Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

RUSVM Pathology I > Neoplasia 2 > Flashcards

Neoplasia 2 Flashcards

1
Q

Neoplasia is a result of an abnormality involved the ________________

A

Cell cycle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Abnormalities in genes controlling what part of the cell cycle can result in neoplasm

A

DNA repair
growth signaling
Growth-inhibition signaling
Evasion of apoptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Defective DNA repair leads to __________

A

Genetic instability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Abnormal cell cycle checkpoints and abnormal responses to DNA damage are due to what

A

Defective DNA repair

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

A normal gene that regulates cell proliferation

A

Proto-oncogene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Protocol-oncogenes regulate?

A

Growth factors
Signal transducers
Transcription factors
Cell cycle component

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

_____________produced oncoproteins

A

Oncogenes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Are proto-oncogene mutations to oncogenes dominant or recessive?

A

Dominant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

___________ gene encodes a receptor tyrosine kinase with growth factor ligand

A

Ckit

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What mutation is common in canine mast cell tumors

A

Ckit (oncogene)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Are mutations in tumor suppressor genes dominant or recessive?

A

Recessive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What usually inhibits cell proliferation, and when absent will lead to growth that is insensitive to inhibition

A

Tumor suppressor genes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Are mutations in a protoncogene OR a tumor suppressor gene inherited in the germ line

A

Tumor suppressor gene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What does p53 encode??

A

DNA binding protein that stimulates many genes involved in arresting cell cycle, and stimulating DNA repair and apoptosis

Eg CDK inhibitor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are normal triggers for apoptosis

A

DNA damage
Loss of essential nutrients/growth factors
Binding of “death factors”
Cytotoxic lymphocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Are mutations that allow evasion of apoptosis dominant for recessive

A

Can be either

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the Rb gene and what is its normal function

A

Tumor suppressor gene

Required for G1/S transition in the cell cycle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Are neoplasms clonal or polyclonal?

A

Clonal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How do neoplasms become heterogenous if they are clonal?

A

Genetic instability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What the tumor cell progression an the effect therapy will have on these cells?

A

Clonal neoplasm -> genetic instability leading to multiple clones -> progression to malignant clone -> overgrowth of malignant cells

Treatment -> selection and growth of resistant cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is tumor invasion ?

A

Malignant tumors do not respect anatomical boundaries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What must cells do be be invasive?

A

Overcome passive growth-> loss of contact inhibition

Loosen cell junctions

Penetrate BM and ECM (enzymatic destruction of collagenase and matrix metalloproteinases)

Migrate actively -> stimulated by growth factors and cleavage products of ECM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Loosening of intracellular junctions is caused by decreased expression of _________

A

Cadherins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Cleavage of matrix components produces substances that have what kind of properties

A

Growth promoting, angiogenic, and chemotactic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Where are growth factors that stimulate migration derived from?

A

Tumors cells and/or degraded ECM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is the metastatic cascade?

A

Clonal expansion-> metastatic subclone -> adhesion and invasion of BM -> pass through ECM ->

intravasation -> interact with lymphoid cells -> form tumor cell embolus (wth platelets) -> adhesion of BM ->

extravasation -> metastatic deposit -> angiogenesis -> growth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Can a tumor progress without angiogenesis ?

A

No

Limited to 1-2mm diameter without new blood vessels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

How do tumor cells recruit endothelial cells and promote angiogenesis ?

A

Release of vascular endothelial growth factor (VEGF)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are the pathways of spread of tumors

A

Tanscoelomic

Hematogenous

Lymphatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is transcoelomic spread and what cancers is this common in?

A

Seeding of body cavities and surfaces -> On surface of organs have fewer atomically barriers

Mesothelioma, ovarian adenocarcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is hematogenous spread and what tumors is this most common in?

A

Invasion of veins (usually not arteries = thicker wall)

Sarcoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is lymphatic spread and what tumors use this route?

A

In lymphatic-> patterned dictated by lymphatic drainage but lymphatic tumors do not arise orderly.

Carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

If metatatic spread is hematogenous or lymphatic where do the metastasis often arise?

A

In the first capillary bed encountered

Lungs(many tumors)

Liverr(enteric tumors)

34
Q

Prostate and mammary carcinoma metastasis have organotrophism for ____________

A

Bone

35
Q

Pulmonary carcinoma in cats has metastatic organotropism for ___________

A

Digits

36
Q

T/F: neoplasms are irreversible proliferation but have the ability to regress

A

T

37
Q

_______________ are proteins and carbohydrates expressed on tumor cell surface

A

Tumor antigens

38
Q

Immune system is capable of recognizing self-antigens expressed on tumor cells and attacking these cells

A

Immunosurveillance

39
Q

What is the most effective anti-tumor defense?

A

CD8+ cytotoxic Tcell

40
Q

CD8+ Tcells recognize what tumor antigens?

A

Product of oncogenes or mutated tumor suppressor gene

Mutated self protein

Overexpressed or aberrantly expressed self protein

Oncogenic virus proteins

41
Q

What immuno-evasive mechanisms can a tumor cell have

A

Alter MHC expression

Loss or masking tumor-specific antigens

Tolerance (antigen shared with normal tissue)

Immunosuppression -> Fas ligand stimulate apoptosis of binding Tcells

42
Q

How can DNA be altered to generate an neoplasm?

A

Mutation

Chromosomal alterations

Epigenetic changes (heritable change in gene expression resulting from something other than DNA sequence)

43
Q

What are the two sources of altered DNA

A

Inherited in germ line

Acquired somatic mutation

44
Q

What is a germline mutation/

A

Mutation passed on in ova or sperm

45
Q

Familial cancer syndrome are most likely due to mutations in what types of genes

A

Recessive genes

Tumor suppressor genes
Gene involved in DNA repair

46
Q

T/F: aquired somatic mutations are passed in germline

A

False

47
Q

What are acquired somatic mutations?

A

Spontaneous mutations (accumulate over lifetime)

48
Q

What are causes of altered DNA?

A 
Spontaneous 
Radiation 
Chemical carcinogens 
Oncogenic virus
Hormonal
49
Q

What are the two types of radiation and what damage do they cause to DNA

A

Ionizing -> strand breaks

Ultraviolet -> pyrimidine dimers

50
Q

What are the mechanisms of injury of chemical carcinogens?

A

Genotoxic -> directly damage DNA

Cytotoxic -> increased cell proliferation due to cell injury

Mitogenic -> increased cell proliferation without cell injury

51
Q

What is a classic veterinary medicine example of a chemical carcinogens?

A

Bracken fern

Aflatoxin
Dioxins, Nitrosamines, Polycyclic aromatic hydrocarbons (cigarette smoke)

52
Q

How do oncogenic viruses interrupt host cell genes?

A

Insert their own oncogene (eg papilloma virus )

Insertional mutagenesis (eg retroviruses)

Immunosuppression

53
Q

How do papilloma viruses cause neoplasia

A

E6/E7 proteins from papilloma virus inactivate p53 and other tumor suppressor genes => loss of cell cycle control

54
Q

How can hormones cause carcinogenesis ?

A

Stimulation and growth of target organ

55
Q

How can chronic inflammation cause carcinogenesis

A

Inflammatory cytokines producing cell proliferation (not well understood)

Eg Spirocerca lupi/ Biliary infection by liver fluke/ Helicobacter

56
Q

What are the mechanisms of host damage of a neoplasm

A

Direct - tissue destruction

Paraneoplasic (indirect)

57
Q

Indirect and usually remote effects caused by tumor cell products rather than the primary tumor and its metastases

A

Paraneoplasic syndromes

58
Q

When does tumor necrosis occur?

A

Secondary to inflammation of tumor
Trauma
Tumor outgrows blood supply

59
Q

What is cancer cachexia

A

Progressive loss of body fat and lean body mass accompanied by profound weakness, anorexia, and anemia

60
Q

What is the difference between cachexia and starvation

A

Cachexia => Lose both fat and muscle, but metabolic rate does not decrease

Decreased metabolic rate in starvation

61
Q

what is the pathogenesis of cancer cachexia

A

TNF, IL1, IL6, and IFNy =>systemic inflammation

  • > anorexia
  • > impaired digestion
  • > metabolic/endocrine changes
62
Q

T/F: cachexia cannot be reversed with extra nutrient support

A

T

63
Q

What is ectopic hormone production?

A

Non-endocrine neoplasms produce hormonally active substances not normally found in tissue

64
Q

Production of parathyroid hormone -like protein by neoplasm is an example of what? And what does it lead to?

A

Edocrinopathy -> ectopic hormone production

Hypercalcemia of malignancy

65
Q

90% of hypercalcemia of malignancy in dogs is due to what type of tumor?

A

Apocrine gland acendocarconoma of the anal sac

66
Q

Hypertrophic osteopathy in cats and dogs is associated with what neoplasm

A

Space-occupying thoracic lesions

Presents clinically with lameness

67
Q

What diagnostic method is faster, cheaper and less invasive then histology

A

Cytologic diagnosis

68
Q

A subset of mesenchymal neoplasm that appear as round cells on cytology

A

Round cell tumors

Shame on your cow, if you didnt get this.

69
Q

What are the round cell tumors ?

A 
Plasma cell tumor
Histiocytoma 
Mast cell tumor 
Lymphoma 
Transmissible venereal tumor
70
Q

How do you decide if your biopsy should be incisional vs excisional ?

A

Incisional - diagnosis might affect surgical plan

Excisional - diagnosis will not affect surgical plan

71
Q

What are the criteria for malignancy

A

Degree of differentiation
Invasion
Mitotic rate
Features of anaplasia

72
Q

What are the features of anaplasia

A 
Pleomorphism 
Anisokaryosis/anisocytosis
Hyperchromasia 
High N:C ratio 
Prominent nuceloli
73
Q

What stain should be used for diagnosis of mast cell tumor

A

Toluidine blue

74
Q

What is Fontana Masson’s stain used for?>

A

Accentuate melanin in amelanotic melanoma

75
Q

What is histopathologic grading used for?

A

Designate now abnormal the cells are

Prognostic factor/indicator to predict behaviour and inform treatment

76
Q

Method that uses dye-labeled antibodies to detect various proteins expressed by a neoplasm

A

Immunohistochemistry

77
Q

An immunohistochemistry that is positive for vimentin means?

A

Mesenchymal cells -> sarcoma

78
Q

An immunohistochemistry that is positive for cytokeratin mean?

A

Epithelial -> carcinoma

79
Q

How can we use clonality assays to determine between hyperplasia and neoplasm

A

High clonality -> neoplastic

Low clonality -> hyperplasia/inflammation

80
Q

What is staging?

A

Indication of extend of tumor growth and spread
Prognostic factor

Uses:

  • size
  • depth of invasion
  • involvement of regional lymph nodes
  • extent of distant metastasis

RUSVM Pathology I (17 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions