Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Haematology > Concepts in malignant haematology and acute leukaemia > Flashcards

Concepts in malignant haematology and acute leukaemia Flashcards

1
Q

What are the kinetics of normal haemopoiesis?

A 
Self-renewal 
Proliferation 
Differentiation or lineage commitment 
Maturation 
Apoptosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How can normal mature, non-lymphoid cells be identified?

A 
Morphology
Cell surface antigens (glycophorin A = red cells) 
Enzyme expression (myeloperoxidate = netrophils)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How can normal progenitors/ stem cells be identified?

A

Cell surface antigens; immunophenotyping (CD34)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is malignant hematopoiesis characterized by?

A

Increased numbers of abnormal and dysfunctional cell

Loss of normal activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is leukaemia characterized by?

A

Dysfunctional haemopoieis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is lymphoma characterized

A

Dysfunctional immune system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What can be encompasses by dysfunctional haemopoesis?

A

Increased proliferation
Lack of differentiation
Lack of maturation
Lack of apoptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is acute leukaemia?

A

Proliferation of abnormal progenitors with block in differentiation/ maturation (AML)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are chronic myeloproliferative disorders?

A

Proliferation of abnormal progenitors but NO differentiation/ maturation block (CML)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is a clone?

A

Population of cells derived from a single parent cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What type of haemopoiesis is polyclonal?

A

Normal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What type of haemopoiesis is monoclonal?

A

Malignant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What do driver mutations confer?

A

Growth advantage on cells

Selected during evolution of cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What do passenger mutations confer?

A

No growth advantage

Present in ancestor cancer cell when a driver mutation was acquired

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How are haematological malignancies classified?

A

Lineage
Developmental stage (precursor) within lineage
Anatomical site involved

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the different types of haematological malignancies based on lineage?

A

Myeloid

Lymphoid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How are haematological malignancies classified based on anatomical site involved?

A

Blood = leukaemia
Lymph node = lymphoma
**CLL can involved blood and lymph nodes **
Myeloma = plasma cell malignancy in marrow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the difference in presentation of acute leukaemias and high grade lymphomas in comparison with chronic leukaemias and low grade lymphomas?

A

Histologically and clinically; acute and high grade are more aggressive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are features of histological aggression?

A

Large cells with high nuclear:cytoplasmic ratio
Prominent nucleoli
Rapid proliferation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are features of clinical aggression?

A

Rapid progression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

How will acute leukaemias be differentiated from chronic leukaemias?

A

Acute leukaemias present with a failure of normal bone marrow function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Which malignancies of the haem system involve the most primitive cells?

A

Chronic myeloid leukaemia/ chronic myeloproliferative disorders - stem cell issue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Which part of haemopoiesis will acute myeloid leukaemia affect?

A

Myeloid progenitor cells - will go on to form erythrocytes, megakaryocytes, granulocytes and monoctytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Which part of haemopoiesis will acute lymphoblastic leukaemia affect?

A

Common lymphoid progenitor cells - will go on to form T cells, B cells and NK cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Which part of haemopoiesis will chronic lymphocytic leukaemia affect?
B cells
26
Which part of haemopoiesis will myeloma affect?
Plasma cells
27
What is acute leukaemia?
Rapidly progressive clonal malignancy of the marrow/ blood with maturation defects Defined as an excess of blasts (>20%) in either the peripheral or bone marrow Los of normal haemopoietic reserve
28
What are the different forms of acute leukaemia?
``` Acute myeloid (AML) Acute lymphoblastic (ALL) ```
29
What is ALL?
Malignant disease of primitive lymphoid cells (lymphoblasts)
30
What is the most common childhood cancer?
ALL
31
What is the clinical presentation of ALL?
Marrow failure; anaemia, infections, bleeding Leukaemic; high count with obstruction of circulation Involvement of areas outside marrow and blood; CNS, testis Bone pain
32
Who will AML affect?
Elderly >60yrs | Can be denovo or secondary
33
What is the presentation of AML?
Similar to ALL | Subgroups may have characteristic presentation; DIC or gum infiltration
34
What are the investigations indicated for acute leukaemia?
Blood count and film Coag screen; PT, APTT and fibrinogen Bone marrow aspirate (posterior iliac crests)
35
What will the blood film show in acute leukaemia?
Reduction in normal cells Presence of abnormal cells - increase in blasts with a high nuclear:cytoplasmic ratio AUER ROD (AML)
36
What feature of the blood film is pathognomonic of AML?
Auer Rod
37
What tests should be performed on the bone marrow aspirate?
Morphology; what do the cells look like? | Immunophenotyping via flow-cytometry; are there lineage specific proteins on cell surface?
38
What is required for a definitive diagnosis of ALL from AML?
Immunophenotyping | Very important because the treatment of AML and ALL differ
39
What does a trephine bone marrow biopsy allow for?
Better assessment of cellularity and helpful when aspirate samples are suboptimal
40
What is the curative treatment of ALL?
Can last up to 2-3 years Different phases of treatment of varying intensity Targeted treatments in certain subsets
41
What is the curative treatment of AML?
Intensive 2-4 cycles of chemo (5-10 days of chemo followed by 2-4 weeks of recovery) Prolonged hospitalisation Target treatments in subsets
42
What is a hickman-line?
Central venous catheter that sits in the SVC and used for administration of chemo
43
What are the problems with marrow suppression?
Anaemia Neutropenia; infections Thrombocytopenia; purpura, petechiae (plt <20), bleeding gums
44
What are the most dangerous bacteria in marrow suppressed patients?
Gram negative bacteria can cause fulminant life-threatening sepsis in neutropenic patients
45
What are the complications of chemo?
``` N+V Hair loss Liver and renal dysfunction Tumour lysis syndrome (during first course of tx) Infection Loss of fertility ```
46
What specific side effect with anthracyclines cause?
Cardiomyopathy
47
What is very important to do if neutropenic occurs in a patient?
Empirical tx with broad spectrum antibiotics specifically covering gram negs
48
What agent should be added on in the instance of persisting fever and neutropenia unresponsive to antibiotics?
Fungal protection
49
What protozoan needs to be covered in ALL Therapy?
PJP
50
What is remission in acute leukaemias?
<5% marrow blasts with recovery of normal haemopoiesis
51
What is an example of targeted treatment in ALL?
Kinase inhibitors in ALL with philadelphia chromosome
52
Which AML subtype predisposes to DIC?
Chromosomal translocation in t(15;17) | Results in DIC
53
What is tumour lysis syndrome?
Increased potassium, urate | AKI
54
What are the symptoms of DIC?
Bruising Bleeding Renal failure
55
What are the blood test signs of DIC?
``` Decreased platelets Increased PT and APTT Decreased fibrinogen Increased d-dimers Blood film; schistocytes ```
56
What are important associations of ALL?
X-rays during pregnancy | Down syndrome
57
What are the si/sy of marrow failure?
Anaemia; decreased Hb Infection; decreased WCC Bleeding; decreased platelets
58
Where can acute lymphoblastic leukaemia infiltrate?
Hepato and splenomegaly Lymphadenopathy Orchidomegaly CNS involvement; meninginism, CN palsy
59
What is the characteristic test results for ALL?
Blast cells on film and marrow | WCC high
60
Are the cure rates high for ALL?
Yes; children cure rate is 70-90%
61
What confers poor prognostic factors in ALL?
``` Adult Male Philadelphia chromosome (BCR-ABL gene fusion due to translocation of chromosomes 9 and 22) Presentation with CNS signs Decreased Hb WCC >100 B-cell ALL ```
62
What is diagnosis of AML dependent on?
Bone marrow biopsy Immunophenotyping Molecular methods AML is differentiated from ALL via auer rods
63
What are myelodysplastic syndromes?
Disorders that manifest as marrow failure with risk of life-threatning infection and bleeding Can develop secondary to chemo or radiotherpay Can transform to acute leukaemia
64
What are the test results for myelodysplastic syndromes?
Pancytopenia Decreased retic count Marrow cellularity increased due to ineffective hematopoiesis Ring sideroblasts
65
Which form of leukaemia is philadelphia chromosome most implicated?
CML Reciprocal translocation between long arm of chromosome 9 and long arm of 22 resulting in a fusion of gene BCR/ABL which has tyrosine kinase activity
66
What are the symptoms of CML?
``` Decreased weight Tiredness Fever Sweats Gout Bleeding Abdo discomfort; splenomeglay ```
67
What are the signs of CML?
Splenomegaly Hepatomegaly Anaemia Bruising
68
What will the tests show in CML?
``` V high WCC (>100) with whole spectrum of myeloid cells; neutrophils, monocytes, basophils, eosinophils Decreased Hb Increased urate Increased B12 Bone marrow hypercellular ```
69
What is the commonest leukaemia?
CLL
70
What is the hallmark of CLL?
Progressive accumulation of a malignant clone of functionally incompetent B cells Mutations, trisomies and deletions influence risk
71
What are the symptoms and signs of CLL?
Often no symptoms; can be anaemic, infection prone or have wt loss, sweats and anorexia Signs; enlarged, rubbery non tender nodes. Splenomegaly, hepatomegaly
72
What will the tests show in CLL?
Increased lymphocytes Autoimmune haemolysis Marrow infiltration; decreased Hb, decreased neutrophils, decreased platelets Bone marrow; smudge/ smear cells
73
What is the natural history of CLL?
1/3rd never progress 1/3rd progress slowly 1/3rd progress actively
74
on the bone marrow, what is pathognomonic of CLL?
Smear/ smudge cells
75
What can cause pancytopenias?
Decreased marrow production; aplastic anaemia, infiltration, megaloblastic anaemia, myelofibrosis Increased peripheral destruction; hypersplenism
76
What is agranulocytosis?
Granulocytes have stopped being made | Commonly via drugs; carbimazole, procainamide, sulphonamides, clozapine, dapsone
77
What is the treatment for tumour lysis syndrome?
Allopurinol
78
In AML and CML which cells in particular will be increased?
Look for an increase in neutrophil count
79
In ALL and CLL what cells in particular will be increased?
Look for an increase in lymphocyte count
80
Which leukaemia in particular is associated with the Philadelphia chromosome?
CML - translocation between chromosome 9 and 22 | Treat with tyrosine kinase inhibitor

Haematology (31 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions