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haematology > red cells + acquired anaemias > Flashcards

red cells + acquired anaemias Flashcards

1
Q

factors influencing ‘normal range’ of haemoglobin levels

A 
age
sex
ethnic origin 
time of day sample taken 
time to analysis
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2
Q

male haemoglobin reference ranges

A

12-70: 140-180

>70: 116-156

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3
Q

female haemoglobin reference ranges

A

12-70: 120-160

> 70: 108-143

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4
Q

general features of anaemia

A 
tiredness
pallor 
breathlessness
swelling of ankles (heart failure) 
dizziness (adjustment of BP)
chest pain - myocardial ischaemia
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5
Q

anaemia causes: problem with production in bone marrow

A

cellularity
stroma
nutrients - not enough iron, folate etc

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6
Q

anaemia causes: problem with red cell

A

membrane
haemoglobin
enzymes

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7
Q

anaemia causes: problems with destruction and loss

A

blood loss
haemolysis
hypersplenism - pooling of blood in spleen

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8
Q

red cell indices

A

automated measurement of red cell size and haemoglobin content

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9
Q

MCH

A

mean cell haemoglobin

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10
Q

MCV

A

mean cell volume (cell size)

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11
Q

hypochromic microcytic anaemia

A

small pale cells

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12
Q

normochromic normocytic anaemia

A

huge number of anaemias

normal amount of Hb and avg normal cell size

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13
Q

macrocytic anaemia

A

big red cells

bigger cells but usually with less Hb - usually pale

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14
Q

hypochromic microcytic anaemia first investigation to do

A

serum ferritin - measure of body iron store

if low = iron deficiency

if normal/inc = thalassaemia, 2ry anaemia (sideroblastic anaemia)

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15
Q

normochromic normocytic anaemic first investigation to do

A

reticulocyte count

if bleeding or haemolysis this count will increase

low if bone marrow nor working

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16
Q

first investigation to do if macrocytic anaemia

A

B12/folate + bone marrow

commonest cause = B12 or folate deficiency

if B12 + folate normal then bone marrow problem e.g. malignancy

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17
Q

hypochromic microcytic anaemia: secondary anaemia

A

normal ferritin with abnormal iron utilisation if background inflammation

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18
Q

intake and loss of dietary iron

A

absorbed by duodenum

lost by intestinal cells (+ menstruation in women)

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19
Q

dietary iron absorption

A
  • iron from diet can be haem or non-haem
  • enter through villi of duodenum, ferroportin transports it across into circulatin
  • bind to transferrin which carries it to liver (if needed for making blood) or to liver where it is stored as ferritin
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20
Q

hepcidin

A

synthesised by hepatocytes in response to increased iron levels, binds to ferroportin and inactivates it

stops you absorbing more iron than you need

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21
Q

iron and inflammation

A

iron can be redirected into inflammatory processes

hepcidin switches on to allow this to happen

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22
Q

signs of iron deficiency

A

kooilonychia
angular chelitis
atrophic tongue

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23
Q

causes of iron deficiency

A

GI blood loss
menorrhagia
malabsorption - gasterectomy, coeliac

24
Q

management of iron deficiency

A

correct deficiency - oral iron usually sufficient (IV if intolerant), blood transfusion rarely indicated

correct cause - diet, ulcer therapy, gynae intervention, surgery e.g. tumour

25
Q

normochromic normocytic anaemia: reticulocyte count increased

A
  • acute blood loss

- haemolysis: inc breakdown of cells

26
Q

normochromic normocytic anaemia: reticulocyte count normal/low

A

secondary anaemia e.g. due to renal impairment, chronic disease
hypoplasia
marrow infiltration

27
Q

secondary anaemia

A

anaemia of chronic disease

mostly hypochromic microcytic

28
Q

secondary anaemia: defective iron utilisation

A
  • increased hepcidin in inflammatin

- ferritin often elevated (acute phase reactant)

29
Q

secondary anaemia: underlying diseases

A

infection
inflammation
malignancy

30
Q

haemolytic anaemi

A

accelerated red cell destruction (low Hb)

compensation by bone marrow (inc reticulocytes)

31
Q

extravascular haemolysis

A

extravascular haemolysis in macrophages of reticuloendothelial cells
normal process
increased in haemolysi s e.g. red cell abnormal shape and removed faster

can get exageration of normal process as cells recognised as foreign by reticuloendothelial system

32
Q

intravascular haemolysi s

A

pathological
red cells bust in circulation
free Hb in circulation toxic to kidneys, free radicals cause inflammation

sick people or haemoglobinopathies e.g. sickle cell

33
Q

congenital haemolytic anaemias

A

hereditary spherocytosis
G6PD deficiency
haemoglobinopathy HbSS

34
Q

acquired haemolytic anemias

A

autoimmune haemolytic anaemia (extravascular) - exaggerated removal of red cells from circulation

mechanical e.g. artificial valve leaking (intravasc)

severe infection/DIC (intravasc)

PET/HUS/TTP (intravasc)

35
Q

immune haemolytic anaemias

A

mostly extravascular

36
Q

non-immune haemolytic anaemias

A

mostly intravascular

37
Q

direct antiglobulin test

A

if suspicion someone has immune haemolysis

detects antibody or complement on red cell membrane

38
Q

direct antiglobulin test: reagent

A

anti-human IgG antibody or
anti-complement antiboy

reagent will bind if there is antibody on red cell surface and cause agglutinatin in vitro (cells stick together)

39
Q

direct antiglobulin test resultd

A

positive - immune mediated

negative - non-immune mediated

40
Q

immune haemolysis: warm autoantibody

A

bind to cells at body temp only

autoimmune
drugs
CLL

41
Q

immune haemolysis: cold autoantibody

A

only bind when cold

CHAD
infections
lymphoma

42
Q

immune haemolysis: alloantibody

A

antibody against transfused cells

transfusion reaction

43
Q

extravascular haemolysis - blood film

A

spherocytes on film - due to damaged membrane

agglutination in cold

AIHA

44
Q

intravascualr haemolysis - blood film

A

red cell fragments - schistocytes

45
Q

haemolytic anaemia investigations

A 
FBC
reticulocyte count 
blood film
serum bilirubin, LDH
serum haptoglobin
46
Q

haemolytic anaemia management

A

support marrow function - folic acid
correct cause - immunosuppression if autoimmune (steroids, treat trigger e.g. lymphoma)
remove site of red cell destruction - splenectomy

consider transfusion

47
Q

macrocytic anaemia investigations

A

B12/folate assay and blood film

megaloblastic = b12/folate deficiency

non-megaloblastic = myelodysplasia, marrow infiltration, drugs e.g.methotrexate

48
Q

vitamin B12 absorption

A

dietary B12 binds to intrinsic factor (made by parietal cells)
B12-IF complex attaches to specific IF receptors in distal ileum
B12 bounded by transcobalamin II in portal circulation for transport to marrow/other tissues

49
Q

B12 deficiency causes

A

pernicious anaemia

gastric/ileal disease

50
Q

folate deficiency causes

A

dietary
inc requirements (haemolysis)
GI pathology e.g. coeliac

51
Q

why do get lemon yellow tinge in B12/folate def anaemia

A

bilirubin, LDH

red cells friable

52
Q

pernicious anaemia

A

commonest cause of B12 def in western pop

autoimmune disease

antibodies against intrinsic factor, parietal cells

malabsorption of dietary B12

53
Q

why to symptoms/signs of pernicious anaemia take 1-2yrs to show

A

takes time to run through b12 stores

bit of passive absorption in small intestine

54
Q

megalobastic anaemia treatment

A

replace vitamin

55
Q

B12 replacement

A

B12 IM injection

loading dose then 3mo maintenance

56
Q

folate replacement

A

oral folate replacement

ensure B12 normal if neuropathic symptoms

57
Q

other causes of macrocytosis

A 
alcohol 
drugs - methotrexate, antiretrovirals, hydroxycarbamine
disordered liver function
hyperthyroidism 
myelodysplasia

haematology (32 decks)

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