occur without symptoms

this can outstrip the maximum dietary iron absorption of iron

40
Q

signs of macrocytic anaemia on FBC

A

Hb low
RBC low
MCV high

41
Q

how can you tell if RBCs are normocytic on a blood film

A

size of the nucleus of a normal small lymphocyte should correspond to the size of RBC

42
Q

what are the causes of macrocytosis

A

genuine

  • megaloblastic
  • non-megaloblastic

spurious

43
Q

what are erythroblasts/normoblasts

A

normal red cell precursors with a nucleus

44
Q

what are the steps of erythroblasts developing into RBCs

A

accumulate Hb
reduce in size
lose nucleus when Hb content optimal

45
Q

at what point to red cell precursors stop dividing

A

late normoblast

46
Q

what are the names of the cells as red cell precursors develop into mature red cells

A 
pronormoblast 
early normoblast 
intermediate normoblast 
late normoblast 
reticulocyte 
RBC
47
Q

define megaloblast

A

an abnormally large nucleated red cell precursor with an immature nucleus

48
Q

how are megaloblastic anaemias characterised

A

predominant defects in DNA synthesis and nuclear maturation but RNA and HB synthesis are preserved

49
Q

what is the result of megaloblastic development

A

reduced division

apoptosis

50
Q

how does megaloblastic development result in anaemia

A

nuclear development is impaired but Hb accumulation is not

once Hb level is optimal, the immature nucleus is removed leaving a bigger than normal cell

the cells are bigger, but there are less of them because they were not able to divide

ANAEMIA

51
Q

causes of megaloblastic anaemia

A 
B12 deficiency 
folate deficiency 
(drugs, congenital abnormalities)
52
Q

why do we need B12 and folate for effective RBC development

A

essential co-factors for nuclear maturation

enable chemical reaction for DNA synthesis and gene activity

53
Q

what is the folate cycle important for

A

nucleoside synthesis

54
Q

what is the methionine cycle important for

A

producing a methyl donor (s-adenosyl methionine) to switch genes on/off

55
Q

causes of B12 deficiency

A

diet (vegans)
stomach (pernicious anaemia, atrophic gastritis, PPIs, gastrectomy)
small bowel (bacterial overgrowth, coeliac, Crohn’s, resection)
inherited deficiencies of things

56
Q

what is pernicious anaemia

A

autoimmune destruction of gastric parietal cells

results in intrinsic factor deficiency with B12 malabsorption and deficiency

57
Q

anaemic patient with family history of autoimmune conditions??

A

pernicious anaemia

58
Q

dietary sources of B12 and folate

A

B12
animal products

folate
liver, leafy veg, fortified cereals

59
Q

how long do B12 stores last

A

2-4 years

60
Q

how long do folate stores last

A

4 months

61
Q

causes of folate deficiency

A

inadequate intake
malabsorption
excess utilisation (haemolysis, increased skin turnover, pregnancy, malignancy)
drugs (anticonvulsants)

62
Q

clinical features of B12 and folate deficiency

A

symptoms/signs of anaemia
weight loss, diarrhoea, infertility
sore tongue, jaundice
developmental problems

63
Q

in which system is B12 deficiency more likely to cause symptoms that folate

A 
neurological system 
posterior/dorsal column abnormalities 
neuropathy 
dementia 
psychiatric manifestations
64
Q

what is pancytopenia

A

all cells low

red and white and platelets

65
Q

what is a macrovalocyte

A

macrocytic RBC that is oval shaped

66
Q

hyperhsegmented neutrophils are a sign of what

A

B12/folate deficiency

67
Q

how to assess for B12/folate deficiency

A 
blood films (for macrovalocytes)
B12/folate levels 
antibody tests (pernicious anaemia)
68
Q

which autoantibodies are useful for investigation of pernicious anaemia

A

anti-intrinsic factor (specific, not sensitive)

anti-gastric parietal cell (sensitive, not specific)

69
Q

treatment of megaloblastic anaemia

A

treat the cause where possible
IM vitamin B12 injections
folic acid tablets
red cell transfusions if life threatening

70
Q

causes of non-megaloblastic macrocytosis

A

alcohol
liver disease
hypothyroidism
marrow failure

red cell membrane changes

71
Q

what is spurious macrocytosis

A

mature red cell volume is normal but the MCV is measured as high

72
Q

causes of spurious macrocytosis

A

reticulocytosis

  • increase in reticulocytes which are bigger than mature red cells
  • the machine measures reticulocytes as RBCs so thinks the MCV is higher

cold agglutinations
- cold temperatures (25 degrees) makes RBCs clump together and be registered as a giant cell

73
Q

why do patients with pernicious anaemia have jaundice

A

intramedullary haemolysis

big cells get stuck in the bone marrow and breakdown, forming bilirubin –> jaundice

74
Q

investigations for anaemia

A 
history/exam/clinical contet
FBC
retic count 
blood film
ferritin/B12/folate 
bone marrow biopsy
75
Q

what is reticulocyte count a marker of?

A

red cell production

76
Q

causes of hypo proliferative anaemia

A 
marrow failure 
hypo metabolic
marrow infiltration (malignancy, fibrosis)
renal impairment
chronic disease
77
Q

how does renal disease cause anaemia

A

kidneys can’t sense hypoxia and/or release epo to induce red cell production

78
Q

pathophysiology of anaemia of chronic disease

A

inflammation causes macrophages to produce IL-6
unregulated hepcidin
hepcidin prevents iron release from tissue by degrading ferraportin

79
Q

when is a retic count indicated

A

if there is evidence of haemolysis eg from history, polychromasia

3 HAEM (20 decks)

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