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Haematology > Haematological Malignancies- Leukaemia > Flashcards

Haematological Malignancies- Leukaemia Flashcards

CML, AML, CLL, ALL

1
Q

Hodgkin’s lymphoma

A

Malignant B cells found in lymphoid tissue. Reed-Sternberg cells

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2
Q

Chronic Lymphoid Leukaemia

A

Malignant transformation of the subset of B cells- ‘B1 cells)

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3
Q

Follicular lymphoma

A

Transformation of the B cells normally found in lymph node follicles

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4
Q

Burkitt lymphoma

A

Leukaemia / Lymphoma not associated with Reed Sternberg cells

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5
Q

What is leukaemia

A

Cancer of a particular line of stem cells in the bone marrow which causes unregulated production of certain types of blood cells (acute / chronic) and the line of cells they effect (myeloid/lymphoid)

the excessive production of a single type of cell can lead to suppression of others (pancytopenia- low RBC anaemia, leukopenia low WBC, thrombocytopenia low platelets)

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6
Q

ages and leukaemia

A

‘ALL CeLLmates have CoMmon AMbitions’

ALL: Acute lymphoblastic leukaemia. <5 and >45

CeLL: CLL: Chronic Lymphoid Leuakemia. >55

CoMmon: CM Chronic Myeloid Leuaemia: >65

AMbitions: Acute Myeloid Leukaemia >75

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7
Q

presentation of leukaemia

A 
Fatigue
Fever
Failure to thrive (children)
Pallor due to anaemia
Petechiae and abnormal bruising due to thrombocytopenia
Abnormal bleeding
Lymphadenopathy
Hepatosplenomegaly
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8
Q

petechiae differentials

A

bleeding under the skin- bruising and petechiae. non blanching rash

thrombocytopenia (low platelets)

  • non-accidental injury
  • leukaemia
  • meningococcal septicaemaia
  • vasculitis
  • HSP
  • idiopathic thrombocytopenia purpura
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9
Q

diagnosis of leukaemia

A

FBC (within 48hrs)

petechiae or hepatosplenomegaly- refer to hospital

blood film (abnormal cells, inclusions)

lactate dehydrogenase (LDH) raised in leukaemia but not specific

bone marrow biopsy- definitive diagnosis

CXR- infection / mediastinal lymphadenopathy

Lymph node biopsy can be used to assess lymph node involvement or investigate for lymphoma.

Lumbar puncture may be used if there is central nervous system involvement.

CT, MRI and PET scans can be used for staging and assessing for lymphoma and other tumours.

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10
Q

bone marrow biopsy

A

Bone marrow aspiration involves taking a liquid sample full of cells from within the bone marrow.

Bone marrow trephine involves taking a solid core sample of the bone marrow and provides a better assessment of the cells and structure.

Bone marrow biopsy is usually taken from the iliac crest. It involves a local anaesthetic and a specialist needle. Samples from bone marrow aspiration can be examined straight away however a trephine sample requires a few days of preparation

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11
Q

ALL

A

Acute lymphoblastic leukaemia

malignant change in one of the lymphocyte precursor cells
the acute proliferation of a single type of lymphocyte (b lymphocytes)

excessive production- replace other cells (panytopenia)

*most common in childhood. children (2-10 years old) (75% of childhood ALL is cured by chemotherapy)

  • adults over 45 (rare in adults, low cure rate)
  • Down’s syndrome

blood film: blast cells

Philadelphia chromosome 9:22 (translocation)

tx: steroids, vincristine, asparagine (intathecal chemo and CN irrigation) them maintenance for 2 years. (limit directed therapies in kids)

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12
Q

CLL

A

Chronic lymphoid leukaemia
the chronic proliferation of a single type of cell (b lymphocytes)

adults >55. most common in adults.

infections, anaemia, bleeding, weight loss (lymphocytosis)
*warm autoimmune haemolytic anaemia. systemic symptoms, sweating and weight loss.

hypogammaglobulinaemia (downregulats immunoglobulin production)
lymphadenopathy, hepatosplenomegaly

can transform into a high-grade lymphoma (Richter’s transformation)

blood films: smear/smudge cells (WBC fragile so rupture= smudge)
immunophenotype

  • can transform into Richter’s syndrome (high grade transformation)
    differentials: prolymphocytic leukaemia, hairy cell leukaemia, NHLs in leukaemia phase.
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13
Q

CML

A

Chronic Myeloid Leukaemia

  • chronic phase
  • accelerated phase
  • blast phase

males 40-60 y/o
clinical features: weight loss, hyper metabolism, massive splenomegaly, scrawny arms, sweaty, anaemic, high WBC, high platelets.

chronic phase; 5 years. asymptomatic. incidental diagnosis of raised WBC

accelerated phase: abnormal blast cells take up a high proportion of bone marrow and blood. more symptoms- anaemia, thrombocytopenia, immunocompromised

blast phase: an even higher proportion of blast cells and blood. severe symptoms, pancytopenia.

CML *philadelphia chromosome 9:22

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14
Q

AML

A

rare
increases in age (any age) (middle age)
the transformation from a myeloproliferative disorder like polycythaemia ruby vera or myelofibrosis.

clinical fears: BM failure, skinner gum infiltration, granulocytic sarcoma, leukaemia meningitis

(wet purpura in gums/cheeks/tongues if easy bruising) (fundoscopy- retinal bleed)

blood film- blast cells
rods, cytoplasm, Auer rods

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15
Q

on the spot leukaemia exam

A

Acute lymphoblastic leukaemia: Most common leukaemia in children. Associated with Down syndrome.

Chronic lymphocytic leukaemia: Most common leukaemia in adults overall. Associated with warm haemolytic anaemia, Richter’s transformation into lymphoma and smudge / smear cells.

Chronic myeloid leukaemia: Has three phases including a 5 year “asymptomatic chronic phase”. Associated with the Philadelphia chromosome.
Acute myeloid leukaemia: Most common acute adult leukaemia. It can be the result of a transformation from a myeloproliferative disorder. Associated with Auer rod

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16
Q

management of leukaemia

A

Treatment will be coordinated by an oncology multi-disciplinary team. Leukaemia is primarily treated with chemotherapy and steroids.

Other therapies include:

Radiotherapy
Bone marrow transplant
Surgery

17
Q

chemotherapy complications

A 
Failure
Stunted growth and development in children
Infections due to immunodeficiency
Neurotoxicity
Infertility
Secondary malignancy
Cardiotoxicity
Tumour lysis syndrome
18
Q

tumour lysis syndrome

A

Release of uric acid from cells that are being destroyed by chemotherapy. The uric acid can form crystals in the interstitial tissue and tubules of the kidneys and causes acute kidney injury. Allopurinol or rasburicase are used to reduce the high uric acid levels. Other chemicals such as potassium and phosphate are also released so these need to be monitored and treated appropriately. High phosphate can lead to low calcium, which can have an adverse effect, so calcium is also monitored.

19
Q

leukaemia

A

cancer of the blood forming cells
either lymphoid or myeloid
starts in bone marrow and can spread to blood stream, can affect lymph nodes, brain and skin

acute: malignant clone of immature cells, proliferation, no differentiation
chronic: malignant clone of a mature cell, proliferation, differentiatoin

20
Q

classification of haematological malignancies

A

leukaemia- acute/chronic (WBC)

lymphoma- hodgkins/non- Hodgkin’s

multiple myeloma
preleukaemic states- myelodysplasia, myeloproliferaitive disorders

can overlap e.g. have CLL but in the lymph nodes, have follicular lymphoma but in the blood.

*mutation one cell and clonal expansion (somatic mutation?)

lymphoma- happens in bone marrow then expands into other lymph nodes

21
Q

NHL can be T / B cell *?

A

GATTA mutation?

22
Q

leukaemia

A

accumulation of malignant bone cells in the bone marrow and BLOOD

consequences-bone marrow failure: anaemia (RBC), infections (WBC), bleeding (platelets)

can accumulate and cause granulocytic sarcoma (gums, skin, brain, other organs)

23
Q

how to classify leukaemia

A

acute/chronic
myeloid/lymphoid

myeloid- granulocytic, monocytic, erythroid, megakaryocytic

lymphoid- b and T cells

causes: virus (EBV Burkett lymphoma, Hodgkin lymphoma), radiation, benzene, family studies, chromosomal disorders, aplastic anaemia, paroxysmal nocturnal haemoglobinuraemai (can’t inhibit complement mediated lysis*), MPD- Jak 2 mutation

24
Q

MPD

A

Jak-2 mutation

25
Q

clinical manifestation of acute leukaemia

A

bone marrow is infiltrated by ‘blast’ cells so you loose the good cells (cytopenias)

anaemia (RBC) pallor, fatigue, dyspnoea
neutropenia (WBC) infection, fever
thrombocytopenia (easy bleeding, bruising, purport, bruising)

blast infiltration of other organs/tissues- brain, testis, liver, skin, kidneys, heat, lungs. (can get infiltration into these areas too but not all drugs can penetrate into those areas)

26
Q

investigation of leukaemia

A 
bloods:
FBC, 
blood culture (if febrile, sepsis 6)
blood film
renal function
clotting studies
fibrinogen
d-dimers

imaging:
CXR

special:
BM aspirate: confirms blast percentage, if there is any underlying dysplasia, genetic molecular mutations
trephine and cytogenetic analysis
cytochemistry (pearls stain?)
immunophenotype (flow cytometry - which cells and where did it come from) (B CLL has a T cell marker cd95?)?

*response to chemo
*genetic mutation
^ predictors of success

27
Q

chromosomal abnormalities for acute leukaemia

A

ALL (4;11) (9;22) (1;19) (12;21) (better prognosis)

AML: 5q, 7q, complex (poor
15;17) (8;21) inv 16 (good risk)

28
Q

myelodysplasia (MDS)

A

clonal stem cell disorder. peripheral blood cytopenia with normocellular or hyper cellular BM after exclusion of other disorders

'dysplasic feature'
increase in blast
clonal BM disorder
increased risk of leukaemia
common cryogenic abnormalities
29
Q

Precursor conditions

A

Jak-2 mutation with polyctemia rivera??

tx: supportive, chemotherapy, splenomegaly, targeted moclecular, hypomethylating agents.

30
Q

multiple myeloma

A

plasma cells
monoclonal malignan B cell disorder
median age diagnosis 66 years
progressive, ultimately fatal course (7 years survival)

31
Q

multiple myeloma

A

plasma cells
monoclonal malignan B cell disorder
median age diagnosis 66 years
progressive, ultimately fatal course (7 years survival)

diagnose with serum protein electrophoresis
albumin, alpha 1 (alpha 1 antitrypsin) alpha 2, beta, gama (haptoglobin)

monoclonal spike
mostly IgG, then IgA, then light chain, then IgD, IgE, then IgM (very rare)

*****becomes a Benz Jones protein (urine)

32
Q

lytic bone lesions in multiple myeloma

A

holes in bones (punched our lesions of the skull)
fractures

tx: watch and wait, oral chemo, combo chemo, transplant, newer agents- thalidomide, velcate.

Haematology (14 decks)

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