2. Blood Cancers and Disorders Flashcards

1
Q

What are our three types of blood cancers?

A

Leukaemia
Lymphoma (arising from lymphatic cells)
Others

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2
Q

How is leukaemia divided?

A

Myeloid (red cells)

Lymphoid (T and B cells)

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3
Q

How are lymphomas divided?

A

Hodgkin

Non-hodgkin

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4
Q

What is leukaemia?

A

Blood cancers that begin in bone marrow and result in high numbers of abnormal blood cells – dysfunctional cells crowd out bone marrow to prevent formation of other important blood cells

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5
Q

What’s the difference between acute and chronic leukaemia?

A

Acute - rapid increase in immature cells, abnormal differentiation and excessive proliferation cause severe leukaemia
Chronic - excessive build up of relatively mature white blood cells, normal differentiation and excessive proliferation (more common in older)

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6
Q

What are features of acute myeloid leukaemia (AML)?

A

Bone marrow failure (neutropenia, aneamia, thrombocytopenia) - pallor, bleeding, infections
Tissue infiltration - swollen gums, mild splenomegaly

Auer rods on cytology, rods in blood cells

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7
Q

What is acute promyelocytic leukaemia?

A

Hyper-aggressive subtype of AML, faggot cells on cytology - lots of auer rods

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8
Q

Features of acute lymphoblastic leukaemia?

A

Bone marrow failure - pallor, bleeding, infections
Tissue infiltration - lymphadenopathy, hepatosplenomegaly, swollen testes, tender bones

> 20% lymphoblasts on marrow biopsy

Often after influenza, common in children

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9
Q

Features of chronic myeloid leukaemia?

A

Caused by philadelphia chromosome, most are asymptomatic

90% have splenomegaly - key features!!

Hyperproliferation of granulocyte precursors (more mature cells than AML) -

Hypermetabolic symptoms - weight loss, malaise, sweating
Bone marrow failure - same as rest
Hyperviscosity - thrombotic events, headaches

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10
Q

What are the phases of CML?

A

Chronic phase
Accelerated phase
Blast crisis - similar to an acute leukaemia

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11
Q

Features of chronic lymphocytic leukaemia?

A

Progressive accumulation of functionally incompetent lymphocytes.
Mostly asymptomatic but sometimes lymphadenopathy or bone marrow failure symptoms

Smear/smudge cells on blood film

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12
Q

Leukaemia investigations

A

Bloods - smear, LDH, FBC
Biopsy - bone marrow aspirate
Other - CXR, immunophenotyping

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13
Q

Treatment of leukaemia?

A

Chemotherapy first line
Bone marrow transplants
Palliative care

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14
Q

What is a lymphoma?

A

A group of cancer developing from lymphocytes, mainly found in lymph nodes

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15
Q

How do patients with a lymphoma present?

A

A lump and systemic/B symptoms - fever, weight loss, night sweats.

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16
Q

What is a hodgkin’s lympoma and its signs?

A

Painless enlarging neck mass, may be painful after alcohol consumptions.
B symptoms

They have reed-sternberg cells on lymph biopsy - look like multiple nuclei

17
Q

How does a non-hodgkin’s lymphoma present?

A

Same as hodgkin’s, but there are NO reed-sternberd cells

18
Q

What is burkitt’s lymphoma?

A

Aggressive subtype of non-hodgkin’s in the jaw.

Starry sky appearance under microscopy.

More common in countries where HIV, EBV and malaria are present (these are risk factors for lymphomas)

19
Q

What is tumour lysis syndrome?

A

Metabolic abnormalities that arise after cancer treatment - especially blood cancers.

20
Q

What abnormalities occur in tumor lysis syndrome, and therefore their presentations?

A
  • Released phosphate from cells form calcium phosphate crystals causing kidney failure and hypocalcaemia
  • Release uric acid that forms urate crystals, causing gout
  • Released potassium causes hyperkalaemia that cause arrythmias.
21
Q

What is a multiple myeloma?

A

Proliferation of plasma cells specifially - production of monoclonal immunoglobulins.

22
Q

Presentations of multiple myeloma?

A

Often older
CRAB
Calcium high - bones, stones, abdo groans
Renal impairment
Anaemia - bone marrow crowding
Bone marrow lesions - increased osteoclasts causing back and rib pain

23
Q

Investigations for multiple myelomas?

A

Bloods - raised ESR, CRP, urea, Cr, Ca, normal ALP
Blood film - rouleaux formation
Serum/urine electrophoresis - bence jones proteins (not very spec)
Bone marrow aspirate - increased plasma cells >10%

24
Q

What is monoclonal gammopathy of unknown significance?

A

Pre-malignant condition with no CRAB symptoms

25
What is a myelodysplasia?
Group of syndromes where immature blood cells don't mature normally Primary - intrinsic marrow problem Secondary - prior chemo/radiotherapy
26
Signs of myelodysplasia?
Chronic pancytopaenia. | Can be split into types by which cells are included.
27
What are the two main types of haemophilia?
A - factor 8 deficiency B - factor 9 deficiency all x-linked, affecting secondary haemostasis so causes deep bleeding or bruising
28
How does haemophilia present?
Haemarthrosis - bleeding into joins Haematoma - painful bleeding into muscles Excessive bruising and haematuria
29
How do we diagnose haemophilia?
Prolonged APTT | Factor assay to confirm diagnosis
30
What is von willebrand syndrome and what does it cause?
VWF deficiency (3 types) causing - Platelet adhesion Platelet aggregation Factor 8 stabilisation (may resemble haemophilia)
31
What are the three types of VWF syndrome?
1. Factor normal, reduced amounts 2. Normal levels, deficient factor 3. No factor
32
How does VWF syndrome present in patients and in investigations?
Superficial bleeding Bruising, epistaxis, menorrhagia Gum bleeding Prolonged bleeding Prolonged APTT and normal PT Reduced VWF except in type 2
33
What is disseminated intravascular coagulation (DIC)?
A predisposing condition that causes unnecessary, widespread clotting. This uses up factors etc. that can cause a side effect of bleeding. Fibrin left over can also destroy red blood cells, causing haemolytic anaemia as a side effect.
34
What are the two types of DIC?
Acute overt - emergency and life-threatening, sudden depletion with lots of bleeding Chronic non-overt - slower rate with time for compensattion, hypercoagulable state
35
How does DIC present?
Underlying pathology - sepsis, pregnancy, cancer Acute - bleeding e.g. purpura, petechiae, epistaxis, resp distress Chronic - clotting issues
36
How do we investigate DIC?
FBC - low pl and hb Clotting - low fibrinogen, high bibrin,, prolonged PT and APTT Blood film - schistocytes Treated by treating underlying pathology, giving factors and treating symptoms.