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Principles of Science > Lymphoreticular and Haemopoietic > Flashcards

Lymphoreticular and Haemopoietic Flashcards

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1
Q

What are the primary lymphoid organs?

A

Bone marrow and thymus

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2
Q

What are the secondary lymphoid organs?

A

Lymph nodes, spleen and MALT

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3
Q

What are the top DAMNITV differentials for pathology of the lymphoreticular system?

A

Infection
Immune-mediated
Neoplasia

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4
Q

Name some diseases of the thymus?

A 
Thymic hypoplasia
Thymic lymphoma (cats)
Thymoma (dogs)
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5
Q

What causes thymic hypoplasia?

A

Developmental abnormalities- associated with primary immunodeficiency e.g. X linked SCID
Systemic viral lymphoid depletion- FeLV, FIV, CDV

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6
Q

What is associated with feline thymic lymphoma?

A

FeLV- infects lymphocytes and undergoes malignant transformation

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7
Q

What are the clinical signs of feline thymic lymphoma?

A

Anorexia, weight loss, dyspnoea

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8
Q

How do you diagnose feline thymic lymphoma?

A 
Thoracic radiography (mass in anterior thorax, effusion)
Cytology of pleural fluid/ FNAB
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9
Q

What is the treatment for feline thymic lymphoma?

A

Chemotherapy

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10
Q

What is canine thymoma?

A

Neoplasia of thymic epithelial cells. Slow growing and low metastatic potential

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11
Q

Which breeds are overrepresented for canine thymoma?

A

GSDs and labrador retrievers

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12
Q

What are the clinical signs of canine thymoma?

A

Dyspnoea, dysphagia, thoracic effusion

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13
Q

How do you diagnose canine thymoma?

A

Thoracic radiography, ultrasound, cytology of fluid/ FNAB

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14
Q

What is the treatment for canine thymoma?

A

Surgical excision +/- chemo

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15
Q

What is the prognosis for canine thymoma?

A

Good if tumour hasn’t spread beyond thymic capsule

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16
Q

What paraneoplastic syndromes are associated with canine thymoma?

A

Myasthenia gravis

Hypercalcaemia

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17
Q

What is the process of lymphocyte recirculation?

A

Circulate in blood visiting secondary lymphoid organs via HEVs. If fail to recognise anything return to blood via efferent lymphatic vessels and thoracic duct.

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18
Q

What are the functions of the LNs?

A

Trap foreign material, optimise exposure of lymphocytes to Ag. Provide best environment for lymphocyte activation, proliferation and differentiation, producing effector T cells and Ab from plasma cells.

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19
Q

How does chylothorax occur?

A

Where the thoracic duct is damaged/ perforated or eroded by a tumour, efferent lymph leaks out into thorax.

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20
Q

What does a chylothorax cause?

A

Can compromise respiratory function. Also disrupts lymphocytes migratory pathway and a lymphopenia may develop.

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21
Q

How do malignant cells cause tumour formation in lymphoid tissue?

A

Attempt to metastasis via lymphatics, become trapped, establish 2ry sites of tumour formation.

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22
Q

Once lymphadenopathy identified what is the 1st thing it is important to determine?

A

Generalised vs Localised.

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23
Q

How do you diagnose a generalised lymphadenopathy?

A

Always FNA. Core biopsy/ Excisional biopsy. Haem- lymphopenia (viral), neutrophilia w/ L shift (bacterial), eosinophilia (parasites)

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24
Q

What are the differentials for a generalised lymphadenopathy?

A

Lymphoma

Reactive LNs to systemic infection

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25
Q

What are the differentials for a localised lymphadenopathy?

A

Reactive to localised infection
Lymphadenitis
2ry metastatic tumour

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26
Q

How does a reactive LN look on histopathology?

A

Normal architecture w/ increased cellularity. Secondary follicles w/ germinal centres in response to Ag.

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27
Q

What is lymphadenitis?

A

An inflammatory reaction due to an active infection within the LN itself.

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28
Q

How does lymphadenitis look on histopathology?

A

Similar to reactive LN except areas of pyogranulomatous inflamm also present. Suppurative, caseous or granulomatous

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29
Q

What is an example of an organism that causes suppurative lymphadenitis?

A

Streptococcus equi (strangles)- abscess in LNs.

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30
Q

What is an example of an organism that causes caseous lymphadenitis?

A

Corynebacterium pseudotuberculosis (sheep and goats)- more like cottage cheese

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31
Q

What is an example of an organism that causes granulomatous lymphadenitis?

A

Mycobacterial infection. TB/ Johnes.

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32
Q

How does lymphoma look on histopathology?

A

Usually complete lack of normal architecture. Large numbers of abnormal lymphocytes present. Mitotic figures (unlikely to see if reactive LN)

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33
Q

How does secondary neoplasia look on histopathology?

A

Areas of normal lymphoid tissue infiltrated by neoplastic cells (focal or diffuse)

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34
Q

Name some diseases of the spleen.

A

Trauma/ rupture/ haematoma (e.g. RTA)
Torsion (w/ GDV)
Infarction (nb CSF)

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35
Q

What causes diffuse splenomegaly?

A

Venous congestion
Lymphoid hyperplasia (systemic infectious/ inflamm/ immune mediated)
Systemic amyloidosis
Neoplasia

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36
Q

What causes nodular splenomegaly?

A 
Nodular hyperplasia (benign- incidental)
Abscess/ cyst (infectious)
1ry neoplasia (lymphoma, haemangioma, HSA)
Metastatic dz (MCT)
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37
Q

Name some viruses that particularly impact on the lymphoreticular system.

A

Malignant catarrhal fever (herpes)
CSF
FeLV/ FIV/ CDV/ FIP
EIA

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38
Q

Name some bacteria that particularly impact on the lymphoreticular system.

A 
Bacillus anthracis (anthrax)
Mycobacterium bovis (TB)/ MAP (Johnes)
Corynebacterium pseudotuberculosis (caseous lymphadenitis)
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39
Q

Name some protozoa that particularly impact on the lymphoreticular system.

A

Leishmania
Babesia
Ehrlichia
Theileria

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40
Q

What is the link between thymoma and hypercalcaemia?

A

PTHrp from tumour cells increases bone resorption and distal tubular Ca resorption

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41
Q

What is the link between thymoma and myasthenia gravis?

A

Tumour may interfere with negative selection of autoreactive T cells, allowing more to leave the thymus. Immune response against an epitope expressed on thymoma cells spills over to NMJ components sharing the same epitope.

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42
Q

What is the classical appearance of sheep LNs with caseous lymphadenitis?

A

Onion ring appearance resulting from alternate layers of fibrosis and necrosis.

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43
Q

What organism causes caseous lymphadenitis in sheep and goats?

A

Corynebacterium pseudotuberculosis

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44
Q

How does the presentation of caseous lymphadenitis differ between sheep and goats?

A

In sheep more often visceral form.

In goats more often occurs as external abscesses around head and neck.

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45
Q

What is the causative agent of chronic lymphadenitis in goats?

A

Mycobacterium avium paratuberculosis (Johnes disease)

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46
Q

How is chronic lymphadenitis in goats diagnosed?

A

Granulomas present in the node. Acid-fast staining of a section of the node.

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47
Q

What are the clinical syndromes associated with Johnes disease?

A

Diarrhoea.

Chronic weight loss.

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48
Q

What are the clinical signs of babesia?

A

Anaemia
Pipe-stem diarrhoea
Icterus
Haemaglobinuria

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49
Q

How is babesia linked to anaemia in the cow?

A

Rapid growth and multiplication of parasite in blood w/ extensive erythrocytic lysis

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50
Q

How is babesia transmitted?

A

Ticks

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51
Q

What cell type in the blood does leishmania multiply in?

A

Macrophages

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52
Q

What are the clinical signs of leishmania?

A

Skin disease, enlarged LNs, eye disease, pallor of MMs, enlarged spleen, cachexia, fever, epistaxis

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53
Q

How is leishmania diagnosed?

A

Suspicion due to clinical signs. Confirmed by ELISA

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54
Q

How is the spleen attached in the abdomen?

A

Dorsal extremity fixed to cranial abdomen by gastrosplenic ligament. Ventral extremity relatively mobile.

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55
Q

Where does the splenic artery arise from?

A

Celiac artery

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56
Q

Where does the splenic vein drain to?

A

Portal vein

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57
Q

Name some important branches of the splenic artery/ vein.

A

Branches to left limb of pancreas, greater curvature of the stomach (L gastroepiploic), fundus of the stomach (short gastrics)

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58
Q

What are the functions of the spleen?

A

Red pulp- RBC maintenance, iron metabolism, blood reservoir, haematopoiesis
White pulp- immune function.

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59
Q

When is total splenectomy indicated?

A

If neoplasia known or suspected.

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60
Q

How is a total splenectomy performed?

A

Large ventral midline incision. Begin removal at tail end and double ligate and transect all the hilar vessels. At head end try and preserve the short gastric vessels and transect the gastrosplenic ligament.

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61
Q

How is a partial splenectomy performed?

A

The hilar vessels to the disease portion are ligated and transected. After a few mins an obvious demarcation between ischaemic and normal used as guidline for resection.

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62
Q

What is the quicker technique for a total splenectomy?

A

Ligate short gastric vessels, L gastroepiploic a+v, splenic a+v distal to branch supplying the pancreas.

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63
Q

What is the association between splenic diseases and cardiac arrhythmias?

A

Dogs w/ splenic masses have high risk of cardiac arrhythmias, esp those w/anaemia and haemoabdomen

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64
Q

Why are coagulation tests recommended prior to splenectomy?

A

DIC can occur w/ both neoplastic splenic lesions and splenic torsion.

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65
Q

What is the main complication following splenectomy?

A

Haemorrhage- monitor vital parameters and PCV/TP regularly post-op

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66
Q

Why are ischaemic pancreatitis and gastritis complications of a splenectomy?

A

If blood supply to these organs is compromised

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67
Q

Is splenomegaly more commonly localised or generalised in dogs? And cats?

A

Localised more common in dogs

Diffuse more common in cats

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68
Q

What are the causes of localised splenomegaly?

A

Non-neoplastic: haematoma, abscess, nodular hyperplasia, infarction, cyst
Neoplasia: benign- haemangioma, leimyoma, fibroma, lipoma; malignant- HSA, FSA, leiomyosarcoma

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69
Q

What are the causes of diffuse splenomegaly?

A

Infection- bacterial, fungal, viral, parasitic
Congestion- drugs (barbiturates), splenic torsion and/or GDV, RCHF
Neoplasia- acute and chronic leukemia, systemic MCT, lymphoma, multiple myeloma, malignant histiocytosis

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70
Q

Why does diagnosis of a localised splenomegaly often require histopathology rather than FNA?

A

FNA often produces just blood when aspirating a localised haematoma or HSA

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71
Q

What is the most common malignant splenic tumour in the dog?

A

Haemangiosarcoma

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72
Q

What are common sites of metastasis for HSA?

A

Liver, omentum, mesentery, brain, right atrium and subcut tissue

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73
Q

What is the recommended tx for HSA w/out mets and what is the px?

A

Splenecomy. Expected survival only 3-12 wks

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74
Q

How long does post op chemo prolong the expected survival following splenectomy for HSA?

A

6 months

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75
Q

How do dogs w/ splenic torsion present?

A

Progressive abdominal pain, distension and shock. Or chronic form- CS are vague and intermittent

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76
Q

What is the classic appearance of a splenic torsion on ultrasound?

A

Snowstorm appearance- large anechoic areas

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77
Q

What is the treatment for a splenic torsion?

A

Pedicle must not be untwisted- remove en mass or gradually divided and ligated.

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78
Q

What is splenic torsion?

A

Spleen twist on its vascular pedicle occluding hilar vessels–> splenic congestion +/- splenic vessel thrombosis

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79
Q

What is a lymphoma?

A

Diverse group of malignant neoplasms that originate from lymphoreticular cells.

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80
Q

What has been suggested to increase risk of feline lymphoma?

A

FeLV +ve status- insertion of retrovirus to DNA–> oncogenic transformation. Immunosuppression may play a role
FIV +ve status- immunosuppression

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81
Q

What is the anatomic predilection site for lymphoma in dogs and cats?

A

Dogs- mainly multicentric (multiple LNs)

Cats- mainly gastrointestinal

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82
Q

How does multicentric lymphoma present?

A

Peripheral lymphadenomegaly. Often asymptomatic- lethargy, malaise, weight loss, anorexia, pyrexia, PD/PU if hypercalcaemic

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83
Q

What are ddx for multicentric lymphoma?

A 
Disseminated infection- lymphadenitis
Immune mediated dz
Other haematopoietic tumours (leukemia, myeloma)
Metastatic/ disseminated neoplasia
Generalised skindz
Sterile granulomatous lymphadenitis
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84
Q

How does feline lymphoma usually present?

A

Single LN/ regional LN enlargement is more common than multiple. More likely to be systemically unwell cf dogs.

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85
Q

How does gastrointestinal lymphoma (common in cats) usually present?

A

Weight loss, anorexia, v+ and/or d+

Localised mass, or multifocal/ diffuse thickened loops of intestine +/- mesenteric LN enlargement on exam

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86
Q

What are the 2 forms of alimentary lymphoma in cats?

A

High grade- mass lesions with rel short hx of illness, may have signs of GI obstruction. Median age 10YO
Low grade- diffuse thickening of intestinal loops or mild lymphadenomegaly, may be more chronic hx. Median age 13YO

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87
Q

What are the ddx for alimentary lymphoma?

A

IBD, other GI tumours, FB, intussuception

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88
Q

What are the clinical signs of mediastinal lymphoma?

A

Dyspnoea, coughing, increased RR (tachypnoea), weight loss, lung sounds decreased ventrally, pooss dysphagia- regurgitation, heart sounds displaced caudally, loss of compressibily, caval syndrome, horners

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89
Q

What are the other sites of lymphoma i.e. extranodal?

A 
Renal
CNS/spinal
Nasal/ nasopharyngeal
Laryngeal/ tracheal
Cutaneous
Occular
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90
Q

How does renal lymphoma present?

A

Large irregular kidneys (often bilateral), signs of kidney dz e.g. PD/PU, anorexia, weight loss

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91
Q

Is extranodal lymphoma more common in dogs or cats?

A

Cats

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92
Q

What are the clinical signs of nasal/ nasopharyngeal lymphoma?

A

Chronic nasal discharge (serosanguinous to mucopurulent), epistaxis, sneezing, stertor, anorexia, facial deformity, exophthalmus, epiphora

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93
Q

Is cutaneous lymphoma more common in dogs or cats?

A

Dogs

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94
Q

What are the 2 forms of cutaneous lymphoma?

A

Epitheliotropic- very superficial epidermis affected

Non-epitheliotropic- deeper layer of skin, sparing the epidermis

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95
Q

What are the 3 stages of the epitheliotropic form of cutaneous lymphoma?

A

Scaling, alopecia, pruritis–>
Erythematous, thickened, ulcerated, exudative–>
Proliferative plaques and nodules w/ progressive ulceration

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96
Q

What are the clinical signs of ocular lymphoma?

A

Uveitis, blepharospasm, infiltration, haemorrhage, retinal detachment

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97
Q

What paraneoplastic syndromes can be seen with lymphoma?

A

Hypercalcaemia
Hypergammaglobulinaemia
Haematological abnormalities- anaemia, thrombocytopenia

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98
Q

How does hypercalcaemia of lymphoma present?

A

PU/PD due to NDI (Ca interferes w/ action of ADH in kidney)
Dehydration, depression, lethargy, weakness, V+, constipation, bradycardia/ bradydysrhytmias, muscle tremors, RF may occur if left untreated

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99
Q

Which LN is it best to avoid when taking FNA for dx and why?

A

Submandibular- shows reactive change to mouth

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100
Q

How is lymphoma graded, what is the usual grade for dogs vs cats?

A

High grade- large cells (blasts)
Low grade- small lymphocytes
Dogs- more are high grade
Cats- intestinal lymphoma can be low or high

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101
Q

What is immunophenotyping?

A

Assesses markers expressed on cell surface
T cell: CD3+, CD4+, CD8+
B cell: CD79a+, CD21+

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102
Q

Why do you immunophenotype lymphoma?

A 
May affect tx plan
Affects prognosis (dogs)
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103
Q

How does immunophenotyping affect prognosis?

A

T cell usually worse prognosis than B cell for high grade lymphomas. Some low grade T cell lymphomas can have prolonged survival.

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104
Q

Why is haematology essential prior to chemotherapy?

A

Ensure there are adequate neutrophils and platelets. Check for anaemia. Also gives an indication of BM involvement.

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105
Q

Why is biochemistry essential prior to chemotherapy?

A

Indicates organ involvement (disease extent and drug metabolism)- liver enzymes, urea and creatinine. Also paraneoplastic syndromes- hypercalcaemia.

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106
Q

What is stage I lymphoma?

A

Involves a single LN

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107
Q

What is stage II lymphoma?

A

Multiple regional LNs involved in a regional area

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108
Q

What is stage III lymphoma?

A

Generalised LN involvement

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109
Q

What is stage IV lymphoma?

A

Liver +/or spleen involvement (+/- stage III)

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110
Q

What is stage V lymphoma?

A

BM involvement +/- other organs

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111
Q

What is the substage of lymphoma?

A

Substage a- w/out systemic signs

Substage b- w/ systemic signs

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112
Q

How do you assess BM involvement in lymphoma?

A

Abnormal circulating cells or cytopenias in >1 cell line

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113
Q

When is surgery indicated as tx for lymphoma?

A

Rare. Solitary site lymphoma (good for Hodgkins like lymphoma in cats), acute intestinal obstruction

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114
Q

When is radiation therapy indicated as tx for lymphoma?

A

Nasal lymphoma
Oral lymphoma
Solitary Lesions

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115
Q

What are the tx options if the O doesn’t want chemo?

A

Corticosteroids e.g. prednisolone for palliation (effect short lived, 2-3m)

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116
Q

Why should you not pre-treat w/ steroids if you are planning to give chemo?

A

Corticosteroids promote multi-drug resistance.

Can use as part of combo protocol from outset

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117
Q

Why are corticosteroids used in chemo protocols?

A

Prednisolone and dexamethasone cause lymphocyte apoptosis

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118
Q

What are the most common lymphoma chemo protocols?

A

COP based

CHOP based

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119
Q

What does the COP based protocol incl?

A

Cyclophosphamide
Vincristine
Prednisolone

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120
Q

What does CHOP based protocol contain?

A

Cyclophosphamide
Doxorubicin
Vincristine
Prednisolone

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121
Q

What is cyclophosphamide’s role in lymphoma chemo protocol?

A

Alkylating agent- substitutes alkyl chain for H+ ions in DNA causing cross-linkage and breakage of DNA strands- interfere w/ replication and transcription. Not cell cycle specific

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122
Q

What is vincristine’s role in lymphoma chemo protocol?

A

Mitotic spindle inhibitor- binds to tubulin–> metaphase arrest. G2/M specific

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123
Q

What is prednisolone’s role in lymphoma chemo protocol?

A

Apoptosis of lymphoid and mast cells

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124
Q

What is doxorubicin’s role in lymphoma chemo protocol?

A

Anti-tumour abx, inhibits topoisomerase II, break and cross link DNA strands. Not cell-cycle specific.

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125
Q

How do COP and CHOP (M-W) protocols compare with regards to cost?

A

Initial outlay more w/ M-W.

Can work out similar over time

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126
Q

How do COP and CHOP (M-W) protocols compare with regards to adverse effects?

A

A bit more likely with M-W than COP

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127
Q

What are the adverse effects of doxorubicin?

A

Cardiotoxocity in dogs (use ECG)
Mast cell degranulation (rare)
Nephrotoxicity in cats
Vesicant if injected perivascularly (apply ice)

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128
Q

How do COP and CHOP (M-W) protocols compare with regards to first remission duration?

A

Longer with M-W

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129
Q

How do COP and CHOP (M-W) protocols compare with regards to median survival?

A

Longer w/ M-W but can be similar w/ COP depending on rescue protocols used
On M-W 20-25% of Ds will live >2y

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130
Q

What is the induction protocol of COP in dogs?

A

C: 50mg/m2 PO q48hr
O: 0.5-0.7mg/m2 IV q7d
P: 40mg/m2 PO daily wk 1 then 20mg/m2 q48hr

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131
Q

How long is the induction phase of COP protocol used for and what next?

A

If in remission after 8 weeks, go onto maintenance protocol

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132
Q

What is the maintenance protocol of COP in dogs?

A

C: 20mg/m2 PO q14d
P: 20mg/m2 PO q48hr

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133
Q

What is usually incorporated in COP protocol in cats for renal/CNS lymphoma?

A

Cytosine arabinoside- on d1 as IV infusion over 4-12hr. Repeat in wk 4.

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134
Q

How does the COP protocol differ in cats from dogs?

A

50mg cyclophosphamide can’t be split. Therefore usually given as pulse dose 200mg/m2 in wk 1 and wk 4 (usually one 50mg tab for most cats)

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135
Q

What is the usual maintenance protocol of COP in cats?

A

Chlorambucil 20mg/m2 q14d and pred 20mg/m2 PO q48hr.

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136
Q

What is the protocol for feline low grade GI lymphoma?

A

Chlorambucil 20mg/m2 q2w
Pred 40mg/m2 q24hr for 7d then 20mg/m2 EOD
Supplement B12 inj if necc
Rescue- cyclophosphamide or lomustine

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137
Q

What is the modified LOPP protocol?

A

Lomustine/ vincristine/ pred/ procarbazine

For high grade T-cell lymphomas

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138
Q

What are the options for low budget protocols which don’t involve injectables?

A

Pred alone- 40mg/m2 daily q7d then 20mg/m2 EOD
Pred plus chlorambucil 20mg/m2 q14d (monitor haem q6-8w)
Lomustine 50-70mg/m2 q21d in Ds, 50mg/m2 q14d in Cs +/- pred (monitor for myelosuppression, hepatotoxicity)

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139
Q

How do you monitor response of LNs to chemo?

A

By PE
CR= LNs not enlarged
PR= >30% reduction in mean sum longest diameters
PD= >20% increase in sum of longest diameters
SD= between PR and PD

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140
Q

Why is regular haematology important for monitoring patients receiving chemo?

A

Check for myelosuppresion ideally before each tx in induction phase

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141
Q

What action should be taken in patient receiving chemo has a neutrophil count of <2x10^9/L?

A

Delay tx for 5-7d

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142
Q

What action should be taken in patient receiving chemo has a neutrophil count of <0.5x10^9/L?

A

Reduce dose of implicated drug by 20-25% next time

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143
Q

What action should be taken in patient receiving chemo has a neutrophil count of <1x10^9/L?

A

Consider prophylactic abx

Consider dose reducion by 10-25% next time

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144
Q

What action should be taken in patient receiving chemo has a platelet count of <75x10^9/L?

A

Delay tx for 5-7d

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145
Q

Why is regular biochemistry important for monitoring patients receiving chemo?

A

Monitor abnormal parameters e.g. Ca.
Organ function- renal/hepatic
Toxicity- e.g. ALT in patients on lomustine (hepatotoxicity)

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146
Q

Why is regular UA important for monitoring patients receiving chemo?

A

SG- renal funcyion
Dipstick/ sediment to check for haemorrhagic cystitis
Increased risk of infection

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147
Q

When is echocardiography used in monitoring patients receiving chemo?

A

Offer prior to doxorubicin- screen for heart dz, assess contractility (FS), esp if exceeding 180mg/m2 cumulative dose

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148
Q

What is recommended for the management of GI disturbances following chemo?

A

Bland diet, little and often

Gut protectants, anti-emetics (maropitant, metoclopramide, ondansetron), probiotics, metronidazole can be useful for D+

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149
Q

What is recommended for the management of anorexia following chemo?

A

Antiemetics
Gut protectants
Appetite stimulants- cyproheptadine, mirtazepine
Feeding tubes?

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150
Q

What is recommended for the management of myelosuppression following chemo?

A

Abx if neutrophils <1x10^9/L e.g. TMS orally

For the febrile neutropenic crisis: BS abx, IVFT, ideally culture open wounds, gut protectants, barrier nurse

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151
Q

What is recommended for the management of haemorrhagic cystitis following chemo?

A

Stop cyclophosphamide. Change to chlorambucil or melphalan, GAGs, NSAIDs if not on steroids, oxybutinin

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152
Q

What are negative prognostic indicators for lymphoma?

A

T cell (high grade). Substage b. Hypercalcaemia. Prolonged pre-tx w/ corticosteroids. > Stage III (vs I +II). Stage V (some studies). Site- primary GI (except for colorectal which can do well), pure hepato-splenic, renal. Failure to achieve CR.

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153
Q

In general do cats have better or worse response rate to COP/ CHOP than dogs?

A

Response rate lower than dogs.

Less predictable- remission 3-8m, survival times variable 3-10m.

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154
Q

What are negative prognostic indicators for cats w/ lymphoma?

A

Failure to achieve complete response, FeLV +ve, high grade vs low grade, LGL lymphoma (large granular lymphocyte lymphoma subtype)

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155
Q

What do you do when lymphoma relapses if not currently on tx?

A

Restart original protocol

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156
Q

What do you do when lymphoma relapses if animal receiving a less intensive maintenance protocol?

A

Go back to original induction protocol

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157
Q

What do you do when lymphoma relapses during induction protocol?

A

Use new drugs that tumour has not been exposed to before. Preferably in combo. e.g. L-asparaginase + lomustine
DMAC protocol.

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158
Q

How you manage para-neoplastic hypercalcaemia?

A

Prompt dx and management of lymphoma. Saline diuresis (0.9% NaCl) at 6mls/kg/hr (if no CI). Once rehydrated into furosemide at 1-2mg/kg to promote calciuresis. Tx underlying cause.

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159
Q

What is leukemia?

A

Malignant neoplasm originating from haematopoietic precursors in BM (or spleen). Neoplastic cells be present in the circulation in large numbers

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160
Q

What are the 2 types of leukemia?

A

Lymphoid or myeloid- depending on which cell line is involved.

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161
Q

What cells come from the myeloid line?

A

Megakaryocyte (thrombocytes), erythrocyte, mast cell, basophil, neutrophil, eosinophil, monocyte (macrophage)

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162
Q

What cells come from the lymphoid line?

A

Natural killer cell
T lymphocyte
B lymphocyte (plasma cell)

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163
Q

How is acute leukemia characterised?

A

Aggressive- rapid. Immature, poorly differentiated cells (blasts) w/ high capacity to divide. Px poor.

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164
Q

How is chronic leukemia characterised?

A

Slow progression, mild signs. Well differentiated late precursor cells, w/ less capacity to divide. Px reasonable (several months to years)

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165
Q

How do you differentiate ALL from stage V lymphoma?

A

ALL- usually sicker, more profound cytopenias on haem and milder lymphadenomegaly
Flow cytometry- ALL CD34 +ve

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166
Q

Which has a poorer px ALL or stage V lymphoma

A

ALL has poorer prognosis than stage V lymphoma

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167
Q

What are the clinical signs of leukemia?

A

Non-specific. Lethargy, weakness, anorexia, GI signs, mild generalised lymphadenopathy, hepatosplenomegaly.
Signs related to myelophthisis- fever, petechial haemorrhages, pallor. Sometimes signs of hypercalcaemia

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168
Q

How do you diagnose leukemia?

A

Cytopenias, often in >1 cells line, abnormal circulating cells
If abnormal cells circulating dx can be made using flow cytometry. May require BM aspirate +/- core.

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169
Q

What is the treatment for acute leukemias?

A

Tx difficult due to severe cytopenias. Poor px.
ALL: L-asparaginase/ pred, cytarabine, lymphoma type protocol
AML: cytarabine

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170
Q

What is the treatment for chronic leukemias?

A

Much better success rate and px.
CLL- chlorambucil and pred, MST 1y
CML (rare)- hydroxycarbamide

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171
Q

How do clinical signs, haem and flow cytometry differ between stage V lymphoma and ALL?

A

Stage V lymphoma- often rel well, LNs often grossly enlarged, cytopenias tend to be mild, CD 34-ve on flow
ALL- often sick, LNs mildly enlarged, cytopenias tend to be marked, CD34+ on flow

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172
Q

What is a myeloma?

A

Plasma cell tumour, starting in BM (spleen) in older animals

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173
Q

What are the clinical signs of myeloma?

A

Pyrexia, lethargy, pallor, lymphadenopathy, hepatosplenomegaly, signs of bone pain
Signs of hyperviscosity (due to Ab production)- neurological, bleeding

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174
Q

What is the classic haem/ biochem and UA for myeloma?

A

Mild non-regenerative anaemia, cytopenias
Hyperglobulinaemia often present due to Ab production by plasma cells (monoclonal spike on serum protein electrophoresis), +/- hypercalcaemia.
UA- Ig light chains (bence-jones proteinuria)

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175
Q

What do radiographs of myeloma often show?

A

Osteolytic lesions (vertebrae, pelvis, long bones) or diffuse osteopenia

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176
Q

How do you dx and tx myeloma?

A

Dx: excess plasma cells in marrow- BM aspirate/ biopsy
Tx: melphalan and pred (Ds)
MST: 12-18m in Ds

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177
Q

How does tx of myeloma differ between dogs and cats?

A

Cats- melphalan can cause marked myelosuppression. Tend to use chlorambucil and pred- px worse

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178
Q

What is polycythaemia vera?

A

Proliferation of erythroid cell series in marrow, with differentiation to mature RBC

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179
Q

What are the clinical signs of polycythaemia vera?

A

Bright red MMs, neurological signs due to hyperviscosity.

180
Q

How do you dx polycythaemia vera?

A

Persistently high PCV w/ low or normal EPO activity. Need to differentiate from dehydration and appropriate causes of increased RBC (hypoxia), also from EPO producing tumours.

181
Q

What is the tx for polycythaemia vera?

A

Phlebotomies and replacement of blood w/ colloids/ electrolytes to alleviate hyperviscosity. Hydroxycarbamide (hydroxyurea)

182
Q

What are the indications for LN sampling?

A

Lymphadenomegaly
Evaluation of mets (based on drainage)
Classification of lymphoma (histo)

183
Q

What does the submandibular LN drain?

A

Head (incl rostral oral cavity)

184
Q

What does the prescapular LN drain?

A

Caudal head (pharynx, pinna), thoracic limb, part of thoracic wall

185
Q

What does the axillary LN drain?

A

Thoracic wall, deep structures of thoracic limb and neck, thoracic and cranial abdominal mammary glands

186
Q

What does the superficial inguinal LN drain?

A

Caudal abdominal and inguinal mammary glands, ventral half of abdominal wall, penis, prepuce, scrotal skin, tail, ventral pelvis, medial part of thigh and stifle

187
Q

What does the popliteal LN drain?

A

Distal to stifle

188
Q

Why is popliteal/ prescapular sampling preferred to submandibular?

A

As submandibular always have additional processes due to mouth

189
Q

How do you evaluate the quality of preparation of a LN aspirate?

A 
Adequate amount of intact cells (immature lymphocytes v fragile, thus lysed cells common)
Adequate spread (fried- egg appearance)
Adequate staining (thick areas tend to under-stain- understained areas always look like lymphoma)
190
Q

What is the systematic approach for looking at lymph node aspirates?

A

Scan entire slide on low magnification (4x), assess cellular arrangement on low power (foreign cells, clusters etc). Uniform/ variable population

191
Q

What are the 5 big categories of cell types present in LN?

A 
Small lymphocyte
Medium lymphocyte
Large lymphocyte
Plasma cell
Macrophage
\+ve others- inflamm cells (neut, eos), mast cells, foreign cells
192
Q

How big is the small/ medium/ large lymphocyte?

A

Small- 1-1.5x RBC
Med- 2-2.5x RBC
Large- >3x RBC

193
Q

What are the 5 LN classifications?

A 
Normal
Hyperplastic/ reactive
Lymphadenitis
Lymphoid neoplasia
Non-lymphoid neoplasia
194
Q

What does a normal LN look like?

A

Dominated by small, mature lymphocytes (>90%)
Low no’s of med to large immature lymphocytes (5-10%)
Occasional macrophages, rare neutophils, eosinophils, mast cells etc

195
Q

What does a small lymphocyte look like?

A

1-1.5x RBC in diameter. Clumped chromatin. Small amount of cytoplasm

196
Q

What does a medium to large lymphocyte look like?

A

2-2.5x RBC and >3x RBC. Finely granular chromatin. Occasionally prominent nucleoli. Increased amount of light to deeply basophilic (blue) cystoplasm

197
Q

What does a hyperplastic/ reactive LN look like?

A

Similar populations as normal but node enlarged.

Increased % of med to large lymphocytes, but less than 50%. Poss incr % of plasma cells and nos of mitotic figures

198
Q

What does a LN w/ lymphadenitis?

A

Incr % of inflamm cells:

  • neut (>5%)- neutrophilic lymphadenitis
  • eos (>3%)- eosinophilic lymphadenitis
  • macrophages- histiocytic/ macrophagic lymphadenitis
  • combo of above, also mast cell % will incr
199
Q

What does lymphoid neoplasia look like?

A

> 50% immature lymphocytes- monotony
Poss incr mitotic figures. Only low nos of small, mature lymphocytes (rare really large). Plasma cells may/ may not be present

200
Q

What does metastatic neoplasia look like?

A

Presence of foreign cells (even w/out ample features of malignancy)

201
Q

What are the main sites of RBC production?

A

Liver/ spleen in foetus
Swaps to BM in neonate
Growing animals- marrow of all bones
At birth all BM is red marrow. With age converted to yellow. Red marrow mainly in flat bones and cancellous material in epiphyses of long bones (yellow marrow in medullary cavity). Liver and spleen maintain erythropoeitic capacity. Yellow marrow can convert back to red.

202
Q

What is the typical erythrocyte lifespan?

A

100d (dog)
70d (cat)
150d (horse, cattle)

203
Q

How are RBCs removed from circulation?

A

Major route- senescent red cells taken up by macrophages, components recycled.
Minor route- intravascular haemolysis- cell membrane damage, haemoglobinaemia

204
Q

How is anaemia (reduced red cell mass) evidenced on bloods?

A

Hb conc
PCV- % of red cells in a vol of blood- manual
Hct- same info as PCV- machine
RBC conc

205
Q

What causes a hypochromic patient?

A

Hb conc. MCHC/ MCH on panel. Decr in iron deficiency/ poor iron incorporation (w/ microcytosis). Incr central pallor.
*hyperchromic not poss

206
Q

What does MCV measure/ indicate?

A

Avg vol of single red cell.
Normocytic- mild non-regenerative anaemia, acute haemorrhage
Microcytic- incr central pallor. PSS, Fe deficiency, hepatic failure. Akitas.
Macrocytic- in regeneration ie polychromatophils, some poodles

207
Q

What is regenerative anaemia?

A

Bodys response to a fall in oxygenation. Kidneys respond to low blood O2 by releasing EPO. Stimulates BM to incr red cell production. Takes 2-3d and younger red cells incr in circulation.
Always indicates blood loss or haemolysis (destruction)

208
Q

What are polychromatophils vs reticulocytes?

A

Same cells- immature RBCs.
On Diff-Quik or Giemsa stained smear, young cells containing ribosomal RNA show up larger and bluer- polychromatophils
w/ NMB- RNA precipitates forming aggregates- reticulocytes

209
Q

How do reticulocytes differ in cats?

A

Released as aggregate retics maturing to punctate retics over time. Retic counts should record either aggregate or both

210
Q

What is the reticulocyte % or corrected reticulocyte %?

A

Reticulocyte %- retics as % of 1000 red cells. Dog- 45%, cat- 35%
Corrected- retic % x patient PCV/ normal PCV. Dog- >1%, Cat- 0.4%

211
Q

What are the reasons for decreased red cell mass?

A

Incr loss- too large/ fast for compensation- haemorrhage (external/ internal, haemolysis)
Decr production- losses not matched by production.

212
Q

What are the causes of for decreased red cell mass?

A

External haemorrhage- melena, urinary tract, epistaxis, post trauma/ sx
Internal haemorrhage- bleeding tumours, trauma, into tissue (bleeding diathesis), sx
Haemolysis- incr internal red cell destruction, intravascular/ extravascular, normal/ damaged

213
Q

What is intravascular immune mediated haemolysis?

A

Anti red cell Ab. Red cells opsonised and either lyse (more common w/ IgM) or are phagocytosed. May agglutinate. Coombs test +ve (for anti-RBC Ab). May be severe/ rapid, usually strongly regenerative.

214
Q

What are ghost cells?

A

Remnants of red cells that have lost Hb. Membrane only. Associated with deposition of complement and intravascular haemolysis.

215
Q

What is extravascular immune mediated haemolysis?

A

RBCs have Ab bound to them. Macrophages (mainly from liver and spleen) try to phagocytose cell or bite chunk out of membrane. Cell fuses back together- loses normal structure- becomes a spherocyte

216
Q

What is a spherocyte?

A

Increased density due to loss of biconcave shape. Denser and smaller because of the partial loss of its membrane, but not its cellular content. Indicative of haemolytic anaemia. Indicates current process as have short 1/2 life.

217
Q

What parasites cause haemolysis?

A

Mycoplasma haemofelis and M.haemominutum. Blood borne, epicellular parasite. Large and small forms. Incr fragility and haemolysis. Cyclical (3-8wks). Pleomorphic- cocci, rings or rods. Dx- PCR (excellent), blood smear exam (not reliable)
Outside UK- babesia (tick borne, pyriform bodies in red cells, tx indoxacarb), cytauxzoon felis

218
Q

What are heinz bodies?

A

Occur due to oxidative damage. Denatured Hb- can see as coming out of RBC. Taken out of circulation therefore cause anaemia.
Onions, paracetamol, vitK, propylene glycol.

219
Q

What are eccentrocytes?

A

Occur due to oxidative damage. Hb uneven distribution within cell. Seen most often in dogs. Horses w/ red maple toxicosis.

220
Q

What is shear injury to red cells?

A

Accompany microangiopathic damage- tumours w/ narrow vessels (HSA) or organ inflamm beds (severe hepatitis, DIC) where there is fibrin stranding.
Schistocytes (associated w/ fibrin deposition, DIC), acanthocytes (projections- splenic dz), keratocytes (helmet shaped cells- intravasc trauma)

221
Q

What is non-regenerative anaemia?

A

Normocytic, normochromic.
Renal- w/ CRF decr EPO
Endocrine- hypothyroidism, hypoadrenocorticism (TH and cortisol facultative effect on red cell production)
FeLV- selective depression of erythropoiesis, dysplastic production, myeloproliferative dz crowding out
Aplastic anaemia- all precursors wiped out
Myelodysplasia- abnormal maturation/ production of cells, may go on to leukemia
Myelopthisis- neoplasia crowding the marrow
Myelofibrosis-response to injury or following prolonged regenerative attempts.
IMHA- if attacks precursors

222
Q

What causes erythrocytosis?

A

May be relative- dehydration (vol contraction), redistribution (splenic contraction)
Primary (polycythemia vera)- myeloproliferative disorder of erythroid stem cells, EPO normal/ decreased
Secondary (appropriate/ inappropriate)- chronic hypoxia, EPO secreting tumours, EPO levels elevated

223
Q

What are the clinical signs of anaemia?

A

Non/ vague if mild/chronic.

Pale MMs, high HR, RR, heart murmur, hyperdynamic pulses

224
Q

What are the differentials for pale MMs and how do you differentiate the two?

A

Poor peripheral perfusion vs anaemia.
CRT <2s- anaemia, prolonged- poor peripheral perfusion
Pulse quality- strong anaemia, weak e.g. hypovolaemia

225
Q

How does TP differ with the cause of anaemia?

A

Decreases with haemorrhage

Increases with haemolysis or non-regenerative anaemia

226
Q

What are the differences between intravascular and extravascular haemolysis?

A

On blood smear, ghost cells- intravascular, spherocytes- extravascular.
Haemoglobinuria- intravascular
Bilirubinuria- extravascular

227
Q

What is the tx for IMHA?

A

IVFT/ blood transfusion
Immunosuppresive- pred (suppression of macrophage activity, impaired complement and Ab binding, suppression of IgG), azathioprine (not cats), cyclosporine or chlorambucil (cats)
Good nursing
Aspirin, clopidogrel for pulmonary TE

228
Q

What is the px for IMHA in dogs?

A

Guarded- icterus, haemoglobinuria/aemia all poor px
Common cause of death is PTE
May relapse in future

229
Q

What are the infectious causes of haemolytic anaemia?

A

Babesiosis in dogs in europe
Mycoplasma in cats (dogs after splenectomy)
Any infection can act as immunological tx- 2ry IMHA

230
Q

What are the miscellaneous causes of haemolysis?

A 
Oxidative damage- paracetamol (cats), onions, garlic, Zn, Cu
Hypophosphataemia- diabetic ketoacidosis
Shear injury (microangiopathic)- damaged endothelium
231
Q

What are the causes of non-regenerative anaemia?

A

Chronic dz
Renal dz
FeLV infection
Miscellaneous- nutrient deficiency, endocrine disorder (hypothyroidism, hypoadrenocortism, hyperoestrogen), liver dz
BM dz- red cell aplasia, aplastic anaemia, neoplasia (myelophthisis), myelodysplasia, myelofibrosis

232
Q

How does chronic dz cause anaemia?

A

Mild/ mod

Due to poor iron storage/ utilisation, shortened red cell survival, impaired erythrocyte production

233
Q

How is the BM sampled?

A

Sedation and local- if aspirate
GA- if biopsy
Use iliac crest or humerus

234
Q

What is the ideal blood donor?

A

Friendly. Clinically healthy. Large breed (25kg+ D, 4.5kg+ C). 1.5-8YO. No hx of travel. No transfusion themselves. Fully vaccinated but not w/in 14d. Free of parasites and infectious dz. Cats tested for FeLV, FIV, mycoplasanma haemofelis.

235
Q

What is the canine donation procedure?

A

12hr fast
PCV and TP
Needle into jugular- collect 405-480g. Moderate pressure over site for 2-5mins. WRap site. Observe for 15-30m. Offer food. Avoid excessive exercise for a few days.

236
Q

What is the feline donation procedure?

A

12hr fast.
PCV/TP
Place IV catheter, admin sedation (ket/midazolam IV). Clip aseptically prepare jugular. Lateral recumbency. Gentle aspiration on syringe.
Moerate pressure over venepuncture site for 2-5m. Wrap site. Observe for 15-30m. Admin 5ml/kg/hr fluid therapy (Hartmanns or 0.9% NaCl) for 3 hrs. Food once fully awake. Kept in for 24hr.

237
Q

What are packed red blood cells and what are their indications for use?

A

Centrifuged whole blood, plasma extractor, additive solutions. Stored at 1-6’
Anaemia w/out hypovolaemia, w/out deficits in other components, w/ risk of vol overload

238
Q

What are the indications for fresh (frozen) plasma?

A

Separated w/in 6 hr. Stored at 1-6’ for 24hr. Frozen for up to 1yr after which clotting factors decrease. High in all clotting factors.
Coagulopathies. Pancreatitis? Immunoglobulin source? Supply of albumin?

239
Q

What are the features of liquid/ frozen plasma and its indications?

A

Refrigerated 24hrs- 6 wks post collection. Frozen for up to 5yrs. Inadequate factors V, VIII, vWF but adequate II, VII, IX and X.
Rodenticide toxicity, haemophilia B, supply of albumin.

240
Q

What is cryoprecipitate and what are its indications for use?

A

Concentrated fraction of plasma by partial thawing and centrifugation of FFP- containing vWF, factors VIII, XI, XII and fibrinogen. Refrozen and stored for up to 1yr. Smaller vols can be given than FFP so less likely transfusion reaction.
Haemophilia A, hypofibrinogenaemia and vWD

241
Q

What is cryosupernatant and its indications for use?

A

Supernatent produced when making cryoprecipitate. Contains vit K dependent clotting factors, albumin and antithrombin.
Rodenticide toxicity, vit K deficiency, haemophilia B and hypoalbuminaemia.

242
Q

What are the canine blood groups?

A

DEA (dog erythrocyte Ag) 1, 3, 4, 5, 7. Can be +ve/ -ve for any of these DEAs in any combo.

243
Q

Why do we test for DEA 1?

A

Naturally occuring Ab v uncommon. Formation of anti-DEA 1 Ab will occur within 1-2wks of transfusion of DEA 1 +ve blood to DEA 1 -ve dog. This is sensitisation and delayed haemolysis of transfusion can result. 2nd transfusion to a sensitised dog can result in acute haemolytic transfusion reaction w/ destruction of all transfused cells within 12hr.

244
Q

What are the feline blood groups and how does this affect transfusion therapy?

A

A, B or AB (rare). Donors and recipients must be typed. Naturally occuring alloAb to the blood proteins they don’t have. Reactions peracute and sometimes fatal to B type recieving A or AB blood. Type A receiving B blood have acute reaction like DEA1 -ve Ds- fever, icterus and destruction of transfused cells within 24hr. Type AB cats should get AB blood but type A is acceptable.

245
Q

What is cross matching?

A

Take serum and EDTA from recipient and donor Centrifuge and then separate off the serum and plasma.
Four slides: donor control- 2 drops donor serum and 1 drop donor RBC; major cross match- 2 drops recipient serum and 1 drop donor RBC; minor cross match- 2 drops donor serum and 1 drop recipient RBC; recipient control- 2 drops recipient serum and 1 drop recipient RBCs. Rock slides for 2 mins, look within 5min. +ve agglutination means incompatible, -ve doesn’t guarentee compatible but major transfusion reaction unlikely.

246
Q

When is cross matching required?

A

Recipient transfused >4d previously.
Hx of transfusion reaction.
Recipients transfusion hx unknown

247
Q

When is fresh whole blood used?

A

Ideal for substantial acute haemorrhage. Rarely available immediately so should be resuscitated with crystalloid or colloid therapy

248
Q

What is the formula for calculating fresh whole blood vol for transfusion?

A

Vol (ml)= 85 (D) or 60 (C) x BWt (kg) x (desired PCV-actual PCV)/donor PCV

249
Q

How are blood/ blood products admin?

A

Slow initial rate 0.5-1ml/kg/hr for 30mins. Then 3-4ml/kg/hr, higher if needed as admin over 4-6hr, max 22ml/kg/hr suggested. Pre-tx PCR/TP, TPR, MM of recipient. Use filter so don’t get microthrombi

250
Q

What are the signs of acute tranfusion reaction?

A

Weakness, tremors, agitation and vocalisation, dyspnoea, tachypnoea, tachy/bradycardia, arrhythmias, hypotension, cardiopulmonary arrest, salivation, nausea, V+/D+, urination, seizures, coma, angioedema and urticaria.

251
Q

How do you manage a transfusion reaction?

A

Stop transfusion. Check ECG and BP. Antihistamines- eg chlorphenamine IV if angiodema of face due to reaction to foreign plasma proteins, can then generally continue.
Incr temp of 1’ or more- stop.
Check ECG and BP- e.g. in haemolytic reaction, O2 therapy, shock crystalloids, drugs for arrhythmias, symptomatic tx w/ adrenaline and steroids as necc.
If dyspnoea due to vol overload give frusemide.
If fever >41’ give antipyretic. Tx seizures w/ diazepam.

252
Q

How long do the effects of a transfusion last?

A

Compatible RBCs have a 1/2 life of 21d in D and 35d in cat, so transfusion should last approx 4-6wks.
W/ delayed haemolytic reactions PCV drops rapidly over 3-5d.

253
Q

What are the features of the foals immune system?

A

Function T cells- 100d gestation
Functional B lymphocytes- 200d gestation
Can mount immune response. But ideally not exposed to pathogens so born immunologically naive. No transfer of Ab across placenta (born agammglobulinaemic). Complement and phagocytosis low in newborns. Maternal Ab suppresses production of foals own Ig. V susceptible to infection

254
Q

What is colostrum and when should foals ingest it?

A

3Produced last 2 wks pregnancy. Soluble componenets- mainly IgG (some IgM and IgA), hormones, GFs, cytokines, lactoferrin, CD14 enzymes. Cellular components- lymphocytes, macrophages, neutrophils, epithelila cells.
1-2L in first 3h. Mesurable in serum 4-6h, peaks 18-24h. Specialised enterocytes allow absorption via pinocytosis for 12-24h

255
Q

What is the nadir of foals Ab?

A

1/2 MDA 20-30d. Foal reaches adult levels at 5-10m therefore nadir level at 1-2m.

256
Q

What are the factors involved in FPT in foals?

A

Maternal- lack of colostrum (premature lactation), poor quality (S.G <1.060
Foal- lack of intake (nursing- sepsis, perinatal asphyxia syndrome, orthopaedic problems; rejectede by mare), lack of absoprtion (ingested too late, GI dz- hypoxic damage)

257
Q

How does IgG conc reflect FPT in foals?

A

8g/L successful transfer.

258
Q

How is FPT in foals diagnosed?

A

Hx- problems standing/ never stood, not nursing until 8-12h, rejected
Colostrum exam- SG <1.060
IgG conc in blood- SNAP test (ELISA)

259
Q

How is FPT in foals treated?

A

Via NGT- foal 8-12hr, systemic signs or no high quality plasma available- IV plasma 1-2L. If reaction, stop, give 1mg/kg flunixin meglumine and IVFT, wait 1-2hr, restart slowly, if still reacts use diff plasma batch/ donor

260
Q

What is neonatal isoerythrolysis?

A

IMHA. Incompatibility between mare and foal blood group. Mare produces Ab against foals RBC Ag (fathers). Ab secreted to colostrum, absorbed by foal, adhere to and destroy foals RBCs. Only affects 2nd foal-mare built up Ab. Intra and extravascular haemolysis.

261
Q

How does neonatal isoerythrolysis present?

A

1-12d of age (usually <3d)

Weakness, depression, not nursing, incr HR aand RR, +/- fever, icterus, neuro signs, may be septic (23%)

262
Q

What are lab findings w/ neonatal erythrolysis?

A

Anaemia, haemoglobinuria, haemoglobinaemia, incr uncjd bilirubin, metabolic acidosis, pre renal/ renal azotaemia, toxic hepatopathy/ hypoxic hepatocellular necrosis, possible despite IgG <4g/L

263
Q

How do you tx neonatal isoerythrolysis?

A

Prevent further olotrum intake- muzzle foat/ separate, provide alternative source of nutrition, alternative passive immunity
Supportive- may require IVFT if severe haemoglobinuria
Blood transfusion- washed RBCs from mare (not plasma), blood donor -ve for Aa and Qa, cross match

264
Q

How do you prevent neonatal isoerythrolysis in mare w/ hx of NI?

A

Determine blood group of sire, test serum for alloAb, prevent colostrum intake if same sire/ other incompatible sire used

265
Q

What is combined immunodeficiency in horses?

A

Auosomal recessive genetic dz of arabian foals. Enzymatic defect- no mature functional T or B cells. Recurrent infections after passive immunity decreases. Fatal at 5m. Dam and sire are carriers. Genetic testing available.

266
Q

How do equine erythrocytes differ from SAs?

A

Large splenic reserve. Circulating life long- 140-145d. Respond slower to anaemic insult. No release of reticulocytes to circulation. Regen vs non-regen only dx by BM aspirate. Howell Jolly bodies normal- don’t indicate responsive anaemia

267
Q

What is the calculation for CaO2?

A 
(1.34xHbxSaO2) + (0.003 x PaO2)
Normal horse- 21ml/dl
Anaemic (PCV 10%)- 4.7ml/dl
Hypoxaemic horse- 16.2ml/dl
ANAEMIA- BIG KILLER
268
Q

What are the clinical and lab signs of inadequate O2 to tissues?

A

Incr plasma lactate
Incr O2 extraction from blood therefore PvO2 decr
Pale MMs, incr HR RR, weakness/ exercise intol/ collapse

269
Q

How does PCV alter with acute bleed in horses?

A

Initially rel proportion of plasma to RBC stays te same. As interstitial fluid replaces vol over time then will see decr in RBC- at least 24hr. (Not surgical colic as PCV and TP normal/ lower than would expect- would haemoconcentrate- consider anaemia)

270
Q

What are the differntials for acute blood loss in horses and associated CS?

A

Haematuria- trauma, pyelonephritis, cystitis/ urolithiasis, idiopathic renal haematuria, neoplasia, coagulopathy/DIC
Epistaxis- trauma, ethmoid haematoma, EIPH, neoplasia, GP mycosis, pulmonary haemorrhage, coaguloopathy/ DIC
Haemothorax- trauma, pulmonary haemorrhage, necrotising pneumonia
Haemoabdomen- trauma, ruptured mesenteric vessel, uterine a rupture, neoplasia

271
Q

What are the most common causes of chronic regenerative blood loss in horses?

A

GI- parasitism, neoplasia

Haemolysis- IMHA, toxic

272
Q

What are the most common causes of non-regenerative chronic blood loss in horses?

A

Chronic dz. BM failure- myelophthisis, myeloproliferative disorders, toxins- phenylbutazone. rhEPO. Iron deficiency- chronic haemorrhage, nutritional (rare)

273
Q

What is the recommended tx for blood loss in horses?

A

Guided by clinical indicators. PCV not good indicator in first 24hr. Attempt to control blood loss- ligate/ external pressure. IVFT to replace circ vol.

274
Q

What are the clinical signs and causes of haemoabdomen?

A

Presenting complaint often colic.
Hypovolaemia- incr HR, slow CRT, incr plasma lactate.
Cuases- trauma, neoplasia, uterine a rupture, mesenteric injury, idiopatic.
Dx- US
Survival approx 50%

275
Q

What is periparturient haemorrhage?

A

Haemorrhage from uterine vessels. Most common after parturition. Cause of pp colic and death. Delivery often uneventful. May be confined by broad ligament or may bleed to abdomen. Tx- CVS stabilisation. Mares prone to repeated bleeding episodes during subsequent pregnancies.

276
Q

How does IMHA present in horses?

A

1ry- uncommon, Ab against patients own RBC Ag
2ry- Ab formation precipitated by 1ry dz process, drug admin, neoplasia, immune-mediated dz.
Dx- coombs test can be attempted, false +ve and -ve poss. Flow cytometry demostrates Ab on RBC
Tx- 1ry dz, stop meds, transfusion if inadequate O2 delivery. Immunosupression- corticosteroids, azothioprine, cyclophosphamide

277
Q

What is EIA?

A

Via insects (lentivirus). Not in UK- risk from imports.
3 syndrome: acute, chronic inapparent. Anaemia- intravasc/ extrvasc haemolysis. BM suppresion. Thombocytopenia common.
Dx- coggins test or ELISA
Euthanasia

278
Q

What are the causes of haemolytic anaemia due to oxidative injury in horses?

A

Drugs (phenothiazine, methylene blue), plants (onions, brassica, red maple).
Heinz bodies- oxidatively dentured Hb precipitates on RBC membrane. Rapidly cleared from circulation.
Red maple- methaemoglobin results from oxidate change of Hb F2+ to Fe3+- not usuable for O2 transport, also heinz body.

279
Q

What are the causes for anaemia due to inadequate erythropoesis in horses?

A

Chronic dz- infamm/infection, neoplasia, sequestraion of Fe, shortened RBC life, defective EPO response.
Mild to mod anaemia, normoctic, normochromic, non-regen
Tx 1ry dz
No tx for anaemia necc
Iron deficiency- chronic blood loss, tx- oral iron supplementation
CRF.

280
Q

What is the role of colostrum for calves?

A

Immune- 1ry protection against neonatal septicaemia and joint/ navel ill, protection against enteropathogens, and enzootic pneumonia. Syetmic protection via IgG and IgM. Local protection of intestine by resecretion of IgG to gut lumen, passage of IgA through gut lumen
Nutrition- 1st feed w/ additional vit and TEs.

281
Q

What is the process for colostrum intake in calves?

A

4-6wks before calving, transfer of Ig to udder. Ingested by calf, absorbed by epithelial cells of SI and passes via lymphatics to peripheral blood circulation

282
Q

How much Ig does a calf get?

A

If 5g/L plasma- protected. 10g/L- no dz, therefore this is the aim. IgG massive uptake into colostrum compared to serum.
In beef suckling usually ok because need a small vol due to high quality colostrum. Dairy- often rely on suckling but prob not best due to dilution etc, sp at first feed traditional, 3-4L more effective

283
Q

What factors influence colostrum uptake in cows?

A

First milking- rapid decrease with each milking.
MY
Beef much better than dairy
Impact- precalving milking or leaking of milk, short dry period, premature calving/abortion, cows typically have richer colostrum than heifers (exposed to more bugs) but higher yields therefore higher dilution, mastitis

284
Q

What factors cause poor colostrum uptake in cows?

A

Calf- weak, acidosis, dystocia, mouth problem (belgium blue- large tongue)
Mother- sore teats, teat shape, teat aligment, dropped udder. Poor mothering, heifers, disturbance/ stress, overcrowding of calving area, C/S, milk fever/ downer cow, slippery floors

285
Q

What factors affect the efficiency of absoprtion of colostrum in calves?

A

Closure of gut depends on presence of protein in intestine, time after calving. Efficiency 12hr-46%, 24hr- 12%, 36hr-7%

286
Q

What factors affects quality of colostrum in cows?

A

Exposure of dam to pathogens

Vaccination e.g. rotavirus- store and allow it fermet, feed stored colostrum for several days (IgA)

287
Q

How do you assess colostrum uptake in calves?

A

Serum of calf- IgG (>10g/L), GGT (200IU/L d1, 100IU/L day 4), TP (>5.5g/L), ZST (>20g/L ZnSo4), sodium sulphate (>18g/L sol)
Colostrum- SG (>1.048), thicker the better, hygrometer

288
Q

How should colostrum be stored?

A

15 C- 24hr
4 C- 7d
-20 C- 6m+
Fermented colostrum not suitable for 1st feed but useful for IgA for rotavirus (local protection)

289
Q

What are the clinical signs of anaemia in farm animals?

A

Pallor. Lack of exercise tol. Weakness. Haemic murmur. Red urine. Jaundice. Dependent oedema. Black faeces. Sweollen udder.

290
Q

What indicates anaemia on clinical pathology in FAs?

A

Low PCV, low Hb, immature of erythrocytes, evidence of regeneration, jaundice

291
Q

What are the normal PCV and Hb values in FAs?

A

Catlle: PCV- 24-46%, Hb 8-15g/dl
Sheep: PCV- 27-45%, Hb 9-15g/dl
Swine: 22-38%, Hb 8-12g/dl

292
Q

What causes haemorrhagic anaemia in FAs?

A

CdVC syndrome, Enzootic haematuria, Ruptured uterine a/aorta, Haemonchosis, Fasciolosis, Lice, mites and ticks, Pyelonephritis, Abomasal ulcer, Intraluminal intestinal
haemorrhage, Gastric ulceration in pigs, Proliferative haemorrhagic enteropathy in pigs (PIA)

293
Q

Causes of haemolytic anaemia in FAs?

A

Leptospirosis, Postparturient haemoglobinuria, Bacillary
haemoglobinuria, Protozoa (Babesia, Eperythrozoon), Chronic copper poisoning, Cold water ingestion, Brassica spp poisoning (Rape, Kale, Cabbages), Drug induced, Blood transfusion, Autoimmune haemolytic anaemia

294
Q

What are the causes of depressed erythrocyte production in FAs?

A

Deficiency of cobalt or copper, Iron deficiency, Acute bracken poisoning (enzootic haematuria), Faciolosis, LSA, Chronic renal dz (amyloidosis, pyelonephritis), Anaemia of inflamm dz, Radiation damage

295
Q

What is used in the tx of anaemia in FAs?

A

Blood transfusion- adult cow may need 5L of blood, 1st transfusion should be safe.
Haemantics- Fe, Cu, vitB12, high protein, fresh foods

296
Q

What are the clinical signs of enzootic haematuria?

A

Haematuria w/ blood clots, fz urination, thickened bladder may/ may not be palpable per rectum, other signs of chronic progressive anaemia, internal bleedings.

297
Q

What are the causes of abomasal ulcer?

A

Sand, displaced abomasum, stress.

Dx- occult blood in faeces/ black, stinking dung, free air in abdomen, abdominal pain

298
Q

How does inflammatory disease cause anaemia in FAs?

A

Alteration in iron metabolism, depressed BM response, shorter lifespan on erythrocytes

299
Q

What happens in chronic copper poisoning of FAs?

A

Sheep more susceptible than adult cattle
Copper stored and accumulated in liver. Some centrilobular necrosis occurs as conc rises. Sudden release from liver to blood–> acute fatal syndrome develops. Can come from the diet (concentrates, phytogenous, hepatogenous- liver damage by PA) or accidental overdose. In sheep >4ppm required for normal health, >12ppm may be dangerous (epends on breed, length of time fed, presence of inhibitors)

300
Q

What are the clinical signs of chronic copper poisoning?

A

Jaundice, pallor, haemoglobinuria, depression, death in 24-48hr

301
Q

How is chronic copper poisoning diagnosed?

A

Clin path- blood Cu elevated (after release), liver Cu elevated (biopsy), as for other acute haemolytic anaemia, incr plasma AST
Necropsy- swollen yellow liver, swollen gunmetal kidneys, jaundice everywhere, take liver for Cu assay and histopath
Haemoglobinuria, jaundice, anaemia

302
Q

What is the tx for chronic copper poisoning?

A

Ammonium tetrathiomolybdate 2.7mg/kg IV at 2-3d intervals for 3-6 treatments
Ammonium molybdate 100mg + sodium sulphate 1g oral daily
Na calcium edetate 70mg/kg IV for 2d
Somnuose 10ml IV
Prevention- keep dietary copper <10ppm, Cu absorption inhibitors- Mo, Zn, Fe and soil, avoid prolonged feeding of concentrates

303
Q

What are the stages in neutrophil production?

A

CFU-G (stem cell)
ProNP (proliferation neutrophil pool)
MatNP (maturation neutrophil pool)
SNP (storage neutrophil pool)

304
Q

What forms does the neutrophil go through in the proliferation neutrophil pool and what is the timeframe?

A

(mitotic pool) Myeloblast–> progranulocyte–> myelocyte

3d

305
Q

What forms does the neutrophil go through in the maturation neutrophil pool and what is the timeframe?

A

(post mitotic) Metamyelocyte–> band neutrophil–> segmented neutrophil.
2-3d

306
Q

What are the CNP and MNP and what is the neutrophil 1/2 life in the blood?

A

CNP- circulating neutrophil pool (sampled during blood collection)
MNP- marginated neutrophil pool (ready to exit circulation and migrate to tissues)
1/2 life: 5-l0hr

307
Q

What is a left shift neutrophilia?

A

If demand high, more immature neutrophils released.

May see toxic change- cytoplasmic foaminess and basophilia, Dohle bodies, giant neutrophils, vacuolation, toxic granules

308
Q

What are toxic vs degenerate neutrophils?

A

Toxic- in peripheral blood, due to accelerated production (no need for toxins)
Degernate/ lytic- in tissues (fluids), fighting w/ bacteria, bacterial toxins

309
Q

How is a left shift classified?

A

Regenerative- neutrophilia, segmented>bands

Degenerative- neutropenia, bands>segmented

310
Q

What are the causes for a neutropenia?

A

Increased demand: peracute bacterial infections, endotoxaemia, immune mediated
Redistribution (marginated): endotoxamiea, anaphylactic shock
Decr production: BM disorders, infectious causes (FeLV, FIV, parvo, ehrlichia), toxicities, myelodysplasia/ fibrosis/ phthisis, congenital

311
Q

What are the causes of a neutrophilia?

A

Increased production: infection, immune mediated (IMHA, PA), 2ry to neoplasia, haemolysis, haemorrhage, necrosis, thrombosis, chronic granulocytic leukemia (well differentiated), acute myeloid leukemia (poorly differentiated)
Incr persistence in circ: stress/ steroid responsive
Redistribution: stress/ excitement (decr margination)

312
Q

What is the recommended tx for neutrophil abnormalities?

A

Neutropenia <2x10e9/l BS abx
Tx underlying cause
Chronic granulocytic leukemias- good short term px
Acute myeloid leukemias- no successful tx

313
Q

What are the causes of a lymphopenia?

A

Incr demand
Redistribution: steroids/ stress (to BM, tissues, trapping in LNs)
Decr production: infectious causes (CDV, parvo, panleukopenia, FeLV, FIV), lympholytic drugs (cyclophosphamide, azathioprine, long term steroids), congenital immunodeficiencies

314
Q

What are the causes of a lymphocytosis?

A

Incr demand: persistent Ag stim, post vaccine, young animals
Incr no: CLL, ALL, stage V lymphoma
Redistribution: physiological leukocytosis, hypoadrenocorticism

315
Q

What are the characteristic features of monocytes?

A

Monoblasts–> monocytes in BM in 6d. No storage pool. Persistence in circulation varies, shortens w/ inflamm- leave circulation to tissues, differentiate into macrophages

316
Q

What are the causes of a monocytosis?

A

Incr demand- infectious, immune mediated, necrosis, trauma, burns, neoplasia
Incr no- 2ry to immune neutropenia, myelomonocytic leukemia, acute monocytic leukemia
Redistribution- steroids (out of marginated pool)

317
Q

What are the causes of an eosinopenia?

A

Corticosteroids- apoptosis, poss neutralisation of histamine/ mast cell degranulation and other mechanisms
Catecholamines

318
Q

What are the causes of an eonophilia?

A

Incr demand- parasite, allergic dz (via sensitised T cells, mast cells)
Incr no: paraneoplastic, hypereosinophilic syndrome (no obvious cause), eosinophilic leukemia (rare)

319
Q

What are the causes of a basophilia?

A

Incr demand- immediate/ delayed hypersensitivity, parasitism, other inflamm responses
Incr no- paraneoplastic (esp w/ MCT), basophilic leukemia (rare)

320
Q

What is a stress leukogram?

A

Response to corticosteroid

Neutrophilia, lymphopenia, monocytosis, eosinopenia

321
Q

What is an inflammatory leukogram- acute vs chronic?

A

Acute: neutrophilia w/ w/out L shift, lymphopenia, monocytosis, +/- eosinopenia
Chronic- neutrophilia w/ w/out L shift, lymphocytosis, monocytosis

322
Q

What changes in WBCs occur with an adrenaline response?

A

Neutrophilia, lymphocytosis

323
Q

How does haematology differ in young animals?

A

Higher nos of WBCs. Lower HCt.

Mild and generally normalised at about 3m

324
Q

What are the typical features of endothelial cells?

A

Flattened cells lining BVs/ Have pro and anticoagulant properties. Normally anticoagulant. Act as a barrier to subendothelial collagen which is procoagulant

325
Q

What is von Willebrands Factor?

A

Produced by endothelium and platelets. Released early in haemostatic process. Responsible for platelet adhesion to collagen.

326
Q

What are platelets?

A

Small, discoid, anuclear cells found in the circulation. 3-5um and are pale basophilic w/ small red granules. Derived from cytoplasm of megakaryocytes in the BM. Mediated by thrombopoietin. Circulate for 5-9d in most sp. OM contains Rs important for adhesion and aggregation. Contain a cytoskeleton w/ actin and myosin that allows for shape change. Contain membrane bound granules- alpha (contain vWF, fibrinogen, factors V and VIII), dense granules (ADP and Ca)

327
Q

What are the surface receptors of platelets?

A

Glycoproteins w/ platelet membrane.
GP Ib- binds vWF. GP IIbIIIa- binds fibrinogen on adjacent platelets and allows platelets to aggregate. Defects in Rs lead to abnormal platelet function and clot formation.

328
Q

What are the main steps of haemostasis?

A

1ry haemostasis- formation of 1ry platelet plug
2ry haemostasis- activation of coagulation cascade and generation of insol fibrin which stabilises the platelet plug
Fibrinolysis- breakdown of fibrin and platelet plug

329
Q

What steps are involved in 1ry haemostasis?

A

Exposure of subendothelial collagen, vWF released from endothelium. Causes platelet to bind to collagen. Shape change–> spherical w/ filopodia- additional Rs for vWF and fibrinogen exposed. Aggregate- form platelet clump/ Rapidly degranulate releasing ADP, fibrinogen, vWF, TXA2–> incr platelet adhesion and aggregation. Also release factors V and VIII

330
Q

What steps are involved in 2ry haemostasis?

A

Simultaneously to 1ry. Endothelium releases tissue factor which activates extrinsic coag pathway. Extrinsic (initiation), intrinsic (amplification) and common pathway. Converts prothrombin to thrombin which converts fibrinogen to fibrin. Fibrin crosslinked and stabalises 1ry platelet plug

331
Q

Which factors are involved in the extrinsic pathway?

A

VII- in presence of Ca

Activates X of common pathway and IX of intrinsic

332
Q

Which factors are involved in the intrinsic pathway?

A

XII, activates XI, which activates IX (Ca required). IX activates X of common pathway (Ca required)

333
Q

What factors are involved in the common pathway?

A

Activation of X, which binds to activaed V and Ca on platelet surface. Converts prothrombin to thrombin, which converts fibrinogen to fibrin. Fibrin crosslinked by activated XIII

334
Q

What are the inhibitors of coagulation?

A

ATIII (incr by heparin from endothelium)- inhibits thrombin and activated X
Protein C- inactivates V and VIII
Fibrinolysis

335
Q

What is fibrinolysis?

A

Enzymatic breakdown of fibrin by plasmin, which is derived from plasminogen found in the platelet membrane and plasma. Plasmin degrades both fibrinogen and fibrin to produce fibrin degradation products

336
Q

How do you evaluate platelet number?

A

Platelet conc- automated from EDTA, good for all sp except cat, sheep and goat (overlap between RBC and platelet size), platelet clumps common
Estimated from blood smear- must be done in cats, also CKCS often thrombocytopaenic w/ giant platelets (counted as erythrocytes)

337
Q

What are the reference ranges wrt platelets?

A

Thrombocytopaenia 1000x10e9/l- incr risk of thrombosis

338
Q

What is the buccal mucosal bleeding time?

A

Length of time for platelet plug to form- 1ry haemostasis and platelet function
Small incision in mucosa, blotted until bleeding stops- incr in thrombocytopaenic, prolonged in vWD/ disorders of platelet function, not incr w/ coagulation def

339
Q

How does a disorder of the platelets generally appear?

A

Haemorrhage if decr or function impaired- ecchymoses or petechiae
If incr- risk thrombosis

340
Q

What causes thrombocytopenia?

A

Incr platelet destruction or consumption- immune mediated destruction, haemorrhage, DIC, sequestration
Decr production
Infectious

341
Q

What is immune mediated thrombocytopenia?

A

Most common. Platelet no extremely low (often <10x10e9/l). If megakaryocytes in BM also affected then decr production
1ry- Ab against platelet Ag
2ry- many causes- other immune dz (SLE), drugs/ vaccine, neoplasia, infectious

342
Q

What is Evans syndrome?

A

Concurrent immune mediated thrombocytopaenia and anaemia

343
Q

How do you diagnose immune mediated thrombocytopaenia?

A

Clinical findings. Profound thrombocytopaenia (recheck). Evidence of petechial or ecchymotic haemorrhages. Hx of bleeding from gums, mucosal surfaces, prolonged bleeding from wounds. Dx of exclusion. May see megakaryocyte hyperplasia. BM exam if platelet nos v low. Anti-platelet Ab. Response to tx.

344
Q

What are the causes of incr consumption thrombocytopaenia?

A

Haemorrhage- should not be <100x10e9/l

DIC- nos may be very low, usually will be signs of a coagulation defect. Check PT, PTT- prolonged, check FDPs- incr

345
Q

What are the causes of sequestration thrombocytopaenia?

A

Rare but may occur w/ splenomegaly or w/ large cavitated mass

346
Q

What are some infectious causes of thrombocytopaenia?

A

No of causes poss incl immune mediated and decr production.

FeLV, BVD, Ehrlichia, Leishmania

347
Q

What are the causes of thrombocytosis?

A

Physiological (transient)- epinephrine induced spleen contraction
Reactive (2ry)- incr thrombopoeitin- inflamm, haemorrhage, iron def
Essential- myeloproliferative disorder (BM megakaryocytes incr, TPO normal/ incr)

348
Q

What is vWD?

A 
Circulates bound to fVIII
Mucosal bleeding (GI, epistaxis, haematuria), bleeding may be absent. No petechiae (differentiate from other platelet disorders). Prolonged BMBT w/out thrombocytopaenia. Clotting times usually normal but PTT may be prolonged due to decr in fVIII. Common in Ds. Rare Cs, Hs.
349
Q

What are the 3 types of vWD?

A

Type 1- all multimers present but at decr conc, variable severity of bleeding but not until conc <0.1%), usually die v quickly, autosomal recessive

350
Q

How do you test for vWD?

A

Measure vWF:Ag levels. EDTA or citrate. Separate plasma immediately, freeze and ship o/n w/ ice. ELISA allows for quantitative measure of vWF using sp specific Abs. Immunoelectrophoresis to separate rel amounts of diff multimers (req for type II)
<35%- vWD. 50-69% borderline. 70-180%- free from vW trait

351
Q

What is the recommended tx for vWD?

A

Transfusion to supply vWF- cryoprecipitate is the best 1 U/10kg. If not available then plasma at 6-12ml/kg. Whole blood if anaemic.
Desmopressin (DDAVP) as pre-op prophylaxis for Ds w/ type 1 vWD, causes release of vWF from endothelium. 1ug/kg SQ 30m prior to sx

352
Q

How do you sample for coagulation tests?

A

Most require citrated plasma. Centrifuger to separate plasma w/in 1hr. Analyse w/in 4 hr or freeze plasma. Incl sp specific control.

353
Q

What is the activated clotting time?

A

Evaluates intrinsic and common pathways. 2ml into ACT tube containing diatomaceous earth. Incubate for 60s at 37’C and check for clot formation every 5-10s. Time to initial signs of clot is ACT (s). Prolonged by thrombocytopenia.

354
Q

What is the PTT (partial thromboplastin time)?

A

Screening for intrinsic and common. Incubate citrated plasma w/ excess phospholipid, contact activator and Ca. Measure time to clot formation. Factor activity must be <30% normal to prolong PTT. Expect prolongation w/ haemophilia (VIII, IX), factor XII def, DIC, vit K def and liver dz. Not affected by thrombocytopaenia

355
Q

What is the PT (prothombin time)?

A

Screening for extrinsic and common pathways. Incubate citrated plasma w/ tissue thromboplastin and Ca. Measure time to clot. Prolongation w/ fVII def, DIC, vit K def, liver failure. FVII decr 1st w/ vit K def so may see prolonged PT w/ normal PTT

356
Q

How do you test fibrinolysis?

A

Serum- separated w/in 30mins. Test immediately or freeze

Incr FDPs w/ DIC. Not specific, may also incr w/ haemorrhage, jugular v thrombosis (horse) and liver dz

357
Q

What is Vit K deficiency?

A

E.g. w/ rodenticides. Factors II, VII, IX and X produced in liver and are activated by vit K dependent carboxylase, this requires Vit K reductase. Extrinsic, intrinsic and common pathways affected. Vit K has shortest 1/2 life so will decr 1st, therefore PT often prolonged 1st. CS- haemorrhage/ Elevation in PT and PTT. Platelet nos and BMBT should be normal but mild thrombocytopaenia poss due to consumption w/ haemorrhage. FDPs may be elevated. Same results in coag 2ry to hepatic dz

358
Q

How is vit K deficiency treated?

A

Emetics, cathartics, activated charcoal if ingestion of rodenticide recent. Transfusions of whole fresh blood or fresh frozen plasma. Vit K therapy. If warfarin or other 1st gen rodenticide used 1 wk tx sufficient. If 2nd/3rd gen need to tx for at least 3 weeks (often up to 6). Check PT 24-48hrs after last dose, if prolonged reinstate tx for another 2wks and recheck PT

359
Q

What are the hereditary defects of coagulation?

A

Factor VII def, haemophilia A (fVIII def), haemophilia B (fIX def), factor XI def, factor XII def
Tx- transfusions of whole blood or plasma to replace factor def and RBCs. Cryoprecipitate (10x more fVIII vs plasma).

360
Q

What is DIC?

A

Mixed haemostatic defect. Excessive coag leads to widespread thrombosis. Eventually haemorrhage as all coag factors consumped. Not 1ry but 2ry to underlying dz (neoplasia, liver, immune mediated, infectious). May be chronic or acute. Thrombocytopaenia, prolonged PT and PTT, elevated FDPs, decr fibrinogen, decr antithrombin III.
Tx: stop the coag process, heparin, transfusion of whole blood, plasma or cryoprecipitate as source of ATIII, aspirin to stop platlet activation. Correct cause. Px poor

361
Q

What is the general approach to the bleeding patient?

A

Haemorrhages ecchymotic or petechial- platelet defect likely
If not- consider coag defect. Check CBC, HCT and platelet nos.
If thrombocytopaenia present check for clots, check smear, recheck nos. If platelets approx 100x10e9/l consider haemorrhage, if <BBT, assay for vWF:Ag. Check clotting function. Check PT and PTT- if both consider Vit K def or DIC. PTT alone consider intrinsic pathways (haemophilia A and B), PT alone (consider early vit K def, liver dz, early DIC)

362
Q

What is FeLV?

A

Non cytopathic retrovirus. Labile, enveloped ssRNA. Reverse transcriptase, integrate into host DNA. Either- destruction of infected cell by immune response, infection +/- virus production, or transformation to neoplastic cell. 1-2% in healthy cats, ~20% in symptomatic

363
Q

What are the 3 major protein groups of FeLV?

A

Core protein p27 (gag)- basis for most diagnostic tests, may circulate free in plasma or excreted in tears/ saliva, envelope masks presence in intact viurion
Envelope protein: p15E (spike)–> immunosuppresion; gp70 (knob) defines subgroup, target for vaccine

364
Q

What is the pathogenesis of FeLV?

A

Oral/ nasal exposure and replication in oropharyngeal lymphoid tissue.. Virus cleared (abortive) p27 -ve, latent in BM, lymphoic tissue. Or can progress to viraemia and replication leading either to a persistent viraemia (progressive) or transient viraemia (regressive) and thus latency.

365
Q

How is FeLV transmitted?

A

Source- PI cats
Shed in saliva, nasal secretions (faeces, urine, milk). Short survival outside body (few hrs). Can be spread to neonates in utero or by nursing. Blood transfusions.

366
Q

What are the clinical findings of FeLV?

A

Many aymptomatic. Varied and non specific. Depend on organ +- 2ry dz. Incl inappetence, weight loss, wasting, poor coat, lymphadenopathy, persistent fever, pale MMs, ocular dz, gingivitis, stomatitis, infections of skin, urinary bladder, URT, persistent d+, seizures, behavioural changes, other neuro disroders, queens- abortion etc. 2ry infections due to immunosuppression. Can have BM suppression due to infection of haematopoeitic stem cells- anaemia, thrombocytopaenia, granulocytopaenia, myelodyspolastic syndrome, leukemia. Lymphoma in 25% cats w/in 2yr dx.

367
Q

How is FeLV diagnosed?

A

Confirmed +ve test only indication of infection, not clinical dz.
Immunoassay- ELISA, p27 Ag, screening test
IFA- p27 in leucocytes and platelets (after marrow infection) confirmatory
PCR- viral nucleic acid sequences, confirmatory
Viral culture- gold standard for confirmation, rare
Ab- not for dx but virus neturalising Ab can be useful.
+ve Ag- transient or persistent viraemia, +ve IFA- BM infection, persistent viraemia
-ve= unexposed, elimination, early infection, latent, localised, false -ve

368
Q

What would a +ve Ag, -ve IFA/ viral isolation of FeLV indicate?

A 
Early infection (not yet replicating), in recovery, false +ve, detection of incomplete virus, localised infection Ag released but not virus, greater Sn of Ag test
Isolate from other cats, repeat bloods in 4wks, if -ve for Ag and virus. likely virus free, confirm by repeating in 8wks. If still discordant recheck in 8wks
369
Q

What is the recommended tx and prevention for FeLV?

A

Systemically well- general preventative health care (nutrition, prevent 2ry infections), neuter if entire, confine indoors.
Sick- supportive care, tx 2ry illness, confine indoors
Vaccinate- test before, assess risk of exposure

370
Q

What is FIV?

A

Lentivirus- retrovirus. 5 subtypes. Most common in free-roaming, aggressive males. 3-6% in healthy cats, 15-19% in sick

371
Q

How is FIV transmitted?

A

Bite wounds- ;large amount in saliva. Less common- vertical (transplacental/ milk),. sexual, low risk by sharing food bowls

372
Q

What are the 5 phases of FIV?

A

Acute
Asymptomatic carrier (up to 10yr, healthy but defects of immun system)
Persistent generalised lymphadenopathy
Terminal- AIDS related complex, AIDS

373
Q

How does the acute phase of FIV present?

A

Several days to weeks. Transient mild illness (+/- fever, lethargy, d+, lymphadenopathy). Early replication in lymphoid tissues (eg thymus) and salivary glands. Later spread to mononuyclear cells in non lymphoid organs- lung, GIT, kidney. +/- neutropaenia, lymphopaenia

374
Q

How does the AIDS phase of FIV present?

A

Only ~10% cats reach this stage. Survival- few weeks to months. Opportunistic infections- FHV, FCV, toxoplasma, cryptosporidium, candida, mycobacterium and demodex. Neuro dz and neoplasia. CBC- leucopaenia, anaemia, CD4+:CD8+ T cell ratio inverted

375
Q

What are the most common findings of FIV?

A

Stomatitis, neoplasia (lymphoma, SCC), occular inflamm (uveitis, chorioretinitis), anaemia and leucopaenia, opportunistic infections, renal insufficiency

376
Q

How is FIV diagnosed?

A

CBC- neutropaenia, anaemia, thrombocytopaenia,l co-infection w/ m.haemofelis–> haemolytic anaemia.
No particular abnormality on serum biochem, +/- polyclonal gammopathy
FIV tests

377
Q

What are the FIV test options?

A

Ab test- Ab to core protein p24 or envelope protein gp41, most develop Ab w/in 60d, interferance from vaccine and MDA
IFA- detects Ab, FIV infected cells fixed to slide, test sample applied, fluorescent 2ry Ab applied
Western blot- detects Ab, confirmatory for +ve ELISA
PCR- commercially available
Viral isolation- only research centres

378
Q

What does an FIV +ve test result indicate?

A

PI, FIV infected queens (test kittens >6m), flase +ve (low prevalence), weak +ve (repeat), if kitten <6m retest every 60d until at least 6m

379
Q

What does an FIV -ve result indicate?

A

Not infected, infected but Ab not detected by test, test error, no Ab response (immunosuppression), early infection (8-12wks post infection, before detectable Ab, retest every 60d if needed)
PCR helpful is suspect MDA interferance, immunosuppressed, detection prior to Ab production (1-3wks)

380
Q

What is the recommended tx for FIV?

A

Supportive- abx, cautious used of GCs in combo w/ abx (gingivitis, stomatitis), lactoferrin (poss in stomatitis).
Antiviral- zidovudine, inhibits new infection by blocking RT of retrovirus but not replication in pre-infected cells

381
Q

How do you prevent FIV infection?

A

Prevent exposure to virus. Readily killed by disinfectatnts, dies within few hrs in environment. Low risk transmission by social contact. Don’t breed from FIV +ve queens. Vaccination (USA only)

382
Q

What is FIP?

A

Fatal dz caused by feline coronavirus. Viral infection in common but clinical dz is uncommon. Infects mascrophages–> systemic infection, clinical dz syndrome resulting from ineffective immune response. Immune complex dz characterised by vasculitis, complement activation, excessive cytokine production

383
Q

What is feline coronavirus?

A

Enveloped, ssRNA virus. Large, pleiomorphic, undergoes mutation. Replicates in cytoplasm, virion acquires envelope from ER and golgi. Released by cell lysis or vesicle fusion w/ plasma membrane. Rel unstable outside host. Present in large portion of healthy cats, oronasal transmission. Replicates in enterocytes. CS- mild/inapparent, V+, D+, URT signs

384
Q

What are the 4 different outcomes of a FCoV infection?

A

Transient infection (60-70%)
Persistent infection (10-15%)
FIP (5-10%)
Resistance to FCoV infection (2-5%)

385
Q

What is the pathophysiology of FIP?

A

Viral Ag+Ab+ complement–> complement fixation–> release of vasoactive amines causing endothelial cell retraction and incr vasc perm

386
Q

What are the clinical signs of FIP?

A

Early, non specific- pyrexia, inappetance/ weight loss, D+, listlessness, dehydration, jaundice
Effusive (60-75%)- abdo effusion, pleural effusion (dyspnoea), pericardial effusion (less common)
Non-effusive- dry/granulomatous, predisposition for eye, CNS, kidney, liver, localised regions of intestine

387
Q

How is FIP diagnosed?

A

Often difficult AM. Hx and CS. PE- incl ocular (+fundic) exam.
CBC- lymphopaenia, neutrophilia (w/mild L shift), mild non-regen anaemia
Biochem-hyperglobulinaemia (polyclonal), Alb:Glob t distinguish infected vs FIP
Histopath- light plaques, adhesions

388
Q

How does fluid analysis of FIP appear?

A

Clear, straw to yellow colour. High protein (>35g/l, >50% globulin). Viscous (may become frothy when shaken). Cellularity variable- <5000/ul, pyogranulomatous MT (exudate less common)

389
Q

What is the tx/px for FIP?

A

Grave- no cure in large majority.
Supportive/ palliative care- abx, SQ fluids, nutrition, rest, thoracocentesis
Immune modulators?- feline IFN, GCs+/- chlorambucil

390
Q

What is used for prevention of FIP?

A

FeCoV vaccine.

Strong cell mediated immune response w/out strong Ab response

391
Q

What is feline infectious anaemia?

A

Mycoplasmas- small epicellular parasites, no cell wall, tetracycline-sensitive. M. haemofelis.
Pleiomorphic-rods, rings, spherical. G-ve. Attach to RBCs–> immune mediated destruction. Often latent- concurrent dz and immunosuppression enhance dz. If recover then chronic infection for variable time, reactivation poss.

392
Q

How is M.haemofelis transmitted?

A

Fleas, blood transfusion, female cats (en utero? nursing?), fighting? oral?- saliva not thought to be infective

393
Q

What are the clinical signs of M. haemofelis?

A

Acute infection- lethargy, innapetence, anorexia, fever, anaemia, splenomegaly, icterus
Chronic- normal to subnormal temo, weakness, depression, weight loss/ emaciation, icterus and splenomegaly less likely

394
Q

How does M.haemofelis appear on bloods?

A

CBC- regen anaemia (if acute onset may be pre-regen), erythrophagocytosis and autoagglutination may be present, leucocyte count variable (leucocytosis w/ monocytosis in acute, normal coutns in chronic, leucopenia in moribund

395
Q

How is M.haemofelis detected?

A

Fresh blood smear- EDTA may displace organism, organisms onlynoted in ~50% of acute dz cases (fluctuating nos), absence doesn’t rule out dx
PCR- Sn, may be -ve when recieving tx

396
Q

What is the recommended tx for feline infectious anaemia?

A

Doxycycline- potential ADE- GI effects (mucosal irritation), abdo discomfort, V+, inappetence/ anorexia, oesophagitis, oesophageal stricture formation
Flea control! esp in FeLV/ FIV +ve cats
Supportive care- blood transfusion, immunosuppressive therapy (pred)

397
Q

What is the px for FIA?

A

No tx- approx 1/3 w/ uncomplicated acute dz die
Regen> destruction–> recovery
Recovery phase- last parasitaemia to PCV stabilisation >1m

398
Q

What are the types of immune mediated disease?

A

Non organ specific (SLE) to organ specific (MG)

Primary (idiopathic) or 2ry (drug usage, neoplasia, infection)

399
Q

What is the pathogenesis of immune mediated dz?

A

Overreacts to normal body tissues or harmless exogenous proteins (loss of tolerance). Humoral and cellular mechanisms
Triggers: release of sequestered Ag, abnormal immunoregulation, molecular mimicry, polyclonal activation of T/ B cells, exposure of cryptic epitopes or haptenisation of foreign molecules to self Ag.

400
Q

How does infection play a role in immune mediated disease?

A

Breakdown of vasc/ cellular barriers- exposure of self-Ag
Promotion of cell death by necrosis causing inflamm
Polyclonal activation of T cells (bacterial superAg)
Molecular mimicry- cross reactivity
Vector borne pathogens

401
Q

What is the likely presentation of immune mediated dz?

A

Likely to be multifactorial. Idiopathic overrepresented in juvenile to middle aged. Generally waxing and waning.
Lameness, MC lesions, lethargy, dyspnoea, weight loss, PU/PD +/- seizures or behavioural changes.
Effusive painful joints; cutaneous erythema, macules, papules, pustules, erosion; pallor +/- petechiae; cardiac arrhythmias; lymphadenomegaly +/- splenomegaly

402
Q

What occurs on the CBC/ coag w/ immune mediated dz?

A 
Anaemia: regenerative- IMHA, or non regenerative- infection, uraemia, chronic bleeding, attack of precursors
Thrombocytopaenia (marked)
Leucopaenia: SLE, IM neutropaenia- drug
Coagulation (incr APTT, PT- SLE, DIC)
*always incl smear*
403
Q

What occurs on the chem panel w/ immune mediated dz?

A

Azotaemia, incr inorganic phosphate- chronic glomerular lesions
Hypoalbuminaemia, hypercholesterolaemia- PLN
Hyperbilirubinaemia- pre hepatic/ haemolysis
Hyperglobulinaemia- inflamm dz, polyclonal B cell activation
Incr CK and LDH- polymyositis +/ myocarditis

404
Q

What occurs on the UA w/ immune mediated dz?

A

Proteinuria- PLN (r/o UTI and occult infections 1st- post glomerular)
Haematuria, pyuria, erythrocyte casts- glomerulonephritis (r/o UTI)

405
Q

What occurs on the radiography and arthrocentesis w/ immune mediated dz?

A

Joint lesions common in polysystemic IM dz- usually non erosive pauciarthropathy. Erosive suggest overlap syndome (rheumatoid arthritis- rare)
Synovial fluid- incr WBC, proportion of neutrophils +/- incr protein content, decr viscosity and poor mucin clot formation

406
Q

What are the common sites for arthrocentesis of IMPA?

A

Antebrachial carpal
Tarocrural
Tibiotarsul
Stifle

407
Q

When is coombs test used?

A

If IMHA suspected try in saline agglutination. If -ve and still suspect- coombs test to detect Ab associated w/ surface of RBCs. Antiserum (IgG, IgM and C3), cross links RBCs. False +ve and -ve.

408
Q

What are AChR autoAb used?

A

Acquired MG- focal, generalised, acute fulminating, paraneoplastic
Immunoprecipitation radioimmunoassay.
False +ves and -ves v rare

409
Q

When is an ANA used?

A

Serum ANA hallmark for canine and feline SLE.
Indirect IFA or immunoperoxidase test
False +ve and -ves may occur

410
Q

What is the treatment for immune mediated disease?

A

Corticosteroids- mainstay

Adjunctive- diet, topical tx, GI protection, blood products

411
Q

How do corticosteroids work?

A

Associate w/ binding proteins (transcortin, Alb). Dissociate from binding proteins and passively diffuse into cell. Bind to cytoplasmic R (>3). Conformational change of R unmasks DNA binding domain- associates w/ GREs following nuclear translocation. Inhibit inflamm cells, epithelium, endothelium, airway smooth m, mucous gland

412
Q

What is the potency, dose and DOA for pred, methylpred, dexamethasone?

A

Pred: potency 1, dose 2-4, DOA 12-36
Methylpred: potency 1.25, dose 2-4, DOA 12-36
Dexameth: potency 7-10, dose 0.2-0.5, DOA >48

413
Q

What are the potential adverse effects of corticosteroids?

A 
Cats much more resistant
CNS- incr excitability/ subdued
MSK- wasting
GIT
Fluid, electrolyte balance
Metabolic
Endocrine- DM
Immune system- 2ry infections
414
Q

What are other immunosuppressive drugs?

A

Alkylating agents
Antimetabolites
Mitotic inhibitors- vinca alkaloids
Calcineurin inhibitors

415
Q

What are the stages of the cell cycle and where do the immunosuppressive drugs target?

A

M- vinca alkaloids
G1- calcineurin inhibitors, leflunomide
S- corticosteroids, antimetabolites, mycophenolate mofetil
G2

416
Q

What are the alkylating agents?

A

Alkylate DNA, causing breaks in molecule and cross-linking of twin strands. Inhibit protein synthesis in resting cells, prevent mitosis and kill diving cells.
Cyclophosphamide (now not really used for IM dz) and chlorambucil (least toxic, myelosupression generally not observed at least for >1m)

417
Q

What are the antimetabolites?

A

Azathioprine: mainstay for 2nd immunosuppresive drug, not in cat- fatal myelotoxicity. Greater decr of cellular than humoral immunity.
Methotrexate

418
Q

What are the vinca alkaloids?

A

Esp for IMT.
Vincristine, vinblastine. Bind to tubulin, blocking polymerisation, also break down pre formed microtubules- incr release of PLTs from megakaryocytes.

419
Q

What are calcineurin inhibitors?

A

Ciclosporin. Tacrolimus.
Ciclosporin- inhibit calcineurin (phosphatase enzyme), inhibit activation of IL-2 (key T-cell 2 factor). IV and oral, large vol distribution, 1ry hepatic metabolism, monitor.

420
Q

What are the guidelines for tx of IM dz?

A

Start w/ pred (3-4mg/kg/d PO). If IMHA or aggressive IM dz consider adjunctive azathioprine (d), chlorambucil (c) from outset. Assess over 7d. If poor response add adjunctive immunosuppressant if not already. If combo from outset consider vincristine, hIVIG. Consider supportive measures- fresh whole blood, PLT-rich plasma
CBC and UA q7-14d. Tapered over 3-4m following initial remission (20-25% decr q4-6wk if remission maintained)

421
Q

Which tick borne pathogens are endemic vs non endemic to the UK?

A

Non endemic- babesia, canis canis, ehrlichia canis

Endemic- borrelia burgdorferi, anaplasma phagocytophilum

422
Q

What is the pathogenesis of babesia?

A

Protozoan parasite of RBCs transmitted by ticks. Trasmitted w/in ticks trans-stadially and trans-ovarially. Sporozoites injected from tick salivary glands, enter circulation, endocytosed by RBCs. IMHA, thrombocytopenia common

423
Q

What are the clinical signs of babesiosis?

A

Haemolytic anaemia: lethargy, depression, inappetence, icterus, splenomegaly (sequestration of RBCs), tachycardia/ tachypnoea

424
Q

How is babesia diagnosed?

A

Lab findings- non specific, anaemia, thrombocytopenia common, many coombs +ve/ autoagglutinate
Microscopic ID- low Sn as wax and wane
PCR- high Sn, extracted from blood/ tissues e.g. LNs, spleen
Serology- usually indirect fluorescence Ab test/ ELISA- don’t seroconvert for wks- months.

425
Q

What is the tx for babesia?

A

Antbabesial drug- imidocarb dipropionate

426
Q

What are the clinical signs of ehrlichia canis?

A

Acute- vasculitis and immune destruction–> thrombocytopaenia and coagulopathy- multi systemic signs, spleen and LN enlargement, CNS/ occular signs.
Either cleared or sequestered in spleen as subclincal carriers. Can recover or become chronic- BM destruction–> pancytopaenia

427
Q

How is erhlichia canis diagnosed?

A

Small obligate intracellular G-ve bacteria.
Morulae (like clumps of grapes) in monocytes in blood smears or macrophages from tissue aspirates.
IFA/ ELISA

428
Q

What is the tx for erhlichia canis?

A

Tetracylcine for 28d
or chloramphenicol
No vaccine, chemoprophylaxis, tick control

429
Q

What is anaplasma phagocytophilym?

A

Small obligate intracellular G-ve bacteria- granulocytic (in neutrophils)
Mild- mod thrombocytopenia, lymphopenia, mild anaemia. Impaired PMN function can predispose to 2ry infections
V rare dz in cats

430
Q

What is borreliosis?

A

Spirochete. Co-infections common
Lethargy, anorexia, pyrexia, inflamm PA, lymphadenopathy, protein losing glomerulonephropathy
Dx complicated- no pathognomonic test, asymptomatic conversion commone, microscopic/ genetic detection often not poss
Empirical abx tx (doxycycline/ amoxicillin)

431
Q

What are the key features of leishmaniosis?

A

Flagellate protozoa. Transmitted by sandfly. Targets macrophages. Systemic infection in hemolymphatic organs. Can persist- chronic infection. Protective immunity mediated by T cells. Signs may develop months to yer after infection (>7y)

432
Q

How does the host immune response determine the clinical outcome of leishmaniosis?

A

TH2 predom response- high serology, decr cellular immunity, high parasite load–> severe non self limiting dz
TH1 predom reponse- low serolgoy, predom cellular immunity, low parasite load–> clinically healthy but infected, self limiting dz

433
Q

What are the clinical signs of leishmaniosis?

A 
Varied
Chornic sustemic dz
Usually visceral and cutaneous signs
Waxing and waning.
E.g. periocular alopecia, erosion of mucocutaneous junction, papillary derm in inguinal region, chronic debilitation etc.
434
Q

How is leishmania diagnosed?

A

Demonstration of parasite- amastigotes in FNA of LN
Serology- high Ab titre highly suggestive
PCR- sensitive- BM, spleen, LN, skin
Clinicopathological findings- hyperglobulinaemia (ineffective B cell response), decr Alb:Glob, thrombocytopaenia, non regen anaemia, proteinuria

435
Q

What is the tx for leishmania?

A

Anti-leishmanial drugs- often clinical remission but persistent parasitaemia
Meglumine antimoniate and allopurinol
Not licensed in UK (needs importation)
Consider euthanasia due to zoonotic risk
Sandfly avoidance, topical insecticide (imidacloprid/ permethrin spot on, deltamethrin collar), vaccine

436
Q

What are the arthopod vector borne infectious diseases of LAs?

A

From ticks

Babesia, anaplasma, louping ill virus, staph pyogenes, borrelia burgdorferi

437
Q

What is bovine babesiosis?

A

Main sp- B.divergens. Ixodes ricinus- common vector. Feeding season- mainly Mar-June
Intravascular haemolysis- pyrexia, anaemia, jaundice, haemoglobinuria, death
Calves <6m resistant, develop immunity and asymptomatic carrier state- endemic stability

438
Q

How is bovine babesiosis diagnosed?

A

Blood smear- fixed and stained w/ giemsa
PCR
Serology- surveillance and export certificate- Ab by IFA/ ELISA

439
Q

How is bovine babesiosis controlled and treated?

A

Acaricides- decr incidence but only takes 1 tick!
Tick habitat removal
Avoid certain pastures/ deliberately graze young on known babesia/ tick pastures
Live attenuated vaccines
Tx- antiparasitic drug imidocarb, supportive

440
Q

What is tick borne fever?

A 
Anaplasma phagocytophilia (ehrlichia)
Ixodes ricinus main vector. Affects cattle, sheep, horses, dogs. Maintained in sylvatic cycle (tick wildlife). Immune suppression- leukopenia, neutropenia, decr phagocytosis
441
Q

What is louping ill virus?

A

Only flavivirus endemic to UK. Upland. In sheep (mostly unvaccinated young)- pyrexia and paresis- neuro signs.

442
Q

What is EIA?

A

Caused by lentivirus. Transmission by horseflies and stable flies, saliva, nasal secretions, faeces, semen, ova and embryos, fomites, in utero. Exotic to UK. Notifiable.
Acute- incubation 1-3 wks, can go unnoticed, fever, thrombocytopenia, lethargy, inappetence, can be fatal, susequent inapparent infection/ recurrent dz episodes
Chronic- anaemia, thrombocytopaenia, weight loss, dependent oedema, occ neuro signs.
Majority episodes subside and become inapparent carriers for life

443
Q

What is the dx and control of EIA?

A

Persistent virus so positive serology confirms infection (AGID, ELISA)
Ab response may not develop for 10-14d. Most seroconvert after 45d
Ab +ve horses culled (statutory)

444
Q

What is Bluetongue?

A

Non enveloped segmented RNA virus. Transmitted by culicoides. Haemorrhagic dz. Replicates in endothelial cells and mononuclear phagocytes. Prolonged cell-associated viraemia.

445
Q

What are the clinical signs of bluetongue?

A

Sheep- pyrexia, salivation, oedema of face and lips, cyanosis of tongue, coronary band haemorrhages.
Cattle- less severe, maybe asymptomatic, important in transmission, oronasal crusts and erosions

446
Q

How do you diagnose Bluetongue?

A

Spleen, red BM, liver, heart, blood, LNs
In hep (for virus isolation, RT-PCR)
Serum (for serology- ELISA)
Notifiable

447
Q

What are the clinical signs of Schmallenberg Virus?

A

Mild dz in adults (cattle> sheep/ goats)- pyrexia, milk drop, diarrhoea
Congenital defects (CNS and MSK), abortions, stillbirths (lambs>calves/kids)
Subsequent immune protection

Principles of Science (5 decks)

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