Equine cardiorespiratory Flashcards
(158 cards)
1
Q
What is the aerobic capacity of a horse?
A
150ml/kg/min
2
Q
Define minute ventilation
A
Tidal volume x breaths/min
3
Q
What is perfusion?
A
Removal of gas from the lungs by the blood
4
Q
CO2 is how many times more diffusible than O2?
A
25
5
Q
CO2 is mostly transported in the blood as what?
A
HCO3-
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)
7
Q
What is EIPH?
A
Exercise-induced pulmonary haemorrhage
Haemorrhage into the airways that occurs at high intensity exercise
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)
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
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
11
Q
What may predispose a horse to EIPH?
A
High pulmonary vascular pressure
12
Q
Give some events that may cause EIPH
A
Extreme vascular pressures High inspiratory pressures Inflammation Locomotory shockwaves Regional differences in dynamic compliance
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
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
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
16
Q
Which 2 diseases compromise ‘allergic’ airway disease in horses or ‘equine asthma’?
A
Recurrent airway obstruction (RAO/heaves)
Inflammatory airway disease (IAD)
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)
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
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
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
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
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
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)
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)
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
