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PAT202 WINTER > cancer management and drugs > Flashcards

cancer management and drugs Flashcards

1
Q

what are the clinical manifestations of cancer?

A

-Paraneoplastic syndromes- symptom complexes that are triggered by a cancer but are not caused by direct local effects of the tumor mass. they are most commonly caused by biologic substances released from the tumor (e.g. hormones) or by an immune response triggered by the tumor
-can be life-threatening
-cachexia- most severe form of malnutrition
leads to protein- calorie malnutrition and progressive wasting

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2
Q

what are the manifestations of cachexia?

A

anorexia, early satiety (unable to eat full meal/ or get full very quickly after eating a small meal) , weight loss, anemia, asthenia ( abnormal weakness) taste alternating, and altered protein, lipid, and carbohydrate metabolism

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3
Q

diagnosing and staging

A

involves the size of the tumour, the degree to which it has invaded and the extend of the spread
stage 1- stage 4

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4
Q

stage 1 cancer

A

is confined to its organ of origin

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5
Q

stage 2 cancer

A

is locally invasive

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6
Q

stage 3 cancer

A

has advanced to regional structures

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7
Q

stage 4 cancer

A

has spread to distant sites

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8
Q

what is grading?

A
  • examines potential cancer cells under a microscope and compares their appearance to normal parent cells
  • normal cells are highly differentiated
  • cancer cells gradually changes and become less differentiated in both structure and function
  • fully undifferentiated cancer cell will look very different from the parent cell and will not carry on the functions of the parent cells
  • grade 1 (G1) is the best prognosis
  • grade 4 cells are grossly abnormal and clearly different from normal cells–> the worst prognosis
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9
Q

tumour markers

A
  • are found on or in a tumour cell, in the blood, in the spinal fluid, or in the urine. can be:
  • hormones
  • enzymes
  • genes
  • antigens
  • antibodies
  • tumour markers are used to screen and identify individuals at high risk for cancer
  • diagnose specific types of tumours
  • follow the clinical course of cancer
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10
Q

immunohistochemical and genetic analysis

A
  • information regarding cellular and molecular alternations inform treatment decisions–> personalized medicine–> sub groups w/ varied prognosis
  • single gene (translocation)
  • a panel of gene (expression of receptors that aid cancer growth)
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11
Q

treatment of cancer- surgery

A
  • is a definitive treatment of cancers that do not spread beyond limits of surgical excision -we want to remove the tumour and have clear margins
  • palliative- indicated for the relief of symptoms
  • in selected high-risk disease, surgery can play a role in preventing cancer
  • mutations of the APC gene has close to a 100% lifetime risk of colon cancer: colectomy
  • women w/ BRCA1/2 mutations have a high risk of breast and ovarian cncer: prophylactic mastectomy or bilateral salpingo-oophorectomy or both
  • surgery must get it all- must achieve adequate margins
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12
Q

radiation therapy

A
  • used to kill cancer cells while minimizing the damage to normal structures
  • ionizing radiation –> damages cells by imparting enough ionizing radiation to cause molecular damage to the DNA –> causes irreversible damage to normal cells & lifetime radiation dose
  • brachytherapy- seeds are implanted
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13
Q

chemotherapy

A
  • eradicates enough tumour cells to enable the body’s natural defences to eradicate the remaining cells
  • can be a single-agent or combination chemotherapy
  • induction chemotherapy- causes shrinkage or the disappearances of tumours
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14
Q

adjuvant chemotherapy

A

Is administered after the surgical excision with a goal of eliminating micrometastases.

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15
Q

Neoadjuvant chemotherapy

A

Is administered before localized (surgical or radiation) treatment

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16
Q

targeted therapy

A
  • designed to address unique growth growth characteristics of a specific class of tumour and directly interfere with that process
  • tumour growth and progression are dependent on a variety of mutations leading to the expression of oncogenes, inactivation of tumour-suppressor molecules, and interactions with inflammatory cells in the tumour microenvironment that foster angiogenesis, resistance to apoptosis and immune-mediated cancer cell death, altered tumour cell metabolism, and metastasis
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17
Q

chemotherapy (pharmacotherapy)

A

kills cells that undergo rapid mitosis

  • transported thorough blood making it more effective at reaching cancer cells
  • can be used with surgery and radiation to maximize chances of eradicating all tumour cells
  • can be used in palliative care
  • can be used prophylactically through it is uncommon
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18
Q

what are the goals of chemotherapy?

A
  • cure- permanent removal of all cancer cells
  • control-preventing growth and spread of tumour
  • palliation- reduction of tumour, easing of pain and other symptoms, improving quality of life
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19
Q

cell cycle- stage G0

A
  • cell is not undergoing mitosis

- cell is performing regular activities

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20
Q

cell cycle -interphase -preparation for mitosis-stage 1- gap 1

A

synthesizing of RNA, proteins, and components needed to duplicate DNA

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21
Q

cell cycle - stage S (synthesis)

A

duplication of DNA

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22
Q

cell cycle stage 2- gap 2

A

additional proteins and spindle apparatus made

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23
Q

cell cycle - stage M

A 
prophase- formation of chromosomes 
metaphase-lining up of chromosomes 
anaphase-chromosome begin to separate 
telophase- cell begins to separate into two daughter cells 
-cytokinesis- cell division is completed
24
Q

what is a growth fraction

A
  • measure of cells undergoing mitosis
  • ratio of number of replicating cells to resting cells
  • goal of chemotherapy is to kill as many cells as possible
  • antineoplastic agents are more effective on tumours with high growth fractions
25
Q

what is the cell kill hypothesis

A
  • in order for a patient’s cancer to be cured, every single cell in a malignant tumour must be eliminated from the body
  • this can be difficult d/t the number, mutations, diversity of cancer cells
  • cell kill hypothesis–> theoretical model that predicts ability of antineoplastic drugs to eliminate a certain percentage of cancer cells
  • if a large enough percentage of tumour cells are killed, body’s defenses can kill the rest
26
Q

how can we improve the success of chemotherapy?

A
  • chemotherapy w/ a single drug will not kill all tumour cells, so we use different strategies
  • combination chemotherapy
  • multiple drugs can attack tumour cells in different stages of cell cycle
  • multiple drugs can attack various clones within tumour
  • lower doses of each agent can be used
  • better ability to attack tumour
  • less risk of adverse effects of therapy
27
Q

Improving Success of Chemotherapy: Dosing schedules and route

A
  • dosing schedule- determined through research to increase effectiveness of antineoplastic agents for a particular type of cancer
  • intermittent scheduling is common- allows pt to recover and allows tumour cells to reenter mitosis phase
  • delays or reductions likely negatively affect treatment
28
Q

route of administration -chemotherapy

A
  • chosen w/ consideration of patient, tumour and risks associated with route
  • antineoplastic agents are available for through enteral, topical, and parenteral routes
29
Q

what are antineoplastic agents?

A

they affect cells that are undergoing rapid mitosis, thus healthy cells that undergo rapid mitosis are also affected

30
Q

Toxicity of Antineoplastic Agents -hematologic system

A
  • reduced production of RBCs, WBCS and platelets until the counts reach a nadir
  • cell counts begin to recover after nadir at time points characteristic of agents
31
Q

Toxicity of Antineoplastic Agents - gastrointestinal system

A
  • nausea and vomiting are common as agents reach chemosensitive trigger zones in brain
  • antieoplastics are sometimes classified by their “emetic potential”
  • mucositis- inflammation of GI mucosa
  • promotes ulcerations of mouth and esophagus
  • causes difficulties in eating and swallowing
  • constipation/diarrhea
  • anorexia
  • cachexia- muscle and tissue wasting
32
Q

Toxicity of Antineoplastic Agents -skin and soft tissue

A
  • extravasation of many antineoplastic drugs cause serious tissue injury; many are vesicants causing blistering/tissue damage
  • alopecia (hair loss)
33
Q

Toxicity of Antineoplastic Agents -reproductive system

A
  • alkylating agents in particular are associated with infertility
  • sterility risk higher in males
  • pregnancy category x- meaning we cannot give it to pregnant mothers
34
Q

Toxicity of Antineoplastic Agents -other adverse effects

A
  • fatigue may be d/t the hematologic effects, GI effects, anxiety and depression
  • repairing and regenerating healthy cells requires energy
  • Secondary malignancy – uncommon however, antineoplastic agents have been known to cause other tumours to develop while primary tumour is treated
35
Q

what are the classification of antineoplastic agents

A
  • Alkylating agents
  • Antimetabolites
  • Antitumour antibiotics
  • Hormones and hormone antagonists
  • Natural products
  • Biologic response modifiers and monoclonal antibodies
  • Miscellaneous antineoplastic drugs
36
Q

Antimetabolites

A
  • Molecules with similar structure to nutrients required for DNA synthesis, metabolic pathways
  • Classes
  • Folic acid analogues–> Folic acid necessary for DNA synthesis
  • Purine analogues –> Similar to adenine and guanine
  • Pyrimidine analogues –> Similar to thymidine and cytosine
37
Q

Methotrexate

A

Indication: choriocarcinoma, osteogenic sarcoma, leukemias, head and neck cancers, breast carcinoma, and lung carcinoma

  • MOA
  • Specific for S phase of the cell cycle
  • Inhibits folic acid reductase enzyme, lack of folate interferes with –DNA synthesis and repair
  • Most effective in cells undergoing rapid mitosis
  • Leucovorin (reduced folate) used to counter effects of methotrexate -normal cells are rescued but cancer cells can’t use it efficiently
  • desired effects- slows/stops cancer cell growth
  • adverse effects- nausea, vomiting, anorexia
38
Q

Hormone-related drugs

A
  • Hormones significantly affect the growth of some tumours
  • Use of natural or synthetic hormones or their antagonists as antineoplastic agents is a strategy used to slow the growth of hormone-dependent tumours
  • Non-cytotoxic, mainly for breast or prostate cancers
  • Examples: SERMs, aromatase inhibitors, GnRH analogues, androgen receptor blockers, corticosteroids
39
Q

Selective estrogen receptor modulator: Tamoxifen

A

indication- Prophylaxis of breast cancer for high-risk patients
-Adjunctive therapy following a mastectomy to decrease potential for cancer in the contralateral breast
MOA-Antagonizes estrogen receptor in breast, agonist in other tissues (ie bone)
-Blocking estrogen receptor in breast reduces tumour growth
-pro-estrogen for the uterus but anti-estrogen in the breast
-adverse effects
-N&V, hot flashes, rash, fluid retention, vaginal discharge, irregular menses, headaches/light-headedness
SERIOUS AE-increased risk of endometrial cancer
-small increased risk of thromboembolic disease (CVA, DVT, pulmonary embolism)

40
Q

biologic response modifiers

A
  • -agents that stimulate the body’s immune system to kill tumour cells
  • interferons –> suppress cell vision in certain cancers and activate macrophages and T cytotoxic cells
  • interleukins- IL-2 activates T cytotoxic cells
  • hematopoietic growth factors- promote formation of blood cells to reduce complications from myelosuppression
41
Q

targeted therapies

A
  • specially engineered molecules that attack cancer antigens
  • monoclonal antibodies (MABs)
  • bind specific antigens on cancer cells
  • act as a target for complement, resulting in destruction of cancer cells
42
Q

Bevacizumab

A
  • Classification: Monoclonal antibody- not chemo
  • Indication: Metastatic carcinoma of the colon or rectum in combination, renal cell carcinoma, glioblastoma, non–small cell lung cancer
  • Mechanisms of action: binds to and inhibits activity of human vascular endothelial growth factor to reduce microvascular growth and inhibition of metastatic disease progression
  • it inhibits angiogenesis
  • Desired effects: decreased tumour size and growth
  • Adverse effects: asthenia, dizziness, impaired wound healing
43
Q

preparing and administration antineoplastics- considerations

A

Nurses preparing and delivering antineoplastics must exercise extreme caution to protect themselves from medication exposure.

44
Q

Nursing Considerations for Patients Receiving Antineoplastic Therapy - what are the assessments?

A
  • Obtain complete health history including allergies and drug history
  • Obtain laboratory values for leukocyte count, platelet count, hematocrit, serum electrolytes, kidney function
  • Assess neurological status
  • Assess for presence of infections that may present if patient immunocompromised following treatment
45
Q

Nursing Considerations for Patients Receiving Antineoplastic Therapy -Planning

A
  • Provide education regarding drug action, possible adverse effects and precautions
  • Patient to experience reduction in growth or size of tumour
46
Q

Nursing Considerations for Patients Receiving Antineoplastic Therapy -Interventions

A

-Monitor hematological and immune status, evidence of myelosuppression
-Monitor cardiovascular status, ECG, vital signs, heart sounds
-Monitor GI status and nutrition
Nausea, vomiting, constipation, occult blood
-Monitor renal status, fluid intake and output, daily weight
-Monitor neurological status
-Peripheral neuropathy
-Ataxia, foot drop
-Photophobia
-depression

47
Q

Safe Handling of Antineoplastic Drugs

A
  • Follow agency policies and procedures for handling antineoplastics
  • Be ready with a chemotherapy spill kit
  • Wear appropriate disposable PPE
  • Carefully check IV line to reduce risk of extravasation, especially with vesicants
  • Dispose of waste materials properly
48
Q

Managing Infiltration of Drugs with Vesicant Properties

A
  • Follow policies and procedures of agency regarding infiltration / extravasation
  • Stop infusion immediately upon recognition of extravasation
  • Disconnect administration line but leave cannula in place
  • Monitor site of injury, elevate limb
  • If necessary, flush the affected tissue with saline
  • Document incident
  • Contact appropriate personnel
49
Q

Filgrastim

A
  • Indication: Neutropenia (not enough WBC)
  • Mechanisms of action: to increase neutrophil production in the bone marrow and to enhance the phagocytic and cytotoxic functions of existing neutrophils
  • Desired effects: shorten the length of neutropenia in cancer clients whose bone marrow has been suppressed by antineoplastic agents or in clients following organ transplants
  • Adverse effects: Bone pain, allergic reaction
  • DO NOT ADMINISTER UNTIL AT LEAST 24 HOURS AFTER A CHEMOTHERAPY SESSION
50
Q

Pathophysiology of Nausea and Vomiting

A

-Nausea and vomiting are often secondary to another condition
-Treatment outcomes should focus on removal of the cause whenever feasible
-Causes: Motion sickness, drugs, toxins, GI infection, stress, pain, pregnancy
-Complications from chronic vomiting may include:
-Dehydration
-Electrolyte imbalances
-Significant weight loss
-Vascular collapse
-Dehydration
Metabolic alkalosis

51
Q

Ondansetron

A

Classification: 5-HT receptor antagonist

  • Indication: Prevention of nausea, vomiting associated with cancer chemotherapy, radiotherapy, and prevention of postoperative nausea, vomiting
  • Mechanisms of action: Blocks serotonin (on vagus nerve and CNS) (5-HT) peripherally, centrally, and in the small intestine
  • Desired effects: Prevent nausea and vomiting
  • Adverse effects: headache, diarrhea, constipation, abdominal pain, fever, urinary retention
52
Q

others drugs reuse for N&V

A

-Anticholinergics (ie scopolamine)
Nausea due to motion sickness
-Antihistamines (ie dimenhydrinate (Gravol))
Nausea due to motion sickness
Cause significant drowsiness
-Serotonin (5HT3) receptor antagonists (ie ondansetron)
Chemotherapy-induced nausea and vomiting
-Phenothiazines (D2 receptor antagonists; ie prochlorperazine)
Antineoplastic therapy
-Cannabinoids
Antineoplastic therapy
-Corticosteroids (ie dexamethasone)
Antineoplastic therapy
Post-surgical nausea and vomiting

53
Q

Glucocorticoids prepare the body for long-term stress and the metabolism of nearly every cell.

A
  • Increase the level of blood glucose (hyperglycemic effect)
  • Increase the breakdown of proteins to amino acids. Amino acids are then converted to glucose and glycogen in the liver  protein depletion
  • Increase the breakdown of lipids (lipolysis)
  • Suppress the inflammatory and immune responses
  • Increase the sensitivity of vascular smooth muscle to the actions of norepinephrine and angiotensin II, thus modifying smooth muscle tone
  • Influence the central nervous system (CNS) by affecting mood and maintaining normal nerve excitability
  • Increase the breakdown of bony matrix  bone demineralization
  • Promote bronchodilation
  • Stabilize mast cells, inhibiting the release of inflammatory mediators
54
Q

corticosteroids- dexamethasone MOA

A
  • Medications work in the same manner as naturally occurring steroid hormones
  • Gonadocorticoids: (androgens) contribute to onset of puberty
  • Mineralocorticoids: recall function of aldosterone
  • Glucocorticoids: (cortisol)
  • Increase blood glucose by inhibiting insulin secretion and promoting gluconeogenesis
  • Breakdown lipids and proteins
  • Suppress the inflammatory response
  • Influence CNS to affect mood
55
Q

corticosteroids- dexamethasone -adverse effects

A
  • heart failure, HTN
  • fragile skin, increased skin of infection and delayed wound healing
  • heading, mood swings, psychiatric impairment
  • insomnia
  • growth suppression Cushing’s syndrome
  • hyperglycaemia
  • peptic ulcers, GI upset
  • osteoporosis
  • increased intraocular pressure-glaucoma
  • cataracts
  • weight gain
56
Q

corticosteroids- nursing considerations

A
  • Careful monitoring for adverse effects
  • Long-term use may cause osteoporosis (decrease absorption & increase excretion of calcium)
  • Long-term use may cause Cushing’s disease/syndrome
  • Oral glucocorticoids should be given in the morning to decrease amount of adrenal suppression
  • Oral glucocorticoids should be given with milk or food to decrease GI upset
  • Growth retardation is possible. Thus, smaller doses should be considered and accurate weekly height and weight must be documented
  • Corticosteroids often aggravate other conditions (i.e. hypertension, CHF, diabetes, infection)

PAT202 WINTER (16 decks)

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