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Chemotherapy drugs Flashcards

1
Q

How do cancers differ?

A
  • based on:
    • phenotype
    • aggressiveness
    • responsiveness to drugs
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2
Q

How are cancers treated? (3)

A
  • surgery
  • radiation
  • pharmacologic agents
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3
Q

What are the different response criterias that the cancer can have to the treatment?

A
  • Cure
    • entirely free of disease, and has the same life expectancy as a cancer free individual
  • complete response
    • complete disappearance of all cancer without evidence of new disease for at least one month
  • Partial response
    • 50% decrease in tumor size or other objective markers
  • Stable disease
    • A patient whose tumor size neither grows nor shrinks by more than 25%
  • Progression
    • 25% increase in tumor size or development of new lesions while on treatment
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4
Q

What is the cycle the cell goes through from one mitotic division to the next?

A
  • M (Mitosis)- 1.5-2 hr
    • cell division
  • G0 (resting)-
    • cells not committed to cell division
  • G1 (postmitotic)
    • enzymes necessary for DNA synthesis are made
  • S (synthesis)- 10-20 hours
    • cell doubles its DNA
  • G2 (premitotic)- 2-10 hours
    • specialized proteins and RNA synthesis
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5
Q

What are the 7 classes of chemotherapy drugs?

A
  • Alkylating agents
  • antimetabolites
  • antitumor antibiotics
  • topoisomerase inhibitors
  • tubulin binding drugs
  • signal transduction modifiers
  • Immunotherapy ( new approach that preserves normal cells and has very different adverse effects compared to traditional chemotherapy)
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6
Q

Why are anti cancer drugs given in combination?

A

to delay drug resistance, decrease toxicity, and improve cancer cell death

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7
Q

Toxicity Summary (side effects) of chemotherapy drugs

A
  • *tissues with high number of proliferating cells
  • Bone marrow suppression
    • leukopenia, thrombocytopenia, anemia
    • may require additional pre-op labs
  • Gi tract damage
    • N/V- electrolyte disturbances, hypovolemia
  • Alopecia
  • mucosal unceration
  • Infertility, teratogenic effects
  • urinary stones
  • extravasation
  • end organ damage and hepatic enzyme induction
    • consider altered response to anesthetics
    • promotion of secondary cancers
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8
Q

What is extravasation?

Symptoms?

A
  • the escape of a chemotherapy drug into the extravascular space, either by leakage from a vessel or by direct infiltration
  • symptoms:
    • pain
    • burning
    • swelling
    • redness
    • lack of blood return
    • may require skin graft/surgery
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9
Q

Which chemotherapies most commonly extravate?

A

anthracyclines

vinca alkaloids

taxanes

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10
Q

What are the Alkylating agents?

(3)

A
  • Nitrogen mustards ( Cyclophosphamide)
  • Nitrosureas (Carmustine)
  • Platinum compounds (Cisplatin, Carboplatin)
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11
Q

What is the MOA of Alkylating Agents?

A
  • Reactive alkyl groups form covalent bonds with nucleotide bases in DNA, RNA
    • Ex: Crosslinks guanines on the DNA helix, makeing DNA “stuck” in supercoil
    • if DNA cannot uncoil, it cannot replicate
    • Disrupts DNA synthesis and cell division
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12
Q

What are the toxicities of Alkylating agents?

A
  • Bone marrow suppression
  • mucositis
  • skeletal muscle weakness
  • sz
  • pneumonitis and pulmonary fibrosis
  • pericarditis and pericardial effusion
  • Inappropriate ADH secretion (water toxicity)
  • uric acid induced nephropathy
  • impaired pseudocholinesterase activity (2-3 weeks)
  • ** the incidence of these toxicities varies among the different agents
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13
Q

Which alkylating agent has similar pulmonary toxicity to bleomycin?

A

Carmustine- pulmonary toxicity similar to bleomycin 20-30% with mortality 24-90%

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14
Q

What are the toxicities of Platinum Compounds?

A
  • Nephrotoxicity
    • cumulative and dose limiting- K and Mg wasting & decreased GFR
    • hydration/supplemental electrolytes
    • may be on lasix/mannitol to prevent
    • hypomagnesium common (affects NMB sensitivity, cardiac dysrhythmia)
  • Peripheral neuropathy
    • presents as tingling around mouth, fingers, toes
    • avoid cold contact
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15
Q

Which Alkylating agent is dose limited because of nephrotoxicity?

A

cisplatin

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16
Q

Which alkylating agent is dose limited for peripheral neuropathy?

A

oxaliplatin

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17
Q

What are the Antimetabolite drugs? (3)

A
  • Folate Analogues- Methyltrexate
  • Pyrimidine analogues- Fluorouracil
  • Purine analogues- Mercaptopurine
18
Q

What is the MOA of Antimetabolites?

A
  • Antimetabolites are structural analogues of natural metabolites, such as nucleic acid synthesis inhibitors
  • They ultimately inhibit replication or repair of DNA by one of the following mechanisms
    • Direct inhibition of enzymes needed for DNA replication or repair
    • incorporation of the antimetabolite, which is structurally similar to nucleotites, directly into DNA
19
Q

What is the Folic acid Analog?

MOA?

A
  • Methotrexate
  • Folate must be taken up by the cell and reduced to FH2, then FH4 by dihydrofolate reductase in order to produce nucleosides
  • Methotrexate has a higher affinity for dihydrofolate reductase than FH2, thereby preventing its reduction to FH4
20
Q

What are the toxicities for Methotrexate?

A
  • Pulmonary fibrosis (8%) and/or non cardiogenic pulmonary edema
  • Neutropenia and thrombocytopenia
  • mucositis and GI ulceration
    • GI perforation possible
  • Renal toxicity (10%)
    • alkalinize urine and hydrate
  • Hepatic toxicity
    • often reversible
21
Q

What is the common Pyrimidine analog?

MOA?

A
  • Fluorouracil (5-FU)
  • Inhibits thymidylate synthetase which inhibits nucleotide production, which inhibits DNA synthesis
22
Q

What are the toxicities of Fluorouracil?

A
  • increased risk of MI for 1 week after administration
  • myelosuppression (leukopenia, thrombocytopenia, and anemia)
  • alopecia
  • neurologic defects
    • ataxia (cerebellum)
  • GI toxicity
    • d/c if stomatitis/mucousitis/diarrhea
    • pt at risk for GI ulceration and perforation
  • Hand-and-foot syndrome
    • tingling, redness, burning, flaking, swelling and blistering of the palms and soles
23
Q

What are the Topoisomerase inhibitors? (2)

MOA?

A
  • Anthracyclines (Doxorubicin, Daunorubicin)
  • Non-anthracyclines (Bleomycin)
  • Inhibition of topoisomerase I and II and intercalation with DNA, causing double stranded DNA to break and inhibits DNA and RNA synthesis
  • Makes hydroxyl free radicals
    • free radical production is greatly stimulated by the interaction of doxorubicin with iron
24
Q

Topoisomerase inhibitors inhibit topoisomeraste I and II. What does Topoisomerase II do?

A
  • relaxes the DNA supercoil and breaks the strand for replication
  • also critical to the DNA strand being put back together
25
Q

What are the Antracyclines drugs? (2)

What are their toxicities?

A
  • Bone marrow suppression
  • Red/orange color urine and sweat
  • cardiotoxicity
    • may be more sensitive to cardiac depressive side effects of anesthetics even if normal resting echo
    • free radical production causes myocardial damage
    • Acute (10%): tachycardia, arrhythmias
    • chronic (2% with 60% fatality): severe cardiomyopathy/CHF
26
Q

What are some protective therapies that can be used agains the cardiotoxicity of antrhracyclines?

A
  • Dexrazoxane- prevents free radical formation
  • Ace inhibitors?
27
Q

What is the Water Soluble Glycopeptide?

MOA?

A
  • Bleomycin
  • Topoisomerase inhibition + binds DNA and chelates iron leading to the formation of free radicals that cause single and double strand DNA breaks
28
Q

Explain the pulmonary toxicity related to Bleomycin

A
  • 4% (1% life threatening)
  • lungs take up high concentrations of drug and lack hydroloase enxyme to inactivate bleomycin
  • Risk increases with: increased cumulative dosing, age, chest radiation, pulmonary co-morbidity, oxygen exposure, other chemotherapy drugs, genetics
  • discontinue if: dry cough, dyspnea, tachypnea and infiltrates on CXR
  • may progress to pulmonary fibrosis and death
  • decreased diffusion capacity
  • keep FiO2 concentration at or below 30% during anesthesia if possible
29
Q

Which cancer patients might have a hypersensitivity reaction to Bleomycin?

A
  • Lymphoma pts
    • fever, chills, confusion, hypotension, wheezing
  • test dose recommended for lymphoma pts before standard doses
30
Q

There are two types of Tubulin-binding drugs. Which are the ones that prevent assembly?

MOA?

A
  • Vinca Alkyloids
    • Vincristine, Vinblastine, Vinorelbine
  • Binds to tubulin to block microtubules assembly, preventing polymerization of dimers
  • cell division is arrested during metaphase and leads to apoptosis
31
Q

What are the toxicities of Tubulin Binding drugs?

A
  • Vincristine
    • very little bone marrow suppression
    • hyponatremia (inappropriate ADH secretion)
    • peripheral neuropathy via damate to neurotubules in almost 100% of pts
      • gets worse with surgery/anesthesia
  • Vinblastine/Vinorelbine
    • bone marrow suppression
32
Q

What are some of the peripheral neuropathy problems seen with Vincristine?

A
  • Sensory loss, weakness, autonomic dysfunction
    • constipation, sinus tachycardia, dry mouth, urinary retention, reflex loss, laryngeal and extraocular dysfunction
  • usually slowly resolves after treatment
  • uncertain safety with regional anesthesia
    • reduce LA doses
    • use ultrasound guidance to avoid intraneural injection
    • no vasoconstrictor additives
33
Q

What are the Tubulin-Binding drugs that prevent disassembly?

MOA?

A
  • Taxanes- Paclitaxel, Docetaxel
  • Stabilizes microtubule bundles and prevents disassembly (by preventing depolymerzation), inhibiting cell devision and producing apoptosis
34
Q

What are the toxicities of Taxanes?

A
  • Peripheral neuropathy- especially hands and feet
  • nuscle and joint pain
  • hypersensitivity reactions (25-30% of pts)
  • cardiac
    • bradycardia, heart block, MI
  • myelosuppression
    • neutropenia develops in almost all pts
      • 1% sepsis related death
      • 11% if liver disease present
35
Q

What are the Signal transduction Modulators?

MOA?

A
  • Antiestrogens (Tamoxifen)
  • Antiandrogens (Flutamide)
  • Disrupt aberrant growth factor:receptor interactions in cancerous cells preventing intracellular signaling that leads to cellular proliferation and survival
  • or target mutated receptors that give a signal to proliferate even without any growth factors bound
36
Q

Tamoxifen is an anti-hormone drug. How does it work?

Side effects?

A
  • acts as an estrogen antagonist in certain cells (breast and ovarian) and and estrogen agonist in other cells (uterus, liver, bone)
  • Side effects related to agonist activity:
    • DVT, endometrial cancer, menopausal symptoms, increased bone density (beneficial), andimproves serum cholesterol panel (beneficial)
37
Q

What are the two Signal Transduction Modulators?

A
  • Monoclonal Antibodies: target specific proteins expressed on immune cells, or that promote pro-survival signaling in cancer cells
    • flu like symptoms common
  • Aromatase Inhibitors: enzyme that converts androgens to estrone peripherally
    • helps to decrease estrone levels in some post-menopausal women with breast ca
38
Q

What is Gleevec (Imantinib)?

A
  • A Monoclonal antibody
  • tyrosine kinase inhibitor/antibody that can treat cancer when tyrosine kinase is mutated to always be “on”
39
Q

What is the Anti-angiogenic?

A
  • Bevacizumab (trade name Avastin)
  • Monoclonal antibody that blocks angiogenesis
  • Inhibits vascular endothelial growth factor-A
  • Without vascularization, tumors cannot survive
40
Q

What are some of the other agents? (2)

A
  • Immunotherapy- flu like symptoms
    • dendritic cells loaded with tumor lysate
    • vaccines targeting tumor-specif epitopes
    • chimeric antigen receptor Tcells
    • autoimmune reactions are major concert with these approaches
  • Biologically directed therapy
    • Engineered viruses
41
Q

What are some general guidelines for chemotherapy?

A
  • these drugs are mutagenic, carcinogenic, and teratogenic
    • protect yourself!
    • avoid contact with the skin, eyes, and mucous membranes
    • follow hospital protocols

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