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U15 Spine > Leukaemia > Flashcards

Leukaemia Flashcards

1
Q

Leukaemia VS Lymphoma

A
  • Leukaemia = term to describe the widesprea dinvolvement of the bone marrow accompanied with a large number of cancer cells in the peripheral blood
  • Lymphoma = Proliferation of lymphoid cells arising as sicrete masses
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2
Q

Haemopoiesis

A
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3
Q

Classifications of WBC neoplasms

A
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4
Q

Acute VS Chronic leukaemia

A
  • Accordign to WHO classification, blasts should be >20% in bone marrow for diagnosis of acute leukamia.
  • So bone marrow biopsy is the investigation of choice for diganosing leukaemia.
  • The FAB (French-americal-british classifciation) diagnostic criteria for aucte leukaemia is the presence of >30% blasts in the bone marrow (Normally <5%) and increased number of cells in the blood
  • Acute leukaemias have a high rate of proiferation without differentiation and their clinical course is rapid
  • Chronic leukaemias have a low rate of proliferation of tumour cells with good differentiation and their clincia course is slow.
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5
Q

WHO classification of the lymphoid neoplasms

A
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6
Q

What is the commonest leukamia seen in childhood with a slight predilection for males?

A

Acute Lympblastic Leukaemia (ALL)

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7
Q

Etiological agents for Acute Lymphblastic leukaemia (ALL)

A
  • Exposure to ionising radiators as X-rays
  • Chemical like benzene
  • Genetic disorders like Down Syndrome
  • Atazia telangiectasia
  • Acquire disorders liek paroxysmal nocturnal haemoglobinuria and aplastic anaemia
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8
Q

WHat are the clinical Features of Acute lymphoblastic Leukaemia (ALL)

A
  • Characterised by sudden onset of symptoms that arise due to replacement of the normal bone marrow cells with blast cells, thereby causing features/symptoms due to decreased number of RBC, WBC and platelets (anemia, infections, increased bleeding tendency respectively).
  • The leukaemic cells also infiltrate the organs of the body like spleen, liver and lymph nodes cuasing splenomegaly, hepatomegaly and lymphaedonpathy
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9
Q

The immunological classification of Acute lymphoblastic Leukaemia

A
  • ALL can be precursor B-cell or T-cell type
  • In the pre-T-cell type, there is presence of mediastinal mass ue to thymus invovlement which can compress either the vessels or airway in the region.
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10
Q

Acute Lymphoblastic leukaemia (ALL) features in bone marrow

A
  • Bone marrow expansion is repsonsible for bone pain and tenderness (usually sternal tenderness) in these patients
  • Testicular invovlement and CNS features like headache, vomiting and nerve palsies are also seen in these patients.
  • Aleukemic leukaemia is diagnosed by the presence of >20% blasts in the bone marrow
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11
Q

Investigations and Blood Findings in Acute Lymphoblastic leukaemia (ALL)

A

Blood:

  • markedly elevated WBC count
  • Uncommonly, some patients may show pancytopenia with few or no blast cells in peripheral blood which is aleukemia leukaemia
  • Diagnosis made by presence of >20% blasts in the bone marrow
  • Blast cells with Periodic Acid Schiff (PAS) positively are seen
  • There is presence of anaemia, neutropenia and thrombocytopenia

Bone marrow: Hypercellular with blast cells >20% of the marrow cells

Biochemical investiagtions:

  • Elevated serum uric acif and phosphate levels
  • Hypocalcaemia (because of hyperphosphatemia)
  • Serum LDH is also increased (due to increased turnover of the cancer cells)

Commonest cytogenic abnormality in ALL is hyperdiploidy.

Apart from CML, philadelphia chromosome is also seen in ALL and is associared with wors eprognosis.

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12
Q

Genetic Associations of ALL

A
  • T cell ALL = associated with gain of funciton mutation in NOTCH1 gene (normally required for T celld evelopment)
  • B cell ALL = associated with loss of function mutation in PAX5, E2A. EBF or balanced t(12;21) affecting TEL and AML1 genes (nromally required for B cell development)

Treatment of choice for ALL is allogenic bone marrow transplantation and cancer drug regime used for induction is VAPD (vincristine + asparaginase + prednisolone + daunoribicin) with intrathecal methotrexate.

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13
Q

What leukaemia affects adults most commonly between 15-39years

A
  • Acute Myelogenous Leukaemia
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14
Q

Etiolgoical agents for Acute Myelogenous Leukaemia (AML)

A
  • Exposure to ionising radiations like X-rays
  • Chemicals like benzene
  • Seocndary to myelodysplastic syndrome
  • Drugs like anti-cancer drugs
  • Genetic disorders like Downs syndrome and Fanconi’s anaemia
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15
Q

Define the characterists of the predominant cell in Acute Myelogenous Leukaemia (AML)

A
  • Myeloblast is the predominant cell
  • Fine nuclear chromatin
  • 3-5 nucleoli
  • High N:C ratio
  • Presence of Auer rods (these are abdnorla aurophilic granules)
  • Staining positively with Sudan black B, myeloperoxidase (MP) and Non Specific Esterase (NSE)
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16
Q

FAB (French - American-British) system for classifiying Acute myelogenous Leukaemia

A

FAB system divides AML into 8subtyes, M0 through to M7, based on the type of cell from which the leukaemia develops and its degree of maturity. This is done by examining the appearance of the malignant cells under light mciroscopy.

17
Q

WHO classification for Acute Myelogenous Leukaemia (AML)

A

Attempts to be more clincially useful than FAB and to produce more meaningful prognostic information. The subtypes are:

  • AML with characteristic genetic abnormlaities
  • AML with multi-lineage dysplasia
  • AML with myelodyslastic syndromes (MDS), therapy related
  • AML not otherwise categorised
  • Acute leukaemias of ambiuous lineage.
18
Q

Clinical features of Acute Myelogenous Leukaemia (AML)

A
  • Similar to ALL
  • Fatigue due to anaemia
  • Bleeding and infections in oral cavty, lungs, etc
  • Bleeding diathests due to DIC which resilts from release of thromboplastic substances in the granules (most common with M3 AML)
  • Infiltration of cells into the organs is relatively less common compared to ALL resulting in only mild hepatosplenomegaly and lymphadenopathy
  • Gum hypertrophy and infiltration of the skin (leukemia cutis) is common particularly with M5 AML
  • Less frequently, patients may present with localised massses in absence of marrow or peripheral blood involvement called myeloblastoma, granulocytic sarcoma or chloroma (turn green in presence of dilute acid due to presence of MP).
19
Q

Positive markers of granulocytic sarcoma (type of AML) and symptoms

A

Lysozyme, CD43, CD45, CD117, MPO

These manifest as proptosis (due to orbital movement) most commonly or may present as bone or periosteal masses.

  • Fever
  • Repeated infections
  • Fatigue
  • Pal skin
  • Difficult in breathing
  • Pain in the bones
  • Tendency for bruising and unusal bleeding
  • Bleeding from nose or gums
20
Q

Blood Findings in Acute Myelogenous leukaemia

A

Blood:

  • Markedly elevated WBC count
  • Findings are similar to that in ALL except that the blast cells show positivity with MPO, NSE or Sudan black
  • There is presence of anaemia, neutropenia and thrombocytopenia

Bone marrow: hypercellular with blast cells>20% of the marrow cells.

Biochemical investiagtions:

  • Elevated serum uric acid and phosphate levels accompanied by hypocalcemia (because of hyperphosphatemia)
  • Serum Muramidase levels is also increased in M4 and M5 AML
  • The fibrin degredation products (FDPs) are levated in M3 AML due to DIC
21
Q

Prognostic factors in AML

A
22
Q

Leukemoid Reaction -what is this

A

Leukemoid reaction = presence of elevated leucocyte count (>50,000 cells/ml) in the peripheral blood resmebling leukaemia in an individual who actually does not have leukaemia

Differentiated by leukaemia by:

  • Immature cells/blasts <5%
  • T leukocyte alkaline phosphatase (LAP) score
  • Dohle bodies + in neutrophils
  • Toxic granulations and in WBC
  • Less hepatosplenomegaly
  • Less lymphadenopathy
  • Less haemorrhage
23
Q

Diagnostic approach to leukaemias

A
24
Q

Myelodysplastic Syndromes (MDS)

A
  • Myelodysplastic syndromes = clonal stem cell disorder resulting in ineffective haematopoiesis and increased risk of development into AML
  • The bone marrow is replaced with multipotent stem cells which can differentiate but in an unorganised and infecctive manner only
  • It has been linked to the exposure to radiation, benzene, alkylating agents and some chromosomal abnormalities like monosomy 5 and 7, deletion of 5q and 7q, trisomy 8 and deletion of 20q.
  • Classification:
  1. Primary MDS - develops slowly usually after 50years of age
  2. Secondary or Therapy related MDS (t-MDS) = usually 2-8years after toxic drug or radiation exposure (secondary MDS gets transformed to AML most frequenlty and has poorer prognosis)
25
Q

What is Chornic Myelogenous leukaemia (CML)

A
  • CML = characterised by the increased number of immature leukocytes, basophilia and splenomegaly seen in adults between the ages of 25-60years
  • An increased risk of CML seen in people exposed to ionising radiation (survivors of nuclear bombs)
  • There is presece of ABL gene (Prot-oncogene) on chromsome 9 and BCR (Break point cluster) gene on chromosome 22
  • A recipocal translocation between these 2 chromsomes causes formation of BCR-ABL fusion gene on chromsoome 22 (called philadelphia chromosome or Ph- This fused gene causes synthesis of 21 kDa duion protein) .
26
Q

Chronic Myelogenous leukaemia key points

A
27
Q

Clinical features of Chronic myelogenous leukaemia

A
  • Intiially = Gradual onset with fatigue, anorexia, weight loss
  • Characteristically there is spelnomegaly caused by infiltration of leukemic cells adn extramedullary haematopoesis
  • Hepatomegaly is also seen but ly,phadenopathy is uncommon in these patients
  • Leukocytic infiltration and hypercellularity can cause sternal tenderness wheras leukostasis can cause priapism (Long-lasting painful erection)< venous thrombosis and visual disturbance.
28
Q

bone marrow and peripheral smeal of CML

A

Bone marrow:

  • 100% cellular in these patients (In normla health, 50%cellular,50%fat)
  • The erythroi precursors are decreased (replaced by myeloid precursors) wheras abnormal megakaryocytes are commonly seen.
  • The presence of scattered histiocytes with blue granules (sea-blue histiocytes or pseudo-gaucher cells) is characteristically seen
  • There is also increased depsoition of reticlin fibres

Peripheral Smear:

  • Thrombocytosis and marked leukocytosis
  • Present of immature white cells, eosinophilia and basophilia
  • The neutrophil Alkaline phosphate (NAP or LAP) is decreased
29
Q

Biochemical findings of CML

A
30
Q

Chronic lymphocytic leukaemia (CLL)/ Small Lymphocytic Lymphoma (SLL) what is it

A
  • It is a proliferation of mature lymphocytes seen in the old patint (abotu 60years)
  • Chronic course of onset (replacement of the bone marrow hematopoietic cells occurs after a few years)
  • Anaemia, thrombocytopenia, and granulocytopenia occur late in this disease
  • TNF-a and TGF-P have a role in CLL
31
Q

Chronic lymphocytic leukaemia (CLL)/ Small Lymphocytic Lymphoma (SLL) clinical features

A
  • More commonly seen in males and is asymptomatic in a large number of cases
  • Fatigue is the comonest presenting complaint associated with lymphadenopathy (Intially, cervical followed by generalised lymphadenopathy)
  • There is also presence of pallor, mild hepatosplenomegaly, skin rash and petechiae
  • Sternal tenderness is absent (seen in acute leukaemia)
  • Cancer cells are not bale to produce normal immunoglobulins resulting in increased susceptibility to infections
  • Present of anaemia, thrombocytopenia and granulocytopenia signify the late stage of the disease.
32
Q

CLL - defects and tests for detecting antiodies

A
33
Q

Diagnostic criteria for CLL

A
  • Peripheral blood lymphocyte count >5000/mm^3 with <55% cells being atypical
  • Bone marrow aspirate showing >30% lymphocytes
34
Q

Investigations for CLL

A

Blood Invetsigation:

  • Low Hb, elevated TLC (total leukocyte count) with lymphocytosis
  • Peripheral smear shows increased number of lymhocytes with scanty cytoplasm

These cells are fragile, so they get disrupted while making a smer and called ‘smudge’ cells or ‘basket’ cells or ‘parachute’ cells

Bone marrow:

  • Is hypercellular with >30% of the nucleated cells being lymphocytes as the idganostic feature of the leukaemia
  • Aggregation of small lymphocytes and large cells called ‘prolymphocytes’ is called proliferation centre which is characteristic finding of CLL

Immunphenotyping:

  • The cancer cells are positive for CD19. CD20. CD23, CD5
  • There is also low level expression of surface immunoglobulin heavy and light chains.

The distinguishing feature of CLL and SLL is that in the former blood involvement is predominant presenting feature whereas in SLL the patients usually have lymph node findings.

U15 Spine (11 decks)

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