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Oncology > Hemangiosarcoma and Mast Cell Tumor > Flashcards

Hemangiosarcoma and Mast Cell Tumor Flashcards

1
Q

What tissue types are sarcomas in general?

A
  • Connective tissue/mesenchymal tumors
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2
Q

How do sarcomas spread?

A

By blood

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3
Q

Tissue origin for HSA

A
  • Vascular endothelial cells (may be of bone marrow origin)
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4
Q

Signalment of HSA

A
  • Large breed dogs - GSD, golden, and labrador retriever overrepresented
  • Older dogs, but can be young
  • Male predominance?
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5
Q

Where can HSA present?

A
  • Anywhere there is blood
  • Spleen, liver, right atrium are typical
  • Kidney, SC tissues/muscle
  • Oral cavity, urinary bladder, pericardium and peritoneum, bone
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6
Q

How does HSA usually present?

A
  • Sudden collapse, weakness, pallor
  • Sudden enlargement of a mass
  • Sudden cardiac tamponade - weakness and arrhythmia
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7
Q

Biologic behavior of HSA

A
  • EXTREMELY aggressive
  • High rate of early development of metastasis
  • Endothelial cells can go anywhere they want
  • 25% have right atrial involvement at diagnosis
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8
Q

Splenic lesions and malignancy rule

A

2/3 are malignant, and of those 2/3 are HSA

  • Evidence of splenic bleeding or rupture makes it a 75% chance of being a hemangiosarcoma
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9
Q

How do you officially make a diagnosis with HSA?

A
  • Histopathology, but you can have a very high degree of suspicion dependent on the clinical picture
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10
Q

Other clinical suspicion for HSA

A
  • Right atrial masses with pericardial hemorrhage
  • Ultrasound appearance of cellular fluid-filled mass anywhere
  • Aspirate for cytology or biopsy yielding only blood
  • Evidence of DIC (elevated coags or D-dimers or FDPs)
  • Plasma troponin 1 concentration high in the pericardial fluid
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11
Q

Plasma troponin 1

A
  • High correlation with hemangiosarcoma

- Not sure if it’s just a correlation with blood

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12
Q

Staging of hemangiosarcoma

A
  • CBC, Chem, UA

- Thoracic Rads are ESSENTIAL

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13
Q

CBC findings of HSA

A
  • Normocytic, normochromic anemia
  • NRBC
  • Fragmented red cells (schistocytes that are HIGHLY suggestive)
  • Neutrophilic leukocytosis, thrombocytopenia (but not horribly low unelss DIC)
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14
Q

Which cell type on blood smear is very suggestive of HSA?

A
  • Schistocytes
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15
Q

Thoracic rad possible findings with HSA

A
  • Chest mets in most cases

- 47% of cardic lesions present are identified

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16
Q

Additional findings for hSA

A
  • Coagulation panel
  • EKG
  • Abdominal ultrasound
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17
Q

What is the best way to identify a cardiac lesion for HSA?

A
  • Cardiac ultrasound

- About 1/4 will have right atrial involvement at outset

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18
Q

Treatment for HSA

A
  • Surgical removal and systemic therapy
  • Really only able to do with spleens and some SC masses
  • Right atrial masses are quite difficult to remove
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19
Q

Chemotherapy - what’s best for HSA?

A
  • Single agent doxorubicin once every 2-3 weeks

- Can do a combination therapy (Doxo + Vincristine + cyclophosphamide)

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20
Q

Biologic therapy for HSA

A

-Liposome encapsulated muramyl tripeptide

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21
Q

Anti-angiogenesis therapy and HSA

A
  • Low dose chemotherapy is best (cyclophosphamide daily, lomustine daily, or chlorambucil daily)
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22
Q

Which anti-angiogenesis agents probably don’t work as well for HSA?

A
  • NSAIDs and Tyrosine kinase inhibitors (although NSAIDs might not be that bad)
  • Minocycline didn’t do anything
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23
Q

Prognosis for HSA in general

A
  • Poor
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24
Q

Prognosis for HSA: surgery alone

A

2-3 months median survival

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25
Q

Prognosis for HSA: surgery + chemotherapy

A
  • 4-6 months (NOT FOR METASTATIC DISEASE)
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26
Q

Prognosis for HSA: Right atrial

  • With doxorubicin, surgery alone, surgery +doxorubicin, radiation
A

Doxorubicin alone: median survival about 4 months

  • Surgery about 4 months with doxorubicin
  • Surgery alone about 1 month
  • Radiation about 2 months
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27
Q

Yunnan Baiyao evidence for helping HSA?

A
  • Limited - seems like it doesn’t help
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28
Q

SC HSA mass treatment

A
  • May benefit from local palliative radiation in addition to chemotherapy (and surgery?)
  • Tend to live longer but the disease still USUALLY metastasizes
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29
Q

WSU Protocol for HSA

A
  • Control local disease (surgery when possible + palliative radiation)
  • Doxorubicin x 4 (chemo)
  • Follow up with metronomic chemotherapy
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30
Q

Survival for WSU protocol

A
  • ~6 months
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31
Q

Who gets cutaneous hemangiosarcoma?

A
  • Light coat color, thinskin dog and cat disease
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32
Q

What likely causes cutaneous hemangiosarcoma?

A
  • Sunlight induce
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33
Q

Prognosis for cutaneous hemangiosarcoma

A
  • If it doesn’t invade into deeper tissues, this is a surgically curable disease
  • 1 cm margins
34
Q

What can Mast cell’s look like?

A
  • ANYTHING!!!! I REPEAT, anything!
35
Q

What is Darier’s sign?

A
  • Tumor disappears

- possible mass that comes and goes could be a mast cell tumor

36
Q

What do mast cell granules contain?

A
  • Histamine
  • Heparin,
  • Other bioactive compounds which can cause systemic signs
37
Q

Paraneoplastic syndromes associated with mast cell tumors

A
  • GI ulceration (vomiting blood)
  • Impaired LOCAL healing
  • Coagulopathy (locally)
  • Hypotensive shock (rare)
  • Urticaria
  • Eosinophilia, basophilia
38
Q

Breeds who get MCT?

A
  • Boxers!
  • Boston Terrier
  • Labrador Retrievers
  • Schnauzers
  • Beagles
  • Pugs
  • Siamese for cats
39
Q

Age for MCT

A
  • Any age in dog, tend to be older cats

- No gender predilection

40
Q

Dog MCT presentation

A
  • Most are external skin masses

- PRIMARY internal tumors are rare

41
Q

Cat MCT presentation

A
  • Equal numbers of external and internal tumors

- Primary symptom is not always a skin mass and MAY be vomiting in a cat

42
Q

Cytology for MCT

A
  • Round cell, often has granules

- Gives you a good idea it is a mast cell tumor so surgery and staging can be planned

43
Q

Histopathology of MCT

A
  • REQUIRED for grading the tumor
  • Don’t forget to submit margins
  • Often just take them out
44
Q

Diagnosis of MCT

A
  • Often start with cytology to give you an idea that it’s a mast cell tumor so that you can take it off with appropriate planning
45
Q

Grading MCT: Pathologists vs Oncologists

A
  • Pathologists prefer a 2 level grading scheme vs 3 levels
  • Not truthful for lowest grade 1 tumors, so oncologists prefer having both systems used and then being able to split the grade 2 tumors additionally into high and low grade grade 2
46
Q

Grade 1 MCT prognosis

A
  • Good
47
Q

Grade 2 MCT prognosis

A

Variable prognosis

48
Q

Grade 3 MCT prognosis

A
  • VERY POOR :(
49
Q

Define a grade 1 MCT

A
  • well differentiated and superficial
50
Q

Define a grade 2 MCT

A

Well to medium differentiation, SQ involvement

51
Q

Define a grade 3 MCT

A
  • Poorly differentiated
52
Q

Mitotic index of MCT - cut off for likelihood to recur or metastasize?

A
  • <5 mitoses/10 HPF is less likely to recur or metastasize

- >5 mitoses/10hpf is more likely to recur or metastasize

53
Q

What are the gold standards for determining prognosis for canine MCT?

A
  • Grade and mitotic index**

- There are other helpful markers too (c-Kit, AgNOR’s, Ki-67)

54
Q

Staging for a grade 1 and lower grade 2 MCT

A
  • Lymph node check and possible imaging
  • CBC/Chem
  • Buffy coat smear
55
Q

Staging for a higher grade 2 and grade 3 MCT

A
  • Lymph node check and possible imaging
  • CBC/Chem
  • Buffy coat smear
  • Abdominal ultrasound +/- spleen and liver aspiration (EVEN IF NORMAL APPEARING)
  • Bone marrow aspirate
56
Q

Staging MCTs

A

0 = one tumor, already excised

I = one tumor

II = one tumor with regional LN involvement

III = multiple dermal tumors, large infiltrating tumors, with or without lymph node involvement

IV = any tumor with distant metastasis or recurrence with metastasis

57
Q

Is LN involvement really bad with MCT?

A
  • No
58
Q

Symptomatic therapy for MCT (not always needed)

A
  • H1 blocker
    (diphenhydramine)
  • H2 blocker (cimetidine, ranitidine, famotidine)
  • Prednisone
59
Q

H1 blocker function in MCT

A
  • Prevent bronchoconstriction, vasodilation
60
Q

H2 blocker function in MCT

A
  • prevent gastric ulceration

- Could give omeprazole too

61
Q

Prednisone function with MCT

A
  • Shrink the tumor prior to surgery
62
Q

General treatment for MCTs

A
  • Surgery
  • Electrochemotherapy
  • Radiation
  • Traditional chemotherapy
63
Q

Surgery for MCTs

A
  • 3 cm margins in ALL directions
64
Q

Electrochemotherapy for MCT - when to use?

A
  • Small low grade tumors
65
Q

Radiation therapy for MCT - when to use?

A
  • Local disease

- Best if minimal disease

66
Q

Traditional chemotherapy for MCT - when to use?

A
  • Used ONLY for high stage/systemic disease (all grade III)

- Minimally effective alone

67
Q

Chemo for canine MCT

A
  • Traditional
  • Prednisone, vinblastine, lomustine (huge)
  • Vinblastine, bred
  • Vinblastine, cyclophosphamide, prednisone
  • Hydroxyurea
68
Q

WSU protocol for canine MCT?

A
  • Vinblastine and lomustine
69
Q

Tyrosine kinase inhibitors for MCTs

A
  • Save for aggressive tumors; about 50% respond for about 2 months
  • There are toxicities - NOT a benign tumor
  • On it for life
70
Q

RTK combination therapy either vinblastine/toceranib or palliative radiation and toceranib for MCT (all grades)?

A
  • Not sure
  • Might be helpful?
  • Might not be helpful?
71
Q

Grade 1 MCT prognosis

A
  • Most cured with surgery
  • Don’t use palladia or chemo with these!
  • can irradiate or use electrochemotherapy when surgery not possible
72
Q

Grade 2 MCT prognosis

A
  • Surgery CAN be curative
  • Often need radiation as follow up
  • Low grade grade 2 electrochemo to follow up
  • Some require systemic therapy (traditional chemo or TK inhibitor)
73
Q

Grade 3 MCT prognosis

A
  • Surgery rarely curative
  • Can irradiate if no confirmed metastasis
  • ALL require systemic therapy
  • Slow progression, not curative
  • In addition to local therapy
  • Best case is surgery, irradiation, and chemotherapy
74
Q

Feline MCT on skin - malignant or benign?

A
  • Usually benign

- Cured with surgery often

75
Q

Feline MCT internally - malignant or benign?

A
  • More aggressive!
76
Q

Two forms of internal feline MCT

A
  • Lymphoreticular

- GI

77
Q

How do cats with internal MCT present?

A
  • Vomiting (often still eating)

- Mass in abdomen, aspirate yields mast cells (solid sheets or pretty normal mast cells)

78
Q

Diagnosis of feline MCTs

A
  • Aspirate of mass in abdomen yields mast cells

- Often circulating mast cells in blood (buffy coat smear on CBC)

79
Q

Treatment for feline internal MCT

A
  • Symptomatic treatment important
  • Corticosteroids, H1, and H2 blockers
  • Splenic form may stop therapy after surgery?
  • Intestinal form may require therapy for life
  • Remove tumor from spleen or intestine
80
Q

TKI and feline internal MCT

A
  • Beneficial but not often necessary
81
Q

Prognosis for feline internal MCT

A
  • Prolonged for splenic (>3 years)
  • Less for GI (11 months)
  • If you can take the spleen out, they often do quite well

Oncology (9 decks)

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