Hematologic Disorders > Leukemias > Flashcards

Leukemias Flashcards

(57 cards)

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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
Study These Flashcards
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
Study These Flashcards
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
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