Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Hematologic Disorders > Leukemias > Flashcards

Leukemias Flashcards

1
Q

Types of AML (3)

A
  • Myeloblastic
  • Monoblastic
  • Megakaryoblastic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Difference between acute and chronic leukemias

A

Acute: very immature, very fast
Chronic: more similar to mature, slow

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

Diagnosis of AML

A

Blast cells >20% or genetic anomalies

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

Causes of AML (3)

A
  • Increase proliferation
  • Decrease apoptosis
  • Block differentiation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

AML age group

A

> 65 years

10-15% childhood

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

AML immunophenotype (4)

A

CD13+ CD33+ CD117+ TdT-

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

AML clinical features (4)

A
  • Infections: Candida, Pseudomonas
  • Normo normo anemia
  • Thrombocytopenia + DIC = bleeding = BRUISES (PML)
  • Gum hypertrophy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are Auer rods made of and in which leukemia are they found?

A

MPO

Myeloid leukemias

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

AML mutations (3)

A

t(8:21) —> RUNX1/CBF1b —> block maturation

t(15:17) —> RARa-PML —> interfere with terminal differentiation = PML

FLT3 —> signals that there’s normal growth —> PML

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

AML mutation with the best prognosis

A

t(15:17) / PML

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

What differentiates PML from AML?

A

***Coagulopaties
Phenotype is arrested differentiation
Best prognosis

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

Labs in PML

Options: cancer procoagulant, factor V, FDP, fibrinogen, D-dimers, platelets, thrombin

A

Decreased:
- Fibrinogen
- Factor V
- Platelets

Increased:
- FDP
- D-dimers
- CP
- Thrombin generation

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

What is the mechanism of coagulopathies in PML? What is the activator called?

A

HYPERFIBRINOLYSIS
- Increase in degradation products
- Decrease in inhibitors: PAI-1, a2 antiplasmin

Annexin A2 = fibrinolytic activator ANA1

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

Myelodysplastic syndrome why are they considered “pre-leukemia”?

A

They only stop maturation, don’t get posterior mutations

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

Why do myelodysplastic syndromes rarely turn into AML?

A

Patients die

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

How to differentiate between AML and MDS?

A

Blast amount
Normal: 2-3%
MDS: <20%
AML: >20%

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

ALL age group

A

CHILDHOOD (3-7)

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

Which leukemias are Tdt +?

A

ALL
CLL

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

Most common ALL mutations (6)

A

t(9;22) - adult
t(12;21) - kids
MLL rearrangements
Diploidy

Abnormal karyotype
NOTCH signaling

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

ALL clinical features (blood 3 and organs 6)

A
  • Anemia normo normo
  • Neutropenia = infections, fever
  • Thrombocytopenia = bruises, purpura
  • Tender bones
  • Lymphadenopathy
  • Hepatosplenomegaly
  • Papilloedema
  • Meningeal sx
  • Rare testicular swelling
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

ALL labs

A

Decrease: cells

Increase:
- Uric acid
- LDH
- Ca2+

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

t(9;22) mutation:

  1. Leukemia type
  2. Age group
  3. Gene
  4. Prognosis
A

“Philadelphia gene”
1. ALL
2. Adults
3. BCR-ABL1
4. Poor prognosis

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

t(12;21) mutation:

  1. Leukemia type
  2. Age group
  3. Gene
  4. Prognosis
A
  1. ALL
  2. Kids
  3. TEL-AML1 or ETV6-RUNX1
  4. Good prognosis
24
Q

t(8;21) mutation:

  1. Leukemia type
  2. Age group
  3. Gene
  4. Prognosis
A
  1. AML
  2. Elder
  3. RUNX1/CBF1b
25
Q

t(15;17) mutation:

  1. Leukemia type
  2. Age group
  3. Gene
  4. Prognosis
A
  1. PML
  2. Elder
  3. RARa-PML
  4. Best prognosis
26
Q

T-ALL pathogenesis

A

NOTCH signaling
EC cleavage mutation —> insert tandem duplications —> IC PEST deletion

Increases rate of cleavage and nuclear translocation

27
Q

T-ALL 3 T’s

A

T-ALL
Thymic mass
Teenagers

28
Q

CLL age group

A

60-80 years
Male 2:1

29
Q

CLL effect on B cells

A

Mature, weak IgM and IgD
Increased production and life span
Decreased apoptosis

30
Q

CLL clinical features

A
  • Symmetrical node enlargement
  • Anemia normo normo or AI hemolysis
  • Thrombocytopenia
  • Splenomegaly
  • Hypogammaglobinemia = immunosuppresion EC
31
Q

Genetics and CLL

A

Chromosome abnormalities:
- del 13q = microRNA loss
- del 11q23 = ATM gene
- T21
- 17p structural = p53 gene

Somatic hypermutation: IGVH gene 50% = poor prognosis

NOTCH1

32
Q

Which leukemia has smudge/fragile cells?

A

CLL

33
Q

CLL lab findings

A
  • B cll increased
  • Smudge cells
  • CD19+ CD5+ CD23+
34
Q

Why autoimmune disorders can develop from CLL?

A

Hemolytic anemia
Thrombocytopenia
Neutropenia
Red cell aplasia

35
Q

In which leukemia are Rai scores used?

A

CLL

36
Q

Rai score indications

A

0 = 12 year survival
IV = < 4 years

37
Q

What is small lymphocytic lymphoma?

A

General lympadenopathy with CLL

38
Q

SLL + mutation = _____

A

Diffuse B cell lymphoma

39
Q

What is the Richter transformation?

A

SLL + mutation = diffuse B cell lymphoma

40
Q

CML genetics

A

BCR-ABL1

41
Q

CML age group

A

40-60 years, neonates, elderly

42
Q

Philadelphia chromosome and which leukemias it causes

A

t(9;22)

ALL
CML

43
Q

Blasts in CML

A

<10%

44
Q

CML clinical findings

A
  • Hypermetabolism
  • Massive splenomegaly
  • Anemia
  • Thrombocytopenia
  • GOUT
45
Q

Labs in CML

A
  • Luekocytosis
  • Basophils, neutrophils, and myelocytes in circulation
  • Normo normo anemia
  • High or low platelets
  • Hypercellular marrow
  • Increase URIC ACID
46
Q

Blastic transformation: which leukemia and what it is

A

CML

> 20% blases in a matter of days-weeks
Hard to control
Survival is rare if they stay for a few months
Tx: imatinib only temporary
- Protein kinase inhibitor replaces ATP in BCR-ABL1 kinase

47
Q

CML phases (3)

A

Chronic = fever & abdominal fullness
<10% blasts

Accelerated = bleeding & opportunists
10-19% blasts

Blast crisis = bone pain
>20% blasts

48
Q

3 main myeloproliferative disorders

A
  • Polycythemia vera
  • Essential thrombocythemia
  • Primary myelofibrosis
49
Q

Mechanism of myeloproliferative disorders

A

TK mutation —> activates without growth factor

50
Q

What leukemia can myeloproliferative disorders turn into?

A

AML

51
Q

Main mutation in myeloproliferative disorders

A

JAK2

52
Q

Clinical features of myeloproliferative disorders

A
  • Facial plethora
  • Conjunctival suffusion
  • Splenomegaly
  • Myelofibrosis
53
Q

What is polycythemia vera?

A

Increase in everything
*** Hb and RBC volume

54
Q

Clinical findings of polycythemia vera

A
  • Hyperviscosity
  • Hypervolemia
  • Hypermetabolism
  • Headache, dyspnea, blurry vision, night sweats
  • Pruritus after hot bath
  • Retinal venous engorgement
  • Splenomegaly 75%
  • Hemorrhage or thrombosis
    GOUT
55
Q

What is essential thrombocythemia?

A

> 450,000 platelets for > 2 months
Thrombosis in head, hands, feed
Bleeding in nose, bruising
Splenomegaly
Tx: aspirin, hydroxyurea, IFNa, plateletpheresis

56
Q

Polycythemia vera treatment

A

Phlebotomy
Hydroxyurea
IFNa

57
Q

What is primary myelofibrosis?

A

Losing architecture in the bone marrow
Hepatosplenomegaly
HSC are surrounded by fibrous and IC substance

Hematologic Disorders (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions