Equine cardiorespiratory Flashcards Preview

Year 4 > Equine cardiorespiratory > Flashcards

Flashcards in Equine cardiorespiratory Deck (158)
1

What is the aerobic capacity of a horse?

150ml/kg/min

2

Define minute ventilation

Tidal volume x breaths/min

3

What is perfusion?

Removal of gas from the lungs by the blood

4

CO2 is how many times more diffusible than O2?

25

5

CO2 is mostly transported in the blood as what?

HCO3-

6

Give some factors that would reduce pulmonary gas exchange and examples of diseases that cause them

Increased pulmonary resistance (URT disorders, turbulence, resistance, small airways- inflammation, blood, hypersecretion)
Decreased alveolar/pulmonary compliance (oedema, hypertension, fibrosis, interstitial disease)
Dynamic airway collapse (inflammatory airway disease, tracheal collapse)
Respiratory muscle/chest wall disease
Decreased cardiac output (decreased lung or tissue perfusion)
Decreased Hb (anaemia)

7

What is EIPH?

Exercise-induced pulmonary haemorrhage
Haemorrhage into the airways that occurs at high intensity exercise

8

How do you diagnose EIPH?

Post-exercise endoscopy into trachea (30-60 mins after exercise; 3 consecutive endoscopies give a better prevalence- 80%)
Can also do bronchoalveolar lavage (look for free RBCs and RBCs ingested by macrophages-haemosiderophages)

9

Describe EIPH distribution in the lungs
Give a histological description

Blue discolouration (accumulation of haemosiderin)
Lesions start caudally and progress craniodorsally
Histologically: peribronchial inflammation and fibrosis

10

Briefly describe the 4 grades of EIPH

Grade 1: flecks of blood/single short stream extending less than a quarter of the tracheal length
Grade 2: one continuous stream of blood extending at least 1/2 the length of the trachea or multiple streams less than 1/3 of the tracheal surface
Grade 3: continuous stream less than half the tracheal width
Grade 4: abundant blood completely covering the tracheal surfaceand pooling at the thoracic inlet

11

What may predispose a horse to EIPH?

High pulmonary vascular pressure

12

Give some events that may cause EIPH

Extreme vascular pressures
High inspiratory pressures
Inflammation
Locomotory shockwaves
Regional differences in dynamic compliance

13

How does EIPH lead to fibrosis?

Intrapulmonary blood invokes influx of macrophages -> reversible disruption of alveolar septal architecture -> thickening and fibrosis -> reduces compliance

14

Give some common and fairly common differential diagnoses of LRT in adult horses

Very common: Recurrent airway obstruction/'Heaves' (RAO)
Inflammatory airway disease (IAD)
Viral and bacterial infections

Fairly common: Exercise induced pulmonary haemorrhage (EIPH)
Pleuropneumonia
Aspiration pneumonia

15

Give some uncommon causes of LRT disease in adult horses

Pulmonary abscesses
Lungworm
Tracheal stenosis/collapse
Interstitial pneumonia
Pulmonary nodular fibrosis
Neoplasia
African Horse sickness/other exotic diseases

16

Which 2 diseases compromise 'allergic' airway disease in horses or 'equine asthma'?

Recurrent airway obstruction (RAO/heaves)
Inflammatory airway disease (IAD)

17

Recurrent airway obstruction (RAO) is associated with which kind of allergens?
What age of horses are typically affected?

Indoor allergens eg organic dusts from hay and bedding, molds, bacteria
Hypersensitivity, non-specific inflammatory response
Older horses (>7 years old)

18

Briefly describe the pathogenesis of RAO (recurrent airway obstruction)

Allergens in bronchi -> inflammation -> muscarinic receptors inititate smooth muscle contraction -> bronchoconstriction
Inflammation -> B2 adrenergic receptors cause reduced bronchodilation -> bronchoconstriction
-> Decreased mucociliary escalator function, mucosal hyperplasia, inflammatory infiltrate/oedema, increased mucous production

19

Give the pathogenesis of chronic RAO

Smooth muscle hypertrophy
Peribronchiolar fibrosis
Epithelial cell hyperplasia
Mucus plugging
-> airway remodelling -> progressive impairment of lung function

20

Give the clinical signs of recurrent airway obstruction

Early: mild exercise intolerance
With time: tachypnoea, increased expiratory effort, cough, nostril flare, nasal discharge
Expiratory+/- inspiratory wheeze
Forced expiration -> 'heaves', heave line
Severe cases: respiratory distress/weight loss

21

How do you diagnose recurrent airway obstruction?

Tracheal aspirate cytology (neutrophils >40%)
Bronchoalveolar lavage cytology (neutrophils >25%)
Response to IV atropine supports diagnosis
Mucus score

22

How do you treat recurrent airway obstruction?

Short-term: bronchodilators, corticosteroids
Long-term: environmental control-reduce dust, moulds, best for horses to live outside, pelleted feeds/pasture, low dust bedding, maximise ventilation

23

How do corticosteroids aid in treating recurrent airway obstruction?
Give some examples

Reduce cell accumulation and activation
Reduce vascular changes
Reduce bronchoconstriction (inhibit release of inflammatory cytokines)

Prednisolone (PO)
Dexamethosone (PO)
Beclomethasone dipropionate (inhaled)

24

When would you give a bronchodilator to a horse with recurrent airway obstruction (RAO)?

Emergency therapy in flare ups
Before other inhaled medication
Before exercise
Diagnostically to see if signs improve
(Don't use as sole therapy)

25

Give some examples of bronchodilators when treating recurrent airway obstruction

B2 agonists (cause bronchodilation):
Clenbuterol (PO), salbutamol (inhaler)

Muscarinic antagonists (smooth muscle relaxation):
Atropine
NBB (buscopan)
Ipratropium bromide (inhaled)

26

Give some pros and cons of inhalation therapy when treating recurrent airway obstruction (RAO)

Pros: lower total dose, rapid onset, fewer systemic side effects, shorter detection times
Cons: expensive, owner compliance, distribution of drug if dyspnoeic

27

What are spacers (used for treating recurrent airway obstruction and inflammatory airway disease)?

Inhaled medications that reach the lungs and have a high local concentration

28

What is pleuropneumonia?

Bacterial pneumonia and secondary pleural effusion

29

Give some bacteria that may cause pleuropneumonia

Aerobic:
B haemolytic strep spp
Actinobacillus spp
Pasteurellaecae
Pseudomonas

Anaerobes:
Bacterioides
Fusobacterium
Eubacterium

30

Give some predisposing factors to pleuropneumonia

Long distance transport (head elevation, aspiration of dust/debris)
Viral respiratory disease (damages resp. epithelium)
Exercise (EIPH, aspiration of debris)
GA/surgery

31

Give the 3 stages of pleuropneumonia

1. Acute exudative stage (inflammation of the lung and pleura-sterile, protein-rich pleural exudate)
2. Fibrinopurulent stage (bacteria invade and multiply in the pleural fluid, fibrin deposits on pleural surfaces, lymphatic obstruction)
3. Organisational stage

32

How do you diagnose pleuropneumonia?

Ultrasound
Thoracocentesis
Culture
Transtracheal wash

33

What are the clinical signs of pleuropneumonia?

Pyrexia
Depression
Increased HR and RR
Soft cough
Pleurodynia
Reduced lung sounds ventrally, dull on percussion

34

How do you treat pleuropneumonia?

Thoracic drainage
Antimicrobials (penicillin, gentamicin, metronidazole if complicated)

35

What is the name of the equine lungworm?
What is the reservoir of infection for horses?

Dictyocaulus amfieldi
Donkeys

36

How do you identify equine lungworm?
How do you treat it?

Identification of worms in tracheal wash or BAL
Ivermectins

37

Aspiration pneumonia is commonly secondary to which conditions?

Oesophageal choke
Gastric reflux
Pharyngeal dysphagia
Iatrogenic

38

Which lung lobes are most affected by aspiration pneumonia?

Ventral

39

What causes multinodular pulmonary fibrosis?

Equine herpes virus-5

40

Give some examples of thoracic neoplasias

Cranial mediastinal lymphosarcoma
Pulmonary granular cell tumour
Malignant melanoma
Haemangiosarcoma
Metastatic adenocarcinoma
Metastatic carcinoma

41

How could you determine if a horse has an infectious respiratory disease?

Compatible clinical signs (fever, dull, outbreaks)
Detection of infectious agent (culture/PCR/virus isolation)
Detection of immune response against infectious agent (antibodies)

42

Give some clinical signs of equine influenza

Fever up to 41oC
Cough: dry and hacking -> moist
Oedema and hyperaemia of URT/trachea
Nasal discharge: serous -> mucopurulent
Lethargy, inappetence +/- muscle soreness

Recovery is usually complete in 1-3 weeks unless secondary infections occur

43

How do you diagnose equine influenza?

Usually outbreaks
Lymphopaenia (neutropaenia initially, later monocytosis, neutrophilia and hyperfibrinogenaemia)
Virus isolation from nasopharyngeal swabs (PCR)
Serology (rising antibody titre over 2-4 weeks)

44

How do you treat equine influenza?

Hydration, NSAIDs
+/- antibiotics for secondary bacterial infections
Generally improve after 7-10 days
Require prolonged period of rest (1 week off for every day of fever)

45

How long do horses excrete equine influenza virus for after initial infection?

Up to 8 days

46

How long can equine influenza virus survive in the environment?

Up to 36 hours
Easily killed by cleaning/disinfection

47

Give the clinical signs of equine herpes virus 1 and 4

Dull +/- mild coughing/serous nasal discharge
Often lasts several weeks

48

How do you treat equine herpes virus 1 and 4?

Symptomatic
Rest, NSAIDs, antibiotics for secondary infections

49

What causes 'rattles'?

Rhodococcus equi

50

Summarise rhodococcus equi infection

Most common in 3 week - 6 month old foals
Causes pyogranulomatous pneumonia
Diagnosis by clinical signs and detection of R.equi by culture/PCR
Treatment= prolonged antimicrobials /

51

What causes 'strangles'?

Streptococcus equi var equi

52

What kind of horses does strangles affect?

1-3 year olds usually

53

What is the incubation period of strangles?

1-14 days

54

What are the 2 phases that follow initial infection with strangles?

Multiplication in the lingual and palatine tonsils
Haematogenous and lymphatic spread to draining lymph nodes

55

What is 'bastard strangles"?

If the bacteria spreads systemically, then abscesses may form in muscle, kidneys, liver or lungs, or may cause peritonitis

56

How long can streptococcus equi survive in the environment?

Up to 12 months

57

How is streptococcus equi spread?

Via nose or mouth contact, fomites

58

What are the early clinical signs of Strangles?

Depression, fever (2-3 days before shedding)
Mucoid nasal discharge
Slight cough
Anorexia
Difficulty swallowing
Swelling (slight) in intermandibular space

59

Give some further clinical signs of strangles

Purulent nasal discharge
Head lymph node enlargement, abscesses and purulent discharge
Retropharyngeal lymph node swelling -> dyspnoea. If ruptures -> gutteral pouch empyema -> chondroids

60

What are chondroids?
Where are they found?
How can you remove them?

The product of chronic gutteral pouch empyema
Found in the gutteral pouch
Remove by breaking up and flushing or surgery

61

Give some complications of strangles

Cellulitis and local tissue damage
Pneumonia and abscessation
Immune-mediated myositis/myocarditis
Purpura haemorrhagica (bleeding from capillaries -> red spots on skin and mucous membranes, plus oedema of limbs and head)

62

How do you diagnose strangles?

Culture or PCR from:
-Nasopharyngeal swabs/lavage
-Gutteral pouch washes/aspirates
-Aspirate from abscess
ELISA

63

How can you confirm that a horse is free of strangles?

Nasal swabs: 3 negative swabs (1 a week for 3 weeks) (85% sure)
Gutteral pouch wash: only need 1 negative to be 88% sure that the horse is free of infection

64

How do you treat strangles?

Symptomatic pain relief (NSAIDs) to help appetite and reduce swelling
At onset of pyrexia, give penicillin for 5-7 days
Soft, wet feed
Hot pack (helps to mature the abscess)
Flush abscesses once draining
A tracheostomy is necessary in horses with respiratory distress

65

Why should you not give antibiotics later in the disease process of strangles (when lymphadenopathy is present)?

Prolongs maturation of abscesses

66

How long does a horse shed streptococcus equi bacteria (strangles) for?

3-6 weeks

67

How would you control a strangles outbreak?

Isolate affected and recovered animals (shed for 3-6 weeks)
Stop movement on and off the yard
Monitor temperature and nasal discharge of all in-contact animals daily
Ideally swab all horses after the outbreak to identify a possible carrier and ensure all horses are free of infection
Deep clean premises

68

How can you prevent strangles?

Vaccination (Equilis Strep E; modified live vaccine)
Quarantine all new animals coming to the yard for 3 weeks
Use ELISA to detect exposure?

69

What is inflammatory airway disease (IAD)?

Non-septic inflammation of lower airways
Part of equine asthma
Common in young/new racehorses

70

Give some risk factors for inflammatory airway disease

Co-mingling
Exercise (strenuous exercise decreases immune function)
Inhalation of dust or cold air
Transport
EIPH
Age-younger horses more at risk
Stable environment esp poor ventilation and bedding

71

Give the clinical signs of inflammatory airway disease

Often no/very subtle clinical signs at rest
Poor performance
Cough
Nasal discharge

72

How do you diagnose inflammatory airway disease?

Endoscopy: mucous in the trachea
Bronchoalveolar lavage (>10% neutrophils)
Tracheal aspirate (>40% neutrophils)
>3% eosinophils and mast cells

73

Where would you palpate the apex beat of the heart?

Apex of heart, across mitral valve

74

Why do you pull the leg forward when listening to the heart?

To pull the triceps out of the way

75

Where should you start when listening to the equine heart?

Start at the mitral valve
Move stethoscope dorsally and cranially to listen to the aortic and pulmonic valves

76

When listening to the heart, where does the aortic valve sound loudest?

On the left

77

When is S4 heard (if present)?

Before S1

78

What do S1 and S2 represent?

S1= shutting of AV valves
S2=shutting of semilunar valves (aortic/pulmonic)

79

What do S3 and S4 represent?
When are they each heard?

S3= end of rapid ventricular filling (just after S2)
S4= atrial contraction (just before S1)

80

Which heart sound is loudest in the apical and basal areas of the heart?

Apical: S1
Basal: S2

81

When is the duration of systole equal to the duration of diastole?

High heart rate

82

When is the duration of systole shorter than diastole?

Normal heart rate

83

What causes a murmur?

Turbulent flow of blood

84

How do you measure Reynolds number (influences turbulence)?

Velocity x diameter x density
/Fluid viscosity

85

Describe the 6 grades of heart murmurs

1: Barely audible
2: Murmur less loud than heart sounds
3: Murmur as loud as heart sounds
4: Murmur louder than heart sounds
5: Very loud, palpable thrill
6: Audible with stethoscope off chest wall

86

If the timing of a murmur is described as 'pan', what does this mean?

Obliterates the heart sounds either side of the murmur ie you can't ehar them

87

If the timing of a murmur is described as 'holo', what does this mean?

Can still hear S1 and S2 either side of the murmur

88

How could you describe the timing of a murmur?

Systolic/diastolic/continuous
-Early
-Mid
-Late
-'Pan'
-'Holo'

89

What 6 features would you describe about a murmur?

Intensity
Timing
Point of maximum intensity
Radiation
Shape of murmur (plateau/crescendo/decrescendo)
Quality of murmur (harsh/coarse/buzzing/honking/musical; high/medium/low-pitched)

90

How would you describe a murmur heard with aortic valve regurgitation?

Holodiastolic (can still hear S1 and S2)
Between aorta and left ventricle
Decrescendo (shape)

91

How would you describe a murmur heard with mitral/tricuspid valve regurgitation? (timing, shape, PMI, radiation)

Holo/pansystolic
Plateau or crescendo
PMI= heart apex
May radiate dorsal and cranial

92

What are the 2 major categories of murmurs?

Physiological/functional (normal blood flow through heart)
Pathological (underlying cardiac disease)

93

What are the 2 main types of physiological/functional murmurs?

Flow murmur
Filling murmur

94

When is a flow murmur heard?
Describe its shape
Where is it localised?

Early-mid systole
Always finishes before S2
Crescendo-decrescendo
Localised over heart base

95

When is a filling murmur heard?
Where is it localised?

Early diastole, left or right side
Squeak/whoop/click
Heard between S2 and S3 (short duration)
Localised over heart base or apex

96

What kind of a murmur is mitral/tricuspid (AV valve) regurgitation?

Pathological systolic murmur

97

When should you investigate a mitral valve regurgitation murmur?

When it is grade 3 or above

98

When should you investigate a tricuspid valve regurgitation murmur?

When it is grade 4 or above

99

What kind of murmur is a ventricular septal defect?

Pathological systolic

100

Regarding ventricular septal defects, where are lesions most commonly seen?

Membranous portion at base of interventricular septum, just ventral to aortic root

101

Is aortic insufficiency more common in older or younger horses?
Describe the associated murmur

Older
Decrescendo, buzzing/cooing
Holodiastolic (can hear S1 and S2)
PMI left heart base
May radiate ventrally
'Uhhh' sound ('teenager murmur')

102

Where would you hear a PDA murmur? (patent ductus arteriosus)

PMI=left heart base, also loud on right heart base
Waxes and wanes in intensity during cardiac cycle

103

Give the 2 physiological murmurs heard in horses

Aortic flow murmurs
Ventricular filling murmurs

104

Give the 4 pathological murmurs heard in horses

Mitral/tricuspid valve regurgitation
Aortic regurgitation
Ventricular septal defect
Patent ductus arteriosus

105

Why don't horses need a high heart rate?

They have a very high vagal tone

106

What is the function of the AV node?

Slows depolarisation down to ensure the atria contract before the ventricles

107

What are the normal equine heart sounds?

B-lub-dup
(S4-S1-S2)

108

What does the P-R segment of an ECG represent?

Delay at AV node

109

Where does ventricular depolarisation start and how does it reach the myocytes?

Starts at AV node -> Bundle of His -> Purkinje network -> Myocytes

110

On an ECG, does the t wave stay the same for different heart rates?

No, it can change morphology or polarity

111

On an ECG, what would a differently shaped P wave tell you?

There is an atrial ectopic pacemaker- atrial contraction originating somewhere other than SA node
Wave of depolarisation spreads across the atria in a different way to normal

112

How would you identify a ventricular premature complex on an ECG?

Slightly wider QRS than normal
No associated P waves

113

Give some examples of common physiologic arrhythmias

1st and 2nd degree AV blocks
Sinus block
Sinus arrhythmia/bradycardia/tachcardia

114

Give some examples of common pathologic arrhythmias

3rd degree AV block
Ventricular fibrillation
Ventricular tachycardia
Atrial premature complexes
Atrial tachycardia
Atrial fibrillation
Junctional escape complexes
Ventricular premature complexes

115

What happens physiologically during a 2nd degree AV block?
How does this appear on an ECG?

AV node stops spread of depolarisation to ventricles every 3-4 beats
Appears as 3-4 normal QRS, followed by a P wave only, followed by 3-4 normal QRS etc

116

How is a 2nd degree AV block resolved?

Increased sympathetic/decreased vagal tone (eg excitement -> vagal tone reduces -> AV block goes away)

117

How would a 1st degree AV block appear on an ECG?

Prolonged P-R

118

What is the difference between aerobic and anaerobic energy production during exercise?

Aerobic: clean, efficient, slow
Anaerobic: generates lactate, rapid, simple but much less efficient

119

How does a sinus block appear on a ECG?

Occasionally no P, QRS or T (ie period of no heart beat)

120

How does a sinus arrhythmia appear on a ECG?

Periodic waxing and waning of R-R interval

121

How does atrial fibrillation appear on an ECG?

No p waves, but instead many fibrillation ('f') waves
Irregular R-R intervals
Normal QRS complexes

122

How could you investigate whether atrial fibrillation was continuous or paroxysmal?

Leave it 48 hours and see if it converts back to normal

123

Give some presenting complaints from owners of horses with atrial fibrillation

Poor performance
Fading during race
Epistaxis

124

What are the 2 main treatment options for horses with atrial fibrillation?

Pharmacological conversion- Quinidine sulphate
Transvenous electrical cardioversion

125

Does atrial fibrillation cause heart failure?

No

126

How is quinidine sulphate administered when treating atrial fibrillation?

Oral
22mg/kg by nasogastric tube every 2 hours until conversion or max. 5 doses
Then prolong treatment interval to every 6 hours or treat in conjunction with digoxin (0.01mg/kg bid 2 days)

127

What is the effect of treating atrial fibrillation with quinidine sulphate?

Increases refractory period for atrial cells

128

When doing transvenous electrical cardioversion to treat atrial fibrillation, where are the electrodes placed?

2 down jugular: 1 in right atrium, 1 in pulmonary artery

129

What can atrial fibrillation predispose to?

Ventricular tachycardia -> ventricular fibrillation

130

How many ventricular/atrial premature complexes are considered significant on an ECG?

(Previously)
>2 isolated premature complexes at peak exercise
>5 pairs or paroxysms post exercise

131

On an ECG, what would a differently shaped QRS/T complex tell you?

There is a ventricular ectopic pacemaker-ventricular contraction originates somewhere other than the AV node
Wave of depolarisation spreads across ventricle in a different way to normal

132

What is the definition of oedema?

Abnormal and excessive accumulation of fluid in the interstitium
(Not a disease, but a sign of disease)

133

'Dependent' oedema is located where?

Accumulation in the lowermost parts of the body (species differences)

134

What is 'anasarca'?

Generalised subcutaneous oedema

135

Give the 4 mechanisms of oedema

1. Increased capillary hydrostatic pressure
2. Decreased capillary oncotic pressure
3. Lymphatic obstruction
4. Increased capillary permeability

136

What is the most common cause of increased hydrostatic pressure?

Congestive heart failure

137

Give some other causes of increased hydrostatic pressure

Portal hypertension (liver disease)
Intra-thoracic mass
Pulmonary oedema from left sided CHF
Venous thrombosis eg jugular thrombosis
Increased intra-abdominal pressure
Elevated Na+

138

Give some causes of decreased colloid oncotic pressure

Protein-losing enteropathy or nephropathy (eg over bowel wall - diarrhoea)
Haemorrhage
Proteinaceous effusions
Chronic hepatopathy
Malnutition

139

Give some causes of lymphatic obstruction leading to oedema

(Lack of lymphatic drainage)
Confinement
Lymphangitis
Tumours
Post partum

140

Give some causes of increased vascular permeability (leads to oedema)

Vasculitis (immune-mediated, infectious, toxic, neoplastic)
Systemic inflammatory response syndrome (SIRS)/Endotoxaemia (inflammatory cascade)
Local inflammation

141

When does a 2nd degree AV block go away and why?

Excitement -> vagal tone reduces -> block disappears

142

How does systemic inflammatory response syndrome (SIRS) lead to oedema?

Causes increased vascular permeability and reduced cardiac output
-> increased capillary hydrostatic pressure
-> fluid leaves capillaries

143

Give some causes of vasculitis

Immune-mediated
Infectious (eg equine viral arteritis, equine herpes virus 1)
Septic
Traumatic
Verminous
Photosensitisation
Toxic
Neoplastic

144

How is equine viral arteritis transmitted and what does it cause?

Causes Panvasculitis
Respiratory or venereal (sexual) transmission

145

What are the clinical signs of equine viral arteritis?
What acts as a reservoir?

+/- pyrexia, dull, oedema, stiff gait, oedematous mm
Respiratory disease
Abortion
Notifiable
Stallion= reservoir

146

What would you see with local and generalised immune-mediated vasculitis?

Local: urticaria, wheals
Generalised: swollen limbs/head
Severe generalised: purpura haemorrhagica

147

Where do arterial aneurysms most commonly form?

From aortic root (ascending aorta; commencing at upper base of left ventricle)
Aneurysm dissects into pericardium or cardiac chamber

148

How would a leg with lymphangitis appear?

Swollen, +/- serum ooze/crusting
Hot
Ulcers can form
Pain on palpation
Still weight-bearing

149

How would you treat lymphangitis ('big leg')?

Anti-inflammatories (NSAIDs +/- corticosteroids)
Antimicrobials (staphs often involved)
Topical cleaning
Local cold support
Encourage walking
Tetanus prophylaxis

150

Give some causes of increased capillary hydrostatic pressure

CHF
Portal hypertension (liver disease)
Intra-thoracic mass
Pulmonary oedema from L-CHF
Venous thrombosis eg jugular thrombosis
Increased intra-abdominal pressure
Elevated Na+

151

Give some causes of decreased colloid oncotic pressure

Protein-losing nephropathy/enteropathy
Haemorrhage
Proteinaceous effusions
Chronic hepatopathy
Malnutrition

152

Give some causes of lymphatic obstruction

Confinement ('stocking up')
Lymphangitis
Tumours
Post-partum
Other local swelling

153

Give some causes of increased vascular permeability

Vasculitis (immune-mediated/infectious/toxic/neoplastic/UV light/traumatic)
SIRS
Local inflammation

154

How is Infectious Equine Viral Arteritis transmitted?

Respiratory or venereal transmission

155

Give some clinical signs of Infectious Equine Viral Arteritis

Variable: +/- pyrexia, dull, oedema, stiff gait, oedematous mm
Resp dz
Abortion

156

Give some infectious causes of vasculitis

Equine herpes virus-1
Equine infectious anamia
Hendra virus
African horse sickness

157

What is the difference between Type 1 and 3 hypersensitivity?

Type 1: IgE-mediated release of histamine and other mediators from mast cells and basophils (eg anaphylaxis)

Type 3: immune complexes are deposited in blood vessel walls -> activates complement and attracts inflammatory cells eg neutrophils -> enzymes released from neutrophils cause damage to endothelial cells of basement membrane

158

Are there any proven treatments for EIPH?

No