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Pathophysiology > Cancer > Flashcards

Cancer Flashcards

1
Q

What are the 4 cancers of highest incidence for men?

for women?

A
  • Men: Prostate > lung and bronchus > colon and rectum > urinary/bladder
  • Women: Breast > lung and bronchus > colon and rectum > uterine
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2
Q

What are the 4 cancers of highest deaths for men?

Women?

A
  • Men: lung/bronchus > prostate > colon and rectum > pancreas
  • Women: Lung/bronchus > breast > colon and rectum > pancrease
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3
Q

Why is cancer increase markedly with age?

A
  • takes years from the time you are exposed to a carcinogen to the time when you present with the disease
  • you get exposed to more carcinogens throughout life
  • as you get older, immune system gets weaker
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4
Q

What are stroma/stromal cells?

A
  • support cells in the tissue
    • connective tissue
    • blood vessels
    • etc
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5
Q

What are parenchyma/parenchymal cells?

A
  • Special cells, uniquely adapted to perform function of organ
    • cardiomyocytes
    • hepatocytes
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6
Q

What are mesenchyme/mesenchymel cells?

A
  • Cells of mesodermal or neural crest origin that give rise to connective tissue, blood, muscle
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7
Q

-oma

A

benign tumor

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8
Q

-carcinoma

A

malignant tumor of epithelial origin

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9
Q

-adenocarcinoma

A

malignant tumor of glandular tissue

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10
Q

-sarcoma

A

malignant tumor of mesenchymal origin

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11
Q

-blastoma

A

malignant tumor of precursor cells

(more common in children)

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12
Q

Invasive neoplasia

A

enlarged growth that has acquired the ability to get through the basement membrane

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13
Q

What does grading measure?

A
  • I: the cell still looks like the cell it is supposed to
  • IV: the cell looks nothing like the cell it is supposed to be
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14
Q

How are tumors staged?

A
  • Tumor: T0-T4
    • T0- no penetration of basement membrane
    • T1- penetrated through basement membrane but still local
    • T4- Invasion into other organs/neighboring tissue
  • Lymph: N0-N4
    • N0- no lymph node involvement
    • N1- local lymph node involvement
    • N4- existensive lymph no
  • Metastasis (M0-M1)
    • M0- no metastasis
    • M1- metastasis
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15
Q

What are the ways cancer can spread?

A
  • Direct contact- grows right on through to the neighbor
  • lymph nodes- drain cancer cells through lymph nodes
  • directly by blood- cancer cell in vein, whole body is accessible
  • biopsy- as needle goes in and comes out cancer cells can be deposited all along needle pathway
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16
Q

Benign Vs Malignant

A
  • Benign (Leiomyoma)
    • small, slow growing and well demarcated (can see where good cells end and bad cells begin
    • noninvasive
    • nonmetastic
    • well differentiated (still looks like the cell type it should be)
  • Malignant (Leiomyosarcoma)
    • Large
    • poorly demarcated
    • rapidly growing with hemorrhage and necrosis
    • locally invasive
    • metastatic
    • poorly differentiated
17
Q

What are the stages of cancer progression?

A
  • Transformation- some kind of carcinogenic induced mutation that gets everything started
  • Progression- the mutated cell had more daugther cells.
  • Proliferation- over time the mutated cells mutate again and again as they continue to grow
    • with all the mutations the tumor has all the special skills required for a cancer to thrive
18
Q

What are the 6 hallmarks of cancer?

A
  1. Self sufficiency in growth signals
  2. insensitivity to antigrowth signals
  3. evading apoptosis
  4. limitless replicative potential
    1. must be able to turn on telomerase
    2. can now double infinite number of times
  5. sustained angiogenesis
    1. as it gets bigger, it will need its own blood supply
  6. tissue invation and metastasis
19
Q

What is a proto-oncogene?

A
  • It is a pre-tumor gene
    • with two copies of everything
  • a normal cell that once it gets one mutation, it can start to proliferate into cancer
20
Q

What is a tumor supressor gene?

How can it change?

A
  • Suppress tumors by negatively regulating the cell
  • If one of the copies of the TSG is mutated, we tend to be ok, it will still function
  • Two inactivating mutations are required for it to no longer function
  • a person born with one TSG already mutated will have a very high rate of cancer
21
Q

What are the proto-oncogenes listed?

(5)

A
  1. bcl-2
  2. HER2/neu
  3. N-myc
  4. C-myc
  5. Ras
22
Q

What happens if a person is born with an active abnormal proto-oncogene?

A

A person would not be born with this mutation because they would not develop properly

23
Q

What is the significance of chromosome translocation?

How are they oncogenic?

A
  • the transcriptional change affects how the genes are controlled
    • the control regulations for one gene are now controlling a different gene
  • Combine to make a new protein. A new protein is never good
24
Q

What are the listed tumor supressor genes?

A
  • p53- most commonly mutated
  • BRCA1, BRCA2
  • APC
  • RBI
  • MSH2
  • NFI, NF2
25
Q

What is Li Fraumeni?

A
  • Mutated p53 at birth
  • only need one other mutation for the tumor supressor gene to no longer function properly
  • Very high cancer rates
26
Q

How does the G-protein coupled receptor (RAS) become cancerous?

A
  • Normally, the RAS is activated when growth hormone hits the receptor
    • after the second signal is completed, normally RAS can convert GTP into GDP, inactivating the pathway until another growth hormone hits the receptor
  • If the RAS cannot convert GTP to GDP, it will remain active and continue to grow
  • RAS is a proto-oncogene, so it only needs one mutation
27
Q

What is an example of insensitivity to anti-growth signals that could cause a tumor to grow?

A
  • RB is a tumor suppression gene
  • If it gets TWO mutations, it could grow uncontrollably into a tumor, causing retinablastoma
    • wont happen until later in life
  • If pt is born with one mutation, they will likely get retinablastoma within 1st year of life because it is relatively easy to get one mutation
28
Q

What is an example of how a cancer can evade apoptosis?

A
  • p53 protects DNA and kills any cell with bad DNA
  • if there are two mutations to the p53 gene, it will no longer work and there will be nothing to kill the cells with bad DNA
  • this is great for a cancer that is trying to acquire mutations.
29
Q

What is an example of how a cancer can have limitless replicative potential?

A
  • if the cancer can “turn on” telomerase, it can replicate infinitely
  • telomerase lengthens DNA telomere caps every time it replicates
30
Q

How does the tumor get sustained angiogenesis?

A
  • Once the tumor becomes too big, it needs its own blood supply
  • The tumor needs VEGF (vascular endothelial growth factor), which determines where blood vessels will grow
31
Q

How is a tumor able to invade tissue and metastasize?

A
  • Normal epithelial cells are tightly bound together but have contact inhibition (down outgrow their position)
  • a tumor cell first has to detatch itself from neighbors
  • then it has to get through the basement membrane
    • has to dissolve the collagen
  • has to grab something and pull itself through
  • this is not normal, must have a superpower
32
Q

What are the ways cancer can spread?

what happens once it escapes its original home?

A
  • direct contact
  • lymph nodes
  • blood
    • extravates (leaves vessel to go into tissue) and will grow in the new environment
    • different cancers will tend to land in different spots, usually somewhere with a similar climate to where they started
33
Q

What are the two main sites of blood borne metastasis?

What are the specific examples he gave?

A
  • Lung- all blood goes through the lungs and there are lots of capillaries–> greater chance of landing there
  • liver- Especially from abdominal cancers because the blood from the abdominal organs all drains through the liver
  • Colon –> liver
  • breast & prostate–> bone
34
Q

What is the difference between primary and secondary metastatic cancer?

A
  • Primary: starts in one place and just becomes one continuous growth
  • Secondary: like sprinkling seeds in a garden
    • each spot starts a new colony, this is why metastatic cancer is so hard to treat
35
Q

How does HPV work?

How does the vaccine work?

A
  • cancer causing HPV has E6 and E7 proteins which attach to p53 and RB, inhibiting their function
    • these are two of the most powerful tumor supressor genes
  • Now there is nothing to kill messed up cells, so mutations occur and those cells survive
    • rate of mutations increases dramatically
  • HPV is responsible for 100% of cervical cancer
  • Vaccine is agains the virus, not cancer
    • causes the body to produce memory cells against the virus, so the body can clear it faster if exposed
36
Q

What HPV types does the HPV vaccine protect against?

A
  • HPV 16 & 18
    • cause about 70% of cervical cancer
  • HPV 6 & 11
    • genital worts
37
Q

Describe the relationship between the tumor cell burden and the phases of cancer treatment. (graph)

A
  • In order for the tumor to get as big as 1mm, the telomerase will have been “turned on” and the cancerous cells will have slipped through the immune system
  • It will be big enough for diagnosis at 1 cm
  • Surgical removal will significantly decreas the tumor cell burden, but might not remove all
  • the cells that remain could be killed with chemo therapy, or if left without treatment, will continue to proliferate
38
Q

What are the adverse effects of cancer chemotherapies?

A
  • Target any kind of rapidly dividing cells, so they will damage other tissues as well
  • GI: esp mucosa of small intesting–N/V
  • Bone marrow: all hematopoetic cells affected
    • anemia (expected); neutropenia is the biggest problem
    • anemia means that the chemo is working (good thing)
    • neurtopenia is dangerous bc you’ll prob get an infection
  • Hair: follicles on head are rapidly replicating, but arent on eyebrows
  • Skin: decreased epidermal renewal rate–will see skin leasions
  • Fetus: chemo is strictly contraindicated in pregnancy

Pathophysiology (26 decks)

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