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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
Describe the 3 classifications of ALL
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
26
What are the signs and symptoms of ALL due to?
Infiltration | Marrow failure
27
Give the signs and symptoms of infiltration in ALL
Hepatosplenomegaly, lymphadenopathy, orchidomegaly, CNS involvement (meningism and CN palsies)
28
Give the signs and symptoms of bone marrow failure in ALL
Anaemia (decreased Hb) Infection (decreased WCC) Bleeding (decreased platelets)
29
What infections are common in those with ALL
``` Bacterial septicaemia Mouth Chest Perianal Skin Zoster CMV Measles Candidasis Pneumocystis pneumonia ```
30
What investigations should be performed in ALL and what may they show?
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
31
Which leukaemia commonly involves the CNS too
ALL
32
Describe the treatment of ALL
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
What is haematological remission of ALL defined as?
No evidence of leukaemia in the blood, normal/recovering blood count and <5% blasts in a normal regenerating marrow
34
What are the cure rates for ALL
``` Children = 70-90% Adults = 40% ```
35
What is associated with a poor prognosis in ALL
``` Adult Male Philadelphia chromosome Presentation with CNS signs Decreased HB WCC >100 B-cell ALL ```
36
What is the Philadelphia chromosome
BCR-ABL gene fusion due to translocation of chromosomes 9 and 22
37
What can be used to detect minimal residual disease?
PCR
38
Which chemo drugs increase prognosis for ALL in adults?
Rituximab/ibrutinib
39
What is acute myeloid leukaemia
Neoplastic proliferation of blast cells derived from marrow myeloid elements
40
Describe the prognosis of AML
Poor - death in 3 months if not treated, 20%3yr survival after treatment
41
Describe the incidence of AML
Commonest acute leukaemia in adults | 1 in 10000 per year
42
What is associated with AML?
``` Increasing age Syndromes such as downs Radiation Myelodysplastic state Long term complication of chemotherapy eg. lymphoma ```
43
Describe the classification of AML
1) AML with recurrent genetic abnormalities 2) AML multilineage dysplasia 3) AML therapy related 4) AML other (M0-M7 maturation sub classification)
44
Describe the signs and symptoms of AML
Marrow failure - Anaemia and bleeding Infiltration - hepatosplenomegaly, gum hypertrophy, skin involvement Fever
45
Which subtype of AML presents with DIC
Acute promyelocytic leukaemia
46
Describe how acute promyelocytic leukaemia causes DIC
Thromboplastin release
47
Describe the diagnosis of AML
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
List the complications of AML
Infection - candida and aspergillus Tumour lysis syndrome Leukostais
49
Describe the treatment for AML
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
What are some complication of bone marrow transplant
GVHD Infection Relapse Infertility
51
What are myelodysplastic syndromes?
Heterogenous group of disorders that manifest as marrow failure and risk of life threatening infection and bleeding
52
What are the causes of myelodysplastic syndromes?
Most primary | Can be secondary to chemo and radiotherapy
53
What do tests show in myelodysplastic syndromes
Pancytopenia with reduced reticulocyte count Marrow cellularity is increased due to ineffective haematopoiesis Ring sideroblasts may also be seen in the marrow
54
Describe the treatment of myelodysplastic syndromes
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
Give an example of a myeloproliferative disorder
Polycythaemia rubra vera - too many red cells
56
What is chronic myeloid leukaemia?
Characterized by an uncontrolled clonal proliferation of myeloid cells
57
What percentage of leukaemia is CML
15%
58
What age does CML occur?
40-60 yo
59
Which gender does CML affect more?
Male
60
What proportion of people with CML is the Philadelphia chromosome present in?
>80%
61
Which patients have a worse prognosis in terms of the Philadelphia chromosome?
Ones without it
62
Give the symptoms of CML
``` Weight loss Tiredness Fever Swears Gout Bleeding Abdominal discomfort ```
63
What are the signs of CML
Splenomegaly Hepatomegaly Anaemia Bruising
64
What tests diagnose CML
``` 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
Describe the natural history of CML
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
Describe the treatment of CML
BCR-ABL inhibitors - monoclonal antibody - imatinib | Stem cell transplant
67
Give the side effects of imatinib
``` Nausea Cramps Oedema Rash Headache Arthralgia Myelosuppression ```
68
Describe CLL
The hallmark is progressive accumulation of malignant clone of functionally incompetent B cells
69
What influences the risk of CLL
Mutations Trisomy's Deletions
70
What staging system is used in CLL
Rai
71
What symptoms present with CLL
Often none, surprise finding on FBC | Patients may be anaemia, infection prone, decreased weight, sweats, anorexia
72
What are some signs of CLL
Enlarged, rubbery, non tender nodes, splenomegaly, hepatomegaly
73
What investigations are done in CLL?
Increased lymphocytes | Later - autoimmune haemolysis, marrow infiltration, decreased Hb, Decreased neutrophils, Decreased platelets
74
What are the complications of CLL
``` Autoimmune haemolysis Increased Infection due to hypogammaglobinaemia (decreased IgG) Bacterial Vital especially herpes zoster Marrow failure ```
75
What is the first line chemo for CLL
Fludarabine Rituximab Cyclophosphamide
76
Describe the natural history of CLL
1/3 never progress (or even regress) 1/3 progress slowly 1/3 progress actively
77
What is death from CLL often due to?
Infection | Transformation to aggressive lymphoma (Richter's)

Oncology, haematology and palliative care (19 decks)

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