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Leukemias Flashcards

1
Q

Types of AML (3)

A
  • Myeloblastic
  • Monoblastic
  • Megakaryoblastic
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2
Q

Difference between acute and chronic leukemias

A

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

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3
Q

Diagnosis of AML

A

Blast cells >20% or genetic anomalies

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4
Q

Causes of AML (3)

A
  • Increase proliferation
  • Decrease apoptosis
  • Block differentiation
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5
Q

AML age group

A

> 65 years

10-15% childhood

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6
Q

AML immunophenotype (4)

A

CD13+ CD33+ CD117+ TdT-

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7
Q

AML clinical features (4)

A
  • Infections: Candida, Pseudomonas
  • Normo normo anemia
  • Thrombocytopenia + DIC = bleeding = BRUISES (PML)
  • Gum hypertrophy
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8
Q

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

A

MPO

Myeloid leukemias

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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

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10
Q

AML mutation with the best prognosis

A

t(15:17) / PML

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11
Q

What differentiates PML from AML?

A

***Coagulopaties
Phenotype is arrested differentiation
Best prognosis

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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

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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

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14
Q

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

A

They only stop maturation, don’t get posterior mutations

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15
Q

Why do myelodysplastic syndromes rarely turn into AML?

A

Patients die

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16
Q

How to differentiate between AML and MDS?

A

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

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17
Q

ALL age group

A

CHILDHOOD (3-7)

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18
Q

Which leukemias are Tdt +?

A

ALL
CLL

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19
Q

Most common ALL mutations (6)

A

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

Abnormal karyotype
NOTCH signaling

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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
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21
Q

ALL labs

A

Decrease: cells

Increase:
- Uric acid
- LDH
- Ca2+

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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

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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
t(15;17) mutation: 1. Leukemia type 2. Age group 3. Gene 4. Prognosis
1. PML 2. Elder 3. RARa-PML 4. Best prognosis
26
T-ALL pathogenesis
NOTCH signaling EC cleavage mutation —> insert tandem duplications —> IC PEST deletion Increases rate of cleavage and nuclear translocation
27
T-ALL 3 T’s
T-ALL Thymic mass Teenagers
28
CLL age group
60-80 years Male 2:1
29
CLL effect on B cells
Mature, weak IgM and IgD Increased production and life span Decreased apoptosis
30
CLL clinical features
- Symmetrical node enlargement - Anemia normo normo or AI hemolysis - Thrombocytopenia - Splenomegaly - Hypogammaglobinemia = immunosuppresion EC
31
Genetics and CLL
Chromosome abnormalities: - del 13q = microRNA loss - del 11q23 = ATM gene - T21 - 17p structural = p53 gene Somatic hypermutation: IGVH gene 50% = poor prognosis NOTCH1
32
Which leukemia has smudge/fragile cells?
CLL
33
CLL lab findings
- B cll increased - Smudge cells - CD19+ CD5+ CD23+
34
Why autoimmune disorders can develop from CLL?
Hemolytic anemia Thrombocytopenia Neutropenia Red cell aplasia
35
In which leukemia are Rai scores used?
CLL
36
Rai score indications
0 = 12 year survival IV = < 4 years
37
What is small lymphocytic lymphoma?
General lympadenopathy with CLL
38
SLL + mutation = _____
Diffuse B cell lymphoma
39
What is the Richter transformation?
SLL + mutation = diffuse B cell lymphoma
40
CML genetics
BCR-ABL1
41
CML age group
40-60 years, neonates, elderly
42
Philadelphia chromosome and which leukemias it causes
t(9;22) ALL CML
43
Blasts in CML
<10%
44
CML clinical findings
- Hypermetabolism - Massive splenomegaly - Anemia - Thrombocytopenia - GOUT
45
Labs in CML
- Luekocytosis - Basophils, neutrophils, and myelocytes in circulation - Normo normo anemia - High or low platelets - Hypercellular marrow - Increase URIC ACID
46
Blastic transformation: which leukemia and what it is
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
CML phases (3)
Chronic = fever & abdominal fullness <10% blasts Accelerated = bleeding & opportunists 10-19% blasts Blast crisis = bone pain >20% blasts
48
3 main myeloproliferative disorders
- Polycythemia vera - Essential thrombocythemia - Primary myelofibrosis
49
Mechanism of myeloproliferative disorders
TK mutation —> activates without growth factor
50
What leukemia can myeloproliferative disorders turn into?
AML
51
Main mutation in myeloproliferative disorders
JAK2
52
Clinical features of myeloproliferative disorders
- Facial plethora - Conjunctival suffusion - Splenomegaly - Myelofibrosis
53
What is polycythemia vera?
Increase in everything *** Hb and RBC volume
54
Clinical findings of polycythemia vera
- Hyperviscosity - Hypervolemia - Hypermetabolism - Headache, dyspnea, blurry vision, night sweats - Pruritus after hot bath - Retinal venous engorgement - Splenomegaly 75% - Hemorrhage or thrombosis GOUT
55
What is essential thrombocythemia?
>450,000 platelets for > 2 months Thrombosis in head, hands, feed Bleeding in nose, bruising Splenomegaly Tx: aspirin, hydroxyurea, IFNa, plateletpheresis
56
Polycythemia vera treatment
Phlebotomy Hydroxyurea IFNa
57
What is primary myelofibrosis?
Losing architecture in the bone marrow Hepatosplenomegaly HSC are surrounded by fibrous and IC substance

Hematologic Disorders (6 decks)

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