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Flashcards in Pharm Chemo Drugs Deck (58):
1

Antimetabolites

Antimetabolites

2

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)

3

Antimetabolites are commonly used to treat what?

leukemias, breast CA, ovary, and the intestinal tract,

4

Fluoropyrimidines
-
-
MOA:

5-Fluorouracil
Capecitabine

MOA:inhibits thymidine synthesis (capecitabine is the prodrug of 5-FU)

5

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

6

what are the side effects of the Fluoropyrimidines

neutropenia, thrombocytopenia, and anemia; Hand–foot syndrome and diarrhea when administered as a continuous IV infusion

7

Cytidine Analogs

Cytidine Analogs

8

Cytidine Analogs

Cytarabine
Gemcitabine

9

what is the MOA of Cytidine Analogs

Cytarabine arabinose analog of cytosine
Gemcitabine- Inhibits DNA polymerase

10

what is a side effect of Cytarabine?

Cellebellar syndrome, ataxia, bone suppression with leukoplenia and thrombocytopenia and anemia.

11

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

12

Purine Antimetabolites (Purine Antagonists)

Purine Antimetabolites (Purine Antagonists)

13

Purine Antimetabolites (Purine Antagonists)
-
-
-
-

Mercaptopurine (6-MP)
Thioguanine (6-TG):
Fludarabine
Cladribine and pentostatin

14

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

15

Fludarabine:
increases the risk of

infection

16

Cladribine and pentostatin
specific MOA of each

cal- resists deactivation by adenosine deaminase

pen- is a potent inhibitor of adenosine deminase

17

Do not combine pentostatin with what?

Fludarabine- risk of fatal pulmonary toxicity

18

Antifolates
-
-
MOA:
what can this cause?

Methotrexate & Pemetrexed

MOA: inhibits dihydrofolate reductates
this can cause pernicious anemia

side effects: Hepatotoxic and Renal tubularnecorisis

19

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

20

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)-

21

Taxanes
Drugs (2)
MOA
SE:
-
-
Requires premedication with what?

Interactions
-
-

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

22

Epothilone
Drugs (2)

May work in those resistant to pactilaxel

Epothilone and Ixabepolone

Epothilone

23

Similar to taxanes for Metastatic breast cancer

Premedicate with what?

Ixabepilone

antihistamine (may/may not need corticosteroid)

24

Estramistine

Estramustine Causes separation of microtubule-associated protein from the microtubultes- inhibits assembly

25

➢Topoisomerase inhibitors

➢Topoisomerase inhibitors

26

MOA of Topoisomerase inhibitors
MOA:
I:
II:
Examples

Manipulated (Break) DNA during replication and transcription-
I= onetime
II= two times
Examples: camptothecins, anthacyclines, epipodopyllotoxins

27

camptothecins

Topotecan and Irinotecan
Etoposide and Teniposide

28

Topotecan and Irinotecan
Inhibits:
S/E:
tx of s/e:

Inhibit topoisomerase 1

Higher risk of diarrhea (treat with loperamide)

29

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

30

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)

31

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

32

➢Alkylating agents

➢Alkylating agents

33

Alkylating agents
MOA:

Damages DNA
Examples: Nitrogen mustards and Nitrosoureas

34

Nitrogen mustard derivatives
example:
used for the treatment:
Side effect:
-
-

Cyclophosphamide and Ifosafamide and Bendamustine

35

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.

36

Bendamustine
active against
used for:

active against quiescent and dividing cells.

used for Chronic lymphocytic leukemia and non hodgkins lymphoma

37

Nitrosouras:

Streptozocin, carmustine (BCNU), Imoustine

38

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

39

Heavy Metals

Heavy metals

40

Heavy metals
called the:
3 drugs

MOA:

Less likely than the

se
-
-
-

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)

41

➢Misc. agents

➢Misc. agents

42

Bleomycin

it is a anti tumor antibiotic that is degraded by aminohydrolase

SE: PULMONARY FIBROSIS

43

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

44

Vorinostat
MOA:
SE

MOA: histone deacetylase inhibitor
SE: PE, DVT, anemia.

45

➢Monoclonal antibodies (MoABs)

➢Monoclonal antibodies (MoABs)

46

➢Monoclonal antibodies (MoABs)
-
-
-

• Rituximab
•Ibritumomab tiuxetan
• Tositumomab

47

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

48

Ibritumomab tiuxetan
MOA:
USE:
SE:

• CD20- can be used if Rituximab fails
• Use: non-hogdkin lymphoma
• SE: anaphylaxis, thrombocytopenia, neotropenia

49

Tositumomab

similar to Ibritumomab tiuxetan

50

Alemtuzumab
MOA:
Used for:
SE:

MOA: Binds to CH 53

B cell lymphocytic leukemia

Black box: Hematologic toxicity and opportunistic infections

51

➢Growth factor receptor and ligand targeting

➢Growth factor receptor and ligand targeting

52

➢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

53

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

54

Tradtuzumab
MOA:
USES:
SE:

• Humanized MoAB bind HER-2
• Use: metstatic breast (alone or with paxlitaxel)
• SE: cardiac failure (esp. if given with anthacylines)

55

Erlotinib
MOA:
SE:

• EGFR-tyrosine kinase inhibitor
•SE: rash, diarrhea- premeditate with steroids and antihistamines

56

Lapatinib
MOA:
SE

• Kinase inhibitor of EGFR and HER-2
• SE: diarrhea, hepatoxicity, rash, QT prolongation

57

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

58

Sunitinib and Sorafenib
MOA:
SE:

• Inhibits VEGFR-2 and platelet derived growth receptor
• SE: CHF-sunitinib and hand foot syndrome –soradenib