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Pathophysiology > module 3 cancer > Flashcards

module 3 cancer Flashcards

1
Q
  1. What are the 2 ways that cancer happens?
  2. What is the suffix for a benign growth?
  3. What is the suffix for malignancy in epithelial tissue?
  4. What is the suffix for malignancy in connective tissue?
  5. If there is cancer of the blood or lymphatic system, is it malignant regardless of the name?
  6. Name 3 special names of cancers that don’t adhere to the naming norms:
  7. If it’s a cancer of CNS, how is it named?
A
  1. genetic disorder (DNA mutation spontaneous), or Heritable (genetic disorder passed down)
  2. “oma”
  3. tissue name + carcinoma ex: adenocarcinoma
  4. tissue name + sarcoma
  5. Yes. ex lymphoma (“oma” sounds benign, but it is malignant)
  6. hodgkins, Wilms, and leukemia
  7. by type of cell affected ex: neuroblastoma
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2
Q
  1. Cells of benign tumors are …………………, whereas cells of malignant tumors are …………….. .
  2. What is anaplasia?
  3. What does anaplasia indicate?
  4. If a tumor is well differentiated (not anaplastic) is it still malignant?
  5. How is invasion different from metastasis?
A
  1. differentiated (adult cells), undifferentiated
  2. an irreversible regression of of differentiated cells back to undifferentiated cells.
  3. aggressiveness of tumor.
  4. Yes. Doesn’t need anaplasia to be malignant. Anaplasia simply demonstrates how aggressive tumor is.
  5. invasion is local into surrounding tissues. Metastasis spreads distantly.
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3
Q
  1. What are the main cancers that men get?
  2. What are the main cancers women get?
  3. What are the main cancers that kids get?
A
  1. Lung, prostate, and colorectal
  2. Lung, breast, and colorectal
  3. bone, lymphomas, leukemias
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4
Q
      1. Name the ten ways that cancer proliferates in the system, and makes a tumor (remember the slide with the multi color wheel)
A
  1. evading growth suppressors
  2. enabling replicative immortality (think telomerase)
  3. Tumor promoting inflammation (feeding the growth)
  4. Activating invasion and metastasis
  5. Genomic instability
  6. Inducing angiogenesis
  7. Resisting cell death
  8. deregulating cellular energetics
  9. proliferation signalling
  10. avoiding immune destruction
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5
Q
  1. What is a proto-oncogene, and give a few examples:
  2. What is an oncogene, and what percentage of cancer involves these mutations?
  3. What are DNA repair genes and give examples:
  4. What are apoptosis genes and give example:
  5. Name the two types of tumor suppressor genes, what do they do, and examples of each?
  6. How many defective genes are needed for cancer to manifest?
  7. Which gene is VERY important is cellular repair, and what percentage of tumors are related to mutations with this gene?
A
  1. A normal gene that regulates cell growth either by favoring proliferation or inciting apoptosis. Ex: HER-2/neu, Ras, Myc, SRC, hTERT
  2. a mutated proto-oncogene, leads to accelerated cell division, 60-75%.
  3. Fix DNA ex: BRCA-1 and BRCA-2 (mutations on these lead to breast cancer)
  4. induce apoptosis when needed BAX and Bcl-2
  5. Governors: put a stop to cell proliferation. Retinoblastoma gene (Rb gene).

Guardians: sense genomic change and do damage control. APC and P53 (70% of tumors result from defects with P53)

  1. 2
  2. P53, 70% of tumors
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6
Q
  1. Describe how P53 works:
  2. If P53 has mutations or doesn’t work, what happens?
  3. What is a telomere?
  4. What is telomerase?
A
  1. When something damages the DNA of a cell, P53 binds to the DNA and causes senescense, doesn’t allow cell to divide until repair is done. or calls upon the BAX gene to incite apoptosis.
  2. Cells w/ damaged DNA will not rest or be repaired. They will divide and produce tumors.
  3. A (protective) region with a repetitive gene sequence at the end of a dna strand. Has a cap on the end of DNA that limits reproduction (cell replicates no more than 50 times).
  4. A cancer enzyme that keeps adding telomeres so reproduction of the cell continues infinitely.
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7
Q
  1. What is angiogenesis and how does it apply to cancer?
  2. What is the Warburg effect?
  3. What is the reverse walburg effect?
  4. What are the high energy fuels of the reverse walburg effect?
  5. Why do cancer patients lose weight without trying?
  6. What is VEGF, Platelet derived GF, and basic fibroblast derived PF?
A
  1. growth of new blood vessels. Cancer wants to be fed by the blood and can secrete angiogenic factors.
  2. Cancer cells use of aerobic glycolysis rather than oxidative phosphorylation despite being in an oxygenated environment. Only renders 4 ATP per one mol of glucose. Not efficient. Not understood why.
  3. When cancer cells are established they recruit normal neighboring cells by releasing reactive oxygen species that cause the cells to produce high energy fuels for the cancer’s use. Like a bully
  4. lactate, ketone bodies, and fatty acids.
  5. cancer/tumors eat all the glucose and then move on to lipid reserves, then protein
  6. Vascular endothelial growth factor: tumors secrete this for angiogenesis as well as platelet and fibroblast GF
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8
Q
  1. How do cancer cells avoid apoptosis?
  2. Which innate immune response is an important factor in cancer? Why?
  3. What are the top cancer-causing infections?
  4. Do viruses cause cancer?
A
  1. defects in the extrinsic/intrinsic pathways
  2. inflammation. cytokine release
  3. H-pylori, hepatitis B and C, HPV, and reflux disease
  4. HIV, EBV, Kaposi sarcoma herpesvirus, HPV, Human T-cell leukemia/lymphoma virus
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9
Q
  1. What are the malignancies that metastasize to bone?
  2. What is the most common site of bone metastasis?
  3. Where do lymphomas metastasize?
  4. Where do abdominal cancers metastasize to?
  5. Why do cancers show up years after remission?
A
  1. breast cancer, lung cancer, thyroid cancer, and kidney or prostate cancer.
  2. the spine
  3. spleen
  4. liver
  5. dormancy/micrometastasis
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10
Q
  1. What are 8 warning signs of cancer?
  2. Is pain a warning sign of cancer? What is pain usually associated with?
  3. What is the most common symptom of early cancer?
A
  1. unusual bleeding or -discharge,
    - bowel/bladder changes,
    - change in wart or mole,
    - wound that doesn’t heal,
    - unexplained weight loss,
    - anemia or persistant fatigue,
    - persistant cough
    - solid lump
  2. not usually. Pain comes from
    psychological effects, or when tumor invades sensitive ares, causes inflammation etc.
  3. Fatigue (can be from a variety of reasons, not all directly from cancer).
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11
Q
  1. What are paraneoplastic syndromes?
  2. What causes them and what does not cause them?
  3. What is cachexia, and what does it do?
  4. Can anemia be a symptom of early cancer? How? What is anemia? Who should never have anemia?
A
  1. group of rare disorders triggered by an abnormal immune response to a tumor.
  2. biological substances released from tumor, immune response. NOT caused by direct local effects.
  3. Severe syndrome (can be paraneoplastic) of weakness and wasting of the body. Involves anorexia, cardiac dysfunction, malabsorption, and wasting of muscle and fats.
  4. Yes because of undetected blood loss to cancer. Decrease of hemoglobin in blood. men
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12
Q
  1. What causes leukopenia and thrombocytopenia?
  2. What is a risk of this when absolute neutrophil and lymphocyte counts fall?
  3. What are the effects of cancer and chemo on the gastrointestinal tract?
  4. What are the effects on skin and hair?
A
  1. Direct tumor invasion to the bone marrow, or effects of chemo (toxic to bone marrow)
  2. Infection
  3. Cancer: oral ulcers. Chemo: malabsorption, diarrhea, nausea
  4. alopecia (chemo), skin break down and dryness
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13
Q
  1. How do we stage cancer when we base it on metastasis?
  2. What is the WHO’s TNM system?
  3. What is Duke’s staging?
  4. Why is it so important to stage cancer?
A
  1. Stage 1: no metastasis
    Stage 2: local invasion
    Stage 3: spread to regional structures
    Stage 4: distant metastais
  2. T = Tumor (T0 = no tumor, T1 = 1 inch, T2 = 2 inch etc)

N = Node involvement (N1 = local nodes, N2 = further away etc)

M = Metastasis (M1 = local, M2 = distant)

  1. Colon cancer staging that gives survival rates after 5 years. A = >90%, B = 55% - 85%, C = 20% - 55%, D = < 5%
  2. Determines seriousness, treatment plan, prognosis
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14
Q
  1. What does “grading” mean in reference to cancer?
  2. What are the grades, 1 - 4?
  3. What are tumor markers? Can there be false positives/negatives?
A
  1. Histopathology. the way the cells look under microscope. Determines how aggressively the cancer will behave.
  2. Grade 1 well-differentiated. Grade 2 moderately differentiated. Grade 3 poorly differentiated. Grade 4 anaplastic
  3. Substances produced by cancer cells that are found on or in tumor cells, in the blood, CSF, or urine. Yes.
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15
Q
  1. What are the goals of radiation? How does it kill cancer?
  2. Name the 4 types of surgery for cancer:
  3. What are the 3 stages of chemotherapy, and what do they do?
  4. Is there any immunotherapy for cancer?
A
  1. Eradicate cancer without excessive toxicity, Avoid damage to normal structures. Radiation damages cancer cell’s dna.
  2. preventative (polyps), biopsy (diagnosis/staging), Lymph node sampling, palliative care
  3. Induction chemotherapy: shrinkage or disappearance of
    tumors

Adjuvant chemotherapy:
Eliminate micrometastasis after surgery

Neoadjuvant therapy:
Given before localized treatment to shrink tumor

  1. Vaccines against cancer-causing viruses are used. Allogenic cancer cell vaccines being tested
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16
Q
  1. What are the 2 inherited breast cancer genes? What type of gene is the first one?
  2. What gene can cause breast cancer that is not heritable?
A
  1. BRCA-1 (chromosome 17) tumor suppressor gene, BRCA-2 (chromosome 13),
  2. HER-2 gene
17
Q
  1. What are the 2 main types of Esophageal cancer and what they are linked to?
  2. T or F most colorectal cancers come from family history?
  3. What is the 2nd most common cancer in men? Is it symptomatic? How to test for?
A
  1. adenocarcinoma- linked to alcohol, smoking, certain foods, and GERD

squamous cell carcinoma - smoking

  1. T
  2. prostate. non-symptomatic until advanced, but can cause difficulty urinating, or incontinence. Digital rectal or PSA blood test
18
Q
  1. What is a TAM
  2. What is Avastin bevicizumab
  3. prevalence:
  4. Incidence:
  5. MOrbidity:
  6. Mortality:
  7. Sensitivity:
  8. specificity:
A
  1. Tumor assisting macrophage. Helps tumor survive and proliferate by secreting cytokines.
  2. A medication that blocks VEGF (an angiogenesis blocker) to starve out tumors
  3. a percentage affected w/ a particular disease at a specific time
  4. number of new cases within a time
    period
  5. risk factor for death
  6. Death rate
  7. correctly identify those with a disease
  8. identify those without the disease

Pathophysiology (11 decks)

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