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pathophysiology 4802 > Neoplasia (Final Exam) > Flashcards

Neoplasia (Final Exam) Flashcards

1
Q

this means “new growth”. implies an abnormality of cellular growth/tumor. it is associated with an altered expression of cellular genes. can be benign or malignant

A

neoplasia

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2
Q

also called surface cells—line papillae and cysts and form tubules. These cells are voluminous eosinophilic cytoplasm and prominent nuclei. Intranuclear inclusions and multinucleation are often observed

A

cuboidal

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3
Q

stromal cells—fill the papillary cores and form the sheets in solid areas. having well-defined borders, clear to eosinophilic cytoplasm, centrally located round to oval nuclei with fine dispersed chromatin, and usually indiscernible nucleoli.

A

round cells

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4
Q

are round cells (stroll cells) usually larger or smaller then cuboidal cells (surface cells)

A

smaller

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5
Q

what does the suffix “-oma” indicate

A

benign tumor

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6
Q

what does the suffix “-carcinoma” or “-sarcoma” indicate

A

malignant tumor

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7
Q

this is a malignant tumour of epithelial origin

A

carcinoma

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8
Q

this is a malignant tumour of mesenchymal origin

A

sarcoma

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9
Q

what are some risk factors for cancer/neoplasia

A
  • tobacco use
  • nutrition
  • obesity
  • sun exposure (skin cancer)
  • sexual exposure to HPV (cervical cancer)
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10
Q

normally cancerous cells are destroyed by _____ and _______

A

cell-mediated immunity and humeral immunity

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11
Q

true or false: normally there is an imbalance in oncogenes and tumor suppressor genes so that you have more tumour suppressor genes so cancer doesn’t occur

A

false - usually have a balance between them. if a mutation occurs then you get an imbalance

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12
Q

these are normal cellular genes transformed into oncogenes by activating mutation. they code for:
- growth factors
- growth factor receptors
- cytoplasmic signalling molecules
- nucelar transcription factors

A

proto-oncogenes

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13
Q

these are small cell-manufactured peptides. are coded for by proto-oncogenes
- they secrete into extracellular space
- diffuse into nearby cells
- interact with receptors on target cell surface
- activate signalling cascade: can produce autocrine signalling if overproduction

A

growth factors (mitogens)

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14
Q

these are transmembrane proteins and are coded for by porto-oncogenes; the mitogen binding area is on ht outside of the cell and the enzyme activating area is on the inside of the cell. will only bind with one particular mitogen. binding activates cell proliferation. HER2 - over expression

A

growth factor receptors

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15
Q

this is coded for by porto-oncogenes. it involves numerous enzymes and chemicals. mutant proto-oncogene is due to overproduction of pathway components
RAS gene: codes defective protein
- unable to hydrolyse GTP
- 30% of all human cancers

A

cytoplasm signalling pathways

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16
Q

these are the three proto-oncogenes that code for transcription factors. they are normally sequestered until appropriate signals occur
examples: lung and breast cancer, leukemia, neuroblastoma

A

Myc, Jun, Fos

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17
Q

true or false: oncogenes become activated proto-oncogenes

A

false other way around
proto-oncogenes become oncogenes!

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18
Q

what are the four ways proto-oncogenes become activated oncogenes?

A
  1. oncogenes introduced to host cell by retrovirus
  2. a mutagenic event
  3. loss/damage of regulatory DNA sequence
  4. error in chromosome replication produce extra copies of proto-oncogene (amplification)
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19
Q

this can cause a proto-oncogene to become an activated oncogene. it is composed of RNA and contains reverse transcriptase enzyme (which directs syntheses of a DNA copy of viral RNA). examples include:
- HIV (Kaposi’s sarcoma)
- Epstein-Barr virus (Burkitt lymphoma)
- Human T-lymphocyte virus type 1 (adult T cell leukemia/lymphoma)

A

retrovirus

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20
Q

these contribute to cancer only when not present, otherwise they inhibit cell proliferations. both copies of these are usually inactivated in order for cancer to develop

A

tumor supressor genes

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21
Q

true or false: one can inherit a defective copy of tumor suppressor genes from one or both parents

A

true

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22
Q

this is a critical tumour suppressor gene that blocks the cell cycle progression by inhibiting transcription factors when unphosphorylated

A

Rb (retinoblastoma) gene

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23
Q

what is the normal process of the Rb gene when a growth factor (such as EGF) binds to its receptor

A

growth factor binds to receptor -> activation of cyclins/Cdk -> phosphorylation of pRB -> release of transcription factors -> gene transcription occurs -> S-phase/DNA replication can occur

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24
Q

this provides instructions for making a protein called tumour protein p53 (TP53) which is a tumour suppressor.

A

p53 gene

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25
Q

when ionizing radiation, carcinogens or mutations are presented to a normal cells (TP53) normal, DNA damage occurs -> TP53 is activated and binds to DNA -> DNA repair -> sucessful cell repair -> normal cells.
what happens when the cell has a mutation or a loss of TP53?

A

after DNA is damaged -> TP53-dependant genes are not activated -> no cycle arrest/DNA repair -> there is an expansion and additional mutations -> malignant tumour

26
Q

these are tumour suppressor genes. e.g. breast cancer genes. early onset compared with sporadic. usually bilateral

A

BRCA1 & BRCA2

27
Q

family history and inherited defect in ______ increases risk of breast (85%) and ovarian (40-60%) cancer

A

BRCA1

28
Q

which of the following will produce a tumour
A. Ras -> anchorage independant
B. Myc -> immortal
C. Ras & Myc -> anchorage independent and immortal

A

C

29
Q

what will happen to cells if there is a homozygous loss of APC locus on 5q

A

cells will look normal

30
Q

what will happen to cells if there is a mutation of ras on 12p

A

cells proliferate and form an adenoma

31
Q

what will happen to cells if there is a homozygous loss of DCC on 18q

A

more proliferation, larger adenoma and cells look abnormal

32
Q

what will happen to cells if there is a homozygous loss of p53 on 17p

A

invasive carcinoma

33
Q

in the multistep nature of carcinogenesis, DNA damage (mutation) leads to

A

initiation

34
Q

in the multistep nature of carcinogenesis, proliferations (growth promoters) leads to

A

promotion

35
Q

in the multistep nature of carcinogenesis, development of the cancerous phenotype leads to

A

progression

36
Q

this stage in the multistep nature of carcinogenesis, genetic mutations occur which inappropriately activate porto-oncogenes and inactivate tumour suppressor genes. proliferation occurs which is required for cancer development

A

initiation

37
Q

this stage in the multistep nature of carcinogenesis, the mutant cell proliferation occurs (activation of another oncogene, inactivation of tumour suppressor gene, nutritional factors, infection).

A

promotion

38
Q

this stage in the multistep nature of carcinogenesis is regulated by many hormonal growth factors such as estrogen and testosterone

A

promotion

39
Q

this stage in the multistep nature of carcinogenesis is where mutant, proliferating cells begin to exhibit malignant behaviour. malignant cells can produce telomerase. cells whose phenotype gives them a growth advantage proliferate more readily

A

progression

40
Q

this is the process by which cancer cells escape their tissue of origin and initiate new colonies of cancer in distant sites - specialized enzymes and receptors enable them to escape their tissue of origin and _______

A

metastasis

41
Q

what are the 4 steps of metastasis

A
  1. loosening of intercellular junctions
  2. degradation
  3. attachement
  4. migration
42
Q

how do cancer cells generally spread

A

circulatory or lymphatic system

43
Q

these are used to help identify parent tissue of cancer origin. some may be released into circulation, others are identified through biopsy. they are usually enzymes and help track the tumour activity

A

tumor markers

44
Q

this is the process by which cancer tumour forms new blood vessels in order to grow. usually does not occur until late stages of development. inhibition of this process is an important therapeutic goal

A

angiogenesis

45
Q

why are tumours graded and staged?

A

to predict clinical behaviour of a malignant tumour and guide therapeutic management

46
Q

does this describe grading or staging of a tumour?
depends on:
- histologic characterization of tumour cells
- degree of anaplasia (cell differentiation)

A

grading

47
Q

does this describe grading or staging of a tumour?
depends on:
- locations and patterns of spread within the host
- tumour size, extent of local growth, lymph node and organ involvement, distant metastasis <- TMN system

A

staging

48
Q

what are the warning signs of cancer

A
  • CAUTION *
    C - change in bowel or bladder habits
    A - a sore that does not heal
    U - unusual bleeding or discharge
    T - thickening or lump in body part
    I - indigestion of difficulty swallowing
    O - obvious change in wart or mole
    N - nagging cough or hoarseness
49
Q

what are the warning signs of cancer in children

A
  • CHILDREN *
    C - continued, unexplained weightloss
    H - headaches and vomitting in the morning
    I - increased swelling or persistent pain in bones or joints
    L - lump or mass in abdomen, neck or elsewhere
    D - development of whitish appearance in the pupil of the eye
    R - recurrent fevers - non infectious
    E - excessive bleeding or bruising
    N - noticeable paleness or prolonged tiredness
50
Q

what would cause pain with regards to cancer

A
  • may be due to metastasis, tissue destruction/inflammation
  • may be caused by cancer tx
51
Q

this is overall weightless and generalized weakness that can be seen with cancer. may be caused by:
- loss of appetite (anorexia)
- increased metabolic rate
- n/v

A

cachexia

52
Q

true or false: the immune system is suppressed by cancer cell secretions

A

true

53
Q

this is due to invasion and destruction of bone marrow cells, poor nutrition and chemotherapy. contributes to anemia, leukopenia and thrombocytopenia - can be managed by blood replacement therapy

A

bone marrow suppression

54
Q

this is a complication of chemotherapy and radiation. it is a primary source for cancer pain and anorexia and could provide a portal for infections

A

mucositis

55
Q

a group of rare disorders that occur when the immune system has a reaction to a cancerous tumor known as a “neoplasm.” e.g hypercalcemia, cushings syndrome secondary to ACTH secretion, hyponatremia and water overload secondary to excess ADH secretion

A

paraneoplastic syndromes

56
Q

true or false: the majority of patients with solid tutors are treated surgically

A

true

57
Q

this type of therapy for cancer
- kills tumour cells by damaging nuclear DNA
- kills cells that are non-resectable due to location, missed by surgery or undetected
- may not kill cells directly but initiates apoptosis
- small doses over several treatments (due to cells being on different cycles)
- some normal cells may also be killed

A

radiation

58
Q

this type of therapy for cancer
- systemic administration of anticancer chemicals to treat cancers known or suspected to be disseminated in the body
- finds cancer cell targets in the body
- most are cytotoxic
- not selective for tumour cells (normal cells may also be killed)

A

drug therapy

59
Q

review!!! describe the cell cycle

A

G0 = resting
G1 = synthesis of components needed for DNA synthesis
S = synthesis of DNA
G2 = synthesis of components needed for mitosis
M = mitosis
G0

60
Q

this type of therapy for cancer primarily involves use of
- interferons: glycoproteins produced by immune cells in response to viral infection
- interleukins: peptides produced and secreted by WBCs
- monoclonal antibodies: antibodies with identical structure that bind with specific target antigens

A

immunotherapy

61
Q

this type of therapy for cancer may have high therapeutic potential and may be used to suppress overactive oncogenes or replenish missing tumour suppressor function.
- genetic alteration to tumour cells to make them more susceptible to cytotoxic agents or immune recognition
- genetic alteration of immune cells to make them more efficient killers of tumour cells

A

gene and molecular therapy

62
Q

this is used to manage life threatening disorders in which patients bone marrow cannot manufacture WBCs, RBCs or platelets.

A

stem cell therapy

pathophysiology 4802 (16 decks)

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