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Small Animal Medicine I > Final Exam-Oncology > Flashcards

Final Exam-Oncology Flashcards

1
Q

What are the cancer statistic for dogs and cats?

A

1 out f 3 dogs and 1 out of 4 cats get cancer

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2
Q

What breeds of dog have a lifetime risk of 50% in developing cancer in their lifetime?

A

Golden retrievers

Boxers

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3
Q

What types of cancers do dogs in urban areas have a higher risks of having?

A

Tonsillar

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4
Q

What increases the risk of hemangiosarcoma in dogs?

A

Radiation

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5
Q

What type of cancer increases in dogs you have been exposed to topical insecticides and dips?

A

Bladder

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6
Q

How can bladder cancer be prevented?

A

Eating vegetables, especially carrots to prevent transitional cell carcinoma

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7
Q

What are the three steps of carcinogenesis? Which are reversible?

A
  1. Initiation - reversible
  2. Promotion
  3. Progression
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8
Q

What are the 6 hallmarks of cancer?

A
  1. Sustained proliferative signaling
  2. Resisting cell death
  3. Inducing angiogenesis
  4. Enabling replicative immortality
  5. Activating invasion and metastasis
  6. Evading growth suppressors
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9
Q

What occurs during the initiation stage of carcinogenesis

A

The carcinogen interacts with the cellular DNA and causes damage.

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10
Q

Why are initiated cells not cancer cells yet?

A

There is no autonomal growth ability

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11
Q

What occurs during the promotion stage of carcinogenesis?

A

Clonal expansion of initiated cells by mutated genes. This action alone ( independent of initiation) can not cause tumor development.

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12
Q

What occurs during the progression stage of carcinogenesis?

A

Tumor obtains ability to grow and invade tissue and metastasis to distant locations with increased genetic instability and nuclear alterations of the cells.

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13
Q

What occurs during sustained proliferative signaling in cancer cells?

A

Cancer cells produce growth factor ligands resulting in autocrine proliferation and paracrine signaling to the stroma around the cell and to other cells.

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14
Q

How can cancer cells die?

A
  1. Apoptosis
  2. Necrosis
  3. Autophagy
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15
Q

Which way in which cancer cells die requires ATP?

A

Apoptosis

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16
Q

What insult must occur in order for their to be apoptosis, necrosis or autophagy of a cancer cell?

A

Apoptosis: Chemotherapy, radiology, withdrawal of growth factors, death signals
Necrosis: Ischemia-reprefusion
Autophagy: Starvation

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17
Q

Which genetic mutation causes most cancer?

A

P53 mutation

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18
Q

What does P53 do for cells?

A

It can recognize damaged DNA , repair, or signal for apoptosis

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19
Q

When is angiogenesis not suppressed?

A
  1. Female cycle
  2. Inflammation
  3. Wound healing
  4. When cancer cells are located 2 mm or more from a vessel become hypoxic and release mediators
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20
Q

What is angiogenic switch-shift?

A

Activators of angiogenesis turn the switch on, while inhibitors, turn it off. There is a balance between these, but in cancer it switches to on.

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21
Q

What is the difference between angiogenic vessels and primary vessels?

A

They are tortuous, dilated, irregularly shaped. Blood pressure may be slow/intermittent, and lead to inefficient delivery of drugs/radiation (makes it harder to treat).

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22
Q

What are some drugs that can be used to treat cancer via inhibiting angiogenesis?

A
  1. Bevacizumab

2. Palladia

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23
Q

What is the angiogenesis-metronomic therapy?

A

Administration of low dose chemotherapy and anti-inflammatory COX2 on a daily or every other day dose

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24
Q

What is angiogenesis-metronomic therapy effective against?

A
  1. Circulating progenitor cells

2. Circulating endothelial cells

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25
Q

What are some benefits to angiogenesis-metronomic therapy?

A
  1. Sensitize endothelium to chemotherapy
  2. Reduce T-cell regulation at malignant site
  3. Normalizes newly formed vessels
  4. Works on tumors resistant to chemotherapy
  5. Reduce production of growth factors
  6. Low toxicity
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26
Q

Why do most patients die of cancer?

A

The results of metastases via the lymphatics and/or hematogenous routes

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27
Q

What are the two theories of activation of invasion and metastasis of cancer cells?

A
  1. Seed and soil

2. Hemodynamic consideration

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28
Q

How does the seed and soil theory of cancer metastasis work?

A

An organ will have matching receptors to tumor cells and will host the tumor

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29
Q

How does the hemodynamic consideration theory of cancer metastasis work?

A

Cancer cells get lodged at capillary beds of rich organs like the liver and lungs where they thrive

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30
Q

What are the phases of metastasis?

A
  1. Primary tumor
  2. Vascularization
  3. Detachment
  4. Intravasation
  5. Circulating tumour cell
  6. Adhesion to blood vessel wall
  7. Extravasation
  8. Growth of secondary tumor
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31
Q

In what cells does lymphoma form in and in what organs does it arise?

A 
Lymphoreticular cells 
Organs:
1. Lymph nodes
2. Spleen
3. Bone Marrow
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32
Q

What is the signalment for a dog with lymphoma?

A

6-9 year old Boxer, bull mastiff, basset hound, St. Barnard, Bulldog and Airdale

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33
Q

What are the etiologies of lymphoma?

A
  1. Genetic: Gain or loss of chromosomes along with P53 mutation and N-ras
  2. Infectious factors: Helicobacter
  3. Environmental factors: 2,4 D, magnetic fields
  4. Immunosuppression
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34
Q

What are the anatomic classifications of canine lymphoma from most common to least common?

A
  1. Multi-centric
  2. Gastrointestinal
  3. Mediastinal
  4. Cutaneous
  5. Hepatosplenic
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35
Q

What are the ways in which canine lymphoma can be classified?

A
  1. Anatomic site
  2. Extranodal vs. Nodal
  3. Histologic: Who system
  4. Grade
  5. Immunophenotype
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36
Q

What are the grades of lymphoma? What is more common?

A

Low grade: small cells

Intermediate to high grade: Large cells and lymphoblasts ( more common)

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37
Q

What are the different immunophentotypes of lymphoma? Why are these important? Which is most common?

A
  1. B cell (more common)
  2. T cell

Determine how patient will response to therapy and survive

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38
Q

What can T cell lymphomas in dogs be associated with?

A
  1. Hypercalcemia

2. Decreased response and survival time

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39
Q

What are the clinical signs of multicentric LSA in dogs?

A
  1. Lymphadenopathy
  2. Hepatosplenomegally
  3. Weight loss, anorexia, lethargy, fever if patient is in substage B
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40
Q

Which type of lymphoma is most likely to result in a patient with substage B?

A

T cell LSA

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41
Q

What are some differentials for lymphadenopathy in dogs?

A
  1. Immune mediated disease
  2. Disseminated infection from virus, bacteria, fungus
  3. Other forms of neoplasia
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42
Q

What are the clinical signs of GI lymphoma in dogs?

A

Weight loss and diarrhea from malabsorption

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43
Q

What are the clinical signs of mediastinal lymphoma in dogs?

A
  1. Regurgitation
  2. Hypercalcemia
  3. PU/PD
  4. Pre-caval syndrome
  5. Dyspnea
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44
Q

What is a paraneoplastic syndrome?

A

Any syndrome associated with cancer but not due to the tumor directly

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45
Q

What are the clinical signs/diagnostic indicators of a dog with paraneoplastic syndrome?

A
  1. Anemia (most common)
  2. Fever
  3. Thrombocytopenia
  4. Hypercalcemia ( T cell LSA)
  5. Monoclonal gammopathies (B cell LSA)
  6. Cachexia
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46
Q

What types of neoplasia can cause hypercalcemia? Why is it important to check for neoplasia if a dog is hyperalcemic?

A
  1. Anal sac carcinomas
  2. Thyomas
  3. T cell LSA ( 10-35%)

2/3 case of hypercalcemic dogs have neoplasia

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47
Q

What is the mechanism behind hypercalcemia with neoplasia? Is this the only mechanism?

A

The tumor increases production of PTHrp

No

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48
Q

How is LSA in dogs diagnosed?

A
  1. Fine needle aspirate with cytology and flow cytometry ( most common)
  2. Biopsy
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49
Q

Why would we do a biopsy in a dog with suspected LSA?

A

If the FNA can’t confirm the diagnosis, the grade the tumor, and give it a subclassification.

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50
Q

Which lymph node should be avoided when doing a biopsy of LSA? Why?

A

Mandibular
It drains the mouth and prevents dental disease, plus has a high chance of masking diagnosis due to high cell reactivity.

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51
Q

How is LSA in dogs staged?

A
  1. CBC/chem
  2. Thoracic rads
  3. Bone marrow aspirate

Staged from I to V with a and b subclassifications

52
Q

Stage I LSA in dogs

A

Single node or lymphoid tissue in single organ

53
Q

Stage II LSA in dogs

A

Multiple lymph nodes in regional area

54
Q

Stage III LSA in dogs

A

Generalized lymph node involvement

55
Q

Stage IV LSA in dogs

A

Liver and/or spleen involvement

56
Q

Stage V LSA in dogs

A

Blood and bone marrow and/or other organ system involvement

57
Q

What are the substages of LSA in dogs?

A

A: Without systemic signs
B: With systemic signs

58
Q

What are the different types of molecular diagnostic techniques that can be used to help diagnosed LSA?

A
  1. PARR: PCR for antigen receptor rearrangement
  2. IHC: Immunohistochemistry
  3. ICC: Immunocytochemistry
  4. Flow Cytometry
59
Q

What is PARR measuring with LSA and what can it tell us about the tumor?

A

Clonality, the hallmark of hematopoietic malignancies. Can tells us if it is lymphoid hyperplasia or lymphoma, B or T cell immunophenotype?

60
Q

What is the difference between ICC and IHC?

A

ICC is done on cytology slides for LSA and IHC is done on histopathology slides for LSA

61
Q

How does ICC and IHC work?

A

A slide from a LSA cytology or biopsy is measured for markers that tell use if the cells are B or T cells based off of an antigen to antibody reaction.

62
Q

What are the markers to identify B lymphocytes with ICC/IHC? Markers for T cells?

A

CD79a and CD 20

CD3

63
Q

What is the best diagnostic test to use with LSA?

A

Flow cytometry, as it evaluates live cells labeled with antibodies

64
Q

What can flow cytommetry tell us about LSA?

A

If the cell population is homogenous or heterogenous and what size the cells are, in addition to the immunophenotype ( it is prognostically significant_

65
Q

What are the prognostic factors of LSA in dogs?

A
  1. WHO clinical stage ( I-V)
  2. WHO clinical substage ( a or b)
  3. Anatomic location
  4. Prolonged steroid treatment before diagnosis
  5. Histologic grade: high grade responds to treatment better
  6. Immunophenotype: T cell worse
  7. Flow cytometry: large cells/ low level MHC worse
  8. Chemotherapy-induced hematologic toxicity
66
Q

Which anatomical locations of LSA are the worse prognostically?

A
  1. Leukemic
  2. Diffuse Cutaneous
  3. Alimentary
67
Q

What is associated with a prolonged first remissions of LSA in a canine patient?

A

Moderate neutropenia from chemotherapy induced hematologic toxicity

68
Q

How is canine LSA treated?

A
  1. Chemotherapy is the standard of care
  2. Prednisolone
  3. Radiation
  4. Surgery
69
Q

If LSA in dog is not treated, how long will the patient survive?

A

4-6 weeks

70
Q

What can prednisone do for a LSA patient?

A

It can slow the disease process and improve quality of life

71
Q

What is complete remission?

A

Disappearance of all signs and symptoms of cancer, although cancer may still be in the body

72
Q

What is the multi-agent chemotherapy protocol for LSA treatment in dogs? How successful is it?

A 
CHOP
C: cyclophosphamide 
H: Doxorubicin (hydroxydaunorubicin)
O: Vincristine (Oncovin) 
P: Prenisone

80-95% remission and survival times of 10-14 months

73
Q

At what point in time after starting chop, do you determine is LSA patient is in complete remission

A

Week 19, where all therapy stops and months re-evaluations are instituted

74
Q

Which drug would you use alone in treating LSA in dogs?

A

Doxorubicin IV every three weeks for 5 treatments and combine with prednisone for last 4 weeks

75
Q

How would you monitor LSA patients who are on chemotherapy?

A
  1. Physical Exam: Weight, body temperature and lymph node measurements
  2. CBC: Cytopenias
76
Q

Why is rescue chemotherapy typically used in LSA?

A

The majority of dogs that achieve a remission will eventually relapse

77
Q

What is the protocol for an LSA patient that relapsed after their first CHOP treatment?

A

DO another CHOP treatment and make sure the cumulative dose of doxorubicin doesn’t go over the limit. If this doesn’t work, give CCNU (lomustine) and L-asparaginase (Elspar)

78
Q

Why is radiation therapy so successful with LSA? What consideration should be taken into account?

A 
It is very sensitive to radiation and can work locally, regionally, and whole body. 
Considerations: 
1. Palliations vs. curative intent 
2. Cost 
3. Length of treatment
79
Q

How is cutaneous lymphoma in dogs treated?

A
  1. Treat underlying infection
  2. CCNU + steroids
  3. CHOP at failure
  4. Regional/whole body radiation
80
Q

How has feline lymphoma changed over the year and why?

A

Lymphoma has been associated with FeLV and before the vaccine, 70% of cats with lymphoma had FeLV, were young and had the mediastinal, multicentric or spinal forms. Since the vaccine, only 25% of cats with lymphoma have FeLV, they are older, and the most common form is GI.

81
Q

What are the etiology/risk factors of feline LSA?

A
  1. FelV with subgroup B (Direct)
  2. FIV (Indirect)
  3. 2nd hand tobacco smoke exposure
  4. Immunosuppression (renal transplants with long term cyclosporine administration)
  5. Chronic IBD
82
Q

How is feline LSA classified?

A
  1. Anatomic location
  2. Histologic criteria
  3. Immunophenotype
83
Q

What are the anatomical classifications of feline LSA from most to least common?

A
  1. Alimentary/GI
  2. Mediastinal
  3. Nodal
  4. Extra-nodal
84
Q

Which part of the body is feline lymphoma most likely to invade?

A

Small intestine

85
Q

What is the most common tumor in the GI tract of cats and the most common form of LSA in cats?

A

Alimentary/GI lymphoma

86
Q

Which lymph nodes are usually affected by mediastinal feline LSA? Which immunophenotype is most common?

A

Thymus, mediastinal and sternal lymph nodes

T- cell

87
Q

Which form of feline LSA is most commonly associated with being FeLV positive?

A

Mediastinal

88
Q

What is the relative frequency, age, B/T cell, FeLV association and prognosis with small cell/low grade GI Feline LSA?

A

It is common, in age 13 , more T cell, rare to be associated with FeLV, and a good prognosis

89
Q

What is the relative frequency, age, B/T cell, FeLV association and prognosis with large cell/high grade GI Feline LSA?

A

It is in moderate frequency, at age 10, more B cell, rare to be associated with FeLV, and a poor prognosis

90
Q

What is the relative frequency, age, B/T cell, FeLV association and prognosis with feline mediastinal LSA?

A

It is uncommon, age 2-4, more T cell, common to be associated with FeLV. and a poor to fair prognosis

91
Q

What is the relative frequency, age, B/T cell, FeLV association and prognosis with feline nasal (extranodal) LSA?

A

It is uncommon, occur at 9.5 years, more B cell, rare to be associated with FeLV and has a good prognosis

92
Q

What is the relative frequency, age, B/T cell, FeLV association and prognosis with feline peripheral nodal LSA?

A

It is uncommon, age at 7, equal T and B cell, uncommon to be associated with FelV, and has a poor to fair prognosis

93
Q

What are the clinical signs of feline low grade small cell alimentary LSA?

A

Weight loss
Vomiting/Diarrea
Anorexia
Abnormal abdominal palpation

94
Q

What are the clinical signs of feline lymphoblastic high grade alimentary LSA?

A

The same as low grade small cell LSA except the sings progress more rapidly and more likely to present with palpable abdominal mass

95
Q

What are the clinical signs of feline mediastinal LSA?

A

Dyspnea
Tachypnea
Dull heart/lung sounds
Pleural effusion

96
Q

What are the clinical signs of feline nodal LSA?

A

Lethargy and decreased appetite unless hodgkin’s like ( asymptomatic)

97
Q

What are the clinical signs of feline nasal LSA?

A

Nasal discharge
Epistaxis
Sneezing
Upper respiratory noise

98
Q

How is feline LSA diagnosed?

A

FNA alone is not as helpful as in the dog and usually require U/S, CT, tissue for histopathology and the use of PARR, IHC, ICC, and flow cytometry.

99
Q

What specifically is needed to diagnose large cell, high grade GI LSA in cats?

A
  1. PE
  2. Abdominal rads and ultrasound
  3. cytologic/histologic evaluation of mass
  4. Enlarged lymph nodes

Less complicated to diagnosed than small cell, low grade GI LSA

100
Q

Why is it difficult to diagnose small cell, low grade GI LSA in cats?

A

It has a similar clinical presentation to IBD and GI thickening may be mild and not appreciable on palpation due to no mass-effect

101
Q

What is specifically needed to diagnosed small cell, low grade GI LSA in cats?

A
  1. Ultrasound
  2. Tissue for histopath
  3. Immunophenotypic tests ( IHC, ICC, flow cytometry)
102
Q

What will be seen on ultrasound in feline GI LSA?

A

Thickening of muscularis propria and lymphadenopathy

103
Q

What type of biopsy should you obtain for feline GI LSA diagnosis for histopath?

A

Full thickness as the location of the disease may only located in certain layers

104
Q

How can you differentiate feline GI lymphoma from IBD in the small intestine?

A

If on histopath there is inflammation, treat it and if it does not respond, do immunohistochemistry and it that stiil is not definitive, do PARR (PCR). PARR is the last step.

105
Q

A cat has a stage I LSA, what does that mean?

A

Single extra nodal tumor or a single nodal tumor

106
Q

A cat has a single extra nodal tumor with a regional lymph node LSA, what stage is this?

A

II

107
Q

A cat has a resectable primary GI tumor with mesenteric node involvement, what stage is this?

A

II

108
Q

A cat with LSA has two or more nodal areas on one side of the diaphragm affected, what stage is this?

A

II

109
Q

If a cat with LSA has two single tumors on opposite sides of the diaphragm, what stage is this?

A

III

110
Q

If a cat has a paraspinal or epidural tumor with LSA, what stage is this?

A

III

111
Q

If a cat with LSA has primary unresectable intrabdominal neoplasia, what stage is this?

A

III

112
Q

What is the difference between stage IV and V with feline lymphoma?

A

Stage V involves the bone marrow and/or CNS along with the liver and spleen while stage IV only involves the liver and/or spleen

113
Q

When do you need to stage a LSA tumor in a cat?

A
  1. If you are trying to decide between surgery/radiation (locoregional) or chemotherapy (systemic)
  2. Prognostic information for owner
  3. Required for a clinical trial
114
Q

What diagnostic tests need to be done in order to stage feline LSA?

A
  1. Bone marrow aspirate/biopsy
  2. Peripheral lymph node cytology
  3. Thoracic radiographs
  4. Abdominal ultrasound
115
Q

What do we base our treatment off of with feline LSA?

A

Whether the patient as low grade or high grade LSA

116
Q

What is the treatment for high grade feline LSA?

A

Similiar to the treatment in dogs…CHOP or COP( don;t use doxorubicin) protocol
with rescue therapy of CCNU, elspar and prednisolone ( not prednisone)

117
Q

How would you treat a cat with low grade, small cell LSA? How effective is this treatment and how long do they typically survive?

A

Prednisolone and Chlorambucil (Leukeran)

90-95% response rate
2 year survival

118
Q

How is feline nodal LSA treated?

A

CHOP or COP if high grade
Chlorambucil/pred combo with low grade
Surgery/radiation with hodgkin’s like

119
Q

What are the good prognostic factors for feline LSA?

A
  1. Complete response/remission with therapy
  2. Negative FeLV status
  3. Early clinical stage
  4. Grade
  5. Not immunophenotyped alone
120
Q

What is the most common cutaneous tumor in dogs?

A

Mast cell tumors

121
Q

What breeds are predisposed to the development of mast cell tumors?

A

Boxers, boston terriers, labradors, pugs, bulldogs, mixed

122
Q

What do mast cell tumors look like and behave like?

A

Anything and have a wide range of biologic behavior

123
Q

What is the most clinical presentation of mast cell tumors?

A

Cutaneous or subcutaneous on the trunk or limbs that comes and goes or appeared overnight with redness, swelling, and pain. A darier’s sign, vomiting, diarrhea, fever, and collapse can occur.

124
Q

What are the two forms of a mast cell tumors?

A
  1. Visceral form

2. Primary GI

125
Q

What is receptor tyrosine kinase (RTK) KIT ?

A

RTK’s conveys growth factor signals from outside the mast cell to the inside and c-kit is a proto oncogene that encodes the KIT. A mast cell tumor may occur because a stem cell factor bins to the KIT and promotes proliferation, differentiation and maturation of the mast cells.

Small Animal Medicine I (2 decks)

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