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Nimna's Flash Cards > Haematology > Flashcards

Haematology Flashcards

1
Q

Which haematological condition is budd chiari associated with?

A

Polycythemia vera

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2
Q

Mutation associated with Polycythemia Vera

A

jAK2 V617F somatic mutation

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3
Q

What is erythromelalgia

A

tenderness or painful burning and/or redness of fingers, palms, heels, or toes

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4
Q

Symptoms of primary myelofibrosis

A

Anaemia, hepatosplenomegaly

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5
Q

BMAT findings in myelofibrosis

A

fibrosis + atypical megakaryocytic hyperplasia and thickening +distortion of the bony trabeculae (osteosclerosis)

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6
Q

MOA of Tranexamic acid

A

synthetic analogue of the amino acid lysine. It serves as an anti-fibrinolytic by reversibly binding four to five lysine receptor sites on plasminogen. This reduces conversion of
plasminogen to plasmin, preventing fibrin degradation

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7
Q

Test which indicates pure red cell aplasia

A

LOW Reticulocyte count

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8
Q

Most common cause for ABO incompatibility

A

Wrong patient identified

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9
Q

Hb is 190. What test is required to diagnose Polycythemia Vera

A

Jak2 V61F mutation

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10
Q

MOA of Warfarin

A

Anti-thrombotic effect: Factor II inhibitor - 3 day half life.
Anti-coagulant effect: Factor VII, IV, X - 12 hour half life.
Inhibition of Protein C - Pro-coagulant effect - warfarin necrosis occurs in patients with an underlying, innate and previously unknown deficiency of protein C

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11
Q

Cause of Warfarin necrosis

A

Inhibition of Protein C - Pro-coagulant effect - warfarin necrosis occurs in patients with an underlying, innate and previously unknown deficiency of protein C

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12
Q

Chemotherapy neutrophil nadir

A

10-14 days

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13
Q

Short term management of bleeding in Von Willibrands disease

A

DDAVP

vWF concentrates

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14
Q

CML mutation

A

Philadelphia chromosome t( 9,22) BCR-ABL translocation.

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15
Q

CML first line treatment

A

TKI - Imatinib.

Others - Nilotinib, Dasatinib

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16
Q

What is factor V leiden?

A

Factor 5a is a procoagulant that has a positive feedback loop with thrombin. Thrombin activates Protein C which negatively feeds back to factor 5.
Factor V leiden is where Factor 5 is resistant to Protein C - leads to procoagulant state.

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17
Q

What is protein S ?

A

Protein S is a co-factor of protein C. It breaks down factor 8a and 5a.

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18
Q

Treatment of ITP

A

High dose glucocorticoids or IVIG - treat only if high bleeding risk or plt <20,000.

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19
Q

Type of inheritance of Von Willebrands disease

A

Autosomal dominant

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20
Q

Management of Haemophillia perioperatively?

A

Give factor 8

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21
Q

Cause of High Hepcidin

A

Chronic inflammation

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22
Q

Low Hepcidin

A

Haemachromatosis

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23
Q

Drug which prolongs survival in MDS

A

Azacitidine

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24
Q

Mechanism of action of antiplatelets

A

inhibits the P2Y12 subtype of ADP receptor, which is important in activation of platelets and eventual cross-linking by the protein fibrin.

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25
Q

Warfarin MOA

A

Vit K epoxide reductase inhibitor

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26
Q

Heparin MOA

A

binds to the enzyme inhibitor antithrombin III (AT), causing a conformational change that results in its activation.

Inhibits Xa and thrombin.

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27
Q

Cause of TTP

A

ADAMTS13 deficiency ( <10%)- usually cleaves large Von Willibrand factor multimers

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28
Q

Pathophys of complement mediated TMA (previously called aHUS)

A

hereditary deficiency of regulatory proteins that
restrict activation of the alternative pathway of complement or mutation of proteins that accelerate this
pathway. leads to uncontrolled activation of complement on cell
membranes.

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29
Q

Warfarin reversal

A
  1. Vitamin K
  2. Prothrombin X (4 factor) - (DO NOT use activated prothrombin)
  3. Tranexamic acid
  4. PRBC
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30
Q

Thrombosis secondary prevention in pregnancy

A

Clexane

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31
Q

4 causes of impaired Haematological cell production

A
  1. Congenital aplastic anaemia
  2. Acquired aplasic anaemia
  3. Bone marrow infiltration
  4. MDS
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32
Q

Cause of acquired aplastic anaemia

A

Auto-immune due to IL 17

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33
Q

Treatment of aplastic anaemia

A

Cell count > 50 - triple immunosuppresion - Cyclosporin + Methyl pred + Anti-thymoglobulin.

Cell count < 50 - HSCT

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34
Q

4 features of Fanconi’s anaemia

A
  1. FANC genes
  2. Cafe au lait spots
  3. Microcephaly
  4. Haematological malignancies
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35
Q

GATA 2 mutation effects

A

Increased mycobacterial infections

MDS/ AML

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36
Q

Findings in hairy cell leukemia

A
  1. splenomegaly
  2. pancytopenia
  3. dry BMAT
  4. CD103, CD25, CD11, CD20
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37
Q

Pathophys of Paroxysmal nocturnal haemaglobinuria

A

Lack of GPI anchor on blood cells, therefore no CD55 or CD59. Causes complement mediated cell destruction.

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38
Q

Pathyophys of Haemophagocytic Lymphohistiocytosis (HLH)

A

Loss of destruction of activated immune cells.

Macrophages phagocytose red cells.

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39
Q

Signs/Symptoms of Haemophagocytic Lymphohistiocytosis (HLH)

A
  1. Fever
  2. Splenomegaly
  3. Cytopenias
  4. High triglycerides and low fibrin
  5. Hemophagocytosis on biopsy
  6. Decreased or absent NK cell activity
  7. High ferritin
  8. Elevated CD25
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40
Q

MGUS criteria

A
  1. M protein <30
  2. BM clonal plasma cells <10%
  3. No MM defining events
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41
Q

Smouldering myeloma criteria

A
  1. M protein > 30
  2. BM clonal plasma cells 10-60%
  3. No MM defining events
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42
Q

Multiple Myeloma criteria

A
  1. BM clonal plasma cells > 10% OR has plasmacytoma

2. MM defining event (CRAB, FLC>100, clonal plasma cells >60%, >1 bone lesion)

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43
Q

Hyperviscosity findings on fundoscopy

A

Flame haemorrhages

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44
Q

Multiple Myeloma genes

A

t(4,14) t(14,16), del(17p)

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45
Q

Causes of renal failure in multiple myeloma

A
  1. Myeloma Cast nephropathy
  2. Light chain deposition disease
  3. Amyloidosis
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46
Q

Myeloma treatement

A

Bortezomib, Thalidomide, Daratumumab

+/- BMAT

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47
Q

AML gene mutations

A
  • FLT3 (Mx with Midastaurin)
  • NPM1 mutation is protective
  • t(8;21)
  • t(16;16)
  • t(15;17) - APML
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48
Q

AML treatment

A

Cytarabine + Anthracycline (rubicin)

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49
Q

APML treatment

A 
Medical emergency 
Vit A (ATRA) + Arsenic

Good prognosis

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50
Q

APML histology and flow cytometry

A

Granulation + Auer rods

Flow cytometry - CD13, CD33, CD45, CD117, MPO. (CD34 and HLA negative)

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51
Q

APML gene mutaion and presentation.

A

t (15,17) - creates fusion of PML and RARA. - Leads to cessation of differentiation and abnormal retinoic metabolism.
Haemorrhage from DIC

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52
Q

Management of Waldenstroms Macroglobulinemia

A

Rituximab + Bendamustine
Dexamethasone + Cyclophosphamide
Ibrutinib.

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53
Q

Management of DLBCL

A

R-CHOP

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54
Q

What is Rasburicase

A

To prevent hyperuricaemia in Tumor lysis syndrome.

Is a urate oxidising agent.

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55
Q

CLL blood film finding

A

smudge cells.

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56
Q

CLL surface proteins

A

CD5, CD19, CD23, CD200

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57
Q

Target for Clopidogrel

A

P2Y12

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58
Q

Von Willibrand Factor function

A

Platelet adhesion + Binds factor 8

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59
Q

Management of Haemophilia A

A
  • 3 weekly injections of clotting factor concentrate.

- If antibodies present - Factor 7

60
Q

How long do NOACs need to be withheld pre-surgery?

A

24hrs if normal renal fn.

61
Q

Dabigatran reversal agent

A

Idarucizumab
If Idarucizumab is not available - use Activated Prothrombin concentrate (aPCC/ FEIBA)
If within 2 hours of last dose - use activated charcoal

62
Q

Apixaban reversal agent

A

Andexanet

63
Q

Hepcidin role

A

Decreases serum iron. Regulates iron transport.

64
Q

What causes HbE

A

Single base substitution.

Only causes symptoms when in combination with b-Thalassemia.

65
Q

Management of a-Thalassemia

A

transfuse >100 to prevent EPO production.

Iron chelation

66
Q

Types of haemolytic anaemia

A

Cold agglutinin disease
Warm AIHA
Microangiopathic Haemolytic anaemia (MAHA)

67
Q

TTP Pentad of symptoms

A
  1. Anaemia
  2. Neurological symptoms.
  3. Renal failure
  4. Fever
  5. Thrombocytopenia
68
Q

Universal plasma donor

A

Type AB

69
Q

TPO receptor agonists

A

Romiplostim

Eltrombopag

70
Q

Aplastic anaemia has overlap with which other disease?

A

Paroxysmal Nocturnal Haemoglobinuria.

71
Q

BMAT findings in MDS

A
  1. Increased blasts <20%
  2. Granulocytic precursor myeloid cells
  3. small mononuclear megakaryocytes.
72
Q

Allergies, anaphylactic symptoms + high tryptase = what diagnosis

A

Systemic mastocytosis. Requires BMAT

73
Q

Lymphoma’s associated with EBV

A
  1. Burkitts
  2. NK cell lymphoma
  3. T cell lymphoma.
74
Q

Lymphoma associated with Hep C

A

Marginal cell lymphoma

75
Q

Lymphoma associated with Helicobacter Pylori

A

MALT lymphoma

76
Q

Salmonella Osteomyelitis is associated with which condition

A

Sickle cell disease

77
Q

Auto-immune gene linked to pernicious anaemia

A

AIRE gene (auto-immune regulator)

  • AIRE mutation also leads to candidiasis, alopecia, hypoparathyroidism and adrenal insufficiency.
  • usually have interferon autoantibodies
78
Q

What is Glanzmann’s thrombasthenia caused by?

A

Glycoprotein 2b3a deficiency

79
Q

Cause of hereditary spherocytosis

A

defect of ankyrin protein

80
Q

What is Feltys syndrome

A 
Splenomegaly 
Anaemia
Neutropenia
Thrombocytopenia 
Arthritis (RA)
  • Santa wears a felt belt
81
Q

Treatment of 5q del (MDS)

A

Lenalidomide

82
Q

Most common cause of renal failure in Multiple myeloma

A

Cast nephropathy

83
Q

Cause of death in Beta thalassemia major

A

Cardiomyopathy from iron overload

84
Q

When to use FFP

A
  • reversal of anticoagulation

- for massive transfusion protocols

85
Q

When to use platelets

A

Stable non-bleeding - use if plt <10
Stable non-bleeding febrile - use if plt <20
Pre- major surgery - use of plt <50
Pre- neuro or eye surgery - use if plt <100

Do not use in ITP/TTP/HITTS - will worsen thrombosis

86
Q

Highest risk of infection for blood products

A

platelets

87
Q

When to use cryoprecipitate

A

When there is low factor 8 or fibrinogen.

After massive haemorrhage

88
Q

Site of coagulation factor activation

A

surface of activated platelets

89
Q

MOA of venetoclax

A

inhibits BCL2

90
Q

complication of ABO incompatible bone marrow transplant

A

Red cell aplasia

91
Q

Poor chemo response gene in CLL

A

del17p

92
Q

Good chemo response gene in CLL

A

del13q - IVGH

93
Q

Predictors of improved survival in ALL with ASCT

A
  1. transplantation in first complete remission
  2. Short time between diagnosis and SCT
  3. HLA matched at DRB1
  4. CMV negative
  5. Philadelphia chromosome negative
94
Q

Best type of donor in ASCT

A

Relapse rates are higher after syngeneic or T cell-depleted grafts compared with unmanipulated sibling grafts.
Best grafts are HLA matched siblings.

95
Q

Highest cause of death in ALL post SCT

A

relapse of disease

96
Q

Binding site of Von-Willebrand factor

A

glycoprotein Ib-IX-V

Von Willibrand work 9-5

97
Q

Management of sickle cell disease

A

Hydroxyurea
Folic acid
avoid iron supplements
Regular Opthalmology for - proliferative sickle retinopathy

98
Q

Management of Antiphospholipid syndrome (anticoagulation choice)

A

WARFARIN.
Target 2-3.

Warfarin has greater efficacy than DOACs in trials.

99
Q

What is Emicizumab used for

A

Binds factor 9+10 together to make a surrogate factor 8 –> used in congenital haemophilia prophylaxis only.

100
Q

Mutations associated with Essential thrombocytosis (ET)

A
  1. JAK2
  2. CALR (Calreticulin) - lower risk of thrombosis
  3. MPL
101
Q

SE of Arsenic

A

Differentiation syndrome - give dex (serositis, effusions, hepatic dysfn, renal dysfn)
Electrolyte disturbance
Torsades de pointes

102
Q

Mx of aHUS

A

Eculizumab

103
Q

Diagnostic criteria for antiphospholipid syndrome

A

least one of the following clinical criteria AND at least one of the following laboratory criteria:

Clinical criteria
1. Deep Vascular thrombosis – One or more episodes of venous. Superficial venous thrombosis does not satisfy the criteria.

  1. Pregnancy morbidity – One or more unexplained deaths of a morphologically normal fetus at ≥10 weeks gestation, or one or more premature births of a morphologically normal neonate before 34 weeks gestation because of eclampsia, preeclampsia, or placental insufficiency, or three or more consecutive spontaneous pregnancy losses at <10 weeks gestation, unexplained by chromosomal abnormalities or by maternal anatomic or hormonal causes.

Laboratory criteria – The presence of one or more antibodies (aPL) on two or more occasions at least 12 weeks apart:

  • IgG and/or IgM anticardiolipin antibodies (aCL)
  • IgG and/or IgM anti-beta2-glycoprotein (GP)
  • Lupus anticoagulant (LA) activity detected according to published guidelines.
104
Q

Von Willibrands disease subtypes

A

●Type 1, an autosomal dominant disease, is the most common, accounting for approximately 75 percent of patients. It represents a partial quantitative deficiency of VWF.

●Type 2, which is usually an autosomal dominant disease, is characterized by several qualitative abnormalities of VWF. Four subtypes have been identified: 2A, 2B, 2M, and 2N.

●Type 3, a total deficiency of VWF, is an autosomal recessive disorder that leads to severe disease with undetectable levels of VWF.

105
Q

Hepatosplenomegaly + femoral bone deformity

A

Gaucher disease
lysosomal storage disease. Imaging shows Erlenmeyer flask deformity.
Associated with Parkinsons disease.

106
Q

What is Gaucher disease

A

lysosomal storage disease - error of metabolism that affects the recycling of cellular glycolipids. components accumulate within the lysosomes of cells (macrophages)

107
Q

What is Sweet syndrome

A

(acute febrile neutrophilic dermatosis) is an inflammatory disorder
characterized by the presence of inflammatory papules, plaques, or nodules on the skin,
systemic symptoms, and neutrophilic infiltration of the skin.

108
Q

Sweet syndrome histology

A

Neutrophilic infiltration

109
Q

Causes of Sweet syndrome

A

Classical - idiopathic
Malignancy related - AML
Drug related - GCSF

110
Q

Treatment of Sweet syndrome

A

Steroids

111
Q

Clexane/Heparin reversal agent

A

Protamine (fish sperm)

Adexanet (clexane only)

112
Q

Reversal for NOACs

A
  1. Adexanet
  2. Prothrombin X
  3. Activated charcoal if within 6 hours.
113
Q

Massive transfusion blood products and amounts

A

improved survival when the ratio of transfused Fresh Frozen Plasma (FFP, in units) to platelets (in units) to red blood cells (RBCs, in units) approaches 1:1:1

114
Q

Complication of massive transfusion

A

Large amounts of citrate are given with massive blood transfusion, since blood is anticoagulated with sodium citrate and citric acid. Metabolic alkalosis and a decline in the plasma free calcium concentration are the two potential complications.

Therefore should give calcium gluconate with infusion.

115
Q

CD200 can be used to differentiate which 2 conditions

A

CD200: a useful marker for differentiation between CLL (positive) and MCL mantle cell lymphoma (negative)

116
Q

CD23+ CD5+ CD200+

A

CLL

117
Q

CD23-, CD5+, CD200-

A

Mantle cell

118
Q

Venetoclax SE and MOA

A

SE: Tumor lysis syndrome, Oedema
MOA: BCL-2 mediates tumor cell survival and has been associated with chemotherapy resistance. Venetoclax binds directly to the BCL-2 protein, restoring the apoptotic process.

119
Q

Ibrutinib MOA and SE

A

irreversible inhibitor of Bruton’s tyrosine kinase (BTK), an integral component of the B-cell receptor (BCR) and cytokine receptor pathways.

SE: Infection, anaemia, HTN, bleeding, arrhythmias.

120
Q

Platelet transfusion is contraindicated in which type of bleeding

A

Intracerebral haemorrhage - increases death and dependence

121
Q

Drug to prevent aplastic anaemia in haemolysis

A

folate

122
Q

Marker for ALL

A

TDT - found only in immature lymphoid cells (lymphoblasts)

123
Q

Indications for AUTOLOGOUS BM transplant

A

Multiple myeloma - autologous is gold standard
relapsed lymphoma
Some auto-immune

124
Q

Indications for ALLOGENEIC BM transplant

A 
AML/ALL/MDS - post initial therapy 
Aplastic anaemia 
SCID 
NHL 
Haematological disease - eg sickle cell
125
Q

How long does immune reconstitution take after allogeneic transplant

A

12-18m

126
Q

Biggest factor in post transplant survival for allogeneic transplant

A

GVHD

Pre-transplant disease severity

127
Q

Biggest cancer increase after bone marrow transplant compared to population risk

A

oesophageal/ oropharyngeal

128
Q

Name of hepatic complication post bone marrow transplant

A

sinusoidal obstruction syndrome

129
Q

Features of DIC

A
  • acute precipitant
  • oozing from wound sites
  • thrombocytopenia
  • coagulopathy
130
Q

Management of MDS

A
  • EPO, antithymocyte, azacitadine. BM transplant.

- Lenalidomide if 5Q mutation.

131
Q

Management of MF

A

Ruxolitinib (JAK2)

or hydroxyurea.

132
Q

Hydroxyurea MOA

A

Hydroxyurea is an antimetabolite that selectively inhibits ribonucleoside diphosphate reductase, preventing the conversion of ribonucleotides to deoxyribonucleotides, halting the cell cycle at the G1/S phase and therefore has radiation sensitizing activity by maintaining cells in the G1 phase and interfering with DNA repair. In sickle cell anemia, hydroxyurea increases red blood cell (RBC) hemoglobin F levels

133
Q

What do lymphocytes attack in transfusion related GVHD

A

recipients bone marrow

134
Q

How to prevent transfusion related GVHD

A

Irradiation (as opposed to leukodepletion in febrile non-haemolytic reactions)

135
Q

Treatment of CML

A

BCR-ABL inhibitors (TKI) - imatinib

136
Q

Mechanism of relapse after CAR-T therapy and immunotherapy

A

Antigenic escape

137
Q

Abdo pain + weakness + psych changes

A

Acute intermittent porphyria

138
Q

Blistering to sun exposed skin

A

Porphyria cutanea tarda

139
Q

Target of Daratumumab in multiple myeloma

A

CD38 - expressed more on MM cells than normal lymphocytes.

140
Q

Multiple Myeloma high risk genes

A
  • t(4;14)
  • t(14;16)
  • Del17p
  • Del13
  • 1q21 amplification
141
Q

Management CLL

A

If high grade then can treat with Ibrutinib and Venetoclax
Traditional therapy - Fludrabine, clyclophosphamide, Rituximab (FCR)
Can watch and wait if indolent

142
Q

High risk mutations in CLL and best treatment.

A

un-mutated IGHV
TP53 aberration
chromosome 11q deletion.

Treatment - good response to Ibrutinib + Venetoclax

143
Q

Type of immunoglobulin in Warm auto immune haemolysis

A

IgG

144
Q

Type of immunoglobulin in Cold auto immune haemolysis

A

IgM

145
Q

Treatment for FLT3 mutation

A

Midastaurin

146
Q

1st line treatment for Philadelphia positive malignancy

A

Imatinib

147
Q

Treatment for T3151 positive malignancy

A

Ponatinib

Nimna's Flash Cards (15 decks)

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