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Clinical Medication: HEENT > Pharm Chemo Drugs > Flashcards

Pharm Chemo Drugs Flashcards

1
Q

Antimetabolites

A

Antimetabolites

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2
Q

MOA of Antimetabolites

A

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)

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3
Q

Antimetabolites are commonly used to treat what?

A

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

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4
Q

-
MOA:

A

5-Fluorouracil
Capecitabine

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

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5
Q

what is the benefit and side effect of Capecitabine

A

it can be taken orally

Black Box: Monitor INR regularly with patients on oral coumadin derivatives-Increased risk of bleeding/death

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6
Q

what are the side effects of the Fluoropyrimidines

A

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

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7
Q

Cytidine Analogs

A

Cytidine Analogs

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8
Q

Cytidine Analogs

A

Cytarabine

Gemcitabine

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9
Q

what is the MOA of Cytidine Analogs

A

Cytarabine arabinose analog of cytosine

Gemcitabine- Inhibits DNA polymerase

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10
Q

what is a side effect of Cytarabine?

A

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

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11
Q 
Azacytidine and Decitabine
MOA:
Indicated for:
Reduces what?
Toxicity :
A

MOA: Nucleoside analog
indicated for: Myelogenous leukemia
It reduces the need for transaction and creates hematopoiesis
Toxic: Myelosupression

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12
Q

Purine Antimetabolites (Purine Antagonists)

A

Purine Antimetabolites (Purine Antagonists)

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13
Q 
Purine Antimetabolites (Purine Antagonists)
-
-
-
-
A

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

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14
Q

Mercaptopurine (6-MP) and Thioguanine (6-TG):
MOA:
Side effects:
Interactions:

A

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

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15
Q

Fludarabine:

increases the risk of

A

infection

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16
Q

Cladribine and pentostatin

specific MOA of each

A

cal- resists deactivation by adenosine deaminase

pen- is a potent inhibitor of adenosine deminase

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17
Q

Do not combine pentostatin with what?

A

Fludarabine- risk of fatal pulmonary toxicity

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18
Q 
Antifolates 
-
-
MOA: 
what can this cause?
A

Methotrexate & Pemetrexed

MOA: inhibits dihydrofolate reductates
this can cause pernicious anemia

side effects: Hepatotoxic and Renal tubularnecorisis

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19
Q 
Microtubular targeting Drugs 
MOA 
Side effects 
CA used for:
Ex
-
-
-
-
A

MOA: work on the M phase
Side effects: Periph N damage
Ca: Breast, lung, Myeloma, Lymphoma

Taxanes
Epothilones
Vinva alkaloids
Estramustine

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20
Q 
Vinca Alkaloids
drugs: (3)
MOA:
from what plant
How is resistance developed?
s/e
A

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)-

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21
Q 
Taxanes
Drugs (2)
MOA
SE: 
-
-
Requires premedication with what?

-

A

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

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22
Q

Epothilone
Drugs (2)

May work in those resistant to pactilaxel

A

Epothilone and Ixabepolone

Epothilone

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23
Q

Similar to taxanes for Metastatic breast cancer

Premedicate with what?

A

Ixabepilone

antihistamine (may/may not need corticosteroid)

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24
Q

Estramistine

A

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

25
Q

➢Topoisomerase inhibitors

A

➢Topoisomerase inhibitors

26
Q 
MOA of Topoisomerase inhibitors
MOA:
I:
II:
Examples
A

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

27
Q

camptothecins

A

Topotecan and Irinotecan

Etoposide and Teniposide

28
Q

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

A

Inhibit topoisomerase 1

Higher risk of diarrhea (treat with loperamide)

29
Q

Etoposide and Teniposide
inhibits:
Resistance:
Side effects:

A

Inhibit topoisomerase 2

Resistance - by increased cells ability to repair type 2 breaks or increased Pgp levels

SE
Severe myelosupression &Bleeding

30
Q 
Anthracene Derivatives (Anthracycline)
Drugs (4)
MOA: (2)
Side effects: 
-
-
-

-what to use for s/e

A

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
Q 
Mitoxantrone
MOA: 
Much less what?
Use in:
S/E
A

Intercalating topoisomerase 2 inhibitor

Much less free radical potential

Uses: MS patients (suppresses Tcells, Bcells, and Macropahges)

SE
Cardiotoxicity
AML

32
Q

➢Alkylating agents

A

➢Alkylating agents

33
Q

Alkylating agents

MOA:

A

Damages DNA

Examples: Nitrogen mustards and Nitrosoureas

34
Q 
Nitrogen mustard derivatives
example: 
used for the treatment:
Side effect: 
-
-
A

Cyclophosphamide and Ifosafamide and Bendamustine

35
Q 
Cyclophosphamide and Ifosafamide
used for the treatment:
Side effect: 
-
-
A

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
Q

Bendamustine
active against
used for:

A

active against quiescent and dividing cells.

used for Chronic lymphocytic leukemia and non hodgkins lymphoma

37
Q

Nitrosouras:

A

Streptozocin, carmustine (BCNU), Imoustine

38
Q

BCNU- IV used for:

A

BCNU- IV used for:
drug impregnated biodegradable wafer (Glindel) for direct application to residual tumor tissue following surgical resection for brain tumors

39
Q

Heavy Metals

A

Heavy metals

40
Q

Heavy metals
called the:
3 drugs

MOA:

Less likely than the

-
-

A

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
Q

➢Misc. agents

A

➢Misc. agents

42
Q

Bleomycin

A

it is a anti tumor antibiotic that is degraded by aminohydrolase

SE: PULMONARY FIBROSIS

43
Q 
Hydroxyurea
-MOA:
Asparaginase
MOA: 
Arsenic Trioxide: antitumor
MOA:
A

Hydroxyurea: Inhibits ribonucleotide reductase, stops cells in S phase

Asparaginase: Inhibit protien synthesis

Arsenic Trioxide: antitumor
just know it is avb

44
Q

Vorinostat
MOA:
SE

A

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

45
Q

➢Monoclonal antibodies (MoABs)

A

➢Monoclonal antibodies (MoABs)

46
Q

-
-

A
  • Rituximab
  • Ibritumomab tiuxetan
  • Tositumomab
47
Q 
Rituximab
moa: 
only used for:
Uses:
SE:
A

• 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
Q

Ibritumomab tiuxetan
MOA:
USE:
SE:

A
  • CD20- can be used if Rituximab fails
  • Use: non-hogdkin lymphoma
  • SE: anaphylaxis, thrombocytopenia, neotropenia
49
Q

Tositumomab

A

similar to Ibritumomab tiuxetan

50
Q

Alemtuzumab
MOA:
Used for:
SE:

A

MOA: Binds to CH 53

B cell lymphocytic leukemia

Black box: Hematologic toxicity and opportunistic infections

51
Q

➢Growth factor receptor and ligand targeting

A

➢Growth factor receptor and ligand targeting

52
Q

➢Growth factor receptor and ligand targeting
what does it do:

-
-
-
-
-
-
A

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
Q

Cetuximab and Panitumumab
MOA:
USES:
SE:

A
  • Chimeric MoAB that binds to EGFR (HER-1)
  • Use: metastaic colorectal, neck , head
  • SE: N/V/D/C, abdominal pain, sudden death
54
Q

Tradtuzumab
MOA:
USES:
SE:

A
  • Humanized MoAB bind HER-2
  • Use: metstatic breast (alone or with paxlitaxel)
  • SE: cardiac failure (esp. if given with anthacylines)
55
Q

Erlotinib
MOA:
SE:

A
  • EGFR-tyrosine kinase inhibitor

* SE: rash, diarrhea- premeditate with steroids and antihistamines

56
Q

Lapatinib
MOA:
SE

A
  • Kinase inhibitor of EGFR and HER-2

* SE: diarrhea, hepatoxicity, rash, QT prolongation

57
Q 
Bevacizumab
MOA: 
SE
-
-
A
  • 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
Q

Sunitinib and Sorafenib
MOA:
SE:

A
  • Inhibits VEGFR-2 and platelet derived growth receptor

* SE: CHF-sunitinib and hand foot syndrome –soradenib

Clinical Medication: HEENT (39 decks)

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