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Haematology Flashcards

1
Q

What cells are characteristic of Hodgkin’s lymphoma?

A

Reed-Sternburg Cells (multinucleate giant polymorphic cells)

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2
Q

What 2 age groups are most likely to have Hodgkin’s lymphoma?

A

Teenager/Young adult

Elderly

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3
Q

Main presentation of Hodgkin’s lymphoma?

A 
Lymphadenopathy - enlarged, painless, non-tender, rubbery superficial lymph nodes
Cervical > Axilla > Inguinal
Cyclical fever
Constitutional B cell symptoms
Worsening symptoms after alcohol
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4
Q

What staging system is used for Hodgkin’s lymphoma?

A

Ann Arbor staging system

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5
Q

What is the treatment for Hodgkin’s lymphoma?

A

Combination chemotherapy (ABVD)

  • Adriamycin (doxorubicin)
  • Bleomycin
  • Vinblastine
  • Dacarbazine
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6
Q

Why are lymphomas more likely to be B cell in origin rather than T cell?

A 
Because B cells undergo class switching and somatic hypermutation in response to invading pathogen.
These processes involve DNA replication and the more DNA replication there is, the more opportunity for mutations to occur. 
T cells do not undergo replication to the same extent.
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7
Q

What cells make antibodies?

A

Plasma cells

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8
Q

Risk factors for Hodgkin’s lymphoma?

A 
Affected sibling
EBV
SLE?
Immunosuppression eg post-transplantation, HIV
Obesity
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9
Q

Risk factors for Non-Hodgkins lymphoma?

A 
Immunodeficiency eg drugs, HIV
HTLV-1
H.pylori
Toxins
Congenital
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10
Q

What haematological malignancy is associated with coeliac disease?

A

Small bowel T cell lymphoma

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11
Q

Which age groups are more likely to have Non-Hodgkins lymphoma?

A

Incidence increases with age

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12
Q

Extranodal presentations of Non-Hodgkin’s lymphoma?

A

Skin - T cell lymphoma
Oropharynx - Waldeyer’s ring lymphoma
Gut - Gastric MALT, Non-MALT gastric lymphomas and small bowel lymphomas

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13
Q

Types of cytopenia?

A 
Anaemia
Thrombocytopenia
Neutropenia
Leukopenia
Pancytopenia
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14
Q

What is the treatment of Non-Hodgkin’s lymphoma?

A 
Combination chemotherapy (R-CHOP)
-Rituximab
-Cyclophosphamide
-Hydroxydaunomycin (doxorubicin)
-Vincristine 
-Prednisolone
Just CHOP for T cell lymphomas
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15
Q

For how long does the patient need to be anticoagulated for DVT and PE?

A

DVT - 3 months

PE - 6 months

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16
Q

What is the definition of multiple myeloma?

A

Clonal proliferation of plasma cells

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17
Q

How is multiple myeloma diagnosed?

A

Serum electrophoresis

Bone marrow biopsy

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18
Q

What are the symptoms of multiple myeloma?

A

C - Hypercalcaemia - stone, bones, groans, thrones, moans
R - Renal failure - N+V, weight loss, lethargy (Uraemia)
A - Anaemia (+thrombocytopaenia - causes viscous blood and soft tissue swelling)
B - Bone lesions - bone pain
I - Recurrent infections

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19
Q

What are the symptoms of hypercalcaemia?

A

Stones - renal stones
Bones - Ostetitis fibrosa cystica, arthritis, osteoporosis
Groans - Constipation, indigestion, nausea and vomiting
Thrones - Constipation and polyuria
Psychiatric moans - Depression, lethargy, psychosis, fatigue, delirium

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20
Q

What is seen on FBC in a patient with myeloma?

A

Normochromic, normocytic anaemia

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21
Q

What are the 3 conditions on the myeloma spectrum?

A

MGUS - multiple gammaopathy of undetermined significance
Asymptomatic myeloma
Multiple myeloma

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22
Q

What is the difference between MGUS and asymptomatic myeloma?

A

Plasma cells are <10% in MGUS and >10% in Asymtomatic myeloma

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23
Q

What does the tallest peak seen on serum electrophoreses represent?

A

Albumin

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24
Q

What genetic abnormality is commonly seen in CML patients?

A

Philadelphia chromosome - reciprocal translocation between chromosome 9 and 22. Results in BCR-ABL fusion gene, which activates tyrosine kinase.

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25
Q

What haematological malignancy is related to Philadelphia chromosome?

A

CML

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26
Q

Name 4 types of myeloproliferative disorders and the cells they derive from?

A

Polycythaemia - RBC
CML - WBC
Essential thrombocytopenia - platelets
Myelofibrosis - Fibroblasts

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27
Q

What are the symptoms of CML?

A

Chronic and insidious constitutional symtoms eg Weight loss, fever, sweats
+/- Gout
+/- Abdominal discomfort (splenomegaly)
+/- Bleeding/bruising (platelet dysfunction)

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28
Q

Treatments for CML

A

Imatinib - Specific BCR-ABL tyrosine kinase inhibitor

Bone marrow transplant - only cure

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29
Q

Treatment for Essential Thrombocytosis

A

Low dose aspirin

Hydroxycarbamide

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30
Q

Secondary causes of thrombocytosis

A

Iron deficiency
Infection/inflammation
Trauma
Bleeding

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31
Q

Difference between absolute and relative polycythaemia

A

Relative - normal RBC, low plasma volume eg due to dehydration
Absolute - Chronic due to hypertension, obesity, smoking, alcoholism

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32
Q

Secondary causes of polycythaemia

A

Hypoxia - high altitudes, congenital heart disease, chronic lung disease, heavy smoking
Increased erythropoietin secretion - renal or hepatocellular carcinoma

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33
Q

What is polycythaemia rubra vera?

A

Primary polycythaemia due to JAK2 mutation resulting in excess proliferation of RBCs, WBCs and platelets, leading to hyper viscosity and risk of thrombosis.
Independent of EPO

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34
Q

What is erythropoietin?

A

A glycoprotein cytokine produced by interstitial fibroblasts in the kidney in response to hypoxia to simulate the production of red blood cells

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35
Q

How can primary and secondary polycythaemia be determined?

A

Serum erythropoietin
Primary - Low
Secondary - High

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36
Q

How is polycythaemia rubra vera treated?

A

Venesection
Hydroxycarbamide
Low dose aspirin

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37
Q

Symptoms of hyper viscosity that may be seen in polycythaemia rubra vera?

A 
Headaches
Dizziness
Tinnitus
Visual disturbance
Itch after hot bath
Erythromelalgia – burning sensation in fingers and toes
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38
Q

What does bone marrow biopsy show in polycythaemia rubra vera?

A

Hyper cellularity (more cells), erythroid hyperplasia (RBC precursors)

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39
Q

What is myelofibrosis?

A

Hyperplasia of megakaryocytes which produce platelet derived growth factor and results in bone marrow fibrosis and myeloid metaplasia.

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40
Q

What conditions can polycythaemia rubra vera progress to?

A

Myelofibrosis

AML

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41
Q

What is seen on blood film for myelofibrosis

A

Teardrop RBCs

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42
Q

What are myelodysplastic syndromes?

A

A group of disorders characterised by bone marrow failure (pancytopenia), either primary or secondary (post chemo or radiotherapy) in cause. Can progress to AML.

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43
Q

What cells are characteristic of myelodysplastic syndrome?

A

Ring sideroblasts

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44
Q

Symptoms of AML

A

Bone marrow failure: bleeding (low platelets), bruising, infection (low WCC), anaemia (low Hb)
Infiltration: hepatosplenomegaly, gum hypertrophy, skin involvement

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45
Q

What cell type, seen on microscopy, is diagnostic of AML?

A

Auer rods

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46
Q

Which age group is most at risk of AML?

A

Incidence increased with age, most commonly affects people 50-60yrs

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47
Q

What is the treatment for AML?

A

Suuportive care
Chemotherapy (daunorubicin and cytarabine)
Bone marrow transplant

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48
Q

How is AML diagnosed?

A

Bone marrow biopsy

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49
Q

Which pathway of the coagulation cascade results in prolonged APTT?

A

Intrinsic

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50
Q

Which pathway of the coagulation cascade results in prolonged PT?

A

Extrinsic

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51
Q

Which factor deficiency causes a prolonged APTT but has no associated bleeding risk?

A

Factor 12

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52
Q

How does factor 13 deficiency first present?

A

Continuous oozing of umbilical cord

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53
Q

Which clotting factors are vitamin k dependant?

A

2,7,9,10

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54
Q

What condition is also known as Christmas disease?

A

Haemophilia B

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55
Q

Which factors are deficient in Haemophilia A and B?

A

A - Factor 8

B - Factor 9

56
Q

What type of inheritance pattern does Haemophilia have?

A

X-linked recessive

57
Q

Which clotting test will be abnormal in haemophilia A?

A

APTT - increased because factor 8 is part of the intrinsic pathway

58
Q

How can you tell if anaemia is due to bone marrow failure or not?

A

Low reticulocytes = bone marrow failure

High reticulocytes = other cause

59
Q

Treatments for Haemophilia A other than recombinant factor 8?

A

Analgesia
Antifibrinolytics eg tranexamic acid
Desmopressin

60
Q

How does desmopressin work in haemophilia?

A

Promote the release of von Willebrand factor with subsequent increase in factor VIII survival secondary to vWF complexing

61
Q

Characteristic appearance of skull xray in myeloma?

A

Pepperpot skull

62
Q

What is the management of vitamin B12 deficiency?

A

If neurological involvement - Hydroxocobalamin 1mg IM on alternate days indefinitely, switch to 3 monthly when no more improvement in neurological symptoms
If no neurological involvement - Hydroxocobalamin 1mg IM 3 times a week for 2 weeks, then 3 monthly

63
Q

What pathogens can precipitate an aplastic crisis in sickle-cell anaemia?

A

Parvovirus B19
Streptococcus
Epstein Barr Virus

64
Q

What does the triad of reticulocytopaenia, symptomatic anaemia and parvovirus IgM antibodies represent?

A

Aplastic crisis in sickle cell precipitated by Parvovirus B19

65
Q

Macrocytic anaemia + neurological symptoms = ?

A

B12 deficiency

66
Q

What investigation would you do for B12 deficiency?

A

Anti-intrinsic factor antibodies

67
Q

What cells produce intrinsic factor?

A

Parietal cells of the stomach

68
Q

Which cause of thrombpcytopaenia is associated with anti-platelet antibodies?

A

Idiopathic thrombocytopaenia purpura

69
Q

What is characterised by the triad of thrombocytopenia, prolonged PT, APTT and low fibrinogen levels?

A

Disseminated Intravascular Coagulation

70
Q

What are the haematological emergencies?

A

Sickle cell crisis

71
Q

Investigations in Hodgkin’s lymphoma?

A

Lymph node CORE NEEDLE biopsy
Imaging (CT)
Raised ESR, low Hb = worse prognosis

72
Q

What is seen on histology for Burkitt’s lymphoma?

A

Starry sky appearance

73
Q

What is seen on blood film ALL?

A

Blast cells

>20% = Acute haematological malignancy

74
Q

What investigations are done for ALL?

A

FBC (bone marrow suppression)
Clotting
Bone marrow aspiration and biopsy
LP - might be CNS involvement

75
Q

What cancer are people with Down’s syndrome at increased risk of?

A

ALL

76
Q

What are the poor prognostic factors for ALL?

A

Adult
Male
Philadelphia chromosome
CNS signs

77
Q

What cell type is affected in AML?

A

Myeloblasts

78
Q

What haematological malignancy present with swollen bleeding gums?

A

AML

79
Q

Which cells are affected in CML?

A

Granulocytes eg eosinophils, basophils, neutrophils

80
Q

What can CML progress to?

A

AML

81
Q

What is the commonest leukaemia?

A

CLL

82
Q

What cells are found on blood film for CLL?

A

Smudge cells (ruptured B cells)

83
Q

What haematological malignancy can present with recurrent shingles?

A

CLL

84
Q

What is the pathology if CLL?

A

Chromosomal abnormalities interfere with B-cell receptors so there is a build up of B lymphocytes and the avoid immunosurveillance and apoptosis

85
Q

What is seen on urine electrophoresis for myeloma

A

Bence Jones proteins (free immunoglobulin light chains)

86
Q

Diagnostic criteria for myeloma?

A

Monoclonal protein bands on serum electrophoresis
Increased plasma cells on bone marrow biopsy
Evidence of end organ damage

87
Q

What drug is used for the induction of treatment for multiple myeloma? What is a SE of it?
What other management options are there?

A

Bortezomib - peripheral neuropathy
(+dexamethasone)
High-dose therapy chemotherapy and stem cell transplant

88
Q

What adjuvant therapies are required in the management of myeloma?

A 
Flu vaccine
Acyclovir 
Bisphosphonates
LMWH (for thrombosis)
Ig replacement
89
Q

What are the features of bone marrow failure?

A

Anaemia
Bleeding
Infection

90
Q

Why is detecting infection in AML difficult?

A

Because AML itself can present with fever, common organisms present differently and few antibodies are made so cant be detected.

91
Q

What is the hallmark of CLL?

A

Accumulation of B cells that have evaded apoptosis and undergone cell cycle arrest in G0/G1 stage

92
Q

What are 3 complications of CLL?

A

Bone marrow failure
Infection due to hypogammaglobulinemia
Autoimmune haemolysis

93
Q

What staging system is used in CLL?

A

Rai Staging

94
Q

Why does ALL management involve intrathecal drugs?

A

Meningeal leukaemia prophylaxis

95
Q

What blood results indicate worse prognosis in Hodgkin’s lymphoma?

A

Increased ESR

Low Hb

96
Q

Causes of microcytic anaemia

A

Iron deficiency
Thalassaemia
Sideroblastic anaemia

97
Q

Causes of normocytic anaemia

A 
Haemolytic 
- Sickle cell disease
- Autoimmune haemolytic anaemia
- Hereditary spherocytosis
- G6PD deficiency
Pyruvate kinase deficiency
Non-haemolytic 
- Aplastic anaemia
- Chronic Kidney disease
- Chronic inflammatory disease
- Acute blood loss
- Pregnancy
98
Q

Causes of macrocytic anaemia

A 
Megaloblastic 
- Pernicious anaemia
- B12 deficiency
- Folate deficiency
- Fanconi anaemia
Non-megaloblastic 
- Hypothyroidism
99
Q

What symptoms are specific to iron deficiency anaemia?

A

Slow eating

Pica

100
Q

Investigations in iron deficiency anaemia

A

FBC: Low Hb, Low ferritin, Increased TIBC

Increased ZPP

101
Q

What is the inheritance pattern of thalassaemia?

A

Autosomal recessive

102
Q

How can you differentiate between alpha and beta thalassaemia?

A

Hb electrophoresis

103
Q

What chains make up normal adult and metal haemoglobin?

A

Adult: 2 x alpha and 2 x beta
Fetal: 2 x alpha and 2 x gamma

104
Q

On what chromosome is the beta haemoglobin gene?

A

Chromosome 11

105
Q

Symptoms of beta thalassaemia major

A 
Failure to thrive
Vomiting
Irritability
Jaundice
Bossing of skull
Maxillary overgrowth
106
Q

Management of beta thalassaemia major

A 
Lifelong RBC transfusions
Iron chelation (sub cut desoferrioxarmine)
Stem cell transplant
107
Q

What is beta thalassaemia?

A

Genetic mutation in beta haemoglobin chain so unable to produce normal adult haemoglobin.

108
Q

Complications of beta thalassaemia major?

A 
Hepatosplenomegaly
Cirrhosis
Infertility
Hyperpigmentation
Heart failure
109
Q

What is alpha thalassaemia?

A

Adults have 4 copies of alpha haemoglobin chain gene (2 x HbA1 and 2 x HbA2, one from each parent).
Abnormal alpha haemoglobin chains.
Manifestation depends on the number of the alpha haemoglobin genes affected.

110
Q

How does alpha thalassaemia major present?

A

Hydrops fetalis in 3rd trimester of pregnancy

111
Q

How is alpha thalassaemia major treated?

A

Intrauterine transfusions followed by lifelong monthly transfusions.

112
Q

What is the pathology of sickle cell disease?

A

Abnormal beta haemoglobin chains due to glutamine to valine amino acid substitution.

113
Q

What is the inheritance pattern of sickle cell disease?

A

Autosomal recessive

114
Q

4 subtypes of sickle cell disease?

A

HbSS - 2 copies of sickle haemoglobin chain mutation
HbSC - 1 copy of sickle haemoglobin chain mutation and 1 haemoglobin C gene mutation
Sickle beta thalassaemia - 1 copy of sickle haemoglobin mutation and 1 copy of beta thalassaemia gene
HbSA - 1 copy of sickle haemoglobin gene and 1 normal copy. Asymptomatic carrier with some protection against falciparum malaria

115
Q

Presentation of sickle cell disease

A 
Jaundice
Susceptibility to infection
Splenomegaly
Dactylitis
Priapism
Vaso-occlusive crises
116
Q

What is a vaso-occlusive crisis?

A

Acute bone pain from microvascular occlusion due to sickled RBC.

117
Q

What is the management of sickle cell disease?

A 
Prophylaxis - Daily oral penicillin and folic acid
Analgesia and fluids for acute crisis
Hydroxycarbamide 
Transfusions
Iron chelation therapy
Stem cell transplant
118
Q

What is a contraindication of hydroxycarbamide?

A

Pregnancy

119
Q

What patients are most commonly affected by sickle cell disease?

A

Afrocaribbeans

120
Q

What patients are most commonly affected by thalassaemia?

A

People from India, middle east and mediterranean countries.

121
Q

In what part of the GI tract is iron principally absorbed?

A

Duodenum

122
Q

What conditions are treated with venesection?

A

Polycythaemia rubra vera

Haemochromatosis

123
Q

What is the inheritance of sideroblastic anaemia?

A

X-linked recessive

124
Q

What is the most common inheritance of hereditary spherocytosis?

A

Autosomal dominant

125
Q

What is the inheritance of autoimmune haemolytic anaemia?

A

Autosomal recessive

126
Q

What are the acquired causes of autoimmune haemolytic anaemia?

A 
CLL
Non-Hodgkin's lymphoma
EBV
CMV
Hepatitis
HIV
127
Q

What is the most common gene mutation in heredity spherocytosis?

A

ANK1

128
Q

How do you tell between B12 and folate deficiency?

A

B12 has autoantibodies (if due to pernicious anaemia), neurological sequelae

129
Q

Vitamin K affects which coagulation factors?

A

II, VII, IX, X

130
Q

Deficiency in which factors cause prolonged aPTT?

A

Those involved in the intrinsic pathway.

XII, XI, IX, VIII

131
Q

Prolonged PT means there is a deficiency in which possible factors?

A

Extrinsic pathway VII, V

132
Q

Causes of schistocytes on blood film

A

DIC
TTP
HUS

133
Q

What is Felty’s syndrome?

A

Triad:
RA
Splenomegaly
Neutropaenia

134
Q

Which causes schistocytes?

A

TTP
HUS
DIC
Mechanical valve

135
Q

What does desmopressin do?

A

Stimulates release of vWF

136
Q

Which cancers cause raised erythropoietin?

A

Renal carcinoma

Hepatocellular carcinoma

137
Q

What conditions are treated with IV Ig?

A 
Kawasaki's disease
Multiple Myeloma
Guillain Barre Syndrome
Lambert Eaton Syndrome
Immune Thrombocytopaenic Purpura

Specialties (7 decks)

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