Brainscape's Knowledge GenomeTM

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


See full index

PVS > Oncology 2 > Flashcards

Oncology 2 Flashcards

1
Q

Outline the role of RNA viruses in cancer and give examples

A
  • Are the biggest cancer causing group
  • Retroviridae especially
  • Avian leukosis (lymphoid, myeloid tumours, sarcomas), feline retroviruses (lymphoid tumours), Jaagsieite sheep retrovirus (lung adenocarcinoma), bovine leukosis (lymphoma)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Outline the role of DNA viruses in cancer and give examples

A
  • Less common
  • Herpesviridae e.g. Marek’s disease virus (lymphoid tumours)
  • Papillomaviridae
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What aspect of cells of viruses affect in order to cause cancer?

A
  • Affect the proto-oncogenes of normal cells
  • Increase expression of these or cause a mutation
  • Affect the cell signalling pathways - any protein in cell signalling are potential oncogenes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the role of oncogenes in cancer?

A
  • Most cellular proto-oncogenes (c-onc) are normal compoentns of growth factor signalling pathways
  • Increased activity leads to increased cell growth
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the mechanisms of retroviral oncogenesis?

A
  • Oncogene capture and transduction
  • Insertional activation
  • Insertion leading to truncation
  • Insertion leading to gene inactivation
  • Other mechanisms e.g. dysregulation of normal cellular metabolism and lead to tumour formation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is required for the mechanisms of retrovial oncogenesis to work?

A
  • A provirus

- At either end have LTR (long terminal repeats)

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

Explain how proviruses work in oncogenesis

A
  • Have LTRs at either end
  • LTRs have promotor and enhancer elements (same as in genome to control gene expression in chromosomes)
  • Act as binding sites to come in and switch on gene expression
  • More active and less controllable than cell’s own mechanisms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Outline the process of transduction in oncogenesis

A
  • Integration of recombinant retrovirus carrying a cellular “onc” gene into host genome
  • Infection of a new cell by a recombinant retrovirus carrying transduced cellular onc gene (v-onc) occurs
  • Viral LTR then drives high level of transcription, leading to over-expression of v-onc mRNA and production of v-onc protein and ending in oncogenic effect
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the consequences to the virus due to acquiring a cellular oncogene?

A
  • Loss of essential retroviral genes
  • Virus defective, requires help to replicate
  • Help from other viruses that exist without the oncogene
  • Defective viruses are generally not transmitted to a new host (except Rous sarcomavirus)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the results of rapid oncogenic transformation in Rous sarcoma?

A
  • Loss of contact inhibition
  • Increased saturation density
  • INcreased growth rate
  • Anchorage-independent growth
  • Tumourigenic in appropriate hosts
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Outline insertional activation of oncogenes by viruses

A
  • Insertion of virus near/next to oncogene
  • LTR of virus close enough to switch on oncogene
  • Can occur over significant distances
  • Virus replication remains competent
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What mechanism of oncogenesis is mainly used by feline leukaemia and avian leukosis viruses?

A

Insertional activation

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

What factors are important determinants of tumorigenesis in Feline Leukaemia virus?

A

LTR (determines kinetics and disease outcome) and surface glycoprotein (determines where disease occurs)

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

Outline the oncogenesis by bovine leukaemia virus

A
  • Virus infects B lymphocytes and becomes latent, no free virus in blood
  • Viral Tax protein transactivates cellular genes
  • Products of transactivated cellular genes may be oncogenic
  • Tax protein must be switched on to activate LTR, but also turns on cytokine proteins and receptors leading to positive feedback loop, growth of cells and neoplastic proliferation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Outline the induction of tumours by Jaagsiekte sheep retrovirus

A
  • Replicates only in type II pneumocytes and Clara cells
  • Replication leads to transformation of every cell
  • Viral Env protein switches on signals for cell division that activates cellular signalling pathway
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Outline bovine papillomavirus oncogenesis

A
  • Persistent viral infecton, latency and co-factors such as immunosuppression/genetic changes
  • Expression og early viral genes activate host signalling pathways
  • Poor immune response
  • Neoplastic progresson slow, multistep, rare
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Describe Marek disease virus

A
  • Oncogenic herpesvirus
  • Tumours derived from T lymphocytes
  • In feather follicles, produces active virus to cause infection at later date
  • Infects resp. tract of birds, into blood, bursa, thymus and spleen to affect macrophages, T-cells and B-cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

List virus-cell interactions that occur in Marek’s disease

A
  • Cytopathic (lytic) and cell-associated (B-cells, macrophages)
  • Non-productive (latent) and cell-associated (tumour cells in T lymphocytes)
  • Cell free and productive (feather follicle cells, source of virus)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the consequences on immune cells due to Marek’s disease virus?

A
  • B lymphocytes and macrophages are killed

- T-lymphocytes are activated to proliferate and form tumour

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

Outline the clinical features of Avian Leukosis

A
  • Retrovirus
  • Transmitted from hen to egg, producing persistently infected chicks that are immunotolerant to viral antigens
  • Incubation period for tumour development >4 months
  • 10 virus subgroups
  • Persistently infected can also pass disease horizontally
  • State of disease depends on infectious dose, immune response, age
  • Can have subclinical infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Outline the clinical features of Bovine Leukaemia virus

A
  • Transmission via infected cells e.g. milk, blood
  • Vertical or horizontal transmission
  • Causes lymphocystosis, lymphoma in older cattle
  • Notifiable in UK
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Outline the clinical features of Ovine pulmonary adenocarcinoma

A
  • Diagnosis by wheelbarrow test (frothy fluid from trachea)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Outline control of Avian leukosis

A
  • Difficult, breed out by breeding resistant birds only
  • Strict biosecurity
  • erdation in breeder flock required
  • Select virus free hens (egg screening), check eggs over 14 day period for ALV anitigen in albumen by ELISA, hatch and rear in isolation, test for ALV antigen in blood, maintain virus free breeders
  • Susceptible to disinfectants but can be transmitted by mating
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Outline the control of Ovine pulmonary adenocarcinoma

A
  • Respiratory secretions are infectious
  • More common in housed sheep
  • Rapid isolation and culling of diseased animals
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

How is ovine pulmonary adenocarcinoma diagnosed?

A
  • Wheelbarrow test

- Histopathology (RT- PCR)

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

Outline the control of Marek’s disease virus

A
  • Disinfection
  • Biosecurity
  • All-in, all-out management
  • Vaccination
  • New strains emerging each more virulent, so new vaccines required at each new mutation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Why is diagnosis and staging important prior to treatment of a tumour?

A
  • Extent of treatment depends on tumour type and stage

- With regards to surgery, need to know the surgical margins that will be required

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

What are the general principles of biopsy?

A
  • Handle tissue gently
  • Position site within probably surgical or radiotherapy field
  • Should be as small as possible, position so as to not increase size of treatment area
  • Sample from different areas of lesion, including junction of normal-abnormal tissue
  • Avoid local dissemination of neoplastic tissue
  • So not breach anatomical planes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are the indications for incision biopsy?

A
  • When mass will not exfoliate well for FNA, not amenable to core biopsy
  • When cytology or core biopsy results are non-diagnostic
  • Lack of core biopsy equipment
  • If is more likely to achieve diagnosis and grade
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What are disadvantages of excisional biopsy?

A
  • Surgical margins unknown, risky
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What are the advantages of an excisional biopsy?

A
  • May be cost saving in some cases
  • Diagnosis and treatment are possible within single surgery
  • Good where diagnosis of tumour type and grade will not affect surgical approach
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What are the roles of oncological surgery?

A
  • Prophylactic e.g. ovariohysterectomy prior to 1st season, cryptorchid testicles
  • Diagnosis and staging
  • Definitive excision
  • Palliative surgery
  • Cytoreduction in order to treat with adjunctive methods
  • Management of oncologic emergencies
  • Surgery for supportive therapy
  • Treatment of metastatic disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What are the 3 possible aims of surgical excision of a tumour?

A
  • Curative
  • Cytoreductive
  • Palliative
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is meant by palliative surgical excision of a tumour?

A

Where removal of a tumour that is causing other problems e.g. blocking nasal passages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Compare primary surgery and revisions with regards to success in treating tumours

A
  • Primary best chance for cure
  • Untreated tumours have more normal surrounding anatomy facilitating surgical removal
  • Recurrent tumours may have seeded to previously unaffected areas, need wider, deeper resection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is meant by surgical dose?

A

How much surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What are the categories that may be used in definitive tumour surgery?

A
  • Debulking/intralesional/cytoreductive excision
  • Marginal resection
  • Wide resection
  • Radical resection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What are the zones of a tumour, going from inner to outer?

A
  • Tumour
  • Pseudocapsule
  • Reactive zone
  • Satellite metastases
  • Skip metastases
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What are skip metastases?

A

Small parts of cancer that are invisible, meaning that taking margins is difficult

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What is the surgical consequence of skip metastases?

A

Require large excisional margins in order to avoid leaving these behind to form new tumour

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Outline debulking/intralesional/cytoreductive excision

A
  • Leaves macroscopic volumes of tumour
  • Will recur unless given adjunctive therapy
  • Done without margins
  • Acceptable as palliative procedure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Why might debulking be appropriate?

A
  • Palliative procedure

- Where need to preserve vital structures e.g. CNS, bladder

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What is marginal excision?

A
  • Excision immediately outside the pseudocapsule

- Are leaving behind microscopic volumes of tumour

44
Q

What does the tumour pseudocapsule consist of?

A

Compressed tumour cells, not connective tissue, around which there are microscopic volumes of tumour cells

45
Q

What is the consequence of marginal excision?

A

Local recurrence likley without adjuvant therapy

46
Q

What is a wide excision?

A

Removal of tumour with complete margins of normal tissue in all directions, so local recurrence is unlikely

47
Q

What tissues are good natural barriers to spread of cancer cells?

A

Collagen rich, relatively avascular tissues e.g. fascia, ligaments, tendons and cartilage

48
Q

What tissues are poor barriers to spread of cancer?

A

Fat, subcutaneous tissue, muscle, other parenchymatous organs

49
Q

What is radical excision?

A

Removal of entire anatomical structure or compartment continuing the tumour e.g. limb amputation, mastectomy. Local recurrence is unlikely

50
Q

What is meant by lateral and deep margins of a tumour?

A
  • Lateral are the margins around the visible lesion (ruler used)
  • Deep margins are the margins below the visible lesion
51
Q

What are some pre-operative considerations with cancer surgery?

A
  • Excision can result in tissue defects, must plan reconstruction
  • Wide clip and prep as plans may change
  • Surgical scars will contain neoplastic cells and should be given the same margins as the tumour
52
Q

Outline histology and margin assessment following surgical excision of a tumour

A
  • Submit all tissue from surgery for histopathology
  • Indicate locations of interest with sutures or ink
  • Take extra biopsy of locations of interest e.g. deep margins
53
Q

In what lesions is a needle only FNA useful?

A

Soft masses and lymph nodes, want to avoid destroying fragile cells with suction

54
Q

In what lesions is a continuous suction FNA useful?

A

Firm masses e.g. firbosarcomas as these do no exfoliate well

55
Q

In what lesions is an intermittent suction FNA useful?

A

Small masses where it is not possible to redirect the needle without exiting the mass

56
Q

What size needle should be used for FNAs?

A

23 gauge

57
Q

What are the indications for a tru-cut biopsy?

A
  • Superficial masses (incl. lymph nodes) that can be palpated and stabilised
  • Internal organs that can be safely accessed via ultrasound guidance
58
Q

What are the contra-indications for a tru-cut biopsy?

A
  • Highly vascular structures
  • Disorders of primary and secondary haemostasis
  • Where structure to be biopsied cannot be stabilised
  • Structure with thin wall that may leak contents following sampling
59
Q

Describe the technique for tru-cut biopsy

A
  • Under heavy sedation or GA
  • Clean and aseptically prepare skin over area to be biopsied
  • Small incision in skin
  • Load needle, advance into sample area
  • Once in, advance stylet to expose the biopsy notch
  • Deploy cutting cannula by depressing the plunger
  • Remove needle from mass
  • Pull plunger back into lock position to remove sample
  • Push stylet forwards to reveal notch with tissue
  • Use fine needle to lift sample off and place in formalin
60
Q

Describe the site preparation for a punch biopsy

A
  • Sedate patient (or GA for ears, nose, toes)
  • Clip with scissors to preserve skin
  • Do not disturb crusts or skin surface, do not prep or scrub skin
  • Draw orientation line along line of hair growth in indelible marker
  • Draw circle around lesion
  • Inject subcut local anaesthetic on this circle, advancing into each previous injection site
61
Q

Outline the method of taking a punch biopsy

A
  • Usually 6-9mm punch, as large as possible
  • Hold perpendicular to skin surface
  • Rotate in one direction only
  • Do not reuse blunt biopsy punches
  • Only through skin, check regularly
  • Grasp sample by subcut tissue and cut connecting tissue
62
Q

What can be used to stabilise thin biopsy samples?

A

Stiff card or wooden tongue depressor, to prevent warping of tissue

63
Q

When should a wedge/ellipse biopsy be used?

A
  • Excision of solitary nodules
  • Transition from normal to lesional skin
  • Vesicles
  • Suspected deep lesions e.g. panniculitis
64
Q

What are the anatomical locations for a percutaneous liver biopsy in the cow?

A
  • 15cm below transverse processes within 11th intercostal space (second to last intercostal space)
  • Can be defined by imaginary lines from wing of ilium to point of elbow, and point of ilium to point of shoulder
65
Q

What are the anatomical locations for percutaneous liver biopsy in the horse?

A
  • Ultrasonographically guided
  • 13th or 14th right intercostal spaces (3rd or 4th from the back)
  • Half way between 2 lines from tuber coxae to point of elbow, and tuber coxae to point of shoulder
66
Q

How are percutaneous liver biopsy in the dog and cat performed?

A

Visualise ultrasonographically, not based on anatomical location

67
Q

How is percutaneous renal biopsy in the cow carried out?

A
  • Rectal palpation and manipulation of left kidney to the paralumbar fossa and fixed in position
  • Biopsied with ultrasound guidance or blind
68
Q

How is percutaneous renal biopsy carried out in the horse?

A
  • Left kidney easier
  • Identify ultrasonographically, fix in position per rectum
  • Biopsy then performed with ultrasound guidance
69
Q

How is percutaneous renal biopsy carried out in the dog and cat?

A
  • Small gauge biopsy needle (16-18G)
  • Ultrasound guided in dogs >5kg and all cats
  • Blind biopsy technique where kidneys palpated and immobilised prior to biopsy more common in cats
  • Right preferred in dogs, caudate lobe of liver provides stability, left may be more accessible in deep-chested dogs
  • In cats both can be stabilised and located easily
70
Q

What are the 3 phases of chemotherapy?

A
  • Induction
  • Maintenance
  • Rescue
71
Q

What is the central principle of chemotherapy?

A
  • Act somewhere in the cell cycle and so stage determines effectiveness of chemo
  • Acquiescent cells are in G0 and so will be non-responsive, dividing cells are responsive
72
Q

What are the classifications of chemotherapeutic drugs?

A
  • Cell cycle non-specific

- Cell cycle specific

73
Q

What is the common outcome of all chemotherapeutic drugs?

A

Prevent cellular division and subsequent cell death

74
Q

What agent types are S phase specific?

A

Anti-metabolites e.g. Cytarabine, 5-fluorouracil

75
Q

What agent types are M-phase specific?

A

Mitotic spindle inhibitors e.g. Vincristine, Vinblastine

76
Q

What agent types are phase non-specific?

A
  • Alkylating agents e.g. Cyclophosphamide Melphalan, Chlorambucil, Lomustine
  • Anti-tumour antibiotics e.g. Doxorubicin, Mitoxantrone
  • Other agents e.g. Cisplatin, Carboplatin, L-asparaginase
77
Q

For what chemotherapeutic agents is peak plasma concentration important?

A

Phase non-specific

78
Q

For what chemotherapeutic agents is concentration over time important?

A

Phase specific

79
Q

What types of resistance to chemotherapeutic drugs may arise?

A
  • Spontaneous
  • Acquired
  • Multi-drug resistance (MDR)
  • Anatomical considerations e.g. BBB
80
Q

What methods of delivery can be used with chemotherapeutic drugs?

A
  • Oral
  • IV
  • Intracavity
  • Intralesional
  • Subcutaneous
81
Q

What are the pharmacological implications of phase specific drugs?

A
  • Need actively replicating cells
  • Kill limited number with single administration
  • Dependent on number of cells in contact with drug, dose dependent (can be altered by multiple administrations or continual infusion)
  • Require steady state of drug concentration to maximise killing
82
Q

What are the pharmacological implications of phase non-specific chemotherapeutic drugs?

A
  • Theoretically active in G0
  • Dose dependent
  • All cells have DNA so will kill any cells, proliferative and non-proliferative
  • Toxic effects only
83
Q

What are the indications for chemotherapy?

A
  • Most effective single therapy for some malignancies e.g. haemolymphatic
  • Adjuvant for highly metastatic tumours when disseminated disease suspected e.g. osteosarcoma
  • Shrinkage of large tumours prior to surgery (neoadjuvant)
  • Radiation sensitisation (damage cells. more sensitive to radiotherapy)
84
Q

What type of pharmacokinetics is cytotoxic cell killing under?

A
  • First Order kinetics

- I.e. number of cancer cells killed by a drug is proportional to the dose

85
Q

What are the negative impacts of cytotoxic drugs?

A
  • Are not cancer specific and will kill other dividing cells
  • Skin, gut lining and bone marrow particularly sensitive
86
Q

What management is used to minimise normal tissue damage through use of cytotoxic drugs?

A

Use maximum dose that will minimal effect on the normal tissues, and apply repeat administrations to allow tissue recovery in between

87
Q

How is the dosing rate of cytotoxic drugs calculated?

A
  • Based on body surface area in m^2 or kg weight

- BSA allows better matching of animal’s capacity to metabolise drugs accurately

88
Q

Outline the common side effects of chemotherapeutics

A
  • Major systems affected are GI and bone marrow
  • Some drug specific side effects
  • Renal and hepatic dysfunction
  • Alopecia in some species/breeds (poodles, Bichon Frise, Old English Sheepdog)
  • Not as severe in humans
89
Q

What is a specific side effect of cyclophosphamide?

A

Sterile haemorrhagic cystitis

90
Q

What is a specific side effect of Doxorubicin?

A

Cardiotoxicity

91
Q

What is a specific side effect of Vincristine?

A

Peripheral neuropathy

92
Q

What is a potential consequence of co-adminstration of chemotherapeutics and NSAIDs?

A

Both are immunosuppressant so careful monitoring and give rest when required

93
Q

List potential pharmacological mechanisms of drug resistance

A
  • Decreased drug accumulation
  • Altered drug metabolism (e.g. drug interactions)
  • Altered drug targets
94
Q

Explain how biological drug resistance to chemotherapeutic drugs may occur

A
  • Kinetics e.g. too many cells in G0 so minimal kill

- Poor vascularisation means reduced drug delivery to tumour

95
Q

Explain how multi-drug resistance to chemotherapeutic drugs may occur

A
  • Decreased drug uptake
  • Increased drug efflux
  • Activation of detoxifying systems
  • Activation of DNA repair mechanisms
  • Evasion of drug-induced apoptosis
96
Q

Explain how pharmacological resistance to chemotherapeutic drugs may occur

A
  • Poor or erratic drug (absorption, excretion, metabolism)
  • Drug interactions
  • Drug targets
97
Q

What tumour types have high chemosensitivity?

A
  • Lymphoma
  • Myeloma
  • Leukaemia
98
Q

What tumour types have moderate chemosensitivity?

A
  • High grade sarcomas e.g. osteosarcoma (adjuvant)
  • Mast cell tumours
  • Haemagiosarcomas (adjuvant)
  • High grade carcinomas (adjuvant)
99
Q

What tumour types have low chemosensitivity?

A
  • Most slowly growing sarcomas
  • Some carcinomas
  • Melanoma
100
Q

How can chemotherapy protocols be modified to target as many tumour cells as possible?

A
  • Use combination protocols
  • Phase specific + non-specific drugs
  • Different toxicities
  • COP or COPH protocols
101
Q

What drugs are included in the COP protocol?

A

Cyclophosphamide, Vincristine, Prednisolone

102
Q

What drugs are used in the COPH protocol?

A

Cyclophosphamide, Vincristine, Prednisolone and Doxorubicin

103
Q

When are single agent protocols commonly used?

A

In adjuvant setting e.g. carboplatin in canine osteosarcoma

104
Q

What other drugs can be used in cancer treatment?

A
  • NSAIDS e.g. meloxicam, peroxicam

- Tyrosine kinase inhibitors e.g. Masitinib, Tocerinib

105
Q

When are NSAIDS indicated as cancer treatment?

A

Transitional cell carcinomas, squamous cell carcinomas, other carcinomas

106
Q

When are tyrosine kinase inhibitors indicated in cancer treatment?

A

Mast cell tumours

PVS (23 decks)

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