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Flashcards in Module 17 Deck (47)
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1
Q

Uncontrolled proliferation of cells.

Cells of this type are often referred to as _________.

A

cancer

neoplastic

2
Q

What are the 5 characteristics of cancer cells?

A
Persistent, uncontrollable cell proliferation
Invasive
Metastatic
Immortal
Angiogenesis
3
Q

The ability of cancer cells to travel to different sites in the body and invade to form new tumours.

A

Metastatic

4
Q

Cancer cells develop their own blood vessels to supply nutrients.

A

Angiogenesis

5
Q

What are the three main treatment modalities for cancer?

A

Surgery
Radiation
Chemotherapy

6
Q

Describe chemotherapy.

A

Drugs target rapidly dividing cells.

7
Q

Describe radiation.

A

High energy radiation causes DNA damage to both cancerous, and non-cancerous cells.

8
Q

Describe the stages of the cell cycle.

A
G1 - the cell prepares to duplicate its DNA
S - synthesis of DNA
G2 - the cell prepares for mitosis
M - mitosis
G0 - resting, cells do not replicate
9
Q

Describe how toxicity to normal cells is an obstacle in chemotherapy.

A

Neoplastic cells are very similar to normal cells.

Cells with very high growth fractions are often affected by the toxic compounds.

10
Q

What are some examples of cells with high growth fractions?

A

Bone marrow, GI epithelium, hair follicles, germinal epithelium of the testes (giving rise to sperm

11
Q

Cure of cancer requires ____% cell kill.

A

100

12
Q

Describe the kinetics of cell death with chemotherapy.

A

1st order

A constant percentage of cancerous cells are killed at a given dose

13
Q

What are the three most prevalent cancers in Men in Ontario?

Women?

A

Men
- prostate, lung, colon and rectum
Women
- breast, lung, colon and rectum

14
Q

Describe the screening protocols (Canadian) for breast cancer.

A

Clinical breast examination every 2 years starting at age 40, for women.
High risk patients are screened more often and screening may begin before age 40.

15
Q

Describe the screening protocols (Canadian) for cervical cancer.

A

Sexually active women should have a Pap smear every 1-3 years.

16
Q

Describe a Pap smear.

A

A speculum is insertred into the vagina, exposing the cervix.
A curette is then inserted into the endocervix.
Cells are scraped from the cervix and examined under a microscope to check for disease.

17
Q

Describe the screening protocols (Canadian) for colorectal cancer/

A

Men and women (not high risk) should have a fecal occult blood test every two years.
Colonoscopy may also be eperformed evert 5 years in high risk patients

18
Q

Describe the screening protocols (Canadian) for prostate cancer/

A

Men over 50 should have the Digital Rectal Exam and/or PSA blood test.

19
Q

Describe the screening protocols (Canadian) for skin cancer.
(What do we look for?)

A

Self-checks should be performed regularly.

in particular, look for changes to birthmarks and/or moles, any new skin growths, and sores that don’t heal properly/

20
Q

Describe the screening protocols (Canadian) for testicular cancer.

A

Males over the age of 15 should regularly perform the testicular self-examination

21
Q

Why do ______ tumours respond poorly to chemotherapy?

A

Solid tumours
Respond poorly to chemotherapy as they have a large fraction of cells in the G0, resting, state. Thus, since chemotherapeutic agents target actively replicating cells, these are largely ineffective.

22
Q

What are some ways in which cancer cells develop resistance to drugs?

A
Decreased drug uptake
increased drug efflux
Decreased drug acgivatoin
Reduced target sensibitiy/increased cellular repair (mostly DNA)
Decreased apoptosis
23
Q

This pump can cause MDR.

A

P-gp

24
Q

Describe intermittent chemotherapy.

A

The intent is to administer chemotherapeutic drugs intermittently, allowing normal cells to recover.
This only works if normal cells grow faster than cancerous cells

25
Q

What are the reasons (3) that combination chemotherapy is more effective than administration of a single drug?

A

Decreased resistance
Increased cancer cell kill
Decreased injury to normal cells

26
Q

Describe how using multiple drugs decreases drug resistance in cancer cells.

A

Resistance may be acquired from random mutations. These mutations are rare and the ability to develop resistance to many drugs simultaneously is very unlikely.

27
Q

How can using more drugs cause decreased injury to normal cells?

A

Using drugs that do not have overlapping toxicities allows us to achieve greater anti-cancer effects more safely than we could with one drug alone.

28
Q

The ____ ______ has a very high growth fraction and therefore is very susceptible to chemotherapy-associated toxicity.

A

Bone marrow

29
Q

Bone marrow suppression may result in these.

A

Neutrophenia
Thrombocytopenia
Anemia

30
Q

Describe digestive tract injury as a result of chemotherapy.

A

Stomatitis (inflammation of the oral mucosa) may develop. If severe enough, this may progress to ulceration.
Diarrhea may also occur secondary to damage to the intestinal epithelium.

31
Q

Serious and common adverse effect associated with chemotherapy. Sometimes these effects are treatment limiting and patients will reufse further treatment because of the frequency.

A

Nausea and vomiting

32
Q

What are some important adjuncts to therapy when nausea and vomiting are prevalent?

A

Anti-emetics, prevention of dehydration, prevention of malnutrtion

33
Q

Anti-cancer drugs can be broken down into two major classes. What are they?

A

Cytotoxic agents

Hormonal and other agents

34
Q

Only effective if the cancer cell is in a specific phase of the cell cycle.
What are they ineffective against?

A

Cell cycle phase specific drugs

Ineffective in cells that are in G0.

35
Q

Can act during any stage of the cell cycle, including G0.

A

Cell cycle phase non-specific drugs

36
Q

Describe the mechanism of action of Alkylating agents.

A

Highly reactive chemicals that act by transferring an alkyl group to cell components (mostly DNA).
They act by forming cross-bridges between nitrogen atoms on guanine nucleotides that make up our DNA.

37
Q

Alkylating agents:

  • effective in which phase?
  • Most widely used drug in this class?
A

cell cycle phase non-specific - effective during any phase of the cell cycle
Cyclophosphamide - most widely used drug in the alkylating agents class

38
Q

Describe cyclophosphamide (i.e. onset of action, activation).

A

Prodrug - converted to active from by the liver

Onset of action is thus delayed.

39
Q

Describe the mechanism of action of platinum compounds.

A

Drugs with platinum in their chemical structure which act by cross-linking DNA. They bind to guanine molecules (similar to alkylating agents) and inhibit DNA replication.

40
Q

Platinum compounds:

  • Cell cycle phase specific/non-specific?
  • Most widely used platinum compound?
A

Cell cycle phase non-specific

Cisplatin is the most widely used platinum compound

41
Q

Cisplatin:

- Side effects?

A

Nephrotoxicity, ototoxicity, emetogenic (nausea and vomiting)

42
Q

Describe the mechanism of action of antimetabolites.

A

Are structurally similar to natural compounds used by the body.
They act by inhibiting particular enzymes or preventing DNA replication.

43
Q

Antimetabolites:

  • Cell cycle phase ___________ ________
  • What are the three subclasses?
A

Cell cycle phase specific –> mostly S phase

i) Folic Acid Analogs
ii) Purine Analogs
iii) Pyrimidine analogs

44
Q

Describe the three classes of antimetabolites and their mechanisms of action.

A

Folic acid Analogs: Block the conversion of Folate to its active form.
Purine/Pyrimidine analogs: Inhibit the synthesis of DNA and RNA

45
Q

Mechanism of action of anti-tumour antibiotics.

A

Kill cancer cells by intercalating DNA –> move between the bases of DNA and bind to DNA, causing a change in DNA structure, which makes the structure not able to be used as a template for DNA replication

46
Q

Describe the administration of Anti-tumour antibiotics.

A

Poorly absorbed and thus given intravenously

47
Q

Describe anthracyclines and their side effects.

A

Antitumour antibiotic, vert effective

Sides: bone marrow suppression, cardiotoxicity