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103 Theme 2 - Blood > Symposium 1 - Anaemia > Flashcards

Symposium 1 - Anaemia Flashcards

1
Q

What is the diameter of a red cell?

A

7-8 microns

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2
Q

Where does erythropoiesis happen?

A

Bone marrow

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3
Q

How much blood is there is ithe body?

A

5L

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4
Q

Complete the diagram of erythropoiesis

A
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5
Q

Complete the diagram of erythropoiesis

A
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6
Q

What molecule is this?

A

Haemoglobin

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7
Q

What molecule is this?

A

Haemoglobin

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8
Q

What are the 4 causes of anaemia?

A
  • Not making enough (synthesis)
  • Getting used up too quickly (consumption)
  • Losing it somewhere (bleeding)
  • Hiding it somewhere (sequestering)
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9
Q

What are the 2 types of problems of synthesis and what are the morphological features of these?

A

•Not enough iron – small pale cells

–microcytic, hypochromic

•Not enough B12 / folate – big cells

–“megaloblastic anaemia”

–macrocytic, right-shifted

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10
Q

What does this blood film show?

A

Microcytic anaemia – Iron deficiency

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11
Q

What does this blood film show?

A

Megaloblastic anaemia – B12/folate

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12
Q

What does this blood film show?

A

Megaloblastic bone marrow

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13
Q

If you see microcytic anaemia, what are the 2 possible conditions?

A
  • Fe deficiency – acquired
  • Thalassaemia – inherited
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14
Q

What blood results would be abnormal in iron deficient anaemia?

A

–Low ferritin

–Low Fe, high transferrin, low transferrin saturation

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15
Q

What blood results would be abnormal in thalassaemia?

A

–Normal ferritin, abnormal Hb electrophoresis/HPLC

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16
Q

If you see macrocytic anaemia, what are the 2 possible causes?

A
  • B12 deficiency
  • Folate deficiency
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17
Q

What does B12 / folate deficiency affect?

A

Defective DNA synthesis; delayed cell maturation

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18
Q

What are the possible causes of B12 deficiency?

A
  • autoimmune pernicious anaemia
  • Lack of intrinsic factor – inadequate absorption
  • Other causes (vegan, gastric surgery, Crohn’s)
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19
Q

What are the possible causes of folate deficiency?

A

–Dietary lack (tea and toast diet); alcohol

–Malabsorption (coeliac); excess utilisation; pregnancy

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20
Q

What are the 2 conditions that causes normacytic anaemia?

A
  • Anaemia of chronic disease
  • Renal failure (lack of erythropoietin)
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21
Q

How does cancer of chronic disease cause normacytic anaemia?

A

–Normal-sized cells

–Iron trapped inside macrophages

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22
Q

Name some examples of diseases which cause anaemia of chronic disease

A
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23
Q

What abnormal blood results would you find with anaemia of chronic disease?

A

–Normal/raised ferritin, normal/low transferrin

–Raised hepcidin (and inflammatory proteins)

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24
Q

How is normacytic anaemia caused by renal failure treated?

A

–Treat with recombinant Epo (weekly sc injection)

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25
Q

How does bone marrow failure cause anaemia?

A

Not making enough red cells

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26
Q

What abnormal blood results would you find in anaemia caused by bone marrow failure?

A

Reticulocyte count is low

Haematinics (iron, B12 and folate) are normal

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27
Q

What are the 2 main causes of bone marrow failure and name some examples

A

Can be congenital

–rare bone marrow failure states

Or acquired, three causes:

–1) Marrow is empty (aplastic anaemia)

–2) Marrow is full (infiltration e.g. leukaemia)

–3) Marrow is not working (e.g. dysplasia)

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28
Q

How does excess consumption cause anaemia and what is the main reason for excess consumption?

A
  • Excess consumption = shortened red cell survival
  • Main reason is haemolysis (red cell lysis)
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29
Q

What are the inherited and acquired causes of excess RBC consumption?

A

–Inherited:

  • Membrane problems
  • Haemoglobin problems
  • Metabolic problems

–Acquired:

  • Immune (antibodies)
  • Non-immune (direct damage)
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30
Q

What are the 3 types of inheritied red cell problems and name some examples

A

•Membrane problems

–e.g. hereditary spherocytosis

•Haemoglobinopathy

–e.g. sickle cell disease (wrong type of Hb)

–e.g. thalassaemia (not enough Hb)

•Metabolic

–e.g. G6PD deficiency

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31
Q

What is hereditary spherocytosis and what is the main treatment?

A

Inheritied red cell membrane problem -

–Red cells are spherical, not biconcave

–Splenectomy can help (may need cholecystectomy for gallstones also)

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32
Q

What is G6PD deficiency and what must be avoided?

A

–X-linked recessive, males, Afro-Caribbean

–Must avoid fava beans, legumes, certain antimalarials and antibiotics

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33
Q

What condition is this?

A

Hereditary spherocytosis

Red cells are spherical, not biconcave

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34
Q

What condition is this?

A

Hereditary elliptocytosis

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35
Q

What disease is this?

A

Sickle cell anaemia

36
Q

Label a sickle cell and a target cell

37
Q

What is the composition of a normal haemoglobin molecule?

A
  • Normal Hb molecule comprises 4 chains
  • This is called HbA = 2α + 2β
38
Q

How does a person develop either thalessaemia trait or thalassaemia major?

A
  • You can inherit mutations in the α gene or β gene
  • You have 4 α genes and 2 β genes
  • Therefore, in β thalassaemia, you can have:

Thalassaemia trait (single defective gene)

Thalassaemia major (both genes defective)

39
Q

Which is the alpha globin gene cluster and the beta globin gene cluster?

40
Q

Draw a genetic diagram for a mother and father both with thalassaemia trait

41
Q

What test is this?

A

Hb electrophoresis

42
Q

What are the morphological features of beta-thalassaemia?

A
  • Microcytic hypochromic blood film
  • Low MCV (same as iron-deficiency anaemia)
43
Q

What is the clinical difference between beta thalassaemia trait and beta thalassaemia major?

A
  • Β-thal trait – no clinical consequences
  • Β-thal major – severe anaemia and transfusion-dependent, with problems of iron-overload and organ failure
44
Q

Name the possible immune and non-immune causes of acquired RBC problems

A

Immune i.e. antibody-mediated (spherocytes)

–Autoimmune (warm IgG vs. cold IgM)

–Alloimmune (red cell transfusion reaction)

Non-immune (red cell fragments)

–Heart valves (mechanical)

–DIC (very sick patients - sepsis, metastatic cancer)

–MAHA (microangiopathic haemolytic anaemia)

45
Q

What does this blood film show?

A

Autoimmune haemolysis

46
Q

What is included in a haemolysis screen?

A

–Direct anti-globulin test (DAT or Coomb’s test)

–Bilirubin level – is patient jaundiced?

–Blood film – are there spherocytes? fragments?

–LDH level – goes up in haemolysis

–Reticulocyte count – goes up in haemolysis

–Haptoglobins – levels go down in serum (binds free Hb)

–Haemoglobinuria = free Hb in urine (dark colour)

–Urine dipstick shows urobilinogen (colourless)

47
Q

What are the 3 main sources of bleeding to cause anaemia?

A

–Bowel

–Menstrual

–Bladder

48
Q

What is sequestering?

A

Internal bleeding

E.g. trauma or vascular rupture

–Abdomen

–Thorax

–Tissues

Big spleen (hypersplenism)

49
Q

How does anaemia result in tissue hypoxia?

A
  • Hb carries oxygen bound to the Fe
  • Oxygen is delivered to the tissues
  • Anaemia results in tissue hypoxia
50
Q

What are the 3 symptoms of anaemia?

A

Tiredness

Breathlessness

Pallor

51
Q

What genetic mutation causes sickle cell anaemia?

A
  • Caused by a point mutation in b globin gene
  • Substitution of valine for glutamic acid at 6th amino acid position (qualitative change)
52
Q

How does the sickle cell mutation cause sickling of RBC?

A
  • On deoxygenation, HbS forms parallel aggregates
  • Valine substitution stabilises this conformational change causing sickling (aggregate formation)
  • Red cell shape is deformed into sickle shape
53
Q

What is the genetic difference between inheriting sickle cell disease and sickle cell trait?

A
  • Inherit 1 copy of b globin gene from each parent
  • If only 1 HbS gene inherited = sickle cell trait
54
Q

What are the symptoms of sickle cell trait?

A

Generally asymptomatic

55
Q

What is HbC and what disease does it cause?

A
  • HbC is genetic variant of sickle Hb (6th aa, lysine)
  • SC disease clinically very similar to SS disease
56
Q

What are the physiological effects of sickled RBC?

A
  • Increased mechanical fragility resulting in shortened lifespan (6-10 days)
  • The rigidity of sickle cells results in increased viscosity with occlusion of small blood vessels
  • Adhesion of sickle cells to endothelium
57
Q

Which does the distribution of sickle cell disease correlate with?

A
  • Distribution correlates with endemicity of Plasmodium falciparum (carried by female Anopheles mosquito)
  • Selective advantage of carrier against infection
58
Q

What is the survival of sickle cell disease without management?

59
Q

Anaemia is compensated by which compound?

A

Increased 2,3-DPG

60
Q

How does an increase in 2,3-DPG compensate anaemia?

A
  • This moves the oxygen dissociation curve to the right
  • Oxy-haemoglobin releases its oxygen to the tissues at higher levels of tissue oxygen
61
Q

Which type of haemoglobin is low affinty?

62
Q

Which curve is adult haemoglobin and which is fetal haemoglobin?

63
Q

Which line is HbA and which is HbS?

64
Q

What are the clinical features of sickle cell disease?

A
  • Presentation in infancy (baby protected by HbF)
  • Anaemia and jaundice
  • Dactylitis, epiphyseal damage can result in shortening of the digits
  • Splenic sequestration only in children
  • Classical vaso-occlusive crises
  • Pneumococcal septicemia
65
Q

What is this?

A

Dactylitis

Finger tips lost due to infarction

66
Q

What are the symptoms of chest syndrome?

A
  • SOB
  • Pleuritic chest pain
  • Patchy shadowing on CXR
  • Progressive hypoxia and fever
67
Q

What pathology does brain syndrome present as?

68
Q

What type of infection is an aplastic crisis associated with?

A

Parvovirus infection

69
Q

What are the 3 types of crisis/syndrome?

A

Chest syndrome

Brain syndrome

Aplastic crisis

70
Q

What are the 4 features you would see on a blood film of sickle cell disease?

A
  • Sickle cells
  • Polychromasia
  • Howell-Jolly bodies
  • Nucleated RBCs
71
Q

What test is this?

Is it positive or negative?

A

Sickle solubility test

Positive

72
Q

What test is this?

What do each of the numbers 1-7 show?

A

Haemoglobin electrophoresis

1,5 = control lanes (Hb A, F, S, C),

2 = normal adult, 3 = normal baby,

4 = sickle cell disease, 6 = sickle cell trait,

7 = SC disease, 8 = sickle cell trait

73
Q

How is a crisis managed?

A

Exclude underlying infection

Intravenous fluids

Oxygen

Analgesia

  • NSAID’s
  • Opiates
  • Avoid pethidine (seizures and addiction)

Antibiotics

Monitor FBC and reticulocyte count

75
Q

How is sickle cell disease managed?

A
  • =Antenatal screening
  • In high prevalence areas
  • But variable clinical course

Prophylaxis against infections

  • Penicillin prophylaxis
  • Vaccination
  • pneumovax / meningovax / haemophilus (HIB)

Prevention of crises

Avoid infections, hypoxia, dehydration

77
Q

When is a patient with sickle cell disease at greatest risk of a stroke?

A

If blood flow >200cm/sec the risk of stroke is significantly increased

78
Q

How are strokes prevented?

A
  • Risk reduced by exchange transfusion
  • Aim to reduce HbS level to below 30%
  • Hydroxyurea is an alternative if unable to transfuse
79
Q

What does an exchange transfusion do?

A

Aim to reduce HbS level to <30%

80
Q

How is an exchanged transfusion done?

A
  • Manually or with cell separator machine
  • Blood-match ABO/Rhesus/Kell/Sickle neg
81
Q

What are the indications for an exchange transfusion?

A
  • Chest syndrome
  • Stroke
  • Major surgery
  • Recurrent severe crises
  • Priapism (painful erections)
82
Q

What are the possible complications of sickle cell disease?

A
  • Sepsis
  • Bone infarcts
  • Avascular necrosis of femoral/humoral heads
  • Gallstones (pigment stones)
  • Proliferative retinopathy
  • Osteomyelitis (Salmonella)
  • Papillary necrosis/renal failure
  • Leg ulcers
83
Q

How does hydroxyurea manage sickle cell disease?

A
  • Hydroxyurea reduced frequency of crises, chest syndrome and transfusions
  • Increase in HbF production
  • Results in reduced sickling of red cells
  • Also, reduction in WCC and platelets
  • Reduction in frequency of crises
84
Q

What is hydroxyurea also known as?

A

Hydroxycarbamide

85
Q

How does hydroxyurea increase HbF?

A
  • Leads to reactivation of gamma globin locus in patients
  • Results in increased production of fetal Hb (HbF)

103 Theme 2 - Blood (10 decks)

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