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MRCP Combined > Haem > Flashcards

Haem Flashcards

1
Q

What is seen on blood smear in ALL?

A

Blast cells

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2
Q

What suggests good prognosis in ALL?

A

FAB L1 type
Pre-B phenotype
Low initial WCC
Deletion of 9p

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3
Q

What suggests poor prognosis in ALL?

A 
FAB L3 type
T or B cell surface markers
Philadelphia translocation
Age <2 or >10
Male
CNS involvement
High initial WCC >100
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4
Q

What is the most common type of AML?

A

M3 - acute promyelocytic

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5
Q

What translocation is seen in APML?

A

t(15;17) - fusion of PML and RAR-alpha genes

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6
Q

What is seen in BM biopsy in AML?

A

Auer rods

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7
Q

What is the treatment of APML?

A

All-trans retinoic acid (ATRA) and anthracycline chemotherapy

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8
Q

What are the poor prognostic features of AML?

A

> 60 years
20% blasts after first course of chemo
Deletion of chromosome 5 or 7

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9
Q

In which leukaemia are smudge cells seen on blood film?

A

CLL

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10
Q

What is the treatment of CLL?

A

FCR (fludarabine, cyclophosphamide, rituximab)

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11
Q

What are the complications of CLL?

A

Hypogammaglobulinaemia leading to secondary bacterial infection
Warm autoimmune haemolytic anaemia
Richter’s transformation

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12
Q

What is Richter’s transformation?

A

Leukaemia cells enter lymph node and change into high grade fast growing NHL

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13
Q

What are poor prognostic features of CLL?

A 
Male
Age >70
Lymphocytosis
Raised LDH
17p13 deletion
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14
Q

What is the genetic mutation in CML?

A

95% philadelphia chromosome - ABL proto-oncogene from C9 fused with BCR gene on C22
Codes for a fusion protein with high tyrosine kinase activity

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15
Q

What is seen on BM biopsy in CML?

A

Hypercellular

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16
Q

What is the treatment of CML?

A

Imatinib (tyrosine kinase inhibitor)

Hydroxyurea and IFN alpha 2nd line

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17
Q

What is a complication of CML?

A

Blast transformation to AML in 80% and ALL in 20%

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18
Q

What mutation is common in hairy cell leukaemia?

A

BRAF

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19
Q

How is hairy cell leukaemia diagnosed?

A

Dry tap despite BM hypercellularity

TRAP stain +ve

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20
Q

What is the treatment of hairy cell leukaemia?

A

Cladribine, pentostatin, rituximab

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21
Q

What is the genetic mutation that can be seen in multiple myeloma?

A

RAS gene mutations

KRAS, HRAS, NRAS

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22
Q

What causes hypercalcaemia in multiple myeloma?

A

Increased osteoclastic bone resorption by IL-1 or TNF released by myeloma cells
Increased renal tubular reabsorption of calcium
Elevated PTH-rP

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23
Q

How is multiple myeloma diagnosed?

A 
IgA paraproteinaemia
IgA in serum and urine (Bence Jones)
BM biopsy - increased plasma cells
X-Ray - raindrop skull
Whole body MRI
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24
Q

What is the treatment of younger myeloma patient?

A

Bortezomib melphalan and prednisolone

with high dose chemotherapy (HDT) with autologous stem cell Tx

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25
Q

What are the complications of myeloma?

A 
Amyloidosis
Macroglossia
Carpal tunnel
Hyperviscosity
Renal failure
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26
Q

MGUS and smouldering myeloma progress to myeloma at what rate per year?

A

MGUS - 1%

Smouldering - 10%

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27
Q

What is poor prognosis in myeloma?

A

Raised B2 microglobulin

Low albumin

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28
Q

50% of Waldenstrom’s macroglobulinaemia patients have which deletion?

A

Chromosome 6q

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29
Q

How is WMG diagnosed?

A

IgM paraproteinaemia >30g
Raised RF
FBC with flow cytometry
Serum protein electrophoresis

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30
Q

How is Waldenstrom’s macroglobulinaemia differentiated from multiple myeloma clinically?

A

No bone lesions/pain

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31
Q

What is the treatment of Waldenstrom’s macroglobulinaemia?

A

Rituximab based chemo

with dex, cyc, fludarabine

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32
Q

Why do WMG patients receiving rituximab need IgM monitoring?

A

Risk of IgM flare which leads to hyperviscosity

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33
Q

How is Hodgkin’s lymphoma diagnosed?

A

LN biopsy - Reed Sternberg cells
Raised LDH
Normocytic anaemia
Eosinophilia

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34
Q

What are risk factors for lymphoma?

A

Chemo/radiotherapy
Immunodeficiency
Autoimmune conditions

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35
Q

What is the treatment of hodgkin’s lymphoma?

A

ABVD

Adriamycin (doxorubicin)
Bleomycin
Vincristine
Dacarbazine

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36
Q

How is Hodgkin’s lymphoma staged?

A

Ann-Arbor

Stage I-IV for lymph nodes
A = pruritus
B = all other B symptoms

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37
Q

Which Hodgkin’s lymphoma has the best and worse prognosis?

A

Best - nodular sclerosing
Worst - lymphocyte depleted

Most common - lymphocyte predominant

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38
Q

What are 3 common types of B cell lymphoma?

A

Mantle Cell
B-cell follicular
Diffuse large B cell

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39
Q

What mutations are seen in Mantle cell and B cell-follicular lymphoma?

A

Mantle cell: t(11;14) –> over-expression of BCL-1

B-cell follicular t(14;18) –> over expression of BCL-2

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40
Q

What is the treatment of NHL?

A

R-CHOP chemotherapy

Rituximab
Cyclophosphamide
Doxorubicin (hydroxydaunomycin)
Vincristine (oncovin)
Prednisolone
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41
Q

25% of low grade B cell follicular lymphoma transform to what?

A

Diffuse large B cell

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42
Q

What are the 2 types of Burkitt’s lymphoma?

A

Endemic African: maxilla/mandible

Sporadic: ileocaecal

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43
Q

What are the risk factors for Burkitt’s lymphoma?

A

EBV and AIDs

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44
Q

What translocation is seen in Burkitt’s lymphoma?

A

t(8;14) - c-myc oncogene translated to Ig gene

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45
Q

What is seen on lymph node biopsy in Burkitt’s lymphoma?

A

Starry sky - lymphocyte sheets interspersed with macrophages containing dead apoptotic tumour cells

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46
Q

What is the treatment of Burkitt’s lymphoma?

A

CYC, MTX, cytosine arabinoside, vincristine

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47
Q

What is the treatment of T and NK cell lymphoma?

A

VHOP

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48
Q

What is the inheritance of factor V leiden and anti-thrombin III deficiency?

A

Autosomal dominant

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49
Q

What is the PPY of factor V leiden?

A

Gain of function in factor V leiden protein - activated factor V is inactivated 10x more slowly by activated protein C

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50
Q

What is the prevalence and risk of VTE in factor V Leiden?

A

Prevalence 5%

Risk of VTE 4% (homozygotes 10% but prevalence 0.05%)

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51
Q

What is the inheritance of protein C deficiency?

A

Autosomal co-dominant

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52
Q

What are the features of protein C deficiency?

A

VTE

Skin necrosis following commencement of warfarin (temporary pro-coagulant state –> thrombosis in venules)

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53
Q

How is protein C deficiency diagnosed?

A

Copperhead snake venom assay

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54
Q

What is the function of anti-thrombin?

A

Inhibits thrombin, factor C, factor IX, and mediates the effects of heparin

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55
Q

What is monitored in anti-thrombin deficiency?

A

Anti-Xa to ensure adequate anticoagulation

As there is a degree of resistance to heparin

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56
Q

What does Protein S do?

A

Activates protein C in the degradation of factor Va and VIIIa

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57
Q

What are the features of anti-phospholipid syndrome

A

Arterial and venous thromboses
Recurrent foetal loss
Thrombocytopenia
Prolonged APTT

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58
Q

What is the mechanism of action of cyclophosphamide and cisplatin?

A

Causes cross-linking in DNA

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59
Q

Name 4 anti-metabolites.

A

Methotrexate
Fluorouracil
6-mercaptopurine
Cytarabine

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60
Q

What is the mechanism of action of vincristine and docetaxel?

A

Acts on microtubules

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61
Q

Which drug stabilises DNA-topoisomerase II complex?

A

Doxorubicin

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62
Q

Which drug inhibits topoisomerase I?

A

Irinotecan

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63
Q

Which drug inhibits ribonucleotide reductase?

A

Hydroxyurea

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64
Q

Which drug has the side effect profile of Low Mg, ototoxicity, and peripheral neuropathy?

A

Cisplatin

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65
Q

What are the side effects of fluorouracil?

A

Myelosuppression
Mucositis
Dermatitis

66
Q

What is the biggest side effect of doxorubicin?

A

Cardiomyopathy

67
Q

Which cytotoxic drugs lead to lung fibrosis?

A

Methotrexate

Bleomycin

68
Q

What percentage of haemophilia is sporadic?

A

30%

69
Q

What are the features of severe haemophilia?

A

Frequent spontaneous deep muscle haematomas and haemoarthroses, usually resulting in joint deformity

Presents <1 year

70
Q

How is haemophilia diagnosed?

A

Prolonged APTT
Normal PT
Normal bleeding time
Normal vWF

Plasma factor VIII and IX assay

71
Q

What is the treatment of severe haemophilia?

A

Factor VIII/IX concentrates

72
Q

What is the treatment of acquired or mild haemophilia?

A

DDAVP

Tranexamic acid

73
Q

What are the features of haemophilia carriers?

A

Asymptomatic

Prolonged APTT

74
Q

What is the cause of acquired haemophilia?

A

Systemic inflammatory conditions - factor VIII antibodies

Drugs: phenytoin, penicillin, sulphonamides

75
Q

How can you differentiate drug induced from genetic haemophilia?

A

In drug induced, APTT remains prolonged after 50:50 mixing study

76
Q

What is the function of vWF?

A

Protein made in endothelial cells and megakaryocytes
Mediates platelet aggregation and adhesion to exposed subendothelium
Binds and stabilises coagulation factor VIII

77
Q

What are the features of von Willebrand disease?

A

Bruising
Mild-mod mucocutaneous bleeding

In type 3 factor VIII is also severely decreased - joint and GI bleeding

78
Q

How is von Willebrand disease diagnosed?

A

Normal or mildly prolonged APTT
Mild thrombocytopenia
Prolonged bleeding time

VWF screening tests: antigen, activity, factor VIII activity

79
Q

What is the treatment of VWD?

A

T1: DDAVP, tranexamic acid
T2: trial of DDAVP (less responsive)
T3: VWF containing concentrates, anti-fibrinolytics

80
Q

What are the biochemical features of DIC?

A 
Thrombocytopenia
Raised d-dimer
Low fibrinogen
Raised FDPs
Prolonged APTT and PT
81
Q

What is the cause of hypogammaglobulinaemia in CLL?

A

Suppression of normal B cell proliferation

Increased proliferation of dysfunction leukaemic B cells that do not produce functional antibodies

82
Q

What does Ca15.3 correspond to?

A

Breast cancer

83
Q

What does S-100 tumour marker correspond to?

A

Melanoma, schwannoma

84
Q

What does alfatoxin cause?

A

HCC

85
Q

What is a risk factor for hepatic angiosarcoma?

A

Vinyl chloride

86
Q

What cancers do aniline dyes, asbestos, and nitrosamines cause?

A

Aniline dye: TCC bladder
Asbestos: bronchial Ca and mesothelioma
Nitrosamines: oesophageal and gastric Ca

87
Q

Where is leucocyte alkaline phosphatase found?

A

Mature WBC

88
Q

How can you differentiate CML and myelofibrosis?

A

Low leucocyte alkaline phosphatase in CML (raised in myelofibrosis)

89
Q

Name 5 causes of secondary polycythaemia.

A

COPD
Altitude
OSA
XS EPO: RCC, hepatoma, cerebellar haemangioma

90
Q

How can you differentiate between primary/secondary (true) polycythaemia, and relative polycythaemia?

A

Red cell mass increased

91
Q

95% polycythaemia vera patients have which mutation?

A

JAK2

92
Q

What are the features of polycythaemia vera?

A 
Hyperviscosity sx
Pruritus after hot bath
Splenomegaly
Bleeding
Plethora
Hypertension
Low ESR
93
Q

What tests are required to diagnose polycythaemia vera if JAK2 is negative?

A 
Red cell mass
Arterial oxygen saturation
Abdo USS
Serum EPO
Bone marrow aspirate and trephine
Cytogenetic analysis
Erythroid burst-forming unit culture
94
Q

10% polycythaemia vera patients progress to…

A

Myelofibrosis or AML

95
Q

What is the treatment of polycythaemia vera?

A

Aspirin
Venesection
Hydroxyurea

96
Q

How is smouldering myeloma differentiated from MGUS?

A

MGUS: paraprotein <30g/L, BM plasma cells <10%, no organ impairment

Smouldering: paraprotein >30g/L, BM plasma cells 10-60%, no organ impairment

97
Q

What is the pathophysiology of myelofibrosis?

A

Hyperplasia of abnormal megakaryocytes

Release of platelet derived growth factor - stimulates fibroblasts

98
Q

What are the features of myelofibrosis?

A

Anaemia sx
Massive splenomegaly
Hypermetabolic sx

99
Q

How is myelofibrosis diagnosed?

A

High WCC and platelets
Anaemia
Blood film - tear drop poikilocytes
High urate and LDH

100
Q

What mutation is seen in essential thrombocytosis?

A

JAK2 in 50%

CALR in 10%

101
Q

What is the characteristic feature of essential thrombocytosis?

A

Burning sensation in hands

102
Q

What is the treatment of essential thrombocytosis?

A

Hydroxyurea

Aspirin

103
Q

What are the features of laboratory tumour lysis syndrome?

A

Uric acid>475
K>6
PO4>1.125
Ca<1.75

OR 25% increase in any component

104
Q

What are the features of clinical TLS?

A

Lab TLS +

Increased creatinine >1.5x normal
Arrhythmia/sudden death
Seizure

105
Q

What are 5 causes of intravascular haemolysis?

A 
Mismatched blood transfusion
G6PD
Red cell fragmentation e.g. heart valves, TTP, DIC, HUS
Paroxysmal nocturnal haemoglobinuria
Cold autoimmune haemolytic anaemia
106
Q

What are 5 causes of extravascular haemolysis?

A 
Haemoglobinopathies
Sickle cell anaemia
Spherocytosis
Haemolytic disease of newborn
Warm autoimmune haemolytic anaemia
107
Q

What is the most common hereditary haemolytic anaemia in Northern Europe?

A

Hereditary spherocytosis

108
Q

What are the features of hereditary spherocytosis?

A 
FTT
Jaundice
Gallstones
Splenomegaly
Aplastic crisis precipitated by parvovirus
109
Q

How is spherocytosis diagnosed?

A

EMA binding test and cryohaemolysis test

110
Q

What is the long term treatment of spherocytosis?

A

Folate replacement

Splenectomy

111
Q

What are the differences between spherocytosis and G6PD def?

A

G6PD: males (X-linked recessive), African/Mediterranean, intravascular haemolysis

Spherocytosis: autosomal dominant, Northern European, extravascular haemolysis

112
Q

Name 5 causes of macrocytic anaemia.

A 
Alcohol
Liver disease
Vit B12/folate def
Pregnancy
Hypothyroidism
113
Q

What proteins are seen in functional asplenia/splenectomy patients?

A

Howell-Jolly bodies

114
Q

What conditions are target cells/codocytes seen?

A

Chronic liver disease
Sickle cell disease
Thalassaemia
Post-splenectomy

115
Q

What causes rouleaux formation?

A

High plasma protein

116
Q

What is the inheritance of sickle cell anaemia?

A

Autosomal recessive

117
Q

When do symptoms of sickle cell arise and why?

A

4-6 months

Abnormal HbSS molecules take over from HbF

118
Q

What causes sickling of HbS?

A

Polar aa glutamate replaced by non polar valine/lysine in haemoglobin beta chains

This decreases the water solubility of deoxygenated Hb

HbS molecules polymerise and cause RBCs to sickle

Homozygous patients sickle at higher pO2s therefore more severe

119
Q

What are the features of sickle cell trait, HbAS?

A

Usually asymptomatic

120
Q

How is sickle cell anaemia diagnosed?

A

Haemoglobin electrophoresis

121
Q

What is the treatment of sickle cell anaemia?

A

Pen V prophylaxis

Hydroxycarbamide

122
Q

What are the characteristics of warm autoimmune haemolytic anaemia?

A

IgG
Haemolysis at body temp
Extravascular haemolysis
Responds well to steroids

123
Q

What are the characteristics of cold autoimmune haemolytic anaemia?

A

IgM
Haemolysis at 4 degrees
Intravascular haemolysis
Responds less well to steroids

124
Q

What is the pathophysiology of sideroblastic anaemia?

A

Ineffective erythropoiesis - poor incorporation of iron into nucleus of erythroblasts

Haem not completely formed

Deposition of iron in mitochondria that forms a ring around the nucleus

125
Q

What are the causes of sideroblastic anaemia?

A 
Delta-aminolevulinate synthase-2 deficiency
Myelodysplasia
Alcohol
Lead
Anti-TB
126
Q

How is sideroblastic anaemia diagnosed?

A

Hypochromic microcytic anaemia
High iron/ferritin/transferrin sats
Blood film - basophilic stippling
BM biopsy - Prussian blue/Perl’s stain - ringed sideroblasts

127
Q

What is seen on blood film in DIC?

A

Helmet cells/schistocytes (indicates MAHA)

128
Q

What is the PPY of TTP?

A

Deficiency of ADAMTS13 which normally breaks down large multimers of VWF

Platelets clump within vessels

129
Q

What are the causes of TTP?

A 
Post infection
Pregnancy
Ciclosporin/COCP/penicillin
SLE
HIV
130
Q

What is the treatment of TTP?

A

Plasma exchange +/- platelet transfusion

131
Q

What is the pathophysiology of ITP?

A

Antibodies directed against glycoprotein IIb/IIIa or Ib-V-IX complex

132
Q

What is the treatment of ITP?

A

Emergency: platelet transfusion, IV methypred, IVIG
Plts<30: oral pred
Plts>30: observation

133
Q

What is the cause of porphyia cutanea tarda?

A

Defect in uroporphyrinogen decarboxylase - inherited or caused by hepatocyte damage

134
Q

What is the treatment of PCT?

A

Chloroquine

Venesection in ferritin >600ng/ml

135
Q

What are the features of PCT?

A 
Photosensitive rash with bullae
Skin fragility on face and dorsal aspect of hands
Hypertrichosis
Skin hyperpigmentation
Dark urine - elevated uroporphyrinogen
136
Q

Low plasma levels of C1 inhibitor protein cause which condition?

A

Hereditary angioedema (AD)

137
Q

What is the treatment of hereditary angioedema?

A

Acute: IV C1 inhibitor concentrate
Chronic: Danazol

138
Q

Which condition features chocolate cyanosis and decreased oxygen saturations, with normal pO2?

A

Methaemoglobinaemia

139
Q

What is methaemoglobinaemia?

A

NADH methaemoglobin deficiency causing oxidation of iron within haemoglobin from Fe2+ to Fe3+.

Fe3+ cannot bind oxygen therefore there is tissue hypoxia (O2 curve moved to left)

140
Q

Which drugs can cause methaemoglobinaemia?

A 
Nitrates
Dapsone
Sulphonamides
Sodium nitroprusside
Haemodialysis (inadequate removal of chloramines)
141
Q

What is the treatment of methaemoglobinaemia?

A

NADH enzyme def: ascorbic acid

Acquired: IV methylthioninium chloride

142
Q

What is the pathophysiology of paroxysmal nocturnal haemoglobinuria?

A

Increased sensitivity of cell membranes to complement, due to a lack of GPI
Lack of CD59 on platelet membranes predisposing to platelet aggregation

143
Q

What are the features of PNH?

A

Increased risk of VTE
Haemolytic anaemia
Pancytopenia
Haemoglobinuria in the morning

144
Q

How is PNH diagnosed?

A

Flow cytometry of blood to detect low levels of CD59 and CD55

145
Q

What is the mechanism of action of tamoxifen?

A

Oestrogen receptor antagonist and partial agonist

146
Q

What are the side effects of tamoxifen?

A

Menstrual disturbance
Hot flushes
VTE
Endometrial cancer

147
Q

What is the mechanism of action of anastrazole and letrozole?

A

Reduce peripheral oestrogen synthesis

148
Q

Name 3 B cell immunodeficiency disorders.

A

Common variable immunodeficiency
Bruton’s X-linked congenital agammaglobulinaemia
Selective immunoglobulin A deficiency

149
Q

What is Chediak-Higashi syndrome?

A

Microtubule polymerization defect –> decrease in phagocytosis –> defect in neutrophils

150
Q

Name 3 combined B and T cell disorders.

A

SCID
Ataxic telangiectasia
Wiskott-Aldrich syndrome

151
Q

Name 5 immune related adverse effects of immunotherapy drugs.

A 
Thyroiditis
Hypophysitis
Adrenalitis
T1DM
Colitis
152
Q

When does acute graft vs host disease occur and what are the features?

A

First 100 days post transplant
Skin rash that starts on palms and soles
Diarrhoea
Jaundice

153
Q

Which chromosomes have mutations in thalassaemia?

A

Alpha: 16
Beta:11

154
Q

How is thalassaemia diagnosed?

A

Disproportionate microcytic anaemia
Elevated serum iron and ferritin
Hb electrophoresis: HbA2>3.5%, HbF raised, HbA absent in b-thalassaemia major

155
Q

What type of cell is seen in alpha thalassaemia?

A

Mexican hat cell

156
Q

What is the management of thalassaemia?

A

Lifelong blood transfusions
Iron chelation: deferiprone + ascorbic acid
Hydroxyurea
Splenectomy

157
Q

Where does erythropoiesis occur?

A

Red bone marrow

Found in flat bones and proximal long bones

158
Q

From where do erythrocytes originate from?

A

Myeloid precursor cells

159
Q

What is the function of EPO?

A

Produced on detection of low oxygen levels

Increases uptake of iron, heme biosynthesis, and globin gene transcription

160
Q

What are the side effects of EPO therapy?

A 
Accelerated HTN
Bone aches
Flu like
Rash
Pure red cell aplasia (antibodies against EPO)
Iron def
161
Q

What are the features of acute haemolytic transfusion reaction?

A

Fever
Chest/abdo pain
Hypotension
Occurs minutes after transfusion is started

162
Q

How do you differentiate TACO from TRALI?

A

TACO - hypertensive

TRALI - hypotensive

MRCP Combined (58 decks)

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