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Onco/Neuro > Oncology > Flashcards

Oncology Flashcards

1
Q

What are some causes of cancer? (4)

A
  1. Viruses- HIV, Hep C,
  2. Chemical factors
  3. Physical factors
  4. Genetics
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2
Q

How do chemical factors cause cancer?

A

Carcinogens causes genetic damage- DNA damage
Tumour suppressor genes are inactivated
DNA repair defects

eg: tobacco smoke

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3
Q

What are 3 physical factors that can cause cancer?

A
  1. Radiation
  2. UV
  3. Asbestos
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4
Q

What are the most common cancers in Australia?

A

Prostate
Lung
Melanoma
Colorectal

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5
Q

What does TMN refer to?

A

T- Primary tumour size
N- Lymph nodes involved?
M- Metastasis frequency

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6
Q

Describe the four stages of cancer?

A

Stage 1: Local disease (local treatment)
Stage 2. Local disease but larger tumour (local treatment but risk of recurring)
Stage 3: Local spread of tumour (removal +systemic therapy)
Stage 4: Metastatic disease (systemic therapy)

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7
Q

What is adjuvant therapy?

A

After definitive local treatment has occur and no evidence of cancer is remaining.
Treatment is given to mop up ‘micro-mets’ to reduce risk of a later relapse

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8
Q

What are 5 treatment options for cancer?

A
  1. Surgery
  2. Radiation
  3. Chemotherapy
  4. Biological therapy
  5. Gene therapy
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9
Q

What is the difference between acute and long tissue effects of radiation?

A

Acute normal tissue effects is crucially affected by the time allowed for repopulation and hence dependent on protraction. It also depends on the cell kill per fraction.
Occurs in renewing tissues (skin, rectum)

Long normal tissue effects appear to depend more on the total dose and size of the radiation fraction than on the protraction

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10
Q

Why are combination chemotherapy preferred over single treatment?

A
  1. Provides maximal cell kill within range of toxicity tolerated by hose for each drug
  2. Provides a broader range of interaction between drugs and tumor cells with different genetic abnormalities
  3. May prevent or slow the subsequent development of drug resistance
  • Only use drugs known to be partially effective against same tumour when used alone
  • Toxicity should not overlap
  • Drugs should be used in their optimal dose and schedule
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11
Q

What is chemotherapy dose based upon?

A

BSA (cap at 2m2 or 2.2m2)

  • always take other parameters into consideration when calculating dose
  • adjust based on drug elimination, other medications etc
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12
Q

Which medications are used for acute N+V in chemotherapy?

A

Metoclopramide or Ondansteron

+/- dexamethasone

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13
Q

Which medications are used to prevent N+V in chemotherapy?

A

5-HT3 antagonist, dexamethasone and aprepitant

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14
Q

What is a common side effect with EGFR inhibition?

A

Rash

Start in first 1-2 weeks, worst at 2-3 weeks and usually resolves 2-3 after ceasing therapy.
Can also improve spontaneously

Therapy should continue if possible
Mx include antibiotics, antifungals, steriods, prevent dry skin

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15
Q

When do hand foot skin reactions occur with sorafenib and sunitnib?

A

Usually 2-3 after starting therapy, with most before the 5th week

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16
Q

Difference between malignant and benign tumour?

A

Malignant tumours have poor differentiation, invasive growth and matastasise frequently

Benign tumours have cells that are differentiated like normal cells, they grow but are encapsulated in the basement membrane

17
Q

What is the difference between stage and grading of cancers?

A

Stage refers to the extent of disease

Grade refers to the extent of tumour cell abnormality

18
Q

Tumourigenesis requires which 7 mechanisms?

A
  1. Self sufficiency in growth signals
  2. Insensivity to anti-growth signals
  3. inflammatory microenviornment
  4. Tissue invasion and metastasis
  5. Limitless replicative potential
  6. Sustained angiogensis
  7. Evading apoptosis
19
Q

What are oncogenes?

A

Genes with the potential to cause cancer

Proto-oncogenes are activated into oncogenes

20
Q

How do oncogenes cause cancer?

A

Cell proliferation is constantly switched on = over proliferation

eg: RAS protein is mutated, emits signal without growth factor binding.

21
Q

What are tumour suppressor genes?

A

Anti growth signals in cells to constrain proliferation

eg: Rb / p53

22
Q

How does a mutation in p53 cause cancers?

A

Mutations in p53 usually occur in the DNA binding domain, hence preventing p53 binding to DNA and regulate cell cycle.

23
Q

Difference between apoptosis and necrosis?

A

Apoptosis is natural cell death occurring in tissue remodelling or genomic damage, cell volume decreases and dead cells are phagocytosed. DNA are evenly fragmented, chromatin condensed

Necrosis occurs without gene activation, is caused by metabolic stresses, absence of nutrients or change in ph or temperature. Cell volume increases causing an inflammatory response and dead cells lysed. DNA randomly degraded, chromatin fragmented

24
Q

What are the 4 apoptosis molecular pathways?

A
  1. Death receptor that can be activated by NK cells, death ligands
  2. Cytotoxic cells creating a pore and inserting granzmes
  3. Caspase cascade
  4. Release of cytochrome c
25
Q

How do tumour cells overcome apoptosis?

A
  1. Down regulate death receptor
  2. Turn off tumour suppressor genes
  3. Oncogenes (RAS turned on constantly)
  4. Mutate caspase
26
Q

What is senescene?

A

Long term residence of cells in a non-growing but viable state

Provoked by physiological stressors

27
Q

How do telomeres affect cancer?

A

Tumour cells escape senescene and crisis by activating telomerase. This continues to elongates telomeric DNA by extending it in hexanucleotide increments causing the cell to be immortal!
They proliferate indefinitely as the signal to die lost.

28
Q

What is angiogensis?

A

Promotion of new blood vessel from factors released by tumours.
Blood supply brings in oxygen, nutrients, growth factors and take out cancer metasasis

29
Q

Tumour microenvironment can re-educate macrophages, how does this affect cancer progression?

A

Tumour associated macrophages promote metastic processes.

  • They promote angiogensis by bringing more growth factors into tumour.
  • Create a pro inflammatory environment
  • Blocks immune response (increase T reg and decrease CD8 cells)
  • Promotes production of proteases that break up surrounding matrix and help tumour escape

Stress triggers more macrophages!

30
Q

4 mechanisms of immune evasion by tumour cells?

A
  1. Repress stress ligands to avoid NK cells
  2. Tumour cells down regulate Fas death receptors to avoid apoptotic killing by NK and CTLs
  3. Cancer cells attract Treg cells. These inhibit and kill CTL and Th cells (good cells)
  4. Re-educate macrophages to promote metastatic conditions

Onco/Neuro (7 decks)

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