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Heme/Onc > HSCT > Flashcards

HSCT Flashcards

1
Q

What are autologous donors?

A

From self or twin (synergeneic)

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2
Q

What are allogeneic donors?

A

From compatible donor

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3
Q

What are other terms for HSCT?

A

Bone marrow transplantation (BMT)

Stem cell transplantation (SCT)

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4
Q

What is the rationale of using autologous HSCT?

A

To facilitate the ability to deliver HD chemotherapy

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5
Q

What is autologous HSCT known as?

A

HD chemotherapy with stem cell “rescue”

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6
Q

What type of toxicity is dose limiting for autologous HSCT?

A

Non-hematopoietic organ toxicity

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7
Q

Which diseases are autologous HSCT used?

A

Lymphomas
Multiple myeloma
Relapsed testicular and germ cell cancers

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8
Q

What is the rationale for allogeneic HSCT?

A

Delivery of HD chemotherapy (with rescue)

Immune reconstitution and graft mediated antitumor activity

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9
Q

What conditions are allogeneic HSCT used to treat?

A

Acute leukemias
CML
Immune deficiency states
Other hematologic disorders

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10
Q

What marker is used to choose donors?

A

HLA

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11
Q

How many HLA antigens are used for matching and what is the gold standard?

A

10

10/10 matching

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12
Q

What type of donor is the gold standard?

A

Matched related sibling donor (MRD)

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13
Q

What is a haploidentical HSCT?

A

HLA “half-math” donor

Donor is parent/child

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14
Q

What type of prophylaxis is required with alloreactive T-cell depleting post transplant cyclophosphamide?

A

Graft-versus-host prophylaxis

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15
Q

What volume is required for a stem cell transplantation?

A

Requires 2-6 x 10^6 stem cells/kg body wt

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16
Q

What are sources of stem cells?

A 
Bone marrow (BM)
Peripheral blood stem cells (PBSC)
Umbilical cord (UC)
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17
Q

Does BM or PBSC have a faster engraftment?

A

PBSCT

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18
Q

Does BM or PBSC need more transfusion support?

A

BM

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19
Q

Does BM or PBSC have early regimen related complications?

A

BM

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20
Q

Does BM or PBSC have a shorter duration of hospitalization?

A

PBSC

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21
Q

Does BM or PBSC have an increased number of stem cells collected?

A

PBSC

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22
Q

Does BM or PBSC have an increased number of T cells collected?

A

10-fold PBSC

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23
Q

Does BM or PBSC have an increased risk of chronic GVHD?

A

PBSC

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24
Q

Does BM or PBSC have an increased risk of acute GVHD?

A

Similar across both

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25
Q

What are the advantages for umbilical cord blood?

A

Large number of stem cells
Greater HLA disparity acceptable
Decreased risk GVHD

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26
Q

What are the disadvantages of umbilical cord blood?

A

Wt limit (<60 kg)
Delayed engraftment
Engraftment failure

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27
Q

What is the mobilization/collection of stem cells?

A

Process by which stem cells are forced into peripheral blood and collected

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28
Q

Where can stem cells be collected from?

A

Direct bone marrow aspiration

Mobilization and peripheral blood apheresis

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29
Q

What does mobilization refer to?

A

Method used to enrich the content of stem cells in the peripheral bleed

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30
Q

What are the 3 methods of mobilization?

A

G-CSF
Plerixafor + G-CSF
Chemomobilization (chemo + G-CSF)

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31
Q

Which type of donor is chemomobilization never used in?

A

Allogeneic donors

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32
Q

What agents are used in G-CSF mobilization?

A

Filgrastim

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33
Q

What are the pros of GCSF mobilization?

A

Well tolerated

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34
Q

What are the SEs of G-CSF?

A

Bone pain
Fever
General malaise

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35
Q

What agents are used with chemomobilization?

A

Etoposide/cyclophosphamide

G-CSF

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36
Q

What are the pros of chemomobilization?

A

More rapid mobilization

Fewer apheresis sessions

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37
Q

What are the cons of chemomobilization?

A

Risks of chemo

Febrile neutropenia

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38
Q

What agent is used with Plerixafor + GCSF mobilization?

A

CXCR4 antagonist

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39
Q

What are the SEs of CXCR4 antagonists?

A

N/D

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40
Q

What is the purpose of conditioning regimens?

A

Myelosuppressive/myeloablative

Immunosuppressive

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41
Q

Which type of donor requires an immunosuppressive conditioning regimen?

A

Allogeneic

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42
Q

How is myelosuppressive/myeloablative conditioning done?

A

Make room in the marrow space for infused stem cells to settle and propagate

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43
Q

Which type of conditioning regimen is required for autologous and allogeneic SCT?

A

Myelosuppressive/myeloablative

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44
Q

What is the major type of antitumor agents used in conditioning chemotherapy?

A

Alkylating agents
Busulfan
Cyclophosphamide
Melphalan

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45
Q

What are busulfan’s dose limiting toxicities?

A

Hepatotoxicity

Mucositis

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46
Q

What are carboplatin’s dose limiting toxicities?

A

Hepatic/renal toxicity
Mucositis
Peripheral neuropathy

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47
Q

What are carmustine’s dose limiting toxicities?

A

Pulmonary

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48
Q

What are cyclophosphamide’s dose limiting toxicities?

A

Cardiac

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49
Q

What are cytarabine’s dose limiting toxicities?

A

Neurotoxicity (cerebellar)

50
Q

What are etoposide’s dose limiting toxicities?

A

Mucositis

51
Q

What are fludarabine’s dose limiting toxicities?

A

Neurotoxicity

52
Q

What are ifosfamide’s dose limiting toxicities?

A

Renal

Neurotoxicity

53
Q

What are melphalan’s dose limiting toxicities?

A

Mucositis

54
Q

What are thiotepa’s dose limiting toxicities?

A

Mucositis

Neurotoxicity

55
Q

Which conditioning regimen is irreversible w/o SC support?

A

Myeloablative

56
Q

Which conditioning regimen should always be given with SC support?

A

Reduced intensity conditioning

57
Q

Which conditioning regimen has an anti-tumor effect based on the graft-vs-tumor effect?

A

Non-myeloablative

58
Q

What are acute toxicities of HSCT?

A

Alopecia
Myelosuppression
N/V
GI mucositis

59
Q

What are the common conditioning regimens for autologous HSCT?

A

Melphalan single agent
BEAM (Carmustine, Etoposide, Cytarabine, Malphalan)
Busulfan/ Cyclophsophamide/ Etoposide

60
Q

To what degree of myelosuppression does autologous HSCT cause?

A

Complete myelosuppression, no immunosuppression needed

61
Q

To what degree of myelosuppression does allogeneic HSCT cause?

A

Varying degrees of myelosuppresson and immunosuppression

62
Q

What are the common conditioning regimens for allogeneic HSCT?

A

Fludarabine/ cyclophosphamide/ TBI*
TBI/ cyclophosphamide
Busulfan/ Melphalan
Busulfan/ fludarabine/ ATG

63
Q

What are the advantages of total body irradiation?

A

Active against a variety of malignancies (chemoresistant as well)
Immunosuppressive effects
Penetrates sanctuary sites (CNS and testes)

64
Q

What is the initial standard combination for total body irradiation?

A

MA with Cy

65
Q

What are the toxicities of total body irradiation?

A

DLT = pulmonary, hepatic, GI

Long term = decreased growth development, pulmonary insufficiency, cataracts, secondary malignancies

66
Q

What is engraftment?

A

Normalization of all peripheral blood counts (WBC< plt, HgB)

67
Q

When does ANC recovery typically accur?

A

14-21 days

68
Q

When does plt transfusion independence typically occur?

A

Before day 35

69
Q

Does engraftment indicate cure/remission?

A

No

70
Q

What is a graft failure?

A

Inadequate hematopoietic function after stem cell transplantation

71
Q

What is primary graft failure?

A

Failure to achieve engraftment by expected time

72
Q

What is secondary graft failure?

A

Failure to maintain graft after initial engraftment

73
Q

What is the treatment for graft failures?

A

Re-collect donor for second infusion

Modification of immunosuppression to allow graft to grow

74
Q

In the first 30 days post transplant, what infection has a big risk and how do we treat it??

A

Candida - fluconazole

75
Q

For days 30-100, which fungus do we worry about?

A

Aspergillus spp

76
Q

How do we treat aspergillus?

A

Voriconazole
Posaconazole
Ampho B

77
Q

How do we diagnose aspergillius?

A

Serum GM
CT findings
Bronchoalveolar lavage (aspiration and biopsy)

78
Q

In days 0-30, which virus are we worried about reactivation?

A

HSV

79
Q

In days 30-100, what viral infections are we worried about and how do we pre-empt it?

A

CMV

Ganciclovir

80
Q

For autologous transplants, when do we discontinue fluconazole prophylaxis?

A

ANC > 500

81
Q

What viral infection are we concerned about after 100 days?

A

VSV

82
Q

What bacterial infection are we concerned about after 100 days?

A

Pneumocytis Carinii pneumonia (PCP)

83
Q

What fungal infections are we concerned about after 100 days?

A 
Mould
Rare fungi (fusarium, zygomycetes)
84
Q

What is acute GVHD?

A

Mediated by mature T cells in infused graft

85
Q

When does acute GVHD typically occur?

A

Within 100 days

86
Q

What is chronic GVHD?

A

Mediated by developing T cells

Host thymus is unable to educate maturing donor T cells to not react to self

87
Q

When does chronic GVHD typically occur?

A

100+ days

88
Q

Is acute or chronic GVHD the major source of morbidity and mortality following allogeneic SCT?

A

Acute

89
Q

What organs are typicaly affected in acute GVHD?

A

Skin
Gut
Liver
(in this order)

90
Q

How do we grade acute GVHD?

A

Based on extent of manifestations in each of the 3 major target organs

91
Q

How do we stage acute GVHD?

A

Based on composite of grading in each organ system and extent of functional impairment

92
Q

What are the most common organs affected in chronic GVHD?

A

Skin

Liver

93
Q

How is chronic GVHD characterized?

A

Sclerosis, contracture of the skin

94
Q

How is chronic GVHD graded?

A

Limited or extensive

95
Q

What is considered limited chronic GVHD?

A

Skin and liver w/o sclerosis

96
Q

What is considered extensive GVHD?

A

Skin sclerosis or involvement of sites outside of skin and liver
Eye, mouth, lungs, GI tract, peripheral nervous system, marrow, vaginal tract involvement

97
Q

What types of medications can be used to prevent GVHD?

A 
Calcineurin inhibitors
M-TOR inhibitors
Inhibitors that block cell growth
Inhibitors that affect salvage of purine nucleotides
Agents that remove T lymphocytes in vivo
98
Q

What are calcineurin inhibitors?

A

Tacrolimus

Cyclopsorine

99
Q

How do calcineurin inhibitors work?

A

Inhibit T cell activation

100
Q

What are the M-TOR inhibitors?

A

Rapamycin

101
Q

How do M-TOR inhibitors work?

A

Inhibition of progression through cell cycle

102
Q

What are inhibitors that block cell growth?

A

MTX

Cyclophsophamide

103
Q

What are agents that remove T lymphocytes in vivo?

A

Alemtuzumab

Anti-thymocyte globulin

104
Q

What are the prophylaxis treatments of GVHD?

A

Cyclophosphamide

Tacrolimus + mycophenolate

105
Q

What are tacrolimus toxicities?

A

Tremor
HA
Electrolyte abnormalities
Nephrotoxicity

106
Q

What are mycophenolate mofetil toxicities?

A

GI toxicity
Infections (BBW)
Pure red cell aplasia

107
Q

Which prophylaxis medication for GVHD is teratogenic?

A

Mycophenolate mofetil

108
Q

What are the toxicities of cyclophosphamide?

A

Hemorrhagic cystitis

Cardiogenic shock

109
Q

What are post transplant cyclophosphamide’s CPs?

A

Empiric diuresis to make net negative on D+2, aggressive diuresis during high IV fluids rate

110
Q

What is the mainstay of therapy for acute GVHD?

A

Corticosteroids

111
Q

What is the antifungal used during corticosteroid use for acute GVHD?

A

Posaconazole

112
Q

What is the treatment of chronic GVHD?

A

Corticosteroids
Rituximab
PUVA/narrow band UVB therapy
Pentostatin

113
Q

What is sinusoidal obstruction syndrome?

A

Obstructive liver disease due to microthrombi in liver sinusoids

114
Q

What causes sinusoidal obstruction syndrome?

A

Damage to hepatic sinusoids and hepatocytes leads to obstruction of sinusoidal flow

115
Q

What are clinical presentations of sinusoidal obstruction syndrome?

A

Fluid retention
Jaundice
Hepatomegaly
Weight gain

116
Q

What are the RFs for sinusoidal obstruction syndrome?

A

TBI, busulfan, or cyclophosphamide containing conditioning regimens
Pre-existing liver dysfunction
Pre-transplant exposure to liver toxins such as gemtuzumab

117
Q

When does sinusoidal obstruction syndrome typically present?

A

W/in 3 weeks of SCT

118
Q

What is the clinical diagnosis of sinusoidal obstruction syndrome?

A

Wt gain
Hyperbilirubinemia
Ascites

119
Q

What are the preventative measures for sinusoidal obstruction syndrome?

A

Busulfan PK monitoring
Ursodiol
Heparin

120
Q

What is the treatment of sinusoidal obstruction syndrome?

A

Defibrotide - if evidence of renal or pulmonary disfunction

121
Q

What do we monitor for with defibrotide?

A

bleeding

122
Q

What is the treatment of diffuse alveolar hemorrhage?

A

HD steroids

Heme/Onc (20 decks)

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