Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Blood and Lymph > Treatment of Cancer Drugs > Flashcards

Treatment of Cancer Drugs Flashcards

(111 cards)

Start Studying
1
Q

Mechlorethamine Class

A

Alkylating Agents

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

Mechlorethamine Use

A

Primary use: Hodgkin’s lymphoma, part of MOPP

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

Meclorethamine Pharmacokinetics/Dynamics

A

IV only—subQ slough/necrosis (often arterial suspply)

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

Mechlorethamine half-Life

A

Half life several minutesreacts rapidly

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

Mechlorethamine Adverse Effects

A

Vesicant, caustic to skin, mucous membranes
Acute—nausea/vomiting
Delayed—decreased blood counts, moderate w/ most doses
- 10-12 days after treatment
- Recovery 3-6 weeks

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

Cyclophosphamide Class

A

Alkylating Agent

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

Cyclophosphamide Use

A

widely used in leukemias and lymphomas

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

Cyclophosphamide Pharmacokinetics/dynamics

A

Oral or IV

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

Cyclophosphamide/Dynamics Activation

A

Pro-drug; activated by host metabolism (primarily liver)

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

Cyclophosphamide AE

A

Acute—nausea/vomiting
Delayed—bone marrow depression (moderate, dose-related)
- Alopecia
- Sterile hemorrhagic cystitis

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

Ifosfamide Class

A

Alkylating Agent

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

Ifosfamide Component of:

A

ICE (Ifosfamide, carboplatin, etoposide)

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

Ifosfamide Use

A

Hodgkin’s and non-Hodgkin’s lymphoma

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

Ifosfamide Analog of:

A

Cyclophosphamide

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

Ifosfamide Pharmacokinetics/dynamicss

A

IV only

high dose for bone marrow/stem cell rescue

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

Ifosfamide Adverse Effect

A

Acute—nausea and vomiting, urinary tract toxicity
More severe bone marrow depression than cyclophosphamide (Leukopenia)
Peripheral neuropathies
CNS effects—hallucinations, coma (may be due to chloroacetaldehyde)

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

Melphalan Use

A

Multiple Myeloma

Myeloablative therapy

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

Melphalan Class

A

Alkylating Agent

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

Melphalan pharmacokinetics/Dynamics

A

highly reactive
chem half life ~50 min
renal excretion

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

Melphalan AE

A

myelosuppression

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

Chlorambucil Class

A

Alkylating Agent

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

Chlorambucil kineticss/dynamicss

A

Oral once daily

Plasma half life~1.5 hours

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

Chlorambucil use

A

was primary drug for CLL but now rarely used

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

Bisulfan Class

A

Alkylating Agent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Bisulfan use
Key for CML prior to imatinib
26
Bisulfan kineticss/dynamics
Oral | IV high dose
27
Bisulfan AE
Profound myelosuppression High dosepulm fibrosis Hepatic veno-occlusive disease
28
Bendamustin Class
non-classic alkylating agent: | alkylates DNA but inhibits mitotic checkpoints
29
Bendamustin use
CLL | Indolent B-cell non-Hodgkin’s lymphoma
30
Bendamustine AE
Nausea vomiting Myelosuppression mucositis
31
Bendamustine kinetics/dynamics
IV | Plasma half life~30 min
32
Dicarbazine Use
Hodgkin’s lymphoma | Multiple myeloma
33
Dicarbazine kinetics/dynamics
IV | Activated by hepatic metabolism
34
Dicarbazine AE
``` Severe acute nausea and vomiting Delayed myelosuppression (dose-limiting) ```
35
Procarbazine Use
Hodgkin’s | Non-hodgkin lymphoma
36
Procarbazine kinetics/dynamics
Oral
37
Procarbazine Class
Non-classic alkylating agent: | inhibits RNA, DNA, protein synthesis-->strand breaks
38
Dicarbazine Class
non-classic alkylating agent
39
methotrexate MOA
Competes with folic acid Dihydrofolate reductase substrate/inhibitor Blocks production of bases for DNA Synthesis (converts Uracil to Thymidine)—depletes pyrimidine
40
methotrexate administration
IV Oral Intrathecal
41
methotrexate kinetics/dynamicss
Excreted in urine High dose rescue • Folinic acid= Leucovorin/Citrovorin for recovery (12-24 hours later)
42
methotrexate AE
Anti-folate effects • Bone Marrow • GI Chronic use: hepatotoxicity
43
6-mercaptopurine MOA
Purine-salvage pathway (hprt) Inhibits AMP and GMP synthesis purine analog
44
6-mercaptopurine route of administration
oral
45
6-mercaptopurine kinetics/dynamics
Inactivated, cleared by thiopurine methyltransferase--controls levels
46
6-mercaptopurine AE
Well-tolerated | Bone marrow suppression at high doses
47
Fludarabine MOA
Diphosphate inhibits ribonucleotide reductase Triphosphate inhibits DNA pol and ligase (incorporated into RNA and DNA) purine analog
48
Fludarabine Use
mono or combo therapy for CLL
49
fludarabine AE
Myelosuppression Nausea Vomiting
50
fludarabine route of administration
Oral or IV as monophosphate
51
fludarabine kinetics/dynamics
Dephosphorylated in plasma and absorbed by cells
52
cladribine (2-chloro-deoxyadenosine, 2-CDA) MOa
Triphosphate incorporated into DNAstrand breaks Inhibits ribonucleotide reductase purine analog
53
cladribine use
hairy cell leukemia CLL low grade lymphomas
54
cladribine route of administration
IV
55
cladribine kinetics/dynamics
activated by deoxycytidine kinase
56
cladribine AE
Bone marrow suppression is dose-limiting toxicity Thrombocytopenia Opportunistic infections
57
cytarabine MOA
Triphosphate incorporated into DNAinhibits elongation and repair pyramidine analog
58
cytarabine use
AML, ALL
59
cytarabine route of administration
IV | intrathecal
60
cytarabine kinetics/dynamics
Activated by deoxycytidine kinase--polymorphic
61
cytarabine AE
More toxic than purines Myelosuppression GI disturbance Stomatitis
62
doxorubicin daunorubicin idarubicin MOA
``` Intercalate into DNAspaces it out Block topoisomerase II Inhibit DNA/RNA synthesis Strand breaks Free radicals ``` antitumor antibiotics
63
doxorubicin daunorubicin idarubicin kineticss/dynamics
biliary clearance | IV
64
doxorubicin daunorubicin idarubicin AE
``` BM suppression GI Alopecia Cardiotoxicity • Cumulative dose • Exacerbated by radiation/other drugs • Arrhythmias • Cardiomyopathy • CHF Free radical mechanism • Administer Dexrazoxane ```
65
bleomycin MOA
``` Mixture of glycopeptides Binds DNA Free radicals Strand breaks Active in G2 antitumor antibiotics ```
66
blemoycin route of administration
IV
67
bleomycin AE
Hypersensitivity Cutaneous rxns Pulm toxicityfibrosis
68
vinca MOA
Inhibits/reverses tubulin polymerizations Disrupts mitotic spindles Metaphase arrest Isolated from Vinca Rosea (Periwinkle)
69
vinca kinetics/dynamicss
IV | biliary excretion
70
vincblastine AE
* Nausea * Vomiting * Alopecia * Bone marrow depletion
71
vincristine AE
* Structurally and mechanistically identical to vinblastine * Less toxic to BM * No nausea/vomiting * Limited to short durationperipheral neuropathy
72
vinca Class
microtubule poisons
73
paclitaxel docetaxel Class info
microtubule poisons
74
paclitaxel, docetaxel MOA
Stabilizes microtubules Blocks progress through mitosis Promising in solid tumors
75
paclitaxel, docetaxel kinetics/dynamics
IV Cremophor/nanoparticles - Not very soluble in water - Premedicated w/ anti-inflammatory
76
paclitaxel, docetaxel AE
``` Acute: Hypersensitivity Nausea Delayed: BM suppression and neuropathy ```
77
eoposide (VP-16) class
topoisomerase inhibitor
78
etoposide MOA
``` Double strand breaks DNA degradation (CCS) ```
79
etoposide administration
oral | IV
80
etoposide AE
Nausea and vomiting Alopecia Bone marrow suppression
81
asparaginase MOA
Catalyzes breakdown of asparagine in blood | Inhibits growth of ALL cells that cell asparagine synthetase
82
asparaginase AE
Allergic responses | Enhances coagulation
83
rituxamab MOA
mAB-->CD20
84
rituxamab use
B-cell lymphomas—CLL, non-hodgkin’s
85
rituxamab kinetics/dynamics
IV | half life~22 days
86
rituxamab AE
Allergic reactions: Hypogammaglobulinemia Autoimmune disorders
87
bortezimib MOA
Inhibits 26S proteasome Disrupts intracellular signaling cascades Leads to apoptosis
88
bortezimib use
Multiple myeloma, mantle cell
89
bortezimib kinetics/dynamics
IV Plasma half life 5.5 hrs Half-life of inhibition 24 hrs
90
bortezimib AE
Thrombocytopenia (28%) Fatigue (12%) Peripheral neuropathy (12%) Hypotension upon fusion
91
ATRA MOA
Used ass mono-therapy or w/ anthracycline or arensic for APL Binds RARalpha receptorpromotes differentiation Promotes degradation of PML-RARalpha fusion protein, activates RARgamma
92
Aresenic Trioxide Use
Inhibits thioredoxin reductaseoxidative stress Promotes modification and degradation of APL fusion protein Cytotoxic and promotes diff
93
lenalidomide MOA & use
Thalidomide derivative (lacks teratogenic, sedative effects of thalidomide CLL Multiple Myeloma
94
lenalidomide kinetics/dynamics
may inhibit rituximab
95
dexamethasone prednisone MOA & use
Suppresses proliferation of immune cells (leukocytes, lymphocytes) Leukemias, lymphomas
96
dexamethasone, prednisone administration
Oral
97
dexamethasone, prednisone AE
Delayed adverse effects: Fluid retention Immunosuppression Diabetes
98
imatinib MOA
Inhibits Bcr-Abl and c-kit tyrosine kinases Blocks growth factor signaling in CML myelosuppressive
99
imatinib use
Hematologic malignancy w/ Philadelphia chromosome
100
imatinib AE
Myelosuppressive Edema and fluid retention hepatotoxicity
101
dasatinib, nilotinib
Newer receptor tyrosine kinase inhibitor Broader spectrum Useful when res to or poor tolerability of imatinib STIs can transform cancer from “curable” disease to a “manageable” disease Some suggestions of cure, but not yet established
102
ibrutinib MOA
Inhibits Bruton’s tyrosine kinase (BTK)
103
ibrutinib use
Mantle cell lymphoma (high activity) | Relapsed/refractory CLL (especially 17p deletion)
104
ibrutinib administration
oral
105
ibrutinib kinetics/dynamics
Metabolized by CYP3A4 | Metabolite 15X more potent as BTK inhibitor
106
ibrutinib AE
``` GI Thrombocytopenia Neutropenia Infections Fatigue ```
107
idelalisib MOA
P13K inhibitor
108
idelalisib use
CLL and SLL | Relapsed follicular B-cell non-hodgkins lymphoma
109
idelalisib administration
oral
110
idelalisib kinetics/dynamics
Metabolized by aldehyde oxidase and CYP3A4 (strong CYP3A4 inhibitor)
111
idelalisib AE
Potentially fatal hepatotoxicity Diarrhea/colitis Pneumonitis Intestinal perforation

Blood and Lymph (3 decks)

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