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ESA 5 - Integrative > Anaemia > Flashcards

Anaemia Flashcards

1
Q

Why might anaemia develop?

A
  • Loss of red cells
  • Reduced erythropoiesis, or dyserythropoiesis
  • Abnormalities in haemoglobin synthesis
  • Abnormal structure of RBCs
  • Abnormal metabolism of RBCs
  • Excessive removal by the reticular-endothelial system
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2
Q

Why might cause reduced erythropoiesis?

A
  • Lack of response to haemostatic loop
  • Problems with bone marrow
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3
Q

What problems with the bone marrow might lead to reduced erythropoiesis?

A
  • Empty bone marrow which cannot response to stimulus from EPO
  • Marrow infiltrated by cancer cells or fibrous tissue, meaning normal haemopoietic cells are reduced
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4
Q

Why might the bone marrow be empty?

A
  • After chemotherapy
  • Toxic insult, such as parvovirus infection or aplastic anaemia
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5
Q

What conditions is dyserythropoiesis seen in?

A
  • Renal disease
  • Inflammatory bowel disease
  • SLE
  • Inflammatory conditions such as RA
  • Chronic infections
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6
Q

What might be seen in blood tests in dyserythropoiesis?

A
  • Increased CRP
  • Increased ferratin
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7
Q

What are the features of dyserythropoiesis?

A
  • Iron not released for use in the bone marrow
  • Reduced lifespan of red cells
  • Marrow shows lack of response to erythropoietin
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8
Q

What kind of anaemia might result from dyserythropoiesis?

A
  • Microcytic
  • Normocytic
  • Macrocytic
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9
Q

What are myelodysplastic syndromes?

A

When there is production of abnormal clones of marrow stem cells

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10
Q

How are diagnoses of myelodysplastic syndromes made?

A

By microscopy of the blood cells and bone marrow cells

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11
Q

How can genetic change often be detected in myelodysplastic syndromes?

A

By looking at the chromosomes in the marrow cells

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12
Q

Describe the red cells in myelodysplastic syndromes?

A

They are defective and large

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13
Q

What is the result of the defective and large red blood cells in myelodysplastic syndromes?

A

They are prematurely destroyed by the RES, and so progressive anaemia or pancytopenia develops

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14
Q

What kind of anaemia develops in myelodysplastic syndromes?

A

Macrocytic anaemia

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15
Q

What can cause haemoglobin abnormalities?

A
  • Lack of iron for haem
  • Deficiency in building blocks for DNA synthesis
  • Mutations in proteins encoding the globin chains
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16
Q

What can cause a lack of iron for haem?

A
  • Iron deficiency
  • Anaemia of chronic disease - functional lack of iron
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17
Q

What buliding blocks might be deficient leading to haemoglobin abnormalties?

A
  • Vitamin B12
  • Folate
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18
Q

Give two diseases where mutations in proteins encoding the globin chains leads to haemoglobin abnormalities

A
  • Thalassaemia
  • Sickle cell disease
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19
Q

How much dietary iron is taken in per day?

A

10-20mg

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20
Q

What % of dietary iron is absorbed?

A

10-20%

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21
Q

What does the bioavailability of iron depend on?

A

Its chemical form

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22
Q

What are the sources of non-haem iron?

A
  • Pulses
  • Green vegetables
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23
Q

What are the sources of haem iron?

A
  • Blood
  • Muscle meat - includes fish, chicken etc
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24
Q

What is better absorbed, haem or non-haem iron?

A

Haem iron

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25
Q

What kind of anaemia is iron deficiency anaemia?

A

Microcytic anaemia

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26
Q

Describe the microscopic appearance of iron deficiency anaemia?

A
  • Variation in size and shape of red cells
  • Hypochromia (lack of Hb)
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27
Q

What kind of anaemia is caused by a deficiency in building blocks for DNA synthesis?

A

Megaloblastic anaemia

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28
Q

How does deficiency of B12 and folate cause macrocytic anaemia?

A

Both B12 and folate are necessary for nuclear divisions and nuclear maturation. When deficient, nuclear maturation and cell divisions lag behind cytoplasm development. This leads to large red cell precursors with inappropriately large nuclei and open chromatin. The mature red cells are also large, leading to macrocytic anaemia

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29
Q

What is vitamin B12 synthesised by?

A

Microorganisms

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30
Q

How do humans acquire B12?

A

By eating foods of animal origin

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31
Q

What happens to vitamin B12 in the body?

A
  1. It is combined with the glycoprotein intrinsic factor (IF), produced by parietal cells in the stomach
  2. IF-B12 complex binds in the ileum, leading to absorption of B12 and destruction of IF
  3. In the portal blood, B12 is bound to plasma protein transcobalamin, which delivers B12 to the bone marrow and other tissues
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32
Q

What could deficiency of B12 result from?

A
  • Dietary deficiency of B12
  • Lack of intrinsic factor
  • Disease of the ileum
  • Lack of transcobalamin
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33
Q

What might cause a dietary deficiency of B12?

A
  • Vegan diet
  • Poor diet
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34
Q

What might cause a lack of intrinsic factor?

A
  • Pernicious anaemia
  • Gastrectomy
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35
Q

What is pernicious anaemia?

A

An autoimmune disease affecting gastric parietal cells

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36
Q

What disease of the ileum might cause anaemia?

A
  • Crohn’s disease
  • Ileal resection
  • Tropical sprue
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37
Q

What might cause a lack of transcobalamin?

A

Congential deficiency

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38
Q

Where can folate be found?

A

In most foods- yeast, liver, and leafy greens are an especially rich source

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39
Q

Where does absorption of folate occur?

A

In duodenum and jejenum

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40
Q

What happens to dietary folates in the body?

A

They are converted to one compound, methyltetrahydrofolate (methylTHF)

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41
Q

What does methylTHF do?

A

Circulates in the plasma

42
Q

What is methylTNF needed for?

A

DNA synthesis

43
Q

What couldd deficiency of folate result from?

A
  • Inadequate folate in the diet
  • Increased use of folate
  • Disease of the duodenum and jejenum
  • Lack of methylTHF
  • Alcoholism
  • Urinary loss of folate in liver disease and heart failure
  • Drugs, e.g. anticonvulsants
44
Q

What could cause increased use of folate?

A
  • Pregnancy
  • Increased erythropoiesis, e.g. haemolytic anaemia, severe skin disease
45
Q

What disease of the duodenum and jejenum could lead to folate deficiency?

A

Proximal small bowel disease, e.g. coeliac disease, Crohn’s disease

46
Q

What might cause lack of methylTHF

A

Drugs which inhibit dihydrofolate reductase enzyme, ​e.g. methotrexate

47
Q

What will the peripheral blood film show when there is a deficiency of vitamin B12/folate, leading to anaemia?

A

Macrocytic red cells and hypersegmented neutrophils

48
Q

What happens as deficiency of vitamin B12/folate progresses?

A

Pancytopenia can develop (low platelets and neutrophils)

49
Q

Other than anaemia, what is B12 deficiency associated with?

A

Neurological disease, where there is focal demyelination affecting the spinal cord, peripheral nerves, and optic nerves. Depression and dementia can also develop

50
Q

What is thalassaemia?

A

Reduced rate of synthesis of normal alpha or beta globin chains

51
Q

What is sickle cell disease?

A

Synthesis of abnormal globin chains

52
Q

What causes sickle cell disease?

A

A point mutation causes substitution of valine for glutamic acid in position 6 of the beta-chain

53
Q

What is the most common cause if severe sickling syndrome?

A

HbSS, or homozygous sickle cell anaemia

54
Q

How can a sickling disorder be produced when HbS (one allele) is inherited?

A

Can be co-inherited with another abnormal Hb, e.g. HbC or ß-thal

55
Q

What does HbS cause?

A

A mild, asymptomatic anaemai

56
Q

What % of West African populations have HbS?

A

Up to 30%

57
Q

Why is HbS found in a high % of West African populations?

A

It conveys protection against malaria

58
Q

What is thalassaemia?

A

A heterogeneous group of genetic disorders

59
Q

What happens in thalassaemia?

A
  • Low levels of intracellular haemoglobin cause red cells to be hypochromic and microcytic
  • The relative excess of other globin chains, e.g. insoluble aggregates of alpha chains, contributes to defective red cells, so most maturing cells are destroyed within the bone marrow, and there is excessive destruction of mature red cells in the spleen
  • You get extramedually haemopoiesis, stimulation of EPO, and iron overload
60
Q

Why does extramedually haemopoiesis occur in thalassaemia?

A

In an attempt to compensate for the lack of RBCs

61
Q

What does extramedually haemopoiesis lead to in thalassaemia?

A
  • Splenomegaly
  • Hepatomegaly
  • Expansion of haemopoiesis in the bone cortex
62
Q

What does expansion of haemopoiesis into the bone cortex due to extramedually haemopoiesis lead to?

A

Impairment of growth and classical skeletal abnormalities

63
Q

What does stimulation of EPO in thalassaemia lead to?

A

Further contributes to the drive to make more red cells

64
Q

What is the importance of iron overload in thalassaemia?

A

It is a major cause of premature death

65
Q

What causes iron overload in thalassaemia?

A
  • Excessive absorption of dietary iron due to ineffective haematopoiesis
  • Repeated iron transfusions required to treat the anaemia
66
Q

How is thalassaemia treated?

A
  • Transfusions
  • Iron chelation
  • Folic acid
  • Immunisation
  • Holistic care, involving cardiology, endocrinology, psychological therapy
  • Stem cell transplantation in some
67
Q

What is ß-thalassaemia major?

A

A severe, transfusion dependant anaemia, where both ß genes are abnormal

68
Q

When does ß-thalassaemia major first manifest?

A

6-9 months after birth

69
Q

Why does ß-thalassaemia major manifest 6 to 9 months after birth?

A

As synthesis switcbes from HbF to HbA

70
Q

What is ß-thalassaemia intermedia?

A

Severe anaemia, but not enough so to require regular blood transfusions

71
Q

What is the genetics of ß-thalassaemia intermedia?

A

Genetically heterogenous

72
Q

What is ß-thalassaemia minor?

A

A usually symptomatic condition with a mild anaemia

73
Q

What is the genetics of ß-thalassaemia minor?

A

Genetically heterozygous

74
Q

What is the silent carrier state of alpha-thalassaemia?

A

Deletion of one alpha-globin gene, that is asymptomatic

75
Q

What is the alpha-thalassaemia trait?

A

When you get deletion of two alpha-globin genes

76
Q

Does the alpha-thalassaemia deletion affect both genes of one chromosome, or one gene or each chromosome?

A

Can be eitehr

77
Q

What is the clinical presentation of the alpha-thalassaemia trait?

A

Minimal or no anaemia, and no physical signs

Clinical findings are identical to those of ß-thalassaemia minor, with microcytosis and hypochromia

78
Q

What is haemoglobin H (HbH) disease?

A

Deletion of three alpha-globin genes, where tetramers of ß-globin, called HbH, are formed

79
Q

What is the clinical presentation of alpha-thalassaemia?

A

Moderately severe anaemia

Resembles ß–thalassaemia, with microcytic, hypochromic anaemia with target cells and Heinz bodies in the blood smear

80
Q

What happens in hydrops fetalis?

A

There is deletion of all four alpha-globin genes, leading to an excess of gamma-globin chains forming tetramers that are unable to deliver oxygen to tissues in the fetus

81
Q

What is the prognosis of hydrops fetalis?

A

Usually intrauterine death

82
Q

What conditions have abnormalities of proteins in the red cell membrane that could lead to anaemia?

A
  • Hereditary spherocytosis
  • Hereditary elliptocytosis
  • Heriditary pyropoikilocytosis
  • Hereditary stomatocytosis
83
Q

Why might red cell membrane defects lead to anaemia?

A

These cells are less flexible and damaged more easily, so break up or are removed more quickly from the circulation

84
Q

What can cause acquired red cell membrane defects?

A
  • Mechanical damage to red cells
  • Heat damage
  • Osmotic change
85
Q

What can cause mechanical damage to red cells?

A
  • Heart valves
  • Vasculitis
  • Microangiopathies
  • Disseminated intravascular coagulation
86
Q

What are the best recognised red cell enzyme defects leading to anaemia?

A
  • Glucose-6-phosphate deficiency
  • Pyruvate kinase deficiency
87
Q

What can cause chronic blood loss?

A
  • Gastric ulceration
  • Gastric cancer
  • Colon cancer
  • Excessive mensturation
  • Bladder cancer
88
Q

How might anaemia caused by chronic blood loss present?

A

Microcytic anaemia caused by development of iron deficiency

89
Q

What organ removes damaged or defective red cells?

A

The spleen

90
Q

What happens in haemolytic anaemias?

A

Red cells are destroyed more quickly, as they are abnormal or damagedf

91
Q

Where can abnormal/damaged red cell destruction occur?

A
  • Within the blood vessels - intravascular
  • Within the RES macropahges in the spleen, liver, and bone marrow - extravascular
92
Q

What happens in autoimmune haemolytic anaemia?

A

Autoantibodies bind to the red cell membrane proteins, and cells in the RES recognise part of the antibody, attach to it, and remove it and the red cell from the circulation

93
Q

What is autoimmune haemolytic anaemia broadly classified as?

A
  • Warm autoimmune haemolytic anaemia
  • Cold autoimmune haemolytic anaemia
94
Q

What antibody is involved in warm haemolytic anaemia?

A

IgG

95
Q

At what temperature is warm autoimmune haemolytic anaemia maximally active?

A

37 degress

96
Q

What antibody is involved in cold autoimmune haemolytic anaemia?

A

IgM

97
Q

What temperature is cold autoimmune haemolytic anaemia maximally active at?

A

4 degrees

98
Q

What are the key laboratory features of haemolytic anaemia?

A
  • Increased reticulocytes
  • Raised bilirubin
  • LDH
99
Q

Why are reticulocytes increased in haemolytic anaemia?

A

As marrow tries to compensate

100
Q

Why is LDH increased in haemolytic anaemia?

A

Red cells are rich in this enzyme

101
Q

What causes anaemia in myelofibrosis?

A
  • Decreased erythopoiesis
  • Increased removal by reticulo-endothelial system
102
Q

On what basis can anaemia be classified?

A
  • By mechanism
  • By size
  • By presence or absense of reticulocytosis

ESA 5 - Integrative (10 decks)

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