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Haematology DA Flashcards

1
Q

Lymphoma -> Jaundice?

A

Compression bile duct
Liver involvement
AIHA

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2
Q

Cancer causing secondary polycythaemia

A

Renal cell carcinoma
Liver cancer

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3
Q

Low ferritin
Low transferrin sat
High TIBC

A

IDA Lab findings

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4
Q

Anaemia is characterised by the presence of red and white cell precursors

A

Leucoerythroblastic anaemia

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5
Q

Tear drop red blood cells (aniso- and poikilocytosis)
Nucleated RBCs
Immature myeloid cells

A

Leucoerythroblastic anaemia

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6
Q

Causes of Leucoerythroblastic anaemia

A

BONE MARROW INFILTRATION:
Leukaemia / Lymphoma / Myeloma
Solid tumours
Myelofibrosis
Miliary TB, severe fungal infection

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7
Q

dry tap on BM aspirate

A

Myelofibrosis

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8
Q

Anaemia caused by reduced red blood cell survival

A

Haemolytic anaemia

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9
Q

Anaemia
Raised reticulocytes
Raised unconjugated bilirubin
Raised LDH
Low haptoglobins

A

Haemolytic anaemia

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10
Q

Inherited Haemolytic anaemia

A

Hereditary spherocytosis (membrane problem)
G6PD deficiency (enzyme problem)
Sickle cell disease, thalassemia (haemoglobin problem)

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11
Q

Acquired Haemolytic anaemia

A

Immune-mediated
Non-immune mediated

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12
Q

DAT +ve

A

haemolytic anaemia is mediated through immune destruction of red cells

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13
Q

Spherocytes

A

Autoimmune haemolytic anaemia

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14
Q

Causes of Autoimmune haemolytic anaemia

A

Cancer involving the immune system (e.g. lymphoma)
Disease of the immune system (e.g. SLE)
Infections (disturbs the immune system)

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15
Q

Non-immune haemolytic anaemia

A

Infection (e.g. malaria)
Microangiopathic haemolytic anaemia (MAHA)

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16
Q

Usually caused by underlying adenocarcinoma
Red cell fragments
Low platelets
DIC/bleeding

A

MAHA features

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17
Q

MAHA MOA

A

An underlying adenocarcinoma produces procoagulant cytokines that activate the coagulation cascade
This leads to DIC and the formation of fibrin strands in various parts of the microvasculature
Red cells will be pushed through these fibrin strands and fragment
NOTE: always consider underlying adenocarcinoma in any patient presenting with MAHA

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18
Q

Causes of secondary polycythaemia

A

Cancer (renal, hepatocellular, bronchial)
High altitude
Hypoxic lung disease
Congenital cyanotic heart disease

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19
Q

Acute vs chronic leukaemia?

A

Chronic - mature white cells are raised
Acute - immature blast cells are raised

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20
Q

causes of neutrophilia

A

Corticosteroids (due to demargination)
Underlying neoplasia
Tissue inflammation (e.g. colitis, pancreatitis)
Myeloproliferative/leukaemia disorder
Infection

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21
Q

Brucella
Typhoid
Viral
??

A

No neutrophilia

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22
Q

Band cells

A

immature neutrophils

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23
Q

Presence of band cells indicate what?

A

presence of immature neutrophils (band cells) show that the bone marrow has been signalled to release more WBCs

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24
Q

Band cells
Toxic granulation
Clinically: infection/inflamm

A

Reactive neutrophilia

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25
Q

Neutrophilia
Basophilia
Immature myelocytes
Splenomegaly

A

Myeloproliferative disorder

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26
Q

Neutrophilia
Myeloblasts

A

AML

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27
Q

Causes of monocytosis

A

Bacteria: TB, Brucella, typhoid
Viral: CMV, VZV
Sarcoidosis
Chronic myelomonocytic leukaemia

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28
Q

Causes of reactive eosinophilia

A

Parasitic infection
Allergy (e.g. asthma, rheumatoid arthritis)
Underlying neoplasms (e.g. Hodgkin’s lymphoma, T cell lymphoma, NHL)
Drug reaction (e.g. erythema multiforme)

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29
Q

FIP1L1-PDGFRa fusion gene

A

Chronic eosinophilic leukaemia

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30
Q

Pox viruses

A

basophilia

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31
Q

causes of reactive lymphocytosis

A

Infection (EBV, CMV, toxoplasmosis, rubella, HSV)
Autoimmune diseases (NOTE: these are more likely to cause lymphopaenia)
Sarcoidosis

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32
Q

Blood film: viral infection vs leukaemia/lymphoma?

A

Viral infection: reactive or atypical lymphocytes (EBV)
CLL or NHL: small lymphocytes and smear cells

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33
Q

raised Hb concentration and raised haematocrit

A

polycythaemia

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34
Q

caused by a lack of plasma (associated with alcoholism, obesity and diuretics)

A

Relative polycythaemia

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35
Q

Philadelphia positive

A

CML

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36
Q

caused by an excess of erythrocytes

A

True polycythaemia

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37
Q

Philadelphia negative

A

polycythaemia vera
essential thrombocythaemia
primary myelofibrosis

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38
Q

AML vs Myelodysplastic syndromes

A

Acute myeloid leukaemia (blasts >20%)
Myelodysplastic syndromes (blasts 5-19%)

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39
Q

Types of myeloid malignancy

A

Acute myeloid leukaemia
Myelodysplastic syndromes
Chronic myeloid leukaemia
Myeloproliferative disorders

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40
Q

Tyrosine kinase

A

myeloproliferative disorders

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41
Q

Genes in Myeloproliferative disorders

A

JAK2 (V617F)
Calreticulin
MPL

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42
Q

JAK2 V617F mutation

A

Polycythaemia vera (100%)
Primary myelofibrosis and Essential thrombocythaemia (60%)

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43
Q

Mutated JAK2

A

constitutively active in the absence of EPO thereby driving cell replication in the absence of a stimulus

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44
Q

Often incidental
Hyperviscosity: headaches, visual disturbance, stroke, fatigue, dyspnoea, light-headedness
Increased histamine release: aquagenic pruritis, peptic ulceration

A

Polycythaemia vera

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45
Q

Tx for polycythaemia vera - reduce Hct and thromobosis risk?

A

Reduce haematocrit (aim for <45%) - venesection, cytoreductive therapy (hydroxycarbamide)
Reduce thrombosis risk - control Hct, aspirin, keep platelets < 400x109/L

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46
Q

Characterised by sustained thrombocytosis > 600 x109/L

A

Essential thyrombocythaemia

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47
Q

Megakaryocyte lineage - chronic myeloproliferative disorder

A

Essential thrombocythaemia

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48
Q

Incidental finding (50%)
Thrombosis (arterial and venous) - CVA, TIA, DVT, PE, gangrene
Bleeding (mucous membrane and cutaneous)
Headaches, dizziness, visual disturbance
Splenomegaly (modest)

A

Essential thrombocythaemia

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49
Q

Tx for Essential thrombocythaemia

A

Aspirin
Hydroxycarbamide
Anagrelide (rarely used)

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50
Q

MOA of Anagrelide

A

specifically inhibits platelet function but rarely used because of side-effects

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51
Q

Hydeoxycarbamide MOA

A

Antimetabolite that suppresses cell turnover

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52
Q

Cytopaenias (anaemia, thrombocytopaenia)
Thrombosis
MASSIVE splenomegaly
Hepatomegaly
Hypermetabolic state (FLAWS)

A

Primary myelofibrosis

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53
Q

Survival primary myelofibrosis

A

3-5 yrs

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54
Q

Poor prognostic indicators - primary myelofibrosis

A

Severe anaemia
Thrombocytopaenia
Massive splenomegaly

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54
Q

Trephine biopsy:
Increased reticulin and collagen fibrosis
Prominent megakaryocyte hyperplasia and clustering
New bone formation

A

Primary Myelofibrosis

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55
Q

Leucoerythroblastic picture
Tear drop poikilocytes (Dacrocytes)
Giant platelets
Circulating megakaryocytes

A

Primary Myelofibrosis

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56
Q

Mutations in Primary myelofibrosis

A

JAK2 and Calreticulin

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57
Q

Characterised by extramedullary haemopoeisis
Reactive bone marrow fibrosis

A

Primary myelofibrosis

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58
Q

Tx for primary myelofibrosis

A

Transfusions
Hydroxycarbamide
Ruxolitinib - JAK2 inhibitor
Allo stem cell transplant
Splenectomy - symptom relief

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59
Q

Leucocytosis (MASSIVE)
Normal or raised Hb and platelets

A

CML

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60
Q

Neutrophils
Basophils
Myelocytes (NOT blasts)

A

CML

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61
Q

CML timeline

A

5-6 years STABLE phase
6-12 months ACCELERATED phase
3-6 months BLAST CRISIS

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62
Q

translocation between 9;22

A

CML -> Philadelphia chromosome - 22q derivative chromosome

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63
Q

Bcr-Abl fusion gene

A

CML - means that the tyrosine kinase component is constitutively activated thereby driving cell proliferation in the absence of a stimulus

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64
Q

BCR-ABL tyrosine kinase inhibitors

A

CML:
- Some people fail to achieve a complete cytogenetic response
- Non-compliance
- Side-effects (fluid retention, pleural effusion)
- Loss of major molecular response (due to resistance mutations)

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65
Q

BCR-ABL inhibitors

A

Imatinib
Dasatinib , Nilotinib
Bosutinib

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66
Q

Cancer of monoclonal plasma cells
Abundance of monoclonal immunoglobulin
Osteolytic bone lesions
Anaemia
Infections (due to deficient polyclonal response)
Kidney failure (due to hypercalcaemia)

A

Multiple myeloma

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67
Q

MGUS?

A

Premalignant MM

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68
Q

MGUS Blood film

A

Serum M <30g/L
Bone marrow clonal plasma cells <10%
No lytic lesions
No myeloma organ or tissue impairment
No evidence of B-cell proliferative disorder

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69
Q

Myeloma vs Lymphoma

A

IgA or G = Myeloma

IgM = Lymphoma

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70
Q

Most common haem malignancy

A

B cell lymphoma

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71
Q

Second most common haem malignancy

A

Multiple myelomma

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72
Q

Mayo criteria

A

Risk stratification MGUS

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73
Q

Smouldering myeloma

A

Between MGUS and Myeloma

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74
Q

Hyperdiploidy
IGH rearrangements (heavy chain gene translocations)

A

MM development mechanisms

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75
Q

Centroblast

A

Activated B cell

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76
Q

CRAB

A

MM symptoms:
Hypercalcaemia (>2.75 mmol/L)
Renal failure (creatinine >177μmol/L or eGFR <40ml/min)
Anaemia (Hb <100g/L or drop by 20g/L)
Bone lesions (One or more bone lytic lesions in imaging

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77
Q

Myeloma defining event

A

BM plasma cells ≥60%
Involved : uninvolved FLC ratio >100
>1 focal lesion MRI >5mm

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78
Q

Criteria for MM diagnosis

A

≥10% plasma cells in bone marrow + ≥1 CRAB or myeloma defining event

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79
Q

Survival in MM

A

3-4 years

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80
Q

Immature plasmablastic cell

A

Prominent nucleoli
Reticular chromatin
Less abundant cytoplasm

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81
Q

Normal plasma cells

A

Nucleus is pushed to one side of the cell
Clumped chromatin
Large cytoplasm (low nuclear-to-cytoplasmic ratio)

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82
Q

+ ve CD138 and CD38

A

MM:
CD138 - commonly used diagnostic marker
CD38 - can be targeted by monoclonal antibodies

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83
Q

-ve CD19, -ve CD20 and surface Ig neg

A

MM

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84
Q

+ve CD20

A

B cell lymphoma and CLL

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85
Q

Cast nephropathy - caused by high serum FLC, which is filtered and precipitates in tubules
Hypercalcaemia - nephrocalcinosis

A

MM

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86
Q

AKI and MM?

A

20-50% AKI at diagnosis

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87
Q

Bence jones protein

A

MM

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88
Q

MM -> AL amyloidosis?

A

Light chains have the potential to misfold and deposit = Amyloid

89
Q

Congo red

A

Amyloid stain

90
Q

Nephrotic (70%)
Proteinuria, Oedema
Unexplained HF - (10%)
Raised NT-pro-BNP
Abnormal Echo and cardiac MRI
Sensory Neuropathy
Abnormal LFTs (9%)
Macroglossia
Malabsorption plus GI symptoms

A

Amyloidosis

91
Q

MM Tx?

A

Cyclophosphamide
Daratumumab
Steroids
Thalidomide
Bortezomib

92
Q

MOA of thalidomide

A

down-regulates pro-survival cytokines and induces apoptosis

93
Q

anti-CD38 antibody

A

Daratumumab - anti-CD38 antibody, binds to cell surface of plasma cells causing complement activation and cell lysis/death

94
Q

Prevalence NHL and HL?

A

NHL = 80%
HL = 20%

95
Q

Oncogenes in Lymphoma/Leukaemia

A

Bcl2
Bcl6
Cyclin D1
c-Myc

96
Q

H. pylori lymphoma

A

Gastri MALT - marginal zone NHL of the stomach

97
Q

Sjogren’s lymphoma

A

marginal zone NHL of the parotid

98
Q

Coeliac disease Lymphoma

A

small bowel T cell lymphoma, enteropathy-associated T cell NHL

99
Q

HTLV1

A

Human T lymphocytrophic virus -> Lymphoma/Leukaemia

100
Q

Loss of T cell function -> lymphoma?

A

EBV established latent infection in B cells which is kept in check by cytotoxic T cell

Loss of T cell function (e.g. HIV, post-transplant immunosuppression) can lead to EBV-driven lymphoma

101
Q

a crescent-shaped region where naïve unstimulated B cells are found

A

Mantle zone - Lymph node

102
Q

where naïve B cells will eventually migrate, and mature B cells will end up in the medulla

A

Germinal centre - Lymph node

103
Q

CD3, CD5

A

T cell markers

104
Q

CD20

A

B cell marker

105
Q

WHO classification of lymphoma

A

Hodgkin lymphoma:
Classical
Lymphocyte predominant
Abnormal B cells

Non-Hodgkin lymphoma:
B cell (MOST COMMON) - (Precursor B cell neoplasm) (Peripheral B cell neoplasm (low and high grade))
T cell - (Precursor T cell neoplasm) (Peripheral T cell neoplasm)

106
Q

11;14 translocation

A

Mantle cell lymphoma

107
Q

2;5 translocation

A

Anaplastic large cell lymphoma

108
Q

Follicular lymphoma
Small lymphocytic lymphoma (CLL)
Marginal zone lymphoma

A

Low-grade lymphoma

109
Q

Diffuse large B cell lymphoma
Burkitt’s lymphoma
Mantle cell lymphoma

A

High-grade lymphoma

110
Q

positive staining for CD10 and Bcl2

A

Follicular lymphoma

111
Q

14;18 translocation involving Bcl2 gene

A

Follicular lymphoma

112
Q

Cells are CD5 and CD23 positivie

A

Small cell lymphoma

113
Q

Richter transformation

A

Small lymphocytic lymphoma -> high grade lymphoma/leukaemia

114
Q

Arise mainly in extra-nodal sites, arise from post-germinal centre memory cells

A

Marginal zone lymphoma

115
Q

middle aged male
Disseminated disease
Lymph in GI tract

A

Mantle cell lymphoma

116
Q

Mantle cell lymphoma survival?

117
Q

Show aberrant expression of cyclin D1 and CD5

A

Mantle cell lymphoma

118
Q

“Angular / clefted nuclei”

A

Mantle cell lymphoma

119
Q

Cyclin D1 overexpression

A

Mantle cell lymphoma

120
Q

Jaw or abdominal mass in children and young adults

A

Burkitt’s lymmphoma

121
Q

EBV lymphoma

A

Burkitt’s

122
Q

Starry sky appearance
Germinal cells

A

Burkitt’s

123
Q

c-Myc translocation (8;14, 2;8 or 8;22)

A

Burkitt’s lymphoma

124
Q

Middle-aged and elderly patients with lymphadenopathy

A

Diffuse large B cell lymphoma
OR
T cell lymphoma - more aggressive

125
Q

p53-positive and high proliferation fraction

A

Poor prognosis Diffuse Large B Cell Lymphoma

126
Q

T cell lymphomas

A

Adult T cell leukaemia/lymphoma - HTLV1
Enteropathy-associated T cell lymphoma - Coeliac disease
Cutaneous T cell lymphoma (mycosis fungoides)
Anaplastic large cell lymphoma

127
Q

Children and young adults with lymphadenopathy - aggressive

A

Anaplastic large cell lymphoma

128
Q

Large epithelioid lymphocytes

A

Anaplastic large cell lymphoma

129
Q

2;5 translocation

A

Anaplastic large cell lymphoma

130
Q

Alk-1 protein expression

A

Good prognosis Anaplastic large clel lymphoma

131
Q

differences between Hodgkin and Non-Hodgkin Lymphoma

A

Hodgkin is more localised (usually one nodal site)
Hodgkin spreads contiguously to adjacent to adjacent lymph nodes

132
Q

Young and middle-aged patients with only a single group of lymph nodes involved
Associated with EBV

A

Hodgkin’s Lymphoma

133
Q

Reed sternberg cells?

A

Bi / multi - nucleated abnormal lymphocyte

134
Q

Hodgkin cell?

A

Mononucleated abnormal lymphocyte

135
Q

+ve CD15 and CD30, (CD20 negative)

A

Hodgkin’s lymphoma - classic

136
Q

Isolated lymphadenopathy
NO association with EBV

A

nodular lymphocyte predominant Hodgkin lymphoma.

137
Q

B cell rich nodules with scattered around L&H cells

A

lymphocyte predominant Hodgkin lymphoma

138
Q

Positive = CD20
Negative = CD15, CD30 (unlike classical Hodgkin lymphoma)

A

Lymphocyte predominant Hodgkin’s lympgoma

139
Q

B symptoms

A

Fever
Night Sweats
Weight loss

140
Q

Lymphoma stages

A

1 = 1 group of nodes

2 = > 1 group of nodes on the same side of the diaphragm

3 = > 1 group of nodes above and below the diaphragm

4 = extranodal spread

Suffic ‘B’ if B symptoms are present

141
Q

Stage lymphoma how?

A

PDG-PET/CT

142
Q

ABVD

A

Hodgkin’s lymphoma chemo regime:
- Adriamycin
- Bleomycin
- Vinblastine
- Dacarbazine

143
Q

Curability of Hodgkin’s

A

Stage I and II: >80%

Stage IV: 50%

144
Q

LDH marker?

A

Of cell turnover

145
Q

R-CHOP

A

Diffuse large b cell lymphoma:
R-CHOP
- Rituximab
- Cyclophosphamide
- Doxorubucin
- Vincristine
- Prednisolone

146
Q

R-CVP

A

Tx for Follicular Lymphoma:
R-CVP (rituximab, cyclophosphamide, vincristine, prednisolone)

147
Q

Epigastric pain, ulceration, bleed
B-symptoms uncommon

A

Gastric MALToma

148
Q

EATL prognosis

A

no response to chemo
usually fatal

149
Q

most common leukaemia in Western world

150
Q

CLL - cells?

A

Prolif of mature B cells

151
Q

Smear cells

152
Q

Lymphocytosis
Smear cells
Normocytic normochromic anaemia
Thrombocytopaenia
Bone marrow lymphocytic replacement of normal marrow elements

153
Q

CD19 positive
CD5 negative

A

Mature B cells

154
Q

CD19 negative
CD5 positive
CD3 positive
CD4 or CD8 positive

A

Mature T cells

155
Q

CD19+ and CD5+

A

CLL or Mantle cell lymphoma

156
Q

Rai and BInet staging system

A

CLL

Binet: stages A-C depending on number of lymphoid areas (< or > 3, Hb and platelets)

157
Q

TP53 mutation - worse prognosis
IgH V gene mutation - better prognosis
CD38 expression

158
Q

Ig levels in CLL

A

Hypogammaglobulinaemia
Malignant B cells suppressing Ab production by B cells

159
Q

Richter transformation risk of CLL

A

1% per year

160
Q

Richter transformation Tc?

161
Q

TP53 intact CLL treatment?

A

FCR - Fludarabine, Cyclophosphamide, Rituximab

162
Q

CAR T therapy for CLL targets?

163
Q

Tx new options for CLL?

A

Bcl2 inhibitor - venetoclax
Bruuton tyrosine kinase inhibitor - Ibrutinib - p53 mutation
PI3K inhibitor - Idelalisib

164
Q

Transient Abnormal Myelopoiesis associations?

A

Down’s syndrome
20% develop Myeloid leukaemia in 4 yrs

165
Q

Transient Abnormal Myelopoiesis - pathophys?

A

Preleukaemic blasts in bone marrow and blood of neonate

166
Q

GLOBIN GENES:
Beta
Delta
Gamma
Epsilon

A

BETA - chromosome 11

167
Q

GLOBIN GENES:
Alpha 1 and 2
Zeta

A

Alpha - chromosome 16

168
Q

Hb - 2 alpha, 2 beta

169
Q

Hb - 2 alpha, 2 delta

170
Q

Hb - 2 alpha, 2 gamma

171
Q

Foetal Hb
2 zeta, 2 epsilon

172
Q

Foetal Hb
2 alpha, 2 epsilon

173
Q

Foetal Hb
2 zeta, 2 gamma

A

Portland 1

174
Q

HbA2 level in adult healthy

175
Q

Birth Hb levels and types

A

1/3 HbA
2/3 HbF

176
Q

homozygosity for HbS gene

A

Sickle cell anaemia

177
Q

Howell-Jolly bodies

A

Splenic dysfunction -> Hyposplenism
Sickle cell anaemmia too

178
Q

Parvovirus causes?

A

Aplastic anaemia

179
Q

clinical features of beta thalassaemia major:

A

Anaemia → heart failure, growth retardation
Erythropoietic drive → bone expansion, hepatomegaly, splenomegaly
Iron overload → heart failure, gonadal failure

180
Q

Beta thalassaemia major Mx

A

Accurate diagnosis and family counselling
Blood transfusion
Iron chelation therapy
Consider child as individual an part of family

181
Q

Iron chelating drug

A

Desferrioxamine

182
Q

Pentose shunt

183
Q

Glycolytic pathway

A

Pyruvate Kinase Def

184
Q

Red cell membrane abnormality

A

hereditary spherocytosis, hereditary eliptocytosis
- Spherocytes = spherocytosis
- Eliptocytes = eliptocytosis

185
Q

Inherited haemolytic anaemia

A

Thalassaemia
Sickle cell
Pyruvate kinase def
G6PD
Hereditary Spherocytosis
Hereditary eliptocytosis

186
Q

Acquired congenital haemolytic anaemia

A

Haemolytic disease of the newborn

187
Q

Low reticulocyte count

A

Aplastic anaemia

188
Q

inheritance pattern of G6PD deficiency

A

X-linked recessive

189
Q

Children - Acquired Haemolytic anaemia

A

Autoimmune haemolytic anaemia (AIHA)
Haemolytic Uraemic syndrome

190
Q

Positive DAT
Spherocytes on blood film

191
Q

Acute renal failure
Microangiopathic haemolytic anaemia
Thrombocytopenia

192
Q

Microangiopathic hemolytic anemia
Thrombocytopenic purpura
Neurologic abnormalities
Fever
Kidney disease

193
Q

Schistocytes

194
Q

Intravascular haemolysis of occuring due excessive shear forces in small vessels

195
Q

Haemarthrosis when starting to walk
Bruises
Excessive post-traumatic or surgery bleeding

A

Haemophilia A and B in infant

196
Q

Mucosal bleeding
Bruises
Post-traumatic bleeding

197
Q

Haemophilia A or B more common?

A

Haemophilia A is 4x more common than B

198
Q

Differentials for ITP

A

Henoch-Scholein Purpura
Non-accidental injury
Coagulation factor defect
Inherited thrombocytopaenia
Acute leukaemia

199
Q

Tx ITP?

A

Observation (most common)
Corticosteroids
High dose IVIG
IV anti-RhD (if RhD positive)

200
Q

Most common leukaemia in children?

201
Q

CD34

A

Stem cell marker

202
Q

Risk of dying from BM transplant

203
Q

autologous stem cell transplantation Mechanism?

A

Growht factor is given to the patient to stimulate the production of cells from the bone marrow
Cells are sampled from the patient’s bone marrow (some of them will be CD34+ stem cells)
These are preserved in a freezer
High-dose chemotherapy is given to the patient to eradicate their bone marrow
Stem cells are re-infused

204
Q

Most common reasons for Autologous HSCT

A

Myeloma
Lymphoma
CLL

205
Q

Allogenic Stem Cell Transplant uses?

A

Acute leukaemia
Chronic leukaemia
Myeloma
Lymphoma
Bone marrow failure
Congenital immune or haematological conditions

206
Q

GvHD which transplant

207
Q

equation that relates the probability of having a sibling with a matching tissue type to the number of siblings a patient has

A

Probability of match = 1 — (3/4) ^ number of siblings

208
Q

HLA for Class I - Present to CD8+ (cytotoxic T cells)

A

HLA-A, B, C

209
Q

HLA for Class II - Present peptide to CD4+ (Helper T cells)

A

HLA-DP, DQ, DR

210
Q

Match rate with parent?

A

1/2

6 HLAs, 2 x parents, match rate = 1/2

211
Q

Allogenic HSCT mechanism?

A

Identify disease unlikely to respond to standard treatment
Treat patient into remission
Identify donor and collect stem cells
Give patient myeloablative therapy
Infuse stem cells
Continue immunosuppression and support patient through period of cytopenia

212
Q

GvHD - acute vs Chronic

A

<100 days = acute
>200 days = chronic

213
Q

GvHD symptoms - acute

A

Skin - painful rash and desquamation
GI tract - abdominal pain and diarrhoea
Liver - jaundice and hepatomegaly

214
Q

GvHD symptoms - chronic

A

Skin - sclerosis, ulcers, nail dystrophy
Mucosal membranes - ulcer
Lungs - bronchiolitis obliterans
Liver - dysfunction and jaundice
Dry eyes
Polymyositits

215
Q

Treatment for acute GvHD

A

Corticosteroids (mainstay)
Calcineurin inhibitors: cyclosporin, tacrolismus
Mycophenolate mofetil
Monoclonal antibodies
Photophoresis
Total lymphoid irradiation

216
Q

Prevention of GvHD

A

Mycophenolate is standard prevention regime

ALSO:
Methotrexate
Corticosteroids
Calcineurin inhibitors
Post-transplant cyclophosphamide

217
Q

GvHD cells involved?

A

Mature lymphocytes, not stem cells

218
Q

Neutropaenic sepsis?

A

Fever >38 for over an hour
Single fever >39
Patient w neutrophils <1 x 10^9

Broad-spec Abx

219
Q

Post-HCST:
Pneumonitis
Retinitis
Colitis
Encephalitis

A

CMV disease post-transplant

220
Q

CMV Tx?

A

Ganciclovir

DEFNE Extra Buzzwords (14 decks)

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