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Chemo Training > Toxicities: Long term > Flashcards

Toxicities: Long term Flashcards

1
Q

What is the mechanism for long-term lung toxicity?

A
  • Progressive and often irreversible inflammation reaction, resulting in drug-induced pneumonitis
  • Damages endothelial lung cells
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2
Q

What drugs are highly implicated in LT lung toxicity?

A
  • Bleomycin
  • Carmustine
  • Lomustine may cause pulm fibrosis
  • Bulsulfan
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3
Q

What are the S&S and timing/onset for LT lung toxicity?

A
  • Long-term use, often greater than 3 years (but can be as quick as 6 weeks)
  • Cough, SOB, dyspnea/tachypnea, rales
  • Low grade fever
  • Hypoxemia
  • Pulmonary fibrosis
  • Capillary leak syndrome (with cytarabine)
  • Interstitial fibrosis (with methotrexiate)
  • Older age, smoking hx, renal dysfunction and thoracic radiation risk factors
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4
Q

What are the treatment and prevention strategies for LT lung toxicity?

A
  • Short term steroid therapy
  • Dry cough suppressant
  • Symptom control (eg. O2 prn)
  • Monitor resp status
  • d/c or alter treatment regime
  • Routine vaccinations (eg. flu vac)
  • Smoking cessation
  • exclude infection
  • pulm function tests
  • education re: breathing techniques and energy/activity
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5
Q

What is the mechanism of action for LT hepatotoxicity?

A
  • Transient increases in hepatic enzymes = hepatomegaly & jaundice
  • Damage to parenchymal cells
  • Rare, but if it occurs can have serious implications (esp since many chemo drugs excreted via liver)
  • Risk factors: prior liver damage (eg. hepatitis), alcoholism, increased age, obesity, any tumor involvement, comorbidities (eg. DM)
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6
Q

What drugs are implicated in LT hepatotoxicity?

A
  • Carboplatin (endings with - platin)
  • Cytrabine (endings with - abine)
  • 5-FU
  • Dacarbazine
  • Methotrexate
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7
Q

What are the S&S and timing/onset of hepatotoxicity?

A
  • Jaundice (urine and stool color changes)
  • Tenderness at site
  • Elevated LFT’s
  • General signs liver failure (eg. decreased clotting, fatigue, ascites)
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8
Q

What is the prevention and management strategies for LT hepatotoxicity?

A
  • Can occur after multiple treatments or 1-4 weeks after starting
  • Monitor LFT’s, adjust tx or stop accordingly
  • Supportive measures if progressed (eg. diuretics, decrease protein intake, lactulose, etc.)
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9
Q

What are common reproductive system dysfunctions that occur and can be a long-term issue? Why?

A
  • Erectile dysfunction in men
  • Pain with intercourse (dyspareunia) with both men and women
  • Decreased libido
  • Affects QOL for the patient and their partner
  • Changes in body image
  • Appears that sexual dysfunction often related to surgery changing the structures, nerves, etc. and/or treatments that can induce reproductive changes (eg. hormonal changes from meds can cause vaginal atrophy in women, decreasing elasticity; radiation therapy; chemotherapy)
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10
Q

Discuss infertility in relation to Ca and it’s treatment:

A
  • Infertility = inability to conceive after one year of unprotected intercourse
  • For adolescents and young adults the risk of infertility with Ca is 50-95%
  • Multiple risk factors in this group (eg. diagnosis, age, type of maligancy and stage, and the treatments - surgery, radiation, hormone manipulation, and the length can lead to delays in pregnancy attempts)
  • There is a lack of information about preserving fertility
  • In women, fertility often d/t premature ovarian failure from antineoplastic treatments
  • In men, infertility is a long-term effect of hypogonadism (azoospermia) d/t germ cells being more sensitive to rad and chemotherapy
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11
Q

What drugs are implicated in altered fertility?

A
  • Bulsulfan
  • Chlorambucil
  • Cyclophosphamide
  • Anti-hormone agents
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12
Q

What are signs of altered sexual function and fertility?

A
  • Irregular menstruation / amenorrhea
  • menopause symptoms - hot flashes
  • Infertility - inability to conceive after trying for a year
  • Erectile dysfunction
  • Pain with intercourse (both male and female)
  • Changes in libido
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13
Q

What are preventative and management strategies for fertility?

A
  • Ensure that provider-pt relationship is open and you demonstrate comfort in discussing
  • Consider the $$ involved in treatments (pt’s may already be under a lot of $ stress)
  • Education re: options for fertility - egg or sperm banking
  • Contraceptive information to avoid pregnancy while on active therapy
  • Emotional support
  • Ensure pt and partner understands the potential for temporary or permanent infertility and sexual changes with treatment
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14
Q

Describe ocular toxicities:

A
  • Relatively uncommon but can occur
  • Can occur in multiple structures, including outside (eyelids) and interior
  • Neurotoxic side effects of chemo tend to be peripheral neuropathies but central neurotoxicities can occur
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15
Q

What drugs are highly implicated in ocular toxicity?

A
  • Most common ocular side effect is blepharitis, inflammation of the eyelids
  • Can also cause excessive tearing, conjunctivitis, dry eyes, and in some cases can cause cataracts and glaucoma to develop secondary to Ca treatment
  • Long-term radiation can cause ocular complications
  • 25-50% of patients receiving 5-FU can experience ocular tox
  • Cetuximab
  • Methotrexate
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16
Q

What are common symptoms of ototoxicity?

A

Damages to inner ear, causing tinnitus, pain, vertigo and hearing loss (unlikely reversible)

17
Q

What are drugs implicated in ototoxicity?

A
  • platins (alkylating agents) such as cisplatin, oxaliplatin, carboplatin
  • stine’s (alkaloids) such as vinblastine and vincristine
  • MAb’s and TKI’s can cause vertigo
  • Radiation therapy (esp for head & neck Ca)
18
Q

What causes otoxocity?

A

Unknown, but believed to be effects to the cochlea and vestibular cells of the inner ear

19
Q

How do you prevent and/or manage ototoxicity?

A
  • Baseline audiogram
  • Monitor for symptoms of tinnitus, hearing loss and vertigo
  • Ensure safety precautions for vertigo, especially if severe
20
Q

What are secondary malignancies?

A
  • Ca caused by treatment by chemo/radiation for the 1st, unrelated Ca, d/t affected normal cells from the treatment
  • can occur months/years later
  • certain groups of Ca and treatment regimes more likely (combo rad/chemo more likely compared c single therapies; groups like childhood leukemia, breast, testicular and ovarian Ca higher risk) and some drugs have higher incidence (cisplatin)
21
Q

What are nursing indications for secondary malignancies?

A
  • Original treatment plan may take into consideration how to prevent secondary malignancies (eg. try to avoid high carcinogenic potential, avoiding radiation therapy, identify regimes that are higher risk)
  • Emotional support
  • Education for what to monitor for (eg. notify doctor immediately of any irregularities) and screening regimes (eg. starting mammography screening sooner)
22
Q

What is the mechanism of action for cardiac toxicity?

A
  • Can be from chemo and targeted therapies, as well as chest radiation
  • Chronic damage to myocardial cells
  • Ca treatments can pose unique direct problems to the heart (myocardial toxicity, ischemia, HTN, arrhythmias) and indirect heart problems (eg. having to make unfavorable lifestyle changes)
  • Cardiac toxicity can even be the cause of mortality over the cancer itself in some groups
23
Q

What are common CV adverse events r/t cardiac toxicity?

A
  • Heart failure - the most serious consequence
  • HTN (TKI’s often causative)
  • Thrombosis and ischemia (combined therapies may increase risk)
  • Rhythm disturbances (QT prolonged wave) leading to arrhythmia’s (some medications like anti-emetics and anti-depressants can contribute to this as well)
  • Radiotherapy induced CV damage (CAD, myocardium damage)
24
Q

What drugs are highly implicated in cardiac toxicity?

A
  • Doxorubicin and daunorubicin (doxo often causes changes in HR and rhythm during or after admin)
  • Paclitaxel
  • Trastuzumab
  • 5-FU
25
Q

What are the S&S of cardiac toxicity?

A
  • Most often asymptomatic until S&S of CHF present

- Changes in HR or rhythm

26
Q

What are preventative and management strategies for cardiac toxicity?

A
  • Baseline studies (eg. ECG, echocardio imaging to determine LVEF, cardiac enzymes [trops]) and periodic monitoring
  • Monitor for S&S cardiac symptoms (eg. SOB, changes in activity tolerance) and educate pt re: changes to monitor for
  • Monitor accumulative life time dosage
  • Cardiac protective agents (eg. beta blockers, anti-hypertensives)
  • Anticoagulants generally not recommended to prevent clots at this time (d/t concern of bleeding complications)
27
Q

What toxicity is second only to myelosuppression as a dose-limiting factor of Ca treatment?

A
  • Neurotoxicity
  • Treatments affect both central and peripheral systems
  • Important to recognize to prevent further injury and to distinguish from nervous system involvement d/t the disease
28
Q

What is the mechanism of injury for neurotoxicities?

A
  • Damage to sensory nerve tissues (85-95%)
  • Heightened immune responses can damage nervous system cells
  • Nervous system cells contain stem cells that replenish some neuron populations and divide (albeit slowly)
  • Radiation therapy can cause damage directly or indirectly by causing vascular damage, endocrine disturbances and fibrosis of structures
  • Often delayed by weeks to years (slow rate of cell turnover)
29
Q

What are central nervous system toxicities that are seen?

A
  • HA and acute altered mental status most common
  • Seizures
  • Encephalopathy
  • Cerebrovascular disease - increase risk strokes
  • Cerebellar dysfunction
  • Movement disorders
  • Radiation necrosis
  • Secondary nervous malignancies
  • Spinal cord syndrome
30
Q

What are peripheral nervous system toxicities?

A
  • Plexopathy (brachial and lumbosacral) - weakness, sensory impairment, pain
  • Peripheral neuropathy - most common and can be dose-limiting
  • Myalgias
  • Acute inflammatory demyelinating polyneuropathy
31
Q

What are highly implicated drugs in nervous system toxicity?

A
  • Platin’s (oxaliplatin)
  • Vincristine
  • Anti-angiogenesis agents (thalidomide)
32
Q

What are S&S of peripheral nervous system toxicities?

A
  • Tingling/numbness distal end of extremities

- Burning sensation and unsteady on feet (changed prioproception d/t altered sensation)

33
Q

What is the most important preventative/management strategy for peripheral neuropathy?

A
    • Identify early and stop or alter the drug! These toxicities are often dose limiting, and it is crucial to recognize and stop to prevent further injury and to distinguish from nervous system involvement d/t other diseases
  • Temporary in most cases but it may take months to years to recover
  • Some cases cause permanent damage
  • Education re: what to monitor for
  • Safety precautions (eg. education for fall prevention if sensation decreased)
  • Assess for risk factors (pre-existing neuropathy from non-Ca causes, like DM or alcohol)
34
Q

What are risk factors for chemo-induced nephrotoxicity?

A
  • Tumor-related kidney effects (eg. primary renal Ca; metabolic changes; volume changes)
  • Innate drug toxicity
  • Patient factors (older age, underlying AKI/CKD) and other nephrotoxic drugs they may be taking
  • Co-morbidities (eg. HTN)
35
Q

What causes nephrotoxicity?

A
  • Acute renal failure if no pre-hydration with some drugs
  • Some drugs can cause renal failure with anemia and HTN
  • Necrosis of renal tubules, huge cause of CHF
  • High dose of drugs can gather in renal tubules and impair GFR (eg. methotrexate)
36
Q

What are preventative and management strategies for nephrotoxicity?

A
  • Pre-hydration to increase urine flow
  • Mannitol (diuretic to force urine production)
  • Encourage + fluids at home, 2-3 L/day
  • Monitor labs and try to obtain baseline renal function
  • Monitor intake/output and weight changes
37
Q

What drugs cause nephrotoxicity?

A
  • Cisplatin
  • Ifosfamide (AA)
  • Cyclophosphamide (AA)
  • Methotrexate

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