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LCB2 > Leukaemia and lymphadenopathy 3 > Flashcards

Leukaemia and lymphadenopathy 3 Flashcards

1
Q

List the side effects caused by all drugs in chemotherapy for lymphoma

A
  • Nausea, vomiting, diarrhoea
  • Hair loss
  • Must drugs will cause neutropaenia
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2
Q

Which side effects are owners most likely to be aware of and worried about with chemotherapy?

A

The signs caused by glucocorticoids i.e. PUPD, hunger, muscle wastage

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3
Q

Outline the treatment for cutaneous lymphoma

A
  • Median survival time only months
  • Lomustine and pred used, also CHOP, in some cases retinoids
  • Surgery if solitary/localised
  • Surgery/radiotherapy for localised epitheliotropic lymphoma of lips/mouth
  • Radiotherapy as are easily accessible
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4
Q

What type of treatment is indicated for well/intermediately differentiated MCTs (Grade I, II) with no evidence of metastasis?

A

Surgical excision

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5
Q

What type of treatment is indicated for well/intermediately differentiated MCT (Grade I, II), with no evidence of metastasis on distal extremities

A
  • If surgery feasible: debulking surgery +/- radiotherapy
  • If not feasible: cytoreduction with pre or vinblastine + pred, +/- debulking surgery prior to radiotherapy (oncologist sees tumour before treatment), or Mastinib, toceranib
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6
Q

What type of treatment is indicated for metastatic of poorly differentiated MCTs (Grade III)?

A
  • Surgery if small and no metastasis - risky and not recommended
  • Radiotherapy
  • Chemotherapy: vinblastine + pred or CCNU
  • Grade III: mastinib, toceranib
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7
Q

Outline the treamtnet options for a Grade II MCT that is too big to resect

A
  • Cytoreductive steroids and surgery
  • Refer for surgery
  • Debulk then irradiate
  • Debulk then monitor
  • Debulk then chemotherapy
  • Tyrosine kinase drugs
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8
Q

Describe the required margins and depth of resection for a Grade I (low grade) mast cell tumour (or grade I soft tissue sarcoma, or well-differentiated dermal squamous cell carcinoma)

A
  • 1cm (wide local) margins

- Down to and including muscle or fascial plane below tumour

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9
Q

Describe the required margins and depth of resection for a Grade II (intermediate grade) mast cell tumour (or poorly differentiated dermal squamous cell carcinoma)

A
  • 2cm margins (wide local)

- Down to and including muscle or fascial plane below tumour

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10
Q

Describe the required margins and depth of resection for a Grade III (high grade) mast cell tumour (grade II and III soft tissue sarcomas (spindle cell sarcomas), feline vaccine associated sarcomas)

A
  • 3cm margins (radical)

- Down to and including 2 muscle or fascial planes below tumour

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11
Q

Name tyrosine kinase inhibitors used in the treatment of lymphoma

A

Masitinib, toceranib

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12
Q

Discuss the use of tyrosine kinase inhibitors in the treatment of mast cell tumours

A
  • Proliferation/survival of mast cells controlled by c-kit receptor tyrosine kinase
  • If use TKIs, life long therapy, will not get rid of tumour
  • Expensive
  • Can cause many side effects
  • Relatively high morbidity
  • Can work well, but need close monitoring
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13
Q

Describe the side effects caused by masitinib and toceranib

A
  • Masivet: protein losing nephropathy
  • Palladia: neutropaenia, muscle cramps
  • Both: anorexia, vomiting, bleeding, can induce thrombocytopaenia
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14
Q

When should lymphoma or mast cell tumour cases be referred?

A
  • If advanced skin reconstruction required
  • For radiotherapy
  • For chemotherapy if unsure of drugs and protocols, side effects and protection of people
  • For incompletely excised tumours
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15
Q

Describe the treatment options for feline mast cell tumours

A
  • Excise cutaneous and splenic ones
  • Radiotherapy possible but often diffuse or benign so questionable value (surgery better)
  • Little published data on chemo
  • Corticosteroids unclear benefit in cats
  • TK inhibitors have had preliminary investigations in cats
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16
Q

Discuss the use of chemotherapy in the treatment of feline mast cell tumours

A
  • Chemo generally reserved for cats with histologically pleomorphic (diffuse) locally invasive and/or metastatic tumours
  • Vinblastine, chlorambucil, lomustine used
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17
Q

Compare the response to treatment of acute and chronic leukaemia

A
  • Acute (poorly differentiated) poor response to treatment

- Chronic (well differentiated) reasonable response to treatment

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18
Q

Outline the pathogenesis of multiple myelomas (plasma cell)

A
  • Secrete excess Igs of one clonal class

- Usually present due to paraneoplastic signs associated with hyperviscosity

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19
Q

Describe the clinical presentation of lymphoid leukaemia in dogs

A
  • Usually middle aged to older
  • Non-specific clinical signs incl: lethargy, weight loss, PUPD, anorexia
  • Anaemia and thrombocytopaenia
  • High numbers of white cells on smear usually, but may have aleukaemic presentation with no peripheral blood component
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20
Q

Describe the acute lymphoblastic form of lymphoid leukaemia in dogs

A
  • Very acute
  • More common than chronic forms
  • Live max. 30 days, but usually only a couple of weeks
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21
Q

What is commonly found in cats with acute lymphoid leukaemia?

A

FeLV positive

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22
Q

How is lymphoid leukaemia diagnosed?

A
  • Blasts in acute, mature lymphocytes in chronic on blood smears
  • Some acute are aleukaemic
  • May have Bence Jones proteinuria
  • Cell markers can be prognostic so flow cytometry can be useful
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23
Q

Outline the treatment of chronic lymphoid leukaemia

A
  • Only if chronically ill

- Prednisolone and chlorambucil

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24
Q

What is polycythaemia vera?

A

Chronic red blood cell leukaemia, more common in dogs than cats and is the most common myeloproliferative disease

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25
Q

Describe the presentation polycythaemia vera

A
  • Chronic non-aggressive
  • Present with bone marrow derived polycythaemia, very high PCV
  • May struggle to get blood through needle due to viscosity
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26
Q

Describe the treatment of polycythaemia vera

A
  • Phlebotomy
  • Hydroxurea (may lead to nail sloughing, otherwise well tolerated), most common drug
  • Iron supplementation
  • Leaches
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27
Q

Describe multiple myelomas

A
  • Clonal proliferation of plasma cells in marrow

- Excessive Ig, M component, may be light chain only (Bence Jones protein)

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28
Q

Describe the presentation of multiple myelomas in horses

A

May become hypercalcaemic and have elevated parathyroid hormone-related protein (PTHrP), and hyperglobulinaemia

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29
Q

Describe the presentation of multiple myelomas in cattle

A
  • Nosebleeds
  • Emaciation
  • Hyperglobulinaemia
  • Amyloid deposition in lymph nodes, kidney, spleen, liver
  • Enlarged lymph nodes
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30
Q

Describe the presentation of multiple myelomas in dogs and cats

A
  • More common in dogs than cats
  • Hyperviscosity (bleeding, renal disease)
  • Hypercalcaemia of malignancy
  • Cytopaenias; anaemia, thormbocytopaenia, neutropaenia
  • Severe bone pain: multiple lucencies (shot gun lesions), fractures, bone marrow affected
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31
Q

How is multiple myeloma diagnosed?

A
  • Bone marrow aspirate
  • Urinary Bence Jones proteins
  • Serum protein electrophoresis (look for clonal Igs from one plasma cell clone population)
32
Q

Outline the treatment and prognosis of multiple myelomas

A
  • Pred and melphalan, plasmapharesis
  • May do well with treatment
  • Median survival time in dogs up to 18 months
33
Q

Outline the behaviour of extramedullary plasmacytomas

A
  • Varies with anatomical location
  • Oral cavity and cutaneous usually benign
  • Intestinal usually malignant, but colonic more favourable prognosis
34
Q

Outline the clinical signs of extramedullary plasmacytoma

A

Relate to location and presence of paraneoplastic conditions

35
Q

Outline the management of extramedullary plasmacytomas

A
  • For solitary disease: surgery and monitoring, oral and cutaneous can be curative
  • For alimentary: surgery followed by chemo when spread documented, recurrence common and metastasis ~1yr or more can be seen
36
Q

Name the disease of importance regarding the thymus of birds

A

Chicken infectious anaemia (chick anaemia virus, Circovirus)

37
Q

List the diseases of importance regarding the Bursa of Fabricius

A
  • Infectious bursal disease (Birna virus, Gumboro disease)

- Tumours

38
Q

List the diseases of importance regarding the spleen of birds

A
  • Tumours: Mareks disease (herpesvirus), Avian leukosis (retrovirus), reticuloendotheliosis (adenovirus)
  • Marble spleen disease of pheasants (adenovirus)
  • Haemorrhagic enteritis of Turkeys (adenovirus)
39
Q

Explain why chicks are most susceptible to infectious bursal disease

A
  • Disease requires presence of functioning bursa
  • Young chicks 3-8wo most susceptible
  • Atrophies with age
40
Q

Describe the aetiology of Infectious Bursal Disease

A
  • Birna virus trophic for B lymphocytes

- Very resistant virus that persists in environment and difficult to eliminate from flock

41
Q

Describe the clinical signs of Infectious Bursal Disease

A
  • Depression, ataxia, ruffled feathers (head and neck)
  • Diarrhoea (stained around vent)
  • Anorexia
  • Acute mortality
  • Varible long term immunsuppression +/- secondary infection in chronic state
42
Q

Describe the gross lesions found in Infectious Bursal Disease

A
  • Bursa enlarged, oedematous, congested, +/- haemorrhagic
  • Muscular haemorrhages
  • +/- swollen kidneys
43
Q

Describe the control of Infectious Bursal Disease

A
  • Cleaning and disinfection of housing
  • Vaccination complicated
  • In broilers: 1 live vaccine at 4 weeks, 1 inactivated at 16 weeks to protect progeny
  • Egg layers: 1 live vaccine around 4 weeks
44
Q

Describe the “gold standard” vaccination protocol for Infectious Bursal disease

A

Obtain blood samples from day old chicks for serology to decide age and vaccine that should be used

45
Q

Describe the aetiology and epidemiology of Mareks disease

A
  • Common presentation of backyard chickens
  • Most common in 2-7mo chickens, also turkey, pheasant, quail
  • Herpesvirus (gallid herpesvirus 2), chronically infected
46
Q

Describe the pathogenesis and transmission of Mareks disease

A
  • Initial viral replication in lungs
  • Cytolytic phase in lymphocytes: immunosuppression
  • Latent phase: transformation and lymphomas
  • Virus shedding from feather follicle epithelium
  • Incubation period: 4 weeks min, usually longer
  • Asymptomatic shedding possible
  • Infected birds viraemic for life
47
Q

Describe the clinical signs of Mareks disease

A
  • Depression, cachexia
  • Presented dead most common
  • Blindness
  • Secondary infection/ill thrift
48
Q

Describe the gross lesions seen with Mareks disease

A
  • Tumours - all parenchymatous organs common
  • Swollen nerves
  • Swollen feather follicles (lymphocytic folliculitis)
  • Iris infiltration (less common)
  • Swollen nerves and iris infiltration are pathognomic
49
Q

Describe the histopathological lesions seen with Mareks disease

A
  • T cell lymphosarcoma
  • Lymphocytic neuritis
  • Perivascular cuffing in brain
50
Q

Outline the treatment and control of Mareks disease

A
  • No treatment
  • Hygiene and disinfection
  • Backyard: Ensure vaccination of new stock (in ovo or as day old chicks)
  • Commercial: long lived birds all vaccinated
  • Several serotypes of vaccine available, all require injection, goo technique important for protection
  • Destocking
51
Q

Describe canine thymoma

A
  • Rare tumour of thymic epithelium
  • Usually self contained, some may spread
  • Usually cranial mediastinum
  • Not usually associated with distant spread
52
Q

Describe the clinical signs of canine thymoma

A
  • Respiratory distress
  • May see cranial caval syndrome (swollen head)
  • Myasthenia gravis
53
Q

Explain how canine thymomas cause cranial caval syndrome

A

Impaired drainage

54
Q

Explain how canine thymomas cause myasthenia gravis

A
  • Paraneoplastic

- Antigen mimicry from thymoma

55
Q

Describe the diagnosis of canine thymoma

A
  • Large thoracic mass on radiology (tracheal displacement and cranial focal soft tissue opacity)
  • Biopsy to distinguish from lymphoma
  • Flow cytometry
  • FNA will showa non-clonal population of lymphocytes
56
Q

Outline the treatment and prognosis for canine thymoma

A
  • Surgery to remove if possible, refer
  • Prognosis good if resectable
  • May involve major vessels and nerves so cannot be resected
57
Q

Describe the identification and possible causes of disease of the spleen in cattle

A
  • Most found at PM
  • key differential for splenomegaly: anthrax
  • Tyre-wire/hardwire possible abscess
58
Q

Describe the diseases of the spleen in pigs

A
  • Rarely the only organ involved
  • Splenic infarcts in swine fever
  • Splenomegaly: PMWS circovirus) and Glasser’s disease (Haemophilus parasuis)
  • Erysipelas: moderate to marked splenomegaly
59
Q

Describe the diseases of the spleen in horses

A
  • Well anatomically protected
  • Can be involved in colic (nephrosplenic entrapment)
  • Other diseases very rare
  • Can be removed if needed
60
Q

Describe the diseases of the spleen in alpacas

A

Splenic haematomas and torsions seen

61
Q

Describe the diseases of the spleen in cats

A
  • Splenic haemangiosarcoma rare

- Splenic MCT more common: mean age ~10yo, splenomegally +/- effusion

62
Q

Describe the diseases of the spleen in dogs

A
  • Splenic masses moderately common
  • Haematoma>neoplasia
  • Common site for metastasis
  • Present as mass or haemabdomen
  • Often incidentally found at vaccine/general exam
  • Can present with circulatory collapse
  • Haemangiosarcoma 36%, 60% benign masses e.g. haematoma, 4% other malignancies
63
Q

Describe the presentation of splenic disease in dogs

A
  • Mid abdominal mass usually ventral, non-painful
  • May have widespread mets if HSA so +/- cough
  • Splenic torsion as part of GDV
64
Q

Describe the presentation of a ruptured splenic mass in dogs

A
  • Pallor
  • Tachypnoea, tachycardia
  • Ascitic/distended abdomen
  • may have palpable fluid thrill
  • SUdden death feasible if huge bleed
  • Waxing and waning signs over moths with repeated bleeding and recovery
65
Q

List the diagnostics included in the investigation of splenic disease in the dog

A
  • Haematology to check PCV
  • Palpation
  • Imaging (radiography + ultrasound)
  • Abdominocentesis if free fluid seen
  • FNA/biopsy mass/splenectomy
66
Q

Discuss the approach to surgery for the treatment of splenic disease in dogs

A
  • Hard to get good diagnosis pre-op
  • Met check thorax
  • Care re. coagulopathy
  • Replace blood volume pre-op
  • Splenectomy better than hemi
  • Care with post-op arrhythmias, monitor 24-48hrs post op
67
Q

Outline the treatment approach to haemangiosarcomas that have metastasised to the spleen

A
  • Commonly in lungs, liver, LNs, brain and potentially skin/SC tissues
  • Surgery primary treatment (check abdo for mets)
  • Post op chemotherapy indicated in almost all cases
68
Q

Discuss the prognosis for splenic haemangiosarcomas

A
  • Splenectomy alone: survival 3 months
  • Splenectomy + chemotheraoy: 6 months
  • Die of diffuse metastatic disease, better prognosis if no splenic rupture
  • Doxorubicin every 3 weeks
69
Q

List the differential diagnoses for a group of calves showing sudden onset bleeding and petechiation

A
  • Anthrax
  • Rat bait poisoning
  • Bracken fern toxicity
  • Bovine neonatal pancytopaenia
  • BVDV
  • Trichothecene mycotoxicosis
  • Sepsis
  • Electrocution
  • Primary haemostatic disorders
70
Q

List the differential diagnoses for a group of calves showing sudden onset lethargy/recumbency and death

A
  • IBR
  • Anthrax
  • Clostridial disease
  • Hypoglycaemia
  • Nutritional deficiency
71
Q

List the differential diagnoses for a group of calves showing submandibular swellgin

A
  • Blocked salivary galnd
  • Enlarged submandibular lymph node
  • Haematomas
  • Infection (lumpy jaw/wooden tongue/calf diptheria), abscess
  • Oedema (cardiovasular origin)
  • Submandibular hypoplasia
72
Q

List the differentials for primary haemostasis disorders in cattle

A
  • Acute bracken fern toxicity
  • BVDV
  • Trichothecene mycotoxicosis
  • Bovine neonatal pancytopaenia
  • Ingestion of other bone marrow suppressive substances e.g. furazolidine nitrofuran antibiotic
  • Platelet malfunction e.g. inherited bovine thrombopathia in Simmental cattle
73
Q

Describe acute bracken fern toxicity in cattle

A
  • Usually young stock affected
  • Pyrexia, bloody diarrhoea, epistaxis, bleeding from eyes or vagina
  • Haematuria and petechial haemorrhages
  • death usually 1-3 days after onset of signs due to bacteraemia and massive haemorrhage into GIT
74
Q

List the differentials for secondary haemostasis disorders in cattle

A
  • Inherited deficiency of coagulation factors
  • Acquired deficiency of coagulation factors
  • Disseminated intravascular coagulation
75
Q

In a group of calves showing sudden onset petechiation and lethargy, what do the following haematological findings indicate?
Non-regenerative normochromic normocytic anaemia, thrombocytopaenia, neutropaenia, leukopaenia, lymphopaenia

A

All indicate bone marrow destruction, suggestive of bovine neonatal pancytopaenia

76
Q

List your differentials for a bilateral submandibular, non-painful swelling

A
  • Infection
  • Neoplasia
  • Non-infectious inflammation
  • Sialocoele
77
Q

List your differentials for PUPD

A
  • Renal disease
  • Endocrinopathy
  • Cystitis
  • Neurogenic/psychogenic polydipsia
  • Hypercalcaemia (neoplasia)

LCB2 (14 decks)

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