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Advanced Pharm- Test 1 > Chemotherapeutic > Flashcards

Chemotherapeutic Flashcards

1
Q

What are characteristics of cancer cells?

A
  • Persistent proliferation
    • unresponsive to feedback mechanisms that regulate cells
  • Invasive growth/formation of mets
    • malignant cells free of constraints that inhibit invasive growth–> cells of solid tumor can penetrate adjacent tissues and spread of cancer
  • immortality
    • cancer cells undergo endless division
    • due to telomerase
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2
Q

What are the 6 hallmarks of cancer cells?

A
  1. Sustaining proliferative signaling
  2. evading growth supressors
  3. activation invasion and metastasis
  4. enabling replicative immortality
  5. inducing angiogenesis
  6. resisting cell death
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3
Q

How do cancers differ?

A

Based on phenotye, aggressiveness, responsiveness to drugs

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4
Q

What 3 ways are cancers treated?

A

surgery

radiation

pharmacologic agents

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5
Q

How does chemotherapy kill cancers (what order?)

A

1st order kinetic matter, generally kill 50% proportion

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6
Q

What is palliative chemo curve representative of?

A

Treatment of a terminal Ca that does not have a cure.

More for symptom management

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7
Q

WHat is adjuvant chemo?

A

Used after surgery to minimize tumor regrowth

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8
Q

What needs to happen in order to reach a cure of cancer

A

Entirely free of disaes, and has same life expectancy as a cancer free individual

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9
Q

What is a complete resposne from chemo?

A

Complete disappearance of all cancer without evidence of new disease for at least 1 month

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10
Q

What is a partial response from chemo?

A

50% decrease in tumor size or other objective markers

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11
Q

What is stable disease?

A

A patient whose tumor size neither grows nor shrinkgs by more than 25%

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12
Q

What is tumor progression?

A

25% increase in tumor size or devleopment of new lesions while on tx

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13
Q

Order of cell cycle events?

A

G0–> G1–> S–> G2–> Mitosis–> G0

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14
Q

What is mitosis?

A

cell division

time span 1/2-1 hour (need high concentration of drugs)

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15
Q

What is G0?

A

Resting

cells not committed to cell divison

(all neurons in resting)

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16
Q

What is G1?

A

Postmitotic

enzymes necessary for DNA synthesis are made

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17
Q

What is S phase?

A

Synthesis

10-20hours

cell doubles its DNA

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18
Q

What is G2?

A

Premitotic phase

2-10 hours

Specialized proteins and RNA synthesis

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19
Q

What are 7 calsses of chemotherapy/antineoplastic drugs?

A
  • Alkylating agents
  • antimetabolites
  • antitumor antibiotics
  • topoisomerase inhibitors
  • tubulin binding drugs
  • signal transduciton modifiers
  • immunotherapy**< new approach
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20
Q

Why are chemotherapy drugs combined?

A

Combination therapy preferred in order to:

  • delay drug resistance
  • decrease toxicity
  • improve cancer cell death
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21
Q

What is a broad summary of toxicity from chemo drugs?

A
  • Bone marrow suppressio (leukopenia, thrombocytopenia, anemia
    • iatrogenic infection
    • may need extra preop lab testing
  • GI tract damage
  • N/V
    • electolyte distubance, hypovolemia
  • Aloplecia
  • mucosal ulceration
    • avoid using oral airways, LMA, esophageal stethoscope
  • Reproductive
    • infertility, teratogenic (1st semester, risk highest)
  • Urinary stones (uric acid crystals)
    • Formed from breakdown DNA following cell death
  • Extravasation: local injury
  • End organ damage and hepatic enzyme induction
    • ​consider altered respones to anesthetics
  • Promotion of secondary cancers
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22
Q

What are the most common chemo drugs to cause extravasation?

A
  1. Anthracyclines
  2. Vinca alkaloids
  3. Taxanes
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23
Q

Symptoms of extravasation?

A
  • Pain
  • burning
  • swelling
  • redness
  • lack of blood return
  • may require skin grafting/surgery
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24
Q

What are some examples of aklylating agents?

A
  • Nitrogen mustards
    • Cyclophosphamide
  • Nitrosureas
    • Carmustine
  • Platinum compounds
    • Cisplatin
    • Carboplatin
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25
Q

What is the MOA of akylating agents

A
  • Reactive alkyl groups form covalent bonds with nucleotide bases in DNA/RNA
    • Makes DNA be stuck in super coil
    • if it cannot uncoil, can’t replicate
    • disrupts DNA synthesis and cell division–> miscoding and strand breaks
26
Q

Common toxicities in alkylating agents?

A
  • Bone marrow suppression- greatest concern
    • neutropenia, hemolytic anemia, thrombocytopenia
  • mucositis
  • skeletal muscle weakness
  • sz
  • pneumonitis and pulm fibrosis
    • carmustine pulm toxicity similar to bleomycin 20-30% with mortality 24-90%
  • Pericarditis and pericardial effusion
  • inappropriate ADH secretion (Water toxicity)
  • uric acid induced nephropathy
  • impaired pseudocholinesterase activity (2-3 weeks)
    • caution succ, mivacurium, esmolol, remi
27
Q

What are the platinum compounds and toxicities?

A

Cisplatin, carboplatin

  • Nephrotoxicity- cumulative and dose limiting; potassium and mag wasting and decreased GFR
    • dose limiting toxicity for cisplatin
    • hydration/supplemental electolytes
    • may be on furosemide/mannitol to prevent
    • hypomagnesium common
      • can also impact NM function
  • Peripheral neuropathy
    • dose limited toxicity fo oxaliplatin
    • presents as tingling around mouth, fingers, toes
    • avoid cold contact
28
Q

What are examples of antimetabolites?

A
  • Folate analogues
    • Methotrexate
  • Pyrimidine analogues
    • Fluorouracil (5FU)
  • Purine analogues
    • Mercaptopurine
29
Q

What is MOA of antimetabolites?

A
  • Strucutral analogues of natural metabolites (nucleic acid synthesis inhibitors)
    • inhibit replication/repair of DNA by:
      • Direct inhibition of enzymes needed for repair
      • Incorporation of antimetabolite, directly into DNA
30
Q

What is methotrexate’s target of action?

A
  • Folate must be taken up by cell and reduced to FH2–> FH4 by dihydrofolate reductase in order to produce nucleosides
  • Methotrexate has higher affinity for dihydrofolate reductase than does FH2, thereby preventing its reduciton to FH4
31
Q

Toxicities of methotrexate?

A
  • Pulmonary fibrosis (8%) and /or noncardiogenic pulmonary edema
  • neutropenia and thrombocytopenia
  • mucositis and GI ulceration
    • GI perf possible
  • Renal toxicity (10%)
    • alkalinize urine and hydrate
  • Hepatic toxicity
    • often reversible
32
Q

What is MOA of fluorouracil? Class of drug?

A
  • Class= pyrimidine analog (antimetabolite)
  • MOA- inhibits thymidylate synthetase–> inhibits nucleotide production–> inhibits DNA synthesis
33
Q

Toxicity associated with fluorouracil?

A
  • Incrased risk of MI for 1 week after admin
    • Low threshold for EKG, echo, beta blocker, art line
  • Myelosuppression (leukopenia, thrombocytopenia, and anemia)
  • alopecia
  • neuro defects
    • ataxia (cerebellum)
  • GI toxicity (d/c if stomatitis/mucositis/diarrhea)
    • Pt at risk for GI ulceration and perf
  • Hand and foot syndrome
    • sx- tingling, redness, burning, flaking, swelling and blistering of palms/soles
34
Q

What are examples of topoisomerase inhibitors?

A
  • Anthracyclines (Doxorubucin, daunorubicin)
  • Non-anthracyclines (Bleomycin)
35
Q

What is MOA of topoisomerase inhibitors?

A
  • Inhibition of topoisomerase I and II and intercalation of DNA–> double strand DNA breaks and inhibition of DNA& RNA synthesis (replication)
    • topoisomerase II relaxes DNA supercoil and breaks strand for replication
    • topoisomerase II also critical to the DAN strande being put back togheter
  • ​Generation of hydroxyl free radicals
    • oxidative damage
36
Q

What are some relatively minor s/e of anthracyclines?

A
  • Bone marrow suppression (anemia, thrombocytopenia, low WBC 70% pt)
  • Red/orange color of urine/swear
37
Q

What is connection b/w cardiotoxicity and doxorubicin?

A
  • May be sensitive to cardiac depressive s/e of anesthetics even in normal resting echo
  • free radical produciton causes myocardial damage
  • Acute (10%): tachycardia and arrhythmias
    • transiet and rare
      • ekg and acute EF reduciton
      • usually lasts 1-2 mon
  • Chornic (2% but with 60% fatality)SEVERE cmp/CHF
    • related to cumulative dose
    • protective therapies
38
Q

What are some protective therapies for doxorubicin?

A
  • Dexrazoxane
    • prevents free radical formation
    • ACE inhibitors
39
Q

When would etomidate vs propofol be perferred in regards to cardiac dysfunction?

A
  • If vasculature issue only, can still use propofol because myocardium hasn’t been affected
  • once myocardium affected, then etomidate is preferred
  • can mix etomidate/propofol or give propofol very slowly and mitigate some effects
  • If RSI and can’t go slow, then etomidate preferred
40
Q

What is MOA of bleomycin? Class?

A

Class= water soluble glycopeptides

  • MOA- Topoisomerase inhibition and binds DNA and chelates iron leading to formation of free radicals that cause single and double strand DNA breaks
41
Q

Main toxicity for bleomycin?

A

PUlmonary toxicity 4% (1% life threatening)

  • Lungs take up high concentration of drug and lack hydrolase enzyme to inactivate bleomycin
  • increased risk with:
    • increased cumulative dosing
    • age
    • chest radiation
    • pulmonary co morbidities
    • oxygen exposure
    • other chemo drugs
    • genetics
  • D/C agent at 1 st sign of dry cough, dyspnea, tachypnea and infiltrates on CXR
    • may progress–> pulm fibrosis–> severe fibrosis–> death
  • decreased diffusion capacity
  • KEEP FIO2 CONCENTRAITON AT OR BELOW 30% DURING ANESTHESIA IF POSSIBLE
42
Q

What can bleomycin cause r/t hypersensitivity?

A
  • Lymphoma pt; fever, chills, confusion, hypotension and wheezing
  • test dose recommended for lymphoma pts before standard doses
43
Q

Is myelosuppression seen with bleomycin?

A

No!

44
Q

What are examples of vinca alkyloids?

A
  • (vincristine, vinblastine, binorelbine)
45
Q

What is MOA of vinca akyloids??

A

aka tubulin-binding drugs

  • binds to tubulin (microtubule dimers) to block microtubules assembly (preventing polymerization (aka forming) of dimers)–> cell division arrested during metaphase –> apoptosis
46
Q

Side effects of vincristine?

(Class of vincristine?)

A

Vincristine= vinka alkaloid (tubulin binding drugs)

  • Very little bone marrow suppression: good in combo therapy
  • hyponatremia (inappropriate ADH secretion)
  • Peripheral neuropathy via damage to neurotubules in almost 100% of aptients (reported to get wrose wiht sx/anesthesia)
47
Q

What are some concerns with peripheral neuorpathy with vincristine?

A
  • sensory loss,
  • weakenss,
  • autonomic dysfunction
    • (constipation, ST, dry mouth, urinary retention, reflex lsos, cranial nerve– laryngeala and extraocular dysfunction)
  • usually resolves after treamtent
  • uncertain w/ regional
    • reduce local doses
    • use US guidance
    • no vasoconstrictors added
48
Q

What is main side effect with vinblastine?

A

bone marrow suppression

49
Q

What are examples of taxanes?

A
  • Taxanes
    • Paclitaxel
    • Docetaxel
50
Q

What is MOA of taxanes??

A

(Taxanes= tubulin-binding drugs)

  • stabilizes microtubule bundles and prevents disassembly (prevents depolymerization)–> inhibitng cell division and producing apoptosis
  • (kind of opposite from vincristine)
51
Q

What are some toxicities associated with taxanes?

A
  • Peripheral neuropathy (esp hand and feet)
  • muscle and joint pain
  • hypersentiivity reactions 25-30% of pt
  • Cardiaac
    • bradycardia, heart block, MI
  • Myelosuppression
    • neutropenia develops in almost all pt
    • 1% sepsis related deaths (11% if liver dx)
52
Q

What are signal transduciton modulators?

A

Antiestrogens (tamoxifen)

antiandrogens (flutamide)

Monoclonal antibodies

aromatase inhibitors

53
Q

MOA of antiestogens/antiandrogens?

A
  • Disrupt aberrant growth factor: receptor interactions in cancerous cells preventing intracellular signaling that leads to cellular proliferation and survivial OR target mutated receptors that give a signal to proliferate even without any growth factors bound
54
Q

How do anti-hormone drugs work?

A
  • Work if the cancer cells expresses the particular receptor (and in proportion to the level of receptor expression)
    • Tamoxifen- act as estrogen antagonist in certain cells (Breast and ovarian) and an estrogen agonist in other cells (uterus, liver, bone)
      • s/e related to agonist activity : DVT, endometrial ca, menopausal symptoms, increased bone density (beneficial) and improves serum cholesterol panel (beneficial)
    • Antiadnrogens (prostate)- gynecomastia, hot flasehs, muscle weakness and osteoporsis
      • Flutamide- methemoglobinemia
55
Q

What is hte MOA of monoclonal ab?

A
  • Antibodies target specific proteins expresssed on immune cells, or that promote pro-survivial signaling in Ca cells
56
Q

What is Gleevac?

A

Gleevac (Imantinib) is a tyrosine kinase inhibitor/antibody that can treat cancer when tyrosin kinase is mutated to be always on (BCR-Abl in chornic myelogenous leukemia)

  • amazing drug that seems to cure problem
  • can cause flu like symptoms
  • used in autoimmune as well
57
Q

What are aromatase inhibitors MOA?

A
  • Aromatase is an enzyme complex that converts androgens to estrone peripherally
  • Helpful to decrease estrone levels in some post-menopausal women with breast Ca
58
Q

What is bevacizumab?

A
  • Anti-angiogenic
  • Trade name: avastin
  • Monoclonal antibody that blocks angiogenesis
  • Inhibits vascular endothelial growth factor-A
  • without vascularization, tumors cannot survive
59
Q

What is the basis for how immunotherapy works in cancer? Major s/e?

A
  • Dendritic cells loaded with tumor lysate, the use of vaccines targeting tumor-sepcific epitopes, the generation of chimeric antigen receptor T cells and checkpoint inhibitors
  • autoimmune reaction major concern with these approches
  • flu like sympetomes
  • Biologically directed therapy
    • ​engineered viruses (oncolytic viral therapy)
60
Q

General counseling guidliens for chemotherapy?

A
  • These drugs are often mutagenic, carcinogenic and tertogenic: protect wourself if you are caring for someone still eliminating chemo!
    • avoid contact with skin, eyes and mucous membrane
    • follow hospital protocols

Advanced Pharm- Test 1 (5 decks)

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