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Veterinary Pathology > Neoplasia > Flashcards

Neoplasia Flashcards

1
Q

Describe what is going on with this lesion

A

diaphragmatic surface of liver

multifocal to coalescing and has a random distribution

variably sized

red

hemangiosarcoma

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2
Q

T/F: All neoplasias (tumors) are metastatic and malignant

A

FALSE

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3
Q

What is neoplasia?

A

derivation from normal tissues, but unresponsive to normal growth controls

benign or malignant

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4
Q

Why should we use caution when using the term cancer?

A

everyone thinks cancer means an automatic death sentence when cancers can be benign

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5
Q

What is the lesion here?

A

pituitary adenoma - benign tumor of glandular cells

Pituitary Pars Intermedia Dysfunction

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6
Q

What are reversible cellular changes examples?

A
  • hypertrophy
  • hyperplasia
  • metaplasia - BUT can LEAD to neoplasia
  • dysplasia
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7
Q

What are irreversible cellular changes examples?

A

anaplasia - can’t even tell cell line (as observed in undifferentiated tumors)

  • cellular atypia, poorly differentiated, more “primitive”
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8
Q

T/F: These cells underwent reversible cellular changes

A

TRUE - have open nuclei

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9
Q

T/F: These cells underwent reversible cellular changes

A

FALSE - does not look like others - irreversible

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10
Q

Which tumors are easier to treat - well-differentiated or poorly differentiated?

A

well-differentiated!

Well-differentiated tumors are easier to treat because they behave more like normal tissue. They grow slowly, are less invasive, and respond better to conventional therapies. Their localized and predictable nature also makes surgical removal and other treatments more effective, giving patients a better prognosis and fewer complications compared to more aggressive, poorly differentiated tumors.

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11
Q

What are the 2 neoplastic cell lineages?

A

mesenchymal cells
- round cells

epithelial cells

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12
Q

What are round cells?

A

type of mesenchymal cell

migrate by themselves - lymphocytes, plasma cells, macrophages

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13
Q

List the types of round cells

A

lymphocytes
plasma cells
macrophages
etc

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14
Q

What do you use for a benign epithelial cell type?

A

“oma”

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15
Q

What do you use for a malignant epithelial cell type?

A

“carcinoma”

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16
Q

What is an adenocarcinoma?

A

malignant tumor of epithelial cells

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17
Q

What is the benign and malignant terminology for mesenchymal cells?

A

benign: “oma”

malignant: “sarcoma”

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18
Q

What is a benign tumor of the cartilage?

A

chondroma

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19
Q

What is a malignant tumor of adipocytes?

A

liposarcoma

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20
Q

What are round cell tumor examples?

A

T and B lymphocytes

mast cells

histiocytes - macrophages

transmissible venereal tumors

plasma cells

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21
Q

A malignant tumor of histiocytes is called a _______. It is from the ______ lineage

A

histiocytic sarcoma

round cells - mesenchymal

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22
Q

T/F: Lymphoma is benign

A

FALSE - malignant
“lymphosarcoma”

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23
Q

What are transmissible venereal tumors?

A

thought to arise from genetic alteration of canine histiocytes

chromosomal abnormalities

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24
Q

What are 3 outcomes of transmissible venereal tumors?

A
  1. spontaneous regression within 6 months
  2. indolent local growth
  3. very rarely progressive growth with metastasis
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25
Q

What round cells have a grade system? 1-2, 1-3

A

mast cells

3 means bad

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26
Q

What is the Tasmanian Devil Facial Tumor?

A

transmissible tumor

bite wounds

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27
Q

What are mixed tumors?

A

believed to arise from single pluripotent or totipotent stem cell

capable of differentiating into a variety of mature cell types

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28
Q

What is a mixed mammary tumor?

A

variable mixture of neoplastic epithelial or glandular elements

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29
Q

How do dogs and cats differ regarding mixed mammary tumors?

A

dogs: benign

cats: malignant

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30
Q

What is a teratoma?

A

mixed tumor

arise from totipotent germ cells

  • usually all 3 embryonic cell lines are expressed in the neoplasm
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31
Q

What are the characteristics of neoplasias?

A

benign
malignant
metastatic

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32
Q

What does benign mean?

A

unregulated neoplastic growth, but cells look like they’re supposed to (well-differentiated)

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33
Q

Do benign cells invade surrounding tissue? Why or why not?

A

No, because they are well-demarcated, +/- encapsulated

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34
Q

T/F: Benign tumors can evolve to become malignant, but not usually metastatic

A

TRUE

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35
Q

How do benign tumors interact with adjacent tissues?

A

expansile, compress adjacent tissues

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36
Q

Benign tumors are [fast/slow growing], and malignant tumors are [fast/slow growing]

A

benign: slow

malignant: fast

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37
Q

Describe the properties of malignant tumors

A

INFILTRATIVE

poorly demarcated, unencapsulated

more likely to become metastatic’ - cells can become poorly differentiated

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38
Q

T/F: You should always use multiple criteria to determine benign vs malignant

A

TRUE

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39
Q

How can you determine malignancy - cellular morphology-wise?

A
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40
Q

How many fields should you look at when counting mitoses?

A

400X (40X lens * 10X ocular piece)
7-10 fields

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41
Q

Which tumors would theoretically be easier to remove and why?

A

benign - because well-demarcated and encapsulated

malignant is infiltrative and harder to remove

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42
Q

What are some tumor-like masses that LOOK neoplastic but aren’t?

A

hamartoma
choriostoma

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43
Q

What is a hamartoma?

A

a lot more present that normal mature tissues/components
- collagenous hamartoma

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44
Q

Biopsy revealed this was not neoplastic. What could it be instead?

A

hamartoma

45
Q

What is a choriostoma?

A

“normal” tissue in an abnormal location

  • “ectopic”
46
Q

What is this an example of?

A

hamartoma - thick part is all cartilage

47
Q

What is this an example of?

A

choriosotma - corneal dermoid

cornea just like the skin so can get haired skin - maybe cause blepharospasm or discharge

48
Q

Where are the checkpoints in the cell cycle?

A

between G1 and S (DNA synthesis stage)

between G2 and M

49
Q

What tumor suppressor gene(s) is/are in the checkpoint between G1 and S?

A

retinoblastoma
p53

50
Q

What tumor suppressor gene(s) is/are in the checkpoint between G2 and M?

A

p53

51
Q

What are the types of tissues regarding cellular division?

A

labile
stable
permanent

52
Q

What are labile tissues? Give an example

A

repeated division

enterocytes

53
Q

What are stable tissues? Give an example

A

“quiet” but can divide

fibroblasts

54
Q

What are permanent tissues? Give an example

A

non-dividing

neuron

55
Q

What are tumor suppressor genes? Give examples

A

genes that control the cell cycle, apoptosis, AND repair

p53, retinoblastoma

56
Q

What is p53?

A

target gene 21
huge player in apoptosis
“guardian of the genome”

checkpoint at G1—>S and G2—>M

57
Q

What is retinoblastoma?

A

inactive gene allows for cell to proceed through G1/S phase

58
Q

Explain how p53 is so important

A

arrests cell cycle: gives time for cell to repair DNA before dividing

if unable to repair, it will activate BCL2-associated X protein (BAX)
- pro-apoptotic molecule

“guardian of the genome”

59
Q

How can tumor cells evade p53?

A

tumor cells lack expression of p53 (or inactive p53’s function), which allows the cell to replicate potentially damaged DNA and resist apoptosis

60
Q

What does apoptosis occur from?

A

withdrawal of growth factors

binding of death receptors (Fas ligand and TNF-alpha)

hypoxia

DNA damage (triggered by p53)

T lymphocytes and NK stimulation

61
Q

What are telomeres?

A

end of chromosomes as buffer

every replication shortens telomeres - eventually are too short and will trigger cell for apoptosis

62
Q

How does neoplasia affect telomeres?

A

cells are able to produce telomerase which replicates telomere ends, essentially producing death-defying cells that resist apoptosis

63
Q

What is latency?

A

time before a tumor is clinically detectable

64
Q

What is the smallest clinically detectable size of a tumor? What is the impact of that?

A

1 cm!

may seem small, but these tumor cells have already divided ~30 times!

65
Q

How many doubling cycles are required for a tumor to go from 1g to 1kg?

A

only 10

66
Q

What are the steps of tumor development (multistage carcinogenesis)?

A

initiation
promotion
progression

67
Q

What is initiation - a step of tumor development (multistage carcinogenesis)?

A

DNA is damaged, but cells are “quiet”
- irreversible changes in DNA

damage by free radicals

68
Q

What is promotion - a step of tumor development (multistage carcinogenesis)?

A

not mutagenic, but cause changes in gene expression giving those “initiated” cells growth advantages over non-initiated cells

these effects can be reversible

69
Q

What is progression - a step of tumor development (multistage carcinogenesis)?

A

benign —> malignant —> metastatic

can start migrating down BM to dermis

squamous cell carcinoma: BM is breached

70
Q

What stage of tumor development is this?

A

promotion

71
Q

What are tumor stromal interactions?

A

humoral cells & the stroma in which they are embedded interact in a variety of ways that serve to modify the growth and behavior of both elements

tumor stroma may both enhance and limit tumor development and spread

72
Q

What is tumor angiogenesis? It produces _______

A

can secrete growth factors

tumor production of:
- pro-angiogenic: VEGF

  • anti-angiogenic: thrombospondin
73
Q

What are the mechanisms of metastases?

A

adhesion

invasion

migration

formation of emboli

74
Q

What happens during adhesion - mechanism of metastases?

A

detach, breach BM, enter ECM

75
Q

What happens during invasion - mechanism of metastases?

A

ECM breakdown via matrix metalloproteinases (MMPs)

76
Q

What happens during migration - mechanism of metastases?

A

growth factors

77
Q

What are pathways for metastasis?

A

transcoelomic

lymphatic

hematogenous

78
Q

What is transcoelomic metastasis?

A
  • multiple tumor masses throughout the abdomen
  • organ surfaces: transitional cell carcinomas, mesotheliomas, pancreatic & ovarian adenocarcinomas
79
Q

What is lymphatic metastasis?

A

regional LN (now metastatic)

  • mostly carcinomas use this route
80
Q

What is carcinomatosis?

A

a condition characterized by multiple tumor masses throughout the abdomen

81
Q

What is hematogenous metastasis?

A

veins > arteries (thickness)

mostly sarcomas

82
Q

What kind of metastasis?

a. transcoelomic
b. lymphatic
c. hematogenous

A

a. transcoelomic

83
Q

What kind of metastasis?

a. transcoelomic
b. lymphatic
c. hematogenous

A

c. hematogenous

84
Q

How do tumor cells inhibit/manipulate immune responses?

A
  • altered major histocompatibility complex expression
  • antigen masking
  • tolerance
  • immunosuppression
85
Q

Explain how having an altered major histocompatibility complex expression regarding tumors inhibits/manipulates immune responses

A

down regulates MHC I and MHC II expression, altered p53

  • no MHC II? No Th (CD4) cell response
86
Q

Explain how antigen masking regarding tumors inhibits/manipulates immune responses

A

no expression of tumor cell antigen on cell surface - mimics other cell-surface antigens & plays it off as their own

87
Q

Explain how tolerance regarding tumors inhibits/manipulates immune responses

A

“self antigens” - identified as self so will not attack

88
Q

Explain how immunosuppression regarding tumors inhibits/manipulates immune responses

A

TGF-alpha production by tumor cells - inhibits growth and function of macrophages and lymphocytes

89
Q

What are paraneoplastic effects?

A

effects due to PRODUCTS of neoplastic cells - not due to tumor size, invasion, etc

90
Q

What are examples of paraneoplastic effects?

A
  • hypercalcemia of malignancy
  • hypoglycemia
  • polycythemia
  • hypertrophic osteopathy
  • cachexia
91
Q

How does an animal get hypercalcemia of malignancy?

A

due to anal gland adenocarcinomas (AGASACA), lymphomas, multiple myeloma

92
Q

What is cachexia?

A

loss of muscle AND fat (different from starvation)

93
Q

How does an animal get cachexia?

A

hormones and inflammatory cytokines

  • prostaglandins
    -leading to anorexia and debilitation
94
Q

What happens with hypertrophy osteopathy - paraneoplastic effects?

A

associated with thoracic tumors

see thickening of long bones - do a radiograph of the chest!

95
Q

Look at this table regarding paraneoplastic syndromes in animals

A
96
Q

What is hypercalcemia of malignancy?

A

hyperparathyroid or PTHrp (increase in calcium)

97
Q

What are some disease with hypercalcemia of malignancy?

A

anal gland adenocarcinoma ( apocrine gland anal sac adenocarcinoma)

lymphoma

multiple myeloma

98
Q

What is happening here?

A

metastatic calcification in the lung, hypercalcemia

99
Q

What is the difference between dystrophic vs. metastatic calcification (mineralization)?

A

dystrophic: localized to areas of tissue damage and occurs without systemic calcium disturbance, NO HYPERCALCEMIA

metastatic: the result of systemic hypercalcemia affecting otherwise healthy tissues.

100
Q

[Dystrophic/Metastatic] calcification has the HARDIONS mneumonic

A

metastatic - because it causes hypercalcemia

101
Q

Does cancer have an etiologic agent?

A

sometimes - may be because of an oncogenic virus like FIV, FeLV, BLV, etc

102
Q

What is the general rule of thumb for biopsies, especially neoplasia?

A

INTERFACE

we want to see the tumor cells, but also what they are doing to the surrounding tumor

103
Q

T/F: This was good sampling technique. Why or why not?

A

TRUE - gets both tumor cells and surrounding tissue

104
Q

T/F: This was good sampling technique (red circle). Why or why not?

A

FALSE - doesn’t show what it’s doing to adjacent tissue

105
Q

What is the difference between incisional vs. excision biopsies?

A

incisional: give me a diagnosis, point is not to remove everything
- be sure to get interface

excisional: did I get it all?

106
Q

What is tumor grading

A

how similar/dissimilar neoplastic cells are to normal counterparts

grade provides indication about biologic behavior

grades 1-3

107
Q

What is tumor staging?

A

indication of the extent of tumor growth and spread in an animal

108
Q

What is the TNM system and what is its function?

A

T: based on size of primary tumor
N: degree of lymph node involvement
M: extent of metastasis

provides a standard measurement by which the natural course of disease and impact of treatment modalities can be compared

Veterinary Pathology (11 decks)

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