Pharm Chemo Drugs Flashcards
Antimetabolites
Antimetabolites
MOA of Antimetabolites
antimetabolites interfere with DNA and RNA formation by substituting for the normal building blocks of RNA and DNA (changing the base then once replication starts it recognizes the change in the base and blocks replication)
Antimetabolites are commonly used to treat what?
leukemias, breast CA, ovary, and the intestinal tract,
-
MOA:
5-Fluorouracil
Capecitabine
MOA:inhibits thymidine synthesis (capecitabine is the prodrug of 5-FU)
what is the benefit and side effect of Capecitabine
it can be taken orally
Black Box: Monitor INR regularly with patients on oral coumadin derivatives-Increased risk of bleeding/death
what are the side effects of the Fluoropyrimidines
neutropenia, thrombocytopenia, and anemia; Hand–foot syndrome and diarrhea when administered as a continuous IV infusion
Cytidine Analogs
Cytidine Analogs
Cytidine Analogs
Cytarabine
Gemcitabine
what is the MOA of Cytidine Analogs
Cytarabine arabinose analog of cytosine
Gemcitabine- Inhibits DNA polymerase
what is a side effect of Cytarabine?
Cellebellar syndrome, ataxia, bone suppression with leukoplenia and thrombocytopenia and anemia.
Azacytidine and Decitabine MOA: Indicated for: Reduces what? Toxicity :
MOA: Nucleoside analog
indicated for: Myelogenous leukemia
It reduces the need for transaction and creates hematopoiesis
Toxic: Myelosupression
Purine Antimetabolites (Purine Antagonists)
Purine Antimetabolites (Purine Antagonists)
Purine Antimetabolites (Purine Antagonists) - - - -
Mercaptopurine (6-MP)
Thioguanine (6-TG):
Fludarabine
Cladribine and pentostatin
Mercaptopurine (6-MP) and Thioguanine (6-TG):
MOA:
Side effects:
Interactions:
rapidly converted to ribonucleotides that inhibit purine biosynthesis
Side effects: Hepatic toxicity
Don’t use with allopurinol, Mercaptopurine metabolism is significantly decreased • REDUCE drug dose by approximately 75% when allopurinol is administered & monitor for toxicity
Fludarabine:
increases the risk of
infection
Cladribine and pentostatin
specific MOA of each
cal- resists deactivation by adenosine deaminase
pen- is a potent inhibitor of adenosine deminase
Do not combine pentostatin with what?
Fludarabine- risk of fatal pulmonary toxicity
Antifolates - - MOA: what can this cause?
Methotrexate & Pemetrexed
MOA: inhibits dihydrofolate reductates
this can cause pernicious anemia
side effects: Hepatotoxic and Renal tubularnecorisis
Microtubular targeting Drugs MOA Side effects CA used for: Ex - - - -
MOA: work on the M phase
Side effects: Periph N damage
Ca: Breast, lung, Myeloma, Lymphoma
Taxanes
Epothilones
Vinva alkaloids
Estramustine
Vinca Alkaloids drugs: (3) MOA: from what plant How is resistance developed? s/e
Vincriostine, Vinblastine, Vinorelbine
Stop assembly of mircotubules
Natural alkaloids from periwinkle plant
resistance: Resistance develops from P-glycoprotein-decreases drug accumulation and retention in tumor cells
S/E extravasation (tx. Warm packs)-
Taxanes Drugs (2) MOA SE: - - Requires premedication with what?
-
Paclitaxel and Docetaxel
MOA: Promote microtubule assembly and interfere with disassembly
S/E Doc: Water retention, Myelosupresion
Pac: Neurotoxicity and hupersensitivtiy
Pre med: corticosteroids
do not give Paclitaxel with solid tumors with baseline PMN normal or Alt/AST > 1.5 normal
Epothilone
Drugs (2)
May work in those resistant to pactilaxel
Epothilone and Ixabepolone
Epothilone
Similar to taxanes for Metastatic breast cancer
Premedicate with what?
Ixabepilone
antihistamine (may/may not need corticosteroid)
Estramistine
Estramustine Causes separation of microtubule-associated protein from the microtubultes- inhibits assembly
➢Topoisomerase inhibitors
➢Topoisomerase inhibitors
MOA of Topoisomerase inhibitors MOA: I: II: Examples
Manipulated (Break) DNA during replication and transcription-
I= onetime
II= two times
Examples: camptothecins, anthacyclines, epipodopyllotoxins
camptothecins
Topotecan and Irinotecan
Etoposide and Teniposide
Topotecan and Irinotecan
Inhibits:
S/E:
tx of s/e:
Inhibit topoisomerase 1
Higher risk of diarrhea (treat with loperamide)
Etoposide and Teniposide
inhibits:
Resistance:
Side effects:
Inhibit topoisomerase 2
Resistance - by increased cells ability to repair type 2 breaks or increased Pgp levels
SE
Severe myelosupression &Bleeding
Anthracene Derivatives (Anthracycline) Drugs (4) MOA: (2) Side effects: - - -
-what to use for s/e
Examples: Doxorubicin, Daunorubicin, Idarubicin, Epirubicin
moa: Intercalating topoisomerse inhibitors- insert or stack between base pairs of DNA AND generation of Free radicals- damage all parts of the cell
S/E:
- all Cardiotoxicity –anthracycline
- Doxorubicin= CHF at doses over 400mg/m2
- AML
use to: ➢ Use Dexrazoxane (Totect) immediately- within 6 hours- if dose puts patient at risk of delayed cardiomyopathy and cold pack if extravagation (remove ice pack 15 prior to Totect)
Mitoxantrone MOA: Much less what? Use in: S/E
Intercalating topoisomerase 2 inhibitor
Much less free radical potential
Uses: MS patients (suppresses Tcells, Bcells, and Macropahges)
SE
Cardiotoxicity
AML
➢Alkylating agents
➢Alkylating agents
Alkylating agents
MOA:
Damages DNA
Examples: Nitrogen mustards and Nitrosoureas
Nitrogen mustard derivatives example: used for the treatment: Side effect: - -
Cyclophosphamide and Ifosafamide and Bendamustine
Cyclophosphamide and Ifosafamide used for the treatment: Side effect: - -
used for the treatment of solid tumors and hematologic malignancies
Side effect: Hemorrhagic cystitis
caused by acrolein metabolite
infuse MESNA to reduce the risk of hemorrhagic crisis
Ifosafamide: causes Encephalopathy which is revisable.
Bendamustine
active against
used for:
active against quiescent and dividing cells.
used for Chronic lymphocytic leukemia and non hodgkins lymphoma
Nitrosouras:
Streptozocin, carmustine (BCNU), Imoustine
BCNU- IV used for:
BCNU- IV used for:
drug impregnated biodegradable wafer (Glindel) for direct application to residual tumor tissue following surgical resection for brain tumors
Heavy Metals
Heavy metals
Heavy metals
called the:
3 drugs
MOA:
Less likely than the
-
-
Called the Platinum Drugs Cisplatin, Carboplatin, Oxaliplatin
MOA: intercalating DNA
Less likely than the alkaylating agents to cause leukemia
SE
Cisplatin: nephrotoxicty, otoxicity, pheripheral neuropathy, emesis, anemia
Carboplatin: hematologic toxicity (potential of above)
Oxaliplatin: peripheral neuropathy (cold induced) (no potential of above)
➢Misc. agents
➢Misc. agents
Bleomycin
it is a anti tumor antibiotic that is degraded by aminohydrolase
SE: PULMONARY FIBROSIS
Hydroxyurea -MOA: Asparaginase MOA: Arsenic Trioxide: antitumor MOA:
Hydroxyurea: Inhibits ribonucleotide reductase, stops cells in S phase
Asparaginase: Inhibit protien synthesis
Arsenic Trioxide: antitumor
just know it is avb
Vorinostat
MOA:
SE
MOA: histone deacetylase inhibitor
SE: PE, DVT, anemia.
➢Monoclonal antibodies (MoABs)
➢Monoclonal antibodies (MoABs)
-
-
- Rituximab
- Ibritumomab tiuxetan
- Tositumomab
Rituximab moa: only used for: Uses: SE:
• CD20 antigen (B cell) agonist (binds to it!)
Only works of ca that are Cd20 +
• Use: non-hodgkin lymphoma, CLL
• SE: Infusion related complex fever, chills, nausea, asthenia, headache
Ibritumomab tiuxetan
MOA:
USE:
SE:
- CD20- can be used if Rituximab fails
- Use: non-hogdkin lymphoma
- SE: anaphylaxis, thrombocytopenia, neotropenia
Tositumomab
similar to Ibritumomab tiuxetan
Alemtuzumab
MOA:
Used for:
SE:
MOA: Binds to CH 53
B cell lymphocytic leukemia
Black box: Hematologic toxicity and opportunistic infections
➢Growth factor receptor and ligand targeting
➢Growth factor receptor and ligand targeting
➢Growth factor receptor and ligand targeting
what does it do:
- - - - - -
HER-1 ( aka EGFR) and HER-2 are know to be over expressed in several cancers, including breast, lung and colon. Activation of theses receptors can lead to uncontrolled cellular growth.
- Cetuximab and Panitumumab
- Tradtuzumab
- Erlotinib
- Lapatinib
- Bevacizumab
- Sunitinib and Sorafenib
Cetuximab and Panitumumab
MOA:
USES:
SE:
- Chimeric MoAB that binds to EGFR (HER-1)
- Use: metastaic colorectal, neck , head
- SE: N/V/D/C, abdominal pain, sudden death
Tradtuzumab
MOA:
USES:
SE:
- Humanized MoAB bind HER-2
- Use: metstatic breast (alone or with paxlitaxel)
- SE: cardiac failure (esp. if given with anthacylines)
Erlotinib
MOA:
SE:
- EGFR-tyrosine kinase inhibitor
* SE: rash, diarrhea- premeditate with steroids and antihistamines
Lapatinib
MOA:
SE
- Kinase inhibitor of EGFR and HER-2
* SE: diarrhea, hepatoxicity, rash, QT prolongation
Bevacizumab MOA: SE - -
- VEGF antagonist- prevents angiogenesis( CA has an over expression of Veg F)
- SE: HTN, bleeding, thombotic events
- GI bleed, CNS hemorrhage, vaginal bleeding
- PE, DVT,MI
Sunitinib and Sorafenib
MOA:
SE:
- Inhibits VEGFR-2 and platelet derived growth receptor
* SE: CHF-sunitinib and hand foot syndrome –soradenib
