Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

MedEd Tutorials > 2. Blood Cancers and Disorders > Flashcards

2. Blood Cancers and Disorders Flashcards

1
Q

What are our three types of blood cancers?

A

Leukaemia
Lymphoma (arising from lymphatic cells)
Others

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How is leukaemia divided?

A

Myeloid (red cells)

Lymphoid (T and B cells)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How are lymphomas divided?

A

Hodgkin

Non-hodgkin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is acute promyelocytic leukaemia?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the phases of CML?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Leukaemia investigations

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Treatment of leukaemia?

A

Chemotherapy first line
Bone marrow transplants
Palliative care

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is a lymphoma?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How do patients with a lymphoma present?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
Q

What is a myelodysplasia?

A

Group of syndromes where immature blood cells don’t mature normally
Primary - intrinsic marrow problem
Secondary - prior chemo/radiotherapy

26
Q

Signs of myelodysplasia?

A

Chronic pancytopaenia.

Can be split into types by which cells are included.

27
Q

What are the two main types of haemophilia?

A

A - factor 8 deficiency
B - factor 9 deficiency

all x-linked, affecting secondary haemostasis so causes deep bleeding or bruising

28
Q

How does haemophilia present?

A

Haemarthrosis - bleeding into joins
Haematoma - painful bleeding into muscles
Excessive bruising and haematuria

29
Q

How do we diagnose haemophilia?

A

Prolonged APTT

Factor assay to confirm diagnosis

30
Q

What is von willebrand syndrome and what does it cause?

A

VWF deficiency (3 types) causing -
Platelet adhesion
Platelet aggregation
Factor 8 stabilisation (may resemble haemophilia)

31
Q

What are the three types of VWF syndrome?

A
  1. Factor normal, reduced amounts
  2. Normal levels, deficient factor
  3. No factor
32
Q

How does VWF syndrome present in patients and in investigations?

A

Superficial bleeding
Bruising, epistaxis, menorrhagia
Gum bleeding
Prolonged bleeding

Prolonged APTT and normal PT
Reduced VWF except in type 2

33
Q

What is disseminated intravascular coagulation (DIC)?

A

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
Q

What are the two types of DIC?

A

Acute overt - emergency and life-threatening, sudden depletion with lots of bleeding
Chronic non-overt - slower rate with time for compensattion, hypercoagulable state

35
Q

How does DIC present?

A

Underlying pathology - sepsis, pregnancy, cancer
Acute - bleeding e.g. purpura, petechiae, epistaxis, resp distress
Chronic - clotting issues

36
Q

How do we investigate DIC?

A

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.

MedEd Tutorials (32 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions