Treatment and Symptom Management Flashcards
What is a peripheral cannula, length, and maximum dwell time?
Is this type of cannula appropriate for prolonged IV therapy?
Short device (up to 2”) usually inserted into hand/forearm for short-term use, with dwell time limit of 96 hours/4 days.
No, not appropriate for prolonged IV therapy.
Describe a Midline catheter:
Peripheral or central device?
Length
Where inserted
Where tip is located
# lumens?
Materials
Maximum dwell time
A Midline catheter is:
- A Peripheral device
- 8-24cm in length
- Inserted AC fossa region
- Tip located in the basilic, cephalic or median cubital veins, below the level of the axilla
- Silicone or polyurethane
- Can be single or double lumen
- Some are CT compatible
- Dwell time 1–4 weeks
What is a CVAD?
Where is tip located?
When indicated? 7 listed.
A CVAD = Central Venous Access Device
- Tip located in the superior vena cava or right atrium.
Indicated when:
1. Poor Peripheral venous access
2. Prolonged IV chemotherapy
3. TPN (total parenteral nutrition)
4. repeated blood products expected
5. IV therapy involves venous sclerosant drugs
6. Continuous therapy
7. Fequent blood sampling / phlebotomy
Name 3 indications for PIV
- Short duration w/non-irritating therapies
- one-time use therapies (ie. IV push)
- Patients with a short life expectancy
Name 5 contraindications to PIVs
- Continuous vesicant therapy
- pH <5 or >9
- Glucose >10%
- protein >5%
- osmolarity >900 mOsm/L
- No definitive recommendation can be made regarding blood specimen collection
Name 3 types of PVADs
- Peripheral (96h/4days)
- Midline: Therapy (1-4 weeks)
- Subcutaneous: Continuous long- or short-term
List 5 General principles of PVAD placement/use.
- Select vein based on type of fluid, rate, and duration
- Use most distal site possible (but proximal to previous venipuncture)
- Smallest gauge and shortest length possible for indicated use
- Avoid extremities/sites with impaired circulation such as:
- antecubital veins
- lymphedema
- injury
- swelling
- hematoma
- site of axillary LN dissection
- infection
- phlebitis
- where previous venipuncture has been performed in the past 24 hours - Assess for blood return and patency prior to use
True or False
Some studies support the practice of changing peripheral lines only as clinically indicated versus every 72 - 96 hours
True
Within what time frame should you AVOID new PVAD placement at same location where previous venipuncture has been performed?
24 hours
List 4 PVAD complications and what is most common?
- Phlebitis (most common)
- Infltration (2nd most common)
- Extravasation
- Infection
What is Phlebitis
What are S&S
How do you prevent?
Phlebitis = the most common complication of PVAD = inflammation of the vein
S&S: Pain, erythema, streak formation, palpable
cord, and edema
Prevent:
- Aseptic technique
- Careful insertion placement
- Maintenance care
What is infiltration?
S&S?
How do you prevent?
Infiltration = second most common PVAD complication caused by leaking around catheter with NON-vesicant therapy
S&S: skin is cool, pale with edema, tenderness, skin tightness, decreased infusion rate
Prevention:
- Use appropriate syringe sizes to prevent vein rupture
What is Extravasation?
S&S?
How do you prevent?
How do you manage?
Extravasation = PVAD complication caused by leaking around catheter WITH vesicant therapy
Burning /stinging, pain, erythema, decreased infusion rate, absence of blood return during or following infusion, followed by blistering, tissue necrosis and ulceration.
Prevention:
- Aseptic technique
- Avoid multiple IV attempts
- Avoid impaired areas
- Avoid previous IV sites
- frequent blood return check during vesicant administration.
Management:
- Stop infusion
- Aspirate residual drug
- Assess site and estimate amount of vesicant extravasated
- give antidote as indicated
- remove peripheral catheter
- apply heat/cold as indicated.
In terms of PVAD, describe infection.
What are S&S
How do you prevent?
Infection = PVAD complication
S&S: Fever, redness, erythema at insertion site, purulent drainage, and warmth to
extremity
Prevention: strict aseptic technique
Name 4 types of CVAD (Central Venous Access Devices)
- Non-tunneled
- Tunneled
- Implanted subcutaneous ports
- PICC
Is a Non-tunneled CVAD common?
What level of care most often?
Name the 3 main insertion sites.
RE: Antimicrobial/antiseptic impregnated catheters:
1. when are these recommended?
2. Name two cons
Yes, Non-tunneled is the most common CVAD.
Most common in acute and critical care.
3 Main insertion sites:
1. Internal jugular vein
2. subclavian vein
3. femoral vein
- Antimicrobial/antiseptic impregnated catheters are recommended for adults at high risk for infection with duration expected <10 days (short term)
- Debate about antibiotic resistance and occasional severe allergic reactions.
When are Tunneled CVAD Recommended?
Higher or lower risk of infection (compared to non-tunneled?
Catheter fixation within how many weeks? How?
Do valved catheters require heparin flush? And cost?
Tunneled CVAD recommended with long-term use >6 months
Associated
with lower infection rates (compared to non-tunneled)
Catheter fixation usually 3–4 weeks of insertion. Cuff induces infammatory
reaction within the subcutaneous tunnel, leading to fibrosis/fixation.
Valved catheters do not
require heparin fushes but may need pressurized infusions for blood products.
MORE cost.
About CVAD: Implanted subcutaneous ports:
When indicated?
What is infection risk of ports compared to other CVAD options (Non-tunneled/ Tunneled)?
Most ports have how many lumens?
Name two drawbacks.
Implanted subcutaneous ports:
Indicated for:
- long-term intermittent therapy
- often in pediatrics and solid-tumor
- poor PIV access
Have lowest rates of catheter-related bloodstream
infections (compared to tunneled and non-tunneled)
Most = single lumen
1.Expensive
2. Larger scars
CVAD Peripherally inserted central catheters (PICCs)
Duration?
Where typically inserted? What vein?
Lumen(s)?
Power injector compatible?
AE drawback?
PICC duration = intermediate
Usually inserted bedside
Antecubital vein
Lumens = single or multiple lumens,
Yes some compatible with power injection
Associated with higher incidence of thrombosis
What is Radiation therapy (RT)?
Radiation therapy (RT) uses high-energy particles or waves, (such as x-rays, gamma rays, electron beams, or protons) to create ionizing radiation (IR) which damages DNA & ultimately destroys targeted cancer cells.
About what percent (%) of patients with cancer receive some type of RT during the course of their treatment?
About half (~50%)
How does RT work?
What are two ways RT can damage cells?
RT kills cancer cells by using high-energy radiation to damage the DNA, leading to cell death (of targeted cancer cells) and tumor shrinking.
DIRECTLY - (energy damaging DNA)
INDIRECTLY - by creating charged particles (free radicals) within the cells that can, in turn, damage the DNA.
Cancer cells whose DNA is damaged beyond repair
stop dividing or die
RT can cause Free Radicals.
What are Free Radicals?
How does RT cause them?
What are the most common type of free radicals produced in living tissue?
Free radicals are highly reactive chemicals that have the potential to harm cells. They are created when an atom or a molecule either gains or loses an electron (a small negatively charged particle found in atoms).
When ionizing radiation hits an atom or a molecule in a cell, an electron may be lost, leading to the formation of a free radical. The production of abnormally high levels of free radicals is the mechanism by which ionizing radiation kills cells (DNA damage).
Free radicals that contain the element oxygen are the most common type of free radicals produced in living tissue. Another name for them is “reactive oxygen species,” or “ROS”
Name the 3 ways that RT can be given
- External radiation (external beam radiation)
- Internal radiation (brachytheraopy)
- Systemic radiation (typically IV or PO)
What is the terminology for RT delivered by a machine from outside the body?
What are 3 beams used in EBRT - What is the machine used to generate the beams?
External-beam RT
- Photon beam RT (x-ray, gamma ray) - Linear accelerator (LINAC)
- Particle Beam (Protons, neutrons) - particle accelerators (such as a cyclotron or synchrotron)
- Electron Beam - Linear accelerator OR particle accelerator can be used
What is the terminology for RT delivered from radioactive material placed in the body near cancer cells?
Internal RT
aka
Brachytherapy
What is Systemic RT?
When radioactive substances are infused to kill cancer cells (ie. radioactive iodine to treat thyroid cancer)
What is Ionizing radiation?
How does it cause cell death?
Ionizing radiation is a form of energy that acts by removing electrons from atoms and molecules.
When ionizing radiation interacts with cells, it can cause cellular damage including damage to DNA leading to cellular death.
What are the 3 goals of RT?
- Cure
- Control (ie PCI)
- Palliation (relieve symptoms)
What RT is the most common?
External beam RT (EBRT)
Is proton therapy a form of EBRT?
Yes
What 2 RT therapies uses particle accelerators (cyclotrons or synchrotrons) to produce charged atoms that destroy tumors?
Particle beam RT (protons or neutrons)
Electron beam RT - NOTE can also be generated by linear accelerator if converted to photons
What type of RT is put inside the body, sealed in needles, seeds, wires, or catheters, and implanted directly into or near a tumor on a temporary or permanent basis?
Internal RT
aka
Brachytherapy
Brachytherapy is a common treatment for what type of cancer (4)?
- Prostate
- Uterus
- Cervix
- Breast
Is RT ever used alone to treat /cure cancer?
Yes
What two cancers are commonly treated by RT alone?
- Prostate
- Larynx
Name a type of cancer / situation where it is common for RT to be given in the adjuvant (post-surgery) setting.
In Breast cancer after breast-conserving surgery.
Name three types of cancer where RT is commonly given in the Neoadjuvant setting.
What is another name for Neoadjuvant therapy?
What are 2 goals for Neoadjuvant RT?
- Esophageal
- Rectal
- Lung
Induction RT
- Improve cure rates
- Make surgery easier to perform
What is the phrase that can be used if multiple treatments used (ie. RT, chemo, surgery)?
What is one cancer where the organ may be preserved in this way?
What are 3 types of cancer that can avoid surgery in this way?
Combined modality therapy
Bladder cancer
- Lung
- Head and neck
- Cervix
A TYPE of EBRT, what is IMRT?
What type of beam is used to generate IMRT?
It is safer for delivery of what type of RT?
Three-dimensional conformal radiation therapy (3D-CRT): delivers radiation beams from different directions designed to match the shape of the tumor.
IMRT = Intensity-Modulated RT, a type of EBRT is generated by a photon beam.
IMRT is like 3D-CRT, but it also changes the strength (intensity) of some of the beams in certain areas. This allows stronger doses to be aimed at certain parts of the tumor and helps lessen damage to nearby normal body tissues.
Safer for delivery of higher than conventional doses of RT
A TYPE of EBRT, what is IGRT?
In what 3 ways is it helpful?
What type of RT therapy is it often used in conjunction with IGRT?
What are the results of combining these therapies?
IGRT = Image-Guided RT. Images are made using CT, ultrasound, x-ray, MRI, or other imaging techniques before EACH treatment session. Can be applied to many RT treatment choices.
Helpful because:
1. more accurate
2. spares surrounding healthy tissue
3. can allow for adjustments during treatment in areas of the body that are prone to movement.
Often used along with IMRT (Intensity-Modulated RT)
Together IGRT + IMRT can deliver precise radiation doses to a malignant tumor or even specific areas within the tumor.
What is Stereotactic radiosurgery (SRS)?
What energy is highly focused in this technique?
How many sessions?
What type of cancer is this often used for?
What is this therapy called when used for other areas of the body?
What are are 3 other names for this type of RT?
Stereotactic radiosurgery (SRS) = a type of EBRT (not a surgery) that uses 3D imaging to determine the exact coordinates of the tumor (ultra-precise) then gives a LARGE dose of radiation to the tumor. Called “radiosurgery” because of how exact it can be in terms of where it delivers the radiation.
Energy used = Photons (Typically high energy X-rays or gamma rays)
Brain cancer
SBRT = Stereotactic body radiation when this type of therapy is used for areas outside of the brain.
- Radiation surgery
- Radiosurgery
- Stereotaxic radiosurgery
Which RT therapy uses radioactive cobalt sources to focus multiple beams of RT on a small area?
Gamma Knife.
Uses about 200 small beams of radiation at one time, creating a very large dose. It’s usually given in one treatment session. It’s important to remember it doesn’t use a knife and there’s no cutting.
What types of RT can linear accelerators (LINAC) deliver?
- Photon beam RT
- Electron beam RT (electrons can be converted to photon beams)
What is radioembolization?
What effect does it achieve?
A RT technique that uses microspheres filled with radioactive isotopes which are then delivered to a tumor.
Radioembolization cuts off blood flow to a tumor (ie in vascular organs such as the liver).
EBRT most often is delivered in the form of what type of energy beams?
Photon (ie high energy x-rays or gamma rays)
What is a photon?
Can the human eye see photons?
Which wavelengths have the least energy, which wavelengths the most?
A bundle of energy, the basic unit of light and other forms of electromagnetic radiation.
Human eyes can see some photon wavelengths (visible light), others wavelengths cannot be seen.
Ordered least-> most energy: Radio waves, microwaves, infrared, (visible spectrum), UV, X-Ray, Gamma ray
Do all photons have the same amount of energy?
No not all photons have the same amount of energy.
Ordered least-> most energy: Radio waves, microwaves, infrared, (visible spectrum), UV, X-Ray, Gamma ray
How does a Linear Accelerator (LINAC) work?
It uses electricity to form a stream of fast-moving subatomic particles = high-energy radiation that can be used to treat cancer.
What type of RT is APBI?
A newer approach for what early-stage cancer?
Accelerated Partial Breast Irradiation = higher fractions and shorter time intervals
A newer approach for early-stage breast cancer.
What is 3D-CRT?
3D-CRT is one of the most common types of EBRT. It uses sophisticated computer software and advanced treatment machines (beams from different direction) to deliver RT to precisely shaped target areas designed to match the shape of the tumor. This helps to reduce radiation damage to normal tissues.
What is Tomotherapy? It is a form of what type of RT?
How is the patient treated?
What is another name for Tomotherapy?
Tomotherapy = A type of EBTR (External Beam Radatian Therapy) called IMRT (Intensity-Modulated RT) where radiation is aimed at a tumor from many different directions.
Patient lays on a table and is moved through a donut-shaped machine. The radiation source in the machine rotates around the patient in a spiral pattern.
Tomotherapy = Helical tomotherapy
How does Proton therapy work?
What type of beam is used?
What does this type of therapy reduce?
What are common cancers in which it is used?
Is this a cheaper therapy alternative?
Proton therapy: A type of EBRT that uses streams of protons to kill tumor cells. The main difference between proton and photon radiation is that protons only travel a certain distance and can be slowed down when they get to the tumor. This means less radiation goes through healthy tissue around the tumor.
Beam = A particle beam.
Reduces radiation damage to healthy tissue near a tumor.
Therefore used to treat malignancies near critical structures such as:
1. Head and neck and organs
2. Brain
3. Eye
4. Lung
5. Spine
6. Prostate
7. Sarcomas near the base of the skull
8. Childhood cancers
Cost = Expensive. Proton radiation is newer, and the machines cost much more than photon radiation machines. Not all insurance companies cover proton therapy and they’re only available at certain treatment centers.
Along with Proton beams, electron beams are also charged particle beams used in RT
Can electron beams be used for internal organs?
Electron beams are NOT used for internal organs as they cannot travel very far through tissue.
Electron beams are used to irradiate superficial tumors, ie skin cancer or tumors near the body surface.
What 3 particles can be used for EBRT?
What BEAM is used to generate them?
- Protons - particle accelerator (cyclotron or synchrotron)
- Neutrons - particle accelerator (cyclotron or synchrotron)
- Electrons - particle accelerator (cyclotron or synchrotron) OR a Linear accelerator (LINAC) if converted to photons
Stereotactic radiosurgery (SRS) and stereotactic body radiation therapy (SBRT) often referred to/ called by the name of the company that makes the machine.
Name 8 machines synonymous with SRS/SBRT therapy.
These machine moves around to target the tumor from many different angles: 1. X-Knife
2. CyberKnife
3. Clinac
4. Synergy-S
5. Edge
6. Novalis
7. TrueBeam.
8. Gamma Knife
What is the typical fraction # for SRS?
When more fractions used, what terms is this given?
Most patients will be given the full radiation dose in one session with stereotactic radiosurgery
Fractionated radiosurgery or Fractionated stereotactic radiotherapy = radiation in several smaller treatments to deliver the same or slightly higher dose
True or false:
Brachytherapy is never permanent
False.
In brachytherapy, radioactive isotopes are sealed in tiny pellets or “seeds.” that are placed in patients using delivery devices (needles, catheters, or other type of carrier). As the isotopes decay naturally, they give off radiation that damages nearby cancer cells.
If left in place, after a few weeks or months, the isotopes decay completely and no longer give off radiation. The seeds will not cause harm if they are left in the body (see permanent
brachytherapy, described below).
What is Interstitial brachytherapy?
Interstitial brachytherapy uses a radiation source placed within tumor tissue, such as within a prostate tumor.
What is Intracavitary brachytherapy?
Intracavitary brachytherapy uses a source placed within a surgical
cavity or a body cavity, such as the chest cavity, near a tumor.
What is Episcleral brachytherapy?
Episcleral brachytherapy uses a source that is attached to the eye, which
is used to treat melanoma inside the eye.
True or False:
Brachytherapy can only be given as low-dose.
False
Brachytherapy can be given as a low-dose OR high-dose treatment.
Low-dose rate treatment = cancer cells receive continuous low-dose radiation from a source over a period of several days.
High-dose rate treatment, a robotic machine attached to delivery tubes placed inside the body guides one or more radioactive sources into or near a tumor and then removes
the sources at the end of each treatment session. High-dose rate treatment can be given in one or more treatment sessions. (ie. MammoSite system used to treat patients with breast cancer who have undergone breast-conserving surgery.)
What is permament brachytherapy?
What type of dosing is this?
Permament brachytherapy = the sources are surgically sealed within the body and remains even after all of the radiation has been given ff. The remaining material (in which
the radioactive isotopes were sealed) does not cause any discomfort or harm to the patient
Permanent brachytherapy =low-dose rate brachytherapy
What is systemic RT?
Name 3 drug examples
Systemic RT, a patient swallows or receives an injection of a radioactive substance.
Examples:
1. Radioactive iodine (oral cocktail) commonly used to help treat thyroid cancer
2. ibritumomab tiuxetan (Zevalin®) = antibody joined to the radioactive substance FDA for certain types of B-cell non-Hodgkin lymphoma (NHL).
3. The radioactive drugs samarium-153-
lexidronam (Quadramet®) and strontium-89 chloride (Metastron®) are
radiopharmaceuticals used to treat pain from bone metastases.
Radiation side effects can be acute or late.
What is the difference in onset Acute vs. Late?
Acute SE occur during treatment, caused by damage to rapidly dividing cells, effects depend on area of RT.
Late SE occur days-years after treatment ends
With RT, are Late effects the same as Chronic effects?
No. Late SE are DIFFERENT from Chronic SE.
Name 5 examples of RT Late effects
- Fibrosis = the replacement of normal tissue with scar tissue
- Damage to the bowels = diarrhea and bleeding
- Memory loss
- Infertility (inability to have a child)
- Rarely, a secondary malignancy
Radiation Safety - What does the Acronym ALARA stand for?
As Low as reasonably achievable
Three main principles of RT safety are
- Time - minimize time of exposure
- Distance - double distance = reduces exposure by a factor of 4
- Shielding - absorber materials Plexiglass for beta particles:. Lead for x-rays and gamma rays.
Brain RT - Nursing Education
Name 8 potential AEs Related to Brain RT
List two items of advice
Potential AE associated with brain RT:
1. headaches
2. hair loss
3. nausea and vomiting
4. hearing loss
5. skin and scalp
changes
6. memory
7. speech
8. seizures.
Advise your patient:
1. Use recommended moisturizers and shampoos on scalp to decrease irritation.
- Protect your
scalp with a hat or frequent application of sunscreen if exposed to the sun.
Breast RT - Nursing Education
List two items of advice
Advise the patient to:
1. avoid bras with underwires, nylon, or lace (OK = breathable cotton bra or camisole)
- OK to use deodorant but avoid shaving the armpits to avoid skin irritation.
Head or neck area radiation:- Nursing Education
List two nursing considerations
- Dry mouth:
- suggest Swish and spit mouthwash either homemade (such as: 1 qt of water, 1 tsp of salt, and 1 tsp of baking soda) OR prescription mouthwash. Repeat several times per day.
- Reduce source of oral infection prior to RT: If possible, dental cleaning/eval recommended prior to initiation of RT to check for severely decayed teeth or an oral infection.
Pelvic radiation: List one important Nursing Education item for younger patients
- Provide information about sexuality and possible infertility before RT begins.
As appropriate:
banking sperm or egg-harvesting options.
RT Early side effects:
Onset time?
Duration, Severity?
When typically end?
What are 3x most common Early SE?
- Occur during or shortly after treatment.
- Tend to be short-term, mild, and treatable.
- Usually gone within a few weeks after treatment ends.
The most common:
1. Fatigue
2.. Skin changes
3. Other early side effects usually are related to the area being treated (ie. hair loss and mouth problems when radiation treatment is given to this area.most common AE
Name facts about RT Late side effects.
1. Onset
2. where in the body
3. Two factors that can influence
- Late side effects can take months to years to develop.
- Late side effects can occur in any tissue in the body that has received radiation.
- The risk of late side effects depends on the area treated as well as the radiation dose that was used.
Radioprotective drugs can reduce RT side effects.
- Name the most commonly used drug.
- What is the MoA?
- What is the typical cancer it is used for and what is the benefit?
- Amifostine is most commonly used Radioprotective drug.
- It is a Cytoprotective Agent. that acts to bind free Radicals (nucleophiles) thereby stabalizing DNA.
- Head and neck cancer - used to decrease dryness in the mouth caused by RT
Acute lymphocytic leukemia (ALL) List 4 Etiology and Risk Factors
- EBV
- human T-cell leukemia virus (HTLV-1)
- exposure to radiation and chemicals
- chromosomal abnormalities
Acute lymphocytic leukemia (ALL) Pathophysiology
- Disease of?
- Originates where in body?
- List 3x Types: L1-L3
- Diagnosed by?
- Malignant disease of lymphoid progenitors (T,B,NK cells).
- Orginates in the marrow, thymus, and lymph nodes
- Three Types of ALL
* L1: childhood (pre-B and T cell); 85% of cases are children
* L2: adult type (pre-B and T cell)
* L3: Burkett type (B cell)
* Diagnosis with marrow blasts > or = to 20%.
Acute lymphocytic leukemia (ALL) Clinical Manifestations (12)
- Recurrent infections
- pancytopenia
- fever
- fatigue
- weight loss
- swollen and bleeding gums
- slow-healing abrasions
- petechiae and bruising
- prolonged bleeding time
- bone pain
- organ infiltration (abdominal pain)
- swollen lymph nodes
Acute lymphocytic leukemia (ALL) Treatment and Management;
Add what for CD20?
Add what for Philadelphia chromosome?
- Hyper-CVAD, methotrexate and cytarabine,
CNS prophylaxis (Ara-C or methotrexate intrathecal) - Add rituximab if CD 20 positive (Burkett)
- Add imatinib if Philadelphia-chromosome– positive
- Bone marrow transplantation recommended
following first remission
Acute myelogenous
leukemia (AML) and acute nonlymphocytic leukemia Etiology and Risk Factors
- Correlated with what three risk factors?
- Peak age?
- Etiology unclear
- Genetics
- Down syndrome
- Correlation with benzene, chemotherapy,
radiation, and tobacco
exposure - Peak age is in the 50s.
Acute myelogenous
leukemia (AML) and acute nonlymphocytic leukemia Pathophysiology
What is early vs late stage?
What %blasts is diagnostic?
- Disease of the pluripotent myeloid stem
cell; chromosomal abnormalities of undifferentiated stem cells - Early stage: depletion of normal myeloid
cells (pancytopenia) - Later stage: Lack of apoptosis in malignant blast cells leads to accumulation in
marrow, blood, and organs. - Blast cells unable to fight infection; more
than 30% blasts in marrow is diagnostic.
Acute myelogenous
leukemia (AML) and acute nonlymphocytic leukemia Clinical Manifestations - name two primary
- Recurrent infections: susceptible to
cytomegalovirus, Pneumocystis carnii pneumonia, herpes simplex virus, and vancomycin resistant enterococcus - Pancytopenia, fever, fatigue, weight loss,
swollen or bleeding gums, slow-healing
abrasions, petechiae and bruising, prolonged bleeding time, bone pain, organ
infiltration (abdomi
Acute myelogenous
leukemia (AML) and acute nonlymphocytic leukemia Treatment and Management
- Cytarabine plus daunorubicin; cytarabine
plus idarubicin; cytarabine, daunorubicin,
and thioguanine; and mitoxantrone plus etoposide - For CNS, cytarabine or methotrexate
- Autologous or allogeneic bone marrow transplantation
- Blood product support (red blood cells,
platelets, and WBCs), broad spectrum antimicrobial, and antifungals
Etiology and Risk Factors Acute
promyelocytic leukemia
- Subtype of acute
myelogenous leukemia
Pathophysiology Acute promyelocytic leukemia
- Myeloid cell line: Myeloid cells can develop into red blood cells, white blood cells (other than lymphocytes NOT B or T cells), or platelets.
Clinical Manifestations Acute promyelocytic leukemia
- Recurrent infections, pancytopenia, fever, fatigue, weight loss, swollen or bleeding gums,
slow-healing abrasions, petechiae and bruising, prolonged bleeding, bone pain, organ
infiltration, swollen lymph nodes, and bleeding (disseminated intravascular coagulation,
fibrinolysis, and proteolysis)
Treatment and Management Acute promyelocytic leukemia
- Arsenic trioxide (the most common treatment), all-transretinoic acid, interleukin-2, and
anthracycline-based chemotherapy regimens - Autologous or allogeneic stem cell transplantation
Burkitt lymphoma (non-Hodgkin lymphoma) Etiology and Risk Factors
- Related to EBV
- Median survival is weeks, if left untreated.
Burkitt lymphoma (non-Hodgkin lymphoma) Pathophysiology
- Very aggressive and fast growing lymphoid progenitor (B or T cells); involvement with bone marrow, meninges, CNS, and blood
- Risk for tumor lysis; CNS a common site of relapse
- Potentially curable with aggressive therapy
Burkitt lymphoma (non-Hodgkin lymphoma) Clinical Manifestations
- Commonly presents at extranodal sites; typically present with rapidly growing, bulky
disease. - Elevated serum uric acid and LDH levels are
commonly found.
Burkitt lymphoma (non-Hodgkin lymphoma) Treatment and Management
- CODOX-M (cytoxan, vincristine, doxorubicin, and high-dose methotrexate)
- Hyper-CVAD —(cyclophosphamide, vincristine, doxorubicin, and dexamethasone)
- High risk: CODOX-M (cytoxan, vincristine, doxorubicin, and high-dose methotrexate) with ifosfamide, etoposide, and cytarabine
- Rituximab and hyper-CVAD (cyclophosphamide, vincristine, doxorubicin, and dexamethasone) alternating with methotrexate and cytarabine
Chronic lymphocytic leukemia (CLL) Etiology and Risk Factors
- No known occupational or environmental
risk factors - Genetic link: high familial risk
- Most common adult
leukemia
Chronic lymphocytic leukemia (CLL) Pathophysiology
- Progressive accumulation of nonproliferating, morphologically mature but immunologically less mature lymphocytes
Chronic lymphocytic leukemia (CLL) Clinical Manifestations
- 40% asymptomatic at diagnosis
- B or constitutional symptoms
- Fatigue; weakness; malaise; bacterial infections; herpes zoster; exaggerated skin
reaction to insect bites or bee sting; and enlarged spleen (less frequently hepatomegaly), abdominal discomfort, and early satiety
Chronic lymphocytic leukemia (CLL) Treatment and Management
- FCR (fludarabine, cyclophosphamide, and rituxan), FC (fludarabine and cyclophosphamide), CFAR (cyclophosphamide, fludarabine, alemtuzumab, and rituximab (campath–found to “clean up” minimal residual disease), and stem cell transplantation
Chronic myelogenous
leukemia (CML) Etiology and Risk Factors
- Also called chronic
granulocytic leukemia - Chromosomal abnormalities
- No known specific
cause except exposure
to ionizing radiation
Chronic myelogenous
leukemia (CML)Pathophysiology
- Disorder of the myeloid stem cells characterized by marked splenomegaly and
increased production of granulocytes - About 90% of patients are Philadelphiachromosome–positive.
- Mature-appearing dysfunctional cells in three phases: chronic, accelerated,
and blast phase; blast crisis presents like acute leukemia, granulocytes replacing marrow - Average age of diagnosis is in 30s–40s; most diagnoses are in the chronic phase.
Chronic myelogenous
leukemia (CML)Clinical Manifestations
- Initial S&S: massive splenomegaly, fatigue, malaise, headache, weakness, weight loss, bone or joint pain, excessive (night) sweats, fever, abdominal pain (left upper quadrant), early satiety, vague abdominal fullness, hepatosplenomegaly,
lymphadenopathy, easy bruising, petechia, elevated basophils and neutrophils, blasts present, high B12 levels, and low alkaline
phosphatase - Chronic phase: high WBC count (10–150 times the normal level).
- Blastic phase presents with hypercatabolism, pancytopenia, and infection.
Chronic myelogenous
leukemia (CML)Treatment and Management
- Interferon alpha, imatinib, dasatinib, nilotinib, and stem cell transplantation (last resort, mostly allogeneic)
Diffuse large B-cell lymphoma (non-Hodgkin lymphoma) Etiology and Risk Factors
- Median age is 64 years;
affects more men than women - Overall survival is 50% at five years.
Diffuse large B-cell lymphoma (non-Hodgkin lymphoma) Pathophysiology
- Most common type of non-Hodgkin lymphoma
- Encompasses a diffuse group of large, neoplastic B lymphocytes with large nuclei.
- Destruction of the normal architecture of the involved lymph node occurs in a diffuse pattern.
- Frequently express B-cell markers (CD19, CD20, CD22, CD79a)
Diffuse large B-cell lymphoma (non-Hodgkin lymphoma) Clinical Manifestations
- Disseminates rapidly
- ”B” symptoms (unexplained fever, night sweats, and unexplained weight loss)
- Anemic
- Most present with nodal and extra nodal (gastrointestinal, skin, sinus, and stomach).
- Potentially curable
- Presents either as primary lymph node disease or at extranodal sites
Diffuse large B-cell lymphoma (non-Hodgkin lymphoma) Treatment and Management
- Stage I: R-CHOP (R-CHOP—rituxan, cyclophosphamide, doxorubicin, vincristine, and prednisone) six times with radiation therapy
- Stage I/II: R-CHOP (rituxan, cyclophosphamide, doxorubicin, vincristine, and prednisone) 6–8 times plus radiation therapy
- Stage III/IV: clinical trial of R-CHOP (rituxan, cyclophosphamide, doxorubicin, vincristine, and prednisone) and
Hyper-CVAD (cyclophosphamide, vincristine, doxorubicin, and dexamethasone) every 14 days or 6–8 courses (rituximab eight times) - Second line: rituxan, ifosphamide, etoposide,
and carboplatin (RICE), R-ESHAP (rituxan, etoposide, methylprednisolone, cytarabine, and cisplatin) salvage (dexamethasone, cisplatin, and cytarabine [DHAP]), and carmustine, etoposide, cytarabine, and melphalan (BEAM)
Follicular lymphoma (non-Hodgkin lymphoma) Etiology and Risk Factors
- Accounts for 35% of
all non-Hodgkin lymphoma cases - Median age is 60;
median survival from
diagnosis is 10 years.
Follicular lymphoma (non-Hodgkin lymphoma) Pathophysiology
- Neoplasm of follicle center (germinal center) B cells
Follicular lymphoma (non-Hodgkin lymphoma)Clinical Manifestations
- B-cell symptoms: unexplained fever, night sweats, and unexplained weight loss
- Lymphadenopathy (cervical, supraclavicular,
and maxillary)
Follicular lymphoma (non-Hodgkin lymphoma)Treatment and Management
- Treatment usually not curative. Responds well initially, but high incidence of recurrence
- Watch and wait, radiation therapy alone, chemotherapy, or chemotherapy with radiation therapy
- High risk: CODOX-M (cytoxan, vincristine, doxorubicin, and high-dose methotrexate) /VAC
- Rituximab and hyper-CVAD (cyclophosphamide, vincristine, doxorubicin, and dexamethasone) alternating with
methotrexate and cytarabine
Hodgkin lymphoma Etiology and Risk Factors
- Affects more men than
women - Genetics, EBV, HIV, herpes virus 6
- Occupational (woodworking, chemical exposures)
Hodgkin lymphoma Pathophysiology
- B-cell origin (Reed-Sternberg cells)
- Nodular sclerosis (grades 1 and 2),
lymphocyte-rich, mixed cellularity, lymphocyte depleted
Hodgkin lymphoma Clinical Manifestations
- Most present with peripheral lymphadenopathy above the diaphragm.
- B cell symptoms: unexplained fever, night
sweats, unexplained weight loss (greater
than 10%) - Pruritis
- Lymphadenopathy (cervical, supraclavicular,
and maxillary) - Fatigue; pain with alcohol consumption
Hodgkin lymphoma Treatment and Management
- Staging dependent
- Radiation therapy
- Chemotherapy: doxorubicin, bleomycin, vinblastine, and dacarbazine (ABVD)
- Mechlorethamine, vincristine, procarbazine,
and prednisone (MOPP) - Stem cell transplantation
Mantle cell (non-Hodgkin lymphoma) Etiology and Risk Factors
- Median age is 60 years;
median survival is 3–5
years. - Aggressive, cure is rare.
Mantle cell (non-Hodgkin lymphoma) Pathophysiology
- B-cell neoplasm
- Strong surface immunoglobulin M
- Monoclonal lymphoid proliferation destroys the architecture of the lymph node.
- A nodular, diffuse, or mantle zone
growth pattern is observed.
Mantle cell (non-Hodgkin lymphoma) Clinical Manifestations
- Hepatomegaly and splenomegaly are common findings.
- Most common extranodal sites reported include the gastrointestinal tract and Waldeyer ring found on the tonsils.
- Anemic
- May include gastrointestinal tract, marrow, blood, liver, brain, and cerebrospinal fluid
Mantle cell (non-Hodgkin lymphoma) Treatment and Management
- First line: hyper-CVAD (cyclophosphamide, vincristine, doxorubicin, and dexamethasone)
- Second line: fludarabine, cytoxan, and rituximab (FCR)
- Pentostatin, cytoxan, and rituximab (PCR)
- Bortezomib
Mycosis fungoids mature T-cell lymphoma (non-Hodgkin lymphoma) Etiology and Risk Factors
- Accounts for 0.5%–3% of non-Hodgkin lymphoma cases
- Median age is 55–60 years; affects more men than women
Mycosis fungoids mature T-cell lymphoma (non-Hodgkin lymphoma) Pathophysiology
- T-cell lymphocytes become cancerous and affect the skin.
- Infiltration of the epidermis and dermis with T cells
Mycosis fungoids mature T-cell lymphoma (non-Hodgkin lymphoma) Clinical Manifestations
- Skin lesions, initially seen on the trunk
- May involve lymph nodes, liver, spleen, lungs, and blood
- Bone marrow involvement is rare
Mycosis fungoids mature T-cell lymphoma (non-Hodgkin lymphoma) Treatment and Management
- Steroids and chemotherapy applied to the skin in early phase
- Treatment usually is palliative.
Myleodysplastic syndrome (MDS) Etiology and Risk Factors
- Unknown
Myleodysplastic syndrome (MDS) Pathophysiology
- Group of hematologic disorders with an increased risk of transformation to acute myelogenous leukemia; occur as result of altered stem cells
- Chromosome abnormalities are present at the level of stem cell in 50% of patients with primary MDS and 75% of patients with therapy-related MDS.
- 80%–90% of patients older than age 50
- Median survival is 28 months.
Myleodysplastic syndrome (MDS) Clinical Manifestations
- Characterized by one or more peripheral blood cytopenias secondary to bone marrow dysfunction
- Anemia, bleeding, easy bruising, and fatigue
Myleodysplastic syndrome (MDS) Treatment and Management
- Bone marrow transplantation (successful if marrow comes from human leukocyte antigen donor and if the patient is younger than
age 55)—only curative therapy - High-dose chemotherapy for ablation can induce remission in 40%–60% of patients.
Multiple myeloma (MM) Etiology and Risk Factors
- Unknown
- Monoclonal gammopathy of undetermined significance (MGUS): possible precursor
- Abnormal level of serum protein that does not cause tumors
Multiple myeloma (MM) Pathophysiology
- Cancer of plasma or B cell
- Serum or urine protein (monoclonal immunglobulin M protein)
- No cure; relapse inevitable
- Plasmablastic cells (plasma stem cell) colonize the bone marrow.
- Research suggests correlation with deletion of chromosome 13 in MM.
- Bone destroyed by osteolytic action of malignant plasma cells
Multiple myeloma (MM) Clinical Manifestations
- Bone pain, anemia, and recurrent infections (related to impaired T cells)
- Lytic bone lesions: risk for fractures, spinal cord compression, and loss of weight bearing ability
- High-protein serum (M protein)
- Pallor: Most common physical finding
- Liver or spleen palpable in many patients
- Mental status changes related to hypercalcemia, hyperviscosity syndrome, or renal insufficiency
- Limitations in range of motion
- Hypercalcemia, elevated blood urea nitrogen, creatinine, and uremia
Multiple myeloma (MM) Treatment and Management
Also Primary vs. Maintenance Therapy
- Bortezomib, thalidomide, and lenalidomide
Primary:
* Melphalan and prednisone
* Vincristine, carmustine, melphalan, cytoxan, and prednisone
* Vincristine, carmustine, doxorubicin, and prednisone
* Vincristine, doxirubicin, and dexamethasone
Maintenance therapy:
* Steroids and interferon
* Radiation therapy: limited, can further deplete bone marrow reserve; used for palliative therapy
* Autologous transplantation
Richter syndrome Etiology and Risk Factors
- Occurs in 1 of 20 patients with chronic lymphocytic leukemia
Richter syndrome Pathophysiology
- Rare, progresses rapidly, aggressive
- Related to EBV
- Richter syndrome transforms into highgrade non-Hodgkin lymphoma, acute leukemia, prolymphocytic leukemia, and Hodgkin leukemia
- Median survival five to eight months.
Richter syndrome Clinical Manifestations
- Rapid onset lymphadenopathy
- Bulky retroperitoneal adenopathy
- Fever, night sweats, and weight loss; massive hepatosplenomegaly; clinical deterioration
- Extranodal involvement (skin, CNS, gastrointestinal tract, eye, testes, lung, and kidney)
Richter syndrome Treatment and Management
- Chemotherapy: lenalidomide, lumiliximab, clofarabine, and dasatinib
- Monoclonal antibodies and biologic therapy
- Allogeneic stem cell transplantation
- Radiotherapy
T-cell Lymphoma Etiology and Risk Factors
- Median age: 61
- Cutaneous T cell: skin involvement and mycosis fungoids
- Viral cause: human T-cell lymphotrophic virus type 1, EBV
- Genetics, radiation, and immunosuppression
T-cell Lymphoma Pathophysiology
Unknown “-“
T-cell Lymphoma Clinical Manifestations
- Lymphadenopathy, ”B” symptoms (unexplained fever night sweats, and unexplained weight loss), and fatigue
T-cell Lymphoma Treatment and Management
- Hyper-CVAD (cyclophosphamide, vincristine, doxorubicin, and dexamethasone) plus etoposide, prednisone, vincristine, cyclophosphamide, and doxorubicin (EPOCH)
- Relapsed: transplantation, DHAP, R-ESHAP (rituxan, etoposide, methylprednisolone, cytarabine, and cisplatin), and ifosphamide, etoposide, and carboplatin (ICE)
- Nontransplantation: velcade, gemcitabine, and ontak
Name two targeted therapy Signal Transduction Inhibitors - EGFR inhibitors
EGFR inhibitors:
e.g., cetuximab, erlotinib
Name two targeted therapy Signal Transduction Inhibitors - HER2 inhibitors
HER2 inhibitors:
e.g., trastuzumab, pertuzumab
Name two targeted therapy Signal Transduction Inhibitors - BCR-ABL inhibitors (also called tyrosine kinase inhibitors)
BCR-ABL inhibitors (also called tyrosine kinase inhibitors):
e.g., imatinib, dasatinib
Name two targeted therapy Signal Transduction Inhibitors - ALK inhibitors (also called multikinase inhibitors)
ALK inhibitors (also called multikinase inhibitors):
e.g., crizotinib, ceritinib
Name two targeted therapy Signal Transduction Inhibitors - BRAF kinase inhibitors (also called multikinase inhibitors )
BRAF kinase inhibitors (also called multikinase inhibitors):
e.g., vemurafenib, dabrafenib
Tumor specific antigen CD20:
What cells express this?
What therapy targets CD20?
Which cancers are treated with this targeted therapy?
Cells: CD20 is expressed on pre-B and mature B cell lymphocytes (Lymphoid lineage)
Therapy: Rituximab = monoclonal antibody that targets CD20 tumor specific antigen
Certain leukemias and lymphomas, including non- Hodgkin lymphoma and lymphocyte predominant subtype of Hodgkin lymphoma
Tumor specific antigen CD33:
What cells express this?
What therapy targets CD33?
Which cancers are treated with this targeted therapy?
Cells: CD33 is expressed primarily on Myeloid lineage cells and some lymphoid cells; Myeloid colony forming cells + Leukemic blasts
- Megakaryocyte (platelet precursor)
- Erythrocyte (RBC precursor)
- Mast cell
- Myeloblast (Basophil, Neutrophil, Eosinophil, Monocyte=Macrophage precursor)
Therapy: Gemtuzumab ozogamicin (removed from market June 2010) targeted CD33
Cancer: Treats AML (acute myeloid leukemia)
Tumor specific antigen CD52:
What cells express this?
What therapy targets CD52?
Which cancers are treated with this targeted therapy?
Cells: CD52: is expressed on 1)Mature lymphocytes (B & T cells), but not on Lymphocyte stem cells 2)Monocytes 3)Macrophage (& dendritic cells)
Therapy: Alemtuzumab
Cancers treated: 1)some types of lymphoma 2)CLL (chronic lymphocytic leukemia)
Name two targeted therapy - Apoptosis Inducers via Proteasome inhibitor
Two targeted therapies - Apoptosis Inducers via Proteasome inhibitor:
bortezomib and carfilzomib
Name two targeted - Angiogenesis Inhibitor PATHWAYS (two) and therapies for each.
Name two targeted therapy - Angiogenesis Inhibitor PATHWAYS:
1)Agents that interfere with the action of vascular endothelial growth factor (VEGF)
- Bevacizumab
2)Agents that target other receptors on the surface of endothelial cells or other proteins in the downstream signaling pathways that stimulate new blood vessel growth (cytosolic TF phosphorylation: RAS, RAF, MAP; Nucleus gene transcription leading to protein synthesis: Fos, ATF-2, Jun, Mac)
- Sorafenib = oral dual action kinase inhibitor with MULTIPLE targets: RAF/MEK/ERK pathway in tumor cells and tyrosine kinases VEGFR/PDGFR in tumor vasculature
- Sunitinib = an oral oxindole receptor tyrosine kinase (RTK) inhibitor with MULTIPLE targets, similar to Sorafenib
Targeted therapy - Small Molecule Agents - Tyrosine Kinase inhibitors (TKIs)
What is MOA, how do TKIs stop cancer cells? What signaling pathways do they inhibit?
What letters do these targeted agents typically end in?
How are they typically administered?
Name drug examples (10)
Tyrosine Kinase inhibitors (TKIs)
TKI MOA: Binds EGFR and/or VEGF inactivates or limits its activity
Orally administered
-tinib
Drug examples:
- dasatinib (CML w/ (+) philadelphia chr)
- erlotinib (advanced NSCLC & pancreatic)
- gefitinib
- ibrutinib (Mantle cell lymphoma, CML)
- imatinib (CML w/(+) philadelphia chr)
- lapatinib
- ponatinib (CML)
- sunitinib (advanced RCC & GIST tumors)
- vandetanib
- odd one out: ziv-aflibercept
Targeted therapy - Tyrosine Kinase inhibitors (TKI) MOABs
What is MOA, how do TKI MOABs stop cancer cells? What signaling pathways do they inhibit?
How are they typically administered?
Name drug examples (2)
Tyrosine Kinase inhibitor (TKI) MOAB
TKI MOAB MOA: Binds EGFR and/or VEGF inactivates or limits its activity
Administered by IV
Drug examples: cetuximab, panitumumab
Targeted therapy - Small Molecule Agents - Kinase inhibitors
What is MOA, how do TKIs stop cancer cells? What signaling pathways do they inhibit?
What letters do these targeted agents typically end in?
How are they typically administered?
Name drug examples (4)
Kinase inhibitors
MOA: target the RAF/RAS/MET pathway
- nib
Administered: PO
Examples:
* Sorafenib,
* Dabrafenib
* Trametinib
* Vemurafenib
Targeted therapy - Small Molecule Agents - PI3K inhibitors
What is MOA, how do PI3K inhibitors stop cancer cells? What signaling pathways do they inhibit?
What letters do these targeted agents typically end in?
How are they typically administered?
Name drug example (1)
PI3K inhibitors
MOA: PI3K inhibitors target the PI3K pathway
- lisib
Administered: PO
Idelalisib - follicular B-Cell non-Hodgkin Lymphoma and relapsed CLL
Targeted therapy - Small Molecule Agents - hedgehog pathway inhibitor
What is MOA, how do hedgehog inhibitors stop cancer cells? What signaling pathways do they inhibit?
What letters do these targeted agents typically end in?
How are they typically administered?
Name drug example (2)
hedgehog pathway inhibitor
MOA: inhibit hedgehog pathway, normally controls cell division of adult stem cells and cell differentiation
- gib
Administered: PO
Examples:
- Sonidegib locally advanced Basal cell carcinoma
- Vismodegib - metastatic or recurrent locally advanced Basal cell carcinoma
The Cell Cycle
GO phase
Action during this phase
Duration
After signal, what is next phase?
G0 phase (resting stage, temporarily out of cell cycle):
The cell has not yet started to divide.
Duration: from a few hours to a few years.
Next phase: When the cell gets a signal to reproduce, it moves into the G1 phase.
The Cell Cycle
G1 phase
Action during this phase
Duration
After signal, what is next phase?
G1 = Gap 1
Action: During this phase, the cell starts making more proteins and growing larger, so the new cells will be of normal size.
Duration: 18–30 hours
Next phase: S phase
The Cell Cycle
S phase
Action during this phase
Duration
After signal, what is next phase?
Synthesis phase
Action: the chromosomes containing the genetic code (DNA) are copied, so both of the new cells formed will have matching strands of DNA.
Duration: from 18–20 hours
Next Phase: G2 phase
The Cell Cycle
G2 phase
Action during this phase
Duration
After signal, what is next phase?
Gap 2 Phase
Action: cell checks the DNA and gets ready to start splitting into two cells.
Duration: form 2–10 hours
Next Phase: M phase
The Cell Cycle
M phase
Action during this phase
Duration
After signal, what is next phase?
Mitosis
Action: Cell splits into two new cells.
Duration: 30-60 min
Next phase: G1 or G0 phase
Are Alkylating Agents
cell-cycle specific?
What does this mean about effectiveness during the cell cycle?
No.
Alkylating agents are cell-cycle NONspecific and therefore exert effects in ALL phases of the cell cycle.
What is Alkylating Agent MOA?
Are they given intermittently?
Alkylating Agents break the DNA helix strand, which interferes with the DNA replication process and results in cell death.
Yes, given intermittently allowing patient to recover.
Name 6 types of alkylating agents (cell-cycle NONspecific)
Types of alkylating agents include:
NON-Platins:
1* Nitrogen mustards (melphalan, ifosfamide, cyclophosphamide, bendamustine)
2* Nitrosoureas (cross the blood-brain barrier) (lomustine, carmustine, streptozocin)
3* Triazines and hydrazines (dacarbasine, procarbazine, temozolomide)
4* Alkyl sulfonates (busulfan)
5* Ethylenimines: (thiotepa and altretamine (hexmethylmelamine)
Platins:
6* Platinums (cisplatin, oxaliplatin, carboplatin)
Name 4 DLTs for alkylating agents (cell-cycle NONspecific) such as:
Nitrogen mustards, Nitrosoureas, Platinums, Triazines and hydrazines, and, Alkyl sulfonates
Alkylating agent - Dose-Limiting Toxicities:
- Bone marrow suppression
- Organ-specific toxicities dependent on medication and dose (e.g., renal, and hepatic toxicities,
pulmonary and cardiac toxicities, urotoxicity). - Hemorrhagic cystitis
- Peripheral neuropathy.
Name the Class of Chemotherapy:
* Nitrogen mustards
Name 3 examples
Type of alkylating agent (cell-cycle NONspecific)
Examples
1. melphalan
2. ifosfamide,
3. cyclophosphamide
4. bendamustine
Name the Class of Chemotherapy:
* Nitrosoureas
Name 3 examples
What is a special feature?
Type of alkylating agent (cell-cycle NONspecific)
Examples
1. lomustine.
2. carmustine
3. streptozocin
**cross the blood-brain barrier
Name the Class of Chemotherapy:
* Platinums
Name 3 examples
Type of alkylating agent (cell-cycle NONspecific)
Examples
1. cisplatin
2. oxaliplatin
3. carboplatin
Name the Class of Chemotherapy:
* Triazines and hydrazines
Name 3 examples
Type of alkylating agent (cell-cycle NONspecific)
Examples
1. dacarbasine,
2. procarbazine,
3. temozolomide
Name the Class of Chemotherapy:
* Alkyl sulfonates
Name 1 example
Type of alkylating agent (cell-cycle NONspecific)
Example
1. busulfan
Common SE of alkylating agents,
cell-cycle NONspecific such as:
Nitrogen mustards, Nitrosoureas, Platinums, Triazines and hydrazines, and, Alkyl sulfonates
Expected SE of alkylating agents:
* GI (e.g N/V anorexia, diarrhea, mucositis, stomatitis).
* Neurological (e.g., peripheral neuropathy).
* Tumor lysis syndrome
* Risk of new malignancy
* Other rapidly dividing cells are affected, often causing alopecia rashes, or infertility.
Pre- and Post- administration considerations for alkylating agents (cell-cycle NONspecific) such as:
Nitrogen mustards, Nitrosoureas, Platinums, Triazines and hydrazines, and, Alkyl sulfonates
Pre- and Post- administration considerations for alkylating agents:
- Monitor blood counts and reference treatment parameters
- GCSF with treatment plan or PRN
- Blood transfusion PRN
- Dose hold vs. reduction PRN
- regular UA depending on treatment plan
- Negative pregnancy test before treatments.
- Conduct baseline assessment, closely monitor during therapy for SE,
intervene early if issues.
What class of chemotherapeutics are derived from compounds produced by the
Streptomyces bacteria?
What is the MOA?
Are these therapies cell cycle specific?
Antitumor Antibiotics
MOA: They work by binding with DNA, thereby inhibiting DNA and RNA synthesis.
NO. This class of chemo is cell cycle phase NON-specific (except
for bleomycin)
What are the TYPES of Antitumor Antibiotic, cell cycle NON-specific chemo derived from the
Streptomyces bacteria?
Types of antitumor antibiotics include:
- Anthracyclines (e.g., daunorubicin, doxorubicin, epirubicin, idarubicin, valrubicin)
- Non-anthracyclines (e.g., bleomycin, mitomycin C, mitoxantrone, dactinomycin)
What are the DLTs of Antitumor Antibiotic, cell cycle NON-specific chemo derived from the
Streptomyces bacteria: Antracyclines and non-anthracyclines?
DLTs of Antitumor Antibiotic, cell cycle NON-specific
- Myelosuppression
- Cardiotoxicity (Anthracyclines)
- Pulmonary fibrosis (Bleomycin w/lifetime dose <400 units)
- Organ-specific toxicities depending on drug/dose (hepatic, renal)
*
What are the expected SE of Antitumor Antibiotic, cell cycle NON-specific chemo derived from the
Streptomyces bacteria: Antracyclines and non-anthracyclines?
Expected SE of Antitumor Antibiotic, cell cycle NON-specific:
- GI (e.g., N/V, anorexia, diarrhea, mucositis, stomatitis).
- Radiation recall =inflammation to areas of prior RT weeks or years after RT completed, especially skin.
- Discolored urine based on medication color (e.g., doxorubicin =
red-colored urine, mitoxantrone = blue- or green-colored urine) - Other rapidly dividing cells are affected causing alopecia, rashes, and hyperpigmentation.
Pre- and Post administration considerations of Antitumor Antibiotic, cell cycle NON-specific chemo derived from the
Streptomyces bacteria: Antracyclines and non-anthracyclines
Pre- and Post administration considerations of Antitumor Antibiotic,
- Monitor blood counts and reference treatment parameters
- GCSF with treatment plan or PRN
- Blood transfusion PRN
- Dose hold vs. reduction PRN
- regular UA depending on treatment plan
- Negative pregnancy test before treatments.
- Conduct baseline assessment, closely monitor during therapy for SE,
intervene early if issues. - vesicant precautions: many antitumor antibiotic agents are vesicants (highly toxic and corrosive to soft tissue).
- IV assessment
- Central line for some meds
- Consider central line for poor venous access
Name 4 Anthracyclines
What class of chemo? Derived from?
Cell cycle specific?
MOA
4x Antracyclines:
1. daunorubicin
2. doxorubicin
3. epirubicin
4 idarubicin
Class of chemo: Antitumor antibiotics, derived from Streptomyces bacteria
No. Cell cycle phase NON-specific (except
for bleomycin)
MOA: bind DNA, thereby inhibiting DNA and RNA synthesis
Nitrosoureas: what class of chemotherapy?
What is MOA?
Cell cycle specific?
Why are they special?
Name 3 examples & how administered
Nitrosoureas are alkylating agents
MOA: Break DNA, interferes with DNA replication
Cell cycle NON-specific
Special: cross the blood–brain barrier
3x Examples:
1. Carmustine (IV or implantation ie wafer)
2. Lomustine (PO)
3. Streptozocin (IV)
Name 4x DLTs for Nitrosoureas, alkylating agents that cross the blood–brain barrier
DLTs for Nitrosoureas, alkylating agents that cross the blood–brain barrier
- Bone marrow suppression (PLT, HGB, and ANC)
Nadir = 4-6 wks = 6-8 week cycle for count recovery - Pulmonary tox (irreversible)
- Implanted wafer (Carmustine) has specific tox: intracranial HTN, seizures, meningitis, delayed neurological surgery wound healing
- Organ spec. tox depending on agent (renal / hepatic etc)
Name 4x expected AEs for Nitrosoureas, alkylating agents that cross the blood–brain barrier
4x expected Nitrosoureas AEs:
- GI
- Secondary malignancy
- Streptozozin can alter glucose metabolism
- Other (fatigue, alopecia, proteinuria, confusion)
5x Pre- and Post administration considerations for for Nitrosoureas, alkylating agents that cross the blood–brain barrier
- Blood counts/reference treatment parameters
- dose hold/reduce PRN - conduct baseline assessment, closely monitor during therapy for SE,
intervene early if issues - Anti-emetic 30-60min pre-dose
- PFTs - Recognize cumulative dose maximums
- IV site assessment prior to administration
Are antimetabolites cell cycle-specific agents?
Yes!
MOA suring S Phase (DNA synthesis/ replication)
Name 4x Types of Antimetabolites, cell cycle-specific (S phase) agents
- Folic acid analogs
- Pyrimidine analogs
- Purine analogs
- Ribonucleotide reductase inhibitors
Name 2x Folic acid analogs, a type of Antimetabolite, cell cycle-specific (S phase) agent
2x Folic acid analogs a type of Antimetabolite
1. Methotrexate
2. Pemetrexed
Name 4x Pyrimidine analogs, a type of Antimetabolite, cell cycle-specific (S phase) agent
4x Pyrimidine analogs, a type of Antimetabolite
- 5-fluorouracil
- cytarabine
- gemcitabine
- azacytidine
Name 4x Purine analogs, a type of Antimetabolite, cell cycle-specific (S phase) agent
4x Purine analogs, a type of Antimetabolite
- fludarabine
- cladribine
- mercaptopurine
- nelarabine
Name 3x Antimetabolite DLTs
3x Antimetabolite DLTs:
- Bone marrow suppression
- Neuro tox. including CEREBELLAR + PSN
- Organ specific depending on agent and dose (ie. renal, hepatic, pulmonary, cardiac)
Name 4x Antimetabolite expected AEs
Name 4x Antimetabolite expected AEs
- GI (N/V, anorexia, diarrhea, mucositis, stomatitis)
- TLS
- secondary malignancy risk
- Other rapidly dividing cell tox. (alopecia, skin issues including rash/photosensitivity, infertility)
Antimetabolite 10x Pre- and Post administration considerations
Antimetabolite 10x Pre- and Post administration considerations
- Monitor cell counts/treatment parameters
- PRN GCSF
- PRN transfusions
- PRN Dose Hold/reduce
- Pregnancy testing Antimetabolites = teratogens - Baseline assessment, monitor, intervene early
- Pre-dose Cerebellar assessment for some meds (ie. high dose cytarabine)
- Anti-emetic pre-meds 30-60min pre-dose
- TLS (ie. allopurinol, hydration)
- PFT & monitoring
- 365day photosensitivity precautions
- assess IV site, vesicant & irritant precautions
- Reference black-box warnings for individual agents
- Fertility preservation
Are Angiogenesis Inhibitor targeted therapy?
Describe the MOA
Name 2x main ways that these treatments work
Angiogenesis Inhibitors are MOA = targeted therapy that interferes with the process of
creating new blood vessels (angiogenesis) which “starve” the tumors
2x Main ways can work:
- Some drugs recognize and bind
vascular endothelial growth factor (VEGF) receptor which disables the receptor. - Other angiogenesis inhibitors work on different parts of the pathway to
block activity downstream or on other molecules.
Name 2x advantages of Angiogenesis inhibitors
- Fewer AE (targets one process0
- Available by PO, allowing continuous administration at lower doses
Name 4x limitations of Angiogenesis inhibitors
4x limitations of Angiogenesis inhibitors:
- Does not kill cancer cells, must be used in combination with other therapies
2* Delayed wound healing (planning around surgeries/procedures)
3* Risks: HTN, internal bleeding, or rare perforation of the intestine
4* Patient adherence PO therapy
Plant Alkaloid:
Vinca alkaloids
Derived from what plant?
Cell cycle specific?
MOA?
Derived from the Madagascar periwinkle plant (Catharanthus rosea)
Yes, cell cycle specific (predominantly M phase)
MOA: Vinca alkaloids are cytoxic to microtubules and cell cycle arrests in metaphases
Plant Alkaloid:
Vinca alkaloids.
Name 4x common AEs
- myelosuppression 2. peripheral neuropathy
- nausea
- vomiting
Plant Alkaloid:
Vinca alkaloids.
Name 3x example drugs
- Vinblastine
- Vincristine
- Vinorelbine
Plant Alkaloid:
Epipodophyllotoxins
(camptothecans and podophyllotoxins)
Derived from what plant?
Cell cycle specific?
MOA?
Camptothecans are derived from the Asian “happy tree” (Camptotheca acuminata)
Podophyllotoxins are derived from the May apple plant.
Yes, cell cycle specific (Late S and G2 phases)
MOA: forms a complex with topoisomerase and DNA resulting in the inhibition of the topoisomerase enzyme
Plant Alkaloid:
Epipodophyllotoxins
(camptothecans and podophyllotoxins)
Name 2x common AEs
- Diarrhea
- Neutropenia
Plant Alkaloid:
Epipodophyllotoxins
(camptothecans and podophyllotoxins)
Name 4 chemo drugs
4x Plant Alkaloid:
Epipodophyllotoxins
chemo drugs:
- Etoposide (VP-16)
- Teniposide (VM 26)
- Camptothecan (CPT)
- Topotecan hydrochloride
Plant Alkaloid:
Taxanes
Derived from what plant?
Cell cycle specific?
MOA?
Plant Alkaloid:
Taxanes
Derived from: Pacific yew tree
Yes, cell cycle specific (M phase, G1 to S transition phase)
MOA: inhibit the microtubules necessary for cellular division
Plant Alkaloid:
Taxanes
1x Potential DLT
Plant Alkaloid,
Taxanes, potential DLT
peripheral neuropathy
Plant Alkaloid:
Taxanes
4x Examples
- Paclitaxel
- Docetaxel
- Cabazitaxel
- Paclitaxel protein bound
Glucocorticoids can be considered chemotherapy or supportive agents:
Glucocorticoids are steroids, naturally occurring hormones, and hormone-like drugs
Name 3x MOA
Glucocorticoids 3x MOA:
- modify transcription and protein synthesis
- reverse capillary permeability
- inhibit glucose transport and phosphorylation to induce apoptosis
Glucocorticoids when used as supportive agents.
Used to prevent/treat what 4x AEs?
Treat what 2x Oncology Emergencies?
Used to prevent 4x AEs:
1. nausea
2. vomiting
3. infusion reactions (hypersensitivity reactions)
4. skin reactions (topical)
Treats 2x Oncology Emergencies:
1. superior vena cava syndrome
2. spinal cord compression
Name 4x Glucocorticoids, steroids, naturally occurring hormones, and hormone-like drugs
- prednisone
- hydrocortisone
- methylprednisolone
- dexamethasone
Hazardous Drug exhibit one or more of 6x characteristics (name the characteristics)
Hazardous drugs (HDs) exhibit one or more of the following characteristics:
- Carcinogenicity
- Teratogenicity
- Reproductive toxicity
- Organ toxicity at low doses
- Genotoxicity
- Any drug similar in structure or toxicity to drugs classified as hazardous
True or False
Use of PPE reduces the risk of absorption of Hazardous Drugs (HDs)
True
Name 5x ways RNs can be exposed to Hazardous Drugs (HDs)
- Absorption
- Injection
- Ingestion
- Inhalation
Name the PPE that protect us from HDs
- gloves
- gown
- mask/shield/goggles
- mask/respirator
Name the 4x standard Chemo PPE items
- 2x pairs gloves tested for HD
- gown: disposable solid front, long sleeves, tight cuffs, back closure
- Eye/face protection
- Respirator PRN (specific drugs or spill clean up)
Steps to don standard chemo PPE
- Wash hands (soap and water)
- 1st pair of gloves on
- Gown on, fasten tie closure at back, gloves INSIDE gown arms/cuffs
- 2nd pair of gloves on (OVER gown cuffs)
- Face/eye protection
steps to doff standard chemo PPE
- Remove outer gloves, turning inside out
- Remove gown, turning inside out
- remove face shield
- Remove 2nd set of gloves
- Dispose of ALL contaminated items
- Remove gloves LAST
- Wash hands (soap and water)
Chemo: Altretamine
(Hexalen®)
What is the:
1. Class of chemotherapeutic
- MOA of this class
- Indications
- DLTs
- Special considerations for this agent
Chemo: Altretamine
(Hexalen®)
- Class: Alkylating agent
- MOA: Break DNA helix
strand, thereby
interfering with
DNA replication - Indications: Ovarian
- DLTs: neuro. tox, PSN, myelosup., n/v, skin rash, hypersensitivity RXN
- Special Considerations for this agent:
- PO administration
- Take after meals and at bedtime
- Monitor for progressive neuro tox.
- AVOID concurrent MAOI Monoamine oxidase Inhibitor anti-depressants -> can cause severe orthostatic hypotension
Chemo: Bendamustine
(Treanda®
Bendeka®)
What is the:
1. Class of chemotherapeutic
- MOA of this class
- Indications
- DLTs
- Special considerations for this agent
Chemo: Bendamustine
(Treanda®
Bendeka®)
- Class: Alkylating agent
- MOA: Break DNA helix
strand, thereby
interfering with
DNA replication - Indications: HEME CLL and Indolent NHL
- DLTs: Myelosup. Pyrexia, n/v, skin RXNs, TLS, hepatic tox. vein irritation
- Special Considerations this agent:
- Irritant and Vesicant
- Infusion RXN cycles 2+
- Monitor for TLS (high risk patients
- Concurrent Allopurinol may increase severe Skin Tox.
- Not compatible with polycarbonate or acrylonitrile-butadiene-styrene lines
Chemo: Busulfan
(IV: Busul-fex®; oral: Myl-
eran®)
What is the:
1. Class of chemotherapeutic
- MOA of this class
- Indications
- DLTs
- Special considerations for this agent
Chemo: Busulfan
(IV: Busul-
fex®; oral: Myl-
eran®)
- Class: Alkylating agent
- MOA: Break DNA helix
strand, thereby
interfering with
DNA replication - Indications: Heme: CML & transplant prep
- DLTs: Myelosup. Pulmonary Fibrosis, profound tachycardia, HTN, chest pain, hyperpigmentation, gamete sup., AMS (confusion), seizures, n/v, mucositis, hyperglycemia, blurred vision, risk of hepatic
sinusoidal obstruction syn-
drome (previously known as
veno-occlusive disease) at
AUC > 1,500 mcm × min - Special Considerations this agent:
- IV (central line) & PO
- Monitor cell counts, dose hold WBC<15,000
- Seizure PPX
- IV admin. asssoc. w/ inflammation and pain during infusion
- IV not compatible with polycarbonate line
Chemo: Carboplatin
What is the:
1. Class of chemotherapeutic
- MOA of this class
- Indications
- DLTs
- Special considerations for this agent
Chemo: Carboplatin
- Class: Alkylating agent
- MOA: Break DNA helix
strand, thereby
interfering with
DNA replication - Indications: Ovarian
- DLTs: Thrombocytopenia, Neutropenia (worse in renal impairment), n/v, hypersensitivity RXN, mild alopecia, skin rash
- Special Considerations this agent:
- AUC dosing
- Irritant
- Hypersensitivity RXN possible with any dose
- Renal tox. < Cisplatin (creatinine prior to each dose)
- Monitor cell counts, most toxic to platelet precursor, monitor for bleeding
Chemo: Chlorambucil
(Leukeran®)
What is the:
1. Class of chemotherapeutic
- MOA of this class
- Indications
- DLTs
- Special considerations for this agent
Chemo: Chlorambucil
(Leukeran®)
- Class: Alkylating agent
- MOA: Break DNA helix
strand, thereby
interfering with
DNA replication - Indications:
Heme: CLL, HL, NHL - DLTs: Myleosup., skin RXN, gamete suppression, n/v, hyperuricemia, pulmonary fibrosis, seizure (increased risk in children with nephrotic syndrome), secondary malignancy
- Special Considerations this agent:
- PO, take on empty stomach
- Caution in pts. w/ seizure Hx & w/i one month RT/Cytotoxic therapy (PULMONARY fibrosis)
Chemo: Cisplatin
What is the:
1. Class of chemotherapeutic
- MOA of this class
- Indications
- DLTs
- Special considerations for this agent
Chemo: Cisplatin
- Class: Alkylating agent
- MOA: Break DNA helix
strand, thereby
interfering with
DNA replication - Indications: Ovarian, Testicular, Bladder
- DLTs: Severe Nephro. tox., myelosuppression, SEVERE acute/delayed n/v, ototoxicity, hyperuricemia, Hypersensitivity RXN, hypomag + electrolyte disturbances, PSN
- Special Considerations this agent:
- Mannitol + aggressive hydration (pre&post), creatine prior to EACH dose (administer next dose when creatinine = BL)
- Delayed n/v up to 6 days post-dose
- Baseline audiogram
- electrolyte correction PRN
Chemo: Cyclophos-
phamide
What is the:
1. Class of chemotherapeutic
- MOA of this class
- Indications
- DLTs
- Special considerations for this agent
Chemo: Cyclophos-
phamide
- Class: Alkylating agent
- MOA: Break DNA helix
strand, thereby
interfering with
DNA replication - Indications: MANY: breast, ovarian, MM, Leukemias, Lymphomas, Neuroblastoma, Retinoblastoma, Mycosis, Fungicides
- DLTs = Hemorrhagic cystitis, + myelosup., n/v, alopecia, maxillary burning if infused too rapidly, gamete failure, secondary malignancy; HIGH DOSE = acute cardiomyopathy & SIADH
- Special Considerations this agent:
- IV & PO admin
- Bladder tox, aggressive hydration + frequent urination + Mesna can help reduce risk for Hemorrhagic cystitis
- Prior or concurrent RT can increase tox.
- Dose holds ANC <1.5, PLT <50,000
Chemo: Dacarbazine
What is the:
1. Class of chemotherapeutic
- MOA of this class
- Indications
- DLTs
- Special considerations for this agent
Chemo: Dacarbazine
- Class: Alkylating agent
- MOA: Break DNA helix
strand, thereby
interfering with
DNA replication - Indications: Melanoma (mets/malignant), HL
- DLTs: Severe
neutropenia and thrombo-
cytopenia (nadir 2–3weeks(+)) - Special Considerations this agent:
- Irritant.
- Protect from light
- Flu-like syndrome possible up to 7 days post-admin; treat symptoms
Chemo: Ifosfamide (Ifex®)
What is the:
1. Class of chemotherapeutic
- MOA of this class
- Indications
- DLTs
- Special considerations for this agent
Chemo: Ifosfamide (Ifex®)
- Class: Alkylating agent
- MOA: Break DNA helix
strand, thereby
interfering with
DNA replication - Indications: Testicular
- DLTs: Hem-
orrhagic cystitis, myelosup-
pression; n/v, alopecia,
neurotoxicity (somnolence,
confusion, hallucinations,
depressive psychoses, and
encephalopathy), urotoxic-
ity, cardiotoxicity, pulmonary
toxicity, Methylene blue
to treat ifosfamide-induced
encephalopathy which may also spontaneously resolve - Special Considerations this agent:
- Hemorrhagic cystitis can be severe w/ risk reduced by mesna + extensive hydration (min 2L/per day).
.
Chemo: Mechlorethamine
(nitrogen mustard, Mustargen®, Valchlor®)
What is the:
1. Class of chemotherapeutic
- MOA of this class
- Indications
- DLTs
- Special considerations for this agent
Chemo: Mechlorethamine
(nitrogen mustard, Mustargen®, Valchlor®)
- Class: Alkylating agent
- MOA: Break DNA helix
strand, thereby
interfering with
DNA replication - Indications: HL, NHL, CLL, CML, Polycythemia vera, Mycosis fungicides, Bronchogenic carcinoma
- DLTs: Severe n/v, alopecia, myelosupression, pain or phle-
bitis at IV site, chills, fever,
testicular or ovarian failure
Topical: Dermatitis, pruritus,
skin infection, ulceration,
hyperpigmentation - Special Considerations this agent:
- Vesicant and irritant.
Administer through the side arm of a free-flowing
IV. Flush with 125–150 ml NS following infusion to minimize phlebitis. If extravasation occurs, antidote = sodium thio-
sulfate.
Use mechlorethamine as soon after preparation as
possible (15–30 minutes); it is extremely unstable.
Chemo: Melphalan
(Alkeran®, Evomela®)
What is the:
1. Class of chemotherapeutic
- MOA of this class
- Indications
- DLTs
- Special considerations for this agent
Chemo: Melphalan
(Alkeran®, Evomela®)
- Class: Alkylating agent
- MOA: Break DNA helix
strand, thereby
interfering with
DNA replication - Indications: Multiple
myeloma Ovarian - DLTs: Dose-limiting toxicity: Myelosuppression, Nausea, vomiting, mucositis,, hypersensitivity reactions
- Special Considerations this agent:
- IV & PO (on empty stomach)
- Ice chips during high-dose to prevent oral mucositis
- Irritant and vesicant
- infuse over 15–20 minutes into fast-running IV solution, inject into into IV tubing; do not administer by direct
PIV injection.
- Alkeran within 1 hour of
reconstitution, Evomela stable 4 hours
- Dose reduce in renal insufficiency (blood urea
nitrogen ≥ 30 mg/dl)
Chemo:
What is the:
1. Class of chemotherapeutic
- MOA of this class
- Indications
- DLTs
- Special considerations for this agent
- Class: Alkylating agent
- MOA: Break DNA helix
strand, thereby
interfering with
DNA replication - Indications:
- DLTs:
- Special Considerations this agent:
Chemo: Oxaliplatin
(Eloxatin®)
What is the:
1. Class of chemotherapeutic
- MOA of this class
- Indications
- DLTs
- Special considerations for this agent
Chemo: Oxaliplatin
(Eloxatin®)
- Class: Alkylating agent
- MOA: Break DNA helix
strand, thereby
interfering with
DNA replication - Indications: Colorectal
- DLTs: Dose-limiting toxicities: -myelosuppression (worsens over time), PSN, COLD intolerance and paresthesia, dysesthesia, or hypesthesia within 1–48 hours, to 14 days, Anaphylactic reaction, nausea,
vomiting, diarrhea, pulmo-
nary fibrosis, fatigue, fever,
increased transaminases and
alkaline phosphatase - Special Considerations this agent:
- Not compatible with NaCl
or other chloride-containing solutions. Flush with D5W
- Persistent (> 14 days) - see DLT section above
- Irritant and vesicant.
- Dose reduce in patients with severe renal impairment (CrCl < 30 ml/min).
Chemo: Thiotepa
What is the:
1. Class of chemotherapeutic
- MOA of this class
- Indications
- DLTs
- Special considerations for this agent
- Class: Alkylating agent
- MOA: Break DNA helix
strand, thereby
interfering with
DNA replication - Indications:
- DLTs:
- Special Considerations this agent:
Chemo: Temozolomide
(Temodar®)
What is the:
1. Class of chemotherapeutic
- MOA of this class
- Indications
- DLTs
- Special considerations for this agent
Chemo: Temozolomide
(Temodar®)
- Class: Alkylating agent
- MOA: Break DNA helix
strand, thereby
interfering with
DNA replication - Indications: Refractory anaplastic astrocytoma
Newly diagnosed
glioblastoma multiforme - DLTs: Dose-limiting toxicity: Myelosuppression; Nausea, vomiting, headache,
fatigue, hepatic toxicity, constipation, rash, alopecia - Special Considerations this agent:
- IV & PO (on empty stomach) to decrease n/v (ie bedtime)
- IV: Infuse 90 min
- Do not administer if patients have allergic RXN to dacarbazine
- compatible with 0.9% NaCl
- PPX: pneumonia pro-
phylaxis (trimethoprim sulfamethoxazole) when RT combo for 42-day regimen
Chemo: Thiotepa
What is the:
1. Class of chemotherapeutic
- MOA of this class
- Indications
- DLTs
- Special considerations for this agent
Chemo: Thiotepa
- Class: Alkylating agent
- MOA: Break DNA helix
strand, thereby
interfering with
DNA replication - Indications: Bladder, Breast, Ovarian, HL, NHL
- DLTs: Myelosuppression;
Fatigue, weakness, fever,
hypersensitivity RXN,
gamete suppression, n/v, pain
at infusion site, rash, alo-
pecia, skin burn, mucositis,
hemorrhagic cystitis - Special Considerations this agent:
- IV, IT, intravesical, intracavitary, PO
- Caution in renal or
hepatic dysfunction
- Dose hold WBCs < 3,000/mm3 or PLT< 150,000/mm3
- used in the transplant setting can cause severe skin irritation. Frequent showering immediately following and during the first 48 hrs help prevent skin tox.
- Avoid tapes / skin adherents during treatment to 48h
- In line 0.22 micron filter
Chemo: Trabectedin
(Yondelis®)
What is the:
1. Class of chemotherapeutic
- MOA of this class
- Indications
- DLTs
- Special considerations for this agent
Chemo: Trabectedin
(Yondelis®)
- Class: Alkylating agent
- MOA: Break DNA helix
strand, thereby
interfering with
DNA replication - Indications: Liposarcoma
Leiomyosarcoma - DLTs: Dose-limiting toxicities: Myelosuppression (neutropenic
sepsis), hepatotoxicity, cardiomyopathy
Rhabdomyolysis, capillary leak
syndrome, nausea, fatigue,
vomiting, constipation,
decreased appetite, diarrhea,
peripheral edema, dyspnea,
headache - Special Considerations this agent:
- 24h continuous infusion and must be given through a central
line with a 0.2 micron filter
- vesicant; extravasation= severe tissue injury
- Premedicate 20 mg IV dex 30min pre-dose
- Dose reduce if hepatic impairment.
- metabolized through CYP3A
pathway; caution when administering concurrently with CYP3A inducers or inhibitors
Chemo: Azacitidine (Vidaza®)
What is the:
1. Class of chemotherapeutic
- MOA of this class
- Indications
- DLTs
- Special considerations for this agent
Chemo: Azacitidine (Vidaza®)
- Class: Antimetabolites
- MOA: DNA hypomethylation and direct cytotoxicity on
abnormal hematopoietic cells in
BM. Abnormal cells (ie cancer) no longer respond to normal growth control mechanisms - Indications: Specific sub-
types of MDS - DLTs: Myelosuppression, elevated SCr, renal failure, hepatic tox.; TLS, n/v, diar-
rhea, fatigue, fever, erythema
at injection site, constipation
IV only: Petechiae, rigors,
weakness, hypokalemia - Special Considerations this agent:
- IV & SC
- SC multiple considerations: roll syringe in hands to resuspend prior to injection -stable 1hr at room temp 8hrs if refrigerated
- Admin. completed within 1hr of reconstitution
- Contraindicated in patients with hypersensitivity to azacitidine, mannitol, and if
advanced malignant hepatic tumors
Chemo: Capecitabine
(Xeloda®)
What is the:
1. Class of chemotherapeutic
- MOA of this class
- Indications
- DLTs
- Special considerations for this agent
Chemo: Capecitabine
(Xeloda®)
- Class: Antimetabolites
- MOA: interfere with one or more enzymes or RXNs necessary for DNA syn-
thesis. Acting as a substitute to metabolites (e.g., antifolates interfere with the use of folic acid). - Indications: Colon and Colon mets, Metastatic breast
- DLTs: Diarrhea, hand-foot syndrome, mucositis; n/v,
myelosuppression, increased
bilirubin, fatigue - Special Considerations this agent:
- PO (with food/water)
- Pt. education: reporting toxicity critical for evaluating dose reductions
- contraindicated in patients with known hypersensitivity to 5-FU
-PT/INR closely because capecitabine increases warfarin effect
- Dose reduce if CrCl < 50 ml/min.
- Uridine triacetate (Vistogard®) is prodrug of uridine (RNA synthesis) = antidote to 5-FU or capecitabine if severe cardiac, CNS, GI, or neutropenia tox. within 96 hours of admin
Chemo: Cladribine
What is the:
1. Class of chemotherapeutic
- MOA of this class
- Indications
- DLTs
- Special considerations for this agent
Chemo: Cladribine
- Class: Antimetabolites
- MOA: interfere with one or more enzymes or RXNs necessary for DNA syn-
thesis. Acting as a substitute to metabolites (e.g., antifolates interfere with the use of folic acid) - Indications: Hairy cell leuke-
mia - DLTs: Myelosuppression, neurotoxicity, Fever, n/v, hyper-
sensitivity, TLS, nephrotoxicity (high-dose therapy) - Special Considerations this agent:
- caution in patients with liver and renal dysfunction.
Chemo: Clofarabine
(Clolar®)
What is the:
1. Class of chemotherapeutic
- MOA of this class
- Indications
- DLTs
- Special considerations for this agent
Chemo: Clofarabine
(Clolar®)
- Class: Antimetabolites
- MOA: interfere with one or more enzymes or RXNs necessary for DNA syn-
thesis. Acting as a substitute to metabolites (e.g., antifolates interfere with the use of folic acid) - Indications: Relapsed or
refractory ALL (age 1–21) - DLTs: myelosuppression,
infection, hepatic and renal tox, n/v, diarrhea RARE: SIRS/capillary leak syn-
drome, cardiotox (tachycardia, pericardial effusion, and left ventricular systolic dysfunction;
TLS, headache, pruritus,
rash, hand foot syndrome - Special Considerations this agent:
- Continuous IV fluid + alkalization of urine 5day pre-dose encouraged to reduce TLS and other AEs.
- D/C for hypotension 5day pre-dose
- PPX steroids to help prevent SIRS/Capillary leak
- PPX allopurinol if hyperuricemia TLS expected
- Monitor RR & BP, renal and hepatic function
- Dose reduce renal impairment
(< 60 ml/min)
Chemo: Cytarabine
What is the:
1. Class of chemotherapeutic
- MOA of this class
- Indications
- DLTs
- Special considerations for this agent
Chemo: Cytarabine
- Class: Antimetabolites
- MOA: interfere with one or more enzymes or RXNs necessary for DNA syn-
thesis. Acting as a substitute to metabolites (e.g., antifolates interfere with the use of folic acid) - Indications: ALL, AML, CML, CNS leukemia
- DLTs: Myelosuppression
n/b, anorexia, fever, mucositis, diarrhea, hepatic dysfunction, rash, pruritus, localized pain and thrombophlebitis
High-dose (1–3 g/m2): Cere-
bellar toxicity, keratitis (treat
with dexamethasone ophthal-
mic drops), dermatologic toxicities - Special Considerations this agent:
- IT, IV, SC
- Determine if standard vs.
high dose
- Toxicities vary depending on rate of high-dose
cytarabine administration. - - - – - Continuous infusion possible pulmonary tox (fluid overload)
- Bolus admin possible cerebellar toxicities
Chemo: Cytarabine liposomal (DepoCyt®)
What is the:
1. Class of chemotherapeutic
- MOA of this class
- Indications
- DLTs
- Special considerations for this agent
Chemo: Cytarabine liposomal (DepoCyt®)
- Class: Antimetabolites
- MOA: interfere with one or more enzymes or RXNs necessary for DNA syn-
thesis. Acting as a substitute to metabolites (e.g., antifolates interfere with the use of folic acid) - Indications: Lymphomatous
meningitis - DLTs: Neurotoxicity, mucositis, chemical arachnoiditis (n/v, headache, fever), seizure, n/v, constipation, weakness
- Special Considerations this agent:
- IT only
-NOT for pediatric patients
- lie flat for 1hr post LP procedure
-PPx dexamethasone 4 mg BID (PO or IV) for 5 days (D1=dosing day) to decrease symptoms of chemical arachnoiditis
Chemo: Decitabine
(Dacogen®)
What is the:
1. Class of chemotherapeutic
- MOA of this class
- Indications
- DLTs
- Special considerations for this agent
Chemo: Decitabine
(Dacogen®)
- Class: Antimetabolites
- MOA: DNA hypomethylation and direct cytotoxicity on
abnormal hematopoietic cells in
BM. Abnormal cells (ie cancer) no longer respond to normal growth control mechanisms - Indications: MDS
- DLTs: Myelosuppression, fever, fatigue, n, cough, diar-
rhea, hyperglycemia, petechiae, peripheral edema - Special Considerations this agent:
- Stable 4 hrs if prepared using cold infusion fluids and refrigerated
- use within 15 minutes if prepared w/ room-temp fluids
Chemo: Floxuridine
What is the:
1. Class of chemotherapeutic
- MOA of this class
- Indications
- DLTs
- Special considerations for this agent
Chemo: Floxuridine
- Class: Antimetabolites
- MOA: interfere with one or more enzymes or RXNs necessary for DNA syn-
thesis. Acting as a substitute to metabolites (e.g., antifolates interfere with the use of folic acid) - Indications: GI adenocarcinoma with mets to liver
- DLTs: Myelosuppression, n/v, diarrhea, stomatitis, mucositis, localized erythema, alopecia, photosensitivity, darkening of the veins, abdominal pain, gastritis, enteritis, hepatotoxicity
- Special Considerations this agent:
-Intra-arterial
- NO pediatric pts
- Irritant
Chemo: Fludarabine
What is the:
1. Class of chemotherapeutic
- MOA of this class
- Indications
- DLTs
- Special considerations for this agent
Chemo: Fludarabine
- Class: Antimetabolites
- MOA: interfere with one or more enzymes or RXNs necessary for DNA syn-
thesis. Acting as a substitute to metabolites (e.g., antifolates interfere with the use of folic acid) - Indications: CLL
- DLTs: Myelosuppression;
TLS, n/v, diarrhea, rash, neurotoxicity, pneumonitis, weakness, hemolytic anemia, cough, infection - Special Considerations this agent:
- IV, PO (with our without food)
- IV = 30-minute infusion
- Monitor PFTs
- PPX Allopurinol and IV hydration new CLL or high tumor burden to prevent TLS
-Contraindicated w/ pentostatin
because possible severe pulmonary toxicity
-Caution with renal impairment
Chemo: Trifluridine and tipiracil (Lonsurf®)
What is the:
1. Class of chemotherapeutic
- MOA of this class
- Indications
- DLTs
- Special considerations for this agent
Chemo:
- Class: Antimetabolites
- MOA: Drug is a combination of a thymidine-based nucleoside analog and a thymidine phosphorylase inhibitor. Incorporates into
DNA, interferes with DNA synthesis - Indications: 2nd + line meta-
static colorectal - DLTs: Anemia, neutropenia, fatigue, nausea, vomiting, diarrhea, abdominal pain, pyrexia, embryo-fetal toxicity
- Special Considerations this agent:
-PO BID within 1 hour after meals (12 hours apart) on days 1–5 and days 8–12 of each 28-day cycle
- Dose hold if ANC < 50,000/mm3 or PLT < 50,000/mm3
Chemo: 5-FU (Adrucil®)
What is the:
1. Class of chemotherapeutic
- MOA of this class
- Indications
- DLTs
- Special considerations for this agent
Chemo: 5-FU (Adrucil®)
- Class: Antimetabolites
- MOA: Nucleoside metabolic inhibitor that interferes with the synthesis of DNA and to a lesser extent inhibits the formation of RNA
- Indications: Colorectal, Breast, Pancreatic, Gastric, Pancreatic
- DLTs: Mucositis, myelosuppression
n/v, anorexia, diarrhea, alopecia, ocular toxicities (e.g., increased lacrimation), photosensitivity), darkening of the veins, dry skin, cardiotoxicity (rare),
neurotoxicity, hand-foot - Special Considerations this agent:
- IV, topical
- year-round photosensitivity precautions & sunscreen
- Leucovorin concurrently to
enhance activity
- ice chips in mouth 10–15min
pre- and post to reduce
oral mucositis- ice chips contraindicated w/capecitabine or oxaliplatin because cold intolerance
Uridine triacetate (Vistogard®) is prodrug of uridine (RNA synthesis) = antidote to 5-FU or capecitabine if severe cardiac, CNS, GI, or neutropenia tox. within 96 hours of admin
Chemo: Gemcitabine (Gemzar®)
What is the:
1. Class of chemotherapeutic
- MOA of this class
- Indications
- DLTs
- Special considerations for this agent
Chemo: Gemcitabine (Gemzar®)
- Class: Antimetabolites
- MOA: interfere with one or more enzymes or RXNs necessary for DNA syn-
thesis. Acting as a substitute to metabolites (e.g., antifolates interfere with the use of folic acid) - Indications: Pancreatic, Breast, Ovarian, NSCLC
- DLTs: Myelosuppression (especially thrombocytopenia)
n/v; flu-like symptoms including fever, headache, arthralgias, and myalgias); rash, peripheral
edema, dyspnea, pulmonary
toxicity with increased infu-
sion time, hepatotoxicity - Special Considerations this agent:
- Irritant.
Infuse over 30min; if > 60min or more than weekly can increase
hematologic toxicity
- caution in patients with renal impairment
- Potential for severe life-threatening tox. when administered within 7 days of RT
Chemo: 6-Mercaptopurine (6-MP; Purinethol®)
What is the:
1. Class of chemotherapeutic
- MOA of this class
- Indications
- DLTs
- Special considerations for this agent
Chemo: 6-Mercaptopurine (6-MP; Purinethol®)
- Class: Antimetabolites
- MOA: interfere with one or more enzymes or RXNs necessary for DNA syn-
thesis. Acting as a substitute to metabolites (e.g., antifolates interfere with the use of folic acid) - Indications: ALL
- DLTs: Myelosuppression, hepatotoxicity, mucositis, n/v, anorexia, hyperuricemia, hyperuricosuria, alopecia, rash, hyperpigmentation
- Special Considerations this agent:
- PO (take on empty stomach)
- Reduce oral dose by 75% when used concurrently with allopurinol
Chemo: Methotrexate
What is the:
1. Class of chemotherapeutic
- MOA of this class
- Indications
- DLTs
- Special considerations for this agent
Chemo: Methotrexate
- Class: Antimetabolites
- MOA: interfere with one or more enzymes or RXNs necessary for DNA syn-
thesis. Acting as a substitute to metabolites (e.g., antifolates interfere with the use of folic acid) - Indications: NHL, Leukemia
CNS mets, Lung, Breast, Head and neck, Gestational trophoblastic tumor, Osteosarcoma, RA, Psoriasis
Gestational choriocarcinoma, Chorioadenoma destruens, Hydatidiform mole - DLTs: Hepatotoxicity, renal toxicity Mucositis, n/v, myelosuppression, oral or
GI ulceration, pneumonitis, photosensitivity, HIGH DOSE: neurotoxicity - Special Considerations this agent:
- IM, IT, IV, PO, SC
- High doses: 1) adjust for renal dysfunction 2)followed by timely administration of leucovorin + alkaline hydration
- Monitor serum levels until ≤ 0.1 mcmol/L
- Monitor urine pH and maintain ≥ 7 before and until serum methotrexate levels ≤
0.05 mcmol/L (depending on clearance, some patients may require additional leucovorin rescue and serum monitoring)
-strict mouth care
- avoid taking multivitamins with folic acid
- Multiple possible drug interactions (ie NSAIDs, alcohol, aspirin, warfarin, aminoglycosides)
- Glucarpidase (Voraxaze®) used when delayed clearance from renal impairment. This drug reduces levels by rapidly converting methotrexate to glutamate and 4-deoxy-4-amino-N10-methylpteroic acid
Chemo: Nelarabine (Arranon®)
What is the:
1. Class of chemotherapeutic
- MOA of this class
- Indications
- DLTs
- Special considerations for this agent
Chemo: Nelarabine (Arranon®)
- Class: Antimetabolites
- MOA: interfere with one or more enzymes or RXNs necessary for DNA syn-
thesis. Acting as a substitute to metabolites (e.g., antifolates interfere with the use of folic acid) - Indications: T-cell ALL, T-cell lymphoblastic lymphoma
- DLTs: Neurotoxicity, myelosuppression, headache, n/v, diarrhea, constipation, cough, fatigue, peripheral neuropathy, dyspnea, neurologic toxicities (somnolence, seizures,
ataxia) - Special Considerations this agent:
-Administer undiluted infusion
2hr adults /1hr pediatrics
- Administer with PPX for hyperuricemia and TLS
- D/C for ≥ grade 2 neurologic events (severe somnolence, seizure, and PSN
- Caution with renal or hepatic dysfunction
Chemo: Pemetrexed (Alimta®)
What is the:
1. Class of chemotherapeutic
- MOA of this class
- Indications
- DLTs
- Special considerations for this agent
Chemo: Pemetrexed (Alimta®)
- Class: Antimetabolites
- MOA: interfere with one or more enzymes or RXNs necessary for DNA syn-
thesis. Acting as a substitute to metabolites (e.g., antifolates interfere with the use of folic acid) - Indications: Mesothelioma
Nonsquamous NSCLC - DLTs: Myelosuppression, fatigue, n/v, anorexia, chest pain, and dyspnea. Vitamin supplementation reduces these AE. Can cause Renal and liver toxicity
- Special Considerations this agent:
- Infuse 10min
- reduce treatment-related hematologic and GI toxicities by administering folic acid 400–1,000 mcg PO daily starting 1 week prior to C1D1 and daily for 3 weeks after final cycle.
- Vitamin B12 injection 1,000 mcg 1 week prior to C1D1 and repeat every 9 for duration
- Dexamethasone 4 mg BID for 3 days starting C1D(-1) to decreas incidence of rash
- HOLD if ANC < 1,500/mm3, platelets < 100,000/mm3, or
CrCl < 45 ml/min
- Monitor renal and hepatic function.
- Concurrent NSAIDs may increase the risk of renal damage.
Chemo: Pentostatin (Nipent™)
What is the:
1. Class of chemotherapeutic
- MOA of this class
- Indications
- DLTs
- Special considerations for this agent
Chemo: Pentostatin (Nipent™)
- Class: Antimetabolites
- MOA: interfere with one or more enzymes or RXNs necessary for DNA syn-
thesis. Acting as a substitute to metabolites (e.g., antifolates interfere with the use of folic acid) - Indications: Hairy cell leukemia
- DLTs: Myelosuppression, acute pulmonary edema, hypotension, fever, chills, n/v, rash, renal toxicity, confusion, hepatic enzyme elevation, infection risk, cough, cardiac
- Special Considerations this agent:
-Administer with 500–1,000ml 5% dextrose in ½NS pre-dose + additional 500ml post-dose
- Do not administer with fludarabine, carmustine, etoposide, or high-dose cyclophosphamide
Chemo: Pralatrexate (Folotyn®)
What is the:
1. Class of chemotherapeutic
- MOA of this class
- Indications
- DLTs
- Special considerations for this agent
Chemo: Pralatrexate (Folotyn®)
- Class: Antimetabolites
- MOA: interfere with one or more enzymes or RXNs necessary for DNA syn-
thesis. Acting as a substitute to metabolites (e.g., antifolates interfere with the use of folic acid) - Indications: Peripheral T-cell lymphoma
- DLTs: Myelosuppression, mucositis, dermatologic RXNS, TLS, hepatotoxicity, edema, fatigue, nausea
- Special Considerations this agent:
- IV push over 3–5min
- Consider dose reduction with impaired renal function (EGFR < 30 ml/min/1.73 m2).
-MUST supplement: folic acid (1–1.25 mg PO daily) + vitamin B12 (1mg IM Q8-10wks)
- Monitor liver and renal function
Chemo: Thioguanine (6-TG; Tabloid®)
What is the:
1. Class of chemotherapeutic
- MOA of this class
- Indications
- DLTs
- Special considerations for this agent
Chemo: Thioguanine (6-TG; Tabloid®)
- Class: Antimetabolites
- MOA: interfere with one or more enzymes or RXNs necessary for DNA syn-
thesis. Acting as a substitute to metabolites (e.g., antifolates interfere with the use of folic acid) - Indications: ANLL
- DLTs: Myelosuppression, hyperuricemia, nausea, hepatotoxicity, diarrhea
- Special Considerations this agent:
-PO
-Monitor hepatic function
Chemo:
What is the:
1. Class of chemotherapeutic
- MOA of this class
- Indications
- DLTs
- Special considerations for this agent
Chemo:
- Class: Anti-Tumor Antibiotics
- MOA: Bind with DNA thereby inhibiting DNA and RNA synthesis
- Indications: Malignant pleural
effusion, Testicular, HL, NHL
[Squamous cell: head & neck, cervix, vulva, penis] - DLTs: Hypersensitivity or anaphylactic (rare), pulmonary
toxicity, Hyperpigmentation, alopecia, photosensitivity, renal toxicity, hepatotoxicity, fever, chills, erythema, rash, mucositis - Special Considerations this agent:
- Ordered in units
- MAX lifetime dose >400units, must track lifetime amounts
- Pulmonary fibrosis (dose-related )
- PFTs baseline, then Q1-2Months during therapy; consider D/C if PFT shows 30%–35% decrease f/ baseline
- Not compatible with D5W
- Lymphoma higher incidence
of anaphylaxis (usually after first or second dose). Institution may test doses of 1–2 units IV, IM, or SC before first regular dose
- PRIOR bleomycin increases risk for pulmonary toxicity to oxygen during surgery. EDUCATION: lifelong necessity of disclosing prior bleomycin for future anesthesia/surgery to prevent fatal pulmonary failure
- Acetaminophen and an antihistamine may decrease
fever and chills in first 24 hours after administration.
- Consider dose reductions in patients with CrCl <50 ml/min.
Chemo: Dactinomycin (Actinomycin-D; Cosmegen®)
What is the:
1. Class of chemotherapeutic
- MOA of this class
- Indications
- DLTs
- Special considerations for this agent
Chemo: Dactinomycin (Actinomycin-D; Cosmegen®)
- Class: Anti-Tumor Antibiotics
- MOA: Bind with DNA thereby inhibiting DNA and RNA synthesis
- Indications: Wilms tumor
Childhood rhabdomyosarcoma, Testicular, Ewing sarcoma, Gestational trophoblastic disease - DLTs: Myelosuppression Nausea, vomiting, alopecia, mucositis, diarrhea, ovarian or sperm suppression, radiation recall (hyperpigmentation of previously irradiated areas), sinusoidal obstruction syndrome, renal & hepatic tox.
- Special Considerations this agent:
-vesicant; extravasation can
result in severe tissue injury
- Administer through the side port of a free-flowing IV
- Highly toxic and corrosive to soft tissues; avoid inhalation and eye contact
- Ordered in mcg (micrograms), check dose carefully
- Contraindicated in concurrent or recent chicken pox / herpes zoster (shingles) due to risk of severe disease
- Avoid within 2 months of RT for right-sided Wilms tumor / RT will exagerate toxicities
Chemo: Mitomycin C (Mutamycin®)
What is the:
1. Class of chemotherapeutic
- MOA of this class
- Indications
- DLTs
- Special considerations for this agent
Chemo: Mitomycin C (Mutamycin®)
- Class: Anti-Tumor Antibiotics
- MOA: Bind with DNA thereby inhibiting DNA and RNA synthesis
- Indications: Pancreatic, Stomach, Bladder
- DLTs: Myelosuppression, n/v, anorexia, fever, renal toxicity, pulmonary toxicity, fatigue
- Special Considerations this agent:
-Intravesical and IV
- Drug is purple/blue in color
-Vesicant; extravasation can result in severe tissue injury
- Administer through the side port of a free-flowing IV
- Nadir within 8 weeks after treatment begins (average 4wks)
- Acute shortness of breath and bronchospasm can occur very suddenly when given with a vinca alkaloid
- Withhold doses for PLT < 100,000/mm3 or WBCs < 4,000/mm3
HOLD if SCr > 1.7 mg/dl
- Hemolytic uremic syndrome possible with a single dose ≥ 60 mg
- Contraindicated if coagulation disorders
Chemo: Mitoxantrone
What is the:
1. Class of chemotherapeutic
- MOA of this class
- Indications
- DLTs
- Special considerations for this agent
Chemo: Mitoxantrone
- Class: Anti-Tumor Antibiotics
- MOA: Bind with DNA thereby inhibiting DNA and RNA synthesis
- Indications: Prostate, ANLL (acute nonlymphocytic leukemia, also called AML, acute myelogenous leukemia or acute myeloid leukemia), Multiple sclerosis
- DLTs: Myelosuppression, cardiotoxicity (risk increased if treated with other cardiotoxic
drugs), n/v, mucositis, alopecia, fever, weakness, hyperuricemia, amenorrhea, blue-green colored urine, bluish skin or sclera - Special Considerations this agent:
-Drug is blue in color
- Fatal if given intrathecally
- Irritant with vesicant potential
- HOLD for ANC < 1,500/mm3
- Cardiotoxicity risk < Doxorubicin; prior anthracycline, chest RT, or cardiac disease increases risk
- Baseline cardiac assessment: MUGA/ECHO, EF eval., ECG
- Contraindicated if hepatic impairment
Chemo: Daunorubicin
What is the:
1. Class of chemotherapeutic
- MOA of this class
- Indications
- DLTs
- Special considerations for this agent
Chemo: Daunorubicin
- Class: Anti-Tumor Antibiotics: ANTHRACYCLINES
- MOA: Bind with DNA thereby inhibiting DNA and RNA synthesis
- Indications: ALL in children, AML
- DLTs: Myelosuppression, cardiotoxicity, n/v, alopecia, hyperuricemia, radiation
recall, red-colored urine - Special Considerations this agent:
- Drug is red in color.
- Vesicant; extravasation can
result in severe tissue injury
- Administer through the side arm of a free-flowing IV
- Dose reduce if hepatic or renal
impairment
- Baseline cardiac EF needed
- Total lifetime dose in adults is - 550 mg/m2 without cardiovascular risk factors and 400 mg/m2 in adults receiving chest RT
Chemo: Daunorubicin and cytarabine liposome (Vyxeos™)
What is the:
1. Class of chemotherapeutic
- MOA of this class
- Indications
- DLTs
- Special considerations for this agent
Chemo: Daunorubicin and cytarabine liposome (Vyxeos™)
- Class: Anti-Tumor Antibiotics: ANTHRACYCLINES
- MOA: Bind with DNA thereby inhibiting DNA and RNA synthesis
- Indications: AML
- DLTs: Myelosuppression, cardiotoxicity, hypersensitivity reaction, Hemorrhage events, copper overload
- Special Considerations this agent:
- Administer over 90 minutes through a central line
-Vesicant; extravasation can
result in severe tissue injury
- LIFETIME dose in adults is 550mg/m2 in those without cardiovascular risk factors and 400mg/m2 in adults receiving chest RT
- Vyxeos contains copper gluconate; copper toxicity is possible in patients with Wilson disease (inability to process copper)
Chemo: Doxorubicin (Adriamycin®)
What is the:
1. Class of chemotherapeutic
- MOA of this class
- Indications
- DLTs
- Special considerations for this agent
Chemo: Doxorubicin (Adriamycin®)
- Class: Anti-Tumor Antibiotics: ANTHRACYCLINES
- MOA: Bind with DNA thereby inhibiting DNA and RNA synthesis
- Indications: MANY: Breast, ALL, AML, HL, NHL, Wilms tumor, Neuroblastoma, Sarcoma, Ovarian, Bladder, Thyroid, Stomach, Bronchogenic carcinoma
- DLTs: Myelosuppression, cardiotoxicity, hepatotoxicity, n/v, alopecia, mucositis,, radiation recall, hyperuricemia, photosensitivity, red-colored urine
- Special Considerations this agent:
- Drug is red in color
- Vesicant; extravasation can
result in severe tissue injury
- Administer through the side arm of a free-flowing IV or via continuous infusion through a central catheter only
- Dexrazoxane if extravasation
- Dose reduce if elevated serum total bilirubin
- Obtain baseline cardiac EF
- LIFETIME cumulative dose max 550mg/m2 (450 mg/m2 if prior chest RT or concomitant cyclophosphamide)
- Consider dexrazoxane (cardio protective) for pediatrics and for patients who have received a cumulative dose of 300mg/m2 and are continuing treatment
Chemo: Doxorubicin liposomal (Doxil®)
What is the:
1. Class of chemotherapeutic
- MOA of this class
- Indications
- DLTs
- Special considerations for this agent
Chemo: Doxorubicin liposomal (Doxil®)
- Class: Anti-Tumor Antibiotics: ANTHRACYCLINES
- MOA: Bind with DNA thereby inhibiting DNA and RNA synthesis
- Indications: Ovarian, AIDS-related Kaposi sarcoma, Multiple myeloma
- DLTs: Myelosuppression, cardiotoxicity, infusion-related reactions, n/v, alopecia, mucositis, arrhythmia, amenorrhea, radiation recall, hand-foot syndrome, hypersensitivity
- Special Considerations this agent:
- Drug is red in color
- Irritant with vesicant properties; caution to avoid extravasation
- The same warnings as conventional doxorubicin regarding cardiovascular complications [- Baseline cardiac EF - LIFETIME cumulative dose max 550mg/m2 (450mg/m2 if prior chest RT or concomitant cyclophosphamide) - Consider dexrazoxane (cardio protective) for pediatrics and for patients who have received a cumulative dose of 300mg/m2 and are continuing treatment]
- Do not substitute for doxorubicin
- Do not use an in-line filter
Chemo: Epirubicin (Ellence®)
What is the:
1. Class of chemotherapeutic
- MOA of this class
- Indications
- DLTs
- Special considerations for this agent
Chemo: Epirubicin (Ellence®)
- Class: Anti-Tumor Antibiotics: ANTHRACYCLINES
- MOA: Bind with DNA thereby inhibiting DNA and RNA synthesis
- Indications: Breast
- DLTs: Myelosuppression, cardiotoxicity, n/v, mucositis, diarrhea, alopecia, amenorrhea, infection, hyperuricemia, radiation recall, flushing, red-colored urine
- Special Considerations this agent:
- Drug is red in color
- esicant; extravasation can result in severe tissue injury
- Infuse into the side port of a free-flowing IV
- HOLD if ANC is < 1,500/mm3
. Consider dose reduction if hepatic and severe renal impairment (SCr > 5 mg/dl)
- LIFETIME cumulative dosing <900mg/m2
- Baseline cardiac EF
Chemo: Idarubicin (Idamycin®)
What is the:
1. Class of chemotherapeutic
- MOA of this class
- Indications
- DLTs
- Special considerations for this agent
Chemo: Idarubicin (Idamycin®)
- Class: Anti-Tumor Antibiotics: ANTHRACYCLINES
- MOA: Bind with DNA thereby inhibiting DNA and RNA synthesis
- Indications: AML
- DLTs: Myelosuppression, cardiomyopathy, Hyperuricemia, n/v, alopecia, vein itching, radiation recall, rash, mucositis, diarrhea, severe enterocolitis with perforation, red-colored urine
- Special Considerations this agent:
- Drug is red-orange in color
- Vesicant; extravasation can result in severe tissue injury
- Inject slowly over 10–15min into free-flowing side-arm infusion
- Cardiotoxicity < Daunorubicin
- LIFETIME cumulative doses >150 mg/m2 associated
with decreased EF
- Local reactions (hives at injection site) may occur
- Consider dose reduction if renal or hepatic impairment
Chemo: Valrubicin (Valstar®)
What is the:
1. Class of chemotherapeutic
- MOA of this class
- Indications
- DLTs
- Special considerations for this agent
Chemo:
- Class: Anti-Tumor Antibiotics: ANTHRACYCLINES
- MOA: Bind with DNA thereby inhibiting DNA and RNA synthesis
- Indications: Intravesical therapy of bacillus Calmette Guérin–refractory in situ bladder cancer
- DLTs: Dysuria, bladder spasm and irritation, urinary incontinence, leukopenia, hyperglycemia; drug may turn the urine red
- Special Considerations this agent:
- Intravesical route ONLY
- Not for use in pediatrics
- Vesicant; extravasation can result in severe tissue injury if perforation of bladder occurs
- non-PVC, non-DEHP containing tubing
Chemo:
What is the:
1. Class of chemotherapeutic
- MOA of this class
- Indications
- DLTs
- Special considerations for this agent
Chemo:
- Class:
- MOA:
- Indications:
- DLTs:
- Special Considerations this agent:
Surgeries Used for Various Purposes
Prophylactic purposes
Surgeries Used for
Prophylactic purposes:
The excision of premalignant lesions
Surgeries Used for Various Purposes
Diagnostic purposes
Surgeries Used for Various Purposes
Diagnostic purposes:
Biopsies for definitive histological diagnosis
Surgeries Used for Various Purposes
Staging purposes
Surgeries Used for Various Purposes
Staging purposes:
The extent of the carcinoma must actually be observed inside the patient
Surgeries Used for Various Purposes
Treatment purposes
Surgeries Used for Various Purposes
Treatment purposes:
The simple removal of the entire carcinomatous tumor for curative reasons
Surgeries Used for Various Purposes
Palliation purposes
Surgeries Used for Various Purposes
Palliation purposes:
Not for altering the outcome of the disease, but to maintain the best quality of life for the patient and to allow death with dignity and maximum comfort
Define Incisional biopsy
Incisional biopsy:
Small sample of suspected tissue is removed for testing
Define Excisional biopsy
Excisional biopsy:
The entire suspected tissue is removed.
Types of Cancer Surgery:
Surgical Excision
Surgical Excision:
Can involve removal of just the involved tissue with a margin of healthy tissue.
It may be more extensive and include removal of the affected tissue and surrounding lymph nodes and other tissues.
Types of Cancer Surgery:
Electrosurgery
Electrosurgery :
Iinvolves applying an electric stimulus to the area affected by the malignancy and destroying the cancer cells.
Types of Cancer Surgery:
Cryosurgery
Cryosurgery:
Involves applying liquid nitrogen to the cancer tissues. This causes destruction of the malignant cells through a freezing process.
Types of Cancer Surgery:
Laser treatments
Laser treatments:
Can be applied directly to the malignant tissue to cause destruction of the malignant cells. This is performed using a specialized scalpel that emits laser stimulus.
Types of Cancer Surgery:
Stereotactic surgery
Stereotactic surgery (SRS):
Is used with brain tumors (or SBRT for tumors next to important body structures outside of the brain) to provide an exact location of the tumor in a three-dimensional appearance. Special equipment is used for positioning the patient to utilize this type of surgery.
Name 3x Lung Surgeries
- Pneumonectomy: complete removal of a lung
- Lobectomy: to remove one lobe of a lung
- Resection: removal of various-sized small portions of the lung
Bowel Surgery
What is an End Stoma?
End stoma:
Created by cutting the bowel and diverting it through the abdominal wall. The rest of the bowel that is left distally may be removed from the body or sewn off.
Bowel Surgery
What is a Loop Stoma?
Loop stomas:
Bring a section (loop) of the colon out through an incision in the abdomen. Usually temporary (ie a bowel obstruction or symptom treatment at the end life). Another surgical procedure can be performed in the future to correct the colostomy so that the bowel will function normally.
Bowel Surgery
What is a Double-barrel stoma?
Double-barrel stomas:
Two stomas present in the abdominal wall. The stoma that is formed from the proximal portion of bowel will excrete stool while the distal portion only secretes mucus.
The consistency of the stool from the proximal end will vary depending on its location;
* More distal in bowel = stool that is more formed.
* More proximal in bowel = stool will be more watery.
Urinary Diversion Surgery
Name the two main types
Urinary Diversion Surgery
Two main types:
1. Incontinent urinary diversions
2. Continent urinary diversions
Urinary Diversion Surgery
Describe Incontinent urinary diversions - one of the two main types
Urinary Diversion Surgery
Incontinent urinary diversions:
Patient cannot control voiding, urine generally drains into the bag as it is made.
Created from a portion of the small intestine. A stoma is created with the small intestine, and the ureters are attached to the section of intestine to drain urine from the body.
Risks:
Urinary reflux can occur and the patient is at a high risk for developing:
1) infections in the urinary tract
2) kidney infections
Urinary Diversion Surgery
Describe Continent urinary diversions - one of the two main types
What are 2x examples (anatomically)
Urinary Diversion Surgery
Continent urinary diversions
Diversions which allow the patient to have control of when they will void.
- One option = diversion by connecting the ureters from the kidneys to a section of the large intestine. Urine flows through the intestine and colon to be exited through the anus. A valve is created which allows the patient to maintain continence.
- Another option = Orthotopic neobladders.
Neobladders are made from a portion of the stomach or intestine, connected to ureters (to collect urine) and connected to the urethra (to enable urine to flow normally out of the body).
This procedure is usually performed when there is bowel disease or damage from disease.
When is Surgical Management of Lymphedema indicated?
Surgical Management of Lymphedema indicated when:
1. Medical procedures have failed.
2. Swelling is extreme enough to prevent use of limb.
3. Significant skin changes.
4. Persistent Infections
Surgical Management of Lymphedema
Name 3x Surgeries to reduce lymphedema by reestablishment of proper drainage
Surgical Management of Lymphedema - Reestablishment of proper drainage:
- Lymphaticovenous anastomosis (LVA):
Jjoins lymphatic vessel to a vein. - Lymphatic-lymphatic anastomosis (L-L), Creates new lymphatic connections
- lymph nodal-venous shunt is also occasionally done.
Surgical Management of Lymphedema:
Excisional procedures
Surgical Management of Lymphedema:
Excisional procedures strive to remove skin layers and subcutaneous tissue where most lymphedema is localized
List 3x Types of bone marrow transplants
- Allogenic: Infusion of bone marrow from one individual to another. Also use of peripheral blood stem cells or cord blood from another.
- Autologous: Infusion of a patient’s own bone marrow previously removed and stored.
- Syngeneic: Infusion from one identical twin to another.
Complications from Bone Marrow Transplantation
What is Hepatic Sinusoidal Obstruction Syndrome (previously known as veno-occlusive disease)?
What % of hematopoietic stem cell transplant patients affected?
What causes it?
Sinusoidal Obstruction Syndrome (previously known as veno-occlusive disease)
- Life-threatening complication that occurs in 15-20% of hematopoietic stem cell transplant patients
- It occurs when fibrous material accumulates, resulting in obstruction of venules in the liver, which in turn causes portal hypertension and destruction of the liver cells.
Complications from Bone Marrow Transplantation
What are 7x clinical mainifestations of Hepatic Sinusoidal Obstruction Syndrome (previously known as veno-occlusive disease)?
Clinical mainifestations of Hepatic Sinusoidal Obstruction Syndrome:
- elevated serum bilirubin
- weight gain
- ascites
- right upper quadrant pain
- hepatomegaly
- splenomegaly
- jaundice
Complications from Bone Marrow Transplantation
Hepatic Sinusoidal Obstruction Syndrome (SOS) (previously known as veno-occlusive disease)
Typical time-frame to occur?
List 3x main treatments
List 3x main prevention steps
SOS Timeframe:
Should be considered in any patient that has these symptoms after stem cell transplant, especially in the first three weeks
SOS Treatment:
1. Maintain intravascular volume
2. Maintain renal perfusion
3. Minimize fluid accumulation
SOS Prevention includes minimizing risk factors
1. decrease hepatotoxic medications
2. iron chelation (for patients with liver disease related to increased iron levels)
3. ursodeoxycholic acid PPx for allogenic transplants, beginning the day before stem cell transplant and continuing three months after the procedure.
Complications from Bone Marrow Transplantation
What is Graft-versus-host disease?
What % of bone marrow recipients can experience this?
What are treatments?
Graft-versus-host disease occurs when the patient develops a rejection reaction to bone marrow received from a donor that may not be a perfect genetic match.
Can affect up to 50% of bone marrow recipients.
- High doses of steroids
- PPx: Other medications that decrease immune reactions for prevention
Complications from Bone Marrow Transplantation
What is Interstitial pneumonitis?
Interstitial pneumonitis is inflammation in lung tissue.
Higher risk:
1. Prior RT to the chest
2. Prior bleomycin
3. Carriers of CMV cytomegalovirus.
Pneumonitis infections can be caused by viruses, bacteria, or fungi. Antimicrobial medications are used to treat this infection.
What is Target Theory of Radiation?
1) Direct hits
Target Theory of Radiation
RT damage results from ionization causing:
1. Direct hits and
2. Indirect hits
Lead to impaired cell function and cell death:
1. Change or loss of a DNA base
2. Hydrogen bond breaks between DNA chains
3. Breaks in one or both DNA chains.
4. Cross-linking after breakage
Ionization of water, the medium surrounding the molecular structures within the cell, which causes a change in the cellular environment.
What is Radiation physics?
Radiation physics is the study of the effects of radiation exposure on cells.
What is Radiobiology?
Radiobiology is the study of the living cell after radiation treatment has been applied to the cell.
Focus:
1. Specific actions that occur to promote cell destruction
2. Length of time necessary for cell death
3. Dose necessary to destroy cells (minimum dose = most desirable)
4. Effects of RT on normal tissues
Name 4x goals of RT in Cancer Treatment and Management
- Cure
- Control
- Adjuvant
- Palliation
List 3x common RT units
- Roentgen (R) = unit of radiation exposure, does NOT reflect dose; established in 1928 in honor of Wilhelm Conrad Roentgen (discoverer of x-rays in 1895)
- rad = Radiation absorbed dose (rad) = 100 ergs absorbed per gram of tissue (1 erg = a unit of energy equal to 10−7 joules (100 nJ))
- Gray (Gy) or sievert (Sv) units = 100 rads = 1 joule absorbed per kg of tissue.
