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Small Animal (Poppy) > Lymphoid and Myeloid > Flashcards

Lymphoid and Myeloid Flashcards

1
Q

Myeloid

A

Anything to do with the bone marrow and the cells it produces

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2
Q

Which cells are myeloid?

A

Granulocytes (neutrophils, eosinophils, mast cells)
Monocytes
Macrophages
Erythrocytes
Thrombocytes
Dendritic cells

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3
Q

Which cells are lymphoid?

A

Lymphocytes

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4
Q

Which tissues are lymphoid?

A

Lymph nodes
Thymus
Spleen
Peyer’s patches

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5
Q

What hormone is associated with physiological leucocytosis (‘fight/flight’)?

A

Epinephrine

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6
Q

What hormone is associated with physiological stress (‘stress leukogram’)?

A

Corticosteroid

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7
Q

What is different about a stress leukogram in hypoadrenocorticism/Addisonian crisis?

A

Insufficient cortisol being produced to stimulate a stress leukogram

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8
Q

In which ways is the myeloid/lymphoid system stimulated?

A

Epinephrine
Corticosteroid
Iatrogenic antigenic stimulation (vaccine)
Inflammation
Infection
Parasites/foreign bodies

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9
Q

Lymph node enlarges as part of immune response to lymphatic drainage from affected site

A

Reactive hyperplasia

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10
Q

Infection or inflammation of the lymph node

A

Lymphadenitis

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11
Q

Non-neoplastic lymphadenopathy pathophysiology (2)

A

Reactive hyperplasia
Lymphadenitis

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12
Q

Investigating a lymphadenopathy

A

History (infection/inflammation/medication)
Physical exam (LN enlargement)
Imaging?
FNA?

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13
Q

What is chyle?

A

Mixture of lymph and chylomicrons

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14
Q

What are chylomicrons?

A

Lipids absorbed from intestine and transported via lymphatics

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15
Q

What are the causes of chylous effusions?

A

Rupture (trauma)
Obstruction of thoracic duct or other major lymphatic vessel (neoplasia)
Often idiopathic

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16
Q

How does chylothorax usually present?

A

Bilateral pleural effusion

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17
Q

Management of chylothorax

A

Thoracocentesis (therapeutic and diagnostic)
Surgical closure of thoracic duct?

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18
Q

Lymphangiectasia pathophysiology

A

Intestinal lymphatics dilate, chyle lost in lumen (protein losing enteropathy)

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19
Q

Causes of lymphangiectasia

A

Idiopathic
Congenital
Acquired obstruction (neoplasia)

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20
Q

Is lymphangiectasia more common in dogs or cats?

A

Dogs

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21
Q

Management of lymphangiectasia

A

Low fat diet
+/- Immunosuppressives (prednisolone)

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22
Q

Diagnosis for lymphangiectasia

A

History (GI signs)
Physical exam (low BCS, ascites)
Biochemistry (hypoalbuminaemia/hypocholesterolaemia)
Haematology (lymphopaenia very suspect, not always seen)
Ultrasound (hyperechoic lacteals)
Biopsy (endoscopic or surgical)

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23
Q

What is seen in endoscopic biopsy of lymphangiectasia?

A

White bumps in lumen where lacteal ducts have dilated

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24
Q

Risk of surgical biopsy in lymphangiectasia

A

Low albumin associated with wound dehiscence

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24
Q

Risk of surgical biopsy in lymphangiectasia

A

Low albumin associated with wound dehiscence

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25
Q

Aplastic anaemia

A

Failure of myeloid cell production

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26
Q

In what order do cell lines become depleted in aplastic anaemia?

A

Neutropaenia, then thrombocytopaenia, then anaemia

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27
Q

Aplastic anaemia is usually secondary to…

A

Toxicity
Adverse drug reaction
Infection (Ehrlichia, parvo, FLV)

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28
Q

Pure red cell aplasia

A

Failure of erythrocyte production
Rare, may be secondary to FeLV

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29
Q

How do bone marrow infiltrates cause non-neoplastic myeloid disease? (Rare)

A

Myelofibrosis
Gelatinous transformation

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30
Q

Myeloid cell neoplasias

A

Mast cell tumour
Histiocytoma
Transmissible venereal tumour

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31
Q

Myeloid leukaemia key features

A

Rare
Acute: immature cells
Chronic: differentiated cells

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32
Q

What is polycythaemia vera?

A

Chronic form of myeloid leukaemia where excess erythrocytes are produced by the bone marrow

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33
Q

Where is the visceral form of mast cell tumour found in cats?

A

Spleen
Lymph nodes
Liver

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34
Q

Histiocytoma key features

A

Common
Young dogs (<2y)
usually benign
Can regress over several weeks

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35
Q

What can a histiocytoma look like?

A

Mast cell tumour

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36
Q

What tumour would you suspect with this presentation?

A

Transmissible venereal tumour

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37
Q

Treatment for transmissible venereal tumour

A

Chemotherapy (e.g. vinchristine)

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38
Q

What tumour is likely to be associated with this cytological finding?

A

Mast cell tumour

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39
Q

Lymphoid neoplasias

A

Lymphoid leukaemia
Plasmocytoma
Lymphoma

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40
Q

Lymphoid leukaemia key features

A

Rare
T/B/natural killer cells
Acute or chronic

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41
Q

Is plasmacytoma malignant or benign?

A

Benign

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42
Q

Does B or T cell lymphoma respond better to therapy?

A

B (remember B = better)

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43
Q

What structure does a T-zone indolent lymphoma usually affect?

A

Submandibular lymph node

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44
Q

What are the problems with treatment of a T-zone indolent lymphoma?

A

Low Ki67 index
Surgical removal of lymph node may be attempted

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45
Q

Rare cutaneous form of lymphoma

A

Epitheliotropic

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46
Q

Reasons for WBC number/morphology change in blood

A

Infection
Stress related (inflammation/endocrine)
Lymphoid/myeloid neoplasia

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47
Q

Where are neutrophils produced?

A

Bone marrow
(Occasionally extramedullary haematopoiesis: spleen/liver etc.)

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48
Q

What are the stages of immature to mature neutrophils?

A

Myeloblast
Progranulocyte
Myelocyte
Metamyelocyte
Band
Segmented

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49
Q

Which neutrophils stages are proliferating and maturing?

A

Myeloblast
Pyogranulocyte
Myelocyte

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50
Q

Which neutrophil stages are just maturing and may be found in blood?

A

Metamyelocyte
Band
Segmented

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51
Q

Stages required for a cell to leave blood vessels

A

Marginalisation
Adhesion
Migration

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52
Q

Factors which cause cells to shift from marginal to circulating pool

A

Epinephrine
Glucocorticoids
Infection
Stress

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53
Q

What happens when cells shift from marginal to circulating pool?

A

Apparent increase in circulating volume without increase in production

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54
Q

How do cells become marginalised?

A

Binding selectin receptors on blood vessels to ligands on cell walls

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55
Q

Causes of neutrophilia

A

Inflammation (infection/immune mediated anaemia/necrosis)
Steroids (stress/therapy/HAC)
Physiological (epinephrine/excitement/fear)
Chronic neutrophil leukaemia
Paraneoplastic
Leukocyte adhesion deficiency

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56
Q

If there are more segmented neutrophils than immature and neutrophil numbers are increased then is the left shift regenerative or degenerative?

A

Regenerative

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57
Q

If there are more immature neutrophils than segmented and neutrophil numbers are increased/decreased/normal then is the left shift regenerative or degenerative?

A

Degenerative

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58
Q

What happens in a right shift?

A

Glucocorticoids down-regulate adhesion molecules, less neutrophils leave circulation

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59
Q

Common causes of neutropaenia

A

Inflammation (per-acute/overwhelming bacterial infections, parvo)
Decreased production (infections, toxicity, neoplasia, marrow necrosis, myelofibrosis)

60
Q

Rare causes of neutropaenia

A

Immune mediated
Chediak-Higashi
Acyclic haematopoiesis (grey collies)
Canine hereditary neutropaenia

61
Q

Causes of neutrophil toxic change

A

Usually severe bacterial infection
Parvo
IMHA
Acute renal failure
DIC
Neoplasia

62
Q

Prognosis when there is lots of neutrophil toxic change

A

Poor

63
Q

What is this cytological finding?

A

Neutrophilic toxic change (foamy cytoplasm, dispersed organelles)

64
Q

What is this cytological finding?

A

Dohle bodies (focal blue grey cytoplasmic structures)

65
Q

Cytological features of reactive lymphocytes

A

More cytoplasm
Most cytoplasmic basophilia
Perinuclear halo
Prominent golgi zone
Larger, eccentric, cleaved nucleus
More large/medium sized (small in peripheral blood)

66
Q

Functional lymphocyte inclusions

A

Large granular lymphocytes

67
Q

Infectious lymphocyte inclusions

A

Ehrlichia
Distemper

68
Q

Metabolic lymphocyte inclusions

A

Lysosomal storage diseases

69
Q

In which age group are reactive lymphocytes more prevalent?

A

Young animals

70
Q

Reasons for lymphocytosis

A

Physiological
Chronic inflammation
Young animals/recent vaccination
Lymphoproliferative disorder (FeLV/BLV)
Hypoadrenocorticism

71
Q

Why is lymphocytosis seen with hypoadrenocorticism?

A

Loss of normal lymphocyte inhibition by glucocorticoids

72
Q

Causes of lymphopaenia

A

Stress/steroid
Acute inflammation
Loss of lymph (chylothorax/lymphagiectasia)
Cytotoxic drugs/radiation
Immunodeficiency
Lymphoma

73
Q

Where are monocytes found?

A

Blood

74
Q

Where are macrophages found?

A

Tissue

75
Q

What are monocytes and macrophages responsible for?

A

Phagocytosis

76
Q

Causes of monocytosis

A

Inflammation
Steroid/stress
Monocytic/myelomonocytic leukaemia

77
Q

Cause of eosinophilia

A

Hypersensitivity
Parasitism
Hypoadrenocorticism
Paraneoplastic (mast cell)
Idiopathic syndromes (canine eosinophilic bronchopneumopathy, myositis, feline eosinophilic granuloma)
Eosinophilic leukaemia (rare)

78
Q

When are nucleated red cells seen in moderate numbers?

A

Regenerative anaemia
Lead toxicity
Extramedullary hematopoiesis/EMH
Splenic contraction
Damaged marrow
Erythroleukaemia

79
Q

How should you confirm WBCC?

A

Smear

80
Q

Neoplastic condition of the bone marrow in which neoplastic cells of lymphoid or non-lymphoid stem cells undergo clonal expansion with or without cellular differentiation

A

Leukaemia

81
Q

Which tissues may be infiltrated by leukaemic cells in the circulation?

A

Liver
Spleen
Lymph nodes

82
Q

What is the cause of clinical signs in leukaemia?

A

Failure of normal marrow function
Infiltrated organ dysfunction
Hyperviscosity
Paraneoplastic syndromes (IMHA, hypercalcaemia)

83
Q

Specific B-cell (plasma cell) neoplasia

A

Myeloma

84
Q

Is AML (acute myeloid leukaemia) or ALL (acute lymphoid leukaemia) more common in dogs and cats?

A

AML more common

85
Q

Is AML (acute myeloid leukaemia) or ALL (acute lymphoid leukaemia) more responsive to aggressive therapy?

A

ALL

86
Q

How are cell types differentiated in acute leukaemias?

A

Not cytology as morphology is similar
Immunophenotyping
(Cytochemistry)
Clonality testing (PARR/ PCR for Antigen Receptor Rearrangements)

87
Q

How are cell types differentiated in chronic leukaemia?

A

Cytology (morphology of cells close to normal but there are too many)

88
Q

4 main reasons there might be a lymphadenopathy

A

Reactive hyperplasia
Lymphadenitis
Metastatic neoplasia
Lymphoma

89
Q

FNA lymph node findings with reactive hyperplasia

A

Cytologically indistinguishable from normal (heterogenous, majority small cells, some plasma cells/macrophages, few neutrophils/eosinophils/macrophages)

90
Q

Lymph node FNA findings in lymphadenitis

A

Increased neutrophils/eosinophils
Inflammatory cells mildly increased or completely replace normal structure

91
Q

Lymph node FNA findings in metastatic neoplasia

A

Carcinoma cells
Mast cells
Melanoma cells

92
Q

Lymph node FNA findings in lymphoma

A

Increased % of large immature lymphocytes (>50%)
More mitoses than reactive
More tingible body macrophages
More lymphoglandular bodies (cell fragility)

93
Q

Reactive or neoplastic lymph node FNA?

A

Reactive

94
Q

Reactive or neoplastic lymph node FNA?

A

Neoplastic

95
Q

What organ is this?

A

Spleen

96
Q

What is the pink?

A

Red pulp
Meshwork of sinusoids with blood and macrophages

97
Q

Function of red pulp

A

Removal and destruction of erythrocytes (damage/antibody coated)
Retrieval of iron from erythrocyte destruction
Blood storage

98
Q

What is the purple?

A

White pulp

99
Q

What is the function of white pulp?

A

T and B lymphocyte system (Ag processing)

100
Q

What are all of these?

A

Incidental findings in older animals, not significant

101
Q

Causes of splenomegaly

A

Infection/reactive hyperplasia
Congestion (barbiturate euthanasia/Anthrax/torsion)
Neoplasia
Autoimmune haemolytic anaemia

102
Q

What can cause a splenic nodule?

A

Haematoma
Hyperplasia
Abscess

103
Q

What is seen in this spleen?

A

Reactive hyperplasia to white pulp lymphoid tissue

104
Q

What is seen in these spleens?

A

Senile hyperplasia

105
Q

Reasons for splenic haemorrhage

A

Haemangiosarcoma
Benign haemangioma
Splenic rupture (GDV)

106
Q

What neoplasia causes blood filled irregular channels on histology of spleen?

A

Haemangiosarcoma

107
Q

Primary neoplasia of the spleen

A

Lymphoma (diffuse and white in bad cases)

108
Q

Site of T cell maturation

A

Thymus

109
Q

What organ is this?

A

Thymus

110
Q

What happens to the thymus after puberty?

A

Involutes (still present)

111
Q

Responses of thymus to injury

A

Lymphoid atrophy/depletion
Haemorrhage/haematoma
Neoplasia
(Inflammation)

112
Q

Are cysts a concerning finding in the thymus?

A

No, incidental and not a problem

113
Q

Viral infections that cause thymus depletion

A

EHV1
FPV
CPV
CDV
FIV

114
Q

When do cats develop thymic lymphoma?

A

FeLV

115
Q

What is SCID/Severe Combined Immunodeficiency?

A

Constellation of entities which vary in severity but all result in failed production of lymphocytes

116
Q

Immunocompromised

A

Any aspect of host defense is deficient

117
Q

Immunosuppressed

A

Immune defense is specifically impaired

118
Q

Immunodeficient

A

Body’s immune response is compromised or absent

119
Q

Morbillivirus, RNA, enveloped virus which destroys a number of cells but has a tropism for lymphocytes?

A

Canine Distemper Virus

120
Q

Infection with canine distemper virus

A

Oronasal infection (inhale aerosol)
Replication in local lymphoid tissue
Enters macrophages
Disseminated into local lymph nodes
Spreads to other haemopoietic organs (spleen, bone marrow etc.)

121
Q

What virus would you suspect with these changes to the nasal planum?

A

Canine distemper virus

122
Q

How is canine distemper virus prevented?

A

Part of core vaccinations

123
Q

Non enveloped DNA viruses that have a tropism for fast dividing cells (GI tract crypts, bone marrow, lymphoid tissue)

A

Canine parvovirus 2 and feline panleukopenia virus

124
Q

What precaution should be taken due to the fact that CPV and FPV are related viruses?

A

Do not isolate puppy in a kitten ward

125
Q

Pathogenesis of CPV/FPV

A

Panleukopaenia: destruction of white blood cell precursors in bone marrow
Vomiting and diarrhoea: sequestration of neutrophils within GI tract = damage to barrier = bacterial translocation (use antibiotics suitable for E. coli)

126
Q

Retrovirus RNA virus in oncovirus family that causes tumours in cats

A

Feline Leukaemia Virus

127
Q

Transmission of FeLV

A

Mutual grooming (‘love virus’)
Bites (rare)
Transplacental

128
Q

Risk factors for FeLV

A

Young (more susceptible, groomed by mother)
Increased population density
Poor hygiene (unwashed bowls)
Shared bowls

129
Q

Clinical stages of FeLV

A

Abortive
Regressive
Progressive

130
Q

Once cats have progressive FeLV what can happen?

A

They can come in and out of regressive/progressive

131
Q

How is FeLV different to FIV?

A

More severe, less selective (pancytopaenia)

132
Q

Retrovirus RNA virus of lentivirus genus that is closely related to HIV

A

Feline Immunodeficiency Virus

133
Q

Do cats have to be clinically affected with FIV to have a positive serology?

A

No

134
Q

Transmission of FIV

A

Deep wounds inoculated with saliva
(Kittens born to persistently infected queens rarely infected but antibodies may be present)

135
Q

Pathophysiology of FIV

A

Infects CD4+ T lymphocytes (helper cells), dendritic cells and macrophages
Functional immunodeficiency leading to AIDS-like deterioration

136
Q

ats at risk of FIV

A

Promiscuous (unneutered)
Old
Male
Stray (free-ranging)

137
Q

What disease is associated with severe stomatitis

A

FIV

138
Q

Control of FIV

A

Vaccination not recommended

139
Q

Enveloped RNA virus causing FIP which is ubiquitous in the feline population

A

Feline Corona Virus/FCoV (enteric virus)

140
Q

Pathophysiology of FIP

A

Mutation allows FCoV to infect monocytes
Extravasation of monocytes (become macrophages)
Increased vascular permeability leading to effusions

141
Q

Clinical sign of FIP

A

Pyrexia
Fluid in abdomen
Uveitis

142
Q

What disease can cause uveitis in cats?

A

FIP

143
Q

Forms of FIP

A

Effusive (‘wet’)
Non-effusive (‘dry’)

144
Q

How does the effusive form of FIP usually present?

A

Fluid in any body cavity (pleural, pericardial, abdominal)

145
Q

How does non-effusive form of FIP usually present?

A

Ocular and neurological presentations

146
Q

What if the main factor in severity of FIP?

A

Cats immune system

147
Q

What is antibody-dependent enhancement/ADE in FIP?

A

The potential for exacerbation of disease by pre-existing antibodies

Small Animal (Poppy) (20 decks)

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