Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
49 Cards in this Set
- Front
- Back
|
What is tyrosine kinase?
|
Good question....
Enzyme (on cytoplasmic side) attached to transmembrane cell receptors (EGFR, VEGF, PDGFR) which, when activated, leads to phophorylation of proteins and ultimately cell proliferation Sum: Ligand --> Receptor --> TK --> phosphorylation --> cell proliferation |
|
|
What are EGFR & VEGF?
|
EGFR: epidermal growth factor receptor; linked to TK --> activation leads to cell proliferation
VEGF: vascular endothelial growth factor; angiogenic signaling (tumor recruits blood supply) |
|
|
What is the role of inhibition of tyrosine kinase in cancer treatment?
|
(ex: cetuximab, trastuzumab)
Disrupt cell-signaling path (now the tumor cannot promote survival, proliferation, motility) MOA: it binds receptor & prevents dimerization |
|
|
What drugs are available that target EGFR?
|
EGFR:
small molecules: erlotinib gefitinib monoclonal Abs: CETUXIMAB, panitumumab, TRASTUZUMAB (for Her2) |
|
|
What drugs are available that target VEGF?
|
VEGF:
Bevacizumab, probably others, but i don't care |
|
|
What is Her2/neu?
In what cancers is it overexpressed? |
1. Her2/neu: oncogene
2. overexpressed in breast cancers |
|
|
What is the name of the monoclonal antibody against HER2?
|
Trastuzumab
|
|
|
Are methotrexate, 5-FU, Ara-C, and 6-MP CCS or CCNS?
|
CCS
|
|
|
What is the MOA of methotrexate?
|
inhibits dihydrofolate reductase which leads to a decrease in dTMP
|
|
|
What is the MOA of 5-FU?
|
converted to active --> 5-FdUMP --> inhibits thymidylatesynthase leading to a decrease in dTMP
|
|
|
What is the MOA of Ara-C?
|
inhibits DNA pol (or inhibits base stacking) leading to inability to elongate DNA
|
|
|
What is the MOA of 6-MP?
|
Activated by HGPRT
inhibits AMP/GMP synthesis! |
|
|
What do you need to replenish when treating w/ methotrexate? What do you give to accomplish this?
|
Leucovorin --> replenishes folate
|
|
|
What are some AE's of methotrexate?
|
Reversible decrease in bone marrow
nephrotox --> give sodium bicarb CNS tox |
|
|
What is a MAJOR AE of 5-FU?
|
ischemia (to the heart)
|
|
|
In what cell cycle phase do methotrexate, 5-FU, Ara-C, and 6-MP act?
|
S phase
|
|
|
What are 2 major AE's of Ara-C?
|
Cerebellar toxicity
Ocular --> conjunctivitis, keratitis (also myelosuppression) |
|
|
What drug interacts w/ 6-MP by inhibiting its metabolism?
|
Allopurinol
(inhibits xanthine oxidase) |
|
|
What are two common SE's of alkylating agents?
|
Bone marrow suppression
Alopecia |
|
|
What is the MOA of busulfan?
Worst AE? |
1. alkylates DNA via cross-linking
2. Pulmonary fibrosis |
|
|
What is the MOA of cyclophosphamide?
|
attacksguanine N7 --> alkylates DNA
|
|
|
What is special about the nitrosureas? (lomustine, carmustine)
|
They cross the BBB!
|
|
|
What are the major AE's of cisplatin?
|
MOA-alkylates
AE: nephrotoxicity (hydrate w/ NS) ototoxicity neurotxic N/V |
|
|
What is the MOA of procarbazine?
|
methylates DNA
|
|
|
What is a common presentation of the major AE of doxorubicin?
|
CHF! (causes cardiomyopathy long-term)
(also see alopecia) |
|
|
What is the MOA of doxorubicin?
|
inhibits topoisomerase II --> intercalates DNA --> breaks --> no replication/translation
|
|
|
What is the MOA of bleomycin?
|
makes free radicals--> damages DNA in G2 phase!
|
|
|
What is the major AE of bleomycin?
|
PULMONARY FIBROSIS
IN ALL CAPS |
|
|
What 4 cancer types do you often use hormone/anti-hormone tx?
|
breast
prostate endometrial adrenal cortex |
|
|
What type of cancer is aromatase-inhibitor used for?
|
breast cancer
|
|
|
What is the MOA of hydroxyurea?
|
inhibit ribonucleotide reductase --> dec dNTP (in S-phase)
|
|
|
What is the MOA of all-trans retinoic acid?
|
inhibits clonal proliferation (in acute promyelocytic leukemia)
|
|
|
What is the general MOA of the plant alkaloids group?
|
inhibit MT's in some way (usually affecting mitotic spindle formation)... so M phase
|
|
|
What is the MOA of vinblastine and vincristine?
|
inhibit MT
AE of cristine --> peripheral neuropathy |
|
|
What is the MOA of docetaxel?
major AE? |
stablize (and immobilize) MT's
AE: hypersensitivity reaction (must prophylax) |
|
|
If a patient cannot make sufficient UGT-1A1, what drug should you avoid?
|
irinotecan
|
|
|
What is the MOA of etoposide?
|
inhibit topoisomerase II --> DNA degradation
|
|
|
This is the term for treating for micromets post surgery or radiation tx.
|
Adjuvant Chemotherapy
|
|
|
This is the term for treating (w/ chemo) prior to surgery (to shrink tumor).
|
Neoadjuvant chemotherapy
|
|
|
What is the MOA of mitomycin C?
|
alkylates DNA
for solid tumors can cause bone marrow suppression |
|
|
Pt. being treated w/ cisplatin may develop what major AE?
What is the treatment? |
AE: nephrotoxicity
Tx: amifostine (forms thiol groups --> binds toxic metabolites) |
|
|
What complication does Dexrazoxane address?
|
cardiotoxicity seen w/ doxorubicin
it is an iron chelator |
|
|
What is the major AE of ifosphamide?
How would you treat this? |
AE: hemorrhagic cystitis
Tx: Mesna (activate thiols --> bind toxicmetabolites) |
|
|
What is the standard of care for treating chemo-induced N/V?
|
5-HT3-R antagonist
NK1-R antagonist corticosteroid |
|
|
What is the DOC for acute chemo-induced N/V?
|
5-HT3 receptor antagonists
(all end in -setron) |
|
|
Pt. on chemo develops anemia. Treatment?
SE's? |
1. ESA's (EPO-stimulating agent)
2. SE: death, DVT, tumor/disease progression (the usual) |
|
|
Pt on chemo develops neutropenia
Treatment? |
CSF's
Ex: filgrastim (G), Pegfilgrastim, Sargramostim(GM) |
|
|
Pt. on chemo develops thrombocytopenia.
Treatment? |
Opreleukin (IL-11)
|
|
|
Pt. on Busulfran develops hyperuricemia.
Treatment? |
allopurinal (xanthine oxidase inhibitor)
or Probenecid (blocks uric acid tubular reabsorption) |
