Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Pharma > Antineoplastics > Flashcards

Antineoplastics Flashcards

1
Q

MOA of methotrexate?

A

inhibits dihydrofolate reductase

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

Indication of methotrexate?

A

ALL lymphomas

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

Indication, Solid Tumor, breast, head neck CA, Osteogenic Sarcoma Anti-inflamm effects (RA, psoriasis, autoimmune)

A

methotrexate

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

Adverse effects of methotrexate? (3)

A

DLT, GIT, severe mucositis

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

Early sign of MTX toxicity?

A

severe mucositis

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

Is MTX able to pass thru BBB?

A

yes

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

Elimination of MTX?

A

renal

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

Antidote for MTX?

A

leucovorin or folinic acid

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

Leucovorin administration after methotrexate when

A

24-36 hrs

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

MOA of leucovorin?

A

FH4 supplement

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

Half life of MTX?

A

triphasic;
Distribution phase : 30-45 mins
Clearance phase : 3-4 hours
Terminal phase: 6-20 hours

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

function of leucovorin? (2)

A

Salvage normal cells, limit toxicity to the bone marrow and GIT (Limitss MTX toxicity)

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

how many times is MTX converted by dihydrofolate reductase?

A

2

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

MOA of 5-FU?

A

Inhibits thymidilate synthetase

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

What phase of the cell cycle is 5-FU?

A

S-phase specific pyrimidine antagonist

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

function of thymidylate synthetase?

A

converts dUMP to dTMP = thymidine

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

What analog is 5-FU

A

Pyrimidine

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

Indication of 5-FU (3)

A

Colon CA, Breast CA, Head/Neck CA

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

AE of 5-FU (5)

A

Myelosuppression (4-7 days) recovery: 14 days
GI, Hepatic, Renal, CNS Toxicity

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

Route of administration of MTX? (5)

A

PO, IM, IV, SC, Intrathecal

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

Route of administration of 5-FU?

A

IV
and Oral, causes degradation of Dihydropyrmidine dehydrogenase = ineffective)

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

Oral version of 5-FU

A

Capecitabine

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

Metabolism of 5-FU

A

Liver: Dihydro fluorouracil

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

Combination of 5-FU

A

FOLFOX (Oxaliplatin)
FOLFIRI (Irinotecan)

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

MOA of Cytobine Arabinoside (ARA-C)

A

Ara-CTP -> Inhibits DNA polymerase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What phase of the cell cycle is ARA-C?

A

S- Phase specific pyrimidine antagonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is ARA C DOC for?

A

Acute Myelogenous Leukemia (AML)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Indication of ARA-C (not DOC)

A

Meningeal Leukemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Adverse effects of ARA-C in the CNS (3)

A

Fever, Seizures, Arachnoiditis (4-7 days)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

AE of ARA-C (3)

A

DLT (transfusion needed) (10 days after treatment, reversible after 21 days)
GI Toxicity Hepatotoxic
CNS Toxicity (Conjuctivitis, & Arachnoiditis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What specimen did ARA-C come from?

A

Cryptotheca crypta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Administration of ARA-C

A

ONLY IV and intrathecal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Elimination of ARA-C

A

Kidney (Ara-U)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

MOA of Fludarabine (2)

A

Inhibits DNA synthesis by incorporating a false nucleotide
Inhibits polymerase, ligase & primase causing chain termination

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

what phase of the cell cycle is Fludarabine?

A

S phase specific pyrimidine antagonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Indication of Fludarabine (3)

A

SINGLE MOST ACTIVE AGENT IN CLL (Chronic lymphocytic leukemia)
Lymphoma
Macroglobulinemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

AE of Fludarabine (3)

A

DLT, GI,
CNS (Progressive encephalopathy, cortical blindness, death in high dose)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

route of administration of Fludarabine

A

IV Only (oral yields fluoroadenine - toxic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

MOA of Hydroxyurea

A

inhibits ribonucleotide reductase -> Inhibits DNA synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Analog of hydroxyurea

A

Urea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Phase of cell cycle Hydroxyurea

A

S- specific antimetabolite

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Indications of Hydroxyurea (5)

A

CML
Blast Crisis (to lower blast count
given with radiotherapy:
Head and neck CA
Essential thombocytosis
Polycythemia Vera

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

AE of Hydroxyurea (4)

A

BMS, Nadir: 6-7 days after tx
Mucositis
Inc lethargy
Maculopapular rash

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

when plasma conc. max of hydroxyurea?

A

1 hr, excreted unchanged by kidneys
well absorbed orally even in high dose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

MOA of Vinca alkaloids?

A

Binds to α & β tubulin subunits -> prevents polymerization -> cell arrest (metaphase)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Vinblastine indication (3)

A

Testicular CA, Hodgkin’s Lymphoma & Bladder CA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What are the Vinca Alkaloids? (3)

A

Vinblastine, Vincristine & Vinorelbine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

AE of Vinblastine (3)

A

DLT (Leukopenia 6-7 after tx) (reversible)
Mucositis (high dose)
Vesicants (Blister agent)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Metab of Vinblastine

A

Liver (CYP450) dos adj required in liver dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Route of administration of Vinblastine

A

IV only

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Vincristine Indication (3)

A

ALL, Lymphoma, Wilms tumor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Vincristine AE (1 early 4 late signs)

A

early signs of toxicity
DLT-> peripheral neuopathy (paresthesia of distal fingers)
late signs of toxicity
Decrease in motor strength (dorsiflexion of the foot)
Constipation, Alopecia
SIADH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Vinorelbine Indications (2)

A

Non-small cell lung CA, Breast CA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Vinorelbine AE (3)

A

DLT (neutropenia) nadir: 7-10 days recovery: 14 days
Mild sensory neuropathy, stomatitis
GI toxicity : constipation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Vinorelbine other use/ important info

A

Non-specific inhibitor of AZT (Azidothymidine/Zidocudine)
(Tx for AIDS kaposi sarcoma)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Taxanes MOA

A

Binds to β tubulin subunit > stabilization of microtubule > inhibition of depolymerization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What are the Taxanes? (2)

A

Paclitaxel, Docetaxel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What phase are the taxanes?

A

M phase specific agents

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Paclitaxel Indication (5)

A

Ovarian, Breast, head and neck, esophageal, non small cell CA - upper body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Paclitaxel AE (3)

A

If formulated in castor oil + alcohol (Cremophor EL)
Histamine stimulated acute hypersensitivity (needs antihistamine / steroids)

Neutropenia,

transient bradycardia, heart block, ischemia (cardiotoxicity)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Importance of paclitaxel (3)

A

Prototype drug
Insoluble in aqueous solution
IV bolus or continuous administration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Docetaxel Indication (4)

A

ANTHRACYCLINE RESISTANT ADVANCED BEAST CA, non small cell lung CA, ovarian, head and neck CA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Docetaxel AE (6)

A

does NOT use cremaphor EL (castor oil + alcohol) = less toxic
SEVERE neutropenia, severe asthma, peripheral neuropathy, stomatitis, myalgia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Importance of Docetaxel (3)

A

Sister drug of paclitaxel
Soluble in aqueous solution
IV only

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Metab of Taxanaes

A

Liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Topoisomerase 1 inhibitor MOA

A

induction of single stranded breaks -> inhibition of DNA synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Function of Topoisomerase 1

A

Repairs/relaxes simple coils by repairing single strand breaks -> DNA synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What phase does topoisomerase 1 inhibitor act on?

A

S phase specific agent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What are the topoisomerase 1 inhibitors? (2)

A

Irinotecan, Topotecan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Irinotecan Indication (2)

A

Advanced colorectal CA, Colon CA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Irinotecan AE (3-4)

A

DIARRHEA, nausea/vomiting
Alopecia, headache

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Route of administration of Irinotecan

A

IV only

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Metab of irinotecan

A

Hepatic & Biliary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Topotecan Indication (3)

A

Advanced colorectal CA, refractory ovarian CA, Small cell lung cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Topotecan AE (1)

A

DLT; Myelosuppression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Route of administration of Topotecan

A

IV only

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Metab of Topotecan

A

Biliary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Topoisomerase 2 inhib MOA

A

induction of double strand break -> prevent religation of DNA -> induces apoptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Function of Topoisomerase 2?

A

Repairs supercoiling of DNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

What are the topoisomerase 2 inhibitors? (2)

A

Etoposide, Teniposide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Indication of TI2 inhib (5)

A

HODGKIN’S disease
Lymphomas
Leukemias
SCLC
Testicular CA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

AE of TI2 inhibs (6)

A

MYELOSUPPRESION

Hypotension with rapid infusion (given slowly)
Alopecia (10-30%)
GI toxicity (10-20%)
inc ALT AST
Leukemogenic with no preceding Myelodysplastic syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

What phase of cell cycle are TI2 inhibs?

A

Late S-G2 Phase specific agents

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Where is TI2 inhibs extracted from?

A

Mayapple root (Podophyllum peltatum)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

route of administration of Etoposide?

A

IV,PO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

route of administration of Teniposide?

A

IV only

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

Metab of Etoposide?

A

Hepatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Metab of Teniposide?

A

Hepatic, Renal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

What are the classical alkylating agents? (4)

A

Cyclophosphamide
Ifosfamide
Melphalan
Chlorambucil

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

Classical Alkylating agents are under what?

A

Cell cycle Nonspecific Agents

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

Cyclophosphamide MOA

A

Inhibition of DNA replication and RNA transcription -> Inhib of nucleic acid synthesis
Becomes 4-hydroxycyclophosphamide
in healthy cells: converted to INACTIVE metabolites
In cancer cells: Aldophosphamide converted into phosphoramide mustard (anticancer)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

Metabolites of Cyclophosphamide? (2)

A

Phosphoramide
Acrolein (Hemorrhagic cystitis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

Indication of Cyclophosphamide

A

Lymphoma (SALVAGE CHEMOTHERAPY) (NOT FIRST LINE)
Breast CA, SCLC, Ovarian CA, BM transplantation, immunosuppresion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

What is the antidote for hemorrhagic cystitis?

A

MESNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

What dose causes nausea and vomiting in cyclophosphamide?

A

> 500mg 8-12 hours after tx
Cyclophosphamide metab -> emetogenic metabolites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

Cyclophosphamide AE (5-8)

A

DLT myelosuppression nadir 10-14 days, recover 21 days
Hemorrhagic cystitis (hematuria)
Nausea and vomiting
Pulmonary fibrosis, acute hemorrhagic carditis, alopecia, SIADH, Veno occlusive disease of liver
Long term:
Infertility and 2ndary malignancies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

Ifosfamide MOA

A

Inhibition of DNA replication and RNA transcription -> Inhibiion of nucleic acid function

97
Q

Ifosfamide Indication (3)

A

Lymphoma (SALVAGE CHEMOTHERAPY)
Breast and ovarian CA,
Sarcoma, Testicular CA

98
Q

Ifosfamide AE (5-8)

A

DLT myelosuppression nadir 10-14 days, recover 21 days
Hemorrhagic cystitis
Nausea and vomiting
Pulmonary fibrosis, acute hemorrhagic carditis, alopecia, SIADH, Veno occlusive disease of liver
Long term:
Infertility and 2ndary malignancies

99
Q

Melphalan MOA

A

Formation of intra strand, inter strand DNA + cross links

100
Q

Melphalan Indication (4) + Combination (3)

A

Multiple myeloma (prednisone, thalidomide, bortezomib)
Myeloablative conditioning regimen for BM transplant
Ovarian CA, Breast CA

101
Q

Chlorambucil MOA

A

Forms DNA cross links resulting in inhibtion of DNA synthesis and function

102
Q

Chlorambucil Indication (2)

A

CLL, low grade non-hodgkin’s lymphoma

103
Q

Chlorambucil AE (5)

A

DLT, Liver abnormalities, Pulmonary fibrosis, Secondary malignancies and leukemia

Well tolerated

104
Q

What are the non-classical alkylating agents? (2)

A

Dacarbazine, Procarbazine

105
Q

Dacarbazine MOA

A

followns intramolecular cyclization
Imidazole carboxamide forms methylcarbonium ion -> attacks N7 guanine

106
Q

Dacarbazine Indication (3)

A

Hodgkin’s disease
Soft Tissue sarcoma
Malignant Melanoma

107
Q

Dacarbazine AE (5)

A

Emetogenic, Myelosuppresion
Flu-like symptoms
Facial FLUSHING
severe pain and necrosis in extravasation (phlebitis, cellulitis)

108
Q

Route of administration Dacarbazine

109
Q

Half life of Dacarbazine

110
Q

Metab of Dacarbazine

111
Q

Route of elim (Dacarbazine

A

Urine as diazomethane

112
Q

MOA of Procarbazine

A

Inhibits transfer of methyl groups of methionine in the RNA -> prevents DNA, RNA and protein synthesis

113
Q

Indication of Procarbazine (4)

A

Hodgkin’s disease
Non-hodgkin’s disease
Lung and Brain CA

114
Q

Procarbazine AE (3)

A

GI toxicity
Neurotoxicity
Severe headache due to MAO inhibitor

115
Q

What is Thiotepa’s drug classification

A

Akyl-alkaline sulfonate based akylating agent

116
Q

Thiotepa MOA

A

Formas DNA cross links -> inhibition of DNA synthesis

117
Q

Thiotepa indication (5)

A

Superficial bladder CA, BM transplantation, Brain tumor, Breast CA, Ovarian CA

118
Q

AE of Thiotepa (5)

A

Myelosuppresion (DLT)
AT high dose: Mucositis, Skin rash, CNS toxicity
Gonadal dysfunction

119
Q

Thiotepa is a blister agent

120
Q

Procarbazine metabolite

A

azoprocarbazine causes DNA scission

121
Q

Route of administration of Procarbazine

122
Q

Half life of procarbazine

123
Q

Route of elim of Procarbazine

124
Q

What are all the platinum compounds? (3)

A

Cisplatin, Carboplatin, Oxaliplatin

125
Q

Platinum compounds MOA

A

Forms platinum coordination complex -> creates interstrands in DNA -> inhibition of DNA synthesis

126
Q

What are the binding sites of platinum compounds? (3)

A

Primary: N7
N3 position of adenine
O6 position of cytosine

127
Q

What phase of the cell cycle do platinum compounds affect?

A

All stages

128
Q

What generation is Cisplatin?

129
Q

Cisplatin indications (4)

A

Broad range solid tumors, Ovarian CA, Testicular CA, Lung CA, head and neck CA

130
Q

Cisplatin AE (6)

A

DLT: Nephrotoxicity -> Renal failure
Caution with inc creatinine

Hypomagnesemia, Severe N&V, Anemia, Hypersensitivity
Neurotoxicity= Hearing loss

131
Q

Antidote of Cisplatin?

A

Amifostine

132
Q

Combination regimen for non seminomatous CA

133
Q

Carboplatin Generation

134
Q

AE of carboplatin

A

DLT; Myelosuppresion

135
Q

What’s the difference of Carboplatin with Cisplatin?

A

Carboplatin has bidentate ligand instead of 2 Cl ligands in cisplatin

136
Q

Oxaliplatin Generation

137
Q

Oxaliplatin indication (1)

A

2nd line therapy for metastatic colorectal CA

138
Q

Oxaliplatin AE (3)

A

DLT; Neurotoxicity -> numbness
Intense pain and hypersensitivity of temp to both hands and feet
Less nephrotoxic

139
Q

Unique characteristic of Oxaliplatin?

A

bidentate oxalate group

140
Q

What are the Antitumor antibiotics? (4)

A

Anthracyclines, Bleomycin, Dactinomycin, Mitomycin

141
Q

Anthracycline suffix?

142
Q

Anthracycline MOA

A

Intercalation of DNA to formation of free radicals
High affinity binding to DNA from intercalation -> inhibits TI2
Generates semiquinone free radicals and oxygen free radicals
Alter’s fluidity and transport of the cell membrane

143
Q

Anthracycline Indications (8)

A

AML, ALL, Hodgkin’s disease, Non-Hodgkin’s disease, Lymphoma
Breast, Lung, Bladder CA

144
Q

Anthracycline AE (3)

A

Most important and dreaded SE:
DLT (Cardiac toxicity)
Acute - Arrythmia, Conduction Abnormalities/ECG changes
Chronic - Dilated cardiomyopathy (when given 450-550mg of daunorubicin)

Adriamycin Flare
Radiation Recall Reaction

145
Q

What’s the Antidote for Anthracycline DLT?

A

Dexrazoxane
-Iron chelating agent
-Started with > 300 mg
-slow infusion
-requires cardiac monitoring
AE: Pain in injection site, neutropenia, thrombocytopenia

146
Q

Route of administration for Anthracycline:

A

IV only (inactivated in the GIT

147
Q

Does anthracycline penetrate BBB?

148
Q

Anthracycline important side effects (2)

A

Cardiac toxicity DLT and imparts discoloration of urine

149
Q

Half life of Anthracycline (2)

A

Distribution phase: 15 mins
Elimination phase: 24-48 hours

150
Q

Metab of anthracycline

A

Liver (Daunomycin/Daunorubicin & Doxorubicinol)

151
Q

Excretion of Anthracycline

152
Q

Which anthracyclines are less toxic to the heart? (2)

A

Epirubicin and Idarubicin

153
Q

MOA of Bleomycin

A

Oxidation of DNA-Bleomycin-ferrous complex -> production of free radicals -> single and double stand break -> inhibition of DNA synthesis

154
Q

What type of agent is Bleomycin?

A

Copper chelating glycopeptide

155
Q

Bleomycin Indication (6)

A

Hodgkin’s disease, Non-Hodgkin’s Lymphoma, Germ cell tumors, head and neck CA
SCC of the skin cervix and vulva, pleural effusion/ascites

156
Q

AE of Bleomycin (2)

A

DLT; Pulmonary Fibrosis
Pneumonitis

157
Q

What specimen is Bleomycin derived from?

A

Streptomyces verticullus

158
Q

Route of administration of Bleomycin (4)

A

SC,IM,IV & intracavitary

159
Q

Antidote for Bleomycin

A

Bleomycin hydrolase

160
Q

Conc. of bleomycin hydrolase from highest to lowest (4)

A

Liver, spleen, lungs, skin

161
Q

Dactinomycin MOA

A

Binds to DNA through INTERCALATION to GUANINE-CYTOSINE base pairs -> dacti DNA complex -> inh of DNA dependent rna synthesis

162
Q

Indications of Dactinomycin (4)

A

Choriosarcoma
Wilms Tumor
Testicular CA
Ewing’s Sarcoma

163
Q

AE of Dactinomycin (3)

A

BMS, NV,
DLT; Leukopenia & Thrombocytopenia (7 days tx)

164
Q

Half life of Dactinomycin

165
Q

Route of administration of Dactinomycin

166
Q

Elimination of Dactinomycin

167
Q

Does Dactinomycin pass the BBB?

168
Q

What specimen is Dactinomycin extracted from?

A

Streptomyces parvulus

169
Q

Mitomycin MOA

A

Cross links DNA strands = DNA synthesis inhibition

170
Q

Indications of Mitomycin (4)

A

tx of solid tumors:
Lungs
Pancreas
Stomach
Head and neck

171
Q

What are the specific toxic doses of Mitomycin?

A

> 30 mg = pulmonary fibrosis
50 mg = HUS (Hemolytic uremic syndrome
70mg = nephrotoxicity

172
Q

Normal adverse effects of Mitomycin?

A

DLT; myelosuppression (occurs 3-5 days after tx)
REcovery (6-8 wks)

173
Q

What type of antibiotic is Mitomycin?

A

Quinine Antibiotic

174
Q

What is the half life of Dactinomycin?

A

25-90 mins

175
Q

Route of administration of Dactinomycin

176
Q

What drug is under “Enzymes”?

A

L-Asparaginase

177
Q

MOA of L-Asparaginase?

A

Convertion to aspartic acid +ammonia = depletion of L asparagine and inhibition of protein synthesis > compromise of cell function = cell death

178
Q

Indication of L-Asparagine (3)

A

ALL
T-Cell leukemia
T-Cell lymphomas

179
Q

What is the MAIN AE of L-Asparagine?

A

Hypersensitivity reaction = skin testing required prior to administration

180
Q

Non important AE of L-Asparginase (4)

A

Neurologic toxicity
Hyperglycemia
altered production of coagulation factions (inc bleeding)
Acute hemorrhagic pancreatitis

181
Q

What specimen is L-Asparaginase isolated from? (2)

A

E. coli & Erwina carotovora

182
Q

Effect of PEGylated asparaginase

A

Dec antibody formation and inc serum half life

183
Q

Adverse effect of PEGylated asparaginase (2)

A

immunologic sensitization to foreign proteins or depletion of asparagine pools and inhibition of protein synthesis

184
Q

Estrogen based Antineoplastic

A

Diethystilbestrol

185
Q

MOA of Diethystilbestrol

A

LH production to inhibit growth of prostatic tissue

186
Q

Indication of Diethystilbestrol (1)

A

Prostatic CA

187
Q

Diethystilbestrol Contraindications (1)

188
Q

Diethystilbestrol AE; Acute (2) Chronic (3)

A

Acute:
Females (NV hyperglycemia, uterine bleeding
Males (loss of muscle, inc body fat loss of libido)

Chronic:
Hypercoagulability
Premature cornary disease
Feminization

189
Q

Anti-estrogen based Anti-neoplastic

190
Q

MOA of Tamoxifen

A

Binds to estrogen receptor in cancer cell & tissue targets

191
Q

Indication of Tamoxifen (1)

192
Q

AE of Tamoxifen; Acute (3) Chronic (3)

A

Acute: Hot flushes, weight gain, nausea, vaginal dryness, loss of libido
Chronic: Thromboembolic disease, Retinitis, Endometrial CA, Hepatotoxicity

193
Q

Androgen base antineoplastic (3)

A

Testosterone Propionate
Fluoxymesterone,
Testosterone enanthate

194
Q

Androgen based antineoplastic MOA:

A

Direct physiologic effect on androgen receptor

195
Q

Indication of Androgen based antineoplastic (2)

A

Metastatic breast CA w/ hormone receptor (+) disease
BM stimulants in BM failure syndromes

196
Q

Contraindication of Androgen based antineoplastic (1)

A

Prostatic CA

197
Q

Adverse effect of Androgen based antineoplastic; Acute (2) Chronic (1)

A

Acute
Cholestatic jaundice
Fluid retention

Chronic
Virilization (mail hair growth)

198
Q

Anti-androgen based antineoplastic (2)

A

Flutamide, Bicalutamide

199
Q

Anti-androgen based antineioplastic MOA

A

Competes with androgens binding to receptors -> blocks action of adrenal or testicular origin -> stimulate growth of malignant and normal prostatic tissue

200
Q

Indication of Anti-androgen based antineoplastic (1)

A

Early stage and metastatic Prostate Cancer

201
Q

AE of Anti-androgen based antineoplastic (3)

A

Gynecomastia, Gi distress
Liver failure (flutamide)
Dec Libido, Hot flushes

202
Q

What is Anti-androgen based antineoplastics combined with? (1)

203
Q

Gonadotropine-releasing hormone agonist (2)

A

Leuprolide and Goserelin

204
Q

MOA of GRHA

A

Inc LNRH -> stimulation of Pituitary -> inc LH & FSH -> reduction of testicular androgen and ovarian estrogen prod

205
Q

Indication of GRHA (2)

A

Prostate & Breast CA

206
Q

AE of GRHA ; Acute (1) Chronic (3)

A

Acute
Transient flare of symptoms
Chronic
Hot flushes, impotence, gynecomastia

207
Q

Aromatase inhibitors (3)

A

Aminoglutethimide, Exemestane, Anastrozol/ Letrozole

208
Q

Aminoglutethimide MOA

A

Non-steroidal inhibition of corticosteroid synthesis -> conversion of cholesterol to pregnenolone -> estrogen inhibition of extra adrenal synthesis of estrone from estradiol
Androstenedione -> estrone

209
Q

Aminoglutethimide Indications (2)

A

Prostate CA
Breast CA

210
Q

AE of Aminoglutethimide ; Acute (1) Chronic (1)

A

Acute: Dizziness
Chronic Rash

211
Q

Exemestane MOA

A

Steroidal irreversible aromatase inhibitor
Inhibits synthesis of estrogen via inhibition of adrenal androgen conversion to estrogen

212
Q

Exemestane Indication

213
Q

Exemestane AE (4)

A

Nausea
Fatigue
Hot flushes
Acne Hair changes

214
Q

Anastrozole/Letrozole MOA

A

Selective non-steroidal aromatase inhibitor with no inhibitory effects in adrenal glucocorticoid synthesis

215
Q

Indication of Anastrazole/Letrozole (1)

A

Post-menopausal women with metastatic breast CA (FIRST LINE TX)

216
Q

Indication of Anastrozole/Letrozole (1)

A

Post-menopausal women with metastatic breast CA (FIRST LINE TX)

217
Q

Difference of Anastrozole/Letrozole VS Aminoglutethimide

A

More potent
More selective
No need for hydrocortisone
No predisposition to endometrial CA
No androgenic side effects

218
Q

What are the Glucocorticoids? (3)

A

Prednisolone, Methylprednisolone, Dexamethasone

219
Q

MOA of Glucocorticoids

A

Lympholytic & Non myelosuppressive = induces cell death

220
Q

Glucocorticoid Indications (6)

A

ALL,
Lymphoma
Multiple Myeloma
Breast CA
Brain metastasis
Spinal cord compression due to malignancy

221
Q

Glucocorticoid AE ; Acute (5) Chronic (4)

A

Acute-
Fluid retention
Hyperglycemia
Mood changes
Hypokalemia
Acute Confusional States

Chronic-
Osteoporosis
Immunosuppression
GI ulcers
Cushingoid appearance, cataracts

222
Q

Progestin based antineoplastic (2)

A

Megestrol acetate
Hydroxyprogesterone

223
Q

Indication of Megestrol acetate/Hydroxyprogesterone (3)

A

Palliative for metastatic breast CA, Endometrial CA, Prostate CA

224
Q

AE of Megestrol Acetate/Hydroxyprogesterone ; Acute (2) Chronic (2)

A

Acute
Inc appetite
fluid retention

Chronic
Weight gain
Thromboembolism

225
Q

Route of Administration of Progestin based antineoplastic

226
Q

What category is Farsenyl Transferase inhibitors and MOA

A

Targeted chemotherapy

Inhibits tumor cell growth by inhibiting farnesyl transferase

227
Q

Important information of Farsenyl Transferase (3)

A

Mutant RAS is constitutively active (found in 30% of cancer cells)
RAS signaling requires linking RAS to inner membrane leaflet -> adding a carbon by the farsenyl transferase
Potent inhibitors of tumor cell growth

228
Q

What are the Tyrosine Kinase Inhibitors (8) *-tinibs

A

Imatinib/Gleevec
Dasatinib/Sprycel
Nilotinib/Tasigna
Gefitinib/Iressa
Erlotinib/Tarceva
Lapatinib/Tykerb
Sorafenib/Nexavar
Sunitinib/sutent

229
Q

Protease Inhibitor antineoplastic

A

Bortezomib

230
Q

Bortezomib MOA

A

Inhibits proteasome
leads to accumulation of regulatory protein (Bax) which leads to cell crisis and apoptosis

231
Q

Bortezomib Indication (2)

A

Multiple myeloma
Plasma cell disorder

232
Q

Bortezomib Important info (skip me)

A

Elevated levels of fibroblast growth factors (FGF) and vascular endothelial growth factor (VEGF) associated with angiogenesis

VEGF is regulated by multiple cytokines
IGF-1R
PKB
C-SRC tyrosine kinase
Inositol triphosphate kinase

233
Q

What antineoplastic is under Matrix metalloproteinase inhib

A

Marimastat

234
Q

Marimastat indication (1)

A

Pancreatic CA

235
Q

Marimistat important info (skipme)

A

MMPS comprise of collegenases, gelatinases, stromelysins and membrane type (MT)

Collagenase cleaves glycine and isoleucine

236
Q

What are the immunotherapy agents? (2)

A

Monoclonal Antibodies
Car T Cells

237
Q

Indications of Moloclonal Antibody (1)

A

Cancer Immunotherapy

238
Q

MOA of Monoclonal Antibody

A

Serve as substitue antibodies that can restore, enhance or mimic the immune systems attack on cancer cells

Cytotoxic Lymphocyte associated antigen 4 (CTLA4) inhibitor
e.x IPILIMUMAB ; functions as a signal dampener to upregulate T-cells against tumor cells
Programmed cell death protein 1 inhibitor (PD1); activates T- cell function against tumor cells

239
Q

Car T Cells MOA

A

Guides T cell directly to the tumor
Triggers T cells fighting power to attack the cancer cells

240
Q

Car T cells Indication

A

Refractory ALL
Non-Hodgkin’s Lymphoma
(Diffuse large B cell lymphoma)

241
Q

Car T Cells AE (2)

A

Cytokine Storm
Autoimmune disease manifesting as colitis or neurotoxicity

Pharma (2 decks)

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