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Equine Clinical Studies * > Respiratory System Diseases > Flashcards

Respiratory System Diseases Flashcards

1
Q

What is the normal respiratory rate of the horse?

A

8-12 bpm

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2
Q

Define the following:
Epistaxis
Haemoptysis
Dyspnoea

A 
Epistaxis = nose bleed
Haemoptysis = coughing up blood 
Dyspnoea = difficulty breathing
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3
Q

What is the normal values for haemoglobin per L in the horse?

A

120g Hg/ L

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4
Q

What is normal PCV in the horse?

A

40

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5
Q

Which lymph nodes are normally palpable in a healthy horse?

A

Non maybe the Submandibular.

The retropharyngeal is NEVER palpable.

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6
Q

How many times will a normal horse cough when you perform a tracheal squeeze?

A

0 to 1 times.

More than 1 cough may indicate tracheal hypersensitivity.

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7
Q

What are the three landmarks for the lung field in horses?

A

Triceps muscle, 17th intercostal space, olecranon

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8
Q

How do you differentiate a crackle, wheezes, stridor and stertor?

A

Crackle - short discontinuous sound eg. oedema
Wheeze- continuous musical sound - reduced airway
Stridor - intense continuous wheezes
Stertor - low pitched sounds

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9
Q

List some ways of diagnosing respiratory problems?

A 
Endoscopy 
Pulse oximetry
Arterial blood gas analysis
Ultrasound 
Tracheal aspirate
Bronchoalveolar lavage 
Thoracocentesis
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10
Q

What is the plica salpingopharyngeus?

A

Guttural pouch access

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11
Q

What is the rima glottis?

A

Opening of the throat

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12
Q

How is oxygen carried in the blood?

A

3% dissolved in plasma

97% haemoglobin bound

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13
Q

What does arterial blood gas analysis analyse?

A

PaO2 and PaCO2 analysis

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14
Q

What does pulse oximetry measure?

A 
Haemoglobin saturation (SaO2) and can use it to calculate PaO2. 
More than 90% of SaO2
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15
Q

What is the bright white line you can see on a normal thoracic ultrasound?

A

Pleural surface

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16
Q

What do comet tails indicate and where will you see them?

A

Comet tails indicate pleural roughening or pulmonary inflammation.
Look at the lungs below the pleural surface.

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17
Q

Describe what pleural effusion looks like on an ultrasound?

A

Wedge of lung tissue - black wedge.

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18
Q

Differentiate tracheal aspirate and bronchoalveolar lavage.

A

TA - all lung fields, for focal disease, taken sterile (bacterial culture).
BAL- needs sedation, caudodorsal lungs/lower lowers, NOT sterile

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19
Q

What are the normal cytological findings of a tracheal wash or bronchoalveolar lavage?

A

Ciliated columnar epithelium & lymphocytes

ANY squamous cells & extracellular bacteria are due ot contamination

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20
Q

What are the highest level of neutrophils for a TA or BAL that are acceptable?

A

Less than 20% TA
Less than 5% BAL
More than this indicates airway inflammation

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21
Q

Describe normal characteristics of a thoracocentesis?

A

Clear, light yellow.
Less than 10 x 10^9 cells/L WBC
Less than 20 g/L protein

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22
Q

What is alar fold stenosis?

A

Flaccidity of alar folds causing a continuous muffled rattling sound.
Can resect folds or use nasal strips

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23
Q

Campylorrhinus lateralis causes what nasal condition?

A

Wry nose

A congenital deviation of the nasal, maxilla, premaxillar and vomer bone.

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24
Q

What is choanal atresia?

A

One or both the nasal cavities doesn’t communicate with the nasopharynx.

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25
Q

How do nasal septum deformities occur?

A

Trauma.
Airflow obstruction.
You will get assymetric airflow and can palpate septum.

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26
Q

What is mycotic rhinitis?

A

Aspergillus fumigates usually secondary to tissue damage. Get a chronic smelly nasal discharge and lymphadenopathy.

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27
Q

Describe how the nasal sinuses communicate with teeth?

A

Caudal maxillary sinus communicates with 10, 11 teeth.

Rostral maxillary sinus communicates with 8, 9 teeth.

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28
Q

How do you get sinusitis?

A

Primary from previous respiratory tract infection usually Streptococcus.
Secondary to dental disease, facial fractures, cysts, neoplasia, ethmoid haematomas.

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29
Q

How do you diagnose sinusitis?

A

Percussion, endoscopy, sinoscopy, nuclear scintigraphy

30
Q

What are some clinical signs of sinusitis?

A

Nasal discharge - mucopurulent, haemorrhagic
Facial swelling
Bad breath
Draining tracts

31
Q

How do you treat sinusitis?

A

Treat underlying disease.
Antibiotics
Feed on ground, low dust environment
Trephination & sinus lavage (under GA)

32
Q

What are the common signs of progressive ethmoid haematoma and how would you treat this?

A

Unilateral epistaxis
Common and idiopathic.
Treat with endoscopic intralesional formalin injections at 2-4 week intervals

33
Q

What is the principle that decreases oxygen delivery in the horse?

A

Reduction in airway diameter causing increase in airway resistance.

34
Q

What is pharyngeal lymphoid hyperplasia?

A

Pharyngitis. Usually in young horses from an immune response of antigens. Just rest. Does look like raised lymphoid nodules in pharynx.

35
Q

What is the most common pharyngeal performance issue?

A

Dorsal displacement of soft palate

36
Q

What will you see clinically with DDSP?

A

Can’t observe epiglottis in nasopharynx.
Soft palate flaps in airway.
Usually from a cyst!
Swallowing restores the normal position.
Horse will be ‘fading rapidly’ during exercise.

37
Q

How would you deal with DDSP?

A

Rest & anti-inflammatories
Tongue tie
Laryngeal tie forwards

38
Q

In what situation might you see retropharyngeal lymph node enlargement?

A

Streptococcus equi subsp. equi.

Get throat swelling, dyspnoea, respiratory distress, dysphagia. Also abscesses in these retropharyngeal LN.

39
Q

How does recurrent laryngeal neuropathy cause respiratory issues?

A

Also called laryngeal hemiplegia from nerve loss or trauma.

Inspiratory issue where the corniculate process of arytenoid cartilage can’t abduct. Get roaring sound.

40
Q

What may occur when laryngeal hemiplegia progresses?

A

Collapse of arytenoids
Vocal cord laxity
Collapse of other vocal cord

41
Q

Which is the most appropriate treatment for laryngeal hemiplegia:

a) Prosthetic laryngoplasty
b) Tie back surgery
c) Ventriculocordectomy
d) Neuromuscular pedicle graft

A

Tricked you! They all are!

None are that great because there is poor prognosis.

42
Q

Define arytenoid chondritis.

A

Arytenoid cartilage infection causing loss of cartilage abduction. Treat with rest for 1-3 months.

43
Q

How would you differentiate dorsal displacement soft palate and epiglottic entrapment?

A

DDSP - epiglottis is hidden

EE - can still see the epiglottis

44
Q

How would you deal with a dorsoventral tracheal prolapse?

A

Emergency situation give oxygen and do tracheostomy

45
Q

How would you differentiate RAO and IAD? (And define both too please!) *****

A

Recurrent airway obstruction- more obvious clinical signs, cough at rest
Inflammatory airway disease- no clinical signs just reduced performance.

46
Q

Define RAO and it’s clinical signs.

A

Recurrent airway obstruction. Get obvious clinical signs with coughing at rest, exercise intolerance and tachypnoea.

47
Q

Describe the pathophysiology of RAO.

A

Get airway inflammation - bronchospasms - airway obstruction - oedema - chronic airway wall remodelling (metaplasia, hypertrophy, fibrosis)

48
Q

How will you diagnose and treat RAO?

A

Diagnosis - abnormal lung sounds, do a tracheal aspirate or bronchoalveolar lavage
Treat - environment control, clenbuterol (bronchodilator), corticosteroids

49
Q

Describe IAD.

A

Inflammatory airway disease. In lower airway of young racehorses. They will get clinical signs during exercise (coughing). See neutrophils on tracheal wash and BAL.

50
Q

What are some normal clinical findings with a tracheal wash and BAL in a patient with inflammatory airway disease?

A

Normally you see lymphocytes and macrophages. If you see neutrophils this is abnormal!

51
Q

Why do most horses get epistaxis during very intense exercise? How do you deal with it?

A

Exercise induced pulmonary haemorrhage.
From a stress failure of pulmonary capillaries during exercise. Give furosemide (decrease BP during exercise but NOT race approved), or just no treatment.

52
Q

What is a major cause of pulmonary oedema?

A

Upper respiratory tract obstruction

53
Q

When is upper respiratory tract obstruction likely to occur?

A

Anaesthetic recoveries when you intubate for example.

54
Q

How would you treat pulmonary oedema?

A

Furosemide (1mg/kg)

55
Q

What is the major predisposing factor for pneumonia development and why?

A

Transport - horse can’t lower head, contamination of airway, reduced mucociliary clearance.

56
Q

What bacteria are the common culprits causing pneumonia?

A

Strep. zooepidemicus
Strep. pneumnia
Bacteriodes

57
Q

List the clinical signs and clinical pathology you are likely to see with pneumonia.

A

Fever, lethargy, exercise intolerance, abnormal resp.

Leukocytosis, neutrophilia, increase acute phase protein (hyperfibrinogenaemia)

58
Q

What’s your treatment choice for pneumonia?

A

Gentamycin or Penicillin (broad spectrum antibiotics) first doing a tracheal aspirate & pleural effusion culture & sensitivity.
Nebulisation
Pleural drainage
NSAIDs

59
Q

What are the four disease presentations of Strangles?

A

Strangles = Streptococcus equi ss equi
Classic Upper Resp Tract Disease (LN localised)
Purpura haemorrhagica (immune mediated vasculitis)
Disseminated abscessation (bastard strangles)
Immune mediated myopathy

60
Q

Explain the principles behind transmission of a classic URT Strangles and the clinical signs most likely to be seen.

A

Transmitted within nasal shedding. The infection persists in horses guttural pouch (can be subclinical).
Get acute fever, mucopurluent nasal discharge, LN swelling, dysphagia, anorexia.

61
Q

What’s purpura haemorrhagica?

A

Immune mediated vasculitis from Strangles infection. Get distal limb oedema, haemorrhages, serum ooze and skin necrosis.

62
Q

Briefly, what is disseminated strangles and what is immune mediated myopathy stranges?

A

Disseminated - strangles spreads to rest of body (look for rough coat, pyrexia, weight loss)
Myopathies - rhabdomyolysis and atrophy

63
Q

You diagnose a case of Strangles in a horse in your clinic, how did you diagnose it and what will you do now?

A

Diagnosis via guttural pouch wash/nasal wash (Strep equi ss equi is NOT normal flora).
Quarantine affected
Treat with penicillin, NSAIDs and drainage with any LN abscessation. Corticosteroids for purpura haemorrhagica and myopathies forms.

64
Q

How does agaltica get caused by a Strangles infection?

A

Absence of milk secretion/abnormal milk secretion.
Secondary to fever, anorexia and lethargy.
Fix with Domperidone (increases prolactin by interfering with dopamine).

65
Q

How do you prevent strangles?

A

Vaccines are no good have to more rely on the horses natural immunity.

66
Q

Which viral disease affected ciliated epithelial cells, doesn’t survive long outside the host and requires rest and NSAIDs for treatment?

A

Equine influenza (type A virus)

67
Q 
What do the following herpesviruses cause: 
EHV-1
EHV-4
EHV-2
EHV-5
A

EHV-1 - respiratory, abortion, neurological
EHV-4- respiratory
EHV-2 - ubiquitous
EHV-5 - equine multinodular pulmonary fibrosis

68
Q

How does EHV-1 & 4 get transmitted and what age horses are most susceptible?

A

Transmission via aerosol/direct/indirect contact.
Most horses infected by 2 years old.
Get fever, cough, nasal discharge, abortions.
Neuro signs in more than 5 years old horses.

69
Q

What is equine viral arteritis?

A

Severe endothelial destruction RNA virus causing vasculitis.
Sheds in nasal, oral secretions, urine, faeces, semen, aborted material!! AND survives in chilled/frozen semen *
NOTIFIABLE DISEASE

70
Q

What is African horse sickness?

A

Exotic in Australia but notifiable disease spread by Culicoides. Get lung form or heart form. Both high mortality.

Equine Clinical Studies * (3 decks)

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