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Haematology Flashcards

1
Q

What is adult haemoglobin made up of?

A

Two alpha and two beta subunits

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2
Q

What is Fetal haemoglobin made up of?

A

Two alpha and two gamma subunits

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3
Q

What is the difference between adult and fetal haemoglobin?

A

FbH has greater affinity to oxygen (binds more easily and more reluctant to let go)

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4
Q

What are on the x and y axis of the oxygen dissociation curve?

A 
X= partial pressure of oxygen
Y= percentage of Hb bound to O2
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5
Q

At what gestation does HbF production begin to decrease?

A

32-36 weeks

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6
Q

At birth, what proportion of haemoglobin is HbF and HbA?

A

50% HbA

50% HbF

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7
Q

By what age do blood cells contain mainly HbA?

A

6 months

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8
Q

What is anaemia?

A

Low level of haemoglobin in the blood

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9
Q

What is the most common cause of anaemia in infancy?

A

Physiologic anaemia of infancy

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10
Q

What are the other causes of anaemia in infancy?

A 
Anaemia of prematurity
Blood loss
Haemolysis
Twin-twin transfusion (unequal distribution)
Haemolysis
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11
Q

What are the most common causes of haemolysis in infancy?

A

Haemolytic disease of the newborn (ABO or rhesus incompatibility)
Hereditary spherocytosis
G6PD deficiency

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12
Q

What is physiologic anaemia of infancy?

A

The normal dip in haemoglobin around 6-9 weeks of age in healthy term babies

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13
Q

What causes physiologic anaemia of infancy?

A

High oxygen levels (caused by high haemoglobin levels at birth) cause negative feedback which suppresses erythropoietin production in the kidneys. This reduces the production of haemoglobin in the bone marrow.

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14
Q

Why are premature neonates more likely to become anaemic?

A

Less time receiving iron from mother
RBC creation cannot keep up with rapid growth in first few weeks
Reduced EPO levels
Blood tests remove large proportion of blood

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15
Q

What test can be done to look for haemolytic disease of the newborn?

A

Direct Coombs test

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16
Q

What are the key causes of anaemia in older children?

A 
Iron deficiency
Blood loss (menstruation)
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17
Q

What are other causes of anaemia in older children?

A 
Sickle cell anaemia
Thalassaemia
Leukaemia
Hereditary spherocytosis/ eliptocytosis
Sideroblastic anaemia
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18
Q

What is a common cause in developing countries of blood loss causing chronic anaemia?

A

Halminth infection (roundwormds, hookworms, whipworms)

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19
Q

How is helminth infection treated?

A

Single dose of albendazole or mebendazole

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20
Q

What are the three types of anaemia?

A

Microcytic
Normocytic
Macrocytic

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21
Q

What are the causes of microcytic anaemia?

A 
TAILS: 
Thallasaemia
Anaemia of chronic disease
Iron deficiency
Lead poisoning
Sideroblastic anaemia
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22
Q

What are the causes of normocytic anaemia?

A 
3A's, 2H's: 
Anaemia of chronic disease
Acute blood loss
Aplastic anaemia
Haemolytic anaemia
Hypothyroidism
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23
Q

What are the two types of macrocytic anaemia?

A

Megaloblastic

Normoblastic

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24
Q

What is the cause of megaloblastic anaemia?

A

Impaired DNA synthesis preventing cell from dividing normally

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25
Q

What causes megaloblastic anaemia?

A

B12 or folate deficiency

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26
Q

What causes normolastic macrocytic anaemia?

A 
Alcohol
Reticulocytosis
Hypothyroidism
Liver disease
Drugs (azathioprine)
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27
Q

What are the symptoms of anaemia?

A 
Tiredness
SOB
Headaches
Dizziness
Palpitations
Worsening of other conditions
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28
Q

What symptoms are specific to iron deficiency anaemia?

A

Pica (strange dietary cravings)

Hair loss

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29
Q

What are the generic signs of anaemis on examination?

A

Pale
Conjunctival pallor
Tachycardia
Raised resp rate

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30
Q

What signs of iron deficiency anaemia may be found on examination?

A

Koilonychia
Angular chelitis
Atrophic glossitis
Brittle hair/ nails

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31
Q

What initial investigations are done into anaemia?

A 
FBC
Blood film
Reticulocyte count
Ferritin
B12/ Folate
Bilirubin
Direct Coombs test
Haemoglobin electrophoresis
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32
Q

What is haemoglobin electrophoresis?

A

Test that measures the different types of haemoglobin in the blood

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33
Q

What are reticulocytes?

A

Immature red blood cells

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34
Q

What does a high level of reticulocytes in the blood indicate?

A

Anaemia is due to haemolysis or blood loss (active production of RBC’s to replace lost cells)

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35
Q

How is anaemia managed?

A

Establish underlying cause (e.g. iron supplements, blood transfusions)

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36
Q

What are the 3 categories of causes of iron deficiency?

A

Dietary insufficiency
Loss or iron
Inadequate absorption

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37
Q

Where is iron mainly absorbed?

A

In duodenum and jejunum

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38
Q

What keeps iron in its soluble ferrous (Fe2+) form?

A

Stomach acid

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39
Q

What happens when there is less acid in the stomach?

A

Soluble ferrous turns into its insoluble ferric (Fe3+) form

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40
Q

What medications can interfere with iron absorption and why?

A

PPIs as they reduce the stomach acid, changing iron into its insoluble form

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41
Q

What conditions can cause inadequate absorption of iron?

A

Those that cause inflammation of the duodenum or jejunum= Coeliac or Crohn’s

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42
Q

In what form does iron travel around the body?

A

Ferric ions (Fe3+) attached to transferrin

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43
Q

What is transferrin?

A

Carrier protein

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44
Q

What is the total iron binding capacity?

A

The total space on transferrin molecules for iron to bing

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45
Q

What is the transferrin saturation?

A

The proportion of transferrin molecules that are bound to iron

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46
Q

How do you calculate transferring saturation?

A

Serum iron/ Total iron binding capacity

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47
Q

What form does iron take when it is stored in cells?

A

Ferritin

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48
Q

When is extra ferritin released from cells?

A

When there is inflammation (infection or cancer)

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49
Q

What does it suggest if there is low ferritin in the blood?

A

Iron deficiency

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50
Q

Can a person with normal blood ferritin levels still have iron deficiency?

A

Yes- may be raised due to infection ect

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51
Q

Why is serum iron on its own not a very useful measure?

A

It varies significantly throughout the day

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52
Q

What happens to both TIBC and transferrin levels in iron deficiency?

A

Increase

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53
Q

What does the transferrin saturation give a good indication of?

A

Total iron in the body

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54
Q

In an adult, what is the normal transferrin saturation?

A

30%

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55
Q

What is the easiest/ best test to look for iron deficiency?

A

Total iron binding capacity

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56
Q

What are the types of leukaemia that affect children (most–> least common)?

A
  1. Acute lymphoblastic laeukaemia
  2. Acute myeloid leukaemia
  3. Chronic myeloid leukaemia
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57
Q

What age does ALL peak?

A

2-3 years

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58
Q

What age does AML peak?

A

<2

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59
Q

What cells does leukaemia affect?

A

Stem cells of the bone marrow

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60
Q

What does leukaemia cause?

A

Excessive production of a single type of abnormal white blood cell

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61
Q

What does excessive production of a single type of cell in leukaemia lead to?

A

Pancytopenia (anaemia + Leukopenia + thrombocytopenia)

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62
Q

What are the risk factors for developing leukaemia?

A 
Radiation exposure furing pregnancy
Down's syndrome
Kleinfelter syndrome
Noonan syndrome
Fanconi's anaemia
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63
Q

What may symptoms of leukaemia include?

A 
Fatigue
Fever
Failure to thrive
Weight loss
Night sweats
Anaemia
Bruising
Bleeding
Lymphadenopathy
Bone/ joint pain
Hepatosplenomegaly
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64
Q

What red flags would cause a child to have immediate specialist assessment for leukaemia?

A

Unexplained petechiae or hepatomegaly

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65
Q

If leukaemia is suspected what initial investigation should be done?

A

FBC within 48 hours

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66
Q

What investigations can be done to diagnose leukaemia?

A

FBC
Blood film
Bone marrow biopsy
Lymph node biopsy

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67
Q

What will FBC show in leukaemia?

A

Anaemia
Leukopenia
Thrombocytopenia
High numbers of abnormal WBC’s

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68
Q

What may blood film show in leukaemia?

A

Blast cells

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69
Q

What further tests may be done into leukaemia?

A

CXR
CT
LP
Genetic analysis

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70
Q

How is leukaemia primarily treated?

A

Chemotherapy

71
Q

What are the complications of chemotherapy?

A 
Failure
Stunted growth/ development
Immunodeficiency/ infections
Neurotoxicity
Infertility
Secondary malignancy
Cardiotoxicity
72
Q

What is the prognosis for ALL?

A

80% cure rate

73
Q

What is ITP?

A

Idiopathic thrombocytopenic purpura

74
Q

What is idiopathic thrombocytopenic purpura?

A

Condition that causes idiopathic low platelet count causing a non-blanching rash

75
Q

What is ITP caused by?

A

Type II hypersensitivity reaction that causes antibodies to destroy platelets

76
Q

What age does ITP usually present?

A

Children under 10

77
Q

What might trigger ITP?

A

Idiopathic or viral infection

78
Q

What are the main symptoms of ITP?

A

Bleeding (gums, nose, menorrhagia)
Bruising
Petechial or purpuric rash

79
Q

What are petechiae?

A

Pin-prick spots (1mm) of bleeding under the skin

80
Q

What are purpura?

A

Larger (3-10mm) spots of bleeding under the skin

81
Q

What is ecchymoses?

A

Large area of blood (>10mm) collected under the skin

82
Q

Is the rash in ITP blanching?

A

Non-blanching

83
Q

How is ITP diagnosed?

A

Urgent FBC for platelet count

84
Q

What other causes of thrombocytopenia should be excluded when diagnosing ITP?

A

Heparin induced thrombocytopenia

Leukaemia

85
Q

How is ITP usually managed

A

Usualy no treatment required and patients monitored until platelets return to normal

86
Q

What percentage of patients remit spontaneously with ITP and how quickly?

A

70% within 3 months

87
Q

What treatments should be given for severe ITP or if the patient is actively bleeding?

A

Prednisolone
IV immunoglobulins
Blood transfusions
Platelet transfusions

88
Q

Why do platelet transfusions only work temporarily when treating ITP?

A

Antibodies against platelets will begin destroying the transfused platelets

89
Q

What key advice should be given to patients with ITP?

A

Avoid contact sports
Avoid IM injections
Avoid NSAIDs, aspirin and anticoagulants
Seek help after any injury that may cause bleeding

90
Q

What are the complications of ITP?

A

Chronic ITP
Anaemia
Intracranial and subarachnoid haemorrhage
GI bleed

91
Q

What is sickle cell anaemia?

A

Genetic condition causing sickle shaped RBC’s

92
Q

What does sickle cell anaemia cause?

A

Haemolytic anaemia

93
Q

What is the pathophysiology of sickle cell anaemia?

A

Patients have abnormal gene for beta-globin on chromosome 11 which codes for abnormal haemoglobin (HbS) which causes RBCs to become sickle shape

94
Q

What kind of genetic inheritance is sickle cell anaemia?

A

Autosomal recessive

95
Q

What does one copy of the abnormal beta-globin gene cause?

A

Sickle-cell trait

96
Q

What do two copies of the abnormal beta-globin gene cause?

A

Sickle-cell disease

97
Q

Where is sickle cell disease more common?

A

Africa, India, Middle East, Caribbean

98
Q

What are the benefits of sickle cell trait?

A

Reduces severity of malaria

99
Q

How is sickle cell anaemia diagnosed?

A

Women at risk tested during pregnancy

Newborn screening heel prick test

100
Q

What are the complications of sickle cell disease?

A 
Anaemia
Increased risk of infection
Stroke
Avascular necrosis of large joints
Pulmonary hypertension
Priapism
CKD
Sickle cell crises
Acute chest syndrome
101
Q

What is the general management of sickle cell disease?

A

Avoid crises triggers
Up to date with vaccines
Antibiotic prophylaxis
Blood transfusion (Severe anaemia)

102
Q

What can be used to protect against sickle cell crises and acute chest syndrome?

A

Hydroxycarbamide

103
Q

What is the action of hydroxycarbamide?

A

Stimulates production of fetal haemoglobin (hbF) which does not lead to the sickling of RBCs

104
Q

What can be used to cure sickle cell anaemia?

A

Bone marrow transplant

105
Q

What may trigger a sickle cell crisis?

A 
Spontaneous
Infection
Dehydration
Cold
Significant life events
106
Q

How are sickle cell crises managed?

A

Supportively:
Treat infection
Keep warm and hydrated
Simple analgesia

107
Q

What is priapsim?

A

Painful and persistent penile erection

108
Q

What are the different types of sickle cell crisis?

A

Vaso-occlusive crisis
Splenic sequestration crisis
Aplastic crisis
Acute chest syndrome

109
Q

What causes a vaso-occlusive crisis?

A

Sickle shaped blood cells clogging capillaries and causing distal ischaemia

110
Q

What is haematocrit?

A

Measurement of the proportion of blood which is made up of cells (Packed cell volume)

111
Q

What is the usual cause of a vaso-occlusive crisis?

A

Dehydration

112
Q

What are the symptoms of a vaso-occlusive crisis?

A

Pain

Fever

113
Q

How is priapism treated?

A

Aspiration of blood from penis

114
Q

What is a splenic sequestrian crisis?

A

When RBCs block flow in the spleen, causing it to become acutely enlarged and painful

115
Q

What can pooling of blood in the spleen lead to?

A

Severe anaemia

Hypovolaemic shock

116
Q

How is a splenic sequestrian crisis managed?

A

Supportive
Blood transfusions
Fluid resuscitation

117
Q

What may be done if there are recurrent splenic sequestration crises?

A

Splenectomy

118
Q

What is an aplastic crisis?

A

Temporary loss of the creation of new blood cells

119
Q

What is the most common trigger of an aplastic crisis?

A

Infection with parvovirus B19

120
Q

How is aplastic crisis managed?

A

Supportive with blood transfusions as necessary

Usually resolves within a week

121
Q

What is acute chest syndrome?

A

Medical emergency caused by sickled cells causing pulmonary infarction/ emboli

122
Q

What must be seen to make a diagnosis of acute chest syndrome?

A

Fever or respiratory symptoms

New infiltrates on CXR

123
Q

What can cause acute chest syndrome?

A

Infection (pneumonia or bronchiolitis)

Non-infective (pulmonary vaso-occlusion or fat emboli)

124
Q

How is acute chest syndrome managed?

A 
Treat underlying cause: 
Antibiotics or antivirals
Blood transfusions
Incentive spirometry
Artificial ventilation
125
Q

What causes thalassaemia?

A

Genetic defect in protein chains that make up haemoglobin

126
Q

What are the two types of thalassaemia?

A

Alpha and beta

127
Q

What genetic inheritance is thalassaemia?

A

Autosomal recessive

128
Q

What does thalassaemia cause?

A

RBCs to be more fragile and break down more easily, leading to anaemia and splenomegaly

129
Q

Why do you get splenomegaly in thalassaemia?

A

The spleen collects all the destroyed red blood cells and there are lots

130
Q

What happens to the bone marrow in thalassaemia?

A

It expands to produce extra RBCs to compensate for chronic anaemia

131
Q

What are the signs and symptoms of thalassaemia?

A 
Microcytic anaemia
Fatigue
Pallor
Jaundice
Gallstones
Splenomegaly
Poor growth/ development
Pronounced forehead/ cheekbones
132
Q

How is thalassaemia diagnosed?

A

FBC (microcytic anaemia)
Haemoglobin electrophoresis
DNA testing
Pregnancy screening test

133
Q

What is the key complication of thalassamiea?

A

Iron overload

134
Q

Why do you get iron overload in thalassaemia?

A

Due to faulty creation of RBCs, recurrent transfusions and increased absorption of iron in the gut in response to anaemia

135
Q

How is iron overload monitored for?

A

Monitor serum ferritin levels

136
Q

How is iron overload managed?

A

Limit transfusions

Iron chelation

137
Q

What are the symptoms of iron overload?

A 
Fatigue
Liver cirrhosis
Infertility
Impotence
Heart failure
Arthritis
Diabetes
Osteoporosis 
Joint pain
138
Q

What gene codes for alpha globin?

A

Chromosome 16

139
Q

How is alpha thalassaemia managed?

A

Blood transfusions
Splenectomy
Bone marrow transplant

140
Q

What chromosome codes for beta globin chains?

A

Chromosome 11

141
Q

What are the different types of beta-thalassaemia?

A

Minor
Intermedia
Major

142
Q

What is thalassaemia minor?

A

When patients are carriers of an abnormally functioning beta globin gene (one abnormal, one normal gene)

143
Q

What does thalassaemia minor cause?

A

Mild microcytic anaemia

144
Q

What is thalassaemia intermedia?

A

When patients have two abnormal copies of the beta globin gene

145
Q

What are the different genes patients may have in thalassaemia intermedia?

A

Two defective genes or one defective gene and one deletion gene

146
Q

What does thalassaemia intermedia cause?

A

More significant microcytic anaemia

147
Q

What is thalassaemia major?

A

When patients have two deletion genes, meaning they have no functioning beta globin genes

148
Q

How does thalassaemia major usually present?

A

Severe anaemia
Failure to thrive
Splenomegaly
Bone defomities

149
Q

How is thalassaemia major managed?

A

Regular transfusions
Iron chelation
Splenectomy
Bone marrow transplant

150
Q

What is iron chelation?

A

Agent (tablet or infusion) given that binds to iron and allows body to excrete the bound particles

151
Q

What is hereditary spherocytosis?

A

Condition where RBCs are sphere shaped, making them fragile and easily destroyed

152
Q

In which population is hereditary spherocytosis most common?

A

Northern Europeans

153
Q

What inheritance pattern in Hereditary spherocytosis?

A

Autosomal dominant

154
Q

How does hereditary spherocytosis present?

A

Jaundice
Anaemia
Gallstones
Splenomegaly

155
Q

What are haemolytic crises?

A

Periods triggered by infections where haemolysis, anaemia and jaundice are more significant

156
Q

What may patients with hereditary spherocytosis develop?

A

Aplastic crisis

157
Q

What happens in an aplastic crisis?

A

The body stops producing enough RBCs, leading to anaemia, haemolysis and jaundice

158
Q

What is the common trigger of an aplastic crisis?

A

Parvovirus

159
Q

How is hereditary spherocytosis diagnosed?

A

By family history and clinical features

Spherocytes on blood film

160
Q

How is hereditary spherocytosis managed?

A

Folate supplementation and splenomectomy

161
Q

What is hereditary elliptocytosis?

A

Autosomal dominant condition causing RBC;s to be an ellipse shape

162
Q

What is G6PD deficiency?

A

Condition where there is a defect in the G6PD enzyme

163
Q

In which patients id G6PD deficiency more common?

A

Mediterranean, Middle Eastern and African

164
Q

What is the inheritance pattern of G6PD deficiency?

A

X-linked recessive

165
Q

Who is usually affected by G6PD deficiency and why?

A

Males because they only have a single copy of the X chromosome

166
Q

What are the key triggers of a G6PD crisis?

A

Infections
Medications
Fava beans

167
Q

What is the action of the G6PD enzyme?

A

Helps protect cells (especially RBCs) from damage by reactive oxygen species (ROS)

168
Q

What are ROS?

A

Reactive molecules that contain oxygen, produced during normal cell metabolism and in higher quantities during stress on the cell

169
Q

What does a deficiency in G6PD lead to?

A

Makes cells more vulnerable to ROS, leading to haemolysis in RBCs, and eventually acute haemolytic anaemia

170
Q

How does G6PD deficiency normally present?

A

Neonatal jaundice

171
Q

What are the key features of G6PD deficiency?

A

Intermittent jaundice
Anaemia
Gallstones
Splenomegaly

172
Q

How is G6PD deficiency diagnosed?

A

Blood film

G6PD enzyme assay

173
Q

What may be seen on blood film of G6PD deficiency?

A

Heinz bodies (blobs of denatures haemoglobin in RBCs)

174
Q

How is G6PD deficiency managed?

A

Avoid triggers to acute haemolysis (fava beans, medications)

Paeds (18 decks)

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