Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Year 5 Pathology Overview > Haematology > Flashcards

Haematology Flashcards

1
Q

In which type of leukaemia is lymphadenopathy most common?

A

CML

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Which type of leukaemia may produce CNS symptoms or testicular swelling?

A

ALL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Which tests are required to make a diagnosis of ALL?

A

Flow cytometry

BM biopsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the presence of an Auer Rod on blood film diagnostic of?

A

AML

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

In which haematological malignancy might “faggot cells” be present?

A

AML

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Which translocation is associated with APML?

A

T(15;17)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Which haematological malignancy is most likely to present with DIC?

A

APML

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the mainstay of treatment in APML?

A

ATRA (All-trans retinoic acid)

This forces cells to differentiate and hals proliferation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Which hamatological malignancy is most likely to present with LUQ pain?

A

CML - due to splenomegaly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Recall 4 features of the blood film that may be seen in CML

A

Leukocytosis
Eosinophilia
Basophilia
Left shift

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Which haematological malignancy may have hypolobated megakaryocytes in the bone marrow?

A

CML

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Which translocation produces the philadelphia chromosome?

A

T(9;22)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Which haematological malignancies are associated with the Philadelphia Chromosome?

A

Comminly CML

20-30% ALL in adults

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the mainstay treatment of CML?

A

Tyrosine kinase inhibitors
There are 3rd generation
Imatinib is an example of a first gen TKI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Which haematological malignancy is most likely to present with ITP/ haemolysis?

A

CLL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Smear/ smudge cells may be seen in which haematological malignancy?

A

CLL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How is CLL diagnosed?

A

Flow cytometry

This identifies light chain restriction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How is CLL similar to small lymphocytic lymphoma?

A

Same pathology, but in the blood rather than the marrow and lymph nodes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Recall the staging of CLL

A

A - no cytopaenia, <3 areas of lymphoid involvement
B - no cytopaenia, 3 + areas of involvement
C - cytopaenias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Describe the stage-depended consideration of treatment for CLL

A

Stage A - watch and wait
Stage B - Consider treatment
Stage C - Treat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the available treatments for CLL?

A
  1. Ibrutinib (Bruton’s tyrosine kinase inhibitor)
  2. FCR (fludarabine, cyclophosphamide, rituximab)
  3. Stem cell transplant
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is Richter’s syndrome?

A

Transformation of CLL to aggressive disease (ALL/ high grade lymphoma)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What platelet level is diagnostic of essential thrombocythaemia?

A

Consistently >450

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

In which myeloproliferative disorders is a JAK2 mutation present in approximately 50% of cases?

A

Essential thrombocythaemia

Myelofibrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is the treatment for essential thrombocythaemia?

A

Aspirin to reduce stroke risk

Hydroxycarbamide to lower count

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What % of patients with polycythaemia vera have a JAK2 mutation?

A

95%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is the treatment for polycythaemia vera?

A

Aspirin to reduce stroke risk
Venesection
Hydroxycarbamide to lower count

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What might polycythaemia be secondary to?

A

Severe COPD
Cyanotic heart disease
Erythropoietin-secreting renal tumours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Which cytopaenias do you get in myelofibrosis?

A

Pancytopaenia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What might be identified on examination of someone with myelofibrosis?

A

Splenomegaly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What abnormal cell may be seen on a blood film of someone with myelofibrosis?

A

Tear drop poikilocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

How is myelofibrosis treated?

A

Stem cell transplant is the only cure

Can use ruloxinib to relieve symptoms - a JAK2 inhibitor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is the most common presentation of myelodystplastic syndrome?

A

Incidental cytopaenia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

At what % of blasts is myelodysplastic syndrome considered to have progressed to AML?

A

> 20%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

How is the risk of a myelodysplastic syndrome progressing to AML calculated?

A

IPSS score

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Describe the typical presentation of Hodgkin’s lymphoma

A

Young, cervical lymphadenopathy made worse on drinking EtOH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Presence of which type of cell is diagnostic of Hodgkin’s lymphoma?

A

Reed-Sternburg cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What is the most common form of Hodgkin’s lymphoma?

A

Nodular sclerosing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What type of haematological malignancy is EBV associated with?

A

Hodgkin’s lymphoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

How is Hodgkin’s lymphoma managed?

A

ABVD chemo + radio

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

How does Non-hodgkin’s lymphoma typically present?

A

With B symptoms and lymphadenopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What is the most common type of indolent Non-Hodgkin’s lymphoma?

A

Follicular

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What would be seen on lymph node biopsy in folliculat non-Hodgkin’s lymphoma?

A

Large number of centroblasts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Which translocation is associated with follicular non-Hodgkin’s lymphoma?

A

T(8;14) –> BCL2 gene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What is the main risk of treatment in high grade lymphoma?

A

Tumour lysis syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What is the typical histological appearance of Burkitt’s lymphoma?

A

Starry sky

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Which translocation is associated with Burkitt’s lymphoma?

A

T(8;14)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What are the 4 B cell subtypes of non-Hodgkin’s lymphoma?

A

Burkitt’s
Diffuse large B cell
Mantle cell
Follicular

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What is the mainstay of treatment for diffuse large B cell lymphoma?

A

R-CHOP chemo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Which translocation is associated with mantle cell lymphoma?

A

T(11;14) - which causes overexpression of cyclin D1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Where is acute T cell lymphoma leukaemia most common?

A

Far East

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Which virus is associated with ATLL?

A

HTLV-1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

In which haematological malignancy are ‘flower cells’ seen on the blood film?

A

ATLL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Recall the name of the staging system used in lymphoma, and how each stage is defined

A 
Ann Arbor staging
Stage 1 = 1 set of LN
Stage 2 = >1 set of LN, one side of diaphragm
Stage 3 = LNs both sides of diaphragm
Stage 4 = involves spleen/ BM
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What is Bence Jones protein?

A

Myeloma paraprotein in urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Recall 2 features of the blood film that may be seen in multiple myeloma

A

Rouleaux

Fried egg cells (plasma cells that are immature)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What are the diagnostic criteria for myeloma?

A

Plasma cells in BM >60%
1+ lesions on MRI
Free light chain ratio > 100

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What is smouldering myeloma?

A

Serum paraprotein >30

Clonal bone marrow plasma cells 10-60%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What are the criteria for MGUS?

A

Serum paraprotein < 30

Plasma cells <10% in BM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What is Waldenstrom’s macroglobulinaemia?

A

Similar to follicular lymphoma but:
Paraprotein is always IgM
Risk of hyperviscosity syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Recall the reversing protocol for warfarin

A

Based on INR
- If at any point there is a major bleed –> hold warfarin, give vit K and FFP/PCC
Otherwise:
- INR <5 –> reduce warfarin dose
- INR 5-8 –> hold warfarin if no bleed, give vit K if minor bleed
INR >8 –> hold warfarin and give vit K

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What is the reversing agent for heparin/LMWH?

A

Protamine sulphate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What is the reversing agent for DOACs?

A

Prothrombin complex concentrate (PCC)

64
Q

What is the reversing agent for aspirin/ clopidegrel?

A

Platelet transfusion

65
Q

Recall the dosing for red cells, platelets and FFP

A

Red cells: ~1 per 10g/l Hb rise
Platelets: ~1 per 25 count rise
FFP: 10-15mls/kg

66
Q

In which blood products does rhesus status matter?

A

Red cells

Platelets

67
Q

At what temperature should platelets be stored?

A

Room temp

68
Q

Over how long should red cells, platelets and FFP be infused?

A

Red cells: 2-3 hours
Platelets: 30 mins
FFP: 30-60 mins

69
Q

By which class of Ig are acute haemolytic transfusion reactions mediated?

A

IgM

70
Q

How can TRALI and TACO be differentiated?

A

TRALI may produce fever, TACO does not

TACO –> features of heart failure, TRALI does not

71
Q

Which blood product is most likely to cause sepsis because of bacterial contamination?

A

Platelets

72
Q

How can febrile non-haemolytic transfusion reactions be prevented?

A

By leukodepletion

73
Q

Which group of patients have the highest risk of anaphylactic reaction to blood products?

A

IgA deficient patients

74
Q

Recall 2 clinical signs of TACO

A

Raised JVP

Raised PCWP

75
Q

What is the main clinical feature of delayed haemolytic transfusion reaction?

A

Extravascular haemolysis

76
Q

By which immunoglobulin is delayed haemolytic transfusion reaction mediated?

A

IgG

77
Q

Recall 3 symptoms of GVHD in blood transfusion

A

Skin desquamation
Diarrhoea
Liver failure

78
Q

What is the pathophysiology of GVHD in blood transfusion?

A

Donor lymphocytes recognise host HLA as foreign

79
Q

How can GVHD in blood transfusion be prevented?

A

Irradiating blood products for immunocompromised patients

80
Q

What leveks of haemoglobin are considered ‘anaemia’ in men and women respectively?

A

M: <135
F: <115

81
Q

What is a normal red cell volume?

A

80-100fL

82
Q

What are the 2 most important tests to do to determine the cause of a microcytic anaemia?

A

Peripheral blood smear

Iron studies

83
Q

What are ‘pencil cells’ pathognomonic for?

A

Iron deficiency anaemia

84
Q

What will be seen as well as anaemia on an FBC in iron deficiency anaemia?

A

Reactive thrombocytosis

85
Q

Which two conditions may have basophillic stippling on a blood smear?

A

Thalassaemia

Sideroblastic anaemia

86
Q

What would iron studies show in sideroblastic anaemia?

A

Same as IDA: high transferrin and TIBC, low iron and ferritin

87
Q

What are the key tests to do to investigate a macrocytic anaemia?

A

Peripheral blood smear
LFTs
TFTs

88
Q

What is elevated in the serum specifically in B12 deficiency?

A

Methylmalonic acid

89
Q

What is the test for pernicious anaemia?

A

Schilling test

90
Q

What drug might cause folate deficiency?

A

Phenytoin - it impairs its absorption

91
Q

Recall 3 causes of non-megaloblastic macrocytic anaemia

A

Pregnancy
EtOH use
Hypothyroidism

92
Q

What are the most important tests to do when investigating a normocytic anaemia?

A

Peripheral blood smear
DAT/Coombs
CRP and ESR

93
Q

Why would you do a CRP/ESR in cases of normocytic anaemia?

A

Would be raised in anaemia of chronic disease

94
Q

Recall 2 inherited causes of haemolytic anaemia

A

Hereditary spherocytosis

G6PD deficiency

95
Q

What are the two tests for hereditary spherocytosis?

A

Osmotic fragility test (less specific)

Eosin-5-maleimide test (more sensitive and specific)

96
Q

How should hereditary spherocytosis be managed?

A

Folate supplementation

Splenectomy

97
Q

What is the inheritance pattern of G6PD deficiency?

A

X linked recessive

98
Q

What is the normal role of G6PD?

A

Generates NADPH via pentose pathway

99
Q

What would be seen on peripheral blood smear in hereditary spherocytosis?

A

Spherocytes and polychromasia

100
Q

What would be seen on peripheral blood smear in G6PD deficiency?

A

Heinz bodies

Bite cells

101
Q

Recall 3 causes of immune haemolytic anaemia

A

Autoimmune (warm/ cold)
ABO incompatibility
Rh incompatibility

102
Q

Describe the differences between warm and cold autoimmune haemolytic anaemia

A

Warm: IgG, extravascular haemolysis (associated with CLL, SLE and methyldopa)

Cold: IgM, intravascular haemolysis (associated with mycoplasma, EBV and Hep C)

103
Q

How can autoimmune haemolytic anaemia be managed?

A

Treat cause
Steroids
Rituximab

104
Q

Recall 3 types of non-immune acquired haemolytic anaemia

A

MAHA
HUS
TTP

105
Q

What is the triad of features in MAHA?

A

HUS, TTP and DIC

106
Q

How can MAHA be distinguished from DIC?

A

MAHA will have normal APTT, PT anf fibrinogen

107
Q

What is the most common cause of HUS in children?

A

E coli O157:H7 - shiga-like toxin

108
Q

In which type of anaemia should antibiotics always be avoided?

A

HUS

109
Q

What is the usual pathophysiology of TTP?

A

ADAMTS13 deficiency –> decreased vWF breakdown

110
Q

What is the triad of features in TTP?

A

HUS + neurology + fever

111
Q

On which chromosomes are the alpha and beta globin chains encoded?

A

Alpha: 16
Beta: 11

112
Q

What are the 3 subtypes of beta thalassaemia?

A

Minor/ intermedia/ major

113
Q

What are the genotypes and corresponding phenotypes of each of the types of alpha thalassaemia?

A

HbBarts - 4 faulty genes - fatal in utero due to hydrops
HbB - 3 faulty genes - severe anaemia
Trait - 2 faulty genes - mild anaemia
Silent - 1 faulty gene

114
Q

What is the mutation that causes sickle cell anaemia?

A

Glu–> Val at codon 6 on the beta globin chain

115
Q

Recall some principles of management of sickle cell disease

A

Vaccinate against encapsulated bacteria
Supplement folate
Hydroxyurea
Supportive care in acute crisis

116
Q

In a patient with sickle cell anaemia, what is the most common pathogen to be implicated in cases of

a) sepsis
b) osteomyelitis?

A 
Sepsis = Strep pneumoniae
Osteomyelitis = salmonella
117
Q

Recall some differentials for disorders of haemostasis

A

Primary haemostatic disorders = to do with platelet function eg. vWF disease, ITP, HIT

Secondary haemostatic disorders = to do with the coagulation cascade = haemophilia A/B, liver disease, vit K deficiency

118
Q

Recall some differentials for thrombotic disorders

A

Inherited: Factor V Leiden, anti-thrombin deficiency, protein C/S deficiency
Acquired: HIT, malignancy, immobilisation

119
Q

What is the inheritance pattern of each of the types of von Willebrand disease?

A

Types 1 and 2 = autosomal dominant

Type 3 = autosomal recessive

120
Q

What are the 3 subtypes of vWF disease?

A

Type 1 = too few platelets
Type 2 = qualitative deficiency
Type 3 = quantitative and qualitative deficiency

121
Q

What would be the exected APTT and PT in vWF?

A

Prolonged APTT

Normal PT

122
Q

Differentiate the presentation of acute vs chronic ITP?

A

Acute: children, self-resolving, preceding infection
Chronic: adults, mostly women, longterm relapsing-remitting

123
Q

How can severe acute ITP/ chronic ITP be treated?

A

Steroids
IV Ig
Splenectomy for chronic

124
Q

What is the inheritance pattern of haemophilia?

A

X linked recessive

125
Q

What is deficient in haemophilia A/B?

A 
A = factor VIII
B = factor IX
126
Q

How is haemophilia treated?

A

Replace missing factor

127
Q

What are the typical symptoms of haemophilia?

A

Deep bleeding

Haemarthroses

128
Q

What would be the exected APTT and PT in haemophilia?

A

Prolonged APTT
Normal PT
(Same as vWF disease)

129
Q

Recall 3 causes of vit K deficiency

A

Malabsorption
Warfarin
Antibiotic therapy

130
Q

Which factor will be the first to be depleted in vit K deficiency?

A

Factor VIII

131
Q

What would be the expected APTT and PT in vit K deficiency?

A

Both prolonged

132
Q

What is the pathophysiology of factor V Leiden?

A

Resistance to Protein C –> failure to degrade factor V –> hypercoagulable state –> predisposition to VTE

133
Q

What is the inheritance pattern of anti-thrombin deficiency?

A

Autosomal dominant

134
Q

What is the main sign of anti-thrombin deficiency?

A

VTEs in weird places (eg spleen, mesenteric veins)

135
Q

How is anti-thrombin deficiency diagnosed?

A

Anti-thrombin deficiency

136
Q

How should anti-thrombin deifciency be managed?

A

Longterm warfarin/ argatroban

137
Q

What is the inheritance pattern of protein C/S deficiency?

A

Autosomal deficiency

138
Q

How can protein C/S deficiency affect the skin?

A

Associated with warfarin-induced skin necrosis: initial hypercoagulable state -> ischaemia of skin vessels

139
Q

How is protein C/S deficiency diagnosed?

A

Protein C/S assay

140
Q

How should protein C/S deficiency be managed?

A

Longterm argatroban

141
Q

What are the key investigations to do in any microcytic anaemia?

A

Peripheral blood smear

Iron studies

142
Q

What are the expected results of iron studies in thalassaemia?

A

All normal

143
Q

What are the key differentials in microcytic anaemia?

A

IDA
Thalassaemia
Siderblastic

144
Q

What are the key investigations to do in macrocytic anaemia?

A

Peripheral blood smear (to see if megaloblastic or not)
LFTs (alcohol?)
TFTs (hypothyroid)

145
Q

What specific marker is elevated in B12 deficiency but not folate deficiency?

A

Serum methylmalonic acid

146
Q

What type of anaemia can be caused by phenytoin use?

A

Folate deficiency –> megaloblastic

147
Q

What 2 tests would be positive in hereditary spherocytosis?

A

Osmotic fragility

Eosin-5-maleimide

148
Q

What are the 2 abnormal cells that can be seen in G6PD in a peripheral blood smear?

A

Heinz bodies

Bite cells

149
Q

What are the difference between hot and cold AIHA?

A

Warm: mediated by IgG, associated with CLL, causes extravascular haemolysis

Cold: mediated by IgM, associated with mycoplasma/ EBV/ Hep, –> intravascular haemolysis

150
Q

How can MAHA and DIC be distinguished?

A

MAHA has normal APTT, fibronogen and PT

151
Q

What are the 5 elements of TTP?

A 
MAHA
Thrombocytopaenia
Acute renal failure
Neurological symptoms
Fever
152
Q

Which inherited clotting disorder carries the highest risk of clots?

A

Antithrombin deficiency

153
Q

What is the most common mode of inheritance of VWD?

A

Autosomal dominant

154
Q

By which class of Ig is ABO incompatibility mediated?

A

IgM

155
Q

With which type of transfusion is bacterial contamination most likely?

A

Platelets (stored at warmer temp)

156
Q

What disorder is most strongly associated with predisposition to anaphylactic reaction to transfusion?

A

IgA deficiency

Year 5 Pathology Overview (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions