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Y4 SA - Respiratory > Coughing in small animals > Flashcards

Coughing in small animals Flashcards

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1
Q

Principle presenting signs of pts with resp tract disease

A

change in rate or character of respiration (dyspnoea, tachypnoea, hyperpnoea, orthopnoea), coughing

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2
Q

Other signs of respiratory tract disease

A

sneezing/nasal discharge, resp noise, cyanosis, weight loss, collapse/syncope, changes in voice (laryngeal lesions), exercise interolance, facial deformity

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3
Q

Stertor - location

A

typically nasopharyngeal

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4
Q

Stridor - location

A

typically URT, laryngeal

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5
Q

What is a cough?

A

closing of the airway, building up pressure in the thorax and suddenly releasing it - so things in the airway are expelled. only stimulated if receptors are stimulated. receptors end in the terminal bronchioles - no cough receptors in the alveoli

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6
Q

Possible causes of acute coughing

A

tracheobronchitis (KC), irritation by smoke/dust/chemical/meds, airway FB (may have been there some time), pulmonary haemorrhage (often with dyspnoea), acute pneumonia (e.g. inhalation, often with dyspnoea), acute oedema (often with dyspnoea, cariogenic/non-cardiogenic), airway trauma

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7
Q

Infectious tracheobronchitis - what is it? causes?

A

infection disease of canine URT. causes include - canine parainfluenza virus, canine adenovirus (2), bordetella bronchiseptica.

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8
Q

Infectious tracheobronchitis vaccines

A

bordetella (live intranasal or inactivate subcut injection), canine parainfluenza and adenovirus (2) (live injection)

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9
Q

Treatment for infectious tracheobronchitis

A

spontaneous recovery 7-10d.
systemic antibacterials often given if - pyrexic, systemically ill, mucopurulent nasal discharge

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10
Q

Anti-tussive use

A

Only want to suppress a cough if the animal has a structural disease of the airway, otherwise we want it - want to expel whatever is in there.

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11
Q

Anti-tussive examples

A

opiates are pretty effective
butorphanol, codeine

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12
Q

Acute/subacute/chronic - time frames

A

acute <1w
subacute <1m
chronic >1m

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13
Q

The chronically coughing dog - causes

A

chronic bronchitis/bronchiectasis, LSHF, Osleurs/Aelurostrongylus infestation, tracheal collapse, airway FB, bronchopneumonia, pulmonary neoplasia (primary or 2ndary), extra-luminal mass lesions (thyroid, abscess, lymphoma), eosinophilic disease (EBP/PIE/allergic airway disease), (pulmonary ‘fibrosis’)

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14
Q

What animals is chronic bronchitis common in?

A

small/toy breed dogs and older animals

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15
Q

What to do with a coughing animal?

A

Radiograph or CT

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16
Q

Canine chronic bronchitis - what is it? what is it characterised by?

A

daily coughing for >2m. characterised by - neutrophilic/eosinophilic infiltration of mucosa and thickening of smooth muscle later + fibrosis + scarring of lamina propria, increased goblet and glandular cell size and number, oxidative injury and inflammatory products damage cells and lead to mucus hyper secretion, loss of ciliated epithelial cells and failure of mucociliary clearance and debris. thick mucus pools in the airways when sleeping so get a cough in the morning/ when wake up. cough receptors are stimulated all the time. The combination of all this leads to thickening of bronchial tissue, overproduction of airway mucus and narrowing of the airways (particularly terminal bronchi)

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17
Q

Canine chronic bronchitis clinical signs

A

wheezing and productive coughing (usually clear/frothy, yellow suggests infection), worse on excitement, often externally well and obese, tracheal pinch positive

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18
Q

Canine chronic bronchitis complications

A

Common - dilation of the airways, airway collapse due to wall weakness (bronchomalacia) - these then cause the airways to constantly be filled with mucus

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19
Q

Aetiology of canine chronic bronchitis

A

may be seen 2ndary to underlying conditions - tracheal collapse, chronic barking, FB, previous infections or inhalant toxins, environmental toxins, chronic smoke inhalation/noxious gas.
cause usually unknown

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20
Q

Chronic canine bronchitis diagnosis

A

typical history and physical findings (often exaggerated sinus arrhythmia due to increased respiratory effort), thoracic radiographs (increased bronchial lung pattern), bronchoscopy and BAL (can often see the airways collapsing - v poor prognosis)

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21
Q

Canine chronic bronchitis BAL results typically show…

A

increased mucus, non-degenerate neutrophils, eosinophils and macrophages, Cushmann’s spirals (airway mucus casts), presence of bacteria/particular matter are less common and if present would suggest underlying cause present

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22
Q

Management of chronic bronchitis

A

general management - weight control, harness vs collar/lead, avoid irritants / smoking environment.
mucus is easier to shift if hydrated - avoid dry environments, steam in the bathroom, chest coupage helps break up the mucus.
glucocorticoids (oral and inhaled), antimicrobials based on evidence of need, don’t use anti-tussives unless absolutely necessary, bronchodilator? (damaged airways may not respond to bronchodilators - so they don’t do much unless bronchoconstriction is part of the problem)

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23
Q

Problems with diagnosing bacterial infection

A

URT and large airways aren’t sterile, vet med BAL often not done until after antibiotic therapy hasn’t resolved signs, antibiotics persist in lung in sufficient quantities for at least 7d, risk of contamination from URT

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24
Q

Treatments for lower airway disease

A

inhaled meds (corticosteroids, bronchodilators, nebulisers), oral therapy - anti-inflammatories (corticosteroids, NSAIDs, anti-leukotrienes), bronchodilators (terbutaline, theophylline), antibiotics, anthelminthics, mucolytics (N-acetyl cysteine (NAC))

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25
How to deliver inhaled meds
mask, space device/chamber, metered dose inhaler (MDI). inhalers are more useful in cats than dogs, if you can get the cat to tolerate it
26
Value of inhaled meds
management of chronic airway disease, minimal absorption into systemic circulation (less systemic side effects, esp with steroids), faster onset of action
27
Drugs that can be delivered by inhalation
Beta 2 agonist (salbutamol, salmeterol [longer acting med]), corticosteroids (fluticasone, beclomethasone), inhibition of mast cell degranulation (unclear efficacy in dogs and cats with airway disease, cromolyn sodium/sodium cromoglicate
28
Salbutamol (Ventolin)
beta 2 agonist, fast onset of action, lasts >3h, cleared renally and metabolism, 10-20% inhaled reaches lower airways
29
Side effects of Salbutamol
tachycardia, arrhythmias, tremors
30
Inhaled glucocorticoids
e.g. Fluticasone propinate (Flixotide in UK), slowly absorbed from lung (long dwell time in lungs), rapid 1st metabolism in liver (less systemic side effects), long T1/2, least bioavailable
31
Side effects of inhaled glucocorticoids
oral infections (e.g. candidiasis), coughing, wheezing
32
Why are inhaled medications valuable?
reduces systemic exposure to GC, dose of GC required is lower, reduced systemic side effects, effective in acute situations - e.g. acute resp distress (beta agonists)
33
Disadvantages of inhaled medications
expensive, time consuming, owner and pt compliance
34
What are the benefits of glucocorticoids on the airway?
bronchodilatory, anti-inflammatory (inhibit both prostaglandin and leukotriene synthesis), potentiate beta-2 adrenergic activity, reduce leukocyte accumulation, reverse increased vascular permeability, alter macrophage function, inhibit fibroblast growth, modulate the immune system
35
What are the benefits of bronchodilators on the airway?
reduce spasm of lower airways, decrease intra-thoracic pressures, decrease tendency of larger airways to collapse, improve diaphragmatic function, improves mucociliary clearance, inhibit mast cell degranulation (reduced release of mediators of bronchoconstriction), possible additional ways that signs are improved - improves pulmonary circulation, improves cardiac function, reducing respiratory effort
36
What bronchodilators are available?
Theophylline, Terbutaline, Etamiphylline camsilate
37
Do most chronic bronchitis cases have a bacterial infection as a causal agent?
No, but if there is secondary infection it requires immediate therapy due to compromised respiratory mechanisms
38
When are antibiotics indicated?
If C&ST + or if intracellular bacteria is seen on BAL cytology
39
Risk of using fluoroquinolone with theophylline
they inhibit metabolism which increases the concentration of theophylline - toxicity risk
40
Prognosis for chronic canine bronchitis?
Long term control is possible but no cure. Dog will always cough - due to irreversible damage to the airways. Major goal is to prevent long term sequelae which includes secondary pneumonia, bronchiectasis/bronchomalacia, emphysema
41
Synonyms for feline bronchial disease
feline asthma, feline allergic airway dz
42
Feline bronchial disease
generally considered to be a type I hypersensitivity condition to inhaled allergens
43
Breed predisposition to feline bronchial disease
Siamese
44
Underlying factors for feline bronchial disease
smoke, feathers, aerosol inhalation, dust, cat litters. seasonality often seen
45
What is the primary problem in acute feline asthma?
Bronchospasms
46
Bacterial bronchopneumonia common pathogens
E.coli, Klebsiella, Pasteurella, staphs (coag positive), streps, mycoplasma, B bronchiseptica. Primary infections are most common with primary pathogens - B bronchiseptica, streptococcus equi subspecies zooepidemicus, Mycobacteria. often mixed infections, obligate anaerobes may account for up to 25% pathogens
47
Are primary infections in otherwise healthy dogs and cats with bacterial bronchopneumonia common?
No - if present you should search for underlying cause
48
Streptococcus Zooepidemicus causing bacterial bronchopneumonia
Has been linked with the outbreak of acute fatal hemorrhagic pneumonia in dogs in several countries. highly contagious sudden onset.
49
Clinical signs of bacterial bronchopneumonia caused by S equi subs. Zooepidemicus
pyrexia, dyspnoea, hemorrhagic nasal discharge and haemopytsis. causes a severe fibrino-suppurative necrotising hemorrhagic pneumonia
50
Factors predisposing to bronchopneumonia
debilitation, prolonged recumbency (e.g. with hospitalisation), systemic immunosuppression (HAC, chemo, red's), immunodeficiency states (Weimaraner's, CKCS), defective respiratory defences, damaged respiratory epithelium, aspiration, airway obstruction, systemic sepsis, bronchiectasis
51
Clinical signs of bacterial bronchopneumonia
occasionally only minor clinical signs, signs often relate to extent of pneumonia. cough, resp distress (if lots of the lung is involved), exercise intolerance. more severe infections may produce hyperthermia and cyanosis. anorexia and lethargy are common signs. increased or decreased lung sounds may be present, may include crackles
52
Diagnosis of bacterial bronchopneumonia
CBC, biochem, UA, faecal, thoracic radiographs, TTW/BAL (culture and cytology on fluid
53
Pattern on thoracic radiograph
alveolar with variable distribution. aspiration - cranial-ventral
54
Treatment of bacterial bronchopneumonia
ABs (broad spec?), supplemental humidified oxygen, IVFT, anti-inflammatories, bronchodilators, mucolytics, physio, nebulisation, surgery
55
Bronchial FB clinical signs
sudden onset of coughing and gagging, history of signs after exercising in agricultural fields, halitosis may be present and progressive, may see weight loss if infection associated with FB becomes significant, more substantial respiratory signs may suggest progression to pleural disease
56
What animals are more likely to get bronchial FBs?
working dogs or those living in rural environments
57
Can you get a secondary pyothorax with a bronchial FB?
yes - if it penetrates the airway and gets into the pleural space
58
Diagnosis for bronchial FB
thoracic radiographs - fully evaluate for signs of pleural involvement, determine if there's suggestion of local lobar involvement or disease seems more diffuse. bronchoscopy - BAL and culture for specific AB therapy, enables visualisation and retrieval of the object
59
Where do most bronchial FBs go?
down the right mainstem bronchus (more straight on than the left), so go into the right diaphragmatic lobe
60
Primary clinical sign for primary pulmonary neoplasia
cough (non-productive), exercise intolerance
61
Where do primary pulmonary neoplasms tend to arise from?
rapidly overlapping cells - the lining of the airways
62
Primary clinical sign of secondary pulmonary neoplasia
breathlessness (it's an interstitial disease)
63
Cancers of the lung in dogs and cats
primary lung tumours are very rare cf humans (1%), dogs>cats, mets more common, weak links with passive smoking
64
Common pulmonary mets in dogs and cats
oral melanoma, thyroid Ca, osteosarcoma, haemangiosarcoma, mammary Ca
65
Primary lung cancer age
median age 11y
66
What type of cancer is commonly seen in primary lung disease
generally carcinomas, classified by location, often hard to tell exact origin. can also see pulmonary lymphoma, pulmonary lymphomatoid granulomatosis, malignant histiocytosis, rare to see mesenchymal tumours in the lung
67
What percentage of primary lung cancers are solitary?
>50%
68
What lung lobe is commonly affected in primary lung cancer?
right caudal lobe
69
Rare paraneoplastic disease of primary lung cancer
hypertrophic osteopathy
70
prognosis of primary lung disease
depends on size, location (re resectability) and spread - adjunctive chemo little use?, best case scenario 50% alive at 1y. adenocarcinoma > SCC survival
71
Direct airway sampling
BAL rarely helpful (neoplastic cells don't readily exfoliate). transthoracic FNA
72
Transthoracic FNA
US guidance in pts with discrete lesions, can also use fluoroscopic or CT guidance, lesions >1cm
73
contraindications of transthoracic FNA
pulmonary bullae or cysts, coagulopathies, PH, pre-existing pneumothorax, suspected infectious process
74
potential complications of transthoracic FNA
pneumothorax, emphysema, bleeding, implantation, seeding of neoplasia
75
Primary CAR parasites
most lungworms are metastrongyloides - Oslerus oiler, Filaroides spp, Crenosoma vulpis, Aelustrongylus abstrusus, Angiostrongylus vasorum Others from trichuroidae - Capilaria aerophila
76
O. osleri - lifecycle
PPP 10-18w, nodules in which worms live appear around 2 months from infection - immune response to adults in trachea and bronchus causes the worm to encapsulate, rare now
77
Clinical signs of O. osleri
may include chronic cough, often dry rasping cough, particularly after exercise, more notable in young dogs: 6-12m
78
Diagnosis of parasites/O. osleri
characteristic nodules (1-1.5cm) can be seen via bronchoscopy particularly at the tracheal bifurcation - most reliable method. small nodules contain immature worms, large nodules often contain tight coils of adult. sampling of tracheal mucus to identify eggs and larvae (characteristically coiled in appearance). L1 in faeces or BAL fluid (+ eosinophils) - faecal L1 counts less reliable - variable shedding.
79
Tx of O. osleri
can be hard to treat, nodules remain, may even calcify and cough persists. fenbendazole - 50mg/kg SID 10d, often need to repeat 4w later
80
Filaroides hirthi lifecycle
same as O.osleri
81
F. hirthi infection
generally asymptomatic, worms live in alveoli
82
Diagnosis of F. hirthi
usually found at PM, radiographs often show diffuse broncho-interstitial patterns. rarely alveolar pattern
83
Tx of F. hirthi
rarely indicated as not pathogenic. when indicated treat as O. osleri
84
Crenosoma vulpis
fox/wolf lungworm that can live in the dog
85
What does C. vulpis cause
chronic bronchopulmonary dz and productive cough
86
Lifecycle of C. vulpis
indirect- slugs/snails as intermediate hosts. PPP = 3w
87
Seasonality of C. vulpis
highest incidence in autumn due to acquisition of infections in summer - due to fluctuations in intermediate snail host
88
Where do adult C. vulpis worms live and what does this cause?
adults live in bronchi and bronchioles where they cause bronchitis - no nodules
89
How to treat C. vulpis
As O. osleri - often more rapid response to tx than O. osleri
90
Investigation of airway dz summary
radiograph/CT, endoscopy, TTW, tracheal wash, BAL, haem, faecal exam if suspect parasites

Y4 SA - Respiratory (12 decks)

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