leukaemia Flashcards
leukimia is the malignancy of— in the bone marrow with an
excess of “ – ” cells i.e. abnormal — — blood cells
* Disease of white blood cells: — or —
* May be acute or chronic
* Symptoms and signs related to
– — replacement
* Reduced RBCs, WBCs and platelets
– —
– +/- Bone pain
– +/- —
white blood cells
blast cells
immature white blood cells
myeloid or lymphocyte
marrow
hypervsicoty
lymphadenopathy
- Flow cytometry/immunophenotyping can help identify the – of blood cell by assessing — , – and — of different cell antigens
- SSC = Side scatter: this assesses the – of the cell
- FSC = Forward scatter: this assesses the – of the cell
type
size
grnaulaty
granularity
size
disorders of white blood cells:
* Reactive increase in number – “philias”/osis
* — : – bacterial sepsis, steroid use
* —- : – viral infection, immune causes
* — : – allergy, parasites, drugs
* Decrease in number – “penias”
– Neutropenia, Lymphopenia & Eosinopenia,
Pancytopenia (reduction in all cells)
– Causes of penias: drugs, viral infections,
radiation, chemotherapy etc.
Learn the language
neurophilia
lymphocytosis
esinotphilia
- —- : increased number of blast cells in bone marrow
and blood - Classification:
– – / –
– — / – - — : Nodal and extra nodal
– Hodgkins
– Non-Hodgkins - Large – lymphoma, – Lymphoma most common
- Other cancers of myeloid lineage
– Myeloproliferative neoplasms
– Myelodysplastic syndromes
leukimia
acute/chronic
myloid/lymphoid
lymphoma
large b and follicular
leukemia is the increased number of — cells in — and —
1-Acute Leukaemias
Broadly divided into:
–Acute myeloid leukaemia (AML)
–Acute lymphoblastic leukaemia (ALL – can be – or – origin)
–Several molecular subtypes of both AML and ALL
2-Chronic Leukaemias
Common examples include:
Chronic myeloid leukaemia ( – lineage)
Chronic lymphocytic leukaemia (– lineage)
b and t cells
myeloid
b cells
clinical features:
The onset of bone marrow failure and symptoms is rapid in – leukaemias
but can be more insidious in – leukeamias
* Bone marrow replacement by blast cells with marrow failure
– Anaemia (low haemoglobin)
– Fever - Infections ( caused by low white cells)
– Bleeding tendency (low platelets and coagulopathy including DIC)
* Bone pain (caused by bone marrow expansion and hypoxia)
* Weight loss
* Night sweats
* Lymphadenopathy (more commonly seen in childhood ALL)
* Enlarged thymus
– Usually presents as SOB in T-ALL in young children, can cause a
widening of mediastinum on chest x-ray
* Enlarged testes – most commonly seen in ALL
* Splenomegaly – more commonly seen in – leukaemias
acute
chronic
chronic
acute myeloid ( myeloblastic) leukaemia aka AML :
* Arises from the –
transformation of a myeloid precursor
* 80% of cases occur in –
* Most frequent leukemia in –
* The incidence increases with –
specific manifestation:
* Low blood counts secondary to bone marrow invasion can lead to initial
symptoms of fatigue, recurrent infections, weight loss, bruising, gum
bleeding and intracranial bleeding causing headache or collapse
* Solid tumours can form from leukaemia in these patients – known as
myeloid sarcoma
* Rarely gum tissue invasion causes gum hypertrophy
* Skin deposits can be seen but this is rare
* Tumour lysis syndrome caused by the rapid breakdown of leukemia cells can cause renal failure – this can be spontaneous or induced by the initiation of cytotoxic chemotherapy
* Coagulopathy – disseminated intravascular coagulation – most commonly associated with a subtype of AML called Acute Promyelocytic Leukaemia–
APML
malignant
adults
neonate
age
( AML-GUM hypertrophy is the infiltration of gums by leuameic cells )
- Accounts for 85% of childhood leukaemia
- In children - most common malignant disease
- Incidence decreases with age, with a second rise after 40
years.
is known as –
-Similar to AML in terms of bone marrow — manifestations
-Clinically can be – to tell the difference between AML and ALL at diagnosis
-More likely to have – , – mass or — involvement
acute lymphoblastic leukaemia ALL
invasion
difficult
adenopathy thymic mass and testicular involvement
investigation of acute leukaemia:
Understand the reason for each test you order!!
* FBC – Hb, platetets, white cell differential count – what does
this mean?
* Blood film – what can you expect to see?
* Coag– PT, APTT, Fibrinogen
* Lactate dehydrogenase
* Renal function, liver function – why is this needed?
* Bone marrow aspirate and trephine
* Immunophenotyping by flow cytometry to determine the type
of cell
* Molecular analysis of DNA inside the leukaemia cells – what
can this tell you?
investigate of acute leukaemia:
1- full blood count:
WCC <1.0x109/l to >200x109/l, white cells and – blast cells
* Anaemia: reduced
haemoglobin normochromic, normocytic
* Thrombocytopenia
(Often <10x109/l)
2- bone marrow aspiration and trephine biopsy:
Confirm acute
leukaemia
Blasts are counted
Flow cytometry
Molecular analysis
Immunohistochemistry
3- immunophenotyping as —- which determine whether the leykimia is — or —
- molecular test help detecte relevant — as:
* t(8;21) AML (Core binding factor AML- good
prognosis)
* t(4;11) ALL (MLL re-arranged ALL- poor
prognosis in adults)
increased
flow cytometry
lymphoid or myeloid
rearrangement
management of acute leukaemia:
- Chemotherapy
- +/- Bone marrow transplant (BMT) – can be from sibling or
unrelated donor - The decision for a BMT or not is complex – depends largely on
cytogenetic subgroup at diagnosis
Supportive care to keep patient alive while chemo is trying to work. - Treat infection with antibiotics
- Treat Bleeding
– Platelet transfusion for bleeding episodes and to prevent
intracranial haemorrhage (ICH)
– Fresh frozen plasma (FFP) to prevent bleeding and ICH
– Fibrinogen to manage DIC – can be fatal despite the leukaemia
itself being a curable disease
– Red cell transfusion for severe anaemia
chronic myeloid leukaemia which is malignancy of —-
* Median age 40-60y
* – chromosome, t(—)
* Marrow replacement +/- failure:
– – , – & —
* Marked — – >50,000
(abnormal)
* Marked – , —
myeloid marrow cells
Philadelphia (9:22)
anemia fever and bleeding
leucytosis
splenomegaly and hepatomegaly
diagnosis of CML:
* Clinical examination and history – what do you expect to hear
and find?
* FBC
* Blood film
* Coagulation screen
* Bone marrow aspirate and trephine
* — testing using PCR or NGS: t(9;22) (Philadelphia chromosome) and – fusion gene
molecular testing
BCR-ABL
principle of treatment of CML:
* Relieve constitutional symptoms of :
– Fluids, hydroxyurea for cytoreduction
– Chemotherapy sometimes needed
– — Inhibitor treatment has been a major breakthrough in cancer
(e.g. Imatinib/Dasatinib/Nilotinib)
– +/- bone marrow transplant in rare refractory cases
leukocytosis, splenomegaly and thrombocytosis
Longterm Tyrosine Kinase
chronic lymphocytic leukaemia CLL which is maligancy of —
* Malignancy of –
* Usually presents in – phase
* Marrow failure – often – development over
years
* – – usually an incidental discovery on FBC with GP, patient otherwise well
* Generalised —
bone marrow lymphocyte
mature lymphocyte
asymptomatic
slow development
lymphocytosis
lymphadenopathy
