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Respiratory CVT Flashcards

1
Q

What are the 2 forms that oxygen is carried in the blood?

A
  1. Dissolved in arterial blood (responsible for diffusion pressure driving oxygen to tissue)
  2. 97% attached to hemoglobin
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2
Q

What are the 2 most important factors influencing amount of O2 in blood?

A
  1. Amount/concentration of hemoglobin in blood

2. % of Hb that is saturated with oxygen (SaO2)

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3
Q

What are 5 conditions that oxygen should be supplemented?

A
  1. Hypoxemia (SaO2 < 90%)
  2. Hypotension (< 18)
  3. Respiratory Distress (RR>24)
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4
Q

Under what conditions are SaO2 and PaO2 within normal limits, but tissue hypoxia present?

A

Low cardiac output, anemia, failure of tissues to use oxygen

In these situations mixed venous oxygen (PvO2) better measure of tissue oxygenation

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5
Q

What is the gold standard for determining if oxygen supplementaion is needed?

A

Arterial PO2; Needed if <80mmHg

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6
Q

What does a venous PO2 value indicate?

A

Influenced by amount of oxygen in arterial blood, tissue perfusion, uptake of oxygen (oxygen extraction ratio)
If < 30mmHg = Low arterial oxygen OR high oxygen extraction ratio

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7
Q

What does a PEEP valve do to pulmonary capacity?

A

PEEP (positive end-expiratory pressure) valve = increases pulmonary functional residual capacity = Decreased work of breathing
Recommended when there is a V/Q mismatch (pulmonary edema, hemorrhage, or parenchymal dz)
Leaves air in the lungs a little longer = increasing time for gas exchange
Aimed at 5-10 mmHg (since 15 mmHg = Barotrauma!)

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8
Q

Name 7 ways that oxygen can be supplemented.

A
  1. Blow By
  2. Oxygen Hood
  3. Oxygen Collar
  4. Nasal Cannula
  5. Nasal Catheters (nasal, nasopharyngeal, or nasotracheal)
  6. Transtracheal catheters
  7. Oxygen Cages
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9
Q

What are the 3 methods to assess supplemental oxygen effectiveness?

A
  1. Clinical Evaluation (CS, lactate, ECG/Echo)

2. Pulse Oximetry (Bad if 65 mmHg)

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10
Q

What does pulse oximetry measure?

A

Peak oxygen saturation of Hb in capillary blood

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11
Q

What does a PaO2 with oxygen supplementation less than 65mmHg indicate?

A

Right to left shunt OR pulmonary dysfunction; Others (pneumothorax, severe hypovolemic shock, cardiogenic shock, obstructive airway disease)

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12
Q

What is CPAP?

A

Continuous positive airway pressure: Maintaining pressure above atmospheric pressure throughout respiratory cycle

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13
Q

What is a side effect of using PEEP?

A

Increased intrathroacic pressure = decreased venous return to heart and increase in dead space

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14
Q

What is a hyperbaric pressure?

A

Pressures higher than sea level

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15
Q

Why is the administration of high concentrations of oxygen bad?

A

Can result in oxygen toxicity - which can cause further lung injury

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16
Q

What are guidelines for ventilation?

A
  1. Failure of Gas Exchange:
    PaCO2 above 50 mmHg
    PaO2 will not rise above 50 mmHg with test of 100% O2 or cannot be maintained with FiO2 0.6 or less
  2. Need to assess the work of breathing in each patient = respiratory muscle exhaustion
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17
Q

What are the 2 classifications of patients that benefit from mechanical ventilation?

A
  1. Primary pulmonary diseases (lung-injured patients) = Noncardiogenic and cardiogenic pulmonary edema, pneumonia, pulmonary contusions, ALI, ARDS, Airway obstruction, smoke inhalation
  2. Neuromuscular Apparatus Failure (nonlung-injured patients) = polyradiculoneuritis
    (coonhound paralysis), myasthenia gravis, tick paralysis, botulism, tetanus,
    cranial cervical spinal cord lesions, brain injury, anesthetic complication, drug overdose, postcardiopulmonary resuscitation, respiratory muscle exhaustion caused by high work of breathing, diaphragmatic herniation, and chest wall trauma
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18
Q

What are the 5 main causes of hypoxemia?

A
  1. Alveolar hypoventilation
  2. V/Q Mismatch
  3. Shunt
  4. Low Insipired FiO2 (high altitudes)
  5. Diffusion Impairment
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19
Q

What is the most common cause of hypoxemia?

A

V/Q Mismatch

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20
Q

What are the two ways that ventilators are cycled?

A
  1. Volume-cycle (good for healthy lungs)

2. Pressure-cycle (good for injured lungs, but lots of variation in tidal volume delivered)

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21
Q

What are the 3 types of patient breaths in a ventilator?

A
  1. Controlled breaths (set interval)
  2. Assisted Breaths (patient can start it, ventilator finished it)
  3. Spontaneous breaths (patient taking own breaths)
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22
Q

What is sensitivity of the ventilator?

A

Sensitivity - responsiveness of the ventilator to patient efforts to initiate breathing (assisted or spontaneous breaths)

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23
Q

What are the breath delivery mode of the ventilator?

A
  1. A/C Mode: (Assist/Control) No spontanous breaths allowed (patients with poor respiratory drive)
  2. SIMV Mode: (Synchronized intermittent mandatory ventilation): allows both mechanical and spontaneous breaths to be delivered according to patient demand
  3. SPONT mode (spontaneous): the ventilator delivers no mandatory mechanical breaths. All breaths are spontaneous = Prewean mode
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24
Q

What are 4 ways that PEEP can improve ventilation?

A
  1. increase in the functional residual capacity
  2. alveolar recruitment
  3. improved V/Q matching
  4. redistribution of the extravascular lung water
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25
Q

What are 2 types of ventilator induced lung injury?

A
  1. High pressures and use of high tidal volumes = Damage capillaries
  2. Opening and closing of alveoli = Shear stress!
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26
Q

What is the trade-off of lung protective strategies for ventilation?

A

Hypoventilation (PaCO2 - 70-80 mmHg) permitted

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27
Q

Which type of patients are harder to keep sedate when using a ventilator?

A

lung-injured patients typically are more difficult to control because of high ventilatory
drive from hypercarbia or hypoxemia

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28
Q

What is a potential cardiovascular cost of ventilation?

A

Declining cardiac output and resultant decreasing oxygen delivery = Eventually it outweighs the benefit of increasing arterial oxygen content

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29
Q

What is a potential sequela of ventilation?

A

Ventilator associated pneumonia (pathogenesis: colonization of the aerodigestive tract with pathogenic microbes early in the course of hospitalization and aspiration of the contaminated secretions)

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30
Q

When would nasal discharge cytology be useful?

A

Eucoleus [Capillaria] boehmi parasitic ova

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31
Q

What 2 bacteria can result in rhinitis in dogs as pure isolates?

A

Bordetella bronchiseptica or Pasteurella multocida (both are very rare; pneumonia may be present)

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32
Q

What are the most common causes of rhinitis in dogs, excluding nasal FB and dental dz)?

A
  1. Neoplasia
  2. Idiopathic chronic (lymphoplasmacytic) rhinitis
  3. Fungal rhinitis
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33
Q

Name the dog nasal mite and nasal nematode.

A

Nasal mites: Pneumonyssus caninum

Nasal Nematode: Eucoleus [Capillaria] boehmi

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34
Q

What is the most common cause of fungal rhinitis in dogs? Name 3 others as well.

A

Aspergillus fumigatus is the most common cause of fungal rhinitis in dogs. occasionally Penicillium spp., Rhinosporidium seeberi, and very rarely Cryptococcus neoformansin dogs

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35
Q

Which nasal fungal infection results in granulomatous masses in the rostral nasal cavity that need to be surgically removed?

A

Rhinosporidium seeberi

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36
Q

Name the 2 breeds that are predisposed to nasal Aspergillus.

A

GSH and Rotties

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37
Q

Name the signalment of dogs with nasal Aspergillus.

A

young to middle-aged dolichocephalic dogs

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38
Q

How is nasal Aspergillus diagnosed?

A
  1. Visualization of fungal plaques on nasal mucosa

2. Demonstration of branching septate hyphae on cytologic or histologic samples

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39
Q

Why are nasal cultures misleading for a diagnosis of Aspergillus?

A

Cultures of nasal discharge may be misleading in that 30% to 40% of cultures from normal dogs
and those with nasal neoplasia can yield Aspergillus or Penicillium spp

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40
Q

What type of treatment is most effective for nasal Aspergillus?

A

Topical therapy is more effective than orally administered antifungal agents

  1. Topical therapy with clotrimazole has become the treatment of choice: As many as 90% of patients may be cured with a single procedure, although some dogs require a second procedure 3 weeks later.
  2. Topical application of enilconazole through surgically placed catheters into the frontal sinuses and nasal chambers has a success rate as high as 90%
  3. Combination of clotrimazole irrigation and depot therapy: 86% of dogs with nasal aspergillosis or penicilliosis established a cure from infection
  4. Oral antifungals only good if cribiform plate compromised and topical antifungals cannot be used (itraconazole, terbinafine, fluconazole, adn voriconazole)
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41
Q

What is the etiology of lymphoplasmacytic rhinitis in dogs?

A

Unknown; potential for aeroallergen, reaction of commensal fungi, etc??

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42
Q

What is the signalment of patients that get lymphoplasmacytic rhinitis in dogs?

A

Young to middle-aged dolichocephalic and mesaticephalic large-breed dogs

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43
Q

Which breed is particularly affected with LP rhinitis in dogs?

A

Dachshunds

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44
Q

What are treatment options for LP rhinits in dogs?

A

Steroids and antihistamines RARELY work
Need immunomodulating antibiotic (doxy or azithromycin) + NSAID (piroxicam) = Needed at least 6 months, but likley longterm

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45
Q

What percent of chronic nasal disease in dogs is from nasal neoplasia?

A

About 1/3 of all dogs with chronic nasal disease

About 2/3 of these are tumors of epithelial origin (mets to LNs and lungs = Rare, late in dz)

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46
Q

What is the treatment of choice for nasal tumors in dogs?

A

Radiation therapy
Median Survival: 16.5-23 months, about 1 year in 54-60% of dogs with nasal neoplasia
NOT cryosurgery or chemo (cisplatin, same as no tx given)

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47
Q

Nasal polyps are rare in dogs, but with cancer has been seen on resection of polypous tissue?

A

Low-grade fibrosarcoma

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48
Q

Which breed gets hyperplastic rhinitis?

A

Irish Wolfhounds

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49
Q

Which feline virus has been suggested as a cause (but not proven) in feline chronic rhinosinusitis?

A

Feline herpesvirus type 1 (FHV-1)

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50
Q

Can feline chronic rhinosinusitis have unilateral nasal signs?

A

Yes!

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51
Q

How is feline chronic rhinosinusitis diagnosed?

A

It is a diagnosis of exclusion = Bx is required to differentiate from other causes

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52
Q

Does rhinoscopic appearance of mucosa predict amount of inflammation present in cats with chronic rhinitis?

A

NO! Rhinoscopic appearance does not predict the presence or absence of substantial inflammation

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53
Q

Since feline rhinitis can have secondary bacterial infections caused by aerobic, anarobic, and Mycoplasma felis, which antibiotics may be considered?

A

Doxycycline
Topical Gentamicin (if Bordetella considered)
Azithromycin
Penicllin-like ones = BAD (do not get Mycoplasma, since they lack cell walls)
Enrofloxacin
Clindamycin (esp if bone involved)

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54
Q

How does lysine work for viral infections?

A

Lysine: an amino acid that competes with arginine for use by the viral machinery in replication

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55
Q

What are the common congenital and acquired abnormalities seen with Brachycephalic Upper Airway syndrome in dogs?

A

Congenital: stenotic nares; shortening, widening, and flattening of the nasal cavity and pharynx; elongation, thickening, and flaccidity of
the soft palate; and decreased glottic size (+/- hypoplastic trachea)
Acquired: From increased respiratory effort = edema and further thickening of the soft palate, eversion of the laryngeal saccules,
edema of the pharyngeal and laryngeal mucosa, enlargement of the tonsils, and progressive laryngeal dysfunction ending with complete laryngeal collapse

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56
Q

Name 5 breeds that are most commonly affected by Brachycephalic Upper Airway Syndrome in dogs?

A

English bulldog, pug, Boston terrier, chow-chow, Pekingese, Shih Tzu and shar-pei

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57
Q

What is the most common CS of Brachycephalic Upper Airway Syndrome in dogs?

A

Progressively worsening inspiratory dyspnea (+/- stridor)

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58
Q

What are the most common nasopharyngeal disease in cats?

A

Cryptococcosis (dependent on location), nasopharyngeal polyps, neoplasia, and foreign bodies

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59
Q

What are the most common nasopharyngeal disease in dogs?

A

Inflammation, neoplasia, foreign bodies, nasal mites (Pneumonyssoides caninum) or congenital abnormalities

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60
Q

What types of CS are specific to nasopharyngeal disease?

A 
Stertor
Reverse sneezing (dogs)
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61
Q

What type of neurologic CS are possible in animals with nasopharyngeal disease?

A

Central nervous signs - if extension of fungus or neoplasia into brain
Vestibular disease - if extension into tympanic bulla, opening of eustachian tube
Horner’s Syndrome (cats) - with invovlement of tympanie bullae
Facial Nerve Dysfunction too (facial assymmetry and absent palpebral reflex)

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62
Q

Why is it important to determine if stertor vs stridor is present?

A 
differentiate stertor (a snoring-type noise arising from the nasopharynx or pharynx, see effect of opening mouth with stertor) from
stridor (a high-pitched noise arising from disturbance of air flow through the larynx or trachea)
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63
Q

What serologic test can be used for Cryptococcus spp?

A

Positive latex cryptococcal antigen agglutination test titer (can be measured for treatment response too)

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64
Q

Name 2 nasopharyngeal parasites.

A 
Pneumonyssoides caninum - found in nasal cavity, nasopharynx, and frontal sinus worldwide
Cuterebra larvea (cats) - Watch for hypersensitivity rxn to hemolymph
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65
Q

Describe the etiology of nasopharyngeal polyps in cats.

A

Unknown: Congenital defect, chronic inflammation of middle ear or eustachian tube, or viral upper respiratory infection

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66
Q

What is the difference in location of nasophyarngeal polyps in cats vs dogs?

A

Cats: Eustachian tube or middle ear
Dogs: Caudal Nasal Turbinates (from chronic rhinitis)

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67
Q

What are the recommended treatment options for cats with nasopharyngeal polyps?

A

Traction/avulsion good first option in cats with no bullae involvement (not all cats will develop involvement of the bullae). Transient Horner’s syndrome is likely; recommended reduced reccurence if anti-inflammatory steroids given after removal
Ventral Bullae Osterotomy

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68
Q

What is nasopharyngeal stenosis?

A

Stricture formation may occur in both cats and dogs following chronic inflammation (infectious diseases, surgery, or other trauma (reflux) or as a congenital abnormality (choanal atresia)

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69
Q

What breed has Nasopharyngeal stenosis resulting from abnormally thickened
palatopharyngeal muscles has also been reported?

A

dachshunds

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70
Q

What is cystic Rathke’s cleft?

A

Embryonic pituitary development proceeds abnormally, resulting in a progressively expansile cystic lesion within the sphenoid bone
May or may not be assoicated with congenital dwarfism

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71
Q

Why do some nasal tumors in dogs respond to piroxicam?

A

81% of canine nasal tumors have been shown to express cyclooxygenase-2 (COX-2)
(Kleiter et al, 2004), and a recent small case series demonstrated that the treatment with oral piroxicam (a
COX-2 inhibitor) in conjunction with alternating doses of doxorubicin and carboplatin was efficacious and well tolerated (Langova et al., 2004)

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72
Q

What are the 2 main factors that need to be present to develop tracheal collapse?

A
  1. Primary cartilage abnormality = Weakness of tracheal rings
  2. Secondary factors capable of initiating progression to the symptomatic state
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73
Q

What is the primary defect responsible for intrinsic weakness of tracheal rings?

A

Reduction in the glycoprotein and glycosaminoglycan content of the hyaline cartilage of the tracheal rings = Reduced capacity of cartilage to retain water

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74
Q

Name potential factors that can contribute to clinical syndrome of tracheal collapse?

A
  1. Cardiomegaly
  2. Pulmonary Edema
  3. Respiratory Infection
  4. Upper Airway Obstruction
  5. Chronic Bronchitis
  6. Allergic Tracheobronchitis
  7. Inhaled irritants (smoke)
  8. Cervical trauma
  9. Obseity
  10. Tracheal intubation
  11. HAC
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75
Q

When does collapse of cervical tracheal segment occur in?

A

Inspiration, decreased pressure within the trachea

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76
Q

When does collapse of the thoracic portion of trachea occur in?

A

Expiration, increased intrathoracic pressure

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77
Q

What creates the cycle of tracheal collapse?

A

• Once clinical signs are apparent, the syndrome is perpetuated by the cycle of chronic inflammation of the tracheal mucosa, which precipitates cough and in turn is exacerbated by the cough
○ Persistent inflammation of the tracheal mucosa leads to a loss of epithelium = fibrinous membrane formation = squamous metaplasia with polypoid proliferation evident in advanced cases
○ Population of ciliated cells is reduced significantly by the metaplastic changes in the mucosa, and the hyperplastic subepithelial glands secrete increasingly viscid mucus = normal ciliary function is replaced progressively by cough as the major tracheobronchial clearing mechanism
○ Once the condition becomes symptomatic, the changes in the dorsal membrane and cartilage are believed to progress beyond those of the original anatomic abnormality

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78
Q

What is the most common signalment for tracheal collapse?

A

Small/toy-breed dogs (mild, intermittent “honking” cough to severe resp distress/obstruction); more common in older (all ages affected)
Toy and miniature breeds = Yorkies, Mini Poodles, Chichuahua, Pomeranians

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79
Q

What percentage of dogs with tracheal collapse are affected by 6 months of age?

A

25%

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80
Q

Do severity of clinical signs related directly to the severity of anatomic changes with tracheal collapse?

A

NO!

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81
Q

What is the gold standard for diagnosing tracheal collapse?

A

Endoscopy - Tracheoscopy

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82
Q

What other organ system has been identified to be dysfunctional in many dogs with tracheal collapse?

A

Hepatic dysfunction

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83
Q

What are the mainstays of treatment for tracheal collapse?

A
  1. Management of Secondary Initiating Causes (weight reduction, CHF, inhaled irritatns, respiratory infections, collars)
  2. Management of cough (antitussives, bronchodilators, glucocorticoids)
84
Q

Name several antitussives that are used for tracheal collapse.

A

Lomotil - Narcotic antitussive
Hydrocodone
Codeine phosphate
Butrophanol

85
Q

What is the rationale for using bronchodilators in tracheal collapse?

A

dilation of pulmonary airways, which decreases intrathoracic pressure during expiration, thereby decreasing the tendency to tracheal narrowing during expiration

86
Q

What are the 2 main types of bronchodilators and which is their MOA?

A
  1. Methylxanthine Bronchodilators: Phosphodiesterase inhibition → smooth-muscle relaxation through accumulation of cyclic adenosine monophosphate (cAMP)
    (theophylline)
  2. B2-Adrenergic Agonists (Terbutaline, Albuterol)
87
Q

How long should steroids be used for tracheal collapse patients?

A

Short periods, in order to reduce inflammation laryngeal, tracheal, or bronchial

88
Q

What 3 factors are considered to be perpetuating factors from chronic pathologic changes in tracheal collapse?

A
  1. Cough
  2. Failure of mucocililary clearance mechanism
  3. Increased mucus production
89
Q

What are the chronic pathologic changes that are seen with tracheal collapse?

A
  1. Epithelial loss
  2. Subepithelial gland hypertropy
  3. Squamous metaplasia
  4. Polyp formation
90
Q

What are the 2 main methods to consider if medical management of tracheal collapse has failed?

A

• Surgical for Extrathoracic Tracheal Collapse: Extraluminal polypropylene ring prostheses (place support rings around trachea via cervical approach)
○ 75-85% overall success rate for ¯clinical signs in 90 dogs (Buback, Boothe, and Hobson, 1996)
§ Complications: 5% died perioperatively, 11% laryngeal paralysis, 19% required permanent tracheostomies (half within 24 hours)
• Interventional Intraluminal Tracheal Stents:
○ Stents: balloon-expandable (Palmaz), self-expanding (stainless steel, laser-cut nitinol, knitted nitinol) stents (Radlinsky et al., 1997; Norris et al., 2000; Moritz, Schneider, and Bauer, 2004)

Clinical improvement in 75-90% dogs with intraluminal, stainless steel, self-expanding metallic stents (SEMSs)

91
Q

What are some of the late complications that can occur with intraluminal tracheal stents?

A

stent shortening, excessive granulation tissue formation, progressive tracheal collapse, stent fracture (severe or life-threatening)

92
Q

Can intraluminal tracheal stents be used for main-stem bronchial collapse?

A

· Debate of using intraluminal stents in patients with main-stem bronchial collapse (no data)
o Can’t stent mainstem bronchi: “cage-off” other bronchi and prevent drainage, secondary/tertiary bronchi will continue to collapse

93
Q

What are the 4 major discussion points for owners regarding tracheal stents?

A

· Procedures do NOT slow progression of disease → Palliative
· Late complications (stent shortening, excessive granulation tissue formation, progressive tracheal collapse, and stent fracture)
· Continued coughing expected in any dog with concurrent bronchial collapse (may be worse prognosis)
· Majority of dogs will require continued life-long medical management!

94
Q

What is a tracheal stent made out of?

A

· Nitinol (shape-memory metal → alloy of nickel (Ni) and titanium (Ti) alloy developed by Naval Ordinance Laboratory)

95
Q

What is foreshortening with tracheal stents?

A

Shortening of stent encountered as it is released from delivery system
o If stent does not achieve full expansion (i.e. lumen in which it is placed prevents complete expansion to its original diameter), stent will be longer than expected
o NOTE: Significantly longer when viewed on delivery system; as stent expands it shortens, and as such the ultimate length of stent is inversely proportional to degree of expansion (the less stent expands, the longer it will remain) → Need to consider during stent selection

96
Q

How does the diameter of the cervical trachea compare to the intrathoracic trachea?

A

cervical trachea is larger in diameter than intrathoracic trachea, and can vary markedly

97
Q

Discuss the post-op care for a tracheal stent?

A

after stenting with 3-4 weeks of tapering dose of prednisone (initial dose 1-2 mg/kg/day PO), continued antitussive (hydrocodone 0.25 mg/kg PO q6–12h or higher if tolerated), +/- antibiotics · If bronchial collapse or “expiratory push” during exhalation: bronchodilator
· Anticipate a dry cough for 3-4 wks that should improve (if lower airway collapse, cough will continue)
· Recheck: 2 wks after stenting or sooner if problems (then every 3-6 months)

98
Q

What is chronic bronchitis?

A

Inflammation (etiology unknown; environmental pollutants, secondhand smoke, or inhaled irritants) of conducting airways → chronic cough o Chronic, low-grade aspiration injury might play a role
o Human Med: Role of bacterial infection in generation/exacerbation is widely debated (NOT established in dogs)
o Disease of exclusion → tx based information from individual at controlling CS (NEVER cured!)

99
Q

What is the hallmark of chronic bronchitis on PE?

A

Expiratory wheezes

100
Q

What are the bronchial casts of airway mucus called?

A

Related to increased mucus

101
Q

What would occur to a flow volume loop (pulmonary function test) in a dog with chronic bronchitis?

A

¯expiratory flow (loop that is on top)

102
Q

What is an alterantive to oral steroids in chronic bronchitis?

A

Fluticasone (Metered-dose inhaler + spacing chamber)

103
Q

Does bronchoconstriction play a large role in chronic bronchitis?

A

No!

104
Q

What are the benefits of using bronchdilators in chronic bronchitis?

A

· Unlikely that bronchoconstriction plays role!
o BUT clinical helpful and allow for reduction in steroid dose (methylxanthine derivatives and β-agonists seem to act synergistically with glucocorticoids to control inflammatory lung disease)
o Other benefits: improving pulmonary perfusion, enhancing cardiac performance, reducing respiratory effort, and stimulating mucociliary clearance

105
Q

Name 2 common antibiotics used in chronic bronchitis.

A

Need to be lipophilic to penetrate airway

  1. Doxycycline (first choice)
  2. Enrofloxacin
106
Q

What is the interaction btwn enrofloxacin and theophylline?

A

§ Enrofloxacin inhibits metabolism of theophylline→ concurrent use results in toxic plasma levels of theophylline (Intorre et al., 1995)
□ At least 30% reduction in theophylline dosage is recommended when enrofloxacin given

107
Q

What is the prognosis for chronic bronchitis?

A

· Chronic dz, that can be controlled but NEVER cured

· Majority have residual cough and CS throughout their life

108
Q

What are the goals of management in chronic bronchitis?

A

control inflammation (to limit CS); to diagnose/treat infection when it occurs; to prevent development of debilitating sequelae → bronchiectasis, cor pulmonale

109
Q

What type of bacteria is Bordetella?

A

§ Gram-negative aerobic coccobacillus

110
Q

Dogs that are co-infected with these two viruses and Bordetella may have more severe disease.

A

□ Dogs with canine parainfluenza virus (CPiV) or canine adenovirus-2 (CAV-2) may experience more severe respiratory dz when coinfected with B. bronchiseptica

111
Q

What bacterial infection can result in fatal pneumonia in young dogs?

A

B. bronchiseptica

112
Q

What are the virulence factors of Bordetella?

A

Encoded by BvgAS locus § BvgAS locus controls 3 distinct phenotypic phases of B. bronchiseptica: Bvg+ (colonization), Bvgi (transmission), and Bvg− (survival/persistence)
o Bordetella virulence genes A and S (BvgA and BvgS): Signaling proteins → expression of several virulence determinants → pathologic consequences

113
Q

What is the most common cause of Most common cause of community-acquired infectious pneumonia in dogs < 1 yr?

A

Bordetella bronchiseptica

114
Q

What 2 factors make it hard to study the prevalence of Bordetella?

A
  1. Infectious respiratory disease is typically associated with other bacterial pathogens (e.g., Mycoplasma spp.) and viruses (e.g., parainfluenza virus, CDV, and calicivirus)
  2. B. bronchiseptica can be isolated from the respiratory tract of healthy dogs and cats
115
Q

What is the most common antibiotic used to treat Bordetella?

A

Doxycycline

116
Q

What type of vaccines are available for Bordetella?

A
  1. Parenteral, cellular antigen extract (dogs)

2. Intranasal avirulent live vaccine (also with MLV parainfluenza +/- CAV-2 MLV) (dogs, cats - only)

117
Q

Does the Bordetella vaccine protect against the disease?

A

NO!
· Effective in reducing the severity of clinical illness (no one vaccine type know to be better), BUT neither prevent infection subsequent to natural exposure

118
Q

Which vaccination can result in hepatic failure if given SQ instead of intranasal, and why does this occur?

A

· Inadvertent SQ administration of avirulent, live intranasal B. bronchiseptica vaccine → Injection site abscess
o Replication of attenuated gram-negative bacteria in SQ → associated with death following liver failure (related to endotoxemia)

119
Q

Does Bordetella bronchiseptica have zoonotic potential?

A

YES! Needs more studies

120
Q

Compare and constrast chronic bronchitis and asthma.

A

o 1. Chronic bronchitis: Inflammatory disorder of lower airways → daily cough, for which other causes of cough (including heartworm disease, pneumonia, lungworms, and neoplasia) are excluded

  1. Asthma: Disorder of lower airways → airflow limitation (combo of airway inflammation, accumulated airway mucus, and airway smooth muscle contraction); Dramatic CS (acute wheeze and resp distress) or daily cough (humans: cough variant asthma); definitive dx based on pulmonary function tests
121
Q

Which lung lobe is the most likley to be atelectic in cats?

A

right middle lung lobe dt mucus accumulation, most commonly involved since it is the only airway with dorsoventral orientation = subject to effects of gravity

122
Q

What is the interaction btwn eosinophils and T-lymphocytes in feline airway disease?

A

· Pathogenesis asthmatic airway hyperreactivity is clearly multifactorial → Interaction btwn T cells and eosinophils (humans; BAL samples have ↑ activated T lymphocytes and eosinophils in patients with asthma)
o Presence of cells correlated to dz severity
o Activated T cells recruited into airways when exposed to aeroallergens (CD4 + lymphocytes, others) → secrete IL-5 to promote eosinophilopoiesis, survival, activation, and recruitment into airways
o Th2-driven cytokine profile → antigen-induced asthma models in cats (Reinero et al., 2004)”

123
Q

Which cat breed to prone to lower airway disease?

A

Siamese

124
Q

What are the 2 mainstays in treatment of feline bronchitis/asthma?

A
  1. Bronchodilation

2. Decrease inflammation with oral or inhaled steroids

125
Q

What organism is cultured from 25% of cats with bronchitis?

A

Mycoplasma - Need to treat with doxycyline or azithromycin

126
Q

Why is cyproheptadine used in bronchitis/asthma in cats?

A

· Antihistamine but also antiserotonin properties (appetite stimulant)
o NOTE: Serotonin (mast cells) primary mediator of bronchoconstriction in cats (NOT in humans)
o Can block serotonin in antigen-induced airway smooth muscle in vitro

127
Q

Briefly describe leukotrience production in relation to airway inflammation?

A

· Leukotrienes (inflammatory mediators from arachidonic acid → eicosanoids)
o Cysteinyl leukotrienes: LTC4, LTD4, and LTE4 → Airway inflammation
§ Produce mucus hypersecretion, ↑ vascular permeability, ↑ mucosal edema; induce potent bronchoconstriction; chemoattractants to inflammatory cells (eosinophils, neutrophils)

128
Q

Discuss the role of anti-leukotriences in feline lower airway disease?

A

· Antileukotriene Drugs: competitive, highly selective, and potent inhibitors of the production/function of LTC4, LTD4, LTE4
Zafirlukast, Montelukast, and Zileuton
o No current evidence that drugs affecting leukotriene synthesis play role in feline or canine resp dz

129
Q

What determines delivery of medication to the lower airways?

A

· Need to deliver to distal airways → depends on size of aerosolized particles + tidal volume and inspiratory flow rate
o In humans: Only about 10-30% of inhaled dose enters the lungs!
o In cats: Passive inhalation via a spacer-mask (Aerokat) is effective for delivering medications (MDI)
§ “Ideal aerosol” based on chamber dimensions
§ Spacer (cats have tidal volume of 5-10mls inspired air per pound BW) – Get drug within 7-10 breaths

130
Q

What are the 2 main portals of entry for bacterial pneumonia?

A
  1. Larynx and trachea (most common in dogs); 2. Hematogenous dissemination (more in cats, Foster, 2004)
131
Q

What is key for colonization of the respiratory tract to result in pneumonia?

A

Bacterial adherence

132
Q

What are risk factors for young dogs with bacterial pneumonia?

A

§ Critical Factors: immunization status, congenital disorders (megaesophagus, ciliary dyskinesia), environment (housing, sanitation, and ventilation), exposure to clusters of dogs, and coinfection (calicivirus or distemper)

133
Q

What are risk factors for adult dogs with bacterial pneumonia?

A

Aspiration pneumonia→ acquired megaesophagus, myasthenia gravis, and laryngeal paralysis § Systemic or local bacterial infection (bacteremia, phlebitis, or periodontitis) → predisposing risk factor for bacterial pneumonia

134
Q

What is the most common Community-acquired infectious pneumonia in dogs< 1 yr?

A

B. bronchiseptica (49%)(Radhakrishnan et al., 2007)

135
Q

Name 7 components of treatment in bacterial pneumonia.

A
  1. Antibiotics
  2. IVF
  3. Bronchodilator = Controversial!
  4. Mucolytic drug (N-acetylcysteine)
  5. Nebulization of Saline (other drugs too - gentamicin for Bordetella)
  6. O2 supplementation
  7. Physical therapy (walking, coupage)
136
Q

Name the 5 most common bacteria in pneumonia for cats.

A
  1. Pasteurella spp
  2. Bordetella bronchiseptica
  3. Streptococcus equi spp zooepidemicus
  4. Pseudomonas spp
  5. Mycoplasma spp
137
Q

Name the 9 most common bacteria in pneumonia for dogs.

A
  1. Bordetella bronchiseptica
  2. Staph spp
  3. Strep spp
  4. Enterococcus spp
  5. E. coli
  6. Pseudomonas spp
  7. Pasteurella spp
  8. Klebsiella spp
  9. Bacteroides
138
Q

Compare and contrast cardiogenic vs noncardiogenic pulmonary edema.

A

· Pulmonary edema → abnormal accumulation of fluid in extravascular spaces of lung (dynamic process)
· Noncardiogenic pulmonary edema → ↑ vascular endothelial permeability rather than ↑vascular hydrostatic pressure (cardiogenic pulmonary edema)
o ↑ vascular endothelial permeability due to injury to pulmonary microvascular endothelium (separates intravascular compartment from pulmonary interstitium and alveoli)
o Unlike cardiogenic PE, ↑ permeability results in extravascular fluid with relatively high protein, leads to ↑ extravascular lung water content at low pulmonary hydrostatic pressures

139
Q

Name causes of noncardiogenic pulmonary edema.

A

o Reflects primary pulmonary injury (aspiration of gastric content, near drowning, inhalation of smoke/toxic gas, blunt trauma, prolonged high inspired O2 contents) or systemic dz (sepsis, neurologic PE, pancreatitis, uremia, SIRS, pulmonary embolism)

140
Q

What changes would you note on a arterial BG in noncardiogenic pulmonary edema?

A

· Arterial BG → pulmonary dysfunction (nonspecific), hypoxemia due to V-Q mismatch, PaCO2 low due to hyperventilation in response to pulmonary parenchymal disease
o Later stages, ¯ pulmonary compliance (inability to ventilate → hypercapnia)

141
Q

What 2 parasites transiently migrate through the lungs during development?

A

Toxocara canis, Ancylostoma caninum

142
Q

What systemic parasitic infection can have pulmonary involvement?

A

protozoan Toxoplasma gondii

143
Q

What parasites lives primarily in the heart and pulmonary arteries?

A

Dirofilaria immitis;, Angiostrongylus vasorum

144
Q

Name 4 nasal parasites. The spp they affect and location.

A 
Eucoleus boehmi (dogs - Epithelial lining of the nasal mucosa, turbinates, and sinuses)
Mammomonogamus ierei (cats - Mucosa of nasal cavity, nasopharynx → mild chronic inflammation)
Pneumonyssoides caninum (dogs - Nasal Cavity and Sinuses)
Cuterebra (cats/dogs - SQ of face, head, and neck region, nasopharynx (rare), wall of cervical trachea)
145
Q

How is Eucloeus boehmi diagnosed?

A

Microscopic: Double-operculated (bipolar) eggs in nasal flushes or fecal float (could be cyclic)
**Misidentified for Capillaria aerophila **
E. boehmi is smaller, distinctive, readily visible space btw egg shell and embryonated contents

146
Q

Name 6 bronchopulmonary nematodes. Name spp and location of infection.

A
  1. Oslerus (filaroides) osleri: Dogs (granulomatous nodules in distal trachea, bifurcation, and first bronchi
  2. Filaroides hirthi: Dogs (deep in lung parenchyma - alveoli and terminal airways)
  3. Andersonstrongylus (Filaroides) milksi: Dogs (rare, similar to F. hirthi)
  4. Aelurostronylus abstrusus: Feline (adult worm in terminal bronchioles, alevaolar ducts)
  5. Crenosoma vulpis: Dogs (bronchi and bronchioles)
  6. Capillaria aerophila (E. aerophilus): Dogs/cats (trachebronchial mucosa - white, coiled masses)
147
Q

What is the intermediate host of the feline lungworm, Aelurostrongylus abstrusus?

A

Snail/slug

148
Q

What is the intermediate host of Crenosoma vulpis?

A

Snail/slug

149
Q

What is the reservoirs of Crenosoma vulpis?

A

Wolves, foxes, raccoon = Endemic in red foxes in NA

150
Q

Which bronchopulmonary parasite can infect dogs, cats, and foxes?

A

Capillaria aerophila

151
Q

What is the lung fluke (trematode) of cats and dogs?

A

Paragonimus kellicotti

152
Q

Which pulmonary parasites can be found on fecal centriguation?

A

Paragonimus kellicotti
Oslerus (Filaroides) osleri
Filaroides hirthi

153
Q

Which pulmonary parasites can be found on fecal float?

A

Capillaria aerophila

154
Q

Which pulmonary parasites can be found on Baerman?

A

Crenosoma vulpis

Aelurostrongylus abstrusus

155
Q

What structures are not included in the lung interstitium?

A

does NOT include the airspaces, the capillary endothelial cells, and the alveolar lining epithelium (but likely involves these structures)

156
Q

Name 7 disease entities that are included in interstitial lung disease?

A

o Pulmonary infiltration with eosinophilia (PIE) (aka eosinophilic bronchopneumopathy)
§ Parasitism (dogs/cats): Filaroides spp. (Oslerus osleri, Filaroides hirhti), Crenosma vulpis, Aelurostrongylus abstrusus, Capillaria aerophilia, and the heartworms Angiostrongylus vasorum and Dirofilaria immitis
o Idiopathic pulmonary fibrosis (IPF)
o Toxin Induced: Paraquat poisoning (dogs)
o Connective tissue disorders
o Vasculitis disorders
o Infiltrative disorders → lymphocytic (humans), neoplasia (LSA)
o Others

157
Q

How do you make a diagnosis of interstitial lung disease?

A

Histopath

158
Q

What 2 breeds are the poster children for idiopathic pulmonary fibrosis?

A

West Highland White Terrier

Carin Terrier

159
Q

What is the effectiveness of azathioprine and antifibrotic colchicine in idiopathic pulmonary fibrosis?

A

Unknown in cats and dogs

Some use in humans

160
Q

Name 4 diseases that can result in pulmonary mineralization?

A
  1. HAC
  2. Pulmonary neoplasia
  3. Idiopathic mineralization
  4. Aging changes
161
Q

What toxin can result in interstitial lung disease?

A

Paraquat

162
Q

Between which ribs should a thoracocentesis be performed?

A

Performed between 7th and 9th rib spaces, above costochondral junction

163
Q

What are the 2 key components of successful treatment in pyothorax?

A
  1. Drainage
  2. ABX - Clavamox is good for nearly all anaerobes, gram positives, and many gram negatives – since not available injectable okay to use Unasyn. Clindamycin also has good anaerobes activity including Bacteroides, but always need second drug for gram negative (usually fluoroquinolones).”
164
Q

Which two organisms can be hard to treat in pyothorax and how do you treat them?

A

Actinmyces or Nocardia (sulfur granules or branching filamentous organisms), penicillins can be used for Actinomyces, but Nocardia are harder to treat (tetracyclines, TMS, aminoglycosides). Actinomyces may be associated with foreign bodies

165
Q

Which spp gets chylothorax more?

A

Cats are 4 X more likely than dogs

166
Q

What are 5 common casues of chylothorax?

A

○ More commonly: right heart failure, mediastinal masses, pericardial disease, paroxysmal AV block, fungal granuloma, heartworm infections – but most are idiopathic

167
Q

What is a pseudochylous effusion and what is it associated with?

A

when fluid cholesterol is higher than serum, but fluid triglycerides the same or less than serum (rare, assoc with tuberculosis)

168
Q

Which 2 cat and 2 dog breeds are overrepresented for chylothorax?

A

Cats: Oriental breeds (Himalayan, Siamese)
Dogs: Afghan hounds and Shiba Inu

169
Q

What is the medical management of chylous effusion?

A

○ Rutin : benzypyrene flavonoid, efficacy unproven
○ Somatostatin analogues: prolong GI transit time, decrease jejunal secretion, stimulation GI water absorption
Octreotide - short term benefit in some cats

170
Q

What are surgical options for chylothorax?

A

TD ligation and pericardectomy

TD ligation with Mesenteric Lymphangiography

171
Q

Name the 3 most common cancer associated with thoracic effusions.

A
  1. Medistinal LSA
  2. Pleural mesothelioma
  3. Metastatic carcinoma
172
Q

What is the prognosis for medistinal LSA in cats?

A

If treated with chem, remission rates as high as 92%, median duration about 6 months, as long as 29 months

173
Q

What is the most common lobe involved in lung lobe torsions in dogs?

A

Right Middle lung lobe

174
Q

What 2 breeds are predisposed to lung lobe torsions?

A

Afghan hounds and Pugs

175
Q

What infectious disease could you consider for an idiopathic pleural effusion?

A

Occult mycobacterium (consider azathiomycin trial)

176
Q

What are the ways to classify a pneumothorax?

A

Traumatic vs spontaneous
Open vs closed
Simple vs tension

177
Q

Which breed is overrepresented for developing spontaneous pneumothorax?

A

Siberian Huskies

178
Q

What are the 3 major risk factors of thrombosis?

A
  1. Endothelial injury
  2. Blood stasis
  3. Alterations in blood constituents that favor thrombosis
    Known as Virchow’s triad
179
Q

What defines hypercaogulability?

A
  1. Platelet hyperaggregability
  2. Excessive activation
  3. Decreased removal of coagulation factors
  4. Deficiencies of natural anticoagulants (antithrombin and protein C)
  5. Defective fibrinolysis
    Acquired disorders in patients with underlying systemic dz known to be associated with an increase risk of thrombosis
180
Q

Name the top 10 diseases that are associated with PTE in dogs.

A
  1. PLN
  2. Neoplasia
  3. Cardiac disease (HW, endocarditis, cardiomyopathy)
  4. Necrotizing pancreatitis
  5. IMHA
  6. HAC (endogenous and exogenous)
  7. Diabetes mellitus
  8. Atherosclerosis
  9. Sepsis
  10. Trauma
  11. Major sx
    All but cardiac dz associated with hypercoagubility
181
Q

Name the top 8 diseases that are associated with PTE in cats.

A
  1. Cardiomypathy
  2. Neoplasia
  3. Pancreatitis
  4. IMAH
  5. PLN
  6. PLE
  7. Hypercorticism
  8. Sepsis
182
Q

Emboli in which part of circulation form PTE?

A

Venous Circulation = PTE

183
Q

Name 4 pulmonary consequeneces of PTE.

A
  1. Ventilation-perfusion mismatch
  2. Bronchoconstriction
  3. Hypoxemia
  4. Hyperventilation
    Later
  5. Regional loss of surfactant
  6. Pulmonary infarction (rare)
    = Atelectasis, Edema, Effusion
184
Q

What is the major burdens of massive PTE?

A

Mechanical Obstruction
Exacerbated by hypoxia-induced vasoconstriction, release of hormonal substances from activated platelets on surface of thrombus

185
Q

What is regional oligemia?

A

Hypovascular lung regions

Appear as areas of increased radiolucency = reduced vascular filling distal to thrombotic occlusion

186
Q

How are d-dimers formed?

A

Firbin Degradation Product: Formed when cross-linked fibrin is proteolyzed by plasmin
Specific for active coagulation and fibrinolysis

187
Q

What is the T1/2 of d-dimers?

A

About 5 hours, thus only good for detecting acute changes

188
Q

What is the goal of anticoagulants in PTE?

A

Do NOT lyse the existing thrombus, instead inhibit propagation and prevent recurrent venous thrombosis

189
Q

Name other diseases in which elevation in d-dimers has been noted.

A
  1. Neoplasia
  2. Hepatic dz
  3. Renal failure
  4. Cardiac failure
  5. Internal hemorrhage
  6. DIC
  7. Following sx
190
Q

What is the primary mechanism of unfractionated heparin?

A

Composed of mucopolysaccharides of varying weights
Primary MOA is AT-III activity leading to inactivation of thrombin, Xa, IXa, XIa, XIIa (thrombin and Xa are most responsive)

191
Q

How is low molecular weight heparin monitored?

A

Anti-Xa assay (since little anti-Iia activity - PTT cannot be used to monitor)

192
Q

What are anti-platelet drugs?

A

Inhibit platelet aggregation = Preventing formation of primary platelet plug

193
Q

Why are anti-platelet used used for arterial thrombi?

A

Arterial thrombi have a large platelet component compared to venous thrombi

194
Q

Why are anti-platelet drugs recommended in PTE?

A

Even though these are venous thrombi (less platelets), in the early stages there is platelet acitvation that resutls in the release of mediators (release of serotonin, ADP, thromboxane A2) that can result in bronhconstriction, vasoconstriction, pulmonary hypertension

195
Q

What is the MOA of aspirin, describe the low dosing of this medication?

A

COX inhibitor, prevents formation of prostaglandins including thromboxane A2 (made by platelets, COX-1, induces platelet aggregation), and prostacyclin PGI2 (produced by endothelial cells, COX-1 and COX-2 derived, inhibits platelet aggregation) § Irreversible, rapid, saturable antiplatelet effects
§ 50x greater COX-1 than COX-2 effects – so need ultra low dose to only inhibit TXA2 and not PGI2

196
Q

What is the MOA of clopidogrel?

A

Inhibit ADP-induced platelet aggregation and so may work synergistically with aspirin (no effect on COX) = Irreversible!

197
Q

What is thrombolysis and name 2 examples?

A

Plasminogen activators that result in production of plasmin = Dissolution of fibrin thrombus
Streptokinase
Tissue plasminogen activator (t-PA)

198
Q

What is the MOA of warfarin?

A

Vitamin K-antagonist - Inhibits the activation of Vit K activated clotting factors

199
Q

What occurs during the first 24-48hrs of warfarin tx?

A

Only factor VII and protein C are significantly affected

Inactivation of Protein C = Prothrombic state!! Thus need to use heparin for first 2 days on warfarin

200
Q

What is monitored during warfarin tx?

A

PT and INR (INR betwn 2-3)

201
Q

Describe the pathogenesis of pulmonary arterial hypertension.

A

Vasoproliferative and vasoconstrictive disorder
Imblance btwn endothelium relaxinf factors (NO and porstacyclin) and endothelium constrictive factors (Endothelium-1, thromboxane, serotonin) = Increased vascular tone, endothelial smooth m proliferation, vascular remodeling, thrombosis

202
Q

What are the 5 categories of pulmonary hypertension?

A

Based on the human Evian Classification

  1. Pulmonary arterial hypertension (idiopathic, familial, condition associated with PH such as HW dz, shunts, drugs)
  2. Pulmonary hypertnesion with left heart disease (most common in vet med)
  3. Pulmonary hypertension associated with lung disease and/or hypoxemia (COPD, interstitial lung dz)
  4. Pulmonary hypertension caused by chronic thrombotic or embloic dz (HW dz, neoplasia)
  5. Other (Central pulmonary vein compression = lymphadenopathy, granulatmous dz, etc)
203
Q

What is the most common cause of pulmonary hypertension in vet med?

A

Pulmonary hypertension with left heart disease (left sided myocardial dz or left sided valvular dz)

204
Q

How can pulmonary hypertension be estimated with doppler echo?

A

If RV-RA systolic regurg (TR) can be quantified = Pulmonary arterial systolic pressure can be estimated
§ Use modified Bernoulli equation: 4 x V^2 = pressure (mmHg)
§ A TR jet of 2.8 M/sec or greater corresponds to an RV-RA gradient of 31 mmHg or greater (PA systolic hypertension)
§ Mild = 30-55 mmHg
§ Moderate = 6-79 mmHg
§ Severe = >80 mmHg

205
Q

What is the MOA of sildenafil?

A

• Phosphodiesterase-5 Inhibitors: Sildenafil (Viagra) inactivates cyclic AMP and GMP, second messengers of NO and prostacyclin, there is lots of PDE5 in the lung tissue versus other PDEs elsewhere in the body, so this is specific (mostly) for the lungs

206
Q

What is the A-a gradient?

A

(A-a) O2 gradient = (PIO2 - 1.25 PaCO2) - PaO2

(A-a) O2 gradient = (150-1.25 PaCO2)-PaO2

  • Values < 15 mmHg = NORMAL
  • If gradient widen = Hypoxemia resulting from V:Q mistmatch
  • If the gradient is normal = Excludes pulmonary dz and suggests some form of central alveolar hypoventilation or abnormality in chest wall or inspiratory mm
  • Values > 25 mmHg = ABNORMAL

Respiratory (4 decks)

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