Respiratory Flashcards

1
Q

How do agents of disease gain entry to the respiratory system?

A
  • Inhalation
  • Haematogenous
  • Direct extension from surrounding tissues
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2
Q

What are the respiratory system defence mechanisms in the airways?

A
  • Aerodynamic filtration
  • Mucociliary escalator
  • Lymphoid tissue (BALT) and IgA secretion in bronchial tissue
  • Protective reflexes
  • Antioxidants
  • Normal bacterial flora in larynx and above
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3
Q

What are the respiratory system defence mechanisms in the alveoli?

A

Macrophages in alveoli and alveolar walls
Antioxidants
Protective reflexes (bronchoconstriction to prevent material getting down there)
IgG

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4
Q

What factors may impair the immune responses and cell functions of respiratory defences?

A
  • Infectious agents – especially some viruses
  • Toxic gases such as ammonia
  • Stress
  • Hypoxia
  • Concurrent diseases
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5
Q

What are the factors impairing mucociliary clearance?

A

Cellular injury and loss of function
Squamous metaplasia (change in cell type, loss of cilia and goblet cells)

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6
Q

What are the factors that contribute to respiratory disease?

A

Host – age, immunity

Pathogen – dose, strain, virulence

Environment – temperature, humidity

Management – stocking density, transport

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7
Q

What are the potential causes of inflammation of the airway system?

A
  • Infectious agents – virus, bacteria, fungi, parasites
  • Physical injury – such as foreign body
  • Secondary to neoplasia
  • Extension form local disease, such as tooth root infections, neoplasia
  • Allergic disease, such as recurrent airway obstruction/equine asthma
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8
Q

What is fungal rhinitis and sinusitis?

A

Fungal infection and necrotic and exudative material within sinuses and nasal cavity

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9
Q

What are the typical pathological features of acute inflammation of the airways?

A
  • Increased secretion from goblet cells and seromucous glands
  • Inflammatory response – vasodilation and increased vascular permeability causing oedema, escape of plasma proteins and emigration of leucocytes = exudate forms on the surface
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10
Q

What is catarrhal discharge and exudate of the respiratory airways?

A

Substantial increase in mucus production from goblet cells/mucus glands. Translucent/clear/slightly opaque, mucoid/tacky.

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11
Q

What is purulent discharge and exudate of the respiratory airways?

A

Typically bacterial infection with necrosis and exudate containing many leucocytes, especially neutrophils. Thick and opaque/coloured discharge.

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12
Q

What is fibrinous/fibrinonecrotic discharge and exudate of the respiratory airways?

A

Typically severe inflammation with exudation containing fibrin. May be mixed with necrotic debris. Soft, yellow/tan/grey fibrin layer on the mucosal surface

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13
Q

How is infectious bovine rhinotracheitis spread?

A

Infection by aerosol or direct or indirect contact

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14
Q

What is the incubation period of infectious bovine rhinotracheitis?

A

2-6 days

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15
Q

What is the pathophysiology of infectious bovine rhinotracheitis?

A
  1. Infection of respiratory epithelium
  2. Viral replication and lysis of respiratory tract epithelium
  3. Dissemination of virus throughout respiratory tree (nasal cavity, pharynx, larynx and trachea mainly)
  4. Mucosal injury and impairment of respiratory defence mechanisms predisposed to secondary bacterial infection in severe IBR
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16
Q

What happens in fatal infectious bovine rhinotracheitis?

A

Fibrinonecrotic exudate on the mucosal surface of the larynx and trachea

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17
Q

How does the respiratory mucosa heal and repair from infectious bovine rhinotracheitis?

A

Immune responses are cell mediated immune responses from 5 days and neutralising antibodies from 10 days

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18
Q

What 2 main features are the result of chronic airway inflammation?

A
  • Increased mucus production
  • Thickening of the mucosa
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19
Q

What can chronic inflammation of the airway result in?

A

Some degree of airways obstruction, may be combined with bronchoconstriction

Inflammatory polyps arising of nasal cavity, nasopharynx, auditory canal/middle ear or airways

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20
Q

How does chronic airway inflammation cause bronchiectasis?

A

Can cause weakening and destruction of the smooth muscle and cartilage in bronchi resulting in permanent dilation of the affected bronchus.

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21
Q

How does chronic airway inflammation cause obstructive atelectasis?

A

The distended bronchi are usually filled with exudate, which can cause obstruction of the airways and secondary collapse of the dependent lung parenchyma in obstructive atelectasis.

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22
Q

What is the most common type of pneumonia?

A

Bronchopneumonia

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23
Q

What are the typical causes of bronchopneumonia?

A

Bacteria including mycoplasma
Viral infections and stress may predispose to bacterial infection
Aspiration of food/gastrointestinal contents

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24
Q

What is the route of entry for bronchopneumonia?

A

Inhalation - infectious agents inspired air or from flora in the nasal passages

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25
Q

What is the distribution of bronchopneumonia?

A

Cranial and ventral regions of the lungs

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26
Q

What is the pathogenesis of acute bronchopneumonia?

A
  1. Bronchiolar infection with initial bronchiolitis
  2. Exudate of fluid, proteins and inflammatory cells into the mucosal surfaces and lumen
  3. Spread of infection to alveoli, resulting in an accumulation of exudate in the alveolar spaces
  4. Involvement of both bronchioles and alveoli = bronchopneumonia
  5. Can spread infection to adjacent alveoli
  6. The interlobular septa may help contain the infection within lobules by acting as a barrier, more pronounced in animals with thicker interlobular septa
  7. Spread to other lobules may occur via the airways/bronchial tree
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27
Q

What are the species differences in interlobular septa?

A

Cattle and pigs have prominent and relatively thick interlobular septa. Sheep, horses, cats and dogs have thinner and less obvious ones

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28
Q

What is the microscopic appearance of bronchopneumonia?

A

Lot of aggregations of small blue dots which represent densely packed inflammatory cells within exudate arising from the inflammatory response. Nearly all alveolar spaces contain inflammatory exudate, which inhibits ventilation of the affected parts of the lung.

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29
Q

Describe the gross appearance of bronchopneumonia.

A
  • Affected regions are red, brown or greyish with time/chronic inflammation
  • Flabby to firm due to exudate filling the airspaces and collapse of alveoli due to airway obstruction
  • Patchwork appearance with affected and unaffected lobules, most prominent in pigs and cattle
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30
Q

What is suppurative bronchopneumonia?

A

Most common type, has mucopurulent exudate exuding from airways on the cut lung surface

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31
Q

What is fibrinous bronchopneumonia?

A

Inflammation may be severe and cause a large amount of plasma protein release in inflammatory exudate in the airways, including fibrinogen, forming fibrin. In animals with prominent interlobular septa, fibrinous bronchopneumonia may expand the interlobular septa with oedema and fibrinous exudate, resulting in a marbled appearance.

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32
Q

What happens if the source of injury causing bronchopneumonia persists?

A

Result in progression to chronic bronchopneumonia.

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33
Q

What changes may chronic bronchopneumonia cause in the airways?

A

Airway obstruction
Bronchiectasis
Abscess formation

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34
Q

What is the gross appearance of chronic bronchopneumonia?

A
  • Dark red-purple with multiple, coalescing, raised, pale pink irregular foci
  • Pale pink foci are firm and nodular, they are dry, caseous necrosis
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35
Q

What is the cause of enzootic pneumonia in pigs?

A

Inhalation and infection with mycoplasma hypopneumoniae

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36
Q

What are the effects of colonisation of the lower airway ciliated epithelium?

A
  • Loss of cilia and epithelial cells
  • Altered mucus composition which affects mucociliary escalator
  • Reduced neutrophil phagocytic function and immunosuppression
  • Lymphoid hyperplasia – can create cuffs around airways
  • Predisposes to secondary bacterial infection > suppurative bronchopneumonia
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37
Q

What is the aetiology of interstitial pneumonia?

A

There is an initial injury to the lung parenchyma, injury directed at any component of the alveolar wall. Inhalation or haematogenous

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38
Q

What are the causes of interstitial pneumonia?

A
  • Viruses, migrating parasites, protozoa
  • Septicaemia
  • Toxins
  • Allergens
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39
Q

What is the distribution of interstitial pneumonia?

A

Most commonly diffuse/generalised

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40
Q

What is the pathogenesis of interstitial pneumonia?

A
  1. Entry to the lungs via the airways or the bloodstream
  2. Diffuse injury to the alveolar walls
  3. Acute inflammatory in alveolar walls - hyperaemia and exudation of fluid, followed by a cellular response with emigration of inflammatory cells.
  4. Initial swelling within the alveolar wall. As the fluid increases it spills over into alveolar spaces
  5. Oedematous fluid/exudate accumulating in the alveolar walls flows into the alveolar spaces, which fill with exudate.
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41
Q

What is the microscopic appearance of interstitial pneumonia?

A

Capillaries are stuffed with red blood cells due to vasodilation and hyperaemia caused by inflammatory response. Pink areas often highlighting the alveolar walls represents hyaline membrane formation, which occurs when plasma proteins leak from the inflamed blood vessels and mix with the surfactant lipids in the alveolar space.

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42
Q

What is the microscopic appearance of the healing phase of interstitial pneumonia?

A
  • Alveolar wall now looks very thick
  • Vasodilation and hyperaemia of the capillaries and there are some inflammatory cells
  • Type II pneumonocytes proliferate to replace the flattened type I pneumonocytes that have been injured
  • To complete healing process when conditions improve, type II pneumocytes will proliferate into type I
  • Alveolar macrophages phagocytose and remove exudate and cellular debris
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43
Q

What is the thickened alveolar walls in chronic interstitial pneumonia due to?

A

Fibrosus
Chronic inflammatory cells
Persistence of type II pneumonocytes

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44
Q

Why is interstitial pneumonia difficult to detect?

A

Difficult to detect grossly because it causes diffuse changes

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45
Q

What are the gross morphological features of interstitial pneumonia?

A
  • Red/grey
  • Lungs fail to collapse when thorax opened
  • Might have rib impressions on surface
  • Heavier than expected
  • Firmer, rubbery or elastic texture
  • In acute interstitial pneumonia, pulmonary oedema may be present
  • Cattle may have interstitial emphysema
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46
Q

How do cattle develop interstitial emphysema?

A
  • Occurs when air escapes from the alveoli and accumulates within the interlobular septa
  • Cattle have thick septa so in cattle, interstitial emphysema can occur where there is partial obstruction of the bronchioles by oedema, fluid or exudate and strenuous respiratory effort
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47
Q

What is fog fever?

A

Acute bovine pulmonary oedema and emphysem

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48
Q

What is the pathophysiology of fog fever?

A
  1. When moved from sparse to lush pasture in which the grass contains high levels of L-tryptophan
  2. Converted to 3-methyl indole in rumen upon ingestion
  3. Absorbed into the blood and reaches the lungs via the circulation
  4. An epithelial cell called club cells convert into a toxic metabolite (bronchiole cells)
  5. Causes necrosis of the bronchial cells and type I pneumocyte injury. Causes acute interstitial pneumonia
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49
Q

What are the microscopic changes of fog fever?

A

Hyaline membrane formation and alveolar oedema

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50
Q

What is the cause of embolic pneumonia?

A

Bacteria – haematogenous of septic emboli containing emboli to the lungs

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51
Q

What is the distribution of embolic pneumonia?

A

Random foci. The lungs have randomly distributed, multifocal to sometimes coalescing discrete, round to irregular, raised, yellow to greenish foci of varying size.

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52
Q

What are some potential causes of septic emboli causing embolic pneumonia?

A

Liver abscesses (cattle)
Bacterial endocarditis (right side of heart)
Umbilical infections
Chronic skin or hoof infections
Mastitis
Endometritis
Intravenous catheterisation

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53
Q

What is the cause of granulomatous pneumonia?

A

Agents that persist in tissues and are resistant to phagocytosis and the acute inflammatory response. Inhaled or haematogenous

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54
Q

What is the pathophysiology of granulomatous pneumonia?

A
  1. Chronic inflammatory response
  2. The cellular infiltrate contains many macrophages
  3. The macrophages may form aggregates or granulomas
  4. Typically present as nodular lesions/masses
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55
Q

What are some examples of causes of granulomatous pneumonia?

A
  • Bacterial – mycobacteria, actinomyces, rhodococcus
  • Parasitic – lungworms
  • Fungal – cryptococcus
  • Viral – feline infectious peritonitis
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56
Q

What is the distribution of granulomatous pneumonia?

A

Variable, focal/multifocal, (nodular)

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57
Q

Describe mycobacterial infections in bovine.

A
  • Multiple nodular to focally extensive, relatively large lesions that would be firm
  • May become mineralised in some cases
  • Parenchyma is being replaced by a yellowish material/granulomatous inflammation and caseous necrosis
  • Variable degrees of granulomatous inflammation and caseous necrosis
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58
Q

Describe mycobacterial infections in cats.

A

Can be nodular and focal or multifocal and mass like in their appearance, can be more generalised to diffuse with extensive coalescing pale brown lesions

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59
Q

What are the potential tumour origins of neoplasia in nasal cavities and paranasal sinuses?

A

Epithelial – such as stratified squamous, transitional, respiratory

Mesenchymal – osteocytes, chondrocytes, endothelium, fibroblasts

Round cell – lymphoid

Others – such as neuroendocrine, melanocytes

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60
Q

What are the most common nasal cavities and paranasal sinus neoplasias in cats and dogs?

A

Dog - carcinomas

Cats - carcinomas and lymphomas

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61
Q

What are the general characteristics of malignant sinonasal tumours?

A
  • Slow growing
  • Space occupying
  • Locally invasive and destructive
  • Late to metastasise
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62
Q

What is the effect of sinonasal tumours?

A

Can be destructive, can cause swelling or distortion of the face and be a cause of nasal discharges (secondary infection) or epistaxis.

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63
Q

What is the pathogenesis of progressive ethmoid haematoma in horses?

A
  • Proliferative but non-neoplastic
  • Presents as an enlarging haemorrhagic nasal mass that can cause obstruction of the nasal passages
  • May cause local distortion and destruction of the soft tissues and bone, ulceration of the mucosa encapsulating the mass may result in mild haemorrhage and epistaxis
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64
Q

How might neoplasia of the larynx and trachea present?

A

Airway obstruction

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65
Q

What are the potential tumour origins of neoplasia of the larynx and trachea?

A
  • Epithelial – stratified squamous, respiratory
  • Mesenchymal – chondrocytes, skeletal muscle, smooth muscle, fibroblasts
  • Lymphoid
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66
Q

What is the likely origin of lung neoplasia?

A

Generally, secondary metastatic spread of tumour to the lung is more common than primary lung neoplasia.

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67
Q

What are the potential tumour origins for primary lung neoplasia?

A
  • Carcinoma and adenocarcinoma are most common. Large airway epithelial origin often near hilus
  • Parenchymal epithelial origin often peripheral.
  • Epithelial – respiratory in airways and glands, alveolar
  • Mesenchymal – chondrocytes (and osteocytes), fibrocytes, mesothelium
  • Lymphohistiocytic
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68
Q

What are the possible routes of metastatic spread of primary epithelial lung tumours?

A
  • Lymphatic invasion – spread within the lung and spread to hilar lymph nodes
  • Intra-airway seeding – spread within the lung
  • Vascular invasion – spread to distant sites
  • Transcoelomic spread – spread within the pleural cavity space
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69
Q

What is ovine pulmonary adenocarcinoma?

A

Ovine pulmonary adenocarcinoma/sheep pulmonary adenomatosis/Jaagsiekte - retroviral-induced neoplasia – Jaagsiekte sheep retrovirus

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70
Q

What is the pathophysiology of ovine pulmonary adenocarcinoma?

A

Neoplastic epithelial cuboidal to columnar cells end up papilliform structures. As masses grow, they tend to compress the surrounding alveoli and may cause a significant increase in collagen that can result in fibrosis.

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71
Q

What is the incubation period of ovine pulmonary adenocarcinoma?

A

Long incubation period
Clinical disease mostly 2-4 years old

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72
Q

What is the gross appearance of ovine pulmonary adenocarcinoma?

A

Solid grey or grey-purple tumour masses, can appear nodular. Cranial and ventral areas of the lungs

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73
Q

What is the sequalae of ovine pulmonary adenocarcinoma?

A
  • Secondary infections and abscesses can occur
  • Production of excessive fluid in the lungs
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74
Q

What are the causes of laryngeal oedema?

A

Local trauma
Irritation or inflammation

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75
Q

What is laryngeal chondritis?

A

An inflammatory condition that principally affects the arytenoid cartilages and the associated mucosa

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76
Q

Why may laryngeal cartilages and mucosa be irregular in laryngeal chondritis?

A

Due to suppurative inflammation, focal areas of ulceration and necrosis on the mucosal surface adjacent to the vocal folds. Can obstruct the larynx or can cause laryngeal oedema that leads to acute respiratory obstruction.

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77
Q

Which systemic conditions cause laryngeal oedema?

A

Oedema disease in pigs by some strains of E.coli
Anaphylaxis/allergic reactions

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78
Q

What is the microscopic appearance of pulmonary oedema?

A

Alveoli contain pale pink staining fluid. The oedematous fluid will have originated with the alveolar walls but has now spilled over into the alveolar spaces, filling them with fluid.

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79
Q

By what mechanisms may pulmonary oedema arise?

A
  • Increased hydrostatic pressure
  • Increased endothelial or alveolar epithelial permeability
  • Decreased colloid osmotic pressure
  • Block lymphatic drainage
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80
Q

What is hydrothorax?

A

Oedema/transudate in the pleural space. Causes include CHF, hypoproteinaemia (other cavities too), intra-thoracic tumours

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81
Q

What are the possible causes of haemorrhage in the respiratory tract?

A
  • Inflammatory diseases – nasal aspergillosis, guttural pouch mycosis
  • Inflammation of the lower RT
  • Neoplastic disease
  • Progressive ethmoid haematoma in horses
  • Exercise induced pulmonary haemorrhage in horses
  • Trauma
  • Coagulopathies
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82
Q

How does pulmonary septic thrombosis cause haemorrhage in the respiratory tract?

A
  1. Liver abscess impinges on the vena cava
  2. Septic thrombus formation
  3. Thromboembolism to the lung
  4. Arterial septic embolic abscess
  5. Erodes into a bronchial wall
  6. Ruptures into airway allowing arterial blood flow into the airway
  7. Fatal epistaxis (exsanguination)
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83
Q

What are the possible causes of haemothroax?

A

Trauma
Erosion of blood vessels by tumours
Clotting disorders

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84
Q

What are the causes of pulmonary infarction?

A
  • Lung lobe torsion
  • Massive pulmonary artery thrombus or thromboembolism
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85
Q

What are the factors predisposing to pulmonary thrombosis or thromboembolism?

A
  • Conditions causing activation of vascular endothelium
  • Conditions promoting procoagulant tendencies/coagulopathies
  • Conditions causing vascular stasis
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86
Q

What are the causes of chylothorax?

A
  • Rupture of the thoracic duct due to a mass
  • Obstruction of the thoracic duct
  • Disease causing occlusion of the cranial vena cava
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87
Q

What is the pathophysiology of paranasal sinus cysts in horses?

A

Fluid filled cyst with a thin wall of bone lined by respiratory epithelium. Causes airway obstruction, facial distortion and compression of surrounding soft tissues and bone.

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88
Q

What are the clinical signs of paranasal sinus cysts in horses?

A

Facial swelling
Epiphora

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89
Q

What is the impact of brachycephalic skulls on the respiratory tract?

A

Skull has shrunk over time while soft tissues have not so excess soft tissues can obstruct airways at various sites. This can result in altered pressures within the respiratory passages.

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90
Q

What are the anatomical problems of BOAS?

A
  • Stenotic nares
  • Elongated soft palate
  • Relatively large tongue
  • Turbinates may protrude into the nasopharynx
  • Hypoplastic trachea in some cases
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91
Q

What are the secondary changes that further contribute to the obstruction of airways in BOAS?

A
  • Inflammation and oedema – palate and larynx
  • Everted tonsils
  • Everted laryngeal saccules
  • Laryngeal collapse from laryngeal cartilage rigidity
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92
Q

What is tracheal/tracheobronchial collapse in dogs?

A

Miniature, toy and brachycephalic dogs. Dorsoventral flattening of the trachea causing tracheal collapse.

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93
Q

Describe tracheal collapse in the extra-thoracic region.

A
  • Lumen pressure reduces below surrounding pressure causing collapse during inspiration
  • Lumen pressure is higher than the surrounding pressure during expiration
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94
Q

Describe tracheal collapse in the intrathoracic region.

A
  • Lumen pressure greater than pleural pressure during inspiration
  • Expiratory forces on the intrathoracic trachea promote collapse during expiration
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95
Q

What are the clinical signs of tracheal/tracheobronchial collapse in dogs?

A

Cough (“goose honk”)
Increased respiratory rate and effort
Exercise intolerance
Respiratory distress
Cyanosis
Collapse

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96
Q

What is the aetiology of laryngeal paralysis?

A

Degeneration of the recurrent laryngeal nerve.

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97
Q

What are the species differences of laryngeal paralysis?

A

Horses – usually unilateral, left sided

Dogs – large breed dogs predisposed, often bilateral

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98
Q

What is the gross appearance of laryngeal paralysis?

A

The muscles on the left side of the larynx are smaller and paler red-brown compared to those on the right side. This is because the muscles on the left are undergoing atrophy due to loss of innervation caused by degeneration of the left recurrent laryngeal nerve.

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99
Q

Describe the pathophysiology of laryngeal paralysis?

A
  1. Atrophy and paralysis of the dorsal, lateral and transverse cricoarytenoid muscles
  2. The dorsal cricoarytenoid muscles abducts the arytenoid cartilage during inspiration
  3. Failure of arytenoid cartilages to abduct during inspiration can result in airway obstruction
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100
Q

What are the potential causes of laryngeal paralysis?

A
  • Primary (idiopathic) neuronal degeneration
  • Secondary to nerve trauma, compression, irritation or injury
  • Component of a generalised polyneuropathy
  • Neurotoxins
  • Liver failure
  • Hypothyroidism in dogs
  • Congenital nerve abnormality
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101
Q

Name 3 bronchodilators.

A

Equine asthma
Feline lower airway disease/feline asthma
Canine chronic bronchitis

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102
Q

What is bronchodilation a function of?

A

Function of sympathetic stimulation – adrenaline acts on alpha and beta adrenoreceptors to cause bronchodilation

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103
Q

Which drug classed cause bronchodilation? Give an example for each.

A

B-adrenergic receptor agonists, such as adrenaline, and anticholinergic drugs such as atropine.

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104
Q

What are some examples of bronchodilators?

A
  • Short acting non-specific – adrenaline
  • Longer-acting β2 specific – terbutaline, Salbutamol, Clenbuterol
  • Sodium chromoglycate
  • Anticholinergic drugs – atropine, ipratropium
  • Methylxanthines – theophylline
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105
Q

How do beta-adrenergic receptor agonists cause bronchodilation?

A
  • Act by working through the cAMP pathway
  • Bronchial smooth muscle relaxes so bronchodilation
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106
Q

What is the effect of beta-adrenergic receptor agonists?

A
  • Stabilises mast cells by inhibiting mast cell degranulation
  • May increase mucociliary clearance
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107
Q

What are the effects of adrenaline, a beta-adrenergic receptor agonist?

A
  • Short acting, non-specific
  • Stimulates α and β adrenergic receptors, so widespread effects - vasopressive and cardiac effects
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108
Q

What is the use of adrenaline?

A

Life-threatening bronchoconstriction – CPR, anaphylactic shock

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109
Q

What is the advantage of long acting beta-adrenergic receptor antagonists?

A
  • Developed to avoid adverse cardiac effects of non-specific drugs
  • Longer acting so suitable for long-term use
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110
Q

What is the use of terbutaline?

A
  • Lasts 6-8 hours
  • Off license for cats with asthma – give prior to bronchoscopy or bronchoalveolar lavage (BAL), injectable in emergencies
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111
Q

What is the use of salbutamol?

A

Used in inhalers

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112
Q

What is the effect of clenbuterol?

A

Partial agonist so may be less effective
Aids mucociliary clearance

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113
Q

What are the side effects of clenbuterol?

A

Sweating
Tremors
Restlessness
Tachycardia

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114
Q

What are the averse effects of beta-adrenergic receptor agonists?

A
  • Cardiovascular – tachycardia, especially with β1 agonists or high dose β2
  • Illegally as a growth promoter in cattle
  • Tolerance with chronic use (weeks) – down-regulation of receptors. Use for short-term treatment of bronchoconstriction
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115
Q

What is the effect of sodium chromoglycate?

A

Stabilises mast cells – inhibit release of histamine and leukotrienes to reduce bronchoconstriction

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116
Q

What is the use of sodium chromoglycate?

A

Equine asthma off license - used in cases with increased mast cells on tracheal wash or bronchoalveolar lavage, usually increased neutrophils so not particularly useful for the majority of cases

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117
Q

What are the effects of theophylline?

A
  • Relaxation of bronchial smooth muscle
  • May also have anti-inflammatory effect
  • Increase mucociliary clearance
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118
Q

What are the uses of theophylline?

A

Dogs for chronic bronchitis
Cats for feline lower airway disease
Not horses due to side effects

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119
Q

What are the side effects of theophylline?

A
  • Mild – nausea, vomiting, diuresis
  • Cardiac – tachycardia, increased contractility, arrhythmias
  • CNS – can cause agitation and seizures (more common with caffeine use/toxin)
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120
Q

What are the potential drug interactions for theophylline?

A
  • Relies on hepatic metabolism and cytochrome P450 enzymes
  • Fluoroquinolones, erythromycin, cimetidine inhibits its metabolism – dose reduction
  • Phenobarbitone, rifampicin active its metabolism – dose increase
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121
Q

What is the effect of anticholinergic drugs?

A

Muscarinic antagonism

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122
Q

What is the use of anticholinergic drugs?

A
  • Equine asthma
  • Mainly for colic but also useful as an emergency bronchodilator (IV)
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123
Q

What is the use and side effects of atropine?

A

In horses IV in emergencies

Side effects – ileus, CNS toxicity, tachycardia

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124
Q

What is the use and side effect of ipratropium?

A

Given to horses by aerosol
Less side effects

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125
Q

What is the mechanism of action of antitussives?

A

Depression of the cough centre in the medulla oblongata, bronchodilation B2 receptor agonist

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126
Q

When should antitussives be used?

A
  • Cough is a protective mechanism
  • Contraindicated if productive, such as pneumonia
  • Chronic cough can increase airway inflammation/irritation
  • Dynamic airway disease, such as tracheal collapse
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127
Q

Name 4 opiate antitussives.

A

Codeine
Hydrocodone
Diphenoxylate
Butorphanol

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128
Q

What drug type is codeine?

A

μ-receptor agonist

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129
Q

What are the side effects of codeine?

A

Sedation and constipation

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130
Q

What type of drug is hydrocodone?

A

μ-receptor agonist

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131
Q

What is the effect of hydrocodone?

A
  • More potent
  • Has anti-cholinergic component to discourage overuse
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132
Q

What type of drug is diphenoxylate?

A

Opioid agonist

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133
Q

What is the effect of diphenoxylate?

A
  • Direct suppression of the cough centre
  • Minimal side effects
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134
Q

What type of drug is butorphanol?

A

κ-receptor agonist

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135
Q

What is the effect of butorphanol?

A

Poor bioavailability orally (1st pass effect) so much higher dose required than when injected

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136
Q

Name 2 non-opiate antitussives.

A

Dextromethorphan

β-agonists also have some effect due to bronchodilation

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137
Q

Why is Dextromethorphan not usually recommended?

A

Often contain other drugs which may be toxic, such as paracetamol

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138
Q

Name a mucolytic drug.

A

Bromhexine (bisolvon)

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139
Q

What are the effects of Bromhexine (bisolvon)?

A
  • Increases secretion of fluid and breakdown of mucus to make it more watery
  • Increase mucociliary clearance in calves with respiratory disease
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140
Q

What are expectorants?

A

Thought to accelerate particle clearance

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141
Q

Name an expectorant.

A

Guaifenesin (glyceryl guaiacolate) and guaiacol

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142
Q

What is the effect of Guaifenesin (glyceryl guaiacolate) and guaiacol?

A
  • Used in veterinary anaesthesia as muscle relaxants
  • May also stimulate bronchial secretions
  • Cough medicine in humans
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143
Q

What is nebulisation?

A

Small droplets of a drug delivered to the airways, possible less systemic absorption, can still see side effects

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144
Q

How is feline lower airway disease managed?

A
  • Management strategies
  • Glucocorticoids
  • Bronchodilators
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145
Q

How are dogs with chronic bronchitis managed?

A
  • Management changes
  • Bronchodilators
  • Glucocorticoids
  • Antibiotics if secondary infections
  • Antitussives occasionally - codeine
  • Mucolytics generally contraindicated
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146
Q

What is canine chronic bronchitis?

A

Chronic bronchial inflammation with over-secretion of mucus in middle aged to older dogs

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147
Q

What are the concurrent morbidities seen with canine chronic bronchitis?

A

Tracheal/bronchial collapse
Mitral valve disease
Pulmonary hypertension

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148
Q

What are the initial predisposing factors of canine chronic bronchitis?

A

Kennel cough
Irritants/allergens
Parasites

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149
Q

What is the pathophysiology of canine chronic bronchitis?

A
  • Smaller airways become obstructed by mucus causing obstructive dyspnoea, emphysema
  • Alteration of mucociliary escalator causing possible concurrent bacterial infections
  • Inflammation of the lower airways – narrowing, bronchomalacia due to weakened cartilage, bronchiectasis due to end-stage bronchial change
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150
Q

What are the clinical signs of canine chronic bronchitis?

A
  • Chronic cough for over 2 months – often productive
  • Gagging/retching
  • Dyspnoea/tachypnoea
  • Pyrexia is concurrent pneumonia
  • Thoracic auscultation – wheezes, crackles (concurrent pneumonia, emphysema)
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151
Q

What is identified from imaging of canine chronic bronchitis?

A

Bronchial pattern
Possible mild interstitial pattern
Mild broncho-interstitial pattern

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152
Q

What is seen on bronchoalveolar lavage with canine chronic bronchitis?

A

Mucus, neutrophils and possibly bacteria. If eosinophils seen, consider angiostrongylus vasorum or eosinophilic bronchopneumopathy

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153
Q

How is canine chronic bronchitis managed?

A
  • Weight control
  • Harness
  • Avoiding airway irritants – tobacco smoke, dust
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154
Q

How is canine chronic bronchitis treated?

A
  • Glucocorticoids – lowest possible dose
  • Bronchodilators – theophylline, methyxanthine
  • Antibiotics if suspicious of bacterial infection, antitussives, mucolytics
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155
Q

When are antimicrobials used to managed canine chronic bronchitis?

A
  • Ideally using culture and sensitivity BAL result
  • Need good airway penetration
  • First line doxycycline – broad spectrum, 7-10 days
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156
Q

Why do canine chronic bronchitis and heart diseases often co-exist?

A

In middle aged small breed dogs with mitral valve disease and chronic bronchitis, stage B2 heart disease can cause a cough due to cardiomegaly without CHF, CHF usually causes tachypnoea/dyspnoea.

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157
Q

What is the stepwise approach to dogs with chronic coughs?

A
  • Cardiac or respiratory?
  • Ideally chest radiographs with/without BAL, with/without faecal parasitology
  • Treatment trials – fenbendazole, bronchodilators, with/without antibiotics
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158
Q

What is the signalment of feline lower airway disease?

A

Young/middle aged cats – Siamese over-represented

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159
Q

What are the initial predisposing factors of feline lower airway disease?

A

Bacterial, virus, parasites, irritants/allergens

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160
Q

What is the pathophysiology of feline lower airway disease?

A
  1. Type I hypersensitivity (IgE mediated) – histamine and serotonin production by mast cells
  2. Smooth muscle contraction – acute bronchoconstriction
  3. Oedema and eosinophilic inflammation of the lower airway
  4. Mucus hypertension
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161
Q

Distinguish obstruction of small and large bronchi in feline lower airway disease.

A

Large – atelectasis of the right middle lung lobe

Small – emphysema, bronchiectasis and possible pneumothorax

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162
Q

What are the clinical signs of feline lower airway disease?

A

No signs/few signs to asthmatic crisis

Cough
Dyspnoea/tachypnoea
Open-mouth breathing
Cyanosis
Wheezes +/- crackles if mucus/emphysema
Dull lung sounds if pneumothorax

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163
Q

How is feline lower airway disease investigated from thoracic radiographs?

A
  • Generalised bronchial/bronchointerstitial pattern with/without alveolar pattern
  • Over-inflated lungs – see flattened diaphragm
  • Possible atelectasis of the right middle lung lobe
  • Possible pneumothorax
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164
Q

How is bronchoscopy done in cats?

A

SC terbutaline the night and the morning before the procedure

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165
Q

What is seen on bronchoscopy with feline lower airway disease?

A

Inflammation, mucus and airway narrowing

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166
Q

What are the emergency treatments of feline lower airway disease?

A

Stress-free
Oxygen
Bronchodilators – terbutaline
Corticosteroids – dexamethasone

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167
Q

How is feline lower airway disease managed?

A
  • Dust free litter
  • Cigarette smoke – no smoking inside the house
  • Reduce use of aerosol
  • Regular parasite control
  • Monitor for secondary infections
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168
Q

How is feline lower airway disease treated?

A
  • Glucocorticoids – lowest effective dose
  • Bronchodilators – oral theophylline long term, inhaled salbutamol for acute bronchoconstriction
  • Doxycycline if mycoplasma infection, fenbendazole if parasitic infection
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169
Q

What is the lifecycle of angiostrongylus vasorum?

A
  1. Infection by eating intermediate host (mollusc) or paratenic host (frog)
  2. L3 larvae are liberated in intestines, travel to the pulmonary vasculature
  3. Adult worms live in the pulmonary arteries and right side of the heart
  4. Larvae migrate into the alveoli and are coughed and swallowed
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170
Q

What are the clinical signs of angiostrongylus vasorum?

A

Chronic cough
Acute dyspnoea
Severe pulmonary hypertension (cor pulmonae – abnormal RV function and structure)
Syncope
Bleeding diathesis
CNS haemorrhage

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171
Q

What may laboratory investigation find with angiostrongylus vasorum?

A

Anaemia
Eosinophilia
Thrombocytopenia
Abnormal coagulation times
Hypercalcaemia

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172
Q

How is angiostrongylus vasorum treated?

A
  • Fenbendazole 10-20 days
  • Moxidectin 2 doses 30 days apart
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173
Q

What are the possible post treatment reactions of angiostrongylus vasorum?

A

Dyspnoea, ascites and sudden death

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174
Q

What are the predisposing causes of bacterial pneumonia?

A

Chronic bronchitis
Bronchiectasis
Immunosuppression
Foreign body
Aspiration

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175
Q

What are the clinical signs of bacterial pneumonia?

A

Cough (soft and productive)
Mixed dyspnoea
Tachypnoea
Exercise intolerant
Crackles and/or wheezes on auscultation
Pyrexia
Lethargy
Inappetence

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176
Q

What might be seen on diagnostic images with bacterial pneumonia?

A

Usually alveolar pattern with ventral distribution, but variable lung patterns:

  • Dorso-caudal distribution = haematogenous spread
  • Aspiration – right middle lung lobe, obtain both lateral views
  • Early pneumonia = interstitial pattern
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177
Q

When are antibiotics used in bacterial pneumonia?

A
  • Empirical treatment – PO doxycycline as it penetrates into airways
  • Aspiration pneumonia – chemical pneumonitis = no antibiotics, IV amoxycillin-clavulanic acid
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178
Q

How are septic bacterial pneumonia patients treated?

A

IV fluoroquinolones + ampicillin or clindamycin
Treat gram positive bacteria and anaerobes
De-escalation as soon as possible

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179
Q

How is bacterial pneumonia treated?

A
  • Oxygen supplementation if hypoxic
  • Fluid therapy as dehydration impairs mucociliary defences
  • Nebulisation increased mucus fluidity
  • Bronchodilators?
  • Treat any gastro-oesophageal reflux disease and oesophagitis with omeprazole and metoclopramide or cisapride
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180
Q

What is the signalment of eosinophilic bronchopneumopathy?

A
  • Usually in young dogs
  • Husky and Malamute are predisposed
  • Previous positive response to steroids
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181
Q

What is the pathophysiology of eosinophilic bronchopneumopathy?

A
  • Immunological hypersensitivity to an allergen
  • Eosinophilic inflammation of the lungs and the bronchi
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182
Q

How is eosinophilic bronchopneumopathy investigated?

A
  • Imaging - broncho-interstitial pattern
  • Bronchoscopy – bronchial wall thickening, lots of green mucus, bronchiectasis
  • BAL – eosinophilic inflammation
  • Negative faecal parasitology
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183
Q

How is eosinophilic bronchopneumopathy treated?

A

Glucocorticoids

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184
Q

What is the signalment of idiopathic pulmonary fibrosis?

A

Old dogs, Westies, bull terriers

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185
Q

What are the clinical signs of idiopathic pulmonary fibrosis?

A

Cough and exercise intolerance, with/without cyanosis
Auscultation – inspiratory crackles, with/without right sided heart murmur

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186
Q

How is idiopathic pulmonary fibrosis diagnosed from imaging?

A

Interstitial pattern
No alveolar pattern
Often cor pulmonae/enlarged right side of the heart due to pulmonary hypertension

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187
Q

How is idiopathic pulmonary fibrosis treated?

A

Sildenafil for pulmonary hypertension

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188
Q

What are the clinical signs of lung tumours?

A

Can be asymptomatic
Cough
Haemoptysis
Systemic signs

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189
Q

What is lung-digit syndrome in cats?

A

Primary pulmonary neoplasm with metastasis to the digits, often present for foot issue/lameness

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190
Q

How are lung tumours diagnosed?

A
  • CT more sensitive than radiographs
  • FNA and lung histopathology – risks of seeding tumours
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191
Q

How do airway foreign bodies present?

A
  • Acute onset cough and respiratory distress
  • Progresses to secondary pneumonia with/without pulmonary abscess
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192
Q

How are airway foreign bodies treated?

A

Bronchoscopic removal
Occasional surgery

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193
Q

What is the most likely diagnosis of a 10 year old labrador with cough, stridor and altered bark?

A

Laryngeal paralysis

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194
Q

What is the most likely diagnosis of a 9 year old overweight border terrier with 3 month history of cough, grade 4 heart murmur and sinus arrhythmia?

A

Chronic bronchitis

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195
Q

What is the most likely diagnosis of a 5 year old Yorkie with goose-honk, worse on excitement?

A

Tracheal collapse

196
Q

What is the most likely diagnosis of a 10 year old CKCS with 2months history of cough and 2 day history of tachypnoea and progressive dyspnoea, grade 5 heart murmur, HR 160bpm?

A

Congestive heart failure

197
Q

What are the treatment options for tracheal collapse?

A

Weight loss
Harness
Avoid excitement
Bronchodilators
Lomotil

198
Q

What are the treatment options for oslerus osleri?

A

Fenbendazole

199
Q

What are the treatment options for chronic bronchitis?

A

Weight loss
Harness
Avoid irritants
Bronchodilators
Corticosteroids

200
Q

What are the treatment options for laryngeal paralysis?

A

Refer for surgery

201
Q

What bronchodilator is common used and licensed in dogs?

A

Theophylline. Terbutaline is used more commonly in cats, especially pre-bronchoscopy and is human licensed.

202
Q

In a dog with chronic bronchitis, what would be a good choice of antibiotic for secondary infections?

A

Doxycycline. Good airway penetration due to lipid solubility and broad spectrum activity including mycoplasmas and is given orally.

203
Q

What injectable bronchodilator is often given to cats prior to bronchoscopy?

A

Terbutaline

204
Q

What clinical signs would you associate with canine angiostrongylus vasorum infection in addition in respiratory signs like chronic cough and acute dyspnoea?

A

Bleeding and neurological signs

205
Q

Define hyperpnoea.

A

Increased respiratory effort (deeper breaths) without dyspnoea.

206
Q

Define orthopnoea.

A

Difficulty in breathing while laying down. Cats often sit or stand to facilitate breathing with elbows abducted and neck extended.

207
Q

Where are the receptors involved in a cough?

A
  • Cough receptors in the large airways and low density cough receptors in nose, sinuses, pharynx, pleura.
  • Mechanical receptors to mucus and foreign bodies and chemical receptors to acid and heat.
208
Q

How may coughing also be associated with heart disease?

A

Enlarged left atrium
Pulmonary oedema causes tachypnoea

209
Q

What are the harmful effects of coughing?

A
  • Exacerbate airway inflammation and irritation
  • Emphysema
  • Pneumothorax
  • Weakness and exhaustion
  • Dissemination of infections
210
Q

What are the potential breed dispositions to coughing and dyspnoea?

A

Working/outdoors lifestyle – airway FB

CKCS (and others) – mitral valve disease

Brachycephalic breeds – BOAS

Toy breed dogs – tracheal collapse

Siamese cat – feline asthma/chronic bronchitis

Westie – idiopathic pulmonary fibrosis

211
Q

Which type of dyspnoea do you typically expect in a patient with BOAS?

A

Obstructive and inspiratory dyspnoea

212
Q

Which type of dyspnoea do you typically expect in a patient with pneumonia?

A

Restrictive and mixed (inspiratory and expiratory) dyspnoea

212
Q

What are the clinical signs of dyspnoea?

A
  • Coughing vs panting
  • Reverse sneezing
  • Gagging
  • Retching
  • Change in sound of bark/purr/meow
  • Cough – initiating factors, productive or non-productive, sound
213
Q

What may be observed before clinical examination from a dyspnoeic patient?

A

Open-mouth
Cyanosis
Anxious expression
Orthopnoea

214
Q

What is palpated on clinical examination of dyspneoic patients?

A

Cranial mediastinal compressibility
Thoracic cavity trauma/deformities
Tracheal pinch

215
Q

What are the differential diagnoses for upper respiratory tract dyspnoea?

A

Obstructive disorders:

Laryngeal paralysis
Tracheal collapse
BOAS

216
Q

What are the differential diagnoses for lower respiratory tract dyspnoea?

A

Obstructive disorders:

Luminal - mucus or FB)
Mural - mass or bronchospasm, feline asthma, chronic bronchitis

217
Q

What are the differential diagnoses for pulmonary parenchyma dyspnoea?

A

Restrictive disorder/reduced lung capacity

Pneumonia
Haemorrhage
Oedema

218
Q

What are the differential diagnoses for pleural space dyspnoea?

A

Restrictive disorder/reduced lung volume = pleural effusion

Obstructive disorder = mediastinal mass

219
Q

What are the possible non-respiratory causes of coughing and dyspnoea?

A
  • Haematological disorders (tachypnoea): decreased oxygen carrying capacity - anaemia or methaemoglobinaemia
  • Metabolic disorders (tachypnoea): compensatory mechanism to acidosis (DKA) - muscular weakness (hypokalaemia)
  • Neurological disorders of the brain, spinal cord, peripheral nerves
220
Q

Summarise the clinical signs, location and differential diagnoses of inspiratory dyspnoea causing stertor.

A
  • Dynamic obstruction of URT causing stertor
  • Nasal/nasopharynx
  • BOAS, polyp, foreign body, tumour
221
Q

Summarise the clinical signs, location and differential diagnoses of inspiratory dyspnoea causing stridor.

A
  • Dynamic URT obstruction causing stridor
  • Larynx
  • Laryngeal paralysis, laryngeal collapse
222
Q

Summarise the findings, clinical signs, location and differential diagnoses of expiratory dyspnoea.

A
  • Dynamic LRT obstruction
  • Wheezes
  • Intrathoracic airways
  • Tracheal collapse, bronchial collapse, asthma, EBP
223
Q

Summarise the clinical signs, location and differential diagnoses of mixed dyspnoea causing prolonged respiratory cycle.

A
  • Laboured breathing
  • Airway obstruction
  • Mass, tracheal collapse
224
Q

Summarise the clinical signs, location and differential diagnoses of mixed dyspnoea causing adventitious lung sounds.

A
  • Crackles, wheezes
  • Pulmonary parenchyma
  • Pneumonia, pulmonary oedema, pulmonary fibrosis
225
Q

Summarise the clinical signs, location and differential diagnoses of mixed dyspnoea causing shallow breathing.

A
  • Muffled lung sounds
  • Pleural space disease
  • Pleural effusion, pneumothorax
226
Q

How is coughing and dyspnoea investigated?

A
  • Imaging of pleural space disease
  • Laryngeal examination
  • Bronchoscopy
  • Haematology – neutrophilia, eosinophilia, thrombocytopenia
  • Biochemistry
  • Test for lungworm
  • BAL
  • Tracheal wash
  • Lung FNA
227
Q

Which lung pattern is best described by doughnuts and tramlines?

228
Q

Which lung pattern is best described as cloudy, fluffy or patchy?

229
Q

Which lung pattern is best described as looking through net curtains?

A

Interstitial diffuse

230
Q

Which lung pattern is best described as cannon balls?

A

Interstitial nodular

231
Q

Describe oxygen supplementation by flow by.

A

During assessment
Easy and well tolerated
Need someone to hold tube
FiO2 of 25-40%

232
Q

Describe oxygen supplementation by mask.

A

Easy
May not tolerate
Useful for recumbent patient
FiO2 of 50-60%

233
Q

Describe oxygen supplementation by nasal prongs.

A

Designed for humans
Easy to place but often dislodge

234
Q

Describe oxygen supplementation by nasal catheter.

A

Longer term supplementation requirement
Well tolerated
Easy access
Easy to place
More invasive and time consuming
Unilateral FiO2 40%
Bilateral FiO2 50%

235
Q

Describe oxygen supplementation by oxygen hood.

A

Risk of hyperthermia
CO2 build up
Humidity
FiO2 30-40%

236
Q

Describe oxygen supplementation by oxygen cage/incubator.

A

Well tolerated
Best suited to small patients
Depends on design
Monitor humidity
FiO2 60%

237
Q

Describe oxygen supplementation by intubation without mechanical ventilation.

A

Upper airway mechanical ventilation
Upper airway obstruction
FiO2 100%

238
Q

What is done on clinical examination of a patient with nasal disease?

A
  • Listen for noises
  • Nasal discharge
  • Facial deformity
  • Pain
  • Nasal planum depigmentation
  • Assess airflow bilaterally
  • Assess regional lymph nodes
  • Retropulsion of the eyeballs/exophthalmia
  • Dental disease?
  • Ophthalmic disease?
239
Q

What are the differential diagnoses for unilateral nasal disease?

A
  • Foreign body
  • Nasal tumour - early course and older patients
  • Aspergillus – early course, younger dogs, nasal depigmentation, dolichocephalic breeds, epistaxis
  • Chronic rhinitis
240
Q

What are the differential diagnoses for bilateral nasal disease?

A
  • Chronic rhinitis – idiopathic
  • URT viruses – vaccination, ocular signs
  • Aspergillus - advanced
  • Nasal tumour – advanced, absent to reduced nasal airflow, CNS signs
241
Q

What is the mechanism of chronic rhinosinusitis present in feline patients?

A

Idiopathic
Unclear role of bacterial and viral infections

242
Q

What are the clinical signs of chronic rhinosinusitis present in feline patients?

A

Sneezing
Nasal discharge
Increased URT noises
Usually bilateral
Often preserved nasal airflow

243
Q

What are the differential diagnoses for unilateral and no nasal airflow?

A

Tumour and fungal rhinitis

244
Q

What are the mechanisms causing chronic rhinitis in dogs?

A

Underlying allergic, irritant, immune-mediated process

245
Q

What are the clinical signs of chronic rhinitis in dogs?

A

Sneezing
Snorting
Mucoid/mucopurulent nasal discharge
Bilateral (can be unilateral)
Possible airflow obstruction
Possible post-nasal drip causing coughing

246
Q

What are the clinical signs of nasal foreign bodies?

A

Sneezing
Gagging
Pawing at the face
Progression to purulent nasal discharge and foul smelling

247
Q

What are the breed predispositions of sino-nasal aspergillosis?

A

Meso/dolichocephalic dog breeds – aspergillosis fumigatus

Brachycephalic cats – sino-orbital, aspergillus felis

248
Q

What are the clinical signs of sino-nasal aspergillosis?

A

Mucopurulent nasal discharge or epistaxis
Unilateral or bilateral
Sneezing
Nasal pain
Nasal depigmentation

Uncommonly stertor, facial deformity, CNS signs

249
Q

What are the clinical signs of nasal neoplasia?

A

Chronic nasal discharge
Sneezing
Dyspnoea
Reduced airflow
Stertor
Facial distortion
Pain
Ocular discharge/exophthalmia

250
Q

What are the diagnostic investigations of nasal disease?

A

Tests for bleeding disorders
Serology for fungal disease
Viral testing in cats
Swabs
Imaging
Rhinoscopy

251
Q

What are the nasal investigations to be taken under GA?

A

Full oral examination use bitch spay hook to the lift the soft palate, otoscope may help visualisation

Dental probing

252
Q

What are radiographs used to identify in nasal disease?

A
  • Foreign bodies
  • Tooth root abscesses/dental disease
  • Turbinate destruction
  • Nasal bone invasion
  • Increased soft tissue opacity
  • Check sinuses
253
Q

How is chronic rhinosinusitis treated in feline patients?

A
  • Steam/nebulise
  • Mucolytics - bromhexine
  • Saline drops
    meloxicam
  • Doxycyline 6 week course
  • Antivirals: famciclovir for FHV
  • Antihistamines - if allergy associated
  • Glucocorticoids – if no bacterial/viral component
254
Q

How is chronic rhinitis treated in dogs?

A
  • Minimise exposure to irritants/allergens
  • Doxycycline
  • Meloxicam
  • Glucocorticoids
  • Humidification/nebulization
  • Antihistamines
  • Hypoallergenic diet
  • Azithromycin
255
Q

How is nasal neoplasia treated?

A

Radiotherapy is usually best treatment, except chemotherapy for lymphoma

Surgery is unrewarding

Meloxicam – analgesia, inhibition tumour growth

256
Q

How is aspergillosis treated?

A
  • Mechanical debridement endoscopically – may require trephination to access frontal sinuses
  • Topical antifungal
  • Non-invasive catheter soaks with clotrimazole:
  • Trephination
257
Q

How is a foley catheter used to treat aspergillosis?

A
  • Use foley catheters in the nasopharynx and rostral nasal cavity
  • Restricts the drug to the nasal cavity
258
Q

How is trephination used to treat aspergillosis?

A
  • Flushing with saline then clotrimazole flush
  • Installation of clotrimazole cream
259
Q

Define bronchomalacia.

A

When bronchial cartilage is weakened and collapses inwards

260
Q

What is the presentation of BOAS?

A

Respiratory noise mild to severe with/without gastrointestinal signs

261
Q

What are the exacerbating factors of BOAS?

A

Obesity
Excitement
Hot weather

262
Q

What are the main possible gastrointestinal signs that could present with BOAS?

A
  • Oesophagitis or megaoesophagus
  • Gastric or hiatal hernia
  • Upper GI issues can lead to secondary intestinal dysfunction
  • Reflex
  • Regurgitation
  • Vomiting or haematemesis
263
Q

What are the respiratory abnormalities of BOAS?

A
  • Mild - snoring, reverse sneezing
  • Severe - cyanosis, collapse
  • Sucking air in rather than breathing passively
  • Stertor
  • Paroxysmal stertor = reverse sneezing
  • Stridor – more high pitched sound than stertor
264
Q

What are the other possible abnormalities that could be present with BOAS?

A

Orthopaedic – luxated patellae to spinal deformities

Ophthalmological – corneal ulcers

Dermatological – skin fold pyoderma

265
Q

What are the respiratory anatomical features of BOAS?

A
  • Nares – sides of the nostrils sucked in as they breathe in
  • Tonsils – can evert
  • Soft palate – can be thickened
  • Laryngeal saccules – can become thickened
  • Aberrant turbinates – restricts air even more
  • Trachea – English bulldogs can have hypoplastic tracheas
266
Q

What are 3 other non-surgical components of BOAS?

A

Nasopharyngeal hyperplasia
Macroglossia
Bronchial collapse

267
Q

What is nares resection BOAS surgery?

A

Alar fold excision/nares resection/rhinoplasty – typically a vertical wedge is removed

268
Q

What is a staphylectomy in BOAS surgery?

A

Soft palate resection/shortening

269
Q

What is a sacculectomy in BOAS surgery?

A

Removing everted saccules, always bilateral. There is an argument to leave alone unless causing obstruction as may risk increased airway swelling.

270
Q

What is a hiatal hernia?

A

The negative intra-thoracic pressure caused by the restriction to airflow from the upper airway anatomy pulls the stomach through the oesophageal hiatus (normal opening in the diaphragm the oesophagus passes through).

271
Q

What is GORD?

A

Gastroesophageal reflex disease

272
Q

How is GORD treated?

A

Always consider medical treatment first, with/without combined airway surgery. Gastrointestinal signs typically improve or resolve post BOAS surgery but may need medical management peri-operatively.

273
Q

What are the possible complications of BOAS surgery post-operatively?

A

Airway swelling > severe dyspnoea
Aspiration
Progression > laryngeal collapse

274
Q

What are the clinical signs of laryngeal collapse?

A

Severe dyspnoea
Syncope
Severe respiratory noise

275
Q

What are the 3 stages of laryngeal collapse?

A

1 = saccule eversion
2 = partial cuneiform collapse
3 = complete collapse

276
Q

What are the treatment options for laryngeal collapse?

A

BOAS surgery
Laryngoplasty
Permanent tracheostomy
Partial arytenoidectomy (laser ablation)
Cuneiformectomy

277
Q

What is GOLPP?

A

Geriatric onset laryngeal paralysis polyneuropathy/polyneuropathies are often immune-mediated. When we see a polyneuropathy that’s when we see progressive hindlimb weakness and dysphagia as well

278
Q

When considering staphylectomy, what is the recommended anatomical landmark for resection?

A

Caudal tonsillar crypt as well as overlap of soft palate with epiglottis

279
Q

What are the mechanisms causing laryngeal paralysis?

A

Most common aetiologies are degenerative, idiopathic and immune-mediated

280
Q

How is laryngeal paralysis diagnosed?

A

Cervical and thoracic radiography - to rule out other things
Laryngoscopy

281
Q

How is laryngeal paralysis surgically treated?

A

Unilateral arytenoid lateralisation via cricoarytenoid sutures (tie back)

282
Q

What are the complications of laryngeal paralysis?

A
  • Haemorrhage leading to airway obstruction
  • Cartilage fracture or suture failure may be associated with barking post operatively
  • Aspiration pneumonia, so soft food initially not wet/liquid
  • Wound issues, such as infection or seroma
283
Q

What is the most common cause of laryngeal paralysis in an elderly dog?

A

Degenerative

284
Q

What are the clinical signs of trachea collapse?

A

Cough
Honk
Stertor
Progression

285
Q

Distinguish inspiratory and expiratory stertor.

A

Inspiratory stertor suggests extra-thoracic airway obstruction

Expiratory stertor suggests intra-thoracic airway obstruction

286
Q

Explain the degenerative/developmental aetiology of tracheal collapse.

A

Tracheomalacia with/without bronchomalacia causing cartilage weak, the trachea collapses inwards, isn’t a rigid tube. This causes dynamic obstruction of the upper airway

287
Q

Explain the infectious/inflammatory aetiology of tracheal collapse.

A
  • Coughing from collapse causes inflammation
  • Inflammatory cycle means you can get sudden deterioration after an infection such as kennel cough
288
Q

How is trachea collapse investigated?

A

Fluoroscopy
Radiography
Bronchoscopy

289
Q

How is tracheal collapse graded?

A

Grade I collapse 25% loss of lumen
Grade II collapse 50% loss of lumen
Grade III collapse 75% loss of lumen
Grade IV collapse total loss of lumen

290
Q

How is tracheal collapse medically managed?

A

Medical management in severe cases – stabilisation, as per any respiratory distress case, with oxygen

291
Q

Can tracheal collapse be surgically managed?

A

Avoided, high rates of complication and can’t cure, only improve

292
Q

How can tracheal collapse be surgically managed?

A

Used if refractory or unresponsive to medical management, severe collapse or medically unstable dogs.

Extraluminal prosthesis
Intraluminal stenting

293
Q

What treatment options are recommended for grade 3 tracheal collapse isolated to the intrathoracic trachea?

A

Intraluminal stenting or euthanasia

294
Q

What is a temporary tracheostomy?

A

Creation of a temporary stoma in the trachea by placement of a tracheostomy tube.

295
Q

What are the indications of temporary tracheostomy?

A

Laryngeal oedema
Extra luminal obstruction
Cervical swelling

296
Q

How are tracheostomy tubes selected by size?

A

Should not be same size as trachea, should be 75% the width of the trachea

297
Q

How is a temporary tracheostomy managed?

A
  • Coupage every 4-6h after nebulisation
  • Cuff – if cuffed, readjust every 4 hours to avoid mucosal damage
  • Cannula – every 2-4h,
  • Suction – every 4-6h
  • Stoma cleaning every 4-6h
298
Q

What are the pos-operative complications of temporary tracheostomies?

A
  • May have trouble sleeping
  • Patient interference/accidental/coughing
  • Blockages common
  • Vagal response, coughing, stimulation of gag reflex upon suction
  • Aspiration pneumonia
  • Tracheal infection
  • Tracheal necrosis
  • Tracheal stenosis
  • Pneumomediastinum
  • Pneumothorax
  • Subcutaneous emphysema
299
Q

What is a permanent tracheostomy?

A

Creation of a permanent stoma in the trachea by removing a section of tracheal rings ventrally and suturing mucosa to skin

300
Q

What are the indications for a permanent tracheostomy?

A

Laryngeal collapse
Neoplasia
Severe crushing trauma

301
Q

Define flange.

A

Side tabs that allow for simple suturing of narrow bore chest drains to skin

302
Q

What is thoracocentesis?

A

Procedure involving the puncture of the pleural space for diagnostic and/or therapeutic purposes. Avoid lateral recumbency

303
Q

Which side of the chest is thoracocentesis done on?

A

Depends on imaging/unilateral or bilateral

304
Q

In which intercostal space is thoracocentesis done?

305
Q

How ventral or dorsal is thoracocentesis done?

A

Ventral for low volume liquid, middle for more volume and dorsal for air as it rises

306
Q

When is a chest drain placed?

A
  • When thoracocentesis is not enough
  • For drainage of large quantity of fluid or air from the chest
  • Recurrent pneumothorax
  • Ongoing formation of fluid/air
  • Fluid too thick to be removed via a butterfly
307
Q

What are the advantages of trocar chest drains?

A
  • Lots of different sizes available
  • Versatile, good for air or fluid, large bore means less likely to block
  • Robust/don’t collapse
  • Once learned, easy to place
  • Most transparent so easy to monitor for stuff that could clog the tube
308
Q

What are the disadvantages of trocar chest drains?

A
  • Typically need a GA to place
  • Likely to have higher complication rate than narrow bore though published evidence minimal
  • Needs careful training
  • Need to learn a good suture technique for anchoring (2nd technique to learn)
  • Less comfy than narrow-bore
309
Q

What are the advantages of narrow bone/seldinger chest drains?

A
  • No GA
  • Easy to place
  • Easy to secure
  • Versatile
  • More comfy
310
Q

What are the disadvantages of narrow bone/seldinger chest drains?

A
  • May not cope with pleural fluid/block
  • Smaller sizes difficult, can be overlong meaning either too much inside the chest (prone to kinking) or too much outside (vulnerable to patient interference)
  • Not as rigid means can end up in weird placement
  • May not be able to do the normal SQ tunnel in a large patient as introducer catheters not that long
311
Q

How are chest drains cared for?

A
  • Wound management – ointments, gels to reduce air leaks, early signs of infection around incisions
  • Tube management – regular checks of sutures, connectors to reduce risk of failure of the drain, flushing as required
  • Body bandage – for increased comfort, reduce infection and reduce risk of patient interference
  • Nursing care and hospitalisation
312
Q

What are the complications of thoracocentesis and chest drain complications?

A

Failure to place
Failure to drain after placement
Patient interference
Iatrogenic

313
Q

What are the reasons to keep chest drains?

A
  • Ongoing treatment via the drain
  • Clinically significant production of fluid/air
314
Q

What are the reasons to remove chest drains?

A
  • Complications
  • Resolution of issue
  • Ongoing need for drainage
315
Q

What is the biggest advantage to large-bore trocar chest drains over small bore seldinger technique chest drains?

A

Better for thick pleural effusions

316
Q

What are the 2 surgical approaches to the thorax?

A

Intercostal/lateral thoracotomy – left/right (depends on target structure), intercostal space

Sternotomy

317
Q

When is a sternotomy used?

A

Sternotomy is used when either disease is bilateral or you can’t be sure which side of the chest might be affected. Not so good for anatomical structures in the dorsal thorax.

318
Q

What are the surgical procedures done during a thoracotomy?

A
  • Exploration
  • Debridement
  • With/without repair
  • With/without foreign body removal
  • With/without lung lobectomy
  • Flushing – remove infection, remove necrotic tissue, check for air leaks post lobectomy
319
Q

What are the complications post thoracotomy?

A
  • Pleural effusion
  • Pneumothorax
  • Lung-associated – pulmonary atelectasis, re-expansion pulmonary oedema, lung lobe torsion
  • Post-operative pain
  • Phrenic nerve injury
320
Q

What are the clinical signs of chest trauma?

A

Shock
Dyspnoea

321
Q

What are the complications of chest traumas?

A

Infection
Inflammation
Delayed healing
Ongoing effusion/pneumothorax

322
Q

What are the clinical signs of diaphragmatic rupture?

A
  • Herniation
  • Depends on size of tear
  • Dyspnoea may be improved if animal thorax raised to allow abdominal organs to leave the chest
  • Tachypnoea and orthopnoea
  • Concurrent ortho injuries
323
Q

What are the tears of diaphragmatic rupture?

A

Circumferential or radial or both

324
Q

How are diaphragmatic ruptures treated?

A

Stabilise with oxygen, analgesia, IVFT

Laparotomy – explore, reposition abdominal content or remove if badly torsed/devitalised, with/without repair, debride as necessary, chest drain

325
Q

What are the complications of diaphragmatic rupture?

A

Organs will become adhesed to pleura within a week or so

326
Q

Distinguish the aetiology of pyothorax in cats and in dogs.

A

Cats idiopathic – bites, extension from pulmonary abscesses

Dogs – foreign bodies, oesophageal tars, pulmonary infections

327
Q

What are the clinical signs of pyothorax?

A

Lethargy
Inappetence
PUO
Dyspnoea
Mild or severe

328
Q

How is pyothorax medically managed?

A

Systemic antibiotics
Chest drain with/without lavage
Good option in cats

329
Q

How is pyothorax surgically managed?

A

Sternotomy: explore, remove, debride, flush and then post-op medical management, typically done early in dogs because of the percentage of foreign bodies

330
Q

What are the complications of pyothorax?

A
  • Non-response to medical therapy/relapse
  • Inflammation – pleuritis/pleural fibrosis, SIRS
  • Thromboembolism
  • Surgical complications
331
Q

What are the aetiologies of pulmonary abscessation?

A

Foreign bodies
Chronic bronchopneumonia
Penetrating wounds
Vascular obstruction
Neoplasia

332
Q

What are the clinical signs of pulmonary abscessation?

A

Non-specific – lethargy, inappetence, PUO

Respiratory – dyspnoea, coughing

333
Q

What are the aetiologies of pericardial effusion?

A

Idiopathic
Neoplastic

334
Q

What is the clinical sign of pericardial effusion?

A

Cardiac tamponade

335
Q

How is pericardial effusion diagnosed?

A

Imaging
Pericardiocentesis

336
Q

How is pericardial effusion treated?

A

Repeat pericardiocentesis
Pericardiectomy

This does not stop the effusion from forming, it prevents the cardiac tamponade and converts into pleural effusion, but this is rarely large enough volume to cause an issue

337
Q

What are the complications of pericardial effusion?

A
  • Recurrence both after draining and surgery – if window removed
  • Long standing effusion causes adhesions
338
Q

What are the clinical signs of pulmonary neoplasia?

A
  • Non-productive cough/dyspnoea
  • Non-specific weight loss
  • Distal limb pain
  • None 25%
  • Hypertrophic pulmonary osteopathy occasionally seen with paraneoplastic syndrome, painful
339
Q

What are the clinical signs of mediastinal masses?

A

Space occupying lesion
With/without pleural effusion
With/without paraneoplastic syndromes
None

340
Q

What are the clinical signs of pulmonary blebs and bullae?

A

Sudden onset dyspnoea
No history of trauma
None
Lethargy
Anorexia
Exercise intolerance)
Progressive = tachypnoea, orthopnoea, coughing
Peracute = tension pneumothorax

341
Q

How are pulmonary blebs and bullae treated?

A
  • Conservative management via intermittent thoracocentesis/indwelling chest tube, but typically pneumothorax continues to reform
  • Surgery thoracoscopy or sternotomy, remove affected lung lobes depending on how many affected
342
Q

What are the complications of pulmonary blebs and bullae?

A

Surgical complications
Staple failure
Recurrence

343
Q

What are the clinical signs of thoracic oesophageal foreign bodies?

A

Retching/gagging
Hypersalivation
Inappetence

344
Q

How are thoracic oesopahgeal foreign bodies?

A

Radiography
Oesophagoscopy

345
Q

How are thoracic oesophageal foreign bodies treated?

A
  • Conservative medical treatment during endoscopy with/without fluoroscopy. Retrieval via mouth, or pushed into stomach
  • Surgical – lateral thoracotomy, chest drain
346
Q

What are the complications of thoracic oesophageal foreign bodies?

A
  • Oesophageal damage – oesophagitis, perforation/tear, stricture (balloon dilation)
  • Surgical complications
  • Suture dehiscence
  • Feeding tube
347
Q

What is PPDH?

A

Peritoneal pericardial diaphragmatic hernia

348
Q

What are the clinical signs of PPDH?

A

None
Intermittent vague signs
Gastrointestinal
Respiratory
Cardiac - tamponade, pericardial effusion

349
Q

How is PPDH treated?

A
  • None if small/asymptomatic
  • Surgery = exploratory laparotomy to explore/replace with/without remove contents
  • Restore normal division between pericardium, diaphragm and abdominal cavity
350
Q

What are the complications of PPDH?

A
  • Adhesions within the pericardium
  • Pericarditis
  • Organ damage
  • Surgical complications
351
Q

What is the agent of Jaagsiekte?

A

Retrovirus

352
Q

How is Jaagsiekte transmitted?

A

Aerosol so needs close contact

353
Q

What is the incubation period of Jaagsiekte?

A

Over 6 months

354
Q

What is the pathogenesis of Jaagsiekte?

A

Epithelial cells produce large amounts of mucoid fluid

355
Q

What are the clinical signs of Jaagsiekte?

A
  • Little until so much lung affected that respiration becomes affected
  • Severe weight loss
  • Hyperpnoea, coughing
  • Fluid crackles on auscultation

Animals can live 3-6 months after initial clinical signs

356
Q

How is Jaagsiekte diagnosed?

A
  • Wheelbarrow test = 50-500ml fluid
  • Fluid production is pathognomonic
357
Q

What are the characteristics of Jaagsiekte on post mortem examination?

A
  • Lungs are larger
  • Heavier than normal with areas of solid grey tumour
  • PCR test may be available in the future
358
Q

Where should sheep be ultrasonographed for Jaagsiekte?

A

Probe at 6-7th intercostal space

359
Q

How is Jaagsiekte in sheep controlled?

A

Slaughter affected animals
Minimise close contact

360
Q

What is Maedi Visna?

A

A lentivirus (a slow virus) affecting the lungs (Maedi) and nervous system (Visna) of sheep

361
Q

How is Maedi Visna transmitted between sheep and flocks?

A

Inhalation
Milk and colostrum

Not placental, ova or semen

362
Q

What are the clinical signs of Maedi Visna?

A
  • Tachypnoeic on exercise and later at rest
  • Dry cough
  • Worsen over 6-12 months
363
Q

What are the characteristics of Maedi Visna on post mortem examination?

A

Large heavy lungs
Grey coloured

364
Q

How is Maedi Visna identified?

A

Blood testing allows identification

365
Q

How is Maedi Visna treated?

A

There is no vaccine, no cure and the disease is fatal

366
Q

Which disease can Maedi Visna be cross infected with?

A

Caprine arthritis encephalitis

367
Q

What is the causative agent of contagious lymphadenitis?

A

CLA bacterial infection caused by corynebacterium pseudotuberculosis

368
Q

What is the aetiology of chronic suppurative pneumonia?

A
  • Rams often neglected outside of tupping season
  • Related to malnutrition
369
Q

What is the pathology of chronic suppurative pneumonia in rams?

A

Damage to lungs from pathogens such as mycoplasma when lungs abscesate following bacterial infection

370
Q

How is chronic suppurative pneumonia treated in rams?

A

3-4 weeks of antibiotic therapy

371
Q

What is the first clinical sign of chronic lung disease in sheep?

A

Weight loss

372
Q

What are the causative agents of pasteurellosis?

A

Mannheimia haemolytica - commonest in UK
Bibersteinia trehalosi

373
Q

Describe the clinical syndrome caused by biotype A pasteurellosis in sheep.

A
  • Under 2 months = hyperacute septicaemia
  • Older lambs = pleurisy and pericarditis
  • Adults = pneumonia
374
Q

Describe the clinical syndrome caused by biotype B pasteurellosis in sheep.

A
  • Acute systemic disease
  • 6 to 12 months old
  • Find dead or recumbent
  • Frothy discharge from mouth
  • Morbidity rarely exceeds 5%
375
Q

What are the clinical signs of pasteurellosis in adult ewes?

A

Find dead
Dull, pyrexic and hyperpnoeic
Adventitious respiratory sounds
Ocular and nasal discharges
Coughing
Mouth breathing
Frothing at the mouth

376
Q

What are the risk factors of pneumonia in cattle, pigs and sheep?

A
  • Poor ventilation in housing
  • Overcrowding when housed
  • Unhygienic conditions (high ammonia) too little bedding or v soiled bedding
  • Recent handling/transportation
  • Inadequate nutrition
  • Concurrent disease
  • Extremes in weather conditions
  • Mixing age groups (lambs> adults)
377
Q

How is bacterial pneumonia treated in sheep?

A

Antimicrobial therapy - oxytetracycline, penicillin, amoxycillin

If severely affected can use NSAID

378
Q

How is bacterial pneumonia treated in sheep?

A

Vaccination:

  • Ovipast plus - M.haemolytica and B trehalosi, lambs from 3 weeks old
  • Heptavac P - inject pregnant ewes colostral protection for 3 to 4 weeks
379
Q

Describe bibersteinia trehalose in sheep.

A
  • Associated with systemic pasteurellosis (speticaemia)
  • Most common cause of death in lambs age 4-10 months
  • Store lambs often affected, as farmers often only vaccinate replacements
380
Q

What is the causative agent on viral pneumonia in sheep?

381
Q

What is the pathophysiology of viral pneumonia in sheep?

A
  • Asymptomatic excretors
  • Consolidation of the cranio-ventral lung lobes
  • Bronchiolar epithelial hyperplasia
382
Q

Describe the pneumonia caused by adenovirus in sheep.

A
  • Apical and cardiac lobes
  • Consolidation and proliferative bronchiolitis
383
Q

What is the causative agent of atypical pneumonia in sheep?

A

Mycoplasma ovipneumoniae = enzootic pneumonia

384
Q

What are the clinical signs of atypical pneumonia in sheep?

A

Chronic, often subclinical

Housed
Morbidity often 40% within a group
Chronic cough
Reduced weight gains
Hyperpnoea
Mucopurulent nasal discharge

385
Q

How is atypical pneumonia in sheep treated?

A

Antibiotics

Oxytetracycline
Tylosin
Tilmicosin
Lincocin

386
Q

How is atypical pneumonia in sheep controlled?

A

Reduce stocking density
Ensure adequate ventilation
Group according to age and size

387
Q

What are the clinical signs of lungworm in sheep?

A

Coughing
Tachypnoea
Weight loss

388
Q

How is lungworm in sheep diagnosed?

A

Baermann technique (larvae)

389
Q

How is lungworm in sheep treated?

A

Anthelmintics, no vaccine in the UK

390
Q

What is the signalment of laryngeal chondritis in sheep?

A
  • Sporadic
  • In rams, especially in texels
391
Q

What is the epidemiology of laryngeal chondritis in sheep?

A

Hereditary predisposition
Laryngeal oedema
Chronic suppuration of the arytenoid cartilage

392
Q

What are the clinical signs of laryngeal chondritis in sheep?

A

Respiratory stridor
Sudden onset
Inspiratory distress
Upper respiratory tract noise

393
Q

How is laryngeal chondritis in sheep treated?

A

Tracheotomy
Corticosteroids
Antibiotics - prolonged course

394
Q

What are the 3 interacting factors of enzootic pneumonia in calves?

A
  • Stress risk factors
  • Immunity of calves
  • Pathogens able to take advantage of conditions
395
Q

How do calves become susceptible to enzootic pneumonia?

A

Organisms they carry in them already can become pathogenic when the calf becomes stressed and the immune system is affected. Many are part of a commensal flora of the RT so isolating a pathogen does not necessarily mean you have isolated the pathogenic causal organism

396
Q

Why is enzootic pneumonia such a problem?

A
  • Calf lungs relatively inefficient due to their position
  • Problems especially with R apical and cardiac lobes
  • Build-up of fluid and debris
  • Cattle lung small for size of animal
397
Q

What are the risk factors of of calf enzootic pneumonia?

A

Calf source
Colostrum
Housing
Temperature
Damp, humidity, ventilation, dust
Nutrition, water
Fear, anxiety
Castration, dehorning
Management

398
Q

Name the pathogens causing enzootic pneumonia in calves.

A

Para-influenza 3 (PI3)
Bovine Respiratory Syncytial Virus (BRSV)
Bovine Herpes Virus 1 (BHV-1/ IBR)
BVD/MD Virus
Coronavirus
Mycoplasma species
Histophilus somni
Mannheimia haemolytica
Pasteurella multocida

399
Q

What is the pathophysiology of parainfluenza-3 virus?

A
  • Take advantage of intensification
  • Acts via a neuraminidase receptor to penetrate the mucociliary layer
400
Q

What are the vaccines available for parainfluenza virus-3?

A

Live and intranasal vaccines available

401
Q

What are the vaccines available for bovine respiratory syncytial virus?

A
  • Both live and inactivated vaccines available
  • Intranasal vaccine
402
Q

What is the pathophysiology of pasteurella multocida?

A
  • Found in nasopharyngeal
  • Responsible for the permanent damage to lungs (consolidation) that can occur in enzootic pneumonia
  • M. haemolytica – potent leukotoxin, specific for ruminant phagocytes
403
Q

What are the clinical signs of enzootic pneumonia in calves?

A
  • Pulse often >120/min
  • Febrile – a key sign
  • Anorexia variable
  • Coughing a major sign, exercise if necessary, deep cough
  • Nasal discharge clear and then mucopurulent
  • Dull depressed, ears down, may have neck extended
404
Q

What are the possible differential diagnoses of enzootic pneumonia in calves?

A

Calves suddenly brought inside
Exclude Dictyocaulus viviparus
White Muscle Disease
Calf Diphtheria
Salmonellosis
Inhalation or aspiration pneumonia
Congenital heart disease
Acute neonatal respiratory distress
Acute pneumonia
Histophilus somni

405
Q

What is white muscle disease in calves?

A
  • Vitamin E deficiency
  • Can get respiratory involvement
  • Very weak
  • Often frothy and bloody nasal discharge
406
Q

What are the clinical signs of inhalation or aspiration pneumonia in calves?

A

Sudden onset
Very dull
Anorexic
Pyrexic
Pain

407
Q

Distinguish severe and less severe inhalation or aspiration pneumonia in calves.

A

If extensive get necrotising pneumonia and death

If less severe need prompt antibiotic treatment to save

408
Q

What is the presentation of respiratory signs due to acute left sided heart failure in calves?

A
  • Commonest is ventricular septal defect
  • Pulmonary oedema
  • Loud systolic heart murmur
409
Q

What is the pathophysiology of acute neonatal respiratory disease in calves?

A
  • Type II pneumonocytes not producing surfactant
  • Severe dyspnoea soon after birth
  • Harsh adventitious sounds
  • No heart murmur but tachycardia
410
Q

What are the clinical signs of histophilus somni in calves?

A

Febrile
Anorexic
Severe pneumonia
Can die
Often history of carrier animal entering herd

411
Q

How is enzootic calf pneumonia treated in calves?

A
  • First line antibiotics – oxytetracycline, nuflor (florfenicol), resflor (florfenicol and flunixin)
  • NSAIDs
  • Steroids – dexamethasone, with great care as these are so immunosuppressive they will affect calves immune response but not part of primary treatment plan
412
Q

How is enzootic pneumonia in calves prevented?

A
  • Preventing risk factors with housing - ridge ventilation, smoke testing
  • Vaccines
413
Q

What is the presentation of mediastinal masses?

A
  • Displacement of lung tissue and/or pleural effusion
  • Reduced compressibility of the cranial thorax (cats)
414
Q

How are mediastinal masses diagnosed?

A

Thoracocentesis and fluid analysis
FNA cytology or Tru-cut biopsy

415
Q

What are the causes of pneumothorax in small animals?

A

Traumatic
Spontaneously – blebs, bullae, chronic airway disease

416
Q

What is the presentation of pneumothorax upon physical examination?

A

No lung sounds audible
Hyper-resonant percussion

417
Q

What is the presentation of a pleural space disease?

A

Inspiratory dyspnoea
Rapid shallow breathing
No URT noise
Muffled heart and lung sounds
Dullness on percussion

418
Q

What components of BOAS are amenable to surgery?

A

Everted laryngeal saccules
Hyperplastic soft palate
Hyperplastic tonsils
Laryngeal collapse
Stenotic nares

419
Q

How can we rule out a false positive (the larynx does not move but is not paralysed) diagnosis of laryngeal paralysis when performing laryngoscopy?

A

Give an injection of a drug to stimulate breathing – GA may be too heavy

420
Q

What drug can we administer intravenously to stimulate breathing that will move no different to laryngeal movement if a patient has laryngeal paralysis?

A

Doxopram IV

421
Q

Why do we sometimes see paradoxical breathing that can give a false negative diagnosis of laryngeal paralysis when performing laryngoscopy?

A

Due to passive movement of the larynx as the dog breathes out

422
Q

How may a dog with respiratory disease who has collapsed and is cyanotic differ in diagnosis based on whether it is a hot or cold day?

A

If this was in winter instead of hot day, potentially has aspiration pneumonia so would administer antibiotics, but on a hot day is likely to be heat stroke.

423
Q

What is the proper name for the surgical treatment of choice for laryngeal paralysis?

A

Unilateral arytenoid lateralisation /laryngoplasty

Lowest complication and highest success rate

424
Q

What are the 2 most significant factors that influence the prognosis of dogs with laryngeal paralysis?

A

Concurrent oesophageal dysfunction
Which tieback technique is used

425
Q

In what circumstances might the surgery need to be done more urgently?

A

Dyspnoea not alleviated by conservative management and stomach in the thorax (stomach through a small hole will start to produce gas in the thorax so then you have a GDV in the thorax, can’t stabilise because it is just going to get worse.)

426
Q

What is the most common cause of spontaneous pneumothorax in dogs?

A

Lung bullae or bleb

427
Q

How does treatment of traumatic pneumothorax differ from treatment of spontaneous pneumothorax?

A

Treatment of traumatic pneumothorax is usually conservative – unusual to be on 1 it of lung, usually on both, but traumatic rupture may be relatively small so chest drain may be able to restore vacuum.

428
Q

What is the prognosis for dogs being treated for spontaneous pneumothorax?

A

Better with surgical treatment than conservative

429
Q

What are the negative prognostic indicators for dogs with pulmonary neoplasia?

A

Distant metastases
Histopathological grade
Presence of a cough
Presence of local metastases
Tumour sensitivity to radiation

430
Q

What is the most commonly selected surgical approach for a lung lobe resection in patients with pulmonary neoplasia?

A

Lateral thoracotomy

431
Q

How are you most likely to treat a dog with pyothorax and why?

A

Surgical management due to an infection associated with ana underlying foreign body

432
Q

How are you most likely to treat a cat with pyothorax and why?

A

Conservative management due to an infection form an underlying pneumonia or an infection spread to the thorax via the bloodstream

433
Q

What is the most appropriate surgical approach for patients with pyothorax?

A

Sternotomy

434
Q

What are the respiratory problems affecting adult cattle at herd level?

A

Parasitic Bronchitis/Dictyocaulus viviparus)
Shipping Fever
IBR (BHV1)
Bovine Farmers Lung
Fog Fever/acute interstitial pneumonia
Dusty feed
Contagious Bovine Pleuropneumonia

435
Q

What are the respiratory diseases affecting adult cattle on a individual level?

A

Acute exudative pneumonia
Chronic suppurative pneumonia
Diffuse fibrosing alveolitis
Caudal vena cava thrombosis

436
Q

What are the possible other causes of respiratory signs in adult cattle?

A

Milk allergy
Tumours
Pulmonary abscess
Tuberculosis

437
Q

What is the epidemiology of post housing pneumonia/pasteurellosis/shipping fever in adult cattle?

A
  • Especially a problem of weaned suckled calves
  • Peak incidence September-December
  • Most outbreaks within 4 weeks of housing
438
Q

What are the stress factors of post housing pneumonia/pasteurellosis/shipping fever in adult cattle?

A

Weaning
Transport
Mixing
Housing
Diet change

439
Q

What are the bacterial pathogens causing post housing pneumonia in cattle?

A

Mannheimia haemolytica (esp. A1)
Pasteurella multocida
Histophilus somni

440
Q

What is the pathophysiology of mannheimia haemolytica causing post housing pneumonia in cattle?

A
  • Initiating agent of pneumonia pasteurellosis but in young calves it is usually secondary to a viral infection
  • Strains A1 and A6
  • Present in nasal cavity of healthy calves
441
Q

How can mannheimia haemolytica be cultured for diagnosis in adult cattle with post housing pneumonia?

A
  • Tracheobronchial/broncho-alveolar lavage
  • Lung lesions at postmortem examination
  • Tonsillar and nasal isolates (not always pathogenic strains)
  • Isolation difficult from animals treated with antibiotics
  • Serology can be performed – paired samples
442
Q

What are the clinical signs of mannheimia haemolytica post housing pneumonia in cattle?

A

Dull
Anorexic
Tachypnoeic
Pyrexia
Nasal discharge
Adventitious lung sounds and coughing

443
Q

What is indicated in cattle post housing pneumonia by rubbing of pleura on auscultation?

A

Fibrinous pleurisy is present

444
Q

How does pasteurella multocida cause post housing pneumonia in adult cattle?

A

Colonises lesions induced by other agents as a secondary pathogen

445
Q

How can pasteurella mulocida be isolated from cattle with post housing pneumonia?

A

Readily isolated from lung lesions of untreated animals – isolates form URT may not be significant

446
Q

How does histophilus somni cause post housing pneumonia in adult cattle?

A
  • Present in URT and LRT of some healthy cattle
  • Thromboembolic mengioencephalitis – rare in UK
447
Q

How can histophilus somni be isolated from cattle with post housing pneumonia?

A

Isolated from calf pneumonias
Difficult to isolate

448
Q

How can pneumonia pasteurellosis be diagnosed in adult cattle?

A
  • History
  • Clinical Signs
  • Nasopharyngeal swabs – culture, can isolate but may not be the organism causing the disease
  • Broncho-alveolar lavage or tracheal wash – culture, may not be diagnostic
  • Postmortem examination
  • Serology – will give some historical perspective but not what will have caused disease at the time
449
Q

How can pasteurellosis in cattle be controlled?

A
  • Decreased stress, housing design, management
  • Vaccination before they are weaned (pre-conditioning)
450
Q

What is infectious bovine rhinotracheitis?

A

The respiratory form of BHV-1

451
Q

How is infectious bovine rhinotracheitis spread?

A
  • Spread by aerosol route
  • Requires close animal contact, slow spread within a group
452
Q

Where does infectious bovine rhinotracheitis infect cattle?

A

Latent infection in the trigeminal nerve ganglia
Stress leads to recrudescence

453
Q

What are the clinical signs of infectious bovine rhinotracheitis?

A

Cough due to inflammation
Decreased appetite = decreased growth rate
Dull
Pyrexia
Nasal discharge
Necrotic plaques on mucosa = halitosis
Ocular discharge/conjunctivitis
Retropharyngeal and submandibular lymphadenopathy
Decreased milk yield
Drooling saliva
Upper airway noise
Rhinitis
Pharyngitis
Abortion

454
Q

How is infectious bovine rhinotracheitis treated?

A
  • Antibiotics to control secondary infection
  • Vaccination in outbreak
  • Never give corticosteroids to not
    immunosuppress these cattle
455
Q

How is infectious bovine rhinotracheitis prevented?

A

Management
Closed herd

456
Q

Describe the live intranasal vaccines used to control infectious bovine rhinotracheitis.

A
  • Live, temperature sensitive
  • Rapid protection within 48-96 hours
  • Vaccine virus spread
  • Useful even in the face of an outbreak
  • Live intranasal vaccines produced nasal gamma-IFN
457
Q

Describe the marker vaccines of infectious bovine rinotracheitis?

A

Glycoprotein-E-deletion, so are able to distinguish between animals that have been vaccinated and have antibody and animals that have any other type of antibody.

458
Q

Why are cattle vaccinated for infectious bovine rhinotracheitis?

A

Improve immunity
Reduce shedding

459
Q

What are the differential diagnoses if infectious bovine rhinotracheitis?

A
  • Photosensitisation
  • Infectious bovine keratoconjunctivitis
  • FMD
  • Mucosal disease
460
Q

How is infectious bovine rhinotracheitis diagnosed?

A

Clinical picture
Virus isolation using fluorescent antibodies
Antibody titre

461
Q

How is bovine herpesvirus-1 spread?

A
  • Transmission via aerosols
  • Spread within the animal via cell-associated viraemia
462
Q

Where does bovine herpesvirus-1 infect?

A

Latent infection of trigeminal (and sciatic) ganglia

463
Q

What is the pathophysiology of bovine herpesvirus-1?

A
  • Focal areas of epithelial cell necrosis causes reduced ciliary clearance
  • Viral infection causes increase in divalent cations, which favour colonisation of the lungs by bacteria
  • Impaired macrophage, neutrophil and lymphocyte function
464
Q

What is the clinical signs of bovine herpesvirus-1?

A

Inflamed nasal mucosa

465
Q

How is bovine herpesirus-1 diagnosed?

A
  • Serology – paired sample
  • Immunofluorescent antibody staining
  • Virus isolation from nasal/nasopharyngeal, ocular/conjunctival and bronchoalveolar lavage swabs
  • Immunohistochemistry
  • PCR
  • ELISA on bulk milk
466
Q

What is bovine farmer’s lung?

A
  • Extrinsic allergic alveolitis
  • An allergic disease of cattle and man
  • Hypersensitivity to fungal spores and bacterial antigens due to exposure of moudly food
467
Q

What are the clinical signs of chronic bovine farmer’s lung?

A

Frequent coughing
Hyperpnoea
Reduced milk yield
Weight loss
Cow still bright
Exercise intolerance
May result in cor pulmonale or diffuse fibrosing alveolitis

468
Q

What are the clinical signs of acute bovine farmer’s lung?

A

Sudden onset
Dyspnoea
Tachypnoea
Milk yield disappears
Anorexic

469
Q

How is bovine farmer’s lung diagnosed?

A

History
Clinical picture
Specific antibodies to Saccharopolyspora

470
Q

How is bovine farmer’s lung treated?

A

Removing source (stop feeding hay or wet straw and move animals onto silage)

Could treat acute cases with corticosteroids to dampen down the immune response but this is likely to cause abortion

471
Q

What is the pathophysiology of fog fever in cattle?

A

Congestion, oedema, interstitial emphysema and epithelialisation of alveoli

Naturally occurring amino acid in pasture converted to pneumotoxin: L-tryptophan > indole acetic acid > 3-methyl indole, which causes a toxic affect that damages the lung.

472
Q

What are the clinical signs in severe and mild cases of fog fever in cattle?

A

Severe:
- Acute distress
- Gross dyspnoea
- Respiratory grunt
- Salivation, often froth at the mouth

Mild - dull, some tachypnoea

473
Q

How is fog fever in cattle treated?

A

Treatment empirical with NSAIDs

Move herd when you can and carefully and restrict grazing to reduce their intake of L-tryptophan

474
Q

What is chronic suppurative pneumonia in adult cattle?

A

Many conditions including chronic bronchopneumonia, bronchiectasis, multiple lung abscessation. Common end stage condition in a small number of animals

475
Q

What are the clinical signs of chronic suppurative pneumonia in cattle?

A

Weight loss/poor growth
Cough
Variable temperature, intermittently febrile
Variable adventitious lung sounds especially cranioventral
Thoracic pain
Halitosis if necrotising

476
Q

How can chronic suppurative pneumonia in cattle be treated?

A

No long term response to treatment
Best culled rather than treated

477
Q

What is the aetiology of diffuse fibrosing alveolitis?

A

Aetiology unknown, but probably repeated allergic reaction

478
Q

What are the clinical signs of diffuse fibrosing alveolitis?

A

Persistent cough
Tachypnoea
Hyperpnoea
Exercise intolerance
Weight loss
Bright thin cows
Widespread squeaks/crackles often over whole of both lung fields
Decreased resonance

Increased lung weight at PME

479
Q

What may be sequalae to diffuse fibrosing alveolitis?

A

May lead to Cor pulmonale and develop right sided heart failure

480
Q

How is diffuse fibrosing alveolitis treated?

A

No treated

481
Q

What does bilateral nasal bleeding indicate?

A

Blood is coming up form the trachea and not the nasal cavities

482
Q

What is the chronic presentation of pulmonary thromboembolism from the caudal vena cava?

A

Cough
Weight loss over a few weeks
Tachypnoeic
Shallow breathing
Coughing
Thoracic pain
Hepatomegaly in 50% of cases

483
Q

Explain the pathophysiology of pulmonary thromboembolism from the caudal vena cava.

A
  1. Young adults being fed a high concentrate diet
  2. Ruminal acidosis resulting in rumenitis/damage to the wall of the rumen
  3. Bacteria get in to the hepatic portal vein and cause abscesses in the liver
  4. Septic thrombus in caudal vena cava causes septic thromboembolus in the pulmonary arteries and lung
  5. Aabscesses causing an embolic suppurative pneumonia as they spread through the lung
  6. If one of these pulmonary abscesses breaks through into the airway, form an aneurism
  7. If this breaks into the airway and ruptures, you get acute haemorrhage and haemoptysis
  8. This will be arterial oxygenated blood that will be very fresh and red.
484
Q

How is pulmonary thromboembolism from the caudal vena cava treated?

A

No treatment invariably fatal – cull

485
Q

What is contagious bovine pleuropneumonia?

A

Exotic notifiable disease
Differential for pneumonia pasteurellosis