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Haematology and Immunology > Haematology > Flashcards

Haematology Flashcards

1
Q

What are the components of blood?

A

Plasma, Buffy coat and red blood cells

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2
Q

What products are found in the Buffy coat?

A

Platelets

White cells

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3
Q

What products are found in the plasma?

A

Clotting, coagulation factors

Albumin
Antibodies

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4
Q

List functions of blood.

A

Transport - Oxygen and CO2, Nutrients, Waste, Messages

Maintenance of vascular integrity

Protection from pathogens

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5
Q

How does blood maintain vascular integrity?

A

Prevent leaks - platelets, clotting factors

Prevent blockage - anticoagulants, fibrinolytic

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6
Q

List leukocytes (white cells).

A 
Meutrophil
Monocyte
Basophil
Eosinophil
Lymphocyte
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7
Q

What cells produce erythrocytes?

A

Erythropblast -> reticulocyte

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8
Q

Stem cell flux is regulated by what?

A

Hormones, growth factors e.g erythropoietin, G-CSF

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9
Q

Where is erythropoietin produced?

A

Made in kidney in response to hypoxia

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10
Q

What can you use to measure red blood cell production?

A

Reticulocytes

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11
Q

What is polycythaemia?

A

Too many red cells - in myeloid malignancies

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12
Q

What are consequences of anaemia?

A

Poor gas transfer, SOB, fatigue

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13
Q

What causes anaemia?

A

Deficiency in hamatinics e.g iron, folate, vit B12

or congenital - thalassaemia

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14
Q

What causes an increased loss in red blood cells?

A

Bleeding, haemolysis

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15
Q

What is polychromasia seen on microscopy?

A

Cells in body that look grey - high reticulocyte count

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16
Q

What is the function of platelets?

A

Haemostasis (and immune)

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17
Q

What developing white cells produce platelets?

A

Megakaryocytes

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18
Q

What regulates production of platelets?

A

Thrombopoietin produced in liver

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19
Q

What do you see in relation to platelets and liver disease/

A

Low platelets

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20
Q

What is the lifespan of platelets?

A

7 days

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21
Q

What is thrombocytopenia?

A

Not enough platelets

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22
Q

What are signs of thrombocytopenia?

A

Marrow failure

Immune destruction

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23
Q

What is thrombocytosis?

A

Too many platelets

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24
Q

What is neutrophilia and what causes it?

A

Too many neutrophils

Infection and inflammation

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25
Q

What regulates production of neutrophils?

A

Granulocyte-colony stimulating factor (G-CSF)

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26
Q

When is G-CSF used therapeutically?

A

Neutropenia

Mobilisation of stem cells

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27
Q

What is neutropenia?

A

Decreased production of neutrophils

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28
Q

What can cause neutropenia?

A

Temporary phenomena in sepsis
Drugs
Marrow failure

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29
Q

What cells make up the reticuloendothelial system?

A

Monocytes

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30
Q

What do monocytes differentiate into?

A

Macrophages

Dendritic cells

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31
Q

What is the function of eosinophils?

A

Parasitic infections

Allergies

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32
Q

List two causes of lymphocytosis.

A

Infectious mononucleosis

Pertussis

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33
Q

What cells are important in the adaptive immune system?

A

Lymphocytes

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34
Q

List causes of lymphopenia.

A

Post-viral

Lymphoma

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35
Q

What are the three subtypes of lymphocytes?

A

B, T, NK cells

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36
Q

Where are lymphocytes produced?

A

B cells - Bone marrow

T cells - thymus

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37
Q

In B cell maturation, when in the pathway can ALL occur?

A

Errors at progenitor V cell splicing in bone marrow

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38
Q

Where do most lymphomas arise from?

A

Within lymph node during somatic hypermutation

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39
Q

What do class 1 HLA molecules display?

A

Internal antigens on all nucleated cells

Self antigen

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40
Q

What do class 2 HLA molecules display?

A

Display antigens eaten by professional APCs

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41
Q

What is the purpose of HLA molecules?

A

Immune cells read HLA- barcode on cells to identify self vs non-self or uninfected vs infected cells

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42
Q

List systemic diseases that affect the blood.

A

RA - Anaemia, Folate deficiency, immune haemolysis, neutrophilia, immune thrombocytopenia

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43
Q

What is felty syndrome?

A

Large spleen and thrombocytopenia linked to that. Early lymphoma.

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44
Q

What is a paraprotein?

A

Malignancy or early malignancy of plasma cell –> one type of cell (too much plasma)

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45
Q

What causes too little plasma proteins?

A

Haemophilia (little clotting factors or abnormal)

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46
Q

What is the normal range of Haemoglobin?

A

Male - 135-170

Female - 120-160

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47
Q

What is the normal range of platelets?

A

150-400

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48
Q

What is the normal range of WBC?

A

4-10

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49
Q

What is the normal range of neutrophils?

A

1.5-7

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50
Q

List diagnostic tools for haematological disorders.

A 
FBC
Clotting times for factors and platelets
Chemical assays - B12, iron, folate
Marrow aspirate and trephine biopsy, lymph node biopsy 
Imaging
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51
Q

List common haematological treatments.

A

Replacement
Transplantation
Drugs

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52
Q

If you are blood group A, what do you have antibodies against?

A

B

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53
Q

If you are blood group B, what do you have antibodies against?

A

A

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54
Q

If you are blood group O, what do you have antibodies against?

A

A and B

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55
Q

If you are blood group AB, what do you have antibodies against?

A

NO antibodies

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56
Q

What blood type is the universal donor?

A

O

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57
Q

What blood type is the universal recipient?

A

AB

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58
Q

If you are blood group A, there is anti-B in the plasma. Who can you donate FFP to?

A

A and O

instead of A and AB in red cells

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59
Q

What happens if RhD- individuals can make anti-D if exposed top RhD+?

A

Transfusion reactions, haemolytic disease in newborns

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60
Q

What are blood donations tested for?

A

HepB/C/E, HIV, Syphilis

Variably for HTLV1, malaria, West Nile virus, Zika virus

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61
Q

List indications for red cell transfusions

A

Correct sever acute anaemia
Improve QoL if uncorrectable anaemia
Prepare patient for recover
Reverse damage caused by own red cells e.g sickle cell

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62
Q

How long do you transfuse blood over?

A

2-4 units

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63
Q

How long do you transfuse platelets over?

A

20-30 minutes

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64
Q

What are indications for platelet transfusion?

A

Massive haemorrhage
Bone marrow failure
Prophylaxis for surgery
Cardiopulmonary bypass

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65
Q

Compare storage temperature and time of red cells and plasma?

A

Red cells - 4 degrees

Platelets - 22 degrees, 7 days help life

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66
Q

In patients receiving chemo, what are platelets used for?

A

Preventing intracranial haemorrhage

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67
Q

Where does 1 unit of FFP come from?

A

1 unit of blood

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68
Q

How is FFP stored?

A

Frozen, need 30 mins to thaw

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69
Q

What are indications for FFP?

A

Massive haemorrhage
DIC with bleeding
Prophylactic

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70
Q

What lab tests are carried out for FFP?

A

PT and APTT

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71
Q

What lab tests are carried out for cryoprecipitate?

A

Fibrinogen

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72
Q

When dealing with the blood bank, what is required to get blood?

A

Blood sample- EDTA

Two sample policy

Group and screen/save

Cross match

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73
Q

What is group and screening?

A

ABO and RhD type
Checked against historical records
Screen for all all-antibodies in serum

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74
Q

What is Coombs test?

A

Used when looking for other IgG antibodies in lab
–> indicates a condition known as hemolytic anemia, in which your blood does not contain enough red blood cells because they are destroyed prematurely.

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75
Q

If you are pregnant and RhD- and developed anti-D (nearly always IgG which crosses placenta). What can happen to baby?

A

If baby RhD+ (inherited from father) –> haemolytic disease - die in utero or at birth

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76
Q

How is haemolytic disease prevented in newborn with mother who is RhD-?

A

Prophylactic anti-D (routine at 28/40)

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77
Q

What should you monitor if giving anti-D?

A

Monitor antibody titres
Doppler USS
Intrauterine transfusions

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78
Q

What causes neonatal alloimmune thrombocytopenia?

A

Similar process to anti-D but for platelets

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79
Q

List cellular therapies that use blood donations?

A

Leucapheresis - bone marrow harvests, donor lymphocyte infusions
Gene therapies

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80
Q

What is anaemia?

A

Reduction in red cells or haemoglobin content

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81
Q

List aetiologies of anaemia.

A

Blood loss
Increased destruction
Lack of production
Defective production

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82
Q

What are reticulocytes?

A

Immature RBCs

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83
Q

What substances are required for red cell production?

A

Metals e.g iron
Vitamins e.g B12, folic acid
Hormones e.g erythropoietin , GM-CSF

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84
Q

How long does a RBC live?

A

120 days

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85
Q

How are RBCs broken down?

A

In reticuloendothelial system

Globin –> AAs reused

Haem –> iron recycled to Hb, uncongucated bilirubin

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86
Q

What 3 components make up RBCs?

A

Membrane
Enzymes
Haemoglobin

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87
Q

What causes congenital anaemias?

A

Genetic defects in RBC - membrane, enzymes, Hb

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88
Q

What happens if there are defects in the cell membrane of RBC?

A

Increased cell destruction

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89
Q

What is hereditary spherocytosis?

A

Red cell membrane disorder - one of most common, autosomal dominant

RBCs are spherical - removed from circulation faster by reticuloendothelial system

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90
Q

How do patients with hereditary spherocytosis present?

A

Anaemia
Jaundice (neonatal)
Splenomegaly
Pigment gallstones

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91
Q

How do you treat hereditary spherocytosis?

A

Folic acid
Transfusion
Splenectomy if anaemia very severe

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92
Q

what are the two main enzyme pathways in RBCs?

A

Glycolysis

Pentose phosphate shunt

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93
Q

Give an example of an enzyme abnormality of RBCs.

A

G6-PD

Cells vulnerable to oxidative damage (since normal function is to protect)

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94
Q

What does G6PD deficiency confer protection against?

A

Malaria

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95
Q

How does G6PD deficiency present?

A

Variable: anaemia, neonatal jaundice, splenomegaly, pigment gallstones

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96
Q

What can precipitate G6PD deficiency?

A

Drugs
Broad beans
Infection
Acute illness

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97
Q

List two enzyme deficiencies of RBCs.

A

G6DP deficiency

Pyruvate kinase deficiency

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98
Q

What happens to the oxygen dissociation curve if acidosis?

A

Shifts to right

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99
Q

What happens to the oxygen dissociation curve if increased temperature?

A

Shifts to right

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100
Q

What happens to the oxygen dissociation curve if increased DBG?

A

Shifts to right

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101
Q

What is normal adult haemoglobin made of/

A

Alpha genes, beta chains, little delta and gamma chains

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102
Q

In terms of chains, what is normal adult haemoglobin made from?

A

Hb A = aabb

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103
Q

What are the two main types of thalassaemias (reduced or absent globing chains?

A

Alpha and beta

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104
Q

Give an example of a mutation that leads to structurally abnormal globing chain/

A

HbS (sickle cell) - beta chain abnormality combined to normal alpha chain

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105
Q

What are consequences of HbS?

A

haemolysis –> vaso-occlusion

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106
Q

How do patients with sickle cell disease present?

A

Painful vaso-occlusive crises - bone
Stroke
Chest crisis
Increased infection risk
Chronic haemolytic anaemia - gallstones, aplastic crises
Sequestrain crises - spleen (Hyposplenia), liver

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107
Q

What is a sickle cell crisis?

A

Severe pain

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108
Q

How do you manage acute sickle cell crisis?

A 
Opiates within 30 mins of presentation for one hour 
Hydration 
Oxygen 
Consider antibiotics
Blood transfusion (HbF doesn't sickle)
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109
Q

What bones present with a painful crisis in children vs adults

A

Adults - long bone, back and hip

Children - small bones

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110
Q

What life long prophylaxis is given for sickle cell disease?

A 
Vaccination 
Penicillin (and malarial) prophylaxis
Folic acid
Disease modifying drugs - hydroxycarbamide
Bone marrow transplant 
Gene therapy
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111
Q

What causes thalassaemia?

A

Reduced or absent globing chain production - in alpha or beta genes

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112
Q

If you don’t inherit any alpha chains from parents, can you make HbF?

A

No, incompatible with life

Also dangerous for mother

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113
Q

If you don’t inherit any beta chains from parents, can you make HbF?

A

Yes with alpha and gamma chains

Compatible with life but severe anaemia - need regular transfusions

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114
Q

Name a transfusion dependent thalassaemia.

A

Beta thalassaemia major

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115
Q

What are signs of beta thalassaemia major?

A 
Failure to thrive 
Bony deformaties 
Splenomegaly 
Growth retardation
Ineffective bone marrow expands
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116
Q

How do you treat beta thalassaemia major?

A

Chronic transfusion support - 4-6 weeks

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117
Q

Why do you need iron chelation for beta thalassaemia major?

A

Prevents iron overloading and reduced life expectancy

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118
Q

Name a curative therapy for thalassaemia.

A

Bone marrow transplant

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119
Q

What factors can affect normal range of haemoglobin?

A 
Age
Sex 
Ethnic origin 
Time of day sample taken 
Time to analyse
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120
Q

What are the reference ranges for haemoglobin?

A

Male 12-70 (140-180) and >70 (116-156)

Female aged 12-70 (120-160), >70 years (108-143)

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121
Q

List clinical features of anaemia.

A 
Tiredness/pallor
Breathlessness
Swelling of ankles 
Dizziness 
Chest pain
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122
Q

What is MCH and MCV?

A

Mean cell haemoglobin

Mean cell volume

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123
Q

How can RBC be described morphologically?

A

Hypochromic, microcytic

Normochromic normocytic

Macrocytic

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124
Q

If macrocytic RBCs seen morphologically, what is this a sign of?

A

B12/folate deficient

or bone marrow problem

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125
Q

If hypochromic microcytic RBCs seen morphologically, what should you test for?

A

Serum ferritin

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126
Q

If normochromic normocytic RBCs seen morphologically, what should you test for?

A

Reticulocyte count - if low - may be aplastic anaemia, malignancy (i.e issue with bone marrow)

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127
Q

If you have hypo chromic microcytic anaemia and serum ferritin is normal or increased, what would this suggest?

A

Thalassaemia
Secondary anaemia
Sideroblastic anaemia

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128
Q

If you have hypo chromic microcytic anaemia and serum ferritin is low, what would this suggest?

A

Iron deficiency

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129
Q

What is the connection of ferritin and CRP?

A

Ferritin = acute phase reactant (goes up with CRP)

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130
Q

What is your total body iron?

A

approx 4g

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131
Q

Where is hepcidin synthesised?

A

Liver

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132
Q

What is the role of ferroportin?

A

Transports iron from enterocytes in gut and macrophages to iron stores by being bound to transferrin

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133
Q

What is the role of hepcidin?

A

When there is increased iron, blocks ferroportin so decreases intestinal iron absorption and mobilisation from reticuloendothelial cells

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134
Q

What is the commonest cause of anaemia?

A

Iron deficiency

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135
Q

What can cause iron deficiency anaemia?

A 
Dyspepsia
Menorrhagia
Diet 
Increased requirement e.g pregnancy
Malabsorption - gastrectomy, coeliac
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136
Q

List clinical signs of iron deficiency anaemia seen on examination.

A

Koilonychia
Angular cheilitis
Atrophic tongue

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137
Q

How do you manage iron deficiency anaemia?

A

Correct deficiency - oral iron, IV iron if intolerant, blood transfusion rare

Correct cause - diet, ulcer therapy, gynaecology interventions, surgery

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138
Q

If normochromic normocytic anaemia with normal/low reticulocyte count what could be the cause?

A

Secondary anaemia

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139
Q

If normochromic normocytic anaemia with high reticulocyte count what could be the cause?

A

Acute blood loss

Haemolysis

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140
Q

What can cause haemolytic anaemia?

A

accelerated red cell destruction (reduce Hb)

Compensation by bone marrow (increased metic count)

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141
Q

What are the two different types of acquired haemolytic anaemia.

A

Immune - mostly extravascular

Non-immune - mostly intravascular

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142
Q

What is the purpose of a direct anti globulin test?

A

Detects antibody or complement on red cell membrane

immune haemolysis - autoimmune issue?

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143
Q

If DAGT positive in haemolytic anaemia, what does this suggest?

A

Immune mediated

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144
Q

How can you work out if patient is haemolysing?

A 
FBC
Reticulocyte count  
Blood film 
Serum bilirubin 
LDH
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145
Q

Should your reticulocyte count be high or low if haemolysing?

A

High

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146
Q

What tests are used in haemolytic anaemia?

A

Hx and Ex
Blood film
Direct antiglobulin test (Coomb’s test)

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147
Q

How do you manage haemolytic anaemia?

A

Support marrow - folic acid

Correct cause - immunosuppression if autoimmune, splenectomy, treat sepsis

Consider transfusion

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148
Q

What is the commonest cause of microcytic anaemia?

A

B12 deficiency and folate deficiency

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149
Q

What is megaloblastic anaemia?

A

B12 and folate deficiency

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150
Q

What can cause B12 deficiency?

A

Pernicious anaemia

Gastric/ileal disease

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151
Q

What can cause folate deficiency?

A

Dietary, increased requirements, GI pathology

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152
Q

What clinical signs would suggest megaloblastic anaemia?

A

“Lemon yellow” tinge

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153
Q

What is pernicious anaemia?

A

Autoimmune disease

Develop antibodies against intrinsic factor

Malabsorption of dietary B12

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154
Q

How do you manage megaloblastic anaemia?

A

Replace vitamin
B12: intramuscular injection - loading dose then 3 monthly maintenance
Oral folate replacement

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155
Q

What additional factors outwith anaemia, can cause macrocytosis (i.e differentials)?

A 
Drugs 
Alcohol 
Disordered LFTs
Hypothyroidism 
Myelodysplasia
156
Q

What is involved in clot formation?

A

Platelets, vWF, coagulation factors

157
Q

How is the clot confined to the site of injury?

A

Natural anticoagulants

158
Q

What causes the clot to vanish after a week?

A

Fibrinolytic system

159
Q

What is the function of nitric oxide and Prostsyacyclyn for endothelial cells in vessels?

A

Non-stick surface

160
Q

What activates resting platelets and coagulation factors to form a clot?

A

Abnormal surface

Physiological activator

161
Q

What is the role of platelets?

A

Adhere
Activate
Aggregation
Provide phospholipid surface for coagulation

162
Q

What are the 3 components of primary haemostats?

A

Vasoconstriction
Platelet adhesion
Platelet aggregation

163
Q

What is a thrombus?

A

Clot in wrong place

164
Q

What is a thromboembolism?

A

Movement of clot along vessel

165
Q

What are the three components of Virchow’s triad?

A

Stasis
Vessel damage
Hypercoagulation

166
Q

What is the common components of arterial thrombus?

A

White clot - platelets and fibrin

167
Q

What does arterial thrombi result in?

A

Ischameia and infarction

168
Q

List examples of arterial thromboemolism

A

Coronary thrombosis - MI, unstable angina

Cerebrovascular - stroke, TIA,

Peripheral - limb ischaemia

169
Q

List risk factors for arterial thrombosis.

A 
Age 
Smoking 
Sedentary lifestyle 
HTN 
DM 
Obesity 
Hypercholesterolaemia
170
Q

How do you manage arterial thrombosis?

A

Primary - lifestyle change, treat risk factors

Acute presentation - thrombolysis, anti platelet/anticoagulant

Secondary prevention

171
Q

How are venous thrombi composed?

A

Fibrin and red cells

172
Q

What does venous thrombi cause?

A

Back pressure –> valvular insufficiency –> post-thrombotic syndrome

173
Q

What commonly causes venous thrombus?

A

Stasis and hyper coagulability

174
Q

Give examples of venous thromboembolism.

175
Q

What are risk factors for venous thrombosis associated with stasis/hypercoagulability?

A 
Age 
Pregnancy 
Surgery 
Obesity 
HRY Trauma
Immobility 
FH 
Systemic disease
176
Q

What systemic diseases

A

Cancer
Myeloproliferative neoplasm (MPNs)
Autoimmune disease e.g IBD, SLE, antiphospholipid syndrome

177
Q

How do you diagnose venous thrombosis?

A

Pretest probability - Wells, Geneva scores

Lab test - D-dimer

Imaging - Doppler, V/Q scan, CTPA

178
Q

What are the aims of management for venous thrombosis?

A

Prevent clot extension, embolisation and recurrence

179
Q

How do you manage venous thrombosis with medication?

A

Anticoagulants (LMWH, Warfarin, DOACs)

Thrombolysis only in selected cases e.g massive PE

180
Q

What is heritable thrombophilia?

A

An inherited predisposition to venous thrombosis

181
Q

What is the main scoring system for DVT?

A

Wells score

182
Q

What should you do for a patient who has high pre-test probability for PE/DVT?

A

Straight to imaging

183
Q

If there is compressibility of veins in ultrasound, what does this suggest?

A

No clot/occlusion

184
Q

What is the treatment duration for clots?

A

Minimal of 3 months then after this, consider if it is long term.

185
Q

List instances which DIC can occur in?

A

Sepsis
Malignancy
Eclampsia

186
Q

What can DIC cause?

A

Gangrene

Organ failure

187
Q

What confines clots? List 3 examples.

A

Natural anticoagulants

  1. Tissue factor pathway Inhibitor
  2. Activate protein C/S system
  3. Antithrombin
188
Q

What is the function of tissue factor and tissue factor pathway inhibitor?

A

Tissue factor = physiological activator, first coagulation factor released

Tissue factor pathway inhibitor = flips and inactivates factors 7 and 10

189
Q

What is the function of antithrombin?

A

Inactivates factors 8, 9, 10, 11 and thrombin

190
Q

What is the function of activated protein C/S system?

A

Inactivates factor 5 and 8

191
Q

How is fibrinolysis activated?

A

Endothelial cells release t-PA or u-PA which converts plasminogen to plasmin which breaks down the clot

192
Q

Give an example of a fibrin degradation products.

193
Q

What does Warfarin inhibit?

A

Factors 4, 5, 7, 10 and prothrombin

194
Q

What does Heparins inhibit?

A

10a and thrombin

195
Q

What do DOACs inhibit?

196
Q

How does Dapigatran and Bivalirudin work?

197
Q

List causes of hypercoaguable states.

A 
Pregnancy
Cancer 
Post-op
HRT 
Combined pills
198
Q

What does PT measure?

A

Prothombin time - measures integrity of extrinsic and common pathways
How long it takes for blood to begin to form clots

199
Q

What does PT help to diagnose?

A

Bleeding disorders and severity of liver disease

200
Q

What factors are present in the primary haemostatic response?

A

Platelet plug
vWF
Wall

201
Q

What factors are present in the secondary haemostatic response?

A

Fibrin plug formation

202
Q

What is haemorrhage diathesis?

A

Any qualitative or qualitative abnormality

203
Q

What can cause haemostatic defects?

A

Problems with platelets, vWF, coagulation factors

204
Q

What points should you consider in a bleeding history?

A 
Has patient got bleeding disorder?
How sever is disorder?
Pattern?
Congenital or acquired? 
Mode of inheritance
205
Q

What clinical signs might indicate history of bleeding?

A 
Bruising 
Epistaxis
Post-surgical bleeding 
Menorrhagia
Post-trauma 
PPH
206
Q

What surgeries are commonly associated with bleeding post-surgery.

A

Dental surgery
Circumcision
Tonsillectomy
Appendicectomy

207
Q

What is the best question to ask when taking a history of bleeding?

A

Post-surgical bleeding

208
Q

Severe unprovoked internal bleeding is a sign of what?

A

Severe haemophilia

209
Q

Where is bleeding seen if abnormalities in platelets/vWF?

A 
Mucosal bleeding 
Epistaxis
Purpura
GI 
Menorhhage
210
Q

If coagulation, factor deficiencies, what is the pattern of bleeding?

A

Articular
Muscle haematoma
CNS

211
Q

Give an example of a condition which commonly presents with mucosal bleeding.

A

Severe thrombocytopenia

212
Q

What pattern of inheritance is haemophilia A and B?

213
Q

In haemophilia A and B, what does severity of bleeding depend on?

A

Residual coagulation factor activity

214
Q

What results from factor 8 deficiency?

A

Haemophilia A

215
Q

What results from factor 9 deficiency?

A

Haemophilia B

216
Q

What is the presentation of haemophilia?

A 
Haemarthrosis
Muscle haematoma
CNS bleeding 
Retroperitoneal bleeding 
Post-surgical bleeding
217
Q

What are common signs of haemarthrosis in haemophilia patients?

A

Key/worst joint = ankle
Weight bearing joints

Hinge joints have worst prognosis

218
Q

Why does synovitis arise from joint bleeding?

A

macrophages eat blood –> inflammatory cytokines produced –> drives synovial hypertrophy –> lose joint cartilage –> endstage haemophilic arthropathy/OA

219
Q

What are clinical complications of haemophilia?

A

Synovitis
Chronic haemophilic arthropathy
Neurovascular compression
Stroke

220
Q

How do you diagnose haemophilia?

A

Clinical
Prolonged APTT
Normal PT
Reduced Factor VIII or Factor IX genetic Analysis - in utero if male or from cord blood at birth

221
Q

How do you treat haemophilia, bleeding diathesis?

A

Coagulation factor replacement (factor 8 or 9)

DDAVP - for mild haemophilia A and VW disease

Tranexamic acid

Gene therapy

222
Q

Apart from medication, how is haemophilia managed?

A 
Splints 
Physiotherapy 
Analgesia 
Synovectomy 
Joint replacement
223
Q

What are complications of DDAVP use?

A

MI

Hyponatraemia

224
Q

What viral infections are common complications haemophilia?

A

HIC
HBV
HCV
vCJD

225
Q

What type of bleeding is seen in von Willebrand disease?

A

Platelet type - mucosal

226
Q

List the types of von Willebrand disease.

A
  1. quantitative deficiency
  2. qualitative, lots of antigens but under function
  3. Complete deficiency
227
Q

How do you manage vW disease?

A

vWF concentrate or DDAVP
Tranexamic acid
Topicals
OCPs

228
Q

List acquired bleeding disorders.

A 
Thrombocytopenia 
Liver failure 
Renal failure 
DIC 
Drugs e.g Warfarin
229
Q

What causes thrombocytopenia?

A

Under production or over consumptionof platelets

230
Q

What can cause decreased production thrombocytopenia?

A

Marrow failure
Aplasia
Infiltration

231
Q

What are clinical signs of thrombocytopenia?

A

Petechia
Ecchymosis
Mucosal bleeding
Rare CNS bleeding

232
Q

Where should you look at petechiae?

233
Q

What causes over consumption thrombocytopenia?

A

Immune ITP
Non immune DIC
Hypersplenism

234
Q

What factors are produced in liver failure?

A

1, 2, 5, 7, 8, 9, 10, 11

235
Q

What does prolonged PT and APTT signs of?

A

Liver failure

236
Q

How do you prevent haemorrhage disease of the baby?

A

Injection of Vitamin K

237
Q

What is pancytopenia?

A

Low WCC, Hb and platelets

238
Q

What do spherocytes suggest?

A

Haemolysis

239
Q

What does aPTT measure?

A

Intrinsic and common coagulation pathways

Evaluates risk of bleeding before surgery

For unexplained bleeding and clotting

240
Q

What is required to convert fibrinogen to fibrin?

241
Q

List roles of platelets.

A

Produce factors that will form a clot and provide phospholipid surface for end-stage coagulation

Adhere
Activate
Aggregate

242
Q

List the 3 receptors found on platelets.

A

ADP
Thrombin
adrenaline

243
Q

List Glycoproteins on platelets.

A

GPIIb/IIIc
GP Ib/V.IX
GP Ia/IIb
GP VI

244
Q

What is the function of the open canalicular system?

A

Secrete granules (alpha and dense) from inside platelet surface which contain thrombin

245
Q

What is the function of platelet receptors?

A

Released at areas of damage allowing platelets to activate and become sticky

246
Q

What activates platelets and coagulation factors/

A

Abnormal epithelium surface and physiological activator

247
Q

What is the first physiological activator released with tissue damage?

A

Tissue factor

248
Q

What enzyme flips the platelet membrane so the phospholipid layer is on the outside?

A

Scramblase

249
Q

Where does DOACs act?

A

GPIIb/IIIa pathway

250
Q

Where does Aspirin act?

A

blocks COX pathway –> preventing conversion of arachidonic acid to thromboxane A2 therefore preventing platelet aggregation

251
Q

Which drugs block the ADP pathway?

A

Clopidogrel
Ticagrelor
Prasegrel

252
Q

What is the function of von Willebrand factor?

A

Allows platelets to adhere to damaged endothelium sites

253
Q

What does von Willebrand Factor bind to?

254
Q

What is the most common type of lymphoma.

A

Non-Hodgkin’s

255
Q

What is the pathogenesis of haematological malignancy?

A

Multi-step process
Acquired genetic alterations in a long lived cell
Proliferative/survival advantage to the mutated cell –> malignant clone –> grows to dominant

256
Q

In what lineages to myeloid malignancies occur?

A

Down myeloid line from myeloid progenitor line

257
Q

In what lineages to lymphoid malignancies occur?

A

Lymphoid line (lymphocytes)

258
Q

What is the difference between leukaemia and lymphoma?

259
Q

what is the difference between acute and chronic leukaemia?

A

Acute - cells don’t differentiate, bone marrow failure, rapidly fatal if untreated

Chronic - cells retain ability to differentiate, proliferative bone marrow failure, survival for a few years

260
Q

Is chronic leukaemia curable?

A

Potentially - Tyrosine kinase inhibitors

261
Q

Why are germinal centres important in lymph nodes?

A

Location of immature B cells are programmed to respond to antigen and if they emerge –> they form memory cells

262
Q

If lymph node localised and painful. What do you think?

A

Bacterial infection in draining site

263
Q

If lymph node localised and painless. What do you think?

A

Rare infections e.g TB
Metastatic carcinoma from drainage site (HARD)
Lymphoma (rubbery)
Reactive, no cause identified

264
Q

If lymph node generalised and painful/tender. What do you think?

A

Viral infections e.g EBV, CMV, hepatitis, HIV

265
Q

If lymph node generalised and painless. What do you think?

A 
Lymphoma
Leukaemia
CT diseases e.g sarcoidosis
Reactive, no cause identified
Drugs
266
Q

What lymphoma most commonly presents with nodal disease?

A

Hodgkin’s lymphoma

267
Q

What lymphoma most commonly presents with nodal disease?

A

Extranodal disease

268
Q

List systemic symptoms of lymphoma.

A 
Fever
Drenching sweats
Loss of weight 
Pruritis
Fatigue
269
Q

When do you prescribe cryoprecipitate?

A

Low fibrinogen

270
Q

When do you prescribe FFP?

A

Low coagulation factors

271
Q

When do you prescribe red cells?

272
Q

When do you prescribe platelets?

A

Thrombocytopenia

273
Q

72 yo lady, haematemesis, Hb 106g/L. Transfusion?

A

Not until you know BP and HR (Assess harm-dynamics)

274
Q

76yo, Hb 54 and blood film consistent with megaloblastic anaemia. Transfusion?

A

No –> give B12 and folate

275
Q

48yo lady admitted for a planned hysterectomy, Hb 95g/L. Transfusion?

A

No likely cause iron deficiency from dysmenorrhoea or malignancy

276
Q

What is the new recommended baseline levels for transfusion?

A

Transfuse so haemoglobin kepyt about 70, except if pre-existing cardiac impairment (use 90 or 100 as baseline)

277
Q

List indications for platelet transfusion.

A 
Prophylactically or therapeutically to stop bleeding 
Dilutional thrombocytopenia
Cardiopulmonary bypass surgery 
DIC if bleeding
Abnormalities of platelet function
278
Q

List indications for FFP.

A

Replace coat factors
DIC
Major haemorrhage
Thrombotic Thrombocytopenia purpura

279
Q

Do you transfuse a bleeding patient with factor VIII deficiency?

A

No - use factor concentrate

280
Q

Do you transfuse a bleeding patient with factor V deficiency?

A

Yes - there isn’t a factor 5 concentrate

281
Q

Do you give bleeding patient on DOAC FFP transfusion?

A

No - use a direct inhibitor

282
Q

Do you give a patient FFP who has a massive haemorrhage but no coagulation results?

283
Q

Do you give FFP to a bleeding patients with DIC?

284
Q

Do you give FFP to a patients with DIC?

285
Q

What are indications for cryoprecipitate prescription?

A

Hypofibrinogenaemia

DIC with bleeding and low fibrinogen

Renal or liver failure and abnormal bleeding

286
Q

Which samples do you send to the lab for blood?

A

Group and screen/save
Cross match
‘Group specific’ blood
Two sample policy

287
Q

If patient is at risk of circulatory overload, what should you do when prescribing red cells?

A

Give 20mg oral furosemide

288
Q

How do you prevent graft vs host disease when transfusing red cells to immunosuppressed patients?

A

Irradiate blood components (done for all platelets)

289
Q

What are risks of transfusion?

A 
Transfusion of ABO incompatibility 
TACO 
TRALI
Hypotension 
nvCJD
Hypotension 
Allergy
290
Q

How do you treat urticaria from transfusion reaction?

A

Antihistamine

291
Q

How do you treat SOB from TACO, TRALI and anaphylaxis from transfusion reaction?

A

Oxygen
Diuretic
Ventilation
Adrenaline

292
Q

How do you treat shock from transfusion reaction?

A 
Adrenaline IV
IV fluid 
ITU admission 
Abx
FFP/Platelets if DIC
293
Q

What are clinical features (triad) of AML?

A

Anaemia
Thrombocytopenic bleeding (purport and mucosal membrane bleeding)
Infection because of neutropenia

294
Q

What are symptoms of AML associated with?

A

Bone marrow failure

295
Q

What are essential investigations for AML?

A

FBC
Blood film
Bone marrow aspirate/trephine (>20% blasts in marrow)
Cytogenetics from leukaemia blasts
Immunophenotyping of leukaemia blasts
CSF examination if symptoms (paediatrics)
Targeted molecular genetics for associated acquired gene mutations
Extended NGS myeloid gene panels

296
Q

How do you treat AML?

A

Supportive care
Anti-leukaemia chemotherapy - Danorubicin and cytosine arabinoside, high dose arabinoside, gemtuzumab, CPX-351
Allogenic stem cell transplant
all-trans retinoid acid and arsenic trioxide in low risk acute prolyelocytic leukaemia

297
Q

What are new developments for AML treatment/

A

Targeted Abs
Targeted small molecules
New chemotherapy delivery systems - CPX-351

298
Q

What indicates remission achieved?

A

Blast count <5%

Blood cell count normal

299
Q

What are signs of CML?

A 
Anaemia
Splenomegaly 
Weight loss 
Hyperleukostasis --> fundal haemorrhage and venous congestion, altered consciousness, respiratory failure 
Gout
300
Q

What lab features will suggest CML?

A

Bone marrow and blood cells contain Philadelphia chromosome - t(9;22)
Bone marrow hyper cellular
Blood film shows all stages of WCC differentiation
Increased basophils
Anaemia
High platelet count
High WCC

301
Q

How do you treat CML?

A

Tyrosine kinase inhibitors: Imatinib, Dasatinib, Nilotinib
Busitinib
Ponatinib

Direct inhibitors of BCR-ABL protein

302
Q

How can lymphoma present?

A

Enlarged lymph nodes
Extranodal involvement
Bone marrow involvement

303
Q

What are systemic (B) symptoms of lymphoma?

A

Weight loss (>10% in 6 months), fever, night sweats, pruritis, fatigue

304
Q

How is the diagnosis for lymphoma made?

305
Q

How is lymphoma staged?

A

Clinical examination and imaging

306
Q

Where do you classically find acute leukaemia?

A

Bone marrow, blood

307
Q

Where do you classically find lymphomas and CLL?

A

Lymph nodes

308
Q

Where do you classically find malignant melanoma?

A

Plasma cells in bone marrow

309
Q

What type of lymphoma is a broad term which has high-grade and low-grade and around 70 subtypes?

A

Non-hodgkin lymphoma

310
Q

Name a type of lymphoma that is a medical emergency and can double in size in 24 hours?

311
Q

List lymphoproliferative disorders.

A

ALL
CLL
Hodgkin lymphoma
Non-hodgkin lymphoma

312
Q

What type of lymphoma is diffuse large B-cell lymphoma?

A

High-grade NHL

313
Q

What is the most common lymphoproliferative disorders?

A

NHL (DLBCL)

314
Q

17 year old male, 1 month impaired vision in both eyes, 1/2 stone weight loss, breathless on minimal exertion. Retinal haemorrhages, marked leukocytosis, thrombocytopenia, low platelets. Bone marrow (0% B lymphocytes. Diagnosis?

315
Q

What are characteristic cells of ALL?

A

Large
Express CD19 - all B cells have this
CD34 TDT - markers of early immature cells

316
Q

What is the standard treatment for ALL?

A

Combination chemo

Stem cells transplantation of high risk

317
Q

Why do patients with ALL require CNS direct treatments - intrathecal methotrexate?

A

High risk of CNS relapse

318
Q

List new therapies for ALL?

A
  • Bi-specific T cell engagers e.g Blinatunumab

- CAR-T

319
Q

How does CAR-T therapy work?

A

T-cells harvested, transfected to express a specific T cell receptor on leukaemia cells (CD19), expanded in vitro, re-infused into patient

320
Q

What are key side effects of T cell immunotherapy?

A

Cytokine release syndrome

Neurotoxicity

321
Q

List poor risk factors for ALL.

A

Increasing age
Increasing WCC
Cytogenetics/molecular genetics (e.g philadelphia chromosome)
Slow-poor response to treatment

322
Q

What is the typical presentation of ALL?

A

Bone marrow failure +/- raised white cell count

Bone pain, infection, sweats

323
Q

How are CLL cells different?

A

Abnormal cells are mature

Grow slowly

324
Q

What is the most common leukaemia worldwide?

325
Q

What is the lymphocyte count required to diagnose CLL?

326
Q

How does CLL present?

A

Often asymptomatic

327
Q

What clinical findings may be found in CLL?

A 
Bone marrow failure
Lymphadenopathy 
Splenomegaly 
Fever and sweats 
Hepatomegaly 
Infections 
Weight loss
328
Q

What staging system is used for CLL?

A

Binet (A,B,C)

329
Q

What are indications of treatment fro CLL?

A 
Progressive bone marrow failure 
Massive lymphadenopathy 
Progressive splenomegaly 
Systemic symptoms 
Autoimmune cytopenias
Lymphocyte doubling
330
Q

How do you treat CLL?

A

Often watch and wait

Cytotoxic chemo
Monoclonal antibodies
Novel agents

331
Q

What are poor prognostic markers of CLL?

A 
Binet stage B or C
CD38+ expression 
Atypical lymphocyte morphology 
Rapid lymphocyte doubling time 
p53 loss/mutation
332
Q

How do patients with lymphoma present?

A

Lymphadenopathy
Extranodal disease
B symptoms
Bone marrow involvement

333
Q

Describe the staging system for lymphoma?

A

Ann Arbour staging
1 - localised, single lymph nodes
2 - 2 or more lymph node regions on same side
3 - 2 or more lymph node regions above and below diaphragm
4 - widespread, multiple organs, with or without lymph node involvement

A = absence of B symptoms

B = fever, night sweats, weight loss

334
Q

What is the origin of most NHL?

335
Q

What is the difference between low and high grade lymphoma?

A

Low = incurable, responds to chemo, often asymptomatic

high = aggressive, fast-growing, combination chemo, can be cured

336
Q

What are the two most common types of NHL?

A

Diffuse large B cell (high grade)

Follicular (low grade)

337
Q

How are DLBCL and follicular lymphoma treated?

A

Combination chemo and antibody (rituximab)

338
Q

List risk factors for Hodgkin Lymphoma?

A

EBV
FH
Geographiocal clustering

339
Q

How is Hodgkin’s lymphoma treated?

A

Combination chemo +/- monoclonal antibodies (anti-CD30)

Immunotherapy

340
Q

How do you assess response to treatment of Hodgkin’s lymphoma?

341
Q

What type of lymphomas are incurable?

A

Low grade NHL

342
Q

What is CD5 a marker for?

343
Q

List conditions associated with paraproteins.

A

Amyloidosis
Waldenstroms macroglobulinaemia
MGUS

344
Q

What is a paraprotein?

A

A monoclonal immunoglobulin present in blood or urine

345
Q

What does the presence of paraproteins indicate?

A

Indicates that somewhere in the body, a B cell or plasma cel is proliferating

346
Q

What qualitative test identifies presence of paraproteins?

A

Serum protein electrophoresis (separates protein according to size and charge)

347
Q

Summarise the tests for paraproteins.

A

Total immunoglobulin levels
Electrophoresis (key to assess antibody diversity and show paraprotein)
Immunofixation (identifies subclass of paraprotein)
Light chains (assess imbalance)

348
Q

What is the purpose of immunofixation?

A

Identifies class of paraprotein

349
Q

What do IgM paraproteins indicate?

A

Lymphoma (since maturing B lymphocytes produce IgM antibodies)

350
Q

What do IgG and IgA paraproteins indicate?

A

Myeloma (mature plasma cells generate these)

351
Q

What is myeloma?

A

Neoplastic disorder of plasma cells resulting in excess production of a single type of immunoglobulin (paraprotein)

352
Q

At what age does myeloma usually affect?

A

Elderly - over 70

353
Q

What are clinical manifestations of myeloma?

A

CRAB

hyperCalcaemia
Renal failure
Anaemia
Bone disease

354
Q

What bone disease features are associated with myeloma?

A 
Lytic bone lesions
Pathological fractures
Cord compression 
Hypercalcaemia 
Infections 
Bone marrow failure
355
Q

List effects of paraproteins.

A

Renal failure (cast nephropathy)
Hyperviscosity
Hypogammaglobulinaemia

356
Q

What are clinical features of hyperviscosity?

A

Retinal, oral, nasal or cutaneous bleeding

Cardiac failure, pulmonary congestion, confusion, renal failure

357
Q

What causes amyloidosis?

A

Characterised by abnormal deposition of fibrillar protein

358
Q

How can amyloidosis manifest/

A 
Nephrotic syndrome 
LVH 
Carpal tunnel syndrome 
Autonomic neuropathy 
Cutaneous infiltration
359
Q

What is MGUS?

A

Monoclonal gammopathy of uncertain significance –> paraproteins present but no effect

360
Q

What is the most common type of paraprotein associated with myeloma?

361
Q

How do you treat myeloma?

A

Chemotherapy (proteosome inhibitors,monoclonal antibodies)
Bisphosphonate therapy
Radiotherapy
Steroids
Surgery - pinning of long bones, decompression of spinal cord
Autologous stem cell transplant

362
Q

What are clinical presentations of IgM paraproteins?

A

Lymphoma

  • bone marrow failure
  • lymphadenopathy
  • heptosplenomegaly
  • B symptoms
363
Q

What are B symptoms?

A

Fever, night sweats, weight loss

364
Q

Patients with prolonged episodes of neutropenia get treated with what?

A

Antibiotics - ciprofloxacin (gram negative protection)

Anti-fungals - fluconazole

Anti-virals - acyclovir

PJP - co-trimoxazole

365
Q

What are supportive measures aimed at reducing sepsis in haematological malignancies?

A 
G-CSF
Stem cell resuce/transplant 
Protective environment 
IV immunoglobulin replacement 
Prophylaxis - antibiotics, anti-fungals, anti-virals
366
Q

What causes neutropenia?

A

marrow failure (higher risk) or immune destruction

367
Q

What are levels of neutropenia?

A 
<0.5 = sig risk 
<0.2 = high risk
368
Q

How long is high risk neutropenia?

369
Q

What can result from disrupted skin/mucosal surfaces in neutropenic patients?

A

Mucositis

GVHD

370
Q

What is the most common bacterial cause of febrile neutropenia?

A

Gram positive bacteria e.g MSSA, MRSA, strep viridian’s, enterococcus faecalis, corynebacterium, bacillus

371
Q

Name gram negative bacteria that cause 30-40% febrile neutropenia.

A

E.coli
Klebseilla
Pseudomonas aeruginosa

372
Q

What are common fungal infections seen in immunocompromised patients?

A

Candida, aspergillus

373
Q

What contributes to increased fungal infection risk in immunocompromised patients?

A

Monocytopenia and monocyte dysfunction

374
Q

How does neutropenic sepsis present?

A

Fever with no localising signs

> 38.5 (1 reading) or >38 (2 readings)

Rigors
Pneumonia
Cellulitis 
UTI 
Septic shock
375
Q

How do you investigate neutropenic fever?

A

Hx
Ex
Blood cultures - Hickman line and peripheral
CXR
Throat swab and other clinical sites of infections
Sputum if productive
FBC, U&Es, LFTs, Coag screen

376
Q

How do you manage neutropenic sepsis?

A

Resuscitation
Braod spectrum IV Abx - Tazocin, Gentamicin

If gram +ve - vancomycin or teicoplanin

If no response in 72 hours, add IV anti fungal e.g caspofungin

CT chest, abdo, pelvis

377
Q

What infections are commonly seen in severely lymphopenic patients?

A

Atypical pneumonia e.g PJP, CMV, RSV
Viral e.g shingles, Herpes, adenovirus, EBV
Fungal e.g candida, aspergillus

378
Q

What is the best treatment regimen for boy with haemophilia A who develops inhibitory antibodies to factor 8?

A

Give factor 8 prophylaxis - small amounts every day or at least 3 times a day

379
Q

What are future treatments for haemophilia?

A 
Gene therapy 
Monoclonal Ab (Emicizumab)
380
Q

What are petechiae, menorrhagia, buccal bleeding and epistaxis suggestive of?

A

Mucosal pattern of bleeding –> Thrombocytopenia

381
Q

List causes of thrombocytopenia.

A

AML
Aplastic anaemia (typically pancytopenia)
IPT

382
Q

How does ITP cause thrombocytopenia?

A

Normal production with increased consumption of platelets

383
Q

What is the likely platelet count for spontaneous bruising and petechiae formation?

A

Less than 10

384
Q

What illnesses are associated with immune thrombocytopenia?

A

HIV
SLE
Glandular fever

385
Q

What increases VTE risk in combination with the COCP?

A

Factor V Leiden

386
Q

List causes of thrombocytosis

A 
Infection 
Post surgery/trauma 
Malignancy 
Iron deficiency 
Inflammation - IBD, RA
Primary myeloproliferative disease
387
Q

What are causes of lymphocytosis?

A 
Viral infections 
Other infections - TB, Brucellosis, syphilis, vasculitis
ALL 
CLL 
Lymphoma

Haematology and Immunology (2 decks)

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