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122 Cards in this Set
- Front
- Back
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What are the two main questions that should be answered before addressing therapy in oncology?
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- What is is? - infection, inflammation, neoplasia
- Has it spread? local, regional, systemic |
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What is the difference between tumor grade and tumor stage?
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- Grade: histological description linked to prognosis
- Stage: systemic extent of tumor linked to treatment, extent of disease |
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Compare and contrast cytology vs. histopathology.
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- Cytology is performed via FNA and is important for tumor staging to determine the spread of a neoplasia
- Histopathology involves the staining of tissue sections to study the manifestation of disease - tumor grade? |
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What is the role of surgery in the treatment of tumors?
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- offers potential cure for localized disease and is also used in combination therapy for many tumor types
- used as debulking - increased efficacy of chemotherapy - or curative - needs to be used aggressively with wide margins - first surgery has the best chance to cure |
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What tissues are affected by acute and chronic side effects of radiation therapy?
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- acute: skin
- chronic: bone, retina, vasculature, CNS |
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What is the difference between specific and non-specific immunotherapy?
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- specific: target tumor specific antigens, but none are expressed solely for tumors. they are overexpressed such as MOAB 231 for canine lymphoma.
- non-specific: stimulates the entire immune system and increases the activity of T cells and phagocytes. proxicam (NSAID) |
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What is the point of a FNA?
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- answer how and where it has spread
- to perform cytology and provide an idea as to the type of lesion (infection, inflammation, tumor) - FNA is important in staging to assess how far along and treatment - systemic extent of the disease |
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What is the point of a biopsy?
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- most important diagnostic test
- tumor grade is evaluated - histologic decription suggestive of prognosis |
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How does palliative RT differ from curative RT?
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- palliative - given in large fractions once a week for 3-6 weeks
- curative - given in small daily fractions for 3 to 4 weeks - side effects occur more commonly with curative RT, acute and chronic |
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What the hell are tyrosine kinase receptor antagonists?
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- block signal transduction within cancer cells, which is critical to their well-being
- Palladia |
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Name some ddx for oral tumors
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- malignant oral tumor -> melanoma, squamous cell carcinoma, fibrosarcoma
- benign tumor -> epulis - melanoma is most common in dogs (11-12 yrs), then SCC (8-10) - SCC most common in cats (10-12) |
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What lymph node is the site of most oral metastasies?
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mandibular - 55%
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What likely canine oral tumors have a high metastatic rate? low?
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high: melanoma and tonsillar SCC
low: FSA and non-tonsillar SCC |
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What likely canine oral tumors are locally aggressive? locally invasice?
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aggressive: melanoma, SCC (tonsillar and non)
invasive: FSA |
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What canine oral tumors are likely to hit the regional LNs? lungs? bony invasion?
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LNs: melanoma
lung: melanoma bone: FSA and melanoma - SCC if in mandible or maxilla; epulis always in bone |
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What is the treatment of choice for canine oral tumors?
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surgery - if local and resectable
RT - if tumor is unresectable or responsive, palliative chemo - if used alone or combo with surgery/RT - FSA is resistant immuno - melanoma with Tyrosinase vaccine >1yr MST |
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What is a Hi-low?
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- histologically low grade, biologically high grade tumor
- FSA, usually large breed dog, often younger - appears benign (fibroma) on histopathology |
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What is the most common feline oral tumor?
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SCC - 70% 10-12 year
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Describe the behavior of feline oral tumors
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- SCC commonly sublingual, bone, gingivial
- SCC and FSA usually bone involvement except sublingual SCC - uncommon to metastisize - SCC usually fast progression compared to FSA |
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What are treatment options for a feline oral SCC?
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- surgery if small, rostral (uncommon)
- most are non-surgical - palliative RT usually, MST 2 to 4 mo |
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What are treatment options for a feline oral FSA?
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- surgery is tx of choice, but similar concerns as SCC die to location and resectability
- poor response to RT or chemo - die of local disease |
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T/F - salivary gland and esophageal tumors are rare
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True, very rare but malignant
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What is the most common salivary gland tumor
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- adenocarcinoma
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What are the types of esophageal tumor?
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SCC and sarcoma (secondary to spirocerci lupi)
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What is the most common canine gastric tumor?
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- very rare
- adenocarcinoma 70-80% metastatic |
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What is the most common feline gastric tumor?
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- very rare
- older cats - lymphoma |
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What treatment options are appropriate for gastric tumors?
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- surgical excision if localized disease
- chemo for cats with gastric lymphoma - prognosis is fair to poor - 6 mo |
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What are the types of intestinal tumors in dogs?
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- rare <1% of all reported malignancies
- 30% adenocarinoma, 30% lymphoma, 23% leiomyosarcoma/GIST - older male dogs |
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What are the types of intestinal tumors in cats?
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- rare like dogs
- lymphoma 75%, adenocarcinoma 17%, MST - older cats, siamese predisposed |
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How is an intestinal tumor treated if carcinoma? sarcoma? lymphoma?
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- carcinoma: surgical excision wth wide margins
- sarcoma: surgery or TKI slower to metastasize than carcinoma - lymphoma: chemo |
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T/F Cats do not have perianal glands therefore are higher risk for anal tumors...
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False - well they dont have perianal glands but they are very low risk
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What type of tumors are found at the perianal region?
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- canine
- adeoma - tenesmus slow growing mass, 70-80%, almost always in intact males and spayed females - adenocarcinoma - quicker growing - anal sac adenocarcinoma |
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What is the definitive method for diagnosing perianal tumors.
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- PE
- biopsy - FNA and cytology - hard to diff adenoma vs adenocarcinoma |
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What treatment options are available for perianal tumors?
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- testosterone dependant, neutering may cause regression
- 90% adenoma cured with neuter +/- surgical removal - adenocarcinoma tx primarily with sx, may metastisize - AGASAC - sx, RT, chemo- high metastatic rate |
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What are the common renal tumor types in cats?
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- rare as primary - carcinoma, 11 yr avg, UNILATERAL 90%
- lymphoma if bilateral, 6 yr, usually seen as part of systemic disease |
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What are the common types of renal tumors in the dog?
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- lymphoma - bilateral usually as part of systemic disease - 8 yr, bilateral
- 2/3 carcinoma if unilateral or 1/3 sarcoma |
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What treatment modalities are employed in renal tumors?
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- if lymphoma chemo, NOT nephrectomy
- carcinoma or sarcoma nephrectomy if GFR is checked prior |
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What is the incidence for urinary bladder tumors?
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- very rare
- cats - 10-15 yr - dogs - 10 yr - Scotties 8X more likely, also WHWT, Beagle, Shetland Sheepdog - TCC, can be due to environmental toxicities such as flea collars, herbicides |
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What treatment options are available for TCCs?
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- surgical resection if localized tumor
- diffuse tumors - chemo, RT not effective? - medical is treatment of choice in dogs as they are trigonal and non-resectable - using mitotoxitrame with proxicam (NSAID) common, but monitor since NSAID is nephrotoxic |
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How do chemotherapeutic agents induce cytotoxicity?
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- by damaging DNA
- interfering with necessary substrates or enzymes required for synthesis and replication of genetic material |
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Sum up the cell cycle phases: G0, G1, S, G2, M
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G0 - not actively dividing, but can divide
G1 - enzymes required for DNA synthesis are produced - the most variable phase of the cell cycle across various types of cells S - DNA is synthesized G2 - where proteins and enzymes required for protein synthesis, RNA synthesis, and mitotic spindle formation are produced M - duplicated DNA is divided equally |
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What are somatic changes vs. germ-line changes?
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somatic - changes to DNA as adult, leads to adult cancers
germ-line - mutations that are born into the gene sequences leading to childhood cancers |
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List the types of chemotherapeutic drugs.
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1 - alkylating agents
2- antimetabolites 3 - antineoplastic antibiotics 4 - microtubule spindle poisons 5 - miscellaneous agents |
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What is the mechanism of alkylating agents?
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- direct results of DNA adducts formation that interferes with the replication of DNA, may lead to cell apoptosis
- non-specific cell cytotoxicity as if affects all phases of cell cycle |
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What is the mechanism of antimetabolite class?
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- inhibition of enzymes or proteins needed for synthesis of DNA
- halts the cell cycle - cell-cycle specific to the S-phase |
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How do antineoplastic antibiotics work?
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- requires water and oxygen
- free radical generation that damages DNA, intercalation of DNA that prevents its synthesis, inhibition of critical enzymes necessary for the unwinding of DNA - cell-cycle-non-specific since it hits the DNA directly, similary to alkylating agents |
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How do microtubule spindle agents work?
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- prevents the formation of the mitotic spindle by inhibiting its formation directly or interfereing with spindle deconstruction halting the cell cycle and leading to cell death
- blocks cells at the M phase where the mitotic spindle is formed - cell-cycle specific |
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T/F The miscellaneous chemotherapeutic agents are considered cell-cycle specific
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False - cell cycle non specific, mechanism is similar to alkylating agents
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Explain the pattern of expansion for tumor growth with respect to the Gompertzian curve.
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- pattern of expansion follows:
1- initial lag phase 2- exponential growth phase 3 - gradual plateu phase - cessaion of 2, usually due to depletion of oxygen and nutrients, or formation of an unfavorable growth environment due to pH or excessive cellular metabolism - size of tumor reflects phase of curve -> small rapdily -> 2 whereas large tumors approaching limits of O2 etc are plateu |
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Why are chemotherapeutics more effective for the treatment of microspic disease burdens?
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- agents are most effective against rapidly dividing cells - via DNA replication interference therefore they are best used when tumors are in the exponential growth phase. This means that the tumors are small, and composed of rapidly dividing cells
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What are the factors that affect or influence chemotherapeutic drug resistance?
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- anatomic compartments - some places are just damn hard to get to, BBB, prostate, eye - can be bypassed with lipophyllic agents
- tumor microenvironment - going back to Gompertzian growth curve large tumors have slowed growth rate due to impaired vasculature, fucked up perfusion, high interstitial presssure etc making drugs hard to get there - inherent drug resistance (Goldie-Coleman) given a population of neoplastic cells some will develop genetic mutation making them resistance - one in every 1 million cells has the potential ---> systemic tx of microscopic tumor burden is likley to be more successful than treating macroscopic burden - aquired drug resistance where cells may be exposed to selective pressures that favor dysregulated growth and neoplastic cells capable of surviving intial chemo agents typically have survival pathways that are beneficial for continued survivial leading to formation of resistance cancer cells |
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What is dose intensity?
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product of drug concentration and time
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How is optimal dose intensity achieved?
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- delivering the maximum tolerated drug dose at the closest possible interval between doses
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Name some benefits to combination chemotherapy.
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- since population is hetergenous use of various agents with several mechanisms of action decreases the likelihood of having a cell resistance to one type of chemo and allows for maximul cytotoxicity
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What is the most common primary bone tumor in dogs?
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OSA
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What is the current standard of care for patients with OSA?
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Surgical resection of the affected site followed by chemotherapy - platinum (cisplatin or carboplatin) or doxorubicin based protocol
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What is the most common sites for OSA in dogs?
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- appendicular skeleton 75-85%
- middle aged to older - common to metaphysis - also an incidence peak of 2 yrs age - bimodal distribution - away from the elbow and towards the knee - equal frequency at the radius, proximal humerus, proximal tibia |
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What are negative prognastic factors for OSA?
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- detectable metastatic lesions
- increased serum ALP levels |
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Which would you rather have...a mandibular OSA or a soft tissue OSA?
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- mandibular OSA - survival rate of 70% at one year versus soft tissue having less than 2 mos
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How would an allograft for a limb-sparing surgery affect the survivial time for OSA?
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- it's been reported that dogs were twice as likely to live longer compared to dogs without an infection - possibly, a non-specific activation of the immune system has been the cause
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What do radiographs of the primary OSA lesion usually present as?
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- bony proliferation and lysis
- mixed osteoproductive with osteodestructive activity - generally does not cross the joint space |
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What is the gold standard for diagnosing OSA? What is seen?
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- biopsy
- FNA may provide diagnosis with less invasive means - see large immature mesenchymal cells that may have intracytoplasmic or extracellular osteoid - FNA or biopsy must be done to rule out fungal or bacterial osteomyelitis (only suspect if sx occured at that site) - ALP stain to differentiate OSA from other sarcomas - suggested to to chest rads and aspirate LNs |
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How is a biopsy for OSA perfomed?
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- biopsy the center, not the peripheral leading edge, which will only indicate reactive bone formation
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What is the biologic behavior of OSA?
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- highly metastatic disease
- pulmonary parenchyma is the most common metastatic site - LN uncommon metastatic site |
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Describe the treatment of OSA
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- surgical resection with 3 to 6 cycles of chemo
- w/o chemo MCT is 4-5 mo, with is 10-14 mo - once metastatic disease is detectable chemo is usually ineffective!!! |
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What is the signalment for most axial OSA cases
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- middle aged
- females outnumber males - mode likely in small dogs |
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What is the biologic behavior of axial OSA tumors?
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- site dependant with mandibular OSA less likely to metastasize that other OSA
- rib origin is the most likely to metastasize |
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What is the recommended treatment for axial OSA?
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- surgical resection followed by chemo
- surgery alone for mandibular |
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Where are canine extraskeletal OSA tumors most commonly found?
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- mammary gland, followed by spleen and other soft tissues
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Describe the biologic behavior of nasal tumors in dogs.
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- 2/3 carcinomas
- 1/3 sarcomas - very locally invasive - low metastatic rate |
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Describe the biologic behavior of nasal tumors in cats.
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- lymphoma is the most common then carcinomas
- usually localized - RT or systemic chemo |
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What is the best method to diagnose nasal tumors?
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- biopsy - cytology rarely helpful except for ruleouts
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What are a few DDx and ways to Dx a nasal tumor?
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- due to epistaxis, look for coagulopathy, foreign body, fungal infection (asp dogs, crypto cats)
- always aspirate the mandibular LNs - staging can also do thoracic rads - facial deformity and exophtalmos are commonly seen |
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What is the therapy of choice for nasal tumors?
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- RT - very effective
- chemo (cisplatin in dogs) 1/3 resolution |
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T/F primary lung tumors are common
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False - rare
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What is the biologic behavior or lung tumors?
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- 2/3 carcinomas (adenocarcinomas)
- or LSA as part of a multi-centric disease - SCC has a worse prognosis, presents with diffuse metastatic disease |
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What is the most important diagnostic test for lung tumors?
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- thoracic rads - will see well demarcated, spherical solitary lung mass within the caudal lung lobes
- excision biopsy or FNA for definitive dx - has risks of pneumothroax hemothorax, etc - ensure not a metastatic lesion....primary lung tumors are rare |
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What is the treatment of choice for lung tumors?
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- surgery, lobectomy
- RT causes too much damage to normal tissues - chemo not widely effective |
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What the fuck are canine pulmonary lymphoid granulomatosis?
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- rare and diffuse pulmonary malignancy
- proliferation of lymphoidreticualr and plasmacytoid cells - highly responsive to chemo and complete remission within 1 to 2 weeks |
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What viruses are associated with feline lymphoma?
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- FeLV: directly causes lymphoma, + cats get it young and its T-cell, mediastinal not GI
- FIV predisposes to lymphoma by suppressing immune system, chronic stimulation |
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What is the common location for lymphoma in cats?
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- GI form FeLV negative
- mediastinal form associated with FeLV infections, as FeLV decreased so does the mediastinal form |
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What is the most common location for lymphoma in dogs?
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- multicentric form - multiple pleripheral LN
- multicentric accociated with hyperCalcemia - most are B cells, T cells worse as they are more resistant to chemo and dont respond as well |
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What is the biologic behavior of LSA?
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- usually arises in lymphoid tissues (LN, spleen, liver, bone marrow) - since its systemic chemo is the therapy
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How is LSA best diagnosed?
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- FNA, but must be staged as it is a systemic disease
- tissue biopsy rarely needed |
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How do you stage LSA?
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- FNA - draining LNs
- CBC - paraneoplastic syndromes - chem - hypercalcemia secondary to malignant production of PTHrP - poor prognostic factor - urinalysis - prior to starting chemo, UTAs, chemo suppreses immune system - throacid rads - evaluate for lung parenchymal involvement - looking for diffuse pattern not nodular - abdominal rads - organomegaly, GI tract - abdomial U/S - cats with GI LSA,usually not done with dogs with multicentric LSA unless GI suspected - bone marrow aspirates - >50% LSA infiltration very poor prognostic factor - tissue biopsy rarely needed except excisional to dx small cell low grads LSA in dogs and some LSA incats |
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What is the staging classified as?
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I - single LN
II - LN in one region III - generalized LN IV - liver/spleen +/- stage III V - marrow/peripheral blood and/or other organs a - clinically normal b - patient is ill |
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What is the treatment for LSA?
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chemo as systemic disease
- 65-90% initial response untreated 4-6 weeks, multidrug 2 years - a 2nd resistance will be shorter than the first etc - resistance due to induction of p-glycoprotein that pumps out toxins from cells cytoplasms |
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Name at least 3 prognostic factors for dogs and cats with LSA?
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- clinically ill?
- FeLV status - + have decreased remission times - response to therapy - cats that go into remission have greatly prolonged survivals |
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What paraneoplasitic syndromes are associated with LSA?
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- hyperCa with mediastinal
- IMHA or thrombocytopenia: may be due to bone marrow infiltration |
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What are the MSTs for multicentric canine LSA untreated, predisone alone, and with multidrug?
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- untreated: 4-6 weeks
- prednisone alone: 11 weeks - Dox: 6-9 mo - COP: 7-8 months - multidrug: 25% 2 years, most 12 mo |
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Describe the biological behavior of STS in dogs.
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- classified as fibrosarcoma, hemangiopericytoma, neurofibrosarcoma, liposarcoma, and malignant fibrous histiocytoma
- have false appearance of encapsulation - will have fingers of malignant cells - slow to metastasize (41% grade 3) - may arise anywhere in the body, but tend to be classified as cutaneous and subcutaneous |
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List the diagnostic steps for a a dog with a subcutanous mass.
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- CBC etc - to determine paraneoplastic syndromes etc
- thoracic rads - 25% met to lungs - other imaging to determine invasiveness - FNA - will most likely reveal mesenchymal cells. if inflammation is present cannot interpret mesenchymal cells - biopsy - incisional or excisional needed for definitive dx. if exc - a 2nd curative is needed |
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What are the treatment options for STS?
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- SX is the tx of choice for most using very side margins
- RT - excellent adjuvant therapy or neoadjuvant, not suceesful as sole tx - chemo - not very effective, may be considered for metastatic disease, when RT is unavailalbe, or in conjunction with RT and in grade 3 tumors |
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What vaccines are associated with VAS in the cat?
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- killed vaccine products
- effects on multiple vx at the interscapular site - 1-> 50%, 2->127%, 3->175% increased risk - rabies or FeLV |
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What treatment options are available for VAS in the cat?
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- SURGERY - if not completely excisable with wide margins it will be fatal
- RT - efficacy is unclear - chemo - may prolong survival, non curative |
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Given the risks of VAS, what is the recommended protocol for administering vaccines in the cat?
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- rabies right rear
- if cat is outdoor and really needs if FeLV in left rear - FVRCP is till over the back and shoulder |
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What is the difference between primary and secondary immune-mediated diseases?
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- primary: antibody is directed against a self antigen
- secondary: antibody is directed against and absorbed antigen on the cells |
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What is autoimmunity?
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- specific recognition of SELF-Ag
- this is not non-specific recognition of Ag such as IBD, or lymp-plas rhinits |
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What is the central tolerance viewpoint for autoimmunity?
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- self-Ag is presented aberrantly by certain subsets of MHC molecules
- allows survival of self-reactive T cells - genetic predisposition |
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What is the peripheral tolerance viewpoint for autoimmunity?
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- self-Ag exposed by nonspevific chronic inflammation
- breaks the sequestration of self-Ag - immune system presents damaged cells |
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Other than the two types of tolerance abnormalitites, what else can lead to autoimmunity?
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- molecular mimicry - such as the weak evidence that foreign Ag mimics self-Ag
- dysregulation: failure of regulatory cells - infectious trigger: overcome the cytokine deviation |
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What is the mechanism of Myastenia Gravis?
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- Ab are directed at the Ach-r on the post synaptic membrane
- this leads to a decrease in the availability, or total number of Ach-R that Ach can bind leading to delays or implairment of transmission - the antibodies can also activate complement that leads to lysis of the post synaptic membrane - Type II HST |
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What are the most commonly affected breeds for MG?
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- female > male
- akitas, terriers, german shorthair pointers, abyssinians, somalis - either <4 yrs or > 9 years |
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What clincial signs are associated with MG?
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- regurgitation since 90% have esophageal dysfunction or megasophagus
- dysphagia - weakness, especially with exercise - dyspnea 2nd to aspiration pneumonia or respiratory muscle weakness |
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How is MG diagnosed?
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- Ach-R AB titers
- tensilon test - given short active Achase inhibiotr to see if immediate improvement - but has some side effects such as vomiting diarrhea, bronchial constriction - must keep atropine on hand and a negative response does not rule out disease |
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How is MG treated?
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- immunosuppresion - controversal with pred, azathioprine
- supportive care - do not give cough suppressant - asp pn most common cause of death - treat megasophagus - guarded, 80% may go into remission with 1/3 recurrence |
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What is SLE?
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- Type III HSR, some II and IV
- loss of control of B cells leading to polyclonal gammopathy, autoAbs produced - triggered by drugs, neoplasia, infection, environment - most likely predisposing factor is genetics - either humoral immunity (autoAb, immune complex deposition) or cell-mediated immunity (complement, phago) |
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What are the clinical signs of SLE?
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- cutanous
- orthopedic - polyarthritis, shifting lameness, muscle wasting - hematologic: thrombocytopenia, hemAnemia, leukopenia - systemic: glom dis, vasculitis, myocarditis, pulm thrombyoembolism |
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How is SLE diagnosed?
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- requires positive ANA (antinuclear antigen) and 2 other symptoms
- ANA: detects Ab vs DNA - LE cells: pahagocy Ab coated cellular material in NP and MP - histopath: immunoflo vs immune complex |
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How is SLE treated?
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- immunosuppresion - specific medications vary so use what works
- supportive care for pain, prevetion and omega-3;s to modulate inflammation |
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What is the prognosis for SLE?
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- guarded
- will be on medication for remainder of life, unless can be weaned - 50% long term survival |
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What is masticatory myositis?
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- myositis of masticator
- due to distinct type of 2M myosin, these fibers are the only affected muslce fibers - distinct embryological origin - severe inflammation of the muscles followed by atrophy and fibrosis |
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What breeds are most affected by masticatory myositis?
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- all breeds, GSD may be predisposed
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What are the acute and chronic clincial signs of MM?
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- actue: fever, muscle swelling, see increased AST (liver-muscle), pain, difficult eating, may be unable to close mouth
- chronic: atrophy and fibrosis of the muscles, may not be able to open mouth |
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How is MM diagnosed?
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- increased AST and CPK
- type 2M Ab titers - muscle biopsy (necrosis and phagocytosis of 2M fibers) - EMG - sponatneous muscle activity, constant crackle |
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What is the treatment for MM?
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- depends on progression and evidence of fibrosis
- treatment will be unsuccessful if fibrosis has occurred - if acute or inflammatory -> immunosuppresive doses of steroids, continue long term or repeat if relapse occurs |
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What type of hypersensitivity is IMHA?
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Type II - antibodies directed against cells or cellular constituents - cell surfaces and cell membranes
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What is the mechanism of IMHA?
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- activation of self-directed Abs by either viral, bacterial infection that tirgger immume dysregulation -> induction of self directed Abs - PRIMARY
- Abs are directed at an infectious agent or drug that is associated with the cell surface - SECONDARY |
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What is the difference between intravascular and extravascular hemolysis?
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- intravascular: Red blood cell lysis occurs in the circulation as a result of activation of the complement system cascade.
- extravascular: Red Blood Cells that are coated with antibodies are specifically recognized in the reticuloendothelial system and destroyed by macrophages. |
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What is the most common type of IHA in dogs? cats?
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- dogs - Primary: may be associated with infection, SLE, idiopathic
- cats: secondary - drugs, infectious agents, neoplasia, vaccine, zinc |
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How is IMHA diagnosed?
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- CBC Chem all that shit
- specific tests such as slide agglutination, Comb's test (only if slide agglutination is negative), test for othere such as Rads, tick panel, FeLV.FIV |
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How is IMHA treated?
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1. stop hemolysis - immune modulators such as steroids
2. maintain tissue oxygenation - RBC transfusion 3. provide adequate perfusion - prevents sludging, decreases organ damage and risk of DIC - IV fluids necessary 4. Prevent side effects - high risk for thromboembolism and DIC |
