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Blurting > Haematology > Flashcards

Haematology Flashcards

1
Q

Presentation of hereditatary haemochromatosis (5)

A 
Diabetes 
Bronzed skin 
Arthritis 
Cardiomyopathy 
Liver disease
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2
Q

Investigation findings in hereditary haemochromatosis

A

Raised LFTs

Raised ferritin

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3
Q

Genetics of hereditary haemochromatosis

A

Autosomal recessive

Chromosome 6

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4
Q

Pathophysiology of hereditary haemochromatosis

A

Decreased synthesis of hepcidin
Hepicidin reduces ferropportin channels
Results in excessive iron absorption
Iron deposition in tissues

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5
Q

Pathophysiology of immune thrombocytopaenic purpura (ITP)

A

Anti-platelet antibodies

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6
Q

Presentation types of ITP

A

Acute - kids

Chronic - adults

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7
Q

Acute presentation of ITP

A

Kids
Sudden and self-limiting
Often post-infectious

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8
Q

Chronic presentation of ITP

A

Adults
Fluctuating
Low platelet - bleeding, menorrhagia, epistaxis

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9
Q

Investigation in ITP

Threshold for Management

A

Platelet count

<20-30 and give prednisolone 1mg/kg to induce remission

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10
Q

Management of ITP

A

Prednisolone

1mg/kg

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11
Q

Causes of anti-phospholipid syndrome

A

Lupus
Drugs
Viral infection

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12
Q

Investigation of anti-phospholipid syndrome

False measurement

A

Anti-cardiolipin antibodies

Cannot trust APTT - falsely prolonged

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13
Q

Pathophysiology of anti-phospholipid syndrome

A

Bind to glycolipid on RBC, change profile of RBC

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14
Q

Presentation of anti-phospholipid (3)

A

Recurrent foetal losses
Thrombosis
Thrombocytopaenia

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15
Q

Management of anti-phospholipid

A

Warfarin

Aspirin

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16
Q

Pathophysiology of myeloma

A

Plasma cell proliferation

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17
Q

Paraprotein in myeloma

A

IgG or IgA

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18
Q

Investigation findings in myeloma

A

Urine electrophoresis
Bence Jones protein
Raised calcium

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19
Q

Management of myeloma (3)

A

Dexamethasone
Thalidomide/similar
Alkylating agent

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20
Q

Paraprotein in Waldenstrom’s Macroglobinuria

A

IgM paraprotein

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21
Q

Pathophysiology of Waldenstrom’s

A

Disorder of intermediate of B and plasma cells

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22
Q

Presentation of Waldenstrom’s

A

Marrow failure

Lymphadenopathy

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23
Q

Management of Waldenstrom’s

A

None

Chemoplasmaphoresis - reduce amount of paraprotein

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24
Q

Group who get ALL

A

Kids

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25
Q

Presentation of ALL (2)

A

Marrow failure

Bone pain

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26
Q

Involvement in ALL

A

CNS and testis

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27
Q

Investigation in ALL

A

See raised lymphoblasts

Often carry out LP as high risk of CNS involvement

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28
Q

Management in ALL

A

Chemotherapy

Consider allogenic stem cell transplant

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29
Q

Subtype of AML

A

t 15:17

Present with catastrophic DIC

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30
Q

Presentation of AML (3)

A

Bleeding
Easy bruising
Anaemia

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31
Q

Group who get AML

A

> 60 years

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32
Q

Pathological findings in AML

A

Aeur rods

Raised myeloblasts which occupy the bone marrow

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33
Q

Presentation of AML

A

Gum infiltration

Marrow failure

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34
Q

Management of AML

A

2-4 cycles of combination treatment

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35
Q

Pathophysiology of TTP

A

Endothelial damage results in microvascular thrombosis
Consumes platelets
Results in thrombocytopaenia

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36
Q

Presentation of TTP (4)

A

Purpura
Fever
AKI
MAHA

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37
Q

MAHA =

A

= microangiopathic haemolytic anaemia

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38
Q

Investigation findings in TTP

A

Haemolysis

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39
Q

Management of TTP

A

Plasma exchange

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40
Q

Pathological findings in myelofibrosis

A

Poikilocytes on blood film

Fibrosis of bone marrow - occupying bone marrow

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41
Q

Presentation of myelofibrosis

A

Marrow failure

= extramedullary haematopoiesis

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42
Q

Management of myelofibrosis

A

Supportive
Transfusion
Allogenic stem cell transplant

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43
Q

What is myelofibrosis

A

Type of chronic leukaemia

A myeloproliferative disorder

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44
Q

Genetics of CML

Protein produced

A

Philadelphia chromosome - t 9:22

Produces BCR-ABL 1 = abnormal phosphorylation

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45
Q

Difference between AML and CML

A

AML - abnormal blasts, maturation block

CML - no maturation block

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46
Q

Presentation of CML (3)

A

B symptoms
Anaemia
Priapism

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47
Q

Who gets CML

A

Elderly

48
Q

Investigation findings in CML (3)

A

Anaemic
Leukocytosis
Thrombocytosis

49
Q

Management of acute presentation of CML

A

Consider transplant

50
Q

Management of chronic presentation of CML

A

Imatinib

51
Q

Involvement in CLL

A

Both blood and lymph nodes

52
Q

Pathology of CLL

A

Proliferation of B cells

53
Q

Who gets CLL

A

Elderly

54
Q

Associations of CLL

A

Warm autoimmune haemolytic anaemia

55
Q

Investigation findings in CLL

A

Normal/low Hb and platelets

Raised WBC

56
Q

Management of CLL

A

Steroids

Chemotherapy

57
Q

Pathological findings in polycythaemia rubra vera

A

JAK2 mutation

BCR-ABL1 negative

58
Q

Presentation of PRV (4)

A

Itching
Worse after hot bath
Fatigue
Headache

59
Q

Investigation of PRV (3)

A

Increased Hb
Erythrocytosis
Haematocrit raised

60
Q

Management of PRV

A

Venesection to lower haematocrit

Hydroxycarbamide

61
Q

Chelation agents

A

Desferrioxamine

62
Q

Who gets Hodgkin’s Lymphoma

A

Two peaks
Young adult
Older

63
Q

Staging of Hodgkin’s Lymphoma

A

1 - single node
2 - 2+ nodes same side of diaphragm
3 - 2+ nodes above and below diaphragm
4 - widespread disease

64
Q

Management of Hodgkin’s Lymphoma

A

Curative with ABVD chemotherapy/combination chemo

Radiation

65
Q

Management of follicular lymphoma

A

Rituximab

CD20+

66
Q

Genetics of follicular lymphoma

Protein lost

A

t 14: 18
CD20+
Loss of BCL2 gene which is the normal apoptosis gene

67
Q

Follicular lymphoma epidemiology

A

2nd commonest in adults

68
Q

Prognosis of mantle cell lymphoma

A

Bad

69
Q

Genetics of mantle cell lymphoma

A

t 11: 14

70
Q

Presentation of mantle cell lymphoma

A

Widespread lymphadenopathy

71
Q

Non-Hodgkin’s Lymphomas (5)

A 
Burkitts
Follicular
Mantle Cell 
Diffuse large B cell 
T cell
72
Q

Most common NHL

A

Diffuse large B cell

73
Q

Pathology of NHL

A

Malignant expansion of lymphocytes at different stages of development

74
Q

Management of NHL

A

CHOP chemotherapy

75
Q

Presentation of fanconi’s anaemia (4)

A

Short stature
Cafe au lait
Anaemia
Hypogenitalia

76
Q

Pathology behind fanconi’s anaemia

A

Cannot correct inter-strand DNA links

77
Q

Investigation findings in fanconi’s anaemia

A

Thrombocytopaenia

Neutropaenia

78
Q

Aplastic anaemia marrow findings

A

Hypocellular marrow

79
Q

Causes of aplastic anaemia (4)

A

Parvovirus
Autoimmune
Chloramphenicol
Penicillamine

80
Q

Pathology of aplastic anaemia

A

T cells target stem cells and CMP

= cannot produce myeloid cells

81
Q

Management of aplastic anaemia (2)

A

Stem cell transplant

Immunosuppression

82
Q

Pathogenesis of myelodysplastic syndrome

A

Ineffective haematopoiesis

83
Q

Investigation findings of myelodysplastic syndrome

A

Dysplastic hypercellular bone marrow

84
Q

Complications of myelodysplastic syndrome

A

AML

85
Q

Who gets myelodysplastic syndrome

A

70-80 years

86
Q

Pre-cursor of AML

A

Myelodysplastic syndrome

87
Q

Genetics of sickle cell

A

Gene 6 of B gene

Change of valine to glutamine

88
Q

Pathophysiology of sickle cell

A

Production of HbS

HbS is prone to depolymerise in hypoxia, producing a RBC defect

89
Q

B-Thalassaemia intermedia genotype (2)

A

Mildly homozygous

Co-dominant with other trait

90
Q

Presentation of B-thalassaemia major (2)

A

Failure to thrive

Severe anaemia

91
Q

Target cells (2)

A

Thalassaemia

Iron deficiency anaemia

92
Q

Management of B-thalassaemia major

A

Transplant

Transfusions for life - chelation agents to prevent iron overload

93
Q

Investigation findings in B-thalassaemia major

A

Target cells

Raised HbF

94
Q

Causes of MAHA (4)

A

Mechanical valve
HUS
TTP
Pre-eclampsia

95
Q

Investigation findings of MAHA

A

Schistocytes

96
Q

Why do schistocytes occur?

A

Intravascular haemolysis with mechanical disruption

97
Q

Pathophysiology of anaemia of chronic disease

A

Increased production of ferritin
Triggers increased hepcidin production
Reduced production of ferroportin
Reduced Fe absorption

98
Q

Pathophysiology of paroxysmal nocturnal haemoglobinuria

A

Stem cell disorder

Results in excessive complement activation (C5)

99
Q

Presentation of paroxysmal nocturnal haemoglobinuria (2)

A

Haemoglobinuria at night

Thrombosis

100
Q

Investigation findings in paroxysmal nocturnal haemoglobinuria

A

Urinary haemosiderin +VE

101
Q

Management of PNH

A

Anti-coagulation

Treatment of stem cells

102
Q

Types of Autoimmune Haemolytic anaemia

A

Warm

Cold

103
Q

Warm Autoimmune Haemolytic anaemia Ig

A

IgG

104
Q

Cold Autoimmune Haemolytic anaemia Ig

A

IgM

105
Q

Intravascular autoimmune haemolytic anaemia

A

Cold AHA

106
Q

Extravascular autoimmune haemolytic anaemia

A

Warm AHA

107
Q

Causes of warm autoimmune haemolytic anaemia

A

Extravascular
SLE
Idiopathic

108
Q

Causes of cold autoimmune haemolytic anaemia

Pathogenesis

A

Intravascular
EBV, mycoplasma
= complement mediated

109
Q

Management of warm autoimmune haemolytic anaemia

A

Steroids 1mg/kg/day

110
Q

Investigation findings in AHA

A

Spherocytes

+VE coombs test

111
Q

A-genes for Hb

A

4 genes

Ch 16

112
Q

B-genes for Hb

A

2 genes

Ch 11

113
Q

Vitamin K dependent clotting factors

A 
Prothrombin (II) 
VII
IX
X 
Protein C
114
Q

Natural anticoagulants

A

Protein C

Protein S

115
Q

Mechanism of unfractionated heparin (main)

A

Increases

Anti-thrombin inhibition of thrombin

116
Q

Mechanism of LMWH (main)

A

Increases

Anti-thrombin inhibition of factor X

Blurting (6 decks)

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