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BVMS 3 > Module 15 Wk 2 > Flashcards

Module 15 Wk 2 Flashcards

1
Q

(Approach to Anaemia in Small Animals)

What is anaemia?

A

Reduction in the haemoglobin concentration of the blood so Reduced oxygen-carrying capacity

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2
Q

T/F with regenerative anaemia, you will see reticulocytes in the circulation.

A

False - you will see the with non- regenerative

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3
Q

What are examples of non-regenerative anaemia?

A
  • Primary bone marrow disease
  • Iron deficiency anaemia – withholding iron from RBC production
  • Anaemia of Inflammatory Disease
  • Chronic renal failure
  • Endocrine disease e.g. hypothyroidism
  • Cobalamin deficiency
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4
Q

What are the two catagories of regenerative anemaia?

A

Haemolysis
Heamorrhage

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5
Q

Give examples of haemolysis and haemorrhagic anaemia.

A

Haemolysis
* IMHA
* Infectious
* Oxidative injury
* Metabolic disorders
Heamorrhage
* Trauma
* GI Ulceration
* Haemostatic disorder
* Ruptured neoplasm

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6
Q

With primary bone marrow disease as the cause of non-regenerative anaemia, what are the main differential diagnoses?

A
  • Pure Red Cell Aplasia – failure of red cell line
  • Aplastic Anaemia
  • Myelofibrosis - fibrous tissue replacing bone marrow
  • Bone Marrow Infiltration
  • Myelodysplastic Syndromes – cats – disordered RBC production, odd cells in blood – uncommon
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7
Q

With Secondary failure of erythropoiesis as the cause of non-regenerative anaemia, what are the main differential diagnoses?

A
  • Anaemia of inflammatory disease
  • Chronic renal failure
  • Endocrine disease
  • Haemoglobin synthesis defects - Fe deficiency
  • Nuclear maturation defects - Cobalamin deficiency
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8
Q

What does the secondary failure of erythropoiesis mean?

A

BM could produce RBC if had sufficient building blocks. Not BM disease.

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9
Q

What are clinical signs of primary bone marrow disease cauing non-reg aneamia?

A
  • lethargy
  • weakness
  • exercise intolerance
  • Relatively BAR
  • Other cell lines may be affected such as thrombocytopenia/neutropenia
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10
Q

When it comes to secondary failure of erythropoiesis, the clinical signs come from the primary disease process. what are the clinical signs for chronic renal failure?

A

PUPD, reduced appetite, weight loss, vomiting

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11
Q

When it comes to secondary failure of erythropoiesis, the clinical signs come from the primary disease process. what are the clinical signs for hyperthyroidism?

A

It is a dermatological disease

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12
Q

When it comes to secondary failure of erythropoiesis, the clinical signs come from the primary disease process. what are the clinical signs of iron deficiency?

A

It is typically associated with chronic low grade external blood loss due to parasitism (internal or external), ulcerative GI disease, chronic urinary losses

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13
Q

When it comes to secondary failure of erythropoiesis, the clinical signs come from the primary disease process. what are the clinical signs of cobalamin deficiency?

A

chronic GI disease, or on rare occasions genetic defects resulting in inability to absorb vitamin B12

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14
Q

What is immune-mediated haemolytic anaemia?

A

It is a condition in which the immune system mistakenly targets and destroys red blood cells, leading to anemia and is characterized by the premature destruction of red blood cells.

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15
Q

If the red blood cells are destroyed in the blood what type of haemolysis is this?

A

intravascular hemolysis

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16
Q

If the premature destruction of red blood cells occurs in organs what type of haemolysis is it?

A

extravascular hemolysis

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17
Q

What are the two classifications of IMHA?

A

Primary and secondary

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18
Q

What is primary IMHA?

A

It is where the immune system directly attacks the red blood cells without an identifiable trigger

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19
Q

Secondary IMHA is triggered by an underlying conditions or external factor, what can these be?

A
  • Infectious - Bacterial or Parasitic
  • Drug-induced - like Sulphonamides, penicillins, vaccines
  • Neoplasia – antibodies cause a secondary IMHA
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20
Q

How would you diagnose Feline infectious anaemia as a cause of IMHA?

A

PCR - often coombs positive

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21
Q

Wha? injury leading to IMHA?

A
  • Paracetamol toxicity
  • Onion toxicity
  • Benzocaine
  • Zinc toxicity
  • Propofol infusion
  • Diabetes mellitus, hepatic lipidosis in cats
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22
Q

What are clinical signs of IMHA?

A
  • Jaundice
  • Haemoglobinuria (intra-vascular)
  • Hepato-splenomegaly
  • Pyrexia
  • Chocolate-coloured oral mm as a sign of MetHb
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23
Q

What lab evaluations should you do for an anaemic patient?

A
  • PCV
  • Blood Smear evaluation
  • Reticulocyte assessment
  • Complete Blood Count
  • Serum biochemistry
  • ISA, Coagulation times
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24
Q

On a PCV is you get 20-30% is it mild, mod or severe?

A

mod

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25
Q

On a PCV if you get less than 20 percent, is the snaemia mild, mod or severe?

A

severe

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26
Q

If your PCV gives you 30-39% is the anaemia mild, mod or severe?

A

mild

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27
Q

T/F Anaemia is non-regenerative if <50% of expected reticulocyte response

A

True

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28
Q

If the patient has other cell lines afftected what do you think the anaemia could be due too?

A

Could the anaemia be due to bone marrow failure

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29
Q

With primary BM disease what do you see from lab results?

A
  • normocytic normochromic anaemia
  • Concurrent bi-cytopenia ( reduction in two of the three) or pan-cytopenia (reduction in all 3)
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30
Q

When it comes to secondary failure of erythropoiesis, what is see on lab results for iron deficiency?

A

microcytic hypochromic anaemia

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31
Q

When it comes to secondary failure of erythropoiesis, what is see on lab results for chronic renal failure?

A

biochemical evidence of renal failure

  • azotaemia = elevated level of nitrogenous waste products, primarily urea and creatinine, in the blood.
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32
Q

What are distinguishing lab features that indicated IMHA

A
  • Regenerative anaemia
  • Spherocytosis
  • Leucocytosis due to a neutrophilia +/- left-shift
  • concurrent immune-mediated thrombocytopenia
  • Hyperbilirubinaemia
  • Evidence of organ dysfunction e.g. increase ALT, increase cPLI
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33
Q

What is spherocytosis?

A

A condition where red blood cells become abnormally spherical in shape, rather than the normal biconcave disk shape. This abnormality affects the cells’ ability to function properly, particularly their ability to pass through small blood vessels and the spleen, leading to hemolysis (destruction of red blood cells) and anaemia.

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34
Q

What further investigations should you do for an anaemic patient?

A
  • Identify and address any underlying disease process
  • Supportive care - transfusion
  • Immunosuppressive drug therapy
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35
Q

What is the mortality rate of patients with anaemia?

A

25-70%

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36
Q

What are the main causes of death in anaemic patients?

A
  • Refractory to Therapy
  • Hypoxaemia
  • Pulmonary Thromboembolism
  • Disseminated Intravascular Coagulation
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37
Q

(Disorders of Haemostasis in Small Animals)

What is the definition of heamostasis and what happens if you reduce and increase it?

A

Haemostasis is the stopping of the flow of blood

  • reduction results in bleeding
  • increment too much results in thrombosis
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38
Q

What is primary haemostasis?

A

The platelet plug is formed via vascular endothelium, platelets, and von Willebrand factors, which bind the subepithelial and platelets and then the platelets into place.

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39
Q

What is secondary haemostasis?

A

The stabilisation of the platelet plug. Coagulation proteins and intrinsic and extrinsic clotting factors are involved here and fibrin is formed.

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40
Q

What is tertiary haemostasis?

A

The breakdown of the platelet plus via fibronlysis

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41
Q

What is primary haemostasis dependent on?

A
  • PLT number
  • PLT function
  • Adequate vWF
  • Normal vessel function
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42
Q

What is thrombocytopenia? and what is haemostasis is it a disorder of?

A

Low platelet count in the blood and its a disorder of primary haemostasis

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43
Q

What is thrombocytopathia? and what is haemostasis is it a disorder of?

A

It is platelet dysfunction and is a disorder of primary haemostasis?

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44
Q

What is Von Willebrands disease and what haemostasis is it a disorder of?

A

It is a genetic bleeding disorder caused by a deficiency or dysfunction of von Willebrand factor and is a disorder of primary haemostasis

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45
Q

When assessing a patient that may have a bleeding disorder, what might be clues given by the owner in the history?

A
  • potential exposure to an anticoagulant rodenticide
  • wormed? - if not, then could be angiostronglus vasorum
  • Travel outside UK - Yes, then could be a vector-borne disease
  • Has the dog or cat been systemically unwell in the run-up to bleeding?
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46
Q

What is thrombocytopenia often associated with clinically?

A
  • Bleeding under the skin like Petechiation (pin point) and ecchymoses (larger areas)
  • Epistaxis - nose bleeds
  • Gastro-intestinal bleeding
  • Clinical signs associated with anaemia due to blood loss
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47
Q

What are clinical signs of Von willebrands disease?

A
  • Prolonged bleeding at surgical sites
  • Prolonged bleeding at oestrus
  • Clinical signs associated with anaemia due to blood loss
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48
Q
A
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49
Q

what are the clinical signs associated with coagulopathies?

A
  • Haematoma formation
  • Haemarthrosis
  • Pulmonary haemorrhage
  • Bleeding into body cavities
  • Clinical signs associated with anaemia due to blood loss
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50
Q

What lab tests should you do for primary haemostasis and what should the results?

A
  • Platelet count - less than 50x10^9/L
  • buccal mucosal bleeding time - longer
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51
Q

What lab test should you perform for secondary haemostasis?

A
  • Prothrombin time
  • activated partial thromboplastin time
  • Fibrinogen
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52
Q

What lab test should you perform with suspected teriary haemostasis?

A
  • Fibrin-degradation products FDPs
  • D-dimers
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53
Q

What is a concerning platelet count?

A

< 50 x 10^9/l

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54
Q

What does buccal mucosal bleeding time assess?

A
  • Platlet Function
  • Vascular response to injury
  • Adequacy of vWF
  • bleeding should cease in 2-4mins if more then problem
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55
Q

What is normal activated patial thromboplastin time in dogs and cats ina VDS lab?

A
  • Normal Dog: 10-17 secs
  • Normal Cat: 15-19 secs
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56
Q

(Upper Respiratory Tract Disease in Small Animals)

What is stretor? And what does it indicate?

A

Stretor is reverbrent airflow in the upper airways which creates a snoring sound. It indicates BOAS

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57
Q

What is stridor? And what does it usually indicate?

A

Stretor is a harsh noise on inspiration. It indicated laryngeal paralysis

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58
Q

What does BOAS stand for?

A

Brachycephalic obstructive airways syndrome

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59
Q

What is BOAS?

A

Brachycephalic breeds have a shortened nasal cavity and altered nasopharyngeal anatomy, which causes turbulent airflow, inflammation, and swelling of soft tissue.

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60
Q

What are the primary components of BOAS?

A
  • Stenotic nares
  • Elongated and thicker soft palate
  • Excess pharyngeal mucosa
  • abnormality in the nasal turbinates
  • Hypoplastic trachea -smaller trachea
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61
Q

What are the secondary components of BOAS?

A
  • Everted laryngeal saccules
  • laryngeal collapse
  • Tonsillar hyperplasia and eversion
  • Regurgitation
  • Hiatal herna - part of the stomach slided into thorax
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62
Q
A
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63
Q

T/F BOAS patients are more likely to develop aspiration pneumonia

A

True so must always be considered

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64
Q

What are the symptoms of aspiration pneumonia?

A
  • cough
  • pyrexia
  • Tachypneoa/dyspnoea
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65
Q

What is the chronic presentation of a BOAS patient?

A
  • Stertor
  • Some exercise intolerance
  • Regurgitation
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66
Q

How would you treat a chronic BOAS patient?

A
  • weight loss
  • harness rather than lead
  • keep cool, avoid stress and manage exercise.
  • early surgery to prevent secondary chnages
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67
Q

How will a acute (emergency) BOAS patient present?

A

with severe dyspnoea

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68
Q

How would you treat an emergency BOAS patient?

A
  • O2
  • cooling
  • steroids
  • sedation
  • GA/intubation
  • Tracheostomy
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69
Q

What can be treated surgically primarily in BOAS?

A
  • Stenotic nares
  • Elongated soft palate
  • Everted laryngeal saccules
  • Tonsillar prolapse
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70
Q

What are more severe cases where symptoms may persist after surgery in BOAS?

A
  • laryngeal collapse
  • Hiatal hernia
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71
Q

What are stenotic snares?

A

It is where the dorsal lateral nasal cartilage collapses after birth creating increased UAW resistance

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72
Q

How can this be corrected via surgery?

A

Via wedge resection, which reduces upper airway resistance and slows the progression of other components

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73
Q

T/F you can diagnose elongated soft palate in a conscious patient?

A

False - under GA with aid of a laryngoscope

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74
Q

What are the markers for a soft palate in a dog?

A

caudal pole of the tonsils and the tip of the epiglottis

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75
Q

What dor everted laryngeal saccules obstruct and how are they like that?

A

They obstruct the ventral half of the glottis, and they are pulled out by negative pressure.

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76
Q

Is laryngeal collapse a primary or secondary condition of BOAS?

A

It is a secondary condition due to increased airway pressures from upper airway disease.

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77
Q

T/F laryngeal collapse causes severe obstruction.

A

True

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78
Q

How would you go about treating a laryngeal collapse?

A
  • Want to correct another airway issue first
  • Modify dog’s lifestyle
  • If unsuccessful, consider laryngeal surgery, but it comes at risk!!!
  • permanent tracheostomy
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79
Q

What causes regurgitation in BOAS?

A

Increased negative pressure in the thorax due to increased inspiritory effort

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80
Q

What is laryngeal paralysis caused by?

A

It is caused by dorsal cricoarytenoid muscle failure, but the vocal cords and arytenoid cartilages remain in paramedian position, causing airway obstruction.

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81
Q

What are the three aetiology of laryngeal paralysis?

A
  • Idiopathic
  • Congenital
  • Secondary
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82
Q

What is the most common form of laryngeal paralysis?

A

idiopathic

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83
Q
A
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84
Q

What kind of dogs are seen to have idiopathic laryngeal paralysis?

A
  • lab retrievers
  • older
  • medium to large breeds
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85
Q

How would you treat a dog with laryngeal paralysis?

A
  • Sedate to calm and reduce resp. rate (acepromazine)
  • Corticosteroids - Dexamethasone
  • Cool
  • Supply oxygen
  • Refer for surgery
  • Temporary tracheostomy
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86
Q

What is aspiration pneumonia?

A

Where the glottis does not close when the patient swallows and food or liquid is aspirated causing pneumonia

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87
Q

What are the clinical signs of aspiration pneumonia?

A
  • dyspnoea
  • pyrexia
  • cough
  • cyanosis
  • inspiratory stridor
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88
Q

How would you diagnose a dog with aspiration pneumonia?

A

Directly looking at the larynx but at the recovery of light plain ana as ana drugs suppress laryngeal function

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89
Q

How do you treat aspiration pneumonia?

A
  • Cricoarytenoid lateralisation – tie back surgery
  • Permanently abduct arytenoid
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90
Q

Where do feline nasopharyngeal polyps originate from and where ca the grow to?

A
  • They origniate in the tympanic bullae
  • Either grow out the ear canal (aural polyp) or they grow down the eustatian tube into the nasopharynx.
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91
Q

How are nasopharyngeal polyps removed?

A

Removed by traction - Approach through oral cavity and retract soft palate rostrally. Grasp and apply steady traction to the polyp until it avulses.

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92
Q

What may removal of nasopharyngeal polyps result in?

A

horner syndrom or vestibular signs

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93
Q

(Therapeutics for Small Animal Haematological Diseases -Transfusion Medicine)

What are the types of immunological transfusion reaction that can occur?

A

Haemolytic and non-heamolytic

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94
Q

What are the non-immunological transfusion reactions?

A
  • Transmission of infectious disease
  • Hypocalcaemia
  • Circulatory overload
  • bacteraemia
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95
Q

What is a haemolytic transfusion reaction?

A

It is a transfusion of incompatible or mismatched blood.

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96
Q

Describe an acute haemolytic transfusion reaction

A
  • Acute intravascular haemolysis
  • Activation of haemostatic system
  • Hypotension
  • Death
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97
Q

Describe a delayed haemolytic transfusion reaction

A
  • Extravascular haemolysis
  • 2-21days after transfusion
  • negates the potential benefits of the transfusion
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98
Q

What does DEA stand for?

A

Dog erythrocyte antigens

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99
Q

What percentages of dogs are DEA 1.1 positive?

A

45%

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100
Q

T/F dogs can receive any blood type as their first tranfusion?

A

True - this is because dogs do not have antibodies to different blood types before they receive a blood transfusion.

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101
Q

How do cats differ from dogs when it comes to blood groups?

A

Cats differ from dogs in that they have naturally occurring alloantibodies. An incompatible transfusion will result in a haemolytic transfusion reaction, even if it’s the first time.

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102
Q

What is cross-matching used for?

A

It is used to detect the presence of antibodies to RBC’s

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103
Q

When do you use cross-matching?

A
  • before blood transfusion in dogs
  • When there is an unknown history
  • When the long-term benefits of RBC transfusion are required
  • In cats, if AB blood typing cards are unavailable.
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104
Q

What are the options for sourcing blood products for canines?

A
  1. buy canine products from blood bank.
  2. collect whole blood from donor dogs in the practice.
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105
Q

What are the options for sourcing blood products for cats?

A

Collect whole blood from donor cats in the practice.

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106
Q

What are the benefits of a blood bank?

A
  • Blood products can be stored on-site for immediate use
  • Products are tailored to individual needs
  • Allowa for donation to be carried out in a calm and controlled setting
  • Convenient for donor/donors owner
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107
Q

How should blood collection goes?

A
  • 3 members of staff
  • sterile scrub solutions, EMLA cream and clippers
  • sedation in cats
  • ideally pre-place catheter
  • for dogs, use a human blood collection bag pre-filled with anticoagulant, scales for weighing the blood unit
  • for cats, three 20ml syringes pre-filled with 2.6mls of anticoagulant
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108
Q

why, when taking blood donations, is the anticoagulant-to blood ratio crucial?

A

If there is too much anticoagulant, it can lead to citrate toxicity.

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109
Q

How much blood are you going to give for anaemia?

A

required volume = k x BW x ((disired PCV- recipient PCV)/ donor PCV)

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110
Q

How much plasma are you going to give for coagulopathies?

A

10-20mls/kg

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111
Q

How quickly should you administer the blood transfusion? start, hypovolaemic, normovolaemic and cardiac or renal patient.

A
  • Start at 0.5-2ml/kg/hr for 30mins
    Then
  • hypovolaemic = 20mls/kg/hr
  • normovolaemic = 5-10mls/kg/hr
  • cardiac or renal = 2mls/kg/hr
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112
Q

(Disorders of the equine lower respiratory tract)

What risk assessments should you take prior to doing an endoscopy on a horse?

A
  • That horse can’t strike out, rear or leap forwards
  • That you are not infornt of the horse
  • Correct PPE
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113
Q

How should you restrain horse for an endoscopy?

A
  • Twitch
  • Stock
  • sedation = Alpha 2 agonist and opioid or detomidine and butorphanol or romifidine and butorphanol
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114
Q

Why do tracheal secreations accumulate in horses?

A

Due to impaired mucociliary clearance mechanism

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115
Q

When doing an endoscopy on a horse and you see oedema of carina what may this indicate?

A

Suggestive of lower airway inflammation, particularly in severe equine asthma.

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116
Q

What can you do to sample lower resp tract?

A
  • tracheal wash
  • Bronchoalveolar lavage (BAL)
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117
Q

What can sampling of the lower resp tract in horses diagnose?

A
  • Inflammatory disorders
  • Haemorrhage
  • Parasitic infections
  • Neoplasia
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118
Q

Where does a tracheal wash collect secretions from?

A

The distal trachea

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119
Q

What are the two methods of tracheal wash?

A
  • Trans-tracheal
  • Trans-endoscopic
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120
Q

Describe how you would perform a Trans-Tracheal wash

A
  • Sedation, sterile prep, local ana and a small incision
  • Introduce catheter and long collection catheter
  • 20mls saline in and then retrieved
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121
Q

What are the two different types of catheters you can use in trans-endoscopic tracheal wash?

A
  • Single lumen for cytology
  • Triple lumen catheter for cytology and microbiology
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122
Q

Describe how you would person and Trans-endoscopic tracheal wash

A

Before you reach the horizontal sump of trachea, instil 20mls of saline, then chase and retrieve saline at the sump.

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123
Q

T/F a trans-tracheal tracheal wash can be used for cytology and microbiology?

A

True

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124
Q

Where does a BAL collect respiratory secretions from?

A

The peripheral lung

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125
Q

What do the secretions from BAL provide information on?

A
  • If diffuse lower resp tract pathology
  • may miss focal pathology
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126
Q

What are the two methods of doing a BAL

A
  1. Blind BAL tube
  2. Via endoscope
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127
Q

Describe how a blind BAL works

A
  • After tracheal wash use the catheter to deliver lignocaine at the carina
  • Pass sterline BAL tube
  • when horse starts to cough, instil more lignocaine
  • pass the tube till wedges then inflate the cuff
  • instil warm fluid then retrieve
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128
Q

What can you use haematology and biochem to detect in horses?

A
  • infectious disease
  • Pneumonia
  • kinda equine asthma
  • parasitism
  • neoplasia
  • immunodeficiency syndromes
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129
Q

When does hyperpnoea start?

A

When the arterial oxygen pressure is less that 70mmHg

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130
Q

What is thoracocentesis useful for in horses?

A
  • Total white cell count and protien concentraction
  • cytological exam
  • microbiological culture and sensitivity
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131
Q

What are the most common causes of pleural effusion in horses?

A
  • Bacterial infection
  • Neoplasia
132
Q

what is equine asthma

A

describes all nonseptic lower airway inflammation

133
Q

what is seen with mild to moderate equine asthma

A

chronic cough/ poor performance
lower airway inflammation

134
Q

what is seen with severe equine asthma

A

lower airway inflammation
reversible obstruction
cough etc

135
Q

what is severe equine asthma

A

adult horses with lower airway inflammation and obstruction associated with frequent coughing and increased resp effort at rest

136
Q

how is severe equine asthma reversed

A

obstruction reversed by bronchodilators or environmental change

137
Q

what is mild to moderate asthma

A

any age horse with chronic cough and/or poor performance
excess tracheobronchial mucous and/or increased ratio neutrophils, eosinophils and/ or mast cells in BAL fluid

138
Q

what are the likely causes of severe equine asthma

A

stabling and/or feeding hay
moulds, bacterial endotoxins
irritants such as ammonia, cold air and dust

139
Q

is severe equine asthma reversible or not

A

reversible

140
Q

what is the pathogenesis of severe equine asthma

A

non-infectious LRT inflammatory disease
neutrophil influx into the airways
mucus accumulation
bronchospasm
bronchial hyper-reactivity
bronchiolitis, bronchiectasis, progressive fibrosis

141
Q

who is predisposed to severe equine asthma

A

no apparent breed/ sex predilection
mature animals
signs are reversible in a low dust environment

142
Q

what are the clinical signs of severe equine asthma

A

variable
mucoid nasal discharge
cough
exercise intolerance
increased expiratory effort
nostril flaring
tachypnoea

143
Q

how do you diagnose severe equine asthma

A

history, clinical signs and physical exam
tracheal endoscopy
tracheal wash
BAL
evidence of obstruction

144
Q

how do you diagnose evidence of obstruction in severe equine asthma

A

history
clinical signs
measurement (pulm function tests)
reversible by change of environment + administer anticholinergic

145
Q

what are the goals of treatment of severe equine asthma

A

treat airway inflammation
relieve airway obstruction
prevent re-occurrence

146
Q

what environmental management do you do with severe equine asthma

A

24 hr turnout
low dust housing
low dust feed
good ventilation
stable management - deep litter bedding, dampen all feeds, groom outside
forage/ straw store location
muck heap location

147
Q

what pharmacological therapy can be used in horses with severe equine asthma

A

systemic=> easier to admin, risk of adverse effects
inhalational => initial set up expensive, efficacious, deliver high concs to airway, compliance

148
Q

what are the aims of therapy in severe equine asthma

A

decreased inflammation
relieve bronchospasm
reduce bronchoconstriction
increased mucociliary clearance
decreased viscosity
stabilise mast cells
suppress immune system

149
Q

what drugs are used to control airway inflammation in severe equine asthma

A

corticosteroids
systemic: prednisolone vs dexamethasone
inhalational: via metered dose inhaler or nebulised

150
Q

what is the licensed inhaled corticosteroid in UK for severe equine asthma

A

aservo equihaler

151
Q

what are the features of aservo equihaler

A

licensed in 2020
ciclesnoide is the active ingredient
anti-inflammatory therapy
decreases airway reactivity
improved pulmonary function

152
Q

what two drugs are licensed for inhalation therapy in the UK for severe asthma

A

aerohippus - space chamber only
flexineb- nebuliser

153
Q

what do bronchodilators do on severe equine asthma
relieve lower airway obstruction providing immediate relief

A

can be systemic or inhalational

154
Q

what IV bronchodilator is given to horses with severe equine asthma

A

clenbuterol

155
Q

when is clenbuterol indicated

A

severe cases with with resp distress in horses with severe equine asthma as they have reduced beta-2 adrenergic receptors

156
Q

what are the side effects of clenbuterol in horses

A

sweating
mild colic
affects uterus= interfere with parturition

157
Q

what inhaled bronchodilator is short acting in horses

A

salbutamol

158
Q

what inhaled bronchodilator can be used long term in horses with severe equine asthma

A

salmeterol

159
Q

features of salbutamol for horses

A

emergency relief or rescue drug
increase cortocosteroid deposition
<4x a week unless together with a corticosteroid

160
Q

features of salmeterol in horses

A

long term control of SEA
duration 6-8hrs
use with corticosteroid

161
Q

what other bronchodilators can be given to provide smooth muscle tone

A

ipratropium- inhaled
atropine- systemic
buscopan- systemic

162
Q

What other medications other than bronchodilators should you consider giving to a horse with severe equine asthma

A

antibiotics
mucolytics
expectorants
mast cell stabilisers

163
Q

what treatment should you do for severe equine asthma in a horse who has a less than desirable environment/ feeding practice

A

change environment/ feeding
no treatment or just oral clenbuterol may be sufficient
reserve further treatment for non-response

164
Q

what treatment should you give a high performance horse or environment/ feeding alterations are less obvious or no response to above or more aggressive treatment warranted

A

further investigation
oral clenbuterol for 2 weeks or inhaled beta-2 agonists combined with longer term inhaled or systemic corticosteroids

165
Q

can you clinically distinguish between severe equine asthma and summer pasture associated-severe equine asthma

A

NO

166
Q

what aeroallergens cause summer pasture associated severe equine asthma

A

seen at pasture
allergy to flower/ crop/ tree/ grass pollens and moulds
seen in summer/ autumn

167
Q

what treatment should you give for summer pasture associated - severe equine asthma

A

use of corticosteroids during expected periods of challenge

168
Q

what is seen during acute exacerbations of summer pasture associated- severe equine asthma

A

dyspnoea and cyanosis
usually on hot humid summer evenings

169
Q

what drug can you give during acute exacerbations of SPA-SEA

A

atropine

170
Q

what horses is mild to moderate asthma normally seen in

A

young athletic horses

171
Q

what are the clinical signs seen with mild to moderate equine asthma

A

exercise intolerance/ poor performance
coughing
increased resp secretions
no increased resp effort at rest but seen at exercise

172
Q

what is the aetiology of mild to moderate equine asthma

A

environmental dusts/ organic particles/ gases
bacteria/ viruses
genetics, immune status
exercise induced pulmonary haemorrhage

173
Q

how do you diagnose mild to moderate equine asthma

A

history and clinical exam
rebreathing bag test
endoscopy
cytology (BAL)
pulmonary dysfunction
pulmonary hypersensitivity

174
Q

what would be seen on a positive diagnosis of mild/ moderate equine asthma on cytology

A

neutrophilia
moderate inflammation 5-20% of differential count
some may have increased eosinophils and mast cells

175
Q

what treatment would you use on mild/ moderate equine asthma

A

low dust environment
corticosteroids- IV or inhaled, possibly in combination with bronchodilators

176
Q

how do you know that the horse is responding to treatment of mild/moderate equine asthma q

A

subclinical so need to repeat BAL to confirm

177
Q

how do you prevent mild/ moderate equine asthma in young horses

A

low dust environment
good ventilation

178
Q

what is the differentiation in signalment of MEA and SEA

A

MEA= usually young adults
SEA = >7 years

179
Q

what is the differentiation in clinical signs of MEA and SEA

A

MEA= no dyspnoea at rest but may have tachypnoea
SEA= dyspnoea at rest

180
Q

what is the differentiation between diagnostic testing results in MEA and SEA

A

MEA- less marked airway inflammation
hay challenge= SEA demonstrate increased resp effort

181
Q

what is the differentiation in prognosis of MEA and SEA

A

MEA= short duration, can resolve spontaneously or with treatment, low risk of recurrence
SEA= long duration, recurrent

182
Q

what is the possible pathogenesis of exercise induced pulmonary haemorrhage

A

stress failure of pulmonary capillaries
assc. with MEA
low alveolar pressure
upper airway obstruction
mechanical forces assoc. with locomotion

183
Q

what are the presenting signs of exercise induced pulmonary haemorrhage

A

none
+/- post exercise/ race epistaxis
+/- poor performance
+/- repeated swallowing post exercise/ race
+/- prolonged recovery post exercise/ race

184
Q

what are the clinical signs of exercise induced pulmonary haemorrhage

A

none
+/- epistaxis
+/- abnormal lung sounds

185
Q

how do you diagnose exercise induced pulmonary haemorrhage

A

endoscopy 30-60 mins post exercise
BAL cytology

186
Q
A
187
Q

what would be seen in BAL cytology of a horse with exercise induced pulmonary haemorrhage

A

free red blood cells
haemosiderophages
+/- neutrophils

188
Q

what does treatment of exercise induced haemorrhages aim to do

A

reduce haemorrhage
minimise sequelae (inflammation and fibrosis)

189
Q

what treatment do you give for exercise induced pulmonary haemorrhage

A

rest for 2-4 weeks
address LRT inflammation
altered training
frusemide before fast exercise but not before racing in UK

190
Q

what is interstitial lung disease an acute or chronic inflammatory process of

A

primarily alveolar walls and adjoining bronchiolar interstitium

191
Q

what does acute interstitial lung disease present as

A

acute respiratory distress

192
Q

what does chronic interstitial lung disease present as

A

SEA

193
Q

what are the causes of interstitial lung disease

A

multifactorial
toxic agents
infectious agents
idiopathic

194
Q

how do you diagnose interstitial lung disease in horses

A

process of elimination and radiography

195
Q

what is equine multinodular pulmonary fibrosis

A

an emerging subset of interstitial lung disease

196
Q

what signalment of horse are most affected with equine multinodular pulmonary fibrosis

A

older horses

197
Q

what clinical signs are seen with equine multinodular pulmonary fibrosis

A

tachypnoea and tachycardia
weight loss
pyrexia

198
Q

how do you diagnose equine multinodular pulmonary fibrosis
differentiate from severe equine asthma

A

differentiate from infectious pneumonia
BAL samples
radiography
ultrasonography

199
Q

what would be seen on radiography of equine multinodular pulmonary fibrosis

A

diffuse nodular interstitial pattern

200
Q

what would be seen on ultrasonography of equine multinodular pulmonary fibrosis

A

diffuse pleural thickening
may identify nodules superficial on lung
biopsy

201
Q

how do you treat equine multinodular pulmonary fibrosis

A

dexamethasone, doxycycline, acyclovir

202
Q

what species of equid get dictylocaulus arnfieldi

A

donkeys. mules and horses

203
Q

are donkeys and mules symptomatic or asymptomatic carriers of dictylocaulus arnfieldi

A

asymptomatic reservoirs of infection

204
Q

what is seen in horses with dictylocaulus arnfieldi

A

chronic cough
increased resp effort
wheeze/ crackles on auscultation

205
Q

how do you diagnose dictylocaulus arnfieldi in horses

A

BAL cytology
may see larvae in tracheal wash
few eggs in faeces as usually not patient infection in horses

206
Q

how do you treat dictylocaulus arnfieldi in horses

A

oral ivermectin/ moxidectin

207
Q

Features of parascaris equorum

A

relatively minor
3 months to become patent infection
larval migration in foals/ yearlings

208
Q

what clinical signs are seen with parascaris equorum

A

lung inflammation and clinical signs
small intestinal obstruction/ intussusception
ill thrift and diarrhoea

209
Q

how do you diagnose parascaris equorum

A

FWEC when patent infection

210
Q

How to you treat/ prevent parascaris equorum

A

deworming

211
Q

what is bacterial pneumonia/ pleuropneumonia

A

bacterial infection of the lung parenchyma
bronchopneumonia, with or without the involvement of the pleural space

212
Q

what is the aetiology of bacterial pneumonia in horses

A

bacterial from nasal or oropharynx

213
Q

what are the gram +ve causative bacteria in bacterial pneumonia

A

strep equi
staph aureus and pneumoniae

214
Q

what are the gram -ve causative bacteria in bacterial pneumonia

A

actinobacillus and pasturella spp.
e.coli
klebsiella pneumoniae
bordetella bronchiseptica

215
Q

what are the common obligate anaerobes in bacterial pneumonia

A

bacteroides fragilis
fusobacterium or clostrisal spp.

216
Q

what does the pathogenic development of pneumonia require

A

overwhelming bacterial challenge
impairment of pulmonary defences

217
Q

what are the presenting signs of bacterial pneumonia

A

pyrexia
inappetence
signs of depression
cough
exercise intolerance
nasal discharge
tachypnoea
hypopnoea
resp distress

218
Q

what would you see systemically on a clinical exam of a horse with bacterial pneumonia

A

evidence of systemic inflammatory response syndrome
tachycardia
mucous membranes
laminitis

219
Q

what would you find on auscultation of a horse with bacterial pneumonia

A

exudate in trachea
increase insp noise with wheezing and crackles ventrally
reduced breath sounds ventrally

220
Q

how do you diagnose bacterial pneumonia in horses

A

history + clinical signs
haematology and biochem
endoscopy
tracheal wash
diagnostic imaging
thoracocentesis

221
Q

what would be seen on ultrasonography of a horse with bacterial pneumonia

A

comet tails
lung consolidation
abscesses
pleural fluid, fibrin etc

222
Q

what antimicrobials would you give first line to treat bacterial pneumonia

A

penicillin + gentamicin +/- metronidazole

depending on sensitivity consider - oxytetracycline, ceftiofur, enrofloxaxin

223
Q

what other supportive treatment can be given to horses with bacterial pneumonia

A

bronchodilation
NSAIDs
remove pleural fluid - esp if in resp distress
supportive care- fluids, good ventilation, low dust environment, no stress

224
Q

what should you monitor for horses with bacterial pneumonia

A

clinical exam
haematology
acute phase proteins
tracheal endoscopy +/- tracheal wash
ultrasonography

225
Q

what complications are seen with bacterial pneumonia and pleuropneumonia in horses

A

abscess formation
pleural adhesions/ abscess

with pleuropneumonia:
cranial mediastinal mass/ abscesses
laminitis
bronchopleural fistula
thrombophlebitis
pneumothorax
pulmonary necrosis

226
Q

what are most cases of bacterial pleuropneumonia an extension of

A

bacterial pneumonia
pulmonary abscess
trauma
oesophageal rupture

227
Q

what is seen with severe acute pleuropneumonia

A

tachycardia, toxic mucous membranes- SIRS
pleural friction rubs on auscultation
pleural pain= shallow breathing, colic signs, pain on palpation of thorax

228
Q

what is seen with chronic pleuropneumonia

A

intermittent fever/ weight loss

229
Q

what causes lung collapse in pneumothoraxes

A

pleural pressure equilibrates with atmospheric pressure

230
Q

how do you diagnose pneumothorax in horses

A

ultrasonography
radiology

231
Q

what is the treatment for an open pneumothorax

A

seal wound with plastic sheet or surgical closure

remove air via trocar

232
Q

what is the treatment for a closed pneumothorax

A

remove all air via trocar until source of entry found

233
Q

discuss bacterial pneumonia in foals

A

3 weeks - 6months of age
acquire by inhalation
can be insidious but progress to acute resp distress and death

234
Q

how do you diagnose bacterial pneumonia in foals

A

auscultation
haematology and biochemistry
ultrasonography/ radiography
TW culture and cytology

235
Q

what is the treatment for bacterial pneumonia in foals

A

antimicrobial needs to have high Vd
long duration 4-9 weeks
rifampin + macrolide
supportive therapy

236
Q

what are other causes of pleural effusion

A

thoracic neoplasia
congestive HF
thoracic trauma
hypoproteinaemia
coagulopathy
chylothorax

237
Q

what changes within vessels cause pleural effusions

A

increased permeability in capillary vessels
increase in hydrostatic pressure
decrease in oncotic pressure
decrease in fluid removal

238
Q

what are causes of increased permeability on capillary vessels

A

infection
inflammation
neoplasia

239
Q

what causes an increase in hydrostatic pressure

A

congestive heart failure
portal hypertension

240
Q

what causes a decrease in oncotic pressure

A

hypoproteinaemia

241
Q

what causes a decrease in fluid removal from vessels

A

impaired lymphatic drainage or obstruction
pleural or parenchymal infiltration

242
Q

what are the 4 main neoplasia found in equine thoraxes

A

lymphoma
mesothelioma
pulmonary granular cell tumour
metastatic neoplasia

243
Q

features of lymphoma neoplasia in the thorax of a horse

A

more common in young adult horses’
rarely leukaemic
most common neoplasm in the thorax
- primary thoracic neoplasia, often cranial mediastinal mass and associated with pleural effusions

244
Q

what are lymphoma neoplasms in the thorax normally classified as

A

multicentric
alimentary
cutaneous
mediastinal

245
Q

is a mesothelioma commonly a primary or secondary thoracic tumour in horses

A

primary

246
Q

what might pulmonary granular cell tumours be misdiagnosed as due to the clinical signs associated

A

SEA

247
Q

what are the common metastatic neoplasias in equine thoraxes

A

adenocarcinomas
melanoma
hemangiosarcoma
squamous cell carcinoma

248
Q

how do you calculate the allowable blood loss in cattle

A

(estimated BV x(initial PCV- MInimum PCV))/ initial PCV

249
Q

what is the BV of a cow

A

55ml/kg

250
Q

what are the common haemorrhages seen in cattle

A

epistaxis with caudal caval syndrome
ruptured middle uterine artery
trauma to udder and mammary vasculature

251
Q

what MM are the most reliable in cattle

A

ocular conjunctival or vulval

252
Q

what is the most common fluid given to cattle in fluid rescue

A

hypertonic saline

253
Q

do you need to cross match before cattle blood transfusions?

A

No

254
Q

How much blood can you easily take from a donor cow

A

8-10 litres

255
Q

why might future neonates be affected if their mother is given a blood transfusion

A

mother will make antibodies against that blood group-> neonates become sensitive to the blood groups

256
Q

what factors are contributing to the change in distribution of different infectious causes of anaemia

A

changes in climate
changes in distribution of vectors

257
Q

what are the methods to diagnose hemoparasites in cattle

A

giemsa stained smears
microscopic examination
pathogen-specific PCR or qPCR

258
Q

what can fleas cause in calves kept in warm wet environment

A

severe anaemia and death

259
Q

what can haemaphysalis longicornis cause throughout asia and oceania in cattle

A

acute, severe and fatal anaemia

260
Q

can rhipicephalus microplus be fatal in cattle

A

yes in exceptional circumstances

261
Q

what can haematobia irritans irritans and H iexigua cause in cattle

A

production loss

262
Q

what diseases do ixodes ricinus carry

A

babesia divergens
anaplasma phagocytophilum
louping ill

263
Q

what diseases do dermacentor reticulatus carry

A

babesia spp.
anaplasma marginale

264
Q

what diseases do rhipicephalus microplus carry

A

babesia bigemina
babesia bovis
anaplasma marginale

265
Q

what diseases do rhipicephalus microplus and rhipicephalus decoloratus carry in africa

A

babesia bigemina
babesia bovis
anaplasma marginale

266
Q

what diseases do amblyomma variegatum and amblyomma hebraeum carry in africa

A

ehrlichia ruminantium
heartwater

267
Q

what diseases do rhipicephalus appendiculatus carry

A

theileria parva

268
Q

what diseases do hyalomma spp. carry

A

theileria annulata

269
Q

what is the treatment for babesia

A

imidocarb dipropionate

270
Q

what are the clinical signs of tsetse and trypanosomes

A

anaemia
ill thrift
pyrexia
lymphadenopathy
haemorrhagic syndrome
death

271
Q

how do you control tsetse and trypanosomes

A

habitat distruction
game reduction
aerial spraying
insecticide treatment of cattle
drug treatment of cattle
traps/ targets

272
Q

what drugs can be used against trypanosomiasis

A

isometamidium
homidium bromide
diminazine aceturate

273
Q

what is the epidemiology of enzootic haematuria

A

low morbidity but mortality can be high
only seen in older mature cattle

274
Q

what is the pathogenesis of enzootic haematuria

A

ptaquiloside-> bladder wall thickening, metaplasia, formation of carcinomas

275
Q

what are the clinical findings of enzootic haematuria

A

intermittent mild haematuria
gradual loss of condition
palpable thickening of the bladder wall on rectal examination in advanced cases

276
Q

what is the aetiology of acute bracken fern poisoning

A

toxic principal in brachen, mulga and rock fern
young fronds more toxic
underground rhizomes highly toxic

277
Q

what is the epidemiology of acute bracken fern poisoning

A

low morbidity but very high mortality
younger animals
seen when other feed scarce
requires ingestion of large amounts

278
Q

what is the pathogenesis of acute bracken fern poisoning

A

radiomimetic effect on bone marrow causing thrombocytopenia and leukopenia

279
Q

what are the clinical signs of acute bracken fern poisoning in cattle

A

pyrexia
inappetance
depression
blood in faeces and urine
haemorrhages in MM
fibrinous broncho-pneumonia

young calves= brachycardia and laryngeal oedema

280
Q

what are the PM findings of acute bracken fern poisoning

A

haemorrhaemorrhages in all tissue
free blood in intestinal lumen
secondary infectious processes

281
Q

what are the inherited disorders of the erythron in cattle (bos taurus)

A

bleeding diathesis
bleeding disorder
factor XI deficiency
haemophilia A
haemolytic anaemia
spherocytosis
thrombopathia

282
Q

do hot or cold blooded horses have more erythrocytes

A

hot

283
Q

do hot or cold blooded horses have a lower volume/kg

A

cold

284
Q

are immature RBC released into the circulation in horses

A

no

285
Q

are there reticulocytes in regenerative anaemia of horse

A

no

286
Q

what might affect haematology of horses before taking their blood

A

exercise
feeding
travel
stress

287
Q

what are clinical signs of acute blood loss in horses

A

tachycardia
tachypnoea
hyperpnoea
MM colour depends on severity of loss

288
Q

What are clinical signs of chronic blood loss

A

exercise intolerance
weight loss
pallor of MM
adaptive tachycardia at <20l/l
haemic murmur due to decreased viscosity and increased turbulence

289
Q

how do you know if the anaemia is regenerative in horses

A

sequential samples for PCV and TSO with constant sampling conditions

290
Q

how long does it take albumins to recover after haemorrhage in horses

A

5-10 days

291
Q

how long does it take globulins to recover after haemorrhage in horses

A

3-4 weeks

292
Q

what is a good sampling site on horses after haemorrhages

A

facial venous plexus

293
Q

what diagnostic tests can you do in anaemic horses

A

strong red cell rouleaux formation
equine platelets clump in EDTA specimens
test for genuine autoagglutination

294
Q

what are specific infectious disease tests to consider in horses

A

equine infectious anaemia
equine piroplasmosis
equine ehrlichiosis
equine trypansomosis

295
Q

where do you collect bone marrow from for evaluation in horses

A

Equine sternum with jamshidi needle

296
Q

what is the normal myeloid:erythroid ratio in bone marrow of horses

A

0.5-2.4

297
Q

what does a <0.5 M:E ratio with >5% reticulocytes indicate in horses

A

adequate regenerative response to anaemia

298
Q

when would IMHA not be regenerative in horses

A

if precursor cells are targeted

299
Q

what are the ways of acute blood loss in horses by trauma or surger

A

intraabdominal
intrathoracic
arterial laceration

300
Q

what are the ways of acute blood loss in horses by the resp system

A

epistaxis
exercise induced
pulmonary artery rupture

301
Q

what are ways of acute blood loss in horses via the GIT

A

mesenteric tear
strongylus vulgaris arteritis

302
Q

what are ways of acute blood loss in horses via the urinary tract

A

renal haemorrhage

303
Q

what are ways of acute blood loss in horses via the uterus

A

uterine artery rupture
foaling complications

304
Q

what % loss is required before collapse in a horse with acute haemorrhage

A

20-30%

305
Q

how much blood does a horse have

A

80-100ml/kg

306
Q

what is an indicator that transfusion is required in horses

A

hyperpnoea caused by hypercapnia/ hypoxaemia

307
Q

how many blood groups do horses have and what are they

A

7

A, C, D, K, P, Q, and U

308
Q

What group is the best donor group of horses

A

AaCa +ve blood group

309
Q

how do you cross- match blood transfusions

A

tube agglutination of washed red cells is standard for major and minor cross matching

310
Q

how do you collect equine blood for transfusions

A

donor must be -ve for piroplasmosis and other blood borne infections
12G catheter placed upwards in jugular after sterile prep

311
Q

how much blood can you collect from a horse

A

1L/ 100Kg

312
Q

what is the cost common anticoagulant for horse blood collection

A

acid citrate dextrose

313
Q

how do you administer blood transfusions to a horse

A

via filter containing blood transfusion set
up to 15 ml/kg
1 drop/ 5s for first 5 mins then increase

314
Q

How much blood is required in a horse with acute haemorrhage

A

BW(Kg) x 80 x desired PCV- (recipient PCV/ donor PCV)

315
Q

what are ways of chronic blood loss in horses via the GIT

A

gastric ulceration
severe colitis
strongylus vulgaris arteritis

316
Q

what are ways of chronic blood loss in horses via resp system

A

exercise induced pulmonary haemorrhage
epistaxis

317
Q

what are ways of chronic blood loss in horses via the urinary system

A

renal haemorrhage
bladder haemorrhage

318
Q

what are ways of chronic blood loss in horses via coagulopathies

A

thrombocytopaenia
factor VIII deficiencies

319
Q

what investigations can be done for chronic GIT blood loss in horses

A

gastroscopic exam
faecal egg count

320
Q

what investigations can be done for chronic resp blood loss in horses

A

endoscopy + cytology
urine sediment cytology

321
Q

what investigations can be done for chronic urinary blood loss in horses

A

assess accurate platelet count

322
Q

what investigations can be done for chronic coagulopathies in horses

A

measure PT and PTT times
assess hepatic function
assay factor VIII conc

323
Q

what will be seen on haematology if the chronic haemorrhage has stopped and is regenerating

A

increased PCV, TSP and MCV

324
Q

features of primary immune-mediated haemolytic anaemia in horses

A

less common form
+ve coombs test
increased erythrocyte fragility
osmotic fragility test more useful than coombs

325
Q

features of secondary IMHA in horses

what are the causes of secondary IMHA
resp tract infections
streptococcal abscesses
drug induced
neoplasia

how do you treat IMHA
identify & discontinue suspect medications
dexamethasone if severe haemolysis
blood transfusion from compatible donors if clinical evidence of requirement
rate of blood loss

what is neonatal isoerythrolysis
immune mediated haemolysis due to RBC ag incompatibility

what clinical signs are seen with neonatal isoerythrolysis
anaemia
icterus
weakness
inc RR
tachycardia
pale MM

how do you diagnose neonatal isoerythrolysis
clinical signs
haematology
rule out DDx
immunological testing
foal RBCs and mare serum/ colostrum

what is the treatment for neonatal isoerythrolysis
supportive care
blood transfusion from a suitable donor

how do you prevent neonatal isoerythrolysis
check blood compatibility before mating
immunological testing
prevent nursing for 24hrs in at risk foals as no Abs are passed transplacentally
give alternate source of colostrum

what makes a foal more predisposed to neonatal isoerythrolysis
a mother who has already had foals and prior mare-stallion incompatibility

what causes non-regenerative anaemia in horses
iron deficiency
chronic diseases
bone marrow failure
coagulopathies
miscellaneous i.e. chronic hepatic + renal disease

what should you investigate when searching for haemorrhage in a horse with non-regenerative anaemia
gastroscopy examination
faecal egg count
endoscopy + cytology
thorax and abdominal US
urine sediment cytology

what should you assess on a coag profile in a horse with non-regenerative anaemia
assess accurate platelet count
measure PT and PTT times
citrate blood tubes
assay factor VIII concs

what should you assess in the metabolic function of a horse with non-regenerative anaemia
assess hepatic function
measure renal function
an inflammatory response?
are acute phase proteins

what is anaemia of chronic disease in horses
shortened erythrocyte lifespan
decreased release of iron
decreased bone marrow response to EPO

what clinical signs are seen with anaemia of chronic disease
pleuropneumonia
internal abscessation
peritonitis
chronic parasitism
neoplasia

what are 3 causes of inadequate erythropoiesis
nutritional deficiencies
myelophthisic anaemia
bone marrow aplasia

what causes nutritional deficiencies that cause inadequate erythropoiesis
prolonged administration of sulphonamides causing decreased folate and vit B12 production by GIT flora

how do you determine if myelophthisic anaemia is the cause of inadequate erythropoiesis
bone marrow aspirate/ biopsy required
cytology and M:E ratio assessed

what is seen with bone marrow aplasia causing inadequate erythropoiesis
neoplastic infiltrate detected on bone marrow aspirate from sternum
likely to have pancytopenia with decreased neutrophils & platelets

least common form

what is seen on blood analysis of acute blood loss anemia
low PCV, Hb and low TSP

what is seen on blood analysis of haemolytic anaemia
low PCV, normal TSP, increased unconjugated bilirubin, increased MCHC, haemoglobinuria

what is seen on blood analysis of chronic disease induced anaemia
low PCV, low Hb, high TSP
may be inflammatory leukogram with increased APPs
may be reduced ferritin and high TIBC

what is equine piroplasmosis
tick-borne haemoprotozoan parasites

what are the 3 kinds of tickborne parasite that cause equine piroplasmosis
theileria equi
babesia caballi

how are theileria equi parasites transmitted
intrastadial and transstadial

when do clinical signs of theileria equi appear
12-19 days after infection

how are babesia caballi transmitted to horses
intrastadial, transstadial and transovarian transmission

when do clinical signs of babesia caballi appear
10-30 days after infection

what is the pathogenesis of equine piroplasmosis
release of merozoites cause haemolysis of RBC
-> decreased survival of non infected red cells
microthrombi and vasculitis
thrombocytopenia is often seen

SIRS and progression to MODS

what can transplacental transmission of theileria equi cause
abortion
neonatal piroplasmosis

where is equine piroplasmosis found
endemic in central and south america, africa, asia, middle east and southern europe

increasing presence in northern europe

what are the risks of equine piroplasmosis to the UK
free movement of horses between UK, france and ROI without border inspection
no specific guidelines re pre import tick treatment
no requirement to test horses moving within EU
tick species likely to be capable of transmission present in UK

what are the clinical signs of acute piroplasmosis
pyrexia, lethargy and haemolysis
systemic signs depend on level of haemolysis= tachycardia, tachypnoea and weakness
petechiations + marked thrombocytopenia
concurrent disease exacerbates

A

multiple possible causes
immune complexes attach to RBC
disease alters RBC membrane
antigen cross reacting
drug interaction

BVMS 3 (10 decks)

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