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Module 17 > Approach to Lymphoma & Leukaemia > Flashcards

Approach to Lymphoma & Leukaemia Flashcards

1
Q

where does lymphoma originate from

A

lymph nodes and peripheral lymphoid tissues

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2
Q

where does leukaemia originate from

A

bone marrow

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3
Q

where does multiple myeloma originate from

A

bone marrow

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4
Q

what are the lymphoid progenitor neoplasias

A

T cell

B cell

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5
Q

what are the myeloid progenitor neoplasia (6)

A
  1. RBC
  2. platelet
  3. basophilic
  4. eosinophilic
  5. neutrophilic
  6. monocytotic
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6
Q

what are the types of hemopoietic neoplasias

A
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7
Q

what is lymphoma also known as

A

malignant lymphoma

lymphosarcoma (LSA)

non hodgkin’s lymphoma

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8
Q

what is lymphoma

A

malignant proliferation of peripheral lymphoid tissues (ex. lymph nodes) but can sometimes infiltrate bone marrow (stage V)

complex disease/group of diseases over 40 different subtypes based on histology, anatomical location immunophenotype

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9
Q

what are the predisposing factors of lymphoma (5)

A
  1. genetics
  2. age
  3. spayed females (dogs)
  4. virus (FeLV and FIV) (cats)
  5. environment (passive smoking in cats and dogs)
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10
Q

what are the clinical signs of lymphoma (4)

A
  1. asymptomatic/clinically well but palpable mass/lymph node
  2. non-specific (general malaise, lethargy, inappetance, fever, weight loss)
  3. paraneoplastic disease (hypercalcemia, more T cell related esp mediastinal mass, hyperviscosity more B cell (Ig) related)
  4. organ specific signs related to anatomical classification
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11
Q

what are organ specific signs of lymphoma (5)

A
  1. multicentric (peripheral nodes)
  2. alimentary (GI)
  3. thymic (mediastinal)
  4. cutaneous
  5. extranodal
    dog: multicentric, GI, mediastinal, cutaneous
    cat: GI, extranodal, peripheral node/mediastinal
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12
Q

what is lymphadenomegaly and how does it form

A

most common multicentric form in dogs

non painful very enlarged LNs, usually generalized

usually derived from B cells of large size ex. immature lymphoblasts –> diffuse large B cell lymphoma (DLBCL)

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13
Q

what is shown here

A

lymphadenomegaly

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14
Q

what is alimentary/GI lesions in lymphoma

A

most common site in cats (older, FeLV negative)

usually in small intestine (focal or diffuse +/- LN enlargement) possibly stomach, colon rare

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15
Q

what are the signs of alimentary/GI lesions in lymphoma

A

vomiting, diarrhea, weight loss, anorexia

palpable abdominal mass, thickened loops intestine

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16
Q

what are the pathology grades in alimentary lesions in lymphoma (2)

A
  1. high grade (poor prognosis): large/intermediate blasts, often B cell
    - usually palpable abdominal mass –> focal, +/- LN enlargement, but can be diffuse too
  2. low grade (poor prognosis): small mature lymphocytes, often T cell
    - thickened intestine –> more diffuse but can appear grossly normal (ddx is IBD)
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17
Q

what might be seen on US with GI LSA

A
  1. mass, lymphadenomegaly
  2. thickening of gut wall
  3. loss of layering
  4. regional/segmental hypomotility –> no peristalsis
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18
Q

what is mediastinal (thymic) lesions in lymphoma common in

A

common younger cats with FeLV positive

common in dogs (often hypercalcemic)

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19
Q

what are the signs of mediastinal lymphoma (3)

A
  1. cough, dyspnea
  2. pleural effusion
  3. dull heart/lung sounds
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20
Q

what can be seen on thoracic xrays with mediastinal lymphoma lesions (3)

A
  1. anterior mediastinal mass on xray
  2. elevated trachea
  3. enlarged tracheobronchial/sternal LN
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21
Q

what is the origin of mediastinal lymphoma most often

A

T cell derived

thymus derived

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22
Q

what virus is mediastinal thymic lymphoma associated with in cats

A

FeLV positive –> poor prognosis

better prognosis in FeLV negative cats

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23
Q

is cutaneous lymphoma more common in cats or dogs

A

more common in dogs

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24
Q

what are the signs of cutaneous lymphoma

A
  1. erythema (redness of the skin or mucous membranes, caused by hyperemia (increased blood flow) in superficial capillaries)
  2. pruritus
  3. ulceration
  4. skin nodules
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25
Q

what is primary skin lymphoma

A

starts in skin as the primary site

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26
Q

what is secondary skin lymphoma

A

spreads to the skin from another site (ex. lymph nodes)

part of multicentric disease

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27
Q

what is the form of primary skin lymphoma almost always

A

T cell derived (2 forms)

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28
Q

what are the two types of primary skin lymphoma

A
  1. primary cutaneous lymphoma (= dermal)
  2. mucosis fungoides (= epitheliotropic/epidermal)
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29
Q

what is the origin of secondary skin lymphoma

A

T or B cell

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30
Q

is extranodal more common in dogs or cats

A

more common in cats

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31
Q

what are the sites of extranodal lymphoma

A

other than LNs –> eyes, nose, brain, spine, kidneys

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32
Q

what are the clinical signs of extranodal lymphoma

A

signs vary with the site

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33
Q

how do you diagnose LSA (4)

A
  1. sample a representative lesion (mass) or LN
  2. examine representative fluid (ex. pleural)
  3. FNA for cytology is diganostic in many cases
  4. large/intermediate size immature lymphoblasts
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34
Q

how is a biopsy used to diagnose LSA

A

needed if any doubt from FNA or for more precise subclassifications/grade of lymphoma

remove whole node if possible to examine LN architecture (follicles intact or ablated – diffuse infiltrate)

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35
Q

what are the histolopathological classifications of LN

A
  1. architecture
  2. cell size
  3. phenotype
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36
Q

what is the most common canine multicentric presentation of lymphoma

A

high grade lymphoma

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37
Q

what is the most common most common feline GI presentation

A

high grade lymphoma

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38
Q

what are the histological features of a high grade lymphoma

A

immature, undifferentiated lymphoblasts, rapidly dividing

needs aggressive chemotherapy

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39
Q

what are the histological features of a low grade lymphoma

A

mature small differentiated lymphocytes, slowly dividing

slowly progressive

difficult to distinguish tumour LC from reactive LCs

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40
Q

how is the cell type determined with LSA

A

use antibody to detect B or T cell protein on the cell surface or inside the cell using immunohistochemistry

41
Q

how can flow cytometry be used to determine the phenotype of LSA

A

collect fresh aspirates of LN and stain with antibodies to cell surface antigens (proteins)

42
Q

how can PCR be used to determine LSA phenotype

A

extract DNA from tumour cells

PCR for antigen receptor gene arragements (PARR)

43
Q

what do clonal products (single size) PCR arrangements suggest

44
Q

what do polyclonal products (multiple sizes) PCR arrangements suggest

A

heterogeneous lymphoid cell population

ie inflammatory/reactive

45
Q

when is PCR for antigen rearragenements useful

A

to confirm lymphoma diagnosis at difficult sites where only small FNA samples possible

useful to determine whether B or T cell depending on whether clone is seen with B or T cell primers

46
Q

what are LSA serum biomarker tests

A
  1. thymidine kinase
  2. neoplasia index (NI)
  3. lactate dehydrogenase (LDH)
47
Q

what is thymidine kinase

A

enzyme that catalyzes pyrimidine salvage pathway

pretreatment values are prognostic useful for monitoring LSA

48
Q

what is neoplasia index

A

thymidine and c-reative protein (CRP) higher in lymphoma

useful for diagnosis and monitoring

49
Q

what are lactate dehydrogenase (LDH)

A

enzyme in glycolysis high in lymphoma but not prognostic

50
Q

how can blood work be used for staging

A

hematology reflects bone marrow cells as baseline prior to chemotherapy and may see circulating LSA cells in the blood

biochem indicates organ involvement and paraneoplastic syndromes

FeLV and FIV status for cats

51
Q

how is lymphoma staged

52
Q

what does concurrent disease affect (4)

A
  1. prognosis
  2. treatment decision
  3. affects choice of chemo agents (drug metabolism or excretion, concurrent use of NSAIDs for arthritis)
  4. may need to extend staging procedures to evaluate disease fully (extra blood tests, echocardiography etc)
53
Q

how is lymhoma treated generally

A
  1. stabilize paraneoplastic syndromes if present (hypercalcemia most common, prevent progressive irreversible renal destruction)
  2. treat the lymphoma (steroids, chemotherapy)
54
Q

how is hypercalcemia treated (2)

A
  1. correct fluid deficit: restore circulating volume and support kidneys (0.9% saline diuresis at 2-3x maintenance)
  2. loop diuretics (frusemide) optional once rehydrated
55
Q

how can refractory hypercalcemia be treated (3)

A
  1. glucocorticoids (IV or oral): decrease bone and intestinal absorption, promote renal excretion, toxic to lymphocytes (do not give prior to diagnosis of LSA)
  2. calcitonin (SC): decrease serum Ca
  3. bisphosphates (IV pamidronate, soledronate or possibly oral alendronate): decrease osteoclast activity, some antitumour activity, potentially analgesic, renal toxicity possible with pamidronate (lots of fluids)
56
Q

what is the mean survival time with no treatment of LSA

A

1-2 months

57
Q

what is the mean survival time with steroid treatment only of LSA

A

2-3 months

58
Q

what is the response rate of LSA to chemo

A

80-90% response rate (complete response and partial response)

59
Q

what is the mean survival time using COP chemo protocol of LSA in dogs

A

6-9 months

60
Q

what is the mean survival time using CHOP chemo protocol of LSA in dogs

A

10-12 months

61
Q

what is the response rate of LSA in cats to chemo

62
Q

what is the mean survival time of high grade LSA in cats

A

6-9 months

63
Q

what is the mean survival time of low grade LSA in cats

A

17-23 months

64
Q

how is LSA treated in cats

A

complete surgical resection (discrete GI mass) + CHOP = 13 months mean survival time

65
Q

what LSA has a good prognosis (7)

A
  1. well patients (substage A)
  2. low clinical stage (I or II)
  3. low histological grade
  4. B cell immunophenotype (dogs – not shown in cats)
  5. nasal site (cats and probably dogs)
  6. CR to treatment (cats)
  7. using doxorubicin in protocol (cats)
66
Q

what is a bad prognosis of LSA (7)

A
  1. sick pateints (substage B)
  2. high clinical stage (V) – bone marrow
  3. T cell immunophenotype (dogs, not done in cats)
  4. certain locations (skin, CNS, ocular)
  5. FeLV/FIV positive (cats)
  6. not achieving complete remission (cats)
  7. prior steroid use (multidrug resistance)
67
Q

where does leukaemia originate

A

hemopoietic malignancy that usually originates in bone marrow

transformation of bone marrow cells and cell proliferation

68
Q

what does leukaemia result in

A

usually results in increased numbers of specific blood cells

can spread to peripheral lymphoid/hemopoietic organs

69
Q

how is leukaemia classified

A
  1. lymphoid (most common) or myeloid
  2. acute or chronic (myeloproliferative neoplasms)
70
Q

what is the difference between lymphoid and myeloid

71
Q

what is acute leukaemia

A

neoplastic transformation early in the cell lineage (proliferation of blasts)

72
Q

what are examples of acute leukaemia

A

ex. myeloblastic, myelomonocytic, monocytic leukaemia (AML)

erythroluekaemia, megakaryblastic leukaemia

73
Q

what is chronic leukaemia

A

myeloproliferative neoplasm (MPN)

neoplastic transformation late in the cell lineage (proliferation of mature differentiated cells)

74
Q

what are examples of chronic leukaemia

A

chronic granulocytic

monocytic leukaemia (CML)

polycythemia vera

essential thrombocythemia

chronic basophilic

eosinophilic leukaemia

75
Q

what is the pathogenesis of leukaemia (3)

A

proliferation of neoplastic cells in the bone marrow causes

  1. crowding out of BM (myelophthisis) leading to cytopenias (severe in acute, mild in chronic)
  2. high numbers of neoplastic cells in the circulation (large buffy coat): immature ‘blasts’ = acute and mature well differentiated cells = chronic
  3. secondary invasion of other organs: LNs, liver, spleen –> hence mild lymphadenopathy, big spleen (EM hemotopoiesis too)
76
Q

how do you differentiate acute vs chronic leukaemia based on appearance

A

chronic: generally well
acute: often quite sick

77
Q

how do you differentiate acute vs chronic leukaemia based clinical exam

A

chronic: clinically normal, mild lymphadenomegaly, big spleen/liver
acute: big spleen/liver, mild lymphadenomegaly, pale mucus membranes

78
Q

how do you differentiate acute vs chronic leukaemia based on hematology

A

chronic: high white cell counts, mild cytopenias of other lines
acute: high/low WBC, immature circulating cells, cytopenias common

79
Q

how do you differentiate acute vs chronic leukaemia based on biochem

A

chronic: PNS may be present
acute: PNS less likely

80
Q

how do you differentiate acute vs chronic leukaemia based on bone marrow

A

chronic: increased # of well differentiated cells, possibly other lines decreased
acute: increased # of blasts, other lines decreased

81
Q

how is leukaemia diagnosed

A
  1. hematology is suggestive: large # of malignant/aberrant cells on blood smear, cyotpenias etc
  2. bone marrow sample: usually diagnostic –> altered cell maturation, malignant cells
  3. flow cytometry (blood or marrow): helps to differentiate cell lineage and precursors using specific antibodies to cell sufrace proteins
82
Q

what is the prognosis of chronic leukaemia

83
Q

what is the prognosis of acute leukaemia

84
Q

what is the difference between acute lymphoid leukaemia and lymphoma

A

both characterized by blast cell proliferation (lymphoblasts)

lymphoma: malignant neoplasms of peripheral lymphoid tissue, can affect bone marrow (stage V), prognosis is reasonable with chemo

acute lymphoid leukaemia: originates within bone marrow, can spread to peripheral tissues, prognosis is poor even with chemo

85
Q

what is the difference in how lymphoma and leukaemia patients present

A

lymphoma:

-usually well

-massive lymphadenopathy

leukaemia:

-often sick

  • mild lymphoadenopathy
  • usually severe hematological abnormalities
86
Q

are lymphoma patients CD34 positive or negative on flow cytometry

87
Q

are leukaemia patients CD34 positive or negative on flow cytometry

88
Q

what is multiple myeloma

A

neoplastic proliferation of plasma cells (antigen stimulated B cells) in bone marrow

89
Q

how does multiple myeloma present

A

myelophthisis (cytopenias)

present as medical/oncological cases

90
Q

what does multiple myeloma cause (2)

A
  1. increased/abnormal Ig production from plasma cells = hyperproteinemia (on biochem) due to hyperglobulinemia
    - impared ability to fight infection
    - light chains excreted –> renal damage
  2. infiltration of other organs by cancer cells
    - bones: skeletal lesions (back pain, skeletal pain or lameness, collapse)
    - kidneys and other tissues
91
Q

how is multiple myeloma diagnosed (4)

A
  1. plasma cells in bone marrow sample (>10%)
  2. osteolytic bone lesions on radiographs (spinous process, pelvis)
  3. myeloma proteins in blood = monoclonal gammopathy –> overproduction of clonal Ig by plasma cells seen as single peak on electrophoresis of serum proteins
  4. myeloma proteins in urine (Ig light chains) = bence jones proteinuria not seen on dipsticks do percipitation test
92
Q

what should you do if serum protein is increased in multiple myeloma

A

do electrophoresis to separate albumin and different globulins by charage

polyclonal gammopathy (non-neoplastic)

monoclonal gammopathy (neoplastic)

93
Q

what is polyclonal gammopathy caused by

A

inflammation/immune mediated disease

FIP in cats

94
Q

what causes monoclonal gammopathy

A

usually from B cell lineage cancer alone

multiple myeloma most common

b cell lymphoma

chronic lymphocytic leukaemia

95
Q

what does high protein lead to

A

hyperviscosity syndrome

96
Q

what are the effects of hyperviscosity

A
  1. increased resistance to blood flow
  2. reduced blood flow
  3. reduced organ perfusion
97
Q

what are the signs of hyperviscosity (5)

A
  1. heart: cardiomyopathy
  2. ocular: retinal lesions/detachment
  3. neurological: lethargy, seizures
  4. kidney: azotemia
  5. coagulopathy

lethargy, seizures, blindness, bleeding

complex medical cases

98
Q

how is myeloma treated

A

chemo to kill neoplastic plasma cells in bone marrow and other sites

lytic lesions may/may not resolve –> very painful

but before chemotherapy need to address paraneoplastic and other problems (hyperviscosity, hypercalcemia, secondary infection due to abnormal Ig)

Module 17 (31 decks)

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