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phase 2 > Haematology > Flashcards

Haematology Flashcards

1
Q

What is the pathophysiology of myeloma

A

Cloned malignant plasma cells all produce the same immunoglobulin in large quantities. Leading to secretion of immunoglobulins

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2
Q

What are histological features of a malignant plasma cell

A

Prominent ER, centrally placed nucleus and hof

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3
Q

What are plasmocytomas

A

Cancers of the plasma, can be within or outside the bone marrow

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4
Q

What is waldenstroms macroglobulinaemia

A

IgM related plasma dysfunction

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5
Q

What are the presentations of myeloma

A

CRAB hypercalceamia, Renal disease, anaemia, bone disease

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6
Q

What causes anaemia in myeloma

A

Plasma cells infiltrating the bone marrow and also excessive WBC reducing the blood volume or RBC

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7
Q

What is rouleaux

A

Stacks of erythrocytes on blood film, caused by high protein. Seen in myeloma

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8
Q

What is the most common cause of death in myeloma

A

Infection due to monoclonal Ig causing immune surpression

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9
Q

What causes renal disease in myeloma

A

Light chain deposition, high calcium, dehydration and NSAIDS

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10
Q

What is amyloidosis

A

Extracellular deposition of fibrillar protein, leads to abnormal clinical signs. Can be due to light chain deposition.

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11
Q

When should you suspect myeloma

A

Rouelaux, back pain, high ESR, high calcium and unexplained anaemia

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12
Q

What should you do if you suspect myeloma

A

Check immunoglobulins in serum and urine

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13
Q

What can cause lumps in the neck

A

Malignancy or reactive lymph nodes due to infection or inflammation

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14
Q

What can cause primary immunodeficiency

A

Ataxia telangiectasia or Wiscott-Aldrich syndrome

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15
Q

What can cause secodnary immunodeficiency

A

HIV, transplant recipients

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16
Q

Which infections can cause lymphoma

A

EBV, HTLI-1 and helicobacter pylori

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17
Q

What causes nodal disease in lymphoma

A

Accumulation of cancerous WBC

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18
Q

Name 3 systemic B symptoms in Lymphoma

A

Loss of apetite, weight loss, drenching night sweats

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19
Q

What causes drenching night sweats in lymphoma

A

Cyotkines from WBC

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20
Q

What is classified as weight loss

A

Unintentional loss of 10% in 6 months

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21
Q

What is WHO performance score 0

A

Asymptomatic, no restriction

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22
Q

What is WHO performance score 1

A

Symptomatic but completely ambulatory, restricted strenuous activity but can carry out light work

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23
Q

What is WHO performance score 2

A

Symptomatic, less than 50% in bed (waking hours). No work but self care

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24
Q

What is WHO performance score 3

A

Symptomatic, more than 50% in bed, not bed bound. Limited self care

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25
Q

What is WHO performance score 4

A

Bedbound, no self care, limited to bed or chair

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26
Q

What is WHO performance score 5

A

Death

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27
Q

Name a low grade NHL

A

Follicular lymphoma

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28
Q

Name a high grade NHL

A

Diffuse Large B cell lymphoma

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29
Q

Name a very high grade NHL

A

Burkitt’s lymphoma

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30
Q

What is the treatment of stage 1-2A hodgkins lymphoma

A

Short course combination chemotherapy followed by radiotherapy

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31
Q

What is the treatment of stage 2B-4 hodgkins lymphoma

A

Combination chemotherapy

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32
Q

Which chemotherapy causes cardiomyopathy

A

Anthracyclines

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33
Q

Which chemotherapy causes lung damage

A

Bleomycin

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34
Q

Which chemotherapy causes peripheral neuropathy

A

Vinca alkaloids

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35
Q

Name a monoclonal antibody used for NHL treatment

A

Rituximab, targets CD-20 on B cells. it is a chimeric antibody with few side effects. CD20 is unique to B cells

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36
Q

Name a radioimmunotherapy used for NHL treatment

A

Zevalin

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37
Q

Name a T cell engaging therapy used for NHL treatment

A

Blinatunomab, bi specific anitbody which targets CD19 on B cells and CD3 on T cells, directing the immune system

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38
Q

What is red marrow

A

Where platelets, rbc and wbc are made

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39
Q

What is white marrow

A

Fat, you get more as you age

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40
Q

Which cells are affected in acute leukaemia

A

Immature

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41
Q

Which cells are affected in chronic leukaemia

A

Mature

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42
Q

Which cells are affected in chronic myeloid leukaemia

A

Basophil, Neutrophil and eosinophil

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43
Q

Which cells are affected in chronic lymphatic leukaemia

A

B lymphocytes

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44
Q

Which cells are affected in chronic lymphoblastic leukaemia

A

Lymphoblast

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45
Q

Which cells are affected in chronic myeloid leukaemia

A

Myeloblast

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46
Q

Name a congenital risk factor for leukaemia

A

Down’s syndrome

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47
Q

Name environmental risk factors for leukaemia

A

Radiotherapy, chemotherapy and benzene and other chemicals

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48
Q

What are signs of anaemia in leukaemia

A

Shortness of breath, fatigue, may not be pronounced in the young

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49
Q

What are the signs of thrombocytopenia in leukaemia

A

Bruising, bleeding (usually mucosal) and rash

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50
Q

What are the signs of infection in leukaemia

A

Fever and rigors

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51
Q

What type of rash does thrombocytopenia cause

A

Pin prick, pink rash which does not go away on touch - purpura, petechiae

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52
Q

What is a sign of lyphoma/ lymphoblastic leukaemia

A

Night sweats

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53
Q

What do blasts look like

A

very little cytoplasm and indistinct nucleioli

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54
Q

Which specialist investigations are used in leukaemia

A

Flow cytometry, cytogenetic analysis and bone marrow biopsy

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55
Q

Who gets acute lymphoblastic leukaemia

A

Young children, median age 3.5 (also 16-24 and old age but rare)

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56
Q

Who gets acute myeloid leukaemia

A

Older adults, peak age 70 (much rarer in children)

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57
Q

What is supportive leukaemia treatment

A

Blood products, symptom relief and reduce the chance of infection

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58
Q

What is a hickman line

A

Allows direct blood access, goes straight into the right atrium

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59
Q

How does aspergillos behave

A

It is a fungus which is angioinvasive and targets vessles

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60
Q

What causes acute relative polycythaemia

A

Dehydration

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61
Q

What causes chronic relative polycythaemia

A

Obesity, HTN, high alcohol and tobacco intake

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62
Q

What is polycythaemia

A

an increase in the haematocrit of the blood

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63
Q

What is polycythaemia vera

A

disease in which there are more RBC and also more WBC and platelets, it is treated with blood letting. Symptoms include head aches, thromboses, plethora, itching and cyanosis

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64
Q

What disease is caused by excessive proliferation of haematoipoietic myeloid stem cells into RBC

A

Polycythaemia vera

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65
Q

What disease is caused by excessive proliferation of haematopoietic myeloid stem cells into RBC

A

Chronic myeloid leukaemia

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66
Q

What disease is caused by excessive proliferation of haematopoietic myeloid stem cells into platelets

A

Essential thrombocytopenia

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67
Q

What disease is caused by excessive proliferation of haematopoietic stem cells into fibroplasts

A

Myelofibrosis

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68
Q

Which mutation is associated with polycythaemia vera

A

JAK2

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69
Q

What is venesection

A

Blood letting

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70
Q

How is polycythaemia treated in high risk/older people

A

Hydroxycarbamide

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71
Q

How is polycythaemia treated in pregnant women

A

Alpha interferon

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72
Q

How is polycythaemia normally treated

A

Venesection

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73
Q

Which chains are present in adult haemoglobin

A

2 alpha, 2 beta

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74
Q

Which chains are present in foetal haemoglobin

A

2 alpha, 2 gamma

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75
Q

When does foetal haemoglobin switch to adult haemoglobin and what is the effect

A

At 6 months, reducing the oxygen affinity

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76
Q

What causes sickle cell structure

A

valine to glutamine point mutation (A to T) in 6th codon in beta globin gene causes the formation of haemoglobin S

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77
Q

What inheritance pattern do sickle cell and thallasaemia show

A

Autosomal recessive

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78
Q

What is priapism

A

persistent and painful erection of the penis

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79
Q

How does sickle cell disease effect RBC

A

Causes polymerisation of haemoglobin molecules this precipitates out, damages red blood cells and renders them useless

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80
Q

How do the causes of alpha and beta thalassaemia differ

A

Alpha mainly caused by mutatations, beta caused by deletions

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81
Q

Define thalassaemia

A

Globin chain disorders resulting in diminished synthesis in one or more globin chains with subsequent reduction in the haemoglobin

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82
Q

What are the different types of thalassaemia

A

Major - transfusion dependent, Intermedia - less severe, can survive without transfusions, Carrier/Heterozygote - asymptomatic

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83
Q

Which type of anaemia does thalassaemia cause

A

microcytic

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84
Q

What would be the blood results for someone with Beta thallasaemia

A

Hb, MCV and MCH very low

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85
Q

What does MCV stand for

A

Mean corpuscular volume

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86
Q

What does MCH stand for

A

Mean corpuscular haemoglobin

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87
Q

What is a consequence of transfusion

A

High Iron, this can lead to deposition in organs causing renal, cardiac and pituitary failure

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88
Q

What is the result of 4 alpha thalassaemia genes

A

Hydrops foetalis - not compatible with life (Barts hydrops)

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89
Q

What happens with increasing numbers of faulty alpha thalassaemia genes

A

Increasing severity, 1 is normal or minimal changes, 2 more marked and 3 moderately severe

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90
Q

Where is alpha thalassaemia found

A

Eastern meditteranean or the far east

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91
Q

Name disease modifying treatment in sickle cell disease

A

Transfusion, stem cell transplant, hydroxycarbamide

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92
Q

What are membranopathies

A

Deficiencies of red cell membrane proteins caused by a variety of autosomal dominant genetic lesions

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93
Q

Name two membranopathies

A

Spherocytosis and elliptocytosis (shape changes)

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94
Q

What is a spherocyte

A

Horizontal membranopathy

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95
Q

What is an eliptocyte

A

Vertical membranopathy

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96
Q

Which RBC membrane protein is commonly missing in membranopathies

A

Spectrin

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97
Q

What causes slapped cheek syndrome

A

Parovirus and haemolytic anaemia. Reduced RBC production and there is already reduced lifespan so leads to has large effect. Occurs in children and in epidemics.

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98
Q

What are common RBC enzyme deficiencies

A

Pyruvate kinase and glucose-6-phosphate dehydrogenase

99
Q

How is G6PDH deficiency diagnosed

A

NADPH screening test

100
Q

What factors can bring on G6PDH deficiency crises

A

Broad beans, infections, drugs (primaquine, sulphonamides, nitrofurantoin, quinolones and dapsone)

101
Q

Define anaemia

A

Low haemoglobin concentration which may be due to low red cell mass or increased plasma volume (eg. in pregnancy)

102
Q

What are the three main causes of microcytic anaemia

A

Iron deficiency, chronic disease, thalassaemia

103
Q

What are the two rarer causes of microcytic anaemia

A

Lead poisoning and congenital sideroblastic anaemia

104
Q

What are the three main causes of normocytic anaemia

A

Acute blood loss, anaemia of chronic disease and combined haematinic deficiency

105
Q

What are the four rarer causes of normocytic anaemia

A

Renal failure, hypothyroidism, haemolysis and pregnancy

106
Q

Name the three main causes of macrocytic anaemia

A

B12/Folate deficiency, Alcohol excess/liver disease and hypothyroidism

107
Q

What are the four examples of haematological causes of macrocytic anaemia

A

Haemolysis, bone marrow failure or infiltration and antimetabolite therapy

108
Q

What is the normal male Hb range

A

131-166g/L

109
Q

What is the normal female Hb range

A

110-147g/L

110
Q

What are the physiological consequences of anaemia

A

Reduced oxygen transport, tissue hypoxia and compensatory changes (increased tissue perfusion, oxygen transfer and RBC production)

111
Q

What are the pathological consequences of anaemia

A

Fatty changes in the myocardium and liver, worsen angina/claudication, skin and nail atrophy, CNS cell death (cortex and basal ganglia)

112
Q

What is intermittent claudication

A

A cramping pain induced by exercise and relieved by rest. Often in the calf.

113
Q

Name something which causes reduced RBC concentration but constant red cell mass

A

Dehydration

114
Q

Name four causes of hypoplastic anaemia

A

Renal failure, endocrine, PRCA, aplastic anaemia

115
Q

Name two causes of dyshaemopoietic anaemia

A

Defective Hb or DNA synthesis

116
Q

Name a cause of post haemorrhagic anaemia

A

Intrinsic RBC abnormalities

117
Q

Name a cause of haemolytic anaemia

A

Extrinsic abnormalities

118
Q

Name some symptoms of anaemia

A

Fatigue, dyspnoea, faintness, palpitations, headaches, tinnitus, anorexia and worsened angina

119
Q

Is high or low ferritin reliable diagnostically

A

Low. High could be caused by acute phase reactions

120
Q

Which two causes of anaemia will show increased serum iron and ferritin and low total iron binding capacity

A

There is iron accumulation. Thalassaemia and sideroblastic anaemia. Both causes of microcytic anaemia

121
Q

Name four causes of iron deficiency

A

Hookworm, menorrhagia, haemorrhage and diet

122
Q

How can you investigate chronic disease in anaemia

A

Clinical investigation, laboratory investigation and renal failure

123
Q

What is the normal range for mean cell volume

124
Q

How can you investigate B12 deficiency

A

IF antibodies, Schilling test, coeliac antibodies.

125
Q

What is the common cause of haematinic deficiency

A

Malabsorption

126
Q

What does a raised reticulocyte count suggest

A

Increased removal of RBC

127
Q

What does a low reticulocyte count suggest

A

Increased production of RBC

128
Q

Which disease can cause RBC fragments

129
Q

What is the Hb cut off for a transfusion

A

below 70g/L

130
Q

In severe anaemia with heart failure what is the treatment

A

Transfusion

131
Q

How does thrombopoietin homeostasis work

A

Low platelets leads to less bound TPO, therefore more free TPO which stimulates megakaryocytes and increases platelets

132
Q

Where is thrombopoietin made

133
Q

What is the normal platelet lifespan

134
Q

How are platelets removed

A

By the spleen

135
Q

What is platelet function

A

Adhesion and aggregation using surface glycoproteins to form a platelet plug by primary haemostasis

136
Q

Name platelet surface proteins

A

ABO, HPA, HLA class I and glycoproteins

137
Q

Which surface protein is used for adhesion to collagen

138
Q

Which surface protein is used for adhesion to vWF

A

GPIb and IIb/IIa

139
Q

What do platelet alpha granules contain

A

PDGF, Fibrinogen, vWF and PF4

140
Q

What do platelet dense granules contain

A

Nucleotides (ADP), Calcium, serotonin

141
Q

Which clotting factors are activated by membrane phospholipids

A

II (prothrombin), V and X

142
Q

Name five causes of bleeding

A

Injury, vascular disorders, low platelets, abnormal platelet function and defective coagulation

143
Q

Clinical features of platelet dysfunction

A

Mucuo-cutaneous features. Mucosal bleeding, easy bruising, petechia, purpura and traumatic haematomas

144
Q

What is epistaxis

A

Bleeding from the nose

145
Q

What is petechia

A

Small, round, flat, dark red spots caused by bleeding beneath/into the skin

146
Q

What is purpura

A

Skin rash from capillaries bleeding into the skin, causes many petechia spots. May be due to either platelet or capillary dysfunction

147
Q

Congenital causes of platelet dysfunction

A

Platelet disorders (Storage pool disorders, Glanzmann or Bernard Soulier) or von Willebrand disease

148
Q

Acquired causes of platelet dysfunction

A

Uraemia or drugs

149
Q

Name a cause of production failure causing low platelets

A

Congenital or acquired(drugs, marrow replacement, suppression, replacement or failure)

150
Q

Name a cause of increased removal causing low platelets

A

Immune, consumption, splenomegaly

151
Q

Name an artefactual cause of low platelets (normal but looks abnormal because of a testing error)

A

EDTA (anticoagulant used in test tubes) induced clumping

152
Q

What is thrombocytopenia

A

A reduction in the number of platelets in the blood

153
Q

What is the cause of congenital thrombocytopenia

A

Few functioning megakaryocytes in the bone marrow

154
Q

Which diseases can cause infiltration of the bone marrow

A

Leukaemia, metastatic malignancy, lymphoma, myeloma and myelofibrosis

155
Q

Name factors which would cause reduced production of platelets by the bone marrow

A

Low B12/folate, Reduced TPO, medication, toxins, infections, aplastic anaemia

156
Q

Name a disease which causes dysfunctional production of platelets in bone marrow

A

Myelodysplasia

157
Q

Name a disease which causes autoimmune destruction of platelets

A

Primary or secondary immune thrombocytopenia

158
Q

Name two diseases which cause hypersplenism

A

Portal hypertension and splenomegaly

159
Q

Name an example of drug related immune platelet destruction

A

heparin induced thrombocytopenia

160
Q

What are causes of platelet consumptin

A

Disseminated intravascular coagulopathy (DIC), Thrombotic thrombocytopenic purpura (TTP), Haemolytic uraemic syndrome (HUS), Haemolysis, elevated liver enzymes and low platelts (HELLP), major haemorrhage

161
Q

Which part of platelet function does clopidogrel target

162
Q

Which part of platelet function does Tirofiban target

A

Gp IIb/IIa

163
Q

Which part of platelet function does aspiring target

A

Cox inhibitor. Prevents thromboxane production from prostaglandin

164
Q

In immune thrombocytopenia which type of immunoglobulin has formed

165
Q

What is the cause of primary immune thrombocytopenia

A

May follow viral infection/immunisation in children

166
Q

What is the cause of secondary immune thrombocytopenia

A

Malignancy or infection eg HIV

167
Q

What causes cytokine release to initiate DIC

A

Systemic inflammatory response syndrome. Causes systemic activation of the clotting cascade

168
Q

What are the consequences of systemic activation of the clotting cascade

A

Consumption of platelets and clotting factors (and therefore bleeding) and microvascular thrombosis (and therefore organ failure)

169
Q

What is thrombotic thrombocytopenic purpura

A

Spontaneous platelet aggregation in the microvasculature of the brain, kidney and heart. Reduction in protease enzyme ADAMTS13 (cant break down vWF multimers)

170
Q

How is the number of platelets investigated

A

Full blood count

171
Q

How is the appearance of platelets investigated

A

Blood film

172
Q

How is the function of platelets investigated

A

PFA and bleeding time

173
Q

How are the surface proteins of platelets investigated

A

Flow cytometry

174
Q

What is tranexamic acid used for

A

Inhibits breakdown of fibrin, so good for mucosal bleeding but not if GU bleeding as causes clot retention

175
Q

What are the common causes of disseminated intravascular coagulation

A

Sepsis or malignancy or obstetric causes

176
Q

What are schistiocytes

A

RBC fragments, microangiopathic haemolytic anaemia

177
Q

Which three system’s microvasculature is commonly affected by thrombocytopenia

A

Renal, CNS and cardiac

178
Q

What is the key treatment for TTP

A

Urgent plasma exchange to replace ADAMTS13 and remove antibodies

179
Q

What is D dimer

A

A protein which is the result of fibrin degradation

180
Q

What are PT and APTT

A

Meaures of coagulation factors

181
Q

What is the genetic abnormality in chronic myeloid leukaemia

A

Philadelphia chromosome

182
Q

What are venous thromboses rich in and what should they be treated with

A

Fibrin rich, should be treated with anticoagulants

183
Q

What are arterial thromboses rich in and what should they be treated with

A

Platelet rich, should be treated with antiplatelets

184
Q

Which DVT are clinically important

A

Proximal thrombosis, between the knee and hip. Large enough to cause fatal PE

185
Q

Risk factors for DVT

A

Surgery, oestrogen (OC pill, pregnancy, HRT), immobility/long haul flights, inherited thrombophilia

186
Q

Name 4 mechanical preventions of DVT

A

Hydration, early remobilisation, compression stockings, foot pumps and

187
Q

Name a chemical prevention of DVT

A

LMW heparin

188
Q

What is a saddle embolus

A

One which blocks left and right pulmonary arteries, it is the most severe

189
Q

Name consequences of a large pulmonary embolism

A

Hypotension, cyanosis, severe dyspnoea, right heart strain/failure

190
Q

What is the consequence of a coronary circulation arterial thrombosis

A

Myocardial infarction

191
Q

What is the consequence of a cerebral circulation arterial thrombosis

A

CVA or stroke

192
Q

What are the consequences of a peripheral circulation arterial thrombosis

A

Claudication, rest pain and gangrene

193
Q

Risk factors for atherosclerosis

A

Smoking, HTN, diabetes, hyperlipidaemia, obesity, stress (type A personality)

194
Q

What are the signs of myocardial infarction

A

diagnosis history, ECG, cardiac enzymes

195
Q

What are the signs of CVA

A

history and examination, CT scan/MRI scan

196
Q

What are the signs of peripheral vascular disease

A

History and examination, ultrasound and angiogram

197
Q

What are the signs of DVT

A

swollen, warm, tender leg

198
Q

What are the signs of pulmonary embolus

A

Pleuritic chest pain, breathlessness, cyanosis, death

199
Q

Genetic causes of venous thrombosis

A

Factor V leiden, PT20210A, antithrombin deficiency, protein C or protein S deficiency

200
Q

Acquired causes of venous thrombosis

A

Antiphospholipid syndrome, lupus anticoagulant, hyperhomocysteinaemia

201
Q

Investigations for DVT

A

D dimer and ultrasound compression test

202
Q

Which type of DVT is more likely to recur

A

Spontaneous rather than provoked

203
Q

What thromboprophylaxis is given to high risk patients

A

Dalteparin s/c od

204
Q

What are the initial investigations in PE

A

CXR, ECG and blood gases

205
Q

What is the standard drug therapy following PE or DVT

A

LMW heparin s/c od for 5 days, Oral warfarin 2.5 INR for 6 months

206
Q

Why are DOACs replacing warfarin

A

They provide coagulation regulation without bleeding

207
Q

What is the best diagnostic test for PE

A

An echo showing right heart strain

208
Q

What does CTPA acheive

A

A 3D moving scan showing the pulmonary arteries either latent or full of filling defect

209
Q

What is thrombosis

A

Blood coagulation within a vessel

210
Q

Whaty does tissue plasminogen activator do (TPA)

A

Generates plasmin and degrades fibrin. Given in MI treatment

211
Q

Name a DOAC

A

Rivaroxaban

212
Q

Describe heparin’s mechanism

A

A glycoaminoglycan it binds to antithrombin to increase its activity. Indirect thrombin inhibitor

213
Q

How does LMWH differ from heparin

A

Smaller molecule with less varation in dose, it is renally excreted and give subcut od

214
Q

Describe aspirin’s mechanism

A

Inhibits COX irreversibly, acts for 7-10 day platelet lifetime. Inhibits thromboxane formation and therefore platelet aggregation

215
Q

Describe clopidogrel’s mechanism

A

Inhibts ADP induced platelet aggregation

216
Q

Describe warfarin’s mechanism

A

Antagonist of Vitamin K it prevents synthesis of factors 1(0)972 and prolongs the prothrombin time

217
Q

How is warfarin measured

A

by INR which is international normalised ratio, derived from prothrombin time. Should be 2-3

218
Q

Describe new oral anticoagulant drugs (NOAC) or DOAC’s mechanism

A

Orally active, acts directly on factors 2 or 10, not used in pregnancy but no monitoring so used for extended thromboprophylaxis

219
Q

What is the normal range of haemoglobin

220
Q

What is the normal range of WBC

221
Q

What is the normal range of platelets

222
Q

What is the normal range of MCV

223
Q

What is polycythaemia

224
Q

Name secondary causes of polycythaemia

A

(response to low oxygen) Smoking, lung disease, cyanotic heart disease, altitude and EPO excess (doping)

225
Q

Name a primary cause of polycythaemia

A

Polycythaemia rubra vera

226
Q

What causes polycythaemia rubra vera

A

JAK2 mutation

227
Q

What is polycythaemia rubra vera

A

Myeloproliferative disorder, overactive bone marrow. Predominantly affects RBC but WBC and platelets as well

228
Q

Clinical presentation of polycythaemia rubra vera

A

Plethoric appearance, thrombosis, itching, splenomegaly, abnormal RBC

229
Q

What is the treatment of polycythaemia rubra vera

A

Aspirin, venesection and bone marrow suppressive drugs

230
Q

What is neutrophilia

A

High neutrophils

231
Q

Name reactive causes of neutrophilia

A

Infection, inflammation and malignancy

232
Q

Name a primary cause of neutrophilia

A

Chronic myeloid leukaemia

233
Q

What is lymphocytosis

A

High white blood cells

234
Q

Name reactive causes of lymphocytosis

A

Infection, inflammation, malignancy

235
Q

Name a primary cause of lymphocytosis

A

Chronic lymphoid leukaemia

236
Q

What is thrombocytopaenia

A

Low platelets

237
Q

What is thrombocytosis

A

High platelets

238
Q

Name reactive causes of thrombocytosis

A

Infection, inflammation and malignancy

239
Q

Name a primary cause of thrombocytosis

A

Essential thrombocythaemia

240
Q

What is neutropaenia

A

Low neutrophils

241
Q

What is classed as severe neutropaenia

A

<0.5 this is a severe infection risk

242
Q

Name two causes of neutropaenia

A

Underproduction and increased removal

243
Q

Name three causes of underproduction of neutrophils leading to neutropaenia

A

Marrow failure, marrow infiltration and marrow toxicity eg drugs

244
Q

Name three causes of increased removal of neutrophils leading to neutropaenia

A

Autoimmune, felty’s syndrome and cyclical

phase 2 (17 decks)

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