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Oncology, haematology and palliative care > Leukaemia > Flashcards

Leukaemia Flashcards

1
Q

List the 4 main types of leukaemia

A

Acute lymphoblastic leukaemia (ALL)
Chronic lymphocytic leukaemia (CLL)
Acute myeloid leukaemia (AML)
Chronic myeloid leukaemia (CML)

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2
Q

List the ways leukaemia patients may become severely ill

A

Infection
Bleeding
Hyper viscosity

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3
Q

What tests should you order for any leukaemia patient who complains they feel ill

A 
FBC
U&E
LFT
CRP
LDH
Blood cultures 
Ca2+
Glucose
Clotting and INR
CXR if clinically indicated
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4
Q

What must you know for any new leukaemia patient

A

The treatment plan - cure, prolong disease free survival or palliation

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5
Q

At what level of neutrophils is considered neutropenic?

A

<0.5X10^9/L

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6
Q

What risk assessment tool is used to predict the risk of serious complications in febrile neutropenia

A

MASCC score (multinational association for supportive care in cancer)

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7
Q

What does a MASCC score >21 indicate

A

Risk of septic complications is low and admission may be avoided

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8
Q

What variables are considered in the MASCC score?

A 
Solid tumour/lymphoma
Outpatient status at onset of fever
Age <60yo
Burden of illness - symptoms 
No hypotension (SBP>90)
No COPD
No dehydration
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9
Q

Give the flaws of the MASCC score

A

Symptom burden is subjective

Omission of potentially vital variables such as CRP

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10
Q

What should the MASCC score be used in conjunction with?

A

Clinical picture

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11
Q

Describe the management for someone with neutropenia

A

Full barrier nursing in side room, hand washing is vital
Avoid IM injection - risk of infected haematoma
Look for infection (mouth,axilla, perineum, IVI site) Take swabs
Check FBC, U&E, LFT, LDH, CRP, cultures x3 blood and hickman line, urine, sputum, stool if diarrhoea, CXR if clinically indicated
Wash perineum after defecation. Swab moist skin with chlorhexidine. Avoid unnecessary rectal exams. Oral hygiene and candida prophylaxis are important
Check vital signs 4hrly
High calorie diet - avoid foods with high risk of microbial contamination
Vases of flowers pose a pseudomonas risk

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12
Q

When should blind combination antibiotic therapy be started?

A

If temp >38 or Temp >37.5 on two occasions greater than an hour apart or if the patient is septic

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13
Q

How long should antibiotics be continued for in a neutropenic patient

A

Until afebrile for 72hrs or 5day course and until neutrophils >0.5x10^9/L

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14
Q

Give the blood results for tumour lysis syndrome

A

Increased potassium, urate and AKI

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15
Q

Describe hyper viscosity in leukaemia patients

A

If WCC>100x10^9/L WBC thrombi may form in the brain, lung and heart (leukostais)

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16
Q

Describe the pathophysiology of DIC

A

The release of procoagulants into the circulation causes widespread activation of coagulation, consuming clotting factors and platelets and causing increased risk of bleeding. Fibrin strands fill small vessels, haemolysing RBCs. Fibrinolysis is also activated

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17
Q

What causes DIC

A

Malignancy
Sepsis
Trauma
Obstetric events

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18
Q

What are some signs of DIC

A

Bruising
Bleeding anywhere (eg. venepuncture sites)
Renal failure

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19
Q

What do test results show in DIC

A

Decreased platelets
Increased PT and APTT
Decreased fibrinogen (correlates with severity)
Increased fibrin degradation products (D-dimers)
Film - broken RBCs (shistocytes)

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20
Q

How do you treat DIC

A

Treat the cause
Replace platelets if <50x10^9/L
Cryoprecipitate to replace fibrinogen
FFP to replace coagulation factors

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21
Q

What can be given to prevent sepsis in neutropenia?

A

Give fluoroquinolone (ciprofloxacin)
Granulocyte colony stimulators (G-CSF) can increase the production of WBCs (granulocytes) from bone marrow, but should not be given routinely in chemotherapy.
Herpes, pneumocystis and CMV prophylaxis has a role

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22
Q

What is acute lymphoblastic leukaemia

A

A malignancy of lymphoid cells, affecting B or T lymphocyte cell lineages, arresting maturation and promoting uncontrolled proliferation of immature blast cells with bone marrow failure and tissue infiltration

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23
Q

Which age group does ALL tend to affect?

A

Children aged 2-5yo

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24
Q

What is ALL associated with?

A

Ionizing radiation

Downs syndrome

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25
Q

Describe the 3 classifications of ALL

A

Morphological - The FAB system divides ALL into 3 types L1,L2,L3 by microscpic appearance

Immunological - surface markers are used to classify ALL into precursor B cell ALL, Tcell ALL and B cell ALL

Cytogenic - chromosomal analysis. Abnormalities are detected in up to 85% which are often translocations. Useful for predicting prognosis (eg. poor with Philadelphia chromosome - 9,22 translocation) and detecting disease recurrence

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26
Q

What are the signs and symptoms of ALL due to?

A

Infiltration

Marrow failure

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27
Q

Give the signs and symptoms of infiltration in ALL

A

Hepatosplenomegaly, lymphadenopathy, orchidomegaly, CNS involvement (meningism and CN palsies)

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28
Q

Give the signs and symptoms of bone marrow failure in ALL

A

Anaemia (decreased Hb)
Infection (decreased WCC)
Bleeding (decreased platelets)

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29
Q

What infections are common in those with ALL

A 
Bacterial septicaemia
Mouth 
Chest
Perianal
Skin 
Zoster
CMV
Measles
Candidasis
Pneumocystis pneumonia
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30
Q

What investigations should be performed in ALL and what may they show?

A

Blood film - characteristic blast cells
Bone marrow - characteristic blast cells
WCC - usually high
CXR and CT - mediastinal and abdominal lymphadenopathy
Lumbar puncture - look for CNS involvement

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31
Q

Which leukaemia commonly involves the CNS too

A

ALL

32
Q

Describe the treatment of ALL

A

Education and motivation - increase pt compliance

Support - blood/platelet transfusion, IV fluids, allopurinol (prevent tumour lysis syndrome), insert SC port/hickman line for IV access

Infections - dangerous due to neutropenia, give IV ABx immediately and start neutropenic regime, give prophylactic antivirals, antifungals and ABx

Chemotherapy - complex, multi-drug, multi-phase regimens that may take many years: remission induction, consolidation and maintenance

Matched related allogenic marrow transplantation - once in 1st remission is the best option in standard risk younger adults

33
Q

What is haematological remission of ALL defined as?

A

No evidence of leukaemia in the blood, normal/recovering blood count and <5% blasts in a normal regenerating marrow

34
Q

What are the cure rates for ALL

A 
Children = 70-90% 
Adults = 40%
35
Q

What is associated with a poor prognosis in ALL

A 
Adult
Male
Philadelphia chromosome 
Presentation with CNS signs
Decreased HB
WCC >100 
B-cell ALL
36
Q

What is the Philadelphia chromosome

A

BCR-ABL gene fusion due to translocation of chromosomes 9 and 22

37
Q

What can be used to detect minimal residual disease?

A

PCR

38
Q

Which chemo drugs increase prognosis for ALL in adults?

A

Rituximab/ibrutinib

39
Q

What is acute myeloid leukaemia

A

Neoplastic proliferation of blast cells derived from marrow myeloid elements

40
Q

Describe the prognosis of AML

A

Poor - death in 3 months if not treated, 20%3yr survival after treatment

41
Q

Describe the incidence of AML

A

Commonest acute leukaemia in adults

1 in 10000 per year

42
Q

What is associated with AML?

A 
Increasing age
Syndromes such as downs 
Radiation
Myelodysplastic state
Long term complication of chemotherapy eg. lymphoma
43
Q

Describe the classification of AML

A

1) AML with recurrent genetic abnormalities
2) AML multilineage dysplasia
3) AML therapy related
4) AML other (M0-M7 maturation sub classification)

44
Q

Describe the signs and symptoms of AML

A

Marrow failure - Anaemia and bleeding
Infiltration - hepatosplenomegaly, gum hypertrophy, skin involvement
Fever

45
Q

Which subtype of AML presents with DIC

A

Acute promyelocytic leukaemia

46
Q

Describe how acute promyelocytic leukaemia causes DIC

A

Thromboplastin release

47
Q

Describe the diagnosis of AML

A

WCC may be high, normal or low
Few blasts in blood film - Auer rods (crystals of coalesced granules)
Diagnosis mainly by bone marrow biopsy, immunophenotyping and molecular methods
Cytogenic analysis guides treatment options and prognosis

48
Q

List the complications of AML

A

Infection - candida and aspergillus
Tumour lysis syndrome
Leukostais

49
Q

Describe the treatment for AML

A

Supportive care
Chemo - daunorubicin and cytarabine for 5 cycles given in 1 week blocks to get remission
Bone marrow transplant - cyclophosphamide and total irradiation, transplant and ciclosporin and methotrexate

50
Q

What are some complication of bone marrow transplant

A

GVHD
Infection
Relapse
Infertility

51
Q

What are myelodysplastic syndromes?

A

Heterogenous group of disorders that manifest as marrow failure and risk of life threatening infection and bleeding

52
Q

What are the causes of myelodysplastic syndromes?

A

Most primary

Can be secondary to chemo and radiotherapy

53
Q

What do tests show in myelodysplastic syndromes

A

Pancytopenia with reduced reticulocyte count
Marrow cellularity is increased due to ineffective haematopoiesis
Ring sideroblasts may also be seen in the marrow

54
Q

Describe the treatment of myelodysplastic syndromes

A

Multiple red cell/platelet transfusions
G-CSF and EPO infusions
Allogenic stem cell transplantation
Low intensity treatments may lead to increased quality of life such as thalidomide analogues (lenalidomide) or hypomethylating agents (azacitidine and decitabine)

55
Q

Give an example of a myeloproliferative disorder

A

Polycythaemia rubra vera - too many red cells

56
Q

What is chronic myeloid leukaemia?

A

Characterized by an uncontrolled clonal proliferation of myeloid cells

57
Q

What percentage of leukaemia is CML

A

15%

58
Q

What age does CML occur?

A

40-60 yo

59
Q

Which gender does CML affect more?

A

Male

60
Q

What proportion of people with CML is the Philadelphia chromosome present in?

A

> 80%

61
Q

Which patients have a worse prognosis in terms of the Philadelphia chromosome?

A

Ones without it

62
Q

Give the symptoms of CML

A 
Weight loss
Tiredness
Fever
Swears
Gout
Bleeding
Abdominal discomfort
63
Q

What are the signs of CML

A

Splenomegaly
Hepatomegaly
Anaemia
Bruising

64
Q

What tests diagnose CML

A 
Increased WCC
Increased neutrophils, basophils, eosinophils, monocytes
Decreased Hb 
Platelets variable
Increased urate
Increased B12
Bone marrow hypercellular
Cytogenetic analysis of blood or bone marrow for Ph
65
Q

Describe the natural history of CML

A

Variable with median survival 5 or 6 years
3 phases
Chronic - lasting months or years of few symptoms
Accelerated phase - increased symptoms, spleen size and difficulty controlling counts
Blast transformation - features of acute leukaemia and death

66
Q

Describe the treatment of CML

A

BCR-ABL inhibitors - monoclonal antibody - imatinib

Stem cell transplant

67
Q

Give the side effects of imatinib

A 
Nausea
Cramps
Oedema
Rash 
Headache
Arthralgia
Myelosuppression
68
Q

Describe CLL

A

The hallmark is progressive accumulation of malignant clone of functionally incompetent B cells

69
Q

What influences the risk of CLL

A

Mutations
Trisomy’s
Deletions

70
Q

What staging system is used in CLL

A

Rai

71
Q

What symptoms present with CLL

A

Often none, surprise finding on FBC

Patients may be anaemia, infection prone, decreased weight, sweats, anorexia

72
Q

What are some signs of CLL

A

Enlarged, rubbery, non tender nodes, splenomegaly, hepatomegaly

73
Q

What investigations are done in CLL?

A

Increased lymphocytes

Later - autoimmune haemolysis, marrow infiltration, decreased Hb, Decreased neutrophils, Decreased platelets

74
Q

What are the complications of CLL

A 
Autoimmune haemolysis 
Increased Infection due to hypogammaglobinaemia (decreased IgG) 
Bacterial 
Vital especially herpes zoster
Marrow failure
75
Q

What is the first line chemo for CLL

A

Fludarabine
Rituximab
Cyclophosphamide

76
Q

Describe the natural history of CLL

A

1/3 never progress (or even regress)
1/3 progress slowly
1/3 progress actively

77
Q

What is death from CLL often due to?

A

Infection

Transformation to aggressive lymphoma (Richter’s)

Oncology, haematology and palliative care (19 decks)

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