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Haematology > Anaemia > Flashcards

Anaemia Flashcards

1
Q

What is anaemia?

A

reduced total red cell mass, Hb is a surrogate marker for this

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2
Q

How can anaemia be measured?

A

using Hb concentration or haematocrit (ratio of the whole blood that is red cells if the sample was left to settle)

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3
Q

Anaemias can be classified by MCV (mean cell volume) as ________

A

normocytic, (hypo chromic) microcytic or macrocytic

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4
Q

Hypochromic microcytic anaemia is due to _________

A

deficient Hb synthesis, a cytoplasmic defect, defects in Hb result in small cells, the cells keep dividing as they try to accumulate Hb

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5
Q

What is the most common cause of microcytic anaemia?

A

iron deficiency anaemia

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6
Q

What is the second most common cause of microcytic anaemia worldwide?

A

thalassaemia

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7
Q

List all the main causes of microcytic anaemia?

A

TAILS

thalassaemia, anaemia of chronic disease, iron deficiency, lead, sideroblastic anaemia

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8
Q

What are the potential causes of iron deficiency anaemia?

A

diet, malabsorption or chronic blood loss

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9
Q

What are some causes of chronic blood loss?

A

menorrhagia, GI bleeding, haematuria

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10
Q

Macrocytic anaemia is due to a problem with ______

A

maturation

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11
Q

Macrocytic anaemia can be ____________

A

megaloblastic or non-megaloblastic

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12
Q

What is a megaloblast?

A

an abnormally large nucleated red cell precursor with an immature nucleus

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13
Q

What are megaloblastic anaemias characterised by?

A

a lack of red cells due to predominant defects in DNA synthesis and nuclear maturation in developing precursors in the bone marrow

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14
Q

Explain how megaloblasts cause a macrocytic anaemia?

A

the megaloblast cytoplasm still develops and they accumulate Hb, once Hb level in the cell is optimal the nucleus is extruded leaving a bigger than normal red cell i.e. a macrocyte

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15
Q

Why do megaloblasts cause an anaemia?

A

compared to normal precursors megaloblasts have reduced division and increased apoptosis which is what causes the anaemia

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16
Q

The larger cell size in megaloblastic anaemia is due to what?

A

failure of precursors to get smaller NOT an increase in size

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17
Q

What are the two major causes of megaloblastic macrocytic anaemia?

A

B12 or folate deficiency

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18
Q

Explain the role of B12 and folate?

A

they are essential cofactors in linked biochemical reactions regulating

1) DNA synthesis and nuclear maturation (this is what causes the blood cell effect)
2) DNA modification and gene activity (what causes the nervous system effect)

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19
Q

What are dietary sources of B12?

A

animal products e.g. meat, fish, milk, cheese, eggs

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20
Q

What are dietary sources of folate?

A

liver, leafy veg and some fortified cereals

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21
Q

___1_____ secreted by gastric parietal cells is what allows B12 to be absorbed

B12 is absorbed in the _____2_____

A

1) intrinsic factor

2) ileum

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22
Q

Folate is absorbed in the ___________

A

duodenum and jejunum

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23
Q

Body stores of B12 last ___1_____

Body stores of folate last __2_____

A

1) 2-4 years

2) 4 months

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24
Q

Why do symptoms of B12 deficiency take longer to manifest than folate?

A

Body stores of B12 are longer (2-4 years vs 4 months) so can have to be deficient for several years before stores can no longer meet demand

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25
Q

How can you assess for B12 or folate deficiency?

A

measure serum folate or B12

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26
Q

List some causes of B12 deficiency?

A

diet (vegan)
pernicious anaemia
surgical resection of the small bowel
gastrectomy

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27
Q

List some causes of folate deficiency?

A

diet, malabsorption in coeliacs or crohns, excess utilisation when stores are low (e.g. haemolysis, exfoliating dermatitis, pregnancy, some malignancies), certain drugs such as AEDs can cause folate deficiency too

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28
Q

What is the most common cause of B12 deficiency in adults?

A

pernicious anaemia

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29
Q

What is pernicious anaemia?

A

an autoimmune condition causing destruction of the gastric parietal cells resulting in intrinsic factor deficiency so malabsorption of B12

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30
Q

What is pernicious anaemia associated with?

A

personal or family history of other autoimmune diseases e.g. atrophic gastritis, vitiligo, addisons and hypothyroid

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31
Q

Is diet more likely to be an issue in folate or B12 deficiency?

A

folate- because body stores are lower

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32
Q

Who does folate deficiency often occur in?

A

alcoholics

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33
Q

What can you check for in pernicious anaemia?

A

anti-gastric parietal cell and anti-intrinsic factor

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34
Q

What are the causes of non-megaloblastic macrocytic anaemia?

A

alcohol, liver disease, hypothyroidism - these are not always associated with an anaemia and can cause macrocytosis on own

marrow failure is another cause and this will always be associated with an anaemia

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35
Q

When can spurious anaemias occur?

A

when there are increases/ decreases in plasma volume which affect the Hb conc relative to the plasma

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36
Q

What can cause a spurious macrocytosis?

A

acute blood loss or haemolysis- there are increased reticulocytes which may raise MCV
cold agglutinins- abnormal proteins produced in infection or cancer cause clumping of cells when not at body temperature

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37
Q

Symptoms of anaemia?

A

can be asymptomatic
fatigue, headaches, faintness
breathlessness
anaemia can exacerbate cardiorespiratory symptoms in the elderly causing angina, palpitations and intermittent claudication

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38
Q

Signs of anaemia?

A

pallor
tachycardia
systolic flow murmur
cardiac failure

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39
Q

Specific signs of iron deficiency?

A 
brittle nails 
koilonychia (spoon nails) 
atrophy of the papillae of the tongue 
angular stomatitis 
brittle hair
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40
Q

Specific signs and symptoms of B12 and folate deficiency?

A 
weight loss
diarrhoea
infertility
glossitis 
pre-hepatic jaundice 
developmental problems 
with B12 only: posterior dorsal column abnormalities, neuropathy, dementia, psychiatric manifestations (these neurological manifestations can be irreversible)
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41
Q

Treatment of iron deficiency anaemia?

A

treat underlying cause
oral ferrous sulfate 200 mg tablets 2-3 a day
can experience GI side effects e.g. nausea, diarrhoea or constipation
monitor Hb and once returned to normal continue for a further 3 months
sodium feredetate is a liquid solution used in children

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42
Q

Treatment of B12 deficiency?

A

IM B12 injections can be given, at first get several over a couple of weeks and then move to every 3 months lifelong

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43
Q

Treatment of folate deficiency?

A

5mg folic acid daily, should be taken for 4 months to replace body stores, any underlying cause should be treated

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44
Q

List some causes of normocytic anaemia?

A

acute blood loss, anaemia of chronic disease, CKD, autoimmune RA, marrow infiltration/ fibrosis, endocrine disease, haemolytic disease

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45
Q

Alpha like genes are on chromosome ________ and their are ______ per chromosome meaning ________

A

16
2 genes
4 overall

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46
Q

Beta like genes are present on chromosome ______ and there _______ per chromosome meaning _______

A

11
1 gene
2 overall

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47
Q

Only _____ chains are present in both adult and fetal Hb

A

alpha

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48
Q

Adult levels of HbA are reached by ___________ and this explains why _______

A

6-12 months of age

beta chain problems dont manifest until this point

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49
Q

What are the haemoglobinopathies?

A

hereditary conditions affecting globin chain synthesis
hundreds of mutations
behave as autosomal recessive disorders
thalassaemias: decreased rate of globin chain synthesis (normal chains though)
structural Hb variants: normal production of abnormal globin chains e.g. HbS

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50
Q

Explain what the thalassaemias are?

A

reduced globin chain synthesis > impaired HB production can be alpha or beta
results in microcytic hypo chromic anaemia
if severe: unbalanced accumulation of globin chains which are toxic to the cell, ineffective erythropoiesis, haemolysis

51
Q

Where are thalassaemias more common and why?

A

Asia and Africa
generally more common in areas where malaria is endemic because the condition offers slight protection against malaria infection

52
Q

What are the three alpha conditions you can have?

A

Alpha thalassaemia trait (1 or 2 missing genes)
HbH disease (only 1 working gene)
Hb Barts Hydrops Foetalis Syndrome (no working genes)

53
Q

Describe the features of alpha thalassaemia trait?

A

one or two alpha genes missing
asymptomatic carrier state
anaemia is usually mild

54
Q

Is treatment usually required for alpha thaalassaemia trait?

A

no

55
Q

Explain what happens in HbH disease?

A

excess B chains form tetramers (B4) called HbH. Red cell inclusions of HbH can be seen with special stains. HbH causes intramedullary and extravascular haemolysis and doesn’t offload O2 to tissues as readily as HbA. This causes hepatosplenomegaly as RBC attempts to increase production.

56
Q

Signs that someone has HbH disease?

A

anaemia with very low MCV and MCH (mean corpuscular Hb)
hepatosplenomegaly
jaundice (due to haemolysis)

57
Q

Treatment of HbH disease?

A

may not be transfusion dependent but can be treated with regular blood transfusions and iron chelating drugs to prevent iron overload

58
Q

What is Hb Barts Hydrops Foetalis Syndrome?

A

severest form of alpha thalassaemia where there are no alpha genes from either parent

59
Q

Explain what happens in Hb Barts Hydrops Foetalis Syndrome?

A

there is minimal or no alpha chain production so HbF and HbA can’t be made
There are no alpha chains to bind to so tetramers of Hb Barts (gamma4) and HbH (beta4) are produced

60
Q

Describe the clinical features of Hb Barts Hydrops Foetalis Syndrome?

A

profound anaemia, cardiac failure, growth retardation, severe hepatosplenomegaly, skeletal and CVS abnormalities
almost all die in utero

61
Q

When should thalassaemia be suspected?

A

if microcytic hypochromic anaemia with normal ferritin

62
Q

What are the three beta conditions you can have?

A

Beta thalassaemia trait/ minor (B+/B) or (B0/B)
Beta thalassaemia intermedia (B+/B+) or (B0/B+)
Beta thalassaemia major (B0/B0)

63
Q

Difference between B+ and B0?

A

B+ is reduced production

B0 is absent production

64
Q

Describe features of beta thalassaemia trait/ minor?

A

individuals are usually asymptomatic with no or mild anaemia

65
Q

What are the clinical features of beta thalasaemia intermedia?

A

causes a moderate anaemia but patients don’t require regular transfusions usually
patients may have splenomegaly and bone deformities, recurrent leg ulcers, gallstones and infections
patients may be iron overloaded even if not having regular transfusions due to excessive iron absorption caused by the underlying dyserthropoiesis

66
Q

Treatment of beta thalassaemia intermedia?

A

patients dont usually require regular transfusions but might need them when they are unwell

67
Q

Describe clinical features of beta thalassaemia major?

A

Most children present in first year of life as Hb falls:

  • failure to thrive and recurrent bacterial infections
  • severe anaemia from 3-6 months (when gamma to beta chain conversion should occur)
  • extramedullary haemopoiesis that soon leads to hepatosplenomegaly and bone expansion
  • skull xr show hair on end appearance due to expansion of cortical bone
  • can get cord compression due to expansion
68
Q

Skull x-ray shows “hair on end” appearance?

A

beta thalassaemia major

69
Q

Management of beta thalassaemia major?

A

regular transfusion programme to maintain Hb at 95-105g/l (this suppresses ineffective erythropoiesis and inhibits over absorption of iron)

long term folic acid supplementation is required

bone marrow transplantation is sometimes an option if carried out before complications can develop

iron overload from transfusions should be managed with iron chelating drugs e.g. desferrioxamine

70
Q

HbS results from a ____________

A

single base mutation/ point mutation at codon 6 in beta globin gene that substitutes glutamine to valine

71
Q

Describe the impact of HbS and sickling?

A

HbS polymerises if exposed to low O2 levels for a prolonged period which distorts the RBC and damages the membrane
sickling of cells is initially reversible but with repeated sickling cells lose membrane flexibility and become irreversibly sickled
sickling can produce a shortened red cell survival and impaired passage of cells through the microcirculation leading to obstruction of small vessels and tissue infarction

72
Q

Where is the sickle gene most common?

A

most common in Africans but is also found in the Middle East, India, and Southern Europe

73
Q

Describe the main features of sickle cell trait?

A

one normal, one abnormal gene
asymptomatic carrier state (300 M worldwide)
few clinical features as HbS level is too low to polymerise
may sickle in severe hypoxia
blood film normal, mainly HbA, HbS < 50%

74
Q

Describe the main features of sickle cell anaemia?

A

two abnormal genes
HbS > 80%, no HbA
episodes of tissue infarction due to vascular occlusion (sickle crisis), chronic haemolysis (shortened RBC lifespan), hyposplenism (due to repeated splenic infarcts)

75
Q

What happens during a sickle cell crisis?

A 
very painful (site depends on where crisis is happening) 
pain is due to occlusion of vessels
76
Q

Precipitants of a sickle cell crisis?

A 
hypoxia
dehydration 
infection
cold exposure 
stress
fatigue
77
Q

Sickle cell crisis treatment?

A 
opiates
hydration 
rest
O2
antibiotics if evidence of infection 
in severe crisis red cell exchange transfusion (venesection- transfuse-venesect etc)
78
Q

Long term management of sickle cell anaemia?

A

manage hyposplenism- give prophylactic penicillin, vaccinate against pneumococcus, meningicoccus, HiB

folic acid supplementation

hydroxycarbamide can reduce severity of disease by inducing HbF production

regular transfusion to prevent stroke in select cases

79
Q

Describe diagnosis of haemoglobinopathies?

A 
FBC, Hb, red cell indices
blood film
ethnic origin 
high performance liquid chromatography (HPLC) or electrophoresis to quantify Hb present 
> this identifies abnormal Hb e.g. HbS
80
Q

Raised HbA2 is diagnostic of what?

A

beta thalasasemia trait

81
Q

Describe the difference between Haem and non-haem iron?

A

Non-haem iron is mainly derived from cereals
Haem iron is derived from haemoglobin and myoglobin in red or organ meats
Haem iron is better absorbed than non Haem iron

82
Q

Most iron is stored in ______

A

Hb

83
Q

Macrophages store iron _______

A

temporarily when red cells are broken down

84
Q

The body iron content is closely regulated by ________ but ___________

A

control of iron absorption but there is no physiological mechanism for eliminating iron from the body

85
Q

Where does iron absorption mainly occur?

A

in the duodenum

86
Q

___1___ facilitates iron export from the enterocyte and passes on to ____2____ for transport elsewhere

A

1) ferroportin

2) transferrin

87
Q

What is the major regulator of iron uptake, what is it produced in response to?

A

hepcidin is the major regulator of iron uptake and it is produced by the liver in response to increased iron and inflammation

88
Q

When do hepcidin levels decrease?

A

when iron is deficient

89
Q

What does hepcidin do?

A

it binds to ferroportin and causes its degradation, iron is therefore trapped in duodenal cells and macrophages

90
Q

3 ways to assess iron status?

A

functional iron > Hb concentration

transferrin saturation (%)

storage iron- serum ferritin (tissue biopsy rarely needed)

91
Q

Describe transferrin saturation as a measurement of iron status?

A

transferrin transports iron from donor tissues to tissues expressing transferrin receptors (erythroid marrow has lots of transferrin receptors)
normally transferrin saturation is around 20-50%
saturation increases in iron overload and decreases in iron deficiency

92
Q

Describe storage iron as a measurement of iron status?

A

serum ferritin isn’t where most iron is stored but tiny amounts reflect the intracellular ferritin synthesis so it is an indirect measure of storage iron
serum ferritin also acts as an acute phase protein so goes up with infection, malignancy etc so can make measurement inaccurate

93
Q

What are the two types of iron overload?

A

primary iron overload due to hereditary haemochromatosis

secondary iron overload due to repeated red cell transfusions, excessive iron absorption due to over-active erythropoiesis

94
Q

What is the commonest form of hereditary haemochromatosis due to?

A

mutations in HFE gene which causes a decreased synthesis of hepcidin resulting in increased iron absorption

95
Q

Clinical features of hereditary haemochromatosis?

A

gradual and insidious, tends to present in middle age, weakness/ fatigue, joint pain, impotence, arthritis, cirrhosis, diabetes, cardiomyopathy

96
Q

Diagnosis of hereditary haemochromatosis?

A

95% will have HFE mutation, transferrin saturation > 50%, serum ferritin > 300 ug/l in men or > 200 ug/l in pre-menopausal women, liver biopsy rarely needed

97
Q

Treatment of hereditary haemochromatosis?

A

weekly venesection, initial aim is to exhaust iron stores (ferritin < 20 ug/l), thereafter keep ferritin < 50 ug/l

98
Q

Why is family screening for hereditary haemochromatosis important?

A

may not be symptomatic until irreversible organ damage has occurred

99
Q

What disorders can you get secondary iron overload in?

A

thalassaemia, sideroblastic anaemia, red cell aplasia, myelodysplasia

100
Q

What is secondary iron overload treated with?

A

iron chelating drugs (can’t venesection because already anaemic)

101
Q

Explain what causes the anaemia of chronic disease?

A

a multifactorial pathophysiology with inflammation (from malignancy, auto immune or infection) as central process, this causes activation of t cells and monocytes which release cytokines which can cause anaemia through a number of mechanisms

102
Q

Explain why anaemia of chronic disease can be normocytic or microcytic?

A

usually normocytic

can be microcytic if the cytokines cause the liver to increase hepcidin causing relative iron deficiency

103
Q

Does shortening of RBC survival always cause anaemia?

A

No

not if there is a compensatory rise in RBC production by the bone marrow

104
Q

What are the consequences of haemolysis?

A

causes erythroid hyperplasia, immature red cells (reticulocytes) are also released prematurely
these cells are larger than mature red cells and stain with light blue tinge on peripheral blood film due to the presence of residual RNA
excess red cell breakdown products e.g. bilirubin will also be present (different products depending on cause)

105
Q

Haemolytic anaemia is normo, macro or micro?

A

normocytic

106
Q

What is more common, extravascular or intravascular haemolysis?

A

extravascular

107
Q

Explain what is meant by extravascular haemolysis and the consequences of it?

A

The RBCs are removed from the circulation by macrophages in the circulation usually by the spleen or liver
there will be hyperplasia at the site of destruction (splenomegaly +/- hepatomegaly)
normal products by in excess
unconjugated bilirubinaemia, urobilogenuria, may cause pigment gall stones

108
Q

What type of haemolysis is being described:

normal products but in excess?

A

extravascular

109
Q

What is meant by intravascular haemolysis and what are the consequences of it?

A

red cells are destroyed in the circulation spilling their contents
abnormal products are produced and this can be life threatening
haemoglobinaemia (due to free Hb in circulation), methaemalbininaemia, haemoglobinuria (pink urine turns black on standing), haemosiderinuria

110
Q

Pink urine turns black on standing?

A

haemoglobinuria - a sign of intravascular haemolysis

111
Q

What type of haemolysis is being described:

abnormal products?

A

intravascular haemolysis

112
Q

Causes of intravascular haemolysis vs extravascular haemolysis?

A 
intravascular has 4 main causes: 
ABO incompatible blood transfusion 
G6PD deficiency 
severe falciparum malaria (blackwater fever) 
rarer causes e.g. PNH or PCH

basically all other causes of haemolysis are extravascular

113
Q

List as many causes as you can of haemolytic anaemia?

A
  • hereditary red cell membrane defects
  • Hb abnormalities e.g. sickle cell or thalassaemia
  • metabolic defects e.g. G6PD deficiency
  • warm or cold autoantibodies
  • alloantibodies e.g. allo-transfusino, HD of newborn
  • acquired membrane defects e.g. paroxysmal nocturnal haemoglobinuria
  • mechanical RBC destruction e.g. prosthetic heart valve
  • secondary haemolysis from renal/ hepatic failure
  • infections e.g. malaria and mycoplasma
  • drugs
  • hypersplenism
  • burns
  • haemolytic uraemic syndrome due to E coli 0157
114
Q

Describe investigations for haemolytic anaemia?

A

1) CONFIRM HAEMOLYTIC STATE:
- FBC and blood film
- retic count
- serum unconjugated bilirubin
- serum haptoglobin
- urinary urobilinogen

2) IDENTIFY CAUSE:
- family history, examine
- blood film
- specialist investigations

115
Q

Spherocytes suggest?

A

RBC membrane damage

116
Q

RBC fragments suggest?

A

mechanical damage

117
Q

Heinz bodies suggest?

A

oxidative damage

118
Q

Describe what Coombs test is used for?

A

can be used to check for auto-immune haemolytic anaemia by identifying if antibody and complement is bound to own RBC

119
Q

Describe management of hereditary haemolytic anaemias causing membrane damage?

A

most of these are treated with splenectomy to relieve symptoms, reverse growth failure and prevent recurrent gallstones,
should be immunised before and go on lifelong prophylactic penicillin

120
Q

Why is serum ferritin so important when diagnosing iron deficiency?

A

tells you if there is an absolute or relative iron deficiency
if ferritin is high- functional/ relative deficiency e.g. anaemia of chronic disease
low ferritin- absolute iron deficiency

121
Q

Microcytosis with normal Hb suggests?

A

thalassaemia trait

122
Q

What are spherocytes?

A

red cells that are spherical in shape and have loss of central pallor
a feature of membrane damage

123
Q

When may MCHC be increased?

A

in spherocytosis

124
Q

When are macrovalocytes seen?

A

in megaloblastic anaemia

Haematology (12 decks)

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