Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Patho/Pharm NP > Cancer > Flashcards

Cancer Flashcards

1
Q

What are the most common adult cancers?

A

Breast, lung, colorectal, prostate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the most common peds cancers?

A

Leukemia, CNS, lymphoma, neuroblastoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the difference between a benign and malignant growth?

A

Benign: slow growth, well-defined, not invasive, well differentiated (resemble cells that they come from), low mitotic index (don’t divide quickly), does not metastasize.
Malignant: rapid growth, not encapsulated, invasive, poorly differentiated: anaplasia, high mitotic index, can spread distantly (metastasis)- usually via bloodstream

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Tell me about the biology of cancer cells.

A
  • predominantly disease of aging
  • clonal proliferation or expansion occurs
  • mutations
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Tell me about mutations in oncology cells?

A
  • alteration in DNA sequence affecting expression or function of a gene
  • a cell that acquires characteristics that allow it to have selective advantage vs. other cells (ex. increased growth rate, decreased apoptosis)
  • multiple mutations are required before cancer develops (due to a good fight from the immune system)
  • immunosuppressed patients may be more at risk of Ca
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the different types of mutations amongst oncology cells?

A

Point mutations: small-scale changes
Driver mutations: “drive” progression of cancer
Passenger mutations: random events “along for the ride”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is gene amplification in oncology cells?

A
  • repeated duplication of chromosome - proliferation
  • 10s or 100s of gene copies made
  • proliferation of cell development
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is chromosome translocation?

A
  • large changes in chromosome structure

- piece of 1 chromosome is translocated to another chromosome (ex. CML)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is clonal proliferation or clonal expansion?

A
  • cancer cell progeny can accumulate faster than non-mutant neighbouring cells
  • identical copy of cell before it
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the stages of human carcinogenesis?

A
  1. Activation of proto-oncogenes: results in hyperactivity of growth-related gene products (called oncogenes)
  2. Mutation of genes: results in the loss or inactivity of gene products that would normally inhibit growth (tumour-suppression genes)
  3. Further mutation of genes- proliferation: results in over-expression of products that prevent normal cell death or apoptosis, thus allowing continued growth of tumours.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Explain the evasion of growth suppressors in cancer development.

A
  • secretion of growth factors (via autocrine stimulation)
  • increase in growth factor receptors
  • mutation of the signal from cell surface receptor in the “on” position
  • mutation in the Ras intracellular signalling protein
  • inactivation of rentinoblastoma protein (Rb) tumour suppressor
  • activation of protein kinases that drive the cell cycle
  • mutation in the TP53 gene (tumour-suppressor gene)- suppression of normal apoptosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Explain the immortality of cancer cells.

A
  • usually normal body cells are not immortal and can divide only a limited number of times (Hayflick limit)
  • telomeres: protective caps on each chromosome that are held in place by a telomerase, become smaller and smaller with each division
  • telomerase: an enzyme that protects the telomeres at the end of the chromosomes, inhibits apoptosis – immortal cell
  • cancer cells can activate telomeres, leading to continued division- increasing production of telomerase
  • cancer cells fail to inhibit telomere growth
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Tell me about angiogenesis in cancer.

A
  • growth of new vessels = neovascularization
  • advanced cancers can secrete angiogenic factors to facilitate feeding of tumour
  • this is done by vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF)
  • some forms of anti-VEGF therapy- which cuts off blood supply to tumour
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Tell me about cancer metabolism.

A
  • cancer performs glycogenesis
  • allows lactate and its metabolites to be used for the more efficient production of lipids and other molecular building blocks needed for rapid cell growth
  • reverse Warburg effect: cancer cells generate large amount of ATP required for cell growth
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Tell me about inflammation in cancer.

A
  • cause of cancer
  • active inflammation predisposes a person to cancer by stimulating a wound-healing response that includes proliferation and new blood vessel growth
  • susceptible organs: GI tract, pancreas, thyroid gland, prostate, urinary bladder, pleura, skin
  • Example: ulcerative colitis for more than 10 years- 30-fold increase in developing colon cancer, Hep B/C- liver cancer risk, H.pylori- stomach cancer risk
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is a tumour-associated macrophage (TAM)?

A
  • key cell that promotes tumour survival
  • develops capacity to block cytotoxic T cell and NK cell functions
  • produces cytokines that are advantageous for tumour growth and spread
  • secretes angiogenesis factors
17
Q

Tell me about immunotherapy (active & passive).

A

Active: immunization with tumour antigens to elicit or enhance the immune response against a particular cancer
Passive: injecting the patient diagnosed with cancer, antibodies or lymphocytes directed against the tumour-associated antigens

  • less toxic than chemo
  • does not effect rapidly growing cells
  • adverse events associated
18
Q

What is metastasis?

A
  • the spread of cancer cells from the site of original tumour to distant tissues and organs throughout the body
    1. Spread (via lymph – circulation – organs)
    2. Survive (attach to specific receptors)
    3. Proliferate in distant locations, destination must be receptive to growth of cancer
19
Q

Tell me about the TNM system.

A

T- tumour (primary tumour size & extent)
N- nodes
M- metastases

20
Q

What are tumour markers?

A
  • substances produced by benign or malignant cells
  • found on or in a tumour cell, in the blood, spinal fluid, urine
  • could be hormones, enzymes, genes, antigens, antibodies
  • ex. PSA (prostate specific antigen)- marker to demonstrate whether tx was successful
  • ex. CEA (carcinoembryonic antigen)- marker that may detect tumour of the bowel
21
Q

Explain the role of surgery in cancer.

A
  • definitive tx for cancers that do not spread beyond the limits of surgical excision (ex.solid tumours)
  • prevention of cancer (if you have at risk genes- BRCA 1/2)
  • biopsy
  • palliative: relief of symptoms (ex. urostomy tubes)
22
Q

Explain the role of radiation in cancer.

A
  • used to kill cancer cells while minimizing damage to normal structures
  • ionizing radiation – damages cells by importing enough ionizing radiation to cause molecular damage to the DNA, causes irreversible damage to normal cells, lifetime radiation dose, problem if relapse occurs

Bradytherapy:

  • seeds are implanted
  • internal radiation
  • ex. prostate cancer tx
23
Q

Explain the role of chemotherapy in cancer.

A
  • most common tx in disseminated cancers such as leukemia and lymphoma
  • eradicates enough tumour cells to enable the body’s natural defences to eradicate the remaining cells
  • single agent or combo chemo
  • curative or palliative intent
  • decreased therapeutic indices (less of the toxic drug needed with combo therapy)

Induction chemo: causes shrinkage or disappearance of tumours

Adjuvant chemo: administered after surgical excision with a goal of eliminating micrometases

Neoadjuvant chemo: administered before localized (surgery or radiation) treatment to “shrink” mass

8 major groups:

  1. Alkylating agents
  2. Platinum compounds
  3. Antimetabolites
  4. Hypomethylating agents
  5. Anti-tumour antibodies
  6. Mitotic inhibitors
  7. Topoisomerase inhibitors
  8. Miscellaneous
24
Q

What are the adverse effects of chemo?

A

common AE: N&V, hair loss, fatigue, diarrhea +/- constipation, neutropenia, bleeding (decreased plts)

  • pneumonitis, colitis, hepatitis, nephritis = refer to oncologist, likely will treat with steroids
  • T1DM, hypo/hyperthyroidism (monitor throughout tx, treat disorder), hypophysitis (inflam. of pituitary gland)- tx steroids
  • febrile neutropenia
  • may induce cancer (ex. leukemia after breast Ca tx)
25
Q

What is febrile neutropenia?

A
  • Decreased WBC and fever = sepsis
  • oncologic emergency- timely tx <1 hr abx- call ER ahead of time
  • Febrile neutropenia in those with solid tumours can often be treated with an outpatient regimen while those with hematological malignancy are often required to stay in hospital.
26
Q

Tell me about anticancer drugs.

A
  • work by targeting unique abilities of cancer cells (grow faster, metastasize)
  • designed to “hit” cell replication through disruption of DNA synthesis at some point in the cell cycle- when a cell is replicating
  • non-specific “buck shot” approach, kill cancer cells only slightly faster than normal cells, toxicities
  • some drugs kill cancer cells only at certain phases of the cell cycle (phase specific)
  • ex. works only when a high proportion of cells are dividing and only on cells that are in the right phase
  • some drugs work throughout the cell cycle (phase non-specific)
  • increase the immune system, hence AE: rash, diarrhea, hypothyroidism, hypophisitis (inflam. of pituitary gland)
  • tx of AE: steroids, treat disorder, stop therapy
27
Q

What is growth fraction?

A
  • some cells are actively dividing and some are in the resting phase
  • the ratio of proliferating cells to resting cells is called the growth factor
  • most chemo drugs are more effective in conditions of high growth fraction
  • the most common cancers (breast, lung, colon, prostate) have low growth fraction
28
Q

List cancers that usually do respond to treatment, may respond and usually do not respond.

A

Do respond: Hodgkin’s lymphoma, acute lymphoblastic (lymphocytic) leukemia, choriocarcinoma, wilm’s tumour, testicular, other germ line cancers
May respond: breast, ovarian, endometrial, myeloma, large intestine, esophageal
Do not respond: thyroid, brain, liver, malignant melanoma, pancreatic, cervical

29
Q

What are some modalities of supportive care with the treatment of cancer?

A
  • abx therapy- prophylactic or responsive (ex. febrile neutropenia)
  • antivirals/antifungals
  • neupogen: help increase WBC’s, to help prevent infection- AE: aches and pains of long bones (stimulation of bone marrow stem cell production) - may need pain management
30
Q

What are the two types of polyps that can develop in the colon/ rectum?

A
  • Adenomatous Polyps (adenoma): considered to be pre-cancerous. Cancer can form in a polyp, grow into the wall of the colon or rectum and then invade blood & lymph vessels; 95% of colorectal cancers are due to adenocarcinomas
  • Hyperplastic polyps: due to inflammation & are not pre-cancerous
31
Q

What is the relationship between DVT’s and cancer?

A
  • Patients with cancer are at four to sevenfold increased risk of venous thromboembolism (VTE) compared to those without cancer, making cancer associated thrombosis a major cause of mortality and morbidity
  • dx: doppler, high rate of false positive d-dimer values in oncology patients
  • tx: dalteparin, LMWH, rivaroxaban, apixaban (monitor for thrombocytopenia and active bleeding)
32
Q

Tell me about biologic response modifiers.

A

Vaccines: immunotherapies to stimulate the immune system
Interferon-α: recombinant cytokine affecting tumor growth (direct antiproliferative effect, immunomodulatory effect on natural killer cells, T & B cells, and macrophages, induction of tumor cell antigens, a differentiating effect on tumor cells). Like the targeted therapies, interferon-α also has anti-angiogenesis effects.
Interleukin 2: recombinantly produced lymphokine that stimulates T and B cell proliferation and differentiation. Lymphoid cells that have been incubated with interleukin 2 were noted to have the ability to lyse tumour cells. Significant dose-related side effects were noted due to diffuse capillary leak that develops with therapy.

33
Q

Tell me about the different screening associated with cervical, colorectal, breast, lung and prostate cancer.

A

See summary notes table
Colon- If average risk: FIT Q 2 years age 50-74. If FIT abnormal, colonoscopy should be done within 8 weeks.
If increased risk: first-degree fam member dx w/ colorectal cancer…
- If diagnosed @ < 60yr, colonoscopy Q 5 yr starting at 50 yrs or 10 yrs before age of dx
- If diagnosed @ > 60 yr, colonoscopy Q 10 yr starting at 50 yrs or 10 yrs before age of dx
Breast If no risk  50-74 years old, mammogram Q 2-3 years. Increased risk 30-60 years old, mammogram + breast MRI Q 1 year
- No clinical breast examinations or teaching about self-assessments
Lung Low-dose CT if age 55-74 with 20 cumulative years of daily smoking (new practice)
Cervical If sexually active or have been PAP Q 3 years age 21-70.
prostate NO screening

Patho/Pharm NP (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions