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Module 17 > Approach to Lymphoma & Leukaemia > Flashcards

Approach to Lymphoma & Leukaemia Flashcards

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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
what is primary skin lymphoma
starts in skin as the primary site
26
what is secondary skin lymphoma
spreads to the skin from another site (ex. lymph nodes) part of multicentric disease
27
what is the form of primary skin lymphoma almost always
T cell derived (2 forms)
28
what are the two types of primary skin lymphoma
1. primary cutaneous lymphoma (= dermal) 2. mucosis fungoides (= epitheliotropic/epidermal)
29
what is the origin of secondary skin lymphoma
T or B cell
30
is extranodal more common in dogs or cats
more common in cats
31
what are the sites of extranodal lymphoma
other than LNs --\> eyes, nose, brain, spine, kidneys
32
what are the clinical signs of extranodal lymphoma
signs vary with the site
33
how do you diagnose LSA (4)
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
34
how is a biopsy used to diagnose LSA
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)
35
what are the histolopathological classifications of LN
1. architecture 2. cell size 3. phenotype
36
what is the most common canine multicentric presentation of lymphoma
high grade lymphoma
37
what is the most common most common feline GI presentation
high grade lymphoma
38
what are the histological features of a high grade lymphoma
immature, undifferentiated lymphoblasts, rapidly dividing needs aggressive chemotherapy
39
what are the histological features of a low grade lymphoma
mature small differentiated lymphocytes, slowly dividing slowly progressive difficult to distinguish tumour LC from reactive LCs
40
how is the cell type determined with LSA
use antibody to detect B or T cell protein on the cell surface or inside the cell using immunohistochemistry
41
how can flow cytometry be used to determine the phenotype of LSA
collect fresh aspirates of LN and stain with antibodies to cell surface antigens (proteins)
42
how can PCR be used to determine LSA phenotype
extract DNA from tumour cells PCR for antigen receptor gene arragements (PARR)
43
what do clonal products (single size) PCR arrangements suggest
lymphoma
44
what do polyclonal products (multiple sizes) PCR arrangements suggest
heterogeneous lymphoid cell population ie inflammatory/reactive
45
when is PCR for antigen rearragenements useful
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
what are LSA serum biomarker tests
1. thymidine kinase 2. neoplasia index (NI) 3. lactate dehydrogenase (LDH)
47
what is thymidine kinase
enzyme that catalyzes pyrimidine salvage pathway pretreatment values are prognostic useful for monitoring LSA
48
what is neoplasia index
thymidine and c-reative protein (CRP) higher in lymphoma useful for diagnosis and monitoring
49
what are lactate dehydrogenase (LDH)
enzyme in glycolysis high in lymphoma but not prognostic
50
how can blood work be used for staging
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
how is lymphoma staged
52
what does concurrent disease affect (4)
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
how is lymhoma treated generally
1. stabilize paraneoplastic syndromes if present (hypercalcemia most common, prevent progressive irreversible renal destruction) 2. treat the lymphoma (steroids, chemotherapy)
54
how is hypercalcemia treated (2)
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
how can refractory hypercalcemia be treated (3)
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
what is the mean survival time with no treatment of LSA
1-2 months
57
what is the mean survival time with steroid treatment only of LSA
2-3 months
58
what is the response rate of LSA to chemo
80-90% response rate (complete response and partial response)
59
what is the mean survival time using COP chemo protocol of LSA in dogs
6-9 months
60
what is the mean survival time using CHOP chemo protocol of LSA in dogs
10-12 months
61
what is the response rate of LSA in cats to chemo
50-70%
62
what is the mean survival time of high grade LSA in cats
6-9 months
63
what is the mean survival time of low grade LSA in cats
17-23 months
64
how is LSA treated in cats
complete surgical resection (discrete GI mass) + CHOP = 13 months mean survival time
65
what LSA has a good prognosis (7)
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
what is a bad prognosis of LSA (7)
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
where does leukaemia originate
hemopoietic malignancy that usually originates in bone marrow transformation of bone marrow cells and cell proliferation
68
what does leukaemia result in
usually results in increased numbers of specific blood cells can spread to peripheral lymphoid/hemopoietic organs
69
how is leukaemia classified
1. lymphoid (most common) or myeloid 2. acute or chronic (myeloproliferative neoplasms)
70
what is the difference between lymphoid and myeloid
71
what is acute leukaemia
neoplastic transformation early in the cell lineage (proliferation of blasts)
72
what are examples of acute leukaemia
ex. myeloblastic, myelomonocytic, monocytic leukaemia (AML) erythroluekaemia, megakaryblastic leukaemia
73
what is chronic leukaemia
myeloproliferative neoplasm (MPN) neoplastic transformation late in the cell lineage (proliferation of mature differentiated cells)
74
what are examples of chronic leukaemia
chronic granulocytic monocytic leukaemia (CML) polycythemia vera essential thrombocythemia chronic basophilic eosinophilic leukaemia
75
what is the pathogenesis of leukaemia (3)
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
how do you differentiate acute vs chronic leukaemia based on appearance
chronic: generally well acute: often quite sick
77
how do you differentiate acute vs chronic leukaemia based clinical exam
chronic: clinically normal, mild lymphadenomegaly, big spleen/liver acute: big spleen/liver, mild lymphadenomegaly, pale mucus membranes
78
how do you differentiate acute vs chronic leukaemia based on hematology
chronic: high white cell counts, mild cytopenias of other lines acute: high/low WBC, immature circulating cells, cytopenias common
79
how do you differentiate acute vs chronic leukaemia based on biochem
chronic: PNS may be present acute: PNS less likely
80
how do you differentiate acute vs chronic leukaemia based on bone marrow
chronic: increased # of well differentiated cells, possibly other lines decreased acute: increased # of blasts, other lines decreased
81
how is leukaemia diagnosed
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
what is the prognosis of chronic leukaemia
good
83
what is the prognosis of acute leukaemia
poor
84
what is the difference between acute lymphoid leukaemia and lymphoma
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
what is the difference in how lymphoma and leukaemia patients present
**lymphoma:** **-**usually well -massive lymphadenopathy **leukaemia:** **-**often sick - mild lymphoadenopathy - usually severe hematological abnormalities
86
are lymphoma patients CD34 positive or negative on flow cytometry
negative
87
are leukaemia patients CD34 positive or negative on flow cytometry
positive
88
what is multiple myeloma
neoplastic proliferation of plasma cells (antigen stimulated B cells) in bone marrow
89
how does multiple myeloma present
myelophthisis (cytopenias) present as medical/oncological cases
90
what does multiple myeloma cause (2)
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
how is multiple myeloma diagnosed (4)
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
what should you do if serum protein is increased in multiple myeloma
do electrophoresis to separate albumin and different globulins by charage ## Footnote **polyclonal gammopathy (non-neoplastic)** **monoclonal gammopathy (neoplastic)**
93
what is polyclonal gammopathy caused by
inflammation/immune mediated disease FIP in cats
94
what causes monoclonal gammopathy
usually from B cell lineage cancer alone multiple myeloma most common b cell lymphoma chronic lymphocytic leukaemia
95
what does high protein lead to
hyperviscosity syndrome
96
what are the effects of hyperviscosity
1. increased resistance to blood flow 2. reduced blood flow 3. reduced organ perfusion
97
what are the signs of hyperviscosity (5)
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
how is myeloma treated
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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