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LCB2 > Leukaemia and lymphadenopathy > Flashcards

Leukaemia and lymphadenopathy Flashcards

Leukaemia, lymphoma, lymphadenopathy, pathology of the lymphoid system

1
Q

Define leukaemia

A

Neoplastic condition of bone marrow where neoplastic cells of lymphoid or non-lymphoid stem cells or their progeny, undergo clonal expansion with or without cellular differentiation

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2
Q

What causes the clinical signs seen with leukaemia?

A
  • Failure of normal marrow function
  • Infiltrated organ dysfunction
  • Hyperviscosity (increased globulin production)
  • Paraneoplastic syndromes (IMHA, hypercalcaemia
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3
Q

What are the 3 types of leukaemic proliferative disorders?

A
  • Lymphoproliferative
  • Myeloproliferative
  • Myelodysplastic
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4
Q

What are the categories of lymphoproliferative disorders?

A
  • Neoplastic B, T or NK cells: lymphoma, lymphoid leukaemia

- Plasma cell neoplasia: Myeloma

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5
Q

What are the categories of myeloproliferative disorders?

A
  • Erythroid
  • granulocytic monocytic
  • Megakaryocytic
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6
Q

Give examples of erythroid myeloproliferative disorders

A
  • Erythroleuakemia
  • Erythemic myelosis
  • Polycythaemia ver
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7
Q

Give examples of granulocytic-monocytic myeloproliferative disorders

A
  • Myeloblastic leukaemia
  • Myelomonocytic
  • Monocytic
  • Eosinophilic
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8
Q

Give examples of megakarycytic myeloproliferative disorders

A
  • Megakaryoblastic

- Thrombocythaemia

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9
Q

What is a lymphoma?

A

Proliferative disorder arising in organ or lymph node

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10
Q

What is lymphoid leukaemia?

A

Proliferative disorder arising in bone marrow/blood

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11
Q

What is a myeloma?

A

Plasma cell neoplasia in the bone marrow, produces antibodies

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12
Q

What cells type are myelomonocytic myeloproliferative disorders affecting?

A

Common precursor for myeloid cells and monocytes

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13
Q

What are myelodysplastic proliferative disorders?

A

Neoplasia in bone marrow, but is not as obvious what type as cells are not released into the circulation

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14
Q

Describe aleukaemic proliferative disorders

A
  • Do not have high white cell count
  • bone marrow full of neoplastic white cells, damaged white cell production
  • Unable to exit into circulation due to abnormality
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15
Q

How does cytopaenia develop with myeloid and lymphoid proliferative disorders?

A
  • Bone marrow crowded by neoplastic cells
  • stops production of other cell types
  • Low white cell count in blood, but those seen will be abnormal
  • Lose neutrophils first, then platelets then RBCs
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16
Q

Why does it take time for the number of RBCs in the blood to drop in myeloid or lyphoid proliferative disorders?

A

RBCs live for ~100 days

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17
Q

Describe the characteristics of acute lymphoid or myeloid leukaemias

A
  • Neoplastic transformation during stem cell proliferation
  • Large numbers of immature (undifferentiated) cells
  • Aggressive rapid disease
  • Cytopaenia very common
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18
Q

How is the acute leukaemia type diagnosed?

A
  • Can be acute lymphoid or acute myeloid
  • Diagnosis by immunophenotyping or clonality testing
  • Bone marrow aspirate and viewing under microscope often wrong
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19
Q

Which type of acute leukaemia is more common?

A

Acute lymphoid leukaemia more common

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20
Q

What is leukaemia defined as based on the proportion of neoplastic blast cells in marrow?

A

> 30% = leukaemia

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21
Q

Outline the methods of immunophenotyping used for acute leukaemias

A
  • Immuno-cytology/histology of marrow aspirates or biopsies

- Immuno-labelled flow cytometry of EDTA blood or marrow

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22
Q

Outline the method for clonality testing for acute leukaemias

A
  • PCR for Antigen Receptor Rearrangements (PARR)
  • Molecular biology looking at DNA of the lymphocyte, specifically the antigen receptor
  • Entire population carrying same antigen receptor = more likely to be neoplastic
  • Reactive population = multiple receptor types
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23
Q

describe the characteristic of chronic leukaemias

A
  • Neoplastic transformation after differentiation
  • Leads to large numbers of mature (differentiated) cells
  • Less organ damage, normal cells but more than normal
  • Slow progression, less aggressive
  • Cytopaenia rare
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24
Q

Describe chronic lymphoid leukaemia

A
  • Easy to identify

- Increased number indicates chronic

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25
Q

Describe chronic myeloid leukaemia

A
  • More difficult to identify
  • Increased numbers may be due to chronic inflammatory condition e.g. abscess
  • Bone marrow aspirates to identify neoplastic cells in bone marrow
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26
Q

Compare the proportion of blast cells in marrow in lymphoma involving the bone marrow and acute lymphoblastic leukaemia

A
  • Lymphoma: <40% in marrow

- Leukaemia: >40% in marrow

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27
Q

Compare the circulating blast count in lymphoma involving the bone marrow and acute lymphoblastic leukaemia

A
  • Lymphoma: lower

- Leukaemia: higher

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28
Q

Compare the cytopaenia in lymphoma involving the bone marrow and acute lymphoblastic leukaemia

A
  • Lymphoma: mild or absent

- Leukaemia: severe

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29
Q

Compare the lymphadenopathy in lymphoma involving the bone marrow and acute lymphoblastic leukaemia

A
  • Lymphoma: massive

- Leukaemia: mild to moderate

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30
Q

Compare the systemic illness lymphoma involving the bone marrow and acute lymphoblastic leukaemia

A
  • Lymphoma: may not be systemically ill

- Leukaemia: usually systemically ill

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31
Q

What are the potential causes of lymphadenopathy?

A
  • Reactive hyperplasia
  • Lymphadenitis
  • Metastatic neoplasia
  • Lymphoma
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32
Q

How can the cause of lymphadenopathy be identified?

A

FNA/FNCS

- NB before steroids (kill lymphocytes)

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33
Q

Compare the appearance of small, medium and large lymphocytes

A
  • Small: very thin rim of cytoplasm, only slightly larger than erythrocytes
  • Medium: distinctly larger than erythrocyte,s, larger rim of cytoplasm seen
  • Large: much larger than erythrocytes, large rum of cytoplasm
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34
Q

Describe the cytological appearance of reactive hyperplasia of the lymph node

A
  • Indistinguishable from normal
  • Heterogenous cell population
  • Marjority 75-95% small lymphocytes
  • low stage medium and large cells (up to 15% in reactive)
  • Occasionally plasma cells
  • Occasionally macrophages (>2% in reactive)
  • Very few neutrophils, eosinophils, mast cells
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35
Q

Describe the cytological appearance of a lymph node with lymphadenitis

A
  • Inflammatory process in the lymph node itself i.e. lymph node is target of insult
  • Increased neutrophils (>5%) or eosinophils (>3%)
  • Macrophages (>3%) incl epitheloid and multinnucleate giant cells in granulomatous inflammation
  • Inflammatory cells may be mildly increased or completely replace normal structure
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36
Q

What does eosinophilic lymphadenitis suggest?

A

Allergy

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37
Q

What does granulomatous or pyogranulomatous lymphadenitis suggest?

A

Fungal or protozoal infection

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38
Q

What may be found on cytology in lymph enlargement as a result of metastatic neoplasia?

A
  • Carcinoma cells drained into lymph node
  • Myeloproliferative disorders
  • Mast cells (>3%)
  • Melanoma cells
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39
Q

Describe the cytological appearance of the lymph node with lymphoma

A
  • Increased % of large immature lymphocytes (confident at 50% either medium or large type in population)
  • More mitotic elements than seen in reactive
  • More tingible body macrophages
  • More lymphoglandular bodies (cell fragility)
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40
Q

What is the role of the spleen?

A
  • Removal and destruciton of erythrocytes by histiocytes (non-specific removal of effete, damage, abnormal RBCs, specific removal of Ab coated RBCs)
  • Retrieval of iron from erythrocyte breakdown
  • Storage of blood
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41
Q

Describe the histological appearance of the spleen

A
  • Red pulp makes up majority (purple), meshwork of sinusoids with blood and macrophages
  • White pulp: lighter/blue, mainly T/B lymphocytes
42
Q

Give examples of common incidental findings on histology of the spleen

A
  • Senile nodular hyperplasia
  • Congestion
  • Siderofiborisis/calcinosis
  • Surface indentations
43
Q

Describe the histological apperance senile nodular hyperplasia of the spleen

A
  • Mixture of red and white pulp tissue
  • Possibly coincidental haemorrhage
  • If found on ultrasound, FNA, examine on slide and send to ClinPath before removal of spleen or euthanasia
44
Q

How does senile nodular hyperplasia occur?

A

Some areas do not work well with age, so others pick up the slack and compensate

45
Q

Describe the gross appearance of splenic congestion

A

When cut open, blood will ooze out

46
Q

How does siderofibrosis/calcinosis of the spleen occur?

A
  • massive haemoglobin iron turnover in spleen

- Over time can lead to accumulations of calcified iron storage leading to fibrosis

47
Q

How do surface indentations of the spleen occur?

A

Normal variation, no clinical relevance

48
Q

List the potential responses of the spleen to injury

A
  • Acute inflammation
  • Hyperplasia of monocyte/macrophage system: granulomatous disease
  • Lymphoid atrophy
  • Storage of blood or contraction to expel reserve blood
  • Neoplasia
49
Q

Describe the appearance of acute inflammation of the spleen

A
  • Hyperaemia
  • Microabscesses, abscesses
  • Swells
  • Dilation of vascular structures
50
Q

Describe the appearance of hyperplasia of monocyte/macrophage system in the spleen, and give examples of causes

A
  • Granulomatous disease
  • May be mycobacterial, fungal, porcine circovirus infecction
  • Chronic condition where macropahges are “losing” against the infectious agent
51
Q

Describe the processes taking place with hyperplasia of the lymphoid system in the spleen and common causes

A
  • Production of plasma cells and antibody
  • Cell mediated immunity
  • Often viral infection
52
Q

Describe the cause of and appearance of lymphoid atrophy of the spleen

A
  • Viral infection affects lymphocytes directly, leading to loss of lymphocyte population
  • If occurs over a prolonged period of time, lose lymphocytes and end up with loss of white pulp = lymphoid atrophy
  • Need to investigate for viruses that affect lymphocytes e.g. parvovirus, distemer
53
Q

What are the 2 types of splenomegaly?

A
  • Diffuse (uniform)

- Focal to multifocal (nodular)

54
Q

What are the potential causes of diffuse splenomegaly?

A
  • Infection/reactive hyperplasia
  • Congestion
  • Neoplasia (leukaemia, systemic tumours e.g. mast cells, haemangiosarcoma, myeloma, lymphoma)
  • Haemolytic anaemia
  • Advanced amyloidosis
55
Q

Outline the potential causes of splenic congestion

A
  • Barbiturate euthanasia
  • Anthrax
  • Torsion/GDV (occludes splenic vein, artery continues to supply blood, may rupture leading to death)
56
Q

List the potential causes of focal to multifocal splenomegaly

A
  • Nodular hyperplasia
  • Focal haematoma
  • Hamengioma/sarcoma, leiomyoma/sarcoma, fibrosarcoma
  • Abscesses e.g. Rhodococcus, Corynebacterium
57
Q

In a case of haemolytic anaemia, the spleen is small and the bilirubinis high. Does this suggest intra or extravascular haemolytic anaemia

A

Intravascular

58
Q

In a case of haemolytic anaemia, the spleen is enlarged. Does this suggest intra or extravascular haemolytic anaemia? Explain why

A

Extravascular, due to proliferation of macrophages leading to enlargement of the spleen

59
Q

What does the appearance of a “milky” spleen indicate?

A

Proliferation of cells

60
Q

Describe follicular hyperplasia of the spleen (appearance, cause)

A
  • Reactive hyperplasia of white pulp lymphoid tissue
  • Multiple white nodules indicating reactive spleen, proliferation of T and B cells due to detection of pathogen in blood
  • Suspicious of viraemia if see this
61
Q

List the different presentations of splenic inflammation

A
  • Can be capsule/peritonitis

- Parenchyma: splenitis or splenic abscesses

62
Q

What is the main concern regarding splenic haemorrhage?

A

Will affect the whole system and can be fatal quickly

63
Q

Describe splenic haemangiosarcomas as a cause of splenic haemorrhage

A
  • Omentalised spleen
  • Bleeds through
  • Underneath is malignant tumour that started in blood vessels of spleen
  • Prone to rupture
64
Q

Describe splenic haemangiomas as a cause of splenic haemorrhage

A
  • Benign vascular umours

- May rupture and be fatal e.g. if rupture too big to clot and close lesion

65
Q

Describe the gross appearance of splenic rupture

A

If animal survives, may get formation of accessory splenic tissue

66
Q

Describe haematomas as a cause of splenic haemorrhage

A

Can rupture, but not usually life threatening as tend to be small, but is not always the case

67
Q

Describe the gross appearance of splenic lymphoma

A
  • Massively enlarged spleen
  • Uniform enlargement, with white area of lymphoid proliferation
  • White shiny lesions, more nodular
  • Multiple variable size tumour emboli in the spleen
68
Q

Describe the histopathological appearance of a haemangiosarcoma

A

Full of blood, create a lot of poor vascular channels that can be seen as spaces on histology - may cause damage to RBCs, show up as schistocytes on smears

69
Q

Describe the development and spread of haemangiosarcomas

A
  • Metastasise early, quickly and widely
  • Focal proliferation
  • Can start anywhere in the circulatory system
70
Q

Describe the normal histological appearance of the thymus

A
  • Cell dense cortex
  • Full of immature T cells
  • Can see thymus and medulla clearly
71
Q

List the potential responses of the thymus to injury

A
  • Lymphoid atrophy
  • Inflammation (very rare)
  • Haemorrhages and haematomas
  • Neoplasia
72
Q

How does thymal injury lead to lymphoid atrophy?

A

No thymus tissue = no maturation of T lymphocytes

73
Q

Give examples of causes of thymal inflammation and describe the appearance

A
  • Porcine circovirus, Rickettsial infection

- Neutrophils and hyperaemia

74
Q

How may thymal haemorrhages and haematomas occur?

A

May occur during seizure/shock

75
Q

List the potential diseases processes that may occur in the thymus

A
  • Cyst formation
  • Hypoplasia
  • Atrophy
  • Depletion
  • Neoplasia
76
Q

Describe thymal cysts

A
  • Involution during puberty and some remnants remain producing cysts
  • Generally do not cause a problem
77
Q

Describe thymal hypoplasia

A
  • Causes immunodeficiency
  • Genetic condition
  • Cannot differentiate between self and non-self
  • No T cels produced
78
Q

Describe thymal atrophy

A
  • Can be stress induced or age related (normal physiological involution)
  • Age related is due to lack of growth factors and proliferative cytokines, accelerated by stress
79
Q

How does thymal depletion occur?

A

Viral infection e.g. EHV-1, FPV, CPV, CDV, FIV

80
Q

Give examples of thymal neoplasms

A
  • Thymic lymphoma (cats and cattle)

- Thymoma

81
Q

Describe thymomas

A
  • Epithelial plus lymphoid cells
  • Some association with myasthenia gravis suggested
  • Usually benign proliferation of all structures within the thymus, including the epithelial structures e.g. Hassle’s corpuscles
82
Q

What is SCID and how does it develop?

A
  • Not single condition, collection of entities varying in severity and molecular basis
  • All result in failed production of functional lymphocytes (splenic and thymic hypoplasia)
83
Q

Which species are classically affected by SCID?

A

Horses, humans, mice, dogs

84
Q

Describe SCID in Arabian horses

A
  • Autosomal recessive in Arabian horse and their crosses
  • All affected foals die by 5mo as a result of infection by variety of pathogens
    E.g. Equine adenovirus, Pneumosystitis carinii, Cryptosporidium parvum, rhodococcus equi
85
Q

Describe the lesions seen in foals with SCID

A
  • Bilateral cranioventral bronchopneumonia
  • Small spleen, lymph nodes and thymus
  • Abscesses common
86
Q

How is SCID diagnosed in horses?

A

PCR to identify genetic condition

87
Q

What are the 2 major molecular mechanisms of SCID of importance in animals?

A
  • Autosomal recessive defect causing inhibition of DNA dependent protein kinase (Arabian foals, JRT, strain of mice)
  • X-linked defect in type I cytokine receptors (Bassett hound, Cardigan Welsh Corgi)
88
Q

Give examples of myeloid neoplasias

A
  • Myeloid leukaemias/dysplasias
  • Histiocytic neoplasias
  • Mast cell tumours
89
Q

Name the anatomical distributions that are possible for lymphomas

A
  • Multicentric (most common, multiple organs affected)
  • Alimentary
  • Medastinal
  • Other e.g. cutaneous, cardiac
  • Ontra and extradural primary lymphoma
90
Q

Describe the metastasis of lymphomas

A
  • Local lymph nodes similarly affected as primary tissue leading to lymphadenomegaly
  • Infiltration of liver and spleen common
  • Spread haematogenously
91
Q

What may lymphomas occur secondary to?

A

Viral infection e.g. FeLV, BLV, bovine enzootic lymphoma

- BLV often abomasal involvement

92
Q

What is the prognosis for lymphomas dependent on?

A
  • Immunophenotype (B or T cell or non-B/non-T)
  • Cellular morphology
  • Histologic pattern (diffuse vs follicular)
  • Biologic behaviour (low to high grade)
93
Q

Describe the characteristics of a high grade lymphoma

A
  • Neoplastic lymphocytes large
  • Large nuclei with dispersed chromatin and prominent nuclei
  • Mitosis figures evident
  • Lots of variability in cells and nuclei
  • Quick, wide, easy metastasis
94
Q

Describe the characteristics of a low grade lymphoma

A
  • Neoplastic lymphocytes small to intermediate size
  • Partially condensed chromatin
  • Look like normal mature lymphocytes mostly
95
Q

What structures are commonly affected by lymphoma in cattle?

A
  • Abomasum
  • Vertebral canal
  • Kidney
  • Heart
  • Retro-orbital space
  • Uterus
96
Q

What structure is usually affected by alimentary lymphomas?

A

Small intestine

97
Q

Describe the gross appearance of splenic lymphoma

A
  • Gross enlargement with pale subscapular nodules

- mottled appearance of spleen due to infiltration of malignant lymphocytes into portal areas

98
Q

Describe the histopathological appearance of splenic lymphoma

A
  • Sheets of round cells effacing normal splenic architecture
  • Absence of normal red or white pulp
99
Q

What is meant by a blast crisis?

A

Sudden switch from chronic to acute leukaemia, unknown cause

100
Q

Describe the bone marrow in a case of chronic leukaemia

A
  • Hypercellular bone marrow

- Consists entirely of haematopoietic tissue (red), no fat

LCB2 (14 decks)

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