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Y3 - Haem > Iron - Anaemia and Overload > Flashcards

Iron - Anaemia and Overload Flashcards

1
Q

What is anaemia?

A

Insufficient amount of red blood cells or Hb

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2
Q

In which circumstances is Hb not a good measure of RBC mass, and why?

A

Acute haemorrhage - there is no change in Hb as even though there is a lot of RBC loss the loss is proportional to other components
Large volume fluid restriction - plasma expands showing a reduction in Hb when there is no RBC loss

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3
Q

What is the general presentation of anaemia?

A 
Exertional SOB
Dizziness
Palpitations
Fatigue
Headache
Fainting
Anorexia
Conjunctival or general pallor
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4
Q

What are the 2 main classifications of anaemia?

A

Microcytic

Macrocytic

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5
Q

What is the pathophysiology of microcytic hypochromic anaemia?

A

Reduction in Hb production which means Hb level in cells takes longer to build up and switch off cell division
Cells divide more so RBCs are smaller and paler

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6
Q

What aspects of Hb can go wrong leading to reduction in Hb production?

A

Haem group
Porphyrin ring
Globin chain

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7
Q

What are the causes of microcytic anaemia, and which components of Hb are defective in each?

A 
Thalassaemia - globin chain
Anaemia of chronic disease - haem group
Iron deficiency - haem group
Lead poisoning - porphyrin ring
Sideroblastic anaemia - porphyrin ring
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8
Q

What is iron deficiency?

A

Anaemia caused by there being insufficient iron to produce haemoglobin
Not a diagnosis - look for a cause

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9
Q

What are causes of iron deficiency anaemia?

A

Chronic blood loss (menorrhagia, GI bleeds)
Malabsorption (coeliac, post-gastrectomy)
Poor dietary intake
Infection (hookworm)
Contributing factors (lots of tea, PPIs, age)

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10
Q

What is the presentation of iron deficiency anaemia?

A

General features of anaemia (fatigue, exertion SOB, dizziness, headache, fainting etc)
Koilonychia
Angular stomatitis, atrophic gastritis
Post-cricoid webs

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11
Q

What do iron studies show in iron deficiency anaemia?

A

Low serum ferritin

Low % transferrin saturation

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12
Q

What is the management of iron deficiency anaemia?

A

Look for a cause, treat that

Oral iron replacement (ferrous sulphate or fumarate)

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13
Q

What are the side effects of oral iron replacement?

A

Nausea
Black stool
Diarrhoea
Constipation

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14
Q

How much should Hb increase on iron replacement?

A

10 per week

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15
Q

Who should be referred for GI screening in iron deficiency anaemia?

A

Iron deficiency anaemia with dyspepsia
Iron deficiency anaemia with rectal bleeding or symptoms of colorectal cancer
Iron deficiency anaemia not responding to treatment

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16
Q

What is sideroblastic anaemia?

A

Disorder of production of the porphyrin ring

This leads to ineffective erythropoiesis, driving iron absorption and deposition in organs other than the liver

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17
Q

What are the causes of sideroblastic anaemia?

A

X linked hereditary
Chemotherapy
Anti-TB drugs
Lead poisoning

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18
Q

What will a marrow biopsy show in sideroblastic anaemia?

A

Ring sideroblasts

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19
Q

What is seen on blood film in sideroblastic anaemia?

A

Atypical blood cells of varying sizes and shapes

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20
Q

What is seen in iron studies in sideroblastic anaemia?

A

High iron
High ferritin
High transferrin saturation

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21
Q

What is the management of sideroblastic anaemia?

A

Treat underlying cause if any

Regular blood transfusions

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22
Q

What is thalassaemia?

A

A group of conditions of defective production of globing chains in Hb
Abnormal cells are small and more susceptible to premature haemolysis

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23
Q

What is the cause of thalassaemia?

A

Hereditary - autosomal recessive

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24
Q

What are the types of thalassaemia?

A

Alpha thalassaemia - trait, HbH disease, Hb Barts hydros fettles
Beta thalassaemia: trait, intermedia, major

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25
Q

What is alpha thalassaemia?

A

Alpha globin chain is affected

One or more alpha genes are deleted

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26
Q

How many alpha genes are there, and which chromosome are they on?

A

4 - chromosome 16

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27
Q

Which types of Hb are affected in alpha thalassaemia?

A

HbA
HbA2
HbF

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28
Q

Which genes are missing in alpha thalassaemia trait?

A

1 or 2 alpha genes

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29
Q

What are the clinical features of alpha thalassaemia trait?

A

Asymptomatic carrier state

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30
Q

What do investigations show in alpha thalassaemia trait?

A

May have microcytic hypochromia

Ferritin will be normal

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31
Q

What is the treatment of alpha thalassaemia trait?

A

None needed

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32
Q

Which genes are missing in HbH disease?

A

3 - only one alpha gene left

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33
Q

What is the pathophysiology in HbH disease?

A

Reduction in alpha chains so excess beta chains form tetramers called HbH

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34
Q

Why is HbH bad?

A

It’s unstable and has an extremely high oxygen affinity, making it ineffective as an oxygen delivery device

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35
Q

What do investigations show in HbH disease?

A

Moderate anaemia

Very low MCV and MCH (disproportionate the the anaemia)

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36
Q

What are the clinical features of HbH disease?

A

Jaundice
Splenomegaly
Leg ulcers
Gallstones

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37
Q

What is the management of HbH disease?

A

May need transfusion in circumstances such as intercurrent infection
If severe - regular transfusions, splenectomy

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38
Q

Which genes are missing in Hb Barts hydros fetalis?

A

All - no functional alpha genes

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39
Q

What are the clinical features of Hb Barts hydros fetalis?

A 
Incompatable with life
Profound anaemia
Cardiac failure
Growth retardation
Severe hepatosplenomegaly
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40
Q

What is the pathophysiology of Hb Barts hydros fetalis?

A

Minimal or no alpha chain production so HbF and HbA can’t be made
Tetramers of Hb Barts and HbH are produced

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41
Q

What is beta thalassaemia?

A

Beta globin chain is affected

Reduced or absent beta chain production

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42
Q

What is the usual mutation in beta thalassaemia?

A

Point mutation

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43
Q

Which types of Hb are affected in beta thalassaemia?

A

Only HbA

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44
Q

How many beta genes are there?

A

2

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45
Q

What genes are affected in beta thalassaemia trait?

A

1 reduced or absent beta gene

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46
Q

What are the clinical features of beta thalassaemia trait?

A

Asymptomatic

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47
Q

What does FBC and Hb analysis show in beta thalassaemia trait?

A

No/mild anaemia
Low MCV, MCH
Raised HbA2

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48
Q

What is the management of beta thalassaemia trait?

A

None needed

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49
Q

What genes are affected in beta thalassaemia intermedia?

A

2 reduced beta genes or 1 reduced and one absent gene

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50
Q

What are the clinical features of beta thalassaemia intermedia?

A 
Similar to HbH disease
(Jaundice
Splenomegaly
Leg ulcers
Gallstones)
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51
Q

What is the management of beta thalassaemia intermedia?

A

Occasional transfusion

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52
Q

What genes are affected in beta thalassaemia major?

A

All - no functional beta genes

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53
Q

What are the clinical features of beta thalassaemia major?

A 
Presents at 6-24 months (as HbF fails)
Pallor
Failure to thrive
Hepatosplenomegaly
Skeletal changes 
Organ damage
Caused by extra medullary haematopoiesis
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54
Q

What does Hb analysis show in beta thalassaemia major?

A

Mainly HbF
High HbA2
No HbA

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55
Q

What is the management of beta thalassaemia major?

A

Lifelong transfusion dependency

Bone marrow transplant may be an option if carried out before complications

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56
Q

What is the risk of treatment of beta thalassaemia major?

A

Iron overload

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57
Q

What is anaemia of chronic disease?

A

Diseases which cause chronic inflammation can cause anaemia
Inflammatory cytokines cause problems with iron utilisation
Iron is being absorbed so stores are high but Hb is low

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58
Q

How do inflammatory cytokines cause problems with iron utilisation?

A

Increase production of hepcidin (which inhibits release of iron from cells)
Reduces erythropoietin (which stimulates erythropoiesis)
Inhibit bone marrow production of erythrocytes
Macrophage red cell destruction is increased

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59
Q

What are some causes of anaemia of chronic disease?

A 
Malignancy
Hypothyroidism
Chronic infection
Connective tissue disease
CKD
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60
Q

What do investigations show in anaemia of chronic disease?

A

FBC: low Hb, can be microcytic or normocytic

High ferritin

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61
Q

What is macrocytic anaemia?

A

Low Hb with large, hyperchromic red cells

62
Q

What is the pathophysiology of macrocytic anaemia?

A

Cells become large due to defective nuclear maturation and DNA synthesis
This leads to growth without division
Due to their size the cells are more prone to early breakdown

63
Q

What is the main classification of macrocytic anaemia?

A

Megaloblastic

Non-megaloblastic

64
Q

What are megaloblasts?

A

Abnormally large, nucleated red cell precursors

65
Q

How do B12 and folate contribute to erythropoiesis?

A

Required for DNA synthesis

66
Q

What are the sources of B12 and folate?

A

B12 - animal foods

Folate - plant foods

67
Q

Where are B12 and folate absorbed?

A

B12 - terminal ilium

Folate - duodenum

68
Q

How is B12 absorbed?

A

By binding to intrinsic factor

69
Q

How long are B12 and folate stored in the body?

A

B12 - 2-4 years

Folate - 4 months

70
Q

What are causes of B12 deficiency?

A

Diet: vegan, alcoholism
Stomach: pernicious anaemia, gastrectomy, PPI, anti-histamines
Small intestine: bacterial overgrowth, coeliac disease, Crohn’s disease, bowel resection
Chronic pancreatitis

71
Q

What is pernicious anaemia?

A

Autoimmune atrophic gastritis causing reduction in intrinsic factor

72
Q

What are the autoantibodies in pernicious anaemia?

A

Anti gastric parietal cell

Anti intrinsic factor

73
Q

What are causes of folate deficiency?

A

Low intake: poverty, old age, alcoholism
Malabsorption: coeliac, tropical sprue
Increased demand: pregnancy, malignancy, myelofibrosis, exfoliating dermatitis, haemolytic anaemia
Drugs: methotrexate, trimethoprim, anticonvulsants

74
Q

What is the presentation of B12 and folate deficiency?

A

Symptoms of anaemia
Mouth - glossitis, angular stomatitis
Jaundice
Psychiatric - irritability, depression

75
Q

What clinical features are seen in B12 deficiency (not folate)?

A

Neurological - numbness, tingling, subacute combined degeneration of the cord (paraesthesia, ataxia, weakness)

76
Q

What do investigations show in B12 and folate deficiency?

A

Low serum B12/folate
FBC - low Hb, high MCV, reticulocytes
Bone marrow biopsy: megaloblasts
Blood film: howel jolly bodies, hyper-segmented neutrophils

77
Q

What is the management of B12 and folate deficiency?

A

Folate - folate tablets

B12 - IM B12 (for life)

78
Q

What are causes of non-megaloblastic macrocytosis?

A 
Alcohol
Pregnancy
Hypothyroidism
Liver disease
Marrow failure: myelodysplasia, aplastic anaemia, myeloma
79
Q

What is seen on blood film in macrocytosis caused by liver disease?

A

Target cells

80
Q

What is spurious macrocytosis?

A

False macrocytosis where the volume of the mature red cell is normal but the MCV is measured as high

81
Q

What are the causes of spurious macrocytosis?

A

Reticulocytosis

Cold-agglutinins

82
Q

What is reticulocytosis?

A

Increase in reticulocyte numbers as a marrow response to acute blood loss or haemolysis
MCV measured as higher as reticulocytes are bigger than mature RBCs

83
Q

What are cold agglutinins?

A

Abnormal proteins produced in certain cancers or infections
Cause clumping of red cells at lower temperatures
The clumps are registered as one giant cell
Causes extraordinarily high MCV

84
Q

What is the pathophysiology of sickling disorders?

A

Mutation of beta globin chain which alters the structure, chainging it from Hb to HbS
This distorts the cell, damaging the membrane and leading to formation of rod/needle-like structures in the cell
Makes it more prone to binding to vascular epithelium - more sticky

85
Q

What are the types of sickling disorders?

A

Sickle cell trait
Sickle cell anaemia
Sickle cell disease
Sickle crisis

86
Q

What genes are affected in sickle cell trait?

A

One normal, one abnormal beta gene

87
Q

What are the clinical features of sickle cell trait?

A

Asymptomatic

May sickle in severe hypoxia, e.g. high altitude, under anaesthesia

88
Q

What do investigations show in sickle cell trait?

A

Blood film normal

Hb analysis: mainly HbA, HbS <50%

89
Q

What genes are affected in sickle cell anaemia?

A

2 abnormal beta genes

90
Q

What do investigations show in sickle cell anaemia?

A

Blood film: sickle cells

Hb analysis: HbS >80%, no HbA

91
Q

What are the clinical features of sickle cell anaemia?

A

Episodes of sickle crisis (severe pain and variable other symptoms)
Chronic haemolysis
Splenic infarcts - leading to hyposplenism

92
Q

What causes splenic infarcts in sickle cell anaemia?

A

Sequestration of sickled RBCs in liver and spleen

93
Q

What genes are affected in sickle cell disease?

A

One beta gene causing HbS, plus another beta chain mutation

94
Q

What are the clinical features of sickle cell disease?

A

Same as sickle cell anaemia

95
Q

What is sickle crisis also known as?

A

Sickle vaso-occlusion

96
Q

What is the pathophysiology of sickle crisis?

A

Sickle cells can get wedged, stick to vessel wall and block microvascular flow
Inflammatory response and recruitment of neutrophils and platelets
Leads to tissue ischaemia and pain

97
Q

What factors precipitate sickle crisis?

A 
Hypoxia
Dehydration
Infection
Cold exposure
Stress/fatigue
98
Q

What is the treatment of sickle crisis?

A 
Opiate analgesia
Hydration
Rest
Oxygen
Red cell exchange in severe crisis (lung, brain)
99
Q

What measures are taken as long-term management of sickling disorders?

A

Prophylactic penicillin and vaccination to reduce the risk of infection
Folic acid supplementation
Hydroxycarbamide (reduces severity by increasing HbF production)
Regular transfusion to prevent stroke in selected cases (e.g. children who have had strokes)

100
Q

What are causes of iron overload?

A

Hereditary haemochromatosis

Long term transfusions

101
Q

What disorders require long-term transfusions?

A

Thalassaemia

Sideroblastic anaemia

102
Q

What is hereditary haemochromatosis?

A

Genetic condition with increased iron absorption due to mutations that reduce the production of hepcidin

103
Q

What is the pathophysiology of hereditary haemochromatosis?

A

Reduced production of hepcidin results in increased iron absorption (as heparin inhibits absorption of iron)
This results in iron deposition in tissues other than the liver, which causes inflammation and end organ damage

104
Q

What are the clinical features of hereditary haemochromatosis?

A

Usually presents in middle age or later
Early: fatigue, arthralgia, weakness
Late: slate grey skin, liver failure, diabetes (to then bronzed diabetes), cardiomyopathy

105
Q

What do investigations show in hereditary haemochromatosis?

A

Abnormal LFTs

Iron studies: high iron, high ferritin

106
Q

What is the management of hereditary haemochromatosis?

A

Regular venesection

107
Q

What causes secondary iron overload?

A

Anaemias can cause overactive erythropoiesis, leading to excessive iron absorption
These patients also require regular blood transfusions which makes this worse

108
Q

What disorders cause secondary iron overload?

A

Thalassaemia
Sideroblasdtic anaemia
Red cell aplasia
Myelodysplasia

109
Q

What is the treatment of secondary iron overload?

A

NOT venesection - as the patients are already anaemic

Iron chelating agents - desferrioxamine, deferiprone, deferasirox

110
Q

What is haemolysis?

A

The premature breakdown of red blood cells

111
Q

What is the body’s response to haemolysis?

A

Erythroid hyperplasia

Reticulocytosis

112
Q

What do reticulocytes look like?

A

Larger and more blue/purple on film

113
Q

What are the different types of haemolysis?

A

Extravascular

Intravascular

114
Q

What is extravascular haemolysis?

A

Breakdown of RBCs outside of the circulation - in the liver and spleen

115
Q

Is extravascular haemolysis pathological or physiological?

A

Both

116
Q

Which breakdown products are detected in extravascular haemolysis?

A

Normal products in excess

Unconjugated bilirubin

117
Q

What are causes of extravascular haemolysis?

A

Autoimmune haemolytic anaemia
Thalassaemia
Sickle cell disease
Hereditary spherocytosis

118
Q

What is intravascular haemolysis?

A

Pathological breakdown of red cells within the circulation

119
Q

Which breakdown products are detected in intravascular haemolysis?

A

Abnormal products
Haemoglobinaemia
Met-haem-albuminaemia
Haemoglobinuria

120
Q

What feature of urine demonstrates haemoglobinuria?

A

Pink urine, turns black when left to stand

121
Q

What are causes of intravascular haemolysis?

A 
Drug-induced
ABO mismatch blod transfusion
G6PD deficiency
Severe malaria
Microangiopathic haemolytic anaemia
122
Q

Does haemolysis always cause anaemia, why?

A

No
In compensated haemolysis Hb is maintained by reticulocytosis
In decompensated haemolysis Hb is not maintained and anaemia results

123
Q

What are the general clinical features of haemolysis?

A

Jaundice
Change in colour of urine
Abdominal pain/swelling

124
Q

What aspects of haemolysis cause which abnormalities on blood film?

A

Membrane damage - spherocytes
Mechanical damage - red cell fragments
Oxidative damage - Heinz bodies
HbS - sickle cells

125
Q

What does the Coomb’s test test for?

A

Direct Coomb’s test - positive in autoimmune disease

Indirect Coomb’s test - positive in immune response to foreign antibodies

126
Q

What ways can causes of haemolysis be classified?

A

Haemolysis of normal red cells
Haemolysis of red cells with abnormal membrane
Haemolysis of red cells with abnormal metabolism
Haemolysis of red cells with abnormal haemoglobin

127
Q

What are the causes of haemolysis of normal red cells?

A

Autoimmune haemolysis

Alloimmune haemolysis

128
Q

What type of haemolysis is autoimmune haemolysis?

A

Extravascular

129
Q

How is autoimmune haemolysis classified?

A

Warm or cold autoantibody - the temperature in which the antibodies bind

130
Q

Which immunoglobulin is responsible in warm autoantibody autoimmune haemolysis?

A

IgG

131
Q

Which immunoglobulin is responsible in cold autoantibody autoimmune haemolysis?

A

IgM

132
Q

What are the causes of warm and cold autoantibody autoimmune haemolysis?

A

Warm - idiopathic

Cold - idiopathic or secondary to leukaemia, lymphoma

133
Q

Is direct or indirect Coomb’s test positive in warm and cold autoantibody autoimmune haemolysis?

A

Warm - direct

Cold - indirect

134
Q

What are the causes of alloimmune haemolysis?

A 
Disseminated intravascular coagulation
Haemolytic uraemia syndrome
Thrombotic thrombocytopenia purpura
Leaking heart valve
Infections (e.g. malaria)
Severe burns
135
Q

Why do leaking heart valves cause alloimmune haemolysis?

A

Red cell fragmentation occurs due to mechanical damage on the damaged valve

136
Q

What cells are seen on blood film in alloimmune haemolysis, and what do they look like?

A

Schistocytes - red cell fragments

Irregularly shaped, jagged, 2 pointed ends

137
Q

What is the main cause of haemolysis of cells with abnormal cell membrane?

A

Hereditary spherocytosis

138
Q

What is the inheritance pattern of hereditary spherocytosis?

A

Autosomal dominant

139
Q

What is the pathophysiology of hereditary spherocytosis?

A

Reduced membrane deformability means increased transit time though the spleen
Oxidant environment in the spleen causes extravascular red cell destruction
Leads to chronic extravascular haemolysis

140
Q

What are the clinical features of hereditary spherocytosis?

A 
Young children with family history of splenectomy
Jaundice
Splenomegaly
Mild anaemia
Increased risk of gallstones
141
Q

What cells are seen on blood film in hereditary spherocytosis?

A

Spherocytes

142
Q

What is the long-term management of hereditary spherocytosis?

A

Folate replacement

Splenectomy is curative

143
Q

What is the management of hereditary spherocytosis in a haemolytic crisis?

A

Supportive

Transfusion if necessasry

144
Q

What is the main cause of haemolysis of cells with abnormal red cell metabolism?

A

G6PD deficiency

145
Q

What is the inheritance pattern of G6PD deficiency?

A

X linked

146
Q

What is the pathophysiology of G6PD deficiency?

A

Deficiency of an enzyme in red cell metabolism - a pathway that prevents against oxidative stress, and generates energy
When exposed to increased oxidative stress the red cells undergo intravascular haemolysis

147
Q

What is the presentation of G6PD deficiency?

A

Rapid onset jaundice and anaemia after exposure to:

  • henna
  • acute illness
  • broad beans
  • drugs: aspirin
148
Q

What are the features of G6PD deficiency on a blood film?

A

Heinz bodies, bit cells

149
Q

What is diagnostic for G6PD deficiency?

A

Enzyme assay - showing reduced G6PD

150
Q

What is the management of G6PD deficiency?

A

Avoid triggers

Transfuse if acutely anaemic

Y3 - Haem (9 decks)

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