Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Heme/Lymph Exam > Chemo 1 > Flashcards

Chemo 1 Flashcards

1
Q

naming conventions - traditional chemotherapy: -platin

A

*platinum alkylating agent
*notes:
-platins are a type of traditional cytotoxic chemo
-MOA: cross-link DNA (cell cycle non-specific)

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

naming conventions - traditional chemotherapy: -rubicin

A

*anthracyclines
*MOA: inhibit topoisomerase II

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

naming conventions - traditional chemotherapy: -tecan

A

topoisomerase I inhibitors

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

naming conventions - traditional chemotherapy: -mycin

A

antitumor antibiotics

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

naming conventions - targeted therapy: -mab

A

monoclonal antibodies; examples:
-rituximab
-bevacizumab
-trastuzamab

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

naming conventions for chemo: -inib/ilib/isib

A

small molecule inhibitors; examples:
-imatinib
-dasatinib
-erlotinib

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

cell cycle and chemo - why it matters

A

*traditional chemotherapy targets rapidly dividing cells
*a subset of the traditional chemo agents work specifically in one portion of the cell cycle:
-G2 = bleomyscin
-M = taxanes, vinca alkyloids, eribulin
-S = cytarabine, fluorouracil, methotrexate
-S/G2 = topoisomerase 1/2 inhibitors
*some agents are cell-cycle independent:
-platinums, alkylating agents, targeted agent

*goal = target as many aberrant, rapidly-dividing cells as possible while avoiding cell cycle of normal, healthy cells

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

how do monoclonal antibodies work in cancer therapy?

A

*all bind extracellularly
*destroys cells through:
-direct tumor effects
-antibody-dependent cellular cytotoxicity
-complement-mediated lysis
-induce apoptosis

*newer molecules contain a conjugated toxin that is delivered to the site of activity by the monoclonal antibody

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

tyrosine kinases for cancer therapy

A

*normally TK -> phosphorylation of proteins resulting in proliferation, differentiation, and survival of cells
*mutation on TK -> uncontrolled replication of cells
*activity tightly controlled in normal cells
*TK inhibitors can be beneficial in blocking reproduction of cancer cells

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

traditional chemotherapy classes

A
  1. nucleotide synthesis (folate antagonists, purine analogues, pyrimidine analogues)
  2. DNA damage (alkylating agents, platinums, antitumor antibiotics, topoisomerase inhibitors)
  3. cellular division - mitotic inhibitors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

methotrexate - drug class & MOA

A

*reduced folate analog (i.e. mimics folate to disrupt nucleotide synthesis)
*MOA:
1. taken up intracellularly by cancer & healthy cells
2. inhibits dihydrofolate reductase -> decreased tetrahydrofolate -> decreased purine and thymidylate
3. lack of purines and thymidylate PREVENTS DNA SYNTHESIS

note - S phase specific antimetabolite

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

leucovorin (folinic acid) - clinical indication

A

*REQUIRED for high dose methotrexate b/c high dose MTX is lethal unless rescue (leucovorin) is given

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

methotrexate - common clinical uses

A

*osteosarcoma
*acute lymphocytic leukemia
*non-hodgkins and CNS lymphomas
*breast/bladder cancer
*non-oncologic uses: rheumatoid arthritis, ectopic pregnancy

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

what is the rescue therapy for high dose methotrexate

A

LEUCOVORIN (folinic acid)

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

leucovorin (folinic acid) - MOA

A

*directly converted into tetrahydrofolate (does not require dihydrofolate reductase, the enzyme that is inhibited by methotrexate)
*allows resumption of DNA synthesis, even in the presence of methotrexate

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

methotrexate toxicities

A

*NEPHROTOXICITY
*MYELOSUPPRESSION
*GI toxicity (mucositis)
*hepatotoxicity
*neurotoxicity
*dermatitis
*death [if not given leucovorin]

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

methotrexate toxicity - risk factors

A

*pre-existing renal dysfunction
*urine pH < 7
*concomitant medications (eliminate these if possible)
*Down syndrome
*third space fluids: ascites, pleural effusions

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

fluorouracil (5-FU) - indications

A

*treatment of SOLID tumors including breast, colorectal, and other GI tumors
*non-oncologic uses: actinic keratoses and noninvasive skin cancers

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

fluorouracil (5-FU) - MOA

A

*fluorinated analog of uracil
*metabolized to FdUMP
*inhibits thymidylate synthetase
*decreases DNA synthesis

note - S phase specific antimetabolite

19
Q

fluorouracil (5-FU) & leucovorin synergy

A

provides higher levels of tumor kill activity

20
Q

fluorouracil (5-FU) - toxicities

A

*myelosuppression (if given as a bolus)
*bloody diarrhea and hand foot syndrome (if given as continuous infusion)
*mucositis (if given as continuous infusion)
*dermatologic
*ocular
*nausea & vomiting (MILD)

21
Q

6-mercaptopurine (6-MP) - MOA

A

*purine analog
*inhibits de novo purine synthesis

22
Q

6-mercaptopurine (6-MP) - clinical uses

A

leukemias (pediatric)

23
Q

6-mercaptopurine (6-MP) - toxicities

A

*myelosuppression
*immunosuppression
*hepatotoxicity

24
Q

hydroxyurea - MOA

A

*inhibits ribonucleotide reductase
*leads to decreased DNA synthesis

25
Q

hydroxyurea - indications

A

*used primarily for CML blast crisis
*non-oncology indications: sickle cell disease (increases HbF)

26
Q

hydroxyurea - toxicity

A

*myelosuppression

27
Q

alkylating agents class - MOA (detailed)

A
  1. one 2-chloroethyl side chain undergoes a 1st order intramolecular cyclization
  2. result is the release of Cl- and formation of a highly reactive aziridinium ion
  3. binds to DNA base pairs, resulting in inter- or intra-strand crosslinking
  4. outcomes of alkylating agent treatment:
    -template being replicated is misread or mismatched during DNA synthesis
    -crosslinking prevents DNA strands from unwinding
    -single or double-strand breaks in DNA occur
    -DNA molecule ineffective

*cell cycle non-specific

28
Q

alkylating agents class - MOA (simple)

A

cross-links DNA

29
Q

common alkylating agents

A
  1. phosphoramide mustards:
    -cyclophosphamide
    -ifosfamide
  2. platinums
    -cisplatin
    -carboplatin
    -oxalitplatin
30
Q

alkylating agents class toxicities

A

*myelosuppression (prolonged/delayed myelosuppression nadir)
*hemorrhagic cystitis
*infertility
*alopecia
*nausea/vomiting
*secondary leukemias

31
Q

cyclophosphamide clinical uses

A

*breast cancer, leukemia, and lymphomas
*bone marrow transplant
*graft-versus-host disease
*immunosuppression in non-malignant diseases: rheumatic disorders, lupus, & autoimmune nephritis

note - cyclophosphamide is an alkylating agent

32
Q

ifosfamide clinical uses

A

*soft tissue/bone sarcomas
*lymphomas

33
Q

cyclophosphamide/ifosfamide metabolism

A

*require bioactivation by liver
*inactive metabolite: acrolein -> NO TUMOR KILLING, just causes toxicities (ifosfamide generates more)
*active metabolite: phosphoramide mustard -> causes the cytotoxities to the tumor

34
Q

hemorrhagic cystitis - dose-limiting toxicity of alkylating agents

A

*caused by accumulation of ACROLEIN (inactive metabolite of cyclophosphamide/ifosfamide) in the bladder wall
*hematuria, urinary frequency, & irritation
*prevent with vigorous hydration & MESNA
*treat with bladder irrigation, alum irrigation, and other therapies
*heme test urine while on therapy

35
Q

what is the prevention for hemorrhagic cystitis associated with use of cyclophosphamide/ifosfamide

A

MESNA

indicated for ANY dose of ifosfamide, but only high doses with cyclophosphamide

36
Q

MESNA

A

*uroprotectant containing sulfhydryl group - binds to acrolein in the bladder to form a nontoxic compound
*not systemically absorbed, so does not interfere with cytotoxic activity
*indicated in:
-cyclophosphamide > 1g/m2/dose
-ifosfamide ANY DOSE
*effective in PREVENTION only

37
Q

cyclophosphamide/ifosfamide - toxicites

A

*hemorrhagic cystitis
*delayed nausea & vomiting
*syndrome of inappropriate anti-diuretic hormone
*pulmonary
*neurotoxicity
*renal Fanconi syndrome (in peds)

38
Q

cisplatin - notes

A

*renally cleared
*nephrotoxicity (if poor renal function, do not use)
*prevent with aggressive hydration
*toxicities: nephrotoxicity, lots of nausea and vomiting, peripheral neuropathy, neurotoxicity, hypersensitivity

39
Q

carboplatin - notes

A

*NOT concentrated in the renal tubules; more efficiently cleared
*dosing based no area under the curve (AUC)
*toxicities: neurotoxicity, vomiting, hypersensitivity

40
Q

platinums - clinical uses

A

*breast cancer
*lung cancer
*testicular cancer
*gyn/onc: cervical and ovarian cancer
*colorectal cancer
*bladder cancer
*lymphoma

41
Q

oxaliplatin

A

*toxicity = peripheral neuropathy, myelopsuppression, hypersensitivity

42
Q

platinum toxicity: hypersensitivity

A

*IgE-mediated process
*increased risk with increased number of doses (>6)
*can be treatment-limiting
*may be revealed using allergen skin testing procedures

43
Q

antitumor antibiotics - MOA

A

DNA strand breakage

44
Q

bleomycin - MOA, uses, toxicities

A

*drug class = antitumor antibiotic
*MOA: induces free radical formation -> BREAKS IN DNA STRANDS
*uses: testicular cancer & Hodgkin lymphoma
*toxicities: PULMONARY toxicity (pulmonary fibrosis), N/V, skin hyperpigmentation

45
Q

dactinomycin - MOA, uses, toxicities

A

*drug class = antitumor antibiotic
*MOA: intercalates into DNA, preventing RNA synthesis
*uses: Wilms tumor, Ewing sarcoma, rhabdomyosarcoma
*toxicities: N/V, myelosuppression

46
Q

mitomycin C - MOA, uses, toxicities

A

*MOA: DNA strand breakage
*uses: GI tumors, intravesicularly in bladder cancer

Heme/Lymph Exam (37 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions