Brainscape's Knowledge GenomeTM

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


See full index

Y4 Cancer > Leukaemia > Flashcards

Leukaemia Flashcards

1
Q

What is acute leukaemia?

A

aggressive disease in which malignant transformation occurs in a haemopoietic stem cell or early progenitor
- accumulation in bone marrow of early haemopoietic cells known as blast cells -> BM fail

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

When would you diagnose an acute leukaemia?

A

presence of atleast 20% of blast cells in BM or blood at clinical presentation
- lineage of blast cells defined with flow cytometry, morphology
- cytogenetic and molecular analysis essential and performed on marrow cells

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

What causes disease burden in acute myeloid leukaemia?

A

uncontrolled proliferation of immature, non-functional white blood cells ‘blasts’

  • causes pancytopenia and haematopoiesis and presents that way
  • blast cells enter blood stream and infiltrate other organs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What cells are involved in the myeloid lineage?

A

monocytes, granulocytes (eosinophil, basophil, neutrophil), erythrocytes, and platelets

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

What are the risk factors of AML?

A
  • myelodysplastic syndrome and other pre-existing haematological disorders
    • MDS, MPD, aplstic anaemia, paroxysmal nocturnal haemogloburia
  • de-novo malignancy
  • congenital disorders: Down’s syndrome, bloom syndrome
  • environmental exposure: prior chemotherapy, radiation, tobacco smoke, benzene
  • no identifiable cause: genetic alterations, isolated gene mutations
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the clinical features of AML?

A

anaemia signs
thrombocytopenia - mucosal bleeding, easy bruising, petechiae, bleeding gums
neutropenia - infection
leukaemia infiltration

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

What clinical signs can be seen in AML?

A
  • weight loss
  • anaemia: pallor and cardiac flow murmur
  • fever, pneumonia signs
  • petechia, dermal bleeding and ecchymoses
  • hepatosplenomegaly, lymphadenopathy and swollen gums
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How would you investigate AML?

A

FBC - pancytopenia
peripheral blood smear - myeloblasts, auger rods
LDH - increased cell turnover
coagulation profile
BM biopsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What diagnoses AML?

A

> 20% myeloid blasts in BM (or peripheral blood) or detecting cytogenetic abnormalities

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

How is AML managed?

A
  • chemo: induction, consolidation, maintenance
  • BM transplant
  • Supportive therapy: blood transfusions, analgesia, abx, allopurinol, anti-emetics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What complications can be caused by AML ?

A

DIC
leukostasis
tumour lysis

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

What is acute lymphoblastic leukaemia?

A

most common childhood cancer with peak age 2-6 years
- arises from a clone of lymphoid progenitor cells
- buildup of these cells causes pancytopenia

*chromosomal translocations seen - t(12;21) most common and Philadelphia t(9;22)

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

What are some risk factors of ALL?

A
  • Trisomy 21, Bloom syndrome, ataxia-telangiectasia
  • pre-natal exposure to XR
  • in-utero exposure to infection
  • delayed post-natal exposure to infection
  • environmental radiation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How might ALL present?

A

marrow failure
tissue infiltration - hepatosplenomegaly, bone pain, mediastinal mass, testicular enlargement
leucostasis
general B sx

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

How might you investigate ALL?

A

FBC - pancytopenia
hyperaemia, high LDH, hypercalcaemia
coagulation screen
bone marrow - 50 to 98% blasts
CSF
CXR
CT CAP
cytogenetics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the general mx of ALL?

A

pre-phase and supportive
induction chemo
maintenance therapy
stem cell transplant
palliative care

*more than 65 out of 100 people (more than 65%) will survive their leukaemia for 5 years or more after being diagnose

17
Q

What are some complications of ALL?

A

tumour lysis
neutropenic sepsis
SVCO
chemo side effets

18
Q

What is the pathophysiology of chronic myeloid leukaemia?

A

cancer of white blood cells specifically myeloid cells raised level of mature granulocytes (neutrophils, basophils and eosinophils), which then interfere with haematopoiesis

*philadephia chromosome - translocation of 9 and 22 activates a cascade of proteins that speeds up cell division and also inhibits DNA repair

19
Q

What are the phases of CML?

A

chronic - 85%, asymptomatic, eventually will lead to accelerated

accelerated - significant progression and BM infiltration, splenomegaly and low cell counts

blast crisis - fever, fatigue, shortness of breath, abdominal pain, bone pain, enlarged spleen, chloroma

20
Q

What are some risk factors for CML?

A
  • radiation exposure - atomic bomb or nuclear reactor accidents
  • increasing age
  • males
21
Q

What are some clinical features of CML?

A

*asymptomatic potentially
upper abdo pain
poor appetite
B sx
gout
infections
anaemia, thrombocytopenia sx
signs - pallor, hepatosplenomegaly, bruising

22
Q

How might you investigate CML?

A
  • FBC - leucocytosis, eosinophilia, basophilia, increased granulocytes, normocytic normochromic anaemia
  • U&E
  • LDH
  • Urate
  • peripheral blood film - all stages of granulocyte maturation, appearances similar to that of BM aspirate
  • BM aspirate - to stage, cytogenetic sampling
23
Q

How might CML be managed?

A
  • tyrosine kinase inhibitors - targets BCR-ABL, inhibiting proliferation of malignant cells
    • imatinib - first line
    • aim to induce clinical, haemtological, cytogenic and molecular remission
    • hydroxycabamide can also be used
  • BM transplant in younger, possible cure
24
Q

How might you define a blast crisis in CML?

A

final phase of evolution of CML and behaves like acute leukaemia, with rapid progression and short survival

  • > 20%myeloblasts orlymphoblasts in the blood or bone marrow
  • Large clusters of blasts in the bone marrow onbiopsy
  • Development of achloroma(a solid focus ofleukaemiaoutside the bone marrow)
25
Q

What is chronic lymphocytic leukaemia?

A

lymphoproliferative disorder of B lymphocytes, which results from abnormal clonal expansion of B cells that resemble mature lymphocytes

  • results in widespread lymphadenopathy and secondary complications like immune deficiency and cytopaenias
26
Q

What is the symptomatic stage of CLL?

A
  • symptomatic stage of CLL is characterised byprogressive lymphadenopathy,
    • includes splenomegaly and hepatomegaly - accumulation of incompetent lymphocytes
27
Q

What are the risk factors for CLL?

A
  • Age - over 50
  • Exposure to certain chemicals
  • Family history - first degree
  • Sex - males
  • Race/ethnicity - caucasian
28
Q

What are some clinical features of CLL?

A

*patients can remain asymptomatic with indolent disease for years

*may be detected on routine blood tests

  • finding of abnormally enlarged, painless nodes
  • B sx
  • lymphadenopathy
29
Q

What are some complications of CLL?

A
  • autoimmune haemolytic anaemia - pallor, dyspnoea, weakness, dizziness
  • ITP - petechiae, bruising, mucosal bleeding
  • Hypogammunaglobulinaemia - reccurrent organ specific infections
30
Q

What are some investigations for CLL?

A

FBC + cytometry
U&E, LFT, bone profile
blood film
haemolysis screen
immunoglobulin
cytogenetics
BM aspirate
CT CAP
LN biopsy
virology

31
Q

What are some indications for CLL tx?

A
  • Bone marrow failure
  • Massive, progressive or symptomatic splenomegaly
  • Massive, progressive or symptomatic lymphadenopathy
  • Progressive lymphocytosis
  • Autoimmune complications not responsive to steroids
  • Symptomatic/functional extranodal sites
  • Disease-related symptoms (e.g. significant weight loss, severe fatigue, >2 weeks of fever or ≥1 month of night sweats without infection)
32
Q

What are some management options available for CLL?

A
  • watch and wait with 3m assessments
  • pharmacological - ibrutinib
  • chemo
  • molecule inhibitors - tyrosine kinase inhibitors - ibrutinib
  • monoclonal antibodies - rituximab
  • steroids - in frail or to treat complications
  • allogenic SCT - fit enough or refractory
  • supportive care - vaccinations, antibiotics, IV immunoglobulins, PJP and herpes zoster prophylaxis
33
Q

What are some complications of CLL?

A
  • autoimmune haemolytic anaemia - pallor, dyspnoea, weakness, dizziness
  • ITP - petechiae, bruising, mucosal bleeding
  • Hypogammunaglobulinaemia - reccurrent organ specific infections
  • histological transformations
  • secondary infections
  • hyperviscosity syndrome
  • secondary malignancies - AML, solid organ

Y4 Cancer (15 decks)

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