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YEAR 4 CANCER CARE > Haem Malignancy- Leukaemia > Flashcards

Haem Malignancy- Leukaemia Flashcards

1
Q

What are the four classifications of leukaemias?

A
  • Acute myeloid leukaemia
  • Chronic myeloid leukaemia
  • Acute lymphoblastic leukaemia
  • Chronic lymphocytic leukaemia
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2
Q

Describe the natural history of acute leukaemias

A
  • develops rapidly - patients gets symptoms quickly (covered in another BS card)
  • these are tumours of immature cells
  • AML = from common myeloid progenitor
  • ALL = from common lymphoid progenitor
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3
Q

How does acute myeloid leukaemia present?
(what are clinical features)

A

Pancytopenia and related symptoms due to marrow FAILURE:
* anaemia –> pallor, lethargy/fatigue, weakness
* neutropenia –> frequent infections
* thrombocytopenia –> bleeding

Signs on examination due to INFILTRATION:
* hepatomegaly
* splenomegaly
* gum hypertrophy

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4
Q

What are the morphological classifications of acute myeloid leukaemia?
(based on WHO histological classification, cytogenics and molecular genetics)

A
  1. AML with recurrent genetic abnormalities
  2. AML multilineage dysplasia (for example, secondary to pre-existing myelodysplastic syndrome)
  3. AML, therapy related (in patients previously treated with cytotoxic drugs)
  4. AML, other (doesn’t fit into classes 1, 2, or 3)
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5
Q

How is AML diagnosed?

A

Blood tests can show high WCC, but it can also be normal or low - not ideal!

For this reason, diagnosis = dependent on bone marrow biopsy, as well as other molecular analyses - immunophenotyping and molecular methods.

  • Characteristic biopsy findings include Auer rods.
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6
Q

How is AML differentiated from ALL when doing a bone marrow biopsy?

A

Auer rods = present in AML only

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7
Q

How does acute lymphoblastic leukaemia present?

A

Just like AML really
* Pancytopenia due to bone marrow failure - anaemia, neutropenia, thrombocytopenia
* Bone pain
* lymphadenopathy (superficial or mediastinal)
* Infiltration of the bone marrow - splenomegaly, hepatomgaly, orchidomegaly, CNS involvment (cranial nerve palsies, meningism)

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8
Q

In patients with acute leukaemias, what types of frequent infections may they mention in PMHx?

A

chest, mouth, perianal and skin
* bacterial septicaemia
* Varicella zoster
* CMV
* measles
* candidiasis
* pneumocystis pneumonia

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9
Q

What investigations would you do for ALL?

A

Blood film and bone marrow biopsy + trephine - would see characteristic blast cells
FBC - WCC usually high
CXR and CT scan - look for mediastinal and abdominal lymphadenopathy
Lumbar puncture - look for CNS involvement

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10
Q

How is ALL treated?

think of preventative / prophylaxis too

A
  • Multidrug chemotherapy
  • Educate and motivate patient to promote engagement with therapy
  • Support - blood/platelet transfusion, IV fluids, allopurinol (prevents tumour lysis syndrome).
  • Infections - can be dangerous for these patients bc of neutropenia - so give immediate abx. Give prophyalctic antivirals, antifungals, antibiotics
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11
Q

What is the prognosis of ALL?

A
  • Cure rates for children = 70 – 90 %
  • Adults = 40 %
  • Poor prognosis if: adult, male, Philadelphia chromosome, presentation with CNS signs, low Hb , WCC > 100 ≈ 10 9 /L , or B -cell ALL .
  • Prognosis in relapsed Ph-negative ALL is poor (but improvable by marrow transplant).
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12
Q

Patient X presents has a blood film and bone marrow biopsy taken after presenting under 2ww with pancytopenia.

Here is his blood film. What is shown?
What is Dx?
Why is it not another type of cancer?

A

Here is his blood film. What is shown?
* BLAST CELLS
What is Dx?
* Acute lymphoblastic leukaemia
Why is it not another type of cancer?
* need Auer rods in AML - these are not present, so is ALL.

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13
Q

How is AML treated?

A

Treatment can be intensive or non-intensive.

  • Support - blood/platelet transfusion, IV fluids, allopurinol (prevents tumour lysis syndrome). Walking exersices can relieve fatigue.
  • Chemotherapy –> intense - can result in long periods of marrow supression with neutropenia and low platelets.
  • Bone marrow transplant - use allogenic stem cell transplant
  • Lower dose chemotherapy for disease control (used in elderly, or where intense chemo has poorer outcomes)
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14
Q

What are complications of bone marrow transplant for AML?

A
  • Graft vs Host disease
  • Opportunistic infections
  • Relapse of leukaemia
  • Infertility
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15
Q

What is the prognosis of AML?

A
  • Death occurs within 2 months without treatment;
  • Still poor in those who undergo treatment, with a 20% 3-year survival rate.
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16
Q

basics

What is the difference between myeloid leukaemia and lymphocytic leukaemia?

A
  • myeloid leukaemia commonly arises from a myeloid precursor cell, such as neutrophils.
  • lymphocytic leukaemia arises from a lymphoid precursor, such as B-cells.
17
Q

What is CML caused by?

hint: chromosome

A

Cytogenetic translocation 9:22 - philadelphia chromosome: BCRABL
* this causes activation of a cell cycle pathway involving tyrosine kinase = get increased cell proliferation.

18
Q

Who does CML predominantly affect?

A

Males
40-60years old

19
Q
  1. What are clinical features of CML?
  2. What are the haematological features?
A
  1. chronic and insidious - weight loss, tiredness, fever, night sweats
  2. bleeding (due to thrombocytopenia), massive splenomegaly (pt feels fullness), gout (due to purine breakdown). Bloods show high WCC - causes hyperviscosity of blood.

Note: may also have anaemia, hepatomegaly and bruising.

20
Q

What is the pathophysiology of CML?

A

There is an issue in the myeloid stem cell - produces normal differentiated cells - but LOTS of them!!
So you get an increase in all myeloid cells = causes high WCC (but low Hb and low plactelets).

21
Q

What investigations would you do for suspected CML? Describe findings for each one you mention.

A

FBC - high WCC with a whole spectrum of myeloid cells - neutrophils, monocytes, basophils, eosinophils, low Hb
Uric acid blood test - will be high for urate
Haemantinics - high B12.
Bone marrow blood film - hypercellular (see pic)
Cytogenic analysis of blood or bone marrow - look for Philadelphia 9:22.

22
Q

Describe the natural history of CML

A
  • median survival is 5-6 years
  • there are three phases:

chronic - can be months or years of few (if any) symptoms
accelerated phase - increasing symptoms, spleen size, difficult to control counts
blast transformation - features of acute myeloid leukaemia –> CML can progress to AML

23
Q

How is CML treated?

A
  • Specifically targerted drug therapy –> tyrosine kinase inhibitors - e.g Imatinib. This allows for long remission and normal life expectancy
  • 2nd generation BCR-ABL inhibitors e.g. dasatinib. Can also use Hydroxycarbamide
  • If have transformation to AML = allogeneic stem cell transplantation.
24
Q

How does chronic lymphocytic leukaemia (CLL) present?
mention:
- Symptoms and signs?
- Haematological findings?

A
  • Can be asymptomatic - incidental finding on routine FBC
  • present with lymphoma type symptoms - LN swelling. can be bilateral in CLL
  • anaemia
  • frequent infections
  • B symptoms if severe = weight loss, sweats, anorexia (if severe)
  • immune dysregulation - may have autoimmune haemolytic anaemia, immune thrombocytopenic purpura.

Signs:
* enlarged, rubbery, non tender LN.
* splenomegaly
* hepatomegaly.

Haematological findings:
* high lymphocyte count
* autoimmune haemolysis
* pancytopenia - anameia, neutropenia, thrombocytopenia.

25
Q

What cells are proliferating in high numbers in CLL?

A

Mature B lymphocytes.

26
Q

How is CLL treated?

A

Chemotherapy
Targeted immune treatments - ibrutinib.

Ox Handbook:
says above +
- steriods for autoimmune haemolysis
- radiotherapy for lymphadenopathy and splenomegaly
- stem cell transplantion in some pts
- supportive care - transfusions, IV immunoglobulins for recurrent infections

27
Q

What is the natural history of CLL?

A
  • 1/3 don’t progress
  • 1/3 slowly progress
  • 1/3 actively progress
  • death often due to infection or transformation to an aggressive non-hodgkins lymphoma (Richter’s syndrome)
28
Q

Define neutropenic sepsis

A

It is defined as a temperature of greater than 38°C or any symptoms and/or signs of sepsis, in a person with an absolute neutrophil count of 0.5 x 109/L or lower (i.e. having anticancer treatment)

29
Q

Causes of neutropenic sepsis?

A

Cytotoxic chemotherapy - chemo causes bone marrow suppression, leading to a temporary reduction in the production of blood cells, including neutrophils, which take time to be replaced (about 5-10 days –> this is why neutropenic sepsis commonly occurs 7-14 days after chemo.
Haemopoeitic stem cell transplantation
immunosuppressive drugs - azathioprine, methotrexate, sulfasalazine, adalimumab, and infliximab

Other causes: Infections (HIV, EBV), Autoimmune (RA, Chron’s), Bone marrow failure

30
Q

Risk factors for neutropenic sepsis?

A

Patients at high risk:

  • Have sustained, significant neutropenia that is expected to last more than 7 days.
  • Are clinically unstable
  • Have an underlying malignancy and are being treated with high-intensity chemo - usually AML
  • Have significant co-morbidities - DM, liver disease, renal disease
  • Age - infants, or over 60
  • On corticosteriods
31
Q

What are the complications of neutropenic sepsis?

A
  • death - delaying treatment is a cause of death; immediate treatments saves lives
  • Organ failure
  • Invasive and atypical infection
  • neutropenic enterocolitis
  • coagulopathy - DIC
  • encephalopathy and delirium
  • physical impairmens - chronic pain and fatigue
  • psych - PTSD, anxiety about recurrent infections
32
Q

What are 4 pathogens involved in neutropenic sepsis?

A

coagulase-negative, Gram-positive bacteria are the most common cause, particularly Staphylococcus epidermidis

see pic

33
Q

A patient has suspected neutropenic sepsis. What would you ask in Hx and do in Ex?

added as could be A-E osce station?

A

History:
* Type and timing of chemo regimen and any other immunosuppressive medication being taken.
* Localizing symptoms e.g right lower-quadrant pain associated with neutropenic enterocolitis
* Recent infections and antibiotics used
* Latent infections are known to reactivate (e.g. TB), sick contacts, blood transfusions
* Co-morbidities
* Any intravascular devices
Examination:
* DRABCDE
* Systems-based examinations
* ENT
* Fundoscopy
* DO NOT perform DRE until antibiotics given)

34
Q

What investigations would you do for neutropenic sepsis?

A

Investigations:
* 2 sets of blood cultures
* Swabs from any indwelling lines
* Blood tests from complete blood cell count, WCC, inflammatory markers, renal and liver function.
* CXR
* Serology and PCR for viruses e.g. CMV
* Sputum, urine, stool samples, CT scans etc. where clinically indicated

35
Q

How do you treat neutropenic sepsis?

A
  • antibiotics must be started immediately, do not wait for the WBC
  • NICE recommends starting empirical antibiotic therapy with piperacillin with tazobactam (Tazocin) immediately
  • (check local guidelines)
  • following this initial treatment patients are usually assessed by a specialist and risk-stratified to see if they may be able to have outpatient treatment
  • Daily measures of fever and baseline bloods until the patient is apyrexial and neutrophil count above 0.5x10^9^
  • When the neutrophil count is normal, has been afebrile for 48 hours and blood tests have normalized, antibiotics can be stopped.

Other added points:
* if patients are still febrile and unwell after 48 hours an alternative antibiotic such as meropenem is often prescribed +/- vancomycin
* if patients are not responding after 4-6 days the Christie guidelines suggest ordering investigations for fungal infections (e.g. HRCT), rather than just starting therapy antifungal therapy blindly

36
Q

What prophylaxis can be given to patients on anti-cancer treatment for neutropenic sepsis?

A

if it is anticipated that patients are likely to have a neutrophil count of < 0.5 * 109 as a consequence of their treatment they should be offered a fluoroquinolone

37
Q

What staging system is used for CLL?

A

Binet staging system

38
Q

What is Richters transformation?

A

Ritcher’s transformation occurs when leukaemia cells enter the lymph node and change into a high-grade, fast-growing non-Hodgkin’s lymphoma. Patients often become unwell very suddenly.

Ritcher’s transformation is indicated by one of the following symptoms:
lymph node swelling
fever without infection
weight loss
night sweats
nausea
abdominal pain

YEAR 4 CANCER CARE (22 decks)

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