Anti Cancer Drugs

Growth fraction of a tumour is constant, therefore, you cannot lower the dose and you can't get to zero cells because you're always killing a certain percentage.

Growth fraction of a tumour is not constant, therefore, dosing will be influenced by whether the tumour is in the early or late stage of growth.

The log-kill model is probably more accurate than the Gompertizian model because the log-kill model takes cell resistance into account.

The log-kill model only applies to terminal cancers.

Lung, liver, bone, and brain

Lung, liver, spleen, and bone

Liver, bone, lymph nodes, and spleen

Spleen, lymph nodes, brain, and colon

tumour size, nodal involvement, and metastases

tumour size, nuclear (cell division rate), and metastases

toxicity, nodal involvement, and metastases

tumour size, nuclear differentiation, and metasteses

How differentiated the cancer cells are (well differentiated = low grade) and how quickly cells are dividing (slower = low grade)

The size of the tumour and the nodal involvement (regional spread)

How quickly the cells are dividing and the nodal involvement

The degree of aggressiveness of the tumour and how rapidly the cells are dividing

Tamoxifen

Aromatase inhibitors

Corticosteroids

Vinca alkaloids

A cell-cycle specific drug, meaning it does not affect cells in G0 (resting stage).

A cell-cycle non-specific drug, meaning it affects cells at all stages of cell growth cycle.

A drug that is only effective for slow growing tumours.

A drug that works by targeting specific antigens on the cell surface, thereby blocking cell signaling and making cells more visible to the immune system.

It is a cell cycle non-specific drug that binds with DNA and interferes with the action of topoisomerase II.

It is a cell cycle specific drug that binds with DNA and interferes with the action of topoisomerase II.

It is a cell cycle non-specific drug that interferes with DNA replication through binding and cross-linking.

It is a highly toxic biologic response modifier that is only approved for experimental use.

It is a biologic response modifier (immunostimulant) that is given as an in situ instillation.

It is an antitumor antibiotic that binds with DNA and interferes with the action of topoisomerase II.

It is an antimetabolite that is effective for high growth fraction tumours.

It is a targeted therapy that has a controversial risk-benefit profile.

A type of targeted therapy that interacts with specific antigens on the cell surface to block cell signalling and make cells more visible to the immune system.

A type of targeted therapy that crosses the cell membrane and interferes with enzymatic activity of target proteins.

A type of cell cycle non-specific drug that interferes with DNA replication via binding and cross-linking.

A type of cell cycle non-specific drug that binds with DNA and interferes with the action of topoisomerase II.

It works against HER2 to inhibit cell proliferation and stimulate apoptosis. The main side effect is cardiotoxicity.

It works against HER2 to inhibit cell proliferation and stimulate apoptosis. The main side effect is increased risk of thrombosis.

It binds to VEGF (vascular endothelial growth factor) receptors to inhibit tumour growth. The main side effect is risk of hemorrhage.

It binds to VEGF (vascular endothelial growth factor) receptors to inhibit tumour growth. The main side effect is cardiotoxicity.

These drugs can only be administered via the parenteral route.

These drugs have a controversial risk/benefit profile and are highly toxic.

These drugs all decrease neutrophils and platelets.

These drugs all come with the risk of cardiotoxicity.

Imatinib

Trastuzumab

Bevacizumab

Cetuximib

Neutropenia and thrombocytopenia

Cardiotoxicity

Increased risk of thrombosis

Interstitial lung disease

Gravol

Lorazepam

Prochlorperazine

Pharmacologic treatment will be ineffective for this patient because this is a case of delayed nausea, which is very difficult to treat

Dexamethasone

Lorazepam

Gravol

Ginger chews

Febrile neutropenia

Anemia

Thrombocytopenia

Hyper-sensitivity reaction

"This is a normal part of the treatment process. The neutropenia will resolve on it's own before your next round of chemotherapy."

"Your oncologist will discuss the next steps with you. She may recommend that we decrease the dose of your next round of chemotherapy. Or, if she decides that the dose will stay the same, she may suggest that you be given a drug called Filgrastim prior to your next round of chemotherapy to prevent you from developing FNE again."

"It is very important that you increase the amount of iron-rich foods you are eating so that your body can heal before the next round of chemotherapy."

"Unfortunately, febrile neutropenia is a common side effect of some drugs. Your physician will likely prescribe an antibiotic for you to prevent infection before your next round of chemotherapy."

"Filgrastim is a drug used to prevent patients from developing febrile neutropenia, which is a condition that increases your risk of infection. It stimulates the production and release of certain cells (neutrophils) from your bone marrow. Therefore, a side effect of this drug is that you may experience some bone pain."

"Filgrastim is a drug that is given as an injection. It stimulates your bone marrow to produce red blood cells."

"You will have to phone your physician and ask him or her to explain to you again why you were prescribed that drug."

"Filgrastim will alter the way that the chemotherapy is metabolized in your body. It will prevent you from developing side effects, such as febrile neutropenia."

rest

oxygen therapy

RBC transfusion

epoetin alpha

filgrastim

Stop the infusion, leave needle in place, and aspirate

Stop the infusion, remove the needle, and monitor the patient closely

Immediately refer to the extravasation kit available in the clinic

Continue the infusion. This is a typical reaction to certain chemotherapies.