{"id":110667,"date":"2023-07-27T11:41:26","date_gmt":"2023-07-27T11:41:26","guid":{"rendered":"https:\/\/learnexams.com\/blog\/?p=110667"},"modified":"2023-07-27T11:41:31","modified_gmt":"2023-07-27T11:41:31","slug":"ons-oncc-chemotherapy-immunotherapy-certificate-exam-2022-2023-with-100-correct-answers","status":"publish","type":"post","link":"https:\/\/www.learnexams.com\/blog\/2023\/07\/27\/ons-oncc-chemotherapy-immunotherapy-certificate-exam-2022-2023-with-100-correct-answers\/","title":{"rendered":"ONS\/ONCC Chemotherapy Immunotherapy Certificate exam 2022\/2023 with 100% correct answers"},"content":{"rendered":"\n

1. Elimination of the Hazard:<\/a><\/p>\n\n\n\n

-highest level of protection from a hazardous exposure

-substitute a less toxic substance for the hazardous material

-not feasible with drug therapy<\/a><\/p>\n\n\n\n

1. Phagocytes
2. Natural Killer Cells
3. Granulocytes
4. Macrophages<\/a><\/p>\n\n\n\n

1.Cells that engulf and destroy invader

2. Cells that sense receptors on self and non-self to determine if they should kill or not

3. Type of WBC that have granules (Neutrophils
Eosinophils – parasites
Basophils – release histamine to stimulate immune response)

4. Large phagocytic cells stimulated by infection<\/a><\/p>\n\n\n\n

2. Engineering Controls<\/a><\/p>\n\n\n\n

-second highest level of protection

-use of machines or equipment that isolate or contain the hazard to reduce worker exposure

-Examples: biosafety cabinets and closed-system drug-transfer devices<\/a><\/p>\n\n\n\n

3. Administrative Controls<\/a><\/p>\n\n\n\n

-third level of protection

-safe handling policies

-procedures

-work practices

-education and training of those responsible for HD handling<\/a><\/p>\n\n\n\n

4. PPE<\/a><\/p>\n\n\n\n

-lowest form of protection

-consisting of garments that provide barriers to protect workers from HDs

-places the primary responsibility for protection on the worker<\/a><\/p>\n\n\n\n

Absolute Neutrophil Count<\/a><\/p>\n\n\n\n

– (%segs + %bands) x (WBC) \/ 100<\/a><\/p>\n\n\n\n

Active Immunotherapy<\/a><\/p>\n\n\n\n

-capitalize on the immune system’s ability to remember a foreign invade

-mount an immune response against the tumor and hopefully remember the cancer cells long after treatment has stopped

-includes cancer vaccines<\/a><\/p>\n\n\n\n

Adaptive Immunity<\/a><\/p>\n\n\n\n

-Stimulated if innate immunity is insufficient

-leads to immune system memory

-Humoral immunity

-Cell-mediated immunity

-Regulatory T-cells<\/a><\/p>\n\n\n\n

Adjuvant therapy<\/a><\/p>\n\n\n\n

-additonal cancer treatment given after the primary treatment to lower the risk that the cancer can recur

-Examples: chemo, radiation therapy, hormone therapy, targeted therapy, or biologic therapy<\/a><\/p>\n\n\n\n

Alkylating Agents<\/a><\/p>\n\n\n\n

-function by causing a break in the DNA helix strand, causing interference with DNA replication, which results in cell death<\/a><\/p>\n\n\n\n

Alkylating Agent Subgroups<\/a><\/p>\n\n\n\n

-Nitrogen mustards (cyclophosphamide{Cytoxin}, ifosfamide{Ifex}, bendamustine{Treanda})

-Platinum-based (cisplatin{Planitol}, carboplatin{Paraplatin}): do not possess an alkyl group

-nitrosoureas<\/a><\/p>\n\n\n\n

B-Cell<\/a><\/p>\n\n\n\n

-each one is programmed to make one specific antibody

-Can recognize antigens whether they are freely circulating in the blood or attached to surface of a microbe

-When dividing, can become plasma cells which will then begin secreting antibodies that are unique to that antigen<\/a><\/p>\n\n\n\n

BCR\/ABL<\/a><\/p>\n\n\n\n

-fusion protein tyrosine kinase formed with a gene translocation occurs between gene 9 and 22

-gene abnormality called the Philadelphia chromosome seen in CML and ALL<\/a><\/p>\n\n\n\n

Benign Tumors<\/a><\/p>\n\n\n\n

-encapsulated and grow in an orderly manner with smooth edges

-Do not invade neighboring tissue

-DO not metastasize to distant sites

-the cells well differentiated in that they look like the parent cell<\/a><\/p>\n\n\n\n

Can I be intimate with my partner during treatment?<\/a><\/p>\n\n\n\n

-you should definiely check with your HCP first to be sure

-traces of chemo may be present in vaginal fluid for up to 48 hours after treatment

-use of a barrier is recommended for this reason for at least the first 48 hours<\/a><\/p>\n\n\n\n

Carboplatin (Paraplatin)<\/a><\/p>\n\n\n\n

-Alkylazing agent

-possibility for a hypersensitivity reaction which is rash, urticaria, erythema, pruritis, rarely bronchospasm and hypotensision

-notify RN if itching, scratchy throat, difficulty breathing, rash

-Blood count, particularly platelets, monitored because thrombocytopenia is a dose-limiting toxicity

-Oral dosage: 1-5mg\/kg\/day<\/p>\n\n\n\n

Cell cycle video and image<\/a><\/p>\n\n\n\n

http:\/\/highered.mheducation.com\/sites\/0072495855\/student_view0\/chapter2\/animation__how_the_cell_cycle_works.html<\/a><\/p>\n\n\n\n

Cell Cycling Time<\/a><\/p>\n\n\n\n

Amount of time from mitosis to mitosis<\/a><\/p>\n\n\n\n

Cell-Mediated Immunity<\/a><\/p>\n\n\n\n

Depends upon cytotoxic T cells and helper T cells and their cyokinds

-more effective against antigens within cells<\/a><\/p>\n\n\n\n

Cells of the Immune System<\/a><\/p>\n\n\n\n

Characteristics of Cancer Cells<\/a><\/p>\n\n\n\n

-Malignant tumors are not encapsulated

-Cell structure is different from parent tissue (no as well differentiated)

-Cell division is uncontrolled

-Cells are loosely adherent without contact inhibition

-Cells are able to invade neighboring tissue

-Cells can migrate and metastasize to distant sites

-Can stimulate the development of new blood vessels to supply the tumor (angiogenesis)<\/p>\n\n\n\n

Check points in the Cell Cycle: Keeping it All Under Control<\/a><\/p>\n\n\n\n

-The cell cycle is carefully controlled through a series of checkpoints

-Variation in duplication or distribution of chromosomes during cell division can alter the genetic information passed on to daughter cells, leading to cellular dysfunction and disease, such as cancer

-These checkpoints monitor for DNA integrity and control progression through mitosis<\/p>\n\n\n\n

Chemotherapy-Induced N\/V (CINV) Risk factors<\/a><\/p>\n\n\n\n

-younger
-have a hx of low or no alcohol consumption
-are female
-hx of morning sickness
-prone to motion sickness
-have had chemo previously<\/a><\/p>\n\n\n\n

Cisplatin (Planitol)<\/a><\/p>\n\n\n\n

-Alkylating agent


-nephrotoxic (IV hydration 2-3 L per day)
-severe N\/V

-ovarian and testicular<\/a><\/p>\n\n\n\n

Cumulative dose<\/a><\/p>\n\n\n\n

total amount of one antineoplastic agent given to the pt, adding up each time that the pt has received it<\/a><\/p>\n\n\n\n

Cumulative lifetime dose<\/a><\/p>\n\n\n\n

-“cumulative dose should not exceed…”

-total amount of specific antineoplastic agents that can be safely given over the course of a pt’s lifetime<\/a><\/p>\n\n\n\n

Cyclophosphamide (Cytoxin)<\/a><\/p>\n\n\n\n

-Alkylating agent)

-hemorrhagic cystitis (dysuria, hematuria, hemorrhage)

-DC treatment if hemorrhagic cystitis

-adequate hydration<\/a><\/p>\n\n\n\n

Cytokines<\/a><\/p>\n\n\n\n

-Secreted by lymphocytes

-Tasked with eliminating the antigen

-Multifunctional subsances having proinflammatory, anti-inflammatory, and regulatory functions in the immune system<\/a><\/p>\n\n\n\n

Cytokines Include..<\/a><\/p>\n\n\n\n

-Interferons (IFNs)

-Tumor necrosis factors

-Transforming GFs

-Interleukins (IL -1, -2, -3, -4, -6, -8, -10, and -15)

-These cytokines regulate antibody production and the functions of B and T cells as well as interact with antigen-presenting cells and NKCs<\/a><\/p>\n\n\n\n

Cytotoxic T-Cells (CD8+)<\/a><\/p>\n\n\n\n

-Directly kill cells for which they are activated to kill

-rapidly divide, become mature cells, and start killing antigens<\/a><\/p>\n\n\n\n

Dimerization<\/a><\/p>\n\n\n\n

two monomers that are side-by-side on the surface of the cell are paired and activated by a ligand, which causes a series of signals<\/a><\/p>\n\n\n\n

Dimerization<\/a><\/p>\n\n\n\n

1. Homodimerization: binding with the same type of receptor, such as an epidermal GF receptor (EGFR) 1 receptor with another EGFR

2. Heterodimerization: binding with a different kind of receptor, such as EGFR1 binding with EGFR2<\/a><\/p>\n\n\n\n

DNA Damage Checkpoints<\/a><\/p>\n\n\n\n

-If DNA damage is present, cells are programmed to stop dividing or undergo apoptosis (programmed cell death)

-The retinoblastoma protein (Rb), p53, and p21 are some of the most well-understood inhibitory proteins (IP)<\/a><\/p>\n\n\n\n

Doffing PPE<\/a><\/p>\n\n\n\n

1. Remove outer gloves turning them inside out

2. remove the gown

3. remove the face shield

4. properly dispose

5.remove inner gloves

6. wash hands<\/a><\/p>\n\n\n\n

Donning PPE<\/a><\/p>\n\n\n\n

1. wash hands

2. inspect gloves

3. apply first pair of gloves

4. put on gown with gloves inside cuff

5. second pair of gloves over the cuff

6. put on eye and face protection<\/a><\/p>\n\n\n\n

Dose density<\/a><\/p>\n\n\n\n

-refers to the drug dose per unit of time

-reduction of time between treatments to achieve higher concentration than in a standard treatment plan<\/a><\/p>\n\n\n\n

Dose intensity<\/a><\/p>\n\n\n\n

-amount of drug delivered over time

-smaller doses of chemotherapy given more frequently<\/a><\/p>\n\n\n\n

During interphase:<\/a><\/p>\n\n\n\n

Cell grows and DNA is replicated through the following three steps:

1: First growth phase (G1 or first gap)

2: Synthesis phase (S phase)

3:Mitotic Phse (M phase)<\/a><\/p>\n\n\n\n

Examples of oncogoenes<\/a><\/p>\n\n\n\n

1. EGFR or Erb-B1 (codes for an epidermal GF receptor in the receptor-tyrosine kinase family ad is associated with head and neck and colorectal cancers)

-EGFR inhibitor therapies are known to cause cutaneous reactions

2. Erb-B2 or HER2\/neu (codes for an EGFR protein in the tyrosine kinase family and is associated with some breast cancers)<\/a><\/p>\n\n\n\n

-Exceptions to this are those that are (Resting in G0 phase)<\/a><\/p>\n\n\n\n

-Exceptions to this are those that are metabollically active, such as

-granulocytes

-and the epithelium of the GI tract<\/a><\/p>\n\n\n\n

Extravasation<\/a><\/p>\n\n\n\n

-leak of a drug capable of causing tissue damage from the vessel in which it is being administered into the surround tissue<\/a><\/p>\n\n\n\n

Factor affecting adherence<\/a><\/p>\n\n\n\n

-provider relationship
-side effects
-necessity
-routinization
-support
-lifestyle fit
-cost
-medication knowledge
-pill burden
-regiment complexity<\/a><\/p>\n\n\n\n

First Growth Phase (G1 or first gap)<\/a><\/p>\n\n\n\n

-cells increase in size

-reproduce RNA

-“quality assurance” test that the cell will be ready to synthesis DNA

-Length of time is variable, can be from hours to days<\/a><\/p>\n\n\n\n

Focusing on Cellular Structure and Function<\/a><\/p>\n\n\n\n

G0 Phase (resting phase)<\/a><\/p>\n\n\n\n

-After mitosis, cells may enter back into the G1 phase or go into a resting phase, known as G0

-Most cells in the human body reside in G0<\/a><\/p>\n\n\n\n

Goals of targeted therapy<\/a><\/p>\n\n\n\n

-disease cure when used as primary or adjuvant therapy

-improving overall response or increase disease-free survival when used in combination with conventional therapies

-controlling or stabilizing disease

-maintaining or enhancing quality of life

-decreasing the severity of toxicities from other therapies<\/p>\n\n\n\n

Growth Signals<\/a><\/p>\n\n\n\n

-cancer cells are able to find their own growth signals making them self-sufficient<\/a><\/p>\n\n\n\n

Helper T-Cells (CD4+)<\/a><\/p>\n\n\n\n

-help other T-Cells by secreting chemicals

-Help B Cells to respond

-rapidly divide, in an effort to stay ahead of the antigen dividsion

-some will turn into effector cells, which secrete different kinds of cytokines

-respond similarly to B-Cells<\/a><\/p>\n\n\n\n

Hierarchy of Hazard Controls aimed at reducing worker exposure<\/a><\/p>\n\n\n\n

1. Elinination of the Hazard

2. Engineering Controls:

3. Administrative Controls

4. PPE:<\/a><\/p>\n\n\n\n

How targeted therapy and chemo differ<\/a><\/p>\n\n\n\n

-targeted therapies act on specific molecular targets on or within the cells that are associated with cancer, whereas standard chemo act on all rapidly dividing cells

-chemo has more SEs

-targeted therapy ae chosen and designed to interact with their target on or within the cells, whereas chemo were IDed becaused they kill cells

-targeted therapies are often cytostatic (they block tumor cell proliferation) whereas chemo agents are cytotoxic (kill tumor cells)<\/p>\n\n\n\n

Humoral Immunity<\/a><\/p>\n\n\n\n

-B-Cells
-Memory B-Cells
-Plasma act to produce immunoglobulins (Igs) or antibodies<\/a><\/p>\n\n\n\n

Hypersensitivity Reaction (HSR)<\/a><\/p>\n\n\n\n

-body mounts an immunologic response to a foreign substance or antigen, resulting in local tissue injury<\/a><\/p>\n\n\n\n

IgE-mediated<\/a><\/p>\n\n\n\n

-immediate (within 5 minute) HSR, present like classic allergic reactions<\/a><\/p>\n\n\n\n

Immunity<\/a><\/p>\n\n\n\n

Immunotherapy works by<\/a><\/p>\n\n\n\n

-stopping or slowing the growth of cancer cells

-stopping cancer from spreading to other parts of the body

-helping the immune system recognize cancer cells and increase its effectiveness at eliminating cancer cells<\/a><\/p>\n\n\n\n

Inhibitory proteins<\/a><\/p>\n\n\n\n

-prevent progression of the cycle when DNA damage is detected

-An example of an inhibitory protein is p53 (AKA TP53)<\/a><\/p>\n\n\n\n

Inhibitory proteins p53<\/a><\/p>\n\n\n\n

-Levels of this IP regulate several important target genes

-Will increase when DNA damage is present

-Protects against inappropriate signal proliferation

-sometimes called the “suicide gene”<\/a><\/p>\n\n\n\n

Innate Immunity<\/a><\/p>\n\n\n\n

-First line of defense against a pathogen

-Does not retain memory of the entity

-Involves the following:
(skin, mucous membranes, and normal flora of the skin and gut)
(Cellular components such as phagocytes, natural killer cells, granulocytes, and macrophages)<\/a><\/p>\n\n\n\n

Interphase and Mitotic Phase<\/a><\/p>\n\n\n\n

Cell division produces two identical cells through these two major phases<\/a><\/p>\n\n\n\n

Intrathecal Chemotherapy<\/a><\/p>\n\n\n\n

-injects chemo directly into the subarachnoid space so it reaches the CNS

-Often used to treat leukemia and lymphoma that has spread to the CNS since most IV chemo does not cross the blood-brain barrier

-only MTX and cytarabine via this route

-IT hydrocortisone is often given at the same time to reduce inflammation

-MUST be preservative free to avoid CNS irritation<\/p>\n\n\n\n

Irritant<\/a><\/p>\n\n\n\n

-causes inflammation, pain, and burning but rarely causes tissue necrosis<\/a><\/p>\n\n\n\n

Kinase<\/a><\/p>\n\n\n\n

type of enzyme that adds chemicals called phosphates to other molecules such as sugars or proteins causing other molecules in the cell to become either active or inactive<\/a><\/p>\n\n\n\n

Lesson 1: Foundations to Set the Stage<\/a><\/p>\n\n\n\n

Lesson 2: Alkylating Agents<\/a><\/p>\n\n\n\n

Lesson 7: Cumulative Dose<\/a><\/p>\n\n\n\n

Lesson 11: Targeted Therapy<\/a><\/p>\n\n\n\n

Lesson 12: Immunotherapy<\/a><\/p>\n\n\n\n

Lesson 13: Safe Handling<\/a><\/p>\n\n\n\n

Ligand<\/a><\/p>\n\n\n\n

a substance that forms a complex with another biomolecule to exert a biologic effect<\/a><\/p>\n\n\n\n

Ligand Binding<\/a><\/p>\n\n\n\n

process by which the ligand attaches to a specific receptor site and activates that receptor, activating the signaling pathway<\/a><\/p>\n\n\n\n

Lines of Defense: The Immune System’s Response to Attack<\/a><\/p>\n\n\n\n

Consists of 2 types of immunity:

1: Innate
2: Adaptive<\/a><\/p>\n\n\n\n

Locations of proteins Cyclins (D, E, A, B) and CDKs<\/a><\/p>\n\n\n\n

-(G0-G1) : Cyclin D and CDK 4\/6

-Early S: Cyclin E and CDK 1\/2

-Late S: Cyclin A and CDK 1\/2

-G2: CDK 1\/2 and cyclin A

-Before M: CDK 1 and Cyclin B<\/a><\/p>\n\n\n\n

Lymphoid Precursor Cells<\/a><\/p>\n\n\n\n

Mature into:
-Specialized WBCs called lymphocytes (Agranulocytes)<\/a><\/p>\n\n\n\n

Major points of cell regulation are entry and exit from<\/a><\/p>\n\n\n\n

-G1 checkpoint

-S Phase

-G2 checkpoint

-M phase<\/a><\/p>\n\n\n\n

mammalian target of rapamycin (mTOR) survival pathway<\/a><\/p>\n\n\n\n

-play a role in resistance to some chemotherapy agents in certain pts by keeping cells that have been exposed to chemotherapy from undergoing apoptosis

-role in angiogenesis<\/a><\/p>\n\n\n\n

Management of DNA-Binding Vesicant Extravasation<\/a><\/p>\n\n\n\n

–Anthracyclines (doxorubicin, epirubicin, daunorubicin, idarubicin)

-Binds to DNA in healthy cells when they extravasate into tissue

-When not immediately treated with dexrazoxane, the vesicant remains in the tissue and invades adjacent healthy tissue

-Likely to result in more tissue damage

-Left untreated, extravasations become larger and deeper, worsening over time (weeks to months)<\/p>\n\n\n\n

Managing Non-DNA Binding Vesicant Extravasation<\/a><\/p>\n\n\n\n

-Vinca Alkaloids (vincristine, vinblastine)

-Do not bind to DNA in healthy cells when they extravasate into tissue. Indirect effect on healthy tissue

-Treat with heat, elevation, and hyaluronidase local injection (spreads the vesicant through the tissue for faster metabolism of the vesicant agent)

-Usually results in less tissue damage

-Improves over a short period of time (days to weeks(<\/a><\/p>\n\n\n\n

mitogen-activating protein kinase (Raf-1\/MAPK) pathway<\/a><\/p>\n\n\n\n

-shown to decrease the benefits of some cancer drugs

-decrease disease-free survival time in some pts<\/a><\/p>\n\n\n\n

Mitotic Phase (M phase)<\/a><\/p>\n\n\n\n

-Replicated chromosomes are aligned, separated, and move into 2 new, identical daughter cells

-takes about 30-60 minutes<\/a><\/p>\n\n\n\n

Monoclonal Antibody Targeted Therapy<\/a><\/p>\n\n\n\n

– end in -mab

-relatively large in size and therefore usually cannot enter cells

-extracellular or transmembrane

-man made version of antibodies that are designed to attack a very specific target on cancer cells

-usually from mice<\/a><\/p>\n\n\n\n

Monomer<\/a><\/p>\n\n\n\n

molecule that can join with other identical monomers to form a structure called a polymer<\/a><\/p>\n\n\n\n

M Phase Checkpoints<\/a><\/p>\n\n\n\n

When the cells prepare to divide, the chromosomes line up in the mitotic spindle.

If the chromosomes are not properly aligned, division is not allowed to continue<\/a><\/p>\n\n\n\n

mTOR<\/a><\/p>\n\n\n\n

-target of rapamycin

-a protein that tells cells when to grow, divide, and survive<\/a><\/p>\n\n\n\n

Mucositis<\/a><\/p>\n\n\n\n

-inflammation of the mucous membrane lining the digestive tract from mouth to anus

-affects 40-100% of pts<\/a><\/p>\n\n\n\n

Myeolid Precursor Cells<\/a><\/p>\n\n\n\n

Mature into:
-RBCS
-Plts
-WBCs (Granulocytes)<\/a><\/p>\n\n\n\n

Nadir<\/a><\/p>\n\n\n\n

-point at which blood cell counts are at their lowest following treatment

-typically, but not always, occurs 7-10 days after the cycle is administered<\/a><\/p>\n\n\n\n

Neoadjuvant Treatment<\/a><\/p>\n\n\n\n

-treatment given as a first step to shrink a tumor before the main treatment, usually surgery

-examples: chemo, radiation therapy, hormone therapy<\/a><\/p>\n\n\n\n

Neutopenia RF<\/a><\/p>\n\n\n\n

-older than 65

-hx of neutropenia with previous chemo

-previous chemo or radiation

-hematologic malignancy, uncontrolled or advanced cancer, or lung cancer<\/a><\/p>\n\n\n\n

Neutropenia<\/a><\/p>\n\n\n\n

-ANC of less than 500\/mm3 or

-less than 1000\/mm3 with the expectation that the count will drop below 500 in the next 48 hours<\/a><\/p>\n\n\n\n

Neutropenic Fever<\/a><\/p>\n\n\n\n

-temp of 38.3 or greater one time

-temp of 38 lasting 1 hour<\/a><\/p>\n\n\n\n

Nitrosoureas<\/a><\/p>\n\n\n\n

-subgroup of alkylating agents

-able to cross the blood-brain barrier (effective in treating some brain tumors, melanomas, lymphomas)

-Carmustine (BiCNU)
-Lomustine (CeeNu)
-Streptozocin (Zanosar)

-pulmonary monitoring recommended<\/a><\/p>\n\n\n\n

Nonadherence<\/a><\/p>\n\n\n\n

-pt takes too few or too many pills<\/a><\/p>\n\n\n\n

Nonspecific Immunotherapy<\/a><\/p>\n\n\n\n

-do no target cancer cells alone but rather stimulate a large immune response

-given adjuvantly to other anticancer treatment drugs

-examples are cytokines, interleukins, and checkpoint inhibitors<\/a><\/p>\n\n\n\n

The Normal Cell Cycle<\/a><\/p>\n\n\n\n

-The cell cycle refers to the ordered seres of processes of DNA replication and mitosis, or cell division

-Cell nucleus regulates these processes by gathering and processing complexes molecular information<\/a><\/p>\n\n\n\n

Oncogene<\/a><\/p>\n\n\n\n

when mistakes in copies of DNA can occur, if a mutation occurs next to a proto-oncogene, it can “turn on” and become a ______<\/a><\/p>\n\n\n\n

Oral Chemotherapy<\/a><\/p>\n\n\n\n

-greater challenge to adherence because the responsibility falls on the pt and caregiver<\/a><\/p>\n\n\n\n

Overadherence<\/a><\/p>\n\n\n\n

-when a pt believes a dose was missed or that “more is better”, too much medication may be taken, leading to increased toxicity<\/a><\/p>\n\n\n\n

Oxaliplatin<\/a><\/p>\n\n\n\n

-Alkylating agent

-irritant and vesicant, extra caution with the IV site

-peripheral neuropathy is a dose-limiting side effect (exacerbated by cold temperatures)

-avoid cold drinks and foods, wearing gloves and warm shoes

-avoid breathing cold air<\/a><\/p>\n\n\n\n

p53<\/a><\/p>\n\n\n\n

-“sucidie gene”

-activates apoptosis when the cell is damaged beyond repair or too old to function

-more than 50% of solid tumors, the gene is mutated and unable to perform its normal function<\/a><\/p>\n\n\n\n

Passive Immunotherapy<\/a><\/p>\n\n\n\n

-initate an antitumor effect but do not result in any immunologic memory

-require repeated administration to be effective

-includes monoclonal antibodies and cytokines<\/a><\/p>\n\n\n\n

Pathways<\/a><\/p>\n\n\n\n

many pathways and crossalks signaling btw and among the different pathways, and they all have the power to control cell behavior in one way or another<\/a><\/p>\n\n\n\n

phosphoinositide 3-kinases (PI3K)<\/a><\/p>\n\n\n\n

-transduction enzymes that activate Akt, leading to cell survival, increased cell proliferation, and growith<\/a><\/p>\n\n\n\n

phosphorylation<\/a><\/p>\n\n\n\n

activation of a chemical process to initiate signaling<\/a><\/p>\n\n\n\n

Plasma Cells<\/a><\/p>\n\n\n\n

-some plasma cells will undergo apoptosis

-Some will go to the BM where they will continue to secrete antibodies sometimes for years<\/a><\/p>\n\n\n\n

Pluripotent Stem Cell<\/a><\/p>\n\n\n\n

-The cells of the immune system are created in the bome marrow from what is know as a ___

-A stem cell that can differentiate into any cell type except for extraembryotic tissue, does not yet have a function<\/a><\/p>\n\n\n\n

Prevention\/Treatment of hand foot syndrome<\/a><\/p>\n\n\n\n

-limit exposure of hands and feet to hot water

-take cool showers

-avoid exposure to sources of heat, such as using saunas or sitting in the sun

-avoid activities that cause unnecessary force or friction on the hands or feet, such as running or aerobics

-avoid contact with harsh chemicals used in detergents and household cleaning products

-avoid activities that require you to press your hand against a hard surface

-elevate your hands and feet when sitting or lying down

-gently apply skin care creams to keep hands moist

-wear loose-fitting, well ventilated shoes<\/p>\n\n\n\n

Progression through the cell cycle is controlled through two proteins:<\/a><\/p>\n\n\n\n

1. cyclines (D, E, A, B)

2. Cyclin-dependent kinases (CDKs)

-Cyclin-CDK complex allows the cell to progress through each phase of the cell cycle<\/a><\/p>\n\n\n\n

Protein tyrosine kinases phosphorylates<\/a><\/p>\n\n\n\n

-turned on by giving up a phosphate molecule

-the message is now send via a “bucket bridage”, or passing the message from one molecule to other signaling molecules until the message gets first into the cell nucleus

-where it is transcribed<\/a><\/p>\n\n\n\n

Proto-oncogene<\/a><\/p>\n\n\n\n

-regulate normal cell growth and division

-large family of genes that code for proteins and enzymes that turn on the cell cyle<\/a><\/p>\n\n\n\n

Receptor<\/a><\/p>\n\n\n\n

-molecule inside or on the surface of a cell that binds to a specific substance causes a specific effect in that cell<\/a><\/p>\n\n\n\n

Regulatory T-cells AKA suppressor T-Cells<\/a><\/p>\n\n\n\n

regulate the immune response to prevent autoimmune reactions and limit inflammatory responses<\/a><\/p>\n\n\n\n

Relative dose intensity (RDI)<\/a><\/p>\n\n\n\n

-calculated by comparing the dose that the pt received to the planned dose of the standard regimen<\/a><\/p>\n\n\n\n

Restriction Point<\/a><\/p>\n\n\n\n

-The transition from the resting phase into an actively dividing phase (G0-G1) is a point where cellular transformation can occur

-During this time, cells pass through a transition phase known as a restriction point

-Extracellular growth factors trigger reentry into G1, and GF are required to send the cells past the restriction point, or the point of no return<\/p>\n\n\n\n

Should I avoid my grandchildren and other family members when I am getting treatment?<\/a><\/p>\n\n\n\n

-it is perfectly safe for you to have contact with your loved ones while getting treatment

-Hugging, kissing, and spending time together while eating are all safe activities

-Safety with bodily fluids is necessary for the first 48 hours after receiving chemo<\/a><\/p>\n\n\n\n

Signal transduction<\/a><\/p>\n\n\n\n

-the communication or passage of a message telling the cell to do a biologic process, such as make a protein, divide, or make new blood vessels<\/a><\/p>\n\n\n\n

Signal transduction steps<\/a><\/p>\n\n\n\n

1. Messages usually sent from outside the cell where the messenger (ligand) first binds to the cell receptor which extended through the cell membrane

2. These receptors ae called receptor tyrosine kinases

3. To send the message through the membrane, the receptor often has to join with another recetor to become active and t autophophorylate

4. This is called dimerization and can be the following:<\/p>\n\n\n\n

Small Molecule Compound Targeted Therapies<\/a><\/p>\n\n\n\n

-end in -ib

-targets located inside the cell because these gents are able to enter cells more easily

-intracellular

-most given orally<\/a><\/p>\n\n\n\n

Specific Immunotherapy<\/a><\/p>\n\n\n\n

-capitalize on tumor markers to specifically target and kill cancer cells

-examples are mAbs and cancer vaccines<\/a><\/p>\n\n\n\n

Stomatitis<\/a><\/p>\n\n\n\n

-specifically inflammatory conditions of the mouth<\/a><\/p>\n\n\n\n

Synthesis Phase (S phase)<\/a><\/p>\n\n\n\n

-DNA replicates

-Results in the formation of identical pairs of DNA (chromatids)

-which are attached a t the centromere

-lasts 2-10 hours<\/a><\/p>\n\n\n\n

targeted therapies work by doing the following<\/a><\/p>\n\n\n\n

1. blocking angiogenesis

2. blocking signals inside or outside the cell

3. delivering toxic substances to the cell

4. stimulating the body’s immune system<\/a><\/p>\n\n\n\n

T-Cell<\/a><\/p>\n\n\n\n

-Can only recognize antigens when they are presented to them by “presenting cells”

-Recognize phagocytized fragments of an antigen that are put on the surface of antigen-presenting cells<\/a><\/p>\n\n\n\n

T-Cell–Mediated<\/a><\/p>\n\n\n\n

-Delayed hypersensitivity reactions, can occur any time after the immediate hypersensitivity window, even days or weeks<\/a><\/p>\n\n\n\n

True statements related to drug dose calculation and administration<\/a><\/p>\n\n\n\n

-the AUC calculation incorporates renal function as part of the equation

-Pts who have had previous radiation therapy or chemo are considered special populations with regard to a potential need for dose modification

-The AUC calculation is used for carboplatin dosing

-Children may metabolize drugs differently than adults; dose modifications are possible<\/p>\n\n\n\n

Tumor suppressor genes<\/a><\/p>\n\n\n\n

-act like brakes in a car, slowing down or stopping cell growth and division

-in the presence of malignancies, they bind to DNA with intention of repairing or activating apoptosis

-for it to be turned on it must be expressed or “opened” in the DNA helix so that it can be transcribed or copied<\/a><\/p>\n\n\n\n

Two ways that angiogenesis inhibitors work<\/a><\/p>\n\n\n\n

1. some intergere with action of VEGF which stimulates n ew blood vessel formation

2. others target their molecules that stimulate new blood vessel growth<\/a><\/p>\n\n\n\n

Type 1 HSR early S\/SX<\/a><\/p>\n\n\n\n

-pruritus
-restlessness, agitation, anxiety, feeling of impending doom
-fever, flushing, chills
-urticaria (hives)
-maculopapular rash
-edema of hands, face, and feet
-N\/V
-dyspnea, wheezing, bronchospasm
-hypotension, cyanosis
-circulatory and respiratory collapse<\/a><\/p>\n\n\n\n

Type IV HSR<\/a><\/p>\n\n\n\n

-pneumonitis
-mucositis
-contact dermatitis
-granulomas
-Graph vs host disease<\/a><\/p>\n\n\n\n

Types of CINV<\/a><\/p>\n\n\n\n

-Acute: occurring within 24 hours

-Delayed: from 24 hour – 5 days after

-Breakthrough: Occurring despite treatment

-Anticipatory: triggered by taste, odor, memories, visions, anxiety r\/t chemo

-Refractory: occurring despite subsequent cycles when treatment failed in earlier cycles<\/a><\/p>\n\n\n\n

VEGF<\/a><\/p>\n\n\n\n

this is the primary angiogenic factor produced by cells<\/a><\/p>\n\n\n\n

Vesicants<\/a><\/p>\n\n\n\n

-causes blistering and significant pain and tissue damage and destruction, leading to tissue death<\/a><\/p>\n\n\n\n

Vesicants in PIVs<\/a><\/p>\n\n\n\n

-Do not use IV in hand, wrist, AC areas

-Do NOT place the IV below a recent ventipuncture site used (<24 hours)

-Use a flexible IV catheter<\/a><\/p>\n\n\n\n

What is a monoclonal antibody, and how is it different from chemo?<\/a><\/p>\n\n\n\n

-mAbs are agents that are derived from human or mouse antibodies or a combination of the two

-mAbs search out proteins on the cells surface

-mAbs recognize and bind to specific anatigens on the cells surface

-natural killer cells and\/or cytotoxic proteins of the immune system recognize and destroy the marked tumor cells

-mAbs can also directly induce cell death as well

-One of the biggest differences is that mAbs cause harm only to those cells that are marked or binded

–<\/p>\n\n\n\n

When a vesicant extravasation occurs or is suspected, take the following steps:<\/a><\/p>\n\n\n\n

1. Immediately STOP administering the vesicant and IV fluids

2. Disconnect the IV tubing from the IV device. Do not remove the IV device or noncoring port needle

3. Attempt to aspirate residual vesicant from the IV device or port needling use a small (1-3 mL) syringe

4. Remove the peripheral IV device or port needle

5. Initiate appropriate management measures<\/p>\n\n\n\n

Xerostomia<\/a><\/p>\n\n\n\n

-dryness of the mouth caused by damage to or dysfunction of the salivary glands<\/a><\/p>\n\n\n\n

3 major phases of cell division:
Interphase
Mitotic phase
Cytokinesis<\/p>\n\n\n\n

3 steps of interphase:
First growth phase (G1)
Synthesis phase (S phase)
Second growth phase (G2)<\/p>\n\n\n\n

4 phases of mitosis:
Prophase
Metaphase
Anaphase
Telophase<\/p>\n\n\n\n

Innate immunity:
Non-specific response, either:<\/p>\n\n\n\n

    \n
  1. Barrier (skin, mucous membranes, flora of skin\/gut)<\/li>\n\n\n\n
  2. Cellular components (phagocytes, natural killer cells, granulocytes, macrophages)<\/li>\n<\/ol>\n\n\n\n

    Adaptive immunity:
    Follows innate immunity if unsuccessful. Memory immunity, including:<\/p>\n\n\n\n

      \n
    1. Humoral immunity (production of antibodies or immunoglobulins)<\/li>\n\n\n\n
    2. Cell mediated immunity (dependent upon T cells)<\/li>\n\n\n\n
    3. Regulatory T -cells (prevent autoimmune reactions and limit inflammatory responses)<\/li>\n<\/ol>\n\n\n\n

      Define mutations
      Variations in the nucleotide sequence of a gene<\/p>\n\n\n\n

      3 main goals of treatment:
      Cure
      Control
      Palliation<\/p>\n\n\n\n

      Define neoadjuvant therapy
      Treatment is given prior to surgery to shrink the tumor<\/p>\n\n\n\n

      Define adjuvant therapy
      Additional cancer treatment given after the primary treatment to lower the risk that the cancer reoccur<\/p>\n\n\n\n

      Define conditioning\/preparative therapy
      Treatments used to prepare a patient for stem cell transplantation<\/p>\n\n\n\n

      2 types of conditioning therapies:
      Myeloablative
      Nonmyeloablative<\/p>\n\n\n\n

      Define dose density
      Drug dose per unit of time<\/p>\n\n\n\n

      Define dose intensity
      Amount of drug delivered over time<\/p>\n\n\n\n

      How is relative dose intensity (RDI) calculated?
      By comparing the dose that the patient ACTUALLY received to the planned dose of the standard regimen<\/p>\n\n\n\n

      How do alkylating agents work?
      By causing a break in the DNA helix strand, interfering with DNA replication and causing cell death<\/p>\n\n\n\n

      3 subcategories of alkylating agents:<\/p>\n\n\n\n

        \n
      1. Nitrogen mustards<\/li>\n\n\n\n
      2. Platinum-based agents (do not possess an alkyl group but still termed alkylating agents as they work similarly)<\/li>\n\n\n\n
      3. Nitrosoureas<\/li>\n<\/ol>\n\n\n\n

        Most common subcategory of alkylating agents:
        Nitrogen mustards<\/p>\n\n\n\n

        Common alkylating agents:
        Cyclophosphamide (Cytoxan)
        Ifosfamide (Ifex)
        Bendamustine (Treanda)<\/p>\n\n\n\n

        Common platinum-based agents:
        Cisplatin (Platinol)
        Carboplatin (Paraplatin)<\/p>\n\n\n\n

        What is unique about nitrosoureas agents?
        Able to cross the blood-brain barrier; can be effective in treating some brain tumors<\/p>\n\n\n\n

        Common nitrosoureas agents:
        Carmustine (BiCNU)
        Lomustine (CeeNu)
        Streptozocin (Zanosar)<\/p>\n\n\n\n

        Hypersensitivity can occur with late doses of:
        Carboplatin<\/p>\n\n\n\n

        These agents are typically categorized as highly emetogenic:<\/p>\n\n\n\n

          \n
        1. Alkylating agents<\/li>\n\n\n\n
        2. Nitrosoureas<\/li>\n<\/ol>\n\n\n\n

          Pre-administration labs for alkylating agents and nitrosoureas:
          BUN
          Creatinine
          CBC w\/ diff<\/p>\n\n\n\n

          What is the medication Mesna used for?
          Bladder protectant with administration of cyclophosphamide or ifosfamide<\/p>\n\n\n\n

          Instruct pts receiving __<\/em><\/strong> to avoid exposure to cold air and consuming cold fluids for 3-4 days following treatment
          Oxaliplatin<\/p>\n\n\n\n

          How do antimetabolites function?
          By blocking DNA and RNA growth by interfering with enzymes needed for normal cell metabolism<\/p>\n\n\n\n

          Antimetabolites work in the _<\/em> phase.
          S<\/p>\n\n\n\n

          What types of cells are best affected by antimetabolites?
          Cells with high division rates<\/p>\n\n\n\n

          Common side effects of antimetabolites:
          Myelosuppression
          GI toxicities
          Photosensitivity
          Hand-foot syndrome<\/p>\n\n\n\n

          Common antimetabolite drugs:
          Azacitidine
          Capecitabine
          5-FU
          Cytarabine
          Decitabine
          Methotrexate<\/p>\n\n\n\n

          The institute for Safe Medication Practices recommends what route of administration for vincristine?
          IV piggyback via gravity<\/p>\n\n\n\n

          Anthracycline antitumor abx work by:
          Interfering with enzymes necessary for DNA to replicate in ALL phases of the cell cycle<\/p>\n\n\n\n

          The two major classifications of antitumor antibiotics are:
          Anthracyclines
          Non-anthracyclines<\/p>\n\n\n\n

          Common anthracycline antitumor abx:
          Daunorubicin
          Doxorubicin
          Epirubicin
          Idarubicin<\/p>\n\n\n\n

          The antitumor abx _<\/strong><\/em><\/strong> is not an anthracycline, but has anthracycline-type properties.
          Mitoxantrone<\/p>\n\n\n\n

          Common non-anthracycline antitumor abx:
          Actinomycin D
          Mitomycin C
          Bleomycin<\/p>\n\n\n\n

          Monitoring necessary with doxorubicin:
          Vesicant –> extravasation
          Cardiac function
          Lifetime dose tracking (cardiotoxicity)<\/p>\n\n\n\n

          Lifetime dose of doxorubicin should not exceed:
          550 mg\/m^2<\/p>\n\n\n\n

          What cardiac protectant medication can be administered prior to doxorubicin?
          Dexrazoxane<\/p>\n\n\n\n

          Significant side effects of doxorubicin are:
          Cardiotoxicity
          N\/V
          Mucositis
          Diarrhea
          Severe myelosuppression
          Hepatic impairment
          Secondary cancers<\/p>\n\n\n\n

          Monitoring necessary with bleomycin:
          Pulmonary toxicity
          Hypersensitivity reactions (esp. in lymphoma patients)
          Cutaneous reactions
          Lifetime dose tracking (pulmonary toxicity)<\/p>\n\n\n\n

          Pulmonary fibrosis is possible when the lifetime dose of bleomycin exceeds:
          400 units<\/p>\n\n\n\n

          What 6 patient characteristics make CINV more likely?<\/p>\n\n\n\n

            \n
          1. Younger than 50 years<\/li>\n\n\n\n
          2. Hx of low alcohol intake<\/li>\n\n\n\n
          3. Female gender<\/li>\n\n\n\n
          4. Hx of morning sickness during pregnancy<\/li>\n\n\n\n
          5. Prone to motion sickness<\/li>\n\n\n\n
          6. Previous chemotherapy<\/li>\n<\/ol>\n\n\n\n

            Types of CINV:
            Acute
            Delayed
            Breakthrough
            Anticipatory
            Refractory<\/p>\n\n\n\n

            Define acute CINV
            Occurring within 24 hours of chemotherapy<\/p>\n\n\n\n

            Define delayed CINV
            Occurring from 24 hours to 5 days after treatment<\/p>\n\n\n\n

            Define breakthrough CINV
            Occurring despite treatment<\/p>\n\n\n\n

            Define anticipatory CINV
            Triggered by taste, odor, memories, visions, or anxiety related to chemotherapy<\/p>\n\n\n\n

            Define refractory CINV
            Occurring during subsequent cycles when treatment failed in earlier cycles<\/p>\n\n\n\n

            Highly emetogenic chemo (HEC) causes CINV in more than _<\/em>% of patients
            90<\/p>\n\n\n\n

            Moderately emetogenic chemo (MEC) causes CINV in patients % to <\/em><\/strong>% of the time
            30-90<\/p>\n\n\n\n

            Patients on low-potential emetogenic chemo develop CINV % to <\/em><\/strong>% of the time
            10-30<\/p>\n\n\n\n

            Minimal-risk emetogenic chemo causes CINV less than _<\/em>% of the time
            10<\/p>\n\n\n\n

            Common IV HEC drugs include:
            Carmustine
            Cisplatin
            Cyclophosphamide
            Dacarbazine
            Mechlorethamine
            Streptozosin<\/p>\n\n\n\n

            Common IV MEC drugs include:
            Carboplatin
            Cytarabine
            Daunorubicin
            Doxorubicin
            Epirubicin
            Idarubicin
            Ifosfamide
            Irinotecan
            Oxaliplatin<\/p>\n\n\n\n

            Common low-potential IV emetogenic chemo drugs include:
            5-FU
            Cytarabine
            Docetaxel
            Etoposide
            Gemcitabine
            Methotrexate
            Mitomycin C
            Mitoxantrone
            Paclitaxel
            Pemetrexed<\/p>\n\n\n\n

            Common minimal-risk IV emetogenic chemo drugs include:
            Bleomycin
            Bevacizumab
            Bortezomib
            Busulfan
            Cetuximab
            Fludarabine
            Trastuzumab
            Vinca alkaloids<\/p>\n\n\n\n

            The 2 most important neurotransmitters involved in vomiting are:<\/p>\n\n\n\n

              \n
            1. Serotonin<\/li>\n\n\n\n
            2. Substance P<\/li>\n<\/ol>\n\n\n\n

              Describe the peripheral pathway of CINV
              Primarily occurs in the GI tract
              Associated with acute CINV
              Neurotransmitter –> serotonin<\/p>\n\n\n\n

              Describe the central pathway of CINV
              Primarily occurs in the brain
              Associated with delayed CINV
              Neurotransmitter –> Substance P<\/p>\n\n\n\n

              Common serotonin 5-HT3 antagonists used for CINV:
              Dolasetron
              Granisetron
              Ondansetron
              Palonosetron<\/p>\n\n\n\n

              Common neurokinin-1 antagonists used for CINV:
              Aprepitant
              Fosaprepitant<\/p>\n\n\n\n

              Common steroids used for CINV:
              Dexamethasone<\/p>\n\n\n\n

              2 types of therapies that commonly have cutaneous reactions:<\/p>\n\n\n\n

                \n
              1. EGFR inhibitor therapies<\/li>\n\n\n\n
              2. Antimetabolites<\/li>\n<\/ol>\n\n\n\n

                Most-common cutaneous reaction seen with 5-FU and Capecitabine:
                Palmar-plantar erythrodysesthesia AKA hand-foot syndrome<\/p>\n\n\n\n

                Antimetabolites that commonly cause cutaneous reactions:
                5-FU
                Capecitabine (Xeloda)<\/p>\n\n\n\n

                Define myelosuppression
                Bone marrow activity is decreased, resulting in fewer RBCs, WBCs and platelets<\/p>\n\n\n\n

                If severe: myeloablation<\/p>\n\n\n\n

                The most common dose-limiting toxicity of chemotherapy
                Myelosuppression<\/p>\n\n\n\n

                Define nadir, and when does it occur?
                The point at which blood cell counts are at their lowest following a treatment cycle.<\/p>\n\n\n\n

                Typically occurs 7-10 days following cycle<\/p>\n\n\n\n

                NCCN defines neutropenia as an ANC < _<\/em><\/strong>\/mm^3
                500<\/p>\n\n\n\n

                Risk factors for developing neutropenia include:<\/p>\n\n\n\n

                \n

                65 years old
                Hx of neutropenia with previous chemotherapy
                Hx of chemotherapy or radiation treatment
                Hematologic malignancy
                Uncontrolled\/advanced cancer
                Lung cancer<\/p>\n<\/blockquote>\n\n\n\n

                Define neutropenic fever
                Fever of 101 F or greater one time
                OR
                Fever of 100.4 F lasting one hour or longer<\/p>\n\n\n\n

                ANC calculation
                (% polys + % bands) x (WBC)\/100<\/p>\n\n\n\n

                Normal WBC count
                4,500-10,000<\/p>\n\n\n\n

                Normal neutrophil count
                54%-62% of WBC<\/p>\n\n\n\n

                An ANC of less that _<\/strong> is considered a risk for infection
                1,000<\/p>\n\n\n\n

                Define thrombocytopenia
                Low platelet count<\/p>\n\n\n\n

                Symptoms of thrombocytopenia
                Petechiae or easily bruising
                Headaches
                Hypotension and tachycardia
                Prolonged bleeding (gums, menstruation)<\/p>\n\n\n\n

                Define anemia
                Deficiency of RBC or hemoglobin in the blood<\/p>\n\n\n\n

                Symptoms of anemia
                Dyspnea
                Fatigue
                Dizziness
                Headaches<\/p>\n\n\n\n

                Acute diarrhea lasts:
                1-2 days and resolves on its own<\/p>\n\n\n\n

                Persistent diarrhea lasts:
                2-4 weeks<\/p>\n\n\n\n

                Chronic diarrhea lasts:<\/p>\n\n\n\n

                \n

                4 weeks<\/p>\n<\/blockquote>\n\n\n\n

                Common constipation-causing agents:
                Vinca alkaloids (vincristine and vinorelbine)
                Thalidomide
                Lenalidomide
                Bortezomib<\/p>\n\n\n\n

                Define mucositis
                Inflammation of the mucous membranes lining the digestive tract from mouth to anus<\/p>\n\n\n\n

                Define stomatitis
                Inflammatory conditions of the mouth specifically<\/p>\n\n\n\n

                AKA oral mucositis<\/p>\n\n\n\n

                Define xerostomia
                Dryness of the mouth caused by damage to or dysfunction of the salivary glands<\/p>\n\n\n\n

                Common diarrhea-causing agents:
                Irinotecan
                5-FU
                Paclitaxel
                Dactinomycin
                Capecitabine<\/p>\n\n\n\n

                Hypersensitivity reaction (HSR) versus anaphylaxis
                HSR- localized tissue injury; generalized<\/p>\n\n\n\n

                Anaphylaxis- severe inflammatory response; systemic; caused by histamine release<\/p>\n\n\n\n

                Immediate HSR can occur:
                Within 5 minutes of start of infusion to 6 hours following infusion<\/p>\n\n\n\n

                Delayed HSR can occur:
                Days or weeks after immediate HSR window<\/p>\n\n\n\n

                Risk factors for HSR and anaphylaxis:
                Administration of a known HSR causing agent
                Hx of allergies
                Hx of hypersensitivity or anaphylaxis
                Premedications not ordered\/administered<\/p>\n\n\n\n

                First thing to do if a HSR occurs:
                STOP THE INFUSION IMMEDIATELY<\/p>\n\n\n\n

                Define cumulative dose
                Total dose of an antineoplastic agent or radiation after repeated exposure to the treatment<\/p>\n\n\n\n

                Define single dose
                Recommended dose of one antineoplastic agent given at a single point in time<\/p>\n\n\n\n

                Define course dose (AKA divided dose)
                Recommended dose of one antineoplastic agent given over a defined period of time<\/p>\n\n\n\n

                Define extravasation
                Leak of a drug capable of causing tissue damage from the intended vessel into the surrounding tissue or unintended sites<\/p>\n\n\n\n

                Agents classified as irritants can cause:
                Inflammation
                Pain
                Burning
                ** Rarely cause tissue necrosis comparable to vesicants<\/p>\n\n\n\n

                Agents classified as vesicants can cause:
                Blistering
                Significant pain
                Tissue damage and destruction
                **Lead to tissue death<\/p>\n\n\n\n

                Define infiltration
                Leakage of non-vesicant\/non-irritant solutions into surrounding tissue<\/p>\n\n\n\n

                Common plant alkaloids:
                Etoposide
                Docetaxel
                Paclitaxel
                Vinblastine
                Vinorelbine<\/p>\n\n\n\n

                Vinca alkaloids are ALL administered (1)<\/em> and should NEVER be administered (2)<\/em>, as this will result in patient death<\/p>\n\n\n\n

                  \n
                1. Intravenously<\/li>\n\n\n\n
                2. Intrathecally<\/li>\n<\/ol>\n\n\n\n

                  How does hormone therapy work?
                  Attempts to add, block, or remove hormones from the body to interrupt cancer cell division<\/p>\n\n\n\n

                  LHRH agonists MOA
                  Produce an initial increase in LH and FSH, which can cause a flare. Then lower testosterone made by testicles and estrogen & progesterone made by ovaries<\/p>\n\n\n\n

                  *Prostate cancer
                  *Estrogen receptor-positive, premenopausal metastatic breat cancer<\/p>\n\n\n\n

                  LHRH antagonists MOA
                  Directly inhibits pituitary from releasing LH and FSH<\/p>\n\n\n\n

                  *No tumor flare<\/p>\n\n\n\n

                  Most common type of breast cancer
                  Hormone receptor (HR)-positive breast cancer<\/p>\n\n\n\n

                  Aromatase inhibitors MOA
                  Block the enzyme aromatase, which turns the hormone androgen into small amounts of estrogen in the body<\/p>\n\n\n\n

                  **Less estrogen is available to stimulate growth of HR-positive breast cancer cells<\/p>\n\n\n\n

                  2 types of aromatase inhibitors<\/p>\n\n\n\n

                    \n
                  1. Steroidal (irreversible)<\/li>\n\n\n\n
                  2. Nonsteroidal (reversible)<\/li>\n<\/ol>\n\n\n\n

                    3 aromatase inhibitors
                    Anastrozole
                    Letrozole
                    Exemestane<\/p>\n\n\n\n

                    Common side effects of aromatase inhibitors (AI):
                    Fatigue
                    N\/V*
                    Weakness
                    HA*
                    Insomnia
                    Dizziness
                    Hot flashes*
                    Weight gain*
                    Higher cholesterol
                    Increased sweating*
                    Bone\/joint pain*<\/p>\n\n\n\n

                    Selective ER downregulators (SERDs) MOA
                    Binding to and degrading ER<\/p>\n\n\n\n

                    Common SERD
                    Fulvestrant<\/p>\n\n\n\n

                    Selective ER modulators (SERMs) MOA
                    Blocking and downregulating ERs<\/p>\n\n\n\n

                    *Can function as ER agonists, antagonists, or mixed agonist-antagonists
                    *Can activate or block estrogen<\/p>\n\n\n\n

                    Common SERMs
                    Tamoxifen
                    Raloxifine
                    Bazedoxifine<\/p>\n\n\n\n

                    Antiandrogens MOA
                    Keeps androgens from binding to androgen receptors found in prostate cancer cells (and in some other tissue cells)<\/p>\n\n\n\n

                    Androgen synthesis inhibitors MOA
                    Stop the adrenal glands from producing androgens<\/p>\n\n\n\n

                    Common androgen synthesis inhibitors
                    Ketoconazole
                    Aminoglutethimide
                    Abiraterone acetate<\/p>\n\n\n\n

                    CYP17 inhibitors MOA
                    Inhibit the key enzyme that catalyzes biosynthesis of androgens from all sources<\/p>\n\n\n\n

                    Common CYP17 inhibitors
                    Abiraterone
                    Orteronel<\/p>\n\n\n\n

                    Adrenolytic agents MOA
                    Suppress testicular and adrenal steroidogenesis, rapidly reducing testosterone levels<\/p>\n\n\n\n

                    Define receptor
                    Molecule inside\/on surface of a cell that binds to a specific substance and causes a specific effect in that cell<\/p>\n\n\n\n

                    Define monomer
                    Molecule that can be bonded to other identical molecules to form a polymer<\/p>\n\n\n\n

                    Define ligand
                    Molecule that binds to a receptor to exert a biologic effect<\/p>\n\n\n\n

                    Define ligand bonding
                    Process by which ligand attaches to specific receptor site and activates receptor, activating the signaling pathway<\/p>\n\n\n\n

                    Define dimerization
                    2 monomers that are side-by-side on cell surface are paired and activated by a ligand, which causes a series of signals<\/p>\n\n\n\n

                    Define kinase
                    Enzyme that adds phosphates to other molecules, causing other molecules in the cell to become either active or inactive<\/p>\n\n\n\n

                    Define phosphorylation
                    Activation of a chemical process to initiate signaling<\/p>\n\n\n\n

                    Targeted therapies work by:<\/p>\n\n\n\n

                      \n
                    1. Blocking angiogenesis<\/li>\n\n\n\n
                    2. Blocking signals inside or outside the cell<\/li>\n\n\n\n
                    3. Delivering toxic substances to the cell<\/li>\n\n\n\n
                    4. Simulating the body’s immune system<\/li>\n<\/ol>\n\n\n\n

                      __<\/em><\/strong> has been described as a way to “fire up the immune system’s response to cancer”
                      Immunotherapy<\/p>\n\n\n\n

                      Immunotherapy works by the following 3 ways:<\/p>\n\n\n\n

                        \n
                      1. Stopping or slowing the growth of cancer cells<\/li>\n\n\n\n
                      2. Stopping cancer cells from spreading to other parts of the body<\/li>\n\n\n\n
                      3. Helping the immune system recognize cancer cells and increase its effectiveness at eliminating cancer cells<\/li>\n<\/ol>\n\n\n\n

                        What sets immunotherapy apart from traditional chemotherapy?
                        Highly specific
                        Trained to remember cancer cells<\/p>\n\n\n\n

                        Immunotherapy categories:
                        Passive
                        Aggressive
                        Specific
                        Nonspecific<\/p>\n\n\n\n

                        Passive immunotherapy MOA
                        Administered to initiate an antitumor effect
                        *Do not result in any immunologic memory<\/p>\n\n\n\n

                        Examples of passive immunotherapy
                        Monoclonal antibodies
                        Cytokines<\/p>\n\n\n\n

                        Active immunotherapy MOA
                        Mount an immune response against tumor
                        *Should remember cancer cells long after treatment has stopped<\/p>\n\n\n\n

                        Examples of active immunotherapy
                        Cancer vaccines<\/p>\n\n\n\n

                        Specific immunotherapy MOA
                        Target tumor markers or tumor-associated antigens (TAAs) to kill cancer cells<\/p>\n\n\n\n

                        Examples of specific immunotherapy
                        mAbs
                        Cancer vaccines<\/p>\n\n\n\n

                        Nonspecific immunotherapy MOA
                        Stimulate a large immune response<\/p>\n\n\n\n

                        *Given adjuvantly to other anticancer treatment drugs<\/p>\n\n\n\n

                        Examples of nonspecific immunotherapy
                        Cytokines, interleukins, checkpoint inhibitors<\/p>\n\n\n\n

                        2 different ways that immunotherapies work against cancer:<\/p>\n\n\n\n

                          \n
                        1. Triggering the immune system to destroy cancer cells<\/li>\n\n\n\n
                        2. Boost immune system’s ability to fight cancer<\/li>\n<\/ol>\n\n\n\n

                          6 main types of immunotherapy<\/p>\n\n\n\n

                            \n
                          1. Monoclonal antibodies<\/li>\n\n\n\n
                          2. Immune checkpoint inhibitors<\/li>\n\n\n\n
                          3. Cancer vaccines<\/li>\n\n\n\n
                          4. Nonspecific immunotherapies<\/li>\n\n\n\n
                          5. Adoptive cell therapy (CAR T-cell therapy)<\/li>\n\n\n\n
                          6. Oncolytic virus therapy<\/li>\n<\/ol>\n\n\n\n

                            mAbs MOA
                            Mark cancer cell surface receptor\/antigen to make the cell visible to the immune system to destroy<\/p>\n\n\n\n

                            Different types of mAbs used in treatment of cancer
                            Naked mAbs
                            Conjugated monoclonal antibodies
                            Bispecific monoclonal antibodies<\/p>\n\n\n\n

                            mAbs ending in “-ximab” source
                            Chimeric human-mouse<\/p>\n\n\n\n

                            mAbs ending in “-zumab” source
                            Humanized mouse<\/p>\n\n\n\n

                            mAbs ending in “-umab” source
                            Fully human<\/p>\n\n\n\n

                            mAbs ending in “-omab” source
                            Murine mouse<\/p>\n\n\n\n

                            Immune checkpoint inhibitors MOA
                            Prevent cancer cells from turning off T cells –> allows T cells to infiltrate a tumor and stop it from growing<\/p>\n\n\n\n

                            Immune checkpoint inhibitors initially cause tumors to swell, making it appear as if the tumor is growing. This is called _<\/em><\/strong><\/em><\/strong>
                            Pseudoprogression<\/p>\n\n\n\n

                            2 main types of cancer vaccines
                            Preventative\/prophylactic
                            Treatment\/therapeutic<\/p>\n\n\n\n

                            Nonspecific immunotherapies MOA
                            Stimulating the immune system in a general way, hopefully leading to a better immune response against cancer cells<\/p>\n\n\n\n

                            Adoptive cell therapy MOA
                            T cells collected from patient
                            T cells grown in laboratory
                            This increases amount of T cells able to kill cancer cells or fight infections
                            T cells given back to patient to help immune system<\/p>\n\n\n\n

                            Oncolytic virus therapy MOA
                            Naturally occurring or genetically engineered virus that can infect and kill a cancer call without harming normal cells<\/p>\n\n\n\n

                            Common side effects of immunotherapies
                            Fatigue
                            Diarrhea
                            Colitis
                            Musculoskeletal pain
                            Dermatitis<\/p>\n\n\n\n

                            Common treatment for immunotherapy side effects
                            Corticosteroids<\/p>\n\n\n\n

                            Results of immunotherapy agents most commonly occur between __<\/strong><\/em><\/strong> after starting therapy
                            12-16 weeks<\/p>\n\n\n\n

                            Hierarchy of controls when controlling workplace hazards
                            Elimination
                            Substitution
                            Engineering controls
                            Administrative controls
                            PPE<\/p>\n\n\n\n

                            4 different types of medication dosing:<\/p>\n\n\n\n

                              \n
                            1. Fixed doses<\/li>\n\n\n\n
                            2. Weight-based doses<\/li>\n\n\n\n
                            3. Body surface area (BSA) doses<\/li>\n\n\n\n
                            4. Area under the curve (AUC) doses<\/li>\n<\/ol>\n\n\n\n

                              G1
                              first growth phase (or first gap)<\/p>\n\n\n\n

                              2
                              How many cells are produced each time a cell divides?<\/p>\n\n\n\n

                              mitosis
                              the process of cell division<\/p>\n\n\n\n

                              interphase
                              The time when a cells grows and replicates DNA in preparation for cell division.<\/p>\n\n\n\n

                              G1
                              most important checkpoint in cell division<\/p>\n\n\n\n

                              cell division
                              Phases of include synthesis phase, G1, G2, M phase<\/p>\n\n\n\n

                              Chemotherapy and immunotherapy
                              These treatments are ALL developed to target specific points in the cell division process.<\/p>\n\n\n\n

                              cyclins and cyclin-dependent kinases
                              Progression through the cell cycle is controlled by these two proteins:<\/p>\n\n\n\n

                              pluripotent
                              _____<\/em><\/strong><\/em><\/strong> stem cells are created in the bone marrow and can differentiate into any type of cell (except embryonic tissue).<\/p>\n\n\n\n

                              undifferentiated
                              Is a pluripotent stem cell differentiated or undifferentiated?<\/p>\n\n\n\n

                              myeloid, lymphoid
                              for hematology a pluripotent stem cell divides producing cells from either _<\/em><\/strong><\/em><\/strong> or _<\/em><\/strong><\/em><\/strong> lineage<\/p>\n\n\n\n

                              myeolid
                              This type of precuros or pre-cell matures into red blood cells, platelets, and white blood cells.<\/p>\n\n\n\n

                              lymphoid
                              this type of stem cell or pre-cell matures into specialized WBCs called lymphocytes.<\/p>\n\n\n\n

                              immunotherapy
                              the use of the body’s own immune system to treat cancer<\/p>\n\n\n\n

                              B, T
                              These two letters make up the two types of lymphocyte cells.<\/p>\n\n\n\n

                              Alkylating agents
                              Classification
                              Break DNA helix strand, thereby interfering with DNA replication<\/p>\n\n\n\n

                              Altretamine (Hexalen)
                              Alkylating Agent
                              PO
                              Ovarian CA
                              Side effects- nausea, vomiting, skin rash, hypersensitivity reaction, diarrhea
                              Dose limiting – neuro-toxicity, peripheral neuropathy, myelosuppression<\/p>\n\n\n\n

                              Bendamustine (Treanda\/Bendeka)
                              Alkylating agent
                              IV
                              CLL or Indolent NHL
                              Side effects- pyrexia, nausea, vomiting, skin reactions, TLS, hepatotoxicity, vein irritation
                              Dose limiting – myelosuppression<\/p>\n\n\n\n

                              Irritant and vesicant properties<\/p>\n\n\n\n

                              infusion reactions likely to occur in 2nd or subsequent infusions<\/p>\n\n\n\n

                              Busulfan (IV busulfex: PO Myleran)
                              Alkylating Agent
                              IV or PO
                              CML and Stem cell prep
                              Side effects – profound tachycardia, HTN, chest pain, hyperpigmentation, alopecia, infertility, confusion, suizures, mucositis, nausea, vomiting, insomnia, hyperglycemia, blurred vision, secondary malignancy, VOD (now sinusoidal obstruction syndrome)<\/p>\n\n\n\n

                              seizure prophylaxis
                              central line only for IV<\/p>\n\n\n\n

                              Carboplatin
                              Alkylating agent
                              IV
                              Ovarian CA
                              Side effects – neutropenia, nausea, vomiting, hypersensitivity, mild alopecia, skin rash
                              Dose Limiting – thrombocytopenia<\/p>\n\n\n\n

                              Irritant
                              AUC dosing<\/p>\n\n\n\n

                              Chlorambucil (Leukeran)
                              Alkylating agent
                              PO
                              CLL, HL, NHL
                              Side effects – infertility, nausea, vomiting, secondary malignancy, hyperuricemia, pulmonary fibrosis, seizure
                              Dose Limiting – myelosuppression, skin reactions<\/p>\n\n\n\n

                              empty stomach
                              caution in pts with seisure history and within 1 month of radiation or other cytotoxic therapy<\/p>\n\n\n\n

                              Cisplatin
                              Alkylating agent
                              IV
                              Ovarian, Testicular, Bladder
                              Side Effects – severe acute and delayed CINV, ototoxicity, hyperuricemia, hypersensitivity, electrolyte abnormalities, peripheral neuropathy
                              Dose Limiting – nephrotoxicity, myelosupression<\/p>\n\n\n\n

                              Mannitol and hydration to prevent nephrotoxicity
                              check creatinine prior to dose
                              nausea up to 6 days after dose<\/p>\n\n\n\n

                              Cyclophosphamide (Cytoxan)
                              Alkylating agent
                              IV, PO<\/p>\n","protected":false},"excerpt":{"rendered":"

                              1. Elimination of the Hazard: -highest level of protection from a hazardous exposure -substitute a less toxic substance for the hazardous material -not feasible with drug therapy 1. Phagocytes2. Natural Killer Cells3. Granulocytes4. Macrophages 1.Cells that engulf and destroy invader 2. Cells that sense receptors on self and non-self to determine if they should kill […]<\/p>\n","protected":false},"author":1,"featured_media":0,"comment_status":"open","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"site-sidebar-layout":"default","site-content-layout":"","ast-site-content-layout":"default","site-content-style":"default","site-sidebar-style":"default","ast-global-header-display":"","ast-banner-title-visibility":"","ast-main-header-display":"","ast-hfb-above-header-display":"","ast-hfb-below-header-display":"","ast-hfb-mobile-header-display":"","site-post-title":"","ast-breadcrumbs-content":"","ast-featured-img":"","footer-sml-layout":"","ast-disable-related-posts":"","theme-transparent-header-meta":"","adv-header-id-meta":"","stick-header-meta":"","header-above-stick-meta":"","header-main-stick-meta":"","header-below-stick-meta":"","astra-migrate-meta-layouts":"default","ast-page-background-enabled":"default","ast-page-background-meta":{"desktop":{"background-color":"","background-image":"","background-repeat":"repeat","background-position":"center center","background-size":"auto","background-attachment":"scroll","background-type":"","background-media":"","overlay-type":"","overlay-color":"","overlay-opacity":"","overlay-gradient":""},"tablet":{"background-color":"","background-image":"","background-repeat":"repeat","background-position":"center center","background-size":"auto","background-attachment":"scroll","background-type":"","background-media":"","overlay-type":"","overlay-color":"","overlay-opacity":"","overlay-gradient":""},"mobile":{"background-color":"","background-image":"","background-repeat":"repeat","background-position":"center center","background-size":"auto","background-attachment":"scroll","background-type":"","background-media":"","overlay-type":"","overlay-color":"","overlay-opacity":"","overlay-gradient":""}},"ast-content-background-meta":{"desktop":{"background-color":"var(--ast-global-color-5)","background-image":"","background-repeat":"repeat","background-position":"center center","background-size":"auto","background-attachment":"scroll","background-type":"","background-media":"","overlay-type":"","overlay-color":"","overlay-opacity":"","overlay-gradient":""},"tablet":{"background-color":"var(--ast-global-color-5)","background-image":"","background-repeat":"repeat","background-position":"center center","background-size":"auto","background-attachment":"scroll","background-type":"","background-media":"","overlay-type":"","overlay-color":"","overlay-opacity":"","overlay-gradient":""},"mobile":{"background-color":"var(--ast-global-color-5)","background-image":"","background-repeat":"repeat","background-position":"center center","background-size":"auto","background-attachment":"scroll","background-type":"","background-media":"","overlay-type":"","overlay-color":"","overlay-opacity":"","overlay-gradient":""}},"footnotes":""},"categories":[],"tags":[],"class_list":["post-110667","post","type-post","status-publish","format-standard","hentry"],"_links":{"self":[{"href":"https:\/\/www.learnexams.com\/blog\/wp-json\/wp\/v2\/posts\/110667","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/www.learnexams.com\/blog\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/www.learnexams.com\/blog\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/www.learnexams.com\/blog\/wp-json\/wp\/v2\/users\/1"}],"replies":[{"embeddable":true,"href":"https:\/\/www.learnexams.com\/blog\/wp-json\/wp\/v2\/comments?post=110667"}],"version-history":[{"count":0,"href":"https:\/\/www.learnexams.com\/blog\/wp-json\/wp\/v2\/posts\/110667\/revisions"}],"wp:attachment":[{"href":"https:\/\/www.learnexams.com\/blog\/wp-json\/wp\/v2\/media?parent=110667"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/www.learnexams.com\/blog\/wp-json\/wp\/v2\/categories?post=110667"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/www.learnexams.com\/blog\/wp-json\/wp\/v2\/tags?post=110667"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}