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Haematology & Immunology > Haematology > Flashcards

Haematology Flashcards

1
Q

what are the three components of blood?

A

red blood cells
plasma
clotting agents

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2
Q

what are the three principal functions of blood?

A

transport
fighting infection
promoting vascular integrity

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3
Q

what are the three general pathogenic mechanisms of haematological abnormalities?

A
  • too many cells
  • not enough cells
  • abnormal function of cells
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4
Q

what aremain components of bone marrow?

A

haemopoietic stem cells

adipose tissue

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5
Q

which types of blood cells are classed as myeloid cells?

A 
erythrocytes
platelets
neutrophils
basophils
eosinophils
monocytes
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6
Q

which types of blood cells are classed as lymphoid cells?

A

B cells
T cells
NK cells

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7
Q

what are the three subtypes of T cells, and what is their function?

A
  • cytotoxic T cells - kill pathogen
  • helper T cells - help cytotoxic T cells kill pathogens and help antibody production
  • regulatory T cells - dampen down immune response
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8
Q

what can reticulocytes be useful for?

A

useful for measuring bone marrow function (ie red cell production)

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9
Q

what is erythropoietin, where is it produced and why?

A

hormone that is produced by the kidneys in response to hypoxia, stimulates red blood cell production by bone marrow

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10
Q

what is the function of erythropoietin?

A

it stimulates haematopoietic stem cells in bone marrow to differentiate into erythrocytes

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11
Q

what are the stages of red blood cell differentiation?

A

haematopoietic stem cell –> myeloid progenitor cell -> erythroblast -> reticulocyte -> erythrocyte

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12
Q

how long does it take for reticulocytes to differentiate into erythrocytes?

A

~24 hours

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13
Q

what is the lifespan of an erythrocyte?

A

~120 days

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14
Q

what hormone regulates platelet production?

A

thrombopoietin

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15
Q

what is the lifespan of a platelet?

A

7 days

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16
Q

where is thrombopoietin produced?

A

in the liver

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17
Q

what is the lifespan of a neutrophil?

A

1-2 days

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18
Q

what stimulates neutrophil production?

A

granulocyte-colony stimulating factors
interleukins
macrophages

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19
Q

what are the stages of platelet differentiation?

A

haematopoietic stem cell -> myeloid progenitor cell -> megakaryocyte -> platelet

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20
Q

what are the stages of neutrophil differentiation?

A

haematopoietic stem cell -> myeloid progenitor cell -> neutrophil

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21
Q

what are monocytes?

A

macrophages that stay in the blood

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22
Q

what name is given to monocytes that have migrated to 1. liver, 2. kidneys, 3. skin, 4. brain?

A
  1. kuppfer cells
  2. mesangial cells
  3. langerhans cells
  4. microglia
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23
Q

what is main function of eosinophils?

A

fighting off parasite infections and mediating allergies

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24
Q

where do B and T cells mature?

A

B cells - bone marrow

T cells - thymus

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25
Q

what is the main role of B cells?

A

antibody production

immune memory

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26
Q

main action of antibodies?

A

opsonisation of pathogen

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27
Q

what is the role of IgG?

A

immune surveillance in circulation long after infection

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28
Q

what is the role of IgA?

A

immune surveillance of mucosa (gut, trachea)

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29
Q

what is the role of IgE?

A

mediation of allergies

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30
Q

what is the role of IgM?

A

first antibody to respond during an infection

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31
Q

what is positive and negative selection in terms of lymphocyte maturation?

A

positive selection - if cell doesn’t react to self-antigens it survives and is taken to periphery
negative selection - if cell reacts to self-antigens it is killed

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32
Q

what is the difference between Class I and Class II HLA?

A

Class I HLA - displays self-antigens on all own cells

Class II HLA - displays foreign antigens eaten by APC’s

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33
Q

what are paraproteins?

A

monoclonal antibodies in the blood which only arise from abnormal proliferation of mature B cells or plasma cells

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34
Q

what is the normal value range for Haemoglobin for men an women?

A

men: 135-170
women: 120-160

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35
Q

what is the normal value range for platelets in the blood?

A

150-400

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36
Q

what is the normal value range for WBC in the blood?

A

4-10

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37
Q

name the main diagnostic tools that are done in haematology

A
  • FBC
  • clotting factors/platelet clotting times
  • chemical assays (haematinics)
  • biopsies (bone marrow, lymph node)
  • imaging (Xray, CT, MRI)
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38
Q

what are the three most common haematinics?

A

iron
folate
vitamin B12

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39
Q

what does a blood group depend on?

A

it depends on the antigens its red blood cells have on their surface

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40
Q

what antibodies does blood group A produce?

A

anti-B antibodies

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41
Q

what antibodies does blood group B produce?

A

anti-A antibodies

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42
Q

what antibodies does blood group O produce?

A

anti-A and anti-B antibodies

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43
Q

why can blood group O give blood to everyone but can only receive from other O?

A

because group O has no antigens, therefore group A and group B won’t trigger an immune response against it. however, group O produces anti-A and anti-B antibodies, therefore it can only receive from blood group O

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44
Q

what kind of antibody do blood groups present?

A

IgM

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45
Q

which antibodies can fix complement?

A

IgM

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46
Q

what are the most common blood groups?

A

A and O

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47
Q

who can blood group O donate to?

A

A, B, AB and O

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48
Q

what is the difference between giving someone red blood cells (RBC) and FFP (fresh frozen plasma)?

A

RBC is literally only a donation of red cells

FFP contains proteins, antibodies and clotting factors but no red cells

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49
Q

name a few indications of RBC transfusion

A

severe acute anaemia
bone marrow failure
prior to major surgery
to replace damaged RBC eg sickle cell

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50
Q

what is the storage temperature for blood?

A

4 degrees

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51
Q

what is the storage temperature for platelets?

A

22 degrees

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52
Q

what is the average transfusion time for blood?

A

2-4 hours

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53
Q

what is the average transfusion time for platelets?

A

20-30mins

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54
Q

what antibodies does AB produce?

A

no antibodies

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55
Q

who can an AB fresh frozen plasma donor give blood to, and why?

A

AB FFP donor can give to A, AB, B and O because their plasma contains no antibodies at all

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56
Q

why is RhD blood group important?

A

because if someone is RhD negative, they can get a transfusion reaction if they are transfused with RhD positive blood

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57
Q

what is apheresis?

A

the process of separating blood into individual components for transfusion

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58
Q

what is contained in the plasma once whole blood is separated?

A

clotting factors
albumin
antibodies

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59
Q

what is contained in the buffy coat layer once whole blood is separated?

A

white blood cells

platelets

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60
Q

name a few indications for platelet transfusion

A

massive haemorrhage
bone marrow failure
prior to surgery
cardiopulmonary bypass

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61
Q

what is the main aim of fresh frozen plasma transfusions?

A

to promote coagulation

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62
Q

what is the main aim of red cell transfusions?

A

to increase hemoglobin and oxygen levels

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63
Q

what is the main aim of platelet transfusions?

A

to correct low platelet levels

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64
Q

what are the processes in place when taking blood to the blood bank?

A
  • EDTA tubes (x2)
  • group and screen (blood type, antibodies)
  • Coombs test
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65
Q

what is the process of the Coombs test in haematology?

A

it involves adding anti-human antibodies to a blood sample; if there are autoantibodies or complement stuck to the RBC, the anti-human antibodies will attach to these, causing the RBC to crosslink and agglutinate

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66
Q

what is the aim of the Coombs test?

A

it is used in haemolytic anaemia to identify whether the cause of the haemolysis is auto-immune or not

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67
Q

what is the difference between direct and indirect Coombs test?

A

Direct - identifies antibodies stuck to RBCs

Indirect - identifies free floating antibodies in plasma

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68
Q

when is a Coombs test positive for antibodies?

A

when the RBC agglutinate on the blood film

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69
Q

what is haemolytic disease of the newborn (HDN) and what causes it?

A

it is the destruction of baby’s red cells by mum’s antibodies, when baby has RhD positive blood and mum has RhD negative blood

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70
Q

for which pregnancy is haemolytic disease of the newborn normally a problem?

A

any pregnancy after the first one with a baby who has RhD positive blood

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71
Q

when is prophylactic anti-D given to pregnant women?

A

as routine during week 28

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72
Q

what is the aim of giving prophylactic anti-D to pregnant women?

A

it neutralises any RhD positive antigens that get into the circulation, so that mum doesn’t form any antibodies against them

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73
Q

in which areas of red blood cells can congenital anaemias occur?

A
  • cell membrane
  • enzymes
  • haemoglobin
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74
Q

what happens to red blood cells in congenital anaemias like spherocytosis and elliptocytosis?

A

structural proteins that maintain the biconcave shape are mutated, causing the red cells to change shape

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75
Q

what are the structural proteins in red cell membranes that, when mutated, can cause congenital anaemias?

A

ankyrin
Band 3
spectrin (alpha and beta)

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76
Q

why are red cells normally biconcave?

A

because this allows them to squeeze through tight capillaries

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77
Q

what is the consequence of congenital anaemias affecting the cell membrane?

A

early haemolysis by the reticuloendothelial system

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78
Q

what system in the body is responsible for getting rid of old or faulty red blood cells?

A

the reticuloendothelial system

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79
Q

what are the main cellular processes which occur in red blood cells? what is the role of each?

A

glycolysis - energy

pentose phosphate pathway - protection against reactive oxygen species

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80
Q

mutation in which red blood cell enzymes can cause congenital anaemias?

A
  • glucose 6 phosphate dehydrogenase (G6PD) deficiency

- pyruvate kinase deficiency

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81
Q

why is G6PD important in red cell metabolism?

A

it forms a link between glycolysis and the pentose phosphate pathway, and protects red cells from oxidation

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82
Q

what is the genetic inheritance of G6PD deficiency?

A

X linked

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83
Q

what triggers haemolytic anaemia in G6PD deficiency?

A

drugs
fava beans
infections
severe disease eg DKA

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84
Q

where does haemolysis occur in anaemia caused by G6PD deficiency?

A

intravascular haemolysis

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85
Q

name a few symptoms/signs of intravascular haemolysis

A
  • anaemia
  • pigment gallstones
  • dark urine
  • jaundice
  • splenomegaly
  • hepatomegaly
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86
Q

what is the pathology behind the signs of intravascular haemolysis?

A

red cells bursting in the circulation, causing haemoglobin to spill into the circulation and bilirubin levels in the blood increasing

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87
Q

what is the general treatment of haemolysis?

A

folic acid and iron replacement

blood transfusion

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88
Q

why is B12 not routinely given as replacement of anaemia, unless there is a specific B12 deficiency?

A

because normally B12 stores in the liver last for about 3 years

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89
Q

what are the main congenital haemoglobinopathies?

A

thalassaemia

sickle cell disease

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90
Q

what is thalassaemia?

A

loss or mutation of certain globin genes, causing a reduction in globin chains and lower haemoglobin levels

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91
Q

what is sickle cell disease?

A

structural abnormality in beta chains of haemoglobin, which cause the chains to crystallise and change the shape of the red cell

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92
Q

what is HbF, and what is it made up of?

A

HbF is fetal haemoglobin

2 alpha chains + 2 gamma chains

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93
Q

what is HbA2 and what is it made up of?

A

HbA2 is a type of haemoglobin that makes up 2% of our total haemoglobin
2 alpha chains + 2 delta chains

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94
Q

what is 97% of our haemoglobin made up of?

A

2 alpha chains + 2 beta chains

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95
Q

what is alpha thalassaemia?

A

it’s a congenital anaemia caused by absence in one or more alpha genes, causing a reduced number of alpha chains and therefore less haemoglobin

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96
Q

why is a lack of alpha globin chains incompatible with life?

A

because formation of haemoglobin depends on 2 alpha chains bound to two beta, delta or gamma chains

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97
Q

what is beta thalassaemia major?

A

it’s a congenital anaemia caused by absence of beta globin genes, resulting in loss of beta chains and therefore very low levels of haemoglobin

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98
Q

what does beta thalassaemia minor look like on a blood film?

A

microcytic and hypochromic red cells

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99
Q

what is sickle cell disease?

A

it’s a congenital anaemia caused by abnormal beta globin chains, which crystallise in low oxygen tension areas and cause the red cell to become sickle shaped

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100
Q

what are the main complications of sickle cell disease, as a result of the abnormal red cell shape?

A

early haemolysis

vaso-occlusion

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101
Q

why is sickle cell disease a risk factor for CVA?

A

because the sickle cell shaped red cells can cause vaso-occlusion

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102
Q

how does sickle cell disease cause anaemia?

A

because of the red cells are haemolysed due to their abnormal shape

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103
Q

why do people with sickle cell anaemia not have any problems with hypoxia?

A

because sickle red cells have slightly lower affinity for oxygen so give it up more readily

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104
Q

what is the appearance of G6PD deficient red blood cells?

A

bite cells

blister cells

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105
Q

how many alpha and beta genes do you get from mother and father?

A

alpha genes - two from mum, two from dad

beta genes - one from mum, one from dad

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106
Q

what is the genetic inheritance of thalassaemia?

A

autosomal recessive

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107
Q

what is the genetic inheritance of sickle cell anaemia?

A

autosomal recessive

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108
Q

what is the appearance of red blood cells in thalassaemia minor?

A

hypochronic microcytic

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109
Q

how is a sickle cell crisis managed?

A

supportive: analgesia, oxygen, fluids, antibiotics if needed

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110
Q

how does sickle cell anaemia affect the spleen?

A

it causes hyposplenism

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111
Q

as a result of vaso-occlusion in sickle cell anaemia, name a few clinical presentations that may occur

A

vaso-occlusion (CVA, bone pain, chest crisis, pain crisis)
sequestration (liver, spleen)
hyposplenism (increased infections)
chronic haemolytic anaemia (gallstones, dark urine, jaundice)

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112
Q

what is the long-term treatment for sickle cell disease?

A

vaccinations and prophylactic antibiotics
folic acid replacement
blood transfusions
hydroxycarbamide

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113
Q

what is the acute treatment for sickle cell disease presentations?

A 
oxygen
analgesia
fluids
antibiotics
blood transfusion if severe
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114
Q

what’s an important complication in beta thalassaemia treatment, and how is it prevented?

A

iron overload

iron chelation therapy is started alongside transfusions to prevent iron overload

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115
Q

how does hydroxycarbamide reduce the amount of sickle cell acute attacks?

A

by increasing the production of fetal haemoglobin, which doesn’t sickle, and therefore reducing the number of sickle cells

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116
Q

in anaemia, what investigation is done to confirm the presence of haemolysis?

A

bilirubin and LDH levels

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117
Q

in anaemia, what investigation is done to assess bone marrow function?

A

reticulocyte count

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118
Q

in anaemia, what investigation is done to assess iron levels?

A

ferritin levels

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119
Q

in anaemia, what investigation is done to test for megaloblastic anaemia?

A

B12/folate levels

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120
Q

what haematinic replacement should anyone with haemolytic anaemia receive?

A

folic acid replacement

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121
Q

what is the presentation of beta thalassaemia major?

A 
severe anaemia from 3 months of age
bone deformities
bone marrow expansion
splenomegaly
growth retardation
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122
Q

why does beta thalassaemia major cause bone deformities?

A

because the lack of haemoglobin causes bone marrow to expand in an effort to create red cells

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123
Q

what is the treatment for beta thalassaemia?

A

blood transfusion every 4-6 weeks

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124
Q

what are the hereditary anaemias caused by abnormalities in haem synthesis steps? name the steps affected

A

mitochondrial step abnormalities - sideroblastic anaemias

cytoplasmic step abnormalities - porphyrias

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125
Q

what is the genetic inheritance of G6PD deficiency?

A

X-linked

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126
Q

what type of haemolysis is caused by a trigger in G6PD deficiency anaemia?

A

intravascular haemolysis

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127
Q

what are the generic features of anaemia?

A 
pallor
tiredness
swollen ankles
breathlessness/dizzyness
gallstones
chest pain
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128
Q

why do men have higher haemoglobin levels than women?

A

because hormones affect Hb production, and testosterone in men causes an increase in Hb production

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129
Q

how does age affect Hb levels?

A

babies are polycythaemic, whereas old people tend to have low Hb

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130
Q

why is acute anaemia more likely to cause hypoxic symptoms than chronic anaemia?

A

because chronic anaemia allow the body to adapt to lower levels of Hb

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131
Q

what are the morphological features of red blood cells that can help identify the type of acquired anaemia?

A

MCV - mean cell volume (size)

MCH - mean cell haemoglobin (colour)

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132
Q

what are the 3 possible morphological features of acquired anaemia?

A
  • hypochromic microcytic
  • normochromic normocytic
  • macrocytic
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133
Q

what is the commonest cause of anaemia?

A

iron deficiency

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134
Q

what diagnostic test should be done if a blood film shows hypochromic microcytic anaemia?

A

serum ferritin levels

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135
Q

in hypochromic microcytic anaemia, what diagnosis do high/normal levels vs low levels of serum ferritin indicate?

A

low levels - iron deficiency

high/normal levels: thalassaemia trait, secondary anaemia

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136
Q

what is the pathology behind secondary anaemia?

A

increased hepcidin levels - ferroportin blocked, not allowing iron to be transported into cells and therefore reducing ability to make red blood cells

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137
Q

in iron metabolism, define the role of ferritin, transferrin, ferroportin and hepcidin

A

ferritin - molecule used to store iron
transferrin - protein used to carry iron in the circulation
ferroportin - endothelial channel that allows iron to enter and exit cells
hepcidin - molecule that regulates iron absorption by opening/blocking ferroportin according to iron levels

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138
Q

which blood cancer is characterised by proliferation of undifferentiated myeloid progenitor cells?

A

acute myeloid leukaemia

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139
Q

in AML, are the proliferating cells differentiated?

A

no

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140
Q

how does AML affect the bone marrow?

A

it causes bone marrow failure, due to the overwhelming amount of undifferentiated blasts taking over the bone marrow

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141
Q

what percentage of cells on the blood film have to be undifferentiated blasts, for it to be classed as AML?

A

> 20% of cells on blood film have to be undifferentiated blasts

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142
Q

what are the three classic features of bone marrow failure? think about the cells involved

A

anaemia (due to low red cells)
thrombocytopaenia (due to low platelets)
neutropaenia (due to low neutrophils)

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143
Q

what symptoms can occur in bone marrow failure, as a result of the pancytopaenia?

A

anaemia - pale, tiredness, fatigue, SoB
thrombocytopaenia - purpura, mucosal bleeding, ecchymosis
neutropaenia - increased risk of infections

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144
Q

what is pancytopaenia?

A

reduction in all blood cell numbers

145
Q

what investigations are essential in diagnosing myeloid malignancies?

A
  • full blood count
  • blood film
  • bone marrow aspirate
  • cytogenetics/immunohistochemistry
146
Q

what is the treatment of AML?

A
  • chemotherapy
  • supportive treatment (prophylaxis for infections)
  • stem cell transplantation
147
Q

why is AML more severe than CML?

A
  • AML develops more rapidly
  • AML causes bone marrow failure as a result of blast proliferation
  • blasts in AML do not function at all, whereas the proliferating myeloid cells in CML still function to a degree
148
Q

which population is more at risk of developing AML?

A

older population

149
Q

in which type of myeloid malignancy is there proliferation of differentiated myeloid cells?

A

chronic myeloid leukaemia

150
Q

what is the pathophysiology of CML?

A

uncontrolled proliferation caused by abnormal tyrosine kinase protein (BCR-ABL) as a result of a translocation between chromosomes 9 and 22 forming the Philadelphia Chromosome

151
Q

what is the treatment of CML?

A
  • tyrosine kinase inhibitors (imatinib = Glivec)

- stem cell transplantation (if TKI fail)

152
Q

what is an important complication in AML chemotherapy treatment?

A

severe bleeding in brain and lungs

153
Q

why is there need for supportive treatment during AML chemotherapy treatment?

A

because chemotherapy completely stops bone marrow function for several weeks, leaving patients severely immunocompromised

154
Q

in which malignancy is the Philadelphia Chromosome found, and what is it formed by?

A

CML

formed by translocation between chromosomes 9 and 22

155
Q

name some features of CML

A

high WBC and platelet count
anaemia
significant splenomegaly
gout

156
Q

why is stem cell transplantation essential after chemotherapy in AML?

A

because it maintains remission of disease

157
Q

what is the myeloproliferative disease which affects red cells?

A

polycytaemia vera

158
Q

what is the pathophysiology of myeloproliferative diseases?

A

constant activation of JAK receptors causing proliferation of certain myeloid cells

159
Q

which myeloid cells are increased in polycytaemia vera?

A

mainly red cells, but also white cells and platelets

160
Q

which myeloid cells are increased in essential thrombocytaemia?

A

mainly platelets

161
Q

what is the treatment of polycytaemia vera, and what is its aim?

A

venesection, aspirin, hydroxycarbamide, JAK inhibitors

aim to reduce haematocrit to <45% and reduce risk of CVA resulting from thrombosis

162
Q

what are some symptoms of polycytaemia vera?

A

itching
headaches
thrombosis - MI, stroke etc

163
Q

what is the treatment of essential thrombocytaemia, and what is its aim?

A

aspirin, hydroxycarbamide, JAK inhibitors

aim to block platelet action and reduce risk of CVA/thrombosis

164
Q

what is a significant risk when a patient develops a myeloproliferative disease?

A

it can develop into AML further down the line

165
Q

blood cancers make up what percentage of total cancers?

A

about 10%

166
Q

which type of leukaemia are children more likely to develop?

A

acute lymphoblastic leukaemia

167
Q

which blood cancers involve proliferation of undifferentiated cells?

A

acute myeloid leukaemia

acute lymphoblastic leukaemia

168
Q

which blood cancers involve proliferation of differentiated myeloid cells?

A

chronic myeloid leukaemia
polycytaemia vera
essential thrombocytaemia

169
Q

which blood cancers are also called myeloproliferative neoplasms?

A

polycytaemia vera

essential thrombocytaemia

170
Q

which blood cancers involve proliferation of differentiated lymphoid cells?

A

chronic lymphocytic leukaemia
Hodgkin’s lymphoma
Non-Hodgkin’s lymphoma

171
Q

what differentiates Hodgkin’s from Non-Hodgkin’s lymphoma?

A
  • Hodgkin’s Lymphoma mainly affects lymph nodes around the head and respiratory tract, without much extra-nodal involvement
  • Non-Hodgkin’s Lymphoma affects symmetrical lymph nodes all over the body and has more frequent extra-nodal involvement
172
Q

where do lymphomas normally arise?

A

in the germinal center of a lymph node

173
Q

which lymphoid cell type is most commonly affected in lymphomas? why is that?

A

B cell most commonly affected, because they proliferate at very high rates to make memory and plasma cells, increasing the risk of an accidental mutation in the process

174
Q

during which process in B cell maturation do lymphomas commonly arise?

A

during somatic hypermutation (extensive proliferation to make plasma and memory cells)

175
Q

when is a swollen, localised lymph node more likely to be an infection or a tumour?

A

if localised and painful - more commonly an infection

if localised and painless - more commonly cancer metastasis

176
Q

when do swollen, painless lymph nodes point towards lymphoma rather than metastatic cancer? explain why

A

when the swollen lymph nodes are generalised - lymphomas spread through lymphatic system, whereas metastases spread through circulation so are unlikely to present in multiple lymph nodes

177
Q

what causes secondary anaemia to develop?

A

increased levels of hepcidin (eg due to inflammation/infection) cause a decrease in iron passing through ferroportin and into cells

178
Q

name a few common causes of iron deficiency anaemia

A 
lack of iron in diet
malabsorption
GI bleed
menorrhagia
increased requirement (pregnancy)
179
Q

what do red cells look like in iron deficiency anaemia?

A

hypochromic and microcytic

180
Q

what feature of anaemia can be seen in nails?

A

koilonychia

181
Q

what features of anaemia can be present in the mouth?

A

atrophic, painful tongue

angular stomatitis

182
Q

what is the first line treatment of iron deficiency?

A

oral iron replacement tablets

183
Q

what investigation is done when a blood film shows normochromic, normocytic anaemia?

A

reticulocyte count

184
Q

what does a low reticulocyte count mean in normochromic, normocytic anaemia?

A

it means bone marrow can’t produce new reticulocytes because there is a lack of available iron ie secondary anaemia

185
Q

what does a high reticulocyte count mean in normochromic, normocytic anaemia?

A

it means the bone marrow is working hard to replace red cells ie haemorrhage or acute haemolysis

186
Q

in secondary anaemia, is serum ferritin high or low? explain why

A

high, because underlying condition is causing an increase in hepcidin which stops ferritin from being absorbed, but it also increases ferritin levels

187
Q

ferritin is an acute phase reactant. what does that mean?

A

it means that during infection or inflammation the ferritin levels in the circulation go up

188
Q

what is haemolytic anaemia?

A

it’s premature destruction/removal of red blood cells from the circulation

189
Q

what are the two possible mechanisms haemolytic anaemia can be acquired? where does each one occur in relation to the circulation?

A
  • autoimmune - occurs extravascularly

- non-autoimmune - occurs intravascularly

190
Q

what red cell abnormalities might cause congenital haemolytic anaemia?

A
  • abnormal red cell shape (spherocytosis)
  • abnormal haemoglobin (sickle cell anaemia, thalassaemia)
  • abnormal enzymes (G6PD deficiency)
191
Q

what organ can be noticeably affected in autoimmune haemolytic anaemia? how and why?

A

the spleen can become very enlarged, because it is working harder than usual to remove the red blood cells it sees as foreign

192
Q

what investigation is done to identify whether haemolytic anaemia is autoimmune or not?

A

Coombs test (ie antiglobulin testing)

193
Q

if a Coombs test result shows agglutinated red blood cells, what does that mean?

A

it means the haemolytic anaemia is autoimmune

194
Q

if a Coombs test result shows non-agglutinated red blood cells, what does that mean?

A

it means the haemolytic anaemia is not caused by an autoimmune response

195
Q

what is an important consideration when interpreting the results of a Coombs test in haematology?

A

some antibodies only activate in warm conditions, and some only in cold conditions. this can point to different causes for immune haemolytic anaemia

196
Q

what blood tests are done to identify whether a patient with anaemia is haemolysing?

A
  • FBC
  • reticulocyte count
  • bilirubin/LDH
  • haptoglobin
  • Coombs test
197
Q

what are the management options of haemolytic anaemia?

A
  • folic acid replacement
  • treating underlying cause
  • immunosuppression
  • transfusion
  • splenectomy
198
Q

what is macrocytic anaemia also called?

A

megaloblastic anaemia

199
Q

what is macrocytic/megaloblastic anaemia caused by?

A

mainly vitamin B12 or folic acid deficiency

also: myelodysplasia, drugs, liver disease, alcohol, hypothyroidism

200
Q

how is vitamin B12 deficiency managed?

A

intramuscular B12 injections (every 3 months)

201
Q

what causes vitamin B12 deficiency?

A
  • pernicious anaemia

- gastrectomy

202
Q

what causes folate deficiency?

A
  • diet
  • increased requirement
  • malabsorption
203
Q

what are the main features of B12/folate deficiency?

A 
anaemia symptoms (pale, fatigue, SoB, jaundice)
neurological symptoms (peripheral neuropathy)
204
Q

what does megaloblastic anaemia look like on a blood film?

A
  • red cells look large and flabby, more friable and prone to haemolysis
  • neutrophils look hypersegmented
205
Q

in anaemia, what specific blood tests help point towards the presence of haemolysis?

A

bilirubin levels
lactate dehydrogenase levels
haptoglobin levels

206
Q

how is folate deficiency managed?

A

oral folate replacement

207
Q

other than anaemia, what can vitamin B12/folate deficiency present with?

A

peripheral neuropathy

208
Q

what are B symptoms in lymphoma?

A 
weight loss
night sweats
fever
pruritis
fatigue
209
Q

what is the commonest physical presentation of lymphoma?

A

lymphadenopathy

210
Q

what is the first line investigation for lymphoma?

A

biopsy of lymph node/bone marrow

211
Q

which type of leukaemia is the commonest in children?

A

Acute lymphoblastic leukaemia

212
Q

what is the commonest type of lymphoma? how aggressive is it?

A

diffuse large B cell lymphoma - high grade

213
Q

what is the commonest low-grade lymphoma?

A

follicular lymphoma

214
Q

which blood cancer involves proliferation of undifferentiated lymphoid cells?

A

acute lymphoblastic leukaemia

215
Q

how can children with ALL present?

A

bone marrow failure
bone pain
limp

216
Q

which lymphoid progenitors are often involved in ALL?

A
  • B cell progenitors
217
Q

how is the type of lymphocyte progenitor identified in ALL?

A

through immunophenotyping - if it expresses CD19 it’s a B-lymphoblast

218
Q

what is the management of ALL?

A

chemotherapy
CNS therapy
stem cell transplant
immunotherapy - RiTe, CAR

219
Q

why is there need for CNS specific therapy in ALL, and how is it administered?

A
  • because chemotherapy drugs normally don’t penetrate BBB, and lymphoblasts often hide in the brain
  • intrathecal methotrexate injection
220
Q

what is the commonest type of leukaemia?

A

chronic lymphocytic leukaemia

221
Q

what is the gender distribution of CLL?

A

2:1 males to females

222
Q

exposure to what virus has been associated with CLL development?

A

EBV virus

223
Q

how does CLL often present?

A

often asymptomatic presentation

224
Q

what is immune paresis?

A

loss of immunoglobulin production

225
Q

what type of blood cancer is immune paresis associated with?

A

CLL

226
Q

what is the staging score used for CLL?

A

Binet staging

227
Q

what are the three stages of CLL according to the Binet score?

A

A - less than 3 lymph nodes involved
B - more than 3 lymph nodes involved
C - 3 or more lymph nodes + cytopaenia

228
Q

name a few indications to treat CLL

A 
bone marrow failure
lymphadenopathy
splenomegaly
systemic symptoms
rapid lymphocyte proliferation
229
Q

if there are no severe symptoms, what is the management of CLL?

A

watch and wait

frequent monitoring

230
Q

what is the management of CLL?

A

chemotherapy

monoclonal antibodies

231
Q

what are some possible signs/symptoms of lymphoma?

A

lymphadenopathy
B symptoms
hepatosplenomegaly

232
Q

what are the main diagnostic investigations for lymphoma?

A

lymph node biopsy
bone marrow biopsy
CT scan

233
Q

what lymphocytic lineage is normally presented by non-Hodgkin lymphoma?

A

B cell lineage

234
Q

why are low grade lymphomas incurable?

A

because they are very slow growing, so it is difficult to target actively proliferating cells

235
Q

what is the management of low grade lymphoma?

A

watch and wait

236
Q

what is the therapeutic management of non-Hodgkin lymphoma?

A

chemotherapy + monoclonal antibody (anti-CD20)

237
Q

what are the commonest age groups to get Hodgkin lymphoma?

A

20-30s

over 60

238
Q

which subgroup of Hodgkin lymphoma patients are more likely to have had EBV exposure?

A

those patients who get Hodgkin lymphoma later in life

239
Q

what is the presentation of lymphadenopathy in Hodgkin’s lymphoma?

A

symmetrical lymphadenopathy in upper respiratory tract and head, with little extranodal involvement

240
Q

what is the presentation of lymphadenopathy in non-Hodgkin lymphoma?

A

lymphadenopathy not symmetrical, can present anywhere, 60% with extranodal involvement

241
Q

what is he treatment of Hodgkin’s lymphoma?

A

chemotherapy
radiotherapy
monoclonal antibodies (anti-CD30)

242
Q

with regards to monoclonal antibody treatment, which cell marker is targeted in non-Hodgkin lymphoma and Hodgkin lymphoma respectively?

A

non-Hodgkin - CD20

Hodgkin - CD30

243
Q

what is the scoring system for lymphoma called, and what are the four stages?

A

Ann Arbor staging score:
1 - one lymph node
2 - two lymph nodes on same side of diaphragm
3 - disseminated lymph nodes on both sides of diaphragm
4 - extranodal disease
+ A (no systemic symptoms) or B (B symptoms)

244
Q

what pattern of bleeding is found in platelet disorders?

A

mucosal bleeding:

ecchymosis, epistaxis, purpura, petechiae, menorrhagia

245
Q

what pattern of bleeding is found in coagulation factor disorders?

A

muscle hematoma
haemarthrosis
CNS bleeding

246
Q

what is haemophilia type A?

A

loss of coagulation factor VIII

247
Q

what is haemophilia type B?

A

loss of coagulation factor IX

248
Q

what is the mode of inheritance of haemophilia A and B?

A

X-linked

249
Q

how can haemophilia affect the joints in the long run, if uncontrolled?

A

it can increase risk of osteoarthritis and haemophilic arthropathy

250
Q

what is the management of haemophilia?

A
  • recombinant factor 8/9 replacement
  • desmopressin
  • tranexamic acid
  • prophylaxis in severe cases
  • gene therapy
251
Q

which bleeding disorders is desmopressin useful in?

A

Type 1 von Willebrand disease

Haemophilia A

252
Q

what are the three subtypes of von Willebrand disease?

A

Type 1 - quantitative, not enough vWF
Type 2 - abnormal function of vWF
Type 3 - complete lack of vWF

253
Q

what is the genetic inheritance of von Willebrand disease?

A

autosomal dominant

254
Q

is von Willebrand disease inherited or acquired?

A

inherited

255
Q

how does desmopressin work in bleeding disorders?

A
  • it releases vWF from the endothelial cells

- it stabilises factor 8

256
Q

which coagulation factors are only involved in the extrinsic pathway?

A

tissue factor
factor VII
factor V

257
Q

which coagulation factors are only involved in the extrinsic pathway?

A

factor XII
factor XI
factor IX
factor VIII

258
Q

does von Willebrand disease cause platelet deficiency type bleeding or coagulation factor deficiency type bleeding?

A

platelet deficiency type bleeding - mucosal, ecchymosis, epistaxis, menorrhagia

259
Q

how common is von Willebrand disease?

A

common - 1 in 200

260
Q

which type of haemophilia is more common?

A

Haemophilia A

261
Q

what investigations are done to diagnose haemophilia, and what might they show?

A

platelet count - normal
prothrombin time (PT) - normal
partial thromboplastic time (APTT) - high
clotting factors - factor 8 or 9 low

262
Q

what do PT and APTT test respectively in haematology?

A

PT - tests extrinsic and common coagulation pathway

APTT - tests intrinsic and common coagulation pathway

263
Q

which clotting factors are vitamin K dependent?

A

factors 2, 7, 9 and 10

264
Q

name a few causes of acquired bleeding disorders

A
  • liver failure
  • renal failure
  • autoimmunity to clotting agents
  • vitamin K deficiency
  • diffuse intravascular coagulation
  • drugs (warfarin, DOACs, aspirin)
265
Q

what are the management options for von Willebrand disease?

A
  • vWF concentrate
  • desmopressin
  • tranexamic acid
  • menorrhagia management
266
Q

what is the mechanism of action of tranexamic acid?

A

tranexamic acid blocks the conversion from plasminogen to plasmin, therefore stopping fibrin degradation

267
Q

why does liver failure lead to bleeding disorders?

A

liver failure affects the liver’s production of clotting factors

268
Q

why does disseminated intravascular failure lead to bleeding disorders?

A

because extensive coagulation uses up all available clotting factors, eventually leading to uncontrolled bleeding

269
Q

what is autoimmune thrombocytopaenic purpura?

A

thrombocytopaenia (low platelet count) as a result of autoimmune reaction against own platelets

270
Q

how is immune thrombocytopaenia treated?

A

steroids
IV immunoglobulin
splenectomy if hypersplenism
thrombopoietin analogues

271
Q

define primary haemostasis and secondary haemostasis

A

primary haemostasis - initial platelet activity and start of fibrin plug formation
secondary haemostasis - coagulation cascade and stabilisation of solid fibrin plug

272
Q

which molecules drive the degradation of fibrin in haemostasis?

A

t-PA: it converts plasminogen into plasmin, and plasmin breaks down fibrin plug

273
Q

where is t-PA released from in haemostasis?

A

t-PA is released from endothelial cells

274
Q

what is t-PA?

A

tissue plasminogen activator - converts plasminogen into plasmin, which breaks down fibrin plug

275
Q

what diagnostic molecule is found in the circulation as a result of fibrin degradation?

A

d-dimer

276
Q

what other conditions is immune thrombocytopaenic purpura associated with?

A

infections (EBV, HIV)
lymphoma
drug related

277
Q

why is Vitamin K injected in babies right after birth?

A

to give their coagulation system a boost and prevent Haemorrhagic Disease of the Newborn

278
Q

when is a diagnosis of haemophilia first made?

A

in children between 6months and 2 years of age

279
Q

what defines haemophilia as mild, moderate or severe?

A

residual coagulation activity:
mild is 5-30%
moderate is 1-5%
severe is <1%

280
Q

what is the monoclonal antibody that can now be used for haemophilia A treatment, and what is its mechanism of action?

A

Emicizubab (Hemlibra)
it replaces factor VIII and binds factor X to factor IXa in order to activate factor X and trigger common coagulation cascade

281
Q

name a few complications of haemophilia treatment

A
  • viral infections (HIV, HBV, HCV)
  • inhibitors (anti-factor 8 antibodies)
  • MI (desmopressin promotes platelet adherence)
282
Q

why does liver failure show prolonged PT and aPTT time on coagulation tests?

A

because the liver produces all coagulation factors, so a lack in production causes deficiency in both extrinsic and intrinsic coagulation pathway

283
Q

which coagulation factors are only involved in the common pathway?

A 
factor X
factor II (prothrombin)
factor I (fibrinogen)
284
Q

vitamin K dependent coagulation factor deficiency is associated with which GI condition and why?

A

cholestasis/biliary tree disease, because it leads to an inability to absorb fat from diet which is essential for factor II, VII, IX and X production

285
Q

what’s the purpose of heparans, thrombomodulin and TFPI in a healthy blood vessel?

A

they inhibit the adhesion of platelets to the endothelial wall

286
Q

what is the physiological activator that triggers platelet adhesion in a damaged blood vessel?

A

tissue factor

287
Q

which platelet surface glycoprotein binds fibrinogen?

A

GP 2b/3a

288
Q

which platelet surface glycoprotein binds to collagen exposed by blood vessel damage?

A

GP Ia/2a

289
Q

what are the most important cell surface receptors on a platelet?

A

ADP receptor
epinephrine receptor
thrombin receptor

290
Q

what are the two granules inside a platelet called, and what does each release?

A

alpha granule - vWF, thrombin

dense granule - calcium, serotonin, ADP/ATP

291
Q

what is von Willebrand Factor released by?

A

platelets and endothelial cells

292
Q

which platelet surface glycoprotein binds to von Willebrand Factor?

A

GP 1b

293
Q

what are the three main actions of platelets?

A

adhere
activate
aggregate

294
Q

how do platelets adhere to damaged blood vessels?

A

they adhere to collagen through GP Ia and to von Willebrand Factor through GP 1b

295
Q

how do platelets activate?

A

they activate through ADP and epinephrine attaching to their receptors, causing arachidonic acid to be converted into thromboxane A2 through COX-1

296
Q

how do platelets aggregate?

A

they aggregate through the action of thromboxane A2, which allows them to shrink and stick together

297
Q

how do platelets facilitate coagulation?

A

platelets help the coagulation process by flipping their phospholipid membrane over

298
Q

what enzyme helps the phospholipid membrane of platelets flip inside out to help coagulation?

A

scramblase

299
Q

what are the three main natural anticoagulants?

A
  • tissue factor pathway inhibitor (TFPI)
  • activated protein S and protein C
  • antithrombin
300
Q

which coagulation factors are switched off by TFPI?

A

factor VIIa and factor Xa

301
Q

which coagulation factors are switched off by activated protein S and C?

A

factor Va and factor VIIIa

302
Q

which coagulation factors are switched off by antithrombin?

A

mainly factor Xa and thrombin, but also factor XIa, IXa and VIIIa

303
Q

what is the purpose of natural anticoagulants in haemostasis?

A

they ensure the fibrin clot is confined to the area of damage

304
Q

how does aspirin inhibit platelet action?

A

it inhibits platelet aggregation by blocking COX-1 pathway, preventing the conversion of arachidonic acid to thromboxane A2

305
Q

how do clopidogrel and ticagrelor inhibit platelet action?

A

they inhibit platelet activation by blocking the ADP/epinephrine receptors and stopping the P2Y12 pathway

306
Q

how do abciximab and tirofiban inhibit platelet action?

A

it they stop fibrinogen binding to GP 2b/3a

307
Q

how does warfarin stop coagulation?

A

it blocks factors 2, 7, 9 and 10

308
Q

how can the effects of warfarin be reversed?

A

by injecting vitamin K

309
Q

how does heparin stop coagulation? which natural anticoagulant does it mimic?

A

it blocks factor Xa and thrombin, mimicking antithrombin

310
Q

how do NOACs like apixaban and rivaroxaban stop coagulation?

A

they stop factor X from being activated, by sitting on the serine site where the inactive zymogen is normally cleaved to activate it

311
Q

what is the serine site on coagulation factors?

A

it’s the area on the protein that is cleaved in order to activate the factor

312
Q

how does dabigatran stop coagulation?

A

it acts as a direct thrombin inhibitor, by binding to its active site

313
Q

what are arterial thrombi mainly made of, and what colour are they?

A

white thrombi containing mostly platelets (and some fibrin)

314
Q

what are venous thrombi mainly made of, and what colour are they?

A

red thrombi containing mostly fibrin (and some red cells)

315
Q

which elements of Virchow’s triad are most likely to lead to venous thrombosis?

A

hypercoagulability ie cancer, pregnancy, OCP

stasis ie long haul flights, immobility

316
Q

which element of Virchow’s triad is most likely to lead to arterial thrombosis?

A

vessel damage - ie atherosclerosis

317
Q

what are the two commonly used pre-test probability scores for DVT?

A

Wells score

Geneva score

318
Q

when is a D-dimer test done for DVT?

A

when the pre-test probability score is low

319
Q

what is the main aim of a D-dimer test for DVT?

A

to rule out the diagnosis of DVT

320
Q

when testing compressibility of a vein, when is it more or less likely to be a DVT?

A

if vein compressible - probably not DVT

if vein non-compressible - probably DVT

321
Q

what imaging tests are carried out for DVT and PE?

A

DVT - doppler USS

PE - V/Q scan

322
Q

which types of long-term conditions can predispose to DVT?

A

cancer
myeloproliferative neoplasms
autoimmune conditions

323
Q

which class of drug is given to patients following a DVT/PE?

A

anticoagulants

324
Q

what is Factor V Leiden?

A

it’s a mutation in factor 5, which makes it resistant to being switched off by activated protein S and C

325
Q

what is the genetic inheritance of Factor V Leiden?

A

autosomal dominant

326
Q

what are microvascular thrombi seen in DIC made up of?

A

can be either platelets, fibrin or both

327
Q

name some risk factors for arterial thrombosis

A 
hypertension
smoking
obesity
diet
sedentary lifestyle
diabetes
high cholesterol
age
328
Q

name some risk factors for venous thrombosis

A 
immobility
pregnancy
long haul flights
older age
obesity
HRT/OCP
surgery
systemic disease (eg cancer, autoimmune disease)
family history
inherited conditions (factor V leiden, antithrombin deficiency)
329
Q

what is the iron level in the blood in polycythaemia vera?

A

almost always low

330
Q

what is the pathogenesis of myelofibrosis?

A

proliferation of abnormal megakaryocytes, leading to fibrosis in bone marrow

331
Q

what is a characteristic sign of myelofibrosis on a blood film?

A

tear-drop shaped red cells
nucleated red cells
large platelets
blast cells

332
Q

name a few signs that point to a diagnosis of myelofibrosis

A

very enlarged spleen
tear-drop shaped red cells on blood film
fibrosis in bone marrow biopsy

333
Q

how can chronic leukaemia and myeloma affect red blood cell count?

A

they can cause anaemia due to autoimmune haemolysis

334
Q

which monoclonal antibody is used to target CD20 B cells in lymphoma?

A

rituximab

335
Q

what chemotherapy drug is used for low grade lymphomas?

A

bendamustine

336
Q

what treatment regimen is used for high grade lymphoma?

A

R-CHOP

  • rituximab
  • cyclophosphamide
  • hydroxydoxorubicin
  • vincristine
  • prednisolone
337
Q

what is the difference between CD19 and CD20 B cells?

A

CD19 is found on all B cells, regardless of their maturity

CD20 is only found on mature B cells

338
Q

what cell marker is expressed on T cells in CLL?

A

CD5

339
Q

which portion of an antibody defines the class of antibody?

A

the heavy chain - Fc portion

340
Q

which immunoglobulin has the highest molecular weight and why?

A

IgM - because it’s a pentamer

341
Q

what are the two possible structures of a light chain in antibody production?

A

kappa

lambda

342
Q

what is the most prevalent class of immunoglobulin?

A

IgG

343
Q

what is the first line investigation for the diagnosis of myeloma? what does it identify?

A

serum protein electrophoresis - identifies presence of paraproteins in the blood

344
Q

name a few examples of lab tests that can be done to help diagnose myeloma

A
  • total immunoglobulin levels
  • serum protein electrophoresis
  • immunofixation
  • light chains levels (kappa vs lambda)
345
Q

proliferation of B lymphocytes leads to which type of blood cancer?

A

lymphoma

346
Q

proliferation of plasma cells leads to which type of blood cancer?

A

myeloma

347
Q

which immunoglobulin is released in lymphoma?

A

IgM

348
Q

which immunoglobulin is released in myeloma?

A

IgG, IgA

349
Q

do plasma cells release IgM?

A

no

350
Q

which immunoglobulins do B cells and plasma cells produce respectively?

A

B cells - IgM

plasma cells - IgG, IgA

351
Q

what is myeloma?

A

it’s a blood cancer resulting in abnormal proliferation of plasma cells and build up of paraprotein

352
Q

what are the classic symptoms of myeloma?

A

CRAB:

  • high calcium
  • renal failure
  • anaemia
  • bone lesions
353
Q

what is a rise in paraproteins in the blood called, if there are no symptoms indicating myeloma?

A

monoclonal gammopathy of uncertain significance (MGUS)

354
Q

name some complications of paraprotein build up in myeloma

A
  • renal disease
  • hyperviscosity
  • hypogammaglobulinaemia (low antibodies)
  • amyloidosis
  • increased risk of infections
355
Q

if there is an abnormal build up of IgM in the blood, what is not the diagnosis and why?

A

it’s not myeloma, as plasma cells do not produce IgM

356
Q

what are the management options for myeloma?

A
  • chemotherapy
  • immunotherapy
  • steroids
  • bisphosphonates
  • stem cell transplant
357
Q

on bone marrow biopsy, what percentage of total cell count needs to be plasma cells for myeloma to be confirmed?

A

more than 10%

358
Q

what type of amyloidosis is caused by multiple myeloma?

A

AL amyloidosis - primary amyloidosis caused by misfolding of immunoglobulin light chains

359
Q

what protein found in the urine can help diagnose multiple myeloma? what is this protein?

A

Bence-Jones protein

it’s a light chain (kappa or lambda) that has spilled out of the circulation and into the urine

Haematology & Immunology (2 decks)

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