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haematology > Anaemia > Flashcards

Anaemia Flashcards

1
Q

Anaemia

A

Reduced total red cell mass

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2
Q

What is the normal response to anaemia

A

Reticulocytosis

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3
Q

Reticulocytosis

A

The increase of production of immature red blood cells

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4
Q

When is a blood film described as polychromatic

A

When there are too many reticulocytes

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5
Q

Why do reticulocytes stain blue/purple

A

Still have remnants of RNA

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6
Q

Symptoms of anaemia (5)

A

Breathlessness
Fatigue
Headaches
Palpitations
Faintness

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7
Q

Investigations for anaemia (3)

A

FBC
blood film
Reticulocyte count

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8
Q

What does haematocrit measure

A

Ratio of the whole blood that is red cells

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9
Q

Microcytic anaemia

A

Anaemia caused by deficient haemoglobin synthesis

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10
Q

Causes of Microcytic anaemia

A

TAILS
Thalassaemia
Anaemia of chronic disease
Iron deficiency anaemia
Lead poisoning
Sideroblastic anaemia

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11
Q

What are the 3 general causes of iron deficiency

A

Insufficient intake
Loosing too much
Not absorbing enough

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12
Q

What can cause you to not absorb enough iron

A

Coeliac disease

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13
Q

What happens to % saturation of transferrin in hereditary haemochromatosis

A

Increases

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14
Q

Where is iron mostly stored in the body

A

Liver

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15
Q

Renal anaemia

A

Anaemia of chronic disease due to failure of erythropoietin production

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16
Q

Why do we get anaemia of chronic disease

A

Protective mechanism to reduce the supply of iron to pathogens

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17
Q

Pathophysiology of anaemia of chronic disease (5)

A
  • inflammatory cytokines result in increased transcription of ferritin mRNA
  • ferritin synthesis increases
  • inflammatory cytokines also causes an increase plasma hepcidin
  • blocks ferroportin-mediated release of iron
  • impaired iron supply to marrow erythroblasts
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18
Q

Clinical features of long standing iron deficiency (6)

A
  • brittle nails
  • koilonychia
  • atrophy of tongue papillae
  • angular stomatitis
  • brittle hair
  • dysphasia and glottitis
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19
Q

Transferrin levels in iron deficiency anaemia

A

Normal or increased

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20
Q

% transferrin saturation in iron deficiency anaemia

A

Reduced

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21
Q

MCV in iron deficiency anaemia

A

Reduced

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22
Q

Serum iron in Anaemia of chronic disease

A

Reduced

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23
Q

Transferrin levels in Anaemia of chronic disease

A

Normal or reduced

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24
Q

% transferrin saturation in Anaemia of chronic disease

A

Reduced

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25
Q

Ferritin levels in Anaemia of chronic disease

A

Normal or increased

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26
Q

MCV in Anaemia of chronic disease

A

Normal (or can be reduced)

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27
Q

When is oral iron recommended to be taken

A

30 mins before a meal or 2 hours before other drugs

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28
Q

What should you avoid taking with oral iron

A

Calcium, antacids, caffeine and high fibre foods

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29
Q

Side effects of oral iron

A

Constipation, N+V , abdominal pains and dark stools

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30
Q

When is IV iron recommended

A

ONLY if oral is unsuccessful

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31
Q

Megaloblastic anaemia

A

Presence of erythroblasts in the bone marrow with delayed nuclear maturation because of defective DNA synthesis

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32
Q

What are the main 2 causes of megaloblastic anaemia

A

Folate and B12 deficiency

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33
Q

Causes of B12 deficiency (7)

A
  • low intake
  • pernicious anaemia
  • PPI and H2 antagonists
  • bypass surgery
  • chronic pancreatitis
  • coeliac disease
  • chronic
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34
Q

Causes of folate deficiency (6)

A
  • low intake
  • coeliac
  • chrons
  • anticonvulsants
  • pregnancy
  • malignancy
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35
Q

Megaloblasts

A

Abnormally large red cell precursor with an immature nucleus

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36
Q

Where are megaloblasts normally found

A

Bone marrow

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37
Q

State 2 biochemical reactions in which folate and B12 are needed

A

DNA synthesis and nuclear maturation
DNA modification and gene activity

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38
Q

Where is B12 absorbed

A

Ileum

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39
Q

Where is folate absorbed

A

Duodenum and jejunum

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40
Q

What extra complications can B12 deficiency cause

A

Neurological

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41
Q

Blood film findings for megaloblastic anaemia (2)

A

Macrovalocytes
Hypersegmented neutrophils

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42
Q

What auto-antibodies might you check for in megaloblastic anaemia (2)

A

Anti gastric parietal cell
Anti intrinsic factor

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43
Q

Management of pernicious anaemia

A

B12 injections for life

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44
Q

Management of folate deficiency anaemia

A

Folic acid tablets

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45
Q

State 4 causes of non-megaloblastic macrocytosis

A
  • alcohol
  • liver disease
  • hypothyroidism
  • marrow failure
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46
Q

What happens in spurious macrocytosis

A

The volume of mature red cells are normal but MCV is measured as high as

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47
Q

State 2 causes of spurious macrocytosis

A

Reticulocytosis in response to acute blood loss or haemolysis
Cold-agglutinins

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48
Q

What is thalassaemia

A

Disorder which causes reduced globin chain synthesis

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49
Q

What kind of inheritance is seen in thalassaemia

A

Autosomal recessive

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50
Q

Alpha thalassaemia

A

Defects in alpha globin chains

51
Q

Beta thalassaemia

A

Defects in beta globin chains

52
Q

What causes alpha thalassaemia

A

Deletion of one or both alpha genes on chromosome 16

53
Q

What causes a patient to have A thalassaemia trait

A

Missing one or two alpha genes

54
Q

Clinical presentation of someone with a thalassaemia trait

A

Microcytic hypochromic red cells with mild anaemia

55
Q

How do you differentiate between iron deficiency anaemia and a thalassaemia trait

A

Low ferritin in iron deficiency anaemia

56
Q

What causes HbH disease

A

Only one alpha gene left

57
Q

What is a consequence of HbH disease

A

Excess b chains form tetrameres

58
Q

Where is HbH disease mostly found

A

SE Asia

59
Q

State 2 key signs of HbH disease

A

Jaundice and splenomegaly

60
Q

What causes Hb Bart’s hydrops fetalis

A

No functional alpha genes

61
Q

Consequence of Hb Bart’s hydrops fetalis

A

No alpha chains so tetrameres of Hb Bart’s and HbH are produced

62
Q

Clinical features of Hb Bart’s hydrops fetalis (5)

A
  • profound anaemia
  • cardiac failure
  • growth retardation
  • severe hepatosplenomegaly
  • skeletal and cardio abnormalities
63
Q

What causes beta thalassaemia

A

Point mutation on chromosome 11

64
Q

Thalassaemia intermedia

A

Beta genes are present but there’s a mutation

65
Q

Thalassaemia major

A

Beta globin genes are missing

66
Q

When do patients with b thalassaemia major tend to present

A

6-24 months

67
Q

Presentation of a patient with b thalassaemia major (4)

A
  • pallor
  • failure to thrive
  • hepatosplenomegaly
  • skeletal changes
68
Q

Management of b thalassaemia major

A

Regular transfusion

69
Q

What kind of anaemia does thalassaemia present with

A

Microcytic hypochromic

70
Q

Hb analysis findings of a patient with b thalassaemia major

A

Mainly HbF , NO HbA

71
Q

What is diagnostic for b thalassaemia trait

A

Raised HbA2

72
Q

How do we quantify haemoglobin present in the body (2)

A
  • electrophoresis
  • high performance liquid chromatography
73
Q

Complication of managing thalassaemia

A

Iron overload

74
Q

Haemolysis

A

Premature red cell destruction

75
Q

Signs of G6PD deficiency on a blood film

A

Heinz bodies

76
Q

Sign of membrane damage on a blood film

A

Spherocytes

77
Q

What do Sickle syndromes affect

A

The structure of haemoglobin

78
Q

What kind of mutation is seen is sickle syndromes

A

Point mutation on codon 6 of the b globin gene

79
Q

What is the consequence of the mutation in sickle syndromes

A

Glutamine is substituted to valine producing bS

80
Q

What happens if a patient with sickle syndrome becomes hypoxic

A

Red blood cells become distorted damaging their membrane

81
Q

Describe haemoglobin in sickle cell trait

A

One normal and one abnormal b gene

82
Q

Is someone sickle cell trait usually symptomatic or asymptomatic

A

Asymptomatic

83
Q

When may a patient with sickle cell trait present

A

Severe hypoxia : high altitude, under anaesthesia

84
Q

Blood film in a patient with sickle cell trait

A

Normal

85
Q

What is the proportion of HbS in sickle cell trait

A

<50%

86
Q

Genetic presentation of sickle cell anaemia

A

2 abnormal b genes

87
Q

Proportion of HbS in patients with sickle cell anaemia

A

> 80%

88
Q

What group of patients are more likely to have sickle cell anaemia

A

Patients with an Afro-Caribbean family background

89
Q

Sickle cell crisis

A

Acute pain due to vaso-occlusion of the small vessels

90
Q

What do people with sickle cell have an increased risk of

A

Infection

91
Q

What is given long term management of sickle cell anaemia (4)

A

Folic acid supplements
Hydroxycarbamide
Regular transfusion
Prophylactic penicillin

92
Q

How do we manage a sickle crisis (6)

A

Opiate analgesia
Hydration
Rest
Oxygen
Antibiotics if sign of infection
Red cell transfusion

93
Q

Lung complication of sickle cell

A

Acute chest syndrome

94
Q

What causes acute chest syndrome (3)

A

Infection
Fat embolism
Pulmonary infarction

95
Q

Clinical presentation of acute chest syndrome

A

SOB, chest pain, pyrexia, hypoxia and consolidation on CXR

96
Q

Haemolysis

A

Premature red cell destruction

97
Q

What are the 5 general causes of haemolysis

A

Immune
Mechanical red cell destruction
Membrane defects
Abnormal red cell metabolism
Abnormal haemoglobin

98
Q

Cold antibodies

A

IgM

99
Q

Warm antibodies

A

IgG

100
Q

Warm autoimmune causes of haemolysis

A

Idiopathic
SLE
lymphoproliferatice disorders
Drugs
infection

101
Q

Name a drug that can cause haemolysis

A

Penicillin

102
Q

Cold immune causes of haemolysis

A

Idiopathic
EBV
Lymphoproliferative disorders

103
Q

State 2 alloimmune causes of haemolysis

A

Haemolytic transfusion reaction
Haemolytic disease of the newborn

104
Q

Name some causes of mechanical red cell destruction

A

Disseminated intravascular coagulation
TTP
Leaking heart valve
Haemolytic uraemia syndrome
Burns
Infections

105
Q

State membrane defect causes of haemolysis

A

Zieves syndrome
Vitamin E deficiency
Hereditary spherocytosis

106
Q

What makes red cells more vulnerable to damage

A

Biconcave
Can’t generate new proteins as no nucleus
Limited metabolic reserve as no mitochondria

107
Q

Haemolytic anaemia

A

Increased rate of red cell destruction exceeding bone marrow capacity for red cell production causes a fall in haemoglobin

108
Q

State 3 consequences of haemolysis

A
  • reticulocytosis by bone marrow
  • bone marrow erythroid hyperplasia
  • excess red cell break down products
109
Q

What are the 2 main classifications of haemolysis

A

Intravascular and extravascular

110
Q

What happens to red blood cells in extravascular haemolysis

A

Red cells are taken up by reticuloendothelial system

111
Q

Are products normal or abnormal in extravascular haemolysis

A

Normal but generated in access

112
Q

Are products of intravascular haemolysis normal or abnormal

A

Abnormal

113
Q

Consequence of extravascular haemolysis

A

Hyperplasia at the site of destruction (splenohepatomegaly)

114
Q

What happens to red cells in intravascular haemolysis

A

Red cells destroyed within the circulation spilling their contents

115
Q

Clinical sign of haemoglobinurea

A

Pink urine that turns black on standing

116
Q

Causes of intravascular haemolysis (4)

A

Incompatible blood transfusion
G6PD deficiency
Severe falciparum malaria
PNH, PCH

117
Q

Reticulocyte count in haemolysis

A

Raised

118
Q

Serum unconjugated bilirubin result in haemolysis

A

Raised

119
Q

Serum hepatoglobins in haemolysis

A

Low

120
Q

Urinary urobilinogen in haemolysis

A

Raised

121
Q

What do spherocytes on blood film suggest

A

Membrane damage

122
Q

What do red cell fragments suggest on blood film

A

Mechanical damage

123
Q

What do Heinz bodies suggest on blood film

A

Oxidative stress due to G6PD deficiency

124
Q

Coombs test result in haemolysis

A

Positive

haematology (11 decks)

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