Tracheal & Bronchial Disorders Flashcards

1
Q

What is the most common sign of tracheobronchial disease? What else is seen?

A

cough (possibly productive)

  • retch/gag
  • increased respiratory effort/dyspnea
  • wheezing
  • inspiratory sounds
  • tachypnea
  • cyanosis
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2
Q

What 2 conditions should be considered if there is a patient with chronic cough?

A
  1. structural disease of the airways, causing weakening of the cartilaginous support
  2. chronic inflammation of airways, resulting in mucus accumulation and secondary bacterial infection
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3
Q

How do the 3 regions of the lower respiratory system indicate tracheobronchial disease?

A
  1. LARYNX = hoarse bark, gagging, inspiratory effort
  2. TRACHEA = cough and respiratory distress
  3. BRONCHI = cough and respiratory distress
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4
Q

What is the general rule out list for patients with a cough?

A
  • Cardiovascular - DOGS with enlarged LA
  • Allergic - asthma, eosinophilic bronchopneumopathy
  • Trauma - FB, collapsing trachea
  • Neoplasia
  • Inflammatory/Infectious - pharyngitis, bronchitis, pulmonary fibrosis, kennel cough, pneumonia, abscess
  • Parasites - lung worms, heart worm, migrating GI parasites
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5
Q

What conditions must be considered in a clinical patient with cough?

A

cardiogenic disorders

  • physical exam (murmur), chest radiographs
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6
Q

What are 4 causes of cough when heart disease is present? What are some signs seen on a radiograph?

A
  1. heart failure leading to pulmonary edema
  2. left atrial enlargement causes pressure on the airways
  3. heartworm disease
  4. heart base tumor
  • pulmonary edema
  • enlarged LA
  • air in stomach from swallowing air
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7
Q

What are some non-cardiogenic causes of cough in clinical patients?

A
  • tracheal collapse
  • hypoplastic trachea
  • infectious tracheobronchitis
  • perihilar lymphadenopathy
  • lower airways and pulmonary parenchyma pneumonia
  • cancer
  • environmental contaminants
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8
Q

What are the 2 major factors that contribute to canine infectious respiratory disease (kennel cough)?

A
  1. HOST FACTORS - stress, immune status, previous exposure
  2. ENVIRONMENT - overcrowding, poor ventilation
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9
Q

In what dogs is kennel cough most common? What plays a huge role in its spread?

A

PUPPIES from breeders, pet stores, and boarding facilities

fomites —> very contagious and spreads quickly at dog shows, kennels, shelters, clinics, and pet stores

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10
Q

What are the uncomplicated and complicated versions of kennel cough?

A

UNCOMPLICATED = not “sick”, only involving the upper airways eliciting a dry cough on tracheal palpation, serous oculonasal discharge, gagging, retching (can evolve!)

COMPLICATED = “sick”, involving both upper and lower airways with a moist cough and more mucopurulent oculonasal discharge (can develop bronchopneumonia)

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11
Q

In what 3 situations is diagnostic testing recommended in patients with kennel cough?

A
  1. patients do not respond to supportive care
  2. signs/evidence of systemic disease
  3. outbreak

usually a presumptive diagnosis is enough and clinically healthy dogs can harbor CIRD pathogens

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12
Q

What are the 2 most common viral causes of kennel cough? What other viruses can contribute?

A
  1. canine parainfluenza virus (CPIV)
  2. canine respiratory coronavirus (CRCoV) - no vaccine
  • canine adenovirus 2
  • canine herpesvirus 1
  • canine distemper virus (more serious)
  • canine influenza virus
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13
Q

What is the most common bacteria that causes kennel cough? How does it cause disease? What are some other bacteria that can contribute?

A

Bordetella bronchiseptica - attaches to cilia of bronchial epithelium and interferes with motility, leading to mucus accumulation and inflammation

  • Mycoplasma cynos
  • Streptococcus equi subsp. zooepidemicus
  • secondary invaders
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14
Q

In what way is Mycoplasma cynos unique? How does it contribute to kennel cough?

A

lacks a cell wall and is the smallest living organism capable of independent existence —> penicillins, like Clavamox, will NOT work

significantly associated with increased severity of respiratory disease, but its role is not well understood

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15
Q

What 5 diagnostics should be evaluated in the complicated form of kennel cough?

A
  1. hemogram: leukocytosis with left shift
  2. thoracic rads: bronchopneumonia signs
  3. tracheal wash cytology and culture
  4. PCR panels (most causes of kennel cough are part of the normal flora…)
  5. fecal float or Baermann for lungworms
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16
Q

What are the 3 major treatments for the uncomplicated form of kennel cough? What is important to note?

A
  1. restrict exercise
  2. isolate
  3. Doxyxyxline if Bordetella is suspected

usually resolves within 2 weeks, but the cough can linger

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17
Q

What 3 systemic antibiotics are recommended for complicated kennel cough? What is not recommended?

A
  1. Doxyxycline
  2. Azithromycin
  3. Enrofloxacin

Penicillin —> poor levels in respiratory secretions

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18
Q

What 4 cough suppressants are recommended for complicated kennel cough? When is their use contraindicated?

A
  1. Butorphanol
  2. Hydrocodone
  3. Codeine derivatives
  4. Dextromethorphan

if bacterial pneumonia is present

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19
Q

What is the best way to diagnose kennel cough?

A

respiratory PCR done simultaneously with a culture —-> gives an idea of what components are involved and culture backs up diagnosis for bacterial components

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20
Q

What are the 2 options for vaccines against kennel cough? How else can infection be prevented?

A
  1. parenteral CAV2 and CPIV vaccine - blocked by maternal antibodies —> repeated every 3-4 weeks until 16 weeks
  2. intranasal CPIV and Bordetella vaccine - not blocked by maternal antibodies and protects within 4-14 days (recommended for high-risk dogs) —> infer superficial antibodies and help prevent disease
  • sanitation with Clorox diluted 1:32
  • proper ventilation in kennels
  • quarantine
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21
Q

What is the most significant canine influenza virus strain in the US? What are the most significant clinical signs? How is it spread? Diagnosed?

A

H3N2 (also H3N8)

coughing and fever that can progress to worsening disease

direct contact with respiratory secretions/fomites

PCR samples within 72 hrs, acute and convalescent titers, viral isolation

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22
Q

In what dogs is an influenza vaccine most important? How does the vaccine help?

A

dogs that attend canine day care centers, travel to dog shows, go to kennels, or go to dog parks

decreases the severity of clinical disease and viral shedding, but does not prevent infection (herd immunity!!)

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23
Q

Why must respiratory PCRs be used carefully for diagnosing kennel cough?

A

NOT PERFECT —> positive results do not imply causation —> modified live vaccine will show positive, some microorganisms are part of the normal flora, co-infection is common

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24
Q

How can we tell if antibiotics are necessary for treating kennel cough?

A

a transtracheal wash is performed and the fluid is cultured and sent out for PCR

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25
Q

What tracheal worm is commonly found in younger dogs in kennels? How do they affect the trachea?

A

Oserlus osleri

larvae are ingested, molt in the small bowel, migrate to lungs, bronchi, and trachea forming cream colored nodules

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26
Q

In what 4 ways can Oserlus osleri infections be diagnosed? What are the most common signs?

A
  1. tracheal mass on x-ray shows nodules on the carina
  2. mass see with bronchoscopy and sampled
  3. fecal or Baermann (can be negative due to intermittent shedding)
  4. cytology of tracheal wash reveals ova or larvae

coughing, wheezing, dyspnea

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27
Q

How is a Oserlus osleri infection treated?

A

Ivermectin or Fenbendazole

(preventatives important!)

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28
Q

In what dogs is tracheomalacia (collapsing trachea) most common? What are the most common clinical findings?

A

toy or small breeds (often obese)

  • history of dry or worsening cough (goose honking)
  • cough worsens with excitement, exercise, eating, or heat
  • cough elicited by tracheal palpation
  • retching of clear secretions
  • episodes of cyanosis or collapse
  • mitral valve disease can exacerbate signs
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29
Q

What is tracheomalacia (collapsing trachea)? What is the most common cause?

A

narrowing of the tracheal lumen, resulting from weakening of the cartilaginous rings, redundancy of the dorsal tracheal membrane, or both

reduction in chondrocytes, glycosaminoglycans, and chondroitin sulfate in the tracheal rings

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30
Q

What dog breeds are most commonly affected by primary tracheomalacia? What causes primary tracheomalacia?

A

Pomeranians, mini and toy Poodles, Yorkies, Chihuahuas, Pugs

chronic inflammation, trauma, external pressure

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31
Q

What are the most common triggers of tracheomalacia (collapsing trachea)?

A
  • obesity
  • cardiomegaly
  • inhalation of irritants and allergens
  • periodontal disease
  • respiratory infections
  • endotracheal intubation
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32
Q

Where is tracheomalacia most often more pronounced? Why is it considered dynamic?

A

cervicothoracic junction

  • CERVICAL trachea collapses during INSPIRATION
  • THORACIC trachea collapses during EXPIRATION
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33
Q

What 3 conditions are commonly concurrent in patients with tracheomalacia?

A
  1. bronchomalacia
  2. airway infection - inflammation of airway mucosa and impaired function of the mucociliary apparatus
  3. hepatomegaly and abnormal liver function tests - hypoxia causes liver disease
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34
Q

What is the gold standard for diagnosing tracheomalacia? What other 2 diagnostics can be done?

A

bronchoscopy —> assesses dynamic change, can look for concurrent disease

  1. thoracic/cervical x-rays - during inspiration and expiration
  2. fluoroscopy
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35
Q

What sedation and cough suppressants are recommended for emergency tracheomalacia treatment? Why are corticosteroids used? What else needs to be done?

A

Acepromazine, Butorphanol, Hydromorphone, Diazepam, Gabapentin

injectible Butorphanol, oral Hydrocodone

single dose is used to decrease inflammation

get into an oxygen-rich environment - O2 cage, nasal catheterization, intubation

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36
Q

What is recommended for chronic management of Grade I or II tracheomalacia? What is important to note?

A
  • weight loss
  • thoracic harness
  • avoid excitement and sedate if necessary
  • avoid smoke, dust, pollen, carpet cleaners, and airway irritats
  • avoid heat and humidity

this is likely a progressive disease that can worsen over time and affect lower airways and bronchi

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37
Q

What 4 cough suppressants are recommended for chronic management of tracheomalacia? What 2 corticosteroid?

A
  1. Butorphanol
  2. Hydrocodone
  3. Cerenia
  4. Lomotil (diphenoxylate)

Prednisone and Fluticasone —> taper over 2-4 weeks

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38
Q

Why are bronchodilators indicated for tracheomalacia? What are 3 examples?

A

help reduce clinical signs in patients with intrathoracic tracheal collapse by dilating small airways and reducing the pressure gradient

  1. extended release Theophylline
  2. Terbutaline
  3. Albuterol
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39
Q

When is surgical intervention recommended for tracheomalacia?

A

30% will not respond to medical management and still experience cyanosis, dyspnea, or syncope; or those with higher grades

  • endoluminal stents are recommended, but a last-ditch effort
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40
Q

Other than tracheomalacia, what are some other causes of a tracheal cough?

A
  • intrathoracic mass/tumor/granuloma pressing on the trachea
  • tracheal injury
  • tracheal foreign body

honking cough = chest rads

41
Q

What is chronic canine bronchitis? What does this typically lead to?

A

chronic cough for at least 2 months with no other known cause and exclusion of other chronic cardiopulmonary diseases (+/- excessive mucus)

chronic obstructive pulmonary disease (COPD)

42
Q

What is the pathophysiology of chronic canine bronchitis?

A
  • inflammatory changes in the bronchial mucosa, increased mucous production, and bronchial wall thickening can result in progressive bronchomalacia
  • poor airflow dynamics and worsened inflammation cause a cough
  • cough continues the cycle of inflammation
43
Q

What is the most common signalment for chronic canine bronchitis? What are the most common signs?

A

6+ y/o small breeds, often obese

  • chronic cough often with a gag (loud and harsh, dry to moderately productive)
  • BAR
  • often have periodontal disease
  • audible wheezes
  • exercise intolerance
  • response to previous medications
  • SEVERE: dyspnea, syncope

(usually come into the office due to exacerbation of signs)

44
Q

What are the 3 most common things heard of auscultation in patients with canine chronic bronchitis? What must be excluded first?

A
  1. end expiratory wheezes
  2. crackles on inspiration and expiration
  3. concurrent tracheal collapse

cardiac causes

45
Q

What are the 4 most common concurrent cardiopulmonary diseases associated with chronic canine bronchitis?

A
  1. tracheobronchomalacia
  2. left atrial enlargement
  3. heart failure
  4. right heart enlargement
46
Q

In what 4 ways can canine chronic bronchitis be diagnosed?

A

DIAGNOSIS OF EXCLUSION —> use labwork to rule out other differentials

  1. thoracic radiographs - bronchial pattern with increased interstitial markings
  2. thoracic CT
  3. transtrracheal wash - non-degenerate neutrophils, some eosinophils, excessive mucus (Curschmann spirals), epithelial hyperplasia, increased goblet cells
  4. bronchoscopic exam - thickened and roughened mucousa, mucus, hyperemia, bronchial dilation
47
Q

What is seen in thoracic x-rays in patients with canine chronic bronchitis?

A

inflammation around airways —> donuts

48
Q

What are the 3 most common complications of canine chronic bronchitis? What 2 conditions are commonly concurrent?

A
  1. bacterial/mycoplasma infections
  2. pulmonary hypertension
  3. bronchiectasis - permanent dilation of airways

tracheal collapse or mitral valve insufficiency

49
Q

How is canine chronic bronchitis treated?

A
  • eliminate irritants
  • improve indoor air quality
  • maintain airway hydration for mucociliary clearance with systemic hydration or vaporizers/nebulizers
  • weight control
  • manage stress/excitement with sedation
  • harness
  • good dental hygiene
50
Q

What is the major cornerstone for treating chronic bronchitis in dogs? Why must they be carefully used?

A

glucocorticoids/anti-inflammatories —> Prednisone/Prednisolone to control signs and development

can cause hyperadrenocorticism (Cushing’s)

51
Q

What drug is recommended in multidose inhalers for controlling canine chronic bronchitis? In what 2 situations is this used?

A

Fluticasone (flovent)

  1. after confirming efficacy of systemic steroids
  2. in patients when prednisone use in contraindicated
52
Q

What bronchodilator is commonly used in dogs with chronic bronchitis? How does it work?

A

Theophylline

can improve mucociliary clearance, decrease muscle fatigue in respiratory muscles, and inhibit the release of mast cell mediators of inflammation, but is not strong enough by itself

53
Q

What drugs does Theophylline commonly interact with? What are 4 possible adverse reactions?

A

fluoroquinolones

  1. GI signs
  2. cardiac arrhythmias
  3. nervousness
  4. seizures
54
Q

What sympathomimetic drugs are used for canine chronic bronchitis? What are 3 possible adverse reactions?

A

Terbutaline, Albuterol

  1. nervousness, tremors
  2. hypotension
  3. tachycardia
55
Q

When are antibiotics indicated for canine chronic bronchitis? What are 5 examples?

A

RARE —> positive culture, sudden exacerbation of clinical signs

  1. Amoxicillin/Clavulanate (also anti-inflammatory)
  2. Doxycycline (Bordetella, Mycoplasma)
  3. Chloramphenicol
  4. Fluoroquinolones
  5. Azithromycin
56
Q

What is the prognosis of canine chronic bronchitis like? What needs to be monitored?

A

incurable and progressive, but if inflammation, coughing, and exacerbation of clinical signs are controlled prognosis is good

monitor and treat pulmonary hypertension

57
Q

What are 2 alternate anti-inflammatories used in canine chronic bronchitis?

A
  1. Maropitant (cerenia) —> 1-2 weeks to show effect
  2. Doxycycline
58
Q

What does canine chronic bronchitis commonly progress to?

A
  • bronchial collapse
  • tracheobronchomalacia
  • pulmonary hypertension
  • bacterial/Mycoplasma infection
  • bronchiectasis: irreversible dilatation of bronchi where elastic and muscular tissue is destroyed by infection/inflammation
  • pneumonia
  • emphysema: coalescence of alveoli into larger space as septa are destroyed
59
Q

What is broncomalacia? Where does it happen most commonly?

A

weakness of bronchial walls due to softening of supportive cartilage leading to collapse of the bronchial walls

left cranial bronchus

60
Q

How is bronchomalacia (bronchial collapse) definitively diagnosed? What clinical signs are most commonly seen?

A

bronchoscopy

  • chronic cough, wheeze, and intermittent respiratory difficulty
  • difficult clearing secretions
  • recurrent bronchitis or pneumonia
61
Q

What is bronchiectasis? What are the 2 most common causes?

A

abnormal and permanent dilation and distortion of subsegmental airways, resulting from chronic airway inflammation that damages elastic components of the bronchi leading to bronchial wall destruction and impaired clearance of respiratory secretions

  1. foreign body aspiration
  2. bronchial obstruction
62
Q

Why is bronchiectasis a vicious cycle?

A
  • dysfunction of mucociliary clearance causes pooling of mucus, exudate, and microbes
  • this causes a host inflammatory response that will ultimately causes further damage to the airway wall and predisposes to recurrent bronchopulmonary infections
63
Q

What is the most sensitive diagnosis for bronchiectasis? What is the treatment like? Prognosis?

A

CT —> can also do radiographs, bronchoscopy (if it can reach), BAL to check for infection

same as bronchitis - long-term broad-spectrum antibiotics, surgery if localized (NO ANTISUSSIVES)

guarded due to recurrent pneumonia

64
Q

Bronchiectasis:

A
65
Q

What is primary ciliary dyskinesia? What is the classic signalment?

A

inherited structural and functional abnormalities of cilia that affects respiratory tract mucosa and other organs, resulting in poor clearance of mucus from airways and mucus plugging and inflammation

young, purebred dog with recurrent respiratory tract infections/signs

66
Q

What is Kartagener’s syndrome?

A

commonly seen triad of clinical signs seen ciliary dyskinesia consisting of bronchiectasis, complete transposition of viscera, and chronic rhinosinusitis

67
Q

Why is diagnosis of ciliary dyskinesia difficult?

A

transmission electron microscopy is needed to see ciliary structure abnormalities after culturing ciliated cells from respiratory, auditory, CNS, or sperm biopsy samples

68
Q

What is canine allergic bronchitis? How does it compare to the same disorder in cats?

A

hypersensitivity reaction to antigens from inhalation or hematogenous spread, causing narrowing of the airways and swelling of bronchi —> mucodal edema, smooth muscle hypertrophy, increased mucus production, and bronchoconstriction

bronchospasm does not occur in dogs (also considered rare in dogs)

69
Q

Other than inhaled allergens, what 2 common causes of canine allergic bronchitis?

A
  1. heartworm/lungworm
  2. fungal infection
70
Q

How is a definitive diagnosis of canine allergic bronchitis reached? What are the most common clinical signs?

A

BAL fluid cytology showing increased eosinophils and inflammation

  • nonproductive cough
  • wheezing
  • increased respiratory effort
71
Q

What are the treatment options for canine allergic bronchitis?

A
  • corticosteroids, cyclosporine, immunosuppressants
  • bronchodilators if there is expiratory effort/bronchoconstriction
  • immunotherapy (hyposensitization)
72
Q

What causes feline asthma? What are the 6 hallmarks?

A

type I hypersensitivity to aeroallergens —> IgE mediated with Th2 cells response

  1. coughing
  2. eosinophilic airway inflammation
  3. goblet sell hyperplasia
  4. reversible bronchoconstriction via serotonin and histamine release from mast cells
  5. inflammatory eosinophilic infiltrate leads to mucosal edema and vascular leakage
  6. airway remodeling
73
Q

How does feline asthma compare to that in dogs? How is it diagnosed?

A

cat airways are more reactive = bronchospams

rule out other active diseases, like pulmonary parasites, heartworm, bacteria/viral bronchitis, Toxoplasmosis, idiopathic pulmonary fibrosis, carcinoma, aspiration pneumonia, idiopathic feline bronchitis, chronic bronchitis

74
Q

What is status asthmaticus?

A

respiratory failure that comes with the worst form of acute severe asthma (asthma attack)

  • comes on quickly and does not respond to regular treatment
75
Q

What is the most common signalment of idiopathic feline bronchitis (asthma)? What are the most common clinical signs?

A

young to middle-aged, common in Siamese

  • cough
  • tachypnea
  • open mouth breathing with abdominal push
  • harsh lung sounds (bronchovesicular), wheezes, crackles
  • increased expiratory effort
  • no systemic signs
76
Q

What is the best way to work up a cat that is coughing/wheezing and asthma is suspected?

A
  • MAKE SURE CAT IS STABLE
  • radiographs
  • fecal exams (+fenbendazole) —> direct and Baermann
  • heartworm test, especially in the south
  • CBC/Chem/UA —> eosinophilia
77
Q

What is the cytology from a transtracheal wash or BAL like in cats with asthma? Bronchoscopy?

A
  • increased eosinophils and neutrophils
  • increased mucus
  • look for bacteria, larvae, ova

mucosal hyperemia with increased mucus

78
Q

What is indicative of feline asthma on radiographs?

A
  • bronchial pattern that outlines airways
  • donuts/tramways
  • collapse of right middle lung lobe due to poor ciliary clearance and mucus plug formation

(clinical signs can precede any radiographic change —> asthmatic cats can have normal radiographs, keep it on the differentials!)

79
Q

How does a collapsed lung lobe look like on radiographs in feline asthma?

A

collapsed right middle lobe will appear as a homogenous opacity, often triangular —> consolidated, small, contracted against the hilus

80
Q

What are the treatment goals for cats with lower airway disease?

A
  • reduce airway inflammation
  • reduce airway hyperreactivity and bronchoconstriction
  • ameliorate airway remodeling
  • remove underlying cause

bronchitis is irreversible; asthma can be reversed

81
Q

What happens to cats with untreated asthma or chronic bronchitis?

A

develop permanent changes with irreversible fibrosis and emphysema

82
Q

What is the general management approach to feline asthma?

A
  • reduce exposure to aeroallergens and environmental irritants
  • oral glucocorticoids with tapering to lowest effective dose
83
Q

What should be the first step in emergency assessment of feline asthma?

A
  • immediately give flow by oxygen or put in an oxygen cage

~ think: respiratory vs cardiac
~ history and signalment: coughing Siamese vs gradual onset Maine Coon
- observe breathing: effort, noise, dyspneic
- temperature: hypothermic
- breadycardia

84
Q

What is the first choice bronchodilator for feline asthma? What else is used?

A

pre-treatment of Terbutaline works within 15-30 mins after parenteral administration

oral or MDI Albuterol

85
Q

What type of corticosteroid is recommended in emergency treatment of patients with feline asthma?

A

IV short-acting Dexamethasone or Prednisone

86
Q

What glucocorticoid is recommended in patients that cannot be medicated orally? Why must it be used carefully?

A

Depo-Medrol

long-acting, lasting for 30 days —> there must be no chances for developing diabetes or heart disease and a definitive diagnosis

87
Q

What glucocorticoid is recommended once signs of feline asthma are controlled with oral medications?

A

Fluticasone (flovent) MDI

88
Q

In what situations are steroids contraindicated for treating feline asthma?

A
  • FeLV or FIV positive
  • possible FHV recurrence
  • obese —> diabetes risk
89
Q

What 4 bronchodilators are recommended for managing feline asthma?

A
  1. Albuterol
  2. Xopenex* (less irritating for chronic use)
  3. Terbutaline
  4. Theophylline
90
Q

When is it contraindicated to use Terbutaline in cats with asthma? What side effects are associated with Theophylline?

A

beta 2 agonist —> should not be administered to cats with hypertrophic myocardial disease

tachyarrhythmias, restlessness, CNS stimulation, increased gastric acid secretion, GI upset

91
Q

What are 3 advantages to metered dose inhaler administration for feline asthma?

A
  1. minimizes systemic steroids (decreases side effects)
  2. easier to treat —> no pill popping
  3. high drug concentrations delivered to site
92
Q

How is immunotherapy used in feline asthma? Which drug is commonly used? What is a major advantage?

A

desensitization with allergen-specific immunotherapy

Cyclosporine —> able ot be used in cats with concurrent disease (diabetes mellitus) that make corticosteroid therapy difficult or contraindicated

93
Q

Why is immunotherapy not commonly done in patients with feline asthma?

A

they require steroids, so there may not be accurate results on tests or therapy

94
Q

What 2 disappointing therapies commonly do not work in patients with feline asthma?

A
  1. nebulization with acetylcysteine (mucolytic agent) increases airway resistance
  2. Cyproheptadine and Cetirizine (H1 antagonist) and other antihistamines do not work
95
Q

What are 3 characteristics of feline chronic bronchitis? In what cats is it most common?

A
  1. NEUTROPHILIC inflammation
  2. mucosal edema
  3. mucus gland hypertrophy with excessive mucus production
96
Q

How do clinical signs of feline chronic bronchitis compare to feline asthma? What does manegement focus on?

A

clinical signs indistinguishable from asthma, though there is rarely life-threatening bronchoconstriction

control of inflammation using corticosteroids

97
Q

What is seen in cats with chronic asthmatic bronchitis?

A

both eosinophilic neutrophilic inflammation

98
Q

Feline asthma vs. chronic bronchitis:

A