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Year 3 > MedED blood cancers and disorders > Flashcards

MedED blood cancers and disorders Flashcards

1
Q

What do all RBCs originate from?

A

Haematopoeitic stem cells

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2
Q

What are the 2 types of haematopoeitic stem cells?

A

Myeloid stem cells

Lymphoid stem cells

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3
Q

What do myeloid stem cells give rise to?

A 
Platelets
RBCs
Basophil
Neutrophil
Eosinophil
Monocyte
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4
Q

What do lymphoid stem cells give rise to?

A

Natural killer cells
T lymphocytes
B lymphocytes

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5
Q

What are the 3 main categories of blood cancers?

A

Leukaemia
Lymphomas
Others

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6
Q

What are the types of leukaemia?

A

Myeloid

Lymphoid

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7
Q

What are the types of lymphoma?

A

Hodgkin

Non hodgkins

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8
Q

What type of cell is there an increase of leukaemia?

A

WBC

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9
Q

What is the key difference between lymphoma and leukaemia?

A

The location of WBCs- were they arise and end up
Leukaemia- originates in the bone marrow
Lymphoma- originates from the lymphocytes themselves (in lymph nodes and lymphatic tissue)

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10
Q

Where are cancer cells in leukaemia likely to be found?

A

In bones and blood

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11
Q

Where are cancer cells in lymphoma likely to be found?

A

Lymph nodes and other lymphatic tissues

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12
Q

How can leukaemia be classified?

A

By onset: chronic or acute

By lineage: myeloid or lymphoid

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13
Q

Why is leukaemia disruptive?

A

The extra cells produced are not useful and crowd out the bone marrow so other useful cells cannot be produced

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14
Q

What are the 4 main types of leukaemia?

A

Acute lymphoid
Acute myeloid
Chronic lymphoid
Chronic myeloid

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15
Q

Out of acute and chronic leukaemia which is more severe?

A

Acute

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16
Q

What type of blood cells arise in acute vc chronic leukaemia?

A 
Acute= immature blood cells 
Chronic= mature white blood cells
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17
Q

What leukaemia is more common in children?

A

Acute lymphoblastic

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18
Q

What leukaemia is more common in adults?

A

Chronic myeloid

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19
Q

How is differentiation of cells in acute vs chronic leukaemia different?

A 
Acute= abnormal differentiation
Chronic= normal (ish) differentiation
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20
Q

What cells proliferate in acute myeloid leukaemia?

A

Myeloblasts

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21
Q

What are the features of acute myeloid leukaemia?

A

Neutropenia
Anaemia
Thrombocytopenia

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22
Q

What happens to the pathway of blood cell differentiation once there is a mutation in one cell?

A

The cells downstream are not produced

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23
Q

What are the risk factors for acute myeloid leukaemia?

A

Increasing age
Downs syndrome
Irradiation
Anti cancer drugs

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24
Q

What are the 2 categories of signs and symptoms of acute myeloid leukaemia?

A

Bone marrow failure

Tissue infiltration

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25
Q

What are the signs and symptoms of acute myeloid leukaemia?

A

Bone marrow failure= pallor, bleeding, infections

Tissue infiltration= swollen gums, mild splenomegaly

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26
Q

What symptom is characteristic of acute myeloid leukaemia and helps differentiate it from other blood cancers?

A

Bleeding gums

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27
Q

What is the buzz word for acute myeloid leukaemia?

A

Auer rods- seen on cytology

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28
Q

What are auer rods?

A

They are seen on cytology in acute myeloid leukaemia

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29
Q

What is acute promyelocytic leukaemia?

A

A hyper agressive AML

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30
Q

What is the genetic translocation for acute promyelocytic leukaemia?

A

t(15;17) fuses the PML gene with the RAR- alpha gene

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31
Q

What is seen on cytology in acute promyelocytic leukaemia?

A

Faggot cells- lots of auer rods

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32
Q

What cell proliferates in acute lymphoid leukaemia?

A

Lymphoblasts

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33
Q

What are risk factors for ALL?

A

More common in children

People who are genetically prone and then they get influenza

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34
Q

What are the 2 catagories of signs and symptoms of ALL?

A

bone marrow failure

tissue infiltration

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35
Q

What are the signs and symptoms of ALL?

A

Bone marrow failure= pallor, bleeding, infections

Tissue infiltration= lymphadenopathy, hepatosplenomegaly, swollen testes, tender bones

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36
Q

In ALL what % lymphoblasts will be seen on bone marrow biopsy?

A

20%

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37
Q

What proliferates in CML?

A

Granulocyte precursors (which also mature into granulocytes)

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38
Q

What are features of CML?

A

Bone marrow failure
Hypermetabolism
Hyperviscosity

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39
Q

What is the difference in cells in AML vs CML?

A

In CML there are mature cells produced too- differentiation continues

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40
Q

What are the 3 phases in CML?

A

Chronic phase, accelerated phase and blast crisis

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41
Q

Out of males and females who is more likely to get CML?

A

Males

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42
Q

What chromosome is involves in CML?

A

Philadelphia chromosome

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43
Q

What fusion gene is made in CML?

A

t(9:22) BCR-ABL1 fusion gene

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44
Q

What is the hallmark of CML and why?

A

Massive splenomegaly- there is time for the cells to accumulate in the spleen

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45
Q

What are signs and symptoms of CML?

A

Massive splenomegaly
Hypermetabolic symptoms= weight loss, malaise, sweating
Bone marrow failure= pallor, bleeding and infections
Hyperviscosity= thrombotic events, headaches

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46
Q

What cells are accumulate in CLL?

A

Incompetent lymphocytes

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47
Q

What is there a failure of in CLL?

A

Failure of apoptosis of CLL

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48
Q

What is the least concerning type of leukaemia?

A

CLL

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49
Q

Out of men and women who is more likely ot get CLL?

A

Men

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50
Q

What are signs and symptoms of CLL?

A

50% of patients are asymptomatic
Occasional non tender lymphadenopathy
Occasional bone marrow failure symptoms

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51
Q

What is the hallmark of CLL?

A

Smudge/ smear cells on blood film

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52
Q

How is CLL diagnosed?

A

Usually on routine blood test when there is lymphocytosis

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53
Q

What are some investigations for leukaemia?

A

First line blood test: FBC, LDH (tumor marker for lots of cancers), blood smear
Biopsy: bone marrow aspirate
Other tests include immunophenotyping (to see what type of specific cancer is it) or CXR

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54
Q

What buzz word should you remember for AML?

A

Auer rods

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55
Q

What buzz word should you remember for ALL?

A

Child under 6

56
Q

What buzz word should you remember for CML?

A

Philadelphia chromosome

57
Q

What buzz word should you remember for CLL?

A

Smudge/ smear cells

58
Q

How is leukaemia managed?

A

First line chemotherapy

Second line bone marrow transplant

59
Q

How do patients with lymphoma classically present?

A 
With a lump
Systemic symptoms (or B symptoms) too like fever, weight loss, night sweats
60
Q

What is a main subtype of non hodgkin’s lymphoma?

A

Burkitt’s lymphoma

61
Q

What virus is HL commonly associated with?

A

EBV

62
Q

What are signs and symptoms of hodgkin’s lymphoma?

A

Painless enlarging neck mass which may become painful after drinking alcohol
B symptoms
Non tender, firm, rubbery lymphadenopathy with splenomegaly and they may not have hepatomegaly

63
Q

What will be seen on lymph node biopsy in HL?

A

Reed-sternberg cells (bi nucleate lymphocytes)

64
Q

What type of lymphoma is more common?

A

Non hodgkins

65
Q

What type of cell is NHL?

A

85% b cell

15% t cell or NK cell

66
Q

What are some risk factors for NHL?

A

EBV, HIV, SLE, Sjogren’s syndrome

Increasing age

67
Q

What are signs and symptoms of NHL?

A

Painless enlarging mass in neck, axilla or groin
B symptoms (less common than in HL)
Organ involvement- skin rash, headache, hepatosplenomegaly (more common than in HL)

68
Q

What is the best way to differentiate NHL and HL?

A

In NHL there will be no Reed-Sternberg cells on lymph node biopsy

69
Q

What are some ways to differentiate NHL and HL?

A

In NHL there will be no reed sternberg cells on blood film
B symptoms are less common than in HL
Organ involvement is more common eg skin rashes, headache, hepatosplenomegaly

70
Q

What are risk factors for burkitt lymphoma?

A

EBV infection
Chronic malaria- this reduces resistance to EBV
HIV

71
Q

How does burkitt lymphoma classically present?

A

A rapidly enalrging lymph node in the jaw

72
Q

What will burkitt lymphoma look like under microscopy?

A

Starry sky appearance

73
Q

What is the buzz word for burkitt lymphoma?

A

Starry sky appearance under microscopy

74
Q

What system is used to stage lymphoma?

A

Ann Arbor staging system

75
Q

How is lymphoma managed?

A

First line chemotherapy

76
Q

What is a common complication of treating blood cancer?

A

Tumor lysis syndrome

77
Q

What is tumor lysis syndrome?

A

Metabolic abnormalities that arise due to cancer treatment, especially leukaemia and lymphoma

78
Q

What is commonly released in tumor lysis syndrome from cancer cells?

A

Phosphate, uric acid and potassium

79
Q

What does the release of phosphate in tumor lysis syndrome lead to?

A

Calcium phosphate crystals are formed

This causes kidney failure and hypocalcaemia

80
Q

What does the release of uric acid in tumor lysis syndrome lead to?

A

Urate crystals causing gout

81
Q

What does the release of potassium in tumor lysis syndrome lead to?

A

Hyperkalemia which causes arrhythmia

82
Q

What is there proliferation of in multiple myeloma?

A

Plasma cells

83
Q

What is produced in multiple myeloma and why?

A 
Monoclonal immunoglobulin (IgG and IgA)
There is proliferation of plasma cells and these produce antibodies
84
Q

What are risk factors for multiple myeloma?

A

Increasing age

Argicultural workers exposed to herbicides/ pesticides

85
Q

What acronym is used to remember signs and symptoms of multiple myeloma?

A

CRAB

86
Q

What are signs and symptoms of multiple myeloma? Explain why they arise

A

C- high calcium= bones, stones, abdominal groans
R- renal impairment
A- anaemia= due to bone marrow crowding (there is also less production of polyclonal IgG which leads to more infections)
B- bone lesions= there is signalling which increases osteoclast activation causing back and rib pain

87
Q

What are investigations for multiple myeloma?

A

First line bloods= DO ALP (will be normal in multiple myeloma so you know its not a bone cancer), raised ESR, CRP, Cr, CA
Blood film= will show rouleaux formation
Serum/ urine electrophoresis= shows bence jones proteins
Bone marrow aspirate= plasma cells will be raised more than 10%

88
Q

What is the buzz word for multiple myeloma?

A

Bence jones proteins

89
Q

How diagnostic are bence jones proteins for multiple myeloma?

A

They are not sensitive or specific but when present alongside hypercalcaemia, kidney failure, anaemia and bone pain are highly diagnostic

90
Q

What is MGUS?

A

Monoclonal gammopathy of unknown significance
It is a pre malignant condition where there is accumulation of some monoclonal plasma cells and it may lead to multiple myeloma
CRAB features will be absent

91
Q

What is myelodysplasia?

A

A group of syndromes where immature blood cells do not mature normally

92
Q

What are the 2 causes of myelodysplasia?

A 
Primary= intrinsic bone marrow problem
Secondary= previous chemo/radiotherapy
93
Q

What does myelodysplasia cause?

A

Bone marrow failure= chronic pancytopenia (anaemia, neutropenia and thrombocytopenia)

94
Q

What are the features of bone marrow failure?

A

Anaemia
Thrombocytopenia
Neutropenia

95
Q

What is the buzz word for myelodysplasia?

A

anaemia with RINGED SIDEROBLASTS

96
Q

What are bence jones proteins?

A

Monoclonal Ig light chain antibodies (can be found in the urine)

97
Q

What are the 2 stages of wound healing?

A

Primary haemostasis

Secondary haemostasis

98
Q

What is primary haemostasis?

A

Platelet aggregation and plug formation

99
Q

What is secondary haemostasis?

A

Fibrin formation to stabilise the platelet plug

100
Q

What does primary haemostasis depend on?

A

VWF

101
Q

What does secondary haemostasis depend on?

A

Clotting factors

102
Q

What type of disorder does disruption of primary haemostasis cause?

A

Superficial bleeding

103
Q

What type of disorder does disruption of secondary haemostasis cause?

A

Deep bleeding and bruising

104
Q

What test measures the intrinsic pathway?

A

APTT

105
Q

What test measures the extrinsic pathway?

A

PT

106
Q

What clotting factors are involved in the intrinsic pathway?

A

XII, XIIa
XI, XIa
IX, IXa
VIII

107
Q

What clotting factors are involved in the extrinsic pathway?

A

VIIa

108
Q

What is haemophilia?

A

A bleeding disorder caused by the inherited deficiency of a clotting factor

109
Q

What stage of haemostasis is involved in haemophilia?

A

Secondary- it involves deficiencies in clotting factors

110
Q

What type of bleeding is present in haemophilia?

A

Deep bleeding and bruising

111
Q

What gender does haemophilia mainly affect and why?

A

Males- it is X linked recessive

112
Q

What are the 2 types of haemophilia?

A

A and B

113
Q

What type of haemophilia is more common?

A

A

114
Q

What is deficient in haemophilia A?

A

Factor 8

115
Q

What is deficient in haemophilia B?

A

Factor 9

116
Q

At what age does haemophilia usually present?

A

Early or after surgery

117
Q

What is the buzz word for haemophilia?

A

Haemarthosis

118
Q

How does haemophilia present?

A

Haemarthrosis= bleeding into joints which are swollen and painful
Haematoma= painful bleeding into muscles
Excessive bruising and haematuria

119
Q

What investigations are done to diagnose haemophilia?

A

Factor assay is done to diagnose it

APTT will be pronged

120
Q

What clotting pathway does haemophilia affect?

A

Intrinsic

121
Q

What are some roles of VWF?

A

Platelet adhesion- forms bridges between damaged subendothelium and platelets via GP1b receptor
Platelet aggregation- facilitates platelets binding to each other
Factor 8 stabilisation- binds to factor 8 and prevent degredation

122
Q

What is type 1 von willebrand syndrome?

A

Reduced levels of normal VWF

123
Q

What is type 2 von willebrand syndrome?

A

Adequate levels of defective VWF

124
Q

What is type 3 von willebrand syndrome?

A

Complete lack of VWF and reduced factor 8

125
Q

How are type 1, 2 and 3 von willebrand syndrome inherited?

A

1 and 2= autosomal dominant

3= autosomal recessive

126
Q

How does VWD classically present?

A

Superficial bleeding eg bruising, nosebleeds, heavy periods, prolonged gum bleeding, prolonged bleeding from minor wounds

In type 3 it is more severe and reduced factor 8 causes deep bleeding into joints and soft tissues

127
Q

How is VWD diagnosed?

A

Depends on type of syndrome
type 1= prolonged bleeding time, reduced VWF, normal platelets
type 2= prolonged bleeding time, normal VWF, normal platelets
type 3= prolonged bleeding time, reduced VWF, normal PT but prolonged APPT due to lack of factor 8, normal platelets

128
Q

What DIC?

A

When an underlying condition causes up regulation of the clotting cascade

129
Q

What happens in DIC?

A

There are blood clots in parts of the body where they are not needed
You are also prone to bleeding because platelets and clotting factors are being used up where they aren’t needed

130
Q

What is deposited in DIC?

A

Fibrin

131
Q

What are the 3 main issues in DIC?

A

Blood clots in the body where you dont need them
Being prone to bleeding as platelets and clotting factors are used up
Deposition of fibrin cutting up RBCs causing anaemia

132
Q

How is DIC classified?

A

By onset
Acute overt= emergency and life threatening, significant platelet and clotting factor depletion presenting with bleeding
Chronic non overt= slower rate, with time for compensatory responses, present more with clotting less with bleeding

133
Q

What is the difference between presentation of acute overt and chronic non overt DIC?

A

acute overt= presents with bleeding and is an emergency

chronic non overt= presents with clotting

134
Q

How does DIC classically present?

A

Signs of underlying pathology eg cancer, sepsis, pregnancy
Acute DIC= bleeding issues (petechiae, purpura, epistaxis etc), respiratory distress
Chronic DIC= DVT or arterial thrombosis

135
Q

How is DIC diagnosed?

A

FBC= low platelets and HB
Clotting= low fibrinogen, high fibrin degredation products, prolonged PT and APTT
Blood film= schistocytes

136
Q

What is a buzz word for DIC?

A

Shistocytes

137
Q

How is DIC managed?

A

Treat underlying cause

Give platelets, fresh frozen plasma and fibrinogen

Year 3 (104 decks)

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