Respiratory Flashcards

1
Q

Where are located the cough receptors?
And the receptors causing espiratory reflex?

A
  • Cough: pharynx, Larynx, Trachea, Bronchy (no bronchioles/alveoli)
  • Spiratory reflex: pharynx, larynx, trachea
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2
Q

When a cough is considered acute/chronis?

A
  • Acute <3w
  • chronic >8w
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3
Q

Which is the neurologic pathway of cough?

A

Receptors stimulation –> vague nerve (aferent) –> oblongata medula –> vague nerve, phrenic nerve, recurrent laryngeal nerve, spiromotor nerve (efferents) –> smooth bronchial mm, dyaphragm, respiratory mm (effector mm)

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4
Q

Which is the most common cause of cough in dogs? And cats?

A
  • Dogs: dinamic and static airway collapse
  • Cats: chronic lower airways inflammatory disease
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5
Q

Which type of antitussigens are there?

A
  • Central acting antitussigens: acting on the medullary cough center (butorphanol, codeine, hydrocodone, dextrometorphane)
  • Peripheric acting antitussigens: relax smooth bronchial mm (beta agonist, methylxantines)
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6
Q

Which are the respiratory patterns?

A
  • Obstructive:
    —- Inspiratory: nose, pharynx, larynx and cervical trachea
    —- Espiratory: thoracic trachea, bronchi, bronchioles
    —- Mixt: fixed airway obstruction, pulmonary parenchyma
  • Restrictive: pulmonary parenchyma, pleural
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7
Q

Which are the different values of PaO2 and SaO2?

A
  • Normal:
    —- PaO2 > 95mmHg
    —- SaO2 > 97%
  • Mild hypoxemia:
    —- PaO2 = 80 mmHg
    —- SaO2 = 95%
  • Severe hypoxemia:
    —- PaO2 < 60mmHg
    —- SaO” < 90%
  • Cyanosis:
    —- PaO2 = 45mmHg
    —- SaO2 = 75%
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8
Q

Which are the causes of metahemoglobinemia?

A

MetaHb = oxidized Hb –> non capacity to transport oxygen.

  • Acquired: acetaminophen, methylene blue, nitrats, nitrits, benzocaine, phenazopyridine
  • Congenital: metaHb reductasa defycit
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9
Q

In which causes of hypoxemia the treatment with oxygent don’t proportion any benefit?

A
  • R to L shunt
  • Altered Hb transport capacity
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10
Q

Which medications can be nebulizated?

A
  • Antibiotics (aminoglycosides)
  • Lidocaine: antiinflammatory and bronchodilator effects, beneficial for feline asthma
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11
Q

Which type of beta agonist can be administered by inhalation?

A
  • Salbutamol (albuterol): used in acute crises, but in chronic administration can produce an inflammatory reaction
  • Levalbuterol: alternative to albuterol if it is used in a chronic way
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12
Q

Which is the formula of DO2?

A

DO2 = CO x CaO2

CaO2 = (1,34 x [Hb] x SaO2) + (PaO2 x 0,003)

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13
Q

Which are the different ways to apport oxygen?

A
  • Oxygen cage
  • Flow by oxygen: FiO2 25-40%
  • Oxygen mask / Elyzabeth Collar: 60%
  • Nasal prongs
  • Nasal catheters: in function of the oxygen flow and unilateral/bilateral (uni: 40-60%, bilateral: 40-80%)
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14
Q

Which are the complications of oxygen therapy?

A

Lipic peroxidation, increase permeability, inflammation

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15
Q

Which are the main causes of nasal disease in cats?

A
  • Rhinitis (50%)
  • Neoplasia (30%): lymphoma > carcinoma
  • Polyp (20%)
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16
Q

Which are the paranasal sinuses?

A
  • Frontal sinus
  • Esphenoidal sinus
  • Maxillary sinus
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17
Q

Which is the innervation of larynx?

A

All muscles are innervated by caudal laryngeal nerve (branch of recurrent laryngeal), except crycothryoid muscle by cranial laryngeal nerve.

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18
Q

Which are the laryngeal collapse grades?

A

Grade I: laryngeal saccules eversion
Grade II: collapse of cuneiform process of arythenoid
Grade III: collapse of corniculate process of arythenoid

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19
Q

In which proportion of dogs with laryngeal paralysis there is a hypoT4 concurrent?

A

30% (but the relatiosnhip is not clear)

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20
Q

Which are the causes of laryngeal paralysis?

A
  • Cogenital: Bouvier des Flandes (autosomal dominant), Siberian Huskies, Bull Terriers, White GSD
  • Acquired:
    —- Trauma to the laryngeal nerve
    —- Compression of the laryngeal nerve
    —- Neuromm disease
    ——– Geriatric onset laryngeal paralysis polyneuropathy (idiopathic)
    ——– Laryngeal paralysis - polyneuropathy complex (genetic: Leonberger, Dalmata, Rottweiler)
    ——– Endocrinopathy: hypoT4 and Addison
    ——– Infectious
    ——– Immunemediated
    ——– MG
    ——– Toxins (lead, organophosphates)
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21
Q

Which are false positive and negatives in the laringoscopy for a laryngeal paralysis?

A
  • false positive: due to the sedation efefct
  • false negative: paradoxial arythenoid movement: close - inspiration, open - espiration –> election anesthetic: doxapram
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22
Q

Which is the prevalence of aspiration pneumonia in surgical management of laryngeal paralysis?

A

10-20%

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23
Q

Which are the indications for nuclear imaging in respiratory diseases?

A
  • Administered IV to evaluate lung perfusion.
  • Administered via nebulization to assess ventilation.
  • Intratracheal or intranasal deposition to assess mucociliary transprt
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24
Q

Which is the BALf culture UFC cuttoff to consider ab treatment?

A

Previously was considered >1700UFC, but it has been seen that it is not possible to establish a cuttoff to decide when to treat with ab –> depends of every case.

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25
Q

What is better to perform, a transtracheal wash or a endotracheal?

A
  • Equivalent results (maybe endotracheal more hypocellular)
  • No difference in oropharyngeal contamination
  • If the cytology is positive, it has a high probability to find a positive culture, but if the cytology is negative, the culture can be both negative or positive (but low positive)
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26
Q

What is the relevance of BALf lymphocytosis?

A

Frequent (20%)
It is indicative of a lung injury, independent of the duration of the process. Specially associated to airway collapse.

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27
Q

Which is the etiology of tracheal collapse?

A
  1. Degeneration of tracheal rings (reduction of GAG and condroitin sulfate)
  2. Predisposing factor (obesity, cardiac disease…)
  3. Vicious cycle due to the inflammation produced
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28
Q

Which grades of tracheal collapse can be distinguished?

A
  • Grade 1: 25% collapse
  • Grade 2: 50% collapse
  • Grade 3: 75% collapse
  • Grade 4: >90% collapse

In function of the clinical signs, can be divided into:
- Those causing only cough
- Those causing collapse
- Those causing cough + collapse
- Malformation

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29
Q

Which parasites can be found in the trachea?

A
  • Dogs: Oslerus osleri, Filaroides
  • Cat: Cuterebra (fly larva)
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30
Q

Which are the main complications of tracheal stents?

A

In ~50%

  • Stent rupture
  • Fibrous tissue proliferation
  • Re-collapse

**in general, the stents don’t produce an icnrease in the bacterial count

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31
Q

How is the BALF cytology of chronic bronchitis?

A

Excess mucus, hyperplasia on epithelial cells, and increased numbers of neutrophils, goblet cells and macrophagues

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32
Q

Which percentage of dogs with eosinophilic broncopneumopathy present with peripheric eosynophilia?

A

60%

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33
Q

How is the BALF cytology of eosinophilic broncopneumopathy?

A

> 50% eosinophils

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34
Q

Which is the gold standard for the diagnosis of bronchiectasia?

A

CT

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35
Q

Which types of bronchomalacia can be distinguished?

A
  • Static: brachycephalyc
  • Dinamic:
    —- Associated with tracheal collapse
    —- As an isolated sign
36
Q

Which prevalence of cats with felina asthma have peripheral eosinophylia?

A

20% (not correlated to the severity of the disease)

37
Q

Which are the characteristics of BALF in feline asthma and chronic bronchitis?

A
  • Asthma: >20% eos and neutros on range, or >50% eos
  • Bronchitis: >7% neutros and eos on range or >50% neutros
  • Mixed
38
Q

Which are the new treatments of feline asthma/bronchitis?

A
  • Allergen specific immunotherapy
  • Omega 3 fatty acids
  • Inhaled lidocaine
  • Tirosine kinase inhibitor (inhibit mastocites activation)
  • Stem cells

No effective: leukotriene antagonists, serotonine antagonists, antihistamine, NAC, doxycycline, NK1 antagonist

39
Q

Which is the interpretation of ratio A-a?

A

A-a = 150 - (PaCO2 + PaO2)

Normal < 10
Suggestive of VQ mismatch >20

40
Q

Which are the most common Influenzavirus species detected in dogs and cats?

A
  • Dogs: H3N2 (avian) and H3N8 (equine)
  • Cats: H5N1 (avian)
41
Q

How is CPR in a pulmonary disorder?

A

It is high in infectious pneumonia (both aspiration pneumonia and infectious broncopneumonia) –> a high CPR can distinguish among a infectious respiratory disorder and non infectious.
But in Bordetella, CPR is on range or mildly increased –> it cannot help in the diagnosis process.

In cases of infectious pneumonia, CRP resolution and clinical signs normalization is a better marker of antibiotic discontinuation than resolution of Rx (normalization CRP 7d, normalization of Rx 15d).

42
Q

Which are the conditions predisposing to aspiration pneumonia?

A
  • Impaired airway protection (anesthesia, seizures, coma, laryngeal paralysis, MG…)
  • Impaired swallowing
  • Regurgitation
  • Vomits
  • Gastric overdistension
  • Forced feeding
43
Q

Which are the diseases that more common produce aerodigestive disorders?

A
  • Pharyngeal
  • Esophagic
44
Q

What is cytidine diphosphocoline?

A

It is an essential precursor for phospholypids synthesis, and its absence produce a dysfunction in type II alveolar cells.
One study demostrates that its use in ARDS secondary to aspiration pneumonia improves hypoxemia and is well tolerated.

45
Q

Which are the hypothetized mechanism of neurogenic edema?

A

Intense pulmoanry vasoconstriction (–> increase hydrostatic pressure) + inflammatory mechanism (–> increase permeability)

46
Q

Which are the most common causes of non cardiogenic edema?

A
  • Neurogenic: asphyxia, seizures, TCE
  • Post obstruction
  • Secomdary to inflammatory systemic diseases
  • Direct pulmonary injury
  • Hypoalbuminemia
  • Impaired lymphatic drainage
47
Q

What is ARDS?

A

Acute respiratory distress syndrome.
Acute pulmonary inflammation and edema secondary to a variety of initial insults –> defined by:
- <1w of the inciting event
- Rx compatible with edema
- Non cardiogenic

48
Q

Which are the characteristics of pulmonary lymphomatoid granulomatosis?

A

It has atypical lymphoid cells infiltrating around and destroying blood vessels. Most are T cells and sometimes B cells.

49
Q

Which is the prevalence of methastases of pulmonary primary tumors at the time of diagnosis?

A

25%

50
Q

Which are the prognostic factors of primary lung tumors?

A
  • Smaller, better prognosis
  • CD204 positive (marker of macrophagues with a immunosupressor paper –> tumor progression), worse prognosis
  • Complete surgical, no mtehastases, no LN affection, no clinical signs, low histologic grade and absence of pleural effusion, better prognosis
51
Q

How can eosinophilic pneumonias be divided?

A
  • Primary:
    —- Isolated eosinophilic pneumonia
    —- Multisystemic disease (hypereosynophilic syndrome)
  • Secondary: parasites, allergy, drugs, etc
52
Q

Which are the causes of lipid pneumonia?

A

Inflammatory reaction against lipids in the alveoli:
- Exogenous: aspiration of lipidic content
- Endogenous: when there is a lung obstructive disease, pneumocytes injury leads to cellular degeneration with release of cholesterol and over production of cholesterol rich surfactant. Lipids are then phagocitized by pulmonary macrophagues and accumulate in alveoli.

53
Q

Whcih biomarkers are potentially useful for lung fibrosis?

A

Increased serum MMP7 and BALF MMP2 and MMP9 (MMP modulate the fibroblast remodelation)

54
Q

Which is the mechanism of action of drowning?

A
  • Water content in alveoli –> VQ mismatch
  • Dilution of surfactant –> alveoli collapse –> VQ mismatch
  • Development of ARDS
55
Q

Which is the action mechanism of smoke inalation?

A
  • Smoke –> airway irritation –> reflex broncoconstriction (–> brocnhodilators can help in the management)
  • Smoke –> pneumocyte damage –> surfactant inactivation –> collapse
  • Cells damage –> ARDS
  • Exfoliation of death cells –> obstruction
  • CO intoxication –> carboxihemoglobin
56
Q

Which is the difference between bulale and blebs?

A
  • Bullae: air pockets within the lung parenchyma
  • Blebs: accumulation of air formed when air escpaed from the lung becomes trapped inside the visceral pleura
57
Q

Which are the most frequently lung lobes affected by lung torsion?

A
  • Middle right
  • Cranial left
58
Q

Which are the main characteristics of lobe lung torsion in cats?

A
  • Very uncommon
  • 2ary (to pleural effusions) > 1ary
  • Main signs dyspnea due to pleural effusion
  • More affected lobes: right cranial = left cranial (40%) > middle right
  • Worse prognosis than dogs
59
Q

Which are the causes of non-recruitable lung associated with pleural effusion?

A
  • Lung entrapment: fibrin avoiding lung expansion
  • Trapped lung: thickening of the visceral pleura
60
Q

Which are the causes of iatrogenic pneumothorax secondary to thoracocentesis for pleural effusion?

A
  • Damage to thickened/fibrotic visceral pleura and lung parenchyma
  • Marked drops in intrapleural pressure which result in the formation of spontaneous tears on the parenchyma
61
Q

What are Light’s criteria?

A

In cats, criterias to evaluate exudate:
- Effusion protein / serum protein > 0.5
- High LDH
Indicative of exudate

62
Q

Which are the most common causes of pleural effusion in cats?

A
  • Cardiogenic (35%)
  • Neoplasia (30%)
  • Pyothorax (9%)
  • FIP (8%)
  • Chylothorax (5%)
  • Miscellaneous (4%)
63
Q

Which is the prevalence of idiopathic chylothorax?

A

50%

64
Q

Which is the response to surgical therapy in chylothorax?

A

50-70% (dogs > cats)

65
Q

Which are the most caracteristics of pyothorax in dogs and cats?

A
  • Cats:
    —- More common cause: bite
    —- More cellularity, more macrophags with intracellular bacteria, more bacterial richness than dogs
    —- Anaerobic bacteria more common than in dogs
    —- Most common bacteria: Actinomyces / Pasteurella
    —- More common medial treatment
    —- More mortality than dogs
  • Dogs:
    —- Most common cause: penetrating FB
    —- Most common bacteria: Actinomyces, E Coli
    —- More common surgical treatment
    —- Better prognosis than cats
66
Q

Which are the causes of pneumothorax?

A
  • Spontaneous: dogs > cats
    —- Primary
    —- Secondary: pneumonia, neoplasia, asthma, bronchitis…
  • Traumatic: most common cause
    —- Open
    —- Close
67
Q

Which are the mediastinal lymph nodes?

A
  • Cranial mediastinal LN: trachea, esophagus, heart, pericardium, pleura, muscles of the neck, thorax and abdomen, scapula, last six cervical vertebrae, thoracic vertebrae, ribs, thyroid, timus and mediastinum
  • Tracheobronchial/hilar: lung and bronchi
  • Sternal: abdomen, diaphragm, ventral thoracic and abdominal walls
68
Q

What is the Macklin effect?

A

When there is a lung trauma or overdistension and rupture of alveoli, it can result in free alveolar air dissecting along the pulmonary interstitium and bronchovascular sheath, into the mediastinal space

69
Q

Which is the relationship between pneumomediastinum and pneumothorax?

A

Pneumomediastinum does not occur secondary to pneumothorax, but a severe pneumomediastinum has the potential to cause a secondary pneumothorax

70
Q

Which are the general causes of pulmonary hypertension?

A

P = F x R
- F: RV cardiac output
- R: mediated by vasodilation/vasoconstriction and platelet activation/inhibition:
—- Hypoxia: vasoconstriction
—- Endothelin: vasoconstrictor
—- Thromboxane: vasoconstrictor + platelet activator
—- Prostaciclines: vasodilation + platelet inhibition
—- Serotonine: vasoconstriction + platelet activator
—- NO: vasodilation + platelet inhibition

71
Q

Which PDE5 inhibitors can we find?

A

Sildenafil (short acting), tadalafil and vardenafil (long acting).
PDE5 inihibitors –> increase the amount of NO –> vasodilation.
Also reduce cardiac remodeling, apoptosis, fibrosis, ventricular hypertrophy, and improve left heart function.

72
Q

How can pulmonary hypertension be calculated from echocardio?

A

Using peak regurgitant flow velocity of tricuspid regurgitation or pulmonic insufficiency.
The regurgitant velocity allows estimation of pulmonary artery pressures by using the Bernouilli equation (pressure gradient = 4x(peak velocity)^4)
- TR velocity >2.8m/s (peak >30mmHg)
- Pulmonary insufficiency >2.2m/s (peak >20mmHg)
suggests pulmonary hypertension

73
Q

Which is the most common cause of pulmonary hypertension in dogs?

A

Secondary to left cardiac disease

74
Q

Which are the most common microbiota on respiratory tract?

A

There is a low biomass but high richness.
Most are Proteobacteria. Also can be found Bacteroidetes and Firmicutes

DOGS:
- Nasal: Moraxellaceae, Psychrobacter
- Oropharyngeal: Pasteurellaceae
- Lung: Pasteurellaceae, Pseudomonaceae

CATS:
- Nasal: Moraxellaceae
- Oropharyngeal: Pasteurellaceae
- Lung: Pseudomonaceae

75
Q

Which type of bronchiolar diseases can be found?

A
  • Primary: damage limited to the bronchioles
    —- Constrictive/obliterans bronchiolitis
    —- Mineral dust airway disease
    —- Infectious
    —- Other
  • Secondary: extension from large airways/interstitial space to bronchioles
    —- Airways: asthma, bronchitis….
    —- Interstitial:
    ——– Obliterans bronchiolitis with organizing pneumonia (cryptogenic organizing pneumonia)
    ——– Bronchiolocentric interstitial pneumonia (airway centered interstitial fibrosis)
76
Q

Which drugs can induce a pulmonary fibrosis?

A
  • Oleic acid
  • Chemotherapeutics: bleomycin, gemcitabine, , cysplatine, cytarabine, paraquat, rabafocsadine
77
Q

How can interstitial lung diseases be divided?

A
  • Primary/idiopathic
  • Secondary/known casues
  • Specific entities
78
Q

Which are the causes of pulmonary hypertension following the Consensus statement?

A
  • Type I: pulmonary arterial hypertension (due to high flow or high artherial resistance)
  • Type I’: associated with pulmonary veno-occlusive diseases or pulmonary capillary hemangiomatosis
  • Type II: associated to left heart disease
  • Type III: associated to hypoxic diseases
  • Type IV: associated with thromboembolic diseases
  • Type V: parasitic diseases (A vasorum, Dirofilaria)
  • Type VI: >1 causes, miscellaneus (myeloproliferative diseases, granulomatous diseases, IMHA, obstruction…)
79
Q

Which is the treatment of choice of cryptogenic organizing pneumonia?

A

Immunosupression

80
Q

In which causes of pulmonary hypertension there is a potential risk of lung edema secondary to the PDE5i treatment?

A
  • Veno-occlusive diseases
    Because higher blood flows don’t accomodate in the fixed capillaries.
  • Left to right cardiac shunts
  • Left heart disease
    When a pulmonary artery vasodilator is administered, the RV cardiac output increase, and the blood flow arriving to LA is higher –> LA enlargement –> increase venous pressure –> pulmonary edema
81
Q

How to treat pulmonary hypertension secondary to left heart failure?

A

If the CHF is decompensated with pulmonary edema, first CHF must be controlled. PDE5i cannot be administered in a patient with pulmonary edema.
If once controlled pulmonary edema, persist signs of pulmonary hypertension, then PDE5i can be administered.
If right CHF signs appeared, then CHF drugs + PDE5i should be started.

82
Q

Which alternatives therapies exist for pulmonary hypertension?

A
  • Pimobenda: PDE3i –> inotropic + vasodilator <– it tends to be used as a general drug for pulmonary hypertension in all types. There is evidence about its efficacy in postcapillary pulmonary hypertension due to left cardiac disease, but there are no evidence in precapillary pulmonary hypertension. However, there are no contraindication to its use.
  • Milrinone: IV PDE3i
  • TK inhibitors: inhibit platelet derived GF –< vasodilation
  • L-arginine: aa essencial, in conjunction with oxigen, to NO synthesis –> vasodilation
83
Q

Which is the best way to monitor pulmonary hypertension?

A

With improve/resolution of clinical signs +/- other tests (arterial gas, NT-proBNP, XR).
Control echocardiography can be performed but proportion less information.

84
Q

Which are the most differences in pulmonary hypertension between dogs and cats?

A

Whereas in dogs the main cause is a left cardiac disease, it is less common in cats, as well as heart worm disease due to adult worms is also less common in cats.

85
Q
A