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ALU 301 > Chapter 10- Advanced Cancer Underwriting > Flashcards

Chapter 10- Advanced Cancer Underwriting Flashcards

1
Q

In large part, what controls the rate of growth and division of cells?

A

genes and gene regulation.

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2
Q

what is the distinction, between genetic changes one is born with and genetic changes acquired through exposure?

A

germ-line mutations (born with) are present in every cell of the body at all times
Acquired mutations tend to produce their effects locally, altering the genome only in the cells exposed.

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3
Q

How are germ-line mutation cancers expressed in the body?

A

gene regulation controls the mutation in way that the particular mutated gene can be expressed at high levels in some tissues, and no other. Which causes those tissues to be at higher risk for developing cancer.

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4
Q

What is happening now that more and more genetic information is gathered from the population?

A

genetic variants are being discovered which can predispose individuals to various cancers.
- note that risk for cancer depends on other genetic and environmental factors that cannot always be quantified.

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5
Q

In terms of Hereditary breast and ovarian cancer (HBOC).

  1. What are the mutated genes?
  2. Cancer types
  3. Countermeasures.
A
  1. BRCA1, BRCA 2
  2. breast, ovarian, pancreatic, prostate cancer.
  3. hormone tx, preventative mastectomy/oophorectomy, increased screening.
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6
Q

In terms of Lynch Syndrome (hereditary non-polyposis colorectal cancer)

  1. What are the mutated genes?
  2. Cancer types
  3. Countermeasures.
A
  1. MLH1, MSH2, MLH3, MSH6, PMS1, PMS, TRGBR2
  2. colon, endometrial, ovarian, stomach, pancreatic, kidney
  3. early screening, pap/endometrial imaging, preventative colectomy or hysterectomy
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7
Q

In terms of Familial adenomatous polyposis

  1. What are the mutated genes?
  2. Cancer types
  3. Countermeasures.
A
  1. APC
  2. colon
  3. increased screening via c-scope or colectomy
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8
Q

In terms of Multiple endocrine neoplasia type 2 syndrome.

  1. What are the mutated genes?
  2. Cancer types
  3. Countermeasures.
A
  1. RET
  2. thyroid, adrenal
  3. monitoring by examination; imaging and lab tests
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9
Q

In terms of Familial malignant melanoma.

  1. What are the mutated genes?
  2. Cancer types
  3. Countermeasures.
A
  1. CDKN2A
  2. melanoma
  3. frequent skin examinations; photographs, biopsies of lesions
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10
Q

What are some environmental factors that play an important role in the development of nearly all cancers?

A

chemical, electromagnetic, and biological agents.

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11
Q

a persons exposures to environemental risks can be expressed by 4 source types. What are they?

A

internal (food)
external (sunlight)
accidental (virus)
deliberate (smoking)

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12
Q

Chemical agents have certain molecules that have structures that make it easy for them to slip into a DNA chain. This can result in cancers if in the right place, right time. These are called intercalating agents- What are some examples of these chemicals that are capable of doing this?

A
  1. naturally occurring dye berberine,
  2. thalidomide (drug)
  3. Aflatoxin
  4. fungal toxin (corn/peanuts)
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13
Q

Electromagnetic radiation can induce cancer-promoting changes in DNA. what are some examples?

A

only Ultraviolet and higher frequency rays can alter the body’s molecules by knocking free the electrons of the molecules that absorb them, creating ionized molecules and therefore becoming reactive. “free-radical”.

*think sun tanning and melanoma.

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14
Q

There are only a few viruses known to promote cancer. What are they?

A
  1. HPV- associated with cervical cancer. several forms called serotypes, certain of them carry higher risk for cervical changes and cancer. All forms are sexually transmitted.
  2. EBV - causing mononucleosis, and lymphoma. exposure is universal, and associated lymphoma is rare.
  3. Hep B virus: liver cancer, often takes years for infection to damage the liver.
  4. HIV: strongly associated with developement of Kaposi sarcoma dn lymphoma. d/t interference with normal task of immune sytem.
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15
Q

What do you term the principle that the immune system can monitor and intervene in the process of cancer development known as carcinogenesis.

A

immune surveillance.
The immune system detect foreign organisms, eliminated them, then chills. this is called the checkpoint pathway.&raquo_space; this system is conterproductive in immune surveillance for cancer, since the cancer might be detected by system is shut down for windown.
* can also have situations where immune surveillance is not functioning which allows for cancer +++++, think tx fo R.A.

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16
Q

What was the type of chemo treatment used in the past, in which chemotherapy agents worked by targetting rapidly dividing cells, but would not distinguish between rapid cancer cells, and normal rapidly dividing nromal cells?

A

Cytotoxic chemotherapy.

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17
Q

What is the newer chemotherapy regime, where chemotherapy drugs target specific proteins which are more abundant or active in cancer cells than normal cells?

A

Target therapy agents or Target chemotherapy.

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18
Q

What is the first and most remarkable target therapy agent?

A

rituximab.
-monoclonal antibody, directed at a single target antigen CD20 (protein on B-lymphocytes)
- good for B-cell cancers (NHL, CLL)
-

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19
Q

How do the class of target therapy agents known as Tyrosine Kinase Inhibitors work?

A

thyrosine kinease is an enzyme in all cells, many types exist and they turn off and on as needed. in some cancers a mutation makes it “on” all the time, and doent follow apoptosis, and results in malignancy. Certain malignancies depending on tyrosine kinease to keep growing. Drugs are targeted to the abnormal tyrosine kinase,

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20
Q

How do the target therapy antigens “Anti-Angiogenesis” work?

A

when solid tumours grow they need food and blood. the process of blood vessel growth is known as angiogenesis. These drugs act to inhibit angiogenesis. They have no yet been developed into effective cancer therapy agents.

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21
Q

How does the specific Targeted therapy: chimeric antigen receptor T-cell (CART) therapy work?

A

combination of targeted chemo, immunotherapy and genetic engineering.

  • focus on B-lymphocyte cancers.
  • they harvest T-cells from pt, then genetically modify them so they express a specific protein which will bind to the CD20 antigen on B-cells. the cells are grown ina . lab and infused back into the pt. they then target the malignant cells,
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22
Q

What is the leading cause of cancer death in the US?

A

Lung Cancer

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23
Q

what is the leading and secondary causes of lung cancer

A
  • smoking,

Secondary: Called relative risk (PR)

  • occupational exposure (asbestos, or other materials such as beryllium, cadmium, mustard gas, silica )
  • household exposure to radon gas,
  • second hand smoke
  • Family history 1.5 ^ risk
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24
Q

How are cancers differentiated?

A

based on the particular lung cells from which the cancer arises

  • Squamous cell or epidermoid: cells lining the lungs
  • lung adenocarcinoma arises from mucous cells.
  • large cell cancers are cells that are neither of the other two.
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25
Q

What are the types of small cell lung cancer?

A
  • Small cell carcinoma (Oat Cell cancer)

- Combined Small Cell Cancer

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26
Q

What are the small cell lung cancers?

A

Small cell carcinoma (oat cell cancer)

Combined small cell cancer

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27
Q

What are the non-small cell lung cancers?

A

Adenocarcinoma
squamous cell cancer (epidermoid carcinoma)
large cell lung cancer

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28
Q

Why is Lung cancer is so deadly?

What are typical lung cancer sxs?

A

There is usually no sxs or mild sxs at early stages.
sxs: chronic coughing, followed by sound changes (if upper airway) as cancer grows there can be localized pain, wight loss, swollen lymph nodes.

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29
Q

How is a lung cancer diagnosed?

A

CXR- initial detection
biopsy- for confirmation
CT: review extent of disease

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30
Q

Prognosis of lung cancer can be strongly influenced by the histology and stages. Explain this.

A

early stage cancer (1-2) have a better prognosis than cancer stages (3-4).
Small cell cancer has a dismal prognosis

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31
Q

What is the 5-year overall relative survival for lung cancer ?

A

17.6%

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32
Q

How is lung cancer treated?

A

surgery => radiation => chemotherapy (can involve targeted agents)

33
Q

If remission is achieved, how is follow-up done?

A

CT’s (regularly) to look for recurrence.

34
Q

What is the third death ranking cancer in the US?

A

Pancreatic

35
Q

Why is there an increase in the rate of diagnosis?

A
  • better detection
  • obesity epidemic
  • Fx, SM, DM, and chronic pancreatitis.
  • growing age.
36
Q

The mass majority of pancreatic cancers are adenocarcinomas, which arise from?

A

the exocrine cells of the pancreas. They make digestive enzymes

3% - of pancreatic cancer arises from endocrine cells (produce hormones)

37
Q

Which type of pancreatic cancer has the best prognosis? In which kind of cells do you find this cancer?

A

Unusual cancers- from the endocrine cells

38
Q

Why is pancreatic cancer diagnosed in the latter stages?

A

signs/sxs are absent or subtle.
- sxs arise if the tumour is at the heart of the pancreas and eventually grows to block the pancreatic duct causing jaundice, dark urine, and abdo pain. Weight loss is common.
If tumour is endocrine variety- sxs associated with excess of the particular hormone.

39
Q

How is pancreatic cancer diagnosed?

A

CT scans- incidental findings or sometimes d/t sxs if present.

40
Q

There are different types of pancreatic cysts. What is the most common?

A

papillary mucinous neoplasm (PMNs)

41
Q

What type of pancreatic cysts have a 60% rate of associated malignancy ?

A

intra-ductal types, specially when near main pancreatic duct.

42
Q

How are pancreatic cysts pathologies diagnosed?

A

Endoscopic produces often used for tissue sampling.

  • Its hard to do a biopsy with a needle because it can lead to chronic pancreatitis.
43
Q

How is pancreatic cancer treated?

A

1 surgery

#2 Chemo
* radiation can be used to prevent recurrence or if surgery is not an option
* no standard chemo agents for pancreatic cancer.

44
Q

What cancers are considered hepatobiliary cancers?

A

cancers of liver and bile ducts.

45
Q

Bile duct cancers are divided into which two subcategories?

A
  1. intrahepatic (including liver)

2. extrahepatic (usually gallbladder)

46
Q

Name risk factors for developing hepatobilitary cancers?

A

viral infections (hep), alcohol-indcued cirrhosis, cirrhosis from any cause&raquo_space; Increases risk for liver cancer

biliary cirrhosis, sclerosing cholamngitis, and IBD&raquo_space;> increase risk of Gall bladder/extrahepatic bile duct cancers

47
Q

Liver cancer is usually diagnosed after/with presence of significant cirrhosis. In what incidence can Liver cancer develop without cirrhosis and how?

A

Hep B can cause cancer without cirrhosis.

There needs to be high levels of viral DNA and presence of ‘e” antigen.

48
Q

How are liver and bile duct cancers diagnosed?

A

imaging (US or CT)
biopsy for confirmation (if needed)
* gall bladder cannot be needle biopsied, so its generally removed.

49
Q

How is liver cancer treated?

A
  • resection if possible (depends on location, and function capacity of the portion of the liver left over)
  • Some cases can be tx’d with ablation, radiation or chemo.
  • liver transplant
50
Q

How is gall bladder and bile duct cancer treated?

A
  • surgical resection (only possible at early stages)

- combine radiation and chemo but overall prognosis is poor

51
Q

What is the survival period for liver and bile duct cancers?

A

low,

bile duct cancer has a better prognosis than liver cancer.

52
Q

what type of malignancies are considered oropharyngeal cancers?

A

malignancies of the lip, mouth, pharynx, larynx, sinuses and salivary glands.

53
Q

What is the most common type of oropharyngeal cancers?
What is the usually cause for this cancer?
Who is more prone to this type of Cancer (male or Females)?

A
  • squamous cell cancers of the oral cavity and throat (lining cells)
  • associated to Tobacco and alcohol use.
  • males > females.
54
Q

Anatomically the oropharyngeal cancers occur where?

A

aerodigestive tract, between boarder of the lips and lowest part of the hypo-pharynx.

55
Q

What regions make up the pharynx?

A

nasopharynx, oropharynx, hydropharynx

56
Q

What increases the risk of developing some forms of the oropharyngeal cancers?

A

tobacco
alcohol
HPV (type 16++) - these cancers have better prognosis

57
Q

What are typical sxs associated to head and neck cancers?

A

lip/tongue/mouth: non-healing lesions or ulcers.

nasal: one side nasal bleeding/obstruction
pharynx: swallowing or dysphonia (hoarseness), hemoptysis (cough blood), mass

58
Q

How is oropharyngeal cancers diagnosed?

A

biopsy (confirmation of diagnosis)
CT scans (determine staging)
CXR (determine metastases)

59
Q

How are head and neck cancers treated?

A 
#1 surgery 
if to large, then can look at radiation/chemo
60
Q

What is occult primary cancer?

How is it treated?

A

malignant cells that appear in the neck lymph-nodes. Initial evaluation fails to demonstrate tumour in the head or neck. Appears with 5% of oropharyngeal cancers.

  • favourable prognosis.
  • tx: radiation and possible removal of lymph node and others.
61
Q

which head/neck cancers are prone to early metastasis?

A

cancers of the base of the tongue.

hemotologies can tell you what type of cancer cells it is and how it was originated.

62
Q

What affects the survival period of head and neck cancer?

A

primary site of malignancy (lips most favourable, hypo-pharynx lease)
stage (early diagnosis is more favourable)
personal health (SM + ETOH can decrease morbidity)

63
Q

What cancer is 4x more common for females than males?

  • It also has a very favourable prognosis.
A

Thyroid cancer

64
Q

What are some increase risk factors to developing thyroid cancer? (3)

A

sex ( females > males)
hx of radiation to the neck
genetics

65
Q

What are the 4 basic forms of thyroid cancer and what is their general prognosis?

A
  1. papillary cancer (most common, good prognosis)
  2. follicular thyroid cancer (good prognosis)
  3. anaplastic (rarest, very poor prognosis)
  4. mixed form (combination of first two, good prognosis)
66
Q

What are the general sxs of thyroid cancer?

A

sxs: mild, soar throat, hoarseness, mass

Usually thyroid cancer is an incidental finding

67
Q

How is thyroid cancer diagnosed?

A

Usually a fine needle aspiration biopsy is done.

  • Diagnosis is complicated by the fact that thyroids commonly have benign nodules and cysts.
68
Q

How is thyroid cancer staged?

A 
size (T-state), number of lymph nodes involved (N-stage), presence of metastases (M-stage) 
and age (before or after 45)

*those before 45, are considered stage 1, irregardless of nodes involved, and cancer is staged class 2 if metastasis is present.

69
Q

how is thyroid cancer treated?

A

surgery (thyroidectomy or hemithyroidectomy)

radioactive iodine can also be used (risk for future cancers)

70
Q

How is thyroid cancer monitored?

A
  • blood work: thyroglobulin since its only made in thyroid tissue, increases in [concentration] usually indicates thyroid concerns.
  • ultrasounds also can be done for thyroid growths/nodules/cysts.
71
Q

What are tumour markers?

A

substances that indicate the presence, size or aggressiveness of a malignancy in the body.
Can also be used to detect recurrence of a cancer.

72
Q

What is the most familiar tumour marker?

A

PSA

abnormally high levels are associated to prostate cancer.

73
Q

What is the tumour marker Human Chorionic Gonadotropin (hCG) linked to?

A

Testicular/prostate cancer

preformed on persons with testicular mass

74
Q

Another tumour marker commonly seen in insurance is Carcinoembryonic Antigen (CEA). When is it elevated?

A

in a number of malignancies including colon, breast, pancreas and thyroid cancers
it is also elevated in non-malignant conditions such as pneumonia, cirrhosis, stomach ulcer and heavy smoking.

75
Q

Why is the tumor-asscoiated protein CA-125 infamous?

A

CA-125 is a poor screening test made infamous by a female who demanded it had been done. But its poor for screening because it can be elevated with benign conditions like endometriosis and fibroids and no reliably elevated with ovarian or peritoneal cancers.

76
Q

what conditions are linked to the tumour marker CA 19-9?

A

Pancreatic cancer. It’s monitored to assess the treatment success of pancreatic cancer.

It can also be elevated in other gastrointestinal malignancies and non-malignant CI diseases.

77
Q

What tumour marker is specific for medullary thyroid cancer?

A

Calcitonin

78
Q

Why is cancer more prone in the elderly?

A
  • They’re exposed to various carcinogenic substances or practices for a longer period of time (ETOH/SM/Fatty diets/ Sun exposure) + less exercise.
  • immune system diminishes with age
  • chronic illness accumulate over time
79
Q

Why is cancer more deadly in the elder ages?

A

less physiological reserves (fatty cells, strength)
complex surgery has a poorer prognosis in the old
they cant’ tolerate chemo/radiation as well
diabetes slows down healing

ALU 301 (14 decks)

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