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exam > 3 Myeloma, Lymphoma and Bleeding > Flashcards

3 Myeloma, Lymphoma and Bleeding Flashcards

1
Q

Risk factors for lymphoma (4)

A

Age
Immunosuppressed - HIV, organ transplant, autoimmune conditions
Infection - EBV, H.Pylori

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2
Q

Difference in cell types between CLL, ALL, lymphoma and myeloma

A

CLL - mature cells in peripheral blood/ marrow
ALL - blastic cells in peripheral blood/ marrow
Lymphoma - mature cells in tissues
Myeloma - mature plasma cells in bone marrow

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3
Q

Difference in cell morphology between high and low grade lymphoma

A

High - Large irregular cells, mitotic bodies (inc proliferation), dispersed chromatin and prominent nucleoli

Low - smaller regular cells, apoptosis rate is low so there is slower accumulation

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4
Q

Difference in presentation and treatment between high and low grade lymphoma

A

High:
Earlier, localised, stage 1/2 usually as more aggressive
Treatment aim is to cure

Low:
Later, more diffuse, as grows slowly
Treatment aim is for symptoms and to prolong life, but there is no cure

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5
Q

What staining/ immunohistochemistry is done for lymphoma and what are the appearances in low/ high grade?

A

Ki67 stain = protein produced by cells in S phase (DNA replication)

Low - not much staining as low proliferation rate
High - lots of staining as very high proliferation rate

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6
Q

4 main types of lymphoma

A

Follicular
Diffuse Large B cell
Burkitt (3 types)
Hodgkins

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7
Q

Treatment and grade (low/high) for Follicular/ DLBCL/ Burkitt lymphoma

A

Follicular (low) = low dose chemo/radio
DLBCL (high) = aggressive chemo, but some resistance
Burkitt (high) = aggressive chemo, very effective (as high rate of cell death)

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8
Q

3 types of Burkitt lymphoma and patient groups

A

Endemic = Africa/Papa NG, children, link to malaria and EBV

Sporadic = western europe, older children/ young adults (mean 30)

Immunodeficiency = HIV, organ transplant

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9
Q

Where in the lymph nodes do Follicular/ DLBCL/ Burkitt lymphoma arise?

A 
Follicular = germinal centres
DLBCL = lymphoid follicle
Burkitt = germinal centres
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10
Q

What mutation is present in Burkitt’s vs follicular lymphoma and what does it cause?

A

Burkitt: MYC gene translocation 14/8, often next to an immunoglobulin which increases MYC role of increasing cell proliferation, and increasing cell death

Follicular: translocation between chromosome 14/18 -> BCL2/IGH protein (BCL2 is an anti-apoptotic protein) and function increased (decreased apoptosis)

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11
Q

Characteristic feature of Hodgkins lymphoma

What else can it be present in?

A

Reed sternberg cells - binucleate, prominent nucleolus, large cytoplasm

Some inflammatory conditions - Infective mononucleosis

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12
Q

Types of Hodgkins lymphoma (2)

A

Classical (94%)

Nodular lymphocyte predominant (6%)

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13
Q

Presentation of follicular vs DLBCL vs Burkitt vs Classical Hodgkins lymphoma

A

Follicular:
>Painless lymphadenopathy ± BM involvement

DLBCL:
>Rapidly enlarging mass (nodes or Waldeyer’s rings/ GIT/ skin/ bone/ CNS)

Burkitt (mostly extranodal)
> All - CNS involvement
> Endemic - jaw and face bones
> Immuno - BM/lymph nodes
> breast/ ovaries/ kidneys

CHL:
>Painless lymphadenopathy
>B symptoms (night sweats/fever/ WL)
>Paraneoplastic phenomenon - sore nodes with alcohol, intractable itch

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14
Q

4 subtypes of Classical Hodgkins lymphoma

A

Mixed cellularity
Nodular sclerosing
Lymphocyte predominant
Lymphocyte depleted

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15
Q

Surface proteins present/ not present on Reed sternberg cells

A

CD10 -

CD30 +++

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16
Q

Features of plasma cell myeloma - X-ray/blood/urine

A

Production of excess immunoglobulin/ fragments (light chains)

X-ray - lytic lesions
Blood - free light chain (fragment), M/para protein (full)
Urine - Bence jones protein (fragment light chains)

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17
Q

Diagnosis criteria of myeloma

A

Neoplastic cells >10% marrow (+ 1 of: )

CRAB:
>hyperCalcemia
>Renal failure
>Anaemia
>Bone lesions - on CT/X-ray

SLiM:
> 60% or more plasma cells in bone marrow
> Light chain ration of >100 (either way, normally 50/50)
> MRI - at least 1 focal bone lesion

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18
Q

Potential cytogenetic abnormalities in myeloma (4)

A

55-70% IGH rearrangement chr 14
50% - monosomy/ partial deletion chr 13
50% MYC rearrangement
Tp53 mutation/ deletion (in many cancers)

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19
Q

Only treatment of myeloma and gene mutation with poorest outcome

A

Bone marrow transplant

Tp53

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20
Q

Define smouldering/asymptomatic myeloma

A

only 10-60% of clonal plasma cells in bone marrow, and none of the SLiM CRAB criteria

Will usually progress to myeloma in around 5 years avg (don’t need treatment til then)

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21
Q

Define Monoclonal Gammopathy of Uncertain Significance

A

Less than 10% clonal cells in bone marrow, low M-protein in blood, absence of end organ damage

Doesn’t need treatment, risk of progression to myeloma is low

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22
Q

Plasmacytoma definition and treatment

A

Single localised bone tumour, may have M-protein, but with no other signs of plasma myeloma

Tx = local radiation, no chemo

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23
Q

Population of incidence of Classical hodgkin’s lymphoma

A

2 age peaks:
Young adults (15-30)
Elderly/ older adults

Mostly males

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24
Q

What does lymphadenopathy in lymphoma feel like compared to other caners/ inflammation

A

Painless and rubbery

Cancer - craggy
Reactive/ inflammation - sore

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25
Q

General lymphoma presentation

A

Splenomegaly
Anaemia
Painless lymphadenopathy - rubbery
B symptoms

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26
Q

Investigations ofr lymphoma/ myeloma

A

Bloods: FBC, ESR (HL, ACD, myeloma), Calcium (severe lymph/myel), LDH (NHL), U+Es/LFT’s (function pre Tx)

Imaging: CT, PET/CT

Bone marrow biopsy: aspirate, trephine

Other: Echo, pulmonary function test (function pre Tx) - lymp

Myeloma only:
Urine, Serum free light chain, serum electrophoresis (M protein/band)

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27
Q

What is the staging classification for lymphoma

A 
Ann-Arbor:
1 - one node group
2 - >1 node group, same side diaphragm
3 - >1 node group, different side diaphragm
4 - extranodal

A - no B symptoms
B - B symptoms

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28
Q

What surface antigen is present on most B cell lymphomas and targeted for treatment (and name of treatment)

A

CD20 - treated with Rituximab monoclonal Ab

29
Q

What are the RCHOP (RCAVP) chemo drugs for lymphoma

A 
R - rituximab
C - cyclophosphamide
H/A - adriamycin
O/V - vincristine
P - prednisolone
30
Q 
What is being tested for in myeloma with:
Serum electrophoresis
Blood film
Immunocytochemistry
Imaging
A

Serum electrophoresis - M band
Blood film - blue background, rouleaux, inc plasma cells
Immunocytochemistry - light chain restriction
Imaging - lytic bone lesions (pepper pot skull)/ fractures

31
Q

What are the ABVD chemo drugs for Hodgkins lymphoma

A

A - ariamycin
B - bleomycin
V - vinblastine
D - dacarbamizine

32
Q

Describe the extrinsic/ activation part of coagulation cascade

A

TF(3a) + 7a > 10a

33
Q

Describe the intrinsic/ propagation part of coagulation cascade

A

12a > 11a > 9a (+8a) > 10a

34
Q

Describe the regulation part of coagulation cascade (3)

A

1) Thrombin stimulates antithrombin which down regulates factors
2) protein C + thrombomodulin > APC (+ protein S) > down regulates factors 5 & 8
3) Factor 10 feedback to TPFI > down regulates factor 7

35
Q

Describe the fibrinolysis part of coagulation cascade and its regulation

A

(Plasminogen>) Plasmin - breaks don fibrin clot

Inhibited by:
PAI 1/2 (plasminogen activation inhibitors)
TAFI - also inhibits plasminogen activators)
alpha2 antiplasmin - inhibits plasmin

36
Q

Requirements for the initiation and propagation steps of coagulation cascade (2)

A

Calcium

Phosphates

37
Q

Analysis of coagulation 1y haemostasis (3)

A

In vivo - bleeding time

Ex vivo:
>FBC (platelets)
> Light Transmission Aggregometry - agonists added to plasma and aggregation measure by light transmission

38
Q

Analysis of coagulation 2y haemostasis (4)

A

Prothrombin time - extrinsic
Activated partial thromboplastin time - intrinsic
Thrombin clotting time - fibrinogen
Individual coagulation factor assays

39
Q

What is added to patient plasma in PT, APTT, TCT?

A

PT - thromboplastin (TF + phospholipids)
APTT - contact factor (12) + phospholipids
TCT - bovine thrombin

40
Q

What would cause prolonged PT, APTT, TCT (@ normal time)?

A

PT (10-13) - extrinsic problems: factor 7

APTT (26-38) - intrinsic problems: F 12,11,9,8; lupus anticoagulant/ some antibodies

TCT - fibrinogen problems; fibrin inhibitors, thrombin inhibitors (heparin/ dibagatran)

PT and APTT - common problems: F 10,5,2(thrombin), 1 (fibrinogen)

41
Q

Describe the pathway of coagulation cascade

A

10a (+5a) > 2a (thrombin) > (fibrinogen (1a)>) fibrin

42
Q

Benefits of LMWH vs UFH

A

Less side effect frequency
Longer half life
More bioavailability and less protein binding
Doesnt require monitoring

43
Q

Uses of heparins (4)

A

> Tx of acute DVT/ PE (LMWH)
Px of acute VTE in obstetrics, cancer, post op (LMWH)
*Cardiac bypass surgery (UFH)
*Acute coronary syndrome (+ antiplts)

44
Q

Target INR for warfarin

A

2-3

45
Q

Uses of warfarin evidence (3)

A

> PE/VTE - recurrence prevention
*AF - stroke prevention
*Prosthetic heart valve - stroke/ valve thrombosis prevention

46
Q

Uses of DOACs

A

> DVT/PE
*AF
*Total hip/knee replacement

47
Q 
Route of administration of:
Heparins
Warfarin
DOACs
Fibrinolytics
A

Heparins - parenteral
Warfarin - oral
DOACs - oral
Fibrinolytics - oral/ parenterally/ catheter

48
Q

Uses of tissue plasminogen activators

A

Acute MI (12 hrs of symptoms onset) - 30 day mortality dec.

Ischemic stroke (4.5 hrs of symptoms onset) - 90 day disability dec.

Massive PE with haemodynaic instability - dec thrombus size and cardiac strain

49
Q

DOAC contraindications (3)

A

Pregnancy/ breast feeding
Liver disease/cirrhosis (± coagulopathy)
Certain drugs

50
Q

Define catheter directed thrombolysis and uses (3)

A

Drug injected directly into clot via catheter
Reduces systemic effect, but not bleeding risk

Uses:
>Acute limb schema
>Massive DVT - proximal and high/ pelvis
>Blocked CVC (Hickman line)

51
Q 
Antiplatelet drug names:
ADP R ax
GPIIb/IIIa R ax
COX1 inhibitor
Phosphodiesterase 3 inhibitor
Thromboxane synthetase / Receptor inhibitors
A

> ADP R ax - clopidogrel/ ticagrelor, ticlodipine
GPIIb/IIIa R ax - abciximab, tirofiban
COX1 inhibitor - aspirin
Phosphodiesterase 3 inhibitor - dypyradimole
Thromboxane synthetase / Receptor inhibitors - picotamide/ ifetroban

52
Q

Uses of antiplatelets in:
CVD - acute MI, 2y prevention
Cerebrovascular: acute stroke/TIA/ 2y prevention, PVD

A

CVD:
>acute MI: aspirin (+ ticagrelor/clop 12 months) (±tirofiban)
>2y prevention: aspirin

Cerebrovascular:
> acute stroke/TIA/ 2y prevention: clopidogrel (2nd- aspirin + dipyramidole)
>PVD: clopidogrel (2nd aspirin)

53
Q 
Antiplatelet drug mechanisms of action:
ADP R ax
GPIIb/IIIa R ax
COX1 inhibitor
Phosphodiesterase 3 inhibitor
Thromboxane synthetase / Receptor inhibitors
A

ADP R ax: irreversibly block ADPR, > prevents expression of GPIIb/IIIa R > no fibrinogen binding

GPIIb/IIIa R ax: prevents fibrinogen binding

COX1 inhibitor: prevents arachidonic acid >thromboxane a2

Phosphodiesterase 3 inhibitor: prevent cAMP> AMP, so increase cAMP > reduced platelet aggregation

Thromboxane synthetase / Receptor inhibitors: reduced platelet aggregation

54
Q

Fibrinolytic drug names:
Kinases
tPAs

A

Kinases - streptokinase, urokinase

tPAs - telecteplase, alteplase, reteplase

55
Q

Define process of DIC and causes (5)

A

Causes: major trauma, sepsis, malignancy, major haemorrhage, pregnancy complications

Inappropriate coagulation > micro thrombi > exhaustion of cascade > excess bleeding

56
Q

Lab tests for DIC

A

> Coagulation tests: APTT, PT, fibrinogen (PT) - raised
D-Dimer
FBC + film platelets - anaemia, thrombocytopenia, RBC fragmentation
Look for underlying cause

57
Q

Treatment of DIC

A

Treat underlying cause

FFP ± platelets (if at high bleeding risk)

58
Q

Management of severe bleed caused by warfarin (3)

A

Stop warfarin
IV vitamin K1, 5mg
IV factor concentrate - Beriplex, Octaplex

59
Q

How does liver disease affect coagulation?

A

> Reduced production coagulation factors
Poor clearance of activated coagulation factors
Reduced thrombopoietin synthesis (low platelets)
Hypersplenism - inc removal WBC/platelets

> DIC
Vit K deficiency - dietary deficiency, malabsorption?

60
Q

Describe haemophilia A and inheritance pattern

A

X linked
Deficiency of factor 8, causing prolonged APTT

Severe - <1% F8
Moderate - 2-5%
Mild 6-40%

61
Q

Treatment of haemophilia A (4)

A

Desmopressin
Replacement factor therapy
Gene therapy

Education for patient/doctor

62
Q

What does von willebrand disease have an effect on (2) and what are the 3 classifications?

A

Platelet aggregation
Binds and increases half life of F8

Type 1 - reduced production (partial quantitative)
Type 2 - produce enough but faulty (qualitative)
Type 3 - complete deficiency (quantitative)

63
Q

2 main severe inherited platelet disorders and their defect

A

Glansmanns Thromboasthenia: Defect/absent GP 2b/3a but normal platelet numbers

Bernard Soulier Syndrome: Defect/absent GP 1b/5/9 and macrothrombocytopenia

64
Q

Characteristics of platelet disorders

A

Mucosal bleeding pattern
Autosomal dominant - parents may be related (asian)
Petechiae

Can have normal numbers in haematology blood test

65
Q

Treatment of severe platelet disorders (5)

A

Platelet transfusion - severe
Pressure - mild

Desmopressin - increase VWF
Tranexamic acid - inhibit fibrinolysis
Recombinant factor 7a - increase thrombin production

66
Q

How does lupus anticoagulant affect coagulation process and tests

A

Phospholipid dependent antibody, if persistent, is prothrombotic

Increases APTT as interferes with phospholipid dependent tests

67
Q

Define antiphospholipid syndrome and its clinical scenarios

A

Persistent lupus anticoagulant (or other phos. dept. Ab)
+ thrombosis/ or recurrent metal loss

Clinical:
Recurrent miscarriage
Young, recurrent thrombosis (arterial/venous)

68
Q

Causes of inherited thrombophilia (5)

A

> Antithrombin deficiency (most common)
Protein S deficiency
Protein C deficiency

> Mutation F5 - factor 5 leiden (resistance to inactivation by APC
Mutation prothrombin gene - increase prothrombin

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