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Haematology Flashcards

1
Q

What does Hb have to be below in anaemia?

A

<135 g/L for men and <115 g/L for women

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2
Q

Name 3 causes of microcytic anaemia

A

Iron deficiency, thalassaemia and sideroblastic anaemia

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3
Q

Name 4 causes of normocytic anaemia

A

Acute blood loss, anaemia of chronic disease, bone marrow failure, renal failure

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4
Q

Name 4 causes of macrocytic anaemia

A

B12/folate deficiency, alcohol excess/liver disease, haemolytic, hypothyroidism

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5
Q

Name 4 causes of iron deficiency anaemia

A

GI bleeding/chronic blood loss, menorrhagia, poor diet, malabsorption

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6
Q

Give 3 investigations for iron deficiency anaemia

A

FBC (low hb, mcv)
Ferritin (low)
Blood film

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7
Q

How do you treat iron deficiency anaemia?

A

Oral iron - ferrous sulphate or IV iron infusion

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8
Q

Give 3 side effects of ferrous sulfate

A

Nausea, abdominal discomfort, constipation

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9
Q

Give 3 causes of anaemia of chronic disease

A

Chronic infection, malignancy and renal failure

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10
Q

Give 4 side effects of erythopoietin treatment

A

Flu like symptoms, hypertension, high platelets and VTE

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11
Q

What is seen on the blood film in B12/folate deficiency?

A

Hypersegmented neutrophils

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12
Q

Give 3 clinical features of B12 deficiency

A

Irritability, peripheral neuropathy, depression

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13
Q

How do you treat B12/folate deficiency?

A 
IM hydroxycobalamin (B12)
Folic acid
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14
Q

Give 5 causes of haemolytic anaemia

A 
Autoimmune (would see spherocytosis)
Sickle cell anaemia
Hereditary spherocytosis
G6PDH deficiency (Heinz bodies)
Drug induced
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15
Q

Give 5 causes of neutrophilia

A 
Bacterial infection
Inflammation eg MI
Drugs (steroids)
Disseminated malignancy
Trauma/surgery/haemorrhage
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16
Q

Give 5 causes of neutropenia

A 
Post-chemotherapy
Severe sepsis
Hypersplenism eg Felty's syndrome
Bone marrow failure (leukaemia etc)
Viral infections
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17
Q

Give 4 causes of raised lymphocytes

A

Viral infections
Chronic infections eg TB and hepatitis
Leukaemias (CLL)
Lymphomas

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18
Q

Give 5 causes of decreased lymphocytes

A 
Steroid therapy
HIV infection
Post chemotherapy
Post radiotherapy
Marrow infiltration
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19
Q

Give 5 causes of raised eosinophils

A 
Allergy
Parasitic infection
Drug reactions eg erythema multiform
Eczema, psoriasis
Eosinophilic leukaemia
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20
Q

Give 7 causes of pancytopenia

A 
Aplastic anaemia
Acute leukaemias
Myelodysplasia
Myeloma
Myelofibrosis
Lymphoma (marrow infiltration)
Hypersplenism - haemolytic anaemias, cirrhosis
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21
Q

Give 2 drugs that can cause agranulocytosis

A

Clozapine and carbimazole

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22
Q

Give 6 causes of thrombocytopenia due to decreased production of platelets

A 
Leukaemias
Lymphoma (marrow infiltrations)
Chemotherapy
Alcohol
Myelofibrosis
Viral infections
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23
Q

Give 6 causes of thrombocytopenia due to decreased platelet survival

A 
ITP
TTP
DIC
Post transfusion
Heparin induced
HELLP syndrome
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24
Q

What can be used to treat ITP?

A 
Prednisolone
IV IG
Rituximab
Splenectomy
TPO receptor agonists
Thrombopoietin analogues
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25
Q

Give 5 symptoms of hyperviscosity syndrome

A 
Lethargy
Confusion
Reduced cognition
Abdominal pain
Visual disturbance
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26
Q

Give 4 causes of hyperviscosity syndrome

A

Polycythaemia vera
Leucocytosis
Myeloma
Waldenstroms macroglobulinaemia

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27
Q

What is the treatment of hyperviscosity syndrome?

A

Underlying cause

Polycythaemia - venesection
Leukapheresis in leukaemia (raised WCC)
Plasmapheresis in myeloma and waldenstroms

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28
Q

Give 6 causes of splenomegaly

A 
CML
Myelofibrosis
Malaria
Portal hypertension
Lymphoma
Haemolytic anaemia
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29
Q

What does the blood film show after splenectomy?

A

Howell-Jolly bodies, pannenheimer bodies, target cells

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30
Q

What organisms are dangerous for people who have had their spleen out?

A

Strep pneumonia, haemophilia influenza and neisseria meningitidis (encapsulated)

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31
Q

What measures are taken to reduce risks for people post splenectomy?

A

Immunisations (pneumococcal, flu and meningococcal)
Lifelong prophylactic antibiotics - penicillin V or erythromycin
Pendants, bracelets or cards for awareness
Caution travelling abroad

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32
Q

Why shouldn’t long term steroids be stopped suddenly?

A

Risk of addisonian crisis due to adrenal insufficiency

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33
Q

What conditions could be made worse by steroids?

A

Diabetes, osteoporosis, hypertension, TB, chickenpox

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34
Q

What are the main side effects of steroids?

A

Weight gain, myopathy, osteoporosis, cushings, depression, psychosis, increased susceptibility to infections

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35
Q

What should you prescribe alongside steroids?

A

Calcium and vitamin D supplements

Bisphosphonates

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36
Q

Which patients require CMV negative blood products?

A

Pregnant women and neonates up to 28 days (CMV can cause sensorineural deafness and cerebral palsy)

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37
Q

Which patients require irradiated blood products?

A

Hodgkin’s lymphoma
Stem cell transplant recipients
Some chemo patients

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38
Q

When are packed red cells indicated?

A

Acute blood loss, chronic anaemia where Hb < 70 or symptomatic anaemia

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39
Q

How long are packed red cells administered over?

A

2-4 hours

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40
Q

When is a platelet transfusion indicated?

A

Haemorrhagic shock, profound thrombocytopenia <20 or preoperatively where platelets <50

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41
Q

How long are platelets administered over?

A

30 mins

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42
Q

What does fresh frozen plasma consist of?

A

Clotting factors

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43
Q

When is fresh frozen plasma indicated?

A

DIC, haemorrhage secondary to liver disease, all massive haemorrhages

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44
Q

How long is fresh frozen plasma administered over?

A

30 mins

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45
Q

What does cryoprecipitate consist of?

A

Fibrinogen, von willebrands factor, factor VIII and fibronectin

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46
Q

When is cryoprecipitate indicated?

A

DIC where fibrinogen is low, von willebrands disease or massive haemorrhage

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47
Q

How long is cryoprecipitate administered over?

A

Stat

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48
Q

What are the main complications of transfusions?

A 
Acute haemolytic reaction
Anaphylaxis
Transfusion Associated Circulatory Overload
Transfusion Related Acute Lung Injury 
Bacterial contamination
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49
Q

What are the clinical features of acute haemolytic reaction from transfusions?

A 
Fever
Hypotension
Urticaria
Abdomen/chest pain
Agitation
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50
Q

What will be seen in investigations for acute haemolytic reaction from transfusions?

A

FBC - low Hb
High LDH
High bilirubin
Positive direct antiglobulin test

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51
Q

What is the management of acute haemolytic reaction from a transfusion?

A

STOP THE TRANSFUSION
Tell haematologist/blood bank
Fluid resuscitation
Give O2

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52
Q

What are the clinical features of transfusion associated circulatory overload (TACO)?

A

Dyspnoea
Raised JVP
Tachycardia
Basal crackles

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53
Q

What is the management of transfusion associated circulatory overload (TACO)?

A

STOP THE TRANSFUSION
Chest X Ray
Oxygen
IV Furosemide 40mg

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54
Q

What are the clinical features of transfusion related acute lung injury (TRALI)?

A 
Dyspnoea
Cough
Hypoxia
Frothy sputum
Fever
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55
Q

What is seen on the chest x ray of TRALI?

A

White out

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56
Q

What is the management of transfusion related acute lung injury (TRALI)?

A

STOP THE TRANSFUSION
100% oxygen
Treat as ARDS
Remove donor from the donor panel

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57
Q

What is the pathophysiology of TRALI?

A

Antileucocyte antibodies in donor plasma causes ARDS

58
Q

What are 3 delayed complications of transfusions?

A

Infection (eg hepatitis, HIV)
Graft vs Host disease (due to HLA mismatch)
Iron overload (especially in repeated transfusions)

59
Q

Which is the most common childhood cancer?

A

ALL

60
Q

What is the peak age of onset of ALL?

A

2-4 years of age

61
Q

What is ALL associated with?

A

Down’s syndrome, Philadelphia chromosome

62
Q

How does ALL present?

A

Pancytopenia - anaemia, infection, bleeding
Bone pain
Lymphadenopathy
Hepatosplenomegaly

63
Q

What is seen on the blood film in ALL?

A

Blast cells

64
Q

What tests need to be done on the bone marrow biopsy?

A

Flow cytometry/immunophenotyping - differentiates between myeloid and lymphoid
Cytogenetics - to look for translocations etc

65
Q

What is the most common translocation in childhood ALL?

A

t(12;21) - TEL-AML fusion gene

66
Q

What chemotherapy induces remission in ALL?

A

Vincristine, prednisolone, L-asparaginase and daunorubicin

67
Q

What is imatinib?

A

Tyrosine kinase inhibitor

68
Q

What is the median age of onset for AML?

A

67 years

69
Q

What is AML associated with?

A
  • Myelodisplastic syndromes
  • Progression from CML
  • Complication of chemotherapy eg for lymphoma
  • Down’s syndrome
70
Q

How does AML present?

A

Fatigue, fever, anaemia, bleeding, gum hypertrophy, hepatosplenomegaly, leukostasis

71
Q

How can Leukostasis present?

A

Respiratory distress and altered mental status

72
Q

What investigations are required in AML?

A

FBC - low Hb, low platelets
LDH - raised
Bone marrow biopsy + flow cytometry and cytogenetics

73
Q

What does the bone marrow biopsy show in AML?

A

Presence of Auer rods found in AML myeloblast cells

74
Q

What is the chemotherapy for AML?

A

Daunorubicin and cytarabine

75
Q

What is the median age at diagnosis for CML?

A

60-65 years

76
Q

Which leukaemia is most associated with the Philadelphia chromosome?

A

CML

77
Q

What is the main association with CML?

A

Philadelphia chromosome - t (9;22) translocation

78
Q

What fusion gene does the Philadelphia chromosome form?

A

BCR/ABL fusion gene (on chromosome 22) which has tyrosine kinase activity

79
Q

Which drug is good at targeting conditions associated with the Philadelphia chromosome like CML?

A

Imatinib (tyrosine kinase inhibitor)

80
Q

What are the 3 stages of CML?

A

1) Chronic phase - asymptomatic for 4-5 years
2) Accelerated phase - getting increasingly anaemic and thrombocytopenia, more blasts taking up blood and bone marrow
3) Blastic phase - blastic transformation (AML)

81
Q

What are some clinical features of CML?

A

Fatigue, night sweats, weight loss, hepatosplenomegaly, fever, symptoms of anaemia

82
Q

What is seen on the blood film of CML?

A

All stages of maturation

83
Q

What is seen on the bone marrow biopsy of CML?

A

Hypercellular, excess myeloid cells

84
Q

How do you manage CML?

A

Imatinib, 2nd gen BCR-ABL inhibitors like dasatinib, hydroxycarbimide, bone marrow/stem cell transplant

85
Q

What is the median survival for CML?

A

5-6 years

86
Q

What is CLL?

A

Progressive accumulation of a malignant clone of functionally incompetent B cells

87
Q

What is the median age at diagnosis for CLL?

A

72 years

88
Q

How does CLL present?

A 
Often asymptomatic
Infection prone
Fatigue
B symptoms
Lymphadenopathy
Splenomegaly
89
Q

What is seen on the blood film for CLL?

A

Smudge cells, lymphocytosis

90
Q

What investigations are needed in CLL?

A

FBC, blood film, bone marrow biopsy, flow cytometry (CD5, CD19, CD20, CD23)

91
Q

What is the natural history of CLL?

A

1/3rd never progress
1/3rd progress slowly
1/3rd progress actively

92
Q

What is Richter’s syndrome?

A

Transformation from CLL to high grade lymphoma

93
Q

How do you treat CLL if indicated?

A

FLudarabine + rituximab + cyclophosphamide
Radiotherapy for lymphadenopathy and splenomegaly
Steroids reduce autoimmune haemolysis
Transfusions when needed
Human IV IG for recurrent infections

94
Q

What are the 3 main myeloproliferative disorders?

A

Polycythaemia vera, essential thrombocythaemia and myelofibrosis

95
Q

What mutations are myeloproliferative disorders associated with?

A

JAK2 (main one)
MPL
CALR

96
Q

Give an example of a JAK2 inhibitor

A

Ruxolitinib

97
Q

What is polycythaemia vera?

A

Malignant proliferation of pluripotent stem cell - excess red blood cells, white blood cells and platelets

Leads to hyperviscosity and thrombosis

98
Q

In what percentage of polycythaemia vera cases is the JAK2 mutation present?

A

> 95%

99
Q

How does polycythaemia vera present?

A 
May be asymptomatic
Headaches, dizziness, visual disturbance (hyperviscosity)
Pruritis - especially after a hot bath
Erythromelalgia
Splenomegaly
Facial plethora
100
Q

What does the bone marrow biopsy show in polycythaemia vera?

A

Hypercellularit with erythroid hyperplasia

101
Q

What investigations would you do in polycythaemia vera?

A

FBC - shows increased all cells
Bone marrow biopsy
Serum erythopoietin would be low

102
Q

How do you mange polycythaemia vera?

A

Venesection in younger people
Hydroxycarbamide
Aspirin 75mg

103
Q

What can polycythaemia transform into?

A

Myelofibrosis in 30%

Acute leukaemia in about 5%

104
Q

What is essential thrombocythaemia?

A

Clonal proliferation of megakaryocytic leading to persistently high platelets

105
Q

How does essential thrombocythaemia present?

A 
Asymptomatic in 50%
Thrombosis
Haemorrhage (if >1500)
Splenomegaly
Headache
Syncope
106
Q

How do you manage essential thrombocythaemia?

A

Plateletphoresis, aspirin 75mg, hydroxycarbimide

107
Q

What can essential thrombocythaemia transform into?

A

Myelofibrosis or polycythaemia vera

108
Q

What are some secondary causes of high platelets?

A

Bleeding, surgery, iron deficiency, inflammation, infection, trauma

109
Q

What is myelofibrosis?

A

Hyperplasia of megakaryocytes - produces platelet-derived growth factor - intense marrow fibrosis and haematopoiesis in the spleen (massive hepatosplenomegaly)

110
Q

How does myelofibrosis present?

A 
Weight loss
Night sweats
Fever
SPLENOMEGALY
Bone marrow failure (anaemia, infections, bleeding)
Bone pain
111
Q

What is seen on the blood film in myelofibrosis?

A

Characteristic teardrop RBCs

112
Q

How do you manage myelofibrosis?

A 
Folic acid and vitamin B6
Cytoreductive drugs
Allopurinol
JAK-2 inhibitors
Splenectomy
Stem cell transpolant
113
Q

What are the two peaks of Hodgkins lymphoma?

A

Young adults in 3rd decade and over 70s

114
Q

What are some risk factors for Hodgkins lymphoma?

A

EBV infection, mononucleosis, HIV

115
Q

What are the characteristic cells in Hodgkins lymphoma?

A

Reed-Sternberg cells (multinucleate giant cells)

116
Q

How does Hodgkins lymphoma present?

A 
Enlarged painless lymph node
B symptoms
Pruritis
Alcohol induced lymph node pain
Hepatosplenomegaly
117
Q

How do you investigate Hodgkins?

A 
FBC
Blood film
LDH, urate, ESR
Lymph node biopsy (excision node biopsy) 
Chest X ray 
CT/PET for staging
118
Q

What is the Ann Arbor staging?

A

I - Confined to single lymph node region
II - 2 or more areas on the same side of diaphragm
III - nodes on both sides of the diaphragm
IV - spread beyond nodes eg liver, bone marrow

A - no symptoms
B - fever, night sweats, weight loss >10% in 6 months

119
Q

What is the chemotherapy for Hodgkins lymphoma?

A

ABVD - adriamycin (doxorubicin), bleomycin, vincristine and dacarbazine

120
Q

What are some complications of the treatment Hodgkins?

A

Infertility, secondary cancers, AML, hypothyroidism from radiotherapy

121
Q

What percentage of Non Hodgkins lymphomas are B cell vs T cell?

A

70% B cell, 30% T cell

122
Q

What are the main high grade non Hodgkins lymphomas?

A

Diffuse large B cell lymphoma, Burkitt’s lymphoma, mantle cell lymphoma

123
Q

What are the main low grade non Hodgkins lymphomas?

A

Follicular lymphoma, MALT lymphoma, waldenstroms

124
Q

What are some risk factors for non Hodgkins lymphoma?

A

HIV, immunodeficiency, EBV, HTLV-1, H pylori

125
Q

How can low grade lymphomas present?

A

Painless, slowly progressive lymphadenopathy
B symptoms
Hepatosplenomegaly
Pancytopenia

126
Q

How can higher grade lymphomas present?

A

Rapidly growing and rapid lymphadenopathy
B symptoms
Hepatosplenomegaly
Obstructive hydronephrosis secondary to retroperitoneal lymphadenopathy

127
Q

How may burkitts lymphoma present?

A

Large abdominal mass and symptoms of bowel obstruction

128
Q

How is high grade non Hodgkins lymphoma managed?

A

Rituximab, Cyclophosphamide, Hydroxydaunorubicin, Vincristine and Prednisolone

129
Q

What is rituximab?

A

Monoclonal antibody against B cells - anti CD20

130
Q

What is myeloma?

A

Malignant proliferation of the plasma cells of the bone marrow - overproduction of a monoclonal antibody - organ dysfunction

131
Q

Which is the commonest myeloma>

A

IgG (2/3rds) followed by IgA (1/3)

132
Q

What is the peak age of onset of myeloma?

A

70 years

133
Q

Which ethnicity is myeloma more common in?

A

Black

134
Q

What are the clinical features of myeloma?

A
  • Hypercalcaemia
  • Anaemia, neutropenia or thrombocytopenia
  • Renal impairment
  • Osteolytic bone lesions
  • Recurrent bacterial infections
135
Q

Why is there renal impairment in myeloma?

A

Due to deposition of light chains in the renal tubules, Hypercalcaemia and hyperuricaemia

136
Q

How do you investigate myeloma?

A
  • FBC, ESR, Plasma viscosity
  • Calcium, U+Es, creatinine
  • Serum protein electrophoresis
  • Urine electrophoresis - bence jones protein
  • Bone marrow biopsy - increased plasma cells
  • Serum free light chain assay
  • Whole body MRI scan or low dose CT
  • X-ray - pepper pot skull, fractures, vertebral collapse
137
Q

How is myeloma managed?

A

Supportive - analgesia for bone pain, transfusion, orthopaedic procedures, rehydration

Chemotherapy - lenolidomide, bortezomib and dexamethasone

Autologous stem cell transplant

138
Q

What are the complications of myeloma?

A

Hypercalcaemia
Spinal cord compression
Hyperviscosity
AKI

139
Q

What are the vacancies of the immunoglobulins?

A

IgM - pentimer - increased risk of hyperviscosity
IgA - dimer
IgG - single

140
Q

What immunoglobulin is associated with waldenstroms macroglobulinaemia?

A

IgM - risk of hyperviscosity

Cancer care (3 decks)

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