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Haematology > Haematology > Flashcards

Haematology Flashcards

1
Q

Worst prognostic factor in AML

A

Age > 60

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2
Q

Who has higher recurrence rates post VTE - men or women?

A

Men

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3
Q

Which vaccines should someone with no spleen have? 4

A

Haemophilus influenza B (HiB)
Influenza (annual)
Meningococcus
Pneumococcus

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4
Q

Which 5 clotting factors are contained in cryoprecipitate

A

Fibrinogen
vWF
XIII
Fibronectin
VIII

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5
Q

What class of drugs can cause a false positive dilute roussel venom viper test?

A

Anti-Xa drugs

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6
Q

What are the types of Haemoglobin?

A 
Hb A (adults)
 - Two alpha, two beta
Hb F (babeh)
 - Two alpha, two gamma

Hb S
- Mutant beta chain

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7
Q

Wells criteria for PE

A
  • *3.0 points - C**linical signs and symptoms of DVT (swelling, tender calves)
  • *3.0 points -** Other Dx less likely than PE
  • *1.5 points - P**ulse >100
  • *1.5 points -** Surgery in previous 4 weeks or immobilisation (>3 days)
  • *1.5 points - P**revious DVT/PE
  • *1.0 point - H**aemoptysis
  • *1.0 point** - Malignancy

Traditional Wells criteria
-High > 6.0
-Moderate 2.0 to 6.0
-Low <2.0
Modified Wells criteria
-PE likely >4.0
-PE unlikely <4.0

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8
Q

Warfarin reversal WITH bleeding

  • lifethreatening and INR > 1.5
  • clinically significant but not life threatening, INR > 2.0
  • any INR with minor bleeding
A
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9
Q

Warfarin Reversal in someone who is NOT bleeding

  • INR <4.5 =
  • INR 4.5 to 10 =
  • INR > 10 =
A
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10
Q

Waldenstrom Macroglobulinaemia

  • Genetic mutation
  • clinical presentation
  • treatment
A
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11
Q

von Willebrand Factor

A
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12
Q

Vitamin K

A
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13
Q

Typical coagulation profiles

A
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14
Q

Typical CLL Immunophenotype

A
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15
Q

TTP

  • define
  • what is the cause of the hereditary form
  • pathogenesis
  • describe symptoms
  • Ix findings
  • 3 components of treatment
  • prognosis with and without treatment
A
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16
Q

Treatment of Waldenstrom Macroglobulinaemia

A
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17
Q

Treatment of ITP

A
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18
Q

Treatment of Hodgkin Lymphoma

A

Two different chemotherapy approaches

  • ABVD (every 14 days in 28 day cycles). Cures:
    • 90-95% Early Stage patients, and
    • 60-70% with Advanced Stage Disease
  • Escalated BEACOPP (every 21 days) – MORE TOXIC BUT
    • Cures more but much more intensive, (can’t use in older patients), much higher incidence of sterility, more premature menopause, and long term risk MDS/AML unresolved

Diminishing role of radiotherapy - Advanced disease: no overall survival difference

New agents:

  • Brentuximab: Anti-CD30 conjugated with MMAE a tubulin toxin, very promising, AE reversible peripheral neuropathy. 75% respond, 2yr OS 65%
  • PD-1 Checkpoint Inhibitors –Pembrolizumab : similar ORR, autoimmune toxicities
  • Both approved in Australia for double relapsed / refractory patients.
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19
Q

Treatment of Haemochromatosis

A
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20
Q

Treatment of CLL

A

When to treat CLL? – ONLY When it threatens trouble.

  • Rituximab (anti-CD20 antibody), Fludarabine and Cyclophosphamide: R-FC in <60yr.
    • ↑ CR, PFS & OS (69% at 6yrs)

UNLESS:

  • 17pdel or TP53 mutation (these patients have a known short term response to other therapies) – Ibrutinib compassionate access in Aust, Venetoclax funded in NZ
  • Obinutuzumab (Type II anti-CD20 with enhanced ADCC) + chlorambucil current frontline treatment for frail elderly (Must have CrCl>30, and cumulative illness rating scale, CIRS>6, or CrCl<70)
  • Oral enzyme inhibitors –for patients with relapsed disease
    • Bruton’s tyrosine kinase inhibitor: Ibrutinib Works very well so long as you stay on it.
    • bcl2 inhibitor: Venetoclax –potential to obtain CR and cease therapy after ≤ 2 years

Because the more effective enzyme inhibitors are not available for most patients in 1st line there is now a tendency to watch closely for intolerance or poor response with a lower threshold for moving to second-line therapies.

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21
Q

Ibrutinib - MoA and indication/useage

A
  • BTK –Bruton Tyrosine Kinase –plays a crucial role in B cell maturation.
  • Ibrutinib oral BTK inhibitor, well tolerated
  • Blocks BTK = blocks BCR signalling / activation. Induces apoptosis, blocks migration / adherence
  • 71% response rate in 85 patients with refractory CLL.
  • Redistribution lymphocytosis (reduced by giving with Rituximab – but no additional benefit of adding rituximab)
  • Prolonged duration of response even if del17p
  • PBS listed for pts with Rel/Ref CLL unsuitable for purine analogue (fludarabine). Strict criteria for suitability based on age/frailty and also 17p del disease by FISH
  • Now available on compassionate basis for 1L del 17p
  • S/E: bruising ++ (withhold 7 days prior to and after major surgery, 3d for minor procedures), diarrhea, fatigue, AF in 7%
  • No clear benefit from adding rituximab except dampens the lymphocytosis.
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22
Q

Treatment algorithm for newly diagnosed MM

A

Side effects

  • Bortezomib/Thalidomide –neuropathy
  • Lenalidamide/Pomalidomide-cytopenias
  • Carfilzomib –cardiac probs
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23
Q

TRALI

  • Which products are highest risk
  • Describe the presentation and the time course
  • What is the 2 hit mechanism
  • Management
  • Single most important prevention strategy
A
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24
Q

Target Hct in PCV?

A

0.40 to 0.45 (aka 40% to 45%)
NEJM 2013

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25
Q

TACO vs TRALI (Blood transfusion)

A
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26
Q

Synthesis and Regulation of Thromboxane A2

A
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27
Q
  • *Summary of platelet activation**
  • Adhesion
    1. GPIb-V-IX receptor complex binds to what?
    2. GP VI and GPIa/IIa receptors bind to what?
  • Secretion
  • What do alpha granules contain
  • What do dense granules contain
A

Adhesion

  • GP Ib-V-IX receptor complex binds to vWF immobilized on collagen
  • GP VI and GP Ia/IIa receptors bind to exposed collagen

Secretion

  • alpha granules - contain fibrinogen, vWF, and factor V
  • dense granules - contain ADP

Aggregation

  • platelet activation triggers conformational change in GP IIb/IIIa from inactive to active state
  • fibrinogen and vWF function as bridges between GP IIb/IIIa rceptors on neighboring activated platelets
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28
Q

Suggested duration of therapy to prevent recurrent VTE

A
  • New trials demonstrating that a finite period of full dose NOACs and then transitioning to prophylactic dose of NOAC demonstrates the same benefit as full dose with less SE of bleeding
  • High risk patients probably unlikely but may be a suitable approach in appropriate patient
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29
Q

Subtype of Hodgkin Lymphoma that is/has

  • Best prognosis
  • Worst prognosis
  • Most common
A

Best prognosis - Lymphocyte predominant (rare)
Worst prognosis - Lymphocyte depleted
Most common - Nodular sclerosing

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30
Q

Some causes of low and high hepcidin

A
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31
Q

Smoldering MM - definition

A
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32
Q

Sickle Cell Anaemia - Cause, Epi and Pathophys

A
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33
Q

Role of compression stockings in DVT

A
  • -Graduated compression stocking reduce incidence and severity of post thrombotic syndrome = use in all patients
  • -Must provide 30 - 40mmHg pressure at ankle and extend to level of the knee
  • -Wear stockings up to 18 months and indefinitely if post thrombotic syndrome is present
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34
Q

Risks of Autologous HCT

A
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35
Q

Risks of allogenic HCT

A
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36
Q

Risk Factors for GVHD

A
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37
Q

Reversal agent for Rivaroxaban/Apixaban

  • how does it work
  • main ADR
A

Andexanet alfa

  • modified factor X fragment which acts as a decoy
  • ADR = thrombosis
  • NOT AVAILABLE IN AUS
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38
Q

Reversal agent for Dabigitran

A

Idarucizumab

  • humanised monoclonal antibody fragment (Fab) that binds to dabigatran with very high affinity (340x fold more than dabigatran binds to thrombin).
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39
Q

Reptilase is normal with

A

HEPARIN THERAPY!

Investigation of patients with a prolonged Thrombin time (clotting). Assists in differentiating the effect of heparin, presence of FDP / D Dimer and dysfibrinogenaemia. A prolonged Thrombin time result will correct to normal using reptilase if this is due to heparin.

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40
Q

Red Blood Cells

A
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41
Q

Prothrombin Time

A

INR is derived from this = (pts PT/control PT) ^ ISI
-ISI = international sensitivity index

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42
Q

Prognostic Factors in B cell lymphoma - APLES

A

Age
Performance status
LDH
Extra nodal involvement
Stage

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43
Q

Preferred imaging modality for staging of Hodgkin lymphoma

A

FDG-PET/CT - chest/abdomen and pelvis

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44
Q

PNH

  • gene mutation
  • classic Sx
  • leading cause of death
  • Rx (requirements to be on this treatment)
  • Other therapies (3)
  • Definitive therapy
A
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45
Q

Platelet disorders vs Coagulation Disorders
-comparison of clinical consequencesd

A
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46
Q

Phenotype/Genotypes of Alpha Thalassaemia

A

Chromosome 16!

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47
Q

Pathophysiology of Alpha Thalassaemia

A
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48
Q

Overview of vWD

  • Function of vWF
  • Classification
  • Epi
  • Presentation
  • Types of tests
  • Treatment
A
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49
Q

Optimal agent to continue on to prevent recurrent VTE

A

Low dose rivaroxaban - superior to aspirin, and placebo
With non inferior rates of major bleeding and non-life threatening bleeding

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50
Q

Obinutuzomab - target

A

CD20

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51
Q

Normal Haemoglobin

  • Describe the structure of HbA, when does it predominate
  • Describe the structure of HbA2, when does it predominate
  • Describe the structure of HbF, when does it predominate
A
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52
Q

Myeloma Diagnostic Criteria

A

Asymptomatic Myeloma = Smoldering Myeloma

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53
Q

Myeloid vs Lymphoid CDs (5 each)

A
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54
Q

Multiple Myeloma Diagnostic Criteria

A
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55
Q

Most signicant APLS antibody - ie conveys greatest risk of thrombosis?

A

Lupus anticoagulant
Weakest = anti-cardiolipin (may have a role in pregnancy)

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56
Q

Most sensitive test for the presence of Rivaroxaban/Apixaban?

A

Anti-Xa
Must specify which agent you think patient is on to get a reference range

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57
Q

Most sensitive test for the presence of Dabigitran?

A

TCT
in higher concentrations APTT will also start to prolong
Can the do a hemaclot specific assay
If TCT and APTT are both negative - excellent NPV

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58
Q

Most common reason for major blood ABO incompatibility

A

Most common cause for acute haemolytic reatcions in Australia =** **INCORRECT PATIENT IDENTIFICATION

  • Failure to obtain pre-transfusion sample from the correct patient
59
Q

Most common genetic mutations in Polycythemia Rubra Vera

A

JAK2v617F (most common) - 95%
JAK2 exon 12 (second most common) - 4%

60
Q

Most common genetic mutations in essential thrombocytosis and primary myelofibrosis

A
  • *1. JAK2 = most common**
    2. CALR = second most common
    3. MPL`
61
Q

Mixing Study

A

MUST correct to normal and stay normal - otherwise there’s an inhibitor

62
Q

MGUS - definition and significance

A
63
Q

Mechanism of Action of Cancer Drugs - just read

A
64
Q

Mastocytosis

A
65
Q

Management of Sickle Cell Disease

A
66
Q

Management of Follicular Lymphoma

A
67
Q

Management of Antiphospholipid syndrome

A
68
Q

Major Components of Haemostasis

A
69
Q

Main Mechanism of Renal Disease in Multiple Myeloma

A
70
Q

Main glycoprotein receptors on platelets

A
71
Q

Lymphoma CD markers

A
72
Q

Lab findings of the different coagulopathies

A
73
Q

ITP

  • define
  • describe pathogesis
  • common precipitant
  • risk factors for severe bleeding
  • Ix findings
  • Mx of severe bleeding
  • Second line options
A
74
Q

Iron and Hepcidin

A
75
Q

Initiation Phase of Coagulation Cascade

A
76
Q

Inhibitors of Fibrinolysis

A
77
Q

Induction therapy for transplant eligible patients with multiple Myeloma

A

Lenalidomide + Bortezomib + Dexamethasone
Usually 4 months prior to cell transplant

78
Q

In young patients treated with radiotherapy what is the most likely **malignancy they will develop in the next 10 years

  • Women
  • Men**
A

Women - breast cancer
Men - thyroid cancer

79
Q

Important causes of aplastic anaemia

  • Telomere diseases
  • Fanconi anaemia - describe the phenotype, gene involved, pathophys
  • GATA2 deficiency - describe the phenotype
  • CTLA4 deficiency - describe the phenotype
A
80
Q

Intravascular vs Extravascular Haemolysis

A
81
Q

Immunophenotypes of CLL

A

Suspect whenever CD19 and CD5 are co-expressed = CLL

82
Q

If your blood causes _____ you should never donate again

A

TRALI
-Transfusion related acute lung injury

83
Q

Hydrops Fetalis (Alpha thalassaemia)

A
84
Q

Hodgkin Lymphoma - defining features and age distribution

A
85
Q

Hodgkin Lymphoma

  • Cell line
  • Classic type - what CDs are expressed and not-expressed
  • Classic presentation
  • Pathogenomic pathology finding
  • Best test of staging
  • What staging system is used and how does it work?
A
86
Q

Hodgkin Lymphoma
-Ann Arbor staging system (describe)

A

A or B - if presence of B symptoms (fever, drenching night sweats, LOW)
X - bulky disease
E - extra-nodal involvement

87
Q

High Risk Features of Multiple Myeloma that convey poor prognosis (4)

A
88
Q

Heyde’s syndrome

A

Aortic Stenosis + Acquired VWD + GI bleeding
-patient can develop angiodysplasia in GI tract
= severe and intractable bleeding

89
Q

HbH Disease (alpha thalassemia)

A
90
Q

Haemolytic uraemic syndrome

  • What is the cause
  • What is the classic triad
  • What is the mainstay of therapy?
A
91
Q

GPIIb/IIIa inhibitors:

A
92
Q

Genetic Mutation of APML

A

Remember - mutation in t(15:17) = GOOD prognosis

93
Q

Frequency of Monoclonal proteins of multiple myeloma

A
94
Q

Follicular Lymphoma

  • Cell type
  • Genetic mutation
  • Presentation
  • What determines tumour grade
  • Risk of transformation into what
A
95
Q

Final Common Pathway of Coagulation

A
96
Q

Fibrinolysis

A
97
Q

Factors which Terminate Coagulation Cascade

A
98
Q

Factors included in Prothrombinex (Prothrombin Complex)

A

II, IX, X
ie 2, 9, and 10
Some countries also include factor VII (7)

99
Q

Endothelial elements inhibiting thrombus formation

A
100
Q

Drugs which are SAFE in the Rx of HITTS (4)

A

Direct thrombin inhibitors - Argatroban, Bivalirudin
Heparinoids - Danaparoid, Fondaparinux
NOT Warfarin as this will decrease level of protein C = risk of venous limb gangrene

101
Q

Drugs and Coagulation Cascade

A
102
Q

Dipyridamole

A
103
Q

Diffuse Large B Cell Lymphoma

  • Important epi fact
  • How does it present
  • What are the B symptoms
  • Most common primary, extra-nodal site?
  • Most common immunophenotype
  • Treatment of limited stage
  • Treatment of advanced stage
  • Prognosis without therapy
A
104
Q

Different Morphology of AML and ALL

A
105
Q

DIC pathogenesis

A
106
Q

Diagnostic Criteria of CLL

A

In CLL: lymphocytes CD5+, CD19+, CD23+

Smudge cells on film.

SLL - small lymphocytic lymphoma = nodal counterpart, same approach

FISH in CLL

Genetic aberrations can be detected in >80%

Unfavourable more commonly seen in advanced disease

  • 17p deletion -median 3yr survival
  • 5% in newly diagnosed,
  • 30% relapsed/refractory
  • Mutation/del p53 → resistance to traditional chemo (e.g. F+C)

Favourable

  • del 13q –median 12yr survival
107
Q

Diagnostic Criteria for Anti-phospholipid syndrome

A
108
Q

Diagnosis of Polycythemia

A

WHO criteria - must fit all 3 major criteria and minor

Major criteria

●Increased hemoglobin level (>16.5 g/dL in men or >16.0 g/dL in women), hematocrit (>49 percent in men or >48 percent in women), or other evidence of increased red cell volume

●Bone marrow biopsy showing hypercellularity for age with trilineage growth (panmyelosis) including prominent erythroid, granulocytic, and megakaryocytic proliferation with pleomorphic, mature megakaryocytes (differences in size)

●JAK2 V617F or JAK2 exon 12 mutation

Minor criterion

●Serum erythropoietin level below the reference range for normal

109
Q

Defining feature of acute leukaemia on BM

A

Presence of >20% blasts on BM morphology

110
Q

Daratumumab - target

A

CD38

Used in MM

111
Q

D-dimer

A
112
Q

Criteria for accelerated phase CML

A

>20% basophils in peripheral blood

113
Q

Clinical Features of Multiple Myeloma in order of prevalence

A
114
Q

Causes of secondary polycythemia (6)
-key examination feature

A
  1. High altitude
  2. COPD
  3. Smoking
  4. Sleep Apnoea
  5. Drugs - EPO, testosterone
  6. Other - Renal, hepatic tumours, hereditary
115
Q

Causes of Prolonged TCT (thrombin clotting time) (4)

A

All other causes of prolonged TCT will prolong reptilase time
Heparin/Enoxaparin will have a normal reptilase time

116
Q

Causes of Prolonged PT/INR (out of proportion to APTT) (3)

A
117
Q

Causes of Prolonged APTT and PT (in proportion) (3)

A
118
Q

Causes of Low Protein C and S

A

Protein C and S
-Drugs: Warfarin, L asparaginase
-Liver disease, vitamin K deficiency, DIC
_______________
Protein S alone
- OCP
- Breast feeding and pregnant women

119
Q

Causes of an Isolated Prolonged APTT (5)

A
120
Q

Anticoagulation test elevated in dabigatran use?

A

Thrombin Time

APTT >PT also elevated,

121
Q

Coagulation study elevated in anti-Xa agents ie apixaban, rivaroxaban?

A

Prothrombin Time!

APTT normal or slightly up

NO EFFECT on thrombin time

122
Q

Brentuximab - target

A

CD30

Used in refractory NHL

123
Q

Blinatumomab - target

A

CD3 on T cells /19 on B cells

used in Philadelphia chromosome-negative relapsed or refractory acute lymphoblastic leukaemia.

124
Q

Beta Thalassaemia pathophysiology and manifestations

A
125
Q

Beta Thalassaemia - predictors of disease severity

A
126
Q

Beta Thalassaemia - genotypes and phenotypes

A
127
Q

Benefits of Tranexamic Acid in adult trauma patients

A

Reduced all cause mortality
Reduced bleeding mortality
with less MI events but no difference in rate of DVT/PE/stroke

No benefit in

  • death due to head injury
  • amount of transfused blood products
  • Benefit lessened if given after 3 hours*
  • *As per CRASH-2 trial**
128
Q
  • *Atypical HUS**
  • define and how is it different from typical
  • most common gene mutation
  • novel Mx, how does it work, serious SE
  • Other options
  • Definitive Mx
A
129
Q

aPTT general principles

A

INTRINSIC PATHWAY

130
Q

Approach to VTE prophylaxis in pregnant women with inherited thrombophilias

A
131
Q

Approach to Bridging Therapy

A
132
Q

APML

  • defining gene mutation
  • strong association with which disorder
  • treatment
  • SE of treatment, management of this syndrome
  • Prognosis without treatment
  • Prognosis with treatment
  • Main cause of death
A
133
Q

Aplastic anaemia

  • Describe 3 features of BM aspirate
  • What is the ideal treatment?
A
134
Q

Antiphospholipid antibodies

A

Lupus anticoagulant
Anticardiolipin antibodies
Anti-beta2 glycoprotein I antibodies

135
Q

Amplification Phase of Coagulation Cascade

A
136
Q

AML treatment

A
137
Q

AML

  • 2 Good Prognostic features
  • 4 Poor Prognostic features (“CAMP”)
A
138
Q

Acute Complications of Blood Transfusion

A

FNHTR = febrile non haemolytic transfusion reaction

  • Common, diagnosis of exclusion
  • More common in platelet transfusion than RBC
  • Frequency decreased with leukoreduced products
  • Pathogenesis - mediated by release of cytokines from the products WBCs
  • Presentation - fever +/- chills with no systemic features
  • Treatment - symptomatic

AHTR = acute haemolytic transfusion reaction

139
Q

7 Unfavourable Prognostic Factors in Hodgkin’s Lymphoma

A
140
Q

4 main factors which activate inactivated platelets

A
141
Q

Synthesis and Regulation of Thromboxane A2

A
142
Q
A
143
Q
A
144
Q
A

Haematology (4 decks)

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