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Year 4 > Equine cardiorespiratory > Flashcards

Equine cardiorespiratory Flashcards

1
Q

What is the aerobic capacity of a horse?

A

150ml/kg/min

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2
Q

Define minute ventilation

A

Tidal volume x breaths/min

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3
Q

What is perfusion?

A

Removal of gas from the lungs by the blood

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4
Q

CO2 is how many times more diffusible than O2?

A

25

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5
Q

CO2 is mostly transported in the blood as what?

A

HCO3-

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6
Q

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

A

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)

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7
Q

What is EIPH?

A

Exercise-induced pulmonary haemorrhage

Haemorrhage into the airways that occurs at high intensity exercise

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8
Q

How do you diagnose EIPH?

A

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)

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9
Q

Describe EIPH distribution in the lungs

Give a histological description

A 
Blue discolouration (accumulation of haemosiderin)
Lesions start caudally and progress craniodorsally
Histologically: peribronchial inflammation and fibrosis
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10
Q

Briefly describe the 4 grades of EIPH

A

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

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11
Q

What may predispose a horse to EIPH?

A

High pulmonary vascular pressure

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12
Q

Give some events that may cause EIPH

A 
Extreme vascular pressures
High inspiratory pressures
Inflammation
Locomotory shockwaves 
Regional differences in dynamic compliance
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13
Q

How does EIPH lead to fibrosis?

A

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

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14
Q

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

A

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

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15
Q

Give some uncommon causes of LRT disease in adult horses

A 
Pulmonary abscesses
Lungworm
Tracheal stenosis/collapse
Interstitial pneumonia 
Pulmonary nodular fibrosis
Neoplasia
African Horse sickness/other exotic diseases
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16
Q

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

A

Recurrent airway obstruction (RAO/heaves)

Inflammatory airway disease (IAD)

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17
Q

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

A 
Indoor allergens eg organic dusts from hay and bedding, molds, bacteria
Hypersensitivity, non-specific inflammatory response
Older horses (>7 years old)
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18
Q

Briefly describe the pathogenesis of RAO (recurrent airway obstruction)

A

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

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19
Q

Give the pathogenesis of chronic RAO

A 
Smooth muscle hypertrophy
Peribronchiolar fibrosis 
Epithelial cell hyperplasia
Mucus plugging
-> airway remodelling -> progressive impairment of lung function
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20
Q

Give the clinical signs of recurrent airway obstruction

A

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

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21
Q

How do you diagnose recurrent airway obstruction?

A

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

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22
Q

How do you treat recurrent airway obstruction?

A

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

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23
Q

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

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

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

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24
Q

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

A 
Emergency therapy in flare ups
Before other inhaled medication
Before exercise
Diagnostically to see if signs improve 
(Don't use as sole therapy)
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25
Q

Give some examples of bronchodilators when treating recurrent airway obstruction

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

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

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26
Q

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

A

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

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27
Q

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

A

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

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28
Q

What is pleuropneumonia?

A

Bacterial pneumonia and secondary pleural effusion

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29
Q

Give some bacteria that may cause pleuropneumonia

A 
Aerobic:
B haemolytic strep spp
Actinobacillus spp
Pasteurellaecae
Pseudomonas

Anaerobes:
Bacterioides
Fusobacterium
Eubacterium

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30
Q

Give some predisposing factors to pleuropneumonia

A

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

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31
Q

Give the 3 stages of pleuropneumonia

A
  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
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32
Q

How do you diagnose pleuropneumonia?

A

Ultrasound
Thoracocentesis
Culture
Transtracheal wash

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33
Q

What are the clinical signs of pleuropneumonia?

A 
Pyrexia
Depression
Increased HR and RR
Soft cough
Pleurodynia 
Reduced lung sounds ventrally, dull on percussion
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34
Q

How do you treat pleuropneumonia?

A

Thoracic drainage

Antimicrobials (penicillin, gentamicin, metronidazole if complicated)

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35
Q

What is the name of the equine lungworm?

What is the reservoir of infection for horses?

A

Dictyocaulus amfieldi

Donkeys

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36
Q

How do you identify equine lungworm?

How do you treat it?

A

Identification of worms in tracheal wash or BAL

Ivermectins

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37
Q

Aspiration pneumonia is commonly secondary to which conditions?

A

Oesophageal choke
Gastric reflux
Pharyngeal dysphagia
Iatrogenic

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38
Q

Which lung lobes are most affected by aspiration pneumonia?

A

Ventral

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39
Q

What causes multinodular pulmonary fibrosis?

A

Equine herpes virus-5

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40
Q

Give some examples of thoracic neoplasias

A 
Cranial mediastinal lymphosarcoma
Pulmonary granular cell tumour
Malignant melanoma
Haemangiosarcoma
Metastatic adenocarcinoma 
Metastatic carcinoma
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41
Q

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

A

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

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42
Q

Give some clinical signs of equine influenza

A 
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

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43
Q

How do you diagnose equine influenza?

A

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

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44
Q

How do you treat equine influenza?

A

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)

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45
Q

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

A

Up to 8 days

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46
Q

How long can equine influenza virus survive in the environment?

A

Up to 36 hours

Easily killed by cleaning/disinfection

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47
Q

Give the clinical signs of equine herpes virus 1 and 4

A

Dull +/- mild coughing/serous nasal discharge

Often lasts several weeks

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48
Q

How do you treat equine herpes virus 1 and 4?

A

Symptomatic

Rest, NSAIDs, antibiotics for secondary infections

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49
Q

What causes ‘rattles’?

A

Rhodococcus equi

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50
Q

Summarise rhodococcus equi infection

A

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 /

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51
Q

What causes ‘strangles’?

A

Streptococcus equi var equi

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52
Q

What kind of horses does strangles affect?

A

1-3 year olds usually

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53
Q

What is the incubation period of strangles?

A

1-14 days

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54
Q

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

A

Multiplication in the lingual and palatine tonsils

Haematogenous and lymphatic spread to draining lymph nodes

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55
Q

What is ‘bastard strangles”?

A

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

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56
Q

How long can streptococcus equi survive in the environment?

A

Up to 12 months

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57
Q

How is streptococcus equi spread?

A

Via nose or mouth contact, fomites

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58
Q

What are the early clinical signs of Strangles?

A

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

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59
Q

Give some further clinical signs of strangles

A

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

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60
Q

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

A

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

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61
Q

Give some complications of strangles

A

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)

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62
Q

How do you diagnose strangles?

A 
Culture or PCR from:
-Nasopharyngeal swabs/lavage
-Gutteral pouch washes/aspirates
-Aspirate from abscess 
ELISA
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63
Q

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

A

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

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64
Q

How do you treat strangles?

A

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
Q

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

A

Prolongs maturation of abscesses

66
Q

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

67
Q

How would you control a strangles outbreak?

A

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
Q

How can you prevent strangles?

A

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

69
Q

What is inflammatory airway disease (IAD)?

A

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

70
Q

Give some risk factors for inflammatory airway disease

A

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
Q

Give the clinical signs of inflammatory airway disease

A

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

72
Q

How do you diagnose inflammatory airway disease?

A 
Endoscopy: mucous in the trachea
Bronchoalveolar lavage (>10% neutrophils)
Tracheal aspirate (>40% neutrophils)
>3% eosinophils and mast cells
73
Q

Where would you palpate the apex beat of the heart?

A

Apex of heart, across mitral valve

74
Q

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

A

To pull the triceps out of the way

75
Q

Where should you start when listening to the equine heart?

A

Start at the mitral valve

Move stethoscope dorsally and cranially to listen to the aortic and pulmonic valves

76
Q

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

A

On the left

77
Q

When is S4 heard (if present)?

78
Q

What do S1 and S2 represent?

A

S1= shutting of AV valves

S2=shutting of semilunar valves (aortic/pulmonic)

79
Q

What do S3 and S4 represent?

When are they each heard?

A 
S3= end of rapid ventricular filling (just after S2)
S4= atrial contraction (just before S1)
80
Q

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

A

Apical: S1
Basal: S2

81
Q

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

A

High heart rate

82
Q

When is the duration of systole shorter than diastole?

A

Normal heart rate

83
Q

What causes a murmur?

A

Turbulent flow of blood

84
Q

How do you measure Reynolds number (influences turbulence)?

A

Velocity x diameter x density

/Fluid viscosity

85
Q

Describe the 6 grades of heart murmurs

A

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
Q

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

A

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

87
Q

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

A

Can still hear S1 and S2 either side of the murmur

88
Q

How could you describe the timing of a murmur?

A

Systolic/diastolic/continuous

  • Early
  • Mid
  • Late
  • ‘Pan’
  • ‘Holo’
89
Q

What 6 features would you describe about a murmur?

A

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
Q

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

A

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

91
Q

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

A

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

92
Q

What are the 2 major categories of murmurs?

A

Physiological/functional (normal blood flow through heart)

Pathological (underlying cardiac disease)

93
Q

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

A

Flow murmur

Filling murmur

94
Q

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

A

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

95
Q

When is a filling murmur heard?

Where is it localised?

A

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

96
Q

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

A

Pathological systolic murmur

97
Q

When should you investigate a mitral valve regurgitation murmur?

A

When it is grade 3 or above

98
Q

When should you investigate a tricuspid valve regurgitation murmur?

A

When it is grade 4 or above

99
Q

What kind of murmur is a ventricular septal defect?

A

Pathological systolic

100
Q

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

A

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

101
Q

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

A 
Older
Decrescendo, buzzing/cooing
Holodiastolic (can hear S1 and S2)
PMI left heart base
May radiate ventrally 
'Uhhh' sound ('teenager murmur')
102
Q

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

A

PMI=left heart base, also loud on right heart base

Waxes and wanes in intensity during cardiac cycle

103
Q

Give the 2 physiological murmurs heard in horses

A

Aortic flow murmurs

Ventricular filling murmurs

104
Q

Give the 4 pathological murmurs heard in horses

A

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

105
Q

Why don’t horses need a high heart rate?

A

They have a very high vagal tone

106
Q

What is the function of the AV node?

A

Slows depolarisation down to ensure the atria contract before the ventricles

107
Q

What are the normal equine heart sounds?

A

B-lub-dup

S4-S1-S2

108
Q

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

A

Delay at AV node

109
Q

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

A

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

110
Q

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

A

No, it can change morphology or polarity

111
Q

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

A

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
Q

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

A

Slightly wider QRS than normal

No associated P waves

113
Q

Give some examples of common physiologic arrhythmias

A

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

114
Q

Give some examples of common pathologic arrhythmias

A 
3rd degree AV block
Ventricular fibrillation
Ventricular tachycardia
Atrial premature complexes
Atrial tachycardia
Atrial fibrillation
Junctional escape complexes
Ventricular premature complexes
115
Q

What happens physiologically during a 2nd degree AV block?

How does this appear on an ECG?

A

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
Q

How is a 2nd degree AV block resolved?

A

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

117
Q

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

A

Prolonged P-R

118
Q

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

A

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

119
Q

How does a sinus block appear on a ECG?

A

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

120
Q

How does a sinus arrhythmia appear on a ECG?

A

Periodic waxing and waning of R-R interval

121
Q

How does atrial fibrillation appear on an ECG?

A

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

122
Q

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

A

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

123
Q

Give some presenting complaints from owners of horses with atrial fibrillation

A

Poor performance
Fading during race
Epistaxis

124
Q

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

A

Pharmacological conversion- Quinidine sulphate

Transvenous electrical cardioversion

125
Q

Does atrial fibrillation cause heart failure?

126
Q

How is quinidine sulphate administered when treating atrial fibrillation?

A

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
Q

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

A

Increases refractory period for atrial cells

128
Q

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

A

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

129
Q

What can atrial fibrillation predispose to?

A

Ventricular tachycardia -> ventricular fibrillation

130
Q

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

A

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

131
Q

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

A

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
Q

What is the definition of oedema?

A

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

133
Q

‘Dependent’ oedema is located where?

A

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

134
Q

What is ‘anasarca’?

A

Generalised subcutaneous oedema

135
Q

Give the 4 mechanisms of oedema

A
  1. Increased capillary hydrostatic pressure
  2. Decreased capillary oncotic pressure
  3. Lymphatic obstruction
  4. Increased capillary permeability
136
Q

What is the most common cause of increased hydrostatic pressure?

A

Congestive heart failure

137
Q

Give some other causes of increased hydrostatic pressure

A 
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
Q

Give some causes of decreased colloid oncotic pressure

A 
Protein-losing enteropathy or nephropathy (eg over bowel wall - diarrhoea)
Haemorrhage 
Proteinaceous effusions
Chronic hepatopathy 
Malnutition
139
Q

Give some causes of lymphatic obstruction leading to oedema

A 
(Lack of lymphatic drainage)
Confinement
Lymphangitis 
Tumours
Post partum
140
Q

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

A

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

141
Q

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

A

Excitement -> vagal tone reduces -> block disappears

142
Q

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

A

Causes increased vascular permeability and reduced cardiac output

  • > increased capillary hydrostatic pressure
  • > fluid leaves capillaries
143
Q

Give some causes of vasculitis

A 
Immune-mediated 
Infectious (eg equine viral arteritis, equine herpes virus 1)
Septic
Traumatic
Verminous 
Photosensitisation
Toxic
Neoplastic
144
Q

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

A

Causes Panvasculitis

Respiratory or venereal (sexual) transmission

145
Q

What are the clinical signs of equine viral arteritis?

What acts as a reservoir?

A 
\+/- pyrexia, dull, oedema, stiff gait, oedematous mm
Respiratory disease
Abortion 
Notifiable 
Stallion= reservoir
146
Q

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

A

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

147
Q

Where do arterial aneurysms most commonly form?

A

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

148
Q

How would a leg with lymphangitis appear?

A 
Swollen, +/- serum ooze/crusting
Hot
Ulcers can form
Pain on palpation
Still weight-bearing
149
Q

How would you treat lymphangitis (‘big leg’)?

A 
Anti-inflammatories (NSAIDs +/- corticosteroids)
Antimicrobials (staphs often involved)
Topical cleaning 
Local cold support
Encourage walking
Tetanus prophylaxis
150
Q

Give some causes of increased capillary hydrostatic pressure

A 
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
Q

Give some causes of decreased colloid oncotic pressure

A 
Protein-losing nephropathy/enteropathy 
Haemorrhage
Proteinaceous effusions
Chronic hepatopathy
Malnutrition
152
Q

Give some causes of lymphatic obstruction

A 
Confinement ('stocking up')
Lymphangitis
Tumours
Post-partum
Other local swelling
153
Q

Give some causes of increased vascular permeability

A

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

154
Q

How is Infectious Equine Viral Arteritis transmitted?

A

Respiratory or venereal transmission

155
Q

Give some clinical signs of Infectious Equine Viral Arteritis

A

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

156
Q

Give some infectious causes of vasculitis

A

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

157
Q

What is the difference between Type 1 and 3 hypersensitivity?

A

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
Q

Are there any proven treatments for EIPH?

Year 4 (51 decks)

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