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NURA 671 Advanced Pharmacology > Cancer Pharmacology > Flashcards

Cancer Pharmacology Flashcards

1
Q

six hallmarks of cancer

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

complete response

A

complete disappearance of all CA w/o evidence of new disease for at least one month

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3
Q

partial response

A

50% decrease in tumor size or other objective markers

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4
Q

stable disease

A

a patient whose tumor size neither grows nor shrinks by more than 25%

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5
Q

progression

A

25% increase in tumor size or development of new lesions while on treatment

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6
Q

cure

A

entirely free of disease, and has the same life expectancy as a CA free individual

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7
Q

cell cycle: M

A

mitosis (1/2 - 1 hour)

cell division

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8
Q

cell cycle: G0

A

resting

cells not committed to cell division

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9
Q

cell cycle: G1

A

postmitotic

enzymes necessary for DNA synthesis are made

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10
Q

cell cycle: S

A

synthesis (10-20 hr)

cell doubles its DNA

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11
Q

cell cycle: G2

A

premitotic (2-10 hr)

specialized proteins and RNA synthesis

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12
Q

tox sum: bone marrow suppression (leukopenia, thrombocytopenia, anemia)

A
  • iatrogenic infection

- may require additional pre-op lab testing; blood products

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13
Q

tox sum: GI tract damage

A

cells lining GI tract turn over rapidly

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14
Q

tox sum: N/V

A
  • consider how they’ll tolerate anesthesia –> aggressive antiemetic plan, inquire what works for them
  • electrolyte disturbances, hypovolemia
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15
Q

tox sum: mucosal ulceration

A

consider avoiding oral airways, LMAs, esophageal stethoscope

sores, pain risk of bleeding

may not be eating/drinking–>Again, fluid/electrolyte status

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16
Q

tox sum: reproductive

A

baby –> highly proliferating

infertility, teratogenic

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17
Q

tox sum: urinary stones

A

uric acid crystals

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18
Q

tox sum: extravasation, s/s, most common culprits

A

local injury

pain, burning, swelling, redness, lack of blood return, may require skin grafting, sx

anthracyclines, vinka alkaloids, taxanes

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19
Q

tox sum: end organ damage and hepatic enzyme induction

A

consider altered responses to anesthetics, additional pre op testing and monitoring requirements, etc

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20
Q

Alkylating agents

A 
nitrogen mustards (cyclophosphamide)
nitrosureas (carmustine)
platinum compounds (cisplatin, carboplatin)
21
Q

alkylating agents: MOA

A

-reactive alkyl groups form covalent bonds with nucleotide bases in DNA, RNA

  • –for example, crosslinks w/ guanines on DNA helix, thereby making DNA “stuck” in its super coil
  • —if dna cannot uncoil, It cannot replicate
  • —-disrupts dna synthesis and cell division –> miscoding, and strand breaks

EXCEPTION: platinating drugs have no alkyl group
–dif structural elements (platinum atom, two amines, two chlorides)

22
Q

alkylating agents: toxicities and anes considerations

A
  • bone marrow suppression (CBC)
  • mucositis (MINDFUL OF AW AND BLEEDING)
  • skeletal muscle weakness (TRY AND AVOID NMB)
  • seizures
  • pneumonitis and pulmonary fibrosis - CARMUSTINE PUL TOX SIMILAR TO BLEOMYCIN 20-30% WITH MORTALITY 24-90% - (THOROUGH RESP WORKUP) - may be difficult to distinguish if exercise tolerance is low or SOB because of anemia/skeletal muscle weakness
  • pericarditis and pericardial effusion
  • inappropriate ADH secretion (water toxicity) - (FLUID/ELECTROLYTE BALANCE)
  • uric acid neuropathy (DNA released from dying cells)
  • impaired pseudocholinesterase activity (2-3 wks after)
  • —CAUTION WITH SUCC, maybe use lowest dose of roc that you can get away with so that you can reverse with sugammadex
23
Q

Platinum compounds: toxicities

A

NEPHROTOXICITY (w/ platinum > alkylating agents)

  • cumulative and dose limiting
  • potassium and magnesium wasting & decrease GFR
  • -dose limiting toxicity for CISPLASTIN
  • -HYDRATION/SUPPLEMENTAL ELECTROLYTES/LABS
  • -may be on furosemide and/or mannitor
  • -hypomagnesemia common
  • —-check level!!!
  • —-NMB SENSITIVITY
  • —-CARDIAC DYSRHYTHMIAS

PERIPHERAL NEUROPATHY

  • dose limiting toxicity for oxaliplatin
  • presents as tingling around mouth, fingers, toes
  • avoid cold contact
  • DOCUMENT PRE EXISTING DEFICITS - make sure unchanged at end of case
24
Q

Antimetabolites: Agents

A 
Folate analogues (methotrexate)
pyrimidine analogues (fluorouracil)
purine analogues (mercaptopurine)
25
Q

Antimetabolites: MOA

A

Structural analogues of natural metabolites (nucleic acid synthesis inhibitors)

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 nucleotides, directly into DNA
26
Q

Methotrexate: Class, MOA

A

folic acid analogue

  • 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 does fh2, thereby preventing its reduction to fh4
27
Q

Methotrexate: toxicities and anes considerations

A
  • pulmonary fibrosis and/or noncardiogenic pulm edema (FULL RESPIRATORY WORK UP)
  • neutropenia and thrombocytopenia (CBC)
  • mucositis and GI ulceration (PAIN, AVOID ORAL AW, MINDFUL OF BLEEDING)
  • renal toxicity (10%) (ALKALINIZE URINE AND HYDRATE)
  • hepatic toxicity (often reversible) (LFTS, JAUNDICE)
28
Q

Fluorouracil (5-FU): Class, MOA

A

pyrimidine analogues

MOA: inhibits thymidylate synthetase –>inhibits nucleotide production –> inhibits DNA synthesis

29
Q

Fluorouracil (5-FU): toxicities and anes. considerations

A
  • inc risk of MI for 1 wk after administration (AVOID SX IF POSSIBLE)
  • –AVOID TACHYCARDIA, MAINTAIN DBP, MORE THOROUGH CV WORK IF YOU HAVE TO TAKE THEM FOR SX)
  • myelosuppression - (CBC, LOWER THRESHOLD FOR BLOOD ADMIN)
  • alopecia
  • neurologic defects - ataxia (cerebellum)
  • GI tox (pts at risk for GI ulceration and perforation) (CAREFUL AW CONSIDERATION, FLUID/ELEC BALANCE)
  • hand and foot syndrome
  • -tingling, redness, burning, flaking, swelling and blistering of the palms and soles (DOCUMENT PRE OP)
30
Q

Topoisomerase inhibitors: Agents

A 
Anthracyclines (doxorubicin, daunorubicin)
non anthracyclines (bleomycin)
31
Q

topoisomerase inhibitors: MOA

A

inhibition of topoisomerase I and II and intercalation with DNA –> doublestrand DNA breaks and inhibition of DNA and RNA synthesis (replication)

  • topoisomerase II relaxes the DNA supercoil and breaks the strand for replication
  • topoisomerase II also critical to the DNA strand being put back together

generation of hydroxyl free radicals (free radical production is greatly stimulated by the interaction of doxorubicin with iron)

32
Q

Anthracyclines: Agents + toxicities

A

doxorubicin, daunorubicin

  • bone marrow suppression (low WBC 70% of patients)(CBC)
  • red/orange color (urine and sweat)
  • CARDIOTOXICITY (free radical production causes mycocardial damage)

related cumulative dose

CONSIDER THOROUGH CV WORKUP NO MATTER HOW FAR OUT THEY ARE

  • -always at risk for HF
  • -HEAVY CONSIDERATION FOR A LINE
  • -consider etomidate?
  • -conservative approach related to cardiac depression
  • -slow titration of anesthetics, avoid abrupt boluses

protective therapies: dexrazoxone (prevents free radical formation), ace inhibitors

33
Q

Bleomycin: Class + MOA

A

topoisomerase inhibitor; water soluble glycopeptides

MOA: topoisomerase inhibition + binds DNA and chelates iron leading to the formation of free radicals that cause single and doublestranded DNA breaks.

34
Q

Bleomycin: hypersensitivity

A

lymphoma pts: fever, chills, confusion, hypotension, and wheezing

test dose recommended for lymphoma pts before standard doses

35
Q

Bleomycin: PULM TOXICITY

A
  • lungs take up high concentrations of drug and lack hydrolase enzyme to inactivate bleomycin
  • inc risk with cumulative dosing, age, chest radiation, pulmonary comorbidity, o2 exposure, other chemo drugs, genetics
  • dec diffusion capacity (reduced ability to eliminate CO2)
  • KEEP FIO2 CONC AT OR BELOW 30% DURING ANESTHESIA IF POSSIBLE

—myelosuppression rarely seen—

36
Q

Tubulin-binding drugs: Agents

A

Vinka alkaloids (vincristine, vinblastine, vinorelbine)

37
Q

tubulin-binding drugs: MOA

A

binds to tubulin (microtubule dimers) to block microtubules assembly (preventing polymerization of dimers) –> cell division arrested during metaphase (i.e. mitosis) –> apoptosis

38
Q

vincristine: Class + toxicities

A

tubulin binding drug; vinka alkaloid

  • very little bone marrow suppression
  • hyponatremia (inappropriate ADH secretion) (FLUID/ELECTROLYTE BALANCE)
  • PERIPHERAL NEUROPATHY via damage to neurotubules in almost 100% of pts (reported to get worse with surgery/anesthesia (VIGILANCE WITH POSITIONING, BP MANAGEMENT (GOOD BLOOD FLOW TO PERFUSE EXTREMITIES))
  • –sensory loss, weakness, autonomic dysfunction (HEMODYNAMIC LABILITY, constipation, sinus tach, dry mouth, urinary retention, reflex loss, cranial nerve - laryngeal and extraocular dysfunction)
39
Q

Vincristine + regional anesthesia: considerations

A

UNCERTAIN SAFETY

  • reduce LA doses
  • use ultrasound guidance to avoid intraneural injection
  • no vasoconstrictor additives
40
Q

Vinblastine/vinorelbine: toxicities

A

vinka alkaloids

significant bone marrow suppression

41
Q

Taxanes (paclitaxel, docetaxel): Class + MOA

A

Tubuline - binding drugs

MOA: stabilizes microtubule bundles and prevents disassembly (prevent depolymerzation) –> inhibiting cell division and producing apoptosis

42
Q

Taxanes: toxicities and anes considerations

A
  • peripheral neuropathy (especially hands and feet) (SAME CONSIDERATIONS AS VINCRISTINE)
  • muscle and joint pain (NO NEED TO RECREATE THE WHEEL, ASK WHAT WORKS FOR THEM, WHAT DOES NOT)
  • hypersensitivity reactions 25-30% of patients
  • cardiac (bradycardIa, heart block, MI) (MORE AGGRESSIVE CV WORK UP)
  • myelosuppression (neutropenia develops in almost all pts; 1% sepsis related death) (INFECTION CONTROL)
43
Q

Tamoxifen: Class, Use, MOA

A

Signal transduction modulator; anti estrogen

acts as an estrogen antagonist in certain cells (breast and ovarian) and an estrogen agonist in other cells (uterus, liver, bone)

44
Q

Tamoxifen: SE and anes considerations

A

SE related to agonist activity

  • DVT (ENSURE DVT PROPHYLAXIS)
  • endometrial CA
  • menopausal symptoms
  • inc bone density (beneficial)
  • improves serum cholesterol panel (beneficial)
45
Q

Flutamide: Class, use, anes consideration

A

signal transduction modulator; anti androgen

METHEMOGLOBINEMIA

46
Q

signal transduction modulators: MOA

A

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

47
Q

Bevacizumab: Class, MOA

A

Trade name: Avastin

monoclonal antibody that blocks angiogenesis

inhibits vascular endothelial growth factor A (without vascularization, tumors can’t survive)

48
Q

Immunotherapy: concerns

A

Autoimmune reactions major concern with these approaches (overactive immune system)

flu like symptoms

won’t really expect same SE profile as chemotherapeutic agents

NURA 671 Advanced Pharmacology (9 decks)

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